J Forensic Sci, January 2016, Vol. 61, No.

S1
doi: 10.1111/1556-4029.12947
PAPER Available online at: onlinelibrary.wiley.com

ANTHROPOLOGY

Lindsey G. Roberts,1 M.A.; Gretchen R. Dabbs,1 Ph.D.; and Jessica R. Spencer,1 M.A.

An Update on the Hazards and Risks of

Forensic Anthropology, Part I: Human
Remains

ABSTRACT: This work reviews the hazards and risks of practicing forensic anthropology in North America, with a focus on pathogens
encountered through contact with unpreserved human remains. Since the publication of Galloway and Snodgrass seminal paper concerning the
hazards of forensic anthropology, research has provided new information about known pathogen hazards, and regulating authorities have
updated recommendations for the recognition and treatment of several infections. Additionally, forensic anthropology has gained popularity,
exposing an increased number of students and practitioners to these hazards. Current data suggest many occupational exposures to blood or
body fluids go unreported, especially among students, highlighting the need for this discussion. For each pathogen and associated disease, this
work addresses important history, reviews routes of exposure, provides an overview of symptoms and treatments, lists decontamination
procedures, and presents data on postmortem viability. Personal protection and laboratory guidelines should be established and enforced in
conjunction with the consideration of these data.

KEYWORDS: forensic science, forensic anthropology, hazard, risk, bloodborne pathogen, occupational exposure

This paper, the first in a two-part series addressing the hazards
of working as a forensic anthropologist, builds upon the seminal
work of Galloway and Snodgrass (1) in reporting on the biologi-
cal hazards associated with contacting human remains during
forensic anthropological analysis. The intent is not to replicate
their work, but instead to update where necessary and supple-
ment where possible. In the fifteen years since their publication,
much has been learned about the hazards they reviewed. The
focus of Part I is on the most common pathogens encountered
when working with human remains in North America; however,
all of the diseases discussed herein are also found in other areas
of the world. One area of rapid increase in forensic anthropolog-
ical research is the number of research facilities studying the
decomposition of human remains, which has increased from one
in 1998 to six in 2014. Along with this, the number of body
donations to outdoor decomposition research facilities has also
increased, thereby increasing the number of faculty, students,
and staff potentially exposed to these hazards.
Although data regarding the incidence and reporting of occu-
pational exposures to blood or body fluids are not available for
forensic anthropology faculty and students, data from health care
workers, the closest comparable field for which research has
been conducted, suggest many exposures are unreported, espe-
cially among students (24). A study at the John Hopkins
University revealed only 12.5% of surveyed medical students
followed appropriate postexposure protocol after exposure to
blood or body fluids (2). In a study at a major teaching hospital
in Illinois, students and healthcare workers did not report 33.0%
of sharps exposures and 82.9% of mucocutaneous exposures, the
most common reason being the exposure was believed to be
insignificant (3). Among medical students at another teaching
hospital, 96.4% were dissatisfied with previous training received
concerning occupational exposure prevention, 48% did not con-
sistently use personal protective equipment, and only 1.4% of
these students officially reported workplace injuries (4). This
paper also serves to bring attention to these issues, highlight the
possible need for more communication between students and
faculty regarding occupational exposures in a teaching setting,
and encourage reporting of all occupational injury.
A hazard refers to the danger of injury from a specific source,
like a scalpel blade or fall in the field (5). A risk refers to the
chance of contracting an infection from a hazard (5). Exposure
to pathogens can occur from splashes of contagious fluids to
mucous membranes or areas of compromised skin, inhalation of
infectious airborne particles, or direct inoculation from sharp
objects (1,5,6). Each pathogen or disease review will include his-
torical and general information about the hazard, routes of expo-
sure, risk of acquiring infection, symptoms of infection,
treatment, pathogen duration of viability postmortem where data
are available, and decontamination measures.

1 Viral Hepatitis
Department of Anthropology, Southern Illinois University, 1000 Faner
Drive (MC 4502), Carbondale, IL 62901. Hepatitis, inflammation of the liver, can be caused by a group

Presented at the 21st Annual Meeting of the Midwest Bioarchaeology and
Forensic Anthropology Association, October 1718, 2014, in Allendale, MI. of five different viruses that target the liver tissue: hepatitis A
Received 1 Oct. 2014; and in revised form 29 Jan. 2015; accepted 3 Feb.
(HAV), B (HBV), C (HCV), D (HDV), and E (HEV) (7). With
2015. over 500 million infected people, chronic hepatitis (caused by

