Providencia Infections



The genus Providencia includes urease-producing gram-negative bacilli that are responsible for a wide range of human infections. Although most Providencia infections involve the urinary tract, they are also associated with gastroenteritis and bacteremia.[1] Providencia infections are uncommon and are usually nosocomial. They represent an emerging problem because of the increasing prevalence of antibiotic resistance secondary to extended-spectrum beta-lactamase (ESBL).

The first species of the genus now known as Providencia was isolated by Rettger in 1904. The bacterium was initially seen in chickens in what was believed to be an epidemic of fowl cholera. The bacterium was not further characterized until 1918, when it was named Bacterium rettgerii by Hadley et al. Organisms belonging to the genus Providencia have undergone many taxonomic changes since their first description, with frequent confusion and overlap between organisms of the closely related genera Providencia, Proteus, and Morganella.

Kauffmann first proposed the genus name Providencia in 1951, referring to a group of organisms studied by Stuart and colleagues at Brown University in Providence, Rhode Island. By 1983, the 4 species in the Providencia genus at that time were fully differentiated with DNA hybridization and urea hydrolyzation. In 1986, Providencia heimbachae was the fifth species discovered.[2]

The 5 species currently in the genus Providencia, in descending order of prevalence, include Providencia stuartii, Providencia rettgeri, Providencia alcalifaciens, Providencia rustigianii, and P heimbachae.[3]


Providencia species are found in multiple animal reservoirs, including flies, birds, cats, dogs, cattle, sheep, guinea pigs, and penguins, and are resident oral flora in reptiles such as pythons, vipers, and boas. Providencia species are also found commonly in soil, water, and sewage. Examples of Providencia infections in animals include neonatal diarrhea due to P stuartii infection in dairy cows and enteritis caused by P alcalifaciens infection in dogs. P rettgeri has been isolated in crocodiles with meningitis/septicemia and in chickens with enteritis.[4] P heimbachae has been isolated in penguin feces and an aborted bovine fetus.[5]

In humans, Providencia species have been isolated from urine (most common), stool, and blood, as well as from sputum, skin, and wound cultures. P stuartii septicemia is primarily of urinary origin. One case study has described P stuartii as the etiology of infective endocarditis.[6] Another case report found P rettgeri to be a cause of ocular infections, including keratitis, conjunctivitis, and endophthalmitis.[7]

P stuartii is frequently isolated in patients with indwelling urinary catheters and is known to persist in the urinary tract after bladder access is attained. In one study, the mean duration of bacterial colonization was 6.4 months.[8] The persistence of bacteria in the urinary tract is thought to be due to an adhesin, mannose-resistant/Klebsiella -like (MR/K) hemagglutinin, which allows bacteria to adhere to urinary catheters (mediated by 3 fimbriae).[8, 9] In a 1994 study by Rahav et al, persistence patterns in males and females were found to differ, with P stuartii showing more persistence in females. Reasons theorized include different receptor characteristics in male and female urinary tracts and a bacterial predilection for Foley catheters over condom catheters, which are used more commonly in males.[8]

ESBL-positive P stuartii is an increasing problem in hospitalized patients. In one study, 52% of 223 P stuartii isolates were found to be positive for ESBL in a hospital population that included ICU, medical, and surgical wards over a 4-year span.[10]

P alcalifaciens, P rettgeri, and P stuartii have been implicated in gastroenteritis. In one study, P rettgeri and P stuartii were found to be highly invasive using in vivo testing with Caco-2, a human colon carcinoma cell line. However, a common virulence plasmid was not identified in Providencia species.[11, 12] Providencia species, most commonly P agalactiae, have been demonstrated in the stool of symptomatic patients, although testing protocols used to identify diarrheagenic bacterial pathogens do not generally include Providencia.



