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At least 19 recordsLinked to original sources
PubMed2026

Nosocomial Outbreak of Lassa Fever in Conakry, Guinea, 2022.

BACKGROUND: Lassa fever is endemic in Guinea, with high seroprevalence in the forest region. However, clinical cases have been only anecdotally reported. In August 2022, a nosocomial outbreak occurred at a private clinic in the capital, Conakry, an area previously considered low risk. METHODS: Suspected cases were confirmed by real-time reverse-transcription polymerase chain reaction within 24 hours. Viremia was monitored during hospitalization, and whole-genome sequencing was performed in-country within 13 days of outbreak detection. Outbreak investigation involved rodent testing in the home village of the suspected primary case. RESULTS: Six cases were laboratory-confirmed, 5 of which were healthcare workers of the clinic. The case fatality rate was 16.7%. Viral RNA remained detectable in blood of survivors for a median of 26 days (interquartile range, 24-41 days) post-disease onset. Epidemiological investigations identified a suspected primary case, who had died of a febrile disease compatible with Lassa fever, had contact with all secondary cases, and had a travel history from Kissidougou area. Three near-complete and 1 partial Lassa virus genomes were recovered from the secondary cases, which phylogenetically clustered with genomes from central Guinea. Consistent with a common transmission source, the 4 genomes were almost identical. Rodent testing revealed a new reservoir area in eastern-central Guinea. CONCLUSIONS: This outbreak highlights the vulnerability of healthcare settings in low-prevalence areas of West Africa to nosocomial Lassa virus transmission due to human mobility. Facilitated by capacity-building programs for viral hemorrhagic fevers, rapid diagnosis, genomic analysis, and ecological assessment enabled an efficient outbreak response and control.

Lassa Fever↗
PubMed1975

Tamiami virus infection in mice and cotton rats.

Tamiami virus produces a lethal encephalitis in suckling mice, and the illness is mediated, at least in part, by cellular immunity. Infection of extraneural organs, including lymphoid organs, is limited. The same virus produces a widespread infection in its natural host, the cotton rat, but neither symptomatic illness nor cytopathology results. Since antibody is produced, as in the murine infection, suppression of cellular immunity to the virus may be responsible for the non-cytolytic infection. Lymphoid tissue is extensively infected in the cotton rat and a relationship between this lymphotropism and immunosuppression is suggested.

Animals↗
PubMed1975

Protection of monkeys against Machupo virus by the passive administration of Bolivian haemorrhagic fever immunoglobulin (human origin).

Bolivian haemorrhagic fever immunoglobulin of human origin, given either prior to or shortly after experimental infection with Machupo virus, protected rhesus and cynomolgus monkeys against initial clinical illness. Some survivors developed severe neurological signs 30-47 days after virus inoculation and died 4-6 days later. Results from one of the experiments suggested that the development of neurological signs was associated more frequently with high doses of immunoglobulin than with intermediate or low doses.

Animals↗
PubMed1975

Dengue haemorrhagic fever in Burma.

Although sporadic from 1965 to 1969, a major outbreak of dengue haemorrhagic fever (DHF) occurred for the first time in Rangoon in 1970. Since then the disease has occurred every year in Rangoon and is now observed to be expanding to other urban areas in the country. The clinical diagnosis of DHF was confused by concurrent outbreaks of influenza A in 1971 and influenza A and B in 1972. A laboratory study of 3,447 clinically diagnosed haemorrhagic fever cases showed that 1643 cases (47.8%) were due to dengue and chikungunya, 296 (8.6%) to influenza A, 85(2.5%) to influenza B, 12(0.3%) to measles and 1411(40.8%) were of unknown aetiology during the 5 year period 1970-1974. Ae. aegypti mosquitoes are widely distributed in the country up to and including 900 meters above sea level but breeding is not found above that altitude. The absolute larval population which is highest in July as well as landing rate correlated with the peak incidence of DHF cases.

Aedes↗
PubMedDate not supplied

Hemorrhagic fevers, with special reference to recent outbreaks in southern Africa.

In considering the diagnosis of a patient admitted to the Johannesburg Hospital, suffering from an illness characterized by high fever and complicated by a hemorrhagic state from which he died, a list of possible causes of his illness was drawn up. This list included the arthropodborne viral infections prevalent in southern Africa, namely, chikungunya fever, Sindbis fever, West Nile fever, yellow fever, and Rift Valley fever; viral infections associated with rodents, such as Lassa fever; the viral infection associated with monkeys, Marburg virus disease; the rickettsial infections; tick-bite fever (the variety of spotted fever of tick typhus occurring in southern Africa) and Q fever; the bacterial infections, especially the coccal infections, plague septicemia, and meningococcal, staphylococcal, and streptococcal septicemia; and the blood protozoal infections malaria and trypanosomiasis. In addition, rubella, Gasser's syndrome, Henoch-Schönlein purpura, and viperine snakebite were briefly described in this review. All of these conditions may be complicated by the development of a hemorrhagic state. The circulation of large numbers of infecting organisms, by they viruses, rickettsiae, bacteria, or protozoa, may initiate the coagulation cascade, the formation of fibrin and its deposition in the finer blood vessels, and the aggregation and entanglement of platelets resulting in marked thrombocytopenia and bleeding. This bleeding tendency is greatly aggravated when the infection specifically involves the parenchymal cells of the liver; such a condition results in defective formation of coagulation factors such as prothrombin. The proper care of patients in whom a hemorrhagic state has developed requires urgent and accurate diagnosis followed by immediate and appropriate treatment that will combat the infection and alleviate the hemorrhagic state and liver disorder. If the hemorrhagic state is due to one of the dangerous infectious fevers, adequate protection of the medical, nursing, and laboratory staff concerned is also vital.

