Search

The objective of this experiment was to investigate the potential influence of inulin on the establishment of new and patent infections of Trichuris suis in growing pigs. Two experimental diets were formulated based on barley flour with either added insoluble fibre from oat husk (Diet 1) or a pure inulin (16%) supplementation (Diet 2). Twenty-eight 10-week-old pigs were divided randomly into 4 groups (Groups 1-4) each of 7 pigs. After 3 weeks adaptation to the experimental diets all pigs were infected with a single dose of 2000 infective T. suis eggs. Group 1 was fed Diet 1 until 7 weeks post-infection (p.i.) and Group 3 until 9 weeks p.i., Group 2 was fed Diet 2 until 7 weeks p.i., Group 4 was fed Diet 1 until week 7 p.i. and was switched-over from Diet 1 to Diet 2 until week 9 p.i. Seven weeks p.i. pigs in Groups 1 and 2 were slaughtered, and pigs in Groups 3 and 4 were slaughtered at 9 weeks p.i. Trichuris suis worm burdens were determined for all pigs. Inulin-fed pigs (Group 2) exhibited an 87% reduction in EPG, compared to the pigs on standard diet (Group 1) (P < 0.0001). The number of worms recovered at week 7 p.i. from pigs on the inulin diet (Group 2) was significantly reduced by 71%, compared to the pigs on standard diet (Group 1) (P < 0.01). At week 9, worm recovery in pigs on the inulin diet switch protocol (Group 4) was reduced by 47% compared to the control pigs in Group 3 (P < 0.01). Further, the inulin-fed pigs exhibited a significant reduction in female worm fecundity and worm large intestine location was more distal compared to those from pigs on standard diet. These results demonstrate that inclusion of the highly degradable fructose polymer inulin in the diet leads to significant reductions in T. suis establishment, egg excretion, and female worm fecundity and can be used as a treatment for patent infections.

A trickle infection experiment was undertaken to study in detail the population dynamics of Oesophagostomum dentatum in pigs. Three groups of 32 pigs were inoculated via the feed twice weekly with 100 (Group A), 1000 (Group B) or 10,000 (Group C) O. dentatum infective larvae (L3). Five pigs from each group were killed 2, 4, 8, 12, 16, and 20 weeks after the first inoculation (p.i.) to determine their worm burdens. Weekly faecal egg counts were determined. At slaughter, worms were counted, differentiated according to sex and developmental stage, and their length measured. Faecal egg counts ranked with dose rate until week 15, but later were more variable. The proportion of the total number of L3 administered which were recovered at slaughter inversely ranked with dose rate. In group C it decreased over time, whereas in groups A and B there was no consistent pattern. Worm fecundities (epg/female) in groups A and B were higher than in group C. The lengths of the female worms increased over time, whereas the lengths of the male worms remained approximately constant from week 8. The study suggests reduced establishment of incoming larvae and lower fecundity of the female worms at high dose levels.

The potential of a recombinant Schistosoma bovis-derived glutathione S-transferase (rSb28GST) to protect cattle against S. mattheei infection was tested in Zambia. All animals were challenged 2 weeks after the second inoculation with either 0.250 mg rSb28GST in adjuvants (vaccinated calves, n = 14) or adjuvants alone (controls, n = 14). In a first experiment, 7 vaccinated and 7 control animals were exposed to 10000 S. mattheei cercariae percutaneously. All animals developed clinical schistosomiasis 7-8 weeks after challenge. At perfusion, 12 weeks after challenge, vaccinated and control groups had averages of 887 and 541 eggs per gramme (epg) faeces, 6515 and 5990 worms, and 4.2 and 3.4 million tissue eggs, respectively. These results indicate that the immunization protocol used did not protect these calves against the massive single experimental challenge. In a second experiment, another 2 groups (n = 7) of vaccinated and control animals were challenged naturally over a period of 9 months on a farm known to be endemic for S. mattheei. The natural infections were much lighter in intensity, as indicated by the mean faecal egg count (13 epg), worm count (139) and tissue egg count (294000) in non-vaccinated controls. In vaccinated calves, significant reductions in female worm burdens (50%), faecal egg count (89%) and miracidial counts (93%) were recorded. Total tissue egg counts were also reduced by 42% in vaccinated animals. It therefore appears that the rSb28GST can provide significant protection in cattle against S. mattheei under conditions of low to moderate natural infection.

The interaction between the 2 nodular worm species in the pig, Oesophagostomum dentatum (O.d.) and Oesophagostomum quadrispinulatum (O.q.), was studied by comparing the development and distribution of the species following single or mixed infections. The faecal egg excretion levels were assessed at regular intervals from week 3 post-inoculation, and indicated a strong negative impact of the introduction of O.q. on the continued egg excretion of O.d. All pigs were killed 9 weeks after the first inoculations to determine the composition and location of the worm burdens in the large intestine. O.q. was found more anteriorly located in the intestine than O.d., thus confirming previous descriptions. When both species were present, the distribution of O.d. was moved further posteriorly and was more spread out than in single-species infections. There appeared to be no adverse effect of O.d. on the establishment and fecundity of O.q. However, the worm recoveries corroborated the egg excretion observations, namely reduced worm burdens of O.d. if O.q. was introduced, or if O.q. was already present. It is uncertain whether this effect is caused by differences in host reaction against the two species, or whether a more specific competition occurs between the two nodular worm species in pigs.

