Providencia species

Authors: Chelsie E Armbruster, PhD., Harry Mobley, PhD.

Previous authors: Robert R. Muder, M.D., Masashi Narita, M.D.


Providencia is a genus within the Enterobacteriaceae family closely related to the Providencia and Morganella genera. There are currently 8 recognized species within the genus: P. alcalifaciens, P. burhodogranaeriae, P. heimbachae, P. rettgeri, P. rustigianii, P. sneebia, P. stuartii,and P. vermicola (22, 61, 66, 71). Like other members of the tribe Proteeae, Providencia species produce the enzyme phenylalanine deaminase, which catalyzes the conversion of phenylalanine to phenylpyruvate.


P. stuartii is the most frequently encountered human pathogen within the genus. The most frequent site of isolation is the urinary tract of chronically catheterized patients (29, 38, 39, 61) in hospitals and long-term care facilities. Among this patient population, P. stuartii is recognized as a persistent colonizer (76, 77). It is common for multiple strains to be present simultaneously in a particular institution (29, 82). The urine of chronically catheterized patients is the usual reservoir of the organism (17). Nosocomially acquired P. stuartii are typically resistant to multiple antimicrobials (54, 65). P. rettgeri is also primarily a cause of nosocomial urinary tract infection (61). Neither organism is likely to cause urinary tract infection in ambulatory persons.

Reservoirs of P. alclifaciens include water, wastewater and soil. It appears to be an agent of gastrointestinal infections in humans (3, 27) and has been reported to cause hemorrhagic pneumonia in piglets (75). Settings in which this agent has been implicated include foodborne enteritis and traveler's diarrhea (3, 13, 27, 58). A large food-borne outbreak of P. alcalifaciens-associated diarrhea occurred in Japan (58). An outbreak of enteritis caused by P. alcalifaciens occurred among Czech Army Field Hospital personnel during their stay in Turkey (13).

Human isolates of P. rustigianii and P. heimbachae are rare; their role, if any, in human disease is uncertain (31, 57). P. vermicola was first isolated from a nematode (71) and later from a diseased rohu fish (56), but this species has not been implicated in human infection. P. sneebia and P.burhodogranaeriae were isolated from fruit flies (36) and have not been reported to cause human infection.

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Clinical Manifestations

The most frequent clinical manifestation of P. stuartii infection is urinary tract infections in the catheterized patient (29, 38, 39, 78). Wound infections and pneumonia may also occur, particularly in critically ill patients (4, 21, 50, 84). P. stuartii bacteremia most commonly arises from urinary tract infection (54, 81). Bacteremia in the course of pneumonia or burn wound infection may occur as well (79). As of 2014, there have been three documented cases of P. stuartii meningitis (67, 70, 73), and P. stuartii has also been isolated from a case of Fournier's gangrene (11).

Clinical P. rettgeri infection presents as nosocomial urinary tract infection in the majority of cases. P. rettgeri has also been isolated from burn wounds (2, 25) and intra-abdominal infections (69).

P. alcalifacians causes an acute enteritis characterized by abdominal pain and watery diarrhea (58). Fever is present in one quarter of patients; tenesmus is uncommon. Based on a common source food-borne outbreak, the mean incubation period is 69 hours.

Laboratory Diagnosis

Providencia species are readily isolated from urine and blood using standard laboratory media. Most commercially available identification systems used in clinical laboratories accurately identify P. stuartii, P. alcalifaciens, and P. rettgeri (61). P. alcalifaciens appears as lactose-negative colonies on MacConkey agar (58). Urease activity is variable but common in Providencia spp., particularly those isolated from urinary tract infections (35, 52). Transfer of large conjugative plasmids from one Providencia species to another can add phenotypic traits that alter the species as identified by commercially available systems (16, 42). These traits include ability to ferment lactose and sucrose.


P. stuartii can directly adhere to urinary catheters (18), and adherence is associated with the presence of the mannose-resistant/Klebsiella-like hemagglutinatin, also known as MR/K fimbriae (50). P. stuartii isolates are also capable of adhering to uroepithelial cells through a process that also appears to involve fimbriae (53). P. stuartii pathogenesis can be investigated using a mouse model of ascending urinary tract infection (6, 34). In this model, infection with P. stuartii results in robust colonization of the bladder and kidneys, and bacteremia in a small percentage of mice (6)

P. alcalifaciens is an invasive enteric pathogen. Strains of P. alcalifaciens, isolated from patients with diarrhea, show invasion of Hep-2 and HeLa cells in vitro (4, 5, 28). Janda et al. reported that some P. alcalifaciens strains, as well as strains of P. stuartii and P. rettgeri, can invade HEp-2 monolayers (33). Injection of an outbreak strain into a rabbit ileal loop caused fluid accumulation, along with evidence of mucosal inflammation on histologic examination (58).

