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Yellow fever
Melaku Yetbarek( MD,Internist)
November,2023
Introduction
• Yellow fever is a mosquito-borne viral
hemorrhagic fever with a high case-fatality rate
• Member of the family Flaviviridae
• Yellow fever virus is a single serotype and is
antigenically conserved
• Yellow fever occurs in tropical regions of sub-
Saharan Africa and South America
Transmission Cycle
• The primary transmission cycle involves
monkeys and daytime biting mosquitoes
(Aedes species in Africa, Haemagogus species
in South America).
• Urban yellow fever(Africa)
• Jungle yellow fever(South America)
Pathogenesis
• An infected female mosquito inoculates approximately
1000 to 100,000 virus particles intradermally during
blood feeding
• Monocyte-macrophages and large histiocytes, appear
to be the preferred cell types for primary replication
• Large amounts of virus are produced in the liver, lymph
nodes, and spleen
• During the viremic phase (days three to six), infection
may be transmitted to blood-feeding mosquitoes.
Pathogenesis
• The midzone of the liver lobule is principally affected
• Injury to hepatocytes is characterized by eosinophilic
degeneration and formation of councilman bodies
• Hemorrhage in yellow fever is as a result of
 Decreased synthesis of clotting factors
 DIC
 Platelet dysfunction
Clinical features
• Yellow fever is a typical VHF accompanied by
prominent hepatic necrosis
• Incubation period of 3–6 days
• Nonspecific febrile illness (fatigue, myalgia,
backache, headaches, photophobia, anorexia,
nausea or vomiting)
• About 15% of cases have severe symptoms
including chills, low back pain, headache, and
fever
Clinical…
• During this stage, the hepatorenal disease is common
and carries a high mortality.
• A physical exam may reveal the Faget sign or pulse
fever dissociation, facial flushing, and conjunctival
injection.
• During the most toxic phase, patients develop
jaundice, dark urine, and vomiting
• May lead to heptatic failure,AKI,myocarditis and
encephalitis
Diagnosis
• Serology(ELISA-presence of IgM antibodies in
a single sample)
• Rapid diagnostic tests-PCR
• Pathology-Postmortem midzone liver necrosis
Treatment
• There is no specific treatment, but severe cases require
aggressive supportive care and hydration.
• Patients should be managed in the intensive care unit
(ICU) and closely monitored for
 Disseminated intravascular coagulation (DIC),
 Hemorrhage,
 Kidney, and
 Liver dysfunction.
• Coagulopathy is managed with fresh frozen plasma,
and
• renal failure may require dialysis
Prevention
• Control of yellow fever mosquitoes
• Live attenuated vaccine
 Starts with in 10 days and protective for 25-35
years
Contraindicated for <6 month age group
Benefit-Risk assessment before for age groups>60
and pregnant ladies
Outcomes
• Higher mortality is usually in patients with liver
and renal damage.
• Deaths tend to occur within the first 10 days of
the toxic phase.
• Both infants and the elderly are more likely to die
than other individuals
• Approximately 20 to 50 percent of patients who
enter the period of intoxication succumb to the
disease
Outcome
Poor prognostic signs include :
• anuria,
• shock,
• hypothermia,
• agitation,
• delirium,
• intractable hiccups,
• seizures,
• hypoglycemia,
• hyperkalemia,
• metabolic acidosis,
• Cheyne-Stokes respirations,
• stupor, and
• coma
Thank you!!!

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Yellow fever.pptx(Epidemiology,Clinical features and prevention)

  • 1. Yellow fever Melaku Yetbarek( MD,Internist) November,2023
  • 2. Introduction • Yellow fever is a mosquito-borne viral hemorrhagic fever with a high case-fatality rate • Member of the family Flaviviridae • Yellow fever virus is a single serotype and is antigenically conserved • Yellow fever occurs in tropical regions of sub- Saharan Africa and South America
  • 3.
  • 4.
  • 5. Transmission Cycle • The primary transmission cycle involves monkeys and daytime biting mosquitoes (Aedes species in Africa, Haemagogus species in South America). • Urban yellow fever(Africa) • Jungle yellow fever(South America)
  • 6. Pathogenesis • An infected female mosquito inoculates approximately 1000 to 100,000 virus particles intradermally during blood feeding • Monocyte-macrophages and large histiocytes, appear to be the preferred cell types for primary replication • Large amounts of virus are produced in the liver, lymph nodes, and spleen • During the viremic phase (days three to six), infection may be transmitted to blood-feeding mosquitoes.
  • 7. Pathogenesis • The midzone of the liver lobule is principally affected • Injury to hepatocytes is characterized by eosinophilic degeneration and formation of councilman bodies • Hemorrhage in yellow fever is as a result of  Decreased synthesis of clotting factors  DIC  Platelet dysfunction
  • 8. Clinical features • Yellow fever is a typical VHF accompanied by prominent hepatic necrosis • Incubation period of 3–6 days • Nonspecific febrile illness (fatigue, myalgia, backache, headaches, photophobia, anorexia, nausea or vomiting) • About 15% of cases have severe symptoms including chills, low back pain, headache, and fever
  • 9. Clinical… • During this stage, the hepatorenal disease is common and carries a high mortality. • A physical exam may reveal the Faget sign or pulse fever dissociation, facial flushing, and conjunctival injection. • During the most toxic phase, patients develop jaundice, dark urine, and vomiting • May lead to heptatic failure,AKI,myocarditis and encephalitis
  • 10. Diagnosis • Serology(ELISA-presence of IgM antibodies in a single sample) • Rapid diagnostic tests-PCR • Pathology-Postmortem midzone liver necrosis
  • 11. Treatment • There is no specific treatment, but severe cases require aggressive supportive care and hydration. • Patients should be managed in the intensive care unit (ICU) and closely monitored for  Disseminated intravascular coagulation (DIC),  Hemorrhage,  Kidney, and  Liver dysfunction. • Coagulopathy is managed with fresh frozen plasma, and • renal failure may require dialysis
  • 12. Prevention • Control of yellow fever mosquitoes • Live attenuated vaccine  Starts with in 10 days and protective for 25-35 years Contraindicated for <6 month age group Benefit-Risk assessment before for age groups>60 and pregnant ladies
  • 13. Outcomes • Higher mortality is usually in patients with liver and renal damage. • Deaths tend to occur within the first 10 days of the toxic phase. • Both infants and the elderly are more likely to die than other individuals • Approximately 20 to 50 percent of patients who enter the period of intoxication succumb to the disease
  • 14. Outcome Poor prognostic signs include : • anuria, • shock, • hypothermia, • agitation, • delirium, • intractable hiccups, • seizures, • hypoglycemia, • hyperkalemia, • metabolic acidosis, • Cheyne-Stokes respirations, • stupor, and • coma