Microbiology Flashcards
1
Q
Learning Outcomes from L23 - Upper RT Infections
A
- relate distribution of normal microbiota to the functional anatomy of the oropharyngeal and respiratory tracts
- describe the defence mechanisms of the URT that are important in containing microbial colonisation
- describe two diseases of the URT
- characteristics of the pathogen
- symptoms
- pathogenesis
- control and treatment
2
Q
- True or False?
Lots of microbes in the Lower Respiratory Tract is normal and usually no problem.
A
False, this applies to the Upper Respiratory Tract.
Lots of microbes in the lower respiratory tract is abnormal and impairs function - gas exchange (O2 rich air in, CO2 enriched air out)
3
Q
- Describe the defence mechanisms of the respiratory tract.
A
Filter barriers and ejection mechanisms:
- noise hairs (vibrissae) - filter large particles out
-
cilia (mucosa) - traps particles before lungs. The upper RT mucosal epithelium is ciliated; the beating of cilia moves mucous upward: mucociliary escalator.
- Mucin constantly moves up and out. For microbes to remain in the RT, they must attach to the epithelial cell surface, resist translocation upwards, or replicate at a greater rate than the mucin is removed.
- mucous - for mucin to be functional, it must be of appropriate volume and viscosity
-
bioactive secretions - control microbe growth and survival in the mucous
- iron limitation - lactoferrin (nutrient competition)
- cell wall destruction - lysozyme (antimicrobial)
- membrane permeabilisation - cationic peptides (antimicrobial)
- histological - epithelial cells tightly oriented
- anatomical - epiglottis
- physiological - coughing/sneezing reflexes, salivation
- microbiological - normal flora of oral and nasal cavities. Impaired defence mechanisms can change relationship with normal microbes; disturbance can lead to endogenous infections
NB - there must be a balance - if filter barriers block the flow of air then they impair respiratory function.
4
Q
- Describe the significance of normal flora.
A
Contribute to normal state (homeostasis)
- maintain characteristics of site such as low nutrients
- Host adapted to them
- tolerates their presence in mucosa (little/no inflammation)
- has specific antibody to them - sIgA limits adhesion to, or penetration of, mucosal barrier. Other Ig’s facilitate rapid control of “accidental breaches”
Exclude potential invaders:
- compete for nutrients
- occupy attachment sites on the host
- produce bacteriocins, lantibiotics
- May* contribute to pathogenesis
- if relationships goes wrong - can invade and cause disease
5
Q
- What are some of the symptoms, predisposing factors and potential complications of URTIs?
A
Symptoms:
- irritated nose or throat, sneezing, watery nasal discarchage, nasal mucous build up, sinuses swell, cough, headache, slight fever
Predisposing factors:
- Immune function (fatigue/stress, poor nutrition)
- respiratory function (smoking)
- exposure (crowded conditions)
Potential complications:
- inflammation (middle ear, sinusitis, bronchitis)
- secondary infection (streptococcal septicemia, pneumonia)
6
Q
- Describe two diseases of the URT wrt:
- characteristics of the pathogen
- symptoms
- pathogenesis
- control and treatment
A
1) The Common Cold
Microorganism: numerous; >200 viruses
- typically rhinovirus - 30-50% of colds
- small 30nm, non-enveloped, icosahedron, ssRNA genome
- 4 protein capsid -> over 100 serotypes
- virus particles must attach to cell for entry (and replication)
- most target ICAM-1 (intercellular adhesion molecule 1) for attachment
- hijack host cell machinery for replication
Symptoms: stuffy nose, sore throat, headache, body aches, congestion, cough, malaise, etc.
Pathogenesis: mild, self-limiting
- incubation period = 2-3 days
- infectious during first 2-3 days
- recover within 1 week
- transmission: twofold, but not highly infectious (30-40% transmission rate)
- aerosols (coughing, sneezing, talking)
- direct contact via hands
Treatment, prevention: none
- manage symptoms
- no antiviral
- no vaccine (antibodies are part of clearance but cold viruses evolve too quickly/frequently for effective vaccination development)
- difficult to target due to antigenic variation and attachment site not immunologically exposed (bottom of deep cleft)
2) Pharyngitis (sore throat)
- bacterial or viral (50:50)
- oral Streptococcus species, most commonly S. pyogenes (GAS; Group A Strep)
Virulence factors
- alpha, beta haemolysins (strain dependent)
- adhesins
- cell envelope/capsule, surface and secreted proteins/antigens
- peptidoglycan layer
symptoms
- often accompanied by pus
- serious secondary effects; septic shock
Infection with GAS dangerous due to wide range of virulence factors and potential for toxic shock
- cell lysis improves access to nutrients - especially iron
- reduces targeting by adaptive immunity
- improves dispersal by releasing from aggregates
- releases nutrients (amino acids, nucleotides)
- cell adhesion
- immune evasion
- superantigens promote tissue damage by inflammation and necrotising fasciitis
Control, treatment
- antibiotics - penicillin (most strains)
7
Q
- LEARNING OUTCOMES L24 LRTI’S
A
- Know the defence mechanisms of the LRT that are important in preventing establishment of disease
- Understand why the LRT is free of normal flora
- Recognise both viruses and bacteria cause LRT infections
- Give examples of LRT infections that are endogenous vs. environmentally acquired vs. contagious
- Able to describe key characteristics of the pathogen, symptoms, pathogenesis, control and treatment
- Relate the significance of selective pressure on bacterial populations to vaccine strategies
8
Q
- What are some of the specific functions of the LRT?
