Leptospirosis hepatitis

Leptospirosis is widespread on all continents. At the end of XIX century. German physician A. Weyl (1886) and Russian researcher N.P. Vasiliev (1889) reported a special form of infectious jaundice, which occurs with liver, kidney and hemorrhagic syndrome. This new nosological form was called Weil-Vasiliev's disease. In 1915, the causative agent of the disease - leptospira was discovered.

Currently, leptospirosis is well studied, including in the Russian Federation.

[1],

Causes of leptospirosis hepatitis

Leptospira are bacteria belonging to the family Leptospiraceae, the genus Leptospira. There are two types of leptospira: pathogenic leptospira L. Interrogans, parasitizing in humans and animals, and saprophytic leptospires - L. Biflexa, not pathogenic for warm-blooded.

The main etiological agents of leptospirosis in humans are representatives of the following serogroups: Icterohaemorhagiae, Pomona, Grippotyphosa, Canicola, Sejroe, Hebdomadis, Autumnalis, Australis, Bataviae.

Leptospira penetrate the human body through damaged skin, mucous membranes of the mouth, digestive tract, eyes, nose. In the site of the entrance gates there are no inflammatory changes. From the entrance gates leptospira get into the blood and then into the internal organs, where they reproduce, especially intensively in the liver and kidneys.

Leptospira produce toxins, along with the products of bacterial decay, which have an activating effect on inflammatory mediators, damaging the liver and kidney parenchyma, as well as the walls of blood vessels. Leptospira can penetrate into 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 an infectious-toxic shock.

With the diversity of serogroups of leptospira, the pathophysiological and pathomorphological nature of the processes that occur when leptospira is infected is the same, and therefore leptospirosis is considered as a single disease. The severity of the disease determines the degree of virulence of the pathogen, the pathway of infection and the state of the macroorganism.

[2], [3], [4], [5]

Morphology

The defeat of the liver is extremely characteristic of leptospirosis. Macroscopically: the liver is enlarged, the surface is smooth, greenish-brown, easily torn. Lymph nodes in the gates of the liver are enlarged, with a diameter of up to 10 mm, juicy.

Histological examination in the liver determines the discomplexation of the hepatic beams, the dystrophic changes in hepatocytes, the irregularity of the dimensions of liver cells and their nuclei, the presence of dual nuclei. Microscopically, the liver looks like a "cobblestone pavement". Inflammatory lymphohistiocytic infiltrates of different degree of severity are noted.

Initially, the infiltration is weak, and as the disease progresses, it can appreciably increase, localizing around the portal tracts and inside the hepatic lobules. In infiltrates, an admixture of single segment neutrophils is noted. Due to the edema of the parenchyma and the discomplexation of the hepatic beams, the yellow capillaries are compressed: cholestasis in the capillaries is markedly expressed. When silvering on the Vartan-Sterry, the crimson leptospira of black color appear on the surface of the hepatocytes.

Symptoms of leptospirosis hepatitis

The incubation period varies from 6 to 20 days. The disease begins acutely, with the rise in body temperature to febrile indices. Patients complain of a headache, insomnia. Characteristic are pain in the calf muscles, back muscles, and the shoulder girdle. On the 3rd-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 extremities, which can be spotty-papular, small-spotted, petechial. On the same days, jaundice of varying severity develops in 30-70% of patients. There is an increase in liver size in almost all patients, while the liver is sensitive and palpable 2-5 cm below the rib margin.

In children, along with icteric, often without jaundiced forms of leptospirosis. In adults, leptospirosis mainly occurs in icteric form - in 61% of cases. In adult patients, in 85% of cases, leptospirosis manifests in severe form with the development of acute renal-hepatic insufficiency.

Children suffer from leptospirosis in mild and moderate form.

In the biochemical analysis of blood, an increase in the level of bilirubin due to the conjugated fraction of the pigment (3-10 times) is recorded. At the same time, the activity of aminotransferases increases very moderately, 2-3 times higher than normal. Characteristic increase in the levels of urea, creatinine and CKK.

Clinical analysis of blood in most patients with leptospirosis is characterized by leukocytosis, a shift of the leukocyte formula to the left, thrombocytopenia, anemia and an increase in ESR.

