Cases reported "Morbillivirus Infections"

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1/3. infection of humans and horses by a newly described morbillivirus.

    OBJECTIVE: To describe the clinical and epidemiological features of an outbreak of a viral infection affecting humans and horses. SETTING: Stables in Hendra, a suburb of Brisbane. SUBJECTS: Affected horses and humans, and at-risk human contacts. RESULTS: A pregnant mare died two days after arrival from a paddock elsewhere in Brisbane. Eight to 11 days later, illness (depression, anorexia, fever, dyspnoea, ataxia, tachycardia, tachypnoea and nasal discharge) was reported among 17 other horses from the same or an adjoining stable. Fourteen horses died or were put down. Five and six days after the index mare's death, a stable-hand and then a horse-trainer, both of whom had had close contact with the sick mare's mucous secretions, developed influenza-like illnesses. The stable-hand recovered but the trainer developed pneumonitis, respiratory failure, renal failure and arterial thrombosis, and died from a cardiac arrest seven days after admission to hospital. A morbillivirus cultured from his kidney was identical to one isolated from the lungs of five affected horses. The two affected humans and eight other horses were seropositive for the infection, which was reproduced in healthy horses following challenge by spleen/lung homogenates from infected horses. There was no serological evidence of infection in 157 humans who had had contact with the stables or the sick horses or humans. CONCLUSIONS: A previously undescribed morbillivirus infected a probable 21 horses and two humans; one human and 14 horses died. That no further cases were detected among humans suggests that the virus was of low infectivity. The source of infection remains undetermined.
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2/3. Ultrastructure of equine morbillivirus.

    The ultrastructure of the equine morbillivirus (EMV) which was implicated in the death of one human and fourteen horses in queensland, australia during September 1994 and a 36 year old man from queensland in October 1995 is described. The ultrastructure of the virus and the intracellular virus-specific structures are characteristic for the family paramyxoviridae. Cytoplasmic nucleocapsids were observed within the infected cells monolayers, endothelial cells (lung) of infected horses and the neurons within the brain of the 36 year old queensland man. Aggregates of smaller nucleocapsid-like structures were also observed within the brain of the same man; these did not react with sera from recovered EMV-infected horses or from a recovered EMV-infected human. Co-examination of rinderpest virus (RPV), bovine parainfluenza-3 (BPIV-3), human respiratory virus (HRSV) and sendai virus revealed that their envelope-associated surface projections are equivalent in length to the 15 nm spikes of EMV. EMV differed from these other viruses in that the majority of virions possessed surface projections of two distinct lengths (18 and 15 nm). Further ultrastructural examinations of plaque purified EMV revealed a small percentage of EM viruses possessed a mixed array of surface projections indicating that the 'double-fringed' (DF) particles may be the result of a post-translational modification(s).
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3/3. Fatal encephalitis due to novel paramyxovirus transmitted from horses.

    BACKGROUND: In September, 1994, an outbreak of severe respiratory disease affected 18 horses, their trainer, and a stablehand in queensland, australia. Fourteen horses and one human being died. A novel virus was isolated from those affected and named equine morbillivirus (EMV). We report a case of encephalitis caused by this virus. FINDINGS: A 35-year-old man from queensland had a brief aseptic meningitic illness in August, 1994, shortly after caring for two horses that died from EMV infection and then assisting at their necropsies. He then suffered severe encephalitis 13 months later, characterised by uncontrolled focal and generalised epileptic activity. Rising titres of neutralising antibodies to EMV in the patient's serum at the time of the second illness suggested an anamnestic response. Distinctive cortical changes were shown on magnetic resonance neuroimaging and histopathological examination of the brain at necropsy. immunohistochemistry and electronmicroscopy of brain tissue revealed pathology characteristic of the earlier cases of EMV infection. PCR on cerebrospinal fluid taken during the second illness, brain tissue, and serum retained from the original illness resulted in an amplified product identical to that previously described from EMV. INTERPRETATION: The results of serology, PCR, electronmicroscopy, and immunohistochemistry strongly suggest that EMV was the cause of this patient's encephalitis, and that exposure to the virus occurred 3 months before the fatal illness.
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