2015 American Academy of Forensic Sciences S5

S6 JOURNAL OF FORENSIC SCIENCES
HBV or HCV) is a global issue and one of the top ten killers
among infectious diseases (8). Over four million Americans are
infected with one or both of these viruses, and many are una-
ware of their infection (7). Additionally, chronic hepatitis is the
leading cause of liver cancer and liver transplants, as well as a
common reason for renal transplants in the United States (U.S.)
(7). HBV, HCV, and, to a lesser extent, HAV are the most con-
cerning to professions that handle human remains. Both HBV
and HCV have been isolated from blood and tissue samples col-
lected from human remains after death, making risk of infection
for forensic anthropologists working with soft tissue a possibility
(912).
HBV is primarily a bloodborne pathogen but can also be
found in smaller concentrations in other body fluids (vaginal
secretions, semen, and fluid from wounds) (13). Transmission
occurs through the introduction of infected blood or body fluids
percutaneously or via mucosal contact (14,15). Viable virus can
survive outside the body on surfaces for at least 7 days (1417),
and any blood, including dried blood, should be considered
infectious (14). HBV DNA was detected in the blood of infected
individuals sampled an average of 4 days postmortem (11), and
the virus was identified in human tissue waste after storage (18).
Contaminated nonporous surfaces should be cleaned with 1:10
dilution of bleach:water (14).
HBV can have a long incubation period lasting from 6 weeks
to 6 months (13). Individuals who contract HBV may have an
acute or chronic reaction that can lead to cirrhosis and cancer of
the liver, and ultimately death. In 2011, the number of newly
reported HBV cases in the U.S. was 2890 individuals, but the
CDC estimated this to be closer to 18,800 individuals, with an
overall estimate of 800,000 to 1.4 million people living with
chronic cases in 2010 in the U.S. (19).
In the U.S., HCV is the most common chronic bloodborne
infection (20). HCV is usually transmitted through repeated or
large punctures. Historically, individuals contracted the virus
through blood transfusions, but contemporarily, it is most com-
monly transmitted through injection drug use (20). Less com-
monly, HCV can be transmitted through occupational skin
pricks and sexual activity. After an occupational sharps injury
with HCV-positive blood, the risk of acquiring infection is
between 0% and 10% (21). Sixty to seventy percent of newly
infected individuals show no symptoms and do not become ill
(20). HCV can be detected 13 weeks after infection; however,
by 6 months, the virus is detectable in 97% of infected individu-
als (21). Though the majority of cases are initially asymptomatic,
infection becomes chronic in 7080% of individuals with at least
6070% experiencing active liver disease (21). HCV can be
fatal, and there is no vaccine for this virus. However, although
costly, there is an effective treatment. In clinical trials on indi-
viduals with chronic HCV, combination antiviral therapy includ-
ing Sofosbuvir and Simeprevir for 1224 weeks resulted in
undetectable HCV RNA in the blood of 8095% of participants
(21). In 2011, there were 1229 newly reported cases of HCV,
although it is estimated this number is closer to 16,500 (19).
Between 2.7 and 3.9 million people in the U.S. were living with
chronic HCV in 2011 (19).
HCV has been found to persist on hard, inanimate surfaces
from 16 h to 4 days (22), and for up to 6 weeks (23), and in liq-
uids for 5 months (24). HCV RNA was identified from blood
samples from one to five days postmortem (11), and after
14 days in whole blood stored at room temperature (25). Spills
of blood can be disinfected using 1:10 dilution of bleach, with
10-min saturation period recommended for large spills (23,26).
The CDC suggests the best way to be protected is to avoid
activities where there is a risk of contracting HCV.
HAV spreads from fecal to oral contact (27). The virus incu-
bates in the liver for 15 to 50 days before a newly infected indi-
vidual becomes ill. High concentrations of the virus are shed in
feces from two weeks before to one week after the onset of
symptoms, and HAV can be transmitted during this time (27).
Viable virus can survive outside the body for months and can be
decontaminated by a 1:10 solution of bleach:water (28). Illness
from HAV can be mild, lasting only a few weeks, to more sev-
ere cases lasting several months. The CDC reported 1398 new
cases of the virus in 2011, and 95 individuals died from HAV in
2010 (19). In situations where forensic anthropologists may han-
dle remains with potential fecal contamination, proper personal
protective equipment (PPE) should be worn accompanied by
proper hand washing.
HDV and HEV pose low risk to forensic anthropologists,
especially if practicing only in the U.S. where these viruses are
uncommon (29,30). HDV only occurs in individuals already
infected with HBV (29). Like HAV, HEV is also transmitted
though fecal contamination and only occurs in acute cases. Both
can be very serious and lead to severe liver disease (29,30).
Anyone potentially exposed to blood or body fluids should
be vaccinated with the HAV and HBV vaccines or the combi-
nation HAV/HBV vaccine, as vaccination is the most effective
method of preventing hepatitis (31). For individuals older than
18 years, the combination vaccine consists of three doses,
given at 0, 1, and 6 months (31). Separate vaccines for hepati-
tis A and B are also available, and the efficacy of these is sim-
ilar to the combination vaccine (80100% overall for at least
15 years) (32,33).
Herpes Simplex Viruses
Herpes simplex viruses are large DNA viruses of which there
are two species: herpes simplex virus-1 (HSV-1), which primar-
ily affects the face, lips, and mouth, and HSV-2, which is
mainly responsible for genital infections (34,35). However, a pri-
mary HSV-2 infection can occur in the mouth, and HSV-1 can
also cause genital lesions (34,35). HSVs are spread through
direct contact of mucous membranes or compromised skin with
oral secretions, sores, or fluid from blisters of an infected indi-
vidual. Primary symptoms begin within a week of exposure,
with a tingly, itchy, or painful feeling occurring at the site of
exposure. Blisters appear, burst, and then transition to painful
ulcers. Primary infection lasts 1014 days (34,35). Subsequently,
the viruses enter dormancy in the dorsal root ganglia of the
trigeminal nerve, reactivating and forming lesions in about 45%
of individuals who experienced primary infection (34). The
infection cannot be cured, but treatments exist that can help
alleviate symptoms.
Researchers estimate 535.5 million (16.2%) of the worlds
population were infected with HSV-2 as of 2003 (36). In the
U.S. between 2005 and 2010, it was estimated 15.7% of individ-
uals aged 1449 years were infected with HSV-2, while 53.9%
were infected with HSV-1 (37). HSVs persist on surfaces from a
few hours to 8 weeks depending on temperature and humidity
(15,3840). They can be disinfected by a 1:101:100 dilution of
5.256.15% sodium hypochlorite (ex. household bleach). Con-
tact time required for inactivation varies depending on the
amount of infectious material with 10 min required for large
spills (26). Viable HSV-1 has been isolated in trigeminal ganglia
several days postmortem (41), but its presence in other tissues
 ROBERTS ET AL.
postmortem is unknown. The risk of acquiring HSVs from
human remains is likely extremely low.
Human Immunodeficiency Virus
Human immunodeficiency virus (HIV), the virus responsible
for causing acquired immune deficiency syndrome (AIDS), is an
enveloped, single-stranded RNA virus within the genus Len-
tivirus and the family Retroviridae (42,43). Two types have been
identified, the more virulent and infectious HIV-1, found glob-
ally, and HIV-2, found in Western and Central Africa (4345).
Both types represent zoonotic infections, with the chimpanzee
(Pan troglodytes) identified as the original reservoir for HIV-1
and the sooty mangabey (Cercocebus atys) the original reservoir
for HIV-2 (4548). The earliest known HIV-1 infection was
identified in a blood sample collected in 1959 from an individual
in Kinshasa, Belgian Congo (now Democratic Republic of the
Congo) (49,50). HIV was first recognized clinically in the early
1980s, and the virus itself, initially named human T-cell lym-
photropic virus-type III/lymphadenopathy-associated virus
(HTLV-III/LAV), was isolated as the causative agent in 1983
(42,43).
HIV transmission is possible if HIV-infected fluids (blood,
semen, vaginal secretions, rectal fluids, breast milk) directly con-
tact a mucous membrane or damaged tissue, or are introduced
into the bloodstream through sharps injury or injection (51).
HIV infects CD4-positive T cells, decreasing the ability of an
infected person to mount an immune response to any onslaught
as HIV levels increase (4244). Primary HIV infection occurs in
5070% of infected individuals 112 weeks (usually 24 weeks)
after contraction of the virus (4244). Symptoms of acute infec-
tion resemble other viral illnesses such as the common cold or
influenza. Fatigue, general malaise, fever, headache, decreased
appetite, muscle aches, swollen lymph nodes, sore throat, and
rash may occur with primary infection (4244). A period of
asymptomatic infection follows and can last up to 15 years
(43,44). With substantial destruction of the immune system, clin-
ical symptoms of infection reappear in conjunction with oppor-
tunistic infections (43,44). Symptoms may include pronounced
weight loss, dry cough, reoccurring fever, night sweats, profound
fatigue, swollen lymph nodes, and persistent diarrhea (4244).
Common opportunistic infections include tuberculosis, pneumo-
nia, candidiasis, meningitis, Kaposis sarcoma, lymphoma, and
Cytomegalovirus disease (4244). Diagnosis of HIV is generally
performed through enzyme-linked-immunosorbent serologic
