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.

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

La leptospirosis es una enfermedad causada por la espiroqueta Leptospira. Se trata de una zoonosis de distribución mundial, con predominio en los trópicos. En España no es frecuente pero sí se observan casos en zonas más húmedas o con presencia de ríos, lagos o estanques, como son Cataluña, Andalucía o la Comunidad Valenciana, donde se relaciona con los arrozales. Los transmisores son múltiples animales como vacas o ratas, contagiándose el ser humano mediante contacto directo con estos animales o su orina, o bien de forma indirecta al consumir o estar en contacto con agua contaminada por la orina de éstos. Las manifestaciones clínicas son muy variables, siendo asintomática o poco sintomática en la mayoría de los pacientes. Aunque no ocurre siempre, la leptospirosis cursa con una primera fase con fiebre, mialgias, afectación renal o hemorragia de distintos órganos, seguida de una segunda fase con presencia de ictericia por afectación hepática. La enfermedad de Weil es una forma de leptospirosis grave caracterizada por afectación hepática con ictericia e insuficiencia renal aguda, asociada a una considerable mortalidad. El diagnóstico se basa en técnicas serológicas y detección de DNA mediante PCR. El tratamiento consta de medidas de soporte y antibioticoterapia. Presentamos un paciente con enfermedad de Weil y hemorragia digestiva por leptospirosis, con una evolución clínica fulminante, y hacemos hincapié en la necesidad de tener presente esta entidad, especialmente en ambientes epidemiológicos favorables como el de este paciente, con el fin de lograr un diagnóstico precoz.

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.

Enfermedades relacionadas con Helicobacter pylori: dispepsia, úlcera y cáncer gástrico / Helicobacter pylori-related diseases: dyspepsia, ulcer and gastric cancer

Las quinolonas de nueva generación, como el sitafloxacino, podrían ser útiles en el tratamiento erradicador de tercera línea. Puesto que la infección por H. pylori no confiere protección, los individuos se pueden reinfectar más de una vez con su propia cepa, lo que podría permitir el empleo de esta bacteria como vector para la administración de diversas vacunas en múltiples ocasiones. A continuación se resumen las principales conclusiones derivadas de las comunicaciones presentadas este año en la Digestive Diseases Week relacionadas con la infección por Helicobacter pylori. Las resistencias antibióticas están aumentando en diversos países. Hay una relación inversa entre H. pylori y enfermedad por reflujo gastroesofágico (ERGE), aunque ello no implica que la erradicación del microorganismo favorezca la aparición de ERGE. El beneficio del tratamiento erradicador en la dispepsia no investigada parece confirmarse a largo plazo. La erradicación de H. pylori mejora los síntomas de un subgrupo de dispépticos funcionales. La frecuencia de úlceras pépticas idiopáticas parece estar incrementándose. La erradicación de H. pylori elimina la práctica totalidad de las recidivas hemorrágicas por úlcera péptica; no obstante, la ingesta de antiinflamatorios no esteroideos (AINE) o la reinfección por H. pylori puede originar una recidiva hemorrágica. Los métodos diagnósticos de H. pylori basados en la biopsia gástrica poseen una reducida sensibilidad en pacientes con hemorragia digestiva. Incluso los pacientes que presentan una hemorragia digestiva mientras reciben AINE están frecuentemente infectados. El origen filogenético de la cepa de H. pylori predice el desarrollo de lesiones gástricas preneoplásicas. Las propiedades electroquímicas de H. pylori permiten su detección en biopsias gástricas con una elevada precisión y rapidez. La realización del test rápido de la ureasa conjuntamente a partir de una (..) (AU)

This article summarizes the main conclusions drawn from the presentations on Helicobacter pylori infection at Digestive Disease Week 2010. Antibiotic resistance is increasing in several countries. There is an inverse relationship between H. pylori and gastroesophageal reflux disease (GERD), although this association does not imply that H. pylori eradication favors the development of GERD. The benefit of eradication therapy in uninvestigated dyspepsia seems to be confirmed in the long term. H. pylori eradication improves symptoms in a subgroup of patients with functional dyspepsia. The frequency of idiopathic peptic ulcers seems to be increasing. H. pylori eradication eliminates almost all episodes of peptic ulcer rebleeding; nevertheless, the use of non-steroidal anti-inflammatory drugs (NSAIDS) or H. pylori reinfection can lead to bleeding recurrence. Diagnostic methods for H. pylori based on gastric biopsy have reduced sensitivity in patients with gastrointestinal bleeding. Even patients showing gastrointestinal hemorrhage while receiving NSAIDs are frequently infected. The phylogenetic origin of the H. pylori strain predicts the development of preneoplastic gastric lesions. The electrochemical properties of H. pylori (..) (AU)

Epithelial cell signaling responses to enterohemorrhagic Escherichia coli infection

Enterohemorrhagic Escherichia coli, including the serotype O157:H7 that is most commonly identified with human disease, cause both sporadic cases and outbreaks of non-bloody diarrhea and hemorrhagic colitis. In about 10 percent of infected subjects, the hemolytic uremic syndrome (hemolytic anemic, thrombocytopenia, and acute renal failure) develops, likely as a consequence of systemic spread of bacterial-derived toxins variously referred to as Shiga-like toxin, Shiga toxin, and Verotoxin. Increasing evidence points to a complex interplay between bacterial products - for example, adhesins and toxins - and host signal transduction pathways in mediating responses to infection. Identification of critical signaling pathways could result in the development of novel strategies for intervention to both prevent and treat this microbial infection in humans.

