Dmp_712 Bact Exam_1 Host Parasite Interactions Section 7 Robertson

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Parasite defn:

Back 1

Parasite defn: a microbe that depends on another living cell for protection and/or nutrients - may or may not cause host damage

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pathogenicity defn:

Back 2

pathogenicity defn: potential (capacity) to cause disease - property of a species

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virulence defn:

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virulence defn: relative pathogenicity - property of a strain within a species

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invasiveness defn:

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invasiveness defn: ability to penetrate, survive and multiply within host tissues

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toxogenicity defn:

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toxogenicity defn: production of chemical substances (toxins) which cause host damage by
1) inhibiting metabolic/biosynthetic step in host cells --> cell death
2) cause cell and/or tissue damage/cytotoxicity with inflmmation and fever

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normal flora defn:

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normal flora defn: microbial population present on skin and mucous membranes within the host

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mucous membranes defn:

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mucous membranes defn: the layer of epithelial cells that line the mount, pharynx, respiratory tract, G.I. tract and urinary tract

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Opportunist defn:

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opportunist defn: a microbe that is normally not pathogenic, but can cause disease upon lowered host resistance or when introduced into a foreign location

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carrier defn:

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carrier defn: an individual host (animal or human) that continually releases infectous microbes, but does not show signs or symptoms of disease

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Infection defn:
2 types & defns:

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Infection defn: presence of microbes in/on host with no symptoms
2 types & defns:
1) dormant infection - microbes can be recovered in clinical specimens from a carrier - the infectious agent can be transferred to a susceptible host
2) latent infection - microbes can not be recovered from usual clinical specimens - also known as subclinical or inapparent infection

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endogenous infection defn:

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endogenous infection defn: an infection that originates from within the animal such as those caused by Fusobacterium necrophorus (liver abscesses and foot rot)

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Exogenous infection defn:

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exogenous infection defn: an infection that originates from outside the animal, such as inhalation of anthrax spores (Bacillus anthracis)

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Primary invader defn:

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primary invader defn: a microbe that can initiate disease with no change in host resistance (e.g. B. abortus)

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secondary invader defn:

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secondary invader defn: a microbe that invades or establishes itself in host tissues due to the presence of a primary invader

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zoonosis defn:

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zoonosis defn: a disease, primarily of animals, but can be transmitted to humans

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vector defn:

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vector defn: host that transmits the pathogen

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reservoir defn:

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reservoir defn: the host from which the vector acquires the infection

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epidemiology defn:

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epidemiology defn: the study of the occurrence, transmission, distribution and control of diseases in populations

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General Aspects of Host Parasite Interactions (6)

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General Aspects of Host Parasite Interactions (6)
1) initial encounter/infection
2) entry - breakdown of local defensens
3) internal spread
4) growth and multiplication in vivo
5) damage - due to pathogen or host response (inflammation)
6) outcome

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General Aspects of Host Parasite Interactions
Initial encounter/infection
begins:
Starts with:

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General Aspects of Host Parasite Interactions
Initial encounter/infection
begins: at birth
Starts with: process begins with exogenous infection from surroundings, can be endogenous after normal flora develops

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General Aspects of Host parasite interactions
Entry - breakdown of local defenses
barriers:
invasion into:

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General Aspects of Host parasite interactions
Entry - breakdown of local defenses
barriers: skin and mucous membranes normally effective
invasion into: skin and epithelial cell barriers not normal healthy skin

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General Aspects of Host parasite Interactions
Internal Spread
limited by:
possible mechanisms (2)
Usually via:

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General Aspects of Host parasite Interactions
Internal Spread
limited by: host factors during early stages
possible mechanisms (2) cell to cell transfer or between cells
Usually via: circulatory system

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General Aspects of Host parasite Interactions
Growth and Multiplication In Vivo
Nutrient availability:
Limited by:

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General Aspects of Host parasite Interactions
Growth and Multiplication In Vivo
Nutrient availabily: good except for Fe++
Limited by: antimicrobial factors (e.g. lysozyme, IgA, complement and Beta-lysins) and phagocytic cells

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General Aspects of Host parasite Interactions
Damage - due to pathogen or host response (inflammation)
inflammation causes:
host experiences:
pathogen causes:

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General Aspects of Host parasite Interactions
Damage - due to pathogen or host response (inflammation)
inflammation causes: mechanical blockage
host experiences: loss of function (e.g. botulism toxin)
pathogen causes: disruption of membranes, metabolic processes, or biosynthetic sequences

