The trypanosomes are elongated, usually pointed, flagellated protozoa (fig. 136) in which the single flagellum, bent under the body, forms the outer limit of a delicate undulating membrane. It arises near one end of the organism from a minute centrosome-like body which is known as the blepheroplast, and at the opposite end extends for a greater or less distance as a free flagellum. Enclosing, or close beside the blepheroplast is the small kinetonucleus. The principal nucleus, round or oval in form, is situated near the center of the body. Asexual reproductions occurs in this stage, by longitudinal fission, the nucleus and the blepheroplast dividing independently of one another. From the blepheroplast of one of the daughter cells a new flagellum is formed.

Among the pathogenic species are to be found the causative organisms of some of the most serious diseases of domestic animals and even of man. It is probable that these pathogenic species secrete a specific poison. The majority of them are tropical in distribution.

Though we are concerned especially with the species which infest man, we shall first consider two of the trypanosomes of lower animals, known long before any of those of man had been found.

Fleas and Lice as Carriers of Trypanosoma lewisi.—Trypanosoma lewisi, the first mammalian trypanosome known, is to be found in the blood of wild rats. Like its host, it appears to be cosmopolitan in distribution, having been reported from several localities in the United States, Brazil, Argentine, England, Germany, France, Italy, Russia, Asia and Africa.

Nuttall concludes that since three distinct kinds of blood-sucking insects are capable of transmitting Trypanosoma lewisi it appears doubtful that this flagellate is a parasite of the invertebrate "host" in the sense claimed by Prowazek and other investigators.

Tsetse-flies and Nagana—One of the greatest factors in retarding the development of certain regions of Africa has been the presence of a small fly, little larger than the common house-fly. This is the tsetse-fly, Glossina morsitans (fig. 165) renowned on account of the supposed virulence of its bite for cattle, horses and other domestic mammals.

The technical characteristics of the tsetse-flies, or Glossinas, and their several species, will be found in a later chapter. We need emphasize only that they are blood-sucking Muscidæ and that, unlike the mosquitoes, the sexes resemble each other closely in structure of the mouth-parts, and in feeding habits.

In 1894, Colonel David Bruce discovered that the fly was not in itself poisonous but that the deadly effect of its bite was due to the fact that it transmitted a highly pathogenic blood parasite, Trypanosoma brucei. This trypanosome Bruce had discovered in the blood of South African cattle suffering from a highly fatal disease known as "nagana". On inoculating the blood of infected cattle into horses and dogs he produced the disease and found the blood teeming with the causative organism. In the course of his work he established beyond question that the "nagana" and the tsetse-fly disease were identical.

Tsetse-flies of the species Glossina morsitans, which fed upon diseased animals, were found capable of giving rise to the disease in healthy animals up to forty-eight hours after feeding. Wild tsetse-flies taken from an infected region to a region where they did not normally occur were able to transmit the disease to healthy animals. It was found that many of the wild animals in the tsetse-fly regions harbored Trypanosoma brucei in their blood, though they showed no evidence of disease. As in the case of natives of malarial districts, these animals acted as reservoirs of the parasite. Non-immune animals subjected to the attacks of the insect carrier, quickly succumbed to the disease.

A question of prime importance is as to whether the insect serves as an essential host of the pathogenic protozoan or whether it is a mere mechanical carrier. Bruce inclined to the latter view. He was unable to find living trypanosomes in the intestines or excrements of the fly or to produce the disease on the many occasions when he injected the excrement into healthy animals. Moreover, he had found that the experimental flies were infective only during the first forty-eight hours and that if wild flies were taken from the infected region, "kept without food for three days and then fed on a healthy dog, they never gave rise to the disease."

Koch had early described what he regarded as sexual forms from the intestine of the fly but it remained for Kleine (1909) to experimentally demonstrate that a part of the life cycle of the parasite was undergone in the fly. Working with Glossina palpalis, he found that for a period of ten days or longer after feeding on an animal suffering from nagana it was non-infective, but that then it became infective and was able to transmit the disease for weeks thereafter. He discovered and described developmental stages of the parasite within the intestine of the insect. In other words, the tsetse-fly (in nature, Glossina morsitans), serves as an essential host, within which an important part of the life cycle of the parasite is undergone. These conclusions were quickly verified by Bruce and numerous other workers and are no longer open to question. Klein and Taute are even inclined to think that mechanical transmission plays practically no rôle in nature, unless the fly is interrupted while feeding and passes immediately to a new animal.

