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Leptospirosis hepatitis
Last reviewed: 12.07.2025

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Leptospirosis is widespread on all continents. At the end of the 19th century, the German physician A. Weil (1886) and the Russian researcher N.P. Vasiliev (1889) reported a special form of infectious jaundice, which occurs with damage to the liver, kidneys and hemorrhagic syndrome. This new nosological form was called Weil-Vasiliev disease. In 1915, the causative agent of the disease, leptospira, was discovered.
Currently, leptospirosis is well studied, including in the Russian Federation.
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Causes of Leptospirosis Hepatitis
Leptospira are bacteria belonging to the Leptospiraceae family, genus Leptospira. There are two types of leptospira: pathogenic leptospira L. interrogans, which parasitize the body of humans and animals, and saprophytic leptospira L. biflexa, which are not pathogenic for warm-blooded animals.
The main etiologic agents of leptospirosis in humans are representatives of the following serogroups: Icterohaemorhagiae, Pomona, Grippotyphosa, Canicola, Sejroe, Hebdomadis, Autumnalis, Australis, Bataviae.
Leptospires enter the human body through damaged skin, mucous membranes of the oral cavity, digestive tract, eyes, nose. There are no inflammatory changes at the entry gate. From the entry gate, leptospires enter the blood and then into the internal organs, where they multiply, especially intensively in the liver and kidneys.
Leptospires produce toxins, which, along with bacterial decay products, have an activating effect on inflammatory mediators that damage the liver and kidney parenchyma, as well as the walls of blood vessels. Leptospires are able to penetrate the cerebrospinal fluid and cause damage to the membranes of the brain. The cause of severe forms, complications leading to death is the development of infectious toxic shock.
With the diversity of leptospira serogroups, the pathophysiological and pathomorphological essence of the processes occurring during infection with leptospira is the same, and therefore leptospirosis is considered a single disease. The severity of the disease is determined by the degree of virulence of the pathogen, the routes of infection and the state of the macroorganism.
Morphology
Liver damage is extremely characteristic of leptospirosis. Macroscopically: the liver is enlarged, its surface is smooth, greenish-brown, easily torn. The lymph nodes in the liver gates are enlarged, up to 10 mm in diameter, juicy.
Histological examination of the liver reveals discomplexation of the liver beams, dystrophic changes in hepatocytes, uneven sizes of liver cells and their nuclei, and the presence of binuclear cells. Microscopically, the liver has a "cobblestone" appearance. Inflammatory lymphohistiocytic infiltrates of varying severity are noted.
Initially, the infiltration is weak, but as the disease progresses, it can significantly increase, localizing around the portal tracts and inside the liver lobules. Infiltrates contain an admixture of single segmented neutrophils. Due to parenchymal edema and discomplexation of the liver beams, the yellow capillaries are compressed: cholestasis in the capillaries is significantly expressed. When silvering according to Vartan-Sterry, twisted black leptospires are detected on the surface of hepatocytes.
Symptoms of Leptospirosis Hepatitis
The incubation period varies from 6 to 20 days. The disease begins acutely, with a rise in body temperature to febrile levels. Patients complain of headaches and insomnia. Characteristic are pains in the calf muscles, back muscles, and shoulder girdle. On the 3rd to 6th day from the onset of the disease, 10-30% of patients develop a rash on the skin of the chest, neck, shoulders, abdomen, and limbs, which can be maculopapular, punctate, or petechial. During these days, 30-70% of patients develop jaundice of varying severity. An increase in the size of the liver is noted in almost all patients, while the liver is sensitive and palpated 2-5 cm below the costal margin.
In children, along with icteric, anicteric forms of leptospirosis are often observed. In adults, leptospirosis occurs mainly in the icteric form - in 61% of cases. In adult patients, in 85% of cases, leptospirosis manifests itself in a severe form with the development of acute renal and hepatic failure.
Children suffer from leptospirosis in mild and moderate forms.
A biochemical blood test shows an increase in bilirubin levels due to the conjugated pigment fraction (3-10 times). At the same time, aminotransferase activity increases quite moderately, 2-3 times higher than normal. An increase in urea, creatinine, and CPK levels is typical.
A clinical blood test in most patients with leptospirosis is characterized by leukocytosis, a shift in the leukocyte formula to the left, thrombocytopenia, anemia, and an increase in ESR.
