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171 Cards in this Set
- Front
- Back
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S. pyogenes
- common name - gram stain - Lancefield group - defining tests - hemolysis |
S. pyogenes
- common name: Group A Strep - gram (+) - Lancefield group: A - defining tests: catalase (-), Beta-hemolytic, PYR (+) |
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What helps S. pyogenes bind to keratinocytes?
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M protein.
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Protein used for serotyping strep, unknown function.
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T protein.
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Group A strep: encounter
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Air-borne (fomites)
Food-borne |
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Three aspects of S. pyogenes that lets it adhere to cells
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1. M protein (binds kerotinocytes)
2. LTA, lipoteichoic acid (binds fibronectin) 3. F protein (binds fibronectin) |
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When are outbreaks of group A strep usually seen?
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Late winter, early spring.
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What are two common areas of colonization of S. pyogenes?
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1. Mucous membranes
2. Skin |
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SpeA
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Toxic shock with Group A Strep
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What causes toxic shock in group A strep? What does it do?
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SpeA (Streptococcus Pyrogenic Exotoxin). Causes release of IL-1, IL-2, TNF-alpha.
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During superantigen release, what two things are brought together?
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T-cells and MHC II.
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SpeB
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Hydrolytic enzyme in S. pyogenes that causes damage.
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Action of streptokinase. Consequence of streptokinase
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plasminogen --> plasmin. As a result, pus is runny. Seen in Group A strep
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What does group A strep have that makes pus runny?
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Streptokinase.
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Digestive enzymes in S. pyogenes
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- Proteases
- Hyaluronidase - DNAase - Streptokinase |
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Group A strep: anti-phagocytic mechanisms
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- M protein binds factor H and disables C3b?
- Hyaluronic Acid Capsule - C5a Peptidase - M-like proteins bind to Fc portion of IgG/IgA to prevent opsonization -Streptolysin-O, forms pores in leukocytes -Sic, inhibitor of complement, disrupts lysis and macrophage function. |
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What in S. pyogenes inhibits chemotaxis?
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C5a peptidase
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Action of Streptolysin-O
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Pore-forming toxin, kills leukocytes.
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Does group A strep have assymptomatic carriers?
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yes.
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Group A Strep: Skin and mucous membrane presentations (3)
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- Strep throat
- Impetigo - Erysipelas |
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Group A Strep: Deep tissue and blood (5)
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- Pneumonia
- Cellulitis - Necrotizing fascitis - Myositis - Puerperal fever |
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Group A strep: toxic manifestations (2)
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- Scarlet Fever
- Toxic Shock Syndrome |
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Group A strep: nonsuppurative complications (2)
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- Acute glomerulonephritis
- Acute Rheumatic Fever |
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Acute rheumatic fever
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- Caused by Group A strep.
- Follows pharyngitis - Must invoke host immune response - Sx: carditis, polyartritis, chorea, subcutaneous nodules |
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Acute glomerulonephritis
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- Caused by S. pyogenes
- Follows pharyngitis or impetigo - Immune complex deposition (IgG + C3) in glomeruli BM |
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Group B Strep
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S. agalactiae
- Normal GI flora - Normal vaginal flora in 25% of women Gram (+) Catalase (-) Beta-hemolytic (complete, clear) Bacitracin resistant |
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Clinical presentation of Group B Strep
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Neonatal sepsis
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Species name of Group B Strep
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S. agalactae
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Alpha/gamma hemolytic, Group D strep
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Enterococcus
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Important source of ABX resistance determinants, but otherwise normal flora
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Enterococcus
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Optichin positive
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Strep Pneumo
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Characteristics of S. pneumoniae
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Gram (+), catalase (-), alpha hemolytic, Lancefield not determined, optichin positive, mucoid diplococci. Also bile soluble.
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Transmission of S. pneumo
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air-borne (fomites)
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Colonization of S. pneumoniae
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nasopharynx
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Carriers of S. pneumo
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pre-schoolers
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Mortality of S. pneumo:
___% for pneumonia, ___% for bacteremia, highest in __________ individuals. |
Mortality of S. pneumo:
5% for pneumonia, 25% for bacteremia, highest in splenectomized individuals. |
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Seasonal peak of S. pneumonia?
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Winter, early spring
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Defense mechanisms of S. pneumoniae (4)
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1. IgA protease
2. Hyaluronic Acid capsule 3. Pneumolysin (pore-forming toxin, impairs mucociliary clearance, not secreted. 4. Autolysin: "altruistic autolysis" |
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What are the stages of pneumococcal pneumonia?
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1. Exudative phase
2. Early consolidation phase 3. Hepatization phase 4. Resolution |
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Clinical features of pneumococcal pneumonia:
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Fever, chills, pleuritic chest pain, egophony, productive cough (green/yellow), crackles, dullness at lung bases.
