FISHERY BULLETIN: VOL. 76, NO. 1 



infections are obvious in fresh squash prepara- 

 tions because PIB's fill every microscopic field. 



Prevalence of virus in feral pink shrimp from 

 several locations on the northern gulf coast of 

 Florida has varied among samples collected. 

 There appears to be no seasonal intensification of 

 prevalence that is statistically significant; how- 

 ever, fall samples have been best for recovering 

 heavy infections. To date, of 4,676 shrimp 

 examined, 808 have been patently infected. In the 

 laboratory, virus prevalence and intensity have 

 increased repetitively in 20- to 30-day periods in 

 different lots or samples of feral shrimp held under 

 crowded, sublethally stressful conditions (Couch 

 1974b). This increase in prevalence associated 

 with crowding provides indirect evidence for the 

 infectious nature of the shrimp baculovirus. There 

 is also increasing evidence, from our research, 

 that exposures to low levels of certain chemicals, 

 such as polychlorinated biphenyl (PCB), enhance 

 spread of virus through captive populations 

 (Couch and Courtney 1977). We have induced a 

 50% increase in prevalence in captive shrimp by 

 exposing shrimp to sublethal levels of PCB's 

 (Aroclor 1254).^ Transmission in nature probably 

 is achieved via cannibalism of infected shrimp by 

 noninfected shrimp. Laboratory transmission has 

 been minimally successful when hatchery-reared 

 or nonpatently infected juvenile or adult shrimp 

 were fed heavily infected hepatopancreas. Only 

 about 20% of fed shrimp show patent infections 20 

 to 30 days after initial feeding. Degree of infection 

 in adult shrimp is not useful in predicting mortal- 

 ity of shrimp. 



Recently the shrimp baculovirus was associated 

 with massive mortality of larval and postlarval 

 brown shrimp in a commercial aquaculture at- 

 tempt. Brown shrimp, hatched and reared to pro- 

 tozoal and mysid stages in laboratory tanks, suf- 

 fered a mass mortality in a 48-h period (95% of 

 several million larvae). Water quality was not 

 found to be at fault and there were no toxicants 

 known to be in the water. Upon careful histologi- 

 cal examination of a sample of surviving and dead 

 larvae, I discovered that 19.4% in - 139) had 

 patent virus infections, mostly heavy, in midgut 

 and hepatopancreatic cells (Table 1). Subsequent 

 electron microscopical study confirmed that 60 to 

 90% of hepatopancreatic cell profiles in larvae had 

 infections, many with prepatent stages of the 



virus. Present in higher prevalences in these 

 dying shrimp were a flagellate protozoon and a 

 ciliate protozoon. The relative roles of the three 

 pathogens in the shrimp mortality will be dis- 

 cussed in later sections of this paper (Tables 1, 2). 



Table l. — Relative prevalence of pathogens in 139 larval (late 

 protozeal and mysid stages) brown shrimp, Penaeus aztecus,^ in 

 April 1974. 



Condition 



Not infected 

 Flagellate 

 Ciliate 

 Virus 



'Whole mount slides with Protargol stain (Bodian-activated protein silver). 



Table 2. — Prevalence and concurrent infections of pathogens in 



139 larval brown shrimp examined in April 1974. 



[Concurrent vs. single infections.] 



■^Reference to trade names does not imply endorsement by the 

 National Marine Fisheries Service, NOAA, or USEPA. 



Bacteria 



The role of bacteria in diseases of penaeid 

 shrimps is presently being investigated seriously 

 for the first time. A few scattered reports deal with 

 bacteria as pathogens, contaminants, or ectocom- 

 mensals in shrimps. 



Cook and Lofton (1973) reported isolation of 

 three genera of bacteria, Beneckea, Vibrio, and 

 Pseudomonas, from penaeid shrimp suffering 

 from "shell disease," also known as black spot dis- 

 ease. This disease (Figure 6) is characterized by 

 brown to black spots on the external carapace or 

 cuticle of shrimp and has been observed in brown, 

 pink, and white shrimps. In advanced cases of the 

 disease, considerable erosion and destruction of 

 the cuticle occurs. This disease has been reported 

 from many other decapod Crustacea (Rosen 1970). 

 Chitinoclastic bacteria such as Beneckea sp. have 

 been thought to be the causative agents of black 

 spot disease, although attempts to experimentally 

 produce the disease in shrimp by innoculating 

 Beneckea have had uncertain results (see section 

 on "shell disease" under Noninfectious Diseases). 

 Mechanical injury to shrimp that results in 

 breakage in the normal cuticle probably plays an 



