Parasites 1 Flashcards
1
Q
characteristics of parasitic disease
A
- high prevalence in developing countries, lower SES
- low mortality and morbidity
- limited drug development
- no vaccines
2
Q
reasons why north americans don’t have parasites
A
- higher standards of education
- general good health
- nutrition
- sanitation
- temperate climate
- absence of certain vectors
3
Q
ectoparasite
A
-live on the outside of the host
4
Q
endoparasite
A
-lives in the body of the host
5
Q
direct life cycle
A
- only humans are hose
- infective stage like ovum, cyst, larva passed out of the body that infects another healthy person
- e histolytca, giardia, ascaris, lumbruicoides
6
Q
indirect life cycle
A
- multiple hosts or involvement of vector
- definitive and intermediate host
- taenia solium, malaria
7
Q
vector importance
A
- geographic distribution and occurrence of many parasitic diseases is related to distribution of vectors that are responsible for the transmission of the parasite and the distribution of secondary or intermediate hosts
- mosquitos, sand fly, tick borne
8
Q
parasitic protozoa
A
- unicellular
- ameba
- flagellates
- ciliates
- sporozoa
9
Q
parasitic helminths
A
- nematodes-ascaris, pinworm
- cestodes-taenia solium
- trematodes
10
Q
blood borne parasites
A
- malaria
- babbesia
- trypanosomes
- leishmania
- filarial infections
11
Q
global impact of malaria
A
- 50 million new cases a year
- 1-3 million deaths per year
- increased global tracel
- drug resistance
- plasmodium falciparium replaced vivax as the main type of malaria in much of africa
- control efforts have decayed-india
12
Q
cause of malaria
A
- plasmodium-have different geographic distributions
- falciparum
- most lethal, majority of 1-3 million deaths
- vivax common-cases in US
- transmitted through infected female in genus anopheles
13
Q
malaria endemic countries
A
- 104
- half world at risk
- africa, asia, south america
14
Q
genetic and immunological protection
A
- absence of duffy antigen prevents vivax
- hereditary elliptocytosis, glycophorin C deficiency and heterozygotes for sickle are less susceptible
- thalassemias or G6PD deficiency offer degree of protection
- untreated infectious patients eventually develop curative immunity against the parasitizing strain
15
Q
life cycle of malarial parasite
A
- sporozoites in salivary glands
- oocytes in stomach wall
- male and female gametocytes
- liver phase (human)
- release of merozoites from liver
- enter red blood cells and burst and spread to new red blood cells causing a cycle of symptoms
16
Q
symptoms of malaria
A
- incubation period is 9-14 for falciparum and 12-18 for vivax
- appear in 7 days, can be as lone as 8-10 months
- fever chills, headache, sweats, fatigue, nausea, vomiting
17
Q
malaria paroxysm
A
- 4-8 hours begins with sudden onset of chills and intense cold despite temp
- then hot stage-heat and headache. fatigue, dizziness, anorexia, myalgia, nausea
- then sweating stage and fever declines then sleep
- then feels fine until next paroxysm
- cold is in RBCs
- hot is burst
- sweating is in new RBCs
- synchronous replication of parasite accounts for this-and can tell which species it is
18
Q
plasmodium falciparum
A
- much more acute and sever than malaria caused by others
- almost all deaths directly from malaria are this
- cerebral malaria, severe anemia, resp failure, renal failure, severe malaria of pregnancy
- sequesters in deep venous microvasculature
- invades young RBCs
- kidneys, liver, brain, GI
- parasitemia low due to adherence of RBCs to capillary walls
19
Q
PfEMP-1
A
- P falciparum erythrocyte membrane protein 1
- binds to CD36
- 60 different variants in parasite
- switches b/n them per generation
- antigenic variation
- causes adhesion to endothelium and vasooclusion
20
Q
cerebral malaria
A
- sequestration of parasites in the cerebral microvasculature (due to CD36 and PfEMP1)
- ring hemorrhages, perivascular leukocyte infiltrates, immunohistochemical evidence of endo activation
- sequestration leads to IF cytokines
21
Q
malaria of pregnancy
A
- placental colonization by infected RBCs results in maternal morbidity and mortality, IUGR, premies, LBW, increased newborn mortality
- selective accumulation of mature parasites in placenta due to CSA, hyaluronic acid and Ig
22
Q
vaccine
A
- only 30% effecting
- targets outer membrane protein of early blood phase
- doesnt work as they get older
23
Q
babesia
A
- world wide
- multiple species
- transmitted by ticks
- B microti in US
- infections in NE similar to p viva
- midwest and west have fulminate febrile hemolytic disease
24
Q
life cycle of babesia
A
- complicated
- involves mouse intermediate
- sporozoites infect us
- goes through trophozoite and metozoite
25
Q
distribution of lyme and babesia
A
-almost the same because they are tick borne
26
Q
babesia infection
A
- more than 100 species infect vertebrates
- obligate erythrocyte parasite-modification and rupture
- asynchronous-lack of periodicity
- erythropoiesis increased- anemia and low level parasitemia explained by clearing not sick RBCs
- hemolytic anemia and non-specific flu like symptoms
- splenomegaly, hepatomegaly, jaundice
27
Q
anaplasma phagocytophilum
A
- NE
- tick vector
- have more than anaplasmosis
- white footed mouse and squirrels
28
Q
anaplasmosis
A
- first symptoms in 1-2 weeks- fever, headache, muscle pain, malaise, cough, confusion
- fatal if not treated correctly
- difficulty breathing, hemorrhage, renal failure, neurological problems
29
Q
chagas disease
A
- american trypanosomiasis
- trypanosoma cruzi
- insect vectors
- only in americas and australia (another species elsewhere- T brucei and tsetse fly)
- transmitted by triatomine insects
30
Q
trypanosome infections
A
- american trypanosomiasis is most frequent in US
- southern to middle texas region
- southern cal
- differences observed in contact of bug-needs and hour
- acute-death within a few weeks
- chronic-symptoms may not present for 5-15 years
31
Q
typanosome life cycle
A
- can infect esophagus, heart, colon
- bites under eye swell because poop releases irritant-romana sign–other places called chagoma
- trypmastigotes infect us
32
Q
leishmaniasis
A
- sandflies
- obligate intracellular
- multiplication in histiocytes-diagnose here
- focal disease
- can survive for decades in asymptomatic people-important for transmission of visceral disease
- neutrophils
33
Q
cutaneous lesihmaniasis
A
- chronic skin ulcers
- may or may not be where bite was
34
Q
mucocutaneous lesihmaniasis
A
-metastatic spread of primary lesions to the mouth, nose, pharynx, destruction of the mucosa and secondary bacterial infection
35
Q
visceral lisihmaniasis
A
-fever weight loss
anorexia
spleno/hepatomegaly
