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microbiology > Spirochetes---Mycoplasma > Flashcards

Spirochetes---Mycoplasma Flashcards

1
Q

Treponema pallidum
gram
shape
LPS?

A

Gram−
spirochete
no LPS

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2
Q

Treponema pallidum flagella/axial filament

A

flagella (3/pole) in an axial filament (between inner &outer membrane)

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3
Q

Treponema pallidum metabolism

A

microaerophile (never grown in culture: host-dependent metabolism)

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4
Q

Treponema pallidum transmission

A

fragile (only survive transmission without exposure):

sexual and congenital (placental) transmission in body fluids and mucous membranes

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5
Q

Treponema pallidum virulence

A

host response causes disease symptoms

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6
Q

Treponema pallidum virulence factors, what causes symptoms?

A

Ø membrane adhesins
Ø hyaluronidase
Ø antiphagocytic coat (fibronectin)
(host response causes symptoms)

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7
Q

Syphilis from?

A

new world to old world

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8
Q

Syphilis transmission

A

sexual or congential

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9
Q

syphilis localities

A

local
desimminated
gummas

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10
Q

local syphilis

infectious?

A

hard chancre/ulcer at site of infection; infectious

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11
Q

disseminated syphilis

infectious?

A

rash, aches; mucous membrane lesions

(“the great imitator”); infectious

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12
Q

gummas
can occur where?
infectious?
form in which stage of disease?

A

damage to blood vessels, eyes, CNS; insanity; not infectious

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

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13
Q

syphilis stages

A

primary
asymptomatic stage
secondary
possible tertiary

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14
Q

Primary syphilis:

A

2-6 weeks; chancre, which heals spontaneously, giving false sense of relief.

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15
Q

Asymptomatic period:

A

2-24 weeks

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16
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)

Microbe persists for 2/3 of secondary infections, with 1/2 exhibiting tertiary syphilis

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17
Q

Tertiary syphilis presentation

A

diffuse, chronic inflammation

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18
Q

congenital syphilis
prevention
lethality
dental abnormalities

A

[completely preventable by penicillin treatment early in pregnancy!):

high lethality in-utero OR when initially born without symptoms: high lethality typical of young children (e.g. 2 yrs old) with facial and dental abnormalities like “Hutchinson’s incisors” and “mulberry molars”.

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19
Q

treatment of 1 and 2 syphilis, vax?

A

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

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20
Q

Borrelia

gram and shape

A

Gram−

spirochete

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21
Q

Borrelia burgdorferi causes what disease?

A

lyme disease

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22
Q

lyme disease cycle

A

zoonosis: caused by Ixodes sacpularis tick
most common in spring/summer as the females lay eggs that hatch into larvae
larvae attach to rodents and acquire B. burgdoferi> detatch and molt into nymphs that can transmit the bacteria to more rodents or to humans

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23
Q

Borrelia burgdorferi virulence factor

A

adhesion proteins

some species with antigenic variation

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24
Q

Borrelia burgdorferi transmission/ reservior

A

ticks

• reservoir: rodents, deer

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25
Q

lyme disease stages

A

local
disseminated
chronic

26
Q

local lyme disease

A

Erythema migrans rash at bite, fever

27
Q

disseminated lyme disease effects on nn and heart, time frame?

A

nerve paralysis with heart arrhythmia (2-8 wks)

28
Q

chronic lyme disease

A

arthritis and CNS paralysis due to persistent immune response
(>6 months)

29
Q

lyme disease vax?

A

none

30
Q

Relapsing Fever of Borrelia spp.due to

A

Relapsing fever due to effective immune response to antigenic variation (small pathogen population maintained)

31
Q

Borrelia spp of relapsing fever

where from?

A

B. recurrentis: from body louse of humans

B. miyamotoi: from soft shell tick from animals

32
Q

Borrelia sp. treatment

A

penicillin
tetracyclines
ceftriaxone

33
Q

Rickettsia gram

A

negative

34
Q

Rickettsia
intra or extracellular?
escape?
result?

A

obligate intracellular parasite: entry into endothelial cells, escape into cytoplasm by phospholipase, slow proliferation, cell lysis and vascular hemorrhages (no laboratory culture)

35
Q

Rickettsia Virulence Factors:

A

intracellular growth

rapid cell-to-cell spread (from cell projections by actin-rockets and through cell lysis)

36
Q

rickettsia transmission

A

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

37
Q

Rocky Mountain spotted fever due to?

species involved?

A

CTL immune disease due to rickettsia

38
Q

Rocky Mountain spotted fever disease presentation/ progression
dissemenation?
mortality without treatment?

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)
39
Q

Rocky Mountain spotted fever vax

A

none

40
Q

Rocky Mountain spotted fever treatment

A

doxy or flouraquinolones

41
Q

Chlamydia trachomatis gram

A

negative

42
Q

Chlamydia trachomatis agent of? commonality?

A

Agent of chlamydia

The most frequent sexually transmitted infection

43
Q

Chlamydia trachomatis intra/extracellular?

A

Obligate intracellular parasite (no laboratory culture; “ATP”-parasite)

44
Q

Chlamydia trachomatis peptdioglycan

A

no synthesis of this/ low LPS

45
Q

what causes Chlamydia trachomatis disease symptoms

A

Inflammatory cytokines released from infected cells cause disease= damaging cell-mediated immune response in various tissues

46
Q

Chlamydia trachomatis
different forms/bodies
cell infection/ spread

A 
elementary body (stable, infectious)
 reticulate body (replicating, fragile, non-infectious)

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

47
Q

Chlamydial diseases caused by:

A

CMI response

48
Q

Chlamydial gonorrheal-like sexual disease

A

caused by 8 serotypes
• 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

49
Q

other chlamydial diseases

A

3 serotypes: lymphogranuloma venereum

4 serotypes: trachoma (endemic chronic eye infection: blindness), ophthalmia neonatorum with conjunctivitis and pneumonia

50
Q

treatment of chlamidyal diseases

A
  • azithromycin: 1 dose

* tetracycline or erythromycin treatment

51
Q

immune protection/ reinfection of chlamidya

A

no immune protection

reinfection: stronger CMI

52
Q

C.pneumoniae strain causes

A

walking pneumonia

53
Q

leading bacterial infection species

A

Chlamydia trachomatis

54
Q

Mycoplasma pneumoniae gram
cell wall?
membrane?

A

non gram staining: (no rigid cell wall: no effect of

penicillin or lysozyme); strong membrane (due to sterols)

55
Q

Mycoplasma pneumoniae sterilization

A

cannot be done with filtration (too small)

56
Q

smallest prokaryote

A

Mycoplasma species are smallest prokaryote (M.

genitalium 580,070 bp – 475 genes)

57
Q

Mycoplasma pneumoniae O2 use? preference for what tissue

A

strict aerobe (preference for bronchial mucosa)

58
Q

Mycoplasma pneumoniae Virulence Factors:

A

Ø P1 adhesin for ciliated respiratory epithelium:
loss of ciliated cells: no mucus clearing from lungs
Ø slow growth

59
Q

Mycoplasma pneumoniae disease

A

atypical, mild pneumonia, the leading cause in schools, students,
and military: aerosol transmission in crowded conditions
• often (>15%) combined with otitis media

60
Q

Mycoplasma pneumoniae vax/ immunity

A

no vaccination; fading protective immunity after recovery

61
Q

pneumonia species, which can be vaxxed against?

A

only pneumococcal can be vaxxed

microbiology (42 decks)

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