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micro immuno 2 > streptococci, enterococcus, pneumococcus and staphylococcus (2/8/18) > Flashcards

streptococci, enterococcus, pneumococcus and staphylococcus (2/8/18) Flashcards

1
Q

what kind of pathogen are streptococci, enterococcus, pneumococcus, and staphylococcus (+/-)

A

all gram possitive

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2
Q

who first described streptococci

A

leuis pastuer in 1879

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3
Q

what is the first microbes identified in cause contagious disease (germ theory)

A

puerperal fever in maternity ward

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4
Q

discovery of streptococci and subsequently germ theory was essential to what in hospitals

A

hygiene and aseptic practices

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5
Q

number of species of streptococcus

A

100+

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6
Q

how were streptococci originally classified

A

lancefield groups

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7
Q

serological classification based on major cell-wall carbohydrate antigens (A-H) (works well for pyogenic strep)

A

lancefield groups

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8
Q

can all strep be classified using lancefield groups

A

no, many strep are un-typeable

no antisera reacts to their cell wall antigens

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9
Q

what lancefield groups of streptococci are pyogenic strep

A

Group a: streptococcus pyogenes

Group b: streptococcus agalactiae

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10
Q

morphology of streptococci

A

gram positive cocci arranged in chains

small and more ovoid than staphylococci

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11
Q

do streptococci react with catalase

A

negative

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12
Q

do streptococci form spores

A

no

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13
Q

are streptococci motile

A

no flagella

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14
Q

do streptococci have a capsule

A

variable (carb or hyaluronic acid

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15
Q

can streptococcus be classified on hemolysis on blood agar

A

yes

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16
Q

alpha hemolysis pattern

A

partial hemolysis and green discoloration of hemoglobin

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17
Q

beta hemolysis pattern

A

clear zone of complete hemolysis (can kill blood cells)

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18
Q

gama hemolysis

A

no zone of clearing

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19
Q

what streptococcus does alpha hemolysis patterns

A

viridans strep mostly in oral cavity

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20
Q

whatstreptococcus does beta hemolysis

A

GBS and GAS

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21
Q

what do biochemical reactions what classifying strep look at

A

particular enzymes

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22
Q

what do DNA sequences look at for classifying strep

A

16s rRNA (doesn’t work well for mitus strep)

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23
Q

types of Group A strep (GAS)

A

primarily infect respiratory tract , blood stream, and skin

  1. suppurative pus diseases: direct damage by organism
  2. toxin mediated disease- systemic response cuased by strep exotoxins secreted in bloodstream
  3. non-suppurative sequelea- late manifestations-autoimmune-aberrant immunological reaction to GAS antigens
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24
Q

who does GAS infect

A

exclusively humans

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25
Q

how does GAS spread

A

respiratory droplets and direct person to person contact

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26
Q

What are the virulence factors of GAS (S pyogenes)

A 
M protein
Protein F
Hyaluronic Acid (HA capsule)
Hyaluronidase
C5a peptidase
streptolysis S and O
Strptokinase
Pyrogenic exotoxins
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27
Q

roll of M protein in GAS( S pyogenes)

A

adhesin binds to keratinocytes (outer layer of skin)

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28
Q

roll of protein F in GAS( S pyogenes)

A

Fibronectin binding protein

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29
Q

roll of hyaluronic acid (HA) capsule in GAS( S pyogenes)

A

anti-phagocytic

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30
Q

roll of hyaluronidase in GAS( S pyogenes)

A

spreading factor that allows S pyogenes to spread through tissues

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31
Q

roll o C5a peptidase in GAS( S pyogenes)

A

degrades complement protein c5a-blocking phagocyte chemotaxis

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32
Q

roll of streptolysin S and O in GAS( S pyogenes)

A

hemolysins the lyse various host cells

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33
Q

roll of streptokinase in GAS( S pyogenes)

A

binds human plasminogen converting it to plasmin-breaks fibrin clots allowing tissue spread

