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With the increased interest and apparent prevalence of encephalitis in
different areas of the world esp India, Nepal and China and with our
knowledge that H5N1 can have this presentation I thought I'd copy some
excepts on enteroviral diseases from 'Tropical Infectious Diseases,
Principles, Pathogens, and Practice' 2nd edition 2006, Richard L.
Guerrant, David H. Walker and Peter F. Weller. This is from Chapter
60 Enterovirus Infections, Including Poliomyelitis by Mark A.
Pallansch and Hamid Jafari
Enteroviruses are among the most common of human viruses, possibly
infecting a billion or more persons annually worldwide. Most
infections are largely inapparent, but enteroviruses may cause a wide
spectrum of acute disease, including mild upper respiratory illness
(common cold), febrile rash (hand-foot-and-mouth disease and
herpangina), conjunctivitis, aseptic meningitis, pleurodynia,
myocarditis, encephalitis, acute flaccid paralysis (paralytic
poliomyelitis), and neonatal sepsis-like disease. Enterovirus
infections result in hundreds of thousands of hospitalizations per
year in the developed world, with aseptic meningitis accounting for
the vast majority of these cases. The disease burden in the
developing world of the tropics is poorly estimated, with the
exception of poliomyelitis. Enterovirus infections are more common in
most developing countries, so it is reasonable to assume that
significant morbidity can be attributed to these viruses globally.
Historically, the classification of enteroviruses into the subgroups
of polioviruses, coxsackieviruses A and B, and echoviruses was based
on the empirical observations of their association with some clinical
syndromes, susceptibility to infection or disease, tissue tropism,
nature of disease in suckling mnice, growth in certain specific cell
cultrues, and in some cases antigenic similarities.
The complete RNA genetic sequences for all the recognized
enteroviruses have been determined, which has allowed a more detailed
description and comparison among these viruses. From these new data
and to avoid the inconsistencies of the previous classification
scheme, the human enteroviruses have been reclassified into five
species: A-D and poliovirus.
Continued characterization of enterovirus clinical isolates has also
identified many new members of the genus, with the naming continuing
from enterovirus 73 sequentially. At this time, very little is known
about any distinctive clinical or epidemiologic features of these new
viurses, but it is clear that there are likely to be many more of
these described with the wider application of sequencing studies to
viruses form the developing world.
The patterns of virus shedding and routes of transmission for
enteroviruses are consistent with only a few exceptions. The virus is
isolated in the highest titer and for the longest time, often several
weeks, in stool specimens but can also be isolated from respiratory
secretions. Therefore, both fecal-oral transmission and spread by
contact with respiratory secretions (person-to-person, fomites, and
large-particle aerosol) are considered the most important modes of
transmission for these viruses. The relative importance of the
different modes probably varies with the virus and the environmental
setting. In addition, enteroviruses that cause a vesicular exanthem
can, presumably, be spread by direct or indirect contact with
vesicular fluid that contains infectious virus. Another exception to
the usual modes of enterovirus transmission are the agents of acute
hemorrhagic conjunctivitis: enterovirus 70 (EV70) and coxsackeivirus
A24 variant (CAV24). These two viruses are seldom isolated from
respiratory tract or stool specimens and are probably spread primarily
by direct or indirect contact with eye secretions.
Enteroviruses are efficiently amplified and transmitted among humans
without intermediaries such as arthropods or other animals.
In tropical regions, especially where sanitation is poor, the
efficiency of transmission is high. Consequently, not only is the
overall prevalence of enterovirus infections higher, but also the
average age of infection is younger. It is not uncommon in these
areas to detect two or three simultaneous infections of different
enterovirus serotypes, often causing no disease.
Enterovirus infections can result in a wide variety of disease
syndromes. The most common result of enteroviurs infection is either
no symptoms or mild upper respiratory tract symptoms. Other mild
enteroviral illness, consisting of fever, headache, malaise, and
occasionally mild gastrointestinal symptoms may also occur. The most
commonly recognized serious manifestation of enterovirus infection is
central nervous syustem (CNS) disease, usually aseptic meningitis, but
sometimes encephalitis or paralysis.
Typically, the primary site of infection is the epithelial cells of
the respiratory or gastrointestinal tract and in the lymphoid
follicles of the small intestine, followed by a viremia that may lead
to a secondary site of tissue infection. Secondary infection of the
CNS results in aseptic meningitis or, rarely, encephalitis or
paralysis.
The key to laboratory confimation of enterovirus infection is the
collection of appropriate clinical specimens for direct detection by
molecular methods, virus isolation, or serologic studies. enterovirus
infection cannot be inferred from the clinical syndrome alone, since
many other infectious agents can cause similar illness.
A general diagnostic caveat, however, is shared among enteroviruses
and other ubiquitous pathogens. Since enterovirus infections are
quite common, especially in childhood, and since most infections are
noninvasive and prolonged, the detected enterovirus infection need not
be the cause of the illness under investigation. It is an issue of
probabilities. If the clinical syndrome is already known to be
associated with the detected agent, then infection is taken as
reasonable evidence of causation. If the presence of the agent is
found in diseased tissue or a relevant body fluid (such as CSF), that
constitutes concrete evidence of invasion, hence causation.
The use of the polymerase chain reaction (PCR) to detect enterovirus
genomes in cell culture, clinical specimens, and tissues promises to
significantly improve the detection of enteroviruses. This technique
is more rapid than isolation and has the potential for providing
diagnostic answers in a timely way for clinical patient management.
