‘Nel tempo che colui, che il mondo schiara,

La faccia sua a noi tien meno ascosa,

Come la mosca cede alla zanzara.’[7]

The practical disappearance as the temperature drops has enabled the

South African traveller to traverse the fly-belts with impunity during

the cooler hours of the night. At nightfall the tsetse seems to retire

to rest amongst the shrubs and undergrowth, but, if the weather be warm,

it may sit up late; and some experienced travellers refrain from

entering a fly-belt, especially on a summer’s night, until the

temperature has considerably fallen.

The sickness and death of the cattle bitten by the tsetse were formerly

attributed to some specific poison secreted by the fly, and injected

during the process of biting. It is now, largely owing to the researches

of Colonel Bruce, known to be due to the inoculation of the beasts with

a minute parasitic organism conveyed from host to host by the fly. The

disease is known as ‘nagana,’ and the organism that causes it is a

species of _Trypanosoma_, a flagellate Protozoon or unicellular

organism, which moves by means of the lashing of a minute, whip-like

process. Since Bruce’s researches a number of _Trypanosomas_ have been

found causing diseases in various parts of the world. Thus _T. evansii_

causes the ‘surra’ disease of cattle, horses, and camels in India. _T.

equinum_ produces the ‘mal de caderas’ of the horse-ranches of South

America, and _T. equiperdum_ is responsible for the North African

disease called by the French the ‘dourine.’ _T. theileri_ causes the

gall-sickness, and there are others. These parasites were first seen by

Gruby, who named them in 1843, in the blood of a frog; they live, not as

does the malaria parasite, in the blood-cells, but in the fluid of the

blood. The particular species of _Trypanosoma_ which causes nagana is

_Trypanosoma brucei_, and it does not attack man, and some goats and

donkeys seem also immune; but, with these exceptions, all domesticated

animals suffer, and in a great percentage of cases the disease

terminates in death. Just as the native children in Africa form the

source of the supply of the malarial parasite without appearing to

suffer much, so the big game of the country abound in _Trypanosoma_

without appearing to be any the worse. They are, in Lankester’s phrase,

‘tolerant’ of the parasite, and a harmony between them and the parasite

has been established, so that both live together without hurting one

another. Under a more natural condition of things than at present

obtains in South Africa, the big game formed the natural prey of the

tsetse; and, indeed, so dependent is the fly on the antelopes, etc.,

that, in places where the game has been exterminated, the fly has also

disappeared. It is from the big game that the disease has spread. In

their bodies the harmful effect of the parasite has through countless

generations become attenuated, but it leaps into full activity again as

soon as the _Trypanosoma_ wins its way into the body of any introduced

cattle, horse, or domesticated animal. Whether the _Trypanosoma_ does

any harm to the fly, or whether it passes through any stages of its

life-history in the body of the fly, is still a debatable point.

Possibly it does not, and the proboscis of the fly acts then simply as

an inoculating needle.

The Report of Colonel Bruce, which was issued three years ago, shows

that the sleeping-sickness which devastates Central Africa, from the

West Coast to the East, is also conveyed by a species of tsetse fly.

