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Toxic-shock syndrome occurred in a mother and possibly in her infant in the immediate postpartum period. Staphylococcus aureus of identical phage type and antibiogram was recovered from mucous membranes in both patients. Staphylococci were transmitted from mother to infant during parturition. These cases represent the first postpartum clinical description and possible vertical transmission of this disease.
Over a 15-month period, seven intravenous drug abusers had 10 admissions because of bacteremia due to methicillin-resistant Staphylococcus aureus. Seven episodes of probable bacterial endocarditis occurred in four patients; one patient had septic thrombophlebitis and two had soft tissue infections. All seven patients patronized a local "shooting gallery" where paraphernalia were provided and drugs were often administered by a "street doctor." All isolates were phage type 29/77/83A/84/85 and demonstrated resistance only to methicillin, oxacillin, and penicillin. This strain of methicillin-resistant S. aureus has a phage type and antibiogram that is distinct from nosocomial methicillin-resistant S. aureus and was probably acquired by intravenous drug abusers during visits to the "shooting gallery". The "shooting gallery" is an integral part of the drug culture and a likely source for the transmission of antibiotic-resistant organisms.
To delineate the pathogenesis and epidemiology of catheter-related infection with Swan-Ganz pulmonary artery (PA) catheters, a prospective clinical study of hospitalized adult medical and surgical patients was done. Role of catheter material was assessed by randomizing insertions to heparin-bonded PA catheters made of polyvinylchloride or polyurethane. Sources of infection and pathogenesis were studied by culturing skin, the introducer, the PA catheter tip, all hubs, infusate from each lumen, and the extravascular portion of the PA catheter beneath the external protective plastic sleeve. Concordance between isolates from sources and infected catheters was determined by speciation, antibiogram, and for coagulase-negative staphylococci, plasmid profile analysis. Risk factors for infection were determined by stepwise logistic regression. Overall, 65 (22%) of 297 Swan-Ganz catheters showed local infection of the introducer (58 catheters) or the intravascular portion of the PA catheter (20 catheters); only two catheters (0.7%) caused bacteremia. Eighty percent of infected Swan-Ganz catheters (the introducer or PA catheter) showed concordance with organisms cultured from skin of the insertion site, 17% with a contaminated hub and 18% with organisms contaminating the extravascular portion of the PA catheter beneath the sleeve. Isolates from infected PA catheters were most likely to show concordance with concomitantly infected introducers (71%). Cutaneous colonization of the insertion site with greater than 10(2) cfu/10 cm2 (relative risk [RR] 5.5; p less than 0.001), insertion into an internal jugular vein (RR 4.3; p less than 0.01), catheterization greater than 3 days (RR 3.1; p less than 0.01), and insertion in the operating room using less stringent barrier precautions (RR 2.1; p = 0.03) were each associated with a significantly increased risk of catheter-related infection. The risk of bacteremic infection with Swan-Ganz catheters is now low, in the range of 1%, with reasonable care. Swan-Ganz catheters are vulnerable to contamination from multiple sources, but the patient's skin is the single most important source of organisms causing invasive infection, which in most cases involves the introducer rather than the PA catheter. Heavy colonization of the insertion site, percutaneous insertion in the internal jugular vein rather than subclavian vein, catheterization longer than 3 days, and insertion with less stringent barrier precautions significantly increase the risk of catheter-related infection. These findings hold promise for application to management of Swan-Ganz catheters and research in catheter design to reduce the risk of catheter-related infection.
An epidemic of methicillin-resistant Staphylococcus aureus (MRSA) infections involving 323 patients occurred at the University of Cincinnati Hospital from 1977 to 1981. Subsequently, endemic MRSA persisted in the hospital for 6 years, until 1987, when a new epidemic began with 223 patients becoming infected over 3 years. Between the two epidemics, there was a major change in the MRSA recovered from infected patients, as demonstrated by three epidemiologic markers. Antibiograms showed that the tetracycline-resistant MRSA involved in the first epidemic was replaced by tetracycline-susceptible MRSA in the second epidemic; bacteriophage typing indicated that the original epidemic strain, D11/83A/85, had been replaced by new strains, many of which were susceptible to phage 54; and restriction endonuclease analysis of plasmid DNA confirmed that a single strain was involved in the first epidemic and that multiple strains were present in the second epidemic. The epidemiology of MRSA infections in the hospital changed with the change in staphylococcal strains. The first epidemic was hospital based with most infections occurring in surgical patients, and the burn unit was the major reservoir. In contrast, 28% of the patients in the second epidemic had community-acquired infections, and nursing home patients were an important source of these infections. Also, 29% of the hospital-acquired infections in this epidemic occurred in nonsurgical patients. This time the burn unit was not a reservoir of infection, but other intensive care units were. The increased diversity of strains of MRSA in the second epidemic might be related to increased transmission in the community and more widespread transmission in the hospital.
