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VIMS Articles
2000
Progression Of Diseases Caused By The Oyster Parasites, Perkinsus Marinus And Haplosporidium Nelsoni, In Crassostrea Virginica On Constructed Intertidal Reefs
Aswani Volety Virginia Institute of Marine Science
Frank O. Perkins Virginia Institute of Marine Science
Roger Mann Virginia Institute of Marine Science
PR Hershberg
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Recommended Citation Volety, Aswani; Perkins, Frank O.; Mann, Roger; and Hershberg, PR, "Progression Of Diseases Caused By The Oyster Parasites, Perkinsus Marinus And Haplosporidium Nelsoni, In Crassostrea Virginica On Constructed Intertidal Reefs" (2000). VIMS Articles. 483. https://scholarworks.wm.edu/vimsarticles/483
This Article is brought to you for free and open access by W&M ScholarWorks. It has been accepted for inclusion in VIMS Articles by an authorized administrator of W&M ScholarWorks. For more information, please contact [email protected]. Journal of She/lfis/1 Resec,rch. Vol. 19. No. I. 341 - 347. 2000.
PROGRESSION OF DISEASES CAUSED BY THE OYSTER PARASITES, PERKJNSUS MAR/NUS AND HAPLOSPORl_DJUM NELSONJ, IN CRASSOSTREA VIRGINICA ON CONSTRUCTED INTERTIDAL REEFS
ASWANIK. VOLETY1·* FRANKO. PERKINS,2 ROGER MANN,3 AND PAUL R. HE.RSHBERG4 1Na1ional Research Council U.S. Environ,nentaf Protection Agency Guf;f Ecology Division J Sabine Island Drive Gu(f Bree:,e, Florida 32561 2 U11iversity of Ha1vaii at Manoa 105 Bac/111101111 Half 2444 Dole Street Honolulu, Ha waii 96822 3 School o,f Marine Science Virginia Institute of Marine Science College of Willia,n and Mary P. 0. Box 1346 Gloucester Point, Virginia 23062 4 Meteorology Deparnnent Florida State University Tallahassee, Florida 32306
ABSTRACT The progression of diseases caused by the oyster para~ites Perki11sus 111ari.J1us and Naplosporidii1111 11elso11i were evaluated by periodic sampling (May 1994-December 1995) of eastern oysters Crassostrea virginica on an artificial reef located in the Piankatank River, Virginia. The infec1ions observed were recorded as a function of: (I) prevalence and intensi1y; (2) oyster size and age; and (3) deplh below mean low water al which the hos! oyster was found on Lhe reef. Only a very small number of oysters were infected wilh the cwo species of pathogens on the oyster ree r during the first 11 monlhs of life. In the second year of oyster li fe, epizootiological patterns of disease development fol lowed temperarure and salinity trends. Oysters at residence depths :S45 cm below mean low water exhibited significantly (P < 0 .000 I ) lower prevalence and intensity of infections than oysters at depths 2 90 cm. In contrast, oysters at resideJ1ce deplhs 290 cm had significantly higher growth rates (P < 0.05) than those at <45 cn1. However, size differences were not significant (P > 0.05) at the end of the Study. Results from this study may be used in managing oyster fisheries on natural or artificial reefs.
