Download Viral Hemorrhagic fever

Viral
Hemorrhagic
Fevers
• All types of Viral hemorrhagic fevers
(VHF) are characterized by fever and
bleeding disorders and can progress to
shock and death in many cases.
• Viral hemorrhagic
fevers (VHFs) is a group of
animal and human illnesses that are caused by
four different RNA enveloped viral families:
oArenaviridae.
oBunyaviridae.
oFiloviridae.
oFlaviviridae.
Arenaviridae
• Lassa virus.
• Junin virus.
• Machupo virus.
Bunyaviridae:
• RVF virus.
• CCHF virus.
Filoviridae:
• Marburg virus.
• Ebola virus.
Flaviviridae:
• Yellow fever virus.
• Dengue virus.
• Alkhumra virus.
Arenaviridae
• Epidemiology:
o Lassa virus: West Africa.
o Junin virus: Argentina.
o Machupo virus: Bolivia.
• Virology:
Round, enveloped viruses. Two segments SS
RNA.
• Viral reservoir:
some are zoonotic
transmitted by rodents.
Transmission:
Arenaviruses are shed in the urine and saliva of
the infected rodents.
• Mucosal exposure to the aerosols e.g. inhalation.
• By direct contact of broken skin with the
infectious material, from infected rodents.
• Ingestion of contaminated food.
• Person to person contact*.
N
Pathogenesis and clinical picture:
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The viruses infect the macrophages and the
endothelial cells of the blood vessels, T-cell
mediated response lead to vascular damage.
o
o
o
o
Liver and spleen necrosis.
Visceral hemorrhages.
Shock and cardiac damage.
Death in 50% of cases.
Bunyaviridae:
• Large group of at least 200 different viruses.
• Most are Arboviruses: transmitted by arthropods.
• Virology:
o Enveloped, spherical, 3 Ss RNA segments.
o The most important specie are Rift Valley
Fever Virus (RVF) & Crimean Congo
Hemorrhagic Fever virus (CCHF).
o RVF was first reported
in livestock in Kenya’s
Rift Valley in the 1910s.
Transmission: Vector-born infection
• Rift valley fever virus is transmitted by
mosquitos, direct contact with infected animals
and rarely between humans.
• CCHF is transmitted by Ticks from animals to
human and from human to humans.
o Vertebrate host: domestic animals such as cattle,
buffalo, sheep, goats, and camels.
o Outbreaks of RVF and CCHF were confirmed in
southern & western borders of Saudi Arabia and
both viruses are now endemic in KSA.
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Pathogenesis and clinical picture:
• Primary viremia: infection of vascular endothelium and
macrophages of RES. Multiply within the RES.
• Secondary viremia:
– Vascular endothelial damage; leakage of plasma and
erythrocytes,
• Cerebral edema and encephalitis.
• Renal hemorrhagic necrosis.
• Hemorrhagic fever.
• Most rift valley fever cases are mild & self-limiting,
febrile illness. However, some patients develop
meningoencephalitis, vision loss or hemorrhagic fever
• CCHF cause sever hemorrhages with mortality rate ≈
RVF
Crimean-Congo -Hemorrhagic fever caused by
Nairovirus:
N
Filoviridae
• Genus: Marburg virus and Ebola virus.
• Virology: filamentous helical enveloped Ss RNA
viruses, encodes seven proteins.
From the Latin "filum," meaning thread-like,
based on their filamentous structure.
• Epidemiology: Endemic in Africa.
• Marburg virus (Kenya and Zimbabwe).
• Ebola virus (Sudan and Zaire).
• Reservoir:
• They are zoonotic
diseases (fruit bats?)*.
Transmission:
• The first infection was first detected among
laboratory workers in Marburg, who had been
exposed to tissue culture of cell line prepared
from African green monkeys.
• Highly transmissible: the virus is present in the
blood and all body fluids including urine, saliva,
sweat, feces, vomit, breast milk, and semen.
• Bats-human contact, monkeys-human contact,
human-human contact and other unknown
routes of transmission.
Pathogenesis and clinical picture:
 Vascular endothelial damage lead to widespread
hemorrhages, edema and hypovolemic shock.
 The virus is disseminated through blood stream to
the liver, spleen, lymph nodes (RES), and lungs.
 Eosinophilic cytoplasmic inclusions are seen in
the infected cells.
 Liver function tests: SGPT (ALT) and AST are
elevated*, and alkaline phosphatase is mildly
elevated.
 Spleen destruction and lymph node enlargements.
 Mortality rate: 50% up to 90%.
Hemorrhagic rash
Ebola Outbreak in Africa (March 2014-2015)
• The largest outbreak of Ebola virus. On17th
October/2014, the cumulative number of
suspected cases was 9216, including 4555 deaths
(case-fatality rate 55 percent).
• On 4th March 2015 24000 cases and 10000 deaths.
• On 26th of April: 26312 cases and 10900 deaths.
• On 9 December: 28 601cases and 11 300 deaths.
• A Saudi citizen was suspected to suffer from
Ebola infection but postmortem samples were
negative.
Flaviviridae:
o Flaviviruses are Arboviruses (transmitted to
man by arthropods).
o Flavus means yellow (jaundice).
o Three genera cause hemorrhagic fever:
• Yellow fever virus:
yellow fever and hepatic dysfunction.
• Dengue virus:
Dengue fever (DF), dengue hemorrhagic fever
(DHF), and dengue shock syndrome (DSS).
• Alkhumra virus*: Alkhumra hemorrhagic
fever. Was first isolated in KSA in 1995.
Virology:
• Enveloped, icosahedral nucleocapsid, positive Ss RNA
viruses. Has glycoprotein spikes (adhesion of virus to
tissue). All Flaviviruses are serologically related.
• Vector: Aedes aegypti female mosquito: Yellow Fever
virus & Dengue virus.
Tick: Alkhumra virus.
• Host: Human and monkeys* (Zoonosis).
• Distribution:
• Dengue fever: Worldwide, especially tropics.
Outbreaks had occurred in KSA.
• Yellow fever: Africa, and South America.
• Alkhumra virus: KSA and Egypt.
Aedes aegypti
Aedes aegypti
Pathogenesis and clinical picture:
The target tissues:
– The endothelial cells of the capillaries.
– The macrophage and monocytes which will
transfer the virus to the reticuloendothelial
system (RES).
• The vector bite host skin and inoculate the
virus with the saliva into the small capillaries.
• Adhesion to the cells by the glycoprotein spikes.
• The virus is then carried through the small
capillaries by the dendritic cells to other organs.
• This will initiate primary viremia (fever, chill,
N
headaches, and flu-like symptoms within 3-7
days).
• Secondary viremia: after efficient replication of
the virus in RES these viruses will infect:
o Liver: hepatitis, and jaundice (yellow fever).
o Brain: encephalitis.
o Vasculature and skin: hemorrhage and shock.
o Kidneys: oliguria and albuminuria.
Pathogenesis of Flaviviruses:
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