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Chapter 8 Classes and Objects: A Deeper Look
Section 8.2 Time Class Case Sudy
8.2 Q1: The _________ of a class are also called the public services or the public interface that the class
provides to its clients.
a. public constructors.
b. public instance variables.
c. public methods.
d. All of the above.
ANS: c. public methods.

8.2 Q2: The static method ________ of class String returns a formatted String.
a. printf.
b. format.
c. formatString.
d. toFormatedString.
ANS: b. format.

8.2 Q3: Which statement is false?

a. The actual data representation used within the class is of no concern to the class’s clients.
b. Clients generally care about what the class does but not how the class does it.
c. Clients are usually involved in a class’s implementation.
d. Hiding the implementation reduces the possibility that clients will become dependent on class-
implementation details.
ANS: c: Clients are usually involved in a class’s implementation.

Section 8.3 Controlling Access to Members

8.3 Q1: Which of the following class members should usually be private?
a. Methods.
b. Constructors.
c. Variables (or fields).
d. All of the above.
ANS: c. Variables (or fields).

8.3 Q2: Which of the following statements is true?

a. Methods and instance variables can both be either public or private.
b. Information hiding is achieved by restricting access to class members via keyword public.
c. The private members of a class are directly accessible to the clients of a class.
d. None of the above is true.
ANS: a. Methods and instance variables can both be either public or private.

Section 8.4: Referring to the Current Object’s Member

with the this Reference
8.4 Q1: When must a program explicitly use the this reference?
a. Accessing a private variable.
b. Accessing a public variable.
c. Accessing a local variable.
d. Accessing an instance variable that is shadowed by a local variable.

© Copyright 1992-2015 by Deitel & Associates, Inc. and Pearson Education, Inc.
ANS: d. Accessing an instance variable that is shadowed by a local variable.

8.4 Q2: Having a this reference allows:

a. a method to refer explicitly to the instance variables and other methods of the object on which the
method was called.
b. a method to refer implicitly to the instance variables and other methods of the object on which the
method was called.
c. an object to reference itself.
d. All of the above.
ANS: d. All of the above.

Section 8.5 Time Class Case Study: Overloaded

Constructors
8.5 Q1: A constructor cannot:
a. be overloaded.
b. initialize variables to their defaults.
c. specify return types or return values.
d. have the same name as the class.
ANS: c. specify return types or return values.

8.5 Q2: Constructors:

a. Initialize instance variables.
b. When overloaded, can have identical argument lists.
c. When overloaded, are selected by number, types and order of types of parameters.
d. Both (a) and (c).
ANS: d. Both (a) and (c).

8.5 Q3: A programmer-defined constructor that has no arguments is called a(n) ________.
a. empty constructor.
b. no-argument constructor.
c. default constructor.
d. null constructor.
ANS: b. no-argument constructor.

8.5 Q4: What happens when this is used in a constructor’s body to call another constructor of the same
class if that call is not the first statement in the constructor?
a. A compilation error occurs.
b. A runtime error occurs.
c. A logic error occurs.
d. Nothing happens. The program compiles and runs.
ANS: a. A compilation error occurs.

8.5 Q5: When implementing a method, use the class’s set and get methods to access the class’s ________
data.
a. public.
b. private.
c. protected.
d. All of the above.
ANS: b. private.

Section 8.6 Default and No-Argument Constructors

© Copyright 1992-2015 by Deitel & Associates, Inc. and Pearson Education, Inc.
8.6 Q1: Which statement is false?
a. The compiler always creates a default constructor for a class.
b. If a class’s constructors all require arguments and a program attempts to call a no-argument
constructor to initialize an object of the class, a compilation error occurs.
c. A constructor can be called with no arguments only if the class does not have any constructors or
if the class has a public no-argument constructor.
d. None of the above.
ANS: a. The compiler always creates a default constructor for a class.

Section 8.7 Notes on Set and Get Methods

8.7 Q1: Set methods are also commonly called ________ methods and get methods are also commonly
called ________ methods.
a. query, mutator.
b. accessor, mutator.
c. mutator, accessor.
d. query, accessor.
ANS: c. mutator, accessor.

8.7 Q2: Using public set methods helps provide data integrity if:
a. The instance variables are public.
b. The instance variables are private.
c. The methods perform validity checking.
d. Both b and c.
ANS: d. Both b and c.

Section 8.8 Composition

8.8 Q1: Composition is sometimes referred to as a(n) ________.
a. is-a relationship
b. has-a relationship
c. many-to-one relationship
d. one-to-many relationship
ANS: b. has-a relationship.

Section 8.9 Enum Types

8.9 Q1: Which statement is false?
a. An enum declaration is a comma-separated list of enum constants and may optionally include other
components of traditional classes, such as constructors, fields and methods.
b. Any attempt to create an object of an enum type with operator new results in a compilation error.
c. An enum constructor cannot be overloaded.
d. enum constants are implicitly final and static.
ANS: c. An enum constructor cannot be overloaded.

8.9 Q2: Which method returns an array of the enum’s constants?

a. values.
b. getValues.
c. constants.
d. getConstants.
ANS: a. values.

© Copyright 1992-2015 by Deitel & Associates, Inc. and Pearson Education, Inc.
Section 8.10 Garbage Collection and Method finalize
8.10 Q1: Which of the following is false?
a. Method finalize does not take parameters and has return type void.
b. Memory leaks using Java are rare because of automatic garbage collection.
c. Objects are marked for garbage collection by method finalize.
d. The garbage collector reclaims unused memory.
ANS: c. Objects are marked for garbage collection by method finalize. (Objects are marked for
garbage collection when there are no more references to the object).

Section 8.11 static Class Members

8.11 Q1: Static class variables:
a. are final.
b. are public.
c. are private.
d. are shared by all objects of a class.
ANS: d. are shared by all objects of a class.

