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Micro > Lecture 10 > Flashcards

Lecture 10 Flashcards

1
Q

syphilis organism

A

Treponema Pallidum

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2
Q

Treponema Pallidum shape

A

long, very thin spirochete

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3
Q

Treponema Pallidum motility

A

endoflagella - within periplasm (3 at each end)

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4
Q

Treponema Pallidum covering

A

has glycosaminoglycan sheath surrounding whole cell
unusual envelope
-no LPS: very loosely anchored OM with cardiolipin in membrane -mostly IM lipoproteins; OM proteins very few

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5
Q

Treponema Pallidum culture

A

-cultivate in rabbit testes

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6
Q

Treponema Pallidum oxygen

A

has microaerophilic metabolism

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7
Q

Treponema Pallidum primary

A

ulcerated, defined papule at site of infection =
chancre; regional lymph nodes swell
-usually genital site, but 10-20% oral or anal or . . . -heals spontaneously, but organisms remain

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8
Q

Treponema Pallidum secondary

A

red maculopapular rash-anywhere on body, including soles and palms
condylomas-white warts in moist areas

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9
Q

Treponema Pallidum tertiary

A

lesions in tissues throughout the body (due to immune response, not bacteria)

  • skin: gummas
  • bones: porous, easily bent, fragile
  • heart: aorta swells, ruptures
  • liver
  • CNS: brain = general paresis; spine = tabes dorsalis
  • neurosyphilis is hard to diagnose, and may occur at 2o or 3o stage
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10
Q

Treponema Pallidum and infants

A

May also cross placenta to infect fetus in utero (few bact. do) -~20% abortion or stillbirth
-~80% congenital defects, which may not appear immediately
-Hutchinson’s triad: interstitial keratitis - blindness : VIII nerve deafness
: Hutchinson’s teeth
-also saddlenose, neural defects, bone deformation
after any stillbirth, mother should be tested for syphilis

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11
Q

Treponema Pallidum epidemiology

A
  • Exclusively human, exclusively STD
  • can artificially infect rabbits, but they never go beyond 1o stage
  • Contagious for first 3-5 years after infection, not thereafter -Incidence in US increasing from 2005 – now (10,000 / yr)
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12
Q

Treponema Pallidum pathogenesis

A
  • highly infectious (10 organisms)
  • hyaluronidase facilitates spread and invasion of tissues
  • rapid motility also a spread mechanism
  • few surface proteins means hiding from immune system - may explain long latent period
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13
Q

Treponema Pallidum control

A
  • includes finding and testing sexual contacts
  • can scrape chancres to look for spirochetes, but not if latent -Serologic Tests for Syphilis (STS) (aka VDRL)
  • Indirect: T. pallidum induces formation of “reagin” in host (IgM + IgA)
  • add cardiolipin to patient’s serum
  • if +, reagin causes cardiolipin to clump - lots of false positives (other infections)
  • Direct: Fluorescent Treponema Antibody (FTA) test
  • bind T. pallidum to slide and add serum from patient
  • add fluorescent anti-human 2o Ab to detect 1o Ab in serum
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14
Q

Treponema Pallidum treatment

A
  • treat with Penicillin G (0.003 U/ml): very sensitive -one i.m. injection for early disease (< 1 year)
  • 3 injections for later disease
  • in use since 1940 without resistance developing -before 1940 treatment was Salvorsan (arsenic paste)
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15
Q

Neisseria gonorrhea shape and stain

A

Gram neg, coffee-bean shaped diplococcus

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16
Q

Neisseria gonorrhea environment and metabolism

A
  • fastidious (grow on MTM or Chocolate blood)
  • better with selective media (vanco, colistin, etc.)
  • aerobic, but prefer 5% CO2 (candle jar)
  • cytochrome c oxidase positive
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17
Q

Neisseria gonorrhea symptoms in general

A
  • Invades mucus membranes of UGT, rectum, eye and throat
  • proctitis (fem usu from vagina, male usu from anal sex) -pharyngitis (oral sex)
  • arthritis (esp of thumbs), dermatitis (rare)
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18
Q

Neisseria gonorrhea in males

A

-urethritis: painful urination, drip of pus from urethra -40% asymptomatic

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19
Q

Neisseria gonorrhea in females

A
  • urethritis, vaginitis
  • cervicitis, salpingitis, PID, peritonitis
  • Fallopian tube scarring, sterility (15% after 1 infection, 80% after 3)
  • 60% asymptomatic
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20
Q