Rectorragia neonatal por Campilobacter jejuni / Neonatal rectal bleeding caused by Campylobacter Jejuni

Se describe un caso de rectorragia en un recién nacido, originada por Campylobacter jejuni. Destacamos la rareza del cuadro y consideramos necesario realizar un coprocultivo anto todo neonato que presente sangre en heces (AU)

Escherichia coli enterohemorrágica en el síndrome hemolítico urémico, en niños chilenos: evaluación de diferentes técnicas de diagnóstico de infección / Enterohemorrhagic escherichia coli in hemolytic uremic syndrome, in chilean children: evaluation of different technics of infection diagnosis

Enterohemorrhagic escherichia coli (EHEC), have been associated with pathogenesis of hemolytic uremic syndrome (HUS) worldwide. Our aim was to determine the association of EHEC ing¿fection and HUS in chilean children. During may 1991 and october 1993, 34 children HUS and 33 age matched controls (children with diarrhea that did not develop HUS) were enrolled in a case/control study. For each child a stool and serum sample were obtained at admission. Stools were processed for common enteropathogen and for EHEC identification. EHEC were identified in stools by gene probes for different virulence factors (EHEC plasmid-associated fimbria, Shiga-like toxin I, Shiga-like toxin II and eae adherence factor) and by detection of free fecal toxin by neutralization assay in Vero cells. Sera were processed for anti-cytotoxin antibodies also by an assay in Vero cells. Enteropathogens were isolated in 20.6 percent and 15.5 percent of HUS and control children respectively (p=NS). 91 percent of the HUS children and 73 percent of the control children were EHEC positive by one or more of the techniques used (p=0.05). Of the 3 detection methods used for EHEC, only free fecal cytotoxin was significantly more common in HUS children than controls (45.5 percent vs 9 percent p=0.007). Genotype patterns of HUS and controls strains were similar except for a trend towards a higher frequency of non-toxigenic strains in the control group. Serogroup 0157 was more common in HUS children than in controls (9 percent vs 0 percent p=0.036). In Chile as in other countries, EHEC infection is common and significantly associated with occurrence of HUS. Infection with EHEC strains 0157 seems to be important risk factor for HUS

Intestinal bleeding and occlusion associated with shiga toxin-producing Escherichia coli 0127: H21

We report a case of a nine-year old boy with vomiting, abdominal pain and fever, who underwent surgery with a diagnosis of appendicitis in Mendonza and from whom a Shiga toxin-producing Escherichia coli (STEC) 0127:H21 strain was recovered. Forty-eight hours after surgery he presented bilious vomiting and two episodes of intestinal bleeding. Loboratory findings included: hematocrit, 35 per cent; blood urea nitrogen, 0.22 g/L. The urinary output was normal. The following day physical examination showed an alert mildy hydrated child, without fever but with distended and painful abdomen. The patient was again submitted to surgery with a diagnosis of intestinal occlusion. Bleeding and multiple adhesions in jejunum and ileum were found. The patient still had tense and painful abdomen and presented two bowel movements with blood; hematocrit fell to 29 per cent and blood urea nitrogen rose to 0.32 g/L. STEC 0127:H21 eae(-)/Stx2/Stx2vh-b(+)/E-Hly(+) was isolated from a stool sample. He was discharged after 10 days of hospitalization and no long-term complications such as HUS or TTP were observed. This is the first report, to our knoweledge, on the isolation of E.coli 0127:H21, carrying the virulence factors that characterize STEC strains, associated to an enterohemorrhagic colitis case. This serotype was previously characterized as a non-classic enteropathogenic E. coli (EPEC). STEC infections can mimic infectious or noninfectious pathologies. Therefore an important aspect of clinical managements is making the diagnosis using different criteria thereby avoiding misdiagnoses which have occasionally led to invasive diagnostic and therapeutic procedures or the inappropriate use of antibiotics.

Intestinal bleeding and occlusion associated with shiga toxin-producing Escherichia coli 0127: H21

We report a case of a nine-year old boy with vomiting, abdominal pain and fever, who underwent surgery with a diagnosis of appendicitis in Mendonza and from whom a Shiga toxin-producing Escherichia coli (STEC) 0127:H21 strain was recovered. Forty-eight hours after surgery he presented bilious vomiting and two episodes of intestinal bleeding. Loboratory findings included: hematocrit, 35 per cent; blood urea nitrogen, 0.22 g/L. The urinary output was normal. The following day physical examination showed an alert mildy hydrated child, without fever but with distended and painful abdomen. The patient was again submitted to surgery with a diagnosis of intestinal occlusion. Bleeding and multiple adhesions in jejunum and ileum were found. The patient still had tense and painful abdomen and presented two bowel movements with blood; hematocrit fell to 29 per cent and blood urea nitrogen rose to 0.32 g/L. STEC 0127:H21 eae(-)/Stx2/Stx2vh-b(+)/E-Hly(+) was isolated from a stool sample. He was discharged after 10 days of hospitalization and no long-term complications such as HUS or TTP were observed. This is the first report, to our knoweledge, on the isolation of E.coli 0127:H21, carrying the virulence factors that characterize STEC strains, associated to an enterohemorrhagic colitis case. This serotype was previously characterized as a non-classic enteropathogenic E. coli (EPEC). STEC infections can mimic infectious or noninfectious pathologies. Therefore an important aspect of clinical managements is making the diagnosis using different criteria thereby avoiding misdiagnoses which have occasionally led to invasive diagnostic and therapeutic procedures or the inappropriate use of antibiotics. (AU)