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

A goat herd severely affected by arthritis was studied. The most representative clinical signs consisted of articular swelling, mainly of the carpal joints, and the subsequent locomotor disorders. Some goats also showed signs of central nervous system involvement. Examinations of joint fluid revealed an increased number of mononuclear blood cells, mostly lymphocytes. Gross and microscopic articular lesions were of inflammatory and degenerative types. Periarticular connective tissue, synovial bursae, tendons and tendon sheaths were predominantly affected. Inflammatory lesions were those of a chronic hyperplastic tenosynovitis with fibrosis of the connective tissue components. Degenerative changes consisted mainly of necrosis and mineralisation of articular-related structures. Histological lesions in the central nervous system were those of a nonpurulent encephalitis initially located in periventricular areas, but in one case extensive encephalomalacia was also seen. Of the 80 animals sampled 82.5 per cent showed seropositive reactions against an ovine progressive pneumonia virus antigen. None was seropositive to brucella and titres to chlamydia were low. Attempts to isolate chlamydia and mycoplasma from affected joints and several organs failed. Different bacteria were recovered from a few samples but did not seem significant. Syncytium-forming viral particles were isolated from several organs, mainly the lungs, synovial membranes and lymphoid tissue of almost all the slaughtered animals. These particles were identified as lentiviruses by electron microscopy. The clinical signs, lesions serological results and microbiological findings, led to a diagnosis of caprine arthritis-encephalitis. This syndrome has not been recognised in Spain previously.
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PMID:Caprine arthritis-encephalitis in the Basque country, Spain. 303 62

After reviewing the immunological anomalies provoked by the human immuno-deficiency virus (HIV) as well as their implications in pulmonary pathology, the authors enumerate the diagnostic and therapeutic methods currently available in the treatment of patients suffering from AIDS and pulmonary diseases. The clinical features as well as the chest radiograph--an essential first line tool--may lead to atypical features. Respiratory function tests and scintigraphy to Gallium may be a useful additional diagnostic technique but for a full pulmonary investigation a bronchoalveolar lavage is required and/or transbronchial biopsy. Open lung biopsy is rarely required, and then only as a last resort. The treatment of pneumocystis remains centred on Trimethoprim sulfamethoxazole and Pentamidine, with a similar efficacy (80% care) but both have side-effects which are less frequent but more severe with Pentamidine. Administration of Pentamidine by aerosol, Eflornithine and Trimetrexate are under study. The level of lactic dehydrogenase (LDH) seems to be a prognostic factor. The value of prophylaxis is discussed. If the treatment of tuberculosis, an infection which is seen more and more frequently, still rests on classical triple therapy, the treatment of atypical mycobacterial infections is even more deceptive than in non-immuno-suppressed hosts. The same is true with pneumonia due to cytomegalovirus. The treatment of lymphoid interstitial pneumonia which is probably a direct result of HIV infection, remains controversial. On the other hand, pulmonary Kaposi's sarcoma is associated with an elevated mortality, and all treatment (interferon and chemotherapy) is disappointing.
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PMID:[Pulmonary manifestations of acquired immunodeficiency syndrome]. 306 2

A 61-year-old women developed progressive neurologic deficits and died with pneumonia and septicemia. An autopsy demonstrated the characteristic intravascular and focal perivascular infiltrate of malignant angioendotheliomatosis (MAE) throughout the body but concentrated in the central nervous system and skin. Ultrastructurally, the neoplastic cells lacked evidence of endothelial differentiation. Immunohistochemical studies showed focal staining for Factor VIII-related antigen, probably on a nonspecific basis, negative staining for Ulex europaeus I lectin (an endothelial cell marker), and intense staining for leukocyte common antigen. The authors' observations provide evidence that at least some examples of MAE are unusual, angiotropic lymphoid neoplasms.
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PMID:Malignant angioendotheliomatosis. An angiotropic lymphoma? 315 8

An autopsy case of a 37-year-old Japanese man, confirmed as an AIDS patient infected by an undetermined route of transmission, is presented. The initial symptoms of full-blown AIDS in this case were neurological, and the patient died of severe pneumonia 9 months after onset. The main histo- and immunopathological features were a marked depletion of helper-inducer T cells and dendritic reticulum cells in the lymphoid tissues, opportunistic infections, and some neuropathologic changes. Very few cells, possibly macrophages, immunoreactive with a monoclonal antibody (VAK-5) against HIV-gag protein P24 were found in the mediastinal lymph nodes. Numerous pathogens had induced opportunistic infections in many organs: severe and generalized cytomegalovirus infection, Pneumocystis carinii pneumonia, bronchopneumonia (possibly due to Pseudomonas aeruginosa), candidiasis in the tongue and oral cavity, and atypical mycobacteriosis in the pulmonic hilar lymph nodes. Vascular proliferation was found in the perinodal regions of some lymph nodes, but this was not neoplastic vascular proliferation compatible with that of localized Kaposi's sarcoma.
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PMID:Histo- and immunopathological features of terminal AIDS. An autopsy case of a Japanese man with neurological signs as initial symptoms. 321 10