From the first days of the disease, signs of kidney damage are noted: oliguria, albuminuria, cylindruria.
The course of leptospirosis hepatitis
The disease usually lasts 4-6 weeks. Fever persists for 3-5 days, intoxication weakens after 5-6 days. Jaundice is very persistent and lasts 7-15 days. Gradually, over 2-4 weeks, the liver returns to normal.
Leptospirosis is characterized by relapses (from one to four) lasting 1-6 days; relapses are milder than the main disease. Complications include infectious toxic shock, pyelitis, eye damage (uveitis, keratitis), and residual effects of meningitis.
In severe icteric forms, especially with damage to the central nervous system and kidneys, mortality reaches 10-48%. Most patients have a favorable prognosis, recovery occurs. The formation of a chronic process is not observed.
Diagnosis of leptospirosis hepatitis
To diagnose leptospirosis, clinical and epidemiological data are taken into account. Staying in a natural leptospirosis hotbed, contact with animals, eating contaminated food, and swimming in forest water bodies are important.
Microbiological diagnostics of leptospirosis hepatitis is aimed at detecting leptospires in biological materials from the patient. In the first week from the onset of the disease, blood is examined to identify the pathogen. Isolation of blood culture is a reliable method for identifying leptospires, giving a positive result in more than 80% of cases.
On the 2nd-3rd week of the disease, a bacteriological examination of urine and cerebrospinal fluid is performed for leptospira. During the recovery period, urine culture is performed.
From the end of the first week of the disease, a serological test is performed for the presence of specific (antileptospirosis) antibodies using the methods of RPGA, RSK, RIGA, ELISA, etc. Among serological methods, preference is given to the microagglutination reaction, which has high sensitivity and serogroup specificity. With the help of this reaction, specific agglutinins of the IgM and IgG class isotypes are detected. In this case, RMA is used to determine specific antibodies both in current leptospirosis and for retrospective diagnostics. In recent years, PCR has been used to detect leptospira DNA in biological materials from patients.
In connection with the appearance of jaundice and hepatomegaly, it is necessary to exclude viral hepatitis. Among the initial diagnoses for leptospirosis, the diagnosis of viral hepatitis is the leading one - up to 10% of cases.
Unlike leptospirosis, viral hepatitis begins gradually, fever is uncharacteristic, the rise in body temperature is short-term - 1-3 days. At the same time, severe pain in the right hypochondrium and epigastrium is noted. The liver is painful on palpation. There is no renal syndrome or meningeal syndrome with viral hepatitis. Unlike leptospirosis, hyperenzymemia is typical for viral hepatitis, when the activity of ALT and AST is 10-20 times higher than normal, including in anicteric forms. A clinical blood test in patients with viral hepatitis is usually normal. Serological testing in patients with leptospirosis shows negative results for viral hepatitis markers.
Differential diagnostics of leptospirosis with hemorrhagic fevers is carried out, since the latter are characterized by intoxication, hemorrhagic and renal syndromes.
Treatment of leptospirosis hepatitis
Patients with leptospirosis are subject to hospitalization. Bed rest and a dairy-vegetable diet are recommended.
Etiotropic therapy consists of prescribing antibiotics of the penicillin or tetracycline groups in the early stages of the disease. In severe forms of leptospirosis, glucocorticoids and cardiovascular drugs are indicated. In renal failure with increasing azotemia, hemodialysis is indicated.
Leptospirosis convalescents are observed for 6 months by an infectious disease specialist; if necessary, consultations with an ophthalmologist and neurologist are conducted.
Prevention of leptospirosis hepatitis
A program of measures for the prevention of leptospirosis has been developed. It provides for monitoring the state of natural and anthropogenic foci endemic for leptospirosis, health education of residents of these regions, as well as vaccination of all those who, due to various circumstances, especially professional ones, are at risk of infection with leptospirosis.
A concentrated inactivated liquid leptospirosis vaccine has been created and is being successfully used. It is a mixture of inactivated concentrated cultures of leptospira of four serological groups (Icterohaemorhagiae, Grippotyphosa, Pomona, Sejroe). The vaccine ensures the development of specific immunity lasting for 1 year. Specific vaccination begins at the age of 7 years.