What Is The Best Antibiotic To Treat Proteus Mirabilis


What Is The Best Antibiotic To Treat Proteus Mirabilis
Treatment / Management – Empirical treatment for an uncomplicated UTI caused by P. mirabilis (much like other uncomplicated UTIs) involves outpatient treatment with either a 3-day course of trimethoprim/sulfamethoxazole (TMP/SMZ) or an oral fluoroquinolone (e.g., ciprofloxacin).

  1. Acute, uncomplicated pyelonephritis can be treated on an outpatient basis with fluoroquinolones, although a regimen of 7 to 14 days is recommended.
  2. An alternative to this treatment is a one-time dose of ceftriaxone or gentamycin followed by either TMP/SMZ, an oral fluoroquinolone, or cephalosporin for 7 to 14 days.

If a patient has a more severe condition or is in an inpatient setting, they may begin antibiotic therapy via intravenous administration of either ceftriaxone, gentamycin, fluoroquinolone, gentamycin plus ampicillin, or aztreonam until fever resolves.

  1. At this point, they may switch to oral therapy with either cephalosporin, an oral fluoroquinolone, or TMP/SMZ for up to 14 additional days.
  2. If a patient presents with a complicated UTI (e.g., a man or woman with a history of an underlying condition that may increase the risk of failure of therapy), they may also be treated in an outpatient setting with oral antibiotics for 10 to 21 days as long as they receive adequate follow-up.

Proteus infection can be avoided with proper sanitation and hygiene, such as adequate sterilization of medical equipment and surfaces. Additionally, catheterization should be reserved for patients for whom there is no other option.

What antibiotic kills Proteus mirabilis?

4. Discussion – Proteus mirabilis is a Gram-negativerod-shaped bacterium that frequently causes catheter-associated UTIs that may be associated with urolithiasis due to the biofilm-forming ability and invasion of urinary epithelial cells by urease, which catalyzes the hydrolysis of urea leading to alkalinization of urine and the development of bladder or kidney stones,

  • In this regard, Proteus mirabilis is the leading cause of struvite formation with magnesium ammonium phosphate and carbonate apatite,
  • UTIs caused by Proteus mirabilis are generally more severe than those caused by E.
  • Coli and are associated with a higher incidence of pyelonephritis,
  • To our knowledge, the characteristics and antibiotic-sensitive patterns of Proteus mirabilis infection in kidney stone patients have not been extensively studied thus far, especially in China; thus, an in-depth understanding of the patterns of antibiotic sensitivity in Proteus mirabilis is necessary to ensure effective treatment.

Therefore, we conducted this study to investigate the characteristics of Proteus mirabilis sensitivity to antibiotics in patients with urinary calculi and to provide evidence for appropriate antimicrobial therapy. Proteus mirabilis may exhibit different epidemiological characteristics due to season, sex, age, and regional differences.

Therefore, regional studies conducted during different seasons are essential for a better understanding of the disease, effective treatment, and prevention of complications. Our review found that Proteus mirabilis infection is more common in women than men as are infective struvite stones, There have been few studies on the susceptibility of Proteus mirabilis to antibiotics associated with urinary tract infection or urinary stones, particularly during various seasons.

UTIs caused by E. coli or Klebsiella are more common during summer and less common during spring, Our study found that UTIs caused by Proteus mirabilis in urolithiasis patients were the most common during autumn and the least common during winter. If sex was considered, Proteus mirabilis infection in females was more common during autumn and less common during spring.

  • Proteus mirabilis infection in males was more common during summer and less common during winter.
  • Therefore, sex, season, and etiological factors should be considered before initiating empiric treatment in light of these findings.
  • Understanding antibiotic sensitivity in the region where patients live will help in selecting the appropriate empiric antibiotic for the treatment of Proteus mirabilis infection.

Over time, however, antibiotic sensitivity patterns in the region are likely to change. Especially in developing countries such as China, antibiotic sensitivity rates are quite low due to the inappropriate use of antibiotics. In a study conducted from 2010 to 2015 in China, the most effective antibiotics for patients with Proteus mirabilis infection and urinary calculi were as follows: furantoin (0.6%), tigecycline (15.4%), sulfamethoxazole (51%), ampicillin (56.5%), cefazolin (55.8%), imipenem (93.4%), meropenem (100%), ciprofloxacin (67.6%), levofloxacin (85.6%), cefoxitin (93.7%), cefoperazone sulbactam (100%), ceftriaxone (93.7%), cefepime (95.6%), and amikacin (97.6%),

A study in Brazil found that effective antibiotics against Proteus mirabilis isolated from patients with community-acquired urinary tract infection were as follows: sulfamethoxazole (78.1%); naphthalinic acid and gentamicin (94.5%); norfloxacin and ciprofloxacin (96.7%); amikacin and amoxicillin + clavulanic acid (99.5%); ampicillin (80.3%); cephalosporin (97.8%); cefuroxime, ceftriaxone and cefepime (98.4%); and ertapenem, meropenem, and piperacillin + tazobactam (100%),

Bandy et al. retrospectively analyzed the antimicrobial spectrum of Enterobacter in a referral hospital in Al Khov, Saudi Arabia, in 2019 and found that the antibiotics used to treat Proteus mirabilis infection that were effective were as follows: furantoin (0.0%), sulfamethoxazole (15.8%), ampicillin (14.0%), cefazolin (55.8%), levofloxacin (13.1%), cefoxitin (78.2%), ceftazidime (25%), ceftriaxone (21.8%), cefepime (23.2%), amikacin (51.4%), and cefuroxime (20%),

Our study found that levofloxacin had a low effective rate when used to treat Proteus mirabilis infection in female and male patients with urinary calculi, which is worthy of attention. The American Medical Association recommends that clinicians treat men and women who have pyelonephritis simply with fluoroquinolones (5 to 7 days) for a short period, depending on antibiotic sensitivity.

Fluoroquinolones are the first line of treatment, Clinical practice guidelines for the antibiotic treatment of community-acquired UTIs (CTIS) published in Korea in 2018 indicate that pyelonephritis patients who have urinary tract obstruction (e.g., urolithiasis) should be administered empiric antibiotics according to the treatment regimen of pyelonephritis alone, and fluoroquinolones can be used as early empiric antibiotics,

  1. The Infectious Diseases Society of America (IDSA) clinical practice guidelines for treating simple cystitis and pyelonephritis also recommend fluoroquinolones as first-line treatment for patients with complicated pyelonephritis,
  2. However, our study found that fluoroquinolone antibiotics are not suitable for the initial treatment of Proteus mirabilis,

In view of the low response rates of Proteus mirabilis strains to sulfamethoxazole, levofloxacin, cefuroxime, and ceftriaxone in China, empiric antibiotic therapy for infections with Proteus mirabilis strains should use the more effective cefoxitin, amikacin, meropenem, imipenem, cefoperazone sulbactam, and piperacillin-tazobactam and should avoid the use of sulfamethoxazole, levofloxacin, and cefuroxime.

  • We also assessed seasonal patterns of urine-isolated Proteus mirabilis sensitivity to antimicrobials.
  • We found that the sensitivity of Proteus mirabilis isolates to cefuroxime and sulfamethoxazole showed a seasonal peak during winter, while levofloxacin sensitivity had a summer and winter peak.
  • Previous studies have demonstrated a temporal association between antibiotic prescription use and enterobacterial susceptibility in the community, although we could not examine this relationship in the current study,

The significant seasonal changes in levofloxacin sensitivity observed here are inconsistent with previous studies of Enterobacter isolated from the urine of patients in Australia, where the authors reported no seasonal changes in quinolone sensitivity in subjects from Tasmania,

  • However, Australia is more restrictive in prescribing fluoroquinolones than China, which may account for the conflicting results.
  • More recently, Martinez et al.
  • Demonstrated an association between ciprofloxacin sensitivity in community Enterobacter urine isolates and ciprofloxacin used during the preceding 3–6 months, suggesting that ciprofloxacin sensitivity is responsive to short-term changes in antibiotic use,

The seasonal variation in sulfamethoxazole sensitivity observed here is inconsistent with previous studies on the seasonal relationship between community antibiotic use and resistance in the United States. The authors suggest that sulfamethoxazole sensitivity is high during summer unlike during other seasons,

What is the drug of choice for Proteus mirabilis?

Medical Care – Cultures with susceptibility data are recommended, when available, to guide antimicrobial therapy. Most Proteus strains are susceptible to commonly used antibiotics, except nitrofurantoin and tetracycline. Like other members of Enterobacteriaceae, multidrug-resistant (MDR) strains of Proteus exist and are increasing in frequency; strains of P vulgaris generally are more resistant.

