Introduction

to
Microbiology

Anas Abu-Humaidan
M.D. Ph.D.
Lecture 18
&
Streptococci / Classification

• The classification of more than 100 species within the genus Streptococcus is complicated because three
different overlapping schemes are used:
- antigenicdifferencesem
i position
of bacterial cell was

• (1) serologic properties: Lancefield groupings (originally A to W);

• (2) hemolytic patterns: complete (beta [β]) hemolysis, incomplete (alpha [α]) hemolysis, and no (gamma [γ])
hemolysis;
• (3) biochemical (physiologic) properties.

• The most important pathogenic streptococcal species for humans include Streptococcus pyogenes (group A
streptococcus/ GAS) , Streptococcus agalactiae (GBS), group D streptococcus (enterococci), Streptococcus
pneumoniae, and Streptococcus viridans.
Streptococci / Classification / hemolytic patterns
Streptococci / Classification / Lancefield groupings
Streptococci / Classification / biochemical (physiologic) properties

interfer

"celldeath
withhe &
*
sensitive
G

Sit
& & GAS
-c
Streptococcus pyogenes
Group E

chairs 33-Hemolytic

& 12 um
after
of
white
> colonies
-

d
2n
sepherical incubation
Itozmmis
size

• S. pyogenes are spherical cocci,&1 to 2 μm in diameter, arranged in chains.

• After 24 hours of incubation, 1- to 2-mm white colonies with large zones of β-hemolysis are observed
O
• Harbors the Lancefield group A antigen, and is often called group A streptococcus (GAS)
 -
d
superantigens
&gts pyogenes

help bacterium
adher

avoid
to epithelial
cels ofo

de oponization
Frotie
>
-
by
*
timulate edi ot immune system
Mongwithtiereasion
tissue
overs have Human
immune
a it miniching
To host tissues

stee och Shin & mucous

mD
syndrome
&
&

&
&
* Je vi r udne or
&

• S. pyogenes has multiple mechanisms for avoiding opsonization and phagocytosis. The hyaluronic acid capsule is a poor
immunogen and interferes with phagocytosis. The M proteins also interfere with phagocytosis by blocking the binding of
the complement component C3b . The M proteins also facilitate adherence to host cells S. pyogenes can invade into
epithelial cells, a process that is mediated by M protein and F protein.
• S. pyogenes has C5a peptidase on the surface. This serine protease inactivates C5a.
inactivating - reduce
it
recriment ofimme cells
Streptococcus pyogenes / Toxins and enzymes
eerthyrogenic
toxins

• The streptococcal pyrogenic exotoxins (Spe), originally called erythrogenic toxins, are produced by lysogenic genome
enta
strain. The toxins act as superantigens. not trigger strong response immune
does
Presence of
active
Obes
in
-remains
• Streptolysin S is an#
oxygen-stable, nonimmunogenic, cell-bound hemolysin that can lyse erythrocytes,
-oleukocytes, and platelets, and is responsible for the characteristic β-hemolysis seen on blood agar media.
antibodies present it - ↑ chance of chomitoid fore & glomo s
>
-

~
some against inactivated by oxygen
• Streptolysin O is an oxygen-labile
- hemolysin capable of lysing erythrocytes, leukocytes, platelets, and cultured
cells. Antibodies are readily formed against streptolysin O (antistreptolysin O [ASO] antibodies), and are
useful for documenting recent group A streptococcal infection (ASO test). patients with cutaneous infections
do not develop ASO antibodies. es localized infection

• Streptokinase lyse blood clots and fibrin deposits and facilitate the rapid spread of S. pyogenes in infected
tissues.
&
• DNases A to D can depolymerize free deoxyribonucleic acid (DNA) present in pus. eliquity bacterial spread
Pus

aiding in
 ①

Espyogen =

3
e
cautions
⑧ -
Toxins
induceoptosis
Streptococcus pyogenes / Epidemiology

• The Centers for Disease Control and Prevention (CDC) has estimated
infection shininfections
that at least 10 million cases of
inroat
noninvasive disease occur annually, with pharyngitis and pyoderma the most common infections. Group A
streptococci can colonize the oropharynx of healthy children and young adults in the absence of clinical
- -

disease.
2

• S. pyogenes disease is caused by recently acquired strains that can establish an infection of the pharynx or
skin before specific antibodies are produced or competitive organisms are able to proliferate.

