33.5 Specific Pathogenic Bacteria Flashcards
What are all of the different important bacterial pathogens listed in the spec?
Gram positive:
- Streptococcus pneumoniae
- Streptococcus pyogenes
- Staphylococcus aureus (including MRSA)
- Clostridium difficile
- Clostridium tetani
Gram negative (O-antigen possessing):
- Escherichia coli
- Shigella
- Salmonella
Gram negative (Non-O-antigen possessing):
- Neisseria gonorrhoeae
- Neisseria meningitides
Mycobacteria:
- Mycobacterium tuberculosis
For Streptococcus pneumoniae, state:
- Gram type
- Diseases it causes
- Gram positive
- Causes: Primary lobular pneumonia
For Streptococcus pyogenes, state:
- Gram type
- Diseases it causes
- Features mentioned in the spec
- Gram positive
- Causes:
- Pharyngitis (sore throat)
- Cellulitis (skin infection)
- Rheumatic fever
- Glomerulonephritis (glomerulus injury)
- Features:
- CO2 may regulate the expression of virulence determinants
For Staphylococcus aureus, state:
- Gram type
- Diseases it causes
- Features mentioned in the spec
- Gram positive
- Causes:
- Abcesses (a form of skin infection)
- Surgical wound and burn infections
- Food poisoning
- Features:
- Examples of adhesins, aggressins (e.g. toxins) and antibiotic resistance genes carried by mobile genetic elements (in Staphs & Streps).
What Streptococcus species makes up most of Streptococcus group A?
Streptococcus pyogenes
What is MRSA resistant to?
Penicillins, such as methicillin.
For Clostridium difficile and Clostridium tetani, state:
- Gram type
- Diseases it causes
- Features mentioned in the spec
- Gram positive
- Causes:
- Clostridium difficile -> Watery diarrhea
- Clostridium tetani -> Tetanus
- Features:
- Anaerobic
- Spore forming
For Escherichia coli, state:
- Gram type
- Diseases it causes
- Features mentioned in the spec
- Gram negative (O-antigen-possessing)
- Causes:
- Travellers’ diarrhoea
- Dysentery (intestinal inflammation and cramps)
- Food poisoning
- Fever
For Shigella species, state:
- Gram type
- Diseases it causes
- Features mentioned in the spec
- Gram negative (O-antigen-possessing)
- Causes:
- Travellers’ diarrhoea
- Dysentery (intestinal inflammation and cramps)
- Food poisoning
- Fever
For Salmonella species, state:
- Gram type
- Diseases it causes
- Features mentioned in the spec
- Gram negative (O-antigen-possessing)
- Causes:
- Travellers’ diarrhoea
- Dysentery (intestinal inflammation and cramps)
- Food poisoning
- Typhoid fever
For Neisseria gonorrhoeae, state:
- Gram type
- Diseases it causes
- Features mentioned in the spec
- Gram negative (Non-O-antigen-possessing)
- Causes:
- Gonorrhoea
- Features:
- There are differences between men and women in terms of asymptomatic carriage
- Main steps of infection and transmission cycle, key interactions, importance of sialylation and capsule for evasion (ADD FLASHCARDS)
For Neisseria meningitides, state:
- Gram type
- Diseases it causes
- Features mentioned in the spec
- Gram negative (Non-O-antigen-possessing)
- Causes:
- Meningitis
- Features:
- Main steps of infection and transmission cycle, key interactions, importance of sialylation and capsule for evasion (ADD FLASHCARDS)
Compare how frequently Neisseria gonorrhoeae infections are asymptomatic in men and women.
Women are much more likely to carry asymptomatic infection.
What is the difference between EHEC and EPEC E.coli?
Enterohemorrhagic Escherichia coli (EHEC) and enteropathogenic E. coli (EPEC) are closely-related bacterial pathogens. EHEC infection causes bloody diarrhea and haemolytic uremic syndrome in developed nations, while EPEC is responsible for paediatric diarrhea in developing countries. Major differences between EHEC and EPEC include:
*EPEC rearranges host cell actin and EHEC does not
*EHEC secretes a Shiga-like toxin and EPEC does not
*EHEC possesses a type III secretion system and EPEC does not
*EPEC passes through the placenta to infect the foetus and EHEC does not
EHEC strains are considered to have evolved from EPEC strains through acquisition of bacteriophages encoding Shiga-like toxins.