Tsetse-flies and Sleeping Sickness of Man—About the beginning of the present century a hitherto little known disease of man began to attract great attention on account of its ravages in Uganda and the region of Victoria Nyanza in South Africa. It was slow, insiduous and absolutely fatal, characterized in its later stages by dullness, apathy, and finally absolute lethargy all day long, symptoms which gave it the name of "sleeping sickness."

It was soon found that the disease was not a new one but that it had been known for over a hundred years on the west coast of Africa. Its introduction into Central and East Africa and its rapid spread have been attributed primarily to the development of the country, the formation of new trade routes and the free mingling of native tribes formerly isolated. It is estimated that in the first ten years of the present century there were approximately two hundred thousand deaths from the disease in the Uganda protectorate. In the British province Bugosa, on the Victoria Nyanza there were thirty thousand deaths in the period from 1902-1905.

While the disease is peculiarly African there are a number of instances of its accidental introduction into temperate regions. Slaves suffering from it were occasionally brought to America in the early part of the last century and cases have sometimes been imported into England. In none of the cases did the disease gain a foothold or spread at all to other individuals.

In 1902 Dutton described a trypanosome, T. gambiense, which he and Forde had found the year before in the blood of a patient suffering from a peculiar type of fever in Gambia. In 1902-1903 Castellani found the same parasite in the cerebro-spinal fluid of sleeping-sickness patients and definitely reported it as the causative organism of the disease. His work soon found abundant confirmation, and it was discovered that the sleeping sickness was but the ultimate phase of the fever discovered by Dutton and Forde.

When Castellani made known his discovery of the trypanosome of sleeping sickness, Brumpt, in France, and Sambon, in England, independently advanced the theory that the disease was transmitted by the tsetse-fly, Glossina palpalis. This theory was based upon the geographical distribution and epidemiology of the disease. Since then it has been abundantly verified by experimental evidence.

Fortunately for the elucidation of problems relating to the methods of transfer of sleeping sickness, Trypanosoma gambiense is pathogenic for many species of animals. In monkeys it produces symptoms very similar to those caused in man. Bruce early showed that Glossina palpalis "fed on healthy monkeys eight, twelve, twenty-four and forty-eight hours after having fed on a native suffering from trypanosomiasis, invariably transmitted the disease. After three days the flies failed to transmit it." In his summary in Osler's Modern Medicine, he continues "But this is not the only proof that these flies can carry the infective agent. On the lake shore there was a large native population among whom we had found about one-third to be harboring trypanosomes in their blood. The tsetse-flies caught on this lake shore, brought to the laboratory in cages, and placed straightway on healthy monkeys, gave them the disease in every instance, and furnished a startling proof of the danger of loitering along the lake shore among those infected flies."

As in the case of nagana, Bruce and most of the earlier investigators supposed the transmission of the sleeping sickness trypanosome by Glossina palpalis to be purely mechanical. The work of Kleine (1909) clearly showed that for Trypanosoma gambiense as well as for Trypanosoma brucei the fly served as an essential host. Indeed, Kleine and many subsequent investigators are inclined to think that there is practically no mechanical transmission of trypanosomes from animal to animal by Glossina in nature, and that the many successful experiments of the earlier investigators were due to the fact that they used wild flies which already harbored the transformed parasite rather than directly inoculated it from the blood of the diseased experimental animals. While the criticism is applicable to some of the work, this extreme view is not fully justified by the evidence at hand.

Kleine states (1912) that Glossina palpalis can no longer be regarded as the sole transmitter of sleeping sickness. Taute (1911) had shown that under experimental conditions Glossina morsitans was capable of transferring the disease and Kleine calls attention to the fact that in German East Africa, in the district of the Rovuma River, at least a dozen cases of the disease have occurred recently, though only Glossina morsitans exists in the district. It appears, however, that these cases are due to a different parasite, Trypanosoma rhodesiense. This species, found especially in north-east Rhodesia and in Nyassaland, is transferred by Glossina morsitans.

Other workers maintain that the disease may be transmitted by various blood-sucking flies, or even bugs and lice which attack man. Fülleborn and Mayer (1907) have shown by conclusive experiments that Aedes (Stegomyia) calopus may transmit it from one animal to another if the two bites immediately succeed each other.

