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For a fungal pathogen to successfully infect, colonize and spread inside a susceptible host, it must have overcome the host immune responses. The early recognition of the fungal pathogen-associated molecular patterns (PAMPS) by the host’s pattern recognition receptors (PRRs) results in the establishment of anti-fungal immunity. Although, our immune system has evolved several processes to combat these pathogens both at the innate and adaptive immune levels. These organisms have developed various escape strategies to evade the recognition by the host\'s innate immune components and thus interfering with host immune mechanisms. In this chapter, we will summarize the major PRRs involved in sensing fungal PAMPS and most importantly the fungal tactics to escape the host\'s innate immune surveillance and protective mechanisms.

The present study was conducted to determine the seroprevalence and pathology of Salmonella infection in white commercial layer birds of District Faisalabad during June 2018 and June 2020. The current study aimed to determine the isolation, identification of Salmonella gallinarum (S. gallinarum), its cultural prevalence, antimicrobial resistance, molecular characterization, and pathological lesions produced in different organs of commercial layer birds. Initial screening of poultry flocks was done through serum plate agglutination test followed by culturing in different media, motility test, molecular confirmation, and histopathology. Based on the serum plate agglutination test, seroprevalence in the commercial white layer in dead and live flocks was 40.09%. The cultural prevalence of Salmonella in the seropositive group was 75.36% and in the seronegative was 31.84%. Cultural prevalence in the liver of dead birds was 62.06%, in spleen 58.62%, and in cloacal swabs was 67.24%. A total of 178 isolates were characterized through cultural characteristic and motility tests, among them 63.48% isolates were S. gallinarum, and 36.51% isolates were S. pullorum. The antibiogram study revealed that all the tested isolates were resistant to amoxicillin, gentamycin, kanamycin, doxycyclin, and tetracyclin. While tested isolates were sensitive to ciprofloxacin against S. gallinarum. Pathologically liver was friable, showing bonze discoloration with focal necrosis, enteritis of various grades, mottled white spleen, and enlarged kidneys were found. Microscopically, leukocytic infiltration with focal necrosis and degeneration, in mucosa and submucosa of intestinal inflammatory cells were observed. In conclusion, the seroprevalence, antibiogram, and molecular characterization of Salmonella help to control the disease in a better way through bacterin production of local isolates.

Chicken type I interferons (type I IFNs) are key antiviral players of the chicken innate immune system and are considered potent antiviral agents against avian viral pathogens. Chicken type I IFNs are divided into three subtypes namely, chIFN-α, chIFN-β, and chIFN-κ. Viral pathogen-associated molecular patterns (PAMPs) recognized by their corresponding specific PRRs (pattern recognition receptors) induce the expression of chicken type I IFNs. Interaction of chicken type I IFNs with their subsequent IFN receptors results in the activation of the JAK-STAT pathway, which in turn activates hundreds of chicken interferon-stimulated genes (chISGs). These chISGs establish an antiviral state in neighboring cells and prevent the replication and dissemination of viruses within chicken cells. Chicken type I IFNs activate different pathways that constitute major antiviral innate defense mechanisms in chickens. However, evolutionary mechanisms in viruses have made them resistant to these antiviral players by manipulating host innate immune pathways. This review focuses on the underlying molecular mechanisms employed by avian RNA viruses to counteract chicken type I IFNs and chISGs through different viral proteins. This may help to understand host-pathogen interactions and the development of novel therapeutic strategies to control viral infections in poultry.

The present study aimed to evaluate the immunopotentiating effect of plant-derived soyasaponin and its immunogenicity in chickens challenged with Newcastle disease virus (NDV). Soyasaponin was extracted from soybean seeds and detected using the phytochemical tests, followed by quantification through the dry-weight method. One-day-old broiler chicks (n = 90) were divided into 3 groups, named as A, B, and C. Group A birds were orally administrated with soyasaponin (5 mg/kg), followed by immunization with inactivated ND vaccine intramuscularly (IM), whereas group B birds were vaccinated with inactivated ND vaccine alone. Group C birds were kept unvaccinated. A booster dose on day 21 was also administered IM to group A and B birds. At day 35, all 3 groups were challenged with NDV. To determine the immunogenicity potential of soyasaponin, antibody titer was measured using the hemagglutination inhibition test before and after the NDV challenge. Histochemical examination was performed to determine the pathological changes associated with NDV infection. Foam formation and hemolytic activity confirmed the presence of saponin in soya bean extract. Group A birds showed a higher antibody response compared with group B and C birds. The disease challenge study showed that soyasaponin-adjuvanted NDV vaccine provided complete protection to group A birds against ND. Moreover, no side effects of soyasaponin were observed on the growth performance of birds during the experiment. Therefore, we can conclude that soyasaponin is a potential immunogenic agent and therefore could be a promising candidate to launch a protective humoral response against ND in chickens.