bb. Male with blackish abdomen, middle tibia with a tubercle beyond

the middle. The larva with spiniferous appendages of which the

dorsal and ventral series are short, the lateral series long and

feathered (fig. 101) _F. scalaris_

aa. Apical cell (R) of the wing more or less narrowed in the margin; i.

e., the bounding veins more or less converging (fig. 108).

b. The mouth-parts produced and pointed, fitted for piercing.

c. Palpi much shorter than the proboscis; a brownish gray fly, its

thorax with three rather broad whitish stripes; on each border

of the middle stripe and on the mesal borders of the lateral

stripes is a blackish brown line. Abdomen yellowish brown; on

the second, third and fourth segments are three brown spots

which may be faint or even absent. The larvae live in dung. The

stable-fly (fig. 110) _Stomoxys calcitrans_

cc. Palpi nearly as long as the proboscis. Smaller species than the

house-fly. The horn-fly (fig. 167) _Haematobia irritans_

bb. Mouth-parts blunt, fitted for lapping.

c. Thorax, particularly on the sides and near the base of the wings

with soft golden yellow hairs among the bristles. This fly is

often found in the house in very early spring or even in the

winter. The cluster-fly, _Pollenia rudis_

cc. Thorax without golden yellow hairs among the bristles.

d. The last segment of the vein M with an abrupt angle. (fig.

108). The larvae live in manure, etc. House-fly, _Musca

domestica_

dd. The last segment of vein M with a broad, gentle curve (fig.

102).

e. Eyes microscopically hairy; each abdominal segment with two

spots. Larvae in dung. _Myiospila meditabunda_

ee. Eyes bare; abdomen gray and brown marbled. _Muscina_

f. With black legs and palpi. _M. assimilis_

ff. With legs more or less yellowish; palpi yellow. Larvae in

decaying vegetable substances, dung, etc. _M. stabulans_

It is almost universally believed that the adults of _Musca domestica_

hibernate, remaining dormant throughout the winter in attics, around

chimneys, and in sheltered but cold situations. This belief has been

challenged by Skinner (1913), who maintains that all the adult flies die

off during the fall and early winter and that the species is carried

over in the pupal stage, and in no other way. The cluster-fly, _Pollenia

rudis_, undoubtedly does hibernate in attics and similar situations and

is often mistaken for the house-fly. In so far as concerns _Musca

domestica_, the important question as to hibernation in the adult stage

is an open one. Many observations by one of the writers (Johannsen) tend

to confirm Dr. Skinner's conclusion, in so far as it applies to

conditions in the latitude of New York State. Opposed, is the fact that

various experimenters, notably Hewitt (1910) and Jepson (1909) wholly

failed to carry pupae through the winter.

[Illustration: 108. The house or typhoid fly (Musca domestica (x4)).

After Howard.]

The house-fly breeds by preference in horse manure. Indeed, Dr. Howard,

whose extensive studies of the species especially qualify him for

expressing an opinion on the subject, has estimated that under ordinary

city and town conditions, more than ninety per cent of the flies present

in houses have come from horse stables or their vicinity. They are not

limited to such localities, by any means, for it has been found that

they would develop in almost any fermenting organic substance. Thus,

they have been bred from pig, chicken, and cow manure, dirty waste

paper, decaying vegetation, decaying meat, slaughter-house refuse,

sawdust-sweepings, and many other sources. A fact which makes them

especially dangerous as disease-carriers is that they breed readily in

human excrement.

The eggs are pure white, elongate ovoid, somewhat broader at the

anterior end. They measure about one millimeter (1-25 inch) in length.

They are deposited in small, irregular clusters, one hundred and twenty

to one hundred and fifty from a single fly. A female may deposit as many

as four batches in her life time. The eggs hatch in from eight to

twenty-four hours.

The newly hatched larva, or maggot (fig. 108), measures about two

millimeters (1-12 inch) in length. It is pointed at the head end and

blunt at the opposite end, where the spiracular openings are borne. It

grows rapidly, molts three times and reaches maturity in from six to

seven days, under favorable conditions.

The pupal stage, like that of related flies, is passed in the old larval

skin which, instead of being molted, becomes contracted and heavily

chitinized, forming the so-called _puparium_ (fig. 108). The pupal stage

may be completed in from three to six days.

Thus during the warm summer months a generation of flies may be produced

in ten to twelve days. Hewitt at Manchester, England, found the minimum

to be eight days but states that larvae bred in the open air in horse

manure which had an average daily temperature of 22.5^o C., occupied

fourteen to twenty days in their development, according to the air

temperature.

After emergence, a period of time must elapse before the fly is capable

of depositing eggs. This period has been tuned the _preoviposition_

period. Unfortunately we have few exact data regarding this period.

Hewitt found that the flies became sexually mature in ten to fourteen

days after their emergence from the pupal state and four days after

copulation they began to deposit their eggs; in other words the

preoviposition stage was fourteen days or longer. Griffith (1908) found

this period to be ten days. Dr. Howard believes that the time "must

surely be shorter, and perhaps much shorter, under midsummer conditions,

and in the freedom of the open air." He emphasizes that the point is of

great practical importance, since it is during this period that the

trapping and other methods of destroying the adult flies, will prove

most useful.

Howard estimates that there may be nine generations of flies a year

under outdoor conditions in places comparable in climate to Washington.

The number may be considerably increased in warmer climates.

The rate at which flies may increase under favorable conditions is

astounding. Various writers have given estimates of the numbers of flies

which may develop as the progeny of a single individual, providing all

the eggs and all the individual flies survived. Thus, Howard estimates

that from a single female, depositing one hundred and twenty eggs on

April 15th, there may be by September 10th, 5,598,720,000,000 adults.

Fortunately, living forms do not produce in any such mathematical manner

and the chief value of the figures is to illustrate the enormous

struggle for existence which is constantly taking place in nature.

Flies may travel for a considerable distance to reach food and shelter,

though normally they pass to dwellings and other sources of food supply

in the immediate neighborhood of their breeding places. Copeman, Howlett

and Merriman (1911) marked flies by shaking them in a bag containing

colored chalk. Such flies were repeatedly recovered at distances of

eight to one thousand yards and even at a distance of seventeen hundred

yards, nearly a mile.

Hindle and Merriman (1914) continued these experiments on a large scale

at Cambridge, England. They "do not think it likely that, as a rule,

flies travel more than a quarter of a mile in thickly-housed areas." In

one case a single fly was recovered at a distance of 770 yards but a

part of this distance was across open fen-land. The surprising fact was

brought out that flies tend to travel either _against_ or across the

wind. The actual direction followed may be determined either directly by

the action of the wind (positive anemotropism), or indirectly owing to

the flies being attracted by any odor that it may convey from a source

of food. They conclude that it is likely that the chief conditions

favoring the disposal of flies are fine weather and a warm temperature.

The nature of the locality is another considerable factor. Hodge (1913)

has shown that when aided by the wind they may fly to much greater

distances over the water. He reports that at Cleveland, Ohio, the cribs

of the water works, situated a mile and a quarter, five miles, and six

miles out in Lake Erie are invaded by a regular plague of flies when the

wind blows from the city. Investigation showed that there was absolutely

nothing of any kind in which flies could breed on the crib.

The omnivorous habits of the house-fly are matters of everyday

observation. From our view point, it is sufficient to emphasize that

from feeding on excrement, on sputum, on open sores, or on putrifying

matter, the flies may pass to the food or milk upon the table or to

healthy mucous membranes, or uncontaminated wounds. There is nothing in

its appearance to tell whether the fly that comes blithely to sup with

you is merely unclean, or whether it has just finished feeding upon

dejecta teeming with typhoid bacilli.

[Illustration: 100. Pulvillus of foot of house-fly, showing glandular

hairs.]

The method of feeding of the house-fly has an important bearing on the

question of its ability to transmit pathogenic organisms. Graham-Smith

(1910) has shown that when feeding, flies frequently moisten soluble

substances with "vomit" which is regurgitated from the crop. This is, of

course, loaded with bacteria from previous food. When not sucked up

again these drops of liquid dry, and produce round marks with an opaque

center and rim and an intervening less opaque area. Fly-specks, then,

consist of both vomit spots and feces. Graham-Smith shows a photograph

of a cupboard window where, on an area six inches square, there were

counted eleven hundred and two vomit marks and nine fecal deposits.

From a bacteriologist's viewpoint a discussion of the possibility of a

fly's carrying bacteria would seem superfluous. Any exposed object,

animate or inanimate, is contaminated by bacteria and will transfer them

if brought into contact with suitable culture media, whether such

substance be food, or drink, open wounds, or the sterile culture media

of the laboratory. A needle point may convey enough germs to produce

disease. Much more readily may the house-fly with its covering of hairs

and its sponge-like pulvilli (fig. 109) pick up and transfer bits of

filth and other contaminated material.

For popular instruction this inevitable transfer of germs by the

house-fly is strikingly demonstrated by the oft copied illustration of

the tracks of a fly on a sterile culture plate. Two plates of gelatine

or, better, agar medium are prepared. Over one of these a fly (with

wings clipped) is allowed to walk, the other is kept as a check. Both

are put aside at room temperature, to be examined after twenty-four to

forty-eight hours. At the end of that time, the check plate is as clear

as ever, the one which the fly has walked is dotted with colonies of

bacteria and fungi. The value in the experiment consists in emphasizing

that by this method we merely render visible what is constantly

occurring in nature.

A comparable experiment which we use in our elementary laboratory work

is to take three samples of _clean_ (preferably, sterile) fresh milk in

sterile bottles. One of them is plugged with a pledget of cotton, into

the second is dropped a fly from the laboratory and into the third is

dropped a fly which has been caught feeding upon garbage or other filth.

After a minute or two the flies are removed and the vials plugged as was

number one. The three are then set aside at room temperature. When

examined after twenty-four hours the milk in the first vial is either

still sweet or has a "clean" sour odor; that of the remaining two is

very different, for it has a putrid odor, which is usually more

pronounced in the case of sample number three.

