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PubMed2002

Venous sinus thrombosis after Proteus vulgaris meningitis and concomitant Clostridium abscess formation.

A 19-y-old woman presented with Proteus vulgaris meningitis as a complication of chronic otitis media. Despite treatment with ceftazidime and amikacin no clinical improvement was observed. Cranial MRI revealed right-sided mastoiditis/otitis media and venous sinus thrombosis. After mastoidectomy, repeat cranial MRI demonstrated abscess formation in the venous sinuses. The abscess was drained. Clostridium spp. was isolated from the abscess culture.

Adult↗
PubMed2006

Proteus mirabilis spondylodiscitis complicating a urinary tract infection.

Infectious spondylodiscitis results from local or haematogenous infection by microorganisms of intervertebral disc spaces, vertebral bodies and surrounding structures. Haematogenous invasion may follow urosepsis. We report on a case of septic spondylodiscitis following urosepsis with Proteus mirabilis, a frequently isolated microorganism in urinary tract infections but rarely in spondylodiscitis.

Aged, 80 and over↗
PubMed1991

The incidence and beta-lactam resistance of Proteus vulgaris in hospital infections: the last decade.

During the period of 1980-1990, 581 Proteus vulgaris strains were obtained in a general hospital. They were considered as the significant isolate in 0.6% of soft tissue infections, 0.6% of urinary tract infections and in 0.2% of bacteremic episodes. Sixty-three percent of the 393 tested strains showed resistance to ampicillin, cefazolin and cefamandole or cefuroxime. About 7% were susceptible to all beta-lactam drugs, and showed a very low beta-lactamase activity and 5% of the strains showed a phenotype of resistance including ampicillin, carbenicillin-ticarcillin, cefazolin and cefamandole or cefuroxime, and presented increased chromosomal beta-lactamase activity. Cefotaxime-resistance was detected in 2% of the isolates which appeared in the period 1987-1990.

Ampicillin Resistance↗
PubMed2003

Swarming of Proteus mirabilis over ureteral stents: a comparative assessment.

BACKGROUND AND PURPOSE: Encrustation on indwelling ureteral stents is commonly related to the presence of urease-producing bacteria that elevate the pH of the urine through the hydrolysis of urea, resulting in the precipitation of calcium and magnesium salts. Using a model previously shown to measure accurately the ability of Proteus mirabilis to swarm over catheter surfaces (Eur J Clin Microbiol Infect Dis 1999;18:206), we investigated the ability of this organism to swarm over three ureteral stents with potential encrustation-resistance properties. MATERIALS AND METHODS: Three commercially available ureteral stents were selected for evaluation: a low surface-energy stent, a hydrogel-coated stent, and a silicone stent. Ten-microliter aliquots of a 4-hour culture of P. mirabilis 296 in Trypticase soya (TSA) broth was inoculated 5 mm from a 1-cm channel cut out from TSA plates. Ten-millimeter stent sections were placed as bridges across the central channel adjacent to the inocula. Time to pathogen crossing was measured. RESULTS: The mean time (+/- SD) to pathogen migration across the three test materials was 15.9 +/- 6.1, 19.8 +/- 9.5, and 29.7 +/- 14.3 hours for the low surface-energy, hydrogel-coated, and silicone stents, respectively. Statistical analysis revealed significant differences between the crossing times of the low surface-energy (P = 0.001) and hydrogel-coated (P = 0.034) stents compared with silicone but not between the low surface-energy and hydrogel-coated stents (P = 0.387). CONCLUSION: Migration of P. mirabilis 296 across silicone stents was significantly reduced compared with low surface-energy and hydrogel-coated stents. These findings suggest that P. mirabilis may have a lower affinity for silicone stents, which may translate into a reduced risk of infection with P. mirabilis and associated stent encrustation.

Equipment Contamination↗
PubMed1978

Influence of pili on the virulence of Proteus mirabilis in experimental hematogenous pyelonephritis.

