Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
43 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
What is associated with?
-Chronic Marginal Gingivitis -Periodontitis -Acute Necrotizing Ulcerative Ging. |
Oral Anerobes
- Infections by normal flora - Polymicrobic Chronic Marginal Gingivitis - Infiltration of CT around teeth - No invasion, only in plaque Periodontitis - Bone resorption due to gingivitis - Invasion possible Acute Necrotizing Ulcerative Ging. - Prevotella, Fusobacterium - Ulceration of gingiva, bone |
|
|
|
What virulence factor is associated with oral anaerobes?
|
inflammation via lymphocyte activators
- Bugs live in plaque |
|
|
|
Oral anaerobe that grows in lymphatics and can drain into thorasic cavity, due to trama such as tooth extraction
Also can be found in intestines. |
Actinomyces israelii
- Normal flora- in GI & resp. mucosa |
|
|
|
Gram (+) rods, filamentous (like fungi)
Sulfur granules- dead cells & Ai Culture pus -slow growing Anerobic/Microaerophilic |
Actinomyces israelii
- Normal flora- in GI & resp. mucosa |
|
|
|
Gram (+) cocci
Catalase (-) Non-lancefield grouped Subacute bacterial endocarditis - Following tooth extraction if damage to heart valve |
Viridans Streptococci
Multiple strains Normal flora - S. mutans ->dental caries NOT Strep pyogenes bc ->G(+) cocci in chains ->rapid aggultination test to id Lancefield Group A -> Catalase (-) -> Bacitracin senstive -> NOT assoc with tooth extraction but with pharyngitis |
|
|
|
Virulence factor for Viridans Streptococci
|
Glucans (complex polysaccharide) permit attachment to teeth
hint: very gooey very = viridans gooey = glucans |
very gooey
|
|
|
Why would a pt develop oral thrush?
|
- Stomatitis
->Oral Thrush, espohagitis - Immunocompromised (leucopenia, corticosteroids, oral inhalers, AIDS, cancer chemotherapy) - Diabetes - inc surface receptors for CA with macrophages -abx txmt ->depresses competing bacterial flora |
|
|
|
virulence factors for Candida albicans?
|
Adhesins- mannoprotein to fibronectin
Invasive hyphae Proteases and elastases |
|
|
|
How is Candida Albican identified clinically?
|
-Specimen collection: Scrapings from infected mucosa
-B. KOH or Gram stains reveal budding round or oval yeast cells with hyphae -C. Germ tube formation can be used to speciate C. albicans |
|
|
|
Major virulence factors for S. pnuemo relevant to ear and sinus infection?
|
Polysaccharide capsule (84 capsular serotypes)
->most imp 1. Primary virulence factor of S. pneumoniae 2. Interferes with classical and alternate complement pathways 3. Anti-capsule antibodies confer immunity Cell wall teichoic acid and peptidoglycan contribute to inflammatory response In LRT infections, strep pneumo key virulence factors are polysac capsule & PNEUMOLYSIN, related to SLO, a hemolysin |
|
|
|
Gram (+) diplococci
Lancet shaped Catalase (-) Optochin susceptibility & Bile solubility |
Streptococcus pneumoniae
(Pneumococcus/Diplococcus) Hint: out (optochin senst) to build (bile senst) a lanct statue |
out to build a lanct statue
|
|
|
What organism can secondarily cause meningitis?
|
Haemophilus Influenzae
(Upper & Middle RT Infections) Meningitis- 2 -> to RT infection |
|
|
|
Gram (-) coccobacills, very small
Chocolate agar, NOT blood agar Satillite Growth around discs of (or in chocolate agar: - Hematin/X Factor - NAD/V Factor Associated with: Acute Otitis Media Sinus Infection Meningitis |
Haemophilus Influenzae
(Upper & Middle RT Infections) |
|
|
|
Virulence factors for Haemophilus Influenzae
|
- Polysaccharide capsule
-> Serotype b = most virulent -> Polyribitol Phosphate capsule - Hib vaccine - IgA protease - Adhesins specific to mucosa hint: hat (haemophilus) is like a (IgA protease & adhesns )cap (capsule - polysaccharide) |
hat is like a cap
|
|
|
Gram (-) coccobacillary
Oropharynx flora Occasional pathogen |
Moraxella catarrhalis
|
|
|
|
What Streptococcus pyogenes
(Group A Strep/ B Hemolytic Strep) virulence factor is associated with: 1. anti-phagocytic and anti-opsonic -Exposed amino terminus antigenically variable⇒ >80 serotypes 2. Re-infection with different M type possible due to antigenic variation (IMP)** 3. Cross-reactive antibodies ⇒ to acute glomerulonephritis & rheumatic heart disease |
M protein
hint: fires (pyro) are monsters (protein M) |
fires are monsters
|
|
|
What Streptococcus pyogenes (Group A Strep/ B Hemolytic Strep) virulence factor is associated with binding to nasopharyngeal epithelium (pharyngitis); regulated by 02 levels?
