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further development; (3) a shell surrounding the germ cell and
vitelline cells, and provided at one end with a cap or operculum. The
eggs escape from the uterus of the adult through the vulva, are
carried to the intestine of the host with the bile, then pass through
the intestines with the contents of the latter, and are expelled from
the host with the fæcal matter. Many of them become dried, and then
undergo no further development; but others are naturally dropped in
the water in marshes, or, being dropped on dry ground, they are
washed into water by the rain, or are carried to a more favourable
position by the feet of animals pasturing or passing through the
fields. After a longer or shorter period of incubation, which varies
with the temperature, a ciliated embryo (miracidium) is developed.
At a temperature of 20° to 26° C. the miracidium may be formed in
ten days to three weeks; at a temperature of 16° C. the development
takes two to three months; at 38° C. it ceases entirely. Experiments
have shown that as long as these eggs remain in the dark the
miracidium will not escape from the egg-shell; accordingly it will not
escape during the night. When exposed to the light, however, or
when suddenly brought into contact with cold water, the organism
bursts the cap from the egg-shell, crawls through the opening, and
becomes a—
Fig. 148.—Embryo of the Fig. 149.—Sporocyst of the
common liver fluke common liver fluke which has
(Fasciola hepatica), developed from the embryo, and
boring into a snail. × 370. contains germinal cells. × 200.
(After Thomas, 1883, p. (After Leuckart, 1889, p. 109, Fig.
285, Fig. 4.) 67 B.)
 Fig. 150.—Sporocyst of the
common liver fluke, somewhat
older than that of Fig. 149, in
which the germinal cells are
giving rise to rediæ. × 200.
(After Leuckart, 1889, p. 109,
Fig. 67 C.)

(c) Free-swimming ciliated miracidium (Fig. 148).—As already

stated, this organism is entirely different from its mother. It
measures about 0·15 mm. long; is somewhat broader in its anterior
portion than in its posterior portion; on its anterior extremity we
find a small eminence, known as a boring papilla; the exterior
surface of the young worm is covered with numerous cilia, which by
their motion propel the animal through the water; inside the body we
find in the anterior portion a simple vestigial intestine and a double
ganglionic mass provided with a peculiar pigmented double cup-
shaped eye-spot; in the posterior portion of the body cavity are found
a number of germ cells, which develop into individuals of the next
generation.

Fig. 151.—Redia of Fig. 152.—

the common liver Redia of the
fluke (Fasciola common liver
hepatica), containing fluke, with
germinal cells which developed
are developing into cercariæ. ×
cercariæ. × 150. 150. (After
(After Leuckart, Leuckart,
1889, p. 269, Fig. 129 1889, p. 270,
A.) Fig. 130.)
 Fig. 153.—Free
cercaria of the
common liver
fluke, showing two
suckers, intestine,
large glands, and
tail. (After
Leuckart, 1889, p.
279, Fig. 137.)

Swimming about in the water, the miracidium seeks out certain

snails (Limnæa truncatula, L. oahuensis, L. rubella), which it
immediately attacks (Fig. 148). The miracidium elongates its papilla
and fastens itself to the feelers, head, foot, or other exterior soft
portion of the body of the snail; some of the parasites enter the
pallial (lung) cavity and attach themselves there. After becoming
securely fastened to the snail the miracidium discards its ciliated
covering, and shortens to about half its former length (0·07 mm. to
0·08 mm.). The parasites now bore their way into the body of the
snail, and come to rest in the liver or near the roof of the pallial
cavity, etc.; the movements gradually cease, and we have before us
the stage known as the—
(d) Sporocyst (Figs. 149 and 150).—The eye-spots, ganglionic
swellings, and vestigial intestine become more and more indistinct,
and are finally lost. The sporocyst grows slowly at first, then more
rapidly, and at the end of fourteen days or so measures 0·5 mm. The
germ cells mentioned as existing in the posterior portion of the
miracidium now develop into individuals of a third generation,
known as—

