Pathogens Flashcards

1
Q

What is an infectious disease?

A

Caused by a pathogenic microorganism such as bacteria, viruses, parasites or fungi, the diseases can be spread directly or indirectly from one person to another
Infection is the largest cause of illness worldwide and one of the largest contributors to global mortality

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2
Q

Why don’t microorganisms call disease?

A

We have tolerance to most of the microbes.
Not all microbes are pathogens.
We have a commensal relationship with some microbes

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3
Q

What are some benefits of the normal flora?

A

Prevents pathogen colonisation
- by physically competing with pathogens for the environment

Antagonises other bacteria
- metabolites produced may kill pathogenic bacteria

Gut microbes make vitamins
- major source of vitamin k2

Make compounds
- nitrite from nitrate
- short chain fatty acids

Effects immune signalling molecules
- microbial signals help dampen immune response

If disrupted can lead to overgrowth of a pathogen
- eg. in the prescription of strong broad spectrum antibiotics

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4
Q

What is commensal bacteria?

A

Commensals are those types of microbes that reside on either surface of the body or at mucosa without harming human health.
The microbes living in harmony with human mostly consist of bacteria which are 10 times more than the cells present in our body.

Commensal bacteria supply the host with essential nutrients and defend the host against opportunistic pathogens. They are involved in the development of the intestinal architecture and immunomodulatory processes.

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5
Q

Why is it good to have a large diversity of commensal bacteria?

A

A high diversity increases the fight between type of bacteria, to help control the growth of infectious disease.

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6
Q

What are the main characteristics of a pathogenic microbe?

A
  • Must be present in every case of the disease
  • Must be isolated from the host and grown in pure culture
  • Must be reproduced when a pure culture is introduced into a non-diseased, susceptible host
  • Microbe must be removable from an experimentally infected host

Must meet all criteria
Theory designed by Robert Koch who discovered germ theory: microbes cause diseases

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7
Q

How can humans become in contact with pathogenic microorganisms?

A

Droplets
- Coughs and sneezes –> eg cold and flu

Skin contact
- e.g. Athletes food, fungal infections

Sexual transmission
- e.g. Herpes, HIV

Direct inoculation
- Insect bites
- Trauma
- Needle prick
- e.g. Malaria, Hepatitis B

Vertical transmission
- Trans-placental
- Perinatal
- Postnatal (milk)
- Germline
- e.g. Hepatitis B

Contaminated food
- e.g. E coli, Campylobacter

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8
Q

What are the differences between a bacteria cell and a human cell?

A

Bacteria
- has a cell wall
- doesn’t have a nucleus, DNA disposition
- has a single chromosome, free in cytoplasm
- has plasmids –> small particles of circular DNA
- has a flagellum which can be identified by immune cells

The differences in characteristics allow bacteria to be identified by immune cells and killed. Means doesn’t attack human cells.

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9
Q

How is bacteria classified?

A

Classification depends on many factors such as
- Staining –> Gram positive and gram negative
- Shape –> Cocci and Bacilli
- Respiration –> Aerobic and anaerobic metabolism
- Shape/ reproduction –> Clusters, chains/ pairs, sporing, non-sporing

Also genus and species

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10
Q

What are the main differences between gram positive and gram negative bacteria?

A

Classification depends on the structure of the cell wall.
Gram positive
- One thick peptidoglycan layer
- Lipid bilayer
- Blue colour when staining

Gram negative
- Two thinner peptidoglycan layers
- Has lipopolysaccharides –> structures that can be identified by immune cells
- Red/ pink colour when staining due to reacting to lipopolysaccharides

Can be identified by staining

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11
Q

What bacteria has lipopolysaccharides?

A

Gram-negative bacteria
Can be identified by immune cells
Turns staining red/pink

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12
Q

Why does respiration type vary in different bacteria

A

Due to oxygen availability
E.g. in the small intestine where oxygen levels are higher, there is a higher abundance of aerobic respiratory bacteria.
Whereas in the large intestine, where oxygen levels are lower, there is a higher abundance of anaerobic bacteria.

The same happens in the mouth, some sites such as close to the teeth or sub mucosa, anaerobic bacteria is more prominent than aerobic.

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13
Q

How does bacteria undergo respiration?

A

Similar to human respiration

  • Uses glucose or fibre, to produce energy

Some species use glucose and release pyruvate where then is used in either aerobic or anaerobic glycolysis.

