Epizootic Infection of a Minimal 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 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 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 of the family 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 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 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 ...

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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 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. Variable degrees of con- a small percentage of pigs, neutrophils in moderate gestion and edema of the lungs, along with increased numbers in the bronchiolar and alveolar spaces. firmness of lung tissue, were the most significant and Basophilic intranuclear inclusion bodies were found consistent lesions. Accompanying this, there was in all lungs and were numerous in several. These were always enlargement and congestion of the bronchial in the vascular endothelium of pulmonary capillaries, and mediastinal lymph nodes. In seven of the 11 whole in the alveolar epithelial cells, and also in macrophages animals examined, all lymph nodes examined were (Figure 4). Nuclei containing inclusions had margin- enlarged. Petechial hemorrhages were commonly ated chromatin. observed in the heart, lungs, intestine, kidneys, and Sections of lymph nodes had diffuse lymphoid lymph nodes (Figure 2). Late in the course of the out- hyperplasia of a very marked degree, giving the impres- break, when sneezing was reported in the nursery, a sion of sarcomatous change. In a few pigs, however, carcass was received with nasal deformity and tur- the lymph nodes appeared severely depleted of binate atrophy. lymphocytes. Inclusion bodies were visible in renal tissue of 12 of 15 pigs in which this tissue was examined micro- 74 L AA'L7 Can Vet J Volume 29, January 1988 ,4 Figure 3. Section of lung tissue from a six-week-old pig Figure 4. Section of lung from the same pig as in Figure 3. with interstitial pneumonia, characterized by thickened and The alveolar septum is infiltrated by lymphocytic cells, and highly cellular alveolar septa. H&E. Bar = 59 ym. an inclusion body is visible in an alveolar epithelial cell nucleus (arrow) with marginated chromatin. H&E. Bar = 14 ttm.

Figure 5. Electron micrograph of a cell in the kidney of Figure 6. Electron micrograph of same kidney as in a 12-week-old pig. N = nucleus. C = cytoplasm. Inner (i) Figure 5. Shown is the cytoplasm of a cell infected with virus. and Outer (0) nuclear membranes are visible with a viral Unenveloped viral particles are visible, free in the cytoplasm, nucleocapsid (arrow) budding through the inner nuclear while those particles seen in the cytoplasmic vacuoles have membrane and acquiring an envelope. Uranyl acetate and acquired an envelope. Uranyl acetate and lead citrate. lead citrate. Bar = 120 nm. Bar = 120 nm. scopically. These inclusions were often in vascular turbinate and renal tissues from the herd. The resulting endothelial cells of the medullary vasa recta or in cells measurements, in nanometers, were 45 to 66, 82 to 92, in the interstitium. Petechial hemorrhages were a and 136 respectively for the electron dense core, the feature of these sections. Inclusion bodies were only capsid and outer double membrane of virus particles occasionally seen in the renal cortex, and rarely in in the turbinate. Equivalent measurements for virus tubular epithelial cells or glomeruli. There was no in the kidney were 61, 95, and 138 nanometers. Based apparent cellular inflammatory response associated on the observed morphology (size, location, cubic sym- with the presence of inclusions. metry, presence of an envelope), the particles were Three young pigs, approximately four-weeks-old, identified as belonging to the family Herpesviridae. had lesions of inclusion body rhinitis, characterized The particle sizes are within the ranges published by by infiltration of the nasal mucosa by neutrophils and Edington for PCMV (8). lymphocytes, associated with numerous very large basophilic intranuclear inclusion bodies within Microbiological Findings enlarged epithelial cells of the nasal mucosal glands. Routine bacteriological examination of multiple tissues from the necropsied pigs yielded no pathogens in most Electron Microscopy cases. Salmonella species were isolated in selenite broth Ultrastructural examination of inclusion bodies in the from the intestines of three pigs. Two isolates were lung, kidney, and