scholarly journals A Complicated Thread: Abdominal Actinomycosis in a Young Woman with Crohn Disease

2017 ◽  
Vol 11 (2) ◽  
pp. 377-381 ◽  
Author(s):  
Ari Nahum ◽  
Gregory Filice ◽  
Ashish Malhotra

Crohn disease is a chronic inflammatory condition that primarily affects the gastrointestinal tract. Typical manifestations include fever, weight loss, fatigue, and abdominal pain, and abdominal abscesses and fistulae are frequent complications. Abdominal actinomycosis is a subacute or indolent disease associated with Actinomyces spp. Symptoms can be very similar to those of Crohn disease, and fistulae are also common. Since ulcerations in the intestinal tract are thought to be caused by Actinomyces escaping from the gut lumen and establishing intra-abdominal infection, it seems likely that abdominal actinomycosis may occur in patients with inflammatory bowel disease. We report a case of abdominal actinomycosis in a woman with active Crohn disease.

2019 ◽  
Vol 15 (4) ◽  
pp. 296-307
Author(s):  
Meng Chen ◽  
Qinglan Li ◽  
Nan Cao ◽  
Yanan Deng ◽  
Lianyun Li ◽  
...  

Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the gastrointestinal tract.


2020 ◽  
Vol 26 (12) ◽  
pp. 1796-1807 ◽  
Author(s):  
Cindy C Y Law ◽  
Deborah Koh ◽  
Yueyang Bao ◽  
Vipul Jairath ◽  
Neeraj Narula

Abstract Objective To assess the impact of inflammatory bowel disease (IBD) medications on postoperative infection risk within 30 days of surgery. Methods We searched multiple electronic databases and reference lists of articles dating up to August 2018 for prospective and retrospective studies comparing postoperative infection risk in patients treated with an IBD medication perioperatively with the risk in patients who were not taking that medication. Outcomes were overall infectious complications and intra-abdominal infections within 30 days of surgery. Results Sixty-three studies were included. Overall infectious complications were increased in patients who received anti–tumor necrosis factor (TNF) agents (odds ratio [OR] 1.26; 95% confidence interval [CI], 1.07-1.50) and corticosteroids (OR 1.34; 95% CI, 1.25-1.44) and decreased in those who received 5-aminosalicylic acid (OR 0.63; 95% CI, 0.46-0.87). No difference was observed in those treated with immunomodulators (OR 1.08; 95% CI, 0.94-1.25) or anti-integrin agents (OR 1.06; 95% CI, 0.67-1.69). Both corticosteroids and anti-TNF agents were associated with increased intra-abdominal infection risk (OR 1.63; 95% CI, 1.33-2.00 and OR 1.46; 95% CI, 1.08-1.97, respectively), whereas no impact was observed with 5-aminosalicylates, immunomodulators, or anti-integrin therapy. Twenty-two studies had low risk of bias while the remaining studies had very high risk. Conclusions Corticosteroids and anti-TNF agents were associated with increased overall postoperative infection risk as well as intra-abdominal infection in IBD patients, whereas no increased risk was observed for immunomodulators or anti-integrin therapy. Although these results may result from residual confounding rather than from a true biological effect, prospective studies that control for potential confounding factors are required to generate higher-quality evidence.


2019 ◽  
Vol 1 (3) ◽  
pp. 124-128
Author(s):  
Linda Nazarko

Inflammatory bowel disease (IBD) is a chronic inflammatory condition affecting the gastrointestinal tract. People with IBD normally present in primary care and may have non-specific symptoms. Diagnosis may be delayed and this can have an impact on response to treatment. This article aims to enable prescribers to be aware of the clinical features, investigations and management of IBD.


