Neuropathology of yellow fever autopsy cases

Carregando...
Imagem de Miniatura
Citações na Scopus
1
Tipo de produção
article
Data de publicação
2023
Título da Revista
ISSN da Revista
Título do Volume
Editora
SPRINGERNATURE
Citação
TROPICAL DISEASES TRAVEL MEDICINE AND VACCINES, v.9, n.1, article ID 1, 7p, 2023
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
BackgroundYellow fever is a viral hemorrhagic fever caused by yellow fever virus, a mosquito-borne flavivirus. Despite an effective vaccine, major outbreaks continue to occur around the world. Even though it is not a proven neurotropic virus, neurological symptoms in more severe clinical forms are frequent. The understanding of this apparent paradox is still rarely addressed in literature.MethodsThe brains of thirty-eight patients with yellow fever confirmed by RT-PCR, who underwent autopsy, were analyzed morphologically to identify and characterize neuropathological changes. The data were compared with brains collected from individuals without the disease, as a control group. Both cases and controls were subdivided according to the presence or absence of co-concurrent septic shock, to exclude changes of the sepsis associated encephalopathy. To verify possible morphological differences between the yellow fever cases groups, between the control groups, and between the cases and the controls, we applied the statistical tests Fisher's exact test and chi-square, with p values < 0.05 considered statistically significant.ResultsAll cases and controls presented, at least focally, neuropathological changes, which included edema, meningeal and parenchymal inflammatory infiltrate and hemorrhages, and perivascular inflammatory infiltrate. We did not find an unequivocal aspect of encephalitis. The only parameter that, after statistical analysis, can be attributed to yellow fever was the perivascular inflammatory infiltrate.ConclusionsThe neuropathological findings are sufficient to justify the multiple clinical neurologic disturbances detected in the YF cases. Since most of the parameters evaluated did not show statistically significant difference between cases and controls, an explanation for most of the neuropathological findings may be the vascular changes, consequent to shock induced endotheliopathy, associated with stimulation of the immune system inherent to systemic infectious processes. The statistical difference obtained in yellow fever cases regarding perivascular infiltrate can be can be explained by the immune activation inherent to the condition.
Palavras-chave
Yellow Fever, Autopsy, Brain, Neuropathology, Sepsis
Referências
  1. Alhakimi HA, 2015, AIMS PUBLIC HEALTH, V2, P132, DOI 10.3934/publichealth.2015.1.132
  2. Amarela Febre, 2018, GUIA PROFISSIONAIS S
  3. [Anonymous], 1966, JAMA, V198, P671
  4. BARRETT ADT, 1986, J GEN VIROL, V67, P631, DOI 10.1099/0022-1317-67-4-631
  5. Bray M, 2005, CURR OPIN IMMUNOL, V17, P399, DOI 10.1016/j.coi.2005.05.001
  6. Duarte-Neto AN, 2019, HISTOPATHOLOGY, V75, P638, DOI 10.1111/his.13904
  7. Duarte-Neto AN, 2019, PLOS NEGLECT TROP D, V13, DOI 10.1371/journal.pntd.0007625
  8. Ekenna O, 2010, West Afr J Med, V29, P91
  9. Faust SN, 2001, NEW ENGL J MED, V345, P408, DOI 10.1056/NEJM200108093450603
  10. Gerin M, 2014, ARCH PEDIATRIE, V21, P384, DOI 10.1016/j.arcped.2014.01.014
  11. Ho YL, 2019, J TRAVEL MED, V26, DOI 10.1093/jtm/taz040
  12. Hutchins GM, 1999, ARCH PATHOL LAB MED, V123, P1085
  13. JAKOB A., 1929, DEUTSCHE ZEITSCHR NERVENHEILK, V111, P111, DOI 10.1007/BF01680492
  14. Johansen ME, 2015, SEMIN THROMB HEMOST, V41, P16, DOI 10.1055/s-0034-1398377
  15. Johansson PI, 2010, MED HYPOTHESES, V75, P564, DOI 10.1016/j.mehy.2010.07.031
  16. Johansson P, 2017, CRIT CARE, V21, DOI 10.1186/s13054-017-1605-5
  17. JONES EMM, 1972, B WORLD HEALTH ORGAN, V46, P653
  18. Kleinert RDV, 2019, VIRUSES-BASEL, V11, DOI 10.3390/v11100960
  19. Kwagonza L, 2018, BMC INFECT DIS, V18, DOI 10.1186/s12879-018-3440-y
  20. Lasnet A., 1929, AFR C YELL FEV DAK A
  21. Liu T, 2001, J VIROL, V75, P2107, DOI 10.1128/JVI.75.5.2107-2118.2001
  22. Ludwig J., 2002, OOK AUTOPSY PRACTICE, DOI [10.1007/978-1-59259-286-9, DOI 10.1007/978-1-59259-286-9]
  23. Marinho PES, 2019, EMERG INFECT DIS, V25, P1567, DOI [10.3201/eid2508.181479, 10.3201/eid2508/181479]
  24. MIMS CA, 1957, BRIT J EXP PATHOL, V38, P329
  25. Monath TP, 2003, ADV VIRUS RES, V60, P343, DOI 10.1016/S0065-3527(03)60009-6
  26. Neumar RW, 2008, CIRCULATION, V118, P2452, DOI 10.1161/CIRCULATIONAHA.108.190652
  27. Opal SM, 2015, J INTERN MED, V277, P277, DOI 10.1111/joim.12331
  28. Ostrowski SR, 2015, CRIT CARE, V19, DOI 10.1186/s13054-015-0918-5
  29. Pan-American Health Organization/World Health Organization, 2018, EP UPD YELL FEV
  30. Paules CI, 2017, NEW ENGL J MED, V376, P1397, DOI 10.1056/NEJMp1702172
  31. Pierrotti LC, 2020, CLIN INFECT DIS, V70, P144, DOI 10.1093/cid/ciz389
  32. Sharshar T, 2004, BRAIN PATHOL, V14, P21, DOI 10.1111/j.1750-3639.2004.tb00494.x
  33. Singer M, 2016, JAMA-J AM MED ASSOC, V315, P801, DOI 10.1001/jama.2016.0287
  34. Stevenson LD, 1939, ARCH PATHOL, V27, P249
  35. THEILER MAX, 1930, ANN TROP MED AND PARASITOL [LIVERPOOL], V24, P249