general characteristics of streptococci Flashcards

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1
Q

Streptococcal pyrogenic exotoxin A (or SpeA), SpeB,are _________. They massively activate the immune system like the staph superantigens that can create cytokine storms, leading to sepsis and death.

A

are superantigens.

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2
Q

Streptococcal pyrogenic exotoxin A (or SpeA), SpeB,are _________. They massively activate the immune system like the staph superantigens that can create cytokine storms, leading to sepsis and death.

A

are superantigens.

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3
Q

which condition is described by the following? Usually occurs age 5-15, with peak in early school years.
Spread by droplets. Crowding enhances spread.
Asymptomatic carriage rates can be 15-30%.

A

pharyngitis

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4
Q

which condition described: 2-4 day incubation period.
Enlarged tonsils with patchy exudates, pain, swollen lymph nodes, fever 101° or higher.
Type specific anti-M antibody protects against recurrence of infection with the infecting serotype.
Usually self-limited, but early treatment with penicillin reduces risk of ARF…but this is not true for AGN.

A

phayrngitis

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5
Q

__________was a streptococcal infection that frequently developed after giving birth.

A

Puerperal fever

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6
Q

what is a superficial purulent skin infection (aka a pyoderma) described by:
Most common in children
May follow insect bites
Weeping vesicles that form honey-colored crusts
Can be focus for more invasive disease

A

GAS impetigo

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7
Q

__________ follows pharyngeal infections, not skin infections.

A

Acute rheumatic fever

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8
Q

_________is a form of impetigo that has invaded more deeply described by annular lesions showing pustular centers and ulceration

A

Ecthyma

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9
Q

A form of streptococcal cellulitis, chararcterized by fiery-red erythema and edema with rapidly advancing, well-demarcated edges

symptoms include: Pain
Fever
Lymphadenopathy

A

erypsipelas

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10
Q

which age group does erypsipelas affect?

A

children and elderly

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11
Q

what is described by the following: An acute inflammatory condition of the skin.

Deeper infection than impetigo or erysipelas (see histological image).

Localized pain, erythema, swelling and heat.

A

cellulitis

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12
Q

_________is commonly associated with a localized infection, such as folliculitis or a carbuncle, a foreign body (splinter, catheter) or surgical wound.

Strep cellulitis is more rapidly spreading and associated with lymphangitis and fever.

A

Staph cellulitis

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13
Q
\_\_\_\_\_\_\_\_\_\_\_\_is a life-threatening deep tissue infection that spreads along fascial planes.
40-70% mortality
Infection often begins innocuously
	Skin trauma, bruise 
Rapid progression of necrosis
	Up to an inch per hour
A

Streptococcal Toxic Shock & Necrotizing fasciitis

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14
Q

these early symptoms describe which condition?Flu-like symptoms
Brawny edema
Extreme pain in infected area way out of proportion to the appearance of the lesion
Spreading erythema (redness of skin), eccymosis (hematoma) with vesicles enlarging to purple bullae

A

streptococcal Toxic Shock & Necrotizing fasciitis

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15
Q

how do you treat streptococaal toxic shock and necrotizing fasciitis?

A

Debridement
Aggressive use of broad spectrum antibiotics immediately
High levels of penicillin and clindamycin if S. pyogenes is detected
Massive amounts of IV fluids may be needed
Monitor cardiac out put closely

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16
Q

__________superantigens cause stretpoccooal toxic shock and necrotizing fasciitis.

A

streptococcal pyrogenic exotoxins

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17
Q

Streptococcal toxic shock also causes a widespread rash that ______ when pressure is applied, but this is not quite as common as with S. aureus TSS.

A

blanches

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18
Q

how do you diagnose STSS?

A

A. Isolation of GAS from a clinically significant specimen in a patient who is hypotensive (systolic BP less than 90 mm HG).
AND
B. Patient has two or more of the following:
i. renal impairment
ii. coagulopathy
iii. liver dysfunction
iv. acute respiratory distress syndrome (ARDS)
v. a generalized erythematous macular rash
vi. soft-tissue necrosis (including necrotizing fasciitis or myositis or gangrene)

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19
Q

What is the Jones criteria for acute rheumatic fever? major and minor manifestations.

