Considerations for Systemic and Topical Treatment of Morganella morganii Septicemia Arising from Maggot Infestation

Introduction. Live maggot infestation (myiasis) of wounds can present a host of ailments. Loosely associated with maggot excreta, Morganella morganii is a widespread, gram-negative rod bacterium commonly found in the intestinal tracts of humans. M morganii has been observed as being pathogenic, particularly in nosocomial and postoperative environments, as well as in immunosuppressed and elderly populations. Case Report. Herein, the authors present a rare, previously unreported case of M morganii septicemia (as confirmed by positive blood culture), secondary to myiasis of the lower extremities. The patient was successfully treated with both systemic and topical interventions. Posttreatment examination revealed resolution of myiasis and negative blood cultures. Conclusions. Myiasis can be invasive, leading to severe systemic infection. In these cases, a broad-spectrum antibiotic combined with systemic and topical antiparasitic therapy should be considered.

Disinfected (sterile) maggots are often used for debridement of necrotic wounds, particularly when revascularization is contraindicated.^1,2 Conversely, parasitic maggot infestation (myiasis) is associated with various symptoms, depending largely on the parasite species and site of infection.³ In rare instances, myiasis has been associated with septicemia.^4,5

Myiasis is a complication of advanced cancer ulcers, poor hygiene, and suppurating lesions that mainly occurs in tropical countries. Lack of adequate medical care, elderly or psychiatric patients, patients with alcoholism, and those with an inability to block flies from depositing eggs or larvae are particularly at risk. Dermatological conditions also are associated with myiasis, such as diverse ulcers (most common) followed by hyperkeratosis. Other dermatological conditions such as psoriasis, leprosy, vascular disease, cutaneous B-cell lymphoma, lymphedema, condyloma acuminatum, hemorrhoids, and basal or squamous cell carcinoma also are associated with myiasis. Because of relatively easy visualization of the larvae that periodically surface in the lesion, biopsy or imaging are rarely indicated for diagnosis.⁶

During myiasis infestations, larvae feed on necrotic tissue and lacerate the fine blood vessels while feeding. Its rapid extension into the surrounding tissues may lead to tissue destruction and morbidity. Mechanical removal of the parasite in association with systemic therapy with ivermectin, or flushing the wound with nitrofurazone or liquid chlorhexidine 0.12%, has been used to minimize the inflammatory process and prevent secondary infections.⁷

The concept that myiasis infestations are noninvasive and only destroy necrotic tissue needs to be reviewed. There are invasive larvae with unique myiasis-related infections leading to serious complications.⁸ Moreover, with increased international trade and immigration, there is a strong likelihood of different larvae and infestations being transported. It becomes vital that providers in nonendemic areas are aware of clinical symptoms, exposure, and presentations of this condition, as early recognition will prevent inappropriate treatments or complications.⁹ To the best of the authors’ knowledge, this is the first reported instance of myiasis-associated Morganella morganii septicemia.

M morganii is a facultative, anaerobic, gram-negative bacterium first discovered by H de R. Morgan in 1906 when describing stool samples collected from infants with “summer diarrhea.”¹⁰M morganii is ubiquitous and typically has a commensal relationship in the gastrointestinal tract of humans.¹¹ The urinary tract is currently the major portal of M morganii entry, followed by hepatobiliary, skin, soft tissue, and blood.¹²M morganii-associated case reports are numerous and often presented in immunocompromised patients; this bacteria is considered an opportunistic pathogen.¹² Infections with M morganii are worrisome because of the bacteria’s increased levels of virulence and resistance due to a great capacity to adapt to the environment. Cases associated with M morganii infection are diverse with high mortality rates reported.¹²

The following case report was prepared via retrospective chart review accompanied with a thorough literature review.

An 82-year-old man with a history of hypertension and peripheral vascular disease was admitted to a rural hospital with chief concerns of respiratory distress, hypotension, fever, and a septic profile. Clinical examination of the patient upon admission revealed poor hygiene and venous stasis disease with significant hyperkeratosis associated with a thick layer of cellular debris. Multiple crevasses in the debris were appreciated, revealing large-scale myiasis infestation of the underlying tissue. Laboratory investigation showed leukocytosis without eosinophilia, and blood cultures were positive for M morganii; urine cultures were negative for M morganii. No stool cultures were obtained.

Local treatment of myiasis initially involved mechanical removal of larvae with forceps and washing the legs with water and chlorhexidine (Figure 1). However, due to a significant amount of myiasis, topical 5% permethrin cream was applied from the knees to toes and covered with plastic cast shower covers for 24 hours to treat the larvae. The patient also received a combination of a carbapenem (Ertapenem; Merck, Kenilworth, NJ) for bacteremia and a 1-time oral dose of an antiparasitic, ivermectin (30 mg), for systemic parasitic treatment.

The patient had a prolonged hospital stay due to decompensated cardiac insufficiency and decline of his respiratory status secondary to congestive heart failure that required intubation. Subsequently, meropenem was substituted for the carbapenem as he was transferred to the intensive care unit (ICU) with concerns of worsening sepsis. Bronchoalveolar lavage showed more than 100 000 colony forming units for Staphylococcus epidermidis, which was likely a contaminant, but no M morganii were detected.

