W&M ScholarWorks
VIMS Articles Virginia Institute of Marine Science
2002
Transmission Of Withering Syndrome In Black Abalone, Haliotis Cracherodii Leach
CS Friedman
W Biggs
Jeffrey D. Shields Virginia Institute of Marine Science
RP Hedrick
Follow this and additional works at: https://scholarworks.wm.edu/vimsarticles
Part of the Marine Biology Commons
Recommended Citation Friedman, CS; Biggs, W; Shields, Jeffrey D.; and Hedrick, RP, "Transmission Of Withering Syndrome In Black Abalone, Haliotis Cracherodii Leach" (2002). VIMS Articles. 471. https://scholarworks.wm.edu/vimsarticles/471
This Article is brought to you for free and open access by the Virginia Institute of Marine Science at 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 Shellfish Research. Vol. 21. No. 2. 8 17-82-1. 2002.
TRANS1VUSSION OF WITHERING SYNDROME IN BLACK ABALONE, HAl,lOTIS CRACHERODIILEACH
CAROLYN S. FRIEDMAN,1.2·* WENDY BIGGS, 1 JEFFREY D. SHlELDS,3 AND RON,.\LD P. HED1UCK2 'California Depart111e1u of Fish a11d Ganze and 2 Deparllnent of Medicine and £pide111iology. Unil'ersiry of California, Bodega Marine Laboratory. P.O. Box 2-17. Bodega Bay. California 94923: 3 Virgi11ia !11s1i1111e of· Marine Science. 771e College o,f ~Villicun and Mory. Gloucester Point. Virginia 23062
ABSTRACT Wi1henng syndrome (\VS) ha, been associated wHh catastrophic declines in blacls. abalone populauons 1n MJU lhern and central California. In an effon to identify the etiological agent or \¥S anu to character11e the progression of th1:, thscasc, we initiated a transmission study 1n wh ich abalone fron1 Ano Nuevo lsland. a locauon free of WS . ,hareJ aquaria with an imals fron1 Vandenberg Airl'orce Base. a locati on where \VS i, epi;,O(> Lic The mean incuba11on period of \VS (time 10 d.:velop oven sign, of the u"ea,e) wa, 245 days with a mean time to death :Lfrer development uf clinical sign, of 4'.! day,. lvledian lime to death was 4 I wk in Lhe experimentally expo,ed Ano Nue,o Island abalone and 16 "kin the positive control Vandenberg abalone. Cun1u la11ve mortality was significantly different between the negaLi ve control (unexpo,ed) Ano Nuevo l,land abalone (25% 1nnnali ty) and both the exposed Ano Nuevo Island abalone /85o/c mortality: P = 0.000 I) and the posit.Ive control Vandenberg abalone ( I OOo/c mortality: P = 0.000 I). In addiLion, significant differences in preva lence, of a recently de~cribed Rickensiales-likc procaryo1e (RLP), ··ca11dida1 11 v Xenohaliotis californiensis." were observed between negative control animals (no RLPsJ and 1ho~e wi th \VS (both the experimemall y exposed Ano Nuevo Island and Vandenberg abalone \\ere infened "ith RLP, : P < 0.00 1) . All abalone infected with the RLP had ;,1gns of WS. including decrea,ed condiLion rndice,. foot muscle atrophy. and uige~tive gland degencrauon (P < 0.05). No correlation between intensity of RLP infection and degree of \VS "as observed, P > 0.051. sugge,1ing a complex relationship between the RLP and clinical di sease in black abalone. Despite thb. these data in conjunction with a Jacls. of observation or any other signifi cant pmhogen, in the abalone provides evidence that the RLP infecting abalone t"Co11dido11,s Xenohalioris californrensis") is the cuolog1cal age nt of \\IS.