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General Aspects of Host Parasite Interactions
Outcome
Types of resistance(2):

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General Aspects of Host Parasite Interactions
Outcome
Types of resistance(2):
1) Innate resistance
2) Acquired resistance
- Humoral response
- Cell mediated response

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Dynamic Nature of Host Parasite Interactions
Host Resistance relationship to Parasite Pathogenicity/Virulence involves:

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Dynamic Nature of Host Parasite Interactions
Host Resistance (involving innate and acquired immunity)
relationship to
Parasite Pathogenicity/Virulence (involving invasiveness and toxigenicity)

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Dynamic Nature of Host Parasite Interactions
Factors that Shift the Balance
Host Side: lowered host resistance due to (4)

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Dynamic Nature of Host Parasite Interactions
Factors that Shift the Balance
Host Side: lowered host resistance due to (4)
1) Change in physiological well being
2) Genetic factors
3) Malignancy
4) Predisposing illness

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Dynamic Nature of Host Parasite Interactions
Factors that Shift the Balance
Pathogen Side:
Virulence factors that mediate invasiveness (3):
Virulence factors with toxicity and host damage (2):

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Dynamic Nature of Host Parasite Interactions
Factors that Shift the Balance
Pathogen Side:
Virulence factors that mediate invasiveness (3):
1) surface molecules that act as adhesins
2) surface molecules that block phagocytosis
3) extracellular enzymes (inactivate complement components, igA or kill phagocytic cells)
Virulence factors with toxicity and host damage (2):
1) Extracellular protein exotoxins
2) Endotoxins - lipopolysaccharides

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Steps in Disease Process (5)

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Steps in Disease Process (5):
1) Exposure
2) Attachment
3) Multiplication
4) Colonization of mucosal surface or tissue
5) Two possible outcomes of exposure

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Steps in Disease Process
Exposure:

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Steps in Disease Process
Exposure: portal of entry is important

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Steps in Disease Process
Attachment
entry:
receptor:
must compete with:
must avoid:

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Steps in Disease Process
Attachment
entry: into body site
receptor: for pathogen must be at site
must compete with: normal flora
must avoid: local defensins

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Steps in Disease Process
Multiplication:

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Steps in Disease Process
Multiplication:
nutritional factors

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Steps in Disease Process
Colonization of mucosal surface or tissue
Shedding:
Important factor:

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Steps in Disease Process
Colonization of mucosal surface or tissue
Shedding: patient is infectious
Important factor: resistance to innate immune mechanism important at this stage

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Steps in Disease Process
Two possible outcomes of exposure:

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Steps in Disease Process
Two possible outcomes of exposure:
1) No signs, symptoms or disease
2) Patient develops symptoms and illness

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Microbial Aspects of Pathogenicity (4)

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Microbial Aspects of Pathogenicity (4)
1) Initiation of Infection
2) Growth and Multiplication In Vivo
3) Host damage due to toxins (exotoxins and endotoxins)
4) Host and tissue specificity

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Microbial Aspects of Pathogenicity
Initiation of Infection
Mode of Transmission:
Contact (2)
Droplets (2)
Ingestion of contaminated food/water (2)

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Microbial Aspects of Pathogenicity
Initiation of Infection
Mode of Transmission: depends on growth requirements of parasite, type of parasite (intracellular or extracellular) and ability to survive outside of host
Contact (2)
1) direct contact - veneral diseases
2) incidental contact - contact with formites such as infected litter, bedding, milking machines

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Microbial Aspects of Pathogenicity
Initiation of Infection
Mode of Transmission:
Droplets (2)
Ingestion of contaminated food/water (2)

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Microbial Aspects of Pathogenicity
Initiation of Infection
Mode of Transmission:
Droplets (2)- microbes carried by water droplets expelled by sneezing or coughing
1) Upper respiratory diseases - BRD complex
2) Lower respiratory disease (M. bovis)

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Microbial Aspects of Pathogenicity
Initiation of Infection
Mode of Transmission:
Ingestion of contaminated food/water (2)

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Microbial Aspects of Pathogenicity
Initiation of Infection
Mode of Transmission:
Ingestion of contaminated food/water (2)
1) food - poultry contaminated with Campylobacter
2) water - E.Coli - carried by cattle causes diarrhea in humans

