Week 1 - DAY 1 notes
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- Embden Meyerhof pathway
- most common breakdown pathway of pyruvate to glucose - in fermentation
- Can obligate intracellular organisms make ATP?
- No
- List the virulence factors of bacteria/
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1.Flagella (V. Cholera has one), Ecoli has many, and Shigella has none.
2. Pili - adhesion, (to attach to specific cell lines)
3. Exotoxin
4. Endotoxin
5. Capsule - Capsules are found in g- or g+?
- in both
- Composition of capsule? what is the best way our body deals with encapsulated organisms?
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1.Polysaccharides
2. Antibiodies - Name two tests to visualize capsulated organisms and how they work?
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1. India ink stain: ink does not penetrate bacteria - result transparent halo (used for cyrptococcus)
2.Quellung- Antibiodies cause the capsule to swell with water for visulization - Name the only two bacteria to have endospores and what group are they in? Best way to destroy spores?
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Both are g+
1.Clostridium and Bacillus
2.Autoclave - Name the 7 faculatative intracellular organisms? What is their common mechanism to stay in the cells?
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1. Listeria (the only g+ with endotoxin)
2. Salmonella
3. Yernia (plaque)
4. Francisella
5. Brucella
6. Legionella
7. Mycobacterium
Prevent fusion with the lysosome and escape H2O2 and superoxide radicals - What type of bac release exotoxins? List the classes of exotoxins?
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1. Both g+ (all except listeria) and g-
2.Exotoxins,Neurotoxins,Enterotoxins,Pyrogenic, Tissue invasive exotoxins, misc. - Types of enterotoxins? Typical mechanism?
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1. Infectious diarrhea -active GI infection (e.g E.Coli, C. Jejuni, Shigella dysenteria)
2. Food poisoning - performed toxins by bacteria (e.g B. cereus, Staph aureus)
General Mechanism
1. Inhibit NACL reabsorbtion
2. Activate NACL secretion - Endotoxins is different from exotoxins?
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1. It is part of the cell wall and shed during lysis.
2. Endo is not made of polypeptide like exotoxin (polysaccharide sugar) - What are the 2 polypeptide units of Exotoxins? (p12 Clinical Simple)
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1. Subunit B or H - binding (or holding)
2. Subnit A or L - Action (or laser)
B/H - Key for the gun
A/L - the Gun - Name the major endogenous mediators of sepsis?
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1. TNF(cachexia)
2. IL-1
they activate a host of other cytokines that lead to sepsis : hypotension,vasodilatation, organ dysfunction. - What is the problem with Antibiodies against endotoxin in treating sepsis?
- You need to know the exact bacteria involved-culture takes time
- Note the experiement that showed 'transformation' of bacteria?
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The experiment with smooth and rough encapuslated staph pneumo.
The rough staph were able to pick up the virulent factor from heat killed staph .
By Griffith 1928 - What is the name of viral integrated genome in bacteria? what is the name of the bacteria?
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1. Prophage
2. Lysogenic - What is an example of lysogenic conversion - required to make this bug virulent? (gene transduction of bac by a temperate phage)
- Corynebacterium diphtheria
- What is the DNA structure of plasmids?
- Circular dsDNA
- Name the types of Transduction of bacteria?
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1. Generalized transduction (from lytic phage-no dna incorporation)
2. Specialized transduction (from prophage next to genome of lysogenic bacteria) - What is F+ bacteria? What is Hfr cell? What is their major role?
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1. F+ is a self transmissible plasmid - circular and dsDNA. can carry many genes such as drug resistance
2. Hfr is bascially an F+ incorporated into the bacterial genome.
- it may transfer the entire bac genome
- or it may be excised (and excised with some adjacent bac gene)
3. Conjugation - Describe Strep? list the different group of Strep?
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A. g+cat-
B.
