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Occasionally a brain abscess has been observed in a neonate. This report presents a unique case of a septic infant who developed a proteus mirabilis brain abscess shortly after birth, which persisted undetected until 21/2 months of age.
Proteus mirabilis, a common cause of urinary tract infection, produces a number of different fimbriae, including ambient temperature fimbriae (ATF). These fimbriae are optimally expressed at 23 degrees C and their contribution to urinary tract infection has so far remained unknown. In the present study, a clinical isolate of P. mirabilis and an isogenic allelic replacement mutant unable to express ATF were tested for their ability to cause infection in the ascending urinary tract infection model in mice. The atf mutant colonised the urinary tract as well as the wild-type strain and was also able to outcompete the wild-type strain in a co-challenge experiment. Different non-clinical P. mirabilis isolates showed a reactive AtfA band after Western blot analysis using a polyclonal rabbit AtfA antiserum. These data together suggest that ATF does not play a role in P. mirabilis urinary tract infection.
The effect of iron deprivation on the expression of outer membrane proteins and the ability to use heme as an iron source by uropathogenic Proteus mirabilis, Pr 6515, was studied. Examination of iron-restricted bacteria showed three outer membrane proteins ranging from 66 to 75 kDa to be affected by iron restriction, as well as a newly expressed 64-kDa protein. These proteins were induced within 15 minutes of iron-deprivation. The strain grew in the presence of ferric citrate, hemin and hemoglobin as iron sources, but could not use transferrin, lactoferrin or siderophores from exogenous sources. The 64- and 66-kDa proteins showed hemin-binding activity by affinity chromatography, and both reacted in Western blots with sera from mice transurethrally infected with the same strain. We suggest that P. mirabilis expresses iron-regulated outer membrane proteins that could be involved in heme uptake and may have a role in pathogenesis.
Ascending pyelonephritis was induced by Staphylococcus saprophyticus and Proteus mirabilis both by inoculating the organisms separately and in combination into rat bladders. Bacterial cultures of tissue homogenates showed that pyelonephritis by both bacteria occurred significantly more often in rats where the two organisms were instilled concomitantly, suggesting a synergistic virulence between the two species. The antibody response to the different organisms was the same either the bacteria were instilled separately or in combination.
Over a 6-year period (1997 to 2002), 56 strains of Proteus mirabilis (12% of the total number of P. mirabilis isolates obtained) resistant to ampicillin, piperacillin, cefazolin and cefoperazone by routine antimicrobial testing method, were isolated in Saitama Medical School Hospital. Of the 56 strains resistant to 4 beta-lactams, 12 strains were studied and were found to produce extended-spectrum beta-lactamases, identified as CTX-M-10 group and Toho-1 group in 8 and 2 strains, respectively. Susceptibility testing showed that 12 strains were resistant to cefotaxime, and cepodoxime, and ceftriaxon but susceptible to ceftazidime. Moreover, all of the beta-lactamases were inhibited by clavulanic acid. Of the 12 strains, one strain showed resistance to cephamycins such as cefoxitin, cefmetazole and cefotetan. Four of the twelve patients had infections caused by ESBL producing P. mirabilis, and eight patients were colonized, as confirmed by clinical and laboratory findings. The infections were urinary tract infections (two episodes), pneumonia (one episode), and sepsis (one episode). These patients had a favorable response to antibiotic therapy including cephalosporin. From these findings, CTX-M-type beta-lactamase producing P. mirabilis strains were confirmed from clinical specimens in our hospital.
