[Acanthamoeba keratitis].
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Biomedical subjects
Publications and source records attributed to E Nohýnková.
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In this review we have summarized published data on two new compounds, which can represent important antiparasitic drugs in the near future, nitazoxanide for treatment of intestinal parasitic infections including cryptosporidiosis and miltefosine for oral treatment of visceral leishmaniasis.
Human babesiosis is a zoonotic tick-borne protozoan infection caused by several species of the genus Babesia. It is a rare disease in Europe. Until recently, 31 cases have been described. Most of them were severe infections caused by a cattle parasite Babesia divergens in splenectomized patients. In contrast, a rodent species Babesia microti was responsible for hundreds of cases of human babesiosis in the U.S.A. In this report we describe the first case of human babesiosis in the Czech Republic. To our knowledge, it is also the first case of symptomatic B. microti infection imported to Europe from the United States.
A 7-year-old previously healthy Czech boy was admitted due to fever, hepatosplenomegaly and pancytopenia. Aspiration of bone marrow revealed no signs of hemoblastosis (nor hemophagocytosis). He was treated with antibiotics and virostatics without effect. Progression of hepatosplenomegaly and pancytopenia induced suspicion of hemophagocytic lymphohistiocytosis (HLH). Five weeks later, bone marrow hemophagocytosis of erythrocytes, nuclear elements and platelets was detected. He was given corticoids and intravenous immunoglobulins and transferred to our haematology department. Laboratory findings of mild pancytopenia, hypofibrinogenaemia, hyperlipidaemia and elevated levels of ferritin, LDH and immunoglobulins were compatible to the diagnosis of HLH. Immunologic evaluation revealed T-lymphocyte activation. Appropriate immunosuppressive treatment with Dexamethasone, etoposide and Cyclosporine A was launched, followed by transient subside of fever and improvement of peripheral blood count, but not regression of hepatosplenomegaly. Four weeks later, relapse of fever and deterioration of blood count led to intensification of immunosuppression. However, no effect was evident. Moreover, hypertrophic cardiomyopathy with ventricular arrhythmia occurred. Treatment with antilymphocytic globulin for resistant course of HLH was planned. Before that, a fifth bone marrow aspiration was performed. Surprisingly, many Leishmania amastigotes were observed within marrow macrophages. Leishmania infection was confirmed by positive serology. Immunosuppressive treatment was withdrawn and changed for causal treatment with liposomal Amphotericin B. Positive clinical effect with subside of fever was evident in ten days, splenomegaly gradually resolved during three weeks, restoration of normal blood count lasted six weeks. No relapses of HLH nor leishmaniasis occurred. In control bone marrow aspirate performed three months later, the parasites were not detected. Ten months after the event, the patient is in complete remission of HLH with normal immunologic parameters. Most probably, he contracted visceral leishmaniasis during a visit of a Neapol area in Italy 3 months before the onset of the disease.
Susceptibility as opposed to resistance of mouse strains (e.g., BALB/c vs C57BL/6) to Leishmania major has been attributed to a defective Th1 and a predominant Th2-response, resulting in increased IL-4 and IgE production, and decreased interferon gamma (IFN gamma) production, macrophage activation and elimination of parasites. Here we report dissection of genetic and functional aspects of susceptibility to leishmaniasis using two contrasting inbred strains BALB/cHeA (susceptible) and STS/A (resistant) and a resistant Recombinant Congenic (RC) Strain, CcS-5/Dem, which carries a random set of 12.5% of genes from the strain STS and 87.5% genes from the susceptible strain BALB/c. Linkage analysis of F2 hybrids between the resistant RC strain CcS-5 and the susceptible strain BALB/c revealed five loci affecting the response to the infection, each apparently associated with a different combination of pathological symptoms and immunological reactions. The correlation between Th2-type immune reactions and the disease in the F2 mice was either absent, or it was limited to mice with specific genotypes at loci on chromosomes 10 and 17. This suggests that the resistance vs susceptibility is influenced by mechanisms additional to the postulated antagonistic effects of Th1 and Th2 responses, and that the host's genotype affects the development of leishmaniasis in a complex way.
