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(2020-21 BY2MI1) Microbiology II > Chlamydia > Flashcards

Chlamydia Flashcards

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1
Q

Show a phylogenetic overview of bacteria and where Chlamydia sp. fits in

A
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2
Q

State the order, family, genus and species of Chlamydia

A

Order- Chlamydiales

Family-Chlamydiaceae

Genus- Chlamydia

Species-C. trachomatis

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3
Q

How many species of chalmydia cause human infections?

A

Three species cause human infections

Others cause animal infections & zoonoses

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4
Q

What are the characteristics of Chlamydia?

A
  • Lack peptidoglycan
  • Cannot be filtered by 0.45µm filter
  • Contain BOTH DNA and RNA
  • Possess ribosomes
  • Make their own proteins, nucleic acids and lipids
  • Possess inner and outer membranes
  • Unique bacterial life cycle
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5
Q
A
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6
Q

What are the characteristics of chlamydias membrane?

A

Gram negative

Typical membrane structure

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7
Q

Bi-phasic life cycle: Extracellular form

A
  • EB – Elementary body
  • Small
  • 0.1-0.3µm
  • No metabolism
  • Highly resistant
  • Non-replicating
  • Spore-like
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8
Q

Bi-phasic life cycle: Intracellular form

A
  • RB – Reticulate Body
  • Larger
  • 1µm
  • Metabolically ACTIVE
  • Sensitive
  • Replicating
  • Fragile
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9
Q

Produce an image of Bi-phasic life cycle

A
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10
Q

Infection ‘Life’ Cycle – key events

A
  1. Infectiouse elementary body (EB) attaches and enters
  2. Phagosome formes
  3. EB to reticulate body (RB) differentiation
  4. Endosome forms
  5. RB multiplication
  6. RB to EB differentiation
  7. Inclusion maturation
  8. Inclusion exocytosis
  9. EBs released
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11
Q

Describe the Growth cycle

A

Phagosome fuses with intracellular membranes

  • Including golgi

C. trachomatis

  • Phagosome fuse to make one large INCLUSION
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12
Q

What are the characteristics of Chlamydia?

A

–Very small genome (<1000 kb) 25% of E. coli

–ca 600 genes

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13
Q

What does chlamydia require a host for?

A

–Energy

•Energy parasites

–Nutrients

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14
Q

Chlamydia – Endotoxin (LOS)

A
  • LipoOLIGOsaccharide
  • Common to all family members
  • Poor endotoxin activity

–Lipid A

–Core

•Smallest naturally occurring

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15
Q

C. trachomatis structure: – OMP1/MOMP

A
  • 40kDa trimer; porin function
  • Unique to each species
  • Abs to variable segments (VS1-4) can neutralise infectivity
  • Defines serological variants
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16
Q

C. trachomatis structure: OMP2

A
  • 60kDa Cysteine-rich protein
  • Structural stability in EB
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17
Q

C. trachomatis structure: POMPs (polymorphic OMPs)

A
  • 90kDa EB surface protein
  • Immune evasion?
18
Q

C. trachomatis structure: Inc proteins

A

–RB specific

–Fusion of inclusion membranes

  • nutrition?
  • Immune evasion?
19
Q

Describe a Chlamydial Infection

A
  • Efficient
  • Poorly understood

–Microfilament-dependent phagocytosis

–Receptor-mediated endocytosis

•No definitive host cell receptor

–GAG; heparan sulphate

•No definitive bacterial adhesin

–GAG; MOMP

Not all Chlamydia use the same mechanism

20
Q

C. trachomatis biovars & serovars

A

Biovar→Trachoma

Serovar (based on MOMP)→15

Biological features→Rel. non-invasive

Target→Mucosal epithelium

21
Q
A

Biovar→ Lymphogranuloma venereum (LGV)

Serovar (based on MOMP)→ 4

Biological features→Can cause systemic effects

Target→Mucosal epithelium

22
Q

Infections

A

•Limited target cell range

•Epithelial cells of mucous membranes

–Urethra

–Cervix

–Endometrium

–Fallopian tubes

–Anorectum

–Respiratory tract

–Conjunctiva

•Presentation

–Cell destruction

–Inflammation

23
Q

Pathogenesis: How does Infection lead to inflammation?

A

–cytokines from infected cells (LOS-dependent)

–Infiltration of

  • NØ (Limited)
  • lymphocytes, macrophages, plasma cells, eosinophils
24
Q

If untreated or not cleared, infection can lead to:

A

–chronic inflammation

–necrosis

–scarring & fibrosis

25
Q

What are the clinical conditions?