We studied 247 strains of Proteus mirabilis collected during the 6 months from November 2003 to April 2004 from 12 clinical laboratories in the Kinki region of Japan for the production of extended-spectrum beta-lactamase (ESBL). Eighteen strains (7.3%) showed MICs for cefpodoxime of > or = 2 microg/mL and 13 strains (5.2%) were positive for the double-disk synergy test. Susceptibility depended on genotype. MICs for cefepime, cefozopran, and cefpirome were high (> or = 8 microg/mL), and that for ceftazidime was low (0.12-0.5 microg/mL). Meropenem showed the lowest MIC (< or = 0.03-0.25 microg/mL) of the calbapenems, while other calbapenems showed somewhat higher values (0.5-2 microg/mL). The MIC of tazobactam/piperacillin was also relatively low (< or = 0.25-1 microg/mL). Analysis of the ESBL genotype by the polymerase chain reaction showed that 12 of 13 strains were CTX-M2 types. CTX-M9 was detected in a single laboratory. The clinical background showed 5 strains in urine samples. Twelve of 13 strains were detected in patients with minimal devices use. No symptoms were found in most cases of established syndrome. Analysis of PCR fingerprint profiles of random amplified polymorphic DNA patterns showed that 6 of 7 strains from hospital 1 showed the same pattern, and 5 of 5 strains from hospital 13 showed the same pattern, suggesting the nosocomial spread of P. mirabilis in each hospital.
The therapeutic effect of cefotiam on experimental urinary tract infections with Proteus mirabilis IFO 3849 in mice was compared with that of cefazolin. The minimal inhibitory concentrations of cefotiam and cefazolin against the test organism were 1.56 and 25 micrograms/ml, respectively. Beginning 3 days after infection, various doses of each cephalosporin were given subcutaneously twice a day for 5 days. Doses of 100 mg of cefotiam per kg or more sterilized the urine within 3 days and effected a marked reduction or complete eradication of bacteria in the bladder walls and kidneys of mice sacrificed the day after treatment was terminated. A dose of cefazolin greater than 800 mg/kg was required for equivalent therapeutic results. Clearance of bacteria from urinary tract organs was as rapid or more rapid with 50-mg/kg doses of cefotiam as with 200-mg/kg doses of cefazolin. Much more rapid clearance was attained with 200-mg/kg doses of cefotiam. The concentrations of cefotiam attained in plasma, kidney, and urine were lower than the cefazolin levels achieved at an equivalent dose. The superiority of cefotiam over cefazolin in treatment of experimental urinary tract infections appears to be due to its greater activity against the test organism.
In previous papers (Y. Ikeda and T. Nishino, Antimicrob. Agents Chemother. 32:1073-1077, 1988; Y. Ikeda, T. Nishino, and T. Tanino, Antimicrob. Agents Chemother. 31:865-869, 1987), we reported that many of the 7-aminothiazolyl cephalosporins, such as cefmenoxime, showed paradoxically reduced activity against Proteus vulgaris at higher concentrations, whereas these paradoxical effects were not observed for other types of cephalosporins, such as cefbuperazone and cefoperazone. In this study, we compare the therapeutic effect of cefmenoxime with that of cefbuperazone and explore the in vivo paradoxical effect of cefmenoxime by using an experimental infection model in mice. In an intraperitoneal infection with P. vulgaris 11, the survival rate with cefmenoxime was increased to 43% at 3.13 mg/kg but was lower at higher doses. On the other hand, cefbuperazone did not show such a paradoxical therapeutic effect. In mice infected with P. vulgaris 11, cefmenoxime levels in both serum and peritoneal washings were rapidly reduced and beta-lactamase activities in the peritoneal cavity were increased at higher cefmenoxime doses. These findings suggested that high levels of cefmenoxime at the infection site induced increased production of beta-lactamase, which then rapidly inactivated the antibiotic. We conclude that the paradoxical therapeutic effect of cefmenoxime against P. vulgaris occurs by the same mechanisms as the in vitro effect and that the high beta-lactamase inducibility and low beta-lactamase stability may account for the paradoxical therapeutic effect of cefmenoxime against P. vulgaris.
A clinical isolate of Proteus mirabilis was found to produce a new variant of the TEM-10 beta-lactamase gene. This is the first report of TEM-10 production by P. mirabilis and the first report of extended-spectrum beta-lactamase production by an isolate of this species recovered in the United States.
TEM-89 (CMT-3) is the first complex mutant beta-lactamase produced by a clinical strain of Proteus mirabilis (strain Pm 631). This new enzyme, which has a pI of 6.28, is derived from TEM-3 and has a single amino acid substitution also encountered in TEM-59 (inhibitor-resistant TEM beta-lactamase IRT-17): Ser-130 to Gly. TEM-89 hydrolyzed penicillins to the same extent that TEM-3 did but lost almost all hydrolytic activity for cephalosporins and, like TEM-59, was highly resistant to inhibitors.
