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MLSCI 242 > LECTURE - Mycoplasmas, Chlamydia, and Treponema > Flashcards

LECTURE - Mycoplasmas, Chlamydia, and Treponema Flashcards

1
Q

Mycoplasma characteristics

A

gram neg but no peptidoglycan; very small genomes; pliable shape makes them look like junk; pleomorphic

  • require lipids and enriched medium to grow
  • live in close association with host cells but on outside (not intracellularly)
  • colonies = fried egg appearance
  • single cell membrane = cholesterol (From medium or host; don’t synthesise it)
  • smallest free-living microorganisms
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2
Q

walking pneumoniae

A

Mycoplasma pneumonia

  • sick but not sick enough to be hospitalaized
  • young adults
  • X-ray = moth-eaten appearance ; typical pneumonia = compact areas of density with clear edges
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3
Q

cells of Mycoplasma pneumoniae hve:

A
  • unique shape
  • show gliding motility
  • special attachment organelle
  • P1 = main protein involved in adherence
  • one end is cytoadherence organelle and the other is gliding end
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4
Q

cell membrane of M. pneumoniae

A
  • asymmetrical

- lipoprotein in outer leaflet cause inflammation like LPS; can possess antigenic differences among different strains

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5
Q

M. pneumoniae pathogenesis

A
  • organisms inhaled
  • bind to base of ciliated cells in lung through its cytadherence organelle
  • depolarize cells and cause ciliastasis
  • lipoprotein of outer leaflet membrane triggers inflammation
  • peroxide and other reactive O2 species => ciliated cell death and phospholipase may damage host cells
  • big virulence = community-acquired resp disease syndrome (CARDS) toxin
  • B cells ad T cells simulated non-specifically = Abs bind to RBCs in cold = cold agglutinins formed
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6
Q

M. pneumoniae pathogenesis

A
  • organisms inhaled
  • bind to base of ciliated cells in lung through its cytadherence organelle
  • depolarize cells and cause ciliastasis
  • lipoprotein of outer leaflet membrane triggers inflammation
  • peroxide and other reactive O2 species => ciliated cell death and phospholipase may damage host cells
  • big virulence = community-acquired resp disease syndrome (CARDS) toxin
  • B cells ad T cells simulated non-specifically = Abs bind to RBCs in cold = cold agglutinins formed
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7
Q

diagnosis of M. pneumoniae

A
  • slow-growing = takes 3-6 wks for positive results
  • paired sera in using a commercial serology test can confirm etiology
  • PCR available but expensive
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8
Q

treatment for M. pneumoniae

A

azithromycin (other macrolide)

- resistant strains are making headway in Asia, so tetracyclines or fluoroquinolones are backup

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9
Q

genital mycoplasmas

A

M. genitalium
M. hominis
Ureaplasma spp.

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10
Q

non gonococcal urethritis and cervicitis

A

Ureaplasma urealyticum

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11
Q

mechanism of Ureaplasma urealyticum

A
  • E production from hydrolysis on urea
  • shapeless mycoplasmas = growth advantage on genital tract
  • production of ammonia may contribute to local tissue destruction and pathology
  • colonize infant at birth but usually disappear by 2 y/o
  • adults acquire bu sexual contact; male exudate is more watery
  • women are more commonly colonized than men
  • lower socioeconomic groups
  • 14 serotypes known
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12
Q

the colonies of this organism shows a fried egg appearance

A

Ureaplasma urealyticum

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13
Q

an emerging cause of STD in women

A

Mycoplasma genitalium

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14
Q

this is similar to gonococcal pillin

A

Mycoplasma genitalium terminal organelle
> MgpB and MgpC = undergo phase and antigenic variation through a reciprocal recombination system similar to gonococcal pillin

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15
Q

This is available for detecting M. genitalium in urine, urethral, and endocervical or vaginal swab

