scholarly journals S3109 Gastric Mucosal Necrosis Due to Mucormycosis in COVID-19 Patient

2021 ◽  
Vol 116 (1) ◽  
pp. S1283-S1284
Author(s):  
Ahmad S. Musmar ◽  
Shaden Almomani ◽  
Laith Al Momani
Keyword(s):  
2017 ◽  
Vol 26 (8) ◽  
pp. 2491-2492
Author(s):  
Caroline de Bataille ◽  
Vincent Sibaud ◽  
Angélique Prioul ◽  
Anne Laprie ◽  
Emmanuelle Vigarios

2001 ◽  
Vol 15 (5) ◽  
pp. 327-331 ◽  
Author(s):  
Isam Alobid ◽  
Manuel Bernal ◽  
Carlos Calvo ◽  
Isabel Vilaseca ◽  
Juan Berenguer ◽  
...  

Rhinocerebral mucormycosis (RCM) is an aggressive fungal infection with a high mortality rate. It frequently develops in patients with uncontrolled diabetes mellitus or immunocompromised patients. RCM typically presents in a rapidly fulminant manner with headache, fever, mucosal necrosis, and ophthalmic symptoms. Although the definitive diagnosis is achieved by histopathological examination, computed tomography (CT) scanning and magnetic resonance (MR) are the best imaging procedures in early diagnosis to assess the extent of the disease.


2000 ◽  
Vol 36 (4) ◽  
pp. 317-321 ◽  
Author(s):  
TL Gieger ◽  
SS Correa ◽  
J Taboada ◽  
AM Grooters ◽  
AJ Johnson

Three adult dogs were evaluated following oral administration of phenol by the owner. All three dogs experienced severe oral and gastric ulceration. Hematological abnormalities included neutropenia with the presence of toxic neutrophils, thrombocytopenia, and increased muscle enzymes. Endoscopic examination was performed, and biopsies yielded a diagnosis of gastric mucosal necrosis in two of the dogs. Following supportive care, the dogs recovered completely. Phenol is a caustic, highly poisonous derivative of coal tar. The dogs of this report were poisoned inadvertently by their owner who received misinformation concerning the use of this chemical via the Internet.


2018 ◽  
Vol 48 (9) ◽  
Author(s):  
Humberto Binsfeld Bonadiman ◽  
Claiton Ismael Schwertz ◽  
Susy Hermes de Sousa ◽  
Ronaldo Michel Bianchi ◽  
Rafaela Albuquerque Caprioli ◽  
...  

ABSTRACT: The objective of this paper is to report the epidemiological, clinical, and pathological aspects of a case of rumenitis due to the ingestion of soybean oil in a bovine. The ox had access to barrels that stored soybean oil and ingested an indeterminate amount of the product. After consuming it, the animal presented hiporexia; liquid, brownish, and greasy feces; severe dehydration (12%); apathy; sternal recumbency; and death with a clinical evolution of 4 days. At necropsy, the rumen was filled with voluminous food and moderate amount of white-gray liquid with a greasy appearance. Upon microscopic examination, hydropic degeneration of the epithelium and areas of mucosal necrosis were observed in the rumen and reticulum. From these findings, we concluded that the bovine developed a state of acidosis and acute rumenitis due to excessive intake of lipids.


Author(s):  
Akira JINGU ◽  
Tomonobu SUZUKI ◽  
Tomoharu ISHIYAMA ◽  
Hidekazu MATSUMOTO ◽  
Takasi YAMAMOTO ◽  
...  

1979 ◽  
Vol 16 (4) ◽  
pp. 450-465 ◽  
Author(s):  
B. P. Wilcock ◽  
H. J. Olander

Swine dysentery was induced in pigs and in ligated colonic segments by inoculation of pure cultures of, or colonic contents containing, Treponema hyodysenteriae. The mildest changes, best seen in ligated segments 48 or 72 hours after inoculation, were congestion and leucocytic margination in mucosal capillaries and depletion of mucigen from goblet cells lining the base of the crypts of Lieberkühn. Superficial mucosal necrosis and crypt cell hyperplasia were later changes. Perfusion studies with India ink did not demonstrate occlusive mucosal ischemia in acute swine dysentery. Mucosa with lesions of swine dysentery contained at least 105 colony forming units of T. hyodysenteriae per gram. Mucosa without lesions had 105 or fewer T. hyodysenteriae per gram. Segments with acute swine dysentery were distended with clear mucoid fluid with electrolyte composition indicative of net colonic secretion. No increase in the concentration of volatile fatty acids was detected in content from intact colons or colonic segments with lesions of acute swine dysentery.


