International Journal of Infection 2022; 6(2) May-August: 40-44


ARTICLE

URINARY TRACT BACTERIAL INFECTIONS: ESCHERICHIA COLI, KLEBSIELLA PNEUMONIAE, PROTEUS MIRABILIS, STAPHYLOCOCCUS SAPROPHYTICUS, ENTEROCOCCUS FAECALIS

Mastrangelo F, Bali N. Urinary tract bacterial infections: Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Staphylococcus saprophytics, Enterococcus faecalis. International Journal of Infection. 2022;6(2):40-44


F. Mastrangelo1* and N. Bali2

1 Department of Clinical and Experimental Medicine, University of Foggia, Foggia, Italy;
2 Department of innovative technology in medicine and dentistry, University “Gabriele D’Annunzio” of Chieti-Pescara, Chieti, Italy.

*Correspondence to:
Dr. Filiberto Mastrangelo,
Department of Clinical and Experimental Medicine,
University of Foggia,
71122 Foggia, Italy.
e-mail: filiberto.mastrangelo@unifg.it

Received: 25 February, 2022
Accepted: 14 July, 2022adobe-pdf-download-icon
ISSN 1972-6945 [online]
Copyright 2022 © by Biolife-publisher
This publication and/or article is for individual use only and may not be further reproduced without written permission from the copyright holder. Unauthorized reproduction may result in financial and other penalties. Disclosure: all authors report no conflicts of interest relevant to this article.

ABSTRACT

Urinary tract infections (UTIs) are very common bacterial infections that occur more often in women than in men and mainly affect the kidneys, ureters, bladder, and urethra. Bacteria enter the urinary tract through the urethra and travel up to the bladder, the route that is responsible for most UTIs. In rarer cases, bacteria can spread to the urinary system from the bloodstream, especially in immunocompromised patients. Once inside the urinary tract, bacteria adhere to the lining cells of the urinary tract using Pili (as in E. coli), type 1 fimbriae that bind to mannose receptors, and P-fimbriae that bind to specific receptors on kidney cells, contributing to pyelonephritis. The classic symptoms of UTIs include the frequent urge to urinate, a burning sensation during urination, the passage of frequent, small amounts of urine, cloudy or strong-smelling urine, and pelvic pain in women and rectal pain in men. If left untreated, these can progress to more serious symptoms and other complications such as kidney infection or sepsis. UTIs are frequently treated with antibiotics such as Trimethoprim-sulfamethoxazole, Nitrofurantoin, Ciprofloxacin (used less frequently due to potential side effects), and Amoxicillin/clavulanate.

KEYWORDS: urinary tract, infection, Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Staphylococcus saprophyticus, Enterococcus faecalis

 

INTRODUCTION

 

Urinary tract infections (UTIs) are predominantly caused by bacteria, although viruses can also contribute to these infections. Understanding the biological and molecular mechanisms of UTIs involves examining how pathogens invade, adhere to, and propagate within the urinary tract. UTIs are infections that affect any part of the urinary system, including the kidneys, ureters, bladder, and urethra. Most infections involve the lower urinary tract in the bladder and urethra. UTIs are typically caused by bacteria entering the urinary tract through the urethra and multiplying in the bladder (1). These infections can lead to persistent or severe symptoms, including high fever, back pain, or blood in the urine, and can be recurring. Proper diagnosis and treatment are essential to prevent complications, such as kidney infections or sepsis, which can arise from untreated UTIs (2).

Common bacteria that cause UTIs include Escherichia coli, Staphylococcus saprophyticus, Klebsiella pneumoniae, Proteus mirabilis, and Enterococcus faecalis (3). Uropathogenic E. Coli (UPEC) is the most common cause of UTI (4). S. saprophyticus is the second- leading cause, especially in younger women (5). In addition to these, other bacteria, viruses, or fungi can also cause UTIs (Table I).

 

Table I. Common bacterial and viral pathogens that cause urinary tract infections (UTIs).

