Diagnosis and Treatment of Clostridium difficile Colitis

Fekety, Robert

doi:10.1001/jama.1993.03500010081036

Cited by 266 publications

(123 citation statements)

References 26 publications

Supporting

Mentioning

122

Contrasting

Unclassified

Order By: Relevance

“…[14][15][16][17][18] Cephalosporins, aminoglycosides and quinolones have all been shown to be principal causative agents of C. difficile associated diarrhoea. 14,19,20 Matters are made worse with long courses of antibiotics and antibiotic 'cocktails'.…”

Section: 12mentioning

confidence: 99%

Clostridium Difficile in Urology

Hossain

Crook

Keoghane

2008

annals

View full text Add to dashboard Cite

INTRODUCTIONThe objective was to determine the incidence of Clostridium difficile infection in a UK urology ward from 2000 to 2005, and correlate and compare the data with other specialty wards and national figures.PATIENTS AND METHODS Urology patients with a positive stool culture for C. difficile between 2000 and 2005 were identified from a hospital database. The medical records of these patients were reviewed and data such as antibiotic use, urological diagnosis and elective/emergency status of the patient were recorded and analysed. The number of C. difficile cases on an elderly care ward, an acute medical ward and an acute surgical ward were also recorded for this period. Data on the number of admissions and occupied bed-days on all 4 wards were compared.

show abstract

Section: 12mentioning

confidence: 99%

Clostridium Difficile in Urology

Hossain

Crook

Keoghane

2008

annals

View full text Add to dashboard Cite

show abstract

“…Anion-exchange resins binding to the toxins or competition by orally administered lactobacilli or nonpathogenic yeasts prove to be promising in the clinic (22)(23)(24). A number of clinical studies indicate that anti-toxin Ab responses in both serum and intestinal secretions may be protective, whereas an inadequate response predisposes to recurrent infection (25).…”

mentioning

confidence: 99%

Polymeric IgA Is Superior to Monomeric IgA and IgG Carrying the Same Variable Domain in Preventing Clostridium difficile Toxin A Damaging of T84 Monolayers

Stubbe¹,

Berdoz²,

Kraehenbuhl³

et al. 2000

The Journal of Immunology

101

View full text Add to dashboard Cite

The two exotoxins A and B produced by Clostridium difficile are responsible for antibiotic-associated enterocolitis in human and animals. When added apically to human colonic carcinoma-derived T84 cell monolayers, toxin A, but not toxin B, abolished the transepithelial electrical resistance and altered the morphological integrity. Apical addition of suboptimal concentration of toxin A made the cell monolayer sensitive to toxin B. Both toxins induced drastic and rapid epithelial alterations when applied basolaterally with a complete disorganization of tight junctions and vacuolization of the cells. Toxin A-specific IgG2a from hybridoma PCG-4 added apically with toxin A alone or in combination with toxin B abolished the toxin-induced epithelial alterations for up to 8 h. The Ab neutralized basolateral toxin A for 4 h, but not the mixture of the two toxins. Using an identical Ab:Ag ratio, we found that recombinant polymeric IgA (IgAd/p) with the same Fv fragments extended protection against toxin A for at least 24 h in both compartments. In contrast, the recombinant monomeric IgA counterpart behaved as the PCG-4 IgG2a Ab. The direct comparison between different Ig isotype and molecular forms, but of unique specificity, demonstrates that IgAd/p Ab is more efficient in neutralizing toxin A than monomeric IgG and IgA. We conclude that immune protection against C. difficile toxins requires toxin A-specific secretory Abs in the intestinal lumen and IgAd/p specific for both toxins in the lamina propria.

show abstract

“…Several recommendations are given regarding adjunctive ICV treatment of C. difficile colitis [59,[74][75][76][77][78][79]. Orally administered vancomycin can result in significant.…”

Section: Discussionmentioning

confidence: 99%

Pseudomemberanous Colitis following Cesarean Delivery with Adjunctive Intracolonic Vancomycin

Ahmadi¹,

Rezaee²,

Tanha³

et al. 2016

J Gynecol Res Obstet

View full text Add to dashboard Cite

Journal of Gynecological Research and Obstetrics 055According to the operation report numerous adhesions were detected during surgery, many of which especially those in the uterine incision site had been released. The patient received one dose of prophylactic cefazolin after clamping of the umbilical cord. Before discharge (discharged with personal consent) she had gas passage and defecation.Three days after C/S the patient was hospitalized with a presumed ileus. At that point she seemed well and had no fever and tachycardia; the abdomen was distended; bowel sounds were normal. On palpation, tenderness in left lower quadrant without rebound was present. In chest auscultation no abnormal finding except dextrocardia was detected (Figures 1,2).Initially the patient was managed conservatively, laboratory tests and surgery consult were ordered.The patient was not allowed to take anything by mouth and it was well emphasised to her to stay mobile. Despite gas passage her abdominal distention fluctuated during the first two days of hospitalization. During this period the laboratory findings were normal, no leucocytosis was present and hemoglobin and electrolytes were normal. Just on abdominal x ray( upright and flat) hyperinflation was to be seen.After the second day, diarrhea and a 38 C fever were added to the patients' signs. The diarrhea contained greenish liquid with white cheese -like parts. The patient was not ill, the abdominal palpation revealed no change and the laboratory findings were still normal.On the third day, abdominal distention was noticeably increased and the abdomen became tenser. Emergent surgery and gastrointestinal consult were ordered and the patient was admitted to the intensive care unit. At that point potassium was as low as 2.4 IntroductionPseudomembranous colitis (PMC) is a type of colitis (and sometimes enteritis), with special pathologic and oftentimes radiologic features, which is usually associated with the overgrowth of a bacterium called Clostridium difficile. Although this condition normally occurs following antibiotic consumption, it may rarely happen in other settings such as bowel ischemia, intestinal obstruction, and intestinal surgery or chemotherapy. Moreover, gastrointestinal infections (e.g. Staphylococcus aureus) can induce a similar condition [1].A recent increase in the incidence rate and severity of clostridium difficile infection has been reported, which is thought to be due to the great use of broad spectrum antibiotics worldwide and the development of a hypervirulant strain of this organism [2][3][4]. The presentation of PMC can vary from a self-limiting diarrhea to toxic megacolon and death [5]. Yet, many cases have confusing clinical features and their condition may not be diagnosed immediately [1]. History of previous antibiotic intake especially cephalosporins and flouroquinolones is the most important risk factor for PMC [6][7][8]. This risk is at its peak within the first month after antibiotic use [9].Immediate diagnosis and treatment of this condition can decre...

show abstract

Diagnosis and Treatment of Clostridium difficile Colitis

Cited by 266 publications

References 26 publications

Clostridium Difficile in Urology

Clostridium Difficile in Urology

Polymeric IgA Is Superior to Monomeric IgA and IgG Carrying the Same Variable Domain in Preventing Clostridium difficile Toxin A Damaging of T84 Monolayers

Pseudomemberanous Colitis following Cesarean Delivery with Adjunctive Intracolonic Vancomycin

Contact Info

Product

Resources

About