Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During the summer and fall of 1969 an outbreak of aseptic meningitis occurred in Montreal and its environs. Forty-four patients were admitted to the infectious disease ward of The Montreal Children's Hospital in August, September and October. Half of the patients were in the age group 6 to 10 years. The ratio of males to females was two to one. Patients showed the typical signs and symptoms of aseptic meningitis, namely fever, vomiting, headache, neck stiffness and pleocytosis of the cerebrospinal fluid.Viruses were recovered from 19 (43%) of the 44 cases. The predominant virus in the outbreak was a non-hemagglutinating strain of echovirus 6. Other virus types isolated in the outbreak were echovirus 7, coxsackievirus A9 and coxsackievirus B4. Serological investigations confirmed the validity of the echovirus isolations and identified additional cases.
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PMID:Aseptic meningitis, Montreal, 1969: a clinical and laboratory study. 510 41

During the summer-autumn of 1999, 390 specimens of cerebrospinal fluid were taken from infants and children younger than 15 years of age. They were suspected of having meningitis and were admitted to Princess Rahma Hospital, Northern Jordan. They were investigated for the presence of enteroviruses using shell vial culture and indirect immunofluorescence assays. Most cases (46.9%) occurred in children younger than 1 year of age in which males represented 71.9%. The common symptoms were fever, vomiting, and headache. Enteroviruses were isolated from 32 (8.2%) cases, coxsackievirus B types 2, 4, and 5 from 15 (46.9%) cases, and echovirus 9 (31.3%) was the most common identified serotype. The virus isolation rate was directly proportional to the number of leukocytes in the cerebrospinal fluid. However, enteroviral isolation was demonstrated in 4 (12.5%) of 32 cerebrospinal fluid specimens without pleocytosis. Leukocyte differential count revealed a predominance of polymorphonuclear cells in 71.4% of the cases. Hospitalization ranged from 1 day to 25 days with a mean of 7 days. The majority of enterovirus-infected patients (88.9%) were treated with at least one type of antibiotic. These results emphasize the importance of shell vial culture assay for diagnosing enteroviruses, especially in laboratories that do not have access to advanced techniques such as polymerase chain reaction.
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PMID:Enteroviral meningitis in Northern Jordan: prevalence and association with clinical findings. 1178 31

Enteroviral infections are more severe in neonates than in older children, and coxsackievirus B is most frequently associated with severe neonatal disease. We summarize the course and clinical data of four neonates with meningitis caused by coxsackievirus B5. Their clinical symptoms and signs were persistent fever, poor appetite, and decreased activity, with vomiting in two. Laboratory analysis of cerebrospinal fluid revealed the following: white blood count, 340-660/mm3; red blood count, 0-250/ mm3; glucose level, 47-59 mg/dl; and total protein level, 70-106 mg/dl. Echocardiography showed normal heart function. Final bacterial cultures of the cerebrospinal fluid showed no growth, whereas viral cultures showed coxsackievirus B5. All patients recovered without intravenous immunoglobulin. No complications occurred at 6-month follow-up.
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PMID:Neonatal meningitis caused by coxsackievirus B5. 1562 70

Coxsackie virus infection may be life-threatening, although in most cases, it is asymptomatic. Coxsackie virus infection can cause rhabdomyolysis. This study reports a 39-year-old female patient with chronic renal failure who presented with fever, myalgia, anuria, edema, vomiting, diarrhea, exacerbation of renal function, elevation of serum CK, CK-MB, CK-MM, myoglobin, and liver function abnormality. Serology for Coxsackie virus IgM antibody was positive at first, and IgG antibody became positive 4 weeks later. Muscle biopsy showed skeletal muscle denaturalization and necrosis. She underwent hemodialysis three times per week and then kidney transplantation. No evidence suggests relapse of Coxsackie virus infection 5 months after transplantation. As illustrated with the present case, serological testing may reveal an early, quick, and simple diagnosis in a case of rhabdomyolysis after a viral illness.
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PMID:Rhabdomyolysis following recent severe coxsackie virus infection in patient with chronic renal failure: one case report and a review of the literature. 1652 25

Enteroviruses (EVs) are the most commonly identified cause of aseptic meningitis. Rapid detection and characterization of EV meningitis is essential in making decisions for patient management and treatment. A total of 52 cases of acute aseptic meningitis that occurred from March 2003 to April 2005 were investigated for EVs using viral culture and/or molecular methods directly in the cerebrospinal fluid (CSF). EVs were detected in 21 out of 52 (40.4%) patients using reverse transcription-PCR (RT-PCR) and/or tissue culture. EVs were isolated from six out of 37 (16.2%) cultured specimens, while 20 out of 52 (38.4%) specimens yielded positive results when 5'non-coding region (5'NCR) RT-PCR assay was used. One specimen that was culture-positive was RT-PCR-negative. Using the VP1-2A RT-PCR and sequence analysis, 14 of the 21 positive EVs were identified as: four strains of Coxsackie virus B5, five echovirus 11, two echovirus 9, one echovirus 5, one echovirus 14, and one Coxsackie virus A9. Fever, headache, vomiting, and stiff neck were the most pronounced symptoms. Pleocytosis with the predominance of lymphocytes and mild elevated protein levels characterized the CSF specimens. Coxsackie virus B5 and echovirus 11 were the predominant serotypes during the study period. Although there was seasonal enteroviral activity (April-November), cases also occurred in the cold months. The 5'NCR and VP1-2A RT-PCR with sequence analysis were found to be superior to conventional methods for direct diagnosis and the typing of EVs.
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PMID:Enterovirus meningitis in Greece from 2003-2005: diagnosis, CSF laboratory findings, and clinical manifestations. 1696 Sep

