Rift Valley Fever: A Deadly Zoonotic Disease of Ruminants and Humans

Rift Valley Fever

Rift Valley fever phlebovirus (RVFV), is a mosquito-borne, zoonotic pathogen in genus Phlebovirus, family Phenuiviridae, order Bunyavirales that typically causes outbreaks in Africa and spread to the Arabian Peninsula in 2000. It has a high colonization capacity, is a potential emergent risk in Europe, Asia and the Americas due to the presence of competent vectors and is a bioterrorism/agroterrorism concern as it could be weaponized. Consequently, it is classified as a category A pathogen by the National Institute of Allergy and Infectious Diseases in recognition of its potential for social disruption requiring significant public health preparedness and is the United States Department of Agriculture Animal and Plant Health Inspection Service’s third most dangerous animal threat after avian influenza and foot-and-mouth disease. In the U.S. RVFV is a Select Agent. All work with virulent RVFV must be conducted minimally at biosafety level 3 enhanced.

The virus replicates in both Aedes spp. and Culex spp. mosquitoes including species native to non-endemic areas. In ruminants, particularly sheep, RVFV infections cause mass abortion and high mortality rates in neonates. Older animals can succumb to liver and kidney failure as well as hemorrhagic fever. Other ruminants, including cattle, goats, a diversity of African wild hoofstock, white-tailed deer, camels and alpacas are also susceptible to RVF. In humans, RVF ranges from flu-like symptoms to hemorrhagic fever, liver and/or kidney failure and can also include encephalitis and retinitis. Increased abortion risk has also been correlated with the presence of RVFV in humans.

Until recently, our understanding of Rift Valley fever pathology in ruminants has come from extant published case reports of natural disease and observations made during experimental animal studies, for which the primary focus was other than improving our understanding of Rift Valley fever (RVF) pathology. These reports are typically focused on a small number of animals and only a few organs, typically liver and lymphoid tissues. Furthermore, pathology information from experimental animal studies while informative has limited value as these studies cannot fully replicate natural disease in its virus format, dose or route of inoculation/exposure.

This talk will present insights regarding RVF pathogenesis in sheep gleaned from macro- and microscopic pathological examinations as well as viral antigen and nucleic acid distribution of Rift Valley fever virus in over 200 naturally infected South African sheep, lambs and fetuses including placenta. These findings will be compared with published information regarding RVF in humans. Additional, topics for discussion will be the importance of type and number of diagnostic samples to collect, limitations of current diagnostic tests and correlation of natural disease findings with those from experimental animal studies. 

Key Learning Objectives:

After attending this webinar, you would be able to:

  • Describe Rift Valley fever virus, its epidemiology, importance and current countermeasures
  • Identify the key pathological findings in cases of Rift Valley fever (RVF) in ruminants and humans
  • Delve deeper into the disease expression in sheep (a natural host)
  • As time allows, review some advances in detection of RVF

Speaker Bio:

Dr. A. Sally Davis, DVM, PhD, DACVP runs the Laboratory of Investigative Pathology in the Department of Diagnostic Medicine/Pathobiology at Kansas State University (K-State). Her research includes the development of tissue-based biomarkers, diagnostic tests and countermeasures against emerging and zoonotic viral pathogens as well as visualization of host-pathogen interactions using a variety of microscopy and analysis techniques. Specific areas of concentration include biospecimen quality, viral pathogenesis, pathogen inactivation and high containment research including work with small and large animals as well as Select Agents. 

Dr. Davis completed a bachelor’s degree in computer science modified with education as well as a graduate certification in middle school sciences education from the Dartmouth College in 1992 then spent over a decade in computer and business consulting industry including in international management positions with fiscal responsibility for multi-million-dollar projects and up to 20 direct reports. She completed a DVM with a focus on zoo, wildlife and aquatic animal medicine in 2007 and a residency in Anatomic Veterinary Pathology in 2009, both at North Carolina State University College of Veterinary Medicine (NCSU CVM). In 2014, she completed a PhD in Jeffery Taubenberger’s laboratory in the NIAID within the Comparative Biomedical Scientist Training program at the NIH joint with NCSU CVM. Dr. Davis is a member of the ASIP and on the Executive Council for the Histochemical Society. She is also extraordinary faculty at University of Pretoria, South Africa, which facilitates work with emerging infectious diseases, such as Rift Valley fever virus, in their endemic country.”

