STREPTOCOCCUS

- Gram (+) cocci in chains (Their form, chains or clusters, depends on their pattern
of growth)
- Large and heterogeneous group of bacteria and no one system suffices to classify
them.
- Catalase (-)
- Nutritionally fastidious organisms w/c is why primary plating media is BAP.
- Some are encapsulated. (Streptococcus pneumoniae)
- Facultative anaerobes.
- Nonmotile, non-spore forming.
***Peptostreptococci are obligate anaerobes.

- Requires enriched medium for growth.

- Requires 5-10% CO2 (Therefore, it requires the candle jar method).
- Not halophilic w/c is why it cannot be grown on MSA.
Clinically Significant Strep:
Group A, Group B, Group D, Streptococcus pneumoniae, Viridans Streptococci
Classifications of Streptococci

A. Hemolysis (Smith and Brown Classification)

- Classified according to Beta-hemolytic, Alpha-hemolytic, or Gamma-hemolytic.
B. Serological Specificity of Cell Wall Group-Specific Substances (Lancefield
Classification)
- SEROLOGICALLY ACTIVE CARBOHYDRATE C-POLYSACCHARIDE.
- Determined by an amino sugar. (Cell wall Carbohydrate)
- Group A Streptococci = rhamnose-N-acetylglucosamine. (S. pyogenes)
- Group B = rhamnose-glucosamine polysaccharide. (S. agalactiae)
- Group C = rhamnose-N-acetylgalactosamine.
- Group D = glycerol teichoic acid containing D-alanine and glucose. (Enterococci)
- Group F = glucopyranosyl-N-acetylgalactosamine.
- Methods for Detection: Extraction of uncentrifuged culture treated with hot
hydrochloric acid, nitrous acid or formamide; By autoclaving of cell suspensions;
By enzymatic lysis of streptococcal cells w/ pepsin or trypsin.
- The extracts produced by the above test yield precipitin reactions w/ specific
antisera.
C. Bergeys/Academic Classification
- According to physiologic requirements and thermal requirements.
- Pyogenic Streptococci = produces pus, mostly Beta-hemolytic and grows at
neither 45C nor 10C.
 - Viridans Streptococci = grows at 45C but not at 10C and is a normal flora in the
mouth. (Streptococcus mutans, S. salivarius, S. mitis, S. sanguis, S. sanginosus)
- Enterococcus = grows at 45C and 10C and is a normal fecal flora. (Enterococcus
faecalis)
- Lactic Group = grows at 10C but not at 45C and causes souring of milk. (S.
cremoris, S. lactis)
Group A Streptococci

- Predominantly pathogenic for man.

- Exhibits beta-hemolysis
- Causes strep throat, rheumatic fever, rheumatic heart disease, post-streptococcal
glomerulonephritis, scarlet fever.

Streptococcus pyogenes

- The most virulent Streptococci in humans.

- It is an obligate human parasite.
- Mode of transmission is via person to person and is spread through respiratory
secretions.
- Known as the prototype human pathogen.
- Produces large zones of beta-hemolysis around colonies.
- PYR-positive because of hydrolysis of L-pyrrolidonyl-B-naphthylamide.
***PYR = Pyrrolidonyl Arylamidase Test.

- Susceptible to 0.04 units of bacitracin (Taxo A).