• The pathogen is spread from person to person through respiratory droplets. Crowding, such as in classrooms
and day-care facilities, increases the opportunity for the organism to spread, particularly during the winter
months
Streptococcus pyogenes / Clinical correlations reddentarget
Exudate
pharyngitis Fo

Fever
scarlet

cellutis bacteria's
,
can cause necrosis e a
flesh eating
pyoderma
Streptococcus pyogenes / Clinical correlations
After Erection
in

• Post-streptococcal glomerulonephritis nephrogic

(PSGN) is an immunologically-mediated strains Endocarditi
sequela of pharyngitis or skin infections antibodies
caused by nephritogenic strains of
Streptococcus pyogenes.
>
-
molecular miniry
• Rheumatic fever (RF) is an inflammatory
auditing a i

S
disease that can involve the heart, joints,
skin, and brain. The disease typically
develops two to four weeks after a
streptococcal throat infection.
·

go
-
jo
scarlet feuer
Streptococcus agalactiae
Stationle B
streptococcus
Group

⑨
• Distinction of GBS from other streptococci can be based on GBS antigen detection or on
O
biochemical reactions including resistance to bacitracin

• Group B streptococci colonize the lower gastrointestinal tract and the genitourinary tract.
Transient vaginal
-
carriage has been observed in 10% to 30% of pregnant women.

• men and nonpregnant women with group B streptococcal infections are generally older and
have debilitating underlying conditions. The most common presentations are bacteremia,
pneumonia, bone and joint infections, and skin and soft-tissue infections
of disease
rately cause
Streptococcus agalactiae Group B

&

magitis
M &
infection of newly Birthed
outsideeith
- Hospital

ov
~

Yesscom

• Neonatal infection is divided into early-onset infection, occurring at less than 7 days of age; and late-onset infection,
occurring at or beyond 7 days of age. Both are characterized by bacteremia or meningitis.
 > Pneumonia & RES
Streptococcus pneumoniae - Piratory
infections
Incomplete Notu
hemolysis
Type
oHood
Agar
ou
pape
greenh

• The pneumococcus is an encapsulated gram-positive coccus. The cells are 0.5 to 1.2 μm in diameter, oval, and
arranged in pairs (commonly referred to as diplococci)

• The α-hemolytic appearance results from production of pneumolysin, an enzyme that degrades hemoglobin,
producing a green product
Streptococcus pneumoniae / Structure

-if itdoesnonenogenic

• Virulent strains of S. pneumoniae are covered with a complex polysaccharide capsule, used for the serologic
classification of strains.
• The most commonly isolated serotypes are used in a polyvalent vaccine.
Streptococcus pneumoniae / Epidemiology
without causing
~ infections !I
• S. pneumoniae is a common inhabitant of the throat and nasopharynx in healthy people, with colonization more
common in children than in adults and more common in adults living in a household with children.

• Pneumococcal disease occurs when organisms colonizing the nasopharynx and oropharynx spread to the lungs
(pneumonia), paranasal sinuses (sinusitis), ears (otitis media), or meninges (meningitis).

• The introduction of vaccines for pediatric and adult populations has reduced the incidence of disease caused by S.
pneumoniae .

is
=
n5
Streptococcus pneumoniae / Pathogenesis
Pneumonihasel
a piTrapped
tvia sie
S ·

• The disease manifestations are caused primarily by the host response to infection rather than the
production of organism-specific toxic factors Pneumolysin

• After colonization in upper respiratory tract (e.g. oropharynx) bacteria can migrate to lower respiratory
tract, Secretory IgA in mucus traps bacteria by binding the bacteria to mucin with the Fc region of the
driea
antibody. The bacterial IgA protease prevents this interaction. Pneumolysin can destroy the ciliated
epithelial cells and phagocytic cells.

• A characteristic of pneumococcal infections is the mobilization of inflammatory cells to the focus of

infection. Amidase, enhances release of the cell wall components (Teichoic acid and the peptidoglycan
fragments) which can activate complement and initiate an immune response.
attatch to human
cells a invade them & funcer of a midage

• Phosphorylcholine present in the bacterial cell wall can bind to receptors for platelet-activating factor ,
and helps in host cell invasion, and is important for &
amidase function.

• The virulence of S. pneumoniae is a direct result of the capsule. Encapsulated (smooth) strains can cause
disease in humans and experimental animals, whereas nonencapsulated (rough) strains are avirulent.
activates immune response
 viral
-
infection &
superimposed Bacterial

opennesses
response
needg virulence
&
oneena
use Lobes"dd
Viridans Streptococci
• The viridans group of streptococci is a heterogeneous collection of α-hemolytic (producing a green
coloration on blood agar plates (hence the name "viridans", from Latin "vĭrĭdis", green)) and nonhemolytic
streptococci.
• The viridans streptococci colonize the oropharynx, gastrointestinal tract, and genitourinary tract.

