Morganella species

Authors: Te-Yu Lin,M.D.  Vivek Kak, M.D.Feng Yee Chang, Ph.D., M.D.


Morganella is the third member of the tribe Proteeae. Proteus and Providencia are the other members of this tribe and share some of the biochemical and clinical characteristics (89).  

In 1906 Morgan described a non-lactose fermenting organism in children with summer infantile diarrhea. This bacterium came to be known as Morgan’s bacillus and was later classified as Bacillus morganii (55). Independently Castellani isolated a bacterium while studying a case of fever in 1905 in Colombo, Sri Lanka. In 1914 he described this bacteria along with two others as Bacterium Columbense (12). Later in 1943 Fulton would classify these strains into the genus Morganella (27). In 1992 using DNA hybridization Jensen et al. defined two subspecies of Morganella (33).  

Morganella are motile, non-lactose fermenting gram-negative bacteria, which share with Proteus the capacity for urease production and presence of phenylalanine deaminase. They can be separated from Proteus species by the lack of swarming activity or gelatin liquefaction or H2S production. Morganella species can ferment mannose and have the enzyme ornithine decarboxylase which Proteus lack (24). Two subspecies, M. morganii subsp. Morganii and M. morganii subsp. Siboniiwith four and three biogroups respectively can be differentiated based on biochemical and genetic features (60).


Morganella species are infrequent causes of disease in healthy individuals. Morganella morganii was originally thought to be a cause of summer diarrhea. The organism has been isolated along with Proteus mirabalis more frequently in patients with diarrhea than in healthy controls (57). M. morganii  is found in the environment and in the intestinal tracts of humans, mammals, and reptiles as part of the normal flora  (23). Therefore,  most M. morganii bacteremia cases were opportunistic community-acquired infections. M. morganii  bacteremia is not common and only accounts for 0.69% of bacteremia reported by Lee et al (41). Custovic et al found 3.6% of  M. morganii  bacteremia among nosocomial infections in newborns (17).

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Clinical infections due to M. morganii often involve the urinary tract, skin and soft tissue and hepatobiliary tract (42).  Urinary tract infection is the most common clinical infection site. Most often these occur in elderly patients in nursing homes with long-term indwelling catheters (84). Morganella is the fifth leading cause of UTIs in nursing home patients (59). In a study of 20 patients with chronic indwelling urinary catheters, Warren et al. found Morganella bacteriuria in 19% of weekly specimens with a mean duration of bacteriuria of 3.3 weeks (83). In a prospective monitoring of all Morganella cultures in a VA microbiology laboratory 60% of isolates were from the urine, 18% from wounds and the remaining 22% from a variety of body fluids or tube drainage (49).  

Morganella usually causes skin and soft tissue infections. Falagas reported 13 patients (54%) suffered from skin and soft tissue infections in  a 4-year period at Greece hospital (23).  In a retrospective review of 19 cases of Morganella bacteremia McDermott found that 37% were related to wound infections (49).

Morganella could also cause intra-abdominal infections. The portals of entry of M. morganii bacteremia involved hepatobiliary tract was 22% by Lee report during one-year period (41).  In a retrospective review of 61 cases of M. morganii bacteremia, Kim found that  64% were related to intra-abdominal infections (included biliary infection, liver abscess and peritonitis) (38).

Morganella may rarely cause bacteremia. In a multicenter study of 2084 cases of bacteremia in Britain, Morganella accounted for 1% of cases and 4 deaths (46). Morganella has been reported as the cause of up to 3% of bacteremias in a nursing home, arising primarily from either the urinary tract or soft tissue infections (56).

Morganella species have been isolated in diabetic foot infections (65), necrotizing fasciitis (40), decubitus ulcer infections (56), septic arthritis (3975), meningitis (304774), otitis media (29), gastroenteritis (2), peritonitis and bacteremia (2833), chorioamnionitis (1134), pericarditis (58) and neonatal sepsis (337173). Isolated case reports have implicated Morganella species in pyomyostis (3), and tubo-ovarian abscess (13, 68). A case of Morganella pericarditis in a bone marrow transplant patient has also been reported (77).