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Complications of pneumococcal pneumonia
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pleural effusions, empyema, recurrent otitis media, septic shock and death, sinusitis, meningitis, bacteremia (seeding pericardium and peritoneum)
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What does S. pneumo do to develop resistance to penicillin?
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It changes its penicillin binding proteins
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What drug is S. pneumoniae resistant to (other than penicillin)?
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cephalosporins
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Vaccine for S. pneumo? What is it based on?
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yes, multivalent vaccine based on capsular polysacharide.
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Subacute bacterial endocarditis
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Viridans Streptococcus
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Dental carries
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Viridans Streptococcus
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Characteristics of Staphylococcus Aureus
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gram (+), catalase (+), Coagulase (+), NOTE: also beta-hemolytic
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How do you distinguish between Group A strep and Group B strep?
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Group A strep is susceptible to bacitracian, Group B strep is not.
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What color colonies does S. aureus make?
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gold colonies
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S. aureus: colonization, carriers
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anterior nares, axilliae, groin, perineum, 25% healthy carriers
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Virulence factors of S. aureus (3)
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1. Peptidoglycan
2. Teichoic acid 3. Protein A |
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Epidermolytic Toxins (Exfoliatin)
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S. aureus, ET-A, ET-B, SSSS
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Enterotoxins (A-E, G)
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S. aureus, food poisoning, heat stable toxins, increase intestinal peristalsis (pre-formed toxin?)
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Enterotoxin F
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S. aureus, TSST-1, Toxic shock syndrome
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Action of catalase
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inactivates bacteriocidal H2O2
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Action of coagulase
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Fibrinogen --> Fibrin
Puts up barrier --> abcess formation --> decrease WBC accumulation (S. aureus) |
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Enzyme that gives S. aureus resistance to penicillins
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beta-lactamase
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Digestive enzymes of S. aureus (3)
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1. DNAase
2. Hyaluronidase 3. Lipase |
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S. aureus: localized infection
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Folliculitis, carbuncles, furuncles, impetigo, cellulitis, wound infections
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S. aureus: deep infections
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Abcesses, bacteremia, many infections, Endocarditis
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Treatment for S. aureus endocarditis
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4-6 weeks of IV ABX
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Infections associated with S. aureus (not abcesses or endocarditis)
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Bursitis, myositis, osteomyelitis, pneumonia (post-influenza bacterial pneumonia), septic arthritis
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S. aureus: Those that are at risk of invasive disease
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Carriers, Post-influenza A pts
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Post Influenza A pneumonia
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S. aureus
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Characteristics of S. epidermis
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Catalase (+)
Coagulase (-) Protein A (-) Novobiocin sensitive White colonies Colonize skin |
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Main pathology of S. epidermis
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biofilms on foreign bodies via exopolysaccharide slime, infection adjacent to prosthetics.
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Resistance genes in S. epidermis carried by:
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plasmids
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Main pathology of S. saprophyticus
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UTI in sexually active women
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What type of Haemophilus influenza is invasive?
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type b
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Transmission, carriers of H. flu
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Air droplets
humans ONLY encapsulated carrier rate = 3-5% capsulated carrier rate = high |
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Colonization of H. flu
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nasopharynx
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Three bacteria that have IgA protease
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SHiN
- Streptococcus - Haemophilus influenza - Nesseria |
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Non-lactose fermenters (4)
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SHYPS
- Shigella - Yersinia enterolytica - Proteus - Salmonella Pseudomonas is also a non-lactose fermenter, but is oxidase positive. |
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Four microbes that increase cAMP
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CAPE
- Cholera - Anthracis (poly D glutamate capsule) - Pertussis (via Gi) - E. coli (LT enterotoxin) |
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Four lactose fermenters
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CEEK
- Citrobacter - Enterobacter - E. coli - Klebsiella |
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Six bacteria with capsules
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Some Killers Have Pretty Nice Capsules
- Strep pneumoniae - Klebsiella - Haemophilus influenzae - Pseudomonas aerginosa - Neisseria meningitidis - Cryptococcus neoformans |
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Most important virulence factor of H. flu
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PRP (polyribose phosphate) capsule
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Clinical presentation of encapsulated H. flu
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- meningitis
- epiglotitis - cellulitis |
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Clinical presentation of non-encapsulated H. flu
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- bronchitis
- otitis media - sinusitis - conjunctivitis |
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Most susceptible population to H. flu (specific ages)
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3 months - 3 years = vulnerable
0 - 3 months = maternal ab protects 3+ years = generates own ab |
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Describe the H. flu vaccine
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toxoid, type b antigen + protein
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ABX prophylaxis for H. flu
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rifamicin
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Similarities between H. flu and S. pneumo (6)
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1. Human only host
2. Nasopharynx 3. Invasive diseae via capsule 4. Protection from disease requires anti-capsular abs 5. Any condition that diminishes phagocyte clearance increases the likelihood of systemic infection 6. Preventing spread involves treatment of potential carriers as well as those that are infected. |
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Characteristics of Listeria monocytogenes
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Gram (+) bacillus, non-spore former, intracellular invasion, facultative anaerobe
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What is required to clear listeria?
