Bacterial Pharygnitis Flashcards
Infectious Pharyngitis
Pharyngitis: inflammation of the oropharynx
Symptoms: sore throat, fever, malaise and pain on swallowing
~30% of cases are caused by bacteria Streptococcus pyogenes (group A ß-hemolytic) = up to 30% Corynebacterium diphtheriae Haemophilus influenzae (type B) Neisseria gonorrhoeae
Streptococcus Species
Background:
Diverse collection Gram-positive cocci
Most are facultative anaerobes
Catalase negative
Ubiquitous organism
Produce many virulence factors: adhesins and toxins
Complex Classification System
Streptococcus species: 1st Level of Classification
1st level: hemolysis pattern; able to RBC or not; can also lyse other cells as well
Agar plate with RBCs and put bacteria on it
Complete lysis: beta hemolytic; yellow color/halo because light coming through agar plate from RBC lysis
Partial lysis: alpha; not as efficient with small yellow coloration halo
Streptococcus species: 2nd Level of Classification
Group structure: 2nd level
Serological properties: amount an immune response to
Lancefield carbohydrate present; if you can measure Ab present; Lancefield groupings (A thru U)
Streptococcus species: Classification System
1st Level
hemolytic patterns
Complete (β), Partial (α) or none (γ)
2nd Level (Group Determination) Serologic properties: Lancefield groupings (A thru U)
3rd Level (Speciation) DNA sequence similarity
Streptococcus Pyogenes
Pharyngitis, impetigo, necrotizing fasciitis, rheumatic fever, glomerulonephritis
Habit: Throat, Skin
Group A beta hemolytic strep
Mechanism of spread: Person-to-Person by aerosol
Streptococcus Pyogenes: 3 Mechanisms of Disease
3 Mechanisms of disease
1. Pyogenic Inflammation
Induced locally at the site of infection
Pharyngitis
- Exotoxin Production
Widespread systemic symptoms
Scarlet Fever - Immunologic
Ab against organism cross-react with host tissue
Rheumatic Fever (Rheumatic carditis, joints, skin, spinal cord, brain)
2-3 weeks after Streptococcus infection
Suppurative vs. Non-suppurative vs. Toxin Mediated Diseases
The suppurative diseases are caused by direct damage by the organism and the secreted enzymes of GAS.
The nonsuppurative sequelae of GAS infection are late manifestations caused by a self-directed immune response.
The toxin-mediated diseases are caused by streptococcal extotoxins that are secreted into the bloodstream.
Suppurative, Non-Suppurative, and Exotoxin Mediated Diseases
Suppurative Diseases: otitis, meningitis, sinusitis, pharyngitis, tonilitis, adenitis, pneumonia, necrotizing fasciitis, osteomyelitis, septic arthritis
Non-Suppurative Diseases: carditis, chorea, polyarthritis, subcutaneous nodules, and erythema marginatum (acute rheumatic fever); also acute post streptococcal glomerulonephritis
Exotoxin Mediated Diseases: scarlet fever and toxic shock syndrome
S. Pyogenes: hyaluronidase, streptokinase, and Dnase
Hyaluronidase: degrades hyaluronic acid (ground substance of subcutaneous tissue)
Streptokinase: activates plasminogen to form plasmin (dissolves fibrin clots)
Dnase: degrades DNA in necrotic tissue and pus
*All help infection spread
S. Pyogenes: Lipoteichoic Acid, Protein F, M Protein, and Capsule
Lipoteichoic Acid: binds fibronectin
Protein F: binds fibronectin
M Protein: adhesion and inhibits phagocytosis (attachment and growth)
*All help with attachment
Capsule: inhibits phagocytosis and promotes growth
S. Pyogenes: Streptolysin O and S, Pyrogenic Exotoxins, and Exotoxin B
Streptolysin O: oxygen labile hemolysin; antigenic ASO titer
Streptolysin S: oxygen stabile hemolysin: non-antigenic
