administration of atoxyl, viz., 2 to 3 gr. of atoxyl are given by
intramuscular injection every third day for at least two years; or
(2) Broden and Rodhain’s method, 7-1/2 gr. of atoxyl by intramuscular
injection every fifth day. For the combined therapy by atoxyl and
antimony they recommend the following:--“An atoxyl injection (3 gr.) is
given every third day or 7-1/2 gr. every fifth day, and sodiotartrate
of antimony (Plimmer’s salt) is administered daily, 2 gr. dissolved
in a large quantity of water (2 pints) by the mouth or by the rectum.
Tartar emetic, however, is best given by intravenous injections, using
solutions of 1 in 100 or 1 in 1,000. The dose of the drug to be given
is 5 to 10 cg. per injection. It is important that none of the fluid of
the injection should escape into the surrounding tissues, as a violent
inflammation may result. These injections should be administered
monthly on ten consecutive days for a long period.”
Macfie and Gallagher (1914) injected 6 gr. of atoxyl intramuscularly
every week in cases infected with _T. nigeriense_ in the Eket district
of Southern Nigeria.
Large doses of atoxyl were often said to cause distressing results
such as optic atrophy, and when the onset of such occurred the
drug was usually discontinued. However, Daniels[432] (July, 1915)
points out that eye troubles, such as iridocyclitis, are symptoms of
trypanosomiasis.
[432] _Journ. Trop. Med. and Hyg._, xviii, p. 157.
Other arsenical preparations such as soamin and arsenophenylglycin have
been used, but less successfully than atoxyl. Fowler’s solution, well
diluted, has been given by the mouth when treatment by injection was
not possible, the doses commencing with 5 minims and increasing to 15
minims.
Salvarsan and neo-salvarsan have also been tried for sleeping sickness.
Plimmer recommended powdered antimony suspended in sterile olive oil.
Ranken used precipitated metallic antimony in normal saline solution
injected intravenously.
Laveran and Thiroux have recommended a combined treatment of atoxyl and
an inorganic salt of arsenic such as orpiment. The orpiment is given as
pills, in doses of 2 gr. of orpiment two or three times daily. Opium is
added to the orpiment to prevent diarrhœa. This treatment is said to
have been used in man with good results.
_Trypanosoma rhodesiense_ seems less amenable to treatment than _T.
gambiense_.
The main preventive measures seem to lie in segregation of the sick in
areas not infested with Glossinæ, and in measures against these flies,
such as bush clearing and destruction, to some extent, of _proved_
reservoirs in big game.
South American Trypanosomiasis.
The chief clinical features of the trypanosomiasis occurring in Brazil
have already been indicated (see p. 87). With regard to treatment,
according to Castellani and Chalmers the indications are the same
as those for African trypanosomiasis, together with treatment for
hypothyroidism. Preventive measures are directed against the Reduviid
bug, _Triatoma megista_, that transmits the disease. The bugs occur in
numbers in the cracks of the houses of the poor of Minas Geraes, and
may be destroyed by sulphur fumigation, lime-washing or whitewashing.
III.--FLAGELLATE DIARRHŒA AND DYSENTERY.
The chief causal agents are _Trichomonas hominis_ (_T. intestinalis_),
_Chilomastix_ (_Tetramitus_) _mesnili_ and allied organisms (see pp. 54
to 57), and _Lamblia intestinalis_ (see pp. 57 to 60 and Appendix
pp. 734 to 736).
These parasites and the associated diarrhœas occur in temperate as
well as in warm climates. Probably some of the diarrhœas in India are
thus caused. The same, or similar parasites occur in various Muridæ,
especially rats and mice, which may act as reservoirs.
(i) Mello-Leitao[433] (1913), writing from Rio de Janeiro, states
that there is a primary flagellate dysentery, due to _Trichomonas
intestinal_is (Leuckart) and to _Lamblia intestinalis_ (_Lambl_),
either separately or in combination. He considers it a benign disease,
and the most frequent form of dysentery in young children. Trichomonas
and Lamblia were found to be pathogenic to children under 3 years of
age.
[433] _Brit. Journ. Children’s Diseases_, x, p. 60.
Escomel[434] (1913) collected 152 cases of dysentery in Peru due solely
to Trichomonas. Examination of the reservoirs containing the water used
for drinking purposes showed the presence of Trichomonas. After the
reservoirs were cleaned no more Trichomonas was found and the cases of
dysentery ceased.
[434] _Bull. Soc. Path. Exot._, vi, p. 120.
Brumpt[435] (1912) described a colitis due to _Trichomonas
intestinalis_ in a patient returned from Tonkin.
[435] _Ibid._, v, p. 725.
Cases of infection by _Chilomastix_ (_Tetramitus_) _mesnili_, with
colitis or dysenteric symptoms, are recorded by Brumpt (1912) from
France, and by Nattan-Larrier[436] (1912) from the Ivory Coast
respectively.
[436] _Ibid._, v, p. 495.
Marques da Cunha and Torres[437] (1914) describe five cases of chronic
diarrhœa in Brazilian children due to the _Chilomastix_ (_Tetramitus_).
[437] _Brazil Medico_, xxviii, p. 269.
Gäbel[438] (1914) described a case of seasonal diarrhœa contracted
in Tunis and caused by a Tetramitid parasite which he named _Difämus
tunensis_, as the discoverer considered that it lacked an undulating
membrane in its large cytostome.
[438] _Arch. f. Protistenkunde_, xxxiv, p. 1.
Derrieu and Raynaud[439] (1914) record a case of chronic dysentery in
Algeria due to a Trichomonad possessing an undulating membrane and
five free flagella. The parasite was named _Hexamastix ardindelteili_,
but the generic name _Hexamastix_ is pre-occupied. Chatterjee’s
_Pentatrichomonas bengalensis_ (1915) is possibly the same organism.
[439] _Bull. Soc. Path. Exot._, vii, p. 571.
_Treatment._--Escomel (1913), finding ipecacuanha and calomel useless,
recommends turpentine for Trichomonad dysentery. Two to 4 gr of essence
of turpentine in an emulsion are given by the mouth, and enemata
containing 15 to 20 drops of turpentine emulsified in the yolk of an
egg to which is added a little water and tincture of opium. Derrieu and
Raynaud found this treatment effective in Algeria. Smithies[440] (1912)
reports two cures of cases of severe dyspepsia, in which Trichomonads
were found in the stomach contents, after administration of a single
dose of 50 to 60 gr. of thymol, given at bed-time, together with 2 gr.
of calomel, and followed by an ounce of Carlsbad salts in the morning.
The patients came from the Southern United States, and had been in the
habit of drinking unfiltered surface water in the localities in which
they lived. Mello-Leitao[441] used magnesium sulphate and water or milk
diet. Sometimes enemata of collargol (1 per cent.) or electrargol were
required. Rosenfeld recommended calomel. Methylene blue has also been
tried. Recently, Escomel[442] (1914) recommends enemata of an aqueous
solution of iodine (1 per 1,000) and farinaceous diet. Lynch[443]
(1915), working in South Carolina, recommends a mouth wash of saturated
solution of bicarbonate of soda three times daily in oral infections. A
similar solution was used as a douche in vaginal trichomoniasis.
[440] _Amer. Journ. Med. Sci._, cxliv, p. 82.
[441] _Brit. Journ. Children’s Diseases_, x, p. 60.
[442] _Bull. Soc. Path. Exot._, vii, p. 657.
[443] _Amer. Journ. Trop. Dis. and Prevent. Med._, ii, p. 627.
Stiles (1913) points out that when amœbæ or flagellates are found in a
large percentage (10 to 40, or even 60) of the members of a community,
means should be taken to improve the methods for the disposal of the
dejecta, so that the food supply may be carefully protected against
fæcal contamination. Cysts of the parasites may be air-borne or
conveyed to food on the bodies of house-flies.
(ii) _Lamblia intestinalis_ in man may cause diarrhœa with
dysenteriform stools. The diarrhœa may be of a chronic recurrent
character. The flagellate, or a variety of it, is fairly common in the
digestive tract of rats and mice.
Mathis[444] (1914) gives an interesting account of cases in Tonkin. In
a child, aged 3, the stools were at first glairy and blood-stained,
containing many encysted Lamblia. The child’s home was infested with
mice. In another case, the house of the patient harboured numerous rats.
[444] _Bull. Soc. Med. Chirurg. Indo-Chine_, v, p. 55.
According to Mathis, prognosis is favourable, but emetine hydrochloride
is without action on Lamblia. Prowazek and Werner[445] (1914), however,
state that emetine will act upon the flagellates, but not upon the
cysts. They recommend uzara (two tablets, three times daily) and
extract of male fern as useful in certain cases. Martin Mayer (1914)
found emetine hydrochloride successful in a case in the Hamburg
Seamen’s Hospital, but Assmy (1914) points out that a suitable diet and
daily doses of magnesium sulphate are sufficient, in his experience, to
effect an improvement, and he doubts the specific action of emetine.
Escomel (1914) recommends milk diet, then calomel succeeded by castor
oil.
[445] Beihefte z. _Arch. f. Schiffs- u. Tropen-Hyg._, xviii, 5, p. 155.
According to Noc, Lamblia may also be water-borne. Healthy carriers of
Lamblia cysts are known. Food should be protected from being soiled by
rats and mice.
IV.--LEISHMANIASES.
A. *Kala-azar.*
(i) _“Indian” Kala-azar due to_ Leishmania donovani.
Indian kala-azar due to _Leishmania donovani_ is a very fatal disease
with a rate of mortality varying from 70 to 98 per cent. of the cases.
The incubation period is very variable and the early symptoms not
well defined. The incubation period seems to range from three weeks
to several months after exposure to infection. The onset seems to
commence with a rigor and attack of irregular, remittent fever, which
may show two remissions per day in a four-hourly temperature chart.
Rogers considers the daily double remission almost diagnostic. The
duration of this first attack is from two to six weeks. The spleen
and liver enlarge, especially the former, and are painful and tender.
Towards the end of the time the temperature declines and the first
period of the disease ends. After this period an apyrexial interval
occurs, which, after some weeks, ends in an attack of fever resembling
the first. Periods of pyrexia and apyrexia alternate. Anæmia commences
and asthenia appears and deepens steadily. The patient is now thin
and wasted, the abdomen much swollen and protuberant, the ribs show
clearly, the limbs are wasted and skin and tongue darker than normal.
In Europeans the skin is of a remarkable earthy hue, and in natives of
India darker than normal, approaching black. Intestinal disturbances,
often in the form of very obstinate and intractable diarrhœa or
dysenteric attacks, are common. Papular eruptions often appear,
particularly on the thighs; hæmorrhages also may occur. The disease
lasts for periods varying from seven months to two years, and usually
ends fatally.
Treatment, unfortunately, has not been very successful up to 1915.
Manson has reported two cases of cure by intramuscular injections of
atoxyl daily or every other day in doses of 3 gr. Rogers has advocated
large doses of quinine, 60 to 90 gr. daily until the temperature falls
and then 20 gr. daily. Castellani and Chalmers consider the best
results are obtained by large doses of quinine given intramuscularly,
supplemented by a course of quinine cacodylate injections or atoxyl
injections. Tartar emetic should be tried (see pp. 627, 629),
especially as L. Rogers (July, 1915) has had promising results in ten
cases. Castellani (1914) and Mackie (1915), have also had successful
results. Leishman states that the administration of red bone-marrow,
either raw or in the form of tablets, may be beneficial. Good nursing
and careful diet are essential, and diarrhœa or dysentery must receive
the appropriate treatment.
With regard to preventive measures, the extermination of bugs and
other biting insects seems to be of most service. Domestic and personal
cleanliness is of great importance. Patients should be segregated. It
would probably be as well if houses in which many cases of kala-azar
occurred were destroyed. Dodds Price, in Assam tea gardens, moves the
coolie lines 300 to 800 yards from old infected ones, with satisfactory
results.
(ii) _Infantile Kala-azar due to_ Leishmania infantum.
This malady is found among children, rarely in adults, along the
Mediterranean littoral.
The disease commences insidiously and is often unrecognized until some
intestinal disturbance occurs. The spleen is then found to be somewhat
enlarged, and the case has often been regarded as one of malaria.
The child becomes anæmic, suffers from diarrhœa, alternating with
constipation, and has attacks of irregular fever. The spleen continues
to enlarge and protrudes from under the cover of the ribs. Hæmorrhages
from the nose and gums and into the skin occur. Anæmia and wasting set
in. The abdomen then becomes very enlarged. The child becomes much less
active both physically and mentally, and looks prematurely old. Death
often occurs from exhaustion, though some cases of spontaneous recovery
are known.
Treatment up till recently has been unsatisfactory. Some of the
remedies tried, as quoted by Castellani and Chalmers, are 15 cg. doses
of atoxyl, benzoate of mercury (2 to 4 mg. as a daily injection),
thiarsol (5 to 15 mg. by subcutaneous injection), salvarsan, etc.
Recently Cristina and Caronia (1915)[446] have given repeated
intravenous injections of 1 per cent. aqueous solution of tartar
emetic, the dose varying from 2 to 10 cg. The treatment in various
cases has lasted from 15 to 40 days.
[446] _Bull. Soc. Path. Exot._, viii, p. 63.
Prophylactic measures seem to lie in the destruction of infected dogs
and diminishing the breeding of fleas (see p. 111).
B. *Oriental Sore, due to Leishmania tropica.*
Oriental sore, known under many other names (see p. 107), is a local
infection of the skin due to _Leishmania tropica_. The incubation
period varies from a few days to some weeks, or even months, and
then one or several small itching papules appear. Each spot becomes
red and shotty, the papules increase slowly in size and the surface
becomes covered with papery scales. After a variable time, usually
not exceeding three to four months, ulceration occurs and a yellowish
secretion is exuded that soon dries into a scab. Under the scab
ulceration continues by erosion of the edges, and subsidiary sores
arise around the parent ulcer and usually fuse with it. Healing
commences after six to twelve months. Granulation begins at the centre
and spreads outwards, and when healing is complete, a depressed,
whitish or pinkish scar remains.
Many treatments for Oriental sore have been devised but do not seem
particularly satisfactory. Castellani and Chalmers state that the
scabs should be removed by boracic acid fomentations, and the ulcers
thoroughly disinfected once or twice daily with a 1 per 1,000 solution
of perchloride of mercury, after which an ordinary antiseptic ointment
is applied.
The use of permanganate of potash has been advocated both by French
and English doctors. Both large and small sores can be treated.
The patient’s skin around the sore is protected by a thick layer
of vaseline, and the surface of the ulcer powdered with potassium
permanganate, which is kept in position by a pad of gauze and a
bandage. The treatment is said to cause great pain for six to eight
hours, but at the most, three treatments are necessary before the sore
becomes a simple ulcer, well on the way to healing. The permanganate
may also be used in ointment. Excision of the ulcer when small is
advisable when the site of the ulcer permits of this. According to
Manson, reports on treatment by radium, salvarsan and carbon dioxide
snow are decidedly promising. Mitchell (1914)[447] reports favourably
on the use of carbon dioxide snow in the form of a pencil, in India.
In Brazil several workers (1914) record successful results from the
intravenous injection of a 1 per cent. solution of tartar emetic in
distilled water. Low (1915) has successfully treated a case by direct
local application of tartar emetic. Row (1912) has treated cases of
Oriental sore by inoculation of killed cultures of the causal organism.
[447] _Journ. Roy. Army Med. Corps_, xxiii, pp. 440–446 (see _Trop.
Dis. Bull._, v, No. 5, p. 276).
As the disease is very contagious, the slightest wound, and any insect
bite, should be thoroughly disinfected with 5 per cent. carbolic acid
or iodine. Destruction of bugs, lice, and other biting insects should
be enforced. As dogs may contract the disease (see p. 108), it is well
not to allow them in the house and not to encourage undue contact with
them.
_Naso-oral Leishmaniasis_ (_Espundia_) _due to_ Leishmania tropica.
This form of Leishmaniasis has been reported from South America and
recently by Christopherson[448] (1914) from the Sudan. In South America
it is often called Espundia, also Buba and Forestal Leishmaniasis. The
primary lesion is found usually on the forearms, legs, chest or trunk.
This ulcer is of the Oriental sore type, and after some months, or
even as long as two years, heals up, leaving a thick scar. While the
ulcer is open, or more often after it has healed, lesions appear on the
mucosa of the mouth and nose. The hard and soft palate, gums and lips
all may be attacked. The mucosa of the nose is usually attacked and the
cartilages become destroyed, producing great deformity. In bad cases
the pharynx and larynx may become infected.
[448] _Annals Trop. Med. and Parasitol._, viii, p. 485.
Till recently it was believed that treatment was of little use unless
the case could be investigated early. Escomel considered that if the
primary cutaneous lesion was excised or destroyed, further progress of
the disease was prevented. When lesions have appeared on the mucosa of
the mouth or nose, little could be done. The ulcers might be cauterized
and mild antiseptic mouth washes used.
In 1913 Vianna, working in Brazil, introduced treatment by tartar
emetic, which is now becoming more widely known and proving
efficacious. Carini[449] (1914) applies it thus. Tartar emetic (that
is, potassium antimonyl tartrate) in 1 per cent. aqueous solution is
introduced slowly into a vein, such as the vein at the bend of the
elbow, in doses of 5 to 10 c.c. daily or on alternate days according to
the tolerance of the patient to the drug. Eighteen to forty injections
have been used. In some of the memoirs on the subject, the drug is
referred to as antimony tartrate.
[449] _Bull. Soc. Path. Exot._, vii, p. 277.
The course of the disease is chronic and may last for twenty to thirty
years, death usually resulting from some intercurrent disease.
At present the actual transmitter of Espundia is not known with
certainty. Various sand-flies (Simulidæ) have been suspected of
transmitting the disease, though so far proof is wanting. It has also
been suggested that the natural food sources of some Simulidæ known to
bite man, namely, certain snakes[450] and lizards,[451] are possible
reservoirs of the disease.
[450] Lindsay (1914), _Trans. Soc. Trop. Med. and Hyg._, vii, p. 259.
[451] Sergent (Ed. and Et.), Lemaire and Senevet (1914), _Bull. Soc.
Path. Exot._, vii, p. 577.
Prophylactic measures would seem to consist in the immediate
disinfection of insect bites by tincture of iodine, and by avoidance of
areas known to be infested with snakes and lizards, and insects that
prey on them and man indifferently. The destruction of the primary
lesion as soon as detected is essential, and the isolation of advanced
cases of the disease seems advisable.
V.--SPIROCHÆTOSES.
A. *Relapsing Fevers.*
The relapsing fevers of Europe and of America, due to _Spirochæta
recurrentis_ and _S. novyi_ (probably a race of _S. recurrentis_),
present much the same symptoms, which differ in some respects from
those due to _S. duttoni_, the excitant of “tick” or “relapsing” fever
in Africa (see pp. 116–122).
The incubation period of _S. recurrentis_ varies from two to twelve
days, during which time a very slight indisposition may be noticed. The
onset is usually sudden, with severe headache, pains in the back, limbs
and stomach and a feeling of weakness. There is a rise of temperature
to 103° F. or 104° F., and the temperature continues high till about
the sixth or seventh day. The skin is yellowish, hot and damp; a rash,
disappearing on pressure, may occur on the trunk and legs, nausea is
always present and thirst is usual. The liver and spleen both enlarge.
The number of respirations and pulse-rate become increased. On the
sixth or seventh day a crisis occurs. There is violent perspiration,
with a rapid fall of temperature, pulse and respiration become normal
and the patient sleeps and awakes better. Improvement continues for
some days, and recovery may ensue, but usually about the fourteenth day
relapse occurs, lasting usually three or four days. A second relapse
is unusual. Numerous complications are known, _e.g._, bronchitis,
pneumonia, diarrhœa and dysentery.
With regard to treatment, the specific appears to be salvarsan.
Castellani and Chalmers recommend salvarsan administered intravenously.
Intramuscular inoculations (for example, into the buttock) of a
suspension of “606” in oil can also be given. The drug is very
efficacious, but large doses should not be given. An intravenous
injection of 4 or 5 gr. does not give rise to unpleasant symptoms but
is sufficient to effect a cure.
The incubation period for the American form of the disease is at least
five to seven days, and the first attack lasts about five to six days.
The treatment is by salvarsan as detailed previously.
As relapsing fever is spread by body lice and possibly by bugs,
preventive measures are directed against these insects. Strict
cleanliness of person, clothing, bedding and dwellings is essential.
