Lecture 8 Flashcards

1
Q

Susceptible host

A

non-infected, non-immune at risk individual

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2
Q

risk

A

Travel to places which have high rates of certain infectious diseases
Unprotected sex
Pneumonia in air spaces in lung lungs. younger more at risk
Immune Senisence: Immune system becoming senile. Diminishing in its capacity with age.
Other illness
Immune deficiency
Other factors

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3
Q

Immune senisence

A

Immune system become senile/diminishing in its capacity with age

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4
Q

What are the possible areas where a pathogen could be caught?

A

Exogenous human to human transmission
endogenous infection (bulk of hospital infectious disaese. bacteria getting to wrong place in the body)
exogenous the environment
Exogenous zoonosis (from animal/other living entity)

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5
Q

Colonisation

A

similar to sub-clinical infection
different to normal body flora
(10x more bacteria living on you than there are cells in your body) -bacteria more unique than dna. Gut flora/bacteria mostly there to help you. if ruin (with antibiotics) can lead to problems
another species invades
20% are colonised with staflacoccus aures nose. never get disease.
1. no symptoms. +/- host immune response. potentially infectious

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6
Q

Primary Pathogens

A

isolation is always pathogenic

-gonorrhoea

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7
Q

Principle pathogen

A
isolation is usually pathogenic
cause infections in otherwise well people with intact defences
-TB
-cough, from sputum
-almost never just hanging around
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8
Q

Opportunistic pathogen

A

Cause infections only when defences are down

older or young people

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9
Q

Gonorrhea

A
Primary pathogen
most people illustrate symptoms
-can cause subclinical infection (more in woman) (esp. throat)
-treated as could be transmissable
Exogenous
Human to human 
risk associated behaviour
Does NOT live in the environment
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10
Q

Setting of infection

A

Infections can occur in the community or in healthcare settings
-community onset (cold/flu upper respiratory tract infections, chickenpox, diarohhea. common, generally pretty mild, no treatment required)
-community acquired (doesnt have to be community onset disease. staph aureas, colonised people has hip operation, gets infected with staph aureas, has been caught in hospital. illness only apparent becuase of hip operation)
-hospital acquired (
-hospital onset (healthcare associated)
nosocomial (health care associated)
Healthcare associated: not hospital required but is anything provokes/related to modern health care. dialisis machines at home, needles into arm blood comes out. opportunities for infection, as blood for a period of time is exposed to outside world, and access for germs to enter into blood. (blood stream infections are more common for people on dialisis than people who aren’t)
-related to environmental exposure.

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11
Q

What is the importance of health care associated infections?

A

often Preventable
-hand hygiene
is a very common complication of health care
kills people (hosts often sicker/older people
is often avoidable
costs NZ: 300 mil each year

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12
Q

What is the single most important activity that you need to do to reduce HAI?

A
hand hygiene
5x moments:
1. before patient contact
2. after patient contact (before going elsewhere)
3.
4.
5. after leaving patient environment
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13
Q

What are one of the large “at risk groups” for infectious diseases?

A

Health care workers

  • Noro virus
  • cough
  • protect via washing hands
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14
Q

Infection and disaese

A

to cause infections an organism must possess an array of factors that regulate interaction with the host
-infection:outcome of replication (something driving it to replicate and produce offspring)
the disease occurs when these factors damage the host and/or incite a substantial host immune response
Virulence factors=in bacteria

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15
Q

Virulence factors

A

in bacteria. usually proteins(sometimes carbs)
the genetic determinants that allow a pathogen to cause disease (interact and damage host cells)
-Adherence/Interaction (scaffolding strut on outside enabling bacteria to bind to human epithleial cells)-bacteria that cant interact themselves often cant cause disease
-Invasion (produce things to enable it to get into tissues)
-Immune evasion (as soon as bacteria interacts/damages human cell, immune system is activated, bacteria need to have some skills to avoid immune system)
-Toxins (proteins bacteria releases outside of themselves (exotoxins) which can damage human tissues)
Ecoli gets into bladder, must be able to bind to bladder cells (some strains cannot bind and therefore do not cause infection). Must be able to invade layers beneath outer lying cells via releasing alpha toxin which damaged bladder lining, enabling it to invoke new response and pain, difficulty with urination/possibly fever

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16
Q

How does a skin infection develop?

