In modern times the plague is confined primarily to warm climates, a condition which has been brought about largely through general improvement in sanitary conditions.

At present, the hotbed of the disease is India, where there were 1,040,429 deaths in 1904 and where in a period of fifteen years, ending with January 1912, there were over 15,000,000 deaths. The reported deaths in that country for 1913 totaled 198,875.

During the winter of 1910-11 there occurred in Manchuria and North China a virulent epidemic of the pneumonic plague which caused the death of nearly 50,000 people. The question as to its origin and means of spread will be especially referred to later.

Until recent years, the plague had not been known to occur in the New World but there were outbreaks in Brazil and Hawaii in 1899, and in 1900 there occurred the first cases in San Francisco. In California there were 125 cases in the period 1900-04; three cases in the next three years and then from May 1907 to March 1908, during the height of the outbreak, 170 cases. Since that time there have been only sporadic cases, the last case reported being in May 1914. Still more recent were the outbreaks in the Philippine Islands, Porto Rico, and Cuba.

On June 24, 1914, there was recognized a case of human plague in New Orleans. The Federal Health Service immediately took charge, and measures for the eradication of the disease were vigorously enforced. Up to October 10, 1914 there had been reported 30 cases of the disease in man, and 181 cases of plague in rats.

The present-day methods of combating bubonic plague are well illustrated by the fight in San Francisco. Had it not been for the strenuous and radical anti-plague campaign directed by the United States Marine Hospital Service we might have had in our own country an illustration of what the disease can accomplish. On what newly acquired knowledge was this fight based?

The basis was laid in 1894, when the plague bacillus was first discovered. All through the centuries, before and during the Christian era, down to 1894, the subject was enveloped in darkness and there had been a helpless, almost hopeless struggle in ignorance on the part of physicians, sanitarians, and public health officials against the ravages of this dread disease. Now its cause, method of propagation and means to prevent its spread are matters of scientific certainty.

After the discovery of the causative organism, one of the first advances was the establishment of the identity of human plague and that of rodents. It had often been noted that epidemics of the human disease were preceded by great epizootics among rats and mice. So well established was this fact that with the Chinese, unusual mortality among these rodents was regarded as foretelling a visitation of the human disease. That there was more than an accidental connection between the two was obvious when Yersin, the discoverer of Bacillus pestis, announced that during an epidemic the rats found dead in the houses and in the streets almost always contain the bacillus in great abundance in their organs, and that many of them exhibit veritable buboes.

Once it was established that the diseases were identical, the attention of the investigators was directed to a study of the relations between that of rats and of humans, and evidence accumulated to show that the bubonic plague was primarily a disease of rodents and that in some manner it was conveyed from them to man.

There yet remained unexplained the method of transfer from rat to man. As long ago as the 16th century, Mercuralis suggested that house-flies were guilty of disseminating the plague but modern investigation, while blaming the fly for much in the way of spreading disease, show that it is an insignificant factor in this case.

Search for blood-sucking insects which would feed on both rodents and man, and which might therefore be implicated, indicated that the fleas most nearly met the conditions. At first it was urged that rat fleas would not feed upon man and that the fleas ordinarily attacking man would not feed upon rats. More critical study of the habits of fleas soon showed that these objections were not well-founded. Especially important was the evidence that soon after the death of their host, rat fleas deserted its body and might then become a pest in houses where they had not been noticed before.

Attention was directed to the fact that while feeding, fleas are in the habit of squirting blood from the anus and that in the case of those which had fed upon rats and mice dying of the plague, virulent plague bacilli were to be found in such blood. Liston (1905) even found, and subsequent investigations confirmed, that the plague bacilli multiply in the stomach of the insect and that thus the blood ejected was richer in the organisms than was that of the diseased animal. It was found that a film of this infected blood spread out under the body of the flea and that thus the bacilli might be inoculated by the bite of the insect and by scratching.

Very recently, Bacot and Martin (1914) have paid especial attention to the question of the mechanism of the transmission of the plague bacilli by fleas. They believe that plague infested fleas regurgitate blood through the mouth, and that under conditions precluding the possibility of infection by dejecta, the disease may be thus transmitted. The evidence does not seem sufficient to establish that this is the chief method of transmission.

