Gram Positive Cocci

Streptococcus
 General characteristics
• Gram positive, spherical, chains
• Catalase negative
• widely distributed in nature, water, dust, dairy
products
• Normal Flora of throat, mouth, intestine,
genital tract, skin
• Beta hemolytic have capsule
• Fastidious require blood for growth
• Facultative anaerobes
 Classification of Streptococci
on basis of hemolysis
• β hemolytic
– [Link], [Link], [Link], Enterococci
• Non β hemolytic
– α hemolytic
– [Link], [Link] ([Link], [Link],
[Link])
– Non hemolytic
– [Link], [Link]
• Variable hemolysis
– Peptostreptococcus
 Lancefield Classification
• Classify β hemolytic streptococci on the basis
of cell wall antigenic carbohydrates into
groups A – U
• Group A: Streptococcus pyogenes
• Group B: Streptococcus agalactiae
• Group D: Streptococcus bovis, Enterococci
• Groups C, E, F, G, H and K – U infrequent
human pathogens
 Streptococcus pyogenes
• β hemolytic, Lancefield group A
• Size 0.5- 1u.
• non spore forming
• capsule (hyaluronic acid)
• 2 antigen
• C Carbohydrate in cell wall
• M protein,
 Pathogenesis
• Virulence factors:
• 2 antigens in Cell wall
– M protein anti-phagocytic, adherence to epithelium – 80
serotypes. Nephritogenic, Rheumatogenic
– C carbohydrate antigenic
• Pili: adherence to epithelium
• Capsule: hyaluronic acid, anti-phagocytic
• Toxins:
• Hemolysins:
• Streptolysin O→β hemolysis, antigenic- ASOT
• Streptolysin S → α/ β hemolysis
• Erythrogenic toxin: like TSST, superantigen, gene on
bacteriophage → Scarlet fever
Fig: Cell surface structure of Streptococcus pyogenes and
secreted products involved in virulence.
• S. pyogenes is the leading cause of uncomplicated bacterial
pharyngitis and tonsillitis commonly referred to a strep
throat. Other respiratory infections include sinusitis, otitis,
and pneumonia.
• Infections of the skin can be superficial (impetigo) or deep
(cellulitis).
• Invasive streptococci cause joint or bone infections,
destructive wound infections (necrotizing fasciitis) and
myositis, meningitis and endocarditis.
• Two post streptococcal sequelae, rheumatic fever and
glomerulonephritis, occur in 1-3% of untreated infections due
to aberrant immunological reactions to Group A streptococcal
antigens.
• Scarlet fever and streptococcal toxic shock syndrome are
systemic responses to circulating bacterial toxins.
 Pathogenesis
• Pyrogenic exotoxin A: superantigen like TSST → Toxic
shock syndrome
• Exotoxin B: protease tissue damage → necrotizing
fasciitis
• Enzymes
– Streptokinase: fibrinolysin activates plasminogen→
plasmin, dissolve clots used in heart attacks
– Streptodornase/ DNase:
– Hyaluronidase: spreading factor
 Pathogenesis
• Transmission
• normal flora of skin and oropharynx
• 3 mechanisms
• Pyogenic inflammation:
• Exotoxin production:
• Immunologic: antibodies against streptococcal
antigens cross react with normal tissue –
damage. Post Streptococcal diseases
 Diseases
• Leading cause of Pharyngitis and Cellulitis.
• Tonsilitis, sinusitis, mastoiditis
• Peritonsilar & Retropharyngeal abscess
• Scarlet fever, Toxic shock syndrome
• lymphadenitis, necrotizing fasciitis,
• Puerperal fever and sepsis, Impetigo
• Septicemia,
• meningitis, brain abscess,
• Arthritis, Endocarditis, glomerulonephritis
Orbital cellulitis
Streptococcus pyogenes and Streptococcal Disease
• Impetigo
A contagious bacterial skin infection forming
pustules and yellow crusty sores.

• Erysipelas and cellulitis are common infections

of the skin. Erysipelas is a superficial infection,
affecting the upper layers of the skin, while
cellulitis affects the deeper tissues.
 Diseases
• Post Streptococcal diseases:
• Children 2 weeks after infecion, antibodies against M
protein cross react with tissues
– Acute Glomerulonephritis after skin infection
(glomerular basement membrane) hypertension,
edema
– Acute Rheumatic fever: joint, heart, brain, after
pharyngitis (fever, polyarthritis, Carditis (mitral,
aortic valves), chorea). ASO titre. Long term
prophylaxis
Rheumatic fever is a systemic illness after a throat
infection with a bacteria “ Streptococcus pyogenes” & It’s
serious illness - can cause permanent damage to the
heart. Most common in children (5 to 15 years old) but
can occur in younger children and adults as well
 Diagnosis and treatment
• Specimen: throat & skin swab, blood
• Microscopy
• Culture: on blood agar – β hemolysis, clear zone around
colonies (small, clear, translucent)
• Catalase negative
• Serologic: ASOT, DNase
• Treatment
• Penicillin G, Amoxycillin
• In allergy Erythrocin or Clindamycin
• Prevention of Rheumatic fever
• monthly Penicillin inj. for several months
 Streptococcus agalactiae
• Group B. flora in vagina, colon
• Pathogenesis: inflammation no toxins. capsule
• Neonates acquire infection during delivery – sepsis,
pneumonia, meningitis. Cause- lack of antibodies in
mother & failure of transfer to fetus.
• Adults arthritis, osteomyelitis, pneumonia, endocarditis,
post partum endometritis.
• Diagnosis:
– Hippurate hydrolysis
– Bacitracin resistance
– Camp test
– DNA detection in vaginal & urethral smears
 Hippurate hydrolysis
• Hippurate hydrolysis test is used to detect the
ability of bacteria to hydrolyse substrate
hippurate into glycine and benzoic acid by
action of hippuricase enzyme present in
bacteria.
• Hippuricase is a constitutive enzyme that
hydrolyzes the substrate hippurate to produce
the amino acid glycine.
 Bacitracin Resistance
• Bacitracin resistance is conferred by the
increased production of the ABC-transporter
BceAB, which removes bacitracin by an
unknown transport mechanism, and reveal
resistance against drug disc.
 The CAMP test
• The CAMP test (Christie–Atkins–Munch-
Peterson) is a test to identify group B β-
hemolytic streptococci (Streptococcus
agalactiae) based on their formation of a
substance (CAMP factor) that enlarges the
area of hemolysis formed by the β-hemolysin
elaborated from Staphylococcus aureus.
 Group D - Enterococci
• flora colon
• UTI especially in hospitalized patients, indwelling
catheter, urinary instrumentation.
• Endocarditis in postoperative
• Intra-abdominal & pelvic infections
• grow in 6.5% NaCl or bile
• VRE – life threatening nosocomial infections
• t/m: Resistant to Penicillin G. Combination
• Linezolid and Daptomycin
•
Pathogenesis and Clinical Manifestations

