Malaria & Babesia Flashcards
apicomplexa
type of protozoan
Plasmodium
has micronemes that make proteins that manipulate RBCs = infection
four species of Plasmodium that cause malaria in humans
P. vivax
P. ovale
P. falciparum (most severe; most deaths)
P. malariae
P. knowlesi
emerging pathogen
aka Monkey Malaria (from long-tailed Maques)
clinically similar to P. malariae
overtaking in Malaysia and Philippines
T or F. The anopheles mosquito is a mechanical vector of Plasmodium
F! biological vector bc part of its life cycle takes place inside mosquito (not all external; mechanical)
incubation of malaria
10-15 days
general symptoms of malaria
headache
nausea
chills
diarrhea
fever (41C)
- due to rupture of RBCs as parasites released
- fragments of RBCs = antigenic components that act as inflammatory response
anemia
splenomegaly
- risk of splenic rupture esp. in ovale and vivax
gold standard for diagnosing malaria
microscopy
but need good equipment and experienced person
rapid diagnostic tests for malaria
- some detect only one species, other several species
- practical; don’t need experienced personnel
- detect antigen so not reliant on good immune functioning
- only need small amt blood
- all detect one or more of: HRP2/histidine-rich protein 2 (only P. falciparum), subtypes of pLDH (plasmodium lactate dehydrogenase) and aldolase (ALL species)
most widespread species of plasmodium
P. vivax and P. falciparum (over 95% mortality)
hypnozoites
P. vivax and P. ovale can remain latent in liver
treatment must eradicate these and treatment is different
this malaria can sometimes be known as benign
P. malariae
can remain infected for up to 40 yrs
same with P. knowlesi
the most deadly form of malaria
P. falciparum
- infects all ages of RBCs
- high % of infected RBC in blood (parasitemia)
complications that arise in P. falciparum malaria
cerebral malaria
blackwater fever
severe anemia
cerebral malaria
- P. falciparum- cerebral anoxia
- increased glucose breakdown
- increased lactate production
= sticky RBC clumps = block vessels
SEQUESTRATION - hard to treat
- altered states of consciousness, confusion, hallucinations, seizures, motor abnormalities, coma
blackwater fever
- P. falciparum
- hemoglobinuria secondary to massive hemolysis (idiopathic?? may be due to hypersensitivity to drugs)
- hepatic, renal, pulmonary complications also seen with severe infection
purpose of gametocyte form?
parasite can communicate with other parasites to let them know they need to differentiate!! want to stay alive
- extracellular vesicles = exosomes formed by endocytosis of segments of plasma membrane
- exosomes secreted by P. falciparum infected RBC act as intracell communication mediators = ring forms release exosomes containing plasmids with genes for antimicrobial resistance or genes for differentiation to gametocytes
what is different about P. falciparum’s pathogenesis?
- ability to sequester in deep vasculature
- sticky, RBCs stiff = rosetting
- blocks blood flow
- accumulation of parasites in organs
what is schizogony?
refers to a replicative process in which the parasite undergoes multiple rounds of nuclear division without cytoplasmic division followed by a budding, or segmentation, to form progeny (merozoites)
define ‘rosetting’
where an infected RBC binds to non-infected RBCs and platelet induced clumping of RBCs
major determinants of pathogenicity of P. falciparum
PfEMP1
- P. falciparum erythrocyte membrane protein 1
- surface of mature RBCs infected with P. falciparum = clonal antigenic variation = bind several different cell receptors
- sequestration for evading spleen-dependent killing
- antigenic variation for evading antibody-dependent killing
PfEMP1
- binds to complement receptor CR1 + blood group antigen A
- binds to CD36 on endothelial cells, monocytes, platelets
- binds to ICAM-1 in brain
- binds to chondroitin sulfate A (CSA) on syncytiotrophoblasts (placenta ,,, different kind of PfEMP1?)
- may bind to downregulate dendritic cell function
lack of glucose and oxygen can lead to this
cerebral malaria
how do we get sick from Plasmodium?
after binding, rosetting and antigen accumulation = increased production of inflammatory cytokines like TNF-alpha = upregulation of ICAM-1 = more sequestration (CYCLE!)
- decreased glucose and O2 = hypoglycemia, also depletion of glycogen and also cerebral malaria
anemia from malaria is due to
lysis of RBC
