Streptococcaceae and Enterococcus species Flashcards

1
Q

Based on hemolysis on 5% Sheep Blood Agar Medium

A

Smith and Brown’s Classification

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2
Q

denotes incomplete lysis of erythrocytes with reduction of hemoglobin and the formation of green pigment

A

α-hemolysis

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3
Q

Streptococci producing such pattern of hemolysis were later on described as “green streptococci”.

A

α-hemolysis

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4
Q

refers to the complete disruption of erythrocytes resulting to clearing of the blood around the bacterial growth.

A

β-hemolysis

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5
Q

signifies absence of hemolysis thereby no change is seen in the medium surrounding bacterial growth.

A

γ-hemolysis

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6
Q

Streptococci producing such pattern of hemolysis were later on described as “indifferent streptococci”.

A

γ-hemolysis

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7
Q

a small zone of intact erythrocytes immediately adjacent to bacterial colony is surrounded with a zone of complete erythrocyte hemolysis.

A

α’ (alpha prime)-hemolysis (wide zone of alpha hemolysis)

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8
Q

This type of hemolysis maybe confused with β-hemolysis.

A

α’ (alpha prime)-hemolysis (wide zone of alpha hemolysis)

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9
Q

Discovered by Rebecca Lancefield in the 1930s based on group-specific antigens which are either cell wall polysaccharides, AKA C-substance, (as in human group A, B, C, F, and G streptococci); or lipoteichoic acids as in the group D streptococci and Enterococcus species These antigens stimulated formation of antibodies with differing specificities.

A

Lancefield Classification

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10
Q

Typing with specific antiserum causing agglutination is generally done only for groups A, B, C, F, and G.

A

Lancefield Classification

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11
Q

Based on temperature for growth particularly at 10OC and 45OC.

A

Academic/ Bergey’s Classification

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12
Q

consists of streptococci that do not grow at both 10OC and 45OC.

A

Pyogenic group

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13
Q

includes streptococci which fail to grow at 10OC but can be recovered at temperatures up to 45OC.

A

Viridans group

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14
Q

are streptococci that grow at both 10OC and 45OC.

A

Enterococcus group

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15
Q

comprise of streptococci that are frequently recovered in dairy products, can grow at 10OC but fail to grow at 45OC.

A

Lactic group

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16
Q

Group A β-Hemolytic Streptococci (GAS): Streptococcus pyogenes: Habitat

A

human throat and skin

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17
Q

Group A β-Hemolytic Streptococci (GAS): Streptococcus pyogenes: Transmission

A

respiratory droplets or contact with cutaneous lesions.

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18
Q

The most common infection caused by S. pyogenes.

A

Pharyngitis or streptococcal sore throat

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19
Q

Although it may occur at any age, it occurs most frequently between the ages of 5 and 15 years.

A

Pharyngitis or streptococcal sore throat

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20
Q

Characterized by acute sore throat, malaise, fever, and headache

A

Pharyngitis or streptococcal sore throat

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21
Q

Typically involves the tonsillar pillars, uvula, and soft palate, which become red, swollen, and covered with a yellowwhite exudate. The cervical lymph nodes that drain this area may also become swollen and tender.

A

Pharyngitis or streptococcal sore throat

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22
Q

Usually self-limiting (illness resolves on its own even without medical intervention). Typically, the fever is gone by the third to fifth day, and other manifestations subside within 1 week.

A

Pharyngitis or streptococcal sore throat

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23
Q
A

Pharyngitis or streptococcal sore throat

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24
Q

Caused by lysogenized strains of S. pyogenes that produce pyrogenic exotoxins A - C

A

Scarlet Fever

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25
Q

Occurs in association with streptococcal pharyngitis

A

Scarlet Fever

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26
Q

The buccal mucosa, temples, and cheeks are deep red, except for a pale area around the mouth and nose (circumoral pallor).

A

Scarlet Fever

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27
Q

Punctate hemorrhages appear on the hard and soft palates, and the tongue becomes covered with a yellow-white exudate through which the red papillae are prominent (strawberry tongue).

A

Scarlet Fever

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28
Q

A diffuse red “sandpaper” rash appears on the second day of illness, spreading from the upper chest to the trunk and extremities.

A

Scarlet Fever

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29
Q

Circulating antibody to the toxin neutralizes its effects.

