2. Introduction
• Pneumococcus, causes pneumonia , concurrently isolated by
George Sternberg ( USA Army Physician) and Louis Pasteur
(French Chemist) in 1881
• Termed Diplococcus pneumoniae (1926) and latter renamed
Streptococcus pneumoniae (1974) due to formation of chains in
liquid media
• Strep. pneumoniae played a central role in ‘transforming
principle of Griffith (1928)
• Normal inhabitants 5 – 40%
• human carriers 40 – 70 %
• 60% all bacteria pneumonia
3. Predisposing factors
• Viral and other respiratory tract infections
• Alcohol or drug intoxication
• Abnormal circulatory dynamics
• Malnutrition
• Sickle cell anaemia
• E.t.c.
4. Microscopy
•Encapsulated Gm positive diplococci or short
chains; Oval or lancet-shaped cells (0.5-1.2um)
•Occurrence in pairs or chains, depends on the
environment
•Capsular antigens occur in virulent strains and
consists of complex polysaccharide and cross
reactive
•Though Gm positive, if poorly stained, may
appear Gm negative especially in old cultures
5.
6. Laboratory Diagnosis
•Specimens include CSF, sputum, blood, aspirates, ear
swab, etc.
•ANO2 and with fastidious growth requirements
•Optimum growth pH 7.4 - 7.8
•Optimum growth Temp: 35 – 370 C
•Grows in media enriched with 5% defibrinated blood
or sheep blood (BA, Choc)
•Requires 5-10 % CO2 , for 24 – 48 hours.
•Colonies dome shaped/draughtsman’s shape/mucoid
7. Laboratory Diagnosis…
•Young cultures due to encapsulation, colonies are
smooth, circular, glistening, dome or draughtsman’s
shape
•Un-encapsulated colonies are rough
8. Identification:
oSusceptibility to Optochin (ethylhydrocupreine
dihydrochloride)
oDetection of pneumococcal antibodies by
radioimmunoassay
oDetection of capsular antigens ( CIE)
oQuellung’s reaction (capsular Ag precipitation)
oBile solubility test (differentiate α-haem streptococci
from Enterococcus)
10. Pathogenesis
• Nasopharynx of 5-10% healthy adults, 20-40% healthy
children
• Attaches to epithelial cells of nasopharynx by adhesins
• In eustachacian tube or nasal sinuses causes otitis media
and sinusitis
• Pneumonia in lungs (viral infection, smoking induced
ciliary paralysis are risk factors)
• Activates complement at site of infection and stimulates
cytokine production to attracts WBCs
11. Pathogenesis …
•Capsules/polysaccharides make it resistant to
phagocytosis
•In absence of anti-capsular antibodies, alveolar
macrophages cannot adequately kill pneumococci
•Haematogeneous spread results in meningitis, brain
abscess, septic arthritis or osteomyelitis
•Pneumococcal surface proteins inhibit complement
activation
•Secretes IgA1 protease that destroys IgA
12. Pathogenesis…
Risk factors:
• Impaired Ig G synthesis
• Impaired phagocytosis or defective clearance of
the pneumococci
• Absence of functional spleen ( due to congenital
asplenia, splenectomy or sickle – cell disease)
13. Virulence factors
• Strept. pneumonae expresses different virulence factors on its cell surface
and inside the organisms
Three classes of virulence factors:
1. Colonization and migration (spreading)
2. Tissue destruction
3. Phagocytic survival
• Cellular components
oComplex polysaccharide capsule is anti-phagocytic by inhibiting C3b
opsonization of the bacterial cells
oPneumolysin lyses the host cells and activate complement
14. Virulence factors…
• Autolysin (LytA) activated form, lyses bacterial cell
releasing contents (.e.g. pneumolysin)
• Hydrogen peroxide causes apoptosis in neuronal cells during
meningitis
• Pilli enhance colonization of the URT and required in large
release of tissue necrotic factor (TNF) in septic shock.
• Choline binding protein A (CbpA) (adhesion) interacts with
the CHO pulmonary epithelia surface
• Protective Antigen (PspA) that inhibits complement-
mediated opsonization of pneumococci
15. Virulence factors…
•Teichoic acid - activates alternative complement
pathway; C5a production mediates inflammation
•Peptidoglycan fragments - activate alternative
complement pathway; C5a production mediates
inflammation
•Secretory IgA protease - assists spreading by
enzymatically cleaving secretory IgA (sIgA) on
the bacteria
16. Host defenses
Immune Response:
• Naturally acquired immunity: Type-specific anti-capsular immunity
• Artificially acquired immunity: Immunization via polyvalent vaccine
prophylaxis
• Purified capsular materials from most common serotypes (23
different polysaccharides covering 94% of clinically relevant
serotypes)
NB: Until recently this vaccine formulation was not effective in young
children or elderly adults or in other high risk groups
17. Diseases caused
•Pneumonia (Pneumococcal, lobar pneumonia)
•Bacterial sinusitis (paranasal sinuses)
•Otitis Media (middle ear inflammation)
•Meningitis: CNS involvement after bacteremia,
sinusitis or otitis media, head trauma
•Bacteremia
•Pericarditis, endocarditis, osteomyelitis, septic
arthritis
•Peritonitis
18. Pneumococcal epidemiology
•Worldwide distribution
•Reservoir are human carriers
•Transmission person to person via respiratory
droplets, respiratory ‘’ autoinoculation’’
•Responsible serotypes that cause infections are
those common in carriers
•Family/house-hold spread influenced by crowding,
season, and presence of URTIs, pneumonia, otitis
media, etc.
19. Epidemiology of pneumococcal serotypes
• Temporal pattern winter and early spring
• Communicability probably as long as the organisms are present in respiratory
secretions
• Over 90 serotypes
• Pneumococcal serotypes causing invasive diseases vary according to:
• Geography,
• Age
• Immune status,
• Race/ethnicity
• Ability to be carried
• Invasiveness
• Disease manifestations and amount resistant strains in circulation.
22. Antibiotics/prevention…
• Pneumococcal polysaccharide vaccine (PeumovaxTM)
•Provides at least 85% protection in under 55 year
olds
•Also good for ≥ 55 year olds
• Revaccination at periodic intervals is recommended
for conditions such as
•Asplenia
•Nephrotic syndrome
