A large outbreak of infections caused by methicillin and aminoglycoside resistant Staphylococcus aureus provided the opportunity to evaluate mechanisms of resistance and compare the usefulness of typing systems. Between January 1979 and December 1980, 63 patients developed infections with S aureus resistant to multiple antibiotics, including methicillin and tobramycin. All isolates had an identical antibiogram and were phage type 47/54/75/77/83A. Beginning in January 1981, a superimposed outbreak caused by S aureus of the same phage type but with a resistance pattern now including gentamicin occurred. The two strains contained different aminoglycoside inactivating enzymes. The initial strain contained a single plasmid of 21.5 mDa molecular weight, whereas the subsequent strain which had acquired gentamicin resistance contained this plasmid plus a heavier one of 33 mDa. Plasmid analysis complements the analysis of antibiograms and phage types and aids in defining epidemiologic patterns of transmission.

We identified 29 episodes of suppurative thrombophlebitis in 27 patients admitted to a large general hospital between May 1980 and May 1984. In 25 patients, the intravenous cannulae had been in place for more than 3 days. Streptococcus faecalis, Pseudomonas aeruginosa or one of the Enterobacteriaceae were implicated in 14 patients. All these patients had recently undergone abdominal surgery or had a major intraabdominal inflammatory process at the time they developed thrombophlebitis. The remaining 13 patients were infected with Staphylococcus aureus, other grampositive cocci or Candida species. Only two of these had an active abdominal process at the time of their infection (x2 = 16.08, P<0.001). There is an apparent association between phlebitis caused by enteric organisms and active intra-abdominal pathology. There were two deaths related to delayed or deferred surgery. Suppurative thrombophlebitis is a lethal, preventable nosocomial infection that requires urgent surgical intervention.

One hundred twelve patients with hematologic malignancies underwent marrow transplantation from HLA-matched sibling donors and were randomized to receive either prophylactic granulocyte transfusions (PG, 67 patients) or prophylactic systemic antibiotics (PSA, 45 patients) as prophylaxis against nosocomial infections. Patients were treated in conventional hospital rooms and studied until day 100 post-transplant. For the entire study period, 26 patients (39%) in the PG group developed septicemia compared to 15 patients (33%) in the PSA group. Twenty-eight patients (42%) in the PG group developed local major infections compared to 19 patients (42%) in the PSA group. Ten patients (15%) in the PG group developed viral interstitial pneumonitis compared to 6 patients (13%) in the PSA group. None of these differences were statistically significant. There was no difference in the incidence of bacterial or fungal infections or viral interstitial pneumonitis between the two groups during the granulocytopenic or post-engraftment period. There was no difference in the incidence and severity of graft-versus-host-disease (GVHD). Inability to carry out the prophylaxis was frequent in the PG group, with complications necessitating discontinuance of transfusion in 24% of the recipients and 13% of the donors. The use of PG as an infection prophylaxis modality in marrow transplantation is not supported by this study, as it is difficult to carry out and because PG did not show any advantage over the use of PSA in preventing nosocomial infections.

Seven nurses working in a newborn unit were infested by Microsporum canis, involving the skin of the left forearm. One infant who was treated in the same unit suffered from a similar lesion on the occipital region. Transmission during bottle feeding was suspected. After the introduction of long sleeves for all nurses, no further cases occurred. Data collected on the nurses in the unit suggested that infection correlated with direct exposure to infants.

This retrospective cohort study reviews the incidence of bacteremia in 48 patients undergoing hemodialysis using subclavian vein dialysis catheters (SDC) as temporary vascular access. Twelve (25%) of these patients had catheter-related bacteremia, and the most frequently isolated organisms were coagulase-negative staphylococci. Three patients developed right-sided endocarditis and one of diem died due to pulmonary embolism. The presence of possible risk factors for SDC-related bacteremia, including duration of catheterization and number of hemodialysis procedures, were not statistically different when patients with and without bacteremia were compared, with the exception of a significantly lower incidence of bacteremia among those patients receiving antibiotic therapy at the time of catheter insertion. The use of resterilized catheters was not a risk factor. Specific guidelines for SDC insertion and care were established and followed, after which the infection frequency was reduced to 7.5% (1 episode per 45.5 patient-weeks of catheter use) in this high-risk population

In 1899, Thiercilin used the term “enterococcus” to describe microscopic organisms seen in pairs or short chains in feces. Later (in the 1930s) the name was used in a more restrictive sense for streptococci that had the hardy capacity to survive under extreme conditions.

Enterococci belong to a group D family of streptococci, as characterized by Lancefield in 1938. In contrast to other groups of streptococci, the group D antigen is not a wall carbohydrate but a glycerol teichoic acid containing glucose and D-alanine. This antigen appears to be related directly to the cytoplasm or plasma membrane.

In the past 15 years, our knowledge of the pathogenesis and etiologic agents of diarrheal disease has expanded rapidly. No longer is it scientifically appropriate or cost effective for the laboratory simply to culture a stool for Salmonella and Shigella and to do a wet mount for amebae. Today we have a plethora of agents including, but not limited to, Campylobacter, Yersinia, Clostridium difficile, Escherichia coli, Aeromonas, Plesiomonas, vibrios, rotavirus, Norwalk agent, Giardia, and Cryptosporidium, which have all been suggested to be agents of diarrheal disease. Given such a wide range of possibilities, what approaches should be taken to determine the etiologic agent of diarrheal disease in the hospitalized patient in an era of cost containment?