Canine Parvovirus Infection in South American Canids

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^1. '' la Reprined from he JOURNAL O THE AERICAN VETERINARY EDICAL ASSOCIATION, Vol. 177, No. 9, Pages 779-78. American Veerinary edical Associaion, 1980. All Righs Reserved. Canine Parvovirus Infecion in Souh American Canids Peer C. ann, DV; ichell Bush, DV; ax J. G. Appel, DV, PhD; Bruce A. Beehler, DV; Richard J. onali, DV SUAAARY Canine parvovirus (CPV) infecions occurred in 5 of 5 Souh American canids a he Deparmen of Conservaion (DC), a breeding faciliy of he Naional Zoological Park in ron Royal, Va. The clinical signs were anorexia, lehargy, diarrhea, and vomiing. Three of he affeced canids survived and had high hemaggluinaion-inhibiion iers o CPV in he recovery period. Necropsy of he 2 ha died revealed exensive necrosis of he inesinal mucosa; CPV paricles were observed by elecron microscopy in he inesinal conens of boh animals. Six of he 0 canids ha remained healhy had high hemaggluinaion-inhibiion iers o CPV prior o he episode of illness, indicaing earlier subclinical exposure. Pe dogs belonging o DC personnel ha were screened as a possible source of he infecion had no evidence of disease. All canids (including pe dogs) on he DC grounds were vaccinaed repeaedly wih a killed feline panleukopenia virus produc afer he episode, wih lile or no effec on exising iers. ain.^"" The disease has been described in 1 Souh American canid, he maned wolf ^^ In he presen repor, we describe CPV infecion in species of Souh American canids. Resuls of sudies of hemaggluinaion-inhibiion (HI) iers are described, and possible roues of infecion of capive Souh American canids are discussed. Hisory Iniially, a cpv-like disease occurred a he Naional Zoological Park's Deparmen of Conservaion (DC), in ron Royal, Va. During he 1s half of Sepember 1979, Souh American canids 1 bush dog (BD 1; Speohos venaicus), 1 maned wolf (W 1; Chrysocyon brachyurus), and 1 crab-eaing fox (CE 1; Cerdocyon hous) developed a disease characerized by anorexia, lehargy, vomiing, and foulsmelling or hemorrhagic diarrhea (Table 1). All animals were hospialized and were given supporive herapy (anibioics, fluids, and muliple viamins). The animals promply recovered and TABLE 1 Souh American Canids Sudied in Episode of CPV Infecion Animal Age (yr) Sex Duraion of illness CANINE PARVOVIRUS (CPV) infecion is a well-recognized syndrome in domesic dogs, wih worldwide disribuion; cases have been seen in he Unied Saes,^"^ Canada,' Ausralia,*^ and Grea Bri- rom lie Deparmens of Paliology (ann, onali) and Animal Healh (Busli, Beeiler), Naional Zoological Park, Smihsonian Insiuion, Washingon, DC 20008, and he James A. Baker Insiue for Animal Healh, New York Sae College of Veerinary edicine, Cornell Universiy, Ihaca, NY 1485 (Appel). Bush dogs BDI BD2 BD BD4 BD5 aned wolves Wl W2 W Crab-eaing foxes CEl CE 2 CE *Died. Clinically normal (9 mo) 2V Vi 2 >6 2V2 2VS 9/8/1979-9/14/1979 10/2/1979-10/6/1979* 9//1979-9/8/1979 10/14/1979-10/19/1979* 9/11/1979-9/14/1979 November 1, 1980 779

