Authors
Harriet Ugboko and Nandita De
Abstract
Salmonella typhi, the causative agent of typhoid fever, is a gram-negative, motile,rod shaped, facultative anaerobe. It is solely a human pathogen and there is noanimal reservoir. Antibiotic therapy is the mainstay for the treatment of typhoid fever and the complications associated with it. The drugs of choice arechloramphenicol, ampicillin, trimethoprim-sulphamethoxazole, quinolones and cephalosporins. Resistance of S. typhi against chloramphenicol was first reported in England in 1950. Several workers have reported occurrence of multidrug resistant S. typhi strains in recent years around the world and in different parts of Nigeria.Mechanisms of antibiotic resistance in S. typhi include inactivation of drug, alteration of the target site, and active efflux. These mechanisms could either be chromosomal or plasmid mediated. Plasmids of incompatibility group HI1 and Care important vectors of antibiotic resistance in some strains of S. typhi. The chromosomal-mediated drug resistance phenomenon against fluoroquinolones has been reported recently and attributed to a single point mutation in the quinolone resistance determining region (QRDR) of the topoisomerase gene gyrA, which encodes DNA gyrase. It has been opined that the initial development of resistance by S. typhi and most other bacterial pathogens occurred as a result of human practices such as over prescription and indiscriminate use of antibiotics as well as inappropriate use in animals. Mass immunization in endemic areas with either the oral live attenuated Typhi 21a or the injectable unconjugated Vi typhoid vaccine, rational use of antibiotics, improvement in public sanitation facilities, availability of safe drinking water, promotion of safe food handling practices and public health education are vital in the prevention of antimicrobial resistance.
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