Hemorrhagic bowel syndrome in dairy cattle: Gross, histological, and microbiological characterization.

Hemorrhagic bowel syndrome (HBS) is a sporadic and fatal disease of predominantly lactating dairy cattle, characterized by segmental hemorrhage and luminal clot formation in the small intestine. Although, Clostridium perfringens and Aspergillus fumigatus have been associated with HBS, the pathogenesis and cause are currently unknown. In this study, 18 naturally occurring cases of HBS (7 necropsied immediately following euthanasia, 11 with 12-48 hour postmortem intervals) were investigated to characterize the pathology and the intestinal microbiome. Hemorrhagic bowel syndrome was characterized by a single small-intestinal, intramucosal hematoma with dissection of the lamina muscularis mucosae. In most cases necropsied immediately after euthanasia (4/7), the intestinal mucosa proximal to the hematoma contained 9 to 14, dispersed, solitary or clustered, erosions or lacerations measuring 4 to 45 mm. In 77% (37/48) of these mucosal lesions, microscopic splitting of the lamina muscularis mucosae comparable to the hematoma was present. These findings suggest the intramucosal hematoma to originate from small mucosal erosions through dissecting hemorrhage within the lamina muscularis mucosae. No invasive fungal growth was observed in any tissue. Bacteriological cultivation and nanopore sequencing showed a polymicrobial population at the hematoma and unaffected intestine, with mostly mild presence of C perfringens at selective culture. Gross and microscopic lesions, as well as the culture and sequencing results, were not in support of involvement of C perfringens or A fumigatus in the pathogenesis of HBS.

Bloody Diarrhea and Shiga Toxin-Producing Escherichia coli Hemolytic Uremic Syndrome in Children: Data from the ItalKid-HUS Network.

OBJECTIVE: To analyze the results of an enhanced laboratory-surveillance protocol for bloody diarrhea aimed at identifying children with Shiga toxin-producing Escherichia coli (STEC) infection early in the course of the disease toward the early identification and management of patients with hemolytic uremic syndrome (HUS). STUDY DESIGN: The study (2010-2019) involved a referral population of 2.3 million children. Stool samples of patients with bloody diarrhea were screened for Shiga toxin (Stx) genes. Positive patients were rehydrated and monitored for hemoglobinuria until diarrhea resolved or STEC-HUS was diagnosed. RESULTS: A total of 4767 children were screened; 214 (4.5%) were positive for either Stx1 (29.0%) or Stx2 (45.3%) or both Stx1+2 (25.7%); 34 patients (15.9%) developed STEC-HUS (0.71% of bloody diarrheas). Hemoglobinuria was present in all patients with HUS. Patients with Stx2 alone showed a greater risk of STEC-HUS (23.7% vs 12.7%) and none of the patients with Stx1 alone developed HUS. During the same period of time, 95 other patients were diagnosed STEC-HUS but were not captured by the screening program (26 had nonbloody diarrhea, 11 came from areas not covered by the screening program, and 58 had not been referred to the screening program, although they did meet the inclusion criteria). At HUS presentation, serum creatinine of patients identified by screening was significantly lower compared with that of the remaining patients (median 0.9 vs 1.51 mg/dL). CONCLUSIONS: Nearly 1% of children with bloody diarrhea developed STEC-HUS, and its diagnosis was anticipated by the screening program for Stx. The screening of bloody diarrhea for Stx is recommended, and monitoring patients carrying Stx2 with urine dipstick for hemoglobinuria is suggested to identify the renal complication as early as possible.

Gastrointestinal manifestations of Talaromyces marneffei infection in an HIV-infected patient rapidly verified by metagenomic next-generation sequencing: a case report.

BACKGROUND: The manifestation of Talaromyces marneffei infection in some HIV-infected patients may be atypical. Cases with gastrointestinal involvement have rarely been reported. It is hard to make a diagnosis when patients are lacking the characteristic rash and positive blood culture. CASE PRESENTATION: Here, we described a patient living with HIV who complained of fever and abdominal pain, and was rapidly diagnosed with Talaromyces marneffei infection by metagenomic next-generation sequencing (mNGS) using formalin-fixation and paraffin-embedded (FFPE) samples of omentum majus tissue. We also reviewed reported related cases. CONCLUSIONS: Talaromyces marneffei is an unusual cause of clinical presentations involving obvious abdominal pain and lower gastrointestinal bleeding, but can be included in the differential diagnosis. As an important diagnostic tool, the significance of mNGS using FFPE samples of lesions provides a more targeted diagnosis.

