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Micro-Bacteria > Sexually Transmitted diseases > Flashcards

Sexually Transmitted diseases Flashcards

1
Q

Physical shape of syphilis

A

-long, very thing spirochete

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2
Q

Visualization of syphilis

A
  • fixed tissues by silver stain

- visualize live by dark field microscope

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3
Q

Sheath surrounding syphilis

A

glycosaminoglycan surrounding whole cell

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4
Q

Motility of syphilis

A
  • endoflagella within periplasm

- 3 at each end

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5
Q

Three other bacteria that have characteristic of spirochete

A
  1. treponema
  2. leptospira
  3. borrelia
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6
Q

Envelope of syphilis

A
  • no LPS, loosely anchored OM with cardiolipin

- mostly IM lipoproteins, few OM proteins

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7
Q

Cultivability of syphilis

A
  • unculturable in lab
  • survive a few weeks, but no growth
  • microaerophilic metabolism
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8
Q

The stages of syphilis

A

Primary, secondary, and tertiary

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9
Q

Description of the primary stage of syphilis

A
  • ulcerated, defined papule at site of infection = chancre
  • regional lymph nodes well
  • usually genital, oral/anal 10-20%
  • heals spontaneously, org. remains
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10
Q

Description of the secondary stage of syphilis

A
  • red macular/maculopapular rash occurring anywhere(in. soles and palms)
  • condylomas in moist areas
  • spont. heals
  • recurrence
  • long latent period
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11
Q

Similarity between primary and secondary stages of syphilis

A
  • unusual primary site indicative of overlap between both stages
  • chin, tonsil, ear, neck, fingers, chest, arm
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12
Q

Description of the tertiary stage of syphilis

A
  • lesions in tissues throughout body(due to immune response)
  • skin: gummas
  • bones: porous, fragile
  • heart: aorta swells, ruptures
  • liver damage
  • CNS: paresis, tabes dorsalis
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13
Q

Birth defects related to syphilis

A
  • abortion or stillbirth
  • Hutchinson’s triad: interstitial keratitis, 8 nerve deafness, H. teeth
  • saddlenose, neural defects, bone deformation
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14
Q

Epidemiology of syphilis

A
  • exclusively human and STD

- contagious for 3-5yrs after infection

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15
Q

Pathogenesis of syphilis

A
  • highly infectious
  • hyaluronidase facilitates spread and invasion of tissues
  • rapid motility
  • few surface proteins
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16
Q

Primary and secondary lesions full of

A

T.pallidum

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17
Q

Tertiary lesions

A

Presentation is a hyperimmune response

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18
Q

Control of syphilis

A
  • Serologic tests for syphilis: STS, VDRL
  • indirect test
  • Fluorescent treponema antibody
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19
Q

Describe indirect test for syphilis

A
  • T pallidum induces formation of ‘reagin’ in host(IgM + IgA)
  • add cardiolipin to patient serum
  • if +, reagin causes cardiolipin to clump
  • lots of false positives
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20
Q

Describe the fluorescent treponema antibody

A
  • can be indirect, detect anti-treponema antibodies
  • bind T.pallidum to slide and add serum from patient
  • add fluorescent anti-human to detect antibody in serum
21
Q

Treatment of syphilis

A
  • treat with penicillin G
  • one i.m. injection for early disease
  • 3 injections for latent disease
22
Q

Physical shape of neisseriae

A
  • gram negative
  • coffee bean shaped diplococcus
  • seen in both inter cellularly and in PMNs
23
Q

Growth of neisseriae

A
  • fastidious
  • aerobic
  • cytochrome c oxidase positive
  • 2 identical chromosomes
24
Q

Clinical presentation of neisseriae

A
  • invades mucus membranes of UGT, rectum, eye, throat
  • proctitis
  • pharyngitis
  • arthritis
25
Q

Male clinical presentation of neisseriae

A
  • urethritis; painful urination, drip of pus from urethra

- 40% asymptomatic

26
Q

Female clinical presentation of neisseriae

A
  • urethritis
  • vaginitis
  • cervicitis
  • salpingitis, PID, peritonitis
  • fallopian tube scarring, infertility
  • 60% asymptomatic
27
Q

