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At least 199 records · Page 11Linked to original sources

Hereditary periodic fever syndrome sans fever or distinct periodicity presenting with psychosis.

The genetic basis for several hereditary periodic fever syndromes has been identified and consequently, the phenotypic spectrum of these disorders has broadened. We describe a young woman with tumor necrosis factor receptor-associated periodic syndrome (TRAPS), proven by mutational analysis, who presented with psychosis but without fever, symptom periodicity, or similar family medical history. This patient represents the first case of TRAPS-associated psychosis. This case illustrates the importance of mutation analysis for this group of disorders in individuals presenting with unexplained inflammatory symptoms and recurrent psychoses.

Adolescent↗

Spotted fever group rickettsiae in immature and adult ticks (Acari: Ixodidae) from a focus of Rocky Mountain spotted fever in Connecticut.

Immature and adult ixodid ticks were collected during 1983 and 1984 in Newtown, Connecticut, an area endemic for Rocky Mountain spotted fever (RMSF), to determine prevalence of infection by spotted fever group (SFG) rickettsiae. Direct fluorescent-antibody (FA) staining revealed SFG organisms in 6 (1.8%) of 332 Dermacentor variabilis larvae, 5 (7.8%) of 64 D. variabilis nymphs, and in 2 (40%) of 5 Ixodes cookei nymphs removed from small- and medium-sized mammals. Hemolymph tests detected rickettsia-like organisms in 15 (8.8%) of 170 D. variabilis adults; 8 specimens retested by direct FA were negative. In contrast, hemocytes from 5 (8.6%) of 58 Ixodes texanus females contained organisms that stained positively in both hemolymph and direct FA tests. An indirect microimmunofluorescence test identified specific antibodies to Rickettsia rickettsii, the etiologic agent of RMSF, in serum samples from a chipmunk, raccoons, and white-footed mice. Results indicate that immature or adult ticks of at least three species may be involved in the maintenance and transmission of SFG rickettsiae at Newtown.

Animals↗

Nosocomial outbreak of viral hemorrhagic fever caused by Crimean Hemorrhagic fever-Congo virus in Pakistan, January 1976.

This paper describes the clinical, epidemiological, and laboratory investigations undertaken to isolate and identify the etiological agent of a nosocomial cluster of hemorrhagic fever cases due to Crimean hemorrhagic fever (CHR)-Congo virus. Since this virus is usually transmitted by ticks it was surprising that the index case, in a nomadic shepherd, occurred during the winter season when ticks are relatively inactive. These are the first cases of CHF-Congo virus found in humans in Pakistan. Investigations on other biological properties, particularly strain differences and virulence, are being continued at the Islamabad laboratory.

Adult↗

[Many faces of West Nile fever--the first case of West Nile fever in the western Galilee, Israel].

West Nile Fever (WNF) is caused by a B arbovirus, which was first isolated in 1937 in Uganda. In Israel the disease bears an epidemic character, and during 1950-1957 several widespread outbreaks of WNF were described in detail. It emerged from obscurity in 1999 when the first incursion of the virus in North America caused 62 cases of encephalitis and 7 deaths in New York. In 1996 an outbreak in Romania signaled that WNF had emerged as clinically important disease in Europe. The virus is transmitted by a mosquito vector. Wild birds serve as amplifying hosts. Human and some domestic animals such as horses, can be infected incidentally. While neurological disease has been prominent in some epidemics, the West Nile virus infection is usually asymptomatic in areas of the world where the virus is endemic. This is a case study of the first patient diagnosed and treated for West Nile Fever in the Western Galilee, Israel. The epidemiology, pathogenesis, clinical manifestations, diagnosis and treatment of the disease are presented in detail.

Aged↗

[Hereditary intermittent fevers, other than familial Mediterranean fevers].

Familial Mediterranean fever is no more the sole hereditary disease characterized by recurrent inflammatory attacks. Three other main entities have now been defined, both at clinical and genetic levels: a dominant disease due to mutations of one of the tumour necrosis factor receptor, called TRAPS for tumour necrosis factor receptor associated periodic syndrome, the hyper-immuno-globulinaemia D and periodic fever syndrome (HIDS), which is a metabolic disorder and the Muckle-Wells syndrome. A thorough diagnosis of these diseases is crucial for appropriate management and treatment.

Diagnosis, Differential↗

[Filovirus haemorrhagic fevers: Ebola fever].

Epidemiological issues, clinical course and laboratory diagnostics of Ebola haemorrhagic fever are reviewed. The structural features of virions and genetic variants of the virus are described along with ecology of Ebola virus. The data on Ebola fever global morbidity are also presented.

