Comparative infectivity of oocysts and bradyzoites of Toxoplasma gondii for intermediate (mice) and definitive (cats) hosts

Tachyzoites, bradyzoites (in tissue cysts), and sporozoites (in oocysts) are the three infectious stages of Toxoplasma gondii. The prepatent period (time to shedding of oocysts after primary infection) varies with the stage of T. gondii ingested by the cat. The prepatent period (pp) after ingesting bradyzoites is short (3-10 days) while it is long (18 days or longer) after ingesting oocysts or tachyzoites. The conversion of bradyzoites to tachyzoites and tachyzoites to bradyzoites is biologically important in the life cycle of T. gondii and it has been proposed that the pp can be used to study stage conversion. In the present study, infectivity of oocysts and bradyzoites released from tissue cysts of a recent isolate of T. gondii, TgCkAr23, to cats and mice was compared. Ten-fold dilutions of oocysts or bradyzoites were administered orally to cats, and orally and subcutaneously to mice. Of the 29 cats each fed 1-10 million oocysts only one cat shed oocysts and the pp was 23 days; all cats remained asymptomatic. In contrast, all mice administered the same 10-fold dilutions of oocysts either orally or subcutaneously died of toxoplasmosis. The results confirm that infectivity of the oocysts to cats is lower than for mice and that oocysts are non-pathogenic for cats. Of the 41 cats each fed 1-1,000 free bradyzoites, 15 shed oocysts with a short pp of 4-9 days, and all remained asymptomatic. The infectivity of bradyzoites to mice by the oral route was approximately 100 times lower than that by the subcutaneous route. The results confirm the hypothesis that the pp in cats is stage and not dose dependent, and that transmission of T. gondii is most efficient when cats consume tissue cysts (carnivory) or when intermediate hosts consume oocysts (fecal-oral transmission).     

Toxoplasma gondii cysts in placentas of experimentally infected sheep

To determine the presence of tissue cysts in ovine placentas, 6 ewes were inoculated orally with 10,000 Toxoplasma gondii oocysts at 60 days of gestation. The ewes were euthanatized and necropsied 21, 52, 56, 57, 57, and 62 days after T gondii inoculation, and placental cotyledons from each ewe were collected and homogenized. To distinguish between the presence of tachyzoites that are killed by acid pepsin solution and bradyzoites (from cysts) unaffected by this solution, a portion of each homogenate was inoculated into mice and another portion was inoculated into mice after digestion in acid pepsin solution. Toxoplasma gondii was isolated in 26 of 34 (76.4%) of mice inoculated with nondigested placentas of all 6 ewes and in 16 of 34 (47%) mice inoculated with digested placenta of 5 of 6 ewes. Seemingly, cysts do occur in placental tissue, but the digestion method was inferior, compared with the nondigestion method for recovery of T gondii from placenta.     

Protective immunity to toxoplasmosis in pigs vaccinated with a nonpersistent strain of Toxoplasma gondii

The RH strain of Toxoplasma gondii is highly virulent; 1 infective organism is uniformly lethal for mice. Three pigs inoculated SC with 10(3) tachyzoites of the RH strain developed fever, but otherwise remained normal, and T gondii was not demonstrated in their tissues by bioassay into mice. To determine whether vaccination with the RH strain could induce protective immunity to oral challenge with T gondii oocysts, 12 pigs were divided into 3 groups (A, B, C) of 4 pigs each. Pigs in groups A and B were inoculated IM with 10(6) tachyzoites of the RH strain and 4 pigs in group C served as uninoculated controls. Except for fever, the pigs remained clinically normal after inoculation with the RH strain and T gondii was not found by bioassay in mice of tissues from 4 pigs euthanatized 64 days after inoculation. Pigs in groups B and C were challenge-inoculated orally with 10(4) (4 pigs) or 10(5) (4 pigs) T gondii oocysts 72 days after vaccination with the RH strain. The previously uninoculated pigs developed fever, anorexia, and diarrhea from 3 to 8 days after the oocyst challenge. One of the 2 pigs given 10(5) oocysts became moribund because of toxoplasmosis and was euthanatized 9 days after inoculation. Pigs vaccinated with the RH strain remained free of clinical signs after challenge with oocysts. Results of the bioassays indicated that fewer tissue cysts developed in the RH strain-vaccinated pigs than in the previously uninoculated control pigs.     

