Toxo- Mycotoxins 1

kelseyfmeyer's version from 2016-10-02 23:31

fungi and toxin intro

Question Answer
what are 2 reasons fungal infections are on the rise?(1) resistance is inc-- antifungal agents used on crops, more resistance to them. So see more and more fungal infxn of plants, particularly grain and other ingredients which go into animal and ppl feed. (2) changes in climate also a prob-- and favor fungi. helps in abundance in fungal infxns all around the globe
what is fungi imperfecti? fungi perfecti?IMPERFECTI- small fungi, you can't see them. PERFECTI- can see them (hence we think they are perfect, bc we can eat them, lol)
Fungi, moulds and yeasts are cosmopolitans- you can find them around the world. the prevalence of the specific toxin often depends on...the climate
The existence of fungi, moulds and yeasts depend on the climate and the availability of substrates: (which 3)?Oxygen (air), water, nutrients
why are plant mycotoxins inc over the years?our climate change is causing this
Deuteromyceta-- are these fungi perfecta or imperfecta? what are the most commonly seen ones?these are fungi imperfecti (cant see them with naked eye) Fusarium - Penicillium - Aspergillus (Alternaria - Botrytis - Trichoderma - Trichocecium)
Fusarium - Penicillium - Aspergillus are what kinda fungi?Fungi imperfecta-- specifically, Deuteromyceta **these three we can see in daily practice that harm animals
what are some Clinical signs after ingestion of putrefied food? (how quickly does this occur?)(tends to develop slowly) (1) Decreased feed conversion, growth retardation (2) Recurrent diarrhoea, maldigestion (3) Thickening of the gastrointestinal mucosa (4) Decreased absorption of nutrients (5) Tympanites (excess gas accumulates in the gastrointestinal tract and causes abdominal distension) (6) Entero-haemorrhagic syndrome
does ingestion of putrefied food cause the GI wall to become thicker or thinner?thickening of the mucosa
Wheat and corn and silage top 3 offenders for mycotic infection***Penicillium <--most common of the 3 for both grains and silage, Aspergillus, Fusarium <--in this order of occurrence too
what are some Environmental factors what fungal growth depends on?Temperature (higher or lower being favorable depends on the specific agent) and humidity, Plant immunity, stress(treating plant for fungal infxn can cause stress, lol), damage (insects), Crop rotation
two factors which might influence if funi will grow at harvest are...Moisture content, ripening
two factors that influence fungal growth in terms of how you store your food?Moisture, use of fungistatics (many fungi resistant to fungistatics)
what is easier to control-- field prob or storage prob?storage-- so preharvest harder to control than post harvest
how does the immune system generally react to mycotoxins?Mycotoxins are VERY SMALL molecules, so they are generally non-immunogenic--- however they are HAPTENS, which means if they attach to a larger carrier molecule/protein then they WILL generate an immune response
generally mycotoxins have HIGH bioavailability (why?)-- what is the exception?generally they are very bioavailable bc they are lipophilic- the exception is fumonisin B1, which isn't lipophilic, so doesnt have great bioavailability
are mycotoxins (in general) lipophilic or hydrophilic?LIPOPHILIC (so high bioavailability)
under what conditions are mycotoxins stable, under what are they unstable?STABLE: heat/cold and pH changes. UNSTABLE UV LIGHT
where in animals/bact/plants are mycotoxins broken down? which type of metabolism?biotransformation! bacterial and in the liver.... Glycosinolate formation in plants


