Lecture 3: Pathogenesis of Parasitic Diseases Flashcards

1
Q

How can location be used for information on life cycle of parasite

A

Egg are ingested

hatched larvae in intestines

eggs in feces

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2
Q

Milk spots in liver and lung damage indicate what life cycle stage for ascaris suum

A

Hatched larvae

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3
Q
A
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4
Q

What does the likelihood and severity of a parasitic disease depend on

A
  1. Status of host defenses
  2. Number of parasites present
  3. Parasite pathogenicity
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5
Q

Pathology may result from….

A
  1. Damage and or loss to host cells, tissues and organs
  2. Alteration of host cellular growth patterns
  3. Interference with host nutrition
  4. Toxins released by the parasites
  5. Host immune response to infection/infestation
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6
Q

What are mixed infections

A

More than one parasite- Additive pathogenic effects on host and may occur with gastrointestinal parasites

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7
Q

What are three ways parasites can cause damage to and or loss of host cells, tissues and organs

A
  1. Destruction/loss due to migrating, developing, feeding or reproducing stages
  2. Obstruction of hollow structures by worms
  3. Compression or distesion of structures by larval or adult worms
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8
Q

How do ancylostoma caninum (hookworm) cause damage to tissue

A

Results in blood loss during feeding and also produces anticoagulants

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9
Q

How does dirofilaria immitis (heart worm) damage host cells, tissues and organs

A

Blocks pulmonary vessels and can cause pulmonary hypertension and heart failure

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10
Q

How does the larval stage (Coenurus) of Taenia multiceps tapeworm damage sheep brain

A

Forms cysts, puts compression on brain, result in Gid (ataxia and circling)

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11
Q

how does Ostertagi ostertagi cause damage to and/or loss of host cells, tissues and organs

A

Larvae develop in gastric glands and damage abomasal mucosa

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12
Q

how can parasites alter host cellular growth patterns

A
  1. Cellular hypertrophy
  2. Hyperplasia
  3. Metaplasia
  4. Neoplasia
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13
Q

What is an example of a parasite that causes cellular hypertrophy

A

Trypanosoma Cruzi in cardiomyoctes

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14
Q

What type of parasite is Trypanosoma cruzi

A

Protozoan

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15
Q

What is an example of a parasite that causes hyperplasia

A

Ostertagia ostertagi acting on abomasal mucous neck cells

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16
Q

How does Ostertagia ostertagi cause hyperplasia in abomasum

A

Causes cells in gastric pits in abomasum to overgrow and can been seen post mortem as bumps on abomasum

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17
Q

What is an example of a parasite that causes metaplasia

A

Trichinella spiralis and skeletal muscle fibers

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18
Q

Where does trichinella spiralis act and what does it do to cells

A

Goes into skeletal muscle fibers and changes cell type so no longer functional muscle cell and becomes hypertrophied

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19
Q

What is an example of a parasite that causes neoplasia

A

Spirocera lupi causes esophageal sarcoma

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20
Q

What are three common examples of parasites that interfere with host nutrition

A

Ascaris suum, dibothriocephalus latus, and giardia

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21
Q

How does ascaris suum interfere with host nutrition

A

Ingestion of chyme

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22
Q

How does dibothriocephalus Altus interfere with host nutrition

A

Absorption of vitamins- B12 (anemia)

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23
Q

How does giardia interfere with host nutrition

A

Causes damage to microvilli and surrounding tissue causing decreased absorption of nutrients

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24
Q

What is a common toxin released by plasmodium (malaria)

A

Hemozoin

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25
Q

What is hemozoin

A

Crystallized dimmers of heme that impair macrophage phagocytic function

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26
Q

What is parasite induced immunopathology

A

Damage that occurs as a result of an inappropriate immune response to infection or infestation

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27
Q

What is an example of parasite induced immunopathology

A

Flea allergy dermatitis- hypersensitivity to allergens in flea saliva

28
Q

Behavioral changes can ____transmission of parasites in taenia multiceps to canids

A

Facilitate

29
Q

What is the definitive host for Taenia multiceps (tapeworm) and where is it found

A

Canids- found in gut

30
Q

What is the intermediate host for taenia multiceps (tapeworm)

A

Sheep; other ruminants

31
Q

What does taenia multiceps (tapeworm) cause in sheep

A

Larva migrate to sheep brain and cause “gid”—> ataxia, circling

32
Q

How is taenia multiceps transmitted from sheep to canids

A

Sheep that are infected and become ataxic are easy prey for canids and transmission is facilitated upon ingestion

33
Q

Behavioral changes are ____ of infection in oestrus Ovis in sheep

A

Side effects

**unlike taenia multiceps which causes ataxia in sheep making them easy targets therefore their behavioral changes make them easy targets for canids and transmission occurs*

