Unit 2 - Blood Borne Parasites Flashcards
what are the 5 blood borne parasites and where they are?
- Malaria - Africa
- Babesia - CNY
- Trypanosomes - Mexico, now in southern CA and AZ
- Leishmania - soldiers returning overseas
- Filarial infections - South America, Africa, and South Asia
who is the intermediate host in most parasitic agents? where does sexual reproduction occur?
man is the intermediate host, with sexual reproduction occurring in vector associated with transmission of the agent
what is the primary factor contributing to the resurgence of malaria?
appearance of drug-resistant strains of the parasite
why is Africa the most affected country by malaria?
- very efficient mosquito (Anopheles gambiae complex) is responsible for high transmission
- predominant parasite is P. falciparum (most likely to cause severe malaria and death)
- local weather conditions allow transmission to occur year-round
- scarce resources and socio-economic instability have hindered efficient malaria control activities
what are factors of more intense transmission?
places where the mosquito lifespan is longer and prefers to bite humans over animals
what are links between genetics and immunological protection?
- absence of Duffy Ag in RBC predominates in West Africans and derived populations, preventing P. vivax malaria
- patients with hereditary elliptocytosis (glycophorin C deficiency = Leach phenotype) and sickle cell carriers are less susceptible to infection
- certain thalassemias or G6PD deficiency offer protection
- untreated infective patients eventually develop curative immunity against parasitizing strain
why does hemolytic anemia occur in malaria?
- rupture of parasitized erythrocytes
- removal of parasitized and unparasitized RBC by spleen
- capillary sequestration
- bone marrow dyserythropoiesis
what is the time from initial malaria infection until symptoms appear (incubation period) for the different species?
falciparum - 9-14 days
vivax/ovale - 12-18 days
malariae - 18-40 days
knowlesi - 11-12 days
but some can be within 7 days to as long as 8-10 months
describe the malaria paroxysm
prodromal symptoms followed by febrile attacks
- cyclic periodicities of 48 hours (vivax/ovale/falciparum) or 72 hours (malariae)
- cold stage: feeling of intense cold with vigorous shivering due to RBC bursting (15-50 minutes)
- hot stage: intense heat and headache due to cytokine response/inflammatory response (2-6 hours)
- sweating stage: exhaustion and weakness cause sleepiness, and upon waking are asymptomatic until next parocysm
explain malaria recrudescence
parasitemia falls below detectable levels and then later increases to a detectable parasitemia
explain malaria relapse
sporozoites invade hepatocytes, in which they develop into schizonts and may not be observed in the circulation and the individual may be asymptomatic
- after a period of time, the hepatocyte ruptures
- each infected hepatocyte liberates 10-30K merozoites that invade circulating RBC
- growth and development of parasites in RBC result in subsequent waves of merozoite invasion
what are most deaths directly attributable to malaria caused by?
severe manifestations of P. falciparum
-cerebral malaria, severe anemia, respiratory failure, renal failure, and severe malaria of pregnancy
what is an important feature of P. falciparum pathogenesis? the most common metabolic complications?
ability to sequester in deep venous microvasculature
- metabolic (lactic) acidosis (due to reduced O2 delivery; primary cause of death)
- pulmonary edema and respiratory distress
- hypoglycemia (cause coma and convulsion, with significant morbidity)
- anemia (excess removal of RBC)
what is the important difference between P. falciparum and other human malarias?
the way P. falciparum modifies surface of RBCs so that asexual parasites and gametoccytes can adhere to the endothelium and asexual parasites can adhere to placenta
- due to PfEMP-1 (P. falciparum erythrocyte membrane protein)
- CD36 is the major receptor for PfEMP-1
describe cerebral malaria?
most severe neurological complication of infection with P. falciparum
- intense sequestration of parasites (infected erythrocytes) in cerebral microvasculature, often accompanied by hemorrhages, perivascular leukocyte infiltrates, and immunohistochemical evidence for endothelial cell damage, causing breakdown of BBB and apoptosis of endothelial cells –> damage and death
- sequestration of parasites stimulates local production of inflammatory cytokines and mediators causing varying degrees of functional obstruction that leads to reduced local delivery of O2 and glucose
explain malaria of pregnancy
maternal morbidity and mortality, intrauterine growth retardation, premature delivery, low birth weight, increased newborn mortality
-mature parasites accumulate in monocytes in placenta due to interaction with syncytiotrophoblastic chondroitin sulfate A(CSA), hyaluronic acid, and Igs
what are the only 2 receptors that provide stable stationary adherence of parasitized RBC to PfEMP-1
- CD36 - major sequestration receptor on microvascular endothelial cells
- condroitin sulphate A (CSA) - receptor on placental intervillous space
rapid diagnostic test for malaria?
only US brand is Binax
- detects 1 Ag specific for P. falciparum, and another found in all 4 human species
- however, cannot tell if double infection
why do P. vivax and ovale have low mortality rates?
strongly favor reticulocytes (as opposed to all RBC like falciparum, or older RBC like malariae)
- don’t exhibit sequestration
- parasitemia <1%
infections with P. vivax and ovale are considered similar to each other clinically
describe P. malariae?
most difficult to diagnose b/c doesn’t have the same intensity as the others
- infects older RBC so parasitemia is low (<2%)
- longest incubation (40 days), but parasites may be found several days (up to a week) before symptoms
- patients present with proteinuria or nephrotic syndrome
- ring forms look like a large signet ring, and infected RBCs are normal or smaller
- merozoites form daisy head arrangement
what is important to know about P. knowlesi?
primate malaria parasite in SE Asia
- emerging infection reported in humans in 1965
- accounts for 70% of malaria cases in SE Asia where it’s mostly found
- replicates and completes blood stage in 24 hour cycles, so high loads of parasite in short periods of time
- similar to P. malariae and unlikely to be diagnosed correctly other than using molecular detection assays
clinical disease of babesia in NE US VS MW and W US
NE: similar picture of P. vivax
MW/W: fulminate, febrile, hemolytic disease
both caused predominantly by Babesia microti (although additional species in MW)
- only ixodid ticks identified as vectors
- severity of infections varies (maybe mild or asymptomatic, or severe)
what are the disease manifestations of human babesiosis caused by?
asexual reproductive stage of organsim in erythrocyte of host and subsequent lysis of host cells
–very broad clinical spectrum probably directly reflective of level of parasitemia in blood
describe anaplasmosis?
first symptoms of anaplasmosis typically start within 1-2 weeks after bite of infected tick
- fever, headache, muscle pain, malaise, chills, nausea/abdominal pain, cough, confusion
- can be fatal if not treated correctly, even in previously healthy people
- -difficulty breathing, hemorrhage, renal failure, neurological problems
what are the causative agents of African sleeping sickness?
2 out of 60 species are pathogenic to men
-Trypanosoma cruzi - American/Chagas disease (kissing Reduvid bugs)
Trypanosoma brucei gambiense and rhodensiense - African sleeping sickness (African trypanosomiasis)
*Trypanosoma brucei brucei causes disease in animals, but not humans
what are the two forms of Chagas disease?
- acute - death within a few weeks
2. chronic - symtpoms may not present until 5-15 years later
