Changing Antibiotic Sensitivity Patterns at a University Hospital, 1992 Through 1999.

ABSTRACT

Background. The emergence of antibiotic-resistant organisms is of great concern in the medical community. Antibiotic sensitivity patterns were studied at a large university hospital.

Methods. From 1992 through 1999, susceptibility testing was done and results recorded for all isolates of Streptococcus pneumoniae, Enterococcus sp, Staphylococcus aureus, coagulase-negative Staphylococcus, Escherichia coli, Haemophilus influenzae, and Pseudomonas aeruginosa. Microbiologic and sensitivity data were reviewed and compiled.

Results. Over the 8-year period, several common bacterial pathogens declined in susceptibility to various antimicrobial agents. Most notable were the decreased sensitivities of S pneumoniae to penicillin (96% to 63%), coagulase-negative Staphylococcus to oxacillin (50% to 38%), and P aeruginosa to aminoglycosides [(gentamicin (85% to 64%), tobramycin (96% to 83%), amikacin (92% to 74%)] and ciprofloxacin (85% to 69%).

Conclusions. These decreased antibiotic sensitivities reflect increased bacterial selection pressure as a result of widespread antibiotic use. A combined approach involving infection-control specialists, infectious disease physicians, and hospital administrators is necessary to address this increasingly difficult problem.

GREAT CONCERN EXISTS about the emergence of antibiotic resistant organisms.[1-1] The goal of this study was to delineate antibiotic sensitivity patterns at a large university hospital.

METHODS

From 1992 through 1999, susceptibility testing was done and results were recorded for all, isolates of Streptococcus pneumoniae, Enterococcus sp, Staphylococcus aureus, coagulase-negative Staphylococcus, Escherichia coli, Haemophilus influenzae, and Pseudomonas aeruginosa. Microbiologic and sensitivity data were reviewed and compiled.

RESULTS

Over the 8-year study period, the susceptibility of several common bacterial pathogens to various antimicrobial agents declined at our institution (Table). Most notable were the decreased sensitivities of S pneumoniae to penicillin (from 96% to 63%), coagulase-negative Staphylococcus to oxacillin (from 50% to 38%), and P aeruginosa to three commonly used aminoglycosides (gentamicin [85% to 64%], tobramycin [96% to 83%], and amikacin [92% to 74%]) and to ciprofloxacin (from 85% to 69%).

DISCUSSION

Antibiotic resistance is influenced by the antibiotic (mechanism of action and molecular composition) and type of resistance. [3] Resistance can develop by chromosomal mutation; acquisition of plasmids, transposons, or antibiotic-resistance genes; or interspecies genetic transformation. [4]

Antibiotic resistance, regardless of antibiotic and bacteria, will occur with sufficient time and drug use. Widespread antibiotic use causes selection pressure: resistant strains survive while susceptible ones are eliminated. Antibiotic resistance is progressive, increasing from low to intermediate to high levels. Furthermore, resistance to one antibiotic is a marker for resistance to others. Antibiotic use by one person also affects others in the immediate and extended environment. Finally, once antibiotic resistance develops, it declines slowly since no counterselective measures exist. The original, susceptible strains of organisms will only reemerge over time if they are not continuously exposed to the antibiotics(s) to which they have developed resistance. All of these principles have been well-documented through the evolution of penicillin-resistant S pneumoniae, [1-4]

Increased antibiotic use in hospitals is often associated with increased frequency of resistance. Changes in antibiotic sensitivity patterns at this hospital reflect all principles of antibiotic resistance already discussed. These findings have profound clinical implications for current and future treatment of common bacterial infections.

How can antibiotic resistance be arrested? A combined approach involving infection-control specialists, infectious disease physicians, and hospital administrators is necessary. Close surveillance of antibiotic use and microbiologic sensitivities is essential. Infection-control specialists can educate faculty, fellows, and residents in each department about the prevalence of antibiotic-resistant strains in the hospital. Reduced antibiotic use can also decrease the prevalence of resistant species in the hospital's microbiologic flora. Infectious disease subspecialists can be instrumental in providing focused, appropriate antibiotic recommendations to minimize indiscriminate antibiotic use. Prompt attention to these findings and continued diligence are crucial, since reduced prevalence of resistant species will most likely take years to become evident.

