[Multilevel tuberculous spondylitis]. / Espondilitis tuberculosa multinivel.

A case of a 20-year-old man with multilevel non-contiguous tuberculous spondylitis (cervical, dorsal 6, dorsal 10 and lumbar) is presented. In the context of disseminated tuberculosis in an HIV-negative patient with serious compromise of his general condition and multiple locations of the disease, some of these with fistulas that secreted caseum. The acute paraplegia led, considering the sensory level at dorsal 6, to a first urgent decompression surgery via the posterior approach. A scheduled surgery was then performed, first in the cervical region via the anterior approach, with corpectomy, placement of a vertebral body replacement plus autologous graft and plate with screws. Subsequently, dislocation of dorsal level 6 was evidenced backwards, compressing the spinal cord and, given the mechanical instability, a third surgical stage was indicated by posterior approach, which included reduction, decompression and fixation, resolving the three levels by posterior approach with bars and screws. The surgical, medical and physiotherapy treatment of this rare form of Pott's disease was successful, with recovery of his mechanical stability and progressive recovery of his neurological status. The surgical, medical and physiotherapy treatment of this rare form of Pott's disease was successful, with recovery of his mechanical stability and progressive recovery of his neurological status.

Se presenta el caso de un varón de 20 años con espondilitis tuberculosa multinivel no contigua (cervical, dorsal 6, dorsal 10 y lumbar). Se trata de un paciente HIV negativo con tuberculosis diseminada con grave compromiso de su estado general y múltiples localizaciones de la enfermedad. Algunas tenían fistulas que secretaban caseum. El paciente presentó paraplejía aguda que requirió, teniendo en cuenta el nivel sensitivo a nivel dorsal 6, una primera cirugía urgente de descompresión por vía posterior. Luego se efectuó la cirugía programada. En primera instancia, la región cervical por vía anterior, con corporectomía, colocación de reemplazo de cuerpo vertebral más injerto autólogo y placa con tornillos. Posteriormente se evidenció luxación del nivel dorsal 6 hacia atrás comprimiendo la médula espinal y, dada la inestabilidad mecánica, se indicó un tercer tiempo quirúrgico por vía posterior que comprendió reducción, descompresión y fijación, resolviendo los tres niveles por vía posterior con barras y tornillos. El tratamiento quirúrgico, médico y kinésico de esta forma poco frecuente del mal de Pott fue exitoso, con recuperación de su estabilidad mecánica y progresiva recuperación de su estado neurológico.

Espondilitis tuberculosa multinivel / Multilevel tuberculous spondylitis

Resumen Se presenta el caso de un varón de 20 años con espondilitis tuberculosa multinivel no contigua (cervical, dorsal 6, dorsal 10 y lumbar). Se trata de un paciente HIV negativo con tuberculosis dise minada con grave compromiso de su estado general y múltiples localizaciones de la enfermedad. Algunas tenían fistulas que secretaban caseum. El paciente presentó paraplejía aguda que requirió, teniendo en cuenta el nivel sensitivo a nivel dorsal 6, una primera cirugía urgente de descompresión por vía posterior. Luego se efectuó la cirugía programada. En primera instancia, la región cervical por vía anterior, con corporectomía, colocación de reemplazo de cuerpo vertebral más injerto autólogo y placa con tornillos. Posteriormente se evidenció luxación del nivel dorsal 6 hacia atrás comprimiendo la médula espinal y, dada la inestabilidad mecánica, se indicó un tercer tiempo quirúrgico por vía posterior que comprendió reducción, descompresión y fijación, resolviendo los tres niveles por vía posterior con barras y tornillos. El tratamiento quirúrgico, médico y kinésico de esta forma poco frecuente del mal de Pott fue exitoso, con recuperación de su estabilidad mecánica y progresiva recuperación de su estado neurológico.

Abstract A case of a 20-year-old man with multilevel non-contiguous tuberculous spondylitis (cervical, dorsal 6, dorsal 10 and lumbar) is presented. In the context of disseminated tuberculosis in an HIV-negative patient with serious compromise of his general condition and multiple locations of the disease, some of these with fistulas that secreted caseum. The acute paraplegia led, considering the sensory level at dorsal 6, to a first urgent decompression surgery via the posterior approach. A scheduled surgery was then performed, first in the cervical region via the anterior approach, with corpectomy, placement of a vertebral body replace ment plus autologous graft and plate with screws. Subsequently, dislocation of dorsal level 6 was evidenced backwards, compressing the spinal cord and, given the mechanical instability, a third surgical stage was indi cated by posterior approach, which included reduction, decompression and fixation, resolving the three levels by posterior approach with bars and screws. The surgical, medical and physiotherapy treatment of this rare form of Pott's disease was successful, with recovery of his mechanical stability and progressive recovery of his neurological status. The surgical, medical and physiotherapy treatment of this rare form of Pott's disease was successful, with recovery of his mechanical stability and progressive recovery of his neurological status.