- Gram (+) cocci in chains w/c divide in a plane perpendicular to the long axis of the
chain.
- Grow as discoid colonies and is beta-hemolytic.
- Carbohydrate utilization is through fermentation, producing lactic acid as by-
product.
- Growth and hemolysis requires incubation at 5-10% CO2 and 37C.
- Called as pyogenes because it is pus-producing.
- Primary plating media is BAP since it is nutritionally fastidious.
- We add trimethoprim-sulfamethoxazole (SXT) since S. pyogenes is resistant to
SXT. Therefore, SXT is selective for S. pyogenes.
Antigenic Structures:
1. Capsule S. pyogenes produces capsules composed of hyaluronic acid.
 - The capsule binds to hyaluronic-acid-binding-protein, CD44, present on epithelial
cells w/c induces disruption of intercellular junctions allowing microorganisms to
remain extracellular as they penetrate the epithelium.
2. M protein It is the major virulence factor of Streptococcus pyogenes.
- Appears as hair-like projections of the streptococcal cell wall.
- When M protein is present, the streptococci are virulent and in the absence of
specific antibodies, they are able to resist phagocytosis by neutrophils.
- S. pyogenes that lack M protein are avirulent.
- Precipitates fibrinogen.
- Clumps platelets & leukocytes, inhibits migration of leukocytes.
- Inhibits activation of complement.
- Plays an important role in the pathogenesis of rheumatic heart disease: a
component of the cell wall of Streptococci with M protein induces antibodies that
react with cardiac muscle tissue.
3. IgG and IgA-binding proteins
- Binds to Crystallizable Fragment of IgG and IgA.
- The binding proteins are specific to IgA since the mode of transmission of S.
pyogenes is person to person via respiratory secretions so we acquire the bacteria
through our upper respiratory tract. In the URT, mucus is abundant and IgA is
found in all types of bodily secretions. Because of IgA in mucus, S. pyogenes is
not virulent as it will signal WBCs to kill the bacteria but because of the presence
of IgA-binding proteins, IgA cannot signal WBCs to kill the bacteria (similar
mechanism of action to Protein A) and therefore contributes to virulence of S.
pyogenes.
4. C5a Protease
- Cleaves C5a component of complement.
- Inhibits neutrophils chemotaxis in vitro.

***Complement System facilitates killing of pathogens.

Classical It starts with the activation of C1 complex w/c cleaves C4 w/c cleaves C2 w/c
cleaves C3 into C3a and C3b, C3b then cleaves C5 into C5a and C5b. C5b then recruits
and assembles C6, C7, C8 and C9 w/c are all coupled and form the MAC (Membrane
Attack Complex) w/c creates a pore or hole in the membrane that can kill or damage
pathogens.

C5a and C3a functions as an anaphylatoxin w/c triggers degranulation (histamine

release) of mast cells leading to increasing vascular permeability (Vasodilation) and
smooth muscle contraction. But these two function most importantly for inducement of
chemotaxis w/c is the migration of macrophage to site of infection. C5a is the
anaphylatoxin with the highest activity while C3a works with C5a for chemotaxis.

***Each cleavage of complexes releases cytokines w/c are chemical messengers aiding
the immune response.
Alternative revolves around the alternate pathway of C3 complex.

Mannose-binding Lectin Pathway functions similar to Classical pathway with the

difference being in C1 complex. In this pathway, Mannose-binding lectin initiates the
complement cascade w/c functions very similar to C1 in the Classical pathway.

5. Lipoteichoic Acid
- It is important for the attachment of Streptococci to epithelial cells. (Adherence)
6. Group-Specific Cell Wall Antigen (Since S. pyogenes is a Group A Strep =
rhamnose-N-acetylglucosamine.)
- The basis of serological grouping (Lancefield Classification).
- It has no relationship to virulence of Streptococci. T substance, an antigen found
in Streptococci, is acid-labile and heat-labile and is obtained from Streptococci by
proteolytic digestion w/c rapidly destroys the M protein .
- R protein.
- P substances.
Toxins and Enzymes

