Host Pathogen Relationship Flashcards
How do commensals differ from pathogens?
Pathogens are always exogenous (sometimes endogenous) and cause disease and can lead to symptoms and health issues when they infect the host
Commensals are endogenous and are part of the normal microbiota, benefiting from the host without causing harm (e.g., Staphylococcus aureus in noses).
==> can be a pathogen in susceptible people, opportunisitc (when immune system is compromised)
Host microbe (parasite/pathogen) interaction
host mounts immune response and parasite no. decreases
= still grows even in harsh immune conditions so it mutates into new versions
= immune system can’t respond to new version, parasite no. increases
= immune systems mounts another response and parasite no decrease
Front: What causes the shift to parasitic relationships in the symbiosis spectrum?
Back: The shift to parasitism can be driven by:
1. increased microbial virulence (ability to cause damage to a host)
2. decreased host immunocompetence (host susceptibility)
3. higher load of microorganisms e.g. poor hygiene, excessive use of chemotherapeutic agents, and environmental changes
microbial virulence
Definition:
Degree or intensity of pathogenicity of a microbe
[Pathogenicity = the ability to cause disease]
increased virulence = increased likelihood of causing harm
Indicated by:
* fatality rates
* ability to invade host tissues and cause disease symptoms
virulence factors
Virulence is influenced by microbial traits (ie. genes) that mainly fall in four
categories:
(1) colonisation : those that affect the ability of the pathogen to replicate/colonise
(2) Penetration those that affect host defense mechanisms (i.e. immune-evasion mechanisms)
==> anitgenic variation OR tough coat to hide antigen
(3) Evasion : those that affect tropism (specific location), spread throughout the host and transmissibility
HIV == T cells
Hep B = liver cells
(4) Damage those that encode products (TOXINS) that directly damage host cells
Colonisation (virulence factors)
Attachment / Adhesion
* Non-specific E.G. biofilms (general tropism), glycocalyces
* Specific e.g. fimbria, spikes, invasions
Adhesins (protein help microorganism to attach to certain tropism) / ligands:
bind to receptors on host cells:
* Specific to receptors
* E.G. Fimbriae (Pili) and spikes
* Outer membrane proteins
Invasions (Trojan Horse):
bacterial surface proteins: tricks cells to phagotyse itself and promotes ingestion
Endocytosis: non-phagocytic cells > Exocytosis: actin tail propulsion
Penetration virulation factor
Hyaluronidase – breaks down hyaluronic acid (cellular cement and maintains tissue integrity)
=> breaks it down to spread bacteria more quickly, deeper penetration
- Collagenase – breaks down collagen (structural protein in skin and hair etc)
=> tissue damage, loss of integrity, easier to penetrate and spread - Hemolysins – breaks down red blood cells
= obtain iron for own growth and replication as well as decreasing oxygen carrying capacity and weakening host
Evasion virulence factors
- Capsules: Mask antigenic sites, protective ie. anti-phagocytic == can’t be engulfed
- Antigen change: antigenic variation/phase variation, protein mimicry = mimicking host proteins
- Microbe produces antibody proteases: destroys immunoglobulins (IgA), breaking the antibodies
- Intracellular survival = enter and survive within host cells, replicate in a protected environment
5.Affect phagocytosis
– Destroy phagocyte/ kill phagocytes
– Inhibit phagocytosis:
* Prevent chemotaxis (Chemotaxis is the movement of immune cells towards a site of infection)
–> pathogens can produce chemicals to disrupt this process
* Inhibit phagosome formation to avoid degradation by lysosome in cells
* Resist lysosomal enzymes
–> Even if the phagosome and lysosome fuse, some pathogens can resist the harsh enzymes and conditions inside lysosomes, allowing them to survive and sometimes replicate within phagocytes.
factors to affect host susceptibility
Impacted by:
i. Host factors - age, socio-economic
status, occupation, sex, also
inherited factors
ii. Non-specific host defenses &
barriers to infection – physical,
chemical, biological
iii. Immune status -
immunocompromised
Damage virulence factors
causes direct damage to host e.g. microbial toxins
exotoxin: gram positive (thick peptidoglycan cell wall)
–> releases toxins, are proteins
endotoxins: gram negative
when its killed, it releases endotoxins (from cell membrane thus lipid)
== causes fever
infectious dose (load )
Definition of Infectious Dose (ID):
Infectious Dose (ID): The number of microbes required to establish an infection in a host. (how much bacteria is required to cause disease)
infectious dose = ID50: The number of organisms required to cause disease in 50% of an exposed population.
Influenced by
1. Initial Inoculum: The quantity of microbes that initially enter the host.
2. Virulence of Microbe
3. Host Susceptibility
e.g.
Very Low Dose (<10 cells): Diseases like tuberculosis
High Dose (10^6 to 10^11 cells): Diseases like cholera (Vibrio cholerae) need a large number of bacteria to overcome stomach acidity and establish infection.
Extremely High Doses in Specific Contexts: Dental caries is an example of a polymicrobial disease where high numbers of various bacteria accumulate in dental plaque, leading to tooth decay.