protozoa II Flashcards
Plasmodium species
coccidian parasites that cause malaria. Four species can cause most cases of malaria in man: P. vivax, P. ovale, P. malariae, and P. falciparum. P. falciparum causes most of the deaths
Plasmodium diagnosis
detecting the asexual forms of the parasites in stained thick or thin blood films or by detecting genus or species specific antigens of Plasmodia in blood (Ab against P. falciparum histidine rich protein or plasmodium LDH for P. falciparum)
Plasmodium life cycle
infected mosquito bites human and injects sporozoites into blood > asexual phase (schizogony) occurs in humans > primary replication in liver > merozoites released in blood > infect RBCs > asexual replication > gametes form in some RBCs > mosquito picks up blood containing gametes > sexual phase (sporogony) occurs in mosquito > gametes fuse in intestine to form zygotes > sporozoites produced in salivary gland
Malaria sx
due to rupture of infected RBCs and release of merozoites- fever paroxysms w/ periodicity if untreated, anemia (lysis of RBcs and phagocytosis), splenomegaly (sequestered RBCs). If hemolysis is extreme, hemoglobinuria (blackwater fever). Jaundice, hypotension (vasodilation) and tachycardia. Inadequate blood supply to vital organs due to vasodilation may cause multi organ failure and death.
Which plasmodium species causes glomerulonephritis
P. malariae- due to immune complex deposition
Erythrocyte Changes in Falciparum Malaria
Infected erythrocytes containing mature asexual forms of P. falciparum stick to small blood vessels (sequestration). Because of sequestration, only ring forms (immature) and sexual forms of P. falciparum are found in circulating erythrocytes
epidemiology of malaria
P. vivax is widely distributed from tropical to temperate zones, but P. falciparum occurs primarily in the tropics and subtropics.
Which diseases have protection from P. falciparum
sickle cell anemia, the thalassemias and glucose-6-phosphate dehydrogenase deficiency. The parasites do not appear to thrive on the hemoglobin S associated with sickle cell disease, nor on certain other abnormal hemoglobins. In thalassemia, there is increased production of fetal hemoglobin, which retards maturation of P. falciparum, while in G6PD deficiency oxidative stress may inhibit parasite growth
HLA subtype associate with recovery from falciparum malaria
HLA-B53
malaria immunity
Both B and T cell responses are involved. Within a few weeks of infection, stage specific anti-plasmodium antibodies are produced. Natural immunity is short-lived, and continual re-infection is required to maintain it. People returning to endemic areas following a long absence may therefore be quite susceptible to re-infection.
which organisms cause sleeping sickness and how are they transmitted
Trypanosomes: T. brucei rhodesiense (in East Africa) and T. brucei gambiense (in West Africa). transmitted to man by Tsetse flies
Cause of Chagas disease and transmission
T. cruzi (in South and Central America) causes Chagas’ disease and is transmitted to humans by triatomine insects (also called reduviid bugs).
Trypanosomes diagnosis
T. brucei rhodesiense and T. brucei gamgiense: flagellated trypomastigote in blood, CSF, lesion aspirates/ lymph nodes, or biopsy of bone marrow/ spleen. IgM in CSF indicates encephalitic phase. T. Cruzi: detection of motile flagellated trypomastigote in blood
African trypanosomes life cycle
Infectious trypomastigote injected into blood by insect > chancre at bite site > spread to blood via lymphatics > IgM production > organism evades immune response by antigenic variation > picked up by insect
African trypanosomes stages of dz
stage I: low-grade parasitemia accompanied by recurrent fever, prominent lymphadenopathy, rash, headache and confusion. Stage II: CNS involvement, convulsion, coma and death in 5-9 months (East African form) OR slower progression (West African form).
T. Cruzi life cycle
Trypomastigote passed by bug in feces on skin > bite is scratched introducin into human host > amistogotes replicate in tissues > cells rupture releasing amistigote > trypomastigote in blood > passed on to insect
Chagas disease clinical features
dvelop on 2 weeks, last 6 months, severe. fever, and enlargement of the lymph glands, liver and spleen, and damage to the heart. Painless edema of the eyelids and periorbital tissues (Romana’s sign) may occur when the conjunctiva is the portal of entry. Children are especially susceptible, and mortality rates may reach 10%.
Leishmania
Hemoflagellates that can cuase- visceral leishmaniasis (L. donovani), cutaneous leishmaniasis, Mucosal lieshmaniasis.
Leishmania transmission
sandflies
Leishmania diagnosis
Macrophages containing amistigotes. Lymph node aspirates or biopsy from lesion for cutaneous forms. Blood, bone marrow, nodes, liver, spleen for visceral form.
Leishmania life cycle
Promastigote injected into human from insect > invasion of reticuloenthothelial cells > amastigote forms in cell > reproduction and invasion of other cells > ingested by flie
Leishmania forms
The amastogote is the only form found in humans, and the infectious promastigote form occurs only in the insect vector
Leishmania clinical features
cutaneous: localized skin ulcers . Mucosal: lesions in the nose and pharynx. More serious than cutaneous lesions. The nasal septum, hard palate and larynx may erode to a degree rendering the victim speechless. Anemia and secondary bacterial infections are common. Visceral: Macrophages of the liver, spleen, bone marrow, lymph nodes and intestine are infected. Symptoms take from 3-12 months to appear, and include fever, diarrhea and malabsorption, hepatosplenomegaly, ascites and lymphadenopathy
Toxoplasma gondii diagnosis
Acute infection: IgM and IgG Abs against organism, tachyzoites in lymph nodes, IgA. Prior infection: cysts containing bradyzoites
Toxoplasma gondii life cycle
Ingesting bradyzoites in cysts in under cooked meat or oocysts in cat feces > infects macrophages > replicates in endosomes > later macrophages acquire ability to kill parasite.
Toxoplasma gondii clincal features
Mono like syndrome. Immuno-compromized patients with AIDS or Hodgkin’s disease have a predilection for developing toxoplasma encephalitis
Transplacental Transmission of T. gondii
•If maternal infection occurs during the first trimester, the incidence of fetal infection is low (15%) but the disease in the neonate is most severe. If maternal infection occurs during the third trimester, the incidence of fetal infection is high (65%). The neonate is usually asymptomatic at birth but may have more learning disabilities and neurological sequelae than uninfected children
