Long's IPM Flashcards
- What do microorganisms use as a source of food?
2. What is microflora?
- Reduced carbons e.g. humans
2. Population of microorganisms. They have a resident population but also transient that can change
What is symbiosis and what are the symbiotic associations with microbes?
Symbiosis are different organisms coming into contact with each other.
Mutualism ↔ commensalism ↔ parasitism
If relationship moves towards mutualism, then re-establishment of a healthy host occurs. If relationship moves towards parasitism then infectious disease process begins.
What is commensalism?
Microorganism associated with host e.g. human for a source of food and shelter but causes no harm to host.
Host can benefit as well from metabolism of commensal microorganisms (normal microflora). If host and commensal are separated both will survive independently. However the defence system in the host must ensure the microorganism stays at a restricted anatomical site and doesn’t replicate above a certain number.
What is mutualism?
Host and microorganism completely dependent on each other. If they are separated, they die. It is not really present in humans but prevalent in animals e.g.) cattles have mutualistic organisms that break down cellulose wall in plants.
What is parasitism?
Microorganism (now parasite) causing harm to host when using it as a good source (moves anatomical site and increases in numbers).
E.coli moving from colon to urinary tract will cause a UTI
Why is the skin not an ideal place for microbial growth?
Impermeable barrier to outside world.
Very inhospitable place for majority of microbes to grow as the horny layer is dead.
Secretions of the skin also make it hostile (salt, oil, enzymes that attack microbes)
Microorganisms that survive tend to be present on mucosal surface (GI tract, inner mouth)
What microorganisms are associated with the skin?
Staphylococcus aureus (gram +ve cocci)
Propionibacterium acnes = anaerobic organism living deep within hair follicle (most common organism on the skin)
Where does most microflora generally reside in the respiratory tract and name two examples.
Mainly in inner layers of the nose and oropharynx (back of throat)
Neisseria Meningitidis (gram -ve cocci) Streptococcus pneumoniae (gram +ve cocci)
These remain commensal in most individuals . These organisms can be colonised by pathogenic organisms yet they do not have signs/symptoms of disease due to immune response. This is colonisation not infection, however one person’s colonisation is another person’s infection.
- Why is there not a huge resident population of microbes in the oral cavity?
- What kind of microbes generally survive and why?
- Secretion of saliva that contains lysosomes that attack glycosidic linkage in peptidoglycan (physical washing removes organisms).
- Some can survive, especially anaerobic gram +ve bacteria in between the teeth that live in the gums (responsible for gum disease and tooth decay). They are resistant to physical degradation of saliva and they attach to enamel.
- The respiratory tract hasn’t got a huge population of organisms and if there are, it is usually transient. Why?
- What are some exceptions to this?
- Due to mucous secretions and cilia to wash away and remove mucous in microorganisms (mechanical motion)
Lower respiratory tract contains cells that feed off microorganisms via phagocytosis (alveolar macrophage) - Pseudomonas aeruginosa, TB, streptococcus pneumoniae, influenza virus)
Why is there isn’t there a huge amount of microorganisms in the upper GI tract (oesophagus and stomach)?
What are some exceptions?
Microorganisms are washed from oesophagus to stomach. In the stomach, there is a hostile environment and microbes are killed by acidic conditions (pH 2) , especially when digesting foods.
Helicobacter pylori, lactobacilli
Discuss the microorganism population in the colon.
Huge number of microorganisms present (faculative anaerobic and aerobic present).
The faeces contains a lot of microorganisms to control numbers within the body.
Discuss the microflora and the Genitourinary Tract
Tends not to have microflora except from the opening of the ureter
Kidneys constantly producing urine which is sterile in a healthy person.
In women, the uterine surface has large mucosal surface. Microflora is restricted to a few species due to acidic environment of the vagina. e.g. Lactobacillus can survive.
Vaginal epithelial surface produces glycogen which is then broken down by enzymes from epithelial surface producing lactose.
Lactobacillus metabolises this which lowers pH in vagina which controls microorganisms and maintains population
How does the environment of the vagina change with the menstrual cycle?
Microflora changes and this is where you can get signs and symptoms of disease such as thrush
Change of metabolism in vagina due to hormonal changes
Koch’s postulate is the criteria to establish a causative relationship between microbe and disease. What are they?
- Organism must be found in all hosts with disease
- Organism must be isolated in pure culture
- Organism should produce the same disease when inoculated into a healthy host
- Organism should be re-isolated in pure culture
What are the disadvantages of Koch’s postulates?
- Doesn’t give you any idea of host as they may have an immune response (some may cause colonisation, some may cause infection)
- Ethics issue
- How do you know the organism is causing the disease and not something else?
