CHAPTER XLIV.

ACUTE INFECTIVE DISEASES.

Acute Infectious Diseases are characterised by certain definite

characters.

1.—_They are usually infectious or contagious._ It is preferable to use

these two terms as interchangeable. The modes in which infection is

received vary greatly with different fevers.

(1) Some can only be propagated by _inoculation_—the introduction

through an abraded surface of a minute quantity of the poison; as in

glanders and hydrophobia. Others, again, _may_ be introduced in this

way, but are usually acquired in another manner, as scarlet fever,

small-pox.

(2) Some are carried through the _atmosphere_. The contagium of

small-pox can be carried as far as any, while that of typhus fever only

traverses a few feet. The atmosphere acts as a conveyer of infection,

and the infectious matter must necessarily, in most instances, be in

the condition of dust to enable it to be wafted by currents of air or

disturbed by the movements of persons in an infected room.

(3) _Clothes_, books, and furniture are not uncommonly carriers of

infection. An old letter, or a lock of hair, has even after many years’

concealment in an enclosed space produced infection on being brought to

light. Woollen articles convey infection more easily than calico, and

dark clothes better than light coloured. A fever nurse’s clothes should

never be woollen, but some washable material.

(4) _Drinking water and food_ often form a vehicle for infection. Milk

and water are the two usual sources of infection; but uncooked food,

especially oysters and mussels, fed in sewage-polluted estuaries,

may produce the same effect. Cholera, enteric fever, dysentery, and

summer diarrhœa are the chief diseases from this source; but scarlet

fever and diphtheria occasionally have a similar origin. Milk may be

infected from having been handed by an infectious patient; or it may

possibly convey infection of the disease from which the cow at the time

is suffering, _e.g._, tuberculosis (see also page 312). Water may be

contaminated with sewage or the excreta of a single infectious patient.

2. _They retain their specific character and origin._ Small-pox never

produces scarlet fever, nor _vice versâ_; and it is found universally

that all the specific fevers “breed true,” each one retaining its

identity. More than this, a previous case of the same fever can nearly

always be detected on careful examination. Overcrowding and other

insanitary conditions diminish the resistance to infection, and may

increase its virulence.

3. _The behaviour of contagia_, when received into the system, is

characteristic of these diseases. There is first of all a period of

latency or _incubation_, during which no symptoms are manifested (see

page 287.) The incubation period is followed by the characteristic

symptoms of the particular fever, which disappear in a variable period,

leaving the patient, as a rule, more or less _insusceptible to a second

attack_ (see page 288).

Throughout the progress of the disease, except in the period of

incubation, the patient is able to communicate his disease to persons

about him who have not been rendered safe by a previous attack. The way

in which he thus communicates his disease varies in different cases. In

scarlet fever, the throat and skin are the chief sources of contagion;

in influenza, whooping-cough, and measles, the secretions from the

respiratory passages; in hydrophobia, the saliva; in enteric fever and

cholera, the vomit and stools.

=Prevention of the Spread of the Chief Acute Infectious Diseases.=—We

may divide these into three classes. (1) Those which are infectious by

contact with the patient or by the atmosphere around him. (2) Those in

which the intestinal and renal evacuations are almost alone infectious;

as enteric fever and cholera. (3) Those in which inoculation through

an abraded surface is generally if not always necessary to produce

infection.

SMALL-POX OR VARIOLA.

The contagium of small-pox is very tenacious of life. All parts of the

body, and all secretions and excretions contain it. As in typhus it

adheres to every article in the room, but unlike typhus is possessed

of great vitality, and if not exposed to the air may be active after

many years. There is considerable evidence indicating that the

contagion of small-pox may occasionally be _conveyed aerially_ for a

considerable distance, for even a quarter or half a mile from hospitals

in which small-pox patients are isolated. Whether this is the aerial

convection of infection, or in part at least due to carelessness of

persons connected with the hospital in their movements to and fro,

may remain an open question; but such hospitals in the midst of towns

are in practice a mistake; and in London small-pox has been found to

be more manageable since its small-pox patients were all conveyed to

extra-urban hospitals. The means for the prevention of small-pox are

(1) Isolation of infectious patients. (2) Disinfection of all infected

articles. For particulars under these two heads, see pages 319 and 324.

They must be carried out most rigidly in this disease. (3) Vaccination

and re-vaccination.

=Inoculation of small-pox= virus was largely practised as a means of

ensuring a comparatively mild attack, until it was made illegal in

1840. Sometimes, however, the attack thus produced was fatal, and every

case of inoculated small-pox became a new focus of infection, and a

source of high mortality, especially among young children.

=Vaccination.= About the year 1795 Dr. Edward Jenner was informed by

a milk-maid that she could not take small-pox, as she had already

contracted the natural cow-pox during milking. Many had previously

heard this same statement made; but Jenner was the first to put the

matter to the test. He took the lymph or virus from a woman who had

accidentally acquired cow-pox (vaccinia) from a cow, and inoculated

a boy with it. Some months later he inoculated the same boy with

small-pox, and a second time five years afterwards, without producing

small-pox on either occasion. Many other experiments were made, all

confirming these results; and in 1798 Jenner published his results.

The practice of vaccination gradually became more general, and was

followed by a progressive decrease in the mortality from small-pox.

Cow-pox or vaccinia is small-pox modified and mitigated by its

passage through the system of the cow, and not a spontaneous disease

of the cow. By its passage through the cow it has become attenuated

and altered. Instead of a general eruption all over the body, there

are vesicles only at the point of inoculation; and vaccinia, unlike

small-pox, is not communicable from person to person except by

inoculation. Furthermore it is in the vast majority of instances an

extremely mild ailment, not involving more than a few days discomfort.

