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 ofreassortment 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.
Lumpy skin disease is an important economic disease of cattle that is controlled by vaccination. This paper presents an investigation into the role of the lumpy skin disease virus (LSDV) superoxide dismutase (SOD) homologue on growth and histopathology of the virus both in vitro and in vivo. SOD homologue knock-out and knock-in recombinants (nLSDV∆SOD-UCT and nLSDVSODis-UCT, respectively) were constructed and compared to the Neethling vaccine (nLSDV) for growth in a permissive bovine cell line as well as on fertilized chick chorioallantoic membranes (CAMs). The infected CAMs were scored for histological changes. Deletion of the SOD homologue from LSDV reduced virus growth both in Madin-Darby bovine kidney (MDBK) cells as well as on CAMs. Furthermore, the knockout virus showed reduced inflammation in CAMs and more ballooning degeneration. A pilot experiment was performed in cattle to compare the lesions produced by the different LSDV constructs in the same animal. One animal developed a larger lesion to nLSDV∆SOD-UCT compared to both nLSDVSODis-UCT and nLSDV. Histological analysis of biopsies of these lesions shows less inflammation and necrosis associated with nLSDVSODis-UCT compared to nLSDV and nLSDV∆SOD-UCT. None of the vaccinated animals showed disseminated LSDV disease, indicating that the candidate vaccines are safe for further testing. Our results suggest that the SOD homologue may improve immunogenicity and reduce virulence.
An incursion of classical swine fever virus (CSFV) into the domestic pig population in South Africa, identified in 2005, raised the concern that infection might spread to wildlife species and be maintained in these hosts. This study sought to determine whether two wildlife Suidae species present in South Africa, the bushpig (Potamochoerus larvatus) and the common warthog (Phacochoerus africanus), could support productive CSFV infection. Both species could be infected with CSFV and transmitted infection to in-contact animals of the same species. Viral antigen and RNA genome were detected in blood/serum and animals that survived initial infection seroconverted approximately 10-14 days post-inoculation. Viral RNA remained detectable in nasal and saliva secretions for prolonged periods until monitoring ended at 42-44 days after initial challenge. These data suggest that both Suidae species could serve to spread circulating CSFV within wild populations, with implications for disease control.
SUMMARYWild African Suidae, the common warthog (Phacochoerus africanus) and bushpig (Potamochoerus On post mortem 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.
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