Pathogens
Infectious microbes that cause symptomatic disease at some point during their infection cycle
Virulence
Measure of the severity of the infection that a pathogen can cause
What determines a person’s susceptibility to an infectious microbe?
- Prior infection with the same or similar strain can provide immunity, reducing infection severity or preventing infection
- People with immune deficiencies are more susceptible to infectious agents
HIV-AIDS - target cell
- Targets specific immune cells called CD4 T cells
- They are white blood cells with a main role in signalling to other immune cells to destroy infectious agents
HIV-AIDS - Disease
- HIV infection results in a loss of CD4 cells which results in an immune deficiency
- Body becomes vulnerable to a wide range of infections that it otherwise would have been able to fight
How does HIV cause a depletion of CD4 cells?
- Infected cells produce cytokines that causes immune activation in both infected and uninfected cells
- Can result in activation-induced cell death of CD4 cells caused by a chronically activated and hyper-inflammatory immune state
How do viruses lead to cancer?
- Viral infection can mutate proto-oncogenes or change their expression
- Mutation or altered transcript levels interfere with normal regulation, causing uncontrolled cell growth (neoplastic transformation) and possibly tumor formation
What viruses are associated with cancer development?
- Human papillomaviruses
- Epstein-Barr virus
- hepatitis B virus
- the oncogenic retrovirus HTLV-1
Retroviruses leading to cancer - package host DNA into viral progeny
- Sometimes retroviruses can package host DNA into viral progeny and can transmit this DNA to the next cell they infect
- If host DNA is a proto-oncogene and is mutated, this can result in conversion of a proton-oncogene to an oncogene
- Transforms infected cell into a cancer cell
Retroviruses leading to cancer - Alteration of protein expression
- Retroviruses can also integrate into the host chromosome and alter the protein expression levels of proton-oncogenes
- Abnormal levels of proteins involved in regulation of cell division can result in uncontrolled growth of the infected cell
Enteropathogenic E. coli (EPEC)
Extracellular pathogens that use TTSS to inject proteins into the host cell that promote the adherence of the bacterium to the cell surface
Type III Secretion used by EPEC - Step 1
- Secretion machinery is assembled
- The needle provides a conduit into the cytoplasm of the host cell
Type III Secretion used by EPEC - Step 2
- Bacterial protein called Tir passes through the needle into the cytoplasm
- Then inserts itself into the membrane of the host cell
Type III Secretion used by EPEC - Step 3
- Next the bacterium is drawn closer to the host cell and the Tir proteins dock with a protein (intimin) on the bacterial surface
- This firmly attaches the bacterium to the host cell surface
Type III Secretion used by EPEC - Step 4
- Host cytoskeletal proteins are recruited to the base of the Tir protein
- Complex assembly of host proteins occurs, forming a pedestal-like structure at the cell surface
How do oral bacteria contribute to dental caries (tooth decay)?
- Commensal bacteria (Streptococcus sanguinis, S. gordonii) form biofilms in the mouth
- Pathogenic Streptococcus mutans attaches to these biofilms on the tooth surface and promotes tooth decay
What causes the shift from oral health to cariogenic species dominance?
Increased fermentable sugar intake lowers pH, creating acidic conditions that promote growth of cariogenic species instead of S. sanguinis and S. gordonii
How can the shift to cariogenic species be prevented?
Better oral hygiene and higher fluoride intake help prevent environmental and ecological changes that favor cariogenic species
Pseudomonas aeruginosa - opportunistic pathogen
- Commonly found in hospitals, health carte institutions and the general envirnemnt
- Being able to develop biofilm is important for P. aeruginosa to be able to infect
4 steps of biofilm formation
- Reversible attachment
- Irreversible attachment
- Maturation (1st stage)
- Maturation (2nd stage)
Why are two-component signalling (TCS) systems essential for biofilm formation?
- Without a specific TCS system, the infection cannot proceed to the next step
- TCS systems coordinate the steps of infection
BfiR/S-P - regulatory steps in biofilm formation
From planktonic form to irreversibly attached
BfmR/S-P - regulatory steps in biofilm formation
Maturing into small areas of biofilm
MifR/S-P - regulatory steps in biofilm formation
Forming large clusters of bacteria embedded in a biofilm
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Module 1: Section 124
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Module 1: Section 236
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Module 2: Section 1A26
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Module 2: Section 1B54
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Module 2: Section 1C8
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Module 2: Section 1D7
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Module 2: Section 2A16
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Module 2: Section 2B6
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Module 2: Section 2C5
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Module 2: Section 2D12
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Module 3: Section 1A15
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Module 3: Section 1B19
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Module 3: Section 1C16
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Module 3: Section 2A18
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Module 3: Section 2B22
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Module 3: Section 2C31
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Module 3: Section 2D23
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Module 3: Section 2E14
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Module 4: Section 1A24
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Module 4: Section 1B24
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Module 4: Section 2A15
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Module 4: Section 2B14
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Module 4: Section 3A34
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Module 4: Section 3B31
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Module 4: Section 3C21
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Module 5: Section 1A15
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Module 5: Section 1B9
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Module 5: Section 1C14
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Module 5: Section 2A30
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Module 5: Section 2B13
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Module 5: Section 2C32
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Module 6: Section 1A15
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Module 6: Section 1B24
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Module 6: Section 1C14
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Module 6: Section 2A14
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Module 6: Section 2B32