Furniture, _e.g._, wooden bedsteads, liable to harbour such insects
should not be used.
The principal and best-known relapsing fever of Africa is that excited
by _Spirochæta duttoni_, and transmitted to man by ticks, chiefly
_Ornithodorus moubata_. The incubation period is usually about seven
days but may be longer. The patient is dull and lethargic, perspires
freely and is often constipated. The temperature rises to 103° F.
or 105° F., there is headache, pains in the back and limbs, general
chilliness and great pain in the region of the spleen, which often
enlarges. The symptoms become worse, there is a fall of temperature
with improvement in the morning, and a rise, with increase of pain,
in the evening. Spirochætes are now found in the blood in greater
numbers. The symptoms last three to four days and end in a crisis with
profuse sweating and fall of temperature below normal. The day before
the crisis there is a pseudo-crisis, when the temperature falls but
there is no improvement. The patient is left weak and tired. Recovery
may follow, but more usually a relapse occurs. The intermission period
varies; five to eight days is common. The symptoms of the relapses are
like those of the first attack. The number of relapses varies, five to
eleven may occur.
The treatment recommended is by salvarsan, as for the European
relapsing fever.
With regard to prophylaxis, localities where ticks abound must be
avoided and the parasites themselves destroyed. Native huts should be
avoided. Mosquito nets, a bed well off the ground and the use of night
lights are advised by Manson to avoid attacks by ticks, which are often
nocturnal in their habits.
In North Africa (Algeria, Tunis, Tripoli, Egypt), and sometimes in
the Anglo-Egyptian Sudan, a spirochætosis due to _S. berbera_ occurs.
According to Castellani and Chalmers, the incubation period varies
somewhat. The fever reaches its height during the first twenty-four
hours, and afterwards shows a morning remission. Jaundice is often
absent, but there may be hepatic tenderness and splenic enlargement.
One or two relapses usually occur. The treatment is on the same
lines as for the other spirochætal fevers. Sergent and Gillot[452]
(1911), working at the Institut Pasteur of Algeria, have had good
results by using injections of salvarsan in doses of 0·75 to 1·0 cg.
per kilogramme weight of the patient. The prophylactic measures are
directed against lice and other biting insects. Personal cleanliness is
most necessary.
[452] _Bull. Soc. Path. Exot._, iv, p. 440.
In Asia, a relapsing fever, due to the spirochæte named _S. carteri_ by
Manson in 1907, producing a mortality of about 18 per cent., occurs.
The symptoms have a general resemblance to those produced by _S.
recurrentis_, but on the fall of temperature to subnormal on the sixth
or seventh day, when profuse perspiration and polyuria occur, instead
of improvement following, the patient often becomes collapsed, with a
clammy skin and feeble pulse. Improvement is slow. The first relapse
occurs about the fourteenth day of the attack, when the temperature may
be higher than for the first attack. There are seldom more than four
relapses. The treatment is by salvarsan, of which doses of not more
than 5 gr. intravenously should be given. Sudden heart failure being
common, Castellani and Chalmers state that cardiac stimulants should be
given. Prophylaxis is the same as for European relapsing fever.
B. *Yaws or Frambœsia tropica.*
Yaws is essentially a tropical disease, though it is found in the
tropical and subtropical zones in all parts of the world, except
in the mountains and cold districts. In 1905, Castellani found the
causal organism, _Treponema pertenue_ (sometimes called _Spirochæta
pertennis_) (see p. 127). The disease shows three periods: (1) The
primary stage, consisting of the development of the primary lesion or
papule, which is usually extragenital. The papule dries into a crust
beneath which an ulcer lies. (2) The secondary or granulomatous stage,
which commences from one to three months after the primary lesion is
first seen. It consists of a general eruption of small papules, some of
which enlarge and become granulomatous nodules covered with a yellowish
crust. They are common on the limbs and face. (3) The tertiary stage,
in which deep ulcerations and gummatous nodules appear. Any of the
tissues may be involved. Osseous lesions may occur. The disease does
not appear to be hereditary; it is usually spread by contact.
The best treatment appears to be by salvarsan or neo-salvarsan.
Castellani and Chalmers recommend intramuscular and intravenous
injections. For intramuscular injection an alkaline or neutral solution
of the drug is preferable, or a suspension of the drug in oil may be
used. The dose varies from 0·3 to 0·5 gr according to the age and sex
of the patient. For use intravenously, a slightly smaller dose is
required. Galyl is also being used.
In countries where frambœsia is endemic, slight skin abrasions should
be carefully treated with antiseptics. Yaws patients should be isolated
till cured, and their dwellings and personal possessions disinfected.
C. *Syphilis.*
Syphilis, due to _Treponema pallidum_ (sometimes called _Spirochæta
pallida_), is prevalent throughout the tropics as well as in
temperate zones. The disease is amenable to treatment by salvarsan
and neo-salvarsan, for administration of which see relapsing fever
and yaws. Galyl is also being used with favourable results. Lambkin’s
mercury cream has been found useful in treating numerous cases in
Uganda. The life-history of the parasite is given on p. 124, and
further medical details hardly come within the purview of this book.
D. *Bronchial Spirochætosis.*
Bronchial spirochætosis, due to _Spirochæta bronchialis_ (see pp. 122,
739) is probably of wide distribution in the tropics. The spirochætes
have been found in cases of chest complaints, especially those with
bronchitic symptoms. The disease may be suspected in atypical cases of
pneumonia and bronchitis, and may be mistaken for incipient phthisis.
Chalmers and O’Farrell[453] (1913), writing from Khartoum, recommended
rest in bed, good food and ventilation, coupled with treatment by
arsenic in some form, preferably associated with glycerophosphates.
These may be given by the mouth, or intramuscularly as an injection
of:--
Sodium cinnamate 0·05 grm.
Sodium cacodylate 0·10 "
Sodium glycerophosphate 0·10 "
[453] _Journ. Trop. Med. and Hyg._, xvi, p. 329.
Taylor[454] (1913–14), writing from Entebbe, Uganda, prescribes
arsenious acid by the mouth in increasing doses. Creosote has been used
in West Africa.
[454] _Annual Med. and Sanit. Rept., Uganda_, for 1913, p. 80.
VI.--MALARIA.
Malaria, known also under the names of ague, paludism, marsh fever,
remittent fever, intermittent fever and climatic fever, among others,
is a very widely spread disease. It is most prevalent in the equatorial
regions and gradually diminishes north and south of the equator. The
various malarial parasites (see pp. 155 to 172) are spread by species
of Anophelines, and hence malaria is present in districts favourable
to these intermediate hosts, that is, in places where there is a
considerable amount of atmospheric moisture and rain, as well as heat.
The principal malarial parasites are: _Plasmodium vivax_, the agent of
simple tertian fever; _Plasmodium malariæ_, the parasite of quartan
malaria, and _Laverania malariæ_ or _Plasmodium falciparum_, producing
malignant tertian or sub-tertian malaria (and quotidian, see p. 167).
These various malarial fevers present certain clinical features in
common, which will be stated here (see also pp. 155 to 157). For
further particulars regarding malaria in all its aspects the reader is
referred to the book by Sir Ronald Ross on “The Prevention of Malaria,”
to the “Manual of Tropical Medicine,” by Drs. Castellani and Chalmers,
and to the “Tropical Diseases” of Sir Patrick Manson.
Typical malarial fevers consist of a series of pyrexial attacks which
recur at definite intervals of twenty-four (quotidian), forty-eight or
seventy-two hours, according to the parasite present in the patient’s
blood. Each attack shows three stages, a stage of rigor, a heat stage
and a stage of profuse perspiration. Following on these three stages,
there is an interval relatively or actually without pyrexia. Then the
fever returns again. A rise of temperature, often accompanied by a
general feeling of malaise, may precede the initial stage of rigor.
When the latter sets in, the patient feels intensely cold, shivers
violently, the skin becomes cold and the features pinched. There may
be violent vomiting and convulsive attacks in young children. The
temperature, however, is really above the normal, and continues to
rise. After about an hour, the shivering abates and the heat stage
succeeds it. The temperature rises rapidly, even to 106° F. The patient
becomes very flushed, the pulse is rapid, headache may be intense and
the skin dry and burning. This stage, that causes acute distress to the
patient, may last for one or often three to four hours, and then the
patient commences to perspire profusely, the clothing and bedding often
being saturated with sweat. After this, the fever rapidly declines, and
when the sweating ceases, the patient may feel almost well although
somewhat languid. The sweating stage persists from two to four hours,
so that the attack lasts as a rule from six to ten hours. After an
interval of one, two or three days, a recurrence takes place. During
the early part of the attack, especially at the stage of rigor, there
is great splenic enlargement. At first the enlargement disappears in
the interval, but in the case of repeated attacks the spleen tends
to become permanently enlarged. During malarial attacks and during
the intermission period, there is a great increase in the amount of
nitrogen excreted by the kidneys, while the excretion of iron and bile
in the fæces is increased.
Stitt[455] (1914) points out that it is characteristic of malignant
tertian paroxysms that they set in with chilly sensations rather than a
frank, definite chill, and that the fever is of the remittent type.
[455] “The Diagnostics and Treatment of Tropical Diseases.” London:
H. K. Lewis.
_Plasmodium malariæ_ and _P. vivax_ rarely produce marked lesions
in the bodies of their hosts, as they sporulate in the circulating
blood and so do not accumulate in any one organ. On the other hand,
_Laverania malariæ_ (_Plasmodium falciparum_) multiplies within the
internal organs of its host, and consequently aggregates or clusters of
the parasites occur therein. The organ in which most sporulation occurs
suffers most. The liver is generally enlarged, soft and congested.
The capsule of the spleen is tense, but the splenic consistency is
less than normal. The bone-marrow is often dark and congested in the
spongy bones and brownish-red in long bones. The blood-capillaries of
the brain and spinal cord are often filled or blocked with sporulating
parasites and large quantities of pigment are found in these organs.
Even if the parasites are absent, the pigment is present in the
endothelial cells. Pigment is found in most organs of the body.
Atypical forms of malaria may occur in which some or all of the
symptoms are much modified. Irregular fevers also may be produced by
successive infections by the same parasite, or by the presence of two
different malarial parasites.
As regards the diagnosis of malaria, according to Manson the three
pathognomonic signs are--periodicity, the effect of quinine, and the
presence of the malarial parasite.
_Treatment._--The great specific for malaria is quinine. It attacks the
merozoites or asexual generation. The drug can be administered by the
mouth, by the rectum, by intramuscular injections or by intravenous
injections, the two latter methods being adopted in serious infections
or where gastric complications are present. When quinine is taken by
the mouth, the more soluble acid salts, _e.g._, quinine bihydrochloride
and bisulphate, are better than the sulphate, the form in which quinine
is usually sold. Tablets, pills and capsules are convenient means of
taking quinine but must not be old or hard, or they may pass unchanged
through the body. In the case of mild tertian or quartan malaria,
Castellani and Chalmers recommend the administration of a dose of
quinine four hours before the sporulation of the parasite is due.
Another modification is to give 10 gr. of quinine by the mouth in the
morning and a second dose of 10 gr. as above. In many cases they give 5
to 10 gr. of the drug three times a day. Administration of quinine _per
rectum_ may be useful but they recommend intramuscular inoculation.
The solutions used must be sterile, and the “sterilettes,” small,
hermetically sealed vials, containing 1 grm.) or 1/2 grm. (7-1/2 grm.)
of quinine in solution, are recommended. A deep injection into the
deltoid or gluteus muscle is usual.
For pernicious infections, intravenous inoculation with not less than
1 grm. at a time is recommended.
After the fever has subsided, the administration of quinine in smaller
doses must be continued for some time, in order to avoid relapses.
Stitt (1914) writes that “there now seems to be a tendency to use
the alkaloid itself instead of its salts, it having been found that
the alkaloid and its very insoluble tannate are absorbed from the
digestive tract equally as well as the soluble salts.” Euquinine or
ethylcarbonate of quinine contains 81 per cent. of quinine, but is
expensive.
During malarial attacks, constipation must not be allowed. Headache can
be relieved by cold applications, and perspiration must be encouraged
in the early stage by hot tea, warm lime drinks, etc. After bad
attacks, a change to a cooler climate is desirable, but the quinine
treatment must not be discontinued.
Preventive measures take two main forms, directed respectively against
the malarial parasites in man, and against the mosquitoes that convey
the parasite from man to man.
With regard to man, houses should be built away from low-lying
marshy ground, and kept free from vegetation such as grass or brush
which furnishes shelter to the mosquitoes. In the tropics, the chief
reservoirs of the malarial parasites are the native children, hence
European quarters should be away from native dwellings as far as
possible. Mosquito nets, having twenty to twenty-four meshes per
square inch, should be used invariably, and houses should be screened.
Malaria-conveying mosquitoes bite chiefly towards evening. Quinine
treatment for preventive purposes is important. A dose of 5 gr. of
quinine daily, with a dose of 10 gr. on the seventh day (Castellani),
is efficacious. Some workers, however, recommend a large dose (15 gr.)
on two consecutive days every eight or ten days for three months, while
others recommend 10 gr. twice a week. Celli administered 3 gr. of
quinine morning and evening.
The second line of attack is directed against mosquitoes, especially
Anophelines, on the lines so well set forth by Sir Ronald Ross.[456]
The accumulation of small quantities of water in various vessels, many
of them unnecessary, should be prevented, as _Stegomyia_ (Culicines)
breed in such receptacles. Anophelines breed in small pools. All
drinking water and household vessels, water-butts and cisterns must be
effectively screened with wire gauze. Cesspools, etc., must also be
screened, and they, and all collections of water, should be oiled with
crude petroleum sprays every week or ten days, or fortnight according
to some workers. The petroleum is a good larvicide and suffocates the
Anopheline larvæ, while its presence renders the site obnoxious to
the adult mosquitoes. The amount of crude petroleum or kerosene will
vary according to the locality concerned, due regard being paid to its
powers of spreading on the surface treated. Different authorities have
used different quantities, such as 1 oz. of oil to 1 square yard or to
15 square feet. Others have used 1 pint of the petroleum to a circle
of 20 feet in diameter, while 1/2 pint for every 100 square feet of
surface has also been recommended. The larvicide used so successfully
in Panama consisted of:--
Average mixture
Crude carbolic acid (containing 15 per cent. phenol) 300 gallons
Caustic soda 30 lb.
Resin 200 lb.
[456] “The Prevention of Malaria.” Second Edition (1911). London: John
Murray.
One part of this mixture in 5,000 parts of water containing mosquito
larvæ destroys them within five minutes; 1 part in 8,000 of water kills
larvæ in thirty minutes. Small fish, such as the “millions” fish, that
feed on the larvæ, can be introduced into collections of water and are
of local service. Ducks may also act as destroyers of larvæ. The growth
of water-weeds and rank vegetation, that affords shelter to the larvae,
must be prevented as far as possible.
Wherever possible hollows should be filled up, swamps and roads should
be well drained. Much good has followed the use of such measures in
Panama, Egypt, British Guiana and other places. The ideal conditions
for malaria reduction appear to consist in a combination of general
quinine prophylaxis with anti-mosquito measures.
VII.--BALANTIDIAN DYSENTERY.
This disease is also known as ciliate or ciliary dysentery. The chief
causal agent is _Balantidium coli_. Others are _Balantidium minutum_,
_Nyctotherus faba_, etc. (see pp. 200–206).
Balantidiasis is insidious and is marked by alternate attacks of
diarrhœa and constipation with vomiting, while mucus is passed in the
motions, which are foul smelling. There may be chronic ulceration of
the colon. Œdema of the face and limbs and anæmia may occur.
Treatment is at present rather unsatisfactory. Castellani and Chalmers
state that “the symptomatic treatment for entamœbic dysentery may
be tried.” Various treatments, more or less empirical, by calomel,
quinine, carbolic acid in pill form, salicylic acid, extract of male
fern, methylene blue, iodine solution, rice water and tannin enemata
are mentioned by Prowazek[457] (1913) and by Seifert. E. L. Walker[458]
(1913) found, from experimental work, that organic compounds of
silver, _e.g._, protargol, were most effective. Local treatment
by large enemata of collargol or protargol seems to be indicated.
Behrenroth[459] (1913) successfully treated a Prussian case with
thymol, given in 4 grm. doses every two days, followed at the end of
a fortnight by de-emetinized ipecacuanha, given in pills containing 6
cg. each, to the number of thirty a day. In about another fortnight
the symptoms had subsided. The thymol checked the diarrhœa, but it
was necessary to give the de-emetinized ipecacuanha to kill off the
balantidia still present. Phillips (1915) also recommends thymol.
Ardin-Delteil, Raynaud, Coudray and Derrieu (1914) found neither
emetine hydrochloride nor protargol of use.
[457] Beihefte z. _Arch. f. Schiffs- u. Tropen-Hyg._, xvii, 6, p. 371.
[458] _Philippine Jl. Sc._, Sect. B, viii, pp. 1–15, 333–349.
[459] _Arch. f. Verdauungs Krankheiten_, xix, p. 42.
As regards prophylaxis Walker states that pigs “should be confined
and not allowed to run in yards and dwellings.” Behrenroth considers
that dirty hands, for example, those of farm workers brought into
contact with pigs, are probably the medium of infection. The personal
cleanliness of such persons is, then, of the greatest importance.
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*PLATHELMINTHES* (Flat Worms).
BY
J. W. W. STEPHENS, M.D., B.C., D.P.H.
FASCIOLIASIS.
Fasciola hepatica.
The symptoms of disease evoked by _Fasciola hepatica_ are rarely
observed in our part of the world, whereas Kermogant[460] states
them to be of frequent occurrence in Tonkin[461]; the parasites are
there called “Douves.” In our experience they are only accidentally
found _post mortem_ in a certain number of cases, as no changes are
manifested during life which would permit of any conclusion being drawn
as to the presence of these parasites. In three cases (Bierner,[462]
Bostroem[463] and Sagarra[464]) icterus was present; in a fourth case,
recorded by Duffek,[465] the parasites had led to a severe and acute
distomiasis of the liver, combined with chronic purulent and ulcerative
cholecystitis, with purulent cholangitis and dilation of the bile-ducts
and numerous small abscesses of the liver. The total number of flukes
found in these cases amounted to about fifty. The parasites passed from
the duodenum into the bile-ducts, and first obstructed the flow of bile
and then set up icterus, followed by cholecystitis and cholangitis.
[460] Kermogant, _Soc. méd. des Hôp._, February 7, 1905.
[461] [The distomiasis of Tonkin is due to _Clonorchis sinensis_ and
not to _F. hepatica_.--J. W. W. S.]
[462] Bierner, _Schweiz. Zeitschr. f. Heilk._, 1863.
[463] Bostroem, _Deutsch. Arch. f. klin. Med._, 1883.
[464] Sagarra, quoted by Duffek.
[465] Duffek, _Wien. klin. Wochenschr._, 1902, xxx.
As regards localization of the liver fluke in the pharynx, see p. 242.
The treatment must be directed to the principal symptoms; prophylaxis
is especially important in districts where distomiasis is of frequent
occurrence. As the embryos live in water, only boiled or filtered
water should be drunk. The attempts of Tappeiner[466] to discover an
effective remedy against liver-fluke disease (liver rot), so prevalent
among sheep, were unsuccessful.
[466] Tappeiner, _Münch. med. Wochenschr._, 1900, l.
Fasciolopsis buski.
This parasite lives in the intestine, not in the liver of man; it
produces bloody stools and typical symptoms--high fever and a condition
of apathy (Odhner).[467]
[467] Odhner, _Centrall l. f. Bakt._, 1902, xxxi.
PARAGONIMIASIS.
Paragonimus ringeri.
The disease produced by the lung fluke is specially endemic in Japan,
also in isolated parts of China, Formosa and Korea. The fact that the
lung-fluke disease is most frequently found in mountainous districts
(Katsurada[468]) is worthy of special attention. The onset of pulmonary
paragonimiasis is generally insidious (Looss[469]); generally the
only symptom is a slight cough, occurring at first at longer, and
later at shorter intervals; it is accompanied by the expectoration
of discoloured sputum, frequently blood-stained. Though now and
then severe hæmorrhages result, up to the present no case has been
established in which they have been the direct cause of death.
[468] Katsurada, Ziegler’s _Beitr. z. path. Anat._, 1900, xxviii.