1. Streptokinase (Fibrinolysin) It converts the plasminogen of human plasma into

plasmin, an active proteolytic enzyme that digest fibrin clot. It is inactivated by a
specific antibody, antistreptokinase. Streptokinase has also been used in
therapeutic treatment for pulmonary emboli, coronary artery and venous
thrombosis.
- Streptokinases degrades clot allowing bacterial spread.
2. Streptodornase (Streptococcal Deoxyribonuclease)
- It is a group of 4 enzymes which depolymerize DNA. Streptodornase and
Streptokinase are used in enzymatic debridement meaning they help liquefy
exudates and facilitate removal of pus and necrotic tissue w/c allows antimicrobial
drugs to gain better access to the sites of infection.
- The DNases protect the bacteria from being trapped in neutrophil extracellular
traps (NETs) by digesting the NETs' web of DNA.
3. Hyaluronidase
4. Pyrogenic Exotoxin (Erythrogenic Toxin)
- 3 types of streptococcal pyrogenic exotoxins: A, B and C.
- Pyrogenic Exotoxin A is the most widely studied and is produced by S. pyogenes
via a lysogenic phage (Bacteriophage T12).
 - It has been associated with Streptococcal Toxic Shock Like Syndrome (TSLS) and
Scarlet Fever and Necrotizing Fasciitis = Exotoxin A.
- Pyrogenic Exotoxin C may also contributes to TSS but Pyogenic Exotoxin Bs
function is unclear.
- They act as superantigens w/c stimulate T cells by binding to class II MHC w/c
leads to enhanced activation of T cells, releasing increased cytokines that mediate
shock and tissue injury. (Mechanism of action is similar to Staphylococcal TSST-
1)
5. Diphosphopyridine Nucleotidase
- Associated with S. pyogenes ability to kill leukocytes.
6. Hemolysin
- Two types of hemolysins: Streptolysin O and Streptolysin S.
- Streptolysin O is a protein that is hemolytically active in the reduced state but
rapidly inactivated in the presence of oxygen (oxygen-labile). It destroys RBCs and
WBCs. It is antigenic meaning it is capable of eliciting an antibody response. It
combines quantitatively with Antistreptolysin O (ASO) w/c is an antibody that
appears in humans following infection w/ any Streptococci that produce
Streptolysin O. An ASO serum titer in excess of 160-200 units suggests recent
infection w/ S. pyogenes or an exaggerated immune response to an earlier
exposure.
- Streptolysin S is responsible for the haemolytic zones around streptococcal
colonies growing on surface of BAP. It is elaborated in the presence of serum w/c
is why it was called Streptolysin S. It is non-antigenic. It is oxygen-stable.

***Hemolysis may be surface or subsurface. Streptolysin S exhibits surface hemolysis

since it is oxygen stable and the BAP surface is subject to oxygen. Streptolysin O
exhibits subsurface hemolysis as it is oxygen labile meaning it is deactivated in the
presence of oxygen so one must puncture deep to the agar where oxygen is not
present anymore for it to exhibit its hemolysis.
Pathogenesis and Clinical Manifestations

A. Pyogenic Disease
1. Erysipelas If the portal of entry of S. pyogenes is skin, it results to erysipelas w/c
is characterized by massive, brawny edema and a rapidly advancing margin of
infection. It is mainly characterized by presence of edema and erythema.
2. Cellulitis It is an acute, rapidly spreading infection of the skin and subcutaneous
tissues. It follows infections associated with trauma, burns, wounds or surgical
incisions. It is characterized by pain, tenderness, swelling and erythema. It is
differentiated with erysipelas by two clinical findings: in cellulitis, lesions are not
raised, and the line between involved and uninvolved tissue is indistinct. It causes
a deeper infection than impetigo.
3. Impetigo (Streptococcal Pyoderma) It is the local infection of superficial layers of
skin. It consists of superficial vesicles that break down and eroded areas whose
surface is covered w/ pus and later encrusted. It is highly communicable. More
widespread infection occurs in eczematous or wounded skin or in burns and may
progress to cellulitis.
4. Streptococcal Pharyngitis (Strep Throat) It is the most common infection due to
S. pyogenes. The bacteria adheres to the pharyngeal epithelium by means of
lipoteichoic acid-covered surface pili and also by means of hyaluronic acid in
encapsulated strains. Fibronectin on epithelial cells serves as lipoteichoic acid
ligands. In adults, it is characterized by intense nasopharyngitis, intense redness
and edema of mucous membranes w/ purulent exudate, enlarged and tender
cervical lymph nodes and high fever. When pneumonia occurs, it is rapidly
progressive and severe. 20% of cases are asymptomatic and a similar clinical
manifestation of the disease occurs with IM, diphtheria, gonococcal infection and
adenovirus infection.
5. Puerperal Fever Streptococcal infection in the uterus after delivery results to
puerperal fever w/c is essentially a septicemia originating in endometritis.
6. Bacteremia/Sepsis Infection in surgical wounds.
B. Toxigenic Diseases
1. Necrotizing Fasciitis (Streptococcal Gangrene)
- Infection of the subcutaneous tissue and fascia. It is characterized by extensive
and very rapidly spreading necrosis of the skin and subcutaneous tissue. Group A
Strep that can cause necrotizing fasciitis are termed as flesh-eating bacteria.
***Pathophysiology:

