ADENOVIRUSES
This group of DNA viruses were so called because they were isolated from
the adenoids (and tonsils) in 1953. They induce latent infections in
lymphoid tissues of man, especially tonsils and adenoids, pharyngitis,
conjunctivitis and serve as helpers for the replication of other
viruses, adeno-associated viruses (AAVs).The infection is subclinical or
mild in normal individuals but it may be severe and fatal in
immunocompromized subjects. Severe and fatal hepatitis with severe
respiratory infection may develop in these individuals. Intranuclear
viral antigen n has been detected in cases of hepatitis. They are
presently classified in 41 serologic types.
COXSACKIE VIRUSES
They were isolated in Coxsackie, New York, in 1948 during studies
poliomyelitis. They rarely produce hepatitis. They commonly induce
epidemic myalgia, myocarditis, pericarditis, aseptic meningitis
pleurodynia, herpangina. Hepatitis is frequently associated with
myocarditis and consists of necroinflammatory changes involving lobules
and porta tracts, to be distinguished from congestive changes due to
heart failure. They are divided in tow groups according to lesions
produced in the suckling mouse. Group A (23 types) produces diffuse
myocytis with inflammation and necrosis of voluntary muscles; group B (6
types) produces brain degeneration, pancreatitis, panniculitis and focal
myocytis of skeletal muscles and myocardium. The virus is similar to
poliovirus. Isolation of the viral agent in each infection is necessary
for diagnosis.
ECHOVIRUSES
Is another group of viruses isolated during studies for poliomyelitis.
It is an enterovirus and produces enteritis, acute respiratory
infection, rash, fever,
encephalitis , aseptic meningitis, paralysis. The liver is rarely
involved but it may be severely affected in severe infections contracted
in the neonatal period.
RUBELLA VIRUS
It was isolated in 1962.It produces a syndrome similar to measles bu
much milder. In 1941 an ophthalmologist in Australia discovered that I
the infection contracted in the first trimester of pregnancy may produce
congenital defects. Circa 20% of children born from infected mothers
(during the first trimester of pregnancy) are affected by the rubella
syndrome which consists of cataracts, deafness, cardiac malformations,
mental retardation, microcephaly. The liver may be involved with
variable degree of acute hepatitis, biliary obstruction and destruction.
The virus can be recovered from the liver.
YELLOW FEVER
A cuban physician, Carlos Finlay associated this infection with
mosquitoes and Dr. Walter Reed of the U.S. army confirmed the theory by
exposing
volunteers to the mosquitoes during the Spanish-american war of 1901 and
demonstrated the viral ultrafiltrability of the agent causing this
disease. The mode of
controlling the infection was found. Until that time, the devastating
effects of this infection in the Caribbean region had bee responsible,
for many deaths and for the France's failure of digging the Panama
canal. The virus is a RNA particle that replicates in the cytoplasm of
infected cells. In the forests (sylvan cycle), the monkeys are the
reservoir of the virus. In urban areas (urban cycle) man are infected
through the aedes aegypti mosquito. The disease may be asymptomatic,
mild and severe fatal. It affects
liver together with heart, kidneys and spleen causing jaundice
hemorrhages and marked albuminuria.Mortality is 50% in severe cases.
Diagnosis is made by virus isolation
and serology. There is an effective vaccine, 17D which confers a
long-standing
immunity (35 years). It is safe for adults but should not be used in
children under 6 months
because it may cause encephalitis.
ARENAVIRUSES
This group comprises Lassa fever (Nigeria 1969), Tacaribe,
Machupo
(Bolivia 1962), Junin (Argentina 1950), Tamiami, viruses.
They are
transmitted through excrements of rodents and produce illnesses of
variable severity with a fatality rate of over 20%.The liver is involved
together with conjunctiva, pharynx, lymph nodes, skin. There is marked
hepatocyte damage in the liver consisting in eosinophilic necrosis of
individual cells but jaundice is rare.
MARBURG VIRUS
It is carried by the african green monkey which is used for biomedical
experiments. The first infection occurred in 1967 among laboratory
personnel in Marburg, Germany and in Yugoslavia with 7 deaths. It is
100% fatal for the monkeys. Fever, rash, diarrhea, hemorrhages are the
clinical manifestations in man. The liver suffers a
necroinflammatory picture suggestive of a viral disease. No other
infections have been reported lately.
EBOLA VIRUS
This virus produces an illness and liver lesions similar to Marburg
virus: hemorrhagic fever, highly fatal. It exploded in East Africa: 70
cases with 33 deaths in Nzara, Sudan; 76 cases with 41 deaths in Maridi
hospital; 237 cases in Zaire with 211
deaths. The virus, like Marburg virus is an RNA particle that has been
named Ebola after a small river in Zaire and belongs to the family of
Filoviridae consisting of filamentous and branched forms. It replicates
in the cytoplasm of infected cells. Maximum security viral laboratories
are needed for the isolation of these deadly viruses. No treatment
exists.
RIFT VALLEY FEVER
This infection which affected sheep in the subsaharan region was
introduced to Egypt in 1977 where it caused an epidemic among humans
with , at least 400 cases with considerable high mortality. No other
cases occurred after that outbreak but the virus may reappear. The virus
is a single strand RNA particle which replicates in the cytoplasm of
infected cells. Clinically it produces hemorrhages encephalitis and
macular degeneration of the eyes. The liver shows focal or diffuse
hepatic necrosis. The pathological damage is more concentrated and more
severe in the sheep. An effective vaccine is available for man and
animals.
CRIMEA CONGO HEMORRHAGIC FEVER
It is an infection caused by a virus affecting man, animals and ticks
in the Middle East up to southern Russia. The virus is similar to Rift
Valley virus, single stranded, RNA particle. Clinical manifestations are
similar to the other hemorrhagic viroses described above: Extensive
perioral and perinasal bleeding followed by thrombocytopenia, leukopenia
and liver involvement. There is high mortality (20-70%) especially when
the infection is acquired from fluids of human patients.
Bibliography
Oxford Textbook of Clinical Hepatology, Mc Intire at al., Editors, pp
630-646.
Pathology of the Liver,R.N.M.MacSween et al., Editors, pp 224-233.
Microbiology, Davis et al., Editors, 2nd ed., pp 1007-1409
Histopathology of the Liver, G.Klatskin & H.O.Conn, pp 317-321
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