A study of the immunomodulatory effects of coconut oil extract in broilers experimentally infected with velogenic Newcastle disease virus.

Objective: This study aims to evaluate the immunomodulatory effects of coconut oil extract (COE) in broilers experimentally infected with velogenic Newcastle disease virus (vNDV). Methods: A total of 150 broiler birds (day-old) were equally divided into five study groups i.e., negative control, positive control, COE-1, COE-2, and COE-3. On day 10, broilers of groups COE-1, COE-2, and COE-3 were supplemented with 1, 2, and 3 ml of COE respectively per liter of drinking water for 15 days. On day 13, 0.1ml/bird (10-5.25 ELD50) of vNDV was inoculated in broilers of positive control, COE-1, COE-2, and COE-3 groups intramuscularly. During this study, growth performance, morbidity, and mortality rates of each study group were recorded. The antibody titer against NDV was determined on days 7, 14, 21, 28, and 35. The levels of IgY and IgM were also determined on the 7th, 14th, and 21st days post-SRBC inoculation. On day 33, avian tuberculin was injected between the 1st and 2nd toes of the left side (intradermally) to measure lymphoproliferative responses. On day 35, the phagocytic activity in the blood was assessed through a carbon clearance assay by injecting carbon black ink into the right-wing vein. The visceral organs having gross lesions were also collected for histopathology. Results: The COE significantly improved the growth performance, and lowered the morbidity and mortality rates of broilers. There was a significant rise in antibody titers against NDV and levels of IgY and IgM antibodies against SRBC in COE-supplemented broilers. The lymphoproliferative response and phagocytic activity were also enhanced. Among COE-supplemented groups, the broilers of the COE-3 group showed a significant increase in growth performance and boosted immune defense. Conclusions: Coconut oil extract has the potential to boost the growth performance and immune status of broilers. It can be used effectively as a feed additive and alternative to antibiotics to prevent the spread of infectious poultry pathogens.

Pathological effects of feeding aflatoxin-contaminated feed on immune status and reproductive performance of juvenile white leghorn males and its mitigation with ∝-tocopherol and Moringa oleifera.

This study was planned to detect the adverse pathological consequences of aflatoxin B1 in White Leghorn (WLH) layer breeder males. Eight-week-old male layer cockerels were separated into six experimental categories: A group was kept as negative control, offered with normal feed only; group B was fed with 400 ppb amount of aflatoxin, while groups F and D fed with normal feed and supplemented with vitamin E 100 ppm and 1% Moringa oleifera, respectively, whereas groups E and C were fed with 400 ppb aflatoxin containing feed and ameliorated with vitamin E 100 ppm and 1% Moringa oleifera, respectively. This study was continued for 2 months and immunologic disorders and reproductive parameters were observed during the trial. To find out immunological status lymphoproliferative response to phytohemagglutinin-P (PHA-P), antibody titers against sheep red blood cells (SRBCs) and carbon clear assay were performed by collecting samples from five birds from each group. The whole data was measured by ANOVA test, and group means were compared by DMR test by using M-Stat C software. Regarding the reproductive status, spermatogenesis, blood testosterone level, testes weight, testes histology, sperm motility, and morphology were negatively affected by aflatoxins, but these deviations positively ameliorated by vitamin E and Moringa. Vitamin E and Moringa found advantageous in boosting the immune status of affected bird. All the immunological parameters including antibody titers against sheed red blood cells, lymphoproliferative response to avian tuberculin and phagocytic potential of macrophages were suppressed by AFB1 however in control, Moringa and vitamin E groups these immunological responses were significantly higher.

Seroprevalence and pathological studies of Salmonella infection in commercial white layer birds.

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.

Anti-chicken type I IFN countermeasures by major avian RNA viruses.

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-ß, 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.

Pathological effects of concurrent administration of aflatoxin B1 and fowl adenovirus-4 in broiler chicks.