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cell-mediated immune response (because lives in cytoplasm)
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What is a facultative anaerobe?
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A bacteria that can switch between anaerobic and aerobic respiration depending on if oxygen is present.
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What is a obligate anaerobe?
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Will die in the presence of oxygen.
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Transmission of listeria
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- food: dairy, deli meats
- oral-fecal - transplacental at birth, NOT in utero |
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Colonization of listeria
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- intestinal epithelium
- intestinal macrophages |
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Listeria: what allows it to lyse phagosome?
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Lysteriolysin lyses the phagosome
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Listeria replicates in the ____
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Listeria replicates in the cytoplasm
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Listeria uses what for motility?
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Host-cell actin
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Most of damage associated with listeria is caused by what?
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host immune response, SEPSIS
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True or false: listeria has no systemic toxins
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True
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Listeria: High risk groups
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Pregnancy, mother, baby
Neonates Immunosuppressed |
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Listeria: most common cause of _______
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meningitis (is this true?)
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Is there neutropenia in listeria?
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NO
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Listeria: get culture from
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CSF, blood
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Listeria: treatment
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ampicillin, penicillin
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General characteristics of E. coli, including serotyping
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Gram (-), facultative anaerobe
H Ag: Flagellar protein O Ag: LPS polysaccharide K Ag: Capsular polysaccharide |
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Colonization of E. coli
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Intestinal epithelium
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Virulence determinants of E. coli (2)
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1. Plasmids (gene exchange)
2. Pathogenicity islands |
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E. coli: intestinal infections
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- colitis
- diarrhea |
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E. coli: neonatal meningitis
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- maternal transmission
- K1 capsule - bacteremia |
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E. coli: opportunistic infection
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- Most important: pneumonia, bacteremia
- siderophore production - predisposing factors: impaired immune function, intestinal trauma or rupture, foreign body |
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Most frequent cause of UTI
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E. coli
- urethritis, cystitis, pyelonephritis, sepsis |
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Important factor in colonization of E. coli
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Pili formation (P type)
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Defense mechanisms of E. coli
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- hemolysin
- siderophores - complement resistance |
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Most common serotype of EHEC
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O157:H7
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Encounter of EHEC
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- person-person
- contaminated meat - contaminated water |
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Transmission of EHEC
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- fecal-oral route
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What is special about the infectious dose of EHEC?
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Very little is needed. Resistant to stomach acid, much like shigella
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Unique proteins from EHEC required for production of characteristic formation
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Tir receptor for intimin delivered to host, required for production of pedestals.
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Toxin of EHEC, inhibits what?
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Shiga-like AB toxin, inhibits 60S ribosomal subunit
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What type of cell does EHEC attack?
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enterocytes, loss of microvilli
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Clinical presentation of EHEC
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mild diarrhea, hemorrhagic colitis, hemolytic uremic syndrome
- most common cause of renal failure under <10 |
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EIEC
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Enteroinvasive E. coli
- no Shiga-like toxin - rare in the US - like less virulent shigella - diarrhea, fever, dysentery |
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EPEC
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Enteropathogenic E. coli
- Similar to EHEC - no Shiga-like toxin - diarrhea with mucous, but little or no blood - malaise, vomiting, fever - childhood fever in developing countries |
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ETEC
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Enterotoxigenic E. coli
- rare in the US - forms pili via Colonization Factor Antigen (CFA) - Diarrhea-producting toxins - Traveller's diarrhea - causes afebrile, watery diarrhea |
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Traveller's diarrhea
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ETEC
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Diarrhea-producing toxins of ETEC
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1. Heat labile toxin (LT), like cholera toxin
2. Heat stable toxin (ST) |
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Characteristics of Salmonella
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Gram (-), non-lactose fermenter, facultative anaerobe
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Three species of vibrio
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V. cholerae
V. parahaemolyticus V. vulnificus |
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Lab test for vibrio species
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Green color on TCBS agar
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Vibrio: encounter
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- food-borne
- water-borne |
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Vibrio: virulence factors in gastroenteric disease
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- adhesins
- cholera enterotoxin - O polysaccharide Ag |
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Vibrio: Sepsis syndrome
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- Ingestion of raw shellfish
- Local invasion of portal circulation (adhesins) - Dissemination in pts with liver disease Cutaneous bullae with hemorrhage Fever, hemorrhage, hypotension, MOSF |
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Vibrio species disseminate in pts with what disease?
