Effect of fenbendazole and pyrantel tartrate on the induction of protective immunity in pigs naturally or experimentally infected with Ascaris suum

An experiment was conducted with 96 weanling pigs (avg initial wt 18.5 kg) divided into six treatment with two replicates of eight pigs each. Pigs in Treatments 1, 2 and 3 were penned in outside pens with dirt lots that previously were contaminated with A. suum ova to induce a natural ascaris infection. Pigs in Treatments 4, 5 and 6 were penned in an open-front building with solid concrete floors and were experimentally infected with 2,000 embryonated A. suum. ova on d 1, 15 and 29 of the experiment. Pigs in Treatments 1 and 4 were medicated with fenbendazole (FBZ, 3 mg/[kg BW.d]) for three consecutive days during three consecutive time periods. Pigs in Treatments 2 and 5 were medicated with pyrantel tartrate (PT, 106 mg/kg feed) for 28 d. Pigs in Treatments 3 and 6 served as infected, unmedicated controls. All pigs were challenged with 100 A. suum eggs 7 d after termination of the final FBZ treatment. All pigs were killed 66 d after challenge and worms were recovered. Fenbendazole treatment resulted in greater (P less than .07) average daily gain than PT treatment in pigs penned outside. Among inside pigs, FBZ treatment resulted in better (P less than .02) feed utilization than in controls. The FBZ and PT treatments reduced (P less than .03) the total number of A. suum, the length and weight of female ascarids and the length of male ascarids compared with controls. A natural continual infection with A. suum was less effective than experimental infection in inducing protective immunity in pigs.     

Susceptibility of fourth-stage Ascaris suum larvae to fenbendazole and to host response in the pig

Fenbendazole given at the rate of 2.5 g/kg of feed for 3 days had 100% efficacy against 4th-stage Ascaris suum larvae in 8 pigs. Eight control pigs had a total of 108 A suum. In 6 pigs infected 3 times with 3rd-stage A suum larvae and treated with fenbendazole after the larvae molted to the 4th stage, the challenge exposure-derived population was decreased by 64%. Similar sequential infections in 6 pigs similarly infected, but not treated with fenbendazole, decreased the challenge exposure-derived population by 98%; however, developing and/or adult worms from the vaccinating infections were present.     

Embryonation and infectivity of Ascaris suum eggs. A comparison of eggs collected from worm uteri with eggs isolated from pig faeces

Ascaris suum eggs were collected from pig faeces or dissected from worms obtained from the same pigs. Eggs from the two sources were allowed to embryonate in 0.1 N H2SO4, in 1% buffered formalin or in tap water. The embryonation of the sulphuric acid and water cultures occurred at the same speed, while the formalin cultures developed slightly more slowly. By experimental inoculation of helminth-free pigs and subsequent counting of white spots in the livers and larvae in the lungs day 7 p.i., the infectivity of eggs dissected from worm uteri and embryonated in sulphuric acid (a normal laboratory procedure) was compared with that of eggs collected from faeces and embryonated in water (i.e. more naturally developed eggs). The results suggest that the two types of eggs were equally infective. For this reason the common practice of using Ascaris eggs dissected from worms for experimental infections might be acceptable.     

Evaluation of fenbendazole as an extended anthelmintic treatment regimen for swine

Fenbendazole was given in the feed to swine at a cumulative dosage of 9 mg/kg of body weight over a period of 3, 6, and 12 days to compare efficacy. Four treatment groups of ten 2- to 3-month-old pigs each, with a mean of 15 kg of body weight per group, received 3 mg of fenbendazole/kg/day for 3 days, 1.5 mg/kg/day for 6 days, 0.75 mg/kg/day for 12 days, and no medication. Medicated feed was scheduled so that all treated pigs reached the last day of treatment on the same day, thus making the time between the last treatment and necropsy equal for all groups. Ascaris suum and Trichuris suis were the target species, their presence before treatment being determined by fecal egg counts and at necropsy by worm counts. At necropsy, 9 control pigs were infected with A suum (mean of 18.0 worms/pig), and all control pigs had T suis infection (mean of 36.5 worms/pig). All 3 treatment schedules were 100% effective in removal of A suum; and for T suis, the 3-day regimen was 100% effective, the 6-day regimen, 99.2%, and the 12-day regimen, 91.0%.     

Concurrent Ascaris suum and Oesophagostomum dentatum infections in pigs.

