Proteus penneri

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Proteus penneri
Electron micrograph of Proteus penneri. Bar represents 200nm.
Scientific classification edit
Domain: Bacteria
Phylum: Pseudomonadota
Class: Gammaproteobacteria
Order: Enterobacterales
Family: Enterobacteriaceae
Genus: Proteus
P. penneri
Binomial name
Proteus penneri
Hickman et al. 1982

Proteus penneri is a Gram-negative, facultatively anaerobic, rod-shaped bacterium.[1] It is an invasive pathogen[2] and a cause of nosocomial infections of the urinary tract or open wounds.[3] Pathogens have been isolated mainly from the urine of patients with abnormalities in the urinary tract, and from stool.[4] P. penneri strains are naturally resistant to numerous antibiotics, including penicillin G, amoxicillin, cephalosporins, oxacillin, and most macrolides, but are naturally sensitive to aminoglycosides, carbapenems, aztreonam, quinolones, sulphamethoxazole, and co-trimoxazole. Isolates of P. penneri have been found to be multiple drug-resistant (MDR) with resistance to six to eight drugs. β-lactamase production has also been identified in some isolates.[5]


Extended biochemical tests have characterized P. penneri as being uniformly salicin negative. The inability to produce ornithine decarboxylase differentiates P. penneri from another indole-negative Proteus species, P.mirabilis.[2] P. penneri isolates are not fermenters of salicin and not users of citrate, but acidify sucrose and maltose.[5] Other chief characteristics of this species that enable its differentiation from other Proteus species include failure to acidify esculin, failure to produce hydrogen sulfide on triple sugar iron agar, and resistance to chloramphenicol.[6] The resistance of P. penneri to cefuroxime and the marked inhibitory activity of cefoxitin against this species also distinguishes P. penneri from the other Proteus.[7] Similar to other Proteus species, P. penneri has a cell-bound hemolytic factor, which has been shown to facilitate penetration of the organism into cultured Vero cells without any cytotoxic effects. It also has a filterable cytotoxic alpha-hemolysin rarely found in other Proteus species.[8] A highly active urease produced by P. penneri may also have a role in the establishment of an infectious process.[6]

The application of molecular techniques such as the polymerase chain reaction to produce DNA fingerprints and other 16S ribosomal RNA gene (ribotyping) methods of strain analysis have been employed to differentiate P. penneri from P. vulgaris and P. mirabilis strains. The RAPD technique, fundamentally a DNA fingerprinting method, has exposed a substantial DNA diversity among P. penneri strains, a characteristic that remained unidentified by other methods.[9]

Distinguishing biochemical features of Proteus penneri.
Test Result
Microscopic morphology Gram-negative rods
Hemolysis (sheep blood agar) Beta
Urease Positive
Indole production Negative
Esculin hydrolysis Negative
Acid from Maltose Positive
Acid from Sucrose Positive
Citrate use Negative
Ornithine decarboxylase Negative
Hydrogen sulfide production Positive


The lipopolysaccharide (LPS) core region of P. penneri strains contains higher structural variability than that observed in other representatives of Enterobacterales.[10] These differences have been used to cluster P. penneri strains into serogroups based on their agglutinating activity when mixed with antibodies directed against specific species of LPS molecules.[11] Presently, 15 O-serogroups have been proposed for P. penneri based on the chemical structure of the O-specific polysaccharide chain (O-antigen) of the lipopolysaccharide.[12][13][14] Certain LPS epitopes have been examined to determine their function in antigenic specificity. The particular groups on the oligosaccharides found to play a dominant role in the specificity of P. penneri LPS are the amide of D-galacturonic acid with L-lysine α-D-GalA-(L-Lys) (and the amide of D-galacturonic acid with L-threonine α-D-GalA- [L-Thr]), respectively.[11]


The occurrence of P. penneri organisms in the normal intestine accounts for their higher frequency in urinary tract infections and for their role as opportunistic invaders after surgery.[15] P. penneri is absent from the intestines of livestock.[9] The optimum growth condition for P. penneri is achieved at 37 °C, which mirrors the intestinal niche colonized by many of these bacteria. Certain strains of P. penneri can differentiate into elongated hyperflagelled cells during development on solid media, resulting in the surface translocation event identified as “swarming”. Swarming motility makes it difficult to isolate single colonies for further study.[16]

