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Flashcards in Blood and tissue parasites Deck (39):

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

Plasmodium falciparum; plasmodium vivax


Where is the highest resistance of malaria?

Central Africa


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

Plasmodium falciparum, plasmodium vivax; falciparum


What are ways to protect against malaria?

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


Life cycle of malarial parasite

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!!


Production of disease by Plasmodium thought to be due to

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


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

Travel history!!
Fever, chills, headache, sweats, fatigue, N/V


Malarial paroxysm:

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


Cyclic pattern of malaria symptoms may

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


Recrudescence describes; relapse is when

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


List P falciparum's pathophysiology:

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


What on P falciparum is central to malaria pathogenesis?

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


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

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


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

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


Easy way to rapidly diagnose malaria?

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


P vivax and ovale with low mortality due to

1. strongly favoring reticulocytes
2. do not exhibit sequestration


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

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


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

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


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

large variety of ticks (Ixodes) with B. microti in US;
vivax, with periodicity of 48 hours and shaking chills; ask about travel history


Primary host for babesia?

Mouse (humans are accidental); maybe deer


Tick for lyme and babesia is

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


Unlike lyme and babesia, anaplasmosis will infect

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


Anaplasmosis can be

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


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

caused by T cruzi with transmission by the reduvid bug;
caused by T brucei (two species) with transmission by Tsetse fly


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

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


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

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)!!!


Toxoplasmosis gondii hosts are

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


Humans get toxoplasmosis

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


Toxoplasma will often produce

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


Congenital toxoplasma infection can

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


Toxoplasma in immunosuppressed can

lead to CNS disease in HIV-infected patients


Leishmania is spread by; causes

sandfly (infects RBC's);
cutaneous leishmaniasis, mucocutaneous leishmaniasis, and visceral leishmaniasis


Lymphatic filariasis; can lead to

is EC and can cause lymphadenitis;
lymphedema and elephantiasis


Malaria transmitted through bites of

Anopheles mosquito (female)


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

trypomastigotes; vertical transmission and blood transfusion


Falciparum and malariae can undergo ___ but not -___

Recrudescence; relapse


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

1. Trypomastigotes;
2. IgG Ab's against T cruzi antigens (ELISA, indirect immunofluorescence, indirect haemagglutination)


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

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


How can one confirm HME/HGA?

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