Bacterial pathogens

 

 

 

 

 

 

·         Uropathogenic Escherichia coli (UPEC): The most common causative agent
·         Klebsiella pneumoniae
·         Proteus mirabilis
·         Staphylococcus saprophyticus
·         Enterococcus faecalis
Viral pathogens ·         Adenoviruses
·         Polyomaviruses: BK virus and JC virus
·         Cytomegalovirus (CMV)

 

DISCUSSION

 

UTIs begin with the colonization of the urethra, and subsequently the bladder, by uropathogens through the action of specific adhesins. UTIs are commonly initiated by UPEC which enter the urinary tract through the urinary meatus and ascend the urethra into the bladder lumen (6). The bacterium can adhere to the urothelium and UPEC strains and uses mannose-sensitive type 1 fimbriae and papG adhesion P pili to adhere to epithelial cells of the bladder and kidney (7,8).

Adhesins are proteins that help bacteria bind to glycoproteins on the surface of uroepithelial cells (9). Pathogenic bacteria begin invasion after attachment to targets and can invade uroepithelial cells, creating intracellular bacterial communities (IBCs) (10). At the intracellular level, these bacteria replicate and evade the host’s immune response (11). Bacteria can form biofilms, which protect them from antibiotics and the host immune system, on urinary catheters and inside the bladder, contributing to chronic and recurrent infections (12).

These bacteria can produce hemolysin, toxins such as alpha-hemolysin produced by E. Coli, capable of lysing host cells and releasing nutrients for bacterial growth (13). The release of bacterial cytotoxins damages host tissues and causes the immune reaction. Additionally, bacterial pathogens produce siderophores to scavenge iron from the host, which is essential for bacterial growth (14). The bacteria are capable of evading the immune system by forming a protective layer around the capsule, which allows them to protect themselves from the phagocytosis of macrophages and polymorphonuclear cells (15).

 

Escherichia coli

E. Coli is the most common cause of UTIs, responsible for up to 80-90% of all cases (16,17). E. Coli bacteria normally live in the intestines and are harmless there. However, when they enter the urinary tract, they can cause an infection. E. Coli can enter the urinary tract from the intestines through several pathways. By ascension through the urethra, E. Coli from the intestines can reach the urethra and travel up into the bladder or can transfer E. Coli from the anal area to the urethra due to improper hygiene (18). Sexual transmission is another route for infection and can facilitate the movement of E. Coli from the vaginal or anal area to the urethra.

Symptoms of UPEC UTIs are similar to those of other UTIs and can include the frequent urge to urinate, a burning sensation during urination, the passage of frequent, small amounts of urine, cloudy or strong-smelling urine, pelvic pain in women and rectal pain in men (19). The diagnosis of the infection is made by collecting urine which is analyzed for the presence of bacteria, white blood cells, and red blood cells. A urine culture is then performed, which helps to identify the specific bacteria causing the infection and determines sensitivity to antibiotics.

E. Coli infections are primarily treated with antibiotics. The choice of antibiotic and duration of treatment depend on the severity of the infection and any patterns of antibiotic resistance. Commonly used antibiotics include Trimethoprim/sulfamethoxazole (Bactrim, Septra), Nitrofurantoin (Macrobid, Macrodantin), Fosfomycin (Monurol), Ciprofloxacin (Cipro), and other fluoroquinolones (usually reserved for more complicated cases) (20).

 

Klebsiella pneumoniae

K. pneumoniae is a bacterium that can cause a variety of infections, including UTIs. This pathogen is known for its ability to acquire resistance to multiple antibiotics, making infections challenging to treat (21). Symptoms of a K. pneumoniae UTI can include the frequent urge to urinate, pain or a burning sensation during urination, cloudy or strong-smelling urine, blood in the urine, lower abdominal pain or discomfort, and fever and chills, particularly if the infection has spread to the kidneys.