Anaerobic:
- Glucose –> pyruvate –> acetyl-CoA –> TCA cycle –> electron transport chain
- then with oxygen –> 38 ATP, CO2 and H20
- with inorganic compounds (e.g. NO3, SO4 etc) –> 34 ATP, NH3, H2S
Can produce energy without oxygen using metabolic ions/ other sources of electrons.
Can produce ammonia to balance pH.
Depends on the bacteria, some bacteria has the capacity to use metabolic ions.
E.g using dietary nitrate to produce nitrite (along with 3 oxygen molecules/ 3 electrons) –> bacteria found in mouth and gut. Cannot be achieved through enzymes, an example of a commensal relationship –> feeding bacteria with a compound the body cannot use, and they produce a compound we can use –> can be used to form nitric oxide.
This process produces energy (ATP) for themselves as they are using electrons

Anaerobic:
- Glucose –> pyruvate –> lactate –> NH3 –> 2 ATP + acids, alcohols etc (incomplete breakdown products).
- Lactate can be used by nitrate reducing bacteria to produce ammonia (acid-base reaction) which can also help balance salivary pH

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14
Q

How does bacteria use nitrate?

A

Aerobic respiration
Can produce energy without oxygen using metabolic ions/ other sources of electrons.
Can produce ammonia to balance pH –> e.g. Saliva pH (around 7)
Depends on the bacteria, some bacteria has the capacity to use metabolic ions.
E.g using dietary nitrate to produce nitrite (along with 3 oxygen molecules/ 3 electrons) –> bacteria found in mouth and gut. Cannot be achieved through enzymes, an example of a commensal relationship –> feeding bacteria with a compound the body cannot use, and they produce a compound we can use –> can be used to form nitric oxide

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15
Q

Describe aerobic respiration pathways in bacteria

A

Anaerobic:
- Glucose –> pyruvate –> acetyl-CoA –> TCA cycle –> electron transport chain
- then with oxygen –> 38 ATP, CO2 and H20
- with inorganic compounds (e.g. NO3, SO4 etc) –> 34 ATP, NH3, H2S
Can produce energy without oxygen using metabolic ions/ other sources of electrons.
Can produce ammonia to balance pH.
Depends on the bacteria, some bacteria has the capacity to use metabolic ions.
E.g using dietary nitrate to produce nitrite (along with 3 oxygen molecules/ 3 electrons) –> bacteria found in mouth and gut. Cannot be achieved through enzymes, an example of a commensal relationship –> feeding bacteria with a compound the body cannot use, and they produce a compound we can use –> can be used to form nitric oxide.
This process produces energy (ATP) for themselves as they are using electrons

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16
Q

Describe the anaerobic respiration pathway of bacteria

A

Anaerobic:
- Glucose –> pyruvate –> lactate –> NH3 –> 2 ATP + acids, alcohols etc (incomplete breakdown products).
- Lactate can be used by nitrate reducing bacteria to produce ammonia (acid-base reaction) which can also help balance salivary pH

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17
Q

How does bacteria cause disease?

A

Adhesion pili
- Adheres to different parts of the body, where they grow and damage tissue/ organ leading to infection
- Immune cells do not respond
- May require antibiotics

Exotoxins
- Cause infections by releasing endogenous molecules, called exotoxins
- Occurs in gram-positive bacteria
- Toxic molecules release –> serious infection if not reversed
- In some cases, if they become chronic, can be life threatening

Endotoxins
- Compounds from gram-negative bacteria
- Less toxic than exotoxins due to it occurring when bacteria die
- Lipopolysaccharides can cause damage in human cells, e.g. endothelial cells
- Can occur when taking antibiotics (side effect), when killing bacteria and some molecules are being released and can cause some damage
- Benefit still outweighs negative/ side effects

Aggressins:
- Molecules that are released from bacteria, can damage organs far from infection site

Immune damage
- Occurs in autoimmune disease
- Chronic inflammatory response can lead to damage
- Release proteins that are recognised by immune cells, but not supposed to be recognised. This stimulates the inflammatory response.
- Can cause organ damage, depending on the condition

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18
Q

What are endotoxins?

A
  • Compounds from gram-negative bacteria
  • Less toxic than exotoxins due to it occurring when bacteria die
  • Lipopolysaccharides can cause damage in human cells, e.g. endothelial cells
  • Can occur when taking antibiotics (side effect), when killing bacteria and some molecules are being released and can cause some damage
  • Benefit still outweighs negative/ side effects
  • Can be dangerous in those who are immunocompromised
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19
Q

What are exotoxins?

