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

On the basis of experimental and clinical study of infections with the aerosol mechanism of infection there was revealed a relationship between the fractional-dispersive composition of the microbial aerosol, the porta of infection and the clinico-pathogenetic peculiarities of the course of the disease. On the example of tularemia, plague and other nosological forms it was demonstrated that coarse-dispersive aerosol caused development of oculo-bubonic and anginous-bubonic form of the disease, whereas the high-dispersive aerosol led to the appearance of primary pneumonia. In experimental aerosol infection with the causative agents in which the infection under natural conditions is not air-borne (botulism, American horse encephalo-myelitis, etc.) specific disease as a rule develops without any primary affection of the respiratory organs.
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PMID:[Effect of the site of microbial aerosol application on the pathogenesis and clinical picture of aerosol infection]. 18 56

In June 1978, three cases of tularemia pneumonia occurred in persons residing in the Washington, DC, area. The patients, all men, became ill three to four days after a brief session training their hunting dogs in an undeveloped wooded area adjacent to a housing complex. One of the dogs, which later died, had captured a wild rabbit during the training session. All three men had handled the rabbit while familiarizing their dogs with the rabbit's scent. The men had no other common exposure that was a likely source of infection.
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PMID:Tularemia pneumonia in Washington, DC. A report of three cases with possible common-source exposures. 57 6

A wide range of microorganisms has been associated with cavitary pneumonia and pulmonary abscess. We present a case of serologically documented tularemia in an animal-hide handler who demonstrated multiple pulmonary infiltrates with cavitation. Inclusion of tularemia in the differential diagnosis of cavitary pneumonia in patients with exposure to animals is emphasized.
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PMID:Cavitary pneumonia associated with tularemia. 63 Sep 47

Imaging of the respiratory system developed with exceptional rapidity in North America during the spring of 1896, after Roentgen's discovery of X-rays in November 1895, largely because of the efforts of a unique physicians, Francis H. Williams. With great zeal, this pioneer used fluoroscopy for early detection of tuberculosis and other life-threatening chest disorders. By the summer of 1896, he had accumulated more than 100 volumes containing tracings of clinical chest fluoroscopy. As a result of his extensive clinical experience, his dedication to patients' welfare, and his sense of scientific inquiry, several inventions and many landmark clinical observations were made in the first few years after the discovery of the X-ray. These included (1) the invention of a "densitometer" for standardized measurements of relative X-ray attenuation of the lung, (2) the invention of a "seehear" device to correlate auscultative findings and fluoroscopic observations, (3) the recognition that fluoroscopy was more accurate than percussion for estimating mediastinal displacement, (4) the discovery that clinically occult tuberculosis and congestive heart failure could be detected with fluoroscopy, (5) the documentation that unilateral chest disease caused decreased ipsilateral ventilatory compliance and increased contralateral ventilation, (6) the identification of the classical imaging characteristics of tuberculosis, pneumonia, pneumothorax, tension pneumothorax, pleural effusion, hydropneumothorax, emphysema, congestive heart failure, and air trapping. In April 1896, Dr. Williams described the "air bronchogram" in a radiograph of a patient with pneumonia.
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PMID:Fleischner Lecture. Imaging the respiratory system in the first few years after discovery of the X-ray: contributions of Francis H. Williams, M.D. 160 79

A 64-year-old man had community-acquired pneumonia that was retrospectively diagnosed as pleuropulmonary tularemia. He was successfully treated with erythromycin. We review the case and briefly discuss the literature on this point.
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PMID:Pleuropulmonary tularemia: successful treatment with erythromycin. 223 78

To identify the factors associated with a poor outcome, we reviewed the records of 28 patients with tularemia diagnosed between 1974 and 1984. Most of the patients were men between the ages of 35 and 45 years, who presented with ulceroglandular tularemia. Twelve patients had the anticipated rapid response to therapy, with resolution of their presenting symptoms within one week (group A). Surprisingly, the majority (16 [58%] of 28) had a more prolonged or fatal illness (group B). Group B patients more often had a serious underlying medical disorder, and waited longer before seeking medical attention. Only patients in group B presented with electrolyte or renal function abnormalities (31%), pneumonia and pleural effusions (25%), elevated serum creatine phosphokinase levels (25%), and Francisella tularensis bacteremia (12.5%). Sterile pyuria, however, was an unexpectedly frequent finding in both groups. Group B patients more often experienced a prolonged delay from the time of physician contact to therapy, and were not treated with an aminoglycoside; relapse (12.5%) and death (6.2%) occurred only in group B. Thus, earlier and more appropriate intervention by the physician may have prevented some of the increased morbidity in our patients. These findings suggest that rapid presumptive aminoglycoside therapy (gentamicin sulfate or streptomycin sulfate) should be considered soon after tularemia is suspected, especially for patients with serious underlying medical disorders.
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PMID:Factors associated with a poor outcome in tularemia. 381 43