 

Proteus mirabilis

P. mirabilis is a gram-negative, facultatively anaerobic bacterium that is a well-known cause of UTIs. P. mirabilis is a rod-shaped bacterium with numerous peritrichous flagella and is very motile. It is characterized by rapid movements with ease of colonizing tissues. P. mirabilis produces the enzyme urease, which hydrolyzes urea into ammonia and carbon dioxide, leading to an increase in urine pH (22). In humans and some animals, it is present in the gastrointestinal tract and can play an important role in the pathogenesis of UTIs (23). It can colonize and infect the bladder and kidneys. P. mirabilis alkalizes urine, promoting the formation of struvite (magnesium ammonium phosphate) and apatite (calcium phosphate) kidney stones (24). P. mirabilis can cause acute cystitis with inflammation of the bladder and painful urination (dysuria), and pyelonephritis with fever. Therapy uses first-line agents such as trimethoprim-sulfamethoxazole, fluoroquinolones, or ampicillin (25). Understanding the specific features and behaviors of P. mirabilis helps in effectively diagnosing and treating UTIs caused by this bacterium, thereby reducing complications and recurrence rates.

 

Staphylococcus saprophyticus

S. saprophyticus is a notable pathogen in the context of UTIs, particularly among young women. S. saprophyticus is a Gram-positive, coagulase-negative bacterium that is a common cause of UTIs. Its ability to adhere to the urinary tract and form biofilms, along with its production of urease, contributes to its pathogenicity (26). Prompt diagnosis and appropriate antibiotic treatment are essential for effective management and to prevent complications. Its incidence in causing UTIs is 5-15% (27) and in addition to women, it can also infect men of all ages. Very often, there is a high rate of infectivity in autumn. S. saprophyticus has the ability to adhere to the lining of the urinary tract (urothelium) using proteins and lipoteichoic acids (28). It can hydrolyse urea into ammonia and increase the pH of urine, an action that contributes to its colonization (29). Some strains of S. saprophyticus can form biofilms that aid their ability to persist in the urinary tract and resist host immune responses (30).

The typical symptoms of UTI infection by S. saprophyticus include painful urination, pain in the lower abdomen, and the presence of hematuria. Untreated or recurring infections can lead to complications such as pyelonephritis. These UTI infections are usually treated with antibiotics such as Nitrofurantoin, Trimethoprim-sulfamethoxazole or Fluoroquinolones of which S. saprophyticus are sensitive (31). However, resistant S. saprophyticus models can also be formed.

 

Enterococcus faecalis

UTIs caused by E. faecalis require careful diagnosis and targeted treatment. Given its potential for antibiotic resistance, appropriate antibiotic selection is crucial (32). Preventive measures and proper hygiene can significantly reduce the risk of UTIs. E. faecalis is a facultative anaerobic Gram-positive bacterium that causes UTI infection, can cause various symptoms such as frequent urination with pain and burning, and can alter the urine making it cloudy and blood-filled. Furthermore, E. faecalis can induce fever and chills and promote the development of UPEC. E. faecalis is part of the intestinal bacterial flora, can become pathogenic under certain conditions, and can develop considerable resistance (32).

 

CONCLUSIONS

 

UTIs are very common bacterial infections caused by several bacterial species. The main bacteria responsible for these infections are E. Coli, K. pneumoniae, P. mirabilis, S. saprophyticus, and E. faecalis. Each of these bacteria has particular characteristics and mechanisms that allow them to cause infection after colonizing the urinary tract and evade the host immune response.

 

Conflict of interest

The authors declare that they have no conflict of interest.

 

