FISHERY BULLETIN: VOL. 69, NO, 3 



sinuses of the lobster. As Parry (1960) had 

 pointed out earlier, this type of aggregation in 

 gills is a common phenomenon in Crustacea. 

 Poisson (1930) observed that, in the few crabs 

 {Carcinus maenas) resistant to the parasitic 

 ciliate Anophrys sarcophaga, masses of dead cil- 

 iates occurred in branchial lacunae, pericardial 

 sinus, and hepatopancreatic sinuses. Degener- 

 ating ciliates eventually formed brownish cysts. 

 Cantacuzene (1923b) observed a similar phe- 

 nomenon in Maia sqn'nmdo inoculated with bac- 

 teria. He pointed out that the lacunar tissue of 

 the branchial lamellae of decapod crustaceans, 

 with its many fixed phagocytes, acts as an ex- 

 tensive and effective bacterial filter. 



Cornick and Stewart suggested that the devel- 

 opment of polysaccharide capsules by G. homari 

 in later stages of infection could be an important 

 device that prevented destruction of the phagocy- 

 tized bacteria and allowed multiplication of the 

 pathogen. They pointed out, as evidence, that 

 unencapsulated G. homari grown in culture were 

 actively phagocytized. As Stewart and Rabin 

 (1970) later reported, however, the unencapsu- 

 lated cultured bacteria were also virulent. It 

 may be that the capsule forms soon after the 

 organisms are injected into the host. This ob- 

 servation of survival and growth of ])hogocy- 

 tized encapsulated bacteria in lobsters is a direct 

 counterpart of the inability of vertebrate phago- 

 cytes to destroy many encapsulated microor- 

 ganisms, and parallels the earlier findings by 

 Cantacuzene (1923b) of a fatal disease in crabs 

 induced by encapsulated gram-positive bacteria. 



Stewart, Dockrill, and Cornick (1969) exam- 

 ined certain insusceptibility factors affecting 

 Gaffkya disease in lobsters. Destruction of the 

 integrity of the integument seemed essential to 

 transmission of the pathogen. Acidity of the 

 gastric fluid was bactericidal and appeared to 

 provide an effective barrier against oral infec- 

 tion. Previous attempts to infect lobsters by 

 feeding infected material had been unsuccessful 

 (Snieszko and Taylor, 1917; Wood, 1965a, 1965b; 

 Rabin and Hughes, 1968). 



Undoubtedly such insuscei)tibility factors are 

 of definite imiMrtance to the epizootiology of 

 gaffkaemia for several reasons: lobsters are 

 cannibalistic; hemolymph of moribund gaffkae- 



mic individuals contains about 10' organisms per 

 ml (Stewart, Arie, Zwicker, and Dingle, 1969); 

 and Gaffkya can be isolated consistently from lob- 

 ster pounds, sea water, bottom mud, and slime of 

 holding containers (Goggins and Hurst, 1960). 

 A thorough study of the effects of temperature 

 on experimentally induced Gaffkya infections in 

 American lobsters was reported by Stewart, 

 Cornick, and Zwicker (1969). Mean time to 

 death was inversely related to temperature 

 (Figure 5). At 1° C no deaths attributable to 

 experimental infections occurred; at 3° C mean 

 time to death was 172 days; and at intermediate 

 higher temperatures mean time to death de- 

 creased drastically to a minimum of 2 days at 

 20° C (which approaches the upper lethal tem- 



175 



150- 



5 125 



X 



I— 

 < 



a 

 O 



z 

 < 



100 



75- 



50- 



25- 



O 

 \ 



1— 

 10 



I 

 15 



20 



25 



TEMPERATURE (°C) 



Figure 5. — Relation of temijoraturc to mean time to 

 ileath in lobsters experimentally exposed to Gaffkya. 

 (From Stewart, Cornick, and Zwicker, 1969.) 



474 



