Epizootic Infection of a Minimal Disease Swine Herd with a Herpesvirus James P
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Epizootic Infection of a Minimal Disease Swine Herd with a Herpesvirus James P. Orr, Elizabeth Althouse, Gilles C. Dulac and Peter J.K. Durham Abstract A totally confined, farrow-to-finish, closed, minimal in herds previously free of infection (9). Infectious disease herd of pigs experienced high death and repro- bovine rhinotracheitis virus and PCMV have been ductive losses during a disease outbreak lasting five shown to cause generalized disease in fetal and weeks, and during the ensuing three months. The losses newborn pigs (4,5,10,11). In addition, IBR virus were caused by infection of pigs of all ages with a has caused genital infections of sows and boars in herpesvirus, with devastating effects on the lungs of Norway (11); porcine cytomegalovirus has occasionally immature pigs and on the reproductive performance been blamed for systemic disease in susceptible older of the sows. pigs (8). In this report, we describe the investigation of a disease outbreak in a minimal disease swine herd, Resume affecting a high percentage of individuals of all age Infection 6pizootique d'un troupeau de porcs groups, and caused by infection with a virus which was taux minimal de maladies, par un herpesvirus almost certainly porcine cytomegalovirus, although Cette etude portait sur un troupeau de porcs a taux attempts to isolate it were unsuccessful. minimal de maladies, completement ferme et garde en reclusion totale, qui comptait des porcelets, des porcs d'engraissement et des sujets de reproduction. Ce History and Clinical Findings troupeau connut un taux eleve de mortalite et de graves This disease outbreak affected a totally confined, problemes de reproduction, tant au cours d'une farrow-to-finish, closed herd of 250 sows. The herd maladie qui dura cinq semaines que pendant les trois was established in 1982 from caesarean-section derived mois qui suivirent. Les pertes resultaient d'une infec- and colostrum-deprived piglets. During 1984 and 1985, tion de sujets de tous les ages par un herpesvirus qui additional caesarean-section derived litters were endommagea gravement les poumons des jeunes et introduced. Herd security is excellent. The herd was affecta la performance reproductrice des truies. classified as a minimal disease herd on the basis of clinical monitoring, serology, and slaughter checks. Can Vet J 1988; 28: 45-SO The course of the outbreak is summarized in Table I. In late October of 1985, pigs in the grower barn experienced reduced feed intake, followed after 48 hours by the sudden deaths of four 12-week-old pigs. At necropsy, three of the four had severe Introduction pulmonary congestion and edema. Fresh and for- Three viruses of the family Herpesviridae have been malinized tissues were transported to the diagnostic previously incriminated as causes of disease in laboratory. More pigs died in the days following, with pigs (1). Two of these, namely pseudorabies virus and similar postmortem findings. Pit gas poisoning or infectious bovine rhinotracheitis (IBR) virus, are other toxic injury was suspected, and blood samples classified as alpha herpesviruses. The third is porcine were drawn for hematological and serological evalua- cytomegalovirus (PCMV), a beta herpesvirus. Canada tion. Within four days, the dry sows were anorexic; is thought to be free of pseudorabies, but has wide- from 10 to 30% of the sows would leave their food spread endemic infection of cattle with IBR virus (2). at any one time, and many had rectal temperature There are a number of reports of PCMV infections peaks of 41.5 to 42.0°C. The temperature would fall in pigs in Canada, based on morphological, virological, rapidly to below normal within 24 to 48 hours. No and serological criteria (3,4,5,6). Infection usually secondary rise was detected. Hematological results causes clinical rhinitis in pigs of two to four weeks, indicated lymphopenia and neutropenia with a left which results from necrosis of epithelial cells lining the shift. No treatment was given. The affected sows had nasal glands (7,8); rhinitis may affect pigs of any age serous, purulent, or hemorrhagic discharge from the external nares. No deaths occurred in sows. Gradual Department of Veterinary Pathology (Orr) and Department recovery followed two to three days off food, and of Veterinary Microbiology (Durham), Western College within a period of ten days almost all sows had of Veterinary Medicine, University of Saskatchewan, shown the above signs and recovered. However, litters Saskatchewan S7N OWO, Animal Management Saskatoon, born to affected sows suffered very high preweaning Services and Pet Clinic Ltd., Box 2439, Humboldt, and Saskatchewan SOK 2A0 (Althouse) and Animal Diseases mortality, associated with starvation, scouring, Research Institute, P.O. Box 11300, Station H, Nepean, general poor viability of piglets. Coughing, pyrexia, Ontario K2H 8P9 (Dulac) inappetance, and dysgalactia were recorded in farrow- Can V 1988 45- Can Vet J Volume 29, January ing