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68 Cards in this Set

  • Front
  • Back
What is a mycorrhizal association?
Symbiotic relationship b/t
plant and fungus •! Plant gives fungus carbs •! Fungus provides plant with
H2O, minerals, dz resistance !! Increased surface area
!!Important in over 90% of all living plants
•! Sterile soil = poor growth
What are four compounds produced by fungi?
•! Antibiotics !! Fungal products mainly toxic to bacteria
•! Digestive aid •! Phytotoxins
!! Fungal products toxic to plants •! Mycotoxins
!! Fungal products toxic to vertebrates and other animal groups
Fungi are ________tic, ________tic, and ________tic.
•! Saprophytic !! Widespread in the environment !! Decomposition of ‘dead’ organic matter !! Cause opportunistic infections
•! Parasitic !! Pathogenic
•! Mutualistic !! Obligatory associations with other
microorganisms, e.g. mycorrhizal association !! Non-pathogenic
Are fungi photosynthetic? How do they obtain their food?
•! Non-photosynthetic heterotrophs - they are not plants.
!! Produce exoenzymes and obtain nutrients by absorption. They extrude their enzymes and then absorb the break-down products.
!! “Live” in their food supply, can’t make it
What are the four phyla of fungi? What's the fake fifth phyla?
Top three distinguished by sexual form.
•! Basidiomycota (basidiomycetes) •! Ascomycota (ascomycetes) •! Zygomycota (zygomycetes)
•! Deuteromycota (fungi imperfecti) !! Sexual form not found
•! Mycophycophyta (lichens)
What phyla of fungi are the club fungi? What do they produce their spores from?
Basidiomycota “Club fungi”
•! What most people think of when they think “mushrooms”
•! ~25,000 species •! Includes species that are delicious, deadly
and hallucinogenic; biodegradation •! Look like umbrellas growing from the ground
or shelves on wood
•! Produce spores (basidiospores) from club- shaped structure (basidium)
What phyla of fungi are the sac fungi? What do they produce their spores from?
Ascomycota “Sac fungi”
•! Include prized morel and truffle mushrooms •! ~25,000 species •! Produce spores (ascospores) from specialized
pods or sac-like structures (asci)
What phyla of fungi are the sac fungi? What do they produce their spores from? Which mold is their best known mold?
Zygomycota “Conjugation fungi”
•! ~600 species •! Most primitive of terrestrial fungi
!! Cell walls do not separate nuclei •! Best known is ‘black bread mold’ or mold seen
on strawberries
•! Zygospores produced when hyphae meet each other, form a bulge (progametangia) & produce spores
What phyla of fungi are the fungi imperfecti? What do they produce their spores from?

What are common species within it?
Deuteromycota “Fungi imperfecti”
•! ~25,000 species •! “Leftovers” that don’t fit well into one of
the other phyla •! Sexual spores not found •! Common species
!! !! !!
Athlete’s foot (Trichophyton) Penicillin production (Penicillium) Yeast infections (Candida albicans)
What is fungi's association with lichen?
•! ~25,000 species •! Not technically another
phylum •! Lichens
!! Symbiotic union b/t fungus and algae or fungus and photosynthesizing bacteria
!! Algae or bacteria provide nutrients while lichen protects them from the elements
What is the morphology of fungi? (two forms)

In what aerobic environment do fungi grow best?

How do the two morphologies grow?
•! Molds !! Exist as branching filaments (hyphae)
•! Yeast !! Unicellular (oval or sphere)

•! Fungi grow best aerobically !! Anaerobically: gut of ruminants, food, beer
•! Molds
!! Lateral branches develop from hyphae at localized areas of plasticity
!! Septa formed by inward growth of cell wall •! Central pores allow passage of nutrients and
organelles !! Extension of hyphae results in formation of
mycelium (interlacing network of hyphae) •! Yeast
!! Single oval, ‘grows’ by asexual reproduction
What is the interlacing network of hyphae of mold called?

What allows passage of nutrients and organelles in mold growth?

Central pores allow passage of nutrients and
What are the cell wall structures of mold and yeast?

