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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute measles is a classic infectious disease of childhood with worldwide distribution. Its causative agent, measles virus (MV), is an efficient pathogen, persisting in nature in populations large enough to support it, even though it is able to cause an acute infection in any individual only once in his lifetime. The characteristic clinical hallmarks of measles, fever and rash, coincide with antiviral immune response. MV-specific T lymphocyte and antibody responses contribute to virus clearance and protection from reinfection, respectively. Concomitant with immune activation immunologic abnormalities arise during MV infection. The ensuing suppression of cellular immune responses is presumably responsible for increased susceptibility to other infections. Additionally, central nervous system (CNS) complications of MV infection with different pathogenesis occur. Autoimmune disease may appear in the form of acute measles encephalomyelitis. Furthermore, MV may persist in the CNS in rare cases without periodic shedding of infectious virus. Measles inclusion body encephalitis can develop on the basis of inadequate virus-specific cell-mediated immune responses and subacute sclerosing panencephalitis occurs many years after primary measles as a slow virus infection. Host cell factors operating in cells of the CNS together with mutations particularly in genes coding for viral envelope proteins initiate and maintain the persistent state of infection with a viral replication cycle that is attenuated at the transcriptional and translational level.
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PMID:Measles virus infections of the central nervous system. 945 Feb 34

The patient is a 10-year-old male who experienced somnolence and incomplete quadriplegia after headache and vomiting, without exanthema, for 3 days. The clinical course and magnetic resonance imaging findings of the brain and spinal cord were compatible with acute disseminated encephalomyelitis. The serologic examination revealed that the patient had rubeola because titers of IgM and IgG antibody to measles virus measured by enzyme immunoassay were 0.91 and 40 (cutoff = 0.80 and 2), respectively, at 5 weeks after the onset, the IgM titer had become negative (0.56), and the IgG titer had decreased to 17.7 at 13 weeks after the onset. Because the patient had received a measles-mumps-rubella vaccine at 12 months of age, the acute disseminated encephalomyelitis was thought to be attributed to the modified measles resulting from measles vaccine failure.
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PMID:Acute disseminated encephalomyelitis with probable measles vaccine failure. 1037 90

The effects of measles are relatively mild in well-nourished children, but are associated with high mortality in those who are malnourished and in those who have other diseases. Complications may include bacterial pneumonia, bronchitis, otitis media, gastroenteritis, myocarditis, hepatitis, and encephalomyelitis. The Expanded Program on Immunization was introduced to India in 1978, but measles immunization did not commence until 1985 under the Universal Immunization Program. Total district coverage was achieved in 1990, followed by a peak immunization coverage figure of 90.9% in 1991. Coverage rates declined, however, to 85.8% in 1992-93. Impressive though they may be, these coverage rates obfuscate the reality that measles remains a major cause of morbidity and childhood mortality in India. Coverage levels remain under 50% in many tribal and remote areas, with 49,453 notified cases at the time of printing. Overall case fatality rates for the country are in the range of 2-15% due to a synergistic relationship between malnutrition and infection. One must therefore not rest in the fight against measles. Sudden outbreaks should be reported immediately and vitamin A supplements and immunization supplies readied in anticipation of epidemic. The many reasons why vaccine coverage rates remain low in some areas include the failure of many parents, health personnel, and some doctors to regard measles as a serious disease; restrictive vaccine administration directives requiring the presence of a physician; physician reticence to open a 10-dose vial for 1-2 patients; and parental and physician reluctance to immunize children who are slightly ill or where minor adverse side reactions such as fever and rash may be anticipated.
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PMID:Measles is down but not out. 1217 72

