Clinicopathological findings of four cases of pure influenza virus A pneumonia.

OBJECTIVE: The purpose of this study was to perform clinicopathological evaluations of patients with pure influenza A virus pneumonia. METHODS: We performed clinicopathological analyses of four cases of pure influenza A virus pneumonia. Patients Among the four cases, three were caused by the pandemic (H1N1) 2009 virus. Three patients were analyzed during autopsy, and one underwent transbronchial lung biopsy. RESULTS: We suggest that the interval between influenza virus A pneumonia onset and our analysis affected the pathological findings. Diffuse alveolar damage was observed during the acute phase. After ten days, organizing pneumonia and marked proliferation of premature type II alveolar epithelium were observed. Clinically, intra-alveolar hemorrhage was observed in two patients. Pathologically, hyaline membrane formation and intra-alveolar hemorrhage were observed in all cases. CONCLUSION: Severe epithelial damage was determined as the main mechanism of respiratory failure caused by influenza A virus pneumonia.

Immunohistochemical findings of an autopsied lung specimen from a patient with pandemic influenza (A/H1N1pdm) virus infection.

A 24-year-old female presented with fever and dry cough. Influenza A virus infection was suspected and the patient was treated with neuraminidase inhibitors. Five days after diagnosis, the patient developed persistent fever and dyspnea, and was diagnosed with severe pneumonia. Despite intensive treatment, the pneumonia worsened and the patient died 14 days after admission. At autopsy, a diffuse alveolar damage (DAD) pattern was observed. Immunohistochemical evaluation indicated severe epithelial damage, resulting in successive regeneration of alveolar type II cells followed by marked proliferation of smooth muscle cells and an increase of collagen fibers at the tip of alveolar orifices.

Necrotizing fasciitis caused by Pseudomonas aeruginosa.

An 85-year-old man patient was admitted to the hospital complaining of fever and bilateral leg pain with swelling and erythema. A laboratory investigation revealed leukocytopenia, thus suggesting sepsis. Gram negative rods were detected in the specimen from the affected skin and empiric antibacterial therapy was initiated. The following day, his symptoms worsened and Pseudomonas aeruginosa was isolated from the blood culture and the skin specimen. Magnetic resonance imaging (MRI) did not show the typical characteristics of necrotizing fasciitis. In spite of intensive medical treatment, the patient's condition became critical, and on day 10 after admission, he died of multiple organ failure. An autopsy revealed necrotizing fasciitis due to P. aeruginosa. This is a rare case and its clinical presentation was atypical. The clinical diagnosis of this infection may be difficult, and therefore such cases warrant the careful attention of physicians.

Intravenous ciprofloxacin versus erythromycin in the treatment of Legionella pneumonia.

BACKGROUND: Erythromycin (EM) and rifampicin (RFP) have mainly been used to treat patients with Legionella pneumonia. Since intravenous ciprofloxacin (CPFX) became available in Japan from 2000, many reports have been published detailing successful treatment of Legionella pneumonia with CPFX. In this study, we compared the evolution of patients with Legionella pneumonia treated with CPFX to those treated with EM. METHODS: The study included nine patients treated with CPFX and eighteen patients treated with EM. Diagnosis of these patients was made by culture, PCR, urinary antigen assay or a serological method. A comparison was made of the patients' characteristics, severity of pneumonia, efficacy of each agent and the clinical course. RESULTS: No significant differences were observed between the two groups, in regard to age, gender, underlying disease or severity of pneumonia. In addition, the period of time from onset of the disease until appropriate therapy did not differ significantly between the two groups. In the CPFX group, all of the patients were cured and in the EM group 16 out of the 18 patients were cured. Although there were no significant differences, the time to apyrexia, normalization of leukocytosis and a 50% decrease in C-reactive protein (CRP) occurred within a relatively shorter time frame in the CPFX group than in the EM group (3.5 versus 4 days, 4 versus 5.2 days, and 2.9 versus 10.3 days, respectively). And, the duration of antibiotic treatment in the CPFX group was significantly shorter than in the EM group. CONCLUSION: CPFX was as effective as erythromycin in the treatment of Legionella pneumonia. The effects of treatment may appear relatively earlier and the duration of treatment was significantly shorter in patients treated with CPFX therapy than with EM therapy.

