Heartwater is a tick-borne disease caused by the intracellular rickettsial parasite Ehrlichia ruminantium and transmitted by Amblyomma hebraeum ticks. Heartwater is problematic in endemic areas because it causes high mortality in ruminants and leads to economic losses that threaten productivity and food security. This may indicate that there is augmented genetic diversity in the field, which may result in isolates that are more virulent than the Ball3 and Welgevonden isolates. The genetic diversity of E. ruminantium was investigated in this study, focussing on the pCS20 gene region and four polymorphic open reading frames (ORFs) identified by subtractive hybridisation. The 16S ribosomal ribonucleic acid gene confirmed E. ruminantium in brain, blood and tick genomic deoxyribonucleic acid samples (n = 3792) collected from 122 farms that were randomly selected from seven provinces of South Africa where heartwater is endemic. The conserved E. ruminantium pCS20 quantitative polymerase chain reaction (qPCR) assay was used to scan all collected field samples. A total of 433 samples tested positive with the qPCR using the pCS20 gene region, of which 167 were sequenced. The known stocks and field samples were analysed, and phylogenetic trees were generated from consensus sequences. A total of 25 new clades were identified; of these, nine isolates from infected blood could be propagated in cell cultures. These clades were not geographically confined to a certain area but were distributed amongst heartwater-endemic areas in South Africa. Thus, the knowledge of strain diversity of E. ruminantium is essential for control of heartwater and provides a basis for further vaccine development.

Heartwater is a tick-borne disease caused by the intracellular rickettsial parasite Ehrlichia ruminantium and transmitted by Amblyomma hebraeum ticks. Heartwater is problematic in endemic areas because it causes high mortality in ruminants and leads to economic losses that threaten productivity and food security. This may indicate that there is augmented genetic diversity in the field, which may result in isolates that are more virulent than the Ball3 and Welgevonden isolates. The genetic diversity of E. ruminantium was investigated in this study, focussing on the pCS20 gene region and four polymorphic open reading frames (ORFs) identified by subtractive hybridisation. The 16S ribosomal ribonucleic acid gene confirmed E. ruminantium in brain, blood and tick genomic deoxyribonucleic acid samples (n = 3792) collected from 122 farms that were randomly selected from seven provinces of South Africa where heartwater is endemic. The conserved E. ruminantium pCS20 quantitative polymerase chain reaction (qPCR) assay was used to scan all collected field samples. A total of 433 samples tested positive with the qPCR using the pCS20 gene region, of which 167 were sequenced. The known stocks and field samples were analysed, and phylogenetic trees were generated from consensus sequences. A total of 25 new clades were identified; of these, nine isolates from infected blood could be propagated in cell cultures. These clades were not geographically confined to a certain area but were distributed amongst heartwater-endemic areas in South Africa. Thus, the knowledge of strain diversity of E. ruminantium is essential for control of heartwater and provides a basis for further vaccine development.

Diplodiosis is an important neuromycotoxicosis of ruminants in South Africa when grazing on harvested maize fields in winter. It is believed to be caused by mycotoxin(s) synthesised by Stenocarpella (Diplodia) maydis. Although several metabolites have been isolated from S. maydis culture material, none of these have been administered to ruminants to reproduce the disease. The objectives of this study were to isolate diplodiatoxin and to administer it to juvenile goats. Diplodiatoxin, considered as a major metabolite, was purified from S. maydis-infected maize cultures (Coligny 2007 isolate). Following intravenous administration of 2 mg and 4 mg diplodiatoxin/kg body weight for five consecutive days to two juvenile goats, no clinical signs reminiscent of diplodiosis were observed. Based on previous experimental results and if diplodiatoxin was the causative compound, the dosage regimen employed was seemingly appropriate to induce diplodiosis. In addition, intraruminal administration of 2 mg/kg diplodiatoxin to one goat for three consecutive days also did not induce clinical signs. It appears as if diplodiatoxin alone is not the causative compound. Other metabolites and/or mixtures of diplodiatoxin and other mycotoxins, when available in sufficient quantities, should also be evaluated.

