Leishmaniasis PDF

LEISHMANIASIS Prof. Ameer kadhim Hussein M.B.Ch.B. FICMS (Community Medicine) Learning objectives about Leishmaniasis The students must understand the following items regarding Leishmaniasis: 1. Types of Leishmaniasis 2. Risk factors of Leishmaniasis 3. Visceral Leishmaniasis: causative agent,...

LEISHMANIASIS Prof. Ameer kadhim Hussein M.B.Ch.B. FICMS (Community Medicine) Learning objectives about Leishmaniasis The students must understand the following items regarding Leishmaniasis: 1. Types of Leishmaniasis 2. Risk factors of Leishmaniasis 3. Visceral Leishmaniasis: causative agent, incubation period, reservoir, mode of transmission, occurrence and methods of prevention and control. 4. Cutaneous Leishmaniasis causative agent, incubation period, reservoir, mode of transmission, occurrence and methods of prevention and control.  Introduction Leishmaniasis is one of the most important vector-borne diseases of humans. This parasitic disease can be caused by many species of Leishmania (over 20 Leishmania species), most of which are zoonotic. In humans, different species of the parasite are associated with different forms of the disease. Many Leishmania spp. cause skin ulcers and nodules. A few of these organisms can also affect the mucous membranes, and may cause disfiguring lesions of the nose. Other species damage the internal organs and cause human visceral leishmaniasis which is a life-threatening condition. Among domesticated animals dogs are the most important species in the epidemiology of this disease. Leishmania transmitted to humans by the bite of infected female phlebotomine sandflies. Over 90 sandfly species are known to transmit Leishmania parasites.  Types There are 3 main forms of the disease: a. Cutaneous Leishmaniasis. b. Mucocutaneous Leishmaniasis. c. Visceral Leishmaniasis. Morphology of leishmania parasites in vertebrate hosts in sandfly vectors Amastigote Promastigote (Leishman body). (Leptomonad). Sand fly Life cycle of species of Leishmania  Risk factors for leishmaniasis Socioeconomic conditions Poverty increases the risk for leishmaniasis. Poor housing and poor domestic sanitary conditions may increase sandfly breeding and resting sites, as well as their access to humans. Malnutrition Diets lacking protein-energy, iron, vitamin A and zinc increase the risk that an infection will progress to a full- blown disease. Population mobility Epidemics of both cutaneous and visceral leishmaniasis are often associated with migration and the movement of non- immune people.  Risk factors for leishmaniasis Environmental changes The incidence of leishmaniasis can be affected by changes in urbanization, and the human incursion into forested areas. Climate change Changes in temperature, rainfall and humidity can have strong effects on vectors and reservoir hosts by altering their distribution and influencing their survival and population sizes.  Visceral Leishmaniasis Identification: It is chronic systemic disease caused by intracellular protozoa of the genus leishmania. The disease is characterized by fever, Hepato- splenomegaly, lymphadenopathy, anemia, leukopenia,thromboocytopenia and progrssive emaciation and weakness. VL also known as kala-azar, the disease is fatal if left untreated in over 95% of cases.  Visceral Leishmaniasis Post-kala-azar dermal leishmaniasis (PKDL) is usually a sequel of visceral leishmaniasis that appears as macular, papular or nodular rash usually on face, upper arms, trunks and other parts of the body. It occurs mainly in East Africa and on the Indian subcontinent, where 5–10% of patients with kala-azar are reported to develop the condition. It usually appears 6 months to 1 or more years after kala-azar has apparently been cured, but can occur earlier. People with PKDL are considered a potential source of Leishmania infection.  Visceral Leishmaniasis Girl suffering from visceral leishmaniasis – a potentially fatal condition, if untreated - with markers showing signs of liver and spleen enlargement. (Ethiopia). Post kala-azar dermal leishmaniasis Patient with post-kala-azar-dermal leishmaniasis. (Ethiopia) Post–kala-azar dermal leishmaniasis Infectious agents: Typically Leishmania donovani , L. infantum and L.infantum/ chagasi. Reservoir: Humans , wild Canidae (foxes and jackals) and domestic dogs. Incubation period: generally 2-6 months ranging from 10 days to years. Period of communicability: Not usually transmitted from person to person but infectious to sandflies as long as parasites persist in the blood or skin of reservoir. Infectivity for phlebotomines may persist after clinical recovery of human patients. Susceptibility: Susceptibility is general. Kala-azar induce lasting homologous immunity. Mode of transmission: 1.Bite of infected female phlebotomine sandflies (P. argentipes). 