first becomes stretched by the developing embryo to finally become
a long, narrow sac encasing the fully developed embryo as it exists
in man. From the lymph stream they reach the general circulation.
In a case of a man with filarial embryos in his peripheral
circulation, who committed suicide one morning, Manson found the
embryos, in large part, contained in the vessels of the lungs.
There were 675 embryos per slide in blood from the lungs for one
from blood from the spleen or liver. It would thus appear that
during the day, when the embryos are absent from the peripheral
circulation, they retire to the lungs. In the case of the filarial
embryo of persons in the Pacific Islands there does not appear
to exist any periodicity. Bahr thinks this absence of nocturnal
periodicity to be connected with the habits of its principal
intermediary host, _Stegomyia pseudoscutellaris_, which feeds by
day. _Culex fatigans_ feeds at night.
With the filarial embryos found in patients in the Philippines
there is also a lack of nocturnal periodicity. In the opinion of
Ashburn and Craig the Philippine filarial worm is a new species,
_Filaria philippinensis_.
Walker, however, recently examined four adult filarial worms in
the Philippines and was unable to note any differences from _F.
bancrofti_.
PATHOLOGY AND MORBID ANATOMY
The adult worms may exist in numbers and over long periods of time
give off great numbers of embryos into the peripheral circulation
without there being any evidence of disease in the patient. There is
apt to be at such time a marked eosinophilia. The process by which
the fibrosis of lymph channels with obstruction to the flow of lymph
occurs is unknown. Some think that with the pouring out of embryos
inflammatory processes, bacterial or otherwise, may be set up. We
know that there is a tendency for these adults to die and become
calcified, in this way bringing about lymphatic obstruction.
Bahr notes the influence of adult filariae in producing an increase
in connective tissue in glands and considers such glands as less
resistant to bacterial infection.
Manson has an idea that some factor may cause the female to give off
immature embryos, which being oval, and of considerable width, may
block the lymphatics.
It has often been claimed that various cocci were the exciting
factors in the lymphangitis associated with filariasis. Recently
Dutcher has reported the isolation of an organism resembling
_B. subtilis_ as the cause of filarial lymphangitis (_Bacillus
lymphangiticus_).
As the result of the lymphangitis and blocking of the channels
the embryos cannot reach the peripheral circulation; hence when
obstruction does occur and symptoms of lymph stasis appear, there
may be an absence of embryos in the circulation.
It is now well established that patients with elephantiasis very
rarely show embryos in the peripheral circulation, and this fact
should be better understood because there is a tendency to negative
a filarial diagnosis when embryos are absent from the peripheral
circulation.
These lymph channel obstructions may at one time cause dilatations
or varices and at another bring about solid oedemas of the
tributary parts. The treatment will be considered under each
special form of the disease. It may be stated however that
salvarsan, arsenophenylglycin and other similar remedies have been
without special effect in destroying the filarial worms.
CLINICAL MANIFESTATIONS
Not only is it important to understand that elephantiasis and other
manifestations of filarial infection may and usually do exist
without there being embryos in the peripheral blood of the patient,
but also, that a high percentage of a population may show filarial
embryos in their blood and yet never or with extreme rarity show
any of the signs of filarial disease. These people, with abundant
embryos in their blood, usually show no disturbance of health. In the
Philippines one may rarely see a case of chylocele but usually there
is nothing clinical to note.
Johnson, in examining 400 people, in Charleston, S. C., found
19% with filarial embryos, yet only 5% showed any symptoms of
filariasis. Croll states that 11.5% of 4000 Europeans admitted
to the Brisbane Hospital (Australia) showed filarial infection
but practically none had symptoms. In South Queensland cases of
lymphangitis, chyluria and varicose groin glands are occasionally
seen and rather frequently hydrocele and filarial abscesses. There
is an absence of elephantiasis.
Elephantoid Fever
The febrile accessions that accompany the recurring attacks of
lymphangitis in elephantiasis, lymph scrotum and other filarial
manifestations, are very important because they may lead to errors in
diagnosis.
Thus in Barbadoes, where there is no malaria, a condition in
which there occurs a high fever of sudden onset with rigors and
associated erysipelatous redness of leg or scrotum, accompanied by
lymphangitis and painful lymphatic glands, has given a suggestion
of a malarial paroxysm. The tense inflamed area, after several
days, shows an exudation of lymph and the redness disappears,
but with some resulting thickening of the affected tissues. Such
attacks may terminate with profuse sweating.
The treatment of the condition is such as would be advisable for
ordinary lymphangitis—rest in bed, elevation of the part, laxatives
and local applications.
Lymph Scrotum
This condition is apt to set in with fever. The scrotal tissues are
somewhat tense and reddened and may show numerous lymphatic varices
which when pricked with a needle, give exit to lymph which may or may
not contain filarial embryos. The lymph continues to exude for a long
time. Erysipelatous manifestations are not uncommon. With recurring
attacks the scrotal tissues become more and more hypertrophied and
may go on to elephantiasis of the scrotum.
Ordinarily local applications with suspension of the scrotum is the
proper treatment. Should the thickening increase to a great extent
the blubbery tissues may be excised, care being exercised to avoid
the testicles and to bring together sound tissue for the enclosing
flaps. These wounds usually heal readily, although there may be
delay in healing from the outpouring of lymph in cases where the
flaps include diseased tissue.
Varicose Groin Glands
Swellings which come on rather slowly and insidiously may involve
the inguinal or femoral groups of glands of one or both sides.
The epitrochlear glands may also be involved. The skin over the
enlarged, rather doughy glands can be freely moved but the glands
themselves are bound down to the deeper tissues. Elephantoid fever
may set in associated with local manifestations of pain and redness.
If such glands are punctured with a hypodermic needle lymph,
which may contain embryos, exudes. This test together with their
slow disappearance on lying down and slow return on assuming the
upright position should differentiate hernia. When the contents of
a hernial sac are omental there is some difficulty in diagnosis. As
a rule it is not advisable to interfere surgically in this filarial
condition.
[Illustration: FIG. 99.—Varicose groin glands and elephantiasis of
scrotum and penis. (From Ruge and zur Verth.)]
Filarial Abscesses
As a rule injury to the adult filarial worms, which results in their
death, is not followed by abscess formation but such termination
may occur. These abscesses have been found deeply seated in the
extremities. Wise and Minett in a careful examination of 28 such
cases found evidences of adult filariae in 22 cases. In 21 of these
abscesses, infections with streptococci or staphylococci were
demonstrated. Very interesting also is the finding of filarial worms
in deep-seated abdominal abscesses.
As regards location, these filarial abscesses were found 31 times
in the pelvis of the kidney, 18 times in the epididymis, 12 times
in the retro-peritoneal tissues, 25 times in the inguinal glands,
4 times in the ilio-psoas muscles and 8 times in the lymphatic
vessels.
They regard the endemic funiculitis to which attention has been
directed by Castellani as simply a similar process involving
the tissues about the spermatic cord. The treatment of filarial
abscesses is similar to that of other abscesses.
Chyluria
As the result of obstruction of the lymphatic vessels varices may
form in the bladder lymphatics and, as the result of their rupture,
milky urine may be passed. If the thoracic duct be occluded the
urine will show an abundance of fat, while if the obstruction exists
only in other lymphatics, the milky fluid will be found to show but
little fat. Blood is usually present in chyluria so that the urine
will show an pinkish tinge.
Chylous urine coagulates rapidly and we have in such a specimen of
urine, upon standing, an upper fatty layer and pinkish sediment at
the bottom, with a clot between.
The sediment shows lymphocytes and at times filarial embryos. When
the exudate is lymph mixed with blood the term haematolymphuria
would be a better one.
Clots may form in the bladder and give rise to obstruction to the
flow of urine from the bladder.
The appearance of the chyluria is often preceded by heaviness about
the loins and pains in the region of the bladder.
The morning urine in such a case is apt to be clear while that
passed later in the day is milky in appearance.
A feature of chyluria is its tendency to disappear and reappear
so that when treating such a case one should be conservative in
considering the treatment as effecting a cure.
It is difficult to understand why chyluria should be common in
India and China while almost unknown in the filarial infections of
the Pacific islands.
In treating a case of chyluria one should enjoin rest in bed,
laxatives and a restriction of fluids and fats. Patients subject
to the condition should refrain from active exercise and other
conditions which might cause fatigue. Drugs are of little value.
Filarial Orchitis and Hydrocele
The condition rather resembles an attack of epididymitis. As a result
of recurring attacks hydrocele develops. The fluid may be lymphous
or chylous in appearance and upon microscopical examination may show
filarial embryos. These filarial hydroceles seemed to be the most
common manifestations of the disease as observed in the Philippines.
These hydroceles or chyloceles do not become very large but may
require tapping.
Elephantiasis
As the result of recurring attacks of lymphangitis the tissues of
the affected part show the effects of lymphatic obstruction by an
hypertrophy of the skin and subcutaneous tissues. It would seem that
the combination of lymphatic obstruction and bacterial infection is
necessary for the production of elephantiasis. The skin of a part
affected with elephantiasis is rough and the hair scanty. In addition
to the lymphoedema of the part there is a great increase in the
connective tissue.
On account of the lymphatic stasis incision into the blubbery
tissue causes the outpouring of much lymph.
Elephantiasis of the lower extremities is by far the most common
situation, giving us probably 90% of such affections. In Fiji
elephantiasis of the upper extremities is quite common.
Other favorite sites are the scrotum, vulva, breasts and penis.
Rarely the scalp or areas about neck or trunk may show involvement.
[Illustration: FIG. 100.—Elephantiasis of the legs. (From Ruge and
zur Verth.)]
Surgical treatment is the one usually followed. When an extremity
becomes too much of a burden, amputation may be indicated. The
employment of the method of lymphangioplasty, which consists in
the introduction of silk threads into the subcutaneous tissues,
to make a channel to the normal lymphatics, does not seem to have
been attended with any degree of success or at any rate permanent
results. These wounds tend to become infected and if this does not
occur the new channels are speedily obliterated.
Castellani recommends the use of Merck’s fibrolysin in injections of
from 2 to 4 cc. daily, for three to six months. After each injection
the part is tightly bandaged with flannel or rubber bandages. The
injections may either be made into the affected part or into the
gluteal region. Massage prior to the bandaging may give better
results. When the limb becomes smaller and the skin smoother, long
strips of skin and subcutaneous tissue may be dissected out and the
adjacent edges sutured.
In considering the advantages of operation in elephantiasis of the
scrotum it is usually stated that the only question involved is the
removal of a burdensome mass which in no way is a source of danger
to the life of the patient. At the same time such patients are
subject to attacks of elephantoid fever, a condition not without
its dangers. There is one factor not usually brought forward and
that is the remarkable effect of a successful operation on the
mental state of the patient. This is well shown in the accompanying
illustrations of the patient before and after operation. If
sexual deficiencies are of so powerful an influence on persons of
education how much greater must they weigh on an uneducated native
with but few of the higher interests of life.
Prior to operation the patient should be kept in bed for a day
or so to lessen the amount of fluid and to secure relaxation of
tissues. Thorough scrubbing with soap and water the day of and the
day before the operation and the use of alcohol as an antiseptic
are important. Some prefer iodine.
[Illustration: FIG. 101.—Elephantiasis of the scrotum. Before
operation. (Fauntleroy.)]
For the operation the lithotomy position is employed. An assistant
supports the scrotal tumor wrapped in a sterile towel. Fauntleroy,
whose method I give, does not recommend a tourniquet to the base of
the tumor as in his opinion it assists but little in controlling
haemorrhage and endangers asepsis. Haemostats answer better and as
the vessels which give most trouble are deeply situated the elastic
cord would not affect them. In some cases there is very little
bleeding. The upper part of the pear-shaped tumor usually affords
sufficient sound skin next the thighs for the flaps. As a rule
the elephantoid tissue does not involve the upper 2 or 3 inches
of the skin anteriorly, which is thus available to cover in the
base of the penis. In addition to this covering for the penis we
have a long prepuce which has been considerably stretched so that
after removing all elephantoid tissue there is enough sound prepuce
remaining to cover the distal 2 or 3 inches, so that usually there
is sufficient sound skin for a 5-inch penis.
[Illustration: FIG. 102.—Elephantiasis of the scrotum. After
operation. Note change in mental state. (Fauntleroy.)]
