Sabin et al. Journal of Physiological Anthropology
https://doi.org/10.1186/s40101-020-00239-5(2020) 39:29

REVIEW

Open Access

Implications of human activities for(re)emerging infectious diseases, including
COVID-19
Nundu Sabiti Sabin1,2,3, Akintije Simba Calliope1,2,3, Shirley Victoria Simpson1,2,3, Hiroaki Arima1,2, Hiromu Ito1,
Takayuki Nishimura4,5 and Taro Yamamoto1,2,3*

Abstract
Since 1980, the world has been threatened by different waves of emerging disease epidemics. In the twenty-first
century, these diseases have become an increasing global concern because of their health and economic impacts
in both developed and resource-constrained countries. It is difficult to stop the occurrence of new pathogens in
the future due to the interconnection among humans, animals, and the environment. However, it is possible toface a new disease or to reduce the risk of its spread by implementing better early warning systems and effective
disease control and prevention, e.g., effective global surveillance, development of technology for better diagnostics,
effective treatments, and vaccines, the global political will to respond to any threats and multidisciplinary
collaboration involving all sectors in charge of good health maintenance. In this review, we generally describe
some factors related to human activities and show how they can play a role in the transmission and spread of
infectious diseases by using some diseases as examples. Additionally, we describe and discuss major factors that are
facilitating the spread of the new pandemic known as COVID-19 worldwide.
Key words: Humans, Factors, (Re)emerging infectious disease, Coronavirus

Background
Emerging infectious diseases (EIDs) are diseases recently
identified or previously unknown infections that cause
public health threats, either locally or internationally [1].
In contrast, reemerging infectious diseases are known
diseases that reappear and increase in incidence but thatin the past may have fallen to levels so low that they
were no longer considered a public health problem [1].
In the twenty-first century, these diseases have increasingly become a global concern [2] due to their healthand economic impacts in both developed and resource* Correspondence: taro.daichi.yamamoto@gmail.com
1
Department of International Health and Medical Anthropology, Institute ofTropical Medicine, Nagasaki University, 1-12-4 Sakamoto, Nagasaki 852-8523,
Japan
2
Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki,
Japan
Full list of author information is available at the end of the article

constrained countries. It has been estimated that out ofapproximately 400 known emerging pathogens, 25%
occur as human pathogens [3]. In other reports, approximately 175 species are associated with emerging diseases, of which approximately 75% are of zoonotic origin[4]. Most of these zoonoses have occurred due to increased contact between humans and animals [5–8].
These zoonoses account for approximately 44%, 30%,
11%, 9%, and 6% of viruses or prions, bacteria or rickettsia, protozoa, fungi, and helminths, respectively [9]. In
the post-1980 period, some zoonotic pathogens were responsible for outbreaks such as Escherichia coli O157 in
the 1980s [10], the avian strain of influenza in HongKong in 1997 [11], West Nile virus in 1999 [12], theoutbreak of chikungunya fever in Italy in 2007 [13], theepidemic of Q fever in the Netherlands [14, 15], the outbreak of severe acute respiratory syndrome (SARS) in© The Author(s). 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License,
which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give
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Sabin et al. Journal of Physiological Anthropology(2020) 39:29