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34
Q

roll of pyrogenic exotoxins in GAS( S pyogenes)

A

superantigens causing fever neutropenia, rash of scarlet fever

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35
Q

how does GAS adhere to mucosal surface via fibronectin

A

pili, M protein, LTA and protein F

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36
Q

how does GAS adhere to sub corneal keratinocytes in the epidermis

A

M protein and protein F

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37
Q

can GAS infecet non-phagocyctic cells

A

yes, but not completely understood

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38
Q

what does GAS do once past host barriers

A

GAS secretes virulence factors that allow host immune evasion and deeper infections to occur

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39
Q

what does M protein look like

A

myosin

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40
Q

function of M protein

A

bind to keratinocytes

prevents opsonization by complemnt

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41
Q

antibody against M protein opsonize where

A

against the hypervariable region

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42
Q

opsonization against M protein hypervariable region is difficult becuase

A

200 distinct M protein serotypes responsbile for subtypes of GAS and inmunity to one serotype does not confer protection to others

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43
Q

regions of M protein of GAS

A

Type specific Ab (hypervariable region)
fibrogen binding region (semi-conserved)
serum factor H (conserved) and inserts into cell wall

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44
Q

what does M protein type determine

A

what disease GAS can cause (different serotypes cause different diseases) with some overlap though

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45
Q

binding of fibrinogen to M protein prevents binding of:

A

C3b

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46
Q

M proteins bind was complement control protein to inhibit alternative compliment pathways

A

Factor H

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47
Q

C5a peptidase degrades what

A

C5a- the peptide mediator of inflammation (degredation leads to prevention of chemotaxis)

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48
Q

purpose of the Hyaluronic acid capsule (HA)

A

antiphagocytic structure by camouflaging against the immune system, pretending to by Non-antigenic (HA is found in connective tissue

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49
Q

problem with Hyaluronic Acid (HA) capsule for pathogens

A

interferes with adherence to epithelial cells

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50
Q

how does S. pyogenes spread through tissue despite having a hyaluronic acid capsule

A

secretes hyaluronidase to digest the capsule

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51
Q

a pore forming toxin the can lyse Red bood cells and kill phagocytes and lse various host cell

A

streptolysin s and o

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52
Q

a toxin the lyses red bllod

A

hemolysin ( Beta-hemolysis on blood agar)

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53
Q

toxin that kills phagocytes

A

leukocidin

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54
Q

why release a toxin to kill host cells

A

release nutrients for growth

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55
Q

stability of streptolysin S and streptolysin O in oxygen

A

S-stable in O2

O- labile in O2

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56
Q

what binds to plasminogen to perform enzymatic conversion to plasmin

A

streptokinase (invasin)

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57
Q

what can plasmin coated GAS do:

A

degrade and spread through fibrin (blood clots) resulting in invasive disease

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58
Q

what do some strains secrete into the blod stream

A

pyrogenic exotoxins (speA, SpeB, and SpeC)

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59
Q

pyrogenic exotoxins cause

A

rash associated with scarlet fever (toxin spread through blood)

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60
Q

the most abundant extracellular protein by GAS

A

SpeB

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61
Q

what is SpeB

A

cysteine protease-degrade immunoglobulins and cytokines preventing complement activation (degrades C3b)

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62
Q

other name for speA and speC

A

superantigens

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63
Q

speA and SpeC non-specificall activate large subsets of what that leads to

A

T-cells cuasing streptococcal toxic-shock syndrome (STSS) (strepSAgs)

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64
Q

most common manifestations of GAS

A 
Acute pharyngitis (strept throat)
pyoderma - GAS infection of skin (impetigo)
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65
Q

who has acute pharyngitis

A

school age children with 20% are asymptomatic carries

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66
Q

who are the most contageous with GAS

A

nasal carriers

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67
Q

who has Pyoderma

A

preschool children

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68
Q

mortaility from S pyogenes (GAS)

