eral individuals. Sprague (1954, 1970, footnote 3), 

 Kruse (1959, 1966), Hutton et al. (1959), Iversen 

 and Manning (1959), Hutton (1964), and Iversen 

 and Van Meter (1964) were early explorers in 

 penaeid shrimp infectious diseases. More recently 

 the works of Overstreet (1973), Lightner (1974, 

 1975), Lightner and Fontaine (1973), Johnson 

 (1974), Feigenbaum ( 1973, 1975), Couch ( 1974a, b, 

 1976) and Sindermann'' have contributed to the 

 general fund of data. Overstreet's 1973 paper is 

 particularly valuable because it gives prevalence 

 data for many of the parasites of penaeid shrimps 

 of the northern Gulf Many other authors of single, 

 significant works on penaeid diseases will be cited 

 in specific sections later in this paper. 



The scientific reports and reviews mentioned 

 above, along with much unpublished experience, 

 present a consensus which impresses me with the 

 high significance of disease to the overall ecology 

 and biology of penaeid shrimps. In its broadest 

 sense, disease is probably second only to predation 

 and periodic physical catastrophes (e.g., freshets, 

 temperature fluctuations) as a continuous en- 

 vironmental factor limiting numbers of penaeid 

 shrimps in nature. In attempts at massive culture 

 of penaeid shrimps, infectious disease may rank 

 below only reproductive and nutritional require- 

 ments as a limiting factor. Toxicants, in the form 

 of pollutants, are threats to the well being of es- 

 tuarine species, particularly in certain chronically 

 polluted regions. Toxic responses in penaeid 

 shrimps have been studied experimentally re- 

 cently, and, therefore, some data are available on 

 this subject. 



This paper is concerned with the present status 

 of diseases, parasites, and toxic responses of four 

 commercial species of penaeid shrimps from the 

 Gulf and South Atlantic region of North America. 

 These are the pink shrimp, Penaeus duorarum; 

 the brown shrimp, P. aztecus; and the white 

 shrimp, P. setiferus. Occasional reference will be 

 made to parasites of P. braziliensis which occupies 

 a marginal portion of the U.S. range of the three 

 other species. The subjects will be treated in the 

 following order: Infectious diseases and parasites; 

 noninfectious diseases and toxic responses; and 

 overview and future research. 



^Sprague, V. 1950. Notes on three microsporidian parasites of 

 Decapod Crustacea from Louisiana waters. Occas. Pap. Mar. 

 Lab., La. State Univ. 5:1-8. 



■•Sindermann, C. J. 1974. Diagnosis and control of mariculture 

 diseases in the United States. Tech. Ser. Rep. No. 2, Natl. Mar. 

 Fish. Serv., NOAA, Highlands, N.J., 306 p. 



FISHERY BULLETIN: VOL. 76, NO. 1 



INFECTIOUS DISEASES AND PARASITES 



Viruses 



To date, only a single virus disease has been 

 described for shrimps. Couch (1974a, b) and Couch 

 et al. (1975) have described a rod-shaped virus 

 (Figures 1-3) which has many characteristics of 

 the baculoviruses (nuclear polyhedrosis viruses) 

 previously described only from insects or mites. 

 The virus has been named Baculovirus penaei 

 (Couch 1974b). 



This virus commonly has been found to infect 

 the hepatopancreas of juvenile and adult stages of 

 pink and brown shrimp in nature. Laboratory- 

 reared larval brown shrimp (protozoea and mysis 

 stages) have been found with virus-infected mid- 

 gut and hepatopancreas. 



Infected hepatopancreatic cells in pink shrimp 

 display striking cytopathological changes when 

 compared with normal, noninfected cells. Nuclear 

 hypertrophy (Figure 3), chromatin diminution 

 (Figure 3), nucleolar degeneration (Figure 3), and 

 polyhedral inclusion body (PIB, Figure 2) produc- 

 tion are characteristic of patent virus infections 

 observable with bright field or phase contrast mi- 

 croscopy. 



Electron microscopy (EM) reveals the rod- 

 shaped virions (269 nm x 50 nm) in infected, 

 hypertrophied nuclei prior to, during, and after 

 the PIB is formed. Various stages of the virus 

 replicative cycle are observable with EM of thin 

 sections of moderately to heavily infected 

 hepatopancreas. The ultimate cytopathological ef- 

 fect of the virus is destruction of the host cell 

 through rupture or lysis. This is accomplished 

 usually by the growth of the PIB to a size too large 

 for the host cell to accommodate (Figure 4), con- 

 comitant with virus-induced nuclear hypertrophy 

 and probable stressing of nuclear membranes. 



The PIB's produced during infections are pat- 

 ently diagnostic for the baculovirus of penaeid 

 shrimp (Figures 4, 5). To find a single characteris- 

 tic PIB in tissue squashes of shrimp hepatopan- 

 creas or midgut is to diagnose infection. Quantita- 

 tion of patent infections (PIB's present) can be 

 made on a relative basis by hemocytometer counts 

 of PIB's in aliquots of fresh tissue. Degree of latent 

 infections, however, may be estimated only with 

 great difficulty through laborious EM examina- 

 tions. Over 2,000 PIB's/mm^ of hepatopancreatic 

 tissue are considered a heavy infection as deter- 

 mined by hemocytometer counts. Heavy patent 