Uncomplicated UTIs in women can be treated on an outpatient basis with an oral quinolone for 3 days or trimethoprim/sulfamethoxazole (TMP/SMZ) for 3 days. Acute uncomplicated pyelonephritis in women can be treated with oral quinolones for 7-14 days, single-dose ceftriaxone or gentamicin followed by TMP/SMZ, or an oral cephalosporin or quinolone for 14 days as outpatient therapy. For hospitalized patients, therapy consists of parenteral (or oral once the oral route is available) ceftriaxone, quinolone, gentamicin (plus ampicillin), or aztreonam until defervescence. Then, an oral quinolone, cephalosporin, or TMP/SMZ for 14 days may be added to complete treatment. Complicated UTIs in men and women can be treated with a 10- to 21-day course of oral therapy (in the same manner as for hospitalized patients) as long as the follow-up is adequate.

Why do I keep getting Proteus mirabilis?

Transmission: – Urinary tract infections caused by P. mirabilis occur usually in patients under long-term catheterization. The bacteria have been found to move and create encrustations on the urinary catheters, Proteus mirabilis can enter the bloodstream through wounds.

Is Proteus mirabilis UTI serious?

These infections can also cause bacteremia and progress to potentially life-threatening urosepsis. Additionally, P. mirabilis infections can cause the formation of urinary stones (urolithiasis).

What is the first line antibiotic for Proteus mirabilis?

Treatment / Management – Empirical treatment for an uncomplicated UTI caused by P. mirabilis (much like other uncomplicated UTIs) involves outpatient treatment with either a 3-day course of trimethoprim/sulfamethoxazole (TMP/SMZ) or an oral fluoroquinolone (e.g., ciprofloxacin).

  • Acute, uncomplicated pyelonephritis can be treated on an outpatient basis with fluoroquinolones, although a regimen of 7 to 14 days is recommended.
  • An alternative to this treatment is a one-time dose of ceftriaxone or gentamycin followed by either TMP/SMZ, an oral fluoroquinolone, or cephalosporin for 7 to 14 days.

If a patient has a more severe condition or is in an inpatient setting, they may begin antibiotic therapy via intravenous administration of either ceftriaxone, gentamycin, fluoroquinolone, gentamycin plus ampicillin, or aztreonam until fever resolves.

At this point, they may switch to oral therapy with either cephalosporin, an oral fluoroquinolone, or TMP/SMZ for up to 14 additional days. If a patient presents with a complicated UTI (e.g., a man or woman with a history of an underlying condition that may increase the risk of failure of therapy), they may also be treated in an outpatient setting with oral antibiotics for 10 to 21 days as long as they receive adequate follow-up.

Proteus infection can be avoided with proper sanitation and hygiene, such as adequate sterilization of medical equipment and surfaces. Additionally, catheterization should be reserved for patients for whom there is no other option.

Why is Proteus mirabilis resistant to antibiotics?

