RESUMEN
A survey to detect antibodies against hepatitis E virus (HEV) was undertaken on 41 Spanish pig farms using an indirect enzyme-linked immunosorbent assay (ELISA). Forty of the farms (97.6%) were positive for anti-HEV IgG antibodies, while 34/41 (82.9%) had IgM positive animals. The highest proportion of IgG positive pigs comprised the adult sows (45/74, 60.8%; P=0.01), followed by young piglets aged 3-6 weeks (79/218, 36.2%). IgM positive pigs were more frequently found to be those animals > or = 12 weeks of age (P<0.001). In a second part of the study, the age distribution of the infection on one HEV infected farm was studied by combining the ELISA test with reverse transcription polymerase chain reaction (RT-PCR). On this farm, viraemia was mostly detected in animals aged 8-12 weeks and faecal shedding of HEV was detected in pigs of the same age. All HEV sequences corresponded to genotype 3. The study confirmed that HEV is spread in pigs in Spain and is probably endemic in many farms.
Asunto(s)
Virus de la Hepatitis E/aislamiento & purificación , Hepatitis E/veterinaria , Enfermedades de los Porcinos/epidemiología , Animales , Anticuerpos Antivirales/análisis , Ensayo de Inmunoadsorción Enzimática/veterinaria , Heces/virología , Hepatitis E/epidemiología , Virus de la Hepatitis E/genética , Virus de la Hepatitis E/inmunología , Carne , ARN Viral/análisis , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa/veterinaria , Estudios Seroepidemiológicos , España/epidemiología , Porcinos , Enfermedades de los Porcinos/sangre , Enfermedades de los Porcinos/etiología , Enfermedades de los Porcinos/virologíaRESUMEN
Previous studies have described a "litter effect" associated with mortality in postweaning multisystemic wasting syndrome (PMWS) affected farms. The main objective of this study was to evaluate litter mortality in different PMWS affected farms and to characterize it in relation to three variables of the sow: parity, porcine circovirus type 2 (PCV2) infectious status and PCV2 antibody titres. The study was performed in seven farms that experienced PMWS in nurseries and/or fattening areas. Fifteen sows from each farm were randomly selected from the same farrowing batch. Serum samples were analyzed for antibodies to PCV2 and for genomic detection of PCV2. Four piglets from each sow (60 piglets per farm) were selected and ear-tagged at birth. Out of 420 initial piglets, 104 (25%) died. Sixty three of them (60%) were necropsied, and 40 (63%) diagnosed as PMWS based on case definition criteria. Our results show that sow PCV2 viremia was significantly related to piglet mortality since more piglets per litter died from viremic than from non-viremic sows. Additionally, a significantly greater proportion of animals died from sows that had low antibody titres against PCV2 (39% vs. 18% from sows with medium to high antibody titres). The present study, of exploratory nature, confirms previous results and further characterizes the so called "litter effect" by establishing that the sow PCV2 status had a significant effect on litter mortality in PMWS affected farms.
Asunto(s)
Infecciones por Circoviridae/veterinaria , Circovirus/fisiología , Síndrome Multisistémico de Emaciación Posdestete Porcino/mortalidad , Hermanos , Animales , Anticuerpos Antivirales/sangre , Infecciones por Circoviridae/complicaciones , Infecciones por Circoviridae/inmunología , Infecciones por Circoviridae/virología , Circovirus/inmunología , Circovirus/patogenicidad , Femenino , Paridad , Síndrome Multisistémico de Emaciación Posdestete Porcino/complicaciones , Síndrome Multisistémico de Emaciación Posdestete Porcino/inmunología , Síndrome Multisistémico de Emaciación Posdestete Porcino/transmisión , Embarazo , PorcinosRESUMEN
Quinolone-resistance determining region (QRDR) of Gyrase A gene was sequenced in 54 Salmonella strains of pig origin that have different quinolone-resistance patterns. Those strains accounted for 12 different serotypes. Mutations at Ser83 or Asp87 were predominant in the studied isolates. However, for serotypes Anatum and Virchow, resistance to quinolones seemed to be linked to specific mutations, namely, Ser83-->Tyr and Ser83-->Phe, respectively. Other mutations found in different positions did not seem to have clinical significance except for changes at Asp82.