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. 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. 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.
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.
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 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.
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.
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]
Snakebites: 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.
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 and a 31-year-old man with pyomyositis.
Bacteremia: 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.
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.
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.
M morganii strains are naturally resistant to penicillin, ampicillin, ampicillin/sulbactam, oxacillin, first-generation and second-generation cephalosporins, erythromycin, 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.
Many hospital-acquired strains express derepressed chromosomal ampC beta-lactamases (Bush group 1) similar to those produced by Pseudomonas aeruginosa and Enterobacter species.
These strains may be resistant to ceftazidime and other third-generation cephalosporins, but they are usually susceptible to cefepime, imipenem, meropenem, piperacillin, the 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 extended-spectrum beta-lactamases (ESBLs). These enzymes hydrolyze drugs such as ceftazidime, cefotaxime, and aztreonam but have little effect on the cephamycins (ie, cefoxitin, cefotetan). ESBLs are inhibited by clavulanic acid.
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.
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).
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.
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.
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.
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.
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.
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.
Douglas A Drevets, MD, Assistant Professor, Department of Medicine, Section of Infectious Disease, Oklahoma University Health Sciences Center
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
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: emedicine $50.00 Author of chapter; MERCK None Other
Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Disclosure: Nothing to disclose.
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