Fig. 154.—Portion of a grass stalk with three encapsuled cercariæ

of the common liver fluke (Fasciola hepatica). × 10. (After
Thomas, 1883, p. 291, Fig. 13.)
 (e) Rediæ
(Figs. 151 and
152).—The
rediæ escape
from the
sporocyst
when the
latter are
from two
weeks (in
summer) to
four weeks
(in late fall)
old. Upon
leaving the
body of the
sporocyst
they wander
to the liver of
the snail,
where they
grow to
about 2 mm. Fig. 155.—Isolated encysted cercaria of the common
long by 0·25 liver fluke. × 150. (After Leuckart, 1889, p. 286, Fig.
mm. broad. 142.)
Each redia
consists of a
cephalic portion, which is extremely motile, and which is separated
from the rest of the young worm by a ridge; under the latter is
situated an opening, through which the next generation (cercariæ)
escape. The posterior portion of the worm is provided, at about the
border of the third and the last fourths of the body, with two
projections. There is a mouth with pharynx situated at the anterior
extremity, the pharynx leading to a simple blind intestinal sac. The
redia, as well as the sporocyst, may be looked upon as a female
organism, and in its body cavity are found a number of germ cells,
which develop into individuals of the next generation, known as—
(f) Cercariæ (Figs. 153—155).—These organisms are similar to the
adult parasites into which they later develop. The body is flat, more
or less oval, and provided with a tail inserted at the posterior
extremity. The oral sucker and acetabulum are present as in the
adult, but the intestinal tract is very simple; on the sides of the body
are seen two large glands, but the complicated genital organs of the
adult are not visible. The cercaria leaves the redia through the birth
opening, remains in the snail for a longer or shorter time, or passes
out of the body of the snail and swims about in the water. After a
time it attaches itself to a blade of grass (Fig. 154) or some other
object, and forms a cyst around itself with material from the large
glands, at the same time losing its tail. It now remains quiet until
swallowed by some animal. Then, upon arriving in the stomach—of a
steer, for instance—the cyst is destroyed, and the young parasite
wanders through the gall-ducts or, as some believe, through the
portal veins to the liver, where it develops into the adult
hermaphrodite.
 Fig. 156.—Drawing from a microscopic preparation, showing a
hæmorrhage in the parenchyma of the liver caused by the common liver
fluke (Fasciola hepatica). a, Atrophic liver tissue; b, round-cell
infiltration; c, a portion of the parasite; d, hæmorrhage. (After Schaper,
1890, Pl. I., Fig. 1.)

From the above we see that this parasite runs through three
generations, namely:
(1.) Ovum, miracidium, and sporocyst ... first generation.
(2.) Redia ... second generation.
(3.) Cercaria and adult ... third generation.
During this curious development, which lasts about ten to twelve
weeks, there is a constant potential increase in the number of
individuals, for each sporocyst may give rise to several (five to eight)
rediæ, each redia to a larger number (twelve to twenty) cercariæ, and
each adult to an enormous number (37,000 to 45,000) of eggs. This
unusual fertility of the parasite is necessary because of the
complicated life history and the comparatively small chance any one
egg has of completing the entire cycle.
Hosts. An interesting and, from an agricultural standpoint, an
important matter connected with this fluke is that it is found in a
large number (about twenty-five) of domesticated and wild animals,
and this fact probably explains to some degree the wide geographical
distribution of the parasite.

Fig. 157.—Drawing from a microscopic preparation, showing the

glandular hyperplasia of the mucosa of a gall-duct caused by the
common liver fluke (Fasciola hepatica). a, Hypertrophied
submucosa; b, interstitial connective tissue; c, compressed lobule;
d, lumen of the gall-duct—thickened fibrous wall of the gall-duct.
(After Schaper, 1890, Pl. I., Fig. 2.)

Symptoms. The symptomatology of this disease may clinically be

divided into three well-marked periods:
 I. Primary period. The primary phase commences with the
penetration of the embryos of the parasite into the body, firstly into
the intestine, and then into the liver by ascending the bile ducts. This
phase occurs during the last months of the year, October, November,
and December, and is rarely accompanied by alarming symptoms. At
this time the sheep appear in good health, the summer being over,
and the animals, being well nourished and fat, are able to resist the
first attacks of the parasite, so that even an observant shepherd only
notices a little dulness, want of condition, and muscular weakness. It
requires a carefully trained eye to note these very general symptoms,
for the bodily condition only changes very slowly and progressively,
the appetite remaining good. Experienced butchers, however, in the
districts where distomatosis is common, readily detect this
condition. The animals make little resistance when handled.
 Fig. 158.—Drawing from a microscopic preparation showing a fluke in
the tissue of the liver. a, Necrotic liver tissue; b, atrophic liver cells; c,
spines on the fluke, showing the outline of the body. (After Schaper,
1890, Pl. III., Fig. 5.)

