week 7 - infections and pathogens Flashcards

1
Q

infection terminology:
superficial

A
  • infections that appear on the skin’s surface and can be caused by numerous external factors
  • limited to the stratum corneum and essentially elicit no inflammation
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2
Q

infection terminology:
Cutaneous

A
  • skin
  • involve the integument and its appendages, including hair and nails. Infection may involve the stratum corneum or deeper layers of the epidermis
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3
Q

infection terminology:
Subcutaneous

A
  • diffuse infection of the skin and subcutaneous tissues characterized by local spreading erythema, warmth, tenderness and swelling
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4
Q

infection terminology:
systemic

A

Circulation/CNS/other organs
- When it gets access to entire body (passed the yellow bit into blood vessels)

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5
Q

Primary pathogen

A
  • A microbe able to cause disease in a otherwise healthy host
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6
Q

Opportunistic pathogen

A
  • A microbe only able to cause infection in a immunocompromised host
    o E.g. HIV, cancer, steroid therapy, pregnancy, diabetes
    o Something else has already weakened the immune system
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7
Q

FUNGAL INFECTIONS
fungi as infectious agents

A
  • Moulds and yeast are widely distributed in the air, dust and normal flora
  • Humans are relatively resistant
    o Body temp 37: huge bottle neck for things that might cause infection
    o Physical barriers
  • Many fungi are non-pathogenic
    o Only approx. 600 species have been linked to disease in animals
     Even small when humans specifically
    o Many. More fungal plant pathogens
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7
Q

FUNGAL INFECTIONS
fungal disease =

A

myocsis

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7
Q

FUNGAL INFECTIONS
pathogenesis of Mycoses

A
  • Infectious agents: spores, yeast, hyphal elements
    o Part of fungus that causes disease is debated
    -
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7
Q

FUNGAL INFECTIONS
pathogenesis of Mycoses
enter the body?

A

Enter body through respiratory, mucous and cutaneous routes
o Primary fungal pathogens tend to enter via respiratory route

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8
Q

FUNGAL INFECTIONS
pathogenesis of Mycoses
normal human flora?

A
  • Dermatophytes and Candida sp. Part of the human normal flora
    o Can be present in healthy amounts
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9
Q

FUNGAL INFECTIONS
pathogenesis of Mycoses
communicable?

A
  • Most mycoses not communicable
    o Don’t generally spread person to person, haven’t developed transmission routes
     Not part of selective pressure to survive
    o EXCEPTION: Dermatophytes and Candid sp. ARE transmissible
     E.g. athletes foot, ringworm
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10
Q

FUNGAL INFECTIONS
fungal diseases can be:

A
  • Superficial
    o Athletes’s foot (Trichophyton)
  • Opportunistic (secondary)
    o Thrush (Candida)
    o Cryptococcosis (Cryptococcus neoformans)
  • But serious primary mycoses exist
    o Coccidioides
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11
Q

FUNGAL INFECTIONS
medically important fungi

A

Primary
- Coccidioides immitis

Opportunistic
- Cryptococcus neoformans
- Candida albicans

(there is more!! this is what we cover)

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12
Q

FUNGAL INFECTIONS
Cryptococcus neoformans
what

A
  • Opportunistic pathogen
    o Associated with people immunocompromised
  • Basidiomycete encapsulated yeast
    o Related to many mushroom forming fungi
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13
Q

FUNGAL INFECTIONS
Cryptococcus neoformans
where from?

A
  • Soil, particular tree species and pigeon droppings
    o Associated with eucalyptus trees
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14
Q

FUNGAL INFECTIONS
Cryptococcus neoformans
most cases in?

A
  • Most cases in HIV+ in sub-Saharan Africa
    o Highest burden of infections
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15
Q

FUNGAL INFECTIONS
Cryptococcus neoformans
infection

A
  • Infection via lung, then disseminating to CNS – cryptococcal meningitis
    o Crossing blood brain barrier
    o High cerebral spinal pressures
    o Keeps growing in spinal fluid
    o Hallucinations
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16
Q

FUNGAL INFECTIONS
Cryptococcus neoformans
chance of survival?

A

40-60% chance of survival
- How quick found
- How good treatment is
o Of the fungi
o Or of existing disease

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17
Q

FUNGAL INFECTIONS
Cryptococcus neoformans
when in body

A

Crossed by extracellular or in the macrophage

Although should be being digested
Its not
So in a sense in a protected environment
* In the macrophage
Instead of all the antifungal stuff in the blood

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18
Q

FUNGAL INFECTIONS
Cryptococcus neoformans
Vomocytosis

A

Can escape from the host cell
Leaving host cell intact
* So immune system isn’t triggered
* Lots of implications if happens at blood brain barrier.
This is vomocytosis

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19
Q

FUNGAL INFECTIONS
Candida albicans
what

A
  • Opportunistic pathogen
    o Also part of normal healthy flora
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20
Q

FUNGAL INFECTIONS
Candida albicans
most common infection

A
  • Most common serious fungal infection is candidiasis
21
Q

FUNGAL INFECTIONS
Candida albicans
where on body

A
  • Commensal on skin/body tracts
22
Q

FUNGAL INFECTIONS
Candida albicans
disseminating infection involved…

A

a DIMORPHIC SWITCH (yeast to hyphal)

  • inflammatory mechanism
23
Q

FUNGAL INFECTIONS
Candida albicans
pathogenic process

A
  1. adhesion and colonization
  2. hyphal penetration and invasion
  3. vascular disemination
  4. endothelial coloization and penetration

Hyphal advantage to fungus
Can puncture tissue and spread to other parts of the body
Hyphal growth to penetrate
Switch to free moving yeast
Ect.