Conclusive experimental proof that fleas transmit the disease is further available from a number of sources. The most extensive series of experiments is that of the English Plague Commission in India, which reported in 1906 that:

On thirty occasions a healthy rat contracted plague in sequence of living in the neighborhood of a plague infected rat under circumstances which prevented the healthy rat coming in contact with either the body or excreta of the diseased animal.

In twenty-one experiments out of thirty-eight, healthy rats living in flea-proof cages contracted plague when exposed to rat fleas (Xenopsylla cheopis), collected from rats dead or dying of septicæmic plague.

Close contact of plague-infected with healthy animals, if fleas are excluded, does not give rise to an epizootic among the latter. As the huts were never cleaned out, close contact included contact with feces and urine of infected animals, and contact with, and eating of food contaminated with feces and urine of infected animals, as well as pus from open plague ulcers. Close contact of young, even when suckled by plague-infected mothers, did not give the disease to the former.

If fleas are present, then the epizootic, once started, spreads from animal to animal, the rate of progress being in direct proportion to the number of fleas.

Aerial infection was excluded. Thus guinea-pigs suspended in a cage two feet above the ground did not contract the disease, while in the same hut those animals allowed to run about and those placed two inches above the floor became infected. It had previously been found that a rat flea could not hop farther than about five inches.

Guinea pigs and monkeys were placed in plague houses in pairs, both protected from soil contact infection and both equally exposed to aerial infection, but one surrounded with a layer of tangle-foot paper and the other surrounded with a layer of sand. The following observations were made:

(a) Many fleas were caught in the tangle-foot, a certain proportion of which were found on dissection to contain in their stomachs abundant bacilli microscopically identical with plague bacilli. Out of eighty-five human fleas dissected only one contained these bacilli, while out of seventy-seven rat fleas twenty-three were found thus infected.

(b) The animals surrounded with tangle-foot in no instance developed plague, while several (24 per cent) of the non-protected animals died of the disease.

Thus, the experimental evidence that fleas transmit the plague from rat to rat, from rats to guinea pigs, and from rats to monkeys is indisputable. There is lacking direct experimental proof of its transfer from rodents to man but the whole chain of indirect evidence is so complete that there can be no doubt that such a transfer does occur so commonly that in the case of bubonic plague it must be regarded as the normal method.

Rats are not the only animals naturally attacked by the plague but as already suggested, it occurs in various other rodents. In California the disease has spread from rats to ground squirrels (Otospermophilus beecheyi), a condition readily arising from the frequency of association of rats with the squirrels in the neighborhood of towns, and from the fact that the two species of fleas found on them are also found on rats. While the danger of the disease being conveyed from squirrels to man is comparatively slight, the menace in the situation is that the squirrels may become a more or less permanent reservoir of the disease and infect rats, which may come into more frequent contact with man.

The tarbagan (Arctomys bobac), is a rodent found in North Manchuria, which is much prized for its fur. It is claimed that this animal is extremely susceptible to the plague and there is evidence to indicate that it was the primary source of the great outbreak of pneumonic plague which occurred in Manchuria and North China during the winter of 1910-11.

Of fleas, any species which attacks both rodents and man may be an agent in the transmission of the plague. We have seen that in India the species most commonly implicated is the rat flea, Xenopsylla cheopis, (= Lœmopsylla or Pulex cheopis) (fig. 89). This species has also been found commonly on rats in San Francisco. The cat flea, Ctenocephalus felis, the dog flea, Ctenocephalus canis, the human flea, Pulex irritans, the rat fleas, Ceratophyllus fasciatus and Ctenopsyllus musculi have all been shown to meet the conditions.

But, however clear the evidence that fleas are the most important agent in the transfer of plague, it is a mistake fraught with danger to assume that they are the only factor in the spread of the disease. The causative organism is a bacillus and is not dependent upon any insect for the completion of its development.

