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17718886
Normal microflora vs pathogens
Description
Microflora in the body and how this can progress into pathogens
No tags specified
human biosciences
biology
biology
Mind Map by
Eleana Landregan
, updated more than 1 year ago
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Created by
Eleana Landregan
over 5 years ago
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Resource summary
Normal microflora vs pathogens
TYPES OF MICROBIAL INTERACTIONS
Pathogens
Can cause disease in individuals with normal host defences
Commensals
The normal microflora found normally on those parts of the body that are exposed to the external environment
COMMENSALS AS OPPORTUNISTIC PATHOGENS
Transfer to normally sterile areas
E.G. infection of GT
E.G. oral streptococci to heart valves
Damage to epithelium
E.G. staphylococci and pseudomonas burns or wounds
E.G. bacterial pneumonia following influenza
Immune supression
E.G. gut flora septicaemia following radiation
E.G. many pathogens following HIV or immunosuppressive drugs
Antibiotic treatment
E.G. clostridium difficile
Opportunistic pathogens
Can cause infection if host defences are impaired
Can often be derived from normal microflora
COMMENSALS OR NORMAL MICROFLORA
Organisms that live on or within the body of healthy individuals
May be of benefit
TYPES OF SYMBIOSIS
Close interactions between organisms
At least one organism gains
Microorganisms may be harmful to host
COMMENSALISM
Neither harm nor benefit the host
MUTUALISM
Both organisms benefit
Microbes get a place to live and nutrients
Microbes may be beneficial to host
PARASITISM
Host is hormed
Parasite gains
NORMAL FLORA
Microbes normally found on healthy individuals
Usually harmless
Microbiota/microbiome
Very abundant
More microbes than host cells in body
Much smaller in size
Transient (impermanent ) microflora
DO NOT INJURE HOST BECAUSE
Survive because they are harmless
If they become less fit = kill or be killed
Fail to gain from damaging host
MICROFLORA PROTECTS US
Inhibits pathogens
Aids digestive processes
Colonization resistance
Competition for space and nutrients with pathogens
Release of bacteriocins and other antibacterials
Substances to prevent pathogen growth
Stimulation of the immune system
Continued antigenic stimulation from commensals
Cross-reaching protective immunity against pathogens
DETRIMENTAL EFFECTS
Dental caries (toothy decay)
Acne and other skin disorders
Body odour
Ulcers
Conversion of compounds to toxic forms (cancer)
FORMATION OF NORMAL MICROFLORA
Foetus is sterile
When born they acquire microflora from mothers vagina (environmental acquisition)
Contact with others
LARGE INTESTINE
Anaerobic environment abundant microbial anaerobic populations
Greatest numbers of normal microflora
Colonization
Colonization of the large bowel occurs in stages
During a vaginal birth lactobactilli are the first colonizers
E.coli soon follows
New born does not start to acquire a complex intestinal fora until weaned
Where do organisms come from?
Oral exposure to faecal microbes
Facultative anaerobes colonise first and strict anaerobes later
Normal flora, mouth
Normal flora, skin
CHANGES IN NORMAL MICROFLORA
New organisms may be acquired
Sterile in utero; neonate colonized from mother during birth
Colonization of gut and URT in hospitalised patients (nosocomial infections)
Cross infection with Colostridium difficile, Methicillin resistant Staphylococcus aureus (MRSA) and Vancomycin resistant Enterococci (VRE)
With changes in physiology and development
Gut flora changes after breast feeding and weaning
Female genital tract and lactobacilli
When antibiotics select for a 'resistant flora'
Candida overgrowth in mouth and vagina (thrush)
Clostridium difficile (antibiotic-associated colitis
About 10^12 bacterial cells/gram in gut
Only 10^13 in human cells
>1kg of bacteria in adult gut
>1000 species of bacteria and archaea (many uncultured)
Composition of normal flora varies from individual to individual
MICROBIAL PATHOGENESIS
Disease
Pathogen
Virulence (severity)
Infection
Non communicable
Microbial intoxications
KOCHS 4 POSTULATES
IDENTIFICATION OF INFECTIOUS DISEASE
1. The microorganism (pathogen) must be present in all cases of the disease
2. The pathogen can be isolated from the diseased host and grown in pure culture
3. The pathogen from the pure culture must cause the same disease when inoculated into a healthy, susceptible laboratory animal
The pathogen must be re-isolated from the new host and shown to be the same as the originally inoculated pathogen
MOLECULAR DETECTION: ADAPTING KOCHS 4 POSTULATES
1. The biochemical or genetic property should always be associated with pathogenic strains
2. Specific inactivation of the gene that specifies a virulence factor should cause a drop in virulence
3. Reversion of the mutated gene or allelic replacement by recombination or complementation should restore virulence
4. Difficulties of defining single 'virulence factors'
VERTICAL DISEASE TRANSMISSIONS
Persistance of the agent
Transmitted from the parent to offspring
Neonatal infection
E.G. gonorrhoea, HIV and Zika
Infection in utero
E.G. rubella and listeria
HORIZONTAL DISEASE TRANSMISSIONS
Inhalation of droplets (aerosols)
E.G. influenza
Faecal-oral
E.G. cholera
Vector-bone
E.G. malaria
Sex or blood exchange
E.G. HIV
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