Cephalopods as hosts

AGENTSTYPE OF AGENTPLACE OF CAPTURE OF THE ANIMAL(HOST) MARINE ANIMALSParagraphMALADYAFFECTED TISSUEAPPEARANCE/EFFECTSURVIVAL (MORTALITY)TREATMENTSTABLES AND FIGURESLITERATURE CITEDnotes
BacteriaVibrio spno information availableLoligo forbesilaboratory cultured squidsdamage from hitting tank walls and bacterial invasionsfin and mantle, abcesses or infections of one or both eyes in a small number of squidsdamage, necrotic tissue30 to 50 % of mortalitiesno information availableno information availableHanlon et al., (1986) Exposure to 0.2 mg/I nifurpirinol (active ingredient) was 100 % lethal within 24 h to L. forbesi suffering severe tail infections.
BacteriaPseudomonas spno information availableLoligo forbesilaboratory cultured squidsdamage from hitting tank walls and bacterial invasionsfin and mantle, abcesses or infections of one or both eyes in a small number of squidsdamage, necrotic tissue30 to 50 % of mortalitiesno information availableno information availableHanlon et al., (1986) Exposure to 0.2 mg/I nifurpirinol (active ingredient) was 100 % lethal within 24 h to L. forbesi suffering severe tail infections.
BacteriaMicrococcus sp.Micrococcus sp.Micrococcus sp.Micrococcus sp.Micrococcus sp.Micrococcus sp.Micrococcus sp.Micrococcus sp.no information availableLoligo forbesilaboratory cultured squidsmechanical abrasion of the external surface of the cornea with subsequent bacterial infectionvitreous humor, posterior lens surface and hemolymphone eye swollen much larger than the other; the cornea of the swollen eye remained clear while the lens was white and nearly opaque; in some cases prior to death, a large allowing direct contact of the sea water with the lens.no information availableno information available Fig. 1-8: Loligo forbesi. A: Normal eye of lab-cultured individual. B: Other eye of same individual,
swollen with opaque lens.C: Ventral view of individual above showing normal versus swollen eye.
D: Individual with hole through cornea. Fig. 1-8: Loligo forbesi. A: Normal eye of lab-cultured individual. B: Other eye of same individual,
swollen with opaque lens.C: Ventral view of individual above showing normal versus swollen eye.
D: Individual with hole through cornea. Fig. 1-8: Loligo forbesi. A: Normal eye of lab-cultured individual. B: Other eye of same individual,
swollen with opaque lens.C: Ventral view of individual above showing normal versus swollen eye.
D: Individual with hole through cornea. Fig. 1-8: Loligo forbesi. A: Normal eye of lab-cultured individual. B: Other eye of same individual,
swollen with opaque lens.C: Ventral view of individual above showing normal versus swollen eye.
D: Individual with hole through cornea. Fig. 1-8: Loligo forbesi. A: Normal eye of lab-cultured individual. B: Other eye of same individual,
swollen with opaque lens.C: Ventral view of individual above showing normal versus swollen eye.
D: Individual with hole through cornea. Fig. 1-8: Loligo forbesi. A: Normal eye of lab-cultured individual. B: Other eye of same individual,
swollen with opaque lens.C: Ventral view of individual above showing normal versus swollen eye.
D: Individual with hole through cornea. Fig. 1-8: Loligo forbesi. A: Normal eye of lab-cultured individual. B: Other eye of same individual,
swollen with opaque lens.C: Ventral view of individual above showing normal versus swollen eye.
D: Individual with hole through cornea. Fig. 1-8: Loligo forbesi. A: Normal eye of lab-cultured individual. B: Other eye of same individual,
swollen with opaque lens.C: Ventral view of individual above showing normal versus swollen eye.
D: Individual with hole through cornea.
Hanlon et al., (1989)Typically there was only unilateral involvement, and the affected
eye swelled to a larger sizeTypically there was only unilateral involvement, and the affected
eye swelled to a larger sizeTypically there was only unilateral involvement, and the affected
eye swelled to a larger sizeTypically there was only unilateral involvement, and the affected
eye swelled to a larger sizeTypically there was only unilateral involvement, and the affected
eye swelled to a larger sizeTypically there was only unilateral involvement, and the affected
eye swelled to a larger sizeTypically there was only unilateral involvement, and the affected
eye swelled to a larger sizeTypically there was only unilateral involvement, and the affected
eye swelled to a larger size
BacteriaGram-negativeno information availableLoligo pealeiwild-caught squids maintained in the laboratorySkin lesions; Gram-negative rods in the tissuefinskin lesionsdeathno information availableHulet et al.(1979); Hanlon et al.,(1983)
BacteriaGram-negativeno information availableLoligo plei
Loligo plei
Loligo plei
Loligo plei
Loligo plei
Loligo plei
Loligo plei
Loligo plei
wild-caught squids maintained in the laboratorySkin lesions; Gram-negative rods in the tissuefinskin lesionsdeathno information availableHulet et al.(1979); Hanlon et al.,(1983)
BacteriaGram-negativeno information availableLolliguncula brevis
Lolliguncula brevis
Lolliguncula brevis
Lolliguncula brevis
Lolliguncula brevis
Lolliguncula brevis
Lolliguncula brevis
Lolliguncula brevis
wild-caught squids maintained in the laboratorySkin lesions; Gram-negative rods in the tissuefinskin lesionsdeathno information availableHulet et al.(1979); Hanlon et al.,(1983)
BacteriaGram-negativeno information availableOmmastrephes pteropuswild-caught squids maintained in the laboratorySkin lesions; Gram-negative rods in the tissuefinskin lesionsdeathno information availableFig. 1-6, D Ommastrephes pteropus. D: Section through dorsal surface of abraded fin on an adult squid fixed 72 h after capture; epidermis is completely absent and arrows indicate exposed surface of the underlying dermis; bacteria (B) are multiplying in the dermis and in adjacent muscle tissue (M).Hulet et al.(1979); Hanlon et al.,(1983)
BacteriaGram-negativeno information availableLoligo opalescenswild-caught squids maintained in the laboratorySkin lesions; Gram-negative rods in the tissuefinskin lesionsdeathno information availableHulet et al.(1979); Hanlon et al.,(1983)Loligo opalescens hatchings cultured from eggs in the laboratory
BacteriaMyxobacteria spp.no information availableLoligo pealeiwild-caught squids maintained in the laboratorybacterial invasionsfin and ventral mantleprogressive necrotic exfoliative dermatitis;
skin lesions and no other marked changes in internal organs;
the third stage of the lesions: total absence of all skin layersprogressive necrotic exfoliative dermatitis;
skin lesions and no other marked changes in internal organs;
the third stage of the lesions: total absence of all skin layersprogressive necrotic exfoliative dermatitis;
skin lesions and no other marked changes in internal organs;
the third stage of the lesions: total absence of all skin layersprogressive necrotic exfoliative dermatitis;
skin lesions and no other marked changes in internal organs;
the third stage of the lesions: total absence of all skin layersprogressive necrotic exfoliative dermatitis;
skin lesions and no other marked changes in internal organs;
the third stage of the lesions: total absence of all skin layersprogressive necrotic exfoliative dermatitis;
skin lesions and no other marked changes in internal organs;
the third stage of the lesions: total absence of all skin layersprogressive necrotic exfoliative dermatitis;
skin lesions and no other marked changes in internal organs;
the third stage of the lesions: total absence of all skin layersprogressive necrotic exfoliative dermatitis;
skin lesions and no other marked changes in internal organs;
the third stage of the lesions: total absence of all skin layers
deathno information availableFig.1-6 B Fairly severe fin damage incurred
initially from transport: C: Same individual in Image B showing amount of damage on posterior fin
and ventral mantle that resulted from hilling transport-tank walls (after Hanlon et al.,1983.).Fig.1-6 B Fairly severe fin damage incurred
initially from transport: C: Same individual in Image B showing amount of damage on posterior fin
and ventral mantle that resulted from hilling transport-tank walls (after Hanlon et al.,1983.).Fig.1-6 B Fairly severe fin damage incurred
initially from transport: C: Same individual in Image B showing amount of damage on posterior fin
and ventral mantle that resulted from hilling transport-tank walls (after Hanlon et al.,1983.).Fig.1-6 B Fairly severe fin damage incurred
initially from transport: C: Same individual in Image B showing amount of damage on posterior fin
and ventral mantle that resulted from hilling transport-tank walls (after Hanlon et al.,1983.).Fig.1-6 B Fairly severe fin damage incurred
initially from transport: C: Same individual in Image B showing amount of damage on posterior fin
and ventral mantle that resulted from hilling transport-tank walls (after Hanlon et al.,1983.).Fig.1-6 B Fairly severe fin damage incurred
initially from transport: C: Same individual in Image B showing amount of damage on posterior fin
and ventral mantle that resulted from hilling transport-tank walls (after Hanlon et al.,1983.).Fig.1-6 B Fairly severe fin damage incurred
initially from transport: C: Same individual in Image B showing amount of damage on posterior fin
and ventral mantle that resulted from hilling transport-tank walls (after Hanlon et al.,1983.).Fig.1-6 B Fairly severe fin damage incurred
initially from transport: C: Same individual in Image B showing amount of damage on posterior fin
and ventral mantle that resulted from hilling transport-tank walls (after Hanlon et al.,1983.).
