Yellow fever is a viral hemorrhagic fever caused by Viscerophilus tropicus, an enveloped single stranded RNA arbovirus belonging to the Flavivirus genus. 1st viral disease to be discovered Not present in india and Russia IP: 2-6 days Quarantine period: 6 days Reservoir: Monkeys, Man, Aedes

1. Yellow fever

2. Outline:
 Introduction
 Epidemiology
 Transmission
 Pathogenesis
 Clinical manifestations
 Diagnosis
 Treatment
 Prevention
 Syndromes
 DDx

3. Introduction:
 Yellow fever is a viral hemorrhagic fever caused byViscerophilus
tropicus, an enveloped single stranded RNA arbovirus belonging
to the Flavivirus genus.
 1st viral disease to be discovered
 Not present in india and Russia
 IP: 2-6 days
 Quarantine period: 6 days
 Reservoir: Monkeys, Man,Aedes

4. Epidemiology:
 As a result of disease control programs in many countries, yellow
fever is now endemic only in parts of sub-SaharanAfrica and
South America.
 It is estimated that there are about 200,000 cases a year resulting
in more than 30,000 deaths annually

6. Transmission:
 Yellow fever is transmitted by female mosquito vectors.
 InAfrica, the Aedes species, particularly A. Eagypti is involved
 while in South America, the Haemogogus species is the dominant
vector.
 Aside from human hosts, yellow fever also has a natural reservoir
in primates.

7. Pathogenesis
 After transmission from a mosquito, the viruses replicate in the
lymph nodes and infect dendritic cells in particular.
 From there, they reach the liver and infect hepatocytes (probably
indirectly via Kupffer cells), which leads to eosinophilic
degradation of these cells and to the release of cytokines.
 Apoptotic masses known as Councilman bodies appear in the
cytoplasm of hepatocytes.
 Fatality may occur when cytokine storm, shock, and multiple
organ failure follow.

8. • Incubation: 3-6
Days
• Period of
Infection
• Period of
Remission
• Period of
Intoxication

9. Clinical
Manifestations
(3 stages)
 The first stage, or period of infection, is one of severe, non-
specific signs of systemic illness corresponding with viremia
associated with fevers, malaise, headache, photophobia, nausea,
vomiting, and myalgias (especially in the knees) for a period of
days.Tender hepatomegaly may also be present as well as
 Faget’s sign, described as pulse-temperature dissociation whereby
there is relative bradycardia despite high fevers.
 Moreover, the tongue may develop characteristic erythema along
the tip and sides with a central white coating.

10.  The second stage, or period of remission, follows with clinical
improvement. For the vast majority (85%) of cases, the disease
ends here. For the unlucky minority (15%), the respite ends after
48 hours.
 Amaryl mask: the patient’s face is purple, with a bluish tinge, eyes
are anxious, bloodshot, sclera are injected, photophobia,
lacrimation is noted.
 The oral mucosa is bright red, edematous.The pulse during this
period is rapid, good filling. Heart tones are muted.
 There are no abnormalities in the lungs.

11.  The final stage, or period of intoxication, is marked by the return
of symptoms seen in the first stage, but further complicated by
jaundice, hemorrhage, oliguria, and metabolic encephalopathy.
 One unique feature of yellow fever is a predominantlyAST
elevated transaminitis as opposed to anALT elevation typically
seen with most viral hepatitides.
 Hemorrhage is a result of thrombocytopenia and inability to
synthesize coagulation factors due to hepatic dysfunction.
Morality rates for those that enter this stage ranges between 20-
50%

12. • Diagnosis
• ELISA todetect
IgMAb
• PCR todetect the
presenceofviral
RNA
A preliminary diagnosis is made based on:
1) Arrival or location in an endemic region(Africa and South
America) – tropics andsubtropics;
2) symptoms of the disease (“saddle” or“two-wave” temperature
curve, hemorrhagic syndrome, jaundice, kidney, liver and spleen
damage);
3) Laboratory data: (in biochemistry – increase bilirubin, ALT,AST,
urea, creatinine, in General the blood oppression shoots blood-
reduction of leukocytes, neutrophils, lymphocytes, reduction of
platelets, acceleration of sedimentation rate, urine
protein,cylinders, erythrocytes)

13. Treatment
 Unfortunately limited to supportive care given that no known
antivirals have been shown to be effective.
 As with other Flavivirus infections, no cure is known for yellow
fever.
 Hospitalization is advisable and intensive care may be necessary
because of rapid deterioration in some cases.
 Certain acute treatment methods lack efficacy: passive
immunization after the emergence of symptoms is probably
without effect; ribavirin and other antiviral drugs, as well as
treatment with interferons, are ineffective in yellow fever
patients.
 Symptomatic treatment includes rehydration and pain relief with
drugs such as paracetamol (acetaminophen).
 Acetylsalicylic acid (aspirin) should not be given because of its
anticoagulant effect, which can be devastating in the case of
internal bleeding that may occur with yellow fever

14. Prevention
Other control measures:
1. Area around airport kept
free of aedes > 400m
2. Vector control (A. Aegypti)
• Mosquito nets
• Mosquito repellents
• Insecticide treatment of
mosquito breeding sites
• Wear proper clothing to
reduce mosquito bites.
When weather permits,
wear long sleeves, long
pants, and socks when
outdoors.
Yellow fever vaccine
 LiveAttenuated
 Strain- 17 D
 Diluent- cold physiological
saline
 Temp=- 30⁰C to +5⁰C
 Validity of certificate- 10 days
to life long
 Reaction to vaccination is
minimal but in some cases it
is sever

15. EYE
(elimination
yellow fever
epidemic)
Strategy
(WHO,UNICEF,GAVI)
 Project at – risk population
 Prevent international spread ofYF
 Rapid containment of outbreak

16. Syndromes
associated
with yellow
fever
1. Intoxication Syndrome
2. Jaundice syndrome
3. Hemorrhagic syndrome
4. Hepatolienial syndrome
5. Hepatic insufficiency syndrome

17. Differencial
diagnosis of
yellow fever
 In a differential diagnosis, infections with yellow fever must be
distinguished from:
 other feverish illnesses such as malaria.
 Other viral hemorrhagic fevers, such as Ebola virus, Lassa virus,
Marburg virus, and Junin virus, must be excluded as the cause.

18. Thank you...