KE Y Yl'ORDS: Crassos1rea virginica. Perkinsus 111ari1111s, Naplosporidium nelsoni. artifi cial reefs. disease progression, growth
INTRODUCTION lack of three-dimensional complexity observed in natural in tertidal communities. Little is known about the colonization and ecology Eastern oysters Crassosrrea virginica were an economic and of C. virginica on intertidal reefs. In addition, the advantages of ecological resource in the Chesapeake Bay until the early 1900s oyster settlement on constructed reefs are not wel I understood. (Hargis and Haven 1999). Years of overharvesting, diseases Therefore, this study was condu cted to detemtlne: ( 1) whether caused by the path ogens Perkinsus 1nari1111s and Haplosporidiun1 residence depth influenced the extent or intensity of disease infec nelsoni. envi ron1nental degradation, and poor resource manage tion: and (2) the size and age at which oysters becan1e infected and ment have led to a dran1atic decline in oyster populations in the the depths that resulted in significant i nJections. Observations from Chesapeake Bay (Andrews 1988, Haskin and Andrews 1988). To the present study are of interest to individuals responsible for day, Virginia's oyster population is less than I o/o of what it was just constructing arti ficiaJ reefs and individuals who must detennine 35 years ago. (Wesson et al. 1999). Various efforts have been when to harvest oysters to a void excess losses. initiated to reju venate dwindling local oyster populati ons. These include spreading of hatchery-reared juvenile oysters on natural l\llETH 0 DS AND MATERIALS oyster beds in estu aries, spreading oyster shell in an attempt to increase hard substrate for settlement of oyster larvae. and con Perki11s 11s 1nari1111s /11fectio 11s struction of artificial reefs. Rejuvenation efforts, such as spreading Oysters were assayed for the presence of P. 111ari1111s using the thin layers of shell over coastal and estuarine bottom for larval Ray's Auid thioglycoll ate n1edium technique (Ray 1954). Samples attachment have had lirn ited success. This may be due in part to the of gi ll and digesti ve gland were incubated in th e medium. Perkins (unpublished data) detennined that these organs can more fre *Current address: Florida Gulf Coast University, I 0501 FGCU Bl vd. South. quently detect the presence of the parasite when infections are , ery Fon Myers. FL 33965; email: [email protected] li ght or light than when n1antle or rectal samples are used. The
34 1 342 V OLETY ET AL. intensity of infections was recorded using a 1uodification of the following spring (April I 4. 1995), another 350 oysters fron1 the Mackjn scale (M ackin 1962) in which O = no infection. l = very sarne Ja1nes River site were placed on the reef and 350 at VIMS as light. 2 = l ight, 3 = lighi- moderate, 4 = 111oderate, 5 = mod in the previous year and sampled until none remained. erate-heavy, and 6 = heavy. Statistical Analyses Haplosporidic11n nelsoni Infections The effects of depth and sampling time (age) of oyster on Hap/osporidit1111 nelsoni was detected using histologi ca l, par disease susceptibility (prevalence and intensity of infection) to P. affin-en1bedded sections stained in hematoxylin and eosin. The 1nari11us and H. 11elsoni \Vere exan1ined using logistic regression scale of Burreson et al. (1988) was en1ployed to record intensities analysis (Agresti 1990). The differences in growth of oysters of infections where O = no infection, I = eel.ls were rare, 2 = sampled at s;45 cm and > 90 cm depths during different sampling fewer than t\vo cells per field of view (40x objective), 3 = t\VO times was assessed using a two-way analysis of variance five cells per field of view, and 4 = more than five cells per field (ANOVA) of view. RESULTS Oyster Sa111pli11g Te111perature and Salinity From M ay 5, 1994 to Decernber 14, 1995, the progression of Ten1peratures and sali nities during the study period showed diseases caused by the oyster parasites P. 1narin11s and H. nelsoni typical seasonal patterns. hjgher ten1peratures during sumrner were evaluated by periodic sa111pling of oysters that had naturally n1 onLhs and lo\ver during \vinter montl1s (Fig. I). Salinity ren1ained set on the artificinl reef located in the Piankatank River. Virginia, fairly constant during the study period. Ten1perature and salinity