Therefore, any blood-sucking insect which feeds upon a plague infected man or animal and then passes to a healthy individual, conceivably might transfer the bacilli. Verjbitski (1908) has shown experimentally that bed-bugs may thus convey the disease. Hertzog found the bacilli in a head-louse, Pediculus humanus, taken from a child which had died from the plague, and McCoy found them in a louse taken from a plague-infected squirrel. On account of their stationary habits, the latter insects could be of little significance in spreading the disease.

Contaminated food may also be a source of danger. While this source, formerly supposed to be the principal one, is now regarded as unimportant, there is abundant experimental evidence to show that it cannot be disregarded. It is believed that infection in this way can occur only when there is some lesion in the alimentary canal.

Still more important is the proof that in pneumonic plague the patient is directly infective and that the disease is spread from man to man without any intermediary. Especially conclusive is the evidence obtained by Drs. Strong and Teague during the Manchurian epidemic of 1910-11. They found that during coughing, in pneumonic plague cases, even when sputum visible to the naked eye is not expelled, plague bacilli in large numbers may become widely disseminated into the surrounding air. By exposing sterile plates before patients who coughed a single time, very numerous colonies of the bacillus were obtained.

But the great advance which has been made rests on the discovery that bubonic plague is in the vast majority of cases transmitted by the flea. The pneumonic type forms a very small percentage of the human cases and even with it, the evidence indicates that the original infection is derived from a rodent through the intermediary of the insect.

So modern prophylactic measures are directed primarily against the rat and fleas. Ships coming from infected ports are no longer disinfected for the purpose of killing the plague germs, but are fumigated to destroy the rats and the fleas which they might harbor. When anchored at infected ports, ships must observe strenuous precautions to prevent the ingress of rats. Cargo must be inspected just before being brought on board, in order to insure its freedom from rats. Even lines and hawsers must be protected by large metal discs or funnels, for rats readily run along a rope to reach the ship. Once infested, the ship must be thoroughly fumigated, not only to avoid carrying the disease to other ports but to obviate an outbreak on board.

When an epidemic begins, rats must be destroyed by trapping and poisoning. Various so-called biological poisons have not proved practicable. Sources of food supply should be cut off by thorough cleaning up, by use of rat-proof garbage cans and similar measures. Hand in hand with these, must go the destruction of breeding places, and the rat-proofing of dwellings, stables, markets, warehouses, docks and sewers. All these measures are expensive, and a few years ago would have been thought wholly impossible to put into practice but now they are being enforced on a large scale in every fight against the disease.

Rats and other rodents are regularly caught in the danger zone and examined for evidence of infection, for the sequence of the epizootic and of the human disease is now understood. In London, rats are regularly trapped and poisoned in the vicinity of the principal docks, to guard against the introduction of infected animals in shipping. During the past six years infected rats have been found yearly, thirteen having been found in 1912. In Seattle, Washington, seven infected rats were found along the water front in October, 1913, and infected ground squirrels are still being found in connection with the anti-plague measures in California.

The procedure during an outbreak of the human plague was well illustrated by the fight in San Francisco. The city was districted, and captured rats, after being dipped in some fluid to destroy the fleas, were carefully tagged to indicate their source, and were sent to the laboratory for examination. If an infected rat was found, the officers in charge of the work in the district involved were immediately notified by telephone, and the infected building was subjected to a thorough fumigation. In addition, special attention was given to all the territory in the four contiguous blocks.

By measures such as these, this dread scourge of the human race is being brought under control. Incidentally, the enormous losses due to the direct ravages of rats are being obviated and this alone would justify the expenditure many times over of the money and labor involved in the anti-rat measures.

CHAPTER VII

We have already emphasized that this is the most important way in which insects may transmit disease, for without them the particular organisms concerned could never complete their development. Exterminate the arthropod host and the life cycle of the parasite is broken, the disease is exterminated.

As the phenomenon of alternation of generations, as exhibited by many of the parasitic protozoa, is a complicated one and usually new to the student, we shall first take up some of the grosser cases illustrated by certain parasitic worms. There is the additional reason that these were the first cases known of arthropod transmission of pathogenic organisms.

