A 48-year-old male farmer from Saptari district (Terai region of Nepal)
Presented with:
•
high-grade fever with chills and night sweats
•
Progressive weight loss and fatigue
•
Abdominal fullness and early satiety
•
Occasional epistaxis and gum bleeding
•
Darkening of skin noticed by family
Two courses of oral antibiotics from a local clinic gave no improvement.
Examination
General:
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Ill looking, cachectic
•
Temperature: 38.7°C
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Pulse: 102/min
•
BP: 100/60 mmHg
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Pallor ++
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Hyperpigmented skin
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Mild pedal edema
Abdominal exam:
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Massive splenomegaly
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Moderate hepatomegaly
•
No ascites
No lymph nodes palpable.
Initial Laboratory Investigations
Hb: 7.8 g/dL
WBC: 2,500/mm³
Platelets: 90,000/mm³
kala-azar
Leishmaniasis
Leishmaniasis is caused by unicellular, flagellate, intracellular protozoa
belonging to the genus Leishmania.
The 21 leishmanial species that cause human disease are responsible for
three clinical syndromes:
A.
Visceral leishmaniasis (VL, kala-azar)
B.
Cutaneous leishmaniasis (CL)
C.
Mucosal leishmaniasis (ML).
Life cycle of leishmania
Transmission of leishmaniasis
Visceral leishmaniasis (kala-azar)
VL is caused by the protozoon Leishmania donovani complex (comprising
L. donovani, L. infantum and L. chagasi).
Incubation period: Usually 1–6 months, but may be several years.
Clinical features
Age group: Adults and children are equally affected.
Onset: Great majority of individuals infected remain asymptomatic and
onset in others may be abrupt.
The first sign of infection is high fever, usually accompanied by rigor and
chills. Fever intensity decreases over time and patients may become
afebrile for weeks to months. This is followed by a relapse of fever. The
fever is intermittent showing a double rise of temperature in 24 hours
(‘camel hump fever’).
Organs involved: It primarily affects the host’s reticuloendothelial system. In
visceral leishmaniasis, monocytes and macrophages of the spleen, liver,
bone marrow and lymph nodes are primarily affected.
Physical findings
Massive splenomegaly and hepatomegaly
Splenomegaly develops in the first few weeks and becomes massive as the
disease progresses. Moderate hepatomegaly develops later.
Lymphadenopathy
Blackish discoloration of the skin
Blackish discoloration of the skin, from which the disease derived its name, kalaazar (the Hindi word for ‘black fever’), is a feature of advanced illness but is now
rarely seen.
Anemia:
Moderate to severe anemia develops rapidly, and can produce congestive
cardiac failure and associated clinical features.
Bleeding manifestations:
Thrombocytopenia, often associated with hepatic dysfunction, may cause
bleeding from the retina, gastrointestinal tract and nose.
Cause of death: Death usually occurs within a year and is either due to
bacterial infection or uncontrolled bleeding.
Complications:
Hypoalbuminemia: May develop in advanced stage and may manifest as
pedal edema, ascites and anasarca.
Immunosuppression: As the disease advances, severe immunosuppression
may lead to secondary infections. These include tuberculosis, pneumonia,
malaria, severe amebic or bacillary dysentery, gastroenteritis, herpes zoster
and chickenpox. Skin infections are common.
Investigations
Blood: Pancytopenia is a common feature (i.e. anemia, granulocytopenia
and thrombocytopenia).
Biochemical findings:
Low serum albumin (hypoalbuminemia) and polyclonal
hypergammaglobulinemia (high serum globulin), chiefly IgG followed by IgM in
advanced cases.
Liver function test: Mildly elevated bilirubin, AST/ALT and alkaline phosphatase
may be seen.
Serological/immunodiagnostic tests:
These are less invasive and are useful in community surveillance studies.
ELISA or immunofluorescence antibody test
Rapid immunochromatographic k39 strip test
Demonstration of amastigotes (Leishman–Donovan bodies) in splenic smears is
the most efficient means of diagnosis , with 98% sensitivity.
Bone marrow or lymph node smears, are less sensitive but are frequently employed.
PCR
Culture: The aspirated material can be cultured in the Novy-MacNeal Nicolle
(NNN) medium for the organism.
Treatment
Nutritional support
Treatment of intercurrent infections
Anemia
Bleeding
First line regimen: Liposomal Amphotericin B
Dose: 10mg/kg over two hours
Safe in pregnant women, severely ill patients, children less than 2 years, old
aged patients and HIV co-infected patients.
Second line treatment:
Any one of the following drug combinations:
a)
Liposomal Ampotericin B 5mg/kg single infusion plus 7 days Miltefosine 50 mg
BD.
b)
Liposomal Ampotericin B 5mg/kg single infusion plus 10 days
Paromomycin(10mg/kg base).
c)
Miltefosine plus Parmomycin for 10 days.
Third line treatment:
Ampotericin B Deoxycholate 0.75-1mg/kg per day by infusion,daily or
alternate day for 15-20 doses.
Post-Kala-azar Dermal Leishmaniasis (PKDL)
After treatment and apparent recovery from VL in India and Sudan, some
patients develop dermatological manifestations due to local parasitic
infection.
2-50% of patients develop skin lesions due to local parasitic infection
concurrent with or after apparent recovery or cure of visceral
leishmaniasis.
In India, dermatological changes occur in a small minority of patients 6
months to at least 3 years after the initial infection.
Clinical features
They are seen as macules, papules, nodules (most frequently) and
plaques, which have a predilection for the face, especially the area
around the chin. The face often appears erythematous
Hypopigmented macules can occur over all parts of the body and are
highly variable in extent.
In Sudan and South Sudan, approximately 50% of patients with VL develop
post-kala-azar dermal leishmaniasis, experiencing skin manifestations
concurrently with VL or within 6 months.
Diagnosis:
Demonstration of parasite in the slit smear or by culture of the dermal tissue.
Q.1Kala-azar in Nepal is mainly transmitted by which vector?
A. Anopheles mosquito
B. Culex mosquito
C. Sandfly (Phlebotomus)
D. Tsetse fly
Q.2 The causative organism of Kala-azar in Nepal is:
A. Leishmania tropica
B. Leishmania donovani
C. Leishmania braziliensis
D. Leishmania major
Q.3 The most common clinical triad of Kala-azar is:
A. Fever, rash, lymphadenopathy
B. Fever, hepatosplenomegaly, pancytopenia
C. Fever, jaundice, ascites
D. Fever, cough, hemoptysis
Q.4 Which laboratory finding is MOST characteristic of Kala-azar?
A. Leukocytosis
B. Thrombocytosis
C. Pancytopenia
D. Polycythemia
Q.6 The recommended first-line treatment for Kala-azar in Nepal under the
elimination program is:
A. Sodium stibogluconate monotherapy
B. Oral miltefosine monotherapy
C. Liposomal amphotericin B single dose
D. Chloroquine
Q.7 The gold standard diagnostic test for Kala-azar is:
A. Peripheral smear
B. Bone marrow/splenic aspirate showing LD bodies
C. ELISA
D. PCR
Thank you
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