The aim of this study was to examine interactions between Ascaris suum and Oesophagostomum dentatum infections in pigs with regard to population dynamics of the worms such as recovery, location and length; and host reactions such as weight gain, pathological changes in the liver and immune response. Seventy-two helminth-na?ve pigs were allocated into four groups. Group A was inoculated twice weekly with 10000 O. dentatum larvae for 8 weeks and subsequently challenge-infected with 1000 A. suum eggs, while Group B was infected with only 1000 A. suum eggs; Group C was inoculated twice weekly with 500 A. suum eggs for 8 weeks and subsequently challenge-infected with 5000 O. dentatum larvae, whereas Group D was given only 5000 O. dentatum larvae. All trickle infections continued until slaughter. Twelve pigs from Group A and B were slaughtered 10 days post challenge infection (p.c.i.) and the remaining 12 pigs from the each of the four groups were slaughtered 28 days p.c.i.. No clinical signs of parasitism were observed. The total worm burdens and the distributions of the challenge infection species were not influenced by previous primary trickle-infections with the heterologous species. Until day 10 p.c.i. the ELISA response between A. suum antigen and sera from the O. dentatum trickle infected pigs (Group A) pigs were significantly higher compared to the uninfected Group B. This was correlated with a significantly higher number of white spots on the liver surface both on Day 10 and 28 p.c.i. in Group A compared to Group B. The mean length of the adult O. dentatum worms was significantly reduced in the A. suum trickle infected group compared to the control group. These results indicate low level of interaction between the two parasite species investigated.     

Influence of an experimental infection of Ascaris suum on performance of pigs

Thirty-two pigs (average 26.6 kg live weight) were individually housed and fed to study the effect of an infection of Ascaris suum (either 0, 600, 6,000 or 60,000 A. suum eggs/pig) on performance of growing-finishing pigs. Increasing the level of A. suum infection produced linear (P less than .07) and quadratic (P less than .09) effects on final weight, weight gain and average daily gain. Feed to gain ratio and number of A. suum worms recovered from the intestines of pigs at slaughter increased linearly (P less than .01) with increasing doses of A. suum eggs. Pigs receiving 60,000 A. suum eggs were 13% less (P less than .01) efficient than the noninfected controls. In each of two trials, eight crossbred barrows (15.7 kg in trial 1 and 16.1 kg body weight in trial 2) were examined for the effects of two levels of A. suum infection (0 and 20,000 eggs/pig) on digestibility coefficients for dry matter, crude protein and gross energy. The infection did not affect (P greater than .05) digestibility coefficients during the first two collection periods (d 6 through 10 and 19 through 23). However, digestion coefficients for dry matter, crude protein and gross energy obtained from the total collection period on d 33 through 37 postinfection were greater (P less than .01) for control pigs than for pigs given 20,000 A. suum eggs each. Also, N retention was greater (P less than .05) for control pigs than for infected pigs.     

Fenbendazole as a therapy for naturally acquired Stephanurus dentatus and gastrointestinal nematodes in feral swine

Adult feral swine, naturally infected with kidney worms (Stephanurus dentatus) and gastrointestinal nematodes, were divided into two groups of 10 pigs each. One group was treated with fenbendazole (Panacur, Hoechst AG, Frankfurt am. Main) mixed in feed at the rate of 3 mg kg-1 body weight for 3 days. The second group received feed only and was designated as non-treated controls. The animals in both groups were necropsied 3 weeks post-treatment and examined for the presence of live and dead adult kidney worms in the perirenal and ureteral area, ureteral penetration, the presence of kidney worm larvae in the liver, hepatic scars due to kidney worm larval migration, and for liver fibrosis. No live adult kidney worms were found in the perirenal and ureteral areas of treated pigs, and the non-treated pigs harbored an average of 42.8 live worms. No liver kidney worm larvae were found in the livers of treated pigs, and the non-treated pigs averaged 6.7 live larvae. At necropsy, urine samples from 8 of the 10 treated pigs contained no kidney worm eggs, and only 2 eggs were found in samples from each of the remaining 2 pigs in this group. In contrast, urine samples from 8 of the non-treated pigs contained numerous kidney worm eggs. Reductions in ascarid (Ascaris suum) and nodular worm (Oesophagostomum dentatum) egg counts were also observed in treated pigs.     

