We analyzed 24,584 cultures obtained from 3371 infants during a three-year period to determine how frequently body surface culture isolates matched those obtained subsequently from body fluids. The sensitivity, specificity, and predictive values of surface cultures were calculated daily for the two weeks up to and including the day that a body fluid culture was obtained. Isolates from cultures of material from the ear canal, nasopharynx, axilla, umbilicus, groin, rectum, stomach, and endotracheal tube were rarely the same as those recovered from blood or fluids of the cerebrospinal, joint, pleural, pericardial, and peritoneal spaces. With a frequency of sepsis of 3.3% among patients in our neonatal intensive care unit, the optimum sensitivity, specificity, and positive predictive values of surface cultures were 56%, 82%, and 7.5%, respectively. These values did not improve substantially for any specific times of surface cultures prior to sepsis, for anatomic sites cultured, or for pathogens recovered. We conclude that surface cultures are of limited value in predicting the etiology of sepsis in neonates.

Drawing upon our experience with 88 cases and a survey of the English literature, we reviewed the clinical, pathophysiological, and epidemiological aspects of tularemia. Tularemia can be thought of as two syndromes--ulceroglandular and typhoidal. This dichotomy simplifies earlier nomenclature and emphasizes the obscure typhoidal presentation. Clinical manifestations suggest that the two syndromes reflect differences in host response. In ulceroglandular tularemia the pathogen appears to be well contained by a vigorous inflammatory reaction. Pneumonia is less common and the patient's prognosis is good. In typhoidal disease there are few localizing signs; pneumonia is more common; and the mortality without therapy is much higher, suggesting that the host response is somehow deficient. Francisella tularensis is an extremely virulent pathogen capable of initiating infection with as few as 10 organisms inoculated subcutaneously. During an incubation period of 3 to 6 days the host responds first with polymorphonuclear leukocytes and then macrophages. Granulocytes are unable to kill the pathogen without opsonizing antibody leaving cellular immunity to play the major role in host defense. One to 2 weeks after infection, a vigorous T-lymphocyte response can be detected in vitro with lymphocyte blast transformation assays and in vivo with an intradermal skin test, which, unfortunately, is not commercially available. Humoral immunity, often used as a diagnostic modality, appears 2 to 3 weeks into the illness. Cellular immunity is long-lasting, accounting for the common reoccurrence of localized disease upon repeated exposures to the pathogen. There are no symptoms that distinguish the ulceroglandular from the typhoidal syndrome. A pulse-temperature dissociation is seen in less than half of the patients. The location of ulcers and enlarged lymph nodes give a clue to the likely vector since lesions located on the upper extremities are more commonly associated with mammalian, and those of the head and neck and lower extremities with arthropod, vectors. Pharyngitis, pericarditis, and pneumonia can complicate both syndromes, although the latter is much more common in typhoidal disease. Hepatitis, usually of a mild degree, is common and occasionally erythema nodosum is seen. No specific laboratory tests characterize tularemia, and cultures of the pathogen are often difficult to obtain because of the special growth requirements of Francisella tularesis and the inability of many clinical laboratories to handle the dangerous pathogen.(ABSTRACT TRUNCATED AT 400 WORDS)

Using clinical isolates of Pseudomonas aeruginosa, we studied the ability of imipenem to antagonize the activity of nine other antipseudomonal beta-lactam antimicrobial agents. Imipenem caused truncation of the zones of inhibition in a disk diffusion test for 91 to 100% of the strains, depending on the beta-lactam tested. Addition of subinhibitory concentrations of imipenem caused a fourfold or greater increase in MICs for 72 of 74 isolates and in 20 to 87% of the tests, again depending on the antibiotic tested. beta-Lactamase assays with both whole-cell suspensions and cell sonicates showed that exposure to subinhibitory concentrations of imipenem resulted in a beta-lactamase production supported the hypothesis that induction of beta-lactamase was responsible for antagonism. In hydrolysis studies with a beta-lactamase extract, most of the antagonized drugs were either not hydrolyzed or only poorly hydrolyzed. We conclude that imipenem induces significantly elevated levels of beta-lactamase in P. aeruginosa. This increase in beta-lactamase is associated with increased resistance of the organism to many other beta-lactam agents.

The Staph-Ident system (Analytab Products) for species identification of coagulase-negative staphylococci was compared with the conventional method of Kloos and Schleifer (21). A total of 101 clinical isolates from urine cultures and 95 clinical isolates from blood cultures were studied: overall agreement between the two methods was 86%. We concluded that the Staph-Ident system is a practical test for most clinical microbiology laboratories and that results obtained from this rapid test are comparable to those obtained from the more cumbersome conventional method. Additional investigations are needed to determine the clinical relevance of such species identification.

Gram-negative bacilli frequently cause epidemics in high-risk newborn intensive care units. Recently, an epidemic caused by a multiply-resistant K. pneumoniae, serotype 21, occurred in the Vanderbilt University intensive care nursery. The background of this outbreak included an increasing endemic nosocomial sepsis rate, operation of the facility in excess of rated capacity, and increasingly inadequate nurse-to-patient staffing ratios. The epidemic lasted 11 weeks; 26 (12%) of the 232 infants at risk in the unit became colonized. Five infants developed systemic illness and one died. Cohorting, reinforcement of strict handwashing and isolation procedures, and closure of the unit to outborn admissions resulted in rapid termination of the outbreak. Followup studies performed on infants colonized with the epidemic bacterium demonstrated persistent fecal shedding up to 13 months following discharge from the hospital. This epidemic had a detrimental influence on high-risk newborn and obstetric health care delivery in an area encompassing portions of three states. Under a system of progressively more sophisticated referral units, nosocomial infections occurring at a tertiary center can have an impact on other hospitals within the network.

The activities of clindamycin and its derivative, pirlimycin (U-57930E), were compared against 100 strains of Staphylococcus aureus, using a microtiter broth dilution technique. Minimal inhibitory concentrations demonstrated that pirlimycin was comparable to clindamycin but offered no increase in activity against either methicillin-susceptible or methicillin-resistant S. aureus.

In recent months several advisory groups have issued recommendations urging hospitals to undertake comprehensive rubella control programs. The primary impetus for these suggestions has been the recognition that, despite a declining rubella incidence in the general population, pregnant women still are being exposed to this infection in hospitals. In 1979 the Vanderbilt University Hospital initiated a limited rubella control program, encompassing new and current employees working in “traditional” high-risk areas of the hospital: obstetrics (wards and clinics), labor and delivery, nursery, pediatrics (wards and clinics), and the emergency department. Medical and nursing students also were included. All persons were tested serologically and immunization was offered to susceptibles, but was not required (except for students and house officers). The Infection Control Committee and hospital administration readily approved this program.