Diplodiosis is an important neuromycotoxicosis of ruminants in South Africa when grazing on harvested maize fields in winter. It is believed to be caused by mycotoxin(s) synthesised by Stenocarpella (Diplodia) maydis. Although several metabolites have been isolated from S. maydis culture material, none of these have been administered to ruminants to reproduce the disease. The objectives of this study were to isolate diplodiatoxin and to administer it to juvenile goats. Diplodiatoxin, considered as a major metabolite, was purified from S. maydis-infected maize cultures (Coligny 2007 isolate). Following intravenous administration of 2 mg and 4 mg diplodiatoxin/kg body weight for five consecutive days to two juvenile goats, no clinical signs reminiscent of diplodiosis were observed. Based on previous experimental results and if diplodiatoxin was the causative compound, the dosage regimen employed was seemingly appropriate to induce diplodiosis. In addition, intraruminal administration of 2 mg/kg diplodiatoxin to one goat for three consecutive days also did not induce clinical signs. It appears as if diplodiatoxin alone is not the causative compound. Other metabolites and/or mixtures of diplodiatoxin and other mycotoxins, when available in sufficient quantities, should also be evaluated.

A study was conducted to investigate the seroprevalence and associated risk factors of Rift Valley fever (RVF) infection in cattle and some selected wildlife species at selected interface areas at the periphery of the Great Limpopo Transfrontier Conservation Area in Zimbabwe. Three study sites were selected based on the type of livestock–wildlife interface: porous livestock–wildlife interface (unrestricted); non-porous livestock–wildlife interface (restricted by fencing) and livestock–wildlife non-interface (totally absent contact or control). Sera were collected from cattle aged ≥ 2 years representing both female and intact male. Sera were also collected from selected wild ungulates from Mabalauta (porous interface) and Chipinda Pools (non-interface) areas of the Gonarezhou National Park. Sera were tested for antibodies to Rift Valley fever virus (RVFV) using a competitive enzyme-linked immunosorbent assay (ELISA) test. AX2 test was used to assess differences between categories, and p 0.05 was considered as significant. In cattle, the overall seroprevalence was 1.7% (17/1011) (95% confidence interval [CI]: 1.01–2.7). The porous interface recorded a seroprevalence of 2.3% (95% CI: 1.2–4.3), the non-porous interface recorded a prevalence of 1.8% (95% CI: 0.7–4.3) and the non-interface area recorded a seroprevalence of 0.4% (955 CI: 0.02–2.5), but the difference in seroprevalence according to site was not significant (p 0.05). All impala and kudu samples tested negative. The overall seroprevalence in buffaloes was 11.7% (95% CI: 6.6–19.5), and there was no significant (p = 0.38) difference between the sites (Mabalauta, 4.4% [95% CI: 0.2–24] vs. Chipinda, 13.6% [95% CI: 7.6–23]). The overall seroprevalence in buffaloes (11.7%, 13/111) was significantly (p 0.0001) higher than in cattle (1.7%, 17/1011). The results established the presence of RVFV in cattle and selected wildlife and that sylvatic infections may be present in buffalo populations. Further studies are required to investigate if the virus is circulating between cattle and wildlife.

