Hendra virus infection in a veterinarian, JN Hanna, WJ McBride, DL Brookes, J Shield

Tags: HeV infection, Jeffrey N Hanna, Carmel T Taylor, Hendra virus, infected, NOTABLE CASES Hendra virus infection, Ina L Smith, Greg A Smith, Queensland Health Scientific Services, Dianne L Brookes, Tropical Population Health Unit, Jack Shield, febrile illness, clinical reports, pre-existing conditions, reported outbreaks, serological evidence, serological studies, laboratory studies, veterinarian, Communicable Disease Control1 William J McBride, Public Health Virology, Population Health Network1 Jack Shield, Scientist4 Ina L Smith, Scientist4 Greg A Smith, Department of Primary Industries, Public Health Nursing Officer, Medicine2 Dianne L Brookes, Clin Infect Dis, Cairns, QLD, Queensland Health, Med J Aust, James Cook University, medical practitioner, Queensland Department of Primary Industries, Nipah virus encephalitis, Young P
Content: NOTABLE CASES
Hendra virus infection in a veterinarian
Jeffrey N Hanna, William J McBride, Dianne L Brookes, Jack Shield, Carmel T Taylor, Ina L Smith, Scott B Craig and Greg A Smith A veterinarian became infected with Hendra virus (HeV) after managing a terminally ill horse and performing a limited autopsy with inadequate precautions. Although she was initially only mildly ill, serological tests suggested latent HeV infection. Nevertheless, she remains well 2 years after her initial illness. Recently emerged zoonotic viruses, such as HeV, necessitate appropriate working procedures and personal protective equipment in veterinary practice. (MJA 2006; 185: 562-564)
H endra virus (HeV) and Nipah virus together comprise the genus Henipavirus within the family Paramyxoviridae (Box 1).1 HeV, formerly called equine morbillivirus, was first described after an outbreak of severe respiratory disease in horses, leading to the deaths of 14 horses and a horse trainer in Brisbane in September 1994.2,3 The trainer had had very close manual contact with frothy nasal and oral secretions,TshoemeMoefdwichalichJowurenrael bolofodA-utisntrgaeldia, from sIeSvSeNra:l0o0f2t5h-e72v9eXry2i0ll Nhorvseems,baesr d2i0d06a
1 Electron micrograph of the Hendra virus
Clinical record In early November 2004, a veterinarian notified the Tropical population health Unit (TPHU) in Cairns that one of his colleagues had become unwell a week after performing an autopsy on a horse. Two other people who had assisted with the autopsy, both members of the family who owned the horse, had apparently also become unwell, and the notifying veterinarian asked about the possibility of HeV infection in the three individuals.
stable1-h8a5n1d0; 5h6e2-d5e6v4eloped an influenzalike il©lnTehsse bMutedmicaadleJaoufurnllalreocfovAeurys.trTahliae
The horse: The horse was a 10-year-old gelding located on a property about
horses20a0n6dwwbwot.hmjap.ecopml.eauwere infected with HNeoVt.a2b,3le Cases
25 km south of Cairns. It had been acutely unwell for 1 day, with restless-
An earlier outbreak of HeV disease was
ness, increased respiratory effort and pro-
not recognised until the death, in 1995,
fuse sweating. On examination, the horse
of a farmer in Mackay. He had assisted his
was febrile (41°C per rectum), tachy-
veterinarian wife with the autopsies of
cardic (120 beats/min), markedly dysp-
two horses that died suddenly from
noeic and very weak; it lay in a lateral
unknown cause in August 1994. He was
recumbent position and could not raise
hospitalised about 2 weeks later with an aseptic meningitis, from which he apparently made a full recovery.3,4 However,
Courtesy, Mr Howard Prior, Senior Technician, Queensland
Department of Primary Industries and Fisheries.

its head. It was very dehydrated, and had injected mucous membranes and large amounts of blood-stained frothy secre-
about a year later he became acutely unwell again, and died from a severe encephalitis caused by HeV.3,4
tions issuing from its nose. A decision was made to euthanase the horse, but it had a convulsion and
The two horses were (retrospectively) shown to have also been infected with HeV.5
expired before this could be performed. Blood-stained froth emanated from its nose and mouth as it died.
