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Elements of Ecology 9th Edition Smith

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Elements of Ecology, 9e (Smith)


Chapter 2 Climate

2.1 Short Answer Questions

1) The temperature, humidity, precipitation, wind, cloudiness, and other atmospheric conditions
that occur at a specific place and time are referred to as .
Answer: weather
Topic: Introduction to Chapter 2
Bloom's Taxonomy: Knowledge/Comprehension

2) The long-term average pattern of weather at local, regional, or global scales is referred to as
.
Answer: climate
Topic: Introduction to Chapter 2
Bloom's Taxonomy: Knowledge/Comprehension

3) Carbon dioxide and are the major gases in the atmosphere that absorb energy from
the sun.
Answer: water vapor
Topic: Section 2.1
Bloom's Taxonomy: Knowledge/Comprehension

4) The absorption and re-radiation of longwave radiation by gases in the atmosphere is called the
.
Answer: greenhouse effect
Topic: Section 2.1
Bloom's Taxonomy: Knowledge/Comprehension

5) Seasonality occurs on planet Earth because of its with respect to the plane it travels
around the Sun.
Answer: axial tilt
Topic: Section 2.2
Bloom's Taxonomy: Knowledge/Comprehension
6) In the Northern Hemisphere, the summer Tropic of
Cancer.
Answer:
1
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solstice Topic: occurs when solar rays fall directly on the
Section 2.2
Bloom's Taxonomy: Knowledge/Comprehension

7) The amount of force exerted over a given area of surface is called atmospheric .
Answer: pressure
Topic: Section 2.3
Bloom's Taxonomy: Knowledge/Comprehension

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8) With increasing altitude, air density .
Answer: decreases
Topic: Section 2.3
Bloom's Taxonomy: Application/Analysis

9) Air masses are deflected to the in the Northern Hemisphere and to the in
the Southern Hemisphere.
Answer: right; left
Topic: Section 2.4
Bloom's Taxonomy: Knowledge/Comprehension

10) The winds formed between the equator and about 30 degrees of latitude, blowing from the
northeast in the Northern Hemisphere and southeast in the Southern Hemisphere, are referred to
as .
Answer: trade winds
Topic: Section 2.4
Bloom's Taxonomy: Knowledge/Comprehension

11) In the Southern Hemisphere, oceanic gyres circulate in a(n) direction.


Answer: counterclockwise
Topic: Section 2.4
Bloom's Taxonomy: Application/Analysis

12) The transformation of water from a liquid to a gaseous state is referred to as .


Answer: evaporation
Topic: Section 2.5
Bloom's Taxonomy: Knowledge/Comprehension

13) is the amount of water vapor in the air expressed as a percentage of the saturation
vapor pressure.
Answer: Relative humidity
Topic: Section 2.5
Bloom's Taxonomy: Knowledge/Comprehension

14) The is the temperature at which atmospheric water condenses.


Answer: dew point
Topic: Section 2.5
Bloom's Taxonomy: Knowledge/Comprehension

15) The narrow region near the equator where trade winds meet is referred to as the .
Answer: Intertropical Convergence Zone
Topic: Section 2.6
Bloom's Taxonomy: Knowledge/Comprehension

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fumigation. Liston allows this gas, developed from ½ ounce KCN, to
act for four hours in a space of 100 cubic feet. The great danger from
the use of this gas in holds of ships is that it tends to collect in
detached spaces or pockets and remains following ventilation of the
hold so that persons entering such spaces suffer the poisonous effects
of the gas. Some cargo ships have a rat-run built to extend fore and aft
and leading to a receptacle in which the rats are caught. Rats naturally
choose a tube or similar opening so they get into this little passageway
which is so constructed that their return is obstructed. This scheme is
used in setting traps, either covering the traps with hay and leaving a
small opening or placing the trap under an inclined plank or placing it
at the end of an iron or terracotta pipe. There is not much danger of
rats getting aboard a ship lying out from the dock. It is when a ship
goes alongside a dock that we can expect rats to come aboard.
Phosphorus paste made up with a glucose base and containing about
4% of phosphorus is spread on pieces of stale bread, 1 inch square and
¾ inch thick. Whatever poison is used, whether strychnine, arsenic or
phosphorus, it should be placed in boxes which have openings large
enough to let the rats in but too small for domesticated animals.
Barium carbonate is a useful rat poison.
Cats will very rarely attack the fierce sewer rat.
Danysz virus.—Many workers, during plague outbreaks, have tried
to exterminate rats by impregnating bread or other bait with bacterial
cultures. The best known of these viruses, as they are called, is that of
Danysz. The organism is closely related to B. enteriditis of Gaertner
and is supposed to bring about a fatal infection in the rats. As a matter
of fact the cultures quickly cease to be virulent and their use has been
generally abandoned. Simpson, however, thinks well of this measure
and employed it with success in South Africa. He kept up the
virulence of his cultures by frequent passage through animals.

