Mycoplasma Gallisepticum Infection Research Articles

Quercetin restores respiratory mucosal barrier dysfunction in Mycoplasma gallisepticum-infected chicks by enhancing Th2 immune response.

Mycoplasma gallisepticum (MG) has long been a pathogenic microorganism threatening the global poultry industry. Previous studies have demonstrated that the mechanism by which quercetin (QUE) inhibits the colonization of MG in chicks differs from that of antibiotics. However, the molecular mechanism by which QUE facilitates the clearance of MG remains unclear. The aim of this study was to investigate the molecular mechanism of MG clearance by QUE, with the expectation of providing new options for the treatment of MG. A model of MG infection in chicks and MG-induced M1 polarization in HD-11 cells were established. The mechanism of QUE clearance of MG was investigated by evaluating the relationship between tracheal mucosal barrier integrity, antibody levels, Th1/Th2 immune balance and macrophage metabolism and M1/M2 polarization balance. Furthermore, network pharmacology and molecular docking techniques were employed to explore the potential molecular pathways connecting QUE, M2 polarization, and fatty acid oxidation (FAO). The findings indicate that QUE remodels tracheal mucosal barrier function by regulating tight junctions and secretory immunoglobulin A (sIgA) expression levels. This process entails the regulatory function of QUE on the Th1/Th2 immune imbalance that is induced by MG infection in the tracheal mucosa. Moreover, QUE intervention impeded the M1 polarization of HD-11 cells induced by MG infection, while simultaneously promoting M2 polarization through the induction of FAO. Conversely, inhibitors of the FAO pathway impede this effect. The results of computer network analysis suggest that QUE may induce FAO via the PI3K/AKT pathway to promote M2 polarization. Notably, inhibition of the PI3K/AKT pathway was found to effectively inhibit M2 polarization in HD-11 cells, while having a limited effect on FAO. QUE promotes M2 polarization of HD-11 cells to enhance Th2 immune response through FAO and PI3K/AKT pathways, thereby restoring tracheal mucosal barrier function and ultimately inhibiting MG colonization.

The house finch ocular microbiome is altered by infection, but does not predict disease transmission

Recent studies have highlighted the importance of host-associated microbial communities in inhibiting growth or colonization of pathogenic species and mitigating disease severity. Much research has been conducted on how the microbiome of individuals may impact their disease susceptibility; however, less attention has been given to the role of microbiomes in population-level disease processes. In this study, we examined the effects of the ocular microbiome on pathogen load, disease severity, and transmission success of the conjunctival bacterial pathogen Mycoplasma gallisepticum (MG) in house finches (Haemorhous mexicanus). Fifteen male house finches were exposed to MG and housed pairwise with uninfected females for 32 days. Swabs for ocular microbiome characterization via 16 S rRNA gene amplicon sequencing were collected from male and female finches before and nine days after MG inoculation. MG load and disease severity were quantified throughout the experiment for all individuals. We examined whether ocular microbiome composition prior to MG infection was associated with pathogen load, disease severity, or transmission efficacy. Although the presence of certain taxa in the ocular microbiome is associated with disease protection in this species, we did not find any evidence that ocular microbiome composition was associated with any metric used to quantify disease transmission. MG infection did alter the resident bacterial communities, which aligns with results from previous studies. However, this was only true for the indicator birds that were directly inoculated with MG. Our results suggest the resident ocular microbiome of house finches shifts in responses to direct contact with pathogens, but may be more resilient, at least at the timescales examined, when host exposure is via an infected conspecific. This suggests that outcomes of interactions between pathogens and resident microbial communities may depend on the mode or dose of pathogen exposure.

