Differences in virulence and oocyst shedding profiles in lambs experimentally infected with different isolates of Cryptosporidium parvum.

A wide spectrum of disease severity associated with cryptosporidiosis has been described, ranging from asymptomatic to fatal in both human and animal hosts. The reasons for the variations in severity are likely to be multifactorial, involving environmental, host and parasite factors. This paper describes two experimental infection trials in lambs, a symptomatic host for the parasite, to investigate variation in the clinical manifestations following infection with two distinct isolates of Cryptosporidium parvum. In the first experiment, groups of naïve lambs were challenged with one of two isolates (CP1 or CP2) at â€‹< â€‹1 week of age, to test the effect of the isolates on disease outcome. In a second experiment one group of lambs challenged at < 1 week of age (CP1) was then re-challenged with the same isolate at 6 weeks of age (CP1), while a second group was challenged for the first time at 6 weeks of age (CP1). This experiment examined age-related disease symptoms, oocyst shedding and the effect of prior exposure to the parasite on a subsequent homologous challenge. The two isolates were associated with significant differences in the demeanour of the animals and in the numbers of oocysts shed in the faeces. There were also differences in the duration and severity of diarrhoea, though these were not significant. The age of the lamb, at the time of a primary challenge (<1 week or 6 weeks), also resulted in differences in clinical outcomes, with younger lambs showing more severe clinical disease than the older lambs (feeding profiles and presentation of diarrhoea), while older lambs showed virtually no signs of infection but still produced large numbers of oocysts.

No Evidence for a Role for Antibodies during Vaccination-Induced Enhancement of Porcine Reproductive and Respiratory Syndrome.

Vaccination is one of the most important tools to protect pigs against infection with porcine reproductive and respiratory syndrome virus 1 (PRRSV-1). Although neutralizing antibodies are considered to represent an important mechanism of protective immunity, anti-PRRSV antibodies, in particular at subneutralizing concentrations, have also been reported to exacerbate PRRSV infection, probably through FcγR-mediated uptake of antibody-opsonized PRRSV, resulting in enhanced infection of, and replication in, target cells. Therefore, we investigated this pathway using sera from an animal experiment in which vaccine-mediated enhancement of clinical symptoms was observed. Three groups of six pigs were vaccinated with an inactivated PRRSV vaccine based on the PRRSV-1 subtype 3 strain Lena and challenged after a single or a prime-boost immunization protocol, or injected with PBS. We specifically tested if sera obtained from these animals can enhance macrophage infections, viral shedding, or cytokine release at different dilutions. Neither the presence of neutralizing antibodies nor general anti-PRRSV antibodies, mediated an enhanced infection, increased viral release or cytokine production by macrophages. Taken together, our data indicate that the exacerbated disease was not caused by antibodies.

Comparison of protection provided by type 1 and type 2 porcine reproductive and respiratory syndrome field viruses against homologous and heterologous challenge.

The objective of this study was to compare protection provided by type 1 and type 2 porcine reproductive and respiratory syndrome virus (PRRSV) against homologous and heterologous challenge based on clinical, virological, immunological, and pathological analysis. At 3 and 8 weeks of age, pigs were inoculated intranasally with either 3mL of tissue culture fluid containing 10(5) TCID50/mL of type 1 PRRSV or 3mL of tissue culture fluid containing 10(5) TCID50/mL of type 2 PRRSV. The homologous challenges resulted in a significant boost of the neutralizing antibodies (NA) and interferon-γ secreting cells (IFN-γ-SC) compared to heterologous challenges. The reduction of secondary challenging PRRSV viremia coincided with the appearance of homologous PRRSV-specific NA and IFN-γ-SC. Homologous challenge reduced the severity of lung lesions and levels of PRRSV viremia significantly in pigs in comparison with heterologous challenge. The differences in homologous and heterologous NA and IFN-γ-SC response may explain the differences in protection against homologous and heterologous challenge between type 1 and type 2 PRRSV. Primary challenge (immunization) with type 1 PRRSV provided protection against the secondary homologous challenge with type 1 PRRSV but failed to provide protection against the secondary heterologous challenge of type 2 PRRSV. Primary challenge with type 2 PRRSV provided protection against both the secondary homologous challenge with type 2 PRRSV and the secondary heterologous challenge with type 1 PRRSV.

Protection to homologous and heterologous challenge in pigs immunized with vaccine against foot-and-mouth disease type O caused an epidemic in East Asia during 2010/2011.

Foot-and-mouth disease (FMD) is a highly contagious infectious disease, and the use of vaccines is known to be effective for its prevention. In 2010/2011, there was an epidemic of the South East Asia (SEA) topotype in East Asian countries. We adapted the SEA topotype virus isolated in November 2010 in Korea in cells to analyze the characteristics of the virus and evaluate its possibility as a vaccine. After cell culture adaptation, the FMD virus particle 146S was purified to develop an inactivated oil vaccine for SEA or other topotypes. To measure its immunogenicity, pigs were inoculated with the experimental vaccine at different concentrations of the antigen. The results indicated that the groups immunized with at least 7.5 µg antigen were protected from homologous challenge. The immunized pigs were also protected against heterologous virus (ME-SA topotype) challenge. The genetic variations between the two field isolates and the adapted vaccine strains were identified in six amino acids by complete genome sequencing.