The mumps virus is similar to the measles virus. It is also spread by airborne contact and multiplies within the upper respiratory tract. It can cause swelling of the salivary glands, testes, pancreas, and inflammation of the central nervous system.
Epidemiology Disease Associations Pathogenesis Laboratory/Radiologic/Other Diagnostic Testing Gross Appearance and Clinical Variants Histopathological Features and Variants Special Stains/
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EPIDEMIOLOGY CHARACTERIZATION SYNONYMS INCIDENCE/PREVALENCE AGE SEX GEOGRAPHY EPIDEMIOLOGIC ASSOCIATIONS
DISEASE ASSOCIATIONS CHARACTERIZATION CONGENITAL IMMUNODEFICIENCY SYNDROMES Pathology of parainfluenza virus infection in patients with congenital immunodeficiency syndromes.
Madden JF, Burchette JL Jr, Hale LP.
Hum Pathol. 2004 May;35(5):594-603. Abstract quote
Infection with parainfluenza virus typically produces a mild, self-limited upper respiratory infection. However, parainfluenza infections have become increasingly recognized as a source of severe morbidity and mortality in immunocompromised patients.
In this retrospective study we identified 6 patients with congenital immunodeficiency and positive respiratory cultures for parainfluenza virus who died and underwent complete autopsy. Tissues obtained at autopsy were studied using hematoxylin and eosin-stained sections, immunoperoxidase staining for parainfluenza virus, and in selected cases, electron microscopy. All 6 patients exhibited typical cytopathic effects of parainfluenza virus, including giant cell formation, in lung and/or bronchial tissues. Parainfluenza virus infection was also documented by giant cell formation and immunohistochemistry in the pancreas (in 3 of 6 patients) and the kidney or bladder (in 2 of 4 patients). Anti-parainfluenza antibody also specifically reacted with cells in the gastrointestinal tract (in 2 of 4), spleen (in 4 of 6), thymus and/or lymph nodes (in 4 of 4), and small blood vessels in various organs (in 4 of 6). Pancreatic, bladder, colon, and thymic epithelial cell lines were susceptible to experimental infections with clinical isolates of parainfluenza virus type 3 in vitro.
Parainfluenza virus infection was serious in patients with congenital immunodeficiencies, contributing directly to death in 5 of the 6 patients studied. Because this virus is capable of infecting tissues in the gastrointestinal and urinary systems as well as in the respiratory tract, body secretions and fluids from each of these locations should be considered potentially infectious.
TRANSPLANT PATIENTS Parainfluenza and influenza virus infections in pediatric organ transplant recipients.
Apalsch AM, Green M, Ledesma-Medina J, Nour B, Wald ER.
Department of Pediatrics, University of Pittsburgh School of Medicine, Children's Hospital of Pittsburgh, Pennsylvania, USA
Clin Infect Dis. 1995 Feb;20(2):394-9. Abstract quote
We retrospectively reviewed parainfluenza and influenza virus infections that occurred in pediatric organ transplant recipients at our hospital from January 1985 through September of 1992.
Cultures of respiratory specimens revealed 45 infections in 42 transplant recipients (32 cases of parainfluenza and 13 cases of influenza virus infection). The following organs were transplanted: liver (28 patients), small bowel with and without liver (4), heart (3), lung with and without heart (5), and kidney (2). Clinical presentations of the patients and outcomes were similar regardless of the type of virus isolated or the type of organ transplanted. There were 20 cases in which patients had upper respiratory symptoms but did not require supplemental oxygen, nine cases in which patients required oxygen supplementation only, and eight cases in which the patients survived with mechanical ventilation.
Eight patients died (five had parainfluenza, three had influenza virus infection); four children had serious concurrent infections (cytomegaloviral pneumonia in one patient, bacteremia in two, bacteremia and pneumonia in one). Factors associated with poor outcome for the entire group were age (increased morbidity and mortality if < 6 months old), augmentation of immunosuppression, and onset of infection within 1 month of transplantation.
In this patient population, parainfluenza and influenza infections were important causes of morbidity and mortality.
CHARACTERIZATION RADIOLOGIC LABORATORY MARKERS
CHARACTERIZATION GENERAL VARIANTS PEDIATRIC Clinical manifestations of parainfluenza infection in children.
Yang TY, Lu CY, Kao CL, Chen RT, Ho YH, Yang SC, Lee PI, Chen JM, Lee CY, Huang LM.
Department of Pediatrics, National Taiwan University Hospital, Taipei, Taiwan, ROC
J Microbiol Immunol Infect. 2003 Dec;36(4):270-4. Abstract quote
Parainfluenza viruses are major pathogens causing respiratory illness, manifesting from mild upper respiratory tract infection to bronchiolitis and pneumonia.
