Cutaneous Leishmaniasis

Synonyms: Oriental sore, Delhi boil, Baghdad boil, Balkan sore, Saldana

Incubation period: a couple of weeks to a couple of months depending on the species

Epidemiology:

Source: http://www.who.int/leishmaniasis/leishmaniasis_maps/en/index.html

Leishmaniasis threatens 350 million people in 88 countries where the disease is endemic. With 12 million cases worldwide, over 1.5 million people report new cases of cutaneous leishmaniasis annually, while many more go unreported. 90% of these cases occur in Saudi Arabia, Afghanistan, Peru, Brazil and Iran. From 2002-2004, 522 new cases of cutaneous leishmaniasis, mostly due to L. major, were reported among troops stationed in Afghanistan, Iraq, and Kuwait.

Pathogenesis:

When an individual is bitten by the sandfly, promastigotes are introduced into the skin and enter small blood vessels and macrophages around the affected area. There, the parasites proflierate as amastigotes. White blood cells, called lymphocytes, then attack the immediate area using white blood cells called lymphocytes and the amastigotes are liberated from the macrophages. A lump then forms and breaks open when the blood flow to the area is compromised. Although the ulcer may become infected, the lesion usually heals as the body builds immunity against the parasite. Once an individual is infected with cutaneous leishmaniasis, it is unlikely that he or she will be re-infected by the same species.

Clinical Manifestations:

• Begins as a red papule that later becomes itchy
• Develops to o ne or more skin ulcers on exposed parts of the body, mostly the face, arms and legs
• Sores can be covered by a scab
• Adenopathy

Photo courtesy of (L-R): http://www3.baylor.edu/~Charles_Kemp/hand.jpg, http://www.ualberta.ca/~medlabsc/leishmaniasis.jpg , http://www.who.int/zoonoses/diseases/Leishmaniasis2_ok.jpg, http://www.yamagiku.co.jp/pathology/image/176/8.jpg

The ulcers may change in size and may appear differently throughout the course of infection. Although most sores may be painless, some may cause extreme disability. The sores can heal spontaneously within a few months, however, they may also leave permanent scars. Recovery depends on the host's immune system. If the sores are not treated appropriately, they can last for many years.

Diagnosis:

• In endemic areas, clinical manifestations are the basis of diagnosis.
• Aspriation of fluid from the ulcer is used to visualize the organism in the amastigote form. (Click for a video, courtesy of http://www.pdhealth.mil/leish.asp)
• Xenodiagnostics with a hamster
• Organisms in the promastigote form may also be revealed when a biopsy is done for a culture.
• Biopsy specimen can also be used to inoculate the nose of a hamster to observe inflammation.
• Molecular techniques, like PCR, DNA hybridization, and antigen detection may be done.
• A Montenegro test (not approved in the US), in which dead promastigotes are injected intradermally, can also be indicative of infection.
• Note: Blood tests are not helpful

Treatment:

Drug	Mechanism of action	Dosing	Therapy Duration	Side effects	Results
Sodium Stibogluconate (Pentostam) *Not licensed for use in the US	Cause parasite death by inhibiting glycolytic enzymes and fatty acid oxidation	Administered intravenously or intra-muscularly	20 mg/kg body weight daily for 20 days	Coughing, headache, vomiting	Cutaneous lesions may not usually require antimonials to heal. After several weeks, the lesions tend to heal on their own.
Glucantime *Not licensed for use in the US	Cause parasite death by inhibiting glycolytic enzymes and fatty acid oxidation	Administered intravenously or intra-muscularly	20 mg/kg body weight daily for 20 days	EKG ab- normalities	Cutaneous lesions may not usually require antimonials to heal. After several weeks, the lesions tend to heal on their own.
Amphotericin B *preferred treatment in India and Mediterranean because of poor response to antimonials	Causes parasite death	intravenously	Gradually increase dose to 1mg/kg lb every other day until 2-3g is given	Slightly toxic	Cutaneous lesions may not usually require antimonials to heal. After several weeks, the lesions tend to heal on their own.
Oral ketoconazole	Alters permeability of cell wall inhibiting fungal enzymes	Oral, topical	Oral: 200-400 mg/day single daily dose, 4-8 wks Topical: rub on affected area 1-2x daily	Headache, vomiting, abdominal pain
Itraconazole	Inhibits cell membrane formation	Oral, intravenously	200 mg, once daily and may increase to 400 mg from 1 day-6 months depending on severity	Gastric acidity
Paromomycin	Interferes with bacteria protein synthesis	oral	25-35 mg, 3 divided doses, 5-10 days	Diarrhea, nausea, eosinophilia
Flucanazole *Antifungal	Inhibits cell membrane formation	oral	200-400 mg/day, duration depends on infection		Complete healing of all lesions

Photos (top-bottom): http://www.usp.org/patientSafety/newsletters/practitionerReportingNews/prn1202004-09-30.html?USP_Print , http://arachosia.univ-lille2.fr/labos/parasito/Internat/medicam/leish_me.html , http://medimpex.com.mx/generic/antimycotics-c-35.html?osCsid=e16e52b335ecd493c77e6140a16d2564

Home

Sources:

http://www.who.int/leishmaniasis/disease_epidemiology/en/index.html

http://www.afip.org/Departments/infectious/lm/01.html

http://www.utdol.com/utd/content/topic.do?topicKey=parasite/16332

Markell and Voges. “Leishmaniasis.” Medical Parasitology . Elsevier Inc. Ninth Edition. 2006.