8.11 Q2: Which of the following is false?

a. A static method must be used to access private static instance variables.
b. A static method has no this reference.
c. A static method can be accessed even when no objects of its class have been instantiated.
d. A static method can call instance methods directly.
ANS: d. A static method can call instance methods directly.

Section 8.12 static Import

8.12 Q1: Which syntax imports all static members of class Math?
a. import java.lang.Math.*.
b. import static java.lang.Math.*.
c. import static java.lang.Math.
d. None of the above.
ANS: b. import static java.lang.Math.*.

Section 8.13 final Instance Variables

8.13 Q1: Instance variables declared final do not or cannot:
a. Cause syntax errors if used as a left-hand value.
b. Be initialized.
c. Be modified after they are initialized.
d. None of the above.
ANS: c. Be modified.

8.13 Q2: A final field should also be declared ________ if it is initialized in its declaration.
a. private.
b. public.
c. protected.
d. static.
ANS: d. static.

© Copyright 1992-2015 by Deitel & Associates, Inc. and Pearson Education, Inc.
Section 8.14 Package Access
8.14 Q1: When no access modifier is specified for a method or variable, the method or variable:
a. Is public.
b. Is private.
c. Has package access.
d. Is static.
ANS: c. Has package access.

8.14 Q2: Which of the following statements is false?

a. If a program uses multiple classes from the same package, these classes can access each other's package
access members directly through references to objects of the appropriate classes, or in the case of static
members, through the class name.
b. Package access is rarely used.
c. Classes in the same source file are part of the same package.
d. Use the access modifier package to give a method or variable package access.
ANS: d. Use the access modifier package to give a method or variable package access.

Section 8.15 Using BigDecimal for Precise Monetary

Calculations
8.15 Q1: Which of the following statements is false?
a. An application that requires precise floating-point calculations such as those in financial applications
should use class BigDecimal from package java.math.
b. We use class NumberFormat for formatting numeric values as locale-specific strings.
c. In the U.S, locale, the value 15467.82 would be formatted as "15,467.82", whereas in many European
locales it would be formatted as "15.467,56".
d. The BigDecimal method format receives a double argument and returns a BigDecimal object that
represents the exact value specied.
ANS: . d. The BigDecimal method format receives a double argument and returns a BigDecimal
object that represents the exact value specied. Actually, the BigDecimal method valueOf receives a
double argument and returns a BigDecimal object that represents the exact value specied.

8.15 Q2: BigDecimal gives you control over how values are rounded. By default:
a. all calculations are approximate and no rounding occurs.
b. all calculations are approximate and rounding occurs.
c. all calculations are exact and no rounding occurs.
d. all calculations are exact and rounding occurs.
ANS: c. all calculations are exact and no rounding occurs.

Section 8.16 (Optional) GUI and Graphics Case Study:

Using Objects with Graphics
No questions.

© Copyright 1992-2015 by Deitel & Associates, Inc. and Pearson Education, Inc.
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 Horse 0·2 lb. per 100 lb. live weight.
Ass and Mule 0·16 lb. „„
Cow and Sheep 1·0 lb. „„
Goat 1·2 lb. „„
Pig 0·3 lb. „„
Rabbit 2·0 lb. „„

Other authorities, however, quote much lower quantities as

necessary to kill the horse and ox, and Pott says that in the case of
horses 150 to 180 grammes (0·33 to 0·4 lb.) is sufficient to cause
death in one-quarter to one-half an hour, without previous
symptoms. Eaten by an animal on a full stomach a small quantity of
Yew may cause little or no dangerous results.
Toxic Principle. The researches of Marmé pointed to the alkaloid
Taxine (C37H52NO10) as the toxic substance. Later investigations of
Thorpe and Stubbs confirmed this view, and it is generally agreed
that this substance is the toxic principle, though doubts as to its
being the only poison have been expressed. Taxine has a bitter
taste, is a heart depressant, and may cause death from suffocation.
The yew also contains a considerable quantity of Formic Acid, and
the acrid, irritant volatile Oil of Yew.
Thorpe and Stubbs (Trans. Chem. Soc., 1902) found in the fresh
leaves of the common Yew from 0·1 to 0·18 per cent. of Taxine. In
an investigation of the Irish Yew (T. baccata var. fastigiata) Moss
found Taxine present as follows:—

Leaves from female tree, fresh 0·596 per cent.

Leaves from female tree, fresh 0·623 „
Seeds from fruit of same tree 0·079 „
Another female tree—leaves 0·323 „
Another female tree—seeds 0·082 „

In the leaves of the male common Yew Moss found 0·082 per
cent. of Taxine, or less than one-half the quantity found by Thorpe
and Stubbs.
Symptoms. The Yew is irritant and narcotic, and the poison is not
cumulative, but on the other hand rapidly effective, so that animals
may die apparently suddenly, no previous symptoms having been
observed.
When small quantities only have been taken the closest attention
is necessary to discern the symptoms, which simply consist in a little
excitement with a slight rise in temperature.
With larger (but not fatal) quantities the first symptom,
excitement, is more pronounced and is followed by nausea, and
(where possible) vomiting. There is a pronounced slackening of
respiration and circulation, the pulse being small, slow, and difficult
to perceive, and the movement of the flanks very slow; sensibility is
diminished. There is a fall in temperature, the skin and extremities
being cold. The head is lowered, the eyes are closed and there is
decubitus. In some cases pregnant animals have aborted. In the
horse there are muscular tremors and frequent urination. In cattle
and sheep rumination is suspended and there is more or less
pronounced tympanites, with eructation, nausea, and sometimes
vomiting. Pigs bury the head in the litter and sleep, their sleep being
interrupted from time to time by nausea and groaning; or the
animals rise, stagger about, and lie down again.
With fatal quantities the foregoing symptoms may be followed by
coma, with death in two hours or more after the poisoning, but more
generally and usually in horses, asses, and mules (but also in cattle)
there is no period of coma, the excitement is less pronounced and
often unobserved, and death appears very sudden. The animals
stop, shake their heads, respiration is modified, there is falling, and
death (sometimes with convulsions) results from cessation of the
heart’s action (Cornevin).
The symptoms given by Müller are roaring, torpidity, stupefaction,
laboured breathing, convulsions and death in from ten minutes to an
hour in the worst cases; or where the course of poisoning is slower,
there is salivation, nausea, vomiting, bloating, retardation of pulse
and respiration, great giddiness and stupefaction, diabetes and
hæmaturia.
The rapidity of the poisoning is confirmed by cases noted in the
veterinary journals. Lander shows that the effects often only appear
in cattle when chewing the cud; whilst quietly chewing, they drop as
if shot. In some examples the animal died while eating the plant, or
was found to have fallen and died suddenly and without evidence of
a struggle. The animal in some cases will stop suddenly whilst
working, start blowing and trembling, stagger, fall on its haunches,
then on its side, and die quietly. Death occurs in about five minutes
with symptoms resembling apoplexy. A colt died after 16 or 17
hours; the plant was taken on a full stomach, but paralysis of the
alimentary system with stoppage of digestion immediately ensued.
In the case of pheasants there was acute inflammation of the
small intestines (Tegetmeier).
REFERENCES.