In rat extermination it is advisable to employ Heiser’s Manila


plan. In this, the location in the city of the plague rats brought into
the laboratory is noted and radiating lines made from such foci.
Plague-infected rats are rarely found more than a few squares from
the focus. The periphery of the infected area is then considered as
an outer zone for the fight and the house-to-house extermination is
carried on toward the center of the area. If, on the other hand, one
should start at the center and work peripherally the infected rats
might be spread all over the city.
Prophylaxis by Immunization.—The best-known bacterial
prophylactic is that of Haffkine. Stalactite bouillon cultures are
grown in flasks for five to six weeks. The organisms are then killed
by heat at 65°C. for one hour. Phenol (½%) is then added and from
0.5 to 4 cc. injected according to the age and size of the individual.
Ten days later a still larger amount is injected. The reaction
following these injections is apt to be quite severe.
Recent reports show that of 118,148 inoculated persons the plague
incidence was approximately 8 per 1000 while among 321,621
noninoculated the incidence was 34 per 1000.
Statistics from Sagaing show 19 cases with 7 deaths among 4284
inoculated persons while there were 134 cases and 128 deaths among
4467 not inoculated.
The plague mortality in cases which had previously been inoculated
was 40% while that among the noninoculated was 78%.

From the above it will be seen that incidence is reduced to about


one-fourth and mortality about one-half as the result of the use of
Haffkine’s prophylactic.
Besides this killed culture other material has been used. Lustig and
Galleotti used the nucleo-proteid from plague bacilli for subcutaneous
injection. Kolle and Strong have recommended a vaccine of living but
nonvirulent plague bacilli. A higher degree of immunity seems to be
conferred by this living vaccine but there are certain dangers in the use
of living organisms which outweigh the advantage noted above.
Yersin’s antiplague serum, which is prepared by injecting horses at
first with killed cultures and later with living plague bacilli, may be
used as a prophylactic as well as in treatment. One point to consider is
that such serum, if used immediately after taking from the horse,
might contain living plague bacilli. The phenol preservative prevents
this. It must be remembered that this is a passive immunization as
against the active one with Haffkine’s prophylactic, hence the
protection is very short, only ten days or two weeks as against the
more enduring immunity of a year or so following Haffkine’s
prophylactic. It must be remembered that anaphylactic manifestations
may follow the repeating of the dose of Yersin’s serum. It is probably
advisable for one who is to be exposed to plague for a short time only
to receive an injection of the serum. As regards pneumonic plague
there seemed to be little protection attaching to either active or passive
immunization.

Treatment.—It may be stated that the only treatment which has


any curative value is that with antiplague serum. This would appear
to be of considerable value in bubonic plague provided it is
administered in the first day or two of the disease. It must be given
in large amounts, from 50 to 100 cc. or even to the extent of 250 cc.
Then too such enormous doses apparently require to be repeated.
Intravenous administration gives a better chance for success in
desperate cases. In septicaemic and pneumonic plague the use of
serum has been without result.
Salvarsan, as might be expected, has been tried but did not prove of
any value.
Connor has reported success with the intravenous injection of one
dram of a dilution of 1 part of tincture of iodine in 10 parts of sterile
water. He gave 6 such injections to a severe case with good result.
In the way of symptomatic treatment one should use ice-bags to
head and cold sponging to the body.
Morphine seems to be the best drug to calm the patient. Cardiac
stimulants, especially strychnine, are indicated for the heart weakness
so much a feature of plague. Some consider incision or enucleation of
the bubo of value in treatment but it has always seemed to me that the
going into the periglandular exudate might serve to set up a
septicaemic condition when otherwise it might not supervene.
CHAPTER XIV

