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Contaminated benzalkonium chloride has been implicated as the source of infection in several nosocomial outbreaks over the past 40 years and was also the most likely source of infection in this cluster of abscesses. Benzalkonium chloride solution from the clinic grew P aeruginosa as did the majority of abscesses, whereas other environmental samples and unopened vials of ТА were not contaminated. The canister containing benzalkonium chloride solution was not disinfected between batches, and once contaminated, could have contaminated successive batches. Two strains of P aeruginosa were identified among three patient isolates and P putida/fluorescens was isolated from one patient’s abscess, suggesting that the canister may have become contaminated with several Pseudomonas strains and species. Unfortunately, the isolate from the benzalkonium chloride solution was discarded before it could be compared with patient isolates.

Contaminated benzalkonium chloride could have led to abscesses in patients via two main pathways. First, use of contaminated benzalkonium chloride solution at the time of injection could have contaminated the hands of the person administering the injection, the skin of the patient at the injection site, and/or the needle used for the injection. Any of these factors could have resulted in infection in patients. Second, the contents of multidose vials could have become contaminated when vial septa were wiped with contaminated benzalkonium chloride and punctured with a needle. Injection of contaminated medication could cause infection, regardless of the disinfectant used at the time of injection. We found that use of benzalkonium chloride on patients at the time of the injection was not a risk factor for abscess development. More than half of the case-patients received injections from clinic personnel who used alcohol to clean injection sites and vial septa. These findings suggest that the first pathway was not a significant contributing factor to infection in patients and that the second pathway (contamination of multidose vials) is a more significant explanation for this cluster of abscesses.
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The clinic did not record from which vial each patient received an injection; thus it was impossible to determine whether case-patients were associated only with injections withdrawn from vials that had been wiped previously with benzalkonium chloride. The one opened vial of ТА available for testing was not contaminated with Pseudomonas spp. The vial may not have been wiped with benzalkonium chloride, however, and the vial was cultured several months after it was opened, allowing sufficient time for any present organisms to have died.

Receiving a corticosteroid injection was a strong risk factor for abscess development in persons receiving IM injections at the clinic (Tables 1 and 2). All case-patients received a corticosteroid injection compared with 48.4% of control-patients. Corticosteroids were the only medication associated with abscess development, although at least nine other medications from multidose vials also were used at the clinic. This outcome may have been due to the immunosuppressive effects of pharmacologic dosages of glucocorticoids (eg, ТА and methylprednisolone). Corticosteroid injections have been involved in other nosocomial outbreaks, including a cluster of abscesses following IM injection of methylprednisolone in New Mexico in 1978.

All case-patients received corticosteroid injections from multidose vials administered in the gluteal muscle. To try to separate the effects of these highly associated variables, we first limited the analysis to patients receiving medications from multidose vials and then to patients receiving injections in the gluteal muscle only. Corticosteroid injection remained a strong, statistically significant risk factor for abscess development in both of these models (exact 95% confidence interval = [4.18, undefined] and [3.45, undefined], respectively), whereas injection site was no longer significant in the first model, and vial type was no longer significant in the second. These results suggest that corticosteroid injection was the most important risk factor of the three; vial type and injection site may have appeared as risk factors only because of their association with corticosteroid injections.

Being female was a risk factor for postinjection abscess development even when controlling for body mass index in the logistic model. Females also were more likely than males to develop abscesses following injections of methylprednisolone in the 1978 cluster of abscesses in New Mexico mentioned earlier. Reasons for this difference between males and females were not clear.
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Although benzalkonium chloride has been documented as a significant nosocomial infection liability for many years, this cluster of abscesses illustrates that some health-care providers remain unaware of the dangers of using it as a disinfectant or skin antiseptic. The use of benzalkonium chloride at this clinic may not be an isolated incident; 12% of respondents of a country-wide survey of hospital epidemiologists reported that benzalkonium chloride was in use for skin disinfection at their hospital. Given the unreliability of benzalkonium chloride as a disinfectant and antiseptic and the availability of more efficacious products, benzalkonium chloride should not be used to clean injection vial septa or the skin of patients before injections. Given the potential for contamination of multidose vials, health care providers should consider using single-dose vials of injectable medications when possible, especially when administering corticosteroids.