5: Fungi and Medical Mycology Flashcards
Clonochis sinesis spread
through undercooked beef, pork, dog
difference between fission and budding yeast
how they divide
how many times can yeasts bud?
24
fission yeast
divide right down the middle over and over (basically limitless)
daughter cells of equal size
schizosaccharomyces pombe
Zygomycete Rhizopus
sexual: mostly haploid, one diploid phase
asexual: all haploid
can live whole life haploid
haploid
one set of chromosomes
diploid
two sets of chromsomes
Zygomycete Rhizopus sexual
if hyphae run into a differntly sexed hyphae (pheremones)
Plasmogomy occurs, zygospore (diploid) produced, a new combo created
plasmogomy
formation of zygospore
fungal sex
zygospore
diploid product of plasmogomy
Zygomycete Rhizopus asexual
hyphase gros
sporangiospore formse
sporangiospore bursts and releases spores
ascomycete: Talaromyces
spore prodcuing structures of sexual and asexual forms look different
more diploid cells in this genus
Basidomycete
thalus (mushroom)
primary function is lifting of spores off the ground for greater travel ability
Fairy Rings
spore lands in the middle, hyphae grow in different directions, encounter different sexed fungi, ring grows
EX of plasmogomy
pretty rare, usually a line or curve not ring
Medical problems caused by Fungi
allergies
poisoning
infections (opportunistic or systematic)
Fungal allergies
reaction of mast cells to fungal spores=allergy
NOT reaction to the spore, reaction to DIFFUSABLE COMPOUNDS from the spore
Type I hypersensitivity
Fungal Allergies: Dust mites
Der p1 from dust mite fecal pellet (Der p1 is a diffusible antigen)
pellet stays in airway, Der p1 diffuses away, runs into dendtritic/mast cells, T cells react
IgE made by plasma cells
antibodies put on mast cells,
mast cells degranulate when they run into Der p1:
allergies in upper respiratory tract
why did “allergy” pathway evolve?
to deal with PATHOGENS, not for dust mite feces diffusables
Fungal Poisoning
aflatoxin
ergot
death cap
psilocybin
Fungal Poisoning: aflatoxin
produced by aspergillus
aflotoxin not toxic, but liver converts it to toxin compound, causes liver problems like cance
found in stored grains
almost all commercial peanut butter has small amoungs of it
no way to store peanuts out of ground w/o aspergillus growing
mostly just a problem if its in ALL your grains, less developed countries.
Aflatoxin and liver cancer world wide
lots of liver cancer due to the toxin in places where grains are stored poorly and for a long time between harvest and consuming
Fungal Poisoning: Ergot
grows in grains after maturation and when very wet
alkaloid ergotamine toxin… causes halucinations
can be good for vasoconstriction of blood vessels
Rye Bread: ergot in it caused hallucinations assocaited with voices heard during Salem witch trials and Preists deciding to kill Jews and Muslims in the Spanish inquisition
Fungal Poisoning: Death Cap
amanita phalloides: death cap mushroom
#1 cause of fatal human fungal ingestion
Phalloidin-toxin and lab reagent binds to polymerized actin
Death Cap action
phalloidin prevents depolymerization of actin
uncompetative inhibition
Fungal Poisoning: Psilocybin
hallucinations, in the new world
Psilobcybe mexicana is a psycedelic mushroom
called “Flesh of the gods” by Aztecs
schizophrenia like psychosis
so what hurts us with fungal toxins?
the METABOLIC BYPRODUCTS that the organisms make
NOT the fungi
its not the goal of fungi to kill us
sometimes fungi use us as a food source though
Superficial Fungal infections
epidermis surface, little or no inflammation
cutaneous fungal infections
skin, hair, nail
how to fungi eat?
