Term
| How do Intracellular and Extracellular pathogens differentially resist phagocytosis? |
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Definition
Extracellular work prior to phagocytosis (produce exotoxins and utilize capsules and surface proteins)
Intracellular work after phagocytosis (inhibit phag/lysosome fusion, escape and resist killing) |
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Term
| Which organisms produce IgA protease to resist phagocytosis? |
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Definition
These are all extracellular pathogens
1) Neisseria gonorrheae (gonorrhea)
2) Neiserria meningitidis (Meningitis)
3) Hemophilus influenzae (EMOP)
4) Strep pneumo (MOPS) |
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Term
| What are 2 examples of toxins used by extracellular pathogens to resist phagocytosis? |
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Definition
1) Streptolysin O from Strep A
2) Leucocidin (PVL in CA-MRSA abscess) |
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Term
| What are 4 types of anti-phagocytic surface structures? |
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Definition
1) Pili (N. gonorrheae)
2) M Protein (Strep A with antigenic variability for disguise and autoantigenicity)
3) Outer membrane (S. typhi with O antigens that block complement)
4) Capsules (S. pneumo, B. anthracis) |
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Term
| What different types of Capsules are responsible for anti-phagocytosis? |
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Definition
1) Polysacharide
- S. pneumo uses D-glucuronic acid:D-glucose
- Group A strep uses Hyalouronic Acid
2) Polypeptide
- Bacillus anthracis uses poly D-glutamic acid
- Y. pestis |
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Term
True or False
Injection of dead capsulated B with live un-encapsulated A can kill mice? |
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Definition
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Term
| What are the 10 pathogens that have virulence involving capsules? |
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Definition
Some Crazy Students Have Not Bathed Since Passing the Kideny Exam
1) Strep pneumo
2) Cryptococcus neoformans
3) Strep pyogenes
4) H. influenzae b
5) Neisseria meningitidis
6) B. anthracis
7) Salmonella typhi
8) Pseudomonas
9) Klebsiella pneumonia
10) E coli K1 |
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Term
| What are 5 ways by which capsules interfere with phagocytosis? |
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Definition
1) Physical (slipper S. pneumo)
2) Bind inhibitory factors (M protein in GAS binds FH)
3) DON'T bind complement-activating factors (pneumococcal wont by complement activation factor B)
4) Enzymes that block complement (Group B strep has C5-a-protease
5) Produce lots of soluble capsule as decoy |
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Term
| Which Streptococci have lancefield groups? |
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Definition
| A and B with Beta hemolysis. |
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Term
A patient's gram stain comes back with gram-positive, alpha-hemolytic (no blood agar), catalase-negative, facultatively anaerobic organism that has a distinct "Lancet" shape.
WHat is the reservoir/transmission of this bug? |
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Definition
This is Strep. Pneumo
1) Human reservoir (rate of carriage higher in young children)
2) Transmission by respiratory droplets (cough, sneeze) and close contact. |
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Term
A gram stain comes back with gram (+) "lancet-shaped" dipplo and monococci.
What is the pathogenesis of this bug? |
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Definition
Strep. pneumo
1) Colonize with droplets (Ab may prevent, but occurs with COPD and smoking, or with preceding virus)
2) Infection of LR through aspiration and entering bloodstream from pharynx or lung (Deficient AB in case of child<2, elderly and immune deficient).
- Local (respiratory tree) and Systemic (bactermia, meningitis) |
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Term
| What virulence factors are associated with S. pneumo? |
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Definition
Neuraminidase and IgA protease for Transmission
Capsule, LTA and Pneumolysin for Infection
1) Adherence (Neuraminidase cleaves sialic acid to open site)
2) Immune evasion (IgA protease)
After Colonization
3) Inflammation (LTA promotes IL-1 and TNF-a)
4) Immune evasion (Capsule deters phagocytosis)
5) Defense damage (pneumolysin damages bronchi, alveoli and ciliated cells, promoting inflammation and spread) |
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Term
| What is the role of the capsule of S. pneumo in pathogenesis? |
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Definition
Required for virulence
1) Prevents phagocytosis
2) Inhibits alternate complement path
**Immune deficiency of IgG production may increase succeptibility |
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Term
| What are common clinical diseases associated with Respiratory and Disseminated form of S. pneumo? |
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Definition
MOPS (meningitis, otitis, sinusitis, pneumonia)
1) UR includes Otitis, Sinusitis and Conjunctivitis
2) LR includes CA-pneumonia (10-30% mortality in adult series)
3) Bacteremia (from pneumonia in adults)
4) Meningitis (IMMUNIZE) |
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Term
| How does an UR, Trachea/bronchi and Small airways/alveoli S. pneumo infections occur? |
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Definition
1) IgA and cilia protect- IgA protease and capsule attack host (most successful in young, old or immunodeficient)
2) Cough and cilia protect- Hijack viral coinfection to attack after mucociliary escalator is damaged)
3) PMNs and Ig protect by opsonization- Capsule and Pneumolysin avoid phagocytes and cause inflammation |
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Term
A patient presents with Fever, Dyspnea, Chest pain:effusions and Cough.
