Koofers

Working...

TESTBANK•PROF RATINGS•GPA HISTORIES•FLASHCARDS•SCHEDULES•TEXTBOOKS•DEALS

Universities » University of Washington (UW) » MICROM - Microbiology » 442 - MED BACTERIOLOGY » Flash Cards

Strep and Entero - Flashcards

Flashcard Deck Information

Class:	MICROM 442 - MED BACTERIOLOGY
Subject:	Microbiology
University:	University of Washington - Seattle
Term:	Summer 2011

- of -

« Previous card

Next card »

INCORRECT

CORRECT

Click Card to flip

Strep Gram Stain and Characteristics

Gram Positive Cocci

defined based on hemolysis type (alpha, beta, gamma) and lance field group

Click Card to flip

Hemolysis

some beta hemolytic strep produce streptolysin, a type of hemolysin that makes a transmembrane channel in erythrocytes aka RBCs->osmolarity disrupted->cell lysis

Strep can be alpha, beta, or gamma hemolytic

respectively slight clearing (leaving greenish color on blood agar), complete lysis, and no lysis

beta hemolytic strep are grouped by lance field grouping

Click Card to flip

Major Pathogens of Strep (Beta Hemolytic)

S.pyogenes

S.agalactiae

Click Card to flip

Viridans Strep

alpha hemolytic some gamma

divided into 4 subgroups

normal microbiota and some pathogens

Click Card to flip

Viridans Strep Subgroups

1. Anginosus Group aka Milleri group

2. Mitis Group

3. salivarius group

4. mutans group

Click Card to flip

Pathogenic viridans strep organisms

1. Anginosus group aka milleri group

S.anginosus
S.constellatus
S.intermedius

2. S.pneumo

Click Card to flip

Lancefield Grouping

way to classify streptococcal organisms

M-protein on cell surface is a virulence factor, each organism has a different serotype and thus latex agglutination with a specific Ab to that protein can be used to classify the organism into:

group a

group b

group c/g

group acfg

Click Card to flip

Lancefield Group A=

S.pyogenes aka GAS

Click Card to flip

Lancefield Group B=

S.agalactiae aka Group B strep
Streptococcus agalactiae is a beta-hemolytic Gram-positive streptococcus.

Click Card to flip

Lancefield Group C&G=

S.dysgalactiae, S.equi, S.canis

Click Card to flip

Lancefield Groups A,C,G,F=

milleri group streptococci (intermedius, constellatus, anginosus)

Click Card to flip

Strep living in Throat

beta-hemolytic strep

Click Card to flip

Strep living on Skin

viridans strep

Click Card to flip

Strep living in GI

Beta-hemolytic strep (S.agalactiae)

viridans strep

Click Card to flip

Strep living in GU

S.agalactiae

Click Card to flip

Strep living in oral cavity

S.pneumoniae

Click Card to flip

S.pyogenes infections

aka Group A Strep

pharyngitis from colonizing epithelia or oropharynx and skin

necrotizing fasciitis and bacteremia and STSS (streptococcal shock syndrome) from penetrating epithelium and becoming invasive

19% patients with invasive gas die in 7 days

STSS increases mortality rate

Click Card to flip

Pharyngitis (Strep Throat)

incubation period: 2-4 DAYS

sudden sore throat, cervical lymphadenopathy, malaise, fever, headache

treated bc of risk of sequelae-> rheumatic fever and acute glomerulonephritis

strep group C/G can cause pharyngitis but not linked to sequelae

Click Card to flip

Rheumatic Fever

Rheumatic fever is an inflammatorydisease that occurs following aStreptococcus pyogenes infection, such asstreptococcal pharyngitis or scarlet fever. Believed to be caused by antibody cross-reactivity that can involve the heart,joints, skin, and brain,[1] the illness typically develops two to three weeks after a streptococcal infection.

Click Card to flip

Acute Glomerulonephritis

a disorder of the glomeruli(glomerulonephritis), or small blood vessels in the kidneys. It is a common complication of infections, typically streptococcal skin infection (impetigo) rather thanstreptococcal pharyngitis, for which it is also known as postinfectious or poststreptococcal glomerulonephritis.