Objection is taken to vaccination for small-pox on the ground that

serious diseases such as syphilis, erysipelas, and tuberculosis may be

inoculated at the same time. With lymph obtained from healthy children

this is impossible. Most of the cases of infection described have been

in reality hereditary disease, the local irritation of vaccination

serving to call into activity the morbid tendencies of the child. The

risk of such infection is infinitesimal; it may be reduced to zero by

moderate care and attention to detail. With modern antiseptic methods,

it is very rare for a vaccination sore to “go wrong.” Erysipelas may be

inoculated from dirt getting into a vaccination sore, as it may be into

any other sore; but with cleanliness this need not occur; and in fact

very seldom does occur. The risks are so small as to be negligible;

and if the protection afforded is one tithe of what is claimed for

it, no parent is justified in withholding this protection from his

infant. The _law as to vaccination_ requires that every infant shall be

vaccinated within six months of its birth, domiciliary visits for this

purpose being made by the public vaccinator. The obligation can only

be avoided by a statement on oath before a magistrate by the parent of

conscientious objection to vaccination.

=Does Vaccination protect against Small-Pox?= The registration of

deaths for the whole country only began in 1837, and before this

period death-rates from small-pox in terms of the population cannot

be accurately stated. Since that time there has been less or more

vaccination, so that it is difficult to obtain a true comparison

between periods with and without vaccination. Some indication of

the facts in London prior to 1801, when the first English census was

taken, may be obtained from the fact that in 1796 (two years before

the date of Jenner’s “Inquiry,”) small-pox reached its highest point,

causing 18½ deaths out of every 100 total deaths from all causes.

In the præ-vaccination period small-pox was 9 times as fatal as

measles, and 7½ times as fatal as whooping-cough (McVail), while

since vaccination has been practised it has sunk to an insignificant

position, when compared with these diseases. Dr. Guy found that in

London there were in 48 years of the seventeenth century ten epidemics,

in the whole of the eighteenth century 19 epidemics, and in the

nineteenth century no epidemic during which the deaths from small-pox

caused one-tenth or more than one-tenth of the total deaths from all

causes in any year. The worst year under obligatory vaccination in

London was 1871, in which barely 4½ per cent. of the total deaths

was due to small-pox, a proportion which was exceeded in the eighteenth

century ninety-three times.

In Sweden, the highest death-rate _before vaccination_ (1774-1800)

was 7·23 per 1,000 inhabitants, the lowest 0·31; under _permissive

vaccination_ (1801-1815) the highest 2·57 per 1,000 inhabitants, the

lowest 0·12; under _compulsory vaccination_ (1816-85) the highest 0·94

per 1,000 inhabitants, the lowest 0·0005. It has been stated that these

results, which might be extended by quotations from the statistics

of other countries, have been obtained not by vaccination, but by

improved sanitation, including in this term not only improved housing

and better water and food supply but also increased means of isolating

the infectious sick. Improved housing may by diminishing overcrowding

aid in diminishing the spread of this disease. Whether in view of the

immense increase in the proportion of the population which lives in

towns, it can be said that this has occurred is doubtful. Hospital

isolation undoubtedly prevents the spread of infection when promptly

effected. But a large share of the improvement in small-pox mortality

occurred before either hospital or home-isolation of small-pox patients

was generally enforced. There is no reason for supposing that impure

water or food, or nuisances about houses have any connection with the

origin or spread of small-pox, any more than they have with the origin

or spread of measles or whooping-cough; which still remain as prevalent

as in the past. Further light can be thrown on the subject by an

examination of the age-incidence of small-pox, and of its attack-rate

and severity in vaccinated and unvaccinated respectively.

The =age incidence of deaths from small-pox= has, since 1847, when

returns classified according to age became available, undergone a

remarkable alteration. Prior to 1870 the small-pox deaths in infants

nearly always formed 20 per cent. or more of the total mortality from

this disease, between 1870 and 1890 they did not greatly exceed 10 per

cent. of the total, while since 1890 they have again begun to form an

increasing proportion of the total small-pox mortality. At ages 1-5 the

change is even more remarkable. Before 1870 deaths at these ages nearly

always exceeded 30 per cent. of the total; since 1870 they have varied

between 5 and 14 per cent. of the total; and since 1890 they have,

like the proportion of deaths under one, again increased. At the higher

ages the proportion of deaths has correspondingly increased, so that

the curves of age incidence have become curiously inverted.

The lowered birth-rate can only account for a small portion of this

transference of the chief mortality due to small-pox from childhood to

adult life.

Furthermore it must not be supposed that the only change which has

occurred is that the deaths which formerly occurred in childhood now

occur in adult life. The death-rate at all ages has greatly declined.

The only explanation which in my judgment satisfactorily explains

this remarkable change in age-incidence of small-pox mortality is

the fact that vaccination protects children from small-pox and that

the protection diminishes, though it never entirely disappears, with

advancing years. This conclusion is confirmed by the evidence obtained

as to the proportion of vaccinated and unvaccinated attacked, and as to

the severity of the attacks occurring when a community is invaded by

small-pox.

=Attack-rate among Vaccinated.=—If the protective effect of

vaccination, like that of a preceding attack of small-pox, wears off,

it will not be expected that no attacks of small-pox will occur among

the vaccinated. For evidence of immunity from attacks we must examine

the records as to =revaccinated= persons exposed to infection. During

the six years 1890-95, out of a staff in the London small-pox hospitals

varying from 64 to 320, the percentage attacked by small-pox was _nil_,

except in 1892 when it was 1·4, and in 1893 when it was 1·9.

Taking the experience of towns in which during recent years epidemics

of small-pox have occurred, the following attack-rates have occurred.

By attack-rate is meant the percentage number of attacks occurring

among persons living in infected houses. By fatality is meant the

number dying out of 100 attacked.