Definitive diagnosis of Morganella infections requires isolation of the bacteria in the clinical laboratory. Morganella grow as flat, colorless 2- to 3-mm colonies on MacConkey’s and sheep-blood agar. However current commercial database systems used in subspecies identification have only M. morganii subsp. morganii listed in their database so far. The phenotypic separation of the Morganella subspecies can be done by the inability of M. morganii subsp. sibonii to ferment the sugar trehalose (60).

The matrix-assisted laser desorption ionization time-of- flight mass spectrometry (MALDI-TOF MS) is a rapid, accurate, and cost-effective method of microbial characterization and identification (1522).This technology generates characteristic mass spectral fingerprints, that are unique signatures for each microorganism and are thus ideal for an accurate microbial identification at the genus and species levels and has a potential to be used for strain typing and  identification.


The ability of Morganella to cause infections in the urinary tract may be due to the MR/K hemagglutinin that enhances adherence to urinary catheters (53). Additionally, Morganella produces a urease that predisposes to encrustation of urinary catheters (78). The Morganella urease also can be activated at a low pH, which may enhance the bacterial survival at low pH (90). Morganella species may also produce a hemolysin, which enhances virulence by lysing erythrocytes due to the formation of hydrophilic pores in the cell wall (86).

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Beta-Lactam Antibiotics

Resistance to β-lactam antibiotics in Morganella species is usually mediated by the presence of chromosomally encoded β-lactamases belonging to the AmpC β-lactamase family. These β-lactamases are typically inducible in the presence of β-lactam antibiotics (10), with only trace amounts being produced in the absence of antibiotics. In the presence of enzyme-inducing antibiotics these enzymes may lead to expression of high-level resistance. As a result, agents such as ampicillin, amoxicillin, and "first-generation" cephalosporins are ineffective. "Second-generation" cephalosporins such as cefuroxime are also ineffective against Morganella with MIC90s ranging from 16 to 64 mg/mL (6467985). Cefoxitin, though a potent beta-lactamase inducer appears more stable against Morganella than Enterobacter (44).

A second mechanism of β-lactam resistance in Morganella is the chromosomally mediated hyperproduction of β-lactamases. These strains have mutations at the ampD locus leading to stable derepression of the β-lactamase gene and permanent production of excessive enzyme levels. These derepressed strains continuously produce β-lactamase without a need for an inducing antibiotic (89). The sequence of the gene encoding one of these β-lactamases has been published (4). The extended-spectrum penicillins and "third-generation" cephalosporins are generally not active against Morganella strains that are constitutive hyperproducers of β-lactamases.  Addition of clavulanic acid or sulbactam to these agents fails to enhance their activity against derepressed organisms. Thus the MICs of ticarcillin and ticarcillin-clavulanate against Morganella are the same (25). Tazobactam, on the other hand, enhances the activity of piperacillin against derepressed strains. Hence, the combination of piperacillin plus tazobactam is five times more active than piperacillin alone (44).

The third-generation cephalosporins ceftriaxone, cefotaxime, and ceftazidime are more active against Morganella, with MIC90s ranging from 0.03 to 32 mg/mL (7). The MICs for cefotaxime and ceftazidime are 0.015 and 0.06 mg/mL for inducible strains but 4 and 8 mg/mL for constitutive hyperproducers, respectively (44).  