[469] Looss, “Handb. d. Tropenkrankh.,” von Mense, 1905, i.
Examination of the thorax frequently fails to reveal anything abnormal.
Inouye[470] states that the most frequently observed changes consist
in retraction of the thorax and in a contraction of its infrascapular
portion. Scheube[471] repeatedly observed that the one side, presumably
that which harboured the worm, moved less freely than the other. The
physical changes are not uniformly spread over the whole lung, but are
localized. The disease may come to a standstill for long intervals and
then set in again, lasting on the whole from ten to twenty years. In
addition to paragonimiasis of the lungs, cysts are frequently found
on the eyelids, which occasionally extend deeply into the orbit and
hinder the movements of the eyes. _Post mortem_, cysts the size of
hazel nuts containing one, two, or three adult worms are found in the
lungs, and in addition, not uncommonly there exist pulmonary emphysema
and bronchiectasis. Besides being present in the lungs and in the
eyelids, the parasites have also been found in the pleura, the liver,
the intestinal wall, the peritoneum, the cervical glands, and in the
scrotum, without actually occasioning any actual symptoms in these
tracts.
[470] Inouye, quoted by Looss.
[471] Scheube, “Die Krankh. d. warm. Länder,” 1896.
The most dangerous locality is in the brain. Otani,[472] Inouye,[473]
Yamagiva,[474] and recently also Taniguchi,[475] have found _post
mortem_ the worms and their ova in tumours of the brain, or, in areas
of softening in cases of Jacksonian epilepsy; in Taniguchi’s case the
eggs were found in masses in the inflammatory areas of softening. In
the nineteen cases of paragonimiasis of the brain collected by Inouye,
the following symptoms were observed: general convulsions on eight
occasions, unilateral convulsions on six occasions, convulsions with
paralysis on the same side and hemiplegia, five times each; in
Taniguchi’s case, attacks of cortical epilepsy, choreiform twitchings
in the right extremities, which gradually become athetotic. The
following were symptoms of rarer occurrence: paresis of the right upper
extremity, vertigo, dementia, and amnesic aphasia, disturbances of
vision. Paragonimiasis of the brain appears to arise by embolism from a
primary pulmonary lesion.
[472] Otani, quoted by Looss.
[473] Inouye, quoted by Looss.
[474] Yamagiva, quoted by Looss
[475] Taniguchi, _Arch. f. Psych. u. Nervenkrankh._, xxxviii.
The diagnosis depends upon the finding of ova in the sputa; if together
with ova in the sputa, cerebral disturbances make their appearance, in
all probability the cause is the presence of worms or ova in the brain.
The prognosis of pulmonary paragonimiasis is favourable; on the other
hand, that of cerebral paragonimiasis is very doubtful.
The treatment of the pulmonary lesion consists only in paying attention
to the general condition (good food, rest, cough remedies), as all
attempts to destroy the worms in the lungs by means of vermicidal
drugs administered internally or by way of inhalation have so far
been without result. The treatment of the cerebral lesion is entirely
hopeless. Trephining has been proposed for cases the condition of which
is more favourable, but it has not reached the stage of performance.
Prophylaxis consists in general management: cleansing and if need be
boiling of everything that is eaten or drunk.
Clonorchis sinensis.
According to our present knowledge _Clonorchis sinensis_ is only
found in China and Japan; even the _post-mortem_ case reported by
Laspeyres[476] was that of an Asiatic sailor who was admitted into the
General Hospital St. George, Hamburg, in a moribund condition with
the clinical diagnosis of beri-beri. The bile-ducts are the usual
site of the parasite, though Katsurada[477] has found them also in
the pancreatic ducts. In addition, it is found not uncommonly in the
upper portion of the small intestine, especially in the duodenum, also,
though decidedly rarely, in the stomach. As these sites, however, do
not afford the conditions necessary to life, they are only found here
on their way out of the body of the host.
[476] Laspeyres, “Dissert. Kiel,” 1904.
[477] Katsurada, Ziegler’s _Beitr. z. path. Anat._, 1900, xxviii.
The initial stage of infection with this fluke generally runs
a symptomless course; in proportion as the worms multiply the
following symptoms are manifested: First there is a morbid sense of
hunger and irregularity in defæcation; at the same time the patient
experiences a feeling of pressure and pain in the epigastrium and
right hypochondrium, or just a dull pain. Pressure increases the
pain considerably. The liver appears to be enlarged, sometimes the
enlargement is specially perceptible over the left lobe of the liver.
The patients maintain a proportionately good general state of health
in this state for a long time and may hope to recover. In severe cases
there occurs copious and generally bloody diarrhœa, also icterus.
The next stages are anæmia, emaciation, epistaxis, ascites, enlarged
spleen, and cachexia, to which the patient finally succumbs. In general
the course of the disease is very chronic and irregular; in winter
and spring there is generally improvement, in the summer and autumn
the patient gets worse. At _post-mortem_ the bile-ducts are enlarged
and thickened, there is interstitial hepatitis with enlargement of
the liver, but not to such an extent as in hypertrophic cirrhosis.
After the initial enlargement contraction of the liver sets in, the
peritoneal coat and capsule proper of the liver become more or less
thickened in places. In the pancreas also dilatation and thickening
of the ducts occur, as well as interstitial inflammatory processes.
Obstructions in the portal circulation may lead to catarrhal changes in
the stomach.
The diagnosis is based on the demonstration of ova in the fæces.
As a radical treatment is still unknown, consequently it can only be
purely symptomatic. Prophylaxis consists in the prohibition of drinking
unboiled water or eating uncooked molluscs, fish, etc., of canal water.
Leaving the epidemic region may bring about gradual recovery.
BILHARZIASIS.
Schistosoma hæmatobium.
The symptoms of bilharziasis are manifested chiefly in the urinary
apparatus, and above all as hæmaturia, at the outset without any
special troubles. Later, however, it is accompanied by subjective
symptoms in the shape of feelings of pain, and of vague pains in the
perinæum and lumbar region, and of burning in the urethra during
the passing of urine. All the symptoms are usually aggravated after
excesses in eating and drinking, and after considerable bodily
exertion. Another condition found, but not often mentioned, is lipuria
(Stock[478]); the highest amount has been 2 per cent. fat in the
urine. Stock found 6 to 20 per cent. of eosinophile cells in ten
cases examined by him. They appear to be increased, especially in
the early cases; Kautsky[479] also called attention to the excessive
degree of eosinophilia, whilst Goebel[480] expresses the opinion that
a specific toxic action on the organism generally is not developed
in bilharziasis. Kautsky[481] assumes a toxic anæmia as in the case
of ancylostomiasis. English authors also have called attention to
the eosinophilia and to a considerable amount of leucocytosis
(Balfour,[482] Douglas and Hardy[483]). The severe forms occur almost
exclusively in men; symptoms of catarrh of the bladder make their
appearance, vesical calculi are frequently found, whilst the formation
of stone in the kidneys and ureters is rare. Urethral fistula occurs
in bilharziasis, often without stricture, and if granulations occur
the fistula is distal to them. Goebel[484] regards the bilharzia
fistula as a chronic burrowing of pus, caused by the irritation set up
by the ova as foreign bodies and consecutive restricted suppuration;
and secondly as due to the passage of urine through the defect in the
epithelium or the wall of the urethra. The fistulæ, which are generally
situated at the neck of the bladder and at the membranous portion, are
very tortuous and frequently very numerous; they often lie embedded
in well-marked tumours--in fact, in granulation tumours with marked
inclination to excessive formation of cicatricial tissue. The opening
generally is in the perineal and scrotal regions. In the case of a
patient, aged 21, from the Transvaal, Kutner[485] found by cystoscopic
examinations the whole summit and walls of the bladder covered with
large and small tumours. In addition to smooth glistening tumours,
others were more or less disintegrated, and scattered large and small
cauliflower-like growths occurred. Like malignant growths, the tumours
were inclined to break down, the process extending from within outwards
towards the surface. Whether the hydrocele so frequent in Egypt has
any connection with bilharzia is not known. A frequent sequela of
bilharziasis is complete sexual impotence (Petrie[486]).
[478] Stock, _Lancet_, September 29, 1906.
[479] Kautsky, _Wien. klin. Rundschau_, 1903, xxxvi.
[480] Goebel, _Arch. f. Schiffs- u. Tropen-Hyg._, 1903, vii.
[481] Kautsky, _Wien. klin. Rundschau_, 1903, xxxv.
[482] Balfour, _Lancet_, December, 1903.
[483] Douglas and Hardy, _ibid._, October, 1903.
[484] Goebel, _Centralbl. f. d. Krankh. d. Harn u. Sexualorgane_, xvii.
[485] Kutner, _ibid._, xvi.
[486] Petrie, _Brit. Med. Journ._, July, 1903.
Bilharziasis of the rectum is manifested by symptoms of dysentery; the
repeated violent attempts at defæcation lead in time to prolapse of the
rectum, which sooner or later induces septic infection and so death.
In the mucosa of the rectum, polypoid growths similar to those in the
bladder are met with, due to the ova of the parasites in the mucosa
and submucosa. In the case of a man, aged 36, who had lived for a long
time in South Africa, Burfield[487] found in the excised vermiform
appendix ova of _Schistosoma hæmatobium_; he assumed this to be a
gradual secondary infection of the appendix, whilst Kelly[488] mentions
a case of primary bilharziasis of the appendix; the eggs lay in the
submucosa directly above the muscularis. Tumours containing numerous
ova are frequently found in the region of the genitalia, thighs and
scrotum. In one case Symmers[489] found numerous male schistosomes
in the portal blood and a copulating pair in the left lung. Though
schistosome eggs have been found by some observers in the lung tissue,
this is nevertheless the first case in which living parasites have been
found in the lesser circulation. Perhaps they got there by way of the
external iliac vein from the veins of the bladder and rectum.
[487] Burfield, _Lancet_, February 10, 1906.
[488] Kelly, quoted by Burfield.
[489] Symmers, _Lancet_, January 7, 1905.
In the female sex bilharziasis is incomparably rarer than in the male
and is generally limited to hæmaturia. Bilharziasis of the vagina,
which takes the form of an acute vaginitis, is frequent according to
Milton.[490] Horwood[491] found in one case a polypoid tumour of the
cervix uteri, and in the connective tissue of the tumour Schistosoma
ova, both in masses and singly. It could not be established whether the
ova reached the vagina and thence the cervix directly, or through the
urine from the bladder.
[490] Milton, quoted by Looss, “Handb. d. Tropenkrankh.,” v. Mense,
1905, i, p. 95.
[491] Horwood, _Brit. Med. Journ._, March 10, 1906.
The course of the disease is chronic, and in slight cases, provided
fresh infections do not occur, is not unfavourable; in severe cases the
cachexia caused by loss of blood, or intercurrent diseases to which the
patients easily succumb--_e.g._, pyelitis, pyelonephritis, pyæmia, or
uræmia--lead to a fatal issue.
In regions in which _Schistosoma hæmatobium_ is endemic, or in patients
from such regions, the diagnosis is easy by microscopically finding the
eggs in the urine.
As regards the treatment of the affection this much must be said, that
so far there is in existence no certain remedy. In countries where
bilharziasis is endemic copaiva balsam is considered a specific. Kutner
(_loc. cit._), however, in the case of his patient who for a long
time had taken no inconsiderable amounts of copaiva, had no success
worth speaking of to record. Urotropin (three times daily, 1 grm.)
has similarly failed, salol (0·75 grm. several times daily) perhaps
affords relief in affection of the bladder (Milton). Methylene blue,
oil of turpentine with extract of male fern (Brock[492]), or the latter
alone and santonin given in small doses for a week at a time, in the
morning, are said by Petrie[493] to be of value. Sandwith[494] and
Harley[495] were not very successful. By way of experiment Kutner for
some time used collargol _per rectum_, proceeding on the assumption
that this preparation, which has proved of such remarkable service
in bacterial infection, would perhaps render a continuance of life
difficult for the bilharzia worms. But this hope proved illusory. In
order so far as possible to limit the loss of blood, Kutner regularly
employed stypticin for long periods (three times daily, two tabloids
of 0·01 grm.) with undoubted success, in so far that the hæmorrhages
became considerably less in amount. As two patients in the course
of enteric fever lost their hæmaturia, Stock accordingly recommends
subcutaneous injections of Wright’s typhoid vaccine. In the early
stages of the rectal lesion suppositories of iodoform, ichthyol, or
narcotics might possibly be of use. In the case of urethral fistulæ,
division, excision and scraping out of the granulation tissue are
recommended; in cystitis with formation of tumours high resection with
curetting of the tumours or their destruction with the cautery; in the
case of vesical calculi, high resection, curetting the bladder, and
then drainage. Tumours of the rectum must also be removed by operation.
[492] Brock, _Journ. of Path. and Bact._, 1893.
[493] Petrie, _loc. cit._
[494] Sandwith, _Annal. of Surgery_, 1904, xxxix.
[495] Harley, _Lancet_, 1870.
Prophylaxis is important; it should be extended to all modes of using
water, only filtered water being drunk, and only boiled water being
used for washing. This advice should be given to tourists who travel
through the infected districts, and is also recommended to soldiers and
officials who are despatched to the Colonies. The favourable influence
of change of climate can only show itself where fresh infections are
avoided.
CESTODES.
GENERAL.
It seems advisable to preface the section on the Cestodes with some
general observations on the symptoms of disease provoked by tapeworms,
especially so far as they relate to the question of toxic effects, and
to include the Nematodes in this discussion. After this will follow
a brief exposition of the most important intestinal lesions causally
connected with intestinal parasites.
It is known to every experienced practitioner that the different
intestinal parasites can give rise to a series of nervous symptoms,
slight or severe, and produce, above all, blood changes--anæmia of the
most varied nature, to the extent of severe progressive anæmia. These
symptoms are regarded by many authors as reflex, or, as in the case of
ancylostomiasis, the main feature from the loss of blood caused by the
habit of life of the intestinal parasites. More frequently, however,
they are regarded as toxic conditions produced by the parasites. In
view of this divergence of opinion there appears to be some advantage
in defining clearly the present position as to the toxic action of
parasites. Most interesting in this respect are _Dibothriocephalus
latus_ and _Ancylostoma duodenale_.
We are indebted to the clinic at Helsingfors for our most detailed
knowledge of bothriocephalus anæmia. Reyher[496] was the first to
demonstrate that this parasite under certain circumstances can produce
a severe, progressive and sometimes fatal anæmia, which can be cured,
generally in a surprisingly short time, by expulsion of the worm.
Among the various hypotheses which have been advanced as to the mode
of origin of bothriocephalus anæmia, the greatest importance has been
attached to the assumption already mentioned by Reyher, but definitely
expressed by von Shapiro,[497] to the effect that _Bothriocephalus
latus_ produces a poison which is absorbed by the intestine and
exercises a deleterious influence on the composition of the blood,
especially on the erythrocytes, perhaps also on the blood-forming
organs. This assumption is supported by no slight number of clinical
and experimental investigations. Podwissotsky[498] observed severe
blood changes in a child, aged 4-1/2, affected with _B. latus._
In the case reported by Pariser[499] the severe anæmia in a girl
disappeared fairly soon after expulsion of the worm. In that reported
by Schaumann[500] high fever accompanied the bothriocephalus anæmia;
he also proved the hæmolytic properties of the broad tapeworm. The
case reported by F. Müller[501] was one of severe anæmia. Also, in
the first of the cases described by Kurimoto[502] of _Diplogonoporus
grandis_ there were present the same symptoms of anæmia as in the case
of _B. latus_. Meyer[503] observed severe anæmia in two youths caused
by _B. latus_. Rosenquist[504] has discussed the proteid metabolism in
anæmia. The presence of _B. latus_ produces in the majority of cases
an increased proteid consumption, to which the blood change generally
corresponds--toxic anæmia; in a further communication he reports on
twenty cases of bothriocephalus anæmia, nineteen of which were cured
by expulsion of the worms, while one case proved fatal, and he again
emphasizes the toxic properties of the intestinal parasites. In the
case reported by Bendix,[505] that of a girl, aged 4-1/2, the anæmia
was moderate, whilst in the case of Zinn[506] (a woman, aged 30) the
anæmia was so excessive that the patient succumbed five days after
expulsion of six bothriocephalus heads. Isaac and van den Velden[507]
have established that in the serum of patients who suffer from anæmia
due to _B. latus_, parasitic products are dissolved, as shown by
a distinct precipitin reaction. Galli-Valerio[508] considers it
likely that toxic substances are secreted by the living helminthes
which produce a lowering or raising of the body temperature, nervous
disturbances and hæmolysis. Tallqvist[509] succeeded in extracting from
_B. latus_ a lipoid-like body which had a strong hæmolytic action. The
experimental anæmia thereby produced differed in no respect from the
severe chronic bothriocephalus anæmia of man. The question as to under
what special conditions severe, and sometimes fatal bothriocephalus
anæmia is developed is answered by Leichtenstern[510] and by
Lenhartz,[511] by the assumption that among the Bothriocephali some are
toxic, that is, manufacture a poison which, when absorbed by the host,
produces a severe anæmia.
[496] Reyher, _Deutsch. Arch. f. klin. Med._, 1886, xxxix.
[497] von Shapiro, _Zeitschr. f. klin. Med._, 1888.
[498] Podwissotsky, _Jahrb. f. Kinderkrankh._, 1889.
[499] Pariser, _Deutsch. med. Wochenschr._, 1892.
[500] Schaumann, Berlin, 1894, and _Deutsch. med. Wochenschr._, 1898.
[501] Müller, _Charité-Annal._, xiv.
[502] Kurimoto, _Zeitschr. f. klin. Med._, xl, and _Kongr. f. inn.
Med._, Karlsbad, 1899.
[503] Meyer, _Mount Sinai Hosp. Reports_, 1903 and 1904, iv.
[504] Rosenquist, _Verein f. innere Med. in Berlin_, May 6, 1901; and
_Zeitschr. f. klin. Med._ xlix.
[505] Bendix, _Deutsch. Aerzte Zeitg._, 1904, i.
[506] Zinn, _Deutsch. med. Wochenschr._, 1903.
[507] Isaac and van den Velden, _Deutsch. med. Wochenschr._, 1904,
xxvii.
[508] Galli-Valerio, _Therap. Monatsh._, 1905.
[509] Tallqvist, _Zeitschr. f. klin. Med._, 1907, lxi.
[510] Leichtenstern, “Handb. d. Therap. v. Pentzoldt-Stintzing,” 1898,
2nd edition, iv.
[511] Lenhartz, _ibid._, 1903, 3rd edition, iv, p. 607.
Certain factors lead him to conclude that an accumulation of poison,
dependent on time and place, occurs in the Bothriocephali.
In the case of ancylostome anæmia, experience so far, according to
Leichtenstern,[512] by no means supports the hypothesis of a difference
in virulence of the worms according to time and locality, ancylostome
anæmia being rather, so far as is known at present, in all races of
man, everywhere and at all times, simply and solely dependent on
the number of ancylostomes, the duration of the disease and--within
certain narrow limits--on the individual capability of resisting the
loss of blood and the toxic effect of the parasites. As is shown by a
short historical résumé of the toxic action that has to be considered
in ancylostome anæmia, we must admit that doubtless here, as in the
case of bothriocephalus anæmia, the toxins secreted by the parasites
exercise a hæmolytic action, even while admitting Leichtenstern’s
contention that the significance of the loss of blood due to
ancylostomes must not be underrated. The toxic hypothesis acquired a
definite standing through a series of experiments of Lussana[513] on
rabbits, where he succeeded in producing anæmia by injecting urinary
extracts of ancylostome patients. Arslan[514] extracted toxins from the
urine of two ancylostome patients and injected them into rabbits, which
thereupon sickened and showed the same blood changes as the ancylostome
patients. Retinal hæmorrhages, so frequent in ancylostome anæmia,
which, according to Fischer[515] and Samelsohn,[516] are not due to
direct loss of blood, must also be ascribed to a parasitic toxin. A
further argument in favour of the toxic hypothesis is furnished by
the blood changes recorded by Zappert,[517] Müller and Rieder,[518]
Bücklers,[519] and Neusser,[520] which must be regarded as the
expression of toxic action, especially with reference to eosinophilia.