Most common pyogenic G+ organisms
Staphs and streps
Staphylococcus - commensalism?
Normally commensal
Staphylococcus activation
Death signals:
- Poor perfusion, tissue necrosis, anaerobic conditions
- Signal host is dead = can no longer survive as commensal
- Activation of destructive enzymes and toxins
Staphylococcus shape
Cocci
Staphylococcus Gram stain
G+
Staphylococcus motility
Non-motile
Staphylococcus ability to form spores
No
Streptococcus shape
Cocci
Staphylococcus catalase test
Positive (oxygen gas bubbles)
Staphylococcus aureus - distinguished from other staphs because (3)
- Coagulase test positivity (coagulase present, coagulates blood plasma)
- Ferments mannitol
- Haemolysis of RBCs
Staphylococcus aureus causes what diseases?
Abscesses, surgical wound and burn infections, food poisoning
Staphylococcus aureus - Gram status and shape
G+ cocci
Staphylococcus aureus - catalase positive; facilitates what?
Breakdown of toxic oxygen products
Salt tolerance
Staphylococcus aureus - commensalism and where (3)?
Common component of normal flora
- Well-oxygenated sites like the skin
- Survives for long periods in the environment; reinfection/recolonisation
- Vagina of ~5% of women (predisposition to TSS)
Staphylococcus aureus - predisposition
- Heavily contaminated environment
- Compromised immune system
- Diabetes
- IV drug use
Staphylococcus aureus - adhesion
Teichoic acids and polymers of ribitol phosphate bind to mucosal cells
Staphylococcus aureus - immune evasion (7)
- Protein A in cell wall binds to Fc portion of IgG at complement binding site, preventing complement activation, C3b production and reducing opsonisation and phagocytosis
- Catalase positive; breaks down PMN’s ROS
- Antiphagocytic capsule
- Coagulase enzyme clots plasma around infection site, forming fibrin barrier impermeable to phagocytes
- Produce toxins, e.g. phospholipase that damage cell membranes
- Produce leukocidins, which kill leucocytes
- Produce IgA protease
Staphylococcus aureus - cause damage by (2)
Exozyme production, e.g. proteases inducing local tissue damage
Aggresin production:
- Alpha toxin causes necrosis of skin, forming holes in cell membrane
- Beta toxin degrades sphingomyelin
mRSA - resistant because
Methicillin-resistant staphylococcus aureus:
- 90%: Spreading of plasmids encoding beta-lactamase
- 20%: Changes in PBP
mRSA - alternative drug and its MOA
Vancomycin - inhibits cell wall synthesis by binding to peptides rather than transpeptidase enzymes
Staphylococcus morphology
Clusters
Streptococcus activation
Death signals:
- Poor perfusion, tissue necrosis, anaerobic conditions
- Signal host is dead = can no longer survive as commensal
- Activation of destructive enzymes and toxins
Streptococcus - commensalism?
Normally commensal
Streptococcus Gram stain
G+
Streptococcus motility
Non-motile
Streptococcus ability to form spores
No
Streptococcus catalase test
Negative
Streptococcus morphology
Chains
Streptococcus pneumoniae causes what disease
Primary lobar pneumonia
Primary lobar pneumonia
Form of pneumonia characterised by inflammatory exudate within alveolar space
Streptococcus pneumoniae - Gram status and shape
G+ diplococcus
Streptococcus pneumoniae distinguished from other Streps because
It is alpha-haemolytic, not beta-haemolytic
Streptococcus pneumoniae adhesion
Lipoteichoic acids bind to fibronectin
Streptococcus pneumoniae immune evasion (2)
- Anti-phagocytic polysaccharide capsule
- Secretion of IgA protease
IgA protease
Enzyme that cleaves IgA. Secreted by S. pneumoniae, H. influenzae type B, and Neisseria (SHiN) in order to colonise respiratory mucosa
Streptococcus pneumoniae cause damage by
- Lipoteichoic acid trigger immune response
- Phagocytosis can’t clear bacteria
- Inflammatory response = damage & pneumonia
Streptococcus pneumoniae susceptible to what drug
Penicillins
Streptococcus pyogenes (Group A) GRT what diseases
- Pharyngitis
- Cellulitis
- Rheumatic fever
- Glomerulonephritis
Streptococcus pyogenes (Group A) - Gram status and shape
Spherical G+ cocci arranged in chains
Streptococcus pyogenes (Group A) - type of pathogen
Facultative aerobe
Streptococcus pyogenes (Group A) - distinguished from other Streps because
Beta haemolytic (complete lysis) and Lancefield typing (group A glycoprotein)
Streptococcus pyogenes (Group A) - commensalism?
