Human Resource Development 5Th Edition Werner Test Bank Full Chapter PDF

Human Resource Development 5th
Edition Werner Test Bank

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APPENDIX 7-1
MORE ON RESEARCH DESIGN
TRUE/FALSE
1. A control group is a group of people of the same age as the trainees.
ANS: F PTS: 1 DIF: Moderate REF: Page 233

NAT: AACSB Analytic | HRM
2. A control group is just a second group of trainees

3. Ideally, the control group and the training group have the same scores before training
ANS: T PTS: 1 DIF: Moderate REF: Page 233

4. Internal validity deals with the question - could something besides the training program have caused the observed change to
occur.

5. External validity means you are comparing your results to those of similar size organizations.

6. History means that unrelated events occur during the training process that influence the training measurements.

7. Statistical power is the probability of concluding there is a difference between the training and the control groups when such a
difference actually exists.

8. A case study involves training followed by post training measurement.

9. Relational research involves measuring two or more variables to see if they are measuring the same thing.

10. Sackett and Mullen begin their analysis of nonexperimental research design by asking the question “How much change has
occurred”.

167
168 Chapter 15—HRD and Diversity: Diversity Training and Beyond
MULTIPLE CHOICE
1. Which of the following is not a form of research design validity?

a. Internal c. Statistical conclusion
b. External d. Statistical initial
ANS: D PTS: 1 DIF: Moderate REF: Page 229

2. Internal validity can be affected by all of the following, except:

a. History c. Differential selection
b. Maturation d. Statistical abnormality

3. Internal validity can be affected by all of the following, except:

a. Instrumentation c. Differential investigation
b. Testing d. Experimental mortality
ANS: C PTS: 1 DIF: Moderate REF: Page 230

4. Maturation refers to:

a. Gaining job experience
b. The effect of a pretest on a posttest score
c. Differential loss of respondents from various groups
d. Using different procedures to select individuals for experimental and control groups
ANS: A PTS: 1 DIF: Moderate REF: Page 230

5. Differential selection refers to:


6. Testing refers to:

ANS: B PTS: 1 DIF: Moderate REF: Page 230

7. A case study research design:

a. Is easy to use to evaluate training
b. Is questionable since there is no pre training information
c. Measures only results
d. Is very commonly used to evaluate training

168
8. A quasi-experimental research design could be:
a. A non equivalent control group
b. A time series
c. A pre post test
d. Both A and B are quasi-experimental designs

9. Collecting data in a pretest and posttest design allows us to:

a. Be certain the training caused any change
b. See what has changed after training
c. Develop the cost effectiveness of our training
d. Know whether or not we should revise the training design.

10. A pre/post comparison is used to evaluate learning so that:

a. we know how much change took place during the program
b. we can calculate a t-test to get nice-looking statistics
c. we can compare the trained group to the control group
d. we know where the group was at the start
ANS: A PTS: 1 DIF: Moderate REF: Page 233

11. A control group is:

a. a second group of trainees
b. of no value in helping us evaluate training programs
c. often critical to determining whether changes were due to a training program rather than some other factor
d. an added cost that is generally too expensive
ANS: C PTS: 1 DIF: Moderate REF: Page 233

12. Ideally, the control group and the training group have:
a. A lot in common c. The same supervisors
b. The same scores before training d. The exact same job description

13. Relational research typically involves the use of what type of statistical measurement?
a. Regression c. A t-test
b. Correlation d. A z-test

14. According to the text what is true about experimental design evaluations:
a. They are easy to use in almost any organization c. They should be the only method used for evaluating
HRD programs
b. They are cheaper to do than case studies d. They are difficult to use due to organizational
constraints

15. To control costs while increasing statistical power Yang et. al. recommend
a. Training more people c. Faking your results
b. Placing more people in the control group d. None of the above

