Lecture 4: Pathogenesis

Question 1

Definition of disease

Answer 1

Alteration in normal cell, tissue, organ, organ system or organismal activity

Question 2

Likelihood and severity of parasitic disease depends on (3)

Answer 2

Status of host defenses (genetics, age, etc)
Number of parasites present
Parasite pathogenicity
*interactions with each other

Question 3

pathogenicity: definition

Answer 3

Ability of infectious agent to damage a host = produce disease

Question 4

Virulence: definition

Answer 4

Relative capacity of infectious agent to cause damage in host

Question 5

Parasite pathogenicity: 2 components

Answer 5

Pathogenicity
Virulence

Question 6

Interaction of pathogenicity and parasite numbers

Answer 6

As virulence increases = fewer parasites needed to cause detectable symptoms in infected host

Question 7

Interaction between host defenses and parasite numbers/pathogenicity

Answer 7

As host defenses weaken = fewer parasites needed to cause disease/mild pathogenic parasites can cause severe disease

Question 8

Pathology can result from (5)

Answer 8

Damage to/loss of host cells, tissues, organs
Alteration of host cellular growth patterns
Interference with host nutrition
Toxins released by parasite
Host immune response to infection/infestation = collateral damage to host

Question 9

Examples of mixed infections with GI parasites (2)

Answer 9

GI protozoan parasites: Coccidia and Giardia
GI nematodes

Question 10

Ostertagia ostertagi: how developing larvae damage host cells

Answer 10

L4 nematode
Develop in gastric glands
Damage mucosa of abomasum

Question 11

Hookworms and ticks: how feeding damages host tissues

Answer 11

Feed on blood and cause tissue damage
Hookworms —> blood leaks from damaged tissues

Question 12

Eimeria: How reproduction damages host cells

Answer 12

With multiplication of intracellular Protozoa = host cell rupture
Cause destruction of enterocytes

Question 13

Tapeworms: How compression of structures damage host tissues

Answer 13

Tissue cysts (larval stages) of various tapeworms compresses nerves, spinal cord, brain

Question 14

Flukes: how distension of structures damages host tissues

Answer 14

Adult liver flukes distend and damage bile ducts

Question 15

Alteration of host cellular growth patterns: 4 types

Answer 15

Cellular hypertrophy
Hyperplasia
Metaplasia
Neoplasia

Question 16

How parasites interfere with host nutrition (2)

Answer 16

Divert nutrients to parasite
Malabsorption of nutrients

Question 17

How does Giardia cause malabsorption of nutrients (2)

Answer 17

Damage to microvilli and apaoptosis of enterocytes
Blocks interaction between brush border enzymes and their substrates

Question 18

Hemozoin: definition, 2 organisms that ingest and produce hemozoin

Answer 18

Crystallized dimers of heme
Plasmodium produce and ingest
macrophages/phagocytes ingest

Question 19

Why plasmodium use hemozoin

Answer 19

Get rid of toxic effects of free heme (free heme lyses membranes and inhibits enzymes)

Question 20

How hemozoin affects macrophages

Answer 20

Can’t be digested by endomembrane system of phagocytes
Builds up in cells and impedes phagocytosis

Question 21

Parasite induced immunopathology definition

Answer 21

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

Question 22

Example of parasite induced immunopathology: flea allergy dermatitis

Answer 22

Hypersensitivity to allergens in flea saliva

Question 23

Parasite induced behavioral pathology: definition, example with Tania multiceps tapeworm

Answer 23

Behavioral changes that facilitate transmission of parasites
Larval stage in sheep brain —> gid = ataxia, circling —> easy prey for canids
*sheep = intermediate host, canids = definitive host

Question 24

example of how behavioral changes are side effects of infection: Oestrus ovis

Answer 24

sheep nasal botfly
larvae infect nasal sinuses of sheep/ruminants –> larvae sometimes migrate into brain and cause “false gid” –> sheep are easy prey but larval botflies die

Question 25

virulence factors definition

Answer 25

traits that confer pathogenicity

Question 26

3 examples of virulence factors from parasitic protozoa: species, how it works

Answer 26

hemozoin - plasmodium
proteases - leishmania, tissue invasion/survival in macrophages/immune modulation
kinases - toxoplasma gondii, disrupt host cell signaling

Question 27

what does immune modulation mean

Answer 27

dampen immune responses so parasite can persist

Question 28

what are metazoan parasites

Answer 28

worms, arthropods

Question 29

3 GENERAL examples of virulence factors from metazoan parasites (worms, arthropods)

Answer 29

proteases
anticoagulants of blood feeding helminths and ectoparasites
excretory/secretory products of helminths

Question 30

examples of host factors that affect likelihood and extent of parasitic disease (5)

Answer 30

age = young and old at risk
sex/reproductive condition = males carry more parasites
nutritional state = malnourishment (decreased resistance)
immunological competency = immunodeficient
genotype

Question 31

explain how immunological competency affects likelihood and extent of parasitic disease

Answer 31

prior exposure –> partial immunity –> reduced number, migration, development and reproduction of parasites

Question 32

premunition definition and function

Answer 32

partial immunity due to chronic, low level infection
protect host against superinfection and more severe pathology

Question 33

factors affecting pathogenic potential of parasite (6): PMSFIT

Answer 33

predilection site
migratory pathway
sites of parasite development
feeding habits
immunopathology
transmission of other infectious agents

Question 34

ostertagia ostertagi: PMFIT

Answer 34

Predilection = abomasum
migration = local within abomasum
site of development = gastric glands of abomasum
feeding = adults feed on abomasal contents
immunopathology = inflammation by larvae and adults
no transmission by other agents

Question 35

how ostertagia ostergati develops in abomasum (and damage)

Answer 35

larval growth erodes parietal and chief cells = increases pH, decreases pepsin = impaired protein digestion, bacterial overgrowth, diarrhea

Question 36

how ostertagia ostertagi causes inflammation

Answer 36

more loss of parietal and chief cells
mucous neck hyperplasia
metaplasia: parietal and chief cells replaced by mucous neck cells
increased vascular permeability = epithelium leaky = loss of serum proteins/diarrhea