assay (ELISA), an antibody screening test on blood or oral fluid
(43,52). Treatment for HIV combines multiple antiretroviral
medications in highly active antiretroviral therapy (HAART) to
decrease both viral load and the rate at which resistance devel-
ops (43,52).
As of 2010, 1.1 million people in the U.S. were infected with
HIV, with an estimated 16% unaware of their infection (53).
Certain groups, including correctional populations, intravenous
drug users, men who have sexual intercourse with men, and the
economically disadvantaged, have a higher incidence of HIV
(54). If HIV status of the deceased is unknown at death, life-his-
tory variables may help identify high-risk autopsies, forensic
anthropology examinations, and body donations.
Exposure to HIV-positive fluids during forensic investigation
is a valid concern, as the virus does not inactivate immediately
upon host death. Several studies have identified infectious HIV
postmortem. Replicating HIV-1 was isolated from plasma 18 h
postmortem (55) and at 142 h (56), and in blood at 16.5 days
. HAZARDS OF FORENSIC ANTHROPOLOGY PART I S7
postmortem, pleural liquid 13.8 days after death, and pericardial
liquid after 15.5 days (57). Replicating HIV was also identified
from a bone fragment, brain, bone marrow, and a lymph node
5.9 days postmortem and from spleen samples stored at room
temperature for 14 days (56). HIV RNA was detected in blood
samples up to five days postmortem (11). The amount of HIV in
tissues postmortem will depend on the viral load at death, the
HIV type, premortem therapies, and storage conditions (58). At
the highest titer of virus ever recorded in the blood of patients,
the virus remained infectious 48 weeks (59). The infectivity of
the virus at lower titers was much reduced (59) and reported to
be at least seven days on surfaces (15,60) and several weeks
within needle syringes stored at room temperature (17). HIV is
inactivated by a 1:101:100 dilution of 5.256.15% sodium
hypochlorite (ex. household bleach). Contact time required for
inactivation varies depending on the amount of blood spilled,
with 10 min required for large spills (26). Many disinfectants
are effective against HIV, and any product with labeling indicat-
ing approval by the EPA for use against HIV may be used to
clean HIV-infective blood as long as all product directions are
followed (26).
The CDC reports an overall 0.3% chance of virus transmission
following exposure to HIV-infected blood (61). The routes of
transmission result in differing risks, with lower chances of
transmission following splashes to mucous membranes or super-
ficial needle sticks and higher chances after deep tissue punc-
tures or lacerations (61). If possible exposure to the virus occurs
via puncture or to compromised skin, gently induce bleeding at
the puncture site while washing the area with soap and water
(61). If potential viral exposure occurs on intact skin or mucous
membranes, wash the area thoroughly with soap and water (61).
Occupational transmission of HIV is extremely rare (61). If
exposure occurs, the recently updated U.S. Public Health Service
Guidelines for the management of occupational exposures to
HIV and recommendations for postexposure prophylaxis (PEP)
include the following: (i) PEP following any occupational expo-
sure, (ii) determination of the HIV status of the source patient,
(iii) PEP medications should begin immediately after virus expo-
sure and be continued for 4 weeks, (iv) medication regimens
should contain three (or more) antiretroviral drugs, (v) seek
expert consultation, (vi) beginning within 72 h of the exposure
event, postexposure follow-up should include counseling, base-
line, and follow-up HIV testing, and continued evaluation for
drug toxicity, and (vii) testing may be concluded 4 months after
exposure if a newer fourth-generation combination HIV p24
antigen-HIV antibody test is utilized for follow-up; if not, fol-
low-up testing is concluded 6 months after virus exposure (62).
Invasive Group A Streptococcus
Invasive Group A Streptococcus (GAS) is the bacterium
responsible for necrotizing fasciitis, also referred to as necrotiz-
ing acute soft tissue injury (NASTI) and flesh-eating disease,
pneumonia, cellulitis, and streptococcal toxic shock syndrome
(STSS) (63,64). GAS causes a range of mild illnesses, such as
strep throat or impetigo, and is often present on the throat or
skin without causing illness (42,64). Invasive disease occurs
when GAS reaches the blood, muscle or other deep tissues, or
the lungs (63,65). Healthy individuals rarely experience invasive
GAS infection. However, discussion of this bacterium is
warranted because of possible introduction into blood or deep
tissues following sharp trauma or fluid splashes to compromised
skin during processing of an infected individual postmortem, as
S8 JOURNAL OF FORENSIC SCIENCES
well as exposure through injuries causing soft tissue trauma
sustained in the field such as insect bites, scrapes, punctures, or
cuts (63,65). Sputum, respiratory droplets, skin lesions, blood,
and wound exudates of infected individuals are infectious (66).
Early signs and symptoms of necrotizing fasciitis are redness,
pain, and swelling around the wound site accompanied by fever
(65). Early signs and symptoms of STSS include dizziness, con-
fusion, flu-like symptoms, and acute onset of severe pain, usu-
ally occurring in an arm or leg (65). Following any break in the
skin during fieldwork or laboratory work, immediately clean the
area with soap and water or available antiseptics. Do not delay
first aid. Treatment of invasive GAS infection includes high-dose
b-lactam antibiotics such as penicillin and clindamycin. Severe
cases may require intravenous antibiotics and surgical removal
of dead tissue (65). There are about 10001500 cases of STSS
and necrotizing fasciitis combined each year in the U.S. (65).
The mortality rate of necrotizing fasciitis is c. 25%, while STSS
has a mortality rate of about 40% (65).
It is unknown how long GAS remains infective in postmortem
tissues. On dry surfaces, the bacterium remains infective for
3 days to 6.5 months (15,67). GAS can be disinfected with 1%
sodium hypochlorite, 4% formaldehyde, 2% glutaraldehyde,
70% ethanol, 70% propanol, 36% hydrogen peroxide, or 0.16%
iodine (66).
Methicillin-resistant Staphylococcus aureus
Methicillin-resistant Staphylococcus aureus (MRSA) is a type
of bacteria that usually causes but is not limited to skin infec-
tions, and is resistant to methicillin as well as the other types of
penicillin and cephalosporin (68). In 1959, forms of Staphylo-
coccus aureus that had become resistant to penicillin were being
treated with methicillin (69). However, in 1961, cases of methi-
cillin-resistant Staphylococcus aureus were starting to be
detected in the United Kingdom. Soon after, cases started show-
ing up in other European countries, Japan, Australia, and the
U.S. MRSA is transmitted through direct skin-to-skin contact
with an infected area of skin, by sharing personal items with an
infected person, as well as by touching surfaces or items that
come into contact with an infected persons wound (70). There
are also documented cases of MRSA transmission to humans
from livestock such as cows, horses, and pigs (71).
MRSA is common, can be a serious problem in hospitals and
nursing homes, and is sometimes fatal (68,72). In 2011, the
CDC (68) reported 80,461 cases of serious MRSA infections,
with 11,285 (14.0%) of these resulting in death in the U.S. In
clinical settings, MRSA is the most common cause of infections
in the bloodstream and at surgical sites, and it is also the most
common cause of ventilator-associated pneumonia (73,74). Indi-
viduals with pre-existing illnesses are at a higher risk of dying
from MRSA (72). Researchers found patients with comorbidities
such as cirrhosis of the liver, cardiovascular disease, and dia-
betes had a higher chance of dying from MRSA (72). MRSA is
the second most common cause (64) of infection found in
patients with central venous catheters (central lines) (75), and
43% of MRSA patients in a recent study acquired their blood
infection from central lines (72).
MRSA can also be found in the community (70,76) and is a
concern in settings in which large groups of people interact in
limited spaces like schools, sports teams, and the military (70).
These individuals also have a high probability of sharing
personal items potentially contaminated with MRSA. MRSA
present in the community usually presents in the form of skin
infections characterized by warm, swollen, painful, red areas on
the skin containing pus and is usually accompanied by fever.
Medical treatment should be sought right away, and treatments
usually include antibiotic regimens and wound draining (77).
MRSA can be resilient, surviving in many different types of
environments (acidic, elevated sodium levels, and varying tem-
peratures), and can remain viable on dust particles, surviving
outside the body from several days to over a week (15,71).
MRSA strains can survive on both porous and nonporous sur-
faces, though last longer on nonporous materials such as plastic
and vinyl (78). Several different types of fomites were found
capable of transferring MRSA to skin for lengthy periods of
time: vinyl up to 63 days, hard plastic at 56 days, ceramic after
21 days, 14 days from cotton towels and sheets, 10 days from
football pads, after 3 days from cedar wood, and only 5 min
from a metal razor blade (78). The range of persistence on non-
porous surfaces is reported between seven days to seven months
(15). Five species of Staphylococcus were cultured from the sur-
faces of anatomy cadavers fixed in formalin (79), but data on
unembalmed individuals are limited. As a result of MRSA likely
persisting after host death, forensic anthropologists should be
cautious. MRSA may be a hazard to forensic anthropologists
and those under their supervision, as human donations to