Several workers have carried out experiments to determine the number of

bacteria carried by flies under natural conditions. One of the most

extended and best known of these is the series by Esten and Mason

(1908). These workers caught flies from various sources in a sterilized

net, placed them in a sterile bottle and poured over them a known

quantity of sterilized water, in which they were shaken so as to wash

the bacteria from their bodies. They found the number of bacteria on a

single fly to range from 550 to 6,600,000. Early in the fly season the

numbers of bacteria on flies are comparatively small, while later the

numbers are comparatively very large. The place where flies live also

determines largely the numbers that they carry. The lowest number, 550,

was from a fly caught in the bacteriological laboratory, the highest

number, 6,600,000 was the average from eighteen swill-barrel flies.

Torrey (1912) made examination of "wild" flies from a tenement house

district of New York City. He found "that the surface contamination of

these 'wild' flies may vary from 570 to 4,400,000 bacteria per insect,

and the intestinal bacterial content from 16,000 to 28,000,000."

Less well known in this country is the work of Cox, Lewis, and Glynn

(1912). They examined over four hundred and fifty naturally infected

house-flies in Liverpool during September and early October. Instead of

washing the flies they were allowed to swim on the surface of sterile

water for five, fifteen, or thirty minutes, thus giving natural

conditions, where infection occurs from vomit and dejecta of the flies,

as well as from their bodies. They found, as might be expected, that

flies from either insanitary or congested areas of the city contain far

more bacteria than those from the more sanitary, less congested, or

suburban areas. The number of aerobic bacteria from the former varied

from 800,000 to 500,000,000 per fly and from the latter from 21,000 to

100,000. The number of intestinal forms conveyed by flies from

insanitary or congested areas was from 10,000 to 333,000,000 as compared

with from 100 to 10,000 carried by flies from the more sanitary areas.

Pathogenic bacteria and those allied to the food poisoning group were

only obtained from the congested or moderately congested areas and not

from the suburban areas, where the chances of infestation were less.

The interesting fact was brought out that flies caught in milk shops

apparently carry and obtain more bacteria than those from other shops

with exposed food in a similar neighborhood. The writers explained this

as probably due to the fact that milk when accessible, especially during

the summer months, is suitable culture medium for bacteria, and the

flies first inoculate the milk and later reinoculate themselves, and

then more of the milk, so establishing a vicious circle.

They conclude that in cities where food is plentiful flies rarely

migrate from the locality in which they are bred, and consequently the

number of bacteria which they carry depends upon the general standard

of cleanliness in that locality. Flies caught in a street of modern,

fairly high class, workmen's dwellings forming a sanitary oasis in the

midst of a slum area, carried far less bacteria than those caught in the

adjacent neighborhood.

Thus, as the amount of dirt carried by flies in any particular locality,

measured in the terms of bacteria, bears a definite relation to the

habits of the people and to the state of the streets, it demonstrates

the necessity of efficient municipal and domestic cleanliness, if the

food of the inhabitants is to escape pollution, not only with harmless

but also with occasional pathogenic bacteria.

The above cited work is of a general nature, but, especially in recent

years, many attempts have been made to determine more specifically the

ability of flies to transmit pathogenic organisms. The critical reviews

of Nuttall and Jepson (1909), Howard (1911), and Graham-Smith (1913)

should be consulted by the student of the subject. We can only cite here

a few of the more striking experiments.

Celli (1888) fed flies on pure cultures of _Bacillus typhosus_ and

declared that he was able to recover these organisms from the intestinal

contents and excrement.

Firth and Horrocks (1902), cited by Nuttall and Jepson, "kept _Musca

domestica_ (also bluebottles) in a large box measuring 4 x 3 x 3 feet,

with one side made of glass. They were fed on material contaminated with

cultures of _B. typhosus_. Agar plates, litmus, glucose broth and a

sheet of clean paper were at the same time exposed in the box. After a

few days the plates and broth were removed and incubated with a positive

result." Graham-Smith (1910) "carried out experiments with large numbers

of flies kept in gauze cages and fed for eight hours on emulsions of _B.

typhosus_ in syrup. After that time the infested syrup was removed and

the flies were fed on plain syrup. _B. typhosus_ was isolated up to 48

hours (but not later) from emulsions of their feces and from plates over

which they walked."

Several other workers, notably Hamilton (1903), Ficker (1903),

Bertarelli (1910) Faichnie (1909), and Cochrane (1912), have isolated

_B. typhosus_ from "wild" flies, naturally infected. The papers of

Faichnie and of Cochrane we have not seen, but they are quoted in

_extenso_ by Graham-Smith (1913).

On the whole, the evidence is conclusive that typhoid germs not only may

be accidentally carried on the bodies of house-flies but may pass

through their bodies and be scattered in a viable condition in the feces

of the fly for at least two days after feeding. Similar, results have

been reached in experiments with cholera, tuberculosis and yaws, the

last-mentioned being a spirochaete disease. Darling (1913) has shown that

murrina, a trypanosome disease of horses and mules in the Canal zone is

transmitted by house-flies which feed upon excoriated patches of

diseased animals and then pass to cuts and galls of healthy animals.

Since it is clear that flies are abundantly able to disseminate viable

pathogenic bacteria, it is important to consider whether they have

access to such organisms in nature. A consideration of the method of

spread of typhoid will serve to illustrate the way in which flies may

play an important role.

Typhoid fever is a specific disease caused by _Bacillus typhosus_, and

by it alone. The causative organism is to be found in the excrement and

urine of patients suffering from the disease. More than that, it is

often present in the dejecta for days, weeks, or even months and years,

after the individual has recovered from the disease. Individuals so

infested are known as "typhoid carriers" and they, together with those

suffering from mild cases, or "walking typhoid," are a constant menace

to the health of the community in which they are found.

Human excrement is greedily visited by flies, both for feeding and for

ovipositing. The discharges of typhoid patients, or of chronic

"carriers," when passed in the open, in box privies, or camp latrines,

or the like, serve to contaminate myriads of the insects which may then

spread the germ to human food and drink. Other intestinal diseases may

be similarly spread. There is abundant epidaemiological evidence that

infantile diarrhoea, dysentery, and cholera may be so spread.

Stiles and Keister (1913) have shown that spores of _Lamblia

intestinalis_, a flagellate protozoan living in the human intestine, may

be carried by house-flies. Though this species is not normally

pathogenic, one or more species of _Entamoeba_ are the cause of a type

of a highly fatal tropical dysentery. Concerning it, and another

protozoan parasite of man, they say, "If flies can carry _Lamblia_

spores measuring 10 to 7u, and bacteria that are much smaller, and

particles of lime that are much larger, there is no ground to assume

that flies may not carry _Entamoeba_ and _Trichomonas_ spores."

Tuberculosis is one of the diseases which it is quite conceivable may be

carried occasionally. The sputum of tubercular patients is very

attractive to flies, and various workers, notably Graham-Smith, have

found that _Musca domestica_ may distribute the bacillus for several

days after feeding on infected material.

A type of purulent opthalmia which is very prevalent in Egypt is often

said to be carried by flies. Nuttall and Jepson (1909) consider that the

evidence regarding the spread of this disease by flies is conclusive and

that the possibility of gonorrhoeal secretions being likewise conveyed

cannot be denied.

Many studies have been published, showing a marked agreement between the

occurrence of typhoid and other intestinal diseases and the prevalence

of house-flies. The most clear-cut of these are the studies of the Army

Commission appointed to investigate the cause of epidemics of enteric

fever in the volunteer camps in the Southern United States during the

Spanish-American War. Though their findings as presented by Vaughan

(1909), have been quoted very many times, they are so germane to our

discussion that they will bear repetition:

"Flies swarmed over infected fecal matter in the pits and fed upon the

food prepared for the soldiers in the mess tents. In some instances

where lime had recently been sprinkled over the contents of the pits,

flies with their feet whitened with lime were seen walking over the

food." Under such conditions it is no wonder that "These pests had

inflicted greater loss upon American soldiers than the arms of Spain."

Similar conditions prevailed in South Africa during the Boer War. Seamon

believes that very much of the success of the Japanese in their fight

against Russia was due to the rigid precautions taken to prevent the

spread of disease by these insects and other means.

Veeder has pointed out that the characteristics of a typical fly-borne

epidemic of typhoid are that it occurs in little neighborhood epidemics,

extending by short leaps from house to house, without regard to water

supply or anything else in common. It tends to follow the direction of

prevailing winds (cf. the conclusions of Hindle and Merriman). It occurs

during warm weather. Of course, when the epidemic is once well under

way, other factors enter into its spread.

In general, flies may be said to be the chief agency in the spread of

typhoid in villages and camps. In cities with modern sewer systems they

are less important, though even under the best of such conditions, they

are important factors. Howard has emphasized that in such cities there

are still many uncared-for box privies and that, in addition, the

deposition of feces overnight in uncared-for waste lots and alleys is

common.

Not only unicellular organisms, such as bacteria and protozoa, but also

the eggs, embryos and larvae of parasitic worms have been found to be

transported by house-flies. Ransom (1911) has found that _Habronema

muscae_, a nematode worm often found in adult flies, is the immature

stage of a parasite occurring in the stomach of the horse. The eggs or

embryos passing out with the feces of the horse, are taken up by fly

larvae and carried over to the imago stage.

Grassi (1883), Stiles (1889), Calandruccio (1906), and especially Nicoll

(1911), have been the chief investigators of the ability of house-flies

to carry the ova and embryos of human intestinal parasites. Graham-Smith

(1913) summarizes the work along this line as follows:

"It is evident from the investigations that have been quoted that

house-flies and other species are greatly attracted to the ova of

parasitic worms contained in feces and other materials, and make great

efforts to ingest them. Unless the ova are too large they often succeed,

and the eggs are deposited uninjured in their feces, in some cases up to

the third day at least. The eggs may also be carried on their legs or

bodies. Under suitable conditions, food and fluids may be contaminated

with the eggs of various parasitic worms by flies, and in one case

infection of the human subject has been observed. Feces containing

tape-worm segments may continue to be a source of infection for as long

as a fortnight. Up to the present, however, there is no evidence to show

what part flies play in the dissemination of parasitic worms under

natural conditions."

