L11 - Bacterial Pathogenesis Flashcards
(31 cards)
How does commensal help protection of diseases?
- commensal = good bactera protect us from colonisation by pathogens
- outcompete nutrient acquisation by pathogens
- production of antimicrobial compounds
- pathogens fight w commensal to obtain short chain fatty acids
- trains our immunological tolerance
What are the harmful effects of commensals?
- displaces commensals can cause infections
- antibiotic induced dysbiosis
- conversion of commonly inserted food substances into carcinogenic substances
- immunocompromised hosts
What are the different ranges of pathogenesis and describe each.
Pathogenic = disease causing bacterial affects all with normal host defences
Non pathogenic = invades individua without causing any obvious detectable symptoms
Asymptomatic = infections detected by presence of these organisms or presence of antibodies
What is the meaning of latent and opportunistic
Organisms can remain latent which means that are not activated with teh recurrence of symptoms
Opportunistic = causes disease under certain conditions
What is the definition of pathogen, commensal, and opportunist
Pathogen = organism that cause infections in individuals w normal host defense
Commensal = organism found on parts of the body that are exposed to external envioenmt ; normal flora
Opportunist = can cause infection in individuals with abnormal host defences.
Give examples of how changes in normal flora can cause pathogen cololnisatons
Changes i hormal physiology (pregnancy child exposed to microbes scarlet fever)
When antibiotic selects for a resistant flora
New organism may be acquired
Outline how harmful effects of alterations in normal fut flora takes place
Antibiotic use -> sensitive gut flora killed -> overgrowth with resistant flora -> c. Difficult toxin production -> diarrhoea
How to treat harmful alterations in normal gut flora?
Stop precipitating antibiotic, give oral metronidazole or vancomycin, recovery requires reestablishment of normal flora ( probiotics?)
How do we know that a given pathogen causes a specific disease.
Koch’s postulates
- pathogen must be present in every case of the disease
- mst be isolated from diseased host and grown in pure culture
- disease must be reproduced when pure culture of pathogen is inoculated into healthy susceptible host
- pathogen must be recoverable from the experimentally infected host
List the modes of transmission of pathogens
Oral oral
Feces oral
Blood
Sexual contact
Animals
Vectors
Environment
Food
List some of the microbial pathogenicity factors
Toxins, iron uptake, adhesins, LPS, enzymes, slime, capsule, invasins
What do bacteria need a huge supply of that is often limiting?
Iron. They have a magnitude of flexibility in how they acquire iron from human and animal hosts
How do commensalism turn into pathogenicity
Exporuse to pathogens -> adherence to skin or mucosa, invasion through epithelium and colonisatio and growth -> toxicity tissue damage and invasiveness
What is the mechanism of b retaking th barrier during bacterial infection
Bacterial interactions with mucous membranes, loose association, adhesion, invasion into submucosal epithelial cells
How are bacterial adhesions flagellate of gram negative bacteria recognised
But innate immune system as a PAMP recognised by TLR5
Describe how bacteria colonise and adhere
- cell wall associated proteins e.g. capsules
- adherence to host cell is fascillitgated by fimbriae and flagella
- prevents bacteria from being washed off by liquid flow
- forms micro colonies
How do bacteria get things to eat in terms of survival and in the host
Adhesins form biofilms, toxins destruct tissue, invasins invasion and multiplication
What are the 3 types of toxins
Exotoxins, endotoxin, enterotoxin
1. Any toxin secreted by bacteria
2. Synonym for LPS of gram negative bacteria (celll surface bound)
3. Exotoxin that is effective in gastrointestinal tract
Describe the mode of action of botulinum toxin from clostridium botulinum
Exotoxins act at teh motor end of the plate to prevent the release of acetylcholine from vesicles resulting in lack of stimulus to the muscle fibres
Normally musecle relaxation is induced by glycine release from inhibitory interneurons and blocks excitation and release of acetylcholine at motor plate. Toxin binds to interneuron to prevent release of glycine so lack of inhibitory signals to motor neurons . Spastic paralyis
What is spastic paralysis
Excess glycine and excess muscle contractions
What are the exoenzymes needed for invading the host (invasion factors)
Proteases, glycosidases, nucleases, lipases
How do lyric toxins damage membranes?
either enzymatically through phospholipases (digest) or physically membrane insertion through binding to cholesterol or non cholesterol (degrade components of the host cell)
What is iron sequestering
Production of iron binding compounds called siderophores to capture from host and bind to bacterial surface.
What is the difference between in classical and hyper virulent kp strains
- normal ones = doesnt produce siderophores
- hyper virulent = produces 4 diff types of siderophores
- there is a correlation between diff types of siderophores and success as a pathogen