KEY ~VORDS: wi thering syndron1e, bl ack abalone. /111/io1,s. rickcttsiaJcs. "Co11dida1t1s Xenohalio1i, califon11 ens1~"
I NTRODUCT ION (2000) observed a significant relationship bet\veen the intensity of RLP infecLion and degree of WS in cultured red abalone. These Withering syndrornc (WSJ has been associated with cata conllicting data indicate further exan1ination of the role of the RLP SLrophic declines in black abalone populations in southern and in \.VS is " 'filTanted. T hi s study \Vas designed to exan1ine Lhe 1rans central California ( Haaker et al. l 992; Steinbecl,. et al. 1992. Fried n1issibility of WS and to cleten11ine the relationship bet,veen RLP m an and H aaker unpublished data). JnitiaJ studies identified a pre infection and \VS i 11 black abalone. viously undescribed coccidian parasite, 1\1/argolisiella ( = Pseudok lossia) haliotis (Fried111an 1991; Friedn1an el al. 1995, Desser & Bower 1997). in black abalone ,viLh VvS that was subsequentl y IVIATE RIA LS AND IVLETHODS detem1ined to be nonpath ogenic a evidenced by field and labo ratory studies (Friedman el al. 1993, 1997). VanBlaricon1 et al. Animals ( L993) doeu111en1ed WS on San Nicolas I~land in April of 1992. T hese researchers a observed Ri ekettsiales-li ke procaryoce (RLP) HealLh y bl:1ck abalone " 'ere collected on March 28. 1995 fro 111 that \Vas recently described as a ne,v taxon and has been given the Ano Nuevo Island. ,vhere WS had never been observed. B lack provisional status of ··candidc1111s Xenohalioti s cali fo rniensis" abalone ,vith WS ,verc collected fron1 Vandenberg Airforce Base (Friedman et al. 2000). T,vo of six abalone with c linical WS har (Vandenberg) mid Cayucos on April 24, 1995. Abalone 1vere trans bored RLPs. \Vherea~ apparentl y healthy ani111als \Vere devoid of ported to the Pathology Quarantine Facility at the Bodega Marine the RLP. The authors indicated that Rickellsiales-like bacteria Laboratory. 1vhcre they were placed in an 88-L aquaria and rc ,vere co111 1nonly observed in 1n arine invertebrates and chat the cei ved ambient (8- J0°C), tlo,v-1hrough, full -strength eawater. pathogenicity o f' these organi s111s ,vas unknown. Gardner el al. 1\1/acrocystis pyrifera was collected fro1n Bodega Bay and was ( 1995) also observed RLPs in association with \VS in black aba surracc sterili7ed by soaking in a tamed iodine solution CPrepo lone from San Nicolas and San Clen1ente Islands in southern Cali dyne: Westagro, Kansas CiLy. MO) for 15 111i n fo ll o" 'ed by a fornia. Healthy abalone from A no Nuevo Island in central Cali freshwater rinse. Ani111als \vere feel M. pyr(fera t"1ice per week. All fornia were not infected with RLPs. suggesting an associati on abalone ,vere tagged and the fo ll o,ving data ,vere coll ected: n1axi bet\veen the RLP and WS. Friedman et al. ( J 997) exa1nined the mum length, foot length and total volu111e (TV). and total " 'eight association bel\veen the RLP. degenerati on of the digestive g land, (TW). A nin1als were bled fron1 the pallial sin us with a tuberculin and 111ortality in a laboratory study. No clear as~ociali ons bet\\'een syringe and a 26-gauge, 0.5-inch needle and the density, cell -Lype, intensity of RLP infection and e ither condition of the digesti ve and condition of circulati ng he 111ocytes was detern1ined using a gland or ti111e to 1nortality \vere observed. RecenLl y, Moore el al. he1nocytometer. Visual condition of the abalone was assessed ac corcli ng to th e fo l lowing scale: (3 ): healthy abitlone with a foot and *Corresponding author. School or Aquatic anc.l Fishery Sciences. viscera that fi ll s the entire shell volume: (2): visible n1ant le retrac Unr versity of \Vashington, Seattle, WA 98 195. E-mail : carolynf@ tion and n1oderate aLrophy of the foot n1u scle: and ( I ): severe u. was hi ngtoo.ed u atrophy of the foot n1usc:le.
8 17 8 18 fRJEDtvlA ET AL.
