and Klcemai), 1939) indicates that the test does not detect all 

 trichina infected swine. 



The evidence shows that the control measures of the past 

 have been palliative and casual and have not controlled trichi- 

 nosis; a basic program should aim at elimination of tlie prin- 

 cipal source of infection of swine — namely, pork scraps in gar- 

 bage or slaughter house waste. The swine sanitation system 

 is of great value where used; pigs are raised on pasture, are 

 not fed swill or garbage, and have little or no opportunity to 

 eat rats or other pigs. As alread.v noted, the incidence of por- 

 cine infection is correlated with the method of feeding pigs. 

 Localities, as England (Van Somereii, 1937), which require 

 cooking of any garbage fed to pigs have a low incidence. A 

 survey made by Wright (1940) shows that in the United States 

 over 50 percent of reporting cities having a population of 

 10,000 or over dispose of municipal garbage in whole or in 

 part by feeding it to swine. Very few cities cook it ; it is 

 evident therefore that municipalities are contributing substan- 

 tially to the spread of trichinosis. The problem of control 

 clearly lies in that field. 



Table 10. — Findings of trichinae in Xational Institute of 



Health nationwide survey* 



Direct microscopic and digest ion-Baermann methods 



Number of Number of 

 diaphragms diaphragms Percent 

 Series examined positive positive 



Base (10 hospitals in Washington, 



D. C, 2 Marine and 4 Naval 



hospitals in eastern seaboard 



cities) ___ _ 3,000 488 16.3 



Random (diaphragms selected at 



random from hospitals selected 



at random throughout U.S. A.) 436 80 1S.3 



Negative (from States in which 



clinical trichinosis has never 



been reported) 140 26 18.6 



Traumatic (persons suffering 



traumatic death and not hos- 

 pitalized) - _.._ 212 3S 17.9 



Jewish (orthodox and unorthodox 



Jews) _... 134 1 0.7 



Totals 3,922 633 16.1 



*As reported by Hall and Collins, 1937; Nolan and Bozice- 

 vich. 193S; Wright, 1939; Kerr, 1940; and Kerr, Jacobs and 

 Cuvillier (in press). 



The F'tlariae 

 D. L. A. 



The superfamily Filarioidea contains a large number of spe- 

 cies of which Wnchereria bancrofti (Colibold, 1877) Seurat, 

 1921 and Onchocerca rolrnlns (Leuckart, 1893) Railliet and 

 Henry, 1910, are important pathogens for man. Less important 

 species that infect man include Loa hia (Cobbold, 1864) Cas- 

 tellani and Chalmers. 1913; Dipelaloiiema perstans (Manson, 

 1891) Yorke and Maple.stone. 1926; and ilansnneUa oszardi 

 (Manson, 1897) Faust, 1929. Several other species have been 

 reported from man which are known only in the immature 

 stages. Of these only Microflnria malai/i (Brug, 1927) appears 

 to be of clinical importance. The following discussion will be 

 limited to the first two species named and Microfilaria malai/i. 



1. BANCROFTIAN FILARIASIS 



The enormous enlargements of parts of the body, particularly 

 of the legs and external genitals, so frequently accompanying 

 Bancroftian filariasis were noted and much studied long before 

 the etiological agent, Wnchereria bancrofti, was discovered. 

 According to Menon (193.1), the first, and a very good descrip- 

 tion of these conditions was written about 600 B. C. by Susliruta 

 in India. The disease was probably also well known in Persia, 

 Arabia, Egypt, and parts of Africa at that time. Hillary 

 (1766) gives a very good account of its occurrence in Barliados, 

 describing the recurring attacks of fever, the lymphangitis, the 

 lymphadenitis, and the slowly increasing swellings of the af- 

 fected part up to the stage at which typical elephantoid appear- 

 ances become definite and iironiinent. Hillary was certain 

 that the disease had been brought to the West Indies from 

 Africa by Negro slaves and, at his time, was observed to be 

 "too frequent among them and among the white people also." 

 Neumann (O'Connor and Beatty, 1938) estimated that 6 per- 

 cent of the population of St. Croix, Virgin Islands, had elephan- 

 tia.sis in 1881. 



