Protective immunity of homologous challenge infection was examined in jirds after drug-abbreviated infection with Brugia pahangi. Mebendazole (MBZ) treatment at the early prepatent (5–7 weeks of post infection) or the late prepatent (7–9 weeks of post infection) period was highly effective in causing almost complete eradication of the primary infection. After challenge infection, the worm burden was significantly reduced 19% (31·1 in average) and 77% (9·5) to that of the controls (38·8 and 41·7), respectively. The magnitude of eosinophil response paralleled the degree of protection. No or only a few microfilariae were seen after challenge infection in jirds treated during the prepatent periods. They were also resistant to intravenous challenge with the microfilariae of B. pahangi. MBZ treatment at the patent period was, on the contrary, incomplete against primarily infected adult worms, and was not able to induce either significant protection (30·1 vs 33·1 in control) or eosinophil response to the challenge infection.

The new organic arsenical R7/45 is a rapidly acting and very potent anthelmintic against adult Brugia pahangi in jirds. Against adult worms implanted into the peritoneal cavity 5 subcutaneous (SC) injections at 2·5 mg/kg of R7/45 killed 100% of adult worms. A single dose SC of 20 mg/kg was 100% effective and 10 mg/kg 76% effective against adult worms. When jirds were autopsied at different times after treatment at 20 mg/kg SC 89% of worms were dead within three days. R7/45 was not active when given by stomach intubation. Pretreatment of jirds with R7/45 had no effect on adult worms subsequently implanted into jirds. R7/45 was highly active against third and fourth stage larvae of B. pahangi in jirds.

Jirds were vaccinated by three to five subcutaneous (SC) injections of infective larvae of Brugia pahangi which had been irradiated at 25, 45 or 90 krads from a 60Co source. They were challenged either SC or intraperitoneally. Vaccination with four doses of 50 larvae irradiated with 25 krads produced 49·3% resistance to IP challenge worms and 39·8% against SC challenge worms. Five doses of larvae irradiated with 45 krads produced 62% resistance to SC challenge. Three doses of larvae irradiated with 90 krads produced 74·9% resistance to SC challenge and five doses produced 76·2% resistance. The reasons why irradiated larvae produce resistance whereas normal larvae do not are discussed.

Worm establishment, development and fecundity of Taenia crassiceps in the intestine of prednisolone (PTBA)-treated, 15- and 4-week-old Mongolian gerbils and 9-week-old inbred mice of 4 strains (AKR/J, BALB/cAn, B10D2/oSn and C57BL/KsJ) were investigated following oral administration of metacestodes. Gerbils were divided into 5 groups of 4 animals each according to the host age and commencement day of PTBA-treatment (day −13, −7 or 0 relative to infection). Worm recovery from the intestine on day 35 postinfection was not affected by host age, but fewer worms were recovered the earlier the commencement of PTBA-treatment. Worm size, determined by wet weight, total length and proglottis number, correlated inversely with worm burden, suggesting they were affected by the crowding effect. Proglottides were released normally in the faeces but were markedly depressed in all groups except for that of young gerbils. Furthermore, egg production and its development in gravid proglottides were markedly depressed in all groups. In PTBA-treated mice of 4 strains, sexually mature but not gravid worms were recovered from all mice of the AKR/J strain on days 20–32 postinfection, but none or few worms from the intestine of the others. PTBA-treatment did not inhibit all protective host defence mechanism(s) in the unnatural or alternative rodent definitive host of T. crassiceps.

Mel W is a second generation anionic organic arsenical which is filaricidal but has sporadic and unacceptable lethal side effects. Eight new cationic derivatives have now been synthesized in an attempt to avoid the side effects and have been examined for their effects upon adult Brugia pahangi in Meriones unguiculatus. They were all shown to be potent filaricides and the two best compounds, Mel Ga and Mel Cy, were at least 95% effective in killing adult B. pahangi at 5x3–13 mg/kg when injected subcutaneously.

