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Microbio Exam 1 > Streptococci > Flashcards

Streptococci Flashcards

1
Q

Streptococci are a diverse collection of ___________ bacterial strains, and typically are found in ___________.

A
  • gram positive

- pairs or chains

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2
Q

3 ways to classify streptococci

A
  1. hemolysis patterns on plates
  2. B-hemolytic can be further divided based on serologic properties (Lancefield groupings) due to different carbs on cell wall
  3. physiologic properties (for non-hemolytic strep)
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3
Q

B- vs. a. vs. y Hemolysis

A
  • Beta: cause complete hydrolysis of RBC
  • Alpha: cause incomplete hydrolysis of RBCs; green color
  • Gamma: no hemolysis
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4
Q

Why is alpha hemolysis green?

A

-hydrogen peroxide produced by the bacterium oxidized hemoglobin to green methemoglobin

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5
Q

Beta-hemolytic strains can further be divided into groups based on serologic properities, with these differences being due to ___________.

A
  • different carbohydrates in the cell wall

- called Group A, B,..etc

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6
Q

Streptococcus pyogenes aka…

A

-Group A streptococcus

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7
Q

Streptococcus agalactiae aka…

A

-Group B streptococcus

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8
Q

Strep are catalase _______ while staph are catalase _______.

A
  • negative

- positive

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9
Q

3 most important strep

A
  • Group A
  • Group B
  • S. pneumoniae
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10
Q

Is Strep a facultative or obligate anaerobe?

A
  • facultative aka aerotolerant

- can use oxygen to make ATP or fermentation

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11
Q

What kind of growth requirements does Strep have?

A
  • autotrophic-complex growth requirements

- as a result, blood or serum-enriched media is needed for isolation

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12
Q

Many strains of strep are B-hemolytic due to expression of ________.

A

-Streptolysin S

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13
Q

Detection of _________ can be used for identification of strep

A

-PYR: L-pyrrolidonyl arylamidase

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14
Q

Where is Strep found within nature?

A

-only humans, it has no environmental reservoir

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15
Q

If gram positive cocci are observed, they are either staph or strep. A ___________ test distinguishes between these 2 major groups.

A

-catalase test

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16
Q

Sensitivity to __________ distinguished Group A from group B strep.

A
  • bacitracin

- GAS are bacitracin sensitive

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17
Q

Group A strep is _____ hemolytic.

A

-Beta (B)

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18
Q

Summary of physiology and structure of GAS (S. pyogenes)

A
  • small gram + coccus
  • pairs and chains
  • growth as white colonies on enriched blood agar
  • B-hemolysis
  • Catalase neg, bacitracin sensitive, PYR-positive
  • cell wall containing Group specific and type-specific antigens
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19
Q

How can GAS infections be recurrent if immunity was built from the first infection?

A

-there are many strains of GAS and immunity to one strain often fails to produce immunity to other strains

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20
Q

3 general categories of things GAS’s virulence factors allow it to do

A

-get through tissue barriers, adhere to sites of inflammation, and inhibit otherwise effective clearance mechanisms

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21
Q

3 characteristics that promote GAS virulence include…

A
  • the ability to adhere to the surface of epithelial cells: ability to invade into and hide in epithelial cells
  • ability to avoid opsonization and phagocytosis
  • ability to cause tissue damage and inhibit clearance by producing toxins akin to snake venom
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22
Q

3 factors allowing GAS to bind to cell surface

A
  1. lipoteichoic acid
  2. M protein
  3. F protein
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23
Q

2 factors allowing GAS to invade host cells

A
  1. M protein

2. F protein

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24
Q

Mechanisms to avoid opsonization and phagocytosis of GAS

A
  1. M protein can bind serum B-globin factor H, which regulated alternative complement pathway
  2. Complement component C3b is destabilized by factor H. So, when C3b clings to the cell surface in the region of the M protein, it is degraded by associated factor H and phagocytosis is prevented
  3. GAS can produce a protease that inactivated C5a which in turn blocks chemotaxis of neutrophils
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25
Q

Factor H degrades C3b which clings to the cell surface of M protein and prevents phagocytosis. This is overcome if a patient ____________.

A

-has antibodies to the strain’s M protein

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26
Q

Exotoxins: 3 examples and what they do.

