Blood and tissue parasites

Question 1

____ has replaced ____ as the main type of malaria in much of Africa?

Answer 1

Plasmodium falciparum; plasmodium vivax

Question 2

Where is the highest resistance of malaria?

Answer 2

Central Africa

Question 3

___ and ___ are the most common malaria; what is the most deadly?

Answer 3

Plasmodium falciparum, plasmodium vivax; falciparum

Question 4

What are ways to protect against malaria?

Answer 4

1. Absence of Duffy antigen in RBC’s (think West African; prevents P vivax as an erythrocyte receptor)
2. H elliptocytosis; glycophorin C deficiency; heterozygous for sickle cell disease (maybe HbS and HbC)
3. Thalassemias or G6PD deficiency

Question 5

Life cycle of malarial parasite

Answer 5

1. Female mosquito regurgitates (sporozoites) into you from salivary glands
2. Parasite goes to liver, infects hepatocytes (develop into merozoites)
3. Hepatocyte rupture and merozoite release into bloodstream, with binding to RBC outer surface
4. Infection of RBC by merozoites and asexual repro cycle and schizonts made from early trophozoites over 48 hrs
5. Schizonts in RBC have daughter merozoites leading to bursting and more RBC’s infected as MEROZOITES are released!!

Question 6

Production of disease by Plasmodium thought to be due to

Answer 6

hemolytic anemia associated with RBC rupture as mech: they can’t move through capillaries and RBC’s stuck in microvasculature

Question 7

What’s a way to distinguish if someone has malaria as opposed to babesia? Early symptoms of malaria?

Answer 7

Travel history!!

Fever, chills, headache, sweats, fatigue, N/V

Question 8

Malarial paroxysm:

Answer 8

1. Cold stage (fever with shaking chills because of RBC rupture; you have circulating schizonts and a cytokine response since body will finally see parasite)
2. Hot stage: inflammatory response (SIRS) and schizonts latch onto RBCs and enter RBC with temp going down
3. Feeling of exhaustion and SWEATING STAGE, and then you become asymptomatic

Question 9

Cyclic pattern of malaria symptoms may

Answer 9

not appear at the beginning of the illness; could come about once malaria actually develop, reproduce, and are released from RBCs; need merozoites from different exoerythrocytic schizonts to synchronize

Question 10

Recrudescence describes; relapse is when

Answer 10

situation when parasitemia falls below detectable levels and then later increases to a detectible parasitemia;
sporozoites invade hepatocytes, when they develop into schizonts and might not be observed in circulation and individual might be asymptomatic until hepatocyte rupture

Question 11

List P falciparum’s pathophysiology:

Answer 11

1. Metabolic (lactic) acidosis: leading cause of death
2. Pulmonary edema and respiratory distress
3. Hypoglycemia
4. Anemia (removal of uninfected erythrocytes)

Question 12

What on P falciparum is central to malaria pathogenesis?

Answer 12

P falciparum erythrocyte membrane protein-1 (PfEMP-1); CD36 in tissues is the major receptor for PfEMP-1

Question 13

What happens in cerebral malaria? (associated with P falciparum)

Answer 13

Adherence of RBC’s along BBB (CD36) such that there is not oxygenation of brain; Infected erythrocytes (with parasites) sequester in cerebral microvasculature and then stimulation of local production of inflamm cytokines and mediators

Question 14

In pregnancy, parasite can stick to _____, leading to what in the fetus?

Answer 14

chondroitin sulfate A (CSA) with infected erythrocytes sequestering in maternal circulation of placenta; lack of oxygenation and potential for stillborn

Question 15

Easy way to rapidly diagnose malaria?

Answer 15

Binax NOW: look for antigen oustide of RBC’s to differentiate if one has falciparum or vivax

Question 16

P vivax and ovale with low mortality due to

Answer 16

1. strongly favoring reticulocytes

2. do not exhibit sequestration

Question 17

P malariae infects ____, and doesn’t have the ______; what would you look for to think P malariae?

Answer 17

older RBC’s; malarial paroxysm necessarily; signet ring, periodicity (72 hours), nephrotic syndrome, travel history

Question 18

P knowlesi is a ____ commonly found in _____; what’s up with its life cycle?