[A case of acute eosinophilic pneumonia that developed after changing cigarette brands].

A 20-year-old man visited a clinic with high fever and a dyspnea. The chest X-ray film and CT showed multiple patchy ground glass opacities in all lung fields with thickened interlobular septa and bilateral pleural effusions. Examination of bronchoalveolar lavage fluid led to a diagnosis of acute eosinophilic pneumonia. The patient was a current smoker and he had changed the brand of cigarette he smoked from one with a filter to another brand without filter, one week before disease onset. His symptoms improved after the administration of methylprednisolone. This case suggested that the presence of a filter or a difference in ingredients, or both, between brands of cigarette might contribute to the development of acute eosinophilic pneumonia.

Elsberg syndrome with eosinophilic meningoencephalitis caused by Angiostrongylus cantonensis.

A 42-year-old man was admitted to our hospital with a history of fever, headache and disorientation. His cerebrospinal fluid revealed eosinophilia and his serum had an antibody against Angiostrongylus cantonensis (A. cantonensis). Then, he was diagnosed as eosinophilic meningoencephalitis caused by A. cantonensis. He was treated with repeated lumbar punctures and oral prednisolone. Although a symptom he had been suffering from at the time of his admission was urinary retention, this symptom disappeared as his general condition improved. Therefore his case was considered to be Elsberg syndrome with eosinophilic meningoencephalitis caused by A. cantonensis.

[A case of multisystem Langerhans' cell histiocytosis with lung deterioration over 15 years].

We report a case of multisystem Langerhans cell histiocytosis (LCH) with lung, bone and pituitary involvement. A 20-year-old man developed thirst, polydipsia and polyuria in 1983. He had right femur pain from 1988 and osseous LCH was diagnosed based on the operated specimen in 1989. From July 1990, he had right chest pain on coughing and dyspnea and was admitted in November 1990. LCH involving the lungs was diagnosed by CT images and diabetes insipidus was also detected. Steroid therapy was started from 1991, but he discontinued it in 1998. Though he stopped smoking, his clinical symptoms worsened and he experienced bilateral pneumothoraces in 2002 and since then he has been receiving home oxygen therapy. Pulmonary LCH is thought to have a good prognosis, but in recent studies, its survival rate appears low. We report a case of multisystem LCH with lung deterioration over about 15 years.

High plasma osteopontin level and its relationship with interleukin-12-mediated type 1 T helper cell response in tuberculosis.

Osteopontin (OPN, also known as Eta-1), a noncollagenous matrix protein produced by macrophages and T lymphocytes, is expressed in granulomatous lesions caused by Mycobacterium tuberculosis infection. In the present study, we compared plasma concentrations of OPN in patients with active pulmonary tuberculosis with those of healthy control subjects and patients with sarcoidosis, another disease associated with granuloma formation. Plasma OPN levels were significantly higher in patients with tuberculosis (n = 48) than in control subjects (n = 34) and patients with sarcoidosis (n = 20). OPN levels correlated well with severity of pulmonary tuberculosis, as indicated by the size of lung lesions on chest X-ray films. Furthermore, chemotherapy resulted in a significant fall in plasma OPN levels. In patients with tuberculosis, plasma OPN concentrations correlated significantly with those of interleukin (IL)-12. In vitro experiments showed that OPN production by peripheral blood mononuclear cells infected with Mycobacterium bovis bacillus Calmette-Guérin preceded the synthesis of IL-12 and interferon-gamma and that the neutralizing anti-OPN monoclonal antibody significantly reduced the production of IL-12 and interferon-gamma. Our results suggest that OPN may be involved in the pathologic process associated with active pulmonary tuberculosis by inducing IL-12-mediated type 1 T helper cell responses.