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PDF The Illustrated Book of Edible Plants Jack Staub Ebook Full Chapter
PDF The Illustrated Book of Edible Plants Jack Staub Ebook Full Chapter
PDF The Illustrated Book of Edible Plants Jack Staub Ebook Full Chapter
Jack Staub
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Table of Contents
Preface
Anise
Apple
Apricot
Artichoke
Asparagus
Basil
Bay Laurel
Bean
Beet
Blackberry
Blueberry
Borage
Broccoli
Brussels Sprout
Cabbage
Carrot
Cauliflower
Celery
Chamomile
Chard
Cherry
Chervil
Chives
Cilantro (Coriander)
Cranberry
Cress
Cucumber
Currant
Dill
Eggplant
Fennel
Fig
Garlic
Goji Berry
Gooseberry
Grape
Grapefruit
Honeyberry
Horseradish
Huckleberry
Kale
Kiwi
Lavender
Leek
Lemon
Lemon Balm
Lemon Verbena
Lemongrass
Lettuce
Lime
Lingonberry
Lovage
Marjoram
Melon
Mint
Mulberry
Mustard
Nectarine
Okra
Onion
Orange
Oregano
Parsley
Pea
Peach
Pear
Pepper
Persimmon
Pineapple
Plum
Potato
Pumpkin
Quince
Radish
Raspberry
Rhubarb
Rosemary
Sage
Savory
Spinach
Squash
Strawberry
Tarragon
Thyme
Tomato
The Illustrated Book Of Edible Plants
Jack Staub, Proprietor Hortulus Farm
Gibbs Smith
P.O. Box 667
Layton, Utah 84041
Orders: 1.800.835.4993
www.gibbs-smith.com
ISBN: 9781423646754
The Illustrated Book Of Edible Plants
Table of Contents
Preface
Anise
Apple
Apricot
Artichoke
Asparagus
Basil
Bay Laurel
Bean
Beet
Blackberry
Blueberry
Borage
Broccoli
Brussels Sprout
Cabbage
Carrot
Cauliflower
Celery
Chamomile
Chard
Cherry
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organs, as the lung, the testicle, the liver, the spleen, etc. The
dependence of miliary tuberculosis of the pia upon previously-
existing caseous or other inflammatory deposits in some part of the
body is acknowledged by most modern pathologists. Seitz3 states
that out of 130 cases, with autopsies, of adults, upon which his work
is based, such deposits were found in 93.5 per cent. General
constitutional weakness, either congenital or resulting from grave
disease or from overwork, from insufficient or unwholesome food,
and from bad hygienic surroundings, also favors the deposit of
tubercle in the meninges. Sometimes two or more predisposing
causes exist at once. Thus, a child born of tuberculous parents may
be fed with artificial diet instead of being nursed, or may live in a
house whose sanitary condition is bad. Hence the disease is
common among the poor, although by no means rare in the higher
classes of society. In some cases it is difficult or impossible to assign
any predisposing cause. A single child out of a numerous family may
be stricken with the disease, while the rest of the children, as well as
the parents and other ascendants, are healthy. For instance, while
writing this article I had under observation a little boy six years old
whose parents are living and healthy, with no pulmonary disease in
the family of either. The only other child, an older brother, is healthy.
While apparently in perfect health the child was attacked with
tubercular meningitis, and died in seventeen days with all the
characteristic symptoms of the disease. At the autopsy there was
found much injection of the cerebral pia everywhere, a large effusion
of lymph at the base of the brain and extending down the medulla,
abundance of miliary tubercles in the pia and accompanying the
vessels in the lateral regions of the hemispheres, lateral ventricles
distended with nearly clear fluid, ependyma smooth, choroid
plexuses covered with granulations, convolutions of brain much
flattened. Careful investigation, however, will usually enable us to
detect some lurking primary cause, either in the family predisposition
or in the history of the patient himself.
3 Die Meningitis Tuberculosa der Erwachsenen, von Dr. Johannes Seitz, Berlin, 1874,
p. 317.
Season appears to have but little influence on the production of the
disease. The largest number of cases is observed during winter and
spring, owing doubtless to the influence of the temperature and
weather, and to the exclusion from fresh air, in favoring the
development of tubercle and the scrofulous diathesis. Males, both
children and adults, are somewhat more frequently attacked than
females.
First Stage: The interval between the prodromic period and the first
stage is usually so gradual that no distinction between the two can
be detected. In other cases the disease is ushered in suddenly by
some striking symptom, such as an attack of general convulsions,
with dilated pupils and loss of consciousness. This is not often
repeated, though partial twitchings of the limbs or of the muscles of
the face may follow at intervals. In young children a comatose
condition, with unequal pupils, is apt to take the place of these
symptoms. The principal phenomena of the first stage are headache,
sensitiveness to light and sound, vomiting, and fever. The latter
varies much in intensity from time to time, but is not usually high, the
temperature seldom rising above 103° F., and usually, but not
always, higher at night than in the morning; but there is no
characteristic curve. The pulse varies in rate, but is usually slow and
irregular or intermittent. The respiration is irregular, with frequent
sighing. The tongue is dryish and covered with a thin white coat. The
bowels are costive. Delirium is frequent at night, and the sleep is
disturbed, the patient tossing about and muttering or crying out. The
eyes are half open during sleep. These symptoms become more
marked from day to day. The pain in the head is more frequent and
severe; the patient presses the hands to the forehead or rests the
head against some support if sitting up. During sleep he occasionally
utters a loud, sharp cry, without waking. There is increasing apathy,
and some intolerance of light, shown by an inclination to turn toward
the wall of the room or to lie with the face buried in the pillow. The
appetite is lost, the constipation becomes more obstinate, the
slowness and irregularity of the pulse persist. With the rapid
emaciation the belly sinks in, so that the spinal column can be easily
felt. Soon the child falls into a state of almost continual somnolence,
from which, however, he can be awakened in full consciousness,
and will answer correctly, generally relapsing again immediately into
slumber. His restlessness diminishes or ceases altogether, and he
lies continuously on the back with the head boring into the pillow. He
becomes more passive under the physician's examination, in strong
contrast to his previous irritability. At the end of a week or more from
the beginning of this stage symptoms of irritation of some of the
cerebral nerves begin to show themselves, in consequence of
pressure from the increasing exudation at the base of the brain and
into the ventricles. Strabismus (usually convergent), twitching of the
facial muscles and grimaces, grinding of the teeth, or chewing
movements of the mouth are noticed. The somnolence deepens into
sopor, from which it becomes more and more difficult to arouse the
patient, who gradually becomes completely insensible.
