ENTERIC FEVER IN THE TROPICS 215 



B. paratyphosus A is prevalent in India and China. Several out- 

 breaks have been traced to fecal contamination. 



Epidemics may be due to the seasonal prevalence of flies, distribu- 

 tion of milk, an infected well or stream, the seasonal use of shell-fish, 

 eating of fried lish so common in the East End of London. 



For a description of the typhosus bacillus, see p. 619. 



Europeans newly entering the tropics should be particularly 

 careful. In Bengal 50 per cent, of the cases in Europeans occurred 

 within one year of their arrival from Europe. 



Rogers noticed that in India 41 "67 per cent, of the cases were in 

 children under 15 years of age. 



Natives are asserted to be somewhat immune to the disease. 



Roberts in explaining this gives some interesting comparisons. 



The gut of the native is longer, more muscular and thicker than 

 that of the European, also Fever's patches are less in evidence. 



Habitat and diet also are important predisposing factors. 



The Native The European 



Food cold and dry. 



Bulky, coarse, much waste. 



Vegetable grains, cereals, pulses ; large 

 cellulose content ; low protein and fat 

 content. 



Food partially cooked, plain and 

 monotonous. 



Meals infrequent, twice daily, long 

 fasts. 



Mastication generally good. 



Life and work in the open air. 



Fascal evacuations twice daily, large, 

 10-12 ounces. 



Strain on stomach and large bowel. 



The majority eat to live. 



Hot and fluid. 

 Concentrated and soluble. 

 Animal food, with high protein and fat 

 content. 



Thoroughly cooked, well mixed, and 

 varied. 



Meals frequent, 4-5 daily. 



Faulty in the extreme. 

 Sedentary and indoors. 

 Small, 5-6 ounces, constipation com 

 mon, purgatives. 



Strain on stomach and small intestine 

 More live to eat. 



PATHOLOGY. 



The disease is a septicemia produced by the invasion of the 

 intestinal lymphoid tissue by bacilli which have entered by the mouth. 

 In this tissue the}' multiply, many passing bv the lymphatics to the 

 abdominal l}-mphatic glands and the spleen increasing rapidlv in 

 each. In the blood they are destroyed if few in number and their 

 toxins neutralized. If it does not proceed beyond this an ambulatory 

 or abortive attack is produced. 



When the bacilli are more numerous but destroyed bv bacteriolysis 

 there may not be sufficient antitoxin to neutralize their toxins, then the 

 fever begins. Ferhaps the antitoxin is formed irregularly and so 

 accounts for the intermittent nature of the disease and the relapse in 

 the tropics. The endotoxin causes the endothelial cells to swell so 

 that the small lymph channels in the liver are blocked and patches of 

 focal necrosis formed. 



