ライフサイエンスコーパス: CDAD

1 CDAD pathology is induced by two exotoxins, toxin A and

2 CDAD predominated in general hospitals versus other faci

3 bes the potential of DNA vaccination against CDAD.

4 dium difficile colitis (CCDC) was defined as CDAD associated with graft loss, total colectomy, or dea

5 with a 5% incidence of antibiotic-associated CDAD (median control group risk), probiotic prophylaxis

6 on model, antibodies to both toxins A and B (CDAD antitoxin) were required to prevent morbidity and m

7 treated without carbapenems were followed by CDAD (P = 0.04).

8 s treated with a carbapenem were followed by CDAD, whereas only 2.1% of infections treated without ca

9 Of these infections, 98 were followed by CDAD.

10 c strains of C difficile isolates that cause CDAD were also recovered from stools of symptom-free pat

11 tomy in the treatment of severe, complicated CDAD resulting in reduced morbidity and preservation of

12 omy improves survival in severe, complicated CDAD, outcomes remain poor with associated mortality rat

13 Confirmed CDAD was lower in fidaxomicin vs placebo recipients (4.3

14 primary endpoint analysis counted confirmed CDAD, receipt of CDAD-effective medications (for any ind

15 ivity analysis, which counted only confirmed CDAD (by toxin immunoassay or nucleic acid amplification

16 symptom-free carriers (1.5 [1.5]) developed CDAD (pooled risk difference -2.3% [95% CI 0.3-4.3], p=0

17 -up 1.7 weeks [SD 1.3]), 22 (3.6%) developed CDAD, whereas only two (1.0%) of 192 primary symptom-fre

18 o (1.1%) of 176 colonised patients developed CDAD (-3.2% [0.4-6.0], p=0.024).

19 illness are at greatest risk for developing CDAD following treatment of polymicrobial infections.

20 le carriers are at higher risk of developing CDAD than patients who are culture-negative.

21 Clostridium difficile-associated diarrhea (CDAD) is an increasingly important diagnosis in solid or

22 Clostridium difficile-associated diarrhea (CDAD) is common during hematopoietic stem-cell transplan

23 f Clostridium difficile-associated diarrhea (CDAD) is highly desirable in the setting of hospital cos

24 f Clostridium difficile-associated diarrhea (CDAD) occurs in 15 to 20% of patients after discontinuat

25 l Clostridium difficile-associated diarrhea (CDAD), a series of recommendations and a pathway to prev

26 r Clostridium difficile-associated diarrhea (CDAD).

27 s Clostridium difficile-associated diarrhea (CDAD).

28 f Clostridium difficile-associated diarrhea (CDAD).

29 Clostridium-difficile-associated diarrhoea (CDAD) are culture-positive or culture-negative before il

30 iated diarrhea due to Clostridium difficile (CDAD) is thought to reflect colonization of a disrupted

31 luation for C. difficile-associated disease (CDAD) among 864 patients was based on clinical criteria

32 Clostridium difficile-associated disease (CDAD) constitutes a large majority of nosocomial diarrhe

33 ed Clostridium difficile-associated disease (CDAD) data from the intensive care unit (ICU) and hospit

34 Clostridium difficile-associated disease (CDAD) due to toxigenic strains is prevented in hamsters

35 decreases the risk of CD-associated disease (CDAD) in humans.

36 tic-induced C. difficile-associated disease (CDAD) that more closely resembles human disease.

37 rhea (AAD), C. difficile-associated disease (CDAD), and other enteric infections in humans.

38 PARgamma in C. difficile-associated disease (CDAD), immunity and gut pathology, we used a mouse model

39 tients with C. difficile-associated disease (CDAD), one of whom died from extensive pseudomembranous

40 stablishing C. difficile-associated disease (CDAD).

41 es Clostridium difficile-associated disease (CDAD).

42 B to treat C. difficile-associated disease (CDAD).

43 with type CF2, three of whom had documented CDAD.

44 risk factors, and outcomes of colectomy for CDAD after solid organ transplantation.

45 umber of patients treated with colectomy for CDAD preceding the initiation of this current treatment

46 have identified significant risk factors for CDAD and predictors of progression to CCDC.

47 ere significant independent risk factors for CDAD.

