The effect of the broad spectrum anthelmintic drug flubendazole (methyl 5-(p-fluorobenzoyl)-2-benzimidazolecarbamate, CAS 31430-15-6), a mebendazole derivative with a molecular weight of 313.29, on Schistosoma mansoni infection in mice was evaluated. Moreover, the relationship between the posttreatment worm burden, hepatic granuloma volume, and serum immunoglobulin profile (immunoglobulin G and immunoglobulin M, IgG and IgM), was also investigated. Two main groups of Swiss albino mice infected with Schistosoma mansoni cercariae were used in the experiment. Group I consisted of infected untreated control mice. The mice of group II were submitted to treatment with flubendazole 100 mg/kg body weight as single oral dose at different time intervals: Group IIa received treatment 24 h before infection. Group IIb received treatment 4 h after infection. Group IIc received treatment 25 days after infection. Mice treated 25 days after infection, compared to those treated in other time intervals, revealed a significant reduction in the recovery of adult schistosomes after portal perfusion (79.5%), a lower immunoglobulin level (IgG and IgM), and the smallest granuloma mean diameter (220.0 +/- 10.3 microns). These data were less salient in mice treated 4 h after, and 24 h before infection.

The possible additive or synergistic effects of both praziquantel (CAS 55268-74-1) and a new antischistosomal drug, Ro 15-5458 (10-(2-diethylamino)thyl)-9-acridanone(thiazolidin-2-yl-i dene)hydrazone, CAS 92928-47-7) were studied in two different strains of Schistosoma mansoni infected mice, namely CD susceptible and SO4 resistant strains. Assessment of cure was performed using the following parameters: hepatic and intestinal tissue egg load and distribution, oogram changes in the small intestine and histopathological examination of the mice livers. In this study, a combination was used between 1/3 the curative doses of praziquantel and Ro 15-5458. This combination therapy proved to be beneficial as regards the percentage parasite reduction and hepatic worm shift (99.4% and 100%, respectively, in the CD susceptible mouse strains, compared to 84.1% and 34.8% in the SO4 resistant strains). Treatment with subcurative doses of praziquantel and Ro 15-5458 resulted in 78.6% intestinal dead ova and 21.4% mature ones. This score shifted to 98.6% and 1.4% dead and mature ova, respectively, in the SO4 resistant strains. Again the range of liver granulomata in the CD susceptible and SO4 resistant strains receiving subcurative doses of both drugs was 4-6 and 2-5, respectively, in five successive low power fields, while in the infected untreated control mice, this range reached 8-11 and 5-9, respectively. Histopathological sections of the liver revealed a small fibrocellular granuloma with few inflammatory cells and excess fibrous collagen tissue deposition in animals undergoing the combination therapy. This contrasts with the large fibrocellular granulomata seen in the infected untreated control mice. These results may be of value in endemic areas of schistosomiasis, due to the unexpected emergence of drug resistance against the currently used antischistosomal drug, praziquantel in these areas.

This study is a trial to demonstrate the effect of the broad spectrum anthelmintic drug flubendazole (methyl 5-(p-fluoro-benzoyl)-2-benzimidazolecarbamate, CAS 31430-15-6), a mebendazole derivative, together with praziquantel (CAS 55268-74-1, EMBAY 8440, Biltricide) in murine schistosomiasis mansoni. Moreover, the relationship between the posttreatment worm burden, oogram pattern, tissue egg load and hepatic granuloma volume was also investigated. Three main groups of Swiss albino mice infected with Schistosoma mansoni cercariae were used in the experiment. Group I included infected untreated control mice. Group II: Subgroup II (a): Animals received 1/3 the dose of praziquantel 25 days post infection. Subgroup II (b): Mice were given 1/3 dose of flubendazole 25 days post infection. Subgroup II (c): Animals received the combination (1/3 dose of flubendazole + 1/3 the dose of praziquantel 25 days post infection. Group III: Subgroup III (a): Mice were given 1/3 the dose of praziquantel 7 weeks post infection. Subgroup III (b): Mice received 1/3 dose of flubendazole 25 days post infection. 24 days later, 1/3 the dose of praziquantel was given. Mice given the consecutive drug regimen (flubendazole 1/3 single oral dose 25 days post infection, then praziquantel 1/3 oral dose for two successive days 24 days later, revealed a significant reduction in the recovery of adult schistosomes after portal perfusion (95.9%), absence of immature stages of ova development, a higher level of dead ova in the oogram and the smallest granuloma mean diameter. These data were less conspicuous in mice given the simultaneous drug regimen.

