Sherwin A. Kabins

Relapsing pneumococcal meningitis: Isolation of an organism with decreased susceptibility to penicillin G

UNTIL RECENTLY, p n e u m o c o c c i i s o l a t e d f r o m h u m a n b e i n g s w e r e u n i f o r m l y h i g h l y s e n s i t i v e to penici l l in. Beg inn ing in 1967, a few p n e u m o c o c c i wi th dec reased suscept ib i l i ty to penic i l l in G were isolated f r o m p a t i e n t s , t h e m a j o r i t y o f w h o m h a d r e c e i v e d penic i l l in G on mul t ip le occas ions . 1, 2 W e isolated a p n e u m o c o c c u s with dec reased suscept ibil i ty to penici l l in G , f rom a pa t i en t wi th sickle cell a n e m i a and meningi t i s . A f t e r initial i m p r o v e m e n t , cl inical s igns of men ing i t i s r ecur red associa ted wi th repea ted isolat ion of p n e u m o c o c c i f rom blood and cereb rosp ina l fluid. Re lapse occu r r ed despi te u n i n t e r r u p t e d t r e a t m e n t with h igh doses of penic i l l in G. W e be l ieve t he re lapse was due in par t to decreased suscept ib i l i ty o f t he p n e u m o c o c c u s to peri ici l l in G.

Acalculous Cholecystitis and Cytomegalovirus Infection in the Acquired Immunodeficiency Syndrome

Excerpt Abdominal symptoms in patients with the acquired immunodeficiency syndrome (AIDS) may be due to multi-organ involvement by various opportunistic infections, Kaposis sarcoma, and non-Hodgki...

Acute Infectious Epiglottitis in Adults

Abstract Epiglottitis is a rapidly progressing disease, often fatal if not recognized and treated promptly. Sore throat followed by dysphagia and rapidly progressive respiratory distress is the cha...

Pseudomonas in the sinks in an intensive care unit: relation to patients.

Sink drains in a medical-surgical intensive care unit (ICU) were cultured during six consecutive weeks as part of a seven month prospective study of acquisition of Pseudomonas aeruginosa by ICU patients. Isolates were typed serologically and by aminoglycoside and chlorhexidine susceptibility patterns. All 11 sinks contained multiple strains of P aeruginosa; some strains persisted for weeks while others were isolated once. Of the sink isolates 56% had high level resistance to gentamicin and tobramycin whereas none of the strains found in patients. In sink isolates chlorhexidine resistance correlated with aminoglycoside resistance and with the presence of a chlorhexidine dispenser at a sink. The sequence of recovery of phenotypically similar isolates suggested that sinks were the source of at most two acquisitions of P aeruginosa by patients during the six weeks. Our study confirms that sinks may be reservoirs for large numbers of highly resistant P aeruginosa but are rarely the source of organisms colonising patients in our ICU.

Outbreak of Clindamycin-Associated Colitis

Excerpt Clindamycin-associated colitis has been reported by the manufacturer to occur once in 50 000 to 100 000 treatment courses (1). Tedesco, Barton, and Alpers (2) reported a 10% incidence in a ...

Structural and phenotypic varieties of gentamicin resistance plasmids in hospital strains of Staphylococcus aureus and coagulase-negative staphylococci.

We previously described a neonatal nursery epidemic of infections caused by a single strain of Staphylococcus aureus bearing a gentamicin resistance plasmid (Vogel et al., Antimicrob. Agents Chemother. 13:466-472, 1978). The same plasmid was present in two isolates of Staphylococcus epidermidis from the patients in this nursery and was transferable interspecifically from either S. aureus or S. epidermidis. During the ensuing 3 years, in the absence of further epidemics, we collected 162 gentamicin-resistant strains of S. aureus and coagulase-negative staphylococci from patients distributed throughout our hospital. Gentamicin resistance plasmids obtained from 41 representative S. aureus and coagulase-negative staphylococcal strains differed as determined by phenotypic and molecular analyses from the plasmid in the neonatal nursery epidemic. Nevertheless, these plasmids were structurally related to each other and to the plasmid of the original epidemic. Our results suggest an evolutionary relationship among these plasmids and support the hypothesis of a genetic reservoir of gentamicin resistance in coagulase-negative staphylococci transferable to S. aureus. Images

In Vitro Comparison of Netilmicin, a Semisynthetic Derivative of Sisomicin, and Four Other Aminoglycoside Antibiotics