Enough has been said to show that the house-fly must be dealt with as a

direct menace to public health. Control measures are not merely matters

of convenience but are of vital importance.

Under present conditions the speedy elimination of the house-fly is

impossible and the first thing to be considered is methods of protecting

food and drink from contamination. The first of these methods is the

thorough screening of doors and windows to prevent the entrance of

flies. In the case of kitchen doors, the flies, attracted by odors, are

likely to swarm onto the screen and improve the first opportunity for

gaining an entrance. This difficulty can be largely avoided by

screening-in the back porch and placing the screen door at one end

rather than directly before the door.

The use of sticky fly paper to catch the pests that gain entrance to the

house is preferable to the various poisons often used. Of the latter,

formalin (40 per cent formaldehyde) in the proportion of two

tablespoonfuls to a pint of water is very efficient, if all other

liquids are removed or covered, so that the flies must depend on the

formalin for drink. The mixture is said to be made more attractive by

the addition of sugar or milk, though we have found the plain solution

wholly satisfactory, under proper conditions. It should be emphasized

that this formalin mixture is not perfectly harmless, as so often

stated. There are on record cases of severe and even fatal poisoning

from the accidental drinking of solutions.

When flies are very abundant in a room they can be most readily gotten

rid of by fumigation with sulphur, or by the use of pure pyrethrum

powder either burned or puffed into the air. Herrick (1913) recommends

the following method: "At night all the doors and windows of the kitchen

should be closed; fresh powder should be sprinkled over the stove, on

the window ledges, tables, and in the air. In the morning flies will be

found lying around dead or stupified. They may then be swept up and

burned." This method has proved very efficaceous in some of the large

dining halls in Ithaca.

The writers have had little success in fumigating with the vapors of

carbolic acid, or carbolic acid and gum camphor, although these methods

will aid in driving flies from a darkened room.

All of these methods are but makeshifts. As Howard has so well put it,

"the truest and simplest way of attacking the fly problem is to prevent

them from breeding, by the treatment or abolition of all places in which

they can breed. To permit them to breed undisturbed and in countless

numbers, and to devote all our energy to the problem of keeping them out

of our dwellings, or to destroy them after they have once entered in

spite of all obstacles, seems the wrong way to go about it."

We have already seen that _Musca domestica_ breeds in almost any

fermenting organic material. While it prefers horse manure, it breeds

also in human feces, cow dung and that of other animals, and in refuse

of many kinds. To efficiently combat the insect, these breeding places

must be removed or must be treated in some such way as to render them

unsuitable for the development of the larvae. Under some conditions

individual work may prove effective, but to be truly efficient there

must be extensive and thorough cooperative efforts.

Manure, garbage, and the like should be stored in tight receptacles and

carted away at least once a week. The manure may be carted to the fields

and spread. Even in spread manure the larvae may continue their

development. Howard points out that "it often happens that after a lawn

has been heavily manured in early summer the occupants of the house will

be pestered with flies for a time, but finding no available breeding

place these disappear sooner or later. Another generation will not breed

in the spread manure."

Hutchinson (1914) has emphasized that the larvae of houseflies have

deeply engrained the habit of migrating in the prepupal stage and has

shown that this offers an important point of attack in attempts to

control the pest. He has suggested that maggot traps might be developed

into an efficient weapon in the warfare against the house-fly. Certain

it is that the habit greatly simplifies the problem of treating the

manure for the purpose of killing the larvae.

There have been many attempts to find some cheap chemical which would

destroy fly larvae in horse manure without injuring the bacteria or

reducing the fertilizing values of the manure. The literature abounds in

recommendations of kerosene, lime, chloride of lime, iron sulphate, and

other substances, but none of them has met the situation. The whole

question has been gone into thoroughly by Cook, Hutchinson and Scales

(1914), who tested practically all of the substances which have been

recommended. They find that by far the most effective, economical, and

practical of the substances is borax in the commercial form in which it

is available throughout the country.

"Borax increases the water-soluble nitrogen, ammonia and alkalinity of

manure and apparently does not permanently injure the bacterial flora.

The application of manure treated with borax at the rate of 0.62 pound

per eight bushels (10 cubic feet) to soil does not injure the plants

thus far tested, although its cumulative effect, if any, has not been

determined."

As their results clearly show that the substances so often recommended

are inferior to borax, we shall quote in detail their directions for

treating manure so as to kill fly eggs and maggots.

"Apply 0.62 pound borax or 0.75 pound calcined colemanite to every 10

cubic feet (8 bushels) of manure immediately on its removal from the

barn. Apply the borax particularly around the outer edges of the pile

with a flour sifter or any fine sieve, and sprinkle two or three gallons

of water over the borax-treated manure.

"The reason for applying the borax to the fresh manure immediately after

its removal from the stable is that the flies lay their eggs on the

fresh manure, and borax, when it comes in contact with the eggs,

prevents their hatching. As the maggots congregate at the outer edge of

the pile, most of the borax should be applied there. The treatment

should be repeated with each addition of fresh manure, but when the

manure is kept in closed boxes, less frequent applications will be

sufficient. When the calcined colemanite is available, it may be used at

the rate of 0.75 pound per 10 cubic feet of manure, and is a cheaper

means of killing the maggots. In addition to the application of borax to

horse manure to kill fly larvae, it may be applied in the same proportion

to other manures, as well as to refuse and garbage. Borax may also be

applied to the floors and crevices in barns, stables, markets, etc., as

well as to street sweepings, and water should be added as in the

treatment of horse manure. After estimating the amount of material to be

treated and weighing the necessary amount of borax, a measure may be

used which will hold the proper amount, thus avoiding the subsequent

weighings.

"While it can be safely stated that no injurious action will follow the

application of manure treated with borax at the rate of 0.62 pound for

eight bushels, or even larger amounts in the case of some plants,

nevertheless the borax-treated manure has not been studied in connection

with the growth of all crops, nor has its cumulative effect been

determined. It is therefore recommended that not more than 15 tons per

acre of the borax-treated manure should be applied to the field. As

truckmen use considerably more than this amount, it is suggested that

all cars containing borax-treated manure be so marked, and that

public-health officials stipulate in their directions for this treatment

that not over 0.62 pound for eight bushels of manure be used, as it has

been shown that larger amounts of borax will injure most plants. It is

also recommended that all public-health officials and others, in

recommending the borax treatment for killing fly eggs and maggots in

manure, warn the public against the injurious effects of large amounts

of borax on the growth of plants."

"The amount of manure from a horse varies with the straw or other

bedding used, but 12 or 15 bushels per week represent the approximate

amount obtained. As borax costs from five to six cents per pound in

100-pound lots in Washington, it will make the cost of the borax

practically one cent per horse, per day. And if calcined colemanite is

purchased in large shipments the cost should be considerably less."

Hodge (1910) has approached the problem of fly extermination from

another viewpoint. He believes that it is practical to trap flies out of

doors during the preoviposition period, when they are sexually immature,

and to destroy such numbers of them that the comparatively few which

survive will not be able to lay eggs in sufficient numbers to make the

next generation a nuisance. To the end of capturing them in enormous

numbers he has devised traps to be fitted over garbage cans, into stable

windows, and connected with the kitchen window screens. Under some

conditions this method of attack has proved very satisfactory.

One of the most important measures for preventing the spread of disease

by flies is the abolition of the common box privy. In villages and rural

districts this is today almost the only type to be found. It is the

chief factor in the spread of typhoid and other intestinal diseases, as

well as intestinal parasites. Open and exposed to myriads of flies which

not only breed there but which feed upon the excrement, they furnish

ideal conditions for spreading contamination. Even where efforts are

made to cover the contents with dust, or ashes, or lime, flies may

continue to breed unchecked. Stiles and Gardner have shown that

house-flies buried in a screened stand-pipe forty-eight inches under

sterile sand came to the surface. Other flies of undetermined species

struggled up through seventy-two inches of sand.

So great is the menace of the ordinary box privy that a number of

inexpensive and simple sanitary privies have been designed for use where

there are not modern sewer systems. Stiles and Lumsden (1911) have given

minute directions for the construction of one of the best types, and

their bulletin should be obtained by those interested.

Another precaution which is of fundamental importance in preventing the

spread of typhoid, is that of disinfecting all discharges from patients

suffering with the disease. For this purpose, quick-lime is the cheapest

and is wholly satisfactory. In chamber vessels it should be used in a

quantity equal to that of the discharge to be treated. It should be

allowed to act for two hours. Air-slaked lime is of no value whatever.

Chloride of lime, carbolic acid, or formalin may be used, but are more

expensive. Other intestinal diseases demand similar precautions.

STOMOXYS CALCITRANS, THE STABLE-FLY--It is a popular belief that

house-flies bite more viciously just before a rain. As a matter of

fact, the true house-flies never bite, for their mouth-parts are not

fitted for piercing. The basis of the misconception is the fact that a

true biting fly, _Stomoxys calcitrans_ (fig. 110), closely resembling

the house-fly, is frequently found in houses and may be driven in in

greater numbers by muggy weather. From its usual habitat this fly is

known as the "stable-fly" or, sometimes as the "biting house-fly."

_Stomoxys calcitrans_ may be separated from the house-fly by the use of

the key on p. 145. It may be more fully characterized as follows:

The eyes of the male are separated by a distance equal to one-fourth of

the diameter of the head, in the female by one-third. The frontal stripe

is black, the cheeks and margins of the orbits silvery-white. The

antennae are black, the arista feathered on the upper side only. The

proboscis is black, slender, fitted for piercing and projects forward in

front of the head. The thorax is grayish, marked by four conspicuous,

more or less complete black longitudinal stripes; the scutellum is

paler; the macrochaetae are black. The abdomen is gray, dorsally with

three brown spots on the second and third segments and a median spot on

the fourth. These spots are more pronounced in the female. The legs are

black, the pulvilli distinct. The wings are hyaline, the vein M_{1+2}

less sharply curved than in the house-fly, the apical cell being thus

more widely open (cf. fig. 110). Length 7 mm.

[Illustration: 110. Stomoxys calcitrans; adult, larva, puparium and

details, (x5). After Howard.]

