Toward the close of 1911 there was a great shortage of the rice crop and the Philippine government bought quantities of rice in order to protect the people from extortionate dealers. Much of this rice was polished rice. The use of this polished rice was commenced at Culion in November, 1911. In January, 1912, there were 35 deaths, of which 2 were from beriberi. In February 86 deaths with 36 from beriberi and in March 82 deaths with 60 from beriberi. In February the use of polished rice was discontinued and unpolished rice substituted. In April the deaths had fallen to 25 with 3 from beriberi and, subsequent to that month, deaths from beriberi cases developing at Culion ceased to be reported.
As regards the length of time necessary for the production of the symptom-complex, Strong’s experiments show that beriberi was produced in from sixty-one to seventy-five days. In Fraser and Stanton’s work no case developed under eighty-seven days and many of the cases did not develop for 120 to 160 days. Hamilton Wright considered that the incubation period for his toxin-producing bacillus was ten to thirty days.
Pathology and Morbid Anatomy
In polyneuritis gallinarum, Vedder and Clark are of the opinion that there may be two vitamines involved, the absence of one from the dietary causing the neuritis, while that of the other leads to general prostration and cardiac degeneration, so that there may be other factors in the production of beriberi than the degeneration of the peripheral nerves and involvement of the vasomotors.
Furthermore, extract of rice polishings rapidly cures the cardiac condition as well as the dropsy, but not the paresis; while Funk’s vitamine base, which will cure the paralysis, will not affect the cardiac disorder.
The blood of beriberics in the acute stage, has been shown to contain a substance capable of profoundly influencing the vasomotor functions, causing venous engorgement and a fall of blood pressure.
In deaths from wet beriberi the tissues are very moist so that incisions tend to fill with fluid. There are generally present pleural and in particular pericardial effusions. Serous fluid in the abdominal cavity may also be present. The lower end of the stomach and the upper portion of the small intestines, in particular the duodenum, show marked congestion with more or less abundant haemorrhagic extravasations. Some authorities do not admit the existence of this duodenal congestion so insisted upon by Wright.
The oesophagus is usually congested as may be also the pharynx and the larynx.
Next to the peripheral nerve degenerations, to be later considered, the most important lesions are found in connection with the heart. All chambers of the heart show a dilatation with hypertrophy as well as dilatation of the right ventricle in cases that have lasted for some time. The heart muscle has the faded-leaf appearance indicative of fatty degeneration. Microscopically there are segmentation and vacuolation of the fibres. The lungs show congestion and at times present the characteristics of pulmonary oedema. The kidneys are congested but show only exceptionally parenchymatous or interstitial changes. As would be expected, the back pressure in the right heart gives a dilatation of the central vein of the liver lobules which at times is productive of atrophy of the adjacent liver cells. The muscles supplied by the affected peripheral nerves show more or less atrophy according to the duration of the disease.
Microscopically, the affected fibres show a loss of striation with a colloid degeneration. These changes are more marked in beriberic residual paralysis. The key to the disease is in the changes present in the peripheral nerves. While these may appear normal yet histological examination shows varying nerve degenerations from slight medullary degeneration in a few fibres to complete destruction of the nerve, giving a Wallerian degeneration (vacuolation and formation of myelin droplets in the medullary sheath with fragmentation of the axis-cylinder).