1-/istology dornly addec.J 10 each of the two experin1en1al aquaria and to each of the two posi tive control aquaria (PC) (Fig. I ). Ani1nals were Selected tissues \vere placed in 1n venebraLe Davidson· s solu rnaintaine
Expe1·imental Design
} Replicate 1
n=l2 n=12 n=12 n=12
} Replicate 2
n=l2 n= l2 n= 12 n= l2
3 (VAFB)1 (EvVS & EA)2 (Ano N uevo l s. ) } A nin1 als
Positive £xperin1 ental Negative } T reatment Control Control Figure I. Expcrin ental Design. The dark circles represent black aba.lone with \~S collected from the fi eld (Vandenber~ Airforce Ba~e _or 1 1 Carucos (VBCS)). The open circles represent healthy, naive (no exposure to \\IS before study) hlack abalone fron1 Ano ue\ O Island. An11nals with \.VS collected from Vandenber i:t Airforce Base and Cayucos in the positive control treatments. 2Animals fron1 VUCS (~\.VS) or Ano Nucvo Island (EA) \Vith a nd without WS, respectively. in experiu1enta l trea1111ents. 3 Animals in the negative contr ol treatments "'1thout \¥S that were collected fron1 Ano uevo Island. \,VJTHERJNG SYNDRONIE fN B LACK ABALOKE 819
,vere also used to test the independence of RLP infection and \VS. tion be tween in itiation of the study and developn1ent of gros& Ani1nals were grouped as infected and uninfected and as above for clinical signs such as n1antle retraction or v1~ ible atrophy of the survival and heaJth parameters. ln a separate analysis to further foot n1usc le. The 1nean incubation peiiod for the EA abalone ,vas assess the independence of specific lesions and RLP infection 245 days (n = 2 1) \Vi th a range of 154-30 I days. The duration intensity an in1 als were grouped as IO\V overall in fection levels between onset of visible signs of \VS and mortality averaged 42 (0-3) and high overall infection levels (4-6) and the response (e.g .. days (11 = 21) with a range of 6- 1 13 days. The t,vo abalone that metaplasia) ,vas grouped as present or absent. Speam1an rank cor died during the initial ,veek of the study fron1 handling stress and relation coefficients \Vere calculated and tested for a (linear) rela the si nQ.le an imal that died at 21 wk did not sho,v siQ.ns of WS or ~ ~ tionship bet\veen intensity of RLP infection and condition of the were too decomposed for assess,nent of WS, respectively. and digestive gland and foot. condition indices, density of circulating were not included in these calculationi,. Cumul ative monality ap hemocytes, cumulative mortality. and time of exposure. Step,vise proached 100%- in the PC aq uari a. 85% of the EA anin1als in the forward and backward regression 1nodels we re used to predict the experin1ental aquari a, and 25% in the NC aq uaria (Fig. 6). A irJtensity of RLP infection in exposed abalone fron1 the follo\ving significantly hi gher proportion of abalone died upon exposure 10 vari ables: condit ion of the digestive gland and foot. weight con \VS (22/2..J.) relative to unexposed animals (6/24: P < 0.0001. Fish dition index. visual condition assessment, and duration of expo er's exact test). Median time to n1ortaliry ,vas significantly differ sure. Multiple logistic regression analysis \vas used Lo predict pres ent between the expo~ed EA ( 4 1 wk) and PC ( 16 wkJ abalone (P ence of RLP in fection by using cotnbinations of the five indepen < 0.000 J. Mann-Whitney tesr). A~ only a fe,v NC abalone died dent variables Iisled above. during the study, median time to death \Vas not calcul ated for this group. RESULTS A significantl y hi gher proportion of abalone exposed to WS (EA and PC) had reduced condition indices, morphologic changes, All abalone fron1 the PC LTeatn1ent and all except three an i1n als and RLP in fections than did unexposed anin1als (NC). Reduced in the experimental treatmen t (EWS and EA) that died in this study condition indice~ ,,ve re observed in 18/24 EA and 19/24 PC aba had visible