Clinical and pathologic features of parvoviral diarrhea in pound-source dogs

From June 1980 through May 1982, 161 pound-source dogs that developed diarrhea while being used in research were evaluated to determine whether canine parvovirus (CPV) type 2 was the etiologic agent. Evaluation included notation of clinical signs, determination of serum CPV-specific immunoglobulin (Ig) M and IgG titers, virus isolation attempts, and histologic examination of tissues. Criteria for diagnosis of canine parvoviral enteritis were serum CPV-specific IgM antibodies, isolation of CPV from feces, and histologic evidence of intestinal crypt cell necrosis. Upon arrival, 67 clinically normal pound-source dogs were evaluated to determine the prevalence of fecal shedding of CPV and to determine their antibody titers to CPV. Parvovirus was not isolated from any of these dogs, although 76% had IgG antibodies and 3% had IgM antibodies. Of the 161 dogs with diarrhea, 40 (25%) had parvoviral enteritis. Of dogs with parvoviral enteritis, 71% had IgG antibodies and 68% had IgM antibodies. Canine parvovirus was isolated from 18 dogs. Serum IgG antibodies were found in 85% of dogs with diarrhea due to other causes. The geometric mean titer of IgG antibodies to CPV was not significantly different among the 3 groups. Clinical signs that appeared significantly (P less than 0.05) more often in dogs with parvoviral enteritis included bloody diarrhea, anorexia, fever (greater than or equal to 39.4 C), and leukopenia (WBC less than 6,000/mm3). Cases occurred throughout the year, without apparent seasonal variation. The duration between arrival and onset of diarrhea was significantly (P less than 0.05) shorter for dogs with parvoviral enteritis.(ABSTRACT TRUNCATED AT 250 WORDS)     

An investigation of ewe to lamb transfer of the itch mite Psorergates ovis

Five outbreaks of acute enteritis and one of myocarditis in 5 to 12-week-old puppies are reported. In cases of enteritis the initial clinical finding of slight malaise was followed within 24 hours by severe vomiting, diarrhoea, dehydration and death in most cases. The lesions of acute necrotizing enteritis and widespread lymphoid depletion were identical to those of feline panleucopaenia. In the outbreak of myocarditis, 3 puppies were founddead and a fourth developed congestive heart failure.

Parvoviral-like particles were found in the faeces of 5 cases of enteritis by electron microscopy and virus was isolated from 2 dogs, using a feline kidney cell line. The isolates demonstrated the physicochemical characteristics of a parvovirus and haemagglutinated porcine red blood cells at 4°C and 22°C but not 37°C. The isolates were antigenically related to feline panleucopaenia virus by immune aggregation, haemagglutination inhibition and immunofluorescence.

Fourteen of 48 sera from local dogs had significant haemagglutination inhibition titres to the virus. The diseases reported here are identical to overseas reports of parvoviral enteritis and myocarditis.     

Prognostic value of serum acute-phase proteins in dogs with parvoviral enteritis

Objective : To evaluate the acute-phase protein response in dogs with parvoviral enteritis as predictor of the clinical outcome. Methods : Canine parvovirus infection was diagnosed based on the compatible clinical findings and confirmed by the canine parvovirus antigen test in 43 dogs of less than six months of age. Blood samples for complete blood cell count and acute-phase proteins (C-reactive protein, haptoglobin, ceruloplasmin and albumin) were collected before treatment. Twenty-three dogs died during or after treatment (non-survival) and the rest recovered (survival). Five healthy dogs were enrolled as control. Results : Serum C-reactive protein, ceruloplasmin and haptoglobin levels in dogs with parvoviral enteritis were higher (P<0·001, P<0·01 and P<0·001, respectively), but serum albumin was lower (P<0·001) than those in controls. Mean C-reactive protein and ceruloplasmin values in non-survival were higher (P<0·01) than those for survival dogs. C-reactive protein was found to be superior to ceruloplasmin, haptoglobin and albumin for distinguishing survival from non-survival dogs. Values higher than 92·4 mg/l for C-reactive protein had a sensitivity of 91% to predict mortality. Clinical Significance : The magnitude of the increase in serum acute-phase proteins in dogs with parvoviral enteritis could be a useful indicator of the prognosis of the disease. In acute-phase proteins, C-reactive protein is a potent predictor of mortality in dogs with parvoviral enteritis.     