It is not possible that insects other than the tsetse-flies (and only certain species of these), play an important rôle in the transmission of the disease, else it would be much more wide-spread. Sambon (1908) pointed out that the hypothesis that is spread by Aedes calopus is opposed by the fact that the disease never spread in the Antilles, though frequently imported there by West African slaves. The same observation would apply also to conditions in our own Southern States in the early part of the past century.

Since Glossina palpalis acts as an essential host of the parasite and the chief, if not the only, transmitter, the fight against sleeping sickness, like that against malaria and yellow fever, becomes primarily a problem in economic entomology. The minutest detail of the life-history, biology, and habits of the fly, and of its parasites and other natural enemies becomes of importance in attempts to eradicate the disease. Here we can consider only the general features of the subject.

Glossina palpalis lives in limited areas, where the forest and undergrowth is dense, along the lake shore or river banks. According to Hodges, the natural range from shore is under thirty yards, though the distance to which the flies may follow man greatly exceed this.

It is a day feeder, a fact which may be taken advantage of in avoiding exposure to its attacks. The young are brought forth alive and full-grown, one every nine or ten days. Without feeding, they enter the ground and under favorable conditions, complete their development in a month or more.

Methods of control of the disease must look to the prevention of infection of the flies, and to their avoidance and destruction. Along the first line, much was hoped from temporary segregation of the sick in regions where the fly was not found. On the assumption that the flies acted as carriers only during the first two or three days, it was supposed that even the "fly belts" would become safe within a few days after the sick were removed. The problem was found to be a much more difficult one when it was learned that after a given brief period the fly again became infective and remained so for an indeterminate period. Nevertheless, isolation of the sick is one of the most important measures in preventing the spread of the disease into new districts. Much, too, is being accomplished by moving native villages from the fly belts. (c.f. fig. 137.)

All measures to avoid the flies should be adopted. This means locating and avoiding the fly belts as far as possible, careful screening of houses, and protection of the body against bites.

Clearing the jungle along the water courses for some yards beyond the natural range of the fly has proved a very important measure. Castellani recommends that the area be one hundred yards and around a village three hundred yards at least.

Detailed studies of the parasites and the natural enemies of the tsetse-fly are being undertaken and may ultimately yield valuable results.

South American Trypanosomiasis—The tsetse-flies are distinctively African in distribution and until recently there were no trypanosomes known to infest man in America. In 1909 Dr. Chagas, of Rio de Janeiro described a new species, Trypanosoma cruzi, pathogenic to man.

The adult trypanosomes, ingested by a Conorhinus megistus, of any stage, first change into Crithidia-like forms and then those which remain in the stomach become ovoid and non-motile. Brumpt found these forms in immense numbers, in a Cornohinus which had been infested fourteen months before. The forms which pass into the intestine quickly assume the Crithidia form and continue to develop rapidly under this form. Some weeks later they evolve into the trypanosome forms, pathogenic for man. They then pass out with the excrement of the bug and infect the vertebrate host as soon as they come in contact with any mucous layer (buccal, ocular or rectal). More rarely they enter through the epidermis.

Brumpt showed that the development could take place in three species; bed-bugs (Cimex lectularius, C. hemipterus) and in the tick Ornithodoros moubata. The evolution proceeds in the first two species of bed-bugs as rapidly as in Conorhinus, or even more rapidly, but they remain infective for a much shorter time and hence Brumpt considers that they play a much less important rôle in the spread of the disease.

Conorhinus megistus, like related forms in our Southern States, very commonly frequents houses and attacks man with avidity. Chagas states that the bites are painless and do not leave any traces. They are usually inflicted on the lips, or the cheeks and thus the buccal mucosa of a sleeper may be soiled by the dejections of the insect and the bite serving as a port of entry of the virus, remain unnoticed.

The possibility of some of our North American Reduviidæ playing a similar rôle in the transmission of disease should not be overlooked.

Leishmanioses and Insects—Closely related to the trypanosomes is a group of intracellular parasites which have recently been grouped by Ross under the genus Leishmania. Five species are known to affect man. Three of these produce local skin infestations, but two of them, Leishmania donovani and L. infantum, produce serious and often fatal systemic diseases.