This fly is widely distributed, being found the world over. It was

probably introduced into the United States, but has spread to all parts

of the country. Bishopp (1913) regards it as of much more importance as

a pest of domestic animals in the grain belt than elsewhere in the

United States. The life-history and habits of this species have assumed

a new significance since it has been suggested that it may transmit the

human diseases, infantile paralysis and pellagra. In this country, the

most detailed study of the fly is that of Bishopp (1913) whose data

regarding the life cycle are as follows:

The eggs like those of the house-fly, are about one mm. in length. Under

a magnifying glass they show a distinct furrow along one side. When

placed on any moist substance they hatch in from one to three days after

being deposited.

The larva or maggots (fig. 110) have the typical shape and actions of

most maggots of the Muscid group. They can be distinguished from those

of the house-fly as the stigma-plates are smaller, much further apart,

with the slits less sinuous. Development takes place fairly rapidly when

the proper food conditions are available and the growth is completed

within eleven to thirty or more days.

The pupa (fig. 110), like that of related flies, undergoes its

development within the contracted and hardened last larval skin, or

puparium. This is elongate oval, slightly thicker towards the head end,

and one-sixth to one-fourth of an inch in length. The pupal stage

requires six to twenty days, or in cool weather considerably longer.

The life-cycle of the stable-fly is therefore considerably longer than

that of _Musca domestica_. Bishopp found that complete development might

be undergone in nineteen days, but that the average period was somewhat

longer, ranging from twenty-one to twenty-five days, where conditions

are very favorable. The longest period which he observed was forty-three

days, though his finding of full grown larvae and pupae in straw during

the latter part of March, in Northern Texas, showed that development may

require about three months, as he considered that these stages almost

certainly developed from eggs deposited the previous December.

The favorite breeding place, where available, seems to be straw or

manure mixed with straw. It also breeds in great numbers in

horse-manure, in company with _Musca domestica_.

Newstead considers that in England the stable-fly hibernates in the

pupal stage. Bishopp finds that in the southern part of the United

States there is no true hibernation, as the adults have been found to

emerge at various times during the winter. He believes that in the

northern United States the winter is normally passed in the larval and

pupal stages, and that the adults which have been observed in heated

stables in the dead of winter were bred out in refuse within the warm

barns and were not hibernating adults.

Graham-Smith (1913) states that although the stable-fly frequents stable

manure, it is probably not an important agent in distributing the

organisms of intestinal diseases. Bishopp makes the important

observation that "it has never been found breeding in human excrement

and does not frequent malodorous places, which are so attractive to the

house-fly. Hence it is much less likely to carry typhoid and other germs

which may be found in such places."

Questions of the possible agency of _Stomoxys calcitrans_ in the

transmission of infantile paralysis and of pellagra, we shall consider

later.

OTHER ARTHROPODS WHICH MAY SERVE AS SIMPLE CARRIERS OF PATHOGENIC

ORGANISMS--It should be again emphasized that any insect which has

access to, and comes in contact with, pathogenic organisms and then

passes to the food, or drink, or the body of man, may serve as a simple

carrier of disease. In addition to the more obvious illustrations, an

interesting one is the previously cited case of the transfer of

_Dermatobia cyaniventris_ by a mosquito (fig. 81-84). Darling (1913) has

shown that in the tropics, the omnipresent ants may be important factors

in the spread of disease.

CHAPTER VI

ARTHROPODS AS DIRECT INOCULATORS OF DISEASE GERMS

We have seen that any insect which, like the house-fly, has access to

disease germs and then comes into contact with the food or drink of man,

may serve to disseminate disease. Moreover, it has been clearly

established that a contaminated insect, alighting upon wounded or

abraded surfaces, may infect them. These are instances of mere

accidental, mechanical transfer of pathogenic organisms.

Closely related are the instances of direct inoculation of disease germs

by insects and other arthropods. In this type, a blood-sucking species

not only takes up the germs but, passing to a healthy individual, it

inserts its contaminated mouth-parts and thus directly inoculates its

victim. In other words, the disease is transferred just as blood

poisoning may be induced by the prick of a contaminated needle, or as

the laboratory worker may inoculate an experimental animal.

Formerly, it was supposed that this method of the transfer of disease by

arthropods was a very common one and many instances are cited in the

earlier literature of the subject. It is, however, difficult to draw a

sharp line between such cases and those in which, on the one hand, the

arthropod serves as a mere passive carrier or, on the other hand, serves

as an essential host of the pathogenic organism. More critical study of

the subject has led to the belief that the importance of the role of

arthropods as direct inoculators has been much overestimated.

The principal reason for regarding this phase of the subject as

relatively unimportant, is derived from a study of the habits of the

blood-sucking species. It is found that, in general, they are

intermittent feeders, visiting their hosts at intervals and then

abstaining from feeding for a more or less extended period, while

digesting their meal. In the meantime, most species of bacteria or of

protozoan parasites with which they might have contaminated their

mouth-parts, would have perished, through inability to withstand drying.

In spite of this, it must be recognized that this method of transfer

does occur and must be reckoned with in any consideration of the

relations of insects to disease. We shall first cite some general

illustrations and shall then discuss the role of fleas in the spreading

of bubonic plague, an illustration which cannot be regarded as typical,

since it involves more than mere passive carriage.

SOME ILLUSTRATIONS OF DIRECT INOCULATION OF DISEASE GERMS BY ARTHROPODS

In discussing poisonous arthropods, we have already emphasized that

species which are of themselves innocuous to man, may occasionally

introduce bacteria by their bite or sting and thus cause more or less

severe secondary symptoms. That such cases should occur, is no more than

is to be expected. The mouth-parts or the sting of the insect are not

sterile and the chances of their carrying pyogenic organisms are always

present.

More strictly falling in the category of transmission of disease germs

by direct inoculation are the instances where the insect, or related

form, feeds upon a diseased animal and passes promptly to a healthy

individual which it infects. Of such a nature are the following:

Various species of biting flies are factors in the dissemination of

anthrax, an infectious and usually fatal disease of animals and,

occasionally, of man. That the bacteria with which the blood of diseased

animals teem shortly before death might be transmitted by such insects

has long been contended, but the evidence in support of the view has

been unsatisfactory. Recently, Mitzmain (1914) has reported a series of

experiments which show conclusively that the disease may be so conveyed

by a horse-fly, _Tabanus striatus_, and by the stable-fly, _Stomoxys

calcitrans_.

Mitzmain's experiments were tried with an artificially infected guinea

pig, which died of the disease upon the third day. The flies were

applied two and one-half hours, to a few minutes, before the death of

the animal. With both species the infection was successfully transferred

to healthy guinea pigs by the direct method, in which the flies were

interrupted while feeding on the sick animal. The evidence at hand does

not warrant the conclusion that insect transmission is the rule in the

case of this disease.

The nagana, or tsetse-fly disease of cattle is the most virulent disease

of domestic animals in certain parts of Africa. It is caused by a

protozoan blood parasite, _Trypanosoma brucei_, which is conveyed to

healthy animals by the bite of _Glossina morsitans_ and possibly other

species of tsetse-flies. The flies remain infective for forty-eight

hours after feeding on a diseased animal. The insect also serves as an

essential host of the parasite.

Surra, a similar trypanosomiasis affecting especially horses and mules,

occurs in southern Asia, Malaysia, and the Philippines where the

tsetse-flies are not to be found. It is thought to be spread by various

species of blood-sucking flies belonging to the genera _Stomoxys_,

_Haematobia_, and _Tabanus_. Mitzmain (1913) demonstrated that in the

Philippines it is conveyed mechanically by _Tabanus striatus_.

The sleeping sickness of man, in Africa, has also been supposed to be

directly inoculated by one, or several, species of tsetse-flies. It is

now known that the fly may convey the disease for a short time after

feeding, but that there is then a latent period of from fourteen to

twenty-one days, after which it again becomes infectious. This indicates

that in the meantime the parasite has been undergoing some phase of its

life-cycle and that the fly serves as an intermediate host. We shall

therefore consider it more fully under that grouping.

These are a few of the cases of direct inoculation which may be cited as

of the simpler type. We shall next consider the role of the flea in the

dissemination of the bubonic plague, an illustration complicated by the

fact that the bacillus multiples within the insect and may be indirectly

inoculated.

THE ROLE OF FLEAS IN THE TRANSMISSION OF THE PLAGUE

The plague is a specific infectious disease caused by _Bacillus pestis_.

It occurs in several forms, of which the bubonic and the pneumonic are

the most common. According to Wyman, 80 per cent of the human cases are

of the bubonic type. It is a disease which, under the name of oriental

plague, the pest, or the black death, has ravaged almost from time

immemorial the countries of Africa, Asia, and Europe. The record of its

ravages are almost beyond belief. In 542 A. D. it caused in one day ten

thousand deaths in Constantinople. In the 14th century it was introduced

from the East and prevailed throughout Armenia, Asia Minor, Egypt and

Northern Africa and Europe. Hecker estimates that one-fourth of the

population of Europe, or twenty-five million persons, died in the

epidemic of that century. From then until the 17th century it was almost

constantly present in Europe, the great plague of London, in 1665

killing 68,596 out of a population of 460,000. Such an epidemic would

mean for New York City a proportionate loss of over 600,000 in a single

year. It is little wonder that in the face of such an appalling disaster

suspicion and credulity were rife and the wildest demoralization ensued.

During the 14th century the Jews were regarded as responsible for the

disease, through poisoning wells, and were subjected to the most

incredible persecution and torture. In Milan the visitation of 1630 was

credited to the so-called anointers,--men who were supposed to spread

the plague by anointing the walls with magic ointment--and the most

horrible tortures that human ingenuity could devise were imposed on

scores of victims, regardless of rank or of public service (fig. 112,

a). Manzoni's great historical novel, "The Betrothed" has well pictured

conditions in Italy during this period.

[Illustration: 111. A contemporaneous engraving of the pest hospital in

Vienna in 1679. After Peters.]

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.

[Illustration: 112 a. A medieval method of combating the plague. The

persecution of the anointers in Milan in 1630. From a copy of "Il

processi originale degli untori" in the library of Cornell University.]

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.