After these two outbreaks, extensive investigations identified fruit bats (Pteropus spp.), commonly known as flying foxes, as the likely natural reservoir of HeV; the infection is probably subclinical in most infected flying foxes.6,7 Although it is not certain how HeV could be transmitted from flying foxes to horses, the isolation of the virus from uterine fluid and aborted fetal tissue of flying foxes suggests that horses could ingest the virus on feed or pasture recently contaminated by birth products (Box 2).6,7 The available
Autopsy on the horse: Because the diagnosis was uncertain, the treating veterinarian performed a limited autopsy on the horse in the paddock where it died. She initially wore gloves, but quickly abandoned these as they were not of an appropriate design and soon became contaminated inside. No other personal protective equipment was used. For the procedure she had to reach deep into the carcass to examine some internal organs. The autopsy resulted in the veterinarian becoming heavily
evidence indicates that transmission of the virus from horses to
contaminated with the horse's body fluids, especially those from
people, albeit rare, occurs through physical contact with nasal and oral secretions emanating from very ill, dying or dead horses.8
the abdominal cavity. Contamination from the thoracic cavity was less, as this was opened only through a relatively small "window"
The third recognised outbreak of HeV disease occurred in
over the heart. The veterinarian had a thorough shower immedi-
January 1999, when a horse in a northern suburb of Cairns died from pneumonia.9 No human infection associated with this equine
ately on returning home after completing the autopsy. The main gross findings at autopsy were massive fluid conges-
HeV case was detected.
tion of the lungs, cardiomegaly with marked thickening of the
We report here the fourth known outbreak of HeV infection and
ventricular walls, and a grossly enlarged liver. The veterinarian
discuss the implications of this recently emerged virus for veteri-
concluded that the horse had died from acute heart failure and
nary practice.
pulmonary oedema of unknown aetiology; no tissue samples were
562
MJA · Volume 185 Number 10 · 20 November 2006
NOTABLE CASES 2 Possible mode of transmission of Hendra virus (HeV) infection
collected for further laboratory studies. At the completion of the autopsy, the horse was deep-buried using a back hoe. The veterinarian: Seven days after performing the autopsy, the veterinarian developed a dry cough and sore throat, associated with cervical lymphadenopathy and a fever lasting 4 days. She had generalised body aches and was very tired. The illness continued for about 8 days, during which time she was unable to work. She was seen 2 days after the onset of symptoms by a medical practitioner who had been informed (by the TPHU) of the possibility of HeV infection. However, the practitioner considered that her illness was consistent with a tonsillar infection and prescribed an antibiotic; blood was collected for HeV laboratory studies only. Follow-up serum samples were collected for further HeV studies at 14, 30, 50, 363, 470 and 559 days after the onset of symptoms. Laboratory studies: HeV RNA was not detected by a reverse transcriptase Polymerase chain reaction (RT-PCR) (TaqMan) assay10 on the initial serum sample. Similarly, HeV IgM and IgG antibodies were not detected by either immunofluorescence assay (IFA) or enzyme-linked immunoassay (EIA).11 However, the subsequent samples demonstrated clear HeV IgM and IgG seroconversions by both IFA and EIA. A serum sample taken nearly a year later was initially reported as having a very high antibody titre on IgG IFA (>1024), but on repeat testing this was revised to a level of 512 (Box 3). Subsequent antibody levels have fallen by one dilution. A plaque reduction neutralisation test11 showed that the serum collected 14 days after the onset of illness neutralised HeV at a dilution of 1 : 5. Autopsy assistants: An adult member of the family who owned the horse held the dying animal's head; two others assisted with the autopsy. All three were exposed to the frothy nasal secretions to varying degrees. Although the two who assisted were reported as
having become unwell after the procedure, further investigation revealed that neither had a febrile illness. Rather, both seemed to have had symptoms of pre-existing conditions. HeV serological studies on samples collected from all three adults 3­4 weeks after the autopsy did not show any evidence of HeV infection. Site visit: A site visit took place on the day of the notification to TPHU, which was about 2 weeks before laboratory confirmation of HeV infection was obtained. The paddock was in a semi-rural area and held seven other horses, all of which appeared in good health. It was surrounded by other paddocks, some of which held horses. There was no obvious flying fox colony nearby; the owner of the property voluntarily quarantined the property (not allowing any horse movement