Leishmania infantum is the cause of the so-called infantile splenic leishmaniasis, occurring in northern Africa, Spain, Portugal, Italy, and possibly other parts of Europe. The parasite occurs habitually in the dog and is only accidentally transferred to children. Alvares and da Silva, in Portugal (according to Brumpt, 1913) have found that the excrement of a flea from a diseased dog contains flagellates, and they suggest that the infection may be transmitted by the accidental inoculation of this excrement by means of the proboscis of the flea, as has been thought to occur in the case of the plague. To this Brumpt objects that they and other workers who thought to trace the development of Leishmania infantum were apparently misled by the presence of a harmless Herpetomonas which infests dog fleas in all countries, even where the leishmaniasis is unknown.

Basile (1910 and 1911) however, carried on numerous experiments indicating that the disease was transferred from children to dogs and from dog to dog by the dog flea, and was able to find in the tissues of the insects forms perfectly identical with those found in children and in dogs suffering from leishmaniasis. He also found that Pulex irritans was capable of acting as the carrier.

Of the cutaneous type of leishmaniasis, the best known is the so-called "Oriental sore," an ulcerative disease of the skin which is epidemic in many tropical and subtropical regions. The causative organism is Leishmania tropica, which occurs in the diseased tissues as bodies very similar to those found in the spleen in cases of Kala-azar. The disease is readily inoculable and there is no doubt that it may be transferred from the open sores to abraded surfaces of a healthy individual by house-flies. It is also believed by a number of investigators that it may be transferred and directly inoculated by various blood-sucking insects.

Ticks and Diseases of Man and Animals

While much of the recent work has dealt with the true insects, or hexapods, it is now known that several of the most serious diseases of animals, and at least two important diseases of man are tick borne. These belong to the types known collectively as babesioses (or "piroplasmoses"), and spirochætoses.

The term babesiosis is applied to a disease of man or animals which is caused by minute protozoan parasites of the genus Babesia, living in the red blood corpuscles. These parasites have usually been given the generic name Piroplasma and hence the type of disease which they cause is often referred to as "piroplasmosis." The best known illustration is the disease known in this country as Texas fever of cattle.

Cattle Ticks and Texas Fever—The cattle disease, which in the United States is known as Texas fever, is a widely distributed, exceedingly acute disease. In Australia it is known as redwater fever and in Europe as hæmoglobinuria, due to the fact that the urine of the diseased animals is discolored by the breaking down of the red blood corpuscles infested by the parasite.

Various workers had described bacteria which they had isolated from the organs of the diseased animals, but their findings could not be verified. In 1889, Smith and Kilbourne discovered a minute, pear-shaped organism (fig. 138) in the red blood corpuscles of a cow which had succumbed to Texas fever. On account of their shape they were given the generic name Pyrososma and because they were usually found two in a corpuscle, the specific name, bigeminum. It is now generally accepted that the parasite is the same which Babes had observed the year before in Roumanian cattle suffering from hæmoglobinuria, and should be known as Babesia bovis (Babes).

By a series of perfectly conclusive experiments carried on near Washington, D.C., Smith and Kilbourne showed that this organism was carried from Southern cattle to non-immune animals by the so-called Southern cattle tick, Boophilus annulatus (= Margaropus annulatus) (fig. 139).

Of fourteen head of native cattle placed in a field with tick-infested Northern cattle all but two contracted the disease. This experiment was repeated with similar results. Four head of native cattle kept in a plot with three North Carolina cattle which had been carefully freed from ticks remained healthy. A second experiment the same year gave similar results.

Still more conclusive was the experiment showing that fields which had not been entered by Southern cattle but which had been infected by mature ticks taken from such animals would produce Texas fever in native cattle. On September 13, 1889, several thousand ticks collected from cattle in North Carolina three and four days before, were scattered in a small field near Washington. Three out of four native animals placed in this field contracted the disease. The fourth animal was not examined as to its blood but it showed no external symptoms of the disease.

In these earlier experiments it was believed that the cattle tick acted as a carrier of the disease between the Southern cattle and the soil of the Northern pastures. "It was believed that the tick obtained the parasite from the blood of its host and in its dissolution on the pasture a certain resistant spore form was set free which produced the disease when taken in with the food." The feeding of one animal for some time with grass from the most abundantly infected field, without any appearance of the disease, made this hypothesis untenable.

In the experimental work in 1890 the astonishing fact was brought out that the disease was conveyed neither by infected ticks disintegrating nor by their directly transferring the parasite, but that it was conveyed by the young hatched from eggs of infected ticks. In other words, the disease was hereditarily transferred to ticks of the second generation and they alone were capable of conveying it.

