Lecture 6: Parasitology 1 Flashcards
What is a parasite?
a eukaryotic organism that is using another for a variety of purposes
T/F
all parasites are worms
false
not all parasites are worms. some can be amoebas, protozoa, etc.
T/F
Parasitic infections can manifest in many different ways.
true
Why do the complex life cycles of parasites make diagnostics and treatment challenging?
- there are multiple stages for the parasite, which can target multiple locations within the body
- makes diagnostics, drug and vaccine development challenging
T/F
Most parasitic infections are not clinical.
true
infections are generally ____ –> most effective parasites are only ____ _____. that is to say, they will ____ but not ____
- chronic
- moderately virulent
- infect
- kill
parasites have the biological imperative to ____, ____, and ___, so not killing the host is beneficial to their existence.
reproduce, find nutrients, and shelter
If you are not the right host, how will a parasite respond?
it will try to get out of you by any means. Often kills the incidental host
T/F
parasites have maintained their responses to the host body since their inception.
false
parasites have evolved to manipulate host immune responses and host
routes of parasitic infection
- ingestion
- arthropod bite
- transplacental penetration
- direct penetration
- transmammary
organisms that use ingestion to infect host
- Giardia
- E. histolytica
- Cryptosporidium spp.
- cestodes
- nematodes
organisms that use arthropod vectors to infect host
- Malaria
- Babesia
- filaria
- Leishmania spp.
- Trypanosomes
Organisms that use transplacental penetration to infect host
Toxoplasma gondii
organisms that use direct penetration to infect host
- hookworm
- Strongyloides
- Schistosomes
how can parasites harm their hosts?
toxic products
- proteases, phospolipase, lytic enzymes, collagenase, elastase
mechanical tissue damage
- intestinal and organ blockage, pressure atrophy, tissue migration
immunopathology
- hypersensitivity reactions, autoimmunity, metaplastic changes, chronic inflammatory changes
Type 1 Reaction: ??
Mechanism: ??
Organism: ??
- anaphylactic
- Ag + IgE –> histamine
- helminths, trypanosomes
Type 2 Reaction: ??
Mechanism: ??
Organism: ??
- cytotoxic
- Ab + Ag + C’ (ADCC)
- T. cruzi
Type 3 Reaction: ??
Mechanism: ??
Organism: ??
- immune complex
- Ab + Ag complex
- Malaria, schistosomes, trypanosomes
Type 4 Reaction: ??
Mechanism: ??
Organism: ??
- delayed
- T cells
- Leishmania, Schistosomes, trypanosomes
What can a type 1 reaction result in?
anaphylactic shock, bronchospasms, local inflammation
what can a type 2 reaction result in?
Ab + Ag on cell surface –> complement activation or ab-dependent cellular cytotoxicity. results in the lysis of cell-bearing microbial antigens
What can a type 3 reaction result in?
inflammation and tissue damage; complex deposition in glomeruli, joints, skin vessels, brain; glomerulonephritis and vasculitis
what can a type 4 reaction result in?
sensitized T-cell reaction with antigen, liberation of lymphokines, triggered cytotoxicity –> results in inflammation, mononuclear accumulation, macrophage activation, tissue damage
What is released when a parasite is destroy and what can it cause?
proteases and phospholipases are released
can cause cell destruction, inflammatory response, and gross tissue pathology
differentiate between parasitic infection and parasitic disease.
parasitic infection is the presence of a parasite in the host; parasitic disease results when the parasitic infection damages the cells or body, thereby harming the host
T/F
most parastic infections are acute
False
most parasite infections are sub-acute or chronic
What determines the outcome of parasitic disease?
- route of exposure
- inoculum size and infective dose
- tissue tropism
- disruption, evasion, and inactivation of host immune system
- host age and immune status
- disease progression –> in for the long haul (unless immunocompromised)
How does Chagas disease demonstrate that parasitic complications can occur YEARS after initial infection?
- can initially see minor skin lesions at time of infection, but years later, the infected can develop complications from damage to cardiac muscle and nerve damage, leading to heart disease, GI issues, etc.
How do schistosome infections demonstrate that parasitic complications can occur YEARS after initial infection?
initial infections may have minor bleeding in the GI or urinary tract from beginning, but years of it develops into obstructions, cancer, etc.
How do eosinophils aid in parasite infections?
- these are the leukocytes that help neutralize infection with worms
what occurs in response to parasites’ surface proteins?