Question Answer
in what geographic regions do aspergillus species tend to form their mycotoxins?toxins usually seen/produced in the tropical regions
ASPERGILLUS: who/where in body does FLAVUS usually affect? Fumigatus?FLAVUS=DOGS=NASAL ASPERGILLOSIS (dogs stick their noses in FLAVORFUL garbage). FUMUGATUS=HORSES=GUTTERAL POUCH MYCOSIS (fumigate that horse)
is aspergillus a pre- or post-harvest problem?post-- occur during storage (if occur during storage- can at least optimize storage to dec infections )
wut dis? aspergillus
is penicillium a pre or post harvest contaminant?post, it's a storage problem (think about your bread).
what kinda pH and temp does penicillium like?like/can adapt to LOW pH and optimal growth at 16-28*C (aka 60-82*F)
wut dis? penicillium-- its actually the thing in roquefort cheese.
what is the mold you commonly find on bread and jam and such? (one of the main sources of spoilage of food)penicillium
wut dis?fusarium
of aspergillus, penicillium, and fusarium, which is the most difficult to control and why?Fusarium, because it is a pre-harvest contaminant which likes to infect young plants. AND it likes to live in the soil
FUSARIUM SPP.-- are they a pre or post harvest contaminant?PRE-- EARTH MOULDS, CONTAMINATES YOUNG PLANTS
what are the two kinds of toxins fusarium species like to produce?tricocethenins and zearalenone
which of these molds is both PARASITIC AND PHYTOPATHOGENIC?fusarium- it parasitize the plant for their own advantage, and parasitism and might harm plant to death (phytopathogenic)
what do fusarium species look like on plant grossly?cotton like
(said in class) what is the most important phytopathogenic fungus (on wheat?) ?Fusarium culmorum
what are the two "bathroom and kitchen" inhabitants (ie the environmental contaminations)RHIZOPUS STOLONIFER AND ALTERNARIA SPP.
how harmful are RHIZOPUS STOLONIFER AND ALTERNARIA SPP.?relatively harmless but might lead to allergic reactions (toxins not as important) allergens can exacerbate resp probs in horses. produce smell, smell irritating to upper airways
so if you probably aren't going to be harmed by rhizopus and alternaria (the enviro/kitchen contaminants) why should you prolly still not eat that moldy bread?because penicillium ALSO causes fungal invasion of food (and rhizopus/alternaria also can cause allergic stuff)
ERGOTISM: What toxin causes this condition, and what fungi is it produced by?This condition is cause by ERGOTAMINE which is produced by CLAVICEPS PURPUREA (a type of ergot fungus).
wut is?This is claviceps purpurea growing on grain- this fungi produces ergotamine
what are the clinical signs of ergotism like? How do people get it?this is caused by ingestion of grain with claviceps purpurea growing on it-- this fungi produces ergotamine, which causes the condition (Aka St Anthony's fire, the devils curse) leads to convulsions, mm spasm, hallucinations(has LSD in it lol), and gangrenous pain at extremities

Moulds and mycotoxins in animal species: inro, aspergillus, endophytes, Equine fescue toxicosis <-- i think this is all endotoxins

