Natural transmission of foot-and-mouth disease virus from African buffalo (Syncerus caffer) to cattle in a wildlife area of Zimbabwe.

An outbreak of foot-and-mouth disease (FMD) occurred during April 1991 in a trypanosomiasis sentinel cattle herd by the Rifa River to the east of Lake Kariba, Zimbabwe. Despite the cattle having been vaccinated biannually for the previous five years the disease was severe. The viruses isolated from the affected animals were typed as FMD virus type SAT 1. Free-living African buffalo (Syncerus caffer) which had been using the same watering place as the affected cattle were sampled and FMD type SAT 1 virus was isolated. Partial nucleotide sequencing of the gene coding for the capsid protein 1D (VP1) of one of the viruses isolated from cattle and two of the viruses isolated from buffalo demonstrated a close relationship between the three viruses. Since no other cattle were present in the area and no outbreaks of SAT 1 had occurred in Zimbabwe since 1989, it was concluded that the disease had been transmitted from buffalo to cattle.

Experimental transmission of foot-and-mouth disease virus from carrier African buffalo (Syncerus caffer) to cattle in Zimbabwe.

Four female cattle and three male African buffalo (Syncerus caffer) which were free of foot-and-mouth disease (FMD) virus were held together on an island in Lake Kariba, Zimbabwe. The buffalo were experimentally infected with FMD virus type SAT2, developed generalised disease and became virus carriers. While the buffalo were in the acute phase of the disease the susceptible contact cattle did not show lesions, no virus was recovered from them and they did not develop serum antibodies. However, five months later the cattle developed severe foot-and-mouth disease. Direct nucleotide sequencing of the virus used to infect the buffalo and of the virus from the in-contact cattle showed that the two isolates were almost identical. The results suggest that in nature it is possible for the virus to be transmitted from buffalo to cattle under the influence of factors not yet defined, and that there was very little change in the nucleotide sequence of the virus during the carrier period of five months.

Point mutations in polypeptide VP1 of foot-and-mouth disease virus affect mouse virulence and BHK21 cell pathogenicity.

Virus produced in the first four days after infection of a BHK21 culture was shown to differ from that produced later in the infection. The early virus caused large plaques in IB-RS-2 cell sheets, had a slow cytopathic effect in BHK21 cultures and showed a high virulence for suckling mice. In contrast, the late virus caused small plaques, was rapid in its cytopathic effect and was of low virulence for mice. Comparison between one clone each of the early and late virus showed that no change in immunogenic specificity had taken place, but that charge changes had occurred both in VP3 and in the large trypsin-resistant fragment of VP1. The early, large plaquing clone gave rise spontaneously to small plaquing virus during the destructive phase of a single passage in BHK21 cultures. Conversely, the late, small plaquing clone gave rise to large plaquing virus after a single passage in mice. Each new virus was cloned and it was shown that they differed in VP1. This indicated that missense mutations in the genome coding for the trypsin resistant fragment of VP1 were responsible for the biological changes observed.