Pare
Enterococcus
• The enterococci are gram-positive cocci, typically arranged in pairs and short chains .
tract
~ digistive
• As their name implies, enterococci are enteric bacteria that are commonly recovered in feces. E. faecalis is
-
found in the large intestine in high concentrations (e.g.,00
105 to 107 organisms per gram of feces) and in the
genitourinary tract. Similar distribution for E. faecium.
~
• The cocci grow both =aerobically and> anaerobically in a broad temperature range (10° C to 45° C), in a wide -

pH range (4.6 to 9.9), and in the presence of high concentrations of sodium chloride (NaCl) and bile salts .
--

helps them
G
O
• Variable hemolysis pattern.
-
which in

surviveintestine

• Virulence is mediated by two general properties: (1) ability to adhere to tissues and form biofilms and (2)
-
antibiotic resistance
-

• enterococci are one of the most common causes of infections acquired in the hospital (nosocomial
infection). The urinary tract is the most common site of enterococcal infections, and infections are
frequently associated with urinary catheterization or instrumentation . &
 Enterococcus from other date n a
& to differentiate bile-escalin
Positive bacteria like
Enterococ ,

S
Positive control (PN): E. faecalis (ATCC
29212)

Negative control (NC): Escherichia coli

(ATCC25923)
O
Test: Positive live
canenvironment G
with bile
salt
E
indicator of inhibit GE
ability
their to

• Principle of Bile Esculin test

&
Bacteria that are bile-esculin positive, first of all, able to grow in the presence of bile salts. Hydrolysis of the
esculin in the medium results in the formation of glucose and esculetin. Esculetin reacts with ferric ions
-

present ferric citrate in the medium to form a phenolic iron complex which produces dark brown or black
color.
 &

-
blood clotting protien
↓

-
-

specific

&
Enterococcus
antige
&

faecalis

=>
-
 immunocomprimized
• Age: 65
-
• Medical History: Type 2 diabetes, hypertension
• Hospitalized post operation with a urinary catheter
• Complaint: Painful urination and fever
• Clinical History:
• Mr. X reports a low-grade fever and a sense of general malaise. Urine is turbid
and he has suprapubic tenderness . >

• Gram stain shows gram positive cocci that is bile-esculin positive

What is the most probable pathogen?

• Age: 7
• Medical History: None significant
• Presenting Complaint:
• Emily is brought to the pediatrician by her parents with complaints of a sore
throat, fever, and a red rash.

• Clinical History:
• Over the past 24 hours, Emily developed a sudden-onset sore throat and fever.
Her parents noticed a fine red rash that started on her neck and spread to her
chest and extremities.
• Physical Examination:

• Vital Signs: Temperature 101.8°F (38.8°C), heart rate 110 bpm, respiratory rate 20/min.
• Throat Examination: Presence of redness and swollen tonsils with yellowish-white exudate.
• Skin Examination: Diffuse red rash with a sandpaper-like texture.
• Diagnostic Tests:

• Throat Culture: Positive for Group A Streptococcus (Streptococcus pyogenes).

• Scarlet Fever Rash Confirmation: The rash, along with the clinical presentation and positive
throat culture, confirms scarlet fever.
• Medical Management:

• Antibiotic Therapy: Initiated with oral penicillin to eradicate the streptococcal infection.
• Symptomatic Relief: Paracetamol for fever and throat lozenges for pain.
• Follow-up:

• 48 Hours Later: Emily's fever subsides, and the rash begins to fade.
• Completion of Antibiotics: The full course of antibiotics is administered to prevent complications
like rheumatic fever.
• Question:

• Describe the clinical features that aid in the diagnosis of scarlet fever in Emily.

• Why is it important to promptly diagnose and treat Group A Streptococcus infections, such as
scarlet fever, and what potential complications should be considered in the management of this
condition in pediatric patients?
Further reading:

• Jawetz, Melnick & Adelberg's Medical Microbiology, 26th edition-

Section 3: Bacteriology-
Chapter 14: The Streptococci, Enterococci, and Related Genera

• Murray - Medical Microbiology 8th Edition

Section 4: Bacteriology
Chapter 19: STREPTOCOCCUS AND ENTEROCOCCUS