The diagnostics and treatment of tropical diseases

by E. R. Stitt

It is possible that infectious material may be disseminated as dust and thus contaminate food.

Pathology

Injection of dysentery bacilli into the peritoneal cavity of guinea pigs causes a muco-sanguinolent diarrhoea with congestion of and haemorrhage into the caecum. There is also a haemorrhagic peritoneal exudate.

In the rabbit lesions similar to those in man are obtained as well as paralysis of the limbs.

It is therefore thought that there are two toxins concerned in the pathology of bacillary dysentery, one a neurotoxin which may cause a peripheral neuritis or joint trouble and the other a toxin which acts on the lower bowel, especially the caecum, with the production of congestion and coagulation necrosis of the mucosa.

Cases have been reported where the adrenals showed congestion and necroses, as if subjected to the action of a toxin.

In man we have an acute inflammation of the mucosa of the large intestines and, in the tropics, we frequently find the lower third of the ileum involved as well. In amoebic dysentery the process rarely extends beyond the ileo-caecal valve. A catarrhal process with hyperaemia and sero-purulent exudate is first noted, to be succeeded by fibrin formation in the mucosa, a process of coagulation necrosis. When the process invades the ileum there is no involvement of Peyer’s patches. Virchow noted the greater intensity of the process in the region of the rectum, sigmoid flexure and ileo-caecal valve.

As a rule, however, the entire large intestine is grayish red, looking like lustreless red velvet. Later on we may have irregular islands of grayish membrane formation surrounded by the red swollen congested gut. The solitary glands are usually swollen and may soften and ulcerate, having the submucosa as a base. Ulceration in bacillary dysentery is superficial rather than deep as with amoebic dysentery. The ulcers of bacillary dysentery involve the free folds of the intestine and extend transversely while amoebic ulcers run longitudinally. The intervening mucosa is unaffected in amoebic ulcerations while in bacillary ones it is inflamed.

Microscopically we note marked congestion of the blood vessels of the mucosa and submucosa with dilated lymph spaces full of polymorphonuclear cells.

In the mucosa we find an outpouring of pus cells which are entangled, along with the glandular structures of the mucosa, in a fibrinous exudate which causes necrosis of the mucosa (coagulation necrosis).