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3.21 Flashcards

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1
Q

Yersenia pestis, cause of plague

characterization

A

Black death

Gram−

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2
Q

Transmission of plague (3)

A

fleas

bubo (infected lymph node with pus): not contagious
• 50-75% mortality if not treated promptly

In 10-20% spread to lungs:
• highly contagious (direct transmission)
• near 100% mortality: black death

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3
Q

Francisella tularensis

characterization (2)

A

Gram−
opportunistic zoonosis
(birds, rabbits, tick bites) (bioterrorism)

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4
Q

Francisella tularensis

Virulence Factors: (1)

A

Ø intracellular growth in macrophages

(prevents phagolysosome fusion) bacteremia

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5
Q

Francisella tularensis

Diseases: rabbit fever, tick fever (2)

A

• ulceroglandular and
oculoglandular tularemia
• pulmonary tularemia

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6
Q 
Brucella
characteriztion  (2)
A

Gram−

opportunistic zoonosis by B.melitensis (or bioterrorism)

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7
Q

undulant fever (brucellosis, “bangs disease”

A

systemic bacteremia starting from infected lymph nodes

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8
Q

skipped

undulant fever

A 
Organisms penetrate mucous
membranes and are carried to heart,
kidneys, and other parts of the body via
the blood and lymphatic system; they
are resistant to phagocytic killing and
grow within these cells
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9
Q

Haemophilus influenzae

characterization (2)

A

Gram−
frequently part of oral flora (carrier rate up to 80%)
6 O-antigen serotypes: a – f: type b is most virulent

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10
Q

Haemophilus influenzae

Virulence Factors:

A

capsule b

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11
Q

Haemophilus influenzaem

Conjugated vaccine

A 
against
capsule b polysaccharides
creates protective IgG,
preventing systemic infections
Vaccine does not protect against
other encapsulated strains and
unencapsulated strains
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12
Q

Haemophilus influenzae type b infections
cases per year before immunization
decrease after

A

20,000

99.7%

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13
Q

before the availability of conjugate vaccines in late 1987 H. influenzae type b was the most common cause of bacterial meningitis in

A

preschool children

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14
Q

Without vaccination: systemic diseases

in children) by encapsulated strains: (2

A
  • meningitis

* septicemia, cellulitis, epiglottitis

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15
Q 
Haemophilus influenzae
Gram- rods, aerobic / facultatively anaerobic
Virulence factors 
Clinical features 
Treatment
EPIDEMIOLOGY (2)
A

polysaccharide capsule b
pili, adhesins
IgA protease

no capsule: otis media,
sinusitis, conjunctivitis,
bronchitis, pneumonia
capsule B: meningitis,
septicemia, cellulitis,
epiglottitis
broad-spectrum
cephalosporin,
azithromycin or
fluoroquinolone
(>30% ampicillin resistance)

aerosol transmission
respiratory tract in
elderly

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16
Q

Legionella pneumophila

characterization (4)

A

Gram−
facultatively intracellular
Growth up to 46C
Relatively resistant to chlorine and other biocides

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17
Q 
facultatively intracellular (prevents endosome-lysosome fusion;
autophagosome-like uptake)
A

Lives and proliferates in the vacuoles of amoebas and

in the endoplasmic reticulum of macrophages

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18
Q

Legionnaires disease: how was it disovered

A

infected roof A/C

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19
Q

Legionnaire’s disease

Virulence Factors:

A

Ø intracellular growth in alveolar macrophages

no phagolysosomal fusion

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20
Q

Legionnaire’s disease

Transmission:

A

aerosol from water sources (living inside amoeba)

No human-to-human transmission

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21
Q

Legionnaire’s disease

A

severe pneumonia, necrotic abscesses

especially in immune-compromised and elderly; mortality 20%

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22
Q

Listeria monocytogenes (6)

A 
• acid-resistant
• cold-resistant (psychrotolerant)
(growth from 1ºC to 45ºC)
• salt-resistant
• motile
• food-borne pathogen
(processed meat like hot dogs,
dairy like Brie cheese; 4ºC stored)
• facultatively intracellular
(enterocytes, macrophages)
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23
Q