Susceptibility profile

Most isolated P. penneri strains are multiple-drug resistant, with 12 being the highest drug-resistance number reported.[2] P. penneri has a distinguishing susceptibility profile, based on the production of the chromosomally induced β-lactamase HugA. HugA determines resistance to aminopenicillins and first- and second-generation cephalosporins, including cefuroxime. However, HugA does not affect cephamycins or carbapenems and is inhibited by clavulanic acid. Similar to other Proteus species, P. penneri is resistant to tetracyclines and nitrofurantoin.[17]

Presently, all tested strains of P. penneri have been found to be highly susceptible to:[18]

Most strains with a few exceptions are also susceptible to:

All tested strains have been found resistant to:


The Proteus penneri group of bacteria was named in 1982. It reclassified a group of strains formerly known as Proteus vulgaris biogroup 1.[19] In 1978, Brenner et al. showed through DNA hybridization studies that P. vulgaris was a heterogenous species.[8] In 1981, Hickman et al conducted experiments on 20 indole-negative strains previously grouped with P.vulgaris and demonstrated the existence of three P. vulgaris biogroups. P. vulgaris biogroup 1, or indole-negative P. vulgaris, was distinguished as a new species within the genus Proteus in 1982.[1] The new species was named Proteus penneri in honor of John Penner, a Canadian microbiologist.[4]


Proteus penneri in blood agar plates

Documented human clinical infections caused by P. penneri have been limited to the urinary tract and to wounds of the abdomen, groin, neck, and ankle.[6] This species is isolated from individuals in long-term care facilities and hospitals and from patients who are immunocompromised or suffering from underlying disease. P. penneri was isolated significantly more often from stools of patients with diarrheal disease than from healthy patients, so P. penneri may play a role in some diarrheal disease.[20] The invasive potential of this microorganism has also been demonstrated in a case of P. penneri bacteremia and concomitant subcutaneous thigh abscess in a neutropenic patient with acute lymphocytic leukemia [6] and in nosocomial urosepsis in a diabetic patient from whom the organism was also subsequently isolated from bronchoalveolar lavage fluid and a pulmonary catheter tip.[21] Furthermore, in an experiment conducted in India, P. penneri strains were isolated as the sole pathogen in all patients having underlying disease postoperatively. Most isolates of P. penneri from the experiment were found to be multiple drug-resistant including resistance to amoxy-clavulanic acid combination.[2] In another study, P. penneri was found to be more resistant to the penicillins and cephalosporins than P. mirabilis and mostly in patients with urogenital infections.[5] Moreover, the urease enzyme of P. penneri is thought to be a significant cause of kidney stone formation. Consistent with this belief, the organism has been isolated from the center of a stone removed from a patient with persistent P. penneri bacteriuria.[22] These data substantiate the need for species-level identification of P. penneri in the clinical setting.

Several virulence factors of P. penneri can make infections from this invasive pathogen more pronounced, persistent, and harder to eradicate.[2] These include adherence due to the presence of fimbriae or afimbrial adhesins, invasiveness, swarming phenomenon, hemolytic activity, urea hydrolysis, proteolysis, and endotoxicity.[23] Swarming motility is the coordinated translocation of a bacterial population driven by flagellar rotation in film or on fluid surfaces.[24] An emerging concept in microbiology, the fundamental role of swarming motility remains unknown. However, it has been observed to be correlated with an elevated resistance to certain antibiotics.[25] Production of IgA proteolytic enzymes has also been reported in P. penneri.[26] Secretory immunoglobulins of the IgA class are produced by mucous tissue and are particularly resistant to enzymatic breakdown by proteases. The ability to degrade a host’s secretory IgA may provide P. penneri with an advantage by permitting it to evade the host immune response, therefore gaining valuable time for the bacterium to establish a foothold for infection. However, the major mechanism of antimicrobial resistance is caused by hyperproduction of the chromosomally encoded β-lactamase, sometimes by plasmids. These inducible β-lactamases hydrolyze primary and extended-spectrum penicillins and cephalosporins,[27] thus making P. penneri strains naturally resistant to penicillin G, amoxicillin, cephalosporins (i.e. cefaclor, cefazoline, cefuroxime, and cefdinir), oxacillin, and most macrolides.[2]