One hundred isolates of Pseudomonas and Enterobacteriaceae, of which 85 were chosen because of their resistance to gentamicin or amikacin, were tested for susceptibility to netilmicin (SCH 20569), a new semisynthetic derivative of sisomicin, and to four other aminoglycosides. Tests were performed in Mueller-Hinton agar and, with 43 of these isolates, also in Mueller-Hinton broth. Most isolates of Escherichia coli, Klebsiella, Enterobacter, Citrobacter, and Serratia that were gentamicin resistant proved to be susceptible to netilmicin and amikacin. Tests of representative isolates of this group showed that they owed their resistance to the production of aminoglycoside-adenylylating enzymes. Four isolates of Serratia, detected by their resistance to amikacin, were also highly resistant to netilmicin but were susceptible to gentamicin. These isolates produced aminoglycoside-acetylating enzymes. Gentamicin-resistant Proteus and Providencia were, in general, highly resistant to netilmicin but were susceptible to amikacin. These isolates also produced aminoglycoside-acetylating enzymes. Most gentamicin-resistant strains of Pseudomonas were resistant to netilmicin, either by enzymatic aminoglycoside modification or by other undefined mechanisms. Thus, like amikacin, netilmicin extends the aminoglycoside susceptibility pattern of Enterobacteriaceae to include gentamicin-resistant isolates that produce aminoglycoside-adenylylating enzymes. It is ineffective against strains, some of them susceptible to amikacin, gentamicin, or tobramycin, that produce aminoglycoside-acetylating enzymes. Images

Infections with Gram-negative bacilli in a cardiac surgery intensive care unit: the relative role of enterobacter

A 7-month prospective survey for cefazolin-resistant Gram-negative bacilli in cardiac surgery patients, receiving cefazolin prophylaxis, showed that 58 (67%) of 87 were colonized with enterobacter, 37 (64%) with citrobacter, 33 (57%) with Pseudomonas aeruginosa, and seven (2%) with Serratia marcescens. About 50% of colonization occurred before cefazolin prophylaxis and was present on admission to the intensive care unit. Typing of strains showed that horizontal transmission accounted for at most 14% of carriage. Cefazolin prophylaxis (and high gastric pH) were associated with increased levels of postoperative colonization, most notably for enterobacter. About 25% of colonization with enterobacter, pseudomonas, and serratia was followed by clinical infection. Enterobacter cloacae was the most common pathogen and pneumonia the most common infection. Infections contributed to eight of 11 deaths; four of the eight involved enterobacter. Potential control measures include eliminating endogenous Gram-negative flora by gut decontamination or at least stemming the increase in level of colonization that occurred after surgery.

Control of aminoglycoside resistance by barrier precautions.

The efficacy of antibiotic resistance (barrier) precautions for control of aminoglycoside resistance was evaluated from 1978 to 1981. Despite increasing aminoglycoside use and a 13-fold increase in aminoglycoside-resistant isolates on a newly opened oncology unit, the hospital-wide frequency of aminoglycoside resistant Enterobacteriaceae remained low, supporting the continued value of barrier precautions which were initiated in our hospital in 1974. This control enabled us to focus on exceptions to the effectiveness of barrier precautions. These were traced to environmental reservoirs, very chronic and heavily infected patients, asymptomatic carriers of Serratia, and oncology patients receiving oral non-absorbable aminoglycosides. In addition, resistance in Pseudomonas aeruginosa paralleled aminoglycoside use and, as in our prior experience, continued to rise. With increasing adoption of barrier precautions by others such exceptions should be anticipated.

Gentamicin-Adenylyltransferase Activity as a Cause of Gentamicin Resistance in Clinical Isolates of Pseudomonas aeruginosa

Gentamicin adenylyltransferase activity was found in extracts of clinical isolates of gentamicin-resistant Pseudomonas aeruginosa. Extracts of one of these isolates, P. aeruginosa POW, inactivated gentamicin in the presence of adenosine 5′-triphosphate. Extracts of strain POW catalyzed the binding of radioactivity from [14C]adenine adenosine 5′-triphosphate to gentamicin components, tobramycin, sisomicin, kanamycin A and B and, to a variable degree, streptomycin and spectinomycin. The substrate profile with these agents and other aminocyclitols was similar to that obtained with R factor-mediated gentamicin adenylyltransferase found in Enterobacteriaceae. Adenylylating activity was absent in gentamicin-susceptible mutants of strain POW. Adenylylation may be added to acetylation as an enzymatic mechanism responsible for gentamicin resistance among strains of P. aeruginosa.