Writing over a hundred years ago of Sierra Leone, Winterbottom mentions

the disease. ‘The Africans,’ he says, ‘are very subject to a species of

lethargy which they are very much afraid of, as it proves fatal in every

instance.’ Early last century it was recorded in Brazil and the West

Indies; and in all probability the deaths which our slave-owning

ancestors used to attribute to a severe form of home-sickness, or even

to a broken heart, were in reality caused by sleeping-sickness. The

severity of the disease, which always terminates fatally, is shown by

the fact that in a single island--Buvuma--the population has recently

been reduced by it from 22,000 to 8,000, whilst whole districts have

been almost depopulated. In one year the deaths in the region of Busoga

reached a total of 20,000; and it is calculated that although the

disease was only noticed in Uganda for the first time in 1901, that by

the middle of 1904 100,000 people have been killed by it. The disease is

caused by the presence of a second species of _Trypanosoma_ in the blood

and in the cerebro-spinal fluid. The existence of this parasite has now

been proved in all the cases recently investigated. Apparently the

_Trypanosoma_ can live in the blood without doing much harm, and only

when it reaches the cerebro-spinal canal does it set up the

sleeping-sickness. It is also found in great numbers in the lymphatic

glands, especially those of the neck, which in patients infected by the

parasite are usually swollen and tender. From the similarity of the

parasite to that causing the cattle disease of South Africa, the idea at

once arose that the _Trypanosoma_ was conveyed from man to man by a

biting insect. Along the lake shores a species of tsetse (_Glossina

palpalis_) abounds; and it was noticed that if the fly, having fed off a

sleeping-sickness patient, bit a monkey, the monkey became infected.

Further, flies which were captured in a sleeping-sickness district were

also capable of conveying the disease to healthy monkeys. The proof that

sleeping-sickness is due to a _Trypanosoma_ known as _T. gambiense_

present in the cerebro-spinal fluid of the patient, and that it is

conveyed from man to man by _Glossina palpalis_, seems now complete.

Fortunately, like its congener, _G. palpalis_ is confined to certain

districts. The knowledge of these, and of the habits of this species of

fly, will suggest preventive measures; and the brilliant research of

Colonel Bruce and his colleagues, Captain Grieg and Dr. Nabarro, may yet

save the much-tried African continent from the most fatal of recent

diseases.

Finally, we come to a last class of disease which is of the utmost

interest to the agriculturist and settler, and yet at present is but

little understood. These diseases are caused by various species of a

Protozoon named _Piroplasma_, and the diseases may collectively be

spoken of as piroplasmosis. When they are present in cattle they are

spoken of in various parts of the world as Texas fever, tick fever,

blackwater, redwater, and many other French, German, Italian, and

Spanish names. Heartwater in sheep is a form of piroplasmosis. Horses

also suffer, and the malignant jaundice or bilious fever, which makes it

impossible to keep dogs in certain parts of this country, is also caused

by a _Piroplasma_. Finally, under the name of Rocky Mountain fever,

spotted or tick fever, the disease attacks man throughout the west half

of the United States.

The organisms which cause the disease live for the most part in the red

blood-corpuscles, but they are sometimes to be found in the plasma or

liquid of the blood. Unfortunately, we know but little about the

life-history of the _Piroplasma_, or of the various stages it passes

through, but we do know how it is transmitted from animal to animal and

from man to man.

We have seen that the carrier or ‘go-between’ in the case of the malaria

is the mosquito, and in the case of the sleeping-sickness is the tsetse

fly. The _Piroplasma_, however, is not conveyed from host to host by any

insect, but by mites or ticks, members of the large group of Acarines,

which include beside the mites the spiders, scorpions, harvestmen, and

many others.

