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ABSTRACT Background Bordetella bronchiseptica is an essential bacterial pathogen characterized by chronic respiratory disease in dogs known as Kennel cough. The presence of causative antibodies in animals can also be detected by lipopolysaccharide antigen‐based enzyme linked immunosorbent assay (ELISA). In recent years, it has been determined that there is a significant relationship between acute phase proteins and diseases, and disease follow‐up can be done within the framework of this relationship. Methods In this study, blood sera from 150 dogs in an animal shelter in Van province were evaluated for B. bronchiseptica by the homemade ELISA method, and their correlations with serum amyloid A (SAA) were investigated. Blood serum samples were analysed for antibodies against B. bronchiseptica using a homemade ELISA method. Positive animals were also molecularly confirmed using nasal swabs by PCR. A commercial ELISA kit determined SAA levels in blood sera. Results Eighteen (12%) of the analysed blood serum samples were found positive by the homemade ELISA method. SAA concentrations in the positive blood sera were elevated from 12.7 to ≤38.98 mg/L. SAA concentrations in blood sera serologically positive for B. bronchiseptica were statistically significant. Conclusions In this study, in which the relationship between SAA concentration and B. bronchiseptica was investigated for the first time in Turkey, it was concluded that SAA concentration analysis may help diagnose and monitor the disease. In addition, the presence and prevalence of this critical and zoonotic agent causing chronic respiratory tract disease in dogs in Van province was revealed for the first time in this study. A study in Van, Turkey examined Bordetella bronchiseptica in shelter dogs using ELISA and PCR. Overall, 12% of blood samples tested positive. Serum amyloid A (SAA) levels were significantly elevated in positive cases, suggesting SAA could be a useful diagnostic marker for this chronic respiratory disease‐causing bacterial pathogen.

The respiratory tract is constantly exposed to the environment and displays a favorable niche for colonizing microorganisms. However, the effects of respiratory bacterial carriage on the immune system and its implications for secondary responses remain largely unclear. We have employed respiratory carriage with Bordetella bronchiseptica as the underlying model to comprehensively address effects on subsequent immune responses. Carriage was associated with the stimulation of Bordetella-specific CD4+, CD8+, and CD4+CD25+Foxp3+ T cell responses, and broad transcriptional activation was observed in CD4+CD25+ T cells. Importantly, transfer of leukocytes from carriers to acutely B. bronchiseptica infected mice, resulted in a significantly increased bacterial burden in the recipient’s upper respiratory tract. In contrast, we found that respiratory B. bronchiseptica carriage resulted in a significant benefit for the host in systemic infection with Listeria monocytogenes. Adaptive responses to vaccination and influenza A virus infection, were unaffected by B. bronchiseptica carriage. These data showed that there were significant immune modulatory processes triggered by B. bronchiseptica carriage, that differentially affect subsequent immune responses. Therefore, our results demonstrated the complexity of immune regulation induced by respiratory bacterial carriage, which can be beneficial or detrimental to the host, depending on the pathogen and the considered compartment.

Bordetella hinzii is commonly acquired from the respiratory tract of diseased poultry but is generally Regarded as nonpathogenic in avian hosts because attempts to demonstrate disease following experimental infection of chickens and turkeys have failed. Recently, with the availability of highly specific DNA-based methods for identification of this agent, it was recognized that some isolates used in previous studies were misidentified at the time of their acquisition as Bordetella avium, B. avium–like, or Alcaligenes faecalis type II, including a subset reported to cause disease in turkey poults. In this study six strains of B. hinzii, genetically distinct and representing all known host species, were evaluated for their ability to colonize and cause disease in turkeys following intranasal administration. Although five strains were able to colonize the tracheas of turkey poults, only a subset induced clinical signs of disease, B. hinzii–specific antibodies, or tracheal lesions. The sixth isolate was undetectable in tracheal swabs obtained 1 or 2 weeks postinfection. Birds of this group displayed no clinical signs and minimal tracheal lesions. All remained B. hinzii seronegative. Three of the six strains, differing in their capacity to colonize and/or cause disease in turkeys, were used to infect chicks intranasally. Only one was able to colonize the trachea but did not induce tracheal lesions. No clinical signs of disease were observed in any chick. These results demonstrate that some strains of B. hinzii are virulent in turkey poults and may asymptomatically colonize chicks, and suggest this agent may be of concern to poultry producers.

Infections with the gram-negative bacteria Bordetella pertussis ( B. pertussis ) have long been recognized as a significant threat to children and are increasingly recognized as a cause of cough in adolescents and adults. Antibiotic therapy, when administered during the virulent stages of the disease, can reduce the duration and severity of symptoms. Unfortunately, there are no effective treatments for the persistent coughing that accompanies and follows the infection. The pathogenesis of B. pertussis infection is briefly reviewed. Also discussed is the evidence supporting the hypothesis that the inflammatory peptide bradykinin may be responsible for the persistent, paroxysmal coughing associated with B. pertussis -initiated illness.