The guidance in this report is for evaluation and treatment of patients with complications from smallpox vaccination in the preoutbreak setting. Information is also included related to reporting adverse events and seeking specialized consultation and therapies for these events. The frequencies of smallpox vaccine-associated adverse events were identified in studies of the 1960s. Because of the unknown prevalence of risk factors among today's population, precise predictions of adverse reaction rates after smallpox vaccination are unavailable. The majority of adverse events are minor, but the less-frequent serious adverse reactions require immediate evaluation for diagnosis and treatment. Agents for treatment of certain vaccine-associated severe adverse reactions are vaccinia immune globulin (VIG), the first-line therapy, and cidofovir, the second-line therapy. These agents will be available under Investigational New Drug (IND) protocols from CDC and the U.S. Department of Defense (DoD). Smallpox vaccination in the preoutbreak setting is contraindicated for persons who have the following conditions or have a close contact with the following conditions: 1) a history of atopic dermatitis (commonly referred to as eczema), irrespective of disease severity or activity; 2) active acute, chronic, or exfoliative skin conditions that disrupt the epidermis; 3) pregnant women or women who desire to become pregnant in the 28 days after vaccination; and 4) persons who are immunocompromised as a result of human immunodeficiency virus or acquired immunodeficiency syndrome, autoimmune conditions, cancer, radiation treatment, immunosuppressive medications, or other immunodeficiencies. Additional contraindications that apply only to vaccination candidates but do not include their close contacts are persons with smallpox vaccine-component allergies, women who are breastfeeding, those taking topical ocular steroid medications, those with moderate-to-severe intercurrent illness, and persons aged < 18 years. In addition, history of Darier disease is a contraindication in a potential vaccinee and a contraindication if a household contact has active disease. In the event of a smallpox outbreak, outbreak-specific guidance will be disseminated by CDC regarding populations to be vaccinated and specific contraindications to vaccination. Vaccinia can be transmitted from a vaccinee's unhealed vaccination site to other persons by close contact and can lead to the same adverse events as in the vaccinee. To avoid transmission of vaccinia virus (found in the smallpox vaccine) from vaccinees to their close contacts, vaccinees should wash their hands with warm soapy water or hand rubs containing > or = 60% alcohol immediately after they touch their vaccination site or change their vaccination site bandages. Used bandages should be placed in sealed plastic bags and can be disposed of in household trash. Smallpox vaccine adverse reactions are diagnosed on the basis of clinical examination and history, and certain reactions can be managed by observation and supportive care. Adverse reactions that are usually self-limited include fever, headache, fatigue, myalgia, chills, local skin reactions, nonspecific rashes, erythema multiforme, lymphadenopathy, and pain at the vaccination site. Other reactions are most often diagnosed through a complete history and physical and might require additional therapies (e.g., VIG, a first-line therapy and cidofovir, a second-line therapy). Adverse reactions that might require further evaluation or therapy include inadvertent inoculation, generalized vaccinia (GV), eczema vaccinatum (EV), progressive vaccinia (PV), postvaccinial central nervous system disease, and fetal vaccinia. Inadvertent inoculation occurs when vaccinia virus is transferred from a vaccination site to a second location on the vaccinee or to a close contact. Usually, this condition is self-limited and no additional care is needed. Inoculations of the eye and eyelid require evaluation by an ophthalmologist and might require therapy with topical antiviral or antibacterial medications, VIG, or topical steroids. GV is characterized by a disseminated maculopapular or vesicular rash, frequently on an erythematous