were reurned o heir compounds wihin 1 week. The iniial laboraory findings from hese animals were considered o be wihin normal limis for hese species. Blood culures were negaive for baceria, and fecal culuring revealed normal flora. ecal floaions were negaive for parasies. Approximaely 6 weeks afer recovery, all animals had high HI iers for cpv (1:640 o 1:5,120), which persised unil early 1980. On Oc 2,1979, a 2-year-old female bush dog (BD 2) became ill. Clinical signs were anorexia, diarrhea, and depression. The animal was hospialized and reaed wih anibioics, fluids, and viamins. Blood and fecal specimens obained a admission were negaive for pahogens. The WBC coun was 4,900/mm^ (normal = 6-10,000/mm^).'' During he nex days, he coun dropped o 800/mm^ The animal became progressively more depressed and coninued o vomi and o have hemorrhagic diarrhea. Despie coninued supporive herapy, he bush dog died on he 4h day of hospializaion. ive monhs earlier, he HI ier for CPV was ^1:20; serum was no available for a ier deerminaion a he ime of illness. Necropsy findings were compaible wih CPV infecion, which was confirmed by idenificaion of CPV paricles on elecron microscopy of inesinal conens. The 2nd maned wolf (W 2) o develop signs of cpv-like disease had been shipped from Roerdam o he Unied Saes on Sep 12, 1979. Afer spending 1 nigh in an animal sheler in New York Ciy, i was placed in he quaranine faciliies a he Naional Zoological Park (NZP). These faciliies are in a separae building from he hospial; personnel don fresh coveralls and rubber boos and cross an anisepic foobah upon enering he quaranine faciliy. On Oc 4, 1979, he wolf was ranspored o he hospial for an iniial physical examinaion. A his ime, he animal was clinically normal. Since he examinaion occurred a he same ime ha BD 2 was in he hospial wih hemorrhagic diarrhea, numerous precauions o preven cross infecion were aken: (1) All procedures excep radiography were performed in a room where he sick bush dog had no been. (2) resh coveralls and rubber boos were donned by clinical personnel before handling he maned wolf () The radiography equipmen (which was used on boh he bush dog and he maned wolf) was horoughly disinfeced wih chlorhexidine,'' he disinfecan of choice a he ime in boh he hospial and quaranine faciliies. This inciden was he only ime he maned wolf was ou of he quaranine faciliies; he exposure in he radiography room was he only known opporuniy for exposure o CPV. Ten days laer, he animal was found in is quaranine faciliy in sernal recumbency, unable o rise. We immediaely insiued inensive care, which included fluids, anibioics, viamins, inesinal proecans, and oral alimenaion. The wolf began o have fluid, foul-smelling "Values for clinically normal Souh American canids in his repor compiled from Naional Zoological Park records. ^Nolvasan, or Dodge Laboraories, or Dodge, Iowa. diarrhea, and vomied he majoriy of any fluids adminisered orally. Inasmuch as we suspeced CPV infecion, 250 ml of whole blood from he recovered maned wolf (W 1) was adminisered in an aemp o confer some degree of passive immuniy. The urine oupu of he affeced animal dropped o 0.5 ml/hr. Dopamine was adminisered (5 xg/kg/min, iv) o simulae urine oupu. The urine oupu increased and over he nex 24 48 hours he animal seemed o improve and was able o sand briefly. Anibioic herapy consised iniially of penicillin, followed by carbenicillin and ampicillin. The animal's condiion began o deeriorae afer 72 hours; diarrhea and vomiing coninued, sernal recumbency recurred, and oliguria progressed o anuria. ive days afer he iniial collapse, he animal died, apparenly of renal failure. The WBC of W 2 had iniially decreased and hen increased o normal numbers during he laer period of inensive care. On he day of suspeced exposure (10/4), he oal WBC coun was 10,400/ mm^. On he 1s day of clinical signs (10/14), he coun had dropped o 2,500/mm^. The nex day (10/15), he coun reached is low poin (1,200/mm''). The couns on hese 2 days consised of approximaely 75% lymphocyes. The