Leishmaniasis: Dr. Kazi Shihab Uddin Mbbs MRCP (Uk) Associate Professor & HOD Department of Internal Medicine

Leishmaniasis
Dr. Kazi Shihab Uddin

MBBS; MRCP (UK)
Associate Professor & HOD
Department of Internal Medicine
 Leishmaniasis is caused by unicellular flagellate intracellular protozoa
belonging to the genus Leishmania. It comprises three broad groups:
● Visceral Leishmaniasis (VL, kala-azar). ● Cutaneous leishmaniasis
(CL). ● Mucosal leishmaniasis (ML).
 Although most clinical syndromes are caused by zoonotic transmission of
parasites from animals (chiefly canine and rodent reservoirs) to humans
through phlebotomine sand fly vectors, humans are the only known
reservoir (anthroponotic) in major VL foci in the Indian subcontinent and
for transmission among injection drug users.

Life cycle
 Flagellar promastigotes (10–20 μm) are introduced by the feeding female sandfly
(Phlebotomus in the eastern hemisphere).
 The promastigotes are taken up by neutrophils, which undergo apoptosis and are
engulfed by macrophages in which the parasites transform into
amastigotes (2–4 μm, Leishman–Donovan bodies).
 They multiply, causing macrophage lysis and infection of other cells. Sandflies pick
up amastigotes when feeding on infected patients or animal reservoirs.
 In the sandfly, the parasite transforms into a falgellar promastigote, which multiplies
in the gut and migrates to the proboscis to infect a new host.

Visceral leishmaniasis (kala-azar
 VL is caused by the protozoon Leishmania donovani complex. India, Sudan,
Bangladesh and Brazil account for 90% of cases of VL.

 The great majority of people infected remain asymptomatic.
Clinical features
● Fever: accompanied initially by rigor and chills, and decreasing over time with
occasional relapses.
● Splenomegaly: develops quickly in the first few weeks and may be massive.
● Hepatomegaly. ● Lymphadenopathy.
● Skin: a blackish discoloration of the skin is a feature of advanced disease,
● Oedema and ascites: secondary to low albumin.
● Haematological abnormalities: severe anaemia, thrombocytopenia and
pancytopenia with retinal, GI or nasal bleeding.
● Secondary infection: profound immunosuppression may result in TB, dysentery,
herpes zoster, chickenpox, skin infections, cellulitis and scabies.

Investigations
 There is pancytopenia with granulocytopenia and monocytosis.
 Polyclonal hypergammaglobulinaemia (IgG, then IgM) and hypoalbuminaemia.
 Splenic smears demonstrate amastigotes (Leishman–Donovan bodies) with 98%
sensitivity as a diagnostic test.

 PCR is only performed in specialised laboratories.
 In developing countries, a highly sensitive and specifi direct agglutination test of
stained promastigotes and an equally effiient rapid immunochromatographic k39

strip test have been developed.
 Differential diagnosis includes malaria, typhoid, TB, schistosomiasis and many
other infectious and neoplastic conditions, some of which may coexist with VL.
Fever, splenomegaly, pancytopenia and non-response to antimalarial therapy may
provide clues to investigate.
Management
 Pentavalent antimonials: Sodium stibogluconate A daily dose of 20 mg/kg is given,
IV or IM, for 28–30 days. Side effects arthralgias, myalgias, raised hepatic
transaminases and pancreatitis, especially in patients co-infected with HIV. Severe
cardiotoxicity, manifested by concave ST elevation, prolong of QTc > 0.5 msec,
ventricular ectopics, ventricular dysrhythmias and sudden death.
 Amphotericin B: Amphotericin B deoxycholate, 0.75–1 mg/kg daily for 15–20 doses, is
an alternative in areas where there is Sb unresponsiveness. It has a cure rate of nearly

100%. Side-effects, e.g. high fever with rigor, thrombophlebitis, diarrhoea and
vomiting. Serious (occasionally fatal) adverse events, such as renal or hepatic toxicity,
hypokalaemia, thrombocytopenia and myocarditis, are not uncommon. Lipid
formulations of amphotericin B are less toxic.
 Miltefosine, paromomycin and pentamidine have also been used to treat VL.
Multidrug therapy is likely to increase to prevent the emergence of resistance.

Post-kala-azar dermal leishmaniasis (PKDL)
 After treatment and recovery from the visceral disease in India and Sudan, some
patients develop dermatological manifestations.

 In India, dermatological changes occur in a small minority of patients 6 mths to
≥ 3 yrs after the initial infection, in contrast to Sudan where 50% of patients
(usually children) develop PKDL rapidly (within 6 mths).
 The diagnosis is clinical, based on the characteristic appearance of macules,
papules, nodules (most frequently) and plaques on the face, especially around
the chin. The face often appears erythematous. Hypopigmented macules can
occur and are highly variable in extent and location.
 There are no systemic symptoms they are a human reservoir for disease.
 Treatment of Indian PKDL is difficult – Sb for 120 days or several courses of
amphotericin B infusions are required. ¾ th cases in Sudan recovery

spontaneously.
Prevention and control
 Sandflies are extremely sensitive to insecticides, and vector control through
insecticide spray is very important. Mosquito nets or curtains treated with

insecticides will keep out the tiny sandflies. In endemic areas with zoonotic
transmission, infected or stray dogs should be destroyed.
 In areas with anthroponotic transmission, early diagnosis and treatment of
human infections, to reduce the reservoir and control epidemics of VL, is

extremely important. Serology is useful in diagnosis of suspected cases in
the field. No vaccine is currently available.
Cutaneous and mucosal leishmaniasis
 Cutaneous leishmaniasis- It (oriental sore) occurs in both the Old World
and the New World, causing two types of leishmaniasis.

