Morganella Infections



Morganella morganii is a gram-negative rod commonly found in the environment and in the intestinal tracts of humans, mammals, and reptiles as normal flora. Despite its wide distribution, it is an uncommon cause of community-acquired infection and is most often encountered in postoperative and other nosocomial settings. M morganii infections respond well to appropriate antibiotic therapy; however, its natural resistance to many beta-lactam antibiotics may lead to delays in proper treatment.

The genus Morganella belongs to the tribe Proteeae of the family Enterobacteriaceae. The Proteeae, which also include the genera Proteus and Providencia, are important opportunistic pathogens capable of causing a wide variety of nosocomial infections. Currently, Morganella contains only a single species, M morganii, with 2 subspecies, morganii and sibonii. M morganii was previously classified under the genus Proteus as Proteus morganii.

In the late 1930s, M morganii was identified as a cause of urinary tract infections. Anecdotal reports of nosocomial infections began to appear in the literature in the 1950s and 1960s. Tucci and Isenberg reported a cluster epidemic of M morganii infections occurring over a 3-month period at a general hospital in 1977.[1] Of these infections, 61% were wound infections and 39% were urinary tract infections.

In 1984, McDermott reported 19 episodes of M morganii bacteremia in 18 patients during a 5.5-year period at a Veterans Administration hospital.[2] Eleven of the episodes occurred in surgical patients. The most common source of bacteremia was postoperative wound infection, and most infections occurred in patients who had received recent therapy with a beta-lactam antibiotic. Other important epidemiological risk factors in these studies included the presence of diabetes mellitus or other serious underlying diseases and advanced age.

In 2011, Kwon et al reported a case of a 65-year-old man with an infected aortic aneurysm in which the pathogen was M morganii. Diagnosis requires a high index of suspicion and imaging tests.[3]


M morganii has been associated with urinary tract infections, sepsis, pneumonia, wound infections, musculoskeletal infections, CNS infections, pericarditis, chorioamnionitis, endophthalmitis, empyema, and spontaneous bacterial peritonitis.



United States

M morganii is a rare cause of severe invasive disease. It accounts for less than 1% of nosocomial infections. M morganii is usually opportunistic pathogen in hospitalized patients, particularly those on antibiotic therapy.




Risk factors for M morganii infection include the following:

Laboratory Studies

Medical Care

Surgical Care


Consultations with a microbiologist, an infection control specialist, and/or an infectious diseases specialist may be warranted.

Medication Summary

Clinical trials are unavailable to assess optimal therapy. Treatment recommendations are based on results with similar gram-negative pathogens. Initiate treatment with an extended-spectrum antipseudomonal cephalosporin or penicillin combined with an aminoglycoside. Preferred beta-lactam antibiotics include cefepime, ceftazidime, aztreonam, piperacillin, and piperacillin-tazobactam. Carbapenems (ie, imipenem, meropenem) and intravenous fluoroquinolones are reserved for resistant cases.

Modify therapy based on the susceptibility test results. Uncomplicated infections often respond to monotherapy. Combination therapy with 2 antibiotics (choice based on susceptibility of organism) is preferred for complicated disease and immunocompromised patients. Duration of therapy should be appropriate for the clinical syndrome.

Cefepime (Maxipime)

Clinical Context:  Fourth-generation cephalosporin. Gram-negative coverage comparable to ceftazidime but has better gram-positive coverage (comparable to ceftriaxone). Cefepime is a zwitter ion; it rapidly penetrates gram-negative cells. Stable against rare isolates of M morganii, which produce ESBLs. Also stable against the more common M morganii isolates with derepressed chromosomal ampC beta-lactamases (Bush group 1).

Class Summary

Many nosocomial M morganii strains express derepressed chromosomal ampC beta-lactamases (Bush group 1) similar to those produced by P aeruginosa and Enterobacter species. These strains may be resistant to ceftazidime and other third-generation cephalosporins but are usually susceptible to cefepime, imipenem, meropenem, piperacillin, aminoglycosides, and fluoroquinolones. The beta-lactamase inhibitors (ie, clavulanic acid, sulbactam) are ineffective against these enzymes; however, the combination of piperacillin and tazobactam is more effective than piperacillin alone. Rare isolates of M morganii produce ESBLs. ESBLs hydrolyze drugs (eg, ceftazidime, cefotaxime, aztreonam) but have little effect on the cephamycins (eg, cefoxitin, cefotetan). ESBLs are inhibited by clavulanic acid.