Long-term persistence of Toxoplasma gondii in tissues of pigs inoculated with T gondii oocysts and effect of freezing on viability of tissue cysts in pork

To study the distribution of tissue cysts in porcine tissues, 16 pigs were fed oocysts of 4 strains of Toxoplasma gondii (4 pigs/strain). Pigs were euthanatized between postinoculation days 103 and 875 and portions of 5 to 14 organs were bioassayed in mice and/or cats for T gondii. For bioassays, 50- to 100-g portions of tissue were incubated in acidic pepsin solution to free bradyzoites from cysts in parenchyma, and washed sediment from the digests of each specimen was inoculated SC into mice (6 mice/organ). For bioassays in cats, a 500-g portion or whole organ was fed to Toxoplasma-free cats (1 cat/organ). Toxoplasma gondii was recovered from tissues of 14 of the 16 pigs (from the brains of 12, hearts of 11, tongues of 10, and diaphragms of 6). Toxoplasma gondii was isolated from commercial cuts of meat from 5 infected pigs; from the arm picnic and ham of 3, Boston butt, spareribs, and tenderloin of 2, and bacon and tailbone of 1. Regarding the 4 pigs euthanatized between postinoculation days 759 and 865, cats shed T gondii oocysts after the ingestion of hearts of all 4; tongues of 3; bacons, hams, arm picnics, Boston butts, spareribs, and diaphragms of 2; and livers, kidneys, and tenderloins of 1. Toxoplasma gondii was found to be inconsistently distributed among the organs and muscles, but overall, tongue and heart were more heavily infected than were other tissues. Tissue cysts in pork were rendered nonviable at -12 C for 3 days.     

Exploring the life cycle of Besnoitia besnoiti - experimental infection of putative definitive and intermediate host species

The biology of Besnoitia besnoiti, the cause of bovine besnoitiosis, is poorly understood. Its definitive host is unknown, and information on potential intermediate hosts is scarce. In order to investigate potential definitive and intermediate hosts for European isolates of B. besnoiti, domestic dogs, cats, rabbits, guinea pigs (Cavia porcellus), gerbils (Meriones unguiculatus), common voles (Microtus arvalis) and NMRI-mice were inoculated with B. besnoiti isolated from naturally infected German cattle. Dogs and cats were fed 5×10(6)B. besnoiti tachyzoites (isolate Bb-GER1), or tissue cysts containing at least 2×10(7)B. besnoiti bradyzoites obtained from the skin of a naturally infected Limousin cow from the same herd where strain Bb-GER1 was isolated. Rodents and rabbits were subcutaneously inoculated with either 5×10(5) Bb-GER1 tachyzoites or 5×10(5) bradyzoites. Groups of 2-4 non-inoculated animals of each species were monitored as negative controls. Feces from all dogs and cats were daily examined by a sedimentation-flotation technique for at least 11 weeks after inoculation but no B. besnoiti oocysts were identified. Cats fed tachyzoites and dogs did not seroconvert, but specific antibodies to B. besnoiti tachyzoites were detected by IFAT (titer≥100) in 2 out of 3 cats fed tissue cysts since 5-7 weeks post infection. By immunoblot, these two cats exhibited a reaction pattern against tachyzoite antigens similar to that observed in naturally infected cattle. Antibodies against B. besnoiti tachyzoites were detected in all inoculated rodent species and rabbits by both, IFAT and immunoblot since 3 weeks post-inoculation. Rabbits and rodents, subcutaneously inoculated with same doses of inactivated bradyzoites remained serologically negative (IFAT titer<50). Clinical signs observed in the inoculated rabbits included fever, serous conjunctivitis and transient swelling of the testes. No clinical abnormalities were noticed in the other tested animal species. Voles developed pneumonia as observed by histological examination. B. besnoiti-DNA was detected by PCR in blood from rabbits, gerbils and voles at 9 days post-infection, and in skin, heart, lung, striated muscle and kidney tissues from voles at 19-21 weeks post-infection. Domestic dogs and cats could not be shown to be definitive hosts of B. besnoiti, but cats seroconverted after feeding on B. besnoiti tissue cysts indicating that B. besnoiti stages had invaded the cats' tissues. The molecular and serological results from this study indicate that European B. besnoiti isolates may infect cats, rabbits, guinea pigs, gerbils, mice and voles; however a persistence of the parasite could be demonstrated only in voles.     