169
170 Chapter 15—HRD and Diversity: Diversity Training and Beyond
170
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INTESTINAL INDIGESTION AND
OBSTRUCTION IN BIRDS.
Causes: Age, debility, atony, matting of feathers, dry or indigestible food, lack of
water, diseased oviducts, sand or gravel, lack of pebbles or power in gizzard.
Lesions: masses of egg, uric acid, or fæces in cloaca, implicating colon and cæca.
Symptoms: dullness, stupor, vertigo, staggering, erect plumage, trailing wings and
tail, bulging anus, covered with matted feathers, impaction felt by finger.
Treatment: extract mass, castor oil, laudanum, chalk, bismuth, pepper,
demulcents, phenol, exercise, silage, green food, pebbles.
Causes. These resemble those already noted for the dog. Old age,
debility, and atony of the bowel, the matting together of feathers
across the anus, dry feeding, indigestible food, scarcity of water, and
lack of exercise are especially to be noted. Malformations or other
changes lead to obstruction of the cloaca, and of defecation. Sand
and gravel passing from an atonic gizzard accumulate in the small
intestine or in the cæca distending them to great excess. Imperfect
trituration in the gizzard, from lack of pebbles, may prove a factor in
stoneless prairies.
Lesions. The most common seat of obstruction is at the cloaca, and
the impacted matter may be yellow partaking of the nature of yolk of
egg, or it may consist of feculent matters and uric acid in various
proportions, white, hard and fœtid. As in the dog this distension may
be continued forward blocking the colon and cæca as well. Lucet
mentions a case in which the impacted mass measured seven inches
long, and eight in circumference at its posterior and larger end.
Symptoms. The bird is dull, sluggish, stupid, giddy or unsteady on
its limbs, with feathers erect, wings, tail and head pendent and loses
flesh rapidly. Often a felted mass of feathers and fæces cover the
anus. In its absence there appears the rounded swelling or on
manipulation the impacted cloaca or rectum can be felt firm and
resistant.
Treatment. Soften and remove the external mass of fæces by the
aid of tepid water, clip off the feathers, which would tend to restore
it, then by the oiled finger and warm water injections break up and
extract the contents of cloaca and rectum. If impaction remains
farther forward give a teaspoonful of castor oil. If diarrhœa has
already set in, give 5 drops laudanum, and mix chalk or bismuth and
pepper in a mush to be fed to the patient. Injections of slippery elm
containing a teaspoonful of carbolic acid in the pint will prove useful.
The bird should be allowed plenty of exercise, its grain being fed
on a floor covered lightly with straw to encourage scratching, and
silage or green food should be allowed. On the prairies where pebbles
cannot be secured, imported gravel or vitrified brick broken into
small pieces should be allowed.
COLIC IN SOLIPEDS FROM VERMINOUS
EMBOLISM. INTESTINAL CONGESTION.
Definition. Causes: presence of sclerostoma in arteries, form, habit, nature,
immature, biology, life in bowel, in submucosa, in arteries, outside the mammal,
pathogenesis, blood-sucking, verminous cysts, verminous aneurisms, seats of
latter, coagula, embolism, stagnation of blood, œdema and thickening of intestine,
mesentery, fermentations, tympany, infective inflammations, blood extravasations,
infection of liver and spleen. Symptoms: sudden attack, violent colics, reckless
movements, frequent defecation followed by its arrest, palsy of peristaltic
movement, of pain, prostration. Course: two to twenty-four hours, death from
indigestion, tympany, obstruction, hemorrhage, poisoning, recovery, sequelæ,
laminitis, intestinal catarrh or atony, debility. Treatment: aneurism worms beyond
reach, treat lesions, venesection, anodynes, stimulants of peristalsis, antiseptics,
compresses, sinapisms. Prevention: expel intestinal worms, exclude embryos,
tartar emetic, iron sulphate, arsenic, phenol, pure water, occasional vermifuges.
Definition. Congestion and spasms of the intestines in connection
with blocking (thrombus or embolism) of the mesenteric arteries,
and verminous aneurism.
Causes. The essential cause is the migration of the sclerostoma
equinum (strongylus armatus, Rud.) into the mesenteric arteries in
its agamous condition. It seems appropriate therefore to here notice
the life history of this parasite.
The sclerostoma equinum (strongylus armatus) is one of the
common pin worms of the horse. It is distinguished by its dull gray
or reddish brown body, thickest at the cephalic end and tapering off
toward the caudal, but ending in a blunt point; by the round, open
mouth furnished with several firm chitinous rings, of which the outer
bears six short symmetrically arranged papillæ, an intermediate row
of rounded blunt tooth-like projections, and the innermost a row of
fine, closely aggregated and very sharply pointed teeth for
penetration of the mucosa. Male ¾ to 1½ inches long, with caudal
membranous alæ in two lateral lobes, joined by a rudimentary
central lobe: two delicate spicula. Female ¾ to 2 inches long, blunt
pointed tail, vulva in posterior half of the body. Eggs ovoid with
slightly raised ring around the centre: oviparous.
Habitats. They are found in solipeds in two stages of existence, the
mature worms in the cæcum and colon, and the immature in the
same organs encapsuled in little pellets of manure, and in cysts in the
mucosa but also apart in the arterial system especially in the anterior
mesenteric artery and other gastric or intestinal trunks.
The mature sclerostomata are found attached to the mucosa of
the large intestine into which the head is sunk for the purpose of
sucking the blood, and they may be gray, brown or red according to
the quantity of blood which they have imbibed. The author has found
them in little hernial sacs of the mucosa hanging from the peritoneal
surface.
The sexually immature sclerostomata are found in little pill-
like masses of ingesta in the large intestines and from which they
project part of the body through a narrow opening. Another habitat
is in cysts of the mucosa of the cæcum and colon and less frequently
of the small intestine, individual cysts varying in size from a pin’s
head to a hazel nut, and containing the young worm rolled upon
itself, and varying in size but always less than the intestinal worm
and always asexual. In some cases the cyst is found empty but with a