research facilities may be received from hospitals or nursing
homes, and have open wounds or catheters, thus increasing the
possibility of MRSA infection. Also, clothing from deceased
individuals encountered in the field or at a research facility
should be handled in accord with MRSAs ability to persist on
cloth (78). The CDC recommends proper PPE procedures be fol-
lowed, and individuals exposed to infectious bodies need to
cover their own cuts and wounds to prevent contracting MRSA
(74).
Smallpox
Smallpox, a disease caused by variola virus, was declared
eradicated by the World Health Assembly on May 8, 1980
(80,81). However, its potential use as a bioterrorism agent, con-
cern over its reintroduction through human remains predating its
eradication, and issues surrounding forgotten or hidden samples
of the virus warrant its inclusion in this paper (80,81). The vari-
ola virus is classified within the genus Orthopoxvirus, which
includes monkeypox, cowpox, camelpox, mousepox, and vac-
cinia (80,81). The origin of the virus is unknown, and the virus
only affects humans (80). The variola virus is transmitted to sus-
ceptible individuals via inhalation of large respiratory droplets
from infected individuals after close contact, inhalation of small,
aerosolized respiratory particles, or direct contact with infected
body fluids (81,82). Objects in close contact with the infected,
like clothing and bedding, can also transmit the virus (81,82).
Smallpox was once prevalent throughout the world and is
thought to be responsible for over half a billion deaths in the
century before its eradication (80).
The symptoms of smallpox began 717 days postexposure
(81,83). Initial symptoms generally lasted two to four days and
included fever (101104F), fatigue, achiness, and sometimes
vomiting (81,83). Following initial symptoms, a rash appeared,
beginning in the mucosa of the mouth and pharynx, progressing
to the face, arms, and legs, and terminating at the hands and feet
(81,83). After the rash appeared, all parts of the body were usu-
ally involved within 24 h (83). The rash transitioned to bumps,
which became round, raised, firm pustules (83). Two weeks after
the initial appearance of the rash, most pustules scabbed over.
 ROBERTS ET AL.
After the scabs fell off (usually three weeks after the rash first
appeared), pitted, depigmented scars frequently remained (83). A
person should be considered contagious from the onset of fever
until the final scab is shed. There are two forms of smallpox
caused by two distinct viruses, variola major and variola minor
(80,81). Variola major caused a more common and severe dis-
ease, with a more extensive rash, higher fever, and higher fatal-
ity rate (30%) (83). Variola major is further divided into four
types: ordinary, modified, flat, and hemorrhagic (83). Variola
minor caused a less severe disease with a 1% fatality rate (83).
The large variola virus is deactivated quickly by UV light, but
may persist as long as 24 h in small respiratory droplets (42).
Smears on glass retained virus from 34 to 84 days (84). The
virus persists in crusts for at least two months (85) to more than
a year (86), and in scabs for at least 13 years (in envelopes in a
laboratory cupboard) (87). Morphologically complete virus was
identified in tissue samples taken from individuals in East Lon-
don crypts over 100 years postmortem, but the virus was not
functionally intact (could not be isolated) (88). During thousands
of extensive investigations into smallpox outbreaks in areas pre-
viously free of the disease for years, researchers were able to
identify the sources of infection in all cases and declared there
was no reservoir in the environment (80). If an outbreak occurs,
spills of blood or tissue containing infective smallpox can be
inactivated on surfaces with 40% ethyl alcohol, 30% isopropyl
alcohol, 100 ppm benzalkonium chloride, 200 ppm sodium
hypochlorite, 0.12% ortho-phenylphenol, or 75 ppm iodophor at
a contact time of 10 min (89).
There is no approved treatment for smallpox except for sup-
portive therapy, but there are effective vaccines, which, if given
within three to four days after virus exposure, lessens symptoms
and decreases mortality (81,90). Routine vaccination ceased
worldwide in 1983, but there is enough vaccine to vaccinate
everyone in the United States who would need it in the event of
a smallpox emergency (81,90). If occupationally exposed to
smallpox, standard postexposure protocol should be followed
and the vaccine should be administered as soon as possible.
Stores of variola virus were previously thought to be protected
in two locations: the Centers for Disease Control and Prevention
in Atlanta, Georgia, and Russian State Centre for Research on
Virology and Biotechnology, Koltsovo, Novosibirsk Region
(91). The WHO recommended destruction of known stockpiles
of smallpox virus in 1994, but destruction has been postponed
on four separate occasions owing to concerns about continued
smallpox research, bioterrorism, and forgotten or hidden stores
of the virus (81). The recent discovery of vials of smallpox virus
in an unused storage room at the National Institutes of Health in
Bethesda, MD, indeed raises concern about other potential
forgotten containers of virus (92).
Transmissible Spongiform Encephalopathies
Transmissible Spongiform Encephalopathies (TSEs) are a
group of neurodegenerative diseases characterized by spongiform
neural lesions, absence of host inflammatory responses, and long
incubation periods (9395). These diseases are caused by infec-
tious and misfolded forms of the prion protein, a neural cell
membrane protein (93,94,96). The protein is encoded by a gene
located on the short arm of chromosome 20, but the physiologic
function of the normal form (PrPC) is still under investigation
(9597). The abnormal form, PrPSC, cannot be broken down
completely by cellular machinery, resulting in its accumulation
in neural tissues over time (93,96). Once present, PrPSC seems
. HAZARDS OF FORENSIC ANTHROPOLOGY PART I S9
to promote further misfolding of normal PrPC through an auto-
catalytic mechanism, creating a cascade of malformation, accu-
mulation, spongiform changes, and neuronal cell death for which
there is no vaccine or treatment (93,96). After the onset of TSE
symptoms (most commonly dementia, loss of coordination, or
balance), TSEs are 100% progressive and fatal. Definitive diag-
nosis is based upon examination of brain tissue obtained from
biopsy or at autopsy (98).
In humans, TSEs are classified as transmissible, but not conta-
gious (96). Human TSEs are generally divided into three cate-
gories: sporadic, acquired, and genetic. Sporadic Creutzfeldt-
Jakob Disease (CJD) is the most common and is thought to be
caused by a rare spontaneous transformation of PrPC to PrPSC
(99). Acquired TSEs include variant CJD (vCJD) (from ingestion
of bovine spongiform encephalopathy (BSE) infected cow meat),
kuru (from mortuary practices involving consumption of infected
tissues), and iatrogenic CJD from exposure during medical pro-
cedures (94,100). Nongenetic prion diseases account for 8590%
of all reported prion cases, with the majority of those being spo-
radic (6,96,101). Genetic TSEs are associated with autosomal
dominant mutations of the gene encoding PrPC and include Ger-
stmannStrausslerScheinker syndrome and fatal familial insom-
nia. Genetic prion diseases account for 1015% of all reported
prion cases (101). Combined, prion diseases infect 1.52.5 indi-
viduals per million worldwide (101). In 2010, about 400 deaths
in the U.S. were caused by CJD (99). Between 1966 and 2006,
26 healthcare workers worldwide (one neurosurgeon, one pathol-
ogist, 24 laboratory workers) were infected with CJD following
blood or body fluid exposure (102).
Prions are extremely resistant to decontamination methods.
They retain infectivity in 1012% formalin for several months,
resist irradiation, high temperatures, and exposure to pH between
2.5 and 10.5, and tolerate most other common sterilization mea-
sures (93,98). It is suggested prions may persist in the environ-
ment for up to at least sixteen years (103). After use with
suspected or confirmed TSE-infected materials, the WHO recom-
mends reusable instruments should be either (i) immersed in 1 N
sodium hydroxide (NaOH) and heated in a gravity displacement
autoclave for 30 min at 121C, ensuring the container is covered
to prevent the release of hazardous gas, (ii) immersed in 1 N
NaOH or sodium hypochlorite (20,000 ppm available chlorine)
for 1 h, transferred to a container of water, and heated in a grav-
ity displacement autoclave for 1 h at 121C, or (iii) immersed in
a 1 N NaOH or sodium hypochlorite (20,000 ppm available
chlorine) for 1 h, removed, rinsed in water, and transferred to a
container to be heated in a porous load (134C) or gravity dis-
placement (121C) autoclave for 1 h. Disposable instruments
should be incinerated (98). Heat-sensitive reusable instruments
and surfaces should be decontaminated by soaking in 2 N NaOH
or undiluted sodium hypochlorite for 1 h, followed by rinsing
with water (98). All of the three above decontamination methods
should be followed by routine cleaning and sterilization (98).
Postexposure response to suspected or confirmed TSE-infected
blood or body fluids depends on route of exposure. After contact
of unbroken skin with infectious material, the area should be
washed well with soap and warm water. For maximum precau-
tion, rinsing with 0.1 N NaOH or a 1:10 solution of bleach water
can be employed (98). After a needle stick or scalpel injury,
gently encourage bleeding while washing with soap and warm
water (98). Following splashes to the eyes or mouth, irrigate with
saline if the eyes are involved, or tap water if the mouth is the
route of exposure. Records involving TSE exposure should be
kept for at least 20 years (98). Previously studied tissues are clas-
S10 JOURNAL OF FORENSIC SCIENCES

