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Unusual patterns of aminoglycoside resistance in Pseudomonas aeruginosa
THE ANTIMICROBIC NEWSLETFER, VOLUME 1, NUMBER 9, SEPTEMBER 1984
75
IN VITRO DIAGNOSTIC PROBLEMS
U N U S U A L PATTERNS OF AMINOGLYCOSIDE RESISTANCE IN PSEUDOMONAS AERUGINOSA In the last two years, we have had numerous reports of Pseudomonas aeruginosa isolates that were apparently resistant to gentamicin and amikacin but susceptible to tobramycin. Most microbiologists and clinicians were surprised at, and skeptical about, this pattern of resistance and thought these results might be in error and could be due to some aberration of the methods used in the test. Most of the results reported to us were by the standard disk diffusion method. We have tested some of these strains and have confirmed these findings both by disk diffusion and by microdilution MICs. We have also obtained P. aeruaeruginosa strains with these susceptible patterns from a multihospi-
tal study in which we are involved, and we are currently studying these strains. Isolates demonstrating similar susceptibility profiles have also been reported to or sent to the Bristol Laboratories, who offer a service to test aminoglycoside resistance in clinical pathogens (personal communication with Dr. Ken Price). When these strains are tested for MICs using cation supplemented Mueller-Hinton broth, we find that they are marginally resistant (or intermediate/interdeminant) to gentamicin and amikacin, but marginally susceptible to tobramycin. We do not have data to definitively establish the mechanism(s) of this pattern of resistance. It is unlikely to be due to aminoglycoside modifying enzymes. We think that it may be
due to changes in permeability to these antibiotics. These changes are enough to create marginal differences to gentamicin and amikacin, but because P. aeruginosa strains are generally more permeable to tobramycin, or because they are innately more susceptible to tobramycin (on a weight basis), they remained susceptible to tobramycin, even though the MICs are somewhat elevated. As indicated above, data would have to be developed to confirm this hypothesis. As far as we know, no clinical studies have been done to determine whether tobramycin is efficacious in infections with these organisms.
C. THORNSBERRY
MEETING HIGHLIGHTS
REPORT O N THE THIRD INTERNATIONAL SYMPOSIUM O N INFECTIONS IN THE I M M U N O C O M P R O M I S E D HOST The Third International Symposium on Infections in the Immunocompromised Host was held at York University, Toronto, Canada between June 24-28, 1984. A multinational committee chaired by Dr. Jack Remington of Stanford University School of Medicine organized a 4-day symposium covering a wide variety of basic and clinically oriented topics related to this growing and ever more complex field. A series of keynote speakers highlighted various aspects of host defense: these included the role of phagocytic cells, immunoregulation of Tlymphocyte functions, cellular im0738.1751184/$0.00+2.00
munity against intracellular parasites, the role of viruses in chronic and latent infections, and current status of the leukotriene cascade in inflammation. More than 100 posters elaborated on the content of abstracts submitted from participants from 30 different countries. In the antimicrobial area, the following studies were highlighted. The prophylaxis of infection in immunocompromised patients remains a controversial subject. Whereas some studies continue to report the beneficial effects of prophylactic trimethoprim/sulfamethoxazole in neutropenid pa-
tients, there is evidence that the side effects of prolonged neutropenia, allergic reactions, and the emergence of resistance are associated significantly with the use of the fixed combination. New agents like the quinolone antimicrobics may be attractive alternatives to prophylactic trimethoprim/sulfamethoxazole. However, the use of some of these compounds has not resulted in a dramatic reduction in gram-positive infections, which are now observed to be a major and increasing component of nonsocomial infections in compromised hosts. Quinolones like ciprofloxacin are now being
© 1984 BY ELSEVIER SCIENCE PUBLISHING CO., INC.
75
IN VITRO DIAGNOSTIC PROBLEMS
U N U S U A L PATTERNS OF AMINOGLYCOSIDE RESISTANCE IN PSEUDOMONAS AERUGINOSA In the last two years, we have had numerous reports of Pseudomonas aeruginosa isolates that were apparently resistant to gentamicin and amikacin but susceptible to tobramycin. Most microbiologists and clinicians were surprised at, and skeptical about, this pattern of resistance and thought these results might be in error and could be due to some aberration of the methods used in the test. Most of the results reported to us were by the standard disk diffusion method. We have tested some of these strains and have confirmed these findings both by disk diffusion and by microdilution MICs. We have also obtained P. aeruaeruginosa strains with these susceptible patterns from a multihospi-
tal study in which we are involved, and we are currently studying these strains. Isolates demonstrating similar susceptibility profiles have also been reported to or sent to the Bristol Laboratories, who offer a service to test aminoglycoside resistance in clinical pathogens (personal communication with Dr. Ken Price). When these strains are tested for MICs using cation supplemented Mueller-Hinton broth, we find that they are marginally resistant (or intermediate/interdeminant) to gentamicin and amikacin, but marginally susceptible to tobramycin. We do not have data to definitively establish the mechanism(s) of this pattern of resistance. It is unlikely to be due to aminoglycoside modifying enzymes. We think that it may be
due to changes in permeability to these antibiotics. These changes are enough to create marginal differences to gentamicin and amikacin, but because P. aeruginosa strains are generally more permeable to tobramycin, or because they are innately more susceptible to tobramycin (on a weight basis), they remained susceptible to tobramycin, even though the MICs are somewhat elevated. As indicated above, data would have to be developed to confirm this hypothesis. As far as we know, no clinical studies have been done to determine whether tobramycin is efficacious in infections with these organisms.
C. THORNSBERRY
MEETING HIGHLIGHTS
REPORT O N THE THIRD INTERNATIONAL SYMPOSIUM O N INFECTIONS IN THE I M M U N O C O M P R O M I S E D HOST The Third International Symposium on Infections in the Immunocompromised Host was held at York University, Toronto, Canada between June 24-28, 1984. A multinational committee chaired by Dr. Jack Remington of Stanford University School of Medicine organized a 4-day symposium covering a wide variety of basic and clinically oriented topics related to this growing and ever more complex field. A series of keynote speakers highlighted various aspects of host defense: these included the role of phagocytic cells, immunoregulation of Tlymphocyte functions, cellular im0738.1751184/$0.00+2.00
munity against intracellular parasites, the role of viruses in chronic and latent infections, and current status of the leukotriene cascade in inflammation. More than 100 posters elaborated on the content of abstracts submitted from participants from 30 different countries. In the antimicrobial area, the following studies were highlighted. The prophylaxis of infection in immunocompromised patients remains a controversial subject. Whereas some studies continue to report the beneficial effects of prophylactic trimethoprim/sulfamethoxazole in neutropenid pa-
tients, there is evidence that the side effects of prolonged neutropenia, allergic reactions, and the emergence of resistance are associated significantly with the use of the fixed combination. New agents like the quinolone antimicrobics may be attractive alternatives to prophylactic trimethoprim/sulfamethoxazole. However, the use of some of these compounds has not resulted in a dramatic reduction in gram-positive infections, which are now observed to be a major and increasing component of nonsocomial infections in compromised hosts. Quinolones like ciprofloxacin are now being
© 1984 BY ELSEVIER SCIENCE PUBLISHING CO., INC.