┌────────────┬───────────────────────────┬──────────────────────────┐

│ │ ATTACK RATE UNDER │ ATTACK RATE OVER │

│ │ 10 YEARS OF AGE. │ 10 YEARS OF AGE. │

│ ├───────────┬───────────────┼───────────┬──────────────┤

│ │VACCINATED.│ UNVACCINATED. │VACCINATED.│ UNVACCINATED.│

├────────────┼───────────┼───────────────┼───────────┼──────────────┤

│_Dewsbury_ │ 10·2 │ 50·8 │ 27·7 │ 53·4 │

│_Leicester_ │ 2·5 │ 35·3 │ 22·2 │ 47·6 │

│_Gloucester_│ 8·8 │ 46·3 │ 32·2 │ 50·0 │

└────────────┴───────────┴───────────────┴───────────┴──────────────┘

=Severity (Fatality) among Vaccinated.=—The experience of the same

three towns comes out as follows:—

┌────────────┬───────────────────────────┬──────────────────────────┐

│ │ ATTACK RATE UNDER │ ATTACK RATE OVER │

│ │ 10 YEARS OF AGE. │ 10 YEARS OF AGE. │

│ ├───────────┬───────────────┼───────────┬──────────────┤

│ │VACCINATED.│ UNVACCINATED. │VACCINATED.│ UNVACCINATED.│

├────────────┼───────────┼───────────────┼───────────┼──────────────┤

│_Dewsbury_ │ 2·2 │ 32·1 │ 2.6 │ 18·7 │

│_Leicester_ │ 0.0 │ 14·0 │ 1.0 │ 7·8 │

│_Gloucester_│ 3·8 │ 41·0 │ 10·0 │ 39·7 │

└────────────┴───────────┴───────────────┴───────────┴──────────────┘

In view of such results as the above it is not surprising that the

Royal Commission, in their majority report, summed up the advantages of

vaccination as follows:

“(1) That it diminishes the liability to be attacked by the disease.

“(2) That it modifies the character of the disease, and renders it

(_a_) less fatal, and (_b_) of a milder or less severe type.

“(3) That the protection it affords against attacks of the disease

is greatest during the years immediately succeeding the operation of

vaccination. It is impossible to fix with precision the length of this

period of highest protection. Though not in all cases the same, if a

period is to be fixed, it might, we think, fairly be said to cover in

general a period of nine or ten years.

“(4) That after the lapse of the period of highest protective

potency, the efficacy of vaccination to protect against attack

rapidly diminishes, but that it is still considerable in the next

quinquennium, and possibly never altogether ceases.

“(5) That its power to modify the character of the disease is also

greatest in the period in which its power to protect from attack is

greatest, but that its power thus to modify the disease does not

diminish as rapidly as its protective influence against attacks, and

its efficacy during the later periods of life to modify the disease is

still very considerable.

“(6) That re-vaccination restores the protection which lapse of time

has diminished, but the evidence shows that this protection again

diminishes, and that, to ensure the highest degree of protection which

vaccination can give, the operation should be at intervals repeated.

“(7) That the beneficial effects of vaccination are most experienced

by those in whose case it has been most thorough. We think it may

fairly be concluded that where the vaccine matter is inserted in three

or four places, it is more effectual than when introduced into one or

two places only—and that if the vaccination marks are of an area of

half a square inch, they indicate a better state of protection than if

their area be at all considerably below this.”

SCARLET FEVER.

Scarlet Fever and Scarlatina are the same disease. It is extremely

infectious, the contagium retaining its virulence for protracted

periods. It occurs in epidemics at irregular intervals. During recent

years the type of scarlet fever has become greatly attenuated, and

this constitutes one of the difficulties of prevention, as the mild

form of the disease is apt to be overlooked. The _fatality_ per 100

persons attacked varies greatly with age. It is highest in children

under four, rapidly declining with increasing age. Hence the importance

of protecting children from attack in early life. Two results follow

from the wise precautions taken to prevent attack early in life. (_a_)

With each successive year of life the liability to attack, when exposed

to infection, diminishes; (_b_) the danger of the attack if it occurs

and its liability to be fatal becomes rapidly less with greater age.

The most common _mode of infection_ is by contact with a previous

patient. Outbreaks due to milk infected by a scarlatinal patient

also occur. Infected cream has also been known to convey infection.

In a milk outbreak the patients would be found chiefly among the

customers of a special dairyman, the cases occur almost simultaneously,

except secondary cases which may be infected from the first. The

_simultaneous_ occurrence of two or more attacks in one house,

especially if the same thing happens in a number of houses should throw

suspicion on the milk supply. It has been suggested that scarlet fever

may originate apart from human infection, from a special disease of the

cow, but the evidence on this point is inconclusive.

The _duration of infection_ is usually reckoned until the desquamation

of the skin is complete, _i.e._ about six or seven weeks from the

onset of the attack. Occasionally it is more protracted even though

desquamation is complete, infection appearing to persist in discharges

from the nose and ear and in sore places inside the nostril and

possibly in other parts. The period of greatest infectivity is in the

earlier part of the disease, when the throat is inflamed. The common

notion that the disease is most infectious during the later period,

that of desquamation, is erroneous. The micro-organism causing scarlet

fever has not certainly been identified. The measures of prevention are

those common to infectious diseases (page 317).

MEASLES.

Measles is an extremely infectious disease, before as well as after the

rash appears on the fourth day of the disease. The infectivity of the

catarrhal stage constitutes one of the main difficulties in preventing

its spread, as measles may be unrecognisable at this stage. The common

notion that measles and whooping-cough are comparatively harmless

infantile complaints will be dissipated by a study of the comparative

death-rate for the five years 1891-5 per million persons living in

England and Wales:—

ENGLAND AND WALES.—DEATH RATES PER MILLION OF POPULATION.