Leibovitz et al., (1977)The first stage was an acute necrotizing dermatitis characterized by epithelial necrosis and desquamation. Amoebocyte infiltration of inner and outer connective tissue layers was prominent in some areas and accompanied by edema and stretching of the surface epithelium. The second stage was a chronic necrotizing ulcerative dermatitis with deeper exfoliation of skin layers resulting in total loss of the dermis containing the iridophore and chromatophore structures. At the base of ulcers, collagen infiltrated with densely packed chains of uniform long bacterial rods was frequently encountered. The third stage of the lesions was a necrotizing bacterial myositis in the total absence of all skin layers. Chains of bacteria were found infiltrating deep into muscle tissue, particularly along the transverse septa of muscle bundles.
BacteriaAeromonas spGalveston Bay, TX, USALolliguncula brevissquid in naturebacteria cellsskin of the dorsal mantle surfaceappeared to be in perfect conditionno information availableno information availableFig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28
Ford et al., (1986)
BacteriaPseudomonas spGalveston Bay, TX, USALolliguncula brevissquid in naturebacteria cellsskin of the dorsal mantle surfaceappeared to be in perfect conditionno information availableno information availableFig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28
Ford et al., (1986)
BacteriaFlavobacterium spGalveston Bay, TX, USALolliguncula brevissquid in naturebacteria cellsskin of the dorsal mantle surfaceappeared to be in perfect conditionno information availableno information availableFig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28
Ford et al., (1986)
BacteriaVibrio spGalveston Bay, TX, USALolliguncula brevissquid in naturebacteria cellsskin of the dorsal mantle surfaceappeared to be in perfect conditionno information availableno information availableFig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28
Ford et al., (1986)
BacteriaProteus spGalveston Bay, TX, USALolliguncula brevissquid in naturebacteria cellsskin of the dorsal mantle surfaceappeared to be in perfect conditionno information availableno information availableFig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28
Ford et al., (1986)
BacteriaVibrio parahaemolyticusGalveston Bay, TX, USALolliguncula brevissquid in naturebacteria cellsskin of the dorsal mantle surfaceappeared to be in perfect conditionno information availableno information availableFig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28
Ford et al., (1986)
BacteriaVibrio alginolyctusGalveston Bay, TX, USALolliguncula brevissquid in naturebacteria cellsskin of the dorsal mantle surfaceappeared to be in perfect conditionno information availableno information availableFig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28
Ford et al., (1986)
BacteriaFlexibacter spFlexibacter spFlexibacter spFlexibacter spFlexibacter spFlexibacter spFlexibacter spGalveston Bay, TX, USALolliguncula brevissquid in naturebacteria cellsskin of the dorsal mantle surfaceappeared to be in perfect conditionno information availableno information availableFig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28
Ford et al., (1986)
BacteriaBacillus sp Bacillus sp Bacillus sp Bacillus sp Bacillus sp Bacillus sp Bacillus spGalveston Bay, TX, USALolliguncula brevissquid in naturebacteria cellsskin of the dorsal mantle surfaceappeared to be in perfect conditionno information availableno information availableFig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28
Ford et al., (1986)
BacteriaStreptococcus spGalveston Bay, TX, USALolliguncula brevissquid in naturebacteria cellsskin of the dorsal mantle surfaceappeared to be in perfect conditionno information availableno information availableFig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28
Ford et al., (1986)
BacteriaMicrococus spGalveston Bay, TX, USALolliguncula brevissquid in naturebacteria cellsskin of the dorsal mantle surfaceappeared to be in perfect conditionno information availableno information availableFig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28
Ford et al., (1986)
BacteriaPlanococcus spGalveston Bay, TX, USALolliguncula brevissquid in naturebacteria cellsskin of the dorsal mantle surfaceappeared to be in perfect conditionno information availableno information availableFig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28
Ford et al., (1986)
BacteriaStaphylococcus spGalveston Bay, TX, USALolliguncula brevissquid in naturebacteria cellsskin of the dorsal mantle surfaceappeared to be in perfect conditionno information availableno information availableFig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28Fig 1-7 A
Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: Table1-2: bacteria isolated from squid skin and sea water pg.28
Ford et al., (1986)
BacteriaAeromonas spAeromonas spAeromonas spAeromonas spAeromonas spAeromonas spAeromonas spGalveston Bay, TX, USALolliguncula brevislaboratory-maintained squidbacteria cellsnormal skin of the dorsal mantle surfaceappeared to be in perfect conditionno information availableno information availableTable1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water
Ford et al., (1986)
BacteriaFlavobacterium spGalveston Bay, TX, USALolliguncula brevislaboratory-maintained squidbacteria cellsnormal skin of the dorsal mantle surfaceappeared to be in perfect conditionno information availableno information availableTable1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water
Ford et al., (1986)
BacteriaVibrio spGalveston Bay, TX, USALolliguncula brevislaboratory-maintained squidbacteria cellsnormal skin of the dorsal mantle surfaceappeared to be in perfect conditionno information availableno information availableTable1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water
Ford et al., (1986)
BacteriaProteus spGalveston Bay, TX, USALolliguncula brevislaboratory-maintained squidbacteria cellsnormal skin of the dorsal mantle surfaceappeared to be in perfect conditionno information availableno information availableTable1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water
Ford et al., (1986)
BacteriaVibrio parahaemolyticusGalveston Bay, TX, USALolliguncula brevislaboratory-maintained squidbacteria cellsnormal skin of the dorsal mantle surfaceappeared to be in perfect conditionno information availableno information availableTable1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water
Ford et al., (1986)
BacteriaVibrio alginolyctusGalveston Bay, TX, USALolliguncula brevislaboratory-maintained squidbacteria cellsnormal skin of the dorsal mantle surfaceappeared to be in perfect conditionno information availableno information availableTable1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water
Ford et al., (1986)
BacteriaVibrio metschnikoviiVibrio metschnikoviiVibrio metschnikoviiVibrio metschnikoviiVibrio metschnikoviiVibrio metschnikoviiVibrio metschnikoviiGalveston Bay, TX, USALolliguncula brevislaboratory-maintained squidbacteria cellsnormal skin of the dorsal mantle surfaceappeared to be in perfect conditionno information availableno information availableTable1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water
Ford et al., (1986)
BacteriaBacillus spBacillus spBacillus spBacillus spBacillus spBacillus spBacillus spGalveston Bay, TX, USALolliguncula brevislaboratory-maintained squidbacteria cellsnormal skin of the dorsal mantle surfaceappeared to be in perfect conditionno information availableno information availableTable1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water
Ford et al., (1986)
BacteriaStreptococcus spGalveston Bay, TX, USALolliguncula brevislaboratory-maintained squidbacteria cellsnormal skin of the dorsal mantle surfaceappeared to be in perfect conditionno information availableno information availableTable1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin and sea water
Ford et al., (1986)
BacteriaAeromonas spGalveston Bay, TX, USALolliguncula brevislaboratory-maintained squiddamage subsequent to injury (skin ulcers opportunistically invaded by bacteria)mantle and muscleskin ulcersno information availableno information availableTable1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).
Ford et al., (1986)
BacteriaPseudomonas spGalveston Bay, TX, USALolliguncula brevislaboratory-maintained squiddamage subsequent to injury (skin ulcers opportunistically invaded by bacteria)mantle and muscleskin ulcersno information availableno information availableTable1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).
Ford et al., (1986)
BacteriaVibrio spGalveston Bay, TX, USALolliguncula brevislaboratory-maintained squiddamage subsequent to injury (skin ulcers opportunistically invaded by bacteria)mantle and muscleskin ulcersno information availableno information availableTable1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).
Ford et al., (1986)
BacteriaVibrio alginolyctusGalveston Bay, TX, USALolliguncula brevislaboratory-maintained squiddamage subsequent to injury (skin ulcers opportunistically invaded by bacteria)mantle and muscleskin ulcersno information availableno information availableTable1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).
