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3.12 Flashcards

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1
Q

Streptococcus
pyogenes

”—“-forming

A

pus

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2
Q

Some streptococci are typically seen

as

A

diplo-cocci:

Streptococcus pneumoniae

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3
Q

b-hemolysis (top) on blood-agar plates causes

A

clearing at and around colonies in

Streptococcus pyogenes

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4
Q

a-hemolysis (bottom) shows greening due to partial lysis of erythrocytes in (2)

A

S.mitis and

S.pneumoniae.

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5
Q 
pneumolysin degrades
hemoglobin  green
Green color sheen has
given the name
--- to many αhemolytic Streptococci
like the caries-causing:
S.mutans, S.mitis,
S.salivarius, S.sanguis
A

viridens

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6
Q

Rapid strep throat test (2)

A

is based on Group A
serological response.
Useful for rapid distinction from viral strep throat
in school children (but culture must be done)

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7
Q

Sequencing of the emm gene for the required virulence factor protein —has
become more important than Lancefield antigens to identify strains.

A

M

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8
Q

M protein - (3)

A

cell wall component, >100 serotypes, membraneanchored: is an important virulence factor

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9
Q

anti-M antibodies prevent infection of S.pyogenes but many serotypes.
So protective immunity is

A

type-specific

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10
Q

• M protein binds —, the main cell type in outer skin layer

A

keratinocytes

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11
Q

M protein binds —, blocking surface from complement system

components

A

fibrinogen

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12
Q

M protein binds complement control proteins

• Inhibits formation of —by complement cascade

A

opsonins

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13
Q

Ø capsule:

A

antibodies are ineffective against glycocalyx-covered surface antigens

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14
Q

Group A strains have capsules of (1), mimicking

mammalian connective tissues, preventing phagocy

A

hyaluronic acid

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15
Q

Ø F protein

A

(cell wall adhesin) provides adherence to the fibronectin of throat epithelial cells

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16
Q

Ø lipoteichoic acid

A

(species-specific form) also adheres to the fibronectin epithelial cell coat

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17
Q

Ø M protein also shows adhesion for — and strong adhesion to —

A

fibronectin

keratinocytes (skin)

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18
Q

Adhesion-based uptake of cocci into epithelial cells is likely a basis for the repeated
nature of

A

strep throat and deep tissue infections.

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19
Q
  1. M protein anti-complement action through
A

Factor H

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20
Q
  1. Capsular C3 peptidase destroys opsonizing — complement opsonization
A

C3b

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21
Q

Thus: CR1 does not work! Phagocytosis only by

A

IgG opsonization (FcR)

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22
Q

Ø G protein (cell surface) binds Fc of IgG, preventing

A

phagocytosis based on FcReceptors

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23
Q

Ø — peptidase in Group A Streptococci

A

C5a

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24
Q

c3b peptidase cleaves the complement component into — fragments

A

inactive

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25
Q

inactivate complement chemotaxin c5a; activate surface of — to — and cleave of c3b

A

plasminogen

plasmin

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26
Q 
membrane damagin toxins (cytotoxins)
fxn
toxin: streptococcus pyrogenes 
name of disease; name of toxin
characteristic of the disease
mechanism
A

disrupts the plasma membrane
pharyngitis and other infections; streptolysin O
accumulation of pus
inserts into membranes, forming pores that allow fluids to enter

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27
Q

streptolysins S, O:

A

lysis of erythrocytes (direct lysis; basis of β-hemolysis) and
of phagocyte lysosomal membranes (indirect lysis of leukocytes)

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28
Q

secretion of tissue degrading enzymes (4)

A

DNase, protease,
hyaluronidase (spreading factor),
streptokinase (degrades blood clots)

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29
Q

streptokinase is clinically useful in early vascular attack treatment because it

A

activates plasminogen

and the resulting plasmin will degrade fibrin clots formed in stroke and heart infarct.

