Streptococcaceae and Enterococcus species Flashcards
1
Q
Based on hemolysis on 5% Sheep Blood Agar Medium
A
Smith and Brown’s Classification
2
Q
denotes incomplete lysis of erythrocytes with reduction of hemoglobin and the formation of green pigment
A
α-hemolysis
3
Q
Streptococci producing such pattern of hemolysis were later on described as “green streptococci”.
A
α-hemolysis
4
Q
refers to the complete disruption of erythrocytes resulting to clearing of the blood around the bacterial growth.
A
β-hemolysis
5
Q
signifies absence of hemolysis thereby no change is seen in the medium surrounding bacterial growth.
A
γ-hemolysis
6
Q
Streptococci producing such pattern of hemolysis were later on described as “indifferent streptococci”.
A
γ-hemolysis
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)
8
Q
This type of hemolysis maybe confused with β-hemolysis.
A
α’ (alpha prime)-hemolysis (wide zone of alpha hemolysis)
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
10
Q
Typing with specific antiserum causing agglutination is generally done only for groups A, B, C, F, and G.
A
Lancefield Classification
11
Q
Based on temperature for growth particularly at 10OC and 45OC.
A
Academic/ Bergey’s Classification
12
Q
consists of streptococci that do not grow at both 10OC and 45OC.
A
Pyogenic group
13
Q
includes streptococci which fail to grow at 10OC but can be recovered at temperatures up to 45OC.
A
Viridans group
14
Q
are streptococci that grow at both 10OC and 45OC.
A
Enterococcus group
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
16
Q
Group A β-Hemolytic Streptococci (GAS): Streptococcus pyogenes: Habitat
A
human throat and skin
17
Q
Group A β-Hemolytic Streptococci (GAS): Streptococcus pyogenes: Transmission
A
respiratory droplets or contact with cutaneous lesions.
18
Q
The most common infection caused by S. pyogenes.
A
Pharyngitis or streptococcal sore throat
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
20
Q
Characterized by acute sore throat, malaise, fever, and headache
A
Pharyngitis or streptococcal sore throat
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
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
23
Q
A
Pharyngitis or streptococcal sore throat
24
Q
Caused by lysogenized strains of S. pyogenes that produce pyrogenic exotoxins A - C
A
Scarlet Fever
25
Occurs in association with streptococcal pharyngitis
Scarlet Fever
26
The buccal mucosa, temples, and cheeks are deep red, except for a pale area around the mouth and nose (circumoral pallor).
Scarlet Fever
27
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).
Scarlet Fever
28
A diffuse red “sandpaper” rash appears on the second day of illness, spreading from the upper chest to the trunk and extremities.
Scarlet Fever
29
Circulating antibody to the toxin neutralizes its effects.
Scarlet Fever
30
Infection of superficial layers of skin
Streptococcal pyoderma (or impetigo)
31
Usually occurs in children ages 2-15 years old, with peak incidence in the 2- to 5- year age group.
Streptococcal pyoderma (or impetigo)
32
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.
Streptococcal pyoderma (or impetigo)
33
Lesions are often seen on the lower extremities and may also involve other pathogens such as S. aureus.
Streptococcal pyoderma (or impetigo)
34
An infection of the dermis and subcutaneous tissues
Erysipelas
35
Organism enters through a small wound or incision on the face or extremities
Erysipelas
36
Characterized by edema and erythematous (red) lesion that is hot, and often vesicular with rapidly advancing, well-demarcated edges
Erysipelas
37
Infection usually occurs on the face and commonly in association with a history of streptococcal sore throat.
Erysipelas
38
Pain, and systemic manifestations, such fever and lymphadenopathy are evident.
Erysipelas
39
An acute, rapidly spreading infection of the skin and subcutaneous tissues.
Cellulitis
40
Occurs following streptococcal infection of preexisting lesions (i.e. mild trauma, burns, wounds, or surgical incisions).
Cellulitis
41
Symptoms include pain, tenderness, swelling, and erythema particularly occurring within the affected area.
Cellulitis
42
Cellulitis:
| Differentiated from erysipelas by two clinical findings:
In cellulitis, the lesion is not raised, and the line between the involved and uninvolved tissue is indistinct.
43
Consists of extensive and very rapidly spreading necrosis of the skin, tissues, and fascia.
Necrotizing fasciitis (streptococcal gangrene)
44
Organism enters at the site of localized trauma or previous surgery, or via hematogenous seeding of subcutaneous muscles and soft tissue.
