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Flashcards in Parasite Infections of the Blood Deck (43):
1

what is the most common species of malarial infection? which is the most deadly?

p falciparum (both questions)

2

what genetic predispositions are protective against malaria?

absence of duffy antigen (vivax), hereditary elliptocytosis, heterozygotes for sickle cell disease, thalassaemia and G6PD deficiency

3

what hemoglobin variants are protective against malaria?

thalassemia, hemoglobin S and HbC

4

why are people without a duffy antigen less likely to get malarial infections?

because it is the erythrocyte receptor for p vivax

5

what is the pathogenicity of malarial infections?

produces anemia by hemolysis and impaired microcirculation

6

what is the range of malarial incubation?

generally around 10-40 days but may take as long as 8-10 months with vivax and ovale

7

what is the malarial paroxysm? how long does it last?

begins with an intense feeling of cold followed by the feeling of intense heat. the fever will then break and the patient will be sweaty and tired takes 4-8 hrs

8

what are the causes of the malaria paroxysm stages?

cold stage- lysis of RBC by schizonts
hot stage- cytokine response to parasite in plasma
sweating stage- parasites infect new RBC and are cleared from circulation

9

when does the malaria cyclic pattern not occur?

it may take time for the schizonts to sync their replication cycle. (beginning of infection).
p falciparum does not exhibit this cycle

10

what is malaria recrudescence?

parasitemia is undetectable for a period of time and later recurs

11

why do relapses of malaria occur?

the sporozoites invade hepatocytes and remain latent there until after a period of time when the hepatocyte ruptures

12

what are the severe manifestations of p falciparum?

cerebral malaria, severe anemia, respiratory failure, renal failure and severe malaria of pregnancy

13

what is an abnormal feature of the pathogenesis of p falciparum?

ability to sequester in the deep venous microvasculature

14

what are the metabolic manifestations of p falciparum infection?

lactic acidosis from impaired O2 delivery and hypoglycemia

15

what causes pulmonary edema and respiratory distress in p falciparum infection?

sequestration of infected erythrocytes in the lungs initiates production of cytokines that increase capillary permeability

16

what is the significance of PfEMP-1?

a ligand for the receptor CD36 that allows RBC to attach to cells in the vasculature

17

what is the classic finding in cerebral malaria?

sequestration of parasites in cerebral microvasculature accompanied by ring hemorrhages, perivascular leukocytes and endothelial cell damage

18

what is the harm of placental malaria?

maternal morbility and mortality, growth retardation, premature delivery, low birth weight and newborn mortality

19

why do mature parasites accumulate in the placenta?

they interact with syncytiotrophoblastic antigens, hyaluronic acid and immunoglobulins

20

what are the benefits for rapid diagnostic testing for malaria? what does it test for?

microscopy is not always available and it detects antigens of p falciparum and p vivax

21

what has been the result of phase three trials for the mosquirix vaccine for malaria?

effectiveness was 35% but stops working after about 6 months in 50% of patients

22

what clinical features are shared by p vivax and p ovale?

they have low mortality because they do not inhibit sequestration and they favor reticulocytes. they also may recur

23

what cells does p malariae often infect? what is the incubation period and what is the usual presentation?

infects older RBC with an incubation period of 40 days. patients present with proteinuria or nephrotic syndrome

24

why has a new species of malaria just recently been found? what does it usually infect?

because p knowlesii is similar to p malariae and is often misdiagnosed. it is primarily a primate parasite

25

what transmits babesia? what does the presentation resemble?

different types of ticks
in the northeast it resembles p vivax infection. in the rest of the country it presents as a fulminate, febrile hemolytic disease

26

what does the distribution of babesia resemble?

lyme disease and anaplasmosis (there is a lot of coinfections)

27

what is a major reservoir for anaplasmosis?

white footed mouse and squirrels

28

what are the first symptoms of anaplasmosis?

constitutional symptoms, nausea, cough and confusion

29

what are some serious clinical presentations of anaplasmosis?

difficulty breathing, hemorrhage, renal failure or neurological problems

30

what disease does trypanosomiasis cause? what is the causative agent?

chagas' disease
trypanosoma cruzi causes it in america

31

what are the two vectors for trypanosomiasis?

the tsetse fly in Africa and the reduvid bug in the americas

32

where is chagas' disease spread and what are the forms of the disease?

in southern california and texas.
acute form- death in weeks
chronic form- symptoms may not present for years

33

how does american trypanosomiasis infect humans?

the reduvid bug excretes the parasite in its feces. when the bug bites a human it leaves the feces behind. the feces cause itching and when the person scratches, it produces breaks in the skin

34

what parasite is a leading cause of foodborne illness death in the US? what is the usual host?

toxoplasmosis
the usual host are cats

35

how is toxoplasmosis transmitted from cats to humans?

oocysts are shed in the cat's feces (especially in kittens) and they infect people by accidental consumption through food or water contamination

36

what nonfeline modes may transmit toxoplasmosis?

may be transmitted via the consumption of undercooked meat that contain infective cysts or may transmit transplacentally

37

what is the progression of toxoplasma infection in healthy people?

most people are asymptomatic or have mild flu like symptoms. the parasite remains in muscle tissue and may reactivate with immunosupression

38

how is congenital toxoplasmosis acquired? what determines severity?

with an acute primary infection of the mother during pregnancy. severity dictated with the trimester of infection (early has more severe symptoms but is less likely to be transmitted)

39

what is the most common presentation of congenital toxoplasmosis infection? what are more severe manifestations?

most are aymptomatic but may develop learning, visual and hearing disabilities later.
may cause miscarriage, still born or abnormal head size

40

what is the manifestation of toxoplasmosis with immunosuppression?

infection will cause severe symptoms with neuro involvement (lesions in brain)

41

what transmits leishmania?

certain species of blood feeding sand flies

42

what are the clinical manifestations of leishmaniasis?

cutaneous-chronic skin ulcers
mucocutaneous- spread of lesion to mouth, nose and pharynx with mucosal destruction
visceral- fever, weight loss, anorexia and hepatosplenomegaly

43

what are the clinical features of lymphatic filariasis?

lymphatic dysfunction causing lymphedema and elephantitis of the lower extremities. Hydrocele and scrotal elephantitis also may occur.