CpG-oligodeoxynucleotides enhance porcine immunity to Toxoplasma gondii

Protection against a challenge infection with Toxoplasma gondii VEG strain oocysts was examined in pigs after vaccination with T. gondii RH strain tachyzoites with or without a porcine specific synthetic oligodeoxynucleotides (ODN) containing immunostimulatory CpG motifs. Six groups of pigs were immunized with incomplete Freund's adjuvant (IFA) and either vehicle, tachyzoites alone or in combination with three different doses of CpG ODN or with CpG ODN alone. Protection from challenge was significantly (P < 0.05) improved in pigs vaccinated using CpG ODN as an adjuvant with tachyzoites compared to all other groups. The CpG ODN tachyzoite-immunized pigs also had higher serum parasite specific IgG antibody, no clinical signs of disease, and 52% had no demonstrable tissue cysts after the challenge infection. These data indicate that CpG ODN is a potential safe and effective adjuvant for the T. gondii RH strain vaccine in pigs.     

Immunity to Hammondia hammondi infection in cats.

Acquisition of immunity to Hammondia hammondi, a newly recognized coccidian of cats, was studied in 18 specific-pathogen-free cats. One cat was given a single oral inoculation, 11 cats were given 2 oral inoculations, and 1 cat was given 3 oral inoculations of homogenized mouse carcasses containing H hammondi. In all cats, oocyst shedding began 6 to 9 days after the 1st inoculation. Oocyst shedding peaked at 1 to 2 days after the onset of shedding and lasted for 1 to 2 weeks. None of the cats became sick. Of the 11 cats inoculated twice (between 2-51 days after the 1st inoculation), 5 shed oocysts 7 to 14 days after the repeat inoculation; however, fewer oocysts were shed at this time. One cat that was inoculated thrice (14 and 51 days after the 1st inoculation) shed oocysts 14 to 17 days after the 3rd inoculation but not after the 2nd inoculation. Spontaneous oocyst shedding was studied in 9 of these 13 H hammondi-infected cats for 5 months. Two cats spontaneously shed oocysts: One cat (inoculated only once) spontaneously re-shed oocysts 21 to 24, 31 to 33, 49 to 50, and 118 to 120 days after inoculation; The other cat (inoculated twice-the 2nd time, 6 days after the 1st inoculation) re-shed oocysts 38 to 48, 85 to 89, and 133 to 136 days after the 1st inoculation. The course of H hammondi infection was studied in 5 cats given weekly injections of 6-methyl prednisolone acetate for at least 7 weeks, starting 18 days before inoculation in 2 cats, and starting 14, 34, and 45 day after inoculation in 3 cats. The induced hyperadrenocorticism did not affect the prepatent period or induce parasitism of extraintestinal organs. The 3 cats infected for 14, 34, and 45 days, re-shed oocysts after hyperadrenocorticism was induced. It was concluded that immunity to H hammondi infection in cats is less stable than immunity to the related coccidian, Toxoplasma gondii.     

Effect of irradiation on the viability of Toxoplasma gondii cysts in tissues of mice and pigs

Muscles from tongue, heart, and limbs of 14 pigs inoculated orally with Toxoplasma gondii oocysts were irradiated with 10, 20, 25, and 30 krad of gamma (cesium-137 and cobalt-60) irradiation. Viability of T gondii cysts was assayed by feeding porcine muscles to T gondii-free cats and/or by inoculation of sediment from acid-pepsin digested porcine muscle into mice. Cats fed 500-g samples of muscles irradiated with up to 20 krad shed T gondii oocysts. Cats fed muscles irradiated with 25 or 30 krad did not shed oocysts. Mice were inoculated with 8 isolates of T gondii, and tissue cysts in their brains irradiated with up to 40 krad were infective to mice; however, there was a 10,000-fold reduction in the viability of organisms in tissue cysts irradiated with 40 krad, compared with that in nonirradiated cysts. At 50 krad of gamma irradiation, there were no detectable infective organisms in infected mouse brains.     