Streptococcus pyogenes w/ M Protein secretes Pyrogenic Exotoxin A w/c activates T

cell nonspecifically w/c is responsible for producing increased cytokines (chemical
messengers). The recipient of these chemical messengers are the macrophages
leading increased stimulation of macrophages releasing free oxygen radicals (kills
MOs in normal levels) but in heightened (nonspecific) immune response, it also kills
subcutaneous tissues.

2. Scarlet Fever
- Caused by Pyrogenic Exotoxin A, B and C.
- It is associated with S. pyogenes pharyngitis or w/ skin and soft tissue infection.
- Signs and Symptoms include sore throat, fever, bright red tongue w/ strawberry
appearance, Forchheimer spots, Rash (most striking sign of scarlet fever)
***Strawberry cervix T. vaginalis infection
3. Toxic Shock Like Syndrome
- Characterized by shock, bacteremia, respiratory failure, multiorgan failure.
 - Tends to follow soft tissue infections.
- Erythema and Desquamative rash may occur.
- Caused by Pyrogenic Exotoxin A and B.
- S. pyogenes grows in soft tissue. The bacteria enters the bloodstream and produce
Pyrogenic Exotoxin A and B resulting to fever, shock, desquamative rash,
bacteremia, respiratory failure.
- 30% death rate.
C. Poststreptococcal Disease (Termed as Sequela)
- The disease is not due to the bacteria itself but because of complications that arise
from the primary infection.
- Caused by improper intake of medicine where bacteria are not killed 100% and
their antigens remain in hosts body.
- Rheumatic is a term relating to joint infections. (Most rheumatic infections are
autoimmune in nature)
1. Acute Glomerulonephritis It develops 1-4 weeks after S. pyogenes skin
infections. It is initiated by antigen-antibody complexes on the glomerular
basement membrane. The most important antigen w/c causes the condition is
streptococcal protoplast membrane. It is characterized by blood and protein in the
urine, edema, high blood pressure and urea nitrogen retention. Severe cases leads
to chronic glomerulonephritis w/c eventually leads to kidney failure.
***Pathophysiology:

Nephritogenic streptococci produce proteins with unique antigenic determinants

and these antigens have a particular affinity for sites w/in the normal glomerulus.
Antibodies against the bacteria then attack the antigen deposited in the glomerulus
leading to additional inflammatory response and recruitment of inflammatory cells
leading to attack of the kidney glomerulus and occlusion of the glomerulus
characterized by decreased GFR and decreased urine output, hypertension, and
eventually kidney failure.

Actual Pathophysiology (From Lecture):

It is basically an inflammation of kidneys and the actual sieving unit of the kidneys
which are the nephrons. The proper term for the disease is actually ACUTE
POSTSTREPTOCOCCAL GLOMERULONEPHRITIS. It usually precedes strep throat or
skin infections caused by S. pyogenes. Strep is antigenic, therefore the body will produce
antibodies w/c will bind and react with the antigens in strep forming an IMMUNE
COMPLEX (Ag-Ab complex). These immune complexes must be eliminated out of the
body so it enters the blood and is filtered by the kidneys. Sometimes, these immune
complexes get stuck in the glomerulus. Since there is an immune complex, there will also
be COMPLEMENT ACTIVATION w/c triggers inflammation and this causes tissue
damage. In the process of killing the antigens, the kidneys (glomerulus) get caught up in
the process leading to destruction of glomerulus. Since the filtering unit is destroyed,
proteinuria (esp. that of albumin) and hematuria occurs.

