Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085593 (chills)
 4,268 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An 81-year-old woman had chills, fever, nausea, vomiting, and epigastric pain. On day 3 she had hematuria and was treated with trimethoprim-sulfamethoxazole. On day 5 she had a cough, hypotension, anemia, azotemia, and elevated hepatic enzyme levels. Her condition deteriorated with thrombocytopenia, anuria requiring dialysis, edema, and hypoalbuminemia. Treatment with chloramphenicol and doxycycline was started on day 10. By day 11, she was in hypotensive shock; on day 12 she had seizures and died. Murine typhus was diagnosed by demonstration of antibodies to Rickettsia typhi by indirect immunofluorescence. Necropsy revealed interstitial pneumonia, pulmonary edema, hyaline membranes, alveolar hemorrhages, petechiae and vasculitis in the central nervous system, interstitial myocarditis, multifocal interstitial nephritis and hemorrhages, splenomegaly, portal triaditis, and mucosal hemorrhages in urinary tract. Immunofluorescent R. typhi were demonstrated in the lungs, brain, kidneys, liver, and heart. This unusual death occurred in an elderly patient without rash who was treated too late with antirickettsial drugs.
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PMID:Histopathology and immunohistologic demonstration of the distribution of Rickettsia typhi in fatal murine typhus. 249 81

Scrub typhus, a mite-transmitted zoonosis caused by Orientia tsutsugamushi, is a disease endemic to Taiwan. Serious complications in scrub typhus were more common in the past 4 years than reported previously. Between August 1993 and July 1997, 33 cases of scrub typhus were admitted at Tri-Service General Hospital. Symptoms and signs were: fever (100%), chills (39%), cough (24%), headache (21%), diarrhea (18%), dyspnea (18%), eschar (60%), adenopathy (33%), and rash (21%). Nineteen percent (6/32) had obvious leukopenia (WBC < 4000/ mm3), 34% (11/32) had leukocytosis(WBC > 10,000/mm3) and 44% (14/32) had thrombocytopenia (platelet count < 100,000/mm3). Elevation of aspartate aminotransferase (AST) and elevation of alanine aminotransferase (ALT) were 81% (26/32) and 75% (24/32), respectively. Serious complications included pneumonitis 36% (12/33), acute respiratory distress syndrome (ARDS) 15% (5/33), acute renal failure 9% (3/33), myocarditis 3% (1/33) and septic shock 3% (1/33). One patient died of ARDS due to delay in diagnosis. Other patients recovered after appropriate antibiotic and intensive supportive treatments. Emerging virulent strains of O. tsutsugamushi in Taiwan might be biologically plausible. Scrub typhus should be considered in a patient with fever, varying degree of respiratory distress, particularly if there is an eschar or a history of environmental exposure in endemic areas. Prompt diagnosis, timely antimicrobial therapy and intensive supportive care are important for ARDS and other life-threatening complications.
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PMID:Serious complications in scrub typhus. 1049 65

A 7-month-old boy was found lifeless in his bed by his grandfather. Near the mouth there were some blood and chyme on the bedlinen. His mother reported a chill during the last 8 days. Autopsy revealed multiple petechia under the capsule of the thymus, subepicardially and subpleurally, the cause of death was tentative supposed to be a sudden infant death. Histologically parts of the myocardium showed a lympho-monocytic myocarditis according to the DALLAS-criteria. Immunohistological investigations demonstrated an enhanced expression of MHC class II antigens, an increased number of leucocytes as well as T-lymphocytes. In situ hybridization and immunohistochemistry revealed myocardial enterovirus infection. Considering that there were regions in the myocardium without the traditional findings of myocardial necrosis and inflammation but with distinct expression of the above mentioned immunohistologic markers, immunohistological investigations turn out to be an appropriate tool to examine infant fatalities with uncertain cause of death for early stages of myocarditis.
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PMID:Lympho-monocytic enteroviral myocarditis: traditional, immunohistological and molecularpathological methods for diagnosis in a case of suspected sudden infant death syndrome (SIDS). 1134 11