in or out). Once the HeV infection in the veterinarian was confirmed, the other seven horses in the paddock were tested for serological evidence of HeV infection (38 days after the horse died); all were negative. The quarantine was subsequently lifted. Discussion All four reported outbreaks of HeV infection have occurred in Queensland, and three have occurred in the northern part of the state. Although no samples were collected from the horse, with hindsight it clearly had an illness consistent with previous clinical reports of HeV disease in horses. The disease is usually fulminant in nature, with fever, tachycardia, respiratory distress and a frothy nasal discharge being the typical reported features in horses.8,12 Facial oedema, physical distress and unease (suggestive of colic), and the close proximity of flying foxes add further support to the clinical suggestion of HeV disease in horses.12 The most obvious gross pathology is marked fluid congestion in the lungs, with a thick, foamy haemorrhagic exudate in the airways.8
3 Hendra virus (HeV) laboratory studies in serum collected from the veterinarian at various intervals after the onset of symptoms. The onset occurred 7 days after the autopsy of the horse
Laboratory studies HeV RNA HeV IgM (IFA) HeV IgG (EIA) HeV IgG (IFA)
2 Not detected <8 Non-reactive <8
14 8 Reactive 256
Days after symptom onset
30
50
363
32 Reactive 256
16 Reactive 128
<8 Reactive 512
470
559
<8 Reactive 256
<8 Not performed 256
IFA = immunofluorescence assay. EIA = enzyme-linked immunoassay.

MJA · Volume 185 Number 10 · 20 November 2006
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NOTABLE CASES
Although there was no obvious flying fox colony nearby, large numbers of flying foxes are usually obvious in the evening sky in the latter part of the year in and around Cairns. The timing of the horse's illness is not only the flying foxes' birthing season,13 but also the season for many domestic and rainforest fruits in Far North Queensland; flying foxes travel considerable distances on nocturnal forays from their colonies in search of these foods. The owner of the horse reported frequently seeing flying foxes in the vicinity of the property. We assume that the veterinarian's symptoms were caused by HeV, occurring after an apparent incubation of 7 days. Unfortunately, haematological and biochemical investigations were not requested after her initial medical consultation. The illness was mild, despite her being heavily contaminated with blood and body fluids during the autopsy. This veterinarian is the fourth person known to have been infected with HeV. All four had direct exposure to secretions and tissues from very ill, dying or dead horses; two were directly involved in autopsies of these horses. Two of the four died, whereas the other two had relatively mild illnesses.2-4 The veterinarian has remained clinically well for 2 years since her initial illness. A rise in the antibody titre 1 year after the initial illness was of concern in view of the observed late neurological relapse (13 months after acute illness), associated with increasing antibody levels, in one of the other cases of HeV infection.4 The closely related Nipah virus has also been associated with late neurological relapse in 7.5% of cases, occurring up to 22 months after initial infection.14 In one case, late-onset Nipah virus encephalitis coincided with rising antibody titres.15 The veterinarian undertook a high-risk procedure, taking less than optimal precautions. She was a relatively recent graduate, and her training may not have adequately impressed upon her the need to undertake such procedures with due care. Just as human health workers have had to accept that several recently emerged viruses (eg, blood-borne viruses and the SARS coronavirus) have changed working procedures, those working in animal health also must accept that recently emerged zoonotic viruses (eg, HeV and Australian bat lyssavirus) necessitate appropriate working procedures and personal protective equipment in veterinary practice. After this HeV incident, the Queensland Department of Primary Industries and Fisheries published revised guidelines for veterinarians handling horses suspected of being infected with HeV.12 These guidelines provide clinical case definitions and the recommended response measures, including the personal protective equipment that should be used when managing a suspected case, and the necessary reporting procedures.12 We suggest that these guidelines should be widely disseminated throughout the Australian veterinary community. Addendum In early December 2004, a horse on a property just south of Townsville died of laboratory-confirmed HeV disease; there were no human infections associated with this fifth recognised outbreak of HeV disease. In mid June 2006, a horse on a property near Peachester on the Sunshine Coast hinterland died of laboratoryconfirmed HeV disease; to date there have been no apparent human infections associated with the sixth outbreak of HeV disease.