[Illustration: 112 b. The modern method of combating the plague. A day's

catch of rats in the fight against plague in San Francisco. Courtesy of

Review of Reviews.]

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 septicaemic

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_,

(= _Loemopsylla_ 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

ARTHROPODS AS ESSENTIAL HOSTS OF PATHOGENIC ORGANISMS

We now have to consider the cases in which the arthropod acts as the

essential host of a pathogenic organism. In other words, cases in which

the organism, instead of being passively carried or merely accidentally

inoculated by the bite of its carrier, or vector, is taken up and

undergoes an essential part of its development within the arthropod.

[Illustration: 113. Dipylidium caninum. The double pored tapeworm of the

dog.]

In some cases, the sexual cycle of the parasite is undergone in the

arthropod, which then serves as the _definitive_ or _primary host_. In

other cases, it is the asexual stage of the parasite which is undergone,

and the arthropod then acts as the _intermediate host_. This distinction

is often overlooked and all the cases incorrectly referred to as those

in which the insect or other arthropod acts as intermediate host.

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

A number of tapeworms are known to undergo their sexual stage in an

insect or other arthropod. Of these at least two are occasional

parasites of man.

_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_.

[Illustration: 114. Dipylidium caninum. Rostrum evaginated and

invaginated. After Blanchard.]

[Illustration: 115. Dipylidium caninum. Immature cysticercoid. After

Grassi and Rovelli.]

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 300u 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 larvae 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.

[Illustration: 116. Dipylidium caninum. Cysticercoid. After Villet.]

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 larvae 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.

[Illustration: 117. One way in which Dipylidium infection in children

may occur. After Blanchard.]

_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 Cyclopidae.

[Illustration: 118. The probable method by which Dipylidium infection

usually occurs.]

Several other cestode parasites of domestic animals are believed to

develop their intermediate stage in certain arthropods. Among these may

be mentioned:

_Choanotaenia 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.

The larvae circulating in the blood are conveniently designated as

microfilariae. In this stage they are harmless and only one species,

_Filaria bancrofti_, appears to be of any great pathological

significance at any stage.

_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.

[Illustration: 119. Elephantiasis in Man. From "New Sydenham Society's

Atlas."]

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 Wucherer 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 Noe (1900), Noe

(1901) and Fulleborn (1910).

The larvae 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 300u x 8u, 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 Fulleborn.

One of the most surprising features of the habits of these larvae 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 larvae, 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 larvae 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 larvae 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 antennae, 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 larvae 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. Fulleborn has cleared up the question by showing that at

this time the filariae escape and, like the hookworm, actively bore into

the skin of their new host.

[Illustration: 120. Filaria in the muscles and labium of Culex. After

Blanchard.]

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 Tabanidae 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.

[Illustration: 121. Dracunculus medinensis; female; mouth; embryo. After

Bastian and Leuckart.]

_Filariae_ 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^o 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 haematoxylin.

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 larvae reach

the exterior after bursting the body of the mother.

[Illustration: 122. Cyclops, the intermediate host of Dracunculus.]

Fedtschenko (1879) found that when these larvae 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 larvae.

_Habronema muscae_ 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.

[Illustration: 123. An Echinorhynchid, showing the spinose retractile

proboscis.]

[Illustration: 124. June beetle (Lachnosterna).]

[Illustration: Larva]

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 larvae 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 larvae. In Europe the usual intermediate hosts are the

larvae 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

ARTHROPODS AS ESSENTIAL HOSTS OF PATHOGENIC PROTOZOA

MOSQUITOES AND MALARIA

Under the name of malaria is included a group of morbid symptoms

formerly supposed to be due to a miasm or bad air, but now known to be

caused by protozoan parasites of the genus _Plasmodium_, which attack

the red blood corpuscles. It occurs in paroxysms, each marked by a

chill, followed by high fever and sweating. The fever is either

intermittent or remittent.

There are three principal types of the disease, due to different species

of the parasite. They are:

1. The benign-tertian, caused by _Plasmodium vivax_, which undergoes its

schizogony or asexual cycle in the blood in forty-eight hours or even

less. This type of the disease,--characterized by fever every two days,

is the most wide-spread and common.

2. The quartan fever is due to the presence of _Plasmodium malariae_,

which has an asexual cycle of seventy-two hours, and therefore the fever

recurs every three days. This type is more prevalent in temperate and

sub-tropical regions, but appears to be rare everywhere.

3. The sub-tertian "aestivo-autumnal," or "pernicious" fever is caused by

_Plasmodium falciparum_. Schizogony usually occurs in the internal

organs, particularly in the spleen, instead of in the peripheral

circulation, as is the case of the tertian and quartan forms. The fever

produced is of an irregular type and the period of schizogony has not

been definitely determined. It is claimed by some that the variations

are due to different species of malignant parasites.

It is one of the most wide-spread of human diseases, occurring in almost

all parts of the world, except in the polar regions and in waterless

deserts. It is most prevalent in marshy regions.

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,

_Mbu_. 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^o

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 amoeboid 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 amoeboid

_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 haemozoin, as they are not related to

melanin. The haemozoin is the most conspicuous part of the parasite, a

feature of advantage in diagnosing from unstained preparations.

[Illustration: 125. Life cycle of the malaria parasite. Adapted from

Leuckart's chart, by Miss Anna Stryke.]

As the schizont matures, its nucleus breaks up into a number of daughter

nuclei, each with a rounded mass of protoplasm about it, and finally the

corpuscles are broken down and these rounded bodies are liberated in the

plasma as _merozoites_. These merozoites infect new corpuscles and thus

the asexual cycle is continued. The malarial paroxysm is coincident with

sporulation.

As early as Laveran's time it was known that under conditions not yet

determined there are to be found in the blood of malarious patients

another phase of the parasite, differing in form according to the type

of the disease. In the pernicious type these appear as large,

crescent-shaped organisms which have commonly been called "crescents."

We now know that these are sexual forms.

When the parasite became known there immediately arose speculations as

to the way in which it was transferred from man to man. It was thought

by some that in nature it occurred as a free-living amoeba, and that

it gained access to man through being taken up with impure water.

However, numerous attempts to infect healthy persons by having them

drink or inhale marsh water, or by injecting it into their circulation

resulted in failure, and influenced by Leuckart's and Melnikoff's work

on _Dipylidium_, that of Fedtschenko on _Dracunculus_, and more

especially by that of Manson on _Filaria_, search was made for some

insect which might transfer the parasite.

Laveran had early suggested that the role of carrier might be played by

the mosquito, but Manson first clearly formulated the hypothesis, and it

was largely due to his suggestions that Ross in India, undertook to

solve the problem. With no knowledge of the form or of the appearance in

this stage, or of the species of mosquito concerned, Ross spent almost

two and a half years of the most arduous work in the search and finally

in August, 1897, seventeen years after the discovery of the parasite in

man, he obtained his first definite clue. In dissecting a

"dappled-winged mosquito," "every cell was searched and to my intense

disappointment nothing whatever was found, until I came to the insect's

stomach. Here, however, just as I was about to abandon the examination,

I saw a very delicate circular cell, apparently lying amongst the

ordinary cells of the organ and scarcely distinguishable from them. On

looking further, another and another similar object presented itself. I

now focused the lens carefully on one of these, and found that it

contained a few minute granules of some black substance, exactly like

the pigment of the parasite of malaria. I counted altogether twelve of

these cells in the insect."

Further search showed that "the contents of the mature pigment cells did

not consist of clear fluid but of a multitude of delicate, thread-like

bodies which on the rupture of the parent cell, were poured into the

body cavity of the insect. They were evidently spores."

With these facts established, confirmation and extension of Ross's

results quickly followed, from many different sources. We cannot trace

this work in detail but will only point out that much of the credit is

due to the Italian workers, Grassi, Bignami, and Bastianelli, and to

Koch and Daniels.

It had already been found that when fresh blood was mounted and properly

protected against evaporation, a peculiar change occurred in these

crescents after about half an hour's time. From certain of them there

were pushed out long whip-like processes which moved with a very active,

lashing movement. The parasite at this stage is known as the

"flagellated body." Others, differing somewhat in details of structure,

become rounded but do not give off "flagella."

The American worker, MacCallum (1897), in studying bird malaria as found

in crows, first recognized the true nature of these bodies. He regarded

them as sexual forms and believed that the so-called flagella played the

part of spermatozoa. Thus, the "flagellated body" is in reality a

_microgametoblast_, producing _microgametes_, or the male sexual

element, while the others constitute the _macrogametes_, or female

elements.

It was found that when blood containing these sexual forms was sucked up

by an Anopheline mosquito and taken into its stomach, a microgamete

penetrated and fertilized a macrogamete in a way analogous to what takes

place in the fertilization of the egg in higher forms. The resultant,

mobile organism is known as the _migratory ookinete_. In this stage the

parasite bores through the epithelial lining of the "stomach"

(mid-intestine) of the mosquito and becomes encysted under the muscle

layers. Here the _oocyst_, as it is now known, matures and breaks up

into the body cavity and finally its products come to lie in the

salivary glands of the mosquito. Ten to twelve days are required for

these changes, after which the mosquito is infective, capable of

introducing the parasite with its saliva, when feeding upon a healthy

person.

Thus the malarial parasite is known to have a double cycle, an

alternation of generations, of which the asexual stage is undergone in

man, the sexual in certain species of mosquitoes. The mosquito is

therefore the definitive host rather than the _intermediate_, as usually

stated.

The complicated cycle may be made clearer by the diagram of Miss Stryke

(1912) which, by means of a double-headed mosquito (fig. 126) endeavors

to show how infection takes place through the biting of the human

victim, (at A), in whom asexual multiplication then takes place, and how

the sexual stages, taken up at B in the diagram, are passed in the body

of the mosquito.

[Illustration: 126. Life cycle of the malarial parasite. After Miss Anna

Stryke.]

The experimental proof that mosquitoes of the Anopheline group are

necessary agents in the transmission of malaria was afforded in 1900

when two English physicians, Drs. Sambon and Low lived for the three

most malarial months in the midst of the Roman Campagna, a region

famous for centuries as a hot-bed of malaria. The two experimenters

moved about freely throughout the day, exposed themselves to rains and

all kinds of weather, drank marsh water, slept exposed to the marsh air,

and, in short, did everything which was supposed to cause malaria,

except that they protected themselves thoroughly from mosquito bites,

retiring at sunset to a mosquito-proof hut. Though they took no quinine

and all of their neighbors suffered from malaria, they were absolutely

free from the disease.