|
Protien F
|
in a fine bind
|
|
|
What Streptococcus pyogenes (Group A Strep/ B Hemolytic Strep) virulence factor is associated with binds the Fc portion of antibodies, covers bacteria with antibodies?
|
Protein G
-a factor that facilitates colonization hint: G looks like C in Fc |
looks like C in Fc
|
|
|
What virulence factor associated with S. pyongens is controlled by lysogeny?
|
Streptococcal Pyrogenic Exotoxins (Spe A-C)
a. Erythrogenic or Scarlet Fever Toxins b. SpeA produced only by minority of lysogenized Group A Streptococcus |
|
|
|
What virulence factor associated with S. pyogens acts as a superantigen?
|
Streptococcal Pyrogenic Exotoxins (Spe A-C)
-Superantigens with sequence homology to staphylococcal exotoxins hint: an eccentric superstar on fire superantigen = strep pyrogenic exotoxin Spec A-C |
an eccentric superstar on fire
|
|
|
What virulence factor S. pyogenes is associated with:
- Induce cytokine release - Fever & rash (scarlet fever) - T-cell stimulation and B cell suppression - Enhanced sensitivity to endotoxic shock |
Streptococcal Pyrogenic Exotoxins (Spe A-C)
hint: fever = fire (pyrogenic) |
fever = fire
|
|
|
What virulence factor associated with S. pyogenes
1. Cause 02-labile or 02 stable β-hemolysis on blood agar plates 2. Form large pores in cell membranes⇒ lysis of leukocytes |
SLO & SLS (exotoxins)
Cause 02-labile (SLO) or 02 stable (SLS) β-hemolysis on blood agar plates |
|
|
|
What is lysogeny?
|
When a bacterial phage carry bacterial genome, integrate it into host chromosome where then toxin is produced
-associated with corynebacterium diphtheriae |
|
|
|
Disease, bug & virulence factor?
rash spreads from mouth & face to trunk & extremities; strawberry tongue |
Scarlet Fever can occur simultaneously with pharyngitis
Caused by pyrogenic exotoxins (Spe), a virulence factor of S. pyogenes |
|
|
|
Most common bacterial cause of pharyngigtis?
|
Group A S. pyogens
|
|
|
|
Disease and bug?
Associated with: Aschoff body Symptoms: fever, subcutaneous nodules, chorea (neurologic), migratory polyarthritis Cardiac: carditis, cardiac enlargement, murmurs, heart failure |
Poststreptococcal Sequelae: Acute Rheumatic Fever
S. Pyogenes |
|
|
|
How is Heart damage developed from S. pyogens?
|
Heart damage caused by anti-streptococcal antibodies that cross-react with cardiac tissue (Strep pyogenes)
1. Anti-streptococcal antibodies are to cell wall, cell membrane, and M protein 2. Epitopes shared with cardiac sarcolemma membranes, smooth muscle cells, valves 3. Recurrent attacks with new M types leads to progressive heart damage 4. SLO, Spe, streptokinase may contribute directly to cardiac damage |
|
|
|
What infection associated with S. pyogens is more likely to be associated with Subacute bacterial endocarditis?
|
respiratory -> pharyngitis -> 3 weeks later post strep sequelae = Acute rheumatic fever
|
|
|
|
What infection associated with S. pyogens is more likely to be associated with deposition of antigen-antibody and complement complexes in glomeruli contribute?
|
Acute Glomerulonephritis
1. Follows skin infection with group A streptococcus 2. Syndrome: - 10 day latent period following infection - Edema, hypertension, proliferative lesion of glomeruli 3. Associated with a few M types (nephritogenic strains) 4. Antibody cross-reactivity and inflammatory response - Anti-M protein antibodies react with glomerular proteins -Deposition of antigen-antibody and complement complexes in glomeruli contribute |
|
|
|
- Gram (+) cocci in chains
- B hemolytic Dx - Catalase (-) - Lancefield classification: Group A Culture - SLO needs CO2 Serologic (Clinical dx) tests: - inc ags. to SLO - Bacitracin sensitive |
Streptococcus pyogenes
also known as: Group A Strep or B - Hemolytic Strep |
|
|
|
anti-SLO antibodies (ASO) is seen in pt with what disease?
|
rheumatic fever - strep pyognes
hint: fires lyse, meaning pyrogens (fire) associated with SLO (streptolysin O) which forms pores to lyse leukocytes |
fires lyse
|
|
|
Bug and virulence factor?