A
  • the leukocydins Streptolysins O (pore forming toxin) and S (B-hemolysin) damage tissue and inhibit clearance
  • pyrogenic exotoxins (SpeA, SpeB, etc) lead to fever by inducing release of numerous cytokines
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27
Q

M protein functions

A
  • provides antigenic variation
  • blocks opsonization by complement alternate pathway, thus evading phagocytosis
  • also plays role in mediating adherence to host cells
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28
Q

Capsule function

A

-thick coat of hyaluronic acid (also found in CT) that confers resistance to phagocytosis

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29
Q

Hyaluronidase function

A

-degrades hyaluronic acid in CT

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30
Q

C5a peptidase function

A

-destroys C5a as a chemotactic signal to neutrophils (PMNs)

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31
Q

Streptokinase function

A

-catalyzes activation of plasmin to lyse blood clots, which may lead to spread of GAS in infected tissues

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32
Q

Streptodornase (DNase) function

A

-helps solubilize pus, thus facilitating spread of infection

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33
Q

Lipoteichoic acid and F protein function

A

-mediated attachment to epithelium, fibronection

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34
Q

The M protein is a major ________ protein expressed by virulent streptococci.

A

-immunodominant

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35
Q

Explain the structure of M protein and why it leads to recurrent infections

A
  • 2 polypeptide chains that are anchored in the bacterial membrane and that extend through the cell wall
  • C terminal portion is inside the cell and is highly conserved
  • N terminal portion is external and highly variable which means that development of immunity to one type leaves an individual still susceptible to all remaining types–recurrent infections!!
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36
Q

T/F. Toxins contribute to disease by GAS

A

-true

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37
Q

In each of the following scenarios, say if the GAS is phagocytosed:
A: GAS with M protein knockout
B: GAS, 1st infection, M protein present
C: GAS, Abs to M protein, M protein present

A
  • Yes
  • No
  • Yes
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38
Q

Streptococci have a predilection for the ________ or ________. Strains that colonize either area are usually distinct “antigenic types” from eachother.

A
  • upper respiratory tract

- skin

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39
Q

GAS commonly colonize ________________. Why is colonization transient?

A
  • oropharynx of healthy children and young adults
  • or the skin
  • transient due to development of M protein-specific immune response requiring 1-4 weeks
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40
Q

If GAS colonization is usually transient and asymptomatic, how does it ever cause disease?

A

-usually caused by a recently acquired strain that can establish an infection prior to the induction of antibodies to the M protein

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41
Q

GAS transmission of pharyngitis

A
  • person to person by respiratory secretions or via fomites

- remember, humans are the exclusive host for GAS, so it must be person-to-person

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42
Q

What are some things that increase risk of pharyngitis?

A
  • crowding (classrooms, military, etc)
  • hospital spread such as post-surgical infection from carriers
  • especially common in children 5-15
  • cold months
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43
Q

Can pharyngitis spread and cause skin issues?

A

-yes, invasive and deep cutaneous diseases are complications of spread from pharynx

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44
Q

What are the post-infectious sequelae of pharyngitis?

A
  • Acute rheumatic fever

- glomerulonephritis

45
Q

How are cutaneous and soft tissue infections from strep spread?

A

-transmitted by bacteremic spread or through breaks in skin after direct contact with oral secretions from infected person, fomite, or arthropod vector

46
Q

Impetigo

A
  • example of skin infection from strep

- more common in warm months and occurs following minor trauma esp. when hygiene is suboptimal

47
Q

What is the only post-infectious sequelae of strep skin and soft tissue infections?

A

-glomerulonephritis

48
Q

GAS is one of the most important human pathogens; Commonly associated with a diverse group of human diseases, including both _________ and _________ diseases.

A

-suppurative (pus-forming) and nonsuppurative diseases

49
Q

3 general categories of GAS virulence factors:

A
  • toxins
  • adhesins
  • anti-phagocytosis
50
Q

Immunity to GAS requires….

A

-type specific (M protein specific) antibodies

51
Q

In summary, 2 ways GAS is spread…

A
  • person to person

- through breaks in skin

52
Q

In winter months, what type of GAS infections do you expect to see? How about summer months?

A
  • pharyngeal in winter

- cutaneous in summer

53
Q

2 types of localized GAS infections

A
  • pharyngeal

- cutaneous

54
Q

3 types of disseminated (invasive) GAS infection

A
  • Bacteremia
  • Septic arthritis
  • Pneumonia
55
Q

Type of GAS infection that is toxin mediated

A

-Toxic shock-like syndrome

56
Q

Pharyngitis chief symptoms

A
  • “strep throat”
  • sore throat, malaise, headache, abdominal pain
  • erythematous posterior pharynx +/- exudate
  • cervical lymphadenopathy
  • ex of a suppurative streptococcal disease
57
Q

How does one determine a viral vs. strep pharyngitis?