A

Scarlet Fever

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30
Q

Infection of superficial layers of skin

A

Streptococcal pyoderma (or impetigo)

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31
Q

Usually occurs in children ages 2-15 years old, with peak incidence in the 2- to 5- year age group.

A

Streptococcal pyoderma (or impetigo)

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32
Q

Characterized by the formation of papules that develop into vesicular lesions and evolve into pustules. These pustules break down over the next 5 to 7 days to form thick scabs.

A

Streptococcal pyoderma (or impetigo)

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33
Q

Lesions are often seen on the lower extremities and may also involve other pathogens such as S. aureus.

A

Streptococcal pyoderma (or impetigo)

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34
Q

An infection of the dermis and subcutaneous tissues

A

Erysipelas

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35
Q

Organism enters through a small wound or incision on the face or extremities

A

Erysipelas

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36
Q

Characterized by edema and erythematous (red) lesion that is hot, and often vesicular with rapidly advancing, well-demarcated edges

A

Erysipelas

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37
Q

Infection usually occurs on the face and commonly in association with a history of streptococcal sore throat.

A

Erysipelas

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38
Q

Pain, and systemic manifestations, such fever and lymphadenopathy are evident.

A

Erysipelas

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39
Q

An acute, rapidly spreading infection of the skin and subcutaneous tissues.

A

Cellulitis

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40
Q

Occurs following streptococcal infection of preexisting lesions (i.e. mild trauma, burns, wounds, or surgical incisions).

A

Cellulitis

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41
Q

Symptoms include pain, tenderness, swelling, and erythema particularly occurring within the affected area.

A

Cellulitis

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42
Q

Cellulitis:

Differentiated from erysipelas by two clinical findings:

A

In cellulitis, the lesion is not raised, and the line between the involved and uninvolved tissue is indistinct.

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43
Q

Consists of extensive and very rapidly spreading necrosis of the skin, tissues, and fascia.

A

Necrotizing fasciitis (streptococcal gangrene)

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44
Q

Organism enters at the site of localized trauma or previous surgery, or via hematogenous seeding of subcutaneous muscles and soft tissue.

A

Necrotizing fasciitis (streptococcal gangrene)

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45
Q

Affected tissues become gangrenous, with sloughing of devitalized tissues and extensive subcutaneous tissue necrosis.

A

Necrotizing fasciitis (streptococcal gangrene)

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46
Q

Group A streptococci that cause necrotizing fasciitis are termed “flesh-eating bacteria”.

A

Necrotizing fasciitis (streptococcal gangrene)

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47
Q

Bacteria other than S pyogenes can also cause necrotizing fasciitis.

A

Necrotizing fasciitis (streptococcal gangrene)

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48
Q

Occurs in women following child birth (either by vaginal or abdominal/Csection) or abortion.

A

Puerperal fever

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49
Q

Organisms colonizing the genital tract or from an obstetrical personnel invade the upper genital tract, causing endometritis, lymphangitis, bacteremia, necrotizing fasciitis, and streptococcal toxic shock syndrome.

A

Puerperal fever

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50
Q

Intrapartum (occuring during pregnancy) transmission of group A streptococci, may lead to severe and often fatal group A streptococcal disease in the neonate.

A

Puerperal fever

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51
Q

Manifestations in the neonate include septicemia, jaundice, and cellulitis, or stillbirth.

A

Puerperal fever

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52
Q

May result from streptococcal infection of traumatic or surgical wounds.

A

Bacteremia or Sepsis

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53
Q

Can be rapidly fatal.

A

Bacteremia or Sepsis

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54
Q

Can also occur with skin infections, such as cellulitis and rarely pharyngitis.

A

Bacteremia or Sepsis

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55
Q

Are non-suppurative sequelae that occur weeks after GAS infection in the throat and/or skin.

A

Post Streptococcal Diseases

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56
Q

Inflammation of the glomeruli of the kidneys caused by the M strains of S. pyogenes (nephritogenic).

A

Acute Glomerulonephritis (AGN)

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57
Q

Begins 1 to 4 weeks after streptococcal pharyngitis or 3 to 6 weeks after skin infection; primarily a disease of childhood.

A

Acute Glomerulonephritis (AGN)

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58
Q

May be initiated by deposition and accumulation of antigenantibody complexes on the glomerular basement membrane

A

Acute Glomerulonephritis (AGN)

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59
Q

Signs symptoms: dark, smoky urine (due to blood and proteins) edema, hypertension, and urea nitrogen retention.

