pathogenicity pt.2

Adherence

The first step of infection following the entry into the host

When the pathogen is more hydrophobic the adherence is greater, where gram - is more hydrophobic

Property of the pathogen that increases adherence

• pili & fimbriae

• Membrane and capsule

• Specialized adhesion molecules ex. Capsid spikes

Adherence virulence factors

Pili & fimbriae

Main adherence virulence factor which mediates ligand-receptor mechanism for adherence

• strains have type 1 pili that adhere to epithelial cell receptors

• Strains that cause UTIs have P-pili

E-coli and adherence

• mediate adherence

• Facilitate invasion

• Allow to evade immune response

• Aid in the formation of biofilms

Functions of proteins A, F, M in the cell wall

• fimbriae made of protein F and M covered in lipoteichoic acids

• Allow for adherence to buccal epithelial tissue

Group A streptococci adherence

Remain in tissues and fluids but do not enter host cells

Extracellular pathogens in invasion

These grow and multiply within host cells and can be subdivided into:

• facultative

• Obligate

Intracellular pathogens invasion

Reside in host cells but can also be grown in pure culture without host support ( in vitro)

Facultative intraceullar pathogens

Incapable of growth and multiplication outside of the host, all viruses are this type other EX. Chlamydia spp. , rickettsias , malarial parasites

Obligate intraceullar pathogens

Lytic enzymes

• coagulase

• Collagenase

• Hyaluronidase

• Hemolysins

Used by pathogens in invasion

1. Attack extracellular matrix and basement membrane

2. Degrade carbohydrate-protein complexes between cells or on the cell surface

Steps of epithelium invasion using lytic enzymes

Intracellular pathogens

These cause conformation changes in host for uptake

• listeria monocytogenes , shigella spp. , rickettsia spp.

• Induce formation of pseudopodia for pathogen engulfment

• Also form actin tail to propel into host

Bacteria that induce polymerization in host cell actin

When bacteria are present in the bloodstream

Bacteremia

Noninvasive as it does not spread from one tissue to another but is blood borne

Clostridium tetani

• produce toxins to be highly invasive

Bacillus anthracis and yersinia pestis

Degrades collagen in connective tissues, produced by clostridium perfringens

Collagenase

Hydrolyze hyaaluronic acid within connective tissues

Hyalronidases

Coagulates plasma, produced by staphylococcus aureus to form fibrin walls around this bacteria to help with invasion

Coagulase

Disrupts normal metabolism of host cells with deleterious effects on host

Toxin

Diseases caused by entrance of toxins into host

Intoxications

Secreted outside of bacterial cell

3 groups:

• AB

• Specific site host

• Membrane disrupting

Exotoxins

Part of the outer membrane of gram - , specifically lipopolysaccharide

Endotoxins

• Often called binary toxins or type III toxins

• A subunit produces toxicity

• B subunit is used for adherence

• EX. Diptheria produced by corynebacterium diphtheriae

AB exotoxins

• neurotoxins, EX. Botulinum to cause botulism or clostridium tetani to cause tetanus

• Cytotoxins: act on specific tissues EX. Hepatotoxins

• Enterotoxins: effect intestines EX. Cholera, E.coli, staphylococcus enterotoxin (TSS)

Specific host site exotoxins

Toxins that disrupt the membrane, EX. Leukocidins that kill phagocytic leukocytes

Membrane disrupting exotoxins

Vaccines made from modified exotoxins against membrane disrupting exotoxins

Toxoids

• pathogens evade phagocytosis by absorbing normal host components to their surface. Ex. S. Aureus that has protein A to bind with igG

• Also some surface factors to avoid phagocytosis: capsules, M protein, pill

• Or production of factors/toxins that inhibit chemotaxis

Antiphagoctic factors

Chromosomes, pathogenicity islands, plasmids, or transposons

Where are genes or pathogenicity found

• E. Coli

• Salmonella serotype typimurium

• Staphylococcus aureus

Pathogens that have pathogenicity islands for pathogenesis