Dr. Sookun Rajeev K

(MD)

Dept of General Medicine

Anna Medical College

Aetiology•The disease is caused by Flavivirus febris of the genus Flavivirus, the family Togaviridae.

•The virus is unstable in the environment.

•It resists drying and can survive in the frozen state for a year.

•In a sealed vial with nitrogen, the virus remains viable for 12 years.

Epidemiology•Two epidemiologically different types of foci are distinguished:

1.Sylvan (rain forest)

2.Urban.

Epidemiology•The reservoir of the virus in the sylvan form are monkeys, possibly rodents, hedgehogsand other animals.

•The vector of transmission in South America are mosquitoes Haemagogus, Sperazzini and other insects.

Epidemiology•In tropic Africa these are mosquitoes Aedessimpsoni, A. africanus, A. aegypti and other species of Aedes.

•Sylvan yellow fever is also called endemic because it usually occurs in the form of endemic foci and less frequently as epidemics.

Epidemiology•Transmission of the virus from epidemic foci to towns and villages, where mosquitoes Aedes aegypti occur, can cause an epidemic outbreak.

•The source of infection in urban foci of yellow fever are human patients; the vector is mosquito Aedes aegypti.

Epidemiology•The mosquito becomes contagious in 6-18 days after sucking blood of a human patient, this period depending on the ambient temperature:

18 days for ambient temperatures under 21 °C

6 days at 31 °C.

Once infected the vector remains infectious for its entire life (1-2 months).

Pathogenesis•As the virus is inoculated into a human by the bite of an infected mosquito, it multiplies during 3-6 days in the regional lymph nodes, in the cells of mononuclear phagocytic system, and enters the blood to cause viraemia.

•The blood carries the virus to the liver, bone marrow, kidneys, spleen, and brain to involve the vascular apparatus and to cause dystrophy and necrosis of their cells.

Clinical Picture

•The incubation period lasts 3-6 days.

•Three periods (phases) are distinguished.

Clinical Picture1. The initial (hyperaemic) phase lasts 3-4 days.

• The onset is acute: the patient develops severe headache, chill, vertigo, lumbar pain, pain in the extremities. • The body temperature rapidly rises to 39-40 °C and higher. • Thirst, nausea and recurrent vomiting with mucus are

characteristic. • The face, the neck and the upper chest are markedly

hyperaemic and swollen from the first days of the disease. • The scleral and conjunctival vessels are injected (rabbit eyes). • The patient complains of insomnia. • The pulse rate is 100-130.

Clinical Picture•On the second or third day, the patient's condition worsens, •He develops cyanosis and then slight jaundice of the skin and

visible mucosa. •Blood studies reveal hyperbilirubinaemia and high

transaminase (mostly AsAT) activity. • The liver and the spleen are slightly enlarged and tender to

palpation. • Tachycardia is followed by bradycardia. • Epistaxis and gingival bleeding are frequent. •Blood is seen in the vomitus ("black vomit").

Clinical Picture2. Remission begins in 4-5 days.

•It lasts from several hours to one day. •The body temperature drops to normal or subfebrile. •The patient's condition improves, vomiting ceases, pain abates. •If the disease runs a mild course, recovery begins with the fall of temperature.

Clinical Picture3. In moderately severe and severe cases, the phase of remission is

followed by the phase of reaction or venous stasis (toxaemia) that lasts 3-4 days.

• Remission can be absent and the initial period can be followed immediately by the reaction phase. • The patient's condition rapidly worsens. The' temperature rises

again, and jaundice intensifies. • The skin is pallid; haemorrhagic rash (petechiae, purpura,

ecchymoses) develops on the trunk and the extremities. •Gingival bleeding, haematemesis, nasal and uterine bleeding

leading to miscarriage, develop. •Arterial pressure falls. •Oliguria or anuria attended by azotaemia develops.

Clinical Picture•Haematologic changes: leucopenia, neutropenia, lymphocytopenia, high globulin and colour index, and accelerated ESR; blood coagulation is delayed. •The fever period lasts 8-9 days, and then the phase of recovery begins with a slow restoration of the upset functions of the organs and tissues. •A fulminating form of the disease leads to death in 3-4 days.

Diagnosis•Yellow fever is diagnosed on the basis of clinical and laboratory findings.

•Virus is isolated in the laboratory from a blood specimen taken during the first 4 days of the disease.

•The virus neutralization reaction is also used.

Diagnosis•Discovery of antibodies to the virus, using the complement fixation test and inhibition of indirect haemagglutination, is diagnostically important too: four-fold increase in the antibody titres in paired serums.

•Serologic studies can confirm the diagnosis retrospectively because the antibodies to the virus can be revealed only on the second week of the disease.

Treatment•Specific therapy is unknown. •Moderately severe forms are treated symptomatically: Vitamin C, Vicasol, Vitamin P, Cardiovascular preparations.

Treatment•Severe and fulminant forms should be treated by:

Intensive therapy

Resuscitation measures may be necessary: correction of haemostasis, complex antishockand detoxicating treatment.

Thank You