in August 1993. The reef was constructed by the Virginia Mari ne ranges during the study period were 2-30 °C and I 0-20 ppt. The Resource Commission using aged oyster shells. Details of reef conversion between oyster age and san1pl ing dates is presented in construction are described else\vhere (Bartol and Mann 1997). Table I . Sampling of oysters was conducted once every 2 co 4 weeks during the study period. Oysters were obtained by hand or by using oyster Perkinsus 111ari1111s Infections tongs, depending on the depth. Six samples of 25 oysters each were obtained for each sample time at two l ocations on the reef. No P. 1nari11us or H. nelsoni cells were foLU1d in the 25 adult T he base of the reef was 2- 3 m below mean low water. Prevalence oysters san1pled before the deployn1ent of the oysters at Pianka and intensity (\veighted prevalence) of P. 1nari1111s, and H. nelsoni tank River and VIMS. P. 111ari11us prevalence (Fig. 2a) and inten infections, oyster size and age, and depth below n1ean low water at sity (Fig. 2b) ln oysters set on the Piankatank reef indicate th at which the hos t oyster was found on the reef were 111easured. The infections did not appear until 14 weeks into the study ,vhen the total nun1ber of reef oysters sampled \Vas 3,908. With respect to oysters \Vere I year old (Table I). For the next 44 weeks or until depth. the data were analyzed according to the oyster's residence the oysters becan1e I year and 10 months old, the number of depth on the reef: s;45 c,11 and ~ 90 crn mean low water. The infected oysters ranged bet1veen 15 and 35o/o; i n the ensuing 2 observations are expressed in terms of number of weeks after months, the prevalence rose rapidly to 100%. Oysters then exhib setting. Most of the set Ln 1993 occurred from A ugust 5 to August ited high prevalence (nearly IOOo/o) until the end of the study, when 12. To facilitate the handling of the data, August I 2 was selected the oysters ,vere almost ?.5 years old. The infection intensities as the date of set. during the plateau phase remained mostly below very I ight until The progress ion of infections in the reef-set oysters ,vere corn the end of the plateau ( I year, IO 111onths old). rose rapidly to pared with the progression through a population of adult oysters. 111oderate to moderate-heavy at 2+ years old, follo'A1ed by a decline Uninfected, adult oysters (350) \Vere obtained fro,11 the upper to light and light-111oderate at the end of the stud y. James River seed beds (Horsehead rock). a region known to have Perki11s11s 111ari1111s prevalence 1,11as significantly higher (P < low P. 111ari1111s and H. r1elso11i infections in oysters (Burreson and Ragone-Calvo 1996). These adult oysters were placed in plastic 35 ~------~ - • - Temperature mesh bags and then were placed on the Piankatank River reef near -Q. the san1ple si tes for the reef oysters: placen1ent was June 16. 1994. .9: 30 -- Salinity -~C the time or the third san1pling of the reef oysters. T he depth of m 25 en placement was about midway between the top and bottorn of the 1! reef {ca. 100 cm belo\v mean low ,vater). At the ti111 e of placement. m 20 a sample of 25 oysters wa~ analyzed for the presence of the two i!! 15 paras ites, using techniques described previously. To confirm that :, Ti! the parasite detection n1ethodology was being properly applied and [ 10 to check for patchine:.s in distribution of the parasites. J:imes E 350 {!!. 5 River oysters from the sarne population used on the Piankatank River reef \Vere pl aced in plastic mesh bags in the York Ri ver o-----~------~-~- behind the Virginia ln~titute of Marine Science (V IMS), an are:1in 30 40 50 60 70 BO 90 100 110 120 •Nhich both disease!> nre con1monly present at high levels. Treat- Oyster age (weeks) 111ent or the 350 oy~ters held at VIMS ,vas the san1e as described figure I. Ten1pcratures and salinities at the reef site during the study for the 350 adult oysters deployed in the Piankatank River. Each ns a fun ction of oyster age. The conversion of oyster age to correspond batch of 350 oysters was sampled ('.!5 oysters per san1pling tin1e) to sampling dates is presented in Table J. Discontinuities in the curves simultaneously with the ree f oyster~ until none ren1ained. Jn the denote lack of data. D ERl\10 AND MSX LN OYSTERS ON ARTIFICLAL REEFS 343
TABLE 1.
