Primary peritonitis due to group A streptococcus.

Primary peritonitis is a rare condition occurring, by definition, in patients without underlying causes, such as perforated viscus, pre-existing ascites, or nephrosis. We report a case of primary peritonitis and shock due to group A beta-hemolytic streptococcus, a rare etiology. A review of the world's literature shows a predilection for women to have this condition. The entry site is obscure in most cases. Asymptomatic genital tract colonization may be a portal of entry in some women. Shock or toxic shock syndrome often accompany the abdominal findings. Laparotomy to exclude a perforated viscus may be unavoidable. Despite the significant morbidity, expeditious and appropriate antibiotic therapy is curative.

Metabolic acidosis with an elevated anion gap.

Determining the cause of metabolic acidosis with a high anion gap may present a diagnostic challenge. Possible causes include ketoacidosis, certain toxic ingestions, renal failure and lactic acidosis. Many of these entities present with nausea, vomiting and changes in mental status; however, there are specific hallmarks in the signs, symptoms and laboratory findings that help to differentiate among them.

Prosthetic valve endocarditis caused by Staphylococcus epidermidis. Development of rifampin resistance during vancomycin and rifampin therapy.

Development of rifampin-resistant Staphylococcus epidermidis was documented in three patients receiving vancomycin and rifampin therapy for prosthetic valve endocarditis. The minimum inhibitory concentrations and minimum bactericidal concentrations of rifampin for the original three isolates were 0.4 micrograms/mL or less. Organisms cultured during relapse or prosthetic valve replacement had minimum inhibitory concentrations of rifampin that were 12.5, 50, and greater than 100 micrograms/mL, respectively. Surgical intervention was necessary in all patients. One died, and one required a second prosthetic valve placement. The patients were treated with vancomycin plus aminoglycoside following identification of rifampin resistance. These observations suggest that vancomycin and rifampin may not be adequate therapy for prosthetic valve endocarditis caused by S epidermidis.

Endotoxin contamination of enzyme conjugates used in enzyme-linked immunosorbent assays.

The specificity of the enzyme-linked immunosorbent assay(s) is thought to depend on the specificity of the antibody used in the assay system. Therefore, the association of broadly reactive antigens like endotoxin with enzyme conjugates or other enzyme-linked immunosorbent assay reagents has the potential of altering the specificity of reactions in the enzyme-linked immunosorbent assay. Using the Limulus amoebocyte lysate assay, we demonstrated that commercially prepared conjugates of goat anti-human immunoglobulin G peroxidase, goat anti-rabbit immunoglobulin G alkaline phosphatase, rabbit anti-human immunoglobulin G, and other enzyme conjugates contained endotoxin. Furthermore, the staphylococcal protein A, horseradish peroxidase, and bovine alkaline phosphatase used to prepare enzyme conjugates also contained endotoxin. Commercially obtained bovine alkaline phosphatase contained as much as 1.0 microgram of endotoxin per ml of enzyme solution. Both commercially prepared enzyme conjugates and those prepared by us contained endotoxin as determined by their absorption to immobilized monoclonal antibody to lipid A or to immobilized Limulus amoebocyte lysate. The results of this study further suggest that the endotoxin was associated with the enzyme component of the conjugate. In a competitive inhibition enzyme immunoassay, 10 micrograms of lipid A per ml inhibited binding of the enzyme conjugate to adsorbed Limulus amoebocyte lysate, thereby confirming that endotoxin mediated the binding of the conjugate in that system. The potential significance of endotoxin bound to enzyme conjugates may be far reaching because of the ubiquity of endotoxin in conjugates and the prevalence of antibodies to endotoxin in mammalian serum.

Campylobacter jejuni-associated hemolytic-uremic syndrome in a mother and daughter.

A mother and daughter with Campylobacter jejuni-associated hemolytic-uremic syndrome (HUS) are discussed. The mother was hospitalized with bloody diarrhea and HUS; C jejuni was isolated from her stool. The 2-year-old daughter had been admitted five days prior to her mother with HUS following a three-day prodrome of vomiting and diarrhea. Multiple stool cultures were negative for enteric pathogens; however, cultures were not obtained until the eighth hospital day and after antibiotic therapy. Extensive investigation failed to identify another cause for the diarrheal illness or HUS in our patients. Indirect immunofluorescent antibody titers for C jejuni were 1:32 and 1:16 for the mother and daughter, respectively. An asymptomatic 9-month-old son had C jejuni isolated from his stool and had an immunofluorescent antibody titer of 1:64. Three other family members were asymptomatic, stool-culture negative, and had immunofluorescent antibody titers less than or equal to 1:4. The susceptibility to develop HUS following an enteric antigenic stimulus is illustrated by the patients presented. The need for systematic investigation of all HUS cases for potential susceptibility markers, as well as an exhaustive etiologic search, is emphasized.