small opening toward the lumen of the bowel showing the means of
escape of the parasite. A third habitat of the immature worm is in the
blood-vessels, especially the posterior aorta and its divisions, and
still more constantly the anterior and other mesenteric arteries.
Biology. The ova of the sclerostoma are segmented in the oviduct
but are hatched out after they have been laid. The hatching may be
effected in the intestine or in manure or water external to the body.
When hatched out in the intestine they may pass out at once with the
manure or they may envelop themselves in pellets of the finer ingesta
and remain for a time in the bowel and finally pass out in this
condition. Baillet has traced their development out of the body. In a
watery or damp medium they are hatched out in a few days as a
cylindroid worm ¼ to ⅓ mm. long, thick in front and with a filiform
tail. In moist environment but especially in damp manure they grow
to 1 mm. or 1.5 mm. and continue for months in this condition, but
remain small and asexual, until taken in, in the drink or green food
of the soliped. Reaching the intestine and especially the cæcum and
colon they bore their way into the mucosa and encyst themselves, or
if they happen to perforate a blood-vessel they make a habitat of that.
In the cyst, development proceeds and when it has reached a certain
stage the worm once more bores its way through the mucosa and
reaching the intestine becomes sexually mature.
In this last migration the young worm is liable to perforate a
blood-vessel in which case it is destined to a period of existence in
the blood. It may, however, have blundered upon a blood-vessel at an
earlier stage when seeking a temporary home in the mucous
membrane, so that the sclerostomata of aneurisms may be derived
from two separate sources. In the blood-vessels the parasite attains a
length of 1 to 8 lines, whereas in the mucous cysts it does not exceed
3½ lines. Yet Neumann holds that after leaving the blood-vessels
they may again encyst themselves in the mucosa before escaping into
the intestine.
Several moultings take place in the asexual condition.
Other views have been advanced as to the development of the
sclerostomata. Colin believed that the ova deposited in the ducts of
the mucous glands and in the perforations made by the parasite in
blood-sucking, hatched in this situation and the embryo at once
encysted itself in the mucosa.
Leuckart imagines that the embryo found in the fæces or in water
outside the body of the soliped, should pass through an intermediate
host before it can return to gain sexual maturity in the horse. But no
evidence of the existence of such intermediate host is furnished, and
the encysted intestinal worms show no indication of a special
development which would have been accomplished in such host.
Willach holds to a hermaphrodite stage passed in the intestine of
the soliped. He found in the bowel small worms apparently related to
the sclerostomata by the appearance of the head and the caudal
membrane, but not exceeding three to five lines in length. Some were
evidently females and contained not only eggs with soft shells, but in
one case embryos. Others had the caudal membrane of the male, yet
contained also a few eggs. There is no vulva and the embryos escape
by rupture of the oviducts. These embryos he supposes are developed
in the same host into the familiar mature sclerostomata.
Whatever may be said of those alleged modes, the first described
series of changes and migrations may be taken as the usual and
regular method of development.
Pathogenesis. Lesions. These embrace perforations of the
mucosa, cysts, aneurisms, embolisms and congestions.
Irritation of the mucosa. The adult worms, like so many
leeches are continually biting and sucking blood from the mucosa
and when present in large numbers, hundreds, thousands, or a
million create an aggregate of irritation which may determine violent
indigestions and congestions.
Verminous Cysts. These are like a pin’s head, a pea or hazel nut,
containing the asexual worm in a mass of purulent debris, or if
empty, presenting a small orifice where it made its exit.
Verminous Aneurisms. These are perhaps the most important
lesions caused by the sclerostome as they are the steppingstone to
the dangerous embolisms, and too often fatal colics and congestions
of the intestines. They are very common in some localities, and rare
in others following the distribution of the sclerostomata. Bollinger
found them in 90 to 94 per cent. of adult horses, and Ellenberger in
84 out of 85 horses dissected. They are found in all ages from six
months up, and are nearly always in the short, stubby trunk of the
anterior mesenteric artery. Often two or three exist in the same
animal, the whole length of the posterior aorta showing patches of
disease, exudations, neoplastic elevations alternating with
depressions, and aneurisms and thrombosis in its different branches.
In 100 horses Bollinger found 168 aneurisms, 153 in the anterior
mesenteric, and its divisions, 4 in the cœliac axis and its divisions, 3
in the hepatic artery, 3 in the posterior mesenteric artery, 3 in the
renal arteries and 2 in the posterior aorta.
The special predisposition of the anterior mesenteric artery is
variously accounted for: 1st. There is the obvious fact that its
branches are distributed to the cæcum and double colon, the home of
the mature parasite, and to the small intestines which are first
reached by the young parasites that are taken in with the water and
the food. These are therefore most likely to get into the branches of
this vessel and to follow them up toward its origin. 2nd. The anterior
mesenteric artery distributes its branches to the small intestines the
most motile portion of the intestinal tract, and the cæcum and colon
the most heavily loaded with solid ingesta, it is therefore the most
subject to traction, and distensions, and the more so that the parent
trunk is extremely short and the divisions pass in all directions and
to a large extent at right angles, so that there is a dragging of the
walls apart as well as an obstruction to the blood flow and an
increase of internal tension. The distension, laceration, inflammation
and softening of the internal coat have accordingly been regarded as
the starting point of an endarteritis upon which the parasites have
been implanted as a further cause of trouble. We must not forget,
