A local granulomatous response leads to the formation of a crateriform lesion
The primary lesion may enlarge to 2cm or more in diameter, be intensely itchy, pruritic and become subjected to secondary bacterial infections Transfusion associated leishmaniasis has been reported has been documented but rare Recovery depends on the development of a CMI response Diffuse cutaneous leishmaniasis (DCL) may occur in patients with impaired immunity
Treatment and Prevention Pantavalent antimony sodium gluconate (Pentostom) and Pentamidine isothionate (Lomidine) Amphotericin B Combination drug regimen exist using either Allopurinol or Gamma interferon along with Pentostom Length of therapy is species dependent
Life Cycle The invading trypomastigotes actively enter histiocytes (phagocytic cells of the RES) and other tissue cells Parasite Transform into amastigotes and multiply by binary fission The parasites may transitionally pass through a promastigote, epimastigote and trypomastigote form within the parasitized cell
Trypanosoma cruzi By day, this reduviid bugs live within the mud and thatch wall of dwellings and emerge at night to feed on human blood Trypanosomes develop in the gut of this insect and passed as they defecate while feeding They bite painlessly about the face Transmitted by triatomine bugs
Diagnosis Demonstration of amastigotes of Leishmania in Giemsa stained smears of biopsy material from the edge of an active ulcer Culture methods will produce the promastigote stage Complement-fixation, direct agglutination and Montenegro skin test
HEMOFLAGELLATE FORMS Characteristic Amastigote Promastigote Epimastigote Trypomastigote Size 5 x 3 m 9-15 m 9-15 m 12-35 m Shape Oval to round Long and slender Long and slightly wider Spindle shaped, U or C shaped in blood films Nucleus One, eccentric One, central One, in posterior end One, anterior to kinetoplast Kinetoplast Present, Consisting of dot- like blepharoplast, with small axoneme and prabasal body Anterior end of the organism, no undulating membrane Anterior to the nucleus, with half body undulating membrane Posterior, gives rise to full- body length undulation membrane Flagellum Absent Single, anterior free flagellum Single, anterior free flagellum Single, anterior free flagellum
Transmission and Pathogenesis The parasite has been acquired through blood transfusion, organ transplant or congenital trans. infection is characterized by 3 progressive stages: o Incubation period: few days to several weeks o Hematogenous spread and lymphatic involvement o Glandular stage: Winterbottoms sign, Kerandels sign
Leishmania chagasi Visceral leishmaniasis in the New World (Central and South America) Foxes and domestic dogs and cats serve as the natural reservoir Sandflies of the genus Lutzomyia serve as the vector
Lab DX Montenegro (Leishmanin) skin test is often used for the screening of large populations at risk. The delayed hypersensitivity(HPS) reaction provoked by a suspension of killed leishmanial promastigotes administered intradermally A local inflammatory reaction appears at the site of injection within 48-72 hours in (+) patients Serologic testing inc. IFA (indirect fluorescent antibody assay)
Transmission and Pathogenesis L. garnhami and L. venezuelensis assosiated with cutaneous leishmaniasis in rural parts of Venezuela Infection with either organism present with a solitary lesion that is usually self-limiting L. mexicana - produces a lesion known as chiclero ulcer or Bay sore common among workers who collect chicle gum from the Chicazapote trees in the rain forest in Nicaragua, Guatemala, Belize and the Yucatan peninsula of Mexico Clinical manifestation: a single cutaneous papule, nodule or ulcer located on the ear or face Lesions generally heal spontaneously but may cause cartilage destruction and gross disfigurement
Transmission and Pathogenesis Acute chagas dse is characterized by bouts of fever and chills, generalized malaise, myalgia (mucle aches), fatigue and may appear in 4days to 2weeks following insect bite Glandular enlargement and abdominal rash may also occur Most severe symptoms are seen in very young children where course of infection is abbreviated and S/S of CNS involvement appear early in infection Marked myocarditis and damage to the CNS lead for eventual death
Transmission and Pathogenesis Invading organism enter fat cells and are ingested by histiocytes and macrophages where they transform into amastigotes and multiply At the site of infection, an acute inflammatory response blocks lymphatic flow and produces an erythematous primary lesion called chagoma Trypomastigotes and amastigotes may be aspirated from chagoma
Lab DX Elevated serum globulin levels Complete Fixation test (CF), Direct agglutination tests(DAT), Indirect fluorescence technique Montenegro skin test (not reactive in people with active disease)
Life Cycle Similar to that of other Leishmanial organisms Morphology is indistinguishable Transmitted by sandflies of the genus Lutzomyia
Life Cycle The infected hosts cell eventually ruptures releasing new parasites to infect additional host cells Trypomastigotes periodically appear in the peripheral circulation as the infection spreads beyond the regional lymph nodes In the insect, T. cruzi is most commonly seen in the epistimastigote stage in the midgut and transforms into the metacyclic trypomastigote which is excreted in the bugs feces
Lab DX Trypomastigotes may be recovered in the peripheral blood during febrile episodes Stained prep of lymph node aspirate may demonstrate the amastigote form Xenodiagnosis CF, EIA, IIFA, PCR, ELISA
Life Cycle Glossina palpalis and Glossina tachinoides both male and female flies bite man and serve as vector Parasites are ingested by the fly when it takes a blood meal on an infected mammal, humans or ungulate (hoofed animals) In the fly, the parasite begins to multiply, develops in the gut and salivary glands
Lab DX Demonstration of the non-flagellated amastigote by Giemsa stain from spleen and liver biopsies Bone marrow and lymph nodes aspirations are advised Culture sample will yield promastigotes Buffy coat preps may reveal intracellular amastigotes
Treatment and Prevention Pentavalent sodium antimony (Pentostam) Cycloguanil pamoate (Camolar) and Amphotericin B Protective clothing, insect repellent, vector control, control of reservoir host, public health educational program
Transmission and Pathogenesis Most common victim is <5 years old As the insect bites, it deposits infective material near the bite wound The bite wound becomes intensely pruritic and T. cruzi is scratched into the bite wound incubation period: 7-14 days An acute local inflammatory reaction results as the organism is carried by the lymphatic to the regional lymph nodes
Treatment and Prevention Melarsoprol. Trivalent arsenic compound much more toxic than Pentamidine or Suramin but is the drug of choice for the later stageof Gambian sleeping sickness. Administered IV and can penetrate the BBB Tsetse flies are attracted tp bright and darf colors; thick khaki or olive drab clothing is preferred Use of bed nets and insect repellant
Treatment and Prevention Sodium stibogluconate (antimony sodium gluconate: Pentostam) administered IM for 10 days May require multiple courses of treatment to induce a clinical response Alternate drug of choice: meglumine antimonite or Glucantime, Amphotericin B, Ketoconazole Prevention lies in vector and reservoir