PubMed · 6460748
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
S A Clift, F Navab. 1982. Current concepts in amebiasis.. https://pubmed.ncbi.nlm.nih.gov/6460748/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Amoebic gill disease of turbot Scophthalmus maximus L. associated with mortalities was repeatedly diagnosed at culture facilities in NW Spain. The agent was assigned to the genus Paramoeba Schaudin, 1896. Trophozoites found in the gill tissue as well as those cultured displayed most of the principal characteristics of P. pemaquidensis Page, 1970. The identity with P. pemaquidensis, known as an agent of gill diseases of salmonids, is yet to be assessed using non-morphological criteria.
The ultrastructure of the Iodamoeba bütschlii cyst from human feces was studied. The glycogen mass appears as a compact dense body in the cytoplasm without any surrounding membrane. The cytoplasm has no mitochondrion. The nucleus shows a distinct nucleolus filled with electron-dense particles. On one side of the nucleolus are electron-dense cytoplasmic masses measuring 200-400 nm. The nuclear membrane is two-layered and shows pores.
We describe a fatal case of amebic encephalitis caused by Balamuthia mandrillaris in a 3-year-old Czech boy who had never traveled abroad. This is the first such infection reported in Europe. The diagnosis was established by brain biopsy, in which abundant trophozoites and a few round amebic cysts were identified. The presence of multiple nucleoli in some trophozoites suggested the organism to be Balamuthia mandrillaris and this was confirmed by indirect immunofluorescence. The amebae invaded brain tissue, including neurons, and blood vessel walls, causing thrombovasculitis. The tissue reaction was a subacute necrotizing and granulomatous encephalitis (GAE) with an infiltrate of CD4- and CD8-positive T-lymphocytes, B-lymphocytes, plasma cells and macrophages. The child, in whom no underlying immunodeficiency was demonstrated, died after 45 days. The mode of infection was not established. Postmortem examination of the brain revealed massive areas of necrosis and microscopic findings like those in the surgical specimen. In vitro isolation of B. mandrillaris was unsuccessful.