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In keeping with their role as nosocomial pathogens, strains of P. stuartii and P. rettgeri are often resistant to multiple antimicrobials. A study from Ethiopia reported that 75% of Providencia isolates were multi-drug resistant (25) and another study identified Providencia spp. as one of the two most common multi-drug resistant urinary tract infection isolates (43). Antimicrobial resistance patterns for 319 Providencia isolates collected over a 10-year period in Portugal are reported in Table 1 (43). Over 90% of isolates were resistant to aminoglycosides (amikacin, gentamicin, isepamicin, and netilmicin), 1st generation cephalosporins (cefazolin and cephradine), and amoxicillin. Approximately 20% of isolates were resistant to other penicillins (augmentin, piperacillin/tazobactam, and pivmecillinam), quinolones (ciprofloxacin, lomefloxacin, norfloxacin, and ofloxacin), and sulfonamides (co-trimoxazole). Roughly 10% of isolates were resistant to 2nd generation cephalosporins (cefoxitin and cefuroxime), and 5% of isolates were resistant to aztreonam. Approximately 99% of isolates remained susceptible to carbapenems (imipenem), 3rd generation cephalosporins (cefadizime, ceftazidime, and ceftibuten), and 4th generation cephalosporins (cefepime). However, it is important to note that these isolates were collected between 1999 and 2009 and may therefore underestimate the current level of antibiotic resistance.

Table 2 shows antibiotic resistance data for P. stuartii and P. rettgeri isolated from diverse sources including urinary tract infections, wounds, Fournier's gangrene, meningitis, blood, pus, and rectal swabs (2, 8, 9, 10, 11, 23, 24, 30, 32, 41, 44, 48, 49, 59, 62, 63, 70, 72, 73, 83, 84). The majority of these strains were isolatedbetween 2005 and 2011.

Providencia stuartii Antibiotic Susceptibility

As shown in Table 2, greater than 40% of P. stuartii isolates were reported to be resistant to aminoglycosides (gentamicin, spectinomycin, streptomycin, tobramycin), 1st generation cephalosporins (cefazolin and cephradine), 2nd generation cephalosporins (cefoxitin and cefuroxime), one 3rd generations cephalosporin (cefotaxime), nitrofurantoin, penicillins (amoxicillin, augmentin, ampicillin, ampicillin-sulbactam, and ticaricillin), quinolones (ciprofoloxacin, fluoroquinolone, levofloxacin, and nalidixic acid), trimethoprim/sulfamethoxazole, polymixins (including colisitin), tetracycline, and chloramphenicol (12, 64, 81). The beta-lactamase enzymes of most strains are not inhibited by clavulanate or sulbactam, but are inhibited by tazobactam; thus, most isolates are susceptible to piperacillin/tazobactam (21, 30). Most isolates remain susceptible to third-generation cephalosporins (20, 37, 81), but cefotaxime resistance has been observed in several cases (9, 41, 83). Virtually all isolates of P. stuartii remain susceptible to meropenem (8, 30, 56, 80, 81). However, carbapenem resistance needs to be carefully monitored. One study reported an outbreak of carbapenem resistance in Brazil, in which approximately 35% of P. stuartii isolates were resistant to ertapenem and imipenem (83), and other P. stuartii isolates have been reported to produce carbapenemases(49).

There has been a recent increase in reports of P. stuartii producing class A and class D extended-spectrum beta-lactamases (ESBLs) (1, 5, 11, 21, 23, 31, 37, 39, 40, 50, 78), which provide resistance to third-generation cephalosporins. Emerging P. stuartii beta-lactamases include the class A TEM, CTX-M, VEB, and the New Delhi metallo-β-lactamase (NDM-1) (2, 9, 32, 41, 44, 47, 48, 49, 59, 83),and the class D OXA-10 (2, 44, 47). Molecular epidemiologic evidence indicates that plasmids encoding ESBLs can be transferred from P. stuartii to other Enterobacteriaceae, including E. coli and Enterobacter aerogenes (2, 7, 9, 32, 41, 59). Although ESBL-producing strains are relatively uncommon in the community, large hospital-associated outbreaks of these strains may occur (9, 49, 74, 83). As is the case with other Enterobacteriaceae, standard susceptibility tests used by clinical laboratories may fail to detect ESBL production by P. stuartii isolates. AmpC-type β-lactamases (CBLs) have also recently been reported in P. stuartii isolates (2, 8, 83). These enzymes are capable of degrading penicillins and most cephalosporins and possibly carbapenems (83), and they are only poorly inhibited by β-lactamase inactivators(8). Spread of CBLs is of great concern if they contribute to carbapenem resistance, one of the few classes of antibiotics effective against P. stuartii.