WBC coun for he nex 4 days (10/16-10/19) showed an increase o a more normal number of leukocyes (11,000/mm^ on 10/19), along wih he reurn of adequae numbers of granulocyes (80% segmened cells, 10% band cells, and 10% lymphocyes). Afer he deah of W 2, HI iers were deermined from serum from his animal. On he dae of his presumed exposure, he ier was ^1:20. A he onse of clinical signs (10 days afer exposure), he HI ier was 1:5,120, and i remained a his level unil he animal died, 5 days laer. eces obained from his animal a necropsy were examined by elecron microscopy; CPV paricles were idenified. Vaccinaion and HI Tiers in Domesic Dogs Afer he episode of CPV infecion, we began o search for he source of CPV. Conversaions wih a veerinary praciioner in ron Royal, Va, revealed ha he had seen faal hémorragie diarrhea in pe dogs in own shorly before he 1s episode of diarrhea was seen a he DC. Since here were no serum samples available (all affeced animals had died), i was impossible o confirm ha illness as CPV infecion. There were, however, 14 pe dogs ha belonged o he DC saff and which lived on he DC campus. Alhough hese animals were kep separaed from NZP animals, we believed i would be advanageous o deermine HI iers and hen o vaccinae hem agains CPV infecion. The dogs were vaccinaed on 10/24/1979 and again 2 weeks laer wih a killed feline panleukopenia virus (PLV) vaccine.'' Before he animals were vaccinaed he 1s ime, blood was drawn from all 14 animals. Approximaely 5 monhs afer he 2nd vaccinaion, HI iers were deermined from 6 randomly seleced dogs ^elocine, Norden Laboraories, Lincoln, Neb. 780 JAVAAA, Vol 177, No. 9

TABLE 2 Hemaggluinaion-lnhibiion liers for cpv in Domesic Dogs a DC, ron Royal, Vo Dog No. 1 2 4 5 6 7 8 9 10 11 12 1 14 Tier, by dae 10/24/1979 /27/1980 <1:10 1:40 <1;10 1:20 <1:20 ND <1;10 ND Vaccinaion for CPV: 10/24/1979 and 11/8/1979. ND = no deermined. : n "'I 'S (Table 2). None of he 14 pe dogs kep on he grounds of he DC ever developed signs ypical of CPV infecion. ;>«"'ííjiíí Vaccinaion, HI Tiers, and Clinical Hisories in Souh American Canids The remaining canids a DC were vaccinaed wih a killed PLV produc' shorly afer he deah of W 2. Each of he canids was vaccinaed on occasions, a 2-week inervals. None of he animals in his series had any evidence of CPV infecion. Tiers for CPV were deermined from serum samples available in he serum bank of he NZP. Some of hese samples were obained prior o he episode of CPV infecion a DC. The resuls are shown in Table. any of he Souh American canids ha did no have signs of CPV infecion had high HI iers. Bush dog had come from rankfur, Germany, on 8/8/1979. I had spen 1 nigh in he same animal sheler in New York Ciy as had W 2, and hen i had been sen o he quaranine faciliies a NZP. This animal has never had any signs of CPV infecion, nor has i ever been o DC, because i wen direcly ino he main zoo collecion afer a 0-day quaranine. Alhough he animal was vaccinaed (killed PLv) on 10/16/1979, 11//1979, and 12/4/1979, he iniial HI ier was deermined from a posquaranine sample (before vaccinaion and before he animal was moved o he park). Bush dog 4 also came o us from rankfur. I TABLE Hemaggluinaion-lnhibiion Tiers for CPV from Clinically Normal Souh American Canids Animal Dae ( ) and ier Bush dogs (8/29/1979) (10/16/1979) (4//1980) BD 1:2,560 1:5,120 1:5,120 (/26/1979) (12//1979) (4//1980) BD4 1:640 1:640 1:640 (10/24/1979) (11/19/1979) BD5 1:640 1:1,280 ND aned wolf (4/0/1979) (10/16/1979) (4//1980) W 1:160 1:160 1:160 Crab eaing foxes (5/12/1979) (/27/1980) CE2 