Spotty liver disease (SLD) has rapidly spread as a major poultry problem, impacting egg-laying flocks in the United Kingdom and Australia, and now causing concern in the United States. SLD is linked to the presence of Campylobacter hepaticus, with more recent findings including Campylobacter bilis. Focal lesions on the livers of avian hosts have been linked to the presence of these organisms. A significant consequence of Campylobacter hepaticus infection is reduced egg production, coupled with decreased feed intake, which results in smaller eggs, and sadly, a sharp increase in mortality amongst valuable laying hens. At the University of Georgia's Poultry Diagnostic Research Center, two flocks (A and B) of organic pasture-raised laying hens, with a history suggestive of SLD, were examined in the fall of 2021. In the postmortem examination of Flock A, five of six hens were discovered to have small, multifocal liver lesions and were determined PCR-positive for C. hepaticus based on pooled swab samples taken from the liver and gall bladder. An examination of Flock B's birds revealed that six out of seven specimens exhibited speckled liver damage. In the pooled bile swabs from Flock B, two hens' PCR results came back positive for C. hepaticus. Five days after the initial visit to Flock A, a follow-up appointment was scheduled, as well as a visit to Flock C, which had not been affected by SLD, functioning as a control group for comparison. Collected from six hens per house were samples of liver, spleen, cecal tonsil, ceca, blood, and gall bladder. Furthermore, feed, water nipples, and environmental water sources (still water located outside the property) were gathered from both the affected farm and the control farm. To ascertain the presence of the organism, all collected samples were processed by direct plating on blood agar and enrichment in Preston broth, subsequently incubated under microaerophilic conditions. Purified bacterial cultures from each sample, through a multi-phase process, were subsequently PCR-analyzed to confirm the presence of C. hepaticus, identifying those showing its characteristics. Flock A samples of liver, ceca, cecal tonsils, gall bladder, and environmental water yielded positive PCR results for C. hepaticus. Flock C's analysis revealed no positive specimens. A further examination, ten weeks subsequent to the initial visit, confirmed the presence of C. hepaticus in the gall bladder bile and feces of Flock A. One environmental water sample also showed a weakly positive response to C. hepaticus. Concerning *C. hepaticus*, Flock C's PCR tests came back negative. To evaluate the prevalence of C. hepaticus, 6 layer hens from 12 different flocks, aged 7 to 80 weeks, and kept in various housing systems, underwent testing for C. hepaticus infection. AP20187 datasheet Following both culture and PCR testing procedures, the 12-layer hen flocks were determined to be free from C. hepaticus. Currently, there are no authorized treatments for C. hepaticus, and no vaccine has been approved for this infection. This study's findings indicate a potential for *C. hepaticus* to be endemic in certain U.S. regions, with free-range laying hens possibly encountering it through environmental sources like stagnant water within their foraging areas.
Eggs from a New South Wales layer flock were implicated in a 2018 food poisoning outbreak in Australia, caused by Salmonella enterica serovar Enteritidis phage type 12 (PT12). Despite ongoing environmental monitoring, this report marks the first documented case of Salmonella Enteritidis infection affecting NSW layer flocks. Most flocks exhibited a minimal level of clinical signs and mortalities, though seroconversion and infection were still observed in some. Researchers investigated the oral dose-response of Salmonella Enteritidis PT12 in commercial laying hens. Caecal, hepatic, splenic, ovarian, magnal, and isthmic tissues, and cloacal swabs were obtained on days 3, 7, 10, and 14 post-inoculation, with additional tissue samples taken at necropsy on days 7 or 14, all of which were processed for isolating Salmonella, per AS 501310-2009 and ISO65792002. Histopathological studies involved the above-mentioned tissues, augmenting with lung, pancreas, kidney, heart, and further intestinal and reproductive tract tissues. Salmonella Enteritidis was reproducibly detected in cloacal swabs during the period from 7 to 14 days after the challenge. The hens challenged orally with 107, 108, and 109 Salmonella Enteritidis PT12 showed complete colonization of the gastrointestinal tract, liver, and spleen; their reproductive tracts, however, were less reliably colonized. Microscopic examination at 7 and 14 days following challenge displayed mild lymphoid hyperplasia in the liver and spleen. Further, the observed conditions included hepatitis, typhlitis, serositis, and salpingitis, with a heightened incidence in the birds receiving higher doses. No Salmonella Enteritidis was found in blood cultures from the challenged hens, nor was diarrhea observed. AP20187 datasheet The NSW isolate of Salmonella Enteritidis PT12 successfully invaded and colonized the reproductive tracts of the birds, as well as a variety of other tissues, which points to the possible contamination of their eggs by these naive commercial hens.