Antibiotic Resistance in Proteus mirabilis: Mechanism, Status, and Public Health Significance – Journal of Pure and Applied Microbiology Review Article | Open Access 1 Department of Biology, Faculty of Applied Science, Umm Al-Qura University, Makkah, Saudi Arabia.2 Research Laboratories Unit, Faculty of Applied Science, Umm Al-Qura University, Makkah, Saudi Arabia.3 Al Hada Armed Forces Hospital, Ministry of Defense, Taif, Saudi Arabia.4 Department of Agricultural Microbiology, Faculty of Agriculture, Fayoum University, Fayoum, Egypt.5 Department of Agricultural Microbiology, Faculty of Agricultural Sciences, Aligarh Muslim University, Aligarh, 202 002, Uttar Pradesh, India. Article Number: 7897 | © The Author(s).2022 Received : 10 June 2022 | Accepted : 25 July 2022 | Published online : 24 August 2022 Issue online: September 2022 Proteus mirabilis is a specific opportunistic pathogen of many infections including urinary tract infections (UTIs). Risk factors are linked with the acquisition of multidrug-resistant (MDR) to 3 or more classes of antimicrobials) strains. The resistance in extended-spectrum alpha-lactamase is rare, but the rising resistance in extended-spectrum beta-lactamase (ESBL) producing strains is a matter of concern. β-lactamases and antibiotic modifying enzymes mainly constitute the ESBLs resistance mechanism by hydrolyzing the antibiotics. Mutation or Porin loss could lead to the reduced permeability of antibiotics, enhanced efflux pump activity hindering the antibiotic access to the target site, antibiotic failure to bind at the target site because of the target modification, and lipopolysaccharide mutation causing the resistance against polymyxin antibiotics. This review aimed to explore various antimicrobial resistance mechanisms in Proteus mirabilis and their impact on public health status. Proteus mirabilis, Antibiotic Resistance, Beta-lactams, Cephalosporins, Fluoroquinolones, Tetracyclines, Public Health Proteus mirabilis, belonging to the class Gammaproteobacteria and family Enterobacteriaceae, is a well-known rod-shaped Gram-negative bacteria that swarm across the agar plates to form characteristic bullseye-shaped motility.1 P. mirabilis strains representing 18 different species have been isolated from various geographical locations.2 P. mirabilis is found in multiple environments such as sewage, soil, water, and especially in the gastrointestinal tract of animals and humans.3 The patients having long-term indwelling catheters or complicated UTIs also suffer from the infection of this opportunistic pathogen.4 Several human infections are associated with this bacterium such as infections of the gastrointestinal tract, wounds, eyes, and UTIs especially catheter-associated urinary tract infections (CAUTI).5 Renal damage and the formation of kidney and bladder stones (urolithiasis) further complicate the P. mirabilis related UTIs and CAUTIs.6 In the urinary tract, P. mirabilis mainly forms two types of crystals including apatite and struvite (CaPO 4 and MgNH 3 PO 4 ), which prevent urine flow.7 The symptoms of P. mirabilis infections such as bacteriuria, acute pyelonephritis, catheter occlusion, and fever could further complicate into bacteremia and sepsis.8 CAUTI is quite common in nursing homes whereas bacteremia mostly occurs following CAUTI or UTI.P. mirabilis associated sepsis and bacteremia comparatively lead to a higher mortality rate than other infections.9,10 Antibiotics resistance exhibited in 48% P. mirabilis strains complicates the treatment of infections.11 The resistant strains are rising sharply and current therapies are becoming unable to cope with the situation. This scenario demands the urgent development of new antibiotic targets. Uropathogenic P. mirabilis might also be resistant to extended-spectrum beta-lactams, cephalosporins, fluoroquinolones, and aminoglycosides.11 P. mirabilis acquire genes encoding antimicrobial resistance via transferable plasmids, insertion sequences, transposons and integrons. Of these mobile genetic materials, integrons, which are not considered as transferable element, but are usually located on mobile plasmids, and play an important role in facilitating the horizontal gene transfer process of cassettes carrying resistance genes, i.e., integrons help incorporate gene cassettes encoding resistance to β-lactams, aminoglycoside and also plasmid-mediates quinolones resistance genes into recipient P. mirabilis cells (Figure 1).11 Integrons contain an integrase gene, attI (recombination site), and a promoter PC for the captured genes’ transcription.12 Integrons link with the mobile DNA elements (plasmids and transposons) to spread resistance determinants. The integrase gene sequence revealed five classes of integrons connected with resistance determinants.13 Integrons belonging to class 1 are mainly associated with MDR.14 Several antibiotic resistance determinants are present in Enterobacteriaceae strains, which are mediated by the integrons. Plasmid-mediated beta-lactamases gene coding and PMQR (quinolone resistance determinants) are complex integrons, which include ISCR1 and resistance genes through the duplication of the 3′ conserved region in addition to the variable part between 5′ and 3′ covered regions.15 Figure 1. Schematic diagram illustrating the role of integron in drug resistance acquisition in Proteus mirabilis Antibiotic resistance mechanisms in Proteus mirabilis Resistance to fluoroquinolones Fluoroquinolones are commonly used antibiotics in Western Europe, North America, and Japan to treat a broad range of infections including UTIs.16 European Antimicrobial Resistance Monitoring Network has reported significantly increased resistance to fluoroquinolones in Europe since 2001.17 Different fluoroquinolones resistance mechanisms have been identified including target enzyme modification in parC and parE encoded topoisomerase IV, gyrA and gyrB encoded DNA gyrase, and changes in the outer membrane to reduce drug accumulation through efflux pumps.18 Gram-negative organisms primarily target DNA gyrase whereas Gram-positive organisms target topoisomerase IV.19 gyrA is the essential target of fluoroquinolones in several Enterobacteriaceae species and its mutation is associated with fluoroquinolones resistance.20 Further mutations in DNA gyrase and topoisomerase IV cause higher resistance to fluoroquinolones.21 DNA sequence analyses have revealed the genetic characterization of mutations in clinical isolates. Quinolone resistance determining regions (QRDRs) have been reported to be extremely conserved.20 QRDRs linked with P. mirabilis resistance to fluoroquinolones exhibit substitutions in parC (S80) and gyrA (S83) whereas gyrB (S464) mutation could result in further higher fluoroquinolones resistance.22 QRDRs’ role in P. mirabilis resistance to fluoroquinolones is not well understood, which requires more data to elaborate its resistance mechanism. Levofloxacin-resistant P. mirabilis has been studied to investigate the fluoroquinolone resistance mechanism. The results depicted that parE (D420) and gyrA (E87) mutations are crucial for a higher resistance in P. mirabilis clinical isolates, which links ParE QRDRs and resistance to fluoroquinolones.18 Different spectroscopic techniques have been employed to identify new ciprofloxacin derivatives (hydroxamic acid, amide, and hydrazide) in addition to levofloxacin analogues. Some of these compounds exhibited significant efficacy against urease splitting P. mirabilis,23 Similar to the GyrA gene, the role of the ParC gene in ciprofloxacin resistance is also important. A couple of mutations in P. mirabilis GyrA and ParC genes could cause resistance to ciprofloxacin. Moreover, the percentage of quinolones resistance should be considered while aiming for other medical options. Therefore, drug susceptibility testing should be conducted for all patients with comparable infections before starting a specific medicine.24 The mutations in target enzymes ( GyrB (Ser-464) and ParC (Ser-80) codons) and AcrAB efflux pump were investigated in relation to P. mirabilis resistance against fluoroquinolones. However, any relationship between mutation numbers in ParC, GyrA, and GyrB genes and the degree of P. mirabilis resistance to fluoroquinolone was not observed. The role of efflux pumps in fluoroquinolones resistance has been estimated by measuring the minimum inhibitory concentrations (MICs) through an efflux pump inhibitor CCCP. The CCCP (12.5 mM) was integrated with Mueller Hinton agar. Fifty isolates with uninfluenced fluoroquinolones susceptibility in response to CCCP were selected from a total of 100 isolates and characterized in terms of MICs and genotype for Levofloxacin (Figure 2).18 Figure 2. Schematic overview of resistance mechanisms to fluoroquinolones in Proteus mirabilis Resistance to tetracyclines Several Gram-positive and Gram-negative bacterial infections are treated with tetracycline antibiotics but high tetracycline resistance rates in Enterobacteriaceae have been reported.25 Tetracycline resistance is presumed to be related to the efflux mechanism. The efflux resistance genes are often associated with the mobile elements such as the class A tetracycline resistance (tet) determinant that was the first to be identified from the RP1/Tn1721 system.26 Tigecycline (9-t-butylglycylamido derivative of minocycline) belongs to the novel class of tetracyclines that is used to treat Gram-negative bacteria.27 Klebsiella pneumoniae was the first tigecycline-resistant strain of Enterobacteriaceae with rpsJ mutation encoding Val57Leu on S10.28 Enterobacteriaceae tetracycline resistance is mostly considered to be linked with tet (A) to tet (E) gene determinants.29 P. mirabilis possesses a natural resistance against tetracycline that could be the main reason for its rising tolerance.30 The rise in acquired resistance of Enterobacteriaceae demands the development of new antibiotics to effectively treat bacterial infections. AcrAB efflux pump, which is a member of the resistance-nodulation-division (RND) superfamily is found in Enterobacteriaceae, This efflux pump has been reported to be involved in P. mirabilis resistance to tigecycline.31 AcrAB provides intrinsic resistance to several structurally diverse lipophilic compounds, antibiotics, dyes, and inclusive detergents.32 P. mirabilis is a notable exemption to tigecycline activity, which normally exhibits 4 µg/ml MICs in tests. A typical clinical isolate was selected to identify the mechanism of decreased tigecycline sensitivity. Two independent transposon insertion mutants were isolated and inserted into the P. mirabilis chromosome. The results revealed a correlation between AcrRAB gene expression and observed MIC changes in various P. mirabilis strains. The classical tetracycline resistance determinants could not affect the tigecycline, however, AcrAB efflux pump identification in P. mirabilis explained its decreased susceptibility to tigecycline. Fortunately, the study did not report a direct threat of spreading tigecycline resistance.33 Nontoxic carbon nanoparticles could inhibit Gram-negative bacterial growth when integrated with tetracycline. This combination has generated tenfold higher activities against tetracycline-resistant bacteria as compared to solely tetracycline. The tetracycline-conjugated carbon nanoparticles could inhibit the efflux mechanism of bacteria. Tetracycline is supposed to direct nanoparticles into efflux pumps to block and inhibit their normal functioning. Qin et al.34 have conducted a study to acquire tigecycline, tetracycline, and colistin-resistant P. mirabilis for NDM-1 Plasmid and further characterized PM58 isolate. Molecular investigation elaborated that the PM58 chromosome contains a novel Salmonella genomic island 1 and conjugative NDM-1 plasmid.34,35 Resistance to β-lactams Lactamase genes are absent on the P. mirabilis chromosome whereas β-lactamase production includes AmpC β-lactamases and broad-spectrum β-lactamases.36 Gene cassette sequence analysis could not relate the resistance patterns and