Cote d'Ivoire↗

Recoverability of Rift Valley fever and sandfly fever Sicilian viruses from infected Phlebotomus papatasi (Diptera: Psychodidae) trapped in various oils.

We studied the effects of various oils used to trap sand flies on the recovery of virus from infected adult Phlebotomus papatasi. Both Rift Valley fever and sandfly fever Sicilian viruses were readily recovered from virus-inoculated specimens held at 26 degrees C on mineral, olive or castor oil-soaked sheets for up to 12 h. However, after 50 h on oil-soaked paper, significantly greater titers were recovered from sand flies trapped with mineral oil than from sand flies trapped with either of the other oils. This indicates that sand flies trapped on oil-soaked paper would be suitable for virus isolation attempts and that mineral oil had the least effect on virus recovery.

Animals↗

Bichat guidelines for the clinical management of Q fever and bioterrorism-related Q fever.

Q fever is a zoonotic disease caused by Coxiella burnetii. Its interest as a potential biological weapon stems from the fact that an aerosol of very few organisms could infect humans. Another route of transmission of C. burnetii could be through adding it to the food supply. Nevertheless, C. burnetii is considered to be one of the less suitable candidate agents for use in a bioterrorist attack; the incubation is long, many infections are inapparent and the mortality is low. In the case of an intentional release of C. burnetii by a terrorist, clinical presentation would be similar to naturally occurring disease. It may be asymptomatic, acute, normally accompanied by pneumonia or hepatitis, or chronic, usually manifested as endocarditis. Most cases of acute Q fever are asymptomatic and resolve spontaneously without specific treatment. Nevertheless, treatment can shorten the duration of illness and decrease the risk of complications such as endocarditis. Post-exposure prophylaxis is recommended after the exposure in the case of a bioterrorist attack.

Bioterrorism↗

Detection of antibodies to Salmonella "O" antigens in typhoid fever by counterimmunoelectrophoresis. II. Assessment in patients with typhoid fever and in a healthy population.

Two different population groups were studied. In one, 50 patients with a confirmed diagnosis of typhoid fever. Serum determinations were made for the detection of antibodies to S. typhi somatic antigen using Widal technique, surface fixation test and counterimmunoelectrophoresis (CIE). In the other group, 350 healthy subjects were studied to determine the minimum diagnostic titer by means of CIE. It was possible to establish that a 1:16 titer was suggestive of typhoid fever when CIE techniques were used. Surface fixation test showed the highest sensitivity levels. CIE with sensitivity levels similar to those found in Widal's reaction exceeds the other test because of its standardization and greater reproducibility.

Adolescent↗

Immunogenicity and reactogenicity of a Q fever chemovaccine in persons professionally exposed to Q fever in Czechoslovakia.

An immunization trial carried out on 1310 persons professionally exposed to Q fever confirmed the suitability of a chemovaccine for field use. Its immunogenicity and reactogenicity differed in three groups of subjects who differed in their previous experience of Q fever and who were given different lots of the vaccine. There was some correlation between reactogenicity of the vaccine and pre-immunization positivity in the microagglutination and skin tests as indicators of a previous exposure. The skin test was more reliable for predicting post-immunization reactions.

Animals↗

Treatment of acute streptococcal pharyngitis and prevention of rheumatic fever: a statement for health professionals. Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease of the Council on Cardiovascular Disease in the Young, the American Heart Association.

Primary prevention of acute rheumatic fever is accomplished by proper identification and adequate antibiotic treatment of group A beta-hemolytic streptococcal (GAS) tonsillopharyngitis. Diagnosis of GAS pharyngitis is best accomplished by a throat culture. Penicillin (either oral penicillin V or injectable benzathine penicillin) remains the treatment of choice, because it is cost effective, has a narrow spectrum of activity, has long-standing proven efficacy, and GAS resistant to penicillin have not been documented. Various macrolides, oral cephalosporins, and other beta-lactam agents are acceptable alternatives, particularly in penicillin-allergic individuals. The individual who has had an attack of rheumatic fever is at very high risk of developing recurrences after subsequent GAS pharyngitis and needs continuous antimicrobial prophylaxis to prevent such recurrences (secondary prevention). The duration of prophylaxis depends on the number of previous attacks, the time lapsed since the last attack, the risk of exposure to streptococcal infections, the age of the patient, and the presence or absence of cardiac involvement. Penicillin is again the agent of choice for secondary prophylaxis, but sulfadiazine or erythromycin are acceptable alternatives in penicillin-allergic individuals. This report is an update of a 1988 statement by this committee. It expands on the previous statement, includes more recent therapeutic modalities, and makes more specific recommendations for the duration of secondary prophylaxis.

