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MSII: Microbio Unit 2 > Parasite Blood Infections (10) > Flashcards

Parasite Blood Infections (10) Flashcards

1
Q

Why is Africa most effected by malaria?

A
  • A mosquito that s a very effective vector
  • P. falciparum is the predominant species
  • Local weather conditions
  • Scarce resources/ socioeconomic factors
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2
Q

Vector for malaria?

A

Anophels mosquito

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3
Q

What are the plasmodium species that cause malaria in humans?

A

P. falciparum
P, vivax
P. malariae
P. ovale

P. knowlesi (but predominantly in monkeys)

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4
Q

Most deadly plasmodium species?

A

P. falciparum

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5
Q

Name the genetic/ immunologic factors that offer protection against malaria?

A

1- Duffy Antigen Negative

2- HE

3- Sickle Cell Trait

4- Thalassemias

5- G6PD deficiency

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6
Q

T/F: The lifecycle of plasmodium requires specialozed protein expression in the verebrate host only

A

False…specialized protein expression is required in both the vertebrate and invertebrate host

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7
Q

What are the 2 reproductive phases of plasmodium in human hosts?

A

Pre-erythrocytic/ tissue

Erythrocytic

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8
Q

After the bite of an infected mosquito, what happens in humans to establish a malarial infection?

A

Within 1 hour the sporozotes enter hepaocytes and begin to divide into exoerythrocytic merozoites.

When merozoites leave the lover they infect erythrocytes and develop into trophozoites

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9
Q

What are parasites called when they start to divide in the RBCs?

A

Schizonts (and they consist of many daughter merozoites)

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10
Q

The pathology of malaria are mostly due to….

A

hemolytic anemia and impaired microcirculation

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11
Q

What causes the anemia in malaria?

A

Rupture of parasitized eythrocytes

Removal of parasitized and unparasitized RBCs by the spleen

Capillary sequestration

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12
Q

Incubation period of the following..

P. falciparumP. falciparum
P, vivax
P. malariae
P. ovale
P. knowlesi
A

P. falciparum–> 9-14 days

P, vivax–> 12-18 days

P. malariae–can be months

P. ovale–> 12-18 days

P. knowlesi–> 11-12 days

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13
Q

Prodrome of malaria?

A

Fever, HA, diaphoresis, N/V

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14
Q

Length of malarial paroxysm of vivax, ovale, and falciparum?

A

48 Hours

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15
Q

Length of malarial paroxysm of malariae?

A

72 hours

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16
Q

How long does it take to establish malarial paroxysm?

A

About 1 week

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17
Q

What are the 3 stages of malarial paroxysm?

A

Cold stage: RBC rupture

Host stage: Cytokine response

Sweating stage: Parasite in new RBC

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18
Q

Is relapse seen in all types of malaria?

A

Not in falciparum and malariae

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19
Q

What causes relapse malaria?

A

Reactivation of infection via hyponozoites (which can last for 30 years)–> the sporozoites invade hepatocytes and over time the hepatocytes rupture

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20
Q

Is recrudescence seen in all types of malaria?

A

Yes

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21
Q

What is recruidescence?

A

Parasitemia falls below detectable levels, later to increase to a detectable parasitemia

22
Q

What are the major complications of P. falciparum infection?

A

1-Metabolic acidosis
2- Pulmonary edema/ respiratory distress
3- Hypoglucemia
4- Anemia

23
Q

What causes pulmonary edema in P. falciparum infections?

A

Sequestration of infected RBCs in the lungs leads to inflammaotry cytokines and increased capillary permeabilit

24
Q

What is PfEMP-1?

A

An antigen of P. falciparum that covers infected RBCs.

It is recognized by CD36 and condroitin sulfate A.

25
Q

What does PfEMP-1 do?

A

Mediates sequestration by microvascular endothelial cells and placenta

26
Q

What 2 conditions can PfEMP-1 lead to?

