Handbook of Medical Entomology Part 25

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 succ.u.mbed 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 s.e.xual 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 role in nature, unless the fly is interrupted while feeding and pa.s.ses 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 sh.o.r.e 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 sh.o.r.e, 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 sh.o.r.e 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 Nya.s.saland, 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. Fulleborn 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 role 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 sh.o.r.e or river banks. According to Hodges, the natural range from sh.o.r.e 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.

[Ill.u.s.tration: 137. Sleeping sickness concentration camp in German East Africa. Report of German Commission.]

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 a.s.sumption 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.

_Trypanosoma cruzi_ is the causative organism of a disease common in some regions of Brazil, where it is known as "opilacao." It is especially to be met with in children and is characterized by extreme anemia, wasting, and stunted development a.s.sociated with fever, and enlargement of the thyroid glands. The disease is transmitted by the bites of several species of a.s.sa.s.sin-bugs, or Reduviidae, notably by _Conorhinus megistus_. The evolution of the parasite within the bug has been studied especially by Chagas and by Brumpt. From the latter's text we take the following summary.

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 _Conorhinus_ which had been infested fourteen months before. The forms which pa.s.s into the intestine quickly a.s.sume 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 pa.s.s 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 role 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 Reduviidae playing a similar role 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.

The first of these, that produced by _L. donovani_, is an exceedingly virulent disease common in certain regions of India and China. It is commonly known as "Kala-azar," or "dum-dum" fever, and more technically as tropical leishmaniasis. Patton (1907) believes that the parasite is transmitted by the bed-bug _Cimex hemipterus_, and has described a developmental cycle similar to that which can be found in artificial cultures. On the other hand, Donovan was unable to confirm Patton's work and believes that the true intermediate host is a Reduviid bug, _Conorhinus rubrofasciatus_.

_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

We have seen that the way to the discoveries of the relations of arthropods to disease was pointed out by the work of Leuckart and Melnikoff on the life cycle of _Dipylidium_, and of Fedtschenko and Manson on that of _Filaria_. They dealt with grosser forms, belonging to well-recognized parasitic groups.

This was long before the role of any insect as a carrier of pathogenic micro-organisms had been established, and before the Protozoa were generally regarded as of importance in the causation of disease. The next important step was taken in 1889 when Smith and Kilbourne conclusively showed that the so-called Texas fever of cattle, in the United States, is due to an intracorpuscular blood parasite transmitted exclusively by a tick. This discovery, antedating by eight years the work on the relation of the mosquito to malaria, had a very great influence on subsequent studies along these lines.

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 _spirochaetoses_.

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 ill.u.s.tration 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 haemoglobinuria, 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.

In their historical discussion, Smith and Kilbourne, point out that as far back as 1796 it was noted that Southern cattle, in a state of apparent health, might spread a fatal disease among Northern herds. As observations acc.u.mulated, it was learned that this infection was carried only during the warm season of the year and in the depth of winter Southern cattle were harmless. Moreover, Southern cattle after remaining for a short time in the North lost their power to transmit the disease, and the same was true of cattle which had been driven for a considerable distance.

Very significant was the fact that the infection was not communicated directly from the Southern to Northern cattle but that the ground over which the former pa.s.sed was infected by them, and that the infection was transmitted thence to susceptible cattle _after a period of not less than thirty days had elapsed_.

Of course a disease as striking as this, and which caused such enormous losses of cattle in the region invaded was fruitful in theories concerning its causation. The most widespread was the belief that pastures were infected by the saliva, urine, or manure of Southern cattle. There were not wanting keen observers who suggested that the disease was caused by ticks, but little weight was given to their view.

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 succ.u.mbed 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 haemoglobinuria, and should be known as _Babesia bovis_ (Babes).

[Ill.u.s.tration: 138. Babesia bovis in blood corpuscles. After Calli.]

[Ill.u.s.tration: 139. The cattle tick (Boophilus annulatus). (_a_) Female; (_b_) male. After Comstock.]