D. H. Smith

Prevalence and transmission of Kaposi's sarcoma‐associated herpesvirus (human herpesvirus 8) in Ugandan children and adolescents

We studied the seroprevalence and transmission of Kaposis sarcoma‐associated herpesvirus (KSHV/HHV8), among 215 Ugandan children, adolescents and young adults. We measured antibodies to a latent nuclear antigen (LANA) and a lytic cycle protein encoded by open reading frame (orf) 65. Infection with KSHV/HHV8 occurred during early childhood and reached adult levels (approx. 50%) before the age of puberty. In children younger than 12 years of age, antibodies to LANA and the orf65 protein were independently associated with hepatitis B infection (p < 0.005). KSHV/HHV8 infection was not associated with antibodies to hepatitis A virus and hepatitis C virus, nor with the quality of the water supply, household size, previous blood transfusions, number of boy/girl friends or marital status. Antibodies to the orf65 protein, but not LANA, were weakly associated with a history of i.v. injections. Our results show that, in contrast to its sexual mode of transmission among homo/bisexual men and sexually transmitted diseases clinic attendees of Northern Europe and the US, transmission of KSHV in Uganda occurs largely before puberty. Among Ugandan children, KSHV transmission follows a horizontal pattern similar to other herpesviruses, in particular the related γ herpesvirus, Epstein‐Barr virus. Transmission of KSHV may be facilitated by living conditions that also promote infection with hepatitis B virus. Int. J. Cancer 77:817–820, 1998.© 1998 Wiley‐Liss, Inc.

Isolation of Trypanosoma brucei gambiense from northern Uganda: evaluation of the kit for in vitro isolation (KIVI) in an epidemic focus

867 individuals from 3 sites near the town of Adjumani in the East Moyo region of north-west Uganda were investigated clinically and serologically for evidence of current trypanosome infections. Blood samples were taken from 94 persons with a positive card agglutination test for trypanosomiasis (CATT) and clinical suspects and inoculated into the kit for in vitro isolation of Trypanosoma brucei gambiense (KIVI). Amongst this group, 30 parasitaemic individuals were identified by microhaematocrit centrifugation and the quantitative buffy coat technique (QBC). Only 80% of these isolates, and one isolate from an aparasitaemic individual, grew in culture. The success or failure of cultures from parasitaemic patients was unrelated to the size of the trypanosome inoculum. The implications of these results and possible reasons for the failure of KIVI are discussed.

A complement fixation test for visceral leishmaniasis using homologous parasite antigen I.

The complement fixation test using homologous parasite antigen was evaluated in 60 individuals with confirmed visceral leishmaniasis and compared with the results obtained in individuals with other parasitic and infectious diseases; 88% of the confirmed cases of visceral leishmaniasis were positive whilst no positive reactions were observed in individuals with other infectious and parasitic diseases. The specificity was partially compromised by anticomplementary activity in 5%, limited to individuals with visceral leishmaniasis, and doubtful (2%) or sero-negative (7%) results.

Treatment of Rhodesian sleeping sickness in Kenya

In a study of 269 sleeping sickness patients treated with Mel-B, 14 (5.2%) died during treatment. With total dosages of at least 30 ml (1.08 g), 1.4% relapsed and another 6.4% died, mostly of unknown causes, within three years of treatment, giving a success rate of 92.1% over the three years. Mel-B was used to treat 55 relapses after suramin therapy with 1.8% deaths during treatment, 3.6% relapses, and 92.7% success over at least three years. Apparent drug resistance to Mel-B was found in three patients who continued to relapse after repeated treatments. During 1980, 51 patients were treated with suramin on the basis of clinical condition without benefit of cerebrospinal fluid (CSF) analysis. Subsequently 49% of these patients relapsed within three years of treatment. When 29 patients were treated on the basis of CSF evaluation only two (7%) relapsed.

Presenting features of Rhodesian sleeping sickness patients in the Lambwe Valley, Kenya

During a recent outbreak of Rhodesian sleeping sickness in the Lambwe Valley no asymptomatic Rhodesian sleeping sickness patients were found although 54% of the primary patients had mild symptoms and 9% were stuporous or comatose at presentation. The duration of symptoms was three months or less in 90% of the patients. Headache, weakness, joint and back pains and weight loss were claimed by at least 75% of the patients, while 82% of the females reported amenorrhoea and 70% of the males claimed impotency. Physical examination revealed lymphadenopathy in 86% but fever in only 36% of the patients, while chancres were found in only 16%. Patients had significantly lower levels of haemoglobin and thrombocytes than controls and their erythrocyte sedimentation rates were elevated. A comparison of both blood group and haemoglobin type between patients and controls yielded no significant differences. Fifty-seven per cent of the primary patients reporting mild symptoms had abnormal levels of leucocytes in their CSF. All relapse patients had abnormal CSF parameters. Levels of serum urea nitrogen were significantly elevated in patients, but SGOT, SGPT and total bilirubin were not. Levels of albumin and beta-globulin in patients were significantly lower than controls while gamma-globulin was elevated. Mean serum IgM levels in patients were elevated to nearly three-fold those of controls, but 35% of the individual patient values fell within the 95% range of control values. Some patients had extended prothrombin and thrombin times while fibrinogen levels were significantly elevated. No patients reported haemorrhage, and none was seen.