2. Acute Rheumatic Fever It is not a secondary infection.

- It usually precedes strep throat.
- M protein is antigenic therefore it has a corresponding antibody, Anti-M protein.
The human heart is said to contain a protein w/ similar structure as the
streptococcal M protein (Antigenic mimicry) w/c is why in the process of killing the
bacteria, the antibodies will also attack the heart. This phenomenon is called cross
reactivity and leads to acute rheumatic fever.
***It is the most serious complication due to S. pyogenes because it causes damage
to heart muscles and valves. Certain strains of S. pyogenes contain cell membrane
antigens that cross-react with human heart tissue antigens. The onset of rheumatic
fever is preceded by S. pyogenes infection 1-4 weeks earlier. Patients with more
severe streptococcal sore throats have greater chances of developing rheumatic
fever. It is the most important cause of heart disease in young people in developing
countries. S/S includes fever, malaise, migratory nonsuppurative polyarthritis, and
inflammation of the heart (endocardium, pericardium, and myocardium). The carditis
leads to thickened and deformed valves and to small perivascular granulomas in the
myocardium called Aschoff bodies that are replaced by scar tissue. ESR, Serum
transaminase levels, EKG/ECG are used to estimate rheumatic activity.
Diagnostic and Laboratory Tests
Specimen: depends upon the nature of infection
Microscopic: Gram (+) cocci in chains
Culture: 18-24 hrs at 37C

- BAP: Beta-hemolytic, discoid, matte or glossy colonies.

- Grows in 10% CO2
- If culture is heavily contaminated, we add SXT.
Biochemical Test:

- Catalase (-)
- Taxo A/Bacitracin Disk Test = Susceptible
- PYR test (+)
- Cotrimoxazole (SXT) = Resistant
 - Leucine aminopeptidase test (+) = similar test to PYR test.

***Principle of PYR hydrolysis. PYR means pyrrolidonyl arylamidase w/c is the enzyme
tested for in the test. It will cleave the substrate, L-pyrrolidonyl-B-naphthylamide, into B-
naphthylamide. B-naphthylamide is then detected by the detection reagent, N,N-
dimethylaminocinnamaldehyde, giving a bright cherry red color as (+).

Serological Test: Antistreptolysin O, Anti-DNase, Antihyaluronidase, Antistreptokinase,

Anti-M type-specific antibodies.
Immunity: Resistance to Streptococcal disease is M type-specific.

Treatment: All S. pyogenes are susceptible to penicillin G and most are susceptible to
erythromycin. Some are resistant to tetracyclines. Antimicrobial drugs have no effects in
cases of glomerulonephritis and rheumatic fever.
Scarlet Fever Susceptibility Tests:

- Dicks Test: Involves injecting 0.1mL toxin and 0.1mL of toxoid. Observe for 24
hrs. Erythematous and edematous skin in test arm (+). (REDNESS IN TEST ARM)
- Schultz-Charlton Test: Inject antitoxin in test arm. (+) result is blanching of
scarlatinal rash. (BLANCHING PHENOMENON since (+) is fading of the rash due
to neutralization of the erythrogenic toxin w/c causes scarlet fever.)

***Schultz-Charlton is performed when rash is already present and we check to see if

rash is that of scarlet fever.

