Phosphorus



1b. Slow poisoning. – On Oct. 8th an old rabbit was put into the box. After 3 weeks it began to emaciate, but did not lose its appetite; suppurating ulcers appeared on tongue and eyelids; the creature grew dejected and apathetic. It was found dead December 4th. Dissection showed tongue almost entirely covered with ulcerations, and the blepharophthalmia had so much increased that the eyes could scarcely be opened; there was, however, no sclerotitis. Venous system was considerably engorged; lungs very much reddened, on some parts black; gall and urinary bladder both very full; all else normal. Another rabbit was put in on Oct. 10th; on Dec. 28th it was found dead. After being 3 weeks in box suppuration of right eye had begun, and increased to such a degree that soon it could not be opened. Dissection showed eye to be sunk, lids adherent, cornea thickened and opaque, pupil filled with pus, but lens and vitreous normal. Veins were full of black fluid blood; muscular parts injected; lungs in some parts showed venous engorgement only, but were mostly hepatized, and here and there tubercles were observable; liver rather congested, and gall – bladder greatly distended with reddish – brown bile.

1c. In order to ascertain if he could produce in rabbits the disease of jaws met with in the human subject, v. Bibra exposed to the fumes some whose jaws he had previously broken. On their death, after about 8 weeks, a large spongy callus was found around the seat of fracture, presenting exactly the characters of the disease in man. The periosteum also was found much separated from the bone, and the whole bathed in unhealthy – looking pus. (v. BIBRA und GEIST, op. cit.)

2. The anatomically demonstrable action of Ph. when given in relatively small doses, incapable of killing either sooner or later, extend principally to two major systems of the body – the digestive apparatus, especially stomach and liver, and the osseous system. [Wegner did not find pneumonia in animals exposed to the fumes any oftener than under ordinary circumstances; and tuberculosis he never observed.]

2a. Let rabbits, cats or dogs be brought under the influence of Ph. in minimum doses, either by exposure to its fumes or by its introduction in pill form per oesophagum, and the dose be gradually increased (but always short of any obvious toxical effect); and very remarkable changes take place. The gastric mucous membrane becomes hyperaemic; it swells; haemorrhages occur here and there, and later on real haemorrhagic infarctions are seen, especially on the summits of the natural folds, where flat pit – like ulcers are found, whose dirty – brown margin and floor show their origin. After the irritation has been going on for months the mucous membrane becomes two or three times thicker than it normally was; it becomes indurated, and of a diffuse smoke – grey or brown colour that is most evident at the fundus. (Here the microscope shows whole masses of pigment in the form of black – brown granules imbedded in the tissue; the glands prolonged; and the interstitial connective tissue, which in the healthy condition is scarcely demonstrable, becomes developed into thick broad threads.)

2b. Alterations in the structure of the liver go hand in hand with the above. The whole organ is swelled and feels harder, and within it and in the connective tissue around the portal vessels there is an intense cellular hyperplasia, and tough fibrous connective tissue is developed from the young cells, constituting a more or less broad stratum at the periphery of the acini. The peripheral zone of the hepatic cells undergoes fatty degeneration, and in the greater part of the acini the cells have an icteric colour, evidently in consequence of the pressure exerted by the new prolifically – developed tissue on the afferent ducts which course with the portal ramifications. In fact, we have interstitial hepatitis in optima forma, the result of which is atrophy of a three fold kind, – either a smooth induration of the liver; or (as sometimes seen in syphilitic human subjects) a “hepar lobatum” with numerous strips of cicatricial tissue dipping deep into the organ and deforming it; or, finally, the typical granular atrophy, the classical cirrhosis. In all these forms icterus is present, and in the last we regularly find those secondary disturbances so well known in human pathology – venous hyperaemia of the mucous membrane of stomach and intestines, indurative hyperplasia of the spleen, and finally death from ascites and hydrothorax. (WEGNER, Virchow’s Archiv,, Bd. lv.)

