M. pneumoniae – F.I.G.H.T for your health! http://lymebook.com/fight Linda Heming describes her Lyme disease healing journey Wed, 06 Nov 2013 05:54:37 +0000 en-US hourly 1 https://wordpress.org/?v=4.9.25 Do infections trigger juvenile idiopathic arthritis? http://lymebook.com/fight/do-infections-trigger-juvenile-idiopathic-arthritis/ http://lymebook.com/fight/do-infections-trigger-juvenile-idiopathic-arthritis/#respond Tue, 22 Dec 2009 07:01:04 +0000 http://lymebook.com/fight/?p=697 Microbiology and Clinical Microbiology Department, Cerrahpasa Medical
Faculty, Istanbul University, Kocamustafapasa, 34303, Istanbul, Turkey.

Juvenile idiopathic arthritis (JIA) is a disease that was prominent with
increased inflammation response in immune system, appeared mostly with
peripheral arthritis and endogenous and exogenous antigens play a role
in the pathogenesis of disease. Two major reasons were thinking to be
considerably important. First of them is immunological predisposition
and the second one is environmental factors.

Infections are considered to be the most important between environmental factors but also stress and trauma are also important in the etiology of the disease. However,
the relation between JIA and infections is not clearly defined but the
relation between adult chronic arthritis and infections was
well-defined. A total of 70 patients, 26 with primer JIA, 20 with
recurrent JIA, 24 healthy control were included in this study.
Mycoplasma pneumoniae, Chlamydophila pneumoniae and C. Jejuni were
detected in 4, 1 and 1 of 10 (38.46%) patients with primer JIA,
respectively. Salmonella enteritidis, EBV, M. pneumoniae, C. jejuni and
Borrelia burgdorferi were detected in 1, 2, 2, 2, and 1 of the 8(40%)
patients with recurrent JIA, respectively. S. enteritidis were isolated
in feces culture and also identified by agglutination method. Infection
was detected in total 18 (39.13%) of patient groups. C. pneumoniae and
C. jejuni were detected in 1 and 1 of 2(8.33) healthy control groups,
respectively. Throat culture positivity was not detected in any of the
patient and healthy control groups. In conclusion, etiopathogenesis of
JIA is not clearly understood and suggested that various factors can
trigger the disease and it is the most common rheumatoid disease of
childhood. However, there are some studies focusing especially on one
infectious agent but this is the first study including such a big range
of infectious agents in the literature for the microorganisms that can
be suggested to have a role in the etiopathogenesis of JIA. We have a
conclusion in the light of our results and suggest that some
microorganisms can trigger and increase the intensity of clinical
situation according to the case. When we evaluate the primer and
recurrent JIA groups; M. pneumoniae and C. jejuni come forward and seen
common in JIA cases. We also suggest that the pre-diagnosis of
microorganisms, which can play a role as primarily or by intervening in
the etiopathogenesis of JIA and adding specific antimicrobial therapy to
the standard JIA therapy, it is possible to perform new, extended,
especially molecular based serial case studies.

PMID: 20012631 [PubMed – as supplied by publisher]

Rheumatol Int.. [Epub ahead of print]

Do infections trigger juvenile idiopathic arthritis?

Aslan M, Kasapcopur O, Yasar H, Polat E, Saribas S, Cakan H, Dirican A,
Torun MM, Ar?soy N, Kocazeybek B.

Microbiology and Clinical Microbiology Department, Cerrahpasa Medical
Faculty, Istanbul University, Kocamustafapasa, 34303, Istanbul, Turkey.

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Association of Mycoplasmal Infections with Malignant Progression, Relapse and Stage in Breast Cancer http://lymebook.com/fight/association-of-mycoplasmal-infections-with-malignant-progression-relapse-and-stage-in-breast-cancer/ http://lymebook.com/fight/association-of-mycoplasmal-infections-with-malignant-progression-relapse-and-stage-in-breast-cancer/#respond Mon, 16 Nov 2009 06:02:26 +0000 http://lymebook.com/fight/?p=450 Association of Mycoplasmal Infections with Malignant Progression, Relapse and Stage in Breast Cancer Patients

Intracellular bacterial infections have historically been proposed as a cause of cancer [1,2].  Although bacterial involvement in malignant transformation and its reversal with antibiotic treatment have been demonstrated in animal models [3], there are few examples of direct involvement of bacteria in clinical transformation of malignant cells [4].  It seems more likely that the release of Reactive Oxygen Species (ROS) and other genotoxic molecules by intracellular bacteria play a role in progression to malignancy rather than the inception of cancer or transformation [5].  Reports in the literature indicate that over one-half of ovarian cancer patients have mycoplasmal infections in their tumors [6], and the incidence of infection in ovarian cancer was related to stage and survival [7].  Some results have been questioned on the basis of contamination in tissue culture [8], but most studies did not use culture procedures.  Therefore, we examined breast cancer patients to determine if there was a relationship between systemic mycoplasmal infections and progression of their breast cancers.  Examination of breast cancer patients showed mycoplasmal infections inside blood leukocytes (~50%+) not blood plasma or serum.  The most common species found were M. fermentans, M. pneumoniae and M. genitalium.  In contrast, in healthy adults the incidence of these species was low [9].  We found an association between stage, progression (measured by relapse after surgery) and presence of mycoplasmal infection(s) (P<0.001) in breast cancer.  The results suggest that intracellular mycoplasmal infections known to be associated with malignant progression are significantly related to progression and relapse due to metastasis of breast cancer.

Prof. Garth L. Nicolson

American Academy of Environmental Medicine 2005 Annual Meeting

The Institute for Molecular Medicine, Email: gnicolson@immed.org

 References
 1. Nuzum JW. Surg Gynecol Obstet 1925; 11:343-353.

2. Plata et al. J Infect Dis 1973; 128:588-598

3. Tsai et al. PNAS 1995; 92:10197-10201.

4. Feng et al. Mol Cell Biol 1999; 19:7995-8002.

5. Nicolson GL. JANA 2003; 6(3):22-28.

6. Chan et al. Gynecol Oncol. 1996; 63(2):258-260.

7. Camolai N. Can J Microbiol 2001; 47(8):691-697.

8. Quirk et al. Gynecol Oncol. 2001; 83(3):560-562.

9. Nicolson  et al.  J Chronic Fatigue Syndr 2000; 6(3):23-39.

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