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MICROBIOLOGY Y1 > week 7 - infections and pathogens > Flashcards

week 7 - infections and pathogens Flashcards

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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

Study These Flashcards
A
  • Most common serious fungal infection is candidiasis
21
Q

FUNGAL INFECTIONS
Candida albicans
where on body

Study These Flashcards
A
  • Commensal on skin/body tracts
22
FUNGAL INFECTIONS Candida albicans disseminating infection involved...
a DIMORPHIC SWITCH (yeast to hyphal) - inflammatory mechanism
23
FUNGAL INFECTIONS Candida albicans pathogenic process
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
FUNGAL INFECTIONS Candida albicans Candodalysin
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
FUNGAL INFECTIONS Coccidioides imitis what
- Primary pathogen o Can infect to healthy individuals
26
FUNGAL INFECTIONS Coccidioides imitis ascomycete
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
FUNGAL INFECTIONS Coccidioides imitis found in?
in desert soilds of South-West USA
28
FUNGAL INFECTIONS Coccidioides imitis causes?
- Causes coccidiodomycosis o Valley / California fever
29
FUNGAL INFECTIONS Coccidioides imitis risk factors
- Construction and severe weather are major risk factors o Spores become air borne (inhalation)
30
FUNGAL INFECTIONS Coccidioides imitis effects and treatment
- Flu like symptoms - Rare-CNS/joints/skin lesions - When becomes chronic treatment can take years (might not even be successful
31
FUNGAL INFECTIONS Coccidioides imitis dimorphic
switches between yeat and hyphae
32
FUNGAL INFECTIONS Coccidioides imitis life cycle
see notes Spherule too large for phagocytosis The cells are huge compared to immune cells * Dimorphic change so resistant to macrophage
33
PROTISTS INFECTIONS Trypanosoma (kinetoplastid) what
- African sleeping sickness - Chagas’ diseases Two different species of Trypanosoma causing two different infections
34
PROTISTS INFECTIONS Trypanosomiasis transmission
- Trypanosoma parasite transmitted by an invertebrate vector:
35
PROTISTS INFECTIONS T. brucei gambeinse disease?
African sleeping sickness
36
PROTISTS INFECTIONS T. brucei gambeinse transmitter
Tsetse fly
37
PROTISTS INFECTIONS T. cruzi disease
Chagas' disease
38
PROTISTS INFECTIONS T. cruzi transmitter
Assassin / kissing bug
39
PROTISTS INFECTIONS T. brucei gambeinse vs. T. cruzi growth
T. brucei gambeinse - Extracellular growth in bloodstream T. cruzi - Intracellular growth
40
PROTISTS INFECTIONS T. brucei gambeinse vs. T. cruzi causes?
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
PROTISTS INFECTIONS T. brucei gambeinse vs. T. cruzi area
T. brucei gambeinse - Sub-Saharan Africa T. cruzi - South and central America
42
PROTISTS INFECTIONS life stages of Trypanosoma
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
PROTISTS INFECTIONS Apicomplexans what
- Apicomplexans are ALL obligate parasites - Included malaria Chosen example - Toxoplasma
44
PROTISTS INFECTIONS Apicomplexans Toxoplasma gondii who does it affect
Affects a lot of mammals Most well known for infection in rodents
45
PROTISTS INFECTIONS Apicomplexans Toxoplasma gondii what does it do?
Manipulates rodents behaviour to make them more likely to be predated on my felines * More likely to be found
46
PROTISTS INFECTIONS Apicomplexans Toxoplasma gondii why switch between rodents and felines?
* 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
PROTISTS INFECTIONS Apicomplexans Toxoplasma gondii humans infected?
Humans can be infected * This is accidently * No evolutionary benefits
48
PROTISTS INFECTIONS Apicomplexans -Toxoplasma gondii Toxoplasmosis
- 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
PROTISTS INFECTIONS Apicomplexans -Toxoplasma gondii Toxoplasma
- 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
is developing antimicrobial for eukaryotic infection difficult? why?
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
summary fungal infections are most often...
opportunistic with serious complications in immunocompromised people
52
summary Protozoan parasitic infection are often (but not always) transmitted by...
a vector and are often primary pathogens

MICROBIOLOGY Y1 (28 decks)

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