gene cassette content. The resistance patterns to beta-lactam antibiotics were more diverse than depicted by integrin-embedded cassettes. Gene screening revealed the presence of bla TEM genes in both genomes. bla TEM-2 encoding beta-lactamases are effective against early cephalosporins and penicillin. Thus, they could not be attributed to ESBL phenotype. Ye et al.37 have reported the involvement of another enzyme in ESBL-positive strains.P. mirabilis is known to possess CMY-2-like AmpC β-lactamases encoding genes, which facilitate to resist against cephamycins and cephalosporins. bla CMY sequence has been reported to conform with P. mirabilis bla CMY-15, Ahn et al.38 have reported chromosome-borne genes coding for MY-15 in P. mirabilis strains in Poland. Colistin serves as a last-resort drug against MDR Gram-negative bacterial infections.P. mirabilis is naturally resistant to colistin due to the presence of the mcr genes, which are mediated by the plasmid. This bacterium can transmit these genes to other bacteria, which are susceptible to colistin.39 ESBL enzyme production confirms the wide-spectrum β-lactam antibiotic resistance. However, the presence of these genes does not necessarily generate phenotypical aspects of ESBLs as reported in several studies.40 Initially, the CTX-M gene appears in combination with the TEM gene but as the predominant gene spreads it replaces others. The selective pressure posed by the antibiotics misuse might provide a favorable environment for the diffusion of ESBLs among Enterobacteriaceae (Figure 3).41 Figure 3. Illustrative diagram of resistance mechanisms to β-lactams and cephalosporins exhibited by Proteus mirabilis Resistance to cephalosporins Cephalosporins are widely prescribed to treat respiratory, abdominal, and urinary infections. Such broad-scale utilization leads to significant selection pressure on Enterobacteriaceae members for resistance. Cephalosporins resistance is either associated with the higher chromosomal ‘ AmpC ‘ b-lactamases production in Enterobacter spp. or transferable ESBLs.42 During a study in China, 2288 clinical isolates (non-repetitive) were collected from five laboratories in four cities to establish cefoselis epidemiological cut-off values (ECOFFs). Disc diffusion and broth micro-dilution methods based on European Committee on Antimicrobial Susceptibility Testing (EUCAST) guidelines were followed to determine MICs of Cefoselis and diameters of isolates inhibition zones. MIC ECOFFs were estimated through visual assessment and ECOF Finder software. Distributed cefoselis MICs ranged between 0.008 to >256 mg/L whereas MIC ECOFFs value was noted as 0.125 mg/L.P. mirabilis zone diameter ECOFF was observed as 26 mm.43 bla CTX, bla OXA-1, tetA, bla CTX-M, and sul1 genes were encoded for cephalosporins-resistance.44, 45 P. mirabilis isolates exhibited significant resistance (57.1%) to Cephalosporins (ceftazidime and cefotaxime).45 P. mirabilis strains are not frequently found in pneumonia patients but they can cause airborne acute infection of the lower airways (pneumonia) or infections that are transferred through the bloodstream from one body part to others.46 Cefepime, an antimicrobial agent that is administered to treat pneumonia patients, was found to be the most effective among six antibiotics used against severe Gram-negative bacterial infections.47 Several studies have confirmed the clinical efficacy of cefepime against drug-resistant organisms.48 However, the efficacy of ceftazidime has reduced over the past decade because of the extraordinary rise in microbial resistance.49 Cefotaxime is used against both types of bacteria (Gram-positive and Gram-negative) but P. mirabilis resistance to cefotaxime has been reported.50 Cefuroxime was found to display better efficiency against rod-shaped Gram-negative bacteria than cephalosporins (first-generation).51 have concluded that carbapenemase genes were not involved in the development of resistance in cephalosporin-resistant strains. The mutations in porin and protein of the outer membrane leading to low antibiotic permeability might have contributed to the resistance of cephalosporin-resistant strains.52 ESBL confirmatory tests revealed that 15 out of 50 cephalosporin-resistant Enterobacteriaceae were ESBL negative depicting that these strains might have acquired cephalosporin resistance via other mechanisms.53 The fosA gene mediated by plasmid could be transferred amidst Enterobacteriaceae species and fosA3 has been reported in 90% of E. coli isolates, which produces ESBL to resist fosfomycin (FOM).54,55 parC, gyrA, and fosA3 mutations might induce resistance to quinolone and further lead to high cross-resistance against fosfomycin (FOM), levofloxacin (LVX), and cephalosporin in UTI-causing bacteria. Ishii et al.56 have reported considerable gyrA and parC mutations based cross resistance of UTI causing bacteria to levofloxacin whereas the presence of fosA3 was linked to fosfomycin resistance. (Figure 3).56 Resistance to aminoglycosides Broad-spectrum aminoglycosides antibiotics are primarily produced through Actinomyces species to treat Gram-negative and Gram-positive bacteria.57 Aminoglycosides have served as successful antibiotics but the resistance and toxicity aspects have hindered their application.58 However, they can still be efficiently used to counter MDR bacterial species.57 Mechanisms of aminoglycoside resistance and aminoglycoside-modifying enzymes (AMEs) have been detected frequently in bacteria.59 AMEs initiate resistance by changing aminoglycoside molecules at specific positions. Based on the modifications, these enzymes are known as aminoglycoside acetyltransferases (AACs), phosphotransferases (APHs), nucleotidyltransferases, and adenyltransferases (ANTs).60 The mobile agents such as plasmids, integrons, or transposons carry the AME coding genes, which often integrate with other resistance mechanisms.57 Recently, 16S ribosomal RNA (rRNA) methyltransferases have been used to code the aminoglycoside-resistance mechanism as these enzymes contain an aminoglycoside linking site in the ribosome to produce higher resistance against all clinically available aminoglycosides.61 Sometimes, the isolates already containing β-lactamases or Metallo-β-Lactamase (MBLs) carry 16S rRNA methyltransferases encoding genes.62 Alteration of membrane protein and ribosome, and raised efflux could be the other mechanisms of aminoglycoside resistance. However, these mechanisms are less spread as compared to AMEs.63 Plazomicin aminoglycoside (semi-synthetic) is obtained from sisomicin. The modifications in the plazomicin molecule structure make it resistant to AMEs-based alterations.64 Carbapenems are highly effective antimicrobial agents to cure hospital-acquired infections (HAIs). However, the development of carbapenemases (GES, VIM, KPC, IMP, OXA-48, and NDM) based resistance has limited their utility.65 Carbapenemases encoding genes are commonly found in plasmids and they might also contain AMEs encoding genes.66 AMEs-based enzymatic inefficiency is common aminoglycosides resistance mechanism followed by 16S rRNA methylation that also imparts significantly higher resistance against gentamicin, tobramycin, and amikacin.67 The studies have reported multiple isolates harbouring bla KPC-2, bla NDM-1, and AMEs encoding genes. The literature depicts the Klebsiella pneumoniae carbapenemase (KPC) insistence over the years that led to the emergence of a new carbapenemase known as NDM. The relationship of bla KPc-2 and bla NDM-1 genes and their association with AME genes in P. mirabilis isolates has been described (Figure 4). This association demonstrates a fast P. mirabilis evolution to obtain and preserve different genes, which urgently require further in-depth elaboration.68 Figure 4. Schematic overview showing aminoglycosides resistance mechanisms in Proteus mirabilis Status of Proteus mirabilis resistance to various antimicrobial agents The first report of ESBL-based resistance in Proteus species emerged in 1987.69 P. mirabilis isolates capable of producing ESBL are now more frequently detected in clinical settings. A study in France (1988 to 1990) revealed the presence of only 0.8% ESBL producing P. mirabilis strains, which has increased up to 6.9% and 9.5% in France and the USA, respectively.70-72 The isolation of ESBL-producing P. mirabilis strains reached 8.8% during 1997–1999.73 An Italian survey in 1999 ranked P. mirabilis as the second-highest ESBL producer in Enterobacteriaceae,74 In France, urine samples of 3340 patients were found positive for P. mirabilis from 1997 to 2002 whereas 45 (1.3%) patients were infected with extended-spectrum b-lactamases producing P. mirabilis,75 In Japan, 45.6% of the P. mirabilis strains were found to produce ESBL during 2009-2010.76 European Committee on Antimicrobial Susceptibility Testing revealed that74% of isolates were resistant to penicillin in 2010 whereas 1.23% of P. mirabilis strains were resistant to third-generation cephalosporins.77,78 In 2019, 8.4% of P. mirabilis isolates were noted to be resistant to various antibiotics such as ciprofloxacin, amoxicillin, gentamicin, amoxicillin/clavulanic acid, and cefotaxime.28.6% of these isolates possessed ESBL genotype ( bla CTX-M-2 ) whereas 71.4% had AmpC/ESBL genotype ( bla CMY-2 /bla TEM-1 ).79 Recently (i.e.2020), 37% of strains produced ESBLs and all ESBLs-producing isolates contained bla TEM, These isolates were susceptible to cefotaxime/clavulanic, cefoxitin, and imipenem.80 Levofloxacine (LVX) resistance average has gradually increased between 2000 and 2005 and a continuous high prevalence (17.5%) has been reported in Europe and Japan since 2004.81,82 Similarly, a high spreading rate (37.0%) of cefotaxime (CTX)-resistant P. mirabilis strain was also noted in 2004. The rise in CTX-resistant P. mirabilis up to 45.6% is comparable to that reported in Japan between 2009 and 2010, 76 whereas the spread of FQ-resistant P. mirabilis strain increased to 17.5% in Japan.18 In 2014, the ciprofloxacin resistance in uncomplicated UTIs in some European countries was reported as Germany (20.3%), France (4.8%), Sweden (7.3%), Spain (30.8%), and the UK (15.3%).83 P. mirabilis resistance rate against a novel antimicrobial agent glycylcycline reached up to 13% in Germany in 2016 47,51 whereas P. mirabilis resistance to imipenem (3.6%) and meropenem (4%) has also been reported in Iran.84 Similarly, decreased efficacy of imipenem (61.5%, 90.9) and ceftazidime-avibactam (72.7%, 93.8%) has been noticed in Canada for ESBL as compared to non-ESBL-producing Enterobacteriaceae in 2015. The situation has led to the lower response of complicated UTI patients to imipenem and ceftazidime-avibactam.85 Problems and Future Concerns The ability of Proteus mirabilis to colonize and form crystalline multidrug-resistant (MDR) biofilms is a major reason for recurrent CAUTIs.86 Multidrug resistance (MDR) in the clinical isolates P. mirabilis is leading to public health anxiety and serious wildlife implications. Therefore, wildlife’s role in spreading resistance to antimicrobials has become a main topic of interest for researchers.87 Several studies have been conducted to understand the P. mirabilis ability to produce swarm cells but it remains unclarified. Peng et al.88 have reported that the swarming migration of the P. mirabilis strain is a rare feature.88 A recent study has revealed the appearance of infectious diseases and the mcr-1gene (colistin-resistant) in MDR Enterobacteriaceae in the Syrian refugee camps’ sewage water.89 These findings further elevate concerns about the health and sanitary conditions in Syrian camps. Similarly, mcr-1 gene has been detected in P. mirabilis samples collected from sewer and domestic waters of Lebanon’s war refugee camps. These results are alarming as P. mirabilis association with healthcare and community infections has already been established. Furthermore, the mcr gene encodes colistin resistance that serves as a last-resort antibiotic to treat complex Gram-negative bacterial infections.39

