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Bacteriology Lectures > STO's and Neisseria meningitidis > Flashcards

STO's and Neisseria meningitidis Flashcards

1
Q

Treponema pallidum shape and visualization techniques

A

Thin spirochete

  • Visualized in fixed tissues by silver stain
  • Visualized live by dark field microscope

*Not visible using light microscopy

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2
Q

Treponema has a _____ that surrounds the whole cell

It is motile due to…..

A

It has a GAG sheath surrounding the whole cell

Motile due to endoflagella within periplasm (THREE at each end)

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3
Q

Treponema envelope composition

A
  • No LPS
  • Loosely anchored OM containing cardiolipin
  • Mostly IM lipoproteins (OM few)
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4
Q

Lab culture technique for treponema

A

Can’t culture in lab!

Cultivate in rabbit testes

*has microaerophilic metabolism

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5
Q

Primary treponema presentation

A
  • Chancre = Ulcerated defined papule at infection site
  • Regional lymph node swelling
  • heals spontaneously, but organisms remain
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6
Q

Secondary treponema presentation

A
  • Maculopapular rash anywhere on body (palms/soles)
  • Condylomas in moist areas
  • Heals spontaneously, recurs for 8 months, then latent for 20 years
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7
Q

How many patients progress to tertiary syphillis?

A

About 40%

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8
Q

Tertiary syphillis: where’s the lesion?

A

throughout the body

*due to immune response, not bacteria

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9
Q

How does tertiary treponema affect particular tissues?

A

Skin: gummas

Bones: porous, fragile

Heart: aorta swells, ruptures

Liver: ??

CNS: paresis in brain, tabes dorsalis in spinal cord

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10
Q

Neurosyphillis can occur…

A

during secondary or tertiary stages

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11
Q

Vertical transmission of treponema?

A

Yes, it can cross the placenta

  • 20% aborted, stillbirth
  • 80% congenital defects
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12
Q

What does congenital syphillis present as?

A

Hutchinson’s triad

  1. Interstitial keratitis (blindness)
  2. 8th nerve deafness
  3. Hutchinson’s teeth

*also saddlenose, cognitive deficits, and bone deformation

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13
Q

Treponema reservoirs and transmission?

A

Only human, only STD

(can artificially infect rabbits, but they don’t progress beyond the Primary stage

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14
Q

When is treponema contagious?

A

Only for the first 3-5 years

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15
Q

Who should be tested for syphilis?

A

High risk populations

Pregnant women at 28 weeks and at delivery

After any stillbirth

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16
Q

Pathogenic factors (4) for treponema

A

Highly infectious (10 organisms)

Hyaluronidase (facilitates spread and invasion)

Motility

Few surface proteins (hide from immune system)

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17
Q

______ lesions are full of treponema organisms

A

Primary and secondary

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18
Q

(General) control measures for treponema

A

ID sexual contacts

Scrape chancres (only if active infection, not latent)

Serologic testing

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19
Q

Indirect serologic tests for treponema

A

induce formation of reagin in host (IgM+IgA)

  • add cardiolipin to patients serum
  • If positive, the reagin will cause cardiolipin to clump
  • ****False positives possible***

FTA test (detect anti-treponema antibodies)

  • bind treponema to slide and add patient’s serum
  • add a fluorescent anti-human 2’ antibody to detect the 1’ antibody
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20
Q

Direct serological tests for treponema

A

FTA test (can also be indirect)

  1. Fix anti-treponema antibodies to slide, and add patients serum
  2. Add fluorescent anti-treponema antibodies to detect organisms
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21
Q

Syphilis Tx

A

Pen G (2.4 MU)

Early disease = One injection

Latent disease = Three injections

*Salvorsan (arsenic) was used before 1940

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22
Q

Neisseria gonorrhea organism shape and location (in cells)

A

Gram (-) , Coffee-bean shaped diplococcus

Intracellular and inside PMN’s

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23
Q

N. gonorrhea growth characteristics

A
  • Fastidious (grow on MTMor chocolate blood agar)……better with selective media (vanco,colistin)
  • Aerobic growth but prefers 5% CO2 (candle jar)
  • Cytochrome C oxidase ++
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24
Q

Ox+, Gram(-) diplococcus =

A

Neisseria

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25
Q

Neisseria genome

A

Two identical chromosomes (diploid) – never heterozygous

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26
Q

Neisseria invades what tissues?