4, 16, 49, 73, 81, 84, 100, 128, 130, 141, 144, 161,
170, 189, 190, 205, 213, 239, 240, 256.
 AROIDEÆ.
Cuckoo Pint (Arum maculatum L.). The well-known Cuckoo Pint,
or Lords and Ladies, is to be regarded as highly poisonous, and
children have died from eating the berries. Animals have
exceptionally eaten the plant, but no record of death has been
found, as it does not appear to be taken in sufficient quantity.
Cornevin records that pigs have eaten the roots, and suffered in
consequence, though the results were not fatal. All parts of the plant
are poisonous, though the virulence is lost on drying. The plant is
acrid, and emits a disagreeable smell when bruised. In Gerarde’s
Herball the following passage occurs: “The most pure and white
starch is made from the rootes of the Cuckowpint; but most hurtfull
for the hands of the laundresse that hath the handling of it, for it
choppeth, blistereth, and maketh the hands rough and rugged, and
withall smarting.” In Dorset the tuber-like corms have been
macerated in water, dried and powdered, and eaten under the name
Portland Sago or Portland Arrowroot, the poisonous property being
dissipated.
Toxic Principle. The Cuckoo Pint does not seem to have received
much attention in this connection, but the poisonous principle is
believed to be a Saponin.
Symptoms. The juice acts as an irritant when in contact with the
mucous membrane. When a pig has eaten several roots rich in sap,
the mouth and tongue redden and tumefy, there is salivation, and
swallowing is difficult on account of the inflammation at the back of
the mouth. Introduced in small quantity into the digestive tract it
acts as an irritant and purgative, and sometimes causes vomiting.
Severe intestinal pains, excitement, some muscular contraction of
the limbs, rocking of the head, and superpurgation with tenesmus
are also symptoms which have been observed. The intestinal pains
continue for some days and the appetite is small. Cornevin states
that animals never take a sufficient quantity to cause fatal poisoning,
but according to Lander, if a dangerous quantity is taken,
convulsions, exhaustion, and death from shock may possibly follow
the foregoing symptoms.
A case in which a horse was poisoned through a wound being
washed with a decoction of arum leaves is cited by Müller. There was
much local swelling, trembling, and rapid breathing, and the heart
beat strongly; the animal died on the third day.
REFERENCES.

73, 81, 130, 141, 170, 190.

 CHAPTER VI
DIOSCORIDEÆ.

Black Bryony (Tamus communis L.). The stem and foliage of

Black Bryony are apparently harmless, being browsed by sheep and
goats with impunity, but the scarlet fruits are decidedly poisonous
and the starchy root is acrid and purgative.
Toxic Principle. This is probably the glucoside Bryonin, which
occurs in Bryonia dioica (p. 35).
Symptoms. Cornevin, in citing experiments on animals, states that
small quantities of the fruits cause uneasiness, somnolence, and
difficult locomotion. Larger quantities cause vomiting, intestinal
pains, and paralysis of hind quarters. Death is rapid. Müller, however,
remarks that paralysis of the hind quarters and convulsions may
result from small quantities, large quantities causing in addition
inflammation of the stomach and intestines.
REFERENCES.

73, 190.
 LILIACEÆ.
Herb Paris (Paris quadrifolia L.). Owing to its habitat—damp
woods—it is unlikely that stock will eat this plant, but it may be
possible where fields border open woods in which it grows. No
records of stock poisoning have been met with, but cases of
poisoning in man are recorded, one due to eating a considerable
number (30 to 40) of the berries, and symptoms of poisoning in a
child four years of age who had eaten a few berries. In smaller
quantities they are very poisonous to poultry. All parts are stated to
be poisonous, especially the berries. Fatal poisonings are nil, or very
rare if recorded.
Toxic Principle. Walz isolated the glucoside Paridin; and Esser
states that the toxic property is due to a Saponin,—the bitter irritant
glucoside Paristyphnin (C38H64O18), which is convertible into Paridin
(C16H28O7 + 2H2O) and sugar.
Symptoms. The plant is emetic, purgative, intensely acrid, and
narcotic. Poisoning up to the present only appears to have been
recorded in fowls, the symptoms being intense local inflammation,
narcotic effects, vomiting, colic, diarrhœa, stupefaction, convulsions,
and paralysis (Müller).
REFERENCES.

4, 16, 73, 76, 81, 130, 141, 190.

