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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transplant recipients living in endemic areas are at high risk of aerosol-transmitted fungal infections because of environmental exposure while on immunosuppressive drugs, as well as reactivation of latent infection from either the patient's or the donor's organs. The latter may account for early development of coccidioidomycosis after transplantation. We describe a case of pulmonary coccidioidomycosis in a lung transplant recipient who acquired the infection from the donor lung and presented with fulminant pneumonia in the immediate postoperative period.
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PMID:Donor transfer of pulmonary coccidioidomycosis in lung transplantation. 1183 38

Mycobacterium tuberculosis produces latent infection or progressive disease. Indeed, latent infection is more common since it occurs in one-third of the world's population. We showed previously, using human material with latent tuberculosis, that mycobacterial DNA can be detected by in situ PCR in a variety of cell types in histologically-normal lung. We therefore sought to establish an experimental model in which this phenomenon could be studied in detail. We report here the establishment of such a model in C57Bl/6 x DBA/2 F1 hybrid mice by the intratracheal injection of low numbers of virulent mycobacteria (4000). Latent infection was characterized by low and stable bacillary counts without death of animals. Histological and immunological study showed granulomas and small patches of alveolitis, with high expression of tumour necrosis factor alpha (TNFalpha), inducible nitiric oxide synthase (iNOS), interleukin 2 (IL-2) and interferon gamma (IFNgamma). In contrast, the intratracheal instillation of high numbers of bacteria (1 x 106) produced progressive disease. These animals started to die after 2 months of infection, with very high bacillary loads, massive pneumonia, falling expression of TNF-alpha and iNOS, and a mixed Th1/Th2 cytokine pattern. In situ PCR to detect mycobacterial DNA revealed that the most common positive cells in latently-infected mice were alveolar and interstitial macrophages located in tuberculous lesions, but, as in latently-infected human lung, positive signals were also seen in bronchial epithelium, endothelial cells and fibroblasts from histologically-normal areas. Our results suggest that latent tuberculosis is induced and maintained by a type 1 cytokine pattern plus TNFalpha, and that mycobacteria persist intracellularly in lung tissue with and without histological evidence of a local immune response.
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PMID:Immunological and pathological comparative analysis between experimental latent tuberculous infection and progressive pulmonary tuberculosis. 1198 12

Simian varicella virus (SVV) is closely related to varicella-zoster virus (VZV) and induces a natural varicella-like disease in nonhuman primates. Therefore, simian varicella is a useful model to investigate varicella pathogenesis and to evaluate antiviral therapies. In this report, we review recent studies on SVV pathogenesis and latency. Experimental infection of African green monkeys is followed by a 7-10 day incubation period during which a viremia disseminates the virus throughout the body. Clinical disease is characterized by fever and vesicular skin rash. Pneumonia and hepatitis may occur during more severe infections. Examination of acutely infected tissues reveals histopathology including necrosis and hemorrhage in the skin, lung, liver, and spleen. In contrast, the neural ganglia exhibit minimal histopathology. SVV DNA, immediate early, early, and late gene transcripts, and viral antigens are detected in the tissues of acutely infected monkeys. Host immune responses are induced which resolve the acute infection within 21 days. During or after acute infection, SVV establishes latent infection in the ganglia of surviving monkeys. The virus may reactivate later in life to cause secondary disease and viral transmission to susceptible monkeys.
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PMID:Pathogenesis of simian varicella virus. 1262 79