A
ARF
Guidelines for Diagnosis of Initial Attack of ARF: The Jones Criteria
Major manifestations
	*Carditis
	*Polyarthritis
	Chorea
	Erythema marginatum
	Subcutaneous nodules
Minor manifestations
	Clinical findings
		Arthralgia
		Fever
	Lab findings
		Elevated acute phase reactants
			Erythrocyte sed rate
			C-reactive protein
		Prolonged PR interval
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20
Q

what are the non-supparative sequelae of S. pyogenes infections?

A

Acute rheumatic fever and Acute glomerulonephritis

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21
Q

ARF usually develops in young children after_________ .

A

pharyngitis

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22
Q

what are the major manifestations of AGN?

A

Major manifestations
Clinical findings
Edema
Hypertension
Hematuria (rust-colored urine)
Proteinuria
Malaise, headache, back pain
Lab findings
Increased glomerular intracapillary cellularity
Ig, complement C3, and strep antigens present
Almost all glomeruli involved, some tubules

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23
Q

what is the treatment and prognosis for AGN?

A

Treatment: Benzathine penicillin ( a slow-release form). However, no treatment alters long-term prognosis, treat to manage acute kidney problems.

Prognosis: usually excellent, especially in children. A small fraction of patients may develop a chronic renal insufficiency.

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24
Q

what is the treatment for most S. pyogenes infections?

A

Most S. pyogenes infections: Penicillin
No resistance to penicillins so far.
Pen is the drug of choice: safe, narrow spectrum, low cost.
For patients with penicillin allergies: clindamycin, azithromycin

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25
Q

how are more serious invasive infections of S. pyogenes treated?

A

Serious invasive infections:
Initiate broad spectrum antibiotics if Group A strep is identified; high levels of penicillin and clindamycin (which is more effective in deep infections)
Surgical debridement required; locate source of infection
Monitor cardiac output carefully
Dialysis and hemoperfusion
IVIG (intravenous immunoglobulin)

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26
Q
this describes which bacteria: 
Diplococci
Reaction positive for Group B antigen
Bacitracin resistant
Hydrolysis of bile esculin
Narrow ring of b-hemolysis
CAMP factor: a GBS factor that synergizes with S. aureus hemolysin to cause increased lysis of red cells.
A

S. agalactiae

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27
Q

what is the major virulence factor for group B strep?why?

A

capsule; Capsule serves as an antiphagocytic factor.

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28
Q

the following describes which disease: Neonatal
Early onset (7 days or younger)
Septicemia, respiratory distress, meningitis
More common in pre-term infants
Mothers had intraamniotic infection
Late Onset (2 wks to 2 mos)
Half of these also are pre-term infants
Bacteremia
Meningitis
Most survivors have permanent neurologic sequelae

A

GBS disease

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29
Q

be aware: Now 2/3 of invasive GBS disease are not associated with pregnancy
Increases with age: incidence for >65 group is 2X that of 50-64.
Fatality rate in GBS pneumonia, for instance, can be up to 85%.
High morbidity and mortality; associated with diabetes, heart disease, malignancy.
High incidence in nursing homes.

A

fyi card

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30
Q

what has reduced the incidence of GBS in neonates?

A

Prenatal screening and intrapartum IV administration of antibiotic (penicillin) to infected mothers and mothers with risk factors has greatly reduced incidence.

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31
Q

when ins intrapartum prophylaxis indicated in a pregrant woman for GBS infection ?

A

previous infant with invasive GBS disease, GBS bacteruria during current pregnancy, and GBS status uknown

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32
Q

the following describes which bacteria:Part of the normal oral microbiota
Usually a-hemolytic
Don’t react antibodies against Lancefield antigens
Distinguished from enterococci by inability to grow in 6.5% NaCl
Distinguished from pneumococci by resistance to optochin (a chemical; ethylhydrocupreine).

A

viridans stretpococci

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33
Q

The viridans or green strep (because of alpha hemolysis) are inhabitants of the________

A

oral cavity

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34
Q

what is a classic biofilm?

A

dental plaque

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35
Q

name four groups of viridans streptococi.

A

S. anginosus, S. mitis, S. mutans, S. salivarius and S. sanguinis groups.

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36
Q

the following describes which bacteria: Present in dental plaque, a classic biofilm.
Contribute to caries, periodontal disease and endocarditis.
S. mutans: caries, glucans, lactic acid, can grow at an acidic pH.

