STIs and Emerging Infectious Diseases Flashcards

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1
Q

What are the 3 major STIs we study? (hint - bacterial infections)
How are they spread?

A

Chlamydia
Gonorrhoea
Syphilis

Spread directly from person-to-person with no animal reservoir

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2
Q

What disease is caused by Neisseria gonorrhoeae?
Traits of bacteria (3 traits)
Contact of what tissue type is needed for transmission?

A

Gonorrhoea

Gram -ve coccus; Diplococci in samples of discharge
Non-motile
Poor survival outside the human host but can be grown in pure culture

Intimate mucosal contact needed for transmission

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3
Q

Gonorrhoea symptoms? (2 gender specific symptoms)

A

Male - Thick urethral discharge; Pain on urination
Female - Vaginal discharge

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4
Q

What occurs in up to 50% of Gonorrhoea infected females?
Without treatment what can this lead to?

A

May be asymptomatic or have mild symptoms

No treatment can lead to infertility, transmission to baby during birth etc.

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5
Q

What is the key virulence factor of Neisseria gonorrhoeae?
Why is it key? (hint - mucosal surfaces)
What happens to importance of certain virulence factors as infection goes on?

A

Surface proteins and structures involved in adhesion and invasion of epithelial cells lining urethra/vagina

Good adhesion essential for a mucosal pathogen to prevent being dislodged by urine

Certain virulence factors become more important than others depending on infection stage

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6
Q

What is molecular mimicry? (hint - sialylation)

A

LPS is modified by attaching sialic acid to it so that it “looks” like host tissue to the immune system; Immune response not provoked

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7
Q

What is antigenic variation? (hint - gonococci)

A

Many surface proteins are highly immunogenic
Gonococci can produce hypervariable sequence variants that make it difficult for the immune system to mount an effective response

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8
Q

What is the method of antigenic variation in Pilin (pilE) gene

A

Partial sequence homology between the silent pilS loci and expressed pilE gene

This allows RecA-mediated recombination to occur, giving rise to a novel PilE variant protein by gene-conversion

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9
Q

What are the threats of asymptomatic carriers and resistant strains of gonorrhoea?

A

Asymptomatic carriers are major reservoirs of infection in the human population
Major problem with multi-drug resistant gonorrhoea; Possibility it becomes untreatable

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10
Q

What disease is caused by Treponema pallidum?
What type of bacterium is this?
- What shape?
Characteristics of growth and infection? (3 characteristics)

A

Causes Syphilis

Treponema pallidum is a spirocahaete; Spiral shape

Fragile and slow growing bacterium
Infection requires intimate sexual contact
Infection is chronic

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11
Q

Why is Syphilis a confusing disease to diagnose?

A

Has many symptoms which can be varied and easily confused with other disease

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12
Q

What are the 3 early stages of syphilis the disease can fluctuate between
- Mild or severe symptoms?
Final stage of syphilis?
- Mild or severe symptoms?
- How long for this to occur?

A

Early stages include:
- Primary
- Secondary
- Latent
These have milder symptoms

Late stage is Tertiary stage
More severe symptoms
Occurs after many years (5-50 years)

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13
Q

How does T. pallidum survive in host long-term? (5 ways)

A

Lack of endo- exotoxins
Invasion of “immune-privileged” tissues
Ability to maintain infection with few organisms
Lack of surface antigens
Low iron requirements and ability to obtain sequestered iron

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14
Q

T. pallidum survival - Lack of endo- and exotoxins (hint - LPS)

A

T. pallidum lacks LPS (endotoxin in Gram -ve outer membrane
This mean attachment of T. pallidum doesn’t harm target cell

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15
Q

T. pallidum survival - Invasion of “immune-privileged” tissues (hint - surveillance)

A

T. pallidum penetrates a broad variety of tissues, including “immune-privileged” tissues where there is less surveillance from innate immunity

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16
Q

T. pallidum survival - Ability to maintain infection with few organisms (hint - failure to trigger)

A

T. pallidum exploits its slow growth to survive in tissues
By maintaining infection with few organisms in distanced anatomical sites , T. pallidum may prevent its clearance by failing to trigger the host’s immune response, which may require “critical antigenic mass”

17
Q

T. pallidum survival - Lack of surface antigens (hint- rare) (hint 2 - host interactions)

A

T. pallidum only has rare integral proteins in outer membrane
- 1% of number in E. coli outer membrane
However these rare proteins are important in interactions with host

18
Q

T. pallidum survival - Low iron requirements and ability to obtain sequestered (removed) iron (3 points)

A

T. pallidum may acquire iron from host proteins
May also overcome iron sequestration by using enzymes that need metals other than iron
Lacks electron transport chain (made from iron using enzymes), decreasing overall iron demand

19
Q

Main treatment for T. pallidum in which little resistance has developed for?
Why are high drug levels required for several weeks?