Ford et al., (1986)
BacteriaVibrio metschnikoviiGalveston Bay, TX, USALolliguncula brevislaboratory-maintained squiddamage subsequent to injury (skin ulcers opportunistically invaded by bacteria)mantle and muscleskin ulcersno information availableno information availableTable1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).
Ford et al., (1986)
BacteriaBacillus spGalveston Bay, TX, USALolliguncula brevislaboratory-maintained squiddamage subsequent to injury (skin ulcers opportunistically invaded by bacteria)mantle and muscleskin ulcersno information availableno information availableTable1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).
Ford et al., (1986)
BacteriaStreptococcus spGalveston Bay, TX, USALolliguncula brevislaboratory-maintained squiddamage subsequent to injury (skin ulcers opportunistically invaded by bacteria)mantle and muscleskin ulcersno information availableno information availableTable1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).Table1-1: total viable bacteria from Loliguncula brevismantle tissue and from sea-water pg.27 ;
Table1-2: bacteria isolated from squid skin pg.30
Fig. 1-7 A Preserved Lolliguncula brevis displaying a range of increasing skin ulcer severity (left to right); mantle muscle of the 2 squids on the right has eroded to the point where the mantle has split. revealing the pen (after Ford and co-authors, 1986.).
Ford et al., (1986)
BacteriaVibrio sppLong Beach harbor near Los Angeles, CA (USA)Octopus bimaculoidesoctopuses in naturepathogenic bacteriamissing varying portions of armsno information availableno information availableno information availableno information availableForsythe and Hanlon (unpubl.);missing arms are presumably lost to predators (Hartwick,1983)
BacteriaPseudomonas sppLong Beach harbor near Los Angeles, CA (USA)Octopus bimaculoidesoctopuses in naturepathogenic bacteriamissing varying portions of armsno information availableno information availableno information availableno information availableForsythe and Hanlon (unpubl.);missing arms are presumably lost to predators (Hartwick,1983)
BacteriaVibrio sppChannel Islands off the California coast (USA)Octopus bimaculatusoctopuses in naturepathogenic bacteriamissing varying portions of armsno information availableno information availableno information availableno information availableForsythe and Hanlon (unpubl.)missing arms are presumably lost to predators (Hartwick,1983)
BacteriaPseudomonas sppChannel Islands off the California coast (USA)Octopus bimaculatusoctopuses in naturepathogenic bacteriamissing varying portions of armsno information availableno information availableno information availableno information availableForsythe and Hanlon (unpubl.)missing arms are presumably lost to predators (Hartwick,1983)
BacteriaVibrio carchariaeno information availableOctopus bimaculoideslaboratory cultured octopusesbacterial invasionsbacterium in arms and in branchial hearts and kidneysno visible external or behavioral symptoms or only a few « 5) very small « 3 mm diameter) skin lesionssudden deathchloramphenicol injected into live or frozen penaeid shrimp at a
dose of 150 mg kg- 1 body weight of octopuses once a day for 7 to 10 days. chloramphenicol injected into live or frozen penaeid shrimp at a
dose of 150 mg kg- 1 body weight of octopuses once a day for 7 to 10 days. chloramphenicol injected into live or frozen penaeid shrimp at a
dose of 150 mg kg- 1 body weight of octopuses once a day for 7 to 10 days. chloramphenicol injected into live or frozen penaeid shrimp at a
dose of 150 mg kg- 1 body weight of octopuses once a day for 7 to 10 days. chloramphenicol injected into live or frozen penaeid shrimp at a
dose of 150 mg kg- 1 body weight of octopuses once a day for 7 to 10 days. chloramphenicol injected into live or frozen penaeid shrimp at a
dose of 150 mg kg- 1 body weight of octopuses once a day for 7 to 10 days.
Fig. 1-6, A Transverse rows of bacteria (arrows) in arm muscle tissue of Octopus bimaculoides: Geimsa stain~ x 1000 (Original).Forsythe and Hanlon (unpubl.);Hartwick (1983)1)In about half of the mortalities, the octopus autotamized I or 2 arms at their midpoint in the last few hours prior to death. On moribund octopuses without such autophagy.palpation of the arms (normally firm due to muscle tone) invariably revealed 1 or 2 arms
having a short soft section in the mid-region.Histological examination of tissue from near the stumps or soft areas of intact arms revealed heavy proliferation of rod-shaped bacteria
2)All afflicted octopuses were at least 6 months old and from individually-cultured laboratory populations having no physical animal-toanimal contact. Furthermore, these octopuses were on diets consisting predominantly of fish and penaeid shrimps frozen after field collection. Vibrio carchariae has previously been implicated as a food-borne pathogen of fishes being fed frozen shrimp (Nelson Herwig, Curator Houston Aquarium, pers. comm., 1988) and this seems to be the most likely route of infection in this case. Chloramphenicol treatment is efficay: however, within 1 to 3 weeks ofstopping this treatment, subsequent mortalities sometimes occurred, requiring reinstitution of drug therapy1)In about half of the mortalities, the octopus autotamized I or 2 arms at their midpoint in the last few hours prior to death. On moribund octopuses without such autophagy.palpation of the arms (normally firm due to muscle tone) invariably revealed 1 or 2 arms
having a short soft section in the mid-region.Histological examination of tissue from near the stumps or soft areas of intact arms revealed heavy proliferation of rod-shaped bacteria
2)All afflicted octopuses were at least 6 months old and from individually-cultured laboratory populations having no physical animal-toanimal contact. Furthermore, these octopuses were on diets consisting predominantly of fish and penaeid shrimps frozen after field collection. Vibrio carchariae has previously been implicated as a food-borne pathogen of fishes being fed frozen shrimp (Nelson Herwig, Curator Houston Aquarium, pers. comm., 1988) and this seems to be the most likely route of infection in this case. Chloramphenicol treatment is efficay: however, within 1 to 3 weeks ofstopping this treatment, subsequent mortalities sometimes occurred, requiring reinstitution of drug therapy1)In about half of the mortalities, the octopus autotamized I or 2 arms at their midpoint in the last few hours prior to death. On moribund octopuses without such autophagy.palpation of the arms (normally firm due to muscle tone) invariably revealed 1 or 2 arms
having a short soft section in the mid-region.Histological examination of tissue from near the stumps or soft areas of intact arms revealed heavy proliferation of rod-shaped bacteria
2)All afflicted octopuses were at least 6 months old and from individually-cultured laboratory populations having no physical animal-toanimal contact. Furthermore, these octopuses were on diets consisting predominantly of fish and penaeid shrimps frozen after field collection. Vibrio carchariae has previously been implicated as a food-borne pathogen of fishes being fed frozen shrimp (Nelson Herwig, Curator Houston Aquarium, pers. comm., 1988) and this seems to be the most likely route of infection in this case. Chloramphenicol treatment is efficay: however, within 1 to 3 weeks ofstopping this treatment, subsequent mortalities sometimes occurred, requiring reinstitution of drug therapy1)In about half of the mortalities, the octopus autotamized I or 2 arms at their midpoint in the last few hours prior to death. On moribund octopuses without such autophagy.palpation of the arms (normally firm due to muscle tone) invariably revealed 1 or 2 arms
having a short soft section in the mid-region.Histological examination of tissue from near the stumps or soft areas of intact arms revealed heavy proliferation of rod-shaped bacteria
2)All afflicted octopuses were at least 6 months old and from individually-cultured laboratory populations having no physical animal-toanimal contact. Furthermore, these octopuses were on diets consisting predominantly of fish and penaeid shrimps frozen after field collection. Vibrio carchariae has previously been implicated as a food-borne pathogen of fishes being fed frozen shrimp (Nelson Herwig, Curator Houston Aquarium, pers. comm., 1988) and this seems to be the most likely route of infection in this case. Chloramphenicol treatment is efficay: however, within 1 to 3 weeks ofstopping this treatment, subsequent mortalities sometimes occurred, requiring reinstitution of drug therapy1)In about half of the mortalities, the octopus autotamized I or 2 arms at their midpoint in the last few hours prior to death. On moribund octopuses without such autophagy.palpation of the arms (normally firm due to muscle tone) invariably revealed 1 or 2 arms
having a short soft section in the mid-region.Histological examination of tissue from near the stumps or soft areas of intact arms revealed heavy proliferation of rod-shaped bacteria
2)All afflicted octopuses were at least 6 months old and from individually-cultured laboratory populations having no physical animal-toanimal contact. Furthermore, these octopuses were on diets consisting predominantly of fish and penaeid shrimps frozen after field collection. Vibrio carchariae has previously been implicated as a food-borne pathogen of fishes being fed frozen shrimp (Nelson Herwig, Curator Houston Aquarium, pers. comm., 1988) and this seems to be the most likely route of infection in this case. Chloramphenicol treatment is efficay: however, within 1 to 3 weeks ofstopping this treatment, subsequent mortalities sometimes occurred, requiring reinstitution of drug therapy1)In about half of the mortalities, the octopus autotamized I or 2 arms at their midpoint in the last few hours prior to death. On moribund octopuses without such autophagy.palpation of the arms (normally firm due to muscle tone) invariably revealed 1 or 2 arms
having a short soft section in the mid-region.Histological examination of tissue from near the stumps or soft areas of intact arms revealed heavy proliferation of rod-shaped bacteria
2)All afflicted octopuses were at least 6 months old and from individually-cultured laboratory populations having no physical animal-toanimal contact. Furthermore, these octopuses were on diets consisting predominantly of fish and penaeid shrimps frozen after field collection. Vibrio carchariae has previously been implicated as a food-borne pathogen of fishes being fed frozen shrimp (Nelson Herwig, Curator Houston Aquarium, pers. comm., 1988) and this seems to be the most likely route of infection in this case. Chloramphenicol treatment is efficay: however, within 1 to 3 weeks ofstopping this treatment, subsequent mortalities sometimes occurred, requiring reinstitution of drug therapy
BacteriaVibrio carchariaeno information availableOctopus mayalaboratory cultured octopusesbacterial invasionsbacterium in arms and in branchial hearts and kidneysno visible external or behavioral symptoms or only a few « 5) very small « 3 mm diameter) skin lesionssudden deathchloramphenicol injected into live or frozen penaeid shrimp at a
dose of 150 mg kg- 1 body weight of octopuses once a day for 7 to 10 days. chloramphenicol injected into live or frozen penaeid shrimp at a
dose of 150 mg kg- 1 body weight of octopuses once a day for 7 to 10 days. chloramphenicol injected into live or frozen penaeid shrimp at a
dose of 150 mg kg- 1 body weight of octopuses once a day for 7 to 10 days. chloramphenicol injected into live or frozen penaeid shrimp at a
dose of 150 mg kg- 1 body weight of octopuses once a day for 7 to 10 days. chloramphenicol injected into live or frozen penaeid shrimp at a
dose of 150 mg kg- 1 body weight of octopuses once a day for 7 to 10 days. chloramphenicol injected into live or frozen penaeid shrimp at a
dose of 150 mg kg- 1 body weight of octopuses once a day for 7 to 10 days.