The clinical diagnosis of trichinellosis is difficult because there are no pathogenic signs or symptoms and in diagnosing the infection epidemiological data are of great importance. Trichinellosis usually begins with a sensation of general discomfort and headache, increasing fever, chills and sometimes diarrhoea and/or abdominal pain. Pyrexia, eyelid or facial oedema and myalgia represent the principal syndrome of the acute stage, which can be complicated by myocarditis, thromboembolic disease and encephalitis. High eosinophilia and increased creatine phosphokinase activity are the most frequently observed laboratory features and the parasitological examination of a muscle biopsy and the detection of specific circulating antibodies will confirm the diagnosis. The medical treatment includes anthelmintics (mebendazole or albendazole) and glucocorticosteroids. Mebendazole is usually administered at a daily dose of 5 mg/kg but higher doses (up to 20 - 25 mg/kg/day) are recommended in some countries. Albendazole is used at 800 mg/day (15 mg/kg/day) administered in two doses. These drugs should be taken for 10 - 15 days. The use of mebendazole or albendazole is contraindicated during pregnancy and not recommended in children aged < 2 years. The most commonly used steroid is prednisolone, which may alleviate the general symptoms of the disease. It is administered at a dose of 30 - 60 mg/day for 10 - 15 days.
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PMID:Opinion on the diagnosis and treatment of human trichinellosis. 1215 Jun 91

Clinical manifestations of Q fever infection are fever, productive cough, decrease in exercise tolerance and chills. Cardiovascular involvement is well recognized and usually presents as endocarditis and infection of an aneurysm or vascular graft. Myocarditis has only rarely been described as a manifestation of acute Q fever infection. In this report we describe a case of a young adult who presented with angina-like symptoms and ECG and biochemical markers indicative of acute coronary syndrome. The diagnosis of myocarditis was ultimately made based on the results of a normal coronary angiography and increased anti-Coxiella burnetii antibody titer. The patient has not developed dilated cardiomyopathy after two years of follow up.
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PMID:Q fever myocarditis. 1892 53

Myocarditis can be totally asymptomatic or can manifest with chest pain syndromes, ranging from mild persistent chest pain of acute myopericarditis to severe symptoms that mimic acute myocardial infarction. About 60% of patients may have antecedent arthralgias, malaise, fevers, sweats, or chills consistent with viral infections 1 to 2 weeks before onset. Here, we report a postpartum young woman who developed postural hypotension as the first manifestation of fulminant myocarditis with initially acute "cold and dry" right-sided heart failure and cardiogenic shock. Common causes of postural hypotension include volume depletion, medications, diabetes, alcohol, infection, and varicose veins as well as dysautonomic syndromes. Fulminant myocarditis can cause cardiogenic shock. Myocardial inflammation more frequently affects localized areas of the left ventricle free wall, rarely right ventricle (RV). However, predominant RV involvement with acute right-sided heart failure and low cardiac output syndrome can be easily overlooked due to lack of typical heart failure signs. On reviewing medical literatures, we had found no report regarding the RV involvement with acute right-sided heart failure as the initial presentation of fulminant myocarditis.
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PMID:Postural hypotension as the initial presentation of fulminant right ventricular myocarditis. 2103 7

Q fever is a bacterial infection affecting mainly the lungs, liver, and heart. It is found around the world and is caused by the bacteria Coxiella burnetii. The bacteria affects sheep, goats, cattle, dogs, cats, birds, rodents, and ticks. Infected animals shed this bacteria in birth products, feces, milk, and urine. Humans usually get Q fever by breathing in contaminated droplets released by infected animals and drinking raw milk. People at highest risk for this infection are farmers, laboratory workers, sheep and dairy workers, and veterinarians. Chronic Q fever develops in people who have been infected for more than 6 months. It usually takes about 20 days after exposure to the bacteria for symptoms to occur. Most cases are mild, yet some severe cases have been reported. Symptoms of acute Q fever may include: chest pain with breathing, cough, fever, headache, jaundice, muscle pains, and shortness of breath. Symptoms of chronic Q fever may include chills, fatigue, night sweats, prolonged fever, and shortness of breath. Q fever is diagnosed with a blood antibody test. The main treatment for the disease is with antibiotics. For acute Q fever, doxycycline is recommended. For chronic Q fever, a combination of doxycycline and hydroxychloroquine is often used long term. Complications are cirrhosis, hepatitis, encephalitis, endocarditis, pericarditis, myocarditis, interstitial pulmonary fibrosis, meningitis, and pneumonia. People at risk should always: carefully dispose of animal products that may be infected, disinfect any contaminated areas, and thoroughly wash their hands. Pasteurizing milk can also help prevent Q fever.
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PMID:Q Fever: an old but still a poorly understood disease. 2321 31