1:20 1:10,240 ND (/27/1980) CE 1:2,560 ND ND = no deermined. ig 1 Phoomicrograph of duodenum specimen from BD 2, showing exensive loss of villi. H&E sain; X 10. arrived a DC in 1976, 2 years before repors of CPV infecion anywhere in he world. This animal has been a residen a DC hroughou he episodes of CPV infecion. I was vaccinaed imes in lae Ocober and early November of 1979. The HI ier of 1:640 was deermined on /26/1979, 6 monhs before he episode of CPV a DC. Bush dog 5 died of hypohyroidism. I never had any signs of CPV infecion. The animal was vaccinaed on 10/15/1979 and 12/24/1979. This animal, along wih he remaining animals in he series (W, CE 2, and CE ), had been housed a he DC faciliies since before he episode of CPV infecion. Pahology The gross and hisopahologic findings in he 2 animals ha died (BD 2 and W 2) were ypical of CPV infecion. ^^'" The mucosa of he small inesine in boh animals and he colon in W 2 were hrown ino hickened hyperemic folds, wih segmens of he inesine being devoid of epihelium. The meseneric lymph nodes were enlarged and edemaous. icroscopic examinaion of he small inesine of BD 2 revealed loss of villi, wih maing of he remaining lamina propria (ig 1) and wih a pauciy of inflammaory cells. Alhough here was no surface epihelium in he small inesine, here were occasional enerocyes deep in he mucosa. Some of hese cells appeared o be regeneraing forms, in ha hey were plump and pleomorphic (ig 2). In he inesinal mucosa of W 2, here was considerable evidence of regeneraion of enerocyes, bu normal villous archiecure had no been reesablished. The lamina propria was hickened and conained irregularly spaced, oruous glands lined by hyperrophied cells wih numerous cryp abscesses (ig ). November 1, 1980 781

/Í*W» # ig 2 Phoomicrograph of ejunal mucosa írom BD 2, showing hyperplasic enerocyes in a cryp adjacen o several empy cryps alered by CPV infecion. H&E sain; X 160. There were areas of perivascular hemorrhage and necrosis in he cerebrum of W 2, wih numerous hrombi in small vessels, some of which conained fungal hyphae consisen wih Phycomycees. ungal elemens were also seen in foci of necrosis in he neuropil, surrounded by inflammaory cells. Posmorem bacerial culures from W 2 revealed Escherichia coli in hear blood, spleen, and colon: findings ha suppor he clinical impression of gram-negaive sepsis. Discussion We assumed ha he animals a DC were exposed o CPV a some poin before Sepember 1979. Alhough possible, i is unlikely ha he sources of CPV were he pe dogs a DC. None of he 14 dogs esed had appreciable HI iers on 10/24/1979, indicaing ha hey had no been exposed o CPV. (In general, HI iers of greaer han 1:256 are considered o be indicaive of clinical exposure o CPV.**''^^^) These domesic dogs received a series of 2 vaccinaions wih PLV vaccine. When HI iers were deermined on hese animals 5 monhs laer, only 2 dogs had a ier: one a 1:20, he oher a 1:40. In general, dogs vaccinaed wih he killed vaccine produc will have an iniial ier in he range of 1:40-1:60 bu will no have a deecable ier afer monhs.^ An HI ier of a leas 1:80 appears necessary o confer proecion agains CPV.^ The Souh American canids ha survived had high HI iers (1:640-1:5,120) shorly afer hey recovered. These findings correlae wih he siuaion in domesic dogs, wherein HI iers are generally quie high (1:640-1:10,240) a he ime of infecion; hese iers do no generally increase ig Phoomicrograph of duodenum specimen from W 2, showing oruous glands and cryp abscesses. H&E sain,-x 25. during convalescence, bu hey do persis for monhs.'