sters from Woods Hole, Mass., and Wood 

 (1965a, 1965b) isolated Gatfkija-Uke organisms 

 from two European lobsters (HoniarKS riil- 

 f/rn/.s' Milne-Edwards) from the North Sea. 

 Wood observed lobster mortalities in storage 

 tanks in southern England in 1962 and recov- 

 ered Gaffkj/a with cultural and biochemical 

 characteristics similar to Canadian and United 

 States isolates. Epizootics of gaffkaemia have 

 been reported from European lobsters in Ire- 

 land (Gibson, 1961), Norway, and the Nether- 

 lands (Roskam, 1957). Gibson noted that dis- 

 eased lobsters were also infested with the "gill 

 maggot," Nicotlwe astaci Audouin and Milne- 

 Edwards, which was absent from uninfected 

 individuals. Cross sections of the parasitic co- 

 pepod were used by Gibson to determine the 

 presence of the disease in the host. 



Experimental studies of host-parasite rela- 

 tionships showed th.it lobsters became infected 

 and died a few days after inoculation with G. 

 honiaii (Rabin, 1965). Prior inoculation with 

 Vihiio endotoxin did not enhance the infection 

 and prior inoculation of heat-killed Gaffkija did 

 not alter the course of infection. Lobster serum 

 .stimulated in vitro growth of G. Jiomari in al- 

 most every test, but growth of Vibrio was some- 

 times inhibited. Studies of possible defense 

 mechanisms of lobsters against G. Iiomari have 

 also been carried out at the Halifax (Nova Sco- 

 tia) and Saint Andrews (New Brunswick) 

 stations of the Fisheries Research Board of 

 Canada (Fisheries Re.search Board of Canada, 

 1966). Lobster serum, as indicated by Rabin's 

 work, had no bactericidal activity against the 

 pathogen but instead promoted its growth. 



A preliminary note by Bell and Ho.skins 

 (1966) described experimental transmission of 

 G. homari to Dungeness crabs and spot shrimps 

 {PcDidaliis platyceros) . Infection was achieved 

 by intramuscular inoculation, but not by inges- 

 tion or contact. Mortalities were produced in 

 both species. 



A .second bacterial disea.se of lobsters, known 

 as "shell di.sease" (Hess, 1937), is caused by 

 chitin-destroying gram-negative bacilli. Hess 

 isolated chitin-degrading bacteria from live lob- 

 sters impounded at Yarmouth, Nova Scotia, but 

 collected from various parts of the Canadian 

 Maritime provinces. This was the first report 

 of attacks by such microorganisms on living 



Crustacea. The disease was characterized by a 

 pitting and sculpturing of the exoskeleton (fig. 

 8) ; although it was first seen in impounded 



Figure 8. — "Shell disease" of American lobster. 



lobsters, similar conditions were later observed 

 in freshly caught lobsters from several widely 

 separated Canadian fishing grounds. Initial le- 

 sions occurred on the walking legs, and were 

 distinguished by white outer margins, from 

 which the bacteria were most readily isolated. 

 Hess found the disease relatively rare in nat- 

 ural populations but noted severe shell erosion 

 and weakening of lobsters stored in pounds over 

 the winter. Microorganisms isolated were bio- 

 chemically and physiologically similar to Bacil- 

 lus fhitinovorouf^ Type II and Type XIV of 

 Benton (1935). All isolates were able to decom- 

 pose pure chitin in saline solution containing 

 no other nitrogen or carbon source. None of 

 Hess' isolates — nor, for that matter, i.solates 



DISEASES OF THE MARINE BIVALVE MOLLUSCA AND CRUSTACEA 



357 



