Cases reported "Hemorrhagic Fevers, Viral"

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1/12. Management of a Sabia virus-infected patients in a US hospital.

    OBJECTIVE: To describe the hospital precautions used to isolate a Sabia virus (arenavirus: arenaviridae)-infected patient in a US hospital and to protect hospital staff and visitors. DESIGN: Investigation of a single case of arenavirus laboratory-acquired infection and associated case-contacts. SETTING: A 900-bed, tertiary-care, university-affiliated medical center. patients OR OTHER PARTICIPANTS: The case-patient became ill with Sabia virus infection. The case-contacts consisted of healthcare workers, coworkers, friends, and relatives of the case-patient. INTERVENTION: Enhanced isolation precautions for treatment of a viral hemorrhagic fever (VHF) patient were implemented in the clinical laboratory and patient-care setting to prevent nosocomial transmission. The enhanced precautions included preventing aerosol spread of the virus from the patient or his clinical specimens. All case-contacts were tested for Sabia virus antibodies and monitored for signs and symptoms of early disease. RESULTS: No cases of secondary infection occurred among 142 case-contacts. CONCLUSIONS: With the frequency of worldwide travel, patients with VHF can be admitted to a local hospital at any time in the united states. The use of enhanced isolation precautions for VHF appeared to be effective in preventing secondary cases by limiting the number of contacts and promoting proper handling of laboratory specimens. patients with VHF can be managed safely in a local hospital setting, provided that appropriate precautions are planned and implemented. ( info)

2/12. Molecular diagnostics of viral hemorrhagic fevers.

    This review addresses the diagnostics of viral hemorrhagic fevers (VHFs). In the first part, an overview is given on classical methods of VHF diagnostics as well as novel molecular diagnostic tools. Currently available polymerase chain reaction (PCR) assays for diagnosis of VHF are summarized and discussed. In the second part, VHF diagnostics are described in particular for lassa fever, yellow fever, and Crimean-congo hemorrhagic fever, based on cases that were imported into or occurred within europe. The third part is focussed on important differential diagnoses of VHF. ( info)

3/12. Acute glaucoma in hemorrhagic fever with renal syndrome (nephropathia epidemica).

    Bilateral eyelid edema, chemosis, conjunctival injection and hemorrhages, shallowing of the anterior chamber with transitory myopia, and acute glaucoma were observed in three patients with hemorrhagic fever with renal syndrome (nephropathia epidemica). One patient had anterior uveitis with posterior synechiae. Two patients had congestion of retinal venules and retinal edema, and one patient had small retinal hemorrhages. fluorescein angiography revealed early leakage of the conjunctival capillaries and delayed filling of the lower retinal arterioles with retinal edema. The acute glaucoma subsided rapidly. The myopia disappeared slowly with a gradual deepening of the anterior chamber after onset of the diuretic phase of the illness. In nephropathia epidemica, the transitory shallowing of the anterior chamber, myopia, and acute glaucoma are due to lesions in the small blood vessels of the ciliary body, resulting in its swelling, with relaxation of the zonules and forward movement of the lens. ( info)

4/12. Fatal hemorrhagic fever caused by west nile virus in the united states.

    BACKGROUND: Most west nile virus (WNV) infections in humans are asymptomatic; severe disease occurs in relatively few patients and typically manifests as encephalitis, meningitis, or acute flaccid paralysis. A few cases of life-threatening disease with diffuse hemorrhagic manifestations have been reported in africa; however, this clinical presentation has not been documented for any of the >16,700 cases of WNV disease reported in the united states during 1999-2004. We describe a case of fulminant WNV infection in a 59-year-old florida man who died following a brief illness that resembled hemorrhagic disease caused by rickettsia reckettsii, dengue virus or yellow fever virus. methods: Traditional and contemporary diagnostic assays, including culture isolation, electron microscopic examination, reverse-transcriptase polymerase chain reaction amplification, and immunohistochemical stains, were used to confirm systemic WNV infection in the patient. RESULTS: WNV was isolated in a cell culture from a skin biopsy specimen obtained from the patient shortly prior to death. Electron microscopic examination identified the isolate as a flavivirus, and reverse-transcriptase polymerase chain reaction amplified specific WNV sequences from the isolate and patient tissue. Quantitative polymerase chain reaction identified approximately 1x10(7) viral copies/mL in the patient's serum. WNV antigens were detected by immunohistochemical stains in intravascular mononuclear cells and endothelium in skin, lung, liver, kidney, spleen, bone marrow, and central nervous system; no viral antigens were identified in neurons or glial cells of the central nervous system. CONCLUSIONS: Although hemorrhagic disease is a rare manifestation of WNV infection, the findings provided by this report may offer new insights regarding the clinical spectrum and pathogenesis of WNV disease in humans. ( info)

5/12. Firsthand clinical observations of hemorrhagic manifestations in Ebola hemorrhagic fever in Zaire.