From the first days of the disease, there are signs of kidney damage: oliguria, albuminuria, cylindruria.

The course of leptospirosis hepatitis

The disease usually lasts 4-6 weeks. Fever persists for 3-5 days, intoxication weakens in 5-6 days. Jaundice is very stubborn and lasts 7-15 days. Gradually, within 2-4 weeks, the liver returns to normal limits.

For leptospirosis relapses (from one to four) lasting 1-6 days are characteristic; relapse occurs more easily than the underlying disease. As complications there are infectious-toxic shock, pyelitis, eye damage (uveitis, keratitis), residual phenomena of meningitis.

In severe icteric forms, especially with CNS and kidney damage, lethality reaches 10-48%. In most patients, the prognosis is favorable, recovery occurs. Formation of a chronic process is not observed.

Diagnosis of leptospirosis hepatitis

Clinical and epidemiological data are used to diagnose leptospirosis. It is important to stay in the natural focus of leptospirosis, communication with animals, eating contaminated foods, bathing in forest reservoirs.

Microbiological diagnosis of leptospirosis hepatitis is aimed at detecting leptospira in biological materials from a patient. In the first week from the onset of the disease, the blood is examined to identify the pathogen. The isolation of the blood culture serves as a reliable method of identifying leptospira, which gives a positive result in more than 80% of cases.

At the 2-3rd week of the disease, a bacteriological study of the urine and liquor on the leptospirae is carried out. In the period of convalescence, uricoculture is isolated.

From the end of the 1st week of the disease, a serological test is conducted for the presence of specific (anti -leptospirosis ) antibodies using the methods of PGA, RSK, RIGA, ELISA, etc. Among the serological methods, a microagglutination reaction with high sensitivity and serogroup-specificity is preferred. With the help of this reaction, specific agglutinins of isotype types IgM and IgG are found. In this case, PMA is used to determine specific antibodies for both current leptospirosis and for retrospective diagnosis. In recent years, for the detection of DNA leptospira in biological: materials from patients using PCR.

In connection with the appearance of jaundice and hepatomegaly, it becomes necessary to exclude viral hepatitis. Among the initial diagnoses with leptospirosis, the diagnosis of viral hepatitis is leading - up to 10% of cases.

Unlike leptospirosis, viral hepatitis begins gradually, the fever is uncharacteristic, the rise in body temperature is short-term - 1-3 days. However, marked pain in the right hypochondrium and epigastrium. With palpation, the liver is painful. With viral hepatitis there is no kidney syndrome, and also meningeal. In contrast to leptospirosis, hyperfermentemia is typical for viral hepatitis, when ALT and ACT activity is 10-20 times higher than normal, including those with anicteric forms. Clinical blood test in patients with viral hepatitis is usually normal. Serologic examination in patients with leptospirosis has negative results on the markers of viral hepatitis.

Differential diagnostics of leptospirosis with hemorrhagic fevers is carried out, since the latter are characterized by intoxication, hemorrhagic and renal syndromes.

[6], [7]

Treatment of leptospirosis hepatitis

Patients with leptospirosis are hospitalized. Showing bed rest and milk-vegetable diet.

Etiotropic therapy consists in prescribing antibiotics of penicillin or tetracycline groups in the early stages of the disease. In severe forms of leptospirosis, glucocorticoids, cardiovascular drugs are shown. With renal failure with increasing azotemia hemodialysis is indicated.

Convalescents of leptospirosis are observed for 6 months by an infectious disease specialist; if necessary, the oculist and neurologist are consulted.

Prevention of leptospirosis hepatitis

A program of measures for the prevention of leptospirosis has been developed. It provides for the control of the state of natural and anthropurgic foci, endemic for leptospirosis, health education of residents of these regions, as well as the vaccination of all those who, under various circumstances, especially professional, are at risk of infection with leptospira.

The leptospirozed concentrated inactivated liquid vaccine has been developed and is successfully used. It is a mixture of inactivated concentrated cultures of leptospira of four serological groups (Icterohaemorhagiae, Grippotyphosa, Pomona, Sejroe). The vaccine provides the development of specific immunity lasting 1 year. Specific vaccination begins at the age of 7 years.