Necrotizing fasciitis (streptococcal gangrene)
45
Affected tissues become gangrenous, with sloughing of devitalized tissues and extensive subcutaneous tissue necrosis.
Necrotizing fasciitis (streptococcal gangrene)
46
Group A streptococci that cause necrotizing fasciitis are termed “flesh-eating bacteria”.
Necrotizing fasciitis (streptococcal gangrene)
47
Bacteria other than S pyogenes can also cause necrotizing fasciitis.
Necrotizing fasciitis (streptococcal gangrene)
48
Occurs in women following child birth (either by vaginal or abdominal/Csection) or abortion.
Puerperal fever
49
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.
Puerperal fever
50
Intrapartum (occuring during pregnancy) transmission of group A streptococci, may lead to severe and often fatal group A streptococcal disease in the neonate.
Puerperal fever
51
Manifestations in the neonate include septicemia, jaundice, and cellulitis, or stillbirth.
Puerperal fever
52
May result from streptococcal infection of traumatic or surgical wounds.
Bacteremia or Sepsis
53
Can be rapidly fatal.
Bacteremia or Sepsis
54
Can also occur with skin infections, such as cellulitis and rarely pharyngitis.
Bacteremia or Sepsis
55
Are non-suppurative sequelae that occur weeks after GAS infection in the throat and/or skin.
Post Streptococcal Diseases
56
Inflammation of the glomeruli of the kidneys caused by the M strains of S. pyogenes (nephritogenic).
Acute Glomerulonephritis (AGN)
57
Begins 1 to 4 weeks after streptococcal pharyngitis or 3 to 6 weeks after skin infection; primarily a disease of childhood.
Acute Glomerulonephritis (AGN)
58
May be initiated by deposition and accumulation of antigenantibody complexes on the glomerular basement membrane
Acute Glomerulonephritis (AGN)
59
Signs symptoms: dark, smoky urine (due to blood and proteins) edema, hypertension, and urea nitrogen retention.
Acute Glomerulonephritis (AGN)
60
Majority recover completely while some develop chronic glomerulonephritis with kidney failure, and a few die
Acute Glomerulonephritis (AGN)
61
Considered as the most serious sequela of S. pyogenes because it results in damage to heart muscle and valves.
Rheumatic fever (RF)
62
Occurs 1–4 weeks after S. pyogenes pharyngitis
Rheumatic fever (RF)
63
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)
Rheumatic fever (RF)
64
Signs and symptoms: fever, malaise, arthritis, carditis, chorea (neurologic disorder characterized by involuntary jerky movements), and skin nodules
Rheumatic fever (RF)
65
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.
Rheumatic fever (RF)
66
Has a marked tendency to be reactivated by recurrent streptococcal infections in contrast with nephritis.
Rheumatic fever (RF)
67
Occur more frequently in tropical countries and is the most important cause of heart disease in young people in developing countries.
Rheumatic fever (RF)
68
major virulence factor of S. pyogenes (those that lack M protein are not virulent).
M Protein
69
Found on the bacterial cell surface associated with fimbriae.
M Protein
70
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;
M Protein
71
Inhibits activation of the complement pathway by destroying C3-convertase thereby prevents formation of the opsonin C3b
M Protein
72
A polysaccharide capsule, which is composed of hyaluronic acid
Capsule
73
A polysaccharide capsule, which is composed of hyaluronic acid
Capsule
74
Prevents opsonized phagocytosis by neutrophils or macrophages.
Capsule
75
Allows the bacterium to mask its antigens and remain unrecognized by its host’s immune system
Capsule
76
Formerly called streptococcal pyrogenic exotoxins (Spe)
Erythrogenic Toxin
77
There are four antigenically distinct streptococcal pyrogenic exotoxins — SpeA, SpeB, SpeC, and SpeF.
Erythrogenic Toxin
78
SpeA has been most widely studied.
Erythrogenic Toxin
79
Elaborated by lysogenic S. pyogenes that contain genes from temperate bacteriophage.
Erythrogenic Toxin
80
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.
Erythrogenic Toxin
81
Responsible for the manifestations of scarlet fever
Erythrogenic Toxin
82
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.
Schultz-Charlton Test
83
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.
Dick Test
84
S. pyogenes elaborates two hemolytic exotoxins, proteins that not only lyse the membranes of erythrocytes but also damage a variety of other cell types.
Streptolysins
85
The “O” refers to this hemolysin being oxygen labile. It is active only in the reduced form.