however, that the sharp circle of teeth of the parasite, by which it
fixes itself on the intima of the vessel are quite enough to produce
initial endarteritis, without any assistance from distension, traction
or laceration.
The irritation of the intima from whatever cause determines here
as elsewhere exudation, and coagulation, and the inflamed walls
losing their tone yield more and more readily to the internal tension.
Sometimes the coagulum lines the aneurism or vessel all round,
leaving a narrow central passage through which the blood still flows;
in other cases the clot extends into the adjacent smaller vessels,
completely blocking them and disturbing circulation and innervation
in the parts which they supply. As a rule the parasites are found in
galleries hollowed out in the clot, and heads or tails may be seen to
project into the circulating blood. Sometimes they are found
imbedded in the arterial coat, or in an adjacent small abscess. The
formation of aneurisms in the other arterial trunks may follow the
same method.
Embolisms. These come very naturally from the formation of
thrombi in the various arteries. The coagulum determined by the
presence of the worms, tends to undergo retrogressive changes
notably fatty degeneration, to which germs brought on the worms or
in their alimentary canals contribute. This together with the
movements of the parasites tends to break up the mass, and minute
portions are washed on into the different smaller vessels. Soon these
reach divisions which are too small to admit them, which are
accordingly occluded and the circulation through them abolished.
The presence of microbes as well as fibrine contributes to cause
further coagulation, more absolute embolism and arrest of the
circulation.
It is further alleged that the sexual instinct in the summer months
(May to August) leads the worms to leave the aneurisms, to pass
through the smaller divisions to the cæcum or colon where alone full
sexual evolution is possible. In these migrations they cause the
thrombosis of the smaller trunks and determine the verminous
congestions of the bowels which are especially common in these
months.
Disturbances of the Intestinal Circulation. As these usually
occur in the lines of distribution of the anterior mesenteric artery a
knowledge of its divisions and their destination and anastomosis, is
essential to an intelligent understanding of the pathogenesis and
lesions. As first pointed out by Lecoq the anterior mesenteric artery
is divided into three primary bundles: (a) a left of 15 to 20 trunks
which are destined to the small intestine; (b) a right which gives off
cæcal branches, one to the double colon, and one to the ilium to
anastomose with the last trunk of the left bundle; and (c) an anterior
which gives one branch to the second division of the double colon
and anastomosis with the colic branch of the right bundle at the
pelvic flexure; and a second branch to the floating colon to
anastomose with the posterior mesenteric artery.
The divisions of the left bundle anastomose so freely with each
other in the mesentery and immediately above the intestine that the
blocking of any one branch cannot entirely arrest the circulation in
the corresponding part of the intestine. It may however produce a
partial local stagnation in the vessels of a short loop of intestine,
resulting in œdematous infiltration and thickening with resulting
induration and stricture of the gut. Chronic and permanent lesions
are produced by such blocking, but only rarely acutely fatal ones.
Acute and fatal congestive lesions of the small intestine from
verminous embolism, occur only when several adjacent divisions of
the artery are blocked at once, and this is a rare occurrence.
The right bundle of branches furnishes the only two arteries which
are supplied to the cæcum and the only artery furnished to the first
half of the double colon. The ileo-cæcal branch is less involved, first,
because being less dependent and smaller, it is less likely to receive
an embolus, and, second, because any lack of blood supply is
counterbalanced by the free anastomosis with the last iliac division
of the left bundle. When the embolus blocks the undivided trunk of
the right bundle this same principle comes into play, the free supply
of blood from the posterior branch of the left bundle supplying blood
through its anastomosis with the iliac and cæcal branches of the
right.
But when the emboli are lower down, in the cæcal branches of the
right bundle, or in these and the colic branch, arrest of the
circulation in the intestinal walls ensues, followed by paresis, passive
congestion and hemorrhage. The cæcum and double colon thus
become the seats of the grave and fatal lesions of verminous
embolism.
The resulting lesions are to be variously accounted for. The
stagnation of blood in the vessels below the embolus, determines a
speedy exhaustion of its oxygen and increase of its carbon dioxide, so
that it is rendered unfit to maintain the normal nutrition and
functions of the part, and the capillary and intestinal walls are alike
struck with atony or paresis. The blood filters into the stagnant
vessels slowly from adjacent anastomosing trunks, and the liquor
sauguinis exudes into the substance of the tissues and lumen of the
intestine, leaving behind the greater part of the blood globules so
that the stagnant blood is rendered more and more abnormal in
composition. The walls of the capillaries soon lose their cohesion as
well as their contractility, and giving way at different points, allow
the escape of blood into the tissues, bowels and peritoneal cavity. It
has been further claimed that the emboli already infected and in
process of degeneration communicate this to the walls of the vessels
and to the stagnant blood, hastening the process of degeneration and
rupture.
Another series of circulatory disorders are liable to take place. The
blocking of the vessels of the right bundle, tends to increase the
blood pressure in the left bundle and the anterior one, and thus to
determine congestions, paresis and inflammations in the small
intestines, the second division of the double colon and the floating
colon. The resulting inflammation and increased vascular tension
may lead indirectly to implications of the brain and lung.
Extravasations so extensive as to appear like blood clots may be
present between the layers of the mesentery or in the mucosa and