What is the principal sterol in plasma membrane? (important)
Cell Wall Structure
•! Hyphae (mold) !! Impart rigidity and osmotic stability !! Composed of chitin macromolecules with cellulose
cross-linkages •! Yeasts
!! Protein complexed with polysaccharides •! Ergosterol = principal sterol (instead of cholesterol)
in plasma membrane
•! Both have nuclei, mitochondria and microtubules with well-defined membranes
How do fungi reproduce? (hint: two methods)
•! Reproduce by spore formation

!! Ascospores, basidiospores or zygospores
!! Individuals communicate via pheromones

!! Mold-aerial hyphae produce spores
!! Yeasts-budding
-Daughter cells separate from parent cells
What do you call disease resulting from invasion of tissue by fungi?
How are fungal organisms usually acquired by the host?
!! Port of entry usually through respiratory tract or
skin •! Acquired via inhalation of spores or from unusual
growth of commensal species normally there
What role do fungi play in disease proceses?
•! Primary pathogens
•! Opportunistic pathogens
What are the three classifications of mycotic disease?
•! Superficial !! Opportunistic infections of the skin, mucous
membranes and keratinized structures •! Subcutaneous
!! Localized fungal invasion of dermis and subcutaneous tissues
•! Systemic
!! Opportunistic infections in respiratory and digestive tracts
What are mycotoxins? When are they produced?

What is intoxication by them called?
•! Mycotoxins !! Secondary metabolites of fungal species
•! Aspergillus, Penicillium, Fusarium !! Produced when toxigenic strains grow under specific
conditions on crops, pasture or stored feed

•! Mycotoxicosis
!! Intoxication (acute or chronic) following ingestion of mycotoxin-contaminated plant material
How are mycotoxins classified?
•! Challenging to classify !! Vary in their chemical structure, biosynthesis,
biological effects !! Produced by a variety of fungal species

By that hasn't stopped people from trying:
•! Clinicians-target organ •! Cell biologists-generic groups (e.g. teratogens) •! Chemists-chemical structure •! Mycologists-fungus that produces them
Are mycotoxins species specific?
Yes. They need particular environments

•Suitable substrate
-Specific host
•Corn, cereals, soybeans, sorghum peanuts, grain, grass/hay
-Specific part of the plant

• Moisture
• Optimal temperature
• Oxygen levels
Are mycotoxins antigenic?

Do they enhance the ability of fungal growth?

Why are they there?
Affect specific target organs

Do not enhance the ability of the fungus to grow in the host, but allows the fungus to be there as a symbiotic relationship with the plant to deter predation by herbivores.
Why do mycotoxins complicate clinical diagnoses?
•! Given mycotoxin may be produced by many fungal species
-Many fungal species may be present on a food source

•! Some fungi can produce many mycotoxins
-Differing biological activities
-Materialize as a variety of clinical symptoms

• Mycotoxins may be unevenly distributed in a batch or lot of plant material
How is mycotoxicoses spread? How is it diagnosed?
•! Outbreaks seasonal and sporadic •! No lateral spread to in-contact animals •! Confirmation requires presence of mycotoxin
!! Feed
!! Tissues of affected animal
What factors determine the development of disease of mycotoxicoses?
Period of exposure
• Duration
• Species, age, sex, time in gestation, health of the animal
• Environmental conditions

Amount of mycotoxin consumed
Are antimicrobial medications effective with mycotoxins? What is their relationship to bacterial infections?
•! Antimicrobial medication ineffective
•! Mycotoxicoses can heighten vulnerability to
bacterial infection
How is mycotoxicoses treated?
•! Relegated to supportive therapy
!! Diet
!! Hydration
•! Binding agents

•! Preventative measures
!! Proper harvest and storage of crops
!! Monitor food supply
!! Dilution of contaminated feed with non-contaminated feedstuff
!! Binding agents
What sort of oxygen situation does dermatophytes prefer? What are the two genera groups that belong to them?
•! Strict aerobes •! Anamorphic genera
!! Microsporum !! Trichophyton !! Epidermophyton
•! Teleomorphic genera !! Arthroderma
Which group of fungi does ringworm belong to? Which species cause it?

What is the infectious form and what environment does it prefer?
Dermatophytosis (Ringworm)

•! Microsporum and Trichophyton
= most common species •! Affects many animal species

Arthrospores = infectious forms
!! Released by fragmentation of hyphae in keratinized structures (superficial) •! Exacerbated from rubbing or insect bites
!! Picked up indirectly from soil (decomposing hair and feathers) or directly from infected animals
!! Viable for over 12 months !! Damp, warm surfaces ideal for germination
Is dermatophytoses zoonotic?