Historically P. stuartii has been susceptible to ciprofloxacin, but two recent studies show that approximately 67% of current isolates are now resistant (8, 30). Quinolone resistant P. stuartii are endemic in a number of long-term care facilities (42, 56); frequent use of quinolones to treat urinary tract infection in these facilities is a pre-disposing factor. A gene that provides quinolone resistance (qnrA) has been identified on a P. stuartii plasmid (47) and detected in several P. stuartii isolates (2, 44, 59). Quinolone resistance via qnrA is readily transferred from P. stuartii to susceptible bacteria (2, 8) and will likely contribute to the spread of resistance. This is particularly troublesome as transfer of qnrA can be coupled with transfer of genes encoding ESBLs and aminoglycoside-modifying enzymes (47, 59)

Providencia rettgeri Antibiotic Susceptibility

The antimicrobial susceptibility patterns of P. rettgeri are generally similar to those of P. stuartii. Resistance is common for penicillins (amoxicillin-clavulanic acid, ampicillin, ampicillin-sulbactam, and piperacillin/tazobactam), polymyxins (including colistin), and 1st and 2nd generation cephalosporins (9, 10, 23, 24, 46, 65, 72, 80, 84). Some strains are aminoglycoside-susceptible, although aminoglycoside resistance is fairly frequent (2, 10, 23, 24, 63, 72, 84). Most strains are susceptible to quinolones, 3rd generation cephalosporins, aztreonam, imipenem, and meropenem (20, 21, 65, 80). However, recent reports of multi-drug resistant P. rettgeri have identified strains resistant to carbapenems (imipenem and meropenem), quinolones (ciprofloxacin), 3rd generation cephalosporins (cefotaxime, ceftazidime, and ceftriaxone), and even 4th generation cephalosporins (cefepime) (2, 10, 23, 24, 40, 63, 72, 84).

ESBLs and CBLs have been reported in several P. rettgeri isolates (2, 9, 45, 63, 69, 72). A Japanese laboratory identified 3 isolates of P. rettgeri that produced a metallo-β-lactamase, an enzyme capable of hydrolyzing imipenem and meropenem (60). NDM-1 has also been detected in P. rettgeri isolates (10, 24, 72, 84), and a qnr gene for quinolone resistance has also recently been detected in P. rettgeri isolates from France and Nigeria (2, 26).

Antibiotic Susceptible of Other Providencia spp.

P. alcalifaciens and P. rustigianii are typically susceptible to ampicillin, cephalosporins, and aminoglycosides (31, 64). The P. alcalifaciens responsible for hemorrhagic pneumonia in piglets had at least intermediate resistance to several aminoglycosides (amikacin, spectinomycin, streptomycin, kanamycin), quinolones (ofloxacin, levofloxacin, and ciprofloxacin), some penicillins (penicillin, piperacillin, and oxacillin), chloramphenicol, vancomycin, trimethoprim-sulfamethoxazole, minocycline, furantoin, tetracycline, medemycin, erythromycin, clarithromycin, polymyxin, and cefazolin (75). The isolate was susceptible to ampicillin, some aminoglycosides (gentamycin, streptomycin, and tobramycin), aztreonam, 2nd generation cephalosporins (cefoxitin and cefuroxime), 3rd generation cephalosporins (ceftriaxone, cefotaxime, and ceftazidime), and 4th generation cephalosporins (cefepime).

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Drug of Choice

Based on emerging patterns of antimicrobial resistance, definitive therapy for infection due to P. stuartii or P. rettgeri requires appropriate antimicrobial susceptibility testing. Because of widespread resistance to multiple antimicrobials and emerging resistance to fluoroquinolones, third generation cephalosporins (cefotaxime, ceftriaxone, and cefepime should be considered first line therapy for infections due to these species. Although there is very little information upon which to base treatment recommendations for infections due to P. alcalifaciens, ampicillin or a 2nd generation cephalosporin would be a reasonable choice based upon in vitro susceptibility testing.

