3. Innate Immunity - 1st Line Defences Flashcards
Which 3 main factors determine the outcome of the host-pathogen relationship?
- Host’s immune response
- Pathogen’s infectivity (ability to infect/adhere to host)
- Pathogen’s virulence (ability to damage host)
Define the term ‘immune system’.
Cells and organs that contribute to immune defences against infectious and non-infectious conditions - recognise self vs non-self.
Define the term ‘infectious disease’.
When the pathogen succeeds in evading and/or overwhelming the host’s immune defences.
State 4 differences between the innate and adaptive immune responses.
Innate:
- fast (seconds)
- non-specific
- no memory
- no change in intensity
Adaptive:
- slow (days)
- specific (differentiates between different types of pathogens)
- immunologic memory
- changes in intensity (eg faster after re-infection due to memory)
Which 4 innate barriers (1st line defences) prevent entry and limit growth of pathogens?
- physical barriers
- physiological barriers
- chemical barriers
- biological barriers
Give 3 examples of innate physical barriers against infection.
- skin
- mucous membranes (mouth, respiratory tract, GI tract, genito-urinary tract) - have own lymphoid tissues to stimulate local immune response
- bronchial cilia - expel mucous-bound pathogens
Give 4 examples of innate physiological barriers against infection.
- diarrhoea (eg food poisoning)
- vomiting (eg food poisoning, hepatitis, meningitis)
- coughing (eg pneumonia)
- sneezing (eg sinusitis)
Not necessarily associated with relevant site of infection (eg pneumonia can also be associated with vomiting)
Give 2 examples of innate chemical barriers against infection.
- low pH (contributed to by presence of normal microflora esp. lactobacillus)
- skin (5.5)
- stomach (1.0-3.0)
- vagina (4.4) - antimicrobial molecules
- IgA (tears, saliva, mucous membrane) - prevents MO attachment
- lysozyme (sebum, perspiration, urine) - hydrolyse bacterial peptidglycan wall
- mucous (mucous membranes) - traps MOs to facilitate elimination
- beta-defensins (epithelium) - form pores in bacterial wall
- gastric acid and pepsin - inhibit bacterial growth and protease
Explain how innate biological barriers prevent infection.
Involves the normal microflora = non-pathogenic microbes present in strategic locations (nasopharynx, mouth, skin, GI tract, vagina (lactobacillus spp) but absent in internal organs/tissues.
- Compete with pathogens for attachment sites and resources
- Produce antimicrobial chemicals
- Synthesise vitamins (K, B12, other B vitamins)
Under which conditions can the normal microflora become pathogenic? Why might this occur?
- Normal flora is displaced from its normal location to a sterile location
i) breaching skin integrity - skin bacteria in blood stream (eg skin loss (burns), surgery, injection drug users, IV lines (esp central line))
ii) faecal-oral route - foodborne infection
iii) faecal-perineal-urethral route (eg UTI in women)
iv) poor dental hygiene/dental work (common cause of harmless bacteraemia) - Normal flora overgrows and becomes pathogenic in immuno-compromised host (eg diabetes, AIDS, malignant diseases, chemotherapy)
Which patients are at high risk of serious infection due to normal flora displacement? What do these patients require?
- asplenic (and hyposlenic) patients
- patients with damaged or prosthetic valves
- patients with previous infective endocarditis
Antibiotic prophylaxis
Why might the normal microflora become depleted? Give examples of diseases this could cause.
Depleted by antibiotics.
- intestine… severe colitis (Clostridium difficile)
- vagina… thrush (Candida albicans)
Which innate immune defences are present in the respiratory system to prevent respiratory infections developing?
- ciliated epithelium - moves particles towards pharynx and down digestive tract
- goblet cells secrete mucus - physical barrier to infections, and contains lysozymes and IgA
- normal respiratory flora - competition
- cough reflex - aids expulsion of harmful substances
- rich vasculature of resp. system - high levels of neutrophils and alveolar macrophages