Parasites III Flashcards

1
Q

What is the difference between a definitive host and an intermediate host?

A

definitive host- sexual reproduction of the parasite happens here
intermediate host- larval development, but NOT sexual reproduction, occurs here

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2
Q

What determines the parasite burden in helminth infection, in MOST cases?

A

the degree of exposure to the infectious form of the parasite..

Note: eggs/larvae may be produced independent of exposure, but usually they don’t mature into an adult parasite in the human- so a person with multiple adult worms usually has had multiple exposures

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3
Q

What are the three most important general ways to prevent and eliminate helminth infections?

A
  1. provide for sanitary disposal of human waste
  2. insure a clean water supply
  3. cook food properly
    FECAL MATTER is a problem
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4
Q

What are the three kinds of helminths?

A

trematodes, aka flatworms/flukes
cestodes, aka tapeworms
nematodes, aka roundworms

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5
Q

What are the four types of trematodes? What is their intermediate host? Generally, how do each of these types enter the body?

A
blood, liver, intestinal, and lung.
liver, lung, and intestinal acquired from undercooked food.
blood trematodes (schsitosoma) invade the body directly from skin contact with contaminated fresh water.
host: snail
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6
Q

Clonorchis sinensis: helminth type, organ infected, and source of infection

A

trematode
liver
fish

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7
Q

Fasciola hepatica: helminth type, organ infected, source of infection

A

termatode
intestinal
uncooked aquatic vegetation

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8
Q

paragonimus westermani: helminth type, organ infected, source of infection

A

trematode
lung
crab

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9
Q

What is one important functional and morphological feature of trematodes?

A

spikes that help them inch through the body

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10
Q

Eosinophilia

What might cause this? What are some associated risks?

A

hallmark of helminth infection
reflects a hypersensitization to antigens released by larvae and eggs
can result in by-stander damage to cardiac tissue, esp. endocardium

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11
Q

What are the three main species of schistosoma that cause human disease?

A

s. mansoni, S. hematobium, S. japonicum

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12
Q

Where do we see schistosoma eggs excreted from the body, and why (multiple answers possible)?

A

schistosoma mansoi and schistosoma japonicum eggs excreted in the feces because these organisms like to live in the mesenteric venules of the portal venous system, near the large intestine
schistosoma hematobium excreated in the urine because this ogranism likes to live in the pelvic venous plexi.

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13
Q

What is a disease that has been correlated with S. hematobium infection?

A

schistosoma hematobium infection has been correlated with ahigh incidence of bladder cancer, perhaps due to the inflammatory response.

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14
Q

Why is schistosomiasis infection rare in the US?

A

it requires a snail vector, which can’t survive in the “cold” US water temperatures

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15
Q

Describe the schistosomiasis lifecycle? (S. mansoni in particular)

A
  1. Carcariae form of the parasite penetrates the skin directly
  2. it migrates to the liver
  3. Adults mate in the liver
  4. Adults migrate to the mesenterics
  5. Eggs are passed to the small intestine, large intestine, and then are excreted.
  6. Eggs hatch in the water
  7. hatched eggs enter the snail
  8. infectious carcariae exit the snail
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16
Q

How is schistosomiasis diagnosed?

A

presence of eggs in excrement, or in host tissues

17
Q

What is the interaction between schistosomiasis eggs and the immune system?

A

Eggs that get trapped in host tissue die. But, even dead eggs elicit a granulomatous immune response caused by hypersensitivity to egg/larval antigens. Leads to a fibrotic, eosiniphilic granuloma (100X the size of the egg itself!)
As egg burden increases, we do see a graudal desensitization to parasite antigens due to parasiite-induced modulation of cytokines that modulate the immune response.
parasite survival enhanced by reducing damage to the host: there is a dynamic balance between the parasite and the host.

18
Q

What is the infectious form of schistosomiasis?

A

cercaria/ cercarial larvae

19
Q

What is unique about schistosomiasis mansoni reproduction?

A

there are male and female worm forms.

all other schistosomiasis worms (S. japonicum and S. mansoni) are hermaphroditic

20
Q

Describe the three phases of schistosomiasis infection.

A
  1. acute phase: rash, fever, abdominal pain
  2. intermediate: immune complexes form- serum-sickness like disease with splenomegaly, diarrhea, and lympadenopathy
  3. chronic: liver and spleen involvement, abdominal swelling due to ascites fluid accumulation (ascities fluid = in the peritoneal cavity). Damage to body mediated by immune response to egg/larval antigens. granuloma formation leads to inc. portal blood pressure leads to incr. portal varicies leads to bleeding and death (major cause of schistosomiasis death).
21
Q

What is concomitant immunity?

A

ongoing infection generates an immune response to adult, egg, and larval antigens. This immunity doesn’t help clear the ongoing infection but will destry a newledy arrived schistosomulum (infectious form- that’s what we call the ceracriae once its in the skin)

22
Q

For what three reasons do we see a decrease in the prevalence and intensity of schistosomiasis infection in people in the 20s (as opposed to kids)?

A
  1. Spontaneous death of adult worms- they only live 3-5 yrs.
  2. Slowly acquired immunity to super-infection mediated by increased numbers of eosinophils that can attack incoming infectious schistosomulums (schistosomula?)
  3. behavior change- less water play
23
Q

What form schistosomiasis is susceptible to immune-mediated destruction?

A

schistosomulum

24
Q

How does the immune system attack the schistosomulum? What factors (cells and antibodies) are important?

A
  1. Antibody dependent cell-mediated cytotoxicity is important: eosinophils + IgE abs is the most toxic. eosinophils + IgG or sensitized macrophages +IgE works too- but NOT IgM. IgM is produced against egg and larval antigens and are called blocking antibodies because they PREVENT the development of protective immunity (cross reactivity with schistosomulum antigens
25
Q

What toxins/systems are used to kill schistosomulums?

A

Complement, ROSs from eosinophils and macrophages, and toxic eosinophil granules: major basic protein, peroxidase, cationic peptides.

26
Q

Why isn’t the adult schistosomiasis worm susceptible to immune attack? Does it have any importance in immunity?

A

thick cuticle. but, abs against adult worm can react with schistosomulum surface

27
Q

Why must the immune system attack the schistosomulum quickly upon entry to the body?

A

otherwise, it can cause disease. also, it acquires host antigens on its surface within 5-7 days that allow it to mask its presence and pass as self.

28
Q

Why/how are IgMs called “blocking antibodies” in schistosomiasis infection?

A

IgM prevent binding of IgG and IgE to epitopes on schistosomulum surface. IgM is pentavalent- Fc portion inaccessible to immune effector cell receptors. IgM can’t participate in antibody dependent cell mediated cytotoxicity.

29
Q

How is concomitant immunity acquired as children age, given that IgM blocking abs exist? How might this be harnessed in the future?

A

At first, IgM predominates. As kids get older, IgE and IgG ab levels rise in comparison with IgM.
vaccine potential- you need to introduce antibodies that promote IgG and IgE immune responses rather than IgM responses.

30
Q

How do we treat schistosomiasis infection? Dosing info?

A

praziquantel- can be effective with a single dose. but, re-infection in endemic areas common, so multiple doses may be necessary. MOA unclear- potential interaction with parasitic use of Ca?

31
Q

What is swimmer’s itch? Where does it occur (geographically)? Reservoir?

A

occurs around the Great Lakes.
caused by ceracriae of schistosomes that infect water fowl and water mammals. in humans it is a cutaneous inflammation caused by death of cercariae in the skin; it is self-limiting.