2.Personto person transmission has been reported in leishmania –HIV co-infected IV drug abuser through exchange of syringes. Occurrence: Visceral leishmaniasis (VL), also known as kala-azar is fatal if left untreated in over 95% of cases. It is characterized by irregular bouts of fever, weight loss, enlargement of the spleen and liver, and anaemia. Most cases occur in Brazil, East Africa and in India. An estimated 50 000 to 90 000 new cases of VL occur worldwide annually, with only between 25 to 45% reported to WHO. It remains one of the top parasitic diseases with outbreak and mortality potential. In 2019, more than 90% of new cases reported to WHO occurred in 10 countries: Brazil, Ethiopia, Eritrea, India, Iraq, Kenya, Nepal, Somalia, South Sudan and Sudan. Status of endemicity of Visceral leishmaniasis Number of cases of Visceral leishmaniasis reported by country Diagnosis based on: 1.Demonstration of intracellular amastigotes in stained smears from bone marrow, spleen, liver, lymph nodes. 2. The PCR technique is the most sensitive, but remains expensive. 3. Serological diagnosis was traditionally based on IFA and ELISA tests. 4. An antigen detection test in urine is also under evaluation. 5. Recombinant k 39 immunochromatographic strip test.  Methods of control A. Preventive measures : No vaccine are currently available although candidate vaccines are in development. Control measures are vary according to the habits of mammalian hosts and habits of vectors and include the following: 1. Case management : detect cases systematically and treat rapidly this applied to all forms of leishmaniasis. 2. Vector control: apply residual insecticide periodically. Phlebotomine are highly susceptible to control by systematic spraying with residual insecticide. Spraying must include stone walls, animal houses and rubbish heaps. Insecticide –treated bed nets are additional vector control measures and should be promoted especially in arthroponotic foci. 3. Eliminate rubbish heaps and other breeding places. 4. Destroy gerbils implicated as reservoirs in local areas by deep plowing and removal the plants they feed on. 5. Avoid sandfly infested forest area especially when sundown and use insect repellents and protective clothes if exposure is un avoidable. 6. Apply environmental management and forest clearance. 7. Control dogs which regard as animal reservoir of parasites. A young gerbil Control patients, contacts and immediate environment 1. Report to local health authority. 2. Isolation with blood and body fluid precautions. 3. Concurrent disinfection, quarantine, immunization of contacts and investigation of contacts and source of infection: not applicable. 4. Specific treatment: Pentavalent antimonials regard as first line treatement in most countries (Sodium stibogluconate and meglumine antimonate). Cases that do not respond to antimony may be treated with amphotericin B or amphotericin B deoxycholate). Liposomal amphotericin B is the most effective drug but it is expensive. Epidemic measures: Effective control must include understanding of the local ecology and transmission cycle and application of practical measures to reduce mortality, stop transmission and avoid geographical extension of the epidemic. The measures used: 1. Case detection and effective treatment. 2. Vector control by indoor residual spray and using insecticide treated bed nets and control of animal reservoir. 3. Effective disease surveillance and program monitoring. Cutaneous and mucosal leishmaniasis Other names Baghdad boil , Delhi boil , oriental sore. In Americas Espundia ,Uta and Chiclero ulcer. It is polymorphic protozoan disease of skin and mucous membranes caused by several species of the genus Leishmania. These protozoa exist as obligate intracellular parasites in humans and other mammalian hosts. The disease starts with a maculae, then a papule that enlarges and typically becomes an indolent ulcer in the absence of bacterial infection. Lesions may be single or multiple, occasionally non- ulcerative and diffuse. Lesions may heal spontaneously within weeks to months, or last for a year or more. In some individual