Restimulation-induced T-cell death through NTB-A/SAP signaling pathway is impaired in tuberculosis patients with depressed immune responses.

Production of IFN-γ contributes to host defense against Mycobacterium tuberculosis (Mtb) infection. We previously demonstrated that Signaling lymphocytic activation molecule-associated protein (SAP) expression on cells from tuberculosis (TB) patients was inversely correlated with IFN-γ production. Here we first investigated the role of NK, T- and B-cell antigen (NTB-A)/SAP pathway in the regulation of Th1 response against Mtb. Upon antigen stimulation, NTB-A phosphorylation rapidly increases and afterwards modulates IFN-γ and IL-17 secretion. To sustain a healthy immune system, controlled expansion and contraction of lymphocytes, both during and after an adaptive immune response, is essential. Besides, restimulation-induced cell death (RICD) results in an essential homeostatic mechanism for precluding excess T-cell accumulation and associated immunopathology during the course of certain infections. Accordingly, we found that the NTB-A/SAP pathway was required for RICD during active tuberculosis. In low responder (LR) TB patients, impaired RICD was associated with diminished FASL levels, IL-2 production and CD25high expression after cell-restimulation. Interestingly, we next observed that SAP mediated the recruitment of the Src-related kinase FYNT, only in T cells from LR TB patients that were resistant to RICD. Together, we showed that the NTB-A/SAP pathway regulates T-cell activation and RICD during human TB. Moreover, the NTB-A/SAP/FYNT axis promotes polarization to an unfavorable Th2-phenotype.

Inusual presentación infecciosa oportunista en pulmón secuelar: reporte de un caso clínico / A Rare Opportunist Infectious Complication in a Lung with Sequelae; Report of a Clinical Case

El aspergiloma se considera la forma clínica más frecuente y mejor reconocida de la aspergilosis pulmonar, que surge como resultado de la colonización por el hongo de una cavidad, quiste o bulla ya existentes, como consecuencia de enfermedades crónicas tales como tuberculosis, bronquiectasias, enfisema bulloso, fibrosis pulmonar o sarcoidosis en estadios avanzados. La presentación de múltiples aspergilomas es infrecuente, lo más común es la presencia de una sola bola fúngica.

Aspergilloma is considered the most common and best known cause of pulmonary aspergillosis, which arises by the fungal colonization of a lung cavity, a cyst or existing bullae resulting from chronic diseases such as tuberculosis, bronchiectasis, bullous emphysema, pulmonary fibrosis and sarcoidosis in advanced stages. The presentation of multiple aspergillomas is infrequent. A single fungal ball-like mass is the most common presentation.

IFNG-mediated immune responses enhance autophagy against Mycobacterium tuberculosis antigens in patients with active tuberculosis.

Protective immunity against Mycobacterium tuberculosis (Mtb) requires IFNG. Besides, IFNG-mediated induction of autophagy suppresses survival of virulent Mtb in macrophage cell lines. We investigated the contribution of autophagy to the defense against Mtb antigen (Mtb-Ag) in cells from tuberculosis patients and healthy donors (HD). Patients were classified as high responders (HR) if their T cells produced significant IFNG against Mtb-Ag; and low responders (LR) when patients showed weak or no T cell responses to Mtb-Ag. The highest autophagy levels were detected in HD cells whereas the lowest quantities were observed in LR patients. Interestingly, upon Mtb-Ag stimulation, we detected a positive correlation between IFNG and MAP1LC3B-II/LC3-II levels. Actually, blockage of Mtb-Ag-induced IFNG markedly reduced autophagy in HR patients whereas addition of limited amounts of IFNG significantly increased autophagy in LR patients. Therefore, autophagy collaborates with human immune responses against Mtb in close association with specific IFNG secreted against the pathogen.