base, which usually occurs 6-9 days after first-time vaccination. This condition is usually self-limited and benign, although treatment with VIG might be required when the patient is systemically ill or found to have an underlying immunocompromising condition. Infection-control precautions should be used to prevent secondary transmission and nosocomial infection. EV occurs among persons with a history of atopic dermatitis (eczema), irrespective of disease severity or activity, and is a localized or generalized papular, vesicular, or pustular rash, which can occur anywhere on the body, with a predilection for areas of previous atopic dermatitis lesions. Patients with EV are often systemically ill and usually require VIG. Infection-control precautions should be used to prevent secondary transmission and nosocomial infection. PV is a rare, severe, and often fatal complication among persons with immunodeficiencies, characterized by painless progressive necrosis at the vaccination site with or without metastases to distant sites (e.g., skin, bones, and other viscera). This disease carries a high mortality rate, and management of PV should include aggressive therapy with VIG, intensive monitoring, and tertiary-level supportive care. Anecdotal experience suggests that, despite treatment with VIG, persons with cell-mediated immune deficits have a poorer prognosis than those with humoral deficits. Infection-control precautions should be used to prevent secondary transmission and nosocomial infection. Central nervous system disease, which includes postvaccinial encephalopathy (PVE) and postvaccinial encephalomyelitis (or encephalitis) (PVEM), occur after smallpox vaccination. PVE is most common among infants aged < 12 months. Clinical symptoms of central nervous system disease indicate cerebral or cerebellar dysfunction with headache, fever, vomiting, altered mental status, lethargy, seizures, and coma. PVE and PVEM are not believed to be a result of replicating vaccinia virus and are diagnoses of exclusion. Although no specific therapy exists for PVE or PVEM, supportive care, anticonvulsants, and intensive care might be required. Fetal vaccinia, resulting from vaccinial transmission from mother to fetus, is a rare, but serious, complication of smallpox vaccination during pregnancy or shortly before conception. It is manifested by skin lesions and organ involvement, and often results in fetal or neonatal death. No known reliable intrauterine diagnostic test is available to confirm fetal infection. Given the rarity of congenital vaccinia among live-born infants, vaccination during pregnancy should not ordinarily be a reason to consider termination of pregnancy. No known indication exists for routine, prophylactic use of VIG in an unintentionally vaccinated pregnant woman; however, VIG should not be withheld if a pregnant woman develops a condition where VIG is needed. Other less-common adverse events after smallpox vaccination have been reported to occur in temporal association with smallpox vaccination, but causality has not been established. Prophylactic treatment with VIG is not recommended for persons or close contacts with contraindications to smallpox vaccination who are inadvertently inoculated or exposed. These persons should be followed closely for early recognition of adverse reactions that might develop, and clinicians are encouraged to enroll these persons in the CDC registry by calling the Clinician Information Line at 877-554-4625. To request clinical consultation and IND therapies for vaccinia-related adverse reactions for civilians, contact your state health department or CDC's Clinician Information Line (877-554-4625). Clinical evaluation tools are available at http.//www.bt.cdc.gov/agent/smallpox/vaccination/clineval. Clinical specimen-collection guidance is available at http://www.bt.cdc.gov/agent/smallpox/vaccination/vaccinia-specimen-collection.asp. Physicians at military medical facilities can request VIG or cidofovir by calling the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID) at 301-619-2257 or 888-USA-RIID.
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PMID:Smallpox vaccination and adverse reactions. Guidance for clinicians. 1261 10