A

Serovars:

  • A, B, Ba, C
  • D-K
  • L1, L2, L2a, L2b, L3

Disease

  • Trachoma
  • GU tract disease
  • Lymphogranuloma venereum
26
Q

Infections Serovars D-K: How are they spread?

A

•Spread by sexual contact

–vaginal intercourse

–anal sex

–less commonly oral sex

•Spread during birth

–Infected mother transmission to non-infected neonate

27
Q

Male GTIs - urethritis

A
  • NGU - non-gonococcal
  • 7-14 day incubation period
  • Dysuria, white/grey discharge (esp. AM)
  • Less purulent than Gonococcal
28
Q

Epididymitis

A
  • Relatively non-specific presentation
  • Testicular pain, masses, inflammation
  • Can lead to obstruction of sperm collecting tubes and infertility
  • Formal diagnosis required
29
Q

Name Female Reproductive tract infections

A
  • Lower GT is prime chlamydial target
  • Cervicitis

–Dysuria

–Soreness

–Discharge

–Asymptomatic

  • Serovars D-K (esp. E)
  • Urethritis
  • Ascending infections
30
Q

Describe Pelvic Inflammatory Disease

A
  • Infection of uterus, fallopian tubes and adjacent pelvic structures
  • Ascending infection
  • Inflammation of uterine lining (endometritis) & fallopian tubes (salpingitis)
  • Asymptomatic ó severe salpingitis
  • Tubal blockage and infertility
31
Q

Describe Infections LGV

A

•Lymphogranuloma venereum biovar

–Serovars L1, L2, L2a and L3

•Causes systemic effects

–Lymphadenopathy

–Inguinal buboes

–Elephantiasis

•Rel scarce STD

32
Q

Describe C. trachomatis epidemiology

A

•Infections can be asymptomatic in a majority of cases

–Varied estimates

•Can lead to

–Sexually active reservoir of infection

•Women are more often asymptomatic

–Often diagnosed after attending clinic with partner

33
Q

C. trachomatis epidemiology stats

A

•Most common sexually transmitted bacterial pathogen

–D-K

•2017 in US

–1.7 million new cases (500 cases per 100,000)

–Underestimate (prob 4+ million) and rising!

  • 200,228 new UK cases in 2014 (46% of all STI in UK)
  • Peak incidence - late teens – early 20s
  • LGV - on the increase in US and Europe
34
Q

C. trachomatis epidemiology – US 2017 data

A
35
Q

Explain the Hosts defence

A

•Innate & Adaptive

–insufficient for clearance

–-> persistence

•Abs

–IgA, G, M BUT no lasting protection

•Cell-mediated immunity

–CD8 Tc exert some protection

•IFN-γ

–indoleamine 2,3-dioxygenase

–iNOS

–decrease transferrin receptor (iron limitation)

36
Q

Describe Host defence - evasion

A

•Intracellular growth

–protects from Ab & complement

•Down-regulation of MHC I

•Inhibition

–phagolysosome fusion

–Apoptosis of host cell

•Chlamydia can infect MØ

–induce apoptosis in T cells

•reduced cell-mediated immunity

37
Q

Diagnosis: Likelihood of infection

A

•Likelihood of infection

–consider symptoms

–age of patient (<25)

–sexual activity

–numbers of partners

•Sampling

38
Q

Diagnosis: Sampling affected area, Culture, Immuno-fluorescence, Enzyme Immuno-Assay, NAATs

A

•Sampling affected area

–Do no harm (endometrial swabs may carry infection higher)

–Non-invasive methods preferred (esp. in men) though not always suitable

•Culture

–Isolation & growth in lab, ID of inclusions

–Highly specific, rel. insensitive

•Immuno-fluorescence

–test for anti-chlamydial Abs (usually against EBs)

•Enzyme Immuno-Assay

–Microplate peptide-based assays to measure anti-chlamydial Abs

•NAATs- nucleic acid amplification tests

–Sensitive, specific, few false positives (e.g.PCR)

39
Q

Therapy

A

•Genital Infection

–Oral tetracycline or doxycycline

•course of antibiotics

–Single dose azithromycin

•ensures compliance

•Complicated infections (e.g. PID)

–Compound, multi-dose therapy

  • Clindamycin (i.v.) plus gentamicin (i.v./i.m.)
  • Cefoxitin (i.v.) + doxycycline (oral/i.v.)
40
Q

Management & Prevention

A

•Partner check

–essential given high rate of asymptomatic carriers

•Prevention

–Abstinence

•Especially whilst receiving treatment

–Barrier protection

41
Q

Remember

A
  • Most bacterial infections of reproductive tract are STDs
  • Most often affects women
  • Women suffer most
  • There’s no effective female-controlled barrier

(2020-21 BY2MI1) Microbiology II (16 decks)

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