Several antibiotics have disulfiram-like effects; we evaluated disulfiram for its antibiotic-like effects. Disulfiram inhibited the in vitro growth of methicillin-resistant Staphylococcus aureus, with an MIC of 1.33 ,ig/ml, but was not effective against members of the family Enterobacteriaceae or Pseudomonas species.The medical management of chronic alcohol abuse frequently includes treatment with disulfiram (DSF) as an aid to maintaining long-term sobriety. A patient who consumes an alcoholic beverage during treatment with DSF will promptly experience the subjectively unpleasant disulfiram-ethanol reaction, which includes palpitations, malaise, flushing, nausea, and vomiting. The molecular basis of this interaction has been ascribed to the noncompetitive inhibition of aldehyde dehydrogenase by DSF, so that the ingestion of ethanol is followed by the accumulation of its first metabolite, acetaldehyde, in toxic quantities (8,10,13,16). However, the disulfiram-ethanol reaction might also be mediated by other enzymes, including dopamine P-hydroxylase (19) and alcohol dehydrogenase (2), which are also inhibited by DSF.It is now well known that patients treated with a number of antimicrobial agents are also at risk for a clinically similar reaction should they consume any alcohol. Disulfiram-like interactions with ethanol have been observed during treatments with cephalosporins, metronidazole, quinacrine, chloramphenicol, and moxalactam (6,12,25).While it is apparent that these antibiotics can simulate the clinical effects of DSF, there is now evidence to suggest that the converse might also be true, i.e., that DSF may in some cases act as an antibiotic. Scheibel et al. (24) found that DSF inhibited the growth of the human malaria parasite Plasmodium falciparum in vitro. The major breakdown product of DSF in vivo is diethyldithiocarbamate (7) (DDC), which has activity against Pityrosporum canis and inhibits the growth of ear mites (Otodectes cynotis) in cats and dogs (17). DDC may also act as an immunomodulator and viricide and may clinically benefit patients suffering from infection with human immunodeficiency virus (14,23 were included in each test run.Preparation of bacterial cultures. Organisms were obtained from stock cultures maintained on cystine-tryptic agar by the Clinical Microbiology Laboratory of St. Vincent's Medical Center of Richmond. S. aureus isolates were identified by colonial morphology, catalase production, and latex particle agglutination (Staphaurex; Wellcome Diagnostics, Research Triangle Park, N.C.). A microtiter identification system was used to identify members of the family Enterobacteriaceae and Pseudomonas species to the species level and to determine antibiotic susceptibility (MicroScan; Baxter Healthcare Corp., West Sacramento, Calif.). Each organism was subcultured from cystine-tryptic agar onto tryptic soy agar containing 5% sheep blood and incubated aerobically at 35°C for 18 h. MRSA was defined as an organism for which the oxacillin MIC was greater than or equal to 4.0 mg/ml and...

Pentoxifylline, which inhibits tumor necrosis factor-alpha (TNF alpha), decreases human immunodeficiency virus replication in peripheral blood mononuclear cells. However, TNF alpha is important in cellular defense against M. avium-intracellulare complex (MAC), a common infection in advanced AIDS. The effect of pentoxifylline on mycobacterial colony counts in macrophages with in vivo MAC infection was evaluated, and differences in lipopolysaccharide (LPS)-induced TNF release in infected and uninfected macrophages were determined. Macrophages with in vivo MAC infection released much less TNF alpha in response to LPS (P = .01). The response was partially restored after antimycobacterial therapy. Pentoxifylline, in a concentration that inhibited LPS-induced TNF alpha by 52.4%, increased MAC counts by 2.5- to 50.0-fold. Thus, macrophages from AIDS patients with disseminated MAC infection are deficient in their ability to release TNF alpha, and further inhibition by pentoxifylline may be detrimental.

The usual presentations and manifestations of systemic lupus erythematosus (SLE) are well known. We describe a patient with SLE that was discovered in the course of evaluation of an abscess, found to be associated with non-0:1 Vibrio cholerue.Systemic lupus erythematosus (SLE) is a common rheumatic disease which has a variety of presentations and manifestations, including the welldescribed malar ''butterfly rash," arthritis, nephritis, serositis, and alopecia. This is the first reported case of SLE presenting as a subcutaneous abscess secondary to non-0: 1 Vibrio cholerue. CASE REPORTThe patient, a 29-year-old woman from the Dominican Republic, presented to the emergency department of a New York City hospital with fever, left hip pain, and pleuritic left chest pain. The medical history was significant for anemia, for which she claimed to be receiving treatment, consisting of "vitamin injections" in the left hip, in the Dominican Republic. The needles and syringes were not disposable and were "cleaned with sea water." On physical examination the patient appeared to be in a toxic condition. The vital signs were as follows: oral temperature 103"F, pulse 101 beatdminute, blood pressure 90/60 mm Hg. There was alopecia, a malar rash, and a maculopapular rash over the torso and extremities. A mild synovitis was present in the left wrist. The left buttock had a 20-cm area of induration, which was Submitted for publication December 1, 1993; accepted in revised form May 11, 1994. firm, red, warm, and tender. The chest radiograph demonstrated a small left pleural effusion. The white blood cell count was 25,300/mm3 with a left shift. The hemoglobin level was 6.4 gm/dl, hematocrit 18.6 gm/ dl, mean corpuscular volume 85.1 pm3, mean cell hemoglobin 29.2 pg/cell. The patient was admitted to the hospital for cellulitis, and empiric treatment with intravenous nafcillin (500 mg every 6 hours) was begun.A left gluteal abscess developed, which drained spontaneously 5 days after admission. The Gram stain demonstrated gram-negative bacilli, which also grew from cultures of blood obtained prior to the initiation of antibiotic treatment. The organism was thought to be V cholerue and was sent to the Public Health Department for serotyping. The antibiotic regimen was changed to intravenous ampicillin (1 gm every 6 hours) and gentamicin (80 mg every 8 hours), and the leukocytosis, cellulitis, and abscess resolved within 10 days.Laboratory evaluation revealed the following: antinuclear antibody (ANA) titer 1 :320 (speckled pattern), anti-RNP antibody titer 1 :512, negative rheumatoid factor, negative anti-Sm antibody, erythrocyte sedimentation rate (ESR) 142 m d h o u r (normal 0-20), C3 51.9 mg/dl (normal 85-193), C4 8.7 mg/dl (normal 12-36 mg/dl), rapid plasma reagin negative. A diagnosis of hemolytic anemia was established based on a reticulocyte index of 3.9%, haptoglobin level of 243 mg/dl (normal 13-163), and Coombs' antibody positivity. The serum creatine level was 4.1 mg/dl, and urinalysis demonstrated persistent proteinuria (>3...

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