ANTHRAQUINONE, C14H8O2, an important derivative of anthracene, first prepared in 1834 by A. Laurent. It is prepared commercially from anthracene by stirring a sludge of anthracene and water in horizontal cylinders with a mixture of sodium bichromate and caustic soda. This suspension is then run through a conical mill in order to remove all grit, the cones of the mill fitting so tightly that water cannot pass through unless the mill is running; the speed of the mill when working is about 3000 revolutions per minute. After this treatment, the mixture is run into lead-lined vats and treated with sulphuric acid, steam is blown through the mixture in order to bring it to the boil, and the anthracene is rapidly oxidized to anthraquinone. When the oxidation is complete, the anthraquinone is separated in a filter press, washed and heated to 120° C. with commercial oil of vitriol, using about 2½ parts of vitriol to 1 of anthraquinone. It is then removed to lead-lined tanks and again washed with water and dried; the product obtained contains about 95% of anthraquinone. It may be purified by sublimation. Various synthetic processes have been used for the preparation of anthraquinone. A. Behr and W.A. v. Dorp (Ber., 1874, 7, p. 578) obtained orthobenzoyl benzoic acid by heating phthalic anhydride with benzene in the presence of aluminium chloride. This compound on heating with phosphoric anhydride loses water and yields anthraquinone,
It may be prepared in a similar manner by heating phthalyl chloride with benzene in the presence of aluminium chloride. Dioxy- and tetraoxy-anthraquinones are obtained when meta-oxy- and dimeta-dioxy-benzoic acids are heated with concentrated sulphuric acid.
Anthraquinone crystallizes in yellow needles or prisms, which melt at 277° C. It is soluble in hot benzene, sublimes easily, and is very stable towards oxidizing agents. On the other hand, it is readily attacked by reducing agents. With zinc dust in presence of caustic soda it yields the secondary alcohol oxan-thranol, C6H4 : CO·CHOH : C6H4, with tin and hydrochloric acid, the phenolic compound anthranol, C6H4 : CO·C(OH) : C6H4; and with hydriodic acid at 150° C. or on distillation with zinc dust, the hydrocarbon anthracene, C14H10. When fused with caustic potash, it gives benzoic acid. It behaves more as a ketone than as a quinone, since with hydroxylamine it yields an oxime, and on reduction with zinc dust and caustic soda it yields a secondary alcohol, whilst it cannot be reduced by means of sulphurous acid. Various sulphonic acids of anthraquinone are known, as well as oxy-derivatives, for the preparation and properties of which see [Alizarin].
ANTHRAX (the Greek for “coal,” or “carbuncle,” so called by the ancients because they regarded it as burning like coal; cf. the French equivalent charbon; also known as fièvre charbonneuse, Milzbrand, splenic fever, and malignant pustule), an acute, specific, infectious, virulent disease, caused by the Bacillus anthracis, in animals, chiefly cattle, sheep and horses, and frequently occurring in workers in the wool or hair, as well as in those handling the hides or carcases, of beasts which have been affected.