Nevertheless, even in this primary phase, the conditions are not

always as above sketched, and a certain number of deaths may occur.
Gerlach has mentioned the possibility of death by cerebral apoplexy,
in consequence of the young distomata penetrating to the brain.
Moussu has certainly never seen such a complication, but has seen
death from hepatitis, perihepatitis, and secondary pericarditis in
animals gravely infested. The young embryos, whether they
penetrate only by the bile ducts, as has been stated, or are carried to
the liver by the blood stream, often excavate canals in the substance
of the gland before establishing themselves in the bile ducts. They
make their way as far as Glisson’s capsule, and may even penetrate
it; and as they carry with them innumerable intestinal germs, when
they arrive viâ the bile ducts, they set up hepatitis, perihepatitis, with
the formation of numerous false membranes, or even infectious
fibrinous peritonitis. Should the patients die during this phase one
finds young distomata at the surface of the liver, or even in the
thickness of the false membranes.

Fig. 159.—Tabular diagram of the occurrence of the

common liver fluke (Fasciola hepatica) during
different months of the year. a, Cattle; b, sheep; c,
swine. (After Leuckart, 1889, p. 301, Fig. 147.)

When infestation is discrete the appearances are quite different.

Careful breeders have even stated that at this period the young sheep
appear to show a greater tendency to fatten.
II. Second period. In the primary phase deaths are exceptional;
they only become common towards the end of the winter. During the
second or middle period (December and January) the patients lose
flesh, appear less active, show less regular appetite and greater thirst.
The conjunctiva becomes pale and swollen, the sclerotic has a bluish
tint, and the eyelids are somewhat infiltrated. The wool appears drier
and less curly; locks of wool part readily from the skin, and the
individual fibres become dry and fragile.
This phase is accompanied by very marked
anæmia, rapid exhaustion during movement,
and inability to run for any length of time.
The different methods of examination
reveal nothing specially striking, except that
the valvular sounds of the heart are sharper,
and that trifling œdema occurs under the
thorax and abdomen.
Microscopic examination of the fæces
reveals the presence of eggs of distomata. The
sheep rapidly become thin from about the end
of January, even although the appetite
persists and nourishing food is given.
III. Third, or wasting, period. The
decline, which sets in about February,
appears extremely obstinate, and resists all
treatment.
The patients become feeble, eat less, and
digest badly. Submaxillary œdema, common
to advanced wasting diseases, then appears. If
the sheep are removed from the fold to
Fig. 160.—The large pasture, the swelling of the submaxillary
American fluke space is very noticeable. It consists in an
(Fasciola magna), indolent œdematous tumefaction, which
natural size. (Stiles, disappears when the animals are travelled,
Annual Report, but reappears when grazing on account of the
U.S.A. Bureau of low position in which the head is then held.
Agriculture, 1901.) The condition then becomes complicated
with diarrhœa, and soon grows alarming. On
examination, extensive dropsy may often be found in the thorax,
pericardium, and abdomen.
Death results from exhaustion; the animals do not appear to
suffer, but become extraordinarily anæmic, and perish without a
struggle. The blood is simply rosy in colour, like gooseberry syrup;
the clot is soft and gelatinous; the number of red blood corpuscles
has fallen from about seven millions to a few hundred thousand.
Icterus is rare, though certain cases have been described where it
has appeared during the last and even during the middle stage.
When animals begin to die in a district which has long been
infested, the losses are enormous, the condition sometimes
constitutes a perfect scourge. It should be remarked, however, that
all those affected do not die; animals kept under good conditions
may even survive for several months, although greatly wasted.
Towards March and April the parasites leave their position, and
are conveyed by the current of bile towards the intestine, to be
rejected with the fæces. This is the period of convalescence and
recovery; but recovery is only relative, for the parasites are never
entirely evacuated. The distomata then recommence their life cycle
outside the animal body.
Unfortunately the mortality caused
by distomata is accidentally aggravated
by other diseases, and the scourge then
becomes an absolute disaster for the
districts where such complications
occur. Thus Besnoit and Cuillé, of
Toulouse have shown that
distomatosis may become complicated
with a form of very rapidly fatal
hæmorrhagic septicæmia, produced by
an ovoid bacterium.
Distomatosis, already sufficiently
grave, then becomes infinitely more
serious, if only from the fact that it
may prove the point of origin of an
absolutely fatal complication.
In bovine animals the symptoms
develop exactly as in sheep, though the
cachectic period is uncommon and the
injury done is often less important
than in sheep. The patients exhibit
irregular appetite, wasting without Fig. 161.—Macerated
appreciable cause, anæmia, and even specimen of large
diarrhœa. In spite of excellent winter American fluke, showing