Fig. 1-6, A Transverse rows of bacteria (arrows) in arm muscle tissue of Octopus bimaculoides: Geimsa stain~ x 1000 (Original).Forsythe and Hanlon (unpubl.);Hartwick (1983)1)In about half of the mortalities, the octopus autotamized I or 2 arms at their midpoint in the last few hours prior to death. On moribund octopuses without such autophagy.palpation of the arms (normally firm due to muscle tone) invariably revealed 1 or 2 arms
having a short soft section in the mid-region.Histological examination of tissue from near the stumps or soft areas of intact arms revealed heavy proliferation of rod-shaped bacteria
2)All afflicted octopuses were at least 6 months old and from individually-cultured laboratory populations having no physical animal-toanimal contact. Furthermore, these octopuses were on diets consisting predominantly of fish and penaeid shrimps frozen after field collection. Vibrio carchariae has previously been implicated as a food-borne pathogen of fishes being fed frozen shrimp (Nelson Herwig, Curator Houston Aquarium, pers. comm., 1988) and this seems to be the most likely route of infection in this case. Chloramphenicol treatment is efficay: however, within 1 to 3 weeks ofstopping this treatment, subsequent mortalities sometimes occurred, requiring reinstitution of drug therapy1)In about half of the mortalities, the octopus autotamized I or 2 arms at their midpoint in the last few hours prior to death. On moribund octopuses without such autophagy.palpation of the arms (normally firm due to muscle tone) invariably revealed 1 or 2 arms
having a short soft section in the mid-region.Histological examination of tissue from near the stumps or soft areas of intact arms revealed heavy proliferation of rod-shaped bacteria
2)All afflicted octopuses were at least 6 months old and from individually-cultured laboratory populations having no physical animal-toanimal contact. Furthermore, these octopuses were on diets consisting predominantly of fish and penaeid shrimps frozen after field collection. Vibrio carchariae has previously been implicated as a food-borne pathogen of fishes being fed frozen shrimp (Nelson Herwig, Curator Houston Aquarium, pers. comm., 1988) and this seems to be the most likely route of infection in this case. Chloramphenicol treatment is efficay: however, within 1 to 3 weeks ofstopping this treatment, subsequent mortalities sometimes occurred, requiring reinstitution of drug therapy1)In about half of the mortalities, the octopus autotamized I or 2 arms at their midpoint in the last few hours prior to death. On moribund octopuses without such autophagy.palpation of the arms (normally firm due to muscle tone) invariably revealed 1 or 2 arms
having a short soft section in the mid-region.Histological examination of tissue from near the stumps or soft areas of intact arms revealed heavy proliferation of rod-shaped bacteria
2)All afflicted octopuses were at least 6 months old and from individually-cultured laboratory populations having no physical animal-toanimal contact. Furthermore, these octopuses were on diets consisting predominantly of fish and penaeid shrimps frozen after field collection. Vibrio carchariae has previously been implicated as a food-borne pathogen of fishes being fed frozen shrimp (Nelson Herwig, Curator Houston Aquarium, pers. comm., 1988) and this seems to be the most likely route of infection in this case. Chloramphenicol treatment is efficay: however, within 1 to 3 weeks ofstopping this treatment, subsequent mortalities sometimes occurred, requiring reinstitution of drug therapy1)In about half of the mortalities, the octopus autotamized I or 2 arms at their midpoint in the last few hours prior to death. On moribund octopuses without such autophagy.palpation of the arms (normally firm due to muscle tone) invariably revealed 1 or 2 arms
having a short soft section in the mid-region.Histological examination of tissue from near the stumps or soft areas of intact arms revealed heavy proliferation of rod-shaped bacteria
2)All afflicted octopuses were at least 6 months old and from individually-cultured laboratory populations having no physical animal-toanimal contact. Furthermore, these octopuses were on diets consisting predominantly of fish and penaeid shrimps frozen after field collection. Vibrio carchariae has previously been implicated as a food-borne pathogen of fishes being fed frozen shrimp (Nelson Herwig, Curator Houston Aquarium, pers. comm., 1988) and this seems to be the most likely route of infection in this case. Chloramphenicol treatment is efficay: however, within 1 to 3 weeks ofstopping this treatment, subsequent mortalities sometimes occurred, requiring reinstitution of drug therapy1)In about half of the mortalities, the octopus autotamized I or 2 arms at their midpoint in the last few hours prior to death. On moribund octopuses without such autophagy.palpation of the arms (normally firm due to muscle tone) invariably revealed 1 or 2 arms
having a short soft section in the mid-region.Histological examination of tissue from near the stumps or soft areas of intact arms revealed heavy proliferation of rod-shaped bacteria
2)All afflicted octopuses were at least 6 months old and from individually-cultured laboratory populations having no physical animal-toanimal contact. Furthermore, these octopuses were on diets consisting predominantly of fish and penaeid shrimps frozen after field collection. Vibrio carchariae has previously been implicated as a food-borne pathogen of fishes being fed frozen shrimp (Nelson Herwig, Curator Houston Aquarium, pers. comm., 1988) and this seems to be the most likely route of infection in this case. Chloramphenicol treatment is efficay: however, within 1 to 3 weeks ofstopping this treatment, subsequent mortalities sometimes occurred, requiring reinstitution of drug therapy1)In about half of the mortalities, the octopus autotamized I or 2 arms at their midpoint in the last few hours prior to death. On moribund octopuses without such autophagy.palpation of the arms (normally firm due to muscle tone) invariably revealed 1 or 2 arms
having a short soft section in the mid-region.Histological examination of tissue from near the stumps or soft areas of intact arms revealed heavy proliferation of rod-shaped bacteria
2)All afflicted octopuses were at least 6 months old and from individually-cultured laboratory populations having no physical animal-toanimal contact. Furthermore, these octopuses were on diets consisting predominantly of fish and penaeid shrimps frozen after field collection. Vibrio carchariae has previously been implicated as a food-borne pathogen of fishes being fed frozen shrimp (Nelson Herwig, Curator Houston Aquarium, pers. comm., 1988) and this seems to be the most likely route of infection in this case. Chloramphenicol treatment is efficay: however, within 1 to 3 weeks ofstopping this treatment, subsequent mortalities sometimes occurred, requiring reinstitution of drug therapy
BacteriaPseudomonas spPseudomonas spPseudomonas spPseudomonas spPseudomonas spPseudomonas spNational Aquarium in Baltimore, Maryland (USA)Octopus dofleinilaboratory cultured octopusesbacterial invasionsskin lesionsno information availableboth susceptible to tetracyclinethe octopuse received tetracycline injected into its live food organismsStoskopf et al., (1987)Stoskopf reported the case of a 7 kg individual had a chronic lesion 1.5 em diameter for 2 months after arrival. After this initial period the lesion
began to enlarge and deepen while additional small lesions (3 to 4 mm diameter) began to appear.