- eosinophilia
- -> accompanied by increased levels of IgE and is triggered by increased IL-5
eosinophilia helps to identify parasitic infection with ___, but doesn’t help much with ____
- helminths
- protozoa
T/F parasites are only a type 2 response.
false
parasites can be either type 1 or type 2
Th Group: Th1 Cell products: ?? Cell receptor: ?? Cell target: ?? Infectious agent(s): ??
- interferon-gamma, IL-2
- IL-12R
- macrophages, DCs
- intracellular bacteria, fungi, viruses, INTRACELLULAR PARASITES
Th Group: Th17 Cell products: ?? Cell receptor: ?? Cell target: ?? Infectious agent(s): ??
- IL-17A, IL-17F, IL-21, IL-22
- IL-23R
- Neutrophils
- Extracellular bacteria, fungi, EXTRACELLULAR PARASITES (?)
Th Group: Th2 Cell products: ?? Cell receptor: ?? Cell target: ?? Infectious agent(s): ??
- IL-4, IL-13, IL-5
- IL4R
- Eosinophils, basophils
- parasites
Types of interference/avoidance
- antigenic variation
- molecular mimicry
- concealment of antigenic site (masking)
- intracellular location
- immunosuppression
mechanism of antigenic variation
variation of surface antigens within the host
mechanism of molecular mimicry
microbial antigens mimicking host antigens leads to poor Ab response
mechanism of masking (concealment of antigenic site)
acquisition of coating host molecules
mechanism of intracellular location
- failure to display microbial antigen on host cell curface
- inhibition of phagolysosomal fusion
- escape from phagosome into cytoplasm with subsequent replication
mechanism of immunosuppression
- suppression of parasite-specific B- and T-cell responses
- degradation of immunoglobulins
trophozoite
motile, feeding stage, causes pathogenesis
- these are the ones interfering with cell lining in the gut, blocking absorption
- “out and about,” so the immune response can recognize them
cyst
infectious (immediately), non-motile, passed in feces (or in tissue and consumed to cause infection)
- often very resistant to immune system or to chemicals
- stage isn’t really doing anything
oocyst
protozoan version of egg; passed in feces; often takes 1-2 days to sporulate and be infectious
sporulate
when oocysts develop from undifferentiated cellular material to sporozoites
merozoite
stage that undergoes asexual reproduction; feeding stage (seen with malaria and coccidia)
schizont
whole cell full of multiplying merozoites; schzogeny is the process by which asexual reproduction may occur
what are the 3 main geohelminths?
- hookworms
- roundworms
- whipworms
T/F
eggs are immediately infectious
false
At which stage is a parasite infectious
L3 stage
Are eggs environmentally resistant or labile
resistant
examples of nematodes
ascarids, strongylids, filarids
ascarids, strongylids, and filarids are examples of what?
nematodes
examples of cestodes
tapeworms
tapeworms are examples of what
cestodes
flukes are examples of what
trematodes
examples of trematodes
flukes
What is one of the leading causes of death in children under 5 years of age
diarrheal illness
what percent of childhood mortality is attributed to diarrhea?
10%
what are the 3 main protozoa that cause diarrhea?
- Giardia
- Cryptosporidium
- Entamoeba histolytica
T/F
illness in early childhood has no longterm physical and cognitive development effects
false
it does
what is the most common intestinal parasite in humans/
Giardia lamblia
what is the route of contamination for giardiasis?
fecal-oral contamination (cysts in feces)
what is the distribution of giardia?
what is it generally associated with?
- world-wide distribution
- water contamination
what is the prevalence of giardia in developed countries?
- 2% in adults, 6-8% of children
what is the prevelance of giardia in developing countries?
33% prevalence
T/F
Giardiasis is rarely zoonotic
true
what could be a reason for the difference in prevalence between developed and developing countries
water purifying systems
What is more likely to affect whether one has Giardiasis: immune status or infectivity?
immune status
which stage of giardia is responsible for transmission of giardiasis?
cysts
how can you diagnose giardiasis?
fecal examination and detecting cysts or trophozoites
what do giardia trophozoites prevent when the affect the intestinal lining?
absorption of fat, leading to diarrhea of a fatty nature
how long can giardia cysts persist in the environment?
several months in cold water
how may trophozoites are released from a cyst?
2
where does giardia typically infect in the body?
small intestine
how do trophozoites multiply?
longitduinal binary fission
when does encystation occur?
as the parasites transit toward the colon
why is person-to-person transmission of giardia possible?
cysts are infectious when passed in the stool or shortly afterward
when trophozoites attach to the intestinal wall with their sucking disks, what do they cause?
