Phenylarsonic organic arsenicals are relatively less toxic than inorganic compounds or aliphatic and other aromatic organic compounds.
Aliphatic organic arsenicals include cacodylic acid and acetarsonic acid. These were historically used as stimulants in large animals, but their use is now uncommon. Some aliphatic arsenicals such as monosodium methanearsonate (MSMA) and disodium methanearsonate (DSMA) are occasionally used as herbicides or grassburr and crabgrass killers. Ruminants, especially cattle, are very sensitive to MSMA and DSMA. Clinical signs, lesions, and treatment of aliphatic organic arsenicals are similar to those of inorganic arsenicals, except that ruminants may have necrosis of the mucosa of the rumen and omasum and gelatinous serosal edema of the omasum and abomasum.
Aromatic organic arsenicals include trivalent phenylorganics, such as thiacetarsamide and arsphenamine for the treatment of adult heartworms in dogs, and pentavalent compounds such as phenylarsonic acids and their salts. Thiacetarsamide and arsphenamine are no longer used commonly, especially since the introduction of melarsomine dihydrochloride (also see Heartworm Disease Heartworm Disease read more ).
Phenylarsonic compounds were widely used as feed additives to improve production in swine and poultry rations and to treat dysentery in pigs. The three major compounds in this class are arsanilic acid, roxarsone (4-hydroxy-3-nitrophenylarsonic acid), and nitarsone (4-nitro-phenylarsonic acid).
Toxicosis results from an excess of arsenic-containing additives in pig or poultry diets. Severity and rapidity of onset are dose-dependent. Signs may be delayed for weeks after incorporation of 2–3 times the recommended (100 ppm) levels or may occur within days when the excess is >10 times the recommended levels. Chickens are tolerant of arsanilic acid; however, roxarsone can produce toxicosis in turkeys at only twice the recommended dose (50 ppm). In pigs, roxarsone also has a higher toxicity than other phenylarsonics.
The earliest sign in pigs may be reduced weight gain, followed by incoordination, posterior paralysis, and eventually quadriplegia. Animals remain alert and maintain good appetite. Blindness is characteristic of arsanilic acid intoxication but not of other organic arsenicals. In ruminants, phenylarsonic toxicosis is similar to inorganic arsenic poisoning. There are usually no specific lesions present in phenylarsonic poisoning. Demyelination and gliosis of peripheral nerves, the optic tract, and optic nerves are usually seen on histopathology. Analyses of feed for the presence of high levels of phenylarsonics confirm the diagnosis.
Phenylarsonic poisoning in pigs should be differentiated from salt poisoning, insecticide poisoning, and pseudorabies. In cattle, arsenic poisoning should be differentiated from other heavy metal poisoning, insecticide poisoning, and infectious diseases such as bovine viral diarrhea.
There is no specific treatment, but the neurotoxic effects are usually reversible if the offending feed is withdrawn within 2–3 days of onset of ataxia. Once paralysis occurs, the nerve damage is irreversible. Blindness is usually irreversible, but animals retain their appetite, and weight gain is good if competition for food is eliminated. Recovery may be doubtful when the exposure is long and the onset of intoxication slow.