Obsei-vations demonstrating the etiology of elephantiasis were 

 initiated in 1863 by the French surgeon Demarquay, who found 

 microfilariae in chylous urine of a person who had lived in 

 Cuba, were continued by the investigations of Lewis (1879) in 

 India and by others, and culminated in the research of Patrick 

 Manson in China between 1876 and 1900. Early in his inves- 

 tigations Manson discovered filarial periodicity and experimen- 

 tally demonstrated that a mosquito. Cule.r fatigans, was an es- 

 sential intermediate host and the agent for dissemination of 

 the parasite. More recent investigations have been largely epi- 

 demiological and pathological. Noteworthv among these arc the 

 studies of Bahr (1912), Low (1913), O'Connor (1923; 1931), 

 Anderson (1924), Fiilleborn (1929), Iyengar (1938), and Payn- 

 ton and Hodgkin (1938). 



The adult worms are parasites only of the lymphatic system 

 of man. They maj' occur at any level of the system, but are 

 found most frequently in the limbs, scrotum and inguinal re- 

 gions. The two sexes are frequently coiled together in the 

 periglandular tissues, the lymphatic vessels of the capsule and 

 in the cortical sinuses. In heavy infections they may also oc- 

 cur in the medulla. 



The microfilariae (for life history see p. 288) occur in the 

 lymph, the blood stream, and, under certain conditions (chy- 

 luria), may be found in the urine. Tliese larvae characteris- 

 tically exhibit a marked nocturnal periodicity. They are found 

 in greatest numbers between 10 o'clock in the evening and 2 

 o'clock in the morning, but during the day they may be en- 

 tirely absent from the blood. In the Philippine Islands and 

 largely throughout Polynesia, however, the microfilariae show- 

 no periodicity; while in Australia and New Guinea, periodicity 

 is the rule, but both types do occur. As far as is known botli 

 types represent one and the same species. In order to continue 

 their life cycle microfilariae must be taken up by an appropriate 

 mosquito. 



GEOGRAPHICAL DISTRIBUTION 



IVnchcreria bancrofti is practically world-wide in distribu- 

 tion, but is largely limited to tropical and subtropical coun- 

 tries. Its spread necessarily depends on the extent of the mi- 

 grations of individuals showing microfilariae in the blood, and 

 on the presence or absence of appropriate mosquitoes in new 

 areas to serve as intermediate hosts. The parasite is eharac- 

 teristicall.y found in island populations or along more or less 

 broad low-lying coastal areas of larger islands and continents. 

 In Asia it is established along coastal areas from Arabia to the 

 Shantung Province in Eastern China, and cases have been re- 

 ported as far north as Manchuria. It is prevalent in the islands 

 of the East China Sea, southern Japan, southern Chosen and 

 throughout Oceania. In Australia its distribution is mainly 

 along the Queensland coasts. 



Bancroftian filariasis is common across tropical Africa, 

 Madagascar, Mauritius and neighboring islands and along the 

 Mediterranean shores. It has been reported to be indigenous in 

 Spain, Hungary and Turkey. It is of very common occurrence 

 throughout the West Indies, the Guianas. and Venezuela, and is 

 less frequent in northern Colombia and eastern Brazil (Bahia). 

 It appears not to have become established along the Pacific 

 coast. A small endemic focus was reported in 191.5 and again 

 in 1919 in North America near Charleston, South Carolina 

 (Francis, 1919). Sporadic cases of infection have been noted 

 from time to time in various parts of the United States, but 

 these, invariably, were of foreign origin or from the Charles- 

 ton area. Thus, it is evident that Bancroftian filariasis has 

 a world-wide geographic distribution. Its distribution within 

 any given country is, however, characteristically and markedly 

 spotted and discontinuous due to the local physical factors and 

 the differences in social standards and .sanitation. 



PATHOLOGY 



It is generall.v held that living microfilariae are not patho- 

 genic. It has been observed that microfilariae readily pass 

 through lymph nodes without phagocytic filtration (Drinker, 

 Augustine and Leigh, 193.5). 'They are exceedingly active in 

 the blood stream. They are not only passively carried about 

 with the blood stream but actively move against the lilood 

 stream in the arterioles, making slow progress by bracing them- 

 selves through the crests of the alternate undulations of their 

 bodies against the walls of the vessel. They frequently- occlude 

 the capillaries and then make their way through the stagnated 

 column of blood cells to reenter the active circulation. They 

 apparently never make permanent plugs or form emboli (Au- 

 gustine, Field and Drinker, 1936; .\ugustine, 1937). 



The serious disorders are brought about by dead micro- 

 filariae and the living and dead adult worms. These disorders 

 in every case can be traced to interference with the lymphatic 

 system. Living worms, however, apparently cause little damage 

 other than varying degrees of blockage of the afferent approach 

 of the vessels in which the3- lie. However, when the adult 



318 