signs of WS, including \veakness, weight loss. and lone. whereas onl y 3/24 NC anim als lost condition ( P = 0.002 and visible arroph y of the foot nn1sc!e (Fig. 2). The two EA abalone in P < O.OOL respectively, X2 test). Morphologic changes were ob the experi n1ental aq uaria tha t died during the first ,veek of the served in the digestive gland of 20/2 1 EA and 17/24 PC abalone. stud y lacked visual and histopathological signs of \VS, RLP in whereas only 1/24 NC abalone had an abnorma l digestive gland fections, or visible injuri es. A third abalone fro n, the experimental architecture (P < 0.00 I, X2 test). Of Lhese. degeneration ,vas ob trearn,ent that di ed during the 21st week of the study was too served in 14/21 EA and 6/ IO PC anin1a l~. 1netaplastic changes in decomposed for gross or hi tologic examination. The six NC aba 9/2 1 EA and 4/10 PC ,tbalone, and in tlainn1ation in 6/21 EA and lone that died during the experin1ent and 18 NC survivors sampled 1/10 PC abalone, whereas 1/24 of the unexposed ani1nals only had upon termination of the srudy did not have visible or microscopic mild digesti ve gland degeneration. Pedal atrophy ,vas observed in signs of WS (Figs. 3 and 4). Both Yandenberg/Cayucos (PC and 15/21 EA. 17/24 PC. and onJy 1/24 NC abalone (P = 0.001 and EWS) and Ano Nuevo lsland (EA) abalone \vith clinical WS had P < 0.00 I. respectively. X2 test). Infecti ons \V ith ·'Ca11didarus Xe histopatho!ogical and he,natological signs of this disease, inclu d nohalioti s califomiensis'· were observed onl y in EA (22/21) and ing degeneration and inflan1mation of and/or n1etaplastic changes PC (24/24) treatn1ents (P < 0.001, X2 test and P < 0.00 I. Fisher's in the di gesti ve gland, depletion of muscle bundles in the foot. exact test). As above. significantly higher proportions or animals (Figs. 3-5). and the presence of necrotic cells. cellular debris. and wi rh RLP in fections died and had clinical signs of WS than did s,nall hemocytes (-4.5 µn1) ,vith a large nucleus to cytoplasmic unexposed abalone (P < 0.001, X2 test). ratio wi thin the hemolyn1ph. In addition. all PC and E\VS anin1al s Speannan rank correlation coefficients for relationships be and all except the two EA abalone th at died du1in g the fi rst week tween intensity of RLP infecti on of individuals in each WS of the study were in fected with the RLP. ,vhereas none of the NC exposed group (EA. EWS. and PC) versus visual condition, con ani1nals ,vere infected. Other than the nonpathogenic renal coccid dition indices. condi tion of the foot and digestive gland, and den ian. Margolisiella ( = Pseudoklossia) haliotis, no other parasites sity of circul ating hen,ocytes \Vere lo,v and ranged between -0.275 \Vere observed in any of the abalone examined in this study. ln this and 0.486 for the Ano Nuevo Island animals and -0.0175 and study, the incubation time for clinical WS is defined as the dura- 0.0567 for Vandenberg anin1als. Except for 1netaplasia and overall
A B
Figu re 2. Black abalone with and without \>VS. A, Healthy animals [ron1 Ano Nuevo Island fron1 a negative control lreatn1ent. B, An (EA) abalone fron1 Ano · 'uevo lsland that contracted WS from infected black abalone in an experin1cnlal treatment. 820 FRIEDMAN ET AL.
- ~ - -! -
Figure 3. Microscopic anaton1y of the foot muscle of hlack ahalonc with and without \·VS. The l'oot n1uscle of an uninfected anin1als are illustrated in A (Vandenberg abalone) and B \Ano Nuevo Island a balone). Note that dense bundles of n1uscle fibers cornprisc n1ost the foot. The pedal n1usd c atrophy of an abalone that contracted \·VS in the tield (C) is also observed in those that acquired \¥S in this laboratory study (D ). Noie the severe reduction in rnuscle fibers and increase in visible connective tissue in affected individuals. Hcnurtoxylin and eosin, bar = J 50 µrn.