TABLE 1Quick facts on human remains pathogen hazards.

Longest Reported Postmortem Viability on Nonporous Decontamination of Nonporous

Pathogen* Vaccine Viability in Human Remains Surfaces, Other Surfaces
Hepatitis B Virus Yes Blood: 4 d (11) At least 7 d (1417) 1:100 dilution of sodium
Human tissue waste after hypochlorite (household
storage: several days (18) bleach)b, 1:10 dilution for large
spills (10 min) (14)
Hepatitis C Virus No Blood: 15 d (11) Up to 6 w (23) 1:10 dilution of household
Blood and serum: 14 d (25) Liquids: 5 mo (24) bleach for 10 min (23,26)
Hepatitis A Virus Yes No data found Months (28) 1:10 bleach solution (28)
Herpes Simplex Virus In development Trigeminal ganglia (HSV-1): Hours8 w (15,3840) 1:101:100 dilution of bleach
several days (41) (10 min for large spills) (26)
Human No Blood: 16.5 d (57) High titer: 48 w (59) 1:101:100 dilution of bleach
Immunodeficiency Plasma: 142 h (56) Low titer: 7 d (15,60) (10 min for large spills) (26)
Virus (HIV) Pleural liquid: 13.8 d (57) needle syringes: several
Pericardial liquid: 15.5 d (57) weeks (17)
Bone, bone marrow, lymph
node, brain: 5 d 22 h (56)
Spleen: 14 d (56)
Invasive Group A No No data found 3 d6.5 mo (15,67) 1:100 dilution of bleach, 70%
Streptococcus ethanol, 36% hydrogen
peroxide, 0.16% iodine (66)
Methicillin-Resistant No Skin of formalin-fixed cadavers, 7 d7 mo (15) 1:100 dilution of bleach, 70
Staphylococcus five species of Staphylococcus: Vinyl: 63 d ethanol, 2% glutaraldehyde,
aureus several weeks (79); animal Hard plastic: 56 d 0.25% benzalkonium chloride
remains: 42 d (116) Ceramic: 21 d (117)
Cotton: 14 d
Metal: 5 min (78)
Variola Virus Yes Crusts: 1 y (86) Scabs: 13 y Respiratory droplets: up Exposure to UV light (42)
(Smallpox) (87) to 24 h (42) 1:10 bleach solution, 30%
Smears on glass: 34 isopropyl alcohol, 40% ethanol
84 d (84) (89)
Transmissible No Likely lengthy in high-infectivity At least 16 y (103) 2 N NaOH (1 h), undiluted
Spongiform tissuesbrain, spinal cord, sodium hypochlorite (1 h) (98),
Encephalopathies retina, optic nerve, spinal and 1 N NaOH and autoclave at
(Prions) trigeminal ganglia, pituitary 121C for up to1 h (98)
gland (93,98,103,105)
Tuberculosis Yes, but it is 36 d (112) Mummified tissues: 1 d4 mo (15,67) 10002500 ppm chlorine, 2%
(Mycobacterium not recommended possibly 200 y (114) cloth, tables, metal aqueous glutaraldehyde (10
tuberculosis) in the U.S. Embalmed remains: 48 h (112) trays: at least 24 h 20 min) (118)
*After any mucocutaneous exposure to these pathogens, rinse the area thoroughly with water. After exposure to blood or body fluids to nonintact skin,
wash well with soap and water. If sharps injury occurs, gently encourage bleeding while washing with soap and water (61). Report all exposures to your
supervisor.
d = days, mo = months, y = years, w = weeks, h = hours, min = minutes.
b Household bleach refers to 5.256.15% sodium hypochlorite. All bleach and bleach products used to disinfect forensic laboratory space should be approved
by the EPA, and the directions on the label should be followed exactly.