revealed Pseudomonas sp. and AcinetobaCler
anitratus, both susceptible to tetracycline. The octopus received tetracycline injected into
its live food organisms at a dosage of 10 mg kg-I body weight once per day. The small
lesions disappeared in 7 days, and the large lesion healed completely in 28 days.Stoskopf reported the case of a 7 kg individual had a chronic lesion 1.5 em diameter for 2 months after arrival. After this initial period the lesion
began to enlarge and deepen while additional small lesions (3 to 4 mm diameter) began to appear.
revealed Pseudomonas sp. and AcinetobaCler
anitratus, both susceptible to tetracycline. The octopus received tetracycline injected into
its live food organisms at a dosage of 10 mg kg-I body weight once per day. The small
lesions disappeared in 7 days, and the large lesion healed completely in 28 days.Stoskopf reported the case of a 7 kg individual had a chronic lesion 1.5 em diameter for 2 months after arrival. After this initial period the lesion
began to enlarge and deepen while additional small lesions (3 to 4 mm diameter) began to appear.
revealed Pseudomonas sp. and AcinetobaCler
anitratus, both susceptible to tetracycline. The octopus received tetracycline injected into
its live food organisms at a dosage of 10 mg kg-I body weight once per day. The small
lesions disappeared in 7 days, and the large lesion healed completely in 28 days.Stoskopf reported the case of a 7 kg individual had a chronic lesion 1.5 em diameter for 2 months after arrival. After this initial period the lesion
began to enlarge and deepen while additional small lesions (3 to 4 mm diameter) began to appear.
revealed Pseudomonas sp. and AcinetobaCler
anitratus, both susceptible to tetracycline. The octopus received tetracycline injected into
its live food organisms at a dosage of 10 mg kg-I body weight once per day. The small
lesions disappeared in 7 days, and the large lesion healed completely in 28 days.Stoskopf reported the case of a 7 kg individual had a chronic lesion 1.5 em diameter for 2 months after arrival. After this initial period the lesion
began to enlarge and deepen while additional small lesions (3 to 4 mm diameter) began to appear.
revealed Pseudomonas sp. and AcinetobaCler
anitratus, both susceptible to tetracycline. The octopus received tetracycline injected into
its live food organisms at a dosage of 10 mg kg-I body weight once per day. The small
lesions disappeared in 7 days, and the large lesion healed completely in 28 days.Stoskopf reported the case of a 7 kg individual had a chronic lesion 1.5 em diameter for 2 months after arrival. After this initial period the lesion
began to enlarge and deepen while additional small lesions (3 to 4 mm diameter) began to appear.
revealed Pseudomonas sp. and AcinetobaCler
anitratus, both susceptible to tetracycline. The octopus received tetracycline injected into
its live food organisms at a dosage of 10 mg kg-I body weight once per day. The small
lesions disappeared in 7 days, and the large lesion healed completely in 28 days.
BacteriaAcinetobacter anitratusNational Aquarium in Baltimore, Maryland (USA)Octopus dofleinilaboratory cultured octopusesbacterial invasionsskin lesionsno information availableboth susceptible to tetracyclinethe octopuse received tetracycline injected into its live food organismsStoskopf et al., (1987)Stoskopf reported the case of a 7 kg individual had a chronic lesion 1.5 em diameter for 2 months after arrival. After this initial period the lesion
began to enlarge and deepen while additional small lesions (3 to 4 mm diameter) began to appear.
revealed Pseudomonas sp. and AcinetobaCler
anitratus, both susceptible to tetracycline. The octopus received tetracycline injected into
its live food organisms at a dosage of 10 mg kg-I body weight once per day. The small
lesions disappeared in 7 days, and the large lesion healed completely in 28 days.Stoskopf reported the case of a 7 kg individual had a chronic lesion 1.5 em diameter for 2 months after arrival. After this initial period the lesion
began to enlarge and deepen while additional small lesions (3 to 4 mm diameter) began to appear.
revealed Pseudomonas sp. and AcinetobaCler
anitratus, both susceptible to tetracycline. The octopus received tetracycline injected into
its live food organisms at a dosage of 10 mg kg-I body weight once per day. The small
lesions disappeared in 7 days, and the large lesion healed completely in 28 days.Stoskopf reported the case of a 7 kg individual had a chronic lesion 1.5 em diameter for 2 months after arrival. After this initial period the lesion
began to enlarge and deepen while additional small lesions (3 to 4 mm diameter) began to appear.
revealed Pseudomonas sp. and AcinetobaCler
anitratus, both susceptible to tetracycline. The octopus received tetracycline injected into
its live food organisms at a dosage of 10 mg kg-I body weight once per day. The small
lesions disappeared in 7 days, and the large lesion healed completely in 28 days.Stoskopf reported the case of a 7 kg individual had a chronic lesion 1.5 em diameter for 2 months after arrival. After this initial period the lesion
began to enlarge and deepen while additional small lesions (3 to 4 mm diameter) began to appear.
revealed Pseudomonas sp. and AcinetobaCler
anitratus, both susceptible to tetracycline. The octopus received tetracycline injected into
its live food organisms at a dosage of 10 mg kg-I body weight once per day. The small
lesions disappeared in 7 days, and the large lesion healed completely in 28 days.Stoskopf reported the case of a 7 kg individual had a chronic lesion 1.5 em diameter for 2 months after arrival. After this initial period the lesion
began to enlarge and deepen while additional small lesions (3 to 4 mm diameter) began to appear.
revealed Pseudomonas sp. and AcinetobaCler
anitratus, both susceptible to tetracycline. The octopus received tetracycline injected into
its live food organisms at a dosage of 10 mg kg-I body weight once per day. The small
lesions disappeared in 7 days, and the large lesion healed completely in 28 days.Stoskopf reported the case of a 7 kg individual had a chronic lesion 1.5 em diameter for 2 months after arrival. After this initial period the lesion
began to enlarge and deepen while additional small lesions (3 to 4 mm diameter) began to appear.
revealed Pseudomonas sp. and AcinetobaCler
anitratus, both susceptible to tetracycline. The octopus received tetracycline injected into
its live food organisms at a dosage of 10 mg kg-I body weight once per day. The small
lesions disappeared in 7 days, and the large lesion healed completely in 28 days.