A

rapid nucleic acid amplification test

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16
Q

M. genitalium is present in the general population at rates between those of __ and ___

A

Chlamydia trachomatis and Neisseria gonorrhoeae

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17
Q

Chlamydial developmental cycle

A
  • attachment and invasion of elementary body (in aa membrane bound inclusion)
  • within inclusion = EBs differentiate into a metabolically active and replicatnig reticulate bodies (RBs); closely interacts with host cell
  • end of developmental cycle = RBs go bak to being EBs = released by cell lysis or by extrustion of inclusion and can start a new round of infection
  • limited growth conditions and antibiotics = reversible arrest of growth or persiistence with RBs transforming into enlarged aberrant bodies (ABs)
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18
Q

1 cause of STI in NA and leading cause of acquired blindness in world

A

Chlamydia trachomatis

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19
Q

three possible diseases caused by Chlamydia trachomatis

A
  1. trachoma = potentially blinding eye infection

STIs:

  1. typical chlamydia infection
  2. Lymphogranuloma Venereum (LGV) = infected lymph nodes (bubos) in groin

type of disease is associated with specific serovars of the organism

20
Q

LGV more common here than in NA

A
  • tropical countries
  • but in NA and Europe there is an increasing incidence of infectious proctitis by LGV strains in MSM with HIV infections
21
Q

most common of the bacterial STIs

A
  • Chlamydia
  • spread by fluids during vaginal and anal intercourse; or from a pregnant woman to her fetus during birth (can happen with gonorrhea too)
  • often asymptomatic in females and sometimes males
  • asymptomatic doesn’t mean safe!!!!; can cause ascending disease; can infect fallopian tubes = sterility , etc.
22
Q

chlamydia infection in women

A
  • bleeding between menstrual periods
  • vaginal bleeding after intercourse
  • abdominal pain
  • painful intercourse
  • low-grade fever
  • painful urination
  • uge to urinate ore often
  • cervical inflammation
  • abnormal vaginal discharge
  • mucopurulent cervicitis (yellowish discharge that may have foul discharge
  • PID (pelvic inflammatory disease)
  • ectopic pregnancy
23
Q

PID

A
  • infection of fallopian tubes, ovaries, and/or uterus characterized by lower abdominal pain during menstruation, irregular menstruatioon, fever, chills
  • scarring may cause infertility by blocking fallopian tubes
24
Q

ectopic pregnancy

A

development of fetus in fallopian tube which causes rupture of fallopian tubes

25
Q

chlamydial infection in males symptoms

A
  • watery or milky discharge from penis, pain or burning when urinating, and swollen or tender testicles
  • epididymitis
  • reactive arthritis (Reiter’s syndrome): more men than women
26
Q

Epididymitis

A

spread from urethra to testicle (fever, swelling, and extreme pain in scrotum)
- can lead to sterility

27
Q

C. trachomatis and trachoma

A
  • passed from eyes of one peson to another by flies, fingers, shared clothing/towels
  • repeated infection = scarring of inner part of upper eyelid = turns lashes inwards so it scratches eyeball and cornea
  • eyelid scarring = poor tea secretion and drying of eye; increase risk of corneal ulceration => impaired vision and irreversible blindness
28
Q

T or F. blindness due to trachoma is irreversible

A

T!
but can be prevented
- SAFE strategy
> surgery for trichiais
> antibiotics to treat C. trachomatis infection
> facial cleanliness
> environmental improvement to reduce transmission

29
Q

Chlamys

A
  • cloak draped around the shoulder = intracytoplasmic inclusions caused by bacterium are draped around infected cells’ nucleus
30
Q

C. trachomatis characteristics

A
  • obligate intracellular pathogen = cant grow C. trachomatis in artificial media; have to be tissue culture
  • gram neg type cell wall but no peptidoglycan
  • smaller diameter than most bacteria
  • small genome
  • EB and RBs (two stages of life)
31
Q

C. trachomatis EB attachment and entry

A
  • EBs internalized by phagocytosis or receptor-medidated endocytosis
  • endosome is not acidified and Inc proteins inhibit function with lysosome; EB cell wall prevents phagolysosomal fusion and hence allows for intracellular surivial
  • endosomes containing EBs fuse together; unique to this organism!
  • phosphorylation of host cell proteins induces changes n actin cytoskeleton causing endosomes to move to the perinuclear region; glycogen is deposited with the inclusion
  • EBs differentiate into RBs
32
Q

how does C. trachomatis avoid lysis without peptidoglycan?

