Recidivance Leishmaniasis (Lupoid)

Old World Visceral Leishmaniasis
(OWVL)

Causative agents & Reservoir hosts of OWVL
L. donovani
India, Bangladesh, Nepal, China and East Africa
Anthroponotic Visceral leishmaniasis
Principal reservoir host: Humans
L. infantum
Europe, Mediterranean, Middle East, Western and Central Asia, China, North and West Africa
Zoonotic Visceral Leishmaniasis
Principal reservoir hosts:
Fox , Jackal , wolf and Rodents
Domestic dogs play the most important role in transmitting the disease to humans
L. archibaldi: Sudan (AVL & ZVL)
L. tropica: Middle East & India

Vectors of OWVL
P. (Eu.) argentipes (India, Bangladesh, Nepal)
P. (La.) oriethalis & P. martini (Africa)
P. (Pa.) alexandri & P. (Ad.)chinensis (China)
P. (La.) major & P. (La.) neglectus (Greece)
P. (La.) tobbi (Cyprus, Caucasus)
P. (La.) perniciosus & P. (La.) arisi (Spain, France)

Mediterranean Kala-azar
Mediterranean regions, south Europe, Western and Central Asia, China
L. infantum
Endemic and sporadic
Infants and children (1 - 5 years old)
Zoonotic visceral leishmaniasis
Wild canids, domestic dogs and Rodents (R. rattus in Europe) are reservoir hosts

African Kala-azar
L. donovani: AVL , East Africa
L. infantum: ZVL , North and West Africa
L. archibaldi: Sudan
Children (5- 9 years old) and adults
Sudan
Sporadic: ZVL / Reservoir: Arvicanthis niloticus
Epidemic: AVL / Reservoir: Humans

African grass Rat

Indian Kala-azar
India, Bangladesh, Nepal, East Africa, China
L. donovani
Humans are principal reservoir hosts
Adults (10 – 20 years old)

Post kala-azar Dermal Leishmaniasis (PKDL)
Occurs after recovery in some cases of visceral leishmaniasis caused b L. donovani
Characterized by macular or nodular rash around the mouth, which spreads
Dermal lesions may contain parasites in great numbers (source of infection for sandflies)
In India, PKDL is seen in 20% of successfully treated (2-10 years after treatment)
In Africa (Sudan and Kenya), PKDL is seen 50% of successfully treated (6 month after treatment)

Visceral Leishmaniasis and HIV co-infection
Leishmania and HIV co-infections have been reported in 35 out 98 countries in which leishmaniasis is endemic
Almost all the cases of co-infection are very prone to VL relapses, even after carefully managed anti leishmanial treatment.
The overlapping geographical distribution of VL and AIDS is due to the spread of the AIDS pandemic and spread of VL from rural to suburban areas

Clinical symptoms in VL in Human
Prolonged Irregular fever
Hepatomegaly
Splenomegali
Anemia , Leukopenia and Thrombocytopenia
Lymphadenopathy
Weight loss , Weakness , Fatigue , Anorexia , Cachexia
Coughing and chronic diarrhea
Darkening of the skin

Clinical symptoms in VL in Human
Splenomegaly, distended abdomen and severe muscle wasting.

Clinical symptoms in VL in Human
Splenomegaly , severe muscle wasting and Cachexia

Clinical symptoms in VL in Human
Hepatomegaly and Splenomegali in an autopsy of an infant dying of visceral leishmaniasis.

Clinical symptoms in VL in Human
Jaundice hands of a VL patient

Clinical symptoms in VL in Dogs
Progressive loss of weight
Localized or generalized loss of hair
Hypertrophy of claws
Cachexia
Opacification of the cornea
Hind legs paraplegia
Apathy
Intestinal bleeding

Diagnosis of VL
The incubation period for VL is 10 days to 1 year (or 2 to 6 months)
Duration of disease about 1 to 20 weeks
Because symptoms are non-specific and often start after redeployment there is usually a delay in diagnosis
Visceral leishmaniasis should be considered in any chronic FEVER patient returning from an endemic area.

Diagnosis of VL
Clinical
Symptoms and clinical signs
Parasitological
Spleen and liver biopsy
Marrow and lymph gland biopsy
Inoculation to sensitive animals (Balb/C, Souri and Golden Hamster)
Serological
Indirect Fluorescent Antibody Test (IFAT)
Direct Agglutination Test (DAT)
Enzyme Linked Immunosorbent Assay (ELISA)
Formol Gel test
Molecular techniques (PCR)