The sequences of the bla(TEM) genes encoding TEM-92 in Proteus mirabilis and Providencia stuartii isolates were determined and were found to be identical. Except for positions 218 (Lys-6) and 512 (Lys-104), the nucleotide sequence of bla(TEM-92) was identical to that of bla(TEM-20), including the sequence of the promoter region harboring a 135-bp deletion combined with a G-162-->T substitution. The deduced amino acid sequence of TEM-92 differed from that of TEM-52 by the presence of a substitution (Gln-6-->Lys) in the peptide signal.
Antimicrobial peptides (APs) are important components of the innate defenses of animals, plants, and microorganisms. However, some bacterial pathogens are resistant to the action of APs. For example, Proteus mirabilis is highly resistant to the action of APs, such as polymyxin B (PM), protegrin, and the synthetic protegrin analog IB-367. To better understand this resistance, a transposon mutagenesis approach was used to generate P. mirabilis mutants sensitive to APs. Four unique PM-sensitive mutants of P. mirabilis were identified (these mutants were >2 to >128 times more sensitive than the wild type). Two of these mutants were also sensitive to IB-367 (16 and 128 times more sensitive than the wild type). Lipopolysaccharide (LPS) profiles of the PM- and protegrin-sensitive mutants demonstrated marked differences in both the lipid A and O-antigen regions, while the PM-sensitive mutants appeared to have alterations of either lipid A or O antigen. Matrix-assisted laser desorption ionization-time of flight mass spectrometry analysis of the wild-type and PM-sensitive mutant lipid A showed species with one or two aminoarabinose groups, while lipid A from the PM- and protegrin-sensitive mutants was devoid of aminoarabinose. When the mutants were streaked on an agar-containing medium, the swarming motility of the PM- and protegrin-sensitive mutants was completely inhibited and the swarming motility of the mutants sensitive to only PM was markedly decreased. DNA sequence analysis of the mutagenized loci revealed similarities to an O-acetyltransferase (PM and protegrin sensitive) and ATP synthase and sap loci (PM sensitive). These data further support the role of LPS modifications as an elaborate mechanism in the resistance of certain bacterial species to APs and suggest that LPS surface charge alterations may play a role in P. mirabilis swarming motility.
A new natural TEM derivative, named TEM-87, was identified in a Proteus mirabilis isolate from an Italian hospital. Compared to TEM-1, TEM-87 contains the following mutations: E104K, R164C, and M182T. Kinetic analysis of TEM-87 revealed extended-spectrum activity against oxyimino cephalosporins (preferentially ceftazidime) and aztreonam. Expression of blaTEM-87 in Escherichia coli decreased the host susceptibility to these drugs.
Twenty-nine Proteus mirabilis isolates from 17 Polish hospitals were analyzed. The isolates were resistant to a variety of antimicrobials, and their patterns of resistance to beta-lactams resembled those of the constitutive class C cephalosporinase (AmpC) producers. Indeed, beta-lactamases with a pI of approximately 9.0 were found in all of the isolates, and they were subsequently identified as four AmpC-type cephalosporinases, CMY-4, -12, -14, and -15, of which the two last ones were novel enzyme variants. The enzymes were of Citrobacter freundii origin and were closely related to each other, with CMY-4 likely being the evolutionary precursor of the remaining ones. The bla(CMY) genes were located exclusively in chromosomal DNA, within EcoRI restriction fragments of the same size of approximately 10 kb. In the CMY-12- and -15-producing isolates, an additional fragment of approximately 4.5 kb hybridized with the bla(CMY) probe as well, which could have arisen from a duplication event during the evolution of the genes. In all of the isolates, the ISEcp1 mobile element, which most probably is involved in mobilization of the C. freundii ampC gene, was placed at the same distance from the 5' ends of the bla(CMY) genes, and sequences located between them were identical in isolates carrying each of the four genes. These data suggested that a single chromosome-to-chromosome transfer of the ampC gene from C. freundii to P. mirabilis could have initiated the spread and evolution of the AmpC-producing P. mirabilis in Poland. The hypothesis seems to be confirmed by pulsed-field gel electrophoresis typing, which revealed several cases of close relatedness between the P. mirabilis isolates from distant centers and showed an overall similarity between the majority of the multiresistant isolates.