Polymerase chain reaction (PCR) amplification of parvoviral DNA from the brains of dogs and cats with cerebellar hypoplasia

Cerebellar hypoplasia in cats is caused most commonly by an in utero or perinatal infection with feline panleukopenia virus (parvovirus). Cerebellar hypoplasia has been reported infrequently in dogs, but no viral etiology has been identified to date. DNA was extracted from archival, paraffin-embedded, cerebellar tissue from 8 cats and from 2 canine littermates with cerebellar hypoplasia, 2 canine littermates with cerebellar cortical abiotrophy, 6 dogs with congenital cerebellar vermal defects, 1 dog with congenital hydranencephaly, and 15 dogs and cats with various encephalitdes. The DNA extracted from each cerebellum was subject to polymerase chain reaction (PCR) amplification by 3 primer pairs specific for parvovirus DNA. Sequence analysis of PCR products from each of the 8 cats and 2 dogs with cerebellar hypoplasia confirmed their identity with parvoviral DNA. The 6 dogs with cerebellar vermal defects, 2 dogs with cortical abiotrophy, 1 dog with congenital hydranencephaly, and all control samples were PCR negative for parvovirus. Parvoviral structural proteins were not identified by immunohistochemistry in either dog with cerebellar hypoplasia. This study shows that parvoviral DNA can be amplified from feline and canine archival brain tissue and that cerebellar hypoplasia in dogs might be associated with in utero parvovirus infection.     

Evaluation of tongue as a complementary sample for the diagnosis of parvoviral infection in dogs and cats.

Diagnosis of canine parvovirus type 2 and feline panleukopenia virus infection in dogs and cats may be hampered by the severity of enteric lesions, secondary bacterial overgrowth, and rapid onset of autolysis. In contrast to small intestine, tongue epithelium is less sensitive to postmortem changes. Sections of tongue and small intestine from 11 dogs and 11 cats with a clinical history and gross and microscopic lesions compatible with canine and feline parvoviral infection were examined for parvoviral infection using real-time polymerase chain reaction (PCR), immunohistochemistry (IHC), and direct fluorescent antibody testing (FA). Parvoviral DNA was detected by PCR in both small intestine and tongue of all but 1 dog. Nineteen of 22 animals (86%) with suspect or positive FA staining in the small intestine also had positive FA and IHC staining in the tongue. Three of 3 dogs (100%) whose carcasses had been frozen and thawed prior to necropsy had more consistently positive staining in tongue than in small intestine by FA and IHC. These data confirm tongue as an excellent complementary sample for parvoviral testing in dogs and cats, especially in cases in which postmortem autolysis has occurred.     

Characterisation of lipid profiles in dogs with parvoviral enteritis

OBJECTIVE: To characterise the lipid profiles in dogs with parvoviral enteritis. METHODS: Blood was collected before treatment from 30 dogs that fulfilled the criteria for severe sepsis including hypo- or hyperthermia, hypotension, leucopenia, thrombocytopenia and evidences of organ dysfunction. Canine parvovirus was detected by haemagglutination and indirect fluorescence antibody tests in the faeces. Twenty control dogs were also enrolled on the basis of normal physical examination results, complete blood count and serum biochemistry profiles. RESULTS: Tachycardia, tachypnoea, hypotension, leucopenia, thrombocytopenia and increased serum markers of tissue injury (alanine aminotransferase, creatinine kinase myocardial isoenzyme [CK-MB], blood urea nitrogen and creatinine) were observed in dogs with parvoviral enteritis. Serum total cholesterol, high-density lipoprotein cholesterol and low-density lipoprotein cholesterol levels were lower, but serum triglyceride level was higher in dogs with parvoviral enteritis than those in control dogs (P<0.001). Circulating tumour necrosis factor alpha correlated negatively with total cholesterol (r=-0.979; P<0.001) but positively with triglyceride (r=0.953; P<0.001) in dogs with parvoviral enteritis. Serum total cholesterol and high-density lipoprotein cholesterol levels were lower in non-survival (n=9) dogs than in survival dogs (n=21, P<0.001). CLINICAL SIGNIFICANCE: Serum total cholesterol and high-density lipoprotein cholesterol levels decreased, but serum triglyceride level increased in dogs with parvoviral enteritis. Low serum total cholesterol and high-density lipoprotein cholesterol levels may be used as an index of the severity of parvoviral enteritis.     

A history of canine parvovirus in Australia: what can we learn?