2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
N. Ananthakrishnan ◽  
G. Parthasarathy ◽  
Vikram Kate

Introduction. The spectrum of gastric injury due to corrosives can vary. This paper presents a single center experience of over 30 years of corrosive gastric injuries of 39 patients with acute gastric injuries from 1977 till 2006. Patients and Methods. Two thirds of the patients in the acute injury group had a concomitant esophageal injury. The age of the patients ranged from 4 years to 65 years with a slight preponderance of males. (M : F ratio 22 : 17). Results. 36 out of 39 acute gastric injuries were due to ingestion of acids. Three patients had history of caustic soda ingestion. Oral hyperemia or ulcers of varying extent were seen in all patients. The stomach showed hyperemia in 10, extensive ulcers in 13, and mucosal necrosis in 10 patients. Fifteen patients (15/39, 38.5%) were managed conservatively. Twenty four patients (24/39, 61.5%) underwent laparotomy: one for frank peritonitis, 10 for gastric mucosal necrosis, and 13 others for extensive gastric ulcerations. Overall the mortality rate was 29.6 %. Conclusion. Although the mortality and morbidity of acute corrosive gastric injuries is high, the key to improve the survival is early identification of perforation, maintenance of nutrition and control of sepsis.


2012 ◽  
Vol 5 ◽  
pp. IDRT.S9818 ◽  
Author(s):  
Patorn Piromchai ◽  
Sanguansak Thanaviratananich

Introduction Invasive fungal rhinosinusitis is a challenging condition that can be found mostly in immunocompromised patients. Failure to diagnose and treat this entity promptly usually results in rapid progression and death. The purpose of this study was to determine clinical presentation, complication and morbidity in patients with acute versus chronic invasive fungal rhinosinusitis. Setting and design Case-control study at Srinagarind Hospital, Khon Kaen University between January 1998 and May 2008. Methods The patient's data with the diagnosis of invasive fungal rhinosinusitis was included. Demographic data, underlying diseases, presenting symptoms, histologic sinonasal tissue evaluations, sinonasal tissue cultures, CT scan findings, surgical interventions, morbidity, and mortality were collected. Results Sixty-five patients were diagnosed as invasive fungal rhinosinusitis between January 1998 and May 2008. The data of six patients were unable to obtain. Fifty-nine patients were included in this study. Patients with immunocompromised status have significant greater risk for acute than chronic IFS, OR = 6.5 ( P = 0.004). Patients with mucosal necrosis have the significant higher risk for acute IFS, OR = 5.5 ( P = 0.01). There was no significant difference in orbital complications proportion between acute and chronic invasive fungal rhinosinusitis, OR = 2.42 ( P = 0.15). Sinus wall erosion have found significantly in chronic IFS group, OR = 0.24 ( P = 0.02). The average hospital stayed was 30.58 ± 26.43 days with no difference between groups ( P = 0.50). Fourteen patients in acute IFS group were dead (31.11%) while all patients in chronic IFS group were survived. Conclusions Invasive fungal rhinosinusitis continues to present a challenge to the otolaryngologist. Acute IFS was found most commonly in immunocompromised patients. The most consistent finding of acute IFS was mucosal necrosis and black crust/debris. The CT finding of sinus wall erosion may help in diagnosis of chronic IFS.


2010 ◽  
Vol 78 (7) ◽  
pp. 2966-2973 ◽  
Author(s):  
Corinne Gurtner ◽  
Francesca Popescu ◽  
Marianne Wyder ◽  
Esther Sutter ◽  
Friederike Zeeh ◽  
...  

ABSTRACT Clostridium perfringens type C isolates cause fatal, segmental necro-hemorrhagic enteritis in animals and humans. Typically, acute intestinal lesions result from extensive mucosal necrosis and hemorrhage in the proximal jejunum. These lesions are frequently accompanied by microvascular thrombosis in affected intestinal segments. In previous studies we demonstrated that there is endothelial localization of C. perfringens type C β-toxin (CPB) in acute lesions of necrotizing enteritis. This led us to hypothesize that CPB contributes to vascular necrosis by directly damaging endothelial cells. By performing additional immunohistochemical studies using spontaneously diseased piglets, we confirmed that CPB binds to the endothelial lining of vessels showing early signs of thrombosis. To investigate whether CPB can disrupt the endothelium, we exposed primary porcine aortic endothelial cells to C. perfringens type C culture supernatants and recombinant CPB. Both treatments rapidly induced disruption of the actin cytoskeleton, cell border retraction, and cell shrinkage, leading to destruction of the endothelial monolayer in vitro. These effects were followed by cell death. Cytopathic and cytotoxic effects were inhibited by neutralization of CPB. Taken together, our results suggest that CPB-induced disruption of endothelial cells may contribute to the pathogenesis of C. perfringens type C enteritis.


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