THE MALARIAL FEVERS 



those organs. After a series of attacks the blood capillaries and 

 lymph spaces in the liver and spleen remain permanently dilated, 

 and separated by only a slight amount of damaged parenchyma 

 tissue. Later, regeneration of the parenchyma takes place, but 

 the organ will remain permanently altered, even though all pig- 

 mentation may have disappeared. 



In the case of the subtertian parasite, serious local damage may 

 be caused to the brain, the intestine, the pancreas, or other organs, 

 by the parasites massing in the capillaries and forming, with free 

 pigment and swollen endothelial cells laden with pigment and 

 parasites, regular thrombi, sufficient to impede the circulation, and 

 thus to still further damage the toxin-poisoned organ. Finally, the 

 toxins are excreted by the skin and by the kidney, and in doing so 

 may damage the latter organ. 



There are two main conditions, the pathology of which must be 

 explained — viz., acute and chronic malaria. In acute malaria there 

 are the effects produced by each of the three parasites, of which the 

 subtertian is liable to seriously damage important organs. 



Chronic malaria should also be described according to the three 

 types, but there is at present lack of material to evolve such a 

 description. Chronic malaria may, however, pass to an advanced 

 condition called ' malarial cachexia,' which shows itself in three 

 ways— as (i) a rare acute cachexia; (2) a more common chronic 

 cachexia ; (3) cachexia with amyloidosis. 



In addition, there are the pathological features of latent malaria 

 and the relapses. 



Before, however, proceeding to describe the actual morbid 

 anatomy of these conditions, a few words must be said upon what 

 we know of the chemical pathology of the disease and on the blood 

 changes which take place. 



Chemical Pathology. — The pyretogenous toxin has already been 

 mentioned among the poisons of animal origin, and, though long 

 suspected of being present, its actual occurrence was first proved 

 by Rosenau and his collaborators. Probably it is the poison which 

 acts deleteriously upon the tissues of the organs and causes meta- 

 bolic changes, but this is only a matter of conjecture. 



We know that the heat output in the cold stage of the attack is 

 markedly diminished — a condition met with in many fevers — but 

 the chemistry of the metabolic changes is but little known. During 

 the attack the urine is at first increased in quantity, which is thought 

 to be due to the rise of blood-pressure internally, owing to the 

 contraction of the cutaneous vessels during the cold stage. Not- 

 withstanding this increase in quantity, the specific gravity is raised, 

 because of the increased metabolism caused by the toxins, as is 

 shown by the large increase in solids. The colour is dark, and the 

 acidity of the urine is increased, as in most fevers. Nitrogen is 

 excreted in excess, which is largely due to the increase of urea. 

 Chlorides, sulphates, and bases, especially potassium, are all in- 

 creased in quantity. Phosphates, however, are diminished during 



