Parasite Infections of the Blood Flashcards

1
Q

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

A

p falciparum (both questions)

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2
Q

what genetic predispositions are protective against malaria?

A

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

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3
Q

what hemoglobin variants are protective against malaria?

A

thalassemia, hemoglobin S and HbC

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4
Q

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

A

because it is the erythrocyte receptor for p vivax

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5
Q

what is the pathogenicity of malarial infections?

A

produces anemia by hemolysis and impaired microcirculation

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6
Q

what is the range of malarial incubation?

A

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

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7
Q

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

A

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

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8
Q

what are the causes of the malaria paroxysm stages?

A

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

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9
Q

when does the malaria cyclic pattern not occur?

A

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

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10
Q

what is malaria recrudescence?

A

parasitemia is undetectable for a period of time and later recurs

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11
Q

why do relapses of malaria occur?

A

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

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12
Q

what are the severe manifestations of p falciparum?

A

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

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13
Q

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

A

ability to sequester in the deep venous microvasculature

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14
Q

what are the metabolic manifestations of p falciparum infection?

A

lactic acidosis from impaired O2 delivery and hypoglycemia

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15
Q

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

A

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

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16
Q

what is the significance of PfEMP-1?

A

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

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17
Q

what is the classic finding in cerebral malaria?

A

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

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18
Q

what is the harm of placental malaria?

A

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

19
Q

why do mature parasites accumulate in the placenta?

A

they interact with syncytiotrophoblastic antigens, hyaluronic acid and immunoglobulins

20
Q

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

A

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

21
Q

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

A

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

22
Q

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

A

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

23
Q

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

A

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

24
Q

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

A

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

25
Q

what transmits babesia? what does the presentation resemble?

A

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
Q

what does the distribution of babesia resemble?

A

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

27
Q

what is a major reservoir for anaplasmosis?

A

white footed mouse and squirrels

28
Q

what are the first symptoms of anaplasmosis?

A

constitutional symptoms, nausea, cough and confusion

29
Q

what are some serious clinical presentations of anaplasmosis?

A

difficulty breathing, hemorrhage, renal failure or neurological problems

30
Q

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

A

chagas’ disease

trypanosoma cruzi causes it in america

31
Q

what are the two vectors for trypanosomiasis?

A

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

32
Q

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

A

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

33
Q

how does american trypanosomiasis infect humans?

A

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
Q

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

A

toxoplasmosis

the usual host are cats

35
Q

how is toxoplasmosis transmitted from cats to humans?

A

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

36
Q

what nonfeline modes may transmit toxoplasmosis?

A

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

37
Q

what is the progression of toxoplasma infection in healthy people?

A

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

38
Q

how is congenital toxoplasmosis acquired? what determines severity?

A

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
Q

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

A

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

40
Q

what is the manifestation of toxoplasmosis with immunosuppression?

A

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

41
Q

what transmits leishmania?

A

certain species of blood feeding sand flies

42
Q

what are the clinical manifestations of leishmaniasis?

A

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

43
Q

what are the clinical features of lymphatic filariasis?

A

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