Streptococcus Lect 20 Micro Exam 2

Front 1

streptococci - gram positve or negative? Appearance?

Back 1

positive. Planar division is perpendicular to long axis. grows in specific orientation with clusters forms, but should be evidence of chain form too.

0.5 to 1 microns; non motile
-most are facultative anaroebs (some are canophilic- requirement for enhanced Co2 to grow)

Front 2

Describe 3 schemes of differentiation for streptococcus

Back 2

dont really behave well when it comes to differentiation

1. hemolysis pattern
2. Lancefiled group (serology of beta hemolytic Strep) based on similar cell wall carbs, groups A to W
3) biochemical properties

Front 3

1) S. Pyogenes common name, hemolysis and Lancefiled cell wall
2) S agalactiae
3) Viridans group - S sanguis, S mutans, S salivarius
4) S pneumoniae
5) others

Back 3

1) Group A, Beta, A, surface protein 100 M protein
2) Group B, Beta or a or none, B, polysaccharides 1a, 1b, 1c, II-VIII (capsule types)
3) Viridans Strep common name, alpha or non
4) Pneumococcus; alpha, usualy 80+ surface polysaccharides
5) Beta, a or none. Lancefiled cell wall C, E-T

Front 4

Describe S pyogenes
-cause
-symptoms

Back 4

Group A Predominant cause of human pharyngitis
(S. pyogenes) Asymptomatic colonization of UR tract and skin
Spread person to person via respiratory droplets
or through breaks in skin

CDC 2005 report indicated 4700 cases of invasive S. pyogenes infection, 129 Streptococcal TSS, and 10 million cases of non-invasive disease

Children at higher risk for disease 5-15 yrs of age

Seasonal incidence (pharyngitis cold months)

Front 5

Group B strep (S. agalactiae)

Back 5

Colonize lower GI tract and GU tract
(S. agalactiae) Most infections are of newborns; acquired from mother
during pregnancy or birth (10-30% carriage in
pregnant women)
Neonates at high risk for infection (~60% of neonates
born to colonized mothers become colonized)
More total cases in adults but incidence higher in neonates
No seasonal incidence

Front 6

Viridans streptococci

Back 6

Colonize oropharynx, GI tract, and
GU tract (rare on skin)
Cause a wide variety of infections
(dental caries, subacute endocarditis
intra-abdominal abscesses)

Front 7

S. pneumoniae

Back 7

Ubiquitous
Colonize naso- and oro-pharynx
(particularly young children)
Infections caused by endogenous spread
People with prior bacterial or viral
respiratory infection have risk
Seasonal incidence observed (cool months)
Spread through aerosols is rare

Front 8

What's the only test to differentiate Streptococci

Back 8

Gram stain

Front 9

1) streptococci is catalse pos/neg?
2) describe basic scheme of lab differentation of streptococci at teh hemolysis stage until you get to group B differentiation

Back 9

neg organisms
2) if its Beta hemolysis, its bacitracin.
can either be S : Group A, or R; B,C, G, F, D. Then do CAMP factor.
Camp - : others, specific antigen analysis
Camp + : Group B

Front 10

What is CAMP test?

Back 10

Christike Atkins, Munch Petersen reaction Group B streptococci produce a diffusible, heat-stable protein (CAMP factor) that enhances -hemolysis of Staphylococcus aureus. S. aureus (streaked vertically) produces sphingomyelinase C, which can bind to erythrocyte membranes. When exposed to the group B CAMP factor

Front 11

1) After alpha hemolysis, wha test do you do?
2) What are the 2 divisions after the Optochin
3) What happens if bile esculin is +?

Back 11

1) Bile esculiin. - : Optochin
+: Group D
2) S: S. pneumoniae R: "Viridans"
3) considered Group D. If you have 6.5% NaCl, - will be non enterococci and + will be Enterococcus

Front 12

Decribe capsule

Back 12

- outermost layer
- carbohydrates
- comprised of glucuronic acid
and N-acetylglucosamine
physical barrier to
phagocytosis as opsonins (Ab
and C’) bind to structures
below the capsule

Front 13

Describe M protein

Back 13

- major type-specific protein
- two polypeptide chains
anchored in CM
- highly conserved molecule
used for serotyping (100+)
- 2 classes
I = C region exposed
(Ab produced- linked to RF)

II = C region not exposed
(Ab not produced)
- Role in attachment and
invasion of host cells
- can bind to factor H thus
inhibiting complement
deposition,

