1

CHAP TER
Chapter
Streptococcus, Enterococcus
and Pneumococcus
63.2
Family Streptococcaceae are catalase negative gram-positive cocci, arranged in pairs or
chains (due to single plane of division).
• Streptococcus, Enterococcus and Pneumococcus are the important members of this family. Typing of Streptococcus:
• However, according to the molecular structure, Enterococcus is now reclassified under • Serogrouping (Lancefield’s):
separate family Enterococcaceae. Based on carbohydrate
antigen, 20 groups
• Serotyping (Griffith typing):
CLASSIFICATION Based on M protein (>100 M
types)
• emm genotyping: Based on
gene coding for M protein,
On the basis of hemolysis, streptococci can be divided into 3 groups >12 emm
1. Hemolytic: (Partial or green hemolysis), e.g. Streptococcus Viridans, Streptococcus
pneumoniae
2. Hemolytic: (Complete or yellowish hemolysis), e.g. haemolytic Streptococcus
3. Hemolytic: (no hemolysis is seen), e.g. Enterococci

Lancefield’s grouping (for β haemolytic streptococci)

Based on carbohydrate antigen in cell wall, the haemolytic streptococci are further
divided into 20 serogroups: Group A to V except I and J.

Carbohydrate antigen extracted by HCl (Lancefield’s method), Formamide (Fuller’s

method), Enzymatic (Maxted’s) or autoclaving.

Streptococcus group A (S. pyogenes) is further subdivided based on

• Griffith typing: Based on M protein (> 100 M serotypes) or
• emm typing: Based on gene coding for M protein, > 124 emm genotypes identified.

STREPTOCOCCUS PYOGENES (GROUP A)

Virulence Factors

Cell wall • Inner thick peptidoglycan layer (confers cell wall rigidity, induces inflammatory
antigens response and has thrombolytic activity)
• C-carbohydrate antigen: Present as middle layer and is group specific
• Outer layer of protein (M, T, R) and lipoteichoic acid (helps in adhesion)
• M protein:
○ Mediates adherence to epithelial cells, inhibits phagocytosis
○ Binds to fibrinogen and neutrophils leadings to release of inflammatory
mediators that induce vascular leakage (streptococcal toxic shock).
○ M protein is further divided into Class I and Class II. Antibodies to class IM
protein are responsible for pathogenesis of rheumatic fever.
Capsule • Expressed by mucoid strains, made-up of hyaluronic acid.
• Capsule is anti-phagocytic, helps in adhesion; but it is not antigenic.
Contd...

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Jeremie R. Galapon, RMT, MT(ASCPi)
Manila Adventist College
Medical Laboratory Science Department

