Hemorrhagic Fever

The available sources characterize hemorrhagic fever as a viral disease category rather than a single uniform entity, with dengue hemorrhagic fever and hantavirus infections both presented as members of the broader group of viral haemorrhagic fevers ^[1][2][3]. Dengue is described as an arboviral disease caused by dengue virus, while hantavirus infection is described as an emergent zoonotic infection with a global distribution ^[1][2][3]. The source set does not provide a single etiologic definition for the page title beyond these linked viral syndromes, so source-backed detail specific to one unified agent is not yet available ^[1][2][3].

The cited literature describes symptomatic dengue infection as ranging from mild dengue fever to potentially fatal dengue hemorrhagic fever and dengue shock syndrome ^[1][3]. For dengue hemorrhagic fever, plasma leakage is identified as the main pathophysiological hallmark, and severe leakage can lead to hypovolemic shock ^[1]. For hantavirus infections, increased vascular permeability is central to pathogenesis, and the main clinical syndromes named are haemorrhagic fever with renal syndrome and hantavirus cardiopulmonary syndrome ^[2]. The sources also note that hantavirus infections can affect diverse organ systems and that HCPS and HFRS share overlapping symptoms, signs, and pathogenic alterations ^[2].

Dengue hemorrhagic fever was first reported in the Philippines in 1953 and subsequently spread to countries in the South-East Asia and Western Pacific regions ^[1]. Hantavirus infections are described as having a global distribution, with HFRS endemic in Europe and Asia and hantavirus cardiopulmonary syndrome endemic in the Americas ^[2]. The hantavirus review further notes that epidemiology and transmission are influenced by climate, environment, social development, rodent-host ecology, and human behavior in endemic regions ^[2]. For dengue, the review emphasizes that understanding virus characteristics and epidemiology is essential to understanding dissemination patterns and disease status ^[3].

For hantaviruses, human infection occurs through exposure to infected rodents in endemic areas ^[2]. The same source states that Andes hantavirus is unusual in that person-to-person transmission can occur ^[2]. For dengue, the provided sources identify the illness as arboviral and caused by dengue virus, but they do not supply a specific transmission mechanism in the snippets available here ^[1][3].

The supplied sources do not define discrete demographic risk groups for this disease label. Source-backed exposure contexts do include people in endemic areas with exposure to infected rodents for hantavirus infection, and populations in regions where dengue and dengue hemorrhagic fever circulate in South-East Asia, the Western Pacific, and other dengue-endemic settings ^[1][2]. Beyond these exposure-linked groups, additional high-risk categories are not yet supported by the provided snippets ^[1][2][3].

The dengue review states that no specific drugs and no licensed vaccines are available for dengue disease in any clinical presentation, and therefore prevention and control are framed as an active area of review and strategy development ^[1][3]. For hantavirus infection, the cited abstract does not give a detailed prevention package, but it links risk to exposure to infected rodents and to ecological and behavioral factors in endemic regions, implying that exposure avoidance is the source-supported preventive focus ^[2]. Source-backed detail on schedules, specific interventions, or programmatic recommendations is not yet available from the supplied snippets ^[1][2][3].

In surveillance settings, this label should be interpreted cautiously because the source material groups together more than one viral hemorrhagic-fever syndrome rather than defining a single agent-specific disease ^[1][2][3]. Hantavirus disease patterns are described as syndrome-specific, with HFRS and HCPS differing by geographic endemicity and clinical emphasis, while dengue hemorrhagic fever is defined by plasma leakage and possible shock ^[1][2]. The sources also indicate that epidemiologic interpretation should consider geography, rodent ecology, human behavior, and environmental context for hantavirus, and dissemination patterns for dengue ^[2][3].

1. 1 Wang WH et al. Dengue hemorrhagic fever - A systemic literature review of current perspectives on pathogenesis, prevention and control. J Microbiol Immunol Infect. 2020 Dec. PMID: 32265181. doi: 10.1016/j.jmii.2020.03.007. PubMed: https://pubmed.ncbi.nlm.nih.gov/32265181/
2. 2 Vial PA et al. Hantavirus in humans: a review of clinical aspects and management. Lancet Infect Dis. 2023 Sep. PMID: 37105214. doi: 10.1016/S1473-3099(23)00128-7. PubMed: https://pubmed.ncbi.nlm.nih.gov/37105214/
3. 3 Khan MB et al. Dengue overview: An updated systemic review. J Infect Public Health. 2023 Oct. PMID: 37595484. doi: 10.1016/j.jiph.2023.08.001. PubMed: https://pubmed.ncbi.nlm.nih.gov/37595484/
4. 4 Hemorrhagic fevers. Tropical Dermatology. 2006. doi: 10.1016/b978-0-443-06790-7.50016-8. DOI: https://doi.org/10.1016/b978-0-443-06790-7.50016-8
5. 5 Hemorrhagic Fevers. History of Arbovirology: Memories from the Field. 2023. doi: 10.1007/978-3-031-22003-6_19. DOI: https://doi.org/10.1007/978-3-031-22003-6_19
6. 6 Hemorrhagic fever. The Journal of Pediatrics. 1954. doi: 10.1016/s0022-3476(54)80201-0. DOI: https://doi.org/10.1016/s0022-3476(54)80201-0

ICD-10

A98.5

ICD-11

1D67.0

Total cases

169K

Total deaths

1K

Peak month

2012-11

Coverage

4 reporting countries · 2010-01-01 → 2017-01-01