Salmonella pp 47-61 | Cite as
Determination of Antimicrobial Resistance in Salmonella spp.
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Abstract
Infections with Salmonella are an important public health problem worldwide. Salmonella are one of the most common causes of food-borne illness in humans. There are many types of Salmonella but they can be divided into two broad categories: those that cause typhoid and those that do not. The typhoidal Salmonella (TS), such as S. enterica subsp. enterica serovars Typhi and S. Paratyphi only colonize humans and are usually acquired by the consumption of food or water contaminated with human fecal material. The much broader group of non-typhoidal Salmonella (NTS) usually results from improperly handled food that has been contaminated by animal or human fecal material. Antimicrobials are critical to the successful outcome of invasive Salmonella infections and enteric fever. Due to resistance to the older antimicrobials, ciprofloxacin [fluoroquinolone (FQ)] has become the first-line drug for treatment. Nevertheless, switch to FQ has led to a subsequent increase in the occurrence of salmonellae resistant to this antimicrobial agent. The exact mechanism of this FQ resistance is not fully understood. FQ resistance has driven the use of third-generation cephalosporins and azithromycin. However, there are sporadic worldwide reports of high level resistance to expanded-spectrum cephalosporins (such as ceftriaxone) in TS and in NTS it has been recognized since 1988 and are increasing in prevalence worldwide. Already there are rare reports of azithromycin resistance leading to treatment failure. Spread of such resistance would further greatly limit the available therapeutic options, and leave us with only the reserve antimicrobials such as carbapenem and tigecycline as possible treatment options. Here, we describe the methods involved in the genotypic characterization of antimicrobial resistance in clinical isolates of salmonellae.
Key words
Salmonella Fluoroquinolones Cephalosporins Clinical and laboratory standards institute Mutations gyrA β-LactamasesReferences
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