-2!~ 60 Sampling C ';fl Oyster Tin1e ~ 40 Sampling Age Elapsed Ten1perature Salinity I Date (weeks) (weeks) (OC) (ppt) f'J 20 May 5. 1994 38 0 NA NA May 26 4 I 3 20 10 June 16 44 6 27.8 12 June 30 46 8 26 17 20 40 60 80 100 120 140 July 15 48 JO 29.8 16 July 28 50 12 27 16 August 12 :,_-, 14 27.5 16 -i 5 • <45cm August 26 54 16 26 16 C Q) • >90cm September 8 56 18 22.8 16 .'.:.- 4 September 23 58 20 21 16 2l C Occober 5 60 22 19 NA Q) 3 October 20 62 24 NA NA "'> November JI 65 27 NA NA a.~ 2 December 8 69 31 I I 16 ~ January 12, I 995 74 36 7 14 ~ 1 'iii February 10 78 40 2 16 :;: March 13 83 45 8 12 0 April I 4 87 49 14 14 May 11 19 14 91 53 20 40 60 80 100 120 140 June 15 96 58 23 16 Oyster age (weeks) June 30 98 60 27.8 18 July 13 100 62 29 L9 Figure 2. P revalences (a) and intensities (weighted incidences) (b) of July 31 103 65 31 19 Perkinsus 111ari1111s infections in Pian katank River reef oysters that set August 24 106 68 27.2 19 in August 1993 ar e presented as a function of oyster age and depth of September 18 110 72 23.5 20 resid.ence below mean low water ($45 cn1 and >90 cm). October 24 I 15 77 18 20 December 14 122 84 NA NA then declined precipitously to ahnost 0% ,vhen the oysters were over 2 years old, fo llowed by a slight increase. which re n1 ained 0.000 I) in oysters collected from depths .::90 cm con1pared to below 10% for the final 4 n1onths of the study. The intensities of th ose from :S45 cm (Fig. 2a). Prevalence significantly increased (P infections peaked at the age of nearly 2 years. which was I n1onth < 0.000 I) in oysters from all depths with increasing age of oysters. before the prevalence peak \vas reached, and declined almost as indicating that continued expos ure to P. 111ori111.1s or increasing age rap idl y as did the prevalence (Fig. 4b). of oysters results in increased infection . Sinular results were ob Similar to P. n1ari11us infections, oysters collected from .::90 served ,vhen P. 111arinus in fect ion was expressed as \Veighted cm depth had a significantl y higher prevalence and intensity of H. prevalence. Although the difference in infection intensity \vas not nelsoni infections compared to lhose from :S45 cm depth (P < as great as the prevalence, it was signi fican tly higher at the greater O.OOOJ) (Fig. 4a,b). In addition, H. 11elso11i prevalence and inten depths (P < 0.01 ) and significantly increased in oysters fro n1 both sity increased with increasing oyster age (P < 0.000 I). depths wi th age ( P < 0.000 I). Haplosporidiun111elso11i infections (Fig. 5a,b) were nearly non Perkinsus ,narinus infection prevalence was the same in adult existent in the Piankatank Ri ver reef oysters during 1994; whereas, oysters held in plaslic mesh bags at the York Ri ver and at the in the York Ri ver stock, infections were above a prevalence of Pi ankatank Ri ver reef during 1994. fn I 995, in fection was ex 60% during the summer nnd fall of 1994. pressed earlier at lhe Pi ankatank Ri ver and reached I00 % 15 weeks before those held in the York Ri ver (Fig. 3a,b). Growth and Si~e
Haplosporidi11111 11elso11i /11fectio11 s The san1pling ti 1ne and the residence depth of oysters signifi cant ly influenced the growth of oysters (P < 0.00 I) (Fig 6). Oys Prevalence of H. nelsoni was n, arkedly different from that of P. ters at both depths grew 'Aii th increasing age (P < 0.001) and n1arinus in reef oysters (Fig. 4a). With the exception of one lightly sampling time ( P 0.00 I). Oysters at depths .::90 cn1 had signifi in fected. 50-\veek-old oyster. the onset of H. 11elso11i infections did cantly greater growth th an oysters at depths :S45 c1n. Although the not occur until the oysters ,vere over 1.5 years old, as opposed to differences in size were pronounced during age 56-1 00 weeks, the appearance of P. ,narinus in I-year-old oysters. Thereafter, the they \vere less pronounced during oyster ages 103-122 \veeks. and infection prevalence of H. nelsoni rose rapidly, reaching a maxi insignificant (P > 0.05) at the end of the study. The rate of oyster mum of 45o/o when the oysters were 21 months old. The infections growth, as es1in1ated from size measuren1ents. decreased 4 weeks 344 V OLETY ET AL. a 100 .------==------..•- ~ - -, • PR •• • <45cm -~ • YR 2"' ~ 80 f • > 90cm 0 I ~ I I ,2 60 I C I 0;,R I ~ 40 I •I 20 I I I ~
