Autopsy risk and acquisition of human immunodeficiency virus infection: a case report and reappraisal.

Autopsy findings have contributed greatly to our understanding of acquired immunodeficiency syndrome. To our knowledge, documented autopsy-acquired infection with human immunodeficiency virus type 1 has not been reported, suggesting autopsy performance is of limited risk. We present a well-documented case of autopsy-acquired human immunodeficiency virus infection in a pathologist who sustained a scalpel wound to the hand.

A multicenter comparative study of the in vitro activity of fleroxacin and other antimicrobial agents.

The in vitro activity of fleroxacin was determined by broth microdilution against 2,079 recent bacterial isolates and compared to the activities of ciprofloxacin, ofloxacin, lomefloxacin, cefaclor, cefuroxime, cefixime, ceftriaxone, amoxicillin/clavulanate, trimethoprim/sulfamethoxazole (TMP-SMX), and, as appropriate, erythromycin and oxacillin. Most Enterobacteriaceae were inhibited by the quinolones at a concentration of < or = 1 microgram/ml; MIC90s of fleroxacin, ciprofloxacin, ofloxacin, and lomefloxacin were 0.25, 0.5, 1 and 1 micrograms/ml, respectively. Fleroxacin was 2-fold more active than ciprofloxacin against Providencia stuartii and Serratia marcescens. Aside from the quinolones, ceftriaxone and TMP-SMX were the most active antibiotics against the Enterobacteriaceae, with MIC90s of 8 and 16 micrograms/ml, respectively. Ciprofloxacin was more active against Pseudomonas aeruginosa than the other quinolones, while fleroxacin was more active against Stenotrophomonas maltophilia: 17.7, 11.2, 20.0, and 22.4% of P. aeruginosa were resistant to fleroxacin, ciprofloxacin, ofloxacin, and lomefloxacin, respectively. Moraxella catarrhalis and Haemophilus influenzae were uniformally susceptible to all antibiotics tested, as were the majority of oxacillin-susceptible staphylococci. The MIC90s of the quinolones and of the beta-lactam antibiotics for oxacillin-resistant staphylococci were 8- to 256-fold higher than for oxacillin-susceptible staphylococci. The beta-lactam antibiotics, TMP-SMX, and erythromycin were more active than the quinolones against streptococci; all antibiotics were poorly active against enterococci. Fleroxacin is active against a broad range of gram-negative bacilli and against oxacillin-susceptible staphylococci and should prove useful for such infections. However, its use cannot be recommended for infections due to oxacillin-resistant staphylococci, streptococci, or enterococci.

Evaluating contrast-enhancing brain lesions in patients with AIDS by using positron emission tomography.

OBJECTIVE: To determine whether a noninvasive method for evaluating contrast-enhancing brain lesions in patients with the acquired immunodeficiency syndrome (AIDS) can accurately differentiate between lymphoma and nonlymphoma diagnoses. This method is based on Toxoplasma serologic testing and positron emission tomography. DESIGN: Prospective, nonrandomized, criterion-standard clinical study. SETTING: An academic center in the mid-southeastern United States. PATIENTS: 20 patients with AIDS and contrast-enhancing brain lesions. INTERVENTIONS: Positron emission tomographic scanning and Toxoplasma serologic testing. MAIN OUTCOME MEASURE: Diagnoses were confirmed by clinical response, autopsy, or brain biopsy. RESULTS: Eight patients had a confirmed diagnosis of toxoplasmosis, six had lymphoma, four had other diagnoses, and two were not evaluable. Seven of eight patients with toxoplasmosis had positron emission tomographic scans; all of these scans showed hypometabolic lesions consistent with a nonlymphoma diagnosis. The six patients with lymphoma all had hypermetabolic lesions on positron emission tomographic scans. The difference between these two sets of results was statistically significant (P < 0.001, Fisher exact test, two-tailed). The anti-Toxoplasma titer was greater than or equal to 1:4 in all patients with confirmed toxoplasmosis who had serologic testing and in three of six patients with lymphoma. CONCLUSIONS: Evaluating contrast-enhancing brain lesions in patients with AIDS by using Toxoplasma serologic testing and positron emission tomography can accurately guide therapy and obviate the need for most brain biopsies in these patients. A larger, national, multicenter study is needed to confirm our findings and to determine the effect of earlier diagnosis and treatment on morbidity and mortality in patients with AIDS and primary central nervous system lymphoma.

Osteomyelitis of the pubic symphysis in athletes: a case report and literature review.

Groin pain is a common problem in athletes. Osteitis pubis, a chronic inflammatory condition involving the pubic symphysis, is a rare cause, and pyogenic osteomyelitis of the pubis is seen even more rarely in healthy athletes. We report one of four cases of pyogenic osteomyelitis of the pubis seen at our institution, review our experience with all four cases, and present a review of the literature (7 cases). The diagnosis is established by the presence of extreme pain, point tenderness at the pubic symphysis, fever, and either a positive culture of blood, needle aspiration, or open biopsy of the pubis. White blood cell count, erythrocyte sedimentation rate, and the results of bone scan and computerized tomography may initially be normal and therefore cannot exclude the diagnosis. Prompt treatment with intravenous (i.v.) antibiotics effective against Staphylococcus aureus (causative organism in all documented cases-9/11) should initially be administered and then guided by culture and sensitivity information. Oral antibiotics should be given if the infection is responsive to i.v. antibiotic treatment. Prompt recognition and treatment with antibiotics may obviate the need for surgical debridement. All athletes who returned to sports activity did so by 6 months after diagnosis.

