Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An antigenically distinct adenovirus is described which was isolated in March 1973 from the lungs and kidney of a 61-year-old woman who died of diffuse interstitial adenovirus pneumonia 55 days after receiving a cadaveric renal allograft. Complement fixation, hemagglutination inhibition, and serum neutralization tests on sequential serum specimens from the patient confirmed that the adenovirus infection occurred in coincidence with her clinical illness and failed to document concomitant infection by any other common respiratory agent. Pathological and virological findings indicated that the pneumonia was only one manifestation of a disseminated adenovirus infection, the source of which may have been a latent infection pre-existing in the donor kidney. The adenovirus, purified by terminal dilution and plaque procedures, has antigenic, morphological, biological, biophysical, host susceptibility, and hemagglutinating properties characteristic of adenovirus group 1A. Buoyant densities in CsCl are 1.340 g/ml for the virion, 1,300 g/ml for the group complement-fixing (hexon) antigen, and 1.290 g/ml for the major soluble complete hemagglutinin (dodecon). The virus was serologically distinct from adenoviruses 1 to 34 in reciprocal serum neutralization tests with antisera to these viruses. We propose this virus as candidate adenovirus type 35 (holden).
 ...
PMID:New human adenovirus (candidate adenovirus type 35) causing fatal disseminated infection in a renal transplant recipient. 7 5

Viral infections and clinical complications were studied during hemodialysis and after renal transplantation. Active cytomegalovirus infection developed in 96% of patients after renal transplantation; reactivation of herpes simplex, varicella-zoster, and Epstein-Barr viruses was found in 35%, 24%, and 0% of patients, respectively. Cytomegalovirus viremia developed in 42% of patients an average of two months after renal transplantation, lasted 1.75 (+/- 1.5) months (except in one patient with chronic viremia), and was followed by chronic viruria. Higher titers of infectious cytomegalovirus were found in the polymorphonuclear than in the mononuclear leukocyte fraction. Reactivation of a latent infection and, less likely, respiratory infection appear to be the most probable mechanisms of cytomegalovirus infection after renal transplantation. One to three months after transplant, cytomegalovirus infection may be related to fever, arthralgia, pneumonitis, and leukopenia; three to four months after transplant, the virus may be related to hepatitis; and 12-30 months after transplant, it may be related to retinitis in patients with chronic viremia. Although other causes of these complications are possible, herpes simplex virus, Epstein-Barr virus, varicella-zoster virus, measles virus, adenovirus, hepatitis B virus, and Toxoplasma gondii appear to be of lesser importance than cytomegalovirus in this respect.
 ...
PMID:Epidemiology of cytomegalovirus infection after transplantation and immunosuppression. 17 15

Cytomegalovirus infections are common throughout the world. Certain populations, including pregnant women and their fetuses, immunosuppressed patients, and recipients of large amounts of transfused blood, are at increased risk. Although the majority of infections in all groups of patients are clinically inapparent, variable symptoms, including fever, rash, pneumonitis, and hepatitis, can occur. The infected host develops antibodies against CMF, but frequently, despite this appropriate immune response, infection becomes chronic with prolonged excretion of virus. In some instances, a latent infection, with disappearance of virus, develops and under a variety of circumstances, including immunosuppression, infection can later be reactivated with reappearance of viral excretion. The human consequences of latent infection with CMV are not yet fully appreciated, and future research on this virus with multifaceted potential will need to focus on this issue.
 ...
PMID:Cytomegalovirus infections. 22 89

Animal models for Pneumocystis carinii, for the most part, have been limited to immunosuppressed rats and ferrets, while a dependable mouse model has been more difficult to develop. A P. carinii mouse model has now been established with several strains of mice, including C3Heb/FeJ, C3HeN, BALB/c, DBA/2N, and BALB/c nu/nu (athymic). In lieu of using invasive methods for initiating P. carinii infections, mice harboring P. carinii transmitted the disease to mice without latent infection via short-term cohabitation. After the exposure period, the seed mice were sacrificed to confirm the presence of acute P. carinii pneumonia. Acute infections in recipient mice developed at approximately 7 to 8 weeks, while control unseeded littermates remained uninfected. All recipient mice and their littermates were maintained in isolation hoods to eliminate the possibility of exposure to other sources of P. carinii. This approach allows investigators to consistently transmit P. carinii to mice and to select the strain of mouse desired for use in a particular study. The results presented here suggest that more attention should be given to the potential for patient-to-patient transmission of P. carinii in immunocompromised patients such as those with AIDS.
 ...
PMID:Mouse model for Pneumocystis carinii pneumonia that uses natural transmission to initiate infection. 154 65