High pressure processing treatment prevents embryonation of eggs of Trichuris vulpis and Ascaris suum and induces delay in development of eggs

High hydrostatic pressure processing (HPP) is an effective non-thermal treatment used to inactivate pathogens from a variety of food and food products. It has been extensively examined using prokaryotic organisms and protozoan's but has had limited study on metazoans. Treatment using HPP has been shown to be effective in inactivating nematode larvae in food and preventing embryonation of Ascaris suum eggs. We conducted experiments using eggs of the canine whipworm Trichuris vulpis collected from naturally infected dogs and A. suum eggs from naturally infected pigs. We observed a delay in development of eggs of T. vulpis in a preliminary experiment and conducted 2 experiments to test the hypothesis that appropriate HPP levels can induce a delay in embryonation of nematode eggs. In experiment 1, nonembryonated T. vulpis eggs in tap water were packaged in sealable bags and exposed to 138-600 megapascals (MPa; 1 MPa=10 atm=147 psi) for 60s in a commercial HPP unit. In a second experiment, nonembryonated eggs of A. suum were exposed to 138-600 MPa and treated for 60s in the same commercial HPP unit. Embyronation of T. vulpis eggs was delayed by 4 and 5 days for eggs treated with 207 and 241 MPa but eventually eggs developed and the numbers of embryonated eggs was similar to controls on day 55. Embryonation of T. vulpis eggs treated with 345 or 350 MPa was delayed by 9 days and never reached more than 5% of eggs embryonated. On day 55 post treatment, 95% of control nontreated T. vulpis eggs were embryonated, 100-65% of eggs treated with 138-276 MPa were embryonated, a maximum of 5% of eggs treated with 345-350 MPa were embryonated, and 0% of eggs treated with ≥ 400 MPa were embryonated. T. vulpis eggs treated with ≥ 400 MPa did not undergo cell division. Embryrnation of A. suum eggs was delayed by 4, 10, and 16 days for eggs treated with 207, 241, and 250MPa, respectively, compared to nontreated control eggs. A. suum eggs treated with 207 MPa eventually embryonated to similar % embryonation values as controls and 138 MPa treated eggs but eggs treated with 241 or 250 MPa were always <5% embryonated. A. suum eggs treated with ≥ 300 MPa did not undergo cell division. On the final day of examination at day 56 after treatment, the % of embryonated eggs was 92% nontreated controls, 94% treated with 138 MPa, 84% treated with 207 MPa, 2% treated with 241 or 250 MPa, and 0% treated with 276, 200, 345, 400, or 414 MPa, respectively.     

Ascaris suum infection in pigs sensitizes lymphocytes but suppresses their responsiveness to phytomitogens

The effect of Ascaris suum infection and treatment with fenbendazole on the blastogenic response of peripheral blood lymphocytes to A. suum antigens and to three phytomitogens was assayed by the lymphocyte transformation technique. Repeated infections with A. suum led to the development of sensitized lymphocytes primarily responding to egg hatching fluid antigen. Treatment with fenbendazole decreased the number of specific sensitized lymphocytes, but favorably increased the resistance of pigs to reinfection. Immunity to reinfection did not correlate with the strength of the blastogenic response to A. suum antigens. Repeated infection with A. suum negatively affected the development of the blastogenic response to phytomitogens in the pigs, leading to a partial depression of the responsiveness of lymphocytes and to the partial suppression by serum. Responses to pokeweed mitogen were affected more than the responses to concanavalin A and phytohemagglutinin.     

Production and distribution of immunoglobulin-bearing cells in the intestine of young pigs infected with Ascaris suum

Pigs of 10 days-1 month old were orally infected with eggs of Ascaris suum at different rates and inoculation schedules. Histological sections from various parts of the small intestines were prepared to observe the production and localization of immunoglobulin-bearing cells. Fluorescent antibody and immunoperoxidase staining methods were used to determine the number of IgM-, IgA- and IgG-producing plasma cells in the intestinal lamina propria. Significant increases in immunoglobulin-bearing cells were observed in those pigs which received single inoculations of A. suum eggs. Pigs infected every 2,4,8 and 10 days with 10,000-20,000 embryonated eggs showed numerical increases in IgM-bearing cells. Increases in IgA-bearing cells were noted in pigs which received the higher number of eggs every 8-10 days. Higher concentrations of IgA- and IgM-bearing cells were observed in the jejunal mucosa of infected pigs as compared to those in the duodenum and ileum.     