Acute primary toxoplasmic hepatitis in an adult cat shedding Toxoplasma gondii oocysts

A 3-year-old 4-kg neutered male domestic shorthair cat died within 5 days after onset of fever and respiratory distress. At necropsy, all tissues were icteric, and the liver had a diffuse reticular pattern. Histologically, hepatitis and encephalitis were associated with Toxoplasma gondii tachyzoites. Toxoplasma gondii female gamonts and oocysts were found in epithelial cells of intact villi and in epithelial cells desquamated into the lumen. Finding of acute hepatitis and T gondii oocysts in an adult cat without detectable immunodeficiency is unusual, because adult cats rarely have clinical signs of toxoplasmosis during the oocyst-shedding phase.     

Prevention of shedding and re-shedding of Toxoplasma gondii oocysts in experimentally infected cats treated with oral Clindamycin: a preliminary study

This work aimed to evaluate the effects of preventive oral Clindamycin in cats infected with Toxoplasma gondii. Twelve short hair cats were divided into two groups (group 1 and group 2). No titres of T. gondii antibodies were detected in these cats before the experiment. The animals from group 1 were infected with tissue cysts of T. gondii and group 2 were infected and treated with Clindamycin (20 mg/kg/day). The infection was done with almost 40-50 tissue cysts for each cat on day 0. The cats from group 2 were treated with Clindamycin by oral rout for 24 days (from day -3 to day 21). At day 45, the groups 1 and 2 were divided into two subgroups with three animals each. Subgroups 1A and 2A were immunosuppressed with dexamethasone (1 mg/kg/day) for30 days and subgroups 1B and 2B were not immunosuppressed. Faecal exam looking for oocyst shedding was made by 30 days after T. gondii infection, and for 30 days after immunosuppression. All kittens from group 1 shedding oocysts after infection, while animals from group 2 did not shed. After immunosuppression period, all animals from group 1A re-shed oocysts and animals from group 2A remained without shed. However, 2 (66.6%) of the kittens from subgroup 2B shed oocysts 19-20 days after re-challenge. Based on this preliminary study, Clindamycin had a complete inhibitory effect on shedding of oocysts by cats, even under severe immunosuppression, which is a new finding not reported elsewhere.     

Diagnosis of transplacentally induced toxoplasmosis in pigs

Seventeen sows were fed 1,000 Toxoplasma gondii oocysts of isolates GT-1 or PT-1 at 32 to 92 days of gestation, and the products of conception were examined for T gondii antibodies and parasites. Twelve of these sows were euthanatized near term between 21 and 62 days after being fed T gondii; fetal body fluids or fetal sera were examined for agglutinating T gondii antibodies, and tissues were bioassayed in mice for T gondii parasites. Six sows produced pigs that had been transplacentally infected with T gondii; one of them aborted a T gondii-infected fetus 17 days after ingesting oocytes. Agglutinating antibodies were detected in fetuses infected in utero, but transplacental transfer of T gondii antibodies was not observed in noninfected fetuses. Transcolostrally acquired T gondii antibodies disappeared by 3 months of age. Diagnosis of transplacental toxoplasmosis was confirmed on the basis of detection of T gondii organisms in fetal tissues by use of histologic examination and bioassay in mice. In conclusion, finding of T gondii antibodies in body fluids could serve as a rapid screening test for transplacental T gondii infection in pigs.     

Isolation and molecular characterization of Toxoplasma gondii from chickens and ducks from Egypt

