FISHERY BULLETIN: VOL. 76, NO. 1 



lethal concentration for 48 h in pink shrimp was 

 0.2 ppb (D. Coppage, pers. commun.). No his- 

 topathogenesis has been reported for penaeids ex- 

 posed to organophosphates. 



Conte and Parker ( 1975) found Malathion ae- 

 rially applied to flooded marshes in Texas caused 

 from 14 to 809c mortality in brown and white 

 shrimps held in cages. They recommended that 

 Malathion not be applied to flooded marshes that 

 maintained shrimp. 



Both organophosphates and carbamates are po- 

 tent acetycholinesterase ( AChe) inhibitors. Little 

 evidence of early, presyndromic inhibition of 

 AChe activity in the ventral nerve cord of pink 

 shrimp was found, but inhibition as high as 75% 

 was found in moribund shrimp exposed to Mala- 

 thion (Coppage and Matthews 1974). 



Carbamate pesticides have not been tested 

 much in regard to penaeid shrimps, but it is known 

 that Sevin is lethal to other shrimps and crusta- 

 ceans when applied to field sites in the marine 

 environment (Haven et al. 1966). J. Lowe (pers. 

 commun.) has found carbaryl (Sevin) to be quite 

 toxic to penaeids (Table 4) in laboratory tests. 



Petroleum 



Very little information exists on the effects of 

 petroleum or oil products on penaeid shrimps. This 

 is surprising because many offshore oil producing 

 areas are also penaeid shrimp producing regions. 



Anderson et al. ( 1974) and Cox^ reported results 

 of studies on the toxicity of No. 2 fuel oil on the 

 brown shrimp. The 24-h median tolerance limits of 

 juvenile brown shrimp exposed to components of 

 No. 2 fuel oil (naphthalenes, methylnaphthalenes, 

 and dimethyl napthalenes) ranged from 0.77 to 

 2.51 ppm. The naphthalenes were the most toxic 

 components of fuel oil. Refined oils. No. 2 fuel oil, 

 and Venezuelan bunker C oil were more toxic to 

 brown shrimp than was Louisiana crude oil. Cox 

 reported that the higher content of toxic aromatics 

 in the refined oils above accounted for their higher 

 toxicity to penaeids. 



Yarbrough and Minchew'° reported several his- 

 tological lesions in penaeids exposed to 2.0 ppm 



^Cox, B. A. 1975. The toxicity of no. 2 fuel oil on the brown 

 shrimp Penaeus aztecus. In Program of the first workshop on the 

 pathology and toxicology of penaeid shrimps. U.S. EPA, Gulf 

 Breeze, Fla., 12 p. 



'"Yarbrough, J. D., and D. Minchew. 1975. Histological 

 changes in the shrimp related to chronic exposure to crude oil. In 

 Program of the first workshop on the pathology and toxicology of 

 penaeid shrimps. U.S. EPA, Gulf Breeze, Fla., 12 p. 



sonified crude oil. Nonspecific lesions were de- 

 scribed in the cuticular chitin, the lining of the 

 gastric mill, and the mouth region of shrimps. The 

 proliferation of cells and necrosis in the basal por- 

 tion of gill filaments was reported as a more 

 specific lesion associated with exposure. These ef- 

 fects should be examined carefully in relation to 

 "shell" disease resulting from natural conditions. 



Heavy Metals 



Cadmium 



Unusually high levels of cadmium have been 

 reported from certain estuarine areas in which 

 penaeid shrimps commonly occur (i.e., Laguna 

 Madre, Corpus Christi, Tex.). This metal is also a 

 pollutant component from several industrial 

 effluents that are emptied into aquatic systems. 



In experiments at Gulf Breeze, Nimmo et al. 

 (1977) observed that in pink shrimp exposed to 

 approximately 760 ppb cadmium (as CdCla) for 9 

 days or longer an unusual darkening of gills oc- 

 curred which eventually led to complete blacken- 

 ing of gills of a significant number of exposed 

 shrimp. Control shrimp did not develop black gills. 

 In other tests, it was found that the hC^^ of cad- 

 mium in 30 days was 718 ppb, and during these 

 tests many exposed shrimp developed the black 

 gill syndrome prior to death (Figure 39). 



I have completed light and electron microscopic 

 studies of gill tissues from exposed blackened gills 

 and control gills of surviving pink shrimp which 

 Nimmo supplied from his tests (Couch 1977). My 

 findings indicate that the gross blackening of gills 

 results from necrosis of subcuticular tissues (gill 

 epithelial tissue) (Figure 40a, b). This necrosis 

 stems from the death of cells in the distal gill 

 filaments (smallest unit in gill of shrimp). Actual 

 cell death occurs prior to gross blackening in tiny 

 foci, followed by gradual involvement of the whole 

 filament. Electron microscopy reveals polymor- 

 phic black deposits in the cytoplasm of moribund 

 or necrotic cells (early around mitochondria, later 

 throughout). A complete loss of structural and, 

 probably, functional integrity of the gill soft tissue 

 (Figures 41, 42a, b) leads to organ necrosis. How- 

 ever, the cuticle and epicuticle remain intact at 

 the ultrastructural level and hold the moribund or 

 necrotic soft tissue within their boundaries. 

 Grossly, apparent melanization of injured gill 

 filaments account for the blackening syndrome. 

 However, EM (Figure 42a, b) does not present 



32 