Chapter 6 - Streptococcus, Enterococcus and Pneumococcus
126 Review of Microbiology and Immunology
Contd...
SPE is associated with the
pathogenesis of:
• Scarlet fever
• Necrotizing fasciitis
• Streptococcal TSS.
Antistreptolysin-O antibodies
(ASO):
• Raised in most of the
streptococcal infections
• Used as a standard marker
for retrospective diagnosis of
streptococcal infections
• Except in glomerulonephritis
and pyoderma; where ASO
titer is low.
Section 3
Manifestations
Streptococcus pyogenes causes both suppurative and nonsuppurative manifestations.
Scarlet fever:
Caused by S. pyogenes, Now
rare, characterized by:
• Pharyngitis and Sandpaper
rashes, strawberry tongue
• Pastia’s lines: prominent
rashes in skin folds
• Pathogenesis is due to SPE
toxin (Dick test ve).
2
SPE • 3 Types (SPE A, B and C): Type A and C are, e.g. of Superantigens
(Streptococcal • Type A and C bacteriophage coded, B toxin chromosomal mediated
pyrogenic • Pathogenic role: Associated with the pathogenesis of scarlet fever, necrotizing
exotoxin) or fasciitis and streptococcal toxic shock syndrome.
Erythrogenic • Dick test: Intradermal injection of SPE produces erythema only in those
toxin children who are susceptible to develop scarlet fever.
• Schultz Charlton reaction (blanching of rash after injection of anti SPE
antibodies): Used for diagnosing scarlet fever in past
Hemolysins Streptolysin O and Streptolysin S (see table below)
Streptokinase Fibrinolysin (activates plasminogen)
Rapid spread: By preventing the formation of fibrin barrier.
Therapeutically used in treatment of coronary thrombosis.
DNase Also called Deoxyribonuclease or Streptodornanse ( types: A, B,C,D)
• Diagnostic use: Anti-DNase B > 300–350 U is useful for the retrospective
diagnosis of skin infections (pyoderma) and acute glomerulonephritis where
ASO titer is low
• Therapeutic use: Preparation containing streptodornase and streptokinase can
be used to liquefy the thick exudates in empyema cases.
Other • Hyaluronidase (spreading factor): Expressed by noncapsulated strains, such
enzymes as M type and 22. It breaks down the hyaluronic acid of the tissues, thus helps
in the spread of infection along the intercellular space
• Serum opacity factor: Lipoproteinase enzyme in nature
• NADase, C5a peptidase and SpyCEP (inactivates IL- 8)
Streptolysin-O (SL-O) Streptolysin-S (SL-S)
Oxygen labile (hence named streptolysin-O ) Oxygen stable
Heat labile Serum soluble (hence named
streptolysin-S)
Hemolysis is seen only in deep colonies (pour plate) as it is Causes hemolysis on the
inactivated in the presence of oxygen surface of blood agar plate
It is cytotoxic for neutrophils, platelets and cardiac tissue It has leucocidal activity
Strongly antigenic Not antigenic
Antistreptolysin-O antibodies (ASO) are raised in most of the Not useful for serological
streptococcal infections and are used as a standard marker for diagnosis of streptococcal
retrospective diagnosis of streptococcal infections (except in infections
glomerulonephritis and pyoderma; where ASO titer is low)
Streptolysin-O is structurally and functionally similar to:
• Tetanolysin of Clostridium tetani
• Pneumolysin of S. pneumoniae
• Theta toxin of Clostridium perfringens
• Listeriolysin O of Listeria
• Cereolysin of Bacillus cereus
Suppurative Manifestations
Respiratory infections:
• Pharyngitis sore throat (MC cause, 20– 0% of all cases)
• Pneumonia and empyema
Scarlet fever (MC cause ): Now rare, characterized by:
• Pharyngitis and Sandpaper rashes, strawberry tongue
• Pastia’s lines- prominent rashes in skin folds
• Pathogenesis is due to SPE toxin (Dick test ve)
Contd...
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Jeremie R. Galapon, RMT, MT(ASCPi)
Manila Adventist College
Medical Laboratory Science Department
 3
Chapter 6 - Streptococcus, Enterococcus and Pneumococcus

Streptococcus, Enterococcus and Pneumococcus 127

Contd...
Suppurative Manifestations
Skin and soft tissue infections:
• Impetigo (pyoderma): (MC cause)
○ Seen in children, poor hygiene, warm climate
○ Characterized by pustular lesions that become honeycomb like crusts, no fever, painless.
○ Associated with higher M types, and nephritogenic strains.
• Cellulitis and erysipelas (MC cause):
○ Tender, bright red, swollen and indurated peaud’orange texture of skin (due to involvement of
the superficial lymphatics) along with fever and chills.
○ MC site- malar area of the face, seen in older people.
Deep soft tissue infections:
• Necrotizing fasciitis or streptococcal hemolytic gangrene- S. pyogenes is MC cause (60%), it is
rapidly spreading, hence S. pyogenes is also called flesh eating bacteria
• Toxic shock syndrome (staphylococcal TSS is MC, but bacteremia is MC in streptococcal TSS)
• Streptococcal myositis (S. aureus is MC cause of myositis)
Complications:
• Puerperal sepsis (Group B Streptococcus is MC cause),
• Others: Otitis media, Quinsy, Ludwig’s angina, pneumonia (post viral), osteomyelitis, meningitis

Nonsuppurative Complications
Streptococcal antigens show molecular mimicry with human antigens. Due to antigenic Nonsuppurative complications
cross reactivity, antibodies produced against previous streptococcal infections cross react of S. pyogenes:
• Acute rheumatic fever
with human tissues to produce lesions. This accounts for a number of nonsuppurative
• Post streptococcal
complications such as: glomerulonephritis (PSGN)
• Acute rheumatic fever • Guttate psoriasis
• Poststreptococcal glomerulonephritis (PSGN) • Reactive arthritis
• Guttate psoriasis • PANDAS
• Reactive arthritis
• Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus
pyogenes (PANDAS)
Antigenic cross reactivity between streptococcal antigens and the corresponding human
antigens
Streptococcal Ag Mammalian Ag
Cell wall M protein (of serotypes M1, M5, M6, and M1 ) Myocardium (tropomyosin and myosin)
Cell wall C carbohydrate Cardiac valves
Cytoplasmic membrane Glomerular vascular intima
Peptidoglycan Skin antigens Systemic Bacteriology
Hyaluronic acid Synovial fluid