CONCLUSIONS

Over an 8-year period at a large university hospital, the susceptibility of several common bacterial pathogens to various antibiotics has declined. This reflects increased bacterial selection pressure as a result of widespread antibiotic use. These findings have profound clinical implications for the current and future treatment of common bacterial infections. A combined approach involving infection-control specialists, infectious disease physicians, and the hospital administration is necessary to address this increasingly difficult problem.

References

(1.) Bartlett JG: Update in infectious diseases. Ann Intern Med 1999;131:273-280

(2.) Chen DK, McGeer A, DeAzavedo JC: Decreased susceptibility of Streptococcus pneumoniae to fluoroquinolones in canada. N Engl J Med 1998;341:233-239

(3.) Levy SB: Multidrug resistance: a sign of the times. N Engl J Med 1998;338:1376-1378

(4.) Swartz MN: Use of antimicrobial agents and drug resistance. N Engl J Med 1997;337:491-492

TABLE. Antibiotic Sensitivity to Bacterial Pathogens, 1992 Through 1999
                                Sensitive Isolates (%)
Organism                  Drug           1992           1993  1994
Streptococcus pneumoniae  PCN             96             96    88
Enterococcus sp           AMP             92             94    94
Enterococcus sp           VANC           100            100    99
Staphylococcus aureus     OX              70             70    63
Staphylococcus aureus     VANC           100            100   100
CN Staphylococcus         OX              50             46    41
CN Staphylococcus         VANC           100            100   100
Escherichio coli          CIPR            99             99    98
Haemophilus influenzae    AMP             55             59    57
Pseudomonas aeruginosa    GENT            85             85    70
Pseudomonas aeruginosa    TOBR            96             95    94
Pseudomonas aeruginosa    AMIK            92             93    82
Pseudomonas aeruginosa    CIPR            85             83    79
Pseudomonas aeruginosa    CEFT            89             89    90
Pseudomonas aeruginosa    IMIP            90             89    89
Pseudomonas aeruginosa    PIP             88             88    90
Organism                  1995  1996  1997  1998  1999
Streptococcus pneumoniae   76    74    73    68    63
Enterococcus sp            93    91    88    93    85
Enterococcus sp            99    98    96    99    92
Staphylococcus aureus      62    61    60    61    64
Staphylococcus aureus     100   100   100   100   100
CN Staphylococcus          42    38    41    39    38
CN Staphylococcus         100   100   100   100   100
Escherichio coli           99    99    99    99    98
Haemophilus influenzae     50    51    57    52    60
Pseudomonas aeruginosa     73    69    59    60    64
Pseudomonas aeruginosa     91    86    85    83    83
Pseudomonas aeruginosa     81    77    73    71    74
Pseudomonas aeruginosa     76    70    70    69    69
Pseudomonas aeruginosa     89    88    87    87    85
Pseudomonas aeruginosa     85    82    80    82    82
Pseudomonas aeruginosa     89    87    83    87    84
PCN = Penicillin; AMP = ampicillin; VANC = vancomycin; OX = oxacillin;
CN = coagulase-negative; CIPR = ciprofloxacin; GENT = gentamicin;
TOBR = tobramycin; CEFT = ceftazidime; IMIP = imipenem;
PIP = piperacillin.

KEY POINTS

* Several common bacterial pathogens declined in susceptibility to various antimicrobial agents at a large university hospital from 1992 through 1999.

* The most notable decreases in antibiotic sensitivity were seen in Streptococcus pneumoniae to penicillin, coagulase-negative Staphylococcus to oxacillin, and Pseudomonas aeruginosa to aminoglycosides, tobramycin, amikacin, and ciprofloxacin.

* Widespread antibiotic use causes selection pressure in the immediate and extended environment: resistant strains survive while susceptible ones are eliminated.

* A combined approach involving infection-control specialists, infectious disease physicians, and hospital administrators is needed to address this increasingly difficult problem.