Revealing the mechanism: the influence of Baicalin on M1/M2 and Th1/Th2 imbalances in mycoplasma gallisepticum infection

Mycoplasma gallisepticum (MG) is a pathogen that induces chronic respiratory illnesses in chickens, leading to tracheal and lung injury, and eliciting immune reactions that support sustained colonization. Baicalin, a compound found in scutellaria baicalensis, exhibits anti-inflammatory, antioxidant, and antibacterial properties. This study aimed to investigate the potential of baicalin in alleviating lung and cell damage caused by MG by restoring imbalances in M1/M2 and Th1/Th2 differentiation and to explore its underlying mechanism. In this research, a model for M1/M2 polarization induced by MG was initially developed. Specifically, infection with MG at a multiplicity of infection (MOI) of 400 for 6 h represented the M1 model, while infection for 10 h represented the M2 model. The polarization markers were subsequently validated using qRT-PCR, ELISA, and Western blot analysis. Baicalin disrupts the activation of M1 cells induced by MG and has the potential to restore the balance between M1 and M2 cells, thereby mitigating the inflammatory damage resulting from MG. Subsequent studies on MG-infected chickens detected imbalances in M1/M2 and Th1/Th2 differentiation in alveolar lavage fluid, as well as imbalances in macrophages and Th cells in the lung. The M1/Th1 model was exposed to MG for 5 d, while the M2/Th2 model was infected with MG for 7 d. The utilization of both light and electron transmission microscopes revealed that the administration of baicalin resulted in a reduction in the number of M1 cells, a decrease in cytoplasmic vacuoles, restoration of mitochondrial swelling and chromatin agglutination, as well as alleviation of alveolar rupture and inflammatory cell infiltration. Furthermore, baicalin restored MG-induced M1/M2 and Th1/Th2 imbalances and inhibited the phosphorylation of p38 and p65 proteins, thereby hindering the activation of the TLR4-p38 MAPK/NF-κB pathway. This study provides insights into the potential long-term effects of baicalin in MG infection and offers a theoretical basis for practical applications.

Alarming and calming: Dual functions of S100A9 on Mycoplasma gallisepticun infection in avian cells

Mycoplasma gallisepticum (MG) is the primary causative agent of chronic respiratory disease (CRD) in chickens, characterized by respiratory inflammation. S100A9 plays a pivotal role in modulating the inflammatory response to microbial pathogens. Our prior investigation revealed a significant upregulation of S100A9 in the lungs of chickens following MG infection. This study delves into the immunomodulatory effects of S100A9 during MG infection, demonstrating a notable increase in S100A9 levels in the lungs, immune organs, alveolar epithelial type II cells (AECII), and macrophage HD11 cells of MG-infected chicks and embryos. In MG-infected AECII cells, S100A9 overexpression significantly enhanced MG proliferation and adhesion, suppressed AVBD1, NFκB, pro-inflammatory factors (IL1β and TNFα), and chemokines, reduced apoptosis, and promoted cell proliferation, thereby facilitating MG infection. Conversely, inhibiting S100A9 produced opposing effects. In MG-infected HD11 cells, S100A9 impeded MG proliferation and adhesion, increased AVBD1, NFκB, pro-inflammatory factors, and chemokines, and induced cell apoptosis while inhibiting proliferation. Additional results demonstrated that S100A9 facilitates MG infection by modulating the TLR7/NFκB/JAK/STAT pathway in AECII/HD11 cells. In summary, S100A9 exhibits a dual role in activating/inhibiting the natural immune response through TLR7/NFκB/JAK/STAT pathway regulation. This dual role promotes MG infection in AECII cells while enabling MG to evade immune surveillance by HD11 cells, ultimately enhancing the overall infection process. These findings advance our understanding of host-pathogen interactions during MG infection and underscore S100A9's potential as a therapeutic target for CRD in chickens.

Evaluation of Internal and External Biosecurity Measures and Their Association with Mycoplasma gallisepticum Infection in Broiler Farms in Khartoum State, Sudan

Evaluation of Internal and External Biosecurity Measures and Their Association with Mycoplasma gallisepticum Infection in Broiler Farms in Khartoum State, Sudan

Seroprevalence and pathology of Mycoplasma gallisepticum infection in layer birds

