Chapter XXXIII: Introduction (2)

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.