feeding they do not regain condition, the digestive system and
and relative recovery only sets in with acetabulum. X 2. (After
the approach of spring. Death from Stiles, 1894, p. 226, Fig. 2.)
simple distomatosis is exceptional, but
in animals so predisposed enteritis
develops more easily, as do all forms of infection of intestinal origin.
The disease is, however, also grave for bovines because successive
reinfection occurs, and the disease may be prolonged for years.
Causation. Distomatosis is due to one cause, viz., the entrance of
embryo flukes into the digestive apparatus of herbivora.
The adult distomata in the biliary ducts continually discharge large
quantities of eggs, though the process is most active between
February and June or July. The eggs are carried away with the bile
and fæces and pass on to the pastures, where they continue their life
cycle, thanks to moisture and the presence of stagnant water. The
embryos, having escaped from the egg, enter the bodies of the snails
found in or near stagnant water (Limnæa truncatula), become
converted into sporocysts, and afterwards into rediæ and cercariæ.
The cercariæ become encysted on the lower surface of blades of grass
in damp pastures, whence they are transferred to the animals’
stomachs along with the grass itself.
As the Limnæa truncatula lives not only in marshy regions, but
also in all damp situations, the embryos of distomata are distributed
over enormous areas, and the disease itself is equally widespread.
The embryo, after ingestion, is set at liberty, and passes from the
intestine into the innermost recesses of the liver, being guided up the
bile ducts by the current of bile. At this point it attaches itself to the
wall of the bile duct, passes through its various stages of evolution,
and attains the adult form. It then begins laying eggs, and thus starts
a new evolutionary cycle.
The life cycle of Distoma lanceolatum is not yet known, and this
variety, moreover, is less widely distributed than the Distoma
hepaticum.
 The bile ducts are more easily
penetrated by the distoma in young
animals, a fact which explains why
calves and lambs are particularly
affected. Adults present a less
favourable nidus, a fact which renders
them less easily infected, but does not
entirely prevent the parasites from
attacking them. Old animals, although
unable to resist entirely, seldom
harbour many of the parasites.
Wet years appear to favour the
extension and propagation of
distomatosis in an extraordinary
fashion, a fact which is easily
understood, if we regard the phases of
evolution of the parasite. The autumn
appears particularly favourable to the
infection of herds. This is explained by
the fact that, during the summer, the
dryness of the fields entirely prevents
Fig. 162.—Limnæa the development of such eggs as may
truncatula. Natural size and be distributed over them; whilst wet
magnified. (After Railliet.) periods during the autumn favour this
development.
On the other hand, the grass
becomes eaten down in autumn, so that the animals gather it almost
level with the ground. As the cercariæ attach themselves to the
lowest leaves they are then ingested in much larger quantities. The
bad effects of wet seasons are not immediately apparent, but appear
during the following spring.
Distomatosis is common throughout almost the whole of Europe,
Africa, and America. In France it is most serious in the moister
regions of Sologne, in Berry, the mountainous and wet districts of the
great central plateau, and particularly in the Pyrenees. It particularly
attacks oxen in the valley of the Meuse, the marshes of Picardy, the
lower regions of Normandy, and in all the mountainous pastures of
the central plateau.
 Lesions. The lesions of distomatosis vary with the stage of
development of the parasites. During the primary phase of invasion
of the bile ducts by young distomata one finds interstitial diffuse
hepatitis, due to perforation of the gland by young parasites,
adhesive perihepatitis, with the formation of false membranes, and
not uncommonly slight peritonitis.
Zoologists state that the young distomata penetrate the liver by
passing upwards against the current of bile. It does not appear
impossible, however, that they may penetrate by another path,
particularly as so-called “erratic” forms of distomatosis like
distomatosis of the lung, heart, lymphatic glands, and various other
tissues are not uncommon. It has been suggested that the young
distomata, arriving in the bile ducts, perforate the gland, giving rise
to these lesions of perihepatitis, peritonitis or erratic distomatosis;
but this view is scarcely in harmony with the fact that the parasites
are usually found in the bile ducts.
During the second phase, corresponding to the development of
almost adult distomata, the perihepatitis and peritonitis set up either
produce fatal results by secondary infection or diminish and
disappear. The parasites develop in the bile ducts, in which they
attain the adult condition. They steadily ascend towards the origins
of the ducts, dilating them in their passage in an extraordinary way.
The number of parasites varies greatly: sometimes there are but few,
and they are only discovered on post-mortem examination; in other
cases the bile ducts are crammed with them, as many as six or seven
hundred or even a thousand being present. The distended bile ducts
always show chronic peripheral inflammation, which steadily