What is the clinical manifestation?
Yes, this is ringworm.

•! Lesion development influenced by virulence of dermatophyte and immunocompetence of host
!! Loss of hair !! Growth of hyphae can result in
epidermal hyperplasia !! Secondary bacterial infection
What is the host immune response to dermatophytosis?

•! Host responds with cell-mediated response !! Delayed-type hypersensitivity ! elimination of
dermatophyte, local resistance to reinfection !! Immunity is transient
•! Antibodies to dermatophyte glycoproteins are ineffective
•! Increased shedding of outer skin layer ! increased permeability of epidermis to inflammatory fluids
How are dermatophytes diagnosed?

•! Dermatophytes tend to be species-specific
•! Specimens = hair, skin from edge of lesions and affected nails
!! Examine microscopically for arthrospores
!! Culture !! Cats and dogs-examine with Wood’s lamp, fungus fluoresces
How is ringworm treated?
•! Isolate animals with lesions !! Monitor in-contact animals
•! Clean the area well !! Clip haircoat
•! Dispose of clippings carefully !! Vacuum !! 5% lime sulphur, natamycin or miconazole
shampoo !! Disinfect grooming equipment and bedding
•! Topical antifungals !! Miconazole and clotrimazole
• Systemic therapy
-Griseofulvin or itraconazole
-Induce neutropenia
What is the most commonly prescribed anti-fungal? How does it work?
•! **‘Azoles’**
!! Inhibit cytochrome P450-mediated synthesis of ergosterol

•! Griseofulvin
!! Binds to keratin precursor cells ! keratin-griseofulvin complex in skin ! enters fungi via transport processes ! binds to microtubules ! interferes with mitosis
•! Amphotericin B !! Associates with ergosterol, forming pore in membrane
leading to K+ leakage !! Saved as a more aggressive therapy
•! Potentially lethal side effects
What are dimorphic fungi?
How do they enter a host?

What are the four species most often associated with disease?
Dimorphic Fungi
•! Occur as a mold and yeast form !! Mold: in the environment !! Yeast: once it's entered animal tissues
•! Enter host through respiratory system, disseminated to rest of body
•! Blastomyces dermatitidis
•! Histoplasma capsulatum
•! Coccidiodes immitis
•! Cryptococcus neoformans
What kind of disease does blastomyces dermatitidis cause? What kind of fungi is this?

What are the symptoms? How is it diagnosed?
Dimorphic fungi

•! Blastomyces dermatitidis
!! Natural habitat unknown •! Isolated from acid soils with organic matter
!! Endemic in Mississippi and Ohio River valleys, SE/south central US
•! Most common in dogs and humans •! Exposed by inhalation of conidia !
transform into yeast in lungs ! pulmonary disease
•! Symptoms !! ~50% cases Io infection asymptomatic !! Coughing, exercise intolerance and dyspnoea !! Can mimic pneumonia, tuberculosis !! Skin lesions also possible

•! Severity determined by immunocompetence of the host
•! Diagnosis (fine needle aspiration,
blood, urine) !! Culture !! Yeast cells seen in affected specimens !! PCR !! Antibodies identified by ELISA
What kind of disease does histoplasma cause? What kind of fungi is this?

What are the symptoms? How is it diagnosed?
Dimorphic fungi
•! Histoplasma capsulatum var. capsulatum !! Found in soil, esp. with bird or bat feces
•! Endemic to Mississippi and Ohio river valleys
•! Most common in dogs and cats
•! Exposed by inhalation of microconidia Distribution of
•! Symptoms !! Generally asymptomatic (>50%) !! Dogs: chronic cough, diarrhea, emaciation,
ulcerative intestinal lesions !! Cats: dyspnoea, depression, fever, weight loss !! Can mimic pneumonia, tuberculosis !! Granulomatous lesions in lungs
•! Disseminated histoplasmosis can be fatal
•! Diagnosis (Fine needle aspiration, blood, urine) !! Culture and stain !! Yeast cells seen in affected specimens !! PCR
•! Treatment !! Mild cases resolve w/o
treatment !! Amphotericin B (initial
therapy) + itraconazole (stabilized patient)
What kind of disease does coccidiodes cause? What kind of fungi is this?