nasal tissues revealed viral particles Salmonella california and one was Salmonella wor- in each location. Nucleocapsids were commonly visible thington. The intestine of a four-week-old pig with in the nucleus and cytoplasm. They were seen to bud enteritis yielded a heavy mixed growth of Escherichia at the inner nuclear membrane, and so acquire an coli (K88 negative) and Pseudomonas aeruginosa. envelope (Figure 5). Membrane-bound vesicles in the Repeated attempts failed to isolate a virus from lung cytoplasm contained numerous enveloped virus par- and kidney tissues, using tissue culture cell lines derived ticles (Figure 6). Virus particle measurements were from porcine fallopian tube and bovine trachea. made from three photographic negatives of affected Paired serum samples from the herd were examined

. . . . .- ^^ a wet 48 Can Vet J Volume 29, January 1988 be a reliable criterion. Our failure to isolate the virus s'- ; - ; is not unexpected for porcine cytomegalovirus in view

I of the difficulties experienced by others in attempting i to isolate this strongly cell-associated virus in cell cultures other than pig lung macrophages (12). Pseud- g*s As - ~~~t- 1:16;.1:1W~~~~~~~16-i2.. A orabies virus would, however, be expected to grow in I 1 * 1:16i- the cell lines used. 5 Swine of all ages may become infected with porcine cytomegalovirus, however clinical disease is usually 8 14 restricted to very young pigs. Under most conditions 11 ~~~~~~1:320 of management, systemic disease or death will occur only in piglets infected in utero or when less than two 3Drdigherd. weeks of age; infection of pigs over two weeks results t o t&ke, may 14, 1934, t c 1:20. sg usually in either a localized rhinitis or subclinical infec- tion (8,13). Pigs exposed for the first time as adults, may however, develop a generalized infection with 3g -ie 1:10 -4 -:;siir '-1i anorexia and lethargy, but, according to Edington (8), {!'-S; ¢No. v-r 4 .1985 ., 2 without pyrexia. In the acute phase of illness, the dry vi e t. 2 1:30 -F: ' sows in the herd described in this report often had -'^-"0' -N 1:160s - N _-ili 'it temperatures of 40.5 to 42.0°C. The same author describes illness in piglets born to sows infected (either or while pregnant; stillbirths were _~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~13 -- ;'1:10 clinically silently) increased, surviving piglets were weak, and often died within two weeks of birth with lesions of a generalized by the ELISA technique (6) for antibody to porcine disease. Microscopic examination of tissues from such cytomegalovirus (Table III). Single sera from a com- cases, and from older piglets with localized rhinitis or mercial herd which supplied piglets to the herd in 1985 subclinical infections, revealed a difference with were titers were in the same ranges also tested. The respect to the predominant cell types attacked by the as those found in surveys of commercial herds (6). No virus. Whereas the milder disease was characterized significant rise in titer occurred in the breeding herd by viral inclusions in, and necrosis of, epithelial cells between the two sampling dates, however a pooled predominantly, the severe form was characterized by was negative sample taken 18 months previously inclusions and injury to vascular endothelium and cells same sera were to indirect (<1:20). The subjected of the mononuclear phagocyte system. immunofluorescence and serum neutralization for Transplacental transmission of virus has been pseudorabies, serum neutralization for infectious demonstrated experimentally in swine (5,10) and is bovine rhinotracheitis virus, and indirect immuno- considered to be an important means of vertical fluorescence for African swine fever and hog cholera, transmission of cytomegalovirus in pigs and in humans were to Indirect and all of these reported be negative. Intrauterine growth retardation and failure to immunofluorescence for porcine cytomegalovirus (14). thrive after birth are reported in congenitally infected was attempted using positive cytomegalovirus swine children. Poor growth rates were recorded here in antiserum on cryostat sections of lung and kidney weeks 4 and 5 of the outbreak for piglets which were tissue which had been stored at - 80°C. No specific born to those pregnant sows infected in week 1. Sows fluorescence could be correlated with the lesions or from this same group also had increased stillbirths, inclusion bodies. weak piglets, and increased preweaning mortality. Discussion Similar