Piperacillin-tazobactam (Zosyn)

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

Class Summary

Many nosocomial M morganii strains express derepressed chromosomal ampC beta-lactamases (Bush group 1). These strains usually are susceptible to piperacillin; however, the combination of piperacillin and tazobactam is more effective. Beta-lactamase inhibitors (eg, clavulanic acid, sulbactam) are ineffective against these enzymes.

Gentamicin (Garamycin)

Clinical Context:  Considered aminoglycoside of choice because of its low cost. Indicated for empiric treatment of life-threatening infections.

Class Summary

These agents bind irreversibly to 30S bacterial ribosomes, thus inhibiting synthesis of proteins. They are bactericidal. They demonstrate concentration-dependent killing and postantibiotic effect (PAE). These latter 2 properties have been instrumental in designing high-dose, extended-interval dosing regimens (ie, high serum concentrations saturate bacterial receptors, resulting in rapid bacterial killing). High doses are administered q24h (or longer), which allow adequate drug clearance. Despite drug elimination, bacterial regrowth is not observed (PAE). These regimens are equivalent or superior to conventional dosing in effectiveness and safety. Extended-interval regimens are also effective in patients with neutropenia.

Aminoglycosides are less effective in anaerobic or acidic environments because their transport (energy and oxygen dependent) is inhibited. Uptake is facilitated by bacterial cell wall synthesis inhibitors (ie, beta-lactams, vancomycin). They are administered parenterally to treat serious infections. They are highly polar; thus, they have low intracellular concentrations and cross the blood-brain barrier poorly. Other tissues where concentrations are suboptimal include eye, bone, and prostate.

Meropenem (Merrem)

Clinical Context:  Slightly increased activity against gram-negative organisms and slightly decreased activity against staphylococci and streptococci, compared to imipenem. Unlike imipenem, does not require a dehydropeptidase inhibitor (cilastatin). Has superior penetration of blood-brain barrier compared to imipenem. Useful to treat meningitis.

Class Summary

These agents are bactericidal broad-spectrum antibiotics that inhibit cell wall synthesis. Bicyclic beta-lactams are effective against most gram-positive, gram-negative, and anaerobic bacteria.

Aztreonam (Azactam)

Clinical Context:  Structurally similar to ceftazidime. Inhibits cell wall synthesis during bacterial growth.

Class Summary

These agents are monocyclic beta-lactam antimicrobials with activity only against aerobic gram-negative bacilli. Monocyclics can be used safely in patients with bicyclic beta-lactam hypersensitivity. No oral form is currently available. They are effective antibiotics; however, they are potent inducers of beta-lactamase production. Because of this, many hospitals restrict their use.

Levofloxacin (Levaquin)

Clinical Context:  Useful for infections due to multidrug-resistant gram-negative organisms, but drug of choice for only a few infections.

Class Summary

These are synthetic broad-spectrum antibacterial compounds. They have a novel mechanism of action, targeting bacterial topoisomerases II and IV, thus leading to a sudden cessation of DNA replication. Oral bioavailability is greater than 90%. Genetic barrier to resistance is not great (only 1-2 mutations).




James R Miller, MD, Assistant Professor, Department of Pediatrics, Uniformed Services University of the Health Sciences; Consulting Staff, Pediatric Infectious Diseases, Naval Medical Center at Portsmouth

Disclosure: Nothing to disclose.

Specialty Editors

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

John W King, MD, Professor of Medicine, Chief, Section of Infectious Diseases, Director, Viral Therapeutics Clinics for Hepatitis, Louisiana State University Health Sciences Center; Consultant in Infectious Diseases, Overton Brooks Veterans Affairs Medical Center

Disclosure: Merck Grant/research funds Other

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.


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