The striking increase in proteid destruction in ancylostomiasis
observed by Bohland,[521] and which ceased after the parasites had been
expelled, also gives additional support to the assumption of toxic
action. The observation of Daniels[522] also deserves consideration in
this connection, according to which the presence of yellow pigment in
the liver and kidney cells is to be attributed to blood destruction by
a verminous toxin absorbed from the gut. Looss[523] considers it not at
all improbable--in fact, almost certain--that Ancylostoma, in addition
to withdrawing blood, exert a kind of toxic action on their host.
[512] Leichtenstern, _Deutsch. med. Wochenschr._, 1899.
[513] Lussana, _Rivista Clin. Arch. ital. di clin. Med._, 1890.
[514] Arslan, _Rev. mens. des Mal. de l’Enfance_, 1892.
[515] Fischer, _Versamml. d. ophthal. Gesellsch._, 1892.
[516] Samelsohn, _ibid._
[517] Zappert, _Wien. klin. Wochenschr._, 1892.
[518] Müller and Rieder, _Deutsch. Arch. f. klin. Med._, xcviii.
[519] Bücklers, _Münch. med. Wochenschr._, 1894.
[520] Neusser, _Wien. klin. Wochenschr._, 1892.
[521] Bohland, _Münch. med. Wochenschr._, 1894.
[522] Daniels, _Lancet_, No. 3,725.
[523] Looss, _Centralbl. f. Bakt._, 1897.
Scheube[524] attributes almost equal importance to the loss of blood,
the digestive disturbances, and the intoxication induced by certain
metabolic products of the parasites. According to v. Jaksch[525]
ancylostome anæmia is not induced solely by loss of blood, but by the
fact that the parasites produce a ferment which has a toxic action
and produces stimulation in those organs in which the eosinophile
cells arise. The hæmolytic action of ancylostomes has frequently been
observed by Galvagno[526] in men employed in sulphur mines. According
to Loeb and Smith[527] the anterior half of the body of ancylostomes
contains a substance which probably causes anæmia. Bauer[528] found in
the urine of ancylostome patients glycuronic acid, which he considers
to be a sign of metabolic disturbance due to parasitic toxins. As has
been demonstrated by Allessandrini,[529] the secretion of glands in
the anterior part of the body has a distinct hæmolytic effect on the
erythrocytes. While the worm attaches itself to the mucosa by means of
its teeth, these glands discharge their secretion, producing hyperæmia.
The extravasated blood is acted on by this secretion, so that it can
serve as food for the parasites. Hynek[530] attributes eosinophilia (up
to 20 per cent.) to a toxic action. Goldmann[531] expresses a similar
opinion, though he assumes that the anæmia is secondary, as the toxin
of the cephalic glands, as the parasites bite, penetrates the mucosa
and thence into the blood, where it dissolves the red blood corpuscles.
Romani[532] discusses the agglutinating hæmolytic action of the serum
of ancylostome patients. Whether Ancylostoma produce toxins and what
is their nature, or whether the loss of blood causes the anæmia,
Liefmann[533] was unable definitely to determine; hæmolytic substances
do not appear to take any part in it.
[524] Scheube, “Die Krankh. der warm. Länder,” 1896.
[525] v. Jaksch, _Münch. med. Wochenschr._, 1902.
[526] Galvagno, _Arch. di Patol. e Clin. inf._, 1902–1904.
[527] Loeb and Smith, _Centralbl. f. Bakt._, xxxvii.
[528] Bauer, _Wien. klin. Wochenschr._, 1904.
[529] Allessandrini, _Policlinica_, 1904.
[530] Hynek, _Klin. Chron._, 1904.
[531] Goldmann, _Wien. klin. Rundschau_, 1905.
[532] Romani, _Gaz. d. Osp._, 1904.
[533] Liefmann, _Zeitschr. f. Hyg._, 1905, l.
Berti[534] also is inclined to attribute the anæmia to metabolic
products of the ancylostomes; he found, in fact, that a serum obtained
from a sheep (after subcutaneous injections of the culture fluid of
ancylostome larvæ) was efficacious in the treatment of ancylostome
anæmia. Peiper[535] likewise assumes that the parasite secretes a cell
toxin. Löbker[536] at the present day still maintains that the cause
of the disease must be looked for really, if not perhaps entirely, in
the continued withdrawal of blood by the parasites; the secretion of
toxins by ancylostomes has not yet, in his opinion, been conclusively
proved. Except in the case of _Bothriocephalus latus_, referred to
previously, toxic action appears to be of quite subordinate importance
for the other Cestodes occurring in man--especially _Tænia solium_
and _T. saginata_, which are most frequently found; thus Cao[537]
flatly denies the presence of toxins in the body of Tæniæ, while
others, such as Messineo and Calmida,[538] Jammes and Mandoul,[539]
consider they are justified from their investigations in concluding
that Tæniæ contain a specific toxin. Messineo[540] injected, with
all bacteriological precautions, extracts of Tænia, dissolved in
physiological salt solution. He invariably obtained severe motor
disturbances and frequently death. The observation by Pereira[541] of
a case of chorea in which rheumatic and cardiac symptoms were absent
and which after expulsion of a Tænia was quickly cured, also favours
the view of a toxic action. Barnabo,[542] however, was unable to
obtain a toxin from _Tænia saginata_. Gagnoni,[543] on account of a
marked eosinophilia which, after expulsion of a _Tænia saginata_, fell
within fourteen days to 1 per cent., assumes the formation of a Tænia
toxin. Dirksen’s[544] observation has reference to a sailor affected
with serious anæmia, who, after expulsion of twelve pieces of _Tænia
solium_, was rapidly cured. A portion of the worm was already breaking
down, the absorption introducing into the body highly toxic hæmolytic
products, to which the anæmia must be ascribed. How far the serious
disturbances of the nervous system, frequently to be observed in cases
of _Hymenolepis nana_, are to be considered as of purely reflex nature
or toxic must remain an open question; the same applies to _Dipylidium
caninum_, in which case Brandt[545] observed serious central nervous
symptoms. Caution is necessary in judging as to any connection between
worm stimulus and nervous symptoms in cases of Ascaris infection.
Peiper[546] is inclined to regard such nervous symptoms not as reflex,
but rather as due to a toxin contained in the helminthes, or metabolic
in origin.
[534] Berti, _Gaz. d. Osp._, 1906.
[535] Peiper, _Deutsch. med. Wochenschr._, 1897.
[536] Löbker and Bruns, _Arb. aus dem kaiserl. Reichsgesundheitsamt_,
1906, xxiii.
[537] Cao, _Riforma Med._, 1901.
[538] Messineo and Calmida, _Centralbl. f. Bakt._, xxx.
[539] Jammes and Mandoul, _Acad. des Sciences_, 1904.
[540] Messineo, _Giorn. med. del regio eserc._, 1903.
[541] Pereira, _Lancet_, September, 1903.
[542] Barnabo, _Sperimentale_, 1906, v.
[543] Gagnoni, _Pediatric._, 1903.
[544] Dirksen, _Deutsch. med. Wochenschr._, 1903.
[545] Brandt, quoted by Pollak in _Centralbl. f. Bakt._, 1889, v.
[546] Peiper, _vide_ Seifert, “Lehrb. d. Kinderkrankh.,” 1897, p. 243.
In cases of pernicious anæmia when the symptoms disappear after
expulsion of _Ascaridæ_ a toxic action must be assumed (Demme[547]).
Additional clinical observations do not, indeed, lead to any definite
conclusion as to the question whether _Ascaridæ_ produce a toxin
which is capable of causing more or less injury either to the nervous
system or to the blood, yet it may be worth while to give a brief
review of this question. In a case of Kutner’s,[548] that of a girl,
aged 12, there was a hæmolysis which was cured after expulsion of
twenty-four _Ascaridæ_. Attacks of opisthotonos in a girl, aged 16,
ceased after seventy-eight _Ascaridæ_ had been expelled (Lutz[549]).
Unusually serious disturbances were observed in a man, aged 26,
who was rapidly cured by Drouillard[550] by the removal of a great
number of _Ascaridæ_. The observations on pseudomeningitis are of
especial interest; they are evidently toxic in origin as in the case
of Annaratone,[551] of a man who was taken ill with gastro-intestinal
symptoms and who died with meningitic symptoms. _Post mortem_ the brain
was normal, but the stomach contained a great coil of _Ascaridæ_.
The cases of Delille,[552] Mériel,[553] Papi[554] (the occurrence of
Cheyne-Stokes respiration has been ascribed to the action upon the
centre in the medulla oblongata of the products of the _Ascaridæ_),
and Taillens[555] related to children in which the meningitic
symptoms (meningismus), partly serious, disappeared with the removal
of the _Ascaridæ_. Máreo[556] designates this disease helminthiasis
meningitiformis, which exhibits all the symptoms of meningitis, but
which is caused by the metabolic products of _Ascaridæ_.
[547] Demme, _vide_ Seifert, _ibid._
[548] Kutner, _Berl. klin. Wochenschr._, 1865.
[549] Lutz, _Centralbl. f. Bakt._
[550] Drouillard, _Journ. de Méd._, 1900. xi.
[551] Annaratone, _Giorn. med. del regio eserc._, 1900.
[552] Delille, _Journ. de Méd._, May 10, 1907.
[553] Mériel, _Annal. de Méd. et Chir. inf._, 1900.
[554] Papi, _Gaz. d. Osp._, 1901.
[555] Taillens, _Arch. de méd. d’Enf._, 1906.
[556] Máreo, _Allg. Wien. med. Zeitg._, 1902.
Schupfer,[557] Duprey[558] (observations in the West Indies, where such
symptoms are said to be of very frequent occurrence), Naab[559] (the
flow of water from the mouth at night is mentioned as a remarkable
fact), and Hammiss[560] assume the action of an Ascaris toxin in the
clinical observations made by them, mostly children with fever and
intestinal symptoms. Schupfer assumes in such cases, as he observed
it once in a man, aged 23, that the disease termed _Lombricoise à
forme typhoïde_ by Chauffard was due to _B. coli_ of marked virulence
due to the action of the _Ascaridæ_. The Widal reaction was negative.
Koneff[561] reports a case in which acute attacks of cramp, trismus,
and rigidity of the pupil disappeared after expulsion of seven
_Ascaridæ_. Tetanus, as observed by Buchholz[562] in a girl, aged 17,
and rapidly cured after expulsion of sixteen _Ascaridæ_, is manifestly
rare, since only Rose[563] mentions this as a cause in his article on
Tetanus. Only a few experimental data exist. Cattaneo[564] could detect
only a very weak toxin in Ascaris, while Messineo,[565] by injecting
into animals extracts in physiological salt solution, invariably
succeeded in producing serious motor disturbances and frequently death.
Interesting also are the observations of Huber,[566] who, after working
with _Ascaridæ_, suffered from itching of the head and neck, blisters,
swelling of the ear, conjunctivitis, ecchymosis and troublesome
palpitation in the head. He consequently assumes that _Ascaridæ_ can
induce irritation by chemical (toxic) means.
[557] Schupfer, _Gaz. d. Osp._, 1901.
[558] Duprey, _Lancet_, 1903.
[559] Naab, _Münch. med. Wochenschr._, 1902.
[560] Hammiss, _Wien. med. Wochenschr._, 1904, iii.
[561] Koneff, quoted by Liesen, “Dissert. Bonn,” 1904.
[562] Buchholz, _Norsk. Mag. for Läge_, 1903.
[563] Rose, Billroth and Pitha, “Chirurgie.”
[564] Cattaneo, _Arch. f. Kinderheilk._, xliv.
[565] Messineo, _Giorn. med. del regio eserc._, 1905.
[566] Huber, _Deutsch. Arch. f. klin. Med._, 1870, vii.
In the case of _Trichocephalus dispar_ no more than in the case of
_Ascaris lumbricoides_ can we speak with certainty of a toxic effect,
even though a number of observations are available which might justify
such an assumption as regards these intestinal parasites. Barth[567]
found the brain normal in a man who had died with meningitic symptoms,
but the intestines were full of _Trichocephalus dispar_; Gibson[568]
records the rapid cure of serious cerebral symptoms after expulsion of
Trichocephalus, so also Pascal,[569] Burchhardt[570] and Rippe.[571]
Moosbrugger[572] was the first to draw attention to grave anæmic
conditions induced by Trichocephalus, Morsasca[573] and Becker[574]
to progressive grave anæmia (trichocephalus anæmia is accompanied by
marked reduction of the number of red blood corpuscles, of the specific
gravity and of the hæmoglobin, well-marked morphological changes of the
red cell, micro-, macro-, and poikilocytosis and nucleated red cells).
Sandler,[575] in his case of a boy, aged 11, who died of anæmia,
assumes a trichocephalus toxin to be the cause of the disease, and
Kahane also reports on anæmic conditions induced by Trichocephalus.
Girard,[576] in addition to symptoms in the gastro-intestinal
tract, calls attention to those arising in the blood--anæmia and
its sequelæ--and also to nervous symptoms: cerebral phenomena,
headache, giddiness, aphonia, symptoms of meningitis. In a case of
Schiller’s[577] high fever was present, which probably set in when
the Trichocephali present in the gut in great numbers commenced their
parasitic activity. Hausmann,[578] in order to explain the adaptability
of Trichocephalus, assumes that according to the _locus minoris
resistentiæ_, at one time the reflex at another the toxic action is
effective, now on one organ, then on another; anæmia being present in
most cases, frequently general and local neuroses and cerebral symptoms
of various kinds.
[567] Barth, reported by Valleix, Paris, 1845.
[568] Gibson, _Lancet_, 1862.
[569] Pascal, quoted by Kahane, _Korrespondenzbl. f. Schweizer_ Aerzte,
1907, viii.
[570] Burchhardt, _Deutsch. med. Wochenschr._, 1880.
[571] Rippe, _St. Petersb. med. Wochenschr._, 1907, i.
[572] Moosbrugger, _Med. Correspondenzbl. f. Württemberg_, 1890.
[573] Morsasca, abstract in _Centralbl. f. innere Med._, 1897.
[574] Becker, _Deutsch. med. Wochenschr._, 1902.
[575] Sandler, _ibid._, 1905.
[576] Girard, _Annal. de l’Inst. Pasteur_, 1901.
[577] Schiller, _Beitr. z. klin. Chir._, 1902, xxxiv.
[578] Hausmann, _St. Petersb. med. Wochenschr._, 1900.
With regard to the toxic action of Oxyuris there is only the single
record of Hartmann,[579] who noticed the disappearance of epileptic
fits and psychic disturbances in a girl, aged 13, after the removal
of Oxyuris. Nervous disturbances and blood changes can but rarely be
attributed to Strongyloides. Silvester[580] and Valdes[581] report on
giddiness, headache and anuria in cases observed by them; whether the
eosinophilia recorded by Bücklers[582] and Bruns[583] is due to the
toxin of Strongyloides must remain an open question.
[579] Hartmann, _Naturforschervers._, Köln, 1889.
[580] Silvester, quoted by Schlüter, “Dissert. Kiel,” 1905.
[581] Valdes, quoted by Schlüter, _op. cit._
[582] Bücklers, _Münch. med. Wochenschr._, 1894.
[583] Bruns, _Münch. med. Wochenschr._, 1907.
Reference has already been made to the possibility that intestinal
ciliates (_Balantidium coli_) can also produce toxins.
The contents of echinococcus cysts appear to contain a substance only
moderately toxic, giving rise to urticaria, in a series of cases where
the fluid has escaped into the abdominal cavity (during puncture). D.
Müller[584] has collected nine such cases out of the literature, to
which may be added six cases of Finsen[585] in which the escape of
fluid into the peritoneal cavity led to severely itching urticaria,
which usually disappeared again after one or two days. On one occasion,
indeed, urticaria occurred after rupture into the pleural cavity.
In the case recorded by Caffarena[586] of echinococcus of the right
lobe of the liver, widespread urticaria developed as the result of
the exploratory puncture. In the case of an echinococcus of the liver
rupturing into the abdominal cavity La Spada[587] ascribed the symptoms
leading to death to toxic influence while the peritoneal symptoms were
less marked. Eosinophilia in hydatid disease is slight according to
the investigations of Bindi[588] and Santucci,[589] and is, according
to Welsh and Barling,[590] no certain sign of echinococcus; it is
independent of the age, sex and temperature of the patient, but upon
rupture of the cyst eosinophilia invariably sets in.
[584] Müller, D., “Dissert. Würzburg,” 1885.
[585] Finsen, quoted by D. Müller.
[586] Caffarena, _Convers. clin. Genova_, 1902.
[587] La Spada, _Gaz. d. Osp._, 1904.
[588] Bindi, _ibid._, 1907.
[589] Santucci, “Clinica moderna,” 1905.
[590] Welsh and Barling, _Scot. Med. and Surg. Journ._, 1907.
The question as to the importance of helminthes in relation to certain
diseases of the gut requires special discussion, but it concerns only
_Ascaris lumbricoides_, _Oxyuris vermicularis_, and _Trichocephalus
dispar_, and the question of appendicitis first of all. The entrance of
intestinal parasites into the vermiform appendix was already known to
medical men in the fifties of last century, as is shown by the works
of Merling[591] (1836), Zebert[592] (1859), Platonor[593] (1853),
and Schachtinger[594] (1861). Most of these authors have considered
intestinal worms, together with other foreign bodies, to be the cause
of appendicitis. As regards the part played by these intestinal
parasites in the etiology of appendicitis, so much discussion has taken
place during the last few years that it is worth while to give a résumé
of the later views on this question, even though at the outset it must
be admitted that the matter is not cleared up. Bergmann[595] records
a case in which an Ascaris perforated the appendix and got into the
peritoneal cavity.
[591] quoted by Rostowzeff, _Bobritsch. Gaz. Botkina_, 1902.
[592] quoted by Rostowzeff, _Bobritsch. Gaz. Botkina_, 1902.
[593] quoted by Rostowzeff, _Bobritsch. Gaz. Botkina_, 1902.
[594] quoted by Rostowzeff, _Bobritsch. Gaz. Botkina_, 1902.
[595] Bergmann, _Prag. med. Wochenschr._, 1890.
Strümpell[596] reckons among the symptoms of Trichocephalus the
possibility of a “typhlitis.” On account of the marked sensitiveness of
the ileo-cæcal region, Boas[597] mentions the possibility of confusing
it with appendicitis. Still[598] regards Oxyuris as a principal
cause of catarrhal affections of the appendix. Arboré-Rally[599]
regarded severe symptoms of appendicitis in a boy, aged 10, as due to
Ascarides. In all cases of appendicitis Metschnikoff[600] requires a
microscopical examination to be made for eggs, and considers treatment
for worms carried out otherwise as a cause of the frequency of
perityphlitis. Matignon[601] does not agree with this opinion, as in
spite of the extraordinary frequency of intestinal worms in China,
he has only seen one case of appendicitis in four and a half years,
and Des Barres[602] expresses himself in similar fashion. Out of
twenty-one cases of appendicitis Kirmisson[603] discovered the ova
of Trichocephalus eighteen times and the ova of Ascarides in three
of these cases; in twelve cases of enteric fever the examination for
eggs was negative nine times. Moty[604] considers Oxyuris to be the
sole cause in his three cases of appendicitis. Girard[605] ascribes to
Trichocephali the _rôle_ of more or less septic foreign bodies which
may bring about the entry of intestinal bacteria into the appendix,
and Triboulet[606] describes a case of appendicitis which he considers
was due to Ascaris. In Morkowitin’s[607] case numerous Oxyuris had
clearly caused the appendicitis. von Genser[608] records the case of
a boy, aged 5, who was operated on for appendicitis, and who passed
through the operation wound a living Ascaris on the eighteenth day
after the operation. In the first case communicated by Schiller[609]
the disappearance of the typhlitic swelling after the discharge of the
Ascarides pointed to the etiological significance of the parasites,
and the same obtained in a further case published at an earlier date
by Czerny and Heddäus.[610] In a case abstracted by Kaposi[611]
Trichocephali appear to have been a contributory cause in the
production of the appendicitis. In a further case reported by Schiller,
where the appendix was removed, it was shown that Oxyuris had given
rise to a pronounced appendicular colic. In a girl, aged 13, who died
from diffuse peritonitis, Schwankhaus[612] found that an Ascaris had
perforated the appendix. Ramstedt[613] found in an extirpated appendix
a whole “tangle” of Oxyuris, and believes in the possibility of their
having provoked the inflammation; he recommends an examination for
entozoa before the operation, without, however, after Metschnikoff’s
example, substituting worm treatment for the operation. Rostowzeff[614]
ascribes only a minimal direct etiological significance to intestinal
worms in the origin of appendicitis; in 163 cases he found worms
in three instances. Wirsaladze[615] expresses himself in a similar
fashion. Oppe[616] observed Oxyuris six times in excised appendices,
and emphasizes the opinion that in appendicitis the question of a
worm cure ought to be taken into consideration. Ascaris and Oxyuris,
if no contra-indication exists, may be expelled, but in the case of
Trichocephalus, which frequently defies all expulsive treatment, no
attempt should be made, but operation proceeded to forthwith. In
a case briefly reported by Hanau[617] Oxyuris was undoubtedly the
etiological starting-point; in a case of Galli-Vallerio[618] Oxyuris
and Trichocephalus. In the opinion of Ssaweljews[619] in some cases of
appendicitis, in addition to other causes, intestinal parasites play
a prominent part. The case recorded by Nason[620] is an interesting
one; in this an Ascaris in the appendix became twisted with it round
a coil of gut, causing obstruction. Spieler[621] argues against the
underestimation by many authors as to the part played by intestinal
worms in producing appendicitis, although he also does not regard
them as a frequent, to say nothing of an exclusive, cause of the
disease. In a case recorded by Bégonin[622] fifteen Oxyuris were found
in the excised appendix (the mucosa showed some ulceration), and in
another recorded by Putnam[623] twenty Oxyuris were present in the
appendix, in which there was no evidence of any change. The standpoint
Schilling[624] takes is to the effect that entozoa irritate the mucosa
and can increase an already existing inflammation, but he considers it
very questionable whether they can produce appendicitis. Blanchard[625]
assumes the possibility of a secondary infection arising from lesions
of the mucosa produced by helminthes (Ascaris and Oxyuris). Moore[626]
considers Trichocephalus the excitant of the appendicitis in his case.
