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The fine structure of trophozoites and especially of merozoites of Babesia herpailuri is described before and after treatment with Imidocarb (Wellcome). The mostly piriform to oval merozoites possess an outer membrane and a supporting membrane below. The intratorium consists of a polar ring, rhoptries micronemes and the sperical body which lies beside the big nucleus and next to mitochondria. The endoplasmic reticulum and invaginations are not clearly formed. The cellular changes of Babesia herpailuri, observed one hour after drug treatment in trophozoites and six hours later in merozoites, concern the form and function of the parasite: widening of the subpellicular endoplasmic reticulum and of the perinuclear space; sporadic dilatation of the endoplasmic reticulum of the merozoites (9 fig.). Damaged membranes, dissolution of the cellular membrane, disintegration of the nuclei as are known effects of the Berenil treatment to Babesia herpailuri, are not noted results after the Imidocarb treatment. The original membrane systems of trophozoites as well as of merozoites, remain unaffected by the drug as long as investigations were carried on (24 h). The satisfying prophylactic effect of Imidocarb as well as the insignificant cellular damages on merozoites may be due to the small feeding of hemoglobin.
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In separate experiments, after repeated oral administration of 3,4,4'-trichlorocarbanilide (TCC) and 3-trifluoromethyl-4,4'-dichlorocarbanilide (TFC) to rats, the biliary metabolites of each were isolated and identified. The major TCC biliary metabolite was found to be 2'-hydroxy-TCC. This compound was isolated mainly from the nonconjugated and the glucuronide fractions. Other metabolites present in substantial quantities were 6-hydroxy-TCC and 2',6-dihydroxy-TCC mainly as glucuronides and 3'-hydroxy TCC mainly as the sulfate conjugate. Small amounts of 3',6-dihydroxy-TCC were isolated from each of the fractions. No unchanged TCC was found in the bile. Only traces of other metabolites were found, and no N-hydroxylated products were observed. The major TFC biliary metabolite was the glucuronide conjugate of 2'-hydroxy-TFC. The only other metabolite of TFC was 3'-hydroxy-TFC, which was the predominant metabolite in the sulfate-conjugated fraction.
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Studies are reported on the localization and quantitative distribution of 3,4,4'-trichloro[14C]carbanilide([14C]TCC) in guinea-pig and human skin, and on the percutaneous absorption of TCC following topical application to guinea pigs. [14C]TCC was applied to guinea-pig skin in various vehicles (conventional, superfatted, 10 percent non-soap detergent (NSD) and 30 percent NSD soap suspensions or in N,N-dimethylformamide [DMF]) and under various conditions (e.g. freshly prepared or equilibrated suspensions; single or multiple washes). Most of the amount of TCC remaining in the skin after rinsing was deposited on the skin surface and only relatively minute amounts actually penetrated through the epidermis into the dermis. Whereas conventional soap facilitated a greater deposition of TCC on the skin surface than NSD, the latter caused greater amounts of TCC to be deposited in the pilosebaceous system and lower dermis than conventional soap. The absence of TCC in the blood and tissues of guinea pigs given topical applications of TCC lends further support to the very low order of percutaneous absorption of TCC. The localisation of TCC followed a similar pattern in human skin as in guinea-pig skin, but the amount deposited was less and the rate of disappearance was more for human than for guinea-pig skin.
The babesicides imidocarb and amicarbalide, which have structural similarities to the antitrypanosomatid diamidines, proved active against Trypanosoma brucei mouse infections: both cured infections when doses were administered daily for 3 days 24 h post-inoculation (curative dose imidocarb, 10 mg/kg; amicarbalide, 25 mg/kg). Mice were considered cured after survival 30 days longer than untreated infected controls, with no trypanosomes present in blood or cerebrospinal fluid smears. Both agents also cured when administered 48 and 72 h after challenge with T. brucei and prolonged the lives of animals 94 h after challenge. The results are discussed in respect to the potential of these carbanilides and their precursors, the antitumor phthalanilides, as lead compounds in chemotherapy of mammalian trypanosomiases.
Skin scrapings from clinical cases of equine skin disorder were examined by culture to determine the micro-organisms involved. In-vitro and in-vivo studies were then made to determine the efficacy of Trichloro-carbanilide as a topical treatment for these cases. The laboratory findings and results of treatment are described, and the value of Trichlorocarbanilide in cases of bacterial, actinomycete and fungal infection assessed.
Treatment of calves with 5 mg/kg Imidocarb (3,3-1-bis-(2 - imidazolin - 2 - yl)carbanilide dipropionate) given intramuscularly 14 days before and 14 days after exposure to Babesia infected Boophilus microplus larvae rendered the next generation of larvae incapable of transmitting Babesia infection. When administered to calves 14 or 28 days before tick exposure, the drug prevented the development of clinical babesiosis; the larval progeny of ticks reared on the calf which was treated 28 days before infestation were infective. Treatment of a calf 42 days before exposure to infective larvae did not prevent the development of a Babesia parasitaemia but appeared to reduce the severity of infection.
The toxic effects of imidocarb dipropionate (3,3'-bis[2-imidazolin-2-yl] carbanilide dipropionate) were studied in calves injected twice intramuscularly with 0, 5, 10 or 20 mg/kg dosages. Transient, dosage dependent signs of toxicosis consisted of excessive salivation, serous nasal discharge, diarrhoea and dyspnoea. Elevations in blood urea nitrogen concentrations and serum glutamic oxalacetic transaminase activities were related to dosage and markedly increased at the high dosage. Renal hyperaemia, hepatomegaly, pulmonary congestion and oedema, hydrothorax, hydroperitoneum, hydropericardium and mortality occurred at the 20 mg/kg dosage. Microscopic lesions observed at the high dosage included acute severe renal tubular necrosis and focal hepatocellular necrosis. Injection site reactions varied from microscopic areas of necrotising myositis at the 5 mg/kg dosage to focal grossly visible areas of necrosis, encapsulated by granulation tissue and surrounded by fascial oedema at the 20 mg/kg dosage.