The bacterium Morganella morganii is an increasingly recognized opportunistic pathogen in hospital settings. This organism belongs to the family Enterobacteriaceae, a large group of Gram-negative bacteria. M. morganii typically lives harmlessly as a commensal organism within the gut flora, but its ability to cause severe infections when it moves to other body sites has drawn significant clinical attention. Its growing prevalence in healthcare-associated infections is compounded by its capacity to develop resistance to multiple classes of antibiotics. Understanding the organism’s characteristics and its mechanisms for evading treatment is important for controlling its spread.
Classification and Habitat
Morganella morganii is characterized as a Gram-negative, rod-shaped bacterium, meaning its cell wall structure does not retain the crystal violet stain used in the Gram staining procedure. The organism is a facultative anaerobe, which allows it to thrive in environments both with and without oxygen. Its cells are generally straight rods.
The bacterium is motile, possessing peritrichous flagella, which are numerous, whip-like appendages that enable movement. This mobility is a factor in its ability to spread within a host and colonize different body sites. Biochemically, M. morganii is active, notably producing the enzyme urease, which breaks down urea and plays a role in its pathogenicity, particularly in the urinary tract.
The natural habitat of M. morganii is diverse, being commonly found in the environment, including soil and water. It is also a normal part of the intestinal microbiota in humans, mammals, and reptiles, where it typically exists without causing disease. Problems arise when the organism translocates from its intestinal niche to sterile sites, often due to a break in the mucosal barrier or a compromised immune system.
Infections and Vulnerable Populations
As an opportunistic pathogen, M. morganii primarily causes infections in individuals whose natural defenses are impaired or whose anatomy has been altered, such as through surgery or catheterization. The clinical spectrum of disease is broad, with the most frequent occurrences involving the urinary tract and soft tissues. Urinary tract infections (UTIs) are common, often associated with long-term indwelling urinary catheters, where the organism’s urease production can contribute to the formation of kidney stones.
M. morganii is also a significant cause of wound and post-surgical infections, particularly in healthcare settings. Furthermore, it can lead to more severe, invasive conditions, including bacteremia and sepsis. Bloodstream infections caused by this organism can carry a high mortality rate, especially when treatment is delayed or ineffective.
The populations most susceptible to M. morganii infections are those in close contact with healthcare environments, making it a common cause of nosocomial or hospital-acquired infections. The elderly are at significantly increased risk, and the incidence of bloodstream infections rises sharply with advancing age. Patients with serious underlying medical conditions are also highly vulnerable, including those with diabetes mellitus, chronic renal disease, and cancer. Immunosuppression from any cause is a major risk factor.
Mechanisms of Treatment Failure
The difficulty in treating Morganella morganii infections stems largely from its inherent and acquired mechanisms of antibiotic resistance. The organism possesses an intrinsic resistance to several common antibiotic classes, including penicillins, ampicillin, and first- and second-generation cephalosporins. This natural resistance is often due to the chromosomal production of a type of enzyme called AmpC beta-lactamase, which actively breaks down the beta-lactam ring structure shared by these antibiotics.
Beyond its intrinsic defenses, M. morganii frequently acquires additional resistance genes, often carried on mobile genetic elements like plasmids and transposons. These mobile elements allow the rapid horizontal transfer of resistance traits between bacteria. A major concern is the acquisition of genes that encode for Extended-Spectrum Beta-Lactamases (ESBLs).
ESBLs are enzymes capable of neutralizing a broader range of beta-lactam antibiotics, including third-generation cephalosporins, which are often the first line of defense against Gram-negative infections. The presence of ESBL-producing strains significantly limits therapeutic options, often requiring the use of last-resort drugs like carbapenems. Some strains have even acquired carbapenemase enzymes, which confer resistance to carbapenems, creating a challenging multi-drug resistant profile. This escalating resistance necessitates careful antibiotic stewardship and the exploration of newer or combination therapies to effectively manage infections caused by this resilient bacterium.