submucosa, and blood, liquid or coagulated, may have accumulated
in the abdominal cavity. Blood effusion into the intestine gives a dark
red coloration to the contents which are further mixed with distinct
clots.
The atonic bowels are always the seat of extensive fermentations
and tympany. The microbes engaged in these fermentations and
their toxins, are accountable for toxic changes occurring in the locally
diseased parts and in distant organs. To this may be attributed the
congestion and softening of the liver and the engorgements and
hemorrhagic centres in the spleen.
Symptoms. An animal, perhaps known to harbor the sclerostoma
equinum, is suddenly attacked with violent and persistent colic. He
trembles, paws, moves his hind feet uneasily, kicks the abdomen,
throws anxious looks at the flanks, crouches, lies down, rolls, gets up,
and at once gets down again. The intensity of the suffering rapidly
increases, the face is drawn and pinched, the eye is extremely
anxious, the patient no longer lies down, but throws himself down
reckless of consequences, when down he is not quiet for an instant,
but now on his breast, then on his side, then on his back, the limbs
struggling and jerked violently, the head turned first to one side and
then to the other, he is a picture of extreme agony. If made to walk
the same indications continue; he walks with head down and limbs
semiflexed ready to drop at any moment, and often he will drop
suddenly in spite of every effort to keep him on his feet. The pulse is
at first strong and full, but as extensive effusion takes place into the
bowels or abdomen, or as the animal is poisoned by toxins, it
becomes small, weak, and it may be imperceptible. Breathing is
quick and catching, and the mucous membranes are dark red.
Sweating which shows first about the elbows or flanks or back of the
ears finally becomes general, the surface cold and the limbs
especially so. Fæces may be passed at first, a few dry balls at a time
from the floating colon or rectum, but soon they are suppressed
entirely. Some patients strain frequently to micturate but pass little
at a time.
In some instances the acute pain seems to suddenly cease, but
there is no general improvement, the patient stands with head
depressed, eyes sunken and expressionless, ears lopped, cold
perspiration, chilly limbs, unsteady gait and imperceptible pulse. It
implies merely a paralysis of the affected bowels in connection with
the extensive congestion and extravasation.
Course. Duration. The more acute cases reach their acme with
great rapidity, death may occur after two hours illness, and in other
cases it may be delayed ten or even twenty-four hours. It may be
caused by indigestion and tympany, by volvulus or invagination, by
excessive hemorrhage, or by poisoning with toxic matters.
Recovery occurs when the vessel blocked is an unimportant one as
a branch of the left bundle so that circulation may be reëstablished
from collateral trunks; or when a more important trunk has been but
partially blocked, and after a time it either clears itself, or collateral
circulation comes in with sufficient compensation. There is a more or
less rapid disappearance of the colics and other symptoms, a free
passage of urine, the rejection of fæces, it may be in a liquid, semi-
liquid or sanguineous condition, yet enough to indicate the
restoration of intestinal tone. The patient begins to pick morsels of
food and soon acquires his former appetite.
In some instances, however, the recovery is not complete. Trasbot
has noted a case of laminitis occurring within fifteen hours after the
improvement, and in other cases there remain chronic debility and
catarrh of the intestines. The appetite remains poor, there are
occasional colics, the bowels are irregular, loose or costive, and the
fæces are dry, glossy and covered with mucus. The back is arched,
the belly tucked up, strength and vigor are both lacking, and the
patient spends much time in the recumbent position.
Complications of various kinds may follow as in other diseases of
the intestines. After even the best recoveries, a relapse is always to be
apprehended as the original cause remains and the animal is liable to
be cut off at any time.
Treatment. This is very unsatisfactory as the original source of
trouble, the worms, being in the blood-vessels, cannot be reached by
vermifuges that would be harmless to the host, and clots blocking the
smaller intestinal vessels, cannot be dissolved and removed.
Moreover, although we could compass the death of the worms in the
aneurisms, we would leave their dead bodies as sources of septic
change, blood coagulation and embolism.
A certain number of cases, however, are not necessarily fatal, and
the worms of the blood-vessels have not an indefinite period of life,
so that there is some encouragement for both therapeutic and
preventive treatment. During the attack we must be content to treat
symptoms. French veterinarians still trust largely to general
bleeding, adopted at the very outset and to the extent of 6 to 10
quarts. It will temporarily lessen the vascular tension, more
permanently dilute the blood, and calm nervous excitement, and in
the most violent cases, as a kind of forlorn hope, it might be tried
with the view of tiding over the acute stage until a freer collateral
circulation could be established.
The use of anodynes will be more generally acceptable to American
practitioners. Two to four grains of sulphate of morphia or codeine
may be given hypodermically in combination with 1½ gr. eserin, 7
grs. barium chloride, or 2 grs. pilocarpin, to secure a speedy
movement of the bowels.
To counteract intestinal fermentation perhaps no better agent can
be got than chloral hydrate, ½ oz. of which may be given by the
mouth in water, and ½ oz. more by the rectum.
Wet compresses to the abdomen, or fomentations with water
rather hotter than the hand can bear or even the application of
mustard is sometimes useful as a soothing or derivative agent.
In the absence of morphia or chloral, laudanum, ether,
chloroform, camphor or assafœtida have been recommended.
It is important to keep the patient on a soft, littered floor to
prevent injury from his throwing himself down, and walking him
around may be resorted to for the same purpose.
Prevention. After a non-fatal attack and in every case in which a
horse is found to harbor the sclerostoma equinum in quantity,
measures should be taken to expel those present in the bowels and to