_Small-pox_ 20

_Measles_ 408

_Scarlet fever_ 183

_Typhus fever_ 4

_Enteric fever_ 174

_Whooping-cough_ 398

_Diphtheria_ 253

_Diarrhœa_ 630

It is a mistake also to suppose that measles and whooping-cough are

only serious when neglected. Such neglect greatly increases the

likelihood of death from bronchitis or pneumonia; but the diseases

themselves, especially measles, are frequently fatal during the acute

early stage. More children are attacked with measles under the age

of five than at any other age, and the greatest number between two

and four years of age. The greatest fatality is in the second year

of life, when it may be 24 per cent. of those attacked, as compared

with between two and three per cent. in the fourth year of life, and

a trifling amount at higher ages. These facts explain the folly of

allowing children to have an infectious complaint when another child in

the house is attacked, “to have it over at one trouble.” Such action

is pregnant with evil results. (1st) Severe cases occur, in which a

fatal result ensues; and even where death does not occur, the child

may be left weakly and very prone to become tuberculous. (2nd) Every

additional case forms a new centre of infection. It is like the old

practice of inoculation for small-pox; the individual is protected, but

becomes a source of danger to all around him. If there is only one

case of measles in a family the risk to neighbouring households is much

smaller than where several children are infected. (3rd) Every year that

a child’s attack can be delayed, increases his chance of recovery if he

is subsequently attacked, and diminishes the likelihood of his being

attacked.

The _duration of infection_ should be reckoned as at least three weeks.

The contagium of measles does not appear to hang about rooms with the

persistence of that of scarlet fever, and less stringent disinfection

is required.

WHOOPING COUGH.

Very few people have reached adult life without having suffered

from this disease, as well as measles. This is chiefly due to

the carelessness in mixing infected with healthy children. One

frequently hears the peculiar and characteristic cough of a child

with whooping-cough, in public assemblies, in railway trains, or in

the out-patient rooms of hospitals. The contagium of whooping-cough

is conveyed chiefly by the expectoration, which becoming dry, may be

scattered like that of phthisis, as dust. Clothing conveys infection

easily; visits to infected children should, therefore, be prohibited to

all who have to mix with susceptible children.

The _duration of infection_ should be reckoned as at least six weeks

from the first recognisable symptoms. It may be longer than this.

DIPHTHERIA.

This disease has become increasingly prevalent in the last ten years

after a period of only slight prevalence for about twenty-five years.

I have shown that epidemics of diphtheria occur during a succession of

years of protracted drought. Diphtheria is more common in girls than

boys, possibly owing to their more affectionate habits; and occurs

chiefly under ten years of age, the fifth year of life being that of

greatest prevalence. Unlike the acute infections hitherto considered,

the bacillus causing diphtheria has been identified and cultivated

in the laboratory (called the Klebs-Loeffler bacillus or diphtheria

bacillus). Direct infection from patient to patient is probably more

common than indirect infection by clothes, etc., though the latter

occurs. The infection may hang persistently about a house and its

belongings, in the absence of complete purification. When diphtheria

is prevalent slighter sore throats occur, sometimes before true

diphtheria is detected. This led to the theory that under conditions

of overcrowding, especially in schools, there occurred in the

micro-organisms causing these sore-throats “the progressive development

of the property of infectiveness.” Possibly these were slight

non-typical attacks of diphtheria. Such attacks occur also during

epidemics of diphtheria, and unless specimens (“throat swabs”) from

these sore-throats are examined bacteriologically, are likely to spread

diphtheria by attendance at school, etc. Aggregation in schools seems

to intensify the contagium of diphtheria. The practices of kissing, of

transferring sweetmeats from mouth to mouth, of cleaning slates with

saliva, are common means of spreading it. Effluvia from foul drains

and sewers have been commonly held to cause diphtheria. If they aid

in producing it, it is rather by lowering the vitality and causing

ordinary sore throat. Sore throats and catarrhs make the subjects of

them much more prone to diphtheria (see also page 117). Damp houses

have been stated to favour the development of diphtheria. Probably

they do so in the same way as effluvia from drains. It is likely that

the diphtheria bacillus has a saprophytic stage of existence in the

soil, as indicated by its excessive prevalence in dry warm years.

Besides direct infection from patient to patient and indirect infection

by _fomites_ (_i.e._ in clothing, etc.), milk occasionally causes

epidemics of diphtheria. The infection has been usually caused by the

handling of the milk by an infectious person. In certain outbreaks no

human contamination of the milk could be discovered; and it has been

surmised that an analogous disease in the cow may cause diphtheria in

man. This is still a moot point. Fowls, cats, and other animals are the

occasional victims of diphtheria, and may convey it to man.

The _duration of infection_ in diphtheria is usually less than six

weeks; but it may be much more protracted. In some instances long after

all naked-eye evidences of diphtheria has disappeared, bacteriological

examination may still show the presence of the diphtheria bacillus for

two or three months; in rare cases even longer. The protection afforded

by one attack of diphtheria against a second is slight and only

temporary. The _means of prevention_ are isolation and disinfection as

for other infectious diseases. Two additional means are available (_a_)

_bacteriological diagnosis_; (_b_) prophylactic injection of antitoxic

serum. Many sore throats without membrane on the throat are due to the

diphtheria bacillus. Even if membrane be present there may be doubt

as to whether the case is true diphtheria. Hence the importance of

bacteriological examination.

The patient’s throat is swabbed with cotton-wool which has been

rolled around a metal probe and sterilised. The wool is then smeared

over sterilised and solified blood serum in a test tube. It is then

incubated over night at a temperature of 37° C. Next morning the

minute growth that has occurred on the surface of the blood serum

is spread on a microscopic cover-glass, appropriately stained, and

examined microscopically. If diphtheria bacilli are present, they can

be recognised by their form and arrangement. The same means enable us

to ascertain when a patient has recovered, whether he is fit to be

released from isolation.

