Short-course chemotherapy for pulmonary tuberculosis with a rifampicin-isoniazid-pyrazinamide combination tablet.

The effectiveness of a tablet containing a combination of rifampicin, isoniazid and pyrazinamide (Rifater; Mer-National) in the treatment of pulmonary tuberculosis was examined by comparing it with a previously evaluated four-drug regimen. Of 150 black goldminers with a first case of pulmonary tuberculosis, 69 were randomly allocated to receive the combination tablet (RHZ), 5 tablets per day on weekdays for 100 treatment-days, and 81 the four-drug regimen (streptomycin, rifampicin, isoniazid and pyrazinamide) (RHZS). Non-compliance was detected in 42% of the RHZ group and in 16% of the RHZS group. Two patients in the RHZ group and 4 in the RHZS group had to have their treatment altered because routine investigations revealed drug-resistant mycobacteria. Treatment was unsuccessful in 10 patients in the RHZ group, with 4 men failing to complete the regimen and being lost to follow-up, 3 cases of failure of conversion of sputum on the regimen, and 3 relapses. The results for the RHZS group were similar, with 4 failures to complete the regimen, 2 treatment failures and 4 relapses. Evaluation of RHZ showed it to be comparable with a previously evaluated, successful short-course regimen (RHZS). The high incidence of non-compliance probably reflects reduced supervision of this wholly oral regimen.

Expression of Rhizobium leguminosarum CFN42 genes for lipopolysaccharide in strains derived from different R. leguminosarum soil isolates.

Two mutant derivatives of Rhizobium leguminosarum ANU843 defective in lipopolysaccharide (LPS) were isolated. The LPS of both mutants lacked O antigen and some sugar residues of the LPS core oligosaccharides. Genetic regions previously cloned from another Rhizobium leguminosarum wild-type isolate, strain CFN42, were used to complement these mutants. One mutant was complemented to give LPS that was apparently identical to the LPS of strain ANU843 in antigenicity, electrophoretic mobility, and sugar composition. The other mutant was complemented by a second CFN42 lps genetic region. In this case the resulting LPS contained O-antigen sugars characteristic of donor strain CFN42 and reacted weakly with antiserum against CFN42 cells, but did not react detectably with antiserum against ANU843 cells. Therefore, one of the CFN42 lps genetic regions specifies a function that is conserved between the two R. leguminosarum wild-type isolates, whereas the other region, at least in part, specifies a strain-specific LPS structure. Transfer of these two genetic regions into wild-type strains derived from R. leguminosarum ANU843 and 128C53 gave results consistent with this conclusion. The mutants derived from strain ANU843 elicited incompletely developed clover nodules that exhibited low bacterial populations and very low nitrogenase activity. Both mutants elicited normally developed, nitrogen-fixing clover nodules when they carried CFN42 lps DNA that permitted synthesis of O-antigen-containing LPS, regardless of whether the O antigen was the one originally made by strain ANU843.

Differences in the regional prevalence of chronic hepatitis B in southern Africa--implications for vaccination.

Chronic hepatitis B infection is an important cause of cirrhosis and subsequent hepatocellular carcinoma in South Africa. The disease can now be prevented by vaccination, but second-generation genetically engineered vaccines still necessitate planned allotment. We have tested 29,312 black southern African mineworkers for hepatitis B surface antigen (HBsAg) to indirectly ascertain the relative prevalence of hepatitis B infection in diverse linguistic and ethnic groups. The overall prevalence of HBsAg in this cohort of predominantly rural men was 9.9%, but the prevalence in men from different regions varied from 5.5% to 14%. The relative prevalence in 200 magisterial districts was ranked; these percentage prevalences ranged from 0% to 17%. A significantly lower mean prevalence was detected in Southern Sotho subjects than in those from coastal districts (Nguni). Based on these data, we believe that there are perhaps 2 million hepatitis B carriers in South Africa. The collected data in this report could provide a basis for a broad-based vaccine campaign whereby hepatitis B vaccine could be targeted to high-priority districts initially. This strategy could rapidly reduce the critical mass of carriers, and hasten control of the disease.

Regional prevalence of hepatitis B, delta, and human immunodeficiency virus infection in southern Africa: a large population survey.

Although hepatitis B infection is endemic in southern Africa, a changing epidemiology of the disease has recently been documented in the region. The authors surveyed migrant southern African male mineworkers during 1986 to establish the prevalence of chronic hepatitis B and D (delta) infection in their areas of origin. Hepatitis B surface antigen (HBsAg) was tested in 29,312 adult male mineworkers from 18 geographic regions, encompassing the diverse tribal and linguistic groups in the region, as well as in expatriate mineworkers from neighboring southern African countries. The same cohort was also tested for antibody to human immunodeficiency virus (HIV). Selected hepatitis B carriers were also tested for hepatitis B virus deoxyribonucleic acid (DNA), antibody to hepatitis D (anti-HD), and alpha-fetoprotein. The overall prevalence of HBsAg in this survey was 9.9%. However, the prevalence varied from 5.5% to 14% in different ethnic groups. A minority of carriers (4.9%) had replicative hepatitis B infection and were hepatitis B virus DNA-positive. Only 0.6% of tested carriers were anti-HD-positive. Alpha-fetoprotein determinations were abnormal in 1.2% of hepatitis B-positive men. These data show that although chronic hepatitis B infection remains widespread in southern Africa, carrier rates vary significantly from region to region. In contrast, hepatitis D co-infection remains extremely uncommon. These baseline seroprevalence data also establish that HIV infection was, in 1986, a rare infection in the indigenous population of South Africa.