This paper reports the experimental transmission of a bird parasite into jirds. Infective larvae of Cardiofilaria nilesi obtained from laboratory colonized Coquillettidia crassipes mosquitoes which had fed on an infected chicken were inoculated subcutaneously into jirds. The number of larvae per jird varied from 10 to 228. Microfilaraemia appeared 22 to 89 days after inoculation of the infective larvae. Experiments were carried out with 24 jirds through six generations extending over a period of 22 months and 17 produced patent infections. At present 8 infected jirds are being maintained in the laboratory; their patent periods ranging from 6 to 13 months. However, the longest patent period observed was about thirteen months. The percentage of adults recovered in autopsied jirds ranged from 0 to 40 with an average of 16. The chicken showed a microfilarial periodicity with the peak microfilarial density around 2200 hours. However, in jirds there was a change in sub-periodicity. This model in the jird may be very useful for the screening of filaricides and in immunological work.

The direct action of diethylcarbamazine (DEC) on the infective larvae of Brugia pahangi was studied. The larvae were cultured in RPMI 1640 supplemented with foetal bovine serum and antibiotics for 22 days. Most of the larvae remained alive for 8 days, but survival rate of larvae decreased rapidly from day 10 onwards. The larvae did not grow in the culture system. The addition of DEC did not affect the morbidity of the larvae and no difference was observed in the morphological characteristics between the larvae cultured in the presence or absence of DEC.

The infective larvae were cultured in vitro for 5 days in the presence or absence of DEC, and inoculated into jirds. The animals were necropsied at intervals, and developing larvae and adult worms were recovered. When the larvae were cultured without DEC and then inoculated subcutaneously into jirds, 29.8% of the inoculum was recovered 3–15 days, and 25% 19–22 weeks, post-inoculation. However, when the larvae were exposed to DEC in vitro and inoculated into jirds, the rate of recovery was reduced to 25% 3–15 days post-inoculation and 2% after 19–22 weeks. When the control larvae cultured in vitro were inoculated intraperitoneally into jirds, 41·3% of inoculum was recovered 3–15 days, and 42·8% 19–22 weeks, post-inoculation. Again the corresponding value for larvae exposed to DEC in vitro was reduced to 19.8% 3–15 days, and 8% 19–22 weeks, post-inoculation. It was observed that the larvae exposed to DEC in vitro were retarded in their development in jirds. These results indicate that DEC has a direct action against the infective larvae of B. pahangi.

Mongolian gerbils were infected with either a benzimidazole-susceptible or a benzimidazole-resistant strain of Trichostrongylus colubriformis larvae. The comparative pathogensis of both strains of T. colubriformis was investigated for 50 days post-infection. The gerbils infected with the drug-susceptible strain of the parasite showed lower survival rates, reduced body weights, higher parasite egg output and higher worm burdens than animals intected with the drug-resistant stram of parasite. There was also evidence of an enhanced hypoalbuminaemia and a more marked gastrointestinal plasma leak in the gerbils infected with the drug-susceptible strain of patasite. Scanning electron microscope examination of the small intestine showed signs of villus atriphy in both groups of ingected grebils.

Groups of 10 Mongolian gerbils. Meriones unguiculatus, were vaccinated with 1,500 gamma-irradiated Trichostrongylus colubriformis infective larvae (L3) or with non-irradiated larvae. 25 days later five gerbils from each group were necropised and the remaining gerbils challenged with 1,500 non-irradiated T. colubriformis infective larvae. Systemic, local intestinal and coproantibody levels were compared in each group of gerbils 25 days after vaccination and 26 days after challenge. Strong local intestinal and faecal antibody responses were detected. Coproantibodies reflected antibody levels in the intestinal contents and in mucosal extracts. The results gave further support to the view that coproantibody measurements provide a sensitive index of immunity at mucosal surfaces to intestinal parasites.