In a second case of appendicitis recorded by Auley[627] operation
became unnecessary owing to the passage of the _Ascaridæ_. Page’s[628]
case is an interesting one; it was that of a man who came up for
operation with a diagnosis of appendicitis. On incising the abdominal
wall numerous Ascarides were found at the base of the wound, lying in
cavities; even after eight days Ascarides escaped from the wound. The
author assumes there was a perforation of the gut wall; it is strange
that the worms were able to exist a proportionately long time in the
muscular tissue. Schoeppler[629] states that there is the danger of an
appendicitis even after the death of an Oxyuris that has found its way
into the appendix. Oui[630] met with two specimens of Trichocephalus
which had become embedded by their thin ends deep in the mucosa.
Frangenheim[631] is not in a position to pronounce any opinion as to
what part intestinal parasites play in the etiology of appendicitis.
In a case recorded by Kahane[632] many Trichocephali were found partly
free in the appendix and partly embedded in the mucosa; microscopically
appendicitis was diagnosed. At a laparotomy for salpingitis Heekes[633]
found the appendix elongated, thickened, and containing about eleven
Oxyuris without the mucosa being in any way changed. In one case
Andrews[634] claims Ascarides to have been the direct cause of the
appendicitis. The literature dealing with this question, so important
in our time, has been collected almost without any omissions, but,
unfortunately, no decisive opinion as to the significance of parasites
in appendicitis can be inferred from it. The vexed question whether
intestinal parasites, especially Ascaris, are able to penetrate the
intestinal wall is just as little finally decided. Leuckart,[635]
Heller,[636] Mosler and Peiper,[637] Henoch,[638] Davaine,[639]
Küchenmeister,[640] and Bremser[641] are opposed to the idea that
the healthy intestinal wall can be penetrated by intestinal worms,
especially Ascarides, whilst a whole series of other authors are of
the opinion that even the healthy intestinal mucosa can be perforated.
Among these is numbered Mondière,[642] who is of the opinion that
Ascaris, by violent pressure against the mucosa, forces it so much
apart that it is enabled to escape through the gap thus formed into
the peritoneal cavity; this opinion is shared by v. Siebold.[643]
Rokitansky[644] considers perforation of the gut by Ascaris as at
least a rare occurrence. Gerhardt[645] does not doubt that the worms
can actively perforate the intestine. Cases like those of Abrault,[646]
Apostolides,[647] Marcus[648] (recorded by Perls as a valid example of
“ascaridophagous” gut perforation), Wischnewsky,[649] Galvagno,[650]
Salieri[651] certainly show that perforation of the healthy gut wall
cannot be denied, but at the same time that this occurrence, compared
with the frequency of _Ascaridæ_, should be regarded as exceedingly
rare. It is another matter as to whether it is possible for the worms
to penetrate an intestinal wall already diseased, especially when
ulcerated; a whole series of observations are in favour of this. In
Lini’s[652] case (fifty-six Ascarides escaped from the umbilicus of
a girl, aged 7), in Gräffe’s[653] (eighty Ascarides escaped from an
inguinal tumour), in Nicolino’s[654] (perforation of the intestinal
wall with strangulated hernia), in Liesen’s[655] (a living Ascaris
in the peritoneal cavity in a woman suffering from a peritoneal
abscess)--in these it is clear that disease processes in the intestine
preceded the exit of the worms. In a case described by Boloff[656] the
Ascarides appear to have produced, by forming a tight coil, necrosis of
the gut with perforative peritonitis. In a case recorded by Lutz[657]
the perforative peritonitis was without doubt provoked by Ascaris, and
in one by Schiller[658] the Ascaris had clearly gained access to the
peritoneal cavity through a gunshot wound opening. In a case observed
by Rehn[659] the worm probably entered through a gangrenous portion
of the intestine in a hernial sac. Broca[660] is unable to determine
whether in his case the intestinal perforation was primary (a worm
escaped from the abdominal wound about two months after a laparotomy
for suppurative peritonitis). The case reported by Lutz[661] is of
special interest: it was that of a young man who had shot himself in
the region of the abdomen, and who died after fifteen days. At the
_post-mortem_ two Ascarides were found in the pulmonary artery; they
had probably escaped from the intestine, and had gained access to the
inferior vena cava. Froelich[662] assumes that in his case (a boy,
aged 11) the Oxyuris were able to penetrate the whole intestinal wall,
but Vuillemin[663] considers this improbable, and is more inclined
to think that the Oxyurides penetrated the rectum at small ulcerated
points, and thus gained access to the perirectal connective tissue.
In females Oxyuris not only have the power of penetrating far into
the sexual organs (Marro[664]), and perhaps causing a parasitic
endometritis (Simons[665]), but also clearly of gaining access to the
peritoneal cavity by way of the tubes, as is to be assumed in the
case recorded by Kolb[666] (that of a woman, aged 42, in whom _post
mortem_ nodules were found over the peritoneum of Douglas’s pouch, in
which the pressure of encapsuled Oxyuris could be demonstrated), in
that reported by Chiari[667] (adult Oxyuris in Douglas’s pouch) and
by Schneider[668] (an Oxyuris encapsuled in the pelvic peritoneum).
Sehrt’s[669] case is worthy of attention; in this an abscess was found
in the omentum with numerous Ascaris ova in the pus and a _nodular_
lesion of the peritoneum, with Ascaris ova encapsuled in the nodules.
Massive accumulation of Ascarides may give rise to a complete occlusion
of the gut. Such an occurrence is not so surprising as might be thought
when one reflects that the number of Ascarides in one individual may
amount to several hundreds. For instance, one boy evacuated within
a single day 600 Ascarides (Fauconneau-Dufresne[670]) and within
three years 5,126 worms. In the case recorded by Tschernomikow[671]
a boy, aged 2-1/2, evacuated during a day 208 worms, partly through
the stomach, partly through the intestine. Coil-formation of such
masses of Ascarides renders possible not only constipation, but also
complete obstruction with symptoms of ileus, as shown by the five cases
quoted by Mosler and Peiper,[672] as well as from observations made by
Raie,[673] Schulhof,[674] Rehberg,[675] Rocheblave,[676] Heller,[677]
Leichtenstern,[678] Huber,[679] and Wilms.[680] In two cases of
Black[681] and Parkinson[682] the intestinal obstruction was caused by
a coil of tapeworms.
[596] Strümpell, “Lehrb. d. spez. Path. u. Therap.,” 1894.
[597] Boas, _Deutsch. med. Wochenschr._, 1895.
[598] Still, _Brit. Med. Journ._, 1899.
[599] Arboré-Rally, _Arch. de Méd. des Enf._, 1900.
[600] Metschnikoff, _Bull. méd._, 1901.
[601] Matignon (abstract), _Münch. med. Wochenschr._, 1901.
[602] Des Barres, _Gaz. des Hôp._, 1903.
[603] Kirmisson, _Annal. de Méd. et Chir. des Enf._, 1901.
[604] Moty (abstract), _Münch. med. Wochenschr._, 1901, p. 910.
[605] Girard, _Annal. de l’Inst. Pasteur_, 1901.
[606] Triboulet, _Soc. méd. des Hôp. de Paris_, 1901.
[607] Morkowitin (abstract), _Centralbl. f. d. Grenzgebiete_, 1902.
[608] v. Genser, _Wien. med. Wochenschr._, 1901.
[609] Schiller, _Beitr. z. klin. Chir._, 1902, xxxiv.
[610] Czerny and Heddäus, _ibid._, xxi.
[611] Kaposi, _ibid._, xxviii.
[612] Schwankhaus, _Amer. Pract._, 1901.
[613] Ramstedt, _Deutsch. med. Wochenschr._, 1902.
[614] Rostowzeff, _Russ. med. Rundschau_, 1903.
[615] Wirsaladze, _Bobritsch. Gaz. Botkina_, 1902.
[616] Oppe, _Münch. med. Wochenschr._, 1903.
[617] Hanau, _ibid._, 1903.
[618] Galli-Vallerio, _Centralbl. f. Bakt._, 1903, p. 1094.
[619] Ssaweljews, _Deutsch. med. Zeitg._, 1903.
[620] Nason, _Journ. Amer. Med. Assoc._, 1904.
[621] Spieler, _Wien. klin. Wochenschr._, 1904.
[622] Bégonin, _Journ. de Méd. de Bordeaux_, July, 1902.
[623] Putnam, quoted by Spieler.
[624] Schilling, “Würzb. Abhandl.,” 1905. v.
[625] Blanchard, _Acad. de Méd._, July 3, 1904.
[626] Moore, _Brit. Med. Journ._, August 18, 1906.
[627] Auley, _ibid._, 1906.
[628] Page, _New York Med. Journ._, January 20, 1906.
[629] Schoeppler, _Centralbl. f. Bakt._, 1906.
[630] Oui, _Rev. prat. d’Obstét. et de Paed._, 1906.
[631] Frangenheim, _Samml. klin. Vortr._, 1906, No. 424.
[632] Kahane, _Schweiz. Korrespondenzbl._, 1907, viii.
[633] Heekes, _Brit. Med. Journ._, March 16, 1907.
[634] Andrews, _ibid._, 1906.
[635] Leuckart, “Die Parasiten des Menschen.”
[636] Heller, “Handb. d. spez. Path.,” v. Ziemssen, vii.
[637] Mosler and Peiper, “Spez. Path. u. Ther.,” v. Nothnagel, vi.
[638] Henoch, “Vorlesungen über Kinderkrankheiten.”
[639] Davaine, “Traité des Entozoaires.”
[640] Küchenmeister and Zürn, “Die Parasiten des Menschen.”
[641] Bremser, “Lebende Würmer im lebenden Menschen.”
[642] Mondière, _Schmidt’s Jahrb._, 1840.
[643] v. Siebold, “Parasiten” in Wagner’s “Handwörterbuch,” 1845.
[644] Rokitansky, “Path. Anat.”
[645] Gerhardt, quoted by Liesen, “Dissert. Bonn.”
[646] Abrault, quoted by Seifert, “Lehrb. d. Kinderkrankh.”
[647] Apostolides, _Lancet_, 1898.
[648] Marcus, quoted by Seifert, “Lehrb. d. Kinderkrankh.”
[649] Wischnewsky, quoted by Seifert, _ibid._
[650] Galvagno, _Arch. de Patol. et Clin., inf._, 1902.
[651] Salieri, _Rif. med._, 1902.
[652] Lini, _Schmidt’s Jahrb._, 1838.
[653] Gräffe, _Protokoll d. Ges. f. Natur u. Heilkunde_, Dresden, 1853.
[654] Nicolino, _Clin. mod._, 1902.
[655] Liesen, “Dissert. Bonn.” 1904.
[656] Boloff, quoted by Seifert, “Lehrb. d. Kinderkrankh.”
[657] Lutz, _Centralbl. f. Bakt._
[658] Schiller, _Beitr. z. klin. Chir._, xxxiv, p. 200.
[659] Rehn, _see_ Schiller, _loc. cit._, p. 201.
[660] Broca, _Rev. mens. des Mal. de l’Enf._, 1904.
[661] Lutz, _Wien. klin. Wochenschr._, 1905, xv.
[662] Froelich, _Rev. mens. des Mal. de l’Enf._, 1897.
[663] Vuillemin, _Centralbl. f. Bakt._, 1902.
[664] Marro, _Arch. per le Sci. med._, 1901.
[665] Simons, _Centralbl. f. Gynäk._, 1899.
[666] Kolb, _Centralbl. f. Bakt._, 1902.
[667] Chiari, _Prag. med. Wochenschr._, 1902.
[668] Schneider, _Centralbl. f. Bakt._, 1904.
[669] Sehrt, _Beitr. z. klin. Chir._, li.
[670] Fauconneau-Dufresne, quoted by Seifert.
[671] Tschernomikow, quoted by Seifert.
[672] Mosler and Peiper, _loc. cit._
[673] Raie, _Lancet_, 1899.
[674] Schulhof, _Münch. med. Wochenschr._, 1903.
[675] Rehberg, “Dissert. Königsberg,” 1907.
[676] Rocheblave, _Gaz. des Hôp._, 1898.
[677] Heller, _loc. cit._
[678] Leichtenstern, “Ziemssen’s Handb.,” vii.
[679] Huber, quoted by Rehberg.
[680] Wilms, _Deutsch. Zeitschr. f. Chir._, xlvi.
[681] Black, _Brit. Med. Journ._, 1872.
[682] Parkinson, quoted by Rehberg.
In the earlier history of medicine the helminthes played a great part
as the excitants of many intestinal diseases and of enteric as well.
Even if to-day they no longer be regarded as such, the conception that
they represent the predisposing factor in typhoid infection through
the injury they inflict on the mucosa (Guiart,[683] Blanchard,[684]
Vivaldi and Tonello[685]) must not be summarily rejected. Vivaldi and
Tonello found helminthes in 80 per cent. of their typhoid patients,
numbering among these _Trichocephalus dispar_, _Oxyuris vermicularis_,
_Ancylostoma duodenale_, and _Ascaridæ_. The report of Leuckart[686] is
here worth citing, to the effect that Thiebault never failed to find
Trichocephalus in his cholera patients at Naples. Blanchard[687] goes
so far as to express the desire that in every febrile affection of the
intestine an anthelmintic treatment with thymol should be undertaken as
early as possible, even before learning the results of serum diagnosis.
[683] Guiart, _Compt. rend. Soc. de Biol._, Paris, March 16, 1901.
[684] Blanchard, _Arch. d. Par._, 1901.
[685] Vivaldi and Tonello, _Gaz. d. Osp._, October 29, 1905.
[686] Leuckart, quoted by Kahane.
[687] Blanchard, _Acad. de Méd._, October 18, 1904.
The lesions of the liver and pancreas due to _Ascaridæ_ are briefly
discussed in the chapter on Ascariasis (p. 687).
A discussion of the intestinal helminthes from the clinical and
therapeutical point of view follows these general considerations.
Dibothriocephalus latus.
From what is known as to the development of _Dibothriocephalus latus_,
the way by which man is infected is self-evident: infection can only
take place through the ingestion of insufficiently cooked fresh-water
fish (pike, burbot, perch, grayling and vendace); what degree of
temperature is necessary to kill the larval forms is still unknown.
_Dibothriocephalus latus_ lives in the small intestine of man, alone
or in some numbers, frequently also together with _Tænia solium_. The
proglottides are passed always united in large pieces, the ova are
deposited through the uterine pore, while the worm is still in the
intestine, so that they are easily found in the fæces. The proglottides
are so characteristic that they cannot be confused with those of
other species. In reference to whether age or sex is spared by _D.
latus_, it is not possible to make any definite statement, especially
so far as the endemic area is concerned, whether a person resides
in it continuously or visits it, so long as his habit of life is in
accordance with those of the country. Bendix[688] certainly emphasizes
the fact that early childhood is as a rule immune: his case was that of
a child, aged 4-1/2 years.
[688] Bendix, _Verein f. innere Med._, Berlin, June 16, 1902.
Sparganum mansoni.
According to our present knowledge (Miyake[689]) the disease occurs
almost exclusively in China and Japan. On the main island it occurs
in all districts, though rarely under observation. It is especially
frequent in the neighbourhood of Kioto and Osaka; these places are very
near together, and between them there is mutually active intercourse,
so that taken together they may be regarded as one district infested by
this worm disease. As regards localization in the body, there appears
to exist a certain predisposition for definite regions, for instance,
the eye and genito-urinary tract. In some cases the parasite manifested
the peculiarity of wandering about the body and of appearing at certain
favourite points (musc. quadriceps femoris) (Hashimoto[690]). Most
patients complain more or less of the onset of attacks of pain and
of sensitiveness to pressure. In those cases in which the patients
evacuated the worm during micturition, the symptoms were variable;
sometimes there was tenesmus of the bladder, sometimes pains in the
inguinal region, sometimes hæmaturia. None of these troubles is
characteristic of the disease, and does no more than represent the
symptoms that follow a mechanical irritation that any kind of foreign
body may produce. Besides the onset of attacks of pain, swelling
of the regions affected, if superficial, may often be recognized,
when a superficial diffuse soft tumour can be felt which often gives
pseudo-fluctuation. Sometimes a peculiar crackling can be detected
internally, as in the making of a snowball. During the further course
an abscess not infrequently forms around the worm. When the situation
of the worm is superficial, “an inflammatory tumour with a tendency
to migrate” is stated by Omi[691] to be an important diagnostic sign.
That, however, is not always the case, as the observation made by
Inoye[692] shows. It would be better to add to this sign the onset of
paroxysmal pain and the temporary change in volume of the tumour. When
once the parasite is removed, the wound heals just as satisfactorily as
any other fresh wounds made at operation.
[689] Miyake, _Mitteil. aus d. Grenzgebiete_, 1904, xiii.
[690] Hashimoto, quoted by Miyake.
[691] Omi, _Iji-Shinshi_, Tokio, 1898.
[692] Inoye, _ibid._, 1897.
*Dipylidium caninum* (_Tænia cucumerina_).
This species belongs to parasites of rare occurrence. Up to the year
1905 Bollinger[693] collected thirty-six cases from the literature,
twenty-nine of which were children and seven adults. Since then some
further cases have come to light, so that the number now observed
amounts to ninety, and among them only eight adults. The youngest
child was 6 weeks old (Köhl[694]), in which the first proglottides
were passed when the child was 40 days old. This preponderating
occurrence in children is clearly connected with the close intercourse
between children and dogs, and also cats. Bollinger believes that _D.
caninum_ in reality occurs more frequently in adults than has hitherto
been supposed. In addition, it must be mentioned that this species
is quite unknown to many physicians, and is occasionally confused
with _Tænia solium_. One notices almost daily a large quantity of
cucumber-seed-like bodies, reddish or whitish-grey, about 1 cm. long
and 2 mm. broad, discharged with the stools. Lindblad[695] remarks
that these bodies have lively movements, that they perish rapidly
in fresh water, and become white and smooth. These Cestodes, in
isolated cases, are parasitic in the intestine in large numbers.
Sonnenschein[696] expelled four fragments in the case of a boy, aged
4 months; Asam[697] three fragments in the case of a child, aged 19
months; and Zschokke[698] as many as five or six in that of a boy, aged
4. They do not always produce such striking symptoms as occurred in
Pollak’s case.[699] In other cases gastro-intestinal disturbances with
or without fever (Krüger[700]), emaciation (Zschokke), or even nervous
symptoms of central origin in the form of convulsions (Brandt[701])
have been observed. From the nature and mode of infection children must
be kept from close contact with dogs and cats as much as possible to
ensure prophylaxis. The appropriate treatment, as it mainly affects
children, deserves special mention, whilst the expulsion of the
remaining Cestodes may be described in this connection. Among the drugs
one may mention flor. kousso 1·0 grm., pulpa tamar. depur. 2 grm.,
syrup of sugar 50·0 grm., one-third to be taken every hour (Lindblad).