Avian mycoplasmosis, caused by Mycoplasma gallisepticum (MG), imposes a significant threat to the poultry industry in Bangladesh, leading to considerable economic losses. This study aimed to determine the seroprevalence of MG and characterize the associated pathology in MG-infected layer birds from different geographical areas within the Nilphamari district. Our hypothesis suggested that the seroprevalence of MG infection in layer birds may vary based on geographical location within the Nilphamari district of Bangladesh, with higher prevalence expected in areas with colder temperatures, such as during the winter season, and in densely populated poultry farming regions. For the serum plate agglutination test, 400 random blood samples were collected, while tissue samples from suspected layer birds with respiratory distress were obtained from 40 commercial layer farms for histopathological analysis. The serum plate agglutination test revealed an overall seroprevalence of MG of 64.25%, with the highest prevalence occurring during the winter season (70%), particularly among layer birds aged 20-40 weeks. Moreover, the seroprevalence of MG was significantly higher in Kishoregonj upazila (68%) compared to Nilphamari sadar (62%). Gross examination of MG-infected layer birds unveiled characteristic features such as tracheal hemorrhages and mucous accumulation, pulmonary edema and hemorrhages, and air sac cloudiness. Histopathological observations included tracheal mucosal sloughing and increased goblet cell numbers, as well as lung edema, hemorrhages, and tissue destruction, alongside significant reactive cell infiltration and exudation in the air sacs. By shedding light on the current MG infection status in layer chickens within the Nilphamari district, this study provides valuable insights to aid poultry industry stakeholders in formulating preventive strategies and enhancing the overall health and welfare of poultry flocks. Asian J. Med. Biol. Res. 2024, 10(1), 58-66

Unmasking the dynamics of Mycoplasma gallisepticum: deciphering HD11 macrophage polarization for innovative infection control strategies

Mycoplasma gallisepticum (MG) is a highly contagious avian respiratory pathogen characterized by rapid spread, widespread distribution, and long-term persistence of infection. Previous studies have shown that chicken macrophage HD11 cells play a critical role in the replication and immunomodulation of MG. Macrophages are multifunctional immunomodulatory cells that polarize into different functions and morphologies in response to exogenous stimuli. However, the effect of MG infection on HD11 polarization is not well understood. In this study, we observed a time-dependent increase in both the expression of the MG-related virulence protein pMGA1.2 and the copy number of MG upon MG infection. Polarization studies revealed an upregulation of M1-type marker genes in MG-infected HD11 cells, suggesting that MG mainly induces HD11 macrophages towards M1-type polarization. Furthermore, MG activated the inflammatory vesicle NLRP3 signaling pathway, and NLRP3 inhibitors affected the expression of M1 and M2 marker genes, indicating the crucial regulatory role of the NLRP3 signaling pathway in MG-induced polarization of HD11 macrophages. Our findings reveal a novel mechanism of MG infection, namely the polarization of MG-infected HD11 macrophages. This discovery suggests that altering the macrophage phenotype to inhibit MG infection may be an effective control strategy. These findings provide new perspectives on the pathogenic mechanism and control measures of MG.

Varying conjunctival immune response adaptations of house finch populations to a rapidly evolving bacterial pathogen.

Pathogen adaptations during host-pathogen co-evolution can cause the host balance between immunity and immunopathology to rapidly shift. However, little is known in natural disease systems about the immunological pathways optimised through the trade-off between immunity and self-damage. The evolutionary interaction between the conjunctival bacterial infection Mycoplasma gallisepticum (MG) and its avian host, the house finch (Haemorhous mexicanus), can provide insights into such adaptations in immune regulation. Here we use experimental infections to reveal immune variation in conjunctival tissue for house finches captured from four distinct populations differing in the length of their co-evolutionary histories with MG and their disease tolerance (defined as disease severity per pathogen load) in controlled infection studies. To differentiate contributions of host versus pathogen evolution, we compared house finch responses to one of two MG isolates: the original VA1994 isolate and a more evolutionarily derived one, VA2013. To identify differential gene expression involved in initiation of the immune response to MG, we performed 3'-end transcriptomic sequencing (QuantSeq) of samples from the infection site, conjunctiva, collected 3-days post-infection. In response to MG, we observed an increase in general pro-inflammatory signalling, as well as T-cell activation and IL17 pathway differentiation, associated with a decrease in the IL12/IL23 pathway signalling. The immune response was stronger in response to the evolutionarily derived MG isolate compared to the original one, consistent with known increases in MG virulence over time. The host populations differed namely in pre-activation immune gene expression, suggesting population-specific adaptations. Compared to other populations, finches from Virginia, which have the longest co-evolutionary history with MG, showed significantly higher expression of anti-inflammatory genes and Th1 mediators. This may explain the evolution of disease tolerance to MG infection in VA birds. We also show a potential modulating role of BCL10, a positive B- and T-cell regulator activating the NFKB signalling. Our results illuminate potential mechanisms of house finch adaptation to MG-induced immunopathology, contributing to understanding of the host evolutionary responses to pathogen-driven shifts in immunity-immunopathology trade-offs.