Infective larvae of Onchocerca lienalis and O.volvulus implanted subcutaneously within micropore chambers into laboratory hosts moulted to the fourth stage (L4) and underwent limited development and growth. Similar recoveries of O. lienalis L4 larvae in the range of 33–66% were obtained from chambers implanted into CBA and BALB/c strains of mice, jirds, and the natural bovine host. A relatively constant proportion of larvae survived up to 24 days post implantation and thereafter recoveries declined, although some worms were still alive after 96 days. Recoveries of O. volvulus L4 larvae from chambers given to normal or T-cell deprived mice were equivalent to one another and to those obtained with O. lienalis. Moulting of O. lienalis in chambers was observed on days 3 and 5, in close accordance with the timing of the third moult in cattle following systemic infection. Moulting of O. volvulus occurred between days 3–6. Morphological changes in developing larvae included a small but significant increase in length, a transient increase in width, and early development of the spicular primordia and genital tube. L4 larvae of O. lienalis, but not those of O. volvulus, exhibited 3 distinct caudal papillae not present on infective larvae.

The study was aimed at developing better orally active albendazole (ALB) formulations. Six formulations (ALB-1 to ALB-6) were prepared and tested against Brugia malayi in Mastomys coucha and jird (Meriones unguiculatus) at 200 mg/kg, orally, for 5 consecutive days. The anti-filarial efficacy was assessed against microfilariae (mf), adult worms and female reproductive potential. Three of the 6 ALB formulations showed greatly improved female worm sterilizing potential (ALB-1: 90%; ALB-3: 63%; ALB-4: 77% of untreated control) in B. malayi – M. coucha model. Sterilization efficacy of ALB-1 was also better than that shown by pure-ALB (P<0·001) or its marketed tablet formulation, Zentel (P<0·01), while that of ALB-4 was better than pure-ALB (P<0·05). The activity of ALB-3, pure-ALB and Zentel was, however, comparable. ALB-1 also showed late microfilaricidal activity with a maximum of 78% fall in microfilarial count. In contrast, neither the pure ALB nor Zentel showed any microfilaricidal activity. In the jird – B. malayi model, ALB-1 and ALB-4 showed marginal sterilizing efficacy whereas pure ALB or Zentel were ineffective. In conclusion the anti-filarial efficacy of ALB-1 was found to be superior to pure-ALB or Zentel.

Trypanosoma (Herpetosoma) grosi, which naturally parasitizes Apodemus spp., can experimentally infect Mongolian jirds (Meriones unguiculatus). Three isolates from A. agrarius, A. peninsulae, and A. speciosus (named SESUJI, HANTO, and AKHA isolates, respectively) of different geographical origin (AKHA from Japan, and the others from Vladivostok), exhibited different durations of parasitaemia in laboratory jirds (2 weeks for HANTO, and 3 weeks for the others). To assess the genetic background of these T. grosi isolates, their small (SSU) and large subunit (LSU) ribosomal RNA genes (rDNA) were sequenced along with those of 2 other Herpetosoma species from squirrels. The SSU rDNA sequences of these 3 species along with available sequences of 3 other Herpetosoma trypanosomes (T. lewisi, T. musculi and T. microti) seemed to reflect well the phylogenetic relationship of their hosts. Three isolates of T. grosi exhibited base changes at 2–6 positions of 2019-base 18S rDNA, at 5–29 positions of 1817/1818-base 28Sα rDNA, or 1–5 positions of 1557–1559-base 28Sβ rDNA, and none was separated from the other 2 isolates by rDNA nucleotide sequences. Since base changes of Herpetosoma trypanosomes at the level of inter- and intra-species might occur frequently in specified rDNA regions, the molecular analysis on these regions of rodent trypanosomes could help species/strain differentiation and systematic revision of Herpetosoma trypanosome species, which must be more abundant than presently known.