Tuberculosis vulvar: Una rara localización / Vulvar Tuberculosis: A Rare Localization

La tuberculosis vulvar es una rara localización de la enfermedad, que debe incluirse en los diagnósticos diferenciales de lesiones ulcerosas o exofíticas dolorosas a ese nivel. Se presenta el caso de una mujer joven, VIH negativa, con grave compromiso del estado general debido a una tuberculosis diseminada con múltiples localizaciones: pulmonar, renal, genital, intestinal y peritoneal. La cepa de Mycobacterium tuberculosis aislada del esputo, orina y tracto genital fue pansensible y la paciente respondió al tratamiento con drogas de primera línea.

The vulvar tuberculosis is an uncommon localization of tuberculosis, which has to be included in the differential diagnosis of painful vulvar ulcerative or exophytic lesions. This report presents a case of an HIV negative young woman with severe compromise of her health status, due to disseminated tuberculosis with multiple localizations: pulmonary, renal, genital, intestinal and peritoneal manifestations. The strain of Mycobacterium tuberculosis isolated from sputum, urine and the genital tract was susceptible to all the antituberculosis medicaments and the patient responded to treatment with first-line drugs.

CD137 differentially regulates innate and adaptive immunity against Mycobacterium tuberculosis.

Protective immunity against Mycobacterium tuberculosis is primarily mediated by the interaction of antigen-specific T cells and antigen presenting cells, which often depends on the interplay of cytokines produced by these cells. Costimulatory signals represent a complex network of receptor-ligand interactions that qualitatively and quantitatively influence immune responses. Thus, here we investigated the function of CD137 and CD137L, molecules known to have a central role in immune regulation, during human tuberculosis (TB). We demonstrated that M. tuberculosis antigen stimulation increased both CD137 and CD137L expression on monocytes and NK cells from TB patients and healthy donors, but only up-regulated CD137 on T lymphocytes. Blockage of the CD137 pathway enhanced the levels of interferon (IFN)-γ and tumor necrosis factor (TNF)-α produced by monocytes and NK against M. tuberculosis. In contrast, CD137 blockage significantly decreased the specific degranulation of CD8(+) T cells and the percentage of specific IFN-γ and TNF-α producing lymphocytes against the pathogen. Furthermore, inhibition of the CD137 pathway markedly increased T-cell apoptosis. Taken together, our results demonstrate that CD137:CD137L interactions regulate the innate and adaptive immune response of the host against M. tuberculosis.

Síndrome DRESS inducido por fármacos anti tuberculosis / DRESS syndrome induced by anti-tuberculosis drugs

Presentamos cuatro pacientes con tuberculosis pulmonar y reacciones adversas graves a los fármacos antituberculosis. Estos pacientes tuvieron farmacodermia, hepatitis, eosinofilia, fiebre y uno de ellos insuficiencia renal, constituyendo el Síndrome DRESS. Este síndromees una reacción grave de hipersensibilidad a diferentes fármacos. Suele ser producido por los anticonvulsivantes, las sulfonamidas, algunos fármacos antivirales, entre otros. Los fármacos anti tuberculosis también pueden producir este síndrome potencialmente fatal. Se destaca la importancia de la farmacovigilancia para su detección y tratamiento precoz.

We present four patients with pulmonary tuberculosis and severe adverse reactions to antituberculosis drugs. These patients had skin rash, hepatitis, eosinophilia, fever, and oneof them had renal failure; all these signs conform the diagnosis of DRESS syndrome. This syndrome is caused by a severe hypersensitivity reaction to different drugs. It is usually caused by anticonvulsants, sulfonamides, some antiviral drugs, among others drugs.Anti-tuberculosis drugs can also cause this potentially fatal syndrome. The importance of surveillance for early detection and treatment of adverse drug reactions is emphasized.

Mycobacterium tuberculosis impairs dendritic cell response by altering CD1b, DC-SIGN and MR profile.