How do each of these symptoms reflect the underlying S. pneumo pathology? |
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Definition
1) Fever- inflammation from LTA and Pneumolysin
2) Dyspnea- inflammation and cell debris in alveoli disturbs O2 uptake (pneumolysin)
3) Cheat pain: effusion- Lung parenchyma infection leads to inflamed pleural lining
4) Cough- fluid in alveoli and debris in bronchi |
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Term
| How do you treat/prevent S. pneumo infections? |
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Definition
Gram positive with thick cell wall
1) Beta-lactams (B-lactamases are REAL PROBLEM, and PBP alteration is somewhat less of a problem)
2) Immunization-
- Capsular polysaccharide for kids >2
- PCV13/Conjugated vaccine solves problem for young kids
** Conjugated is better for children, but not adults** |
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Term
| What bug is associated with a "spider-like bite" that leads to elevated Liver enzymes and "sunburn-like" rash? |
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Definition
S. aureus!
Encapsulated, gram-positive, catalase-positive, coagulase-positive Cocci in clusters.
Grows golden on chocolate agar |
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Term
A culture on chocolate agar reveals golden clusters of gram-positive bacteria.
What is the reservoir/transmission of this bug? |
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Definition
S. aureus (golden because of anti-oxidant pigment)
1) Humans in warm, moist sites with common carriage (increased by immune suppression, indwelling catheterization or skin disease)
2) Droplet transmission is RARE, but durable on fomites, where it can persist. |
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Term
True or False.
S. aureus is most likely to be transmitted by respiratory droplets than S. pneumo? |
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Definition
False!
The opposite is true!
S. aureus is found on fomites |
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Term
| What are the virulence factors associated with S. aureus. |
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Definition
1) Adherence (Protein A, Clumping factors binding fibrinogen, Collagen BP, Fibronectin BP, Plasmin-sensitive protein promotes binding to nasal epithelial)
2) Exotoxins
- Hemolysins a through y
- Enterotoxins A-J (diffuse immune activation in severe disease)
- Exfoliative epidermolytic toxin A and B (superantigens leading to scalded skin)
- TSST-1
3) LTA/Peptidoglycan
- Capsule less important
- Peptidoglycan anchors for adherence molecules
- LTA for inflammatory cytokine release
4) Resistance
- Altered PBP2A (mecA) in MRSA and TEM class b-lactamase |
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Term
| What exotoxins are associated with S. aureus? |
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Definition
1) Hemolysins a through y (role unclear)
2) Enterotoxins A-J (diffuse immune activation in severe disease)
3) Exfoliative epidermolytic toxin A and B (superantigens leading to scalded skin)
4) TSST-1 |
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Term
| What cell wall components are associated with S. aureus? |
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Definition
1) Capsule less important than S. pneumo
2) Peptidoglycan anchors for adherence molecules
3) LTA for inflammatory cytokine release |
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Term
| What clinical diseases are seen in S. aureus infection? |
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Definition
Remember, Abscess, TSS and Central Venous Catheterization!
1) Skin/Soft tissue
- Abscess*****
- Cellulitis, Osteomyelitis, Myositis, Septic arthritis
2) Disseminated
- TSS******
- Septicemia and Endocarditis
3) Device infections
- Central venous catheterization*****
- Implant and post-surgical |
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Term
| What peculiarities are associated with CA-MRSA infections? |
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Definition
EPIDEMIC
1) Predilection for skin and abscess disease
2) Absense of bacteremia or other invasive manifestation
3) Mild antibiotic resistance compared to HA-MRSA
4) Panton-Valentine leukocidin gene |
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Term
True or False:
TSS presents without bactermia |
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Definition
True!
Remember, it is an INTOXICATION involving local multiplication followed by TSST-1 secretion into bloodstream |
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Term
A patient presents with fever, diffuse rash, hypotension and multi-organ system dysfunction.
What is going on? |
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Definition
TSS- They are in shock with endothelial leakage and organ system failure.
- INTOXICATION involving local multiplication followed by TSST-1 secretion into bloodstream
- TSST-1 is a superantigen that stimulated 20% o f T cells and leads to secretion of TNF-a and IL-2 |
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Term
| Why do Device MRSA infections require special care? |
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Definition
Common b/c S. aureus produces numerous adhesion molecules that predispose for clot formation (Fibrinogen-binding, collagen-binding ect).
1) Propensity for endocarditis
2) Relapse without antibiotics
3) Infected clots and vascular endothelium |
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Term
| How do you treat/prevent S. aureus infections? |
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Definition
1) Resistance is common with altered PBP (mecA from SCC), B-lactamases, Macrolide and FQ resistance.
- Choose by epidemiology (CA-MRSA you want clindamycin)
- Vancomycin, Daptomycin and Linezolid
2) WASH YOUR HANDS |
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