_Antitoxic serum_ has been found to be a valuable prophylactic and

curative agent.

The serum is obtained as follows: Sterilised broth is inoculated with

virulent diphtheria bacilli, and grown at 37° C. for a week or more.

The broth is then filtered through a Pasteur filter. The filtrate

contains _toxine_ free from bacilli. Some of this toxine is injected

under the skin of a horse. A few days later the dose is repeated,

gradually increasing amounts being injected until injection of further

quantities of the toxine is found experimentally not to increase

the antitoxic value of the horse’s blood serum. Next the horse is

bled. Its serum is found to have acquired the power of protecting a

guinea-pig against doses of the toxine of diphtheria which would

otherwise be fatal. Ten times the quantity of the horse’s serum which

will protect a guinea-pig (of 250 grammes weight) against ten times

the minimum fatal dose of the toxine is called an antitoxic unit.

The treatment of diphtheria in man by the antitoxic serum thus obtained

has proved to be remarkably successful. Furthermore, if a susceptible

person who has been exposed to the infection of diphtheria, is injected

with a small dose of antitoxic serum, he becomes temporarily immune,

and does not fall a victim to diphtheria. This is a most important

point especially for young children, who may already be incubating a

disease which but for this prophylactic injection might occur and prove

fatal.

TYPHUS FEVER.

This disease was formerly known as spotted or jail-fever, and for many

ages has been the scourge of prisons and armies, and all collections

of people living in overcrowded and insanitary districts. The history

of typhus is the history of human misery. It is essentially associated

with filth, overcrowding, and destitution; but when once established

by these conditions, it can be carried by infection to others who

live amidst healthy surroundings. It generally occurs in winter, when

overcrowding is greatest. With free ventilation, the disease cannot be

carried more than a few feet. It can be transmitted by clothing. The

micro-organism causing it has not been discovered. With the clearance

of the rookeries of our great towns, it is rapidly decreasing, and

appears likely to become extinct. The _means of prevention_, in

addition to the abatement of nuisances, including overcrowding, are

isolation and disinfection (pages 319 and 325).

RELAPSING FEVER.

This disease was formerly common in this country, but except in

some parts of Ireland has entirely died out. It is caused by a

micro-organism (_Spirillum Obermeieri_) which can be detected in the

blood. Inoculation of this will produce the disease in man or in

monkeys.

Epidemics of relapsing fever commonly follow in the track of typhus

fever; overcrowding and filth being especially associated with typhus,

and starvation with relapsing fever, hence its name of “famine fever.”

ENTERIC OR TYPHOID FEVER.

Enteric fever causes its highest death-rate in early adult life,

though it is not peculiar to any age. Eberth in 1880 discovered the

_Bacillus typhosus_ in the spleen and other organs of enteric fever

patients. This is commonly known as Eberth’s bacillus, and is the cause

of enteric fever. A few years later it was isolated and can now be

grown on agar or gelatine in laboratories. It closely resembles other

bacilli which are normal inhabitants of the human intestine; but can

be distinguished by certain tests. It is a small rod, rounded at its

ends, and from 2 to 4 µ long and three times as long as broad. In the

living state it is freely motile, and possesses a number of minute

cilia or flagella. Apart from other means of distinction between it

and other bacilli, _Grüber’s serum reaction_ enables its identity to

be ascertained. The bacillus suspected to be the _Bac.-typhosus_ is

cultivated in broth in the bacteriological laboratory. A small quantity

of blood is taken from the finger of a patient known to be suffering

from enteric fever. The serum is separated from the blood corpuscles

of this blood by a centrifugalising machine. A drop of the blood serum

is diluted with 100 drops of broth culture of the suspected bacillus.

If the latter is not the _Bac.-typhosus_, the individual bacilli when

a drop of the mixture is examined under the microscope, will continue

to move about freely; if it is the _Bac.-typhosus_, the bacilli will

adhere together in “clumps” and become immobile. Conversely a valuable

means of ascertaining whether a suspected case is really suffering from

enteric fever is secured, as this blood added to 30 times the amount of

a pure culture of the _Bac.-typhosus_ in broth will cause the latter to

“clump” within half-an-hour (_Widal reaction_). Higher dilutions are

usually unnecessary.

The chief means of spread of enteric fever is by the urine and fæces;

and nurses who have to empty bed-pans unless very careful to wash

their hands afterwards, using the nail-brush, are very liable to

become infected, probably when eating food afterwards. The urine in a

considerable proportion of cases, contains the typhoid bacilli, and

it is therefore most important that care should be exercised in the

cleansing of all chamber utensils, and that the urine as well as the

fæces should be rigidly disinfected (see page 331). The infectivity

of enteric fever has been underrated in the past. When patients with

this disease are nursed at home by relatives who do not appreciate the

full importance of the necessary precautions, it is rather the rule

than the exception for them to fall victims to its infection. Probably,

sometimes the infection has been scattered as dust, owing to small

particles of fæces or of urine having become dried on bed linen. The

most absolute cleanliness is essential in nursing this disease. In hot

climates there is reason to believe that infective dust may be blown

about from privies.

_Insanitary local circumstances_ are an important means of spreading

enteric fever. It is more prevalent where there are privies than

where there are pail-closets; and more prevalent where there are

pail-closets, than where water-closets are the rule. Defective drains

or soil-pipes are frequently found in houses in which enteric fever

originates, and there can be little doubt that the former are at least

partially responsible for the latter. The exact link is doubtful.

Probably infective dust is blown or aspirated into the room and is

inhaled.

The most common cause of enteric fever is _infected food or water_.

Of foods _milk_ not infrequently has been the means of spread of

enteric fever. Large epidemics have been traced to this source.