United States

P stuartii and, to a lesser extent, P rettgeri are the most common Providencia species that cause human infection. While uncommon in most clinical settings, these organisms tend to cause cystitis in patients with bladder catheters and are primarily associated with complicated urinary tract infections. In a Canadian study in 2001, Providencia species were isolated in 18% of complicated urinary tract infections.[13] In contrast, Providencia bacteriuria in acute hospital settings is rare (0.3-1%).[8]

The prevalence of Providencia infections are generally low, although it is increasing. More significantly, Providencia infections with antimicrobial resistance patterns are increasing. In 2003, a study at an Italian university hospital with medical, surgical, and intensive care units found that the prevalence of ESBL-producing P stuartii in the general patient population increased from 31% in 1999 to 62% in 2002. Over a 4-year span, P stuartii was isolated in 0.08% of patients. Of these isolates, 87% were found in urine, 10% in blood, and 3% in respiratory tract secretions.[10]

P stuartii is most often found in complicated urinary tract infections in patients with chronic indwelling urinary catheters or condom catheters. Providencia species are rarely a cause of uncomplicated urinary tract infections. In a study of patients with urinary catheters living in a retirement home, P stuartii was the most commonly isolated bacteria, found in 59% of urine specimens. (The next most common was Escherichia coli, at 32%.)[8]

Providencia species, specifically P alcalifaciens and P rettgeri, have also been shown to be an infrequent cause of foodborne gastroenteritis. In 1996, a large outbreak of foodborne P alcalifaciens infections occurred in Japan at multiple schools, affecting student and teacher populations.[14] This was the first reported outbreak of foodborne P alcalifaciens gastroenteritis. Providencia species, especially P rettgeri, have also been implicated as cause of traveler’s diarrhea. In a Japanese study, 130 patients with diarrhea were evaluated at the Kansai Airport quarantine station, and Providencia species were isolated in 15.4% of stool samples. Most travelers who reported diarrhea had traveled to Southeast Asia.[11]


Providencia species are found worldwide. A study that examined ESBL-producing Enterobacteriaceae distribution worldwide (including Providencia species) found that the prevalence of ESBL-positive bacteria varied across geographical boundaries. The highest percentage of ESBL-positive isolates as found in Latin America (44%) and the lowest in Netherlands and Germany (2% and 2.6%, respectively).[15]


The mortality rate in patients with Providencia bloodstream infection ranges from 6-33%. The rate is greater in polymicrobial infection.


All races appear to be equally susceptible to Providencia infection.


Males and females appear to be equally susceptible to Providencia infection. In one study, however, a significant difference was seen in the persistence pattern of bacteriuria in women versus men among nursing-home patients with long-term urinary catheterization (88.25% vs 50.5%).[8]





Laboratory Studies

Imaging Studies

Other Tests

Medical Care

Surgical Care




Medication Summary

Medical therapy is directed at eradication of the infecting Providencia organism with an antimicrobial agent to which the organism is susceptible.

Aztreonam (Azactam)

Clinical Context:  A monobactam (not a beta-lactam) antibiotic that inhibits cell wall synthesis during bacterial growth. Active against gram-negative bacilli but very limited gram-positive activity and not useful for anaerobes. Lacks cross-sensitivity with beta-lactam antibiotics. May be used in patients allergic to penicillins or cephalosporins.

Duration of therapy depends on severity of infection and should be continued for at least 48 h after symptoms resolve asymptomatic or evidence of bacterial eradication obtained. Doses smaller than indicated should not be used.

Transient or persistent renal insufficiency may prolong serum levels. After initial loading dose of 1 or 2 g, reduce dose by one half for estimated ClCr of 10-30 mL/min/1.73 m2. When only serum creatinine concentration available, the following formula (based on sex, weight, and age) can approximate ClCr. Serum creatinine should represent a steady state of renal function.

Males: ClCr = [(weight in kg)(140 - age)] / (72 X serum creatinine level in mg/dL)

Females: 0.85 X above value

In patients with severe renal failure (ClCr < 10 mL/min/1.73 m2), those supported by hemodialysis, usual dose of 500 mg, 1 g, or 2 g, is given initially.

Maintenance dose is one fourth of usual initial dose given at usual fixed interval of 6, 8, or 12 h.

For serious or life-threatening infections, supplement maintenance doses with one-eighth of initial dose after each hemodialysis session.

Elderly persons may have diminished renal function. Renal status is a major determinant of dosage in these patients. Serum creatinine may not be an accurate determinant of renal status. Therefore, as with all antibiotics eliminated by kidneys, obtain estimates of ClCr and make appropriate dosage modifications. Insufficient data are available regarding IM administration to pediatric patients or dosing in pediatric patients with renal impairment. Administer IV only to pediatric patients with normal renal function.

