Term
| Oral Anaerobes: Virulence Factors |
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Definition
Lymphocyte Activators: induce inflammatory response
Complement activation/PMN content release: tissue damage |
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Term
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Definition
Oral Infection
Caused by normal flora
Polymicrobic
Form localized abscesses |
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Term
| Oral Anaerobes: Pathogenesis |
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Definition
Chronic Marginal Gingivitis: between teeth and gums
-PMNs/lymphocytes enter CT attached to tooth (inflammation)
-No bacterial invasion
-Can occur in 2 weeks w/o tooth care
Periodontitis: teeth and supp. tissue
-Progressive gingivitis (bone resorption, loss of ligament, loss of entire tooth)
-Bacterial invasion may occur
Acute Necrotizing Ulcerative Gingivitis (Trench Mouth):
-Ulceration of gingiva (bone resportion and tooth loss)
-Bacterial invasion occurs |
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Term
| Oral Anaerobes: Clinical ID |
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Definition
Diagnosis: via Sx
Mixed anaerobes not differentiated
Abscesses may be sampled: must be cultured in anaerobic conditions
-Mostly G(-) rods and PMNs |
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Term
| Actinomyces israelii: Etiology |
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Definition
Oral Infection
Normal flora: colonizes mucosal surfaces (oropharynx to lower intestine)
Endogenous infection: only occurs upon penetration of epithelial barrier (low O2 tension) |
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Term
| Actinomyces israelii: Pathogenesis |
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Definition
Follows mouth trauma:
-Inflammatory sinuses fill with pus and bacteria from initial site of infection
-Slow progressing
Thoracic Actinomycosis: may occur if sinus extension or aspiration occurs
Polymicrobic infection: also GNRs in sinuses |
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Term
| Actinomyces israelii: Clinical ID |
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Definition
Shape: G(+) filamentous rod- looks like fungi
Culture:
-Sulfur granules (yellow granules- diagnostic)
-Anaerobic or microaerophilic
-Slow growth |
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Term
| Viridans Streptococci: Virulence Factors |
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Definition
| Glucans: polysaccharides that permit attachment to teeth |
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Term
| Viridans Streptococci: Etiology |
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Definition
Oral Infection
Normal flora: of oral and nasopharyngeal cavity |
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Term
| Viridans Streptococci: Pathogenesis |
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Definition
Dental Cavities: S.mutans
Subacute Bacterial Endocarditis: tooth extraction leads to transient bacteremia and colonization of damaged heart valves |
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Term
| Viridans Streptococci: Clinical ID |
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Definition
Shape: G(+) cocci
Biochemical:
-Catalase (-)
-No Lancefield group |
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Term
| Candida albicans: Virulence Factors |
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Definition
Adhesion: mannoprotein binds fibronectin receptors
Invasion:
-Invasive hyphae bind fibronectin, collagen, and laminin
-Proteases and elastases |
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Term
| Candida albicans: Etiology |
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Definition
Oral Infection
Predisposing Factors:
-Abx (diminish normal flora)
-Compromised immune system
-Disruption of mucosa (ie. catheter or cancer chemotherapy)
-Diabetes (increased glucose and surface R) |
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Term
| Candida albicans: Pathogenesis |
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Definition
Stomatitis: inflammation of the oral cavity
-Oral Thrush: multiple white plaques loosely adherent to tongue or palate
-Inflammatory patches on esophagus |
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Term
| Candida albicans: Clinical ID |
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Definition
Specimen: scrapings of infected mucosa
-KOH or Gram stain shows budding round yeast with hyphae
-Germ tube formation |
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Term
| Streptococcus pneumoniae: Virulence Factors |
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Definition
Polysaccharide Capsule: primary VF
-Anti-phagocytic
-Prevents complement deposition
-Abs to it confer immunity
Cell Wall TA and PG: inflammation |
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Term
| Streptococcus pneumoniae: Etiology |
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Definition
Ear/Sinus Infection
Predisposition for URTIs:
-High carriage rate
Predisposition for Acute Otitis Media:
-Viral infection
-Allergies
-Infant (short/pliant Eustachian tubes)
Predisposition for Sinusitis:
-Viral Infection
-Allergies
-Anatomical blockage |
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Term
| Streptococcus pneumoniae: Pathogenesis |
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Definition
Acute Otitis Media: middle ear inf.