RLP burden in the EA abalone ( P < 0.05 ). al I coefficients \Vere DISCUSSION nonsignificant (P > 0.05). This relationship ,vas also 1nirrorcd in X" analysi~ 111 which a higher proponion (8/9) of EA abalone ,vith The present study describes the transmission of WS fro111 black high overall RLP burdens (scores of 4-6) had n1etaplas tic changes aba lone \Vi th WS LO pre viously healthy black abalone held in the as the :-ole or partial re~pOn\e LO RLP infection~ than tlid tho~e ,vith sa111e aquaria. The sin1ilarity in physical. histopa th ological. and Jo,\ {~core~ or 0- 3) infection, ( I /7 . P < 0.0 I ). Several of the PC hen1atologica l characteristic~ of \VS between black abalone ex abal one ,vere too necrotic LO as~ess ~pecific lesions in the diges tive posed 10 WS in the laboratory and fi eld. co n1 bi ned with a lack of gland, a tissue that degrades 1nore quickly than other tissues these signs 111 the negative control anin1als. confinned that the (Friedn1an. personal observa tion). and resu lted in s111 all sa1nples cxperi111ental abalone contracted \VS in this stud y (Haaker et al. sizes for this ~pccific analysi~. Intensity of RLP infection in labo 1992. VanBJ,u·ico 111 et al. I 993. Gardner et al. 1995. Shields et al. ratory EA abalone ,vai,. predicted fro n1 tJ1e duraLion of exposure 1996, Fried111a n el al. 1997). These data also suggest that \VS i~ (Lime) ,vith weight condition index. vi, ual condition. condition or direc1l y trans n1 issible bet\vccn sy 1npatric abalone by cohabitaLion. Lhe foot antl digestive gland. and 1in1e as independent variables in WS is a cnronic, slow-progress ing n1 alacly in \v hich clinical th e n10Jel ( P = 0.0 156. For,v,1rd and Back,vard stepwise regres signs appear in the final sLage;, or the disease. The presence of sions). No prediction or presence of RLP infection could be n1ade advanced n1icro~copic 111orphologic chan ges throughout the pedal using Multiple logisitic regression analyse, u~ing all possible com n1uscle and digestive gland of affected abalone supports this con binationi, of the five independent variable, u~ed in this study (P > clusion (Figs. 2-5). Our data also ~uggests a long incubation pe 0.500). We did ob,erve a significant correlation bet\ve.:n hen1 ocyte riod for WS (- 35 \Vk) follo,ved rapidly by 111ortali1y (--12 days) nun1bers antl we ight condition index of the EA abalone (P = under the conditions used in this stu dy. As sho,vn in Figure 6. once 0.0-169). PC abalone {P = 0.0016) and NC abalone {P = 0.00 15). the animals tlevelopecl clinical \VS. the slope~ of th e n1ortali1y C'orrelat1o n coefficient,, however. ~1ere IO\\' lo n1oderale and curves l"ron1 the experi1nentally (EA) and field-exposed (PC) ani ran!!etl- bet ~1een 0.2668- 0.5612. n1als ,vere \'Cry sitnilar. However. n1edian survival tin1es bel\veen WITH.ERi G SYNDROME 1.N BLACK ABALONE 8'2 I
·, .... -<. • 1' ,. • I
• • • • • • .. • :B
Figure 4. Microscopic anatorny of the di gesti ve gland of black abalone with and without \ 10 A ~ UJ 1 I (/) +I ~ Body Mass Condition Index (/) Q) 0 I u ' Weighl/Length3 Ratio u ~ Visual Conditio n C C 0 o, 0 .:, u C 0 u 0 001 ,-.·= } .r:: '{ ; : Experimental Pos Control Neg. Control Treatment B ~ UJ 3 Cl) +I ~ C Foot Muscle 0 ' :fi Digestive Gland u !ll!l!W'&! Connective Tissue C 0 c== Transport Duct Metaplasia u 2 Inflammation Q) ···-· > - :",: .;:;; (I) Q) - - 0::: ":..:, .: ~ .,...... : '.: l .,___ _ _ Experimental Pos. Control Neg Control Treatment w 5 -r------~ Cl) C C 4 0 ·.;:, u Q) C Postesophagus - 3 0... -~I • , I Digestive Gland _J 0::: ~ Pooled Intensity -O 2 c (/) C Treatment Figure 5. l\llicroscopic rnorphologic changes of black abalone that acquired \.YS in the field (Pos. Control) or in lhe laboratory (Experimental) relative lo unexposed (Neg. Control) animals. A, Anin1al condition; 8, relative condition or the foot n1uscl e and digesti ve gland. C. RLP intensity of infection. Each bar represents the n1ean or 12 abalone in each or two replicate lreatrn enls ± standard error (SE}. lected fro1n Vandenberg and held at I 8°C, lhe