13 - Vector-borne Apicomplexans Flashcards

1
Q

What are Apicomplexans (sporozoa)?

A

Organisms that infect liver and plasma cells.

All are obligate intracellular parasites with an apical complex for attachment and invasion.

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2
Q

What are two notable diseases caused by apicomplexans?

A

Malaria and Babesiosis.

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3
Q

What is the severity of Malaria in terms of public health? What is the geographical distribution?

A

214 million new cases in 2015; Economic toll is well over 12 billion/year.

3.2 billion humans at risk.

Subsaharan Africa is disproportionately affected (81% of cases)

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4
Q

What are the five types of plasmodium species that infect humans? Which is the most deadly? What type of cells do they infect?

A

P. falciparum (most deadly), P. vivax, P. ovale, P. malariae, P. knowlesi.

Infects erythrocytes and hepatocytes.

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5
Q

How is malaria transmitted?

A

Vector-borne (anopheles mosquito)

Blood transfusions

IV drug use

Congenital (rare)

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6
Q

What is Schizogony? What is pigment?

A

Schizogeny is asexual reproduction that takes place in humans. This is the amplification stage that occurs in P falciparum that’s makes it more severe.

Pigment (aka hemozoin) is produced in the infected RBC and is a source of toxicity when RBCs lyse.

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7
Q

What is the life cycle of malaria?

A
  1. Mosquito injects person with sporozoites.
  2. Sporozoites go to infect liver cells.
  3. Schizogony occurs and makes schizont that infect RBCs (when symptoms occur)
    - some develop into gametocytes such as falciparum and these are banana shaped.
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8
Q

What is a particularly clinical point about P. vivax and P. ovale?

A

They can establish latent infections in the liver as hypnozoites.

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9
Q

What is the geographical distribution of P. falciparum, P. vivax, and P. Knowlesi?

A

P. falciparum: 80-90% cases in Africa

P. vivax: 70-90% cases in Asia and S. America. Uncommon in Africa.

P. Knowlesi: Malaysia and SDE asia

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10
Q

What is the incubation period of P. falciparum, P. vivax, and P. Knowlesi, P. ovale, and P. malariae?

A
P. falciparum: shortest, 7-10 days
P. vivax: 10-17 days 
P. ovale: similar to vivax
P. malariae: longest, 18-40 days  
P. Knowlesi: 12 days
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11
Q

What two species of plasmodium are associated with drug resistance? Why does this make sense?

A

P. falciparum and P. vivax

This makes sense because they are the most common and thus are treated the most often and susceptible to drug resistance.

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12
Q

What is the time period between paroxysms (fever and chills) for each species of plasmodium?

A

Falciparum: initially quotidian (daily), then tertian (every other)

Vivax: Tertian

Ovale: tertian

Malariae: quartan (every 72 hours)

Knowlesi: Quotidian

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13
Q

Which species are malignant (very infectious)? Which are benign? Which have liver persistance that leads to relapse?

A

Falciparum and knowlesi are malignant (most virulent)

Vivax and ovale are both benign and can lead to liver persistence.

Malariae is benign.

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14
Q

Which is the most common cause of severe malaria? Which is observed in compromised patients? What accounts for about 6-10% of malaria cases?

A

Severe: falciparum

Observed in compromised pts: vivax

6-10%: knowlesi

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15
Q

The species of plasmodium and _____ dictate the outcome of the disease?

A

The immune status of the patient - ie pregnancy, elderly, immunocompromised.

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16
Q

What are physical findings and common presenting symptoms seen in uncomplicated malaria?

A

Physical: fever, splenomegaly early on, jaundice from hemolysis, anemia from RBC destruction.

Fever, chills, sweats, nausea, vomiting, body aches and general malaise.

17
Q

Nearly all deaths from severe malaria are caused by ______? What are some characteristics of severe malaria? What are the three most common symptoms?

A

P. falciparum.

Vital organ dysfunction, abnormal clotting, metabolic complications such as acidosis and hypoglycemia.

Cerebral malaria, acute respiratory distress syndrome, and severe anemia.

18
Q

What is cerebral malaria (CM)? Who are particularly at risk? What is the cause?

A

Unarousable coma attributed to Malaria infection only.
-Only 1% of P. falciparum infections with 20% mortality.

Children older than 2 who’s maternal Abs are waning.

Infected RBCs adhere to the vascular endothelium plugging up blood vessels in the brain.

19
Q

What causes acute respiratory distress syndrome (ARDS) seen in malaria pts?

A

When pulmonary capillaries and venules are packed with parasitized red cells and inflammatory cells.

Pro-inflammatory processes increase vascular permeability, leading to severe edema.

20
Q

What are some causes of severe anemia seen in pts with malaria?

A

Microbe-mediated hemolysis of parasitized RBCs.

Antibody-mediated destruction of non-parasitized RBC’s coated with parasite proteins (opsinization and/or complement-mediated lysis).

Decrease in erythropoiesis due to toxic products released by RBCs when they die.

21
Q

How is malaria diagnosed?

A

Microscopy with Giema stains.

Thick smears to detect presence of parasites.

Thin spears used for species-level identification and to determine the level of parasitemia (% of RBCs infected).

22
Q

What are distinguishable features of P. falciparum?

A

Multiple rings (immature trophozoite stage) and RBC often seen near the edge of the membrane (accole position).

Crescent shaped gametocytes

23
Q

How does Malaria evade the immune system? Describe the immunity associated with malaria infection?

A

Anatomical seclusion, RBC lack MHC class 1, antigenic variation of surface antigens on infected RBCs. Recrudescence (no symptoms).

Short-lived and incomplete immunity; but may be enough to render host asymptomatic (premunition).

24
Q

How can malaria be prevented? Is there a vaccine?

A

Avoidance: bed nets and insecticides

Drug prophylaxis.

No vaccine currently available.

25
Q

Describe the genetic resistance to malaria?

A

Inheritable anemias provide malaria resistance: sickle-cell, thalassemia, and others.

Duffy blood group negative phenotype lacks the receptor for P. vivax and P. knowlesi.

26
Q

What is Babesiosis?

A

Intracellular sporozoan parasites that morphologically resemble plasmodia.

27
Q

What causes babesiosis? What cells are infect? What are the hosts?

A

Babesia microti

RBCs infected.

Definitive host: loxdes scapularis (deer tick)
Int. host: white-footed mice
Accidental: humans

28
Q

How is babesiosis transmitted? Where is it found geographically? How long is the incubation phase?

A

During the nymph stage of the tick, through blood transfusions (can’t be tested for in blood), and congenitally during pregnancy and delivery.

Wooded areas of New England, NY, NJ, WI, and MN

Incubation: 1-9 weeks

29
Q

How is the life cycle of babesiosis similar to that of falciparum?

A

They both have a trophozoite ring stage.

30
Q

What are symptoms of babesiosa? How is it diagnosed? How can you prevent it?

A

Asymptomatic, flu-like symptoms, anemia, mild jaundice, severe complications and death in immunocompromised.

Blood smears, but false negatives are common due to low parasitemia (low number of RBCs infected)

Prevent with insecticides and repellants.