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A study was conducted to examine the clinical signs, hematological, biochemical and histopathological changes in vitamin D3 toxicity at a dose rate 2 mg/kg b.wt. of vitamin D3 and to assess the protective effect of Aloe vera in vitamin D3 toxicity. The clinical signs observed were anorexia, progressive weight loss, difficulty in movement and respiration, diarrhea, epistaxis, subnormal body temperature and nervous signs before death. Mortality was observed in treated rats between day 10 and day 19 of treatment. The gross postmortem changes observed were severe emaciation, white chalky deposits on epicardial surface of heart, pin point white deposits on cortical surface of kidneys with pale yellow discoloration and diffused white deposits on serosal surface of stomach and intestine with bloody ingesta in lumen. The hematological changes included non-significant increase in hemoglobin and total leukocyte count and significant increase in relative neutrophil count. The biochemical changes observed were significant increase in plasma concentration of calcium, phosphorus and blood urea nitrogen, whereas a significant decrease in the concentration of albumin and total plasma protein was observed. The histopathological lesions included calcification of various organs, viz., tongue, stomach, intestines, kidney, heart, aorta, larynx, trachea, lungs, spleen, choroid plexus arteries of brain and vas deferens. The Aloe vera juice (2.5% in drinking water) has no protective effect on vitamin D3 toxicity (2 mg/kg b.wt.).

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Avian Infectious coryza, a highly opportunistic respiratory tract infection caused by Avibacterium paragallinarum is now believed to be evolving as a re-emerging disease of poultry birds. Albeit adoption of strong precautionary/prophylactic measures i.e. vaccine/vaccination practice, the infection continues as complicated pattern of disease course worldwide that results in massive economic and production losses. India, being a major admirer of poultry products suffers tremendously with this insidious infectious insult every year, thus strives for some better optional measures to curtail this curse. This review article blazons some significant development(s) that took place over the period of last decade with regards to its epidemiologic spectrum, characterization of its etiologic agent and important improvement(s)/advancement(s) in its diagnostic as well as prophylactic approach (es). Although, the major achievements to identify and restrict this disease has been carried out in early 80s and 90s, however precarious nature of this organism has largely left scientific and farming community abstruse over its ambit on host specificity and geographic limitation(s). Following strong vaccinal/prophylactic measures, the causative organism(s) further acquired superlative advantages having bypassing host immune surveillance mechanisms acquired through existing vaccine components, besides violating constitutive immunity of host. The plausible reason behind such immunity exclusion is hitherto unknown, when it comes to host's response against pathogen. Resultantly, a detailed study to this effect is highly warranted to avoid further sinister in our poultry operation(s) due to Avibacterium paragallinarum infection. Most of the recent studies endeavoured to work on serovar B of Avibacterium paragallinarum organism which is quite prevalent at the moment at varied places across the globe. This warrants concerted/dedicated diagnostic techniques employing high end bio-molecular approaches for better comprehension of the disease, and to have a blue print with regard to adoption of newer therapeutic strategy towards containment of the infection for fruitful future.

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Lindane is very commonly used organochlorine pesticide and has been reported to cause several toxic effects including respiratory insufficiency. However, effects of low concentration of lindane alone or in combination with microbial molecules on lungs are not fully understood. To understand the effects a preliminary study was designed on Swiss albino mouse. Male mice were divided into treatment and control group (20; each). Treatment mice were given lindane in ground nut oil orally at 0.25 mg kg−1 day−1 for 60 days. After treatment, 10 mice were challenged with intranasal Escherichia coli lipopolysaccharide (LPS; 80 μg per mice) and remaining 10 with normal saline. The mice were euthanized 16 h post-LPS exposure. Control mice (10 each) were given normal saline or the LPS alone. Mice exposed with lindane and in combination with LPS had increase in total cell counts and leukocyte counts in broncho-alveolar lavage. Histological examination showed lung injury in the lindane-treated mice. The histopathological changes were more pronounced in lindane along with LPS-exposed mice. Lindane alone and in combination with LPS showed expression of immunopositive Toll-like receptor (TLR)-4 and tumour necrosis factor-alpha (TNF-α) positive reaction in various cells of lungs. While LPS induced acute inflammation in the lungs, combination of lindane and LPS exacerbated histological signs of the inflammation. The data indicate that lindane alone or in combination with LPS caused changes in lung morphology and altered TLR-4 and TNF-α expression which may have led to altered response to LPS challenge.