The ability of heavily and lightly piliated Proteus mirabilis to infect the renal parenchyma was compared in a model of hematogenous pyelonephritis. Cortical abscesses occurred in 13 of 24 rats injected with lightly piliated P. mirabilis but in none of 24 rats challenged with heavily piliated organisms (P less than 0.001). Lightly and heavily piliated organisms were cleared from the vasculature equally rapidly and were also delivered to the kidney in equal numbers. During the first 24 hr, however, titers of the lightly piliated organisms in the kidney increased by 4 logs, whereas the heavily piliated P. mirabilis were virtually all eliminated. Pili are believed to mediate attachment to cell surfaces, and heavy piliation has been correlated with enhanced virulence when P. mirabilis invades the kidney across the pelvic mucosa. The results in this study suggest, however, that pili may adversely affect bacterial survival within the renal parenchyma.

Animals↗
PubMed1979

A nosocomial outbreak of infections due to multiply resistant Proteus mirabilis: role of intestinal colonization as a major reservoir.

An outbreak of nosocomial infections involving an unusual strain of multiply resistant Proteus mirabilis (phage type 8888) occurred in 15 patients, 14 of whom were in the surgical intensive care unit at that time. No common source of infection was identified, and person-to-person transmission was the most likely mode of spread. Case-control analysis indicated a significantly increased risk infection related to length of hospital stay (P less than 0.005), number of operations (P less than 0.005), proximity to another case (P less than 0.01), number of antibiotics received (P less than 0.02), and use of a respirator (P less than 0.01). Only the number of operations (P less than 0.01) and proximity to another case (P less than 0.05) remained significant risk factors when related parameters were controlled by multivariate analysis. Thirteen of 14 patients prospectively cultured were colonized by the epidemic organism in the intestinal tract, while rectal carriage preceded infection by the same strain in at least four patients. These data suggest that intestinal colonization may have been an important reservoir for this outbreak, and the findings may explain the unduly prolonged course of intrahospital spread as well as the difficulty encountered in the eradication and control of the outbreak.

Cross Infection↗
PubMed1990

Hemagglutinin, urease, and hemolysin production by Proteus mirabilis from clinical sources.

Proteus mirabilis, a common cause of urinary tract infection, can lead to serious complications including pyelonephritis. Adherence factors, urease, and hemolysin may be virulence determinants. These factors were compared for bacteria cultured from 16 patients with acute pyelonephritis and 35 with catheter-associated bacteriuria and for 20 fecal isolates. Pyelonephritis isolates were more likely (P less than .05) to express the mannose-resistant/Proteus-like (MR/P) hemagglutinin in the absence of mannose-resistant/Klebsiella-like (MR/K) hemagglutinin than were catheter-associated or fecal isolates. Pyelonephritis isolates produced urease activity of 63 +/- 27 (mean +/- SD) mumol of NH3/min/mg of protein, not significantly different from catheter-associated or fecal isolates. Hybridization of Southern blots of P. mirabilis chromosomal DNA with two urease gene probes demonstrated that urease gene sequences were conserved in all isolates. Geometric mean of reciprocal hemolytic titers for pyelonephritis isolates was 27.9; for urinary catheter isolates, 18.0; and for fecal isolates, 55.7 (not significantly different, P greater than .1). Although in vivo expression of urease and hemolysin may not be reliable indexes of virulence, MR/P hemagglutination in the absence of MR/K hemagglutination may be necessary for development of pyelonephritis.

Acute Disease↗
PubMed1994

Extended-spectrum beta-lactamase in Proteus mirabilis.

Over a period of one month, five isolates of Proteus mirabilis resistant to extended-spectrum cephalosporins colonized or infected five patients of the same intensive care unit. The antibiotic resistance phenotype and the metabolic profiles of the five strains were identical. All five produced a plasmid-mediated extended-spectrum beta-lactamase closely related to TEM-3/CTX-1 according to its pI (6.3), to its substrate profile and to the hybridization of the corresponding gene with blaTEM-3 specific oligonucleotide probes. Ability to produce this enzyme transferred by conjugation to Escherichia coli along with aminoglycoside and sulphonamide resistance. These resistance markers were encoded by a plasmid, (pAP1) which was identical in all five isolates but which was different from the TEM-3 beta-lactamase plasmids found in other Enterobacteriaceae. Plasmid pAP1 differed by its smaller size (47 kb), its EcoRI restriction pattern, its resistance co-markers (AAC(6') and sulphonamide only) and its much lower transfer frequency (2 x 10(-8)). Furthermore this plasmid did not belong to any known Enterobacteriaceae incompatibility group.