A

500,000 death/year worldwind (influenced by strain, host and portal of entry)

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69
Q

symtoms of scarlet fever

A

high fever (101 degrees F)
deep red cheecks (white around mouth and nose-circumoral pallor)
red tongue with yellow-white exudate that peals after a few days (straberry tongue)
sand paper rash develops after several days

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70
Q

how to treat S pyogenes (GAS upper repiratory tract infections

A

10 days of penicillin

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71
Q

strep throat is characterized by

A

swollen white pus on the tonsils

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72
Q

skin infections cuased by GAS

A

impetigo-infection of the epidermise
erysipelas
Cellulitis- acute inflamatory process involving subcutaneous tissue

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73
Q

symptomes of impetigo

A

transient skin colonization+ trama (insect bite)
intraepidermal vesicles filled with exudate- eventually crust over
not systemic, but nephrogenic GAS can lead to post streptococccal glomerulonephritis

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74
Q

sysmpotms of erysipelas

A

superficial erythematous and edematous lesions
spreads in superficial ymp of the dermis
rash is confluent, salmon red, with sharp demarcations

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75
Q

symptos of cellulitis

A

red, heat, tender
indistinct boarders
rapid progression to septicemia

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76
Q

autoimmune diseases (non-suppurative infections) due to S. pyogenes (GAS)

A

acute Rheumatic Fever (ARF)

Acute Post streptococcal Glomerulonephritis (APSGN)

77
Q

what does ACute Rheumatic fever follow

A

pharyngeal infections by rheumatogenic strains

78
Q

what does Acute post streptococcal Glomerulonephritis follw

A

pharyngeal or skin infections by nephritogenic strains

79
Q

Hypersensitivity reaction cuased by cross-reacting antibodoies ( M proteins) to effect the heart, joint, skin and brain.

A

Acute Rheumatic Fever (ARF)

80
Q

when does ARF appear

A

1-4 weeks after strep throat (even asymptomatic infection) but only 10% of people are susceptible

81
Q

who sees ARF

A

not-developed counties

82
Q

Since ARF has a high susceptibility for recurrence, what is done

A

prophylactic antibiotics into adulthood or life is required (3-4 week IM dose)

83
Q

how to prevent ARF

A

treating strep throat with a full course of Penicillin

84
Q

symptoms of ARF

A 
Fever
Painful joints (arthritis)
Chorea- (fidgety or abrnormal movement)
heart murmur
non-itchy erytheme marginatum rash
85
Q

who gets acute post streptococcal glomerulonephritis

A

2-12 years old after strep throat or impetigo 5-21 says before

86
Q

incidence of Acute Post streptococcal Glomerulonephritis

A

rare(6-20: 100,000 in the west)

87
Q

what strain of GAS causes acute post streptococcal glomerulonephritis

A

only nephritogenic GAS strains (type M12 and 49)

88
Q

what cuases acute post streptococcal glomerulonephritis

A

immune complexes (antibody-antigen) containing steptococcal antigens are deposited in affected glomeruli causing type III hypersensitivty

89
Q

symptoms of Acute Post Streptococcal Glomerulonephritis

A

Edema
Gross Hematuria )tea colored urine)
Hypertension)

90
Q

how to treat acute post streptococcal glomerulonephritis

A

sodium restirction
diuretics
(95% recovery)

91
Q

what severe invasive infections can S pyogenes (GAS) cause

A

subdermis (cellulitis)
Connective FAscia (necrotizing fasciitis, i.e. flesh-eating disease)
muscle(myositis)
Blood (septicemia, streptococcal toxic shock syndrome)

92
Q

streptococcal toxic shock syndrome can occur with what

A

necrotizing fasciitis- nausea, vomiting, diarrhea, hypotension, shock, organ failure…

93
Q

what is effective against GAS

A

penicillin G

Beta-lactams and macrolides also work

94
Q

becuase antibodies are protective against future infections with the same M type, they are considered