Reconstitution of the trypanolytic factor from components of a subspecies of human high-density lipoproteins.

Trypanosoma brucei brucei is non-infectious to man due to the sensitivity of these parasites to the lytic activity of normal human serum. Apolipoproteins (apo) have been purified, under non-denaturing conditions, from the subclass of human high-density lipoprotein (HDL), termed trypanosome lytic factor (TLF), which is responsible for the cytotoxicity of human serum to T. b. brucei. The TLF apolipoproteins were purified by anion exchange chromatography in the presence of the nonionic detergent octylglucoside and a reconstitution method was developed which allowed the role of the individual apolipoproteins and different lipids to be assessed. The results suggest that the TLF lipids do not have a direct role in lysis but are necessary for the correct assembly of the lytic HDL particle. Apo A-I, apo L-III and apo L-I contribute to lysis in reconstituted particles but individually they are not cytotoxic. Apo A-II was not required in the reconstituted TLF particle for trypanosome lysis. Formation of a lytic HDL particle required apo L-III suggesting its potential role as a toxin. Thermal inactivation of TLF activity correlated with the amount of denatured apo L-I, indicating that apo L-I was involved in lysis of T. b. brucei by native TLF.

Endocytosis of a cytotoxic human high density lipoprotein results in disruption of acidic intracellular vesicles and subsequent killing of African trypanosomes.

The host range of Trypanosoma brucei brucei is restricted by the cytolytic effects of human serum high-density lipoprotein (HDL). The lytic activity is caused by a minor subclass of human serum HDL called trypanosome lytic factor (TLF). TLF binds in the flagellar pocket to specific TLF-binding sites. Internalization and localization of TLF to a population of endocytic vesicles, and ultimately large lysosome-like vesicles, precedes lysis of T. b. brucei. The membranes of these large vesicles are disrupted by the accumulation of TLF particles. Inhibitor studies with lysosomotropic amines have shown these large vesicles to be acidic in nature and that prevention of their rupture spares the cells from TLF-mediated lysis. Furthermore, leupeptin inhibition suggests that a thioprotease may be involved in the mechanism of TLF-mediated lysis of T. b. brucei. Based on these results, we propose a lytic mechanism involving cell surface binding, endocytosis and lysosomal targeting. This is followed by lysosomal disruption and subsequent autodigestion of the cell.

Role of nucleotide pyrophosphatase in enflurane-induced reduction of UDP-glucuronic acid concentration in mouse liver.

Because hepatic UDP-glucuronic acid levels decrease upon exposure to volatile anesthetics, the present study was designed to determine the mechanism by which enflurane decreases UDP-glucuronic acid in mice by measuring the concentrations of intermediates and the activities of enzymes in the UDP-glucuronic acid pathway. UDP-glucuronic acid concentrations were decreased by 40% in both male and female mice after 10 min of enflurane-induced narcosis. Concentration of UDP-glucose and the activities of diethylstilbestrol UDP-glucuronosyltransferase and UDP-glucose dehydrogenase were not affected by enflurane treatment. In contrast, nucleotide pyrophophatase activity was increased approximately 50% in both sexes. Thus, the decrease in hepatic UDP-glucuronic acid upon exposure of mice to enflurane is probably due to increased degradation by nucleotide pyrophosphatase.

Q fever endocarditis.

Q fever endocarditis, which is seen most often in Great Britain and Australia, has been rarely observed in the United States. A patient with an eight month febrile illness who had signs and symptoms of endocarditis and serologic studies diagnostic of Q fever endocarditis is reported. A history of extensive travel makes it unclear where he originally contracted the disease. Q fever endocarditis is probably underdiagnosed and should be looked for in any case of culture negative endocarditis or chronic fever of unknown origin.

Cefotaxime aminoglycoside interactions.

Minimum inhibitory concentrations and minimum bactericidal concentrations were determined for cefotaxime, gentamicin, tobramycin and amikacin and for the combination of cefotaxime and each of the aminoglycosides in vitro against 200 strains of Enterobacteriaceae. 91% were susceptible to cefotaxime, 93.5% were susceptible to gentamicin, 89.5% were susceptible to amikacin and 68% were susceptible to tobramycin. There were 95 strains which could be evaluated for synergistic killing by the antimicrobial combinations. Synergism was shown against 78% of strains by cefotaxime and amikacin, against 71% by cefotaxime and tobramycin and against 64% by cefotaxime and gentamicin. In 19 of 22 instances where a bacterial strain was resistant to both cefotaxime and the aminoglycoside, synergistic killing with clinically achievable levels of both antimicrobial agents was demonstrated. There was no significant decrease in concentration of any of the three aminoglycosides after incubation with cefotaxime at 37 degrees C for 0, 4 or 24 h.