A
  • Cause infections by releasing endogenous molecules, called exotoxins
  • Occurs in gram-positive bacteria
  • Toxic molecules release –> serious infection if not reversed
  • In some cases, if they become chronic, can be life threatening
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20
Q

What are adhesion pili?

A
  • Cause infections by releasing endogenous molecules, called exotoxins
  • Occurs in gram-positive bacteria
  • Toxic molecules release –> serious infection if not reversed
  • In some cases, if they become chronic, can be life threatening
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21
Q

What is biofilm?

A

An aggregate of interactive bacteria attached to a solid surface or to each other, encased in a extracellular polysaccharide matrix
Formed by aerobic bacteria on the outside and anaerobic bacteria on the inside (take compounds from body tissue, e.g. proteins, sugar).
Can damage body tissues

Dental plaque biofilms where there first place bacteria were discovered –> main cause of peridontal disease

Biofilms can occur on air/water, water/oil, solid/water and solid/air interfaces

Cannot be removed by antibiotics as they don’t have the capacity to enter the biofilm, cannot enter the matrix to kill the bacteria. Must be removed mechanically –> dentist/ hygeinist

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22
Q

What are some examples of bacterial disease?

A

Tuberculosis
- Mycobacterium tuberculosis

Food poisoning
- Escherichia Coli
- Salmonella spp

Tooth decay (caries)
- Streptococcus mutans

Meningitis
- Streptococcus pneumonia

Tetnaus
- Clostridium teanii

Cholera
- Vibrio cholera

Sepsis
- Gram-negative bacteria

Anthrax
- Bacillus anthracsis

23
Q

How are viruses classified?

A
  • Nucleic acid
  • Arrangement of nucleic acid –> single or double strand
  • Structure of virus particle –> envelope or no envelope
  • Symmetry –> icosahedral, complex
24
Q

What is one of the main differences between bacteria and viruses?

A

Bacteria can survive outside of the host.
Viruses require a host to multiple, grow and survive

25
Q

What are the 3 categories of viruses?

A

DNA viruses
- can be single or double strand
- can replicate using the host transcription and translation machinery to replicate their own DNA

RNA viruses
- can be single or double strand
- Often use their on RNA polymerase in order to replicate their genome. Don’t reply on host machinery
- Can use host cell translation machinery
- e.g. COVID-19 –> double stranded, has it’s own machinery for replication

Retroviruses
- Single strand
- Convert RNA into DNA in the host cell
- Have a protein that the virus can recognise, binds to the protein on the cell membrane and infects the cell. The the virus uses the RNA to produce DNA and grow and replicate and then affect T-helper cells
- e.g. HIV

Depends on the genetic material the virus has as to what type it is

26
Q

Describe the anatomy of a virus

A

Designed to protect DNA material as much as they can.
Has an envelope –> formed by glycoproteins
Protein matrix
Nucleocapsid where they have the DNA or RNA molecule
Need a host cell to multiply and grow
Haemaglutanin 1-16 –> binds sialic acid on host cell
Neuraminidase 1-9 –> cleaves sialic acid bond, allowing virus spread

27
Q

How do viruses spread disease?

A

Attachment
- Virus bind to host cell receptor

Penetration
- Virus enters the cell

Uncoating
- Once in the cell, they open up and release all genetic material (capsid shed)

Replication
- Synthesis of viral mRNA (direct or via host machinery)
- Synthesis of viral protein for new capsids
- Synthesis of viral nucleic acid

Assembly
- Capsids form around replicated nucleic acid
- Form new molecules of virus and damage and kill infected cell

Release
- Release new molecules of virus and infect new cells
- Released by budding forming envelope or by cytolysis using no envelope

28
Q

What are some examples of viral diseases

A

Common cold
- Rhinovirus

Coronovirus
- Respiratory syncytial virus
- Parainfluenza

Influenza
–> Influenza B, Swine flu, Bird flu, ‘Aussie’ flu

Acquired immunodeficiency syndrome (AIDS)
- Human immunodeficiency virus

Shingles

Cold sores

Genital warts

Chicken pox

Hepatitis

Ebola Haemorrhagic Fever
- Ebolavirus spp

29
Q

Why is research more focus on bacteria rather than viruses?