Adolescent↗
PubMed1975

Experimental biology and pathogenesis of Junin virus infection in animals and man.

A fatal disease resembling Argentine haemorrhagic fever of man has been produced in guinea-pigs and mice by inoculation with Junin virus. Infected guinea-pigs show macroscopic and microscopic haemorrhagic lesions, marked bone marrow changes, decreased leukocytes and platelets in the peripheral blood, and impairment of immunological response. This response permits differentiation between pathogenic (XJ) and attenuated (XJ Cl(3)) strains. Guinea-pigs inoculated with the XJ Cl(3) strain develop an inapparent infection accompanied by slight haematological changes, the appearance of antibody, and protection against challenge with the pathogenic strain. The attenuated strain has been used successfully as an immunizing antigen in 636 human volunteers. Guinea-pigs infected with Tacaribe virus show cross-protection against Junin virus, with the presence of heterologous neutralizing antibodies. Suckling mice infected with Junin virus develop a typical viral encephalitis; the pathogenicity of the virus decreases with increasing age of the mice. Experiments with thymectomized mice and with mice treated with antithymocyte serum suggest that the pathogenicity of Junin virus in this host is related to the integrity of the thymus-dependent immune system. There is evidence that humoral antibodies do not play any role in the development of the encephalitic lesions but rather protect mice against Junin virus infection. A recent serological survey among laboratory workers and inhabitants of the endemic area has demonstrated the presence of inapparent infection with Junin virus.

Animals↗
PubMed1975

Ultrastructural and immunohistochemical study of the human kidney in Argentine haemorrhagic fever.

In six lethal cases of Argentine Haemorrhagic Fever (AHF) a disease caused by Junin virus, kidney samples were studied by means of immunofluorescent and electron microscopic techniques.--The ultrastructural studies showed that the distal and collecting tubes presented a large number of virus like intracytoplasmic particles. Those particles were present in the lumen of the endoplasmic reticulum cisternae and showed two distinct morphological aspects. Some of them were of high electron density and contained a few granules. The others were larger in size, electron lucid, and contained a variable number of ribosome like granules. Both types of particles originated from the endoplasmic reticulum wall by a process of budding. The presence of these particles was coincident with a severe cell damage which lead to necrosis and desquamation; and with large quantities of Junin virus antigen as demonstrated by immunofluorescence.--On the basis of these observations it is assumed that in AHF the cell damage is due to direct viral replication within the affected cells.

Antigens, Viral↗
PubMed1975

Epidemiological features of dengue and chikungunya infections in Burma.

A serological survey for antibody to dengue and chikungunya was carried out in all 14 divisions and states and 2 border towns in Burma during 1973-74. Dengue HI antibody prevalence rate of less than 10% was observed in Arakan and Shan States, 10 to 30% in the Irrawaddy, Pegu, Mandalay Divisions and Kachin, Mon and Karen States, 31 to 60% in Sagaing Division, and over 60% in Rangoon, Magwe and Tenasserim Divisions. Similarly, chikungunya HI antibody prevalence rate of less than 10% was observed in Arakan State, 10 to 30% in the Irrawaddy, Pegu, Mandalay and Sagaing Divisions and Kachin State, 31 to 60% in Rangoon Division and Mon State. Both dengue and chikungunya antibodies were detected where Aedes aegypti mosquitoes were prevalent but the antibody prevalent rates were not directly proportional to the premises index. No HI antibody to dengue nor chikungunya was detected in Aedes aegypti free hilly areas, Chin and Kayah States, but was detected in the Shan State, Dengue and chikungunya infections were observed both in rural and urban populations. Dengue and chikungunya infections affected all socioeconomic classes in Rangoon equally but in Mandalay high socioeconomic class was nearly 3 times less affected than lower socioeconomic class. The infrequencies of dengue and chikungunya infections were observed to be 2 to 3 times higher in residents of Rangoon City than those of other towns. In Rangoon the antibody prevalence rates to dengue increased progressively with age while in other towns no appreciable increase in rates with age was observed. Both sexes were equally affected. This study provides strong circumstantial evidence that dengue and chikungunya viruses are highly and widely distributed throughout Burma, and that new outbreaks of haemorrhagic fever could occur in previously free areas following introduction of dengue viruses into populations previously exposed to one type of dengue.

Aedes↗