TULARAEMIA

D S

Definition.—This is a plague-like disease of various rodents,


transmissible to man, caused by an organism Bacterium tularense,
which is not closely allied to any other species. A number of human
cases have been reported from Utah, where the disease is prevalent
among the jack rabbits, and the transmission to man is through the
bite of a horsefly, Chrysops discalis, which has previously sucked
the blood of infected jack rabbits.
The site of the bite in man is usually marked by a punched-out ulcer,
which is associated with swelling and suppuration of the glands
draining the area. The general symptoms are sudden onset, with rigors,
followed by an irregular fever of three or four weeks’ duration and by
a prolonged convalescence. Several cases have been reported in the
middle west due to handling infected rabbits. There have been a
number of infections in laboratory workers where the local signs have
been absent. In man death rarely results from the disease.

Synonyms.—Deer-fly fever (in man). Plague-like disease (in


rodents).

H G D

History.—In 1911 McCoy and Chapin discovered the B. tularense in


a plague-like disease, first described by McCoy in the California
ground squirrel. They described the organism, succeeded in cultivating
it on special media, transmitted the infection to various rodents by
feeding, nasal inoculation and injection of infected blood, and
demonstrated the probable natural mode of transmission by the squirrel
flea.
In recent publications, Francis, Lake and Mayne, and Wayson have
recorded the transmission of the disease experimentally by the house
fly (Musca domestica), the horsefly (Chrysops discalis), the stable fly
(Stomoxys calcitrans), the rabbit louse, the mouse louse and the
bedbug, and have shown that the freshly recovered organism can be
grown on other than the special media previously recommended.
Geographical Distribution.—The first case of infection occurring
in man was reported from Ohio by Wherry and Lamb in 1914. Since
then a number of cases have been reported by Francis among rural
residents of Utah and by Francis and Lake among laboratory workers
handling animals infected with B. tularense.

E E

Etiology.—Bacterium tularense is a small nonmotile Gram-


negative cocco-bacillus, from 0.3 to 0.7µ long and gives the
appearance in stained preparations of being surrounded by capsular
material. It is very difficult to cultivate and until recently it has been
grown only on coagulated egg yolk as used by McCoy and Chapin.
F . 70.—Chrysops discalis. The transmitting agent of tularaemia.

Recently Francis has shown that the organism will grow scantily on
serum or blood agar. However, by adding a piece of fresh sterile spleen
to such media he has obtained a more satisfactory culture medium,
although for routine work the egg yolk medium is preferred. The
organism refuses to grow on ordinary media such as nutrient broth or
agar. Material from a culture, or pus from bubo, or an emulsion of the
spleen of an infected guinea pig, when rubbed into the abraded skin of
an experimental animal brings about infection, in this respect showing
a similarity to plague infection. Upon autopsy of such an
experimentally infected guinea pig we find haemorrhagic oedema at
the site of inoculation with caseation of lymph glands and small
necrotic foci in spleen and liver. Smears from the spleen show the
organism in varying numbers. In infected rodents the organism is often
found abundantly in the blood and in man a bacteriaemia may occur.

Epidemiology.—The infection of ground squirrels with this


organism was noted by McCoy in his plague work in California.
Francis in studying the disease in man in Utah found infection of
the jack rabbits and ground squirrels of the region and showed that
the transmission of the disease could be carried out by a biting fly
(Chrysops discalis) and reported this fly as the common
transmitting agent of the human infection. He regarded the sick and
dying jack rabbits as the reservoir of virus. Tularaemia is chiefly a
disease of the rural population attacking those at work in the fields.
As a result of accidental laboratory infections it would seem that
almost 100% of those carrying on extensive animal experimentation
with this organism become infected.
The louse infesting jack rabbits Haemodipsus ventricosus, can
transmit the infection from rabbit to rabbit so that the infection in the
jack rabbits is probably kept up by this agency. Recent experiments
have shown that the infection in white mice can be transferred by the
bites of the mouse louse and also by bedbugs. Again if the mice are fed
on infected bedbugs transmission is found to take place by such
feeding experiments. The faeces of such bedbugs prove infectious.
Guinea pigs injected subcutaneously with the urine of white mice
suffering from the disease die acutely with typical lesions of
tularaemia.
Mice fed on the liver of a rabbit dying of the disease succumbed to
the infection within five days.

