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.


Urinary tract infections

M morganii is commonly recovered from urine cultures in patients with long-term indwelling urinary catheters.

In a study of 135 consecutive patients with symptomatic, complicated, multidrug-resistant urinary tract infections, nearly 10% were infected with M morganii.

Like Proteus species, M morganii has properties that enhance its ability to infect the urinary tract; these include motility and the ability to produce urease.

Urolithiasis is associated with both genera. Members of the tribe Proteeae account for approximately 50% of cases of urolithiasis associated with urinary tract infections in children.

Perinatal infections

M morganii has been associated with perinatal infection. Four cases of chorioamnionitis and one case of postpartum endometritis have been reported, and each case involved immunocompetent women.[4, 5]

Three of the women had received parenteral treatment with ampicillin prior to delivery.

In 2 of the pregnancies, the neonates were not infected.

A third neonate developed early-onset sepsis and M morganii bacteremia. He was treated successfully with 10 days of cefotaxime and gentamicin. A fourth neonate, born at 24 weeks' gestation, died within the first 38 hours of life. M morganii was recovered from this neonate's blood, pleural fluid, and peritoneal fluid cultures.

The fifth case occurred in a mother who had repeated exposures to beta-lactam antibiotics in the months prior to delivery for rheumatic fever prophylaxis and pharyngitis and then had intrapartum ampicillin for chorioamnionitis. Her neonate, born at 35 weeks' gestation, was treated empirically with intravenous ampicillin and gentamicin immediately after delivery, but he developed respiratory distress and petechial and purpuric skin lesions on the second day of life. A chest radiograph revealed a lobar infiltrate. Blood culture findings were positive for M morganii that was resistant to ampicillin and susceptible to cefotaxime and gentamicin. He recovered following a 14-day course of cefotaxime and gentamicin. His mother remained febrile after delivery, with evidence of endometritis and subsequent M morganii urinary tract infection. Her isolate was resistant to ampicillin and gentamicin and was treated successfully with imipenem-cilastatin.

Two cases of early-onset neonatal sepsis in the absence of maternal infection have been reported. Both involved 32-week–premature neonates born to mothers who had received dexamethasone and ampicillin prior to delivery. Both neonates were treated with cefotaxime and amikacin. One neonate's sepsis responded to treatment; the other neonate died from M morganii infection.

Late-onset neonatal infection

Late-onset neonatal infection has been reported in 2 neonates: (1) a neonate born at term who presented on the 11th day of life with fever, irritability, and M morganii bacteremia and (2) a 15-day-old neonate with M morganii meningitis and brain abscess.[6]

Necrotizing fasciitis

Fatal necrotizing fasciitis caused by M morganii and Escherichia coli was reported in a 1-day-old neonate who had been inadvertently dropped into a toilet bowl during a home delivery.[7]

Skeletal infections

Four cases of M morganii septic arthritis have been reported in adults. All presented as chronic indolent infections. In contrast to the aggressive and destructive joint disease associated with Proteus mirabilis septic arthritis, the cases of M morganii arthritis were remarkable for their benign clinical presentations and lack of joint damage despite a prolonged course.[8, 9, 10]


M morganii is commonly found in the mouths of snakes. As a result, it is one of the organisms recovered most often from snakebite infections. Jorge (1994) recovered M morganii from 57% of abscesses occurring at the site of Bothrops (ie, the American Lanceheads) bites.[11]

Scombroid poisoning

M morganii produces the enzyme histidine decarboxylase, which reacts with histidine, a free amino acid present in the muscle of some species of fin fish, including tunas, mahimahi, sardines, and mackerel. When these fish are improperly stored, spoilage from M morganii may cause the decarboxylation of histidine into histamine. Scombroid poisoning, an anaphylacticlike clinical syndrome, is caused by ingestion of the histamine-containing fish.[12, 13]

Infections in people with AIDS

Two case reports of M morganii infection in patients with AIDS exist: a 45-year-old man with meningitis[14] and a 31-year-old man with pyomyositis.[15]


In a retrospective review of 73 patients with M morganii bacteremia in Taiwan, 70% cases were community acquired and 45% were associated with polymicrobial bacteremia. The most common portals of entry were the urinary tract and hepatobiliary tract. Polymicrobial infection was most commonly associated with hepatobiliary disease. The overall mortality rate was 38%. The most important risk factor for mortality was inappropriate antibiotic therapy.[16]

CNS infections

CNS infections are rare. Six adult cases have been reported, including 3 cases of meningitis and 3 cases of brain abscess. The most common presentation was fever and altered mental status. Two of the patients with meningitis died. Two patients with brain abscess survived, one with long-term neurological sequelae.[17]


Physical findings are similar to those of other gram-negative infections.

Ecthyma gangrenosum–like eruptions and hemorrhagic bullae have been associated with M morganii sepsis.

One 15-year-old girl with recurrent episodes of Henoch-Schönlein purpura was found to have a tuboovarian abscess caused by M morganii. Treatment of the infection resulted in complete remission of the vasculitis.[18]


Risk factors for M morganii infection include the following:

Laboratory Studies

Identification of M morganii is made by recovery of small oxidase-negative catalase and indole-positive gram-negative rods on blood agar or MacConkey agar.