Although chemical immunosuppression has been shown to benefit patients with chronic progressive multiple sclerosis (MS), it appears that chemotherapy has an appreciable oncogenic potential in patients with multiple sclerosis. Accordingly, we developed a modified total lymphoid irradiation (TLI) regimen designed to reduce toxicity and applied it to a randomized double blind trial of TLI or sham irradiation in MS. Standard TLI regimens were modified to reduce dose to 1,980 rad, lowering the superior mantle margin to midway between the thyroid cartilage and angle of the mandible (to avert xerostomia) and the lower margin of the mantle field to the inferior margin of L1 (to reduce gastrointestinal toxicity by dividing abdominal radiation between mantle and inverted Y), limiting spinal cord dose to 1,000 rad by custom-made spine blocks in the mantle and upper 2 cm of inverted Y fields, and also protecting the left kidney even if part of the spleen were shielded. Clinical efficacy was documented by the less frequent functional scale deterioration of 20 TLI treated patients with chronic progressive MS compared to to 20 sham-irradiated progressive MS patients after 12 months (16% versus 55%, p less than 0.03), 18 months (28% versus 63%, p less than 0.03), and 24 months (44% versus 74%, N.S.). Therapeutic benefit during 3 years follow-up was related to the reduction in lymphocyte count 3 months post-irradiation (p less than 0.02). Toxicity was generally mild and transient, with no instance of xerostomia, pericarditis, herpes zoster, or need to terminate treatment in TLI patients. However, menopause was induced in 2 patients and staphylococcal pneumonia in one. Our data suggest that this modified TLI regimen has clinical efficacy and sufficiently low toxicity to make it suitable for investigative immunosuppressive treatment of patients with progressive MS or other non-malignant conditions.
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PMID:Total lymphoid irradiation for multiple sclerosis. 327 1

The effect of high-dose cyclophosphamide (Cy), either alone or in combination with irradiation, upon the development of interstitial pneumonitis (IP) after bone marrow transplantation (BMT) was investigated in a Brown Norway rat model. The parameters that were examined included ventilation rate, mortality, and histopathology. No damage to the lungs was observed in rats given Cy alone in supralethal dosages plus BMT, and mortality resulted from severe aplasia of hemopoietic and lymphoid tissues with multifocal hemorrhages, secondary infections, and sepsis. Two separate periods of mortality were observed within the first 180 days following whole thorax irradiation with a high dose rate (HDR; 0.8 Gy/min) or a low dose rate (LDR; 0.05 Gy/min). The addition of Cy prior to irradiation resulted in an increased mortality in the first period (before day 100) in all experimental groups. The influence of Cy on mortality at 180 days however, was different for the HDR and LDR experiments. The LD50-180 after HDR irradiation, dose range 8 to 18 Gy, was not significantly altered by the addition of Cy (100 mg/kg) 1 day prior to irradiation, whereas Cy (100 mg/kg) 1 day prior to LDR irradiation, dose range: 16 to 24 Gy, caused an enhancement of radiation damage with a decrease of the LD50-180 by 1.33 Gy. The dose modification factor (DMF) was 1.07. This enhancement was no longer significant after splitting up the dose of Cy in two dosages of 50 mg/kg given on 2 consecutive days prior to irradiation with a LDR. The extrapolation of the data in this rat model to available dose-response curves on IP after BMT and radiation pneumonitis in humans, implied that non-infectious IP is a radiation pneumonitis that is only slightly enhanced by Cy.
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PMID:Lung damage following bone marrow transplantation: II. The contribution of cyclophosphamide. 330 44

The mouse model of acute murine respiratory mycoplasmosis was used to screen 18 strains of Mycoplasma pulmonis for their ability to establish respiratory infections and produce gross lung lesions in the susceptible C3H/HeN mouse strain. All experiments were designed to minimize host, environmental, and microbial differences to ensure that experimental results would reflect differences in mycoplasmal virulence. There were differences in the 50% infectious dose (range, 3 X 10(2) to greater than 10(7) CFU) and the 50% gross pneumonia dose (range, 10(3) to greater than 10(7) CFU) among the 18 mycoplasmal strains. Only 10 strains (UAB CT, M1, UAB 5782C, UAB 6510, 66, UAB T, UAB 8145D, Nelson C, Peter C, and Negroni) established respiratory infections, and only 2 of the 10 strains (UAB CT and M1) produced gross lung lesions. Strains UAB CT, UAB T, M1, UAB 5782C, and PG34(ASH) were chosen for qualitative and quantitative evaluation of lung lesions in C3H/HeN and C57BL/6N mice. Lesion incidence and severity was dependent on the mycoplasmal strain and the mouse strain. Microscopic lesions varied among mycoplasmal strains and mouse strains in the amount of lymphoid infiltrate, neutrophilic exudate, and consolidation, as well as overall severity. The most virulent strain, UAB CT, produced acute pneumonitis in the 10(7) CFU dosage group and required a threshold dose of 10(3) CFU to consistently produce microscopic lung lesions. These results suggest that M. pulmonis virulence is multifactorial and different strains of mycoplasmas yield disease expressions that differ both qualitatively and quantitatively.
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PMID:Differences in virulence for mice among strains of Mycoplasma pulmonis. 339 87