The ticks differ from the insect bearers of disease inasmuch as the tick

that attacks an ox or a dog does not itself convey the disease, but it

lays eggs--for I regret to say here, as with the _Anopheles_, it is the

female only that bites--and from these eggs arises the generation which

is infective, and which is capable of spreading the disease. The tick

which conveys the _Piroplasma_ from dog to dog is called _Hæmophysalis

leachi_. The brilliant researches of Mr. Lounsbury have shown that even

the young are not immediately capable of giving rise to the disease. The

female tick gorges herself with blood, drops to the ground, and begins

laying eggs. From these eggs small six-legged larvæ emerge. These larvæ,

if they get a chance, attach themselves to a dog, gorge themselves, and

after a couple of days fall off. If their mother was infected they

nevertheless do not convey the parasite. After lying for a time upon the

ground the larval tick casts its skin and becomes a nymph, a stage

roughly corresponding with the chrysalis of a butterfly. This nymph, if

it has luck, again attaches itself to the dog and has a meal, but it

also fails to infect the dog. After a varying time it also drops to the

ground, undergoes a metamorphosis, and gives rise to the eight-legged

adult tick. Here at last we reach the infective stage; the adult tick is

alone capable of giving the disease to the animal upon which she feeds,

and then only when she is descended from a tick which has bitten an

infected host. Think what a life-history this parasite has! Living in

the blood-corpuscles of a dog, sucked up by an adult tick, passed

through her body until it reaches an egg, laid with that egg, being

present while the egg segments and slowly develops into the larva,

living quiescent during the larval stage and the nymph stage, surviving

the metamorphosis, and only leaping into activity when the adult stage

is reached. This most remarkable story probably indicates that the

_Piroplasma_ undergoes a series of changes comparable to those of the

malaria organism when it is inside the mosquito; what these stages are

we do not at present know, but Dr. Nuttall and Mr. Smedley at Cambridge,

and many other observers elsewhere, are at work on the problem, and soon

we shall have more light.

With regard to bovine piroplasmosis, Koch, and others have distinguished

redwater fever, which is conveyed by _Rhipicephalus annulatus_, and in

Europe probably by _Ixodes reduvius_ from the Rhodesian fever, which is

conveyed by _Rhipicephalus appendiculatus_, and I regret to say by a

species dedicated to myself, _Rhipicephalus shipleyi_.

The heartwater disease of sheep and goats is similarly conveyed by

_Amblyomma hebræum_, the Bont tick, and many farmers accuse _Ixodes

pilosus_ of causing the well-known paralysis from which sheep suffer in

the early autumn; and there are many others, diseases such as the

chicken disease of Brazil, which is so fatal to poultry yards, and which

is conveyed by the _Argas persicus_.

I will not weary you with more diseases. I think I have said enough to

show that within the last few years a flood of light has been thrown

upon diseases not only of man and his domestic animals, but upon such

insignificant creatures as the mosquito and the tick. I have tried to

show how these diseases interact, and how both hosts are absolutely

essential to the disease. We can now to a great extent control these

troubles; the old idea that there is something unhealthy in the climate

of the Tropics is giving way to the idea that the unhealthiness is due

to definite organisms conveyed into man by definite biting insects. We

have at last, I think, an explanation of why Beelzebub was called the

Lord of Flies.

THE DANGER OF FLIES

_And Moses said, Behold, I go out from thee, and I will entreat the

Lord that the swarms of flies may depart from Pharaoh, from his

servants, and from his people, to-morrow._--EXODUS.

It is one of those facts which not unfrequently occur in science that we

know less about the life-history and habits of the commonest insects

than we know about scarce and remote species. For instance, the

life-history of the common house-fly, one of the most widely distributed

insects in the world, is as yet very incompletely known.

It was Linnæus who first described this insect and named it _Musca

domestica_, and de Geer who, in the middle of the eighteenth century,

first described its transformation. In 1834 Bouché described the larva

of the insect as living in the dung of horses and fowls. In 1873 the

well-known American entomologist, A. S. Packard, reinvestigated the

question, and L. O. Howard has recently written on the subject. In our

own country C. Gordon Hewitt is publishing a monograph on the house-fly,

which will, when completed, fill a long-felt want. Packard noted that in

the August of 1873 the house-fly was particularly abundant, especially

in the neighbourhood of stables. He was able to observe the insects

laying their ova in clumps containing some 120 eggs in the crevices of

stable manure, ‘working their way down mostly out of sight.’ The eggs

hatched in about twenty-four hours, but he noticed that those hatched in

confinement required from five to ten hours longer, and that these

larvæ when hatched were smaller than those hatched out in the open. The

eggs are oval and cylindrical, one twenty-fifth to one-twentieth of an

inch long and about one-hundredth of an inch wide, and of a dull,

chalky-white colour.