Click Card to flip

Flesh Eating Disease

Necrotizing fasciitis, commonly known as flesh-eating disease or Flesh-eating bacteria syndrome, is a rare infection of the deeper layers of skin and subcutaneous tissues, easily spreading across the fascial plane within the subcutaneous tissue.

patients present with: erythemia progressing to formation of bullae (blisters) and tissue destructions w/in HOURS

Click Card to flip

Components of GAS that lead to disease 1 of 2

-liptotechoic acid and pili adhere to epithelia

-matrix binding proteins like fibronectin binding proteins allow epithelial cells invasion

-M protein mediates adhesion to epithelial cells AND resistance to phagocytosis (essential for GAS virulence)

-evasion by hyaluronic acid polysac in capsule (looks like host)

-evasion by SIC=strep inhibitor of complement (no complex)

-streptolysin O forms pore in host cells: neutros, macs, epi cells

-streptokinase: plasminogen-> plasmin degrades blood clots to allow for dissemination

Click Card to flip

Components of GAS that lead to disease 2 of 2

-hyraluronidase hydrolyzes hyaluronic acid in deeper tissues

-strep pyrogenic exotoxins (SPE) are super antigens that can cause STSS (toxic shock)

Click Card to flip

GBS clinical manifestations (S.agalactiae)

neonatal sepsis

meningitis (leading cause of both in the US)

acquired when fetus passes thru birth canal

Click Card to flip

Neonatal sepsis/meningitis from GBS

GBS has virulence mechanisms in common with GAS but takes advantage of the lack of immune system of neonates

iagA gene allows bacteria to invade the blood-brain barrier-> meningitis

Click Card to flip

Adults GBS infections

rare in the healthy

elderly have a higher risk for strep meningitis due to weaker IS

GBS UTI in pregnant women

Click Card to flip

Enterococci characteristics

gram positive cocci

pairs or short chains

typically alpha-hemolytic

able to live in GI and GU can survive harsh conditions

Click Card to flip

2 species of entero pathogens

E.faecalis and E.faecium

Click Card to flip

Pathogenesis of entero

opportunistic

infections can be caused by translocation from GI to another site

common sites: UT, blood, abdomen

Click Card to flip

Meachanisms of entero caused disease

(poorly understood)

-colonize human tissues bc of MSCRAMMs interacting with proteins in host extracellular matrix

-pili allow adhesion to human cells

-pili allow for biofilm formation (contributes to uti and endocarditis)

-antimicrobial resistance (intrinsic resistance) make immunocompromised more at risk

- INCORRECT - CORRECT - SKIPPED

Shuffle Remaining Cards Show Definitions First Take Quiz (NEW)

Hide Keyboard shortcuts

Next card

Previous card

Mark correct

Mark incorrect

Flip card

Start Over

Shuffle

Mode: CARDS LIST ? pages

PRINT EXIT

Strep Gram Stain and Characteristics	Gram Positive Cocci defined based on hemolysis type (alpha, beta, gamma) and lance field group
Hemolysis	some beta hemolytic strep produce streptolysin, a type of hemolysin that makes a transmembrane channel in erythrocytes aka RBCs->osmolarity disrupted->cell lysis Strep can be alpha, beta, or gamma hemolytic respectively slight clearing (leaving greenish color on blood agar), complete lysis, and no lysis beta hemolytic strep are grouped by lance field grouping
Major Pathogens of Strep (Beta Hemolytic)	S.pyogenes S.agalactiae
Viridans Strep	alpha hemolytic some gamma divided into 4 subgroups normal microbiota and some pathogens

Generated by

Koofers.com

Viridans Strep Subgroups	1. Anginosus Group aka Milleri group 2. Mitis Group 3. salivarius group 4. mutans group
Pathogenic viridans strep organisms	1. Anginosus group aka milleri group S.anginosus S.constellatus S.intermedius 2. S.pneumo
Lancefield Grouping	way to classify streptococcal organisms M-protein on cell surface is a virulence factor, each organism has a different serotype and thus latex agglutination with a specific Ab to that protein can be used to classify the organism into: group a group b group c/g group acfg
Lancefield Group A=	S.pyogenes aka GAS

Generated by

Koofers.com

Lancefield Group B=	S.agalactiae aka Group B strep Streptococcus agalactiae is a beta-hemolytic Gram-positive streptococcus.
Lancefield Group C&G=	S.dysgalactiae, S.equi, S.canis
Lancefield Groups A,C,G,F=	milleri group streptococci (intermedius, constellatus, anginosus)
Strep living in Throat	beta-hemolytic strep

Generated by

Koofers.com

Strep living on Skin	viridans strep
Strep living in GI	Beta-hemolytic strep (S.agalactiae) viridans strep
Strep living in GU	S.agalactiae
Strep living in oral cavity	S.pneumoniae