Age distribution, history of vaccination against measles, clinical signs and symptoms were investigated among a total of 113 adult measles patients admitted in our hospital between January, 2000 and December, 2002. The maximum body temperature, duration of fever, presence of Koplik spot and exanthema among these adult inpatients were compared with those among 1-to-5-year-old inpatients having measles. Concerning age distribution, the peak was found at the age of 20-24 years. Most of adult inpatients had not contracted measles until then and had not been vaccinated against measles. The infection route was unknown except a small number of inpatients. Clinical signs and symptoms among adult inpatients were about the same of those in pediatric inpatients except a sore throat. Complications occurred in 17 cases out of 113 adult inpatients, 4 of them had encephalitis or acute disseminated encephalomyelitis and the other 4 cases contracted pneumonia. Among the 45 child inpatients, whereas, 23 had complications, 13 of them had pneumonia, 3 contracted otitis media, and an additional 3 suffered from both pneumonia and otitis media. From the results it is reasonably concluded that clinical signs and symptoms among adults impatients with measles are comparable with those of pediatric measles inpatients or slightly severer.
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PMID:[Clinical investigation on adult inpatients contracted measles; comparing with pediatric measles inpatients]. 1460 14

In developing guidelines for the improved management of herpesvirus infections of the central nervous system (CNS), the International Herpes Management Forum (IHMF) has considered human herpesvirus (HHV) type 6 and type 7 disease. Although HHV-6 is generally asymptomatic, it has been associated with exanthema subitum, febrile convulsions and encephalitis in infants and immunocompromised adults and may play a role in multiple sclerosis, Guillain-Barre syndrome and acute disseminated encephalomyelitis. As HHV-6 is present in the brain tissue of healthy individuals, its role as an aetiological agent in CNS disorders is unclear. While polymerase chain reaction (PCR) is a method useful for diagnosis of other viral CNS infections, it has no value for diagnosing HHV-6. HHV-7 has not been shown to cause a specific disease but is associated with febrile convulsions and has been implicated as a cause of encephalitis. Ganciclovir and foscarnet, either alone or in combination, may be used for the management of HHV-6-related neurological disease. Although ganciclovir is unlikely to be effective against HHV-7-related CNS disease, foscarnet may be useful but prospective trials are needed.
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PMID:Human herpesvirus type 6 and human herpesvirus type 7 infections of the central nervous system. 1531 97

Alphaviruses are mosquito-borne, enveloped, plus-strand RNA viruses that cause a spectrum of diseases in humans that include fever, rash, arthritis, meningitis, and encephalomyelitis. Sindbis virus (SINV) is the prototype alphavirus, causes encephalomyelitis in mice, and provides a model system for studying the pathogenesis of alphavirus-induced neurological disease. Major target cells for SINV infection in the central nervous system (CNS) are neurons, and both host and viral factors determine the fate of infected neurons. Young animals are most susceptible to fatal disease. This correlates with the ability of SINV to induce apoptosis in immature neurons. In vitro, apoptotic death of neuroblastoma cells can be induced by fusion of the virus envelope with the endosomal membrane and does not require infectious virus. This fusion process activates acid sphingomyelinase that cleaves sphingomyelin to release ceramide, an initiator of apoptosis. Within an hour, poly(ADP-ribose) polymerase is activated, and this is followed by release of cytochrome c and activation of effector caspases. SINV-induced cell death can be delayed or prevented by treatment with antioxidants or caspase inhibitors and by intracellular expression of Bcl-2, Beclin-1, or protease inhibitors. Older animals survive infection unless infected with a neurovirulent strain of SINV. In these mice, anterior horn motor neurons die by a primarily necrotic process that is influenced by excitotoxic amino acids and inflammation, whereas hippocampal neurons can be either apoptotic or necrotic. Death also occurs in uninfected neurons in the vicinity of infected neurons and can be delayed or prevented by treatment with glutamate receptor antagonists.
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PMID:Neuronal cell death in alphavirus encephalomyelitis. 1579 51

This study investigated the clinical manifestations and outcomes of central nervous system (CNS) infection by enteroviruses. Cases with CNS involvement among all enterovirus-culture-positive cases from January 1995 to June 2003 were retrospectively reviewed. Among 1028 enterovirus-culture-positive cases, there were 333 cases involving the CNS. Of these, the ratio of male to female subjects was 1.78, and the mean (+/- standard deviation) age was 6.83 +/- 5.9 years; 21 were premature neonates, and 10 failed to thrive. Disease entities included 282 cases of aseptic meningitis (84.7%), 44 cases of encephalitis (13.2%), and 7 cases of encephalomyelitis/polio-like syndrome (2.1%). Of these cases, 97.9% (326/333) had fever with peak body temperature at 38.9 degrees C, 85% had headache and vomiting, 70% had meningeal signs, 64% had neck stiffness, 16.6% (55/333) had change of consciousness, 5.4% (18/333) had seizures and 5.2% (17/333) had myoclonic jerks. Mannitol was administered in 77.2% of patients (257/333), along with intravenous immunoglobulin in 6.6% (22/333). Twelve cases received ventilator support. One patient died of hand-foot-and-mouth disease, encephalitis plus cardiopulmonary failure, and 2 premature neonates died of hepatic failure, disseminated intravascular coagulation, sepsis-like syndrome and myocarditis. Eighteen had neurologic sequelae, including 7 with limb weakness, 5 with epilepsy, 2 with sixth cranial nerve palsy, 3 with cerebral palsy, 4 with psychomotor retardation, 2 with spasticity, and 1 with hearing loss. Factors associated with unfavorable outcomes (death or sequelae) included younger age (p=0.0003), higher peak white blood cell count (WBC) [p=0.0009] and skin rash (p=0.005). Younger age and higher peak WBC were poor prognostic factors of severe enterovirus CNS infection. Death was related to neonatal enterovirus infection and enterovirus 71 infection in young children.
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PMID:Clinical features and factors of unfavorable outcomes for non-polio enterovirus infection of the central nervous system in northern Taiwan, 1994-2003. 1634 42

