Parasites Flashcards
Leishmaniasis - Vector
female sand fly
Leishmaniasis - Reservoir
dogs, rodents, humans
Leishmaniasis - Pathogen
Leishmania donovani
• Intracellular amastigotes (no flagella) inside WBCs.
• Promastigotes (with flagella) in sand fly vector.
Leishmaniasis - Transmission
- Bite of a female sand fly.
* Rarely, transplacental, vaginal birth, blood transfusion, needle sharing, sexual transmission.
Leishmaniasis - Pathogenesis
- Protozoan engulfed by macrophages, divides within and destroys cells –> lesions, ulcer at bite site.
- Spreads through the RES, damaging spleen liver, and bone marrow –> visceral leishmaniasis (splenomegaly, thrombocytopenia, anemia and leukopenia).
- Secondary infections due to weakened immune state cause death.
- Cell-mediated immunity controls infection. Deficient CMI is a factor that promotes development of mucosal and visceral disease. Life-long immunity to reinfection.
Cutaneous Leishmaniasis
o Old World Cutaneous – dry and scaly lesions; found in the Mediterranean, Africa/Middle East. (Species - major, tropica, aethiopica.)
o New World Cutaneous – wet chronic lesions; seen in South America, potentially Texas. (Species - panamensis, guyanesis, amazonensis, mexicana, braziliensis, etc.)
Papules are NOT painful, progress slowly (wks) to an ulcer with rolled margins, induration. Often, multiple subcutaneous nodules. NO response to antibiotics.
Mucosal Leishmaniasis
Usually a late complication of New World CL (Mucosal Belt, south of Nicaragua).
Lesions appear months to years after skin lesions. Starts with nasal stuffiness, inflammation –> ulceration of nasal mucosa/septum –> lips, cheeks, palate, pharynx, larynx.
Visceral Leishmaniasis
L. donovani (human reservoir in Indian subcontinent)
L. infantum (dog reservoir in Western Med.)
Can be asymptomatic, subclinical, or overt (malnourished children, travelers); determined by infectious dose, CMI status, environmental factors, etc.
Fever, splenomegaly (massive), hepatomegaly, weight loss, LAD, cytopenias. Fever spikes TWICE in 24 hours.
Kala Azar – fever, weight loss, hepatosplenomegaly, pancytopenia, and hypergammaglobulinemia.
DEATH due to secondary infection – pneumonia, measles, sepsis, Tb, dysentery.
Leishmaniasis - Diagnosis
CL - histology, look for kinetoplast (little blue dot disease).
ML - PCR (low protozoan count in lesions).
VL – serology (ELISA rK39), bone marrow or spleen biopsy.
Leishmania skin test is positive in CL ONLY.
Leishmaniasis - Treatment
CL - wound care, topicals, etc. Self-limited disease.
ML - liposomal amphotericin (preferred), pentavalent antimony.
VL - liposomal amphotericin (preferred), pentavalent antimony, miltefosine.
Sleeping Sickness - Parasite
West - Trypanosoma brucei gambiense
East - Trypanosoma brucei rhodesiense
Sleeping Sickness - Vector
tsetse fly – large and bite is very painful
characteristic ‘cleaver cell’ wing
Sleeping Sickness - Reservoir
humans (West/gambiense)
antelope/cattle (East/rhodesiense)
Sleeping Sickness - Pathogenesis, Symptoms
(1) Host immune response causes a hard red chancre at inoculation site.
(2) Hemo-lymphatic stage – enlarged LNs, fever, myalgia, anemia, and hepatomegaly. Winterbottom’s Sign – posterior cervical adenopathy.
(3) Meningo-encephalitis stage – encephalitis/meningitis caused by infection of the CNS; causes headache, personality change, somnolence (“sleeping sickness”), and coma.
* Antigenic variation of the variant surface glycoprotein (VSG) allows protozoan to evade immune response. Causes remitting/relapsing course of disease; fever every 2 weeks.
Sleeping Sickness - Diagnosis
“C” shaped, flagellated protozoan in blood, LN aspirate, of CSF. Must see a kinetoplast for diagnosis.
CATT (card agglutination trypanosomiasis test) – T. b. gambiense screening only!