A

Acute Glomerulonephritis (AGN)

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60
Q

Majority recover completely while some develop chronic glomerulonephritis with kidney failure, and a few die

A

Acute Glomerulonephritis (AGN)

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61
Q

Considered as the most serious sequela of S. pyogenes because it results in damage to heart muscle and valves.

A

Rheumatic fever (RF)

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62
Q

Occurs 1–4 weeks after S. pyogenes pharyngitis

A

Rheumatic fever (RF)

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63
Q

Is an autoimmune disease, i.e., antibodies formed against streptococcal antigens cross react with the molecules of the host that trigger inflammation and injury of tissues (of the heart, joints, CNS)

A

Rheumatic fever (RF)

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64
Q

Signs and symptoms: fever, malaise, arthritis, carditis, chorea (neurologic disorder characterized by involuntary jerky movements), and skin nodules

A

Rheumatic fever (RF)

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65
Q

Pathologic processes of S. pyogenes infection can extend to the heart. The cross-reaction between streptococcal-induced antibodies and heart proteins have a gradual destructive effect on atrioventricular valve. Scarring and deformation change the capacity of the valves to close and shine the blood properly leading to Rheumatic Heart Disease.

A

Rheumatic fever (RF)

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66
Q

Has a marked tendency to be reactivated by recurrent streptococcal infections in contrast with nephritis.

A

Rheumatic fever (RF)

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67
Q

Occur more frequently in tropical countries and is the most important cause of heart disease in young people in developing countries.

A

Rheumatic fever (RF)

68
Q

major virulence factor of S. pyogenes (those that lack M protein are not virulent).

A

M Protein

69
Q

Found on the bacterial cell surface associated with fimbriae.

A

M Protein

70
Q

There are more than 200 types of S. pyogenes M proteins; immunity to infection with GAS is related to the production or presence of typespecific antibodies against M protein; subsequent infections may occur with different M serotypes;

A

M Protein

71
Q

Inhibits activation of the complement pathway by destroying C3-convertase thereby prevents formation of the opsonin C3b

A

M Protein

72
Q

A polysaccharide capsule, which is composed of hyaluronic acid

A

Capsule

73
Q

A polysaccharide capsule, which is composed of hyaluronic acid

A

Capsule

74
Q

Prevents opsonized phagocytosis by neutrophils or macrophages.

A

Capsule

75
Q

Allows the bacterium to mask its antigens and remain unrecognized by its host’s immune system

A

Capsule

76
Q

Formerly called streptococcal pyrogenic exotoxins (Spe)

A

Erythrogenic Toxin

77
Q

There are four antigenically distinct streptococcal pyrogenic exotoxins — SpeA, SpeB, SpeC, and SpeF.

A

Erythrogenic Toxin

78
Q

SpeA has been most widely studied.

A

Erythrogenic Toxin

79
Q

Elaborated by lysogenic S. pyogenes that contain genes from temperate bacteriophage.

A

Erythrogenic Toxin

80
Q

Act as superantigens which stimulate monocytes and T cells. When activated, these cells proliferate and produce tumor necrosis factor, which in high quantities leads to damage of the plasma membrane of blood capillaries.

A

Erythrogenic Toxin

81
Q

Responsible for the manifestations of scarlet fever

A

Erythrogenic Toxin

82
Q

is a skin test for scarlet fever that uses antitoxin to the erythrogenic toxin of Streptococcus pyogenes subcutaneously: a positive reaction is blanching of the rash in the area around the injection site.

A

Schultz-Charlton Test

83
Q

is a skin test performed to determine an individual’s susceptibility to scarlet fever. It consists of intradermal injection of diluted scarlet fever toxin on the arm of a suspected patient. Development of a red rash with a diameter of 10 mm or greater indicates lack of immunity to the disease.

A

Dick Test

84
Q

S. pyogenes elaborates two hemolytic exotoxins, proteins that not only lyse the membranes of erythrocytes but also damage a variety of other cell types.

A

Streptolysins

85
Q

The “O” refers to this hemolysin being oxygen labile. It is active only in the reduced form.