What are the infections that this causes?

A

invades mucus membranes of the UGT, rectum, eye, throat

Proctitis, pharyngitis, arthritis, dermatitis (rare)

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27
Q

Male N. gonorrhea infections

A

Urethritis

*40% asymptomatic

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28
Q

N. gonorrhea female infections

A
  • Urethritis, vaginitis
  • Cervicitis, salpingitis, PID, peritonitis

–>> fallopian tube scarring and infertility (even if asymptomatic…60%)

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29
Q

Neonatal N. gonorrhea infection

A

Conjunctivitis

(from infected birth canal)

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30
Q

Animal carriers of N. gonorrhea

A

None. Exclusively human

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31
Q

Infection and coinfectino rates of N. gonorrhea

A

75% of people who sex an infected person (50% after one time)

40% coinfect with Chlamydia

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32
Q

N. gonorrhea diagnosis

A

Males = gram stain of urethral discharge

Females = culture of cervical/vaginal swab

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33
Q

N. gonorrhea virulence factors

A
  1. Pili
  2. Proteins 1-3
    1. Por
    2. Opa
    3. Rmp
  3. IgA protease
  4. LOS
  5. Peptidoglycan release
  6. Fbp
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34
Q

N. gonorrhea virulence factors for ATTACHMENT

A

pili (initial)

  • Antigenic variation via cassette switching – avoid host immune response
    • One promoter (PiliE), many genes (PiliS)
    • recombine new piliS gene or part of gene with piliE

OPA protein = “Protein 2” (tight attachment)

  • antigenic variation by DNA slippage of repeats
  • infections in females change Opas during menstrual cycles
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35
Q

N. gonorrhea virulence factors for EVASION (3)

A

Por = protein 1

  • Outer membrane porin
  • Prevents phagolysosome fusion

Rmp = protein 3

  • Prevents antibody binding to Por and LOS in the outer membrane

IgA protease

  • prevents complement activation
  • Stops IgA response (first-response Ab in mucus membranes)
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36
Q

N. gonorrhea virulence factors for TOXICITY (2)

A

Lipooligosaccharide (rather than LPS)

  • Lipid A = toxic in all Gram (-) bacteria (endotoxin)
  • Oligosaccharide mimics hist cell membrane structure
  • NANA transferase = sialylates bacterial LOS with host NANA

Peptidoglycan release by autolysins

  • At low temperature or alkaline pH
37
Q

“Other” N. gonorrhea virulence factor

A

Fbp

Scavenges iron from human lactoferrin and transferrin

38
Q

What is PPNG?

A

Penicillinase-producing N. gonnorhea

* produces beta-lactamases

39
Q

Other type of resistant gonorrhea?

A

Pan-resistant NG

**to ALL available antibiotics

40
Q

Tx for N. gonorrhea

A

Ceptriaxone (i.m.) + Cefixime (oral)

PLUS

Doxy or erythromycin for chlamydia co-infection

**NO DOXY DURING PREGNANCY

41
Q

Treat N. gonorrhea sexual partners with…

A

Cefixime

42
Q

Neonatal N. gonorrhea infection treatment?

A

Tetracycline drops (for conjunctivitis)

**no longer use AgNO3

43
Q

Neisseria meningitidis structure

A

Like the gonococcus, but has polysaccharide capsule

44
Q

Types of N. meningitidis

A

12 types

Common: A, B, C, Y, W135

45
Q

N. meningitidis initially invades ______, causing ________ (infection)

It presents as ________ and small hemorrhages. Why?

A

Invades bloodstream–> meningococcemia

Purpura (75%) – because blood vessels become more permeable in response to the toxic effects of LOS and soluble peptidoglycan

46
Q

15% of N. meningitidis cases involve

A

meninges (meningococcal meningitis)

  • acute headache, vomiting, stiff neck
47
Q

Cellular findings in meningococcal meningitis?

