Acute Pulmonary Infection Research Articles

The responses of γδ T-cells against acutePseudomonas aeruginosapulmonary infection in mice via interleukin-17

Interleukin (IL)-17-producing T-lymphocytes play a crucial role in inflammation, yet the potential roles of the cells in acute bacterial pulmonary infection remain unclear. Here, we investigated the role of IL-17-producing γδ T-cells in a mouse model of acute Pseudomonas aeruginosa pulmonary infection. Results showed that augmentation of IL-17, IL-22 and IL-23 was associated with the development of acute bacterial pulmonary infection. However, IL-17 was markedly reduced following the blockade of γδ T-cell activity in vivo. The levels of the chemokines, including granulocyte colony-stimulating factor (G-CSF), keratinocyte chemoattractant (KC), macrophage inflammatory protein-1α (MIP-1) and macrophage inflammatory protein (MIP-2), were also noticeably decreased in the anti-γδ T Cell Receptor(TCR) mice after 8 h infection. Following the depletion of γδ T-cells, the bacterial load was consistently increased. Anti-TCRγδ-treated mice had changes similar to those in the the anti-IL-17-treated mice. The mRNA and protein levels of IL-22 and IL-23, and the mRNA level of RORγt were all markedly decreased in the anti-TCRγδ mice. Overall, our results demonstrated that at the early stage of acute P. aeruginosa pulmonary infection, γδ T-cells are the major source of IL-17 and play a pivotal role in the host immune response and defense against bacteria.

Time course of early histopathological lung changes in an ovine model of acute lung injury and pulmonary infection

ABSTRACTLarge animal models are valuable tools in biological and medical lung research. Despite the existence of established large animal models, the scientific progress requires more detailed description and expansion of established methods. Previously, we established an ovine model of acute lung injury and subsequent bacterial instillation into the lungs. The current study was designed to assess the time course of early lung histopathological alterations in a large animal model. Injury was induced by smoke inhalation and instillation of live Pseudomonas aeruginosa into the lungs. After 4, 8, 12, 18, and 24 hours, respectively, lung tissue was harvested and histopathological changes were evaluated (n = 4 each). Additional four sheep received no injury and only lung tissue was taken. In injured animals, bronchial obstruction score increased over time and was significantly elevated from 12 to 24 hours (P < .05 versus no injury). Inflammation score was significantly increased at 12 and 18 hours (P < .05 versus no injury). Hemorrhage score was increased at 8 and 12 hours (P < .05 versus no injury). Alveolar edema score was significantly higher in injured sheep at 8, 18, and 24 hours (P < .05 each versus no injury). In conclusion, bronchial obstruction and alveolar edema scores significantly increased over time and reached a plateau, while both inflammation and hemorrhage scores were transiently increased peaking around the 12-hour time point. This information improves the understanding of lung histopathological alterations following acute lung injury and pulmonary infection and may help optimizing the timing of study interventions and evaluation time points in future experiments with this model.

Outcomes in critically ill chronic lymphocytic leukemia patients

Although recent studies have demonstrated an improvement in the prognosis of critically ill cancer patients, little is known regarding the prognosis of patients with non-aggressive underlying malignancies. The aims of this study were to assess the prognosis of critically ill patients with chronic lymphocytic leukemia (CLL) and to evaluate risk factors for hospital mortality. In retrospective mono-center cohort study, consecutive adult patients with CLL requiring ICU admission from 1997 to 2008 were included. Sixty-two patients of 67 years (62-75) were included. Median time interval between CLL diagnosis and ICU admission was 6.7 years (2.6-10.8). Nine patients (15 %) had stage C disease at the time of ICU admission, and seven patients (11 %) had Richter syndrome. Most ICU admissions were related to bacterial or fungal pulmonary infections (n = 47; 76 %). ICU, in-hospital, and 90-day mortality were 35 % (n = 22), 42 % (n = 26), and 58 % (n = 36), respectively. Only three factors were independently associated with in-hospital mortality: oxygen saturation lower than 95 % when breathing room air (odds ratio (OR) 5.80; 95 % confidence interval (CI) 1.23-27.33), need for vasopressors (OR 27.94; 95 % CI 5.37-145.4), and past history of infection (OR 6.62; 95 % CI 1.34-32.68). The final model did not change when disease-related variables (Binet classification, Richter syndrome, long-term steroids) or treatment-related variables (fludarabine, rituximab, or alemtuzumab) were included. Acute pulmonary infections remain the leading cause of ICU admission in patients with CLL. The severity at ICU admission and past history of infection were the only factors associated with hospital mortality. Neither disease characteristics nor previous cancer treatments were associated with outcome.