Information on the treatment of P. penneri infections is limited, but the use of gentamicin, tobramycin, netilmicin, and amikacin have been indicated as possible drugs of choice for the treatment of systemic infections caused by susceptible P. penneri strains. In vitro studies of ceftizoxime, ceftazidime, moxalactam, and cefoxitin suggest these agents also may prove to be clinically useful in treating infections caused by P. penneri.[18]


The proportion of P. penneri strains isolated in clinical specimens is unknown.[7] Since P. penneri was only recently recognized as a new species, many bacteriologists are either generally unaware of it, or have made limited attempts to discover its clinical significance. Thus, reports on the isolation of P. penneri from infected patients is limited.[2] Although increasing numbers of laboratories are now identifying P.penneri strains, the numbers reported in susceptibility studies are relatively small for a general assessment of the incidence of the species.[7] Likewise, the epidemiology of P.penneri is also unknown for these reasons.

See also


  1. 1.0 1.1 Hickman FW, Steigerwalt AG, Farmer JJ, Brenner DJ (June 1982). "Identification of Proteus penneri sp. nov., formerly known as Proteus vulgaris indole negative or as Proteus vulgaris biogroup 1". Journal of Clinical Microbiology. 15 (6): 1097–102. doi:10.1128/jcm.15.6.1097-1102.1982. PMC 272260. PMID 7050147.
  2. 2.0 2.1 2.2 2.3 2.4 2.5 2.6 Kishore J (2012). "Isolation, identification & characterization of Proteus penneri--a missed rare pathogen". Indian J Med Res. 135 (3): 341–5. PMC 3361870. PMID 22561620.
  3. Kaistha, N; Bansal, N; Chander, J (July 2011). "Proteus penneri lurking in the intensive care unit: An important often ignored nosocomial pathogen". Indian Journal of Anaesthesia. 55 (4): 411–3. doi:10.4103/0019-5049.84842. PMC 3190523. PMID 22013265.
  4. 4.0 4.1 O'Hara CM, Brenner FW, Miller JM (2000). "Classification, identification, and clinical significance of Proteus, Providencia, and Morganella". Clin Microbiol Rev. 13 (4): 534–46. doi:10.1128/cmr.13.4.534-546.2000. PMC 88947. PMID 11023955.
  5. 5.0 5.1 5.2 Stock I (2003). "Natural antibiotic susceptibility of Proteus spp., with special reference to P. mirabilis and P. penneri strains". J Chemother. 15 (1): 12–26. doi:10.1179/joc.2003.15.1.12. PMID 12678409. S2CID 28138251.
  6. 6.0 6.1 6.2 6.3 Engler HD, Troy K, Bottone EJ (1990). "Bacteremia and subcutaneous abscess caused by Proteus penneri in a neutropenic host". J Clin Microbiol. 28 (7): 1645–6. doi:10.1128/jcm.28.7.1645-1646.1990. PMC 268005. PMID 2380386.
  7. 7.0 7.1 7.2 Piccolomini R, Cellini L, Allocati N, Di Girolamo A, Ravagnan G (1987). "Comparative in vitro activities of 13 antimicrobial agents against Morganella-Proteus-Providencia group bacteria from urinary tract infections". Antimicrob Agents Chemother. 31 (10): 1644–7. doi:10.1128/aac.31.10.1644. PMC 175007. PMID 3435110.
  8. 8.0 8.1 Rozalski A, Kotełko K (1987). "Hemolytic activity and invasiveness in strains of Proteus penneri". J Clin Microbiol. 25 (6): 1094–6. doi:10.1128/jcm.25.6.1094-1096.1987. PMC 269143. PMID 3597752.
  9. 9.0 9.1 Costas M, Holmes B, Frith KA, Riddle C, Hawkey PM (1993). "Identification and typing of Proteus penneri and Proteus vulgaris biogroups 2 and 3, from clinical sources, by computerized analysis of electrophoretic protein patterns". Journal of Applied Bacteriology. 75 (5): 489–98. doi:10.1111/j.1365-2672.1993.tb02806.x. PMID 8300450.
  10. Palusiak A, Sidorczyk Z (2010). "Characterization of epitope specificity of Proteus penneri 7 lipopolysaccharide core region". Acta Biochim Pol. 57 (4): 529–32. doi:10.18388/abp.2010_2439. PMID 21060898.