The flaps which are to cover the penis and testicles should be
mapped out with shallow incisions and care must be exercised that
only sound skin is included in these flaps. A horseshoe shaped
incision is made commencing at the left side of the base of the
tumor about 1 inch from the thigh and about at the level of the
penis in health. The incision is carried downward and passes just
below the opening of the penis on the tumor surface. A similar
incision on the right side completes the horseshoe curve. Next a
downward incision in the sound skin is made over the posterior
surface of the tumor, thus encircling the base of the scrotum. The
anterior horseshoe incision is now deepened to free the penis,
care being taken not to injure the spermatic cord. Next the
incisions are deepened laterally until the testicles are reached.
The testicles are usually in the center of the tumor imbedded in
a blubbery tissue from which they can be easily stripped. The
remains of the gubernacula are then hooked up and cut close to the
testicles. The tunicae vaginales are often thickened and contain
fluid which has to be drawn off.
In 60% of Fauntleroy’s cases it was necessary to remove one
testicle on account of extensive disease. One must also bear in
mind the possibility of hernial complications and undescended
testicle.
A sound is now introduced into the urethra and the septum of the
scrotum divided close to the sheath of the penis, then dissecting
away the blubbery tissue. At this stage there may be considerable
bleeding.
The testicles and spermatic cords are then dissected away from the
tunicae vaginales. The penis is now freed by a circular incision
around and above the opening in the anterior part of the mass.
The remainder of the horseshoe flap is now dissected up and the
penis freed. The proximal covering for the penis is made from this
horseshoe flap which is stitched to the distal one shaped from the
prepuce, carefully trimmed of elephantoid tissue.
The lateral flaps are brought together with linen or silk-worm gut
sutures leaving space for a drainage tube and we thus form a new
scrotum for the testicles.
The mortality is usually given as 5% but Fauntleroy did not lose a
case among 149 such operations, the tumors varying from 10 to 85
pounds in weight.
Chylous Hydrocele
Filarial affections of the tunica vaginalis or the testicle itself
are not rare. In the milky fluid obtained by tapping such a hydrocele
we may find filarial embryos.
Besides chylous hydrocele we may have a chylous ascites or a
chylous diarrhoea. Where there is no obstruction to the thoracic
duct there is less fat and the condition is more properly a
lymphocele rather than a chylocele. The same distinction is
applicable to the other conditions connected with lymphatic varices
due to lymphatic obstructions other than that of the thoracic duct.
LABORATORY DIAGNOSIS
The blood from a needle prick of the finger tip or the lobe of the
ear can be examined as a fresh preparation. It is advisable to make a
vaseline ring around the drop of blood on the slide and then apply a
cover-glass. Such a preparation will permit of the examination of the
living embryos for a day or more.
Smear preparations may be made by the Ehrlich method of drawing
cover glasses apart or by the Daniels method on slides. Some
prefer making a thick smear of a drop of blood and, after it
has dried, carefully to dehaemoglobinize it with water and then
staining with dilute haemotoxylin. Staining with Leishman’s or
Wright’s stain gives beautiful pictures. Fixation with methyl
alcohol or with heat, by burning off a film of alcohol, and then
staining with Giemsa’s stain or some haematoxylin preparation, is
to be recommended. On the whole I consider haematoxylin the most
desirable staining reagent, as such preparations hold their color
for a long time. The paper-like sheaths are seen as if twisted
about the larvae with their violet-stained cells. One should note a
break in the violet-stained cell column which is 50µ from the head
end of _F. bancrofti_ and 40µ for _L. loa_.
A V spot is seen posterior to the break in the cell column and
shows best with very light staining.
The break in the column of the cell nuclei marks the position of
the nerve ring, which is distant from the head one-fifth the total
length. The anterior spot, below the break in the cell column, is
distant about 30% of the total length. It is the location of the
excretory pore. In _F. bancrofti_ the cell nuclei extend to 95% of
length, thus differing from those of _L. loa_, which fill up the tail
end. At about 82% of the length from the head is located the anal
pore.
Ruge’s thick film method for malarial parasites gives excellent
results in staining filarial embryos. Either the Giemsa or
haemotoxylin staining may be employed.
Embryos may be found in the lymph from varicose groin glands or in
the exudate from a chylous hydrocele, as well as in the urinary
sediment from a case of chyluria.
The failure to find embryos in no way negatives the existence of a
filarial infection.
Adult filariae, either alive or dead and calcified, may be found in
the lymphatic glands or in the contents of filarial abscesses.
The blood shows an eosinophilia.
LOA LOA
This filarial infection is at present only known for the West Coast
of Africa. In the Cameroons and in Old Calabar the infection is quite
common.
As noted in the table previously given, the adults which are a
little more than an inch long have cuticular protuberances or
bosses, about 12 to 15 microns in height. The sheathed embryo is
very similar to that of _F. bancrofti_, but has a more twisted
tail and shows a complete filling up of the tail end with rather
elongated cells. The lines of the curves of the embryo show
irregularities and are not the smooth lines characteristic of _F.
bancrofti_ embryos.
The periodicity is diurnal, for which reason the parasite was
originally termed _F. diurna_.
Leiper has reported two species of _Chrysops_, one of the tabanid
biting flies, as transmitting agents and considers that the embryos
undergo development in the salivary glands of the fly.
The life history is not well understood but as a rule a period of
several years elapses after infection before adult filariae or
filarial embryos are found. Again, for some reason, adult filariae
may be noted and when extracted be found full of embryos and yet
embryos not be found in the peripheral circulation.
The adults are noted for their tendency to move about in the
subcutaneous connective tissues having been found in such tissues
in the region of scalp, trunk, penis and extremities.
Most frequently, however, they are noted in the tissues about the
region of the eyes and even under the conjunctivae, from which
location they have been frequently extracted. It is this which has
caused the name _Filaria oculi_ to be given the worm.
[Illustration: FIG. 103.—_L. loa_ above. _Acanthocheilonema
perstans_ below. (From Greene, after Fülleborn.)]
The course of the wandering worm is usually marked by an oedematous
track. In his own case, recently reported by a medical man, the
first symptoms were transient painless swellings about the joints,
associated with stiffness. Various diagnoses, such as rheumatism,
erythema nodosum and angioneurotic oedema were made in his case.
Although two adult filariae were removed at different times the blood
examinations were negative for embryos.
As a rule the appearance of the worms in the subcutaneous tissues
is characterized by itching sensations and a feeling of tension.
Warmth causes them to appear in the superficial tissues while
cold makes them confine themselves to the deeper structures.
Eosinophilia is rather pronounced.
=Calabar Swellings.=—Although we have no absolute proof that these
usually painless swellings, which occur rather suddenly on various
parts of the body having only a thin layer of connective tissue, as
forearms, face, ankles, hands, are connected with an infection with
_L. loa_, yet such is the general view. These swellings are about the
size of a hen’s egg, do not pit on pressure and last for about three
days. There is marked tension over the swellings and they may itch
greatly.
[Illustration: FIG. 104.—_L. loa_ in the subcutaneous tissues, twice
normal size. (From Greene, after Fülleborn.)]
Rarely does one note more than one swelling at a time. Eosinophilia
is quite marked during the attacks. Manson thinks the oedema
results from the extrusion of embryos from the female at the site
of the swelling. Ward considers the cause to be toxic material
excreted by the worm.
There is very little of importance in connection with treatment.
When the worms, which travel in the tissues about the eye, at the
rate of about ½ inch per minute, are noted, some local anaesthetic
may be used and the worm seized with forceps and extracted through
a small incision. Elliot recommends the application of hot
fomentations to the eye and upon the appearance of the worm under
the conjunctiva to instill cocaine solution, seize the worm with
forceps and then pass a silk ligature through the conjunctival
fold taking in the worm. The ligature is tied and an incision made
through which the worm is extracted. Cooling local applications, or
an ichthyol ointment, may be applied to the Calabar swellings.
ONCHOCERCA VOLVULUS
This name is given to a filarial worm, found principally on the
West Coast of Africa, which causes the formation of subcutaneous
tumors. In certain localities as many as 10% of the population may be
infected. More recently the parasite has been reported from Guatemala.
It is supposed that the adult worms cause an inflammation of the
lymphatic vessel in which they may lie and that a formation of
new connective tissue results, giving rise to a tumor-like mass,
which is most often found in the axilla or about the sides of the
thorax. This tissue stroma encompasses the worms except for the
anterior extremity of the female, with its uterine opening, and the
posterior extremity of the male carrying the spicules, which ends
lie loose in a sort of cyst-like dilatation, which is filled with
a viscid fluid swarming with unsheathed embryos. These tumor-like
masses cause very little discomfort, last indefinitely and do not
tend to ulcerate.
It was formerly thought that these larvae were absent from the
peripheral circulation but more recent investigations in cases of
onchocerciasis have shown sheathless larvae in the blood, which had
the characteristics of those in the contents of the tumors. Such
findings, however, are of extreme rarity, the blood examination being
almost invariably negative.
The cysts are usually found on the sides of the chest and are quite
superficial, with the skin freely movable over them. They may be as
large as a hen’s egg but usually are smaller. They are also found
over trochanters or along the crests of the ilium.
Dubois states that the embryos may be found in juice from puncture of
groin glands.
The tumors are easily enucleated.
In the American infections the tumours are more common in the
regions near the eye and it has been thought that certain cases of
keratitis may be due to onchocerciasis.
DRACUNCULUS MEDINENSIS
The disease caused by infection with this parasite is usually termed
dracontiasis and the parasite _Dracunculus medinensis_ or the Guinea
worm.
The geographical distribution includes India, Arabia, the West Coast
of Africa and Brazil.
_Life History._—The male has not surely been seen in man so that
the pathological condition is entirely connected with the female
worm. Almost invariably the female worm, which measures about
two feet long by 1/12 inch broad, tends to wander down to the
connective tissue structures of the lower extremity. In about 10%
of the cases the worm may present elsewhere, as scrotum, back or
arms. At the posterior extremity there is a sort of anchoring hook.
With the anterior extremity the worm presses against the overlying
skin and causes the formation of a blister-like lesion.
This vesicle later on bursts and, if water is applied to the
spot, a delicate tube, the uterus, is extruded and there exude a
few drops of a milky fluid, which swarms with the sharp-tailed,
striated, sheathless embryos. It is thought that the pouring forth
of embryos, when water touches the part, is in order that the
embryos may reach the water of a pool through which the infected
native may be wading. Once in the water of such a pool, the larvae
are swallowed by _Cyclops_ and gaining the body cavity of this
little crustacean, they continue to develop for about one month.
During this period there are two ecdyses, the first after about two
weeks, when the tail becomes blunt.
When one takes these infected cyclops into the stomach, by drinking
water containing them, the cyclops is killed by the gastric juice
and the Guinea worm larva breaks out of the dead intermediary host
and bores its way through the stomach wall and possibly goes to the
tissues about the retroperitoneal region. As a matter of fact we are
in ignorance of the exact cycle which goes on, until the fertilized
female, with her embryo-distended uterine tube, reaches the lower
extremity. A cross section of the female shows the body of the worm
to be almost entirely made up of uterus, with an insignificant
alimentary canal pressed to one side.
The period of incubation is from 8 to 12 months.
Usually there are no other symptoms than discomfort from the
blister and a feeling of heaviness about the affected extremity. At
times there may be pain and fever. The parasite may fail to gain
exit to the skin surface or die before reaching maturity. In such
cases she may become calcified or give rise to abscess formation.
The _x_-ray plate may show a convoluted cord-like structure with
frequent breaks in the line.
[Illustration: FIG. 105.—Guinea worm (_D. medinensis_). Rolled on a
stick for gradual extraction. (From Greene’s Medical Diagnosis.)]
_Treatment._—By douching the point of exit we may cause the uterus
to empty itself in about three weeks. At that time we may commence
extraction by intermittent traction by winding the worm around a
large toothpick or similar object. If undue force is exerted the worm
may break off and abscess formation or sloughing result.
Macfie has reported success in treating 23 cases of dracontiasis
with tartar emetic. He gave 1 grain intravenously every other day
and found that it was not necessary to give more than 6 grains in
the course of treatment. The inflammation quickly yielded and the
discharge from the sore ceased rapidly.
CHAPTER XXIII
THE SCHISTOSOMIASES
GENERAL CONSIDERATIONS
There is a group of diseases, caused by trematodes of the family
Schistosomidae, to which we apply the name schistosomiasis. The
Schistosomidae differ from other human flukes (Trematoda) by not
being hermaphroditic and by having nonoperculated eggs. From these
eggs a ciliated embryo (miracidium) emerges which gains entrance to
certain species of molluscs. In this intermediate host the miracidium
gives rise to a sporocyst, which latter forms daughter sporocysts.
These emerge from the mother cyst and enter the digestive gland of
the mollusc and produce cercariae.