Inflammatory responses and barrier disruption in the trachea of chicks following Mycoplasma gallisepticum infection: a focus on the TNF-α-NF-κB/MLCK pathway

Mycoplasma gallisepticum (MG) can induce persistent inflammatory damage to the tracheal mucosa of poultry and cause chronic respiratory diseases in chickens. To further investigate the mechanism of MG-induced injury to the tracheal mucosa, we used chick embryo tracheal organ culture (TOC) as a model to study the invasion and reproduction of MG, the effect of MG on tracheal morphology, and the potential factors that promote MG tissue invasion. The results showed that MG infection significantly damaged the tracheal epithelial structure and weakened tracheal epithelial barrier function; MG also increased the occurrence of bacterial displacement, with a significant (p < 0.05) increase in the bacterial load of the infected TOCs at 5 and 7 days post-infection. In addition, MG significantly (p < 0.05) increased the expression levels of inflammatory cytokines, such as TNF-α, interleukin-1β (IL-1β), and IL-6, and activated the NF-κB signalling pathway, leading to increased nuclear translocation of NF-κB p65. Simultaneously, the map kinase pathway (MAPK) was activated. This activation might be associated with increased myosin light chain (MLC) phosphorylation, which could lead to actin-myosin contraction and disruption of tight junction (TJ) protein function, potentially compromising epithelial barrier integrity and further catalysing MG migration into tissues. Overall, our results contribute to a better understanding of the interaction between MG and the host, provide insight into the mechanisms of damage to the tracheal mucosa induced by MG infection, and provide new insights into the possible pathways involved in Mycoplasma gallisepticum infection in vivo.

Респираторные заболевания у кур и индеек, вызванные Mycoplasma gallisepticum

Mycoplasma gallisepticum (MG) is a prokaryote, intermediate between bacteria and viruses, and lacks a cell wall. MG mainly causes chronic respiratory disease in chickens and other poultry and infectious sinusitis in turkeys. In addition, MG infection can cause poor carcass sorting and feed processing efficiency in broiler chickens. Egg production and hatching rate in laying hens tends to decrease with increasing numbers of weak broods. Several methods are available for isolation of the microorganism: culturing, PCR diagnosis, etc. There is no definite treatment against this disease, but there are a number of attenuated vaccines produced by different countries as prophylaxis. At this point in time, the question remains both the need for further identification of a more sensitive and specific diagnostic system for the invention, as well as more in-depth studies of mycoplasma at the molecular level, which will allow further production of vaccines with a large number of strains.

Quadrivalent hemagglutinin and adhesion expressed on Saccharomyces cerevisiae induce protective immunity against Mycoplasma gallisepticum infection and improve gut microbiota

Mycoplasma gallisepticum (MG) infection causes infectious respiratory diseases in poultry, causing economic losses to the poultry industry. Therefore, this study aims to develop a safe, convenient, and effective multivalent recombinant Saccharomyces cerevisiae vaccine candidate and to explore its potential for oral immunization as a subunit vaccine. Mycoplasma gallisepticum Cytadhesin (MGC) and variable lipoprotein and hemagglutinin (vlhA) are associated with the pathogenesis of MG. In this study, a quadrivalent recombinant Saccharomyces cerevisiae (ST1814G-MG) displaying on MGC2, MGC3, VLH5, and VLH3, proteins was innovatively constructed, and its protective efficiency was evaluated in birds. The results showed that oral immunization with ST1814G-MG stimulates specific antibodies in chickens, reshapes the composition of the gut microbiota, reduces the Mycoplasma loading and pulmonary disease injury in the lungs. In addition, we found that oral ST1814G-MG had better protection against MG infection than an inactivated vaccine, and co-administration with the inactivated vaccine was even more effective. The results suggest that ST1814G-MG is a potentially safer and effective agent for controlling MG infection.

