Abolnik C.,Onderstepoort Veterinary Institute |
Gerdes G.H.,Onderstepoort Veterinary Institute |
Sinclair M.,Western Cape Provincial Veterinary Laboratory |
Ganzevoort B.W.,Africa co |
And 7 more authors.
Avian Diseases | Year: 2010
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. © 2010 American Association of Avian Pathologists.
Abolnik C.,Onderstepoort Veterinary Institute |
Abolnik C.,University of Pretoria |
Olivier A.J.,Klein Karoo International Laboratory |
Grewar J.,Provincial Government of the Western Cape |
And 2 more authors.
Avian Diseases | Year: 2012
The third outbreak of highly pathogenic avian influenza (HPAI) H5N2 in less than seven years affected ostriches of South Africa's Western Cape during 2011. Twenty farms tested PCR positive for the presence of HPAI H5N2 between March and November 2011. Three HPAI H5N2 (AI2114, AI2214, AI2512) and 1 H1N2 (AI2887) viruses were isolated during this period, but H6N2 and H1N2 infections of ostriches were also confirmed by PCR. HPAI H5N2 isolate AI2114 produced an intravenous pathogenicity index (IVPI) score of 1.37 in chickens whereas isolate AI2214 produced an IVPI score of 0.8. The former virus had an additional, predicted N-linked glycosylation site at position 88 of the hemagglutinin protein as well as an E627K mutation in the PB2 protein that was lacking from AI2214. Four variations at HA0 were detected in the PCR-positive cases. Phylogenetically, the branching order of outbreak strains indicated a lack of reassortment between outbreak strains that implied a single outbreak source and a wild duck origin for the progenitor outbreak strain. The 2011 outbreak strains had no genetic relationships to the previous 2004 and 2006 HPAI H5N2 outbreak viruses. Molecular clock analysis based on the N2 neuraminidase genes estimated a recent common ancestor for the outbreak tentatively dated at September 2010. Deep sequencing results of 16 clinical PCR-positive samples yielded data in the range of 573 to 12,590 base pairs (bp), with an average of 4468 bp of total genomic sequence recovered per sample. This data was used to confirm the lack of reassortment and to assign samples into one of two epidemiologic groups to support epidemiologic tracing of the spread of the outbreak. One farm (no. 142), thought to have played a major epidemiologic role in the outbreak, was confirmed by deep sequencing to contain a mix of both epidemiologic virus groups.
PubMed | Western Cape Provincial Veterinary Laboratory and University of Pretoria
Type: Comparative Study | Journal: Transboundary and emerging diseases | Year: 2015
Wild African Suidae, the common warthog (Phacochoerus africanus) and bushpig (Potamochoerus larvatus), were experimentally infected with classical swine fever (CSF) virus following the diagnosis of CSF subtype 2.1 in domestic pigs in South Africa in 2005. No data regarding the susceptibility or potential lesions of these African wild suids are available. Seven subadult warthogs and six bushpigs were captured and infected intranasally with the South African isolate. Two in-contact control animals of the same species in each experiment verified intra-species transmission. Surviving animals were euthanized after 44 days. Formalin-fixed tissue samples collected from them as well as animals euthanized during the trial were evaluated for histological lesions. The warthogs, which were clinically normal throughout the study, developed histological lesions that were inconsistently present and sometimes subtle. Three individuals, including one in-contact control, developed distinct lympho-plasmacytic cuffing in their brains. Subtle lesions included scant lympho-plasmacytic infiltration of various organs, occasionally accompanied by perivascular cuffing. In contrast, the bushpigs developed overt clinical signs similar to CSF in domestic pigs. Four of six animals, including two in-contact controls, died or were euthanized during the trial. On postmortem examination, intestinal necrosis and ulceration, purulent rhinitis and pneumonia were present. Affected animals developed lymphoid necrosis and depletion whilst surviving individuals showed perivascular cuffing in multiple organs. From the present work, we conclude that these wild Suidae are susceptible to CSF virus and intra-species transmission under experimental conditions can occur.
Howerth E.W.,University of Georgia |
Olivier A.,Klein Karoo International |
Franca M.,University of Georgia |
Stallknecht D.E.,University of Georgia |
Gers S.,Western Cape Provincial Veterinary Laboratory
Avian Diseases | Year: 2012
In 2011, over 35,000 ostriches were slaughtered in the Oudtshoorn district of the Western Cape province of South Africa following the diagnosis of highly pathogenic avian influenza virus H5N2. We describe the pathology and virus distribution via immunohistochemistry in juvenile birds that died rapidly in this outbreak after showing signs of depression and weakness. Associated sialic acid (SA) receptor distribution in uninfected birds is also described. At necropsy, enlarged spleens, swollen livers, and generalized congestion were noted. Birds not succumbing to acute influenza infection often became cachectic with serous atrophy of fat, airsacculitis, and secondary infections. Necrotizing hepatitis, splenitis, and airsacculitis were prominent histopathologic findings. Virus was detected via immunohistochemistry in abundance in the liver and spleen but also in the air sac and gastrointestinal tract. Infected cells included epithelium, endothelium, macrophages, circulating leukocytes, and smooth muscle of a variety of organs and vessel walls. Analysis of SA receptor distribution in uninfected juvenile ostriches via lectin binding showed abundant expression of SAα2,3Gal (avian type) and little or no expression of SAα2,6Gal (human type) in the gastrointestinal and respiratory tracts, as well as leukocytes in the spleen and endothelial cells in all organs, which correlated with H5N2 antigen distribution in these tissues.