Streptolysin O (SLO)
86
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
Streptolysin O (SLO)
87
It lyses a variety of host cells including leukocytes, platelets, as well as RBCs
Streptolysin O (SLO)
88
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.
Streptolysin O (SLO)
89
ASO combines quantitatively with streptolysin O and is measured in the Anti-streptolysin O Test
Streptolysin O (SLO)
90
a test performed to determine whether an individual has had a recent infection with S. pyogenes.
Anti-Streptolysin O Test (ASTO or ASOT)
91
It involves detection and quantitation of Anti-Streptolysin O antibodies in the serum
Anti-Streptolysin O Test (ASTO or ASOT)
92
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.
Anti-Streptolysin O Test (ASTO or ASOT)
93
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).
Anti-Streptolysin O Test (ASTO or ASOT)
94
Is responsible for hemolysis seen around colonies (surface hemolysis) incubated aerobically
Streptolysin S (SLS)
95
It is oxygen stable, lyses leukocytes, and is non-immunogenic — does not stimulate antibody production in the host.
Streptolysin S (SLS)
96
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.
Streptokinase
97
Its action is blocked by non-specific serum inhibitors and anti-streptokinase antibody.
Streptokinase
98
has been given intravenously for treatment of pulmonary emboli, coronary artery, and venous thromboses.
Streptokinase
99
Liquefies purulent discharges by hydrolyzing DNA which promotes spread of the pathogen into the tissues.
Streptodornase
100
Are antigenic and an antibody develops after streptococcal infections (especially after skin infections).
Streptodornase
101
Dissolves hyaluronic acid, an important component of the ground substance of host’s connective tissue.
Hyaluronidase
102
Aids in spreading the pathogen (spreading factor) into the host’s tissues.
Hyaluronidase
103
Are antigenic and antibodies produced are specific for each bacterial or tissue source.
Hyaluronidase
104
Causes lysis of host’s white blood cells.
Leukocidin
105
Group B β-Hemolytic Streptococci (GBS): Streptococcus agalactiae: HABITAT
Part of the normal vaginal flora in approximately 5–30% of women; may also colonize lower gastrointestinal tract.
106
Group B β-Hemolytic Streptococci (GBS): Streptococcus agalactiae: TRANSMISSION
is during birth by passage through the colonized birth canal (vertical transmission).
107
GBS remains as a significant cause of invasive disease in the newborn
Neonatal meningitis and septicemia
108
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.
Neonatal meningitis and septicemia
109
Neonatal GBS disease is associated with two clinical syndromes:
Early onset infection and Late onset infection
110
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.
Early onset infection
111
Acquired either by ascending infection before delivery, through
ruptured fetal membranes, or during passage through a birth canal
Early onset infection
112
Pathogen invades the pulmonary endothelial and epithelial cells, and
gains access to the bloodstream.
Early onset infection
113
The disease spectrum includes bacteremia, pneumonia, meningitis,
septic shock, and neutropenia.
Early onset infection
114
Becomes clinically evident 7 days to 3 months (average 3 to 4 weeks)
after birth.
Late onset infection
115
Results from postnatal acquisition of the organism acquisition from the
mother, other caregivers, or nosocomially
Late onset infection
116
Bacteremia is the predominant clinical presentation, and about 25% of
these infants also develop group B streptococcal meningitis.
Late onset infection
117
GBS were known for many years as the cause of mastitis in cattle.
Bovine mastitis
118
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.
Bovine mastitis
119
is the major virulence factor for GBS
Capsule of Enterococcus species and Group D streptococci (nonenterococcus)
120
A polysaccharide capsule consisting primarily of sialic acid
Capsule of Enterococcus species and Group D streptococci (nonenterococcus)
121
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.
Capsule of Enterococcus species and Group D streptococci (nonenterococcus)
122
Promotes resistance to opsonin-mediated phagocytosis by inhibiting
deposition of C3b on the bacterial cell surface
Capsule of Enterococcus species and Group D streptococci (nonenterococcus)
123
A diffusible, heat-stable, pore-forming protein
Christie-Atkins-Munch-Peterson (CAMP) Factor of Enterococcus species and Group D streptococci (nonenterococcus)
124
Promotes lysis of host’s cell by formation of pores on the cell membrane
Christie-Atkins-Munch-Peterson (CAMP) Factor of Enterococcus species and Group D streptococci (nonenterococcus)
125
Binds to Fc region of immunoglobulins preventing opsonin-mediated
phagocytosis
Christie-Atkins-Munch-Peterson (CAMP) Factor of Enterococcus species and Group D streptococci (nonenterococcus)
126
Acts on sphingomyelin that causes lysis of a variety of host cells.