Differences between acute rheumatic fever and poststreptococcal glomerulonephritis

Acute rheumatic fever Poststreptococcal glomerulonephritis
Feature (ARF) (PSGN)
Prior history of infection Pharyngitis strains Mainly pyodermal strains, or rarely
with pharyngitis strains
Serotype Most of the strains of Pyodermal strains: , 53–55, 5 –61 and
S. pyogenes Pharyngitis strains: 1, 12
Immune response Marked Moderate
Complement level Unaltered Low (due to deposition in glomeruli)
Genetic susceptibility Present Absent
Repeated attacks Common Uncommon
Penicillin prophylaxis Indicated Not indicated
Contd...

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Jeremie R. Galapon, RMT, MT(ASCPi)
Manila Adventist College
Medical Laboratory Science Department

Chapter 6 - Streptococcus, Enterococcus and Pneumococcus
128 Review of Microbiology and Immunology
Serology:
• ASO Ab: Titer > 200 Todd
unit ml in most streptococcal
infections except in pyoderma
and PSGN
• Anti-DNase-B Ab – Titer >
300–350 units ml is diagnostic
of PSGN and pyoderma.
Treatment of Necrotizing
fasciitis:
• Surgical debridement (most
crucial) plus
• Penicillin G plus
• Clindamycin
Section 3
Rheumatic fever:
• Treatment: Benzathine
penicillin G, IM single dose; or
oral Penicillin V for 10 days
• Long-term maintenance
therapy, with penicillin G
monthly
○ For 5 years or until 21
years of age, (without
carditis)
○ For 10 years (with carditis)
○ Up to 0 years of age
lifelong (with residual heart
disease)
4
Contd...
Acute rheumatic fever Poststreptococcal glomerulonephritis
Feature (ARF) (PSGN)
Course Progressive Spontaneous resolution
Prognosis Variable Good
Hypersensitivity reaction Type II Type III
Laboratory Diagnosis of Streptococcus Pyogenes
• Transport medium: Pike’s medium
• Direct smear microscopy: Pus cells with gram-positive cocci in short chains
• Culture:
○ Blood agar: Pinpoint colony with a wide zone of -hemolysis
○ Selective media: Crystal violet blood agar and PNF (polymyxin B, neomycin,
fusidic acid) media
○ Liquid media: Granular turbidity with powdery deposit
• Biochemical identification: Catalase negative, Bacitracin sensitive and Pyrrolidonyl
Arylamidase (PYR) test is positive
• Typing:
○ Lancefield grouping: Shows group A Streptococcus
○ Typing of group A Streptococcus: Griffith typing and emm typing
• Serology: ASO antibodies and Anti-DNase B antibodies
○ ASO antibodies titer is elevated > 200 Todd unit/ml in most streptococcal infec-
tions except in pyoderma and PSGN.
○ Anti-DNase-B Ab – Titer > 300–350 units/ml is diagnostic of PSGN and pyoderma.
○ Other antibodies elevated are Antihyaluronidase and antistreptokinase antibodies.
Treatment of streptococcal infection
Penicillin is the drug of choice for all type of streptococcal infections
Conditions Treatment recommended
Pharyngitis Benzathine penicillin G, IM single dose
or oral penicillin V for 10 days
Erysipelas Cellulitis Mild- Procaine penicillin
Severe- Penicillin G
Necrotizing fasciitis Surgical debridement (most crucial) Penicillin G Clindamycin
Pneumonia and empyema Penicillin G drainage of empyema
Streptococcal TSS Penicillin G Clindamycin immunoglobulin (to SPE)
Rheumatic fever Benzathine penicillin G, IM single dose;
or oral Penicillin V for 10 days
Long-term maintenance therapy with penicillin G monthly:
• For 5 yrs or until 21 yrs of age, (without carditis)
• For 10 yrs (with carditis)
• up to 0 yrs of age lifelong (with residual heart disease)
PSGN Benzathine penicillin G, IM single dose;
or oral penicillin V for 10 days
Treatment of asymptomatic carriers
Pharyngeal carrier Penicillin V rifampicin
Rectal carriers Vancomycin rifampicin
Prophylaxis
Long-term maintenance therapy with penicillin (alternative-sulfadiazine or erythromycin in
penicillin allergy) is required for children who develop early signs of rheumatic fever. This
prevents streptococcal reinfection and further damage to heart.
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Jeremie R. Galapon, RMT, MT(ASCPi)
Manila Adventist College
Medical Laboratory Science Department
 5
Chapter 6 - Streptococcus, Enterococcus and Pneumococcus

