Mitral valve replacement at Tygerberg Hospital: a 5 year follow-up: mitral valve replacement

"This study provides 5-year follow-up data of isolated mitral valve replacements with mechanical prosthesis at a large South African tertiary hospital. It also assessed the significance of pre-operative parameters to predict mortality. This is a retrospective study of 187 patients that underwent isolated mitral valve replacement at Tygerberg Hospital from Jan 1998-Dec 2002. Twenty seven patient's data was incomplete and they were excluded from the study. All patients had rheumatic mitral valve disease and the valve lesions included mitral incompetence; mitral stenosis and mixed mitral valve disease. All patients had a mechanical prosthesis implanted (St Jude medical or Orbis bileaflet valves). The mean follow-up time was 5.41-years. The 30 day mortality was 5.62and the 5-year survival was 80. Pre-operative risk factors that significantly increased mortality were pulmonary hypertension and mitral stenosis. Valve-related complications were more common in this series compared to other First World populations but our results compare well with other Third World population groups. Valve thrombosis 4.32(0.8/yr); thromboembolism 8.71(1.61/yr); anticoagulant related haemorrhage 6.87(1.27/yr); prosthetic valve endocarditis 3.08(0.57/yr) and re-operation 8.12(1.5/yr). Conclusion: Mechanical valve replacement for mitral valve disease that requires valve replacement is still a good treatment option even in third world population groups. In our series; severe pulmonary hypertension; mitral stenosis and reoperation was statistically significantly more common in the ""non-survivors"" group."

Some epidemiological and economic aspects of a bluetongue-like disease in cattle in South Africa--1995/96 and 1997.

In December 1995 to March 1996 and the early summer of 1997 South Africa experienced above average rainfall which favoured the occurrence of Culicoides transmitted diseases. During this period several outbreaks of an uncommon disease of cattle occurred over a large part of the country. The clinical signs were similar to those of infection with the viruses of bluetongue (BT) and epizootic haemorrhagic disease of deer (EHD). Virus isolation from cattle and Culicoides yielded both viruses. Dual infections occurred on several farms. Typing of BT isolates yielded types 2, 3, 6 and 8. On at least two farms more than one BT virus serotype was involved. On one farm only EHD virus could be isolated from cattle and Culicoides. Serological tests confirmed that on this farm the disease was caused by EHD. In 1932/33, when a similar disease was reported conditions were vastly different. Rainfall figures show that the 1932/33 season was exceptionally dry. Techniques available at that time could not identify EHD and the cause was reported to be BT. The occurrence of BT in a dry season and over a much wider area than the distribution in South Africa of Culicoides imicola, the only proven vector for BT, is a clear indication that other species less dependent on high rainfall are involved. The present isolation of BT virus from three of five pools of parous C. bolitinos is evidence that this species, which breeds in cattle dung, may be an additional vector for BT.

Epidemiology of African horse sickness and the role of the zebra in South Africa.

Zebra are the only equine species native to South Africa. These animals roamed over much of the country in the 17th century when horses and donkeys were first imported. The first cases of African horse sickness (AHS) then occurred in the horses of hunters who entered zebra territory. AHS continued to occur on a country-wide basis until the beginning of the 20th century, though the number of outbreaks decreased as the populations of zebra collapsed through overhunting. For most of the 20th century almost all free-living zebra have been confined to the north-eastern parts of South Africa which are now the only areas in the country where AHS is endemic; though when climatic conditions are favourable, temporarily, it spreads beyond these areas. The minimum size of a zebra population necessary to maintain a focus of AHS virus is unknown but the small, isolated populations that have inhabited the majority of South Africa for most of the 20th century are apparently insufficient to maintain the virus in the long term. In this context, the restocking of many parts of the country with zebra should be viewed with caution since conditions may be generated that will facilitate the re-establishment of permanent foci of AHS virus.

Transmission and distribution of African horse sickness virus serotypes in South African zebra.

The prevalences of African horse sickness (AHS) virus serotypes in zebra foals from the Kruger National Park, South Africa were examined for possible associations between serotypes. Serotypes known to cross-react were combined for analysis. The distributions of serotypes between zebra were not always independent; in 7-8 month old zebra positive pairwise associations were observed between 3 serotypes. This could be generated by biological interactions between serotypes or heterogeneity in host-vector transmission. The data were also used to estimate the basic reproduction number, R0. For AHS virus overall, estimates of R0 ranged from 31-68. This underlines the need for a better understanding of serotype transmission and interactions in AHS.

Antibodies against some viruses of domestic animals in southern African wild animals.