A

Penicillin

Slow growing bacterium so high drug level needs to be maintained

20
Q

What type of parasite is the Chlamydia bacterium?
- Wall?
What is the life cycle? (hint - 2 functionally distinct cell forms)

A

Obligate intracellular parasite; Wall-less

Elementary Body (EB) - Survives outside of host cells and initiates infection

Reticulate Body (RB) - Differentiate from the EB and is responsible for intracellular growth

21
Q

Male and Female symptoms of Chlamydia?
- Which is more often asymptomatic?

A

Male:
- Thin, watery urethral discharge
- Pain on urination
- Can be asymptomatic

Women:
- Cervix infection
- Urethritis
- Infertility and ectopic pregnancy
- Very often asymptomatic

22
Q

Why is screening of Chlamydia important?
What are some treatments of Chlamydia? (hint - Wall-less)

A

Screening is important due to often asymptomatic infection

Chlamydia are insensitive to β-lactam antibiotics; No peptidoglycan
Alternatives include tetra-/doxycycline, but these have side effects

23
Q

What factors result in the constant change of prevalence and patterns of infectious diseases? (3 factors)
These factors can result in changes in identification of pathogens. What does this cause? (hint - “new”

A

Changes in:
- Pathogen
- Environment
- Host population

Change sin identification can cause an existing pathogen to be identified as “new”

24
Q

What are factors responsible for Emergence and Re-emergence of pathogens (5 factors)
- Look at reasoning for each

A

Globalisation and environmental change
New ways of growing and handling food
Natural disasters and breakdowns in public health
Changes in pathogens
Recognition of “new” pathogens

25
Q

What was originally thought to cause gastric ulcers (3 things)
What did early gastric ulcer treatments do?
- Symptomatic relief or cure?
What bacteria was discovered to cause stomach ulcers?

A

Diet, stress and hereditary factors

Early treatments inhibited secretion of excess stomach acid
- Symptomatic relief but ulcers were not cured

Caused by Helicobacter pylori

26
Q

Traits of Helicobacter pylori? (4 traits)
What does it produce to survive?

A

Gram -ve spiral shaped bacterium
Found in only humans
Small genome; Typical of highly adapted bacterium
Microaerophilic; Cultivates at very low O2 and CO2 concentrations

Produces highly active urease enzyme, protecting against stomach acid

27
Q

Method of Helicobacter pylori pathogenesis
How does this form stomach ulcers?

A

Essentially forms a bubble micro environment with little urea so it can survive

Results in degradation of mucosal layer in stomach; Stomach acid can degrade stomach lining and form ulcers

28
Q

What is encoded by Helicobacter pylori pathogenicity island? (2 things)
What do each of them do?
What does cagA do?
- Type of protein?

A

Island encodes vacuolating cytotoxin (VacA) and a type IV secretion system (T4SS)

VacA - Pore forming toxin
T4SS - Secretes toxins

CagA is an effector protein that remodels host cell cytoskeleton; Impacts signalling pathways and makes cell do what the bacteria wants

29
Q

What are the 3 outcomes of Helicobacter pylori infection? (hint - differently located ulcers)

A

Duodenal ulcer (stomach bottom)
Gastric ulcer (stomach top)
Mild/mixed chronic gastritis

30
Q

How is Helicobacter pylori treated? (hint - 3 compounds)
- Length of treatment?

A

Combination of 2 antibiotics as well as drug to stop stomach aid production
Given for 1-2 weeks

31
Q

Since 1950s Helicobacter pylori infections have decreased and rates of esophageal cancer and gastroesophageal reflux disease (GERD) have increased. What does this mean about Helicobacter pylori?

A

Helicobacter pylori may protect against these diseases; Could be better to not cure patients with Helicobacter pylori

32
Q

What disease does Legionella pneumophila cause?
Traits of Legionella pneumophila? (3 traits)
Where is it common and how does it survive here? (hint - amoebae)

A

Legionaries’ disease

Gram -ve bacteria
Motile with polar flagella
Very specific nutritional requirements

Common in water bodies; Survives by entering amoebae and growing intracellularly

33
Q

What immune cell in humans is similar to amoebae?
How does Legionella pneumophila utilise this?

A

Macrophages

Legionella pneumophila grows inside macrophages

34
Q

How does Legionella pneumophila grow in macrophage?
What does this form?

A

Bacteria uses type IV secretion system (Dot/Icm) to deliver effector proteins into macrophage cytoplasm and prevent phagolysosome formation
Allows Legionella pneumophila to grow inside vacuole

Forms Legionella Containing Vacuole (LCV)

35
Q

How is Legionella pneumophila infection controlled and prevented? (3 ways)

A

Heating water to disinfect potential Legionella pneumophila
Biocides added to air conditioning systems to prevent Legionellae from growing
Chlorine dioxide treatment of water

36
Q

How is Legionella pneumophila treated? (2 types of compounds)

A

Fluoroquinolone antibiotics e.g. Ciprofloxacin
Macrolides e.g. Azithromycin