These cercariae show an absence of a pharynx and upon the rupturing
of the sporocyst are discharged from the mollusc and furnish the
infecting stage for penetrating the skin of man or other animal.
There are those who think the entrance is effected through mucous
membranes, especially those of the mouth, genitalia and anus and even
the nasal mucosa.
It is generally admitted that infection by drinking water, containing
the ciliated embryos, is impossible, owing to the rapidity of their
destruction by solutions of HCl of similar strength to that of the
gastric juice.
Infecting mice with _S. japonicum_ cercariae from snails mashed on
the abdominal surface of the mouse, it was found by Suyeyasu that
after penetrating the skin the cercariae went to the right heart by
way of venous and lymphatic channels. From the pulmonary vessels they
penetrate the lungs and go by way of the mediastinum or pleura to the
diaphragm which they penetrate and make their way to the abdominal
cavity next penetrating the liver and entering the portal vein.
It is probable that the earlier stages of development take place
in the portal vein and that having reached maturity the female
attaches herself to the male and together they go, by way of
the inferior mesenteric vein, to the haemorrhoidal or vesical
terminals. The male is in the shape of a narrow leaf, about ½
inch long with a ventrally turned oral sucker and a closely
adjacent ventral sucker. The female is a somewhat longer and
cylindrical worm almost an inch in length and, like the male, has
two suckers. There is a dark brown zig-zag stripe which shows
prominently in the posterior part of the female and outlines the
blood-filled intestinal tract. When the female applies herself to
the ventral surface of the male there is an infolding of the sides
of the flattened surface giving the male a cylindrical outline
and resulting in the formation of a canal containing the female
(gynaecophoric canal).
[Illustration: FIG. 106.—_Schistosoma japonicum_ (male and female).
The sharp edges of the borders at the beginning of the gynaecophoric
canal formed by the male are an accidental appearance. (From Mense.)]
The males of the flukes which cause the vesical (_Schistosoma
haematobium_) and the rectal (_Schistosoma mansoni_) involvement are
covered externally with small tubercles and have a ventral sucker
only slightly larger than the oral one. The Japanese schistosome
(_Schistosoma japonicum_) is slightly smaller, has a smooth surface
and shows a prominent pedunculated ventral sucker of much larger size
than the oral one.
Both suckers are larger than those of the other species.
The eggs of _S. haematobium_ have a terminal spine and measure from
115 to 175 by 60 microns; those of _S. mansoni_ have a lateral
spine and measure from 110 to 125 by 50 microns while those of _S.
japonicum_ are devoid of spinous projections and measure about 100
by 70 microns.
Clinically, the three infections differ as will be noted further on.
Looss claims that the two tuberculated species are identical and
that the lateral spined egg is the product of an unfertilized
female. He has more recently regarded the egg as produced
parthenogenetically. Other helminthologists have noted slight
anatomical differences as to ovaries and testicles so that the
consensus of opinion is that vesical and rectal bilharziases are
caused by different species of the genus _Schistosoma_.
[Illustration: FIG. 107.—Ovum of _Schistosoma japonicum_. By J. A.
Thomson. (Jefferys and Maxwell.)]
Recently Leiper has found cercariae showing the absence of a pharynx
(characteristic of the genus) in a Japanese mollusc. Such molluscs
were teased out in water and laboratory bred mice immersed therein.
One of these mice was killed a month later and adult schistosomes
were found in the portal vessels. Leiper has also found cercariae
showing absence of pharynx in four different species of molluscs
in Egypt. With such molluscs he was able to infect white rats and
other animals. He states that infection with these cercariae from the
mollusc host can bring about infection either by way of the mouth or
through the skin. Sodium bisulphate in a strength of 1 to 1000 killed
these cercariae almost immediately.
It would therefore seem proven that all human schistosome
infections take place following cercarial and not miracidial
development. As proof that _S. haematobium_ and _S. mansoni_ are
different species, Leiper notes that mice infected by molluscs of
the genus _Bullinus_ showed schistosomes with terminal spined eggs,
the ovary lying in the lower half of the female. The male had four
or five large testes. In mice infected by molluscs of the genus
_Planorbis_, the eggs were lateral spined, the ovary was in the
anterior half of the body and the male had eight small testicles.
The mollusc host of _S. japonicum_ is _Blanfordia nosophora_. The
shell of this snail is of cornucopia shape.
As these flukes are found in the blood vessels they are often
referred to as the blood flukes.
HISTORY
Vesical schistosomiasis has undoubtedly existed in Egypt since
ancient periods as vesical calculi are frequent in the mummies of
various dynasties. Ruffer has found calcified schistosome ova in the
kidney of a mummy.
The French troops suffered greatly from the disease in 1800. It was
Bilharz in Cairo, in 1851, who first associated the haematuria with
the presence of the parasite and it is from his name that we get
the designation bilharziasis or bilharziosis for the disease.
In 1903, Manson found lateral spined eggs in a patient from the
West Indies who was suffering from rectal rather than bladder
symptoms. In 1907 Sambon, considering the points of difference
between the eggs and the involvement of rectum rather than bladder,
established a new species, _S. mansoni_.
In the West Indies, as shown by the reports of Surgeon Holcomb from
Porto Rico, rectal bilharziasis is rather common.
For a number of years Japanese physicians had noted the existence
of a disease characterized by splenic and hepatic enlargement,
ascites and cachexia. In August, 1904, Katsurada discovered ova
with a ciliated embryo in the stools of patients with this disease.
He found schistosomes in the portal vessels of dogs and cats
containing eggs similar to those seen in the human cases. He named
this trematode _S. japonicum_. In November, 1904, Catto discovered
the parasite at an autopsy on a Chinaman. In 1910 Lambert, in
China, described a disease, which he called urticarial fever,
and a short time afterward Houghton established the connection
between this disease and the more advanced stages of Japanese
schistosomiasis.
[Illustration: FIG. 108.—Ovum of _Schistosoma haematobium_. By
William Pepper. (Jefferys and Maxwell.)]
[Illustration: FIG. 109.—Ovum of _Schistosoma mansoni_. By William
Pepper. (Jefferys and Maxwell.)]
PATHOLOGY
The pathological lesions are almost entirely due to the irritation
of the eggs with resulting connective tissue increase or ulcerative
processes. For some reason these flukes select the inferior
mesenteric vein and make their way to the vesical plexus of veins in
the case of _S. haematobium_ and to the haemorrhoidal vessels for the
other species. At times the ova or worms may be carried over to the
systemic veins by way of the channels of anastomosis. In the terminal
vessels the female gives off the eggs which penetrate the adjacent
mucosa giving rise to inflammatory thickenings and the extrusion of
the irritating eggs into the lumen of the bladder or rectum.
In the bladder these terminal spined eggs cause haematuria and form
the nucleus for vesical calculi. The mucosa may also show wart-like
excrescences. If the eggs are swept back through the portal vessels
to the liver an interlobular cirrhosis results which would seem to
be due entirely to the irritation of these egg emboli and not to
toxic products of the worms themselves. Marked ureteral and kidney
lesions may result as complications of cystitis or primarily from
irritation by ova. In women the vagina, vulva and cervix uteri may
show papillomatous thickenings. Bilharzial lesions of the male
urethra are not uncommon and may lead to fibroid thickenings and
fistula.
In searching for the flukes at autopsy we should make a
longitudinal slit in the portal vein and with a spoon scoop out the
blood and search for the parasites in a glass dish.
In the intestinal form of schistosomiasis the rectum may be studded
with polypoid tumors which when projecting from the anus may ulcerate
and lead to a diagnosis of cancer of the rectum. In sections from
these masses great numbers of lateral spined eggs may be found.
The connective tissue increase is in the submucosa. The gut section
may also present small abscess-like areas.
Eggs have been found in the appendix as well as in the large
intestines and the small intestine has been found involved in one
case. In rare instances ova have been found in the lungs, spleen
and even in the brain and spinal cord.
By digesting selected tissues in 4% NaOH at 75°C. and centrifuging
one may find eggs which otherwise would be overlooked. Statistics
from Cairo usually note 30 to 40% of infection in natives but
Ferguson employing all methods found 61% infected at autopsies on
600 males. In all forms of schistosomiasis but particularly in the
Japanese infection, eosinophilia is pronounced.
In Japanese schistosomiasis the intestines may show thickenings at
the site of aggregations of eggs. In the liver a marked interlobular
cirrhosis occurs with numerous eggs in the connective tissue
increase. Rarely, eggs may lodge in the brain, giving granuloma-like
areas. The irritating eggs may also give rise to similar areas in the
lungs.
SYMPTOMATOLOGY
Vesical Schistosomiasis or Endemic Haematuria
This form of the disease is chiefly found in Egypt, Syria, Uganda
and South Africa. It is caused by _S. haematobium_ and the period of
incubation is approximately six months.
[Illustration: FIG. 110.—Vesical schistosomiasis showing fistulous
tracts opening from penis and scrotum. (From Ruge and zur Verth.)]
The first symptoms are pricking sensations about urethra and slight
haematuria which comes on at the end of the act of micturition.
Excesses or fatigue are apt to increase the haematuria. The diagnosis
is made by finding the ova in the sediment of the centrifuged urine.
Symptoms of cystitis and even pyelitis may follow the early
bladder and urethral manifestations. Pain in the back or symptoms
suggesting renal colic may be present. Anaemia and physical
weakness gradually develop. An important sequel is vesical
calculus. It is a question whether the eggs or some other product
of the infection form the nucleus of such a stone. Not only can
stone be recognized by cystoscopy but rather distinctive are
small, glazed yellowish nodules with areas of granulation tissue.
Papillomatous growths may also be seen upon cystoscopy.
Perineal fistulae in the male and vaginitis in the female may be
noted.
When reinfection does not occur the haematuria tends slowly to
disappear but recovery does not usually take place for several
years. The vesical schistosome (_S. haematobium_) often causes
pathological changes in the rectum so that a case may show both
vesical and rectal symptoms. The rectal schistosome (_S. mansoni_)
does not give rise to vesical trouble.
Rectal Schistosomiasis
While terminal spined eggs may be found in rectal lesions, but
usually combined with lateral spined eggs, in countries where the
vesical form of the disease exists, yet there are many parts of
the world where, with the exclusive existence of an intestinal
bilharziasis, only lateral spined eggs are found. The infection
resulting from _S. mansoni_ is the sole one in the West Indies, Congo
Free State and in North-eastern South America.
The symptoms are usually those of a chronic dysentery with more or
less tenesmus and straining. Prolapse is a common result and is the
cause of the ulcerations which may cause the disease to be diagnosed
as cancer. Cirrhosis of the liver is more apt to occur than in pure
vesical schistosomiasis.
Most writers fail to mention other than the later manifestations
of rectal bilharziasis, the earlier symptoms being overlooked
or attributed to other causes. The same was true of Japanese
schistosomiasis in which the initial “urticarial fever” was only
recognized as connected with the late manifestations of liver
cirrhosis and ascites a few years ago.
In 1916 Lawton noted in a number of Australian soldiers, encamped
in Egypt, a fever of about 7 to 10 days’ duration in which the
evening rise approximated 103°F. A diarrhoea and abdominal pain
accompanied the fever and along with this a cough and patchy
consolidation. Most of the cases showed urticaria which lasted from
one to seven days. All cases showed a well marked eosinophilia.
The diagnosis, but frequently only after prolonged and continued
search, was made by the finding of the lateral spined eggs of _S.
mansoni_. The period of incubation in these cases seemed to be from
one to three months.
Japanese Schistosomiasis
This is also called Katayama disease and in its early stages
urticarial fever or Yangtse fever. It is caused by the
nontuberculated species, _S. japonicum_, which is characterized by
the egg without a spine.
Laning, in a study of 7 well-controlled cases, has shown that the
disease sets in after two or three days from the time of exposure
to infection, by wading through paddy fields or still waters of
infected ponds or lakes. The disease occurs in China, Japan and
possibly in the Philippine Islands.
[Illustration: A B
FIG. 111.—A and B, Case of _Schistosoma japonicum_. Severe infection
of three years’ duration. Ova very abundant in stools. Liver dullness
diminished. Spleen not enlarged. (From Jefferys and Maxwell.)]
The course of the disease may be divided into 3 stages: the 1st, that
of urticarial, pulmonary and febrile manifestations, which lasts
about a month; the 2d, where ova begin to show in the small mass of
bloody mucus which may cap the stool, and finally the 3d stage with
cirrhosis of the liver, ascites, cachexia and death.
In the 1st stage we have headache and an evening rise of
temperature to about 101°F. or 102°F. Shortly after the onset
urticarial lesions, which may be 2 or 3 inches in diameter, may
appear and disappear on various parts of the body.