Six male patients with chronic bronchitis, who were known previously to have excreted Streptococcus pneumoniae and/or Haemophilus influenzae, both at the times of exacerbations and during remission, were studied for 43 to 52 months. Sputum was examined fortnightly and at the time of exacerbations. Strains of Strep. pneumoniae were serotyped and those of Haemophilus species were typed by antibiograms along with other supporting methods. Sera collected before or at the time of an exacerbation and seven and 30 days afterwards were examined by complement fixation tests against respiratory viruses and Mycoplasma pneumoniae. In 18 out of 25 exacerbations there was evidence of a new type of Strep. pneumoniae and/or Haemophilus spp. or of a current virus infection, suggesting exogenous infection in the majority of these cases. There was a possible reason for failure to detect a new pathogen in three of the seven cases in which none was found. In five further exacerbations adequate investigation was not possible.
Faeces or rectal swabs from 689 diarrhoeic and non-diarrhoeic animals were cultured for thermophilic campylobacters and their antibiograms were determined. Three hundred and fifteen (45.7%) samples were positive for Campylobacter. Piglets had the highest prevalence, 79.3% (233/294) and lambs, the lowest with 17.9% (15/84) being positive. The difference was statistically significant (P < or = 0.01; chi 2). In calves, 20.5% (60/293) and in kids 38.9% (7/18) were positive for campylobacters. The prevalence of infection was not significantly (P > or = 0.05; chi 2) different between diarrhoeic (46.1%) and non-diarrhoeic (45.1%) animals nor between male (47.5%) and female (43.8%). The frequency of isolation of campylobacters harvested from semi-intensively managed animals (75.4%) was, however, significantly higher (P < or = 0.001; chi 2) than from intensively or extensively managed animals. Overall, C. coli strains (32.8%) were more frequently isolated than C. jejuni strains (12.9%) and the difference was significant (P < or = 0.001; chi 2). Biotype I accounted for 67.3% (152/226) of C. coli and 64.0% (57/89) of C. jejuni strains isolated. A total of 245 (77.8%) strains of Campylobacter exhibited resistance to one or more antibiotics and was highest to streptomycin (76.5%), kanamycin (28.6%) and neomycin (26.7%). It was concluded that Campylobacter infections were widespread in livestock in Trinidad, particularly C. coli in piglets.
The American Heart Association recommends prophylactic administration of penicillin before each dental session to patients susceptible to infective endocarditis. Such preventive treatment, however, may trigger the transient appearance of penicillin-resistant bacterial strains. In order to investigate the behavior of oral streptococci, 29 healthy volunteers who did not harbor penicillin-resistant viridans streptococci received 4 gm of phenoxymethyl penicillin orally over a period of 10 hours. This amount constituted the sole dose of antibiotics administered in the entire experiment. Daily specimens of oral flora were obtained for 14 successive days from each participant and incubated aerobically with a penicillin-saturated disk for 24 hours. Viridans streptococci were considered resistant when bacterial colonies grew adjacent to the disk for 1 day or more. The study population was divided into high- and low-resistance groups, according to the individual antibiograms. Resistant viridans streptococci were already detected at 6 hours after penicillin ingestion in nine (31%) of the subjects. Six months later, oral specimens were taken from ten randomly selected participants; these specimens served as a control. The difference in bacterial resistance between the high- and low-resistance groups was significant for the duration of 9 days, as was that between the high-resistance and control groups (p less than 0.05 in both cases). In order to minimize the odds that penicillin-resistant bacterial strains will develop in patients susceptible to infective endocarditis, elective dental treatments in these persons should be scheduled in intervals of not less than 10 days.
