Hendra Virus Infection in Dog, Australia, 2013

Kirkland, Peter D.; Gabor, Melinda; Poe, I; Neale, Kristie; Chaffey, Kim; Finlaison, Deborah S.; Gu, Xingnian; Hick, Paul; Read, Andrew J.; Wright, T.; Middleton, Deborah

doi:10.3201/eid2112.151324

Cited by 39 publications

(32 citation statements)

References 6 publications

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“…Although some dogs developed subtle, non‐specific and short‐lived signs of infection, others remained clinically well throughout the period of virus replication; virus clearance was temporally associated with the development of virus neutralising antibody. These observations are consistent with the two canine field cases, in which neutralising antibodies against HeV were found in reportedly asymptomatic dogs that were tested during investigation of HeV events in horses and from which infectious virus was not recovered.…”

Section: Discussionsupporting

confidence: 51%

“…More recently, antibody to HeV has been found in asymptomatic dogs on two properties that were experiencing HeV outbreaks in horses . In at least one of those cases, the infected dog may have had exposure to the blood of an infected horse . The close relationship between dogs and people has raised a question regarding the potential of dogs to act as a source of transmission of HeV to people.…”

mentioning

confidence: 99%

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Experimental Hendra virus infection of dogs: virus replication, shedding and potential for transmission

et al. 2017

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Objective Characterisation of experimental Hendra virus (HeV) infection in dogs and assessment of associated transmission risk. Methods Beagle dogs were exposed oronasally to Hendra virus/Australia/Horse/2008/Redlands or to blood collected from HeV‐infected ferrets. Ferrets were exposed to oral fluids collected from dogs after canine exposure to HeV. Observations made and samples tested post‐exposure were used to assess the clinical course and replication sites of HeV in dogs, the infectivity for ferrets of canine oral fluids and features of HeV infection in dogs following contact with infective blood. Results Dogs were reliably infected with HeV and were generally asymptomatic. HeV was re‐isolated from the oral cavity and virus clearance was associated with development of virus neutralising antibody. Major sites of HeV replication in dogs were the tonsils, lower respiratory tract and associated lymph nodes. Virus replication was documented in canine kidney and spleen, confirming a viraemic phase for canine HeV infection and suggesting that urine may be a source of infectious virus. Infection was transmitted to ferrets via canine oral secretions, with copy numbers for the HeV N gene in canine oral swabs comparable to those reported for nasal swabs of experimentally infected horses. Conclusion HeV is not highly pathogenic for dogs, but their oral secretions pose a potential transmission risk to people. The time‐window for transmission risk is circumscribed and corresponds to the period of acute infection before establishment of an adaptive immune response. The likelihood of central nervous system involvement in canine HeV infection is unclear, as is any long‐term consequence.

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Section: Discussionsupporting

confidence: 51%

mentioning

confidence: 99%

Experimental Hendra virus infection of dogs: virus replication, shedding and potential for transmission

et al. 2017

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“…A second confirmed HeV infection in a dog was reported in 2013. The dog tested positive to HeV by quantitative reverse transcription PCR (q-RT-PCR) during the apparent early stages of an acute infection and had appeared to have become naturally infected with HeV following close exposure to blood from a euthanized HeV infected horse [35]. This dog was euthanized and extensively analyzed via postmortem examination.…”

Section: Hendra Virus and Nipah Virus Emergencementioning

confidence: 99%

“…Although the dog had appeared clinically healthy, histopathologic findings of widespread necrotizing vasculitis was noted, with the most severe lesions recorded in the kidney, brain and lymph nodes, with little involvement of the lungs. Additionally, HeV RNA was detected in multiple tissues [35]. Presently, the extent of HeV transmission from bats to dogs in Australia is an unknown concern and should be the focus of future studies.…”

Section: Hendra Virus and Nipah Virus Emergencementioning

confidence: 99%

Hendra virus and Nipah virus animal vaccines

Broder

Weir

Reid³

2016

Vaccine

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Hendra virus (HeV) and Nipah virus (NiV) are zoonotic viruses that emerged in the mid to late 1990s causing disease outbreaks in livestock and people. HeV appeared in Queensland, Australia in 1994 causing a severe respiratory disease in horses along with a human case fatality. NiV emerged a few years later in Malaysia and Singapore in 1998-99 causing a large outbreak of encephalitis with high mortality in people and also respiratory disease in pigs which served as amplifying hosts. The key pathological elements of HeV and NiV infection in several species of mammals, and also in people, are a severe systemic and often fatal neurologic and/or respiratory disease. In people, both HeV and NiV are also capable of causing relapsed encephalitis following recovery from an acute infection. The known reservoir hosts of HeV and NiV are several species of pteropid fruit bats. Spillovers of HeV into horses continue to occur in Australia and NiV has caused outbreaks in people in Bangladesh and India nearly annually since 2001, making HeV and NiV important transboundary biological threats. NiV in particular possesses several features that underscore its potential as a pandemic threat, including its ability to infect humans directly from natural reservoirs or indirectly from other susceptible animals, along with a capacity of limited human-to-human transmission. Several HeV and NiV animal challenge models have been developed which have facilitated an understanding of pathogenesis and allowed for the successful development of both active and passive immunization countermeasures.

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“…2 Infected horses are further able to transmit HeV to other horses, dogs and humans, acting as an amplification host for the virus. 3,4 Clinical signs of HeV infection in horses are highly variable and non-specific, and infection has been confirmed in some cases in the absence of or with only minimal clinical signs, including, in some instances, a lack of pyrexia. 5 Acutely infected horses usually display depression and a range of general, respiratory and/or neurological signs, mediated by an endothelial vasculitis, such as fever, loss of appetite, abdominal pain, muscle fasciculations, terminal nasal discharge, ataxia and apparent loss of vision.…”

mentioning

confidence: 99%