The pulse rate is usually low. Very characteristic and early
manifestations are those of the pulmonary involvement. Here
oedematous patches may give the signs of crepitation and
consolidation to rapidly disappear and reappear in another part of
the lungs.
These pulmonary manifestations and the associated fever frequently
cause a diagnosis of broncho-pneumonia to be made. A dry hacking
cough appears early and with the fever, etc., may make one think
of tuberculosis. The urticarial lesions often cause a diagnosis of
ptomaine poisoning to be made. The blood examination shows a marked
eosinophilia, of from 30 to 60%.
The 2d stage shows more or less intestinal disturbance with at times
bloody mucus containing ova. The ova may not be present for long
intervals or may never be found. Where reinfection does not take
place the patient tends to recover but if exposure to infection be
kept up then the 3d stage sets in with rather marked dysenteric
manifestations, emaciation, anaemia, ascites, dropsy and a terminal
cachexia.
The bladder never seems to be involved in Japanese schistosomiasis.
The eggs, however may be carried to the brain and produce symptoms
of Jacksonian epilepsy.
LABORATORY DIAGNOSIS
This consists in the search for ova in the centrifuged urine of
vesical bilharziasis or in the bloody mucus of the intestinal
manifestations of the disease. If one adds water to the urine the
ciliated embryo will be noticed to break out of the shell in a few
minutes and move about actively as if in search for some host.
The eosinophilia is of great diagnostic value and is usually
associated with an increase in the leucocyte count.
Fairley has introduced a complement fixation reaction in diagnosis,
using an extract of the livers of infected snails as antigen. The
reaction appears early in the infection but disappears in the later
stages. It is a group reaction as the livers of Bullinus answer for
the _S. mansoni_ serum as well as for the specific _S. haematobium_
serum.
PROPHYLAXIS
Bathing should be allowed only in filtered water, there being an
absence of the infecting cercariae in such a supply.
Then, too, if a water which does not contain fresh water snails is
stored for three or four days the cercariae which might have been
present in the freshly pumped up water will have died out, such
free cercariae only surviving for about this period. The gastric
juice will destroy cercariae so that it would seem impossible for
an infection to occur by the alimentary tract atrium with the
exception that cercariae might bore their way through the buccal
mucosa as well as through the skin. The sterilization of the urine
of cases of vesical bilharziasis and of the faeces in other forms
should be carried out where practicable. It is now considered
practicable to eradicate carriers of the infection with antimony
treatment.
TREATMENT
The most important matter is to avoid places where the infection is
known to exist. If one must wade through infected waters the body
should be protected by canvas or other closely woven garments.
Of various treatments, having in view the destruction of the worm,
such as salvarsan, etc., none seem to have been of any value except
antimony.
Robertson has reported relief of symptoms from the administration
of 2 grains of thymol dissolved in half a drachm of benzine. The
treatment is continued for a few weeks. Others have not had good
results from this treatment. Local treatment is necessary in
treating the cystitis and prolapse of rectum. Operative procedures
are indicated where calculi exist.
The results obtained by treatment with tartrate of antimony during
the past three years justify us in considering bilharziasis as a
disease which has a specific for its cure. Almost all cases will
yield to a course of intravenous injections of from one-half to two
grains of the drug, commencing with the smaller dose. The drug should
be well diluted (25 to 50 cc. sterile saline). Some use a 1% solution
but the higher dilutions are safer from a standpoint of avoiding
phlebitis. Intravenous injections are made twice weekly and the total
amount of drug given during the course should rarely exceed 25 to 30
grains. For details see under treatment of leishmaniasis.
CHAPTER XXIV
MINOR HELMINTHIC INFECTIONS
PARAGONIMIASIS
General Considerations
This is an infection with a trematode, _Paragonimus westermanni_ (_P.
ringeri_) (_Distoma pulmonale_). It is rather common in some parts of
Japan and Formosa.
[Illustration: FIG. 112.—_Paragonimus westermanni_: natural size; to
left showing ventral surface; to right showing dorsal surface. (Braun
after Katsuruda.) (From Tyson.)]
Arce has recently reported cases of paragonomiasis in three
Peruvians who had been in contact with Japanese immigrants.
In 1880, Baelz found the ova in the sputum of a case of haemoptysis
in a Japanese, as did also Manson in a Chinaman. Manson’s case
subsequently died and when autopsied showed in his lungs a fluke
which was responsible for the eggs seen by Manson. The fluke itself
is a little more than ⅓ of an inch (8 mm.) long and is almost round
on transverse section, there being, however, some flattening of
the ventral surface. The acetabulum is conspicuous and opens just
anterior to the middle of the ventral surface.
The branched testicles are posterior to the laterally placed uterus
and the genital pore opens below the acetabulum. The branched ovary
is opposite the uterus on the other side.
It is rather flesh-like in appearance and is covered with
scale-like spines. The flukes are usually found in tunnels in the
lungs, the walls of which are thickened connective tissue. These
tunnels result from hypertrophy of the bronchioles. There may be
also cysts formed from the breaking down of adjacent tunnel walls.
In addition to lung infection with this fluke, brain, liver and
intestinal infections may be found.
The life history and mode of infection of man, further than the
miracidium stage, has been unknown until recently. If the eggs in the
sputum are shaken up with water and the water renewed from time to
time a ciliated embryo or miracidium develops after a few weeks and,
at this time if one presses on a cover-glass covering some of these
more mature ova, the miracidium will break through the operculated
extremity of the egg and swim about actively in the surrounding
water.
[Illustration: FIG. 113.—Sputum of man containing eggs of the lung
fluke, greatly enlarged. (After Manson.)]
Nakagawa has found that the miracidia infest certain fresh water
molluscs and become cercariae in this first intermediate host. From
this host the cercariae go to certain fresh water crabs and encyst
in this second intermediate host, either in the liver or in the
gills. In Japan one of these crab hosts, _Potamon dehaanii_, is
eaten both raw and cooked.
[Illustration: FIG. 114.—_Paragonimus westermanni_; photograph from
a sexually immature specimen. (From Tyson.)]
Experimental feeding of puppies on infected crabs brought about
infection with the lung fluke. It is thought that the fluke, after
leaving the cyst, goes through the intestine to the abdominal
cavity. Thence it perforates the diaphragm and enters the pleural
cavity, finally penetrating the lung to become encysted there. The
lung is the favorite site but wandering flukes may invade other
tissues and organs even invading the central nervous system.
Besides man, dogs, cats and especially hogs may be infected.
Symptomatology, Diagnosis and Treatment
The case is usually considered as one of chronic bronchitis on
account of the occurrence of cough and morning expectoration of a
gelatinous sputum which is usually brownish. It is popularly known
as endemic haemoptysis for the reason that after violent exertion, or
at times without manifest reason, attacks of haemoptysis of varying
degrees of severity come on. The signs on percussion are usually
insignificant while those on auscultation at the time of haemoptysis
are often marked. The symptoms often disappear for months to again
reappear.
[Illustration: FIG. 115.—Anatomy of trematoda (flukes) of man. _O
S_, oesophageal sucker. _Ph_, pharynx. _Oes,_ oesophagus. _O P_,
genital pore. _V S_, ventral suckers or acetabulum. _Ut_, uterus.
_Int_, intestines. _Ov_, ovary. _Sh G_, shell gland. _T_, testicles.
_T G_, yolk glands or vitellaria. _Exc_, excretory pore.]
The course of the disease is very chronic, often lasting many
years. As a rule the patient is fairly well nourished although
recurring attacks of haemoptysis may bring on a rather marked
anaemia. Jacksonian epilepsy has been reported as occurring
in paragonomiasis, the ova being found in cysts of the brain.
There is some question as to whether some of the reports as to
paragonomiasis may not have been connected with infections with
Japanese schistosomiasis.
The diagnosis of endemic haemoptysis is readily made by finding the
operculated eggs in the more or less sanguinolent sputum. These eggs
are of a light yellow color and average 90 × 65 microns. One often
sees Charcot-Leyden crystals in the sputum.
As prophylactic measures we should forbid uncooked crabs or crayfish.
The sputum should be sterilized.
The treatment is entirely symptomatic.
[Illustration: FIG. 116.—Ova of _Clonorchis sinensis_. After Bell
and Sutton. (Jefferys and Maxwell.)]
CLONORCHIOSIS
This is an infection due to a trematode, _Clonorchis endemicus_
(_Opisthorchis sinensis_). It is also referred to as human liver
fluke disease. It is true that the common liver fluke of sheep,
_Fasciola hepatica_, may occur in man but such infections are rare,
only 23 cases having been reported. Another liver fluke of ruminants
is the lancet fluke, _Dicrocoelium lanceatum_, but it is also
unimportant for man, only 7 cases having been reported.
_Clonorchis_ infections are common in China and Japan, the fluke
being about ½ inch long by ⅛ inch wide. There is considerable
dispute as to whether we have a pathogenic and nonpathogenic
_Clonorchis_; the name _C. endemicus_ applying to the former and
_C. sinensis_ to the latter.
Looss considered the nonpathogenic _C. sinensis_ to be larger
(13-19 mm.), to show pigment in its parenchyma and to have breaks
in the vitelline glands. _C. endemicus_ was reported as smaller (10
to 13 mm.), and without pigment or breaks in the continuity of the
vitellaria.
The eggs of this fluke show slightly concave bending of the sides
at the operculated end and are about 30 × 16 microns. These flukes
are found within the thickened bile ducts and may be present in
great numbers. They may invade the pancreas as well as the liver.
These flukes are found in dogs and cats as well as man.
This fluke is supposed to produce most serious symptoms as
indigestion, swelling and tenderness of liver, bloody diarrhoea,
ascites, oedema and a fatal cachexia.
The course of the disease is insidious and chronic with periodic
improvement.
As a matter of fact, many physicians in China attribute very little
pathogenic importance to it. The disease is diagnosed by the presence
of the ova in the stools. The source of infection is probably through
the eating of uncooked fish.
[Illustration: FIG. 117.—_Clonorchis sinensis._ (Jefferys and
Maxwell.)]
Kobayashi has examined various molluscs and fish for trematode
larvae. He succeeded in infecting nine kittens and two cats by
feeding them with certain fresh water fishes whose flesh contained
trematode larvae. These fishes were found in districts where human
distomiasis was common.
Further experiments by Kobayashi have shown that the larval flukes
leave the cyst and start for the biliary passages. When the flukes
are very numerous the size is smaller. Maturity is reached in four
weeks. This investigator believes that the primary intermediate
host is a mollusc as cercariae found in these hosts are very
similar to the larval forms found in fish.
He does not consider that there are two species concerned in
_Clonorchis_ infections, as he has found variations in continuity
of vitellaria in small as well as large flukes. Number of parasites
present influences size. Age influences pigment production.
Another human fluke, _Opisthorchis felineus_, inhabits the gall
bladder and bile ducts of man and it is stated that the infection is
quite common in Siberia.
It is also a parasite of cats and dogs.
Both _Clonorchis_ and _Opisthorchis_ have the testicles in
the posterior end with the uterus anterior. The testicles of
_Clonorchis_ are branched (dendritic) while those of _Opisthorchis_
show as two lobes. In _Dicrocoelium_ the lobed testicles are
anterior to the uterus, which fills up the posterior end of the
fluke.
The mode of infection as well as the life history is not known but is
probably connected with the eating of raw fish.
The symptoms are similar to those caused by _C. endemicus_.
The fluke has two-lobed testicles as against the dendritic one of _C.
endemicus_.
INTESTINAL DISTOMIASIS
The most important intestinal fluke is undoubtedly _Fasciolopsis
buski_. It is now thought that this infection is more common than
was previously stated. Goddard states that more than 5% of stools
examined in Shaohing, China, show eggs of this parasite. It is a
very large fluke with an acetabulum 4 times the diameter of the oral
sucker. It is characterized by a very long and prominent cirrus.
_F. buski_ and _Fasciola hepatica_ are much alike in size and
outline. The acetabulum of the latter is only 1.6 times the
diameter of the oral sucker and the alimentary tract shows
branching which is best seen in the cone-shaped projection of its
anterior extremity. _F. hepatica_ is a liver fluke rarely found in
man.
_F. buski_ is found in China, Assam and India. It is a parasite of
hogs as well as man. The eggs measure from 80 to 120 microns, are
nearly colorless and have a thin shell with a very small operculum.
The symptoms are chiefly those of a chronic diarrhoea followed by
anaemia and wasting. The stool is light yellow in color, exceedingly
offensive and does not contain blood. Goddard thinks that they live
in the upper part of the small intestines.