- malabsorption
- inflammation
- hyperplasia
50% of infected indivduals are ____
asymptomatic
symptoms of giardiasis
- fatty diarrhea
- gas
- abdominal cramps
- nausea
- vomiting
dehydration
in children with giardiasis, malnutrtion may result in what?
delayed physical and mental growth
what age group is most likely to be infected with giardia?
ages 1-4
what are the two crypto species most common in humans? Which is zoonotic
- C. hominis
- C. parvum (zoonotic)
distribution of Crytposporidium
world wide
T/F
cryptosporidium has a transplacental route of contamination
false
fecal oral contamination, possibly even respiratory secretions
is the cryptosporidium oocyst environmentally labile or resistant?
resistant
what are large risk factors for c. hominis?
daycare and swimming
how can one acquire C parvum zoonotically?
from neonatal calves
how does cryptosporidiosis occur?
- the protozoa colonizes microvilli on the apical surface of the epithelial cells, predominantly in the small intestine
symptoms of cryptosporidiosis
- watery diarrhea
- dehydration
- cramps
- weight loss
- nausea
- occasionally may see resp. symptoms
when might one consider cryptosporidiosis zoonotic?
in immunocompromised individuals, like those with AIDS
T/F in healthy individuals, crypto is generally self-limiting and symptoms resolve after ~10 days
true
how has water been treated to prevent crypto infection?
with UV treatments
where are most people getting infected with cryptosporidium
recreational water parks
what is the pathogenesis of both giardia and cryptosporidium
- interaction between Crypto/Giardia and the apical surface of the epithelial cells of the GI wall results in a localized activation of signalling cascades, culminating in barrier disruption and polymerization of actin filaments in the region with host-parasite interaction
- several molecules result in cellular damage, enhancing fluid secretion from the crypts and supporting diarrhea due to active secretion and malabsorption, which can lead to cell death
- essentially, they come in, and penetrate or bloc the cell, which gets your immune system involved. The activation of the immune system can disrupt the barrier through cell death, and other forms of disruption
which parasite is responsible for human coccidosis?
cyclospora spp.
cyclospora distribution
worldwide, but most tropical and subtropical
prevalence of cyclospora in
- endemic areas.
- developed countries
- 2-18% in endemic areas
- 0.1-0.5% in developed countries
T/F
cyclospora oocysts are not initially infective, thus fecal-oral transmission cannot occur.
true
when does Cyclospora sporulation occur?
- after days or weeks at 22C-32C
what can serve as the vehicle for cyclospora sporulated oocyst transmission
fresh produce and water
Where do Cyclospora oocysts excyst in the host?
GI tracted, thus freeing sporozoites which invade the epithelial cells of the Small Intestine.
what symptoms are seen with human coccidiosis?
- watery diarrhea
- dehydration
- cramps
- weight loss
- nausea
- occasionally may see resp. symptoms
Cyclospora is ____ in healthy individuals and ____ in immune-compromised individuals
- self-limiting
- chronic
What is the route of infection for Entamoeba histolytica?
fecal-oral contamination
infective stage of Entamoeba histolytica
the cyst
motile feeding stage of entamoeba histolytica
trophozoite
distribution of Entamoeba histolytica
worldwide, but mostly tropical and subtropical areas
what can lead to increased risk of E. histolytica infections
poor sanitation / contaminated water
prevalence of E. histolytica
- globally
- US
- 10-15%
- 1-2%
Is one more likely to get E. histolytica in a crowded or low-density area?
crowded
which stage of E. histolytica are you more likely to find in feces?
cysts
Where does E. histolytica generally stay in the host?
where can it migrate to if it leaves that location?
- the gut
- can go to the bloodstream –> liver –> lungs or brain
T/F
an individual may be an asymptomatic carrier of Entamoeba histolytica
true
Entamoeba histolytica
intestinal amebiasis symptoms
- related to tissue destruction in LI
- -> abdominal pain
- -> cramping
- -> colitis
- -> bloody diarrhea
- -> necrosis in intestine (flask-shaped lesions)
entamoeba histolytica
extraintestinal amebiasis symptoms
- invasion into deeper mucosa & peritoneal cavity (liver, heart, & brain may be affected)
- systemic fever
- rigors
- abcess formation and enlargement of liver from filtering trophozoites, hepatomegaly
Intestinal Protozoa
- Giardia
- Cryptosporidium
- Cyclospora
- Entamoeba histolytica
blood and tissue protozoa
- plasmodium (4 spp.)
- Trypanosoma cruzi
- Trypanosoma brucei spp.
- Leishmania spp.
- Toxoplasma
- Babesia spp.