• Two virulence factors of viridans streptococci

play vital roles in pathogenesis. The first is
dextran which facilitates binding to fibrin
platelet aggregates on damaged heart valves.
• Another is that these can form biofilms that
assist in forming dental plaques.
 Contd…
• Viridans streptococci can bind to oral mucosa
and tooth surfaces colonizing the oral cavity.
Most common dental infections include dental
caries, abscesses, and periodontal disease.
– If trapped in an oral cavity, a Sucrose-rich diet
converts into dextrans, that creates a favorable
environment for bacteria for demineralization and
decay of teeth. The dental procedures, which may be
invasive, leading to endocarditis. Hence patients with
an existing heart problem need to use prophylactic
antibiotics before surgery or dental procedure.
 Streptococcus viridans
• Alpha hemolytic, flora oropharynx – enter blood after
dental surgery
• S. mutans synthesize polysaccharides- dental plaque- caries
• S. mutans, [Link], [Link], [Link]– infective
endocarditis – fatal unless antibiotic given. Penicillin/
Vancomycin + Aminoglycoside
• [Link], [Link], [Link] - mixed infection with
mouth anaerobes. brain & abdominal abscess
• Diagnosis: Resistant to Bile and Optochin
– Alpha hemolytic
Fig: Viridans streptococci (right) are optochin resistant.
Optochin-containing paper disc is added on blood agar
previously inoculated with S. viridans. On incubation, it shows
no zone of inhibition around the disc.
 Peptostreptococci
• Flora of mouth, gut, FGT
• Anaerobic, microaerophilic
• variable hemolysis
• Most common cause, Cause mixed anaerobic
infections, abscess in brain, lung, abdomen &
pelvis
• Brain abscesses following dental surgery
• Treatment: Penicillin G
 Streptococcus pneumoniae
• Alpha hemolytic, diplococci, or
Short chains, lancet shaped. Flora
in oropharynx of 5-50% population
• considered non communicable
• Pathogenesis
• Virulence factors
– Capsular polysaccharides of >85 antigenic types
– Pneumolysin -α hemolysis
– IgA protease - colonize URT mucosa
– Lipo-teichoic acid activates complement → induce
inflammatory cytokines → inflammation & septic shock
syndrome in immuno-compromised
– C -Polysaccharide/ C-substance reacts with serum CRP
 Streptococcus pneumoniae
• Pathogenesis
• Predisposing factors
– Alcohol & drug intoxication
– Cerebral impairment depressing cough
reflex
– Head injury (CSF leaking through nose)
– Respiratory irritants, RTI, bronchial
obstruction, pooling of mucus
– Abnormal CVS dynamics: Pulmonary
Congestion, cardiac failure
– Splenectomy, Sickle cell anaemia
– Chronic diseases, Nephrosis,
 Streptococcus pneumoniae
• Pathogenesis: pneumococci colonize upper respiratory
tract, mutiply in tissues , cause inflammation. In alveoli,
out poring of fluids, WBCs, RBCs result in consolidation of
lung. Phagocytosis of bacteria and debri leads to
resolution
• Diseases:
• mostly endogenous Pneumonia. Purulent bronchitis
clinical features: chill, fever, cough, pleuritic pain, rusty
sputum. Spontaneous recovery may occur in 5-10 days.
• Sinusitis, mastoiditis, conjunctivitis
• Meningitis,
• Osteomyelitis, Arthritis
• Endocarditis
• Peritonitis
• Sepsis
 Streptococcus pneumoniae
• Diagnosis:
• Specimen: blood, sputum, CSF
• Microscopy: Diplococci, lancet shape
• Culture blood agar: Alpha hemolytic
• Bile soluble colonies
• Growth inhibited by Optochin
• Quellung reaction using antisera
• Rapid diagnosis by detecting capsular polysachcarides and C –
Polysaccharide
• Treatment: Penicillin V & G, Erythromycin. Vancomycin for
resistant pneumococci. Levofloxacin, Ceftriaxone. MDR strains
• Prevention: Polyvalent polysaccharides vaccine for elderly &
immuno-compromised
 Thank you
Success is not final
Failure is not fatal
It is the courage to continue that counts
Winston Churchill