Lipocalin 2 Regulates Inflammation during Pulmonary Mycobacterial Infections

Pulmonary tuberculosis (TB), caused by the intracellular bacteria Mycobacterium tuberculosis, is a worldwide disease that continues to kill more than 1.5 million people every year worldwide. The accumulation of lymphocytes mediates the formation of the tubercle granuloma in the lung and is crucial for host protection against M.tuberculosis infection. However, paradoxically the tubercle granuloma is also the basis for the immunopathology associated with the disease and very little is known about the regulatory mechanisms that constrain the inflammation associated with the granulomas. Lipocalin 2 (Lcn2) is a member of the lipocalin family of proteins and binds to bacterial siderophores thereby sequestering iron required for bacterial growth. Thus far, it is not known whether Lcn2 plays a role in the inflammatory response to mycobacterial pulmonary infections. In the present study, using models of acute and chronic mycobacterial pulmonary infections, we reveal a novel role for Lcn2 in constraining T cell lymphocytic accumulation and inflammation by inhibiting inflammatory chemokines, such as CXCL9. In contrast, Lcn2 promotes neutrophil recruitment during mycobacterial pulmonary infection, by inducing G-CSF and KC in alveolar macrophages. Importantly, despite a common role for Lcn2 in regulating chemokines during mycobacterial pulmonary infections, Lcn2 deficient mice are more susceptible to acute M.bovis BCG, but not low dose M.tuberculosis pulmonary infection.

Electrophysiological and motor function scale association in a pre-symptomatic infant with spinal muscular atrophy type I

A term infant, at familial risk for spinal muscular atrophy (SMA), had the diagnosis genetically confirmed on day 3 of life. Clinical evaluation, the CHOP INTEND motor scale and the CMAP amplitude were obtained on days 5 (pre-symptomatic), 20 (mildly weak), 34 (moderately weak) and 63 (severely weak). Palliative care was provided and he expired of an acute pulmonary infection on day 81. The CMAP amplitude and INTEND scores were initially in the normal range, then followed a corresponding decline to a nadir at day 34 and remained so at the 4th assessment. A log-transformed plot of CMAP amplitude from days 5-34 was linear. These data suggest that early motor neuron loss in SMA type I may be logarithmic and demonstrates that the INTEND motor scale closely follows the CMAP electrophysiological biomarker. This single case report supports the consideration that early intervention with a potential therapy is necessary, before the pool of functional motor neurons has plummeted. Further study of these parameters in pre-symptomatic infants with SMA type I will help guide the design of future intervention studies.

Extracellular Superoxide Dismutase Promotes Phagocytosis During Acute Pulmonary Infection

Extracellular Superoxide Dismutase Promotes Phagocytosis During Acute Pulmonary Infection

Syndrome de MacLeod et pneumothorax : une source d’erreur diagnostique et thérapeutique

MacLeod syndrome, also known as Swyer-James syndrome, is a rare syndrome characterized by unilateral lung hyperlucency. It is a form of constrictive bronchiolitis which is caused by repeated acute bronchiolitis and/or pulmonary infections during infancy. The patient was a 26-year-old man who had had a first left pneumothorax at the age of 21. He smokes tobacco. When he was 1-year-old he had experienced repeated episodes of acute bronchiolitis. At age 26, he suffered from a second left pneumothorax which was wrongly diagnosed as a recurrent drain-resistant pneumothorax. Misdiagnosed, he underwent a chemical pleurodesis during thoracoscopy. As a hyperlucency remained in the left upper part of the lung on chest X-ray, further investigations were undertaken and a diagnosis of MacLeod syndrome was made. MacLeod syndrome is rare. It can be associated with pneumothorax which can be a source of misdiagnosis and error in the management of these patients. Therefore, the diagnostic criteria and therapeutic indications are reiterated. The probable mechanism of association between pneumothorax and Macleod syndrome is also discussed.