  • CONFLICT OF INTEREST The authors declare that there is no conflict of interest.
  • AUTHORS’ CONTRIBUTION All authors listed have made a substantial, direct, and intellectual contribution to the work, and approved it for publication.
  • FUNDING None.
  • DATA AVAILABILITY All datasets generated or analyzed during this study are included in the manuscript.
  • ETHICS STATEMENT This article does not contain any studies with human participants or animals performed by any of the authors.
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© The Author(s) 2022. Open Access, This article is distributed under the terms of the which permits unrestricted use, sharing, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

What kills Proteus bacteria?

Since Proteus mirabilis is a form of bacteria, infections caused by Proteus mirabilis are usually treated using antibiotics. Antibiotics are used to kill bacteria in the body.

Does amoxicillin treat Proteus mirabilis?

Amoxicillin is not the first choice to treat the infections against Proteus mirabilis and Staphylococcus aureus because they showed resistance 96.1% and 61.3% against Proteus mirabilis as compare to tetracycline is the first choice to treat infection which is caused by Staphylococcus aureus and Proteus mirabilis

Where is Proteus mirabilis found in the body?

Proteus species are most commonly found in the human intestinal tract as part of normal human intestinal flora, along with Escherichia coli and Klebsiella species, of which E coli is the predominant resident. Proteus is also found in multiple environmental habitats, including long-term care facilities and hospitals.

What foods can cause Proteus mirabilis?

An outbreak of Proteus mirabilis food poisoning associated with eating stewed pork balls in brown sauce, Beijing , March 2010, Pages 302-305 Proteus mirabilis, which is widely distributed in soil and water in the natural environment, is a member of the Enterobacteriaceae family of Gram-negative bacilli and resides in normal flora of human gut. Though approximately one quarter of the human population have P.

mirabilis in their feces (Mansy et al., 1999), it still give rise to opportunistic infections through the urinary tract and wounds resulting in septicemia. In addition, it can also cause food poisoning when consumed in contaminated food such as meat, vegetables, and seafood. A few cases of food poisoning caused by P.

mirabilis have been reported in the last several decades (Gritsenko et al., 1970, Petrilia, 1964, Tomasoffova et al., 1965, Zietze, 1984, Cooper et al., 2005). An outbreak of food poisoning involving 13 persons occurred in Beijing in August 2008. We began an immediate investigation to ensure proper treatment of the ill persons, identified and interviewed the persons exposed to the implicated food, and obtained clinical and food samples for laboratory testing.

  • An epidemiological investigation and microbiological testing indicated that a meal of Stewed Pork Balls in Brown Sauce was the probable source.
  • The 13 patients and the remaining 107 unaffected persons were interviewed with a standard questionnaire requesting information on clinical symptoms (fever, abdominal pain, diarrhea, vomiting) and food history.
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Based on the interview results, a case-control study including 13 patients and 107 controls was conducted. Odds ratios (ORs) from univariate analysis were calculated by using maximum-likelihood estimates, including 95% exact confidence intervals (CIs) by the Fisher exact test (Epi-Info On August 4, 2008, around 17:00 o’clock, 120 consumers had dinner in a restaurant in Beijing.

After 40 min, one consumer started to have abdominal pain, vomiting, and diarrhea, followed by 13 cases with similar symptoms until August 5. All 13 patients were identified as consumers at the restaurant between August 4 and 5, 2008 (Fig.1). The incubation period was 0.67–9 h and the attack rate was 10.8%.

All patients were male, whose median age was 23 years old (range 19–30 years old). The clinical The authors are grateful to Dr. Xuejie Yu in the Department of Pathology, the University of Texas Medical Branch at Galveston for reviewing the manuscript. This work was supported by grants from the Chinese Ministry of Science and Technology 863 Project (No.2007AA02Z144) and the Beijing Natural Science Foundation (No.7002033).

K.E. Cooper et al. V.K. Gritsenko et al. Z. Hu et al. X. Liu et al. X. Liu et al. M.S.M. Mansy et al.

The role of Proteus mirabilis on food safety has not been investigated before. Three P. mirabilis strains (swupm1, swupm2 and swupm3) isolated from fresh-cut fruits were shown to vary in swarming motility, with strains swupm1 and swupm2, but not swupm3 exhibiting the characteristic bull’s-eye phenotype. Strains swupm1 and swupm2 grew faster and produced stronger biofilm than swupm3. These strains were all multidrug resistant and exhibited high virulence in Galleria mellonella (100% mortality at around 100 CFU inoculum) with swupm1 being the most virulent one.P. mirabilis was shown to be able to survive in fresh-cut cantaloupe at 4 °C and facilitate the growth of other bacteria. At 25 °C, P. mirabilis could significantly accelerate the decay of fresh-cut fruits. Headspace gas chromatography–ion mobility spectrometry (HS-GC-IMS) analysis showed that P. mirabilis strain swupm1 could cause dramatic changes in the volatile components of fresh-cut cantaloupe, such as ethyl acetate, ethanol and formic acid. This study indicates that P. mirabilis can accelerate the decay of fresh-cut fruits and that the virulence level of these strains seems to be closely associated with the adverse effect of such strains on food quality. Proteus mirabilis is an important pathogen involved in human urinary tract infections, and also more isolated from stools of patients with diarrheal disease than from healthy patients. The role of food, especially poultry products as source for human infection and multi-resistant strains remains unclear. As a resident in broilers’ intestines, P. mirabilis can contaminate broiler carcasses due to slaughter practices, and be a risk for human infection. The present study evaluated the performance of five isolation media, and subsequently examined the presence of P. mirabilis on broiler carcasses at retail. Additionally, isolates were characterized by the Dienes’ test, repetitive element PCR fingerprinting and pulsed-field gel electrophoresis, and their antibiotic resistance profile determined. Using a combined isolation protocol on blood agar, xylose lysine deoxycholate agar and violet red bile glucose agar, P. mirabilis was isolated from 29 out of 80 broiler carcasses (36.25%) with a mean contamination level of 2.25 ± 0.50 log 10 CFU/g. A high strain heterogeneity was present in isolates from broilers and human stool. The same strains were not shared, but the antibiotic resistance profiling was similar. A role of poultry products as source for human infection should be taken into account. Proteus mirabilis is the second most common cause of urinary tract infections after Escherichia coli, Due to the recent increase in the prevalence of this microorganism, this study aimed to evaluate the genetic linkage among P. mirabilis isolated from patients suffering from UTI. A total of 292 urinary samples were collected from January to June 2018. Using routine microbiological and biochemical methods, 60 P. mirabilis isolates were isolated, all of which were subjected to the ERIC-PCR method to analyze their genetic linkage. All 60 P. mirabilis isolates were typeable by ERIC-PCR technique and the genetic fingerprints showed a total of seven clusters (A–G) with cluster C being the predominant one. Only two strains () were grouped in G cluster. Strains 3 and 27 had also the same banding patterns and were grouped into the B cluster. These results indicated the genetic diversity of the studied clinical P. mirabilis isolates. ERIC-PCR showed to be an appropriate fingerprinting technique for P. mirabilis isolates, which can be used for epidemiological studies and infection control strategies. The microbial risk involved with natural food fermentation is largely unknown. Here, we report the prevalence of enteric bacterial pathogens in the traditional fermented foods marketed in Northeast region of India. A total of 682 samples of 39 food types (broadly categorized into fermented soybean, bamboo shoot, fish, milk and pork products) collected over four different seasons from seven states of India were analyzed in this study. Cultivation-independent analysis by MiSeq amplicon sequencing of V4-V5 region of the 16S rRNA gene showed the bacterial community structure in the foods. Among the WHO prioritized foodborne bacterial pathogens, we detected the prevalence of phylotypes related to Clostridium botulinum, Bacillus cereus, Staphylococcus aureus, Clostridium perfringens, Listeria monocytogenes, and Escherichia coli in these ethnic foods. We also observed the occurrence of other well known human enteric pathogens like Proteus mirabilis, Clostridium difficile, and Yersinia enterocolitica, Further pathogen-specific qPCR assays confirmed a higher population (>10 7  cells/g) of B. cereus, P. mirabilis, and a C. botulinum related phylotype in the fermented soybean, fish, and pork products. We noticed a general trend of higher pathogen occurrence during the colder months without any seasonal variation of total bacterial load in the fermented foods. Further qPCR analysis on toxigenic and pathogenic potential, and toxins production by immunoassays showed that all the soybean samples and the isolated B. cereus cultures were positive for diarrheal toxins (Nhe and Hb1), and nearly half of the samples were positive for emetic toxin (cereulide). Similarly, the food samples and associated swarming P. mirabilis cultures were positive with the pathogenic factors like hemolysin ( hpm ), urease ( ure ) and multidrug resistance. However, we could not confirm the presence of botulinum neurotoxin (toxins A, B, E, and F) in the C. botulinum positive food samples. This is the first baseline data of the enteric bacterial pathogens prevalent in the traditional fermented foods of India, which will support the sustained effort of WHO to estimate the global foodborne disease burden. The unusual presence of P. mirabilis in the fermented foods marketed in the Indian region with high incidence of urolithiasis cases is a concern. Our study emphasizes the need of the hour to have a coordinated action to control and prevent the spread of enteric bacterial pathogens through fermented foods marketed in India. Moreover, replacing the indigenous process with a defined starter culture based controlled fermentation will enhance the safety of Indian fermented foods. Diseases caused by opportunistic pathogens have been generally overlooked where a pathogen causes mild clinical signs with sporadic mortality at the farm level. Here, we identified an opportunistic Gram negative bacterium, Proteus mirabilis, from Indian major carp, Labeo rohita, exhibiting disease and mortality in the culture farm and subsequently confirmed for its virulence in experimental challenge study. The bacterium was identified as P. mirabilis based on phenotypical, biochemical characters and 16s rDNA PCR followed by virulence/species specific gene PCRs targeting urease, metalloprotease and haemolysin genes. Experimental challenge of healthy rohu juveniles with 10 7  cfu/fish reproduced the clinical signs and caused 100% mortality within 3 days of challenge. The affected fish, as well as the experimentally infected fish exhibited haemorrhages on the body along with red patches over the operculum and lower abdomen before dying. Histopathological analysis of the posterior kidney of infected rohu revealed significant renal damage showing massive glomerular congestion, focal periglomerular necrosis and periglomerular mononuclear aggregation. Skin tissues showed massive inflammatory reaction in epidermis, dermis, and myositis below the dermal layer. Further, the presence of amplicons for integrons I and II was also determined by concurrent analysis, thus implying significant horizontal stability and mobility in the gene capture system of this isolate along with enhanced resistance to antibiotics. This isolate was found to be multi-drug resistant showing resistance to 10 classes of antibiotic groups. Phylogenetic analysis based on 16s rRNA gene revealed its close association with other reported P. mirabilis from different locations with common ancestry and formed a distinct cluster along with other Proteus species. This study seems to be first record of sole involvement of MDR P. mirabilis causing mortality in fish farm, which was mostly considered as a favourable microbe in aquaculture systems. Foodborne bacteria are some of the most important human pathogens and can cause many diseases. In this study, multiplex PCR amplification combined with microchip electrophoresis (MCE) was studied to simultaneously and sensitively detect Staphylococcus aureus, Proteus mirabilis, and Enterobacter sakazakii, In order to simultaneously and accurately detect the aim bacteria, three pairs of primers were specially designed for the multiplex PCR amplification of the target genes of three bacteria, which were the specific genes corresponding to these bacteria respectively. After the DNA fragments of three bacteria were simultaneously extracted, the multiplex PCR amplification was performed by adding the three pairs of specific primers in the mixed DNA fragments solution. The multiplex PCR products of the three food-borne pathogens were analyzed by MCE and the limits of detection of target DNA fragments were 1.2–2.2 ng μL −1, (S/N = 3). The limits of detection of the aim bacteria were calculated as 53 CFU mL −1 for Enterobacter sakazakii, 32 CFU mL −1 for Proteus mirabilis, 28 CFU mL −1 for Staphylococcus aureus, respectively. Satisfactory results were obtained when this method was applied to detect the three foodborne bacteria in milk samples. The experimental results show that this method has the advantages of quickness, less sample consumption, high selectivity and high sensitivity.