Normal flora of skin and oropharynx
(small numbers, less common than staph. aureus)
Streptococcus pyogenes (Group A) - adhesion (2)
Protein F and lipoteichoic acids allow binding to fibronectin
M proteins allow binding to cell surface sugars
Streptococcus pyogenes (Group A) - adherence to pharyngeal epithelium (pharyngitis)
Pili covered in lipoteichoic acid and M proteins
Streptococcus pyogenes (Group A) - immune evasion (3)
- M proteins bind the Fc region of IgA/IgG and prevent complement activation/opsonisation
- Anti-phagocytic hyaluronic capsule
- Molecular mimicry; hyaluronic acid is normal in body
Streptococcus pyogenes (Group A) - cause damage by (2)
Production of:
- Exoenzymes
- Toxins and haemolysins
Streptococcus pyogenes (Group A) - main exotoxin and its function
Exotoxin B - protease that rapidly destroys tissue and is produced in large amounts
Streptococcus pyogenes (Group A) - quorum sensing
Detects CO2 levels to up regulate virulence factors in the body when they are greater (death signal)
Streptococcus pyogenes (Group A) - treatment
- Susceptible to penicillins unless rheumatic fever or acute glomerulonephritis arise
- Can use macrolides, but resistant stains have emerged
Clostridia Gram stain
Positive
Clostridia shape
Bacillus/rod
Clostridia catalase test
Negative
Clostridia haemolysis test
Negative
Clostridia oxidase test
Negative
Clostridia oxidative-fermentative
Anaerobic
Clostridia fermentation
Mannitol, glucose, fructose, mannose
Clostridia ability to form spores
Yes
Clostridia motility
Non-motile
Clostridia - commensalism?
Normal part of flora found in intestinal
tract (anaerobic)
Clostridia strains on spec
- Clostridium difficile
- Clostridium tetani
Clostridium difficile infection causes what
Diarrhoea and colic
Clostridium tetani causes what
Tetanus - sustained muscular contraction due to rapid series of nerve impulses, e.g. lockjaw
Clostridium tetani - reservoir
Soil
Three most common enteric O-antigen-possessing G- bacteria
E. coli
Shigella
Salmonella
Common virulence factors of E. coli, Shigella and Salmonella (3
- LPS (endotoxin)
