Secondary myelofibrosis in visceral leishmaniasis--case report.

A 39-year-old woman with a history of travel to the Montenegrin coast presented with a 9-month long history of fever and weakness, and on examination was found to be emaciated with hepatosplenomegaly and pancytopenia. Marrow aspiration showed poor cellularity with abundant Leishman Donovan (LD) bodies in the macrophages. Bone marrow trephine biopsy revealed a marked myelofibrosis (Manoharan classification: grade III) with osteosclerosis. The impression smears of a trephine biopsy stained with Güiemsa also showed LD bodies. The patient did not exhibit evidence of any risk factors for visceral leishmaniasis (VL). She was treated with meglumine antimoniate (Glucantime) without any adverse effect. The spleen returned to a normal volume after 4 months and bone marrow trephine biopsy performed 6 months after initiation of the therapy had returned to normal. A diagnosis was difficult to establish as VL is rarely encountered in the continental parts of Yugoslavia, and with the presence of associated myelofibrosis it could easily have been mistaken for chronic idiopathic myelofibrosis. The association of myelofibrosis with visceral leishmaniasis has been reported in the literature only three times; we thus feel that documentation of this case is merited.

[Neurologic manifestations in trichinosis]. / Neuroloske manifestacije u toku trihinoze.

Neurologic manifestations are present in about 10-20 percent of patients with trichinosis. They could be a serious diagnostic problem in the absence of corresponding epidemiological data and typical symptoms and signs of the disease. In untreated patients the mortality rate is about 50%. Several pathogenic mechanisms are responsible for the neurological complications in trichinosis: obstruction of brain blood vessels by larvae, cysts or granulomas, toxic vasculitis with secondary thrombosis and haemorrhages, granulomatous inflammation of the brain parenchyma and allergic reaction. Neurotrichinosis is manifested with clinical symptoms and signs of meningitis, encephalitis, polyradiculoneuritis, poliomyelitis, myastenia gravis, paresis and paralysis, with the clinical picture of systemic disease of the connective tissue involving the nervous system and, extremely rare, as a sinus thrombosis. Thus, the broad spectrum of neurological lesions in trichinosis is, probably, the results of the fact that Trichinella spiralis larvae, during haematogenic dissemination has no special affinity for particular parts of the nervous system. We present five patients with encephalitis and focal cerebral lesions in trichinosis. In one patient the neurologic manifestations were the only sign of the disease. We believe that all pathogenic mechanisms mentioned above, were involved in the onset of neurological manifestations in our patients. The diagnosis of the disease was based on the clinical picture, epidemiological data, microscopic identification of larvae in the muscular tissue, the presence of antibodies against Trichinella spiralis in cerebrospinal fluid (with preserved blood brain barrier) and in serum confirmed by IIF method, computerised tomography and magnetic resonance imaging of the brain, eosinophilia in the peripheral blood picture. One patient died, and in the remaining patients the course of the disease was favourable; they were discharged from the hospital with minimal neurologic sequelae.

[Pulmonary manifestations of acquired immunodeficiency syndrome (AIDS)]. / Plucne manifestacije sindroma stecene imunodeficijencije (AIDS-om).

The lungs are the principal target organ in the infectious complications of acquired immunodeficiency syndrome (AIDS) and this predisposition to infections is not the regional manifestation of systemic immunologic deficiency induced by human immunodeficiency virus (HIV) only, because HIV also affects lung's own complex system of local defense mechanisms. It was demonstrated that pulmonary host defenses were compromised by.direct infection of alveolar macrophages with HIV and decreased production of solubile factors by lymphocytes derived from bronchoalveolar lavage fluid was shown. The most common infectious causative agents are facultative intracellular pathogens including Pneumocystis carinii, Cryptococcus neoformans, Mycobacterium tuberculosis and cytomegalovirus, which reflects the specific defects of cell-mediated immunity. AIDS patints have, in addition, an increased incidence of infections with capsulated bacteria such as Haemophilus influenzae and Sterptococcus pneumoniae which are associated typically with the impairment of the humoral immune response. High-grade pathogens such as M. tuberculosis tende to reactivate early in the progression of immunodeficiency whereas low-grade pathogens such as P. carinii only emerge when the defect is more advanced. The profound immunodeficiency in AIDS patients means that clinical features may be quite atypical and blunted.