Usually this has arisen by washing the milk cans with or wilfully

adding contaminated water to the milk. _Water_, whether added to milk

or taken independently, must have contained the specific contagium

(the _Bac.-typhosus_) of enteric fever, to enable it to cause enteric

fever. Hence water from a contaminated stream is more likely to have

produced this effect than well-water, unless a patient has had enteric

fever in the house to which the well is attached, and his dejecta

have contaminated the water. Surface waters or spring waters may be

contaminated with sewage (as at Maidstone) or deep well waters through

fissures (as at Worthing) and thus widespread epidemics be produced.

After floods, rivers and wells are most likely to contain the specific

contagium of enteric fever, as at such times surface impurities from

middens, etc., are apt to be washed into the water. (See also pages 91

and 224).

The _means of prevention_ of enteric fever are the discovery and

removal of the cause of an outbreak, and the isolation of each patient

and disinfection of all discharges. An early means of diagnosis is

secured by Widal’s reaction. This is especially useful in cases not

presenting characteristic clinical symptoms. The recognition of a

disease or at least the suspicion of its presence is an indispensable

first step for the taking of precautionary measures.

CHOLERA.

Cholera, which was formerly so prevalent, now seldom occurs in this

country, and at each successive visit to England its inroads have

become less serious. At its last visit in 1893 it scarcely obtained

a footing in the country. Thus in the epidemic of 1854 in England it

caused 1080, in that of 1866 it caused 672, and in that of 1893 only

45 deaths per million of population. In this country at least it is

chiefly spread by infected water and foods, especially by infected

water; and the preceding figures form an excellent testimony to our

improvement in this respect. For particulars of the Hamburg outbreak,

see page 93. In its mode of prevalence and propagation it is very

similar to enteric fever, being infectious by means of the evacuations.

The means of prevention are the same as for enteric fever. Cholera was

shown by Koch to be caused by what is known as the _comma bacillus_ or

_spirillum_ of Asiatic cholera, so called because of its curved shape.

It is from 1·5µ to 2·6µ long and ·5µ broad. For the supposed connection

of enteric fever and cholera with movements of the ground-water, see

page 225.

SUMMER OR EPIDEMIC DIARRHŒA

is a most fatal disease among infants in the third quarter of

each year. It is chiefly a disease of urban life, and occurs to a

preponderant extent among the children of the artisan and still more

of the unskilled labouring classes. It is much less abundant in towns

which have adopted the water-carriage system of sewage than in those

retaining the conservancy methods of removal of excrement (page

198). Towns with the most perfect domestic and street scavenging

arrangements have the least epidemic diarrhœa. An impervious soil

favours a low diarrhœal mortality; while persons living on porous

soils usually have much diarrhœa. I have shewn elsewhere that given

two towns equally placed so far as social and sanitary conditions are

concerned, their relative diarrhœal mortality is proportional to the

height of the temperature and the deficiency of rainfall of each town,

particularly the temperature and rainfall of the third quarter of each

year. In other words there is a general inverse relationship between

rainfall and diarrhœa and a direct relationship between temperature and

diarrhœa. Thus wet and cool summers are adverse to diarrhœa. Ballard

concluded that the summer rise of diarrhœal mortality does not commence

until the mean temperature recorded by the 4-foot earth thermometer

has attained somewhere about 56° F., no matter what may have been the

temperature previously attained by the atmosphere. This is a convenient

index, as the summer warmth does not immediately cause diarrhœa. All

the above facts point to the conclusion that the fundamental condition

favouring epidemic diarrhœa is an unclean soil, the particulate

poison from which infects the air, and is swallowed most commonly

with food, especially milk. Thus, diarrhœa, like enteric fever, is a

“filth-disease.” As the contagium appears to gain entrance by food, the

following card of precautions which is distributed each year in the

poorer districts of Brighton may be reproduced here:

HOW TO PREVENT DIARRHŒA.

During the summer a large number of infants die from diarrhœa.

Scarcely a single baby who was being suckled dies from this cause.

It is evident, therefore, that in the prevention of this very fatal

summer disease, precautions as to food are most important.

Attention to the following points would save many infants’ lives:—

1. _Do not wean your infant during the hot months_ of July, August

and September. To begin artificial feeding during hot weather is very

dangerous.

2. If feeding by hand is absolutely necessary, carefully follow these

directions:

(_a_) _All milk should be boiled_ before being given to the infant.

(_b_) The infants’ food must be _prepared fresh each time_. (For

particulars see below.) Milk and water, and still more “pap” or patent

foods, if left two or three hours, “go bad,” and are then very highly

dangerous to the infant.

(_c_) _All jugs_ or other utensils used _for storing milk must be

scalded out_ and kept absolutely clean. They should be covered to

prevent access of dust.

(_d_) _The feeding bottle must be thoroughly scalded after each meal_,

and the tube thoroughly cleansed. It is best to use alternately

two boat-shaped bottles without tubes. If the bottle smells sour,

something is not clean, and the infant will suffer.

3. _Decomposing refuse_, such as decaying vegetables, bones,

fish-heads, &c., _is a fertile source of Diarrhœa_. _It should be

burnt_, and not placed in the dust-bin.

4. _Scrupulous cleanliness_ of the house, especially of the rooms where

food is stored, is most important. Dust in every form is dangerous to

health, and for removing it wet cleansing is preferable to dry. Thus

washing and scrubbing are safer means of cleansing floors, &c., than

sweeping.

5. _Report to the Sanitary Office_, Town Hall, any smells or choked

closet or drain.

DIRECTIONS FOR PREPARATIONS OF INFANTS’ FOOD.

=For a Child aged= =Mix and then boil= =For each Meal=

(1 part _fresh_ milk )

Under 6 weeks {2 parts water } 4 tablespoonsful.

(1 teaspoonful cream )

=Mix and then boil=

(1 part fresh milk )

6 weeks old {1 part water } 8 tablespoonsful.

(2 teaspoonsful cream)

=Mix and then boil=

(2 parts fresh milk )

From 3 to six months old {1 part water } 8 tablespoonsful.