BacteriaVibrio alginolyticusno information availableOctopus joubinilaboratory cultured octopusesbacterial invasionssevere skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
no information availablecourse to deathOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated area
Fig.1-4,A-E pg.30; Fig.1-5, A-D; Table 1-3 treatment of skin ulcers pg.32; Fig. 1-5, C, D healingHanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
BacteriaPseudomonas stutzerino information availableOctopus joubinilaboratory cultured octopusesbacterial invasionssevere skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
no information availablecourse to deathOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated area
Fig.1-4,A-E pg.30; Fig.1-5, A-D; Table 1-3 treatment of skin ulcers pg.32; Fig. 1-5, C, D healingHanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
BacteriaAeromonas cavia
Aeromonas cavia
Aeromonas cavia
Aeromonas cavia
Aeromonas cavia
no information availableOctopus joubinilaboratory cultured octopusesbacterial invasionssevere skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
no information availablecourse to deathOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated area
Fig.1-4,A-E pg.30; Fig.1-5, A-D; Table 1-3 treatment of skin ulcers pg.32; Fig. 1-5, C, D healingHanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
BacteriaBacillus sp
Bacillus sp
Bacillus sp
Bacillus sp
Bacillus sp
no information availableOctopus joubinilaboratory cultured octopusesbacterial invasionssevere skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
no information availablecourse to deathOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated area
Fig.1-4,A-E pg.30; Fig.1-5, A-D; Table 1-3 treatment of skin ulcers pg.32; Fig. 1-5, C, D healingHanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
BacteriaAcinetobacter spno information availableOctopus joubinilaboratory cultured octopusesbacterial invasionssevere skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
no information availablecourse to deathOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated area
Fig.1-4,A-E pg.30; Fig.1-5, A-D; Table 1-3 treatment of skin ulcers pg.32; Fig. 1-5, C, D healingHanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
BacteriaPleisiomonas spno information availableOctopus joubinilaboratory cultured octopusesbacterial invasionssevere skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
no information availablecourse to deathOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated area
Fig.1-4,A-E pg.30; Fig.1-5, A-D; Table 1-3 treatment of skin ulcers pg.32; Fig. 1-5, C, D healingHanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)
Cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. Cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. Cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. Cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. Cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
BacteriaFlavobacterium breveno information availableOctopus joubinilaboratory cultured octopusesbacterial invasionssevere skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
no information availablecourse to deathOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated area
Fig.1-4,A-E pg.30; Fig.1-5, A-D; Table 1-3 treatment of skin ulcers pg.32; Fig. 1-5, C, D healingHanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)
Cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. Cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. Cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. Cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. Cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
BacteriaVibrio damselano information availableOctopus joubinilaboratory cultured octopusesbacterial invasionssevere skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
no information availablecourse to deathOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated area
Fig.1-4,A-E pg.30; Fig.1-5, A-D; Table 1-3 treatment of skin ulcers pg.32; Fig. 1-5, C, D healingHanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
BacteriaVibrio parahaemolyticusno information availableOctopus briareuslaboratory cultured octopusesbacterial invasionssevere skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
no information availablecourse to deathOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated area
Fig.1-4,A-E pg.30; Fig.1-5, A-D; Table 1-3 treatment of skin ulcers pg.32.Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)
cultured from water-culture-system samples
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. cultured from water-culture-system samples
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. cultured from water-culture-system samples
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. cultured from water-culture-system samples
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. cultured from water-culture-system samples
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
BacteriaVibrio damselano information availableOctopus briareuslaboratory cultured octopusesbacterial invasionssevere skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
no information availablecourse to deathOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated area
Fig.1-4,A-E pg.30; Fig.1-5, A-D; Table 1-3 treatment of skin ulcers pg.32.Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
Bacteria Pseudomonas stutzeri
Pseudomonas stutzeri
Pseudomonas stutzeri
Pseudomonas stutzeri
Pseudomonas stutzeri
no information availableOctopus briareuslaboratory cultured octopusesbacterial invasionssevere skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
no information availablecourse to deathOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated area
Fig.1-4,A-E pg.30; Fig.1-5, A-D; Table 1-3 treatment of skin ulcers pg.32.Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
BacteriaBacillus sp.
Bacillus sp.
Bacillus sp.
Bacillus sp.
Bacillus sp.
no information availableOctopus briareuslaboratory cultured octopusesbacterial invasionssevere skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
no information availablecourse to deathOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated area
Fig.1-4,A-E pg.30; Fig.1-5, A-D; Table 1-3 treatment of skin ulcers pg.32.Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)
cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
BacteriaAcinetobacter sp.
Acinetobacter sp.
Acinetobacter sp.
Acinetobacter sp.
Acinetobacter sp.
no information availableOctopus briareuslaboratory cultured octopusesbacterial invasionssevere skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
no information availablecourse to deathOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated area
Fig.1-4,A-E pg.30; Fig.1-5, A-D; Table 1-3 treatment of skin ulcers pg.32.Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)
cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
BacteriaPleisiomonas spno information availableOctopus briareuslaboratory cultured octopusesbacterial invasionssevere skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
no information availablecourse to deathOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated area
Fig.1-4,A-E pg.30; Fig.1-5, A-D; Table 1-3 treatment of skin ulcers pg.32.Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)
cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
BacteriaFlavobacterium breve
Flavobacterium breve
Flavobacterium breve
Flavobacterium breve
Flavobacterium breve
no information availableOctopus briareuslaboratory cultured octopusesbacterial invasionssevere skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
severe skin ulcerations:last stage: spread of lesions onto the head and arms
no information availablecourse to deathOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated areaOnly nifurpirinol significantly reduced mortality by stopping ulcer penetration and promoting healing
Complete healing of lesions
required 1 to 2 months. Ulcers typically progressed to the next stage of damage during the
first week of treatment with nifurpirinol. Healing became evident thereafter with the
formation of a smooth, continuous epidermis across the ulcerated area
Fig.1-4,A-E pg.30; Fig.1-5, A-D; Table 1-3 treatment of skin ulcers pg.32.Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)Hanlon et al., (1984)
Forsythe et al., (1990)
cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus. cultured from water-culture-system samples

1st stage: extensive damage to the microvillous epidermis of the dorsal mantle and dysfunction of the underlying chromatophores due to destruction of the nerves and radial muscles involved with their expansion and retraction
2nd stage: the epidermis and dermal chromatophores were totally destroyed, leaving a clear or white lesion. The infection then penetrated through the dermis and into the underlying muscle layers of the mantle.
3rd stage: lesions spread to the lateral or ventral surfaces of the mantle and penetrated deep into or through the muscle layers, exposing the gills or other internal organs.
4th stage: lesions spread onto the head and arms

The ulcerations were due to secondary bacterial invasions of skin abrasions caused by octopusoctopus interactions under crowded conditions. The first signs of disease were seen in O.joubini at 2 months post-hatching, and at 1 month in O. briareus.
BacteriaVibrio pelagiusno information availableSepia officinalislaboratory cultured cuttlefishesbacterial infectionsdorsal surface of the mantle (rarely, on the ventral mantle skin and musculature) a long narrow ridge (5-10 cm):swollen haematoma, blue in color due to large amounts of oxygenated haemocyanin death consequent to a massive destruction of the dorsal epidermis in the 12 to 24 h following the appearance of the ridgechloramphenicol (40 mg kg-I) and
gentamycin (20 mg kg-I) administered by intramuscular injection or via food have been
highly effective in halting progression of the disease (see notes for details)chloramphenicol (40 mg kg-I) and
gentamycin (20 mg kg-I) administered by intramuscular injection or via food have been
highly effective in halting progression of the disease (see notes for details)chloramphenicol (40 mg kg-I) and
gentamycin (20 mg kg-I) administered by intramuscular injection or via food have been
highly effective in halting progression of the disease (see notes for details)chloramphenicol (40 mg kg-I) and
gentamycin (20 mg kg-I) administered by intramuscular injection or via food have been
highly effective in halting progression of the disease (see notes for details)chloramphenicol (40 mg kg-I) and
gentamycin (20 mg kg-I) administered by intramuscular injection or via food have been
highly effective in halting progression of the disease (see notes for details)
Fig. 1-8, F Labcultured adult showing longitudinal ridge-like haematoma (arrow) along the mantle: systemic
bacterial infection suspected. (Original.);
Fig. 1-8, F Labcultured adult showing longitudinal ridge-like haematoma (arrow) along the mantle: systemic
bacterial infection suspected. (Original.);
Fig. 1-8, F Labcultured adult showing longitudinal ridge-like haematoma (arrow) along the mantle: systemic
bacterial infection suspected. (Original.);
Fig. 1-8, F Labcultured adult showing longitudinal ridge-like haematoma (arrow) along the mantle: systemic
bacterial infection suspected. (Original.);