- O-antigen in LPS (outermost portion); protective against bile salt
- Anti-phagocytic polysaccharide capsule
E. coli - Gram stain and shape
G- bacillus
E. coli - distinguished from shigella and salmonella because
Ferments lactose
E. coli - commensalism?
Some strains commensal, others pathogenic
E. coli - enterotoxinogenic strain invasion
Invade epithelium
E. coli - enteropathogenic strain invasion
Do not invade epithelium
E. coli - adhesion
P pili
E. coli - motility
Motile due to flagellar protein
E. coli - enterotoxigenic strains cause damage by
- Produce heat-labile toxin and/or heat-stable toxin (enterotoxins)
- Inhibit channels leading to salt and water retention in lumen = watery diarrhoea
E. coli - enteropathic strains cause damage by
- Disruption of microvilli in small intestine
- Alter absorption and inflame epithelium
- Bloody diarrhoea (dysentery)
Salmonella - Gram stain and shape
G- bacilli
Salmonella - distinguished from Shigella and E. coli because
Does not ferment lactose (different to E.coli) but does produce H2S (different to Shigella)
Salmonella - motility
Motile due to flagellum
Salmonella - pathogenesis
- Penetrates epithelium in terminal SI, taken up by M cells and then spreads
- Migrates to lamina propria and initiates inflammatory response
- Prostaglandins activate adenylate cyclase, increase cAMP and disrupt NaCl absorption
- Causes diarrhoea, sometimes dysentery
- Severe strains invade, causing chronic inflammation and fever due to LPS presence
Salmonella - reservoirs
Many animal reservoirs; associated with food poisoning
Salmonella - SPI-1 function
Produces T3SS
Salmonella - SPI-2 function
Prevent lysosomal fusion and improve replication
Shigella - Gram stain and shape
G- bacillus
Shigella - distinguished from salmonella and E. coli because
Do not ferment lactose (unlike E. coli) and does not produce H2S (unlike Shigella and E. coli), also non-motile
Shigella - motility
Non-motile
Shigella - pathogenesis
- Shigella enters epithelial cells of the large intestine through endocytosis mediated by plasma-encoded membrane proteins
- Escapes from phagosome and begins to move cell-to-cell using actin filaments
- Movement causes mucous dysentery
Mycobacterium tuberculosis shape (M. TB)
Bacillus
M. TB - cell wall structure
Very thick lipid wall containing mycolic acids that confer negative charge to OM
M. TB - immune evasion
- Few surface targets
- Resistant to phagolysosomal killing
- Macrophage subversion
M. TB - culture time
Slow growing, 4-6 weeks to culture
M. TB - Features of primary infection
Ghon focus and granuloma formation
M. TB - Ghon focus Vs Granuloma
Tissue inside granuloma dies due to caseous necrosis; necrotic area known as Ghon focus
M. TB - granuloma formation
- Mtb phagocytose by alveolar macrophages
- TLR2 recognises lipids, triggers MyD-88 dependent signalling
- Secretion of TNF-alpha recruits phagocytes, development of granuloma
- VEGF recruits small vessels, allowing more lymphocytes, macrophages and DCs to the infection
M. TB - granuloma structure
Immune cells (foamy macrophages, giant cells and CD4 T cells) surround bacteria, which becomes enclosed in a fibrous cuff
M. TB - latency
Granuloma becomes hypoxic due to fibrous cuff, bacteria enter dormant phase
M. TB - reactivation
Cavitation due to increasing bacterial load
M. TB - treatment
Antibiotic cocktail over long period of time due to latent infection
Examples of non-O-antigen-possessing G- bacteria
Neisseria gonorrhoea and neisseria meningitidis
Professional non-O-antigen-possessing G- bacterial pathogen
Neisseria gonorrhoea
Non-professional non-O-antigen-possessing G- bacterial pathogen
Neisseria meningitidis
Neisseria meningitidis - Gram stain and shape
G- diplococci
Neisseria meningitidis - commensalism
Normally colonises nasopharynx as harmless commensal
Neisseria meningitidis - spread from nasopharynx
Colonisations spread to blood/CSF but not evolved, disease-causing phenotype because bacteria can’t be transmitted once in CSF; disease causing strains are not infectious
Neisseria meningitidis - pathogenesis (3)
- Pilus with adhesive properties and molecular mimicry of host structures
- Opacity (Opa) proteins bind to epithelial cells and macrophages, allowing invasion
- LPS
Neisseria meningitidis - immune evasion (2)
- IgA protease production
- Anti-phagocytic polysaccharide capsule (virulent strains = sialic acid also found in human membranes)
Neisseria meningitidis - treatment
Penicillin
Neisseria gonorrhoea - Gram stain and shape
G- diplococcus
Neisseria gonorrhoea - commensalism
No - normally colonises genital tract, almost always leading to infection go gonorrhoea
Neisseria gonorrhoea - difference in pathogenesis to neisseria meningitidis
N. meningitidis causes immune response when in blood, N. gonorrhoea rapidly induces pus formation at infected surface
Neisseria gonorrhoea - men Vs women symptoms
Men have more noticeable symptoms: urethritis, dysuria and purulent discharges
Women can be asymptomatic carriers with undetected local tissue damage (aids transmission because no precautions taken)
Neisseria gonorrhoea - adhesion
Pili and Opa proteins, important to prevent washing away of bacteria by urine/discharge
Neisseria gonorrhoea - immune evasion
- Anti-phagocytic pili (no capsule)
- IgA protease; without this would be unable to attach to the mucosa
- Porin protein in cell walls inactivated C3b complement fragment
Neisseria gonorrhoea - pathogenesis
Local damage due to inflammatory response
Neisseria gonorrhoea - treatment
Penicillin, but more strains becoming resistant due to plasmids for penicillinase transport
