Pathogen Case Studies Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

Why could STIs be easy to control?

A

As infection is linked to human social and sexual behaviour, we have more opportunity to stop infection (e.g. condoms) (it is difficult to control human behaviours however).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are 3 reasons to why STIs are increasing in numbers still?

A
  1. Use of pill has replaced barrier methods of contraception that help prevent spread of STIs.
  2. Change in public attitudes to sex – increased numbers of sexual partners in many western countries, as well as dating apps, leading to more opportunities for STIs to spread.
  3. Other factors: Problems of drug resistant strains of bacteria, poor attendance at STI clinics by some infected individuals, lack of appropriate sex education advice, introduction of Viagra has increased STIs in old people homes etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the 3 major bacterial STIs in the UK, the bacteria that causes it, and what is a common property of all of these bacteria?

A
  1. Gonorrhoea – Neisseria gonorroheae
  2. Syphilis – Treponema pallidum
  3. Chlamydia – Chlamydia trachomatis

> All of these bacteria are highly host-adapted strict pathogens and cannot survive long outside of the human body (non-commensal). They are spread directly from person-to-person with no animal reservoir.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are 5 general properties of Neisseria Gonorrhoeae?

A
  1. Gram negative (outer-membrane) coccus, characteristically seen as diplococci in samples of discharge (2 cells stuck together after cell division)
  2. Non-motile
  3. Humans are the only host: No animal reservoir. Transmission is directly from person-person
  4. Poor survival outside the human (can be grown as pure culture)
  5. Intimate mucosal contact is needed for transmission (vagina, penis, throat and rectal mucosa).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the symptoms of Gonorrhoea in a) Males b) Females?

A

a) Male: Thick urethral discharge.

b) Pain on urination Female: vaginal discharge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What can cause Gonorrhoea to lead to more serious complications and some examples?

A

> Up to 50% of infected females may be asymptomatic or only have mild initial symptoms. They may not seek treatment and this can lead to serious complications:

  1. Pelvic Inflammatory Disease (PID)
  2. Damage to fallopian tubes, leading to infertility
  3. Passed to baby at birth making them blind (why screens are needed on pregnant women)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the protein involved in the early and later stages of infection of Neisseria gonorrhoeae (for Gonorrhoea)

A
  1. Initial attachment through long ranged Pili (not high affinity but reach long distances)
  2. Outer membrane proteins mediate interment attachments
    a. Protein II- OM (Opacity protein) protein
    for intimate attachments
    b. Capsule- Helps resist phagocytosis
    c. Protein I- Outer membrane porin
    needed for survival in phagocytes
  3. Later stage of infection
    a. IgA protease- destroys secretory IgA
    b. Transferrin/ lactoferrin binding proteins-
    Fe uptake (won’t be a lot of iron present in
    sex mucosal surfaces)
    c. LPS/LOS- Inflammation at site of
    infection (pain)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Why are so many surface proteins on Neisseria gonorrhoeae involved in adhesion onto epithelial cells lining the urethra or vagina?

A

Good adhesion is essential for a mucosal pathogen in this environment to prevent being dislodged by urine flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the gonococcal strategy for evading the immune system?

A
  1. Molecular Mimicry
    >The LPS can be modified by attaching sialic acid residues (very common in human cells) to it (sialylation) so that it “looks” like host tissue to the immune system and so does not provoke an immune response.
  2. Antigenic variation
    >Many of the surface proteins (e.g. pilin PilE and PII) are highly immunogenic, but gonococci can continuously produce sequence variants (able to vary sequence of proteins so antibodies don’t recognise them) that make it difficult for the immune system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe how antigenic variation is present in the Pilin of Neisseria gonorrhoeae and how this is done

A

> The variable region of Pilin (section detected by antibodies and T-cells) varies in populations of Neisseria gonorrhoeae so is difficult for immune system to target.

> PilE encodes for the major subunit of Pilin. pilS is similar to PilE but sequence variation with many different copies with changed sequences.
PilE is expressed with different recombined silent genes (pilS genes).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why is tracing and treatment important for Gonorrhoea?

A

As asymptomatic carriers are major reservoirs of infection in the human population (up to 50% of females, and 10% of males)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What antibiotics is Neisseria gonorrhoeae a) resistant to b) resistance becoming more common to?