Streptococcus, Enterococcus and Pneumococcus 129

GROUP B STREPTOCOCCUS (S. AGALACTIAE)

Pathogenesis: Approximately 30% of women are vaginal or rectal carriers of group B
Streptococcus. Hence, the infection is common in neonates and in pregnancy. It is a major
cause of:
• Neonatal sepsis and meningitis: Neonatal sepsis can be of two types-early onset and late
onset type
• Puerperal sepsis and peripartum fever
• Infections in elderly people with underlying illness, such as diabetes mellitus or
malignancy: Cellulitis and soft tissue infections, UTI, pneumonia, and endocarditis.
Group B Streptococcus
aboratory Diagnosis: It can be differentiated from Group A Streptococcus by following Causes:
biochemical tests (see table) • Neonatal sepsis and
• CAMP positive, Hippurate hydrolysis test positive, Bacitracin resistant and PYR test is meningitis
negative • Puerperal sepsis and
peripartum fever
• Orange pigment production- enhanced in Islam’s medium.
• Infections in elderly people
• hemolytic colonies, which are mucoid and slightly larger (2 mm). with underlying illness
• It has a capsular polysaccharide, which can be typed into nine serotypes.

Early and late onset Group B Streptococcus disease in neonates

Characteristics
Age of onset
Increased risk following
obstetric complications
Mode of transmission to
the baby
Common clinical
manifestations
Common serotypes
Case fatality rate
Early-onset disease Late-onset disease
0–6 days of birth 7– 0 days of birth
Prematurity and prolonged labor Not associated
During or before birth from the colonized Contact with a colonized
maternal genital tract mother and nursing personnel
Pneumonia and or respiratory distress Bacteremia and meningitis
syndrome followed by meningitis (most common)
Ia, III, V, II, Ib III predominates
.7% 2.8%

Characters S. pyogenes S. agalactiae

Lancefield group Group A Group B
Bacitracin sensitivity test Sensitive Resistant
P R test Positive Negative
Hippurate hydrolysis test Negative Positive
CAMP test Negative Positive
Systemic Bacteriology
hemolytic colonies 0.5–1 mm, pin point Mucoid, larger (2 mm)

ENTEROCOCCUS
The enterococci were initially grouped under group-D Streptococcus, but later, it has been
reclassified as a separate genus Enterococcus under family Enterococcaceae.
• Enterococci are the part of normal flora of human GIT. At the same time, they are also
increasingly important agents of human disease especially in hospitals mainly because
of their resistance to antibiotics.
• E. faecalis is the most common species found in clinical specimens; whereas E. faecium is
more drug resistant than E. faecalis.

Various Clinical Manifestations Include

• Urinary tract infections (cystitis, urethritis, pyelonephritis and prostatitis)
• Bacteremia and mitral valve endocarditis (in IV drug abusers)
• Intra-abdominal, pelvic, and soft tissue Infection

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Jeremie R. Galapon, RMT, MT(ASCPi)
Manila Adventist College
Medical Laboratory Science Department

