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Morganella Infections Clinical Presentation

  • Author: James R Miller, MD; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD  more...
 
Updated: Oct 05, 2015
 

History

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]

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.[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]

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.[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]

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Physical

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]

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Causes

Risk factors for M morganii infection include the following:

  • Prior exposure to ampicillin and other beta-lactam antibiotics
  • Diabetes mellitus
  • Advanced age
  • Surgical procedures
  • Perinatal exposure
  • Abscesses or soft tissue infections following snakebite
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Contributor Information and Disclosures
Author

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

James R Miller, MD is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Specialty Editor Board

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

John W King, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Federation for Medical Research, Association of Subspecialty Professors, American Society for Microbiology, Infectious Diseases Society of America, Sigma Xi

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

Pranatharthi Haran Chandrasekar, MBBS, MD is a member of the following medical societies: American College of Physicians, American Society for Microbiology, International Immunocompromised Host Society, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

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