sows. Respiratory distress and sneezing were growth rates, but continued to sneeze. Repeat blood observed in nursery pigs, and several deaths occurred samples were obtained from five sows only, since the in this group also. other sows bled at the first sampling had been removed All of the sows were eating better by the third week, from the herd. but many were farrowing prematurely; 20% of the Long-term effects on reproductive performance piglets were stillborn; those surviving had low viabil- were evident during the subsequent three months ity. Groups weaned at this time recorded 30-47% pre- (Table II). Mummified fetuses occurred at rates up to weaning mortality. Illness and deaths continued to 20% of piglets in some groups of farrowing sows, in occur in the nursery, with respiratory distress and conjunction with a number of stillbirths. Live-born raised temperatures in affected pigs, and pulmonary pigs were correspondingly reduced in numbers. Sows edema as the major postmortem lesion. which had been in early pregnancy at the time of the Premature farrowings continued in the fourth week, initial outbreak, subsequently produced small litters. with up to 50% of piglets stillborn. Sows were eating The cumulative effects of increased culling and low and seemed to be producing more milk, however mor- conception rates were experienced several months later tality rate amongst the piglets remained high. Mortality in reduced farrowings, so that five to seven months consisted of sudden deaths at 10-14 days of age, and after the initial outbreak, approximately 200 fewer pigs the slower deaths of sick weakly pigs. In the nursery, per month were marketed. there was obvious sneezing and many pigs had purulent Gross inspection of nasal turbinates and lungs from nasal discharges. One pig with a short deformed snout 15 and 25 slaughter pigs respectively, in January and was destroyed and submitted to the laboratory. July of 1986 revealed only two pigs with slight tur- By the fifth week, sows and feeder pigs were eating binate atrophy in January. All other turbinates and normal amounts. At weaning, emaciated sows were all lungs were considered normal. culled or destroyed. The remaining weaned sows were As of May 1986, reproductive performance of the in poor condition with the result that their weaning- herd is gradually returning to normal. It has proved breeding interval was prolonged and their conception difficult to increase the body weight of those sows rate was reduced. Stillbirths, sudden deaths, and which were very thin after weaning. Sneezing is occa- piglets dying with scours continued in the young age sionally heard in the nursery, but there is little evidence groups with up to 670o preweaning mortality. Several of turbinate atrophy. of these were sent to the laboratory for postmortem examination. The young weaned pigs had marked Necropsy Findings dyspnea along with purulent nasal discharges. Pigs The veterinarian attending the herd (E.A.) reported with rhinitis in the nursery had reduced appetite, and consistent gross necropsy findings in the first three growth rate was adversely affected. Low weaning deaths. There was severe pulmonary edema, hydro- weights contributed to difficulties in weaning pigs onto thorax, and hydropericardium. Petechial hemorrhages feed. The older pigs in the nursery achieved good were observed on the small intestines and in the 4646 Can Vet J Volume 29, January 1988 ... -.::...-..:::A ::::-... :.: Z.::X" .': in/.'lvf~ Figure 1. Severe pulmonary congestion and edema in the Figure 2. Diffuse cortical petechiation in a kidney from a left lung from an eight-week-old pig. 17-day-old pig. meninges. Portions of fresh and fixed tissue were Histopathological Findings transported to the diagnostic laboratory, along with Lesions of interstitial pneumonia were found in lungs two whole carcasses of eight-week-old pigs which had from all 21 pigs. Pigs which died after a brief illness died on the following day. had diffuse pulmonary congestion, alveolar edema with.-°:...i.t8.::f:i' increased numbers of alveolar macrophages, and The prominent gross lesion in the two pigs necrop- sied at the laboratory was very severe diffuse increased cellularity of the alveolar septa. Pigs sur- pulmonary congestion and edema (Figure 1), accom- viving for more than about two days had thickened panied by excessive clear fluid in pleural and peri- and cellular alveolar septa, along with alveolar and cardial cavities. Small confluent gray firm areas in the interlobular edema, and perivascular hemorrhages lungs were restricted to the dependent tips of the (Figure 3). Histiocytes, lymphocytes, and neutrophils middle lobes. The broncial and mediastinal lymph could be identified within the alveolar septa. Small nodes were enlarged fivefold and very congested. groups of cells scattered in the interstitial tissues had During the course of the outbreak, carcasses and the morphology of erythrocyte precursors. There were tissues of 20 pigs with an age range of 2-20 weeks were increased numbers of alveolar macrophages, and, in transported to the laboratory.