certain strain (from Western Hemisphere) can disseminate to cause mucosal lesions even years after healing of cutaneous lesions. Occurrence Cutaneous leishmaniasis (CL) is the most common form of leishmaniasis and causes skin lesions, mainly ulcers, on exposed parts of the body, leaving life-long scars and serious disability or stigma. About 95% of CL cases occur in the Americas, the Mediterranean basin, the Middle East and Central Asia. In 2019 over 87% of new CL cases occurred in 10 countries: Afghanistan, Algeria, , Brazil, Colombia, Iran (Islamic Republic of), Iraq, Libya, Pakistan, the Syrian Arab Republic and Tunisia. It is estimated that between 600 000 to 1 million new cases occur worldwide annually. Mucocutaneous leishmaniasis leads to partial or total destruction of mucous membranes of the nose, mouth and throat. Over 90% of mucocutaneous leishmaniasis cases occur in Bolivia, Brazil, Ethiopia and Peru. Cutaneous leishmaniasis Child with cutaneous leishmaniasis in Kabul, Afghanistan Classic Leishmania major lesion from a case in Iraq shows a volcanic appearance with rolled edges Diagnosis is based on: 1. Microscope identification of the non-motile, intracellular form (amastigote) in stained specimens from lesions. 2. An intra-dermal (Montenegro) test with leishmanin, an antigen derived from promastigotes, is usually positive in established disease but it is not helpful with very early lesions and immuno-suppressed patients. 3. Serological (IFA or ELISA) testing. Infectious agents: Eastern hemisphere: Leishmania tropica , Leishmania major , Leishmania aethiopica. Western hemisphere: Leishmania braziliensis and Leishmania mexicana. Reservoir: locally variable including humans, wild rodents, and domestic dogs. Incubation period: At least a week up to many months. Mode of transmission: 1.Bite of infective female phlebotomine sandfly. (P. papatasi and P. sergenti). 2. Rarely through blood transfusion. Period of communicability: Not directly transmitted from person to person but the patient infectious for sand fly as long as parasites remain in the lesions. In untreated cases they can remain few months to 2 years. Susceptibility: is general. Life long immunity may be present after healing of lesions due to L.tropica and L.major but not protect against other L. species. Status of endemicity of cutaneous leishmaniasis Data by country Number of cases of Cutaneous leishmaniasis reported by country  Methods of control A. Preventive measures: As mentioned in visceral leishmaniasis. B. Control patients , contacts and immediate environment: 1. Report to local health authorities. 2. Isolation, concurrent disinfection, Quarantine and immunization of contacts: Not applicable. 3. Investigation of contacts and source of infection: Interrupt the local transmission cycle in the most practical fashion. 4. Specific treatment: Medicines called antimony-containing compounds are the main drugs used to treatment. These include: Meglumine antimoniate. Sodium stibogluconate. Other drugs that may be used include: Amphotericin B. Ketoconazole. Miltefosine. Paromomycin. Pentamidine.  Epidemic measures Control the disease by: 1. Provision of adequate diagnostic and treatment facilities. 2. Provision of adequate measures against sandflies and mammalian reservoirs.  Leishmania-HIV co-infection Leishmania-HIV coinfected people have high chance of developing the full-blown clinical disease, and high relapse and mortality rates. Antiretroviral treatment reduces the development of the disease, delays relapses and increases the survival of the coinfected patients. High Leishmania-HIV coinfection rates are reported from Brazil, Ethiopia and the state of Bihar in India.  Summary There are 3 main forms of leishmaniases – visceral (often known as kala-azar and the most serious form of the disease), cutaneous (the most common), and mucocutaneous. Leishmaniasis is caused by the protozoan Leishmania parasites which are transmitted by the bite of infected sandflies. The disease affects some of the poorest people on the planet, and is associated with malnutrition, population displacement, poor housing, a weak immune system and lack of resources. Leishmaniasis is linked to environmental changes such as deforestation, building of dams, irrigation schemes and urbanization.  Summary An estimated 700 000 to 1 million new cases occur annually. Only a small fraction of those infected by Leishmania parasites will eventually develop the disease. Thank you