ライフサイエンスコーパス: M. ulcerans

1 M. ulcerans causes Buruli ulcer, a severe human skin les

2 M. ulcerans is an opportunistic environmental pathogen;

3 M. ulcerans pathogenesis may not only be an individual a

4 M. ulcerans produces the polyketide-derived macrolide my

5 M. ulcerans was s.c. inoculated in three consanguine mou

6 rocess and did not confer protection against M. ulcerans.

7 ze the relationship between M. liflandii and M. ulcerans, strains were analyzed for the presence of t

8 se soils were Mycobacterium tuberculosis and M. ulcerans, M. tuberculosis (macrolide-lincosamide-stre

9 s revealed a significant association between M. ulcerans and Aedes notoscriptus.

10 ulation of responses such as effects between M. ulcerans, mycolactone, and S. aureus virulence that w

11 The relationship between M. ulcerans, mycolactone, and Ae. aegypti further sugges

12 non-random, co-correlated clustering of both M. ulcerans positive possum excreta and human BU cases.

13 colactone, a lipid-like exotoxin secreted by M. ulcerans, inhibits the Sec61 translocon, driving tiss

14 rtance of innate immune responses to control M. ulcerans infection.

15 culture-positive samples were able to detect M. ulcerans DNA in all 21 culture-confirmed patients.

16 We evaluated the IS2404-based PCR to detect M. ulcerans DNA in tissue specimens from 143 BUD patient

17 ment membranes were disrupted in vivo during M. ulcerans infection in the mouse model.

18 stological diagnosis, a positive culture for M. ulcerans, or a smear positive for acid-fast bacilli (

19 specimens of which 11% were PCR positive for M. ulcerans-specific DNA.

20 single-nucleotide-polymorphism profiles for M. ulcerans detected in mosquitoes, possum excreta and h

21 Possums are a local wildlife reservoir for M. ulcerans and, although mosquitoes have been implicate

22 ective, simple, cheap and safe treatment for M. ulcerans disease.

23 terized a macrolide toxin, mycolactone, from M. ulcerans.

24 One member of the genus, M. ulcerans, causes a necrotizing skin disease called Bu

25 rveys show that locales where possums harbor M. ulcerans overlap with human cases of BU, raising the

26 However, M. ulcerans infections are not limited to skin, and oste

27 was to assess using statistical modeling if M. ulcerans surveillance of possum excreta provided usef

28 Our data suggest that additional factors in M. ulcerans may be involved in Buruli ulcer pathogenesis

29 At the molecular level, M. ulcerans is distinguished from M. marinum by the pres

30 rs of M. ulcerans-positive Ae. notoscriptus, M. ulcerans-positive possum excreta and Buruli ulcer cas

31 conducted extensive field survey analyses of M. ulcerans prevalence among mosquitoes in the Morningto

32 For 70 clinically diagnosed cases of M. ulcerans disease, the modified PCR was 98% sensitive

33 tistics revealed overlap between clusters of M. ulcerans-positive Ae. notoscriptus, M. ulcerans-posit

34 and histopathology in making a diagnosis of M. ulcerans disease in a field setting.

35 he difficulties associated with diagnosis of M. ulcerans osteomyelitis, with one-fourth of patients h

36 s important to understand the interaction of M. ulcerans with other bacteria encountered during skin

37 This in vivo model of M. ulcerans infection now paves the way for new avenues

38 tter understanding of the pathophysiology of M. ulcerans infection, and the development of new therap

39 bstacle to understand the pathophysiology of M. ulcerans infection.

40 interval, 68 to 82%) showed the presence of M. ulcerans DNA by PCR.

41 Australian native possums are reservoirs of M. ulcerans and that they shed the bacteria in their fec

42 ationship between possum excreta shedding of M. ulcerans and humans developing BU.

43 nce of a toxin in the culture supernatant of M. ulcerans which causes a cytopathic effect on the mous

44 lipid toxin from the culture supernatant of M. ulcerans which is capable of causing the cytopathic e

45 ure of mycolactone F is identical to that of M. ulcerans mycolactones, but a unique side chain struct

46 s, but the specific route of transmission of M. ulcerans to humans remains unclear.

47 ost detailed field data in space and time on M. ulcerans and Buruli ulcer available today, we assess

48 ycolactone congeners from the human pathogen M. ulcerans, the frog pathogen Mycobacterium liflandii,

49 tients with polymerase chain reaction-proved M. ulcerans infections.

50 of combination antibiotic therapy for small M. ulcerans lesions.

51 For selected small M. ulcerans lesions, 6 weeks may be as effective as 8 we

52 is on cultured cells but is less potent than M. ulcerans mycolactones.

53 Together, these data demonstrate that M. ulcerans infection causes systemic perturbations in t

54 The M. ulcerans genome strain has a deletion in RD1 and lack

55 The M. ulcerans toxin does not cause cell death but instead

56 In contrast to M. ulcerans and conventional M. marinum, mycolactone F-p

57 cobacterium liflandii, is closely related to M. ulcerans and Mycobacterium marinum, and as further ev

58 e as all other mouse strains with respect to M. ulcerans infection, presented a spontaneous healing a

59 ts suggest that the human immune response to M. ulcerans is similar to that seen with some other myco

60 molecule appears so far to be restricted to M. ulcerans.

61 Mycolactone is unique to M. ulcerans and an immunological Ag capture assay would

62 indicate Ae. notoscriptus probably transmit M. ulcerans in southeastern Australia and highlight mosq

63 cterial species isolated from areas in which M. ulcerans infection is endemic.

64 Infection with M. ulcerans results in persistent severe necrosis withou

65 d radiological features in all patients with M. ulcerans infections with bone involvement, identified