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.
D000293:Adolescent; D000328:Adult; D017677:Age Distribution; D000368:Aged; D000369:Aged, 80 and over; D000818:Animals; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D002771:Cholera / Q000453:epidemiology* / Q000382:microbiology; D004269:DNA, Bacterial / Q000032:analysis; D004196:Disease Outbreaks; D005260:Female; D006801:Humans; D007223:Infant; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D011815:R Factors; D012998:Somalia / Q000453:epidemiology; D013753:Tetracycline Resistance / Q000235:genetics*; D014734:Vibrio cholerae / Q000187:drug effects / Q000235:genetics*; D014871:Water Microbiology
D004269:DNA, Bacterial