Drug-induced eosinophilic myocarditis is uncommon with few cases reported in the literature. It is a rare but potentially life-threatening disease.We report the case of an 11-year-old girl without medical history who developed an acute malaise and chills, followed by severe shortness of breath and a cardiopulmonary arrest 1 hour after an intramuscular injection of penicillin.At autopsy, we observed in the external examination nonspecific asphyxia signs, an injection mark, and the absence of traumatic signs. The organs examination showed a heart with a normal shape and a transmural, diffuse, tannish discoloration of the myocardium. The lungs were severely congested with a diffuse edema. Histological examination of the ventricular walls and septum revealed suggestive signs of eosinophilic myocarditis. Immunohistochemical analysis for the phenotypic characterization of the inflammatory cells revealed the positivity of the CD3 antibody without any stain for CD20.The diagnosis of fulminant myocarditis with an eosinophilic infiltrate was established as the cause of death. The manner of death was stated as natural.
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PMID:Penicillin-Induced Fulminant Myocarditis: A Case Report and Review of the Literature. 2800 85

Myocarditis as a result of malaria infection is uncommon. However, we report a case of a Pakistani emigrant who presented with respiratory distress, fever, chills, and nausea at the emergency room. The patient had traveled to visit his relatives in Pakistan without receiving antimalarial chemoprophylaxis. (Travel clinic advises travelers to Pakistan to take antimalarial drugs as prophylaxis.) Cardiorespiratory examination revealed bilateral crepitation in all lung fields, as well as triple heart sounds. Examination of blood smear showed trophozoites and schizonts of Plasmodium vivax with low parasite density. Echocardiography showed diffuse hypokinesia with an ejection fraction of 22% consistent with acute myocarditis. The patient was given chloroquine phosphate, digoxin, perindopril arginine, furosemide, and spironolactone and gradually improved.
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PMID:Imported Plasmodium vivax malaria complicated by reversible myocarditis. 3157 56

Pheochromocytomas are rare catecholamine-secreting neuroendocrine tumors that can occasionally progress to life-threatening disease, including a multisystem crisis. Patients with Neurofibromatosis type 1 (NF1) may develop pheochromocytomas, and the consequent chronic elevation of plasma catecholamine levels could further complicate various cardiovascular and pulmonary manifestations they may have. A 37-year-old African American female with NF1 presented with severe dyspnea, chills, myalgia, vomiting, and abdominal pain. Within several hours of hospital admission, she developed progressive agitation and died from circulatory collapse. An autopsy revealed disseminated histoplasmosis with necrotizing granulomatosis in her lungs, mediastinum, liver, and spleen, as well as bilateral pheochromocytomas with one tumor showing marked hemorrhage. Additionally, she had cardiac hypertrophy, myocarditis, pulmonary edema, apical bullae, features of pulmonary hypertension and interstitial fibrosis. Disseminated histoplasmosis caused by the fungal organism Histoplasma capsulatum is rarely described in immunocompetent individuals. This case is presented to illustrate that chronic hypercatecholaminemia caused by pheochromocytomas may potentially mask disseminated fungal infections which in turn could induce pheochromocytoma multisystem crisis in susceptible patients with neurofibromatosis.
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PMID:Pheochromocytoma Multisystem Crisis and Masquerading Disseminated Histoplasmosis in a Neurofibromatosis Type 1 Patient With Bilateral Adrenal Tumors. 3298 95


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