protozoa II Flashcards Preview

ID test III > protozoa II > Flashcards

Flashcards in protozoa II Deck (27)
Loading flashcards...
1
Q

Plasmodium species

A

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

2
Q

Plasmodium diagnosis

A

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)

3
Q

Plasmodium life cycle

A

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

4
Q

Malaria sx

A

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.

5
Q

Which plasmodium species causes glomerulonephritis

A

P. malariae- due to immune complex deposition

6
Q

Erythrocyte Changes in Falciparum Malaria

A

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

7
Q

epidemiology of malaria

A

P. vivax is widely distributed from tropical to temperate zones, but P. falciparum occurs primarily in the tropics and subtropics.

8
Q

Which diseases have protection from P. falciparum

A

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

9
Q

HLA subtype associate with recovery from falciparum malaria

A

HLA-B53

10
Q

malaria immunity

A

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.

11
Q

which organisms cause sleeping sickness and how are they transmitted

A

Trypanosomes: T. brucei rhodesiense (in East Africa) and T. brucei gambiense (in West Africa). transmitted to man by Tsetse flies

12
Q

Cause of Chagas disease and transmission

A

T. cruzi (in South and Central America) causes Chagas’ disease and is transmitted to humans by triatomine insects (also called reduviid bugs).

13
Q

Trypanosomes diagnosis

A

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

14
Q

African trypanosomes life cycle

A

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

15
Q

African trypanosomes stages of dz

A

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).

16
Q

T. Cruzi life cycle

A

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

17
Q

Chagas disease clinical features

A

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%.

18
Q

Leishmania

A

Hemoflagellates that can cuase- visceral leishmaniasis (L. donovani), cutaneous leishmaniasis, Mucosal lieshmaniasis.

19
Q

Leishmania transmission

A

sandflies

20
Q

Leishmania diagnosis

A

Macrophages containing amistigotes. Lymph node aspirates or biopsy from lesion for cutaneous forms. Blood, bone marrow, nodes, liver, spleen for visceral form.

21
Q

Leishmania life cycle

A

Promastigote injected into human from insect > invasion of reticuloenthothelial cells > amastigote forms in cell > reproduction and invasion of other cells > ingested by flie

22
Q

Leishmania forms

A

The amastogote is the only form found in humans, and the infectious promastigote form occurs only in the insect vector

23
Q

Leishmania clinical features

A

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

24
Q

Toxoplasma gondii diagnosis

A

Acute infection: IgM and IgG Abs against organism, tachyzoites in lymph nodes, IgA. Prior infection: cysts containing bradyzoites

25
Q

Toxoplasma gondii life cycle

A

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.

26
Q

Toxoplasma gondii clincal features

A

Mono like syndrome. Immuno-compromized patients with AIDS or Hodgkin’s disease have a predilection for developing toxoplasma encephalitis

27
Q

Transplacental Transmission of T. gondii

A

•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