observations were made in Australia during an We have concluded that the herpesvirus associated epidemic in 1959 and 1960 (9). with this epizootic was porcine cytomegalovirus. The Epidemiological studies of pregnant women infected most important differential we considered was pseud- with the human strain indicate that the immune status orabies, and there were several criteria to be considered of the mother is a major determining factor in fetal in reaching our etiological diagnosis. The macroscopic infections (14). Briefly, these studies show that fetal lesions could equally well be associated with either infection is more likely to result from a primary mater- disease. The microscopic lesions, however, favored nal infection than from a subsequent infection. porcine cytomegalovirus over pseudorabies. In the The age range of pigs with severe systemic disease latter disease in swine, focal necrotizing lesions in and death (0-5 months) and the prevalence of adult various tissues have usually been associated with the clinical infections in this herd, with consequences for inclusion bodies, and involvement of the central ner- the unborn litters, suggest that most of the pigs were vous system has been common. Neither lesion was found exceptionally susceptible and very likely experiencing in this outbreak. The serological studies for evidence a primary infection. This is supported to some extent of active infection with porcine cytomegalovirus were by the seroconversion to PCMV, which occurred in inconclusive, but did provide evidence of seroconver- the intervening 18 months. We consider it likely that sion since the pre-epizootic sampling eighteen months PCMV was introduced in the summer or fall of 1985 earlier. The serology for pseudorabies was negative. by caesarean-derived litters, which were from a The virus particle size is suggestive of porcine serologically-positive commercial herd (Table I1I) with cytomegalovirus, although on its own, this would not clinical evidence of rhinitis. Pigs from these litters were Can Vet J Volume 29, January 1988 49 in the barn at the time of the outbreak, sharing a in Saskatchewan has experienced a similar epizootic common airspace with the affected pigs, though not outbreak during the winter of 1986/87, with clinical in direct physical contact. effects on the adult breeding herd comparable to those In addition to the widespread vascular injury, dif- described in this paper. So it seems to us that porcine fuse interstitial pneumonia was consistently present in cytomegalovirus is emerging as an economically sig- affected pigs from this herd. In both natural and nificant pathogen for swine herds with minimal disease experimentally-induced infections in pigs, interstitial status. If this is correct, the capacity for transplacental pneumonia has been described and inclusions found transmission of the agent will present some difficulties in cells in the lungs (4,8). Experimentally, interstitial in preventing the entry of the virus into herds of this pneumonia with inclusion bodies occurred in pigs inoc- type via infected caesarean-derived pigs. ulated at up to eight-days-old and either dying or killed at 16-27 days, and cytomegalic inclusions have been Acknowledgments observed in the lungs of pigs up to 34-days-old (13). We wish to acknowledge the technical expertise of Corner and co-workers (4) concluded that enzootic Mr. Ian Shirley and Mrs. Louise Stevenson in process- pneumonia was present in the pigs they examined and ing tissues for electron microscopy and developing the this obscured any effects of PCMV on the lungs. We photographs, respectively. did not consider the pneumonia in pigs from this out- break to be consistent with pneumonia caused by References Mycoplasma hyopneumoniae. The diffuse interstitial 1. GILLESPIE JH, TIMONEY JF. Hagan and Bruner's infec- character of the lesion, without evidence of specific tious disease of domestic animals. 7th ed. Ithaca: Cornell is different from of University Press,. 