MGY277H1 Lecture Notes - Lecture 11: Phagolysosome, Streptolysin, Phagosome

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Unit 11Principle of Pathogenesis
Terminology
Colonization the microbe establishing itself on/In body surface or mucosal layer
Infection can be used to refer to colonization by a pathogen
Can be subclinicalNO or mild symptoms
Infectious disease or illness noticeable impairment in a person
Symptomessubjective effects experienced by patients (e.g pain and
nausea)
Signs objective evidence (e.g rash, swelling) can be physically measured
Primary infection initial infection
Damage can predispose individual to “secondary infection” (e.g measles
impairs immune system leading to pneumonia by other microbes)
Primary pathogenmicrobe or virus that causes disease in otherwise healthy
individual
Diseases such as plague, malaria, measles, influenza,etc
Opportunistic pathogen (opportunist)casue disease ONLY when body’s innate
or adaptive defenses are compromised or when introduced into unusual location
Can be members of normal microbiota or common in environment
Virulence degree of pathogenicity
Virulence factorstraits that allow microorganisms to casue disease (e.g toxic a
microbe produces)
Attribute of a microbe that promote pathogenicity
Infectious dose number of microbes necessary to establish infection (an
experimentally derived number)
ID50a number of microbes sufficient to casue infection in 50% of those
people/animals to which the microbes are administrated
Communicable or contagious diseases easily spread when they have a low
infectious dose
Course of infectious Disease
Incubation periodtime between exposure and onset of symptoms
Varies considerably (days to years)
Depends on growth rate/host condition/infectious dose
May be preceded by prodromal phase (vague symptoms)
Convalescencerecuperation, recovery from disease
Carriermay harbour and spread infectious agent for long periods of time in
absence of signs or symptoms
The most challenging population to control disease since they don’t show
signs
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Actue
Illness is short term
Symptoms develop quickly
but last short time
The pathogen is eliminated
by the host defense
Person is usually immune to
reinfection
E.g strep throat
Chronic
Symptoms develop slowly
Illness persists over a long period of time (month or year)
e.g tuberculosis, HIV
Latent
Infectious agent never completely eliminates
May exist in host tissue without causing symptoms
Illness may recur if immunity weakens
Latent is NOT contagious when hiding (diff from Carrier)
E.g Chicken poxshingles
Distribution of Pathogen
Localized infectionmicrobe limited to small area
(boil cause by staphl aureus)
Systemic Infectionagent disseminated throughout body (e.g measles)
oSuffix –emia = “in the blood
oBacteremiabacteria circulating in blood
Not necessarily a disease state
oSepticemia or sepsisacute, life threatening illness caused by
infectious agent or product in blood stream
oToxemiatoxins circulating in bloodstream
oViremiaviruses circulating in blood stream
Evolution of bacterial pathogens
There are 10 times more Microbial cells in you body than human cells in your body
So why aren’t we sick all the time?
3 closely related microbes
1. E.coli strain HS (O9)Harmeless commensal of human
2. E.coli strain EDL 933 (O157:H7)Pathogenic ( cause fever and diarrhea,
priduces toxins, haemolytic, uremic syndrom
3. Salmonell entericapathogenic (cause fever and diarrhea, produces toxins)
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Genomic
islandlarge blocks of newly
acquire
genes
If they are involved in diseasepathogenicity islands
All strain aand species of Salmonella have at least 3 major pathogenicity
island pick up in the early evolution system
How are ne genes acquired?
1. Competence/Transformation
Some bacteria have energy driven protein complexes in their
membrane that actively pump naked d DNA from the environment into
their cytoplasm
Usually the bacteria wants the DNA as food but sometimes this DNA is
incorporated into the genome
2. Conjugation/Jumping plasmids
Some plasmid encode a gene that help them jump from cell to cell
This allows the plasmid to find new hosts and are often packed with
genes to promote survival of their hosts including drugs resistance
genes/phage/ resistance genes/immune evasion genes
It’s NOT the host that is taking up the DNA but rather the plasmid DNA
that is forcing itself into a new host
3. Phage/Transduction
Phage (bacteriaphare) are viruses that infect bacteria
Before they kill a bacterial cell they pack their virions with copies of their
own phage DNA
However sometimes by accident, a few virions will package a fragment of
DNA from their batieral host
When those virions go and infect they next cell they DONOT kill the new
cell because they ARENOT delivering viral DNAthey are delivering a
segment of DNA from the previously infected cell (That DNA can get
incorporated into the genome)
Transductiondefected phage particle accident carry bacteria DNA
instead host DNA (Major jumping mechanisms of gene)
4. Phage encoded genes (lysogeny)
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