The life history is unknown but Goddard states that fresh water
snails are much eaten by the people of Shaohing. Nakagawa notes that
the eggs of _Fasciolopsis_ hatch in two to three weeks. The miracidia
penetrate various species of snails in which the cercariae may encyst
and infect pigs eating such snails. The cercariae may also leave
the snail and encyst on blades of grass, to later infect an animal
feeding on the grass, this latter method of infection resembling that
of _Fasciola hepatica_.
Noc has reported success with treatment with thymol and Goddard with
beta-naphthol.
Other intestinal flukes such as _Cladorchis watsoni_, _Gastrodiscus
hominis_, _Heterophyes heterophyes_, and _Fascioletta ilocana_
are of less importance. _Heterophyes_ is probably a rather
common parasite but owing to its very small size (2 mm.) has been
generally overlooked at autopsy.
STRONGYLOIDES STERCORALIS
It was formerly supposed that a chronic form of diarrhoea in Cochin
China was due to an infection with the parthenogenetic female of
_Strongyloides stercoralis_. It is now known that the parasite is
widely distributed over the tropical and subtropical world and that
it rarely gives rise to manifest symptoms although some observers
regard it as capable of producing diarrhoea and more or less anaemia.
[Illustration: FIG. 118.—Ovum of _Fasciolopsis buski_. Bell and
Sutton. (Jefferys and Maxwell.)]
[Illustration: FIG. 119.—_Fasciolopsis buski._ Cleared in glycerin.
(From Jefferys and Maxwell.)]
It seems to be capable of setting up quite an eosinophilia at the
time the adult female is penetrating the crypts of Lieberkühn, so
that it is probably of pathogenic importance.
[Illustration: FIG. 120.—A, Egg of _Strongyloides intestinalis_
(parasitic mother worm) found in stools of case of chronic diarrhoea;
B, Rhabditiform larva of Strongyloides intestinalis from the stools.
(William Sydney Thayer, in Journal of Experimental Medicine.)]
The parasitic or intestinal form (also known as _Anguillula
intestinalis_) is represented only by females. These are about 1/12
of an inch (2 mm.) long and reproduce parthenogenetically. They have
a pointed, four-lipped mouth, and a filariform oesophagus which
extends along the anterior fourth of the body. The uterus contains
a row of 8 to 10 elliptical eggs which stand out prominently in the
posterior part of the body by reason of being almost as wide as the
parent worm.
They usually live deep in the mucosa and the embryos emerge from
the ova laid in the mucosa. The embryos escape from the eggs
while still in the intestines, so that in the faeces we only find
actively motile embryos. The eggs, which are strung out in a
chain, never appear in the faeces except during purgation. As they
greatly resemble hookworm eggs this is a point of great practical
importance.
In fresh faeces we find hookworm eggs and _Strongyloides_ embryos.
The embryos are rather common in stools in the tropics. These embryos
have pointed tails and are about 250 × 13 microns. They have a double
oesophageal bulb. They are about 250 microns when they first emerge
but may grow until they approximate 500 microns in the faeces. The
mouth cavity of the embryo of the hookworm is about as deep as the
diameter of the embryo at the posterior end of the mouth cavity; that
of _Strongyloides_ is only about one-half as deep as the diameter.
If the temperature is low, below 15°C., these rhabditiform embryos
develop into filariform embryos, which form the infecting stage.
It has been demonstrated by Fülleborn that infection of man takes
place through the skin. If the temperature is warm, 25° to 35°C.,
these embryos develop into the free-living form. In this we have
males and females, with double oesophageal bulbs, the male about
1/30 of an inch (¾ mm.) long with an incurved tail and 2 spicules
and the female about 1/25 inch (1 mm.) long with an attenuated
tail. These copulate and we have produced rhabditiform larvae,
which later change to filariform ones. At this time the length is
about 550 microns. These start up the parasitical generation.
For treatment thymol is usually recommended. Stiles speaks highly
of sulphur.
CHAPTER XXV
TABLE OF IMPORTANT ANIMAL PARASITE DISEASES
PROTOZOAL DISEASES
-----------------+--------+----------+-----------+-----------------------
Parasite | Defin. | Inter- | Important | Transmission and
| host | mediate | reservoir | pathogenicity
| | host | of virus |
-----------------+--------+----------+-----------+-----------------------
Entamoeba |Man. |Not |Man-carrier|Cysts in food or water.
histolytica. | | required.| stage | Flies may act as
| | | (feces). | carriers. Ingestive.
| | | | Amoebic dysentery.
-----------------+--------+----------+-----------+-----------------------
Balantidium coli.|Man |Not |Man-carrier|Transmission probably
| (hogs).| required.| stage | same as for E.
| | | (hogs). | histolytica. Found
| | | | in those having care
| | | | of hogs. Ingestive.
| | | | Balantidium dysentery.
| | | | Anaemia.
-----------------+--------+----------+-----------+-----------------------
Lamblia (Giardia)|Man |Not |Man-carrier|Transmission probably
intestinalis. | (mice | required.| stage | same as for E.
| and | | (mice and | histolytica. Rat
| rats). | | rats). | feces on human food
| | | | important. Ingestive.
| | | | Lamblia dysentery.
| | | | Giardiasis.
-----------------+--------+----------+-----------+-----------------------
Spiroschaudinnia |Louse |Man.(*) |Man |Cyclical development in
(Spironema) | (P. | | (blood). | louse. Bite puncture
recurrentis, | vesti- | | | contaminated by
carteri, etc. | menti).| | | crushed louse.
(louse group.) | | | | Relapsing fever.
-----------------+--------+----------+-----------+-----------------------
Spiroschaudinnia |Tick |Man.(*) |Man |Excretions of tick
(Spironema) |(species| | (blood). | contaminating
duttoni, novyi. |of | | | tick-bite. Tick
(Tick group.) |Ornith- | | | fevers. Relapsing
|dorus or| | | fever.
|Argas). | | |
-----------------+--------+----------+-----------+-----------------------
Treponema |Man. |Not |Man. |T. pallidum. Usually
(pallidum and | | required.| | venereal. Syphilis.
pertenue). | | | | T. pertenue. Flies or
| | | | contact. Yaws.
-----------------+--------+----------+-----------+-----------------------
Leptospira |Man |Not |Rat. |Common infection of
ictero- | (rat). | required.| | rats. Present in
haemorrhagiae. | | | | blood. Excreted in
| | | | urine. Ingestion.
| | | | Weil’s disease.
-----------------+--------+----------+-----------+-----------------------
Leptospira |Mosquito|Man. |Man |Cyclical development
icteroides. |(Stego- | | (blood). | in mosquito--12
|myia | | | days. Inoculative.
|calopus)| | | Yellow fever.
-----------------+--------+----------+-----------+-----------------------
PROTOZOAL DISEASES (Continued)
-----------------+--------+----------+-----------+-----------------------
Parasite | Defin. | Inter- |Important | Transmission and
| host | mediate |reservoir | pathogenicity
| | host |of virus |
-----------------+--------+----------+-----------+-----------------------
Leptospira |Man |Not |Rat. |Man inoculated by
morsus-muris. | (rat). | required.| | bite of infected rat.
| | | | Rat bite fever.
-----------------+--------+----------+-----------+-----------------------
Trypanosoma |Fly |Man. |Man--game |Cyclical development
gambiense |(Glossina| | animals? | in tsetse fly.
and rhodesiense.|species)| | (blood). | Inoculative. Sleeping
| | | | sickness.
-----------------+--------+----------+-----------+-----------------------
Schizotrypanum |Lamus |Man. |Man. |Cyclical development
cruzi. |megistus| | | in bug. Inoculative.
| | | | Brazilian
| | | | trypanosomiasis.
-----------------+--------+----------+-----------+-----------------------
Leishmania |Not |Man. |Man. |L. donovani—Bed bug?
(donovani, | surely | | | kala-azar. L. infantum
infantum, and | known. | | | —dog flea? infantile
tropica). | | | | leishmaniasis. L.
| | | | tropicum--biting
| | | | insects? Oriental
| | | | sore; American
| | | | leishmaniasis.
-----------------+--------+----------+-----------+-----------------------
Plasmodium |Mosquito|Man (with |Man (blood)|Cyclical development
malariae, |(Anoph- | schiz- | (with | in mosquito—12
vivax and | eline | onts). | gametes). | days. Inoculative.
falciparum. |species)| | | Malaria.
-----------------+--------+----------+-----------+-----------------------
Rickettsia |Man. |Louse (P. |Man (blood)|Cyclical development in
prowazeki. | | vesti- | | louse. Bite puncture
| | menti). | | inoculated by
| | | | louse feces. Typhus
| | | | fever.
-----------------+--------+----------+-----------+-----------------------
Dermacentroxenus |Man |Tick |Goats and |Excretions of tick
rickettsi. |(goats, |(Dermacen-| rodents. | contaminating
|rodents,|tor ander-| | tick-bite. Rocky
| etc.). |soni). D. | | Mountain fever.
| | venustus.| |
-----------------+--------+----------+-----------+-----------------------
Bartonella |Man. |Unknown. |Man (blood)|Transmission unknown.
bacilliformis. | | | | Species of
| | | | Phlebotomus suggested.
| | | | Oroya fever.
-----------------+--------+----------+-----------+-----------------------
NOTE.—(*) Some authorities give man as definitive host of
Spiroschaudinnia (Spironema). Diseases often classified as filterable
virus ones of protozoal affinity are (1) Dengue. Cause unknown.
Transmitted by Stegomyia species. (2) Pappataci fever. Cause unknown.
Transmitted by Phlebotomus species. Other protozoal diseases are (1)
Tsutsugamushi. Probably a protozoan. Transmitted by Kedani mite. (2)
Trench fever. Probably Rickettsia. Transmitted by louse.
HELMINTHIC DISEASES—TREMATODES
-------------+--------+-------------+-----------+-----------------------
Parasite | Defin. |Intermediate |Important | Transmission and
| host | host |reservoir | pathogenicity
| | |of virus |
-------------+--------+-------------+-----------+-----------------------
Clonorchis |Man |1st, snail |Man. |Not definitely known.
sinensis. | (cats, | (Melania | | Eating raw fish.
|dogs and| libertina)? | | Ingestive. Human liver
| hogs). | and 2d, fish| | fluke disease.
-------------+--------+-------------+-----------+-----------------------
Opisthorchis |Man |1st, mollusc.|Cats and |Man infected by eating
felineus. | (cats | 2d, fish. | dogs. | raw fish. Ingestive.
| and | | | Liver fluke
| dogs). | | | disease.
-------------+--------+-------------+-----------+-----------------------
Fasciolopsis |Man |Possibly 1st,|Hog. |Not definitely known.
buski. | (pig). | mollusc. | | Intestinal
| | Cercariae | | Distomiasis.
| | encyst on | |
| | grass. | |
-------------+--------+-------------+-----------+-----------------------
Heterophyes |Man |1st, probably|Dogs and |Not definitely known.
heterophyes.| (dogs | mollusc. | cats. | Intestinal Distomiasis.
| and | 2d, probably| |
| cats). | fish. | |
-------------+--------+-------------+-----------+-----------------------
Paragonimus |Man |1st, snail. |Cats, dogs |Eating raw crabs
ringeri. | (dogs, | 2d, crab. | and hogs. | containing cercariae.
|cats and| | | Ingestive. Lung fluke
| hogs). | | | disease.
-------------+--------+-------------+-----------+-----------------------
Schistosoma |Man. |Snail |Man |Bathing or drinking
haematobium.| | (Bullinus). | (urine). | water containing
| | | | cercariae. Penetrative.
| | | | Vesical bilharziasis.
-------------+--------+-------------+-----------+-----------------------
Schistosoma |Man. |Snail |Man (feces)|Bathing or drinking
mansoni. | | (Planorbis).| | water containing
| | | | cercariae. Penetrative.
| | | | Rectal bilharziasis.
-------------+--------+-------------+-----------+-----------------------
Schistosoma |Man. |Snail |Man (feces)|Bathing or drinking
japonicum. | |(Blanifordia)| domesticated | water containing
| | | animals). | cercariae. Penetrative.
| | | | Katayama disease.
-------------+--------+-------------+-----------+-----------------------
NOTE.—Rare trematodes of man are (1) Fasciola hepatica. Chiefly
disease of sheep. Cercariae from snail (Limnea) encyst on grass.
(2) Dicrocoelium lanceatum. Chiefly disease of cattle. (3)
Heterophyes nocens. A very small intestinal fluke of man. (4)
Metagonimus yokogawai. Another very small intestinal fluke of man.
Intermediate hosts: mollusc and gold fish. (5) Echinostoma ilocanum.