Kamala appears to have no effect, although Huber[702] recommends it
in small doses according to age from 0·5 to 3·0 grm. He warns against
_Filix mas_ preparations, which otherwise, even in early childhood,
under careful dosage gives the best results. Young children are given
1·0 to 2·0 grm. extr. fil. maris, with mint syrup or raspberry syrup
30·0 grm., in the morning twice an hour by the mouth, or 1·0 grm.
extr. fil. maris is mixed with syrup of mint, and given by means of a
stomach tube (Rosenberg[703]). A few hours afterwards a mild laxative
may be taken--one to two tablespoonfuls of aqueous tincture of rhubarb
(Asam)--or an enema may be given. In a case reported by Sonnenschein
decoction of pomegranate root had no effect, as it was vomited up.
[693] Bollinger, _Deutsch. Arch. f. klin. Med._, 1905, lxxxiv.
[694] Köhl, _Münch. med. Wochenschr._, 1904.
[695] Lindblad, _Hygiea_, xlv.
[696] Sonnenschein, _Münch. med. Wochenschr._, 1903.
[697] Asam, _Münch. med. Wochenschr._, 1903.
[698] Zschokke, _Centralbl. f. Bakt._, 1905.
[699] Pollak, _Wien. klin. Wochenschr._, 1907.
[700] Krüger, _St. Petersb. med. Wochenschr._, 1887.
[701] Brandt, _Centralbl. f. Bakt._, 1889.
[702] Huber, suppl. to Asam, _Münch. med. Wochenschr._, 1903.
[703] Rosenberg, _Ges. f. innere Med._, February 16, 1904.
Hymenolepis nana.
This species, very rare in Central and Northern Europe, inhabits
the small intestine, especially of children; it burrows very deeply
into the mucosa. Not uncommonly several thousand have been found in
one case (Nicolo,[704] E. Stoerk and Haendel[705]). It is remarkable
that these Cestodes have been found so frequently _post mortem_ and
after vermifuges given for other reasons. Thus the clinical symptoms
must often be very indefinite (Stoerk and Haendel), so that one may
assume that only a slight percentage of cases of _Hymenolepis nana_
come under observation and are published as such. On the other hand,
it is certainly conceivable that with the large number of parasites
that frequently occur in one individual a whole series of symptoms,
in part quite severe, are capable of being produced. These are partly
symptoms of intestinal catarrh, consisting of abdominal pains,
constipation, alternating with attacks of diarrhœa, perverse appetite,
and boulimia, abdominal pains of a cramp-like nature, followed by
emaciation, headache, sleeplessness, pallor, lassitude, and in part
nervous symptoms--epileptiform attacks without loss of consciousness,
weakness of memory, melancholia, irregular febrile attacks (Lutz[706]).
Possibly, too, _Hymenolepis nana_ infects the urinary organs, producing
true chyluria (Predtetschensky[707]). Stoerk and Haendel are inclined
to think that this species, unlike other Cestodes parasitic in man
and domestic animals, needs no intermediate host for its development,
and that the larval forms (cysticercoid) live in the same host as the
adults. The diagnosis is based on the demonstration of ova in the
stools. As far as expulsion of this Cestode is concerned, santonin,
kamala, kousso flowers and thymol appear to have no effect of
importance; whilst extract of male fern, recommended by Grassi[708] as
a result of his considerable and successful experience, has been given,
with the result that the worms really are expelled, and that after the
treatment neither worms nor ova are any longer demonstrable in the
stools of patients. In his cases of chyluria Predtetschensky prescribed
ol. terebinth. 20 drops three times daily for a fortnight, then
acid. gallic. 0·5 grm. three times a day for two days, then 1·0 grm.
three times a day; the urine became clear, but whether permanent cure
resulted remained doubtful.
[704] Nicolo, _Gaz. d. Osp._, 1904.
[705] Stoerk, E., and Haendel, _Wien. klin. Wochenschr._, 1907, xxix.
[706] Lutz, _Centralbl. f. Bakt._, 1894.
[707] Predtetschensky, _Zeitschr. f. klin. Med._, xl.
[708] Grassi, _Centralbl. f. Bakt._, 1887.
_Hymenolepis diminuta_, _H. lanceolata_, _Davainea asiatica_, and _D.
madagascarensis_ possess no actual clinical interest; with regard to
the latter it need only be pointed out that Bordier[709] in studying
a case of chyluria found this species in the kidneys of a person in
Madagascar.
[709] Bordier, quoted by Predtetschensky, _loc. cit._, p. 95.
Tænia solium.
_Tænia solium_ inhabits the small intestine of man; single proglottides
or whole worms may get into the abdominal cavity and the bladder
through fistulæ, and penetrating the abdominal wall escape outwards
or become discharged with the urine. Symptoms of intestinal stenosis
are certainly very rare, as in the case recorded by Steinhaus[710]
of a child, aged 9, the stenosis ceasing after the expulsion of the
segments. The usual position of the worm in the small intestine is with
the head closely adherent to the mucosa and the proglottides lying
along the intestine; from time to time portions are discharged with
the fæces _per rectum_. Its position can also be reversed, and the
proglottides in the gut become thus discharged by vomiting.
[710] Steinhaus, _Deutsch. med. Wochenschr._, 1903.
The diagnosis depends upon the proglottides being generally discharged
in pieces in the stools, or eventually an examination for eggs.
Larval infection (_Cysticercus cellulosæ_) occurs also in man through
auto-infection or through food.
_Cysticercus cellulosæ_ of the skin and subcutaneous tissue occurs
very seldom singly; as a rule they are found in hundreds and thousands
in the same individual. They occur in different parts of the body,
especially on the flexor surfaces of the extremities (generally
symmetrically), small globular swellings, the size of a pea or a hazel
nut, smooth, of a tough cartilaginous consistence, fairly movable under
the skin, in the muscles less so. They never degenerate or cause the
surrounding skin to lose its colour. It is an interesting fact that
in the case described by Posselt[711] nodules on the face, namely in
the neighbourhood of the left cheek and behind the left ear, reformed.
The following are, according to Posselt, characteristic for cutaneous
tumours due to cysticerci: (1) the position in the subcutaneous
connective tissue (and almost always simultaneously in the muscles);
(2) the approximately equal size and regularly rounded oval form; (3)
the peculiar density, almost reminding one of cartilage in its hardness
and the sensation of tightly distended thick-walled bladders; (4)
proportionately slight mobility; (5) with painlessness, absence of any
cutaneous reaction (hyperæmia or swelling of the skin or pigmentation).
The very gradual appearance generally of the tumours supports the
diagnosis, and in addition to this evidence we may emphasize the
preponderating liability of the upper part of the body to attack and
the symmetrical arrangement of the nodules. Cutaneous and muscular
cysticerci cause the most varied symptoms, sensory disturbances,
abnormal sensations, depression and a feeling of weariness whenever
the diseased parts are moved, weakness in the lower extremities,
pains in the course of the sciatic nerve, in addition to those which
simulate cramp in the calves, numbness in the hands, pains upon their
being moved. In the case of a cysticercus situated in the elbow-joint,
painful dragging sensation in the course of the ulnar nerve persisted.
In other cases the arm was almost paralysed, or it could not be
completely extended; stiffness and bending of the little finger were
noticed. Cysticerci of the gluteal muscle cause trouble upon sitting
and upon defæcation. Remittent unilateral headaches were present in
the case of a cysticercus of the region of the right eyebrow; pains of
a neuralgic character radiated from the diseased temporal region. The
cysts may be inflamed and may suppurate; this especially happens in the
case of solitary cutaneous and muscle cysticerci. The best treatment
consists in puncture of the cysts with a Pravaz syringe and subsequent
injection of a drop of 1 per cent. sublimate solution. Tincture of
iodine has similarly been proposed (Wolff[712]). Frangenheim[713]
recommends early extirpation (this, however, only in the case of
solitary cysts). Pelagutti[714] believes that in his case diminution
in the size of the cysts was obtained by the use of anthelminthic
remedies continued over a long period combined with potassium iodide
and calcium salts (internally). Cysticercus is very rarely found in
the tongue; there the worms generally lie in front of the sulcus
terminalis, corresponding to the middle of the tongue, according to
Glas.[715] In the case recorded by Gaetano[716] (a boy, aged 10) there
was a nodule on the left side of the tongue which grew very rapidly
till it reached the size of a nut; it was embedded in the muscle and
covered over by normal mucosa. Cysticerci are just as rare in the
pleuræ, in the lungs, in the intestinal submucosa, in the submucosa
of the small intestine, in the mesenteric glands, in the liver,
pancreas, spleen and kidneys, in the mamma, in the heart, in the bones
and in the great vessels (Huber[717]). Cysticercus of the eye deserves
special mention; in rare cases the cysticercus has been met with in the
subcutaneous cellular tissue of the eyelid, once in the muscle bundles
of the musculus orbicularis. Subconjunctival cysts are found chiefly
in youthful individuals. Their position is most varied, generally in
the neighbourhood of the inner angle of the eye. Dilated vessels pass
right over the cysts, which are generally movable, together with the
base they rest upon, producing a spherical protrusion. The head of the
worm can sometimes be seen shining through as a whitish speck. The only
symptoms are those of a slight irritation of the connective tissue and
some difficulty in closing the lid; larger cysts dislocate the globe.
The diagnosis has the rapid growth of the cystic tumour to support
it; there is the possibility of its being mistaken for a foreign body
(Kaldrovils[718]). After division of the connective tissue capsule
extraction is easily performed. It is most rare for the cysticercus
to occur in the orbit. Suppuration of the cyst may have serious
consequences for the eye. It is only exceptionally that the cysticerci
gain access to the anterior chamber of the eye.
[711] Posselt, _Wien. klin. Wochenschr._, 1899.
[712] Wolff, “Lesser’s Encyclop. d. Haut- u. Geschlechtskrankh.,” 1900.
[713] Frangenheim, _Volkm. klin. Vortr._, No. 424.
[714] Pelagutti, _Giorn. ital. delle mal. vener._, 1900.
[715] Glas, _Wien. klin. Wochenschr._, 1905.
[716] Gaetano, _Giorn. int. delle Sci. med._, 1904.
[717] Huber, “Bibliographie der klin. Helminthologie,” 1891, pt. 2.
[718] Kaldrovils, _Wien. med. Wochenschr._, 1902.
Subretinal cysticerci or those localized in the vitreous are more
frequent. Upon examination with the ophthalmoscope there is seen in the
vitreous a bluish bladder with a smooth surface. The head is seen as
a white patch, and the circle of hooks and the suckers also come into
view, also the frequent movements which the head and neck make in the
vitreous. Operation generally yields good results; in rare instances
the globe is atrophied and must be enucleated.
Formerly cysticerci in the brain were met with in fair frequency, but
the number of such cases has generally decreased of late years in a
remarkable way, in correspondence with the diminution of cysticerci,
which is to be attributed to compulsory meat inspection. Whilst, for
example, the _post-mortem_ records of the Pathological Institute in
Berlin before the year 1875 showed 20 per cent. cysticerci affecting
the brain, this number declined later to 16·3 per cent., and of late
years has fallen to 1 per cent. (Orth[719]). Nevertheless even now
cysticercus still plays no inconsiderable part in the etiology of
cerebral diseases. For example, in the clinic of de Amicis at Naples,
among seven cases of cysticerci of the skin, they were found four
times also in the brain (Sipari[720]). Cysticerci may occur in the
dura mater, arachnoid, pia mater, choroid plexus, the surface of
the cerebral hemisphere, the medullary substance, the ventricles,
the aqueduct, the corpus striatum, corpora quadrigemina, the pineal
gland, the pons, the cerebellum, the olfactory trigone, the bulb, the
medulla oblongata, and the olive. They are most frequently found in the
cortical substance and in the ventricles; the frequency of the latter
situation may be explained by the flow of the fluid (Henneberg[721]).
The severity of the symptoms is not always in proportion to the number
of cysticerci. Cases have been known in which ten, twenty and forty
cysticerci have been found (Hagen-Thorn[722]), and yet the clinical
symptoms have been remarkably slight. On the other hand, solitary cysts
may both run a course completely without symptoms and also cause the
severest symptoms when located in specially important parts of the
brain (crus, pons, central convolutions). In the case mentioned by
Jacobson[723] the invasion of the brain by cysticerci was immense; the
largest cyst was found in the cerebral cortex. The chief symptoms of
cysticercus of the brain substance consist in the onset of cortical
epilepsy, which sometimes runs a very pernicious course, frequently
with psychical disturbances, whilst paralyses are absent. Perhaps, too,
the localization of pain, spontaneous and on pressure, corresponding
with the points observed on the cranium, is of importance. Cysticerci
may also change their position in the brain; patients who had earlier
suffered from epileptiform convulsions later showed intra-ocular
cysticerci after the cerebral symptoms had completely disappeared.
Treatment can only be surgical; v. Bergmann[724] operated in two
cases with well-marked improvement. Parasites in the ventricles are
especially dangerous, more especially so when free in the ventricles,
and so capable of giving rise to the danger of sudden closure of
the foramen of Majendie (Simmonds,[725] Versé[726]). Stern[727]
states the symptoms of cysticercus in the fourth ventricle to be the
following: general cerebral pressure symptoms (headache, vertigo,
vomiting, somnolence, congested disc caused by internal hydrocephalus);
in addition, there are symptoms which point to disease of the
hind-brain--pain and stiffness in the neck, vertigo and cerebellar
ataxy, violent and persistent vomiting, slowness of pulse; and lastly
those rare but certain symptoms of a lesion of the bulb, such as
diabetes, respiratory disturbances and paralysis of cerebral nerves,
especially of the abducens. These are far less marked than the general
symptoms of cerebral pressure. One characteristic is the remarkable
alternation between severe general symptoms and periods of complete
sense of well-being; in this way a functional nervous affection may
be simulated (Jolasse[728]). Brun’s symptom (in the widest sense,
sudden onset of violent cerebral symptoms upon change of head-posture)
is a specially characteristic sign of free cysticercus in the fourth
ventricle; the disease generally terminates with sudden death from
cessation of the heart’s action. Defects in motor power, convulsions,
implication of other nerves, are rare and unessential complications
(Hartmann[729]). Carefully carried out, lumbar puncture may possess
some diagnostic and therapeutic value. Treatment is purely symptomatic,
or eventually Neisser’s ventricle puncture may be considered.
[719] Orth, _Berl. med. Ges._, June 29, 1904.
[720] Sipari, “Angelo Trani Neapel,” 1900.
[721] Henneberg, _Berl. klin. Wochenschr._, 1906, xxxii.
[722] Hagen-Thorn, abstract by Posselt.
[723] Jacobson, _Berl. klin. Wochenschr._, 1906.
[724] v. Bergmann, quoted by Frangenheim, _loc. cit._, p. 470.
[725] Simmonds, _Münch. med. Wochenschr._, 1907, xxvii.
[726] Versé, _Münch. med. Wochenschr._, 1907, xi.
[727] Stern, _Zeitschr. f. klin. Med._, lxi.
[728] Jolasse, _Münch. med. Wochenschr._, 1896.
[729] Hartmann, _Wien. klin. Wochenschr._, 1902.
At the base of the brain the cysticerci, as a rule, assume that form
which is designated as _C. racemosus_, and consists of rows of delicate
grape-like bladders in groups, sometimes also markedly branched, but
generally sterile, which develop in the meshes of the soft meninges
and may envelop the nerves and vessels of the base of the brain.
Such tumours bring about hydrocephalus and chronic leptomeningitis,
which must be regarded as the causes of the clinical disturbances
(cysticercus meningitis), attacks of loss of consciousness, dementia
and apathy, dulness and confusion and headaches. In the case recorded
by Meyer[730] symptoms which resembled paralysis agitans were
noteworthy, and defects in speech in the case recorded by Durst[731]
(_C. racemosus_ in the region of the left Sylvian fossa). According
to Markwald[732] _C. racemosus_ of the fourth ventricle is said to
represent a characteristic clinical picture: violent headaches,
attacks of vertigo followed very soon by deep coma and death in a few
days. Treatment in _Cysticercus racemosus_ is ineffectual. In the
diagnosis of cerebral cysticerci in general the recognition of multiple
cysticerci in the skin and muscle and of the tapeworm is of importance.
In cases of cerebral diseases in which cysticerci may be a possible
cause, Remmert[733] recommends that the skin of the whole body should
be palpated.
[730] Meyer, _Deutsch. med. Wochenschr._, 1906.
[731] Durst, _Lieven. viestnik_, 1902.
[732] Markwald, _Münch. med. Wochenschr._, 1895.
[733] Remmert, “Dissert. Berlin,” 1893.
Cysticercus in the spinal cord and in the vertebral column is
occasionally observed; as a rule, other organs, above all the brain and
its membranes, are simultaneously affected. Here, too, the cysticercus
occurs in two forms--sometimes the cysts are roundish or oval, solitary
or multiple, and at other times _Cysticercus racemosus_ occurs.
Tænia saginata.
Occurs in the small intestine of man. It is characteristic of the
habit of life of this parasite that once it has become mature its
proglottides are dropped off daily in increasing numbers because its
growth is extraordinarily rapid. The joints are discharged generally
spontaneously during the whole day without a stool. An extraordinarily
unpleasant sensation is produced by the damp, cool joints slipping
down into one’s lower garments and over one’s legs when walking; women
especially, in whom the proglottides slip through their petticoats on
to their legs, complain bitterly of this troublesome symptom. Another
unpleasant symptom is superadded in the shape of the proglottides
tickling the rectum, and this excites irritable people to the last
degree. Different species of tapeworms are not mutually exclusive.
_B. latus_ and _T. solium_ frequently occur side by side, so also _T.
solium_ and _T. saginata_--for instance, in a butcher’s assistant we
once expelled twelve _T. solium_ and one _T. saginata_ at the same
time. The greatest number of Tæniæ which have been observed at one
time amounted to forty _T. solium_ (Kleefeld[734]). Even though the
cysticercus of _T. saginata_ is not, as in the case of _T. solium_,
particularly dangerous to man, a parasite, nevertheless, which requires
so much nutrient material during its rapid growth, and thereby sets up
manifold disturbances in the general condition of health, ought to be
expelled as rapidly and thoroughly as possible.
[734] Kleefeld, _see_ Seifert _loc. cit._
Tapeworms are found not uncommonly with other intestinal parasites,
such as Ascaris, Oxyuris, Trichocephalus or Ancylostoma. Prunac[735]
described a case in which a woman passed a Tænia through the anus while
she vomited a _Fasciola hepatica_.
[735] Prunac, _see_ Eichhorst, “Handb. d. spez. Path. u. Therap.,” ii,
p. 281.
The symptomatology of these three large species of Cestodes,
_Dibothriocephalus latus_, _Tænia solium_, and _T. saginata_, may
very well be summarized together, as, apart from some peculiarities,
the clinical symptoms, especially so far as their localization in the
intestine is concerned, are practically the same for all three species.
In a large number of cases the hosts have no suspicion whatever that
they are harbouring a tapeworm; they feel quite well and free from any
disquieting symptoms whatever, and only become aware of the fact that
they are the carriers of a tapeworm when the discharge of the segments
takes place; on the other hand, it is often difficult to rid people
of the idea that they are harbouring a Tænia (Küchenmeister calls
such _Tænia imaginata_); usually it is undigested fibrous shreds of
beefsteak which are regarded by the patients as proglottides of tæniæ.
In a large number of cases, disturbances of the intestinal tract set
in, _e.g._, sense of pressure in the abdomen, which sometimes becomes
constant on one and the same side, or sometimes changes, now at the
umbilicus and again at the epigastrium; here and there colicky pains
are present. Derangements of appetite and digestion are frequently
complained of; the most frequent are the sensations of morbid hunger or
irregular appetite, nausea and vomiting. Thus, at the Third Congress
of Internal Medicine, Senator recorded a case in which there were
symptoms of nervous dyspepsia, cured after a successful vermifuge.
