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SUMMARYCats are essential in the epidemiology ofToxoplasma gondiibecause they are the only hosts that can excrete the environmentally resistant oocysts in nature. Samples of serum, feces, and tissues from feral cats from St Kitts, West Indies were examined forT. gondiiinfection. Antibodies toT. gondiiwere assayed by the modified agglutination test, and found in 71 of 96 (73·9%) of cats with titres of 1:10 in six, 1: 20 in six,1:40 in seven,1: 80 in three, 1: 160 in 10, 1:320 in 13, 1:640 in nine, and 1:1,280 or higher in 17. Tissues of 10 cats were bio-assayed in mice.Toxoplasma gondiiwas isolated from tissues of 7 cats; from hearts of 6, from tongue of 5, and brains of 3 cats. All 7 isolates were avirulent for mice.Toxoplasma gondiioocysts were not found in the feces of 51 cats. Genotyping of these 7T. gondiiisolates by 10 multi-locus PCR-RFLP markers, including SAG1, SAG2, SAG3, BTUB, GRA6, c22-8, c29-2, L358, PK1, and an apicoplast marker, Apico, revealed 4 genotypes, including clonal Type II, Type III and 2 unique genotypes. Five of the 7 cats had infection with 2 genotypes, indicating high frequency of mixed infection in the cat population on the St Kitts island.

Serum samples from 315 horses from Costa Rica, Central America, were examined for the presence of antibodies against Sarcocystis neurona, Neospora spp., and Toxoplasma gondii by using the surface antigen (SAG) SnSAG2 enzyme-linked immunosorbent assay (ELISA), the NhSAG1 ELISA, and the modified agglutination test, respectively. Anti-S. neurona antibodies were found in 42.2% of the horses by using the SnSAG2 ELISA. Anti-Neospora spp. antibodies were found in only 3.5% of the horses by using the NhSAG1 ELISA, and only 1 of these horses was confirmed seropositive by Western blot. Antibodies to T. gondii were found in 34.0% of the horses tested, which is higher than in previous reports from North and South America. The finding of anti-S. neurona antibodies in horses from geographical areas where Didelphis marsupialis has wide distribution suggests that D. marsupialis is a potential definitive host for this parasite and a source of infection for these horses. Se examinaron muestras de suero de 315 caballos de Costa Rica América Central, se examinaron para detectar la presencia de anticuerpos contra Sarcocystis neurona, Neospora spp. y Toxoplasma gondii mediante la prueba de inmunoabsorción superficie (SAG) SnSAG2 mediante el ensayo inmunoenzimático (ELISA), el ELISA NhSAG1 y la prueba de aglutinación modificada, respectivamente. Se encontraron anticuerpos anti-S. neurona en el 42,2% de los caballos mediante la prueba SnSAG2 ELISA. Los anticuerpos anti-Neospora spp. sólo se encontraron en el 3,5% de los caballos mediante la prueba ELISA NhSAG1, y sólo 1 de estos caballos fue seropositivo por Western blot. Los anticuerpos contra T. gondii fueron en el 34,0% de los caballos examinados, lo que es más elevado que en los informes anteriores de América del Norte y del Sur. El hallazgo de anticuerpos anti-S. neurona en caballos de zonas geográficas en las que Didelphis marsupialis tiene una amplia distribución sugiere que D. marsupialis es un potencial huésped de este parásito y una fuente de infección para estos caballos. Universidad Nacional, Costa Rica Escuela de Medicina Veterinaria

Prevalence of antibodies to Toxoplasma gondii was investigated in 673 domestic dogs from northeastern Portugal, using the modified agglutination test (MAT) with 1∶20 as cutoff for seropositivity; antibodies were found in 256 dogs (38.0%). Differences between seroprevalence levels in males (36.7%) and females (41.8%) and between pure-breed (42.1%) and mixed-breed dogs (35.2%) were not statistically significant. Multiple logistic regression analysis identified age above 12 mo (odds ratio [OR] = 4.0), chance of eating birds or small mammals (OR = 4.0), housing exclusively outdoors (OR = 1.5), home-cooked meals (OR = 3.0), and eating raw meat or viscera (OR = 7.7) as risk factors for the canine T. gondii infection. Some control measures are suggested based on these findings.