— is rare (2500 cases/yr)
But exposure is common (10%
asymptomatic carriers)

A

Listeriosis

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24
Q

Listeria monocytogenes

VF

A

listeriolysin O

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25
Q

listeriolysin O

A

pore-forming toxin (phagosome escape)

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26
Q

Intracellular infections by Listeria monocytogenes

A

listeria or other bacteria cross the mucous membrane into tissues by passing through M cells

(b) macrophages engulf bacteria
(c) pathogen released from macrophages enters host cells by endocytosis
(d) bacteria move from cell to cell propelled by actin filaments

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27
Q

Cooperation of CD4+ and CD8+ T cell CMI responses

Observations: (2)

A

In mutant Listeria that lack lysteriolysin,
the oxidative burst in infected
macrophages, stimulated by CD4+ T cell
IFNg, will eradicate the infection.
Cooperation of CD4+ and CD8+ T cell CMI responses
In wild-type Listeria, where the bacteria
escape to the cytoplasm, the additional
lytic action by CD8+ CTLs is required
before the infection is eradicated.

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28
Q 
Listeria monocytogenes
Gram+ rods, aerobic / facultatively anaerobic
Virulence factors 
Clinical features 
Treatment 
EPIDEMIOLOGY (5)
A

Listeriolysin O
internalins
ActA-intracellular motility
growth at 4ºC

neonatal abscess,
meningitis
like-flu in adults
systemic disease in CMI- deficient persons

ampicillin or penicillin
− or + gentamicin
Increasingly:
plasmid-acquired
antibiotic resistance
immune compromised
neonates
elderly
pregnant women
contaminated food
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29
Q 
Mycobacteria 
characterizations (4)
A

Mycolic acids in cell wall
Gram+ weak staining: use acid-fast stain
or specific fluorescent detection
Facultative intracellular growth (in macrophages)
Obligate aerobe (growth in lung macrophages)

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30
Q

Koch identified Mycobacterium tuberculosis

as cause of TB in 1882: (2)

A

• Humans are reservoir
• airborne transmission (as few as 10 cells
can result in infection)

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31
Q

Acid-fast stain

A
  1. hot carbol fuchsin: acid fast cells, red
  2. acid-alcohol (decolorizer): nonacid fast cells, blue
    methylene blue (counter stain)

Mycobacteria can be subjected to Gram staining but this requires a
pre-treatment:
1. treat with alkaline-alcohol to extract lipid mycolic acids
2. do Gram stain: result Gram+

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32
Q

skipped
Structural mycobacterial cell wall components which are Virulence Factors
(4)

A

cord factor (glyco-lipid)
mycolic acid
mannose-cappde lipoarabinomanah
arabinogalatan

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33
Q

Mycobacteria Virulence Factors

A

Slow, cord-like growth
strongly correlates
with virulence.

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34
Q

Cord-like growth results from

A

adherence of cell surface

lipid mycolic acids and glyco-lipids

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35
Q

Virulence Factors (2) M.tuberculosis and M.leprae

While many “virulence factors” are listed, their virulence results from the challenge that
they provide to the immune response (typically DTH: CD4+ T-cells + macrophages)
because

A

(in most cases) the disease is caused by the immune response,
NOT by the mycobacteria.

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36
Q

Facultative intracellular growth in alveolar and other macrophages:

A

inhibition of phago-lysosome fusion

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37
Q

CMI to Mycobacterium tuberculosis

A

TB granuloma surrounded by punctate nuclei
of lung tissue and inflammatory leukocytes.
Central area of necrosis where nuclei have
been destroyed.
Mycobacterium tuberculosis is a “life-long” pathogen:
once infected, you may be asymptomatic but never cured.

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38
Q

CMI to Mycobacterium tuberculosis

Aerosol transmission

A

Effective CMI is capable of localizing and stopping infection by M.tuberculosis. Chronic TB is
typical.

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39
Q

CMI to Mycobacterium tuberculosis

Exception:

A

young children under 5 years have a high risk for developing progressive TB due
to insufficient immune system development/activation.