Neisseria gonorrhea in infants

A

conjunctivitis from infected birth canal

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21
Q

Neisseria gonorrhea Epidemiological

A

-Exclusively a human STD
~75% of people who have sex with infected person get infected, ~50% after one encounter
-other co-infections contribute to symptoms (40% Chlamydia+)
-large number of asymptomatic carriers allow continued spread
-major problem in US (0.2 to 0.5% infection prevalence, 600,000 new cases / yr. reported)

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22
Q

Neisseria gonorrhea diagnosis

A

-diagnosis in males is by gram stain of urethral drip, in females by culture of cervical or vaginal swab

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23
Q

Neisseria gonorrhea adhesion

A
  • initial - pili:
  • pilus antigenic variation by recombinational “cassette switching” – very common, >2% of pop with variant pili
  • one promoter (pilE), many genes (pilS)
  • recombine new pilS gene or part of gene with pilE to make new pili (note the advantage of being diploid)
  • avoid host immune response -tight - Opa (Protein II)
  • named for opacity phenotype of colonies on petri dish -antigenic variation by DNA slippage of repeats
  • infections in females change Opas during menstrual cycle
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24
Q

Neisseria gonorrhea evasion

A
  • Por (Protein I): outer membrane porin, but also prevents phagolysosome fusion in host
  • Rmp (Protein III): Host Abs bind to it, prevents Ab binding to Por and LOS in outer membrane
  • IgA protease: IgA is the bactericidal, complement activating, first response Ab
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25
Q

Neisseria gonorrhea toxicity

A
  • LOS rather than LPS:
  • lipid A part is toxic as in all G- bacteria (endotoxin) -oligosaccharide mimics host cell membrane structure
  • NANA transferase to sialylate bacterial LOS with host NANA
  • PG released by autolysins at low temp or alkaline pH -typical PG inflammatory effects
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26
Q

Neisseria gonorrhea other virulence factors

A

-Fbp: scavenges Fe from human lactoferrin and transferrin

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27
Q

Neisseria gonorrhea Tx

A
  • resistance acquired very easily
  • PPNG produce β-lactamases, make penicillin less effective
  • Pan-resistant (to all available antibiotics) Ng from Sweden reported in 2011 – in North America 2012
  • preferred treatment is ceftriaxone (i.m.) or cefixime (oral) for the N.g. PLUS doxycycline or erythromycin (not doxy in pregnancy) for Chlamydial co-infections
  • must locate and treat sexual contacts, too (expedited partner therapy with cefixime)
  • tetracycline drops in eyes of newborns (used to use AgNO3)
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28
Q

N. Meningitidis structure

A 
Antiphagocytic capsule (about 12 types)
B type with sialic acid very hard to detect
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29
Q

Where does N. meningitidis first attack?

A

Blood stream

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30
Q

How does N. meningitidis first present?

A

Purpura (75%)
Small hemorrhages
In response to LOS

31
Q

What are the second and third infections associated with N. meningitides?

A
  1. Meningitis

3. DIC and circulatory collapse (Waterhouse-Friderichsen syndrome)

32
Q

When does N. meningitides become virulent?

A

Pilin modification

Phosphatidylglycerol disrupts colonies and allows organisms to spread

33
Q

How does N. meningitidis spread?

A

Respiratory droplets

34
Q

Most epidemics of N. meningitidis are due to what?

A

Specific capsular antigen type (B, C, Y in North America)

35
Q

How does N. meningitidis breach BBB?

A

Special pili recruit tight junctions and open

36
Q

How can you treat N. meningitidis and why?

A

PCN G
BBB is permeable at this point
3rd gen Cephalosporins if allergy to PCN

37
Q

What is prophylactic treatment for N. meningitidis in epidemic setting?

A

Rifampin

38
Q

Moraxella catarrhalis belongs to what family?

A

Neisseria

39
Q

Moraxella catarrhalis causes what?

A 
Opportunistic
OM in children
Sinusitis
Bronchitis
Pneumonia
40
Q

Moraxella catarrhalis in adults specifically causes what?

A

Exacerbates COPD symptoms

41
Q

Moraxella catarrhalis treatment and why?

