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 Salmonella enterica 

Samantha Go
Bio 113, Dr. Ruscetti, Fall 2010


 
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  Salmonella enterica 


    

   


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  Salmonella
enterica 
 
   
Salmonella is the leading cause of food-borne illness, with an estimated
annual 1.4 million infections in the United States alone. Most occur as a result
of eating contaminated food, particularly those of animal origin. Antimicrobial
agents are not essential for the treatment of most salmonella infections, but
they can be lifesaving in cases of severe infection.
Use of ampicillin, chloramphenicol, and trimethoprim-sulfamethoxazole
is now limited because of increasing antimicrobial resistance to these agents.
Fluoroquinolones, such as ciprofloxacin, which work by targeting the bacteria¶s
DNA gyrase A, are commonly used.
The use of antimicrobial agents creates selection pressures that favor
the survival of antibiotic-resistant pathogens. Overuse of antibiotics has dire
implications, evidenced by emerging resistance to fluoroquinolones. As a ³last   Total quarterly numbers of S. enterica ser choleraesuis isolates from the fourth
resort´ drug, resistance to it would result in no effective method of treating quarter of 1996 through the third quarter of 2001 (bars) and the percentage of these
isolates that were resistant to ciprofloxacin (curve).
those particular Salmonella infections.  ! Lanes 1, 8, and 14 show S. enterica ser. Newport controls; lanes 2 through 7 and 9
through 11 show isolates from the Oregon patients; lane 12 shows the environmental isolate from
‡In March 2000 there was a dramatic and rapid increase in the incidence of a foam mattress; lane 13 shows the isolate obtained in 1995 from the New York patient.
ciprofloxacin resistance in S. enterica serotype choleraesuis
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‡In the third quarter of 2001, the rate of resistance reached a high of 60% ‡The four control isolates had different patterns on pulsed-field gel
electrophoresis and were sensitive to ciprofloxacin
 
  

  Salmonella enterica 
 



  Salmonella enterica 
 
    

    ‡All isolates associated with the outbreak had similar patterns on pulsed-field

  


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gel electrophoresis, which were also similar to the sample of S. enterica
serotype Schwarzengrund isolated from the New York patient.

   
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number of isolates

*MIC denotes minimal inhibitory concentration, MIC90 the lowest antibiotic concentration


 Isolates were collected from Chang Gung Memorial Hospital and Chang
Gung Children's Hospital from 1991 through 2000.

‡Before 1991, most S. enterica serotype choleraesuis isolates were susceptible
to ampicillin, chloramphenicol, and trimethoprim-sulfamethoxazole.
‡By 2000, resistance to at least one of the three antibiotics was found in
approximately 90% of the isolates, and 78% of the isolates were resistant to all
three antibiotics.
‡There were no reports of resistance to ciprofloxacin in S. enterica serotype
choleraesuis through 1999.
Figure 2 shows the total quarterly numbers of S. enterica serotype
choleraesuis isolates from Chang Gung Memorial Hospital and Chang Gung
Children¶s Hospital in Taiwan. Ciprofloxacin was not available in these
hospitals before October 1996.


that inhibited the growth of 90% of the organisms.
The amino acids at codons 83 and 87 were found on comparison with the sequences of the
gene for DNA gyrase A (gyrA) from Escherichia coli.
Á The amino acids at codons 83 and 87 were the same as those of gyrA from E. coli.
‡The quinolone-resistance-determining region of the gene for DNA gyrase A
was PCR-amplified and sequenced
‡The base substitutions Ser83Phe and Asp87Asn were identified in all
ciprofloxacin-resistant isolates
‡Most susceptible strains had a single amino acid change, either Ser83Phe or
Asp87Asn, indicating that the two mutations are equally important in permitting
S. enterica ser. choleraesuis to attain resistance to ciprofloxacin
Figure 3 and Table 2 show isolates from a 1997 Oregon outbreak of
fluoroquinolone-resistant salmonella infection, caused by S. enterica ser.
Schwarzengrund. The four control isolates of S. enterica ser. Schwarzengrund
were collected in Oregon between 1995 and 1998 but not associated with the
outbreak. Comparisons were made to the only previous isolate of
fluoroquinolone-resistant salmonella in the US, a sample of S. enterica ser.
Schwarzengrund isolated in New York in 1995.
‡The 9 ciprofloxacin-resistant isolates had the same two point mutations in the
region of gyrA that determines quinolone resistance, whereas the control
isolates had the wild-type sequence
‡The two point mutations were identical to those seen in the New York patient
 
‡The most common mutations (Ser83Phe and Asp87Asn) associated with
fluoroquinolone resistance in S. enterica ser. choleraesuis are the same mutations
responsible for fluoroquinolone resistance in S. enterica ser. Schwarzengrund
‡Certain antibiotics are critical to human medicine because they are effective
against pathogens that are resistant to other antibiotics. Fluoroquinolones are
among the few remaining antibiotics to which Salmonella is still sensitive, so the
emergence of fluoroquinolone-resistant S. enterica serotypes is potentially a
serious problem.
‡In order to prevent widespread Salmonella antimicrobial resistance, clinicians
should be advised to use antimicrobial agents judiciously per the indications
outlined in the standard of care.

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‡Chiu CH, Wu TL, Su LH, et al. (2002) The emergence in Taiwan of fluoroquinolone resistance in Salmonella enterica serotype choleraesuis. New England Journal of Medicine 346:6, 413-419.
‡Molbak K, Baggesen D, Aarestrup F, et al. (1999) An outbreak of multidrug-resistant, quinolone-resistant Salmonella enterica serotype typhimurium DT104. New England Journal of Medicine 341:19, 1420-1425.
‡Olsen SJ, DeBess EE, McGivern TE, et al. A nosocomial outbreak of fluoroquinolone-resistant Salmonella infection. (2001) New England Journal of Medicine 344:21 , 1572-1579.
‡Waltner-Toews, David. Food, Sex, and Salmonella: Why Our Food Is Making Us Sick. Vancouver: Greystone, 2008. Print.
‡White DG, Zhao S, Sudler R, et al. (2001) The isolation of antibiotic-resistant Salmonella from ground meats. New England Journal of Medicine 345:16, 1147-1154.