Cephalosporinase↗
PubMed1995

Imipenem resistance in clinical isolates of Proteus mirabilis associated with alterations in penicillin-binding proteins.

Two strains of Proteus mirabilis, IpR1 and IpR2, resistant to both imipenem and mecillinam, but susceptible to other beta-lactams were isolated from blood cultures of patients who had been treated with imipenem. Strain IpR1 was isolated in the same sample as a P. mirabilis IpS1 which was susceptible to imipenem and mecillinam. Strains IpR1 and IpR2 did not produce a beta-lactamase and their outer membrane protein profiles were similar to those of IpS1 and P. mirabilis ATCC 29906. Electrophoretic profiles of penicillin-binding proteins (PBPs) showed a decrease in PBP 1A of strains IpR1 and IpR2 compared with IpS1 and ATCC 29906. Competition experiments revealed a decrease in affinity of PBP 2 for imipenem from strain IpR1. These findings suggest that imipenem resistance in P. mirabilis might result from altered PBPs, as reported for Acinetobacter baumanii and Pseudomonas aeruginosa.

Amdinocillin↗
PubMed2000

Clinical relevance of Proteus mirabilis in hospital patients: a two year survey.

A retrospective study was performed on 1072 non-duplicate isolates of Proteus mirabilis, taken in the period April 1996 to March 1998, and on 100 patient charts randomly selected during the same period. P. mirabilis isolates accounted for 7.7% of Enterobacteriaceae. The isolates were predominantly from urine (70.2%); of the total, 38.0% were penicillinase-producing isolates, 6.9% were extended-spectrum beta-lactamase (ESBL)-producing isolates and 3.6% produced inhibitor-resistant beta-lactamase (IRB). ESBL-producing isolates were observed in long-stay and intensive care and IRB-producing isolates in paediatric units. Of the 95 patients whose charts were examined, 69 had a confirmed infection, which in 42 cases was nosocomial.

Anti-Bacterial Agents↗
PubMed2002

Characterization of CMY-type beta-lactamases in clinical strains of Proteus mirabilis and Klebsiella pneumoniae isolated in four hospitals in the Paris area.

We isolated five clinical strains (three Proteus mirabilis and two Klebsiella pneumoniae) with beta-lactam resistance phenotypes consistent with production of an AmpC-type beta-lactamase. The predicted amino acid sequences of the enzymes were typical of class C beta-lactamases. The enzymes were identified as CMY-2, CMY-4 and a new CMY-variant beta-lactamase, CMY-12. The AmpC beta-lactamases from the two K. pneumoniae isolates were found to be encoded on self-transferable plasmids. The genes encoding the AmpC-type beta-lactamase produced by the three P. mirabilis isolates were chromosomal. Four of the five clinical isolates were from patients transferred from Greece, Algeria and Egypt; one of the K. pneumoniae strains was recovered from a French patient. PFGE analysis and rep-PCR fingerprinting showed that the two P. mirabilis isolates from Greek patients were closely related.

Cross Infection↗
PubMed2004

Nosocomial outbreak by Proteus mirabilis producing extended-spectrum beta-lactamase VEB-1 in a Korean university hospital.

OBJECTIVES: To examine the molecular mechanisms involved in the beta-lactam resistance of multidrug-resistant Proteus mirabilis isolates that showed an unusual synergy between imipenem and ceftazidime in a Korean hospital. METHODS: Over an 11 month period, a total of 12 P. mirabilis isolates showing resistance to ampicillin, gentamicin, ceftazidime, cefotaxime, cefuroxime, cefalothin, cefepime, piperacillin, trimethoprim/sulfamethoxazole and ciprofloxacin, were recovered from the sputum and urine specimens of nine patients who were hospitalized in the neurosurgery ward. The extended-spectrum beta-lactamases were screened with a double disc synergy test using ceftazidime, cefotaxime, aztreonam, cefepime and clavulanate. The ESBL types were determined by PCR using specific primers for bla(TEM-1), bla(SHV-1), bla(CTX-M-1), bla(CTX-M-2), bla(CTX-M-8), bla(CTX-M-9), bla(PER-1), bla(GES-1), bla(VEB-1), bla(OXA-10) and bla(OXA-13) followed by sequencing. All the isolates underwent molecular typing by PFGE. The transferability was examined by conjugation. RESULTS AND CONCLUSIONS: All the isolates showed a marked synergy between the extended-spectrum cephalosporins and clavulanate together with an unusual synergy between cefoxitin and the cephalosporins (cefalothin, cefuroxime, ceftazidime, cefotaxime) and between imipenem, and ceftazidime and cefotaxime. Isoelectric focusing of the crude bacterial extracts showed a beta-lactamase band with a pI value of 5.4, which was inhibited by clavulanate. PCR and sequencing identified the gene to be bla(VEB-1). In addition, the aadB gene was detected, conferring aminoglycoside resistance. The resistance was not transferred by conjugation. The outbreak was of a clonal origin as shown by PFGE demonstrating an identical banding pattern. This is the first report of VEB-1-producing Enterobacteriaceae in Korea.