A

a) Penicillin and Fluoroquinolones

b) Cephalosporins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the morphology of Treponema Pallidum

A

Spiral with flagellum in periplasmic space.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What disease does Treponema Pallidum cause?

A

Syphilis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What disease does Neisseria gonorrhoeae cause?

A

Gonorrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the general properties of Treponema pallidum?

A
  1. Fragile
  2. Slow growing
  3. Poor survival outside host
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What phylum does Treponema pallidum belong to?

A

Spirochaetes due to spiral shape

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How is infection of Treponema pallidum caused and what are the mortality rates?

A

> Infection requires intimate sexual contact, and is aided by minute tissue abrasions that occur during sex

> Infection is CHRONIC and in untreated cases may last decades, with maybe 30-50% mortality.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the stages of Syphilis infection

A

Occurs over a very long time frame (Stages go from more localised to disseminated)

  1. Primary Syphilis (can jum straight to latent phase)
    >Chancre sores (short lived sores)
  2. Secondary Syphilis
    >Rash, fever, neuro symptoms
  3. Latent
    >No symptoms
    >Can go back and repeat secondary Syphilis many times.

§ First 3 are early syphilis (under a year)

  1. Tertiary stage
    >5-50 years
    >50% fatality.
    >Gumma (a nodule or tumour-like growth in organs), bone, cardiac, nerve disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are 5 ways T.pallidum survives in the host long-term?

A
  1. Lack of endo- and exotoxins
    >T. pallidum lacks LPS, the endotoxin found in the outer membranes of many Gram-negative bacteria. The attachment of T. pallidum to cells does not harm the cells.
  2. Invasion of “immune-privileged” tissues
    >Cells in CNS, eye, and placenta, where there is less surveillance by the host’s innate immune system.
  3. Ability to maintain infection with few organisms
    >Maintaining infection with very few organisms in anatomical sites distant from one another, T. pallidum may prevent its clearance by failing to trigger the host’s immune response, which was may require a “critical antigenic mass”.
  4. Lack of surface antigens
    >Only rare integral proteins in its outer membrane (less antigens)
  5. Low iron requirements, ability to obtain sequestered iron
    > may be able to acquire iron from host proteins. It may also overcome the iron sequestration problem by using enzymes that need metals other than iron as their cofactors.
    >Also it lacks an electron transport chain, which is made up of enzymes that use iron as a cofactor, which decreases its overall demand for iron.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is used to treat Syphilis and why is it difficult?

A

> Penicillin

> Because the bacterium is so slow growing it is essential that a high level of penicillin is maintained in the body for several weeks (to make sure all cells are dead); many people give up and keep the disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does Syphilis infection effect HIV infection?

A

Infection with syphilis makes it several times more likely that HIV infection occurs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the structure of Chlamydia and what issues does this cause?

A

Small wall-less bacteria (still gram negative) which are obligate intracellular parasites (cannot be cultured on agar in lab, cannot survive outside host cell- virus like)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What bacterium causes Chlamydia?

A

Chlamydia

25
Q

What two forms can Chlamydia be found in and what is their purpose?

A
  1. “Elementary body” (EB) – survives outside of host cells and initiates infection
  2. “Reticulate body” (RB) - Differentiates from the EB and is responsible for intracellular growth

Can differentiate between these many times.

26
Q

Describe the life cycle of Chlamydia in 4 steps

A
  1. EB (Elementary body) infects host cell
  2. EB differentiates to RB (Reticulate body) inside vacuole
  3. Grows inside vacuole, some differentiate back into EBs
  4. The ones back as EBs leave and infect other cells.
27
Q

What strains (serovars) of Chlamydia cause STIs?

A
  1. D,K – cause Urethritis (men) and Cervicitis (women) - STI
  2. L1-L3 – cause Lymphogranuloma venereum (LGV) – STI
28
Q

What are the symptoms of Chlamydia in a) Men b) Women?

A

a) Men
>Thin, watery urethral discharge
>Sometimes pain on urination
>Can be asymptomatic

b) Women
>Infection of the cervix
>Urethritis
>Infertility and ectopic pregnancy
>Very often asymptomatic

29
Q

Why are screening programmes important against Chlamydia?