Question Answer
what are "mycoses"? which fungi usually cause these problems?This is where the animal itself is infected with the mold. Your main contenders are: Trichophyton - Trichosporum - Trichoderma - Microsporum a.o (dermatomycoses)
what are "Mycotoxicoses"? examples of fungi which cause these problems?This is where the animal is intoxicated with the mycotoxins. Examples are Lolitrem, ergot alkaloids, fumonisins
what are "Toxico-infections"? examples of fungi which causes these problems?Infections with fungi that result in the production of toxins in the animal(or plant) Aspergillus flavus (Aflatoxins), Aspergillus fumigatus (Gliotoxin)
so what are the fungi where its not just that you ate some toxin, but that they infect you and produce toxin inside of you?aspergillus! think gutteral pouch and nasal
*mycotoxicoses vs toxico-infections?myco: intoxication with mycotoxins. TI: Infections with fungi that result in the production of toxins in the animal(or plant)
Aspergillus flavus makes what toxin?aflatoxin (flavus= dog noses)
aspergillus fumigatus makes what toxin?gliotoxin (gutter pouch in horses, cattle also affected)
Aspergillus fumigatus can be an OPPORTUNISTIC pathogen (toxico-infection)-- what are the clinical symptoms you'd see in CATTLE? WHERE in their body is affected (in order of most to least)(1) GI: Omasum > rumen > reticulum... necrohemorrhagic lesions, neutrophilia, thrombosis, pneumonia (2) mycotic ABORTION (3) mycotic MASTITIS
how do you know if a cow is toxico-infected with aspergillus?you will be able to detect the mold itself in the tissues
if there is silage/roughage contamination, aspergillus can cause what systemic dz in cattle?Lymphogenic generalised multi-organ aspergillosis
Respiratory diseases in horses--> Recurrent airway obstruction is a major health and welfare problem with horses-- what is a factor responsible for a large amount of resp. inflammatory reactions in horses?mainly caused by hay/straw and an indoor environment-- and aspergillus fumigatus are present in what is called the "haydust sample" and inhalation leads to an inc in the inflammatory response in the airway. The graph shows that the aspergillus fumigatus showed the LARGEST inflammatory response of all the things tested to see inflammatory response. (hay dust has LPS and aspergillus in it) (his slide also said they are Non-histaminic and proinflammatory-- so maybe dont cause allergies just inflammation?)
why is it hard to prevent aspergillus in the hay?its a soil borne fungus which lives in the environment and in the hay.
sheep with "Staggers" are suffering from what mycotic problem?they have consumed ryegrass with endophytes ( NEOTYPHODIUM LOLII - LOLITREM B) on it
what IS an endophyte?fungi that live IN the plant-- so cant see them!
what kinda grass does neotyphodium lolii particularly like to grow in? what toxin does it produce?ryegrass (think ryegrass staggers in sheep)-- produces the toxin lolitrem B
what likes to live on ryegrass and what toxin does it produceneotyphodium lolii makes lolitrem B, likes to live on ryegrass
what causes ryegrass staggers?lolitram B
what kinda toxin (class) is lolitram B? and what is lolitram B resposible for causing?ergoline alkaloids-- ryegrass staggers
who is affected by ryegrass staggers?sheep know well known for being affected, horses can be affected too tho.
after ingesting neotyphodium lolii infected ryegrass, how long before you see signs of ryegrass staggers? what are the clinical signs?see signs in 7-14d of ingestion-- CSs are: staggering gait, falling over, ill thrift, heat stress, reduced fertility, lower milk production, and tremors, loss of direction of movement. Can even lead to accidental death.
Explain the MOA of lolitram B It leads to inhibition of potassium channels (specifically Ca++ activated K+ channels). Inhibiting the K+ channels is what leads to the ataxia and tremors. So when they are at rest there are no clinical signs (maybe slight tremor) but when they move then you see the signs more. [danger in moving a 500kg horse which can't tell where it is going.] STUFF ON SLIDE THAT HE DIDNT SAY: Alpha subunit is responsible for tremorgenic effects, the Beta-4 subunit is important in ataxia effects (so A tremor Beats Ataxia-- which i guess is true IRL lol)
how much lolitram B results in visible clinical sympoms? how much does NOT cause visible symptoms?> 1.2 ppm lolitrem B result in visible clinical symptoms.... < 0.8 ppm lolitrem B does not result in clinical symptoms.
so lolitram B molecules can degrade in the environment-- what does the rate of degradation depend on?storage conditions
how can you treat lolitram B intoxications?THEY ARE REVERSIBLE!! :D :D Ataxia and instability decrease within 48hrs after hay withdrawal, Full recovery > 6 weeks
what does lolitram B intoxication MOST look like (ddx)? How can you tell them apart? (then list the other ddxs which are on the slide but he didnt mention in class)Equine Herpes Virus 1 infection (neuro form) (they have ataxia as well)... how to tell apart? Well first, lolitram B is completely reversible. EHV1 is not (might get a little bit better with the neuro form but not by much). ALSO in EHV1 infection the horse will have a very large bladder ..... (OTHER lolitram B ddx's include: Equine degenerative myelo-encephalopathy, Equine motor neuron diseases (EMND), Equine grass sickness (equine dysautonomia), Clostridium botulinum type C toxin (Group III), Polysaccharide storage myopathy, Iliac thrombosis)
which type of fescue is involved in Equine fescue toxicosis?Festuca arundinacea: tall fescue
what is the mycotic agent involved in equine fescue toxicosis? what is it growing on again?Neotyphodium coenophalium which likes to grow on tall fescue (Festuca arundinacea)
Neotyphodium coenophialum (implicated in what dz) makes WHAT kinda toxin?Ergopeptide alkaloids: ergotamine (so kinda like the claviceps purpurea) [implicated in equine fescue toxicosis]
clinical signs of equine fescue toxicosis?abortion - prolonged gestation (abortion and prolonged gestation? weird) - premature separation of the chorionic membrane - thickened placenta - retained placenta - agalactia..... this is all mostly bc it does cause quite severe contractions of the uterus-- and depending on when that happens in the peg, can cause one or the other.
what other problem aside from equine fescue toxicosis does Tall fescue-->Neotyphodium coenophialum--> Ergopeptide alkaloids: ergotamine cause? CSs?causes fescue foot in cattle, you will see heat intolerance and a very poor meat quality
what kinda (class) is Neotyphodium coenophialum?ENDOPHYTE: ie you cannot see it with your eye (lives in the plant)