Pilot Study Indicates Helicobacter pylori Infection May Induce Small Intestinal Mucosal Injury.

BACKGROUND AND AIM: Helicobacter pylori infection is a primary cause of gastroduodenal ulcers. To investigate whether there is an association between H. pylori infection and small intestinal mucosal injury. METHODS: Patients were selected from a general pool of subjects who underwent capsule endoscopy for current or past obscure gastrointestinal bleeding. Characteristics including age, gender, history, treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) and/or acid suppressant, diagnosis, and H. pylori infection were investigated. Patients infected with H. pylori had positive test result, ranging 30 days before to 30 days after capsule endoscopy. Patients diagnosed with inflammatory diseases, malignant tumors, etc. were excluded. All video images were re-evaluated to count small intestinal mucosal breaks. Eligible patient variables were compared. RESULTS: A total of 92 patients (30 infected with H. pylori/62 uninfected) were eligible. By univariate analysis of the number of mucosal breaks, patients treated with NSAIDs were found to have more mucosal breaks than patients untreated (38%: 8/21 vs. 18%: 13/71; p = 0.004), and the possible association was detected between patients infected with H. pylori and those who were not (67%: 14/21 vs. 37%: 26/71; p = 0.081). When comparing the H. pylori infected and uninfected patients, the rate of patients with mucosal breaks was greater in infected patients (47%: 14/30 vs. 11%: 7/62; p = 0.001). After excluding patients treated with NSAIDs, the number of mucosal breaks was also greater in patients infected with H. pylori (1.2 ± 1.5 vs. 0.38 ± 0.62; p = 0.001). CONCLUSION: There is a possibility that H. pylori infection induces small intestinal mucosal injury.

Massive Lower Gastrointestinal Bleeding Due to Fulminant Necrotizing Amebic Colitis: A Diagnostic and Therapeutic Challenge.

Acute fulminant necrotizing amebic colitis rarely presents with massive lifethreatening lower gastrointestinal bleeding without diarrhea. Diagnosis is difficult as colonoscopy is suboptimal due to active bleeding, stool testing is often negative and a positive serology cannot confirm the diagnosis. We herein report a case of a 39-year-old male who presented with profuse bleeding per rectum, without associated significant antecedent history of fever or diarrhea. Colonoscopy was inconclusive as active bleeding obscured the vision. Computed tomography of abdomen revealed non-specific thickening of the caecum. Emergency laparotomy with right hemicolectomy and temporary ileostomy was performed. Microscopic examination of colonic mucosa revealed Entamoeba histolytica trophozoites with erythrophagocytosis suggestive of fulminant amebic colitis. Intravenous metronidazole was given subsequently and patient recovered completely. Ileocolonic anastomosis was done after closing the ileostomy three months later. This case highlights this exceedingly rare presentation of fulminant amebic colitis which poses a diagnostic challenge and can be life threatening without early surgical intervention.

Black esophagus: a case report.

INTRODUCTION: Acute esophageal necrosis, also known as black esophagus, is a rare digestive complication, frequently manifested by an upper gastrointestinal hemorrhage and occurs in patients with comorbidities. AIM: To report the case of a patient with a black esophagus revealed by an upper gastrointestinal hemorrhage. OBSERVATION: A 72-year-old patient with a history of diabetes mellitus, hypertension and ischemic heart disease was hospitalized in surgical intensive care unit for hemorrhagic shock induced by cholecystectomy. On the 7th postoperative day, the patient developed acute hematemesis. Gastroscopy showed circumferential necrosis, localized in the middle and lower third of the esophagus and stopped abruptly at the gastroesophageal junction. Gastric mucosa was strictly normal. The bulb and the first part of duodenum showed multiple superficial ulcers without signs of recent hemorrhage. The patient was placed on absolute diet and total parenteral nutrition associated with high-dose intravenous proton pump inhibitor. Second-look gastroscopy, performed six days later, showed a significant improvement in esophageal lesions. The evolution was marked by the occurrence of pneumonia complicated by septic shock which caused patient's death. CONCLUSION: Black esophagus is a rare pathology of multifactorial etiology. Treatment is based on proton pump inhibitors in combination with resuscitation measures to control comorbidities. Mortality remains high due to the seriousness of comorbid disease states often associated with this condition.