To complete the proof, mosquitoes which had fed in Rome on malarious

patients were sent to England and allowed to bite two volunteers, one of

them Dr. Manson's own son, who had not been otherwise exposed to the

disease. Both of these gentlemen contracted typical cases of malaria and

the parasites were to be found in abundance in their blood.

[Illustration: 127. Eggs of Anopheles. After Howard.]

Since that time there have been many practical demonstrations of the

fact that malaria is transmitted exclusively by the bite of mosquitoes

and that the destruction of the mosquitoes means the elimination of the

disease.

We have said that the malarial parasite is able to undergo its

development only in certain species of mosquitoes belonging to the

Anopheline group. It is by no means certain that all of this group even,

are capable of acting as the definitive host of the parasites, and much

careful experiment work is still needed along this line. In the United

States, several species have been found to be implicated, _Anopheles

quadrimaculatus_ and _Anopheles crucians_ being the most common. The

characteristics of these species and the distinctions between them and

other mosquitoes will be discussed in Chapter XII.

In antimalarial work it is desirable to distinguish the anopheline

mosquitoes from the culicine species in all stages. The following

tabulation presents the more striking distinctions between the groups as

represented in the United States.

_Anopheles_ _Culex, Aedes, etc_.

_Eggs_: Laid singly in small Deposited in clumps in the

numbers upon the surface of the form of a raft (Culex group) or

water. Eggs lie upon their sides deposited singly in the water or

and float by means of lateral on the ground in places which

expansions (fig. 127). may later be submerged.

_Larva_: When at rest floats in When at rest (with few exceptions)

a horizontal position beneath the floats suspended in an

surface film. No respiratory oblique or vertical position, or

tube but instead a flattened more rarely nearly horizontal,

area on the eighth abdominal with the respiratory tube in

segment into which the two contact with the surface film

spiracles open (fig. 128). (fig. 128).

_Adults_: Palpi in both sexes Palpi short in the female, in

nearly or quite as long as the the male usually elongate.

proboscis. Proboscis projecting Proboscis projects forward at an

forward nearly on line with the angle with the axis of the body.

axis of the body. When at rest When at rest on a vertical wall

on a vertical wall the body is the body is usually held parallel

usually held at an angle with the or the tip of the abdomen inclined

vertical (fig. 128). Wings frequently towards the wall (fig. 128).

spotted (fig. 130). Wings usually not spotted.

[Illustration: 128. (_a_) Normal position of the larvae of Culex and

Anopheles in the water. Culex, left; Anopheles, middle; Culex pupa,

right hand figure.]

These malarial-bearing species are essentially domesticated mosquitoes.

They develop in any accumulation of water which stands for a week or

more. Ponds, puddles, rain barrels, horse troughs, cess-pools, cans,

even the foot-prints of animals in marshy ground may afford them

breeding places.

[Illustration: 128. (_b_) Normal position of Culex and Anopheles on the

wall.]

It is clear from what has been said regarding the life cycle of the

malarial parasite that the mosquito is harmless if not itself diseased.

Hence malarial-bearing species may abound in the neighborhood where

there is no malaria, the disease being absent simply because the

mosquitoes are uninfected. Such a locality is potentially malarious and

needs only the introduction of a malarial patient who is exposed to the

mosquitoes. It is found that such patients may harbor the parasites in

their blood long after they are apparently well and thus may serve as a

menace, just as do the so-called typhoid carriers. In some malarious

regions as high as 80-90 per cent of the natives are such

malaria-carriers and must be reckoned with in antimalaria measures.

Based upon our present day knowledge of the life cycle of the malarial

parasite the fight against the disease becomes primarily a problem in

economic entomology,--it is a question of insect control, in its

broadest interpretation.

[Illustration: 129. Larva of Anopheles. After Howard.]

The lines of defence and offence against the disease as outlined by

Boyce (1909) are:

1. Measures to avoid the reservoir (man):

Segregation.

Screening of patients.

2. Measures to avoid Anopheles:

Choice of suitable locality, when possible.

Screening of houses and porches.

Sleeping under mosquito nets.

3. Measures to exterminate the Anopheles:

Use of natural enemies.

Use of culicides, oiling ponds, etc.

Drainage and scavenging to destroy breeding places.

Enforcement of penalties for harboring larvae or keeping stagnant

water.

Educational methods.

4. Systematic treatment with quinine to exterminate the parasites.

MOSQUITOES AND YELLOW FEVER

Yellow fever was until recently one of the most dreaded of epidemic

diseases. It is an acute, specific and infectious disease,

non-contagious in character but occurring in epidemics, or endemics,

within a peculiarly limited geographical area. It is highly fatal, but

those who recover are generally immune from subsequent attacks.

It is generally regarded as an American disease, having been found by

Cortez, in Mexico, and being confined principally to the American

continents and islands. It also occurs in Africa and attempts have been

made to show that it was originally an African disease but there is not

sufficient evidence to establish this view.

There have been many noted outbreaks in the United States. Boston

suffered from it in 1691 and again in 1693; New York in 1668 and as late

as 1856; Baltimore in 1819. In 1793 occurred the great epidemic in

Philadelphia, with a death rate of one in ten of the population. In the

past century it was present almost every year in some locality of our

Southern States, New Orleans being the greatest sufferer. In the latter

city there were 7848 deaths from the disease in 1853, 4854 in 1858, and

4046 in 1878. The last notable outbreak was in 1905. Reed and Carroll

(1901) estimated that during the period from 1793 to 1900 there had not

been less than 500,000 cases in the United States.

[Illustration: 130. Anopheles quadrimaculatus, male and female,

(x3-1/2). After Howard.]

As in the case of the plague, the most stringent methods of control

proved ineffective and helplessness, almost hopelessness marked the

great epidemics. A vivid picture of conditions is that given by Mathew

Cary, 1793 (quoted by Kelly, 1906) in "A Short Account of the Malignant

Fever Lately Prevalent in Philadelphia."

[Illustration: 131. Anopheles punctipennis. Female, (x4). After Howard.]

"The consternation of the people of Philadelphia at this period was

carried beyond all bounds. Dismay and affright were visible in the

countenance of almost every person. Of those who remained, many shut

themselves in their houses and were afraid to walk the streets. * * *

The corpses of the most respectable citizens, even those who did not die

of the epidemic, were carried to the grave on the shafts of a chair

(chaise), the horse driven by a negro, unattended by friends or

relative, and without any sort of ceremony. People hastily shifted their

course at the sight of a hearse coming toward them. Many never walked on

the footpath, but went into the middle of the streets to avoid being

infected by passing by houses wherein people had died. Acquaintances and

friends avoided each other in the streets and only signified their

regard by a cold nod. The old custom of shaking hands fell into such

disuse that many shrunk back with affright at even the offer of the

hand. A person with a crape, or any appearance of mourning was shunned

like a viper. And many valued themselves highly on the skill and address

with which they got to the windward of every person they met. Indeed, it

is not probable that London, at the last stage of the plague, exhibited

stronger marks of terror than were to be seen in Philadelphia from the

24th or 25th of August until pretty late in September."

[Illustration: 132. Anopheles crucians. Female (x4). After Howard.]

Such was the condition in Philadelphia in 1793 and, as far as methods of

control of the disease were concerned, there was practically no advance

during the last century. The dominant theory was that yellow fever was

spread by _fomites_, that is, exposed bedding, clothing, baggage, and

the like. As late as 1898 a bulletin of the United States Marine

Hospital Service stated:

"While yellow fever is a communicable disease, it is not contagious in

the ordinary acceptance of the term, but is spread by the infection of

places and articles of bedding, clothing, and furniture."

Based upon this theory, houses, baggage, freight, even mail, were

disinfected, and the most rigid quarantine regulations were enforced.

The hardships to which people of the stricken regions were subjected and

the financial losses are incalculable. And withal, the only efficient

check upon the disease seemed to be the heavy frosts. It was found that

for some reason, the epidemic abated with cold weather,--a measure

beyond human control.

[Illustration: 133. Culex sollicitans. Female (x4). After Howard.]

It is not strange that among the multitude of theories advanced to

explain the cause and method of dissemination of the disease there

should be suggestions that yellow fever was transmitted by the mosquito.

We have seen that Beauperthuy (1855) clearly urged this theory.

More detailed, and of the greatest influence in the final solution of

the problem were the arguments of Dr. Carlos Finlay, of Havana. In 1881,

in a paper presented before the "Real Academia de Ciencias Medicas,

Fisicas y Naturales de la Habana," he said:

"I feel convinced that any theory which attributes the origin and the

propagation of yellow fever to atmospheric influences, to miasmatic or

meteorological conditions, to filth, or to the neglect of general

hygienic precautions, must be considered as utterly indefensible."

He postulated the existence of a material transportable substance

causing yellow fever,--"something tangible which requires to be conveyed

from the sick to the healthy before the disease can be propagated" and

after discussing the peculiarities of the spread of the disease and the

influence of meteorological conditions, he decides that the carriers of

the disease must be sought among insects. He continues:

"On the other hand, the fact of yellow fever being characterized both

clinically and (according to recent findings) histologically, by lesions

of the blood vessels and by alterations of the physical and chemical

conditions of the blood, suggested that the insect which should convey

the infectious particles from the patient to the healthy should be

looked for among those which drive their sting into blood vessels in

order to suck human blood. Finally, by reason of other considerations

which need not be stated here, I came to think that the mosquito might

be the transmitter of yellow fever."

"Assimilating the disease to small-pox and to vaccination, it occurred

to me that in order to inoculate yellow fever it would be necessary to

pick out the inoculable material from within the blood vessels of a

yellow fever patient and to carry it likewise into the interior of a

blood vessel of a person who was to be inoculated. All of which

conditions the mosquito satisfies most admirably through its bite."