Animals.—As affecting wild as well as domesticated animals and man, anthrax has been widely diffused in one or more of its forms, over the surface of the globe. It at times decimates the reindeer herds in Lapland and the Polar regions, and is only too well known in the tropics and in temperate latitudes. It has been observed and described in Russia, Siberia, Central Asia, China, Cochin-China, Egypt, West Indies, Peru, Paraguay, Brazil, Mexico, and other parts of North and South America, in Australia, and on different parts of the African continent, while for other European countries the writings which have been published with regard to its nature, its peculiar characteristics, and the injury it inflicts are innumerable. Countries in which are extensive marshes, or the subsoil of which is tenacious or impermeable, are usually those most frequently and seriously visited. Thus there have been regions notorious for its prevalence, such as the marshes of Sologne, Dombes and Bresse in France; certain parts of Germany, Hungary and Poland; in Spain the half-submerged valleys and the maritime coasts of Catalonia, as well as the Romagna and other marshy districts of Italy; while it is epizootic, and even panzootic, in the swampy regions of Esthonia, Livonia, Courland, and especially of Siberia, where it is known as the Sibirskaja jaswa (Siberian boil-plague). The records of anthrax go back to a very ancient date. It is supposed to be the murrain of Exodus. Classical writers allude to anthrax as if it were the only cattle disease worthy of mention (see Virgil, Georg. iii.). It figures largely in the history of the early and middle ages as a devastating pestilence attacking animals, and through them mankind; the oldest Anglo-Saxon manuscripts contain many fantastic recipes, leechdoms, charms and incantations for the prevention or cure of the “blacan blezene” (black blain) and the relief of the “elfshot” creatures. In the 18th and 19th centuries it sometimes spread like an epizootic over the whole of Europe, from Siberia to France. It was in this malady that disease-producing germs (bacteria) were first discovered, in 1840, by Pollender of Wipperfürth, and, independently, by veterinary surgeon Brauell of Dorpat, and their real character afterwards verified by C.J. Davaine (1812-1882) of Alfort in 1863; and it was in their experiments with this disease that Toussaint, Pasteur and J.B. Chauveau first showed how to make the morbific poison its own antidote. (See [Vivisection].)
The symptoms vary with the species of animal, the mode of infection, and the seat of the primary lesion, internal or external. In all its forms anthrax is an inoculable disease, transmission being surely and promptly effected by this means, and it may be conveyed to nearly all animals by inoculation of a wound of the skin or through the digestive organs. Cattle, sheep and horses nearly always owe their infection to spores or bacilli ingested with their food or water, and pigs usually contract the disease by eating the flesh of animals dead of anthrax.
Internal anthrax, of cattle and sheep, exhibits no premonitory symptoms that can be relied on. Generally the first indication of an outbreak is the sudden death of one or more of the herd or flock. Animals which do not die at once may be noticed to stagger and tremble; the breathing becomes hurried and the pulse very rapid, while the heart beats violently; the internal temperature of the body is high, 104° to 106° F.; blood oozes from the nose, mouth and anus, the visible mucous membranes are dusky or almost black. The animal becomes weak and listless, the temperature falls and death supervenes in a few hours, being immediately preceded by delirium, convulsions or coma. While death is usually rapid or sudden when the malady is general, constituting what is designated splenic apoplexy, internal anthrax in cattle is not invariably fatal. In some cases the animal rallies from a first attack and gradually recovers.
In the external or localized form, marked by the formation of carbuncles before general infection takes place, death may not occur for several days. The carbuncles may appear in any part of the body, being preceded or accompanied by fever. They are developed in the subcutaneous connective tissue where this is loose and plentiful, in the interstices of the muscles, lymphatic glands, in the mucous membranes of the mouth and tongue (glossanthrax of cattle), pharynx and larynx (anthrax angina of horses and pigs), and the rectum. They begin as small circumscribed swellings which are warm, slightly painful and oedematous. In from two to eight hours they attain a considerable size, are cold, painless and gangrenous, and when they are incised a quantity of a blood-stained gelatinous exudate escapes. When the swellings have attained certain proportions symptoms of general infection appear, and, running their course with great rapidity, cause death in a few hours. Anthrax of the horse usually begins as an affection of the throat or bowel. In the former there is rapid obstructive oedema of the mucous membrane of the pharynx and larynx with swelling of the throat and neck, fever, salivation, difficulty in swallowing, noisy breathing, frothy discharge from the nose and threatening suffocation. General invasion soon ensues, and the horse may die in from four to sixteen hours. The intestinal form is marked by high temperature, great prostration, small thready pulse, tumultuous action of the heart, laboured breathing and symptoms of abdominal pain with straining and diarrhoea. When moved the horse staggers and trembles. Profuse sweating, a falling temperature and cyanotic mucous membranes indicate the approach of a fatal termination.