Lily-of-the-Valley (Convallaria majalis, L.). This beautiful plant is
only likely to induce poisoning of domestic animals at very rare
intervals, as it occurs wild in only a few woods from Moray
southwards, being, however, abundant in some districts. All parts are
stated to be poisonous, especially the flowers. It has an acrid, bitter
taste. Few cases of poisoning are recorded. Sheep and goats are
believed to eat the leaves with impunity. The extract is so poisonous
that four drops injected into the blood stream sufficed to kill a dog in
ten minutes (Cornevin). The leaves have been known to kill geese
and fowls.
Toxic Principle. All parts of the plant contain the bitter poisonous
glucoside Convallamarin (C23H44O12), the glucoside Paridin
(C16H28O7 + 2H2O), and the glucoside Convallarin (C34H62O11)—the
first a dangerous purgative, and the last a cardiac poison resembling
Digitalis. Convallamarin is a very poisonous crystalline substance,
with at first a bitter and afterwards a sweetish taste.
Symptoms. The action of this plant on the animal organism is not
yet clearly known, but it is stated to have marked emetic and
purgative action. Taken in moderate quantities a period of
retardation of the heart and lung action is followed by a period in
which the heart action is intermittent, and there are stoppages in
respiration, and vomiting. Taken in large quantities, the first of these
periods is extremely short, the pulse soon becomes rapid and small,
respiration is quickened, and the heart action ceases (Cornevin).
Pott observes that the leaves cause stupefaction, convulsions, and
death after a few hours in the case of geese. He cites a case in
which ten fowls ate the leaves and nine died.
REFERENCES.

52, 73, 76, 81, 190, 203, 205, 213.

Meadow Saffron (Colchicum autumnale L.). The Meadow
Saffron, Autumn Crocus, or Naked Ladies, as it is variously named,
occurs in meadows in many districts in England and Wales. All parts
are poisonous, both in the green state and when dried, as it possibly
may be, in hay. It has caused extensive losses of live stock, and the
greatest care should be taken to eradicate it from grass land. The
leaves and seed-vessels are produced in spring, and the flowers
from August to October—and it is at these two periods that cases of
poisoning by this plant are most frequent, though, as stated, it may
be included in hay. Many horses, cattle, and pigs have been killed by
Meadow Saffron, though cattle commonly avoid it. Sheep and goats
are believed to be very slightly affected. Children and fowls died at
Schorren (Canton Berne) from eating the seeds, and there have
been many cases of human poisoning due both to eating the seeds
and the bulbs. In Staffordshire, Mr J. C. Rushton reported some
years ago[4] that in one year a farmer lost seventeen milking cows;
in 1908 he lost seven calves; and in 1909 he lost a number of sheep
and cows. It was then discovered that the field in which the animals
grazed contained “any quantity of Meadow Saffron and Water
Hemlock,” and this was the cause of the losses. Horses and cattle
are more commonly poisoned than other domesticated animals.
Johnson and Sowerby record the case of a woman who ate the
corms in mistake for onions at Covent Garden, and died; and state
that deer and cattle have been killed by the leaves. Kanngiesser
notes that this species is the most toxic of German plants, and that
in cases of human poisoning the mortality is 90 per cent., children
being chiefly affected. Cornevin’s experiments showed that 8 to 10
grammes of green leaves per kilogramme of live weight—say 3 to 5
lb. for an average cow—was sufficient to kill ruminants; while 30
centigrammes of corms per kilogramme of live weight sufficed to kill
pigs—say 4½ oz. for a pig of 200 lb. live weight. Barret and
Remlinger (Veterinary Journal, 1912, p. 306) record the sudden
illness of 31 out of 51 cattle, and 5 of them died.
4. Staffordshire Weekly Sentinel, Aug. 21st, 1909.
The toxic principle is cumulative, that is, small quantities of the
plant eaten regularly may result in poisoning, owing to the poison
being slowly eliminated by the kidneys. Indeed, cases have been
recorded in which the poison has been secreted and eliminated in
the milk of cows and so has caused poisoning of both calves and
infants.
Toxic Principle. Meadow Saffron contains in all parts the acrid,
poisonous alkaloid Colchicine (C22H25NO6) stated by Esser to occur
to the extent of 0·2 per cent. in the corms, 0·4 to 0·6 per cent. in
the seed coats, but only traces in the leaves. Hertel obtained 0·38 to
0·41 per cent. of alkaloid from the seeds, Farr and Wright from 0·46
to 0·95 per cent., and Carr and Reynolds 0·12 to 0·57 per cent.; the
U.S. Pharmacopœia, 1905, required a Colchicine content of 0·45 per
cent. in the seeds, and 0·35 per cent. in the corms (Allen).
Symptoms. After small, but not fatal doses there is loss of
appetite, suppression of rumination, salivation, light colic, diarrhœa
and voiding of small quantities of urine. Blood has been observed in
the milk of affected cows. Larger and fatal quantities cause total loss
of appetite and sensation, stupefaction, loss of consciousness,
dilatation of pupils, unsteady gait, and even paralysis of limbs,
sweating, severe colic, and bloody diarrhœa, strangury and bloody
urination; rapid, small, and finally imperceptible pulse, laboured
breathing; and death in from one to three days. Where recovery
takes place it is very slow (12 to 14 days according to Cornevin).
Cornevin draws attention to the fact that, as the symptoms do not
occur until several hours after ingestion, by which time the poison
must be partly distributed, the poison is very dangerous and difficult
to combat, attempts at vomiting or evacuation, whether
spontaneous or caused therapeutically, having little chance of ridding
the organism of the poison. Cornevin’s account of the symptoms
shows that at first there is abundant salivation, with constriction of
the throat, and dysphagia; then nausea with vomiting; colic;
abundant, repeated and diarrhœic evacuations, which at the end
become dysenteric with painful tenesmus; abundant urination; short,
accelerated and difficult respiration, with incoordination in the
thoracic and abdominal movements. The circulatory functions are
modified only in fatal cases, when the pulse is small and intermittent
towards the end. There is finally a notable drop in temperature,
shown by the coldness of the skin. Death occurs in from 16 hours to
6 days after ingestion. During the last few hours the animals are
stretched at full length and are incapable of getting up. There may
be prolapsus of the rectum; the eye is deeply sunk; sensibility is
deadened and death is due to stoppage of respiration.
In the horse, there are spasmodic movements of the hind-quarters
and excessive excitement of the urinary genital organs. In cattle
there is cessation of rumination, grinding of teeth, dryness of
muzzle, ptyalism, groaning, painful colic, dysentery, deeply sunken
and watery eyes, anus wide open, and evacuation of very fœtid,
blackish, glareous matter round the excrement. In cows there may
be suppression of milk, and abortion. In the pig there is abundant
salivation and vomiting, and the animal keeps its snout buried in the
litter. There is also extremely fœtid diarrhœa, with dysentery.
REFERENCES.