M morganii ferments glucose and mannose but not lactose.

M morganii is motile, facultatively anaerobic, and nonencapsulated, and it hydrolyzes urease and reduces nitrates.

Unlike Proteus species, swarming does not occur.

M morganii urinary tract infections are often associated with an alkaline urine pH.

Medical Care

M morganii strains are naturally resistant to penicillin, ampicillin, ampicillin/sulbactam, oxacillin, first-generation and second-generation cephalosporins, erythromycin, tigecycline, colistin, and polymyxin B.

Most strains are naturally susceptible to piperacillin, ticarcillin, mezlocillin, third-generation and fourth-generation cephalosporins, carbapenems, aztreonam, fluoroquinolones, aminoglycosides, and chloramphenicol.

The widespread use of third-generation cephalosporins has been associated with the emergence of highly resistant M morganii, as follows:

Surgical Care

Drain any abscesses. Aggressive surgical drainage is required for brain abscesses caused by M morganii.

Debride any surgical wounds.


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).


Prevent M morganii infection by observing appropriate infection control practices and judiciously using beta-lactam antibiotics.


The prognosis depends on the type of infection and the particular host.

Data suggest that inappropriate antimicrobials (ones that an organism is resistant to) are associated with a worse outcome.


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: Received salary from Medscape for employment. for: Medscape.

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: Nothing to disclose.

Chief Editor

Pranatharthi Haran Chandrasekar, MBBS, MD, Professor, Chief of Infectious Disease, Program Director of Infectious Disease Fellowship, Department of Internal Medicine, Wayne State University School of Medicine

Disclosure: Nothing to disclose.


