In vitro toxicity of bithionol and bithionol sulphoxide to Neoparamoeba spp., the causative agent of amoebic gill disease (AGD).

The objective of the present study was to evaluate the in vitro toxicity of bithionol and bithionol sulphoxide to Neoparamoeba spp., the causative agent of amoebic gill disease (AGD). The current treatment for AGD-affected Atlantic salmon involves bathing sea-caged fish in freshwater for a minimum of 3 h, a labour-intensive and costly exercise. Previous attempts to identify alternative treatments have suggested bithionol as an alternate therapeutic, but extensive in vitro efficacy testing has not yet been done. In vitro toxicity to Neoparamoeba spp. was examined using amoebae isolated from the gill of AGD-affected Atlantic salmon and exposing the parasites to freshwater, alumina (10 mg l(-1)), seawater, bithionol or bithionol sulphoxide at nominal concentrations of 0.1, 0.5, 1, 5 and 10 mg l(-1) in seawater. The numbers of viable amoebae were counted using the trypan blue exclusion method at 0, 24, 48 and 72 h. Both bithionol and bithionol sulphoxide demonstrated in vitro toxicity to Neoparamoeba spp. at all concentrations examined (0.1 to 10 mg l(-1) over 72 h), with a comparable toxicity to freshwater observed for both chemicals at concentrations > 5 mg l(-1) following a 72 h treatment. Freshwater remained the most effective treatment, with only 6% viable amoebae seen after 24 h and no viable amoebae observed after 48 h.

Liquid chromatographic determination of depletion of bithionol sulfoxide and its two major metabolites in bovine milk.

A liquid chromatographic method is described for determining bithionol sulfoxide and its metabolites, bithionol and bithionol sulfone, in milk. Samples are treated with HCl to precipitate proteins and to permit extraction of bithionol sulfoxide in nonionized form. Tetrahydrofuran is added to the organic phase to facilitate extraction in diethyl ether; the dried residue is dissolved in chloroform, hexane, and sodium hydroxide and subjected to LC analysis. Residues of bithionol sulfoxide and its 2 metabolites were determined in milk of lactating cows. Holstein-Friesian dairy cows were administered a single oral dose of bithionol sulfoxide (50 mg/kg). Milk samples were analyzed with a reliable detection level of 0.025 microgram/mL for each compound. Residues of bithionol sulfoxide and bithionol were detected during 30 and 16 milkings, respectively; bithionol sulfone was never present at detectable levels.

Mutagenicity of bithionol sulfoxide and its metabolites in the salmonella/mammalian microsome test.

The mutagenic effects of bithionol sulfoxide and its two major metabolites, bithionol and bithionol sulfone, on 4 Salmonella typhimurium strains (TA97, TA98, TA100 and TA102) were investigated. Bithionol sulfoxide was found to be mutagenic to TA98 and TA100. However, mutagenicity was abolished in the presence of rat-liver S9 fractions.

[Autoradiographic study of the distribution of 14C bithionol sulfoxide in mice (author's transl)]. / Etude autoradiographique de la distribution du 14C bithionol sulfoxyde chez la souris.

The distribution of a single oral dose of 14C bithionol sulfoxide in mice was determined by whole body autoradiography. The bithionol sulfoxide was found in the whole organism mainly in richly vascularized organs, liver, kidney, lung. It did not pass through the blood-brain barrier and did not accumulate in any particular organ but persisted in the blood. Observations were performed in 18-day pregnant mice in order to investigate an eventual placental transfer. Six hours after the administration, radioactivity was detected in blood and fetal vascularized tissues.

Metabolic detoxication of bis-(2-hydroxy-3, 5-dichlorophenyl)-sulfoxide in man.

The metabolic detoxication of bis(2-hydroxy-3, 5-dichlorophenyl)sulfoxide (BTS) in man was investigated. Bis(2-hydroxy-3, 5-dichlorophenyl)sulfide (BT) was identified in beta-glucuronidase treated urine following the administration of BTS by thin-layer chromatography, gas chromatography, ultraviolet spectrum and quantitative analysis. No other metabolites were detectable. BT-glucuronide was also identified in urine. It was assumed that BTS was reduced to BT and successively conjugated with glucuronide in man, and excreted as BT-glucuronide in the urine.

Morphological changes after treatment of bovine cysticercosis with droncit and oxichloron.

Droncit and Oxichloron in total doses of 100 (50 mg/kg for two days) and 300 mg/kg (100 mg/kg for three days) of body weight were applied for the treatment of cysticercosis 12 (Droncit) and 6 (Oxichloron) weeks after experimental infection. Four or six weeks after the treatment dead cysticerci or their remnants were found. There occurred a striking vacuolization of the larval tegument, but even six weeks after the treatment, muscles, portions of subtegumental cells and remnants of excretory canalicular system and microtriches were discernible. The structure of microtriches was still well preserved in some cases. The dominating component of tissue reaction around the dead larvae was the hyperplasia of lymphoid tissue forming sometimes folliculoid structures, and blastic transformation of lymphocytes. Nodules with dead larvae were separated from the surrounding tissue by connective tissue.

[The prevention and therapy of fascioloidiasis using bithionol sulfoxide]. / Prevence a terapie fascioloidózy skotu bithionolsulfoxidem.

The elimination of the sources of invasion, i. e. hay and forage coming from the infested biotopes, combined with the administration of bithionol sulphoxide, resulted in a reduction of the invasion of cattle by Fascioloides magna from 21.1 to 3.2% within two years. The Czechoslovak-produced bithionol sulphoxide, administered at a rate of 40 to 50 mg per kg body weight as medicated feed, showed 100% effectiveness. At doses higher than 30 mg per kg body weight, the protective period should be prolonged to three or four weeks.