34
Q

What is oestrus ovis

A

Sheep nasal botfly

35
Q

How is oestrus ovis transmitted to sheep

A

Adult flies deposit bot egg in sinus and larvae then infect nasal and paranasal sinuses

36
Q

Oestrus ovis rarely migrates to brain to cause behavioral changes like taenia multiceps but if it does why does it not facilitate transmission

A

Although they are easy prey, the botflies die and therefore aren’t transmitted to predator

37
Q

What are virulence factors

A

Traits that confer pathogenicity

38
Q

How does hemozoin produced by plasmodium spp. (malaria) act as a virulence factor

A

Hemozoin inhibits phagocytic effect of macrophages therefore allowing plasmodium to survive

39
Q

What does leishmania spp. use as virulence factor and how does that work

A

Proteases, causes tissue invasion, survival in macrophages, and immune modulation

40
Q

What virulence factor is used by toxoplasma gondii and how does that work

A

Kinases- disrupt host cell signaling and cause immunomodulation

41
Q

Are Plasmodium spp., Leishmania spp., and Toxoplasma gondii parasitic Protozoa or metazoan parasites

A

Parasitic Protozoa

42
Q

What virulence factor do nematodes, tapeworms and trematodes take advantage of and how does that work

A

Proteases- tissue invasion and immune modulation

43
Q

What virulence factordo ticks, mosquitoes and other ectoparasites take advantage of and how does that work

A

Proteases- diminish pain at bite wound

44
Q

What virulence factor do blood-feeding helminths and ectoparasites use

A

Anticoagulants

45
Q

What do helminths secrete to act as virulence factors and cause immune modulation

A

Proteins, glycoproteins, peptides, glycine, glycolipids, eicosanoids that function in immune modulation by the parasite (downregulate immune response)

46
Q

Which age groups are most at risk for parasitic disease

A

Young and geriatric

47
Q

Are males or females more likely to carry parasite

A

Males- because of androgens

48
Q

What females are more susceptible to parasitic disease

A

Pregnant, postpartum and lactating females

49
Q

How does nutrition impact likelihood of getting parasitic disease

A

Malnourishment causes decreased resistance and resilience, increasing likelihood

50
Q

How does immunological competency impact likelihood of getting parasitic disease (4)

A
  1. Immunodeficiency vs immunocompetent
  2. Prior exposure gives partial immunity—> reduced number, migration, development and reproduction
  3. Premunition- partial immunity due to chronic, low level infection, protects host against superinfection and more severe
  4. Immunization status
51
Q

How does genotype contribute to likelihood of developing disease

A

Hosts resistance to infection has a genetic component

52
Q

What factors influence pathogenic potential of a parasite (6)

A
  1. Predilection site
  2. Migratory pathway
  3. Sites of parasite development
  4. Feeding habits
  5. Immunopathology
  6. Transmission of other infectious agents
53
Q

What does osteratagia ostertagi cause in cattle

A

Chronic abomastitis in young cattle

54
Q

What is the predilection site of ostertagia ostertagi

A

Abomasum

55
Q

What is the migratory pathway for ostertagia ostertagi

A

Local (within abomasum)

56
Q

What is the site of development for ostertagia ostertagi

A

Gastric glands of abomasum

57
Q

What are the feeding habits of ostertagia ostertagi

A

Adults feed on abomasal contents and epithelial tissue

58
Q

What is the immunopathology of ostertagia ostertagi

A

Inflammation induced by larvae and adults

59
Q

Is there transmission of other infectious agents for ostertagia ostertagi

A

No

60
Q

Parasitic development of ostertagia ostertagi In the gastric glands of abomasum does what to parietal (pH) and chief cells (pepsin)

A

Erodes parietal and chief cells therefore increasing pH (parietal secretes HCl) and decreased pepsin

61
Q

What is the consequence of ostertagia ostertagi larva in gastric glands of abomasum

A

Impaired protein digestion and bacterial overgrowth (no pepsin and less acidic)

This results in diarrhea

62
Q

What do the ostertagia ostertagi Adults damage in gastric glands of abomasum

A

Epithelium

63
Q

What is the consequence of ostertagia ostertagi Adults

A

Loss of serum proteins- leaking out and causing diarrhea due to osmotic effect

64
Q

The immunopathology of ostertagia ostertagi Results in inflammation and causes what 4 things

A
  1. Further loss of parietal and chief cells
  2. Mucous neck cell hyperplasia
  3. Parietal and chief cells are replaced by mucous neck cells (metaplasia)
  4. Increased vascular permeability, loss of serum proteins, diarrhea
65
Q

In ostertagia ostertagi Parietal cells are replaced by mucous neck cells, what is this an example of

A

Metaplasia- parasite replaces cell types

**other example was trichniella spiralis in skeletal muscle

66
Q

Overall ostertagia ostertagi Results in what 3 things

A
  1. Impaired protein digestion
  2. Bacterial overgrowth
  3. Diarrhea