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MICROBIOLOGY II > Lecture 9 - Chlamydia > Flashcards

Lecture 9 - Chlamydia Flashcards

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Biology 101 flashcards
1
Q

What are two genera

A

Chlamydia - c.trochomatis - human pathogens
Chlamydophila - contain two human pathogens c.psittaci (birds), c.pneumoniae (if think have cold or flu may have infection)

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2
Q

What does c abortus do

A

Case spontaneous in sheep

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3
Q

Name some strand characteristics that chlamydia have that make it more virus like

A

No peptidoglycan
Cannot be filtered by 0.45um filter (most bacteria 1um in length)
Contain both DNA and RNA
Own ribosomes very unlike virus
Make own proteins, nucleus acid and lipids ( nt reading upon cell)
Possess inner and outer membrane

MUST LIVE WITHIN CELL TO SURVIVE

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4
Q

What is strange that doesnt have peptidoglycan

A

Has machinery to make it but doesn’t have it

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5
Q

Does chylamida have LPS or LOS

A

LOS

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6
Q

Desrcribe the life cycle of chyladia

A

BIPHASIC

Extracellular form and intracellular form

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7
Q

Describe extracellular form and compare to intracellular

A

E - have elementary body EB whereas Intra has reticulate body (RB)
E is small whereas I is larger
E 0.1-0.3 I- 1um
E - no metabolism I - Metbaolically active
E - highly resistant, non replicating. I - Senstiive, replicating.
E - spore like I - fragile

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8
Q

Why does it not matter is RB is sensitive

A

Live in cell at this tim - nice environment

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9
Q

How do chlamydia replicate

A

Binary fission

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10
Q

Describe life cycle part 1

A

EB bind cell

Be contained and survive within phagosome vesicles as RB. Divide inside vesicle (called inclusion)

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11
Q

Life cycle part 2 (back to EB)

A

Reorganised into EB
Inclusion contain EB and RB
COntinued reorganisation
Extrusion of mass of EB by reverse endocytosis

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12
Q

Describe lifecycle in hours from EB to EB release

A

3hrs have EB in cell. Organism need to condense DNA to replicate
At 9hrs organism dividing
15 hrs Incluson body got bigger and lots of membrane. Organism need membrane to expand inclusion as organism keep dividing
40 hrs fewer RB more EB some intermediate bodies start to condense dna so can EB again
Lytic release - burst cell open like lytic viruses

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13
Q

Describe inclusion of c trochomatis

A

Phagosome fuse to make one large inclusion (lots of membrane )

Stain with iodine see huge spot (incluson body full of it)

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14
Q

How many genes does chlamydia have

A

600 genes, approx 1/4 of ecoli
Parasitic so dont need big genome

Require host for energy - energy parasites . Nutrients

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15
Q

What is interesting about LPS of chlamydia

A

SMALLEST NAUTRALLY OCCURING LPS
Only lipid A anchor and key sugars - same to family so use antibodies to identify all chlamydia as all have sameebdotoxin

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16
Q

Why do we not know a lot about structure of chlamydia

A

Need to see condensed form to replicating form

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17
Q

What OMP do for chla

A

Form porin - allow it to get what it needs from cell

Variability or protection so antibodies may not be able to bind and protect as MOMP Aldo on infectious form

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18
Q

What gives structure to c tromachtic

A

Cysteine rich - disulphides bridges - no need or peptidoglycan

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19
Q

Why is typical suggestion for why something is hugely variable

A

Immune evasion

20
Q

What are inc proteins

A

In inclusion membranes - allow us to do nutrition and parasitising. Also immune evasion - preevent lysosomes fusing with phagosome - avoid killing

RB SPECIFIC

21
Q

What is a biovar

A

Biological varient - behave different biologically

Trachoma

Lymphogranuloma (LGV)

22
Q

What is serovar

A

Based on MOMP
Variation of serum so different antibody response
Use antibody to bind to organisms and differentiate them.

E..g antibody 1 bind to this serovar etc
15 and 4 are serovars

23
Q

What are biological features of two biovars of c trochomatis

A

Trochoma - serovar 15 -
- Relatively non invasive

Lymphogranuloma venereum (LGV) - serovar 4- 
CAUSE SYSTEMIC EFFECTS
24
Q

What is target for c trochomatis biovars

A

Mucosal epitheliaum for both

25
Q

What little do we know about chylamdial infection mechanisms

A

Efficient
No efinitive host cell receptor - use GAG complex sugars coming off proteins called heparan sulphates e.g. CD44 on HUMAN CELLS

We know MOMP on bacterial cell has some role of adhesion.

Use cytoskeleton to be uptaken
Different uptake mechanism for each chylamdia

26
Q

Why is persisting form troublesome

A
  • inhibit lysosome fusion
  • inhibit cell death mechanisms. Just sit inside cell not replicating.

AS NOT REPLICATING ANTIBIOTICS NEED ORGANISM TO REPLICATE TO DESTROY IT.