0 +-tllii~---r---.---,------.;:..-----,----,--1 0 10 20 30 40 50 60 70 80 90 30 40 50 60 70 80 90 100 110 120 b 2.------~ ;:;. • < 45 cm • PR -.iii -.~ C • >90cm (/) 5 • YR Q) C C Q) - -C 2l 4 C Q) ~ 3 I ~ a. '"/ Ii ~ j 2 I .c J 0, I ~ 1 I • o+-.._.• 0 --f-,. 30 40 50 60 70 80 90 100 110 120 0 10 20 30 40 50 60 70 80 90 Oyster age (weeks) Sampling time (weeks) Figure 4. Prevalences (a) and intensities (weighted incidences) (b) of Figure 3. Prevalence (a) and intensity (weighted incidences) (bJ of Haplosporidi11 111 11elso11i infections in Piankatank River reef oysters Perkins11s 111ari1111s for adult oysters i111ported Crom the upper .Jan1es that set in August 1993 as a function of oyster age and depth of resi River and placed on the Piankatank Ri ver reef and in the Yor k River dence below mean low water (915 cn1 and e::90 cm ). behind the Virginia Institute of Marine Science. Oysters (350 at each site) were twice placed at the sites and assayed until the popul ations were depleted by sampling and natural 1nortalities. The disease organ clearly indicates that residence depth of oysrers significantly in ism data arc expressed as a function of site and san1pling time in the fluences prevalence and intensity of P. 111ari1111s and H. 11elso11i study. infeclions. Oysters that are growing at ::S45 c1n depth can be expected to have lower prevalences and it1tensities of infections of both patho before the first P. 111ari1111s infections ( 10 weeks and 1-l ,veeks into the study) (Fig. 6). gens con1pared to those living at >90 c111 depth (figs. 2a.b. and -la.b). The prevalence and intensity of P. 111ari1111s in reef oysters DISCUSSION from the current study, v,hile agree ing with those of Mackin ( 1962). differ from studies by Quick and Mackin ( 197 1) in the Interpretation of epizootiological data such as Lhose generated Atlantic and Gulf of Mexico coasts of Florida. Weighted inci in this study is confounded by n1any factors that dictate disease dences (intensities) in their study sho"•ed a decrease with increas prevalence and intensity. These include ten1perature. salinity, \Va ing depth and no effect of depth on prevalences Fro n, intertidal to ter quality, density or oysters. patterns of water n1overnent, oyster 3 111 below n1ean low ,vater. Sin1ilarly. Bu1Tell et al. ( 1984) found age and/or size. genetic strains. physiological condition. food higher prevalences and intensities of P. 111ari1111s in intertidal oys availabi lity (density and species composition of planktonic food ters than in subtidal oysters. M ackin ( 1962) speculated that lower organis1ns prese nt). and nun1bers and levels of other parasitic spe infection prevalences and intensities in intertidal oysters 1nay be cies causing stress on the oysters. A further complication is the fact because these oyster~ are not exposed to a~ many infective cells as that the reservoir of H. nel.1011i infecLive cells is unkno,vn. and subtidal oysters by virtue or the increased an1ount of time they are tran sn,ission of infections is not frorn oyster-to-oyster as \ViLh P. closed and not feeding. 