Pathogens Flashcards

1
Q

What are pathogens?

A

An organism that causes disease- some are not pathogenic all the time and infect individuals the same way

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2
Q

Name and define the types of pathogens

A

Primary pathogens – cause disease frequently, rarely found in healthy individuals. Directly and quickly attacks a host using toxins or other mechanisms

Opportunistic pathogens – have potential to cause disease, but only when host is in a particular (weakened) state– considered to be pathobiont

Commensal – can colonise and persist on/within a host, but does not cause overt disease. May help to exclude primary/opportunistic pathogens- this is host specific, so pathogens of one host can be commensal in others

Amphibiosis – process by which microbe can be either pathogen or symbiotic depending on other factors

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3
Q

Define: pathogenic potential

A

the capacity of an organism to cause disease

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4
Q

Define: Pathobiont

A

only harmful when host has particular genetic/acquired traits.

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5
Q

What does infection by pathogens depend on?

A

Seesaw between microbial and host factors:
- some organisms are more likely to be pathogenic than others- have specialised mechanisms to help them infect and survive
- Host must be susceptible to infection- reduced via host defence, vaccination, lockdowns to prevent spread

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6
Q

Define: microbiome and how is divided?

A

total microbial content of an environment (usually a living host), which are complex and help to resist invading microbes

Commonly divided into regions/habitats e.g. human gut microbiome, skin, plant leaf and root

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7
Q

How do microbiomes resist invading microbes and how are they disturbed?

A

Resist via most niches occupied and lots of competition for scarce resources

Disturbance from antibiotics, surgery, implants, medical devices

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8
Q

What alterations may lead to disease + examples?

A
  • Transfer of bacterium from one site to another e.g. Staphylococcus aureus:
    normal on skin due to dry environment = slow growth
    Tranfer to internal site = faster growth + toxin production as environment is wetter, nutrient rich and faster growth
  • Loss of competitor microbes
    Clostridiodes difficile
    problems after antibiotic treatment, causes damage to intestine- treated with microbial transplant to replace lost microbes
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9
Q

What are the functions of the human microbiome?

A
  • Make vitamins that humans can’t
  • Alters how body processes drugs- important for chemotherapy
  • Make signals that interact with brains and body
    Hunger and nutrition
    Insulin signalling- recent data = artificial sweetners poision bacteria and alter insulin signalling + low-calorie sweetners alter bacterial gene expression to more pathogenic states
  • Immunomodulation- trains and controls immunity + inflammation
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10
Q

What do primary pathogens have to compete with?

A

Resident microbes

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11
Q

Name + define 4 examples of primary pathogens

A

Vibrio cholerae = gut bacterial pathogen causing cholera
Bacillus anthracis = non-motile, gram + and forms spores
Borrelia burgdorferi + treponema pallidum = spirochaete bacteria causing Lymes or syphillis
Influenza = virus- non cellular obligate intracellular pathogen causing respiratory disease- flu

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12
Q

How does V. cholerae cause disease?

A
  1. Bacteria ingested in contaminated water
  2. Bind to gut lining and secrete 2 part cholera toxin (AB)
  3. 5 B subunits deliver A subunit to cytoplasm and toxin disrupts cell signalling
  4. Large amounts of cAMP are produced by gut- bacteria metabolise this and replicate
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13
Q

What does V.cholerae cause and how is it treated?

A

Lots of diarrhoea = loss of water and salts can result in death
Treatment = oral and IV rehydration

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14
Q

What is the cholera toxin carried on and how was this acquired?

A

integrated bacteriophage acquired by viral infection

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15
Q

What is bacillus anthracis most commonely found?

A

soils, animal skins and furs in tropical areas

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16
Q

What 3 main diseases does anthrax cause and what does this result in?

A
  • Cutaneous- woolsorters disease = spores enter via skin break and cause leathery black lesion
  • Gastrointestinal- diarrhoea, sepsis and swelling in lymph nodes + abdomen = can cause death
  • Inhalation/pulmonary = flu-like symptoms then death due to respiratory failure caused by toxins
17
Q

Describe some anthrax virulence factors

A
  • Cells have protective capsules = polymer of D-glutamic acid to form negatively charged shell that helps to resist phagocytosis
  • 2 toxins which both have a protective antigen that carries them into host cells:
    EF causes fluid accumulation by making more cAMP
    LF mechanisms not understood
  • All of these are carries on plasmids which can be shared with other bacteria
18
Q

Why is anthrax so successful?

A

found in arid, tropical environments with poor, dry sandy soils
1. Grazing animal dies and carcass enriches local soil boosting plant growth
2. Plants grow = attracts grazers
3. Spores or live cells transmitted to new hosts during grazing

19
Q

What are spirochaetes?

A

Gram negative, long helical bacteria that have an internal flagella between inner and outer membranes

20
Q

Why are spirochaetes considered to be stealthy pathogens?

A

Move via corkscrew motion of whole cell – allows access to body sites by burrowing through tight junctions between mammalian cells

Internal flagellum and low number of surface proteins makes them hard for immune system to spot – they can also bind host plasminogen

Very slow growth

21
Q

Name 2 diseases that spirochaetes cause

A
  1. Syphilis
  2. Lymes
22
Q

Describe the stages of syphilis

A
  1. Primary lesion upon 1st infection- painless ulcer resolves
  2. Secondary lesions can occur on hands, feet, mouth or vagina
  3. Latent stage can last for many years with no symptoms
  4. Tertiary stage- gummas, neurological + heart problems
  5. Congenital- transmission to baby
23
Q

How is lyme disease transmitted and what does it result in?

A

Transmitted by deer tick bites resulting in a bullseye rash
can cause:
Slow growth in joints, periodic fevers, rashes due to exposure of bacteria
Low-level inflammation can lead to joint damage, autoimmunity

24
Q

What is a privileged site?

A

an area of the body that does not typically elicit strong immune responses

25
Q

What do spirochaetes have to do and how is this achieved?

A

They have to cross internal barriers to privileged sites = CNS and joints- these are protected by epithelia where cells are held together by tight junctions
- these barriers need to be crossed but it is unclear and how this is achieved

26
Q

Define: obligate pathogen

A

can only survive and reproduce inside a host

27
Q

Describe the structure of influenza and how is it spread

A

Carries no machinery for protein production – just a genome, envelope and few proteins

Spread via aerosol directly, or contact with contaminated surfaces

Crosses species barriers – pigs, birds, humans

Yearly epidemics as segmented genome allows easy exchange of genetic material between flu viruses

28
Q

How does influenza evoke an immune response?

A

2 main antigens- H and N, but there are variants :

  • H proteins are required for cell attachment to promote infection
  • N protein cleaves sialic acids from cell surface = promotes envelope assembly and coating

Both proteins are strongly antigenic which evokes good immune responses

29
Q

What does cross-protective mean?

A

Exposure to varient can induce resistance against other varients

30
Q

Is influenza cross protective and what does this cause?

A

No many varients are not cross-protective and therefore a new vaccine is need each year
- due to long production time, the vaccine produced are best guesses to match the likely new strains from Southern hemisphere winter

31
Q

What does an influenza vaccine consist of?

A

4 or more types of purified H proteins made in tissue culture or eggs

32
Q

How are new viral strains created?

A

Viral recombination creates new strains:

Flu viruses have RNA genomes split into 8 segments
There is a higher mutation rate for RNA replication than DNA – so small changes are common

Reassortment allows greater changes
- Shuffling of segments between viruses when a cell is infected with two or more different viruses
- New variants/combinations caused by packaging or segments from different “parents”

This can therefore occur anywhere wild viruses meet