Gram Positive Cocci 4/1

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General Features of Streptococci

Back 1

1. gram positive spherical/ovoid cocci
(usually in chains)

2. non spore forming, non motile

3. some form capsules of polysaccharide or hyaluronic acid

4. grow best in ENRICHED media
(sheep blood agar most common)

5. grows best 35-37 degrees
(warmer than room temp!)

6. range from aerobes to strict anaerobes

7. Catalase negative
(no mechanism to deal with H202)

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Classification of streptococci

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1. Hemolysis on blood agar
-complete/clear = Beta
-incomplete/green = alpha
-none = gamma

2. serologic properties w/respect to cell wall carbohydrates
- Lancefield groups A-H, K- M, O-V

3. Biochemical/ physiological properties

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Group A Strep Diseases

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pharyngitis
scarlet fever
impetigo/pyoderma
erysipelas
cellulitis
necrotizing fascititis
toxic shock syndrome
Non-supporative complications
-rheumatic fever
-glomerulonephritis

Front 4

Group B Strep Diseases

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Neonatal infections

chorioamnionitis, endometritis

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S. pneumoniae Diseases

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pneumonia
meningitis
sinusitis
otitis media

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Group C and G Strep Diseases

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skin and throat infections, endocarditis

bone / joint infections

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S. milleri / anginosus group Diseases

*smell like caramel

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associated w/ polymicrobial abcesses (brain, liver, abdomen)

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Viridans strep (non-milleri)

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dental caries

endocarditis

bacteremia in neutropenia

includes S. mutans and S. sanguis

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Group A VIRULENCE

1. adherence to host epithelial cells

2. invasion of epithelial cells

3. avoidance of opsonization, phagocytosis

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1. Hyaluronic acid capsule (antiphagocytic)

2. lipoteichoic acid, PROTEIN F (works for adhesion)

3. M protein
(adhesion to kerantinocytes and antiphagocytic)

3. M Protein,

Front 10

Group A VIRULENCE

4. production of enzymes

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ENZYMES

1. streptokinase
-lyses blood clots and promotes tissue spread of bacteria

2. C5a peptidase
-interferes w/complement activation and involved in adhesion

3. Hyaluronidase
-hydrolyzes hyaluronic acid in host

4. DNases A-D
(will have antibody to DNase B as evidence of past infection)

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Group A VIRULENCE

5. production of toxins

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Streptolysins S and O

1. toxic for neutrophils, RBC, platelets

2. S toxin = hemolysis on agar

3. S = non antigenic

4. o highly antigenic
- can use ASO titer to determine recent infection

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GROUP A virulence

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Streptococcal pyrogenic exotoxins (SPE)

1. produced by some strains

2. responsible for SCARLET fever rash

3. can act as superantigens

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Pathogenesis of GAS infection

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STEP 1: Adherence
-lipoteichoic acid and protein F bind fibronectin on epithelial cells of nasopharynx or skin
-M protein binds keratinocytes

STEP 2: Invasion
-invasion of epithelial cells via M and F proteins

STEP 3: Evasion of host immune system
-M protein
-C5a peptidase interferes with complement activation

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GAS- Strep Pharyngitis

"beefy red throat"

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SIGNS:
fever, absence of cough, sore throat, malaise, tender lymphadenopathy, lasts 1 week

DIAGNOSIS:
(physical exam)
1. exudative pharyngitis
2. palatal petechiae
(lab exam)
1. throat culture
-beta hemolysis
-bacitracin susceptible
-catalase negative

2. rapid immunoassay
-nitrous acid extraction of carbohydrate antigen

TREATMENT:

Penicillin (no resistance)
or
Erythromycin (some resistance)

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GAS- Strep Pharyngitis

COMPLICATIONS

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SUPPURATIVE
1. retropharygeal abscess
2. peritonsillar abscess
(aka Quizny?)
3. cervical adenitis
4. meningitis/brain abscess

TOXIN MEDIATED

1. Scarlet Fever

IMMUNOLOGICALLY MEDIATED

1. Rheumatic Fever
2. Glomerulonephritis

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GAS- SCARLET FEVER

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1. diffuse erythematous rash
-circumoral pallor
(no rash around mouth)
-sandpaper texture
-spares palms/soles
-"pastia lines" exaggeration at skin creases
-desquamates later
(skin falls off!)

2. strawberry tongue

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GAS Skin/Soft Tissue infections

Impetigo/ pyoderma

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HONEY COLORED CRUSTY RASH

effects kids (2 to 5 y/o) with poor hygiene

skin ulceration on face or lower extremities

seen at sites of skin trauma or insect bites

TREATMENT:

topical mupirocin ointment or penicillin by mouth if needed

COMPLICATIONS:

glomerulonephritis

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GAS Skin/Soft Tissue infections

Cellulitis

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demarcation of normal/abnormal tissue not as clear

could be from staph or strep

TREATMENT: empiric with broad spectrum drug to cover staph or strep so cephalosporin

GAS surgical wound infections

1. occur within 24 hours of surgery

2. watery discharge

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GAS Skin/Soft Tissue infections

Erysipelas

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specialized form of cellulitis affects cheeks and lower extremity

clear demarcation of red, raised skin, peau d'orange, tender, warm, bullae can form

Systemic manifestions: fever and leukocytosis

TREATMENT:

penicillin

*must beware of staph infection

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Necrotizing Fascitis

GAS implicated in ~60% of cases

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enters through skin via trauma or inoculation of bowel flora

onset = acute, severe pain out of proportion to exam, fever, chills

RAPID progression over hours

surgical intervention, antibiotics, IV fluids, inotropic support

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Acute Rheumatic Fever

GAS- in 3% of untreated, 1% of treated

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MAJOR CRITERIA
J: joint involvement
O: carditis
N: nodules, subcutaneous
E: erythema marginatum (pink rings on arms and legs)
S: sydenham's chorea (emotional lability, purposeless movements--rapid uncontrolled)