Epidemiology: Nasal discharges of a person harbouring S. pyogenes are the most

dangerous source for spread of the bacteria.
Streptococcus agalactiae
- Group B Streptococci.
- Typically beta-hemolytic.
- They hydrolyze sodium hippurate and give a positive reaction in the CAMP test
(Christie, Atkins, Munch-Peterson).
- Part of normal vaginal flora, URT, lower GIT flora of females.
- Has a polysaccharide capsule w/ sialic acid. (Sialic acid is also found surrounding
RBCs, responsible for singling them out.)
o Antiphagocytic
o Inactivates complement system
o Host mimicry (enhances its pathogenicity)
- It causes bovine mastitis and is the leading cause of neonatal meningitis and
septicemia.
- ***Causes fulminant sepsis, meningitis or respiratory distress in infants.
 - ***Predisposing factors include diabetes mellitus, cancer, advanced age, liver
cirrhosis, corticosteroid therapy, HIV and other immunocompromised states.
- ***Infection by GBS is characterized by bacteremia, skin and soft tissue infection,
respiratory infection and GUT infection.
- Mode of Transmission:
o Adults: Group B Strep are part of the normal vaginal flora in adult females.
o Children: More susceptible to GBS infection than adults.
o Infants/Neonates: GBS ascend from the vagina and infect the amniotic fluid
through the placental membranes. Its passage is through the birth canal.
- Diagnostic Laboratory Test:
o CAMP Test in BAP (+) = formation of an arrowhead in the presence of S.
aureus. (enhanced zone of hemolysis)
o Hydrolysis of Sodium hippurate
0.4mL of 1% Sodium hippurate + GBS + Incubation at 32C for
10mins + 0.2mL Ninhydrin solution + Reincubate 37C for 10mins =
Deep purple color w/in 5-10mins.
Principle: Sodium hippurate is hydrolysed to benzoic acid and
glycine by the enzymatic action of hippuricase (present in GBS). The
benzoic acid may be detected using Ferric Chloride (FeCl3) though
this is not often used. The glycine end product is detected by addition
of ninhydrin reagent. This results to a deep purple color.
Group D Streptococcus (Enterococcus)

- ***8 species in the genus Enterococci, many of which do not cause infections in
humans.
- Divided into an Enterococcal Group and Non-enterococcal group.
- Normal GIT and fecal flora.
- Streptococcus bovis is of most importance to human disease.
- Non-hemolytic (Most often) or alpha-hemolytic.
- May be weakly catalase (+)
- Grows on Bile Esculin Agar. (Indicated by blackening of the agar)
- Associated with UTI, Endocarditis, Abscesses, Wound Infection.
- Epidemiologically associated with colon carcinoma.
- 2 Classifications:
o Enterococcal group S. faecalis, S. durans, S. faecium, S. avium. (6.5%
NaCl (+) w/ growth, Penicillin resistant, PYR (+), Leucine aminopeptidase
test (+)
o Non-enterococcal group S. bovis, S. equinus. (6.5% NaCl (-) w/out
growth, Penicillin susceptible, PYR (-)
Streptococcus pneumoniae (Pneumococcus)
 - Formerly Diplococcus pneumoniae.
- Gram (+) lancet-shaped diplococcus. (Bullet-shaped)
- Tends to form chains that is why Streptococcus.
- Encapsulated, non-motile, non-spore forming, facultative anaerobe.
- Capnophilic (5-10% CO2), always alpha-hemolytic, fastidious organisms.
- Often seen in sputum or pus.
- Easily distinguished from Viridans group because pneumococci easily lyse in the
presence of bile salts (Sodium deoxycholate) while viridans strep do not.
- Inhibited by Optochin disk while viridans strep are not.
Major Virulence Factors:
Virulence

o Capsule The capsule is highly antigenic w/c is why it has a vaccine

component due to its highly antigenic property since the antigen is used in
the vaccine. (ANTIPHAGOCYTIC)
o Pneumolysin - A cytotoxin responsible for the alpha-hemolysis of S.
pneumoniae in BAP. It facilitates host adhesion during colonization,
damages host cells by forming spres during invasion and interferes w/
immune responses during infection.
It is a normal flora in the nasopharynx of humans.

It colonizes the Respiratory Tract and may travel to the Sinuses and Middle Ear causing
SINUSITIS AND OTITIS MEDIA.