A

viridans streptococci

37
Q

fyi: Transient bacteremia every time you brush your teeth.
Bacteremia during most dental procedures.
S. sanguis and other viridans strep are strongly associated with endocarditis of damaged heart valves.
Damage of heart valves leads to exposure of fibronectin and deposition of fibrin amd platelets.
Viridans strep have adhesins for fibronectin, fibrin and other host proteins that accumulate on injured valves.
Once they adhere, they form biofilms called vegetations.
So, if you’ve had ARF, you’ll have penicillin prophylaxis before dental work.

A

fyi card

38
Q

what is described by the following: Formerly a Group D streptococcus
Shows reaction for Lancefield Group D antigen, but clearly a different genus
A commensal of GI tract
Over a dozen species, but faecalis and faecium are the main clinical problems
Usually a- or g-hemolytic
Can grow in high salt, at 45°C and are bile esculin positive
Diplococci and short chains

A

enterococcus

39
Q

__________ treatment alters the dynamic in favor of enterococci because they are naturally tolerant to a wide variety of commonly used antibiotics.

A

Antibiotic

40
Q

Altering pH of the stomach (e.g. using proton pump inhibitors) can alter gut pH and favor growth of _________

A

enterococci

41
Q

enterococci are a leading cause of __________

A

nosocomial infections

42
Q

when do enterococci cause problems?

A

They commonly cause problems after a course of antibiotics because they are resistant to so many.

Also, while they are normally a small fraction of GI microbiota, killing competing organisms with antibiotics leads to overgrowth.

43
Q

E._______ cause more problems because they are resistant to more antibiotics.

A

E. faecium

44
Q

describes which organism:
Once they increase in number, they can gain access to lymphatics or blood. They don’t make lots of toxins like staph and strep, but any organism in large numbers in the bloodstream can be fatal.

A

enterococcus

45
Q

One particular reason enterococci are a big problem is because they are extremely proficient at taking up______ and passing it along to other species. VRE E. faecium (1988) was the likely source of a transposon (Tn1546) that brought vancomycin resistance to S. aureus (2002).

A

One particular reason enterococci are a big problem is because they are extremely proficient at taking up DNA (e.g. plasmids, transposons) and passing it along to other species. VRE E. faecium (1988) was the likely source of a transposon (Tn1546) that brought vancomycin resistance to S. aureus (2002).

46
Q

list the virulence factors for Group A streptococci.

A
M-Protein
M-like proteins
Streptolysin O 
Streptolysin S 
Hyaluronidase 
SpeA(streptococcal pyrogenic exototoxin A), B, C, F, Ssa (the superantigens)
Protein S 
T-antigen 
C5a peptide
 streptokinase
Proteinase(SpeB)
47
Q

which condition is described by the following? Usually occurs age 5-15, with peak in early school years.
Spread by droplets. Crowding enhances spread.
Asymptomatic carriage rates can be 15-30%.

A

pharyngitis

48
Q

which condition described: 2-4 day incubation period.
Enlarged tonsils with patchy exudates, pain, swollen lymph nodes, fever 101° or higher.
Type specific anti-M antibody protects against recurrence of infection with the infecting serotype.
Usually self-limited, but early treatment with penicillin reduces risk of ARF…but this is not true for AGN.

A

phayrngitis

49
Q

__________was a streptococcal infection that frequently developed after giving birth.

A

Puerperal fever

50
Q

what is A superficial purulent skin infection (aka a pyoderma) described by:
Most common in children
May follow insect bites
Weeping vesicles that form honey-colored crusts
Can be focus for more invasive disease
Staph also causes impetigo (usually with pus)

A

GAS impetigo

51
Q

__________ follows pharyngeal infections, not skin infections.

A

Acute rheumatic fever

52
Q

_________is a form of impetigo that has invaded more deeply described by annular lesions showing pustular centers and ulceration

A

Ecthyma

53
Q

A form of streptococcal cellulitis, chararcterized by fiery-red erythema and edema with rapidly advancing, well-demarcated edges

symptoms include: Pain
Fever
Lymphadenopathy

A

erypsipelas

54
Q

which age group does erypsipelas affect?

A

children and elderly

55
Q

what is described by the following: An acute inflammatory condition of the skin.

Deeper infection than impetigo or erysipelas (see histological image).

Localized pain, erythema, swelling and heat.