The most active β-lactam antibiotics against the derepressed and inducible isolates are cefipime and cefpirome. These agents are the most β-lactamase stable and have MICs against the derepressed isolates of 1 to 4 mg/mL versus more than 64 mg/mL for cefotaxime (44). Cefipime appears to be the most active cephalosporin (MIC90s, 0.03-0.25 mg/mL). Washington found MIC90s to cefipime below 1mg/mL for all isolates (85); Kessler found that 100% of isolates had MICs below 8 mg/mL and that cefipime was more active than ceftazidime, ceftriaxone, or imipenem (37). This increase in cefipime activity is due to an increased resistance to enzymatic hydrolysis compared  to the other cephalosporins. MICs for aztreonam range between 0.06 and 0.12 mg/mL (61). Jean found  remarkably high imipenem-non-susceptible rates were documented for M. morganii in 2009 (32). Meropenem appears to be the most active of the carbapenems, and is active even against some imipenem-resistant isolates (67). The new carbapenem ertapenem at a concentration of 4mg/mL inhibited 100% of isolates of AmpC-producing Morganella morganii (54).  

A third mechanism of resistance of β-lactam resistance in Morganella strains is due to extended-spectrum β-lactamase (ESBL) production. ESBLs are plasmid-mediated enzymes that can confer resistance to third generation cephalosporins such as cefotaxime, ceftriaxone, ceftazidime as well as the monobactamaztreonam but are generally susceptible to β-lactam + β-lactamase inhibitor combinations. The carbapenems however still maintain their activity against ESBL-producing strains of Morganella. The occurrence of ESBLs in Morganella morganii has been reported (1669), and a few have been characterized at the molecular level (581). Since 1990,Morganella isolates possessing the extended spectrum TEM-13, TEM-10, TEM-21 and TEM-72 enzymes have been reported (55064, 81). In a 1992 survey of 1000 isolates of Enterobacteriaceae, Liu found several Morganella isolates possessing SHV, TEM, or OXA plasmid-mediated β-lactamases (43).

Non β- Lactam Antibiotics

Aminoglycosides are usually active against Morganella (19). Between 71 and 100% of Morganella isolates from the Medical College of Virginia remained susceptible to aminoglycosides (45). At the Mayo Clinic, 91 and 98% of 163 isolates of M. morganii were reported susceptible to less than 2 mg/mL of gentamicin and less than 8 mg/mL of amikacin, respectively (20). Aminoglycoside resistance among Morganella is rare and mediated by a variety of complex combinations of enzymes, the most frequent of which is the modifying enzyme ANT(2")- I which confers resistance to gentamicin, tobramycin, and kanamycin (52).  

The fluroquinolones are highly active against Morganella, with the MIC90s for most isolates below 0.25 mg/mL (264679). Ciprofloxacin is twice as active as ofloxacin in vitro (46). In a study of 390 clinical isolates, 97% were ciprofloxacin susceptible (1). Decreased quinolone uptake has been described in laboratory mutants of Morganella, due to enhanced efflux as well as decreased permeability of the quinolones in those strains (18).

Trimethoprim-sulfamethoxazole is also active against some Morganella (MIC50s-0.06 mg/mL; MIC90s 16 mg/mL) (46).

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Therapeutic choices for infections due to Morganella are primarily based upon in vitro susceptibility data, since little information is available from clinical trials. The antibiotic of choice depends upon the site of infection, the nature of the host and the local pattern and prevalence of resistance.

Specific Infections


Initial therapy for patients with suspected bacteremia due to Morganella should be selected on the basis of local susceptibility patterns. A third-generation cephalosporin has been suggested as the drug of choice for Morganella infections (51).  This recommendation certainly holds for initial empirical treatment for Morganella infections in areas where local susceptibility patterns indicate absence of ESBL producing strains. However, while using these drugs, clinicians need to be aware of a potential drug resistance to emerge in vivo due to the constitutive production of the AmpC β-lactamase as has been seen in Enterobacter (14). Addition of an aminoglycoside to a cephalosporin may decrease the potential of emergence of resistance to broad-spectrum cephalosporins (36). In areas where bacteremia may be due to presence of an ESBL producing strain, the carbapenems should be regarded as drugs of choice (62). The published experience in using carbapenems against ESBL producing organisms is most with imipenem though  meropenem appears to be more active than it in-vitro (67). Ertapenem also has good in vitro activity against Morganella (54). In addition to a cell wall active agent, some physicians would recommend combination therapy with the addition of an aminoglycoside active against Morganella in cases of bacteremia.