4, 16, 27, 73, 81, 128, 130, 141, 148, 151,

190, 192, 203, 217, 255.
 GRAMINEÆ.
Darnel (Lolium temulentum L.). The grass known as Darnel, of
the same genus as rye-grass, has been recognized for centuries as a
harmful species, and it is considered by some authorities that it is
really the tares of Scripture which the enemy sowed among the
wheat. Its effect on eyesight was known to the ancients[5], and its
objectionable character was noted by Shakespeare:—
5. E.g. Ovid says “Let the fields be clear of darnel that weakens the eyes.” In
Plautus’ comedy, The Braggart Soldier, one servant says to another, “’Tis a wonder
that you are in the habit of feeding on darnel with wheat at so low a price.” “Why
so?” “Because you are so dim of sight.” [Agric. Jour. Union of S. Africa, Jan. 1914,
p. 82.]

“Want ye corn for bread?

I think the Duke of Burgundy will fast
Before he’ll buy again at such a rate:
’Twas full of darnel: Do you like the taste?”
—I Henry VI, Act III, Sc. 2.

Its effect when mixed with flour was also referred to by Gerarde
(1597): “The new bread wherein Darnell is, eaten hot, causeth
drunkenness; in like manner doth beere or ale wherein the seede is
fallen, or put into the mault.”
Before the seeding stage is reached Darnel seems to be quite
suitable as a food for stock, only the seed or grain being poisonous,
and this not invariably so. The chief danger perhaps is that the grain
may not be thoroughly removed from cereal grains, and may thus
find its way into bread or cereal stock foods. Though it has caused
many cases of human poisoning, fatal results seem to be rare: Dr.
Taylor could record no fatal case up to 1859. Darnel mixed with
barley caused the poisoning of pigs (Veterinarian, 1842). Johnson
and Sowerby (1861) state that Darnel has in several cases proved
fatal to horses and sheep. The same authorities quote a case in
which 80 inmates of Sheffield Workhouse were attacked by violent
vomiting and purging from the use of oatmeal containing Darnel. At
the Veterinary School at Lyons a horse was killed by giving it 2
kilogrammes (4·4 lb.) of Darnel. Cornevin concluded that the
amounts of Darnel necessary to kill certain animals would be as
follows:—

Horse 0·7 lb. per 100 lb. live weight.

Ruminants 1·5 to 1·8 lb. per 100 lb. live weight.
Poultry 1·5 to 1·8 lb. „„
Dog 1·8 lb. „„

He found pigs very little affected. As regards man 30 grammes (1

oz.) of the flour appear to be about the most that can be taken
without showing dangerous symptoms.
The presence of Darnel flour in flour of the cereal grains may be
determined by an examination of the starch granules, which are
given by Cornevin as only 5 to 8µ; in diameter (compared with 25 to
4µ for rye), simple in general, but sometimes in groups of 2 to even
5, polyhedral or partly rounded, with a nucleus or fusiform nucleal
cavity, and readily coloured blue with iodine; they resemble those of
maize but are only about one-eighth the size.
Toxic Principle. The grains only are harmful, and contain the
narcotic alkaloid Temuline (C7H12N2O), which Hofmeister showed to
be a strong nerve poison, and which is said to occur to the extent of
0·08 per cent. in the seeds. Other authorities impute the toxic
property to Loliine, while Smith states that the toxic principle is
Picrotoxin. In relation to the grain fungal hyphæ have usually been
found, though not invariably, 20 to 30 per cent. of the plants
sometimes being free from it. The fungus (Endoconidium
temulentum) is propagated vegetatively by means of mycelium. It
appears to live symbiotically in the maturing grain, and perhaps to a
slight extent renders possible the assimilation of nitrogen from the
atmosphere; but Freeman observed that though generally
stimulating to the Darnel, it is occasionally injurious to it. Esser sums
it up by saying that according to most authorities who have
investigated Darnel the fungus alone contains the toxic substance—
the Temuline—and hence the grains in which the fungus does not
occur should be harmless. The fungus is found in Darnel grain in all
countries—Chile, Brazil, S. Africa, Persia, Spain, France, Sweden,
Germany, etc. So far as can be ascertained there have been no
feeding experiments to determine the difference in toxic character
between fungus-infested and fungus-free grains. The dangerous
properties are said to be most pronounced in wet seasons.
Symptoms. In France Darnel is called Ivraie, because, when
brewed with barley, it acts as a narcotic intoxicant.
Darnel poisoning induces giddiness, drowsiness, uncertain gait,
and stupefaction (Müller), and, in the older animals, vomiting,
convulsions, loss of sensation and death (Pott).
The symptoms in the horse are dilatation of pupils, vertigo,
uncertain gait, and trembling. The animal falls, the body is cold and
the extremities are stiff, respiration is laboured, the pulse is slow and
small, and there are convulsive movements of the head and limbs.
There is rapid enfeeblement, and death may occur within thirty
hours.
In pigs, foaming, convulsions and paralysis have been observed;
the stomach and intestines were inflamed and the lungs congested.
REFERENCES.