Thirty battery-hatched chukar partridges (Alectorts graeca) were inoculated orally with oocysts of the ME 49 or the GT-1 strain of Toxoplasma gondii. All six chukars given 10,000 GT-1 strain oocysts died or were euthanized between postinoculation day (p.i.d.) 3 and 6. Fifteen of 24 chukars given 10,000, 1000, 100 or 10 ME 49 strain oocysts died or were euthanized between p.i.d. 6 and 14. Nine chukars that were not ill by p.i.d. 14 remained clinically normal until euthanized in good health p.i.d. 47 and 67; T. gondii was found by bioassay in mice inoculated with tissues of these nine chukars. From the tissues of five chukars bioassayed individually in mice, T. gondii was isolated from brains of four of four tested, and from the hearts and skeletal muscles of five, and livers of three of five chukars tested. Major lesions in chukars that died or those euthanized when ill were enteritis, splenic necrosis, myocarditis and encephalitis. Myocarditis and encephalitis persisted in chukars examined p.i.d. 47, 53 and 67. All chukars examined p.i.d. 10 developed anti-T. gondii antibodies. Anti-T. gondii antibodies detected in the modified agglutination test were higher than those in latex and haemagglutination tests. The Sabin-Feld-man dye test did not detect T. gondii antibodies in sera of chukars. The ME 49 strain of T.gondii was more pathogenic to chukars weighing >/= 300 g than to the 25 g Swiss Webster mice.

Toxoplasma gondii is a significant worldwide parasitic protozoan. In the present study, prevalence of antibodies of T. gondii was examined from 29 free-ranging black bears (Ursus americanus) from south-central Florida where the host species was listed as state threatened during this project. Overall T. gondii prevalence was found to be 44.8%, specifically 46.2% in male and 43.8% in female U. americanus, using a modified agglutination test (1∶25 titer). Seroprevalence differences between sexes were not significant (P > 0.05). Results of the present study add supportive data to the growing body of evidence suggesting that U. americanus has one of the highest T. gondii seroprevalences among all known intermediate hosts. In addition, our data emphasize the importance of understanding parasitic disease dynamics from a conservation perspective.

Clinical neosporosis was diagnosed in a litter of five pups born to a Beagle bitch from Virginia, USA. Four of the pups developed limb weakness starting at 4 weeks of age. The dogs were suspected to have neosporosis based on clinical signs and empirically treated with Clindamycin (75 mg, oral, twice daily, total 150 mg) starting at 9 weeks of age and the dosage was doubled at 13 weeks of age. Antibodies to Neospora caninum were detected in sera of the dam and pups when first tested serologically at the age of 4 months. The owner donated the pup with the worst clinical signs and the dam for research; both dogs were euthanized. Viable N. caninum was isolated in gamma interferon gene knock out (KO) mice and in cell culture from the pup killed at 137 days of age. Tissue cysts, but no tachyzoites, were found in histological sections of brain and muscles. The isolate was also identified as N. caninum by PCR and sequence analysis and designated NC-9. N. caninum was neither isolated by bioassay in KO mice nor found in histological sections of tissues of the bitch. Clinical signs in the remaining three pups improved considerably after a 6-month treatment with Clindamycin; N. caninum antibody titers were still persistent in these pups at 23 months of age. Results indicate that medication with Clindamycin can improve clinical condition but not eliminate N. caninum infection.