Chapter 6 - Streptococcus, Enterococcus and Pneumococcus
130 Review of Microbiology and Immunology
All cocci are Nonmotile except:
• Enterococcus gallinarum
• ne u a e ifla u
Section 3
Pathogenic Viridans
streptococci:
• S.mutans: Causes dental
caries and plaques
• S.sanguis: Causes subacute
bacterial endocarditis
• S.milleri group: Produces
suppurative infections
6
• Late-onset neonatal sepsis and meningitis
• Infection on burn surface.
Laboratory Diagnosis
Enterococci show the following characteristics that help in the identification:
• They are gram-positive oval cocci arranged in pairs (spectacle eyed appearance)
• Nonmotile cocci (except E. gallinarum and E. casseliflavus)
• Blood agar: It produces nonhemolytic, translucent colonies (rarely produces or
hemolysis)
• MacConkey agar: It produces minute magenta pink colonies.
• Bile aesculin hydrolysis test is positive
• PYR test is positive
• Growth occurs in presence of:
○ 6.5% NaCl, 40% bile and pH 9.6
○ Heat tolerance test: They are relatively heat resistant, can survive 60°C for
30 minutes.
Treatment
Most strains of enterococci are resistant to penicillins, aminoglycosides and sulfonamides.
They show intrinsic resistance to cephalosporins and cotrimoxazole.
• Resistance is overcome by combination therapy with penicillin and aminoglycoside
(due to synergistic effect) and is the standard therapy for life-threatening enterococcal
infections; however in UTI, monotherapy with ampicillin or nitrofurantoin is sufficient.
Resistance to this combination therapy may also develop.
• Vancomycin is usually indicated in resistant cases but resistance to vancomycin has also
been reported.
Vancomycin Resistant Enterococci (VRE)
Vancomycin resistance in enterococci has been increasingly reported nowadays.
• RE is mediated by Van gene, which codes for altered target site for vancomycin in the
cell wall (i.e. D-alanyl-D-alanine side chain of peptidoglycan layer is altered to D-alanyl-
D-serine or D-alanyl-D-lactate) and this altered side chains have less affinity for binding
to vancomycin.
• Van gene has 9 genotypes. mportant ones are: VanA to VanE.
○ Strains with VanA gene show high level resistance to both glycopeptides- vancomy-
cin and teicoplanin.
○ Strains with VanB gene show low level resistance to vancomycin, but sensitive to
teicoplanin.
○ E. gallinarum and E. casseliflavus possess VanC genes which is chromosomal coded
(other genotypes transposon coded), and they show intrinsic resistance to both gly-
copeptides.
• Screening of patients for RE is carried out by: Rectal swab culturing on Bile esculin
azide agar with 6 g/ml vancomycin
VIRIDANS STREPTOCOCCI
Viridans streptococci are hemolytic, commensal of mouth:
• S. mutans: Causes dental caries and plaques
• S. sanguis: Causes subacute bacterial endocarditis
• S. milleri group: Produces suppurative infections, differ in hemolytic pattern (may be ,
or hemolytic).
Treatment: Usually sensitive to penicillin (except neutropenic patients with bacteremia;
where vancomycin is given).
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Jeremie R. Galapon, RMT, MT(ASCPi)
Manila Adventist College
Medical Laboratory Science Department
 7
Chapter 6 - Streptococcus, Enterococcus and Pneumococcus

Streptococcus, Enterococcus and Pneumococcus 131

STREPTOCOCCUS PNEUMONIAE OR PNEUMOCOCCUS

Virulence Factors and Pathogenesis Virulence Factors of
S. pneumoniae:
S. pneumoniae possesses a number of virulence factors such as:
• Capsule (detected by Quellung
• Capsular polysaccharide: It protects the cocci from phagocytosis: reaction)
○ It is type specific (> 90 capsular serotypes are recognized), serotypes are detected • C carbohydrate antigen: CRP
by Quellung reaction. is named after this
• Pneumolysin
○ uellung reaction: Capsular swelling occurs when colonies are added with type-
• Autolysin: Responsible for bile
specific antiserum and methylene blue dye. solubility and draughtsman
○ It diffuses (soluble) into culture media, tissue and exudates, hence also called solu- colony
ble specific substance.
• C-carbohydrate antigen (C-polysaccharide or C-substance): It is species specific. CRP
(C-reactive protein) present in sera of patients with acute inflammation. It is so named
because; it precipitates with pneumococcal C-antigen.
• Pneumolysin: It is a membrane damaging toxin, inhibits neutrophil chemotaxis.
• Autolysin: It is an amidase enzyme that cleaves peptidoglycan leading to autolysis of
cells. This property is responsible for bile solubility and draughtsman appearance of
pneumococcal colonies.

Clinical Manifestation
S. pneumoniae is the most common cause of:
• Lobar pneumonia
• Pyogenic meningitis in all ages (except in neonates)
• Noninvasive manifestations such as otitis media and sinusitis. S.pneumoniae is the most
common cause of:
ther invasive manifestations: S. pneumoniae can cause osteomyelitis, septic arthritis, • Lobar pneumonia
• Pyogenic meningitis in all ages
endocarditis, pericarditis, primary peritonitis, rarely, brain abscess and hemolytic-uremic
(except in neonates)
syndrome. Empyema and parapneumonic effusion may occur as complications of pneumonia. • Noninvasive manifestations,
such as otitis media and
sinusitis.
Epidemiology
• Source of infection in humans is upper respiratory tract of carriers (less often patients).
• Carrier rate > 90% of children of 6 months to 5 yrs of age harbor S. pneumoniae in the
nasopharynx.
• Mode of transmission is by inhalation of contaminated droplet nuclei.