A history of sleeping sickness in Kenya

Gambian sleeping sickness entered what is now Kenya from Uganda in about 1901 and quickly spread along the Kenyan shores and islands of Lake Victoria, reaching Tanzania in 1902. By 1910 the disease had spread 25 miles inland along the Kuja and Migori rivers and their tributaries. Sleeping sickness waxed and waned in these areas despite attempts to control tsetse fly populations by various methods. It was not until 1950, when the use of insecticides (DDT) applied by backpack sprayer proved successful against Glossina fuscipes at Kibigori, that eradication of G. fuscipes and Gambian sleeping sickness seemed possible. Subsequently the Kuja-Migori endemic area was cleared of flies and disease, as well as the South and Central Nyanza lake shores and islands. By 1965 Gambian sleeping sickness had virtually disappeared from Kenya. A more virulent form of the disease, Rhodesian sleeping sickness, may have also spread to Kenya from Uganda, although its appearance in diverse areas of the Gambian disease suggest that local ecological factors may have played a role in enhanced virulence of trypanosomes stocks. The Rhodesian form of sleeping sickness appeared in the Lambwe Valley, South Nyanza, in about 1959, and despite attempts to eradicate this disease it still persists as the only remaining endemic area in Kenya at this time. The usual transmission of Rhodesian sleeping sickness by G. pallidipes in Kenya was altered when an outbreak occurred at Alego, in Central Nyanza, in 1964. It was discovered that G. fuscipes was the vector and that domestic cattle were an important reservoir of infection. Glossina fuscipes was also the vector of Rhodesian sleeping sickness in an outbreak in Samia in 1976 and another along the lakeshore in South Nyanza in 1981. Sleeping sickness has been restricted primarily to the Western and Nyanza Provinces of Kenya (Fig. 1).

Outbreak of botulism in Kenyan nomads

During disease surveillance in Kenya, a series of deaths were investigated among a group of nomadic Gabra in Marsabit. The cause was identified as botulism (Clostridium botulinum Type A), contracted from sour milk prepared traditionally in a gourd. Reported outbreaks of botulism in Africa would appear to be extremely rare.

Epidemiology of Rhodesian sleeping sickness in the Lambwe Valley, Kenya

A total of 912 cases of sleeping sickness have been recorded from the Lambwe Valley from 1959 to 1984. After a period of decreasing prevalence in the 1970s an outbreak of disease occurred between 1980 and 1984. The incidence of disease for this five-year period was highest in areas adjoining the Ruma National Park, reaching 54% in Area I. Attack rates were highest in the 50+ age group (125) and children had significantly lower attack rates (8%) in this area of peridomestic transmission. Sex ratios of patients (M/F) were near 1.0 in areas in closest proximity to the thickets in the National Park, while in distant areas the ratios rose to 6.0. The distribution of the number of patients within different households was studied; fewer households than expected had 0 or one patient, and more than expected had three or more patients. No difference in attack rates were found between Nilotic and Bantu groups. Twelve different zymodemes were found in 136 stocks of Trypanosoma brucei rhodesiense. Four new zymodemes appeared in 1980 in the latest outbreak and accounted for 73% of the stocks isolated from man during this outbreak. Neutralization tests indicated that each trypanosome zymodeme may also represent a different serodeme.

Immunodiagnostic tests on cerebrospinal fluid in the diagnosis of meningoencephalitic Trypanosoma brucei rhodesiense infection

Fourteen cerebrospinal fluid (CSF) samples obtained from Rhodesian sleeping sickness patients from the Lambwe Valley at relapse were positive for the presence of anti-trypanosomal antibody by both IFAT and ELISA. The mean optical density (o.d.) in the ELISA test was 0.804 +/- 0.362 and ranged from 0.258 to 1.363. CSF from five patients from the same area without evidence of meningoencephalitis were all negative by ELISA (mean o.d. 0.023 +/- 0.016, range 0.011-0.051). Control CSF samples from U.K. patients without Rhodesian sleeping sickness but with elevated levels of CSF total protein were also negative. Antibody detected by ELISA declined after Mel-B treatment of relapse and most samples had returned to negative within two years of treatment. We present evidence that serological evaluation of the CSF by ELISA and/or IFAT can provide supportive evidence of the trypanosomal origin of the infection. This is especially important at the time of relapse, when parasitological diagnosis may be impossible and records of treatment for the primary infection may not be available.

A complement fixation test for visceral leishmaniasis using homologous parasite antigen II: Results in an endemic area in Kenya

Further studies of the complement fixation test using homologous parasite antigen in an endemic area for visceral leishmaniasis have showed that 82% of individuals with proven visceral leishmaniasis were positive initially whilst 92% were positive at some stage during their illness. Titres fell slowly following effective treatment and anticomplementary activity, confined to confirmed visceral leishmaniasis, was usually lost during treatment. Individuals with alternative causes of hepatosplenomegaly from the same population were negative apart from those with a presumptive diagnosis of visceral leishmaniasis but without parasitological confirmation. Less than 1% of people in the same endemic area without visceral leishmaniasis were positive, suggesting that preliminary serodiagnostic investigation would limit the need for invasive investigation under field conditions.