In favorable cases recovery takes place in one or two days. There is a return of life and appetite, a gradual improvement in pulse and breathing, the respirations becoming deeper and longer, and in a few hours all the more violent symptoms may have disappeared. With a more gradual improvement recovery may still be complete in four or five days. _Lesions._ When the subject has died suddenly the appearances are essentially those of uniform engorgement of the pulmonary capillaries with blood. The general aspect is a dark red, varying from reddish brown to black, the darkest shades corresponding to circumscribed areas of actual hæmorrhage. In the worst cases the whole mass may appear like black currant jelly. The lungs do not collapse when the chest is opened, they are more or less friable at various points, and different portions will sink or float in (not on) water, according as it may be more or less airless. A dark liquid blood exudes freely from the torn or cut surface. Sections of the lung tissue hardened and examined under the microscope show the alveoli and bronchioles devoid of exudate, but having their cavities compressed and obliterated by the pressure of the swollen mucosa, and its investing blood clot. The heart is overdistended with fluid blood. In asphyxiated cases the general venous system is filled with black, liquid blood, and the serosæ spotted with petechiæ. _Nature._ The nature of this disease is variously understood. It differs from inflammation in the absence of active cell proliferation, and migrations of inflammatory exudation, and of fever at all proportionate to the extent of the lesions. All these may and do supervene if the patient survives but they are practically absent for a length of time at the outset. Some attribute it to paresis of the vaso-motor centres for the lungs, as the result of their over stimulation and of the retrocession of blood from the chilled surface to the internal organs. But congestions caused by cutting the cervical branch of the sympathetic nerve or the sciatic plexus are not marked by a similar blood extravasation and destruction of tissue. The delicate structure of the lung tissue and the comparative absence of mechanical support will account for this in part, the great force of the circulation overloading the capillaries, under the impulse of the heart so closely adjacent, has doubtless a certain effect, and the venous nature of the blood thus forced into the lungs and calculated to arrest all normal function has a potent influence. If we add to this, for the _over-exertion_ cases, the sudden advent into the circulatory stream of unchanged peptones and other ingredients of the portal blood of highly fed and plethoric animals we find a sufficiently pathogenic combination. In all acute cases however the adiposity, poor condition and susceptibility to speedy exhaustion must be given their full share of responsibility.