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Microbiology and immunology > Streptococci and enterococcus > Flashcards

Streptococci and enterococcus Flashcards

1
Q

What are the principles used to categorize streptococci?

A
  • Colony morphology and hemolytic reactions on blood agar
  • Serologic specificity of the cell wall group-specific substance (Lancefield antigens)
  • Biochemical reactions and resistance to physical and chemical factors
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2
Q

What are the different outcomes of tests for hemolysis with streptococci?

A
  • Complete (β) hemolysis, leaving clear medium
  • Incomplete (α) hemolysis, leaving a green pigment
  • No (γ) hemolysis
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3
Q

How is the Lancefield grouping determined for different streptococci?

A

Antibody development to different antigens present on the surface of the bacterial strain

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4
Q

Which streptococcus is group A streptococcus (GAS)?

A

Streptococcus pyogenes

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5
Q

Which streptococcus is group B streptococcus (GBS)?

A

Streptococcus agalactiae

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6
Q

What are the β-hemolytic streptococci?

A
  • S. pyogenes
  • S. agalactiae
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7
Q

How can the β-hemolytic streptococci be differentiated?

A
  • Sensitive to bacitracin: S. pyogenes
  • Not sensitive to bacitracin: S. agalactiae
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8
Q

How can the α-hemolytic streptococci be differentiated?

A
  • Sensitive to optochin: S. pneumoniae
  • Not sensitive to optochin: S. viridans group
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9
Q

What are the α-hemolytic streptococci?

A
  • S. pneumoniae
  • S. viridans group
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10
Q

What are the morphologic features of S. pyogenes?

A
  • Spherical cocci
  • 1–2 µm in diameter
  • Arranged in short chains in clinical specimens
  • After 24 hours of incubation, small white colonies with large zones of β-hemolysis are observed
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11
Q

How does S. pyogenes avoid opsonization and phagocytosis?

A
  • Its hyaluronic acid capsule is poorly immunogenic and interferes with phagocytosis
  • M proteins also interfere with phagocytosis by blocking the binding of C3b. They are the most important anticomplement virulence factors
  • S. pyogenes has a C5a peptidase on its surface, degrading the chemotactic agent
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12
Q

How does S. pyogenes adhere to host cells?

A

Several antigens, notably M proteins and F proteins

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13
Q

What is the significance of streptococcal pyrogenic exotoxins (Spe)?

A

Superantigens

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14
Q

What is streptolysin S?

A
  • An oxygen-stable, nonimmunogenic, cell-bound hemolysin
  • Lyses erythrocytes, leukocytes, and platelets
  • Is the enzyme responsible for β-hemolysis
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15
Q

What is streptolysin O?

A
  • An oxygen-labile hemolysin
  • Lyses erythrocytes, leukocytes, platelets, and cultured cells
  • Antistreptolysin O (ASO) antibodies are used to document recent GAS infection (unless the infection was cutaneous)
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16
Q

What is streptokinase?

A
  • Two forms: streptokinase A and B
  • Lyse blood clots and fibrin deposits and facilitate the rapid spread of GAS in infected tissues
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17
Q

What is the role of DNases A–D in S. pyogenes pathogenesis?

A
  • Depolymerizes free DNA present in pus
  • This reduces the viscosity of the abscess material and facilitates the spread of the bacteria
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18
Q

What is the epidemiology of S. pyogenes infections?

A
  • Pharyngitis and pyoderma are the most common infections
  • GAS can colonize the oropharynx of healthy children and young adults in the absence of clinical disease
  • Infection is established by recently acquired strains of the bacteria before specific antibodies are formed or competitive organisms are able to respond
  • Spread from person to person via respiratory droplets
  • Crowding, such as in classrooms or day-care centers, facilitates spread
  • Pyoderma can be transmitted by insect bites or traumatic implantation
19
Q

What are the diseases caused by S. pyogenes?

A

Suppurative

  • Pharyngitis
  • Scarlet fever
  • Pyoderma
  • Erysipelas
  • Cellulitis
  • Necrotizing fasciitis

Nonsuppurative

  • Rheumatic fever
  • Acute glomerulonephritis
20
Q

What are the features of streptococcal pharyngitis?

A
  • Sore throat, fever, malaise, and headache
  • The posterior pharynx appears erythematus with an exudate, and cervical lymphadenopathy can be prominent
21
Q

What is scarlet fever?

A
  • A complication of GAS pharyngitis that occurs when the infecting strain is infected with a bacteriophage that mediates production of a pyrogenic exotoxin
  • A diffuse erythematous rash initially appears on the upper chest and then spreads to the extremities
22
Q

What are the features of streptococcal necrotizing fasciitis?

A
  • Infection deep in the subcutaneous tissue that spreads along the fascial planes
  • Characterizied by extensive destruction of muscle and fat
  • Introduced to the tissue through a break in the skin (e.g. cuts, trauma, burns, surgery)
23
Q

What are the features of streptococcal erysipelas?

