Oral Myiasis: Etiology, Pathogenesis, Clinical Presentation, Diagnosis, and Treatment

Myiasis is a parasitic disease caused by fly larvae from the order Diptera, which lay eggs in human or animal tissues.

Oral myiasis is a subgroup of myiases, characterized by the involvement of oral cavity tissues. The condition is rare, and adequately assessing its prevalence is challenging. In general, the literature cites isolated cases. Between 1990 and 2020, 157 cases of oral myiasis were reported in English-language literature (based on PubMed, Ovid, Web of Science, Scopus, and LILACS). The disease is most prevalent among low-income populations in tropical regions. It develops due to parasite invasion in untreated open wounds of the oral cavity.

Predisposing factors include:

• Poor oral hygiene;
• Low social and economic status;
• Severe musculoskeletal disorders;
• Neurological and mental disorders;
• Lack of access to timely medical care.

Epidemiology

• Geography: more common in tropical and subtropical areas (Latin America, Southeast Asia, and Africa). It may be sporadically registered in any region.
• Age: extreme age groups — children <10 years old and elderly >60 years old.
• Gender: men ≈ women (differences are driven by social and hygienic factors rather than gender ones).
• Risk groups:
  • The homeless;
  • Patients with mental disorders;
  • Alcoholism / drug addiction;
  • Severe somatic diseases (musculoskeletal disorders, neurological and mental disorders).

Etiology

Main causative agents (larvae)

• Chrysomya bezziana: the most aggressive species;
• Cochliomyia hominivorax;
• Lucilia sericata (green bottle fly);
• Sarcophagidae;
• Dermatobia hominis;
• Oestrus ovis: more rarely, but oral cases are documented;
• Musca domestica.

Factors contributing to infection

• Inadequate oral hygiene;
• Untreated open wounds, ulcers, extraction sockets;
• Neuropathy/paresis;
• Immunodeficiency.

Pathogenesis and pathophysiology

To lay eggs, an adult female fly searches for accumulations of decomposing organic matter, which can be represented by an untreated wound in the oral cavity. Adult female flies instinctively lay eggs where a less mobile larva will be provided with a sufficient amount of food.

Depending on the fly species, the eggs hatch within 8–24 hours, and the resulting larvae start feeding on surrounding tissues, causing both mechanical and physical damage due to toxins that destroy host tissues. The larvae complete their development within 5–7 days, then crawl out of the wound and fall to the ground to pupate.

1. Inoculation: the female fly deposits 100–300 eggs on the surface of the wound.
2. Incubation: within 8–24 hours, stage I larvae emerge and penetrate host tissues.
3. Mechanical destruction: oral hooks and proteolytic enzymes of the larvae lead to tissue necrosis and the development of secondary infections.
4. Formation of the immune response: in response to parasite invasion, the human body forms an immune response both at the systemic and local levels:
   • Systemic: acute inflammatory infiltration (elevated WBC counts are detected in the blood: neutrophils, eosinophils);
   • Local: formation of granulation tissue and a fibrous capsule/pseudocyst.
5. Cycle completion (cycle duration is 5–7 days): upon completing development, the larvae exit host tissues and pupate in the environment.

Clinical presentation

Complaints

Patients complain of:

• Discomfort, pain (from mild to severe) in the area of larval accumulation;
• Swelling;
• Presence of bleeding ulcers;
• Enlargement of lymph nodes;
• Purulent discharge from the affected area;
• General symptoms of body intoxication: increased temperature, fever, weakness (more severe in patients with decreased immunity against the background of concomitant chronic diseases).

Local manifestations (Status localis)

The clinical presentation primarily depends on the localization of the affected area by larvae. For instance, when the parasite is localized in the wound area of the upper lip, facial asymmetry will be observed due to collateral edema of the soft tissues of the upper lip. Whereas when the inflammatory process is localized in the hard palate area, the configuration of the face will not be altered.

Common signs and symptoms of the affected area include:

• Edema, mucosal hyperemia;
• Presence of a painful infiltrate;
• Visual presence of larvae.

When secondary infection occurs, purulent discharge from the affected area and a putrid odor may also be observed. Regional lymph nodes (often submandibular) may be enlarged, mobile, soft, painful/slightly painful on palpation.

Diagnosis

1. Medical history and physical examination

• The specific medical history may include low social and economic status, severe musculoskeletal disorders, neurological and mental disorders;
• Complaints of pain and swelling in the area of open wounds of the oral cavity;
• Symptom duration often ranges from 2 to 7 days, reflecting the life cycle duration of the parasites.

2. Clinical examination

Direct visualization of white/creamy larvae and/or eggs.

3. Instrumental methods

CT of the maxillofacial area, if deeper spread into the soft tissues is suspected (rare).

4. Laboratory tests

• Complete blood count: leukocytosis with eosinophilia (up to 15%);
• Bacterial culture from the wound: to determine secondary microflora and sensitivity to antibiotics.

The diagnosis is primarily based on the visualization of larvae or parasitic eggs in the patient’s wound!

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Treatment

1. Mechanical removal (gold standard)

• Tool: sterile Crane tweezers or curette.
• Technique:

1. Infiltrative anesthesia with local anesthetics (lidocaine 2%, articaine 4% with epinephrine);
2. If necessary, enlarging the entry point with a scalpel for better visualization;
3. Extraction of the whole larvae using tweezers or curette (avoiding rupture of the larvae);
4. Local irrigation with local antiseptics (e.g., 0.05% aqueous chlorhexidine solution).

2. Pharmacotherapy

Due to the rarity and low social significance of the disease, there are no universally accepted treatment protocols. Among the agents used for treatment, four groups can be conditionally distinguished:

1. Asphyxiation agents: turpentine, mineral oils, chloroform, ethyl chloride, mercuric chloride, creosote, and phenol. Asphyxiation agents create an anaerobic atmosphere within the wound, forcing aerobic parasitic larvae to surface, facilitating their removal.
2. Antiparasitic drugs: 1% ivermectin gel, 5% thiabendazole in an oromucosal paste (locally 2 to 3 times a day).
3. Systemic antibiotic therapy (used for secondary infections): amoxicillin/clavulanate 875/125 mg (1 tablet twice daily for 5-7 days), clindamycin 300 mg (1 tablet 2-3 times daily for 5-7 days).
4. Non-steroidal anti-inflammatory drugs (NSAIDs) as needed: ibuprofen 400 mg up to 3 times a day.

3. Surgical therapy (recommended in case of complications)

Depending on the neglecting of the process, additional interventions are recommended:

• For deep granulating defects: curettage and primary wound closure.
• For extensive defects: plastic surgery to restore damaged tissues.
• For mandibular osteomyelitis: sequestrectomy combined with antibiotic therapy.

4. Prevention of recurrences

• Education on adequate oral hygiene;
• Sanitary treatment of the oral cavity (0.12% chlorhexidine twice a day for 1 week);
• Correction of comorbidities;
• Social measures: improved hygiene, health education activities, insect protective nets.