During his ICU stay, he developed an acute kidney injury that subsequently improved. He was extubated and completed his 2-week course of carbapenem therapy. Five days after initial treatment, blood cultures revealed no growth of M morganii. Further, upon gross observation, the myiasis of the bilateral lower extremities had resolved (Figure 2).

Throughout his hospital course, the patient received daily hydrotherapy to the bilateral lower extremities using 0.0125% Dakin’s solution as a supplemental disinfectant. The patient was discharged and continued compressive therapy to treat his chronic bilateral lower extremity venous stasis (Figure 3).

M morganii is a normal variant in human and other mammalian gut flora.¹² About 40 years ago, M morganii was established as an opportunistic pathogen, particularly in nosocomial environments.^13,14 Further investigation revealed an enhanced ability to infect the urinary tract due to motility and production of urease.¹⁵ Twenty years after initial reports of pathogenic M morganii infection, O’Hara et al¹⁶ reviewed published instances of soft tissue infection, skin infection, and meningitis arising from this surprisingly adaptable bacterium. In recent years, reports have implicated M morganii in cases of pyomyositis,¹⁷ neonatal and adult sepsis,^18–20 osteomyelitis,^1,21 necrotizing fasciitis,²² and recently a fatal case of rhabdomyolysis.²³ In addition, M morganii, Providencia spp, and Proteus spp have been isolated in the larval gut of the house fly.²⁴

Bacteremia from M morganii is typically found in immunocompromised or elderly patients or in patients with another underlying disease. Notably, to the best of the authors’ knowledge, M morganii has been only loosely associated with live maggot excreta/secreta.²⁵ Early identification of M morganii on the present patient’s blood cultures following initial presentation permitted aggressive systemic intervention in addition to topical care. Follow-up examination showed successful treatment of both the primary myiasis infestation and secondary septicemia.

Septicemia secondary to myiasis is highly atypical in the United States. However, increasing travel to endemic regions, global trade, immigration, and changing global climates increase the likelihood of new forms of myiasis spreading to previously untouched areas.⁹ Reports have suggested at least 3 patients have developed Ignatzschineria (Schineria) indica septicemia from maggot infestations.⁴ Other cases have been reported in France and Asia Minor^5,26 (Table). Previously described cases^4,5,26 of myiasis-related septicemia were treated with broad-spectrum antibiotics with varying results (Table). In addition to a broad-spectrum antibiotic, the present patient received a 1-time oral dose of ivermectin and topical application of 5% permethrin cream. Ivermectin has been used successfully to treat cutaneous,²⁷ oral,²⁸ and rhino-orbital myiasis²⁹ and has been established as a proven treatment for general myiasis.³⁰ Previously reported cases demonstrating permethrin cream used successfully in conjunction with oral ivermectin guided the authors’ decision for topical and systemic combination therapy.^31–33

Providers should be aware of the severe complications associated with large myiasis infestations. Early diagnosis, treatment, and active surveillance play an important role in prevention of complications. Appropriate diagnosis and management is critical and should include at least empiric antibiotic treatment, tetanus prophylaxis, bedside debridement, and pharmacological antiparasitic treatment in association with the underlying cause.^8,12 Based on this case report, the authors contend that in febrile patients presenting with myiasis infestation, M morganii infection could be considered, especially when clinical improvement is not observed following narrow-spectrum empiric antimicrobial therapy. Recognizing and implementing an effective ivermectin and permethrin cream regimen earlier in the time-course of patient treatment may lead to decreased morbidity and mortality. Additional study of M morganii infection and its association with myiasis infections should be conducted to accurately characterize its prevalence, which may necessitate expansion of empiric treatment for severe myiasis infections to include M morganii.

In addition, while medicinal maggot therapy is a controlled, artificially induced myiasis with the intent of destruction of necrotic tissues, there are significant potentially negative effects, including transformation into invasive myiasis. McGraw and Turiansky³⁴ found that 87% of human wound myiasis in the United States were caused by flies of the Calliphoridae family. These include Luicilia sericata (the green bottle blowfly and also used most commonly as sterile maggot) and Phormia regina (the black blowfly).³⁴ Therefore, the authors also contend that empiric antibiotic treatment should be considered in patients who are at high risk for maggot-associated septicemia while receiving sterile maggot treatment for wound debridement, such as patients with new onset fever.

The authors suggest myiasis can be invasive, leading to severe systemic infection. Moreover, patients presenting with significant myiasis infestation of wounds who are susceptible for M morganii septicemia — notably immunosuppressed, elderly, postoperative, and nosocomial patient populations — should be evaluated for, diagnosed, and treated both systemically and topically. M morganii can be highly virulent and lead to high mortality when treatment is delayed. The present case, in light of infection due to M morganii, suggests a combination treatment that consists of a carbapenem antibiotic coupled with topical and systemic antiparasitic therapy. Future studies should be conducted to evaluate the need of speciation of larvae causing infestation. Moreover, use of an empiric antibiotic treatment in febrile patients with significant myiasis or receiving maggot therapy and susceptible to M morganii septicemia such as immunosuppressed patients should be considered.

Affiliation: West Virginia University School of Medicine, Morgantown, WV

Correspondence: Ian Lambourne McCulloch, MRes, West Virginia University School of Medicine, 16 Willow Lane, 1 Medical Center Drive, Morgantown, WV 26506; imccullo@mix.wvu.edu

Disclosure: The authors disclose no financial or other conflicts of interest.