Second Stage: This period is not separated from the preceding one
by any distinct change in symptoms. The patient lies in a state of
complete insensibility, from which he can no longer be aroused by
any appeal. The face is pale or of an earthen tint, the eyes are half
closed. If the anterior fontanel be still open, the integument covering
it is distended by the pressure beneath. Often one knee is flexed, the
opposite leg extended; one hand applied to the genitals, the other to
the head. Sometimes one leg or arm is alternately flexed and
extended. The head is apt to be retracted and bores into the pillow.
The pupils are dilated, though often unequal and insensible to light:
the sclerotica are injected; a gummy exudation from the Meibomian
glands forms on the edges of the lids. The patient sighs deeply from
time to time, and occasionally utters a loud, piercing cry. Paralysis,
and sometimes rigidity of one or more of the extremities, are often
observed, and occasionally there is an attack of general convulsions.
The pulse continues to be slow and irregular, the emaciation
progresses rapidly, and the abdomen is deeply excavated. The
discharges from the bladder and rectum are involuntary. The
average duration of the second stage is one week.
I have already observed that the division of the disease into definite
stages is purely arbitrary, and is employed here merely for
convenience of description; in fact, few cases pursue the typical
course. A period of active symptoms and another of depression can
often be observed, but these frequently alternate. Stupor and
paralysis may characterize the early stage, and symptoms of
irritation, with restlessness, screaming, and convulsions,
predominate toward the end. Certain characteristic symptoms may
be wholly or in part wanting, such as vomiting, constipation, or
stupor.
In the early stage of the disease the pupils are usually contracted
and unequal. They are sluggish, but still respond to the stimulus of
light. At a later period they become gradually dilated, and react even
more slowly to light or not at all, the two eyes often differing in this
respect. Ophthalmoscopic examination frequently shows the
appearance of choked disc and commencing neuro-retinitis. In rare
cases tubercles are seen scattered over the fundus of the eye. They
are about the size of a small pin's head, of a yellowish color, and of
sharply-defined contour. Neuro-retinitis and choked disc are not, of
course, pathognomonic of tubercular meningitis, and choroidal
tubercles are so rarely seen as to be of little avail in diagnosis. In
fact, they are less frequent in this disease than in general
tuberculosis without meningitis. In twenty-six cases of tubercular
meningitis examined by Garlick at the London Hospital for Sick
Children they were found only once.6 The effect upon the conjunctiva
of the unclosed lids has been already described.
6 W. R. Gowers, M.D., Manual and Atlas of Medical Ophthalmoscopy, Philada., 1882,
p. 148. See, also, Seitz, op. cit., p. 347; Steffen, op. cit., pp. 452 and 472; and
“Tubercle of the Choroid,” Med. Times and Gazette, Oct. 21, 1882, p. 498.
FIG. 30.
Autopsy.—General lividity of surface, much emaciation. Much fine
arborescent injection on outer surface of dura mater. Numerous
Pacchionian bodies. Yellow matter beneath arachnoid along course
of vessels on each side of anterior lobes. Abundant fine granulations
along course of vessels on each anterior lobe, on upper margins of
median fissure, along fissure of Sylvius, and on choroid plexuses.
Very little lymph at base of brain. Six or eight ounces of serum from
lateral ventricles, and abundant fine transparent granules over
ependyma of both. Numerous opaque granulations in pia mater of
medulla oblongata. Surface of right pleura universally adherent.
Mucous membrane of bronchia much injected; a considerable
amount of pus flowed from each primary bronchus. No tubercles in
lungs nor in peritoneum. No ulcerations in intestines. No other
lesions.
The above-described lesions are not confined to the brain, but may
extend to the cerebellum, the pons, the medulla, and the spinal cord.
If examinations of the latter were more frequent in autopsies of this
disease, we should doubtless find, as has been done in some
instances, that the membranes often show the characteristic
alterations of tubercular meningitis, and even the presence of
granulations in the cord itself. The lesions may extend throughout
the cord, and are especially noticed in the dorsal region and in the
vicinity of the cauda equina. Their presence explains some of the
symptoms evidently due to spinal origin, such as retraction of the
head with rigidity of the neck and of the trunk, contractions of the
limbs, tetanic spasms, priapism, paralysis of the bladder and rectum,
etc., which are common in simple spinal meningitis.
The deposit of miliary tubercles in the pia mater, with little or no
accompanying meningitis, is met with in rare instances. The
tubercles are few in number, but vary in dimensions, being
sometimes united together in masses of considerable size, which are
frequently encysted. Beyond thickening and opacity of the
membrane, their presence seems to excite but little inflammatory
reaction, but they are generally accompanied by ventricular effusion
which by its pressure gives rise to characteristic symptoms.