Monitoring of bronchiolar lesions and their relation with Mycoplasma gallisepticum and Infectious bronchitis virus infections in broilers with severe respiratory distress

Monitoring of bronchiolar lesions and their relation with Mycoplasma gallisepticum and Infectious bronchitis virus infections in broilers with severe respiratory distress

STAT5-mediated transcription of miR-33-5p in Mycoplasma gallisepticum-infected DF-1 cells

ABSTRACT Mycoplasma gallisepticum (MG) represents the primary causative agent of chronic respiratory disease (CRD) in chickens. CRD is a prevalent ailment in the global poultry industry, resulting in substantial economic losses. In our previous work, we reported that miR-33-5p inhibits MG-induced apoptosis, inflammatory factor production, and MG replication by specifically targeting JNK1 in chickens. Nevertheless, the regulatory mechanisms governing miR-33-5p expression during MG infection remain poorly understood. Therefore, the objective of this study was to explore the regulation of miR-33-5p gene expression during MG infection. In this study, we observed an upregulation in the expression of pri-miR-33-5p and pre-miR-33-5p following MG infection, suggesting that their regulation takes place at the transcriptional level. Moreover, we characterized the transcriptional regulatory region of miR-33-5p and discovered the presence of a binding motif for STAT5, a recognized transcription factor responsible for gene expression regulation. Luciferase reporter assays and mutational analyses unequivocally showed that STAT5 binds to the miR-33-5p promoter element, thereby modulating miR-33-5p transcription in response to MG infection. Ultimately, the overexpression of STAT5 led to an elevation in miR-33-5p expression while concurrently suppressing JNK1 expression. Our findings elucidate that STAT5 governs the upregulation of miR-33-5p during MG infection. This research offers a comprehensive understanding of MG pathogenesis and the exploration of therapeutic approaches for MG-induced CRD. RESEARCH HIGHLIGHTS MG-HS regulates the expression of transcription factor STAT5. Transcription factor STAT5 can target miR-33-5p promoter element. MG-influenced STAT5 regulates miR-33-5p and its target gene expression.

Depletion of tilmicosin residue in Gushi chickens following oral administration via drinking water.

This study aimed to examine the depletion of tilmicosin residues in Gushi chickens following the administration at a concentration of 75 mg/L in their drinking water for three consecutive days. Plasma, liver, kidney, lung, muscle, and skin + fat samples were collected from 6 chickens at 6 h, 1, 3, 5, and 7 days after the treatment. Tilmicosin concentrations in the samples were determined using a high-performance liquid chromatography (HPLC) method. The findings revealed that the highest tilmicosin residues were detected in the liver, followed by the kidney, lung, skin + fat, muscle, and plasma. Notably, at 7 days post-treatment, no drug residue was detected in all samples except for the liver and kidney. The non-compartmental model was employed to calculate relevant pharmacokinetic parameters. The elimination half-lives (t1/2λz ) of tilmicosin were as follows, ranked from long to short: skin + fat (45.42 h), liver (44.17 h), kidney (40.06 h), plasma (37.64 h), lung (31.39 h), and muscle (30.05 h). Considering the current residue depletion and the maximum residue limits (MRLs) set by Chinese regulatory authorities, the withdrawal times for tilmicosin were estimated as 18.91, 10.81, and 8.58 days in the kidney, liver, and skin + fat, respectively. A rounded-up value of 19 days was selected as the conclusive withdrawal time. Furthermore, based on the observed tilmicosin concentrations in plasma and lung, combined with previously reported minimum inhibitory concentration (MIC) values against Mycoplasma gallisepticum, the current dosing regimen was deemed adequate for treating Mycoplasma gallisepticum infections in Gushi chickens.

Quercetin and AMPK: A Dynamic Duo in Alleviating MG-Induced Inflammation via the AMPK/SIRT1/NF-κB Pathway.