β-hemolysin of Enterococcus species and Group D streptococci (nonenterococcus)
127
Together with CAMP factor, produces synergistic hemolysis.
β-hemolysin of Enterococcus species and Group D streptococci (nonenterococcus)
128
Were previously termed "enterococcal group D streptococci", but now
reclassified into new genus Enterococcus
Enterococcus species
129
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.
Enterococcus species
130
Are important agents of nosocomial infections; may enter the bloodstream
during GIT or GUT manipulation.
Enterococcus species
131
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.
Enterococcus species
132
May cause endocarditis in adults, and meningitis and bacteremia in neonates.
Enterococcus species
133
Less than one third are associated with human diseases.
Enterococcus species
134
is the most common and causes 85–90% of
| enterococcal infections
Enterococcus faecalis
135
causes 5–10% of
| enterococcal infections
Enterococcus faecium
136
Termed the "nonenterococcal Group D streptococci" that remain in the genus
Streptococcus
Group D streptococci
137
Compose only a small part of the enteric flora of humans and animals
Group D streptococci
138
Implicated in UTI, endocarditis, and septicemia.
Group D streptococci
139
is the most important species to humans (animal species in
| the bovis group have been assigned to the species Streptococcus equinus)
Streptococcus bovis
140
A normal colonizer of the upper respiratory tract of 5–40% of humans.
Streptococcus pneumoniae ; Common name: Pneumococcus
| HABITAT
141
Disease develops by endogenous spread of the organism from its habitat, esp.
among individuals with weakened respiratory defenses.
Streptococcus pneumoniae ; Common name: Pneumococcus
| HABITAT
142
Person-to-person transmission rarely occurs by respiratory droplets, usually from a
healthy carrier.
Streptococcus pneumoniae ; Common name: Pneumococcus
| TRANSMISSION
143
S. pneumoniae is the most common cause (about 80%) of community-acquired
bacterial pneumonia esp. the elderly (after 65 years), but also in infants.
Pneumococcal pneumonia
144
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.
Pneumococcal pneumonia
145
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.
Pneumococcal pneumonia
146
Bacteremia is present in 10–20% of cases particularly evident early in the disease,
when the fever is high.
Pneumococcal pneumonia
147
Predisposing conditions for pneumonia:
. Antecedent influenza or measles infection: damage to mucociliary elevator
. Chronic obstructive pulmonary disorders
. Congestive heart failure
. Alcoholism
. Asplenia predisposes to septicemia
148
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.
Sinusitis and otitis media
149
Most common cause of meningitis among adults, when organisms from the
respiratory tract reach the CNS; may also endocarditis and septic arthritis.
Systemic complications / Other infections
150
Classifies pneumococci into more than 90 serotypes
Polysaccharide capsule
151
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.
Polysaccharide capsule
152
Delays ingestion by phagocytes thereby promoting multiplication of the
organism in the tissues of the host.
Polysaccharide capsule
153
Enzyme that cleaves IgA, allowing bacteria to adhere to and colonize mucous
membranes.
IgA protease
154
Exhibits toxicity for pulmonary endothelial cells and direct effect on cilia that
contributes to the disruption of endothelial barrier.
Pneumolysin O
155
Facilitates the access of pneumococci to the alveoli and eventually their
spread beyond into the bloodstream.
Pneumolysin O
156
Lyses phagocytes and suppresses host inflammatory and immune functions.
Pneumolysin O
157
Also referred to as spreading factor
Neuraminidase
158
It hydrolyses neuraminic acid, an important component of mucus that covers
cells of the respiratory tract and protects them from bacterial attachment.
Neuraminidase
159
Is an autolysin that causes lytic dispersal of pneumolysin and hemolysin
Amidase
160
Causes dermal hemorrhage in experimental animals
Purpura-producing principle
161
The most prevalent members of the normal microbiota of the
| oropharynx.
Viridans streptococci
162
The most frequent cause of subacute bacterial endocarditis
| (SBE) in individuals with damaged (or prosthetic) heart valve.
Viridans streptococci
163
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.
Viridans streptococci
164
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
S. mutans
165
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.
Biofilm formation
166
S. mutans and other bacteria in plaque produce
| large amounts of acids that will break down the enamel of the teeth.
Carbohydrate fermentation