Fig. 1-8, F Labcultured adult showing longitudinal ridge-like haematoma (arrow) along the mantle: systemic
bacterial infection suspected. (Original.);
Hanlon et al., (1983); Elston (1984)If antibiotics are given immediately when the first sign of ridge swelling appears, symptoms will disappear completely within 18 h (overnight). Once signs of haematoma appear, intramuscular injections for 2 days preceding oral administration of antibiotics are necessary to assure survival. When
injected, chloramphenicol and gentamycin concentrations should not exceed 100 mg ml- 1 and 40 mg ml- I respectively to avoid excessive tissue toxicity at injection sites. A single injection is usually divided among 4 sites, often 4 different arm bases, to avoid tissue traumaIf antibiotics are given immediately when the first sign of ridge swelling appears, symptoms will disappear completely within 18 h (overnight). Once signs of haematoma appear, intramuscular injections for 2 days preceding oral administration of antibiotics are necessary to assure survival. When
injected, chloramphenicol and gentamycin concentrations should not exceed 100 mg ml- 1 and 40 mg ml- I respectively to avoid excessive tissue toxicity at injection sites. A single injection is usually divided among 4 sites, often 4 different arm bases, to avoid tissue traumaIf antibiotics are given immediately when the first sign of ridge swelling appears, symptoms will disappear completely within 18 h (overnight). Once signs of haematoma appear, intramuscular injections for 2 days preceding oral administration of antibiotics are necessary to assure survival. When
injected, chloramphenicol and gentamycin concentrations should not exceed 100 mg ml- 1 and 40 mg ml- I respectively to avoid excessive tissue toxicity at injection sites. A single injection is usually divided among 4 sites, often 4 different arm bases, to avoid tissue traumaIf antibiotics are given immediately when the first sign of ridge swelling appears, symptoms will disappear completely within 18 h (overnight). Once signs of haematoma appear, intramuscular injections for 2 days preceding oral administration of antibiotics are necessary to assure survival. When
injected, chloramphenicol and gentamycin concentrations should not exceed 100 mg ml- 1 and 40 mg ml- I respectively to avoid excessive tissue toxicity at injection sites. A single injection is usually divided among 4 sites, often 4 different arm bases, to avoid tissue traumaIf antibiotics are given immediately when the first sign of ridge swelling appears, symptoms will disappear completely within 18 h (overnight). Once signs of haematoma appear, intramuscular injections for 2 days preceding oral administration of antibiotics are necessary to assure survival. When
injected, chloramphenicol and gentamycin concentrations should not exceed 100 mg ml- 1 and 40 mg ml- I respectively to avoid excessive tissue toxicity at injection sites. A single injection is usually divided among 4 sites, often 4 different arm bases, to avoid tissue trauma
BacteriaVbrio splendidusno information availableSepia officinalislaboratory cultured cuttlefishesbacterial infectionsdorsal surface of the mantle (rarely, on the ventral mantle skin and musculature) a long narrow ridge (5-10 cm):swollen haematoma, blue in color due to large amounts of oxygenated haemocyanin death consequent to a massive destruction of the dorsal epidermis in the 12 to 24 h following the appearance of the ridgechloramphenicol (40 mg kg-I) and
gentamycin (20 mg kg-I) administered by intramuscular injection or via food have been
highly effective in halting progression of the disease (see notes for details)chloramphenicol (40 mg kg-I) and
gentamycin (20 mg kg-I) administered by intramuscular injection or via food have been
highly effective in halting progression of the disease (see notes for details)chloramphenicol (40 mg kg-I) and
gentamycin (20 mg kg-I) administered by intramuscular injection or via food have been
highly effective in halting progression of the disease (see notes for details)chloramphenicol (40 mg kg-I) and
gentamycin (20 mg kg-I) administered by intramuscular injection or via food have been
highly effective in halting progression of the disease (see notes for details)chloramphenicol (40 mg kg-I) and
gentamycin (20 mg kg-I) administered by intramuscular injection or via food have been
highly effective in halting progression of the disease (see notes for details)
Fig. 1-8, F Labcultured adult showing longitudinal ridge-like haematoma (arrow) along the mantle: systemic
bacterial infection suspected. (Original.);
Fig. 1-8, F Labcultured adult showing longitudinal ridge-like haematoma (arrow) along the mantle: systemic
bacterial infection suspected. (Original.);
Fig. 1-8, F Labcultured adult showing longitudinal ridge-like haematoma (arrow) along the mantle: systemic
bacterial infection suspected. (Original.);
Fig. 1-8, F Labcultured adult showing longitudinal ridge-like haematoma (arrow) along the mantle: systemic
bacterial infection suspected. (Original.);
Fig. 1-8, F Labcultured adult showing longitudinal ridge-like haematoma (arrow) along the mantle: systemic
bacterial infection suspected. (Original.);
Hanlon et al., (1983); Elston (1984)If antibiotics are given immediately when the first sign of ridge swelling appears, symptoms will disappear completely within 18 h (overnight). Once signs of haematoma appear, intramuscular injections for 2 days preceding oral administration of antibiotics are necessary to assure survival. When
injected, chloramphenicol and gentamycin concentrations should not exceed 100 mg ml- 1 and 40 mg ml- I respectively to avoid excessive tissue toxicity at injection sites. A single injection is usually divided among 4 sites, often 4 different arm bases, to avoid tissue traumaIf antibiotics are given immediately when the first sign of ridge swelling appears, symptoms will disappear completely within 18 h (overnight). Once signs of haematoma appear, intramuscular injections for 2 days preceding oral administration of antibiotics are necessary to assure survival. When
injected, chloramphenicol and gentamycin concentrations should not exceed 100 mg ml- 1 and 40 mg ml- I respectively to avoid excessive tissue toxicity at injection sites. A single injection is usually divided among 4 sites, often 4 different arm bases, to avoid tissue traumaIf antibiotics are given immediately when the first sign of ridge swelling appears, symptoms will disappear completely within 18 h (overnight). Once signs of haematoma appear, intramuscular injections for 2 days preceding oral administration of antibiotics are necessary to assure survival. When
injected, chloramphenicol and gentamycin concentrations should not exceed 100 mg ml- 1 and 40 mg ml- I respectively to avoid excessive tissue toxicity at injection sites. A single injection is usually divided among 4 sites, often 4 different arm bases, to avoid tissue traumaIf antibiotics are given immediately when the first sign of ridge swelling appears, symptoms will disappear completely within 18 h (overnight). Once signs of haematoma appear, intramuscular injections for 2 days preceding oral administration of antibiotics are necessary to assure survival. When
injected, chloramphenicol and gentamycin concentrations should not exceed 100 mg ml- 1 and 40 mg ml- I respectively to avoid excessive tissue toxicity at injection sites. A single injection is usually divided among 4 sites, often 4 different arm bases, to avoid tissue traumaIf antibiotics are given immediately when the first sign of ridge swelling appears, symptoms will disappear completely within 18 h (overnight). Once signs of haematoma appear, intramuscular injections for 2 days preceding oral administration of antibiotics are necessary to assure survival. When
injected, chloramphenicol and gentamycin concentrations should not exceed 100 mg ml- 1 and 40 mg ml- I respectively to avoid excessive tissue toxicity at injection sites. A single injection is usually divided among 4 sites, often 4 different arm bases, to avoid tissue trauma
BacteriaPseudomonas stutzerino information availableSepia officinalislaboratory cultured cuttlefishesbacterial infectionsdorsal surface of the mantle (rarely, on the ventral mantle skin and musculature) a long narrow ridge (5-10 cm):swollen haematoma, blue in color due to large amounts of oxygenated haemocyanin death consequent to a massive destruction of the dorsal epidermis in the 12 to 24 h following the appearance of the ridgechloramphenicol (40 mg kg-I) and
gentamycin (20 mg kg-I) administered by intramuscular injection or via food have been
highly effective in halting progression of the disease (see notes for details)chloramphenicol (40 mg kg-I) and
gentamycin (20 mg kg-I) administered by intramuscular injection or via food have been
highly effective in halting progression of the disease (see notes for details)chloramphenicol (40 mg kg-I) and
gentamycin (20 mg kg-I) administered by intramuscular injection or via food have been
highly effective in halting progression of the disease (see notes for details)chloramphenicol (40 mg kg-I) and
gentamycin (20 mg kg-I) administered by intramuscular injection or via food have been
highly effective in halting progression of the disease (see notes for details)
Fig. 1-8, F Labcultured adult showing longitudinal ridge-like haematoma (arrow) along the mantle: systemic
bacterial infection suspected. (Original.);
Fig. 1-8, F Labcultured adult showing longitudinal ridge-like haematoma (arrow) along the mantle: systemic
bacterial infection suspected. (Original.);
Fig. 1-8, F Labcultured adult showing longitudinal ridge-like haematoma (arrow) along the mantle: systemic
bacterial infection suspected. (Original.);
Fig. 1-8, F Labcultured adult showing longitudinal ridge-like haematoma (arrow) along the mantle: systemic
bacterial infection suspected. (Original.);
Hanlon et al., (1983); Elston (1984)If antibiotics are given immediately when the first sign of ridge swelling appears, symptoms will disappear completely within 18 h (overnight). Once signs of haematoma appear, intramuscular injections for 2 days preceding oral administration of antibiotics are necessary to assure survival. When
injected, chloramphenicol and gentamycin concentrations should not exceed 100 mg ml- 1 and 40 mg ml- I respectively to avoid excessive tissue toxicity at injection sites. A single injection is usually divided among 4 sites, often 4 different arm bases, to avoid tissue traumaIf antibiotics are given immediately when the first sign of ridge swelling appears, symptoms will disappear completely within 18 h (overnight). Once signs of haematoma appear, intramuscular injections for 2 days preceding oral administration of antibiotics are necessary to assure survival. When
injected, chloramphenicol and gentamycin concentrations should not exceed 100 mg ml- 1 and 40 mg ml- I respectively to avoid excessive tissue toxicity at injection sites. A single injection is usually divided among 4 sites, often 4 different arm bases, to avoid tissue traumaIf antibiotics are given immediately when the first sign of ridge swelling appears, symptoms will disappear completely within 18 h (overnight). Once signs of haematoma appear, intramuscular injections for 2 days preceding oral administration of antibiotics are necessary to assure survival. When