This may progress to…

A

PMN lymphocytes in CSF (d/t increased vascular permeability)

Brain covered in purulent exudate with PMNL’s and N. meningitidis

–> may progress to DIC and circulatory collapse = meningococcal septicemia

48
Q

N. meningitidis is ______ in 10% of people

A

resident flora

49
Q

N. meningitidis spread is helped by __________

A

pilin modification

–with phosphatidylglycerol

–disrupts microcolony and spreads the organism

50
Q

N. meningitidis is chiefly spread by

A

respiratory droplets, especially in crowded areas and with susceptible populations

51
Q

Common environments (examples) for spread of N. meningitidis

A

College dorms and military barracks

52
Q

Once N. meningitidis epidemic begins, there is a ____ carrier rate. This necessitates ________

A

80% carrier rate

Prophylaxis for control of epidemic

53
Q

Most N. meningitidis epidemics are due to…

A

specific capsular antigen types

54
Q

N. meningitidis virulence factors…

A

all of the ones from N. g.

PLUS

  1. Antiphagocytic polysaccharide capsule
    • Antigen B is sialylated = much more disguised
  2. Special Pili that attach to BBB and recruit junction complexes, depleting them in other areas of the BBB (increasing permeability)
  3. Additional Adhesins (in outer membrane)
55
Q

N. meningitidis vaccines

(current and newly approved)

A

NmA vaccine = general prophylaxis

ACWY conjugate vaccine = US use (dorms, army, etc)

NmB vaccines = recently approved

  • Bexsero = 3Nm proteins + PorA
  • Trumenba = 1 recombinant lipidated proteinfrom 2 NmB strains
56
Q

Preferred N. meningitidis treatment

A

3rd gen Ceph

(may include acyclovir too if CSF suggests herpes present (RBC/WBC)

57
Q

Initial treatment of N. meningitidis should be…

A

broad spectrum antibiotic

including Vancomycin (will penetrate BBB)

58
Q

_____ or ______ can be used for prophylactic N. meningitidis treatment in epidemic settings. Why these in particular?

A

Rifampin or 3rd gen Ceph

** they cross the BBB

**can also use high-dose ciprofloxacin

59
Q

Other Neisseria

(Carrier rate, infections in kids and adults, and Tx)

A

Moraxella catarrhalis

  • 50% carrier in school aged kids
  • infections = opportunistic sinusitis, bronchitis, PNA
  • May also present as Otitis Media (3rd most common cause)
  • Exacerbates COPD in adults (attach to ECM)
  • Produce BETA LACTAMASES = Treat wth Ceph3 or with Cipro (or not at all?)
60
Q

Chlamydia trachomatis organism, genome,and structure

A
  • Obligate intracellular parasite
  • Small genome (lacks metabolic genes, steals ATP from host)
  • Cell wall lacks MurNAC, but has PBP’s
    • Susceptible to Penicillin but not to lysozyme (PEN NOT USED TO TREAT)
61
Q

Chlamydia trachomatis has ___ serovariants, baed on ____

A

15 serovariants

based on LPS antigens

62
Q

Must cultivate Chlamydia trachomatis on ________

A

eukaryotic host cells

(embryonated chicken eggs, McCoy cells in monolayer tissue cultures, mouse brains)

63
Q

Two life cycle forms of Chlamydia trachomatis

A

Elementary bodies

  • .3um in diameter, electron dense nucleoid tough membrane (S-S)
  • INFECTIVE FORM (the form that enters cell)

Reticulate bodies

  • 1um diameter, diffuse EM staining, fragile (SH-HS), more ribosomes
  • REPLICATIVE FORM (the one that divides)
64
Q

Chlamydia trachomatis life cycle (7 steps)

A
  1. Entry
  2. Initial attachment (surface sugars), actin remodeling, induced uptake
  3. Vacuole
  4. Elementary body metabolism
  5. Develops into RB
  6. RB matures
  7. Release
65
Q