Mycoplasma gallisepticum (MG) is recognized as a principal causative agent of avian chronic respiratory disease, inflicting substantial economic losses upon the poultry industry. However, the extensive use of conventional antibiotics has resulted in the emergence of drug resistance and various challenges in their clinical application. Consequently, there is an urgent need to identify effective therapeutic agents for the prevention and treatment of mycoplasma-induced respiratory disease in avian species. AMP-activated protein kinase (AMPK) holds significant importance as a regulator of cellular energy metabolism and possesses the capacity to exert an anti-inflammatory effect by virtue of its downstream protein, SIRT1. This pathway has shown promise in counteracting the inflammatory responses triggered by pathogenic infections, thus providing a novel target for studying infectious inflammation. Quercetin possesses anti-inflammatory activity and has garnered attention as a potential alternative to antibiotics. However, there exists a gap in knowledge concerning the impact of this activation on MG-induced inflammatory damage. To address this knowledge gap, we employed AlphaFold2 prediction, molecular docking, and kinetic simulation methods to perform a systematic analysis. As expected, we found that both quercetin and the AMPK activator AICAR activate the chicken AMPKγ1 subunit in a similar manner, which was further validated at the cellular level. Our project aims to unravel the underlying mechanisms of quercetin's action as an agonist of AMPK against the inflammatory damage induced by MG infection. Accordingly, we evaluated the effects of quercetin on the prevention and treatment of air sac injury, lung morphology, immunohistochemistry, AMPK/SIRT1/NF-κB pathway activity, and inflammatory factors in MG-infected chickens. The results confirmed that quercetin effectively inhibits the secretion of pro-inflammatory cytokines such as IL-1β, TNF-α, and IL-6, leading to improved respiratory inflammation injury. Furthermore, quercetin was shown to enhance the levels of phosphorylated AMPK and SIRT1 while reducing the levels of phosphorylated P65 and pro-inflammatory factors. In conclusion, our study identifies the AMPK cascade signaling pathway as a novel cellular mediator responsible for quercetin's ability to counter MG-induced inflammatory damage. This finding highlights the potential significance of this pathway as an important target for anti-inflammatory drug research in the context of avian respiratory diseases.

Protection of Chickens from Mycoplasma gallisepticum through the MAPK/ERK/JNK Pathway by a Compound of Ten Chinese Medicine Formulas1

Mycoplasma gallisepticum (MG) is a common avian pathogen that mainly infects poultry, causing significant reductions in body weight gain and egg production, along with damage to immune organs and immunosuppression. MG is susceptible to co-infections with other pathogens, leading to increased mortality rates and significant economic losses in the global poultry industry. While antibiotics have been extensively applied worldwide to treat MG infections in poultry production, concerns regarding antibiotic resistance and residue remain prevalent. Traditional Chinese medicine (TCM), renowned for its natural, safe, and non-toxic properties, has shown significant anti-inflammatory and immune-enhancing effects. This study aimed to investigate the protective effect of TCM on production performance and its impact on MG-induced immunosuppression through the MAPK/ERK/JNK signaling pathway in chickens. Our results showed that TCM alleviated the negative effects of MG infection on production performance, as evidenced by improvements in body weight gain, feed conversion rate, survival rate, and immune organ index. TCM exhibited direct inhibition of the MG proliferation in vitro and in vivo. Furthermore, TCM treatment promoted the normalization of trachea and lung tissue structure in MG-infected chickens, leading to a significant reduction in inflammatory damage. Moreover, following the treatment with the TCM, the production of pro-inflammatory cytokines Interleukin-1β (IL-1β) and Tumor Necrosis Factor-α (TNF-α) decreased significantly, accompanied by the downregulation of pro-apoptotic genes caspase3, caspase9, and BAX, both in vitro and in vivo. A mechanism-based study showed that in vitro and in vivo treatment with the TCM significantly reduced the expression of key proteins, including early growth response gene1 (EGR1), p-ERK, p-JNK, and p-JUN. Altogether, TCM improved body weight gain, inhibited pro-inflammation responses, and alleviated tissue damage by inhibiting the MAPK/ERK/JNK signaling pathway to protect the performance and immune system of MG-infected chickens.

An overview of the Pathogenesis and Virulence of Mycoplasma gallisepticum infection – a review

Mycoplasma gallisepticum (Mg) belongs to the class Mollicutes, the smallest and simplest microorganisms which lack a cell wall and are capable of self-replication outside a host. Mg is the primary etiological agent of chronic respiratory diseases in poultry, and causes major economic losses. Recently, owing to advances in scientific knowledge, large data sets have become available for Mg, providing sequencing data, new typing strategies, diagnostic methods, and means for comprehensive studies. The aim of this review is to summarize the current knowledge regarding the virulence, variable surface lipoproteins, invasion of host cells, adhesion, antigenic variation, biofilm formation, and modulation of the host immune system. Moreover, the broader picture includes the emergence of Mg successfully combating host immunity and adapting to the new host or niches, having evolved a number of strategies and mechanisms, contributing to the pathogenesis and dissemination of Mg infection.