sified as having high infectivity, low infectivity, and no currently
detectable infectivity. The most infective tissues of TSEs in
humans include the following: brain, spinal cord, retina, optic
nerve, spinal and trigeminal ganglia, and the pituitary gland
(104,105). The infectivity of blood in cases of TSEs is still being
debated, but if infective, blood is likely of low infectivity (104).
It is currently unknown how long after host death prions survive,
but based on their extended survival on surfaces and resistance to
decontamination, it may be a lengthy period (105). Despite this,
the extreme rarity of TSEs and the confinement of titers of infec-
tion to neural tissues likely result in a very low risk of prion
transmission to forensic anthropologists (102,105).
Tuberculosis
Mycobacterium tuberculosis is the bacterium responsible for
tuberculosis (TB), an infection of the lungs that can spread to
other parts of the body such as the spine and brain (106). TB is
transmitted through the air when bacteria are expelled from the
lungs, infecting others through inhalation of aerosolized
respiratory particles. TB can follow an asymptomatic latent
course or progress to active disease, the symptoms of which
may include a lasting cough producing blood or sputum, fatigue,
anorexia, weight loss, and fever. TB manifests more frequently
in individuals with compromised immune systems and is the
leading cause of death in individuals with HIV (107). TB is one
of the worlds greatest killers, infecting approximately one-third
of the worlds population (107,108). Worldwide in 2012, nine
million individuals were newly infected, and 1.3 million cases
resulted in death (107). In 2012, 9,945 individuals contracted
TB in the U.S. However, the CDC (107) reports the rates of TB
in the U.S. are on the decline. TB can become resistant to medi-
cation if taken improperly, referred to as multidrug-resistant TB
(MDR-TB) (109). Most cases of MDR-TB are found outside the
 ROBERTS ET AL.
U.S.; however, the cases of MDR-TB that are in the U.S. are
expensive and time consuming to treat, with patients often suf-
fering severe morbidity.
Mycobacterium tuberculosis can be contracted from human
remains when air is expelled from the lungs, as occurs during
early decomposition when blood and fluid bubble out of the
mouth and nose, during the later bloat stage when gasses are
released from remains, or during the movement of an individual
postmortem (110112). When the bacilli become aerosolized,
they can remain infectious for extended periods of time. Dried
fluids containing M. tuberculosis may be aerosolized when dis-
turbed (113). M. tuberculosis can persist on dry, inanimate sur-
faces for one day to four months (15,67). Tissue cutting and
histological preparation of samples from M. tuberculosis-infected
individuals can also aerosolize bacteria. Historically, medical
examiners have contracted TB from cutting through bone (113).
Additionally, traces of M. tuberculosis have been found on
objects in autopsy rooms (cloth, tables, metal trays, etc.) up to
24 h postautopsy (113). In the U.S., staff in laboratories, mor-
gues, and autopsy rooms are between 100 to 200 times more
likely to contract TB than individuals in the community and ten
times more likely than other hospital workers (113). Research
found U.S. funeral directors have higher morbidity and mortality
rates from occupationally acquired TB infection than the
community (110).
The postmortem survivability of M. tuberculosis surpasses
that of most other pathogens (111). Viable M. tuberculosis was
identified in unembalmed remains up to eight days postmortem
at temperatures between 20 and 25C, and up to 14 days at
4C (113). Recently, researchers found M. tuberculosis in
human remains 36 days after death (112). It is suggested
M. tuberculosis may be revived from mummified tissues up to
200 years postmortem (114). Embalmed remains should also be
considered a hazard. Embalmed cadavers from anatomy depart-
ments may contain viable M. tuberculosis (12), and research
suggests these bacilli are able to survive up to 48 h after
embalming (112). During a recent investigation, M. tuberculosis
was not detected in remains three weeks after embalming
(112).
Undiagnosed M. tuberculosis-infected individuals pose the
greatest risk to pathologists, medical students, and laboratory
workers (113). Forensic cases frequently involve unidentified
individuals, and thus individuals with unknown health histories,
making occupational TB exposure a continual risk to forensic
practitioners. Individuals may show no outward signs of disease
status; however, forensic anthropologists can reduce occupational
exposures to TB by obtaining complete health histories of body
donations to research facilities and wearing proper PPE during
casework, which should include high filtration masks in sus-
pected or confirmed cases of TB (112). During cases, if remains
are suspected to be infected with TB, a cloth should be placed
over the deceaseds nose and mouth if the remains are being
moved and proper ventilation should be utilized in laboratories.
While cutting bone or soft tissue, especially with saws that can
aerosolize particles, proper PPE should be worn (113). The vac-
cine for tuberculosis has a long, controversial history in terms of
efficacy and is generally not recommended in the U.S. except
under very specific circumstances (108).
Conclusions
This work has highlighted necessary information about patho-
gen hazards and the many updates regarding the risks of forensic
. HAZARDS OF FORENSIC ANTHROPOLOGY PART I S11
anthropology in the more than 15 years since the seminal
publication of Galloway and Snodgrass (1). Table 1 briefly sum-
marizes pathogens highlighted in this work, including viability
after host death and on surfaces, along with decontamination
procedures. The authors suggest it would be best used posted in
laboratory settings with other informational materials. Being cog-
nizant of potential hazards of human remains can help prevent
occupational injury and exposure to blood and blood products.
Attention should be placed on appropriate PPE, training, and
vaccination requirements at specific institutions, as well as ensur-
ing those under supervision abide by all regulations. Students
and personnel may view some occupational exposures as
insignificant, and this attitude should be discouraged. Addition-
ally, individuals under supervision may feel occupational expo-
sures are perceived as indicative of incompetence and may be
concerned about potential negative consequences after reporting.
Forensic anthropologists should attempt to create an environment
in which injury reporting is encouraged and knowledge about
hazards and risks is increased. To review the pathogens encoun-
tered by forensic anthropologists while working in the field as
well as chemical hazards of the laboratory, see An Update on
the Hazards and Risks of Forensic Anthropology, Part II: Field
and Laboratory Considerations by the same authors (115).
Acknowledgments
The authors wish to extend our gratitude to Logan Banadyga,
Ph.D., and Laura Ross, M.D., for their constructive comments
and assistance in ensuring the accuracy of this work. We would
like to thank Ami Ruffing of the SIU Center for Environmental
Health and Safety for providing guidance on some topics dis-
cussed, although any errors of interpretation belong to us. Also,
the authors thank the reviewers and editors for their time and
effort in reviewing this manuscript.
References
1. Galloway A, Snodgrass JJ. Biological and chemical hazards of forensic
skeletal analysis. J Forensic Sci 1998;43(5):9408.
2. Bernard JA, Dattilo JR, LaPorte DM. The incidence and reporting of
sharps exposure among medical students, orthopedic residents, and fac-
ulty at one institution. J Surg Educ 2013;70(5):6608.
3. Kessler CS, McGuinn M, Spec A, Christensen J, Baragi R, Hershow
RC. Underreporting of blood and body fluid exposures among health
care students and trainees in the acute care setting: a 2007 survey. Am
J Infect Control 2011;39(2):12934.
4. Souza-Borges FR, Ribeiro LA, Oliveira LC. Occupational exposures to
