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

A retrospective analysis of absolute numbers in 802 white blood counts and 396 sedimentation rates of 407 children, admitted between 1973-78, with 9 "classic" infections was done and evaluated for diagnostic usefulness. As diagnostic meaningful it was found: Lymphocytosis in pertussis; lymphocytopenia and slight increased sedimentation rate in measles; nothing particular in mumps; slight increased sedimentation rate in chicken pox; increase in mononuclear cells, particularly atypical lymphocytes and sedimentation rate in infectious mononucleosis; leucocytopenia caused by neutrocytopenia and lymphocytopenia in exanthema subitum (roseola infantum); increased sedimentation rate in scarlet fever; lymphocytopenia and a high sedimentation rate in mycoplasma-pneumonia; leucocytopenia with lymphocytopenia in rubella.
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PMID:[Leucocyte number, differential count and sedimentation rate in 9 "classic" childhood infections. (author's transl)]. 719 42

Human herpesvirus-6 (HHV-6) infects the majority of children under the age of 2 years causing roseola infantum. Following short self-limited disease, the virus enters into a latency phase in peripheral blood lymphocytes (PBL). It has been previously reported that HHV-6 reactivation from latency, in immunocompromised patients undergoing bone marrow transplantation (BMT), could result in febrile illness, pneumonitis, meningitis, and/or encephalitis. In our study, 14 BMT patients received two different antiviral prophylactic therapies: 8 patients received acyclovir, whereas 6 patients received ganciclovir. Clinical manifestations and virus recovery were monitored pre- and post-BMT by polymerase chain reaction tests of cord blood cells cultured with the patients' PBL. No HHV-6 recovery was shown in the 6 patients treated with ganciclovir, whereas 3 of the 8 acyclovir-treated patients experienced virus reactivation 20-21 days post-BMT. One of the 3 patients was asymptomatic but had late engraftment; the second patient had prolonged fever, skin rash, and hemorrhage; the third patient experienced prolonged fever, pneumonitis, marrow rejection, and fatal encephalitis. It is concluded that viral reactivation may be prevented by prophylactic treatment with ganciclovir. Our observation awaits further documentation in prospective randomized trials in high-risk BMT recipients.
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PMID:Antiviral prophylaxis may prevent human herpesvirus-6 reactivation in bone marrow transplant recipients. 1212 21

Human herpesvirus 6 (HHV-6) infections occur in > 95% of humans. Primary infection, which occurs in early childhood as an asymptomatic illness or manifested clinically as roseola infantum, leads to a state of subclinical viral persistence and latency. Reactivation of latent HHV-6 is common after liver transplantation, possibly induced and facilitated by allograft rejection and immunosuppressive therapy. Since the vast majority of humans harbor the virus in a latent state, HHV-6 infections after liver transplantation are believed to be mostly due to endogenous reactivation or superinfection (reactivation in the transplanted organ). In a minority of cases, however, primary HHV-6 infection may occur when an HHV-6 negative individual receives a liver allograft from an HHV-6 positive donor. The vast majority of documented HHV-6 infections after liver transplantation are asymptomatic. In a minority of cases, HHV-6 has been implicated as a cause of febrile illness with rash and myelosuppression, hepatitis, pneumonitis, and encephalitis after liver transplantation. In addition, HHV-6 has been associated with a variety of indirect effects such as allograft rejection, and increased predisposition and severity of other infections including cytomegalovirus (CMV), hepatitis C virus, and opportunistic fungi. Because of the uncommon nature of the clinical illnesses directly attributed to HHV-6, there is currently no recommended HHV-6-specific approach to prevention. However, ganciclovir and valganciclovir, which are primarily intended for the prevention of CMV disease, are also active against HHV-6 and may prevent its reactivation after transplantation. The treatment of established HHV-6 disease is usually with intravenous ganciclovir, cidofovir, or foscarnet, complemented by reduction in the degree of immunosuppression. This article reviews the current advances in the pathogenesis, clinical diagnosis, and therapeutic modalities against HHV6 in the setting of liver transplantation.
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PMID:Human herpesvirus 6 infections after liver transplantation. 1949 84

Human herpes virus 6 (HHV-6) infects > 95% of humans. Primary infection which occurs mostly during the first 2 years of life in the form of roseola infantum, non-specific febrile illness, or an asymptomatic illness, results in latency. Reactivation of latent HHV-6 is common after liver transplantation. Since the majority of human beings harbor the latent virus, HHV-6 infections after liver transplantation are most probably caused by endogenous reactivation or superinfection. In a minority of cases, primary HHV-6 infection may occur when an HHV-6-seronegative individual receives a liver allograft from an HHV-6-seropositive donor. The vast majority of HHV-6 infections after liver transplantation are asymptomatic. Only in a minority of cases, when HHV-6 causes a febrile illness associated with rash and myelosuppression, hepatitis, gastroenteritis, pneumonitis, and encephalitis after liver transplantation. In addition, HHV-6 has been implicated in a variety of indirect effects, such as allograft rejection and increased predisposition to and severity of other infections, including cytomegalovirus, hepatitis C virus, and opportunistic fungi. Because of the uncommon nature of the clinical illnesses directly attributed to HHV-6, there is currently no recommended HHV-6-specific approach prevention after liver transplantation. Asymptomatic HHV-6 infection does not require antiviral treatment, while treatment of established HHV-6 disease is treated with intravenous ganciclovir, foscarnet, or cidofovir and this should be complemented by a reduction in immunosuppression.
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PMID:Impact of human herpes virus 6 in liver transplantation. 2116 Oct 19

Human herpesviruses 6 and 7 are ubiquitous herpesviruses that normally infect their hosts early in life. There are two variant groups of human herpesvirus 6 (HHV-6): variants A (HHV-6A) and B (HHV-6B). Variant A has not been unambiguously associated with a specific disease but may contribute to disease in immunocompromised patients; variant B is the major etiologic agent of roseola (roseola infantum or exanthem subitum) and other febrile illnesses of young children, and has been associated with disease in immunocompromised patients. HHV-6B is frequently present in plaque regions in the brains of multiple sclerosis patients, although an etiologic association has not been proven. Human herpesvirus 7 (HHV-7) has been associated with some cases of roseola. The clinical spectrum of these viruses remains to be completely defined. Braun et al. (1) recently described three clinical scenarios that might warrant the use of antivirals to treat HHV-6 infections: (1) transplant recipients with idiopathic pneumonitis (2), multiple sclerosis patients, and (3) patients with HHV-6-associated encephalitis. For HHV-7, cases of neurologic involvement during primary infection might warrant investigation (2).
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PMID:Antiviral screening assays for human herpesviruses 6 and 7. 2133 5