What are the symptoms? How is it diagnosed?
Dimorphic fungi

•! Coccidiodes immitis and C. posadasii !! Found in soil (esp. dust) of arid and semi-arid low-
lying areas •! C. immitis in San Joaquin valley •! C. posadasii in Texas, New Mexico, Arizona, S. America •! Species can co-exist
!! a.k.a ‘valley fever,’ ‘desert fever’ •! Affects many species including humans
!! Dog is most common, esp. young adult (large breed) •! Exposed by inhalation of arthroconidia •! Symptoms
!! ~50% asymptomatic !! Non-specific: cough, fever, inappetence !! Pulmonary lesions
•! Dissemination results in inflammation of bone with lameness and bone destruction
•! Diagnosis (Fine needle aspiration, blood, urine) !! History of animal-originated from endemic area !! Culture !! Spherules found in affected specimens
!! PCR

•! Treatment
!! May recover spontaneously !! Amphotericin B, fluconazole,
keto- or itraconazole
What kind of disease does cyptococcus neoformans cause? What kind of fungi is this?

What are the symptoms? How is it diagnosed?
•! Caused by the yeast Cryptococcus neoformans
!! Three varieties: C. neoformans v. gattii (Cryptococcus gattii), C. neoformans v. neoformans, and C. neoformans v. grubii
!! In soil and manure (esp. pigeons); trees •! Worldwide distribution, esp. temperate regions
•! Route of infection: lungs and skin !! Inhalation of spore or contamination of wounds Cryptococcus gattii !! Few actually infected compared to # that inhale yeast-
laden air •! People with AIDS, cancer •! Cats with FIV and FeLV, dogs with chronic corticosteroid use

•! Diagnosis !! History of visiting infected area
•! Worldwide distribution !! Hot spots: Vancouver Island
Wright’s stain of C. neoformans (Arrow indicates budding)
!! Culture in nasal or skin exudate, CSF, sputum •! Serum, urine or blood can also be used
•! Treatment: fluconazole, itraconazole or amphotericin B
What is the most common fungal disease of cats? What are the signs of chronic infection? What would make you suspect a fungal disease? What are the symptoms differences between dogs and cats?

Cats: can lead to chronic infection of nose and sinuses and
skin ulcers •! Impt differential when sneezing cat is unresponsive to antibiotics

•! Symptoms
!! Cats: sneezing/nasal discharge, polyp masses in nostrils; cutaneous lesions; CNS: depression, seizures, change in temperament; blindness
!! Dogs: fewer respiratory signs, more CNS/eye symptoms
What disease causing fungus is a commensal yeast found on skin of birds and mammals? What is its relationship with oxygen? What are the common presentations and diagnoses?
Malassezia pachydermatis
•! Commensal yeast found on skin of birds and mammals
!! Areas rich in sebaceous glands •! Anal region, external ear canal, lips, interdigital skin of dogs
•! Aerobic, non-fermentative •! Otitis externa and seborrhoeic dermatitis
!! Yeast present in high numbers
!! Ass’d with immunosuppression •! Diagnosis
!! Culture !! Unique budding structure identified microscopically
with methylene blue !! PCR
What causes otitis externa usually?

What are the signs?
The fungus Malassezia pachydermatis
•! Otitis externa !! Proteolytic enzymes from
M. pachydermatis damages
mucosa of ear canal !! Excessive production and retention of wax !! Inflammatory exudate and necrotic debris accumulate
in ear canal !! Excessive itching, rubbing and head shaking
•! Mucosa of ear is painful and swollen !! Treatment
•! Correct underlying causes and keep ears clean •! Ear drops with drugs or topical antifungal •! Chronic cases-surgical intervention
How does malassezia pachydermatis interact with skin? What predisposes animals to it?

What are the signs?
•! Seborrhoeic dermatitis
!! Prediposed: hypersensitivity disorders, keratinazation defects,immunosuppression, moist skin folds
•! Lesions occur more frequently in skin folds
!! Itching, erythema, foul- smelling exudate
!! Treatment: miconazole- chlorhexidine shampoo or ketoconazole
How do you minimize mycotoxin production? (eight ways)
1)! Harvest at maturity and as soon as the moisture content allows for minimum grain damage
2)! Adjust harvesting equipment for minimum seed or kernel damage
3)! Dry all grain to at least 15% moisture as quickly as possible
4)! Cool the grain after drying and store at moisture below 13%
5) Thoroughly clean grain and all bins before storage
6)! Store in water-, insect- and rodent-tight structures
7)! Periodic aeration and probing for “hot spots” through storage period
8)! When feasible, choose grain varieties that are resistant to insects, diseases and mechanical damage
What are the four carcinogens of Aflatoxicosis? What is the most carcinogenic?