Mongolian jirds, Meriones unguiculatus, are susceptible to infection with Trypanosoma grosi, which naturally parasitizes Apodemus spp. The present study investigated T cell dependence of elimination of T. grosi from the bloodstream of jirds by in vivo T cell depletion using a monoclonal antibody (HUSM-M.g.15). In T cell-depleted jirds, elimination of T. grosi, particularly the dividing forms, from the bloodstream was significantly delayed, occurring at around week 3 p.i. The kinetics of serum levels of IgM and IgG specific to trypanosomes in T cell-depleted and control immunocompetent jirds were different; peak levels of IgM were noted on days 6–8 p.i. around the time of peak parasitaemia (day 6 p.i.) in immunocompetent jirds, whereas the serum levels began to increase abruptly after day 10 p.i., peaking at around day 18 p.i. in T cell-depleted jirds. Similarly, serum IgG increased after day 6 p.i. in immunocompetent jirds, in contrast to after day 12 p.i. in T cell-depleted jirds, and the level increased steadily even after disappearance of parasitaemia. Our findings indicate that T cells play a major role at least in the ‘first crisis’ during elimination of dividing T. grosi from the bloodstream.

Non-pathogenic trypanosomes of the subgenus Herpetosoma are normally host specific, and laboratory models include Trypanosoma lewisi in rats and Trypanosoma musculi in mice. Two isolates of Trypanosoma grosi, originating from Apodemus agrarius and Apodemus peninsulae, grew well in Mongolian jirds, Meriones unguiculatus, after intraperitoneal inoculation of 2×105 or a minimum 500 bloodstream forms. The course of T. grosi infection in jirds resembled T. musculi infection in mice, rather than T. lewisi infection in rats. At week 2 to 3 p.i. trypanosomes disappeared from the bloodstream, and neither prednisolone treatment nor splenectomy prevented parasite elimination from the bloodstream. However, these treatments induced a marked increase in peak parasite counts. Regardless of prednisolone treatment or splenectomy, all jirds after day 21 p.i. became resistant to the reinfection. Although no trypanosomes were detected in the bloodstream of recovered jirds, dividing parasites persisted in the medullary capillaries of the kidney, like T. musculi infection in mice. We propose the T. grosi infection in jirds as an additional laboratory model for the study of non-pathogenic trypanosomes.

The Mongolian gerbil has been used as laboratory animal since 1935. Breeding gerbils as an isolated laboratory population for decades may have led to a domestication process whose effects include changes in brain size. Quantitative changes in testicular activity could be assumed. Comparative intraspecific measurements were performed in 34 adult males of the laboratory strain (LAB) and in males raised as offspring of wild Mongolian gerbils (WILD) caught in central Mongolia (F1, n = 16; F2, n = 17). LAB and WILD were examined in January. Testicular spermatozoa were counted, proportions of different cell types were analysed using DNA flow cytometry, and mitotic and meiotic activity was calculated from DNA histograms. Intratesticular testosterone concentrations were measured with an enzyme immunoassay. In the WILD, testicular activity was lower and varied more. The overall weight, the efficiency of spermatogenesis (sperm/g testis) and resulting total sperm per testis were significantly less in offspring of wild gerbils. This corresponded with lower levels of haploid cells, total germ cell transformation of diploid cells to spermatids and meiotic transformation of spermatocytes to spermatids. The most profound difference was found in testicular testosterone concentration: the mean level was 405.7 ± 41.2 ng/g testis in LAB vs 6.4 ± 2.0 ng/g in WILD F1. All parameters changed in WILD F2 generation compared with F1 and diminished the differences with LAB. Differences between F1 and F2 were significant for testis mass, testis/body weight ratio, percentages of haploid cells and cells in G2/M phase, both germ cell transformations and testosterone concentration. The results suggest rapid, adaptive changes of male reproductive physiology in the early offspring generations from wild populations under laboratory breeding conditions. The breeding of Mongolian gerbils in the laboratory has influenced the testicular function resulting in increased spermatogenic activity and highly stimulated testosterone production.