Efficacy of dichlorvos, fenbendazole, and ivermectin in swine with induced intestinal nematode infections

Anthelmintic efficacies of dichlorvos, fenbendazole, and ivermectin were compared in specific-pathogen-free crossbred weanling pigs inoculated with Ascaris suum, Trichuris suis, and Oesophagostomum dentatum. On postinoculation day (PID) 50, 24 pigs in each treatment group were treated orally with 43 mg of dichlorvos/kg of body weight, 3 X 3 mg of fenbendazole/kg, or 300 micrograms of ivermectin/kg, SC. Twenty-four pigs were not treated. On posttreatment day 7 (PID 57), 12 pigs from each treatment group (phase I) were slaughtered, and the anthelmintic efficacy of each treatment was determined. Efficacies against A suum, T suis, and O dentatum, respectively, were: dichlorvos, 100%, 99.9%, and 100%; fenbendazole, 100%, 99.8%, and 100%; and ivermectin, 98.7%, 53.9%, and 87.6%. Weight gains and feed conversions of the remaining pigs were monitored until they reached market weight (phase II). The average weight gains (kg) and feed conversions (kg of feed/kg of gain) at posttreatment day 81 (PID 131), respectively, were: 73.6 and 3.44 for nontreated controls, 78.9 and 3.31 for dichlorvos-treated pigs, 72.1 and 3.36 for fenbendazole-treated pigs, and 74 and 3.48 for ivermectin-treated pigs. Differences in average weight gains and feed conversions were not significant (P greater than 0.05).     

Immunity of swine to Ascaris suum

Swine were hyperimmunized to Ascaris suum by giving multiple oral inoculations of embryonated eggs. Sera and lymphocyte lysate from these pigs were administered parenterally to 4-week-old pigs. The latter animals were no more resistant to larval migration than control pigs receiving sera or lymphocyte lysate from non-immunized pigs. Other pigs were infected with transmissible gastroenteritis (TGE) virus, allowed to recover and challenged with embryonated ascarid eggs. They likewise were no more resistant to ascarid larval migration than control pigs.     

Effects of milbemycin on adult Toxocara canis in dogs with experimentally induced infection

To determine the efficacy of a formulation of milbemycins in treating patent infection with Toxocara canis, 8 male and 7 female, 10-week-old, ascarid-free Beagles each were given 125 embryonated eggs of T canis. All dogs developed patent infection within 56 days. On post-infection day 70, the dogs were assigned to 1 of 3 groups of 5 dogs each; members of 1 group were given a placebo, while dogs of the other 2 groups were given either 5.68 or 34.08 mg of the milbemycin formulation, respectively. In both groups of dogs given the drug, the number of eggs passed per gram of feces decreased precipitously. However, a few eggs still were found in the feces of several dogs of each group on the day of necropsy (postinfection day 75). Worms or fragments of worms were passed by the treated dogs from the day of treatment until the day on which necropsy was performed; however, most worms were passed during the first 2 days after treatment. At necropsy, only dogs of the control group were found to harbor adult T canis.     

Effect of fenbendazole on Toxocara canis larvae in tissues of infected dogs.

The effect of fenbendazole therapy was studied in six dogs fed 10,000 embryonated Toxocara canis eggs. At 47 days after they were fed T canis, four dogs were given fenbendazole in two divided doses totaling 50 mg/kg of body weight each day for 14 days. Two infected dogs were not given fenbendazole. All dogs were necropsied at the end of treatment and the foci were counted in the lungs; their skeletal muscles were digested in 1% trypsin for the recovery of larvae. The T canis larvae were not recovered from the skeletal muscle of the four infected dogs treated with fenbendazole; 15 and 42 larvae/100 g of skeletal muscle were recovered from the two nonmedicated infeected dogs. The number of grossly visible foci on surfaces of lungs in treated dogs was markedly less than in the nonmedicated infected dogs. The results indicate that fenbendazole might be effective in preventing prenatal infection in dogs.     