Canine parvovirus (CPV) has been reported throughout the world since the late 1970s. Published information was reviewed to draw insights into the epidemiology, pathogenesis, diagnosis, treatment and outcomes of CPV disease in Australia and the role of scientific research on CPV occurrence, with key research discoveries and knowledge gaps identified. Australian researchers contributed substantially to early findings, including the first reported cases of parvoviral myocarditis, investigations into disease aetiopathogenesis, host and environmental risk factors and links between CPV and feline panleukopenia. Two of the world's first CPV serological surveys were conducted in Australia and a 1980 national veterinary survey of Australian and New Zealand dogs revealed 6824 suspected CPV cases and 1058 deaths. In 2010, an Australian national disease surveillance system was launched; 4940 CPV cases were reported between 2009 and 2014, although underreporting was likely. A 2017 study estimated national incidence to be 4.12 cases per 1000 dogs, and an annual case load of 20,110 based on 4219 CPV case reports in a survey of all Australian veterinary clinics, with a 23.5% response rate. CPV disease risk factors identified included socioeconomic disadvantage, geographical location (rural/remote), season (summer) and rainfall (recent rain and longer dry periods both increasing risk). Age <16 weeks was identified as a risk factor for vaccination failure. Important knowledge gaps exist regarding national canine and feline demographic and CPV case data, vaccination coverage and population immunity, CPV transmission between owned dogs and other carnivore populations in Australia and the most effective methods to control epizootics.     

Experimental viral myocarditis: parvoviral infection of neonatal pups

Myocarditis was produced in seronegative five-day-old pups by oral and by intraperitoneal inoculation of canine parvovirus. The disease was subclinical. Histologic lesions were compatible with, but less extensive than, those seen in naturally occurring canine parvoviral myocarditis. In pups necropsied 23 days after inoculation, scattered cardiac myocytes contained intranuclear inclusion bodies, and virus-infected myocytes were demonstrated by immunofluorescence. Degeneration and loss of cardiac myocytes usually was not associated with a cellular infiltrate. At 51 days after inoculation, the myocardium contained an extensive lymphocytic infiltrate which was sometimes associated with fragmented myocytes, and was often contiguous with areas of interstitial fibrosis. At 108 days after inoculation, inflammatory lesions had regressed, and there were multifocal areas of myocardial fibrosis.     

Phosphorus deficiency in cattle on two farms in canterbury

A New Zealand canine herpesvirus isolate was inoculated into three 2-day-old puppies via the intraperitoneal route, two other puppies from the same litter being retained as in-contact controls. All pups were left suckling the bitch.

One inoculated pup died of misadventure. The remaining inoculated pups, and one in-contact pup, died with clinical signs of herpesvirus infection, the virus being subsequently recovered from a number of tissues. The remaining in-contact pup also developed typical disease, but recovered, virus being detected only in the tonsils. Lesions were detected in the diseased puppies in a wide variety of organs, and were consistent with previously published reports. No evidence of disease was detected in the bitch, but both she and the recovered pup developed neutralizing antibodies to the virus.     

Treatment of canine parvoviral enteritis with interferon-omega in a placebo-controlled challenge trial

Canine parvoviral enteritis continues to cause significant morbidity and mortality in dogs worldwide, and efficacious antiviral therapies are lacking. The present trial was aimed at evaluating the therapeutic efficacy of a recombinant feline interferon (type omega) preparation in the treatment of parvoviral enteritis in dogs. A double-blind, placebo-controlled challenge trial was performed in beagle pups (8-9 weeks); clinical signs, body weight, hematologic parameters, and mortality were monitored for a period of 14 days after challenge. Fourteen animals were inoculated with virulent canine parvovirus; 10 animals that developed clinical signs thereby meeting the inclusion criteria were admitted to the treatment phase in two randomly selected groups (placebo and IFN) of equal size. The IFN group received daily intravenous injections of rFeIFN-omega (2.5 MU/kg) for three consecutive days. The placebo group received daily injections of saline without IFN. Both groups of animals received individual supportive treatment consisting of adjusted diet and electrolyte solution.All five dogs in the placebo group developed fulminating enteritis with typical clinical signs and died within 10 days post-inoculation (or 6 days post-treatment). In the IFN-treated group, one animal died on day 2 after the treatment was started, whereas the other four dogs survived the challenge and gradually recovered. Our data confirm that the rFeIFN-omega can exert a significant therapeutic effect on dogs with parvoviral enteritis by improving clinical signs and reducing mortality.     

Evaluation of a killed feline panleukopenia virus vaccine against canine parvoviral enteritis in dogs

Immunogenic potency of a killed feline panleukopenia virus vaccine against canine parvoviral enteritis in dogs was examined. The vaccine elicited hemagglutination-inhibition antibodies to canine parvovirus (CPV) in all of the 72 dogs which were vaccinated. The vaccine was protective in dogs against both experimentally induced and naturally occurring CPV-induced disease. By statistical analysis, 4 weeks was found to be the optimal spacing between 2 vaccinal doses resulting in hemagglutination-inhibition antibody titers up to 1:5,120. Adverse reactions to the vaccine were not observed. Atypical lymphocytes were found consistently in the CPV-infected control dogs.     

