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Biomedical subjects

J J Rahal

Publications and source records attributed to J J Rahal.

At least 37 records · Page 2Linked to original sources
PubMed1994

Clinical and molecular epidemiology of acinetobacter infections sensitive only to polymyxin B and sulbactam.

A nosocomial outbreak of infections due to imipenem-resistant Acinetobacter baumannii occurred in a New York hospital after increased use of imipenem for cephalosporin-resistant klebsiella infections. We identified all A baumannii isolates over 12 months, reviewed corresponding patient records, and compared strains with different antibiotic susceptibility patterns by restriction endonuclease analysis. Environmental surveillance cultures were done before and after institution of control measures. 59 patients harboured imipenem-resistant A baumannii, and 18 were infected. Isolates from patients were resistant to all routinely tested antibiotics, including imipenem. Further studies showed susceptibility to polymyxin B and sulbactam. These isolates were identical by restriction endonuclease analysis to A baumannii isolates susceptible to imipenem alone, or to imipenem and amikacin, but differed from broadly susceptible isolates. Surveillance cultures showed hand and environmental colonisation by imipenem-resistant strains. Infection and colonisation were eliminated by intensive infection control measures, and irrigation of wounds with polymyxin B. Increased use of imipenem against cephalosporin-resistant klebsiella may lead to imipenem resistance among other species, particularly acinetobacter. Such resistance appears to derive from a prior multi-resistant clone, in contrast to one which retains susceptibility to several antibiotics.

Acinetobacter↗
PubMed1994

Identification of TEM-26 beta-lactamase responsible for a major outbreak of ceftazidime-resistant Klebsiella pneumoniae.

An epidemic of nosocomial ceftazidime-resistant Klebsiella pneumoniae was correlated with production of a ceftazidime-hydrolyzing enzyme with an isoelectric point of 5.6 (BMH-1). BMH-1 was encoded on a large transferable plasmid conferring multiple antibiotic resistance. The gene that encodes BMH-1 was identical to the gene that encodes the TEM-26 extended-spectrum beta-lactamase.

Base Sequence↗
PubMed1994

Mycobacterium-avium complex.

The ubiquitous MAC causes disseminated disease in a large proportion of patients with AIDS. It will become an increasingly important clinical pathogen as more patients survive within the context of prolonged immunodeficiency. The primary risk factor for DMAC is CD4 < 100 mm3 and thus the institution of adequate prophylaxis will significantly reduce its presentation in advanced HIV infection. For those patients presenting with DMAC, therapy with a multiple drug regimen including a macrolide is indicated. Because of potential toxicities and interactions in these debilitated patients, however, the ideal approach is to employ a minimum number of drugs with maximal clinical activity.

AIDS-Related Opportunistic Infections↗
PubMed1993

Nosocomial outbreak of Klebsiella infection resistant to late-generation cephalosporins.

OBJECTIVE: To describe the epidemiology, antimicrobial susceptibility, and control of widespread ceftazidime-resistant Klebsiella pneumoniae infections in a North American hospital and circumstances that led to delayed detection. DESIGN: A 2-year epidemiologic, microbiologic, and clinical cohort study. SETTING: A 487-bed general hospital in New York City. PATIENTS AND CLINICAL ISOLATES: Patient records were reviewed retrospectively and prospectively. Isolates were obtained from the Clinical Microbiology Laboratory. RESULTS: Four hundred thirty-two isolates of ceftazidime-resistant Klebsiella pneumoniae were recovered during a 19-month study period. The peak incidence reached 17.3% of all Klebsiella isolates. One hundred fifty-five patients were colonized or infected, representing more than 70 per 1000 average daily census. Infections occurred in 39% of patients from whom ceftazidime-resistant Klebsiella was isolated. These included 14 bacteremias and 17 pulmonary infections among 52 infected patients. The outbreak coincided with increasing use of ceftazidime therapy for multiresistant Acinetobacter infections. Reduction in ceftazidime use and barrier precautions markedly reduced the incidence of colonization and infection. Ceftriaxone, ceftizoxime, cefotaxime, and cephamycins were inhibitory, but not bactericidal, against ceftazidime-resistant Klebsiella and appeared effective by routine disc diffusion tests. In contrast, imipenem provided consistent bactericidal activity. Preliminary studies indicated that the outbreak was caused by one or more plasmid-mediated beta lactamases. CONCLUSIONS: Nosocomial ceftazidime-resistant Klebsiella pneumoniae may be resistant to the bactericidal activity of all cephalosporins and cephamycins. Such isolates appear susceptible to cephalosporins other than ceftazidime by routine disc diffusion testing. Ineffective therapy, delayed detection of resistance, and epidemic spread are potential consequences. Imipenem provides consistent bactericidal activity. Ceftazidime restriction and barrier precautions for colonized and infected patients are effective control measures.