111ari1111s. Despite these con1plicating fac tors, patterns of dise:1se Growth or oysters at both the depths (::S-l5 cm and .::90 cm) progression of both the diseases and oyster growth al differen t decreased fron, age 74 weeks, and coincided ,vith increased P. residence depths we re apparen t. The residence depth of the oysters n1ari1111s incidence in oysters. The decrease in gro,vth of oysters relative to mean low water is of considerable interc~t. because the upon acquisition of P. 111arinus infections upport the findings of pre111i ~c behind construct ion of artificial ree fs is that Lhe survival of Paynter and Bun·eson ( 1991 ) who observed a decrease in the oy~ter~ in the presence of P. 111ari1111s anll H. 11elso11i wi II be en gro\vth rate of juveni le and adult oysters in1111ediare ly after or j ust hanced if they are grown in the n1orc natural environn1ent of an before infection. Haplosporidi11111 11elso11i did not see 1n for n1ore oy~ ter shell reef off the hotto111 of the estuary. In fact, this study than 7 1nonths after the change in gro,vth rate, and it is concluded D E~10 AND MSX IN OYSTERS ON ARTIFICIAL REEFS 345 a 100 70 PR • <45cm -~ ~ • "'Q) . YR • 60 >90cm 80 • ->, - ,~ .I... ~ "'0 "'O I I •• Q) 50 I' ~ -u l .. E ~ 60 - • I C I E Ir 40 -Q) Q~ N ~ I ~~\ cii Q) 40 . •I u I \ I C I \ 30 f .!!? l it' m I ~ . I ~ 20 a. I • 20 / I I t 10 ~~~~~-~~~~~~~~~~~~ 0 ~ - ., ' ' ' ' ' 20 40 60 80 100 120 140 0 10 20 30 40 50 60 70 80 90 Oyster age (weeks) Figure 6. Piankatank Ri ver reef oysters that set in August 1993 and b 4-,------, PR were sampled for the disease studies. Sizes are presented as a function ~ ?;- • ·oo • YR of oyster ages and depth of residence below mean low water (<45 cn1 C Q) ~ and >90 cm). -C 3 ~ I~ • Q) u C areas into containers in an enden1i c area (Ray 1953, 1954. Mackin Q) m l • 1962. Paynte r and Bun·eson 199 L). Place,nent in containers pro > 2 Q) I' • a.~ vides a greater degree o f experin1enral cono·ol. but artificial den "'O I Q) I sities o f oysrers can lead to results different from those in naturally ,::- I I "\ Ol 1 set popul ations, where distances vary from oyster to oyster. Q) I ,. \ ~ I • The prevalence and incensi1ies of infections of P. ,na rinus in • I reef oysters generally follo\ved the patterns dictated by tempera I rure and salinity tre nds observed in earlier studies (e.g. . Soniat 0 10 20 30 40 50 60 70 80 90 1985, Andre\vs 1988. Burreson 199 1, Burreson and R agone-Calvo Sampling time (weeks) 1996. Ray 1996). P. 111ari11us in fections in oysters rose in the spring. peaking in October and November. and declined in the Figure 5. Prevalence (a) and intensity (weighted incidences) (h) of \Vinter n1onths into the spring. Intensities of infections were more Haplosporidi11111 11elso11i for adult oysters imported from the upper nearly ret1ective of previous reports in that the peaks for ihe t\vo James River and placed on the Piankatank Rj ver reef and in the York Ri ver behind the Virgirua Institute of l\1arine Science. Oysters (350 at depths 1vere in October and November and the minima in M ay of each site) were twice placed at the sites and assayed until the popula the fol101ving year (Fig. 2b). Therefore. assuming that te mperature tions were depleted by sampling and natural n1ortaUties. The disease and salinity values approximate those of the stud y period and organism data are expressed as a function of site and sampling time in given the infection intensities and levels, oyster mortalities fron1 P. the study. n1arinus can be expected to begin 13 n1onths after setting, rising most signi ficantly 22 months after setting. that P. 111arinus ,vas responsible for the decreased growrh rate. The Considering the face that the salinity values recorded during the decline in oyster sizes after the age of 2 years (65 \veeks inro the first year after setting did not go belo1v 10 ppt. and most of the ti1ne study) is believed to be arributable 10 death of the larger oysters were > L6 ppt. it is reasonable to assun1e that infections fron1 these from infections of the t,vo pathogens. two diseases did not occur before May 5. 