A
  • Acute infection of the skin
  • Localized pain, inflammation, lymph node enlargement, and systemic signs (chills, fever, leukocytosis)
  • The involved skin area is typically raised and distinctly differentiated from the uninvolved skin
24
Q

What is rheumatic fever?

A
  • A nonsuppurative complication of S. pyogenes pharyngitis
  • Characterized by inflammatory changes involving the heart, joints, blood vessels, and subcutaneous tissues
  • Involvement of the heart manifests as pancarditis (endo-, peri-, and myocarditis) and is often associated with subcutaneous nodules
  • Chronic progressive damage to the heart valves may occur
25
Q

What are the features of post-streptococcal glomerulonephritis (PSGN)?

A

Acute inflammation of the renal glomeruli with edema, hypertension, hematuria, and proteinuria

26
Q

What types of streptococci cause PSGN?

A

Specific nephritogenic strains of S. pyogenes

27
Q

How is S. pyogenes identified?

A
  • GAS antigen detection
  • β-hemolysis with no resistance to bacitracin
28
Q

How is S. agalactiae identified?

A
  • GBS antigen detection
  • β-hemolysis with no resistance to bacitracin
29
Q

What is the epidemiology and disease features of S. agalactiae infections?

A
  • Colonize the lower GI tract and the genitourinary tract
  • Transient vaginal carriage occurs in pregnant women
  • Men and nonpregnant women with infection are generally older and have debilitating underlying conditions
  • Most common presentations are bacteremia, pneumonia, bone and joint infections, and skin and soft-tissue infections
30
Q

What are the types of neonatal GBS infection?

A
  • Early-onset: younger than 7 days
  • Late onset: 1 week–3 months
  • Both are characterizied by bacteremia and meningitis
31
Q

Which organism is called pneumococcus?

A

Streptococcus pneumococci

32
Q

What are the physiologic and structural features of pneumococcus?

A
  • Encapsulated, Gram-positive coccus
  • Cells and oval and arranged in either pairs (diplococci) or short chains
  • Are α-hemolytic on blood agar if incubated aerobically
  • The hemolytic activity is mediated by the enzyme pneumolysin, and produces a green pigment from hemoglobin
  • Virulent strains are covered with a polysaccharide capusle which is used for serologic classification and for use in a polyvalent vaccine
33
Q

What is the epidemiology of pneumococcus infections?

A
  • Pneumococcus is a common inhabitant of the throat and nasopharynx in healthy people, especially children and adults who live with children
  • Pneumococcal disease occurs when orgnanisms in the nasopharynx and oropharynx spread to the lungs (pneumonia), paranasal sinuses (sinusitis), ears (otitis media), or meninges (meningitis)
  • Vaccination in pediatric and adult populations has reduced the incidence of disease
34
Q

What is the cause of the clinical disease manifestations of pneumococcal infection?

A

The host response rather than bacterial toxic factors

35
Q

How does pneumococcus colonize parts of the body?

A
  • Initial colonization of the oropharynx is mediated by surface protein adhesins
  • Migration to the lower respiratory tract is mediated by secretory IgA protease (which inactivates the IgA in mucus by preventing mucin from binding to the Fc region) and pneumolysin (which destroys ciliated epithelial cells and phagocytes)
36
Q

How is the complement activated in response to pneumococcus?

A
  • Teichoic acid and peptidoglycan fragments activate the alternative pathway
  • This is augmented by the bacterial enzyme amidase, which enhances the release of cell wall components
37
Q

How does pneumococcus enter cells to avoid phagocytosis?

A

Phosphorylcholine present in the bacterial cell wall can bind to receptors for platelet-activating factor

38
Q

What is the significance of the capsule of pneumococcus?

A
  • Provides anti-phagocytic protection
  • Nonencapsulated strains are avirulent
39
Q

What are the species included under viridans group streptococci?

A
  • S. mitis
  • S. mutans
40
Q

What are the diseases caused by viridans group streptococci?

A
  • S. mitis: subacute endocarditis, sepsis in neutropenic patients, pneumonia, meningitis
  • S. mutans: dental caries, bacteremia
41
Q

What are the physiologic and structural features of enterococci?

A
  • Gram-positive cocci
  • Arranged in pairs or short chains
  • Grow aerobically and anaerobically in a broad temperature range, a wide pH range, and in the presence of high concentrations of NaCl or bile salts
  • Can appear α-hemolytic, β-hemolytic (rarely), or γ-hemolytic
42
Q

What is the epidemiology of enterococci?

A
  • Enteric bacteria that are commonly recovered in the feces of humans and other animals
  • E. faecalis is found in the large intestine and the genitourinary tract
  • E. faecium is also found
43
Q

What are the virulence factors of enterococci?

A
  • Ability to adhere to tissues and form biofilms
  • Inherent antibiotic resistance
44
Q

What are the features of enterococcal infection?

A
  • One of the most common nosocomial infections
  • The urinary tract is a common site of nosocomial infection due to catheterization (with a Foley catheter)

Microbiology and immunology (33 decks)

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