Lecture 7- Infection, Pathogenicity + Virulence- Bacterial Toxins Flashcards
(21 cards)
Pathogenicity
The ability of an organism to cause disease
Virulence
The ability of the pathogen to infect a host + cause disease
-degree of pathogenicity
Virulence factors
-molecules
-cellular structures
-regulatory systems that enable microorganisms to cause disease
Bacterial toxins
-virulence factor
-protein, peptide/ any other substance produced by bacteria which is highly poisonous for living cells in other organisms
Why do bacterium’s harm its host?
Main goal of bacteria cell= multiply
Killing host= kills bacteria = no nutrients
Successful bacteria= obtain nutrients + spread with the least amount of energy and host damage
Host damage=
-facilitate invasion (weakened barriers/ immune responses)
-access/liberate nutrients
-reduce competition from other microbes
Host response vs disease
Immune response too weak to be effective= no benefit to the host
Immune response excessive= damaging to the host
Extracellular enzymes
Hyaluronidase and Collagenase (used by bacteria like Streptococcus pyogenes):
Bacteria attach to the surface of epithelial (skin/mucosal) cells.
They release enzymes hyaluronidase and collagenase.
These enzymes break down the “glue” between cells, allowing bacteria to move deeper into body tissues.
This helps the bacteria invade and spread into areas under the skin.
S. aureus enters the body (e.g., through a cut) and produces coagulase, which forms a clot around the bacteria.
This clot protects the bacteria from the immune system and helps them grow.
Later, kinase is released to break down the clot, allowing bacteria to escape and spread.
Lab Tip:
Coagulase tests help identify bacteria:
If the sample clumps: Coagulase positive (e.g., S. aureus).
If no clumping: Coagulase negative (e.g., S. epidermidis).
Bacterial toxins
Contribute significantly to bacterial disease
Primary causes = anthrax + tetanus
-highly potent
-act away from where they are secreted
Bacterial toxins
Endotoxins;
-produced when bacteria die/ phagocytosed
-gram negative bacteria only e.g. endotoxic septic shock
Exotoxins;
-secreted by bacteria
-can travel through the body + have an effect far from the site of infection e.g. botulism, tetanus etc
Types of toxins
Endotoxin; a lipopolysaccharide component of the gram - bacteria cell = released during active cellular growth + cell lysis
Exotoxin; group of soluble proteins that are secreted by the bacterium; enter host cells + catalyse the modification of a host cell component
Enterotoxin; a protein exotoxin released by a microorganism that targets the intestines. Involved in diarrhoea + food poisoning
Impacts of bacterial toxins
-changes to target cells
-facilitate bacterial spread through tissues
-damages cell membranes
-dampen the host immune system
-inhibit protein synthesis
Bacterial cell envelope
2 major categories; gram + and gram -
Gram + = no LPS= no endotoxin
LPS release can cause host immune system to be hyper-activated
Immune response to endotoxins
-they have pattern recognition receptors that recognise pathogen specific moieties
-known as pathogen-associated molecular patterns (PAMPs)
Examples;
-flagellin, LPS, DNA, chitin and peptidoglycan
Endotoxins- host immune system hyperactivation
Inflammation= increases permeability of tissue to immune cells and promotes healing
Uncontrolled, systemic inflammation + septic shock
Inflammatory response can fail to localise + deal with the pathogen ;
-immune cells become overwhelmed
-bacteria spread to other areas of the body
-large amounts of LPS can enter blood circulation
Endotoxins- host immune system hyperactivation
Antibiotics?
-antibiotic therapy can aggravate symptoms of massive gram-negative sepsis
-LPS is released simultaneously from all cells being destroyed
Toxoids
-exotoxins = may lose toxicity but retain their antigenic properties
-toxin= inactivated (chemically/heat-treated)= known as toxoid
Cytotoxins
Known as= cytolytic forms/ haemolysins
-disrupt cytoplasmic membrane of host cells
-destruction of erythrocytes = haemolysis
-liberate nutrients from the destroyed RBC
Example; pore-forming cytotoxin
Superantigens + Streptococcal toxic shock syndrome
Dealt with= slide 23-25
Streptococcal toxic shock syndrome
1.invade body via wounds in the skin + can release cytotoxins;
- cleaves host cell junction proteins
- loosens tight gap junctions
- cytotoxicity destroys cels in deeper layers of the skin
Results in=
- tissue damage and hyper-inflammation
- invades deeper into the body
-soft tissue infections
- GAS infections are complicated by superantigens
- cytokine storm -> sepsis -> organ dysfunction
- toxic shock syndrome
Two subunit AB toxins
A subunit= actual toxin, enzymatically active
5 B-subunits= involved in delivery + attachment to target site
-recognises receptors on eukaryotic cell surface; toxins are specific and can exert its effect at a different site to where the bacterial infection is
Examples; cholera toxin, shiga toxin, tetanus toxin and pertussis toxin
AB toxins
-all share the AB5 structure
-interfere with signal transduction
-block release of neurotransmitters + protein synthesis
Examples; slides 29-43 (cholera)
*go over cholera toxin, Botox and tetanus toxin= mode of action slide 34, 40 + 44
Summary
Pathogenicity= ability to produce disease
Virulence= disease producing power of an organism, degree of pathogenicity within a group of species
-AB toxins have different effects on the same target protein
-G protein= cholera and pertussis toxins
-AB toxins= range of mechanisms affecting the same system
-motor neurons= tetanus + botulism toxins
