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American oysters Crassostrea virginica exposed to high concentrations (600 mg I-') of nnitrosodiethylamine (DENA) during winter (February to May) showed significant enhancement of an epizootic apicomplexan parasite, Perkinsus rnarinus. The parasite reproduced and caused atypical lesions in exposed oysters in water temperatures at its lower range (20°C). The reasons for this enhancement are not clear but may reflect damage to the oysters' nonspecific, cellular defense mechanisms by the DENA without concomitant negative effects on the parasite. INTRODUCTION ginica, with the chemical carcinogen DENA. Histopathological consequence of the infections and possiPerkinsus marinus, formerly Derrnocystidium manble reasons for the enhancement phenomenon are also num, is epizootic in American oysters Crassostrea virdiscussed. ginica and a significant cause of mass mortality in Gulf coast and mid-Atlantic estuaries of the USA (Mackin 1951, Ray 1954a,b, Dunnington 1956, Mackin & HopMATERIALS AND METHODS kins 1962, Lauckner 1983, Sparks 1985). The taxonomy, morphology and pathology of P. marinus have American oysters Crassostrea vjrginica were colbeen extensively reviewed (Perkins 1976, Levine 1978, lected from East Bay, Santa Rosa County, Florida, USA, Lauckner 1983, Sparks 1985). in November 1986 and held in flow-through seawater Previous investigators indicated that Perkinsus tanks until experiments were begun in February 1987. marinus infections in oysters are enhanced by tenlA baseline sample (50 oysters) was taken at the collecperatures above 20°C (Maclun 1962, Quick & Mackin tion site and 17 individuals were sampled for histologi1971, Andrews 1976), salinities above 15 %O (Mackin cal examination 3 d prior to tests. Exposed and control 1956, Scott et al. 1985), close proximity or crowding oysters were held in static 12 l aquaria during each test. (Mackin 1962, Andrews 1965, 1979), and spawning No attempt was made to feed exposed or control oysstate of the oysters (Ray 1954a, Andrews & Hewatt ters during tests. Temperature and salinity were niain1957, Mackin 1962, Sinderman 1970). Scavengers tained at 20°C and 20%0, respectively. Expenmental (Hoese 1964) and ectoparasitic snails (White et al. 1987) oysters were exposed to 600 mgl-l of n-nitrosodiethywhich feed on oysters infected with the parasite may lamine (Sigma N0258) for up to 28d. act as vectors in transmitting the disease to other oysFour separate tests were conducted over a 14wk ters. period (Tables 1 and 2). Test 1 was designed to deterThis paper reports the first experimentally induced mine acute effects of high concentrations of the carenhancement of Perkinsus mannus in Crassostrea vircinogen on exposed oysters. Samples of 3 exposed and 2 control oysters were taken for histological examinaContribution No. 645 of the Environmental Research Lation at 2 j 4 , l1 and l4 . Additionally1 4 boratory exposed and 3 controls were taken when tests were O Inter-Research/Printed in F. R. Germany 206 Dis. aquat. Org. 5: 205-213, 1988 Table 1. Crassostrea virginica. Results from tests exposing oysters to DENA (600 mg I ' ) . In Test 1 , 22 oysters were taken for histological examination during test (+); 23 survivors were transferred to clean seawater and held for 3 wk after test termination before histological examination ( ' ) Test Date of test No exposed Days exposed No. left at test end Percent sampled at test end with Perk~nsus marin us enhancement 1 Feb 87 45+ 27 23' 100 2 Mar 87 20 I7 5 100 3 Apr 87 20 28 6 67 4 May 87 20 26 7 86 Table 2. Crassostrea virginica. Control oysters from DENA exposure tests. In Test 1, 15 samples were taken during 27 d (+) Test Date of test No. of controls Days held No. left at test end Percent sampled at test end with Perkinsus marinus enhancement 1 Feb 87 25 + 27 10 0 2 Mar 87 20 17 20 0 3 Apr 87 20 28 20 0 4 May 87 20 26 20 0 terminated (27 d). Surviving exposed oysters (23 total) observing 6 microscopic fields on each of 10 slides were transferred to clean seawater and histologically prepared from control oysters and 10 each from examined 3 wk later. exposed and baseline oysters. Values for respective Tests 2, 3 and 4 were conducted between March and groups of 10 slides were averaged to obtain the infecMay 1987 to verify the Perkinsus marinus enhancetion values. Light infections averaged 3 observable ment observed in Test l . In each test, 20 oysters were parasites per field, moderate infections averaged 16, exposed to the carcinogen and sampled for histological and heavy infections averaged more than 170. examination after mortalities were greater than 50 %. Test2 was terminated after 17 d with 5 surviving test specimens and Tests3 and 4 were terminated after 28 RESULTS and 26d with 6 and 7 survivors, respectively (see Tables 1 and 2) . Control, oysters were also sampled at Histological examination of baseline oysters sampled the same time exposed oysters were taken. 