Answer 18

primate malaria parasite; SE Asia; replicates and completes its blood stage cycle in 24 hour cycels resulting in fairly high loads of parasite densities

Question 19

Babesia is transmitted by_____; what does it resemble clinically but how can you differentiate?

Answer 19

large variety of ticks (Ixodes) with B. microti in US;

vivax, with periodicity of 48 hours and shaking chills; ask about travel history

Question 20

Primary host for babesia?

Answer 20

Mouse (humans are accidental); maybe deer

Question 21

Tick for lyme and babesia is

Answer 21

Ixodes scapularis (more East Coast, Northeast); Ixodes pacificus (more West Coast)

Question 22

Unlike lyme and babesia, anaplasmosis will infect

Answer 22

WBC’s (but still uses the same vector; uses squirrels and white-footed mice as hosts)

Question 23

Anaplasmosis can be

Answer 23

fatal/serious illness if not treated correctly, even in previously healthy people (difficulty breathing and hemorrhage of the internal organs)

Question 24

In the US, trypanosoma is; in Africa, it is

Answer 24

caused by T cruzi with transmission by the reduvid bug;

caused by T brucei (two species) with transmission by Tsetse fly

Question 25

For American trypanosomiasis in the US, there are two forms of the disease, namely

Answer 25

acute (death within a few weeks); chronic (symptoms may not present until 5-15 years later)

Question 26

The reduvid bug goes for; what can we see chronically?

Answer 26

the soft tissue around the eye, takes a dump and you scratch and have inoculated yourself with the infected form (Romana’s sign!!);
Megacolon (involves rectum, sigmoid, descending colon), cardiomyopathy (most common, have myocarditis leading to heart issues), megaesophagus (dysphagia, regurgitation, malnutrition)!!!

Question 27

Toxoplasmosis gondii hosts are

Answer 27

felines that can shed oocysts in feces and transmitt parasite by this means to e.g. pregnant women

Question 28

Humans get toxoplasmosis

Answer 28

through consumption of feline fecal material, through food or water with fecal contamination, consumption of undercooked meat with infective cysts, transplantation, or transplacentally from mother to fetus

Question 29

Toxoplasma will often produce

Answer 29

no symptoms because immune system keeps parasite from causing illness; can become reactivated if person becomes immunosuppressed

Question 30

Congenital toxoplasma infection can

Answer 30

be due to transmission of infection across placenta to unborn baby; can lead to miscarriage, stillborn, enlargement/smallness of the head; down the road, there could be learning, visual, and hearing disabilities later in life

Question 31

Toxoplasma in immunosuppressed can

Answer 31

lead to CNS disease in HIV-infected patients

Question 32

Leishmania is spread by; causes

Answer 32

sandfly (infects RBC’s);

cutaneous leishmaniasis, mucocutaneous leishmaniasis, and visceral leishmaniasis

Question 33

Lymphatic filariasis; can lead to

Answer 33

is EC and can cause lymphadenitis;

lymphedema and elephantiasis

Question 34

Malaria transmitted through bites of

Answer 34

Anopheles mosquito (female)

Question 35

Trypanosoma cruzi releases _____ in feces; how else can Chagas be transmitted?

Answer 35

trypomastigotes; vertical transmission and blood transfusion

Question 36

Falciparum and malariae can undergo ___ but not -___

Answer 36

Recrudescence; relapse

Question 37

For acute Chagas, what can be seen in blood; for chronic phase, what can be seen?

Answer 37

1. Trypomastigotes;

2. IgG Ab’s against T cruzi antigens (ELISA, indirect immunofluorescence, indirect haemagglutination)

Question 38

How can you diagnose babesiosis? What can be used to treat if severe?

Answer 38

Examine blood specimens under microscope and see Babesia parasites in RBC’s;
clindamycin and quinine

Question 39

How can one confirm HME/HGA?

Answer 39

Detection of morulae/EB in peripheral blood or CSF leukocytes; detect Ehrlichia/Anaplasma DNA with blood PCR or CSF; direct detection of either by IHC