To determine the susceptibility and disease processes of Eurasian tree sparrows (Passer montanus), wild-caught specimens were inoculated with genotype VII velogenic Newcastle disease virus (NDV) APMV1/chicken/Japan/Fukuoka-1/2004. The intranasal inoculation of two groups, one with a high dose and the other with a low dose of virus, led to the death of certain birds in both groups between days 7 and 15 post-inoculation. In a small sample of birds, a range of symptoms including neurologic deficits, ruffled feathers, difficulty breathing, profound weight loss, diarrhea, depression, and ataxia were noted, unfortunately leading to their demise. Inoculation with a higher viral burden resulted in a greater frequency of mortality and a higher rate of detection for hemagglutination inhibition antibodies. Sparrows, having endured the 18-day observation period post-inoculation, displayed no observable clinical symptoms. Pathological lesions were noted in the nasal mucosa, orbital ganglia, and central nervous system tissues of deceased avian specimens, accompanied by immunohistochemically detectable NDV antigens. From the oral swabs and brains of the deceased birds, NDV was isolated, but not from any of the other organs – the lung, heart, muscle, colon, or liver. Further experimentation involved intranasal inoculation of tree sparrows with the virus, subsequent observation 1-3 days later, to study early disease development. Birds that received the inoculation displayed nasal mucosal inflammation containing viral antigens, and virus was isolated from some oral swabs taken on days two and three following inoculation. The investigation suggests a susceptibility of tree sparrows to velogenic NDV, potentially leading to fatal outcomes, yet some birds may exhibit either no or mild symptoms of infection. The pathogenesis of velogenic NDV, uniquely characterized by neurologic signs and viral neurotropism, was evident in infected tree sparrows.
The pathogenic flavivirus Duck Tembusu virus (DTMUV) is a significant factor in the notable decrease in egg production and severe neurological disorders affecting domestic waterfowl. AP20187 datasheet Ferritin nanoparticles self-assembled with E protein domains I and II (EDI-II) of DTMUV (EDI-II-RFNp) were prepared, and their morphology was observed. Independent experimental procedures were used twice. Cherry Valley ducks (14 days old) were inoculated with EDI-II-RFNp, EDI-II, and phosphate-buffered saline (PBS, pH 7.4), along with virus-neutralizing antibodies, interleukin-4 (IL-4), and interferon-gamma (IFN-γ). Subsequent analyses focused on serum antibody and lymphocyte proliferation measures. Vaccinated ducks, receiving EDI-II-RFNp, EDI-II, or PBS, were exposed to virulent DTMUV; clinical signs were evaluated on day seven post-infection. At both seven and fourteen days post-infection, mRNA levels of DTMUV were measured in the lungs, liver, and brain tissue. The experimental findings demonstrated near-spherical nanoparticles, labeled EDI-II-RFNp, with diameters measured at 1646 ± 470 nanometers. In the EDI-II-RFNp group, levels of specific and VN antibodies, IL-4, and IFN-, as well as lymphocyte proliferation, were markedly greater than those found in the EDI-II and PBS groups. Within the DTMUV challenge test framework, clinical signs and mRNA levels within tissues served as metrics for evaluating the protective impact of EDI-II-RFNp. Milder clinical signs and decreased DTMUV RNA loads were observed in the lungs, liver, and brain tissues of EDI-II-RFNp-vaccinated ducks. The EDI-II-RFNp intervention effectively prevented DTMUV infection in ducks, signifying its potential as a safe and reliable vaccine to curtail this viral threat.
Since 1994, when the bacterial pathogen Mycoplasma gallisepticum traversed from poultry to wild avian species, the house finch (Haemorhous mexicanus) has been widely considered the primary host species among wild North American birds, exhibiting a disease prevalence exceeding that of all other avian counterparts. Our study in Ithaca, New York, concerning purple finches (Haemorhous purpureus), examined two potential explanations for the recently observed increase in disease. The hypothesis posits that the evolutionary trajectory of *M. gallisepticum*, characterized by growing virulence, is accompanied by amplified adaptability to a broader range of finch species. Correctly identifying the strain of M. gallisepticum is critical; early isolates are predicted to induce less severe eye lesions in purple finches than in house finches, whereas more recent isolates are forecast to create eye lesions of similar severity in both species. The decline of house finches post-M. gallisepticum epidemic, according to Hypothesis 2, is correlated with a relative increase in purple finch abundance around Ithaca, thus heightening their contact with and potential exposure to M. gallisepticum-infected house finches.