A

-throat swab

58
Q

5 other suppurative diseases other than pharyngitis

A
  • puerperal sepsis (assoc. with childbirth)
  • Lymphangitis (inflammation of lymphatic vessels)
  • Pneumonia
  • Bacteremia (bacteria in blood)
  • Septicemia (sepsis)
59
Q

Septicemia definition

A

-systemic disease associated with persistent presence of bacterial cells, bacterial toxins, or other bacterial products in the blood causing multi-system failure and mortality approaching 40%

60
Q

5 cutaneous/soft tissue infections from GAS

A
  1. Pyoderma/Impetigo
  2. Erysipelas
  3. Cellulitis
  4. Necrotizing fasciitis
  5. Scarlet Fever
61
Q

Pyoderma/Impetigo

A
  • generally caused by strains of different M type from pharyngitis and other infections and is generally seen in young children
  • impetigo is contagious pyoderma with superficial yellow weeping-crusty lesions
62
Q

Erysipelas

A
  • acute superficial cellulitis of skin with lymphatic involvement
  • face, lower extremities, skin and subcutaneous tissues
  • associated with local pain
  • involved area is typically raised and distinct from adjoining, uninvolved areas
  • most comon in young children and older adults
63
Q

Cellulitis

A
  • involvement of DEEPER subcutaneous tissues than erysipelas
  • deeper invasion with systemic symptoms
  • involved areas not well demarcated
  • many other organisms can cause cellulitis so you cannot assume it is GAS
64
Q

Cellulitis vs. Erysipelas

A

-E: less deep and well demarcated; local pain

C: deeper tissue and not well demarcated; systemic symptoms

65
Q

Necrotizing fasciitis

A
  • aka flesh-eating bacteria

- infection deep in subcutaneous tissues that spreads along fascial planes, destroying muscle and fat

66
Q

Describe progression of necrotizing fasciitis and treatment

A
  • begins with cellulitis, followed by bullae (fluid filled blisters), gangrene, systemic toxicity, multiorgan failure and mortality more than 50%
  • cannot treat with just antibiotics, need to surgically debride affected area
67
Q

Scarlet fever

A
  • complication of streptococcal pharyngitis with “scarletina” rash on upper chest spreading to extremities
  • results from infection with a strain that is lysogenized with a temperate bacteriophage that genetically encodes for pyrogenic exotoxin
68
Q

Rheumatic Fever

A
  • inflammatory disease that may develop after an infection with GAS but not other bacteria
  • may involve heart, joints, skin, and brain
  • diagnose via modified-Jones criteria
69
Q

5 major diagnostic criteria of rheumatic fever

A
  1. carditis
  2. polyarthritis
  3. chorea
  4. erythema marginatum
  5. subcutaneous nodules
    - requires evidence of recent GAS infection
70
Q

Why are physicians more worried about rheumatic fever in people who have had it before?

A

-carditis has cumulative, negative effects

71
Q

Rheumatic heart disease

A

-can be due to chronic, progressive heart valve damage

72
Q

Rheumatic fever primarily affects children between ages 6 and 15, and occurs approximately _____ after strep throat or scarlet fever.

A

-20 days

73
Q

The recurrence of rheumatic fever is relatively common in the absence of ___________.

A

-maintenance of low dose antibiotics, esp during first 3-5 years

74
Q

Major heart complications that cause rheumatic heart disease

A
  • mitral stenosis and aortic stenosis

- may be long term and severe

75
Q

Define acute glomerulonephritis

A

-acute inflammation of renal glomeruli

76
Q

Signs of acute glomerulonephritis

A
  • dark, smoky (coke) urine with red and white blood cells
  • depressed serum complement
  • decreased GFR
  • hypertension
  • granular accumulations of Ig due to deposition of immune complexes within kidney
  • can cause renal failure
77
Q

Latent period of acute glomerulonephritis

A

-1-2 weeks after skin infection and 2-3 weeks after pharyngitis

78
Q

Streptococcal toxic shock syndrome

A

-multisystem “systemic” toxicity following soft tissue infection progressing to shock (low blood pressure) and organ failure; erythematous rash

79
Q

Scarlet fever rash is caused by pyrogenic exotoxins that used to be called _______. What are some key symptoms of scarlet fever?

A
  • erythrogenic toxins

- sand paper like rash and strawberry tongue

80
Q

_________ of skin is common following Strep infections

A

-desquamation

81
Q

Sydenham’s chorea

A

-chorea associated with febrile illness rheumatic fever

82
Q

What toxins cause Streptococcal toxic shock like syndrome?

A

-pyrogenic exotoxins (SpeA,B, C,F) which are superantigens made by some strains

83
Q

What do superantigens in strep TSLS do?

A
  • interact directly with T cells to release cytokines
  • effects include shock (vascular collapse), erythematous rash, and organ failture
  • it is the host response via cytokines that is problematic!!
84
Q

Strep toxic shock is similar to TSS seen in staph infections except…

A

-GAS infections are disseminated rather than localized

85
Q

Toxic Shock Syndrome via Strep is due to ______________.

A

-non-specific stimulation of T cells by superantigen rather than effects of a toxin

86
Q

You can diagnose Strep by a throat swab from posterior oropharynx or from skin lesioned and follow up by doing 1 of what 2 things?