For patients with allergy to β-lactams and or carbapenems an attractive option would be the use of quinolones such as ciprofloxacin. In general the newer quinolones offer no therapeutic advantage over ciprofloxacin for treatment of Morganella infections. In the future though, increasing in-vitro resistance to the quinolones by ESBL producing organisms may limit this option. Another option for susceptible strains would be the use of high dose trimethoprim-sulfamethoxazole and aminoglycosides.

The exact duration of treatment for these infections has not been studied but a course of at least 2 weeks appears reasonable.

Urinary Tract Infection

UTI’s due to Morganella should be treated with oral quinolones like ciprofloxacin. The absence of high levels of resistance so far to this class of drugs in Morganella makes this an attractive choice. Other options include the third generation cephalosporins and trimethoprim-sulfamethoxazole.  

For UTI’s caused by ESBL-producing strains of Morganella a quinolone still is probably the drug of choice, though there have been several reports of urinary tract infection due to ESBL-producing organisms being successfully treated with cephalosporins, despite the results of in-vitro susceptibility tests (24). Other treatment options for these infections include trimethoprim-sulfamethoxazole (for susceptible strains) or carbapenems.

 In cases of uncomplicated UTI’s due to Morganella a course of 3 to 5 days of therapy should be adequate; however Morganella UTI’s are generally associated with complicating features such as indwelling catheters. In such cases the duration of therapy should be at least 2 to 3 weeks.

Wound Infection

Nosocomial wound infections can often be due to Morganella species (284987). These infections can be polymicrobial or monobacterial in origin. An important caveat in management of these infections is adequate debridement of the infected tissues. In general these infections should be treated with the use of a broad-spectrum agent such as piperacillin-tazobactam. Other options include the use of third generation cephalosporins like ceftriaxone, cefipime or a quinolone with an antianaerobic drug. For infections caused by an ESBL-producing strain, the drug of choice is generally a carbapenem. The once daily administered, ertapenem is an attractive option in severe wound infections caused by ESBL producing strains of Morganella morganii.

Intra-abdominal Infection

Morganella species are often involved in intra-abdominal infections (41). These infections can be polymicrobial or mixed with anaerobic bacteria. Treatment emphasizes the importance of adequate drainage or removal of the infected tissues. Broad-spectrum antibiotic such as  piperacillin-tazobactam was the first choice;  other options include the use of third generation cephalosporins like ceftriaxone, cefipime or a  fluoroquinolone. Carbapenem, especially meropenem or ertapenem was indicated if  ESBL-producing strain was considered.

Neonatal Infections

Though Morganella species are an extremely rare cause of neonatal infections, recently increasing case reports have implicated this organism as a cause of neonatal brain abscess (82), neonatal sepsis, as well as necrotising fascitis (40). It is thought that the neonate acquires the infection probably from overt or subtle chorioamnionitis in the mother. The other risk factor of acquisition of these bacteria in a neonate may be use of   ampicillin as prophylactic therapy during pregnancy. Antibiotic therapy of these infections in a neonate should be with a combination of a third generation cephalosporin such as cefotaxime and an aminoglycoside.

Underlying Diseases

The majority of infections caused by Morganella are in patients who have been hospitalized and may have urinary catheters or intravenous lines or wounds that can get infected (8, 616380). Other cases have been reported in individuals with underlying immune defects due to diabetes, AIDS, splenectomy, Hodgkin’s disease, cirrhosis of liver, solid organ malignancy and autoimmune disease (42).

Alternative Therapy

In general use of alternative drugs for treatment of Morganella infections must be guided by the isolated organisms in-vitro susceptibility pattern. The use of combination therapy using a β-lactam antibiotic with an aminoglycoside has been traditionally used in serious Morganella infections although no data exists from controlled studies supporting such a practice.