4, 16, 73, 81, 106, 128, 130, 141, 190, 203, 204,
205, 213, 233, 235, 254.
 EQUISETACEÆ.
Horsetails (Equisetum sp.). A very great deal has been written
on the subject of Equisetosis or Equisetum poisoning, and even at
the present day opinion is divided as to which species are poisonous
and to what extent. From the time of Linnæus there has been
uncertainty as to the species, which has generally been given as E.
arvense. Two German papers, by Weber and Lohmann respectively,
published by the German Agricultural Society in 1903 and 1904,
have done much to remove doubt on the matter, but cannot be said
to have settled the question absolutely. These two papers seem to
have been overlooked by some recent writers on the subject, but
Lohmann’s appears to be the most authoritative paper yet written.
Both are referred to below.
It seems to be definitely proved that certain species of Equisetum
really are poisonous, hesitating statements notwithstanding. Chesnut
and Wilcox state that there are cases of poisoning of both horses
and sheep by E. arvense in the United States, though they are not
common, and the opinion is expressed that “the plant, if deleterious,
is evidently so only on account of its harsh scouring action in the
mouth and intestinal tract.” On the other hand Rich and Jones record
poisoning of horses by E. arvense in hay, but while adding that
horses seem to develop a depraved appetite for the weed, they state
that they have no evidence that horses grazing upon the green plant
are poisoned. Güssow’s experience has been that cattle do not suffer
any inconvenience at all from this species, or only very slight
disturbance of the digestive organs, but that horses are
conspicuously subject to fatal poisoning by it. Examination of hay on
which a considerable number of poisoned horses were fed revealed
in every case the presence of E. arvense. When the food was
changed, horses, if not too seriously affected, made rapid recovery.
(Treatment suggested is to change to easily digested food, give a
sharp purgative, and follow by small doses of nux vomica three
times a day.) Pammel says that in recent years a disease of horses in
Vermont has been attributed to hay and fodder containing the weed;
that it is proved by experiment that when ingested in sufficient
quantity E. arvense is capable of causing fatal poisoning in horses,
and is at times the cause of extensive losses; and that young horses
are most susceptible, while grain-fed horses are less susceptible
than others. He adds that sheep are supposed to be slightly
affected, but cattle eat hay in which it occurs in large proportion
with impunity.
Coming to the two German reports, it is stated by Weber (1903)
that E. palustre contains a specific poison for cattle and other
ruminants, but sheep and goats are able, owing to their fine
muzzles, to separate it in fodder, and hence suffer less. Horses and
pigs, he says, seem to suffer very little. Young animals and stock,
from districts where the species does not occur, suffer more than
those from places where it occurs—the latter appearing to learn
early to avoid it.
Lohmann conducted feeding experiments with guinea-pigs with E.
arvense, E. palustre, E. pratense, E. sylvaticum, E. maximum, and E.
heleocharis (not British). He also fed E. arvense and E. palustre to
horses, cattle, sheep, pigs, and geese in considerable quantities for
many days on end; and made experiments with aconitic acid on
guinea-pigs and horses. The feeding experiments with guinea-pigs
showed that of the species named only E. palustre and to a less
extent E. sylvaticum are poisonous plants (to guinea-pigs). With the
large domestic animals the experiments showed E. arvense to be a
harmless plant, and E. palustre to be really injurious to cattle but
avoided by other stock. Lohmann considers that the many
statements in the literature agree in part with this result, and that
the divergent observations may be traced to various causes, among
which perhaps an abnormal chemical composition of the weed fed
plays a principal part.
In this connection, however, the American results must be
carefully borne in mind, and E. arvense must not too hastily be
regarded as blameless.
 Toxic Principle. It was for some years believed that the apparent
toxic symptoms induced by Horsetails were due to Silica or to
Aconitic acid—the latter a substance found by Matz and Ludwig. The
conclusion come to by Weber, however, was that the poisoning by E.
palustre is of an organic character, not due to silica. The young
shoots, which contain little silica, were found in general to be much
more poisonous than the old plants, which contain much silica. It
was long since found by Wiggers that dried plants of E. palustre
contained 8·88 per cent. of silica, but all species contain this
substance in greater or less degree, and it varies considerably in
amount, even in the same species. The feeding experiments
conducted by Lohmann, with certain species of Equisetum, and the
observed symptoms of illness after the consumption of some of
them, particularly E. palustre, serve to show that the ill effects are
neither to be attributed to greater or less digestibility, nor to the
silica present. Neither are the aconitic acid and other organic
substances, in part found in previous investigations, responsible for
the poisoning. However, an active compound named Equisetine, a
substance belonging to the alkaloid group, was isolated; this occurs