Thus was explained the fact that Texas fever did not appear immediately along the route of Southern cattle being driven to Northern markets but that after a certain definite period it manifested itself. It was conveyed by the progeny of ticks which had dropped from the Southern cattle and deposited their eggs on the ground.

These results have been fully confirmed by workers in different parts of the world,—notably by Koch, in Africa, and by Pound, in Australia.

The disease is apparently transmitted by Boophilus annulatus alone, in the United States, but it, or an almost identical disease, is conveyed by Ixodes hexagonus in Norway, Ixodes ricinus in Finland and France and by the three species, Boophilus decoloratus, Hyalomma ægypticum (fig. 140 and 141), and Hæmaphysalis punctata in Africa.

In spite of the detailed study which it has received, the life cycle of Babesia bovis has not been satisfactorily worked out. The asexual reproduction in the blood of the vertebrate host has been described but the cycle in the tick is practically unknown.

More successful attempts have been made to work out the life cycle of a related species, Babesia canis, which causes malignant jaundice in dogs in Africa and parts of Southern Europe. In this instance, also, the disease is transmitted by heredity to the ticks of the second generation. Yet the larval, or "seed ticks," from an infected female are not capable of conveying the disease, but only the nymphs and adults. Still more complicated is the condition in the case of Babesia ovis of sheep, which Motas has shown can be conveyed solely by the adult, sexually mature ticks of the second generation.

In Babesia canis, Christopher (1907) observed developmental stages in the tick. He found in the stomach of adult ticks, large motile club-shaped bodies which he considered as oökinetes. These bodies pass to the ovaries of the tick and enter the eggs where they become globular in form and probably represent an oocyst. This breaks up into a number of sporoblasts which enter the tissues of the developing tick and give rise to numerous sporozoites, which collect in the salivary glands and thence are transferred to the vertebrate host. A number of other species of Babesia are known to infest vertebrates and in all the cases where the method has been worked out it has been found that the conveyal was by ticks. We shall not consider the cases more fully here, as we are concerned especially with the method of transfer of human diseases.

Ticks and Rocky Mountain Spotted Fever of Man—Ever since 1873 there has been known in Montana and Idaho a peculiar febrile disease of man, which has gained the name of "Rocky Mountain spotted fever." Its onset is marked by chills and fever which rapidly become acute. In about four to seven days there appears a characteristic eruption on the wrists, ankles or back, which quickly covers the body.

According to Ricketts (1907) the experimental evidence in support of this hypothesis was first afforded by Dr. L. P. McCalla and Dr. H. A. Brereton, in 1905. These investigators transmitted the disease from man to man in two experiments. "The tick was obtained 'from the chest of a man very ill with spotted fever' and 'applied to the arm of a man who had been in the hospital for two months and a half, and had lost both feet from gangrene due to freezing.' On the eighth day the patient became very ill and passed through a mild course of spotted fever, leaving a characteristic eruption. The experiment was repeated by placing the tick on a woman's leg and she likewise was infected with spotted fever."

The most detailed studies were those of the late Dr. H. T. Ricketts, and it was he who clearly established the tick hypothesis. In the summer of 1906 he found that guinea pigs and monkeys are very susceptible to spotted fever and can readily be infected by inoculation of blood from patients suffering from the disease. This opened the way to experimental work on tick transmission. A female tick was fed upon an infected guinea pig for two days, removed and isolated for two days and then placed upon a healthy guinea pig. After an incubation period of three and a half days the experimental animal contracted a well-marked case of the disease.

A similar result was obtained at the same time by King, and later in the season Ricketts proved that the male tick was also capable of transmitting the disease. He found that there was a very intimate relation of the virus to the tick and that the transmission must be regarded as biological throughout. Ticks remained infective as long as they lived and would feed for a period of several months. If they acquired the disease in the larval or nymphal stage they retained it during molting and were infective in the subsequent stages. In a few cases the larvæ from an infected female were infective.

The evidence indicated that the tick suffers from a relatively harmless, generalized infection and the virus proliferates in its body. The disease probably is transferred through the salivary secretion of the tick since inoculation experiments show that the salivary glands of the infected adult contain the virus.