Effect of Linezolid on the 50% Lethal Dose and 50% Protective Dose in Treatment of Infections by Gram-Negative Pathogens in Naive and Immunosuppressed Mice and on the Efficacy of Ciprofloxacin in an Acute Murine Model of Septicemia

Murine models of infection were used to study the effect of linezolid on the virulence of Gram-negative bacteria and to assess potential pharmacodynamic interactions with ciprofloxacin in the treatment of these infections, prompted by observations from a recent clinical trial. Naive and immunosuppressed mice were challenged with Klebsiella pneumoniae 53A1109, K. pneumoniae GC6658, and Pseudomonas aeruginosa UC12120 in acute sepsis and pulmonary infection models, using different serial dilutions of these pathogens (groups of 8 animals each). Linezolid (100 mg/kg/dose) was administered orally at 0.5 and 4.0 h postchallenge in the sepsis model and at 4 h postchallenge followed by 2 days of twice-daily treatment in the pulmonary model. Further, ciprofloxacin alone and in combination with oral linezolid was investigated in the sepsis model. Survival was assessed for 4 and 10 days postchallenge in the systemic and respiratory models, respectively. The data were fitted to a nonlinear regression analysis to determine 50% lethal doses (LD(50)s) and 50% protective doses (PD(50)s). A clinically relevant, high-dose regimen of linezolid had no significant effect on LD(50) in these models. This lack of effect was independent of immune status. A combination of oral ciprofloxacin with linezolid yielded lower PD(50)s than oral ciprofloxacin alone (ciprofloxacin in combination, 8.4 to 32.7 mg/kg; oral ciprofloxacin, 39.4 to 88.3 mg/kg). Linezolid did not improve the efficacy of subcutaneous ciprofloxacin (ciprofloxacin in combination, 2.0 to 2.4 mg/kg; subcutaneous ciprofloxacin, 2.0 to 2.8 mg/kg). In conclusion, linezolid does not seem to potentiate infections caused by Gram-negative pathogens or to interact antagonistically with ciprofloxacin.

Nicotinamide nucleotide transhydrogenase (NNT) acts as a novel modulator of macrophage inflammatory responses

Nicotinamide nucleotide transhydrogenase (NNT) is a mitochondrial redox-driven proton pump that couples the production of NADPH to the mitochondrial metabolic rate. In this study, we demonstrated for the first time that NNT has a significant effect in the modulation of the immune response and host defense against pathogens. We found that NNT mRNA is enriched in immune system-related tissues and regulated during macrophage activation. Overexpression of NNT in a macrophage cell-line resulted in decreased levels of reactive oxygen species (ROS) and nitric oxide upon induction of the macrophage inflammatory responses. These cells failed to fully activate MAPK signaling pathways, resulting in defective secretion of proinflammatory cytokines in response to LPS, and were inefficient in clearance of intracellular bacteria. We have shown that C57BL/6J mice, which have a deletion in the Nnt gene, exhibited greater resistance to acute pulmonary infection with Streptococcus pneumoniae. Macrophages from these mice generated more ROS and established a stronger inflammatory response to this pathogen. Our results demonstrate a novel role for NNT as a regulator of macrophage-mediated inflammatory responses.

Venlafaxin-induziertes Syndrom der inadäquaten ADH-Sekretion (SIADH) - Therapie mit Tolvaptan

A 74-year-old woman with known COPD was admitted to hospital because of dyspnoa. Clinical and laboratory tests showed an acute pulmonary infection which was treated with antibiotics. Additionally she was found to have a moderately severe episode of depression for which she had the preceding three weeks been treated with venlafaxine, a selective serotonin re-uptake inhibitor. During the subsequent days she gradually developed a hyponatremia with serum sodium levels down to 108 mmol/l. After excluding common causes of hyponatremia such as a cerebral or pulmonal malignancy or endocrine disorders by computed thomography and laboratory tests, a venlafaxine induced syndrome of inappropriate ADH secretion (SIADH) was assumed to be the cause of the hyponatremia. As neither discontinuation of venlafaxine nor strict fluid restriction led to a rise in the natrium level and the patient had a generalized seizure, oral treatment with the tolavaptan, a vasopressin-2-receptor antagonist, was initiated. This resulted within 48 hours in a rise of the sodium level to 131 mmol/l and there were no further seizures. Hyponatremia is a relatively common side effect of medical treatment with SSRI or SSNRI in elderly patients. The therapy of choice in case of a hyponatremia due to a SIADH is to discontinue the antidepressive drugs and institute strict fluid restriction. Tolvaptan has recently emerged as a promising new therapeutic option for SIADH.