During a chronic infection such as tuberculosis, the pool of tissue dendritic cells (DC) must be renewed by recruitment of both circulating DC progenitors and monocytes (Mo). However, the microenvironment of the inflammatory site affects Mo differentiation. As DC are critical for initiating a Mycobacterium tuberculosis-specific T-cell response, we argue that interference of M. tuberculosis with a correct DC generation would signify a mechanism of immune evasion. In this study, we showed that early interaction of γ-irradiated M. tuberculosis with Mo subverts DC differentiation in vitro. We found that irradiated M. tuberculosis effect involves (1) the loss of a significant fraction of monocyte population and (2) an altered differentiation process of the surviving monocyte subpopulation. Moreover, in the absence of irradiated M. tuberculosis, DC consist in a major DC-specific intercellular adhesion molecule 3-grabbing non-integrin receptor (DC-SIGN(high))/CD86(low) and minor DC-SIGN(low)/CD86(high) subpopulations, whereas in the presence of bacteria, there is an enrichment of DC-SIGN(low)/CD86(high) population. Besides, this population enlarged by irradiated M. tuberculosis, which is characterized by a reduced CD1b expression, correlates with a reduced induction of specific T-lymphocyte proliferation. The loss of CD1molecules partially involves toll-like receptors (TLR-2)/p38 MAPK activation. Finally, several features of Mo, which have been differentiated into DC in the presence of irradiated M. tuberculosis, resemble the features of DC obtained from patients with active tuberculosis. In conclusion, we suggest that M. tuberculosis escapes from acquired immune response in tuberculosis may be caused by an altered differentiation into DC leading to a poor M. tuberculosis-specific T-cell response.

NK cells from tuberculous pleurisy express high ICAM-1 levels and exert stimulatory effect on local T cells.

Tuberculous pleurisy, one of the most common manifestations of extrapulmonary tuberculosis, is characterized by a T-cell-mediated hypersensitivity reaction along with a Th1 immune profile. In this study, we investigated functional cross-talk among T and NK cells in human tuberculous pleurisy. We found that endogenously activated pleural fluid-derived NK cells express high ICAM-1 levels and induce T-cell activation ex vivo through ICAM-1. Besides, upon in vitro stimulation with monokines and PAMP, resting peripheral blood NK cells increased ICAM-1 expression leading to cellular activation and Th1 polarization of autologous T cells. Furthermore, these effects were abolished by anti-ICAM-1 Ab. Hence, NK cells may contribute to the adaptive immune response by a direct cell-contact-dependent mechanism in the context of Mycobacterium tuberculosis infection.

Spontaneous or Mycobacterium tuberculosis-induced apoptotic neutrophils exert opposite effects on the dendritic cell-mediated immune response.

Polymorphonuclear neutrophils (PMN) modulate the adaptive immune response through interactions with immature dendritic cells (iDC) while spontaneous apoptotic neutrophils PMNapo (PMNapo) may have an inhibitory effect on DC functions. We investigate the effect exerted by PMNapo in DC maturation and the role of Mycobacterium tuberculosis (Mtb)-induced PMNapo in the cross-presentation of mycobacterial antigens. We demonstrate that Mtb triggers the maturation of iDC while it is impaired by the presence of PMNapo, which abrogate Mtb-induced expression of costimulatory and HLA class II molecules, reducing IL-12 and IFN-gamma release by DC and partially inhibiting Mtb-driven lymphocyte proliferation. This inhibitory effect is not observed in already Mtb-matured DC, and it involves a direct interaction between DC and PMNapo, as supernatants from PMNapo cultures do not reveal this effect. Although PMNapo do not alter Mtb/DC-SIGN interaction, they affect the intracellular signals leading to DC maturation without requiring their entry into DC. Phagocytosis of Mtb-induced PMNapo by iDC leads to lymphoproliferation, which is significantly reduced by blocking CD36 and not DC-SIGN on iDC. Therefore, cross-presentation of Mtb antigens is taking place. Our findings suggest that the inflammatory milieu is subjected to a fine balance between non-infected and Mtb-induced PMNapo: non-infected PMNapo limiting inflammation and Mtb-induced PMNapo generating a specific immune activity.

Tratamiento de la tuberculosis: guia practica elaborada por la Seccion Tuberculosis, Asociacion Argentina de Medicina Respiratoria / Tuberculosis treatment: a practical guide elaborated by the Tuberculosis Section, Argentine Association of Respiratory Medicine

La tuberculosis es una enfermedad prevalente en todo el mundo. La emergencia de cepas multirresistentes del Mycobacterium tuberculosis ha incentivado la búsqueda de nuevos fármacos. Existen diversas guías de tratamiento de la enfermedad, internacionales y a nivel programático local. Un grupo de especialistas argentinos elaboró una guía práctica basada en criterios clínicos y en la bibliografía nacional e internacional sobre el tema a través de reuniones de consenso, abarcando tópicos como: fármacos antituberculosos disponibles en la Argentina, modalidades de tratamiento inicial y retratamiento, tratamiento en situaciones especiales, reacciones adversas a fármacos antituberculosos, indicaciones actuales de tratamiento quirúrgico y nuevos fármacos en estudio para el tratamiento de la enfermedad.