Pneumocystis carinii is a frequent cause of interstitial pneumonitis in patients with cell-mediated immunodeficiencies. Extrapulmonary P carinii infection is a rare manifestation of disease caused by this organism. Nevertheless, reports of extrapulmonary P carinii infection are increasing in the setting of the acquired immunodeficiency syndrome (AIDS). We report two cases of extrapulmonary P carinii infection in patients with AIDS and review the literature on this subject. We identified 37 such cases: in 19 cases, P carinii pneumonia was present concurrently; in 18 cases, involvement was exclusively extrapulmonary. A minority of patients were receiving aerosolized pentamidine isethionate therapy. Most patients had a history of P carinii pneumonia, and other AIDS-related illnesses, such as cytomegalovirus infection, mycobacterial disease, candidiasis, Kaposi's sarcoma, and cryptococcosis were common. Concurrent cytomegalovirus infection indicated a poor prognosis, while otic pneumocytosis was associated with a favorable outcome. Pathologic evidence suggested that extrapulmonary pneumocystosis occurred by hematogenous and lymphatic dissemination from the lungs in most cases. In other cases, extrapulmonary pneumocystosis appeared to be due either to reactivation of latent infection in extrapulmonary sites or to primary infection of these sites. Further studies are needed to determine the true frequency of extrapulmonary involvement in P carinii infections and to define risk factors for acquisition of extrapulmonary pneumocytosis.
 ...
PMID:Extrapulmonary Pneumocystis carinii infections in the acquired immunodeficiency syndrome. 204 23

Pneumocystis carinii has been recognized as a cause of pneumonia in immunocompromised patients for over 40 years. Until the 1980s, Pneumocystis pneumonia (pneumocystosis) was most often seen in patients undergoing chemotherapy for malignancy or transplantation. Infection could be prevented by trimethoprim-sulfamethoxazole prophylaxis; thus, it was an uncommon clinical problem. With the onset of the AIDS epidemic, Pneumocystis pneumonia has become a major problem in the United States because it develops in approximately 80% of patients with AIDS and because almost two-thirds of patients have adverse reactions to anti-Pneumocystis drugs. Thus, physicians and laboratories in any community may be called upon to diagnose and provide care for patients with Pneumocystis pneumonia. The classification of the organism is currently controversial, but it is either a protozoan or a fungus. P. carinii appears to be acquired during childhood by inhalation and does not cause clinical disease in healthy persons but remains latent. If the person becomes immunosuppressed, the latent infection may become activated and lead to clinical disease. Damage of type I pneumocytes by Pneumocystis organisms leads to the foamy alveolar exudate which is characteristic of the disease. Diagnosis is established by morphologic demonstration of Pneumocystis organisms in material from the lungs. Current efforts to find better anti-Pneumocystis drugs should provide more effective therapy and prophylaxis.
 ...
PMID:Pneumocystis carinii, an opportunist in immunocompromised patients. 207 Mar 42

Although infection with cytomegalovirus (CMV) continue to be recognized relatively frequently after organ transplantation, a decrease in their severity has been described with the use of newer immunosuppressive regimens. In particular whereas antithymocyte globulin was associated with an increase in morbidity and mortality, the use of cyclosporin A has resulted in a decrease in the frequency of symptomatic infections. Several sources of CMV infection in transplant recipients are: immunosuppression secondary to drug therapy can result in reactivation of the latent infection present before transplantation; blood transfusion, either pretransplant red blood cell transfusion or blood required at the time of surgery can also result in transmission of CMV and primary infection; the transplanted kidney or heart, particularly in situations in which seropositive organs are transmitted into seronegatives can serve as the vehicle for transmission. Recent data suggest that transmission of organ donor CMV can occur even in seropositive recipients. The clinical manifestations of CMV infection in transplant recipients range from asymptomatic or mild mononucleosis syndromes to severe infection. It is generally accepted that primary infections in patients who were seronegative before transplantation are more severe than reactivated infections. Involvement of multiple organ systems has been common, with retinitis, pneumonitis and gastrointestinal manifestations occurring most commonly. A specific CMV infection of the kidney has also been described but its manifestations are variable. The association of CMV infections with rejection remains controversial in human transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Cytomegalovirus infections in renal, heart, heart-lung and liver transplantation. 245 12