Generated by

Koofers.com

S.pyogenes infections	aka Group A Strep pharyngitis from colonizing epithelia or oropharynx and skin necrotizing fasciitis and bacteremia and STSS (streptococcal shock syndrome) from penetrating epithelium and becoming invasive 19% patients with invasive gas die in 7 days STSS increases mortality rate
Pharyngitis (Strep Throat)	incubation period: 2-4 DAYS sudden sore throat, cervical lymphadenopathy, malaise, fever, headache treated bc of risk of sequelae-> rheumatic fever and acute glomerulonephritis strep group C/G can cause pharyngitis but not linked to sequelae
Rheumatic Fever	Rheumatic fever is an inflammatorydisease that occurs following aStreptococcus pyogenes infection, such asstreptococcal pharyngitis or scarlet fever. Believed to be caused by antibody cross-reactivity that can involve the heart,joints, skin, and brain,[1] the illness typically develops two to three weeks after a streptococcal infection.
Acute Glomerulonephritis	a disorder of the glomeruli(glomerulonephritis), or small blood vessels in the kidneys. It is a common complication of infections, typically streptococcal skin infection (impetigo) rather thanstreptococcal pharyngitis, for which it is also known as postinfectious or poststreptococcal glomerulonephritis.

Generated by

Koofers.com

Flesh Eating Disease	Necrotizing fasciitis, commonly known as flesh-eating disease or Flesh-eating bacteria syndrome, is a rare infection of the deeper layers of skin and subcutaneous tissues, easily spreading across the fascial plane within the subcutaneous tissue. patients present with: erythemia progressing to formation of bullae (blisters) and tissue destructions w/in HOURS
Components of GAS that lead to disease 1 of 2	-liptotechoic acid and pili adhere to epithelia -matrix binding proteins like fibronectin binding proteins allow epithelial cells invasion -M protein mediates adhesion to epithelial cells AND resistance to phagocytosis (essential for GAS virulence) -evasion by hyaluronic acid polysac in capsule (looks like host) -evasion by SIC=strep inhibitor of complement (no complex) -streptolysin O forms pore in host cells: neutros, macs, epi cells -streptokinase: plasminogen-> plasmin degrades blood clots to allow for dissemination
Components of GAS that lead to disease 2 of 2	-hyraluronidase hydrolyzes hyaluronic acid in deeper tissues -strep pyrogenic exotoxins (SPE) are super antigens that can cause STSS (toxic shock)
GBS clinical manifestations (S.agalactiae)	neonatal sepsis meningitis (leading cause of both in the US) acquired when fetus passes thru birth canal

Generated by

Koofers.com

Neonatal sepsis/meningitis from GBS	GBS has virulence mechanisms in common with GAS but takes advantage of the lack of immune system of neonates iagA gene allows bacteria to invade the blood-brain barrier-> meningitis
Adults GBS infections	rare in the healthy elderly have a higher risk for strep meningitis due to weaker IS GBS UTI in pregnant women
Enterococci characteristics	gram positive cocci pairs or short chains typically alpha-hemolytic able to live in GI and GU can survive harsh conditions
2 species of entero pathogens	E.faecalis and E.faecium

Generated by

Koofers.com

Pathogenesis of entero	opportunistic infections can be caused by translocation from GI to another site common sites: UT, blood, abdomen
Meachanisms of entero caused disease	(poorly understood) -colonize human tissues bc of MSCRAMMs interacting with proteins in host extracellular matrix -pili allow adhesion to human cells -pili allow for biofilm formation (contributes to uti and endocarditis) -antimicrobial resistance (intrinsic resistance) make immunocompromised more at risk