As noted under etiology the most important method of spread of


the disease to man is by the bite of an infected horsefly (Chrysops
discalis). From experimental studies it would seem that any biting
arthropod might prove a transmitting agent. In view of the fact that
the infected deer fly tends to lose its infectivity after about five days
Francis is of the opinion that the fly is only a mechanical
transmitter of the organism.
Wherry reported the infection as manifested by conjunctivitis with
glandular involvement and due to handling infected wild rabbits.
Lake and Francis have reported that of six investigators from the
Hygienic Laboratory working with this infection all have contracted
the disease. There were fortunately no fatalities. Such an experience
demonstrates the great infectivity of this virus and must lead to the
conclusion that the few cases so far reported of the disease do not
represent the importance of tularaemia in man. With a knowledge of
the existence of such an infection and with satisfactory methods of
laboratory diagnosis we shall probably have other reports of the
infection. We now know that the ground squirrels of California and
Utah, the jack rabbits of Utah and the wild rabbits of the middle west
furnish important reservoirs of virus.

In experimental animals we have lesions which cannot well be


differentiated from those of plague. There is not sufficient data for a
statement as to the pathology in man.
In experimental animals we have a definite bacteriaemia but in man
the organism has only in rare instances been obtained from the blood.

It has been difficult to determine the period of incubation but in


one laboratory infection the disease set in seven days after the
patient began tularaemia work. There do not seem to be any
prodromata.
F . 71.—Temperature chart of a case of laboratory infection (tularaemia.)

In Utah most of the cases showed local lesions at the site of the
fly-bite and subsequent swelling and suppuration of adjoining
lymph glands. The local lesions were generally observed about the
head or on parts of the body not covered by the clothing. There is a
rather sudden onset with chilliness or rigors, generally associated
with dizziness, prostration and malaise. Headache is usually present
and there may be complaints of pains in the back and limbs. The
temperature rises rapidly and when first taken during the rigors may
reach 103° or 104°F. An irregular fever course follows for two or
three weeks. There is practically no apathy, thus differentiating the
mental state of typhoid fever or the marked clouding of the
consciousness of plague. At times we may have rhinitis and
epistaxis.
Physical examination is almost invariably negative. The spleen is not
palpable. The pulse is rather rapid and the blood pressure
uninfluenced.
The white and differential counts vary but little from normal.
The main feature of the disease, aside from local lesions when these
are present, is prostration and this continues marked during the several
weeks or months of convalescence.

It is a disabling illness rather than a dangerous one though a fatal


case is recorded.
In the six laboratory infections above referred to, there were no local
lesions except in the case of one man who had had previously an attack
of the disease. In the second attack, two years after the first one, there
was noted a papule on one finger with subsequent involvement of the
epitrochlear and axillary glands. A guinea pig inoculated with blood
taken from the papule became infected and showed the typical lesions
of tularaemia.
There was no fever or malaise in this second attack, thus showing a
degree of immunity. In cases showing conjunctival ulcerations with
glandular involvement Wherry and Lamb obtained cultures of B.
tularense from inoculated animals.

There is very little in the clinical picture, other than the local
lesions, to indicate a diagnosis.
Material from ulcers or glands should be inoculated into guinea pigs
or white mice. The organism is almost invariably absent from the
blood of human cases so that blood cultures or animal inoculation from
such blood are almost always negative.
Complement fixation and agglutination tests are the methods of
diagnosis to be relied on. In the Hygienic Laboratory an antigen is
prepared by washing off the 72 hour growth from egg yolk medium
with small amounts of saline. The suspension is heated for 30 minutes
at 56°C. and then preserved by the addition of O.3% tricresol. Such an
antigen is used for each type of test.
P

This disease is but rarely followed by death. It is however a most


incapacitating disease by reason of the three or four months of
convalescence during which time the strength and energy of the
patient are markedly affected.