Tuberculosis is a worldwide prevalent disease. The emergence of multidrug-resistant strains spurred the search for new drugs. There are several tuberculosis treatment guidelines, international and local in a programmatic approach. An Argentinean specialists panel draw practical guidelines based in clinical criteria and the local and international bibliography through consensus meetings, including issues as: antituberculosis drugs available in Argentina, initial and re-treatement modalities, special situations treatment, adverse reactions to antituberculosis drugs, current indications of surgical treatment and new drugs under study for the treatment of the disease.

Mycobacterium tuberculosis triggers apoptosis in peripheral neutrophils involving toll-like receptor 2 and p38 mitogen protein kinase in tuberculosis patients.

Polymorphonuclear neutrophils (PMN) exposed to Mycobacterium tuberculosis display bactericidal responses and produce inflammatory proteins. This PMN-mediated inflammatory response is regulated by an activation of the apoptotic program, which collaborates to avoid tissue injury. In vitro, circulating PMN from patients with tuberculosis (TB) show an increased spontaneous apoptosis, and M. tuberculosis-induced activation accelerates the PMN apoptosis. In this study, we evaluated the mechanisms involved in spontaneous and M. tuberculosis-induced apoptosis. We demonstrate that apoptosis of PMN is not induced by lipoarabinomannan or by a whole-cell lysate of M. tuberculosis and that neither tumor necrosis factor alpha nor CD11b, CD14, and Fcgamma receptors are involved. Apoptosis of PMN from patients with active TB (TB-PMN) is induced by the interaction with the whole M. tuberculosis via Toll-like receptor 2 (TLR2), and, in contrast to spontaneous apoptosis, it involves the p38 mitogen-activated protein kinase (MAPK) pathway. These results correlate with a high expression of phosphorylated p38 (p-p38) in circulating TB-PMN and with the ability of M. tuberculosis to induce in vitro the expression of p-p38 in PMN. Therefore, when the bacterial burden is low, TB-PMN could be detecting nonopsonized M. tuberculosis via TLR2, leading to the activation of the p38 MAPK pathway, which in turn would induce PMN activation and apoptosis. This mechanism needs further confirmation at the site of infection.

Expression of signaling lymphocytic activation molecule-associated protein interrupts IFN-gamma production in human tuberculosis.

Production of the Th1 cytokine IFN-gamma by T cells is considered crucial for immunity against Mycobacterium tuberculosis infection. We evaluated IFN-gamma production in tuberculosis in the context of signaling molecules known to regulate Th1 cytokines. Two populations of patients who have active tuberculosis were identified, based on their T cell responses to the bacterium. High responder tuberculosis patients displayed significant M. tuberculosis-dependent T cell proliferation and IFN-gamma production, whereas low responder tuberculosis patients displayed weak or no T cell responses to M. tuberculosis. The expression of the signaling lymphocytic activation molecule (SLAM)-associated protein (SAP) on cells from tuberculosis patients was inversely correlated with IFN-gamma production in those individuals. Moreover, patients with a nonfunctional SAP gene displayed immune responses to M. tuberculosis similar to those of high responder tuberculosis patients. In contrast to SAP, T cell expression of SLAM was directly correlated with responsiveness to M. tuberculosis Ag. Our data suggest that expression of SAP interferes with Th1 responses whereas SLAM expression contributes to Th1 cytokine responses in tuberculosis. The study further suggests that SAP and SLAM might be focal points for therapeutic modulation of T cell cytokine responses in tuberculosis.

Tubeculosis generalizada por Mycobacterium Bovis en un paciente inmunocompetente (presentación de un caso y revisión de la bibliografía) / Generalized tuberculosis by Mycobacterium bovis in a immunocompetent patient (case report and bibliographic review)

El Mycobacterium bovis es una variedad del complejo M. tuberculosis que afecta principalmente al ganado vacuno. Raramente puede producir tuberculosis pulmonar y extrapulmonar en el hombre. Presentamos el caso de una paciente de 72 años, con serología negativa para HIV y sin otras evidencias de inmunosupresión que se internó por tuberculosis pulmonar miliar, ósea y cutánea por M. bovis. El diagnóstico se confirmó por el examen directo y cultivo del esputo y la biopsia de piel. Al ingreso presentaba severa afectación de su estado general, pero luego de tres meses de tratamiento antituberculoso su evolución clínica y radiológica fue favorable. Analizamos la incidencia, las características del bacilo y las vías de contagio. Este es un caso poco frecuente de tuberculosis generalizada por M. bovis en un paciente inmunocompetente