The current study was designed to investigate pathological effects of fowl adenovirus in broilers exposed to aflatoxin B1. Fowl Adenovirus-4 (FAdV-4) infection is remerging in all types of poultry birds in Pakistan. Poultry feed contamination with mycotoxin (aflatoxin) is another important global issue. A total of 125-day old broiler birds were divided into six equal groups. Group A served as control. B and C groups were administered with aflatoxin B1 (AFB1) 100 and 200 µg/kg feed. Group D was infected with FAdV-4, while groups E and F administered with both AFB1 (100 & 200 µg/kg) along with FAdV-4. These birds were monitored for clinical signs and mortality. Feed intake, body weight (BW), relative organ weights and gross & histopathological lesions were recorded. The highest mortality was observed in group F (FAdV-4 + AFB1 200 µg/kg feed) and the lowest mortality was observed in group B (AFB1 100 µg/kg feed). Body weights of all the groups were significantly (p < 0.05) lower as compared with control group. Relative weight of liver and kidneys in groups E and F were significantly higher as compared with control. Grossly, liver was swollen, anemic with round margins in groups D, E and F. Kidneys were also swollen with whitish areas indicating dead tissue. Microscopically intranuclear inclusion bodies were observed in group D-F. The hepatic parenchyma was also indicating necrotic changes along with vacuolar degeneration. In renal parenchyma, acute tubular necrosis was observed in groups C, E and F. It was concluded that AFB1 intoxication lead to dose dependent changes in liver and kidneys. Severity of the changes was increased in interactive groups of AFB1 with FAdV-4. Therefore, feed should be regularly monitored for AFB1 levels and day old chicks for vertically transmitted FAdV-4 to prevent losses.

Toxicopathological effects of lambda-cyhalothrin in female rabbits (Oryctolagus cuniculus).

The aim of this study was to investigate effects of lambda-cyhalothrin (LCT) on clinical, hematological, biochemical and pathological alterations in rabbits (Oryctolagus cuniculus). New Zealand white female rabbits (n = 24) of 4-5 months age having 997.92 ± 32.83 g weight were divided into four equal groups. Group A (control) received normal saline intraperitoneally (ip). Animals in groups B, C and D were treated with LCT 1.0, 4.0 and 8.0 mg/kg bw ip. Each group received seven consecutive doses at an interval of 48 hours. Blood and serum samples were collected at an interval of 96 hours. Blood analysis revealed a significant (p < 0.05) decrease in red blood cell and white blood cell counts, hemoglobin concentration and lymphocytes, while mean corpuscular hemoglobin concentration, mean corpuscular volume, neutrophils, monocytes and eosinophils were increased. Serum biochemical analysis revealed significant (p < 0.05) decrease in serum total proteins and serum albumin, while an increase was seen in serum alanine aminotransferase and aspartate aminotransferase activities compared with the control group. Serum globulin values varied non-significantly in all treatment groups as compared to control group. A dose-dependent increase in the incidence of micronucleated polychromatic erythrocyte was observed. All gross and histopathological lesions observed in LCT-treated rabbits were dose-dependent. Liver of the treated rabbits exhibited extensive perihepatitis, hyperplasia of bile duct, necrosis, hemorrhages and congestion. In lungs, there were hemorrhages, thickened alveolar walls, congestion, emphysema, collapsed alveoli and accumulation of extensive inflammatory cells. Kidneys were congested and hemorrhagic whereas renal parenchyma and stroma were normal. Microscopically, heart showed congestion of blood vessels and nuclear pyknosis, myodegeneration. It was concluded from the study that LCT produced toxicopathological alterations in rabbits in a dose-dependent manner. On the basis of the results, it can be suggested that overdosing of LCT be avoided while treating animals for ectoparasites.

Toxic effects of cypermethrin and methamidophos on bovine corpus luteal cells and progesterone production.

This study was planned and executed with the aims to explore corpus luteal primary cell culture as an "animal alternate testing system" in toxicity studies and in vitro toxic effects of cypermethrin (CY) 90% (pyrethroid) and methamidophos (MTP) 73% (organophosphate) on morphology and progesterone secretory activity of bovine corpus luteal cells and tissue. For this purpose, primary cell cultures of bovine corpus luteum (CL) cells were maintained in Dulbecco's Modified Eagle Medium (DMEM) supplemented with 5% fetal calf serum (FCS). Toxicity evaluation were based on viable CL cell counts, morphological changes in CL cells, ability of CL cells to produce progesterone and histological changes in CL tissue at different hours post exposure to CY and MTP. The changes induced by both the insecticides were time and dose dependant. Viable cell counts and progesterone concentration decreased significantly (P<0.05) with the treatment of CY and MTP when compared to control. Corpus luteal cells exposed to CY showed more severe toxic effects as compared to MTP, though the difference was non-significant. Cellular or tissue alterations included degenerative changes in luteal cells, pleomorphic changes, nuclear degeneration and vacuolation, cell shrinkage and rupture, cloudy swelling and hydropic degeneration, less cytoplasmic granulation, cell elongation, hyalinization and cytoplasmic haziness and stripling and necrosis. It was concluded that both the insecticides induce toxic effects in terms of viable counts, morphological and histological changes and progesterone production of bovine CL cells. Cypermethrin exhibited more adverse toxic changes in viable cell counts, progesterone production and histological findings as compared to methamidophos.