P T

Prophylaxis.—In view of the very great liability to infection of


those carrying on autopsies of animals experimentally infected with
the disease it would seem advisable to wear rubber gloves when
doing such work. It would appear that house flies, stable flies and
horseflies may transmit the disease in nature and we know that
bedbugs and lice can transmit the disease among experimental
animals. When we consider the natural infection of ground squirrels
and jack rabbits in California and Utah and wild rabbits in the
middle west, the problem of prophylaxis looms to great proportion.
Treatment.—At present treatment is entirely symptomatic.
Those who go to bed at once and remain in bed during the stage of
fever seem to be less seriously affected.
CHAPTER XV

CHOLERA

D S

Definition.—Cholera is a disease caused by a spirillar type of


bacterium, Spirillum cholerae asiaticae. The organism multiplies in
the small intestines and, undergoing lysis, liberates an endotoxin,
which is responsible for the desquamation of the epithelium of the
mucosa and other manifestations of the disease. Cholera appears to
be endemic in the delta of the Ganges and the various world-wide
epidemics can generally be traced to that source. The rice-water
stool of cholera teems with the spirilla, and infections of water or
food supplies can be traced to such a contamination. The
importance of the cholera carrier has been thoroughly demonstrated
from the time of the Hamburg epidemic of 1892. The clinical
course of the disease is divided into a stage of evacuation, in which
we have diarrhoeal discharges of rice-water character along with
very painful cramps of the muscles. Following increasing cyanosis
we have almost a cessation of circulation often associated with
anuria, the algid stage. With the return of activity of circulation and
urinary secretion we have the stage of reaction.
Synonyms.—Cholera Asiatica.

H G D

History.—Although the word χολέρα, meaning flow of bile, is


found in the writings of Hippocrates, it certainly does not refer to
the disease we now recognize as cholera. The older writers noted
the characteristics of bilious discharges in the disease they termed
cholera, which could not apply to the bile-free rice-water
discharges of what we now term cholera. Koch rather doubted the
antiquity of cholera but Susruta, in India, in the 7th century A. D.,
described a disease in which there were diarrhoea and vomiting,
stabbing pains, cyanosed lips and nails, with sinking in of the eyes
and weak voice.
Detailed accounts of the presence of cholera in India were published
from the 16th to 18th centuries when the Portuguese, English and
French were carrying on their wars of conquest in India. These wars
naturally spread the disease all over India.
It is thought that true cholera did not exist in China until 1669 when
it was carried there from India. It is first described from Japan in 1821
although an epidemic which devastated Tokyo in 1718 may have been
cholera.
A great pandemic of cholera started in India, in 1817, extending
over Asia but not invading Europe. The second great pandemic is of
importance as being the first to invade Europe. It started in India in
1826 and advancing slowly reached Persia in 1829, going thence by
way of Astrakhan to Russia, Sweden, Northern Europe and England.
By 1832 it had spread over the whole of Europe.
In the same year, 1832, it reached Canada and thence spread to Fort
Dearborn where it infected the soldiers who subsequently carried the
disease down the Mississippi valley. It was also introduced into New
York and spread thence South and West so that by 1836 cholera was
present all over the U. S., not disappearing until 1838. It disappeared
from Europe in 1839.
The next European outbreak or third pandemic lasted from 1846 to
1862 and was traced to India by way of land and sea, that by land
following the caravan route by way of Persia and Russia and that by
sea from Indian pilgrims going to Mecca and there causing the
infection of Mahommedan pilgrims from Egypt and European Turkey.
This pandemic reached the U. S. in 1848, starting at New Orleans and
going up the Mississippi valley. Central and South America and the
West Indies were also invaded by the third pandemic.
The fourth great pandemic invaded Europe by the usual routes and
continued from 1863 to 1875. During its continuance there were two
outbreaks in the U. S., one in 1867 and another in 1873.

