What is Mucocutaneous Leishmaniasis (Espunda)?
Cutaneous mucous leishmaniasis (Espundia, cutaneous mucous Brazilian leishmaniasis) is a type of cutaneous leishmaniasis of the New World, a disease of the skin and mucous membranes caused by the simplest parasite Leishmania braziliensis.
Causes of Mucocutaneous Leishmaniasis (Espundia)
The causative agent of mucocutaneous leishmaniasis – Leishmania braziliensis. Distributed in the forests of South America to the east of the Andes, it proceeds with extensive skin lesions, subsequently mucous membranes, usually the upper respiratory tract, sometimes with deep destruction of soft tissues and cartilage.
Pathogenesis during Mucocutaneous Leishmaniasis (Espundia)
The disease is transmitted by mosquitoes to the genera Phlebotomus. In South America, carriers of cutaneous leishmaniasis pathogens are mosquitoes of the genus Lutzomyia. Moreover, in the body of mosquitoes, the parasite is in flagellate form, and in the human body – in the leishmanial (intracellular) form.
Reservoir of infection – large forest rodents. Usually recorded among workers employed in forest and road works, among the population of forest villages.
Leishmaniasis is a zoonotic infection and affects rodents and canids on all inhabited continents, with the exception of Australia. The prevalence of leishmaniasis varies: on the shores of the Mediterranean Sea, they affect 4–10% of dogs, and in the southern regions of our country – 80–95% of gerbils; many of them have subclinical invasion. The spread of the disease occurs when the female of a mosquito of the genus Lutzomyia swallows amastochites during bloodsucking on infected mammals. In the stomach of an insect, amastigotes turn into promasigotes, migrate to the proboscis, and at the next sucking enter the skin of the new host. The production of mosquitoes occurs in a warm humid microclimate – in the holes of rodents, termite mounds, in clusters of rotting vegetation. A person becomes infected with leishmaniasis, getting into such a natural focus. The presence of infection in domestic dogs serves as an important reservoir of leishmaniasis in cities. Transmission of leishmaniasis from person to person, except in cases of Indian kala-azar, occurs very rarely. Even less often, transmission can occur through blood transfusions, injections and sexual intercourse. According to estimates, there are over 12 million people in the world affected by leishmaniasis.
Promasigotes enter the skin in a small accumulation of blood that is formed during mosquito bloodsucking. Leishmania fix complement on its surface through an alternative path and quickly penetrate the macrophage thanks to the type 3 complement receptor (RKZ) and the mannosyl / flucosyl receptor. Promastigotes are transformed into amastigoty inside phagolysos and multiply by binary division. In the end, they tear apart the cell and penetrate into neighboring macrophages.
Further development of the disease is determined by the level of cellular immunity of the host, as well as the specific form of the pathogen. In mucocutaneous leishmaniasis, after some time after complete or partial healing of the primary element, metastatic lesions of the skin and mucous membranes may appear. The destructive nature of metastatic lesions is associated with the development of hypersensitivity to the simplest antigens. The exception to the typical nature of the development of cutaneous leishmaniasis is diffuse cutaneous leishmaniasis, in which there is no infiltration by lymphocytes and plasma cells or a decrease in the number of pathogens; The leishmanin reaction remains negative, and the skin lesion becomes chronic, progressive and widespread. At the same time, patients, apparently, have a selective anergy to Leishmania antigens, which is mediated, at least partially, by adjacent suppressor cells. The ability of Leishmania to cause progressive disease may be associated with the formation of T-lymphocyte suppressors in the host organism. After recovery, immunity to this strain of the pathogen remains.
Symptoms of Mucocutaneous Leishmaniasis (Espundia)
Symptoms of mucosal leishmaniasis appear 1-4 weeks after a carrier bite. The clinical picture: characterized by painless, deforming lesions of the mouth and nose, metastatic to adjacent areas with the appearance of fungal and erosive ulcers on the tongue, cheek and nose mucosa; relapses are possible several years after the spontaneous disappearance of primary foci.
Mucous lesions occur in the presence of open ulcers, but more often a lesion of the nasopharynx occurs after scarring of skin ulcers. Accompanied by the destruction of the nasal septum, soft palate, pharyngeal cartilage and larynx.
The disease is accompanied by fever, weight loss and secondary bacterial infections.
Complications of mucosal leishmaniasis:
- In the late stages of the disease, edema, cachexia, and hyperpigmentation are possible.
- Bacterial superinfections and bleeding from the gastrointestinal tract can cause the death of untreated patients with visceral leishmaniasis.
- In 3-10% of treated patients, skin changes develop in the form of depigmented spots and wart nodules on the face and the extensor surface of the limbs.
- Metastatic destructive lesions of the nasopharyngeal mucosa are possible in patients with mucopurulent leishmaniasis.
Diagnosis of the Skin and Mucous Leishmaniasis (Espundia)
For the diagnosis of the disease, material from lymph nodes, ulcers, and a blood test are analyzed. In visceral leishmaniasis, the results of a blood test show an increase in ESR, a decrease in albumin, an increase in the level of globulins, anemia, and thrombocytopenia. An additional indication of the possibility of the disease is the patient’s stay in areas that are endemic for leishmaniasis in the last year or two.
Treatment of Mucocutaneous Leishmaniasis (Espundia)
Treatment of mucocutaneous leishmaniasis is carried out with specific drugs only on prescription. In addition to the main treatment, antibiotics are prescribed to prevent the development of adverse bacterial infections. Also prescribed vitamins, anti-anemia, spend infusion of erythrocyte mass and plasma.
Drugs of choice: Antimonil Sodium Gluconate – 20 mg / kgv / w or / m 1 r / day for 20-30 days. Meglumine antimoniat (glucantim) – 20-60 mg / kg deep in / m 1 r / day for 20-30 days. When the disease recurs or the treatment is not effective enough, a repeated course of injections should be given within 40-60 days. Effectively the additional appointment of allopurinol 20-30 mg / kg / day in 3 ingestion.
Alternative drugs for the relapse of the disease and the causative agent’s resistance to the drugs of choice: Amphotericin B – 0.5-1.0 mg / kg IV per day, or Pentamidine – IM / mg 3-4 mg / kg 3 r / week for 5 -25 weeks In the absence of the effect of chemotherapy, additional human recombinant y-interferon.
Current and forecast. With early diagnosis and timely treatment, more than 90% of patients recover. Even against the background of chemotherapy, mortality reaches 15-25%. If untreated, 95% of adults and 85% of children die within 3–20 months.
Prevention of Mucocutaneous Leishmaniasis (Espundia)
Carry out the destruction of insect vectors, rodents and stray dogs in areas adjacent to human settlements. Individuals visiting endemic foci are recommended to use personal protective equipment (repellents, mosquito nets, etc.). Timely treatment of patients with leishmaniasis.