prevent the entry of embryos. The infested horse may be purged and
put on two drachms each of tartar emetic and sulphate of iron every
morning in a handful of feed half an hour before the first meal. After
six doses he may take a second active purgative. In case of need the
addition of 6 grains arsenious acid and a drachm of carbolic acid to
each dose will render them much more effective. All water must be
withheld that comes from streams running by farm-yards, from
ponds or open wells in barn-yards, from uncovered cisterns and from
any source which receives drainage or leaching from land occupied
by solipeds or spread with their manure.
A course of vermifuge medicine should be given at intervals of two
or three months to get rid of the worms which have passed in the
interval from the cysts of the colon, into the intestine.
NON-VERMINOUS INTESTINAL
CONGESTION IN SOLIPEDS.
Causes: sudden changes to green food, or leguminous fodder, newly harvested
fodder, frosted food, iced water, microbian infection, toxin poisoning, intestinal
fermentations, experiments, volvulus, invagination, strangulation, compression,
atony. Symptoms: as in verminous aneurisms. Diagnosis: absence of worms,
presence of other causes. Treatment.
Causes. Acute intestinal congestion apart from verminous
aneurisms is ascribed to a variety of causes. Sudden changes of food
especially to green food, in spring, or to some of the leguminous
fodder plants (alfalfa, cowpea, clover, tares, vetches), newly
harvested grain or hay, fodders covered with hoarfrost, iced water,
and microbian infection or poisoning with toxins or other irritant
products of intestinal fermentations. Experimentally the injection
into the circulation of pyogenic toxins and putrid matters has
determined intestinal congestion and hemorrhage. In the same way
musty hay or grain have proved the occasion of these attacks. Finally
mechanical blocking of the circulation of the intestine as by volvulus,
invagination, strangulated hernia, or even compression by bulky
food has seemed to operate in this way.
It ought to be borne in mind that the habitual microbes of the
healthy bowel may become pathogenic when brought in contact with
a mucosa which is the seat of irritation, atony or any condition of
debility.
Symptoms and Lesions. The verminous aneurisms and thrombosis
aside, the symptoms and lesions of this form of congestion so closely
resemble those of the verminous affection that it seems needless to
repeat them.
Diagnosis is difficult but the absence of worms in the affected
animals and their fellows, and the presence of some one of the other
recognized causes may lead to a fair conclusion.
Treatment of the affection is more hopeful than in the verminous
affection, and may be conducted on the same general lines.
PSEUDOMEMBRANOUS (CROUPOUS)
ENTERITIS IN SOLIPEDS.
Definition. Causes: As in ordinary enteritis, with added infections or toxins.
Symptoms: As in enteritis, nervous symptoms, diarrhœa. Lesions: Congested
mucosa, whitish or grayish false membranes, in patches or tubular casts, granular,
mucous, albuminoid, fibrinous. Diagnosis: False membranes in stools. Treatment:
Glauber salts, calomel, alkaline carbonates or tartrates, oils, antiferments,
demulcents, careful diet, bitters.
Definition. An inflammatory affection of the bowels characterized
by the ejection with the fæces of false membranes.
Causes. It has been long attributed to the causes which produce
other forms of enteritis and indigestions, as youth, rich stimulating
feeding, sudden change to green food in spring, sudden chills, over-
fatigue, confinement indoors, and prolonged costiveness. In man it is
found as a sequel of infectious diseases (pneumonia, pyæmia), in
Bright’s disease, cirrhosis of the liver and cancer, and in poisoning by
lead, mercury or arsenic (Osler). Cadeac, who found great numbers
of streptococci in the false membranes in animals, is certain it is a
microbian disease, and this is doubtless true, if qualified by the
statement that the microbe as is so often the case with other
intestinal affections, requires an occasion in the form of a diseased or
debilitated condition of the mucosa to enable it to become
pathogenic. The disease is not known to propagate itself indefinitely
or without such a predisposing occasion.
Symptoms. There are dullness, prostration, langor, hyperthermia,
accelerated pulse, and colics which may be slight or very severe. In
some cases nervous symptoms have been observed, such as
irritability or stupor and somnolence with icterus and fœtid stools.
The fæces are usually semi-liquid, implying an excessive liquid
secretion as well as the exudation of the membranous matter.
Lesions. There is a pink congestion of the intestinal mucosa more
or less generally distributed. Whitish false membranes cover patches
chiefly on the terminal portion of the small intestine, but frequently
also on the cæcum and colon, covering an especially red and angry
mucosa. They may occur as simple patches, as ribbon shaped pieces,
or as hollow cylinders lining the entire circumference of the
intestine. They appear as if fibrillated, but contain abundance of
granular matter and seem to be composed mainly of mucus with
albuminoid matter and probably a little fibrine. The deeper layers, in
contact with the inflamed surface are soft and gelatinoid. It is alleged
that coexisting wounds on other parts of the body become covered by
a soft pultaceous false membrane.
Diagnosis is based on the presence of the false membranes of a
considerable thickness, so that they can be distinguished from the
film of mucus which covers the fæcal balls in constipation or enteric
catarrh.
Treatment. Facilitate the secretion from the mucosa, and the
separation of the false membrane by giving 1 lb. Glauber salts, or give
this agent in doses of 5 or 6 ozs. per day. Calomel 1 dr. may be used
instead and has the additional advantage of acting as a disinfectant.
The alkaline carbonates or tartrates or even olive or castor oil may be
used as substitutes. Antiferments like salol, naphthol, salicylic acid,
and salicylate of soda have been prescribed to check the
multiplication of the germ. Flaxseed tea, elm bark, and other
mucilaginous agents may also be given. An easily digestible and
laxative diet and a course of bitters may follow.
ENTERITIS IN CATTLE.
Causes: as in solipeds, youth, overfeeding, plethora, dietetic blunders,