That in 1873, when it was introduced into three widely separated


parts of the country, was the last appearance of cholera in the U. S.
The fifth pandemic began in 1883 and affected particularly the
Mediterranean seaports of France, Spain and Italy. It was during this
epidemic, in 1883, that Koch, working in Egypt, discovered the cause
of cholera, the Spirillum cholerae asiaticae.
A very serious outbreak of cholera, which originated in 1891, in
pilgrims from the delta of the Ganges, reached Europe in 1892, almost
a million deaths occurring in Russia. It was during this epidemic that
cholera appeared in Hamburg and gave opportunity for those careful
studies as to transmission of the disease to be later referred to.
It is usual to recognize a sixth pandemic which began in 1902 and
spread over India, China and the Philippines. This pandemic
continuing was a cause of great mortality among the soldiers of the
recent Balkan war. During the World War there was much cholera
among the Austrian forces in Galicia. It also prevailed in Bulgaria,
Greece and Turkey.
Geographical Distribution.—Practically every pandemic when
studied can be traced back to India and particularly to the delta of the
Ganges, which may be considered the enduring focus of the disease.

E E

Etiology.—The cholera vibrio, Spirillum cholerae asiaticae, was


discovered by Koch in 1883 and is a short curved organism which,
from its shape, is often called the comma bacillus. In addition to
single spirilla there may be “S” shapes from attachment of pairs. In
cultures in peptone solutions long filamentous forms may be seen
which however are exceedingly rare in the rice-water stools. A
stained smear from a fleck of mucus gives the fish-in-the-stream
appearance. Besides comma-shaped organisms we may have
coccoid or rod-shaped forms. In old cultures marked pleomorphism
is often seen.

F . 72.—Cholera vibrios, short forms. (MacNeal from Kolle and


Schurmann after Zettrow.)

It is Gram-negative and stains best with a dilute (1-10) carbol


fuchsin. There is a single terminal flagellum, which endows the
organism with great motility, which may best be termed scintillating.
It has been estimated that its motility is five times greater than that of
the typhoid bacillus. It grows best on media with an alkaline reaction
(—0.4%) and it is this tolerance for media of high alkalinity that
permits the separation of the cholera spirillum from the ordinary
faecal bacteria by the use of Dieudonne’s alkaline blood agar or
similar media. This is equal parts of defibrinated ox blood and N/1
NaOH, 3 parts of which are added to 7 parts of nutrient agar. It thus
has 15% of normal sodium hydrate, instead of the 1% acid reaction of
the usual media. Unfortunately, other spirilla tolerate this high
alkalinity.
The cholera organism is strongly aerobic and grows quickly and
luxuriantly in the upper part of a tube of Dunham’s peptone solution,
this property enabling one to separate it from other organisms of
faeces by taking up loopfuls from the surface layer to plate out on agar
of about 0 or -0.3% reaction. When grown in peptone solution the
cholera spirillum produces a nitroso body so that one obtains an indol
reaction (cholera red) by simply adding 5 or 6 drops of concentrated
H2SO4.
When this test is employed it is necessary to determine whether the
peptone used is suitable for the reaction. As a matter of fact this test is
now rather discredited. Blood serum is digested. Recently much
discussion has arisen as to the value of the haemolytic power
possessed by noncholera vibrios on blood agar plates.
It is true that the digestive action which true cholera has on the red
cells of the medium may give the appearance of a zone of haemolysis.
Therefore, for the demonstration of this haemolytic action of
noncholera spirilla, fluid blood media should be used. The El Tor
spirillum, isolated from Egyptian pilgrims without symptoms of
cholera, is haemolytic, but gives the immunity reactions of the true
cholera vibrios which are not haemolytic.
Gelatine is liquefied and the stab shows an air bubble liquefaction at
the summit of the stab. On gelatine plates a powdered glass center
with an encircling zone of liquefaction was formerly considered
characteristic of cholera, but at the present time gelatine cultures have
been almost abandoned in practical work.
As a rule animals cannot be infected by feeding them cholera
material unless the acidity of the gastric juice be neutralized and
intestinal peristalsis checked by opium (procedure of Koch). Injected
intraperitoneally, the cholera vibrio produces a fatal peritonitis.
Recently monkeys have been infected after purgation with sulphate of
soda and administration of bicarbonate of soda. They died in from one
to forty-eight hours with symptoms of cholera.