absorption
secrete enzymes, absorb
subcutaneous fungal infections
dermis infection (bellow skin)
systemic fungal infections
deep tissue
pulmonary
opportunistic
superficial mycosis
common in tropics easy to treat cosmetic problem hair (piedras) skin (tinea nigra, pityriasis versicolor)
Hair infections
black piedra white piedra grow in hair follicle sometimes nodules in hair used to be seen as a sign of health (so did lice)
black piedra
hair
adherent, black, hard, gritty nodules
in the tropics
Trichosporon ovoides
white piedra
subtropics and temperate (US)
several Trichosporon species
used to test w/ UV light bc they had floursesnce protein, but we basically killed off this species bc we could ID them easily
cutaneous mycosis
30 species of fungi infect human skin
hair, nails, epidermis only
direct contact with infected person or pet
indirect contact with shower flower, barber clippers, wet floor
ringworm
tinea
broken down medically by where it occurs
DISEASE not genus
tinea pedis
feet
ringworm
tinea capitis
scalp
defoliates hair, temporary baldness
micosporum canis: species from dogs to humans
(ringworm)
tinea unguium
nails
ringworm
tinea corpus
body
ringworm
tinea cruvis
groin
ringworm
tinea barbae
beard
ringworm
Dermatomycoses-dermatophytes
cellular immune response invoked
ring worm (tinea)
ID’d by disease, not genus
disease vs. species
disease: group of symptoms medically ID’d, can be caused by multiple species
Species: organism
Opportunistic Fungal Infections
ppl who are abnormal: immunocompromised, antibiotic use, organ transplant
candidia albacians
Aspergillus (grain and immunosuprresed ppl)
NOT transmitted person to person, just from environment
aspergilus as an opportunistic infection
asthmatic attacks
bronchitis
can invade issue and organs
candida infection
due to change in normal flora
vaginal candidias
yeast infection
lost of cases
diabetes, antibiotics, oral contraceptives, preganancy, are risk factors
cutaneous candida
diaper rash
interiginous candidiasis
moist, warm, soft areas of body that touch (esp in overweight ppl)
thrush
oral infection, usually after antibiotic treatment
immunocompomsied ppl
grows in throat
opportunisitic in aids
IDing Candida
germ tubes
KOH test
Germ Tubes
candidia is dimoprhic (2 forms)
growth of germ tubes shows that you have candida
Dimorphic candida
yeast form: 37C (body temp)
fungal form: 25C (room temp)
KOH test
diagnose candida infection
10% potassiu hydroxide kills bacteria, not fungus
dissolves bacteria, not fungal, cell walls
Systemic infections
Histoplasma capsulatum
coccidioides immitis: valley fever
both dimorphic
Histoplasma capsulatum
Ohio and Mississippi River Valleys subclinical infection usually inhalation of airborne spores occasional serious and fatal outbreaks can cause fungal pneumonia and kill you Midwest... to dry in AZ sero-conversion
“subclinical”
shows no symptoms
Histoplasma capsulatum outbreak in Indiana HS
due to changing of flower bed where birds pooped
aersolized the fungus (which grew in bird droppings)
Histoplasma capsulatum as dimorphic
yeast form in body (37C)
spore form in soil (25C)
coccidioides immitis
valley fever
mostly subclinical, but poor diet and fatigue can make it worse… resembles tuberculosis
symptoms: chest pain, fever, coughing, weight loss
sero-conversion rate in AZ of 30%/year
sero-conversion 30%/year
live in Tucson 1 year, 30% of people make antibodies to inhaled and growing fungal spores
2 years, 60% of population sero-convert
95% chance of sero-conversion after 4 years
dimorphic coccidioides immitis
spores inhaled are fungal
spores in lung are yeast like (see slide 32)
coccidioides immitis lifecycle
SLIDE 33! athrosopres produced earth distrubed spores inhaled live in lings if you get really sick, the spherule may break, spores released, you get pneumonia
athrospores
aren’t really spores
broken bits of hypahe
spread only when you disturb the earth, aren’t usually airborne
Theory of coccidioides immitis spread
cadaver model of spread
cadaver model of spread
coccidioides immitis doesnt spread in air or normal human to human: spread from cadaver to human
humans migrate, people die, living inhale spores, spores live in lung, it happens again
as humans migrated from CA to AZ and south america, they carried occidioides immitis with them
and dogs carry it too