New clinical paradigms for treating and preventing antiplatelet gastrointestinal bleeding.

PURPOSE OF REVIEW: To quantify antiplatelet-related gastrointestinal bleeding (GIB), characterize patients at greatest risk and summarize risk-management strategies emphasizing evolving knowledge in acute management of antiplatelet-related bleeding. RECENT FINDINGS: New paradigms for acute management of antiplatelet-related GIB exist in the domains of resuscitation and the transfusion of blood products, strategic use of proton pump therapy and identification and eradication of Helicobacter pylori. This review will also highlight the importance of prompt resumption of cardiac aspirin and dual antiplatelet therapy following endoscopic hemostasis to minimize the risk of future cardiac events. SUMMARY: This review will provide pragmatic strategies for the management of acute antiplatelet-related GIB. Emerging areas of clinical knowledge will be addressed and knowledge gaps requiring further research to inform clinical practice will be highlighted.

[Gastrointestinal bleeding and acute hepatic failure by leptospirosis: an entity that should not be forgotten]. / Hemorragia digestiva e insuficiencia hepática aguda por leptospirosis: una entidad que no debemos olvidar.

Leptospirosis disease is caused by the spirochete Leptospira. It is a worldwide distribution zoonosis, with predominance in the tropics. In Spain, it is not frequent but some cases have been noticed especially in humid areas surrounded by rivers, lakes or ponds, such as Catalonia, Andalucia or the Valencian Community. It is transmitted by a variety of animals such as cows or rats, that are infected either by direct contact with these animals or their urine, or indirectly by consuming or being in contact with water contaminated by their urine. The clinical manifestations are very variable, being asymptomatic or not very symptomatic in most of the patients. Unusually, leptospirosis presents with a first phase with fever, myalgias, liver injury or different organs hemorrhage, followed by a second phase with the presence of jaundice due to hepatic failure. Weil's disease is a kind of severe leptospirosis characterized by hepatic failure with jaundice and acute renal failure, associated with high mortality rates.The diagnosis is based on serological techniques and DNA detection by PCR. The treatment consists of life support measures and antibiotic therapy. A patient with Weil's disease and leptospirosis digestive bleeding is presented, with a fulminant clinical course. In order to achieve an early diagnosis, the need to keep this entity in mind must be emphasized, especially in favorable epidemiological environments as the one of this patient.

Fecal microbiota transplantation for severe clostridium difficile infection after left ventricular assist device implantation: a case control study and concise review on the local and regional therapies.

BACKGROUND: We report herein a case of fecal microbiota transplantation (FMT) used for severe Clostridium difficile infection for a 65-year-old Lebanese man who underwent left ventricular assist device implantation. To the best of our knowledge this is the first case report from Lebanon and the region presenting such technique. CASE PRESENTATION: The patient experienced diarrhea and rectal bleeding and was diagnosed of pseudomembranous colitis (PMC). His condition failed to improve on maximal pharmacological therapy. Protocolectomy, an invasive operation consisting in resection of the entire colon and rectum seemed to be the last resort before the patient responded to FMT given through gastroscopy. CONCLUSION: Despite the increasing experience with FMT for C. difficile infection, published evidence in severe related cases from this region is very limited. Hence, we promote adjunctive FMT, an effective noninvasive method, to be considered as a promising early treatment option in severe C. difficile infection.

Clinical characteristics and outcomes of spontaneous bacterial peritonitis caused by Enterobacter species versus Escherichia coli: a matched case-control study.