Disseminated cutaneous histoplasmosis in an immunocompetent adult

Histoplasmosis, a systemic mycosis caused by the dimorphic fungus Histoplasma capsulatum var capsulatum and Histoplasma capsulatum var duboisii is endemic to many parts of the world. The clinical manifestations range from acute or chronic pulmonary infection to a progressive disseminated disease. After initial exposure to the fungus, the infection is self-limited and restricted to the lungs in 99% of healthy individuals. The remaining 1%, however, progress to either disseminated or chronic disease involving the lungs, liver, spleen, lymph nodes, bone marrow or rarely, the skin and mucous membranes. Mucocutaneous histoplasmosis is frequently reported in patients with acquired immune deficiency syndrome (AIDS), but it is rare in immunocompetent hosts. A 60-year-old male presented with asymptomatic swelling of the hard palate and crusted papules and nodules over the extremities, face and trunk. Clinically, the diagnoses of cutaneous cryptococcosis versus histoplasmosis was considered in this patient. A chest X-ray revealed hilar lymphadenopathy. Enzyme-linked immunosorbent assay (ELISA) for human immunodeficiency virus (HIV) was nonreactive. Skin biopsy revealed multiple tiny intracellular round yeast forms with a halo in the mid-dermis. Culture of the skin biopsy in Sabouraud's dextrose agar showed colonies of Histoplasma capsulatum. Despite an investigation including no evidence of underlying immunosuppression was found, he was started on IV amphotericin-B (0.5 mg/kg/day). However, the patient succumbed to his disease 2 days after presentation. We report a rare case of disseminated cutaneous histoplasmosis in an immunocompetent individual.

Wheeze in Preschool Age Is Associated with Pulmonary Bacterial Infection and Resolves after Antibiotic Therapy

BackgroundNeonates with airways colonized by Haemophilus influenzae, Streptococcus pneumoniae or Moraxella catarrhalis are at increased risk for recurrent wheeze which may resemble asthma early in life. It is not clear whether chronic colonization by these pathogens is causative for severe persistent wheeze in some preschool children and whether these children might benefit from antibiotic treatment. We assessed the relevance of bacterial colonization and chronic airway infection in preschool children with severe persistent wheezing and evaluated the outcome of long-time antibiotic treatment on the clinical course in such children.Methodology/Principal FindingsPreschool children (n = 42) with severe persistent wheeze but no symptoms of acute pulmonary infection were investigated by bronchoscopy and bronchoalveolar lavage (BAL). Differential cell counts and microbiological and virological analyses were performed on BAL samples. Patients diagnosed with bacterial infection were treated with antibiotics for 2–16 weeks (n = 29). A modified ISAAC questionnaire was used for follow-up assessment of children at least 6 months after bronchoscopy. Of the 42 children with severe wheezing, 34 (81%) showed a neutrophilic inflammation and 20 (59%) of this subgroup had elevated bacterial counts (≥104 colony forming units per milliliter) suggesting infection. Haemophilus influenzae, Streptococcus pneumoniae and Moraxella catarrhalis were the most frequently isolated species. After treatment with appropriate antibiotics 92% of patients showed a marked improvement of symptoms upon follow-up examination.Conclusions/SignificanceChronic bacterial infections are relevant in a subgroup of preschool children with persistent wheezing and such children benefit significantly from antibiotic therapy.

Interleukin-23-Mediated Inflammation in Pseudomonas aeruginosa Pulmonary Infection

Pseudomonas aeruginosa is an opportunistic pathogen that is capable of causing acute and chronic pulmonary infection in the immunocompromised host. In the case of cystic fibrosis (CF), chronic P. aeruginosa infection causes increased mortality by promoting overly exuberant airway inflammation and cumulative lung damage. Identifying the key regulators of this inflammation may lead to the development of new therapies that improve P. aeruginosa-related mortality. We report here that interleukin-23 (IL-23), the cytokine most clearly tied to IL-17-mediated inflammation, also promotes IL-17-independent inflammation during P. aeruginosa pulmonary infection. During the early innate immune response, prior to IL-17 induction, IL-23 acts synergistically with IL-1β to promote early neutrophil (polymorphonuclear leukocyte [PMN]) recruitment. However, at later time points, IL-23 also promoted IL-17 production by lung γδ T cells, which was greatly augmented in the presence of IL-1β. These studies show that IL-23 controls two independent phases of neutrophil recruitment in response to P. aeruginosa infection: early PMN emigration that is IL-17 independent and later PMN emigration regulated by IL-17.