There is either constipation or diarrhœa, so that many of such patients
are brought for treatment with the diagnosis of “chronic intestinal
catarrh” and correspondingly treated. As to the treatment of toxic
action of the Tæniæ when such arises, _see_ the special section on the
subject (bothriocephalus anæmia, p. 644). The frequent disturbances of
the general condition, so-called reflex phenomena, so far as the action
of toxic substances is not in question, may be explained by the fact of
their occurrence in specially sensitive individuals who are affected
by such phenomena. The proof that a diseased condition is produced by
a tapeworm will be forthcoming with some degree of certainty if the
symptoms cease immediately after the removal of the parasites. As a
whole series of troubles, which certainly have nothing to do with them,
are erroneously ascribed to the tapeworm, as is frequently assumed, one
will do well to be somewhat critical in this respect.
The treatment is of a threefold nature: prophylactic, symptomatic and
radical.
Under any circumstances, the best prophylaxis is that which consists
in only eating the flesh of those animals in which any of the three
larval forms occur (pig, cattle, salmon, pike, burbot, etc.) so
prepared that the larval forms have been destroyed and the food thus
rendered innocuous. For domestic and public use the rule prescribed by
Küchenmeister is under all circumstances most easily understood, namely
to roast or boil till the flesh appear greyish-white and sufficiently
done by reason of the coagulation of the albumen and decolorization
of the blood. The general prophylaxis simply concerns the tapeworm
carriers trying to limit as far as possible the further extension of
the parasites in the animal world by carefully rendering the expelled
segments and worms harmless (pouring sulphuric acid over the fæces
and burning the worms) and also by strictly adhering to official
regulations. The official system of meat inspection in this respect
has been of immense service, and much can still be done by means of
thorough official control over cleanliness in abattoirs and butchers’
shops. Galli-Valerio[736] very rightly desires the abolition of the
custom of manuring fruit-plants such as strawberries, vegetables and
salad with the contents of privies, and would extend the use of privies
in the country.
[736] Galli-Valerio, _Therap. Monatsh._, 1900.
Symptomatic treatment consists, in the case of those Tæniæ which resist
radical attempts at expulsion, of repeated use of drugs injurious to
the worm as soon as ever new proglottides are formed, or in special
cases, as in the case of persons weakened by diseases or operations,
or frail old people, or patients with severe heart failure, gastric or
intestinal carcinoma, or in pregnancy, in effecting the expulsion of a
large chain of proglottides by the mildest measures possible.
Radical treatment of the Tænia is not always equally easy in all three
species, even when the means used are the same; the easiest to expel
is _T. solium_, then _D. latus_, and the most difficult _T. saginata_.
That as yet no certain cure exists for Cestodes is clear from the large
number of drugs recommended from time to time, and the increase of
bungling treatment in this respect; in addition, there is no department
in which there is so much quackery as in vermifuges. The treatment
proper should always be preceded by thorough preparatory treatment,
the purpose of which is to render the gut as empty as possible once
for all, and on the other hand to put the worms themselves into a
diseased condition. How far the host himself has been made ill by
such preliminary cures (herring, pickle, garlic, onions, preserved
strawberries), many a person who has had to do with such things can
recount. In the opinion of Fischer[737] strict preparatory treatment
appears to favour the development of toxic substances, or else it
disposes to vomiting; as a rule it causes the patient far more
discomfort than the treatment itself. In recent times far less weight
is attached to these preparatory treatments than to carefully prepared
and correctly dosed drugs; the preparation is generally limited to
relieving the intestine in a simple way, the day before the treatment,
of the densest fæcal masses, by a simple aperient or water enema.
[737] Fischer, Stockholm, Nordin and Josephson, 1904.
We recommend the following, which has always proved itself to be the
best and simplest remedy against _T. saginata_. The patient takes
early in the evening before the treatment nothing but a plate of soup
or a glass of milk, and then takes a laxative (electuar. lenit or
infus. sennæ compos. or an enema), so that later in the evening one
to two stools are passed. In this connection we fail to agree with
Grawitz[738] and Boas,[739] who consider that at least preliminary
evacuation of the intestines can be dispensed with. On the following
morning the patient should take a cup of black coffee or tea without
anything else, and half an hour later the vermifuge.
[738] Grawitz, _Münch. med. Wochenschr._, 1899.
[739] Boas, _Deutsch. med. Wochenschr._, 1889.
The best drug is extract. filicis maris æther., which also forms
the main constituent of most of the secret remedies recommended for
tapeworms. Earlier mishaps with this preparation had their origin
principally in insufficient dosage. Also, in addition to correct
dosage, extract. filic. maris needs very careful preparation if
satisfactory results are to be attained. If preparations with the trade
mark “Helfenberg” or “Wohnar” are not used, but the male fern extract
has been prepared by a chemist, one must make certain that the roots
of the _Aspidium filix-mas_ have been collected in May or October, and
only green sappy specimens selected, and that the attached paleæ have
been separated, that they have been broken up small and ether poured
over them with a little spirits of wine while quite fresh. The whole
mass is to be kept in a cool place, but not too closely covered. If
at any time a certain quantity is to be used, it is taken out, the
ether carefully distilled in a retort till the extract has a suitable
fluid consistency. Fischer attaches great importance to the direction
in the Pharmacopœia being exactly followed, to the effect that the
extract is to be carefully stirred before prescribing, as the active
substances undergo partial crystallization if kept for any length of
time and sink to the bottom, so that the preparation has a different
strength and toxicity in different layers. Of this extract 10 to 12
to 15 grm. are to be taken in gelatine capsules within half an hour.
We consider it unjustifiable to give greater doses than 15 grm. to
adults, as many cases are known in which to some extent severe toxic
symptoms have followed, such as headache, sensation of giddiness,
dyspnœa and cyanosis, yellow vision (xanthopsia), delirium, stupor,
the most severe cramps in the extremities, rapidly fatal trismus and
tetanus. The most serious are defects of vision of various kinds,
which may end in amblyopia and amaurosis, with permanent blindness. A
complete collection of toxicological literature up to the year 1903
is to be found in Marx’s[740] Dissertation. Since that time further
instances of such intoxications have been made known. Nagel[741]
observed them only in severe cases. O. Meyer[742] lays special
stress on the bad prognosis of the disturbances of vision evoked by
poisoning with extract. filicis maris. Studt[742] has seen two cases
of optic neuritis, one with circumscribed, the other with diffuse
retinal œdema. Uhthoff[743] has only seen one case; in that reported
by Noiszewski[744] the toxic retinitis was cured; in Viereck’s[745]
case bilateral concentric limitation of the field of vision followed
three days after taking 8·0 grm. extract. filicis maris. Stuelp[746]
attributes the amaurosis occurring after taking filix mas to a toxic
action on the muscularis of the central retinal artery; there followed
paralysis of the vessel, vascular engorgement, and thereby nutritional
defects of the nervous elements followed. In children one has to
diminish the dose correspondingly, as with them, still more so than
with adults, severe disturbances arise. Huber[747] claims that this
drug should not be given to children indiscriminately. The view is
frequently expressed that a combination of extractum filicis maris
with fatty oils in which the active constituents are soluble favours
intoxication. Marx[748] also argues from this standpoint and assumes
that the ideal preparation, free from objection, would be got if from
filix-mas extract a preparation free from fatty oils could be made, and
he considers it advisable to limit the use of castor oil as an aperient
before and after taking the “cure” and to prescribe instead a saline
laxative, such as Epsom salts or Glauber’s salts. Sonnenschein[749]
also advises against the simultaneous exhibition of extractum filicis
maris with oleum ricini, as is the case with Helfenberg’s capsules,
and Boas[750] is likewise anxious that ol. ricini should be avoided.
Lenhartz[751] appears to consider the warning against the simultaneous
combination of the extract with fats or ethereal oils, and especially
against the employment of castor oil as an after-treatment, as without
justification, and we, too, in the course of our many filix treatments,
have never yet witnessed any unfavourable effect from the use of
castor oil in the after-treatment. The surest way of obviating the
toxic effects of extractum filicis is to give a laxative (ol. ricini)
as soon as the extract has left the stomach, say, about half an hour,
so that it need not stay longer than necessary in the gut and become
absorbed. Perhaps in most cases of poisoning, transgressions against
this rule have been the cause of the toxic action. The nausea that
sets in the day after taking the drug and the inclination to vomit are
best resisted by giving iced coffee, iced tea, iced pills, peppermint
tea, cognac, one to two wafer powders of menthol and sacch. lactis
āā 0·2 grm. (Apolant[752]) half an hour before the drug is taken.
Fischer[753] considers that lying still in the horizontal position is
the best remedy. Boas[754] recommends the injection of the drug into
the stomachs of patients who tolerate extractum filicis badly, in the
form of a thin emulsion (with gi. arab.). In the case of children
the extract is prescribed with honey as an electuary. The method
recommended by Fowler[755] is without doubt too detailed; he prescribes
before the treatment two to three to four days’ rest in bed; special
diet, tablets of cascara sagrada three times daily, on the fourth
day senna infusion, and then to give the extractum filicis maris in
capsules in four doses, to be taken every quarter of an hour.
[740] Marx, “Diss. Würzburg,” 1903.
[741] Nagel, _Deutsch. med. Wochenschr._, 1903.
[742] Meyer, O., _Berl. klin. Wochenschr._, 1905.
[743] Studt, _ibid._, 1905.
[744] Uhthoff, _ibid._, 1905.
[745] Noiszewski, “Postepokuhst,” 1906.
[746] Viereck, _Arch. f. Schiffs- u. Tropen-Hyg._, 1906.
[747] Stuelp, _Arch. f. Augenheilk._, 1906, li.
[748] Huber, M_ünch. med. Wochenschr._, 1903.
[749] Marx, _loc. cit._
[750] Sonnenschein, _Münch. med. Wochenschr._, 1903.
[751] Boas, _loc. cit._
[752] Lenhartz, _loc. cit._
[753] Apolant, _Deutsch. med. Wochenschr._, 1905, xliv.
[754] Fischer, _loc. cit._
[755] Boas, _loc. cit._
[756] Fowler, _Brit. Med. Journ._, 1906.
Under Jaquet’s[757] direction, Kraft has prepared an amorphous acid
from the fern root extract which is designated filmaron. As a vermifuge
the drug is prescribed for children of 2 to 5 years of age in doses up
to 0·2 to 0·3 grm., for children of from 8 to 12 years in doses up to
0·5 to 0·7 grm., and for adults up to 0·7 to 1·0 grm., so as to expel
the parasites. Bodenstein[758] gives the filmaron oil introduced into
commerce by the firm of Boehringer (one part filmaron and nine parts
castor oil) in still greater dosage, either fasting or, in the case of
sensitive patients, one hour after a cup of tea; he gives peppermint
tablets against possible nausea. Brieger[759] tested the preparation
in twenty-three cases; in twenty-one of these he prescribed it as an
ether-castor oil mixture, and in two as capsules. The action always
took effect in from two to five hours, and only in three cases were
unpleasant after-effects in the shape of colic observed; in sixteen
cases the result was positive, in seven negative.
[757] Jaquet, _Therap. Monatsh._, 1904.
[758] Bodenstein, _Wien. med. Presse_, 1906.
[759] Brieger, “Therap. d. Gegenwart.,” 1905.
The attempts made by Goldmann[760] to prepare from the bark of _Musenna
abyssinica_, a plant of the order _Myrsinaceæ_, indigenous to Persia,
the active substance, namely sebirol, have shown that when this is
given alone it certainly acts as a vermicide, but not as a vermifuge;
on the other hand, the results of a combination of sebirol with
thymol and salicylates were surprisingly good; this mixture has been
introduced into commerce as tæniol, in the shape of pastilles prepared
with chocolate for children. The method of giving tæniol is as follows:
On the day before the administration a light diet and thorough purging
with calomel are ordered; and then on the day of the treatment itself,
after a breakfast consisting of a cup of tea, in the case of adults,
thirteen to fifteen tæniol pastilles are taken in some red wine at
intervals of ten minutes respectively. In the middle of this treatment
an interval of some hours is interposed. After the pastilles have
been taken a calomel purge is again given. The results obtained by
Liermberger[761] are sufficiently encouraging to be put to further test.
[760] Goldmann, _Wien. klin. Wochenschr._, 1905.
[761] Liermberger, _Berl. klin. Wochenschr._, 1905.
Fischer[762] has tested in some of his cases extracts of some new
species of fern root; he employed the extract from the rhizomes of
_Aspidium spinulosum_ and _A. dilatatum_, two fern roots indigenous to
Sweden, and obtained remarkable results (doses of 4 grm.). Laurén[763]
had previously recorded similar results, and recently Friedjung,[764]
using extr. aspid. spinulos.
[762] Fischer, _loc. cit._
[763] Laurén, _Therap. Monatsh._, 1899.
[764] Friedjung, _Ges. f. innere Med._, Wien, March 8, 1906.
Cortex radicis granati as fresh bark is a very good drug, and is
usually given as a decoction: 180·0 bark to 1,000·0 water, boiled
for forty hours to 240·0, and a small cupful to be given every
half an hour; colic, vomiting and diarrhœa, are, however, easily
induced. The chief constituent of the granate root, pelletierinum,
possesses vermicidal properties, and is much recommended, especially
in France. Sequelæ easily arise (vertigo, hazy vision, malaise,
vomiting, quickened heart’s action, muscular tremors, cramps in the
calves), especially in delicate persons and children, so that one
should refrain from giving it to the latter especially (Drivon[765]).
Sometimes, judging by the experience of Sobotta[766] and Boas,[767]
the action is problematical. Where it is desired to employ it in the
case of adults, the following is prescribed: pellet. sulfur. 0·3 to
0·4 grm., acid. tannic. 0·5 grm., sir. rub. jd. 30·0 grm., to be taken
at one time, and a quarter to half an hour after a purgative (senna
infusion). In the case of children it is better to employ semina
cucurbitæ maximæ instead of extractum filicis maris. Sixty to 100
pumpkin seeds are pounded up with sugar, which yield a pleasant-tasting
electuary, and which are taken all at once; half an hour afterwards a
laxative is taken (Storch,[768] Pick[769]), Jungklauss’s preparation
is nothing else than a pumpkin extract; its action is favourable;
it is, however, too expensive (Ritter[770]). Flores kousso up to 15
to 20 grm. in compressed form or in sugar or honey in the form of
electuaries (children 2·0 to 10·0 grm. according to age) is not to be
relied upon; kussin, prepared from kousso flowers (Bedall, Munich),
is not a pure body; when taken it is divided into four parts up to
1·0 to 2·0 grm. with elæosaccharum menthæ, at half-hourly intervals;
it is said to be less unpleasant than treatment with flores kousso
(Liebreich and Langgard[771]). Kosinum crystallisatum (dose 1·5 to
2·0 grm.) is prepared by the firm of Merck. Kamala is the least potent
of the tapeworm drugs in use, and is principally to be recommended in
the treatment of children: 1·5 to 3·0 grm. in electuaries. According
to Leichtenstern[772] and White[773] chloroform, even in toxic
doses, cannot do any harm to the tapeworm, nevertheless it has been
recently recommended by Carratú[774]; chloroform 6·0, sirup. 60·0, one
teaspoonful to be taken every hour (fasting). Salol is recommended by
Galli-Valerio[775] as an absolutely harmless tapeworm drug; thymotal (a
derivative of thymol) by Pool,[776] 3 grm. to be given up to three to
four times on four consecutive days.
[765] Drivon, _Lyon méd._, 1902.
[766] Sobotta, _loc. cit._
[767] Boas, _loc. cit._
[768] Storch, _see_ Lenhartz, _loc. cit._
[769] Pick, _Ges. f. innere Med._, Wien, March 8, 1906.
[770] Ritter, _Prag. med._ Wochenschr., 1904, v.
[771] Liebreich and Langgard, “Kompendium der Arzneiverordnung,” 1907.
[772] Leichtenstern, “Therap. der Gegenwart.,” 1899.
[773] White, _Scot. Med. and Surg. Journ._, 1900.
[774] Carratú, _Giorn. med. del regio eserc._, 1903.
[775] Galli-Valerio, _Therap. Monatsh._, 1900.
[776] Pool, _Med. Woche_, 1901.
The drug well known long ago, cuprum oxyd. nigr., has been recently
brought into fresh notice by Dörr.[777] It is also the chief
constituent of the tapeworm drug introduced into commerce by the
firm of Dehlsen (Itzehoe) (Koch[778]). The coconut is absolutely
ineffectual, also naphthalin, croton-chloral, ether, gallanol,
strontium lactate, glycerine and bromide of potash.
[777] Dörr, “Therap. der Gegenwart.,” 1901.
[778] Koch, _Med. Klinik_, 1907.
Where possible one should endeavour to discover the head or the heads
of the tapeworm in the stools, so as to make certain whether the
treatment has been successful; this search is best carried out by
immediately and carefully pouring water over the total quantity of
evacuations collected in the night stool, without stirring them up,
till only the tapeworm is found lying at the bottom of the vessel.
NEMATODES.
*Strongyloides stercoralis.*
The pathological significance of this intestinal parasite is not
yet fully demonstrated. In Seifert’s[779] observation, on what
Leichtenstern[780] called the celebrated Würzburg case, the patient
had suffered many times from attacks of blood-stained diarrhœa with
tenesmus, as in Zinn’s[781] case of a three year old boy who had bloody
purulent diarrhœa. Schlüter[782] speaks of a hæmorrhagic enteritis
produced by Strongyloides. In other cases besides diarrhœa (either
with or without blood) there were noted: pains in the body (Schlüter),
tenderness of the abdomen, loss of appetite, gastric troubles of
a general kind, headache, giddiness, fainting attacks, anæmia
(Silvestri,[783] Valdes,[784] and Trappe[785]), so that even if in
isolated cases (Fülleborn[786]) symptoms are absent, some significance
cannot be denied these parasites as a matter of course (Bruns,[787]
Leichtenstern[788]). According to Kurlow,[789] in Siberia there is a
form of sporadic bloody diarrhœa which has its origin in the presence
of _Strongyloides stercoralis_. The parasite does not live only in the
intestinal lumen, but also in the intestinal wall, where it causes
abscesses, fistulæ and effusions of blood.
[779] Seifert, “Sitzungsberichte der phys.-med. Ges. in Würzburg,” 1883.
[780] Leichtenstern, _Arbeiten aus d. kaiserl. Gesundheitsamte_, 1905,
xxii.
[781] Zinn, _Berl. klin. Wochenschr._, 1900, xlix.
[782] Schlüter, “Diss. Kiel,” 1905.
[783] Silvestri, _see_ Schlüter _loc. cit._
[784] Valdes, _ibid._
[785] Trappe, _Deutsch. med. Wochenschr._, 1907.
[786] Fülleborn, _Biol. Abt. d. ärztl.-Vereins in Hamburg_, October 14,
1902.
[787] Bruns, _Münch. med. Wochenschr._, 1907, xix.
[788] Leichtenstern, _Deutsch. med. Wochenschr._, 1898.
[789] Kurlow, _Centralbl. f. Bakt._, 1902.
Diagnosis is easily made by the detection of the actively moving larvæ
in the stools.
Treatment is rather difficult, as it is not always successful in
getting rid of the parasites. Authors differ as to the effectiveness
of extr. fil. maris. Goldmann[790] still considers this preparation
as the most effective; he recommends preliminary treatment with
calomel 0·2 grm. and tuber. jalapæ 0·5 grm. a day before the special
treatment, which consists of gelatine capsules of 15·0 grm. extr.
fil. maris (to be taken in the course of four hours); afterwards
rectified oil of turpentine in gelatine capsules. The thymol treatment
(_vide_ Ancylostomiasis, p. 682), thymol alone or in combination with
calomel (Schlüter,[791] Valdes,[792] Soussino,[793] Goldmann[794]),
has often caused diminution of the number of larvæ, but also often
remains resultless. Teissier[795] maintains that by degrees he procured
complete cure by the administration of mercury in the form of blue
pill. In our case neither thymol nor calomel, santonin, extr. fil.
maris, decoct, rad. granat., had any result whatever. Davaine[796]
believes he attained decrease and final disappearance of the larvæ
by protracted milk-cure. Santonin, tannalbin and other preparations
seem ineffectual. Tannin enemata (Mildner[797]), high injections with
starch enemata (Schlüter[798]), may alleviate in persistent diarrhœa.
Travellers who are visiting regions the native home of Strongyloides
must exercise the most extreme care and scrupulous cleanliness,
and these are also necessary in patients already suffering from
Strongyloides, to prevent auto-reinfection (Trappe[799]).
[790] Goldmann, _Deutsch. Aerzte-Zeitg._, 1903.