Insects as Intermediate Hosts of Tapeworms

Dipylidium caninum (figs. 113 and 114), more generally known as Taenia cucumerina or T. elliptica, is the commonest intestinal parasite of pet dogs and cats. It is occasionally found as a human parasite, 70 per cent of the cases reported being in young children.

In 1869, Melnikoff found in a dog louse, Trichodectes canis, some peculiar bodies which Leuckart identified as the larval form of this tapeworm. The worm is, however, much more common in dogs and cats than is the skin parasite, and hence it appears that the Trichodectes could not be the only intermediate host. In 1888, Grassi found that it could also develop in the cat and dog fleas, Ctenocephalus felis and C. canis, and in the human flea, Pulex irritans.

The eggs, scattered among the hairs of the dog or cat, are ingested by the insect host and in its body cavity they develop into pyriform bodies, about 300µ in length, almost entirely destitute of a bladder, but in the immature stage provided with a caudal appendage (fig. 115). Within the pear-shaped body (fig. 116) are the invaginated head and suckers of the future tapeworm. This larval form is known as a cysticercoid, in contradistinction to the bladder-like cysticercus of many other cestodes. It is often referred to in literature as Cryptocystis trichodectis Villot.

As many as fifty of the cysticercoids have been found in the body cavity of a single flea. When the dog takes up an infested flea or louse, by biting itself, or when the cat licks them up, the larvæ quickly develop into tapeworms, reaching sexual maturity in about twenty days in the intestine of their host. Puppies and kittens are quickly infested when suckling a flea-infested mother, the developing worms having been found in the intestines of puppies not more than five or six days old.

Infestation of human beings occurs only through accidental ingestion of an infested flea. It is natural that such cases should occur largely in children, where they may come about in some such way as illustrated in the accompanying figures 117 and 118.

Hymenolepis diminuta, very commonly living in the intestine of mice and rats, is also known to occur in man. Its cysticercoid develops in the body cavity of a surprising range of meal-infesting insects. Grassi and Rovelli (abstract in Ransom, 1904) found it in the larvæ and adult of a moth, Asopia farinalis, in the earwig, Anisolabis annulipes, the Tenebrionid beetles Akis spinosa and Scaurus striatus. Grassi considers that the lepidopter is the normal intermediate host. The insect takes up the eggs scattered by rats and mice. It has been experimentally demonstrated that man may develop the tapeworm by swallowing infested insects. Natural infection probably occurs by ingesting such insects with cereals, or imperfectly cooked foods.

Hymenolepis lanceolata, a parasite of geese and ducks, has been reported once for man. The supposed cysticercoid occurs in various small crustaceans of the family Cyclopidæ.

Several other cestode parasites of domestic animals are believed to develop their intermediate stage in certain arthropods. Among these may be mentioned:

Choanotænia infundibulformis, of chickens, developing in the house-fly (Grassi and Rovelli);

Davainea cesticillus, of chickens, in some lepidopter or coleopter (Grassi and Rovelli);

Hymenolepis anatina, H. gracilis, H. sinuosa, H. coronula and Fimbriaria fasciolaris, all occurring in ducks, have been reported as developing in small aquatic crustaceans. In these cases, cysticercoids have been found which, on account of superficial characters, have been regarded as belonging to the several species, but direct experimental evidence is scant.

Arthropods as Intermediate Hosts of Nematode Worms

Filariasis and Mosquitoes—A number of species of Nematode worms belonging to the genus Filaria, infest man and other vertebrates and in the larval condition are to be found in the blood. Such infestation is known as filariasis. The sexually mature worms are to be found in the blood, the lymphatics, the mesentery and subcutaneous connective tissue. In the cases best studied it has been found that the larval forms are taken up by mosquitoes and undergo a transformation before they can attain maturity in man.

Filaria bancrofti in its adult state, lives in the lymphatics of man. Though often causing no injury it has been clearly established that they and their eggs may cause various disorders due to stoppage of the lymphatic trunks (fig. 119). Manson lists among other effects, abscess, varicose groin glands, lymph scrotum, chyluria, and elephantiasis.