1. Group A beta-hemolytic strep
2. Group B Strep (strep agalactiae)
3. Viridans Strep
4. Group D strep (enterococci -fecalis,faecium, non enterococci-bovis, equinus)
5. Strep pneumoniae (No lancefield antigens) - How many species of strep? how many are pathogenic?
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1. 30
2. 5 are pathogenic (A,B,D,S.pneumonia and Viridans group) - Name two major ways that you can group strep?
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1. Hemolytic abilities
2. Lancefield antigens (C-carbohydrate of cell wall) -
What the Strep strains
Beta hemolytic? (clear-complete)
Alpha hemolytic? (greenish-partial)
Gamma hemolytic? (no hemolysis) -
1. Beta: Group A Strep Pyogenes (bac+)
Group B Strep Agalactiae (bac-)
-test with Bacitracin
2. Alpha: Strep pneumoniae. Quellung+,optochin+, bile+
Viridans strep QL-,Optochin-,bile-
3. Gamma: Enterococcus
Peptostreptococcus (anaerobe) - List the components of S. pyogenes cell wall? Virulent enzymes?
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1. i. C carbohydrate: group A
ii. M protein: Inhibits complement,antigenic
2 i.Streptolysin O: used in ASO titers. O for O2 labile. RBC,WBC killer
ii.Streptolysin S: O2 stable, beta hemolytic, -antegenic
iii. Pyrogenic exotoxin: cause of scarlet fever- only in some strains. - Name the 4 disease by Strep pyogene due to direct effect? Due to Delayed mediated diease?
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1. Strep. pharyngitis, Strep. skin infection, Scarlet fever, Strep. TSS
2. Rheumatic fever, Post-strep glomerulonephritis - Is Strep still penicillin G sensitive?
- Yes
- Describe Scarlet fever?
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1.By some b-hemolytic A strep - due exotoxin.
2.Causes Fever and Scarlet -red rash (spares face)
3.Skin may peel during healing - What are the manifestations of Rheumatic fever? Usu. due to what strep infection?
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i. Fever,
ii. Myocarditis (valves,as well)
iii.Joint swelling (acute polymigratory arthritis)
iv.Chorea,
v.Subcutaneous nodules (rubbery underskin)
vi.Erythema Marginatum (red margin that spreads out)
2. Untreated Pharyngitis (no strep skin infec.) - Cause of post-strep glomerulonephritis?
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1.Strep infec. of Pharynx or Skin
2. Type II (complex deposit in kidney-activates complement) -
How many % of women carry S.agalactiae (group B) in their vagina?
Complication to fetus by S. agalactiae? -
1. 25%
2. Neo-natal meningitis - presents atypically - Vomiting, irritable, poor feeding, fever
(lumbar puncture and treat) - Name the three main bugs for meningitis of neonates<3months?
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1. S.agalactiae
2. E. Coli
3. Listeria - List the 3 major pathology of Strep Viridans group?
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1. Dental infection: S.mutans
2. Endocarditis: Subacute endocarditis-Strep viridans
3. Abscesses: S. Intermedius (if in blood immediately asses for abscess) - Major cause of Subacute endocarditis?
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1. Strep Viridans
2. Group D Enterococci (faecalis, faecium) - What is a major problem with Enterococus (group D strep)?
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1.Resistance to Drugs
2. Now Resistant to Ampicillin,Vancomycin(VRE)
1st treat with Amp + Aminoglycoside, then Vancomycin, then pristinomycin
(can't use Vanco alot inorder to reduce the chances of Staph aureus resistance) - Growth requirement for Enterococcus?non Enterococcus?
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1. 40% bile or 6.5%NaCl (entero)
2. 40%bile (non-entero) - Most common cause of Otitis media in children? Most common cause of meningitis in Adults?
- Streptococcus Pneumoniae
- What are Strep Pneumonia becoming resistant to? Treatment and prevention?
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1. Penicillins (mainly intermediate resistance (10%US))
2. Vaccine - Pneumovax
Treat with high doses of penicillin and cephalosporins. - How is catalase tested?