A
  • Harder to identify viruses
  • More time consuming and expensive sequencing to identify viruses
30
Q

What is bacteriophage?

A

When viruses infect bacteria to help them stay alive

31
Q

What are the two basic structures of fungi?

A

Yeast –> unicellular, spherical or ovoid (tissue)
Mould –> multicellular, hyphae

Dimorphic fungi is capable of existing in both forms

32
Q

What is the criteria for pathogenic fungi?

A
  • Grow and live in higher temperature or up to 37’
  • Must be able to reach tissue they are going to infect –> e.g skin, oral mucosa, gut mucosa - anatomical barriers can prevent this
  • Must overcome immune response –> not be killed by immune cells. A lot of immune cells can identify these pathogens and kill them before they cause an infection, so to be pathogenic they must overcome this response
33
Q

Are fungal infections common in humans?

A

Not in healthy humans.
However in immunosuppressed/ immunocompromised individuals it is one of the most challenging form of infection, because not all cases respond to anti-fungal treatments and approaches.

34
Q

What are the different forms of fungal disease?

A

Superficial mycoses:
- Yeast infections of the mucosa (thrush) –> can occur in the mouth after dental implant
- Dermatophyte infections of the skin (ringworm)

Subcutaneous mycoses:
- Subcutaneous tissue, traumatic implant of environmental fungi
- Chronic disease, tissue destruction and formation of sinuses
- e.g. Sporotrichosis ‘rose gardener’s disease’

Systemic (deep) mycoses:
- Often fatal, respiratory acquisition
- e.g. Histoplasmosis

35
Q

What are prions?

A

Transmissible, untreatable and fatal brain diseases of mammals. From animals to humans - causing serious neurological disorders
e.g. Mad cow disease

Mis-folded abnormal prion proteins invading lymphatic tissues e.g tonsils, lymphatic areas of the gut and the spleen.
Can travel in the nerves from the gut to the spinal cord and brain (autonomic nervous system) and can cause neurological disorders
- Psychiatric and behavioural symptoms
- Persistent pain in lower limbs
- Unsteadiness develops and cognition becomes affected
- Neurodegenerative due to damage in the brain from the presence of the proteins
- Death usually within 14 months

36
Q

What is protoza?

A

Parasites that require a host to multiply and survive
Unicellular
e.g Cryptosporidum, Plasmodium (malaria), Toxoplasma gondii (toxoplasmosis)

37
Q

What are Helminths?

A

Parasites/ microbes that do not need host to multiply and survive.
Multicellular
e.g. Tapeworms, Nematodes (tricuris trichure, whipworm)

38
Q

What is the transmission of parasitic infections?

A
  • Food
  • Water –> toxoplasmosis
  • Animal transmission –> mosquitos transmit malaria from infected people to non-infected people’s blood
39
Q

What are antimicrobials?
Types?

A

Main treatment for bacterial infections (antibiotics)

Bactericidal
- Kill bacteria by destroying it’s cell wall
- Target cell wall synthesis (e.g. penicillin, beta-lactams)

Bacteriostatic
- Don’t kill the bacteria, just prevent it’s growth

40
Q

What are the main target sites of antibiotics?

A

Nucleic acid synthesis inhibitors –> stop synthesis of DNA
- e.g. Quinolones
- Bacteriostatic

Cell wall synthesis –> destroy cell wall of bacteria
- e.g. Penicillin
- Bactericidal

Metabolic pathways (PABA-folate) –> stop metabolic pathway of bacteria, down regulate synthesis of folic acid. Stop capacity to multiply
- e.g. sulfonamides
- Bacteriostatic

Cell membrane function –> prevent synthesis of cell membranes and slow down synthesis of proteins that form it
- Bacteriostatic

41
Q

What is the main pathway of bactericidal antibiotics?

A

Cell wall synthesis

Providing molecules that bind to the cell wall of bacteria and destroy it and therefore killing the bacteria.
This also speeds up and increases the immune response as the immune response can identify some particles of intracellular bacteria due to being exposed by the broken down cell wall. The immune cells then are activated and increase the immune function.

42
Q

What type of bacteria is penicillin used for?

A

Gram-positive bacteria
- because penicillin is capable to attach to cell wall and change its permeability. The gradient of ions changes between intracellular and extracellular which kills the bacteria.

Not affective in killing gram-negative bacteria as it isn’t very efficient in going pass the lipopolysaccharides.