3 d before tests showed all individuals with healthy Sampled oysters were grossly examined and l c m digestive gland epithelia and vesicular connecbve thick transverse cuts were taken across the digestive tissue (VCT). Most individuals had light to moderate gland, fixed in Davidsons' fluid (Shaw & Battle 1957) infection5 of Perkinsus marinus in gut epithelia conand embedded in Paraplast". Tissue was sectioned at comitant with some hemocytic response to the patho7,um and stained with Hanis' hematoxylin and eosin gen but no severe histologic damage was observed (Luna 1968). (Fig. 3). Fig. 1 illustrates the general experimental design Results of the 4 tests are shown in Tables 1 and 2. used to evaluate Perkinsus marinus enhancement in Experimental oysters in Tests 2, 3 and 4 began to have oysters exposed to DENA. Microscopic quantification significant mortalities 17 d postexposure to DENA; only of P. marinus infections in test oysters was done to 18 individuals (30%) survived when the tests were obtain relative prevalencehntensity values. The terminated (Table l ) . In contrast, no control oysters number of parasite stages per field (at 4 0 0 ~ ) i.nfecting died (Table 2). Histological examination of moribund or the outer gut loop epithelia (Fig. 2) was quantified by 'gaper' oysters indicated the probable cause of death to be heavy Perkmsus marinus infect~ons. Examination of @ Mention of trade names or commercial products does not exposed and control oysters, after tests were termiconstitute endorsement or recommendation for use nated, showed very heavy infections of P. marinus in ( ~ x ) ' ( s ~ o l l e ) s a n l e h A l ~ s u a l u ~ / a s u a ~ e ~ a ~ d s n u r r e c u s n s u . c p a d j o u o ~ ~ e ~ ~ j ~ ~ u e n b s r d o x o i s ! u r a u ~ u ~ a l a p 0 1 p a s n ( s ~ o l l e ] s d o o ~ ~ e u ! j s a l u l l a i n 0 z a q l a l o N . p a u r u r e x a e a i e l e i a u a 6 a q t 6 u w o q s s d p d a q l M o l a q 1 s n I s s e r r r l e i a x ! A a q l q 6 n o 1 q 1 u a y e l l a j s k o u e j o u o q s a s s s 0 1 3 x ~ s r u , r 6 ~ r ~ e a r l s o s s e r 3 . z 6 ! j 4 0 s u o ~ a 3 a ~ u ~ L ~ e a q U O J J X i l l e 1 ~ o w p u e s L s o q a e d ' b a l s u a a u 1 p a s e a J 3 u 1 ' I p p a s o d x 3 s l l n s a 8 ( a S ~ 0 d S a ~ 3 ~ a K 2 o w a q a w o s 4 7 p i u e a ! u o m o 3 s u o b 2 2 a j u ! ( s a s a q a i ~ d e d a s p ) a l e ~ a p o u 0 3 1 4 6 ~ 1 v 1 r ~ % U U I ) s b e p 8 2 o a L T J O J ' u a h o q l e d 4 0 b a ! s u a ? u l w e a m a l V N 3 d 4 0 l _ l f i u l 0 0 9 ~ h a ~ d * U I w a l a p 0 3 5 l S a 3 a J O J a g 0 1 p a s o d x a s J a l s r ( 0 s A p p a u ~ w e x a X I l e 3 ~ 6 o l o a s ~ ~ s d n o ~ 6 p a s o d x a s e s q u e a 6 u ~ p l o q i e 3 L a u a p t U ! p w l e a U L e u l a n q ' W N ~ U 0 1 p a s o d x a 3 0 U S J J ? S & ) s i s a l p a s o d x a v ~ g a j o s l l n s a l a l e n p h a 0 1 p a s n s p o q l a m j o u 6 ! s a p ~ e l u a u r ~ l a d x g 1 B y ' S J J ~ S X Q u o t a ~ n s o d x a ~ ~ 3 0 4 0 S I ~ ~ J J J a y 1 C p n l s o a p a s n u b l s a p ( ~ l u a w l ~ a d x j 1 a ~ n b l j 208 Dis. aquat. Org. 5: 205-213, 1988 gut epithelia from 15 of 18 (83 % ) experimental oysters Test 1 had no mortalities in experimental or control (Figs. 4 and 5) and only light infections in gut epithelia oysters. Of 18 exposed and 14 control oysters histologiof controls (Fig. 6). cally examined 14 d postexposure, 83 '10 of exposed and Winstead & Couch: Enhancement of infection in oysters exposed to a carcinogen 209 100 % of control oysters showed light infections with the parasite. After 27 d, all exposed oysters sampled (4) showed heavy infections of Perkinsus marinus in gut epithelia identical to Tests2, 3 and 4 (Figs. 4 and 5) while all controls had only light infections of the para-

diseases of aquatic organisms

Enhancement of protozoan pathogen Perkinsus marinus infections in American oysters Crassostrea virginica exposed to the chemical carcinogen n-nitrosodiethylamine (DENA)