Comparative studies of experimental oral inoculation of pigs with Ascaris suum eggs or third stage larvae

This experimental study was designed to compare the acquired resistance in pigs to Ascaris suum eggs following 4-weekly oral immunizations with either 200 A. suum infective eggs or 50 A. suum third stage larvae (L3). The two immunized groups (n = 7) together with an unimmunized control group (n = 7) of pigs were challenged orally with 50 infective A. suum eggs per kilogram bodyweight on day 19 after the last immunization. Seven days post-challenge the group immunized with eggs showed signs of resistance as evidenced by reduced lung larval counts compared with the challenge control group. Such significant resistance was not observed in the L3-immunized group. However, a markedly increased inflammatory liver reaction and white spot formation was demonstrated in the L3-immunized pigs after challenge compared with both control animals and egg-immunized pigs. On the day of challenge only the egg-immunized pigs mounted an anti-Ascaris antibody response both in serum and in lung lavage fluid. Ascaris-antigen induced increased histamine release from peripheral leucocytes following both immunization and challenge could only be demonstrated in the egg-immunized pigs. On day 7 post-challenge local IgA-anti-Ascaris antibodies were further demonstrated in bile of the egg-immunized group and in the small intestine of both immunized groups. In conclusion, oral A. suum egg immunization of pigs induced a significant reduction in lung larval counts upon challenge. In contrast, oral L3 immunization seemed to prime the pigs as observed by the presence of stunted lung larval growth and increased liver reaction post-challenge with A. suum eggs.     

Ecological influences on transmission rates of Ascaris suum to pigs on pastures

A study was conducted to determine the distribution and transmission rate of Ascaris suum eggs and Oesophagostomum dentatum larvae in a pasture/pig house facility, which during the preceding summer was contaminated with helminth eggs by infected pigs. In May, four groups of 10 helminth na?ve tracer pigs were exposed to fenced sections of the facility for 7 days and necropsied for parasite recovery 9-10 days later (trial 1). The highest rate of A. suum transmission (201 eggs per day) occurred in the pig house (A). On the pasture, egg transmission decreased with the distance from the house: 8 eggs per day in the feeding/dunging area (B); 1 egg per day on the nearest pasture (C); <1 egg per day on the distant pasture (D). Only a few O. dentatum infections were detected, indicating a poor ability of the infective larvae to overwinter. Soil analyses revealed that the highest percentage (5.8%) of embryonated A. suum eggs were in the house (A). Subsequently, the facility was recontaminated with A. suum eggs by infected pigs. A replicate trial 2 was conducted in the following May. A major finding was the complete reversal of egg distribution between the 2 years (trials 1 and 2). In contrast to previous results, the highest rates of transmission (569 and 480 eggs per day) occurred in pasture sections C and D, and the lowest transmission rates (192 and 64 eggs per day) were associated with the feeding/dunging sections and the house (B and A). Soil analyses again supported the tracer pig results, as the pasture sections had the highest concentrations of embryonated eggs. Detailed soil analysis also revealed a non-random, aggregated egg distribution pattern. The different results of the two trials may be due to the seasonal timing of egg deposition and tracer pig exposure. Many eggs deposited during the summer prior to trial 1 may have died rapidly due to high temperatures and dessication, especially when they were not protected by the house, while deposition in the autumn may have favored egg survival through lower temperatures, more moisture, and greater sequestration of eggs in the soil by rain and earthworms. The latter eggs may, however, not have become embryonated until turnout the next year. The results demonstrate that yearly rotations may not be sufficient in the control of parasites with long-lived eggs, such as A. suum, and that a pasture rotation scheme must include all areas, including housing.     

Presence of immunoglobulins and antigens in serum, lung and small intestine in Ascaris suum infected and immunised pigs

The immunodetection of local Ascaris suum antigens and local and systemic antibodies were analysed in pigs reinfected with eggs or immunized with the 14, 42 and 97 kilodalton (kDa) fractions from A. suum. Twenty-one Iberian pigs were divided in 7 groups of 3 pigs. Groups 1 and 2 were uninfected and challenge control groups, respectively. Groups 3 and 4 were infected weekly with increasing doses of A. suum eggs and Group 4 was additionally treated with pyrantel pamoate. Groups 5, 6 and 7 were immunised with the 14, 42 or 97 kDa fractions from adult worms, respectively. Groups 2-7 were challenged with 10,000 infective eggs. Animals of Groups 3 and 4 showed a pulmonary granulomatous reaction with moderate number of eosinophils and leukocytes, while Groups 5-7 presented higher number of cells, especially in animals immunized with the 42 kDa fraction. These immunized groups presented abundant deposition of Ascaris body fluid (BF) and body wall (BW) antigens as well as the 14 and 42 kDa fractions in the pulmonary and intestinal tissues, while lower deposition of antigens was observed in animals of Groups 3 and 4. The immunized pigs of Groups 5 and 6 showed the highest systemic IgG titres in serum and these antibodies were negatively correlated with the number of larvae recovered in the lungs, suggesting that the IgG response may have a protective function against the ascariosis. The highest concentrations of IgA-bearing cells were observed in animals of Groups 3 and 4 compared to the immunised pigs (Groups 5-7), suggesting that local IgA production may be involved in the protection against migrating larvae. The main localisations of IgA-bearing cells were the bronchial and peribronchial areas of lungs and the lamina propia of duodenum. Low numbers of local IgG-bearing cells were observed in all animals and no IgM-bearing cells were detected in the local tissues.     