A

use virulence principles

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17
Q

Virulence

A

description of the capacity of the bacteria to cause disease

  • the capacity to cause disease in hosts with intact defences (highly virulent e.g. Staph aureaus - can causes disease without any invitation. Micobacterium TB- can causes disease in otherwise perfectly health human)
  • requires some breach of host defence(s)
  • commensal that rarely causes disease
  • commensal that “never” causes disease (low virulence)
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18
Q

Humans covered in bacteria

A

human flora
approx 5000 different species live in humans
1 quadrillion bacteria mostly in the gut (there are 100 trillion cells in the body)

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19
Q

Gut flora

A

anaerobic bacteria
enterobacteriaceae (E coli)
Enterococcus faecalis
non-uniform : germs in small intestine are different to germs in large intestine. germs in saliva have different properties to the germs under the gum
-organisms adapted to grow where oxygen levels are low, tolerate bile
help breakdown carbohydrates such as lactose

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20
Q

Skin Flora

A

non-uniform
“Leg” contains scalptuous germs, different to arm and chest 200ish per region. “poo germs”
-re placing a drip into someone. lower risk if insert higher, because if insert in leg/femoral artery higher risk of infection, as germs have a higher capacity to invade

21
Q

Pyogenic infection

A

Main bacterial infection
“acute” infection
tissue invasion, multiplication and immune response in a sterile site
e.g. N.meningitidis enters CSF and provokes innate immunity (phagocytes) results in meningitis

22
Q

Granulomatous/chronic infection

A

Uncommon
Evade innate immune system: cellular immunity required
activated macrophages fuse and surround the antigen: incomplete host response = granuloma
e.g. Mycobacterium tuberculosis. Treponema palidum syphillis
trying so hard to avoid immune system, infectious process clump in different way

23
Q

Intoxication change in host physiology

A

change in host physiology
vibrio cholerae toxin
-bacteria that dont damage tissues but release a toxin whihc interferes with tissue
-Cholera characterised by passing huge amounts (up to 20 L per day) of watery diarohhea (huge in developing world)
-hard to replace this water loss, so young people, babies and elderly will die of dehydration.
cholera does this by releasing toxin which makes cells in the colon release water(lose salt)

24
Q

Intoxication tissue destruction

A

tissue destruction
Clostridium Perfindens: gas gangrene (myonecrosis) caused by histotoxin which splits phospholipids (skin and muscles cells killed/ limb or foot will literlaly rot off)

25
Q

Immune mediation

A

antigen mimicry

  • Streptococcus pyogenes pharyngitis
  • glomoerulonephritis
  • rheumatic fever
  • campylobacter jejuni dysentery
  • Guillan Barre Syndrome
26
Q

Cancer

A

Some bacteria are Oncogenic (have the capacity to cause cancer)-viruses are more common examples of oncogenic pathogens (HPV leading to cervical, anal, penile, throat cancer etc)
stomach cancer caused by Helicobacter Pylori
-Carcinogens
-spirally/curvy bacteria living in stomach
-more in developing walls
-low levels of inflammation in stomach over long periods of time, leading to gastric cancer

27
Q

Cholera

A

Intoxication cause change in host physiology
-infection with Vibrio cholerae. often from unsanitary water supply. Profuse watery diarrhoea
Cholera divides in bowel and releases a toxin.
cholera toxin inhibits GTPase enzyme.
cGMP builds up inside the call and causes a pump on the cell membrane pump chloride ions out of the cell
Chloride, sodium and water is lost into bowel lumen causing diarrhoea