Front 14

1) F protein
2) pyrogenic exotoxins

Back 14

1) - appear to be predominantly
involved with attachment to
host cells
2) - originally called erythrogenic
toxins
- 4 immunologically distinct types
(SpeA, SpeB, SpeC, SpeF)
act as superantigens
many systemic effects are
caused by host secreted
cytokines:
TNF-a
IL-1, IL-2, IL-6
Ifn-γ
(specifically shock and organ
failure)
linked to rash characteristic of scarlet fever, as well as to necrotizing fasciitis, and streptococcal TSS

Front 15

1) Streptolysin S
2) Streptolysin O

Back 15

Streptolysin S
- cell bound
- oxygen-stable hemolysin
- produced in presence of serum
- non-immunogenic
- responsible for b-hemolysis

Streptolysin O
- oxygen-labile hemolysin
Immunogenic
- Useful diagnostic for recent group A infection
- Inhibited by cholesterol thus no Ab during skin infections

Front 16

Streptokinase

Back 16

- At least 2 types (A and B)
- Cleave plasminogen resulting in plasmin which on turn cleaves fibrinogen and fibrin (digest clots)
- Anti-streptokinase Ab are
useful as marker of infection

Front 17

Deoxyribonucleases (DNases)

Back 17

- 4 types A to D
- are not cytolytic, but
depolymerizes DNA in pus
facilitates spread
- Ab against DNAse B are good
markers of cutaneous S. pyogenes infection (as no streptolysin O Ab generated)

Front 18

1) C5a peptidase

Back 18

1) inhibits leukocyte activation
and recruitment by
degrading C5a

Front 19

Mechanisms of attachment of S pyogenes to host cells

Back 19

- Group A possess a broad array of structures that mediate attachment to host cells (epithelial) via specific receptors

- More than 10 distinct adhesins have been identified

- The most important adhesins include: Lipoteichoic acid
M-proteins
F-proteins

- After attachment, invasion of cells occurs where M- and F-proteins play significant roles

Front 20

Describe the colonization and migration virulence factors of S. pneumonia

Back 20

Surface adhesins Bind to cells
Secratory IgA protease Disrupts IgA-dependent clearance
Pneumolysin Cytotoxin - binds to cholesterol; may
destroy ciliated epithelial cells

Front 21

Virulence factors in tissue destruction

Back 21

Teichoic acid 2 forms, Activates alternate C’ pathway
Peptidoglycan Activates alternate C’ pathway
Pneumolysin Activates classical C’ pathway; stimulates
IL-1 and TNF-a from leukocytes
Hydrogen peroxide Reactive oxygen intermediates cause tissue
damage
Phosphorylcholine Binds phosphodiesterase-activating factor
promoting entrance into cells
Phagocytic survival

Front 22

Virulence factors in phagocytic survival

Back 22

Capsule Antiphagocytic; unencapsulated are avirulent
Pneumolysin Suppresses oxidative burst associated with
phagocytosis

Front 23

Name diseases caused by S. pyogenes

Back 23

Streptococcal pharyngitis (Strep throat)

- Cutaneous infections
Pyoderma (Impetigo): purulent infection of skin
(common 2-5yr old)

Erysipelas: acute skin infection (also group C or G Strep). - acute skin infection
- young children or older
adults
- face or extremities
- raised, painful, warm
- usually following S.
pyogenes but also
group C or G
Cellulitis: similar to erysipleas but invovles deeper tissues

Necrotizing fasciitis (streptococcal gangrene)
deep subcutaneous tissues
treatment usually requires surgical debridement

Streptococcal toxic shock syndrome - due to bacteremia. M proteins 1 and 3.

Front 24

What are 3 complications of Group A pharyngitis

Back 24

-Scarlet fever
-Rheumatic fever
-Acute glomerulonephritis

Front 25

Scarlet fever

Back 25

rapid onset after pharyngitis (1 -2 days)

: toxin-mediated, red rash

: starts on chest and radiates to extremities

: yellow-wound develops on tongue leads skin is shed revealing raw tongue surface “strawberry tongue” characteristic of SF

: rash disappears 5 – 7 days with desquamation

Front 26

Rheumatic fever

Back 26

- Prior S. pyogenes pharyngitis and presumably development of cross-reactive antibodies (specifically those of M protein type 1, 3, 5, 6, and 18)

- Characteristics: non-suppurative complication
: inflammatory changes to heart, joints, blood vessels and sub-cutaneous tissues

- Chronic heart valve damage can occur, can lead to arthritis with involvement of multiple joints (can have migratory pattern)