Useful to use penicillin when cause of infection is known. If not known then a wide spectrum antibiotic may be prescribed

43
Q

What is difference between narrow and broad-spectrum antibiotics?

A

Narrow-spectrum antibiotics –> are more specific and are only active against certain groups or strains of bacteria
- cause of infection known

Broad-spectrum antibiotics –> inhibit a wider range of bacteria

44
Q

What can be used to treat gram-negative infections?

A

Tetracylines, macrolides or clindamycin –> can pass through cell wall and target plasmids. Bind to the plasmids and reduce their replication to help control/ slow bacterial growth

45
Q

Why are narrow-spectrum more likely/ preferred to prescribes, as of recently?

A

Due to antibiotic resistance.
Bacteria is starting to develop anti-microbial mechanisms quite quickly.
Narrow-spectrum affects a smaller group of bacteria.
Also a lot of bacteria in the body is not pathogenic and does not need to be killed. This can compromise some metabolic and physiological functions as bacteria is needed in the body to keep it healthy.

46
Q

Why are antibiotics not useful to treat viral infections?

A

Bacteria and viruses have very different structures and antibiotics are designed for the structure of bacteria.
Doesn’t have a cell wall like with bacteria, so wouldn’t work for bactericidal antibiotics.
Bacteriostatic antibiotics cannot enter through the envelope of the virus to kill the DNA material.
Once the virus has enter the cell and caused replication the antibiotic is not able to identify the pathogen.

47
Q

What increases the risk of antimicrobial resistance?

A
  • Emergency surgery
  • Routine surgery
  • Caesarean section
  • Chemotherapy
  • Organ transplants
  • Immunosuppression
  • Common bacteria infections
48
Q

What are some causes of antibiotic resistance?

A
  • Over-prescribing of antibiotics
  • Patients not finishing their treatment –> keep some bacteria alive which can lead to resistance
  • Over-use of antibiotics in livestock and fish farming
  • Poor infection control in hospital and clinics
  • Lack of hygiene and poor sanitation
  • Lack of new antibiotics being developed
49
Q

What is antibiotic resistance?

A

When bacteria change and become resistant to the antibiotics used to treat the infections they cause.

50
Q

What are the different approaches/ pathways of antibiotic resistance?

A
  1. Acquired. evolved an efflux pump (antibiotic enters the cell but its pumped out again). Develop this from expressing some resistant genes that produce proteins that can identify antibiotic and remove it from the bacteria.
  2. Reduced diffusion/ transport in to the cell. Some bacteria can change cell membranes to stop antibiotic function - change structure/ composition (type of proteins and lipids in the membrane)
  3. Acquired detoxification genes (antibiotic destroyed) Express genes that can reduce the activity of antibiotics and down-regulate their action.

4 Acquired transformation genes (antibiotic converted to a less toxic form) Antibiotic less effective and doesn’t harm/ destroy the bacteria. Antibiotic not destroyed just has a much weakened effect.

51
Q

How is antibiotic resistance spread?

A

Vertical gene transfer:
- Once bacteria express a resistant gene this can be passed to daughter cell

Horizontal gene transfer:
- Have the capacity to identify resistant genes from other microbes (e.g. fungi) and absorb the resistant gene and use it to express the protein that can reduce the activity of antibiotics and help them survive

52
Q

What is multi-drug resistant TB?
Different forms?

A

TB resistant to many antibiotics
Arises due to improper use of antibiotics
- administration of improper treatment regimens
- failure to ensure that patients complete the whole course of treatment e.g. areas with weak TB control programmes

3 emerging form:
- Drug resistant TB
- Multi-drug resistant TB
- Extensively drug resistant TB

High levels of MDRTB in eastern Europe and central Asia. In several of these countries, up to 32% of new cases and more than 50% of previously treated cases have MDRTB

450,000 people developed multi-drug resistant TB snd at least 180,000 deaths were caused by MDRTB in 2012.

53
Q

Which of the following characteristic is common to both bacteria and viruses?
A. Contain genetic material
B. Can be killed using antibiotics
C. Have a cell membrane
D. Have a protein coat
E Contain plasmids

A

A. Contain genetic material

54
Q

Antibiotics inhibiting folate mechanism are:
A. Bacteriostatic
B. Medium-spectrum
C. Bactericidal
D. More effective than penicillin
E Less effective than penicillin

A

A Bacteriostatic