REFERENCES

  1. Flores-Mireles AL, Walker JN, Caparon M, Hultgren SJ. Urinary Tract infections: epidemiology, Mechanisms of Infection and Treatment Options. Nature Reviews Microbiology. 2015;13(5):269-284. doi:https://doi.org/10.1038/nrmicro3432
  2. Zhang L, Zhang F, Xu F, et al. Construction and Evaluation of a Sepsis Risk Prediction Model for Urinary Tract Infection. Frontiers in Medicine. 2021;8. doi:https://doi.org/10.3389/fmed.2021.671184
  3. Fazly Bazzaz BS, Darvishi Fork S, Ahmadi R, Khameneh B. Deep insights into urinary tract infections and effective natural remedies. African Journal of Urology. 2021;27(1). doi:https://doi.org/10.1186/s12301-020-00111-z
  4. Terlizzi ME, Gribaudo G, Maffei ME. UroPathogenic Escherichia coli (UPEC) Infections: Virulence Factors, Bladder Responses, Antibiotic, and Non-antibiotic Antimicrobial Strategies. Frontiers in Microbiology. 2017;8(1566). doi:https://doi.org/10.3389/fmicb.2017.01566
  5. Hovelius B, Mardh PA . Staphylococcus saprophyticus as a Common Cause of Urinary Tract Infections. Clinical Infectious Diseases. 1984;6(3):328-337. doi:https://doi.org/10.1093/clinids/6.3.328
  6. Loubet P, Ranfaing J, Dinh A, et al. Alternative Therapeutic Options to Antibiotics for the Treatment of Urinary Tract Infections. Frontiers in Microbiology. 2020;11. doi:https://doi.org/10.3389/fmicb.2020.01509
  7. Martinez JJ. Type 1 pilus-mediated bacterial invasion of bladder epithelial cells. The EMBO Journal. 2000;19(12):2803-2812. doi:https://doi.org/10.1093/emboj/19.12.2803
  8. Coşar G, Hoşgör M, Ozgenç O, Hilmioğlu S, Taşli H. Expression of P fimbriae of uropathogenic Escherichia coli strains. Le infezioni in medicina. 2001;9(2):98-100.
  9. Dufrêne YF, Viljoen A. Binding Strength of Gram-Positive Bacterial Adhesins. Frontiers in Microbiology. 2020;11. doi:https://doi.org/10.3389/fmicb.2020.01457
  10. Lewis AJ, Richards AC, Mulvey MA. Invasion of Host Cells and Tissues by Uropathogenic Bacteria. Microbiology Spectrum. 2016;4(6). doi:https://doi.org/10.1128/microbiolspec.uti-0026-2016
  11. Thakur A, Mikkelsen H, Jungersen G. Intracellular Pathogens: Host Immunity and Microbial Persistence Strategies. Journal of Immunology Research. 2019;2019:1-24. doi:https://doi.org/10.1155/2019/1356540
  12. Soto SM. Importance of Biofilms in Urinary Tract Infections: New Therapeutic Approaches. Advances in Biology. 2014;2014:1-13. doi:https://doi.org/10.1155/2014/543974
  13. Wiles TJ, Mulvey MA. The RTX pore-forming toxin α-hemolysin of uropathogenic Escherichia coli: progress and perspectives. Future Microbiology. 2013;8(1):73-84. doi:https://doi.org/10.2217/fmb.12.131
  14. Page MGP. The Role of Iron and Siderophores in Infection, and the Development of Siderophore Antibiotics. Clinical Infectious Diseases. 2019;69(Supplement_7):S529-S537. doi:https://doi.org/10.1093/cid/ciz825
  15. Cress BF, Englaender JA, He W, Kasper D, Linhardt RJ, Koffas MAG. Masquerading microbial pathogens: Capsular polysaccharides mimic host-tissue molecules. FEMS microbiology reviews. 2014;38(4):660-697. doi:https://doi.org/10.1111/1574-6976.12056
  16. Foxman B. Urinary Tract Infection Syndromes. Infectious Disease Clinics of North America. 2014;28(1):1-13. doi:https://doi.org/10.1016/j.idc.2013.09.003
  17. Hooton TM. Uncomplicated Urinary Tract Infection. New England Journal of Medicine. 2012;366(11):1028-1037. doi:https://doi.org/10.1056/nejmcp1104429
  18. Klein RD, Hultgren SJ. Urinary tract infections: microbial pathogenesis, host–pathogen interactions and new treatment strategies. Nature Reviews Microbiology. 2020;18(4):211-226. doi:https://doi.org/10.1038/s41579-020-0324-0