What plants are affected?
B1, B2, G1, G2
!! B1 is most potent natural carcinogen known

Plants most affected: cereals, figs, oilseeds, nuts, tobaccos
What are the three levels of immune response to aflatoxicosis? What factors influence the response? What are the sensitive/resistant species?
•! Acute !! Results in ataxia, massive hemorrhaging & bruises,
death •! Sub-acute
!! Results in inappetence and reduced growth rate
!! Decreased protein synthesis •! Chronic
!! Results in cancer, immune suppression
•! Response influenced by species, age, sex, weight, diet, exposure to infectious agents
•! Large species-susceptibility !! Sensitive: calves, birds, fish and dogs !! Resistant: adult cattle, pigs, sheep, horses, goats
What is the target organ of aflatoxicosis?

What is the mechanism of toxicity?
•! Target organ: Liver
!! Mechanism of toxicity: cytochrome P450s convert aflatoxins to reactive 8,9-epoxide form
!! Binds to DNA and protein which results in GC to TA transversions (arrow) mutate p53
What is aflatoxin contamination associated with?
•! Highly variable !! Usually ass’d with drought stress or when kernels are
damaged !! Stored under conditions to favor mold growth (high
moisture in crop & high humidity of surroundings) !! Pet food recall: Diamond Pet Food 2005 (corn)
•! Has been linked to increased mortality in farm animals and humans
!! China and third world countries !! Meat & milk can contain metabolized form of aflatoxin B1 leads to human health threat
How do you diagnose and control/prevent aflatoxicosis?
•! Diagnosis !! Besides acute outbreaks, clinical signs are
vague !! Tissues
!! Presence of Aspergillus
!! Presence of aflatoxins !! Feed samples analyzed for aflatoxins
•!Control & Prevention !! Proper harvest and storage of crops !! Monitor food for aflatoxin
!! Treat contaminated feed with ammonia gas at high T &P
!! Dilution of feed !! Binding agents
What is the non-steroidal estrogen associated with mycoestrogenism? What is its prevalence?

•! Prevalent in winter and early spring !! Fungus needs low temp to produce large amounts of zearalenone
What species are effected by mycoestrogenism? What are the clinical signs?

How is it diagnosed? How is it treated?
•! Species affected !! Pigs
!! Results in vulval edema, hypertrophy of mammary glands and uterus and vaginal/rectal prolapse
!! Cattle and sheep !! Low conception-reduces ovulation rates !! Vaginal discharge, nymphomania and abnormal mammary development
$$$Financial loss through poor reproductive performance$$$
•! Diagnosis !! Chromatography of zearalenone, #- and "-zearalenol (metabolites) !! ELISA of pasture samples and urine
•! Treatment !! Stop intake of infected feed
!! Reproductive functions return in 1-4 weeks
What are the three mycotoxins of fusarium graminearum?

What species do they infect and clinical signs do they result in?
Trichothecene toxicoses

Vomitoxin (deoxynivalenol, DON): Species most commonly affected
!! Pigs
!! More recently, dogs •! Clinical signs
!! Food refusal and emetic syndrome !! contaminated feed refused, vomition, poor growth/weight gain

Diacetoxyscirpenol (DAS) and T-2 toxin: Species most commonly affected !! Cattle, pigs, poultry
•! Clinical signs
!! Haemorrhagic syndrome !! Necrotic lesions in skin or oral cavity, bloody diarrhea
What fungi produces ergot? What kind of plant does it inhabit? What is its mechanism of action?
Claviceps purpurea colonizes cereal grains and grasses

Results in stimulation of #-adrenergic receptors !! Contracts smooth muscle and induces convulsions !! Chronic exposure leads to necrosis of extremities
!! Clear line of demarcation between non-viable and viable tissues !! Exacerbated by cold or warm temperatures
•! Dopamine agonists
!! Inhibit prolactin secretion !! Poor mammary development
! suppresses lactation !! Low litter sizes !! Premature births and abortions
What species is ergotism commonly seen in?

