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, and cachexia.

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

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Morphology

The liver is macroscopically enlarged, has a blurred pattern. Microscopically: dystrophic changes in hepatocytes are observed. Sharp hypertrophy of stellate reticuloendotheliopsies is revealed, many of them, especially on the periphery of the lobules, contain a large number of leishmania; individual cells containing leishmania are deflated.

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

Microscopically: the structure is poorly discernible due to the replacement of lymphoid tissue by large reticular cells. The cytoplasm of many of them contains leishmania. There are a large number of plasma cells. The endothelium of the sinuses is swollen. There are hemorrhages in the pulp, accumulations of neutrophilic leukocytes; ischemic infarctions may be observed.

Symptoms of Leishmaniasis Hepatitis

The incubation period lasts from 2 weeks to several months. The disease begins gradually, with malaise, loss of appetite, lethargy against the background of subfebrile temperature. By the end of the 1st week of the disease, the body temperature begins to rise to 40 ° C, then the fever becomes remittent. The patient's condition steadily worsens, weight loss is noted.

The skin is pale with a waxy or earthy tint. Anemia develops. All patients have hepatosplenic syndrome, with a more significant increase in the spleen, its density and soreness.

If left untreated, cachexia develops by 2 months from the onset of the disease. Patients are emaciated, they have no subcutaneous fat layer. Edema is observed. The abdomen is swollen, the liver and spleen are very large, and the spleen is palpated in the small pelvis. During the period of cachexia, patients suffer from various purulent lesions of the skin, ears, etc.

Changes in peripheral blood are extremely characteristic. Hypoglobinemia, anisocytosis, toxic granularity of erythrocytes, leukopenia, neutropenia, thrombocytopenia, relative lymphocytosis and monocytosis, and a sharply increased ESR are observed. Bone marrow is depleted, and signs of hematopoietic hypoplasia and agranulocytosis are detected in it.

The course of leishmanial hepatitis

In young children, visceral leishmaniasis may have an acute course with a rapid increase in severe anemia and gastrointestinal disorders, purulent complications. In this variant, high mortality is observed without treatment.

In older children and adults, chronic visceral leishmaniasis is observed with persistence of hepatosplenic syndrome, weight loss, asthenia, pale waxy skin and pathological changes in the peripheral blood.

Diagnosis of leishmanial hepatitis

The diagnosis of visceral leishmaniasis is based on epidemiological anamnesis data (living in regions endemic for leishmaniasis) and clinical and laboratory manifestations. The clinical symptoms include fever, often of a remitting type, significantly expressed hepatosplenic syndrome, progressive anemia, and weight loss of the patient.

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

A definitive diagnosis of visceral leishmaniasis is made by detecting leishmania in blood smears or bone marrow preparations stained according to Romanovsky.

Serological diagnostics for the detection of antileishmanial antibodies has not become widespread due to the ambiguity of the results obtained.

At present, there is no great concern about visceral leishmaniasis. Doctors are poorly informed about the main manifestations of the disease, its course, and epidemiology. This leads to late diagnosis of visceral leishmaniasis.

The presence of pronounced hepatosplenic syndrome in both acute and chronic variants of the disease is a reason to suspect viral hepatitis. However, unlike viral hepatitis, visceral leishmaniasis does not show hyperfermentemia or increased levels of conjugated bilirubin. In addition, with viral hepatitis, peripheral blood indices are almost always normal. Only with pronounced activity of chronic hepatitis can moderate anemia and thrombocytopenia be recorded.

It is possible to exclude viral hepatitis based on negative results of serological testing for hepatitis virus markers.

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

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Treatment of leishmanial hepatitis

Etiotropic treatment for visceral leishmaniasis is based on the use of antimony-containing drugs. These include organic antimony compounds - stibosan, surmin, pentostam. High (almost 100%) effectiveness of these drugs in this disease is noted. Detoxification therapy, treatment of anemia with iron-containing drugs, and if they are ineffective - transfusion of red blood cells are also carried out. A high-energy diet is prescribed. In the development of cachexia, parenteral nutrition is carried out with solutions containing amino acids and fat emulsions.

The effectiveness of therapy is assessed by the disappearance of fever, anemia, weight gain, normalization of clinical blood tests, and gradual return of the spleen and liver sizes to normal limits.

Prevention of leishmanial hepatitis

In endemic foci of visceral leishmaniasis, it is necessary to destroy or treat sick dogs, and fight against the carriers of leishmania - mosquitoes. To destroy mosquito larvae, it is necessary to disinfect yards and treat premises with repellents.

Specific prevention of visceral leishmaniasis has not been developed.