This study was conducted to evaluate the efficacy of praziquantel (CAS 55268-74-1, EMBAY 8440, Biltricide) in different grades of Schistosoma mansoni infection. Moreover, the relationship between the post treatment worm burden, hepatic granuloma volume, and serum immunoglobin profile was also investigated. Four groups of Swiss albino mice infected with Schistosoma mansoni cercariae were used: Highly infected untreated control mice (infected with 120 Schistosoma mansoni cercariae) and their corresponding praziquantel treated group. Lightly infected untreated control mice (infected with 60 Schistosoma mansoni cercariae) and their corresponding praziquantel treated group. Praziquantel was given seven weeks post infection in a dose of 500 mg/kg body weight for two consecutive days. Animals were sacrificed two weeks post treatment. Praziquantel achieved better cure rates in mice with heavy infection than in less intensely infected animals. The drug reduced the hepatic granuloma in animals with light intensity infection. This reduction was more accentuated in highly infected animals. The serum immunoglobulin profile (immunoglobulin G and immunoglobulin M) showed a higher level in highly infected treated mice (1.2 +/- 0.6 optical density unit and 1.1 +/- 0.5 optical density unit, respectively) and was reduced in animals with low intensity infection (1.18 +/- 0.6 optical density unit and 0.7 +/- 0.6 optical density unit, respectively). This study may be of value in tropical regions, where schistosomiasis with low worm burden is a common occurrence.

This work is a trial to evaluate the effect of the combination of the anthelmintic drug praziquantel (CAS 55268-74-1, PZQ, EMBAY 8440, Biltricide) with the antifibrotic agent beta-aminopropionitrile-monofumarate salt (BAPN, CAS 2079-89-2). It is also a trial to elucidate the repercussions of this drug combination upon worm and tissue egg loads and oogram pattern. Moreover, it aims to study their effects on the hepatic granuloma size and the resistance to reinfection in experimental murine schistosomiasis mansoni. A group of 120 Swiss albino mice was used. This group was further subdivided into six small subgroups. Subgroup I comprised infected untreated control mice. Subgroup II comprised infected untreated challenged control mice. Subgroup III comprised challenged control mice. Subgroup IV comprised infected mice treated with PZQ 500 mg/kg b. w. orally for two successive days. Subgroup V comprised infected mice given BAPN daily as 5 mg powder in 0.5 ml saline for 14 successive days. Subgroup VI comprised mice given both PZQ + BAPN. Animals were sacrificed 12 weeks post primary infection. Mice given the combination regimen PZQ + BAPN, compared to those given each drug solely, revealed absence of worm recovery at perfusion and only dead ova in the oogram (99.2 + 0.6). Inspite of the marked reduction in the hepatic and intestinal tissue egg loads recorded, this drug combination revealed the highest score of percent resistance to reinfection (91.2 + 0.5%). The data were less salient in mice given PZQ or BAPN alone.

Objectives. This work is a trial to elucidate the parasitological and histopathological sequelae of giving the antimalarial drug (artesunate) in experimental intestinal amoebiasis. Methods. A group of 24 hamsters was infected by Entamoeba histolytica cysts orally using a canula. This group was subdivided into two main subgroups. Subgroup I: given 6000 E. histolytica cysts orally by a canula, then sacrificed five weeks postinfection. Subgroup II : given the same infective dose, then two weeks later, treated with artesunate 10 mgm/Kg b. wt/hamster over 3 consecutive days. Again sacrifice was performed five weeks postinfection. Multiple stool examinations, and histopathological examination of the caecal end of the large intestine were resorted to, in order to assess the antiamoebic effect of the drug. Faecal smear examination revealed absolute disappearance of E. histolytica cysts in the treated group. Again, histopathology of the mucosal scrapings of the caecum showed complete absence of Entamoeba histolytica trophozoites in the treated group, when compared to the control animals (P < .001). This study may be beneficial, especially in areas endemic with amoebiasis to help overcoming the emerging resistance to the usually available antiamoebic drugs.

Diclofenac could be used successfully as a preventive agent against schistosomiasis mansoni infection in endemic areas.