This longitudinal study suggests that low-level RVFV transmission occurred among African buffalo in Kruger National Park during 2000–2006. Although no South African epizootics were reported to the World Organisation for Animal Health during the study, we detected nine buffalo seroconversions during the program follow-up.29
Evidence of IEP transmission was also provided by detection of seropositivity among the youngest age group of animals (1–3 years of age) born during the study period. The apparent continuing low-level transmission to wild ruminants during periods of average rainfall suggests that such undetected transmission may be important to the maintenance of RVFV in natural habitats. Continuing local transmission could be an important factor in earlier and more rapid RVFV amplification and transmission to humans during recognized epizootic/epidemic periods.
Initial RVFV seroprevalence was high in our buffalo sample, consonant with rates detected in previous cross-sectional surveys of RVFV seroprevalence among wild ruminants in Kenya and Zimbabwe.12,13
Overall, in our Kruger National Park sample, seropositivity was highest in the first year of study (2000–2001), likely secondary to anomalous heavy rainfall that had occurred in 2000 (). Transmission of RVFV is associated with excessive rainfall in high-risk areas because of the abrupt increase in mosquito numbers after flooding events.3,6,7
Thus, it is possible that many of the buffalo that we documented to be RVFV seropositive at the onset of the study had just recently seroconverted during this preceding heavy rainfall season. In addition, an RVFV outbreak was reported to have occurred in 1999 among wild fauna in South Africa, although its location was not described.29
Furthermore, two RVFV outbreaks were reported among cattle in nearby Zimbabwe during 2001. Those outbreaks resulted in 791 cases in cattle and 4 animal deaths.29
Among the study animals sampled, the observed RVFV seroprevalence waned over the study period. This finding could have been the result of several causes, including loss of immunity over time, insensitive testing (variable detection of HAI levels), or selective loss of seropositive individuals over the study period. Although the observed seroprevalence decreased in later years of the study, there were nine negative-to-positive seroconversions documented during the 2001–2004 interval. These conversions occurred after more typical November–April wet seasons had average rainfall, suggesting a connection between local seasonal weather patterns and RVFV transmission. This pattern appears more subtle than the large outbreaks of zoonotic RVFV disease seen after extreme rainfall events.3,6,7
It is possible that these lower levels of seroconversion may represent echo events of heavy RVFV transmission that occur during extremely heavy rainy seasons. These findings suggest the likelihood of continuing low-level transmission of RVFV to buffalo and other animals during non-flooding off years in suitable RVFV vector habitats.
Seroprevalence of RVFV, indicating past exposure to viral infection, was not associated with worsened survival during long-term follow-up of a closely monitored cohort of animals. Among humans, RVFV infection can be the cause of long-term neurologic sequelae and visual impairment caused by retinitis and anterior chamber eye inflammation.2,30
For buffalo survivors of RVFV infections, we were unable to detect a persistent health impact. Given the limited size of our available longitudinal sample, the confidence interval for the adjusted hazard ratio associated with RVFV seropositivity remains fairly broad, and it is possible that we missed a clinically significant effect caused by type II error in statistical inference. In addition, the RVFV testing performed yields evidence only of past RVFV infection, and we cannot comment on whether acute RVFV-related disease has a significant impact on buffalo survival. Previous analysis found no detectable delayed effects of the capture interventions of the study on buffalo survival.18
This study has several limitations. First, the RVFV study was a sub-study of a larger program that focused on infectious disease dynamics, particularly bovine tuberculosis (TB), among African buffalo. Our RVFV results may be biased because recaptures of African buffalo were intended to exclude those that were known to be TB positive from prior capture. Because TB-negative buffalo are more likely to be younger, recaptures were more likely to be younger. However, in years 2–6 of the study, buffalo > 8 years of age were adequately represented in serologic testing (> 30% of all animals sampled), such that the rates measured were unlikely to be markedly influenced by age bias.
Second, the method of RVFV testing in this study was HAI. Although HAI has been shown to have 100% sensitivity and specificity compared with plaque-reduction neutralization testing in sheep samples, no published studies have reported the test characteristics for buffalo.22
Five buffalo that initially tested positive by HAI (titers 1:5, 1:20, 1:40, 1:80, and 1:160, respectively) seroreverted during the course of the study, which may indicate a higher false-positive rate of HAI in buffalo than in sheep, or a loss of antibody levels, a loss of immunity, or both, in these buffalo over time.
In summary, in a prospective longitudinal African buffalo survey in Kruger National Park during 2000–2006, serologic testing for antibodies against RVFV showed a buffalo seroprevalence of 21% and 7% of retested individuals seroconverted, highlighting the potential importance of local interepidemic RVFV transmission among wildlife in perpetuating regional risk for RVFV transmission. Although there may be considerable variation of RVFV transmission across regional habitats and over time, it is evident that transmission continues on a regular basis in suitable locales. Better definition of the long-term patterns of transmission will provide better insights for planning for vector and population-based RVF prevention and control.