Weil's Disease

Weil's Disease, an acute infectious disease characterized by jaundice, early enlargement of the liver and spleen, and often also by significant changes in the kidneys. - Virchow's theory of catarrhal jaundice as a local process was most popular in the second half of the 19th century, despite the fact that clinical pathology and anatomy did not always confirm this view. S.P. Botkin was the first to oppose Virchow's view. Based exclusively on his clinical observations, he came to the conclusion that icterus catarrhalis in all cases is an acute infectious form, in which gastrointestinal catarrhal jaundice, changes in the liver, spleen and kidneys are merely symptoms of infection. Following Botkin, Chauffard and Landouzy expressed the same point of view. In 1886, A. Weil described a special form of acute infection, characterized by enlargement of the liver and spleen, jaundice and nephritis. According to Weil, this disease may occur sporadically and epidemically. Goldschmidt named this form morbus Weili. Although many authors tend to distinguish Weil's form from other clinical forms of infectious jaundice, familiarity with the clinic of jaundice convinces that it is completely impossible to draw a line between cases of simple, so-called catarrhal jaundice and mild cases of Weil's form, on the one hand, and severe cases of Weil's form and icterus gravis, often ending in acute yellow atrophy of the liver, on the other hand. All these forms are observed during the same epidemic; even members of the same family may have different forms of jaundice. Schwager collected 1,343 cases of B.-V. disease from mild to severe, with a whole series of intermediate forms, and noted a definite rise in diseases in the autumn, as well as the fact that this disease, without ceasing, flares up through strictly defined intervals - namely, every 4 years. The factor that brings all these forms together is the same specific causative agent. - Etiology. Discovered in 1915 by the Japanese Inado, together with Ido, Hoki, Kanneko and Ito, the causative agent of epidemic jaundice, named by them Spirochaeta ictero-haemorrhagica, was also found in catarrhal jaundice and in icterus gravis. With the discovery of the causative agent of epidemic jaundice, the exact systematic name of which is Leptospira ictero-haemorrhagica, it became possible to study the epidemiology of this disease more correctly. Research by Japanese and German bacteriologists (Hübener and Reiter, Uhlenhuth and Fromme) proved that rats are carriers of epidemic jaundice spirochetes. While remaining completely healthy, spirochete carriers from time to time may excrete spirochetes with urine, which, getting into the soil, water or food products, are easily carried from there into the human digestive tract, or through the skin and conjunctiva directly into the blood. From an epidemiological point of view, it is extremely important that Weil's jaundice spirochetes are widely distributed in contaminated waters, from which they can penetrate the human body in various ways (drinking, bathing) and cause characteristic infection (see Spirochetes). The incubation period lasts from one to two weeks. Patients with epidemic jaundice also excrete spirochetes with urine, which in turn are a source of infection for rats. Epidemic jaundice is apparently observed everywhere. Rat spirochetosis is particularly widespread in Japan and in some states of America. - In pathoanatomical terms, epidemic jaundice represents a general septic disease characterized by jaundice, hemorrhages in the skin, mucous membranes, muscles and internal organs, and degenerative changes in all parenchymatous organs. The liver shows no specific changes; it is usually enlarged, markedly jaundiced; under the microscope, a poorly expressed dissociation of trabeculae and 'pericapillary' edema are found, i.e., expansion of the lymphatic spaces located between the capillaries and trabeculae. The presence of fat in Kupffer cells, infiltration of connective tissue with lymphoid elements, and phenomena of regeneration of liver cells at the periphery of lobules are often observed. Sometimes the liver shows changes characteristic of acute yellow atrophy of the liver. Obstructions or catarrhal swelling of the large bile ducts are never found. The small bile ducts and capillaries are often inflamed, and their lumen is closed with plugs of desquamated epithelium and leukocytes, which, however, cannot be considered as an obstacle to the movement of bile. In the kidneys, necrotic nephrosis and infiltration of the interstitial tissue are observed; quite typical is the change in muscles in the form of foci of wax-like degeneration with hemorrhages. C l i n i c a l. 1-2 weeks before the onset of the disease, patients experience severe headaches, pains in the lower back, calves and joints; then gastrointestinal phenomena, chills and even chills with significant increases in temperature join in. The temperature usually remains at high figures for about 5 days, then falls lytically and remains normal for 4-8 days, only to give a new rise at the end of the second or beginning of the third week. Usually during the first febrile period, and sometimes at the beginning of the interfebrile period, jaundice suddenly develops, accompanied by enlargement and density of the liver and spleen. In its nature, jaundice in V.-V. d. is considered as diffuse jaundice, depending on damage to liver cells by infection, as a result of which bile begins to enter not the bile capillaries, but directly into the blood (paracholic jaundice). The second moment causing jaundice lies in the enhanced delivery to the liver of bilirubin formed from disintegrating red blood cells. Since part of the bile constantly enters the bile ducts, the stool in epidemic jaundice, as a rule, is not acholic. There are indications that sometimes B.-V. d. may occur without or almost without jaundice. The phenomena of hemorrhagic diathesis that develop during epidemic jaundice must be put in a causal relationship with intoxication, and not with jaundice as such, since they can occur very early and do not always correspond to the degree of jaundice. A number of phenomena from the nervous system are very often noted - insomnia, clouding of consciousness, cerebral phenomena. Changes in urine are detected very early; in it are found: bile pigments, slight albuminuria, significant cylindruria, renal epithelium, leukocytes and erythrocytes. In the blood - phenomena of moderate leukocytosis with absolute lymphopenia and slight anemia. During the first period of the disease, in the blood, in transmitted light, spirochetes are sometimes found. By inoculating an animal with the patient's urine, and sometimes by direct bacterioscopic examination of smears from the urine sediment stained by Giemsa, it is possible to detect spirochetes. Depending on the severity of the clinical course, three forms of epidemic jaundice are distinguished. The mildest form, ic. infect. benignus, better known under the name ic. catarrhalis; a form of moderate severity, which is mainly given the name of Weil's disease, and the severe form - ic. gravis, often ending in acute yellow atrophy of the liver. Based on the observation of an epidemic of jaundice on the Romanian front during the imperialist war, Buhstab and Oke believe that the clinical picture of B.-V. d. is not uniform. There were patients in whom a disease that began mildly ended in acute yellow atrophy of the liver. In general, this is a severe infectious disease affecting mainly three organs: the liver, spleen and kidneys, but accompanied by general phenomena of an intoxication nature. The total duration of the disease is 3-4 weeks. Recovery occurs very slowly. The mortality rate for epidemic jaundice in Europe averages 3-4%, in Japan it reaches 25%. After the disease, a stable immunity remains. T r e a t m e n t of B.-V. d. is symptomatic. Specific serotherapy is willingly used by Japanese doctors. When cases of epidemic jaundice appear, the doctor's attention should be directed to taking preventive measures, consisting in drying the soil, deratization and disinfection of all patient excretions.

L. Buznptab, A. Oke. Weil's Disease in children is observed, mainly, in the form of mild catarrhal jaundice, rarely taking a very severe course (cholemia, death). Family (Krasnobayev) and intra-hospital epidemics have been observed. Children of all ages, starting from the first months of life, get sick. Very often there is no increase in temperature. It was rarely possible to find spirochetes in the urine or blood of patients. The enlarged and very dense liver sometimes remains for a long time. Relapses were often observed. The seasonality of the disease is very characteristic - mainly in the autumn (Schwager). The mortality rate ranges from 2 to 7. A second case of B.-V. d. in children has not been observed.