Biomedical Engineering Reference
In-Depth Information
were infected but morbidity and mortality were low and
concentrated in very young and very old patients.
Nonhuman primates housed outdoors were exposed and the
infection rate was between 30% and 50% in one colony.
Clinical disease was not noted except in rare instances.
Infections in nonhuman primates were not considered to be
reservoirs for spread to the human population (
Ratterree
et al., 2003
).
Primary infection with herpes B in macaques may result
in gingivostomatitis with characteristic mucosal lesions,
but infection occurs frequently without such signs. Thus,
the absence of oral lesions is not a justifiable reason to relax
biosafety standards when handling individual macaques,
although the presence of such lesions mandates the most
extreme adherence to handling guidelines. The virus
remains latent in the host and may reactivate spontaneously
or in times of stress, resulting in shedding of the virus in
saliva and/or genital secretions. It has been speculated that
herpes B may be sexually transmitted among macaques
because less than 25% of monkeys under 3 years of age are
antibody positive, whereas 72
e
100% of adult rhesus
monkeys are reported to be antibody positive (
Palmer,
1987
).
Herpes B infection in humans is commonly believed to
be transmitted by exposure to contaminated monkey saliva
through bites and scratches; however, such exposure has
not been consistently documented. Nearly all human cases
of herpes B virus infection have occurred in persons
exposed to monkeys or monkey tissues. One instance of
person-to-person transmission has been reported (
Centers
for Disease Control, 1987a
). The wife of an infected animal
handler became infected after applying ointment to the
perpetic lesions on her husband and then to a small area of
dermatitis on her own hand (
Holmes et al., 1990
).
The human disease is characterized by a variety of
symptoms which usually occur within 5 days to 1 month after
exposure. These include, but are not limited to, any or all of
the following: vesicular skin lesions at or near the exposure
site; aching; chills and other flu-like symptoms; persistent
fever; nausea; lethargy; chest pain and difficult breathing;
and neurological symptoms such as itching or tingling at or
near the exposure site, numbness, dizziness, double vision,
difficulty swallowing, and confusion. If untreated, these early
signs and symptoms progress rapidly to coma, respiratory
failure, and death (
Elmore and Eberle, 2008
).
Prevention of herpes B infection in people is of utmost
importance. The ultimate protection may be achieved only
by using herpes B-free macaques obtained from breeders
and sources known to be free of this zoonotic pathogen. To
ensure their negative status, these monkeys must be
obtained directly from the supplier, transported, and at all
times housed and maintained with no contact with other
macaques with unknown or questionable herpes B status.
Supplies of monkeys free of herpes B are limited, and
purchase prices are commensurate.
Currently, most macaques used in biomedical and
behavioral research are known or suspected to harbor
herpes B. Guidelines for preventing this infection in
monkey handlers were published in 1987 (
Centers for
Disease Control, 1987b
) and updated in 2003 (
Murphy and
Roberts, 2003
). Most institutions that use macaques have
developed their own SOPs for handling these species. The
Herpesvirus Infections
The herpesviruses are among the most prevalent and
important of the endogenous primate viruses because
a virus that usually produces asymptomatic carriers of
latent infection in the native or reservoir host species
may regularly cause severe and often fatal disease in
another primate species. This is true to such an extent
that the latter have sometimes been called “fatal hosts.”
Infected individuals in the latent phase may shed the
virus at any time, particularly when undergoing stress;
thus, the potential for spreading infection to workers or
other animals is always present. An excellent review of
simian herpes viruses and the risk to humans can be
found here (
Estep et al., 2010
).
Herpesvirus Simiae
Herpes B virus, also known as Herpes simiae, B virus,
simian B or monkey B virus, cercopithecine herpesvirus 1,
and, more recently, macacine herpesvirus 1, was first
identified in a polio research scientist who died of a rapidly
progressive encephalitis in 1932 following a macaque bite
(
Sabin and Wright, 1934
). Since then, this virus has been
found to be enzootic among Old World monkeys of the
genus Macaca, particularly among rhesus monkeys
(M. mulatta), with prevalence of infection ranging up to
80% or higher. Thousands of rhesus monkeys have been
distributed throughout the world in research facilities, zoos,
and, not infrequently, in private homes, and people who
work with or care for these animals are often exposed to the
herpes B virus through bites, scratches, contaminated
needlesticks, and other routes. Although the virus usually
causes a minimal or undetectable disease in its natural
simian hosts, it may cause a rare but rapidly progressive
ascending neuropathy and encephalomyelitis associated
with high mortality in humans. There have been at least 31
published cases of human herpes B (
Palmer, 1987
); of the
24 cases reported in detail, 16 (67%) were fatal. In the 14
years preceding 1987 no human cases of herpes B infection
were reported. Then there was a cluster of four human cases
in Florida (
Centers for Disease Control, 1987a
), followed
by three additional cases in Michigan in 1989 (
Centers for
Disease Control, 1989
) and one case in Texas in 1991
(
Dalgard, 1991
).