A

Streptolysin O (SLO)

86
Q

Is responsible for hemolysis on sheep blood agar (SBA) plates incubated anaerobically or subsurface hemolysis when growth occurs in cuts (stabs) made deep into the blood agar plates

A

Streptolysin O (SLO)

87
Q

It lyses a variety of host cells including leukocytes, platelets, as well as RBCs

A

Streptolysin O (SLO)

88
Q

It is highly immunogenic, and infected individuals readily form antibodies against it known as anti-streptolysin O (ASO) which blocks hemolysis caused by streptolysin O.

A

Streptolysin O (SLO)

89
Q

ASO combines quantitatively with streptolysin O and is measured in the Anti-streptolysin O Test

A

Streptolysin O (SLO)

90
Q

a test performed to determine whether an individual has had a recent infection with S. pyogenes.

A

Anti-Streptolysin O Test (ASTO or ASOT)

91
Q

It involves detection and quantitation of Anti-Streptolysin O antibodies in the serum

A

Anti-Streptolysin O Test (ASTO or ASOT)

92
Q

An abnormally high serum titer suggests either recent infection with S. pyogenes or persistently high antibody levels caused by an exaggerated immune response to an earlier exposure in a hypersensitive person.

A

Anti-Streptolysin O Test (ASTO or ASOT)

93
Q

is also related to the retro-diagnosis of rheumatic fever (to check whether rheumatic fever is caused by a previous streptococcal infection or by other etiologies).

A

Anti-Streptolysin O Test (ASTO or ASOT)

94
Q

Is responsible for hemolysis seen around colonies (surface hemolysis) incubated aerobically

A

Streptolysin S (SLS)

95
Q

It is oxygen stable, lyses leukocytes, and is non-immunogenic — does not stimulate antibody production in the host.

A

Streptolysin S (SLS)

96
Q

Transforms the plasminogen of human plasma into plasmin, an active proteolytic enzyme that digests fibrin and other proteins allowing bacteria to escape from blood clots.

A

Streptokinase

97
Q

Its action is blocked by non-specific serum inhibitors and anti-streptokinase antibody.

A

Streptokinase

98
Q

has been given intravenously for treatment of pulmonary emboli, coronary artery, and venous thromboses.

A

Streptokinase

99
Q

Liquefies purulent discharges by hydrolyzing DNA which promotes spread of the pathogen into the tissues.

A

Streptodornase

100
Q

Are antigenic and an antibody develops after streptococcal infections (especially after skin infections).

A

Streptodornase

101
Q

Dissolves hyaluronic acid, an important component of the ground substance of host’s connective tissue.

A

Hyaluronidase

102
Q

Aids in spreading the pathogen (spreading factor) into the host’s tissues.

A

Hyaluronidase

103
Q

Are antigenic and antibodies produced are specific for each bacterial or tissue source.

A

Hyaluronidase

104
Q

Causes lysis of host’s white blood cells.

A

Leukocidin

105
Q

Group B β-Hemolytic Streptococci (GBS): Streptococcus agalactiae: HABITAT

A

Part of the normal vaginal flora in approximately 5–30% of women; may also colonize lower gastrointestinal tract.

106
Q

Group B β-Hemolytic Streptococci (GBS): Streptococcus agalactiae: TRANSMISSION

A

is during birth by passage through the colonized birth canal (vertical transmission).

107
Q

GBS remains as a significant cause of invasive disease in the newborn

A

Neonatal meningitis and septicemia

108
Q

A predisposing factor in the acquisition of disease is the immunologic immaturity of neonates as antibody production does not begin until several months after birth.

A

Neonatal meningitis and septicemia

109
Q

Neonatal GBS disease is associated with two clinical syndromes:

A

Early onset infection and Late onset infection

110
Q

Occurs during the first 5 to 6 days of life, however, in more than half the
cases, infants become ill within the first 12 to 20 hours after birth.

A

Early onset infection

111
Q

Acquired either by ascending infection before delivery, through
ruptured fetal membranes, or during passage through a birth canal

A

Early onset infection

112
Q

Pathogen invades the pulmonary endothelial and epithelial cells, and
gains access to the bloodstream.

A

Early onset infection

113
Q

The disease spectrum includes bacteremia, pneumonia, meningitis,
septic shock, and neutropenia.

A

Early onset infection

114
Q

Becomes clinically evident 7 days to 3 months (average 3 to 4 weeks)
after birth.