A

type specific immunity

95
Q

Vaccine agianst GAS

A

none yet but specific M-protein vaccines that do not cross react with host protein are being tested with good results

96
Q

what group of strep is streptococus pneumoniae

A

mitis

97
Q

morphology of streptococcus pneumoniae

A

gram-possitive oval cocci found in pairs (diplococcus)

98
Q

hemolysis of streptococcus pneumoniae

A

alpha-hemolytics (partial hemolyisis, green colonies on blood agar)

99
Q

capsule on streptococcus pneumoniae>

A

yes, required for virulence with antigenic carbs

100
Q

lysis of streptococcus pneumoniae

A

autolytics

101
Q

where does pneumococcal colonize

A

nasopharynx in 5-40% of healthy perons, highest in children in winter months

102
Q

how does pneumoccal spread

A

person to person via direct contact, microaerosoles

103
Q

what pneumococcal serotypes produce disease

A

20 of the 90 serotypes produce more disease due to enhanced virulence factors

104
Q

Virulence factors for Pneumococci

A

Capsule (necessary)
Choline-binding Proteins_asherence to host tissues
Pneumolysin- transmembrane pore-forming toxin
Neuraminidase- cleaves sialic acid present in host mucin, glycolipids, and glycoproteins- exposing binding sites

105
Q

how is pneumolysin released

A

pneumococci must lyse itself to release the pneumolysin

106
Q

pathogensis for pneumococcal pneumonia

A

aspiration of respiratory secretion containing pneumococci
adherence to host epithelial cells in aveoli of lungs
neuraminidase aids in addition recetpors being exposed
capsule acts to block phagocytosis disrupting complement-C3b
Bacterial cells lyse causing release of pneumolysin injurying host cells

107
Q

what normally clears pneumococcal pneumonia when breathed into the lungs

A

the mucocilliary blanket

108
Q

what helps with binding of pneumococcal pneumonia to epithelial cells of aveoli

A

cell-wall choline binding proteins and carbs on host cells

109
Q

what causes the lungs to fill with fluid in pneumococcal pneumonia

A

the neutrophils come in in response to injury of host cells due to pneumolysin

110
Q

what makes up the capsle ofpneumococci

A

high molecular weight polysaccharide polymers with 90 different serotypes with unique antigens

111
Q

how does the capsule work in pneumococci

A

interferes with deposition of complement protein C3b on bacterial cell surface

112
Q

if antibodies recognize the capsule of pneumococci, what happens

A

opsonophagocytosis

113
Q

what is pneumolysin related to

A

staph alpha-toxin and streptolysin O produced by GAS

114
Q

action of pneumolysin

A

cytokines relase
pore formation
discupts cilia of human respiratory epithelial cells

115
Q

pneumococcal disease is the leading cuase of

A 
pneumonia (500k cases)
otitis media (ear infections- millions of cases)
acute purulent meningitis (3000 cases)
bacteremia
other infections
116
Q

who dies from pneumococcal disease

A

5 million deaths in children per year

117
Q

symtoms of pneumococcal pneumonia

A

shaking chill and high fever initally
Productive cough with pink and rusty color(blood)
Sharp chest pain when inhaling and exhaling
Pulmonary consolidation (fluid filled lungs)

118
Q

when do symptoms of pneumococcal pneumonia clear

A

5-10 days due to adaptive immunity-opsonizing antibody arrival

119
Q

after the sysmptoms of pneumococcal pneumonia clear what may happen

A

bacteremia is common and may be followed by pneumococcal meningitis

120
Q

who is at risk for pneumonia

A

people over the age of 50

121
Q

how to treat pneumococcal pneumonia

A

penicillin works on susceptible strains
cephalosporins also used
fluoroquinolones