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40
Q

CMI to Mycobacterium tuberculosis
OUTCOMES of untreated primary TB [results for non-immune-compromised patents]: (3)

  • –% no disease
  • –% clinical TB (2% pulmonary + 3% extrathoracic + 1% both)
  • –% progressive systemic disease and death.
A
  • 91% no disease
  • 6% clinical TB (2% pulmonary + 3% extrathoracic + 1% both)
  • 3% progressive systemic disease and death.
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41
Q

CMI to Mycobacterium tuberculosis
However, acute (‘open’) TB [also known as “secondary tuberculosis” or in older terms “— —” caused by “— —” of prior infection - while rare (life-time risk is assessed as <12% for carriers, or less) it is VERY contagious!
Isolation of acute TB cases is mandatory.
Endogenous reactivation is stimulated by stress, malnutrition and HIV

A

galloping consumption

endogenous reactivation

42
Q

CMI to Mycobacterium tuberculosis

Actually, the “disease” (except for the infection risk of “Open TB”) arises from

A

tissue destruction
by our immune defenses and not by damage caused by the bacterial infection.
The repeated attempts to remove foci of infection by lung macrophages cause the granulomatous
lung tissue that impairs lung function.
Breathing impairment in TB is not due to tuberculosis bacilli but by the macrophage-induced tissue
destruction

43
Q

Mantoux Reaction

A 
A positive tuberculin test to
subdermal PPD (processed
protein derivative of the cell
wall of the opportunistic
intracellular pathogen
Mycobacterial tuberculosis).
44
Q

Mantoux Reaction
Positive test: >– mm redness
Strongly positive: >–mm red

A

10

20

45
Q

Mantoux Reaction
Vaccination
Exposure to living attenuated mycobacterium, known as Bacille Calmette-Guérin (BCG), a
derivative of M.bovis (which may be identical to M.tuberculosis based on whole genome sequencing): (3)

A

• little virulence in humans (but infectious in immune-compromised persons)
• some protective immunity (when given to young children)
• BCG vaccination is discouraged in USA because it gives a positive tuberculin test, thus removing
an important diagnostic screening tool. (And M.bovis causes disease in immune-compromised persons.)

46
Q

Mycobacterium leprae: diverse CMI responses

TH1-response

A

macrophages kill nerves;

macules and plaques without sensation

47
Q

Mycobacterium leprae: diverse CMI responses

Loss of CMI

A

(or TH2-response
CTL lysis and
loss of tissue)
(including nerves)

48
Q

Tuberculoid vs Lepromatous Leprosy

Multidrug therapy:

A

Dapsone + rifampin + clofazimine

Rising resistance is becoming a problem.

49
Q 
Mycobacterium
Gram+ rods (branched), strict aerobic, mycobacteria
M.species 
M.tuberculosis
(obligate aerobic)
(doubling time: 1 d)

Virulence factors (1)
Clinical features (1)
Treatment (2)
Epidemiology (3)

A

Ability to survive
and live in lung
macrophages

pulmonary (and
extrapulmonary)
tuberculosis

multidrug therapy:
isoniazid (INH)º +
rifampin +
ethambutol +
pyrazinamide *
6-12 months
Aerosol
(person-to-person)
All ages
Highest risk if
immune
compromised (HIV)
50
Q 
Mycobacterium
Gram+ rods (branched), strict aerobic, mycobacteria
M.species 
M.leprae
(doubling time: 12 d)

Virulence factors (1)
Clinical features (1)
Treatment (2)
Epidemiology (1)

A

Ability to survive
and live in
macrophages

tuberculoid-tolepramatous
leprosy

multidrug therapy:
dapsone +
rifampicin + (for
lepramatous form)
clofazimine
2+ years

Close physical
contact

51
Q

All pathogenic mycobacterial species have (very) — growth rates

A

slow

52
Q 
Nocardia
characterization (2)
A

• Gram+ (poor staining)
• mycolic acid in cell wall: “partially acid-fast”
(Test to distinguish Nocardia from fungal look-alikes)

