2 results
Experimental plague infection in South African wild rodents
- A. J. Shepherd, P. A. Leman, D. E. Hummitzsch
-
- Journal:
- Journal of Hygiene / Volume 96 / Issue 2 / April 1986
- Published online by Cambridge University Press:
- 19 October 2009, pp. 171-183
-
- Article
-
- You have access Access
- Export citation
-
Susceptibility studies were undertaken to determine the response of some South African wild rodent species to experimental plague (Yersinia pestis) infection.
A degree of plague resistance was found in three gerbil species captured in the plague enzootic region of the northern Cape Province, these being the Namaqua gerbil, Desmodillus auricularis, (LD50 1 × 106 organisms), the bushveld gerbil, Tatera leucogaster, (LD50 9·1 × 105) and the highveld gerbil, T. brantsii (LD50 4 × 102). Animals from a population of the four-striped mouse, Rhabdomys pumilio, captured in the plague area of Port Elizabeth, proved moderately resistant to experimental plague infection (LD 50 1·3 × 104) while those from another population of the same species captured in a plague-free area of the Orange Free State were extremely susceptible (LD50, 5 organisms). The response of both populations however was a heterogeneous one. Marked differences in susceptibility were also found between two populations of multimammate mice, Mastomys natalensis (2n = 32) although both originated from areas outwith the known distribution of plague in southern Africa.
The 50% infectious dose was relatively high in T. leucogaster (3·2 × 102) and D. auricularis (1·7 × 103), but was low (2–16 organisms) in the other rodent species tested.
The plague antibody response, determined by enzyme-linked immunosorbent assay (ELISA), was extremely short-lived in T. leucogaster, only 10% of inoculated animals remaining seropositive at low titres after 11 weeks. Antibodies persisted for only slightly longer in the sera of T. brantsii which were reinoculated with 2 × 103 plague organisms 6 weeks after initial challenge.
The demonstration of the existence of both susceptible and resistant populations of R. pumilio and M. natalensis indicates that these species must be considered as potential plague reservoir hosts in parts of South Africa.
The results suggest that resistance to plague infection in previously epizootic hosts in the northern Cape Province such as Tatera sp. and D. auricularis has arisen through continual selective pressure of the organism. If the findings are applicable to gerbil populations in other plague enzootic regions of South Africa it is probable that acquired plague resistance has been responsible for the absence of gerbil epizootics and consequently for the dramatic decline in human plague outbreaks in South Africa since 1950.
Comparative pathogenicity and antigenic cross-reactivity of Rift Valley fever and other African phleboviruses in sheep
- R. Swanepoel, J. K. Struthers, M. J. Erasmus, S. P. Shepherd, G. M. McGillivray, A. J. Shepherd, D. E. Hummitzsch, B. J. Erasmus, B. J. H. Barnard
-
- Journal:
- Journal of Hygiene / Volume 97 / Issue 2 / October 1986
- Published online by Cambridge University Press:
- 19 October 2009, pp. 331-346
-
- Article
-
- You have access Access
- Export citation
-
Homologous and heterologous haemagglutination-inhibition (HAI), complement- fixation (CF), immunodiffusion (ID) and mouse neutralization tests were performed with the Lunyo (LUN) and a Zimbabwean strainof Rift Valley fever (RVF) virus, the prototype and a South African strain of Arumowot (AMT) virus and prototype strains of Gordil (GOR), Saint-Floris (SAF) and Gabek Forest (GF) viruses, using immune mouseascitic fluids prepared against these viruses. Reactions of identity occurred in all tests between LUN and the Zimbabwean strains of RVF and between the two strains of AMT virus. Otherwise, cross-reactions occurred between all the phleboviruses in HAI tests, while reactions in CF, ID and neutralization testswere monospecific for virus serotypes, except that weak cross-reaction occurred between GOR and SAF viruses in CF and ID tests.
Four sheep infected subcutaneously with the Zimbabwean strain of RVF virus developed transient fever, viraemia, leucopaenia, relative thrombocytopaenia, haemoconcentration and raised serum enzyme levels, which indicated that the sheep had developed necrotic hepatitis. Disseminated focal necrotic hepatitis was confirmed in a sheep killed for examination on day 4 post-infection. The other three sheep recovered uneventfully after only mild depression and anorexia. Groups of three sheep infected with SAF, GOR, AMT and GF viruses had no demonstrable viraemia or other sign of infection or illness, except that the sheep infected with AMT developed mild fever lasting less than 24 h.
Antibody responses were monitored at intervals over a period of 24 weeks in all sheep by homologous and heterologous HAI, CF and cell culture neutralization (CPENT) tests. Homologous antibody responses were marked in the RVF-infected sheep and their sera cross-reacted strongly in HAI tests with antigens of the other viruses. The sera of the RVF-infectes sheep cross-reactes less marledly in CF and CPENT tests. Homologous antibody responses were poor in all the sheep infected with phlebovirused other than RVF, and the cross-reactivity of their sera RVF antigen or virus was negligible. All sheep were challenged with RVF virus 48 weeks after their initial infection. The sheep which had originally been infected with RVF virus were immune and developed neither fever nor viracmia. All other sheep developed fever, viraemia and antibodies to RVF virus.
It was concluded that the African phleboviruses, other than RVF, are unlikely to cause disease in livestock ot to induce antibodies which could cause confusion in the diagnosis of RVF.