    About 5 weeks after the beginning of the outbreak of Ebola virus fever in Yambuku, Zaire, several acute cases of the disease were observed. All of those affected had the following common signs and symptoms: sudden onset of high fever, with chills, headache, myalgia, anorexia, nausea, abdominal pain, sore throat, expressionless face, and profound prostration. In some cases, on around the fifth day of the acute phase, the appearance of an exanthematous rash on the trunk announced the hemorrhagic manifestations: hemorrhagic conjunctivitis, bleeding ulcerations in the mouth and on the lips, gingival bleeding, hematemesis, and melena; epistaxis, ear bleeding, hematuria, and postpartum hemorrhages were also reported. All these hemorrhagic cases had a fatal outcome within about a week. The hemorrhagic manifestations were less severe in the cases that occurred by the end of the outbreak than in the first reported cases. Hemorrhagic manifestations were less frequent and less severe, or even absent, in the nonfatal cases (convalescents, serologically confirmed). No biologic investigation of the hemostatic impairment could be performed under the emergency conditions of this field study. ( info)

6/12. Haemorrhagic manifestations with Sindbis infection. Case report.

    Sindbis infection in man occurs rarely in australia. Most recorded cases are either asymptomatic or result in a fever sometimes accompanied by a macular or vesicular rash. This case is of particular interest because of the severe haemorrhagic vesicular rash and the repeated recurrence of symptoms over a 5 month period together with the persistence of IgM antibodies to sindbis virus. ( info)

7/12. The hemorrhagic fevers of Southern africa with special reference to studies in the South African Institute for Medical research.

    In this review of studies on the hemorrhagic fevers of Southern africa carried out in the South African Institute for Medical research, attention has been called to occurrence of meningococcal septicemia in recruits to the mining industry and South African Army, to cases of staphylococcal and streptococcal septicemia with hemorrhagic manifestations, and to the occurrence of plague which, in its septicemic form, may cause a hemorrhagic state. "Onyalai," a bleeding disease in tropical africa, often fatal, was related to profound thrombocytopenia possibly following administration of toxic witch doctor medicine. Spirochetal diseases, and rickettsial diseases in their severe forms, are often manifested with hemorrhagic complications. Of enterovirus infections, Coxsackie B viruses occasionally caused severe hepatitis associated with bleeding, especially in newborn babies. Cases of hemorrhagic fever presenting in February-March, 1975 are described. The first outbreak was due to marburg virus disease and the second, which included seven fatal cases, was caused by rift valley fever virus. In recent cases of hemorrhagic fever a variety of infective organisms have been incriminated including bacterial infections, rickettsial diseases, and virus diseases, including Herpesvirus hominis; in one patient, the hemorrhagic state was related to rubella. A boy who died in a hemorrhagic state was found to have congo fever; another patient who died of severe bleeding from the lungs was infected with leptospira canicola, and two patients who developed a hemorrhagic state after a safari trip in Northern botswana were infected with trypanosoma rhodesiense. An illness manifested by high fever and melena developed in a young man after a visit to zimbabwe; the patient was found to have both malaria and marburg virus disease. ( info)

8/12. Ebola hemorrhagic fever: Tandala, Zaire, 1977-1978.

    Ebola virus was recovered from a nine-year-old girl who died of acute hemorrhagic fever in June 1977 at Tandala Hospital in northwestern Zaire, in the first reported recognized case of this disease since the discovery epidemics of 1976 in Zaire and sudan. Investigations undertaken in the Tandala region revealed that two previous clinical infections with Ebola virus had occurred in 1972 and that about 7% of the residents had immunofluorescent antibodies to the virus. Females younger than 30 years of age had a higher prevalence of antibodies than males of comparable age, but above the age of 30 years there was no sex difference. No other clues to the still-mysterious natural reservoir of Ebola virus were uncovered. ( info)

9/12. Virologic investigation of a case of suspected haemorrhagic fever.

    After travelling in subSaharan africa, an area known for sporadic cases of Marburg virus infection, a young Swedish man presented with a classical picture of severe viral haemorrhagic fever complicated by disseminated intravascular coagulation and septicaemia. serum samples examined by electron microscopy revealed particles of a size compatible with filovirions. Indirect fluorescent antibody tests indicated transient seroconversion to Marburg virus. In lymphocyte transformation assays of cells isolated from the patient 11 months after the onset of acute disease, Marburg viral antigen was able to stimulate lymphocyte proliferation 3.9-fold; however, exhaustive attempts to isolate virus from acute phase blood cultured in vitro or in vivo from guinea pigs and monkeys failed. Data suggest that this patient may have been infected with a filovirus. This case demonstrates the difficulties that may occur in laboratory diagnosis of viral haemorrhagic fevers. ( info)

10/12. Adenovirus-associated hemorrhagic cystitis treated with intravenous ribavirin.

    Adenovirus hemorrhagic cystitis following bone marrow transplantation occurs in 2 to 16% of the patients. While usually self-limiting, this disease can cause significant morbidity and even mortality in the immunocompromised patient. risk factors include graft versus host disease and pre-transplant seropositivity to adenovirus. Standard treatment of this disorder consists of hydration, diuresis and analgesics. Failure of these measures leads to multiple blood transfusions, severe patient morbidity and possible death. When conservative therapy is unsuccessful, there is no proved standard of care. We recently used ribavirin, a broad-spectrum antiviral agent against adenovirus infection in vitro, to treat refractory adenovirus hemorrhagic cystitis after bone marrow transplantation. The hematuria and urinary symptomatology resolved without demonstrable side effects. We present ribavirin as a therapeutic alternative when conservative treatment for adenovirus hemorrhagic cystitis fails. ( info)
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