It is the major cause of community-acquired pneumonia and lobar pneumonia. (S.

pneumoniae)

***Lobar pneumonia is a form of pneumonia that affects a large and continuous area of a
lobe of the lung.
***Community-acquired pneumonia is common to people of all ages presenting w/
pneumonia but has not come into contact with hospitals and its symptoms occur as a
result of oxygen-absorbing areas of the lungs, alveoli, filling up with fluid.
RUSTY RED SPUTUM is usually suggestive of S. pneumoniae infection.
Diagnostic Laboratory Tests
Microscopic: Gram (+) lancet-shaped or bullet-shaped diplococcic

Culture: Mucoid colonies (Mucoid signifies capsule formation), dome-

shaped w/c develops to a crater-like appearance.
***S. pneumoniae is mucoid also partly due to the abundance of M protein.
***The crater-like appearance is due to S. pneumoniae being autolytic.

Biochemical Tests: Optochin (Taxo P): Susceptible (Utilizes

Ethylhydrocuprein w/c is a 6mm disk, a (+) test is indicated by a zone of inhibition of
14mm or greater.)

Bile Solubility Test: Susceptible (Utilizes bile salts, sodium

deoxycholate and taurochoate, and a (+) test is indicated by a clear solution due to S.
pneumoniaes autolytic properties.

Quellung Test: (+) (Utilizes an antisera w/c contains antibodies

against capsule of S. pneumoniae added to the sample of bacteria. This results to a (+)
test indicated by swollen capsule due to an inflammatory reaction via antigen-antibody
reaction. The test is also known as Newfeld Reaction.
Leucine Aminopeptidase Test (+).
Viridans Group

- Not yet grouped under Lancefields classification.

- Exhibits alpha hemolysis on BAP. (greenish discoloration)
- Bile Solubility and Optochin RESISTANT.
- Normal flora of the Upper Respiratory Tract.
- Seen in nasopharynx and gingival crevices.
- S. mitis, S. salivarius, S. constellatus, S. sanguis, S. mutans, S. intermedius.
- 3 Types of Infection Caused by Viridans Strep:
1. Dental Infections The bacteria binds to teeth and ferments sugar =
acid leading to dental carries.
2. Endocarditis Bacteria are implanted on endocardial surfaces of the
heart causing damaged heart valves. The bacteria cling to these valves
causing subacute bacterial endocarditis.
3. Abscesses Caused by S. intermedius, S. constellatus, S. anguinosus
w/c forms abscesses in the brain or abdominal organs.
Nutritionally Variant Strep (Abiotrophia or Granulicatella)

- Require other nutrients such as cysteine and pyridoxal (Vit. B6).

- AKA Pyridoxal-requiring Strep, Thiol-requiring Strep or Satelliting Strep.
- They are called as Satelliting Streptococci because they grow on the sides of S.
aureus colonies, revolving around them. S. aureus produces excess pyridoxal for
the growth of Pyridoxal-requiring Strep.
- Examples include S. defectivus named so because they are defective, still
requiring cysteine and pyridoxal. Another is S. adjacens named for its adjacent
growth with S. aureus colonies.
 - Usually alpha-hemolytic.
- Abiotrophia requires pyridoxal.
Group C Strep

- Normal flora of the body but can be opportunistic.

- Pathology ranges from simple wound infections to severe endocarditis.
- Examples are S. dysagalactiae, S. zooepidemicus, S. equisimitis.

Treatment and Control

- Penicillin G (Super variant of penicillin) = Group A Strep and Pneumococci.

- Clindamycin = Toxic Shock Like Syndrome.
- Erythromycin = Most sensitive drug for Strep infections.
- Ampicillin/Vancomycin = Enterococci and Pneumococci.
- 1st Generation Cephalosporin = Pneumococci.
- 3rd Generation Cephalosporin w/ or w/o Vancomycin = Meningitis.
- Azithromycin = Community-acquired pneumonia (Taken once per day due to its
high half-life, it stays longer in the blood.)
Control: Multivalent pneumococcal vaccine (Splenectomized and immunocompromised)
SUMMARY SO FAR:

Gram Stain. If Gram (+) cocci, perform catalase test. If catalase (+), perform coagulase
test. If coagulase (+), then S. aureus. If coagulase (-), then CoNS.

