Studies on the pathogenesis of heart lesions in dogs infected with pseudorabies (Aujeszky's disease) virus

Olson, Greg R.

doi:10.31274/rtd-180813-6854

Cited by 9 publications

(15 citation statements)

References 19 publications

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“…Following primary replication, the virus is taken up by sensory nerve endings and spreads by retrograde axonal transport first to the sensory nerve ganglia and subsequently to the central nervous system. 19 In addition to ganglioneuritis and encephalitis, PRV may also cause myocardial degeneration with ganglionitis of the cardiac autonomic plexuses 30 and degeneration of intestinal myenteric ganglia. 15 To test for PRV, fresh cerebellum and medulla from dogs 1 and 2 were used for virus isolation and identification (virus isolation and PCR results are summarized in Table 1).…”

Section: Discussionmentioning

confidence: 99%

Pseudorabies virus infection in Oklahoma hunting dogs

et al. 2011

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Pseudorabies is caused by Suid herpesvirus 1, a member of the Alphaherpesvirinae subfamily. Although pigs are the natural host of Pseudorabies virus (PRV), the virus has a broad host range and may cause fatal encephalitis in many species. The United States obtained PRV-free status in 2004 after the virus was eradicated from domestic swineherds, but the virus is still present in feral swine populations. The current report describes PRV infection in 3 dogs that were used to hunt feral swine. The dogs developed clinical signs including facial pruritus with facial abrasions, dyspnea, vomiting, diarrhea, ataxia, muscle stiffness, and death. Two were euthanized, and 1 died within approximately 48 hr after onset of clinical signs. The salient histologic changes consisted of neutrophilic trigeminal ganglioneuritis with neuronophagia and equivocal intranuclear inclusion bodies. Pseudorabies virus was isolated from fresh tissues from 2 of the dogs, and immunohistochemistry detected the virus in the third dog. Virus sequencing and phylogeny, based upon available GenBank sequences, revealed that the virus was likely a field strain that was closely related to a cluster of PRV strains previously identified in Illinois. Though eradicated from domestic swine in the United States, PRV is present in populations of feral swine, and should therefore continue to be considered a possible cause of disease in dogs and other domestic animals with compatible clinical history and signs. Continued surveillance is necessary to prevent reintroduction of PRV into domestic swine.

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Section: Discussionmentioning

confidence: 99%

Pseudorabies virus infection in Oklahoma hunting dogs

et al. 2011

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“…Examination of several other organs by histopathological immunohistochemical and ISH methods was negative, including the heart. Previous studies have described severe myocardial necrosis and viral replication (OLSON and MILLER, 1986). It has been proposed that cardiac lesions could occur in relation to a haematogenous dissemination of ADV or neurocardiotropism, but this could not be verified in these cases.…”

Section: Discussionmentioning

confidence: 88%

“…I n these animals, Aujeszky's disease virus (ADV) can establish latent infections from which the virus can be reactivated (RZIHA et al, 1986;BROWN et al, 1990). Aujeszky's disease is always lethal in other animal species including carnivores (OLSON and MILLER, 1986;GRATE and MONTALI, 1987).…”

Section: Introductionmentioning

confidence: 99%

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Diagnosis of Aujeszky's Disease Virus Infection in Dogs by Use of Immunohistochemistry andIn‐SituHybridization

Quiroga

Nieto

Sur

et al. 1998

Journal of Veterinary Medicine Series A

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Aujeszky's disease (AD) was diagnosed in seven dogs by histolog~cal examination, immunohistochemistry and DNA in-situ hybridization. All dogs which lived on two swine farms died spontaneously showing an acute neurological syndrome (hypersalivation, vomiting, pruritus, depression and coma). The most significant histopathological lesion was a non-suppurative encephahtis located in the brain stem, mainly near the floor of the IVth ventricle. Aujeszky's disease virus (ADV) antigen and ADV nucleic acid hstribution coincided with the histopathologcal lesions. However, little ADV antigen and ADV nucleic acid was found in severely damaged areas. A few neurons stained intensely by immunohistochemistry and in-situ hybridization in non-inflamatory areas. Both immunohistochemistry and in-situ hybridization techniques are valid techniques to confirm ADV infection in paraffin-embedded tissues and will be useful for characterizing the pathogenesis of ADV in the central nervous system (CNS) in carnivores.

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“…Electrocardiographic (ECG) changes associated with viral infection of the heart have been studied in animal models, primarily coxsackie B and encephalomyocarditis viruses in mice (14)(15)(16)(17), although the effects of western equine encephalitis virus, influenza A virus, and pseudorabies virus infections in the heart have also been described (18)(19)(20). In an effort to further evaluate and char-acterize the RbCV model system, this study was designed to describe the ECG and pathologic changes associated with RbCV infection.…”

mentioning

confidence: 99%

ECG changes after rabbit coronavirus infection

Alexander

Keene

Yount

et al. 1999

Journal of Electrocardiology

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This study examines the electrocardiographic (ECG) changes following rabbit coronavirus (RbCV) infection. We have shown that infection with RbCV results in the development of myocarditis and congestive heart failure and that some survivors of RbCV infection go on to develop dilated cardiomyopathy in the chronic phase. Serial ECGs were recorded on 31 RbCV-infected rabbits. Measurements of heart rate; P-R interval; QRS duration; QTc interval; and P-, QRS-, and T-wave voltages were taken. The recordings were also examined for disturbances of conduction, rhythm, and repolarization. The acute and subacute phases were characterized by sinus tachycardia with depressed R- and T-wave voltages as well as disturbances of conduction, rhythm, and repolarization. In most animals in the chronic phase, the sinus rate returned to near-baseline values with resolution of the QRS voltage changes. The ECG changes observed during RbCV infection are similar to the spectrum of interval/segment abnormalities, rhythm disturbances, conduction defects, and myocardial pathology seen in human myocarditis, heart failure, and dilated cardiomyopathy. Because animals often died suddenly in the absence of severe clinical signs of congestive heart failure during the acute phase, RbCV infection may increase ventricular vulnerability, resulting in sudden cardiac death. RbCV infection may provide a rare opportunity to study sudden cardiac death in an animal model in which the ventricle is capable of supporting ventricular fibrillation, and invasive techniques monitoring cardiac function can be performed.

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Studies on the pathogenesis of heart lesions in dogs infected with pseudorabies (Aujeszky's disease) virus

Cited by 9 publications

References 19 publications

Pseudorabies virus infection in Oklahoma hunting dogs

Pseudorabies virus infection in Oklahoma hunting dogs

Diagnosis of Aujeszky's Disease Virus Infection in Dogs by Use of Immunohistochemistry andIn‐SituHybridization

ECG changes after rabbit coronavirus infection

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