Establishment of Ascaris suum in the pig: development of immunity following a single primary infection

Development of immunity after a single primary infection of Ascaris suum in pigs was investigated with regard to the worm population dynamics of a superimposed A. suum infection, host immune response and gross liver pathological changes. Group A was given a primary infection of 60,000 infective A. suum eggs and group B was left uninfected. Four weeks later both groups A and B were inoculated with 1,000 A. suum eggs, and subgroups were slaughtered 7, 14 and 21 days post challenge infection (p.c.i.). An uninfected control group C was slaughtered on day 21 p.c.i. The challenge worm recovery in group A was reduced compared to group B by 12%, 50% and 75% on day 7, 14 and 21 days p.c.i., respectively. In both groups was the expulsion of worms initiated between day 14 and 21 p.c.i. However, in group A the worms were recovered more posteriorly in the small intestine and 21 days p.c.i. the mean worm length was significantly shorter than in group B (p = 0.01). The results above were associated with significantly higher (p < 0.05) antibody response and higher eosinophil counts in group A compared to group B. The present results suggest that the larval growth and survival of a challenge infection are decreased, probably due to higher antibody and eosinophil attack during the migratory phase.     

Ascaris suum antigens incorporated into liposomes used to stimulate protection to migrating larvae

Four- to 8-week-old SPF pigs were immunized, using antigens of Ascaris suum incorporated into liposomes, via intestinal cannula or orally. Avridine was also incorporated in the liposomes in one experiment and interleukin-2 (IL-2) injected into pigs in another experiment. A priming dose of embryonate eggs (80-470 eggs/pig) were given in four of six experiments. Compared to control animals, the greatest protection of pigs to migrating ascarid larvae from a challenge dose of 10,000 embryonated eggs occurred where pigs received (1) a priming dose of eggs plus second-stage ascarid larval wall incorporated into liposomes, with or without avridine or IL-2, or (2) a priming dose of eggs plus ascarid intestinal aminopeptidase incorporated into liposomes with IL-2. The degree of protection was not statistically significant due, in part, to the variability in the responses of animals in the same treatment groups and the small number of animals per group. In general, only low titers of specific serum antibodies were detected and specific antibodies were not detected in the intestinal washing.     

Influence of helminth parasite exposure and strategic application of anthelmintics on the development of immunity and growth of swine

Infection of pigs with the intestinal roundworm parasite Ascaris suum and strategic application of anthelmintic drugs during the growing phase of development were observed for specific effects on 1) development of immunity in feeder pigs and 2) growth rate during the finishing phase. Management treatments included maintenance in a parasite-free concrete environment, maintenance in a concrete environment and inoculation with 1,000 infective A. suum eggs every other day over a 52-d period, and maintenance on a dirtlot contaminated with A. suum and Trichuris suis eggs. Within each management environment, pigs were either untreated, treated with ivermectin or treated with fenbenzadole at strategic times during parasite exposure. Protective immunity, assessed by a challenge inoculation with A. suum eggs following management treatments, was not affected by ivermectin or fenbenzadole treatment during exposure, but adult worm burdens were reduced and the pattern of A. suum larval antigen serum antibody responses were different from those in control pigs not treated with drugs. Exposure to A. suum and treatment with anthelmintics during the growing phase reduced adult worm burdens following the finishing phase of growth. Rate, but not efficiency, of gain was significantly improved by anthelmintic treatment following natural exposure to parasites. Strategic treatment of pigs with anthelmintics following inoculation with A. suum eggs in a concrete management environment had no effect on rate of gain. Results suggest that natural exposure to parasites during the growing phase without therapeutic treatment causes permanent damage to growth potential.