Clonal relationship among Vibrio cholerae O1 El Tor strains causing the largest cholera epidemic in Kenya in the late 1990s.

Eighty Vibrio cholerae O1 strains selected to represent the 1998-to-1999 history of the largest cholera epidemic in Kenya were characterized by ribotyping, antimicrobial susceptibility, and random amplified polymorphic DNA patterns. Except for 19 strains from 4 local outbreaks in North Eastern Province along the Somalia border, the other 61 strains from 25 outbreaks occurring in districts scattered around the country were all ribotype B27 and resistant to chloramphenicol, spectinomycin, streptomycin, sulfamethoxazole, and trimethoprim. The 61 strains showed similar and specific amplified DNA patterns. These findings indicate that the predominant strains that caused the Kenyan epidemic had a clonal origin and suggest that ribotype B27 strains, which first appeared in West Africa in 1994, have had a rapid spread to eastern Africa.

A rapid method for restriction analysis of large plasmids from enteric pathogens.

A modified version of the method of Kado and Liu (J Bacteriol 1981, 145: 1365) has been developed for rapid detection and direct cleavage analysis of large plasmids from Vibrio cholerae and other enteric pathogens.

Vibrio cholerae in the horn of Africa: epidemiology, plasmids, tetracycline resistance gene amplification, and comparison between O1 and non-O1 strains.

The prevalence of Vibrio cholerae O1 and non-O1 has been investigated in numerous Somali regions of the Horn of Africa from 1983 to 1990. From January 1983 to January 1985 and between December 1986 and December 1990, no strains of V. cholerae O1 and 226 strains (5.3%) of V. cholerae non-O1 were isolated from 4,295 diarrhea cases. During a cholera epidemic in 1985 and 1986, the overall case-fatality rate was 13% and the attack rate was 3-3.5 per 1,000 population. Matched case-control studies identified a waterborne route of transmission. A drug-susceptible Ogawa strain from Ethiopia caused the introduction of the disease into northern Somalia. There were two major resistant derivatives of the original strain, and the one resistant to ampicillin, kanamycin, streptomycin, sulfonamide, and tetracycline (TC) predominated in the spreading disease. In 1986, susceptible Ogawa strains quickly displaced this resistant strain. The two incompatibility group C plasmids responsible for the resistance patterns had complex and scattered differences in their structures. Physical analysis of the plasmid DNA region coding for TC resistance demonstrated its genetic amplification in highly resistant variants of Ogawa strains.

Visceral leishmaniasis in Somalia: prevalence of markers of infection and disease manifestations in a village in an endemic area.

Prevalence and disease manifestations of visceral leishmaniasis (VL) were studied in a Somali village in an area which has long been known to be endemic for VL. Demographic data were collected from 102 households, comprising 438 inhabitants. Clinical examination was performed of 306 individuals, 72% of the 426 eligible persons. Of these, 276 (90%) agreed to give blood and 246 (80%) to be skin tested with leishmanin. Leishmanin reactions were positive; in 26% anti-Leishmania antibodies were detected in 11%, and splenomegaly was recorded in 14% (23% of those who were seropositive). Malaria was hypoendemic and therefore unlikely to be responsible for more than 10% of the cases with splenomegaly. Three of the seropositive villagers with splenomegaly complained of feeling ill. The remaining 91 sero- and/or leishmanin-positive individuals had no complaint regarding their health and had not experienced any long period of illness. There was a slight over-representation of males in the group of sero- and/or leishmanin-positive villagers, possibly due to a gender-associated difference in exposure to the parasite. Among the patients with clinical VL treated at Mogadishu hospitals during 1989 and 1990, the male/female ratio was 3.3:1, which may indicate a selection of male patients for hospital care. Most patients were < or = 15 years old, suggesting that the highest risk of becoming clinically ill was among children.

Characterization of endemic Shigella flexneri strains in Somalia: antimicrobial resistance, plasmid profiles, and serotype correlation.

One hundred twelve Shigella flexneri strain isolated from children with diarrheal disease in Somalia in 1983, 1984, 1988, and 1989 were analyzed for serotype, plasmid profile, and genetic location of antimicrobial resistance determinants. The prevalent serotypes were 4 (46% of the isolates), 1b (16%), 2a (16%), 3a (12%), and 6 (8%). Each serotype was associated with a characteristic predominant plasmid profile, whereas no specific correlation between antimicrobial resistance patterns and single serotypes was found. All but three of the strains were resistant at least to ampicillin, chloramphenicol, spectinomycin, and tetracycline. Of these resistant strains, 41 were resistant to sulfonamide and streptomycin and 14 were resistant to trimethoprim or trimethoprim and kanamycin. The genes for resistance to ampicillin, chloramphenicol, spectinomycin, and tetracycline formed a linkage group located on the chromosome of the strains of all serotypes. The genes for resistance to sulfonamide and streptomycin were located on a 6.3-kb plasmid in strains of serotypes 1b, 2a, and 4. Conjugative trimethoprim or trimethoprim and kanamycin resistance plasmids with lengths of 80 to 110 kb were present in strains of serotypes 1b, 2a, 3a, and 4. The systematic presence of a chromosomal component in this uncommon genetic plasmid-chromosome configuration may play a role in the emergence of increased genetic stability of resistance patterns in S. flexneri.

The growth chart--a road to health chart? Maternal comprehension of the growth chart in two Somali villages.

Growth monitoring is so far not implemented on a large scale in the Somali health services. Available reports indicate that growth faltering is common. However, the use of growth charts as a tool for health education has been questioned. This study examines the ability of 199, predominantly illiterate, rural Somali mothers to understand the growth chart message after an intensive period of growth chart use and education. During a home-based interview the mothers were asked to combine a set of four growth curves with a set of four pictures, showing the corresponding developments of four children. The mothers managed significantly better to interpret the charts than could be expected by chance alone. Maternal age, number of children and literacy did not differ much between those who correctly and incorrectly combined pictures and charts. Almost all mothers recognised the value of the growth chart as being good for the control and promotion of their children's health and/or growth. We conclude that the growth chart may be an applicable and appropriate tool even with illiterate mothers, provided that other prerequisites for successful growth monitoring, e.g. appropriate health services, are available.