  11. 11.0 11.1 Manos, J.; Belas, R. (2006). "The Genera Proteus, Providencia, and Morganella". The Prokaryotes. p. 245. doi:10.1007/0-387-30746-x_12. ISBN 978-0-387-25496-8.
  12. Cedzyński M, Knirel YA, Rózalski A, Shashkov AS, Vinogradov EV, Kaca W (1995). "The structure and serological specificity of Proteus mirabilis O43 O antigen". Eur J Biochem. 232 (2): 558–62. doi:10.1111/j.1432-1033.1995.tb20844.x. PMID 7556207.
  13. Sidorczyk Z., Zych K., Kołodziejska K., Drzewiecka D. and Zabłotni A. (2002) Progress in serological classification of further strains from genus Proteus and determination of epitopes and new serogroups. Second German-Polish-Russian Meeting on Bacterial Carbohydrates, Moscow, September 10–12, 2002.
  14. Zych K, Kowalczyk M, Knirel YA, Sidorczyk Z (2002). "New Serogroups of the Genus Proteus Consisting of Proteus Penneri Strains only". Genes and Proteins Underlying Microbial Urinary Tract Virulence. Advances in Experimental Medicine and Biology. Vol. 485. pp. 339–44. doi:10.1007/0-306-46840-9_47. ISBN 978-0-306-46455-3. PMID 11109127.
  15. Krajden S, Fuksa M, Lizewski W, Barton L, Lee A (1984). "Proteus penneri and urinary calculi formation". J Clin Microbiol. 19 (4): 541–2. doi:10.1128/jcm.19.4.541-542.1984. PMC 271113. PMID 6715521.
  16. Belas R, Schneider R, Melch M (1998). "Characterization of Proteus mirabilis precocious swarming mutants: identification of rsbA, encoding a regulator of swarming behavior". J Bacteriol. 180 (23): 6126–39. doi:10.1128/JB.180.23.6126-6139.1998. PMC 107696. PMID 9829920.
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  18. 18.0 18.1 Fuksa M, Krajden S, Lee A (1984). "Susceptibilities of 45 clinical isolates of Proteus penneri". Antimicrob Agents Chemother. 26 (3): 419–20. doi:10.1128/aac.26.3.419. PMC 176184. PMID 6508270.
  19. Krajden S, Fuksa M, Petrea C, Crisp LJ, Penner JL (1987). "Expanded clinical spectrum of infections caused by Proteus penneri". J Clin Microbiol. 25 (3): 578–9. doi:10.1128/jcm.25.3.578-579.1987. PMC 266001. PMID 3571463.
  20. Müller HE (1986). "Occurrence and pathogenic role of Morganella-Proteus-Providencia group bacteria in human feces". J Clin Microbiol. 23 (2): 404–5. doi:10.1128/jcm.23.2.404-405.1986. PMC 268658. PMID 3517057.
  21. Latuszynski DK, Schoch P, Qadir MT, Cunha BA (1998). "Proteus penneri urosepsis in a patient with diabetes mellitus". Heart Lung. 27 (2): 146–8. doi:10.1016/s0147-9563(98)90023-1. PMID 9548071.
  22. Griffith DP, Musher DM, Itin C (1976). "Urease. The primary cause of infection-induced urinary stones". Invest Urol. 13 (5): 346–50. PMID 815197.
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  24. Fraser GM, Hughes C (1999). "Swarming motility". Curr Opin Microbiol. 2 (6): 630–5. doi:10.1016/S1369-5274(99)00033-8. PMID 10607626.
  25. Kim W, Killam T, Sood V, Surette MG (2003). "Swarm-cell differentiation in Salmonella enterica serovar typhimurium results in elevated resistance to multiple antibiotics". J Bacteriol. 185 (10): 3111–7. doi:10.1128/JB.185.10.3111-3117.2003. PMC 154059. PMID 12730171.
  26. Loomes LM, Senior BW, Kerr MA (1990). "A proteolytic enzyme secreted by Proteus mirabilis degrades immunoglobulins of the immunoglobulin A1 (IgA1), IgA2, and IgG isotypes". Infect Immun. 58 (6): 1979–85. doi:10.1128/iai.58.6.1979-1985.1990. PMC 258753. PMID 2111288.
  27. Swenson, JM; Hindler J A, Peterson L R. (1999). Murray, P.R. (ed.). Manual of clinical microbiology. Washington, D.C. pp. 1563–1577.

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