A

Screening programmes are important because of the often asymptomatic nature of the infections

30
Q

Why can’t normal treatments be used for Chlamydia and what alternatives are used instead?

A
  1. Chlamydia are insensitive to beta-lactam antibiotics as they have no peptidoglycan.
  2. Have to use alternatives like Tetracycline/doxycycline or Azithromycin, which have some side-effects.
31
Q

Why are the prevalence and patterns of infectious diseases constantly changing?

A

Due to changes in the pathogen, the environment and/or the host population

32
Q

What are the reasons for the emergence of “new” pathogens and the re-emergence of “old” ones?

A
  1. Globalisation and environmental change.
    >Increased urbanisation in tropical countries has lead to massive increases in insect borne viral diseases
    >Clearing forests in Africa has led to the emergence of Ebola virus by new zoonotic transfer to humans (forcing the infectious agents into closer proximity to humans)
    >Climate change (global warming) allows vector borne diseases to spread into new areas.
    >Increased international travel and commerce
  2. New ways of growing and handling food.
    >Strains take advantage of modern high-volume meat production methods (less infection control and more infection between animals) and inadequate cooking (zoonotic transfer of pathogens)
  3. Natural disasters and breakdowns in public health.
    >Natural disasters, wars, inadequate take-up of vaccines (e.g. MMR).
  4. Changes in pathogens.
    >Development and spread of antibiotic resistance
    > High mutation rates in some viruses (HIV)
33
Q

What is the structure of Helicobacter Pylori (H. pylori)?

A

A Gram-negative spiral shaped bacterium, with a bundle of polar flagella (all at one end) with terminal “bulb”.

34
Q

What does H. pylori cause?

A
  1. Gastritis
  2. Gastric ulcers
  3. Duodenal ulcers
  4. Some types of gastric cancer
35
Q

What species is H. pylori found in?

A

Only found in humans

36
Q

What size genome does H. pylori have and what is this associated with?

A

Small genome, typical of a highly host adapted bacterium (usually the more host adapted, the smaller the genome as need less genes to survive in less of a range of environment)

37
Q

How is H. pylori transmitted?

A

Cannot grow outside a human host (no environmental reservoir) – transmitted person-to-person

38
Q

Why is H. pylori highly motile and chemotactic?

A

Highly motile and chemotactic due to polar flagella

39
Q

How does H. pylori survive the acidic pH of the stomach?

A

> Produces a highly active and abundant UREASE enzyme

> Urease protects against stomach acid, protects from acid by producing alkaline ammonium (Urea -> NH3/ ammonium (alkaline) + CO2)

40
Q

What are the 8 steps of pathogenesis of H. Pylori?

A
  1. Reaches mucus layer of stomach, bacteria senses nutrient gradient so know where epithelial cells are.
  2. Using polar flagella and aided by corkscrew shape, swims through mucus to reach epithelial cells lining stomach.
  3. Secrete urease converting urea (acidic) to ammonia (alkaline) creating a bubble of neutralised area protecting against gastric acid. (doesn’t diffuse away as mucus is viscous)
  4. Form a colony in neutralised bubble
  5. Produce enzyme (mucinase) which degrades mucus as a nutrient source generating gaps in mucus layer
  6. Stomach acid reaches epithelium and degrades lining of stomach.
  7. H. pylori also cause inflammation which also causes more pain.
  8. This damage can lead to genomic changes leading to cancer.
41
Q

How do H. Pylori use a) VacA b) Type IV secretion system?

A

a) VacA is a pore forming toxin
>Punch holes into membrane of epithelial cells to leak nutrients
>Can cause apoptosis of epithelial cells lining the stomach

b) Type IV secretion system
>Like a syringe that injects proteins into host cells, inject CagA which remodels host cell cytoskeleton and signalling pathways to change epithelial cell behavoiur to benefit bacteria.

42
Q

What are the three main outcomes of being infected with H. Pylori and what are the % of each?

A
  1. In 80% of cases no significant disease is caused after the mild/ mixed chronic gastritis.
  2. In 10-15% of cases, increased acid production and degrades mucus at the bottom of stomach causing Duodenal ulcer.
  3. In 2-5% of cases, at corpus (top) of stomach, low stomach acid production (no pain associated) leading to a gastric ulcer or cancer.
43
Q

How is infection with H. Pylori treated?