Presence of antibody to adenylate cyclase toxin (ACT) has been noted following Bordetella pertussis infection. Because ACT is not presently in any acellular pertussis vaccines, it has been considered as a possible antigen to use in B. pertussis diagnostic enzyme-linked immunosorbent assay (ELISA) studies. We determined antibody to B. pertussis ACT by ELISA and Western blot tests in serum samples obtained from unvaccinated children, from children vaccinated with several diphtheria and tetanus toxoid vaccines (DTP vaccines), from children vaccinated with vaccines containing acellular pertussis components in combination with diphtheria and tetanus toxoids (DTaP vaccines), and from children and adults with pertussis. Primary infections with either B. pertussis or Bordetella parapertussis stimulated a vigorous antibody response to ACT. In contrast, patients in whom DTP and DTaP vaccines failed had minimal ACT antibody responses. The lack of a significant ACT antibody response in children in whom the vaccine failed is of interest but would seem to preclude the use of ACT in diagnostic tests.

To analyze a Bordetella holmesii isolate from a patient with sickle cell anemia and to compare it with other B. holmesii strains and isolates and with strains of B. pertussis and B. bronchiseptica, two well-characterized species of the Bordetella genus. The bacteriological characteristics and proteins produced by the B. holmesii isolate and the reference strain (ATCC 51541) were analyzed and compared with those of B. pertussis and B. bronchiseptica using sera from patients infected with B. pertussis, B. bronchiseptica or B. holmesii. The bacteriological characteristics of the B. holmesii isolate studied here were similar to those of the B. holmesii reference strain and other isolates. Some of the proteins produced by B. holmesii isolates were similar to those produced by B. pertussis and B. bronchiseptica, but none of these proteins was similar to the toxins and adhesins involved in the pathogenicity of B. pertussis and B. bronchiseptica. The phenotypic diversity of the proteins produced by B. holmesii isolates and the reference strain was striking. Our results suggest that either, the expression of B. holmesii proteins is regulated as in B. pertussis and B. bronchiseptica, with the B. holmesii strain exhibiting different phases, or the proteins produced in B. holmesii are different.

Blood samples collected from 31 free-roaming peafowl from three zoos in Michigan were tested serologically. Antibody titers were present against avian adenovirus and Bordetella avium in 19.3% and 61.3% of the samples, respectively. Serum plate agglutination tests were positive for Mycoplasma meleagridis and Mycoplasma synoviae in 3.2% and 38.7% of the samples, respectively. All birds were seronegative for avian influenza, Newcastle disease virus, West Nile virus, Mycoplasma gallisepticum, Salmonella pullorum, Salmonella typhimurium, and Giardia sp. No parasites were seen in blood smears. Cloacal swabs were cultured for anaerobic, aerobic, and microaerophilic bacteria. Clostridium perfringens type A and Escherichia coli were cultured most frequently from 64.5% and 29% of the samples, respectively, whereas Salmonella sp. and Campylobacter sp. were not isolated. Fecal samples contained moderate numbers of ascarid and Capillaria sp. ova and coccidian oocysts. Female biting lice (Goniodes gigas) were identified on three birds.

Plasma triiodothyronine (T3), thyroxine (T4), and corticosterone (CS) were measured in fasted and nonfasted control and Bordetella avium-infected poults. The stress of B. avium infection increased plasma CS, and fasting for 24 hours caused a further significant increase in CS levels. Plasma T3 was not affected by the infection, but fasting caused a significant reduction in both control and infected poults. Plasma T4 of fasted poults was increased in both control and infected groups, but infection attenuated the plasma T4 response. Total iodothyronines were increased in the control-fasted poults more than in infected-fasted poults, indicating a reduced responsiveness to stress by the thyroids of infected poults. Changes in plasma thyroid hormones and CS partially explain the decreased body weight gain and decreased body temperature after exposure to B. avium

We calculated the effectiveness of pertussis vaccine in preventing parapertussis among Oregon children 2 months to 10 years of age using 2 methods. During 2011–2016, the 2 VE methods found 66% (95% CI, 59–75%) and 82% (95% CI, 69–90%) effectiveness against parapertussis. Pertussis vaccine may induce cross-immunity.

Cystic fibrosis (CF) is an autosomal recessive disease caused by dysfunctional cystic fibrosis transmembrane conductance regulator (CFTR) protein, and is marked by an accumulation of mucus in affected airways resulting in persistent infection and chronic inflammation. Quantitative differences in inflammatory markers have been observed in CF patient serum, tracheal cells, and bronchoalveolar lavage fluid, in the absence of detectable infection, implying that absent CFTR function alone may result in dysregulated immune responses. To examine the relationship between absent CFTR and systemic inflammation, 22 analytes were measured in CF mice (F508del/F508del) sera using the MSD multiplex platform. Pro-inflammatory cytokines IL-2, TNF-α, IL-17α, IFN-γ, IL-1β, and MIP-3α are significantly elevated in infection-naïve CF mice ( p  < 0.050). Anti-inflammatory cytokines IL-10 and IL-4 are also significantly increased ( p  = 0.00003, p  = 0.004). Additionally, six general markers of inflammation are significantly different from non-CF controls ( p  < 0.050). To elucidate the effects of chronic infection on the CF inflammatory profile, we examined CF mice exposed to spontaneous Bordetella pseudohinzii infections. There are no statistical differences in nearly all inflammatory markers when compared to their infection-naïve CF counterparts, except in the Th2-derived IL-4 and IL-5 which demonstrate significant decreases following exposure ( p  = 0.046, p  = 0.045). Lastly, following acute infection, CF mice demonstrate elevations in nearly all inflammatory markers, but exhibit a shortened return to uninfected levels over time, and suppression of Th1-derived IL-2 and IL-5 ( p  = 0.043, p  = 0.011). These results imply that CF mice have a persistent inflammatory profile often indistinguishable from chronic infection, and a dysregulated humoral response during and following active infection.