 Old World CL: A mild disease found around the Middle East and Central
Asia as far as Pakistan, and in sub-Saharan West Africa and Sudan. It is

caused by Leishmania major, L. tropica and L. aethiopica.
 New World CL: A disfiguring disease, largely found in Central, South
America caused by Leishmania mexicana complex and Viannia subgenus.

 The incubation period is 2–3 mths (range 2 wks to 5 yrs). The characteristic
lesions of CL are ulcerated papules that form at the site of a vector bite. They
may be single or multiple, and may measure up to 10 cm in diameter .
 There can be satellite lesions, regional lymphadenopathy, pain, pruritus and
secondary bacterial infection.

 Mucosal leishmaniasis- The Viannia subgenus (New World CL) is
responsible for deep sores and mucosal leishmaniasis (ML).

 Young men with chronic lesions are particularly at risk, and between 2 and
40% of infected persons develop ‘espundia’, metastatic lesions in the mucosa

of the nose or mouth. This is characterised by thickening, erythema and
later ulceration of nasal mucosa, starting at the junction of the nose and
upper lip. The lips, soft palate, fauces and larynx may be invaded and
destroyed.
 There is no spontaneous healing, and death may result from severe
respiratory tract infections due to massive destruction of the pharynx.

Investigations
 CL is often diagnosed on the basis of the lesions’ clinical characteristics.
However, parasitological confirmation is important because clinical

manifestations may be mimicked by other infections.
 Amastigotes can be demonstrated on slit-skin smear with Giemsa staining;
alternatively, they can be cultured from the sores early during the infection.
 Culture of fine needle aspiration material has been reported to be the most
sensitive method.
 ML is more difficult to diagnose parasitologically. The leishmanin skin test
measures delayed-type hypersensitivity to killed Leishmania organisms. A

positive test is defined as induration of more than 5 mm 48 hours later.
 PCR is used increasingly for diagnosis and speciation and selecting therapy
Management of CL and ML
Treatment of CL should be individualised on the basis of the causative organism,
severity of the lesions, availability of drugs, tolerance of the patient for toxicity, and
local resistance patterns.
Small lesions may self-heal or be treated by freezing with liquid nitrogen or curettage.
Topical paromomycin 15% plus methylbenzethonium chloride 12% is benefiial in CL.
Intralesional antimony is also rapidly effective and generally well tolerated in CL.
For CL with multiple lesions and for ML, parenteral Sb (20 mg/kg/day) should be
used. CL requires 20 days of systemic Sb; ML is treated for 28 days.
Refractory CL or ML should be treated with amphotericin B. Other effective drugs
include pentamidine, fluconazole, ketoconazole and itraconazole.
Personal protection against sandfly bites, no effective vaccine is yet available.

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Leishmaniasis

Dr. Kazi Shihab Uddin

belonging to the genus Leishmania. It comprises three broad groups:

● Visceral Leishmaniasis (VL, kala-azar). ● Cutaneous leishmaniasis

(CL). ● Mucosal leishmaniasis (ML).

 Although most clinical syndromes are caused by zoonotic transmission of

parasites from animals (chiefly canine and rodent reservoirs) to humans

reservoir (anthroponotic) in major VL foci in the Indian subcontinent and

for transmission among injection drug users.

(Phlebotomus in the eastern hemisphere).

engulfed by macrophages in which the parasites transform into

amastigotes (2–4 μm, Leishman–Donovan bodies).

up amastigotes when feeding on infected patients or animal reservoirs.

in the gut and migrates to the proboscis to infect a new host.

Bangladesh and Brazil account for 90% of cases of VL.

● Skin: a blackish discoloration of the skin is a feature of advanced disease,

● Oedema and ascites: secondary to low albumin.

● Haematological abnormalities: severe anaemia, thrombocytopenia and

pancytopenia with retinal, GI or nasal bleeding.

● Secondary infection: profound immunosuppression may result in TB, dysentery,

herpes zoster, chickenpox, skin infections, cellulitis and scabies.

 Polyclonal hypergammaglobulinaemia (IgG, then IgM) and hypoalbuminaemia.

 Splenic smears demonstrate amastigotes (Leishman–Donovan bodies) with 98%

sensitivity as a diagnostic test.

 In developing countries, a highly sensitive and specifi direct agglutination test of

stained promastigotes and an equally effiient rapid immunochromatographic k39

an alternative in areas where there is Sb unresponsiveness. It has a cure rate of nearly

Multidrug therapy is likely to increase to prevent the emergence of resistance.

patients develop dermatological manifestations.

 Treatment of Indian PKDL is difficult – Sb for 120 days or several courses of

amphotericin B infusions are required. ¾ th cases in Sudan recovery

insecticide spray is very important. Mosquito nets or curtains treated with

human infections, to reduce the reservoir and control epidemics of VL, is

and the New World, causing two types of leishmaniasis.

Asia as far as Pakistan, and in sub-Saharan West Africa and Sudan. It is

America caused by Leishmania mexicana complex and Viannia subgenus.

secondary bacterial infection.

responsible for deep sores and mucosal leishmaniasis (ML).

40% of infected persons develop ‘espundia’, metastatic lesions in the mucosa

respiratory tract infections due to massive destruction of the pharynx.

However, parasitological confirmation is important because clinical

measures delayed-type hypersensitivity to killed Leishmania organisms. A

local resistance patterns.

Topical paromomycin 15% plus methylbenzethonium chloride 12% is benefiial in CL.

used. CL requires 20 days of systemic Sb; ML is treated for 28 days.

Refractory CL or ML should be treated with amphotericin B. Other effective drugs

include pentamidine, fluconazole, ketoconazole and itraconazole.

Personal protection against sandfly bites, no effective vaccine is yet available.

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