Salmonella enterica is a well-known pathogen commonly acquired from the consumption of contaminated food. It has been estimated to affect millions of humans and cause hundreds of thousands of deaths per year globally. Pork, one of the most commonly consumed meats worldwide, has been identified as one of the main sources of human salmonellosis. In this study, we aimed to detect and characterize S. enterica from slaughtered swine and generate antimicrobial resistance profiles of select isolates. Tonsils and jejunum with mesenteric lymph nodes (MLN) were collected from a total of 240 swine from eight abattoirs (five accredited and three locally registered abattoirs) across Metro Manila.S. enterica were isolated using conventional culture methods and confirmed by PCR amplification of the invA gene. Isolates were further characterized based on somatic antigen by multiplex PCR. We report that there is no significant difference (P = 0.42) between the incidences of S. enterica in swine slaughtered in accredited (44.0%) and in locally registered abattoirs (46.7%). Most samples were contaminated with S. enterica under serogroup O:3,10. Antimicrobial susceptibility testing of 183 isolates using the VITEK ® 2 system revealed high resistance to ampicillin (67.8%) and trimethoprim/sulfamethoxazole (80.3%). Multidrug-resistance was found in 124 (67.8%) isolates. Proteus penneri is an opportunistic pathogen, which may cause severe diseases, most frequently urinary tract infections in immunocompromised patients.P. penneri Br 114 exhibiting a good swarming growth ability as an S-form strain was isolated from a wound of a patient in Łódź, Poland. Serological studies using ELISA and Western blotting and chemical analyses along with 1 H and 13 C NMR spectroscopy showed that the O-antigen (O-polysaccharide) of this strain is unique among the known Proteus serotypes O1–O79. It possesses a linear pentasaccharide repeating unit containing a partially O-acetylated amide of d -glucuronic acid (GlcA) with l -serine having the following structure: These data are a basis for creating a new Proteus serogroup, O80, so far represented by the single Br 114 isolate. The O80 is the 21st O-serogroup containing P. penneri strains and the fourth serogroup based on Proteus spp. clinical isolates from Łódź, Poland. The objective of this study was to investigate the molecular characteristics and horizontal transfer of florfenicol resistance gene-related sequences in Proteus strains isolated from animals. A total of six Proteus strains isolated from three farms between 2015 and 2016 were screened by polymerase chain reaction (PCR) for known florfenicol resistance genes. Proteus cibarius G11, isolated from the fecal material of a goose, was found to harbor both cfr and floR genes. Whole genome sequencing revealed that the strain harbored two copies of the floR gene: one was located on the chromosome and the other was located on a plasmid named pG11-152. Two floR -containing fragments 4028 bp in length were identical and showed transposon-like structures. The cfr gene was found on a plasmid named pG11-51 and flanked by a pair of IS 26 s. Thus, mobile genetic elements played an important role in floR replication and horizontal resistance gene transfer. Therefore, increasing attention should be paid to monitoring the spread of resistance genes and resistance in real time. Proteus mirabilis is ubiquitous in soil and water. It is an important catheter-associated urinary tract pathogen and has reportedly been associated with antimicrobial-resistant infections. This study reports the draft genome of a multidrug-resistant P. mirabilis isolated from raw retail chicken meat in Singapore. The P. mirabilis strain was isolated on Brilliance TM ESBL Agar and was screened for antimicrobial susceptibility against 29 antimicrobial agents using a MicroScan® Neg MIC Panel Type 44. The double-disk synergy test (DDST) was used for confirmation of extended-spectrum β-lactamase (ESBL) production. Genomic DNA from the pure culture isolate was extracted and was sent for sequencing based on Illumina HiSeq 2500 technology. Further bioinformatics analysis was performed using online tools available at the Center for Genomic Epidemiology. Species identification of the isolate was performed by KmerFinder. Antimicrobial susceptibility testing of the isolate showed multidrug resistance to broad-spectrum β-lactams, fluoroquinolones and aminoglycosides, among others. ESBL production was confirmed by the DDST. A total of 29 antimicrobial resistance genes were detected by ResFinder. To the best of our knowledge, this is the first report of the whole-genome sequence of a multidrug-resistant P. mirabilis producing an ESBL from raw chicken meat in Singapore. This indicates that raw meat in Singapore can be a reservoir for drug-resistant pathogens. This study was designed to investigate the antifungal activity of Bacillus pumilus 344-3 against toxigenic fungi. In vitro co-incubation assay revealed that A. carbonarius AC82, A. niger AN8 and P. digitatum PD43 are most sensitive fungi to bacterial antifungal compounds with zone of inhibition of 29.2 mm, 27.7 mm and 27.1 mm, respectively. The addition of Bacillus pumilus 344-3 culture supernatant at low concentration in the fungal growth medium stimulated A. carbonarius biomass, but inhibited ochratoxin A (OTA) synthesis significantly ( p ≤ 0.05). Conidial germination of A. carbonarius was not affected in a medium containing 10% and 20% of the bacterial culture supernatant, while it was completely inhibited in 100% bacterial extract. Storage of bacterial culture supernatant at temperature ranging from −20 °C to 100 °C for 1 h, didn’t affect its antifungal potential. In vivo application of bacterial extract on the maize kernels, showed 95% protection against A. carbonarius infection. Application of B. pumilus 344-3 culture supernatant on the surface of maize kernels provided 99% reduction in OTA production potential of A. carbonarius AC82. Because of its strong activities against the growth of A. carbonarius AC82 and OTA-synthesis, B. pumilus 344-3 can be considered as a very promising biocontrol agent. Urinary tract infections (UTIs) are common nosocomial infections. Proteus mirabilis is a frequent cause of these infections in individuals with abnormal urinary tracts or using indwelling catheters (CAUTIs). Since most research on non- E. coli uropathogens has been conducted on P. mirabilis, this organism serves a model of pathogenesis for these types of infections. To establish and infect the urinary tract, P. mirabilis must possess virulence factors to adapt to the local environment and to evade the host immune response. The virulence factors known to be involved in UTIs caused by P. mirabilis include adhesins, motility, biofilm formation, immunoavoidance, toxins and nutrient acquisition. The annotation of the P. mirabilis genome and transcriptome profiling have allowed for better understanding of the disease process caused by this bacteria in the urinary tract. This chapter reiterates previous works discussed in the first edition and introduce current research being performed on this uropathogen.

