Twenty-four 8 to 9 week-old Pasteurella multocida -free rabbits were divided into three equal groups, the first group was pretreated with hydrocortisone and inoculated intranasally with pasteurella multocida serotype A:3. The second group was inoculated intranasally with P. multocida without hydrocortisone treatment. The third group was inoculated with phosphate buffered saline only and used as a control group. Pasteurella multocida was isolated from the nasal cavity of all infected rabbits in group 1 and 2 and from the trachea of seven rabbits in group 1 and five rabbits in group 2. This study was conducted to observe the ultrastructural changes of the upper respiratory tract of hydrocortisone treated and non-treated rabbits infected with P. multocida serotype A:3. The ultrastructural changes detected in infected rabbits were ciliary destruction and deciliation of the ciliated epithelial cells, cellular swelling, goblet cell hyperplasia and endothelial cell damage. Pasteurella multocida was observed attached to the degenerated cilia, microvilli and mucus. Pasteurella multocida infection was associated with inflammatory responses, which may have caused tissue damage. It is possible that hydrocortisone modulates the severity of infection as an immune suppressor and an inhibitor of goblet cell secretion.
The objectives of this study were to determine the prevalence, characterization and antibiotic resistance of Pasteurella multocida isolated from calves with respiratory infection in Iran. P. multocida was detected in 141/169 bovine respiratory infection cases on Iranian dairy and beef farms. P. multocida were grouped into serogroups A (126/141), D (12/141), and B (3/141). Of the P. multocida isolates, all harboured the psl, ompH, oma87, fimA, ptfA, nanB, and nanH genes, 139/141 had hsf-2, and 115/141 pfhA, and tadD. The isolates were most frequently resistant to penicillin G (43/141 resistant isolates; 30.5%) and streptomycin (31/141; 22%).
A paramyxovirus virus termed Nipah virus has been identified as the etiologic agent of an outbreak of severe encephalitis in people with close contact exposure to pigs in Malaysia and Singapore. The outbreak was first noted in late September 1998 and by mid-June 1999, more than 265 encephalitis cases, including 105 deaths, had been reported in Malaysia, and 11 cases of encephalitis or respiratory illness with one death had been reported in Singapore. Electron microscopic, serologic, and genetic studies indicate that this virus belongs to the family Paramyxoviridae and is most closely related to the recently discovered Hendra virus. We suggest that these two viruses are representative of a new genus within the family Paramyxoviridae. Like Hendra virus, Nipah virus is unusual among the paramyxoviruses in its ability to infect and cause potentially fatal disease in a number of host species, including humans.
A human isolate of Nipah virus from an outbreak of febrile encephalitis in Malaysia that coincided with a field outbreak of disease in pigs was used to infect eight 6-week-old pigs orally or subcutaneously and two cats oronasally. In pigs, the virus induced a respiratory and neurological syndrome consistent with that observed in the Malaysian pigs. Not all the pigs showed clinical signs, but Nipah virus was recovered from the nose and oropharynx of both clinically and sub-clinically infected animals. Natural infection of in-contact pigs, which was readily demonstrated, appeared to be acute and self-limiting. Subclinical infections occurred in both inoculated and in-contact pigs. Respiratory and neurological disease was also produced in the cats, with recovery of virus from urine as well as from the oropharynx. The clinical and pathological syndrome induced by Nipah virus in cats was comparable with that associated with Hendra virus infection in this species, except that in fatal infection with Nipah virus there was extensive inflammation of the respiratory epithelium, associated with the presence of viral antigen. Viral shedding via the nasopharynx, as observed in pigs and cats in the present study, was not a regular feature of earlier reports of experimental Hendra virus infection in cats and horses. The findings indicate the possibility of field transmission of Nipah virus between pigs via respiratory and oropharyngeal secretions.