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
What do spirochaetes have to do and how is this achieved?
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
Define: obligate pathogen
can only survive and reproduce inside a host
27
Describe the structure of influenza and how is it spread
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
How does influenza evoke an immune response?
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
What does cross-protective mean?
Exposure to varient can induce resistance against other varients
30
Is influenza cross protective and what does this cause?
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
What does an influenza vaccine consist of?
4 or more types of purified H proteins made in tissue culture or eggs
32
How are new viral strains created?
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