A
  1. culture: bacitracin sensitivity for beta hemolytic strep; negative catalase used to differentiate from staph
  2. Rapid ID tests: agglutination reactions based on extraction of GAS carbohydrate directly from swab and agglutination in presence of antibody
87
Q

ASO test:

A
  • detection of antibodies against the conserved toxin streptolysin O confirms a recent group A strep infection
  • retrospective diagnosis only used in suspected acute rheumatic fever
88
Q

Anti-DNase B test

A
  • try to detect antibodies against DNase B
  • unlike ASO test, anti DNase B is useful for diagnosing recent GAS infection in cases of rheumatic fever and glomerulonephritis
89
Q

Antibodies to ASO or Anti-DNase B are useful to confirm recent GAS infection for diagnosis of __________.

A

-post-infectious complications

90
Q

Treatment of strep infections are aimed at ______________.

A
  • prevention of suppurative complications and the nonsuppurative sequelae of rheumatic fever and glomerulonephritis
  • pharyngitis is generally self-limited, so youre treating for sequelae
91
Q

GAS Pharyngitis drug of choice and alternatives

A
  • oral penicillin or intramuscular benzathine penicillin; treatment failure may be due to neighboring cells release of beta-lactamases
    alternatives: erythromycin (but increasing macrolide resistance), clindamycin, cephalexin (oral cephalosporin)
92
Q

Treatment of Acute Rheumatic Fever

A
  • salicylates and corticosteroids for acute symptom reduction and control of long-term sequelae
  • prevention of reoccurences by preventing strep infection with long-term prophylactic antibodies
  • decrease inflammation and then to prevent future episodes
93
Q

Treatment of acute post-streptococcal glomerulonephritis

A
  • therapy directed at secondary phenomenon of renal failure: volume excess, hypertension and seizures;
  • sodium restriction, diuretics, anticonvulsants
94
Q

Is there a GAS vaccine?

A

-no

95
Q

There is antibiotic prophylaxis if have had rheumatic fever, but is there the same treatment for glomerulonephritis?

A

-no, no antimicrobial treatment or prophylaxis

96
Q

T/F: Treat GAS asymptomatic carriers with penicillin.

A

-False; do not treat asymptomatic carriers

97
Q

Group B strep physiology and structure (gram stain, shape, hemolysis, catalase, bacitracin, etc)

A
  • small, gram positive coccus
  • grow in pairs and chains
  • facultative anaerobe, autotrophic complex growth requirements
  • growth as buttery colonies on enriched blood agar
  • B or non-hemolytic
  • catalse negative
  • bacitracin resistant UNLIKE GAS
  • cell wall contains group specific and type-specific antigens
  • type specific antibodies are more diverse than GAS which is HA
98
Q

S. agalactiae epidemiology

A
  • colonizes lower GI
  • GU tract
  • transient vaginal colonization
99
Q

How does GBS spread?

A

-maternal-fetal in utero (early onset disease) or at birth/after (later onset disease)

100
Q

What is GBS the leading cause of?

A

-neonatal infection

101
Q

Risk factors for GBS infection

A
  • prematurity because have less maternal antibodies
  • prolonged rupture of chorioamniotic membranes
  • teenage pregnancy
102
Q

4 differences between GAS and GBS

A
  • niche: skin and oropharynx for GAS and lower GI and GU for GBS
  • GBS has animal reservoir and is cause of bovine mastitis
  • bacitracin resistant (GBS)
  • cause different diseases
103
Q

GBS has capsules made of __________. What are the advantages of capsules?

A
  • sialic acid (a polysaccharide) which is different from GAS HA capsule
  • these thick layers are anti-phagocytic by inhibiting opsonization
  • specific antibody to the capsular polysaccharide type is protective but there are many chemically and antigenically distinct capsule types
104
Q

GBS major clinical disease is infection of newborns (

A

-puerperal sepsis in mothers immediately following delivery

105
Q

Following maternal-fetal transmission (vertical transmission) before delivery (early-onset disease), the infant is susceptible to _____________.

A

-invasive infections (pneumonia, sepsis, meningitis)

106
Q

GBS is also a cause of _________ in adults.

A

-UTI

107
Q

GBS prevention

A
  • since idea of immunizing mothers during pregnancy to provide IgG by transplacental transfer is not well accepted, prevention is aimed at identifying mothers carrying GBS late in gestation and treating them with antibiotics to reduce burden of organisms
  • newborns at high risk are given prophylactic treatment (premature rupture of membranes, signs of infection like fever)
108
Q

How to diagnose GBS?

A

-PCR (colonization) or routine culture (infection)

109
Q

GBS remains ______ susceptible.

A

-penicillin

Microbio Exam 1 (13 decks)

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