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81 Cards in this Set

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Embden Meyerhof pathway
most common breakdown pathway of pyruvate to glucose - in fermentation
Can obligate intracellular organisms make ATP?
List the virulence factors of bacteria/
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?
2. Antibiodies
Name two tests to visualize capsulated organisms and how they work?
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?
Both are g+
1.Clostridium and Bacillus
Name the 7 faculatative intracellular organisms? What is their common mechanism to stay in the cells?
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?
1. Both g+ (all except listeria) and g-
2.Exotoxins,Neurotoxins,Enterotoxins,Pyrogenic, Tissue invasive exotoxins, misc.
Types of enterotoxins? Typical mechanism?
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?
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)
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?
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?
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?
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?
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?
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?
A. g+cat-
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?
1. 30
2. 5 are pathogenic (A,B,D,S.pneumonia and Viridans group)
Name two major ways that you can group strep?
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?
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?
1. Strep. pharyngitis, Strep. skin infection, Scarlet fever, Strep. TSS
2. Rheumatic fever, Post-strep glomerulonephritis
Mom my throats, my skin is disintegrating and my urine is tea-colored
Is Strep still penicillin G sensitive?
Describe Scarlet fever?
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?
i. Fever,
ii. Myocarditis (valves,as well)
iii.Joint swelling (acute polymigratory arthritis)
v.Subcutaneous nodules (rubbery underskin)
vi.Erythema Marginatum (red margin that spreads out)

2. Untreated Pharyngitis (no strep skin infec.)
Fig 4-3.
John travolta with joint,heart,chorea arms)
Cause of post-strep glomerulonephritis?
1.Strep infec. of Pharynx or Skin
2. Type II (complex deposit in kidney-activates complement)
Mom my urine in Tea colored (hematouria)
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?
1. S.agalactiae
2. E. Coli
3. Listeria
List the 3 major pathology of Strep Viridans group?
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?
1. Strep Viridans
2. Group D Enterococci (faecalis, faecium)
What is a major problem with Enterococus (group D strep)?
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?
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?
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?
1. Staph Aureus -Cat+ Coag+
2. Staph Saprophyticus - Cat+ Coag-
3.Staph epidermis - Cat+ Coag -

Coag+ in aureus - coagulates blood by activating Pro-thrombin
Staff with gold medal with cats around
What are the virulence factors Staph aureus?
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
What are Strep Pneumonia becoming resistant to? Treatment and prevention?
1. Penicillins (mainly intermediate resistance (10%US))
2. Vaccine - Pneumovax

Treat with high doses of penicillin and cephalosporins.
Problem with treating Staph?
1.penicillinase resistant.
2.Some strains are becoming methicillin resistance Staph aureus - MRSA
What are Staph aureus tissue destroying proteins?
1. Hyalondinase: breaksdown proteoglycan
2. Lipase
3. Staphylokinase: lyses fibrin
Name the 3 Toxins of Staph aureus?
1. Exfoliatin: Scalded Skin Syndrome
2. Enterotoxin: food poisoning
3. TSST1
Name the clinical diesases caused by staph aureus due to its direct invasion?
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
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?
Staph Saprophyticus is clinical significant in? Treat with?
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?
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?
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?
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
1. Penicillin G, Vanco
. Vaccine (of PA antigen)
What are toxin types of B. Cereus?
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?
Be serious - no treatment because its pre-formed.
For the bacteria- its is penicillin resistant- So
The various diseases caused by the Clostridium family?
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
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?
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)?
1. 2 subunits
Binding unit: entry into neural and cardiac cells
Action unit: EF-2 inhibitor- inhibiting protein synthesis.
The Human Antibiotic (similar to the action of tetracycline on bacteria)
How do you clinically identify C.diptheria?
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?
1.Tellurite potassium agar (get dark black colonies)
2. Loffler's medium: stain with methylene blue -Reddish granules
For C.diptheria - Be sure to TELlur INtern and don't LOaf arround
What are the charateristics of Listeria Monocytogenes?
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?
1. Unpasturized milk or cheese
2. Vaginal canal (during birth)
What is complication of meningococcemia?
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
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?
1. Endotoxin -LPS cause blood vessel destruction
2.IgA1 protease
3. Extracts Iron from transferrin
Who are high risk for N. Meningitidis?
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?
(babies have atypical presentation- vomiting, irritable, poor feeding)
In older kids with meningococcemia meningitis - what signs can you illict?
1. Kernig sign
2. Brudzinski's sign
The Thayer Mayer VCN agar is for what organisms? What does VCN stand for?
1.Chocolate agar(heated agar) to culture Neisseria Meningitidis and Gonorrhea
Complication of Gonorrhea infection?
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?