Leishmaniasis hepatitis

Leishmaniasis is an infectious disease caused by Leishmania parasites. It is characterized by remittent fever, anemia, a sharp increase in the spleen, liver, cachexia.

As a result of invasion, leishmania develops hyperplasia of reticuloendothelial elements in the liver, spleen, lymph nodes and bone marrow. The next stage is the fatty degeneration of the parenchymal organs, functional impairment and exhaustion; develops bone marrow hypoplasia.

[1], [2], [3], [4], [5], [6], [7], [8]

Morphology

The liver is macroscopically enlarged and has a blurred pattern. Microscopically: dystrophic changes in hepatocytes are observed. There is a sharp hypertrophy of stellate reticuloendotheliocytes, many of them, especially on the periphery of the lobules, contain a large number of leishmanias; individual cells containing leishmania are released.

The spleen is macroscopically dark red or cyanotic in color, hyperplastic, compacted; its mass is increased several times.

Microscopically: the structure is poorly discernible as a result of replacement of lymphoid tissue with large reticular cells. Many of them contain leishmania in the cytoplasm. There is a large number of plasmocytes. The endothelium of the sinuses is swollen. In the pulp there are hemorrhages, accumulations of neutrophilic leukocytes; may be observed ischemic heart attacks.

Symptoms of leishmaniasis hepatitis

The incubation period lasts from 2 weeks to several months. The disease begins gradually, with malaise, impaired appetite, lethargy against a background of subfebrile temperature. By the end of the first week of the disease, body temperature rises to 40 ° C, then fever takes on a remitting character. The patient's condition is steadily deteriorating, weight loss is observed.

The skin is pale with a waxy or earthy tinge. Anemia develops. All patients expressed hepatolyenal syndrome, with a greater increase in the spleen, its density and tenderness.

In the absence of treatment, cachexia develops to 2 months from the onset of the disease. The patients are exhausted, they have no subcutaneous fat layer. There are edemas. The abdomen is swollen, the liver and spleen are very large, while the spleen is palpable in the small pelvis. In the period of cachexia patients suffer from various purulent lesions of the skin, ears, etc.

Changes in peripheral blood are very characteristic. Hypoglobinemia, anisocytosis, toxic granularity of erythrocytes, leukopenia, neutropenia, thrombocytopenia, relative lymphocytosis and monocytosis, sharply increased ESR are observed. The bone marrow is exhausted, signs of hematopoiesis hypoplasia and agranulocytosis are revealed in it.

The course of leishmaniasis hepatitis

In young children, visceral leishmaniasis can have an acute course with a rapid increase in severe anemia and abnormalities of the gastrointestinal tract, purulent complications. With this option, without treatment, there is a high mortality rate.

In older children and adults, a chronic course of visceral leishmaniasis with preservation of hepatolienal syndrome, loss of body weight, asthenia, pale waxy skin lesions and pathological changes in the peripheral blood is observed.

Diagnosis of leishmaniasis hepatitis

Diagnosis of visceral leishmaniasis is based on epidemic data (living in regions endemic in leishmaniasis) and clinico-laboratory manifestations. Clinical symptoms include fever, often remitting type, marked hepatolienal syndrome, progressive anemia, weight loss of the patient.

In peripheral blood, attention is drawn to a significant reduction in hemoglobin, the number of erythrocytes, leukoneutropenia, thrombocytopenia.

The final diagnosis of visceral leishmaniasis is made when leishmania is detected in blood smears or bone marrow preparations stained according to Romanovsky.

Serological diagnostics for the detection of anti-leishmaniasis antibodies did not spread due to the ambiguity of the results obtained.

At present, there is no great alertness towards visceral leishmanosis. Doctors have little knowledge of the main manifestations of the disease, its course, epidemiology. This leads to late diagnosis of visceral leishmaniasis.

The presence of severe hepatolienal syndrome, both acute and chronic, is a cause of suspected viral hepatitis. However, unlike viral hepatitis, visceral leishmaniasis does not show hyperfermentemia, an increase in the level of conjugated bilirubin. In addition, with viral hepatitis, almost always normal values of peripheral blood. Only with severe activity of chronic hepatitis can moderate anemia and thrombocytopenia.

It is possible to exclude viral hepatitis from the negative results of a serological test for the markers of hepatitis viruses.

Differential diagnostics of visceral leishmaniasis with malaria, typhoid, leukemia and other oncological diseases is also carried out.

[9], [10], [11], [12], [13], [14]

Treatment of leishmaniasis hepatitis

Etiotropic treatment for visceral leishmaniasis is based on the use of antimony containing drugs. These include organic compounds of antimony - stibozan, antimony, pentostam. There is a high (almost 100%) effectiveness of these drugs in this disease. Detoxication therapy, treatment of anemia with iron-containing drugs, and ineffective transfusion of erythrocyte mass are also conducted. A food ration of high energy value is prescribed. With the development of cachexia, parenteral nutrition is provided with solutions containing amino acids, fat emulsions.

The effectiveness of therapy is assessed by the disappearance of fever, anemia, weight gain, normalization of the clinical blood test, and a gradual return to the boundaries of the norm of the size of the spleen and liver.

Prevention of leishmaniasis hepatitis

In endemic foci of visceral leishmaniasis, it is necessary to destroy or treat sick dogs, to fight vectors of leishmanias - mosquitoes. To destroy the larvae of mosquitoes, it is necessary to conduct disinfection of the yards and treatment of the premises with repellents.

Specific prevention of visceral leishmaniasis is not developed.