Recommended Reading:

  1. Odendaal L#, Davis AS#, Venter EH. Insights into the Pathogenesis of Viral Hemorrhagic Fever Based on Viral Tropism and Tissue Lesions of Natural Rift Valley Fever. Viruses.2021; 13(4):709. doi: 10.3390/v13040709.
  2. van Schalkwyk A#, Gwala S, Schuck KN, Quan M, Davis AS, Romito M, Odendaal L. Retrospective phylogenetic analyses of formalin-fixed paraffin-embedded samples from the 2011 Rift Valley fever outbreak in South Africa, through sequencing of targeted regions. J Virol Meth. 2021; 287:114003. doi: 10.1016/j.jviromet.
  3. Anthony T, van Schalkwyk A, Romito M, Odendaal L, Clift SJ, Davis AS#. Vaccination with Rift Valley fever virus live attenuated vaccine strain Smithburn causes meningoencephlitis in alpacas. J Vet Diag Invest. 2021; 33(4):777-781. doi 10.1177/10406387211015294.
  4. Odendaal L#, Clift SJ, Fosgate GT, Davis AS#. Ovine fetal and placental lesions and cellular tropism in natural Rift Valley fever virus infections. Veterinary Pathology. 2020; 57(6):791-806. doi: 10.1177/0300985820954549.
  5. Odendaal L#, Davis AS#, Fosgate GT, Clift SJ. Lesions and cellular tropism of natural Rift Valley fever virus infection in young lambs. Veterinary Pathology. 2020;57(1):66-81. doi: 10.1177/0300985819882633.
  6. Ragan IK, Schuck KN, Upreti D, Odendaal L, Richt JA, Trujillo JD, Wilson WC, Davis AS#. Rift Valley Fever Viral RNA Detection by In Situ Hybridization in Formalin-Fixed, Paraffin-Embedded Tissues. Vector Borne Zoonotic Dis. 2019; 19(7):553-556, doi 10.1089/vbz.2018.2383.
  7. Odendaal L#, Clift SJ, Fosgate GT, Davis AS. Lesions and cellular tropism of natural Rift Valley fever virus infection in adult sheep. Veterinary Pathology. 2019; 56(1):61-77, doi: 10:1177/0300985818806049.
  8. Baudin M, Jumaa AM, Jomma HJE, Karsany MS, Bucht G, Naslund J, Ahlm C, Evander M, Mohamed N. Association of Rift Valley fever virus infection with miscarriage in Sudanese women: a cross-sectional study. Lancet Glob Health.2016;4(11):e864-871. Doi: 10.1016/S2214-109X(16)30176-0.
  9. Wilson WC, Davis AS*, Gaudreault NN, Faburay B, Trujillo JD, Shivanna V, Sunwoo SY, Balogh A, Endalew A, Ma W, Drolet B, Ruder MG, Morozov I, McVey DS, Richt JA. Experimental Infection of Calves by Two Genetically Distinct Strains of Rift Valley Fever Virus. Viruses. 2016; 8(5), doi: 10.3390/v8050145.
  10. Faburay B, Gaudreault NN, Liu Q, Davis AS, Shivanna V, Sunwoo SY, Lang Y, Morozov I, Ruder MG, Drolet B, McVey DS, Ma W, Wilson WC, Richt JA#. Development of a sheep challenge model for Rift Valley fever. Virology. 2016; 489:128-40, , doi: 10.1016/j.virol.2015.12.003.
  11. Arishi H.M., Aqeel A.Y., Al Hazmi M.M. Vertical transmission of fatal Rift Valley fever in a newborn. Ann. Trop. Pediatr. 2006;26:251–253. doi: 10.1179/146532806X120363.
  12. Al-Hazmi M., Ayoola E.A., Abdurahman M., Banzal S., Ashraf J., El-Bushra A., Hazmi A., Abdullah M., Abbo H., Elamin A., et al. Epidemic Rift Valley fever in Saudi Arabia: A clinical study of severe illness in humans. Clin. Infect. Dis. Off. Publ. Infect. Dis. Soc. Am. 2003;36:245–252. doi: 10.1086/345671.

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