Examination of milk from goats yielded 41 strains from 40 clinically affected halves; 15 were Staphylococcus aureus, 6 Staph. epidermis, 1 Streptococcus agalactiae, 2 Strept. dysgalactiae, 5 Strept. uberis, 2 Corynebacterium pyogenes, 3 Escherichia coli, 3 Pasteurella spp. and 4 Mycoplasma spp. One half had dual infection of Staph. aureus and Strept. dysgalactiae. Twenty two of the 297 milk samples from apparently normal halves also harboured pathogens comprising of 9 Staph. aureus, 1 Strept. agalactiae, 2 E. coli, 2 Pasteurella spp., 2 Candida albicans and 6 Mycoplasma spp. Most of the bacterial isolates were sensitive to many broad spectrum antibiotics. Twenty of the 24 Staph. aureus isolates were phase typable by a set of 23 human Staphylococcal International Phages suggesting the utility of these phages for the typing of goat strains. The isolates were grouped into 15 phage-types, many of which have been reported from human infections in Iraq. This indicates the possibility of association of human strains of Staph. aureus in caprine mastitis. No definite correlation could be noted between antibiogram and phage types of Staph. aureus strains.
Amongst a herd of 250, approximately 22 weeks old, Dutch Friesian veal calves, 84 were condemned on meat inspection because of typical pathology of salmonellosis, confirmed by isolation of Salmonella dublin from spleens. From the condemned animals 15 carcasses were randomly selected for further investigation. Their livers, kidneys and samples of their longissimus dorsi muscles were examined for Salmonella using Rappaport-Vassiliadis' and Muller-Kauffmann's enrichment media. In addition, livers were macroscopically scanned for necrotic foci. Signs of (multiple) miliary liver necrosis were not consistently related to isolation of Salmonella from the three tissues examined. Although all spleens had been found positive for Salmonella, from only 53% of the livers, 33% of the kidneys and 27% of the muscles could salmonellae be isolated by one or both enrichment procedures. The Rappaport-Vassiliadis enrichment medium was found to be slightly superior for the isolation of salmonellae. All Salmonella-isolates were serotyped as Salmonella dublin. Their antibiograms showed the expected resistance to chloramphenicol and tetracyclines but, surprisingly, sensitivity to ampicillin, kanamycin, neomycin and streptomycin.
During a period of 6 months, an 'epidemic strain' of Acinetobacter calcoaceticus was isolated from 10 pre-term neonates in a special care baby unit (scbu). Of these, nine had pulmonary infections. The tenth was found to have conjunctival colonization only. The 'epidemic strain' was characterized by serotyping, biotyping, bacteriocin typing and antibiograms. An identical strain was isolated from an 'Ambu' resuscitation device but not from other environmental samples or from staff on the unit. The outbreak ceased after the colonized resuscitator was removed and an appropriate disinfection policy implemented for the replacement resuscitators.
We studied 50 strains of coagulase-negative staphylococci (CNS) isolated from 50 patients with hospital-acquired bacteraemia, identified by prospective surveillance at the University of Virginia Hospital between March 1981 and September 1982. Using the Staph-Ident System for speciation, we found that 37 strains (74%) were Staphylococcus epidermidis, 7 (14%) Staph. hominis, 3 (6%) Staph. haemolyticus and 3 (6%) Staph. warneri. 33 (66%) of the strains produced slime and a higher proportion of the Staph. epidermidis group (75%) than the non-epidermidis group (46%), did so. Minimal inhibitory concentrations (MIC) were determined by a microdilution technique with 20 different antibiotics. There was no difference in geometric mean MICs between slime producers and non-slime producers within either the epidermidis or non-epidermidis group. The most potent antibiotics against Staph. epidermidis (MIC90 mg l-1) were rifampin (0.05), netilmicin (0.05), amikacin (2.9), thienamycin (0.75), teichomycin (0.85), vancomycin (1.0) and nafcillin (0.39). On the other hand strains were resistant to tobramycin (15), moxalactam (50), fosfomycin (greater than 64), and clindamycin (greater than 64). Overall, eight (16%) of the CNS strains were resistant to methicillin, three of which were Staph. haemolyticus. The non-epidermidis strains were more resistant than the Staph. epidermidis strains to most beta-lactam antibiotics. Differences in antibiograms indicate that speciation of CNS may prove useful for clinical and epidemiologic purposes.
An outbreak of urinary-tract infection involving a strain of Proteus mirabilis resistant to gentamicin and several other antibiotics affected 90 patients in Southampton between July 1980 and May 1985. The outbreak strain was also resistant to chlorhexidine and this, in combination with the antibiogram and Dienes' test, permitted differentiation from other P. mirabilis strains. The outbreak had features in common with other Enterobacteriaceae outbreaks, although certain aspects of the population involved have made it particularly difficult to control. The outbreak commenced shortly after the introduction of a catheter care policy which involved the use of chlorhexidine, and although the majority of the cases were colonized before this policy was enforced, chlorhexidine had been used extensively for other procedures within the district. Preliminary evidence suggests that there is no genetic linkage between the chlorhexidine and multiple antibiotic resistance.