3a. Let rabbits be confined for weeks or months in an atmosphere pervaded with the fumes of Ph., and we shall see that, after the primary bronchial irritation has subsides, they get accustomed to it. In the cranial bones we see nothing abnormal except minute and hardly visible osteophytic sub – periosteal deposits on the bones forming (Wegner did not find pneumonia in animals exposed to the fumes by oftener than under ordinary circumstances; and tuberculosis he never observed.) The boundaries of the nasal cavities. But in an insignificant minority of them there arises, generally without any evident external cause, a tumefaction on the upper and lower jaws; the bone pushes out processes, the sort parts often swell monstrously from extensive caseous infiltration, respiration becomes difficult, and mastication is interfered with. The thickening of the bone advances continually, the sort parts have become hard as a board, until, finally, movement of the jaws becomes impossible, and the animal succumbs from inanition. After the extremely firmly – adhering, caseously – infiltrated soft parts are stripped off (or, better, rolled off), we see extensive and often enormously thick osseous deposits of very dense structure on the old superficies of the jaw, generally starting from the alveolar margin. There are in filled with caseous exudations, and having crateriform everted edges, – in a word, ulcerations partial necrosis. The process is essentially the maxillary periostitis with masses of osteophytic new growth and necrosis, so well known from observations on the human subject. (Dr. Wegner now discusses the question why a few only among animals and workpeople as thus affected, and concludes that as carious teeth are generally the starting point in the latter, some corresponding lesion must exist in the former, the process starting thus from a local irritation produced by the fumes. He admits, however, that there are exceptions to the rule of carious teeth being present in the work people, and that in one only of the animals effected could he discover any such; so that, he says, “we must fall back upon the hypothesis of an opportune wounding of the periosteum.” If this is induced artificially, animals hitherto untouched become the subjects of the Ph. bone disease.)

3b. If we give to a rabbit, dog, cat, or fowl – while yet immature – minute doses of Ph. in pill, so insignificant that they produce no changes in stomach or liver; or if we cause them to inhale air moderately charged with its fumes; and subsequently, after a relatively short time (10 day in those that are quickly growing, 3 weeks in others), carefully examine their bones, we shall find changes of a more or less different kind, and which evidence their presence in different ways, according to the stage of growth of the animals. In all those places where, physiologically, there is developed from cartilage spongy osseous substance, having wide meshes and much red medullary tissue, there is formed under the influence of Ph. a tissue that, seen with the naked eye, appears perfectly homogeneous, solid, and compact, just like the cortex of the long bones. That part of the spongy tissue which was developed before the feeding began remains perfectly unchanged. The substance of the Ph. stratum shows itself under the microscope to be real well – formed bone.

3c. If the feeding with Ph. be continued, dense osseous substance is always added to the cylindrical bone from the intermediary cartilage, [Intermediary, that is, between the shaft and its epiphyses and apophyses EDS, ] while the spongy substance formed before the feeding obeys the physio – logical law by being disintegrated and absorbed to form the medullary canal. Thus one sees, after a certain period, according to the rate of growth, the entire normal cancellous structure at the extremities of the diaphyses replaced by a compact solid bony mass. If we continue the feeding still longer, we find that the abnormally formed bone – substance likewise follows the physiological law for the formation of the medullary canal, – the oldest layers, which are pushed nearest to the centre, again become rarefied, and at last melt down into red medullary tissue. (If the feeding with Ph. be arranged with intervals of abstinence, we find developed from the intermediary cartilage strata of dense compact substance alternating with others of ordinary spongy structure.)

3d. If Ph. be given in small doses to animals after their bones have ceased to grow, the spongy tissue in the epiphyses, vertebrae, &c., gets a little thicker; the osseous spiculae and lamellae are a little broader and thicker, without, however, any approach to a sclerosis of the spongy part as we have seen it in the newly – deposited layers of growing animals. The compact substance, also, of the cylindrical and of the flat bones becomes more dense from the narrowing of the vascular canals. Just as the medullary tissue, in the meshes of the cancellous substance and around the circumference of the vessels in the Haversian canals, in part becomes changed into bone, so also, in consequence of continued feeding with Ph., does a part of the medullary substance which fills the large medullary canal under go an ossificatory process; and it is the peripheral layers that ossify, so that while the circumference of the bones remains constant the medullary canal becomes contracted, and the compact crust grows thicker by the deposit of new layers within. In fowls we can at last succeed, by feeding several months with Ph., in obtaining a complete occlusion of the medullary canal with real osseous substance, – in this sequence; first the bones of the tarsus, then the tibia, the bones of the forearm, the femur, and lastly the humerus.

Richard Hughes
Dr. Richard Hughes (1836-1902) was born in London, England. He received the title of M.R.C.S. (Eng.), in 1857 and L.R.C.P. (Edin.) in 1860. The title of M.D. was conferred upon him by the American College a few years later.

Hughes was a great writer and a scholar. He actively cooperated with Dr. T.F. Allen to compile his 'Encyclopedia' and rendered immeasurable aid to Dr. Dudgeon in translating Hahnemann's 'Materia Medica Pura' into English. In 1889 he was appointed an Editor of the 'British Homoeopathic Journal' and continued in that capacity until his demise. In 1876, Dr. Hughes was appointed as the Permanent Secretary of the Organization of the International Congress of Homoeopathy Physicians in Philadelphia. He also presided over the International Congress in London.