- Incidence is on the decline and primarily affecting school-age children

- No specific diagnostic test available, thus clinical diagnosis is required (culture +ve, group A antigen, anti-streptolysin O, or other)

- Can recur with subsequent re-infection if appropriated prophylactic antibiotic is not administered

Front 27

Acute glomerulonephritis

Back 27

- Acute inflammation of glomeruli

- Characteristics : non-suppurative complication
: edema, hypertension, hematuria, proteinuria

Diagnosis is based on clinical presentation and recent S. pyogenes
infection

- Usually young patients recover; however, progressive and
irreversible loss of kidney function can occur

Front 28

Disease caused by S. agalactiae
-early and late onset neonatal disease

Back 28

Early onset neonatal disease (serotypes Ia, III, V)
within 7 days of birth present with symptoms
of pneumonia, meningitis, and sepsis

Late onset neonatal disease (serotype III)
More than 1 week (to 3 months) after birth
present with symptoms of meningitis and
bacteremia

Front 29

What are the consquences of S. alagalactiae in Group for pregnant and non - pregnant females

Back 29

Pregnant Women
Urinary tract infections, Amnionitis, Endometritis
Bacteremia (with rare complications of endocarditis,
meningitis, and osteomyelitis)

- Non-pregnant females and men (serotypes Ia, V)
Usually associated with older individuals and an
underlying condition (depressed immunity)
Bacteremia, pneumonia, bone and joint infections
Skin and soft tissue infections

Front 30

Viridans Streptococci dissease
-Subacute bacterial endocarditis ex. any others?

Back 30

1) S. gordonii, S. mitis, S. mutans, S. oralis

Abscesses
S. intermedius, S. anginosus, S. constellatus

- Dental Caries
S. mutans, S. oralis, S. sanguis

- Bacteremia (neutropenic individuals)
S. mitis

- GI infections
S. bovis

Front 31

Describe microbial relationship in dental caries

Back 31

S. mutans can be present in dental plaque but a person doesn't need to have caries.
Lactobacillius alone - dont get disease.

if you have both present, you see errosion of enamel. considered primary and secondary cariogen.

Front 32

Describe the diseases causes by S. pneumonaie and clinical presentations of these diseases

Back 32

Pneumonia:
Clinical manifestations
fever 39-41ºC, productive cough, chest pain
radiograph supports lobar pneumonia

- Meningitis: CNS infection via bacteremia

- Sinusitis: usually preceded by viral infection and PMN
infiltrate occludes the sinus

- Otitis media: usually preceded by viral infection and
PMN infiltrate occludes the ear canal

- Bacteremia: Bacteria in blood (blood should be sterile)
can lead to endocarditis

Front 33

Treatment and control for
1) S. pyogenes
2) S. agalacitae
3) S. pneumoniae

Back 33

1) S. pyogenes
Penicillin is the drug of choice (erythromycin and cephalospirin)
Beginning antibiotics within 10 days of pharyngitis prevents
Rheumatic fever
Prophylactic antimicrobial chemotherapy to limit endocarditis
(common prior to dental procedures)
2) Penicillin G is drug of choice (penicillin and aminoglycoside for
serious infections; vancomycin if patient is allergic to
penicillin)

High-risk pregnancies penicillin 4h prior to delivery
3) Penicillin is the drug of choice (resistance on increase;
fluoroquinolones, vancomycin also)

7-valent conjugate vaccine is recommended for all children
under age of 2

23-valent vaccine for adults
(not protective against all clinically relevant strains but is
suggested for high risk)

Front 34

Enterococcus; epi, transmission; pathogenesis; clinical findings; lab diagnosis; treatment

Back 34

A. Epidemiology and Transmission
1. Present as part of the normal flora of the colon, urethra and female genital tract.
2. They cause up to 10% of all hospital-acquired infections.

B. Pathogenesis and Immunity
1. No significant virulence factors or exotoxins have been identified.

C. Clinical Findings
1. Enterococcus faecalis is commonly found in hospitals and can cause urinary tract
infections, bacteremia and endocarditis, and wound infections.

D. Laboratory Diagnosis
1. Gram-positive cocci
2. Can be α, β, or non-hemolytic.
3. Grows in 6.5% NaCl and hydrolyzes esculin in the presence of bile; characteristics used
in diagnostic lab tests.

E. Treatment and Prevention
1. Many of these strains are multiply antibiotic resistant, including to vancomycin.
2. No vaccine.