International audience | A study was conducted to investigate the seroprevalence and associated risk factors of Rift Valley fever (RVF) infection in cattle and some selected wildlife species at selected interface areas at the periphery of the Great Limpopo Transfrontier Conservation Area in Zimbabwe. Three study sites were selected based on the type of livestock-wildlife interface: porous livestock-wildlife interface (unrestricted); non-porous livestock-wildlife interface (restricted by fencing) and livestock-wildlife non-interface (totally absent contact or control). Sera were collected from cattle aged >= 2 years representing both female and intact male. Sera were also collected from selected wild ungulates from Mabalauta (porous interface) and Chipinda Pools (non-interface) areas of the Gonarezhou National Park. Sera were tested for antibodies to Rift Valley fever virus (RVFV) using a competitive enzyme-linked immunosorbent assay (ELISA) test. AX2 test was used to assess differences between categories, and p < 0.05 was considered as significant. In cattle, the overall seroprevalence was 1.7% (17/1011) (95% confidence interval [CI]: 1.01-2.7). The porous interface recorded a seroprevalence of 2.3% (95% CI: 1.2-4.3), the non-porous interface recorded a prevalence of 1.8% (95% CI: 0.7-4.3) and the non-interface area recorded a seroprevalence of 0.4% (955 CI: 0.02-2.5), but the difference in seroprevalence according to site was not significant (p > 0.05). All impala and kudu samples tested negative. The overall seroprevalence in buffaloes was 11.7% (95% CI: 6.6-19.5), and there was no significant (p = 0.38) difference between the sites (Mabalauta, 4.4% [95% CI: 0.2-24] vs. Chipinda, 13.6% [95% CI: 7.6-23]). The overall seroprevalence in buffaloes (11.7%, 13/111) was significantly (p < 0.0001) higher than in cattle (1.7%, 17/1011). The results established the presence of RVFV in cattle and selected wildlife and that sylvatic infections may be present in buffalo populations. Further studies are required to investigate if the virus is circulating between cattle and wildlife.

A study was conducted to investigate the seroprevalence and associated risk factors of Rift Valley fever (RVF) infection in cattle and some selected wildlife species at selected interface areas at the periphery of the Great Limpopo Transfrontier Conservation Area in Zimbabwe. Three study sites were selected based on the type of livestock–wildlife interface: porous livestock–wildlife interface (unrestricted); non-porous livestock–wildlife interface (restricted by fencing) and livestock–wildlife non-interface (totally absent contact or control). Sera were collected from cattle aged ≥ 2 years representing both female and intact male. Sera were also collected from selected wild ungulates from Mabalauta (porous interface) and Chipinda Pools (non-interface) areas of the Gonarezhou National Park. Sera were tested for antibodies to Rift Valley fever virus (RVFV) using a competitive enzyme-linked immunosorbent assay (ELISA) test. AX2 test was used to assess differences between categories, and p < 0.05 was considered as significant. In cattle, the overall seroprevalence was 1.7% (17/1011) (95% confidence interval [CI]: 1.01–2.7). The porous interface recorded a seroprevalence of 2.3% (95% CI: 1.2–4.3), the non-porous interface recorded a prevalence of 1.8% (95% CI: 0.7–4.3) and the non-interface area recorded a seroprevalence of 0.4% (955 CI: 0.02–2.5), but the difference in seroprevalence according to site was not significant (p > 0.05). All impala and kudu samples tested negative. The overall seroprevalence in buffaloes was 11.7% (95% CI: 6.6–19.5), and there was no significant (p = 0.38) difference between the sites (Mabalauta, 4.4% [95% CI: 0.2–24] vs. Chipinda, 13.6% [95% CI: 7.6–23]). The overall seroprevalence in buffaloes (11.7%, 13/111) was significantly (p < 0.0001) higher than in cattle (1.7%, 17/1011). The results established the presence of RVFV in cattle and selected wildlife and that sylvatic infections may be present in buffalo populations. Further studies are required to investigate if the virus is circulating between cattle and wildlife.

The first known severe disease caused by a coronavirus (CoV) in humans emerged with the severe acute respiratory syndrome (SARS) epidemic in China, which killed 774 people during its 2002/2003 outbreak. The Middle East respiratory syndrome (MERS) was the second human fatal disease, which started in 2012 in Saudi Arabia and resulted in 858 fatalities. In December 2019, a new virus, SARS-CoV-2 (COVID-19), originating from China, began generating headlines worldwide because of the unprecedented speed of its transmission; 5.2 million people were infected and 338 480 had been reported dead from December 2019 to May 2020. These human coronaviruses are believed to have an animal origin and had reached humans through species jump. Coronaviruses are well known for their high frequency of recombination and high mutation rates, allowing them to adapt to new hosts and ecological niches. This review summarises existing information on what is currently known on the role of wild and domesticated animals and discussions on whether they are the natural reservoir/amplifiers hosts or incidental hosts of CoVs. Results of experimental infection and transmission using different wild, domesticated and pet animals are also reviewed. The need for a One Health approach in implementing measures and practices is highlighted to improve human health and reduce the emergence of pandemics from these zoonotic viruses.