injected, chloramphenicol and gentamycin concentrations should not exceed 100 mg ml- 1 and 40 mg ml- I respectively to avoid excessive tissue toxicity at injection sites. A single injection is usually divided among 4 sites, often 4 different arm bases, to avoid tissue traumaIf antibiotics are given immediately when the first sign of ridge swelling appears, symptoms will disappear completely within 18 h (overnight). Once signs of haematoma appear, intramuscular injections for 2 days preceding oral administration of antibiotics are necessary to assure survival. When
injected, chloramphenicol and gentamycin concentrations should not exceed 100 mg ml- 1 and 40 mg ml- I respectively to avoid excessive tissue toxicity at injection sites. A single injection is usually divided among 4 sites, often 4 different arm bases, to avoid tissue trauma
BacteriaVibrio anguillarumno information availableSepioteuthis lessonianalaboratory cultured squidsbacterial infectionsinfections of the eye,primarily involving damage to the corneaone eye had a slightly whitish clouding of the cornea (Vibrio harveyi); the other eye was more severely damaged with a part of the cornea actually missing and the lens opaque (V. anguillarum and V. carchariae).no information availableno information availableHanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio harveyino information availableSepioteuthis lessonianalaboratory cultured squidsbacterial infectionsinfections of the eye,primarily involving damage to the corneaone eye had a slightly whitish clouding of the cornea (Vibrio harveyi); the other eye was more severely damaged with a part of the cornea actually missing and the lens opaque (V. anguillarum and V. carchariae).no information availableno information availableHanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio carchariaeno information availableSepioteuthis lessonianalaboratory cultured squidsbacterial infectionsinfections of the eye,primarily involving damage to the corneaone eye had a slightly whitish clouding of the cornea (Vibrio harveyi); the other eye was more severely damaged with a part of the cornea actually missing and the lens opaque (V. anguillarum and V. carchariae).no information availableno information availableHanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio splendidusno information availableSepioteuthis lessonianalaboratory cultured squidsbacterial infectionsovarian infectionclear and opaque (Pseudomonas) eggs clear and opaque (Pseudomonas) eggs clear and opaque (Pseudomonas) eggs clear and opaque (Pseudomonas) eggsno information availableno information availableFig. 1-8, E Ventral view of opened mantle
cavity revealing 2 very large. normal white nidamental glands and. posterior to them (left). various
dead embryos (white) amidst normal translucent embryos in the ovary. Fig. 1-8, E Ventral view of opened mantle
cavity revealing 2 very large. normal white nidamental glands and. posterior to them (left). various
dead embryos (white) amidst normal translucent embryos in the ovary. Fig. 1-8, E Ventral view of opened mantle
cavity revealing 2 very large. normal white nidamental glands and. posterior to them (left). various
dead embryos (white) amidst normal translucent embryos in the ovary. Fig. 1-8, E Ventral view of opened mantle
cavity revealing 2 very large. normal white nidamental glands and. posterior to them (left). various
dead embryos (white) amidst normal translucent embryos in the ovary.
Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaPseudomonas spno information availableSepioteuthis lessonianalaboratory cultured squidsbacterial infectionsovarian infectionclear and opaque (Pseudomonas) eggs clear and opaque (Pseudomonas) eggs clear and opaque (Pseudomonas) eggs clear and opaque (Pseudomonas) eggsno information availableno information availableFig. 1-8, E Ventral view of opened mantle
cavity revealing 2 very large. normal white nidamental glands and. posterior to them (left). various
dead embryos (white) amidst normal translucent embryos in the ovary. Fig. 1-8, E Ventral view of opened mantle
cavity revealing 2 very large. normal white nidamental glands and. posterior to them (left). various
dead embryos (white) amidst normal translucent embryos in the ovary. Fig. 1-8, E Ventral view of opened mantle
cavity revealing 2 very large. normal white nidamental glands and. posterior to them (left). various
dead embryos (white) amidst normal translucent embryos in the ovary. Fig. 1-8, E Ventral view of opened mantle
cavity revealing 2 very large. normal white nidamental glands and. posterior to them (left). various
dead embryos (white) amidst normal translucent embryos in the ovary.
Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaAcinerobacter lwoffiMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaAeromonas caviaeMarine Biomedical Institute biology laboratoryOctopus splaboratory cultured octopusesdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaAeromonas hydrophilaMarine Biomedical Institute biology laboratoryOctopus splaboratory cultured octopusesdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaAeromonas sobriaMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaAlcaligenes faecalisMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaCytophaga spMarine Biomedical Institute biology laboratoryOctopus splaboratory cultured octopusesdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaCytophaga spMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskin and haemolymphno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaFlavobacterium spMarine Biomedical Institute biology laboratoryOctopuslaboratory cultured octopusesdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaKlebsiella pneumoniaeMarine Biomedical Institute biology laboratoryOctopus splaboratory cultured octopusesdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaPlesiomonas shigelloidesMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseasehaemolymphno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaProteus spMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaPseudomonas alcaligenesMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaPseudomonas diminutaMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskin and haemolymphno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaPseudomonas maltophiliaMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaPseudomonas putrifaciensMarine Biomedical Institute biology laboratoryOctopus splaboratory cultured octopusesdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaPseudomonas putrifaciensMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaPseudomonas vesicularisMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskin and haemolymphno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaPseudomonas stutzeriMarine Biomedical Institute biology laboratoryOctopus splaboratory cultured octopusesdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaPseudomonas stutzeriMarine Biomedical Institute biology laboratorySepia splaboratory cultured cuttlefishesdiseasehaemolymphno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio alginolyticusMarine Biomedical Institute biology laboratoryOctopus splaboratory cultured octopusesdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio alginolyticusMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskin and haemolymphno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio anguillarumMarine Biomedical Institute biology laboratoryOctopus splaboratory cultured octopusesdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio anguillarumMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseeyeno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio carchariaeMarine Biomedical Institute biology laboratoryOctopus splaboratory cultured octopusesdiseasemuscle and haemolymphno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio carchariaeMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskin, haemolymph and eyeno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio cambelliMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskin and haemolymphno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio costicolaMarine Biomedical Institute biology laboratoryOctopus splaboratory cultured octopusesdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio cholerae (non-01)Marine Biomedical Institute biology laboratoryOctopus splaboratory cultured octopusesdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio damselaMarine Biomedical Institute biology laboratoryOctopus splaboratory cultured octopusesdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio damselaMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskin and haemolymphno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio fluvialisMarine Biomedical Institute biology laboratoryOctopus splaboratory cultured octopusesdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio fluvialisMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio harveyiMarine Biomedical Institute biology laboratoryOctopus splaboratory cultured octopusesdiseasehaemolymphno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio harveyiMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseeyeno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio hollisaeMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskin and haemolymphno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio mediterraneiMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio metschnikoviiMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio mimicusMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio natriegenesMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio ordaliiMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio parahaemolyticusMarine Biomedical Institute biology laboratoryOctopus splaboratory cultured octopusesdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio parahaemolyticusMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskin and haemolymphno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)Hanlon and
Forsythe (1990)
BacteriaVibrio parahaemolyticusMarine Biomedical Institute biology laboratorySepia splaboratory cultured cuttlefishesdiseasehaemolymphno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)
BacteriaVibrio pelagiusMarine Biomedical Institute biology laboratoryOctopus splaboratory cultured octopusesdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)
Vibrio pelagius (biovar 2)
BacteriaVibrio pelagiusMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)
Vibrio pelagius (biovar 2)
BacteriaVibrio pelagiusMarine Biomedical Institute biology laboratorySepia splaboratory cultured cuttlefishesdiseasehaemolymphno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)
Vibrio pelagius (biovar 2)
BacteriaVibrio splendidusMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskin, eye and ovaryno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)
Vibrio splendidus (biovar 2)
BacteriaVibrio splendidusMarine Biomedical Institute biology laboratorySepia splaboratory cultured cuttlefishesdiseasehaemolymphno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)
Vibrio splendidus (biovar 2)
BacteriaVibrio tubiashiMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskin and haemolymphno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)
BacteriaVibrio vulnificusMarine Biomedical Institute biology laboratoryLoligo splaboratory cultured squidsdiseaseskinno information availableno information availableno information availableTab. 1-4 pag 39Hanlon and
Forsythe (1990)