Francisella tularensis is an infection acquired from animals. Although the pathogen is not a cause of nosocomial infections, it is a major hazard to workers in the clinical microbiology laboratory and could easily become a problem for the infection control officer in this setting. The organism can be cultured from many sites but is difficult to recover unless the appropriate media are used. A number of clinical syndromes are caused by this pathogen. Most are characterized by an ulceration and regional lymphadenopathy. Typhoidal tularemia, however, can present as an obscure fever often complicated by pneumonia. The therapy of choice for tularemia is streptomycin although gentamicin and tobramycin are reasonable alternatives.
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PMID:Francisella tularensis. 385 Aug 62

Drawing upon our experience with 88 cases and a survey of the English literature, we reviewed the clinical, pathophysiological, and epidemiological aspects of tularemia. Tularemia can be thought of as two syndromes--ulceroglandular and typhoidal. This dichotomy simplifies earlier nomenclature and emphasizes the obscure typhoidal presentation. Clinical manifestations suggest that the two syndromes reflect differences in host response. In ulceroglandular tularemia the pathogen appears to be well contained by a vigorous inflammatory reaction. Pneumonia is less common and the patient's prognosis is good. In typhoidal disease there are few localizing signs; pneumonia is more common; and the mortality without therapy is much higher, suggesting that the host response is somehow deficient. Francisella tularensis is an extremely virulent pathogen capable of initiating infection with as few as 10 organisms inoculated subcutaneously. During an incubation period of 3 to 6 days the host responds first with polymorphonuclear leukocytes and then macrophages. Granulocytes are unable to kill the pathogen without opsonizing antibody leaving cellular immunity to play the major role in host defense. One to 2 weeks after infection, a vigorous T-lymphocyte response can be detected in vitro with lymphocyte blast transformation assays and in vivo with an intradermal skin test, which, unfortunately, is not commercially available. Humoral immunity, often used as a diagnostic modality, appears 2 to 3 weeks into the illness. Cellular immunity is long-lasting, accounting for the common reoccurrence of localized disease upon repeated exposures to the pathogen. There are no symptoms that distinguish the ulceroglandular from the typhoidal syndrome. A pulse-temperature dissociation is seen in less than half of the patients. The location of ulcers and enlarged lymph nodes give a clue to the likely vector since lesions located on the upper extremities are more commonly associated with mammalian, and those of the head and neck and lower extremities with arthropod, vectors. Pharyngitis, pericarditis, and pneumonia can complicate both syndromes, although the latter is much more common in typhoidal disease. Hepatitis, usually of a mild degree, is common and occasionally erythema nodosum is seen. No specific laboratory tests characterize tularemia, and cultures of the pathogen are often difficult to obtain because of the special growth requirements of Francisella tularesis and the inability of many clinical laboratories to handle the dangerous pathogen.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Tularemia: a 30-year experience with 88 cases. 389 22

Three patients with tularemia pneumonia developed adult respiratory distress syndrome and required positive end-expiratory pressure for adequate oxygenation. Rapid improvement was noted following appropriate antibiotic therapy, and mechanical ventilation was successfully discontinued after six to eight days.
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PMID:Adult respiratory distress syndrome secondary to tularemia pneumonia. 402 75

The pathogenesis of tularemia was studied in groups of rhesus monkeys (Macaca mulatta) that inhaled graded 10-fold doses ranging from 10 through 10(6) organisms of Francisella tularensis 425, a strain highly virulent for the white mouse but of reduced virulence for the domestic rabbit. Mean incubation periods ranged from 3 to 6 days followed by acute illness lasting 5 to 11 days with subsequent recovery of most animals. The higher inhaled doses resulted in shorter incubation periods, longer and more severe acute illnesses, and 18% mortality at the highest dose. Strain 425 multiplied in the lungs, disseminated to the regional lymph nodes, and became systemic. Maximal bacterial populations in tissues were reached by the 7th day after exposure of the animals regardless of the number of organisms inhaled. F. tularensis was no longer recoverable from any of six tissues examined 2 months after exposure. The most significant tissue changes occurred in the lungs; these consisted of foci of liquefaction necrosis, lobular consolidation, and pleural effusion and adhesions. The data indicate that the inhaled dose of strain 425 determined the maximal growth of the organism in the lungs which in turn influenced the severity of the usually self-limiting pneumonia and systemic infection. Although the monkey is less resistant to tularemia than is man, this laboratory animal when infected with F. tularensis 425 provides a useful model for the self-limiting type of human pulmonary tularemia usually observed in Europe and Asia but to a lesser extent in North America.
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PMID:Pathogenesis of tularemia in monkeys aerogenically exposed to Francisella tularensis 425. 462 51


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