Pathology

The main pathogenic feature is the intracellular reproduction of the bartonella inside the cytoplasm of

Figure VIII.22.2. Verrucose eruptions: (top) miliary form, diffuse and generalized; (middle) nodular form, two intradermic nodules; (bottom) mular form. In the pseudotumoral eruption (bottom), the granulomatous lesions are seated in the deep tissue; sometimes the eruption becomes painful when a secondary infection develops or when bleeding increases. (From O. Urteaga-Ballón and J. Calderón. 1972. Dermatología Clínica, by permission of the author.)

the endothelial cell. Microscopically these cells are swollen with tremendous numbers of bacteria, which push the nucleus of the cell eccentrically (Figure Vni.22.3A,B). The pressure resulting from the multiplication of the bartonellas causes the cell membrane to rupture, releasing millions of bacteria,

Figure VIII.22.3. Intracellular reproduction cycle of the Bartonella bacilliformis (top) the cytoplasm of a histiocytic bone marrow cell, and (bottom) the endothelial cells of a lymph node. (From O. Urteaga-Ballón and J. Calderón. 1972. Dermatología Clínica, by permission of the author.)

which then start a new intracellular colonization in other endothelial cells. Also, the bartonellas act as parasites on the peripheral erythrocytes, inducing the anemia syndrome.

Histopathological study of the anemia of Carrion's disease reveals massive hyperplasia of the phagocytic reticuloendothelial cells in the spleen, lymph nodes, liver, and bone marrow. Erythrophagocytosis is responsible for the anemia. The macrophages initiate the destruction of the parasitized erythrocytes. The extraordinary phagocytic hyperplasia characterizes the cellular immunoresponse of this disease. The macrophages contain, in their cytoplasm, 2 to 10

Figure VIII.22.4. Erythrophagocytosis of parasitized erythrocytes in (top) peripheral blood; and (bottom) spleen. Bottom panel, showing extraordinary phagocytic hyperplasia, and macrophages containing more than 10 erythrocytes, illustrates the mechanism responsible for the anemia. (From O. Urteaga-Ballón and J. Calderón. 1972. Dermatología Clínica, by permission of the author.)

Figure VIII.22.4. Erythrophagocytosis of parasitized erythrocytes in (top) peripheral blood; and (bottom) spleen. Bottom panel, showing extraordinary phagocytic hyperplasia, and macrophages containing more than 10 erythrocytes, illustrates the mechanism responsible for the anemia. (From O. Urteaga-Ballón and J. Calderón. 1972. Dermatología Clínica, by permission of the author.)

erythrocytes with bartonellas (Figures VIII.22.4 A,B). Severe cases show thrombosis and infarction in the spleen, centrolobular necrosis of the liver, and lung congestion.

At the end of the anemia stage, an immunore-sponse is mounted against the active basilar bartonellas, which then are converted to the resistant coccoid stage. This is the most dangerous period of the disease. The "anoxemia" is extremely severe, with the red blood cell count falling to below 1 million. In at least 30 percent of the cases, the untreated patient dies after physical collapse. Another 40 percent die from secondary complications. The nonspecific immunoreaction decreases to the "anergic stages," but some quiescent chronic infection in the patient will exacerbate to an acute stage. The most frequent complications are salmonellosis, tuberculosis, malaria, and amebiasis in carrier cases.

From the clinical point of view, the patient has recovered. He or she appears to be normal, but the bartonellas still live in the adventitial cells surrounding the subcutaneous capillaries. Blood and bone marrow cultures are still positive. There is an unstable balance between the intracellular bacteria and the immune response. In time, when this equilibrium breaks down, the bartonellas start a new cycle of reproduction in the histiocytes. The second stage of the disease appears as a disseminated verrucose eruption. This histiocytic proliferation, with the in situ presence of the microorganism, is a clear example of cellular immunity. Sometimes the histiocytic proliferation is so great that the lesion appears like a tumor, a histiocytic lymphoma.

The histopathology of the granulomatous phase shows an angioblastic proliferation with large, pale histiocytes and endothelial cells, some filled with coccobacillus bartonellas. The rupture of these cells results in the dissemination of the bartonellas through the skin, with the appearance of new verrucose eruptions. The eruptive phase tends to heal spontaneously without scars.

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