usually, perhaps only, in E. palustre, at any rate in sufficient quantity
to be dangerous to animals. Lohmann then, following up the
investigations of Paucerzynski, Matz, Meyer, Weber and others,
ascertained definitely that E. palustre contains an alkaloidal nerve
poison, to which the name Equisetine was given, and the
experiments were held to decide that this is the poisonous substance
in this species. (As stated above, E. arvense was held to be
harmless.)
Symptoms. At first, excitement and anxiety, followed by
uncertainty of movement, reeling and staggering; paralysis of hind
limbs at least, falling, possibly general paralysis, insensibility to
external irritants, unconsciousness, and coma. Pulse accelerated,
appetite at first normal, but in course of time great disturbance of
nutrition; sugar in the urine. Course sometimes very acute, death
occurring in a few hours, but sometimes protracted (two to eight
days), and at times even chronic (one to several weeks).
 In cattle, after excessive eating, continuous diarrhœa is
characteristic, with paralysis; while, if the food be persisted with,
cachexia and hydræmia combined with weakness bordering on
paralysis make their appearance (Friedberger and Fröhner, via
Pammel). In addition to cachexia, Pott also mentions colic, stoppage,
bloody urination, abortion, and loss of teeth.
Young animals appear to succumb sooner than older ones, while
grain-fed animals are more resistant than others. Referring to E.
arvense Pammel says it produces paralysis of the rear extremities,
and when death occurs spasms are noted. In relation to the
poisoning of horses by the same species in hay Rich and Jones note
unthriftiness, the animal appearing thin and the muscles wasted. In
from two to five weeks, according to the age of the horse and the
manner of feeding, the animal begins to lose control of the muscles,
and there is swaying and staggering, though the eye is bright and
the appetite good. If the plant is regularly ingested the horse loses
the power of standing, becomes nervous, struggles to rise, the legs
become more or less rigid, and at times all the muscles of the body
seem convulsed. Even in this condition one well-nursed patient lived
two weeks. The horses are generally willing to eat, although unable
to rise, but become sore and tired from struggling, finally dying from
exhaustion. Life is much prolonged by turning from side to side three
or four times in twenty-four hours, thus preventing congestion. The
pulse is slow till near the end, when it is rapid and weak; the
temperature is below normal at first, but when the animal is down
there is fever; the extremities are usually cold; and the lining
membrane of the mouth, nose, and eye becomes pale.
Of Equisetum sp. Stebler and Schroeter say that they induce
diarrhœa in cattle, which become poor, and in cows the milk yield is
checked or ceases. Weber also refers to the effect on milk yield of E.
palustre, which he says causes the milk of affected cows to become
watery, poor in fat, and gives rise to a greasy, unappetising butter,
while the yield may soon quite fail.
REFERENCES.
2, 20, 57, 111, 176, 203, 204, 213, 220, 221, 222, 237, 260, 261.
 FILICES.
Bracken (Pteris aquilina L.). The Bracken, Brake Fern, or “Fern” is
of very considerable importance to farmers for four reasons: (1) It is
a most pernicious weed; (2) it forms an excellent litter for stock and
treads down into good manure; (3) it is said to have been
successfully converted into silage; but (4) it has been accused of
poisoning cattle.
In regard to possible poisonous properties, it must be said that the
facts are at present somewhat uncertain, but a number of
authorities clearly regard the Bracken as poisonous. (a) Müller
(1897) records the poisoning of horses which ate it for some weeks
with chaff—and some died. (b) Chesnut and Wilcox (1901) say that
cases of poisoning of horses and cattle have been reported from
England and a few localities in the United States. (c) Pott states that
when eaten in quantity by cattle Bracken causes hæmaturia, and in
horses nervous symptoms (brain trouble), sometimes with fatal
effects. (d) Pammel also remarks on the believed poisonous
character of this plant. (e) In view of its suspected poisonous
character feeding experiments were conducted by the Board of
Agriculture and Fisheries with a large quantity of Bracken, but the
results were negative, yielding no experimental proof of the plant
being poisonous. One animal—a heifer—consumed 60 lb. of Bracken
between Aug. 14 and Aug. 20, and after two meals containing about
30 lb. of Bracken showed only symptoms of indigestion. After the 60
lb. there were no symptoms of illness. It has been thought possible
that the so-called Bracken poisoning is due to Potentilla Tormentilla
(q.v.).
In 1893 Storrar dealt with the question and expressed the view
that any disorder due to Bracken was probably not a toxic effect but
a digestive trouble simply (Jour. Comp. Path., 1893).
 Toxic Principle. Continental authorities say that Bracken contains
the poisonous Pteritannic acid, which is identical with the Filicic acid
of the Male Fern (Aspidium filix-mas).
Symptoms. In the cases of horses which died Müller gives the
symptoms as timidity, slower movement or action, loss of balance,
dilated pupils, reddening followed by yellowing of the conjunctivæ,
and slowing of the pulse.
Pammel notes Bracken as an astringent and anthelmintic, and also
says it causes enteritis, spasms, and paralysis.
REFERENCES.

