Lecture 7- Infection, Pathogenicity + Virulence- Bacterial Toxins Flashcards
Pathogenicity
The ability of an organism to cause disease
Virulence
The relative 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
Slides 9-10
Bacterial toxins
Contribute significantly to bacterial disease
Primary causes of some diseases= 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
- necrotising 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