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30
Q 
superantigens:
fxn
toxin: streptococcus pyogenes (certain strains)
name of disease; name of toxin
characteristic of the disease
mechanism
A

overrides the specificity of the t cell response
streptococcal toxic shock; streptococcal pyrogenic exotoxins (SPE)
fever, vomitting, diarrhea, muscle aches, rash, low bp
systemic toxic effects due to the resulting massive release of cytokines

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31
Q

Cytokines:

A

IL2, TNF-β, IFN-γ , and through macrophage activation: TNF-α, IL1, IL6 (inflammation, shock)
Cause of scarlet fever, toxic shock, flesh-eating fasciitis

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32
Q

scarlet fever: toxin

A

Streptococcus pyogenes

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33
Q

scarlet fever

Virulence factor:

A

a superantigen SPE

Streptococcal Pyrogenic Exotoxins

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34
Q

Other results of pyrogenic SPEs (2)

A

Pyoderma (impetigo)
pyo = pus
derma = skin
skin infections of face, arms, legs

Erysipelas
erythros = red
pella = skin
bullae = blisters

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35
Q

Flesh-Eating: toxin

A

Strept.pyogenes

“streptococcal gangrene”

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36
Q

Progression to deep, systemic

infection leads to

A

multi-organ

failure and death.

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37
Q

—- is caused by streptococcus pyogenes

A

necrotizing fasciitis

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38
Q

Acute Pharyngitis = Strep throat (2) symptoms

A 
glomerulonephritis (type 3 hypersensitivity)
rheumatic fever (type 2 hypersensitivity)
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39
Q

acute rheumatic fever symptoms (2)

A

myocarditis

arthritis

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40
Q

Rheumatic Heart Disease by —

A

Streptococci

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41
Q 
Acute Rheumatic Fever:
• non---- sequela with some strains
• <---% of population is susceptible
• fever is non-responsive to --- because disease is autoimmune
•frequency of reoccurrence?
A

suppurative
10
penicillin
high

42
Q 
Streptococcus agalactiae
Group B (4)
A

β-hemolytic (<2% non-hemolytic), chain-like growth, aerobic, polysaccharide capsule

43
Q

Group B,
Normal occurrence in the —
Does not cause disease in healthy people

A

lower gastrointestinal tract

44
Q

Group B,

where is it found? (4)

A

• pneumonia in neonates (neonates: <7 days of birth)
• bacteremia and meningitis (neonates: >7 days of birth)
• various symptoms in elderly suffering from chronic diseases
(often complicated by penicillin allergy)
• urinary infections, bacteremia (pregnant women)

45
Q

— against group B polysaccharide Ag develop quickly and protect.

A

Neutralizing antibodies

maternal Abs prevent infection of neonate

46
Q

Strains different from S.pyogenes or S.agalactiae may cause opportunistic

e. g. in HIV-immune-compromised cases.

A

streptococcal toxic shock syndrome

47
Q

Enterococcus faecalis

virulence

A

Ø high, multiple antibiotic resistances (plasmid and chromosomal)*

48
Q

Enterococcus faecalis

Epidemiology

A

elderly
long hospitalization
(high nosocomial risk
antibiotic resistance)

49
Q

Streptococcus pneumoniae (3)

A

α-hemolytic, Gram+ diplococci

50
Q

Streptococcus pneumoniae

causes per year in USA

A

500,000

51
Q

Streptococcus pneumoniae
Only — strains
(smooth colonies) are
virulent

A

encapsulated

52
Q

pneumococcal pneumonia (2)
epidemiology
prevention/tx

A

high carrier rates for s pneumoniae

capsular vaccine available

53
Q

klebsiella pneumonia (4)
cauative agent
epidemiology (2)
prevention/tx

A

an enterbacterium
often resistant to antibiotics
fatal nosocomial pneumonias
no vaccine available

54
Q

mycoplasmal pneumonia

prevention/tx

A

no vaccine available

55
Q

Streptococcal pneumonia

treatment of choice

A

penicillin

56
Q

S.pneumoniae virulence factors (3)

A

α-hemolysis
capsule
secretory IgA protease

57
Q

meningitis

A

S.pneumoniae

58
Q

Neisseria sp. (5)

A

• Gram− diplococci
• Lipooligosaccharide (vs. LPS): lack O antigen extensions
• common oral flora and other mucous membranes
• facultative anaerobe
• pathogens: N.gonorrhoeae and N.meningitidis
Host: only humans

59
Q

Ø — variation and — variation of pilin genes

A

phase

antigenic

60
Q

Virulence Factors of N. gonorrhoeae

vaccination?

A

not possible

61
Q

Virulence Factors of N. gonorrhoeae

capsule?

