[8 April, 1907] Staggers in Horses. 245 



identical with that which is considered to cause the disease in man (the 

 diplococcus intracellular is meningitidis) is a question that is still un- 

 decided. According to Nocard's latest work (1903), the German 

 veterinary, Johne, concludes that they are identical, but Ostertag, another 

 German, denies this, and Nocard remarks that ' the very incomplete 

 descriptions furnished by Johne and Ostertag will not, from a bacterio- 

 logical point of view, allow of the deciding of the question.' In the 

 meantime, it may be observed that the disease changes in the brain in 

 man and in the horse have not always everything in common. In man, 

 inflammation of the brain covering (meningitis) is constant, but in horses 

 it is not so, there being many cases in which no changes in the brain 

 coverings can be discovered. The germ is supposed to belong to the 

 family of 'moulds' or saprophytes, i.e., those which usually live on dead 

 matter. They exist in the soil, and are conveyed to the animal either by 

 water, food, or bedding, but the exact mode in Avhich the germ invades 

 the body and penetrates into the nerve centres (brain and spinal cord) has 

 not been determined. It has been suggested that it may pass direct from 

 the no'strils through the nasal apertures (in the • ethmoid bone) to the 

 biain. 



" When animals become affected while at grass, it is in that season of 

 the year when the herbage is dry and ripe, and it used to be considered 

 that in over-ripe grass there was developed, in certain seasons, a poisonous 

 or narcotic principle, which caused the disease, in much the same way as 

 prussic acid is developed in sorghum during certain stages of its growth. 

 It is more probable, however, that when in a certain stage of ripeness 

 or deadness the grass- — more particularly rye grass — becomes attacked 

 by the germ or mould which causes the disease. Amongst stabled horses, 

 the disease attacks those housed in damp and badly -ventilated buildings, 

 and the connexion between the occurrence of the disease and the eating of 

 musty and mouldy forage, or the drinking of slimy water, has been in 

 many cases distinctly traced. Under such circumstances, it will be easily 

 understood how, without being transmitted from one animal to another 

 by infection, the disease attacks a number of animals placed under similar 

 conditions of food and water supply at the same time, and assumes the 

 cliaracter of an outbreak. 



" Symptoms. 



" Whatever may be still undecided regarding the pathological pheno- 

 mena and nature of the disease, the records of observations regarding- its 

 s> mptoms and progressive manifestations are fairly complete and accurate. 

 The usual symptoms are at first a drowsiness and aimlessness of move- 

 m.ent, the appetite is not lost, but the animal eats slowly and mechanicallv, 

 the breathing is slow, deep, and often snoring, pulse less frequent than 

 natural, a sleepiness comes over the animal, which, if suddenly disturbed, 

 is followed by shivering and evident excitement or fright. If made to 

 walk, the gait is straggling, and there is want of proper control of the 

 movements of the hind limbs, which are often crossed, the body wobbling 

 meanwhile and sometimes falling. The animal places its head against a 

 wall, or fence, or tree, or anything solid, and paws the ground automati- 

 cally, or moves the limbs as if walking. These symptoms are succeeded 

 by those of approaching delirium or convulsions. There will be great 

 excitement, the head will be tossed; horses will whinny and cattle bellow; 

 spasmodic twitchings of the muscles ofi neck, breast, and hindquarters will 