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: An outbreak of Proteus mirabilis food poisoning associated with eating stewed pork balls in brown sauce, Beijing

Is Proteus mirabilis rare?

3. Discussion – Native valve infective endocarditis is a relatively rare pathology accounting for 2 to 10 cases per 100,000 people per year, Staphylococcus aureus is the most common cause of IE with a nearly 30% occurrence rate, followed by Streptococcus viridans at nearly 20%, other streptococci at 17.5%, and enterococci at 10.5%.

  1. These organisms account for approximately 80–90% of all cases of IE,
  2. Gram-negative bacteria, such as Escherichia coli, can cause bacteremia, however, rarely cause IE.
  3. Proteus spp are Gram-negative bacilli and facultative anaerobes that are part of the Gammaproteobacteria bacterial lineage and are often associated with urinary tract infections, not IE,P.

mirabilis possesses a number of different virulence factors including fimbriae and urease which allow it to evade the host immune system, This high virulence may explain how P. mirabilis bacteremia may lead to IE, According to a recent systematic review in 2020, there are only 16 cases of IE secondary to Proteus spp,

There is also another recent case reporting multivalvular IE, All of these cases were in patients who presented with bacteriuria. Our case demonstrates a patient with a rare causative organism for IE with P. mirabilis, and it is the first known presentation without a concurrent UTI or asymptomatic bacteriuria.

The clinical cure rate, based on this 2020 systematic review, is noted at 62.5%, and mortality was 43.8%, Our patient was treated with meropenem and ultimately deescalated to ceftriaxone and ciprofloxacin. Repeat blood cultures returned negative four days after initiating antibiotic therapy and remained negative.

The patient was successfully discharged on IV antibiotics for five more weeks. There are case reports about systemic infection related to AICD placement. The risks of systemic infections due to AICD cannot be overlooked in this case. This risk ranges from 1.7–4% in 6 months to 2 years, respectively. These cases are more related to subcutaneous infection rather than endocarditis.

AICD leads are located in the right atrium and ventricle of the heart. This patient’s infection is likely unrelated to AICD as he had no evidence of subcutaneous infection and simply by location of the vegetation in the aortic valve. Additionally, there was no evidence of the vegetation on the AICD leads.

Can Proteus be cured?

Proteus syndrome results from assymetric and patchy overgrowth of various tissues including bones and connective tissues. Most of the time there are no signs at birth. The overgrowth is usually not cancerous but can cause significant medical issues related to function, appearance and compression of blood vessels and organs.

Is Proteus mirabilis normal in urine?

Proteus mirabilis urinary tract infection and bacteremia: Risk factors, clinical presentation, and outcomes , June 2012, Pages 228-236 Author links open overlay panel,,,,, Under an Elsevier open archive Proteus mirabilis is a common pathogen responsible for complicated urinary tract infections (UTIs) that sometimes causes bacteremia. Most cases of P. mirabilis bacteremia originate from a UTI; however, the risk factors for bacteremia and mortality rates from P. mirabilis UTI have not been determined. A retrospective, case-control study was performed between May 2008 and November 2010 to identify the risk factors and markers for P. mirabilis bacteremic UTI. Each subject in the case group (all patients were diagnosed with P. mirabilis bacteremia from a urinary tract source) was matched by age and gender to two subjects in the control group (patients diagnosed with P. mirabilis UTI but with negative blood culture results). Clinical presentation and laboratory data were analyzed to determine the risk factors and markers of P. mirabilis bacteremic UTI. Sixty-seven bacteremic UTIs and 124 nonbacteremic UTIs were included in this study. Community-acquired infection ( p = 0.017), hydronephrosis ( p = 0.017), band neutrophils accounting for >10% of the white blood cell count ( p = 0.001), hyperthermia or hypothermia ( p = 0.047), and a serum C-reactive protein concentration >100 mg/L ( p = 0.002) were identified as independent risk factors for P. mirabilis bacteremic UTI. Seventeen patients died in hospital, including 11 in the bacteremic group and 6 in the nonbacteremic group. The bacteremic group had a higher mortality rate ( p = 0.016). Bacteremic UTI ( p = 0.049), shock ( p = 0.014), and a low body mass index (BMI) 2 ( p = 0.033) were identified as independent risk factors for mortality. Because bacteremic P. mirabilis UTIs are associated with higher mortality, clinicians should carefully manage cases that present with the risk factors for bacteremia, including community-acquired infection, hydronephrosis, band neutrophils accounting for >10% of the white blood cell count, hyperthermia or hypothermia, and a high level of C-reactive protein.

Bacteremia Multidrug resistance Proteus mirabilis Urinary tract infection

Copyright © 2012 Published by Elsevier Taiwan LLC. : Proteus mirabilis urinary tract infection and bacteremia: Risk factors, clinical presentation, and outcomes

Does Proteus mirabilis UTI smell?

Proteus mirabilis Proteus mirabilis is a Gram-negative, rod-shaped, motile bacterium that produces high levels of urease, a protein that hydrolyzes urea to ammonia.P. mirabilis can be detected in the lab by its unique characteristic to swarm when grown on agar plates. Additionally, this bacterium gives off a strong fishy odor.

Is Proteus mirabilis a kidney infection?

I. Introduction – Proteus mirabilis, a Gram-negative rod-shaped bacterium, is well-known for its urease production and distinctive ability to differentiate into elongated swarm cells and characteristic bull’s-eye pattern of motility on agar plates.P.

Mirabilis belongs to the class Gammaproteobacteria, and has long been recognized as a member of the order Enterobacteriales, family Enterobacteriaceae, However, one group recently created a reconstructed phylogenetic tree based on shared core proteins, ribosomal proteins, and four multilocus sequence analysis proteins, and has proposed that the order Enterobacteriales be reclassified, placing Proteus within a new Morganellaceae family ( 1 ).P.

mirabilis can be found in a wide variety of environments, including soil, water sources, and sewage, but it is predominantly a commensal of the gastrointestinal tracts of humans and animals ( 2, 3 ). While the bacterium is capable of causing a variety of human infections, including those of wounds, the eye, the gastrointestinal tract, and the urinary tract, it is most noted for infections of the catheterized urinary tract, known as catheter-associated urinary tract infections (CAUTI) ( 4 – 9 ).

  • These infections are common in long-term catheterized patients, such as those who reside in nursing homes and chronic care facilities, and may be of particular danger to spinal cord injury patients ( 10 ).
  • Urinary tract infections (UTIs) and CAUTIs involving P.
  • Mirabilis are typically complicated by the formation of bladder and kidney stones (urolithiasis) and permanent renal damage ( 11 – 13 ), and may progress to bacteremia and sepsis ( 14, 15 ).

Indeed, CAUTI is the most common source of bacteremia in nursing homes, bacteremia involving P. mirabilis most frequently occurs following UTI or CAUTI compared to other sources of infection, and bacteremia and sepsis due to P. mirabilis carry a high mortality rate ( 14 – 17 ).

What are the complications of Proteus infection?

Clinical Manifestation, Pathogenesis, and Treatment – Proteus can cause gastroenteritis, urinary tract infections, and wound infections. The ingestion of food contaminated by Proteus may contribute to the sporadic and epidemic cases of gastroenteritis, which may cause symptoms such as vomiting, fever, abdominal pain, severe nausea, diarrhea, and dehydration.

  • The incubation period is short, usually 1–3 days.
  • The illness duration is approximately 40 h.
  • Sometimes, blood can be found in patients’ vomitus.
  • Proteus mirabilis and P,
  • Penneri are often isolated from diarrheal fecal samples of gastroenteritis patients.
  • The incidence rate of acute intestinal infection of Proteus is higher in young children as well as older and immunosuppressed persons, due to their low immunity.

Proteus is thought to increase the pathogenicity of other microbes. When Proteus infection occurs together with other microbes, infant diarrhea is more severe. As a secondary pathogen, P, vulgaris has been frequently observed in coinfection with streptococci, staphylococci, Bacillus coli, Bacillus lactis aerogenes, Bacillus welchii, Bacillus diphtheriae, etc.