A rare intestinal fluke of the Philippines. (6) Two genera of
Paramphistomidae—Cladorchis and Gastrodiscus. Intestinal flukes.
HELMINTHIC DISEASES (Continued). NEMATODES
-------------+--------+-------------+-----------+------------------------
Parasite | Defin. |Intermediate |Important | Transmission and
| host | host |reservoir | pathogenicity
| | |of virus |
-------------+--------+-------------+-----------+------------------------
Filaria |Man. |Mosquito |Man |Indirect in mosquito.
bancrofti. | | (various | infected | Mature larva
| | species). | (blood). | penetrates skin.
| | | | Elephantiasis, etc.
-------------+--------+-------------+-----------+------------------------
Loa loa |Man. |Fly. Species |Man |Probably indirect
(F. loa). | | of Chrysops | infected | (cyclical) in Chrysops.
| | (mangrove | (blood). | Probably inoculative.
| | flies). | | Ocular filariasis, etc.
-------------+--------+-------------+-----------+------------------------
Acantho- |Man. |Not |Man |Transmission by
cheilonema | | definitely | infected | mosquitoes and ticks
perstans (F.| | known. | (blood). | suggested. No
perstans). | | | | pathogenicity.
-------------+--------+-------------+-----------+------------------------
Dracunculus |Man. |Species of |Man |Larvae enter cyclops.
medinensis. | | cyclops. | infected | Infected cyclops in
| | | (subcuta- | drinking water.
| | | neous | Ingestive. Guinea
| | | tissue). | worm infection.
-------------+--------+-------------+-----------+------------------------
Onchocerca |Man. |Not |Man |Possibly Glossina.
volvulus (F.| | definitely | (blood?). | Subcutaneous tumor
volvulus). | | known. | | and lymphangitis.
-------------+--------+-------------+-----------+------------------------
Strongyloides|Man. |Not required.|Man (feces)|Parasitic filariform
stercoralis.| | | | larva penetrates skin.
| | | | Pathogenicity doubtful.
-------------+--------+-------------+-----------+------------------------
Necator |Man. |Not required.|Man (feces)|Encysted strongyloid
americanus | | | | larvae penetrate skin.
and | | | | Ancylostomiasis.
Ancylostoma | | | |
duodenale. | | | |
-------------+--------+-------------+-----------+------------------------
Trichinella |Man (rat|Hog (man and |Hog |Encysted larva in raw
spiralis. | and | rat). | (muscle). | or insufficiently
| hog). | | | cooked pork. Ingestive.
| | | | Trichinosis.
-------------+--------+-------------+-----------+------------------------
NOTE.—Ascaris, Trichuris and Oxyuris do not require intermediate
host. With Ascaris and Trichuris, larva gradually develops in egg
passed in faeces. Infection by ingestion of embryo-containing eggs.
Embryo-containing eggs contaminate fingers from crushing female
Oxyuris in perineal region.
HELMINTHIC DISEASES. CESTODES
-------------+--------+-------------+-----------+-----------------------
Parasite | Defin. |Intermediate |Important | Transmission and
| host | host |reservoir | pathogenicity
| | |of virus |
-------------+--------+-------------+-----------+-----------------------
Dibothrio- |Man. |1st, cyclops?|Man |Eating raw fish
cephalus | | 2d, fish. | (feces), | containing pleocercoid
latus. | | | dog and | larvae. Broad Russian
| | | cats. | tapeworm disease.
-------------+--------+-------------+-----------+-----------------------
Hymenolepis |Man. |Not required.|Children |Man intermediate and
nana. | | | (feces). | definitive host.
| | | | Ingestive. Dwarf
| | | | tapeworm disease.
-------------+--------+-------------+-----------+-----------------------
Taenia |Man. |Cattle (ox). |Man (feces)|Eating insufficiently
saginata. | | | | cooked beef containing
| | | | cysticerci. Ingestive.
| | | | Beef tapeworm
| | | | disease.
-------------+--------+-------------+-----------+-----------------------
Taenia |Man. |Hog. |Man (feces)|Eating insufficiently
solium. | | | | cooked pork containing
| | | | cysticerci. Ingestion.
| | | | Pork tapeworm
| | | | disease.
-------------+--------+-------------+-----------+-----------------------
Taenia |Dog. |Man, sheep |Dog (feces)|Dogs infected at
echinococcus.| | and hogs. | | abattoir. Hydatid
| | | | disease.
-------------+--------+-------------+-----------+-----------------------
NOTE.—Rare cestodes of man are (1) Dipylidium caninum. A parasite
of the dog with louse or flea as intermediate host. (2) Hymenolepis
diminuta. A parasite of rats. Intermediate host in insects. (3)
Species of Davainea. Intermediate host possibly cockroach. These
cestodes are probably accidental parasites of man.
ARTHROPODAN DISEASES
--------------+---------------------------+------------------------------
Parasite | Life history | Disease and manifestations
| | and remarks
--------------+---------------------------+------------------------------
Linguatula |Adult in nasal cavity of |Porocephaliasis. Man may
serrata | dogs, etc. Eggs in nasal | harbor adult or larva. Larvae
(Lingua- | mucus contaminate grass. | usually in lungs or liver
tulidae). | Rabbits, cattle infected. | and do not seem to cause
| Larvae in liver, lungs. | symptoms.
--------------+---------------------------+------------------------------
Porocephalus |Adults in lungs of snakes. |Porocephaliasis. Larvae wander
armillatus | Eggs contaminate water | in abdominal cavity or lungs
(Lingua- | or food. Larvae in liver, | in which latter they produce
tulidae). | lungs, etc., of lions, | a chronic bronchitis which
| monkeys, man, etc. | may resemble phthisis.
--------------+---------------------------+------------------------------
Demodex |All stages passed within |Demodectic acariasis. Causes a
folliculorum | hair follicles or | resistant itch in dogs. In
(Demodicidae).| sebaceous cysts especially| man, may invade eyelids or
| about nose. Adult may | meibomian glands, and has
| wander. | been reported as causing
| | various forms of dermatitis.
--------------+---------------------------+------------------------------
Sarcoptes |Female lives in burrow of |Scabies. Burrows show as
scabei | skin giving off eggs which| blackish lines, especially
(Sarcoptidae).| hatch into larvae. | between fingers, flexor
| | surfaces of arms and penis.
| | Itching worse at night.
--------------+---------------------------+------------------------------
Pediculoides |Female lives on wheat straw|Grain itch. The mites leave
ventricosus | worm or grain moth. Larval| wheat straw or grain and
(Tarson- | mites develop inside | attack harvesters or those
emidae). | mother. | sleeping on straw mattresses.
| | Attack upper trunk, neck and
| | arms. Erythematous or
| | vesicular eruption with
| | constitutional symptoms.
---------------+--------------------------+------------------------------
Microtrombidium|Adults live in fields or |Autumnal erythema. The larval
pusillum | woods. The larval mite | mites known as red bug or
(Trombidoidae).| lives on grasshoppers or | jigger attack man causing a
| small rodents. | severe itch.
---------------+--------------------------+------------------------------
Dermanyssus |Mites live in chicken |Poultryman’s itch. The mites
gallinae | houses and feed on fowls. | attack man producing
(Gamasidae). | | eczematous dermatitis on
| | backs of hands and forearms.
--------------+---------------------------+------------------------------
Dermacentor |Adults live on cattle, |Tick paralysis. The bite of
venustus | sheep, etc. May bite man. |this tick or Ixodes holocyclus
(Ixodidae). | | may produce paralysis in
| | sheep. An ascending type of
| | paralysis due to tick bites
| | has been several times noted
| | in man, chiefly in children.
--------------+---------------------------+------------------------------
Pediculus |Adults live on clothing or |Pediculosis—Phthiriasis.
humanus | hair and feed on man. | Produce skin irritation with
(Insecta, | | later on pigmentation
Pediculidae).| | (Vagabondismus).
--------------+---------------------------+------------------------------
Dermatophilus |Impregnated female |Sandflea or chigoe
penetrans. | penetrates skin of man or | infestation. Site of penetr-
(Sarco- | animals, especially toes | ation shows as black spot
psyllidae). | and feet. | with whitish induration
| | surrounding it. Apt to form
| | ulcers.
--------------+---------------------------+------------------------------
ARTHROPODAN DISEASES (Continued)
--------------+---------------------------+------------------------------
Parasite | Life history | Disease and manifestations
| | and remarks
--------------+---------------------------+------------------------------
Dermatobia |Eggs of fly become attached|A cutaneous myiasis. Larva at
cyaniventris | to mosquitoes or ticks. | first club shaped (ver
(Oestridae: | These latter bite man and | macaque), later worm shaped
Bot Flies). | larva penetrates skin. | (torcel). Larva causes a
| | swelling with black opening.
| | May invade eye.
--------------+---------------------------+------------------------------
Hypoderma |Larvae of this or other |Creeping eruption. Larva
lineata | flies burrow under skin. | migrans. The burrows make
(Oestridae). | | zig-zag lines on face or
| | soles of feet. Causes
| | itching.
--------------+---------------------------+------------------------------
Chrysomyia |Fly deposits eggs in |Screw worm infection. Nasal
macellaria, | nostrils. Larvae wander to| myiasis. Larvae in their
and C. dux | nasal sinuses. May invade | wandering destroy tissues of
Muscidae). | aural canal. | nasal cavities, or of ear,
Oestrus ovis | | and may cause death. May
(Oestridae). | | infest wounds or vagina. C.
| | macellaria causes American
| | nasal myiasis, C. dux causes
| | Indian nasal myiasis and O.
| | ovis causes African nasal
| | myiasis.
--------------+---------------------------+------------------------------
Ochromyia |An African fly, which |Larvae bore under skin,
(Cordylobia) | deposits eggs on children | causing boil-like lesions
anthropophaga| and animals. | with central opening. Larvae
(Muscidae). | | mature in two weeks.
--------------+---------------------------+------------------------------
Auchmeromyia |An African fly deposits |Congo floor maggot. The bite
luteola | eggs on floors of native | is not painful.
(Muscidae). | huts. Larvae bite man. |
--------------+---------------------------+------------------------------
Calliphora |Blow and bluebottle flies, |Larvae may be cause of obscure
vomitoria | depositing eggs on tainted| abdominal conditions; may be
and Lucilia | meats. Larvae may be found| found in nasal cavities,
caesar and L.| in feces. | causing serious symptoms, or
serricata | | in ear.
(Muscidae). | |
--------------+---------------------------+------------------------------
Musca |Eggs presumably deposited |Larvae have been found in male
domestica | near genitalia or ear. | urethra and in the ear.
(Muscidae). | |
--------------+---------------------------+------------------------------
Sarcophaga |Viviparous. Larvae are |Larvae gain access to wounds,
carnaria | deposited on decaying | nasal cavities, etc., at
(Sarcoph- | flesh (wounds, orifices | times causing death. Commonly
agidae). | of body). | found in intestinal myiases.
| | May occur in vagina.
--------------+---------------------------+------------------------------
Anthomyia |Larvae deposited in body |Occasionally reported as found
pluvialis | orifices. | in ear.
(Anthomyidae).| |
--------------+---------------------------+------------------------------
Fannia |Eggs deposited near |Symptoms of urinary irritation
canicularis | external genitalia and | or obstruction. Has been
(Anthomyidae).| larva penetrates urethra. | found in gastro-intestinal
| | tract.
--------------+---------------------------+------------------------------
SECTION V
INFECTIOUS GRANULOMATA OF THE TROPICS
CHAPTER XXVI
YAWS OR FRAMBOESIA
HISTORY AND GEOGRAPHICAL DISTRIBUTION
=History.=—Some authorities think that a disease described by the
Arabian physicians of the 10th century was yaws, but the first
description of what was undoubtedly yaws was that of Oviedo, who in
the 16th century described such an affection as existing in the West
Indies. Bontius, later on, noted the existence of the disease in the
East Indies as well as in the West Indies.
It is known that yaws often occurred in epidemic form on board the
slave ships and it is thought that this disease may have been an
African importation into the new world.
=Geographical Distribution.=—Yaws is essentially a disease of
tropical regions.
In Africa it is very prevalent in the equatorial region, especially
in the Congo Free State. It is also found more rarely in Tripoli
and Algiers and to a less extent in the Sudan region. It is common
in the West Indies and tropical America.
In Asia it is very prevalent in the Malay Peninsula, Siam, the East
Indian Islands and in the Philippines. It does not exist in Japan.
In many of the islands of the Pacific it is exceedingly prevalent,
particularly in Samoa. It is also present in Northern Australia.