Hand, foot, and mouth disease (HFMD) is caused by human enteroviruses, especially by enterovirus 71 (EV71) and coxsackievirus A16 (CA16). Patients infected with different enteroviruses show varied clinical symptoms. The aim of this study was to determine whether the etiological spectrum of mild and severe HFMD changed, and the association between pathogens and clinical features. From 2009 to 2013, a total of 2,299 stool or rectal specimens were collected with corresponding patient data. A dynamic view of the etiological spectrum of mild and severe HFMD in Shenzhen city of China was provided. EV71 accounted for the majority proportion of severe HFMD cases and fatalities during 2009-2013. CA16 and EV71 were gradually replaced by coxsackievirus A6 (CA6) as the most common serotype for mild HFMD since 2010. Myoclonic jerk and vomiting were the most frequent severe symptoms. Nervous system complications, including aseptic encephalitis and aseptic meningitis were observed mainly in patients infected by EV71. Among EV71, CA16, CA6, and CA10 infection, fever and pharyngalgia were more likely to develop, vesicles on the hand, foot, elbow, knee and buttock were less likely to develop in patients infected with CA10. Vesicles on the mouth more frequently occurred in the patients with CA6, but less in the patient with EV71. Associations between diverse enterovirus serotypes and various clinical features were discovered in the present study, which may offer further insight into early detection, diagnosis and treatment of HFMD.
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PMID:Characterization of severe hand, foot, and mouth disease in Shenzhen, China, 2009-2013. 2595 88

In this case study, a co-infection with coxsackievirus A5 (family Picornaviridae) and norovirus GII.4 (family Caliciviridae) was detected by RT-PCR in a faecal sample from a six-year-old girl with symptoms of severe acute encephalopathy subsequently diagnosed as the intermittent form of maple syrup urine disease (MSUD). The two co-infecting viruses, which had been detected previously, appeared to have triggered the underlying metabolic disorder. Here, we describe the genotyping of the viruses, as well as the chronological course, laboratory test results, and clinical presentation of this case, which included recurrent vomiting without diarrhoea, metabolic acidosis, unconsciousness, seizure and circulatory collapse, but with a positive final outcome.
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PMID:Co-infection with coxsackievirus A5 and norovirus GII.4 could have been the trigger of the first episode of severe acute encephalopathy in a six-year-old child with the intermittent form of maple syrup urine disease (MSUD). 2824 3

In this study, we investigated the epidemiology and molecular characteristics of enteroviruses associated with severe hand, foot and mouth disease (HFMD) in Shenzhen, China, during 2014-2018. A total of 137 fecal specimens from patients with severe HFMD were collected. Enterovirus (EV) types were determined using real-time reverse transcription polymerase chain reaction (RT-PCR), RT nested PCR, and sequencing. Sequences were analyzed using bioinformatics programs. Of 137 specimens tested, 97 (70.8%), 12 (8.8%), and 10 (7.3%) were positive for EV-A71, coxsackievirus A6 (CVA6), and CVA16, respectively. Other pathogens detected included CVA2 (2.9%, 4/137), CVA10 (2.9%, 4/137), CVA5 (0.7%, 1/137), echovirus 6 (E6) (0.7%, 1/137) and E18 (0.7%, 1/137). The most frequent complication in patients with proven EV infections was myoclonic jerk, followed by aseptic encephalitis, tachypnea, and vomiting. The frequencies of vomiting and abnormal eye movements were higher in EV-A71-infected patients than that in CVA6-infected or CVA16-infected patients. Molecular phylogeny based on the complete VP1 gene revealed no association between the subgenotype of the virus and disease severity. Nevertheless, 12 significant mutations that were likely to be associated with virulence or the clinical phenotype were observed in the 5'UTR, 2Apro, 2C, 3A, 3Dpol and 3'UTR of CVA6. Eight significant mutations were observed in the 5'UTR, 2B, 3A, 3Dpol and 3'UTR of CVA16, and 10 significant mutations were observed in the 5'UTR, VP1, 3A and 3Cpro of CVA10. In conclusion, EV-A71 is still the main pathogen causing severe HFMD, although other EV types can also cause severe complications. Potential virulence or phenotype-associated sites were identified in the genomes of CVA6, CVA16, and CVA10.
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PMID:Molecular epidemiology of enteroviruses associated with severe hand, foot and mouth disease in Shenzhen, China, 2014-2018. 3266 45