Journal Scan: Benzodiazepines Reduce Ketamine-Related Emergence Reactions in Adults

Journal Scan: Benzodiazepines Reduce Ketamine-Related Emergence Reactions in Adults

Acute pulmonary oedema in chronic dialysis patients admitted into an intensive care unit

Acute pulmonary oedema (APO) in patients undergoing chronic dialysis (CD), a common cause of hospital admission in this population, is poorly documented. The objective of this study was to determine the causes, profile, clinical course and outcomes of APO in CD patients admitted in an intensive care unit (ICU). Medical charts of all CD patients consecutively admitted for APO in the renal ICU of the Tenon Hospital (Paris, France) between January 2000 and December 2007 were considered. Data collection included patient characteristics, etiologic factors for chronic renal failure and co-morbidities, past history of APO, precipitating factors, clinical evolution and outcomes. Of the 112 files considered, 102 (65% men) were included in the final analysis. Patients were aged 20-88 years and had been dialysed for a median duration of 2 years. Hypertension (36.3%), chronic glomerulonephritis (25.5%) and diabetes mellitus (17.6%) were the main etiologic factors of chronic renal failure; 38.2% had a past history of APO. Acute pulmonary infection (26%), excessive interdialytic weight gain (25%) and inappropriate dry weight prescription (23%) were the leading causes of APO. The duration of hospitalization was <4 days in 60% of participants. Nine deaths (four being of cardiac origin) were recorded. Being referred from another hospital service was the main predictor of death. APO fuelled in part by chest infection, excessive interdialytic weight gain and inappropriate dry weight are important causes of hospitalization in CD patients. Mortality is high among those referred from other services usually in critical conditions.

Protective Immunity against Experimental Pulmonary Cryptococcosis in T Cell-Depleted Mice

Individuals with defects in T cell-mediated immunity (CMI) are highly susceptible to infection with Cryptococcus neoformans. The purpose of these studies was to determine if protection against experimental pulmonary cryptococcosis can be generated in T cell-deficient hosts. BALB/c mice were depleted of CD4⁺and/or CD8⁺ T cells or given an isotype control antibody prior to vaccination with a C. neoformans strain, designated H99γ, previously shown to induce protection against C. neoformans infection in immunocompetent mice. Mice depleted of CD4⁺ or CD8⁺ T cells, but not both subsets, survived an acute pulmonary infection with C. neoformans strain H99γ and a subsequent second challenge with wild-type C. neoformans strain H99. We observed a significant increase in the percentage of CD4⁺ and CD8⁺ T cells expressing the activation marker CD69 in the lungs of mice immunized with C. neoformans strain H99γ prior to a secondary challenge with wild-type cryptococci. CD4⁺ T cells within the lungs of immunized mice also appeared to acquire a predominantly activated effector memory cell phenotype (CD69⁺ CD44⁺ CCR7⁻ CD45RB⁻ CD62L⁻) following a second pulmonary challenge with wild-type C. neoformans, compared to CD4⁺ T cells from naïve mice. Lastly, immunization of immunocompetent mice with C. neoformans strain H99γ prior to depletion of CD4⁺ and/or CD8⁺ T cells resulted in significant protection against a second challenge with wild-type C. neoformans. Our studies demonstrate that protective immunity against pulmonary cryptococcosis can be generated in immunosuppressed hosts, thus supporting the development of cryptococcal vaccines.

Pulmonary Complications of Endocrine and Metabolic Disorders

There are many important respiratory manifestations of endocrine and metabolic diseases in children. Acute and chronic pulmonary infections are the most common respiratory abnormalities in patients with diabetes mellitus, although cardiogenic and non-cardiogenic pulmonary oedema are also possible. Pseudohypoaldosteronism type 1 may be indistinguishable from cystic fibrosis (CF) unless serum aldosterone, plasma renin activity, and urinary electrolytes are measured and mutation analysis rules out CF. Hypo- and hyperthyroidism may alter lung function and affect the central respiratory drive. The thyroid hormone plays an essential role in lung development, surfactant synthesis, and lung defence. Complications of hypoparathyroidism are largely due to hypocalcaemia. Laryngospasm can lead to stridor and airway obstruction. Ovarian tumours, benign or malignant, may present with unilateral or bilateral pleural effusions. Metabolic storage disorders, primarily as a consequence of lysosomal dysfunction from enzymatic deficiencies, constitute a diverse group of rare conditions that can have profound effects on the respiratory system.