temperament, over-exertion, chill when heated, gestation, foul water, irritants,
drastics, infections. Symptoms: as in enteritis with false membranes,
complications. Duration. Lesions: false membranes, extent, color, structure,
composition, congested mucosa. Treatment: Glauber and other salts, pilocarpin,
potassium iodide, antiseptics, sulphites, sulphides, borax, bismuth, naphthol,
creolin, muriatic acid, bitters.
Causes. The same causes are quoted as in solipeds, youth, extra

high condition, rich feeding, sudden change to the green food of
spring, climatic vicissitudes of the same season, a sanguineous
(Reynal) or lymphatic (Friedberger and Fröhner) temperament,
overwork, exhausting travel, suppressed perspiration, gestation,
plethora, foul drinking water, special irritant plants (chicory,
Huzard), and drastic purgatives. Cadeac suggests bacteria, quoting
instances of a fifth or a fourth of a herd suffering at once. The same
would come from any other cause acting on the whole herd and it
seems probable that a microbian factor is present but can find
occasion for its pathogenesis only in given morbid conditions of the
mucous membrane. This would explain the failure of the affection to
propagate itself like a plague, and at the same time its tendency to
manifest itself extensively in given herds with a common
predisposing condition.
Symptoms. There are indications of enteric inflammation and
fever, rigors, slight hyperthermia, drying up of the milk secretion,
impaired or suspended appetite and rumination, constipation, colicy
pains, increasing dullness and prostration. As the disease advances
the excrements become soft, pultaceous or watery, with floating hard
baked pieces, dark and even glistening on the surface and more or
less false membranes. These are sometimes stained with blood,
which may also be mingled with the liquid debris. As in solipeds
these membranes constitute the only true diagnostic symptom. They
may appear as shreds, bands or complete cylindroid casts of the
intestine.
Other complications, like pseudomembranous exudate on wounds,
abortions and profound weakness are sometimes noted. The disease
may last eight days before ending in recovery. When death takes
place it is about the fourth or sixth day.
Lesions. The false membranes are found on the ilium and colon, in
thin films or in thick masses, or tubular casts. In extreme cases the
membrane has covered an extent of 24 feet in length, and if recent it
is soft and friable. If older it may be firm, consistent and yellow or
stained by the blood or ingesta. As in solipeds it shows a reticulated
network and a fine granular structure, and is composed mainly of
inspissated mucus with albuminoids and fibrine. The exudate covers
a surface of extreme redness, with points of darker blood-staining
and even abrasion or ulceration. The surrounding mucosa is also
congested, the villi hypertrophied, the mucous follicles swollen.
Treatment. In the early stages a laxative of soda sulphate is of
especial value in depleting from the inflamed mucosa, liquefying the
secretions and dissolving and loosening the false membranes. Epsom
salts, cream of tartar, Rochelle salts, calomel, and pilocarpin are
more or less valuable substitutes. Iodide of potassium is most
valuable in dissolving the exudate and acting as a microbicide (dose
3–4 drs.).
Other alkaline salts may be substituted or as antiseptics the
sulphites, hyposulphites, or sulphides of potash or soda. Borax,
bismuth, naphthol and creolin have also been recommended.
Enemata of warm water are desirable.
In very adynamic conditions, muriatic acid (½ dr. doses) may be
given with vegetable bitters and the same may be allowed during
convalescence.
ENTERITIS IN SHEEP.
Causes: As in cattle, draughts in folds, overfeeding. Symptoms: fever,
inappetence, weakness of hind parts, diarrhœa, tenesmus, false membranes, blood
in stools, tympany. Treatment: change diet of dam, exercise, Glauber salts,
potassium iodide, bismuth, flaxseed, elm bark, mallow, gum, carminatives, bitters,
antiseptics.
Causes. The same causes are claimed as for cattle. Clavel
attributed it to too rich milk, and exposure to cold draughts, in
folded lambs.
Symptoms. To the general symptoms of fever are added refusal of
the teat, weakness or paresis of the hind limbs, looseness of the
bowels and the ejection of false membranes with an unusual amount
of straining. The dejections may be watery and mixed with blood. In
some cases defecation is suppressed, the intestines being blocked by
the membranes, and then acute indigestion and fatal tympany may
follow.
The pathological anatomy and lesions resemble those seen in the
ox.
Treatment. Change the diet of the ewe, and allow more outdoor
exercise. Give the lamb Glauber salts (½ to 1 oz.) with potassium
iodide (10 grs.), and bismuth (1 dr.). Decoctions of flaxseed, or
solutions of elm bark, mallow or gum arabic are desirable, and
infusions of aromatic plants or oils of peppermint, anise, or fennel
may be added with quinia. As in the other animals such antiseptics
as salol, naphthol, naphthalin, boric acid, or salicylate of soda may be
administered.
ENTERITIS IN DOGS.
Complication of other diseases like distemper. Symptoms: fever, retching,
vomiting, tense, tender, tympanitic abdomen, irregular bowels, false membranes.
Lesions: stomach empty, congested, croupous exudate, extravasations. Treatment:
sodium sulphate, boric acid, sodium salicylate, salol, bismuth, by mouth or enema,
strychnia, vermifuges.
In dogs the formation of false membranes on the intestinal mucosa
seems to have less of an individual character, and is found associated
with other affections, like canine distemper and parasitism. In the
absence, however, of accurate knowledge of the specific cause of
croupous enteritis in other animals it seems permissible for the
present, to arrange the whole in one class characterized by the
presence of false membranes.
Symptoms. Along with the general symptoms of fever and the
special ones of the existing specific disease there is more or less
disturbance of the digestive organs, anorexia, vomiting, tense,
tender, perhaps tympanitic abdomen, irregularity of the bowels and
the passage of the false membranes. A morose disposition and
tendency to snap has been noticed by Röll.
Lesions. The stomach is empty with red or dark mottled mucosa,
the intestinal mucosa is congested covered with a layer of
mucopurulent exudate, and at intervals patches of false membranes
which are also found in shreds floating in the glairy contents. The
exudates are of a yellowish gray color, more or less streaked with
blood, and the mucosa infiltrated, swollen, highly congested and with
spots of extravasation of blood.
Treatment. Small doses (1 to 2 drachms) of sulphate of soda may
be given by the mouth, or boric acid (1 scruple), salicylate of soda (10
grains), salol (5 grains), or bismuth nitrate (½ drachm). Injections of
boric acid, borax, sodium hyposulphite, or even Glauber salts prove
useful, and powdered nux vomica (1 grain twice daily) may be added.
In case of intestinal parasites vermifuges must be resorted to.
ENTERITIS IN BIRDS.
In pigeons: Ærobic, non-motile bacillus, in lesions, membrane and internal
organs, pathogenesis, in chickens pathogenesis differs, also in man, parts attacked,
exudate, other symptoms, mortality early and late in outbreak, American form,
pathogenesis to rabbits and Guinea-pigs. Prevention: Avoidance of infection,
quarantine of birds, separation of sick, disinfection, accidental bearers of infection,
pigeons, buzzards, carrion crows, dogs, men, cleanliness. Treatment: Locally
antiseptics, phenol, boric acid, generally, phenol.
This has been especially seen in pigeons in which it has been
studied by Löffler, Cornil and Megnin, and Babes and Puscarin.
Löffler found an ærobic, non-motile, non-liquefying bacillus in the
false membranes, inflamed tissues, liver, lungs and blood, even in
the leucocytes. It formed irregular masses, and grew in nutrient
gelatine, blood serum and potato. It proved pathogenic to pigeons,
linnets, rabbits and mice, but not to hens, Guinea-pigs, rats or dogs.
Chickens, however, suffer from an acute diphtheritic affection caused
by a nearly allied bacillus, and it remains to be seen whether the
varying pathogenesis may not be due to the habit of long continued
growth in a particular genus and an acquired unfitness for growing
in the other. The pathogenesis is also different from the bacillus of
diphtheria of man, and the two diseases are not usually inter-
communicable, in spite of the fact that in rare instances infection has
appeared to have taken place from man to birds.
In pigeons and fowls the upper parts of the air passages and
digestive tract are mainly involved, the tongue, fauces, corners of the
mouth, nares, larynx, and conjunctiva. The bowels suffer less
frequently and mostly concurrently with the mouth, nose and throat.
The mucosa is deeply congested and in part covered by a yellowish
exudate which may accumulate in masses, and dry into a firm
substance. The disease affects particularly high bred birds, kept in
close warm houses, and is often imported by prize animals returned
from a show. There may be dullness, listlessness, sunken head,
trailing wings and tail, erect plumage, diarrhœa, and, if the nose and
throat are affected, a modification of the voice as in roup. Death may