^ Two of he recovered Souh American canids had iers persising 6y2 monhs afer infecion. The HI iers in he clinically normal Souh American canids (BD, BD 4, BD 5; W ; CE 2, CE ) indicaed exposure o CPV a some poin before Sepember 1979, he ime of he CPV infecion a DC. The only animals o die (BD 2, W 2) had iers of <1:20 before hey developed clinical signs, indicaing lack of prior exposure. The regeneraion ha occurred in he inesine of W 2, along wih he reurn of a normal WBC coun, implies ha his animal migh have survived he CPV infecion had i no developed gramnegaive sepsis and mycoic encephaliis. The fac ha he exposure of W 2 evidenly occurred afer horough disinfecion of he faciliies wih chlorhexidine furher underscores he resisance of CPV in he environmen and he need o use proper disinfecans. Afer he deah of W 2, he enire hospial area was placed under quaranine, wih all enrances and exis equipped wih foobahs consising of 5.25% sodium hypochlorie dilued 1:0 wih waer. This mixure is he acceped disinfecan^" for areas conaminaed by CPV. None of he affeced Souh American canids had any cardiopulmonary signs of CPV infecion, as described in domesic dogs.'*'" However, all domesic dogs so affeced were pups, whereas he Souh American canids of his repor were all aduls, wih he excepion of BD 1, which was 9 monhs old. References 1. Appel JG, Cooper BJ, Greisen H, e al: Canine viral eneriis. I. Saus repor on corona- and parvo-like viral eneriides. Cornell Ve 69:12-1, 1979. 2. Appel JG, Sco W, Carmichael LE: Isolaion and immunizaion sudies of a canine parvo-like virus from dogs wih hemorrhagic eneriis. Ve Rec 105:156-159, 1979.. Appel JG, Cooper BJ, Greisen H, e al: Saus repor: Canine viral eneriis. JAm VeedAssoc 17:1516-1518,1978. 782 JAVAAA, Vol 177, No. 9

4. Black JW, Holscher A, Powell HS, e al: Parvoviral eneriis and panleukopenia in dogs. V SAC 174:45-50, 1979. 5. Kramer J, eunier P, Pollock R: Canine parvovirus; Updae. V SAC: In press, Oc, 1980. 6. Eugser AK, Bendele RA, Jones LP: Parvovirus infecion in dogs. J Am VeedAssoc 17:140-141, 1978. 7. Gagnon AN, Povey RC: A possible parvovirus associaed wih an epidemic gasroeneriis of dogs in Canada. Ve Rec 104:26-264, 1979. 8. Johnson RH, Sprodbrow PB: Isolaion from dogs wih severe eneriis of a parvovirus relaed o feline panleukopenia virus. Aus Ve J 55:151, 1979. 9. Walker ST, eilen CP, Sabine, e al: A serological survey of canine parvovirus infecion in New Souh Wales, Ausralia. Ve Rec 106:24-25, 1980. 10. ccandlish lap, Thompson H, Cornwell HJC, e al: Parvovirus infecion in dogs. Ve Rec 105:540, 1979. 11. ccandlish lap Thompson H, Cornwell, HJC, e al: Isolaion of a parvovirus from dogs in Briain. Ve Rec 105:167-168, 1979. 12. lecher KC, Eugser AK, Schmid RE, e al: Parvovirus infecion in maned wolves. J Am Ve ed Assoc 175:897-900, 1979. 1. Plecher J, Tof JD, rey R, e al: Hisopahologic evidence for parvovirus infecions in dogs. J Am Ve ed Assoc 175:825-828, 1979. 14. Nelson DT, Eusis SL, cadaragh JP, e al: Lesions of sponaneous canine viral eneriis. Ve Pahol 16:680 686, 1979. 15. cadaragh JP, Nelson DT, Eusis SL, e al: Experimenal sudies of canine parvovirus: Evaluaions of diagnosic procedures. In Proceedings, Am Assoc Ve Lab Diagnosicians, 1979, pp 405-lO. 16. Carpener JL, Robers R, Harpser NK, e al: Inesinal and cardiopulmonary forms of parvovirus infecion in a lier of pups. J Am Ve ed Assoc 176:1269-127, 1980. 17. Hayes A, Russell RG, Babiuk LA: Sudden deah in young dogs wih myocardiis caused by parvovirus. J Am Ve ed Assoc 174:1197-120, 1979. November 1, 1980 78