ADP-ribosylates elongation factor 2 (ADPR-EF2) of any eucaryotic cell |
Corynebacterium diphtheria
Diptheria Toxin - B subunit- binding ->endocytosis - A subunit- enzymatic (like pseudomon) - Released by redn. in vesicle - ADP ribosylation of EF2 -> stops ribosome translocation - tox gene carried by bacteriophages -> lysogenic conversion - Iron inhibits toxin exp. - low Fe in host -> toxin expression |
|
|
|
Gram (+), club shaped rods
-> “chinese letter” Toxin produced in culture |
Corynebacterium diptheriae
hint: chinese dip |
chinese dip
|
|
|
What is the genetics of C. Dyptheria and how is it regulated?
|
tox gene carried by bacteriophages β and ϖ
DT synthesis negatively regulated by iron note: once Diptheria toxin gene enters bacteria with help of phage, it goes through lytic or lysogenic cycle to either produce multiple progeny toxin gene and lyse cell or become integrated into host genome to produce diphtheria toxin |
|
|
|
What organism is used to develop toxin chimeras directed against tumor cell and HIV-infected cells?
|
C. diphtheria
Diptheria Toxin subunit A |
|
|
|
Name of virulence factor and associated bug?
-Adhesin for binding to ciliated mucosal epithelial cells - directs to macrophages - can agglutinate erythrocytes |
Filamentous Hemagglutinin (Fha) and Pili
Bordetella pertussis Whooping Cough hint: filmsy board needs a tack |
filmsy board needs a tack
|
|
|
What is the virulence factor and associated bug?
Enzymatic subunit ADP-ribosylates Gi protein |
Pertussis Toxin (Ptx) is the major virulence factor of B. pertussis
Enzymatic subunit ADP-ribosylates Gi protein -Renders cells unable to cease production of adenylate cyclase - ↑Adenylate cyclase levels in cells⇒ ↑cAMP levels⇒ physiologic effects on cells |
|
|
|
What virulence factor of Bordetella pertussis causes the following effects:
1. Enters cells and directly stimulates cAMP production 2. Requires mammalian cell calmodulin (Ca++-binding protein) for activation 3. Net effect: Interference with chemotaxis & superoxide production by PMNs |
Invasive Adenylate Cyclase
|
|
|
|
How is virulence factors of Bordetella pertussis regulated?
|
Signal Transduction Regulation
1. Signal or Temp (37C) - BvgS phosphorylates BvgA via histadine kinase 2. BvgA= transcriptional activator - Pili and Fha expression FIRST - adherence to cilliated epithelium - Ptx & Invasive Adenylate cyclase SECOND Allows delay of triggering immune response so infection can take hold before toxins are produceds -> Key: Is the 2 step process of sensory and activation**** hint: temp stimulates before activates, inc temp to 37C or ion change causes BvgS to activate BvgA which then activates trascription of Fha and Pilli and later Ptx and Inv AC |
temp stimulates before activates
|
|
|
Gram (-) coccobacillus, small
Culture - Charcoal BAP + cephalosporins (inh. Gram (+)’s) - Slow growth |
Bordetella pertussis
|
charcoal BaP
|
|
|
Disease and bug?
-paroxysmal (sudden / violent) cough - Disease seen most in infants and preschoolers -only infects the human respiratory tract -highly contagious, spread by droplet -Immunized individuals have mild symptoms - Adult carriers can be source of infection of newborns -May cause edema and hemorrhages in brain |
Pertussis/Whooping Cough
Bordetella pertussis |
|
|
|
What is the pathogenesis of B. pertussis?
|
1. Fha directs B. pertussis to adhere to bronchial epithelium
2. AB Toxins kill ciliated cells and interfere with phagocytosis 3. Systemic effects due to toxin, not bacteria 4. Local inflammatory response to bacteria in bronchi leads to cough hint: Filimsy (Fha) board (bordetella) need to be tacked (ab toxin) down |
Filimsy board need to be tacked down
|
|
|
What 2 lab tests should be done to clinically ID B. pertussis?
|
Direct fluorescent antibody detection is available but should be confirmed by culture
|
|
