Lyme disease (LD) is a tick-borne infection caused by the bacterial pathogen Borrelia burgdorferi. Current diagnostic tests mostly use borrelial lysates or select antigens to detect serum antibodies against B. burgdorferi. These immunoassays are not entirely effective, especially for detection of early infection. We have recently characterized an in vivo-induced antigen, BBK07, as a serodiagnostic marker for LD. We now report that in a line blot assay, recombinant BBK07 protein-based detection is 90% sensitive and nearly 100% specific against B. burgdorferi infection in humans. Using an overlapping peptide library of 23 peptides encompassing fulllength BBK07, we identified the immunodominant epitopes of BBK07 during human infection. We show that a select combination of amino-terminal peptides significantly enhanced BBK07-based diagnostic accuracy compared to that with the full-length protein. Although in enzyme-linked immunosorbent assay (ELISA) studies BBK07 peptides had overall lower sensitivity than established serodiagnostic peptides, such as the VlsE peptide C6 and OspC peptide pepC10, for the detection of early human LD, a subset of serum samples that failed to recognize either VlsE or OspC peptides were preferentially reactive to BBK07 peptides. These results highlight the fact that BBK07 peptides could be useful to complement the efficacy of VlsE and OspC peptidebased serodiagnostic assays. Finally, using a panel of canine sera, we show that BBK07 peptide is also effective for LD diagnosis in infected dogs. Together, our data show that peptides from the B. burgdorferi surface protein BBK07 are highly specific and sensitive serodiagnostic markers, and we suggest their future use in LD diagnostic assays.

In this paper, we report on the evaluation of five influenza antigen detection tests by avian influenza H5N 1 virus-positive swab samples to estimate their diagnostic sensitivity. The tests included two chromatographic immunoassays, an H5 avian influenza-specific antigen detection enzyme-linked immunosorbent assay (ELISA), an influenza A antigen detection ELISA, and an H5 rapid immunoblot assay. The results showed that the overall sensitivities of these tests ranged from 36.3% to 51.4% (95% confidence interval ranging from 31.0% to 57.0%), which were comparable to Directigen Flu A antigen detection tests but substantially lower than genome detection methods. Diagnostic sensitivity performance is a function of the concentration of antigens in samples and the analytical sensitivity of the individual test. The test sensitivities were significantly higher for sick and dead birds by cloacal, tracheal, or tissue swabs than for fecal swabs from apparently healthy birds, and these tests would not be suitable for surveillance testing of clinically healthy birds. Furthermore, the sensitivity for testing tracheal and cloacal swabs from waterfowl and wild birds was not as good as for chickens. This was most likely to be associated with variation in virus titers between specimens from different bird species. However, the tests showed good sensitivities for testing brain swabs from clinically affected waterfowl species. The results indicate that these antigen detection tests could be used for preliminary investigations of H5N 1 outbreaks as a low-cost, simple flock test in sick and dead birds for the rapid detection of H5N1 infection. However, the relatively low sensitivity of the tests as individual bird tests means that they should be used on optimal clinical specimens from diseased birds, testing birds on a flock basis, or testing samples as close to the onset of disease as possible before viral titers diminish. They should be followed up by confirmatory tests, such as reverse transcription polymerase chain reaction or viral culture, wherever possible but could assist in facilitating rapid investigations and control interventions.

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Hematocrits, histopathology, concanavalin A-induced lymphocyte proliferation, intracellular calcium signaling, and lymphocyte subpopulations were analyzed over a 6-week period in individual chicks inoculated with the CL-1 isolate of chicken anemia virus. Lymphoid depletion/atrophy was present in the thymus and bone marrow by 11 days post-infection (PI). Anemia was present at 14 days PI. The mean lymphocyte proliferation stimulation index (SI) of the inoculated group was significantly lower than that of the control group at 11 days PI. This response was reversed at 18 days PI, when the SI of the inoculated group was significantly higher than that of the controls; values subsequently returned to baseline. The increase in intracellular calcium levels in CAV-infected chicks and controls paralleled the proliferative response. Percentages of CD3-, CD4-, CD8-, and natural-killer-positive-staining cells decreased significantly at 18 and 25 days PI. The most dramatic decrease occurred in the CD8-positive-staining cell population at 18 and 25 days PI.

Seven-week-old chickens infected oro-nasally with the lentogenic V4 strain of Newcastle disease virus showed no clinical signs and minimal gross pathology. There was slight ulcerative tracheobronchitis but the main system response was a rapid and progressive lymphoproliferative hyperplasia in the respiratory system, gastrointestinal tract, bursa and spleen which tended to peak after three weeks. By using an indirect immunoperoxidase technique with antibody prepared against homologous virus, viral antigen was localised chiefly in the cytoplasm of lymphoreticular cells, persisting for at least 28 days in the caecal tonsil. Positive cells were not seen in the bursa or brain.