The prevalence of Toxoplasma gondii in free range chickens is a good indicator of the prevalence of T. gondii oocysts in the environment because chickens feed from the ground. In the present study, prevalence of T. gondii in 121 free range chickens (Gallus domesticus) and 19 ducks (Anas sp.) from a rural area surrounding Giza, Egypt was assessed. Blood, heart, and brain from each animal were examined for T. gondii infection. Antibodies to T. gondii, assayed with the modified agglutination test (MAT), were found in 49 (40.4%) chickens in titers of 1:5 in 11, 1:10 in four, 1:20 in four, 1:40 in eight, 1:80 in 10, and 1:160 or more in 12 chickens. Antibodies were found in three ducks each with a titer of 1:80. Hearts and brains of seropositive (MAT > or = 1:5) chickens and ducks were bioassayed in mice. Additionally, hearts and brains of seronegative (MAT<1:5) animals were bioassayed in T. gondii-free cats. T. gondii was isolated from 19 of 49 seropositive chickens (one with a titer of 1:5, two with a titer of 1:20, one with a titer of 1:40, five with a titer of 1:80, three with a titer of 1:160, and seven with a titer of > or = 1:360). One cat fed tissues pooled from 15 seronegative chickens shed T. gondii oocysts, while two cats fed tissues of 34 seronegative chickens did not shed oocysts. T. gondii was isolated from one of the seropositive ducks by bioassay in mice. The two cats fed tissues from 16 seronegative ducks did not shed oocysts. Genotyping of 20 chicken isolates of T. gondii using the SAG 2 locus indicated that 17 isolates were type III and three were type II. The duck isolate of T. gondii was type III. The mice inoculated with tissue stages of all 21 isolates of T. gondii from chickens and ducks remained asymptomatic, indicating that phenotypically they were not type I because type I strains are lethal for mice. Infections with mixed genotypes were not found.     

Experimental infection of budgerigars (Melopsittacus undulatus) with a low virulent K21 strain of Toxoplasma gondii

In total 53 budgerigars (Melopsittacus undulatus) were divided into six groups and orally infected with a suspension of oocysts of low virulent Toxoplasma gondii K21 strain in the doses of 10(2), 10(3), 10(4), 10(5) and 10(6), respectively. Blood was collected from the birds prior to the inoculation and then on days 10, 20 and 30 post infection. Latex-agglutination test (LAT) was used for the detection of antibodies in the inoculated birds. The infected birds showed no apparent signs of disease. The antibodies were found in all but two birds inoculated a dose of 10(2) oocysts. Haematological values remained unchanged after infection. T. gondii was isolated by bioassay in mice from all 37 birds fed 10(3) or more oocysts and 6 of 9 fed 10(2) oocysts. The results demonstrate that budgerigars are resistant to T. gondii infection.     

Genetic and biologic characteristics of Toxoplasma gondii isolates in free-range chickens from Colombia, South America

The prevalence of Toxoplasma gondii in free-ranging chickens is a good indicator of the prevalence of T. gondii oocysts in the soil because chickens feed from the ground. The prevalence of T. gondii in 77 free-range chickens (Gallus domesticus) from Colombia, South America was determined. Antibodies to T. gondii were assayed by the modified agglutination test (MAT), and found in 32 (44.4%) of 72 chickens with titers of 1:5 in 4, 1:10 in 3, 1:20 in 1, 1:40 in 1, 1:80 in 8, 1:160 in 8, 1:320 in 3, and 1:640 or higher in 4. Hearts and brains of 31 seropositive chickens were pooled and bioassayed in mice. Tissues from 32 (16+16) seronegative chickens were pooled and fed to two, T. gondii-free cats, and tissues from nine chickens without matching sera were fed to one T. gondii-free cat. Feces of cats were examined for oocysts. T. gondii oocysts were excreted by a cat that was fed tissues of 16 seronegative chickens. T. gondii was isolated by bioassay in mice from 23 chickens with MAT titers of 1:20 or higher. All infected mice from 16 of the 23 isolates died of toxoplasmosis. Overall, 82 (81.1%) of 101 mice that became infected after inoculation with chicken tissues died of toxoplasmosis. Genotyping of these 24 isolates using polymorphisms at the SAG2 locus indicated that seven T. gondii isolates were Type I, 17 were Type III, and none was Type II. Phenotypically, T. gondii isolates from chickens from Colombia were similar to isolates from Brazil but different from the isolates from North America; most isolates from chickens from Brazil and Colombia were lethal for mice whereas isolates from North America did not kill inoculated mice. Genetically, none of the T. gondii isolates from Colombia and Brazil was SAG2 Type II, whereas most isolates from chickens from North America were Type II. This is the first report of genetic characterization of T. gondii isolates from Colombia, South America.     

