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

Choosing appropriate antimicrobial therapy for patients with pneumonia requires knowledge of the etiologic agents seen in specific kinds of patients at specific times and places. For community-acquired pneumonia, there is an important difference in the agents seen in the normal and the compromised host. The normal host most often presents with viral, mycoplasmal, or pneumococcal pneumonia. The exact place of Chlamydia pneumoniae is still under study. A normal host who aspirates is at risk of anaerobic pneumonia. Normal hosts with influenza may acquire superinfection with Streptococcus pneumoniae, Haemophilus influenzae, or Staphylococcus aureus. Under specific epidemiologic conditions, community-acquired pneumonia may be due to Legionella species, Yersinia pestis, Francisella tularensis, Coxiella burnetii, Chlamydia psittaci, a mycotic agent, or tuberculosis. Patients with chronic bronchitis and emphysema are predisposed to H. influenzae, Moraxella catarrhalis, and S. pneumoniae infections. HIV-infected patients are likely to have Pneumocystis carinii pneumonia and pneumonia due to cytomegalovirus, S. pneumoniae, and H. influenzae. Patients with diabetes, nursing-home patients, hospitalized patients, immuno-compromised patients, and patients with recent antibiotic therapy are predisposed to pneumonia due to Gram-negative aerobic bacilli of enteric and environmental origin. Initial therapy should be directed at the likely organism or organisms based on hospital susceptibility surveillance. In the normal host with community-acquired pneumonia, the therapy will often be penicillin G or erythromycin. In the patient predisposed to Gram-negative pneumonia, a third-generation cephalosporin with or without an aminoglycoside is the usual choice.
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PMID:Pneumonia. Patient profiles, choice of empiric therapy, and the place of third-generation cephalosporins. 173 Jan 86

The clinical, clinicopathologic, and pathologic features of 119 cases of plague in cats from 1977 to 1988 in New Mexico were reviewed. Fifty-three percent were bubonic, 10% were pneumonic, 8% were septicemic, and 29% with neither buboes nor pneumonia were unclassified (but presumed septicemic). Three quarters of the lymphadenopathy was submandibular, and almost half of this was bilateral. One third of all cats had the triad of lethargy, anorexia, and fever in addition to buboes; one quarter had this triad plus abscesses. The overall mortality rate was 33%, with the greatest risk of death in pneumonic cases. For confirmatory diagnosis with a single laboratory test, fluorescent antibody was most frequently used (39% of cases). Cultures and passive hemagluttination titers were also used for confirmation. Gross and histologic findings depended on the type of plague, with Yersinia pestis organisms visualized in buboes of cats with bubonic plague and in the alveolar spaces and respiratory tubules of cats with pneumonic plague.
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PMID:Clinical, clinicopathologic, and pathologic features of plague in cats: 119 cases (1977-1988). 175 74

We evaluated the clinical characteristics of patients with Francisella philomiragia (formerly Yersinia philomiragia) isolated from normally sterile sites. Isolates from 14 patients were received by the Centers for Disease Control between 1975 and 1987: 9 were from blood; 2 from lung biopsies; and 1 each from pleural, peritoneal, and cerebrospinal fluid. Underlying problems included chronic granulomatous disease in 5 patients, near-drowning in 5, and a myeloproliferative disease in 2. All 13 patients for whom records were available had a febrile syndrome compatible with bacterial infection. Pneumonia and fever-bacteremia were the commonest clinical syndromes reported. In 7 cases, F. philomiragia was the only sterile-site isolate, and the clinical syndrome did not resolve without appropriate antibiotics. Familiarity with this organism is important because of its ability to cause serious disease in chronic granulomatous disease and near-drowning patients. Further study may yield new insights into pathogenic and host defense mechanisms.
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PMID:Infection caused by Francisella philomiragia (formerly Yersinia philomiragia). A newly recognized human pathogen. 254 46

Circulating immune complexes are thought to play an essential part in the pathogenesis of necrosing angiitis. This theory also allows a role to be attributed to certain infectious agents (viral, bacterial, parasitic) in the development of periarteritis nodosa (PAN). An infectious syndrome was found in all our 9 patients, aged 26 to 69 years, with histologically confirmed PAN: previous infection (over 15 days before hospital admission): otitis, hepatitis B, tonsillitis, ascaris (Case n.7), pulmonary tuberculosis, brucellosis, seropositivity for Chlamydia trachomatis (Case n.9), paratyphoid (Case n.5), seropositivity for Yersiniosis pseudo-tuberculosis (Case n.2), seropositivity for Chlamydia trachomatis (Cases 3 and 4), seropositivity for toxoplasmosis (Cases 4 and 6), seropositivity for rubella (Case n.8). Recent infection (less than 15 days before hospital admission): staphylococcus aureus septicaemia (Case n.1); Group A betahemolytic streptococcal urinary infection (Case n.2); Group A betahemolytic streptococcal otitis media; pseudomonas aeruginosa and Klebsiella septicaemia; enterococcal cystitis (Case n.4); progressive pulmonary tuberculosis (Case n.6), acinetobacter pneumonia (Case n.9). The HBs antigen was only found in one patient (Case n.6), who had an active hepatitis.
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PMID:[The role of infection in the precipitation of periarteritis nodosa]. 290 81