Neosporosis in a pup

CASE: A 13-week-old female boxer pup was found to be suffering from rigidity of the left hindleg. Antibiotic and anti-inflammatory treatment over a 3-week period failed to improve the condition and the pup was humanely killed. METHODS: Serological examination for Neospora antibodies was carried out by the indirect fluorescent antibody test and for Toxoplasma gondii antibodies with a latex agglutination test. A variety of tissues were examined histologically, and the central nervous system by immunohistochemistry and the polymerase chain reaction. RESULTS: The IFAT for anti-Neospora antibodies showed a titre of 1:51 200 in the clinically affected pup while the latex agglutination test for Toxoplasma antibodies was negative. The dam and one of two tested litter-mates had anti-Neospora IFAT titres of 1:1600, the other litter mate was negative. All three were not clinically affected. Histological, immunohistochemical and polymerase chain reaction examinations of the affected pup confirmed the diagnosis of Neospora infection. CONCLUSION: In the live animal, serological examination is thought to be the most useful specific test. Post-mortem examination by traditional histology, immunohistochemistry and the polymerase chain reaction confirmed the diagnosis. The case is discussed in the context of present knowledge about Neospora infection in New Zealand.     

Sudden death in young dogs with myocarditis caused by parvovirus.

Sudden death of pups in the 4- to 6-week age range has recently been occurring in western Canada as a result of severe, primary, nonsuppurative myocarditis. At necropsy, the prominent macroscopic lesion was pulmonary edema, and microscopically, characteristic intranuclear inclusion bodies were found within cardiac myofibers in association with myocarditis. Ultrastructurally, numerous small particles resembling parvoviruses were found within the intranuclear inclusion bodies, which were positive by direct fluorescent antibody test for canine parvovirus. Of three pups inoculated with homogenate from affected myocardium, one developed lesions resembling canine parvoviral enteritis.     

Experimental infection in pigs with encephalomyocarditis virus

Non-suppurative myocarditis in pigs that were experimentally infected with encephalomyocarditis (EMC) virus is reported. Two of the four pigs that were infected with the virus died suddenly from myocardial failure, and all four had gross and microscopic changes consistent with EMC infection. This confirms the pathogenic potential of some strains of EMC virus for young pigs.     

Amelioration of oxidative stress using N‐acetylcysteine in canine parvoviral enteritis

Previously, antioxidants have not been evaluated for treatment of parvoviral diarrhea in dogs. In this study, antioxidant potential of N‐acetylcysteine (NAC) in dogs infected with canine parvovirus with a nonblinded randomized clinical trial has been carried out. A total 18 parvo‐infected dogs were randomly divided into two groups: nine parvo‐infected dogs were treated with supportive treatment and nine parvo‐infected dogs were treated with NAC along with supportive treatment. Simultaneously, nine healthy dogs were kept as healthy control. In parvo‐infected dogs, marked hemoconcentration, leucopenia, neutropenia and oxidative stress were noticed compared to healthy dogs. The NAC treatment progressively improved the leukocyte, neutrophil, monocyte, and eosinophil counts over the time in parvovirus‐infected dogs compared to dogs that received only supportive treatment. In addition, NAC treatment significantly improved glutathione S‐transferase (GST) activity and decreased nitrite plus nitrate (NOx) and malondialdehyde (MDA) concentrations on day 3 and 5 compared to supportive treatment in parvo‐infected dogs. However, supportive treatment alone failed to ameliorate oxidative stress in the infected dogs till day 5. The results of this study suggest that NAC represents a potential additional treatment option that could be considered to improve the health condition and minimize the duration of hospitalization in case of canine parvoviral diarrhea.     

Canine distemper infection associated with acute nervous signs in dogs.

Eight vaccinated dogs suddenly developed progressive ataxia, paresis or paralysis of short duration. A histopathological examination revealed a non-suppurative meningoencephalitis suggestive of a viral infection, and immunohistochemical examination confirmed the presence of canine distemper virus antigen in five of the dogs. Distemper had not been suspected from the clinical examination of the dogs.     