Pyrogenic Exotoxins A, B, and C: superantigen; toxic shock syndrome and scarlet fever
Exotoxin B: destroys tissue (cysteine protease); necrotizing fascitis
S. Pyogenes: M Protein
Adhesin
Binds fibronectin
Antiphagocytic
Bind complement factor H (regulatory factor)
Destabilizing C3b
Antigenic
Anti-M Protein Ab are protective
>80 antigenic types of M Proteins
Complement factor H: prevents our cells from complement protein attachment so does not undergo lysis
Immune response to M proteins: reinfection is likely due to a strain with a different protein M structure
S. Pyogenes: Pharyngitis Clinical Presentation
Clinical Presentation 20% are asymptomatic Sore throat Exudate and Inflammation Fever Tender cervical lymph nodes
S. Pyogenes: Pharyngitis Dx
Diagnosis (3 part)
1. Throat Culture on Blood Agar - beta hemolytic
2. Gram-Stain
3. Rapid Antigen Detection Test (Rapid Strep Test)
Detects Group A carbohydrate antigen
60-90% sensitive 98-99% specific
Swab patient’s throat and put into lysis solution with Ab; Ab recognize Lancefield carbohydrate only present in strep pyogenes; put in strip that have Ab on it, and they recognize group A carbohydrate; that gives you the positive dye line
S. Pyogenes: Scarlet Fever
Caused by Pyrogenic toxin= superantigen
“Strawberry tongue”
Rash - sand paper like
12-48 hours after fever
Usually starts on Chest
Fades in 3-4 days then skin peals
S. Pyogenes: Rheumatic Fever
Serious post-infection sequela: rare in the US
Antibodies that cross-react to heart tissue antigens (Anti M-protein Ab): class I M Proteins
Onset 2-3 weeks after infection
Symptoms: fever, malaise, migratory poly-arthritis
Cardiac sequelae: inflammation of heart tissue and thickened and deformed valves
Reactivate by subsequent S. pyogenes infections
S. Pyogenes: Host Defense, Prevention, and Tx
Host Defense Phagocytosis polymorphonuclear leukocytes Opsonizing antibody M Protein specific
Prevention: no available vaccine
Treatment: penicillin
Corynebacterium diphtheriae
Gram-positive rod: club shaped
Non-spore forming (only gram positives have this capability)
Asymptomatic carriers
Humans are the only host transmitted via aerosol
Infection in throat
Causes diphtheria
Corynebacterium diphtheriae: Pathogenesis
Diphtheria Toxin: Inhibits protein synthesis Encoded by phage Systemic spread Very Potent Very Stabile
AB toxin associate with receptor on cell and are endocytosed
A adds a sugar to EF2 (protein synthesis factor) and shuts down protein synthesis in eukaryotic cell (our cells)
B binding portion, and A is active
Corynebacterium diphtheriae: Host Response and Clinical Findings
Host Response:
Anti-toxin AB - block receptor binding and local Inflammation
Clinical Findings: thick grey “pseudomembrane” over tonsils and throat
Pseudomembrane can extend onto the larynx and trachea causing airway obstruction; made of dead cells and bacteria
Corynebacterium diphtheriae: Lab Dx and Tx
Laboratory Diagnosis:
Throat culture - 3-4 days for growth
PCR for toxin gene
PCR =Polymerase chain reaction - only takes 2 hours
Treatment: penicillin and antitoxin (horse Ab), which binds toxin and prevents binding to eukaryotic cell; must give both
Corynebacterium diphtheriae: Prevention
Prevention: diphtheria toxoid vaccine
Toxin is treated with formaldehyde to generate toxoid vaccine
Vaccine given at 2,4, and 6 months of age with boosters at 1 and 6 yrs of age. After that, it is recommended every ten years
Non-active form of toxin, but looks similar to it; body will take care of bacteria, but ultimately you need to inactivate toxin to survive