Aged↗
PubMed1993

Effect of sulbactam on infections caused by imipenem-resistant Acinetobacter calcoaceticus biotype anitratus.

A recent outbreak of multiresistant strains of Acinetobacter calcoaceticus biotype anitratus was observed mostly, but not exclusively, in the surgical intensive care unit in our hospital. Disk diffusion and microdilution susceptibility studies demonstrated resistance to imipenem, all aminoglycosides, and all individual beta-lactam antibiotics. Only ampicillin plus sulbactam, cefoperazone plus sulbactam, and polymyxin produced zone sizes and MICs in the susceptible ranges. Determination of MICs and MBCs demonstrated that sulbactam was the antimicrobial agent responsible for the killing of these organisms. Nine of 10 patients who were infected with imipenem-resistant Acinetobacter strains and received ampicillin plus sulbactam for > 3 days improved clinically, and in many cases organisms were eradicated from the site of isolation.

Acinetobacter Infections↗
PubMed1991

Effect of a beta-lactamase inhibitor, tazobactam, on growth and penicillin-binding proteins of Borrelia burgdorferi.

The effects of tazobactam, a relatively new beta-lactamase inhibitor, were investigated on growth and penicillin-binding proteins (PBPs) of Borrellia burgdorferi. A previous communication from our group demonstrated several proteins capable of binding labelled penicillin in this organism. Of these proteins, 94-kDa and 57-kDa PBPs possessed the highest affinity for penicillin and were assumed to be essential proteins involved in cell-wall synthesis. In these experiments, tazobactam was used in competition binding experiments as well as on whole spirochetes. Only the 94-kDa and 57-kDa PBPs were affected by increasing amounts of tazobactam during competition-binding experiments and growth of B. burgdorferi was also inhibited. These results may explain the in vitro activity of beta-lactamase inhibitors in general and suggest a utility for these compounds when examining PBPs with hydrolysing activity and/or organisms with beta-lactamases.

Bacterial Proteins↗
PubMed1991

Role of candida in pathogenesis of antibiotic-associated diarrhoea in elderly inpatients.

The part that candida plays in antibiotic-associated diarrhoea was investigated in 24 elderly inpatients (mean age 74 years) who tested negative for Clostridium difficile toxin and other intestinal pathogens. 7 had intestinal overgrowth of Candida species (greater than or equal to 10(5) cfu/ml). None of the 24 matched, antibiotic-treated controls without diarrhoea had candida overgrowth. All 5 patients with diarrhoea and candida overgrowth treated with oral nystatin responded with resolution of diarrhoea and lowering of faecal counts to less than 10(4) cfu/ml within 7 days of start of antifungal therapy despite continuation of antibacterial therapy. In the other 2 patients with candida overgrowth, the diarrhoea subsided spontaneously and faecal candida counts returned to normal (less than 10(4) cfu/ml) after antibacterial agents were withdrawn. In patients without candida overgrowth, diarrhoea persisted until antibiotics were withdrawn, at a mean of 16 days after study entry.

Aged↗
PubMed1990

Penicillin-binding proteins in Borrelia burgdorferi.

Penicillin-binding proteins were identified in Borrelia burgdorferi membranes. A 94-kilodalton penicillin-binding protein was the first to be labeled with tritiated penicillin and was the first band to disappear in a competition experiment. Its binding ability was destroyed when membranes were preboiled. In addition, several of these penicillin-binding proteins comigrated with bands previously identified as surface proteins.

Bacterial Proteins↗
PubMed1988

Choices of new penicillins and cephalosporins in the DRG era.

Several new penicillins and cephalosporins have provided important advances in the therapy of infections caused by gram-negative aerobic bacilli. Older agents, alone or in combination, possess equivalent or greater activity against gram-positive and anaerobic organisms and most community-acquired gram-negative enteric pathogens. Thus, newer agents are useful primarily for the treatment of highly resistant hospital-acquired gram-negative infections. Financial pressures created by the DRG era may favor their broader application, thus creating further resistance by selection or induction. However, prudent use of these agents for selected serious infections or for individuals threatened by aminoglycoside toxicity will yield the most durable cost-effective results.

Bacterial Infections↗
PubMed1986

Pentamidine-associated fatal acute pancreatitis.

Severe hemorrhagic pancreatitis developed in a patient with the acquired immunodeficiency syndrome (AIDS) during pentamidine isethionate treatment for Pneumocystis carinii pneumonia. Despite prompt withdrawal of administration of the drug, the patient died of complications of pancreatitis. Pentamidine is known to be toxic to pancreatic islet cells, causing both hypoglycemia and hyperglycemia in clinical use. However, it rarely causes symptomatic pancreatitis. A review of the literature indicates that this is the second report of fatal pancreatitis associated with pentamidine therapy.

Acquired Immunodeficiency Syndrome↗