The first known severe disease caused by a coronavirus (CoV) in humans emerged with the severe acute respiratory syndrome (SARS) epidemic in China, which killed 774 people during its 2002/2003 outbreak. The Middle East respiratory syndrome (MERS) was the second human fatal disease, which started in 2012 in Saudi Arabia and resulted in 858 fatalities. In December 2019, a new virus, SARS-CoV-2 (COVID-19), originating from China, began generating headlines worldwide because of the unprecedented speed of its transmission; 5.2 million people were infected and 338 480 had been reported dead from December 2019 to May 2020. These human coronaviruses are believed to have an animal origin and had reached humans through species jump. Coronaviruses are well known for their high frequency of recombination and high mutation rates, allowing them to adapt to new hosts and ecological niches. This review summarises existing information on what is currently known on the role of wild and domesticated animals and discussions on whether they are the natural reservoir/amplifiers hosts or incidental hosts of CoVs. Results of experimental infection and transmission using different wild, domesticated and pet animals are also reviewed. The need for a One Health approach in implementing measures and practices is highlighted to improve human health and reduce the emergence of pandemics from these zoonotic viruses.

All effects taken together, bovine tuberculosis (bTB) has a long-term detrimental effect on bovine herds and many wildlife species in South Africa. The disease is not only found in domestic cattle but also in African buffaloes and has to date been diagnosed in 21 wildlife species, including several rare and endangered species, thus having a potentially serious effect on conservation and biodiversity. In cattle, bTB is mostly characterised by sporadic outbreaks, but bovine herds chronically infected with the clinical disease are not uncommon. Presently, the recognised bTB control strategy in South Africa is based on ‘test and slaughter’, using the intradermal tuberculin test, followed by the slaughter of animals that have tested positive. Affected herds are placed under veterinary quarantine with movement restrictions until the outbreak is eradicated; this can take several years or last indefinitely if the outbreak cannot be eradicated. The same measures apply to infected buffalo populations, often with no prospect of ever being eradicated. This strategy is neither practical nor viable in the context of a communal farming system and becomes unethical when dealing with valuable wildlife reservoir hosts. Transmission of bTB between wildlife and cattle has been demonstrated and emphasises the need for an effective, affordable and culturally acceptable control strategy to curb the spread of bTB in South Africa. In countries with similar challenges, vaccination has been used and found to be promising for treating wild and domestic reservoir species and may hence be of value as a complementary tool for bTB control in South Africa.

All effects taken together, bovine tuberculosis (bTB) has a long-term detrimental effect on bovine herds and many wildlife species in South Africa. The disease is not only found in domestic cattle but also in African buffaloes and has to date been diagnosed in 21 wildlife species, including several rare and endangered species, thus having a potentially serious effect on conservation and biodiversity. In cattle, bTB is mostly characterised by sporadic outbreaks, but bovine herds chronically infected with the clinical disease are not uncommon. Presently, the recognised bTB control strategy in South Africa is based on ‘test and slaughter’, using the intradermal tuberculin test, followed by the slaughter of animals that have tested positive. Affected herds are placed under veterinary quarantine with movement restrictions until the outbreak is eradicated; this can take several years or last indefinitely if the outbreak cannot be eradicated. The same measures apply to infected buffalo populations, often with no prospect of ever being eradicated. This strategy is neither practical nor viable in the context of a communal farming system and becomes unethical when dealing with valuable wildlife reservoir hosts. Transmission of bTB between wildlife and cattle has been demonstrated and emphasises the need for an effective, affordable and culturally acceptable control strategy to curb the spread of bTB in South Africa. In countries with similar challenges, vaccination has been used and found to be promising for treating wild and domestic reservoir species and may hence be of value as a complementary tool for bTB control in South Africa.