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Liver disease
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Vibrio: wound infections
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- bullous formation
- hemorrhagic infections |
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Characteristics of campylobacter
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Gram (-)
Bacilli polar flagellae motile non-spore former slow growth |
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Encounter of C. fetus
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contaminated food
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Encounter of C. jejuni
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- animal exposure
- contaminated food (summer peak) |
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Virulence factor of C. fetus
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S-layer protein prevent complement/abs binding
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Clinical presentation of C. fetus
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- bacteremia
- meningitis - vascular infections |
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Clinical presentation and post-infectious sequelae of C. jejuni
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- Gastroenteric disease, 12-24 hour prodrome
- Post infectious sequleae (1-3 weeks), Guillain-Barre syndrome - 1.3/100,000 cases |
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Characteristics of Helicobacter pylori
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- gram (-)
- helical - slow growth - microaerophilic |
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Encounter of H. pylori
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- oral-oral
- vomitus |
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Transmission of H. pylori
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- oral-fecal
- gastric-oral |
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Colonization of H. pylori
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Mucous layer lining the human gastric mucosa.
Protects from gastric acid and the host response (IgA, IgG, neutrophils) |
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Infection with H. pylori lasts how long?
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At least decades
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Virulence factors of H. pylori (4)
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1. Adhesins (RBC agglutinization)
2. CagA virulence island 3. Urease 4. LPS |
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Function of urease in H. pylori
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assists with local CO2 production, allows survival in acidic environment.
Altruistic autolysis |
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Chronic gastritis
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H. pylori
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Gastric cancer (adenocarcinoma)
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CagA+ H. pylori
Also see with MALT Lymphoma, etc. |
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_____ H. pylori strains protect against ______
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CagA+ H. pylori strains protect against GERD
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Peptic ulcer disease
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- H. pylori
- increased acid production |
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What is the breath test for H. pylori?
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ingest 14C labelled urea, assay breath for 14CO2
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Serology for H. pylori?
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Anti H. pylori IgG
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Salmonella colonize what?
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human macrophages
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How does salmonella survive in a cell?
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It prevents fusion of the phagosome with the lysosome.
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Gallbladder colonization with a long-lived carrier state.
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S. typhi
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Characteristics of Enteric Fever (typhoid)
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Salmonella typhi
- systemic infection with fever, abdominal symptoms - slow, insidious --> severe disease - Rose spots = macropapular rash on trunk (30%) |
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Rose spots
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macropapular spots on trunk (30% of those with typhoid fever)
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Type III secretion
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Salmonella
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Notable about salmonella gastroenteritis
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organism shed for several weeks after symptoms disappear
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Characteristics of Nesseria gonorrhoeae
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gram (+) diplococci
non-maltose fermenting |
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Encounter of N. gonorrhoeae
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Asymptomatic carriers (F 30% > 10%)
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Transmission of N. gonorrhoeae
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- perinatal (conjunctivitis)
- sexual |
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Colonization on N. gonorrhoeae
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- non-ciliated columnar epithelium (cervix, urethra)
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Spread of N. gonorrhoeae
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- attachment to sperm
- reflux of menstrual blood |
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Mucosal attachment: N. gonorrhoeae
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- pili
- Opa proteins - LPS ? |
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Survival of mucosal immunity: N. gonorrhoeae
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- IgA1 protease?
- Iron acquistion (receptors for human transferrin and lactoferrin) - Phagocytosis prevention (variant Opa-strains) |
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Variation: N. gonorrhoeae
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- Phase variation: Pili, Opa
- Ag variation: Pili, Opa, LPS |
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Does N. gonorrhoeae have a capsule?
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NO
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Clinical presentation of N. gonorrhoeae
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- Purulent discharge
- Salpingitis - Pelvic inflammatory disease - Can spread to skin and joints |
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Treatment for N. gonorrhoeae
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- cephalosporins
- quinolones - difficult to make vaccine because of variation |
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Most common serotypes of N. meningitidis?
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B and C
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Encounter: N. meningitidis
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Asymptomatic carriers in urban centers
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Colonization: N. meningitidis
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non-ciliated upper respiratory epithelium
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Virulence factors: N. meningitidis
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1. Pili + Opa mediated attachment
2. IgA protease 3. Sialated LPS (serum resistance) 4. Phase and Ag variation |
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True or false: there is a vaccination for N. gonorrhoeae
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False.
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Vaccination: N. meningitidis
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for type A, C
not very immunogenic |