This retrospective study aimed at providing clinical and epidemiologic data addressing the parainfluenza virus infection in Taiwan. A total of 39 patients were enrolled in this study from March 1999 to December 2000. Infants and young children were the major susceptible population, with 87.2% of them younger than 3 years. No seasonal trend was noted for parainfluenza type 1 and type 2 infections. One clustering of parainfluenza virus type 3 infections occurred in late spring of 2000 based on collected results. Parainfluenza type 1 viral isolates accounted for all of the cases of croup. Most isolates of parainfluenza virus type 3 were associated with upper and/or lower respiratory tract infections. A substantial proportion of the patients had skin involvement; the identification of one case of possible parainfluenza virus-related erythema multiforme is particularly interesting, especially because the chances of a causal relation between viral infection and skin symptoms are formerly thought to be slight.
The identification of parainfluenza virus in illnesses classically considered to be due to other viruses is intriguing and may have important implications in the management of childhood illness clinically.
HISTOLOGICAL TYPES CHARACTERIZATION GENERAL
CHARACTERIZATION SPECIAL STAINS IMMUNOPEROXIDASE ELECTRON MICROSCOPY
DIFFERENTIAL DIAGNOSIS KEY DIFFERENTIATING FEATURES
TREATMENT CHARACTERIZATION GENERAL VACCINE
- MMR vaccination and febrile seizures: evaluation of susceptible subgroups and long-term prognosis.
Vestergaard M, Hviid A, Madsen KM, Wohlfahrt J, Thorsen P, Schendel D, Melbye M, Olsen J.
The Danish Epidemiology Science Centre, Department of Epidemiology and Social Medicine, Aarhus University, Aarhus, Denmark.
JAMA. 2004 Jul 21;292(3):351-7. Abstract quote
CONTEXT: The rate of febrile seizures increases following measles, mumps, and rubella (MMR) vaccination but it is unknown whether the rate varies according to personal or family history of seizures, perinatal factors, or socioeconomic status. Furthermore, little is known about the long-term outcome of febrile seizures following vaccination.
OBJECTIVES: To estimate incidence rate ratios (RRs) and risk differences of febrile seizures following MMR vaccination within subgroups of children and to evaluate the clinical outcome of febrile seizures following vaccination.
DESIGN, SETTING, AND PARTICIPANTS: A population-based cohort study of all children born in Denmark between January 1, 1991, and December 31, 1998, who were alive at 3 months; 537,171 children were followed up until December 31, 1999, by using data from the Danish Civil Registration System and 4 other national registries.
MAIN OUTCOME MEASURES: Incidence of first febrile seizure, recurrent febrile seizures, and subsequent epilepsy.
RESULTS: A total of 439,251 children (82%) received MMR vaccination and 17,986 children developed febrile seizures at least once; 973 of these febrile seizures occurred within 2 weeks of MMR vaccination. The RR of febrile seizures increased during the 2 weeks following MMR vaccination (2.75; 95% confidence interval [CI], 2.55-2.97), and thereafter was close to the observed RR for nonvaccinated children. The RR did not vary significantly in the subgroups of children that had been defined by their family history of seizures, perinatal factors, or socioeconomic status. At 15 to 17 months, the risk difference of febrile seizures within 2 weeks following MMR vaccination was 1.56 per 1000 children overall (95% CI, 1.44-1.68), 3.97 per 1000 (95% CI, 2.90-5.40) for siblings of children with a history of febrile seizures, and 19.47 per 1000 (95% CI, 16.05-23.55) for children with a personal history of febrile seizures. Children with febrile seizures following MMR vaccinations had a slightly increased rate of recurrent febrile seizures (RR, 1.19; 95% CI, 1.01-1.41) but no increased rate of epilepsy (RR, 0.70; 95% CI, 0.33-1.50) compared with children who were nonvaccinated at the time of their first febrile seizure.
CONCLUSIONS: MMR vaccination was associated with a transient increased rate of febrile seizures but the risk difference was small even in high-risk children. The long-term rate of epilepsy was not increased in children who had febrile seizures following vaccination compared with children who had febrile seizures of a different etiology.
Henry JB. Clinical Diagnosis and Management by Laboratory Methods. Twentieth Edition. WB Saunders. 2001.
Rosai J. Ackerman's Surgical Pathology. Ninth Edition. Mosby 2004.
Sternberg S. Diagnostic Surgical Pathology. Fourth Edition. Lipincott Williams and Wilkins 2004.
Robbins Pathologic Basis of Disease. Sixth Edition. WB Saunders 1999.
DeMay RM. The Art and Science of Cytopathology. Volume 1 and 2. ASCP Press. 1996.
Weedon D. Weedon's Skin Pathology Second Edition. Churchill Livingstone. 2002
Fitzpatrick's Dermatology in General Medicine. 5th Edition. McGraw-Hill. 1999.
Weiss SW and Goldblum JR. Enzinger and Weiss's Soft Tissue Tumors. Fourth Edition. Mosby 2001.
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