Moderate to marked interstitial pneumonitis with many Pneumocystis organisms was found in rabbits treated with cortisone and antibiotics and instilled intranasally with a suspension of lung tissue from either a patient or a rabbit with this infection. Organisms and pulmonary lesions of similar severity and frequency were present in controls treated in the same manner but instilled with either saline or a boiled suspension of normal human lung tissue. The administration of antibiotics and infected rabbit lung suspension only produced less marked lung changes with fewer organisms. Rare organisms and minute foci of pneumonitis were encountered in normal rabbits which had received neither hormone, antibiotics, nor inoculum. The pulmonary lesions in the cortisone-treated rabbits resembled closely the findings in patients with the subclinical form of Pneumocystis pneumonitis. They did not reproduce the massive lesions of widespread Pneumocystis pneumonia in infants. The findings indicate that latent pulmonary Pneumocystis infection was widespread in these rabbits but do not establish the transmission of the disease. The activation of latent infection was dependent on an impairment of host resistance which in these experiments was produced most effectively by the administration of cortisone. The differences between the experimental lesions and those of typical Pneumocystis pneumonia in infants suggest that in man an unknown defect of host defenses other than that induced by prolonged hormone administration accounts for the increased susceptibility to the infection. It is concluded that in the presence of widespread latent Pneumocystis infection the development of active disease is a manifestation of altered host resistance.
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PMID:Experimental pulmonary Pneumocystis carinii infection in rabbits. 1366 76

Simian varicella virus (SVV) causes a natural varicella-like disease in nonhuman primates. Epizootics of simian varicella occur sporadically in facilities housing Old World monkeys. SVV is antigenically and genetically related to varicella-zoster virus (VZV), the etiologic agent of varicella (chickenpox) and herpes zoster (shingles) in humans. The SVV and VZV genomes are similar in size and structure, share 70%-75% DNA homology and are co-linear with respect to gene organisation. Simian varicella is a highly contagious disease characterised by fever and vesicular skin rash and may progress to pneumonia and hepatitis. Infected monkeys may resolve the disease within 2 weeks although epizootics are sometimes associated with high morbidity and mortality. SVV, like VZV, establishes life-long latent infection, as indicated by detection of viral DNA within neural ganglia. Subsequently, SVV may reactivate to cause secondary disease and spread of the virus to susceptible monkeys. The relatedness of VZV and SVV and the similarities in the clinical symptoms and pathogenesis of human and simian varicella make SVV infection of nonhuman primates an excellent animal model to investigate VZV pathogenesis and latency, and to evaluate potential antiviral strategies.
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PMID:Simian varicella: a model for human varicella-zoster virus infections. 1538 93

Pneumocystis carinii is an opportunistic eukaryotic pathogen most common causing pneumonia in immunocompromised host. DNA P. carinii f. sp. hominis has been frequently detected in air samples collected from environments of P. carinii pneumonia (PCP) patients and nasal swabs samples from contact health care workers and family. Epidemiological studies suggested not-only the possibility of person-to-person infection transmission. First hypothesis of reactivation latent infection of the causing the new episode of PCP based on serological studies. Recently findings based molecular studies has suggested new acquired infection may to be cause of many cases of PCP. Early diagnosis, therapy and effective prophylaxis of PCP is a very important strategy to reduce morbidity and mortality among infected patients. The combination of trimethoprim (TMP) and sulfamethoxazole (SMX) is effective for prophylaxis and treatment P. carinii pneumonia. Empiric therapy in immunocompromised host also including AIDS patients with anti-Pneumocystis prophylaxis is also not recommended. Both dapsone and sulfamethoxazole act inhibiting the folate biosynthetic enzyme DHPS. Mutations identified in P. carinii in gene coding this enzyme are associated with resistance to sulfonamide. P. carinii may also developing resistance to atovaquone, second-line therapeutic and prophylactic agent.
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PMID:[New aspects of epidemiology and treatment of Pneumocystis carinii infection]. 1575 52

Human cytomegalovirus (HCMV) is a beta herpes virus with a double stranded DNA genome of 240kbp. The virus is prevalent and establishes a latent infection in most adults. HCMV is an opportunistic pathogen for patients with impaired cellular immunity. HCMV pneumonia is a common presentation of HCMV disease in immunocompromised patients. The incidence of HCMV pneumonitis can be as high as 90% in lung transplant recipients. This paper takes a fresh look at the challenging perspectives of molecular, immunologic, cellular, diagnostic, clinical, and therapeutic characteristics of HCMV infection as future targets for development of antiviral strategies.
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PMID:Pneumonitis in human cytomegalovirus infection. 1664 74