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Besides optimal antibiotics, adjunctive therapy is important for treatment of Morganella infections. The urinary catheter should be replaced in urinary tract infections. Intravenous lines should also be replaced in cases of bacteremias and wounds should be adequately debrided. In cases of diabetic foot infections due to Morganella the vascular supply of the infected areas should be assessed to determine the presence of any arterial insufficiency.


In general once appropriate therapy is initiated against Morganella infections, patients, if febrile initially, should defervesce in 48-72 hours. In cases of urinary tract infections failure to defervesce should prompt an evaluation of the kidney to exclude any obstruction to the collecting system and or any abscesses. Deep wound infections should also be evaluated for any underlying osteomyelitis. Generally there is little need for follow-up cultures to document bacteriological cure if the patient responds clinically.


There are no vaccines in development against Morganella.


Over the last few years the antibiotic susceptibility of Morganella species has gradually shown a trend towards increased resistance, with certain strains also showing the presence of ESBLs. In areas where ESBL-producing organisms have been recently documented, infection control methods should be implemented to limit spread of these organisms. These may include checking for rectal colonizers of these organisms, vigorous handwashing practices, use of contact isolation for infected or colonized patients. If there are multiple different clones of ESBL producing organisms in a hospital, changes in antibiotic use policy in the hospital may have a role in decreasing the number of these organisms (70).

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TABLE 1.  Comparative Activity of Antibiotic Against Morganella morganii

Antibiotic No. Isolates MIC50 MIC90
Amoxicillin 9 128 128
Amoxicillin-clavulanate 39 16 64 >64 >64 >64
Ticarcillin 165 <1 16
Ticarcillin-clavulanate 165 <1 16
Cefaclor 16 39 >64 >64 >64 >64
Cefuroxime 39 39 62 >64 >64 >16 >64 >64 >16
Cefoxitin 9 39 16 8 512 >64
Cefixime 19 16 0.008 2 0.008 32
Cefpodoxime 19 0.06 0.5
Ceftriaxone 39 33 0.5 <0.03 8 2
Cefotaxime 9 33 8 0.06 16 2
Ceftazidime 9 62 33 8 <0.25 0.25 32 <0.25 2
Cefipime 62 33 <0.25 0.03 <0.25 0.12
Cefoperazone 33 1 16
Imipenem 33 2 4
TMP-SMXa 39 0.06 16
Fleroxacin 39 0.06 0.12
Ciprofloxacin 39 0.06 0.06
Ofloxacin 39 0.12 0.25
Lomefloxacin 39 0.12 0.25

a TMP-SMX, trimethoprim-sulfamethoxazole.

Adapted from references 920,29,34,52,58,62,70 by Orenstein R, Wong ES. Morganella Species- In: Yu VL, MerriganJr TC, Barriere SL. Antimicrobial Therapy and Vaccines. Wilkins and Wilkins .1999.

TABLE 2.  Recommendation For Treatment Of Infections Caused By Morganella.

Site of Infection Non-ESBL-Producing ESBL-Producing
1st Line 2nd Line 1st Line 2nd Line
Bacteremia III Generation Cephalosporin a Ciprofloxacinb Carbapenemsc   Ciprofloxacin
Urinary Tract Infection Ciprofloxacin III Generation Cephalosporin a Ciprofloxacin III Generation Cephalosporin a


Adult Dose
aIII Generation Cephalosporin
Cefotaxime 1-2 gm I.V q. 8h.
Ceftriaxone 1-2 gm/ I.V q. day
  500-750 mg orally b.i.d.
  400 mg I.V b.i.d.
Meropenem 0.5-1 gm I.V q8-12h.
Imepenem 0.5-1 gm I.V q.6-8h
Ertapenem 0.5-1 gm I.V qd
Doripenem 0.25-0.5 gm I.V q.8-12h

*In vitro data showed ESBL producing strain more susceptible to meropenem; in vivo data was not available.

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