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Yellow fever
(YF) is an infectious, non-contagious disease
caused by an RNA virus of the family
Flaviviridae
(that cause
dengue
and other hemorrhagic fevers), which is
transmitted to man by the bite of hematophagous mosquitoes.
First
described in the Caribbean, yellow fever is the oldest known viral
hemorrhagic fever.
It
is a re-emerging infectious disease that currently is at risk of
urbanization due to the advance of the Aedes aegypti vector.
Geographic distribution:
The disease affects about 200,000 individuals annually, mainly in
tropical Africa and South America, including both jungle and urban
settings.
It is a
significant hazard to unvaccinated travelers to these endemic areas.
Recent
increases in the density and distribution of the urban mosquito
vector, Aedes aegypti, as well as the rise in air travel increase the
risk of introduction and spread of yellow fever to North and Central
America, the Caribbean, the Middle East, Asia, Australia, and Oceania.
Mode of Infection:
The usual
reservoir is tree dwelling monkeys, virus being passed among them in
the forest canopy by mosqitoes. These monkeys are a good reservoir
because the virus neither kills them nor makes them ill . Humans
acquire jungle yellow fever by entering the forest and being bitten
and inoculated by Aedes mosquitoes. Felling trees increases the risk
because mosquitoes are brought down with the tree. On returning to the
village or city, the victim becomes the reservoir for epidemic yellow
fever in the urban setting , where Aedes aegypti is the vector.
Hence, virus
transmission occurs between humans, mosquitoes, and monkeys. The
mosquito, the true reservoir of YF, is infected throughout its life,
and can transmit the virus transovarially through infected eggs. Man
and monkeys, on the other hand, play the role of temporary amplifiers
of the virus available for mosquito infection.
Clinical presentation:
This is an
acute illness manifested by abrupt onset of chills and fever, conjunctival injection, leukopenia, a brief period of
remission, and then reappearance of fever and jaundice, punctate
hemorrhages of the soft palate, epistaxis, and gingival and
gastrointestinal bleeding (black vomit).
Approximately
50% of the patients develop relative bradycardia in relation to the
degree of fever.
Death occurs
in the second week after onset,and is preceded by coma.
Pathogical features:
The yellow fever virus
(YFV) is viscerotropic
causing the most damage in the heart,
kidneys, central nervous system, gastrointestinal tract and liver. The
gross features in fatal cases are not specific
Heart:
The heart
when involved is flabby and pale with scattered pericardial and
petechial hemorrhages. Microscopically there is degeneration of
myocardial fibers and accumulation of fat.
Kidneys:
May show
edema ; Microscopically the features are those seen in cases of
tubular necrosis. Hemoglobin casts may be seen. The most characterisitic pathologic changes are seen in the liver. The
appearance of the lesions is typical between the seventh and ninth day
of illness.
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CLICK ON THE
IMAGE: Liver biopsy in a patient suffering from Yellow Fever
: The biopsy shows mid-zonal necrosis and numerous acidophilic
Councilman bodies. |
Liver:
The liver is
grossly normal in size, pale and yellow because of fatty
metamorphosis.
The histopathological pattern is characterized by mid-zonal steatosis, lytic
necrosis and hepatocyte apoptosis associated with a moderate
mononuclear inflammatory infiltrate.
The inflammatory component mainly
consisted of CD4+ T lymphocytes, followed by CD8+ T lymphocytes, which
showed a preferential portal and midzone distribution.
The midzonal
necrosis in severe cases may extend to become panlobular. [
A new
hypothesis has been proposed that the mid-zonal necrosis is consequence
of action of combined factors mainly the direct cytopathic effect of
YFV associated with a potent immune response in which CD4+ and CD8+
lymphocytes and the cytokines, especially TGF-beta, but also TNF-alpha
and IFN-gamma play an important role.]
Intracellular
condensations of cytoplasm that appear as round to oval,
well-demarcated, eosinophilic inclusions are termed Councilman bodies.
These are found in the cytoplasm of Kupffer cells. These inclusions
are not composed of virus particles and are nonspecific for the
disease. They are periodic acid Schiff (PAS) positive.
Rarely,
eosinophilic intranuclear inclusions (Torres bodies) are present.
Fatty change
may be prominent.
The surviving
liver shows ballooned hepatocytes and regenerative hyperplasia ;
multinucleate hepatocytes are common ; Cholestasis is
unusual.
Biopsies taken
from survivors upto 2 months after the acute illness show a
non-specific intra-acinar hepatitis.
A distinctive
feature of the lesion is the fact that despite massive necrosis, the
reticulin framework of the hepatic lobule is preserved.
This
characteristics pattern of liver injury in yellow fever is also
observed in conditions of low-flow hypoxia and other infections such
as viral hepatitis, dengue, Weil's disease and Rift Valley fever.
Brain:
Edema and
petechial hemorrhage.
Spleen and Lymph nodes:
Follicular hyperplaasia.
Skin ; Gingiva and
Gastrointestinal Tract :
Hemorrhage.
Diagnosis:
The
diagnosis is usually confirmed by the serological demonstration of
specific IgM by an ELISA method, or by virus isolation from blood.
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