Parvoviral enteritis and salmonellosis in raccoons with sudden death

Eight of 9 juvenile raccoons at a rehabilitation center died without obvious prior clinical signs. Gross changes were unremarkable except for mildly distended intestines. Microscopically, crypt loss, distension, necrosis, and regeneration with intranuclear viral inclusions were observed in the small intestine, with marked lymphoid depletion and necrosis in Peyer patches and mesenteric lymph nodes. Immunohistochemistry with a canine parvovirus antibody showed intensive signals of parvoviral antigens in the crypts and lymphoid germinal centers. Metagenomic sequencing allowed assembly of a complete parvoviral genome with >99% identity to canine parvovirus 2a, as well as Salmonella enterica subsp. enterica. Also, S. enterica subsp. enterica serovar Thompson with multiple antimicrobial resistance was isolated from the intestinal contents. Concurrent infection with parvovirus and Salmonella should be included as a differential diagnosis in raccoons with sudden death.     

Polymerase chain reaction analysis for viruses in paraffin-embedded myocardium from dogs with dilated cardiomyopathy or myocarditis

OBJECTIVE: To perform polymerase chain reaction (PCR) analysis on paraffin-embedded myocardium from dogs with dilated cardiomyopathy (DCM) and dogs with myocarditis to screen for canine parvovirus, adenovirus types 1 and 2, and herpesvirus. SAMPLE POPULATION: Myocardial specimens from 18 dogs with an antemortem diagnosis of DCM and 9 dogs with a histopathologic diagnosis of myocarditis were evaluated. PROCEDURE: Paraffin-embedded myocardial specimens were screened for viral genome by PCR analysis. Positive-control specimens were developed from cell cultures as well as paraffin-embedded tissue specimens from dogs with clinical and histopathologic diagnoses of viral infection with canine parvovirus, adenovirus types 1 and 2, and herpesvirus. The histologic characteristics of all myocardial specimens were classified regarding extent, location, and type of inflammation and fibrosis. RESULTS: Canine adenovirus type 1 was amplified from 1 specimen from a dog with DCM. Canine parvovirus, adenovirus type 2, and herpesvirus were not amplified from any myocardial specimens. Histologic analysis of specimens from dogs with DCM revealed variable amounts of fibrosis; myocardial inflammation was observed in 1 affected dog. Histopathologic analysis of specimens from dogs with myocarditis disclosed variable degrees of inflammation and fibrosis. CONCLUSIONS AND CLINICAL RELEVANCE: Viral agents canine parvovirus, adenovirus types 1 and 2, and herpesvirus are not commonly associated with DCM or active myocarditis in dogs. Additional studies evaluating for nucleic acid from viruses that less commonly affect dogs or different types of infectious agents may be warranted to gain insight into the cause of DCM and myocarditis in dogs.     

The seroprevalence of canine respiratory coronavirus and canine influenza virus in dogs in New Zealand

Abstract

AIM: To determine whether canine respiratory coronavirus (CRCoV) and canine influenza virus (CIV) are present in dogs in New Zealand.

METHODS: Serum samples from 251 dogs of varying age, breed and clinical histories were tested for the presence of antibodies to CRCoV and CIV, using indirect fluorescent antibody (IFA) analysis. The population sampled represented a wide geographic area but principally encompassed the central and lower North Island of New Zealand.

RESULTS: Seventy-three of the 251 samples (29%) were seropositive for CRCoV. Dogs <2 years old were less likely to be seropositive for CRCoV than older dogs. None was seropositive for CIV.

CONCLUSIONS: This study revealed the presence of antibodies to CRCoV in dogs in New Zealand. Young dogs are less likely to be seropositive than older dogs, probably due to increased opportunity for exposure to CRCoV over time. Serum antibodies to CIV were not detected in any of the dogs sampled, suggesting that this virus is unlikely to be present in dogs in New Zealand.

CLINICAL RELEVENCE: Canine respiratory coronavirus is present in New Zealand. Although the role of this virus in canine infectious tracheobronchitis has not been fully elucidated, evidence suggests that it may have a causal role in this disease. Veterinarians should consider CRCoV as a differential diagnosis in cases of respiratory disease in dogs in New Zealand. While CIV appears not to be currently present in New Zealand, veterinarians should consider infection with this virus as a differential diagnosis in dogs presenting with respiratory signs.     

Canine viral enteritis: Prevalence of parvo-, corona- and rotavirus infections in dogs in the Netherlands

Summary After a brief review of the present knowledge about canine viral enteritis, the role played by parvoviral, coronaviral and rotaviral infections in contagious diarrhoea in dogs in the Netherlands is discussed. For this purpose a serologic survey, pathologic findings in dogs, and the demonstration of parvoviral antigen with an immunofluorescence test and with a newly developed haemadsorption-elution-haemagglutination assay (HEHA) are presented. It is concluded that infections with canine parvovirus, coronavirus and rotavirus appear widespread among dog populations in the Netherlands.