Cockleburs (Xanthium spp.) are widely distributed in the midwestern US and grow as weeds in fencerows, ditches, and low or marshy areas. The toxic principle, carboxyatractyloside, is present in the seeds and young seedlings of the plant, especially during the cotyledonary (“two-leaf”) stage of growth. Seedlings may be ingested by pigs on pasture especially after spring rains when burs sprout in low-lying areas. Also, seeds may be ingested in mixed or ground feeds. Pigs may be found dead after consuming only modest number of seedlings. Because the clinical course of disease is only several hours, signs may not be observed and lesions may be absent from dead pigs. Mortality is sporadic unless plants are numerous.
In experimentally poisoned pigs, signs include depression, hypoglycemia, occasional nausea, incoordination, convulsions, and death. Lesions include serofibrinous effusions in body cavities and subcutaneous edema. There sometimes can be edema of the gall bladder wall and mild gastroenteritis. Microscopic lesions include centrilobular hepatotoxicosis with centrilobular accentuation of the liver pattern.
Diagnosis is often difficult unless cocklebur seedlings can be found in significant numbers in the pasture or seeds can be found in the feed. An “on-the-knees” search for the two-leaf stage sometimes reveals seedlings deep within lush pasture. Cocklebur poisoning must be differentiated from poisonings caused by ingestion of clay pigeons, aflatoxin, and gossypol.
In pigs showing clinical signs, mineral oil administered per os may delay absorption of the toxic principle until it can be eliminated. Injecting physostigmine has been reported to be of value in affected pigs.
Phenylarsonic (Organic Arsenical) Poisoning
Roxarsone and arsanilic acid are used to promote growth and to treat swine dysentery and eperythrozoonosis. Roxarsone is more toxic than arsanilic acid but most features of poisoning are similar in both cases. Poisoning is dose-related. Chronic poisoning may occur when low doses are given over a long period of time. Acute poisoning occurs when large amounts are consumed in a short period of time.
Signs of chronic poisoning with arsanilic acid include goose-stepping, hind limb ataxia, limb paresis, and blindness. Blindness is not typical of poisoning with other organic arsenicals. Paralyzed pigs remain alert. If provided with feed and water, they will continue to eat and drink. There are few or no associated gross lesions. Signs of acute poisoning include cutaneous erythema, ataxia, vestibular disturbances, and terminal muscular weakness. An acute gastroenteritis will often be present in these cases. Although signs and lesions of roxarsone poisoning will often be similar, an additional syndrome has been described that includes repeated convulsive seizures following exercise without the blindness produced by arsanilic acid. Microscopic lesions associated with chronic poisoning by these compounds include neuronal degeneration of optic and peripheral nerve trunks, including the sciatic nerves. Neuronal lesions may not be present in acute cases.
A tentative diagnosis can often be based on a history of misuse of the compounds and the presence of characteristic clinical signs in chronically affected swine. Diagnosis may be assisted by toxicologic assays of kidney, liver, muscle, and feed.
Prevention of organic arsenical poisoning can be achieved simply by correct management of these legal compounds during feed preparation or medication. In particular, water treated with these compounds should not be given to thirsty pigs, as they are likely to consume a toxic dose. Directions provided with the compounds should be followed carefully. The neurotoxic effect of poisoning sometimes is reversible if the compound is removed within two or three days of the appearance of signs. Blindness and long standing peripheral nerve damage may be permanent.
Pigs allowed access to pastures or lots containing pigweed (Amaranthus retroflexus) may be poisoned.
Most poisonings occur in the late summer or fall. Signs appear within five to ten days after exposure and include trembling, weakness, incoordination, knuckling, and almost complete rear leg paralysis. Morbidity is variable; mortality can be high (75-80%) in pigs showing signs.
Lesions are those associated with acute nephrosis and heart failure. There is a marked perirenal edema. The kidneys are normal in size but may appear blanched. Other lesions include ascites, hydrothorax and edema of the ventral body wall; long-standing cases may have chronic fibrosing nephritis. Microscopic lesions in the kidneys of acutely affected pigs include necrosis of both proximal and distal convoluted tubules with numerous casts in tubules. Many glomeruli will be atrophic and have a distended Bowman’s capsule containing filtrate. Diagnosis can usually be made after identification of the plants, obtaining a history of sudden access to them, and observing the clinical signs and rather unique kidney lesions. The toxic principal is not known.
There is no widely accepted treatment. Pigs should be denied access to the plants immediately, but new cases may develop for as long as ten additional days.
Salt Poisoning (Water Deprivation; Sodium Ion Toxicosis)
Salt poisoning can occur in pigs either as a consequence of water deprivation or from sudden ingestion of too much salt.
Poisoning in water-deprived pigs can occur in pigs consuming a proper level of salt but it is more likely if the salt level in the feed is excessive. Signs often are precipitated, or worsened, by allowing the pigs sudden, unlimited access to water. Water deprivation can occur for many reasons but commonly may be the result of freezing of the water source, plugged water nipples, or inadvertently leaving a water valve closed. Operators may not always be forthright in admitting human errors related to water deprivation. Poisoning has occurred following prolonged shipping without access to water, followed by unlimited access.
Following sudden heavy rains, salt poisoning can occur in swine after ingestion of salty brine from overflowing, loose-salt boxes provided for other livestock and is also reported following ingestion of whey. This type of poisoning is more likely in water-deprived pigs.
Clinical signs of sodium ion toxicosis are caused by the acute cerebral edema that occurs as a result of multiple central nervous system (CNS) lesions. Because the condition most often occurs secondary to water deprivation (rather than a primary toxic intake of salt), salt poisoning is frequently apparent at a “pen” or “herd” level. Signs include aimless wandering, blindness, deafness and head pressing. Affected pigs sometimes “dog-sit”, slowly raise their nose upward and backward, and fall on their side in spasms that may be followed by paddling of the legs. They then may arise and continue their wandering.
Diagnosis associated with water deprivation may be suggested by history, signs, and elevated sodium levels in serum or cerebrospinal fluid. Gross lesions may be absent or limited to gastroenteritis. Gastroenteritis is more likely in pigs consuming salty brine and may be accompanied by diarrhea. A valuable but not infallible diagnostic aid is the microscopic observation of rather unique meningeal and cerebral perivascular cuffing by eosinophils in brain. Later and less reliably there may be laminar subcortical polioencephalomalacia or necrosis. Salt poisoning must be differentiated from all other encephalitic diseases. In an affected pen, a clue to the occurrence of water deprivation will be the absence of any urine or wet feces on the pen floor.
Water-deprived or affected pigs should be reintroduced to water slowly, given only small amounts of water at frequent intervals. This may suppress mortality. Pigs showing clinical signs usually die regardless of treatment.