What is the molecular version of Koch’s postulates?
- Genes/their products have pathogenic potential
- Genes should be found in all pathogenic strains but not in a virulent strain
- Disruption of gene results in reduced virulence
- Non-virulent strain can be transformed into virulent strain via gene cloning
- Gene must be expressed during infectious process
- Gene should elicit an immune response
What is a virulence factor?
Enables a host to cause a disease and contains characteristics responsible for transmission.
They can be endotoxins or exotoxins
What are the stages of infection?
- Transmission of pathogen
- Adhesion and colonisation of the host
- Invasion of pathogen
- Growth and multiplication
- Evasion of immune response
The first stage of infection is transmission of pathogen. How can a pathogen be transmitted?
- Direct/indirect contact
- Airbourne
- Dustbourne
- Via insect vector
The second stage of infection of adhesion and colonisation of the host. In what ways can adhesion occur?
- Via pili to certain receptors. Pili = protein fibre bundles that can break down easy so is very transient adhesion. E.coli attaches this way onto epithelial surface on urinary tract. It can be advantageous as an immune defence system can kick and attack its own pili.
- Adhesion via F proteins (afibral) = much tighter adhesion
- Biofilm formation- microorganisms can secrete mucous polysaccharide polymers, sticking to epithelial surface, which is a safer place for microorganisms to grow and more mucous is secreted e.g.) Pseudomonas.
Biofilms can move against gravity causing an ascending infection, such as E.coli moving up to kidneys especially those who have catheters as biofilms are formed in plastic tubes
Discuss the third stage of infection, invasion of pathogen and the different ways in which invasion occurs.
- Physically move its way between junctions between cells
- Transportation
- Make cells (which are normally phagocytic-causing cells) to rearrange actin skeleton
- Use bacterial resin to attach
Discuss the fourth stage of infection, growth and multiplication.
- Free iron is limiting in natural environments
- Siderophores ( catechols/hydroxymates) chelate free iron
- Exotoxins can release bound iron from cells
Discuss the fifth stage of infection, evasion of immune response
Will cause symptoms and signs of disease if it evades immune system
What is opsonisation?
Immune system process where particles such as bacteria are targeted for destruction via phagocytes. Process where a pathogen is marked in order for it to be phagocytosed.
Opsonisation with antibody greatly increases adherence to phagocytes
What are exotoxins and give examples of them
Proteins produced by vegetated microbial cells secreted into the environment
- A-B toxins (Diphtheria, Cholera)
- Hydrolytic enzymes
- Bacterial Products:
Neurotoxin (C.tetani)
Enterotoxin (Escherichia coli, salmonella)
Cytotoxin (S.aureus, C.Difficile)
What are A-B toxins?
- Exotoxins
- Divided by structure (A and B portion)
- A portion is catalytic active subunit
- B portion is binding subunit specificity
- Linked by disulphide bond which breaks and separates A and B
- ADP ribosylates the toxin
- Removes ADP ribose from NAD, then uses ADP ribose to ribosylate target protein - effect depends on protein (usually inactivates it)
What is the mode of action of the exotocin, botulinum toxin?
- Normally, acetylcholine induces contraction of muscle fibres
- The toxin blocks release of acetylcholine inhibiting contraction from pre-synaptic membrane
- Induces flacid paralysis
What is the mode of action of the exotoxin, tetanus toxin?
Normally, glycine releases stops acetylcholine release and allows muscle relaxation
Tetanus bind to inhibitory interneurons preventing glycine release - spastic paralysis
What are super antigens?
- Normal antigen presentation- a small subset of t cells are not produced and cascade pathway occurs to form antibody
- Superantigens cause non-specific activation of T cells causing XS IL-2 production, which stimulates TNFa anf other cytokines by other cells to induce shock
- Can start to attack the body due to this massive immune response resulting in tissue breakdown
e. g) streptococcus pyogenes:
- Membrane activating
- Also produces a-toxin which affects pore formation causing swelling, cell lysis, releasing the cell contents as a food source for microorganisms
Explain the exotoxin Lecithinase of Clostridium Perfringens
- Membrane activating
- Phospholipase breaks phosphate groups in glycerol
- Phosphate groups by themself are charged making them unstable and the membrane breaks down
- RBCs are also broken down to try and get a source of iron
Explain the exotocin effect of hydrolytic enzymes
- Lipase, amylase
- Virulence factors
- Hyaluronidases and proteases disrupt tissue structure
- This allows spread and nutrients
- Necrotising fascilitis caused by Group A streptococci
- Treat with Broad spectrum ABX and ITU