It is probable that in nature the reservoir of the virus of spotted fever is some one or more of the native small animals. Infected ticks have been found in nature, and as various wild animals are susceptible to the disease, it is obvious that it may exist among them unnoticed. Wilson and Chowning suggested that the ground squirrel plays the principal rôle.

Unfortunately, much confusion exists regarding the correct name of the tick which normally conveys the disease. In the medical literature it is usually referred to as Dermacentor occidentalis, but students of the group now agree that it is specifically distinct. Banks has designated it as Dermacentor venustus and this name is used in the publications of the Bureau of Entomology. On the other hand, Stiles maintains that the common tick of the Bitter Root Valley, and the form which has been collected by the authors who have worked on Rocky Mountain spotted fever in that region, is separable from D. venustus, and he has described it under the name of Dermacentor andersoni.

Mayer (1911) has shown experimentally that spotted fever may be transmitted by several different species of ticks, notably Dermacentor marginatus, Dermacentor variabilis and Amblyomma americanum. This being the case, the question of the exact systematic status of the species experimented upon in the Bitter Root Valley becomes less important, for since Dermacentor occidentalis, Dermacentor venustus and Dermacentor andersoni all readily attack man, it is probable that either species would readily disseminate the disease if it should spread into their range.

Hunter and Bishop (1911) have emphasized the fact that in the eastern and southern United States there occur several species which attack man, and any one of which might transmit the disease from animal to animal and from animal to man. The following species, they state, would probably be of principal importance in the Southern and Eastern States: the lone star tick (Amblyomma americanum); the American dog tick (Dermacentor variabilis); and the gulf-coast tick (Amblyomma maculatum). In the extreme southern portions of Texas, Amblyomma cajennense, is a common pest of man.

Since the evidence all indicates that Rocky Mountain spotted fever is transmitted solely by the tick, and that some of the wild animals serve as reservoirs of the virus, it is obvious that personal prophylaxis consists in avoiding the ticks as fully as possible, and in quickly removing those which do attack. General measures along the line of tick eradication must be carried out if the disease is to be controlled. That such measures are feasible has been shown by the work which has been done in controlling the tick-borne Texas fever of cattle, and by such work as has already been done against the spotted fever tick, which occurs on both wild and domestic animals. Detailed consideration of these measures is to be found in the publications of the Public Health and Marine Hospital Service, and the Bureau of Entomology. Hunter and Bishopp give the following summarized recommendations for control or eradication measures in the Bitter Root Valley.

(1) A campaign of education, whereby all the residents of the valley will be made thoroughly familiar with the feasibility of the plan of eradication, and with what it will mean in the development of the valley.

(2) The obtaining of legislation to make it possible to dip or oil all live stock in the Bitter Root Valley.

(3) The obtaining of an accurate census of the horses, cattle, sheep, mules, and dogs in the valley.

(4) The construction of ten or more dipping vats.

(5) The providing of materials to be used in the dipping mixture.

(6) The organization of a corps of workers to carry on the operations.

(7) The systematic dipping of the horses, cattle, sheep, and dogs of the valley on a definite weekly schedule from approximately March 10 to June 9.

(8) The treatment by hand of the animals in localities remote from vats, on the same schedule.

They estimate that after three seasons' operations a very small annual expenditure would provide against reinfestation of the valley by the incoming of cattle from other places.

Supplementary measures consist in the killing of wild mammals which may harbor the tick; systematic burning of the brush and debris on the mountain side; and in clearing, since the tick is seldom found on land under cultivation.

CHAPTER X

Arthropods and Spirochætoses of Man and Animals

African Relapsing Fever of Man—It has long been known to the natives of Africa and to travelers in that country, that the bite of a certain tick, Ornithodoros moubata, may be followed by severe or even fatal fever of the relapsing type. Until recent years, it was supposed that the effect was due to some special virulence of the tick, just as nagana of cattle was attributed to the direct effect of the bite of the tsetse-fly. The disease is commonly known as "tick-fever" or by the various native names of the tick.

Ornithodoros moubata (fig. 142), the carrier of African relapsing fever, or "tick-fever," is widely distributed in tropical Africa, and occurs in great numbers in the huts of natives, in the dust, cracks and crevices of the dirt floors, or the walls. It feeds voraciously on man as well as upon birds and mammals. Like others of the Argasidæ, it resembles the bed-bug in its habit of feeding primarily at night. Dutton and Todd observed that the larval stage is undergone in the egg and that the first free stage is that of the octopod nymph.