-Eustachian tube inflammation
-Bacteria enters middle ear from nasopharynx
Sinus Infection: acute and chronic sinusitis in all ages |
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Term
| Streptococcus pneumoniae: Clinical ID |
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Definition
Diagnosis: clinical exam
-OM: swollen tympanic membrane (pus formation)
-S: symptoms and radiography
Needle Aspiration: difficult cases
-OM: pus behind tympanic membrane
-S: sinus wall puncture or catheterization
Shape: G(+) lancet shaped diplococcic
Biochemical:
-No Lancefield group
-Optochin sensitive |
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Term
| Haemophilus influenzae: Virulence Factors |
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Definition
Polysaccharide Capsule: primary VF
-Antiphagocytic
-Antigenic variation
-Polyribitol phosphate capsule with 6 serotypes (a-f)
IgA Protease: colonization
Non-Pilus Adhesins: tissue tropism (direct to mucosal surfaces) |
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Term
| Haemophilus influenzae: Etiology |
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Definition
Ear/Sinus Infection
Normal Flora: high carriage rate in URT
-Most have no capsule (non-typeable)
Predisposing Factors for Otitis Media/Sinusitis:
-Viral infection
-Displacement of flora to sterile sites |
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Term
| Haemophilus influenzae: Pathogenesis |
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Definition
Otitis Media and Sinusitis:
-Most causes of OM are non-typeable (therefore, not affected by Hib vaccine)
-Common in kids under 5
-If caused by Hib, can lead to meningitis |
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Term
| Haemophilus influenzae: Clinical ID |
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Definition
Diagnosis: clinical exam
Needle aspirate: in difficult cases (as above)
Shape: G(-) coccobacillus
Growth: fastidious (needs factor X and V)
Capsular serotyping |
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Term
| Streptococcus pyogenes (GAS): Virulence Factors |
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Definition
Facilitating Immune Evasion:
M protein:
-Anti-phagocytic
-80 different serotypes
-Antigenic variation
Protein G:
-Binds Fc portion IgG Abs
Hyaluronic Acid Capsule:
-Antiphagocytic
Facilitating Colonization:
Protein F:
-Bind nasopharyngeal epithelium
-Regulated by O2 levels
M Protein:
-Binds epidermis (impetigo)
Exotoxins:
SLO: oxygen labile
SLS: oxygen stable
-B-hemolysis
-Form pores in cell membranes
Spe A-C (Erythrogenic/Scarlet Fever Toxins):
-SpeA only produced by some lysogenized GAS
-Superantigens (similar to Staph exotoxins)
-Cytokine release
-Toxic Shock Like Syndrome |
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Term
| Streptococcus pyogenes (GAS): Etiology |
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Definition
Pharynx Infection
Transmission: person to person spread via droplets |
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Term
| Streptococcus pyogenes (GAS): Pathogenesis |
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Definition
Most common bacterial cause of pharyngitis: but usually due to viruses
Scarlet Fever: may occur with pharyngitis (due to Spe)
-Rash (Face trunk and extremities)
-Strawberry tongue
Post-Streptococcal Sequelae:
-Rheumatic Heart Disease (~3 weeks after pharyngitis)
-Acute Glomerulonephritis (more commonly following skin infection) |
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Term
| Streptococcus pyogenes (GAS): Clinical ID |
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Definition
Throat swab of tonsils and pharynx:
-Culture on BAP for B-hemolysis
-Aggulitination test for Lancefield group A (rapid)
Biochemical Tests:
-Catalase (-)
-Bacitracin sensitive
High titers anti-SLO Abs: in patients with rheumatic fever |
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Term
| Corynebacterium diphtheria: Virulence Factors |
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Definition
Diphtheria Toxin: only VF
-AB toxin (polypeptide with nicked chain between A and B)
-B binds EGF precursor on cell membrane
-A is enzymatic subunit (ADP-ribosylates elongation factor 2 to halt translation)
Tox Genes:
-Carried by bacteriophages
-Synthesis negatively regulated by iron (production is on when iron is low, such as in human host) |
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Term
| Corynebacterium diphtheria: Etiology |
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Definition
Pharynx Infection
Rare in US: due to immunization
Only lysogenized strains produce DT: required for pathogenesis (can lysogenize in vivo and convert to toxin producing strain)
Transmission: droplet spread or contact with cutaneous infection/fomite
-Can have asymptomatic carriers of toxinogenic strains |
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Term
| Corynebacterium diphtheria: Pathogenesis |
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Definition
Bacterial Toxinosis with NO invasion:
-DT responsible for ALL pathogenesis
Manifestations of DT Cytotoxicity:
-Pseudomembrane formation (can cause suffocation)
-Systemic manifestations (organ damage to heart and CNS) |
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Term
| Corynebacterium diphtheria: Clinical ID |
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Definition
Diagnosis: based on clinical symptoms
Throat swab: difficult because it is a normal resident flora in many people
Shape: G(+) club shaped rods (remain attached after division-“Chinese Letters”) |
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Term
| Bordetella pertussis (Whooping Cough): Virulence Factors |
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Definition
Filamentous Hemagglutinin (FHA) and Pili:
-Adhesin for binding mucosal epithelial cells
-Directs organism to MØ
-Agglutinates RBCs
Pertussis Toxin (Ptx):
-AB toxin
-B subunit made of 5 non-identical subunits (binding)
-A subunit (enzymatic) ADP-ribosylates Gi, preventing Gs from being turned off (increase cAMP)
Invasive Adenylate Cyclase:
-Enters cell directly to ↑ cAMP
-Requires calmodulin |
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Term
| Bordetella pertussis (Whooping Cough): Etiology |
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Definition
Pharynx Infection
Only infects humans: often seen in infants and preschoolers
Transmission: HIGHLY contagious; droplet spread
-Adults can be carriers and a source of infection for unvaccinated newborns |
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Term
| Bordetella pertussis (Whooping Cough): Pathogenesis |
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Definition
Whooping Cough: acute bronchitis with violent/paroxysmal cough
-Can also cause edema and hemorrhages in the brain
Pathogenesis:
-FHA directs organism to adhere to bronchial epithelium
-Toxins kill ciliated cells and interfere with phagocytosis
-Systemic effects due to TOXIN
-Local inflammatory response to BACTERIA in bronchi leads to cough |
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Term
| Bordetella pertussis (Whooping Cough): Clinical ID |
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Definition
Deep Nasopharyngeal Cultures: needs to be cultured immediately (does not survive well)
Growth:
-CAP with cephalosporins (to inhibit G positive)
Shape: G(-) coccobacillus (resembles H.flu)
Direct fluorescent Ab detection: should still confirm with culture |
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