Yellow Fever

Introduction Epidemiology Lifecycle of vector Transmission of disease Clinical features and diagnosis Control

Introduction

Yellow fever is an acute mosquito-transmitted viral infection which is endemic and occasionally epidemic in many countries of tropical Africa and South America. It is also refered to as yellow jack, black vomit, American plaque, and Asian Fetish Main vectors are Aedes and Haemagogus mosquitoes

Epidemiology

Yellow Fever is now found only in Sub-Saharan Africa, the Amazonian region of South America, and occasionally in Trinidad. Africa accounts for around 90% of the cases. Yellow fever is grossly underreported due to unrecognized cases, unavailability of laboratory facilities to make the diagnosis, and poor surveillance. The WHO estimates that there are 200,000 cases a year with 30,000 deaths. Yellow fever appears to be on the rise due to deforestation, urbanization, and the increases of global travel.

Epidemiology

Yellow fever epidemics Philadelphia 1793 Haiti 1805 Norfolk, Virginia 1855

Epidemiology
Yellow fever belt in Africa lies between latitude 15 to 10 south of the equator Nigeria 1986/7 10,000 cases with about 5,000 deaths were reported. In Ghana in 1996 a total of 27 cases of yellow fever with 5 deaths has been reported over a period of a few weeks in the Upper East Region of the country

Lifecycle of vector

The female Aedes mosquito lays eggs above water as compared to other mosquitoes Eggs are laid singly or in a group (raft). These eggs have the ability to survive in dry conditions hence increasing the spread of the disease. Eggs hatch into larvae which extend in the water and have short siphons and may dive to bottom if disturbed After 4 molts the larvae develop to become pupae which have 2 trumpets and after 4 days they become the adult mosquito which flies to find a mate

Yellow Fever Virus

It is a flavivirus 45-60nm An RNA enveloped virus Also classified ecologically as an arbovirus as its cycle involve the arthropods as vector and it has been observed that viral infection does not harming the vector

Transmission

The vector is the Aedes aegypti or Haemagogus mosquito. There are two modes of transmission of the virus-vertical and horizontal Vertical transmission occurs when the virus is passed on to the mosquito's ovum. This is advantageous for continuation of the life cycle during the dry season when the eggs may lay dormant. When the rainy season returns, the eggs hatch, allowing the virus to carry on. Horizontal transmission occurs when either an animal (typically monkeys) or humans are infected by the mosquito.

Transmission

There are several different transmission cycles in yellow fever: sylvatic, intermediate, and urban. All three occur in Africa, but only sylvatic and urban occur in South America. Sylvatic (or jungle ) yellow fever occurs in tropical rainforests where monkeys are infected. Here humans are infected as a result of entering the forest. Risk groups include hunters, farmers, chain saw operators, construction workers.

Transmission

Intermediate yellow fever occurs in the humid or semi-humid savannahs of Africa where small epidemics occur in villages. Here mosquitoes infect both monkeys and humans at this zone of emergence. Urban yellow fever can occur in large epidemics where the virus is passed from human to human via domestic Aedes mosquito.

Sylvatic or Jungle yellow Fever

Sylvatic yellow fever is spread to humans by the bites of Haemagogus spp (south America) and A. africanus (Africa) mosquitoes. These mosquitoes are infected when they feed on viraemic monkeys or because they inherited the infection by transovarial transmission from their mother. Sylvatic yellow fever is usually sporadic, but it is also the ultimate source of urban yellow fever. Sylvatic yellow fever is maintained in a natural enzootic cycle between a number Aedes species which breed in tree holes and the monkeys they feed upon. A. simpsoni, A furcifer and A. luteocephalus found at the edge of forests are also important vectors.

Urban Yellow Fever

Urban yellow fever occurs in more populated areas and is usually transmitted by Aedes aegypti which deposit their eggs in any container which can hold water, in or around houses perpetuating a mosquitoto-human-to-mosquito transmission cycle. Their ability to rear offspring in household water makes Aedes aegypti a threat for yellow fever transmission in areas of very low rainfall, or during the dry season (when water is stored inside houses or very close by). Thus, these mosquitoes complete their life cycle from eggs to adults in very close proximity to humans.

