Enteric fever is a major public health problem in developing countries. Due to the problem of resistance to first-line drugs and fluoroquinolone, cephalosporins are currently used for treatment of enteric fever. Cephalosporin resistance in Salmonella spp. is mainly due to production of extended-spectrum β-lactamases (ESBLs). The majority of ESBLs in Salmonella are derivatives of the TEM and SHV β-lactamase families. The objectives of this study were to detect antibiotic susceptibility patterns, ESBL production and TEM-, SHV- and CTX-M-encoding genes (blaTEM, blaSHV and blaCTX-M) among clinical isolates of Salmonella spp. A total of 134 Salmonella isolates [Salmonella Typhi (n=101), Salmonella Paratyphi A (n=31), Salmonella Paratyphi B (n=1) and Salmonella Typhimurium (n=1)] were included in this study. Multidrug resistance was seen in 5/134 (3.73 %) isolates, all of which belonged to serotype S. Typhi. A better susceptibility profile was observed for first-line drugs (ampicillin, chloramphenicol, co-trimoxazole and tetracycline) and cephalosporins (cefotaxime, ceftazidime, ceftriaxone, cefixime and cefepime). However, 131 (97.76 %) of the 134 isolates were resistant to nalidixic acid and one (0.75 %) was resistant to ciprofloxacin. TEM-1-type β-lactamase (blaTEM-1) was detected in six (4.47 %) of the 134 isolates, which belonged to the serotype S. Typhi. All six TEM-positive isolates were negative for the blaSHV gene and none of the isolates was positive for the blaCTX-M gene. The presence of the blaTEM gene encoding TEM-1 β-lactamase is believed to confer resistance only to penicillins and early cephalosporins; however, the resistance spectrum of TEM-1 descendants may extend to second-, third- and fourth-generation cephalosporins. The ESBLs derived from TEM-1 differ from their progenitors by as few as 1 aa, and have the ability to hydrolyse third-generation cephalosporins. Therefore, appropriate selection and rotation of antibiotics as well as continuous monitoring of antibiotic susceptibility profiles could help to control the emergence and spread of resistant strains.