1981; 551-594. peribronchiolitis that Mycoplasma 2. FRANK JF, MAGWOOD SE, GRAY DP. Infectious bovine (15), and paralleled the distribution of inclusion rhinotracheitis in Canada. Bull Off Int Epizoot 1975; 1 1 1: 1-10. bodies. Interstitial pneumonia is described in infants 3. MITCHELL D, CORNER AH. An outbreak of "inclusion infected congenitally or postnatally with human body" rhinitis in pigs. Can J. Comp Med 1958; 22: 199-202. cytomegalovirus. It is also a common lesion in adults 4. CORNER AH, MITCHELL D, JULIAN RJ, MEADS EB. A generalized disease in piglets associated with the presence of following renal allografts, in association with immuno- cytomegalic inclusions. J Comp Pathol 1964; 74: 192-199. suppressive therapy. The lesions described are similar 5. L'ECUYER C, CORNER AH, RANDALL GCB. Porcine in adults and young: pneumocytes are enlarged and cytomegalic inclusion disease; transplacental transmission. Proc contain intranuclear inclusion bodies, and alveolar 2nd Congress International Pig Vet Soc Hannover, 1972: 99. are 6. ASSAF R, BOUILLANT AMP, DI FRANCO E. Enzyme septa infiltrated by mononuclear and plasma linked immunosorbent assay (ELISA) for the detection of anti- cells (14). Hyaline membranes are sometimes present. bodies to porcine cytomegalovirus. Can J Comp Med 1982; The pulmonary macrophage of the pig has been shown 46: 183-185. to be particularly sensitive to infection with 7. DONE JT. An "inclusion body" rhinitis of pigs (preliminary PCMV (12). report). Vet Rec 1955; 67: 525-527. 8. EDINGTON N. Porcine cytomegalovirus infection. In: Leman The kidneys have been a common site of involve- AD, Glock RD, Mengeling WL, Penny RHC, Scholl E, Straw ment in pigs and other species, with inclusions in B, eds. Diseases of swine. 5th ed. Ames, Iowa: The Iowa State tubular epithelium, glomeruli, vascular endothelium, University Press, 1981: 271-277. and interstitial tissue (4,8,14,16,17). In our case herd, 9. CAMERON-STEPHEN ID. Inclusion body rhinitis of swine. were seldom in tubular Clinical aspects. Aust Vet J 1961; 37: 87-91. inclusions observed epithelial 10. EDINGTON N, WATT RG, PLOWRIGHT W, WRATHALL cells or in glomeruli but frequently in capillary AE, DONE JT. Experimental transplacental transmission of endothelium and interstitial tissue of the renal medulla. porcine cytomegalovirus. J Hyg (Camb) 1977; 78: 243-251. It should also be noted that we did not find lesions 11. EUGSTER AK, ANGULO AB, SCHWARTZ WL. Isolation of interstitial nephritis, such as recorded in pigs by of infectious bovine rhinotracheitis (IBR) virus from stillborn and neonatal piglets. Proc Am Assoc Vet Lab Diagnost Buffalo, others, especially in association with tubular epithelial New York, 1978: 1-14. cytomegalovirus inclusions (17). 12. WATT RG, PLOWRIGHT W, SABO A, EDINGTON N. A At the ultrastructural level, the viral particles seen sensitive cell culture system for the virus of porcine inclusion in nasal glands, pulmonary and renal tissues from pigs body rhinitis (cytomegalic inclusion disease). Res Vet Sci 1973; in this herd in 14: 119-121. were similar morphology and dimensions 13. EDINGTON N, PLOWRIGHT W, WATT RG. Generalized to those described previously as porcine cytomegalovirus porcine cytomegalic inclusion disease: distribution of (18,19,20). These characteristics are, however, not cytomegalic cells and virus. J Comp Pathol 1976; 86: 191-202. specific to this member of the family Herpesviridae. 14. HANSHAW JB, DUDGEON JA, MARSHALL WC. Viral Anemia was not shown to be a significant part of diseases of the fetus and newborn. Toronto: W.B. Saunders Company, 1985: 92-131. the clinical or pathological picture in this herd. Mild 15. WHITTLESTONE P. Enzootic pneumonia of pigs (EPP). Adv anemia was detected in two of four sick nursery pigs Vet Sci Comp Med 1973; 17: 1-55. blood sampled, and in a single anorexic sow out of 16. HARTLEY WJ, DONE JT. Cytomegalic inclusion body disease four farrowing sows sampled. Nine dry sows, two in sheep: a report of two cases. J Comp Pathol 1963; 73: 84-87. and 17. KELLY DF. Pathology of extranasal lesions in experimental boars, three feeder pigs were also sampled but inclusion-body rhinitis of pigs. Res Vet Sci 1967; 8: 472-478. were within the normal range for packed cell volume 18. DUNCAN JR, RAMSEY FK, SWITZER WP. Electron micro- and hemoglobin level. scopy of cytomegalic inclusion disease of swine (inclusion body The economic significance of porcine cytomegalovirus rhinitis). Am I Vet Res 1965; 26: 939-947. in commercial herds in Canada has been limited to 19. VALICEK L, SMID B, PLEVA V, MENSIK I. Porcine cytome- galic inclusion disease virus: electronmnicrospic study of the nasal rare sporadic deaths of very young piglets, and the mucosa. Arch Virusforsch 1970; 32: 19-30. more common occurrence of mild rhinitis in piglets 20. VALICEK L, SMID B, MENSIK I. Electron microscopy of over three weeks of age. Another minimal disease herd porcine cytomegalovirus. Arch Virusforsch 1973; 41: 344-353. 50 Can Vet J Volume 29, January 1988