A

no

62
Q

Pathogenesis of Gonorrhea

Antigenic variation of bacterial surface proteins (4)

A

ØPilE single chromosomal copy of pilin structural gene
ØStrains contain 10-15 copies of PilE variants lacking promoter and 5-end
of gene called PilS genes
ØPilS genes recombine with PilE creating unlimited antigenic variants of PilE
ØResult is that antigenic structure of pilus protein is constantly changing

63
Q

Phase Variation:

A

on/off switch for surface protein expression

64
Q

In Neisseriae:

A

Slipped Strand Mispairing resulting from presence of multiple
identical repeated sequences at 5-end of gene. Replication errors due to strand
misalignment creates reading frame errors.
Often, premature stops, but also results in ON/OFF switch.

65
Q

Multiple Opa (Colony Opacity) protein copies scattered across genome;

A

Slipped
strand mispairing results in frequent variation in Opa protein expression or
complete absence of Opa

66
Q

Pathogenesis of Gonorrhea (2)

A

Ø Phase Variation: on/off switch
Ø E. coli and other Gm- rods simple inversion
of promoter

67
Q

— mediate bacterial attachment to non-ciliated epithelia

bacteria proliferate and shed into secretions; can also ente

A

Pili

68
Q

Virulence Factors of N. gonorrhoeae

Ø secreted IgA protease:

A 
Usefulness of cleaving IgA:
Coating of bacteria with IgA
Fab fragments (does not
activate complement and
also blocks binding by other
IgG and IgM)
69
Q

Serum-resistant virulent strains cause disseminated gonococcal infections: (2)

A

• Strains lack Opa proteins (colony opacity proteins = outer-membrane proteins)
Neutrophils unable to engulf bacteria lacking Opa proteins.
• Sialic acid on LOS (Lipidoligosaccharide of outer membrane) binds complement
regulatory proteins, prevents complement-based phagocytosis.

70
Q

Ø Shedding of lots of — (LOS of these bacteria)
Binds TLR-4 (especially on dendritic cells, macrophages,
& B cells) secretion of pro-inflammatory — (TNFalpha, IFN-gamma, IL-1,-12, & -18) & nitric oxide shock

A

endotoxin

cytokines

71
Q

Gonorrheal Diseases

transmission

A

§ Sexual transmission - urogenital infections

72
Q

Gonorrheal Diseases
§ Frequently (almost) —
o — in men, urethral pus secretion
(leukocytes with many gonococci)
o — in women, frequently some urination
sensitivity but no other symptoms
(infection tracing is important to prevent re-infection)

A

asymptomatic
urethritis
cervicitis

73
Q 
Gonorrheal Diseases
Opthalmia Neonatorum (2)
A

o destructive eye infection, acquired during birth
o Application of erythromycin ointment into both
eyes of newborns is mandatory in many states
and is considered standard neonatal care

74
Q

Gonorrheal Diseases

Pelvic Inflammatory Disease (PID) in women (3)

A

Initial infection of cervix, fallopian tubes and vaginal wall glands can lead to PID (15-30%):
o gonococci enter abdominal cavity, cause liver disease
o tissue scarring causes fallopian tube abnormalities which lead to ectopic pregnancies
and sterility

75
Q

Gonorrheal Diseases

Urethral and testicular tubule scarring, resulting from epididymitis, leads to (2)

A

sterility

and increased urethral infections by other microbes

76
Q

Disseminated Gonococcal Infection (without apparent genital infection) causes (3)

A

skin

lesions, suppurative arthritis of a major joint, heart valve destruction.

77
Q

Little or no — (pilin variability!) is observed

after recovery from an infection with N.gonorrhoeae.

A

protective immunity

78
Q

factors affecting intravascular survival (2)

A

capsule: protects against complement mediated bacteriolysis and phagocytosis
acquisition of iron from transferrin

79
Q

crossing of the blood brain barrier

A

multiplication in subarachnoid space

80
Q

Neisseria meningitidis

Symptoms

A

start like a mild cold, progress to throbbing headache, fever, stiffness in neck and back, nausea and vomiting, deafness and coma.
Shock and death (100% if untreated) may occur within 24 hours, but frequently
is slower so that effective treatment can be given (<10% death in treated
cases).

81
Q

Neisseria meningitidis

Obstruction of release of increased fluid pressure (due to PMN attempts at eradication: pus and clotting) impairs

A

brain, causes paralysis of motor nerves
and coma. Loss of blood supply to brain is one of the frequent symptoms just
prior to death

82
Q

Neisseria meningitidis
LOS/endotoxin release from blood-circulating meningococci (which have a high tendency to auto-lyse and thus spread LOS widely) causes —.