Laboratory findings in an adult bull terrier presented with a history of anorexia and weight loss included the following: severe anaemia, leukocytosis, neutrophilia, lymphopaenia, thrombocytopaenia, Ehrlichia canis morulae in monocytes, hypergammaglo-bulinaemia, a bleeding tendency, icterus and proteinuria. In addition, a high Haemobartonella canis parasitaemia, non-encapsulated yeasts on urinalysis and a localised Demodex canis infestation were present. Treatment for ehrlichiosis was initiated but the dog died. Lesions found were a severe cryptococcal granulomatous pneumonia and cryptococcal colonies in the lungs, bronchial lymph nodes, kidneys, liver, spleen, heart, meninges, eyes and thoracic cavity. In addition, hyphal forms resembling Filobasidiella neoformans, the teleomorph of Cryptococcus neoformans, were seen in lung fine needle aspiration smears, impression smears and lung sections. C. neoformans was cultured from urine, lung and liver. Lung and kidney also yielded Salmonella typhimureum. Cortical atrophy with T-cell depletion of lymph nodes as well as splenic lymphoid follicular atrophy, typical of chronic ehrlichiosis-induced cell mediated immunosuppression, could have predisposed to the fatal disseminated cryptococcis.
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PMID:Fatal disseminated cryptococcosis and concurrent ehrlichiosis in a dog. 350 65

Pregnant rats were exposed to N-methyl-2-pyrrolidone (NMP) at atmospheric concentrations of 0.1 and 0.36 mg/liter for 6 hr/day on Days 6 through 15 of gestation. Except for sporadic lethargy and irregular respiration in several rats the first 3 days of exposure, there were neither abnormal clinical signs nor pathological lesions in the maternal rats. Exposure did not affect either the outcome of pregnancy or embryonal growth rate. No abnormal development was detected in the vital organs and skeletons of the fetuses. Rats were exposed to an aerosol-vapor mixture of NMP at concentrations of 0, 0.1, 0.5, and 1.0 mg/liter for 6 hr/day, 5 days/week for 4 weeks. At 0.1 and 0.5 mg/liter exposure levels, rats did not show any significant clinical signs or pathological lesions. However, lethargy, respiratory difficulty, and excessive mortality were found in rats exposed to 1.0 mg/liter. These rats had focal pneumonia, bone marrow hypoplasia, and atrophy of lymphoid tissue in the spleen and thymus. These lesions were reversible in surviving rats following 2 weeks of recovery. Increases in the relative and absolute numbers of neutrophils were observed during exposure at 1.0 mg/liter, but returned to normal limits after 2 weeks of recovery. Rats were exposed to vapor of NMP at concentrations of 0, 0.04, or 0.4 mg/liter for 6 hr/day, 5 days/week for 2 years. Male rats at 0.4 mg/liter showed slightly reduced mean body weight. No life-shortening toxic or carcinogenic effects were observed in rats exposed for 2 years to 0.04 or 0.4 mg/liter of NMP.
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PMID:Toxicity of N-methyl-2-pyrrolidone (NMP): teratogenic, subchronic, and two-year inhalation studies. 365 66

Groups of F344/N rats and B6C3F1 mice were exposed to aerosols of nickel subsulfide (Ni3S2) 6 hr/day for 12 days not including weekends. Actual exposure concentrations were within 3% of target (target = 10.0, 5.0, 2.5, 1.2, 0.6, and 0.0 mg Ni3S2/m3). Nickel lung burdens of exposed rats and mice increased linearly with exposure concentration. Two male rats and all mice exposed to 10.0 mg Ni3S2/m3 died before the end of the exposures. Exposure to Ni3S2 had no effect on the natural killer cell activity of mouse spleen cells. Lesions in rats and mice related to inhalation of Ni3S2 were found in the nasal epithelium, lung, and bronchial lymph nodes. The most extensive lesions were found in the lung and included necrotizing pneumonia. Emphysema developed in rats exposed to 5.0 or 10.0 mg Ni3S2/m3, while fibrosis developed in mice exposed to 5.0 mg Ni3S2/m3. Degeneration of the respiratory epithelium and atrophy of the olfactory epithelium of the nose occurred in rats exposed to as low as 0.6 mg Ni3S2/m3 and mice exposed to 1.2 mg/m3. Results indicate that inhalation exposure of rats and mice to Ni3S2 aerosol concentrations near the current threshold limit value (TLV) for nickel compounds (1 mg/m3 for Ni metal and roasting fume and dust and 0.1 mg/m3 as Ni for soluble compounds) can produce lesions in the respiratory tract. Atrophy of lymphoid tissues (spleen, thymus, and bronchial lymph nodes) was found in animals of the highest exposure concentration. Degeneration of the testicular germinal epithelium was also observed in mice and rats that survived 5.0 or 10.0 mg/m3 exposure concentrations.
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PMID:Comparative inhalation toxicity of nickel subsulfide to F344/N rats and B6C3F1 mice exposed for 12 days. 365 67


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