In an unusual nosocomial outbreak, 13 staff and 11 patients in an acute and chronic health care facility were infected with the zoophilic dermatophyte, Microsporum canis. The dermatophyte was apparently introduced into the facility by a single infected patient. Likely modes of subsequent disease transmission include person-to-person contact, handling of contaminated laundry, and use of a shared razor. Infection control measures for managing such outbreaks are discussed.
SUMMARYA 53-year-old man developed a widespread erythematous eruption which rapidly evolved into fluidfilled bulla mostly involving the distal areas of all four limbs and erosions on the oral as well as anogenital mucosa. Based on clinical presentation, chronology of drug exposure, past events and histopathology as diagnosis of widespread bullous fixed drug eruption was made over Steven Johnson-toxic epidermal necrolysis syndrome. Steroids were deferred and the lesions healed with minimal pigmentation within a week. Differentiating between the two entities has been historically difficult, and yet can have significant therapeutic and prognostic implications. BACKGROUND
A 35-year-old male presented to us with oedema discoloration of eyes and urine, gradually progressive lower limb oedema and abdominal distension since a month. On examination, vital signs were within normal limits but pallor, icterus, clubbing and bilateral pitting pedal oedema were noted. Systemic examination revealed an enlarged liver, up to 4cm below the lower costal margin and signs of ascites. There was no personal or family history of previous blood transfusions, joint pains or recurrent jaundice. There was no history of alcohol intake.Laboratory investigations [Table/ Fig-1] were suggestive of severe anaemia (hemoglobin 4.3 gm/dl; normal range 14-17 gm/dL). Increased reticulocyte count (16.5 %), lactate dehydrogenase (1562 U/L; normal range 225-450 U/L) and hyper bilirubinemia pointing to a hemolytic aetiology. Multiple drepnocytes (sickle cells) were noted on peripheral smear. A hemoglobin electrophoresis study showed a broad abnormal band (89.2%) corresponding to Hemoglobin S, suggestive of sickle cell anaemia. Other investigations suggestive of chronic liver disease included thrombocytopenia (85,000 normal range 150000-450000) elevated Aspartate Transaminase (92 U/L; normal range <49 U/L), alkaline phosphatase (211 U/L: normal range 28-111 U/L), hypoalbuminemia (2.2gm/dl; normal range 3.6-4.4 gm/dl) and an elevated prothrombin time (test 25 seconds, control 15 seconds INR 1.75; normal range <1.2). Ultrasound of the abdomen showed hepatomegaly (166mm) with an altered echopattern suggestive of cirrhosis. The gall bladder showed thickened oedematous walls with hypo echoic sludge within. Portal vein dilation (15.6 mm) was reported however, splenomegaly was not seen. Free fluid in the peritoneal cavity was also noted which on analysis revealed a SAAG of 1.8 supporting portal hypertension. Upper endoscopy revealed grade 2 non bleeding varices. Other investigations including renal function test, an electrocardiogram and an echocardiogram revealed no abnormalities. Viral markers for chronic hepatitis B and C were negative and serum ferritin was normal. Considering the risk of bleeding a liver biopsy was decided against.The patient was treated with folic supplementation and transfused. A regimen of salt restriction, spironolactone and beta-blockers was begun for his ascites and liver disease and a considerable clinical improvement with reduction in bodyweight and oedema was noted on follow up six months after presentation. Pneumococcal vaccination and hydroxyurea were also administered following hematological consult. Green et al., first described the aetiology of liver disease in sickle cell patients. His autopsy records on several patients showed hyperplasia of Kupffer cells, sinusoidal dilatation and erythrophagocytosis, which resulted in hypoxia, necrosis and cirrhosis at a later stage [3]. Various aetiologies for cirrhosis in SCD include (1) hypoxic injury due to sickling (2) viral hepatitis due to repeated transfusions (3) gallstones due to hemolysis (4) iron overload due to repeated transfusions and abse...
Introduction: Obesity is associated with metabolic syndrome. Obesity is a leading preventable cause of death worldwide, with increasing rates in adults and children. Obesity is associated with vitamin D insufficiency and hyperparathyroidism, secondary hypercalcemia. The purpose of this study is to test effect of obesity on Vitamin D and calcium level. Methods: The present study investigated effect of obesity on Vitamin D and calcium level. We studied 150 Subjects with no pre-existing disease and not taking any nutritional suppliments for vitamin D. At a baseline they were asked about their family history of obesity. Subjects are investigated for 25-hydroxyvitamin D [25(OH) D] and serum Total calcium level to study effect of obesity on vitamin D and calcium status. Results: Out of 150 subjects included in the study, 107 had obesity and 43 subjects was non-obese. The Body Mass Index less than 30 is taken as cut off point for defining obesity. The mean value of 25-hydroxyvitamin D was 13ng/ml in the group of obese people and the same was 28ng/ml in the group of non-obese individuals. This change was statistically significant (p<0.05). The mean value of serum Total calcium level was 13mg/dl in the group of obese people and the same was 10mg/dl in the group of non-obese individuals. This change was statistically significant (p<0.05). Conclusions: It is concluded that obese individuals are increased risk of developing Vitamin D Deficiency and secondary hypercalcemia.
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