Toxicopathological effects of feeding aflatoxins B1 in broilers and its ameliosration with indigenous mycotoxin binder.

Mycotoxicosis is the second most important problem faced by the Pakistan poultry industry, after high feed prices. The present experimental study was designed to investigate the toxicopathological effects of aflatoxin B1 (AFB1) in commercial broiler chicks and its amelioration with locally produced mycotoxin binder. Total of 125 broiler chicks was divided into five equal groups (A-E). Group A served as negative control, group B (300 µg AFB1/kg feed) as positive control, group C (300 µg AFB1/kg + Local Mycotoxin Binder (LMB), 1 g/kg feed), group D (300 µg AFB1/kg + 2 g LMB/kg feed), and group E (300 µg AFB1/kg + Commercial Mycotoxin Binder (CMB), 2 g/kg of feed). Parameters studied included mortality, feed intake, bodyweights, absolute and relative organ weights, and gross and microscopic lesions in visceral organs. Clinical signs including alertness, fecal consistency, and feather shine were significantly lower in group B compared with control group A. The feed intake of 2 g/kg LMB treated group was significantly higher than that of the positive control group B. Also mean bodyweights of group D birds was higher than that of group B birds indicating an ameliorative effect of LMB. Histopathological results showed that moldy feed produced necrotic changes in the liver and kidneys in group B birds. However, in group D and E birds, the hepatic and renal parenchyma was normal, showing a protective effect of LMB. In the present study, a higher dose of LMB (2 g/kg) in group D showed higher bodyweights and feed intake. In group D, birds hepatic and renal parenchyma was also normal. The results suggested that local mycotoxin binder ameliorated the toxicopathological effects of AFB1 in mortality, feed intake, bodyweights, organ weights and, gross and microscopic lesions in visceral organs. These ameliorative effects of LMB were dose-dependent. The results of the present study concluded that AFB1 intoxication leads to decrease in bodyweights, feed intake in dose-related manner. The mortality was also dose-dependent. Gross and microscopic changes in the aflatoxin groups were more pronounced, however, all these deleterious effects were ameliorated in higher dose of LMB (group D) and CMB (group E). In group C, these deleterious effects were partially ameliorated. Local mycotoxin binder is an economical solution for aflatoxicosis problem, making poultry production more cost-effective.

Pathophysiology of peste des petits ruminants in sheep (Dorper & Kajli) and goats (Boer & Beetal).

Peste des petits ruminants (PPR), an economically important viral transboundary disease of small ruminants is not only prevalent in Pakistan but also in other countries where people rely on agriculture and animal products. The present study was aimed at describing the pathology and antigen localization in natural PPR infections in local (Kajli sheep; Beetal goats) as well as imported small ruminant breeds (Dorper sheep; Australian Boer goat). Morbidity and mortality rates were significantly (P < 0.001) higher in indigenous Kajli sheep (75.37 and 32.80%) and Beetal goats (81.10 and 37.24%) as compared to Dorper sheep (6.99 and 1.48%) and Australian Boer goat (5.01 and 2.23%). Affected animals exhibited high fever, severe diarrhea, abdominal pain, respiratory distress and nodular lesions on lips and nostrils. Thick mucous discharge was oozing out from nostrils. On necropsy, lungs were congested and pneumonic, with nodular and cystic appearance. Intestines were hemorrhagic with zebra stripping. Characteristic histopathological lesions of PPR were noted in intestines, lymphoid organs and lungs. In GI tract, stunting and blunting of villi, necrotic enteritis, and infiltration of mononuclear cells in duodenum, jejunum and ileum. Small intestines exhibited diffuse edema of the submucosa along with proliferation of fibrocytes leading to thickened submucosa which has not been reported previously. Lymphoid organs showed partial to complete destruction of lymphoid follicles. Lesions of the respiratory tract included depictive of bronchopneumonia, severe congestion of trachea and apical lobe of lungs with deposition of fibrinous materials. Histopathological lesions of respiratory tract were severe and characteristic of broncho-interstitial pneumonia, bronchopneumonia, interstitial pneumonia and fibrinous pneumonia. The alveoli were filled with edematous fluid mixed with fibrinous exudate, numerous alveolar macrophages, mononuclear cells along with thickened interalveolar septa and presence of intranuclear eosinophilic inclusion bodies. One-Step RT-PCR using NP3 and NP4 primers confirmed a PPR virus of 352 bp size in spleen, lungs and mesenteric and brachial lymph node samples. It was concluded that morbidity and mortality due to PPR were significantly higher in indigenous breeds of sheep and goat as compared to imported sheep and goat breeds. PPR has rendered various lesions in GI and respiratory tract which are characteristic in nature for the diagnosis of the disease under field condition.