Anti-Bacterial Agents↗
PubMed2006

Role of type II topoisomerase mutations and AcrAB efflux pump in fluoroquinolone-resistant clinical isolates of Proteus mirabilis.

OBJECTIVES: We conducted a study to determine the role played by amino acid mutations in DNA gyrase and topoisomerase IV, and the AcrAB efflux pump in resistance to fluoroquinolones in clinical isolates of Proteus mirabilis. METHODS: Nine clinical isolates of P. mirabilis containing eight fluoroquinolone-resistant isolates and one fluoroquinolone-susceptible isolate as the causative pathogen were collected from different patients with urinary tract infections. Fluoroquinolone resistance was characterized by PCR and DNA sequencing. The role of the AcrAB efflux pump was investigated by semi-quantifying the transcriptional expression of the acrB gene. RESULTS: Double mutations were found in GyrA, at S83I and E87K, and single mutations in GyrB (S464F) and ParC (S80I) in four isolates with ciprofloxacin MICs of 16 to >128 mg/L. In three isolates (ciprofloxacin MICs of >128 mg/L), the level of acrB expression was 2.1- to 3.2-fold higher than that in the wild-type control strain (ciprofloxacin MIC of < or =0.12 mg/L) and these isolates also had increased MICs of minocycline (>64 versus 8-16 mg/L) and chloramphenicol (>256 versus 4-8 mg/L) compared with the five other fluoroquinolone-resistant isolates. CONCLUSION: Our findings demonstrate that two mechanisms--mutations in GyrA (at S83I and E87K), GyrB and ParC, and overproduction of the AcrAB efflux pump--might synergistically contribute to a highest level of resistance to fluoroquinolones in clinical isolates of P. mirabilis.

Anti-Bacterial Agents↗
PubMed2006

Proteus mirabilis clinical isolate harbouring a new variant of Salmonella genomic island 1 containing the multiple antibiotic resistance region.

OBJECTIVES: A clinical isolate of Proteus mirabilis strain 18306, which displayed the multidrug resistance phenotype of Salmonella genomic island 1 (SGI1), was examined for the presence of this island including its multiple antibiotic resistance genomic region. METHODS: P. mirabilis 18306 was isolated in March 2006 from a patient in Palestine with diabetic foot infection. Antibiotic susceptibility tests and various molecular techniques, including PCR, cloning and DNA sequencing were used for detection and characterization of SGI1 in P. mirabilis 18306. RESULTS: P. mirabilis 18306 showed the typical multidrug resistance phenotype of SGI1 as it was resistant to ampicillin, chloramphenicol, streptomycin, sulphonamides and tetracycline, in addition to trimethoprim and nalidixic acid. Molecular characterization showed that P. mirabilis 18306 harboured a structure similar to SGI1, except that the aadA2 gene, which confers resistance to streptomycin and spectinomycin, of standard SGI1 had been replaced with dfrA15, which confers resistance to trimethoprim. Furthermore, the nucleotide sequence of the extrachromosomal circular form of SGI1 in P. mirabilis was found to be identical to that of Salmonella Typhimurium DT104. However, PCR results showed that P. mirabilis 18306 was negative for the left and right junctions which represent the integration sites of SGI1 into Salmonella enterica chromosome. Hence, this new variant of SGI1 may be integrated at a different site into the chromosome of P. mirabilis 18306. Tn1826-derived class 2 integron, which carries only two gene cassettes, sat2 and aadA1, was also identified in this strain. CONCLUSIONS: In this study, we identified a new variant SGI1 containing the multiple resistance genomic region in a multidrug-resistant strain of P. mirabilis. This is the first report for SGI1 in a genus other than Salmonella.