Imipenem and cilastatin (Primaxin)

Clinical Context:  For treatment of multiple organism infections in which other agents do not have wide spectrum coverage or are contraindicated due to potential for toxicity.

Piperacillin and tazobactam sodium (Zosyn)

Clinical Context:  Antipseudomonal penicillin plus beta-lactamase inhibitor. Inhibits biosynthesis of cell wall mucopeptide and is effective during stage of active multiplication.

Ceftazidime (Ceptaz, Fortaz, Tazicef, Tazidime)

Clinical Context:  Third-generation cephalosporin with broad-spectrum, gram-negative activity, including pseudomonas; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to one or more penicillin-binding proteins, which, in turn, inhibit the final transpeptidation step of peptidoglycan synthesis in bacterial cell wall synthesis, thus inhibiting cell wall biosynthesis. The condition of the patient, severity of the infection, and susceptibility of the microorganism should determine the proper dose and route of administration.

Cefotaxime (Claforan)

Clinical Context:  Third-generation cephalosporin with broad gram-negative spectrum, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms. Arrests bacterial cell wall synthesis by binding to one or more of the penicillin-binding proteins, which in turn inhibits bacterial growth. Used for septicemia and treatment of gynecologic infections caused by susceptible organisms.

Third-generation cephalosporin with gram-negative spectrum. Lower efficacy against gram-positive organisms.

Amikacin (Amikin)

Clinical Context:  Irreversibly binds to 30S subunit of bacterial ribosomes; blocks recognition step in protein synthesis; causes growth inhibition. For gram-negative bacterial coverage of infections resistant to gentamicin and tobramycin. Effective against Pseudomonas aeruginosa.

Use patient's IBW for dosage calculation. The same principles of drug monitoring for gentamicin apply to amikacin.

Meropenem (Merrem IV)

Clinical Context:  Bactericidal broad-spectrum carbapenem antibiotic that inhibits cell-wall synthesis. Effective against most gram-positive and gram-negative bacteria. Has slightly increased activity against gram-negatives and slightly decreased activity against staphylococci and streptococci compared with imipenem.

Class Summary

Selection of empiric antimicrobial therapy must take into account the likely pathogens given the clinical setting. Selection of final antimicrobial therapy, once the identity of the infecting organism is known, should favor the safest and most cost-effective agent with the narrowest spectrum of activity to which the infecting pathogen is susceptible.

Further Inpatient Care

Further Outpatient Care

Inpatient & Outpatient Medications






Joshua S Hawley-Molloy, MD, Staff Physician, Infectious Disease Service, Associate Program Director, Internal Medicine Residency, Department of Medicine, Tripler Army Medical Center

Disclosure: Nothing to disclose.


Ebbing Lautenbach, MD, MPH, Director of Infection Control, Presbyterian Medical Center, Assistant Professor, Department of Medicine, Division of Infectious Disease, University of Pennsylvania School of Medicine

Disclosure: Nothing to disclose.

Evan G Brown, DO, Resident Physician, Department of Internal Medicine, Tripler Army Medical Center

Disclosure: Nothing to disclose.

Leanne B Gasink, MD, MSc, Assistant Professor, Department of Medicine and Faculty-Fellow, Center for Clinical Epidemiology and Biostatistics at the University of Pennsylvania School of Medicine; Associate Hospital Epidemiologist, Hospital of the University of Pennsylvania

Disclosure: Johnson and Johnson Salary Employment

Specialty Editors

Kenneth C Earhart, MD, Deputy Head, Disease Surveillance Program, United States Naval Medical Research Unit #3

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Charles V Sanders, MD, Edgar Hull Professor and Chairman, Department of Internal Medicine, Professor of Microbiology, Immunology and Parasitology, Louisiana State University School of Medicine at New Orleans; Medical Director, Medicine Hospital Center, Charity Hospital and Medical Center of Louisiana at New Orleans; Consulting Staff, Ochsner Medical Center

Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Disclosure: Nothing to disclose.

Additional Contributors

The views expressed in this abstract/manuscript are those of the authors and do not reflect the official policy or position of the Department of the Army, Department of Defense, or the U.S. Government.


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