ETIOLOGY AND EPIDEMIOLOGY
=Etiology.=—In view of the fact that many great authorities,
especially J. Hutchinson, insisted upon the syphilitic nature of
yaws it was a matter of great interest when Castellani, in 1905,
discovered the causative organism which is characterized by the same
sharp-cut, corkscrew spirals that are noted with the syphilitic
spirochaete discovered by Schaudinn in the same year. _Treponema
pertenue_ is found in the epidermis of the yaws granuloma and has
been demonstrated in lymphatic glands and spleen. Although it has not
been demonstrated in the blood, through microscopical examination, it
must exist there as monkeys infected with the blood of yaws patients
develop the lesions of yaws in which the spirochaetes are present.
Another name for the organism is _Spirochaeta pallidula_; this
however is only a synonym.
Inoculation experiments as well as clinical manifestations show
yaws and syphilis to be distinct. Thus Charlouis, in 1881,
inoculated a native suffering from typical yaws wistations
of syphilis followed. There have been many instances of the
development of yaws, naturally and by inoculation, in those
affected with syphilis. Nichols has shown that a rabbit which had
been infected intratesticularly with _T. pallidum_ and then cured
by salvarsan did not show immunity to _T. pertenue_ when the latter
was used to infect the testicle.
In the monkey inoculation over the eyebrow gives a flat dry and
scaly lesion with syphilitic material while yaws inoculation gives
a softer, more oedematous one.
Levaditi and Nattan Larrier have noted that monkeys which had been
inoculated with syphilis were immune to yaws inoculation but yaws
monkeys could be infected with syphilis, thus indicating that yaws
was a mild form of syphilis. In Guam, it has recently been shown
that 68% of cases of gangosa, a disease supposed to be a tertiary
form of yaws, give a positive luetin reaction. This would indicate
a close relationship between yaws and syphilis.
Salvarsan is more specific for yaws than it is for syphilis and the
percentage of positive Wassermann tests is as great in yaws as in
syphilis.
Notwithstanding the above points, which would indicate a close
relationship, all authorities are now agreed that clinical and
pathological evidence show the two diseases to be separate entities.
=Epidemiology.=—Charlouis inoculated 32 Chinese prisoners with
scrapings from yaws lesions. The disease developed in 28 of them,
first showing itself at the site of inoculation.
Paulet inoculated 14 negroes with yaws material and after a period
of incubation of from twelve to twenty days a primary lesion
appeared, to be followed by the generalized eruption. In naturally
acquired yaws the period of incubation is from three to six
weeks. These experiments are in line with the known fact that any
skin abrasion which comes in contact with a yaws lesion becomes
infected, as when the mother nurses an infant with lesions on its
face and develops a yaws lesion at the site of some fissure about
the nipple.
Yaws shows a striking limitation to the tropics and in a disease so
communicable by direct contact it seems remarkable that it does not
spread from the occasional case introduced into temperate regions.
In the tropical world it seems limited to low level areas. Another
feature of yaws epidemiology is the vastly greater susceptibility
of colored races, even those of mixed white blood showing a certain
degree of immunity.
All evidence is against a congenital form of yaws.
In particular are flies important factors in the transmission of the
disease, transferring the secretions from yaws lesions to abrasions
or ulcers on the skin of healthy persons.
The greater the attention to personal hygiene the less probable is
the spread of yaws, so that Europeans are rarely infected while the
disease may be prevalent in the native population.
In countries where it is prevalent it is chiefly a disease of
children, the adults possessing immunity as the result of attacks
in childhood.
PATHOLOGY
The primary yaws lesion is histologically the same as the lesions of
the generalized eruption of the second stage. In these lesions we
fail to find the endothelial proliferations and perivascular round
cell infiltrations so characteristic of syphilis. There is great
thickening of the interpapillary pegs of the epidermis which dip down
deeply into the corium. Areas are noted in the epithelium containing
swollen degenerated epithelial cells, polymorphonuclears and granular
débris. There is marked oedema in the corium with dilatation of the
blood vessels and lymphatics.
There is less oedema of the corium in yaws than in a syphilitic
condyloma thus accounting for the greater dryness of the former. The
main point in the pathology of a yaws lesion is the predominating
involvement of the epidermis and the comparatively slight change in
the corium.
In a Levaditi-stained specimen the spirochaetes are found in the
epidermal layers instead of in the corium as with syphilis.
The visceral organs and central nervous system are not affected
although Harper has reported cases of tabes and general paresis in
Fijians following yaws. He excludes syphilis.
SYMPTOMATOLOGY
It is usual to consider the clinical course of yaws as exhibiting
two stages, the primary one, which comes on from 2 to 5 weeks after
introduction of the virus and is characterized by a papular initial
lesion, which later shows the fungoid appearance of a typical yaws
tubercle, and the secondary stage in which yaws lesions similar to
the initial one develop as a generalized eruption.
Some authorities recognize a tertiary stage in which gumma-like
nodules, with subsequent ulceration, appear. There is much evidence
to indicate that a destructive ulceration of the nasopharyngeal
region, in natives of Guam, is a tertiary manifestation of yaws.
[Illustration: FIG. 121.—Yaws. This case shows an abundance of
yaws tubercles on face. Distribution on trunk and extremities less
extensive. (From Ruge and zur Verth.)]
_The Primary Stage_.—During a period of incubation, averaging three
weeks, vague digestive troubles, nocturnal headache, joint pains
and an irregular fever may be noted which often abate upon the
appearance of the initial papule at the site of inoculation. There
may be enlargement and tenderness of the lymphatic glands about the
time of the appearance of the eruption. This initial lesion may be
single or there may be several papules grouped together. In some
cases it may be impossible to get any history of a primary lesion or
it may have been overlooked. The primary lesion is almost invariably
extra-genital and it has the same appearance as the lesions of the
secondary stage, thus differing from syphilis.
[Illustration: FIG. 122.—Child with yaws. (From U. S. Naval Medical
Bulletin.)]
The yaws lesion, whether primary or secondary, starts as a papule
which in a few days enlarges to the size of a small pea. It is
conical and surrounded by an inflammatory areola. At this time the
thickened epidermis begins to crack and a yellowish sero-purulent
fluid exudes from the underlying fungoid base. They bleed easily
but are not painful. It is this fungoid yellowish or yellowish-red
tubercle which has been thought to resemble a raspberry, hence
the name framboesia. French authors liken it to a fig which has
been turned inside out. The moist or crusting surface soon shows
an underlying ulcer, which may dry up leaving a pigmented spot or
become exuberant and appear as a mass of fungating granulations, 1
to 2 inches in diameter. Such lesions are given the name “mother
yaw.”
_The Secondary Stage_.—In from six weeks to three months after the
appearance of the initial lesion, which may have dried up and left
only a scar, or which more commonly is still present, there again set
in malaise, headache and joint pains with an irregular inconstant
fever.
The secondary eruption is made up of lesions having the same
character and course as the primary yaws tubercle. In the general
eruption, the papules appear frequently in the region of the
junction of skin and mucous membrane as about mouth, nose and anus.
In such regions they may become very moist and resemble the mucous
patches of syphilis.
Besides their location on face and about the perineal region they
are numerous on neck, arms, legs, and buttocks. They are rare on
the trunk and scalp.
In their ordinary locations the yaws tubercles are not painful
unless pressed firmly but when located on the palms of the hands or
soles of the feet the thick skin of these regions exerts pressure
so that in such situations the lesions are painful.
In this stage yaws does not involve mucous membranes or affect the
viscera.
The secondary stage lasts from 3 or 4 months to 2 or 3 years, the
yaws tubercles coming out in successive crops in long standing
cases.
_The Tertiary Stage_.—Daniels noted in the Fiji Islands destructive
lesions of the naso-pharyngeal region which he thought might be
associated with a preceding yaws attack. He noted cutaneous lesions
which resembled lupus vulgaris. Boissiere has noted not only the
nasopharyngeal lesions and lupus-vulgaris-like ones but also tibial
involvement, joint swellings and dactylitis.
Numa Rat describes various tertiary manifestations. There may
be subcutaneous nodules about ankle or leg which soften and may
produce bone lesions and deformities. He notes destructive lesions
of nares, pharynx and palate which may set in years after an
attack of yaws. His description of the process starting as an
ozoena or sore throat followed by destruction of the uvula, velum
palati and septum nasi is much like gangosa. Howard has noted the
greater frequency of destructive lesions of the nasopharynx in
those parts of Africa where yaws is prevalent than in parts where
syphilis prevails.
[Illustration: FIG. 123.—Tertiary jaws, “Gomma”. (Johns Hopkins
Bull., Moss and Bigelow.)]
According to Castellani the characteristic lesions of tertiary yaws
are gummatous nodules and deep ulcerations. Such ulcerations may
give rise to contractures.
In Guam the view now prevails that the condition known as gangosa
is a form of tertiary yaws.
Other than a moderate anaemia there is very little in the blood of
yaws which differs from the normal.
_Peculiar Types of Yaws_.—When yaws tubercles develop in the
palms of the hands or soles of the feet we have a very painful
and incapacitating condition resulting. The pressure of the thick
unyielding epidermis on the tubercles beneath gives rise to marked
pain, thus differing from tubercles on other parts of the body.
Eventually these tubercles break through and the affected sole may
have a worm-eaten appearance. The name “crab yaws” is a common
one for such a condition involving the soles of the feet and is
so-called from the difficulty in walking which has a resemblance
to the locomotion of a crab. In some cases the yaws tubercles
adjoin one another to form a circle enclosing unaffected skin. Such
an arrangement of lesions is often described under the name of
“ringworm yaws.”
[Illustration: FIG. 124.—Tertiary yaws. Clavus or Crab-yaws. (Johns
Hopkins Bull., Moss and Bigelow.)]
DIAGNOSIS
=Clinical Diagnosis.=—Bromide eruptions may greatly resemble yaws
but the history of the taking of the drug and the effect upon
withdrawal should differentiate.
_Syphilis and Yaws._—Degorce gives a very complete table of the
points of difference between syphilis and yaws, some of the more
important of which are the following:
YAWS
1. Primary lesion of soft consistency, or very little infiltrated,
with granulating or pimply surface, situated almost invariably
extragenitally, resembling the secondary lesions. Lymphadenitis not
marked.
2. Roseola resembling that of syphilis but rarer.
3. Secondary cutaneous lesions at first in the form of conical
elevations of a light red color, not infiltrated at base, appearing
in close groups. The lesions are similar to those of syphilis,
namely, on the scalp in the form of encrusted papules; on
thin-skinned regions in the form of ulcerating papules, and in the
case of the palm of the hands and plantar surface of the feet, in
the form of simple papules.
4. Circinate lesions with the edges more raised than in syphilis,
covered with yellow crusts.
5. On the face lesions of the same type, but more striking and with
irregular projections.
6. Cutaneous lesions do not itch.
7. Perionychia similar to that of syphilis, but occasionally giving
rise to pimply lesions.
8. Alopecia has not been described.
9. Lesions in the buccal and pharyngeal mucosa often absent. No
erythema. No typical mucous patches. Sometimes fissures at the
angles of the mouth. The typical lesions are raised, pure white and
occasionally covered with intact epithelium.
10. Lesions with prominent edges or even pustular with yellowish
crusts, occasionally also ulcerations resembling mucous patches.
11. Similar condylomata, but larger and more raised.
SYPHILIS
1. Primary lesion infiltrated and indurated, with flat and
smooth surface, ordinarily situated on the genital organs; often
accompanied by abundant lymphadenitis. Phagedenic processes
frequent.
2. Roseola present.
3. Secondary cutaneous lesions papular from the first, dark red,
infiltrated and fairly regularly scattered.
4. Circinate lesions with pink edges, slightly raised, with fine
scales.
5. Seborrheic syphilides on the face.
6. Cutaneous lesions do not itch.
7. Perionychia present.
8. In syphilis, alopecia rather the exception.
9. Lesions in the buccal and pharyngeal mucosa are not numerous
and are slight in degree. Erythema of the soft palate and pharynx
occurs. Mucous patches. Ulcers of the lips and at the angles of the
mouth.
10. In the glans, prepuce or vulva, the lesions are more or less
typical mucous patches.
11. Moist condylomata at the margin of the anus.
The authorities generally discuss extensively the points of
distinction between yaws and syphilis. This is probably more
connected with possible relationship than practical importance in
diagnosis.
=Laboratory Diagnosis.=—The staining of the juice from yaws
tubercles by the India ink method or with Giemsa’s stain is the usual
procedure.