BACKGROUND: Enterobacter species are important nosocomial pathogens, and there is growing concern about their ability to develop resistance during antimicrobial therapy. However, few data are available on the clinical characteristics and outcomes of Enterobacter spontaneous bacterial peritonitis (SBP). METHODS: We retrospectively identified all patients with SBP caused by Enterobacter species admitted to a tertiary care hospital between January 1997 and December 2013. Each case was age- and sex-matched with four patients with Escherichia coli SBP. RESULTS: A total of 32 cases with Enterobacter SBP and 128 controls with E. coli SBP were included. Twenty-one (65.6 %) cases and 111 (86.7 %) controls had Child-Pugh class C (P = 0.006). Cases were significantly more likely to have hepatocellular carcinoma (65.6 % vs. 37.5 %, P = 0.004) and upper gastrointestinal bleeding (28.1 % vs. 9.4 %, P = 0.005). The initial response to empirical therapy (81.3 % vs. 81.2 %, P = 0.995) and the 30-day mortality (37.5 % vs. 28.9 %, P = 0.35) were not significantly different between the groups. Drug resistance emerged in one case and in no controls (4.3 % [1/23] vs. 0 % [0/98], P = 0.19). CONCLUSIONS: Compared with E. coli SBP, patients with Enterobacter SBP more frequently had hepatocellular carcinoma and upper gastrointestinal bleeding, yet clinical outcomes were comparable. Development of resistance during third-generation cephalosporin therapy was infrequent in patients with Enterobacter SBP.

A case of multiple recurrence of Clostridium difficile infection with severe hematochezia in an immunocompromised host.

Clostridium difficile infection (CDI) is increasing in incidence and severity. Clinically, diarrhea frequently occurs, but severe hematochezia is rarely seen with CDI. We describe here a hematopoietic stem cell transplantation (HSCT) recipient who experienced life-threatening gastrointestinal bleeding due to severe CDI. Subsequent stool surveillance and molecular typing observed the patient who had two episodes of recurrence with a new strain of C. difficile distinct from the initial infection. We analyze C. difficile strains obtained from the patient, and also discuss the diagnosis and treatment of this case.

Pentaplex PCR assay for detection of hemorrhagic bacteria from stool samples.

Diarrheal diseases cause illness and death among children younger than 10 years in developing countries. Conventional testing for the detection of hemorrhagic bacteria takes 2 to 5 days to yield complete information on the organism and its antibiotic sensitivity pattern. Hence, in the present study, we developed a molecular-based diagnostic assay that identifies common hemorrhagic bacteria in stool samples. A set of specific primers were designed for the detection of Salmonella spp., Shigella spp., enterohemorrhagic Escherichia coli (EHEC), and Campylobacter spp., suitable for use in a one-tube PCR assay. The assay in the present study simultaneously detected five genes, namely, ompC for the Salmonella genus, virA for the Shigella genus, eaeA for EHEC, 16S rRNA for the Campylobacter genus, and hemA for an internal control. Specific primer pairs were successfully designed and simultaneously amplified the targeted genes. Validation with 20 Gram-negative and 17 Gram-positive strains yielded 100% specificity. The limit of detection of the multiplex PCR assay was 1 × 10(3) CFU at the bacterial cell level and 100 pg at the genomic DNA level. Further evaluation of the multiplex PCR with 223 bacterium-spiked stool specimens revealed 100% sensitivity and specificity. We conclude that the developed multiplex PCR assay was rapid, giving results within 4 h, which is essential for the identification of hemorrhagic bacteria, and it might be useful as an additional diagnostic tool whenever time is important in the diagnosis of hemorrhagic bacteria that cause diarrhea. In addition, the presence of an internal control in the multiplex PCR assay is important for excluding false-negative cases.

[Detection rate of Helicobacter pylori and its clinical significance in children with Meckel's diverticulum].

OBJECTIVE: To determine the detection rate of Helicobacter pylori (Hp) in children with Meckel's diverticulum (MD) and its clinical significance among children with MD. METHODS: Eighty-one children with MD were divided into two groups according to the presence (n=45) or absence (n=36) of digestive hemorrhage. The detection rates of Hp in MD tissues and stomach tissues were determined by immunohistochemistry. The detection rates of Hp were compared between the two groups and between the MD tissues with different clinical features in the hemorrhage group. RESULTS: The detection rate of Hp in MD tissues for the hemorrhage group was 76% (34/45), which was significantly higher than that for the non-hemorrhage group (47%, 17/36) (P<0.05). The detection rate of Hp in stomach tissues for the hemorrhage group (87%, 39/45) was insignificantly higher than that for the non-hemorrhage group (67%, 24/36) (P>0.05). Among patients in the bleeding group, the detection rate of Hp in MD tissues showed no relationship with age, sex, preoperative hemorrhage frequency, amount of hemorrhage, length of MD, basal diameter of MD, and pathological type (P>0.05), but was related to location of MD, presence or absence of ulcer, and depth of ulcer (P<0.05). For the hemorrhage group, a significant positive correlation was found between the detection rates of Hp in MD tissues and stomach tissues (P<0.05), as shown by the Spearman correlation analysis. CONCLUSIONS: The detection rate of Hp in MD tissues is increased in children with MD complicated by digestive hemorrhage. Hp infection may play some role in the hemorrhage process among children with MD.

