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Flashcards in Bacterial Pharygnitis Deck (23):

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

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

2. Exotoxin Production
Widespread systemic symptoms
Scarlet Fever

3. 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

Binds fibronectin

Bind complement factor H (regulatory factor)
Destabilizing C3b

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
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
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