A
- gas exchange: absorb oxygen, remove CO2
- maintain air flow: removal of obstructions
- mucociliary escalator keeps lungs free of mucus accumulation, foreign particles and microbes
- protection from infection:
- mucous provides a medium to concentrate defence molecules
- antimicrobial substances: lactoferrin, lysozyme, cationic peptides
- secretory IgA
- alveolar macrophages
- humoral factors
- IgG
- mucous provides a medium to concentrate defence molecules
9
Q
- How might infection of the LRT occur?
A
Aerosols (from outside) and aspirates (from oral microbiota) contain potentially infectious particles of varying size and hygroscopicity:
- 6-10 um - trapped in nose
- < 6 um, non-hygroscopic - impeded in trachea, bronchi; may be cleared by escalator
- < 3um, hygroscopic - make way to alveoli - clearance requires immune function (macrophages, humoral factors)
10
Q
- Describe the defences of the LRT against microbes.
A
LRT has less exposure to microbes than URT and additional defences to remove the few microbes that get there.
- Immune: macrophages, humoral factors
Macrophages - many roles
- Antibacterial affector - recognises pathogen, produces alarm and coordinated response to infection
- Antibacterial effector - apoptotic death reduces pneumococcal burden - antibacterial
- Proresolution, Anti-Inflammation - efferocytosis (clearance of dying leukocytes), signalling to the epithelium to dampen inflammatory signalling
- Bad - necroptosis/pyroptosis - outcome reflects bacterial toxins - uncontrolled death risks inflammatory injury and infection risk - pathological
11
Q
- Describe the LRT: Pneumonia
A
Microbial infection of bronchial tubes/lungs (parenchyma/lining)
Microbes:
- Bacteria - Legionella, Mycoplasma, Streptococcus
- Viruses - influenza
- Protozoa - Pneumocystis
- Fungi - Aspergillus, Cryptococcus
Infection routes and reservoirs:
- aspiration - normal URT microbes
- inhalation - aerosol generators (mechanical devices, air-breathing animals, any habitat of spore-forming organisms)
Compounding factors:
- depressed cough reflex
- immunosuppression
- mucus accumulation - genetic defect (CF), co-infection/epithelial damage
Virulence attributes pertinent to LRT infection:
- readily aerosolised/aspirated
- resist macrophages
- avoid humoral immunity
- RT-specific adhesins
Viral Pneumonia: see #12
12
Q
- Describe viral pneumonia
- examples
- cellular targets
- symptoms
A
~200 million cases/yr
Adults: typically influenza, coronavirus
- Bacterial 70%, viral 30%
Children: typically respiratory syncytial virus (RSV), parainfluenza
Dual viral infections exist, as do dual-viral (30% of cases).
Target:
- LRT via RT-specific epithelial receptors
- eg influenza binds to sialic acid moiety on ciliated cells
- result: motility ceases, cells desquamate, cough triggered
Symptoms:
- 3-4 day fever = infection of RT
- rapid onset: chills, fever, cough
- malaise, myalgia
- hyperventilation
- hyperinflation (of lungs)
- fluid accumulates in lungs
13
Q
Describe Bacterial Pneumonia, mentioning reservoir, infection route, colonisation success and pathogenesis.
A
- Grav +ve diplococci
- Reservoir: normal microbiota of the nasopharynx (~50% children carriers)
- Infection route: aspiration, an endogenous infection
- Colonisation success: large polysaccharide capsule protects from phagocytosis
-
Pathogenesis : multiplication in alveolar spaces; toxin destruction of cells (pneumolysin)
- alpha-haemolytic
- alpha-haemolytic
-
Incidence:
- children: rate reflects immature immune system
- elderly/sick: increased incidence reflects decline in lung function (tissue resilience) plus declining immune function
14
Q
- Discuss Legionnaires’ Disease with regard to its virulence and survival characteristics.
A
High mortality rate ~20%; a frequent cause of pneumonia.
Genus Legionella:
- ubiquitous - soil and aquatic ecosystems
- slender, weakly staining, pleiomorphic G- rods
- requires iron, cysteine-dependent
- habitat: biofilms on wet surfaces (air conditioning towers, condensers, shower roses, irrigation spray heads, potting mixes)
- survives in moist environments at relatively high temperatures
Intracellular survivor:
- phagocytic uptake via coiling endocytosis
- vacuole formation: intracellular phagosome, survival
- multiplication within macrophage phagosome, ruptures, host cell lysis, bacteria escapes - further infection
Pathogenesis:
- environmentally acquired , no person-person transmission
- eg biofilm droplets containing Legionella -> inhaled, deposits in lung -> resists macrophage killing; growth; promotes inflammation -> systemic dissemination
Pathology/symptoms:
- cough
- headache
- fever
- chills
Treatment/control:
- antibiotics
- control incidence by cooling tower hygiene and source tracking to identify hygiene failure or infection risk
15
Q
- Describe the symptoms and pathology of Whooping Cough (Pertussis)
A
- Acquired, contagious infection
- affects mainly infants and small children
- incubation period 1-3 weeks
- begins like cold
- dry, unproductive cough develops:
- paroxysmal, “whoop” sound
- severe
- post-tussis vomiting -> weight loss
- haemorrhage in eyes
- cough lasts 3 months: “100 day cough”
Bordetella pertussis:pathology is due to a variety of toxins
- pertussis toxin
- incr. tissue susceptibility to histamine and serotonin
- incr. lymphocyte response
- adenylate cyclase toxin
- invasive
- haemolytic
- inhibits host response: chemotaxis, phagocytosis, phagocytic killing
2 Gram-negative endotoxins (cell well associated):
- tracheal cytotoxin (peptidoglycan fragment)
- kills tracheal epithelial cells
- paralyses cilia
- LPS
- inflammation
- shock
Control/treatment strategies:
- hygiene (including quarantine)
- vaccination - historically very effective (but not currently… see #16)
