Bacterial Pharygnitis Flashcards

1
Q

Infectious Pharyngitis

A

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
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2
Q

Streptococcus Species

A

Background:
Diverse collection Gram-positive cocci
Most are facultative anaerobes
Catalase negative

Ubiquitous organism

Produce many virulence factors: adhesins and toxins

Complex Classification System

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3
Q

Streptococcus species: 1st Level of Classification

A

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

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4
Q

Streptococcus species: 2nd Level of Classification

A

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)

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5
Q

Streptococcus species: Classification System

A

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
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6
Q

Streptococcus Pyogenes

A

Pharyngitis, impetigo, necrotizing fasciitis, rheumatic fever, glomerulonephritis

Habit: Throat, Skin

Group A beta hemolytic strep

Mechanism of spread: Person-to-Person by aerosol

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7
Q

Streptococcus Pyogenes: 3 Mechanisms of Disease

A

3 Mechanisms of disease
1. Pyogenic Inflammation
Induced locally at the site of infection
Pharyngitis

  1. Exotoxin Production
    Widespread systemic symptoms
    Scarlet Fever
  2. Immunologic
    Ab against organism cross-react with host tissue
    Rheumatic Fever (Rheumatic carditis, joints, skin, spinal cord, brain)
    2-3 weeks after Streptococcus infection
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8
Q

Suppurative vs. Non-suppurative vs. Toxin Mediated Diseases

A

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.

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9
Q

Suppurative, Non-Suppurative, and Exotoxin Mediated Diseases

A

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

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10
Q

S. Pyogenes: hyaluronidase, streptokinase, and Dnase

A

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

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11
Q

S. Pyogenes: Lipoteichoic Acid, Protein F, M Protein, and Capsule

A

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

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12
Q

S. Pyogenes: Streptolysin O and S, Pyrogenic Exotoxins, and Exotoxin B

A

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

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13
Q

S. Pyogenes: M Protein

A

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

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14
Q

S. Pyogenes: Pharyngitis Clinical Presentation

A
Clinical Presentation
20% are asymptomatic
Sore throat
Exudate and Inflammation
Fever
Tender cervical lymph nodes
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15
Q

S. Pyogenes: Pharyngitis Dx

A

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

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16
Q

S. Pyogenes: Scarlet Fever

A

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

17
Q

S. Pyogenes: Rheumatic Fever

A

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

18
Q

S. Pyogenes: Host Defense, Prevention, and Tx

A
Host Defense
Phagocytosis
polymorphonuclear leukocytes
Opsonizing antibody
M  Protein specific

Prevention: no available vaccine

Treatment: penicillin

19
Q

Corynebacterium diphtheriae

A

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

20
Q

Corynebacterium diphtheriae: Pathogenesis

A
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

21
Q

Corynebacterium diphtheriae: Host Response and Clinical Findings

A

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

22
Q

Corynebacterium diphtheriae: Lab Dx and Tx

A

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

23
Q

Corynebacterium diphtheriae: Prevention

A

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