initiation of n1or by a lack or observation of any pathogens besides "Ca11dida111s ta lity al 15 wk was sin1i lar lO that observed in the PC and EWS Xenohaliotis ca liforniensis.. in any abalone exarnjned in this stud y. abakine in the current study and also supports a long incubation Transr11i ssion of this RLP is thought to be via a \vater-born e/fecal period for WS (Friedman & Fan 1998). oral rou te because of the presence of bacterial foci in the digesti ve The observalion of RLPs in th e EA Ano Nuevo Island ani,nab epitheliun1 and the observation of both intact and lysed RLP foci and not in lhe NC Ano Nucvo Island animals (Fig. 5) suggests that in lun1ina of the digestive tract (unpublished observations). M or this bacteriun1, like WS. is horizontally transn1 itted by cohabitation talities of the European Saint-J:icques scal lop. Pecren 11raxi11111s. and is the etiological agenl of this disease. This is further supported have been associated with a branchial RLP infection (Le Gall et al. Wrr HER TNG SYts.'DROME IN B LACK A BALONE 813 Black Abalone Cohabitation Study to Lhe bacLeriun1· s growth rate. Significant correlations between Survivo rship Curves intensity of RLP infection and degree of WS have recently been observed in both field and laboratory studies u, ing wild and cul 100 tured red abalone (Moore el al. 2000. Friedn,an. unpublished ob servation). The author, :iJso suggested that differences in correla 90 tions bet\veen intensity of RLP infec tion and disease in red and 80 black abalone 111i ghL rel ate to species differences in host response 70 to infections. Red abalone respond to the RLP infections predon1 i ~ -0 nantly by a n1etaplastic change in which digesti ve gland tubules C. 60 .c are replaced by Lransporl duct epitheliu1n (M oore et al. 2000) . ~ 50 "'0 Black abalone respond LO RLP infec tion by a co1nbinaLion of di > ~ 40 gestive tubule degeneration and. to a lesser ex tent, Lransport duct :, n1 elaplasia (Gardner et al. J 995. Friedn,an et al. 1997} ( Figs. 4 and "' 30 5). BoLh of these ti ssue changes result in a loss of key functi onaJ 20 ti ss ue in the digesti ve gland, the tenninal tubu les (Yollzow 1994), 10 v,hich may lead to starvation and accoun t for the uli I ization of fool 0 n1uscle as an energy source follo,ved by death as observed in 0 5 10 15 20 25 JO JS 40 45 abalone with WS ( Friedman unpublished data.). As the RLP in nme (Weeks) fects transport duct epithelia and not tennin:LI digesti ve tubules, this 111ay result in an increase in RLP intensity of infection in red -+- Negative Control and not in bl ack aba lone as the infections progress and clinical ~ Posttrve Control disease develops. Figure 5. however. does illustrate alterations in Experimentally Exposed condition indices and changes in th e condition of the fool and Figure 6. Survivorship curve of abalone in the cohabitation study. The dige ri ve gland only in abalo-ne ,vith RLP infections. This provides closed circles represent the negative control anirnals. the open circles further evidence that the RLP is the etiological agent of WS. RLPs represent positive control ani1nals, and the closed triangles represent have been associ:ued with atrophy and degenera tive changes in the (EA) Ano Nuevo Island anin1als in the ex peri1nental lreatn1ent. other invertebrate ~pecies (Min & Benzer l 997). Infections with RLPs have been reported in a variety or mol 1988. l 99 1) . Traas1uission of this scallop-pathogenic RLP via luscs and crustaceans, including the sea sca l lop, P/acopec1e11 ,na· horizontal. waler-borne transmission has also been docu1nen1ed gella11ic11 s G1nelin (Gulka & Chang 1984a), the blue 1nusseL M.,·ci (Le Gall ei al. 199 l ). Field and laboraLory studies suggested that /11s ed11/is Linne (Gulka & Chang 1984b), the 111ani la clam. Tapes trans mission of the sca llop RLP occurred between - 5-28 \Vk of japonica Adams and Reeve and the Japanese scallop. Pati11opec1e11 exposure (Le Gall et al 199 l ). Additional fi eld studi es reported ye.1·l·oe 11 sis (ElsLon 1986), die European flat oyster, Ostrea