53
Q

Nocardia

VF

A

Opportunistic pathogen

in immuno-compromised patients

54
Q 
Nocardia
Gram+ rods (branched), mycobacteria
Virulence factors 
Clinical features 
Treatment 
Epidemiology
i
A

ntracellular survival +
growth
catalase
superoxide dismutase

bronchopulmonary
cutaneous infections
brain abscesses

sulfonamides
amikacin, carbapenems
or cephalosporins

opportunistic pathogen
(if pulmonary disease or
T deficiency)

55
Q

Treponema pallidum

characteristics (3)

A

Gram− spirochete but no LPS
flagella (3/pole) in an axial filament (between inner &outer membrane)
fragile (only survive transmission without exposure):
sexual and congenital (placental) transmission in body fluids and
mucous membranes

56
Q

Treponema pallidum

VF

A

host response causes disease

symptoms

57
Q

Syphilis

A new-world ®

A

old-world

disease thanks to Columbus

58
Q

Syphilis

Transmission: (2)

A

• sexual (human reservoir)
• congenital (spirochete
crosses placenta: late lethality)

59
Q

Syphilis

Stages: (3)

A 
1.local: hard chancre/ulcer at
site of infection; infectious
2.disseminated: rash, aches;
mucous membrane lesions
(“the great imitator”);
infectious
3.gummas; damage to blood
vessels, eyes, CNS;
insanity; not infectious
60
Q

Primary syphilis:

A

2-6 weeks; chancre, which heals

spontaneously, giving false sense of relief.

61
Q

Asymptomatic period:

A

2-24 weeks

62
Q

• Secondary syphilis:

A

2-6 weeks; 50% of primary
infections go on to secondary; symptoms typically
resolve spontaneously (but recurrence in 25% with 1 yr)

63
Q

Microbe persists for – of secondary infections, with –

exhibiting tertiary syphilis

A

2/3

1/2

64
Q

Tertiary syphilis:

A

diffuse, chronic inflammation

65
Q

gummas –

A

These form in tertiary syphilis
granuloma lesion = inflammatory mass which can perforate, e.g. roof of
mouth or any other tissues

66
Q

congenital syphilis

A

[completely preventable by penicillin treatment early in pregnancy!)

67
Q

high lethality in-utero OR

when initially born without symptoms:

A

high lethality typical of young children (e.g. 2 yrs old) with facial
and dental abnormalities like “Hutchinson’s incisors” and “mulberry molars”.

68
Q

syphilis tx

A

penicillin for 1º and 2º infections, which contain actively growing spirochetes
No vaccine

69
Q

Borrelia

characteristics

A

Gram− spirochete

70
Q

Lyme Disease: Borrelia burgdorferi

A

Ixodes scapularis Tick

The tick transmission cycle sustains the bacteria, B. burgdorferi, that cause Lyme
disease. Lyme disease risk is greatest in spring and summer, but can occur during all
four seasons. Nymphs, which feed in the late spring and early summer, are responsible
for transmitting the majority of infections to humans.

71
Q

Lyme Disease: Borrelia burgdorferi

transmission (2)

A
  • ticks

* reservoir: rodents, deer

72
Q

Lyme Disease: Borrelia burgdorferi

disease (3)

A
  1. acute, local: fever
  2. disseminated: nerve
    paralysis (with heart
    arrhythmia)(2-8 wks)
  3. chronic: arthritis,
    CNS paralysis (due
    to persistent immune
    response)(>6 months)
73
Q

Lyme Disease: Borrelia burgdorferi

vaccine

A

no effective vaccine

74
Q

Lyme Disease: Borrelia burgdorferi

rash

A

Erythema
migrans
rash

75
Q

Relapsing Fever: Borrelia spp.

