MALARIAL CACHEXIA REMOTE EFFECTS OF MALARIA TREATMENT


When a patient is continually exposed to the malaria miasm which gives rise to chills and fever, he no longer displays the typical, recurrent symptoms of an intermittent fever….


WHEN the malarial poison, instead of being eliminated from the system, remains to pursue its ravages, a series of constitutional effects follow, which are called the Malarial Cachexia.

The symptoms of this Cachexia vary from those which mark merely chronic disease to those which indicate remote changes in functions and tissues.

When a patient is continually exposed to the miasm which gives rise to chills and fever, he no longer displays the typical, recurrent symptoms of an intermitting fever; except, perhaps, in the height of the “season” when, a fresh supply of the poison arouses the system from its condition of non-resistance. But he is constantly suffering from a series of symptoms which indicate that depraved state of the body we call Cachexia. As this state becomes more and more fixed, nutritive changes develop and increase, and finally a condition is reached which constitutes what we may term the remote effects of Malaria.

We are to consider, then, tow conditions differing only in degree the one the ultimate effect of the other.

In the early manifestations of the Malarial Cachexia, the patient suffers from general Malaise. Clear, crisp days days are enjoyable, but every damp day, especially every warm and wet change, makes him gloomy, weary and cold.

One suffers from biliousness; another from diarrhoea; a third is tormented with Neuralgia. Still another feels tolerably well, but the onset of any disease is the occasion for an arousing of the malarial poison, greatly to his discomfort as it complicates his case and renders recovery tardy and uncertain. As the Cachexia becomes more permanent, the victim displays more constant symptoms, indicative of organic lesions. He is pale or sallow, jaundiced when the liver is diseased or its ducts obstructed, but yellow whether icteric or not. The mouth is dry, there is bitter taste and the tongue is furred. He is melancholic, suffers from tinnitus aurium, and complains of spinal irritation and even of paretic symptoms. He is always dizzy, even when not bilious.

Soon he becomes anaemic; and liver and spleen are enlarged forming what are termed “ague-cakes” a term most frequently applied to an enlarged spleen, though no less applicable to the swollen liver, too.

Still later, there develops a sort of cirrhosis of liver spleen and kidneys “Ague-cakes” are now replaced by contracted organs, congestion and haemorrhage giving place to softened pulp, fatty degeneration, amyloid changes and hypertrophy of the connective tissues. The basement membrane of the kidneys is thickened and uriniferous tubules are filled with cast off epithelium.

The heart, like muscular tissue elsewhere, becomes softened and flaccid; finally it is dilated.

Anaemia is an early and progressive symptom. Dependent at first upon defective manufacture of blood, arising from diseased spleen, etc., it soon finds other causes in the advance stage of the Malarial Cachexia; especially in imperfect digestion and in defective assimilation from intestinal catarrh and alterations in the intestinal glands.

Disintegration of red corpuscles leads to two sets of accidents; one haemorrhage, which most commonly appears as epistaxis; the other, the effects of emboli. These emboli, if they may be so- called, arise from a clogging of small vessels with pigment granules, derived from the broken down blood-cells in the spleen.

A common symptom is Dropsy. This may appear as oedema of the ankles, as Ascites, or as Anasarca, according as it arises simply from anaemia or from lesions of liver, spleen, heart or kidneys.

Finally, as still more remote effects of Malaria, we may refer to the wrinkled and half-imbecile state referred to by Watson, as, resulting from a protracted residence in miasmatic districts. Children reared in such places are dwarfed and idiotic; adults are shrivelled, stoop-shouldered and also mentally impaired.

E. A. Farrington
E. A. Farrington (1847-1885) was born in Williamsburg, NY, on January 1, 1847. He began his study of medicine under the preceptorship of his brother, Harvey W. Farrington, MD. In 1866 he graduated from the Homoeopathic Medical College of Pennsylvania. In 1867 he entered the Hahnemann Medical College, graduating in 1868. He entered practice immediately after his graduation, establishing himself on Mount Vernon Street. Books by Ernest Farrington: Clinical Materia Medica, Comparative Materia Medica, Lesser Writings With Therapeutic Hints.