Review of epidemic aminoglycoside resistance worldwide.

Epidemic aminoglycoside resistance may be caused by the spread of a species with distinctive chromosomal genes (e.g., Pseudomonas aeruginosa), or it may be due to the dissemination of plasmids or transposons between genera. Although strains of P. aeruginosa resistant to aminoglycosides because of impermeability may cause nosocomial outbreaks, most of the acute increases in aminoglycoside resistance are due to the spread of inactivating enzymes by plasmids. The index species for intergeneric outbreaks is usually Klebsiella pneumoniae carrying the ANT(2") or AAC(3) gene; however, the distribution of resistance varies greatly by location and species. The AAC(6')-I gene is most common in Serratia marcescens and in East Asian isolates of other species, whereas the AAC(3) gene is common in Chile. In the United States, the ANT(2") and AAC(3) genes are particularly common among Enterobacteriaceae, except for Proteus and Providencia, which often carry the AAC(2') gene. The most common patterns of epidemic resistance lead to the inactivation of gentamicin and, less frequently, tobramycin, but only rarely affect amikacin.

Pertussis epidemic in Oklahoma. Difficulties in preventing transmission.

From Jan 1 to Dec 31, 1983, 351 cases of pertussis were reported in Oklahoma. Overall, 59% of the cases were among children 3 months to 6 years of age, the target age group for pertussis vaccination; only 42% of the patients in this age group were appropriately immunized for age with diphtheria and tetanus toxoids and pertussis vaccine (DTP). A survey of 185 households in the neighborhoods of three cases found that only 65% of 57 children 3 months to 6 years of age were appropriately immunized for their age. Aggressive control of the outbreak was attempted in Oklahoma County with recommendations for widespread vaccination against pertussis. However, the effort failed to immunize 82% of the 931 children in the initial target group. Nonetheless, analysis of the reported cases suggested that less than one fourth of the cases were potentially preventable by a single additional dose of DTP, ie, in individuals 3 months to 6 years of age with a history of at least one prior dose of DTP who were not appropriately immunized for age. The optimal solution to outbreak control is outbreak prevention by ensuring that the maximal number of children younger than 7 years of age receive routine age-appropriate DTP vaccination.

An outbreak of Clostridium difficile necrotizing enterocolitis: a case for oral vancomycin therapy?

During a 2-month period, 13 infants in this neonatal intensive care unit developed necrotizing enterocolitis, increasing the prevalence in inborns from 5.2 to 20.5/1,000 live births. Fifty-seven perinatal and neonatal factors, many of which have previously been associated with necrotizing enterocolitis, were compared between the infants with necrotizing enterocolitis and 17 unaffected inborn control infants admitted concurrently. Clostridium difficile cytotoxin was detected in the stools of 12 affected infants (92.3%) in comparison with two control infants (11.8%) (P less than .001), and the organism was isolated in eight affected neonates (61.5%) compared to none of the control infants (P less than .001). The outbreak was terminated upon institution of oral vancomycin therapy in cases and infant contacts, and strict antiinfective measures in the neonatal intensive care unit. This indicates an etiologic role of C difficile in the outbreak. Oral vancomycin in the management of necrotizing enterocolitis was assessed by therapeutic response, drug levels, and occurrence of side effects. Oral vancomycin therapy is indicated in necrotizing enterocolitis outbreaks in units where C difficile is endemic.

Endemic aminoglycoside resistance in gram-negative bacilli: epidemiology and mechanisms.

Isolates of gentamicin-resistant gram-negative bacilli from clinical specimens peaked at nine to 10 per month in 1973-1974. Instituting barrier-type precautions during 1974-1977 was associated with a sustained 87% reduction in resistant Enterobacteriaceae. The number of resistant Pseudomonadaceae fell temporarily by 28%, paralleling gentamicin usage. During an endemic 15-month period in 1976-1977 nonenzymatically mediated resistant Pseudomonas aeruginosa often emerged after aminoglycoside therapy in patients who had prior carriage of sensitive strains of the same serotype (P = 0.002); this resistance was associated with wound or sputum isolates (P = 0.003). Resistant Enterobacteriaceae more often demonstrated the converse, that is, spread of urinary tract isolates with enzymatically mediated resistance from patients not on aminoglycoside therapy. These findings suggest that control measures to minimize occurrence of resistant bacilli include barrier-type precautions for patients with resistant Enterobacteriaceae, evaluation of transfers and readmissions as a source of resistant organisms, and reduction of aminoglycoside use to decrease the selection of nonenzymatic resistance.