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Microbial Aspects of Pathogenicity
Initiation of Infection
Mode of Transmission:
Adherence to mucous membranes (4):

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Microbial Aspects of Pathogenicity
Initiation of Infection
Mode of Transmission:
Adherence to mucous membranes (4): colonization of mucosal surfaces
1) mucosal cells - often first point of contact
2) specific colonization by normal flora
- begins hrs after birth
- normal flora limits adherence by pathogens
3) invasion may follow
4) pathogen can block local defenses (e.g. produce proteases that cause tissue damage or inactivate IgA)

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Interactions with Mucous Membranes (3)

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Interactions with Mucous Membranes (3)
1) loose association
2) adhesion
3) invasion

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Control on Mucosal Surfaces by Normal Flora (3)

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Control on Mucosal Surfaces by Normal Flora (3)
1) Deplete essential nutrients (probably the most important)
2) Maintain unfavorable environment (e.g. low pH, Eh or toxic levels of H2O2)
3) Produce an antibiotic-like substance called a colicin - toxic to closely related bacteria

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Challenges for Pathogens on Mucosal Surfaces
In order for pathogens to grow and multiply on mucosal surfaces (5)

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Challenges for Pathogens on Mucosal Surfaces
In order for pathogens to grow and multiply on mucosal surfaces (5)
1) Must establish close proximity - efficient delivery of exotoxins)
2) Avoid being swept away by tears, saliva, urine, etc.
3) Acquire essential nutrients
4) Replicate at a rate to expand numbers
5) Resist local defenses (e.g. IgA, PMNs, macrophages, bactericidal peptides)

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Bacterial Adherence to Cell Surfaces
Bacterial adhesins
mecchanism:
overcome negative charges:

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Bacterial Adherence to Cell Surfaces
Bacterial adhesins
mecchanism: interact with specific host cell receptors - result is tight binding
overcome negative charges: on both cells by hydrophobic interactions

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Examples of Bacterial Adhesins
ETEC:
Bordetella:
Strep. agalactiae:

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Examples of Bacterial Adhesins
ETEC: fimbriae - assembly of protein subunit
Bordetella: filamentous hemagglutinin (FHA) - high molecular weight OM protein
Strep. agalactiae: polysaccharide capsule

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Virulence, Fimbriae and Adherence
Correlation:

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Virulence, Fimbriae and Adherence
Correlation: strong correlation between adherence to mucosal surfaces and virulence
Specifically:
1) fimbria increase relative adherence and relative infectivity

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Importance of enterotoxins and suface fimbriae to intestinal colonization and clinical disease

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Importance of enterotoxins and suface fimbriae to intestinal colonization and clinical disease
surface fimbriae are important for intestinal colonization
both surface fimbriae and enterotoxins are necessary for severe clinical disease

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Adherence and Formation of Biofilms
Adherence due to:
Binds:
Structure:
Causes changes in bacterial population (2)

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Adherence and Formation of Biofilms
Adherence due to: polysaccharide capsule
Binds: bacteria to each other and to surface
Structure: complex, resemble islands separated by channels
Causes changes in bacterial population(2)
1) cells become almost dormant
2) antibiotics lose effectiveness
-due to slow growth rate
-phagocytic cells may not be present or bacteria can not be ingested

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Medical Problems Caused by Biofilms 2 mechanisms with examples

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Medical Problems Caused by Biofilms 2 mechanisms with examples
1) bacteria in biofilms become aerosolized - pneumoophilia in water towers
2) biofilms on body surfaces and catheters - dental plaque, catheters

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Growth and Multiplication In Vivo
Nutritional adaptation to host and/or tissues
varries with:
adequate nutrition:
poor nutrition:

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Growth and Multiplication In Vivo
Nutritional adaptation to host and/or tissues
varries with: type of parasite (extracellular vs intracellular) and growth requirements
adequate nutrition: in most tissues except for Fe, eg. blood, serum, lung edema
poor nutrition: skin, GI tract

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Growth and Multiplication in Vivo
Avoid or Inhibit:
2 types & examples:

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Growth and Multiplication in Vivo
Avoid or Inhibit: local defenses
2 types & examples:
1) Surface macromolecules
-polysaccharide capsule - antiphagocytic
-lipopolysaccharide - antiphagocytic and confers complement resistance
2) Production of extracellular enzymes
-proteases and phospholipases that cause tissue damage and restrict blood supply
-protease specific for IgA - cleaves hinge region of heavy chain