Emphysematous gastritis due to Sarcina ventriculi infection in a diabetic liver-kidney transplant recipient.

Emphysematous gastritis (EG) is a rare and potentially lethal process caused by invasive, gas-producing bacteria leading to inflammation and gas dissection of the stomach. The most common etiologic agents are Clostridium infections, but other organisms, including enterobacteria, staphylococcus, and fungi have also been identified. We report the first case of EG due to Sarcina ventriculi in a solid organ transplant recipient, who presented with epigastric pain and vomiting. The patient had a history of type 1 diabetes mellitus (DM) with recurrent episodes of ketoacidosis and systemic diabetic complications, including severe gastroparesis. CT scan studies demonstrated EG with venous air, and endoscopy showed severe gastritis and ulcerations. In the gastric biopsies, abundant Sarcina ventriculi were noted in areas of mucosal/submucosal necrosis. Antibiotic treatment was instituted at admission, and subsequent endoscopy demonstrated the disappearance of Sarcina, with some improvement of the gastric inflammation; however, the patient developed septic shock with multiorgan failure and expired. This case highlights the need to consider other infectious etiologies in transplant patients, in addition to the well-known opportunistic infections.

Emphysematous gastritis due to Sarcina ventriculi infection in a diabetic liver-kidney transplant recipient

Emphysematous gastritis (EG) is a rare and potentially lethal process caused by invasive, gas-producing bacteria leading to inflammation and gas dissection of the stomach. The most common etiologic agents are Clostridium infections, but other organisms, including enterobacteria, staphylococcus, and fungi have also been identified. We report the first case of EG due to Sarcina ventriculi in a solid organ transplant recipient, who presented with epigastric pain and vomiting. The patient had a history of type 1 diabetes mellitus (DM) with recurrent episodes of ketoacidosis and systemic diabetic complications, including severe gastroparesis. CT scan studies demonstrated EG with venous air, and endoscopy showed severe gastritis and ulcerations. In the gastric biopsies, abundant Sarcina ventriculi were noted in areas of mucosal/submucosal necrosis. Antibiotic treatment was instituted at admission, and subsequent endoscopy demonstrated the disappearance of Sarcina, with some improvement of the gastric inflammation; however, the patient developed septic shock with multiorgan failure and expired. This case highlights the need to consider other infectious etiologies in transplant patients, in addition to the well-known opportunistic infections.

Graft dysfunction in simultaneous pancreas kidney transplantation (SPK): Results of concurrent kidney and pancreas allograft biopsies.

Simultaneous pancreas and kidney transplants offer significant therapeutic advantages but present a diagnostic approach dilemma in the diagnosis of rejection. Because both organs are from the same donor, the kidney has been treated traditionally as the "sentinel" organ to biopsy, presumably representing the status of both allografts. Truly concurrent biopsy studies, however, are needed to confirm this hypothesis. We examined 101 concurrent biopsies from 70 patients with dysfunction in either or both organs. Results showed concurrent rejection in 23 of 57 (40%) of cases with rejection; 19 of 57 (33.5%) and 15 of 57 (26.5%) showed kidney or pancreas only rejection, respectively. The degree and type of rejection differed in the majority (13 of 23, 56.5%) of cases with concurrent rejection, with the pancreas more often showing higher rejection grade. Taking into account pancreas dysfunction, a positive kidney biopsy should correctly predict pancreas rejection in 86% of the instances. However, the lack of complete concordance between the 2 organs, the discrepancies in grade and type of rejection, and the tendency for higher rejection grades in concurrent or pancreas only rejections, all support the rationale for pancreas biopsies. The latter provide additional data on the overall status of the organ, as well as information on nonrejection-related pathologies.

Histopathological analysis and demonstration of EBV and HIV p-24 antigen but not CMV expression in labial minor salivary glands of HIV patients affected by diffuse infiltrative lymphocytosis syndrome.

BACKGROUND: The diffuse infiltrative lymphocytosis syndrome (DILS) in HIV patients is characterized by the persistence of CD8-circulating lymphocytes and lymphocytic infiltration, predominantly in salivary glands. METHODS: We examined seven HIV-positive patients with bilateral parotid enlargement and sicca symptoms. Minor labial salivary gland biopsies were performed in all patients and submitted for histopathological analysis and immunohistochemistry for CD4, CD8, cytomegalovirus (CMV), LMP-EBV protein, and HIV p-24 protein. RESULTS: In all cases, lymphocytic infiltration of the minor salivary glands, mainly periductal, was found. Acinar atrophy, ductal ectasia, and mild to moderate fibrosis were also observed. We noticed strong immunohistochemical reaction for LMP-EBV and p-24 proteins in ductal cells in all cases, while staining for CMV was consistently negative. The lymphocytes were positive for CD8, but consistently negative for CD4. CONCLUSIONS: A role of Epstein-Barr virus (EBV) and HIV, but not CMV, in the pathogenesis of DILS, is suggested by our immunohistochemical findings.