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At least 253 records · Page 14Linked to original sources
PubMed1987

Haemophilus aegyptius bacteraemia in Brazilian purpuric fever. Brazilian Purpuric Fever Study Group.

Brazilian purpuric fever (BPF) is a fulminant, often fatal childhood illness that was first recognised in 1984. An outbreak in Serrana, São Paulo State in March to May, 1986, resulted in 11 cases. Haemophilus aegyptius was isolated from normally sterile body fluids in 10 children (9 from blood and 1 from cerebrospinal fluid contaminated with blood), consistent with a direct role for H aegyptius in the pathogenesis of BPF. The ability to define cases by positive blood cultures permitted an evaluation of the spectrum of illness of this disease. 5 culture-positive cases were clinically similar to those previously described; the other 5 had milder illness without petechial or purpuric skin manifestations at the time the bacterium was isolated. Blood cultures were a sensitive means of diagnosing BPF; cultures were positive in 5 of 6 patients that met the full clinical case definition. Treatment of conjunctivitis did not appear to prevent BPF. However, children treated with intravenous antimicrobials early in the systemic illness had a trend toward better survival, suggesting that early therapy may prevent progression of the illness.

Brazil↗
PubMed1981

Studies on immunopathogenesis in epidemic hemorrhagic fever: sequential observations on activation of the first complement component in sera from patients with epidemic hemorrhagic fever.

Sequential measurements of activation of the 1st component of complement (C1) in the sera of 29 patients hospitalized with epidemic hemorrhagic fever (EHF) were performed according to a method recently developed. These patients were treated with supportive, routine therapy, but not immunosuppressive agents. This paper describes the kinetic observations on the activation of C1 in the 29 cases. The data confirm that an apparently increased extent of activation occurred in their sera. It was found that the more severely ill the patients were, the more apparent the activation. Additionally, beginning with the 15th day of disease, the extent of C1 activation diminished in most of the moderate and severe types of patients, but not in those with moribund illness and fatal ones. On the basis of the study, it may be reasonably concluded that C1 activation was correlated well with the severity and clinical course of EHF, indicating that the classical C pathway was activated in these patients. We feel that our findings are important to an understanding and elucidation of the immunopathogenetic mechanisms of EHF.

Adolescent↗
PubMed1982

Rocky Mountain spotted fever in areas of high and low prevalence: survey for canine antibodies to spotted fever rickettsiae.

Antibodies to Rickettsia rickettsii were detected by indirect immunofluorescence in sera from 149 of 467 dogs (32%) examined from 4 military installations located in Kentucky, North Carolina, Pennsylvania, and Virginia. The prevalence at individual installations ranged from 4.3% at Fort Knox, Ky, to 63.4% at Fort Bragg, NC. Most of the seropositive dogs were in the working and sporting groups of dogs. The difference in antibody prevalence between sexes was not significant. Serologic responses were related to R rickettsii infection, although antibodies to R montana also were detected in a few of the sera. Comparison of serodiagnostic methods indicated that the indirect fluorescent antibody test was more sensitive than was the indirect hemagglutination test for obtaining survey data on the prevalence of Rocky Mountain spotted fever in the area.

Animals↗
PubMed1993

[Structural protein of hemorrhagic fever renal syndrome virus in uric fusion cells in hemorrhagic fever renal syndrome].

The efoliative cells in the urine of 21 hemorrhagic fever patients with renal syndrome (HFRS) were examined with Swiss blue staining. Fusion cells were found in the urine of 18 HFRS patients. The quantity of fusion cells was closely related to the severity of patients' condition and renal damage. Specific antigen of HFRS virus (HFRSV) was found immunohistochemically in all fusion cells. Specific monoclonal antibodies (McAb) of membrane protein and nucleocapsid protein from HFRSV were used for analyzing antigen in fusion cells. The positive rate of membrane protein antigen was 72.2%. Nucleocapsid protein was not found in all fusion cells. The above results suggested that the forming of fusion cells in the urine of HFRS patients is related membrane protein of HFRSV.

Adolescent↗
PubMed1993

[Teflon fever--a differential diagnosis of acute fever].

Two case-histories are presented with onset while at work of fever, leucocytosis and general malaise, all of short duration. Both men had previously experienced similar episodes in connection with work, and both were occupationally exposed to teflon powder. The episodes ceased after there was no further exposure to teflon. It is concluded that the episodes were most likely caused by inhalation of combustion products of teflon originating from teflon-contaminated cigarettes.

Acute Disease↗
PubMedDate not supplied

Dengue fever and dengue haemorrhagic fever: challenges of controlling an enemy still at large.