Let's stick together: Infection enhances preferences for social grouping in a songbird species.

Acute infections can alter foraging and movement behaviors relevant to sociality and pathogen spread. However, few studies have directly examined how acute infections caused by directly transmitted pathogens influence host social preferences. While infected hosts often express sickness behaviors (e.g., lethargy) that can reduce social associations with conspecifics, enhanced sociality during infection might be favored in some systems if social grouping improves host survival of infection. Directly assaying social preferences of infected hosts is needed to elucidate potential changes in social preferences that may act as a form of behavioral tolerance (defined as using behavior to minimize fitness costs of infection). We tested how infection alters sociality in juvenile house finches (Haemorhous mexicanus), which are both highly gregarious and particularly susceptible to infection by the bacterial pathogen Mycoplasma gallisepticum (MG). We inoculated 33 wild-caught but captive-held juvenile house finches with MG or media (sham control). At peak infection, birds were given a choice assay to assess preference for associating near a flock versus an empty cage. We then repeated this assay after all birds had recovered from infection. Infected birds were significantly more likely than controls to spend time associating with, and specifically foraging near, the flock. However, after infected birds had recovered from MG infection, there were no significant differences in the amount of time birds in each treatment spent with the flock. These results indicate augmented social preferences during active infection, potentially as a form of behavioral tolerance. Notably, infected birds showed strong social preferences regardless of variation in disease severity or pathogen loads, with 14/19 harboring high loads (5-6 log10 copies of MG) at the time of the assay. Overall, our results show that infection with a directly transmitted pathogen can augment social preferences, with important implications for MG spread in natural populations.

Comparing the suitability of the serologic tests in diagnose Mycoplasma gallisepticum

Mycoplasma gallisepticum (MG) infection in chickens results in significant economic losses because it reduces egg production. Chickens infected with MG are stated to have a higher susceptibility to other disease agents. Therefore it is vital to monitor the presence of MG in layer farms. Monitoring through serological tests is the easiest option to apply. Rapid Agglutination Serum (RSA) is an option because of its fast and inexpensive application. In addition, ELISA has also been used to confirm the RSA test. This study compares the suitability of two serological tests, the RSA and ELISA. Serum samples of 155 taken from laying hens were tested by RSA and ELISA. RSA test results obtained 99 (63.9%) seropositive and 105 (67.7%) ELISA seropositive. As many as 68 (64.8%) were seropositive on the RSA and ELISA tests, while 19 (38%) were seronegative. The proportion of conformity by the Mc Nemar test between the RSA and ELISA tests did not show a significant difference of 0.545 (P>0.005). The kappa value between the two serological techniques was low (k=0.027). The statistical analysis results of these two serological tests show that these two tests can be used as initial monitoring for screening for MG.

Concentration of Interferon - gamma in Respiratory Disease Infected Chickens Caused by Mycoplasma gallisepticum

Mycoplasma gallisepticum is commonly involved in the polymicrobial "chronic respiratory disease" in broiler chickens, leading to increased condemnations in the processing plant. In layers and breeders, it is usually subclinical, but causes a reduction in the number of eggs laid per hen over the production cycle. The present study aim to sero-identification of the Mycoplasma gallisepticum and study the concentration of interferon gamma. Sixty seven broiler chickens with respiratory signs (infected group), and fifteen healthy chickens considered as control group were used in this study. Blood samples were collected from all groups to perform in enzyme-linked immunosorbent test to identification antibodies for Mycoplasma gallisepticum and the level of interferon gamma. The result was shown (32/67) sample from infected chicken was positive for Mycoplasma gallisepticum and the level of INF-Gamma is significantly higher in the positive chicken for Mycoplasma gallisepticum infection at (102.34 ± 31.37) pg/ml when compared to control group at found (74.68 ± 12.75) pg/ml. The conclusion that increasing the level of INF-Gamma was affected in the increasing the susceptible to Mycoplasma gallisepticum infection and caused chronic respiratory disease infected to chickens in Iraq