Toxins

In livestock, typically, exposure is through what?

• contaminated feed/water or too high a dose of an otherwise safe feed/water additive/med

• access to poisonous plants, pesticides, and rodenticides

• envenomation

• exposure to noxious gases

• topical application

what are household pets more likely to be exposed to

human-associated hazards

how are toxins typically diagnosed

based on hx of exposure, signs, and lesions on post-mortem

how are toxins generally treated

• removal of toxin and supportive care, potentially lavage or “flush” GIT if ingestion was recent

• induce vomiting for some recently ingested toxins (not recommended in livestock)

• if topical bathe animal

• specific commercial tx → general binding agents or anti-toxins

what is the primary concern with toxicosis

dose- exact amount of exposure/intake

what is the amount of toxin required to cause pathology generally correlated to

body weight

what other factors are important for toxicosis

duration and frequency, route of exposure

what are variations in toxicosis

absorption, metabolism, excretion, nutrition/dietary factors, hormonal/health status, organ pathology, stress, environmental factors

samples collected for potential toxicosis analysis include what

• dead or recently euthanized animals tha showed signs

• feed and drinking water that was available when signs were present

• label or picture of product/plant/animal that is suspected to have caused toxicity

what are the two families of venomous snakes in North America

• Elapidae- coral snakes

• Crotalidae- pit vipers (rattlesnakes, copperhead, cottonmouth moccasin)

what is the only venomous snake native to NH

timber rattlesnake

where do livestock typically get bit by snakes

tongue, nose, face

what are signs for elapid envenomation

systemic neurologic signs → paresis, ataxia, depressed gag reflex w drooling, muscle twitching, quiet mentation, rapid shallow breathing

pain/swelling at the bite are minimal

what are the signs for crotalid envenomation

severe local tissue damage that spreads → tissue discoloration w/i a few minutes, bloody fluid oozing from wounds, skin may slough

neurologic less likely, mostly muscle twitching

what does the prognosis for snake bites depend on

• type/species of snake

• location of bite

• size of victim

• degree of envenomation

• time between bite and start of tx

what can tx include

• preventing/controlling cardiovascular shock

• neutralizing venom

• preventing or controlling clotting issues

• minimizing tissue necrosis

• prevent secondary infection

what is the only direct and specific means of neutralizing snake venom

antivenom → if administered in first 6 hr after bite

what mechanisms can rodenticides act through

• anticoagulants

• neurotoxins

• kidney failure

• multisystem organ failure

what do anticoagulant rodenticides do

interfere with ability of blood to clot → internal hemorrhage (lungs, intestines, body cavity)

how may anticoagulant rodenticides be treated

with vit K if exact product known

what is the increased susceptibility of skin to damage caused by UV light

photosensitization

during photosensitization, what accumulates in the skin

photodynamic chemicals → stimulated by sunlight on exposed and non pigmented areas

what can photosensitization cause

damage to small vessels by free radicals → skin necrosis and sloughing

what is photosensitization most common in

cattle, sheep, goats, horses

what does the time interval between exposure to photodynamic agent and onset of signs depend on

• type of agent

• dose

• exposure to sunlight

what photosensitization occurs when the photodynamic agent is either ingested, injected, or absorbed through the skin

primary, results in skin cell membrane damage

what is an example of primary photosensitization

hypericin from St. John’s wort and fagopyrin from buckwheat

what photosensitization causes liver damage that results in accumulation of photodynamic substances

secondary → more frequent

what are plant derived photosensitizing agents

phytophorphyrins

what are signs for photosensitization

head shaking, restlessness, redness of unpigmented skin, edema/swelling of eyelids, muzzle, ears, and tail

what photosensitization has better prognosis

primary > secondary

tx for photosensitization

• remove offending substance

• manage complicating infections ± liver damage

  • provide shade- graze at night

what comes from exposure to feed/bedding contaminated with toxins produced during growth of various fungi/molds on cereals, hay, straw, pastures, etc.

mycotoxins

how are mycotoxins diagnosed

presence of a dz documented to be cause by a known mycotoxin, detection of mycotoxin in feed or animal tissues

some mycotoxins are what (allow pathogens to create secondary disease that complicates diagnosis)

immunosuppressive

what to do if suspected mycotoxicosis

• change feed

• inspect storage bins, mixing equipment, feeders for caking, molding, or musty odors

• clean equipment and sanitize with dilute bleach

• analyze for known mycotoxins → spore counts, fungal cultures

• use commercially available mold inhibitor, mycotoxin adsorbent if appropriate

• save sample of each diet until animals are at 1 mo beyond when the feed was consumed

methods of mycotoxicosis prevention:

