Apesar do diagnóstico da anemia infecciosa e mais evidências recentes de infecção em campo (Brentano & Ottati, 1999), não havia até hoje dados disponíveis da prevalência do vírus da anemia das galinhas (CAV) no Brasil. Uma vez que o conhecimento da prevalência do vírus e da distribuição de anticorpos nos lotes de matrizes é essencial para o delineamento de estratégias de controle da doença, realizamos um levantamento em 5 Estados com produção comercial intensiva de linhas de corte, abrangendo lotes de aves com diferentes idades. De 2.355 soros testados por ELISA, 89% foram positivos, indicando a alta prevalência do CAV no Brasil, em todos os Estados testados. A análise do soro de aves das 6 até as 70 semanas de idade demonstrou que lotes de 6 a 18 semanas apresentam desuniformidade na imunidade ao CAV, caracterizada por títulos de anticorpos abaixo dos níveis considerados protetores e aves ainda negativas para o CAV. A desuniformidade nos títulos de anticorpos e a ausência dos mesmos são evidentes ainda, mas em menor proporção também até as 24 semanas, enquanto que apenas partir das 25 semanas há 100% de soroconversão, acompanhada de significativa redução da desuniformidade no título de anticorpos das matrizes para menos de 2,5% das aves. Esses resultados fornecem evidência de uma progressiva disseminação do vírus em matrizes de corte, mas com riscos da presença de aves ainda susceptíveis à transmissão vertical e inadequada transferência de imunidade passiva no início do período de postura, que podem culminar em surtos da doença na progênie.

Although the isolation and identification of CAV as well as other recent diagnosis of the virus in broiler flocks have provided evidence for chicken anemia virus, Brentano & Ottati (1999), the prevalence of CAV had not yet been determined in Brazil. Since the knowledge of the prevalence of the virus and the level of antibodies against CAV in breeders flocks provide key information for designing control measures against chicken infectious anemia, we conducted a serological survey in broiler breeders of different ages, in five States with intensive commercial broiler flock production. Of a total of 2,355 sera tested by a commercial ELISA assay, 89% were found positive for antibodies to CAV, indicating a high prevalence of the virus in Brazil, in all the surveyed states. The analysis of antibodies to CAV in 6 to 70 week-old breeders showed that flocks between 6 and 18 weeks of age have the highest number of seronegative and low antibody titer chickens, thus representing the age group with the most uneven level of immunity against CAV. Chickens with negative or low antibody titers were still detected until 24 weeks of age, whereas at 25 weeks there was a 100% seroconversion to CAV and a reduction to less than 2,5% in the number of chickens with low antibody titers. These results provide evidence for a gradual and progressive virus spread in broiler breeder flocks, with the occurrence of a small percentage of chickens with low antibody titers at beginning of lay and therefore susceptible to inadequate transfer of passive immunity and vertical transmission of CAV to their progeny.

A survey of Isospora suis performed in 177 faecal samples from 30 swine farms detected thin wall type I. suis oocysts in seven samples. This type of oocyst measuring 23.9 by 20.7 mm had a retracted thin wall similar to that of the genus Sarcocystis. This type of oocysts, isolated from four different faecal samples, was inoculated in four-five-days-old piglets free of contamination in order to verify the life cycle and pathogenicity of the species. The pigs were kept in individual metal cages and fed with cow milk. Daily faecal collections and examinations were performed until the 21st day after infection. MacMaster and Sheather' s methods were used for oocyst counting and identification. Infected piglets produced yellowish-pasty diarrhoea with slight dehydration. The prepatent and patent periods were respectively from 6 to 9 and 3 to 10 days after infection. Oocyst elimination was interrupted on the 10th and 11th days after infection with biphasic cycles. Thin and thick wall oocysts were detected in the same faecal samples. Thin walls were not observed in unsporulated oocysts. The observations suggest that this type of oocysts could appear in specific strains which occur in the later stages of their development. These oocysts seem to be responsible for clinical and pathogenic signs of neonatal isosporosis in pigs.