Clinical and epidemiological peculiarities of hemorrhagic colitis complicated by hemolytic-uremic syndrome.

The aim of the research: identification of etiological structure of acute diarrheas and hemorrhagic colitis in Georgia, manifestation of clinical peculiarities and predictors of hemorrhagic colitis complicated by HUS ( Hemolytic-Uremic syndrome). In 2011-2013 we studied 274 hospitalized patients at the Center of Infectious Diseases, AIDS and Clinical Immunology (160 hemorrhagic colitis and 114 non-bloody diarrhea). Causative agents of hemorrhagic colitis (160 patients) were determined in 110 (69%) cases; etiology of the non-bloody diarrhea (114 patients) was established in 46 (40%) cases. Enteronterohaemorrhagic E. coli (EHEC) strains are major causes of hemorrhagic colitis. For the confirmation of STEC infection by the bacteriological investigation some significant additional methods were used: serologic examination of feces on shiga- toxin molecular markers by ImmunoCard STAT and PCR methods. Thus, these above mentioned investigations contribute to diagnosis STEC infection at the early stage of the disease. Based on our findings we were able to reveal predictors of complications of hemorrhagic colitis by HUS. They include: Delayed hospitalization, rural residents, premorbid background, onset of the disease with low-grade fever accompanied with abdominal cramps, manifestation of bloody diarrhea on the 2-3-rd days of the disease, frequent bowl movement (>20 times a day), development of oliguria and edema on the following days, leucocytosis in hemogram, elevation of LDH, creatinine and urea, hypoalbuminemia and development of ascites.

Plasma proteome signature of canine acute haemorrhagic diarrhoea syndrome (AHDS).

Acute haemorrhagic diarrhoea is a common complaint in dogs. In addition to causes like intestinal parasites, dietary indiscretion, intestinal foreign bodies, canine parvovirus infection, or hypoadrenocorticism, acute haemorrhagic diarrhoea syndrome (AHDS) is an important and sometimes life-threatening differential diagnosis. There is some evidence supporting the link between Clostridium perfringens toxins and AHDS. These toxins may be partially responsible for the epithelial cell injury, but the pathogenesis of AHDS is still not fully understood. Recent studies have suggested that severe damage to the intestinal mucosa and associated barrier dysfunction can trigger chronic gastrointestinal illnesses. Besides bloodwork and classical markers for AHDS such as protein loss and intestinal bacterial dysbiosis, we focused mainly on the plasma-proteome to identify systemic pathological alterations during this disease and searched for potential biomarkers to improve the diagnosis. To accomplish the goals, we used liquid chromatography-mass spectrometry. We compared the proteomic profiles of 20 dogs with AHDS to 20 age-, breed-, and sex-matched control dogs. All dogs were examined, and several blood work parameters were determined and compared, including plasma biochemistry and cell counts. We identified and quantified (relative quantification) 207 plasmatic proteins, from which dozens showed significantly altered levels in AHDS. Serpina3, Lipopolysaccharide-binding protein, several Ig-like domain-containing proteins, Glyceraldehyde-3-phosphate dehydrogenase and Serum amyloid A were more abundant in plasma from AHDS affected dogs. In contrast, other proteins such as Paraoxonase, Selenoprotein, Amine oxidases, and Apolipoprotein C-IV were significantly less abundant. Many of the identified and quantified proteins are known to be associated with inflammation. Other proteins like Serpina3 and RPLP1 have a relevant role in oncogenesis. Some proteins and their roles have not yet been described in dogs with diarrhoea. Our study opens new avenues that could contribute to the understanding of the aetiology and pathophysiology of AHDS.