  19. Hannan TJ, Totsika M, Mansfield KJ, Moore KH, Schembri MA, Hultgren SJ. Host–pathogen checkpoints and population bottlenecks in persistent and intracellular uropathogenic Escherichia coli bladder infection. FEMS Microbiology Reviews. 2012;36(3):616-648. doi:https://doi.org/10.1111/j.1574-6976.2012.00339.x
  20. Jancel T, Dudas V. Management of uncomplicated urinary tract infections. Western Journal of Medicine. 2002;176(1):51-55. doi:https://doi.org/10.1136/ewjm.176.1.51
  21. Moya C, Maicas S. Antimicrobial Resistance in Klebsiella pneumoniae Strains: Mechanisms and Outbreaks. Proceedings. 2020;66(1):11. doi:https://doi.org/10.3390/proceedings2020066011
  22. Grahl MVC, Uberti AF, Broll V, Bacaicoa-Caruso P, Meirelles EF, Carlini CR. Proteus mirabilis Urease: Unsuspected Non-Enzymatic Properties Relevant to Pathogenicity. International Journal of Molecular Sciences. 2021;22(13):7205. doi:https://doi.org/10.3390/ijms22137205
  23. Armbruster CE, Mobley HLT. Merging mythology and morphology: the multifaceted lifestyle of Proteus mirabilis. Nature reviews Microbiology. 2012;10(11):743-754. doi:https://doi.org/10.1038/nrmicro2890
  24. Armbruster CE, Mobley HLT, Pearson MM. Pathogenesis of Proteus mirabilis Infection. EcoSal Plus. 2018;8(1). doi:https://doi.org/10.1128/ecosalplus.esp-0009-2017
  25. Danilo de Oliveira W, Lopes Barboza MG, Faustino G, et al. Virulence, resistance and clonality of Proteus mirabilis isolated from patients with community-acquired urinary tract infection (CA-UTI) in Brazil. Microbial Pathogenesis. 2021;152:104642. doi:https://doi.org/10.1016/j.micpath.2020.104642
  26. Lawal OU, Barata M, Fraqueza MJ, et al. Staphylococcus saprophyticus From Clinical and Environmental Origins Have Distinct Biofilm Composition. Frontiers in Microbiology. 2021;12:663768. doi:https://doi.org/10.3389/fmicb.2021.663768
  27. Jhora ST, Paul S. Urinary Tract Infections Caused by Staphylococcus saprophyticus and their antimicrobial sensitivity pattern in Young Adult Women. Bangladesh Journal of Medical Microbiology. 2011;5(1):21-25. doi:https://doi.org/10.3329/bjmm.v5i1.15817
  28. Teti G, Chiofalo MS, Tomasello F, Fava C, Mastroeni P. Mediation of Staphylococcus saprophyticus adherence to uroepithelial cells by lipoteichoic acid. Infection and Immunity. 1987;55(3):839-842. doi:https://doi.org/10.1128/iai.55.3.839-842.1987
  29. Gatermann S, John J, Marre R. Staphylococcus saprophyticus urease: characterization and contribution to uropathogenicity in unobstructed urinary tract infection of rats. Infection and Immunity. 1989;57(1):110-116. doi:https://doi.org/10.1128/iai.57.1.110-116.1989
  30. Hashemzadeh M, Dezfuli AAZ, Nashibi R, Jahangirimehr F, Akbarian ZA. Study of biofilm formation, structure and antibiotic resistance in Staphylococcus saprophyticus strains causing women urinary tract infection in Ahvaz, Iran. New Microbes and New Infections. 2020;39:100831. doi:https://doi.org/10.1016/j.nmni.2020.100831
  31. Martins KB, Ferreira AM, Pereira VC, Pinheiro L, de Oliveira A, da Cunha MLRS. In vitro Effects of Antimicrobial Agents on Planktonic and Biofilm Forms of Staphylococcus saprophyticus Isolated From Patients With Urinary Tract Infections. Frontiers in Microbiology. 2019;10. doi:https://doi.org/10.3389/fmicb.2019.00040
  32. Kristich CJ, Rice LB, Arias CA. Enterococcal Infection—Treatment and Antibiotic Resistance. In: Gilmore MS, Clewell DB, Ike Y, Shankar N, eds. Enterococci: From Commensals to Leading Causes of Drug Resistant Infection. Boston: Massachusetts Eye and Ear Infirmary; February 6, 2014.

You may also like...