Twenty-four species of South African wild animals were tested for the presence of antibodies against the viruses of 16 common diseases of domestic animals. Positive results were obtained for African horsesickness, equine encephalosis, equid herpes virus-1, infectious bovine rhinotracheitis, Allerton disease (Herpes mammillitis), lumpy skin disease, parainfluenza, encephalomyocarditis, bluetongue, Wesselsbron disease, bovine ephemeral fever, and Akabane disease complex. No antibodies could be demonstrated against the viruses of equine influenza, equine infectious anaemia, equine viral arteritis and Rift Valley fever. The negative results substantiate observations that the latter diseases, with the exception of equine viral arteritis, are absent in South Africa. The number of animal species found positive for a specific virus, ranged from 0-16. No antibodies were found in crocodiles and warthogs, whereas antibodies against Wesselsbron and bovid herpes virus-1 were present in 16 species. Antibodies against viruses of horses were found almost exclusively in zebras and, although elephants reacted to African horsesickness, no neutralizing antibodies against it could be demonstrated in their sera. Zebras were also found to be positive for Wesselsbron and Akabane, which are usually regarded as viruses of ruminants. Antibodies against most viruses were encountered in all vegetation zones in South Africa but, as a rule, most viruses were more prevalent in the high-rainfall zone in KwaZulu-Natal.

Transmission and distribution of virus serotypes: African horse sickness in zebra.

The prevalence of African horse sickness (AHS) serotypes in zebra foals from the Kruger National Park, South Africa was examined for possible associations between serotypes and to estimate the basic reproduction number, R0. The distributions of serotypes between zebra were not independent in the 6- and 7-8-month-old age classes (P < 0.005). This does not necessarily imply biological interactions between serotypes, as heterogeneity in host-vector transmission rates can generate non-independent distributions of serotypes. Both age and month of capture were significant factors in the number of serotypes infecting each zebra (P < 0.0001). Pairwise, positive associations between non-cross-reacting serotypes were found in the 7-8-month-old class only. For AHS overall, estimates of R0 ranged from 31-68. Assuming serotypes are transmitted independently, estimates of R0 for individual serotypes ranged from 10 for serotype 1 to 23 for serotype 6. The wide range of estimates emphasizes the need for a better understanding of serotype transmission and interactions in AHS.

Some factors governing the entry of Culicoides spp. (Diptera: Ceratopogonidae) into stables.

The entry of Culicoides species into stables was examined by comparing the numbers of midges caught with identical light-traps under different conditions. The comparison was made between collections made inside an empty stable, a regularly cleaned stable and a dirty stable and those made outside the stables in a sleeping space open on two sides. The work was first done in the presence of cattle and sheep in adjoining paddocks and then repeated in their absence. A positive correlation was found between the numbers of C. imicola females caught out of doors and inside a clean stable. Removal of the cattle and sheep resulted in a reduction in the numbers of C. imicola caught inside and outside the stables. In contrast, the numbers of Culicoides spp. that prefer to feed on birds was not affected by the removal of the cattle and sheep. Their entry into the stable was proportionate to the size of the entrances into the sleeping space and the size of the stable door and presumably occurs passively. On the other hand, the numbers of C. imicola females entering the same stables were somewhat enhanced by the presence of horses inside the stables and by odours associated with dirty stables.

Transmission of the South African asinine strain of equine arteritis virus (EAV) among horses and between donkeys and horses.

Lateral and sexual transmission of EAV among horses and lateral transmission between donkeys and horses were attempted by experimental infection with the South African asinine strain. Clinical, immunological and virological responses were evaluated. All intramuscularly inoculated horses developed very mild clinical signs, were viraemic, shed virus from nasopharynx, and seroconverted. Lateral infection was demonstrated in one in-contact mare. Reinfection of two stallions by intranasal instillation was shown by virus recovery from buffy-coat cultures. After nasal instillation of virus, one stallion which did not become infected by in-contact exposure, showed slight serous nasal and ocular discharge, contained virus in a blood and nasopharynx and seroconverted. Attempts to transmit the virus from seropositive stallions to seronegative mares by breeding, were not successful; no virus was isolated from semen. All inoculated donkeys and three in-contact horses showed clinical signs consistent with an EAV infection. Although virus was isolated from donkey buffy-coat preparations and the nasopharynx, and they seroconverted, no virus was isolated from the horses, and they failed to seroconvert; it was assumed that their clinical signs were due to factors unrelated to EAV. The South African strain of EAV appears to be poorly transmissible to horses, supporting the findings of other field studies which indicate a widespread distribution and long-standing presence of the virus among South African donkeys, but a very restricted prevalence of seropositive horses.

The use of sucrose-acetone-extracted Rift Valley fever virus antigen derived from cell culture in an indirect enzyme-linked immunosorbent assay and haemagglutination-inhibition test.