Isolation and characterization of Toxoplasma gondii strains from stray cats revealed a single genotype in Beijing, China

Cats are essential in the epidemiology of Toxoplasma gondii because they are the only hosts that can excrete the environmentally resistant oocysts in nature. This study was aimed to determine the seropositivity, distribution of genotypes and mouse virulence of T. gondii from stray cats in Beijing, China. A total of 64 serum samples, 23 feces and tissue samples were collected from stray cats in Beijing. Antibodies to T. gondii were assayed by the modified agglutination test (MAT). 57.8% (37/64) of these stray cats had titers of 1:20 or higher and were considered positive with infection. T. gondii oocysts were not found in feces of the 23 cats. Tissues of 23 cats were bioassayed in mice and 11 T. gondii isolates were obtained. The genotype of these isolates were identified by 11 PCR-RFLP markers, including SAG1, (3'+5')SAG2, alt.SAG2, SAG3, BTUB, GRA6, c22-8, c29-2, L358, PK1, and an apicoplast marker, Apico. Only one genotype was identified. This genotype, designated as ToxoDB genotype #9, was previously reported in cats, pigs and human from Guangdong and Gansu provinces in China and animals from a few other countries. To determine mouse virulence of this lineage of parasites, one isolate was randomly selected and inoculated into BABL/c mice, the result showed that it is intermediately virulent to mice. These results indicated that an atypical, intermediately virulent T. gondii lineage is widespread in China. The high seropositivity of T. gondii in stray cats posts potential risk of transmission of the parasite to human population in the region.     

Genetic and biologic characteristics of Toxoplasma gondii infections in free-range chickens from Austria

The prevalence of Toxoplasma gondii in free-ranging chickens is a good indicator of the prevalence of T. gondii oocysts in the soil because chickens feed from the ground. The prevalence of T. gondii in free-range chickens (Gallus domesticus) from 11 Bio-farms in Austria was determined. Antibodies to T. gondii assayed by the modified agglutination test (MAT) were found in 302 of 830 (36.3%) chickens with titers of 1:10 in 50, 1:20 in 69, 1:40 in 53, 1:80 in 40, 1:160 or higher in 90. Hearts of 218 chickens with MAT titers of 10 or higher were bioassayed individually in mice. Tissues from 1183 chickens were pooled and fed to 15, T. gondii-free cats. Feces of the cats were examined for oocysts; 11 cats shed T. gondii oocysts. T. gondii was isolated from 56 chickens by bioassay in mice. Thus, there were 67 isolates of T. gondii from these chickens. Genotyping of these 67 isolates using the SAG2 locus indicated that all 33 were Type II. Phenotypically and genetically these isolates were different from T. gondii isolates from Brazil. None of the isolates was virulent for mice. This is the first report of isolation of T. gondii from chickens from Austria.     

Serological survey and risk factors for Toxoplasma gondii in domestic ducks and geese in Lower Saxony, Germany

To obtain estimates for the prevalence of Toxoplasma gondii infection in ducks and geese in Germany, enzyme-linked immunosorbent assays (ELISA) were established based on affinity-purified T. gondii tachyzoite surface antigen 1 (TgSAG1) and used to examine duck and goose sera for T. gondii-specific antibodies. The results of 186 sera from 60 non-infected ducks (Anas platyrhynchos) and 101 sera from 36 non-infected geese (Anser anser) as well as 72 sera from 11 ducks and 89 sera from 12 geese inoculated experimentally with T. gondii tachyzoites (intravenously) or oocysts (orally) and positive in a T. gondii immunofluorescent antibody test (IFAT) were used to select a cut-off value for the TgSAG1-ELISA. Sera obtained by serial bleeding of experimentally inoculated ducks and geese were tested to analyze the time course of anti-TgSAG1 antibodies after inoculation and to assess the sensitivity of the assays in comparison with IFAT. In ducks, IFAT titres and ELISA indices peaked 2 and 5 weeks p.i with tachyzoites, respectively. Only three of six geese inoculated with tachyzoites at the same time as the ducks elicited a low and non-permanent antibody response as detected by the IFAT. In the TgSAG1-ELISA, only a slight increase of the ELISA indices was observed in four of six tachyzoite-inoculated geese. By contrast, inoculation of ducks and geese with oocysts led to an increase in anti-TgSAG1 antibodies within 1 or 2 weeks, which were still detectable at the end of the observation period, i.e. 11 weeks p.i. Inoculation of three ducks and three geese with oocysts of Hammondia hammondi, a protozoon closely related to T. gondii, resulted in a transient seroconversion in ducks and geese as measured by IFAT or TgSAG1-ELISA. Using the newly established TgSAG1-ELISA, sera from naturally exposed ducks and geese sampled in the course of a monitoring program for avian influenza were examined for antibodies to T. gondii; 145/2534 (5.7%) of the ducks and 94/373 (25.2%) of the geese had antibodies against TgSAG1. Seropositive animals were detected on 20 of 61 duck and in 11 of 13 goose farms; the seroprevalences within positive submissions of single farms ranged from 2.2% to 78.6%. Farms keeping ducks or geese exclusively indoors had a significantly lower risk (odds ratio 0.05, 95% confidence interval 0.01-0.3) of harboring serologically positive animals as compared with farms where the animals had access to an enclosure outside the barn.     