The geographical distribution of this parasite is usually given as coextensive with that of elephantiasis, but it is by no means certain that it is the only cause of this disease and so actual findings of the parasites are necessary. Manson reports that it is "an indigenous parasite in almost every country throughout the tropical and subtropical world, as far north as Spain in Europe and Charlestown in the United States, and as far south as Brisbane in Australia." In some sections, fully 50 per cent of the natives are infested. Labredo (1910) found 17.82 per cent infestation in Havana.

The larval forms of Filaria bancrofti were first discovered in 1863, by Demarquay, in a case of chylous dropsy. They were subsequently noted under similar conditions, by several workers, and by Wücherer in the urine of twenty-eight cases of tropical chyluria, but in 1872 Lewis found that the blood of man was the normal habitat, and gave them the name Filaria sanguinis hominis. The adult worm was found in 1876 by Bancroft, and in 1877, Cobbold gave it the name Filaria bancrofti. It has since been found repeatedly in various parts of the lymphatic system, and its life-history has been the subject of detailed studies by Manson (1884), Bancroft (1899), Low (1900), Grassi and Noé (1900), Noé (1901) and Fülleborn (1910).

The larvæ as they exist in the circulating blood, exhibit a very active wriggling movement, without material progression. They may exist in enormous numbers, as many as five or six hundred swarming in a single drop of blood. This is the more surprising when we consider that they measure about 300µ × 8µ, that is, their width is equal to the diameter of the red blood corpuscle of their host and their length over thirty-seven times as great.

Their organs are very immature and the structure obscure. When they have quieted down somewhat in a preparation it may be seen that at the head end there is a six-lipped and very delicate prepuce, enclosing a short "fang" which may be suddenly exserted and retracted. Completely enclosing the larva is a delicate sheath, which is considerably longer than the worm itself. To enter into further details of anatomy is beyond the scope of this discussion and readers interested are referred to the work of Manson and of Fülleborn.

One of the most surprising features of the habits of these larvæ is the periodicity which they exhibit in their occurrence in the peripheral blood. If a preparation be made during the day time there may be no evidence whatever of filarial infestation, whereas a preparation from the same patient taken late in the evening or during the night may be literally swarming with the parasites. Manson quotes Mackenzie as having brought out the further interesting fact that should a "filarial subject be made to sleep during the day and remain awake at night, the periodicity is reversed; that is to say, the parasites come into the blood during the day and disappear from it during the night." There have been numerous attempts to explain this peculiar phenomenon of periodicity but in spite of objections which have been raised, the most plausible remains that of Manson, who believes that it is an adaptation correlated with the life-habits of the liberating agent of the parasite, the mosquito.

The next stages in the development of Filaria nocturna occur in mosquitoes, a fact suggested almost simultaneously by Bancroft and Manson in 1877, and first demonstrated by the latter very soon thereafter. The experiments were first carried out with Culex quinquefasciatus (= fatigans) as a host, but it is now known that a number of species of mosquitoes, both anopheline and culicine, may serve equally well.

When the blood of an infested individual is sucked up and reaches the stomach of such a mosquito, the larvæ, by very active movements, escape from their sheaths and within a very few hours actively migrate to the body cavity of their new host and settle down primarily in the thoracic muscles. There in the course of sixteen to twenty days they undergo a metamorphosis of which the more conspicuous features are the formation of a mouth, an alimentary canal and a trilobed tail. At the same time there is an enormous increase in size, the larvæ which measured .3 mm. in the blood becoming 1.5 mm. in length. This developmental period may be somewhat shortened in some cases and on the other hand may be considerably extended. The controlling factor seems to be the one of temperature.

The transformed larvæ then reenter the body cavity and finally the majority of them reach the interior of the labium (fig. 120). A few enter the legs and antennæ, and the abdomen, but these are wanderers which, it is possible, may likewise ultimately reach the labium, where they await the opportunity to enter their human host.