In the course of his study of the problem, Finlay made detailed studies

of the life history and habits of the common mosquitoes at Havana, and

arrived at the conclusion that the carrier of the yellow fever was the

_Culex mosquito_ or _Aedes calopus_, as it is now known. With this

species he undertook direct experimental tests, and believed that he

succeeded in transmitting the disease by the bite of infected mosquitoes

in three cases. Unfortunately, possibility of other exposure was not

absolutely excluded, and the experiments attracted little attention.

Throughout the next twenty years Finlay continued his work on yellow

fever, modifying his original theory somewhat as time went on. Among his

later suggestions was that in the light of Smith's work on Texas fever,

his theory must be "somewhat modified so as to include the important

circumstance that the faculty of transmitting the yellow fever germ need

not be limited to the parent insect, directly contaminated by stinging a

yellow fever patient (or perhaps by contact with or feeding from his

discharges), but may be likewise inherited by the next generation of

mosquitoes issued from the contaminated parent." He believed that the

bite of a single mosquito produced a light attack of the disease and was

thus effective in immunizing the patient. Throughout the period, many

apparently successful attempts to transmit the disease by mosquitoes

were made. In the light of present day knowledge we must regard these as

defective not only because possibility of other infection was not

absolutely excluded but because no account was taken of the incubation

period within the body of the mosquito.

In 1900, while the American army was stationed in Cuba there occurred an

epidemic of yellow fever and an army medical board was appointed for

"the purpose of pursuing scientific investigations with reference to the

acute infectious diseases prevalent on the island." This was headed by

Walter Reed and associated with him were James Carroll, Jesse W. Lazear

and Aristides Agramonte, the latter a Cuban immune. For a detailed

summary of this work the lay reader cannot do better than read Dr.

Kelly's fascinating biography "Walter Reed and Yellow Fever."

Arriving at the army barracks near Havana the Commission first took up

the study of _Bacillus icteroides_, the organism which Sanarelli, an

Italian physician, had declared the causative agent in yellow fever.

They were unable to isolate this bacillus either from the blood during

life or from the blood and organs of cadavers and therefore turned their

attention to Finlay's theory of the propagation of yellow fever by means

of the mosquito. In this work they had the unselfish and enthusiastic

support of Dr. Finlay himself, who not only consulted with them and

placed his publications at their disposal, but furnished eggs from which

their experimental mosquitoes were obtained. Inoculations of eleven

non-immunes through the bite of infected mosquitoes were made, and of

these, two gave positive results. The first of the two was Dr. Carroll

who allowed himself to be bitten by a mosquito which had been caused to

feed upon four cases of yellow fever, two of them severe and two mild.

The first patient had been bitten twelve days before.

Three days after being bitten, Dr. Carroll came down with a typical case

of yellow fever. So severe was the attack that for three days his life

hung in the balance. During his convalescence an incident occurred which

showed how the theory of mosquito transmission of the disease was

generally regarded. We quote from Dr. Kelly: "One of his nurses who came

from Tennessee had had considerable experience with yellow fever, having

indeed, lost her husband and several children from it. One day early in

his illness Dr. Carroll mentioned to her that he had contracted the

disease through the bite of a mosquito, and noticed that she looked

surprised. Some time later, when well enough to look over the daily

records of his condition, he found this entry: 'Says he got his illness

through the bite of a mosquito,--delirious'."

The second case was that of an American who was bitten by four

mosquitoes, two of which had bitten severe (fatal) cases of yellow fever

twelve days previously, one of which had bitten a severe case (second

day) sixteen days before and one which had bitten a severe case eight

days before. Five days later, the subject developed a well pronounced

but mild case of the disease.

In the meantime, another member of the Commission, Dr. Lazear, was

accidentally bitten by a mosquito while collecting blood from yellow

fever patients. Five days later he contracted a typical case which

resulted fatally.

So clear was the evidence from these preliminary experiments that the

commission felt warranted in announcing, October 27, 1900, that, "The

mosquito serves as the intermediate host for the parasite of yellow

fever, and it is highly probable that the disease is only propagated

through the bite of this insect."

In order to extend the experimental evidence under conditions which

could leave no possibility of infection from other sources, a special

experimental sanitary station, named in honor of the deceased member of

the Commission, was established in an open field near the town of

Quemados, Cuba. Here there were constructed two small buildings known

respectively as the "infected clothing building" and the "infected

mosquito building."

The infected clothing building, 14 x 20 feet in size, was purposely so

constructed as to exclude anything like efficient ventilation, but was

thoroughly screened to prevent the entrance of mosquitoes. Into this

building were brought sheets, pillow-slips, blankets, etc., contaminated

by contact with cases of yellow fever and their discharges,--many of

them purposely soiled with a liberal quantity of black vomit, urine, and

fecal matter from patients sick with yellow fever. Nothing could better

serve as the fomites which were supposed to convey the dread disease.

Three non-immunes unpacked these articles, giving each a thorough

handling and shaking in order to disseminate through the air of the room

the specific agent of the disease. They were then used in making up the

beds which the volunteers occupied each night for a period of twenty

days. The experiment was repeated three times, volunteers even sleeping

in the soiled garments of yellow fever victims but in not a single case

was there the slightest symptom of disease. The theory of the spread of

yellow fever by fomites was completely demolished.

The infected mosquito building, equal in size to its companion, was the

antithesis as far as other features were concerned. It was so

constructed as to give the best possible ventilation, and bedding which

was brought into it was thoroughly sterilized. Like the infected

clothing building it was carefully screened, but in this case it was in

order to keep mosquitoes in it as well as to prevent entrance of others.

Through the middle of the room ran a mosquito-proof screen.

On December 5, 1900, a non-immune volunteer who had been in the

quarantine camp for fifteen days and had had no other possible exposure,

allowed himself to be bitten by five mosquitoes which had fed on yellow

fever patients fifteen or more days previously. The results were fully

confirmatory of the earlier experiments of the Commission--at the end of

three days, nine and a half hours, the subject came down with a well

marked case of yellow fever.

In all, ten cases of experimental yellow fever, caused by the bite of

infected mosquitoes were developed in Camp Lazear. Throughout the period

of the disease, other non-immunes slept in the little building,

separated from the patient only by the mosquito-proof screen, but in no

circumstances did they suffer any ill effects.

It was found that a yellow fever patient was capable of infecting

mosquitoes only during the first three or four days after coming down

with the disease. Moreover, after the mosquito has bitten such a

patient, a period of at least twelve days must elapse before the insect

is capable of transmitting the disease.

Once the organism has undergone its twelve day development, the mosquito

may remain infective for weeks. In experiments of the Commission, two of

the mosquitoes transmitted the disease to a volunteer fifty-seven days

after their contamination. No other volunteers presenting themselves,

one of these mosquitoes died the sixty-ninth and one the seventy-first

day after their original contamination, without it being determined

whether they were still capable of transmitting the disease.

So carefully carried out was this work and so conclusive were the

results that Dr. Reed was justified in writing:

"Six months ago, when we landed on this island, absolutely nothing was

known concerning the propagation and spread of yellow fever--it was all

an unfathomable mystery--but today the curtain has been drawn--its mode

of propagation is established and we know that a case minus mosquitoes

is no more dangerous than one of chills and fever."

The conclusions of the Commission were fully substantiated by numerous

workers, notably Dr. Guiteras of the Havana Board of Health, who had

taken a lively interest in the work and whose results were made known in

1901, and by the Brazilian and French Commission at Sao Paulo, Brazil,

in 1903.

Throughout the work of the Army Commission and down to the present time

many fruitless efforts have been made to discover the specific organism

of yellow fever. It was clearly established that the claims of Sanarelli

for _Bacillus icteroides_ were without foundation. It was found, too,

that whatever the infective agent might be it was capable of passing

through a Berkefeld filter and thus belongs to the puzzling group of

"filterable viruses." It was further found that the virus was destroyed

by heating up to 55^o C for ten minutes. It is generally believed that

the organism is a Protozoan.

The question of the hereditary transmission of the yellow fever organism

within the mosquito was left unsettled by the Army Commission, though,

as we have seen, it was raised by Finlay. Marchoux and Simond, of the

French Commission devoted much attention to this phase of the problem

and basing their conclusions on one apparently positive case, they

decided that the disease could be transmitted through the egg of an

infected _Aedes calopus_ to the second generation and thence to man. The

conclusion, which is of very great importance in the control of yellow

fever, has not been verified by other workers.

Once clearly established that yellow fever was transmitted solely by

mosquitoes, the question of the characteristics, habits, and

geographical distribution of the insect carrier became of vital

importance.

_Aedes calopus_, more commonly known as _Stegomyia fasciata_ or

_Stegomyia calopus_ (fig. 134) is a moderate sized, rather strikingly

marked mosquito. The general color is dark-brown or reddish-brown, but

the thorax has a conspicuous broad, silvery-white curved line on each

side, with two parallel median silvery lines. Between the latter there

is a slender, broken line. The whole gives a lyre-shaped pattern to the

thorax. The abdomen is dark with silvery-white basal bands and silvery

white spots on each side of the abdominal segments. Legs black with

rings of pure white at the base of the segments.

Size of the female 3.3 to 5 mm.; male 3 to 4.5 mm.

[Illustration: 134. The yellow fever mosquito (Aedes calopus). (x7).

After Howard.]

It is preeminently a domesticated species, being found almost

exclusively about the habitation of man. "Its long association with man

is shown by many of its habits. It approaches stealthily from behind. It

retreats upon the slightest alarm. The ankles and, when one is sitting

at a table or desk, the underside of the hands and wrists are favorable

points of attack. It attacks silently, whereas other mosquitoes have a

piping or humming note. The warning sound has doubtless been suppressed

in the evolutionary process of its adaptation to man. It is extremely

wary. It hides whenever it can, concealing itself in garments, working

into the pockets, and under the lapels of coats, and crawling up under

the clothes to bite the legs. In houses, it will hide in dark corners,

under picture moldings and behind the heads of old-fashioned bedsteads.

It will enter closets and hide in the folds of garments."--Howard.

It was claimed by the French Commission, and subsequently often stated

in discussions of the relation of the mosquito to yellow fever that the

mature _Aedes calopus_ will bite only at night. If this were true it

would be of the greatest importance in measures to avoid the disease.

