Parasites Flashcards
pathophysiology of malaria
from anophiline mosquito. sporozoites enter and go to liver. they invate hepatocytes and either become dormant (P ovale and P vivax only) or mature to schizonts. schizonts give off merozoites which enter RBCs and reproduce asexually. merozoites mature into trophozoites or gametocytes. Gametocytes make be picked up by mosquito for sexual reproduction that leads to eggs and infective sporozoites. trophozoites can form more schizonts
P. falciparum
no dormant liver stage. all sporozoites later become schizonts which make thousands of merozoites. can infect RBCs at all stages of RBC development and multiple merozoites can infect a single RBC. P. falciparum forms RBC membrane knobs that adhere to vascular endothelium. this can block blood flow in small vessels and cause hypoxia in kidneys and brain.
P vivax and P ovale
cause fevers every 2 days.
P vivax need duffy antigen on RBCs to attach and enter. Many ppl in sub-saharan africa lack duffy antigen.
P vivax and P ovale can form hypnozoites that remain dormant in the liver. They can both only infect young RBCs- this decreases parasitic load compared with P falciparum
P malariae.
classically, see a fever ever 3 days.
no dormant phase but can cause low grade, chronic fever for up to 30 yrs! only infects older RBCs- low levels of parasitemia
Clinical presentation of malaria
vraiable incubation (often 9-40 days). hallmark is fever. P falciparum can also cause kidney, liver, lung, and brain damage. liver damage: high levels of parasitemia -> profound hemoptysis -> enough hemoglobin to overwhelm the liver -> jaundice and black pee. Cerebral malaria can lead to confusion, then quickly to seizures, coma, and death
Blood tests in malaria
inc. LDH, bilirubin, thrombocytopenia, serum creatinine, hypoglycemia
diagnosis of malaria
giemsa stain- examine every day for 3-4 days to r/o infection. Necessary for quantification of parasitemia levels. or ELISA.
treatment on non-falciparum or susceptible falciparum malaria (rare)
Chloroquine. this accumulates in the parasitic food vacule and complexes with heme. only treats the blood stage. resistance in variants that don’t transport drug to the food vaccule.
For the liver stage, treat with primiquine. but be careful, because primiquine can cause SEVERE hemolytic anemia in people who are G6PD deficient
treatment of resistant falciparum
artemisinin combo therapies, like CoArtem. produces lethal free radicals in parasites
Malarone
used for uncomplicated falciparum infection if pt didn’t used malarone as prophylaxis.
2 parts:
1. atovaquone: inhibits parasitic mitochondrial electron transport (also used for toxoplasmosis, babesiosis, pneumocystis pneumonia)
2. proquanil: ihibits dehydrofolate reductase. metabolized by Cyp450- lots of drug interactions. This combo attacks both liver and blood stages
quinine
decreases O2 uptake and carb metabolism. intercalates into DNA. can cause QT prolongation, torsades de pointes, CNS infection, rash, GI symptoms. drug interactions (CYP 450). safe in pregnancy. use with doxy, clindamycin, or fansidor (?)
nefloquine
treatment and prevention of malaria. use in combo with doxycycline or femisinin (?)
has some CNS side effects.
OK as pregnancy prophylaxis
resistance along Thai/Cambodian border
What is complicated falciparum infection
paresitemia more than 5% and/or major organ dysfunction. this is an emergency. treat with quinine and artemisins (like CoArtem). treat IV. If from SE asia also give doxycycline or clindamycin. artemisinins can be given rectally to kids to reduce mortality
Babesiosis: pathophysiology
bitten by deer tick. sporozoites in blood. attack RBCs. mature into trophozoites. undergo asexual binary fission. become tetrads in RBCs. these are merozoites that can rupture RBCs. causes fever and chills
Clinical babesiosis
fever and chills. no massive hemoptysis because bursting of RBCs is asynchronous. no liver stage.
should suspect for flu-like symptoms in summer in NE US. if normal host should be mild and self-limiting.