It was formerly supposed that when the infested mosquito punctured the skin of man, the mature larvæ were injected into the circulation. The manner in which this occurred was not obvious, for when the insect feeds it inserts only the stylets, the labium itself remaining on the surface of the skin. Fülleborn has cleared up the question by showing that at this time the filariæ escape and, like the hookworm, actively bore into the skin of their new host.

Once entered, they migrate to the lymphatics and there quickly become sexually mature. The full grown females measure 85-90 mm. in length by .24-.28 mm. in diameter, while the males are less than half this size, being about 40 mm. by .1 mm. Fecundation occurs and the females will be found filled with eggs in various stages of development, for they are normally viviparous.

Filaria philippinensis is reported by Ashburn and Craig (1907) as a common blood filaria in the Philippine Islands. As they describe it, it differs from Filaria bancrofti primarily in that it does not exhibit periodicity. Its development has been found to occur in Culex quinquefasciatus, where it undergoes metamorphosis in about fourteen or fifteen days. There is doubt as to the species being distinct from bancrofti.

Several other species occur in man and are thought to be transferred by various insects, among which have been mentioned Tabanidæ and tsetse-flies, but there is no experimental proof in support of such conjectures.

Filaria immitis is a dangerous parasite of the dog, the adult worm living in the heart and veins of this animal. It is one of the species which has been clearly shown to undergo its development in the mosquito, particularly in Anopheles maculipennis and Aedes calopus (= Stegomyia). The larval form occurs in the peripheral blood, especially at night. When taken up by mosquitoes they differ from Filaria bancrofti in that they undergo their development in the Malpighian tubules rather than in the thoracic muscles. In about twelve days they have completed their growth in the tubules, pierce the distal end, and pass to the labium. This species occurs primarily in China and Japan, but is also found in Europe and in the United States. It is an especially favorable species for studying the transformations in the mosquito.

Filariæ are also commonly found in birds, and in this country this is the most available source of laboratory material. We have found them locally (Ithaca, N. Y.) in the blood of over sixty per cent of all the crows examined, at any season of the year, and have also found them in English sparrows.

In the crows, they often occur in enormous numbers, as many as two thousand having been found in a single drop of the blood of the most heavily infested specimen examined. For study, a small drop of blood should be mounted on a clean slide and the coverglass rung with vaseline or oil to prevent evaporation. In this way they can be kept for hours.

Permanent preparations may be made by spreading out the blood in a film on a perfectly clean slide and staining. This is easiest done by touching the fresh drop of blood with the end of a second slide which is then held at an angle of about 45° to the first slide and drawn over it without pressure. Allow the smear to dry in the air and stain in the usual way with hæmatoxylin.

Other Nematode Parasites of Man and Animals Developing in Arthropods

Dracunculus medinensis (fig. 121), the so-called guinea-worm, is a nematode parasite of man which is widely distributed in tropical Africa, Asia, certain parts of Brazil and is occasionally imported into North America.

The female worm is excessively long and slender, measuring nearly three feet in length and not more than one-fifteenth of an inch in diameter. It is found in the subcutaneous connective tissue and when mature usually migrates to some part of the leg. Here it pierces the skin and there is formed a small superficial ulcer through which the larvæ reach the exterior after bursting the body of the mother.

Fedtschenko (1879) found that when these larvæ reach the water they penetrate the carapace of the little crustacean, Cyclops (fig. 122). Here they molt several times and undergo a metamorphosis. Fedtschenko, in Turkestan, found that these stages required about five weeks, while Manson who confirmed these general results, found that eight or nine weeks were required in the cooler climate of England.

Infection of the vertebrate host probably occurs through swallowing infested cyclops in drinking water. Fedtschenko was unable to demonstrate this experimentally and objection has been raised against the theory, but Leiper (1907), and Strassen (1907) succeeded in infesting monkeys by feeding them on cyclops containing the larvæ.