Acute Disease↗

[Detection of hemorrhagic fever virus-RNA in renal tissue and peripheral blood in patients with hemorrhagic fever with renal syndrome].

Hemorrhagic fever virus (HFV) RNA in renal tissue and blood samples from 21 patients with epidemic hemorrhagic fever with renal syndrome (HFRS) were examined by either in situ or blot hybridization using digoxigenin labelled HFV-cDNA probe. HFV associated antigen and immune complex (IC) in renal tissue were also investigated simultaneously using immunofluorescence (IF) technique. HFV-RNA was detected in the renal specimen particularly renal tubular in 8/21 HFRS patients mostly of severe type illness. However, the deposition of IC in the renal tissue in this group of patients occurred mainly in the mild type apparently in a different manner of HFV-RNA. We conclude that both the HFV-RNA and immune complexes deposition are contributable to the pathogenesis of renal lesion in HFRS.

Adolescent↗

Tumor necrosis factor in Plasmodium falciparum malaria: high plasma level is associated with fever, but high production capacity is associated with rapid fever clearance.

In the present study, we investigated 91 patients with Plasmodium falciparum malaria of different severity in a highly endemic area. Patients were examined at least twice daily until clearance of parasites and fever. Plasma cytokine concentrations without and after ex vivo PHA stimulation of whole blood were determined. On admission we found elevated plasma concentrations of TNF, IFN-gamma, and IL-10 compared to levels during and after chemotherapy. Plasma TNF levels on admission were significantly different between patients with severe and mild malaria (differentiated in schoolchildren and adults). The PHA elicited TNF production capacity of peripheral blood leucocytes was suppressed during the acute phase of malaria. High TNF production capacity was associated with faster fever clearance and parasite clearance and, in patients with severe malaria, with higher blood glucose levels. In conclusion we observed circulating TNF concentrations in malaria patients dependent on the severity of disease, which is itself dependent on age, and an association of a high TNF production capacity with parameters for accelerated cure and good prognosis.

Adolescent↗

African swine fever and classical swine fever: a review of the pathogenesis.

This paper describes major pathogenetic mechanisms of African and Classical Swine Fever virus infections. The interactions between both viruses and the monocyte-macrophage-system result in the release of mediator molecules, which are important for the further progression of the diseases. The causes of the thrombocytopenia and the mechanisms of the haemorrhages, which are characteristic in both infections, are described. Apoptotic cell death is regarded as the predominant cause of lymphopenia in both virus infections.

African Swine Fever↗

Dengue NS1-specific antibody responses: isotype distribution and serotyping in patients with Dengue fever and Dengue hemorrhagic fever.

To understand the antibody responses to dengue (DEN) nonstructural 1 (NS1) glycoprotein and their roles in protective immunity or pathogenesis of dengue fever (DF) and dengue hemorrhagic fever (DHF), we have analyzed the NS1-speccific IgM, IgA and IgG antibodies from patients with DF and DHF. An isotype-specific, indirect enzyme-linked immunosorbent assay (ELISA) was established by coating a NS1-specific monoclonal antibody (MAb), D2/8-1, to capture soluble NS1 antigens secreted in the culture supernatants of Vero cells infected with DEN virus. We observed strong anti-NS1 antibody responses in all of the convalescent sera of patients with DF and DHF. Similar NS1-specific isotypic and serotypic antibody responses were found in the sera from DF and DHF patients. The results showed that all DEN infections induced significant NS1-specific IgG, whereas 75% and 60% of primary DF patients vs. 40% and 90% of secondary DF patients produced IgM and IgA antibodies, respectively. Specificity analysis showed that DEN NS1-specific IgG and IgA antibodies cross-react strongly to Japanese encephalitis (JE) virus NS1 glycoprotein, whereas DEN NS1-specific IgM antibodies do not cross-react to JE virus NS1 glycoprotein at all. The serotype specificity of NS1-specific IgM, IgA and IgG were found to be 80%, 67% and 75% for primary infections, and 50%, 22% and 30% for secondary infections in positive samples of DF patients. Similar pattern was found in DHF patients. The results showed that all of the DF and DHF patients produced significant NS1-specific antibodies. We did not observe direct correlation between the anti-NS1 antibody responses and DHF because sera from patients with DF and DHF showed similar anti-NS1 antibody responses.

Antibodies, Monoclonal↗