Biomedical Engineering Reference
In-Depth Information
The initial outbreaks occurred in remote areas, and
human infection was primarily the result of contact with
infected blood from injections with reused syringes and
needles at rural hospitals. Some person-to-person trans-
mission resulted from intimate contact with infected
persons. Recent evidence indicates that bats may be
reservoirs for Ebola and other filoviruses (
Towner et al.,
2007
).
The Ebola virus produces high mortality (30
e
90%) in
humans and rhesus monkeys by causing fulminating
hemorrhagic fever and shock (
Feldmann and Geisbert,
2011
). It has several pathological features in common with
other severe viral hemorrhagic fevers such as Lassa fever,
and the rhesus monkey model has been used to study the
pathophysiology of its shock and hemorrhage (
Fisher-Hoch
et al., 1985
).
In 1989, infections caused by a filovirus closely related
to the Ebola virus were detected in cynomolgus (Macaca
fascicularis) monkeys imported from the Philippines and
held in quarantine facilities in Virginia and Pennsylvania.
Transmission among monkeys in the quarantine facilities
occurred; many of the animals died. Four of five animal
handlers who had a high level of daily exposure to infected
macaques at one facility were found to have serological
evidence of recent infection with a strain of filovirus iso-
lated from the infected monkeys, though none had unex-
plained febrile illness (
Centers for Disease Control, 1990a
).
These episodes documented the first known instances of
Ebola-related filovirus infection in imported nonhuman
primates in the USA. There have been three different but
antigenically related filoviruses implicated in the episodes
in the USA.
The incubation period of naturally occurring hemor-
rhagic diseases in humans and experimental infection in
monkeys is typically 5
e
9 days (range 2
e
15 days). In
humans the disease is rapid in onset and is usually
characterized by severe fatigue, headache, high fever,
muscle and joint pain, and sore throat. Some patients also
have conjunctivitis, jaundice, diarrhea, abdominal pain,
and a skin rash. In monkeys, the illness may consist of
fever, depression, coma, and death. On postmortem
examination, monkeys may have hemorrhages in the liver
and other organs and may have blood and fluid in all body
cavities. The gross pathology is very similar to that
observed with simian hemorrhagic fever (
Feldmann and
Geisbert, 2011
).
Although the serological evidence suggests that this
filovirus can infect humans, it has much lower pathoge-
nicity than do its African counterparts. The high level of
transmission to animal handlers in this single facility and
the possibility of importation of other virulent viruses
underscore the importance of strict adherence of quarantine
measures for handling monkeys (
Centers for Disease
Control, 1990a
).
Prevention
Biosafety Level 4 practices, containment
equipment, and facilities are recommended for all activities
using materials of human or animal origin that may be
infected with the filoviruses. These include blood, urine,
respiratory and throat secretions, semen, and tissues.
Respiratory exposure to infectious aerosols, mucous
membrane exposure to infectious droplets, and accidental
parenteral inoculation are the primary hazards to laboratory
or animal care personnel (
Centers for Disease Control/
National Institutes of Health, 2009
).
Simian Hemorrhagic Fever
Although no cases of human disease from the filovirus that
causes simian hemorrhagic fever (SHF) have been repor-
ted, persons who have had contact with monkeys infected
with the Ebola-Reston virus have demonstrated asymp-
tomatic serum conversion (
Many et al., 1991
). The
potential exists for human infection with any virus that
infects nonhuman primates.
This extremely virulent disease causes death by dissem-
inated intravascular coagulation within as few as 3 days from
onset of the clinical symptoms. These symptoms include
epistaxis, ecchymosis, ataxia, anorexia, and lethargy. Clin-
ical laboratory findings include patterns consistent with
disseminated intravascular coagulation. Abnormal coagula-
tion factors with fibrin degradation products are the earliest
indicators of disease, followed by elevation of the liver
enzymes lactate dehydrogenase,
g
-glutamyltransferase, and
aspartate aminotransferase and elevated blood urea nitrogen
and creatinine from kidney involvement. Pathognomonic
lesions found at necropsy include duodenal necrosis and
splenic infarction (
Renquist, 1990
). Confirmation tests
include serology, a rhesus peritoneal macrophage assay,
immunochemistry, and antigen capture procedures and most
recently an ELISA test (
Godney, 2002
).
Outbreaks of SHF are not frequent, but eight have been
reported with 100% mortality of exposed rhesus and cyn-
omolgus (M. fascicularis) macaques. Patas monkeys
(Erythrocebus patas), baboons (Papio spp.), and African
green monkeys can be asymptomatic carriers of the virus.
Failure to exercise good laboratory practices and to observe
strict separation of species was responsible for an outbreak in
1972 inwhich rhesusmonkeys were infected because a bottle
of ketamine was contaminated with patas monkey blood
(10
12
dilution). The disease also spreads by contact with
infected animals in a room. During one of several outbreaks
in 1989, 400 macaques died or were killed to prevent further
spread throughout the facility (
Renquist, 1990
).
Prevention
Any macaque having epistaxis with ecchy-
moses and unexplained death should be considered to have
SHF, and Animal Biosafety Level 2 procedures for
protection of other animals and personnel should be