Habronema muscæ is a worm which has long been known in its larval stage, as a parasite of the house-fly. Carter found them in 33 per cent of the house-flies examined in Bombay during July, 1860, and since that time they have been shown to be very widely distributed. Italian workers reported them in 12 per cent to 30 per cent of the flies examined. Hewitt reported finding it rarely in England. In this country it was first reported by Leidy who found it in about 20 per cent of the flies examined at Philadelphia, Pa. Since then it has been reported by several American workers. We have found it at Ithaca, N. Y., but have not made sufficient examinations to justify stating percentage. Ransom (1913) reports it in thirty-nine out of one hundred and thirty-seven flies, or 28 per cent.

Until very recently the life-history of this parasite was unknown but the thorough work of Ransom (1911, 1913) has shown clearly that the adult stage occurs in the stomach of horses. The embryos, produced by the parent worms in the stomach of the horse, pass out with the feces and enter the bodies of fly larvæ which are developing in the manure. In these they reach their final stage of larval development at about the time the adult flies emerge from the pupal stage. In the adult fly they are commonly found in the head. frequently in the proboscis, but they occur also in the thorax and abdomen. Infested flies are accidentally swallowed by horses and the parasite completes its development to maturity in the stomach of its definitive host.

Gigantorhynchus hirudinaceus (= Echinorhynchus gigas) is a common parasite of the pig and has been reported as occurring in man. The adult female is 20-35 cm. long and 4-9 mm. in diameter. It lacks an alimentary canal and is provided with a strongly spined protractile rostrum, by means of which it attaches to the intestinal mucosa of its host.

The eggs are scattered with the feces of the host and are taken up by certain beetle larvæ. In Europe the usual intermediate hosts are the larvæ of the cockchafer, Melolontha vulgaris, or of the flower beetle, Cetonia aurata. Stiles has shown that in the United States the intermediate host is the larva of the June bug, Lachnosterna (fig. 124). It is probable that several of the native species serve in this capacity.

A number of other nematode parasites of birds and mammals have been reported as developing in arthropods but here, as in the case of the cestodes, experimental proof is scant. The cases above cited are the better established and will serve as illustrations.

CHAPTER VIII

Mosquitoes and Malaria

So commonplace is malaria that it causes little of the dread inspired by most of the epidemic diseases, and yet, as Ross says, it is perhaps the most important of human diseases. Figures regarding its ravages are astounding. Celli estimated that in Italy it caused an average annual mortality of fifteen thousand, representing about two million cases. In India alone, according to Ross (1910) "it has been officially estimated to cause a mean annual death-rate of five per thousand; that is, to kill every year, on the average, one million one hundred and thirty thousand." In the United States it is widespread and though being restricted as the country develops, it still causes enormous losses. During the year 1911, "in Alabama alone there were seventy thousand cases and seven hundred and seventy deaths." The weakening effects of the disease, the invasion of other diseases due to the attacks of malaria, are among the very serious results, but they cannot be estimated.

Not only is there direct effect on man, but the disease has been one of the greatest factors in retarding the development of certain regions. Everywhere pioneers have had to face it, and the most fertile regions have, in many instances been those most fully dominated by it. Herrick (1903) has presented an interesting study of its effects on the development of the southern United States and has shown that some parts, which are among the most fertile in the world, are rendered practically uninhabitable by the ravages of malaria. Howard (1909) estimates that the annual money loss from the disease in the United States is not less than $100,000,000.

It was formerly supposed that the disease was due to a miasm, to a noxious effluvia, or infectious matter rising in the air from swamps. In other words its cause was, as the name indicated "mal aria," and the deep seated fear of night air is based largely on the belief that this miasm was given off at night. Its production was thought to be favored by stirring of the soil, dredging operations and the like.

The idea of some intimate connection between malaria and mosquitoes is not a new one. According to Manson, Lancisi noted that in some parts of Italy the peasants for centuries have believed that malaria is produced by the bite of mosquitoes. Celli states that one not rarely hears from such peasants the statement that "In such a place, there is much fever, because it is full of mosquitoes." Koch points out that in German East Africa the natives call malaria and the mosquito by the same name, Mbù. The opinion was not lacking support from medical men. Celli quotes passages from the writings of the Italian physician, Lancisi, which indicate that he favored the view in 1717.

Dr. Josiah Nott is almost universally credited with having supported the theory, in 1848, but as we have already pointed out his work has been misinterpreted. The statements of Beauperthuy, (1853) were more explicit.