Specific Infections

Urinary Tract Infection: Infections due to P. stuartii or P. rettgeri may be treated with third-generation cephalosporins. Seriously ill patients, or those unable to take oral medications, should receive parenteral therapy. Appropriate regimens include ceftriaxone 1 gm daily, cefotaxime 1 gm every 6-8 hours, and cefepime 0.5 – 1 gm every 12 hours. Stable patients able to take oral medications may receive an oral expanded-spectrum cephalosporin such as cefixime 500 mg daily or cefpodoxime 200 mg every 12 hours. Oral cephalosporin therapy may be particularly appropriate for treatment of urinary tract infections in nursing home patients, in whom parenteral therapy may be impractical. Because urinary tract infections due to these organisms is nearly always complicated by catheterization or other anatomic or functional abnormality of the urinary tract, treatment duration should be 10-14 days.

Bacteremia: Bacteremic infection due to P. stuartii or P. rettgeri most frequently arises from the urinary tract, although bacteremia may occur secondary to pneumonia or burn wound infection. Patients should receive treatment with a third-generation cephalosporin as outlined above. As ESBL production by P. stuartii and P. rettgeri is on the rise, it would be reasonable to test blood isolates for ESBL production since it may not be detected by routine clinical laboratory susceptibility tests.

Enteritis: Enteritis due to P. alcalifaciens appears to be of mild-to-moderate severity in healthy adults and children. It is likely that the majority of infections resolve spontaneously without treatment; there are no published studies of therapy. It would be reasonable to treat patients with severe or prolonged diarrhea with ampicillin or amoxicillin, 500 mg four times daily.

Alternative Therapy

Infections Due to P. stuartii or P. rettgeri: Aztreonam is an appropriate alternative to cephalosporins in patients with cephalosporin allergy. Aminoglycosides are another alternative if the infecting isolate is susceptible, but resistance to multiple aminoglycosides is common. If the isolate produces an ESBL, imipenem or meropenem would be appropriate. Parenteral or oral quinolones could be considered based on susceptibility. However, frequent use of quinolones in a facility tends to foster widespread quinolone resistance among multiple different strains of Providencia. Thus routine quinolone use is not recommended.

Enteritis Due to P. alcalifaciens: Reasonable alternatives to ampicillin or a cephalosporin include certain aminoglycosides, aztreonam or tetracycline, based on the results of susceptibility testing.

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Urinary catheters of patients with urinary tract infections should be removed or changed; this is particularly important for infections due to P. stuartii, since the continuing presence of adherent organisms on the catheter may provide a nidus for recurrent infection. Fluid and electrolyte replacement are essential in the treatment of P. alcalifaciens enteritis.


In patients with urinary tract infection and bacteremia, defervescence and clearing of the organism from the urine or blood are appropriate endpoints.


There are no available vaccines.


Because of the strong association of Providencia urinary tract infections with urinary catheterization, avoidance of urinary catheterization, removal of catheters after they are no longer needed, appropriate catheter care, and hand hygiene by healthcare workers may reduce the transmission of Providencia spp. in hospitals and nursing homes. Although data are limited, safe food handling practices designed to prevent transmission of other enteric pathogens should be effective in preventing food-borne transmission of P. alcalifaciens.

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Table 1.: Resistance of Providencia Species to Selected Antibiotics

Antibiotics aResistant Isolates/Total Number Tested (%)
Amikacin 285/307 (92.8%)
Gentamicin 288/307 (93.8%)
Isepamicin 262/282 (92.9%)
Netilmicin 289/306 (94.4%)
Spectinomycin NR
Streptomycin NR
Tobramycin NR
Ertapenem NR
Imipenem 4/308 (1.4%)
Merepenem NR
1st Generation Cephalosporins:
Cefazolin (Cephazolin) 298/311 (95.8%)
Cephradine 300/310 (96.8%)
2nd Generation Cephalosporins:
Cefoxitin 26/308 (8.4%)
Cefuroxime 32/317 (10.1%)
3rd Generation Cephalosporins:
Cefadizime 3/269 (1.1%)
Cefotaxime (Cefatam) NR
Ceftazidime 0/313 (0%)
Ceftibuten 0/313 (0%)
Ceftriaxone (Rocephin/Epicephin) NR
4th Generation Cephalosporins:
Cefepime 0/314 (0%)
Aztreonam 16/310 (5.2%)
Nitrofurantoin 268/307 (87.3%)
Amoxicillin 311/314 (99.0%)
Amoxicillin-Clavulanic Acid (Augmentin) 57/309 (18.4%)
Ampicillin NR
Ampicillin-Sulbactam NR
Piperacillin/Tazobactam 80/300 (26.7%)
Pivmecillinam 69/285 (24.2%)
Ticarcillin NR
Ciprofloxacin 57/312 (18.3%)
Fluoroquinolone NR
Levofloxacin NR
Lomefloxacin 51/272 (18.7%)
Nalidixic Acid NR
Norfloxacin 59/307 (19.2%)
Ofloxacin 60/310 (19.3)
Trimethoprim-sulfamethoxazole (Co-trimoxazole) 70/303 (23.1%)
Colistin (Polymyxin E) NR
Polymyxin B NR
Tetracycline NR
Tigecycline NR
Dichloroacetic Acid Derivatives:
Chloramphenicol NR