Unfortunately, the claim was illy founded and numerous workers have

clearly established that the exact converse is more nearly true, this

mosquito being pre-eminently a day species, feeding most actively in

early morning, about sunrise, and late in the afternoon. On cloudy days

it attacks at any time during the day. Thus there is peril in the

doctrine that infected regions may be visited with perfect safety during

the daytime and that measures to avoid the mosquito attack need be taken

only at night.

[Illustration: 135_a_. Aedes calopus. Pupa. After Howard.]

Dr. Finlay maintained that the adult, even when starved, would not bite

when the temperature was below 23^o C, but subsequent studies have shown

that this statement needs modification. The French Commission, working

at Rio de Janeiro, found that _Aedes calopus_ would bite regularly at

temperatures between 22^o and 25^o and that the optimum temperature was

between 27^o and 30^o C, but their experiments led them to believe that it

would bite in nature at a temperature as low as 17^o C.

The yellow fever mosquito breeds in cisterns, water barrels, pitchers

and in the various water receptacles about the house. In our own

Southern States it very commonly breeds in the above-ground cisterns

which are in general use. Often the larvae (fig. 135b) are found in

flower vases, or even in the little cups of water which are placed under

the legs of tables to prevent their being overrun by ants. They have

been repeatedly found breeding in the holy water font in churches. In

short, they breed in any collection of water in close proximity to the

dwellings or gathering places of man.

The life cycle under favorable conditions is completed in from twelve to

fifteen days. These figures are of course very dependent upon the

temperature. The Army Commission in Cuba found that the cycle might be

completed in as brief a period as nine and a half days. Under less

favorable conditions it may be greatly lengthened.

The adults are long lived. We have seen that during the experimental

work in Cuba specimens were kept in captivity for sixty-nine and

seventy-one days, respectively, and that they were proved to retain

their infectivity for at least fifty-seven days. Dr. Guiteras

subsequently kept an infected adult for one hundred and fifty-four days.

Low temperatures have a very great effect not only on development, but

on the activity and even life of the adults. Long before the method of

transmission of yellow fever was discovered it was well known that the

epidemics were brought to a close by heavy frosts, and it is now known

that this is due to the killing of the mosquitoes which alone could

spread the disease.

[Illustration: 135_b_. Aedes calopus; larva. (x7). After Howard.]

_Aedes calopus_ has a very wide distribution since, as Howard says,

being a domestic mosquito, having a fairly long life in the adult stage,

and having the custom of hiding itself in the most ingenious ways, it is

particularly subject to carriage for long distances on board vessels, in

railway trains, even packed in baggage. In general, its permanent

distribution is from 40 degrees north latitude to 40 degrees south

latitude (Brumpt), in a belt extending around the world. In the United

States it breeds in most of our Southern States.

Thus, as in the case of malaria, there are many places where the insect

carrier is abundant but where yellow fever does not occur. Such, for

instance, are Hawaii, Australia and Asia. An outbreak may occur at any

time that a patient suffering from the disease is allowed to enter and

become a source of infection for the mosquitoes. In this connection

various writers have called attention to the menace from the Panama

Canal. When it is completed, it will allow of direct passage from

regions where yellow fever is endemic and this will greatly increase the

possibility of its introduction into these places where it is now

unknown. The result, with a wholly non-immune population, would be

appalling.

On the other hand, there are places wholly outside of the normal range

of _Aedes calopus_ where the disease has raged. Such are New York,

Boston, and even Philadelphia, which have suffered notable epidemics.

These outbreaks have been due to the introduction of infected mosquitoes

during the heat of summer, when they have not only conveyed the disease

but have found conditions favorable for their multiplication. Or,

uninfected mosquitoes have been thus accidentally brought in and

developed in large numbers, needing then only the accidental

introduction of cases of the disease to start an epidemic.

Methods of control of various diseases have been revolutionized by the

discovery that they were insect-borne, but in no other case has the

change been as radical or the results as spectacular as in the case of

yellow fever. The "shot-gun quarantine," the sufferings and horrors, the

hopelessness of fighting absolutely blindly have given way to an

efficient, clear-cut method of control, based upon the knowledge that

the disease is carried from man to man solely by the mosquito, _Aedes

calopus_. The lines of defense and offense are essentially as follows:

In the first place, when a case of yellow fever occurs, stringent

precautions must be adopted to prevent the infection of mosquitoes and

the escape of any already infected. This means that the patient must be

removed to a mosquito-proof room, or ward beyond reach of the insects,

and that the infected room must be thoroughly fumigated at once, to kill

the mosquitoes hiding within it. All cracks and openings should be

closed with strips of paper and fumigation with burning sulphur or

pyrethrum carefully carried out.

It should be remembered that if the first case noted is that of a

resident rather than imported, it means that the mosquito carriers

became infected more than two weeks before the case was diagnosed, for

as we have seen, the germ must undergo a twelve-day period of

development within its insect host. Therefore a careful search must be

made for mild cases which, though unrecognized, may serve as foci for

the spread of the disease.

In face of a threatened epidemic one of the most essential measures is

to educate the citizens and to gain their complete cooperation in the

fight along modern lines. This may be done through the schools, the

pulpit, places of amusement, newspapers and even bulletin boards.

Emphasis should be placed on the necessity of both non-immunes and

immunes using mosquito curtains, and in all possible ways avoiding

exposure to the mosquitoes.

Then the backbone of the fight must be the anti-mosquito measures. In

general, these involve screening and fumigating against adults, and

control of water supply, oiling, and drainage against the larvae. The

region involved must be districted and a thorough survey undertaken to

locate breeding places, which must, if possible, be eradicated. If they

are necessary for water supplies, such as casks, or cisterns, they

should be carefully screened to prevent access of egg-laying adults.

The practical results of anti-mosquito measures in the fight against

yellow fever are well illustrated by the classic examples of the work in

Havana, immediately following the discoveries of the Army Commission and

by the stamping out of the New Orleans epidemic in 1905.

The opportunities for an immediate practical application of the theories

of the Army Commission in Havana were ideal. The city had always been a

hotbed of yellow fever and was the principal source from which the

disease was introduced year after year into our Southern States. It was

under martial law and with a military governor who was himself a

physician and thoroughly in sympathy with the views of the Commission,

the rigid enforcement of the necessary regulations was possible. The

story of the first campaign has been often told, but nowhere more

clearly than in Dr. Reed's own account, published in the _Journal of

Hygiene_ for 1902.

Closer home was the demonstration of the efficacy of these measures in

controlling the yellow fever outbreak in New Orleans in 1905. During the

spring and early summer of the year the disease had, unperceived, gained

a firm foothold in that city and when, in early July the local Board of

Health took cognizance of its existence, it was estimated that there had

been in the neighborhood of one hundred cases.

Conditions were not as favorable as they had been under martial law in

Havana for carrying on a rigid fight along anti-mosquito lines. The

densely populated city was unprepared, the public had to be educated,

and an efficient organization built up. The local authorities actively

began a general fight against the mosquito but in spite of their best

efforts the disease continued to spread. It was recognized that more

rigid organization was needed and on August 12th the United States

Public Health and Marine Hospital Service was put in absolute charge of

the fight. Up to this time there had been one hundred and forty-two

deaths from a total of nine hundred and thirteen cases and all of the

conditions seemed to threaten an outbreak to exceed the memorable one of

1878 when, as we have seen there were four thousand and forty-six

deaths.

With the hearty cooperation of the citizens,--physicians and laymen

alike,--the fight was waged and long before frost or any near approach

thereto the disease was stamped out,--a thing unheard of in previous

epidemics. The total loss of life was four hundred and sixty--about 11

per cent as great as that from the comparable epidemic of 1878. If the

disease had been promptly recognized and combated with the energy which

marked the fight later in the summer, the outbreak would have made

little headway and the great proportion of these lives would have been

saved.

CHAPTER IX

ARTHROPODS AS ESSENTIAL HOSTS OF PATHOGENIC PROTOZOA (Continued)

INSECTS AND TRYPANOSOMIASES

By trypanosomiasis is meant a condition of animal parasitism, common to

man and the lower animals, in which trypanosomes, peculiar flagellate

protozoa, infest the blood. Depending upon the species, they may be

harmless, producing no appreciable ill-effect, or pathogenic, giving

rise to conditions of disease. A number of these are known to be

transferred by insects.

In order that we may consider more fully the developmental stage of

these parasites within their insect host, it is necessary that we

describe briefly the structure of the blood-inhabiting stage.

[Illustration: 136. Trypanosoma brucei. After Bruce.]

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.

This species is usually regarded as non-pathogenic, but in experimental

work, especially with white rats, heavy infestations often result

fatally, and naturally infested specimens sometimes show evidence of

injury. Rats which have been infested exhibit at least temporary

immunity against new infection.

_Trypanosoma lewisi_ is transmitted from rat to rat by fleas and by

lice. Rabinowitsch and Kempner (1899) first found that healthy rats

which were kept with infested rats, showed trypanosomes in their blood

after about two weeks. They found the trypanosomes in the alimentary

canal of fleas which had fed on the diseased rats. On teasing such fleas

in physiological salt solution and inoculating them into fresh rats they

were able to produce the infection. Finally, they showed that the fleas

which had fed upon infested rats were able to carry the parasites to

healthy rats. Corresponding experiments with lice were not successful.

Prowazek (1905) found in the rat louse (_Haematopinus spinulosus_)

organisms which he regarded as developmental stages of the _Trypanosoma

lewisi_. He believed that the sexual cycle was undergone in this insect.

Nuttall (1908) readily transmitted the trypanosomes through the agency

of fleas, (_Ceratophyllus fasciatus_ and _Ctenopthalmus agyrtes_). He

believes that these insects are probably the chief transmitters of the

parasite. He was also able to transmit it from diseased to healthy rats

through the agency of the rat louse. He was unable to trace any

developmental stages in the louse and inclined to the opinion that

Prowazek was deceived by the presence of extraneous flagellates such as

are known to exist in a number of blood-sucking arthropods.

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 Muscidae 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 role 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.