A

Most have beta-lactamases

Treat with 3rd gen cephalosporins or cipro

42
Q

Chlamydia trachomatis metabolism

A

Obligate intracellular parasite

lacks many metabolic genes, steals ATP from host

43
Q

What is distinct about Chlamydia trachomatis cell wall?

A

Lacks MurNAc

but still has PBPs

44
Q

Chlamydia trachomatis mostly resemble what, GramPos or GramNeg?

A

GramNeg

45
Q

What are the two life cycles of Chlamydia trachomatis?

A

Elementary bodies-infective (small)

Reticulate bodies-replicative (large)

46
Q

Chlamydia trachomatis enters the cell during what phase of life cycle?

A

Elementary (this is the infective stage)

47
Q

What are the five manifestations of Chlamydia trachomatis?

A
  1. Trachoma (eyes)
  2. Inclusion conjunctivitis (eyes, newborns)
  3. Neonatal pneumonia
  4. Chlamydia
  5. Latent infection (lymphogranuloma venereum)
48
Q

How does one get trachoma?

A 
Infected birth canal 
Or vectors (such as from flies)
49
Q

Trachoma symptoms?

A 
Pus in eyes
Keratinized corneas (pannus formation)
Corneal obscuration
Eyelid involvement (trichiasis)
May lead to eventual blindness
50
Q

Trachoma Tx?

A

Maybe azithromycin

51
Q

How does one get inclusion conjunctivitis?

A

Mostly from infected birth canal

52
Q

What can be sequela to inclusion conjunctivitis?

A

Respiratory problems

“Neonatal pneumonia” can be secondary

53
Q

Male chlamydia symptoms?

A
  • nongonococcal urethritis!
  • epididymitis!
  • prostatitis!
  • usually self-limiting!
54
Q

Female chlamydia symptoms?

A

!-urethritis!
! !-cervicitis!
! !-salpingitis / PID (invasive)!

55
Q

What is the most common cause of PID?

A

Chlamydia

56
Q

Latent infection caused by Chlamydia trachomatis symptoms (lymphogranuloma venereum)?

A

May begin as a small abscess that heals quickly
Can get inguinal buboes which can turn black
Associated with fever and pain

57
Q

What is a long term complication of lymphogranumoa venereum?

A

May form fibrous restrictions:

Can lead to elephantiasis or bowel obstruction

58
Q

Trachoma has what epidemiological implication?

A

Leading cause of infectious blindness in the world

59
Q

Chlamydia trachomatis mechanism for invading cells (during elementary body phase)?

A

Bind host receptors
Induce pathogen-mediated endocytosis
(T3SS effectors remodel cytoskeleton)

60
Q

How does Chlamydia trachomatis survive in a cell?

A

Inhibit phagolysosome fusion

61
Q

How does Chlamydia trachomatis induce inflammation once residing in a cell?

A

Induce cytokines

Especially IL-1

62
Q

Why are vaccines ineffective against Chlamydia trachomatis?

A

Intracellular location

63
Q

What is most common test for Chlamydia trachomatis?

A

PCR

64
Q

How can you prevent corneal keratinization with trachoma?

A

Pull out eyelashes

65
Q

Treatment for Chlamydia trachomatis?

A

One does azithromycin

tetracycline or macrolides also work

66
Q

Chlamydia pneumoniae is found in what percentage of population?

A

Almost 100%

Most asymptomatic

67
Q

Chlamydia pneumoniae may be implicated in what diseases?

A 
Atherosclerosis 
CAD
Asthma
Stroke
Alzheimers
68
Q

Chlamydia psittaci causes what disease?

A

Parrot fever

69
Q

Parrot fever symptoms?

A

Acute, severe pneumonia and sepsis

Patchy, well-defined lung involvement

70
Q

How is Chlamydia psittaci transmitted?

A

Always via psittacine birds

71
Q

Chlamydia psittaci treatment?

A

Tetracycline

72
Q

Rickettsiae shape and stain

A

Small rods

GramNeg

73
Q

Rickettsiae metabolism

A

Obligate intracellular parasite (cultured in yolk sac of eggs)

74
Q

What are the four groups of Rickettsiae?

A
  1. Typhus
  2. Spotted fever
  3. Ehrlichia/anaplasma
  4. Coxiella burnetti (actually genetically related to Legionella)

Micro (13 decks)

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