A sucrose-acetone-extracted, Madin-Darby-bovine-kidney (MDBK)-derived Rift Valley fever virus (RVFV) antigen was tested both in an indirect ELISA and a haemagglutination-inhibition test for its ability to detect serum antibodies to RVFV. Optimal conditions for antigen concentration, serum and conjugate dilutions for the ELISA were established by checkerboard titration. The specificity and sensitivity of ELISA were determined by the use of paired pre- and post-vaccination sheep-serum samples. Compared with the virus neutralization test, the overall ELISA specificity and sensitivity were 97.4 and 97.3%, respectively. There was a 100% correlation between the results obtained in haemagglutination-inhibition tests with a RVFV sucrose-acetone-extracted antigen derived from hamster liver, and from MDBK cells. A total of 10 582 field-serum samples (84 cattle, 3,659 sheep, 6,839 goats) collected in 1994-1995 from animals of unknown vaccination status in different regions of South Africa were tested with ELISA for antibodies against RVFV. There were no seropositive cattle, 0.16% seropositive sheep and 0.12% seropositive goats. This study demonstrates the potential diagnostic application of cell-culture-derived, sucrose-acetone-extracted RVFV antigen in an indirect ELISA and HI test.

Epidemiology of African horsesickness: antibodies in free-living elephants (Loxodonta africans) and their response to experimental infection.

The presence of low levels of group- and type-specific antibodies against African horsesickness virus in the serum of some free-living elephants was reconfirmed. Experimental infection resulted in conflicting results. No detectable viraemia nor virus could be demonstrated in the organs of the six elephant calves and none of them mounted significant levels of neutralizing antibodies against the virus. On the other hand, all calves showed a slight rise in ELISA titres. This rise, however, was modest when compared with the rise in experimentally infected zebra. The presence of low levels of group- and type-specific antibodies in the serum of some free-living elephants is judged to be the result of natural hyper-immunization due to frequent exposure to infected biting insects. Elephants should therefore, despite the presence of low levels of antibodies, be regarded as poorly susceptible and unlikely to be a source of African horsesickness virus.

Sexual and in-contact transmission of asinine strain of equine arteritis virus among donkeys.

Two in a group of five naturally seropositive donkey stallions were found to shed equine arteritis virus (EAV) in their semen as demonstrated by virus isolation. Direct intramuscular inoculation of sonicated semen from one virus-shedding stallion (S3) caused clinical disease in two donkeys from which virus was recovered and in which seroconversion was detected. Sexual transmission was confirmed in two mares mated to S3 when after a febrile response during which EAV was isolated from huffy coats and nasal and ocular exudates, both mares were found to have seroconverted. In-contact transmission in a susceptible stallion was demonstrated after its exposure to a sexually infected mare. The 3' end of the asinine virus was amplified directly from donkey semen with EAV-specific primers, and its nucleotide sequence was found to be homologous to that of the prototype Bucyrus virus isolated from horses. These results indicate that EAV and its disease transmission are analogous in donkeys and horses.

An outbreak of encephalomyocarditis-virus infection in free-ranging African elephants in the Kruger National Park.

A cluster of four deaths in late December 1993, marked the onset of an outbreak of disease of African elephants (Loxodonta africana) in the Kruger National Park (KNP) in South Africa, which has an estimated population of 7,500 elephants. Mortalities peaked in January 1994, with 32 deaths, and then declined steadily to reach pre-outbreak levels by September, but sporadic losses continued until November. During the outbreak altogether 64 elephants died, of which 53 (83%) were adult bulls. Archival records revealed that, in addition to the usual losses from known causes such as poaching and intraspecific fighting, sporadic deaths from unexplained causes had, in fact, occurred in widely scattered locations from at least 1987 onwards, and from that time until the perceived outbreak of disease there had been 48 such deaths involving 33 (69%) adult bulls. Carcases had frequently become decomposed or had been scavenged by the time they were found, but seven of eight elephants examined early in 1994 had lesions of cardiac failure suggestive of encephalomyocarditis (EMC)-virus infection, and the virus was isolated from the heart muscles of three fresh carcases. The results of tests for neutralizing antibody on 362 elephant sera collected for unrelated purposes from 1984 onwards and kept frozen, indicated that the virus had been present in the KNP since at least 1987. Antibody prevalences of 62 of 116 (53%) 18 of 139 (13%) and seven of 33 (21%) were found in elephants in three different regions of the KNP in 1993 and 1994. Studies had been conducted on myomorph rodents in the KNP for unrelated purposes since 1984, and trapping attempts were increased during the perceived outbreak of disease in elephants. There was a striking temporal correlation between the occurrence of a population explosion (as evidenced by markedly increased catch rates per trap-night) and a surge in prevalence of antibody to EM virus in rodents, and the occurrence of the outbreak of disease in elephants.