Generated by

Koofers.com

List View: Terms & Definitions

Hide All 30 Print

	Front	Back
	Strep Gram Stain and Characteristics	Gram Positive Cocci defined based on hemolysis type (alpha, beta, gamma) and lance field group
	Hemolysis	some beta hemolytic strep produce streptolysin, a type of hemolysin that makes a transmembrane channel in erythrocytes aka RBCs->osmolarity disrupted->cell lysis Strep can be alpha, beta, or gamma hemolytic respectively slight clearing (leaving greenish color on blood agar), complete lysis, and no lysis beta hemolytic strep are grouped by lance field grouping
	Major Pathogens of Strep (Beta Hemolytic)	S.pyogenes S.agalactiae
	Viridans Strep	alpha hemolytic some gamma divided into 4 subgroups normal microbiota and some pathogens
	Viridans Strep Subgroups	1. Anginosus Group aka Milleri group 2. Mitis Group 3. salivarius group 4. mutans group
	Pathogenic viridans strep organisms	1. Anginosus group aka milleri group S.anginosus S.constellatus S.intermedius 2. S.pneumo
	Lancefield Grouping	way to classify streptococcal organisms M-protein on cell surface is a virulence factor, each organism has a different serotype and thus latex agglutination with a specific Ab to that protein can be used to classify the organism into: group a group b group c/g group acfg
	Lancefield Group A=	S.pyogenes aka GAS
	Lancefield Group B=	S.agalactiae aka Group B strep Streptococcus agalactiae is a beta-hemolytic Gram-positive streptococcus.
	Lancefield Group C&G=	S.dysgalactiae, S.equi, S.canis
	Lancefield Groups A,C,G,F=	milleri group streptococci (intermedius, constellatus, anginosus)
	Strep living in Throat	beta-hemolytic strep
	Strep living on Skin	viridans strep
	Strep living in GI	Beta-hemolytic strep (S.agalactiae) viridans strep
	Strep living in GU	S.agalactiae
	Strep living in oral cavity	S.pneumoniae
	S.pyogenes infections	aka Group A Strep pharyngitis from colonizing epithelia or oropharynx and skin necrotizing fasciitis and bacteremia and STSS (streptococcal shock syndrome) from penetrating epithelium and becoming invasive 19% patients with invasive gas die in 7 days STSS increases mortality rate
	Pharyngitis (Strep Throat)	incubation period: 2-4 DAYS sudden sore throat, cervical lymphadenopathy, malaise, fever, headache treated bc of risk of sequelae-> rheumatic fever and acute glomerulonephritis strep group C/G can cause pharyngitis but not linked to sequelae
	Rheumatic Fever	Rheumatic fever is an inflammatorydisease that occurs following aStreptococcus pyogenes infection, such asstreptococcal pharyngitis or scarlet fever. Believed to be caused by antibody cross-reactivity that can involve the heart,joints, skin, and brain,[1] the illness typically develops two to three weeks after a streptococcal infection.
	Acute Glomerulonephritis	a disorder of the glomeruli(glomerulonephritis), or small blood vessels in the kidneys. It is a common complication of infections, typically streptococcal skin infection (impetigo) rather thanstreptococcal pharyngitis, for which it is also known as postinfectious or poststreptococcal glomerulonephritis.
	Flesh Eating Disease	Necrotizing fasciitis, commonly known as flesh-eating disease or Flesh-eating bacteria syndrome, is a rare infection of the deeper layers of skin and subcutaneous tissues, easily spreading across the fascial plane within the subcutaneous tissue. patients present with: erythemia progressing to formation of bullae (blisters) and tissue destructions w/in HOURS
	Components of GAS that lead to disease 1 of 2	-liptotechoic acid and pili adhere to epithelia -matrix binding proteins like fibronectin binding proteins allow epithelial cells invasion -M protein mediates adhesion to epithelial cells AND resistance to phagocytosis (essential for GAS virulence) -evasion by hyaluronic acid polysac in capsule (looks like host) -evasion by SIC=strep inhibitor of complement (no complex) -streptolysin O forms pore in host cells: neutros, macs, epi cells -streptokinase: plasminogen-> plasmin degrades blood clots to allow for dissemination
	Components of GAS that lead to disease 2 of 2	-hyraluronidase hydrolyzes hyaluronic acid in deeper tissues -strep pyrogenic exotoxins (SPE) are super antigens that can cause STSS (toxic shock)
	GBS clinical manifestations (S.agalactiae)	neonatal sepsis meningitis (leading cause of both in the US) acquired when fetus passes thru birth canal
	Neonatal sepsis/meningitis from GBS	GBS has virulence mechanisms in common with GAS but takes advantage of the lack of immune system of neonates iagA gene allows bacteria to invade the blood-brain barrier-> meningitis
	Adults GBS infections	rare in the healthy elderly have a higher risk for strep meningitis due to weaker IS GBS UTI in pregnant women
	Enterococci characteristics	gram positive cocci pairs or short chains typically alpha-hemolytic able to live in GI and GU can survive harsh conditions
	2 species of entero pathogens	E.faecalis and E.faecium
	Pathogenesis of entero	opportunistic infections can be caused by translocation from GI to another site common sites: UT, blood, abdomen
	Meachanisms of entero caused disease	(poorly understood) -colonize human tissues bc of MSCRAMMs interacting with proteins in host extracellular matrix -pili allow adhesion to human cells -pili allow for biofilm formation (contributes to uti and endocarditis) -antimicrobial resistance (intrinsic resistance) make immunocompromised more at risk

The information provided on this site is protected by U.S. and International copyright law, and other applicable intellectual property laws, including laws covering data access and data compilations. This information is provided exclusively for the personal and academic use of students, instructors and other university personnel. Use of this information for any commercial purpose, or by any commercial entity, is expressly prohibited. This information may not, under any circumstances, be copied, modified, reused, or incorporated into any derivative works or compilations, without the prior written approval of Koofers, Inc.