Prevalence of Toxoplasma gondii in free-range chickens (Gallus domesticus) is a good indicator of the environmental contamination with oocysts because chickens become infected mainly by feeding from ground, feed, or soil contaminated with oocysts. The seroprevalence of T. gondii antibodies in 125 free-range chickens from the Addis Ababa, Ethiopia, was determined. Antibodies to T. gondii were assayed by the modified agglutination test; 48 of 125 (38.4%) chickens were seropositive, with titers of 1:5 in 14, 1:10 in 12, 1:20 in 14, 1: 40 in 3, 1: 80 in 1, 1:160 in 1, 1:320 in 1, and ≥1:640 in 2 chickens. The hearts of 115 chickens were bioassayed for T. gondii infection. Hearts of 72 seronegative (modified agglutination test [MAT]1:5) chickens were pooled in 4 groups (20 + 18 + 19 + 15) and fed to 4 T. gondii -free cats; none of these 4 cats shed oocysts in their feces examined 3-21 days after feeding chicken tissues. Hearts of 43 seropositive chickens (MAT ≥ 1:5) were bioassayed individually in mice. Toxoplasma gondii was isolated from only 1 chicken, with a MAT titer of 1:80. This isolate was designated TgCKEt1 and was not pathogenic for outbred mice. Restricted fragment length polymorphism (RFLP) genotyping using 10 loci indicated the TgCKEt1 was ToxoDB polymerase chain reaction-RFLP genotype #1 (Type II clonal). Results of this study indicate very low environmental contamination with T. gondii oocysts around Addis Ababa.

Twenty-four 5-month-old battery-hatched Japanese quail were inoculated orally with 105 (ME 49 strain, group A, 6 birds), 103 (ME 49 strain, group B, 6 birds), 105 (GT-1 strain, group C, 6 birds), and 103 (GT-1 strain, group D, 6 birds) Toxoplasma gondii oocysts. All birds in group C died or were euthanized within 8 days after inoculation (DAI). Five of the 6 birds in group D died or were euthanized 8, 9, 15, 19, and 23 DAI. One of the 6 quail in group A died 9 DAI, and 1 of the 6 birds in group D died 16 DAI. The 11 quail (1 from group D and 10 from groups A and B) were euthanized 63 DAI; T. gondii was isolated by bioassays in mice from the brains of 10, hearts of 10, and skeletal muscles of all 11 quail. Quail that survived marked small intestinal and splenic toxoplasmosis lived long enough to develop severe protozoal pneumonia, myocarditis, or meningoencephalitis. The quail that survived only to be examined at 63 DAI had moderate multifocal nonpurulent encephalitis and myositis and had a hypertrophic spleen that contained hemosiderin-laden macrophages. Toxoplasma gondii antibodies were found in the sera of all quail examined 63 DAI. Antibody titers to T. gondii in the modified agglutination test were higher than in the indirect hemagglutination and latex agglutination tests. Antibodies were not detected in quail sera examined by the Sabin-Feldman dye test.

A nematicidal toxin was purified fromPleurotus ostreatus NRRL 3526 grown on moistened, autoclaved wheat straw for 30 days at room temperature (21-33°C). The active compound, at a concentration of 300 ppm, immobilized 95% of test nematodes (Panagrellus redivivus) within 1 hr. Immobilized nematodes did not recover, even after being rinsed with deionized water. The toxin was identified astrans-2-decenedioic acid.

Infection and immunity to toxoplasmosis induced by the RH strain of Toxoplasma gondii was compared in Sprague-Dawley (SD) and Wistar rats and in outbred Swiss Webster mice. All rats injected with up to 1,000,000 RH-strain tachyzoites remained clinically normal, whereas mice injected with only 1 live tachyzoite died of acute toxoplasmosis. Rats could be infected with 1 tachyzoite of the RH strain as shown by antibody development and by bioassay in mice. However, after 8 days, RH-strain organisms were recovered only inconsistently from SD and Wistar rat brains. Contrary to a report of sterile immunity to T. gondii infection in rats after immunization with live RH tachyzoites, we found infection immunity after challenge with the VEG strain. Toxoplasma gondii tissue cysts of the VEG strain could be recovered from most SD and Wistar rats, first injected with live RH-strain tachyzoites and then challenged with oocysts of the VEG strain. Our RH strain, and probably many others, passed for 50+ yr as tachyzoites has lost not only the capacity to form oocysts, but also shows a marked reduction or absence of tissue cyst (bradyzoites) formation.