Clinical features and outcome of 2009 H1N1 influenza virus in the paediatric setting is ill-defined. The epidemiologic and clinical features of children with confirmed H1N1 influenza virus infection admitted to an Italian tertiary paediatric hospital from August through December 2009 were evaluated. A total of 63 children (mean age 4.3 years) were studied; of these, 29 (46%) had chronic underlying diseases. The most frequent symptoms and signs at admission were fever (97%), cough (60%) and respiratory disturbances (24%). Forty patients (63.5%) had H1N1-related complications: 32 (51%) pulmonary diseases, three (5%) neurological disorders, such as acute encephalitis or acute disseminated encephalomyelitis, and two (3%) haematological alterations. Three patients were admitted to the Intensive Care Unit. Most children (81%) were treated with oseltamivir: one developed rash during treatment; no other adverse events were noticed. All children survived without sequelae. In conclusions, 2009 H1N1 influenza virus infection in children is associated with a wide spectrum of clinical manifestations. Neurological disorders are not exceptional complications. Oseltamivir therapy seems safe also in infants.
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PMID:Clinical features of hospitalised children with 2009 H1N1 influenza virus infection. 2120 58

The aim of this review is to present briefly background information on 27 tick-borne viruses ("tiboviruses") that have been detected in Europe, viz flaviviruses tick-borne encephalitis (TBEV), louping-ill (LIV), Tyuleniy (TYUV), and Meaban (MEAV); orthobunyaviruses Bahig (BAHV) and Matruh (MTRV); phleboviruses Grand Arbaud (GAV), Ponteves (PTVV), Uukuniemi (UUKV), Zaliv Terpeniya (ZTV), and St. Abb's Head (SAHV); nairoviruses Soldado (SOLV), Puffin Island (PIV), Avalon (AVAV), Clo Mor (CMV), Crimean-Congo hemorrhagic fever (CCHFV); bunyavirus Bhanja (BHAV); coltivirus Eyach (EYAV); orbiviruses Tribec (TRBV), Okhotskiy (OKHV), Cape Wrath (CWV), Mykines (MYKV), Tindholmur (TDMV), and Bauline (BAUV); two thogotoviruses (Thogoto THOV, Dhori DHOV); and one asfivirus (African swine fever virus ASFV). Emphasis is laid on the taxonomic status of these viruses, range of their ixodid or argasid vectors and vertebrate hosts, pathogenicity for vertebrates including humans, and relevance to public health. In general, three groups of tibovirus diseases can be recognized according to main clinical symptoms produced: (i) febrile illness-usually with a rapid onset, fever, sweating, headache, nausea, weakness, myalgia, arthralgia, sometimes polyarthritis and rash; (ii) the CNS affection-meningitis, meningoencephalitis or encephalomyelitis with pareses, paralysis and other sequelae; (iii) hemorrhagic disease. Several "European" tiboviruses cause very serious human (TBEV, CCHFV) or animal (LIV, ASFV) diseases. Other arboviruses play definite role in human or animal pathology though the disease is usually either less serious or infrequently reported (TYUV, BHAV, AVAV, EYAV, TRBV, DHOV, THOV). The other European arboviruses are "orphans" without a proven medical or veterinary significance (BAHV, MTRV, MEAV, GAV, PTVV, ZTV, SAHV, UUKV, SOLV, PIV, AVAV, CMV, OKHV, CWV, MYKV, TDMV, BAUV). However, certain arbovirus diseases of free-living vertebrates (but also those of domestic animals and even man) may often pass unnoticed or misdiagnosed and eventually, they might potentially appear as emerging diseases. Active search for new tiboviruses or for new, pathogenic variants of the known tiboviruses in Europe should therefore continue.
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PMID:Tick-borne viruses in Europe. 2252 90


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