2021 ◽  
Author(s):  
Anita C. Parker ◽  
Nathaniel L. Seals ◽  
Cecile L. Baccanale ◽  
Edson R. Rocha

The opportunistic, anaerobic pathogen and commensal of the human large intestinal tract, Bacteroides fragilis strain 638R, contains six predicted TonB proteins, termed TonB1-6, four ExbBs orthologs, ExbB1-4, and five ExbDs orthologs, ExbD1-5. The inner membrane TonB/ExbB/ExbD complex harvests energy from the proton motive force (Δp) and the TonB C-terminal domain interacts with and transduces energy to outer membrane TonB-dependent transporters (TBDTs). However, TonB’s role in activating nearly one hundred TBDTs for nutrient acquisition in B. fragilis during intestinal colonization and extraintestinal infection has not been established. In this study, we show that growth was abolished in the ΔtonB3 mutant when heme, vitamin B12, Fe(III)-ferrichrome, starch, mucin-glycans, or N-linked glycans were used as a substrate for growth in vitro . Genetic complementation of the ΔtonB3 mutant with the tonB3 gene restored growth on these substrates. The ΔtonB1 , ΔtonB2 , ΔtonB4, ΔtonB5, and ΔtonB6 single mutants did not show a growth defect. This indicates that there was no functional compensation for the lack of TonB3, and it demonstrates that TonB3, alone, drives the TBDTs involved in the transport of essential nutrients. The ΔtonB3 mutant had a severe growth defect in a mouse model of intestinal colonization compared to the parent strain. This intestinal growth defect was enhanced in the ΔtonB3 ΔtonB6 double mutant strain which completely lost its ability to colonize the mouse intestinal tract compared to the parent strain. The ΔtonB1 , ΔtonB2 , ΔtonB4, and ΔtonB5 mutants did not significantly affect intestinal colonization. Moreover, the survival of the ΔtonB3 mutant strain was completely eradicated in a rat model of intra-abdominal infection. Taken together, these findings show that TonB3 was essential for survival in vivo . The genetic organization of tonB1 , tonB2 , tonB4, tonB5, and tonB6 gene orthologs indicates that they may interact with periplasmic and nonreceptor outer membrane proteins, but the physiological relevance of this has not been defined. Because anaerobic fermentation metabolism yields a lower Δp than aerobic respiration and B. fragilis has a reduced redox state in its periplasmic space - in contrast to an oxidative environment in aerobes - it remains to be determined if the diverse system of TonB/ExbB/ExbD orthologs encoded by B. fragilis have an increased sensitivity to PMF (relative to aerobic bacteria) to allow for the harvesting of energy under anaerobic conditions.


2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
F. Scaldaferri ◽  
V. Petito ◽  
L. Lopetuso ◽  
G. Bruno ◽  
V. Gerardi ◽  
...  

Inflammatory bowel disease (IBD) is a chronic inflammatory condition characterized by an abnormal immune response against food or bacterial antigens in genetically predisposed individuals. Several factors of innate and adaptive immune system take part in the inflammatory process, probably actively contributing in endoscopic and histological healing at molecular level. Although it is difficult to discriminate whether they are primary factors in determining these events or they are secondarily involved, it would be interesting to have a clear map of those factors in order to have a restricted number of potentially “good candidates” for mucosal healing. The present review will present a class of these factors and their modulation in course of therapy, starting from pathogenic studies involving several treatments associated with good clinical outcomes. This approach is meant to help in the difficult task of identifying “good candidates” for healing signatures, which could also be possible new therapeutic targets for clinical management of IBD patients.


2020 ◽  
Vol 26 (30) ◽  
pp. 3733-3747 ◽  
Author(s):  
Mariana Ferreira-Duarte ◽  
Joana Beatriz Sousa ◽  
Carmen Diniz ◽  
Teresa Sousa ◽  
Margarida Duarte-Araújo ◽  
...  

The endothelium has a crucial role in proper hemodynamics. Inflammatory bowel disease (IBD) is mainly a chronic inflammatory condition of the gastrointestinal tract. However, considerable evidence points to high cardiovascular risk in patients with IBD. This review positions the basic mechanisms of endothelial dysfunction in the IBD setting (both clinical and experimental). Furthermore, we review the main effects of drugs used to treat IBD in endothelial (dys)function. Moreover, we leave challenging points for enlarging the therapeutic arsenal for IBD with new or repurposed drugs that target endothelial dysfunction besides inflammation.


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