If catalase (-), culture on BAP. If Beta-hemolytic, perform Bacitracin Disk Test. If w/o
growth or susceptible, then S. pyogenes. If w/ growth or resistant, then S. agalactiae. If
Alpha-hemolytic, perform Optochin Test. If w/o growth or susceptible, then S.
pneumoniae. If w/ growth or resistant, then Viridans Strep.

ADDTL JAWETZ NOTES:

Other groupings of Strep:
Capsular Polysaccharide

- Classifying S. pneumoniae into over 90 types and to type the group B Streptococci
(S. agalactiae).
Biochemical Reactions
 - Includes sugar fermentation reactions, test for presence of enzymes, test for
susceptibility of resistance to certain chemical agents.
- Used for species that do not react with antibodies commonly used in the Lancefield
Classification.
Group C and G

- Have similar appearance to S. pyogenes on BAP and are only differentiated from
them by their reactions w/ specific antisera for Group C and G.
Anginosus Group

- Under which are S. constellatum and S. intermedius.

- These 2 are under Viridans group and are Vogues-Proskauer test (+).
Lactic Group (Group N) = Lactococcus

- Causes souring of milk.

- S. lactis and S. cremoris.
Viridans Group

- Important cause of endocarditis on abnormal heart valves.

- Subacute endocarditis involves abnormal valves. Viridans strep reaches the
bloodstream and establishes itself on thrombotic lesions that develop on
endothelium injured as a result of circulatory stresses.
Peptostreptococcus

- Grow under aerobic or microaerophilic conditions.

- Normal flora of mouth, URT, bowel and GUT of females.

***Type of antiserum used in Quellung Test is a polyvalent antiserum w/c contains

antibodies to all antigen types. It is also called as an omniserum.
***Viral and other respiratory tract infections lower humans natural resistance against
pneumococci. Also, alcohol and drug intoxication depresses phagocytic activity w/c
contributes to pneumococci infection. Abnormal circulatory dynamics and other
mechanisms such as malnutrition, sickle cell anemia, nephrosis, complement deficiency
and etc.
Pathology of Pneumococci:

Pneumococcal infection causes an outpouring of fibrinous edema fluid into the

alveoli, followed by RBCs and WBCs, w/c results in consolidation of portions of lung.
Many pneumococci are found throughout this exudate and may reach bloodstream via
the lymphatic drainage of the lungs.
Enterococci
- Among the most frequent cause of nosocomial infections, particularly in ICU.
HENRYS ADDTL INFO:

***Enterococcal group may exhibit alpha, beta or gamma hemolysis on BAP. Most
common species is Enterococcus faecalis and Enterococcus faecium. These 2 species
may be vancomycin resistant.

***Most common clinical manifestation for Group A strep is pharyngitis. This may be
accompanied by scarlet fever, w/c is characterized by an erythematous rash which later
desquamates. (Diffuse erythema)
***ARF may develop 1-5 weeks prior to GAS pharyngitis infection while APG may develop
10 days-3 weeks after GAS pharyngitis and skin infection.

***Culture media used for enhancement or isolation of GBS are Lim broth, carrot broth,
Granada agar. In Granada agar, GBS present with orange colonies due to organisms
own pigment. Pigmentation in this medium does not occur with any other Streptococci or
other organisms making the Granada agar specific for GBS. Biochemical tests is not
necessary for confirmation anymore.
***Taxo P/Optochin uses ethylhydroxycupreine hydrochloride (ethylhydrocuprein).

***Milleri streptococci (S. intermedius, S. constellatum, S. anginosus) are recognized by

their characteristic caramel odor.