Risk factors: Systemic Bacteriology

• Children (< 2yrs)
• Splenectomy, sickle cell disease and other hemoglobinopathies: As spleen is the site of
destruction of capsulated bacteria, the conditions where the opsonization and clearance
of circulating bacteria by the spleen is hampered, there is increase risk of pneumococcal
Nature of infecting serotypes of
infection. Pneumococcus:
• Underlying comorbid diseases, such as chronic lung, heart, kidney and liver disease, • In children: Serotypes , 6B,
cochlear implants, diabetes mellitus and immunosuppression (e.g. HIV). V, 1 , 18C, 1 F, and 23F are
• Underlying viral upper respiratory tract infections (e.g. Influenza). common
• In adults: Serotypes 1–8 are
• Nature of infecting serotypes: common
○ In children: Serotypes 4, 6B, 9V, 14, 18C, 19F, and 23F are common • Virulent serotypes: Serotype 3
○ In adults: Serotypes 1–8 are common followed by 7 are more virulent
○ Virulent serotypes: Serotype 3 followed by 7 are more virulent and they produce and they produce mucoid
colonies.
mucoid colonies.

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Jeremie R. Galapon, RMT, MT(ASCPi)
Manila Adventist College
Medical Laboratory Science Department

Chapter 6 - Streptococcus, Enterococcus and Pneumococcus
132 Review of Microbiology and Immunology
Treatment of Pneumococcal
Infections:
• Penicillin G remains the DOC
• Ceftriaxone can be given
alternatively.
• Oral amoxicillin is
recommended for children with
acute otitis media.
Contraindications to PPV-23
include:
• Malignancies
• Pregnancy
• Children of < 3 years
Section 3
81
Laboratory Diagnosis
S. pneumoniae can be differentiated from Viridans streptococci by various features:
Properties Pneumococcus Viridans streptococci
Morphology Lanceolate or flame shaped Round oval
Arrangement Gram-positive cocci in pairs Gram-positive cocci in long chains
Capsule Present Absent
On blood agar Draughtsman or carom coin colony Convex shaped colony
Liquid medium Uniform turbidity Granular turbidity
Bile solubility Soluble in bile Insoluble in bile
Inulin fermentation Fermenter Nonfermenter
Optochin Sensitive Resistant
Mice Pathogenicity Pathogenic Nonpathogenic
Treatment
Penicillin G remains the drug of choice; cephalosporins, such as ceftriaxone can be given
alternatively.
Oral amoxicillin is recommended for children with acute otitis media.
Prevention (Capsular Polysaccharide Vaccines)
Two types of pneumococcal vaccines are available.
23-Valent Pneumococcal Polysaccharide Vaccine (PPV23)
PPV23 includes capsular polysaccharide of 23 serotypes of pneumococci. It gives protection
for about 5 years.
Indication: It is recommended for people with
• Asplenia or splenic dysfunction • Diabetes mellitus
• Sickle cell disease or celiac disease • Cochlear implants
• Chronic lung, heart, kidney and liver disease • Cerebrospinal fluid leaks
• Immunocompromised patients (HIV) • Age above 65 years
Contraindication to PPV-23 include:
Malignancies, pregnancy and children of < 3years: As capsular antigens are examples of T-
independent antigen, they are poorly immunogenic to children of < 3 years. Hence, PPV-23
is not useful among children of < 3 years.
7-Valent Polysaccharide Conjugate Vaccine (PCV-7)
It consists of capsular polysaccharide of 7 serotypes added to a protein conjugate. It mainly
includes the childhood serotypes (such as 6B, 9V, 14, 19F, 23F, and 18C):
• When a protein conjugate is added, it increases the immunogenicity of capsular antigen
(act as adjuvant), hence can be given to children of < 3years.
• Schedule: 4 doses administered at 2, 4, 6, and 12–15 months of age.
• As, resistance to antibiotics is most often noted in pneumococcal serotypes 6, 9, 14, 19,
and 23; hence use of PCV-7 has shown to decrease pneumococcal resistance.
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Jeremie R. Galapon, RMT, MT(ASCPi)
Manila Adventist College
Medical Laboratory Science Department