In HIV-infected patients, cytomegalovirus (CMV) disease diagnosis is usually difficult and disease results from reactivation of latent infection or reinfection in the context of severe immunosupression. Although the introduction of highly active antiretroviral therapy (HAART) has resulted in a important decline of CMV disease, it has considerable morbidity and mortality rate. We present a case of a patient who presented fever, pulmonary infiltrates and abdominal pain after P.jirovecii pneumonia, with isolated of CMV (positive shell-vial) from LBA and gastric biopsy. We propose a possible diagnosis of digestive and pulmonary CMV disease and we initiated treatment for this with clinical response. It results surprising the rapid progression to SIDA of the patient and we can suggest that a co-infection HIV-CMV could be the cause for the rapid immunological damage.
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PMID:[Pulmonary infiltrates and fever in a HIV infected patient after Pneumocystis jirovecii pneumonia]. 1827 97

Toxoplasmosis is a life-threatening opportunistic infection that affects haematopoietic stem cell transplant (HSCT) and solid organ transplant (SOT) recipients. Its incidence in these patients is closely related to the prevalence of toxoplasmosis in the general population, which is high in Europe. In SOT recipients, toxoplasmosis results mainly from transmission of the parasite with the transplanted organ from a Toxoplasma-seropositive donor to a Toxoplasma-seronegative recipient. This risk is high in cases of transplantation of organs that are recognized sites of encystation of the parasite, e.g. the heart, and is markedly lower in other SOT recipients. Clinical symptoms usually occur within the first 3 months after transplantation, sometimes as early as 2 weeks post transplant, and involve febrile myocarditis, encephalitis or pneumonitis. In HSCT recipients, the major risk of toxoplasmosis results from the reactivation of a pre-transplant latent infection in seropositive recipients. The median point of disease onset is estimated at 2 months post transplant, with <10% of cases occurring before 30 days and 15-20% later than day 100. Toxoplasmosis usually manifests as encephalitis or pneumonitis, and frequently disseminates with multiple organ involvement. Diagnosis of toxoplasmosis is based on the demonstration of parasites or parasitic DNA in blood, bone marrow, cerebrospinal fluid, bronchoalveolar lavage fluid or biopsy specimens, and serological tests do not often contribute to the diagnosis. For prevention of toxoplasmosis, serological screening of donors and recipients before transplantation allows the identification of patients at higher risk of toxoplasmosis, i.e. seropositive HSCT recipients and mismatched (seropositive donor/seronegative recipients) SOT recipients. Preventing toxoplasmosis disease in those patients presently relies on prophylaxis via prescription of co-trimoxazole.
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PMID:Prevention of toxoplasmosis in transplant patients. 1901 9

The goal of the present study was to discover etiological role of Pneumocystis carini/jiroveci and to determine frequency of pneumocystic infection in the structure of bronchopulmonary pathology among armenians-liquidators of accident consequences in the Chernobyl Nuclear Power Plant. For the study, 65 patients-liquidators with diagnosed pneumonia, 44 liquidators with chronic bronchitis and 34 with bronchial asthma were examined. The control group was included 65 patients with pneumonia, 44 with chronic bronchitis, 34 with bronchial asthma which were unlinked with radionucleotide aggression. Mean age in main group was 46,9 and in control group- 47,6 years old. Main and control groups were randomized by sexual characteristics also. Serologic examinations were performed by the ELISA (enzyme-linked immunoSorbent assay) and method of immunofluorescent detection of P.carinii. Circulation of pneumocystosis etiologic agent among patients-liquidators of accident consequences in the Chernobyl Nuclear Power Plant with different bronchopulmonary pathology was established and high percentage of seropositivity was revealed. Overall these data revealed high probability of Pneumocystis carini/jiroveci in the etiology of bronchopulmonary pathology among liquidators of accident consequences in the the Chernobyl Nuclear Power Plant. Even among immunocompromised patients, liquidators of accident consequences, represent an exclusive group, that is in risk for activation of latent infection or new infection with P. carini/jiroveci. Therefore these findings suggest that there is a need for regular complex epidemiological monitoring of these patients.
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PMID:[Pneumocystosis distribution among accident liquidators in the Chernobyl nuclear power plant in remote period]. 1964 5


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