General preventive measures include enteric precautions and good
personal hygiene. Enteroviruses can be a cause of nosocomial
infection. Hospital staff can inadvertently carry the virus between
patients or become infected themselves and spread the virus
different areas of the world esp India, Nepal and China and with our
knowledge that H5N1 can have this presentation I thought I'd copy some
excepts on enteroviral diseases from 'Tropical Infectious Diseases,
Principles, Pathogens, and Practice' 2nd edition 2006, Richard L.
Guerrant, David H. Walker and Peter F. Weller. This is from Chapter
60 Enterovirus Infections, Including Poliomyelitis by Mark A.
Pallansch and Hamid Jafari
Enteroviruses are among the most common of human viruses, possibly
infecting a billion or more persons annually worldwide. Most
infections are largely inapparent, but enteroviruses may cause a wide
spectrum of acute disease, including mild upper respiratory illness
(common cold), febrile rash (hand-foot-and-mouth disease and
herpangina), conjunctivitis, aseptic meningitis, pleurodynia,
myocarditis, encephalitis, acute flaccid paralysis (paralytic
poliomyelitis), and neonatal sepsis-like disease. Enterovirus
infections result in hundreds of thousands of hospitalizations per
year in the developed world, with aseptic meningitis accounting for
the vast majority of these cases. The disease burden in the
developing world of the tropics is poorly estimated, with the
exception of poliomyelitis. Enterovirus infections are more common in
most developing countries, so it is reasonable to assume that
significant morbidity can be attributed to these viruses globally.
Historically, the classification of enteroviruses into the subgroups
of polioviruses, coxsackieviruses A and B, and echoviruses was based
on the empirical observations of their association with some clinical
syndromes, susceptibility to infection or disease, tissue tropism,
nature of disease in suckling mnice, growth in certain specific cell
cultrues, and in some cases antigenic similarities.
The complete RNA genetic sequences for all the recognized
enteroviruses have been determined, which has allowed a more detailed
description and comparison among these viruses. From these new data
and to avoid the inconsistencies of the previous classification
scheme, the human enteroviruses have been reclassified into five
species: A-D and poliovirus.
Continued characterization of enterovirus clinical isolates has also
identified many new members of the genus, with the naming continuing
from enterovirus 73 sequentially. At this time, very little is known
about any distinctive clinical or epidemiologic features of these new
viurses, but it is clear that there are likely to be many more of
these described with the wider application of sequencing studies to
viruses form the developing world.
The patterns of virus shedding and routes of transmission for
enteroviruses are consistent with only a few exceptions. The virus is
isolated in the highest titer and for the longest time, often several
weeks, in stool specimens but can also be isolated from respiratory
secretions. Therefore, both fecal-oral transmission and spread by
contact with respiratory secretions (person-to-person, fomites, and
large-particle aerosol) are considered the most important modes of
transmission for these viruses. The relative importance of the
different modes probably varies with the virus and the environmental
setting. In addition, enteroviruses that cause a vesicular exanthem
can, presumably, be spread by direct or indirect contact with
vesicular fluid that contains infectious virus. Another exception to
the usual modes of enterovirus transmission are the agents of acute
hemorrhagic conjunctivitis: enterovirus 70 (EV70) and coxsackeivirus
A24 variant (CAV24). These two viruses are seldom isolated from
respiratory tract or stool specimens and are probably spread primarily
by direct or indirect contact with eye secretions.
Enteroviruses are efficiently amplified and transmitted among humans
without intermediaries such as arthropods or other animals.
In tropical regions, especially where sanitation is poor, the
efficiency of transmission is high. Consequently, not only is the
overall prevalence of enterovirus infections higher, but also the
average age of infection is younger. It is not uncommon in these
areas to detect two or three simultaneous infections of different
enterovirus serotypes, often causing no disease.
Enterovirus infections can result in a wide variety of disease
syndromes. The most common result of enteroviurs infection is either
no symptoms or mild upper respiratory tract symptoms. Other mild
enteroviral illness, consisting of fever, headache, malaise, and
occasionally mild gastrointestinal symptoms may also occur. The most
commonly recognized serious manifestation of enterovirus infection is
central nervous syustem (CNS) disease, usually aseptic meningitis, but
sometimes encephalitis or paralysis.
Typically, the primary site of infection is the epithelial cells of
the respiratory or gastrointestinal tract and in the lymphoid
follicles of the small intestine, followed by a viremia that may lead
to a secondary site of tissue infection. Secondary infection of the
CNS results in aseptic meningitis or, rarely, encephalitis or
paralysis.
The key to laboratory confimation of enterovirus infection is the
collection of appropriate clinical specimens for direct detection by
molecular methods, virus isolation, or serologic studies. enterovirus
infection cannot be inferred from the clinical syndrome alone, since
many other infectious agents can cause similar illness.
A general diagnostic caveat, however, is shared among enteroviruses
and other ubiquitous pathogens. Since enterovirus infections are
quite common, especially in childhood, and since most infections are
noninvasive and prolonged, the detected enterovirus infection need not
be the cause of the illness under investigation. It is an issue of
probabilities. If the clinical syndrome is already known to be
associated with the detected agent, then infection is taken as
reasonable evidence of causation. If the presence of the agent is
found in diseased tissue or a relevant body fluid (such as CSF), that
constitutes concrete evidence of invasion, hence causation.
The use of the polymerase chain reaction (PCR) to detect enterovirus
genomes in cell culture, clinical specimens, and tissues promises to
significantly improve the detection of enteroviruses. This technique
is more rapid than isolation and has the potential for providing
diagnostic answers in a timely way for clinical patient management.
General preventive measures include enteric precautions and good
personal hygiene. Enteroviruses can be a cause of nosocomial
infection. Hospital staff can inadvertently carry the virus between
patients or become infected themselves and spread the virus
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