24
Q

FUNGAL INFECTIONS
Candida albicans
Candodalysin

A

see notes for diagram

attacks host’s cholesterol-containing membrane

Make Ece1 toxin
Secreted as candidalysin toxin
Makes pores in the membrane (fungal toxin that causes damage)
So not just hyphae physical force rupturing cells
Also chemical
Important for ability to cause disease
has various adhesion molecules so it can better adhere to cells

25
Q

FUNGAL INFECTIONS
Coccidioides imitis
what

A
  • Primary pathogen
    o Can infect to healthy individuals
26
Q

FUNGAL INFECTIONS
Coccidioides imitis
ascomycete

A

o Hyphae can segment and every other cell can become a pore
o So a switch to a spherule –> which are full of endospores
o Example of differentiation

27
Q

FUNGAL INFECTIONS
Coccidioides imitis
found in?

A

in desert soilds of South-West USA

28
Q

FUNGAL INFECTIONS
Coccidioides imitis
causes?

A
  • Causes coccidiodomycosis
    o Valley / California fever
29
Q

FUNGAL INFECTIONS
Coccidioides imitis
risk factors

A
  • Construction and severe weather are major risk factors
    o Spores become air borne (inhalation)
30
Q

FUNGAL INFECTIONS
Coccidioides imitis
effects and treatment

A
  • Flu like symptoms
  • Rare-CNS/joints/skin lesions
  • When becomes chronic treatment can take years (might not even be successful
31
Q

FUNGAL INFECTIONS
Coccidioides imitis
dimorphic

A

switches between yeat and hyphae

32
Q

FUNGAL INFECTIONS
Coccidioides imitis
life cycle

A

see notes

Spherule too large for phagocytosis
The cells are huge compared to immune cells
* Dimorphic change so resistant to macrophage

33
Q

PROTISTS INFECTIONS
Trypanosoma (kinetoplastid)
what

A
  • African sleeping sickness
  • Chagas’ diseases
    Two different species of Trypanosoma causing two different infections
34
Q

PROTISTS INFECTIONS
Trypanosomiasis
transmission

A
  • Trypanosoma parasite transmitted by an invertebrate vector:
35
Q

PROTISTS INFECTIONS
T. brucei gambeinse
disease?

A

African sleeping sickness

36
Q

PROTISTS INFECTIONS
T. brucei gambeinse
transmitter

A

Tsetse fly

37
Q

PROTISTS INFECTIONS
T. cruzi
disease

A

Chagas’ disease

38
Q

PROTISTS INFECTIONS
T. cruzi
transmitter

A

Assassin / kissing bug

39
Q

PROTISTS INFECTIONS
T. brucei gambeinse vs. T. cruzi
growth

A

T. brucei gambeinse
- Extracellular growth in bloodstream

T. cruzi
- Intracellular growth

40
Q

PROTISTS INFECTIONS
T. brucei gambeinse vs. T. cruzi
causes?

A

T. brucei gambeinse
- Fever, lethargy, mental disturbance (+trouble sleeping), death

T. cruzi
- Acute infection (fever/headaches), chronic >20 yrs, latent/asymptomatic
Some cardiac complications

41
Q

PROTISTS INFECTIONS
T. brucei gambeinse vs. T. cruzi
area

A

T. brucei gambeinse
- Sub-Saharan Africa

T. cruzi
- South and central America

42
Q

PROTISTS INFECTIONS
life stages of Trypanosoma

A

Epimastigote
- In the Tsetse fly/kissing bug
- Become trypomastigotes in the salivary gland/rectum

Trypomastigote
- In humans
- Can multiply by binary fission

Amastigote
- In humans
- Intracellular replicating form T. cruzi

43
Q

PROTISTS INFECTIONS
Apicomplexans
what

A
  • Apicomplexans are ALL obligate parasites
  • Included malaria
    Chosen example
  • Toxoplasma
44
Q

PROTISTS INFECTIONS
Apicomplexans
Toxoplasma gondii
who does it affect

A

Affects a lot of mammals

Most well known for infection in rodents

45
Q

PROTISTS INFECTIONS
Apicomplexans
Toxoplasma gondii
what does it do?

A

Manipulates rodents behaviour to make them more likely to be predated on my felines
* More likely to be found

46
Q

PROTISTS INFECTIONS
Apicomplexans
Toxoplasma gondii
why switch between rodents and felines?

A
  • In rodents can only divide asexually in gut
  • In felines and divide sexually in gut and make oocytes
    o Felines are the divinitve host
    o Need to mix up genes
47
Q

PROTISTS INFECTIONS
Apicomplexans
Toxoplasma gondii
humans infected?

A

Humans can be infected
* This is accidently
* No evolutionary benefits

48
Q

PROTISTS INFECTIONS
Apicomplexans -Toxoplasma gondii
Toxoplasmosis

A
  • Usually asymptomoatic but transmission to foetus is very serious
    o Foetus cant protect itself
    o Miscarriages
  • Humans are accidental hosts latent CYSTS form in the brain
  • Asymptomatic carriage in humans varies greatly from country to country
49
Q

PROTISTS INFECTIONS
Apicomplexans -Toxoplasma gondii
Toxoplasma

A
  • Human is an (inadvertent) intermediate host
  • But still get some behavioural manipulations
    o Higher incidence of mental illness in infected humans
    o Higher incidence of infection in drivers who crash
  • Evidence is patchy
50
Q

is developing antimicrobial for eukaryotic infection difficult?
why?

A

yes really difficuly

because:
- Similar to our cells
- Not a lot of options for mechanism of action
o Only a handful that work
- Which first?
o Cells die or fungi die first

51
Q

summary
fungal infections are most often…

A

opportunistic with serious complications in immunocompromised people

52
Q

summary
Protozoan parasitic infection are often (but not always) transmitted by…

A

a vector and are often primary pathogens