Acknowledgements We wish to thank the veterinarian, her colleague who first notified the incident, and the owners of the horse. We also wish to thank the medical practitioner concerned.
Competing interests None identified.
Author details Jeffrey N Hanna, DTCH, MPH, FAFPHM, medical director, Communicable disease control1 William J McBride, FRACP, FRCPA, PhD, Professor of Medicine2 Dianne L Brookes, MPH&TM, Public Health Nursing Officer, Tropical Population Health Network1 Jack Shield, BVSc, Veterinary Officer3 Carmel T Taylor, BSc, Scientist4 Ina L Smith, PhD, Research & Development Coordinator4 Scott B Craig, BSc(Hons), Scientist4 Greg A Smith, PhD, Scientific Manager4 1 Queensland Health, Cairns, QLD. 2 James Cook University, Cairns, QLD. 3 Department of Primary Industries and Fisheries, Cairns, QLD. 4 Public Health Virology, Queensland Health Scientific Services, Brisbane, QLD. Correspondence: [email protected]
References 1 Wang L, Harcourt BH, Yu M, et al. Molecular Biology of Hendra and Nipah viruses. Microbes Infect 2001; 3: 279-287. 2 Selvey LA, Wells RM, McCormack JG, et al. Infection of humans and horses by a newly described morbillivirus. Med J Aust 1995; 162: 642-645. 3 Paterson DL, Murray PK, McCormack JG. Zoonotic disease in Australia caused by a novel member of the Paramyxoviridae. Clin Infect Dis 1998; 27: 112-118. 4 O'Sullivan JD, Allworth AM, Paterson DL, et al. Fatal encephalitis due to a novel paramyxovirus transmitted from horses. Lancet 1997; 349: 93-95. 5 Hooper PT, Gould AR, Russell GM, et al. Retrospective diagnosis of a second outbreak of equine morbillivirus disease. Aust Vet J 1996; 74: 244-245. 6 Field H, Young P, Yob JM, et al. The natural history of Hendra and Nipah viruses. Microbes Infect 2001; 3: 307-314. 7 Halpin K, Young PL, Field HE, Mackenzie JS. Isolation of Hendra virus from pteropid bats: a natural reservoir of Hendra virus. J Gen Virol 2000; 81: 1927-1932. 8 Westbury HA. Hendra virus disease in horses. Rev Sci Tech 2000; 19: 151159. 9 Field HE, Barratt PC, Hughes RJ, et al. A fatal case of Hendra virus infection in a horse in north Queensland: clinical and epidemiological featureS. Aust Vet J 2000; 78: 279-280. 10 Smith IL, Halpin K, Warrilow D, Smith GA. Development of a fluorogenic RT-PCR (TaqMan) for the detection of Hendra virus. J Virol Methods 2001; 98: 33-40. 11 Daniels P, Ksiazek T, Eaton BT. Laboratory diagnosis of Nipah and Hendra virus infections. Microbes Infect 2001; 3: 289-295. 12 Queensland Department of Primary Industries and Fisheries. Handling suspect Hendra virus cases in all equines: guidelines for veterinarians. June 2005. http://www2.dpi.qld.gov.au/health/16503.html (accessed Jun 2006). 13 Hall L, Schulz M, Richards G. Bats. In: Ryan M, Burwell B, editors. Wildlife of tropical north Queensland. Brisbane: Queensland Museum, 2000: 313327. 14 Tan CT, Goh KJ, Wong KT, et al. Relapsed and late-onset Nipah encephalitis. Ann Neurol 2002; 51: 703-708. 15 Wong SC, Ooi MH, Wong MN, et al. Late presentation of Nipah virus encephalitis and kinetics of the humoral immune response. J Neurol Neurosurg Psychiatry 2001; 71: 552-554.
(Received 30 Jun 2006, accepted 12 Sep 2006)

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