48 pecific objectives: (1) conduct a review for CDAD and prevention; (2) develop statements based upon p

49 uggests that use of a probiotic strategy for CDAD prevention in humans receiving antibiotics might be

50 nosed with severe, complicated ("fulminant") CDAD and were treated at the University of Pittsburgh Me

51 erage, it does not reduce the risk of future CDAD.

52 Metronidazole had no association with future CDAD.

53 ICU CDAD rates increased significantly only in hospitals wit

54 light of the recent substantial increases in CDAD incidence and severity, this model will be valuable

55 prophylaxis results in a large reduction in CDAD without an increase in clinically important adverse

56 fficile spores is the first required step in CDAD.

57 edications (for any indication), and missing CDAD assessment (for any reason, including death) as fai

58 However, most failures were due to non-CDAD events.

59 CCDC occurred in 15.8% of CDAD cases.

60 t disinfection (7/8); (8) early detection of CDAD in symptomatic patients (7/8); (9) usage of protect

61 re known to contribute to the development of CDAD, the role of preventive antibiotics is unproven.

62 r to be sufficient for accurate diagnosis of CDAD.

63 cile test as an adjunct for the diagnosis of CDAD.

64 animals that survived an initial episode of CDAD showed no evidence of diarrhea or colitis after sub

65 assays positive or chart review evidence of CDAD, 97 (14.8%) stool specimens were positive by one or

66 Typical histologic features of CDAD were evident.

67 The peak frequency of CDAD was between 6 and 10 days posttransplantation.

68 Probiotics reduced the incidence of CDAD by 66% (pooled relative risk, 0.34 [95% CI, 0.24 to

69 micin significantly reduced the incidence of CDAD in HSCT recipients.

70 is associated with an increased incidence of CDAD in this population.

71 The incidence of CDAD was 12.4% (165 patients); it increased from 4.5% (1

72 nly carbapenem use affected the incidence of CDAD: 3.5% of infections treated with a carbapenem were

73 effective in the treatment and management of CDAD in humans.

74 We have developed a mouse model of CDAD that closely represents the human disease.

75 s used to identify independent predictors of CDAD.

76 We evaluated fidaxomicin for prevention of CDAD in HSCT patients.

77 analysis counted confirmed CDAD, receipt of CDAD-effective medications (for any indication), and mis

78 d by Health Canada for the risk reduction of CDAD in hospitalized patients.

79 ry end point for the study was resolution of CDAD.

80 We calculated the difference in risk of CDAD between colonised and non-colonised patients in eac

81 ation is associated with a decreased risk of CDAD.

82 itivity of each test method for screening of CDAD was as follows: bacterial culture, 95%; culture wit

83 In 13 trials, data on CDAD were missing for 5% to 45% of patients.

84 To prevent CDAD during treatment with antibiotics, we gave a Cm-res

85 sistant nontoxigenic C. difficile to prevent CDAD must be balanced against the risk that resistance m

86 Failure to prevent CDAD was associated with failure of colonization with no

87 strain B1 on days 5, 7, or 9, M13 prevented CDAD in 100% of the hamsters.

88 Oral vancomycin prevented CDAD in all mice, but 68% died from colitis after treatm

89 ith 3 nontoxigenic CD strains for preventing CDAD after exposure to toxigenic CD.

90 CD strains is highly effective in preventing CDAD in hamsters challenged with toxigenic CD strains, w

91 to investigate the epidemiology of recurrent CDAD in 18 patients.

92 es for prevention and treatment of recurrent CDAD, which is often recalcitrant to existing therapies.

93 fecal communities in patients with recurrent CDAD were highly variable in bacterial composition and w

94 rgrowth (8/8); (4) staff education regarding CDAD preventive measures (8/8); (5) appropriate hand hyg

95 uated for antibiotic coverage and subsequent CDAD.

96 These results indicate that CDAD antitoxin may be effective in the treatment and man

97 In contrast to vancomycin, CDAD antitoxin prevented relapse and subsequent C. diffi

98 The primary endpoint was CDAD incidence through 30 days after study medication.

99 II) score were independently associated with CDAD by multiple logistic regression analysis.

100 leen and colonic lamina propria of mice with CDAD.

101 ofiled the fecal microbiota of patients with CDAD (both initial and recurrent episodes) by culture-in

102 Patients with CDAD were identified from a prospective transplant datab