Neonate clinical presentation of neisseriae

A

-conjunctivitis from infected birth canal

28
Q

Epidemiology of neisseriae

A
  • exclusively a human STD
  • -75% infection rate
  • 50% after one encounter
  • co infection chlamydia
  • large number of asymptomatic carriers
29
Q

Diagnosis for neisseriae

A
  • males: gram stain of urethral drip

- females: culture of cervical swab or vaginal swab

30
Q

Pathogenesis of neisseriae- light binding

A
  1. attachment
    - pili
    - pilus antigenic variation by recombination
    - 1 promoter(pilE), many genes(pilS)
    - recombine new pilS gene or part of gene with pilE to make new pili
31
Q

Pathogenesis of neisseriae-tight binding

A
  • Opa(protein II)
  • named for opacity phenotype of colonies
  • antigenic variation by DNA slippage of repeats
  • infections in females change Opas during menstrual cycle
32
Q

Three proteins involved in the evasion process of neisseriae

A

-Por, Rmp, IgA protease

33
Q

Function of Por in neisseriae

A

Por(protein 1): outer membrane porin, but also prevents phagolysosome fusion in host

34
Q

Function of Rmp in neisseriae

A

Rmp(protein 3): Host abs binds to it, prevents Ab binding to Por and LOS in outer membrane

35
Q

Function of IgA protease

A

IgA is the bactericidal, complement activating, first response Ab in mucus membranes

36
Q

Toxicity associated with neisseriae

A

LOS
-lipid A part is toxic
-oligosaccharide mimics host cell membrane structure
-NANA transferase to sialylate bacterial LOS with host NANA
PG
-released by autolysis at low temp or alkaline pH
Fbp
-scavenges Fe from human lactoferrin and transferrin

37
Q

Control of neisseriae

A
  • resistance acquired very easily
  • PPNG produce B-lactamases
  • Pan resistant
38
Q

Treatment of neisseriae

A
  • cephtriaxone or cefixime
  • doxycycline or erythromycin for co-infections
  • tetracycline drops in eyes of newborns
39
Q

Difference of neisseria meningitidis

A

-spread via aerosol transmission and not via STD

40
Q

Physical appearance of neisseria meningitidis

A

-gonococcus, but also has a polysaccharide capsule

41
Q

Clinical presentation of neisseria meningitidis

A
  • invades bloodstream, meningococcemia
  • presents as purpura and small hemorrhages as blood vessels become permeable
  • toxic effects of LOS, soluble PG
42
Q

Involvement of meninges of neisseria meningitidis

A
  • acute headache, vomiting, stiff neck
  • disoriented, lethargic
  • coma, death
  • PMNL found in CSF, BS permeability
  • brain covered with purulent exudate
  • progress to DIC and circulatory collapse, meningococcal septicemia
43
Q

Epidemiology of neisseria meningitidis

A
  • transient or resident flora in 10%
  • pilin modification with phosphatidylgylcerol disrupts micro colony of Nm
  • spread via respiratory droplets
44
Q

Treatment of widespread neisseria meningitidis

A

-prophylaxis is necessary in epidemic settings

45
Q

Pathogenesis of neisseria meningitidis

A
  • like gonococcus(pili, prot I,II,III, LOS)
  • antiphagocytic polysaccharide capsule
  • antigen B is sialylated, much more disguised than the others
  • special pili attach to BBB endothelial cells and recruit junctional complexes
  • additional adhesins
46
Q

Vaccines of neisseria meningitidis

A
  • ACWY conjugate vaccine

- 2 NmB vaccines

47
Q

Medical treatment for neisseria meningitidis

A
  • 3rd generation Cephlasporin
  • initial broad spectrum with vancomycin
  • acyclovir if herpes present
  • Rifampin or 3rd generation Ceph for prophylaxis
  • high dose Cipro
48
Q

Description of Moraxella catarrhalis, a type of Neisseria

A
  • 50% carrier rate in school age
  • opportunistic sinusitis, bronchitis, pneumonia
  • present as otitis media in children
  • COPD problems
  • B lactamases production
49
Q

Treatment of Moraxella Catarrhalis

A
  • 3rd generation Ceph

- Ciproxin

Micro-Bacteria (32 decks)

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