A

cellulitis

56
Q
\_\_\_\_\_\_\_\_\_\_\_\_is a life-threatening deep tissue infection that spreads along fascial planes.
40-70% mortality
Infection often begins innocuously
	Skin trauma, bruise 
Rapid progression of necrosis
	Up to an inch per hour
A

Streptococcal Toxic Shock & Necrotizing fasciitis

57
Q

these early symptoms describe which condition?Flu-like symptoms
Brawny edema
Extreme pain in infected area way out of proportion to the appearance of the lesion
Spreading erythema (redness of skin), eccymosis (hematoma) with vesicles enlarging to purple bullae

A

streptococcal Toxic Shock & Necrotizing fasciitis

58
Q

how do you treat streptococaal toxic shock and necrotizing fasciitis?

A

Debridement
Aggressive use of broad spectrum antibiotics immediately
High levels of penicillin and clindamycin if S. pyogenes is detected
Massive amounts of IV fluids may be needed
Monitor cardiac out put closely

59
Q

Streptococcal toxic shock also causes a widespread rash that ______ when pressure is applied, but this is not quite as common as with S. aureus TSS.

A

blanches

60
Q

how do you diagnose STSS?

A

A. Isolation of GAS from a clinically significant specimen in a patient who is hypotensive (systolic BP less than 90 mm HG).
AND
B. Patient has two or more of the following:
i. renal impairment
ii. coagulopathy
iii. liver dysfunction
iv. acute respiratory distress syndrome (ARDS)
v. a generalized erythematous macular rash
vi. soft-tissue necrosis (including necrotizing fasciitis or myositis or gangrene)

61
Q

What is the Jones criteria for acute rheumatic fever? major and minor manifestations.

A
ARF
Guidelines for Diagnosis of Initial Attack of ARF: The Jones Criteria
Major manifestations
	*Carditis
	*Polyarthritis
	Chorea
	Erythema marginatum
	Subcutaneous nodules
Minor manifestations
	Clinical findings
		Arthralgia
		Fever
	Lab findings
		Elevated acute phase reactants
			Erythrocyte sed rate
			C-reactive protein
		Prolonged PR interval
62
Q

what are the non-supparative sequelae of S. pyogenes infections?

A

Acute rheumatic fever and Acute glomerulonephritis

63
Q

ARF usually develops in young children after_________ .

A

pharyngitis

64
Q

what are the major manifestations of AGN?

A

Major manifestations
Clinical findings
Edema
Hypertension
Hematuria (rust-colored urine)
Proteinuria
Malaise, headache, back pain
Lab findings
Increased glomerular intracapillary cellularity
Ig, complement C3, and strep antigens present
Almost all glomeruli involved, some tubules

65
Q

what is the treatment and prognosis for AGN?

A

Treatment: Benzathine penicillin ( a slow-release form). However, no treatment alters long-term prognosis, treat to manage acute kidney problems.

Prognosis: usually excellent, especially in children. A small fraction of patients may develop a chronic renal insufficiency.

66
Q

what is the treatment for most S. pyogenes infections?

A

Most S. pyogenes infections: Penicillin
No resistance to penicillins so far.
Pen is the drug of choice: safe, narrow spectrum, low cost.
For patients with penicillin allergies: clindamycin, azithromycin

67
Q

how are more serious invasive infections of S. pyogenes treated?

A

Serious invasive infections:
Initiate broad spectrum antibiotics if Group A strep is identified; high levels of penicillin and clindamycin (which is more effective in deep infections)
Surgical debridement required; locate source of infection
Monitor cardiac output carefully
Dialysis and hemoperfusion
IVIG (intravenous immunoglobulin)

68
Q
this describes which bacteria: 
Diplococci
Reaction positive for Group B antigen
Bacitracin resistant
Hydrolysis of bile esculin
Narrow ring of b-hemolysis
CAMP factor: a GBS factor that synergizes with S. aureus hemolysin to cause increased lysis of red cells.
A

S. agalactiae

69
Q

what is the major virulence factor for group B strep?why?

A

capsule; Capsule serves as an antiphagocytic factor.