MINOR CRITERIA
-evidence of infection
-elevated ASO
-arthralgia (joint pain)
-fever
-elevated ESP, CRP

**2 major or 1 major and @ minor = ARF

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ARF

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-onset is 3 weeks after pharyngitis

-autoimmunity due to molecular mimicry of M protein to myosin, heart and brain components

-most ARF patients have elevated ASO, hyaluronidase, streptokinase titers

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ARF treatment

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high dose aspirin for 4-6 weeks to normalize ESR and CRP

10 day course antibiotics

culture and treat family

prophylaxis for future via penicillin

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ARF complication

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Acute Glomerulonephritis

diffuse inflammation of glomeruli

edema, hypertension, hematuria, proteinuria

resolves in weeks-months

can progress to renal failure

deposition of ag/ab complexes = pathogenesis

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GROUP B STREPTOCOCCI

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1. leading cause of neonatal sepsis and meningitis

2. colonize GI and GU tracts

3. virulence via capsular polysaccharide, beta hemolysin, alpha protein

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GBS DISEASES

(sequelae of newborn meningitis - seizures, sensorineural deafness, developmental delay)

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early onset:
less than 7 days of age
(ascending infection = bacterial growth in amniotic fliud, infant aspirates this, GBS replicates in alveoli and disseminates)

late onset:
7 days to 3 months of age

Infections of pregnancy
1. UTI
2. Chorioamnionitis
3. endometritis
4. bactermia

ADULTS:
diabetes
chronic liver/renal disease
malignancy
immunocompromised
10-15% mortality

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GBS DX, TX, and prevention

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culture of CSF and blood

all pregnant women are screened

chemoprophylaxis 4 hours pre-delivery via penicillin or ampicillin

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Viridans streptococci

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normal flora of oral cavity, teeth, nasopharynx, skin, genitourinary tract

lacks specific antigens/toxins

low virulence except when host defenses are altered

COMPLICATIONS
1. 40% of Subacute bacterial endocarditis (affects previously damaged heart valves)
*treat w/penicillin and gentamicin

2. Bacteremia in neutropenic patients w/cancer

DISEASE:

1. dental caries (s. mutans)

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Streptococcus pneumoniae

(most common cause of community acquired pneumonia)

(most common secondary infection of influenza)

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oval diplococci

virulent strains are encapsulated (round glistening)

alpha hemolytic

sensitive to optochin

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S pneumoniae Extracellular Factors

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1. Adhesins- mediate binding to epithelial cells

2. Pneumolysin- released during autolysis, shares properties with SLO, inhibits ciliary fctn, epithelial cytotoxin

3. cell wall associated factors- teichoic acid, petidoglycan, phosphorylcholine (CRP)

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S pneumoniae capsule

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1. high MW and complex polysaccharide polymer

2. unique for each serotype and antigenic

3. major component of vaccines
*pneumovax 23 valent
*prevnar 7 valent conjugated
to diphtheria protein

4. inhibits alternate pathway of complement activation

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S pneumoniae pneumonia

*most common cause of community acquired pneumonia
*underlying chronic disease important predisposing factor

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1. aspiration into lung (normally cleared by defenses, but targets impaired individuals and multiples)

2. fever, chill, productive cough, and chest pain

3. lobar consolidation in children & young adults- diffuse distribution in older

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Other S pneumoniae diseases

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A. sinusitis- otitis media
*40-50% of cases

B. meningitis
*leading etiologic agent
among bacteria
*complication of
1. bacteremia/pneumonia
2. mastoiditis/sinusitis
3. skull fracture/cochlear
implants
4. immune deficiency
5. mortality 60-80%

C. spontaneous bacterial
peritonitis
1. nephrotic syndrome,
wasting of serumb Ab

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DX of S pneumoniae

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1. gram stain of sputum, CSF, blood

2. lancet shaped diplococci

3. alpha hemolysis, optochin sensitive, sensitive to bile salts

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TX of S pneumoniae

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penicillin

*resistance seen, but overcome by high dose amoxicillin or cephalosporin or vancomycin

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Enterococci and group D streptococci

(entero grow in bile salts and 6.5% NACL, group D do not)

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Enterococci
1. E. faecalis (most common)
2. E. faecium (more likely vanco resistant)

Group D
1. S. bovis

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Group D streptococci

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dieases
1. native valve endocarditis
2. bacteremia
*association w/colon
malignancies

treat

1. penicillin
2. gentamicin

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Enterococcal Diseases

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1. endocarditis
2. infections of foreign body
3. opportunistic UTI
4. wound infections/abdominal
abscesses

Front 39

Enterococci treatment

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FOR ENDOCARDITIS
1. sensitive strains are more resistant to penicillin and vancomycin
2. need synergy of PCN/VCN and aminoglycosides (Bactericidal agents in cell wall disruption)

3. VRE: treat with linezolid, quinupristin/dalfopristin or daptomycin

FOR OTHER INFECTION

single agent for 2 week: PCN, Vanco, linezolid, daptomycin, quinupristin/daflopristin

treatment for condition at hand (debridement, abscess drainage, line removal)

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E faecalis vs E faecium

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80% of clinical isolates, 20% are VRE isolates, no Synercid use = E. faecalis

20% clinical isolates, 80% VRE isolates, YES synercid

**synercid = infusion related adverse events (phlebitis) w/ requires larger bore venous catheter & causes arthralgia and myalgia

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VRE prevention

Back 41

spread by fecal shedding, skin contamination, hospital personnel and fomites

previous van use is risk

**VRE can transfer VR genes to S. Aureus = VRSA