body fluids and behaviors regarding their prevention and post-exposure
among medical and nursing students at a Brazilian public university.
Rev Inst Med Trop Sao Paulo 2014;56(2):15763.
5. Burton JL. Health and safety at necropsy. J Clin Pathol 2003;56
(4):25460.
6. Davidson SS, Benjamin WH Jr. Risk of infection and tracking of
work-related infectious diseases in the funeral industry. Am J Infect
Control 2006;34(10):65560.
7. http://www.cdc.gov/hepatitis/ (accessed July 21, 2014).
8. http://cdc.gov/Features/dsHepatitisAwareness/ (accessed August 4,
2014).
9. Watkins BP, Haushalter RE, Bolender DL, Kaplan S, Kolesari GL.
Postmortem blood tests for HIV, HBV, and HCV in a body donation
program. Clin Anat 1998;11(4):2502.
10. Cattaneo C, Nuttall PA, Molendini LO, Pellegrinelli M, Grandi M,
Sokol RJ. Prevalence of HIV and hepatitis C markers among a cadaver
population in Milan. J Clin Pathol 1999;52(4):26770.
11. Eriksen MB, Jakobsen MA, Kringsholm B, Banner J, Thomsen JL,
Georgsen J, et al. Postmortem detection of hepatitis B, C, and Human
Immunodeficiency Virus genomes in blood samples from drug-related
deaths in Denmark. J Forensic Sci 2009;54(5):10858.
S12 JOURNAL OF FORENSIC SCIENCES
12. Demiry urek D, Bayramoglu A, Ustacelebi S . Infective agents in fixed
human cadavers: a brief review and suggested guidelines. Anat Rec
2002;269(4):1947.
13. http://www.cdc.gov/hepatitis/HBV/index.htm (accessed July 27, 2014).
14. http://www.cdc.gov/hepatitis/HBV/HBVfaq.htm (accessed August 5,
2014).
15. Kramer A, Schwebke I, Kampf G. How long do nosocomial pathogens
persist on inanimate surfaces? A systematic review BMC Infect Dis
2006;6:130.
16. Bond WW, Favero MS, Petersen NJ, Gravelle CR, Ebert JW, Maynard
JE. Survival of hepatitis B virus after drying and storage for one week.
Lancet 1981;1(8219):5501.
17. Thompson SC, Boughton CR, Dore GJ. Blood-borne viruses and their
survival in the environment: is public concern about community
needlestick exposures justified? Aust N Z J Public Health 2003;27
(6):6027.
18. Park H, Lee K, Kim M, Lee J, Seeong SY, Ko G. Detection and haz-
ard assessment of pathogenic microorganisms in medical wastes. J
Environ Sci Health A Tox Hazard Subst Environ Eng 2009;44
(10):9951003.
19. http://www.cdc.gov/hepatitis/Statistics/index.htm (accessed July 21,
2014).
20. http://www.cdc.gov/hepatitis/HCV/index.htm (accessed July 27, 2014).
21. http://www.cdc.gov/hepatitis/HCV/HCVfaq.htm (accessed August 5,
2014).
22. Krawczynski K, Alter MJ, Robertson BH, Lu L, Spelbring JE,
McCaustland KA, et al. Environmental stability of hepatitis C virus
(HCV): viability of dried/stored HCV in chimpanzee infectivity stud-
ies. Hepatology 2003;38(Suppl):428A.
23. Paintsil E, Binka M, Patel A, Lindenbach BD, Heimer R. Hepatitis C
virus maintains infectivity for weeks after drying on inanimate surfaces
at room temperature: implications for risks of transmission. J Infect
Dis 2014;209(8):120511.
24. Ciesek S, Friesland M, Steinmann J, Becker B, Wedemeyer H, Manns
MP, et al. How stable is the hepatitis C virus (HCV)? Environmental
stability of HCV and its susceptibility to chemical biocides. J Infect
Dis 2010;201(12):185966.
25. Weber DJ, Rutala WA. The emerging nosocomial pathogens Cryp-
tosporidium, Escherichia coli 0157:H7, Helicobacter pylori, and hep-
atitis C: epidemiology, environmental survival, efficacy of disinfection,
and control measures. Infect Control Hosp Epidemiol 2001;22(5):306
15.
26. Rutala WA, Weber DJ, Healthcare Infection Control Practices Advi-
sory Committee (HICPAC). Guideline for disinfection and sterilization
in healthcare facilities, 2008. Atlanta, GA: Centers for Disease Control
and Prevention, 2008.
27. http://www.cdc.gov/hepatitis/HAV/index.htm (accessed July 22, 2014).
28. http://www.cdc.gov/hepatitis/HAV/HAVfaq.htm (accessed August 5,
2014).
29. http://www.cdc.gov/hepatitis/HDV/index.htm (accessed July 27, 2014).
30. http://www.cdc.gov/hepatitis/HEV/index.htm (accessed July 27, 2014).
31. Barnett ED, Kozarsky PE, Steffen R. Vaccines for international travel.
In: Plotkin SA, Orenstein WA, Offit PA, editors. Vaccines, 6th edn.
Philadelphia, PA: Elsevier Saunders, 2013;127089.
32. Murphy TV, Feinstone SM, Bell BP. Hepatitis A vaccines. In: Plotkin
SA, Orenstein WA, Offit PA, editors. Vaccines, 6th edn. Philadelphia,
PA: Elsevier Saunders, 2013;181204.
33. Van Damme P, Ward J, Shouval D, Wiersma S, Zanetti A. Hepatitis B
vaccines. In: Plotkin SA, Orenstein WA, Offit PA, editors. Vaccines,
6th edn. Philadelphia, PA: Elsevier Saunders, 2013;20534.
34. Hawker J, Begg N, Blair I, Reintjes R, Weinberg J. Communicable
disease control handbook, 2nd edn. Hoboken, NJ: Wiley, 2008.
35. http://www.cdc.gov/std/Herpes/STDFact-Herpes-detailed.htm (accessed
August 11, 2014).
36. Looker KJ, Garnett GP, Schmid GP. An estimate of the global preva-
lence and incidence of herpes simplex virus type 2 infection. Bull
World Health Organ 2008;86(10):80512.
37. Bradley H, Markowitz LE, Gibson T, McQuillan GM. Seroprevalence
of herpes simplex virus types 1 and 2 United States, 19992010. J
Infect Dis 2014;209(3):32533.
38. Mahl MC, Sadler C. Virus survival on inanimate surfaces. Can J
Microbiol 1975;21(6):81923.
39. Turner R, Shehab Z, Osborne K, Hendley JO. Shedding and survival
of herpes simplex virus from fever blisters. Pediatrics 1982;70
(4):5479.
40. Nerurkar LS, West F, May M, Madden DL, Sever JL. Survival of her-
pes simplex virus in water specimens collected from hot tubs in spa
facilities and on plastic surfaces. JAMA 1983;250(22):30813.
41. Saitoh H, Momma Y, Inoue H, Yajima D, Iwase H. Viable herpes sim-
plex virus type 1 and varicella-zoster virus in the trigeminal ganglia of
human cadavers. J Med Virol 2013;85(5):8338.
42. Turkington C, Ashby BL. The encyclopedia of infectious diseases, 2nd
edn. New York, NY: Facts On File Inc, 2003.
43. Wertheim HFL, Horby P, Woodall JP, editors. Atlas of human infec-
tious diseases. Chichester, U.K.: Wiley-Blackwell, 2012.
44. http://www.cdc.gov/hiv/basics/whatishiv.html (accessed August 11,
2014).
45. Gao F, Bailes E, Robertson DL, Chen Y, Rodenburg CM, Michael SF,
et al. Origin of HIV-1 in the chimpanzee Pan troglodytes troglodytes.
Nature 1999;397(6718):43641.
46. Hirsch VM, Olmsted RA, Murphey-Corb M, Purcell RH, Johnson PR.
An African primate lentivirus (SIVsm) closely related to HIV-2. Nature
1989;339(6223):38992.
47. Huet T, Cheynier R, Meyerhans A, Roelants G, Wain-Hobson S. Ge-
netic organization of a chimpanzee lentivirus related to HIV-1. Nature
1990;345(6273):3569.
48. Wertheim JO, Worobey M. Dating the age of the SIV lineages that
gave rise to HIV-1 and HIV-2. PLoS Comput Biol 2009;5(5):
e1000377.
49. Zhu T, Korber BT, Nahmias AJ, Hooper E, Sharp PM, Ho DD. An
African HIV-1 sequence from 1959 and implications for the origin of
the epidemic. Nature 1998;391(6667):5947.
50. Worobey M, Gemmel M, Teuwen DE, Haselkorn T, Kunstman K,
Bunce M, et al. Direct evidence of extensive diversity of HIV-1 in
Kinshasa by 1960. Nature 2008;455(7213):6614.
51. http://www.cdc.gov/hiv/basics/transmission.html (accessed August 2,
2014).
52. http://www.cdc.gov/hiv/basics/testing.html (accessed August 2, 2014).
53. http://www.cdc.gov/hiv/basics/statistics.html (accessed August 2,
2014).
54. http://www.cdc.gov/hiv/risk/index.html (accessed August 2, 2014).
55. Henry K, Dexter D, Sannerud K, Jackson B, Balfour H Jr. Recovery
of HIV at autopsy. N Engl J Med 1989;321(26):18334.
56. Nyberg M, Suni J, Haltia M. Isolation of human immunodeficiency
virus (HIV) at autopsy one to six days postmortem. Am J Clin Pathol
1990;94(4):4225.
57. Douceron H, Deforges L, Gherardi R, Sobel A, Chariot P. Long-
lasting postmortem viability of human immunodeficiency virus: a
potential risk in forensic medicine practice. Forensic Sci Int 1993;60
(12):616.
58. Ganczak M, Boron-Kaczmarska A, Dziuba I. Pathologist and HIV
are safe autopsies possible? Pol J Pathol 2003;54(2):1436.
59. van Bueren J, Simpson RA, Jacobs P, Cookson BD. Survival of
human immunodeficiency virus in suspension and dried onto surfaces.
J Clin Microbiol 1994;32(2):5714.
