Bacteriology

PYOGENIC COCCI

I. STAPHYLOCOCCI

Morphology and culture characteristics

• Gram-positive cocci, facultative anaerobic, relatively resistant to - heat, drying, and high-salt
environments
• Growth: grow singly, in pairs, in short chains, or in irregular clusters; cluster formation more
often seen in isolates of solid media culture than in clinical specimens.
• Three species of medical importance are:
a) S. aureus: colonies may appear golden, coagulase-positive, ferments glucose anaerobically,
sensitive to novobiocin
b) S. epidermidis: colonies appear white, coagulase-negative, ferments glucose anaerobically,
sensitive to novobiocin
c) S. saprophyticus: coionies appear either yellow or white, coagulase-negative, fails to
ferment glucose anaerobically, resistant to novobiocin

Transmission
Normal component of human flora, carried asymptomatically (S. aureus, S. epidermidis). A human
can serve as endogenous source to himself or exogenous source to others. S. saprophyticus is only
occasionally found on human skin

Clinical disease
Staphylococcus aureus causes:
Characteristic feature is abscess formation in any part of the body
a) CUTANEOUS INFECTIONS-furuncles, carbuncles, impetigo, scalded skin syndrome generalized
exfoliative dermatitis, bullous impetigo, staphylococcal scarlet fever)
b) OSTEOMYELITIS, septic arthritis, septic bursitis (either as a complication of S. aureus sep-
ticemia or secondary to local trauma or injury)
c) SEPTICEMIA AND ENDOCARDITIS
d) PNEUMONIA (aspiration or hematogenous spread) and pleural empyema
e) TOXIC SHOCK SYNDROME (high fever, hypotension, diarrhea, erythroderma, mental con-
fusion, and renal failure)-Staphylococcus aureus, from phage group I, producing enterotoxin
F and exotoxin C (may be identical)
f) FOOD POISONING-preformed heat-stable enterotoxin B produced by the toxigenic strains
growing in contaminated food
g) PERICARDITIS (from hematogenous spread or perforating chest injury)

Staphylococcus epidermidis
a) Endocarditis-native or prosthetic valves
b) Intravenous catheter infections; vascular graft infections
c) Peritoneal dialysis catheter-associated peritonitis
d) Cerebrospinal fluid shunt infections
e) Urinary tract infections (usually in hospitalized patients with urinary tract complications)
f) Osteomyelitis (sternal osteomyelitis due to infection of the median sternotomy wound after
cardiothoracic surgery, bone infection surrounding a prosthetic joint, hematogenous
osteomyelitis from hemodialysis shunt infections)
g) Ocular infections-commonly endophthalmitis following ocular surgery

Staphylococcus saprophyticus
Urinary tract infection in young, sexually active females

Diagnosis
 • Presumptive evidence of staphylococcal infection by smear gram stain, showing gram-positive
cocci in clusters
• Culture of pus, purulent fluid, blood, sputum, urine, etc.
• Coagulase and novobiocin testing

Treatment
1. S. Aureus-most produce penicillinase
• DRUG OF FIRST CHOICE-penicillinase-resistant penicillin (dicloxacillin, nafcillin)
• "METHICILLIN-RESISTANT" S. aureus-initially seen in drug addicts, now more common;
Vancomycin is the drug of choice.
2. S. epidermidis-Vancomycin is the drug of choice
II. STREPTOCOCCI

Morphology and culture characteristics

Gram-positive cocci, cell division in one plane resulting in pairs or chains, most are facultative
anaerobic, although some are obligate anaerobes (includes members of the family
Peptostreptococcaceae), catalase-negative, nonmotile.
Classification
Hemolysis and Lancefield groups. The Lancefield groups are based on the antigenic "C carbohydrate"
found in the cell wall of many streptococci.
• Alpha hemolytic (incomplete, may produce greenish discoloration)
• Beta hemolytic (complete hemolysis of RBC in the medium)-Lancefield group A (S. pyogenes),
group B (S. aga/actiae), group C (S. equisimilis, S. zooepidemicus, S. equi), group D
(enterococcus and nonenterococcus), group F (S. anginosus), group G, groups E, L, M, P, U, or
V, or non-typables
• Gamma hemolytic (no hemolysis)-Lancefield group D (enterococcus and nonenterococcus) bile-
esculin positive, S. pneumoniae (negative bile-esculin reaction; bile soluble, positive zone
inhibition around optochin disk), S. viridans (negative bile-esculin reaction, not bile soluble,
negative zone of inhibition around optochin disk)