Immuno-pathologic effects of oral administration of chlorpyrifos in broiler chicks.

This study sought to assess if chlorpyrifos (CPF) induced immunotoxic effects in orally-treated day-old broiler chicks. Groups of chicks received per os CPF diluted in xylene at 5, 10, and 20 mg/kg body weight (CPF-5, CPF-10, and CPF-20) orally daily for 15 days. Xylene and control groups received xylene alone (1 ml/kg BW) and physiological saline, respectively. At various times during/after the exposure regimens, different immune end-points were analyzed in the birds. Humoral immunity was examined by assessing antibody responses to sheep red blood cells. Cell-mediated immunity was measured via lymphoproliferative responses to avian tuberculin. Leukocyte phagocytic ability was measured using a carbon clearance assay. Results showed that CPF administered to broiler chicks caused a dose-dependent decrease in humoral immunity, cell-mediated immunity, and phagocytic activity. Dose- and time-related pathological changes were observed in bursa of Fabricius, spleen, and thymus in treated birds. These changes were mild, moderate, and severe, respectively, in the 5, 10, and 20 mg/kg CPF groups. The Bursa of Fabricius in treated birds showed increased inter-follicular connective tissue proliferation, severe moderate cytoplasmic vacuolation, edema, and degenerative changes such as pyknosis and fragmentation of nuclei that depleted the follicles of lymphoid cells. In the spleen, disorganization of follicular patterns, severe congestion, cytoplasmic vacuolation, degenerative changes, and hyperplasia of reticular cells were noted. The thymus in treated birds exhibited congestion, hyper-cellularity, and a presence of immature monocytes in the medullary region, as well as myoid cell necrosis. Taken together, these studies clearly demonstrated that chlorpyrifos could induce immunotoxicities in broiler birds.

Toxicological effects of diclofenac in four avian species.

The objective of the present study was to investigate the toxico-pathological effects of diclofenac in different avian species including broiler chicks (Gallus gallus, 15 days old), pigeons (Columba livia, 3 months old), Japanese quail (Coturnix japonica, 4 weeks old) and mynah (Acridotheres tristis, independent young). For each species, five groups each containing 10 birds were maintained and administered diclofenac sodium orally at dose rates of 0, 0.25, 2.5, 10 and 20 mg/kg body weight, respectively, for seven consecutive days. Clinical signs in all species included depression, somnolence, decreased body weight and mortality. Severity of clinical disease increased in a dose-related manner and was most severe in broiler chicks, followed by pigeons, Japanese quail, and was least severe in mynah. Serum creatinine levels were elevated in all species. Serum urea levels varied non-significantly in broiler birds, significantly decreased in pigeons and significantly elevated in Japanese quail and mynah. Broiler chicks and pigeons administered 10 and 20 mg diclofenac/kg had visceral gout; however, this was not observed in Japanese quail and mynah. The kidneys and liver were enlarged in all species. Histologically, the kidneys of all species showed acute renal necrosis and the livers had fatty change and necrosis of hepatocytes. The kidneys and liver of broiler chicks and pigeons given 10 and 20 mg/kg diclofenac also exhibited uric acid crystal aggregates (tophi) and associated lesions in the parenchyma.