The clearest early presentation of the circumstantial evidence in favor of the theory of mosquito transmission was that of A. F. A. King, an American physician, in 1883. He presented a series of epidemiological data and showed "how they may be explicable by the supposition that the mosquito is the real source of the disease, rather than the inhalation or cutaneous absorption of a marsh vapor." We may well give the space to summarizing his argument here for it has been so remarkably substantiated by subsequent work:

1. Malaria, like mosquitoes, affects by preference low and moist localities, such as swamps, fens, jungles, marshes, etc.

2. Malaria is hardly ever developed at a lower temperature than 60° Fahr., and such a temperature is necessary for the development of the mosquito.

3. Mosquitoes, like malaria, may both accumulate in and be obstructed by forests lying in the course of winds blowing from malarious localities.

4. By atmospheric currents malaria and mosquitoes are alike capable of being transported for considerable distances.

5. Malaria may be developed in previously healthy places by turning up the soil, as in making excavations for the foundation of houses, tracks for railroads, and beds for canals, because these operations afford breeding places for mosquitoes.

6. In proportion as countries, previously malarious, are cleared up and thickly settled, periodical fevers disappear, because swamps and pools are drained so that the mosquito cannot readily find a place suitable to deposit her eggs.

7. Malaria is most dangerous when the sun is down and the danger of exposure after sunset is greatly increased by the person exposed sleeping in the night air. Both facts are readily explicable by the mosquito malaria theory.

8. In malarial districts the use of fire, both indoors and to those who sleep out, affords a comparative security against malaria, because of the destruction of mosquitoes.

9. It is claimed that the air of cities in some way renders the poison innocuous, for, though a malarial disease may be raging outside, it does not penetrate far into the interior. We may easily conceive that mosquitoes, while invading cities during their nocturnal pilgrimages will be so far arrested by walls and houses, as well as attracted by lights in the suburbs, that many of them will in this way be prevented from penetrating "far into the interior."

10. Malarial diseases and likewise mosquitoes are most prevalent toward the latter part of summer and in the autumn.

11. Various writers have maintained that malaria is arrested by canvas curtains, gauze veils and mosquito nets and have recommended the rise of mosquito curtains, "through which malaria can seldom or never pass." It can hardly be conceived that these intercept marsh-air but they certainly do protect from mosquitoes.

12. Malaria spares no age, but it affects infants much less frequently than adults, because young infants are usually carefully housed and protected from mosquito inoculation.

Correlated with the miasmatic theory was the belief that some animal or vegetable organism which lived in marshes, produced malaria, and frequent searches were made for it. Salisbury (1862) thought this causative organism to be an alga, of the genus Palmella; others attributed it to certain fungi or bacteria.

In 1880, the French physician, Laveran, working in Algeria, discovered an amœboid organism in the blood of malarial patients and definitely established the parasitic nature of this disease. Pigmented granules had been noted by Meckel as long ago as 1847, in the spleen and blood of a patient who had died of malaria, and his observations had been repeatedly verified, but the granules had been regarded as degeneration products, and the fact that they occurred in the body of a foreign organism had been overlooked.

Soon after the discovery of the parasites in the blood, Gerhardt (1884) succeeded in transferring the disease to healthy individuals by inoculation of malarious blood, and thus proved that it is a true infection. This was verified by numerous experimenters and it was found that inoculation with a very minute quantity of the diseased blood would not only produce malaria but the particular type of disease.

Laveran traced out the life cycle of the malarial parasite as it occurs in man. The details as we now know them and as they are illustrated by the accompanying figure 125, are as follows:

The infecting organism or sporozoite, is introduced into the circulation, penetrates a red blood corpuscle, and forms the amœboid schizont. This lives at the expense of the corpuscle and as it develops there are deposited in its body scattered black or reddish black particles. These are generally called melanin granules, but are much better referred to as hæmozoin, as they are not related to melanin. The hæmozoin is the most conspicuous part of the parasite, a feature of advantage in diagnosing from unstained preparations.