Phylogenetic analysis of influenza A viruses (H6N8, H1N8, H4N2, H9N2, H10N7) isolated from wild birds, ducks, and ostriches in South Africa from 2007 to 2009.

Influenza A strains emerging from wild birds are a constant threat to South Africa's valuable ostrich industry. In 2004 and again in 2006, low pathogenicity avian influenza H5N2 strains introduced from a wild bird reservoir mutated in ostriches to high pathogenicity avian influenza (HPAI), with serious economic consequences and export bans imposed by the European Union. Although no outbreaks of notifiable avian influenza have occurred in South Africa since 2006, the H9N2 virus caused a localized outbreak where ostriches displayed symptoms of green urine, depression, and mild morbidity. Most recently, an outbreak of H10N7 in farmed Pekin ducks (Anas platyrhynchos domestica) caused increased mortalities, but this was exacerbated by a secondary Escherichia coli infection, because an intravenous pathogenicity index of 0.00 was recorded. Each of the eight gene segments of the five strains isolated from 2007 to 2009 from farmed ostriches in the Oudtshoorn region (H6N8, H9N2), Pekin ducks (H10N7, Joostenburgvlakte region), and wild Egyptian geese (Alopochen aegypticus; H1N8, Baberspan wetlands; H4N2, Oudtshoorn region) were sequenced, genetically analyzed, and compared to previous South African isolates and viruses in the public data banks. An H5N8 strain was also detected by reverse-transcription PCR in cloacal swabs from swift terns (Sterna bergii) in the Mosselbaai region during 2007, although a virus could not be isolated. Initial phylogenetic results indicate that H6N8 and H9N2 ostrich and H10N7 Pekin duck viruses originated in the wild bird population that is geographically dispersed throughout southern Africa, based on the reassortment of viral genes from birds sampled outside of the ostrich farming areas. No evidence of internal genes associated with Asian HPAI H5N1 strains were detected in the South African isolates.

Characterisation of a highly pathogenic influenza A virus of subtype H5N2 isolated from ostriches in South Africa in 2004.

OBJECTIVES: The HPAI H5N2 strain that caused an outbreak in ostriches of the Eastern Cape Province, South Africa in 2004 was characterized. DESIGN: Haemagglutination inhibition (HI) and agar gel immunodiffusion (AGID) were performed on sera from ostrich farms in the outbreak region, and intravenous pathogenicity (IVPI) tests, reverse-transcriptase-polymerase-chain reaction (RT-PCR), nucleic acid sequencing and phylogenetic comparisons were performed on the HPAI H5N2 virus isolated during the outbreak. RESULTS: The deduced amino acid sequence at the HA0 cleavage site determined by RT-PCR and nucleotide sequencing was PQREKRRKKRGLF and thus the virus fell within the definition of a highly pathogenic virus, but in an IVPI test in chickens on the virus isolated from the index case and a value of 0.63 was recorded, which is below the criterion for highly pathogenic viruses in this in vivo test. After a further passage in embryonated eggs a second IVPI was carried out and an elevated value of 1.19 was obtained. Cloacal swabs were taken from the initial IVPI birds, inoculated into embryonated chickens eggs and a third IVPI was then performed on the resulting haemagglutinating, infective allantoic fluid. An index of 2.73 was recorded. CONCLUSIONS: HI tests appeared to be the more sensitive test compared to AGID when testing for antibodies to avian influenza in sera. An ostrich-derived virus with a virulent HA0 cleavage site was not initially virulent in chickens but after passage in the latter the virulence increased. Phylogenetic analyses demonstrated the link between AI viruses carried by wild ducks and those infecting ostriches.

Lineage 2 west nile virus as cause of fatal neurologic disease in horses, South Africa.

Serologic evidence suggests that West Nile virus (WNV) is widely distributed in horses in southern Africa. However, because few neurologic cases have been reported, endemic lineage 2 strains were postulated to be nonpathogenic in horses. Recent evidence suggests that highly neuroinvasive lineage 2 strains exist in humans and mice. To determine whether neurologic cases are being missed in South Africa, we tested 80 serum or brain specimens from horses with unexplained fever (n = 48) and/or neurologic signs (n = 32) for WNV. From March 2007 through June 2008, using reverse transcription-PCR (RT-PCR) and immunoglobulin (Ig) M ELISA, we found WNV RNA or IgM in 7/32 horses with acute neurologic disease; 5 horses died or were euthanized. In 5/7 horses, no other pathogen was detected. DNA sequencing for all 5 RT-PCR-positive cases showed the virus belonged to lineage 2. WNV lineage 2 may cause neurologic disease in horses in South Africa.

Rift valley fever.

Rift Valley fever virus is an arthropod-borne Phlebovirus endemic in sub-Saharan Africa. Outbreaks also have occurred in Egypt, Madagascar, and most recently in the Arabian peninsula. Large epizootics occur at irregular intervals in seasons of above-average rainfall with persistent flooding and the appearance of large numbers of floodwater-breeding Aedine mosquitoes. The virus is transmitted transovarially and can remain dormant in mosquito eggs during dry interepizootic periods. Low-level virus circulation occurs in high-rainfall forested areas, although individual cases of the disease rarely are recognized. RVF is characterized by abortion in pregnant animals and a high mortality in newborn lambs, kids, and calves. Susceptibility to disease is related to age and breed, with severe disease occurring in the young of exotic sheep and cattle breeds. RVF is a zoonosis, and human beings experience an influenza-like illness and, more rarely, complications such as encephalitis or retinitis. The virus causes a severe hepatitis, particularly in aborted fetuses and newborn lambs. The disease must be differentiated from other conditions that cause death with hepatitis and jaundice. Both an inactivated and a live attenuated vaccine are available. New-generation vaccines are being tested, because the existing mousebrain-attenuated strain induces fetal teratology or abortion in a percentage of pregnant animals. Diagnosis is based on histopathology or the demonstration of viral antigen or antibody.