There have been instances where cholera has been caused in


laboratory workers by the accidental ingestion of cholera cultures,
thus Orgel was infected from sucking up peritoneal fluid in doing
Pfeiffer tests for bacteriolysis and died.
Emmerich and Pettenkofer swallowed cholera cultures, the former
experiencing a severe attack of cholera and the latter a diarrhoea in
which cholera spirilla were present. On the other hand similar
experiments have resulted negatively but this is what should be
expected from the epidemiological facts as to carriers.
The virulence of the cholera vibrio can be exalted by passage
through guinea pigs—successive culturing of the peritoneal exudate of
intraperitoneally infected animals alternating with culture media
growth inoculations. Such a fixed virus, the virulence of which cannot
be exalted, is the material used by Haffkine in his cholera vaccine. The
toxicity of cholera is supposed to be due to an endotoxin which is set
free when the vibrios undergo disintegration when lying between the
basement membrane and epithelial lining of Lieberkühn’s glands.
Others think the vibrios may enter the blood stream, there to be
immediately disintegrated with toxin production. The usual idea,
however, is that the cholera spirilla never invade the blood stream—
they are confined to the alimentary canal. Macfadyen obtained the
endotoxin by grinding the frozen spirilla. This toxin was destroyed by
a temperature of 60°C.

The spirillum of cholera has but little resistance to disinfecting


agents or to drying. It is also rapidly overgrown by putrefactive
bacteria and tends to disappear from sewage-contaminated water in
a short time. In stools the vibrio dies in about one or two days in
summer and in about a week in winter.
The inoculation of animals by cholera cultures tends to produce an
immune serum which is remarkable for its high agglutinating power,
the titre at times going as high as 1 to 20,000. For agglutination tests
in proving spirilla isolated from stools to be true cholera ones we use a
serum of at least 1 to 4000 for its specific vibrio. Such a serum should
agglutinate any true cholera spirillum in a 1 to 500 or 1 to 1000
dilution. The occurrence of bacteriolysis, when a small loopful of the
culture emulsified in 1 cc. of 1 to 1000 dilution of the immune serum
and then introduced into the peritoneal cavity of a guinea pig, is the
surest proof that a suspected organism is that of cholera.
This is shown when, upon removing a drop of the peritoneal fluid
fifteen to twenty minutes afterward, there is noted an absence of
motility and disintegration of the spirilla (Pfeiffer’s phenomenon).
Complement fixation tests, using the rice-water stools or peptone
solution cultures as antigen, are of less value than those above noted.
Agglutination is the practical test and is almost as specific as that for
bacteriolysis.

Epidemiology.—Until recently our attention as to the methods


of transmission of cholera was directed almost exclusively to the
water and food supply, with a certain degree of consideration of
danger from fomites, especially to that connected with clothing
soiled by cholera discharges, it having been noted that those who
wash such clothing showed a high incidence of infection. Later on
the importance of flies in the spread of the disease was strongly
insisted upon. At the present time we consider the cholera carrier
the most important factor in cholera epidemiology and it is to the
detection and isolation of such persons that we now chiefly direct
our attention in the keeping out of a country of this dread disease.
It will be remembered that Pettenkofer and Emmerich insisted upon
the factors of soil and ground water in the spread of cholera.
Emmerich now admits that the spirilla excreted by carriers can
produce cholera but that such transference never gives origin to
epidemics. For this to take place he thinks that the vibrios excreted by
a carrier must come in contact with a soil which has been impregnated
with a suitable medium drawn to the surface from the deeper layers of
the soil by capillary suction. In such medium the vibrios flourish and
acquire the property of actively producing nitrites from nitrates.
Emmerich considers that the symptoms of cholera are those of
nitrite poisoning so that only such organisms as possess this nitrite-
forming function in high degree can produce virulent outbreaks of
cholera.
All facts in connection with the spread of cholera by land or water
routes can be best explained by the cholera carrier; the individual who
is excreting vibrios, while in apparent health, being far more
dangerous than the one excreting such organisms in the rice-water
stools of a well-recognized case of the disease.

Water Transmission.—There are two types of outbreaks of


cholera according as the general water supply is contaminated or
when such contamination is localized to certain wells, cisterns or
other nongeneral supplies. In the former the onset is explosive and
cases occur almost simultaneously and with equal distribution in all
parts of the city, to disappear with almost equal suddenness.
In the latter mode of infection, cases will appear from day to day
and often peculiarly localized to certain definite districts of a city or to
certain definite users of a particular water supply.

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