How is it diagnosed/prevented?
•! Most common in cattle, sheep, pigs, chickens •! Diagnosis
!! Presence of sclerotia in grasses or grain
!! Identify ergot alkaloids by HPLC •! Prevention
!! Regular grazing or topping to prevent seed-head formation
!! Grain with ergots should not be fed to animals
So What’s the Trouble with Fescue? (in relation to mycotoxicoses)
•! Infected with Neotyphodium coenophialum
!! endophyte that lives in seeds and leaves !! good for the plant: stress tolerance & drought resistance
!! bad for livestock: produces ergot alkaloids !! responsible for insect and mammalian toxicoses
What is the mechanism of fescue toxicosis?
•! #-Adrenergic agonists !! stimulate smooth muscle cell contraction !
vasoconstriction !! necrosis and sloughing of extremities !! "ed weight gain (ADG)
•! Dopamine agonists !! Inhibit production of prolactin !! "ed milk production and reproductive efficiency
What is summer syndrome or summer slump?
Fescue Toxicosis
•! Summer syndrome or summer slump !! heat intolerance !! !d grazing = !d weight gain !! reproductive difficulties
What is fescue foot?
Fescue Toxicosis
!! cold intolerance !! necrosis " gangrene " sloughing "terminate
What is the bioavaliability of ergot alkaloids?

How do they transport across the tissue wall?
Remenal metabolism of ergot alkaloids

•! Bioavailability !! relatively unknown
•! Transport across tissue wall !! rumen > omasum > reticulum !! ergoline alkaloids > ergopeptides
•! Rumen fluid !! degradation of ergovaline and other ergot
alkaloids to lysergic acid
In addition to the rumen, what other organ contributes to metabolism of ergot alkaloids?
Hepatic Metabolism of Ergot Alkaloids
•! Cytochrome P450s
!! rats, humans, livestock: CYP3A
!! hydroxylation on proline ring
!! excrete in bile within 6 hours
How can we apply genomic technologies to fescue toxicosis and ryegrass staggers?
•! Significant data gaps in our understanding of cellular and metabolic changes
!! Mechanism of toxicity not fully developed
!! Limits development of effective therapies

These technologies will hopefully help us fill in these gaps.
How could we prevent pre-harvest contamination of crops with fescue toxicoses?
!! Develop host resistance through plant breeding and enhancement of antifungal genes
!! Genetic engineering
!! Targeting regulatory genes in mycotoxin development
What fungus infects perenial ryegrass?

What mycotoxin does it produce? What is the name of the syndrome seen in livestock?
•! Infected with Neotyphodium lolii !! Endophyte, produces loline alkaloids
!! good for the plant: deters insect pests !! bad for livestock: responsible for staggers
What is lolitrem B?

What fungus is it associated with?

What clinical effects does it produce?
!! Indole diterpene alkaloid

Neotyphodium lolii

!! Tremorgen !! Neurological effects including
muscular tremors, ataxia, incoordination and convulsive seizures. Perennial ryegrass staggers
What species are most effected by ryegrass staggers?

What are the signs/treatment?
•! Most common in sheep, cattle, horses, farmed deer
!! Individual susceptibility varies •! Signs develop over a couple
of days !! Fine tremors and nodding movements of
the head !! Running is stiff, uncoordinated !! Gross incoordination when disturbed !! Limbs not flexed !! Fall easily, struggling violently when attempting to rise !! Death is rare
•! Treatment of an “inconvenient disease”
!! Animals recover quickly if removed from contaminated plant material
What are the five stages of ryegrass staggers?
0) No clinical signs
1)! Low-intensity tremor and incoordination with
2)! Moderate-intensity tremors and incoordiantion with handling
handling !! Stiffness
!! Head and neck tremors
3)! Resting: spontaneous low-intensity tremors and
incoordination; moderate to severe tremors and incoordination with handling
!! “Goose” stepping
4)! Resting: pronounced tremors and incoordination; convulsive tremors and severe incoordination with handling
!! Falling, incoordination
5)! Resting: severe spontaneous tremors and incoordination, usually accompanied by convulsive episodes
What mechanism causes the tremors of ryegrass staggers?
Calcium-activated potassium channels
!! Molecular site of motor impairment
What is the final resting place of lolitrem alkaloids in the animal tissues?
Adipose tissue

!! Concerns have been raised about the public health safety of lolitrem B residues in beef fat

(from ryegrass staggers)