To determine the number and efficacy of respiratory isolation facilities in St. Louis hospitals and to assess the mechanisms in place for evaluating function of hospital ventilation systems.

A prospective multi-hospital surveillance study using direct observation and a standardized questionnaire.

Seven hospitals (including university-affiliated large teaching, private community, private teaching, and private nonteaching adult hospitals, and one pediatric teaching hospital) in St. Louis, Missouri.

Actual direction of airflow in rooms designated for respiratory isolation was measured using smokesticks. Hospital demographic information, respiratory isolation policies, and frequency of ventilation tests were provided by infection control personnel.

One hundred twenty-one (3.4%) of 3,574 hospital rooms were designed to have negative pressure ventilation suitable for respiratory isolation. The percentage of isolation rooms in each institution ranged from 0.4% (92 of 486) to 93% (39 of 42). Only three (43%) of seven hospitals had intensive care respiratory isolation rooms, and none had isolation rooms in the emergency department. No hospital had tested routinely the efficacy of the negative pressure ventilation, and two (28%) of seven had tested airflow for the first time in the past year.

We tested 115 (95%) of 121 isolation rooms. With the doors closed, 52 (45%) of 115 designated negative pressure rooms actually had positive airflow to the corridor. The number of negative pressure rooms and the presence or absence of anterooms did not predict correct direction of airflow. There was a significant difference among hospitals in the percentage of designated isolation rooms that had truly negative pressure (P<0.0001). Hospital age, size, and type corre-latedwith correct direction of airflow (R<.0001).

In the hospitals studied, only a small number of rooms were designated for respiratory isolation, and the performance of these was not tested routinely. High-risk areas including intensive care units and emergency rooms were not equipped to provide respiratory isolation. The direction of airflow in respiratory isolation rooms was not always correct and should be evaluated frequently. (Infect Control Hosp Epidemiol 1993;14:623-628.)

To assess risk factors for colonization and nosocomial infection with ampicillin-resistant enterococci (ARE).

Patients with ampicillin-resistant enterococci were compared retrospectively by logistic regression analysis with controls harboring susceptible strains. ARE were characterized by whole plasmid DNA analysis and restriction enzyme analysis of plasmid (REAP) DNA with EcoRI.

The study was done at a 1,125 bed, tertiary-care teaching hospital in North Carolina with patients from whom enterococci were isolated from June 1, 1989, to March 30, 1991.

The final study group comprised 44 cases with nosocomially-acquired colonization or infection with ARE and 100 controls with ampicillin-susceptible strains. Clinical and epidemiological risk factors for ARE were abstracted by chart review.

After controlling for age and site of infection, patients with ARE were more likely to have been admitted previously to our hospital and to have received third-generation cepha-losporins and clindamycin. However, only advanced age and clindamycin therapy were independently associatedwith presence of ARE. REAP with EcoRI showed 20 groups of enterococci on 19 different wards.

These results suggest that ARE are endemic and multifocal in origin in our hospital and that advanced age and use of clindamycin are important selective risk factors for ARE colonization and infection (Infect Control Hosp Epidemiol1993;14:629-635).

To determine risk factors for Mycobacterium xenopi isolation in patients following a pseudo-outbreak of infection with the organism.

Retrospective cohort analysis of mycobacteriology laboratory specimen records and frequency-matched case-control study of hospital patients.

General community hospital.

See also page 642

For the case-control study, 13 case patients and 39 randomly selected controls with mycobacterial cultures negative for M xen-opi, frequency matched by specimen source, whose specimens were submitted from June 1990 through June 1991.

Between June 1990 and June 1991, M xenopi was isolated from 13 clinical specimens processed at a midwestern hospital, including sputum (n = 6), bronchial washings (2), urine (4), and stool (1). None of the patients with M xenopi- positive specimens had apparent mycobacterial disease, although five received antituberculosis drug therapy for a range of one to six months. Specimens collected in a nonsterile manner were more likely to grow the organism than those collected aseptically (3.1% versus 0, relative risk= infinity, P= 0.003). M xenopi isolation was attributed to exposure of clinical specimens to tap water, including rinsing of bronchoscopes with tap water after disinfection, irrigation with tap water during colonoscopy, gargling with tap water before sputum collection, and collecting urine in recently rinsed bedpans. M xenopi was isolated from tap water in 20 of 24 patient rooms tested, the endoscopy suite, and the central hot water mixing tank, but not from water in the microbiology laboratory. The pseudo-outbreak occurred following a decrease in the hot water temperature from 130°F to 120°F in 1989.

Maintenance of a higher water temperature and improved specimen collection protocols and instrument disinfection procedures probably would have prevented this pseudo-outbreak (Infect Control Hosp Epidemiol 1993;14:636-641).

The purpose of this study was to determine current regulations and policies in the United States concerning maximal water temperatures in acute care hospitals.

A standardized questionnaire administered by telephone to health department officials from 50 states and the District of Columbia.

See also page 636

State Health Departments in the 50 states and the District of Columbia.

All states responded to the survey. Respondents from 39 states (77%) reported regulating maximum allowable hospital water temperature at a mean of 116°F (median, 120°F; mode 110°F; range, 110°F to 129°F). Twelve states (23%) have no regulations for maximum water temperature. Of the 39 states regulating maximum water temperature, 30 (77%) routinely monitor hospital compliance. Nine states (23%) conduct inspections only in response to a complaint or incident.

There is great variation among the states with respect to the existence, enforcement, and specific regulations controlling hospital water temperature. Risk-benefit and cost-effectiveness analyses would help to assess the risk of scald injuries at water temperatures that will inhibit microbial contamination (Infect Con-trol HOsp Epidemiol1993;14:642-645).