A

Late onset infection

115
Q

Results from postnatal acquisition of the organism acquisition from the
mother, other caregivers, or nosocomially

A

Late onset infection

116
Q

Bacteremia is the predominant clinical presentation, and about 25% of
these infants also develop group B streptococcal meningitis.

A

Late onset infection

117
Q

GBS were known for many years as the cause of mastitis in cattle.

A

Bovine mastitis

118
Q

It was not until Lancefield defined streptococcal classification in the 1940s that their role in human
disease was recognized. S. agalactiae was identified in the 1970s as a significant cause of invasive
disease in the newborn.

A

Bovine mastitis

119
Q

is the major virulence factor for GBS

A

Capsule of Enterococcus species and Group D streptococci (nonenterococcus)

120
Q

A polysaccharide capsule consisting primarily of sialic acid

A

Capsule of Enterococcus species and Group D streptococci (nonenterococcus)

121
Q

Responsible for the resistance to clearance by innate immune defenses in
the bloodstream as a consequence of molecular mimicry because sialic
acid is present on human cells.

A

Capsule of Enterococcus species and Group D streptococci (nonenterococcus)

122
Q

Promotes resistance to opsonin-mediated phagocytosis by inhibiting
deposition of C3b on the bacterial cell surface

A

Capsule of Enterococcus species and Group D streptococci (nonenterococcus)

123
Q

A diffusible, heat-stable, pore-forming protein

A

Christie-Atkins-Munch-Peterson (CAMP) Factor of Enterococcus species and Group D streptococci (nonenterococcus)

124
Q

Promotes lysis of host’s cell by formation of pores on the cell membrane

A

Christie-Atkins-Munch-Peterson (CAMP) Factor of Enterococcus species and Group D streptococci (nonenterococcus)

125
Q

Binds to Fc region of immunoglobulins preventing opsonin-mediated
phagocytosis

A

Christie-Atkins-Munch-Peterson (CAMP) Factor of Enterococcus species and Group D streptococci (nonenterococcus)

126
Q

Acts on sphingomyelin that causes lysis of a variety of host cells.

A

β-hemolysin of Enterococcus species and Group D streptococci (nonenterococcus)

127
Q

Together with CAMP factor, produces synergistic hemolysis.

A

β-hemolysin of Enterococcus species and Group D streptococci (nonenterococcus)

128
Q

Were previously termed “enterococcal group D streptococci”, but now
reclassified into new genus Enterococcus

A

Enterococcus species

129
Q

Are part of the normal enteric microbiota and are transmitted by direct
contact with fecally-contaminated materials; urethra and female genital tract
can be colonized.

A

Enterococcus species

130
Q

Are important agents of nosocomial infections; may enter the bloodstream
during GIT or GUT manipulation.

A

Enterococcus species

131
Q

Show resistance to penicillin and other antimicrobial agents to which other
streptococci are generally susceptible; E. faecium is usually much more
antibiotic-resistant than E. faecalis.

A

Enterococcus species

132
Q

May cause endocarditis in adults, and meningitis and bacteremia in neonates.

A

Enterococcus species

133
Q

Less than one third are associated with human diseases.

A

Enterococcus species

134
Q

is the most common and causes 85–90% of

enterococcal infections

A

Enterococcus faecalis

135
Q

causes 5–10% of

enterococcal infections

A

Enterococcus faecium

136
Q

Termed the “nonenterococcal Group D streptococci” that remain in the genus
Streptococcus

A

Group D streptococci

137
Q

Compose only a small part of the enteric flora of humans and animals

A

Group D streptococci

138
Q

Implicated in UTI, endocarditis, and septicemia.

A

Group D streptococci

139
Q

is the most important species to humans (animal species in

the bovis group have been assigned to the species Streptococcus equinus)

A

Streptococcus bovis

140
Q

A normal colonizer of the upper respiratory tract of 5–40% of humans.

A

Streptococcus pneumoniae ; Common name: Pneumococcus

HABITAT

141
Q

Disease develops by endogenous spread of the organism from its habitat, esp.
among individuals with weakened respiratory defenses.

A

Streptococcus pneumoniae ; Common name: Pneumococcus

HABITAT

142
Q

Person-to-person transmission rarely occurs by respiratory droplets, usually from a
healthy carrier.