10, 25, 57, 190, 203, 204, 213.

 FUNGI .
[6]

Ergot (Claviceps purpurea). This fungus, parasitic on rye and a

number of grasses, has long been known to induce distinct
poisonous effects on man and domestic animals when ingested in
sufficient quantity.
6. Poisonous parasitic fungi generally are not dealt with in this volume, but
ergot is included because it is widely distributed and perhaps the best known,
while its effects have been fully studied.
Ergot must be regarded as a cause of abortion in cows, though
somewhat divergent views have been expressed as to the facts,
some authorities considering the belief well founded, while others
consider that there is little ground for it. It is quite clear, however,
that when taken in sufficient quantity Ergot induces serious
poisoning of domestic animals. Horses have died in two or three
days from eating ergoted hay and wild rye. Extensive outbreaks of
ergotism have occurred in the United States, and serious losses have
been recorded in the Central and Western States. Ewart remarks
that “a comparatively small number of fresh Ergot grains suffice to
injure or kill a horse, cow, or sheep.” The effects of the poisoning of
animals will be found under Symptoms below.
Toxic Principle. Ergot of rye is used in medicine. It contains 0·20 to
0·25 per cent. of Ergotinine. In the British Pharmaceutical Codex,
1911, the grains (sclerotia) of Ergot (see Frontispiece) are described
as longitudinally furrowed, 1 to 4 cm. long, slender, curved, tapering
to both ends; they break with a short fracture, and are somewhat
triangular in transverse section; they have a characteristic and
disagreeable odour and taste, are dark violet to black in colour, and
whitish within. Ergot contains the physiologically active alkaloid
Ergotoxine or Hydroergotinine (C35H41O6N5), also known as
amorphous Ergotinine, and, when formerly obtained in an impure
state, as Cornutine and Ecboline. It is the hydrate of the crystalline
base Ergotinine (C35H39O5N5). There are also other physiologically
active constituents derived from amino-acids.
Symptoms. In man Ergot has induced two types of epidemic
ergotism, caused by the prolonged use of ergoted rye bread. The
two forms are rarely or never found together. One is a gangrenous
form characterized by agonizing pain in the extremities, followed by
dry gangrene of the peripheral parts of the body. The second type of
ergotism is much more rare—a nervous epidemic characterized by
paroxysmal epileptiform convulsions.
Owing to the fact that at the outset ergotism causes irritation in
the hands and feet it is termed “Kribbelkrankheit” in Germany.
The three substances noted above as isolated by Kobert are stated
to cause poisoning—the first producing inflammation of the serous
and mucous membranes, disintegration of the red blood cells, and
widespread ecchymoses; the second excites the central nervous
system and causes general convulsions; and the last induces
gangrene.
In one case a horse ate ergoted hay: next day the left hind leg
was stiff, and moist with cold sweat; on the second day it was badly
swollen and gangrene of all the tissues became apparent, and after
the skin of the leg and a considerable part of the muscular tissue
had sloughed off the animal died on the third day. In other cases
horses showed symptoms twenty-four hours after eating ergoted
hay: fatigue, indisposition to work, cold sweat, particularly on the
neck, paralysis of the tongue and muscles concerned in swallowing,
and then generalized paralysis, very slow and deep respiration,
subnormal temperature, normal pulse at first and then weaker till
scarcely distinguishable, death in six or eight hours (Chesnut and
Wilcox).
According to Pammel ergotism manifests itself among animals
chiefly in the chronic form, the poison being acquired in small
amounts and accumulation taking place slowly. Two distinct forms of
the disease are recognized, the spasmodic and gangrenous.
“Symptoms referable to the digestive tract, such as nausea,
vomiting, colic, diarrhœa, or constipation occur in both forms.
Pregnant animals very frequently abort.”
“In the spasmodic type of the disease, symptoms due to
overstimulation of the central nervous system appear. These are
tonic contraction of the flexor tendons of the limbs, anæsthesia of
the extremities, muscular trembling, general tetanic spasms,
convulsions and delirium. Death usually occurs from secondary
causes.”
“Gangrenous ergotism is characterised by coldness and
anæsthesia of the extremities, followed ultimately by dry gangrene
of these parts. The effects of this dry gangrene are often very
serious and amount to sloughing of the feet, tips of the ears, tip of
the tail, shedding of the hair, teeth, etc. Death takes place from
exhaustion.
“Acute poisoning is characterized by vomiting (in dogs), profuse
salivation, dilatation of the pupils, rapid breathing and frequent
pulse. The animal cries out, has convulsive twitchings, staggering
gait, paraplegia, intense thirst and coma, terminating in death.”
In an extensive outbreak of ergotism in the United States in 1884
Law and Salmon reported as a prominent symptom ulceration of the
mucous membrane of the tongue and mouth cavity, this and lesions
on the extremities giving the appearance of foot-and-mouth disease.
Affected animals showed weakness, dullness, and paralytic
conditions of certain groups of muscles. When in pregnant animals
the uterus is acted upon, labour pains occur, and the fœtus is
expelled. The straining in those cases is often very painful and may
be so severe that prolapsus of the uterus or even the rectum is the
result. When Ergot produces gangrene, it usually affects the
extremities, like the lower parts of the legs, the ears, tail or teats in
cattle, and the comb, wattles, toes, wings or tongue of poultry. It is
preceded by redness, coldness, and painful swelling of the parts
affected. After a while sensibility of the dying region is lost and the
line of demarcation between it and the living tissue becomes
manifest. The dead portion commonly dies and is cast off. In some
cases the gangrene is accompanied by symptoms of a septic nature.
 “The possible result of the poisoning depends largely on the
amount of Ergot taken and on the severity of the symptoms
produced thereby. When small amounts are taken and only a slight
dullness or digestive disturbance results the outlook may be quite
favourable. Even Ergot abortion with rather severe symptoms usually
is followed by recovery, but in the gangrenous cases, fatal
terminations are common. The animals which through this cause
have lost one or more parts are not only crippled, but septic or
embolic complications may lead to a fatal termination. Paralytic
cases do not permit of a favourable prognosis, especially if muscle
groups containing important functions are involved.” (N. Dakota Exp.
Sta. Rept.)
REFERENCES.

1, 4, 13, 16, 35, 57, 81, 82, 128, 154, 161, 203, 242, 251.
 CHAPTER VII
PLANTS SUSPECTED OF BEING POISONOUS.

A very large number of plants have at various times been

suspected of possessing poisonous properties and causing harm to
live stock. Of these it is quite probable that many are in practice
entirely harmless, but some must be included as possibly
deleterious, complaints having been made which vary in gravity from
a slight irritation to causing death.
Purging Flax (Linum catharticum L.). It is perhaps doubtful
whether this plant is really poisonous unless taken in considerable
quantity by animals—as it is quite unlikely to be. It may, however, be
included here, as it is stated to contain a glucoside which is
purgative and which on fermentation yields prussic acid.
Furze or Gorse (Ulex europæus L.). In view of the fact that
Gerrard isolated from the seeds of Gorse the alkaloid Ulexine, which
is identical with Cytisine (p. 27) and that the alkaloid is also
contained in less quantity in the bark of young shoots, this plant has
been suspected of possessing toxic properties. Experiments (179)[7]
with the alkaloid definitely showed it to be a nerve and muscle
poison, 3 milligrammes having killed a chloroformed cat with
convulsions in three minutes, though the animal could be kept alive
as long as artificial respiration was kept up. As, however, Gorse has
long been used very widely and in considerable quantities as a
fodder the percentage content of the alkaloid must in general be
exceedingly small, and no harmful effects need be feared from the
consumption of the cut and bruised plant. Possibly the seeds might
prove injurious if eaten in quantity.
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