70
Q

the following describes which disease: Neonatal
Early onset (7 days or younger)
Septicemia, respiratory distress, meningitis
More common in pre-term infants
Mothers had intraamniotic infection
Late Onset (2 wks to 2 mos)
Half of these also are pre-term infants
Bacteremia
Meningitis
Most survivors have permanent neurologic sequelae

A

GBS disease

71
Q

be aware: Now 2/3 of invasive GBS disease are not associated with pregnancy
Increases with age: incidence for >65 group is 2X that of 50-64.
Fatality rate in GBS pneumonia, for instance, can be up to 85%.
High morbidity and mortality; associated with diabetes, heart disease, malignancy.
High incidence in nursing homes.

A

fyi card

72
Q

what has reduced the incidence of GBS in neonates?

A

Prenatal screening and intrapartum IV administration of antibiotic (penicillin) to infected mothers and mothers with risk factors has greatly reduced incidence.

73
Q

when ins intrapartum prophylaxis indicated in a pregrant woman for GBS infection ?

A

previous infant with invasive GBS disease, GBS bacteruria during current pregnancy, and GBS status uknown

74
Q

the following describes which bacteria:Part of the normal oral microbiota
Usually a-hemolytic
Don’t react antibodies against Lancefield antigens
Distinguished from enterococci by inability to grow in 6.5% NaCl
Distinguished from pneumococci by resistance to optochin (a chemical; ethylhydrocupreine).

A

viridans stretpococci

75
Q

The viridans or green strep (because of alpha hemolysis) are inhabitants of the________

A

oral cavity

76
Q

what is a classic biofilm?

A

dental plaque

77
Q

name four groups of viridans streptococi.

A

S. anginosus, S. mitis, S. mutans, S. salivarius and S. sanguinis groups.

78
Q

the following describes which bacteria: Present in dental plaque, a classic biofilm.
Contribute to caries, periodontal disease and endocarditis.
S. mutans: caries, glucans, lactic acid, can grow at an acidic pH.

A

viridans streptococci

79
Q

fyi: Transient bacteremia every time you brush your teeth.
Bacteremia during most dental procedures.
S. sanguis and other viridans strep are strongly associated with endocarditis of damaged heart valves.
Damage of heart valves leads to exposure of fibronectin and deposition of fibrin amd platelets.
Viridans strep have adhesins for fibronectin, fibrin and other host proteins that accumulate on injured valves.
Once they adhere, they form biofilms called vegetations.
So, if you’ve had ARF, you’ll have penicillin prophylaxis before dental work.

A

fyi card

80
Q

what is described by the following: Formerly a Group D streptococcus
Shows reaction for Lancefield Group D antigen, but clearly a different genus
A commensal of GI tract
Over a dozen species, but faecalis and faecium are the main clinical problems
Usually a- or g-hemolytic
Can grow in high salt, at 45°C and are bile esculin positive
Diplococci and short chains

A

enterococcus

81
Q

__________ treatment alters the dynamic in favor of enterococci because they are naturally tolerant to a wide variety of commonly used antibiotics.

A

Antibiotic

82
Q

Altering pH of the stomach (e.g. using proton pump inhibitors) can alter gut pH and favor growth of _________

A

enterococci

83
Q

enterococci are a leading cause of __________

A

nosocomial infections

84
Q

when do enterococci cause problems?

A

They commonly cause problems after a course of antibiotics because they are resistant to so many.

Also, while they are normally a small fraction of GI microbiota, killing competing organisms with antibiotics leads to overgrowth.

85
Q

E._______ cause more problems because they are resistant to more antibiotics.

A

E. faecium

86
Q

describes which organism:
Once they increase in number, they can gain access to lymphatics or blood. They don’t make lots of toxins like staph and strep, but any organism in large numbers in the bloodstream can be fatal.

A

enterococcus

87
Q

One particular reason enterococci are a big problem is because they are extremely proficient at taking up______ and passing it along to other species. VRE E. faecium (1988) was the likely source of a transposon (Tn1546) that brought vancomycin resistance to S. aureus (2002).

A

One particular reason enterococci are a big problem is because they are extremely proficient at taking up DNA (e.g. plasmids, transposons) and passing it along to other species. VRE E. faecium (1988) was the likely source of a transposon (Tn1546) that brought vancomycin resistance to S. aureus (2002).

88
Q

list the virulence factors for Group A streptococci.

A
M-Protein
M-like proteins
Streptolysin O 
Streptolysin S 
Hyaluronidase 
SpeA(streptococcal pyrogenic exototoxin A), B, C, F, Ssa (the superantigens)
Protein S 
T-antigen 
C5a peptide
 streptokinase
Proteinase(SpeB)