Eye infection of Chlamydia trachomatis

(Aquisition and symptoms/pathology)

A

Trachoma

  • infection at birth or early childhood via flies
  • mucopurulent discharge –> pannus forms (keratinized cornea)
  • Corneal obscuration and trichiasis
  • Permanent blindness

Tx = oral Azithromycin (mass trial showed reduced infective rate by 50%)

66
Q

Other eye infection of Chlamydia trachomatis (the less severe one)

(who does it infect, and possible complications)

A

Inclusion conjunctivitis

  • mostly in neonate (adult from self-innoculation of conjunctiva)
  • may be respiratory complications
67
Q

Chlamydia trachomatis neonatal (non-eye) infection

(Symptoms and Dx?)

A

Neonatal PNA

  • Shortness of breath
  • NO FEVER
  • suspect if infant has inclusion conjunctivitis
68
Q

STD version of Chlamydia trachomatis?

A

Chlamydia

69
Q

Male Chlamydia STD symptoms

A
  • non-gonococcal urethritis
  • epididymitis
  • prostatitis

(usually self-limiting)

70
Q

Female chlamydia STD symptoms

A
  • urethritis
  • cervicitis
  • salpingitis/PID (most common cause)

(**Fallopian scarring may lead to infertility or predispose to ectopic pregnancies – 10 fold increase in likelihood)

71
Q

Most common cause of acquired infertility in females?

A

Chlamydia induced PID

72
Q

Latent infection of Chlamydia trachomatis?

General infection timeline?

A

Lymphogranuloma venereum

(small abcess–> heals quickly –> inguinal buboes later)

**must Ddx from PLAGUE buboes

73
Q

Latent Chlamydia infection may become ______. This could lead to ______ or ______ due to fibrous restrictions of lymphatic system.

A

Chronic

elephantiasis or bowel obstruction

74
Q

Specific manifestation of latent Chlamydia depends on…

A

Serovar of the organism

75
Q

Probability of infection by sex with partner who is infected with Chlamydia trachomatis?

A

68%

76
Q

Most common Chlamydia trachomatis infections in North/South America and Europe?

What about Asia and Africa?

A

NA/SA/Eur = STD

Asia/Africa = Trachoma

77
Q

Why do we need to treat both epidemiological localizations of Chlamydia trachomatis the same?

A

They can cross-infect

78
Q

Chlamydia trachomatis infectiveness is caused by _______

A

Elementary Bodies

–binding to a host receptor and inducing Pathogen-mediated endocytosis

79
Q

_____ remodels the host cytoskeleton in Chlamydia trachomatis pathogenesis

A

T3SS

80
Q

Chlamydia inhibits ______ so it can proliferate intracellularly

A

phagolysosome fusion

81
Q

Chlamydia trachomatis induces _______

A

Cytokine (IL-1) production

82
Q

Chlamydia vaccine?

What is the preferred treatment? Prevention?

A

Vax = ineffective d/t intracellular location

Tx = Azithromycin (one dose oral)

  • Can also treat with Tetracycline or macrolides

Prevention = surgery or epilation for trichiasis to prevent keratinization of the cornea

** ID partners – expidited partner therapy, legal in 35 states

83
Q

C. pneumoniae may have originated as a _____ from what?

A

zoonosis from koalas

84
Q

C. pneumoniae infection rate

A

100%, but mostly asymptomatic

85
Q

C. pneumoniae may progres to….

A

Walking PNA (like mycoplasma)

86
Q

C. pneumoniae is found in ______, which suggests…

A

atherosclerotic plaques

suggests link to atherosclerosis and coronary artery disease

** also associated with asthma, stroke, and late-onset Alzheimer’s

87
Q

C. pneumoniae Tx

A

usually untreated

Tetracycline may help

88
Q

C. psittaci presentation, transmission, and Tx/control

A
  • Severe PNA, sepsis with patchy, well-defined lung involvement
  • Transmitted via contact with psittacine birds (bites or inhalation of dried feces)
  • Control with tetracycline and quarantine of imported birds

Bacteriology Lectures (14 decks)

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