1994. when sampling The higher gro\vth of oysters residing at depths 2:90 cm than began. This assun1pti on is based on other studies that observed those at <45 cm is urprising. Given ihe higher infection preva when a popul ation becon1es in fected, the infections do not disap lence and intensities of both P. 1nari1111s and H. nelso11i in oysters pear (or decline) unless the salinity decreases belo\V 10 ppt for an at depths 2:90 cm, \Ve would expect that these oysters wou Id gro,v extended period (Andrews and Hewan 1957, Ragone and Burreson less because of d isease pressure. The biological. che mical. and 1993. Burreson and Ragone Calvo 1996). physical processes associated with ihe bottom ,vaters 111ay influ Previous studies have noted that oysters are refractory to ac ence the physiological and defense responses of organisn1s inhab quiring infections in the first year of life (Ray 1953. 1954) and iting these areas. Organic n1 atter near the bottom of the reef close becon1e increasingly 111ore susceptible into the second year, with to Lhe sedin1ent has been speculated (Dahlback and Gunnarsson significant prevalence, incidence. and mortali ty being observed 1981) to have contributed to the increased growth in oysters from then (Andrews and Hewitt 1957). That pattern was observed in the >90 cm. However, at the end of the study, the differences in sizes present study (Figs. 2a.b and 4a.b). As menti oned above. the con1 - of oysters fro m the t\VO depths were noL significant. plicating factor was Lhe low level of infection pressure from H. The presen1 dataset is unique. because it is the first ti,ne a nelsoni in the first year of li fe at the reef. P. 111arin11s infections in population of naturally set oysters of kno\vn age has been assayed oysters are dose-dependent (Mackin 1962. Chu and Volety 1997). in si111 for progression of infections by P. 1nari1111s and H. 11elsoni and small oysters probably fil ter less volun1es of water to acquire over an extended period of Lin1e. Other epizootiological studies enough infective cells of the parasite ro initiate an infection (Bur have involved placing naturally set or hatchery set oysters of reson 1991, Burreson and Ragone Calvo 1996). Results fron1 the known age in containers in an endemic area or placing adult oys current study indicate that in th e first LI 1nonths of life, only a \'ery ters of unknown ages from nonendemi c or marginally ende1nic s1nall number of oysters on the oyster reef become infected \vith 346 Y OLETY ET AL. the two species of pathogens. The question that cannot be an 4a). and the population did not otherwise begin to show infections swered is whether the prin1ary factor in encouraging or pern1itting until the oysters ~1ere over 1.5 years old. It is possible that this lag a rapid increase in prevalence was temperature. oyster age. or can be attributed to: ( J) th e oysters being young and, thus, less salinity. The best answer probabl y is that aU three played interac susceptible, as has been reported fro1n other studies; and (2) the tive roles. fact that even the susceptible, imported adu lt oysters did not ac Data for adult oysters imported from the upper James Ri ver quire very many infections at the Piankatank Ri ver reef (Fig. Sa) seed beds, whi ch represent a di sease-susceptible population, con in the first year of life. It was clear that H. 11elso11i was present in firmed that the two pathogens were present in the study area and strength in the nearby York Ri ver (Fig. 5a) bu t not in the reef area, in the neighboring area of the lower York River (Figs. 3a,b and thus iUustratLng the patchiness in distribution of the reservoir of 5a,b). They were used pri1narily to indicate presence or absence of infective ceUs, at least in that part of the Chesapeake Bay. The H. 11elsoni, because it is known to fluctuate greatly, sotne years decline in prevalence and Lntensity of H. 11e/soni in reef oysters