Attempeted transmission of feline coccidia from chronically infected queens to their kittens

Eight female, 12- to 34-month-old, specific-pathogen free cats were inoculated orally with Toxoplasma gondii cysts on day 0, then with Isospora felis and Isospora rivolta oocysts on day 39, and cysts of Hammondia hammondi on day 86 after inoculation with Toxoplasma. All cats shed oocysts of all 4 of these coccidia within 11 postinoculation days. The female cats were caged with 4 male Toxoplasma-free cats, starting 66 days after inoculation with Toxoplasma, until they were 5 to 6 weeks pregnant. Kittens that were born were housed with their mothers until necropsied or weaned. One 42-day-old kitten shed T gondii oocysts in feces. It was necropsied 2 days later and asexual stages of Toxoplasma (types D and E), gametocytes, and oocysts were demonstrated in sections of superficial epithelial cells of its small intestine. Lesions or forms of Toxoplasma were not demonstrated histologically in tis extraintestinal organs. Toxoplasma was not isolated from feces or tissues of the remaining 47 kittens born to these 8 queens. Toxoplasma was not isolated from the 4 male cats that were caged with infected females for 53, 59, 217, and 217 days. The source of toxoplasma infection in the kitten remained unknown but was considered unlikely to be congenital or through fecal contamination. Oocysts of I felis, I rivolta, and H hammondi were not found in the feces of any kittens, indicating that these coccidia are unlikely to be transmitted congenitally.     

Sarcocystis capracanis and Toxoplasma gondii infections in range goats from Texas

Specimens of tongues, esophagi, diaphragms, or abdominal muscles of 115 range goats from San Angelo, Tex, were examined for Sarcocystis and Toxoplasma gondii infections. Sarcocystis spp zoites were found microscopically in pepsin digests of muscles of 60.8% goats and sarcocysts of S capracanis were found in histologic sections of 27.8% goats. Sarcocysts were more common in sections of tongue (19.1%) than in those of other muscles (9.9% to 10.7%). A dog fed Sarcocystis-infected tissues shed sporocysts in feces, whereas 2 cats fed the same tissues did not shed sporocysts. Toxoplasma gondii was neither seen in histologic sections of goat tissues nor found by bioassays in mice or cats. Mice inoculated with pepsin digests of muscles did not develop T gondii infection and 2 cats fed goat tissues did not shed oocysts. Also, antibody to T gondii was not found in serum samples from goats. The low prevalence of T gondii infection in range goats may be because of the relative absence of domestic cats on Texas ranges.     

Antibody reactivity in mice and cats to feline enteroepithelial stages of Toxoplasma gondii.

The reactivity of antibodies in mice and cats to feline enteroepithelial stages of Toxoplasma gondii was examined by means of an indirect immunofluorescent antibody test. Mice immunized with feline enteroepithelial stage (FES) parasites produced antibodies not only against FES, but also against tachyzoites, sporozoites/oocysts, tissue cysts and one part of the infected feline enterocytes. After absorption with tachyzoites, the titer of antibodies reactive to enterocytes was significantly reduced. In contrast, the titer of antibodies reactive to FES remained unchanged. The antibodies from cats immunized with FES, reacted specifically to FES, but not to tachyzoites, tissue cysts or enterocytes. These results suggest that FES parasites may have stage-specific antigen(s).