Mokola virus infection: description of recent South African cases and a review of the virus epidemiology.

Five cases of Mokola virus, a lyssavirus related to rabies, are described. The cases occurred in cats from the East London, Pinetown and Pietermaritzburg areas of South Africa from February 1996 to February 1998. Each of the cats was suspected of being rabid and their brains were submitted for laboratory confirmation. Four of the cases were positive, but with atypical fluorescence, and 1 was negative. Mokola virus infection was identified by anti-lyssavirus nucleocapsid monoclonal antibody typing. As in rabies cases, the predominant clinical signs were of unusual behaviour. Aggression was present, but only during handling. Four of the 5 cats had been vaccinated for rabies, which is consistent with other studies that show that rabies vaccination does not appear to protect against Mokola virus. Since Mokola may be confused with rabies, the incidence of Mokola virus may be more common in Africa than is currently reported. As human infections may be fatal, the emergence of this virus is a potential threat to public health.

Brucella melitensis biotype 1 outbreak in goats in northern KwaZulu-Natal.

Brucella melitensis biotype 1 was confirmed in indigenous, outbred goats in three northern districts of the KwaZulu-Natal province following the diagnosis of human Malta fever in the same area. Six foci of infection were found during an extensive serological survey involving 6266 goats carried out in most of the districts of the KwaZulu-Natal province. The prevalence in the positive herds varied between 17% and 100%. The diagnosis was confirmed by culturing milk samples from serologically positive animals. Infected goats were found in only three districts (Ubombo, Ingwavuma and Pongola) and all infected herds fell within a 50-km radius.

NAD (V-factor)-independent and typical Haemophilus paragallinarum infection in commercial chickens: a five year field study.

An unusual bacterium causing respiratory disease in chickens emerged in South Africa in February 1989. The disease resembled infectious coryza but the organism differed from typical Haemophilus paragallinarum especially in that it did not require V-factor for growth. It has been termed an NAD-independent H. paragallinarum. A study of avian haemophili isolated from diseased chickens in Kwazulu-Natal over the past five years revealed the presence of typical H. paragallinarum, NAD-independent H. paragallinarum and H. avium (now transferred to the genus Pasteurella). Before the end of 1989 the NAD-independent H. paragallinarum had become the predominate isolate and thereafter was isolated from commercial chickens in other regions of South Africa. The disease affected all strains of chickens in an overall age range of 14 days to 64 weeks. The organism was responsible for upper respiratory disease of broilers and layers and implicated in lower respiratory disease of broilers. It was commonly isolated from diseased adult birds previously vaccinated against typical H. paragallinarum. Broilers were most commonly infected from 3 weeks of age and layers within the placement to peak production period. Whole cell protein profiles of NAD-independent H. paragallinarum isolates from five different commercial poultry units were identical but differed from that of a typical isolate.

Phenotypic and molecular characterization of V-factor (NAD)-independent haemophilus paragallinarum.

In South Africa from early 1989 onward, strains of Haemophilus paragallinarum not requiring nicotinamide adenine dinucleotide (NAD) have been isolated from commercial chickens suffering from infectious coryza. Fifteen of these field isolates were characterized by biochemical typing, serotyping, restriction endonuclease analysis (REA), and ribotyping. The chosen isolates represented diversity in geographic location, time of disease outbreak, and type of flock. All were typical of the species in biochemical properties, except that they were NAD-independent, and all were Page serovar A. REA was performed with three enzymes: HindIII, HpaII, and SspI. All isolates gave identical REA profiles with all three enzymes. Ribotyping was performed using a probe that consisted of the plasmid pUC19 into which the 16S rRNA operon of H. paragallinarum had been inserted. All 15 isolates gave the same ribotyping profile using each of the three enzymes. As a group, the NAD-independent strains gave REA profiles and ribotypes that were very different from a range of classic South African strains isolated before 1989. Our results strongly suggest that the NAD-independent isolates are clonal in nature.

Case study of a high-risk neonate failing to thrive post-extracorporeal membrane oxygenation and post-necrotizing enterocolitis.

Infants discharged from neonatal intensive care units (NICUs) often face a long journey of chronic illness, family stresses, and financial burdens. Health care professionals involved in acute care need to be aware of the far-reaching repercussions of neonatal illness. This report presents a case study of a low-income, single mother from a rural community and her son, a neonatal intensive care unit (NICU) graduate post-extracorporeal membrane oxygenation (ECMO) and post-necrotizing enterocolitis (NEC) discharged with a gastronomy tube (g-tube) and failure to thrive (FTT), from his birth to 10 months of age. Family-focused interventions aimed at improving growth and developmental delays and providing family support will be discussed.

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)

An upper respiratory disease of commercial chickens resembling infectious coryza, but caused by a V factor-independent bacterium.

From early 1989 the emergence of an infectious bacterial disease resembling infectious coryza was seen in several commercial chicken flocks in Natal Province of South Africa. Clinical signs were facial swelling and nasal discharge. An organism was routinely isolated from the infra-orbital sinus or trachea of infected chickens. The organism was found to be a Gram-negative rod, non-motile, V factor (nicotinamide adenine dinucleotide, NAD)-independent, catalase negative, oxidase positive and urease and indole negative. No gas was produced from carbohydrates and acid was produced from glucose, mannitol, inositol and sorbitol. Experimental inoculation of this organism into the infraorbital sinus of SPF chickens and conventional broilers produced an acute upper respiratory disease. The organism could be recovered for up to 7 days post-inoculation. The organism is closely related to Haemophilus paragallinarum, the cause of infectious coryza, but because it is NAD-independent it cannot be classed as an Haemophilus species.

Thromboembolic meningoencephalitis diagnosed in Natal.

Nine feedlot cattle showed clinical signs consistent with those expected in thromboembolic meningoencephalitis. These signs included pyrexia, ataxia, posterior paresis, paralysis and coma. Brown necrotic foci with haemorrhagic borders were observed in the brains of three animals that had died. In these foci vasculitis, thrombosis, infarction and neutrophil infiltration were observed during microscopical examination. Haemophilus somnus was isolated in pure culture from the brains.

A brucellosis serological survey on beef cattle slaughtered at Cato Ridge Abattoir.

A total of 5059 sera were collected from adult female beef cattle at Cato Ridge Abattoir and tested for Brucella abortus antibody levels over the period November, 1981 to August, 1982. The sera were screened using the Rose Bengal Plate Test, and the Complement Fixation Test was used as the definitive test. Seventy-seven sera (1,5%) had titres of 30 IU complement fixing B. abortus antibody per ml serum or greater.