Legionella Pneumophila Transcriptome during Intracellular Multiplication in Human Macrophages

Legionella pneumophila is the causative agent of Legionnaires’ disease, an acute pulmonary infection. L. pneumophila is able to infect and multiply in both phagocytic protozoa, such as Acanthamoeba castellanii, and mammalian professional phagocytes. The best-known L. pneumophila virulence determinant is the Icm/Dot type IVB secretion system, which is used to translocate more than 150 effector proteins into host cells. While the transcriptional response of Legionella to the intracellular environment of A. castellanii has been investigated, much less is known about the Legionella transcriptional response inside human macrophages. In this study, the transcriptome of L. pneumophila was monitored during exponential and post-exponential phase in rich AYE broth as well as during infection of human cultured macrophages. This was accomplished with microarrays and an RNA amplification procedure called selective capture of transcribed sequences to detect small amounts of mRNA from low numbers of intracellular bacteria. Among the genes induced intracellularly are those involved in amino acid biosynthetic pathways leading to l-arginine, l-histidine, and l-proline as well as many transport systems involved in amino acid and iron uptake. Genes involved in catabolism of glycerol are also induced during intracellular growth, suggesting that glycerol could be used as a carbon source. The genes encoding the Icm/Dot system are not differentially expressed inside cells compared to control bacteria grown in rich broth, but the genes encoding several translocated effectors are strongly induced. Moreover, we used the transcriptome data to predict previously unrecognized Icm/Dot effector genes based on their expression pattern and confirmed translocation for three candidates. This study provides a comprehensive view of how L. pneumophila responds to the human macrophage intracellular environment.

Acute Lung Inflammation in Klebsiella pneumoniae B5055-Induced Pneumonia and Sepsis in BALB/c Mice: A Comparative Study

Lungs play an important role in the body's defense against a variety of pathogens, but this network of immune system-mediated defense can be deregulated during acute pulmonary infections. The present study compares acute lung inflammation occurring during Klebsiella pneumoniae B5055-induced pneumonia and sepsis in BALB/c mice. Pneumonia was induced by intranasal instillation of bacteria (10(4) cfu), while sepsis was developed by placing the fibrin-thrombin clot containing known amount of bacteria (10(2) cfu) into the peritoneal cavity of animals. Mice with sepsis showed 100% mortality within five post-infection days, whereas all the animals with pneumonia survived. In animals suffering from K. pneumoniae B5055-induced pneumonia, all the inflammatory parameters (TNF-α, IL-1α, MPO, MDA, and NO) were found to be maximum till third post-infection day, after that, a decline was observed, whereas in septic animals, all the above-mentioned markers of inflammation kept on increasing. Histopathological study showed presence of alternatively activated alveolar macrophages (or foam cells) in lungs of mice with pneumonia after third post-infection day, which might have contributed to the induction of resolution of inflammation, but no such observation was made in lungs of septic mice. Hence, during pneumonia, controlled activation of macrophages may lead to resolution of inflammation.

Postinfectious bronchiolitis obliterans in children: Clinical and pulmonary function findings

Postinfectious bronchiolitis obliterans (PIBO) is an infrequent yet potentially severe disorder following acute lower pulmonary infection (ALRI) in children. In infants and young children PIBO have been strongly associated with Adenovirus (Ad). The purpose of this study was to analyze the clinical features and pulmonary function findings in children with PIBO. Cases caused by Ad were compared with cases in which no viral agent was identified. Fifty-eight children with PIBO were prospectively studied. Clinical data and pulmonary function tests (spirometry and plethysmography) were evaluated. Patients were divided in two groups according to the identification of the causal agent. Group 1 (G1): Adenovirus (+) Group 2: No etiologic agent identified. Fifty-eight patients (male/female ratio 3.4:1); median age 8 years; mean age at initial injury 11 months; median time of hospitalization at acute stage of disease 60 days. Spirometry: FVC 68 ± 13%, FEV1 40.5 ± 11%, FMMF(25-75%) 16.7 ± 7.5%. Pletysmography: TLC 136 ± 22%, FRC 208 ± 50%, RV 343 ± 102%, RV/TLC 59 ± 10, SGaw 0.05 ± 0.02. When clinical, spirometric and plethysmographic data were compared, no statistically significant difference was found between the two groups. PIBO is an extremely crippling lung disease with significant obstructive pattern in PFT. Both analyzed groups shared similar characteristics in the acute phase of the disease and in the severity of the sequelar pulmonary disease.