A

> For successful eradication, a combination of TWO antibiotics PLUS a drug to stop acid production (Proton pump inhibitor) given for 2 weeks and the proton pump inhibitor for years (90% successful)

> e.g. Amoxycillin + metronidazole + omeperazole

44
Q

What does evidence suggest H. Pylori effects are body for?

A

In some people H. pylori causes Gastric disease but in the 80% with no development of significant disease it seems to protect them against.

45
Q

What are the 8 key virulence factors of H. Pylori and their role?

A
  1. Flagella
    >Polar clusters of flagella allow of motility and chemotaxis to colonize under mucosa.
  2. Urease
    >Neutralize gastric acid by ammonia production
  3. Lipopolysaccharides
    >Adhere to host cells and cause inflammation
  4. Outer proteins
    >Adhere to host cell
  5. Exotoxins
    >Vacuolating toxin (vacA) causing gastric mucosal injury
  6. Secretory enzymes
    >Mucinase, protease, lipase leading to gastric mucosal injury
  7. Type IV secretion system
    >Pilli-like structure for injection of effectors.
  8. Effectors (cagA)
    >Actin remoddling, IL-8 induction, host cell growth and apoptosis inhibition.
46
Q

What are two examples of an unknown pathogen causing a disease?

A
  1. H. Pylori causing stomach ulcers
  2. Legionella pneumophilia causing Legionnaires’ Disease
47
Q

What does infection with Legionella pneumophilia cause?

A

Legionnaires’ Disease

48
Q

What was Legionella pneumophilia the first example of?

A

Legionella was a “new” genus of Gram-negative bacteria from the gamma sub-division of the proteobacteria.

49
Q

What are the general properties of Legionella pneumophilia?

A

Motile with polar flagella, and have fastidious nutritional requirements

50
Q

What type of agar does Legionella pneumophilia grow on?

A

Growth is best on “charcoal agar” which adsorbs toxic compounds and reactive oxygen species.

51
Q

What were the 6 steps of figuring out Legionella caused Legionnaire’s disease and how does this link to Koch’s Postulates?

A
  1. Got samples of patients lungs
  2. Observed under microscope.
  3. Cultured samples in eggs to grow bacteria
  4. Developed charcoal agar to grow pure culture
  5. Infected guineapigs (model organisms) from pure cultures which replicated the Legionnaire’s phenotype
    Re-isolate bacteria in agar culture and view on microscope

> Koch’s postulates, took pathogen from host, made pure culture, re-infected model organism which showed disease symptoms/ phenotypes, then isolated and grew the bacteria.

52
Q

How does Legionella pneumophilia grow?

A

It is very common in water bodies, both natural and man-made and survives by entering amoebae and growing intracellularly.

53
Q

What were the 4 main sources of Legionella pneumophilia?

A
  1. Water cooling towers
  2. Air-conditioning systems
  3. Shower-heads
  4. Windscreen wiper wash bottles in cars

All these sources create aerosols that spread the bacteria/amoebae

54
Q

As well as amoebae, what else can Legionella grow in and why?

A

It Is a bacterium that has evolved to survive being eaten by amoebae; very similar to macrophages so can hijack macrophages and not be targeted by immune system.

55
Q

How do Legionella grow in macrophages?

A

The bacteria use a type IV secretion system (Dot/Icm) to deliver effector proteins into the macrophage cytoplasm that prevent phagolysosome formation but instead allow them to replicate inside a vacuole forming the Legionella containing vacuole (LCV). Eventually macrophage bursts and Legionella spreads.

56
Q

What are 4 ways to avoid Legionella growing in water?

A
  1. Biocides can now be added to air-conditioning systems
  2. Chlorine dioxide treatment
  3. Heating water above 60°C inhibits growth
  4. Regularly turning on taps to flush out Legionella from pipes.
57
Q

What antibiotics are given to treat Legionnaires’ Disease?

A

For respiratory infections, fluoroquinolone antibiotics like ciprofloxacin, or macrolides like azithromycin are effective.

58
Q

How does Legionella pneumophila survive and replicate in macrophages? (extra knowledge from Mol Cell)

A

Legionella pneumophila can recruit rab1 to the cell surface to create an ER like compartment where it can replicate inside macrophages.