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.
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The cellular division of trophozoites of Giardia intestinalis group was followed microscopically in stained preparations from axenic cultures. Eleven successive stages were described, documented by photomicrographs and their survival times calculated.
Giardia infections were detected in 14 out of 32 weaned, 1 to 2-month-old pigs, used in experiments with coccidia. Giardia trophozoites were present in the small intestine from the duodenum to the ileum with maximum numbers in the cranial part of the upper jejunum. They were localized mainly on the surface of intestinal crypts. No histological changes accompanied the infection and the infected animals were asymptomatic. Giardia trophozoites obtained from the intestines of necropsied pigs were isolated in axenic culture in a bile-supplemented TYI-S-33 medium. Morphological features of the trophozoites revealed by both light and scanning electron microscopy proved that the organism belongs to the Giardia intestinalis group.
Bloodforms of Trypanosoma brucei brucei STIB 247 taken from rats and containing more than 80 per cent short stumpy forms, differentiated in vitro to procyclic forms in medium SDM 79 (Brun and Schönenberger 1979), enriched with 3 mmol.dm-3 cis-aconitate. Cell division was abolished by the addition of hydroxyurea (200 micrograms.ml-1) or arabinosyl adenine (20 micrograms.ml-1 to the cultivation medium, or by the omission of serum from the medium. The ultrastructure of exponentially growing controls was rearranged within 24 h. The endogenous respiration and the respiration stimulated by proline, succinate, and 2-oxoglutarate were detectable within 12 h; after 48 h the respiration rates were comparable to those found in the established procyclic forms. After 12 h the respiration was inhibited by 200 mumol.dm-3 KCN, and by 20 mumol.dm-3 antimycin to the extent found in procyclic forms. Hydroxyurea did not significantly affect respiration. Activities of procyclic-stage enzyme markers malate dehydrogenase, threonine dehydrogenase, succinate: cytochrome c reductase, and NADH: cytochrome c reductase rose within 48 h of differentiation to values which were close to those found in established procyclic forms. The activity of glutamate dehydrogenase (NAD-specific), however, was only 1/3 of that in the procyclics, and no citrate synthase was detected in differentiating culture. Glycosomal malate dehydrogenase was detected after 6 h. In the presence of hydroxyurea or arabinosyl adenine, or in the absence of serum, respiration rates, marker enzyme activities, and glycosomal malate dehydrogenase developed to the extent comparable to the untreated controls. The results suggest that it is possible to separate the process of differentiation from cell proliferation. Cell division is not a necessary prerequisite of differentiation.
Thirty one Giardia isolates, established from six species of hoofed livestock by axenic culture or growth in suckling mice, were compared genetically by analysis of DNA amplified from loci encoding variant surface proteins or the enzyme glutamate dehydrogenase and by allozyme analysis. The isolates were heterogeneous, but all showed affinity with genetic Assemblage A--one of two major assemblages defined previously by analysis of Giardia from humans. Three distinct genotypes were evident. Ten isolates (eight axenic and two established in suckling mice) from an alpaca, pig, horse, cattle and sheep were indistinguishable from human-derived G. intestinalis belonging to a previously designated genetic group (Group I). This genotype seems to have broad host specificity, including a zoonotic potential for humans. Five isolates (two axenic and three established in suckling mice) from an alpaca, a horse and sheep had close affinity with human-derived Group I and Group II G. intestinalis genotypes. The other 16 isolates (comprising both axenic and suckling mouse-propagated cultures derived from cattle, sheep, alpaca, a goat and pigs in Australia and Europe) differed from all other Giardia with "duodenalis" morphology that have been examined by these methods and they segregated as a highly distinct sublineage (referred to herein as 'Novel livestock') within genetic Assemblage A. The predominance of 'Novel livestock' genotypes in the test panel and their apparent exclusive association with artiodactyl hosts indicates that they may be confined to this group of mammals. Assemblage B genotypes, which are prevalent in humans and some other animal species, were not detected.