becomes aggravated, producing pericanalicular atrophying sclerosis.
This condition is followed by change in and disappearance of a
certain quantity of hepatic tissue, and by various forms of vascular
and secretory disease.
This is the period of greatest disturbance, not only in consequence
of the actual presence, but also of the mode of living, of the parasites.
Moussu declares that the parasites live principally on blood, at
least during the first and second stage of their sojourn in the liver,
adducing as proof that if one completely injects the vascular system
of the liver (arteries and veins), some of the injected matter will be
found a day afterwards in the digestive apparatus of the parasites.
 The disturbances which they produce are therefore due to their
actual presence and its consequences, to their mode of life, and to the
intercurrent infections of which they are sometimes the initial cause.
It is idle to object that the part played by these parasites is less
important than has been suggested, and that the mortality results
from intercurrent infection, and not from the parasites themselves. It
is equally idle to point out that carcases of animals suffering from
severe infection with distomata, particularly the carcases of sheep,
are frequently found in slaughter-houses, in perfectly fat condition,
and with the appearance of not having suffered in any way. These
observations are perfectly correct and well founded. But it matters
little that death results from an infection superadded to the
distomatosis, if the presence of distomata is the determining factor
in causing the superadded infections, and if such infection is, as
Moussu believes, almost inevitable in animals already exhausted by
the action of the parasites.
The fact that animals suffering from distomatosis and slaughtered
for food are well nourished is not a valid objection; for it has long
been known that wasting and anæmia are not immediate
consequences, and that before they are clearly apparent the
distomata must have been present in the liver for several months.
Bakewell and the Marquis of Behague have shown that in moderately
infected animals there is a tendency to lay on flesh during the first
and a portion of the second stage of development of the disease.
If the animals are slaughtered before the period of progressive
decline sets in, it is quite possible to form entirely wrong views
regarding the importance of these parasites.
The wasting process commences towards the end of the second
phase of the disease, and then makes rapid progress. The parasites,
which have then been continuously drawing on the blood for their
nourishment for a long time, produce anæmia, and some infection of
the bile ducts, and usually a certain degree of icterus.
The third phase is accompanied by general signs of cachexia,
which need not again be described. They are similar to those of all
progressive cachexias. In animals which survive this phase and are
ultimately slaughtered the liver always shows very marked sclerosis,
commencing around the biliary ducts. Even after the parasites have
been evacuated, these ducts appear indurated, thickened, fibrous,
and sometimes encrusted with biliary deposits or obstructed with
true calculi. These calculi may or may not contain parasites;
sometimes they simply contain eggs: they are open, tubular, and
perforated, but always irregular on the surface.
When in addition complications have appeared, one usually finds
general lesions of septicæmia and blood infection.
In erratic distomatosis, which is of no importance clinically,
distomata may become encysted in the lung or other viscus, and in
time die. The cysts, which only contain one and rarely two parasites,
present a fibrous shell, enclosing a blackish, pultaceous, grumous
magma, which sometimes has undergone a certain amount of
calcareous infiltration. The parasite may be entirely destroyed.
Diagnosis. Early diagnosis is difficult, and can only be
established by microscopic examination of the excreta and the
discovery of eggs. On an average one may find one egg in each
preparation when the liver contains 80 to 100 flukes. When wasting
is very marked, and particularly when there has already been a
number of deaths, diagnosis becomes extremely easy. It is sufficient
to find flukes in any form (Distoma hepaticum rel lanceolatum) to
be assured as to the cause of disease.
Prognosis. In severely infested cases the prognosis is extremely
grave, because no efficient method of treatment exists. Embedded in
the liver, the parasites resist the action of all drugs, and we know of
no anthelmintic eliminated by the bile which in any way affects their
vitality. When the disease is recognised early, the most economical
method is to fatten the animals as rapidly as possible and prepare
them for slaughter.
Treatment. There is no reliable curative treatment. The drugs
which one might employ would kill the animal before poisoning the
parasites embedded in the liver. Various mixtures containing
sulphate of iron, juniper leaves, etc., have been recommended; but
rich food constitutes the best of all treatment, both from a curative
and a prophylactic standpoint.
With the view of preventing the disease, however, and protecting
flocks from attack in places where the disease is common, certain
precautions should be adopted. They comprise—(a) providing a free
supply of rock-salt, either in masses placed in the mangers or