28
Q

How do bacteria cause disease? why? Pathogenesis of appendicitis

A

Inflammation of the appendix
appendix: off small intestine, attaches to colon. outer coldersac. part of immune system. Contains large amount of immune cells and important in development of gut immune system in early childhood. Less important when older
1/3 chance of finding Faecolith upon removal of inflamed infected appendix
Faecolith- hard lump of rich dirt from gut that blocked the appendix.
if blocked will have bacteria trapped. many bacteria will propagate and divide and chew up resources, eat sugars. dont have capacity to cause disease.
-sometimes trapped behind faecolith (sometimes will fall off) Ecoli/something similar, which has potential to interact and damage human tissue (normal ecoli doesnt attach, but when trapped and fighting with bacteria that are also consuming resources, Porum sensing triggered (the population of that species, get message that there are something else diminishing resources, or resources are become scarce. Some bacteria commit suicide, releasing DNA for other bacteria of the same species to share it/to recombine and have sex. Others develop SAS branch to find other neighbourhoods to attack (SAS)). Others will try to remain, bind to epithelial cells lining appendix, releasing toxins to attack those cells, immune system starts to fight back=inflammed appendix.
-Faecoliths might stick or might go. If go, the bacteria propagate spill into bowel, calm down, SAS switches turned off (now have plenty of resources
-Inflamed appendix= contains lots of immune cells (WBC), bacteria, dead bacteria(killed by immune sys) and dead WBC (killed by bacteria) = pain (nerve fibres to gut, not well defined(rare to be poked), vs parts of body exposed to external environment more precise sensation (large part of brain))
-Gut nerves enter 10thish thoracic vertebrae. T10 also innervates skin around bellybutton. Appendix inflamed to point that noxious nerve fibres are stimulated by inflammation, proteins, dead bacteria, dead WBCNerve triggered, first belly button pain, then inside of abdominal wall (parietal peronium) (visceral isnt precise) (parietal precise, but not as precise as skin)(1/2 day 12-16 hours = poor bellybutton pain –> local sharp pain in right lower quadrant /where appendix touches partieal peratoneum. - pain moves due to where inflammation stimulates nerve fibres at different areas of abdomen

29
Q

What is the pain transition in appendicitis?

A

nerves from the appendix enter the spinal cord at the levels of the umbilicus, so initial pain is felt there.
In time inflammation spreads to the parietal peritoneum, which has more precise innervation and the pain shifts to the right illiac fossa

30
Q

Outcomes of appendicitis

A

The inflamed appendix is encased by omentum (apron of fat over gut) and forms a chronic inflammatory appendical mass
-form painful lump in belly that over few lumps will settle down
The appendix ruptures –> peritonitis –> sepsis –> death
-bacteria leaks into peritoneal cavity around bowel. Infection goes from being localised in 5cm appendix, to being localised to 1/3 of body. Infection quickly becomes overwhelming, and immune system must work alot harder, then somebody quickly go into shock and die
-unusual for somebody to recover from this

31
Q

Management of appendicitis

A

Diagnose pain relief, fluids, surgery, antibiotics
Antibiotics given peri-operatively reduce risk of surgical wound infection
surgery= reduce pain, and rupture/shock/death
Antibiotics dont do much for appendicitis. important more to prevent surgical wound from getting infected- prevent healthcare associated wound infection (not to treat appendicitis)
-antibiotics arent wonder drug, different for each situation

32
Q

Disease is an outcome of replication

A
Get to host - be transmitted
Get to & recognise environment
Adhere or interact
Compete
-other organisms and hosts replicate
Symptoms: destroy cells and immune response
Be transmitted
33
Q

Adherence

A
to enable adherence, some pathogens are:
viable in the environment
Transmitted to their niche
motile
able to use chemotaxis
able to use specific host targets to bind
34
Q

Compete with other organisms

A

almost all sites of infection are already colonised with commensal flora
need to adapt and compete for space and nutrients
-can utilise metabolic by-products of host or other commensal microbes
-can use virulence factors to concentrate nutrients in environment
some illnesses develop when the pathogen enters a sterile site, devoid of any competition

35
Q

Compete with the host

A

in all infectious diseases the microbe comes into contact with the host immune system
the pathogen must have a strategy to overcome every specific host defence

36
Q

Human immune system

A

list and understand the elements of the human immune system

  1. Adaptive: (anitbodies produced to provide immunity) T cells(fight speicific infections in powerful ways), B cells, Antibody, Nodes and spleen
  2. Innate: (always there and ready to fight) anatomical barriers, inflammation, complements, cellular, other
37
Q