  1. Tucci V, Isenberg HD. Hospital cluster epidemic with Morganella morganii. J Clin Microbiol. 1981 Nov. 14(5):563-6. [View Abstract]
  2. McDermott C, Mylotte JM. Morganella morganii: epidemiology of bacteremic disease. Infect Control. 1984 Mar. 5(3):131-7. [View Abstract]
  3. Kwon OY, Lee JS, Choi HS, Hong HP, Ko YG. Infected abdominal aortic aneurysm due to Morganella morganii: CT findings. Abdom Imaging. 2011 Feb. 36(1):83-5. [View Abstract]
  4. Johnson JR, Feingold M. Case of chorioamnionitis in an immunocompetent woman caused by Morganella morganii. J Matern Fetal Med. 1998 Jan-Feb. 7(1):13-4. [View Abstract]
  5. Ranu SS, Valencia GB, Piecuch S. Fatal early onset infection in an extremely low birth weight infant due to Morganella morganii. J Perinatol. 1999 Oct-Nov. 19(7):533-5. [View Abstract]
  6. Verboon-Maciolek M, Vandertop WP, Peters AC, et al. Neonatal brain abscess caused by Morganella morgagni. Clin Infect Dis. 1995 Feb. 20(2):471. [View Abstract]
  7. Krebs VL, Koga KM, Diniz EM. Necrotizing fasciitis in a newborn infant: a case report. Rev Hosp Clin Fac Med Sao Paulo. 2001 Mar-Apr. 56(2):59-62. [View Abstract]
  8. Gautam V, Gupta V, Joshi RM, et al. Morganella morganii-associated arthritis in a diabetic patient. J Clin Microbiol. 2003 Jul. 41(7):3451. [View Abstract]
  9. Katz LM, Lewis RJ, Borenstein DG. Successful joint arthroplasty following Proteus morganii (Morganella morganii) septic arthritis: a four-year study. Arthritis Rheum. 1987 May. 30(5):583-5. [View Abstract]
  10. Schonwetter RS, Orson FM. Chronic Morganella morganii arthritis in an elderly patient. J Clin Microbiol. 1988 Jul. 26(7):1414-5. [View Abstract]
  11. Jorge MT, Ribeiro LA, da Silva ML, et al. Microbiological studies of abscesses complicating Bothrops snakebite in humans: a prospective study. Toxicon. 1994 Jun. 32(6):743-8. [View Abstract]
  12. Lopez-Sabater EI, Rodriguez-Jerez JJ, Hernandez-Herrero M, et al. Incidence of histamine-forming bacteria and histamine content in scombroid fish species from retail markets in the Barcelona area. Int J Food Microbiol. 1996 Jan. 28(3):411-8. [View Abstract]
  13. Otwell WS. Scombroid Poisoning. US Food and Drug Administration, Sea Grant Extension Fact Sheet. 1995.
  14. Mastroianni A, Coronado O, Chiodo F. Morganella morganii meningitis in a patient with AIDS. J Infect. 1994 Nov. 29(3):356-7. [View Abstract]
  15. Arranz-Caso JA, Cuadrado-Gomez LM, Romanik-Cabrera J, et al. Pyomyositis caused by Morganella morganii in a patient with AIDS. Clin Infect Dis. 1996 Feb. 22(2):372-3. [View Abstract]
  16. Chen HW, Lin TY. Tumor abscess formation caused by Morganella morganii complicated with bacteremia in a patient with gastrointestinal stromal tumor. Clin Res Hepatol Gastroenterol. 2011 Sep 14. [View Abstract]
  17. Abdalla J, Saad M, Samnani I, et al. Central nervous system infection caused by Morganella morganii. Am J Med Sci. 2006 Jan. 331(1):44-7. [View Abstract]
  18. Pomeranz A, Korzets Z, Eliakim A, et al. Relapsing Henoch-Schonlein purpura associated with a tubo-ovarian abscess due to Morganella morganii. Am J Nephrol. 1997. 17(5):471-3. [View Abstract]
  19. Choi SH, Lee JE, Park SJ, et al. Emergence of antibiotic resistance during therapy for infections caused by Enterobacteriaceae producing AmpC beta-lactamase: implications for antibiotic use. Antimicrob Agents Chemother. 2008 Mar. 52(3):995-1000. [View Abstract]
  20. Bagel J, Grossman ME. Hemorrhagic bullae associated with Morganella morganii septicemia. J Am Acad Dermatol. 1985 Mar. 12(3):575-6. [View Abstract]
  21. Bensman A, Roubach L, Allouch G, et al. Urolithiasis in children. Presenting signs, etiology, bacteriology and localisation. Acta Paediatr Scand. 1983 Nov. 72(6):879-83. [View Abstract]
  22. Casanova-Roman M, Sanchez-Porto A, Casanova-Bellido M. Early-onset neonatal sepsis caused by vertical transmission of Morganella morganii. Scand J Infect Dis. 2002. 34(7):534-5. [View Abstract]
  23. Cox CE. Aztreonam therapy for complicated urinary tract infections caused by multidrug-resistant bacteria. Rev Infect Dis. 1985 Nov-Dec. 7 Suppl 4:S767-71. [View Abstract]
  24. Cunningham ET Jr, Whitcher JP, Kim RY. Morganella morganii postoperative endophthalmitis. Br J Ophthalmol. 1997 Feb. 81(2):170-1. [View Abstract]
  25. Del Pozo J, Garcia-Silva J, Almagro M, et al. Ecthyma gangrenosum-like eruption associated with Morganella morganii infection. Br J Dermatol. 1998 Sep. 139(3):520-1. [View Abstract]
  26. Dutta S, Narang A. Early onset Neonatal Sepsis due to Morganella morganii. Indian Pediatr. 2004 11 7. 41(11):1155-1157. [View Abstract]
  27. Gebhart-Mueller Y, Mueller P, Nixon B. Unusual case of postoperative infection caused by Morganella morganii. J Foot Ankle Surg. 1998 Mar-Apr. 37(2):145-7. [View Abstract]
  28. Isobe H, Motomura K, Kotou K, et al. Spontaneous bacterial empyema and peritonitis caused by Morganella morganii. J Clin Gastroenterol. 1994 Jan. 18(1):87-8. [View Abstract]
  29. Lee IK, Liu JW. Clinical characteristics and risk factors for mortality in Morganella morganii bacteremia. J Microbiol Immunol Infect. 2006 Aug. 39(4):328-34. [View Abstract]
  30. Müller HE. Occurrence and pathogenic role of Morganella-Proteus-Providencia group bacteria in human feces. J Clin Microbiol. 1986 Feb. 23(2):404-5. [View Abstract]
  31. O'Hara CM, Brenner FW, Miller JM. Classification, identification, and clinical significance of Proteus, Providencia, and Morganella. Clin Microbiol Rev. 2000 Oct. 13(4):534-46. [View Abstract]
  32. Piccolomini R, Cellini L, Allocati N, et al. Comparative in vitro activities of 13 antimicrobial agents against Morganella-Proteus-Providencia group bacteria from urinary tract infections. Antimicrob Agents Chemother. 1987 Oct. 31(10):1644-7. [View Abstract]
  33. Rowen JL, Lopez SM. Morganella morganii early onset sepsis. Pediatr Infect Dis J. 1998 Dec. 17(12):1176-7. [View Abstract]
  34. Salen PN, Eppes S. Morganella morganii: a newly reported, rare cause of neonatal sepsis. Acad Emerg Med. 1997 Jul. 4(7):711-4. [View Abstract]
  35. Samonis G, Anatoliotaki M, Apostolakou H, et al. Fatal septicemia and meningitis due to Morganella morganii in a patient with Hodgkin's disease. Scand J Infect Dis. 2001. 33(7):553-5. [View Abstract]
  36. Stock I, Wiedemann B. Identification and natural antibiotic susceptibility of Morganella morganii. Diagn Microbiol Infect Dis. 1998 Mar. 30(3):153-65. [View Abstract]
  37. Williams EW, Hawkey PM, Penner JL, et al. Serious nosocomial infection caused by Morganella morganii and Proteus mirabilis in a cardiac surgery unit. J Clin Microbiol. 1983 Jul. 18(1):5-9. [View Abstract]
  38. Vinogradov E, Nash JH, Foote S, Young NM. The structure of the Morganella morganii lipopolysaccharide core region and identification of its genomic loci. Carbohydr Res. 2015 Jan 30. 402:232-5. [View Abstract]