VIBRIO-CHOLERAE IN THE HORN-OF-AFRICA - EPIDEMIOLOGY, PLASMIDS, TETRACYCLINE RESISTANCE GENE AMPLIFICATION, AND COMPARISON BETWEEN O1 AND NON-O1 STRAINS

Citation
A. Coppo et al., VIBRIO-CHOLERAE IN THE HORN-OF-AFRICA - EPIDEMIOLOGY, PLASMIDS, TETRACYCLINE RESISTANCE GENE AMPLIFICATION, AND COMPARISON BETWEEN O1 AND NON-O1 STRAINS, The American journal of tropical medicine and hygiene, 53(4), 1995, pp. 351-359
Citations number
38
Categorie Soggetti
Public, Environmental & Occupation Heath","Tropical Medicine
ISSN journal
00029637
Volume
53
Issue
4
Year of publication
1995
Pages
351 - 359
Database
ISI
SICI code
0002-9637(1995)53:4<351:VITH-E>2.0.ZU;2-7
Abstract
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. Fr om 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. chole rae non-01 were isolated from 4,295 diarrhea cases. During a cholera e pidemic in 1985 and 1986, the overall case-fatality rate was 13% and t he attack rate was 3-3.5 per 1,000 population. Matched case-control st udies identified a waterborne route of transmission. A drug-susceptibl e Ogawa strain from Ethiopia caused the introduction of the disease in to northern Somalia. There were two major resistant derivatives of the original strain, and the one resistant to ampicillin, kanamycin, stre ptomycin, sulfonamide, and tetracycline (TC) predominated in the sprea ding disease. In 1986, susceptible Ogawa strains quickly displaced thi s resistant strain. The two incompatibility group C plasmids responsib le for the resistance patterns had complex and scattered differences i n their structures. Physical analysis of the plasmid DNA region coding for TC resistance demonstrated its genetic amplification in highly re sistant variants of Ogawa strains.