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Biomedical subjects

H B Tanowitz

Publications and source records attributed to H B Tanowitz.

At least 109 records · Page 6Linked to original sources
PubMed1983

Diagnosis of giardiasis by two methods. Immunofluorescence and enzyme-linked immunosorbent assay.

Antibody response in giardiasis was measured by indirect fluorescent antibody (IFA) and enzyme-linked immunosorbent assays (ELISA) on serum samples of 125 patients. Twenty-nine of these patients had symptomatic giardiasis; 30 were asymptomatic (carriers); 40 had other parasitic infections; 16 had inflammatory bowel diseases; ten were normal subjects. It was found that those patients with symptomatic giardiasis had higher IFA titers compared with all patients who did not have giardiasis and patients who had asymptomatic giardiasis. Serum samples with titers of 1:64 or greater in Giardia IFA were absorbed with Giardia and other parasite antigens. Only absorption with Giardia caused the titers to fall significantly. The ELISA technique was less specific than the IFA technique. Giardiasis elicits a specific host antibody response that may be used as an adjunct in its diagnosis.

Antibodies↗
PubMed1982

The effect of adenosine analogues on the in vitro growth of Trypanosoma cruzi.

Trypanosoma cruzi (Brazil strain) was maintained in liver infusion tryptose and medium supplemented with 5 or 10% foetal calf serum at 27 degrees C on a rotating shaker platform. 85 to 95% of the organisms under these conditions are epimastigotes and the medium supported logarithmic growth for up to 24 hours. The effect of S-isobutyl adenosine and Sinefungin against cultured T. cruzi epimastigotes was studied: growth rate was slowed by both in a dose-dependent fashion; 500 micrometer Sinefungin caused complete inhibition which was irreversible after 24-hour exposure but the effect of S-isobutyl adenosine (100 micrometer) was reversible. Motility and morphology appeared to be unaffected.

Adenosine↗
PubMed1982

Infection of organotypic cultures of spinal cord and dorsal root ganglia with Trypanosoma cruzi.

Although the involvement of the nervous system in Chagas' disease is well described, the mechanism of the neuronal destruction is unclear. Immunologic, toxic mechanisms and direct invasion have been advocated. Organotypic cultures of spinal cord and dorsal root ganglion derived from Swiss outbred mice were infected with the Brazil strain of Trypanosoma cruzi. Light microscopic and ultrastructural studies were performed at regular intervals. It was found that trypomastigotes were rapidly taken up by glial and other supporting cells. Neurons were rarely parasitized and demyelination was not evident. Loss of several cytoskeletal components was seen. Dendrites were swollen and axons lost their normal filamentous structures but synaptic membranes remained intact. Mitochondrial swelling was evident even in nonparasitized neurons from infected cultures. By 7-10 days of infection the majority of neurons lost their typical morphology and were eventually destroyed by mechanisms other than direct parasite invasion. Organotypic cultures exposed to T. cruzi-conditioned medium exhibited no change in morphology. Since neurons were found only rarely to be parasitized, it is suggested that neuronal destruction is an indirect result of the parasitism of supporting cells such as glial cells and macrophages.

Animals↗
PubMed1982

Successful chemotherapy of transfusion babesiosis.

We describe babesiosis transmitted by transfusion. The infected blood donor was identified and a minimum period of infectivity of the donor's blood was established. We report a new modality for chemotherapy consisting of quinine plus clindamycin, and a new endemic focus for this zoonosis on Fire Island, New York. There are insufficient data to establish a reasonably safe period after which visitors and residents of Babesia-endemic foci can become blood donors. Screening of such persons by a rapid serologic test, such as the ELISA or immunofluorescent antibody tests, is suggested.

Adult↗
PubMed1981

Taxol, a microtubule stabilizing agent, blocks the replication of Trypanosoma cruzi.

Taxol, an experimental antitumor agent and stabilizer of microtubules, inhibits in vitro replication of the human pathogenic hemoflagellate Trypanosoma cruzi. Micromolar concentrations of the drug prevent the completion of cell division in these organisms but allow the multiplication of cell organelles such as the nucleus, kinetoplast, and flagellum. The result is the formation of motile organisms that have extra organelles but cannot fully replicate. Division proceeds to a relatively fixed locus on the long axis of the organism, suggesting the presence of a specific affected structure or function at this site. It is postulated that taxol produces these effects by stabilizing a portion of the microtubular cytoskeleton of T. cruzi.

Alkaloids↗
PubMed1980

Effect of sodium cyanate on Plasmodium falciparum in vitro.

Sodium cyanate at concentrations as low as 0.5 mM inhibited the growth of Plasmodium falciparum (FCR-3 Strain) utilizing the Trager-Jensen continuous culture system. At concentration higher than 1 mM, the parasites were irreversibly destroyed. Utilizing synchronized cultures, the relative susceptibilities of early and late trophozite forms were examined, and it was found that both developmental forms were equally susceptible to the action of cyanate. Pretreatment of red cells with sodium cyanate prior to infection did not alter the intracellular growth of the parasite. Consequently, the effect of the drug is likely to be on the parasite per se rather than the red cell. The mechanism of action is probably the carbamylation of essential, parasite proteins that eventually impair growth and/or function. Published pharmacological studies in humans would predict that the level of cyanate at which growth inhibition occurs in vitro can be achieved in vivo and that the adverse effects will likely be minimal for short treatment periods.

Animals↗
PubMed1977

Infective endocarditis caused by Streptococcus mutans. A complication of idiopathic hypertrophic subaortic stenosis.

Three patients with endocarditis caused by Streptococcus mutans were seen during a six-month period. All had clinical features of subacute bacterial endocarditis, including fever, heart murmurs, and positive blood cultures. One had underlying aortic insufficiency and two had idiopathic hypertrophic subaortic stenosis. All patients were treated with parenteral antibiotics and were cured. Streptococcus mutans is a pleomorphic, microaerophilic organism that is associated with dental caries and plaque. Differentiation of S mutans from enterococcal endocarditis is important because the former condition can be treated for a shorter period of time with penicillin alone, without the addition of aminoglycoside antibiotics.

Cardiomyopathy, Hypertrophic↗