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Adenoid hypertrophy is common in children. Size of the adenoid increases up to the age of 6 years, then slowly atrophies and completely disappears at the age of 16 years. Adenoid hypertrophy in adults is rare. Present study shows that adenoid hypertrophy is now increasing in adults because of various causes. Study has been conducted in the Department of ENT and Head & Neck Surgery, Alluri Sitarama Raju Academy of Medical science, Eluru, Andhra Pradesh, India. Study shows that incidence of adenoid hypertrophy is increasing as the cause of nasal obstruction in adults. This study identified the different causes of adenoid hypertrophy in adult patients. The common causes of adenoid hypertrophy in adults are chronic infection and allergy. Pollution and smoking are also important predisposing factors. Sometimes it is also associated with sinonasal malignancy, lymphoma and HIV infection. Study shows that 21 % of adult nasal obstruction is due to adenoid hypertrophy. But in case of the patient with chronic tonsillitis only 9 % were associated with adenoid hypertrophy. Males are more commonly involved (70 %) then female, may be because of out door activities and more commonly exposed to pollutants. And most commonly involved age group is 16-25 years (60 %). Majority of the cases with adenoid hypertrophy are associated with infection and allergy i.e. descending infection in 33.3 % cases, ascending infection in 20 % cases and allergic rhinitis in 30 % cases. Association of malignant sinonasal tumors, non Hodgkin's lymphoma and HIV infections are rare i.e. 3.3 % each. So any cases of adult adenoid hypertrophy should be treated seriously to exclude the dangerous causes.

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The present study reports the clinico-pathologic changes observed in spontaneous hepatic coccidiosis caused by Eimeria stiedae in rabbits at Bannerghatta Biological Park (BBP) in Karnataka state of India. The clinical signs observed in the affected rabbits included sudden death, stunted growth, anorexia, weight loss, diarrhoea and abdominal pain. Increased liver enzymes and bilirubin was noticed upon biochemical examination. At necropsy, lesions included grossly enlarged liver (hepatomegaly) with presence of discrete yellowish-white nodules ranging from 1mm to 5mm size throughout the parenchyma containing a thick creamy white fluid. Faecal sample examination demonstrated the presence of Eimeria oocyts. The impression smears from the liver and intestinal mucosa also showed Eimeria oocysts, degenerative changes, necrotic cells and mononuclear cell aggregation to form oocyst granuloma. Histological observation revealed distension of bile duct, hyperplasia of epithelium along with numerous coccidian oocysts at the centre. Granulomatous tissues were observed to have encircled the bile duct with infiltration of inflammatory cells. Microscopic examination of exudates from liver also revealed numerous oocysts of E. stiedae. Multiple areas of coagulative necrosis of hepatic cells surrounded with inflammatory cells were also found.