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Human Resource Development 5th

Edition Werner Test Bank

1. A control group is a group of people of the same age as the trainees.

ANS: F PTS: 1 DIF: Moderate REF: Page 233

2. A control group is just a second group of trainees

ANS: F PTS: 1 DIF: Moderate REF: Page 233

ANS: T PTS: 1 DIF: Moderate REF: Page 233

ANS: T PTS: 1 DIF: Moderate REF: Page 229

ANS: F PTS: 1 DIF: Moderate REF: Page 229

ANS: T PTS: 1 DIF: Moderate REF: Page 230

ANS: T PTS: 1 DIF: Moderate REF: Page 235

8. A case study involves training followed by post training measurement.

ANS: T PTS: 1 DIF: Moderate REF: Page 231

ANS: F PTS: 1 DIF: Moderate REF: Page 231

ANS: T PTS: 1 DIF: Moderate REF: Page 232

1. Which of the following is not a form of research design validity?

ANS: D PTS: 1 DIF: Moderate REF: Page 229

2. Internal validity can be affected by all of the following, except:

ANS: D PTS: 1 DIF: Moderate REF: Page 230

3. Internal validity can be affected by all of the following, except:

ANS: C PTS: 1 DIF: Moderate REF: Page 230

4. Maturation refers to:

ANS: A PTS: 1 DIF: Moderate REF: Page 230

5. Differential selection refers to:

ANS: D PTS: 1 DIF: Moderate REF: Page 230

6. Testing refers to:

ANS: B PTS: 1 DIF: Moderate REF: Page 230

7. A case study research design:

ANS: B PTS: 1 DIF: Moderate REF: Page 231

ANS: D PTS: 1 DIF: Moderate REF: Page 235

9. Collecting data in a pretest and posttest design allows us to:

ANS: B PTS: 1 DIF: Moderate REF: Page 233

10. A pre/post comparison is used to evaluate learning so that:

ANS: A PTS: 1 DIF: Moderate REF: Page 233

11. A control group is:

ANS: C PTS: 1 DIF: Moderate REF: Page 233

ANS: B PTS: 1 DIF: Moderate REF: Page 233

ANS: B PTS: 1 DIF: Moderate REF: Page 231

ANS: D PTS: 1 DIF: Moderate REF: Page 234

ANS: B PTS: 1 DIF: Moderate REF: Page 237

Causes: as in solipeds, youth, overfeeding, plethora, dietetic blunders,

Causes. The same causes are quoted as in solipeds, youth, extra

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