Anti-Bacterial Agents↗
PubMed1976

Nosocomial infection with highly resistant, Proteus rettgeri. Report of an epidemic.

Over 22-1/2 months an epidemic of at least 127 cases of nosocomial infection developed from a strain of Proteus rettgeri resistant to all antibiotics commonly tested in hospital laboratories. Although there were at least four cases of septicemia and one related death, the majority of cases consisted of asymptomatic bacteriuria or clinically mild urinary tract infection. Indwelling urinary tract devices and antibiotic therapy were important predisposing factors. Data supported an association between increasing use of gentamicin and increasing rates of resistant infection. No common source was found, and contact spread appeared more likely. Control measures included efforts to reduce unnecessary exposure to the incriminated risk factors and to improve asepsis in the management of catheterized patients. An additional 36 cases and one related death were identified in the 7-1/2 months following the investigation and institution of control measures. Nosocomial infection with extremely resistant organisms may pose a serious hazard wherever indwelling urinary tract devices and antibiotics are used together intensively.

Bacteriuria↗
PubMed2005

Successfully treated mitral valve Proteus mirabilis endocarditis.

Infective endocarditis caused by Proteus mirabilis is rare and is fatal in most cases. A case of a 64-year-old man presenting with fever, dysuria, and murmur is reported. P mirabilis endocarditis was diagnosed based on clinical presentation, blood culture findings, and the presence of a large mitral valve vegetation seen on echocardiogram. The patient survived after long-term antibiotics and surgical replacement of the mitral valve. The clinical characteristics and complications from reported cases of P mirabilis endocarditis are reviewed.

Anti-Bacterial Agents↗
PubMed1990

Septic sacroiliitis due to Proteus mirabilis.

This case demonstrates the difficulty frequently encountered in making an early diagnosis of septic sacroiliitis. The proper use of appropriate laboratory tests and radiologic examinations can narrow the differential diagnosis significantly, with confirmation resting on culture results. Appropriate antibiotic therapy will depend on the organism isolated. When confronted by the typical clinical findings and supporting ancillary data of septic sacroiliitis, the physician should consider the possibility of an unusual organism such as Proteus mirabilis and should direct antibiotic therapy accordingly.

Adolescent↗
PubMed1980

Genetic recombination between Proteus mirabilis and Providencia alcalifaciens.

Chromosome transfer occurred in plate matings between Proteus mirabilis strain PM5006 and Providencia alcalifaciens strain P29 in either direction with the use of plasmid D or R772 as sex factor. Auxotrophic chromosomal markers of recipients were converted to prototrophy and the galactose fermentation marker of donor PM5006 could also be selected. Recombination frequencies for a group of selected markers in PM5006(D) x P29 matings varied between 3 x 10(-5) (trp+) and 1.2 x 10(-7) (lys+) per donor. In the reverse cross, plasmid D mobilized markers on the P29 chromosome randomly with a recombination frequency of about 1.7 x 10(-7) per donor for all selected P29 markers. R772 produced random mobilization of markers on both chromosomes yielding recombinants at a frequency of about 1.8 x 10(-7) per donor. Unselected markers separated by no more than about 10 min from selected markers on the PM5006 chromosome were cotransferred from P29 by both plasmids. Despite the low degree of DNA homology existing between the two species, all hybrids behaved as stable haploids. Progeny from P29(D or R772) x PM5006 auxotroph matings displayed similar sets of naturally occurring P29 unselected markers irrespective of the selected prototroph allele. In reverse crosses, a similar range of PM5006 naturally occurring unselected markers registered in P29 recipients, although differences existed in the sets of markers mediated by the two plasmids. Weak linkage was detected between PM5006 gal+ allele(s) and some P29 auxotroph markers. Adsorption of donor-specific phages 5006M or PL25 to hybrids could not be demonstrated and many recombinants failed to express some or all of the plasmid markers.

Chromosomes, Bacterial↗