Corneal intrastromal inoculation of guinea pigs with approximately 10(4) plaque-forming units of live, adapted varicella-zoster virus (VZV) resulted in reproducible, acute, superficial corneal disease in all animals. The culture-positive VZV ocular infection progressed to involve 30% to 40% of the corneal surface in a diffuse punctate keratitis and 10% to 15% of this surface with microdendrites, characteristic of VZV-induced ocular disease. Retrograde dissemination of VZV to the trigeminal ganglia, midbrain, cerebellum, and superior cervical ganglia was demonstrated by whole-cell coculture VZV recovery. Central nervous system VZV dissemination, manifested by transient neurologic symptoms and pneumonitis, was evident in 60% of the animals. Varicella-zoster virus spread to the trigeminal ganglion during acute and early-latent infection was evident by electron microscopy.
 ...
PMID:Ocular varicella-zoster virus infection in the guinea pig. A new in vivo model. 254 23

Varicella zoster (VZV) and herpes simplex (HSV) viruses commonly cause self-limited infection of the skin and mucous membranes. However, certain groups of subjects, including neonates, cancer patients, organ and bone marrow transplant recipients and those with congenital or acquired deficiencies of cell mediated immunity, are at increased risk for dissemination of either virus to the lungs and/or other viscera. The highest risk for VZV pneumonitis is in bone marrow transplant recipients, 44%, and in children with acute leukemia, 32%. The mortality from this complication of VZV infection in the preantiviral era was at least 25%. Except for neonates, dissemination and mortality rates for HSV infections are less than for VZV infections in the high risk groups. Cell-mediated immunity has a major role in both recovery from primary infection and modulation of latent infection, but antiherpes antibodies also have an important role in moderating the extent and severity of infection. Both viruses cause a patchy nodular pneumonia with scattered necrotic and hemorrhagic foci. Physical examination is often misleading and rapid progression of pneumonia can occur within hours. Intravenous acyclovir, administered early in the course of HSV and VZV infection at dosages of 250 mg/m2 and 500 mg/m2 every eight hours, respectively, has nearly eliminated the risk of severe symptomatic pneumonitis. Treatment of established pneumonitis with acyclovir at these doses has also reduced the mortality of herpesvirus pneumonias.
 ...
PMID:Varicella zoster and herpes simplex virus pneumonias. 332 Dec 72

Since 1959, the Pig Health Control Association (PHCA) has run a national health-control scheme for pig herds believed to be free from enzootic pneumonia. During this time, many herds developed this disease without a simple explanation. From 1968, 55 such unexplained breakdowns have been studied in detail. The first signs in 50 breakdowns were either coughing in growing pigs (52 per cent of outbreaks), illness in adult stock (34 per cent of outbreaks) or pneumonia in routinely slaughtered pigs (14 per cent of outbreaks). In some outbreaks, enzootic pneumonia appeared to grow out of a pre-existing respiratory infection, which was not identified as enzootic pneumonia, in suckling pigs, suggesting that either Mycoplasma hyopneumoniae was already present in a latent state, or it more readily seeded damaged respiratory tracts from outside. In three outbreaks of this type, where pathological material was collected during the transition period, no laboratory evidence was obtained for the presence of M hyopneumoniae in the primary respiratory disease. Analysis of breakdowns in two national testing stations indicated that clinical/pathological signs might not develop until three to five months after the introduction of an infected group of weaners. It is possible, therefore, that a pig herd might not show obvious signs of the disease until up to six months or more after initial infection. There was little evidence to indicate that unexplained breakdowns arose from long term latent infection in other herds from which stock had been imported. There was considerable evidence, however, to suggest that breakdowns arose from extraneous sources.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Apparent reinfection of enzootic-pneumonia-free pig herds: early signs and incubation period. 649 92


1 2 3 4 5 6 Next >>