41. Chlamydia & Mycoplasma Flashcards

1
Q

Chlamydia general characteristics?

A

gram negative

obligate intracellular

unique developmental cycle

ubiquitous to humans and animals

highly conserved small genome (highly reombinant)

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2
Q

chlamydia growth/metab

A
  • EB = spore-like for extracellular survival/ transmission and is metab. Dormant
  • after internalization becomes RB = less dense, grow in contact w/inclusion membrane, metabolically active (multiplies by binary fission), NON infectious
  • late differentiation RB>EB 20-40 hrs post infection, outer memb rigidification and condensing of chromosomal DNA
  • fully mature inclusion has 1000 EBs and 1+ inclusion per cell
  • cycle closed when inclusion and infected host cell lyse (or inclusion is exocytosed)
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3
Q

chlamydia pathogenesis

A

Secretion/translocation of chlamydial effector protein into the host cell is key to pathogenesis:
- type III secretion (T3S) (early T3S effectors assoc w/EBRB; mid assoc w/growth; late assoc w/RB detachment / T3S disruption and late RBEB)
- autotransport (T5S)
- outer membrane blebs
Primary infection is freq asymptomatic and responds to Abx, pathology caused by inflammatory response
Chronic infection due to extensive remodeling and scarring of tissue often at remote sites
Repeat infection or persistence common

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4
Q

chlamydia virulence factors

A
  • cytotoxins related to clostridial cytotoxins

- co-option of metabolites from the host and local microbiota promotes chlamydial growh**

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5
Q

chlamydia disease

A
  • Long-lasting in the absence of treatment
  • repeat infections common
  • often asymptomatic
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6
Q

C. trachomatis pathogenesis?

A

Direct contact, house flies; enhanced by poor hygienic conditions; genital: 10% of sexually active adults

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7
Q

C.trachomatis disease?

A

Primary = inclusion conjunctivitis
Repeated = follicular conjunctivitis (may resolve = immunity)
Chronic = trachoma (pannus, blindness, trichiasis)
Ophthalmia neonatorum = 5-12 days post-natal; abx eye drops at delivery
Genital  PID, ectopic, infertility

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8
Q

C.trachomatis treatment?

A

Primary = Abx

But Abx therapy has no effect past childhood! (disease is immune-response mediated)

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9
Q

c. pneumoniae disease?

A

Common cold-like sxs to atypical CA-PNA

  • chronic infection (bronchitis, asthma, COPD exacerbation)
  • disseminated chronic infections (arthritis, AAA, stroke, atherosclerosis)
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10
Q

C.penumoniae dx and tx?

A

dx Not usually attempted (Ag possible)

10-14 days doxycycline, erythromycin, quinolones

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11
Q

C.psittaci disease?

A

Flu-like to severe pna-like syndrome

Avian, occupational hazard

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12
Q

C. psittaci dx and tx?

A

Rarely dx
- CF test, hx of bird exposure

-Doxycycline, tetracycline
B-list bioweapon

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13
Q

mycoplasma characteristics?

A

Broad group, 100+ species

  • wall-less pleiomorphic bacteria, evolved from Gram+ by mutational loss
  • few pathogenic to humans
  • fastidious orgs (difficult to manipulate in vitro)
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14
Q

mycoplasma virulence factors?

A
  • hemolysins (alpha or beta)
  • surface structures (attachment to ciliated epith cells of respiratory tract)
  • polysaccharide capsule
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15
Q

M. pneumoniae general characteristics?

A
  • super tiny colonies
  • mulberry colonies
  • Leading cause of pna in school-age kids and young adults
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16
Q

M. pnemoniae pathogenesis and virulence factors?

A

Some immune response is beneficial (IgM, IgG, CMI)
BUT 50% develop cold agglutinins

  • CARDS (community acquired respiratory distress syndrome) toxin of M.pneumoniae: ADP ribosylating and vacuolating toxin
17
Q

M. pneumoniae disease??

A

Cough, malaise, fever, CA-PNA = walking pneumonia

18
Q

M. pneumoniae dx and tx?

A

Serology and PCR (because hard to culture): IgG or IgM by ELISA

  • Doxycycline
  • ciproflaxin
  • erythromycin
  • azithromycin
  • levoflaxin
19
Q

M. hominis, M. genetalium & U. urealyticum?

A

Members of normal GU flora

Opportunistic pathogens

STI – PID?
Spontaneous abortions?
Non-gonococcal urethritis (10%) - asymptomatic

20
Q

M. fermentans & M. petrans?

A

Assoc w/HIV infection (HIV grows better in vitro if host cells are already infected w/these mycoplasma, and assoc w/AIDS pts)

Why assoc w/HIV?

  1. mycoplasma are opportunistic
  2. mycoplasma infection enhances HIV virulence
  3. AIDS-assoc mycoplasma are pathogenic in their own right