Spotty liver disease (SLD) is now a significant health concern for egg-laying poultry in nations like the United Kingdom and Australia, and it has also become prevalent in the United States. Among the organisms responsible for SLD are Campylobacter hepaticus, and, significantly, Campylobacter bilis. Infected avian livers show focal lesions, a direct result of these organisms' activity. The presence of Campylobacter hepaticus infection results in a decline in egg output, a decrease in feed consumption leading to smaller egg sizes, and a rise in death among high-value hens. Two flocks (A and B) of organically raised pasture-laying hens, displaying potential symptoms of SLD, were taken to the Poultry Diagnostic Research Center at the University of Georgia during the autumn of 2021. The postmortem examination of Flock A indicated that small, multifocal liver lesions were present in five of six hens, and subsequent PCR testing on pooled swab samples from the liver and gall bladder confirmed the presence of C. hepaticus. Flock B's necropsy results indicated that six of the submitted seven birds exhibited irregular liver markings. In samples of pooled bile from hens, two out of seven birds from Flock B exhibited a PCR-positive result for C. hepaticus. Flock A's follow-up visit was scheduled for five days from now, along with a visit to Flock C, where SLD had not been documented, acting as a control group for comparison. Six hens per house were the source of samples from their liver, spleen, cecal tonsils, ceca, blood, and gall bladder. The affected and control farms provided samples of feed, water nipples, and outside water (standing water outside the farms). Incubation under microaerophilic conditions, after direct plating on blood agar and enrichment in Preston broth, was used to detect the organism in all collected samples. 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. A PCR analysis of liver, ceca, cecal tonsils, gall bladder, and environmental water from Flock A indicated the presence of C. hepaticus. Flock C's analysis revealed no positive specimens. Following a subsequent visit conducted ten weeks later, Flock A's gall bladder bile and fecal matter PCR tests returned positive results for C. hepaticus. A single environmental water sample displayed a weak positive test for C. hepaticus. The PCR test for *C. hepaticus* on Flock C specimens was negative. The prevalence of C. hepaticus in layer hens was determined by examining 6 hens from each of 12 different layer hen flocks, ranging in age from 7 to 80 weeks, and maintained in different housing systems, to ascertain the prevalence of C. hepaticus infection. Unesbulin No C. hepaticus was found in the 12-layer hen flocks, according to the results of both culture and PCR analysis. As of today, no accepted treatments are available for C. hepaticus, nor is a vaccine currently in use. 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.
The 2018 New South Wales food poisoning outbreak, attributed to Salmonella enterica serovar Enteritidis phage type 12 (PT12), was traced back to eggs consumed from a local layer farm. In NSW layer flocks, this report spotlights the first instance of Salmonella Enteritidis, an unexpected finding in the context of continuous environmental monitoring. Although most flocks exhibited minor clinical signs and mortalities, seroconversion and infection were identifiable in some flocks. Researchers investigated the oral dose-response of Salmonella Enteritidis PT12 in commercial laying hens. Cloacal swabs obtained at 3, 7, 10, and 14 days after inoculation, along with caecal, hepatic, splenic, ovarian, magnal, and isthmic tissues collected from necropsy at either 7 or 14 days post-inoculation, underwent processing for Salmonella isolation, according to procedures outlined in AS 501310-2009 and ISO65792002. The above-mentioned tissues, in conjunction with lung, pancreas, kidney, heart, and additional intestinal and reproductive tract tissues, underwent histopathological procedures. Cloacal swabs consistently revealed Salmonella Enteritidis between 7 and 14 days following the challenge. Hens orally challenged with 107, 108, and 109 Salmonella Enteritidis PT12 isolates showed complete colonization of their gastrointestinal tract, liver, and spleen, but less consistent colonization of the reproductive tracts. Pathological analysis of liver and spleen samples, taken at 7 and 14 days post-challenge, revealed mild lymphoid hyperplasia, coupled with the presence of hepatitis, typhlitis, serositis, and salpingitis. Higher-dose groups showed a more substantial occurrence of these effects. In challenged layers, Salmonella Enteritidis was absent from the heart blood cultures, and no instances of diarrhea were noted. Unesbulin Invasive colonization of the reproductive tracts and numerous other tissues occurred in birds infected with the Salmonella Enteritidis PT12 strain from NSW, signifying the potential for naive commercial hens to introduce this contamination into their eggs.