being nearly absent from the lower York Ri ver region. (Andrews (Fig. 5a.b) was 1nore precipitous that has been previously reported 1988, Haskin and Andrews 1988). using imported susceptible adult oysters (Haskin and Andrews ll is interesting to note that P. n1arin11s infection prevalence was 1988). In 1995. a different pi cture of H. nelsoni infection distri the san1e in oysters held in the York Ri ver and at the Piankatank butions in the in1ported, adult oysters was observed (Figs. 5a.b). Ri ver reef during 1994, but in 1995 was expressed earlier in the The prevalences and intensi ties were quite sinl.i lar at the two sta Pianka tank Ri ver and prevalence reached I 00%, J5 weeks before tions, with the infections appearing earli er at the York River sta those held in the York Ri ver. One would have expected that the tion and lasting longer in the popul ation. Nine more weeks of data oysters held in the York Ri ver woul d have shown a higher preva were obtained fro1n the York Ri ver stock. because the stock at the lence, because salini ties were about 5 ppt above those of the Pi reef was depleted by 1nortalities earlier, probably caused by P. ankatank River and th us woul d have presented 111ore favorable n1ari11us infecti ons (Fig. 5a,b). salinities for expression of P. 1nari11us. On the other hand. in 1994, Given the decreased susceptibi lity of oysters to P. rna ri11us and H. 11elsoni infections were nearl y nonexistent in the Piankatank H. nelsoni at residence depth of < 45 cm compared \vith oysters at River reef oysters: whereas. in the York River stock, infections > 90 cm, it seems that pil ing of shells and constructing arti ficial \Vere above a prevalence of 60 o/o during the summer and fall of reefs is a better strategy for rej uvenating oyster stocks th an spread l 994 (Fig. 5a). These observations reaffinn the necessity of havin g ing thin layers of oyster shells on the bonom in estuari ne and a stock of susceptible, adult oysters present in a study where ju coastal areas. Future studies should in vesti gate the survival di ffer veni le and young oysters are being observed. ences in oysters at di fferent depths and the factors responsible for The reef oysters > 2 years old can reasonabl y be compared to differences in growth rates of oysters at di fferent depths. the imported oysters in terms of response 10 the diseases. A It hough P. rnari11us prevalences and intensities of infections were similar in ACKNOWLEDGMENTS Lhe two groups of oysters at the reef, H. 11e/so11i data suggest that the reef-set oysters were n1ore resistant to those infections. Ln1- This project was fu nded. in part. by the Virginia Council on the poned oysters at the reef reached a peak of 68% in fec ti on (Fig. 5a); Environment's Coastal Resources Management Program through whereas, the reef oysters peaked at 36 and 45%, depending upon Grant NA370Z0360-0l (task 16) of the National Oceanic and At the depth of residence (Fig. 4a). Likewise, the intensities of H. rnospheri c Adn1inistrati on, Office of Ocean and Coastal Resource 11el:so11i in fections had a mean level of 2 in imported oysters as Management Act of 1972 as amended. We thank Kenneth Walker opposed to 1.3 in the reef oysters. Therefore. soo,e advantage and Lan Bartol for assistance in field operati ons, and Ms Juanita seems to have been obtained for the reef-set oysters, if we can Walker for her techn ical assistance. Insightful con1nJen1s on the neglect 111 in or age differences. previous drafts of th is manuscript by Dr. Wi ll ia1n S. Fisher are The data for H. 11elso11i was son,e\vhat surprising, because onl y greatly appreciated. Contribu tio n number I 062 of the U.S. Envi one oyster was found to be infected in the fi rst year of li fe (Fig. ronmental Protecti on Agency. Gul f Ecology Di vision.
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