(2 or 3 teaspoonsful )

cream.

The infant should _be fed at regular intervals only_, at first every

two hours, the interval being gradually increased.

The infant should _be fed slowly_.

If the milk as prepared above disagrees, _freshly boiled barley water_

should be used instead of water.

The _addition of cream is necessary_ because cows’ milk is poorer in

cream than mothers’ milk, and because it is very often made poorer

still by mixing with separated milk before sale. _Deficiency of cream

causes rickets._ A little sugar may also be added to the milk, but this

must not be regarded as a substitute for the cream.

TETANUS.

Tetanus or lockjaw is not infectious, but is conveyed to man by the

inoculation of a wound by dirt or earth which contains the tetanus

bacillus. For this reason it is more apt to follow injuries to the

hands or feet. Extreme cleanliness of wounds is the only practicable

preventive means. Little is known of the history of the tetanus

bacillus outside the body; and as to what soils contain it most

abundantly. Wounds contaminated by horse manure appear to be especially

dangerous.

GLANDERS.

Glanders is common in horses. It attacks the mucous membrane of the

nose, causing ulceration. It is extremely infectious. =Farcy= is a more

chronic form of the same disease, in which the so-called “farcy-buds”

are produced. Its prevention can best be ensured by killing both

actually diseased and suspected animals, if the latter give a reaction

to mallein. _Mallein_ is a product allied to tuberculin, obtained from

cultivations of the bacillus of glanders. It sets up febrile reaction

in glandered, but not in healthy horses. Further preventive measures

are the temporary closing of public drinking fountains for horses, and

the thorough cleansing and disinfection of stables. Men, especially

grooms, are sometimes infected by the horse, and the disease is

commonly fatal.

HYDROPHOBIA.

Hydrophobia is the disease in man which is caused by the bite of a

dog or other animal suffering from =rabies=. It is seldom if ever

communicated otherwise than by inoculation. The _incubation period_ in

the dog varies from three to six weeks, and in man is usually about the

same; but occasionally it is much longer, occasionally even more than a

year.

At the Pasteur Institute, Paris, patients who have been bitten by rabid

dogs are treated by the inoculation of an attenuated virus of rabies

derived from rabbits, with promising results.

Dogs only acquire rabies from dogs or other animals already rabid.

So far as is known, it does not arise _de novo_. Hence the necessity

for an extensive area of muzzling when cases of rabies occur. The

enforcement of this plan has greatly reduced the amount of hydrophobia

in this country in recent years. There has been much misplaced sympathy

with dogs on this score. In the dog the symptoms of rabies occur in

three stages: a _premonitory_ stage, in which the dog’s habits change,

he becomes morose and quiet, and dribbles; a _second_ stage, in which

he has paroxysms of fury, his voice is high-toned and croupy, and he

cannot swallow water; and a third or paralytic stage, in which his jaws

drop, he drags his hind legs and soon dies.

ERYSIPELAS.

Erysipelas occurs on various parts of the skin. It is caused by the

inoculation through an abraded surface of a virulent form of the same

streptococcus that commonly causes suppuration. It occurs chiefly in

debilitated subjects. Some persons are specially prone to it, and may

have many attacks. Erysipelas, like scarlet fever, occurs most in years

in which there is deficient rainfall; and is probably conveyed by dust.

It may spread, though exceptionally, from case to case.

YELLOW FEVER.

Yellow fever never occurs in England, except when imported from the

West Indies or other countries in which it is endemic. It clings to

seaport towns in hot countries; and as a permanent disease is only

found when the mean winter temperature is at least 68°-72° F. A frost

always stops an epidemic of this disease. The germs of this disease

are communicated by mosquitoes, which act as an intermediate host. Dr.

J. W. Lazear, although isolated from yellow fever cases, died of it

seven days after submitting to the puncture of an infected mosquito,

thus proving the communicability of this disease, and entitling himself

to an honoured position among scientific martyrs.

PLAGUE.

Plague is an Eastern disease, which occasionally shows a tendency

to become widely epidemic. It is due to a rod-shaped bacterium,

averaging ·8 µ to 1·6 µ in length, which does not form spores. In

its characteristic form patients suffering from this disease have

inflammatary swellings (buboes) of various glands: hence the name

_Bubonic Plague_. In other cases it simulates ordinary pneumonia,

typhus or septicaemia; or the patient may be so slightly ill as to

be able to walk about. It appears probable that the bacillus enters

the body through cracks or other lesions of the skin, possibly also

by inhaling infective dust. The rat is an important factor in the

spread of plague. Very commonly plague has been widely prevalent and

fatal among them before it attacks human beings. Rats also bring it in

ships from infected ports. Hence one of the most important preventive

measures is to kill all rats on board ship, before the cargo is

unloaded. This has been done by sulphurous acid fumigation in the

holds. The use of carbonic oxide gas will probably be found practicable

for the same purpose. Manson has put the importance of this point

tersely as follows: “To prevent cholera the tea-kettle, malaria the

mosquito net, and plague the rat-trap.” Flies may carry the infection

(page 281). It has been suggested that the fleas of rats carry the

infection (page 281).

ANTHRAX.

Anthrax is a very fatal disease in cattle and sheep, occasionally

in pigs. Butchers may inoculate themselves with it when dressing a

diseased carcase; the tanners similarly when handling the hide; and

woolsorters may inhale it when sorting wool derived from a diseased

animal (page 107). To prevent the latter, suspected wool must be

disinfected by steam, and special arrangements made for carrying off

the dust produced during sorting.

PUERPERAL FEVER

occurs after childbirth. It is caused like erysipelas by the

inoculation of septic material. This may be conveyed by dirty

instruments (syringes, etc.), or by dirty hands. Hence the importance

of extreme cleanliness of hands, finger-nails, and all articles used

during and after childbirth.