Dengue virus infections are a serious cause of morbidity and mortality in most tropical and subtropical areas of the world: mainly Southeast and South Asia, Central and South America, and the Caribbean. Understanding the pathogenesis of dengue haemorrhagic fever (DHF), the severe form of dengue illness, is a very important and challenging research subject. Viral virulence and immune responses have been considered as two major factors responsible for the pathogenesis. Virological studies are attempting to define the molecular basis of viral virulence. The immunopathological mechanisms appear to include a complex series of immune responses. A rapid increase in the levels of cytokines and chemical mediators apparently plays a key role in inducing plasma leakage, shock and haemorrhagic manifestations. It is likely that the entire process is initiated by infection with a so-called virulent dengue virus, often with the help of enhancing antibodies in secondary infection, and then triggered by rapidly elevated cytokines and chemical mediators produced by intense immune activation. However, understanding of the DHF pathogenesis is not complete. We still have a long way to go.

Animals↗
PubMedDate not supplied

Malignant catarrhal fever in cattle experimentally inoculated with a herpesvirus isolated from a case of malignant catarrhal fever in Minnesota USA.

A malignant catarrhal fever (MCF)-like syndrome was experimentally induced in three steers, which were under immunization trials with a herpesvirus previously isolated from a case of MCF in a cow in Minnesota USA. The clinical signs observed in the three steers, and the pathological and histological lesions observed in two of these steers which succumbed to the disease syndrome were indistinguishable from those described for MCF. Although seroconversion was readily demonstrated in the three animals, virus was not re-isolated from the blood leucocytes, secretions and tissues obtained from the two animals which succumbed to the syndrome during the course of the disease and after death. However, a herpesvirus which showed cell rounding cytopathic effects (cpe) in bovine thyroid cells (Bth), was re-isolated from the one steer which survived the disease.

Animals↗
PubMed1987

The status of dengue fever virus in South Africa--serological studies and diagnosis of a case of dengue fever.

To assess the possibility of a dengue epidemic occurring in South Africa 3 groups of survey sera and 2 groups of patients' sera, from a dengue high risk area of South Africa, were tested for antibodies to several flaviviruses. 3.8% (75/1951) of the survey sera and 9.2% (26/282) of the patients' sera had haemagglutination inhibition antibodies to one or more of the flaviviruses tested. One of 1951 survey sera had a spectrum of complement fixation antibody consistent with a primary dengue infection, and 5 of 282 patients' sera also had complement fixation antibodies to flavivirus antigens. These 5 positive patients had recently travelled to India but in only one was there an antibody spectrum unequivocably consistent with a primary dengue infection. Dengue virus type 1 was successfully isolated from this patient's acute serum. The susceptibility of the population to dengue virus infection, the presence of the main vector of dengue virus and the occurrence of imported cases of dengue fever emphasize the need for continuous vigilance.

Antibodies, Viral↗
PubMed1989

An infant rat model of bacteremia with Brazilian purpuric fever isolates of Hemophilus influenzae biogroup aegyptius. Brazilian Purpuric Fever Study Group.

Brazilian purpuric fever (BPF) is a newly recognized fulminant pediatric infection caused by bacteremia with Hemophilus influenzae biogroup aegyptius (Hae). Following intraperitoneal inoculation, each of five disease isolates caused bacteremia more frequently than control, conjunctival isolates of Hae in complement-depleted 6-d-old rats. Sustained but self-limited bacteremia was observed in normal infant rats after inoculation with a disease strain. These rats developed meningitis and had depressed hemoglobin concentration and platelet counts. Pathologic examination showed meningitis and contiguous otitis. Pretreatment of infant rats with immune adult rat serum raised against disease isolates protected rats from bacteremia. Normal adult rat serum or immune rat serum against control strains failed to protect infant rats. Thus, strains of Hae isolated from patients with BPF are more virulent than control strains. Antibody against antigens unique to disease isolates protects infant rats from bacteremia.

Animals↗
PubMed1992

Brazilian purpuric fever identified in a new region of Brazil. The Brazilian Purpuric Fever Study Group.

Brazilian purpuric fever (BPF) is a life-threatening pediatric infection that is preceded by conjunctivitis and caused by Haemophilus influenzae biogroup aegyptius. BPF was first recognized during 1984 in the state of Sao Paulo. BPF was not reported in Brazil outside of Sao Paulo and the neighboring state of Parana until December 1989, when children with BPF were identified in the state of Mato Grosso. By April 1990, 10 children with confirmed BPF were identified from six widely separated cities in Mato Grosso. The overall attack rate for the combined population was 6/100,000 children less than 10 years of age. Six (60%) of the 10 children with BPF died. The recognition of BPF in Mato Grosso suggests that the H. influenzae biogroup aegyptius strain responsible for BPF has a wider geographic distribution than previously appreciated or may be capable of spreading.

Brazil↗