The little larva has not been seen emerging from the egg-case, but

probably, as in the case of the meat- or blow-fly, _Musca vomitoria_, the

eggshell splits longitudinally and the maggot pushes its way out. The

length of the newly-hatched larva in its first stage (or instar) is

seven-hundredths of an inch, and it remains in this stage about

twenty-four hours, when it casts its skin and appears as a larger maggot

three-twentieths of an inch long. In this condition it remains from

twenty-four to thirty-six hours. After a second moult the maggot attains

the length of one-quarter of an inch, and in this stage it remains five

or six days. During its life the larva moves actively about amongst its

surroundings, eating up the decaying matter, but avoiding bits of straw

and hay. There is some evidence to believe that, if pressed for food,

larvæ may devour one another. After living altogether some five to seven

days, the larva somewhat suddenly turns into a dark brown pupa or

chrysalis. The transition takes place very rapidly--in the course of a

few minutes--and the pupa remains enclosed in the last larval skin.

After another period of five to seven days in normal circumstances the

insect hatches out, at first running around with soft and baggy wings,

which, however, soon stretch out, harden, and dry. It is worthy of note

that whereas Howard found the complete metamorphosis to take ten days,

and Packard from ten to fourteen days, in the cooler climate of

Manchester Hewitt finds it takes from twenty to thirty days. The last

named gives some interesting particulars as to the effect of the weather

upon the rate of development. It is believed that many flies pass the

winter in the pupa state; the adult fly also survives the cold weather

hidden away in cracks and crevices, from which it may from time to time

emerge when the sun shines warmly.

When the larvæ are reared in too dry manure, they attain only one-half

their usual size. Too direct warmth and the absence of moisture and

available semi-liquid food also tend to dwarf them.

A word may be said about the distribution of the insect. It is

practically cosmopolitan. As Mr. Austen records:

‘The British Museum collection, though very far from complete,

includes specimens from the following localities: Cyprus;

North-West Provinces, India; Wellesley Province, Straits

Settlements; Hong Kong; Japan; Old Calabar; Southern Nigeria; Suez;

Somaliland; British East Africa; Nyassaland; Lake Tanganyika;

Transvaal; Natal; Sokotra; Madagascar; St. Helena; Madeira; Nova

Scotia; Colorado; Mexico; St. Lucia; the West Indies; Pará, Brazil;

Monte Video, Uruguay; Argentine Republic; Valparaiso, Chili;

Queensland; New Zealand.’

It is carried all over the world in ships and trains, and seems to be

equally at home in the high latitudes of Finmark or in the humid heat of

Equatorial Brazil.

The diseases which flies convey from man to man--which rendered them by

no means the least formidable of the plagues of Egypt, and fully

justified Beelzebub’s title of the ‘Lord of Flies’--are for the most

part conveyed mechanically. The proboscis acts as an inoculatory needle.

No part of the life-history of the disease-causing organism must

necessarily be carried on in the body of the fly; it is conveyed

mechanically and without change from an infected to a healthy subject.

The mouth parts can pick up the anthrax bacillus, and if the fly then

alight upon a wounded surface it will set up woolsorter’s disease. It,

together with the flea, is accused of transmitting the plague bacillus,

not only from man to man, but from rat to man. Flies are active agents

in disseminating cholera; and anyone who has watched them clustering

around the inflamed eyes of the children in Egypt, or in Florida, will

not readily acquit them of being the active agents in the spread of

inflammatory ophthalmia or of ‘sore eye.’

It is worthy of note that after exhaustive experiments on the tsetse fly

(_Glossina palpalis_), which conveys that most fatal of diseases,

sleeping-sickness, Professor Minchin and his colleagues, Mr. Gray and

Mr. Tulloch, have come to the conclusion that the Protozoon

(_Trypanosoma gambiense_) which causes the disease does not--as might be

expected--pass through certain stages of its life-history in the fly,

but is mechanically conveyed upon the biting mouth parts of the insect.

The deadly parasite is, indeed, so easily cleaned off these appendages

that a single bite is sufficient to wipe them off. A tsetse fly which

has bitten an infected person will set up the disease in the next person

(or monkey) it bites; but the insertion of the proboscis, quick and

instantaneous as it is, serves to clean it--to wipe off adhering

trypanosomes, and if it now bite a second person (or monkey), it fails

to convey the disease. This is a most important discovery, and contrary

to what we should have expected; but our knowledge of the history of the

genus _Trypanosoma_ is still too small to justify generalization,

difficult as it is to avoid it. The diseases which in our country are

disseminated by flies are all bacterial and all mechanically conveyed.

