sábado, 27 de julio de 2013

E. Coli Meningitis

E. coli Meningitis Presenting in a Patient with Disseminated Strongyloides stercoralis.


Gomez JB1, Maque Y, Moquillaza MA, Anicama WE.

1Department of Internal Medicine, Guillermo Almenara Irigoyen National Hospital, Lima, Peru.

 

Abstract

Introduction. Spontaneous Escherichia coli meningitis is an infrequent condition in adults and is associated with some predisposing factors, including severe Strongyloides stercoralis (SS) infections. Case Presentation. A 43-year-old Hispanic man, with history of travelling to the jungle regions of Peru and Brazil two decades ago, and who received prednisone due to Bell's palsy for three weeks before admission, presented to the Emergency Department with diarrhea, fever, and hematochezia. A week after admission he developed drowsiness, meningeal signs, abdominal distension, and constipation. A cerebrospinal fluid culture showed extended spectrum β -lactamase producing E. coli. A colonoscopy was performed and showed pancolitis. Three days after the procedure the patient became unstable and developed peritoneal signs. He underwent a laparotomy, which ended up in a total colectomy and partial proctectomy due to toxic megacolon. Three days later the patient died in the intensive care unit due to septic shock. Autopsy was performed and microscopic examination revealed the presence of multiple Strongyloides larvae throughout the body. Conclusion. Strongyloides stercoralis infection should be excluded in adults with spontaneous E. coli meningitis, especially, if gastrointestinal symptoms and history of travelling to an endemic area are present. Even with a proper diagnosis and management, disseminated strongyloidiasis has a poor prognosis. 

Case Rep Infect Dis. 2013;2013:424362. doi: 10.1155/2013/424362. Epub 2013 Nov 13.

http://www.hindawi.com/journals/criid/2013/424362/

Md. MSc. Yvan Maque. Ex-miembro del GII.

Chlamydia trachomatis e Inmunidad

Human female genital tract infection by the obligate intracellular bacterium Chlamydia trachomatis elicits robust Type 2 immunity.


Vicetti Miguel RD1, Harvey SA, LaFramboise WA, Reighard SD, Matthews DB, Cherpes TL.

1Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.

 

Abstract

While Chlamydia trachomatis infections are frequently asymptomatic, mechanisms that regulate host response to this intracellular Gram-negative bacterium remain undefined. This investigation thus used peripheral blood mononuclear cells and endometrial tissue from women with or without Chlamydia genital tract infection to better define this response. Initial genome-wide microarray analysis revealed highly elevated expression of matrix metalloproteinase 10 and other molecules characteristic of Type 2 immunity (e.g., fibrosis and wound repair) in Chlamydia-infected tissue. This result was corroborated in flow cytometry and immunohistochemistry studies that showed extant upper genital tract Chlamydia infection was associated with increased co-expression of CD200 receptor and CD206 (markers of alternative macrophage activation) by endometrial macrophages as well as increased expression of GATA-3 (the transcription factor regulating TH2 differentiation) by endometrial CD4(+) T cells. Also among women with genital tract Chlamydia infection, peripheral CD3(+) CD4(+) and CD3(+) CD4(-) cells that proliferated in response to ex vivo stimulation with inactivated chlamydial antigen secreted significantly more interleukin (IL)-4 than tumor necrosis factor, interferon-γ, or IL-17; findings that repeated in T cells isolated from these same women 1 and 4 months after infection had been eradicated. Our results thus newly reveal that genital infection by an obligate intracellular bacterium induces polarization towards Type 2 immunity, including Chlamydia-specific TH2 development. Based on these findings, we now speculate that Type 2 immunity was selected by evolution as the host response to C. trachomatis in the human female genital tract to control infection and minimize immunopathological damage to vital reproductive structures.

PLoS One. 2013;8(3):e58565. doi: 10.1371/journal.pone.0058565. Epub 2013 Mar 13.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0058565

Md. Rodolfo Vicetti. Ex-miembro del GII.

miércoles, 24 de julio de 2013

Dermatología e Inmunología


Melanocitos en vitíligo y melanoma: una lección
entre autoinmunidad e inmunidad tumoral

  Julio E Valdivia-Silva1, Claudia Ramírez1

1Chemokines Biology Research Laboratory, Instituto de Investigaciones Biomédicas, UNAM, México D.F., México.

ABSTRACT 

Classically, vitiligo has been deined as a skin disease in which melanocytes (MC) are eradicated from lesional epidermis by MC-reactive T cells, as well as other non-immune and immune components, resulting in disiguring loss of pigment. Moreover, the absence or damage on MC has frequently been associated to a major risk to develop skin cancer including melanoma. However, patients with vitiligo have also shown 'non-pigmented' MC in epidermis similar to individuals with albinism, and these cells are apparently conferring resistance of developing melanoma. These seemingly contradictory facts are further complicated because, the MC antigens which are immunologically recognized are shared for both diseases producing fairly different results. An analysis of the similarities and differences between the autoimmunity observed in vitiligo and the tumour immunity observed in melanoma might lead to a better understanding of the MC' roles and the development of new therapies for both diseases. 

Dermatol PerU 2013; vol 23 (3)



Md PhD Julio Valdivia Silva. Fundador del GII