Anatomical barriers of innate immune system

A

skin, sweat (has antibacterial properites-kills bacteria that gets in the wrong place), desquamation flora

38
Q

Inflammation of the innate immune system

A

damaged cells release chemicals
-trigger macrophages
physical barrier: promote healing, recruit other cells

39
Q

Complements of the innate immune system

A

Complement: a biochemical cascade is triggered by:
bacterial sugars bound to immune protein called mannose binding lectin (MBL)
Antibody bound to bacterial components
Complement can form spontaneously on the surface of bacteria
Outcome:
a) Complement enhances chemotaxis
b) Complement binds to bacteria (opsonisation) to increase recognition by immune cells
c) Complement can make holes in bacterial cell wall to kill bacteria

40
Q

Cellular of the innate immune system

A

Phagocytes: neutrophils, macrophages, dendritic cells. engulf, destroy and present antigens (peptides) to T cells
Non-phagocytes: mast cells, basophils, eosinophils. release chemicals which aids inflammation. recruitment of phagocytes and which are toxic to pathogens
Natural killer cells: destroy compromised host cells lacking MHC I

41
Q

Other components of the innate immune system which arent anatomical barriers, cellular, inflammation or complements?

A

coagulation cascade
platelets
antimicrobial proteins
other proteins (e.g. lactoferrin)

42
Q

Streptococcus pyogenes

A
  1. colonises pharynx in up to 40% of children
    - in throat of 10-15% of healthy children
  2. common cause of pharyngitis(sore throat) and skin infection (cellulitis)
  3. RARELY some children develop rheumatic fever or glomerulonephritis following the infection
    - sometimes rheumatic fever occurs without strep throat, therefore is not just disease that leads to rheumatic fever. is also colonisation, group A (strep pyogenes) interacting with immune system
43
Q

Rheumatic fever symtpoms

A

“illness of poverty”
fever - immune system is acitivated
painful joints - swollen. changes between joints every day
inflammation of connective tissue and muscle in the heart - carditis (most kids surivive this. unless there is repeated episodes, and heart stuructre becomes damaged)
an interesting rash
chorea- distressing but benign (doesnt lead to long term damage) . serpintim involvuntary writhing movements (sydinums chorea)
-distressing but relatively minor on its on (not death)
-but as a Subsequent illness, can attack heart and lead to death. - major complications re heart damage

44
Q

Rheumatic fever

A
  1. Innate immune system activation and S pyogenes toxins damage cells in pharynx
  2. inflammation in pharynxs
  3. pain, erythema, swelling, purulent exudate
  4. S pyogenes has surface proteins that it uses to bind to the cells in the pharyns. M proteins which bind factor K to destroy convertase
  5. Antibodies that form against these bacterial proteins sometimes also bind to human tissues
  6. If antibodies binds to human tissue, heart, joints, kidneys etc, (misdirected antibody, activates immune system) local inflammation occurs.– what causes the disease. unrelated to initial site of infection (if you aspirated fluid out of knee joint of rheumatid fever child, wouldnt grow Strp. pyogenes, as would only be the antibodies)
  7. symptoms of rheumatic fever OR glomerulonephritis after an interval
45
Q

Function of Streptococcus pyogenes M protein

A

on outside
used for adherence
also has capacity to bind complements (protein cascade which helps fight infections)
- binds a regulator (which turn off complements)
-therefore whichever complement comes to attack, is turned on by human protein it is disguising itself in (immune evasion factor)

46
Q

I you aspirated fluid out of knee joint of rheumatic fever child could you grow and culture Streptococcus pyogenes?

A

Now. You wouldnt grow Strp. pyogenes

  • joint is sterile
  • would only be the antibodies)
47
Q

Alexander Fleming

A

discovered penicillen mold

  • bacteria colonies close to mould are small and scant and weedy
  • but bacteria further away were going well and were larger
  • mould producing something to kill the bacteria
  • Penicilin
48
Q

Prescription of antibiotics

A

antibiotics prescribing leads to development of resistance

  • more antibiotics used in winter
  • used for colds, but do nothing for viruses (0% chance of improvement. 20% chance of harming person)
  • more antibiotics used = more resistance
  • Netherlands have low rates