We compared the infections encountered in 23 renal transplant patients given the monoclonal anti-T-cell antibody, Orthoclone OKT3 (OKT3), for treatment of steroid-resistant rejection in 1986 and in 23 control patients from 1984 to 1985 with resistant rejection matched demographically, for severity of rejection and for risk factors predisposing to infection, who did not receive OKT3; recipients of OKT3 received substantially less prednisone, cyclosporine, and antilymphocyte globulin (ALG) than control patients for treatment of the rejection episode. Fourteen (61%) patients given OKT3 developed one or more infections in the 3-month period following treatment as compared with 9 control patients (39%) given conventional antirejection therapy with high-dose steroids and, usually, ALG. Patients given OKT3 were significantly more likely to develop serious infections (pneumonia, bacteremia, meningitis, or severe viral infection; 16 episodes vs. 4, P = .02). Six recipients of OKT3 (26%) acquired infections typically encountered in states associated with depressed cell-mediated immunity (CMI)--Listeria sepsis (2), disseminated nocardiosis and Mycobacterium tuberculosis infection (1), cytomegalovirus (CMV) pneumonia (1), Yersinia infection with severe dermatophytosis (1), and Epstein-Barr virus-associated lymphoproliferative syndrome (1)--as compared with 1 case of mild CMV infection in the control group (P = .08). Trimethoprim-sulfamethoxazole (TMP-SMZ) was given to 19 patients in each group; all 4 recipients of OKT3 who did not receive TMP-SMZ prophylaxis developed life-threatening infection, 3, bacteremia (2 with Listeria) and 1, disseminated nocardiosis and M tuberculosis infection. These data suggest that OKT3 given for treatment of resistant rejection in renal transplantation predisposes the patient to serious infection, particularly with opportunistic pathogens characteristically associated with depressed cell-mediated immunity. Prophylaxis with TMP-SMZ, which is safe, well tolerated, and effective for reducing the incidence of infection in renal transplantation, may be especially important during OKT3 therapy.
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PMID:Increased infections associated with the use of OKT3 for treatment of steroid-resistant rejection in renal transplantation. 327 66

After one week of nonspecific symptoms, pneumonia and an extremely tender and enlarged cervical lymph node developed in a 12-year-old girl who lived in an area of New Mexico known to have plague-infected rodents. Cultures from an aspirate of the node, her sputum, and blood all showed growth of Yersinia pestis. She was treated successfully with aminoglycosides and tetracycline. As the pneumonia resolved, areas of consolidation were replaced by cavitary lesions.
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PMID:Multiple lung cavities in a 12-year-old girl with bubonic plague, sepsis, and secondary pneumonia. 372 14

Micronodular pneumonia and persistent sepsis with mild symptoms caused by Yersinia enterocolitica serotype 3 is described. Two of 4 patients had pneumonia as their only clinical manifestation, while the others had diarrhea as well. Pneumonic changes disappeared quickly during antimicrobic therapy. The course of the disease was fundamentally different from septicaemias caused by other gram-negative bacteria.
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PMID:Interstitial pneumonia and sepsis caused by Yersinia enterocolitica serotype 3. 373 35

Experimental infections with Yersinia pestis were followed in groups of rock squirrels. Development of coagulopathy and pneumonia were observed in 2-4% and 11-12% of the test animals, respectively. Susceptibility to experimental infection was heterogeneous with some animals surviving inoculation with large numbers of organisms and others succumbing after inoculation with small numbers. Production and longevity of serum antibody titers, as measured by passive hemagglutination tests, were variable as well, and apparently unrelated to dose. The data presented attest to the need for care in interpreting serologic tests results for individual animals.
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PMID:Experimental plague in rock squirrels, Spermophilus variegatus (Erxleben). 403 20

Yersinia pseudotuberculosis was isolated from placenta and abomasal contents of triplet goat kids, two of which were aborted and one of which died shortly after birth. Necropsy findings in the kids were suppurative placentitis and suppurative pneumonia. The public health implications in intrauterine Yersinia infection in goats are discussed.
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PMID:Abortion and early neonatal death of kids attributed to intrauterine Yersinia pseudotuberculosis infection. 405 3

Infection of several strains of laboratory mice with a virulent strain of Yersinia enterocolitica was followed by performing viable bacterial counts on homogenates of selected tissues at intervals after intragastric, aerogenic, or intravenous infection. It is observed that CD-1 mice are more susceptible to Y. enterocolitica infection than either the C(57)B1/6 or B6D2 strains. Development of an enteric infection is dose dependent; less than 5 x 10(7) organisms by mouth yields sporadic, low levels of systemic infection, with many of the animals showing no apparent infection. Increasing the challenge inoculum by a factor of 10 eliminates the variability among the animals, giving rise to an enteric infection in all of the mice that moves quickly to the mesenteric lymph node. The bacterial population in the lymph node multiplies rapidly, and the infection is disseminated to the spleen, liver, and lungs, ultimately killing most of the animals. Exposure to an aerogenic challenge of less than 1,000 organisms resulted in a fulminating pneumonitis with an invariably fatal outcome. Intravenous challenge with 500 organisms caused a rapidly fatal, systemic infection. The growth of the bacteria in the intravenously infected mouse depends upon the temperature at which the challenge inoculum had been grown in vitro. At temperatures below 26 C, the bacteria are cleared from the blood at a slower rate and are more resistant to intracellular killing, as compared to organisms grown at 37 C. This effect results in the inoculum increasing to greater numbers in the tissues in a shorter period of time.
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PMID:Experimental Yersinia enterocolitica infection in mice: kinetics of growth. 459 77


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