A

Cerebral malaria–> cytoadherarence of infected RBCs and sequestration of infected RBCs in the brain, which leads to the breakdown of the BBB

Placental malaria–> accumulation of infected RBCs and monocytes in the placenta which leads to a imune response and early labor

27
Q

What is specific to P. vivax and P. ovale infections?

A

They prefer reticulocytes and there is no RBC sequestration

28
Q

What is specific to P. malariae infections?

A

Prefer older RBCs and patients present with proteinuria or nephrotic syndrome

29
Q

Vector for Babesia?

A

Ixodid ticks

30
Q

Clinical presentation of babesia?

A

NorthEastern US: similar to P. vivax

Midwest/ Western US: fulminate, febrile, hemolytic disease

31
Q

Describe the life cycle of babesia?

A

Requires a biological stage in a rodent or deer host:

Ticks introduce sporozoites into rodent when taking a blood meal

Sporozoites enter RBC and begin cyclical development between trophozoites and merozoites

Some merozoites produce gametocytes which ticks take up when attache for blood meal

Gametocytes fertilize gut of the tick and develop into sporozoites in the salivary glands

32
Q

What is the distribution of babesia?

A

Same as lyme

33
Q

How is babesia treated?

A

Clindamycin if it doesnt resolve on its own

34
Q

What do erhlicia and anaplasma infect? What transmits them?

A

Tick transmits them and they infect WBCs

35
Q

Symptoms of anaplamsa?

A

Fever, chills, HA, myalgia, Add pain, cough, myalgia

Serious: difficulty breathing, renal failure, neuro problems

36
Q

Symptoms of erhlichia?

A

Neuro manifestations possible, pancytopenia

37
Q

Which parasite causes Chagas disease?

A

Trypanosoma cruzi

38
Q

What transmits chagas disease?

A

Reduviid bug (kissing bud) or tsetse fly

39
Q

What is a typical presenting sign of chagas?

A

Roman’s sign–> swelling of the eyelid near bite or where bug feces was rubbed into eye

40
Q

Clinical features of acute chagas?

A

lasts 4-8 weeks

asymptomatic or self limiting febrile illness

IgM and IgG present

41
Q

Clinical features of chronic chagas?

A

10-30 years after initial infection

involvement of heart (chagas heart disease), esophagus (megaesophagus), colon (megacolon), or a combo

IgG only is present (no IgM)

42
Q

What is chagas heart disease?

A

insidious myocarditis

impairment of contractile function and deletion of the chambes

sudden death posible

43
Q

What causes toxoplasmosis?

A

Toxoplasma gondii

44
Q

How is toxoplasmosis contracted?

A

Foodborne illness–> consumption of infected tissue or fecal matter by naive feline–> they then shed infected ooytes–>people then become infected by eating food/ water contaminated with feline fecal matter

45
Q

Toxoplasmosis symptoms in healthy, nonpregnant people?

A

No symptoms b/c immune response

Flu like symptoms

Parasite can remain in inactive state and be reactivated if immunosuppressed

46
Q

Symptoms of congenital toxoplasmosis?

A

Results from a primary infection of the mother during pregnancy

symptoms depend on the trimester

Can have sequele later in life (developmental issues)

47
Q

Symptoms of toxoplasmosis in the immunosuppressed?

A

Neuro symtoms, fever, N/V, HA

** leading cause of focal CNA diseae in AIDS

48
Q

What speads leishmania?

A

Sand flies

49
Q

What are the 3 manifestations of leishmania?

A

Cutaneous: skin ulcers

Mucocutaneous: destruction of mucosa of mouth, nose, pharynx

Visceral: fever, weightloss, hepatosplenomegaly

50
Q

What causes lymphatic flariasis?

A

Several different agents

51
Q

Clinical features of lymphatic flariasis?

A

Lymphatic destruction

Elephantitis of lower extremities

MSII: Microbio Unit 2 (10 decks)

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