[791] Schlüter, “Diss. Kiel,” 1905.
[792] Valdes, _loc. cit._
[793] Soussino, _see_ Schlüter _loc. cit._
[794] Goldmann, _loc. cit._
[795] Teissier, _Arch. d. Méd. exp._, 1895.
[796] Davaine, _see_ Seifert, _Deutsch. med. Zeitg._, 1885.
[797] Mildner, _Berl. med. Ges._, July 24, 1907.
[798] Schlüter, _loc. cit._
[799] Trappe, _loc. cit._
*Dracunculus medinensis* (Dracontiasis).
The guinea worm develops in the dermis of human beings without any
symptoms; only when it is completely grown does it form boil-like,
extremely painful abscesses, in the greater majority of cases in
the legs, in the region of the ankle, and is accompanied by general
disturbance and a feeling of heaviness, dragging and pricking of the
affected part; it occurs more rarely in the arms, certain parts of the
back, the head, neck, scrotum and penis; in a superficial position the
worm can occasionally be felt through the skin. In most cases there is
only one worm and one abscess, but here and there one finds patients
with three, four or even up to eight worms, and very exceptionally
still more, as in the cases described by Poupée-Desportes[800] (fifty
worms) and by Harington[801] (seventeen worms).
[800] Poupée-Desportes, _see_ Looss, “Handb. d. Tropenkrankh.,” 1905, i.
[801] Harington, _Brit. Med. Journ._, 1906.
Diagnosis offers no difficulty when the worms are presenting or can be
felt under the skin.
The inhabitants of the native home of the guinea worm, as a rule,
quietly wait till it has got so far out that it can be conveniently
grasped; it is then bound round with thread and fastened between the
tips of a split piece of wood and slowly wound out. In ten to twelve
days it can be wound out in this way. Emily[802] makes injections of
a 1 in 1,000 solution of sublimate either in the neighbourhood of the
worm or directly into its body. Mense[803] managed to remove the worm
in one sitting by laying a wad of cotton wool soaked in chloroform on
the exposed portion, thus stupefying it. Our therapeutic observations
(Frangenheim[804]) favour the free laying open of the existing abscess
and the consequent complete extraction of the worm.
[802] Emily, _see_ Looss _loc. cit._
[803] Mense, _ibid._
[804] Frangenheim, _Volkmann’s Samml. klin. Vorträge_, 424.
Prophylaxis depends on care in the use of water in the guinea worm
countries, especially dangerous being permanent waters infested by
_Cyclops_ sp.
*Filaria bancrofti.*
The parasitism of this filaria leads to the formation of lymphangitis,
elephantiasis, chyluria, orchitis, chylocele, abscesses, lymphatic
varices, perhaps also to chylous ascites and chylous diarrhœa.
Lymphangitis usually attacks the extremities, beginning generally with
a rigor and swelling of the lymphatic vessels with adjoining lymph
glands. The lymphatics become hard, knotty and extremely painful, the
overlying skin red and swollen in longitudinal lines (Looss), high
fever sets in with, to some extent, severe general disturbance. After
some days the attack subsides, the swelling then partially disappears,
but not completely, and often abscesses develop in consequence of
the lymphangitis. Children, as a rule, suffer from such lymphangitic
attacks (Finucane[805]).
[805] Finucane, _Lancet_, 1907.
Diagnosis is not easy, for many other causes frequently produce
lymphangitis.
Treatment consists in rest, raising the affected limb, applications of
vinegar and alum or liquor plumbi, in some cases incisions into the
swollen part under antiseptic precautions.
_Elephantiasis_ (_Arabian_) is usually situated in the lower
extremities, in men in the scrotum and penis, in women in the labium
pudendi, mons veneris, and the mammæ; more rarely it attacks the upper
extremities or, indeed, the head. The disease develops during repeated
attacks, which occur at irregular intervals of weeks, months or years,
of fever accompanied by symptoms of lymphangitis and erysipelas
(_elephantoid_ fever), and especially as the result of different
accidental occurrences such as chills, bodily exertions, external
irritation. The extremities become shapeless, heavy cylinders, the
scrotum occasionally a colossal tumour, the female genitalia and the
mammæ smaller or larger tumours; the penis often shares in the general
thickening, the inguinal glands form large hard prominent masses, and
enormous deformity is caused. The cause is more often seen in men than
women, rarely in children over 10, never in younger children.
Treatment of elephantiasis of the extremities consists in raising the
affected part, massage, bandaging, vapour baths; the large elephantoid
tumours of the genitalia and mammæ can only be treated by operative
removal.
Chyluria (hæmato-chyluria), as a rule, begins by a series of attacks
and often ceases for weeks or months, the attacks being accompanied by
fever, pain in the back and lumbar region, about the kidneys and in the
perinæum. The attacks are separated by intervals of months’ or even
years’ duration, a continuous chyluria being quite rare. The disease
may last many years without the constitution being markedly weakened,
but in other cases anæmia and debility ensue and result in death from
marasmus. In chyluria the urine becomes completely opaque like milk;
but sometimes, from the presence of blood, is of a peach-like redness:
the sediment contains clotted blood, and microscopically one finds
fine dust-like fat granules and red cells and leucocytes, and usually,
but not always, filaria larvæ. Sclerodermia may possibly be caused by
Filaria (Bancroft[806]).
[806] Bancroft, _Lancet_, 1885.
Treatment, consists in administration of ol. santali, methylene blue
(0·12 grm. dose several times daily), ichthyol (in pills from 0·5 to
1·5 grm. per day), ol. terebinthinæ (0·5 to 1·5 gr. per day), thymol
(Ziemann[807] had no result from either thymol or methylene blue),
together with absolute rest in bed, diminution of all fatty nourishment
and administration of light purgatives.
[807] Ziemann, _Deutsch. med. Wochenschr._, 1905, xi.
Orchitis is in acute attacks a relatively frequent symptom in the East;
the chylocele is rarely marked; the fluid usually shows numerous
larvæ; in the case of abscesses they are generally caused directly by
the adult parasites, as they have often been found in them; varices of
the lymphatic vessels are either superficial or deep; lymphorrhagia
arises from rupture of the dilated vessels; chylous ascites and chylous
diarrhœa may also be produced by Filariæ.
*Loa loa.*
_Loa loa_, according to modern investigations, is a parasite of
the subcutaneous connective tissue of man, and its appearance in
the conjunctiva somewhat accidental; in earlier times it seems to
have been less common (Ziemann[808]). A number of cases are seen in
Europe of patients who have lived in filaria regions, and on return
have been found to have this Nematode in the subconjunctival tissue.
Pick,[809] in the case of a man who had lived in the Cameroons, found
the parasites in active motion under the connective tissue of the
eyeball right over the cornea; extraction was easy. Ziemann[810] noted
three cases of _Loa loa_ in the eye accompanied by temporary migratory
swellings in different parts of the body. In one case, observed by
Wurtz and Cleri[811] (a woman from the French Congo), _Loa loa_ was
the cause of intermittent elastic swellings in the subcutaneous and
subconjunctival tissue (marked eosinophilia). In the case recorded by
Pollack[812] (for thirty years police commissioner in the Cameroons)
the worm under the connective tissue of the left eye by its snake-like
movements caused an unpleasant itching. With cocaine and adrenalin
the worm can be made visible, and by means of a strabismus hook can
be drawn out of a small wound in the connective tissue. Martens[813]
exhibited a Filaria extracted from the eyelid under local anæsthesia.
[808] Ziemann, _Deutsch. med. Wochenschr._, 1905.
[809] Pick, _ibid._
[810] Ziemann, _loc. cit._
[811] Wurtz and Cleri, _Arch. Méd. expér._, 1905, ii.
[812] Pollack, _Berl. ophthal. Ges._, May 17, 1906.
[813] Martens, _Berl. med. Ges._, July 24, 1907.
*Trichuris trichiura.*
Whilst many authors consider the whip-worm as a harmless parasite
of the large intestine (Leichtenstern,[814] Eichhorst,[815]
Askanazy[816]), the number of severe and even fatal cases of diseases
caused by it (trichocephaliasis) increase so much that the _Trichuris
trichiura_ must be excluded from the group of harmless intestinal
parasites. (For disturbances of the nervous system and of the blood
[anæmia] from trichocephaliasis, _see_ p. 650). Infection in human
beings results from the eggs that have developed outside the body,
which probably reach the digestive tract on the hands soiled with dirt
or earth, or possibly through drinking water. (Moosbrugger[817] and
Kahane[818] mention in their cases that the children had an absolute
passion for earth-eating.) Possibly, too, patients reinfect themselves
anew, as an intermediate host is not necessary.
[814] Leichtenstern, “Handb. d. Therap. v. Pentzoldt-Stintzing.”
[815] Eichhorst, “Handb. d. Spez. Path. u. Therap.”
[816] Askanazy, _Deutsch. Arch. f. klin. Med._, 1896.
[817] Moosbrugger, _Med. Corresp.-Bl. f. Württemburg_, 1890.
[818] Kahane, _Korrespondenzbl. f. Schweiz. Aezte_, 1907, viii.
The anterior part of the body of the parasite is usually fixed in the
mucous membrane, and according to Askanazy feeds on the blood of its
host. Moosbrugger,[817] Schulze,[819] Kahane,[818] Vix,[820] Girard[821]
and Blanchard[822] all found changes in the mucous membrane of the
gut, showing that the parasites had been in the gut for a considerable
time. Kahane[818] had an opportunity of seeing at the Pasteur Institute
Trichocephali with the anterior part of the body penetrating not
only the mucosa but also deep into the muscularis of the gut wall.
From this mode of attachment to the wall it is easily understood how
Trichocephali, especially when they are numerous in the gut, cause
local irritation and inflammatory conditions consisting of frequent
attacks of diarrhœa, sometimes twenty times a day, lasting for months,
resisting all remedies, and often accompanied by colicky pains and
symptoms of peritonitis. The stools often have blood mixed with the
fluid, very glassy, jelly-like mucus, more or less abundantly as in
the cases of Moesasca, Moosbrugger,[817] Kahane,[818] Girard,[821]
Poledne,[823] and Rippe.[824] Nausea and vomiting are rarer symptoms.
[819] Schulze, _Deutsch. med. Wochenschr._, 1905.
[820] Vix, _Zeitschr. f. Psychiat._, xvii.
[821] Girard, _Annal. d. l’Inst. Pasteur_, 1901.
[822] Blanchard, _Acad. de Méd._, July 3, 1906.
[823] Poledne, _Wien. med. Wochenschr._, 1906.
[824] Rippe, _St. Petersb. med. Wochenschr._, 1907.
Diagnosis as a rule can only be made by microscopical examination of
the stools; together with the eggs, regular and beautifully formed
Charcot-Leyden crystals occur.
The prognosis is unfavourable in severe infections, in slighter cases,
where only a few worms are present, the danger of important symptoms
is less. Treatment consists in administration _per os_ of vermicides
and in local treatment of the large gut. A remedy which was once much
used was calomel, which is much lauded by Gibson and given as follows:
calomel 0·06 grm., rheum. 0·3 grm., tinct. ferri sesquichlor. 1·2 c.c.,
aq. dest. 90·0 grm., six dessert-spoonfuls three times daily. Rippe
appears to have got no result from the use of this prescription.
Thymol, especially in conjunction with local treatment of the large
intestine, had unquestionably some effect in certain cases, such as
those of Girard, Poledne, Hausmann, Kahane and Schiller. The local
treatment of the large bowel is most effectual when high injections
of water and benzine are given. Becker[825] obviously used too much
benzine (1 dessert-spoonful to 1 litre of water), for severe irritation
was set up, whilst Peiper[826] used only a few drops of benzine, 5
drops to 1 litre of water being enough (Schiller). Instead of benzine
enemata, garlic, 1 per cent. thymol solution, and physiological saline
injections have been used, but the benzine enemata seem to be far and
away the most effective. In Schiller’s case 2,000 worms came away
on the first day as the result of such a combined treatment (thymol
internally and benzine enemata).
[825] Becker, _Deutsch. med. Wochenschr._, 1902.
[826] Peiper, quoted by Seifert, _loc. cit._, p. 248.
Trichinella spiralis.
Trichinosis is, happily, becoming so much rarer that many doctors get
no opportunity, either in their student days or in private practice,
of seeing this severe disease; we ourselves remember having observed
one typical case of a peasant, aged 17, from Metz in Med.-Rat Merkel’s
clinic in Nuremberg in the year 1879. In the description of the disease
we follow Merkel’s[827] observations.
[827] Merkel, “Handb. d. Therap. v. Pentzoldt-Stintzing,” i.
The eating of flesh containing Trichinæ is often followed, if not
invariably so, by gastric disturbances of different kinds, especially
by vomiting and diarrhœa, with colic, great muscular fatigue, œdema of
the eyelids, muscular swellings with hardness and extreme painfulness,
disturbance of ocular movements, of deglutition and of breathing,
hoarseness, aphonia, intestinal hæmorrhage, bleeding of the nose,
ecchymosis of the skin and mucosæ, prurigo, herpes, miliaria, pustules,
boils, severe sweating, œdema of the extremities, and, finally,
desquamation of the skin; more rarely there is considerable decubitus,
bronchial catarrh, hypostatic and catarrhal pneumonia, with dry and
purulent pleurisy, and in severe cases symptoms of collapse with
delirium close the scene. Slight cases last from three to six weeks,
severe ones for several months, and in the latter convalescence is very
slow. It is remarkable that in cases of trichinosis of long duration,
cancer of the breast was observed at the same time (Klopsch,[828]
Langenbeck,[829] Babes[830]). Death during epidemics occurred in 30 per
cent. of all cases. The disease begins generally from one to ten days
after eating trichinous flesh, yet there have been cases noted in which
the disease began several weeks after.
[828] Klopsch, quoted by Babes.
[829] Langenbeck, _ibid._
[830] Babes, _Centralbl. f. Bakt._, 1906, xlii.
Diagnosis in the presence of several cases, or in epidemics, is not
difficult, but in isolated cases, on the other hand, it is not easy.
If there is a suspicion of trichinosis, from the muscular fatigue and
the œdema of the eyelids, the diagnosis can be made by excision of a
piece of muscle and by finding the Trichinæ in the tissue, taken with
the results of the examination of the previously eaten sausage or meat.
In contradistinction to this circumstantial process, there is the
examination of the blood, which, according to Schleip[831] (Homburg
trichinosis epidemic, August 19 to 26, 1903, 130 cases), is the most
valuable method of diagnosing trichinosis when the Trichinæ have not
yet penetrated the muscles, for a blood examination shows a large
increase in the numbers of the eosinophile cells; Stäubli detected
his seven cases in this way, four of the severe ones showing a marked
hyperleucocytosis, and a combination of Kernig’s sign with absence of
the patellar reflex. On account of the rarity of these two signs in
combination in other infective diseases, they have a certain diagnostic
value. Stäubli[832] also observed in trichinosis the constant
appearance of a remarkably strong positive diazo-reaction of the urine.
[831] Schleip, _Deutsch. Arch. f. klin. Med._, lxxx.
[832] Stäubli, _ibid._, lxxxv.
Prophylaxis in trichinosis is fully considered under _Trichinella
spiralis_ (p. 429).
Treatment consists in those cases where it is known that trichinous
flesh has been swallowed in the first place of washing out the stomach,
but still more in a thorough evacuation of the bowels, for which
calomel (0·5 grm.), ol. ricini (a dessert-spoonful till the action
becomes marked), infusion of senna with sulphate of magnesia and large
enemata are employed, and should be repeated at intervals during the
first few weeks. Alcohol (cognac up to 250 c.c. a day) is recommended
by some, also glycerine (150 grm. at a dose) and large doses of dilute
hydrochloric acid. Beside these, a large number of other remedies are
recommended, of which, perhaps, benzine and thymol, especially in the
form of enemata, are worthy of notice.
When the disease is fully developed the treatment should be
symptomatic; a protracted practically continuous luke-warm bath is
especially useful.
Eustrongylus gigas.
_Eustrongylus gigas_ is most frequently found in the pelvis of the
kidney. Infection in the majority of cases leads to pyelitis. The
inflammation extends to the capsule from the pelvis, resulting in a
purulent nephritis. In infections of longer duration, the affected
kidneys become changed into so-called kidney sacs, while the kidney
itself continuously shrinks. Owing to the worm fixing its posterior end
in the ureter, and owing to an inflammatory swelling of the mucosa of
the ureter, the passage of urine becomes very difficult.
The symptoms resemble those caused by a foreign body, _e.g._, kidney
pain, suppression of urine, dysuria, discharge of blood and pus with
the urine. But these symptoms are not sufficient for a diagnosis; this
can only be established by finding eggs or the parasite itself in the
urine.
Moscato[833] records a case with chyluria, pain in the region of the
right kidney, and hysterical symptoms. During an hysterical attack
a specimen of _Eustrongylus gigas_ was discharged in the urine, and
the chyluria and nervous affections disappeared. In a case described
by Stuertz[834] of an Australian with chyluria due to _Eustrongylus
gigas_ the chyluria had existed for seven years. In the urine the eggs
of _Eustrongylus gigas_ were found. The cystoscopic examination showed
that turbid urine was discharging from the left ureter. Nephrectomy was
considered.
[833] Moscato, quoted by Predtetschensky, _Zeitschr. f. klin. Med._, xl.
[834] Stuertz, _Ges. d. Charité-Aerzte in Berlin_, June 26, 1902.
*Ancylostoma duodenale* (Ancylostomiasis).
Whilst up to quite modern times it has been generally maintained that
the great majority of worm diseases cause more or less marked symptoms,
the exact investigations of the last few years have made it plain
that the great majority of people with worms are not only perfectly
healthy, but the most careful clinical observations show no single sign
of any ill-effect of the intestinal parasites on the health of the
host (Löbker and Bruns[835]). If infection has led to the development
of only a few ancylostomes, then injury to the general health is, as
a rule, scarcely noticeable. In order to produce severe illness the
presence of several hundred worms in the intestine is necessary, and
in general the intensity of illness varies in exact proportion to the
number of worms. Then the duration of the infection comes into play:
the longer the human organism is submitted to the injurious effect
of the parasite, the clearer is the effect on the host. Besides, the
resistance of the individual has to be considered. Whilst a more robust
person can harbour without ill-effect for a longer time a larger number
of ancylostomes, the symptoms of the disease become more markedly and
much sooner apparent in weakly persons or in those weakened by other
diseases.
[835] Löbker and Bruns, _Arb. aus. dem. kaiserl. Gesundheitsamte_,
1906, xxiii.
The first symptom is disturbance of the digestive system; more often
there is a feeling of pain in the epigastrium, more severe upon
pressure, heartburn, nausea, vomiting of mucus or food at different
times of the day (occasionally ancylostome ova have been found in the
vomit). Whether the eggs which reach the frontal sinus with the vomit
can develop into larvæ there is questionable, but the records of v.
Ziemssen[836] and Huppertz,[837] to the effect that in some instances
ancylostomes have been discharged from the frontal sinus, are of
interest. The five cases recorded by the latter had a fatal termination
from œdematous swellings of the face with severe inflammation of the
meninges. The tongue is furred, and extensive catarrhal stomatitis
and ptyalism are recorded. The appetite is variable, increasing or
diminishing, there is loathing of nourishment or a marked longing for
acid food and unripe fruit, whilst ordinary meals are rejected. At
first there is often constipation, later diarrhœa with abundant mucus,
and often blood in the stools; microscopically eggs and Charcot-Leyden
crystals were found.
[836] v. Ziemssen, quoted by Haenisch, “Diss. Strasburg,” 1901.
[837] Huppertz, quoted by Haenisch, “Diss. Strasburg,” 1901.
In the further course of the disease symptoms due to increasing anæmia
predominate; the hæmoglobin of the blood diminishes from one-fourth
to one-fifth of the normal (Baravalle[838]), the eosinophile cells
increase considerably (Boycott,[839] Lohr[840]), yet in regard to
diagnosis eosinophilia cannot be regarded as of equal value to
a microscopical examination of the fæces (Bruns, Liefmann, and
Meckel[841]). The disturbances of the circulatory system take the form
of more or less severe palpitation, pain in the region of the heart,
quick pulse, œdema of the eyelids, of the face, of the lower limbs, and
even of the whole body. Disturbance of the sexual functions (impotence,
irregular menstruation, delayed onset of puberty) are not infrequently
observed.
[838] Baravalle, _Progresso medico_, 1903.