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ABBEY MSII Unit 2 > Micro U2 L1 pt 2. > Flashcards

Micro U2 L1 pt 2. Flashcards

1
Q

How does transmission of most parasitic infections spread?

A

mosquitos, ticks, specific flies, other arthropods

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2
Q

What is human to most parasitic infections?

A

intermediate host. sexual reproduction occurs in vector associated with transmission of agent

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3
Q

Plasmodium

A

protozoan parasite - malaria

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4
Q

Which area of the world is most affected by malaria and why?

A

africa - very efficient mosquito (anophele gambiae complex); predominant parasite species is plasmodium falciparum; warm weather = year round

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5
Q

What transmits malaria?

A

anopheles mosquitos - usually by female mosquitos

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6
Q

What are the four parasite species that cause malaria in humans?

A

plamodium falciparum, vivax, malariae, ovale

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7
Q

Plasmodium falciparum

A

most fatal outcomes - sub saharan africa, SE asia, S america

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8
Q

Plasmodium vivax

A

most common, seen in US - NOT seen in sub saharan africa

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9
Q

Plasmodium malariae

A

all malarious areas, but spotty

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10
Q

Plasmodium ovale

A

tropical areas - africa; SE asia, S america

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11
Q

What are the clinical symptoms of malaria due to?

A

schizont rupture and destruction of erythrocytes

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12
Q

What are the prodromal symptoms of malaria?

A

fever, chills, headaches, diaphoresis

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13
Q

What are malarial paroxysms?

A

febrile attacks following the prodromal symptoms - exhibit periodicities (24 hrs for vivax, ovale, falciparum and 72 hr for malariae)

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14
Q

What are natural protections against malaria?

A
  1. hg C, S (sickle cell) 2. Duffy antigen - lack this = low incidence 3. thalassemia
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15
Q

What are the stages of the malaria paroxysm?

A
  1. cold stage (lysis of RBC) - intense cold feeling, shivering, 15-20 min 2. hot stage - due to circulating and innate immune response - intense heat, dry burning skin, throbbing headache, 2-6 hr 3. sweating stage due to infection of additional erythrocytes and immune system shutting off - profuse sweating, declining temp, exhausted and weak, 2-4 hr
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16
Q

What are the major complications of severe malaria?

A

cerebral malaria, pulmonary edema, acute renal failure, severe anemia, bleeding

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17
Q

What are the most common metabolic complications of malaria?

A

acidosis and hypoglycemia

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18
Q

PfEMP-1 antigen

A

on 100% of RBCs

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19
Q

What causes stable stationary adherence of the parasitized RBCs?

A

CD36 and chondroitin sulphate A (CSA) - surface of P falciparum trophozoite and schizont infected RBCs is covered with knob-like excrescences made up of the PfEMP-1 antigen

20
Q

How does p falciparum modify the surface of RBCs so that asexual parasites and gametocytes can adhere to the endothelium and asexual parasites can adhere to the placenta?

A

knob-like excresences made up of PfEMP-1 antigen

21
Q

Cerebral malaria

A

most severe neurological complication of infection with plasmodium falciparum - breakdown of BBB due to cytoadherence of infected RBCs and vascular sequestration of infected erythrocytes

22
Q

Placental malaria

A

accumulation of parasitized erythrocytes and monocytes in the placenta, direct adverse birth outcomes

23
Q

Malaria relapse

A

reactivation of infection via hypozoites released from the liver (with vivid and ovale only) - second drug should be given with these types to help prevent relapses

24
Q

Malaria recrudescence

A

parasitemia falls below detectable levels and later increases to detectible level = re-attack of malaria due to surviving malaria parasites in RBCs. Due to: 1. incomplete or inadequate treatment 2. antigenic variation 3. multiple infections

25
Q

Malaria Treatment

A

chloroquine (RBC stage) and paraquinine (liver stage for ovale and vivax)

26
Q

American Trypanosomiasis

A

Chagas disease - chronic, systemic parasitic infection by trypanosoma cruzi - NOT intracellular

27
Q

Who does Chagas disease affect?

A

Latin america

28
Q

What do people with chagas disease develop later on?

A

cardiomyopathy, digestive megasyndromes (esophagus and colon esp), or both

29
Q

What transmits Cagas disease to humans?

A

large, bloodsucking reduviid bugs (tick like) - also by blood transfusion and mother to infant

30
Q

What is the method of transmission from reduviid bug to human?

A

bug takes blood meal and releases trypomastigotes in feces near bite wound - enters through wound or intact mucosal membranes (conjunctiva)

31
Q

What is the classic sign for Chagas infection?

A

Romana’s sign - swelling of the eyelids near the bite or where the feces was rubbed into eye

32
Q

What are the clinical manifestations of Chagas disease?

A

initial infection - acute infection 4-8 weeks, chronic for life

33
Q

Acute phase of Chagas disease

A

asymptomatic - might have self-limiting febrile illness - resolve spontaneously in about 90% of infected individuals

34
Q

Chronic chagas disease

A

cardiac, diestive, cardidigestive disease usually 10-30 years after initial infection

35
Q

Chagas heart disease

A

low intensity, slowly progressive that leads to impairment of contractile function and dilatation of all four chambers. most frequent and serious manifestation of chagas

36
Q

What are the causes of death in chagas heart disease?

A

sudden death, refractory heart failure, thromboembolism

37
Q

Gastrointestinal dysfunction

A

mainly megaesophagous, megacolon, or both. megacolon = end segments causing abdominal distention, large bowl obstruction, prolonged obstipation. megaesophagus = dysphagia with odynophagia, epigastric pain, regurgitation , ptyalism (excessive saliva), malnutrition (severe)

38
Q

Diagnosis of chagas

A

acute: microscopic detection of trypomastigotes in blood. chronic: presence of IgG antibodies against T cruz antigens

39
Q

Toxoplasmosis

A

T gondii - coccidian parasite- humans intermediate host so uncommonly cause disease in humans

40
Q

When does toxoplasmosis cause disease?

A

usually fetuses and immunologically impaired individuals - typically by food borne transmission (undercooked meat) or CATS MEOW (litter box)

41
Q

Congenital Toxoplasmosis

A

Classic triad: chorioretinitis, hydrocephalus, intracranial calcifications. Transmission risk greatest during 3rd trimester, but earlier the infection = more severe symptoms

42
Q

Pathogenesis of toxoplasmosis in healthy people

A

often no symptoms - if there are = flu-like - also most common cause of posterior uveitis - parasite remains in body in inactive state

43
Q

Toxoplasma ocular infection

A

results from congenital infection or infection after birth. symptoms: eye pain, photophobia, tearing of the eyes, blurred vision

44
Q

How does reactivation of ocular infection appear on exam?

A

white fluffy cottony lesions

45
Q

What is the diagnostic method to determine infection with toxoplasma?

A

toxoplasma specific antibodies

46
Q

Lesihmania

A

found in desert - affect military - usually cause skin lesions and liver shit

ABBEY MSII Unit 2 (19 decks)

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