The influence of host dietary protein on acquired immunity and intestinal helminth population dynamics during repeated infection was studied using the mouse-Trichuris muris experimental model. CBA/Ca mice fed a 2% (by mass) protein diet ad libitum maintained body weight during the experiment, but when fed diets containing either 4% or 16% (by mass) protein gained weight steadily. Infection with T. muris did not affect the growth of the latter mice but significantly reduced the growth of animals fed on the 2% protein diet. When repeatedly infected with either 5 or 50 eggs every 10 days, the mice fed the 2% or 4% protein diet accumulated adults in proportion to infection dose. The results show that this is due to both the establishment of larvae at each repeated infection and the survival of established adults. In contrast, very few worms were recovered from animals fed the 16% protein diet, principally as a result of the development of strong acquired immunity to reinfection. T. muris egg output/mouse increased with infection dose in animals fed the low protein diets, but no parasite eggs were detected in the faeces of hosts fed the 16% protein diet. Mouse antibody responses to adult worm excretory/secretory antigen were time- and infection dose-dependent in all 3 dietary groups. The major finding was that the specific antibody response was more intense, both quantitatively (serum OD levels) and qualitatively (antigen recognition by IgG1), in mice fed the low protein diets, even though they remained susceptible to infection. This study shows that host dietary protein deficiency, even at levels irrelevant to normal growth, can markedly potentiate the transmission of T. muris via alterations in host resistance. The high levels of antibody in susceptible animals suggest that this defect in resistance is unlikely to be due to nutrient deficiency-associated defects in humoral immunity.

The course of infection with a Malaysian dog strain of Ancylostoma ceylanicum was investigated in 15 inbred strains of mice, in outbred and inbred mice immunosuppressed with prednisolone, and in immunodeficient hypothymic mice. Oral, percutaneous and subcutaneous routes of infection, in both sexes of mice, were assessed. In only one instance was a single small adult male worm found. Following oral infection, larvae migrated from the stomach to the large bowel and then a proportion of worms penetrated the perianal skin. This was followed by the appearance of larvae in the lungs. Living 3rd-stage larvae were seen in the anterior small intestine, perianal skin and lungs for the 6 weeks of the study, with peak recoveries being at 12 h, 8 days and 3 weeks, respectively. It is clear that systemic migration of larvae occurs after oral infection, and it is possible that recirculation may occur. Only a small percentage of larvae penetrated the abdominal skin after being administered percutaneously. In subcutaneous infections, a small proportion of larvae moved rapidly from the site of injection and were recovered from the lungs 2 h after infection. Most larvae, however, migrated from the injection site over the ensuing few days. Living 3rd-stage larvae were seen in the lungs and in the small intestine for the 4 weeks of observation. The strain of A. ceylanicum employed does not complete its development in mice. Nevertheless, this model offers significant potential for studying the immune responses, as well as investigating the means by which these parasites evade host defences.

In young (6- to 8-week-old) NIH strain inbred mice expulsion of a primary infection of Trichinella spiralis began on day 8 and was virtually complete by day 11-5. In older mice expulsion occurred 1 or 2 days earlier. Experience of a primary infection elicited strong immunity to challenge, whether the challenge was given immediately after worm expulsion (day 14) or delayed (day 42). Challenge infections were expelled rapidly the majority of worms being lost during the first day. Immunity to challenge was elicited by low-level primary infections and was effective against large ventionally accepted parameters of immunity to T. spiralis in mice which, it is considered, are applicable only to mice with a genetically determined low-level of responsiveness to the parasite.

Eimeria flavescens and E. irresidua from the domestic rabbit are redescribed. The relatively smaller ovoidal oocysts of E. flavescens which measure on average 31.7 X 21.4 micrometer, possess a wide micropyle at the broad end. First-generation schizonts of this species develop deep in the glands of the lower small intestine. Merozoites migrate to the caecum and colon where second, third and fourth-generation schizonts develop in the superficial epithelium followed by the fifth-generation schizonts and gametocytes which form in the glands. In young Dutch rabbits E. flavescens is very pathogenic; low doses of oocysts produce a severe enteritis with high mortality and morbidity. The larger, broadly ellipsoidal oocysts of E. irresidua measure on average 38.4 X 23.2 micrometer and often possess a very small cryptic oocyst residuum. The endogenous stages develop in the small intestine only; first-generation schizonts in the glands and second-generation schizonts in the lamina propria whilst third and fourth-generation schizonts and gametocytes develop in the villous epithelium. E. irresidua is not pathogenic in young Dutch rabbits; even heavy infections produce only a transient pause in weight gain.

The results are presented of an experimental study of the population biology of chronic Trichuris muris (Nematoda) infection in cortisone-treated CBA/Ca mice. Attention is focused upon both the validity of the common use of faecal egg counts to demonstrate density dependence in helminth fecundity, and the identification of other possible density-dependent mechanisms that may regulate worm numbers in chronic trichuriasis. The results show that faecal egg counts, although demonstrating high daily variation, are not an artefact of host faecal output but a significant density-dependent function of worm burden. This finding contrasts with the observations on Heligmosomoides polygyrus infection in outbred MFI mice, but accords with similar studies in a wide variety of host - helminth systems. Worm establishment in the murine host is found to be a density related function of infection dose. This is attributed to the probable existence of a physical gut-carrying capacity in the murine host for T. muris. Worm distribution in the gut is also shown to the density dependent, with worms being displaced from the caecum to the colon at increasing intensities of infection. The sex ratio of the adult parasites, however, is found to be both unitary and independent of worm burden. Evidence for a significant density-dependent decline in female T. muris growth or size is presented. The results also show a significant positive association between female T. muris weight and per capita fecundity. These findings indicate that the stunted growth of individual worms at high parasite densities may be a potential mechanism underlying density dependence in helminth fecundity.