A case of pseudomembranous colitis presenting with massive ascites

Tsourous, G I; Raftopoulos, Leonidas; Kafe, Eleni E.; Manoleris, E.; Makaritsis, Kostas P.; Pinis, Sotirios G.

doi:10.1016/j.ejim.2006.09.034

Cited by 13 publications

(12 citation statements)

References 7 publications

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“…C. difficile infection can cause systemic complications including ascites, pleural effusion, cardiopulmonary arrest, hepatic abscess, abdominal compartment syndrome, acute respiratory distress syndrome, and renal failure [ 162 , 163 , 164 , 165 , 166 , 167 , 168 ]. Additionally, mental status changes have been often reported in complicated CDI cases [ 169 ].…”

Section: Are Severe Clinical Manifestations Associated To the Amoumentioning

confidence: 99%

Clostridium difficile Toxins A and B: Insights into Pathogenic Properties and Extraintestinal Effects

Bella

Ascenzi

Siarakas

et al. 2016

Toxins

183

203

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Clostridium difficile infection (CDI) has significant clinical impact especially on the elderly and/or immunocompromised patients. The pathogenicity of Clostridium difficile is mainly mediated by two exotoxins: toxin A (TcdA) and toxin B (TcdB). These toxins primarily disrupt the cytoskeletal structure and the tight junctions of target cells causing cell rounding and ultimately cell death. Detectable C. difficile toxemia is strongly associated with fulminant disease. However, besides the well-known intestinal damage, recent animal and in vitro studies have suggested a more far-reaching role for these toxins activity including cardiac, renal, and neurologic impairment. The creation of C. difficile strains with mutations in the genes encoding toxin A and B indicate that toxin B plays a major role in overall CDI pathogenesis. Novel insights, such as the role of a regulator protein (TcdE) on toxin production and binding interactions between albumin and C. difficile toxins, have recently been discovered and will be described. Our review focuses on the toxin-mediated pathogenic processes of CDI with an emphasis on recent studies.

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Section: Are Severe Clinical Manifestations Associated To the Amoumentioning

confidence: 99%

Clostridium difficile Toxins A and B: Insights into Pathogenic Properties and Extraintestinal Effects

Bella

Ascenzi

Siarakas

et al. 2016

Toxins

183

203

View full text Add to dashboard Cite

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“…In addition to gastrointestinal pathology, systemic complications of infection such as ascites[6, 7], pleural effusion[8, 9], cardiopulmonary arrest[10, 11], hepatic abscess[12], abdominal compartment syndrome[13], acute respiratory distress syndrome[14], multiple organ dysfunction syndrome[15], and renal failure[16] have been reported in human cases. The mechanisms by which C. difficile causes these systemic effects are not entirely understood, but the toxins produced by the bacterium, especially toxins A and B, are likely involved.…”

Section: Introductionmentioning

confidence: 99%

Piglet Models of Acute or ChronicClostridium difficileIllness

Steele¹,

Feng²,

Parry³

et al. 2010

J INFECT DIS

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We have examined the piglet model for CDI in humans since swine are naturally susceptible to C. difficile. The piglet is a reproducible model for acute or chronic CDI with characteristic pseudomembranous colitis (PMC). Germfree piglets were consistently and extensively colonized when orally challenged with the human 027/BI/NAP1 strain, establishing an infectious dose-age relationship. This allowed a demarkation between acute fatal and chronic models. The clinical manifestations of disease inclusive of gastrointestinal and systemic symptoms and characteristic mucosal lesions in the large bowel including PMC are described. Additionally, we demonstrate the presence of toxins in feces, body fluids and serum, and a significant elevation of IL-8 in animals with severe disease. We conclude that piglets infected with C. difficile mimic many of the key characteristics observed in humans with CDI, and are suitable animals in which to investigate the role of virulence attributes, drug efficacy and evaluation of vaccine candidates.

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“…However, CDI-associated mortality may be attributable to systemic sequelae of the disease (12). Although large-scale epidemiological studies are lacking, reported systemic complications include hepatic abscesses (13), ascites (14), pleural effusion with acute respiratory distress (15,16), and severe sepsis and multiorgan dysfunction (17).…”

mentioning

confidence: 99%

Memory B Cells Encode Neutralizing Antibody Specific for Toxin B from the Clostridium difficile Strains VPI 10463 and NAP1/BI/027 but with Superior Neutralization of VPI 10463 Toxin B

et al. 2016

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T he role of immune cell memory in Clostridium difficile infection (CDI) remains poorly understood. CDI is complicated by a high frequency of recurrence, often after disease has apparently resolved, and can be associated with progressively worsening pathology and ultimately death (1). However, patients that develop antibodies (Ab) capable of neutralizing two toxins secreted by C. difficile (TcdA and TcdB) are less likely to experience recurrence (reviewed in reference 2). This suggests that memory B (Bmem) cells may contribute to resistance to reinfection by encoding toxin-neutralizing Ab. Bmem cells have typically undergone affinity maturation and Ab class switch in the germinal centers of secondary lymphoid organs (3). Bmem cells are therefore poised to respond rapidly to booster vaccinations or infection, by rapidly differentiating into plasma cells that secrete class-switched, highaffinity Ab (4). Such plasma cells may display a range of short-toextreme longevity, be associated with transient or sustained Ab titers, or secrete neutralizing or nonneutralizing Ab (5-7).In earlier studies, a correlation between bacterial load and advanced age was observed during CDI, with older individuals lacking toxin-neutralizing Ab (8). In more recent work, the probability of HIV-positive patients experiencing CDI increased as their CD4 ϩ T-cell counts declined (9), which could be partly attributable to altered CD4 ϩ T-cell-dependent B cell function (10). Indeed, there is growing concern about CDI in a variety of immunocompromised individuals, including organ transplant recipients (reviewed in reference 11). These observations highlight the wellrecognized importance of B cell responses and production of toxin-neutralizing antibodies in resisting CDI. However, the underlying characteristics of the Bmem cellular response and their contributions to production of toxin-neutralizing Ab have not been described.CDI is best known as a disease of the gastrointestinal tract, causing diarrhea, and this infection may progress to a severe pathological condition in which pseudomembranous colitis and toxic megacolon are evident (1, 2). However, CDI-associated mortality may be attributable to systemic sequelae of the disease (12). Although large-scale epidemiological studies are lacking, reported systemic complications include hepatic abscesses (13), ascites (14), pleural effusion with acute respiratory distress (15, 16), and severe sepsis and multiorgan dysfunction (17).TcdA and TcdB are large clostridial toxins that contribute sub-

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A case of pseudomembranous colitis presenting with massive ascites

Cited by 13 publications

References 7 publications

Clostridium difficile Toxins A and B: Insights into Pathogenic Properties and Extraintestinal Effects

Clostridium difficile Toxins A and B: Insights into Pathogenic Properties and Extraintestinal Effects

Piglet Models of Acute or ChronicClostridium difficileIllness

Memory B Cells Encode Neutralizing Antibody Specific for Toxin B from the Clostridium difficile Strains VPI 10463 and NAP1/BI/027 but with Superior Neutralization of VPI 10463 Toxin B

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