An outbreak with a strain of methicillin-resistant Staphylococcus aureus began in The London Hospital in 1982 and continues to be associated with significant morbidity and mortality. This particular strain, termed epidemic methicillin-resistant S. aureus, is recognized by its characteristic antibiogram, phage-type and plasmid profile. In this outbreak various means of control have been attempted. Sideroom isolation did not curtail spread of the organism and containment was only achieved with the combination of extended screening, mupirocin for treatment of carriage and the use of an isolation ward.
Clinical microbiologists normally identify important isolates to the level of species and determine their susceptibility to antibiotics. These activities generate a species identification and provide some differentiation below the level of species in the form of a biotype and an antibiogram. Most other typing methods should be reserved for special studies or to investigate possible infection problems or outbreaks. Specialized techniques should usually be done in reference laboratories. These include serotyping, (complete antigenic analysis), bacteriophage susceptibility, and bacteriocin production or susceptibility.
We report the first outbreak of Acinetobacter species meningitis in a group of children with acute leukaemia following the administration of intrathecal chemotherapy. Eight of twenty patients receiving methotrexate injections on a single day developed signs and symptoms of meningitis within 18 h of treatment, and cases were clustered by time of administration. A cohort study comparing case and non-case patients did not identify any specific host factor associated with meningitis. Acinetobacter calcoaceticus var anitratus was isolated from the cerebrospinal fluid (CSF) of five patients; three patients died. Our investigation determined that the methotrexate was extrinsically contaminated by reused needles, used for reconstitution and administration, which had been inadequately sterilized. Acinetobacter calcoaceticus var anitratus was isolated from an autoclaved needle and a vial of methotrexate used for chemotherapy; these and the clinical isolates had similar antibiograms. After introduction of single-use disposable needles no subsequent cases occurred.
An outbreak of infection due to multiply resistant Pseudomonas aeruginosa occurred from March to April 1986 in a neonatal unit. Affected neonates were receiving ventilation support and the mortality rate was high. Plasmid analysis and antibiograms indicated that the outbreak was due to a single strain. A survey of bacteria isolated from respirators, potable water and hands of personnel working in the unit failed to recover the outbreak strain. Lack of sterilization of respirators and overcrowding were considered to be the causes of the outbreak and reinforcement of the importance of aseptic techniques helped in its termination.
Two hundred and sixty Acinetobacter isolates were recovered from 237 patients over a 2-year period; 156 isolates from 135 spinal cord injuries unit (SCIU) patients and 104 isolates from 102 patients in all the other hospital units. In SCIU patients, 133 isolates were recovered from the urine, 21 from wounds and aspirates, one from sputum and one from blood culture. In non-SCIU patients, 12 isolates were recovered from urine, 43 from wounds and aspirates, 48 from sputum and one from blood culture. Sixty-nine percent of isolates from SCIU patients showed resistance to gentamicin compared to 3% from non-SCIU patients. Gentamicin-resistant Acinetobacter anitratus was recovered from many environmental sites in the SCIU wards and from the hands of seven of 94 SCIU staff members tested. Serial rectal swabs were obtained from 79 newly-diagnosed SCIU patients. Ninety-two percent of those patients followed for up to 5 months acquired gentamicin-resistant Acinetobacter anitratus in their intestinal tract. API 2ONE profiles and antibiograms suggested that two distinct gentamicin-resistant strains of A. anitratus had become endemic in the SCIU and that nosocomial transmission was a frequent occurrence.
During the last few years, among nosocomial pathogens, Acinetobacter spp. have given rise to an increasing number of nosocomial infections. Acinetobacter strains are widely distributed in nature; in hospitals, the human skin is the likely source for most outbreaks of hospital infections. The organism has been frequently found in the inanimate environment, especially in moist situations and it has been isolated from various types of opportunistic infections (septicaemia, endocarditis, meningitis, pneumonia, skin and wound sepsis and urinary tract infection). For epidemiological studies, various typing methods such as biotyping, bacteriocin typing and serology have been developed. More recently electrophoretic patterns of cell-envelope proteins and plasmid analysis have proved useful in differentiating outbreak strains. Antibiogram typing may be useful but the antibiotic resistance of Acinetobacter spp. has changed rapidly within the last few years and thus antibiotyping must be complemented by other typing systems. New methods such as electrophoretic analysis of isoenzymes, definition of plasmidotype profiles or restriction endonuclease digestion of chromosomal DNA are under investigation.