In passing, it is worth recording that, contrary to the usual statement

that tsetse flies are confined to the continent of Africa, Captain R. M.

Carter[8] has recently brought some back from the Tabau River and from

other localities in South Arabia. Mr. Newstead has recognized the

specimens as belonging to the species _Glossina tachinoides_. It

evidently does not live on big game here, since, except the gazelle,

game is absent. The Bedouins say that it bites donkeys, horses, dogs,

and man, but not camels or sheep. It is at times so troublesome as to

force the natives to shift their camps.

The common house-fly has been known for some time to be an active agent

in the dissemination of bacterial diseases. In intestinal

disorders--such as cholera and enteric fevers, which are caused by

micro-organisms, the flies convey the bacteria from the dejecta of the

sick to the food of the healthy. In the recent war in South Africa they

are described in the standing camps as dividing their activities

‘between the latrines and the men’s mess-tins and jam rations.’[9] In

the Spanish-American War in Cuba, and in the South African War, and in

several recent outbreaks of enteric fever in the British army in India,

flies have been proved to be the carriers of the _Bacillus typhosus_.

Dr. Veeder[10] writes:

‘In a very few minutes they may load themselves with dejections

from a typhoid or dysenteric patient, not yet sick enough to be in

hospital or under observation, and carry the poison so taken up

into the very midst of the food and water ready for use at the next

meal. There is no long roundabout process involved. It is very

plain and direct; yet when thousands of lives are at stake in this

way the danger passes unnoticed.’

Similar records come from the Boer camp at Diyatalawa in Ceylon. The

bacilli are conveyed direct, just as they might be by an inoculating

needle. They do not pass into the body of the fly, neither do they

undergo any part of their life-history in its tissue.

Dr. Sandilands[11] has recently investigated outbreaks of epidemic

diarrhœa. He points out that the prevalence of diarrhœa follows

the earth’s temperature, and does not follow the temperature of the

atmosphere. It is a well-known fact that this illness is more prevalent

in the houses of the poor than in the mansions of the rich. As Dr.

Newsholme, late Medical Officer of Health for Brighton, said:

‘The sugar used in sweetening milk is often black with flies which

have come from neighbouring dust-bins or manure heaps; often from

the liquid stools of diarrhœa patients in the neighbouring

houses. Flies have to be picked out of the half-emptied can of

condensed milk before it can be used for the next meal. When we

remember the personal uncleanliness of some mothers, and that they

often prepare their infants’ food with unwashed hands, the

inoculation of this food with virulent colon bacilli of human

origin ceases to be a matter of surprise.’

Compared with cow’s milk, which nourishes a very numerous progeny of

bacteria, the bacterial content of Nestlé’s milk is very low, according

to Dr. Sandilands. In certain seasons the cow’s milk is exposed to

temperatures which favour an enormous multiplication of bacteria, and

yet it is not then a frequent source of diarrhœa--in fact, mere

numbers have little or no influence on the incidence of the illness. The

greater number of cases are due to infection conveyed from some patient

in the near neighbourhood and conveyed mechanically by flies.

The great attraction of the sweetened condensed milk for flies to some

extent explains the greater prevalence of infantile diarrhœa among

children fed on this preparation.

As was stated above, one of the most remarkable features in the

prevalence of infantile diarrhœa is that it follows the rise and fall

of the earth’s temperature, and not that of the air. In the same way the

number of house-flies does not reach its maximum with the first burst of

hot weather. The prevalence of these insects follows rather than

coincides with periods of great heat. The flies, in fact, lag behind the

air temperature and persist for a time after the hot weather has ceased.

In other words, the meteorological conditions associated with an

increase or a diminution of the prevalence of diarrhœa exercise a

similar influence on the prevalence of flies.

Pearls & Parasites · 第 13 / 18 段