Bloodstream infection (BSI) due to Proteus mirabilis strains is a relatively uncommon clinical entity, and its significance has received little attention. This study was initiated to evaluate risk factors and treatment outcome of BSI episodes due to P. mirabilis producing extended-spectrum beta-lactamases (ESBLs). Twenty-five BSI episodes caused by P. mirabilis occurred at our hospital (Ospedale di Circolo e Fondazione Macchi, Varese, Italy) over a 7.5-year period. Phenotypic and molecular methods were used to assess ESBL production. Clinical records of BSI patients were examined retrospectively. Demographic data, underlying diseases (according to McCabe and Jackson classification and Charlson weighted index), risk factors, and treatment outcome were investigated by comparing cases due to ESBL-positive strains to cases due to ESBL-negative strains. Eleven isolates were found to express ESBLs (TEM-52 or TEM-92). The remaining 14 isolates were ESBL negative and were uniformly susceptible to extended-spectrum cephalosporins and monobactams. Comparison of the two groups showed that previous hospitalization in a nursing home (P = 0.04) and use of bladder catheter (P = 0.01) were significant risk factors for infections due to ESBL-positive strains. In addition, cases due to ESBL-positive strains showed a significantly higher mortality attributable to BSI (P = 0.04). BSI cases due to ESBL-negative isolates uniformly responded to therapy, whereas 5/11 cases due to ESBL-positive isolates failed to respond (P < 0.01). Use of carbapenems was associated with complete response independently of ESBL production. Therapeutic failure and mortality may occur in BSI episodes caused by ESBL-positive P. mirabilis isolates. Thus, recognition of ESBL-positive strains appears to be critical for the clinical management of patients with systemic P. mirabilis infections.
In animals developing experimentally induced unilateral pyelonephritis, both the infected kidney (IK) and the contralateral noninfected kidney (NIK) showed an immediate increase in renal lysozyme activity of about 5 days' duration after the unilateral injection of viable Proteus mirabilis into the renal cortex. Lysozyme activities of the NIK were consistently higher than those of the IK. This initial increase was followed by a second increase which lasted throughout the period of observation (17 days), and enzyme activities of the NIK were consistently higher than those of the IK. In saline punctured kidneys of control animals, both the saline punctured kidney (SP) and the non-saline punctured kidney (NSP) showed only the immediate increase in renal lysozyme activity, which persisted until the SP was completely healed. These enzyme activities were less than those observed in the infected animals, but the response of the NSP was greater than that of the SP. Trauma not directed to the kidney does not produce a similar response of renal lysozyme. The elevated renal lysozyme of the NIK could not be shown to protect it from bacterial infection.
An outbreak of nosocomial urinary-tract infection was caused by a strain of Proteus rettgeri that fermented lactose overnight and was resistant to all antimicrobial drugs tested. The nonmotile isolates shared an O (somatic) antigen that differed from those of wild-type P. rettgeri. The organisms proved markedly serum-sensitive. In rats, the isolates elicited an acute interstitial nephritis with associated transient bacteriuria. Attempts to transfer the lac(+) trait and drug-resistance markers to recipient strains of Escherichia coli K-12 failed; exposure of the isolates to acridine orange yielded small numbers of non-lactose-fermenting variants which, however, were still as drug-resistant as before. Epidemiological studies failed to uncover the source of this unique strain and appeared to indicate exogenous spread of infection.
This review presents the current taxonomy of the genera Proteus, Providencia, and Morganella, along with the current methods for the identification of each species within the three genera, incorporating both conventional biochemical and commercial methods. While all of these organisms are ubiquitous in the environment, individual case reports and nosocomial outbreak reports that demonstrate their ability to cause major infectious disease problems are presented. Lastly, anticipated antimicrobial susceptibility patterns are reviewed. Many of these organisms are easily controlled, but the advent of newer and more powerful antimicrobial agents has led to some problems of which laboratorians need to be aware.