- Add H2O2 and see if O2 (bubbles) are produced. (All Staph are Cat+, all strep are Cat-)
- Name the 3major Staph? Tests to distinguish the groups?
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1. Staph Aureus -Cat+ Coag+
2. Staph Saprophyticus - Cat+ Coag-
3.Staph epidermis - Cat+ Coag -
Coag+ in aureus - coagulates blood by activating Pro-thrombin - What are the virulence factors Staph aureus?
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1. Protein A (binds Fc of IgG)prevents opsoniation
2. Coagulase: fibrin to protect Staph
3. Hemolysins (alpha,beta,gamma,delta) and Leukolydins to kill RBC and WBC
4. Penicillinase - Problem with treating Staph?
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1.penicillinase resistant.
2.Some strains are becoming methicillin resistance Staph aureus - MRSA - What are Staph aureus tissue destroying proteins?
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1. Hyalondinase: breaksdown proteoglycan
2. Lipase
3. Staphylokinase: lyses fibrin - Name the 3 Toxins of Staph aureus?
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1. Exfoliatin: Scalded Skin Syndrome
2. Enterotoxin: food poisoning
3. TSST1 - Name the clinical diesases caused by staph aureus due to its direct invasion?
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1. Pneumonia - Rare - but the causes lobar pneumonia, destruction of lung parenchyma
2. Meningitis
3. Osteomyelitis(in Boys<12)
4. Septic arthritis (PMN>100,000,g+)
5. Bacteremia/Sepsis
6. UTI
7. Skin infection: best buddy Strep Pyogenes cause very similar (treat with dicloxacillin to cover both) - How do you treat MRSA strains? methicillin resistant staph aureus
- Vancomycin
- Why is Stap epidermis - so pathogenic in prosthetic materials?
- Because its polysaccharide capsule very adhere to these devices (catheters, prosthetic valves, joints)
- Treatment of Stap. epidermis?
- Vancomycin. resistant to multiple drugs.
- All the Staph are facultative anaerobes T/F?
- True
- Staph Saprophyticus is clinical significant in? Treat with?
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1.UTI of sexually active women.
2.Surprisingly with Penicillin - What are the two spore forming g+ rods?
- 1.Bacillus and Clostridium
- What are the manifestations of Anthrax infection?
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1. Skin Anthrax infection: can lead to death - exotoxin causes necrosis. Painless lesion is black with rim of edema
2. Lung Anthrax infec: Woolsorter's disease. Exotoxin damages
3. GI anthrax: rare - lead to vomiting,bloody diarrhea, abdominal pain - The Anthrax exotoxins is made of?
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1. Action factor: Edema factor - extracellular adenylyl cyclase. Taken up by PMN and Macrophage. Increase CAMP and deactivates these cells
2. Binding factor: Protective antigen (PA) promotes entry of Edema factor
3. Lethal factor: destroy macrophages- func. not really well known. - How B. cereus different from B.anthracis?
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B. Cereus is
1. Motile, non-encapsulated and resistant to penicillin - What is the unique Anthrax capusule made of?
- Polymer gamma-D-glutamic = anti-phagocytic
- What is the most common clinical manifestation of anthrax?
- 95% cutaneous
- Treatment?
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1. Penicillin G, Vanco
. Vaccine (of PA antigen) - What are toxin types of B. Cereus?
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1. Heat labile (like e-coli, V. cholera)
2. Heat Stable (Staph aureus like food poisoning) - What is the treatment of food poisoning of B. cereus?
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Be serious - no treatment because its pre-formed.
For the bacteria- its is penicillin resistant- So
1.Vancomycin
2.Clindamycin - The various diseases caused by the Clostridium family?
