Infection 3: Bacterial pathogenesis and infectious disease Flashcards
How can bacteria be described? (4)
Staining Growth Conditions e.g atmosphere Morphology Microscopic Macroscopic (colonies on agar) Typing
Describe the bacterial envelope structure of gram+ and gram- bacteria
Gram+ thick peptidoglycan
Gram- additional lipopolysaccharide layer
Describe how the atmosphere affects bacterial growth and give an example for each (3)
Some are aerobes e.g S. aureus
Use O2 as final electron acceptor (very efficient)
Some are anaerobes (obligate anaerobes) e.g. Clostridium Spp
Fermentation - Yields final electron acceptor is organic molecule
ok when substrates are plentiful
Oxygen usually toxic to anaerobic bacteria
Many are ‘facultative anaerobes’ e.g. E. coli
Can switch between aerobic and anaerobic metabolism
Describe the appearance on agar when classifying streptococci
alpha’ haemolysis = partial
‘beta’ haemolysis = complete
‘gamma’ haemolysis = none
Describe how typing is used to group bacteria
Relatedness of strains within a species e.g. E. coli O157:H7 (sero-) group A N. meningitidis M3T3 S. pyogenes Primarily serological types Antibodies to expressed antigens Now frequently correlating genotypes e.g. S. pyogenes emmtype ≈ M type
The pathogenicity of a bacteria depends on what factors?
The immune status of the patient.
The site / sample in question.
The disease causing properties of the bacteria (virulence).
What is the role of coagulase on S.aureus ?
Coagulase
Stimulates clotting
Role in immune evasion
Not expressed by less virulent ‘coagulase negative’ staphs
What is the role of adhesins in s.aureus?
Adhesins: bind host proteins Tissue adherence Colonisation Deep infections Immune evasion ‘cloaking’
What is the role of protein A on S.aureus
protein A is an adhesin which binds to the Fc portion of the IgG
What are the 3 types of staphylococcal toxins ?
Cytotoxins Pore forming toxins, lyse host cells Panton-valentine leukocidin (PVL) – lyses polymorphs Exfoliative toxins Proteases Target epidermal structural proteins Enterotoxins (superantigens) Stimulate massive T cell activation ?immune evasion
how does Ritter’s disease happen and its features
What is the diagnosis ? What organism and toxin is responsible for this? Ritter’s disease Exfoliative toxins (ET)A, B etc Serine proteases - specific for desmoglein I Outbreaks in nurseries ET+ve strains No immunity Local infection – e.g. umbillicus Distant bullae Sheet-like desquamation
What are the clinical features you would expect to see in toxic shock syndrome? (5)
Superangtigen exotoxins Rash Renal failure Septic shock Multiorgan failure Skin desquamation on recovery
how does staph aureus cause vomiting
S. aureus superantigens = ‘enterotoxins’ Ingestion → Rapid brief illness Vomiting +++ Minimal diarrhoea Contamination of food Manufacture Preparation
what is a coagulase - staph and where does it occur?
S. epidermidis most commonly Central venous line infection Endocarditis (prosthetic valve) Orthopaedic surgical infections Foreign material in a ‘sterile’ place grafts, implants etc
features of nec fasc
Caused by S. pyogenes infection of deep tissues Production of tissue-destructive enzymes by organisms in stationary phase Pain out of proportion to physical signs Bruising and blistering Generalised toxaemia Renal impairment Very high inflammatory response (CRP) Raised Creatine Kinase Diagnosis by surgical exploration