60. Barre-Sinoussi F, Nugeyre MT, Chermann JC. Resistance of AIDS
virus at room temperature. Lancet 1985;2(8457):7212.
61. http://www.cdc.gov/hiv/risk/other/occupational.html (accessed August
1, 2014).
62. Kuhar DT, Henderson DK, Struble KA, Heneine W, Thomas V, Che-
ever LW, et al. Updated US Public Health Service guidelines for the
management of occupational exposures to human immunodeficiency
virus and recommendations for postexposure prophylaxis. Infect Con-
trol Hosp Epidemiol 2013;34(9):87592.
63. Howie WO. Anesthetic implications of necrotizing fasciitis. AANA J
2003;71(1):3740.
64. http://www.cdc.gov/groupAstrep/about/index.html (accessed June 24,
2014).
65. http://www.cdc.gov/groupAstrep/about/faqs.html (accessed June 24,
2014).
66. http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/strep-pyogenes-eng.php
(accessed August 2, 2014).
67. Mitscherlich E, Marth EH. Microbial survival in the environment: bac-
teria and rickettsiae important in human and animal health. Berlin,
Germany: Springer, 1984.
68. http://www.cdc.gov/drugresistance/threat-report-2013/ (accessed June
24, 2014).
69. Enright MC, Robinson DA, Randle G, Feil EJ, Grundmann H, Spratt
BG. The evolutionary history of methicillin-resistant Staphylococcus
aureus (MRSA). Proc Natl Acad Sci U S A 2002;99(11):768792.
 ROBERTS ET AL.
70. http://www.cdc.gov/mrsa/community/index.html (accessed June 24,
2014).
71. Daum RS. Staphylococcus aureus vaccines. In: Plotkin SA, Orenstein
WA, Offit PA, editors. Vaccines, 6th edn. Philadelphia, PA: Elsevier
Saunders, 2013;11638.
72. Pastagia M, Kleinman LC, Lacerda de la Cruz EG, Jenkins SG. Pre-
dicting risk for death from MRSA bacteremia. Emerg Infect Dis
2012;18(7):107280.
73. Huang SS, Septimus E, Kleinman K, Moody J, Hickok J, Avery TR,
et al. Targeted versus universal decolonization to prevent ICU infec-
tion. N Engl J Med 2013;368(24):225565.
74. http://www.cdc.gov/mrsa/healthcare/index.html (accessed June 24,
2014).
75. Burton DC, Edwards JR, Horan TC, Jernigan JA, Fridkin SK. Methi-
cillin-resistant Staphylococcus aureus central lineassociated blood-
stream infections in US intensive care units, 19972007. JAMA
2009;301(7):72736.
76. Bancroft EA. Antimicrobial resistance its not just for hospitals. JAMA
2007;298(15):18034.
77. http://www.cdc.gov/mrsa/community/clinicians/ (accessed August 2,
2014).
78. Desai R, Pannaraj PS, Agopian J, Sugar CA, Liu GY, Miller LG. Sur-
vival and transmission of community-associated methicillin-resistant
Staphylococcus aureus from fomites. Am J Infect Control 2011;39
(3):21925.
79. Tabaac B, Goldberg G, Alvarez L, Amin M, Shupe-Ricksecker K,
Gomez F. Bacteria detected on surfaces of formalin fixed anatomy
cadavers. Ital J Anat Embryol 2013;118(1):15.
80. Henderson DA. Smallpox: the death of a disease. New York, NY: Pro-
metheus Books, 2009.
81. Kennedy RB, Lane MJ, Henderson DA, Poland GA. Smallpox and
vaccinia. In: Plotkin SA, Orenstein WA, Offit PA, editors. Vaccines,
6th edn. Philadelphia, PA: Elsevier Saunders, 2013;71845.
82. Milton DK. What was the primary mode of smallpox transmission?
Implications for biodefense. Front Cell Infect Microbiol 2012;2:150.
83. http://emergency.cdc.gov/agent/smallpox/overview/disease-facts.asp (ac-
cessed June 25, 2014).
84. Walther BA, Ewald PW. Pathogen survival in the external environment
and the evolution of virulence. Biol Rev Camb Philos Soc 2004;79
(4):84969.
85. Huq F. Effect of temperature and relative humidity on variola virus in
crusts. Bull World Health Organ 1976;54(6):7102.
86. MacCallum FO, McDonald JR. Effect of temperatures of up to 45
degrees C on survival of variola virus in human material in relation to
laboratory diagnosis. Bull World Health Organ 1957;16(2):4413.
87. Wolff HL, Croon JJ. The survival of smallpox virus (variola minor) in
natural circumstances. Bull World Health Organ 1968;38(3):4923.
88. Baxter PJ, Brazier AM, Young SE. Is smallpox a hazard in church
crypts? Br J Ind Med 1988;45(5):35960.
89. http://emergency.cdc.gov/agent/smallpox/response-plan/files/guide-f.pdf
(accessed June 24, 2014).
90. http://emergency.cdc.gov/agent/smallpox/faq/smallpox_disease.asp (ac-
cessed June 24, 2014).
91. Henderson DA. Smallpox: clinical and epidemiologic features. Emerg
Infect Dis 1999;5(4):5379.
92. http://www.usatoday.com/story/news/nation/2014/07/08/forgotten-vials-
of-smallpox-found-in-storage-room/12363365/ (accessed June 25,
2014).
93. Franco DA. An introduction to the prion diseases of animals: assess-
ing the history, risk inferences, and public health implications in the
United States. Alexandria, VA: The National Renderers Association,
2005.
94. Beringue V. Introduction. In: Beringue V, editor. Prion biology:
research and advances. Waretown, NJ: Apple Academic Press, 2013;
xviixix.
95. http://www.cdc.gov/ncidod/dvrd/prions/ (accessed July 30, 2014).
. HAZARDS OF FORENSIC ANTHROPOLOGY PART I S13
96. McDonnell G. Prion diseases and device reprocessing: a time gone or
a time bomb? Br J Neurosci Nurs 2013;9(5):22933.
97. Jayanthi P, Thomas P, Bindhu PR, Krishnapillai R. Prion diseases in
humans: oral and dental implications. N Am J Med Sci 2013;5(7):399
403.
98. http://www.cdc.gov/ncidod/dvrd/cjd/qa_cjd_infection_control.htm (ac-
cessed July 31, 2014).
99. http://www.cdc.gov/ncidod/dvrd/cjd/index.htm (accessed July 31,
2014).
100. Takada LT, Geschwind MD. Prion diseases. Semin Neurol 2013;33
(4):34856.
101. Jung M. Spongious encephalopathy (19202010). Croat J Infect
2010;30(4):17794.
102. Tarantola A, Abiteboul D, Rachline A. Infection risks following acci-
dental exposure to blood or body fluids in health care workers: a
review of pathogens transmitted in published cases. Am J Infect Con-
trol 2006;34(6):36775.
103. Georgsson G, Sigurdarson S, Brown P. Infectious agent of sheep scra-
pie may persist in the environment for at least 16 years. J Gen Virol
2006;87(Pt12):373740.
104. World Health Organization. WHO guidelines on tissue infectivity dis-
tribution in transmissible spongiform encephalopathies. Geneva,
Switzerland: WHO, 2006.
105. Bradford BM, Piccardo P, Ironside JW, Mabbott NA. Human prion
diseases and the risk of their transmission during anatomical dissection.
Clin Anat 2014;27(6):82132.
106. http://www.cdc.gov/tb/topic/basics/default.htm (accessed August 1,
2014).
107. http://www.cdc.gov/tb/statistics/default.htm (accessed August 2, 2014).
108. Smith KC, Orme IM, Starke JR. Tuberculosis vaccines. In: Plotkin
SA, Orenstein WA, Offit PA, editors. Vaccines, 6th edn. Philadelphia,
PA: Elsevier Saunders, 2013;789811.
109. http://www.cdc.gov/tb/topic/drtb/default.htm (accessed August 2,
2014).
110. Morgan O. Infectious disease risks from dead bodies following natural
disasters. Rev Panam Salud Publica 2004;15(5):30712.
111. Kirkis EJ. A myth too tough to die: the dead of disasters cause epi-
demics of disease. Am J Infect Control 2006;34(6):3314.
112. Correia JC, Steyl JL, De Villiers HC. Assessing the survival of My-
cobacterium tuberculosis in unembalmed and embalmed human
remains. Clin Anat 2014;27(3):3047.
113. Collins CH, Grange JM. Tuberculosis acquired in laboratories and
necropsy rooms. Commun Dis Public Health 1999;2(3):1617.
114. Lemma E, Zimhony O, Greenblatt CL, Koltunov V, Zylber MI, Ver-
non K, et al. Attempts to revive Mycobacterium tuberculosis from
300-year-old human mummies. FEMS Microbiol Lett 2008;283(1):54
61.
115. Roberts LG, Dabbs GR, Spencer JR. An update on the hazards and
risks of forensic anthropology, part II: field and laboratory considera-
tions. J Forensic Sci. 2016; In press.
116. Spickler AR, Roth JA, Gaylon J, Lofstedt J, editors. Emerging and
exotic diseases of animals, 4th edn. Ames, IA: Iowa State University,
2009.
117. http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/staphylococcus-aureus-
eng.php (accessed August 2, 2014).
118. http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/tuber-eng.php (accessed
August 2, 2014).
Additional information and reprint requests:
Lindsey G. Roberts, M.A.
Department of Anthropology
Southern Illinois University
1000 Faner Drive (MC 4502)
Carbondale, IL 62901
E-mail: lindseyroberts@siu.edu