122
Q

vaccines for pneumococcal pneumonia respond because

A

capsular polysaccharides

123
Q

types of vaccines for pneumococcal pneumonia

A

PPV23-pneumococcal polysaccharide vaccine-
purified polysaccharide from 23 serotypes of invasive S pneumoniae
PPV13- pneumococcal conjugate vaccine- from 13 strains conjugated with protein for type 2 response

124
Q

who is recommended for the PCV13 vaccine

A

children 2 months to 2 years of age

125
Q

the leading cause of neonatal sepsis and miningitis in newborns

A

Group B streptococci (GBS) - S. agalactiae (aeobic)

126
Q

where is GBS/S. Agalactiae found

A

inhabit lower GI and female genital tracts

127
Q

how babies get GBS/S. agalactiae

A

during burth because 15-40% of women are carriers

128
Q

how to prevent babies from getting GBS/S. agalactiae

A

screen female at 35-37 week of gestation and if possitive, mother takes intrapartum antibiotics

129
Q

GBS/ S. agalactiae causes what in adults with chronic diseases

A

Cellulitits, arthritis, and meningitis

130
Q

roll of polysaccharide sialic acid capsule of GBS

A

prevent opsonization and phagocytosis

131
Q

how may one become immune to GBS

A

because the polysaccharide sialic acid capsule has type-specific antibodies, infection leads to immunity along the complement pathway

132
Q

serotypes of GBS polysaccharide sialic acid capsule

A

9 serotypes, with type III most common in neonatal sepsis in USA

133
Q

what are Group C and G streptococci

A

commensal bacteria that live in the airway, skin, and Digestive tract and female genitals

134
Q

what does s. dysgalactiae cause

A

bovine mastitis

135
Q

what does s. equi cause

A

strangles in horses

136
Q

what do C and G streptococi have that make them similar to other streptococci

A

M proteins that bind fibrinogen and secreate similar extracellular enzyme

137
Q

does C or G streptococci have a hyalueonic acid capsule

A

Group C

138
Q

what infections can group c and G streptococci cause

A

Similar to GAS- tonsillitis, respiratory and deep tissue

139
Q

gRoup C and G streptocci are implicated in what

A

AGN no ARF

140
Q

hemolytic type of group D

A

alpha or gamm

141
Q

are group D streptococi enterococci or non-enterococci

A

both!

142
Q

where are group D streptococci found

A

in the normal flora of GI and genitourinary tracts

143
Q

why are enterococci coined as the worlds toughest pathogenic bacteria

A

grow in high salt and detergents (bile)
Inhibited but not killed by penicillin (Altered PBP’s)
resist most antibiotics

144
Q

what does Enterococci cause

A

nosocomial opportunistic infections

145
Q

how to kill enterococci

A

antibiotic synergism(penicillin-weakens cell wall and aminoglycoside-reaches inside

146
Q

why are Vacomycin resistant enterococci emerging

A

subtle changes in peptidoglycan precurses, so beta-lactams bind much less

147
Q

the last resort antibiotic for enterococci

A

linezolid

148
Q

who does Enterococci give its Vancomycin resitance to in a lab

A

staphylococci

149
Q

main virulence factor of enterococci are from

A

resisting environmental and antimicrobial agent stress

150
Q

hemolytic description of viridans (greening streptococci)

A

alpha

151
Q

where is Viridans(greening streptococci found

A

30-60% of oropharyngeal flora

152
Q

what does Viridans greening strptococci causea s a pathogen

A

if introduced into the blood stream by dental procedues, can cause subacute bacterial endocarditis, affecting abnormal heart valves

153
Q

what is used to treat Viridans (greening) streptococci in high risk patients

A

prophylaxis antibiotics

154
Q

what is subacute bacterial endocarditis

A

bacterial infection on endocardium when abnormal values or heart disease is present

