Clinical, laboratory, and pathologic findings in nine of the 12 patients who died from toxic shock syndrome in Minnesota are reported. All patients met the toxic shock syndrome case definition except for desquamation, which occurred in only one patient. Eight were menstruating and at least four were wearing tampons at the time of the acute illness. One patient was using napkins only. Noncardiogenic pulmonary edema was the only clinical development that could be used to predict a fatal outcome. Specific pathologic findings included various degrees of fatty metamorphosis of the liver; pronounced hemophagocytosis by reticuloendothelial macrophages; and a characteristic vaginal lesion consisting of mucosal separation beneath the basal layer with ulceration, severe vasodilatation, inflammation and thrombosis, but with minimal bacterial invasion. This vaginal lesion was noted in two tampon users, but an identical lesion was found in a menstruating patient who used only napkins.

Previous investigators have suggested that opsonization of two Bacteroides species is mediated exclusively by the alternative complement pathway and requires immunoglobulins. In this study, the nature of the opsonic factors in nonimmune human serum for four species of Bacteroides was investigated by measuring uptake of [3H]thymidine-labeled bacteria by human polymorphonuclear leukocytes. Normal human serum, C2-deficient serum, immunoglobulindeficient serum, and serum chelated with ethylene glycol-bis(,f-aminoethyl ether)-N,N-tetraacetic acid (EGTA), MgEGTA, and ethylenediaminetetraacetic acid (EDTA) were used as opsonic sources. Heat inactivation of each of these sera significantly reduced its opsonic activity for all four Bacteroides species, suggesting that serum complement was essential for effective opsonization. All strains were opsonized in the absence of the classical complement pathway; however, kinetics studies revealed that opsonization proceeded at a significantly faster rate when the classical complement pathway was intact. Although two strains were opsonized in immunoglobulin-deficient sera, opsonization was less efficient and appeared to occur via the alternative complement pathway. Unexpectedly, all strains were well opsonized by the classical complement pathway in 10% serum which had been effectively chelated with EGTA or EDTA. The explanation for this finding is unknown; however, it is possible that cell wall cations of Bacteroides species may participate in the activation of complement in chelated serum, resulting in effective opsonization. It was also found that Bacteroides, when incubated with an Escherichia coli strain in normal serum, could compete for opsonins and thereby reduce phagocytosis ofE. coli. It is possible that competition for opsonins among bacterial species contributes to the synergistic role these organisms share in mixed floral infections. An effective osponic source including complement or immunoglobulin is required to prepare bacteria for maximal phagocytosis by polymorphonuclear leukocytes (PMNL). Anderson et al.(1) have shown that encapsulated strains of Haemophilus influenzae are opsonized in immune serum by the classical complement pathway, whereas Quinn and co-workers (26) found that these same strains were opsonized by the alternative complement pathway in nonimmune serum. Other investigators (31, 34) have shown that several bacterial species can be opsonized by the complement system in the relative absence of immunoglobulin. In contrast to unencapsulated organisms, encapsulated bacteria appear to require specific antibodies for optimal opsonization (3, 24).Casciato et al. (4) were the first to study opsonization and phagocytosis of Bacteroides species. They demonstrated that B. thetaiotaomicron could be opsonized only by heat-la-bile serum opsonic factors and that phagocytosis by PMNL occurred equally well under anaerobic and aerobic conditions. Recently, Bjornson and Bjornson (2) studied two species of Bacteroides and concluded that optimal opsonization required bot...

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The susceptibilities of 347 urine isolates of enterococci (Streptococcus faecalis, 44%; S. faecalis subsp. zymogenes, 37%; S. faecalis subsp. liquefaciens, 19%) to ampicillin, azlocillin, mezlocillin, piperacillin, vancomycin, gentamicin, erythromycin, rosaramicin, rifampin, rifampin plus trimethoprim (1:4), trimethoprim-sulfamethoxazole (1:20), and chloramphenicol were determined by the agar dilution technique. There were no significant differences in susceptibility to individual agents among the subspecies of S. faecalis. Azlocillin and mezlocillin (MIC for 90% of isolates, 0.78 micrograms/ml) and piperacillin, ampicillin, and vancomycin (MIC for 90% of isolates, 1.56 micrograms/ml) were the most active agents and were significantly more potent than the other reference antibiotics tested.

We studied 28 women and two men, with a median age of 20 years, who first had toxic shock syndrome between 1 February 1980 and 15 July 1981. Two of these patients died. All patients had intense myalgia, high fever (greater than or equal to 38.9 degrees C), hypotension or syncope, skin rash and desquamation, and abnormalities in at least three organ systems. Over half had sterile pyuria; immature granulocytic leukocytosis; coagulation abnormalities; hypocalcemia; low serum albumin and total protein concentrations; and elevations of blood urea nitrogen, alanine transaminase, bilirubin, and creatine kinase. Staphylococcus aureus was isolated from cultures from sites of soft-tissue infection in both male patients and from 13 of 19 vaginal and eight of 12 cervical cultures. All isolates produced both pyrogenic exotoxin C and enterotoxin F. All patients with a febrile, exanthematous, multisystem illness, particularly one associated with menstruation or a staphylococcal infection, should be promptly evaluated and empirically treated for toxic shock syndrome.

Toxic shock syndrome is a recently recognized illness with serious morbidity and mortality that occurs primarily in healthy menstruating women who use tampons. Thirteen women and two men were evaluated; two of the women died in spite of seemingly appropriate therapy. All patients had a temperature of 38.9 degrees C or greater, hypotension of syncope, a skin rash with subsequent desquamation, mucous membrane inflammation, and laboratory evidence of multiple organ dysfunction. Staphylococcus aureus was isolated from the cervix or vagina in eight women and from soft-tissue infections in both men. Two patients were bacteremic. The significant heterogeneity in the clinical manifestations, laboratory abnormalities, and therapeutic requirements among patients may result in diagnostic confusion and inappropriate therapy. Although toxic shock syndrome appears to be associated with tampon usage and S. aureus, the pathogenesis remains unknown.

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We evaluated the efficacy and toxicity of moxalactam during treatment of 45 documented infections in 36 patients. A majority of patients received 4.5 g of moxalactam per day. There was a good clinical response in 42 of the 45 (94%) infections, including 3 bacteremias, 20 skin and soft tissue infections, 6 gramnegative lower respiratory tract infections, 6 purulent diabetic foot ulcers, 3 wound infections, 3 urinary tract infections, and 4 miscellaneous infections (meningitis, suppurative phlebitis, peritonitis, bursitis). Previously, 11 of these patients had failed to respond to other antibiotics. Our three treatment failures were attributed to abnormal host defense in two patients and to a resistant enterococcal urinary tract infection in another. Moxalactam was tolerated well and produced minimal renal, hepatic, and hematological toxicities. The only serious adverse effects were the development of documented pseudomembranous colitis in one patient and progressive renal dysfunction in another. Acquisition of resistance among noneradicated isolates during therapy was not demonstrated.Moxalactam is a new 1-oxa-f3-lactam antibiotic which has a broad spectrum of in vitro activity against aerobic gram-positive cocci and aerobic and anaerobic gram-negative bacilli, including multiply antibiotic-resistant isolates (2, 4, 7). A majority of the Enterobacteriaceae and streptococci are inhibited at a concentration of <1 jLg/ml, staphylococci are inhibited at 4 to 8 jig/ml, and Pseudomonas aeruginosa is inhibited at 16 jig/ml; these are levels which can be achieved easily after 1-g intravenous infusions (8). In