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1. Tetanus - C.tetani
2. Botulism- C.botulinum
3. Gas gangrene -C.perfringens
4. Pseudomembranous colitis-C.Difficle - Are all Clostridium motile?
- Yes except for C. Perfrigens is non-motilie
- Action of the tetanus toxin? Botulism toxin? Alpha toxin? Toxin A and B
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1. Tetanus toxin inhibits the release of inhibitory NT - Glycine and GABA
2. Botulism toxin binds and inhibits Ach receptor
3. Alpha toxin of C. perfrigens - splits lecithinase into phosphocholine and diglyceride.
4. Toxin A causes diarrhea and toxin B is cytotoxic to colonic cells - these are the toxins of C.Difficle - Treatment of C.difficle?
- Metronidazole and Vancomycin
- Is Impetigo infectious? usual location in body?
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1.Yes - it is very contagious
2. Face
3.Strep pyogenes -
1.Is Corynebacterium diptheria motile? Catlase +?
2. What are the major organs affected by C. diptheria? -
1.non-motile and catalase +
2. Heart and CNS - 1.What are the major exotoxins of C. diptheria (g+cat+ rod)?
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1. 2 subunits
Binding unit: entry into neural and cardiac cells
Action unit: EF-2 inhibitor- inhibiting protein synthesis. - How do you clinically identify C.diptheria?
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1. Child with fever and sore throat
2. Pseudomembranous layer - grayish color on pharynx
3. Myocarditis(10%)
4. Neural - peripheral nerve palsies and Guillian Barre like syndrome - How do you culture C. diptheria?
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1.Tellurite potassium agar (get dark black colonies)
2. Loffler's medium: stain with methylene blue -Reddish granules - What are the charateristics of Listeria Monocytogenes?
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1. g+, H,O(streptolysin),
2. Motile (tumbling in 20oC)
3. Facultative intracellular parasite (best in Macrophages of neonates and immunocomprismed patients) - you need you cell mediated immunity to kill these guys
4. Facultative anaerobe - Where can we get listeria monocytogenes infection from?
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1. Unpasturized milk or cheese
2. Vaginal canal (during birth) - What is complication of meningococcemia?
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Life threatening - Septic shock
Waterhouse-Fredrichsen Syndrome
1.Bilateral hemorrhage into adrenal glands - drop in BP,tachycardia
2. Rapidly enlarging Petechiae
3. DIC
4. Death (6-8hrs) - Who has the capsule Gonococcus or Meningococcus? What are the properties of the capsule
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1. Neisseria Meningitidis
2. Polysaccharide capsule (K),antigenic, 9serotypes but just A,B,C cause Meningitis - What are other virulent factors of N. meningitidis other than K antigen -capsule?
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1. Endotoxin -LPS cause blood vessel destruction
2.IgA1 protease
3. Extracts Iron from transferrin - Who are high risk for N. Meningitidis?
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1. Babies (6mths - 2yrs)
2. Army Recruits
A. normal pop. asymmptomatic N.meningitidis in nasopharynx of carriers= 5%
B. In Army recruits - 40% in that population with varing serotypes - the camp makes the recruits immune weakened.
C. Babies within that age dont have IgG2 for capsulated organisms yet. - A bulging open anterior fontanelle may be a sign of ------- in neonates?
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Meningitis
(babies have atypical presentation- vomiting, irritable, poor feeding) - In older kids with meningococcemia meningitis - what signs can you illict?
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1. Kernig sign
2. Brudzinski's sign - The Thayer Mayer VCN agar is for what organisms? What does VCN stand for?
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1.Chocolate agar(heated agar) to culture Neisseria Meningitidis and Gonorrhea
2.
V-Vancomycin
C-Colistin
N-Nystatin - Complication of Gonorrhea infection?
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1.Women- PID: salpingitis, endometritis, oophoritis.
a. Ectopic pregnancy due to scarring for the falopian tube
b. Abcesses
c. peritonities
2.Urethral discharge
3. Gonococcal Bacteremia
4. Septic Arthritis
5. Opthalmia neonatorum (infants) - To treat against ocular infection of gonorrhea and chlamydia during birth- what are all babies treated with?
- Erythromycin drops
- Treatment of gonorrhea?
- Ceftriaxone