A

Streptococcus pneumoniae ; Common name: Pneumococcus

TRANSMISSION

143
Q

S. pneumoniae is the most common cause (about 80%) of community-acquired
bacterial pneumonia esp. the elderly (after 65 years), but also in infants.

A

Pneumococcal pneumonia

144
Q

Entrance of bacteria into the lungs initiates acute and massive inflammatory
response that fills the lungs (and bronchioles) with fluid; consolidation of fluid leads
to lobar pneumonia.

A

Pneumococcal pneumonia

145
Q

Produces a lobar pneumonia with symptoms that include high fever, chills, rapid
breathing, chest pain, and rust-colored sputum from blood coughed up from the
lungs.

A

Pneumococcal pneumonia

146
Q

Bacteremia is present in 10–20% of cases particularly evident early in the disease,
when the fever is high.

A

Pneumococcal pneumonia

147
Q

Predisposing conditions for pneumonia:

A

. Antecedent influenza or measles infection: damage to mucociliary elevator
. Chronic obstructive pulmonary disorders
. Congestive heart failure
. Alcoholism
. Asplenia predisposes to septicemia

148
Q

Occuring readily in children, bacteria gain access to the paranasal sinuses
causing sinusitis; or into the chamber of the middle ear by way of the eustachian
tube and cause middle ear infection called otitis media.

A

Sinusitis and otitis media

149
Q

Most common cause of meningitis among adults, when organisms from the
respiratory tract reach the CNS; may also endocarditis and septic arthritis.

A

Systemic complications / Other infections

150
Q

Classifies pneumococci into more than 90 serotypes

A

Polysaccharide capsule

151
Q

The primary virulence factor of pneumococci, with some capsular types more
virulent than the others. In adults, capsular types 1–8 are responsible for about
75% of cases of pneumococcal pneumonia and for more than half of all
fatalities in pneumococcal bacteremia; in children, types 6, 14, 19, and 23 are
frequent causes of infection; no virulence if without capsule.

A

Polysaccharide capsule

152
Q

Delays ingestion by phagocytes thereby promoting multiplication of the
organism in the tissues of the host.

A

Polysaccharide capsule

153
Q

Enzyme that cleaves IgA, allowing bacteria to adhere to and colonize mucous
membranes.

A

IgA protease

154
Q

Exhibits toxicity for pulmonary endothelial cells and direct effect on cilia that
contributes to the disruption of endothelial barrier.

A

Pneumolysin O

155
Q

Facilitates the access of pneumococci to the alveoli and eventually their
spread beyond into the bloodstream.

A

Pneumolysin O

156
Q

Lyses phagocytes and suppresses host inflammatory and immune functions.

A

Pneumolysin O

157
Q

Also referred to as spreading factor

A

Neuraminidase

158
Q

It hydrolyses neuraminic acid, an important component of mucus that covers
cells of the respiratory tract and protects them from bacterial attachment.

A

Neuraminidase

159
Q

Is an autolysin that causes lytic dispersal of pneumolysin and hemolysin

A

Amidase

160
Q

Causes dermal hemorrhage in experimental animals

A

Purpura-producing principle

161
Q

The most prevalent members of the normal microbiota of the

oropharynx.

A

Viridans streptococci

162
Q

The most frequent cause of subacute bacterial endocarditis

(SBE) in individuals with damaged (or prosthetic) heart valve.

A

Viridans streptococci

163
Q

May enter the blood stream through dental procedure (tooth
extraction, or dental prophylaxis) or by simply brushing the
teeth; form biofilm that bind vegetations (consist of fibrin,
platelets, blood cells, and bacteria) on the damaged heart
valves; the clinical course of the diseases is gradual, but is
invariably fatal in untreated cases.

A

Viridans streptococci

164
Q

is a normal flora of the oral cavity and is responsible
for dental caries (tooth decay) due to the following activities
of bacteria when they are not removed regularly through
brushing and flossing

A

S. mutans

165
Q

S. mutans synthesizes large
polysaccharides, dextrans, that build up on the surfaces of the teeth, entrap
bacteria and food debris. The combination of dextrans, bacteria, and debris is
known as dental plaque, which fosters dental caries.

A

Biofilm formation

166
Q

S. mutans and other bacteria in plaque produce

large amounts of acids that will break down the enamel of the teeth.

A

Carbohydrate fermentation