A

shock

83
Q

Neisseria meningitidis
Contrary to other meningitis-causing infections, small local skin hemorrhages are observed: Localized loss of vascular integrity: effect of

A

inflammatory cytokines release induced by endotoxin activation of macrophages.

84
Q

Neisseria meningitidis

Purpura fulminans:

A

blood spots, bruising, and discoloration

of skin from coagulation in small blood vessels

85
Q

Neisseria meningitidis

Can progress to disseminated intravascular coagulation:

A

blood clots throughout the circulatory system resulting in
blockages and excessive bleeding elsewhere (clotting
factors depleted)

86
Q

Virulence Factors of N.meningitidis (4)

A

Ø Large capsule
Ø IgA protease
Ø Pili
Ø Shedding of lots of Endotoxin shock

87
Q

Ø Large capsule leads to

A

disseminated intravascular coagulation (DIC)
Some virulent strains have capsules with sialic acid on LOS (like
N.gonorrhea): reduces phagocytosis further

88
Q

Effective vaccination against capsular polysaccharides (2)

A

MenACWY Vaccine – CDC recommended since 2005
Protection from 4 major disease-causing strains:
A, C, W135 and Y (serotyping: 12 antigenic groups)
MenB vaccine – approved in 2014 & also recommended
B capsule poly-sialic acid; Andy Marso’s case involved
serogroup B bacteria.
European MenB vaccine was used in outbreaks at
Princeton and UC Santa Barbara in 2013-2014

89
Q

q Mandatory vaccination for students living in dorms

in many states, military recruits, and jail inmates

A

N.meningitidis

90
Q

N.species: N.gonorrhoeae “gonococci”
Virulence factors
Clinical features
Epidemiology

A

pili, Ag-variation
adhesins, OPA
IgA protease
endotoxin/LOS

gonorrhea (Ch.69)
pelvic inflammatory
disease
arthritis (Ch.65, 70)

sexual transmission
asymptomatic carrier

91
Q 
N.species: N.meningitidis "meningococci"
Virulence factors 
Clinical features 
Prevention
Epidemiology
A 
polysaccharide
capsule
endotoxin/LOS
Pili
IgA protease

meningitis (Ch.61)
meningococcemia
(bacteremia)

Prevention:
MenACWY &
MenB vaccines

asymptomatic carrier
aerosol transmission
children/young adults

92
Q

Gram− bacteria of the human colon/oral cavity

A

Bacteroides

93
Q

Bacteroidales (3)

A

Strict anaerobes
Commensals
Opportunistic pathogens

94
Q

Bacteroides fragilis (2)

A
  • most frequently isolated from clinical specimens of abscesses caused by intestinal bacteria
  • most oxygen-resistant Bacteroides
95
Q

Bacteroidales

Virulence Factors: (3)

A

Ø Superoxide dismutase - detoxifies oxygen radicals
Ø Catalase - breaks down hydrogen peroxide
Ø Polysaccharide capsule

96
Q

Ø Superoxide dismutase - detoxifies oxygen radicals
Ø Catalase - breaks down hydrogen peroxide
allows for

A

survival in well oxygenated peritoneal cavity

Also helps bacteria resisting killing by phagocytosis

97
Q

Bacteroidales
Disease
caused when
examples (2)

A

bacteria are introduced into deep tissues

  • peritonitis - rupture of infected appendix/diverticulum
  • pulmonary abscess - aspiration of oropharyngeal bacteria
98
Q

Bacteroides fragilis is one component in these diseases
— —
— - start with acute inflammation
progress to formation of localized abscesses
— as disease progresses
100’s of different species in inoculum
few species in abscess
due to response of the host and features of individual bacterial
species

A

polymicrobial diseases
biphasic
bacterial composition changes

99
Q

Bacteroidales

Course of disease

A

perforation of intestine/spillage of intestinal fluid
neutrophils mobilized
surviving bacteria resistant to phagocytosis
B. fragilis has a capsule
oxygen-sensitive bacteria are killed
peritoneal cavity well-oxygenated
facultative anaerobes grow first (E. coli)
some strict anaerobes survive
site becomes anaerobic
surviving strict anaerobes become predominant

100
Q

Bacteroidales

treat with

A

Surgery and antibiotic combinations (target aerobes and anaerobes)

Microbiology (42 decks)

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