  1. Infection by the genus Providencia, another member of the tribe of Proteeae, is rare.
  2. Proteus alcalifaciens, P,
  3. Heimbachae, P,
  4. Rettgeri, and P,
  5. Rustigianii are usually related to gastroenteritis whereas P,
  6. Stuartii is usually related to urinary infections.
  7. The Providencia -associated gastroenteritis leads to abdominal pain, vomiting and diarrhea.

Some patients may have fever. Most case reports of the Providencia -associated gastroenteritis are related to fecal contamination. The common incubation period from the ingestion of contaminated food is 80–90 h. Proteus alcalifaciens has been identified as an enteric pathogen.

Both in vitro cell invasion tests and animal models have proved the pathogenicity of P, alcalifaciens, The third member of the tribe Proteeae is Morganella sp. The presence of common food spoiled by M, morganii is fish, including mackerel, marlin, mahi-mahi, tuna, and bluefish. Both Proteus spp. and M,

morganii have the histidine dehydrogenase activity to produce histamine. The temperature of 15 °C is a critical point for histamine production of M, morganii, When the temperature is lower than 15 °C, the histamine production by M, morganii is significantly reduced.

  1. In general, M,
  2. Morganii does not produce toxic concentration of histamine below 7 °C.
  3. The elevated level of histamine and the factors influencing histamine absorption synergistically lead to symptoms after the ingestion of spoiled food.
  4. The symptoms include headache, diarrhea, redness of the face and neck, a feeling of heat, itching, etc.

The time elapsed between food intake and symptom onset ranges from minutes to 3 h. Usually, 100 mg dL −1 of histamine is the minimum level to cause symptoms, although 20 mg dL −1 of histamine may cause symptoms in some individuals. The histamine level in fresh fish is normally 1 mg dL −1, and 50 mg dL −1 is the hazardous level.

The cases of M, morganii outbreaks have been found associated with either raw fish or processed fish consumption. Therefore, cooking is not an effective way to eliminate the toxicity. In terms of treatment, Proteus spp. have varied sensitivity and resistance to antibiotics. Most Proteus spp. are sensitive to penicillin, gentamicin, furagin, ciprofloxacin, levofloxacin, and nevigramone, but they are resistant to nitrofurantoin, tetracycline, bacitracin, cecropin, polymyxin, and colistin.

The antibiotic resistance of Proteus spp. is transferred through plasmids encoding antibiotic-resistant genes. Proteus spp. have a high content of phosphate-linked 4-aminoarabinose in their LPS. The less acidic bacterial surface makes them inherently resistant to polycationic antibiotics, such as cecropin and polymyxin.

  • Polymyxin B binds to the negatively charged lipid A portion of LPS. In P,
  • Mirabilis, l -arabinoso-4-amine substituting the ester-linked phosphate group of lipid A can lead to the resistance to polymyxin B.
  • The first-choice antibiotic against P,
  • Mirabilis is ampicillin and the alternative antibiotics are aminoglycoside and cephalosporin.

Resistance to fluoroquinolones has been seen in P, mirabilis isolates. Most P, mirabilis strains are sensitive to ampicillin and cephalosporin, but P, vulgaris and P, hauseri are not sensitive to them. The first-choice antibiotics to treat P, vulgaris and P,

Hauseri are cefotaxime and ceftizoxime, and the alternative antibiotics are cefoxitin and trimethoprim (TMP)-sulfamethoxazole (SMX). In addition, P, vulgaris and P, hauseri are sensitive to ceftazidime, ceftriaxone, imipenem, ciprofloxacin, netilmicin, sulbactam, meropenem, and levofloxacin. In contrast to other Proteus spp., P,

penneri is resistant to chloramphenicol. Therefore, combinations of antibiotics are more effective treatment against Proteus, such as gentamicin with carbenicillin, gentamicin with ampicillin, monomycin with ampicillin, Zosyn (piperacillin and tazobactam), and Unasyn (ampicillin and sulbactam).

Most M, morganii strains are resistant to penicillin and cephalosporin and are susceptible to aztreonam, aminoglycoside, and quinolone. Providencia is highly resistant to penicillin G, ampicillin, chloramphenicol, colistin, polymyxin B, nitrofurantoin, and nalidixic acid, but it is sensitive to aminoglycoside, quinolone, carbapenem, aztreonam, and modern cephalosporin.

Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780123786128001086

How is Proteus mirabilis diagnosed?

Diagnosis – An alkaline urine sample is a possible sign of P. mirabilis, It can be diagnosed in the lab due to characteristic swarming motility, and inability to metabolize lactose (on a MacConkey agar plate, for example). Also P. mirabilis produces a very distinct fishy odor.

Is Proteus mirabilis sensitive to ciprofloxacin?

According to the studies presented, 40.0% of the P. mirabilis strains were resistant to ciprofloxacin. This percentage is higher when compared to that of the results obtained by Hernández et al., who indicated that 16.2% of strains are resistant to this fluoroquinolone.

Which drug is sensitive to Proteus mirabilis?

P mirabilis is likely to be sensitive to ampicillin; broad-spectrum penicillins (eg, ticarcillin, piperacillin); first-, second-, and third-generation cephalosporins; imipenem; and aztreonam.

How do you prevent Proteus mirabilis?

To prevent colonization of animals with P. mirabilis, the animals must be raised in strict bioexclusion housing, such as would be necessary for immunodeficient mice.P. mirabilis is susceptible to most common disinfectants used in animal facilities.

Is Proteus mirabilis a gut bacteria?

A specific gut bacterium, Proteus mirabilis, is identified from the genera Proteus which is isolated from the commonly increased Enterobacteriaceae family in the feces of PD mice models – Enterobacteriaceae is a representative pathogenic bacterial family that changes in disease states 25,

  • It has been reported that the Enterobacteriaceae family triggers colonic inflammatory conditions and is distinctly increased in the colon of PD patients 22, 26, 27, 28,
  • As shown in Fig.1A, we explored whether these bacterial colonies changed in PD mice models induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), MPTP/probenecid (MPTP/p), and 6-OHDA toxicity.

The number of Enterobacteriaceae increased significantly compared with those of each control group for three PD mice models (Fig.1B–D ). We found that, in the Enterobacteriaceae, the number of Proteus sp, was increased significantly in MPTP/p mice versus the normal group, whereas Escherichia coli ( E.

  1. Coli ) and Klebsiella sp,
  2. Hardly differed from each normal group (Fig.1E ).
  3. We confirmed that Proteus sp,
  4. Was increased significantly in MPTP-induced PD mice (Fig.1F ).
  5. Then, we identified the increased Proteus sp,
  6. As Proteus mirabilis by 16 S rRNA gene sequencing (Table S1 ).
  7. Next, we assessed whether treatment with P.

mirabilis influenced the mouse brain as well as colon. Figure 1 P. mirabilis is an isolated bacterium from the increased bacterial colonies in PD animal models. ( A ) Schematic diagram of isolation and identification processes of P. mirabilis, ( B – D ) The colonies of Enterobacteriaceae were increased in the feces of MPTP/p, MPTP, and 6-OHDA-induced PD mice compared with the normal group, respectively. ( E ) The colonies of Proteus sp, in MPTP/p mice were only increased compared with the normal group whereas those of E. coli and Klebsiella sp, were no different from each normal group. ( F ) The colonies of Proteus sp. in MPTP mice were also increased compared with the normal group. Values were expressed as means ± SEM. #p < 0.05 and ##p < 0.01 vs. each normal group (unpaired t-test; n = 4).n.s; not significant, CFU; colony-forming unit.

What kills Proteus bacteria?

Since Proteus mirabilis is a form of bacteria, infections caused by Proteus mirabilis are usually treated using antibiotics. Antibiotics are used to kill bacteria in the body.

Does amoxicillin treat Proteus mirabilis?

Amoxicillin is not the first choice to treat the infections against Proteus mirabilis and Staphylococcus aureus because they showed resistance 96.1% and 61.3% against Proteus mirabilis as compare to tetracycline is the first choice to treat infection which is caused by Staphylococcus aureus and Proteus mirabilis

Is Proteus mirabilis resistant to ciprofloxacin?

Mirabilis and P. vulgaris were susceptible to ciprofloxacin. However, among the 20 strains of P. mirabilis three (15.0%) were classified as the intermediate group.

Is Proteus mirabilis sensitive to ciprofloxacin?

According to the studies presented, 40.0% of the P. mirabilis strains were resistant to ciprofloxacin. This percentage is higher when compared to that of the results obtained by Hernández et al., who indicated that 16.2% of strains are resistant to this fluoroquinolone.