Enfermedades intersticiales del pulmón: incidencia, etiología y estrategia diagnóstica en un centro especializado / Interstitial lung diseases: incidence, etiology and diagnostic strategy in a specialized center

Las enfermedades intersticiales del pulmón (EIP) son un grupo muy amplio y heterogéneo de enfermedades que comprometen difusamente el parénquima pulmonar afectando predominantemente al intersticio. Con el objetivo de determinar la incidencia y etiologías de las EIP y conocer la estrategia empleada para llegar al diagnóstico, se revisaron retrospectivamente las historia clínicas (HC) de los pacientes que consultaron por primera vez durante el período 2/1/99 al 30/12/00. Se seleccionaron las que cumplían con uno o más de los criterios aceptados para su diagnóstico. Se evaluó cada método de diagnóstico empleado, clasificándolos en métodos no invasivos (MNI): HC, Rx, TAC de tórax, pruebas de laboratorio y de función pulmonar; y métodos invasivos (MI): lavado broncoalveolar (LBA), biopsia transbronquial (BTB) y biopsia quirúrgica (BQ). De las 4518 HC revisadas, 88 (1,94 por ciento) presentaron EIP. En 67 pacientes (76 por ciento) se llegó a un diagnóstico específico (DE). Las etiologías más frecuentes fueron: TB 16 (18 por ciento), silicosis 14 (16 por ciento), sarcoidosis 8 (9 por ciento) y FPI 6 (6,8 por ciento). Utilizando solamente MNI se obtuvo el diagnóstico en 31 de los 67 pacientes (46 por ciento). En el resto, 36 pacientes (54 por ciento), el diagnóstico se hizo por MNI y MI. El LBA se realizó en la mitad de los casos (44 pacientes). En 13 (30 por ciento) permitió hacer DE y en 31 (70 por ciento) no contribuyó al diagnóstico. La BTB fue realizada en 32 pacientes (36 por ciento). En 9 (28 por ciento) permitió hacer el diagnóstico y en 23 (72 por ciento) no fue útil para el mismo. La BQ se practicó en 5 pacientes (6 por ciento) obteniéndose diagnóstico en 4 (80 por ciento). De los 21 pacientes sin DE, a 10 se le realizaron MI y a pesar de ello, no se pudo obtener el diagnóstico. Conclusiones: La incidencia de EIP fue baja (2 por ciento) si se la compara con otras enfermedades del aparato respiratorio. Las causas más frecuentes fueron: TB y silicosis. Esto podría deberse a que en nuestro hospital se derivan pacientes con estas patologías. En casi la mitad de los pacientes, el DE se realizó sólo por MNI. El rendimiento del LBA y la BTB fue de alrededor de 30 por ciento. En cambio, el de la BQ fue 80 por ciento. En 24 por ciento de los pacientes no pudo obtenerse DE. Esto podría deberse a que la BQ se realizó en sólo 5 pacientes. Recomendamos realizar la BQ con más frecuencia.

Síndrome de inmunodeficiencia adquirida y eosinofilia pulmonar / Acquired immunodeficiency syndrome and pulmonary eosinophilia

La Enfermedad Pulmonar Eosinófila es producida por diferentes patologías, en las cuales hay un aumento de los eosinófilos tisulares y circulantes. Los mecanismos patogénicos, en la mayoría de las causas están pobremente aclarados. Entre los desórdenes que pueden desencadenarla se encuentran hipersensibilidad a drogas; secundaria a enfermedad parasitaria; micosis; vasculitis y otras enfermedades infecciosas como la tuberculosis. También puede acompañar a neoplasias como carcinoma broncogénico y enfermedad de Hodgkin. Se presenta el caso de un paciente de sexo masculino, de 45 años de edad con SIDA y Tuberculosis Pulmonar, que durante el tratamiento desarrolla eosinofilia periférica e infiltrados fugases (periféricos y bilaterales) en la radiografía de tórax. Se concluye que los pacientes con Sida y Tuberculosis, tienen mayor proporción de reacciones adversas a drogas, y que la Tuberculosis puede desencadenar per se una Eosinofilia Pulmonar Simple o Idiopática.