RHEUMATIC FEVER

has been commonly attributed to a damp condition of the atmosphere and

soil. I have elsewhere shown that this is a mistake, probably arising

from the fact that these conditions produce what are called “rheumatic”

pains, though they have no true relationship with acute rheumatism

(rheumatic fever). I have shown that rheumatic fever occurs chiefly in

very dry years, the excess of prevalence in such years being sufficient

to justify the use of the term “epidemic.” There is strong reason to

believe that rheumatic fever is an infective disease, derived, not from

other patients suffering from the same disease, but from some outside

micro-organism which is ordinarily saprophytic. It follows the rule

that when the lesion produced by an infective disease is deepseated

(in the joints in this instance), no infection can be communicated to

other persons. Some families are much more prone to rheumatic fever

than others.

INFLUENZA

is, like diphtheria, a somewhat mysterious infectious disease. Like

the latter it almost disappeared for a series of years, and then again

became epidemic in 1889. The previous epidemics of influenza in the

19th century had occurred in 1803, 1833, 1837-8, and 1847-8. The causes

of this recurrence of influenza are unknown. It is spread from person

to person by direct infection, the infection being conveyed by the

mucous discharge from the nose, throat, and lungs. Pocket-handkerchiefs

probably are largely responsible for conveying the infection as dust.

The disease is particularly fatal to the old; and these should not

expose themselves to possible sources of infection, as in public places

of assembly, during an epidemic. Every patient attacked with the

disease should remain indoors for at least ten days. This is in his own

interest, as he thus minimises the risk of such dangerous complications

as pneumonia; and it is his duty in the interest of the rest of the

community. Many lives might have been saved, had not influenzal

patients “struggled about” during the early stages of the disease.

MALARIA.

=Malaria=, or =Ague=, is a generic name given to a disease caused by

the invasion of the body by the _plasmodium malariæ_, discovered by

Laveran in 1880. It occurs in two chief types, remittent fever and

intermittent fever. For many generations it has been regarded as due

to a marshy condition of the soil, associated with decaying vegetable

matter, and a moderately high temperature. It is now clear that these

conditions are necessary, only because they are necessary for the

life of the mosquito. The well-known danger of being out of doors at

night in a malarious country is explained by the nocturnal habits of

the mosquito. The higher salubrity of the upper stories of houses is

explained by the fact that the mosquito does not rise high from the

ground; and of high-lying localities by their greater dryness. The

value of the mosquito net, of smoke, and of fire as protections from

malaria are due to their keeping mosquitos at a distance. The mosquito

clings to the puddle or swamp where she was born, and where she will

deposit her eggs. Hence the special danger of the immediate vicinity

of such collections of water. Thus the prevention of malaria resolves

itself chiefly into means for preventing the development of certain

species of Anopheles (page 282). The conditions necessary for the

multiplication of these are (1), an atmospheric temperature from 75°

to 104° F.; (2) collections of fresh or slightly brackish water; and

(3) the presence in these of low forms of animal and vegetable life. We

have already described the cycle of life of the _plasmodium malariæ_

(page 282). Man is the chief, if not the only source, from which

the mosquito derives this parasite. In native communities the young

children, even when apparently not ill with malaria, nearly always

harbour these parasites in their blood corpuscles. Hence the importance

of Europeans having their dwellings as remote as possible from native

houses. Mosquitos do not travel far.

Instances of the prevalence of malaria in the absence of mosquitos are

not substantiated. The outbreaks of malaria where the soil has been

disturbed after long lying uncultivated, probably mean the formation of

puddles favourable to the breeding of the larvæ of mosquitos.

The necessary preventive measures are classified by Manson as:

1. Suppression of mosquitos.

2. Prevention of infection of mosquitos.

3. Prevention of infection by mosquitos.

The =suppression of mosquitos= involves the draining or filling in of

swamps and ponds, the cleansing and canalisation of sluggish streams,

and the afforestation of hills to prevent floods. Cultivation of rice

and other plants entailing the prolonged flooding of land should

be restricted to fields remote from dwellings. Subsoil drainage is

helpful. The “painting” of stagnant waters with petroleum, which should

be renewed every week or two, frees water for a considerable time from

the larvæ of mosquitos. Eucalyptus and other balsamic trees may help to

dry up pools, &c.

The =prevention of infection of mosquitos= is secured by insisting on

all malarial patients using mosquito nets. This prevents the access of

mosquitos. At the same time patients should vigorously and persistently

take quinine, which kills the malarial parasites in the blood, and thus

diminishes and finally removes the danger to other persons produced by

the intermediation of the mosquito.

The =prevention of mosquito bites= is secured by rendering the house

mosquito-proof by filling in all openings by fine wire gauze, and by

having mosquito curtains to all beds; also by fumigating the rooms

occasionally with the dried flowers of the chrysanthemum, by strict

cleanliness of rooms, and by flushing them with sunlight. The proof of

the mosquito theory as to the causation of malaria has been recently

supplied by two test experiments. (_a_) In the first, a number of

mosquitos which had been fed on the blood of malarious patients were

sent to London from Rome. These were allowed to bite Dr. Manson’s

son, who had never previously had malaria. A few days later he had a

characteristic attack of fever. Malarial parasites were found in his

blood. He recovered in a week’s time after free dosage with quinine,

and the parasites disappeared from his blood. He suffered from a slight

relapse about a year later. (_b_) On a fever-haunted spot in the Roman

Campagna a wooden hut was built, and Drs. Sambon and Low, and three

others took up their abode here during the malarious season, the only

precautions taken being the use of mosquito nets and wire screens in

doors and windows. They went about the country daily, but were always

home before sunset. They all remained at the end of the season free

from malaria.

Hygiene: a manual of personal and public health (New Edition) · 第 44 / 48 章