155
Q

symptoms of subacute bacterial endocarditis

A 
fever
chills
muscle aches
abdominal pain
heart murmur
156
Q

morphology of staphylococcus

A

large and more round than strptococci and bunch together

157
Q

hemolytic properties of staphylococcus

A

beta-hemolytic

158
Q

motility of staphylococcus

A

non-motile

159
Q

spore of staphylococcus

A

non-spore forming

160
Q

catalase reaction with staphylococcus

A

positive

161
Q

coagulase of staphylococcus

A

positive(variable)

162
Q

where staphylococcus can be found

A

in the normal flora

163
Q

cell wall of staphylococcus aureus

A

contains peptiodglycan with lots of Teichoic acid (TA)
also polysaccharide capsule
and surface proteins

164
Q

surface proteins of staphylococcus aureus

A

Clumping factors (bind fibrinogen)
FnBP (bind fibronectin)
Surface protein A (bind the Fc portion of IgG molecules- stimulates cytokines (TNF-alpha), platelets and activates B cells

165
Q

virulence factros of S. aureus

A 
cytolyitc toxins (alpha, beta gamma, delta) that cause cell lysis
PVL
exfoliatin toxin
Staphylococcal superantigens
toxic shock syndrom toxin
166
Q

what toxin is secreted by all S. aureus except coagulase negative strains to create pore

A

alpha toxins

167
Q

what is active against platelelts and neutrophils to cuase tissue necrosis

A

Panton-Valentine leukocidin (PVL)

168
Q

protease that cleaves specific cell membrane fatty acids forn in keratinized epidermis of skin to disrupt intraepidermal junction

A

exoliatin toxin

169
Q

what does exfoliatin toxin cause

A

staphlococcal scald skin syndrome (SSSS)- fluid filled blisters

170
Q

secreted proteins that stimulate systemeic effects when absorbed in the gut or when produced in vivo by multiplying bacteria

A

SAgs(staphylococcal superantigen)

171
Q

Enterotoxins cause

A

vomiting and diarrhea

172
Q

resistance of enterotoxins

A

V. stable to boiling and digestive enxymes

cause toxic shock syndrome (TSS)

173
Q

toxic shock syndrom toxin leads to

A

massive cytokine release, binding to class II MHC to activate T cell non-specifically

174
Q

primary infection by staphlococcal diseases lead to

A

Furuncle (boil)
impetigo
deep tissue lesions
pneumonia

175
Q

where do furuncles begin

A

in hiar follicle, sebaceous gland, or sweat glands

176
Q

multiple boils under the surface

A

carbuncle

177
Q

what is impetigo secondary to

A

GAS infection

but can also act as a primary infection

178
Q

deep tissue lesions of staphylococcal diseases

A

in bones, joints, and soft tissues

179
Q

toxin mediate disease can result from

A

primary infections via staphlococcus with strains that produce toxins

180
Q

what are toxin mediated disease

A

Scaldd skin syndrome
toxic shock syndrome
staphylococcal food poinsing

181
Q

how does one get infected by staphylococcus aureus

A

normal transmission via nasal carriers (10-30% of population has it in their nose)
hospital spread- hands of medical personnel

182
Q

what can staphylococcus aureus

A

survives drying-spread from contaminated clothing

183
Q

pathogensis of staphylococcus

A

inital atachement via nBP
alpha-toxin injures keratinocytes to allow in
immune evasion
inflammator cells create the boil
and spontaneously resolves via drainage of puss

184
Q

how does stphylococcus evade the immune system

A

antiphagocytic properites of protein a
pVL limited innate defence
Coagulase and CIF-limit host phagocytes

185
Q

what causes toxic shock syndrom

A

toxin from a local infection enters blood stream

186
Q

what is the most common superantigen adsorbed across the mucosal membranes

A

TSST-1

187
Q

what does TSST-1 bind to

A

T-cell receptors andclass II MHC receptors- stimulating massive cytokine release (IL-1 and TNF)

188
Q

what other way can Toxic shock syndrom occure

A

non-mentrual TSS without TSST-1

micro immuno 2 (8 decks)

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