Pathological bacterial translocation in cirrhosis: pathophysiology, diagnosis and clinical implications.

Bacterial translocation (BT) is defined by the passage of viable indigenous bacteria from the intestinal lumen to mesenteric lymph nodes (MLNs) and other territories, and its diagnostic criteria rely on the isolation of viable bacteria in MLNs. Small intestinal overgrowth, increased intestinal permeability and immunological alterations are the main factors involved in its pathogenesis. BT is obviously difficult to identify in patients with cirrhosis, and alternative methods have been proposed instead. Bacterial DNA detection and species identification in serum or ascitic fluid has been proposed as a reliable marker of BT. Bacterial products, such as endotoxin, or bacterial DNA can translocate to extra-intestinal sites and promote an immunological response similar to that produced by viable bacteria. Therefore, pathological BT plays an important role in the pathogenesis of the complications of cirrhosis, not only in infections, but by exerting a profound inflammatory state and exacerbating the haemodynamic derangement. This may promote in turn the development of hepatorenal syndrome, hepatic encephalopathy and other portal hypertension-related complications. Therapeutic approaches for the prevention of BT in experimental and human cirrhosis are summarized. Finally, new investigations are needed to better understand the pathogenesis and consequences of translocation by viable bacteria (able to grow in culture), or non-viable BT (detection of bacterial fragments with negative culture) and open new therapeutic avenues in patients with cirrhosis.

Mucormycosis as a rare cause of severe gastrointestinal bleeding after multivisceral transplantation.

Mucormycosis, an emerging fungal infection in solid organ transplant patients, is mostly located in rhino-orbito-cerebral, pulmonary, and cutaneous areas, or disseminated with poor prognosis. A 4-year-old girl with chronic intestinal pseudo-obstruction syndrome underwent a modified multivisceral transplantation, including half of the stomach, the duodeno-pancreas, the small bowel, and the right colon. On postoperative day 5, a digestive perforation was suspected. Surgical exploration found a small necrotic area on the native stomach, which was externally drained. The next day, massive gastric bleeding occurred. During the emergency laparotomy, 2 hemorrhagic ulcers were found and resected from the transplanted stomach. Pathology and fungal culture showed mucormycosis caused by Lichtheimia (formerly Absidia) ramosa in both the transplanted and native stomach. High-dose intravenous liposomal amphotericin B was immediately started. No other site of fungal infection was found. The child recovered, and 3 years after transplantation, is alive and well, off parenteral nutrition. The originality of this case is the very early presentation after transplantation, the unusual site, and the complete recovery after rapid medico-surgical management. The origin of the fungus and treatment are discussed.

Gross blood in stools of premature neonates, a clinical and microbiological follow-up study.

AIM: To characterize the clinical course and the gut microecology of premature infants with macroscopic gross blood in stools. METHODS: We studied 14 premature infants receiving breast milk supplemented with probiotics, according to our units practice, with macroscopic blood in stools without signs of ileus or systemic infection upon occurrence of the symptom and 14 days later. Controls were matched prospectively by gestational and postnatal age and type of feeding. Gut microbiota composition was analysed by quantitative real-time polymerase chain reaction (qPCR), and the presence of enteric viruses in the stools was assayed by PCR and by reverse transcription reaction followed by PCR (RT-PCR). RESULTS: The symptom was transient, benign and self-limiting and none of the background factors explained it. No enteric viruses were detected, and the bacterial analyses showed no statistically significant differences between the infants with or without gross blood in stools. The characterization of the gut microbiota revealed low bacterial diversity. CONCLUSION: Gross blood in the stools of premature infants without other clinical signs of infection can be an innocuous and self-limiting symptom. This cohort of preterm infants receiving breast milk supplemented with probiotics showed no alterations in gut microecology to be associated with the symptom.

Tuberculous pancreatitis complicated by ruptured splenic artery pseudoaneurysm.

Tuberculosis involving the pancreas is rare. We report a patient with pancreatic tuberculosis complicated by haemorrhage from a splenic artery pseudoaneurysm. As far as we are aware, the development of a splenic artery pseudoaneurysm in association with a large caseating mass of tuberculous pancreatic lymph nodes has not been reported previously. We review the literature and discuss the varied presentations of tuberculosis involving the pancreas or the pancreatic bed and its draining lymph nodes.