VF

A

Relapsing fever due to effective

immune response to antigenic variation

76
Q

infection: relapsing fever, epidemic (louse born)
reservoir
vector

A

humans
body louse
B. recurrentis

77
Q

infection: relapsing fever, epidemic (tick born)
reservoir
vector

A

rodents, soft shelled ticks
soft shelled tick
B. miyamotoi

78
Q 
Spirochetes
Species: Treponema pallidum
Virulence factors 
Clinical features 
Treatment 
Epidemiology
A

adherence
hyaluronidase
coat
host response

Syphilis: 1º, 2º, 3º,
congenital

penicillin

sexual or
congenital
transmission
(human reservoir)

79
Q 
Spirochetes
Species: Borrelia sp.
Virulence factors 
Clinical features 
Treatment 
Epidemiology
A

surface binding
proteins
antigenic variation
(relapsing fever)

Lyme disease:
erythema migrans
neurologic, cardiac,
rheumatic
Relapsing fever

penicillin
tetracyclines
ceftriaxone

Ticks, lice from
animal reservoir

80
Q 
Rickettsia
characteristics  (3)
A 
Gram−
obligate intracellular parasite
entry into endothelial cells, escape 
vascular hemorrhages
(no laboratory culture)
81
Q

Transmission of this zoonosis: (2)

A
  • wood tick (including transovarian transmission from adult ticks into tick eggs)
  • reservoir: wild rodents
82
Q

Rocky Mountain spotted fever: CTL immune disease

Disease: (3)

A

• rash of extremities, then trunk
• hemorrhagic lesions (with disseminated vascular
CTL lysis of endothelial cells) ► spots
• dissemination to heart, kidneys, etc ► shock, death
(mortality = 20-40% if no treatment)

83
Q

Chlamydia trachomatis

Agent of

A

chlamydia
The most frequent sexually transmitted infection (followed by
gonorrhea, AIDS and syphilis)

84
Q

Chlamydia trachomatis (3)

A

Obligate intracellular parasite (no laboratory culture; “ATP”-parasite)
No “peptidoglycan” synthesis (although the bacterial cell wall looks ‘normal G−’)
Inflammatory cytokines released from infected cells cause disease
manifestations

85
Q

Inflammatory cytokines released from infected cells cause disease
manifestations:

A

damaging cell-mediated immune response in various

tissues.

86
Q

Chlamydia trachomatis

EB:

A

epithelial cell adhesion to microvilli ► RB in phagosomes (no fusion with
lysosomes) ► replication and division ► EB ► cell lysis / exocytosis

87
Q

EB =

A

elementary body

stable, infectious

88
Q

RB =

A

reticulate body
(replicating, fragile,
non-infectious)

89
Q

Chlamydial diseases caused by CMI responses

8 serotypes:

A

gonorrheal-like sexual disease
• Mucopurulent urethritis, cervicitis, salpingitis (fallopian tube
infection)
• mobility by adhesion to sperm (► epididymitis prostatitis in men)
• PID (pelvic inflammatory disease) ► scarring ► ectopic pregnancy
+ decreased fertility

90
Q

Chlamydial diseases caused by CMI responses

3 serotypes:

A

lymphogranuloma venereum

91
Q

Chlamydial diseases caused by CMI responses

4 serotypes:

A

trachoma (endemic chronic eye infection: blindness)

ophthalmia neonatorum with conjunctivitis and pneumonia

92
Q

Chlamydial diseases caused by CMI responses (2)

A

ü no immune protection

ü reinfection: stronger CMI

93
Q

C.pneumoniae strain causes

A

“walking pneumonia”

94
Q

Mycoplasma pneumoniae

characteristics (3)

A

non-Gram staining (no rigid cell wall: no effect of
penicillin or lysozyme); strong membrane (due to sterols)
no sterilization by filtration (0.45μm)
Mycoplasma species are smallest prokaryote (M.
genitalium 580,070 bp – 475 genes)
strict aerobe (preference for bronchial mucosa)

95
Q

Mycoplasma pneumoniae

Disease:

A

• atypical, mild pneumonia, the leading cause in schools, students,
and military: aerosol transmission in crowded conditions

96
Q

Mycoplasma pneumoniae

tx

A

no vaccination; fading protective immunity after recovery

97
Q

pneumococcal Pneumonia

tx

A

capsular vaccine available

98
Q

klebsiella Pneumonia

tx

A

no vaccine available

99
Q

mycoplasmal Pneumonia

tx

A

no vaccine available

100
Q

Mycoplasma pneumonia is also known as “walking pneumonia” because

A

it is typically mild and without the need for hospitalization.

Microbiology (42 decks)

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