Urban Yellow Fever_2

When a female Aedes aegypti feeds on blood infected with yellow fever virus, her salivary glands and her ovaries become infected, and she passes this infection into her eggs through her ovaries (transovarial transmission). The infected eggs develop into infected adults, and the adult females are able to transmit yellow fever virus to humans as soon as they begin feeding on humans. This ability of Aedes mosquitoes to transmit virus transovarially and thus to rapidly multiply the numbers of infected adult mosquitoes is the reason why it is important to use insecticide treated-bednets with yellow fever patients. After several mosquito generations, transovarial transmission ends if yellow fever virus is not consumed naturally in a blood meal.

Pathophysiology

Bite from an infected mosquito leads to viral spread to lymph nodes where they multiply and from there enter the circulation Localises in the liver, spleen, bone marrow, and lymph glands persisting for days in these areas. Localisation and propagation of the virus in a particular organ constitutes the lesions of yellow fever Haemorrhage in the mucosa of the pylorus of the stomach, kidney and liver necrosis (mid zonal, with councilman bodies), perivascular infiltraion of the brain with mononuclear cells Degenerative changes in heart, spleen lymph nodes also occur Bleeding is the result of a hemorrhagic diathesis

Incubation period

Extrinsic incubation period- 12-14 days period when an infected vector is not infectious Incubation period-3to 6 days period when an infected individual is asymptomatic

Clinical findings 1

Fever, chills, headache and backache followed by nausea and vomiting, suffused conjunctivae, retro bulbar pain. On about the fourth day the period of intoxication starts with a slow pulse relative to a high fever (Fagets sign), and moderate jaundice

In severe cases marked proteinuria and haemorrhagic manifestations, black vomitus, epigastric pain The degree of jaundice and black vomitus correlated with severity of disease and hence fatality After 3 to 5 days of the disease, either the patient recovers or goes onto the next stage of fulminate disease.

Clinical Findings 2

In fulminant disease there is significant hepatic injury with jaundice occurring, hence the name "yellow fever." Renal failure is not uncommon. A hemorrhagic diathesis may occur causing of epistaxis, oozing at the gums, petechiae, ecchymosis, haematemesis: ("black vomit"), melena, haematuria, thrombocytopenia, and disseminated intravascular coagulation. Myocarditis, encephalopathy, and shock may also ensue. From 20% to 50% of patients with classic symptoms die, with deepening scleral icterus, hemorrhages, shock, encephalopathy, and renal failure. If one survives, a full recovery can be expected.

Immunity

Disease presentation can be subclinical, however, once an individual acquires the infection one acquires a life long immunity.

Diagnosis

Clinical Serology Culture Biopsy

Differential Diagnosis
The differential diagnosis of yellow fever includes: Leptospirosis, Relapsing fever, Malaria, Typhoid, Viral hepatitis (especially hepatitis E)

Treatment

Treatment for yellow fever is supportive in nature. Bed rest under insecticide treated nets Analgesics Fluid and electrolyte balance

Control

Vaccination Vector control

Surveillance

Control

The 17D yellow fever vaccination is the only strain available. It is a live, attenuated vaccine and has several contraindications including: children under 9 months of age, pregnancy, immunosuppression. International regulations require a booster every 10 years to enter or depart from endemic yellow fever regions.

Control
Vector control Elimination of breeding sites Insecticides Repellant creams ITN Surveillance Prompt detection and management of cases

References

Monath TP. Yellow Fever: A medically neglected disease. Report on a seminar. Reviews Infect Dis 1987;9(1):165 Cahill KM, O'Brien W. Tropical Medicine A Clinical Text. Mount Salus Press, Dublin ,1989, p104-105 World Health Organization, Yellow Fever Fact Sheet, WHO Fact Sheets 1999 August, #100 Guerrant RL, Walker DH, Weller PF. Tropical Infectious Diseases. Churchill Livingstone. Philadelphia 1999, p 1262