Epidemiology of African horsesickness: duration of viraemia in zebra (Equus burchelli).

The viraemic period of African horsesickness is significantly longer in experimentally infected zebra than in horses. The virus could be isolated 40 d post-infection from blood and 48 d post-infection from spleen. The introduction of zebra into African horsesickness-free countries should therefore be considered carefully, and preferably be restricted to serologically negative zebra.

Rabies in southern Africa.

The first confirmed outbreak of rabies in Africa, believed to have followed the importation of an infected dog from England in 1892, occurred in the eastern Cape Province of South Africa, and was brought under control in 1894. An unconfirmed epidemic of rabies in dogs occurred in western Zambia in 1901. By the following year the disease had apparently spread along a major trade route, to cause an outbreak in Zimbabwe which engulfed most of the country before being eradicated in 1913. The existence of endemic rabies of viverrids (mongooses and genets) was confirmed in South Africa in 1928, and since then the viverrid disease has continued to occur widely on the interior plateau of the country with spill-over of infection to cattle and a variety of other animals. From about 1947 onwards, an invasive form of dog rabies spread from southern Zambia and/or Angola into Namibia, across northern and eastern Botswana into Zimbabwe and the northern Transvaal by 1950, entered Mozambique in 1952, and spread from there to Swaziland in 1954. Dog rabies extended from southern Mozambique into Natal in 1961 to cause a major epidemic which was brought under control in 1968. The disease re-entered northern Natal from Mozambique in 1976 and since then dog rabies has proved difficult to control in the peri-urban settlements of Natal-KwaZulu. The disease spread from Natal to Lesotho in 1982, and into the Transkei region of the eastern Cape Province in 1987, to reach the Ciskei by 1990. The spread of the disease in dogs was followed by the emergence of rabies of jackals and cattle in central Namibia, northern Botswana, Zimbabwe and the northern Transvaal. A unique outbreak of rabies in kudu antelope occurred in central Namibia from 1977 to 1985, apparently involving oral spread of infection between individuals. A few cases of rabies in the bat-eared fox were recognized each year in Namibia from 1967 onwards, and from the 1970s the occurrence of the disease in the fox has emerged as a distinct problem in the northern Cape Province and spread to the west coast. The rabies-related viruses, Lagos bat, Mokola and Duvenhage, associated with bats, shrews and rodents in Africa, are known to have caused isolated cases of disease in South Africa, and on one occasion a small outbreak involving six cats and a dog in Bulawayo, Zimbabwe.(ABSTRACT TRUNCATED AT 400 WORDS)

Prevalence of antibodies against some equine viruses in zebra (Zebra burchelli) in the Kruger National Park, 1991-1992.

The presence of antibodies against equine encephalosis virus (EEV) and equid herpesvirus 1 and 4 in zebra in the Kruger National Park (KNP) was demonstrated. The ability of zebra to maintain immunity against EEV is illustrated by the appearance of neutralizing antibodies in most zebra foals within months of losing their maternal immunity. This occurs in every month of the year, even in winter. The high proportion of serologically positive foals in winter is ascribed to the presence of large numbers of susceptible foals and sufficient numbers of Culicoides vectors even at that time of the year. The high prevalence of antibodies against both herpesviruses is similar to the situation in horses and suggests that herpesvirus infection is endemic among zebra in the KNP.

Circulation of African horsesickness virus in zebra (Equus burchelli) in the Kruger National Park, South Africa, as measured by the prevalence of type specific antibodies.

In the Kruger National Park 75% of zebra foals are born in October-March and they lose their passive immunity against African horsesickness virus (AHSV) when they are 5-6 months old. One month later infection with different serotypes of AHSV amounts to 31% and thereafter infections increase rapidly to almost 100% before the foals are 12 months old. The capability of zebra to maintain AHSV is clearly illustrated by the continuing infections during every month of the year with a peak period in winter. This peak is ascribed to the presence of large numbers of susceptible foals in the presence of active Culicoides species.

Serological evidence of equine arteritis virus in donkeys in South Africa.

This paper reports the first serological evidence of exposure of donkeys to equine arteritis virus. Seven hundred and thirty-four serum samples collected between 1989 and 1992 from donkeys in different areas of South Africa were examined for the presence of antibodies against this virus by a microneutralization test. Seventeen percent of serum samples tested positive. The distribution of seropositive animals varied from none in the western Cape Province and the Transvaal Highveld to 30% in the northern Transvaal. The country-wide distribution of serologically positive donkeys suggests a longstanding presence of the virus in South Africa.