Transmission
Part of normal human flora, can induce disease from any portal of entry.

Clinical disease
Streptococcus pyogenes: M protein (in the cell wall) is closely associated with virulence
a) More than 20 toxins are elaborated by S. pyogenes
 • Streptokinase-activates plasminogen
• Hyaluronidase-lyses important component of ground substance, therefore the propensity for
spread versus formation
• Erythrogenic toxin-causes rash in scarlet fever
• Streptolysin O-this antigenic material is the basis of the titer of anti-streptolysin 0 (ASO) as
an indication of recent Group A strep infection
b) PHARYNGITIS, scarlet fever, suppurative complications of pharyngitis (peritonsillar cellulitis,
peritonsillar abscess, retropharyngeal abscess, bacteremic metastatic spread); unsuppurative
complications of pharyngitis (acute rheumatic fever, poststreptococcal glomerulonephritis)
c) ERYSIPELAS
d) PYODERMA (impetigo)
e) OTHER-cellulitis, lymphangitis, perianal cellulitis, puerperal sepsis, meningitis, pneumonia,
emphysema.

Treatment
Penicillin G, if allergic-erythromycin

Streptococcus pneumoniae
a) PNEUMONIA (most common cause of bacterial pneumonia); local complications- empyema,
lung abscess, and/or pericarditis; bacteremia (in 25-30% patients with pneumococcal
pneumonia)
 b) UPPER RESPIRATORY TRACT INFECTION-otitis media, mastoiditis, sinusitis
c) EXTRAPULMONARY-meningitis, endocarditis (acute, < 1 % of cases, normal or damaged
valves, local tissue destruction common), arthritis, peritonitis

Treatment
Although there have been reports of sporadic resistance, the overwhelming majority of S.
pneumoniae are exquisitely sensitive to penicillin

Group D streptococci causes

Endocarditis (both enterococcal and nonenterococcal), bacteremia (usually S. faecalis), urinary tract
infection (S. faecalis), intra-abdominal abscess (bacteremia less common), soft tissue infection
(often present, pathogenicity unclear), neonatal meningitis, pneumonia (rare)

Treatment
a. Nonenterococci-penicillin
 b. Enterococci-requires synergy between penicillin and aminoglycoside

Group B streptococci
• EARLY-ONSET (first 5 days of life) neonatal infection; bacteremia
• LATE-ONSET (7 days-3 months of age) neonatal infection; bacteremia, fulminant meningitis,
osteomyelitis, septic arthritis
• POSTPARTUM WOMEN- Endometritis, caesarian section wound infection, bacteremia
• IMMUNO-COMPROMISED HOSTS- Pyelonephritis, pneumonia, tracheobronchitis, cellulitis, septic
arthritis, meningitis, endocarditis, bacteremia

Treatment
Penicillin G

Viridans streptococci (Streptococci viridans)

• ENDOCARDITIS (5. mitior, S. sanguis more common)

• SUPPURATIVE INFECTlON-(S. mille'; most common); intra- abdominal, brain abscess, meningitis,
bone and joint, skin, respiratory, and oral infection

Treatment
Penicillin

Lab Diagnosis of Streptococci

Smears and cultures of clinical specimens
Group A: ASO, anti-DNase B, anti-hyaluronidase, type-specific antibody
Pneumococcus: Quellung reaction, counterimmunoelectrophoresis
Group D: Smear and Culture
Group B: CIE, latex particle, agglutination, (+) cAMP test