A

EB membranes contain proteins with multiple disulfide cross-links
major outer membrane protein (MOMP) = porin and maybe attachment
polymorphic outer membrane protein (POMP)
small and large cysteine-rich proteins = functional equivalent to peptidoglycan since they allow for intracellular division and extracellular survival

RBs protected by high osmolarity in interior of human cell

33
Q

detecting Chlamydia

A 
- traditional way
 > cultivate bacteria in tissue culture cells
- current way
 > PCR
 > fluorescent monoclonal antibody

** presence of glycogen within incisions detected by iodine staining **

34
Q

prevention and treatment for Chlamydia

A
  • abstinence and safe sex
  • antibiotics = doxycycline (tetracycline) or azithromycin (macrolide)
  • erythromycin ophthalmic ointment for newboarns
35
Q

best target for a vaccine for Chlamydia

A

proteins that affect EB entry bc once inside cell, Chlamydia is protected from Abs

> human cells infected do NOT display bacterial antigens on surface; so T cells attracted by CTLs not very effective

36
Q

cause of atypical pneumonia

A

Chlamydia pneumoniae

  • same structure and same life cycle
  • atypical pneumonia esp. in young adults
  • associated with atherosclerotic plaques in heart
37
Q

Chlamydia pneumoniae invades…

A

endothelial cells and triggers a profound inflammatory response

38
Q

chlamydial infection in infants symptoms

A
  • 20-50% of children born to women with chlamydia will be infected
  • conjunctivitis or pneumonia (can be fatal) so all babies should be treated with appropriate antibiotics (erythromycin)
  • prematue delivery, miscarriage, stillbirth, or low birthweight
39
Q

C. trachomatis inside host cells

A
  • RBs replicate
  • endosome enlarges to fit all; T3SS expressed (for cytoplasmic nutrients acquisition?)
  • RB Inc (inclusion) proteins insert into endosomal membrane = fuses with Golgi fragments = RBs differentiate into EBs = move to center of endosome
  • 40h post infection = endosomal membrane disintegrate = release EBsinto host cytoplasm = infect adjacent cells OR…
  • endosome fuses with host cytoplasmic membrane to release EBs and RBs (lyse rapidly) into extracellular space
40
Q

how are spirochetes unique?

A

genetically distinct from other bacteria, despite their overall gram neg-like structure

41
Q

spirochetes structure

A
  • stain lie a gram neg; has IM and OM
  • no LPS in OM, instead = lipoproteins
  • Ab to OM proteins can kill organisms if complement is activated
  • corkscrew motility due to flagella (axial filament) that is attached at both poles of the cell
  • long, thin with distinctive wavelength and amplitude of coils
42
Q

spirochetes causing human infection

A
  • Treponema pallidum = syphilis
  • Treponema pertenue = yawm a tropical multi-organ disease spread by physical contact
  • Leptospira interrogans = Weil’s disease; water-contaminated w infected rodent urine is ingested or enters wounds, causes multi-organ infection (eg: renal failure)
  • Borrelia hermsii or B. burgdorferi (tick-borne); B. recurrentis (louse-borne) relapsing fever
43
Q

T. pallidum

A
  • gram neg spirochete but no antigenic variation
  • virulent strains grown in rabbit testes bc they cannot be cultivated in artificial medium; avirulent grown on artificial media
  • can be transmitted transplacentally
  • STD
44
Q

stages of syphilis

A
  • primary: typically painless raised and ulcerated lesion (chancre)
  • secondary: rash and fever as organisms invade multiple organs
  • latent: Ab rises but organisms are not easily detected
  • tertiary: slowly progressing inflammatory disease with neurological symptoms, heart damage,, disfiguring lesions in skin
45
Q

this is a good screen for T. pallidum

A

Cardiolipin

- released from mitochondria by several diseases so Ab to it is not specific but a good screen

46
Q

reliable diagnosis for syphilis

A

serology

- specific serologic tests based on a patient Ab to T. pallidum antigens

47
Q

T or F. syphilis is still treatable with penicillin

A

T!

MLSCI 242 (39 decks)

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