Genotype VII velogenic Newcastle disease virus (NDV) APMV1/chicken/Japan/Fukuoka-1/2004 was used to experimentally infect wild-caught Eurasian tree sparrows (Passer montanus) to determine their susceptibility and the course of the ensuing disease. Birds in two groups, inoculated intranasally with either high or low viral doses, experienced mortality in some members of both groups from days 7 to 15 after inoculation. A few birds displayed neurologic signs, ruffled feathers, labored breathing, marked emaciation, diarrhea, a depressed state, and ataxia, and ultimately died. Mortality and hemagglutination inhibition antibody detection rates both increased following inoculation with a higher viral load. No discernible clinical signs were present in the tree sparrows that survived the 18-day observation period subsequent to inoculation. Avian fatalities showed histological changes in the nasal mucosa, orbital ganglia, and central nervous system; these were associated with NDV antigens, demonstrable by immunohistochemical means. The oral swabs and brains of the deceased birds proved positive for NDV, but this virus was not found in the other organs, including the lung, heart, muscle, colon, and liver. In a control group, tree sparrows underwent intranasal inoculation of the virus, and were monitored 1-3 days later to study the early pathogenesis of the disease. Following inoculation, birds exhibited inflammation in their nasal mucosa, containing viral antigens, and virus was isolated from some oral swab samples taken on the second and third post-inoculation days. This research indicates that tree sparrows are susceptible to velogenic NDV, with the infection capable of being fatal; however, some birds may exhibit only mild infection or no symptoms at all. A unique pathogenesis, particularly concerning neurologic signs and viral neurotropism, was displayed by velogenic NDV in infected tree sparrows.
Domestic waterfowl afflicted with the Duck Tembusu virus (DTMUV), a pathogenic flavivirus, experience a considerable decline in egg production and serious neurological issues. Unesbulin Ferritin nanoparticles, self-assembled with E protein domains I and II (EDI-II) sourced from DTMUV (EDI-II-RFNp), were produced, and their morphology was observed. Duplicate experimental procedures were employed, independently. At 14 days of age, Cherry Valley ducks were vaccinated with EDI-II-RFNp, EDI-II, and phosphate-buffered saline (PBS, pH 7.4), alongside specialized virus-neutralizing antibodies, interleukin-4 (IL-4), and interferon-gamma (IFN-γ). Subsequently, serum antibody and lymphocyte proliferation assays were performed. Ducks, administered EDI-II-RFNp, EDI-II, or PBS, were exposed to virulent DTMUV; clinical observations commenced at seven days post-inoculation. DTMUV mRNA levels were quantified in the lung, liver, and brain at days seven and fourteen post-inoculation. The results showed EDI-II-RFNp nanoparticles to be nearly spherical, with a diameter of 1646 nanometers, plus or minus 470 nanometers. The EDI-II-RFNp group significantly outperformed both the EDI-II and PBS groups in terms of specific and VN antibody levels, IL-4 and IFN- levels, and lymphocyte proliferation rates. To gauge the protective effect of EDI-II-RFNp in the DTMUV challenge trial, clinical signs and mRNA levels in tissue samples were analyzed. Vaccinated EDI-II-RFNp ducks displayed milder clinical indications and reduced DTMUV RNA quantities in the pulmonary, hepatic, and cerebral tissues. Results indicate EDI-II-RFNp provides significant protection against DTMUV in ducks, positioning it as a vaccine candidate for safe and effective disease control strategies.
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. In our recent study focused on purple finches (Haemorhous purpureus) in Ithaca, New York, we sought to explain the increase in disease prevalence by evaluating two proposed hypotheses. As *M. gallisepticum* evolved greater virulence, its capacity for adaptation within other finch species correspondingly increased. 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. In light of the M. gallisepticum epidemic's impact on house finch populations, Hypothesis 2 proposes that purple finches around Ithaca experienced a relative increase in abundance, potentially leading to more encounters with and exposure to M. gallisepticum-infected house finches.