edulis heavy RLP infections in scal lops during the winter 1nonths fol Linne (Friedn, an et al. 1989). the black abalone, Haliotis crach lo\ved by n1onalities in the spring (Le Gal l et al. 1991). suggesting erodii Leach (YanBlaricon, et al. 1993). and the penaeid shrimp, a re latively long incubation period for the scallop rickett ial di~ Pe11ae11s 111argi11a11,s Randall (Brock el al. 1986). These infections ease as we have observed for the RLP-induced WS in th is study. va ried grea tly in tissue specificity (nonspecific to highly specific), The relationship between the RLP and WS in black abalone is length of incubation period. and pathogenicity. ranging fron1 no co1nplex as evidenced by higher proportions of n1011aJity and clini app,ll'ent harn1 ful effects LO lethal effects in the host (Gu lka & cal WS i 11 groups of abalone either exposed to \.VS-affected ani Chang 1984a, Brocl.. et al. 1986. Frel ier et al. 1993, Gardner ct al. mals or infected with the RLP. WiLh one exception. a lack of 1995. Bower et al. 1996). In addition. the pathogenicity of a spe significant correlation existed between intensity of RLP infection ci fi c RLP has been sho\vn to vary between hos t species (Brock et and WS in both the experin1entaJ and PC animals coupled ,vith a al. 1986). As in th ese srudies, which document that RLPs are lack of ability to predjct intensity of R LP based on gross or his pathogenic for marine invertebrates. our data provides evidence tologic signs that characterize WS (regression n1 odels). The single that "Ca11didc,111s Xenohaliotis californiensis:· the recently identi significant positive correlation between overall intensity of RLP fi ed RLP observed in abalone in Califo111ia. is the etiological agent infection and degree of 1netaplasia in the EA abalone that re of WS. Future studies that exan1ine the interaction bet\veen host sponded. in pan, with this 1norphologic change suggests that sus gastrointestinal cells and the RLP n1ay provide insight into the tained high RLP burdens may lead to metaplasia in black abalone cellular ph ys iology of the host and the physiology and disease as has been observed in red aba lone (M oore et al. 2000). This n1echanisrns of the bacteriun1. re lationship was not observed in the sn1all nun1ber ( I OJ of PC abalone in which the presence or absence of n1etaplasia was quan ACKNOWLEOGiVIENTS tified: the sn1alJ san1pl e size may account for an inability co detect a relationshjp. However. when the overall DG condition (alteration fron1 nom,al, including all three specific n1orphologic changes) We appreciate the editorial con1 ments of Jan1es D. l'vtoore. Thjs was assessed in the EA and PC, these relationships were not ob work was supported, in pan. by the National Sea Grant College served. T his lack of con·elation between RLP infection and DG and the Sa ltonstall-Kennedy Progran,s of the National Oceanic and overal I condition in black abalone n1ay relate to the host response A tmospheric Adn1inistratio11 , U.S. Department of Co1n1nerce u11- to RLP infection (prin,arily degeneration of digestive tubules) der grant nun1bers NA36RG0537. Project No. R/F- 153 (through ( Figs. 4 and 5) combined with the high turnover rate of the target the California Sea Grant College Progran1) and NA 76FD0046. ti ssue (digestive epid1elia) infected by the WS-bacteriun, relative respecti vely. Additional support was provided by die Ca lifornia 8:?A FRIEDM AN ET A L. State Re!>ources Agency. California Depart n1c nl of Fi, h and Ga111e ,Lnd do not nece~,ar ily refl ect the vie\v:, of NOAA or any of its and the Aquacultu re anti Fisherie& Progran1. Univer~ity of Cali ,ubagencie,. T he U.S. Govcr11111ent is authori7,cd to reproduce and fornia. Da\'i~. The view, exprcs,cd herein are tho~e uf the auLhor, distribute this \\'Ork for govern1nental purpo~e,. REFER ENCES Bower. S. Jvl., G. R. Meyer & .I . A. Bou1i llicr. 1996. Stained prawn d,~ea,e Gulka. G. & P. \V. C hang. 1984a. Pa1hogen1ci1y and infecti vi ty of a nck (SPI)) of Pn11dalt11 p/a1yu! r1" in Britbh Cnlumbrn. Canad:,, c·au,e