commensal Bac

what are the symbiotic relationships ?

• Mutalism - muralist + host are metabolic dependent of each other and may have recipircol benefit in both partners

• Commensalism- both are not dependent of each other metabolism. can survive on their own . host is neither helped our harmed

• Parstism - harms the host at the expense of living

One person colonisation is another person infection

Colonisation → bac is at a site without causing a disease

Microbiome Respiratory tract

1. Nasal : staphylocccus aureus+ epidermis

2. Nasopharynx - small number of dangerous pathogen but they lack virulence factor so the person carries them as commensal

3. Mouth : microbes is in juvenile groove , gums , saliva

4. Alveoli no microbes

5. Lysozyme is present in nasal mucus to ctrl the microbes

Microbiome Geniutory tract

• the upper GU tract is sterile only few genera is found in the distal portion of urethea → staphyloccuc epidermis , enterococcus facesils

• Female GU has complex microbiome

  • Lactobacilli ferment glycogen → lactic acid → ph 4.5-4.6 in vagina

Microbiome Digestive tract

• no microbes in stomach → very acidic

• Jejunum : Enteroccocci + Lactobacillus

• Colon : has lot

Microbiome of skin and how it not favourable to micropbes

• periodic drying

• Epidermis has slight acidic ph - pool + sweat

• Has enzymes - Lysozyme which controls the microbiome

• associated to staphylococcus epidermis , germ + anaerobe - propionic bacterium Acnes ?

What is Kosch’s postulates and why and how was is it changed into ?

Kosch pustules : is way to prove that an organism is pathogenic - 4 rules

1. organism must be found in all. host with diease

2. organist must be isolated in pure culture - this wasn’t practical

3. it should also produce a disease when involuting to healthy person - not ethical

4. organism should be re-isolated in pure culture - virulence factor can be lost

changed to Molecular version

• Genes are pathogenic

• Genes are found in all pathogenic strain but not avirulent strain

• Disruption of the gene → reduce virulence

• Avirulent can be transformed to virulent

• gene is expressed in the infectious process

• fene product should give rise to immune response

Adhesion + colonisation of there host

to colonise first needs to adhere

1. Pilli formation

   • attaches it self to receptor on the cell surface

   • these formation are weak

   • antibitotic can attach to tip of the pilli this reduces the bac effectiveness

   • however if the bac able to replace the pilli - antibiotic resistance seen in UTI

   • to get a tighter binding u can get fibril adhesion

2. Biofilm

   • 1st layer of microorganism to attach to the cell surface

   • then other lay is attached to basal lay by polysaccharide matrix

   • can form biofilm if the pt is immobile

3. Colonisation: Bac can colon the mucosal membrane so to avoid being trap in the mucus layer : secretes an enzyme so it breaks down the surface and allow it to invade

Invasion of pathogen

1. It can enter by endocytosis → rearrange the cytoskeleton so the cell can it is copy to find a new environment for nutirent

   • Lyosome fusing iWITH vACULE THT PHAGOCYTOSED C.ALBICANS ?

what do they need to grow and how do they get

• Free iron is limited environment therefore bac need virulence factor to extract

  1. Siderphores- catechols / hydroxamates: protein that request any free iron out of the cell and then allows the bac to absorb it

  2. Extotoxins protein tht released to break down tissue to release free iron

Evasion form immune system

1. produce lipid capsid which protects itself.

2. BAC CSN INHIBT PROTEIN FORM THE COMPLENT PATHWAY

3. anti- phagocytic stargeies

what are the virus factor ?

• Adhere

• Invade

• Gorw

• Evade