• testing of suspect feed at harvest

• maintaining clean/dry storage facilities

• using additive to control mold growth in storage

• efficient air exclusion in silage storage

• reduce storage time of prepared feeds

what is produced by toxigenic strains of Aspergillus flavus and A parasiticus, is common on peanuts, soybeans, corn, etc when moisture content and temp are sufficiently high

alfatoxicosis

what species does aflatoxicosis affect

growing poultry (especially ducklings and turkey poults), pigs, calves, and dogs

Where is alfatoxicosis metabolized

liver → high dosages cause necrosis of liver cells, prolonged low dosages result in reduced growth rate, immunosuppression, liver enlargement

what does acute aflatoxicosis entail

death after short period of inappetence, vomiting, hemorrhage, jaundice

what does chronic aflatoxicosis entail

more common, unthriftiness, weakness, anorexia, reduced growth and feed efficiency, occasional death

how is aflatoxicosis diagnosed

dz hx, microscopic examination of liver (biopsy or necropsy), presence and levels of aflatoxins in feed should be determined

what is the ingestion of sclerotia of parasitic fungus Claviceps purpura

ergotism

what grains/forage plants are related to ergotism

rye, bluegrasses, fescues, ryegrasses

what species are most commonly involved in ergotism outbreaks

cattle, sheep, pigs, poultry, but most other species are susceptible

what does ergotism primarily cause (sign)

vasoconstriction by direct action on muscle of arterioles, repeated doses injures blood vessels → initially reduce blood flow and eventually leads to necrosis of extremities

how does ergotism appear in ruminants

• lameness (2-6 wk or more after initial ingestion), hindlimbs b4 forelimbs, within ~1 wk, sensation is lost in affected part the dry gangrene sets in

• tip of tail or ears become necrotic and slough off

• body temp, pulse, respiration rates increase

• stimulation of CNS followed by depression (sheep)

how does ergotism present in pigs

• reduced feed intake and weight gain

• occasionally necrosis of tips of ears or tail

• in pregnant gilts/sows → lack of udder development w agalactia at parturition, piglets smaller and starve to death w/i few days

how is ergotism diagnosed

find causative fungus in grains, hay, pastures provided to livestock showing signs

control for ergotism

immediate change to ergot-free diet, under pasture conditions, frequent grazing or topping of pastures prone to ergot infestation during summer months reduces sclerotia production

what species are particularly sensitive to copper toxicosis

sheep

copper toxicosis signs

sudden release of a large amount of copper from liver to blood → stress and liver damage or disease (e.g. flukes) → hemolysis = anemia with jaundice

• depression, anorexia, diarrhea, weakness

copper toxicosis lesions

most tissues will be yellow, but kidneys are black because of accumulation of RBC breakdown products

how is copper toxicosis diagnosed

measure Cu level in blood or kidneys

copper toxicosis tx

usually unrewarding, fluid therapy, supplemental molybdenum, minimize stress

Copper toxicosis prevention

feeding 5-10 ppm of Cu in total diet and less than a 10:1 ratio of copper to molybdenum

what is polioencephalomalacia

edema, swelling and necrosis of brain gray matter, may cause brain to herniate

signs of polioencephalomalacia

ataxia → recumbency, head pressing, central blindness, opisthotonos, muscle tremors, seizure, nystagmus, decreased mentation

causes of polioencephalomalacia

thiamine deficiency, sulfur toxicosis, lead toxicosis, salt toxicosis

what deficiency is most often associated with rumen acidosis

vit B1 (thiamine)

how is vit B1 deficiency prevented

provide good quality roughage, slowly adapting to diet changes, avoiding toxic plants

possible feed sources for sulfur toxicosis

gypsum, urinary acidifiers, molasses, cruciferous crops, water

what toxicosis makes the rumen smell like eggs as a result of H2S gas production

sulfur

diagnosis for sulfur toxicosis

demonstrate exposure and possibly by measuring H2S

sulfur toxicosis tx

no specific tx, remove offending substance and supportive care

what are environmental lead contaminants

insecticides, herbicides, lead-acid batteries, lead paint, gasoline, shot gun pellets

lead toxicosis mechanism

once absorbed, lead irreversibly binds to RBCs, deposits in bones, kidneys, and liver, can cross placental border

lead toxicosis signs

CNS, GI irritation (colic, anorexia, diarrhea), osteoporosis (lameness, paralysis)

how is lead toxicosis diagnosed

measure blood or tissue lead levels

lead toxicosis tx

removal of ingested toxin and chelation therapy (binds lead in blood and aids in excretion)

term for excessive salt concentration in blood

hypernatremia

what species is most sensitive to salt toxicosis

swine, mortality >50%

how to control salt toxicosis

slowly bring down salt concentration in blood, controlled access to fluids over multiple days