a319 isolates were included in the study; NR=not reported

Table 2. Antibiotic resistance of recent P. stuartii and P. rettgeri isolates

Antibiotic aP. stuartii bP. rettgeri
Resistant Isolates/Total Number Tested (%)
Amikacin 71/1067 (6.6%) 16/20 (80.0%)
Gentamicin 649/1064 (61.0%) 11/11 (100%)
Isepamicin NR NR
Netilmicin NR NR
Spectinomycin 67/67 (100%) NR
Streptomycin 70/72 (97.2%) NR
Tobramycin 70/71 (98.6%) NR
Ertapenem 11/31 (35.5%) NR
Imipenem 11/32 (34.4%) 15/23 (65.2%)
Merepenem 11/1012 (1.1%) 10/12 (83.3%)
1st Generation Cephalosporins:
Cefazolin (Cephazolin) 874/990 (88.3%) NR
Cephradine NR NR
2nd Generation Cephalosporins:
Cefoxitin 13/21 (61.9%) 11/14 (78.6%)
Cefuroxime 486/989 (49.1%) 5/7 (71.4%)
3rd Generation Cephalosporins:
Cefadizime NR NR
Cefotaxime (Cefatam) 19/20 (95.0%) 6/7 (85.7%)
Ceftazidime 140/1082 (12.9%) 18/18 (100%)
Ceftibuten NR NR
Ceftriaxone (Rocephin/Epicephin) 37/990 (3.7%) 5/8 (62.5%)
4th Generation Cephalosporins:
Cefepime 71/1007 (1.7%) 8/14 (57.1%)
Aztreonam 58/989 (5.9%) 5/5 (100%)
Nitrofurantoin 6/6 (100%) NR
Amoxicillin 68/72 (94.4%) NR
Amoxicillin-Clavulanic Acid (Augmentin) 6/6 (100%) 5/6 (83.3%)
Ampicillin 851/994 (85.6%) 3/3 (100%)
Ampicillin-Sulbactam 4/4 (100%) 8/12 (66.7%)
Piperacillin/Tazobactam 33/1002 (3.3%) 16/18 (88.9%)
Pivmecillinam NR NR
Ticarcillin 12/12 (100%) NR
Ciprofloxacin 716/1071 (66.9%) 12/12 (100%)
Fluoroquinolone 11/11 (100%) NR
Levofloxacin 14/15 (93.3%) 2/8 (25.0%)
Lomefloxacin NR NR
Nalidixic Acid 18/18 (100%) NR
Norfloxacin NR NR
Ofloxacin NR NR
Trimethoprim-sulfamethoxazole (Co-trimoxazole) 445/1068 (41.7%) 2/3 (66.7%)
Colistin (Polymyxin E) 4/4 (100%) 15/15 (100%)
Polymyxin B 11/11 (100%) NR
Tetracycline 74/74 (100%) NR
Tigecycline NR 6/10 (60.0%)
Dichloroacetic Acid Derivatives:
Chloramphenicol 74/74 (100%) NR

a Compiled results for 1098 isolates from thirteen separate studies.
b Complied results for 25 isolates from eight separate studies.
NR=not reported


Baron EJ. Flow Diagram for Gram Neg Rods on BAP & MacConkey (NOT for stool isolates)

Review Article: Bush K, et al. MiniReview: Updated Functional Classification of β-lactamases. Antimicrob Agents Chemother 2010;54:969-976.

Review Article: Pitout JD. Enterobacteriaceae Producing ESBLs in the Community: Are They a Real Threat? Infect Med 2007;24:57-65.

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