27
Q

Where can you find infections of chlamydia and what are 2 key presentations

A 
- urethra
Cervix 
Endometrium
Fallopian, 
Anorectum
Respiratory tract 
Conjunctiva

Present via inflammation and cell death

28
Q

How is pathogenesis of chlamydia an issue

A

Relatively uncontrolled inflammation
Cytokines from LOS
Infiltration of nueutrohils and other immune cells

Try to prevent fibrosis from chronic inflammation - loss of tissue function. Can also get necrosis

29
Q

What are the serovars and their associated disease

A

A,B,Ba,C - trachoma - eye infection
D-K - GU (genital urinary) tract disease
L1,L2,L2a,L2b,L3 - lymphogranuloma venereum

30
Q

How are serovars D-k Spread

A

Spread by sexual contact

  • vaginal intercourse
  • anal sex
  • less commonly oral sex
31
Q

For male GTI - urethritis

A 
If discharge is yellow gonococcal 
NGU - non gonoccos like urethritis - if discharge grey/white especially in the morning 
Dysuria - pain on urination (NGU) 
Less purulent than gonococcal 
7-14 dy incubation period
32
Q

Describe epididymitis infection

A

Relatively non specific presentation
Testicular pain, masses, inflammation
Can lead to obstruction of sperm collecting tubes and VERY rearley infetility
Formal confirmation required. Symptoms not enough to diagnose

33
Q

IN female reproductive tract infections

A 
Harbour ascending infections better than men - route to other big organs 
- cervicitis - cervical inflammation 
- dysuria 
Soreness
Discharge 
Asymptomatic (primarily)

Serovars D-K (especially E)

Can get urethritis - less common in women

34
Q

Describe pelvic inflammatory disease

A

Infection of uterus, fallopian tubes and adjacent pelvic structures
Ascending infection
Inflammation of uterine lining (endometritis) S F fallopian tubes (salpingitis)

Can go from asymptomatic to sever salpingitis
Tubul blockage and infertility

35
Q

As LGv is more invasive, as well as Mucosa what else does it efffect

A

Secondary lymphoid tissues - inflammation of lymph nodes - stop fluid drainin due to blockage so swell up as buboes and ultimately elephantiasis

36
Q

What does it mean if people are asymptomatic

A

Sexually active reservoir of infection

Women often diagnosed from partner check from boyfriend

37
Q

How many mil new cases are in us each year

A

1.5 mil 2011
8% increase on 2010 estimated actually 4+ million

Peak incidence later teens early 20s

38
Q

Where is LGV on increase

A

US and Europe

39
Q

What defences are there for chlamydia

A

Innate and adaptive - not enough to clear it. Persist in body
Will get antibodies but will not protect from repeat infection - can be common. Get IgA and IgG and IgM,

Cell mediated immunity - T cell CD8 Tc - some protection

IFNy - see other flashcard for more info

40
Q

What is main defence against chla

CONTROL BUT NOT CLEAR

A

Indoleamine 2,3-dioxygenase - break down tryptophan - so bacteria cannot use it to

Nitric oxide synthase anther defence, catabolise arginine to create nitrous oxide (iNOS)

Can also decrease transferrin receptor (iron limitation)

41
Q

How does chlamydia evade

A

Hide in cell. - antibodies and complement not touch bacteria

Down regulate MHC class I 
Inhibit phagolysosome fusion

CAN INFECT MACROPHAGES - induce apoptosis of T cells - reduced cell mediated immunity.

Get arthritis or athersclerosis - due to chalamydia being hidden in macs and been delivered there

42
Q

What are risk factors for infections (also how it diagnosed)

A 
Lots of partners 
Unprpotected sex 
Age of patient <25) 
Sexual activity 
Numbers of partners

Diagnose via above and taking a sample

43
Q

What are tests that can be used to diagnose

A

Sampling affected area - swabs. BUT can drive infection further

To detect:
- culture - isolation and growth in lab, ID of inclusions but relatively insensitive

  • can use antibodies against EB’s - good for eye infections (flourescent)
  • can use ELISA - look for antibodies present - challenge is may have antibodies because have respiratory infection - wont tell you what route we get infection.
  • PCR!!!!! THIS METHOD IS USED AS SENSITIVE, SPECFIC, FEW FALSE POSTIVE.
44
Q

WHAT THERAPIES ARE AVAILABLE

A

EASY TO TREAT:
Genital infection - oral tetracycline or doxycycline - course of antibiotics
OR single dose azithromycin (ensures compliance - need to abstain from sex for seven days and finish course of antibiotics)

HARDER TO TREAT - CHRONIC DISEASES E.G. PELVIC INFLAMMATORY DISEASE - PID) as dependant on compliance.

  • need intravascular and intramuscular injections of antibiotics
  • compound therapy - multiple antibiotics for long periods of time.
  • clindamycin (i.v) plus gentamicin (i.v./i.m.)
  • Cefotoxitin (i.v.) + doxycycline (oral/i.v.)
45
Q

What is management and protection for chlamydia

A

Partner check - essential given high rate of asymptomatic carriers

Prevention - abstinence, especially when receiving treatments, barrier protection.

46
Q

Points to remember

A

Most bacterial infection of reproductive tract are STDs
Most affect women
Women suffer most
Theres no effective female controlled barrier - more on males - take power away from women

MICROBIOLOGY II (9 decks)

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