Baermann gives the percentage of positive Wassermann reactions in
untreated, clinically positive cases, as 80 to 100%; in treated
cases, 50%, and in the latent ones as from 35 to 40%. In an
examination of the serum of 281 cases of gangosa, Halton obtained
37.3% positive Wassermann reactions. Kerr found that 73.8% of 2,429
natives of Guam had had yaws, usually in childhood.
Among other diseases which may be confused with yaws, particularly
as regards the nasopharyngeal ulcerations of tertiary yaws, may be
mentioned American cutaneous leishmaniasis. The differentiation
rests in finding _Leishmania tropica_ in such lesions.
Sections from a yaws tubercle treated and sectioned according
to Levaditi’s method show the treponemata in the region of the
thickened interpapillary pegs of the epidermis.
PROGNOSIS
This is almost entirely favorable as regards danger to life. The
death rate is approximately ½ of 1% and such fatalities generally
occur in young children in whom secondary infections develop on the
site of the ulcerating yaws lesions.
PROPHYLAXIS AND TREATMENT
=Prophylaxis.=—Daniels thinks the frequency of infection about the
angles of the mouth, which frequently show fissures, is explained by
the exchange of particles of food or other substances by children,
thus transferring the infection.
Of course care should be taken to prevent articles of clothing
contaminated with yaws discharges from acting as infecting agents.
The main point in prophylaxis is to prevent flies from having
access to abrasions on the skin, so that all cuts or sores should
be protected by dressings. The sound skin is a barrier to infection.
=Treatment.=—It can certainly be stated that in salvarsan we have an
absolute specific for yaws, the results which obtain in a few days
being almost miraculous when one considers the protracted normal
course of the disease.
The drug is given intravenously although neosalvarsan
intramuscularly is more convenient for those not prepared to give
intravenous injections.
The methods of administration are exactly as for the treatment of
syphilis. The drug gives best results when used early in the course
of the disease.
Doses of 0.4 gram of salvarsan usually suffice and frequently
one dose effects a cure. The dose for women, children and thin
individuals should be less than for strong adult men. Atoxyl does
not seem to be effective in yaws. In other words the methods of
treatment are the same for the two treponemata, except that the
effect of salvarsan may be termed specific for yaws and less so
for syphilis. Bergen found that about 4% of cases treated with
salvarsan or neosalvarsan relapsed. The average time to effect a
cure was eleven days.
Many of the older writers have reported the value of mercury in the
treatment of yaws but the present view is that this drug has very
little if any place in the therapy of the disease. Potassium iodide
does seem to be a very useful drug in the absence of opportunity
for obtaining some arsphenamine product. Where the specific remedy
cannot be secured the next best treatment is Castellani’s yaws
mixture. The formula for the preparation is the following:
Tartar emetic one grain (0.06 gm.)
Potassium iodide twenty grains (1.3 gms.)
Sodium salicylate ten grains (0.6 gm.)
Sodium bicarbonate fifteen grains (1 gm.)
Chloroform water and syrup one ounce (30 cc.)
The above is a single dose and it is given well diluted about three
times daily. This treatment is continued for about a week and after
an interval of another week is resumed according to the response
to such treatment. In children between seven and fifteen years the
dose is reduced one-half and for younger children correspondingly.
It would seem well to start treatment with a smaller dosage than
the standard one, being guided by the ability of the patient to
stand an increase in the dose of the drugs.
For local treatment use antiseptic dusting powders as iodoform or
boric acid.
CHAPTER XXVII
GANGOSA
HISTORY AND GEOGRAPHICAL DISTRIBUTION
=History.=—It is known that in 1828 a Spanish Commission,
investigating the diseases of the Ladrone Islands, reported the
existence, in those islands, of a disease which was called gangosa,
by reason of the muffled character of the voice, the Spanish word
_gangosa_ meaning muffled voice. The Commission recommended that
cases of this disease, as well as those with leprosy, be isolated,
thus showing that the disease was differentiated from leprosy at that
time.
Daniels, who studied similar naso-pharyngeal lesions in Fiji,
considered the disease as a sequel of yaws and stated that if it
were not a stage of yaws it was probably a separate and distinct
disease. Leys, who studied gangosa in Guam, in 1904, gave it the
name rhino-pharyngitis mutilans and described it as a disease _sui
generis_.
=Geographical Distribution.=—The disease is very prevalent in
Guam, and is also present in other islands of the Caroline group.
It exists in Fiji and many cases have been reported by Numa Rat
from the island of Dominica, in the West Indies. Cases have also
been reported from the Philippines and Ceylon.
ETIOLOGY AND EPIDEMIOLOGY
=Etiology.=—The two most prominent views as to its etiology are that
it is a sequel of either yaws or syphilis. The fact that gangosa
responds to antisyphilitic treatment is no proof as to its luetic
origin because yaws yields equally well to such remedies.
Gangosa cases also give a considerable percentage of positive
Wassermann reactions, 105 positives in 281 cases. Halton who made
these tests found 100% positive reactions in cases of yaws and 46%
of positives in those who had had yaws several years previously.
The main points against the syphilitic nature of the disease are
absence of either congenital or acquired syphilis among the natives
of Guam. There is an absence of Hutchinson’s teeth and interstitial
keratitis. Leys states that neither primary nor secondary syphilis
had been seen in a native of Guam during a year in which a very
large number, including several prostitutes, had been treated.
Recently a positive luetin reaction has been obtained in 253 out of
369 cases of gangosa, of which 143 were papular type reactions,
65 pustular and 45 torpid reactions (taking ten days or more for
the reaction to manifest itself). The syphilitic and yaws antigens
seem to be reciprocal so that these tests do not throw out yaws.
The great stumbling block of the advocates of the luetic etiology
has been to show the presence of syphilis among the people of Guam.
Under tropical ulcer it will be noted that Jeanselme failed to find
the eye or teeth signs of congenital syphilis among natives of
Indo-China with the disease.
[Illustration: FIG. 125.—Cases of Gangosa from Guam. (U. S. Naval
Medical Bulletin.)]
Kerr, who has been an advocate of the yaws etiology, has shown that
of 315 cases of gangosa, 205 could show yaws scars and knew where the
mother yaw had been and of the entire 315 only 18 claimed never to
have had yaws and failed to show scars.
Rossiter, who observed active ulcerations of the nasal septum and
hard palate in the case of a two-year old Samoan child, following
yaws, states that he found yaws treponemata in smears from the
ulcerated areas.
=Epidemiology.=—If gangosa is a sequel of yaws then the same factors
which are operative for yaws apply to gangosa.
PATHOLOGY
Sections made from the ulcerating margins of the nasopharyngeal
lesions have failed to show treponemata when stained by Levaditi’s
method. In sections of such tissue stained by Giemsa’s method I noted
a rather marked infiltration with lymphocytes and a great number of
mast cells. Fordyce has noted the presence of giant cells.
From the histological study one can only state that the lesions
present the characteristics of the granulomata.
A remarkable feature of the disease is the rapidity with which
ulceration destroys cartilage and bone. The nasal duct seems to be
prone to attack and it is through this channel that the process
reaches the eye to bring about its destructive tendency in that
organ.
Of 81 cases studied by McLean and Mink the eye was involved in 21.
The larynx was involved in 33 of these cases. It is the frequent
perforation of the hard palate that gives these patients the nasal
voice, whence the name of the disease is derived.
SYMPTOMATOLOGY
Patients with the disease have rarely been observed prior to the full
development of the mutilating ulcerations. In a few cases, however,
it was noted that a patch of membrane first appeared in the region
of the soft palate. This membrane rapidly became honeycombed and an
examination three or four days later showed underneath a deep ulcer,
surrounded by an area of marked congestion.
The ulcerating process advances rapidly, destroying bone as well as
soft parts. The process seems to extend from within outward, giving
a funnel-shaped loss of tissue. The ulceration advances upward and
forward, destroying the nasal septum and structures forming the
tip of the nose, leaving the upper lip as the lower border of this
external opening.
The active process tends to become quiescent in one or two years,
the cases then showing extensive loss of tissue with cicatricial
borders. Occasionally active ulceration may again set in after a
period of quiescence.
The voice character is that of any case where there is a
perforation of the hard palate and is not distinctive of the
victims of this disease.
During active ulceration there is a malodorous sero-purulent
discharge which makes the patients very objectionable. These cases
seem to suffer very little impairment of the general health even
when the process is active.
Although the destructive lesions about the nasopharynx and the region
of the face are the most striking ones it would appear that similar
ulcers on the extremities are of the same nature as those more
prominently situated.
In an examination of the blood of 10 of these cases in Guam I did
not observe any abnormal findings, other than an eosinophilia,
which was present to an equal degree in those unaffected. Musgrave
and Marshall reported a slight leucocytosis in their case.
DIAGNOSIS
Gangosa is chiefly to be differentiated from leprosy, syphilis and
lupus vulgaris. Its more rapid course should distinguish it from
leprosy and lupus and the history from syphilis.
TREATMENT
Odell found that a thorough antisyphilitic treatment cured these
ulcerations. He used mercurial injections. Recently salvarsan has
been used with striking curative results. It has been thought that
local application of tincture of iodine was effective in stopping the
progress of the early ulcerations but this would seem doubtful, it
being advisable immediately to give salvarsan.
On account of the offensive odor of the discharge solutions of
permanganate of potash have generally been used.
CHAPTER XXVIII
MYCETOMA
GENERAL REMARKS
Various destructive processes of different parts of the body, but
more commonly of the foot, which are caused by invasion and growth
of fungi are generally designated mycetomas. Chalmers and Archibald
have studied these conditions most carefully and have grouped most
of them under maduro-mycoses and actinomycoses. The mycetomas are
characterized by the presence of fungi in the form of grains composed
of hyphae, and at times chlamydospores, imbedded in a matrix. These
grains may be imbedded in the tissues or present in the discharge
from the sinuses. Eosinophile bodies are usually present. The
maduro-mycoses have grains with large segmented mycelial filaments,
possessing well defined walls and usually chlamydospores. We have
white or yellow, black and red ones according to the colour of the
grains. The actinomycoses have very fine nonsegmented mycelial
filaments with ill-defined walls and no chlamydospores. We have
black, yellow and red grain actinomycoses. In addition to the
mycetomas we recognize paramycetomas and pseudomycetomas, the former
of which show fungi which do not show any grain formation and the
latter failing to have present either fungi or eosinophile bodies.
The pseudomycetomas are associated only by reason of clinical
resemblance.
HISTORY AND GEOGRAPHICAL DISTRIBUTION
=History.=—The disease was first described by Kaempfer about 200
years ago, but at that time was often confused with elephantiasis.
The first exact clinical description of the disease, with its
pathology, in which was noted the fungus nature of the granules given
off in the discharges from the sinuses, was that of Vandyke Carter,
whose studies were carried on from forty to fifty years ago.
=Geographical Distribution.=—The name Madura foot takes its origin
from the great prevalence of the affection about Madura, in the
Madras Presidency of India. It is less frequent in other parts of
India. It also occurs in Ceylon. The disease is rather widespread
in Africa, having been reported from Algiers, Tripoli, Tunis, Egypt
and the Sudan as well as from Madagascar. Cases have also been
reported from Italy and Greece in Europe and from the West Indies
and some of the South American countries. Several cases have been
reported from North America and Sutton, in 1913, reported two cases
from Kansas, one in a Mexican and one in a native of Texas.
ETIOLOGY AND EPIDEMIOLOGY
=Etiology.=—The disease is caused by the penetration of certain
species of fungi into the tissues of the foot, although rarely the
hand or some other part of the body may be affected. These species
of fungus develop in granulomatous areas from which sinuses lead to
the surface of the foot, in the discharges from which are found small
granules resembling those found in the discharges from actinomycosis
lesions.
As a rule only one kind of fungus is found in a single case.
The most common infection is that due to _Discomyces madurae_
(_Nocardia madurae_) which is the fungus of the fish-roe-like
granules of the pale or white variety of mycetoma. These, like the
fungus of actinomycosis, _Discomyces bovis_, show a felted mycelium
in the center and peripheral club-like structures. These granules
are yellowish-white and vary in size from a pin’s head to a small
pea. The mycelial threads are very narrow, 1 to 1½ microns. It
grows aerobically and the cultures show slender mycelial threads
which are Gram-positive. This is the organism of Carter’s white
mycetoma.
Other species of the pale, white or ochroid group of mycetoma
fungi are _Indiella mansoni_ (Brumpt’s white mycetoma),
_Nocardia asteroides_ (Musgrave and Clegg’s white mycetoma),
_Sterigmatocystis nidulans_ (Nicolle’s white mycetoma) and several
others.
The cases caused by the black varieties are more rare and are
characterized by the presence in the discharges from the sinuses of
black gunpowder-like grains.