2002 caused by very virulent strains of new coronaviruses [16–18], Middle East respiratory syndrome
coronavirus (MERS-CoV) in 2012 [19], and avian influenza, such as A/H1N1 in 1997 in Hong-Kong [20], A/
H7N7 in 2004 in the US [21], A/H7N2 in 2007 in theUK [22], and A/H7N9 in China [20, 23]. Recently, major
outbreaks of Ebola virus disease (EVD) threatened populations in West African countries between 2013 and2016, with 28,603 cases and 11,310 deaths [24], and in
the Democratic Republic of Congo (DRC) from 2018 to2020, with 3444 cases and 2264 deaths [25]. Currently,
the entire world is facing an unprecedented pandemic
caused by a new strain of coronavirus called coronavirus
disease 2019 (COVID-19) [26].
Wolfe et al. [27] identified five stages leading to endemic human disease, where a pathogen restricted to infecting animals may be transformed into a humanpathogen. The first stage is when a pathogen is present
in animals but has not yet been detected in humans
under natural conditions; the second is when a pathogen
has been transmitted from animals to humans, but there
is no evidence of human-human transmission (e.g., tetanus, rabies); the third is when a pathogen can undergo
only a few cycles of secondary transmission between
humans and shortly die out, where a subsequent wave
will require the involvement of animal hosts (e.g., Ebola
virus, Marburg virus, monkeypox virus); the fourth iswhen a pathogen undergoes long sequences of secondarytransmission between humans without the involvementof animal hosts (many vector-borne diseases, e.g.,
dengue virus, yellow fever virus, cholera, influenza A,
typhus); and the fifth is when a pathogen previously
restricted to animals later evolves into an exclusively
human pathogen (e.g., smallpox, measles, syphilis,
falciparum malaria, rubella, mumps, hepatitis B, tuberculosis, AIDS) [27]. Consequently, the passage from one
stage to another depends on the host-pathogenenvironment interconnection [28]. The emergence of
infection is influenced by the interconnecting domainsof determinants such as physical and environmental
factors; ecological factors; genetic and biological factors; and social, political, and economic factors [29].
Therefore, these determinants may influence the emergence and spread of infectious diseases. According toChareonsook et al. [30], human demographic changes
and behavior, travel and commerce, ecological changes,
technology and industry, microbial adaptation andchange, and the breakdown of public health measures
are sufficient factors for the emergence and spread of
infectious diseases. Subsequently, Lederberg et al. [29]identified additional factors such as human vulnerability, economic development, land use, lack of politicalwill, poverty and social inequality, war and famine, andintent to harm.

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In the twenty-first century, many outbreaks have occurred around the world, such as EVD, avian influenza,
and coronaviruses (SARS, MERS, COVID-19), becauseof factors related to human activities. Here, we will
describe some human-related factors and give someexamples.

Human-related factors influencing thetransmission and spread of infectious diseases
Globalization (international travel and trade)

The twenty-first century has ushered in an era where infectious diseases are occurring at an unprecedented
frequency and speed. A coordinated global response isneeded; however, in this globalized environment ofinterdependent trade, travel, and migrations, pathogens
have no geopolitical borders [2, 31].
Recently, EIDs such as COVID-19, EVD, Lassa fever,and SARS have been an issue of global concern. With
globalization, the risk of the emergence of new diseases
is increasing since humans have more chances to be exposed to new pathogens. Additionally, the risk of international spread of infectious diseases is increasing
because of increased international travel. The process ofglobalization potentially influences a broad range of biological, environmental, and social factors that affect theburden of many critical human infections [32]. Various
international organizations and governments have been
trying to establish better global systems to respond to
EIDs. However, the SARS outbreak in 2003, the EVD
outbreak in West Africa in 2014, and the current
COVID-19 pandemic have highlighted that the current
global system is still not fully ready for such (re)emerging infectious diseases [33]. These EIDs threaten publichealth, as well as the global economy, and are sustainedby increasing global trade and travel. However, the disruption of the human-ecological system is another potential factor. Travelers could play a role in importing
EIDs and could be a carrier of major epidemics [34]. It
has been observed that (re)emerging infectious diseases
are imported by travelers or tourists in Europe, such as
chikungunya and dengue in France and Italy as well as
COVID-19 in France from China [35–37]. Cross-border
movements of people, as well as trade in goods and services, are increasing the challenges for infectious disease
control. As an example, in 2005, evidence of outbreak
importation through international travel was found with
the isolation of H5N1 type A influenza virus from two
mountain hawk eagles that were illegally imported fromThailand in an airline cabin carry-on baggage to Belgium[38]. The risk of infectious diseases rises with the increased mobility of people, growth in the international
trade in food and biological products, and social and environmental changes. It is evident that trade and international travel are essential to humankind. However,Sabin et al. Journal of Physiological Anthropology(2020) 39:29

some preventive measures, such as travel restrictions
and creation of awareness among trade and travel stakeholders, are paramount to flatten the curve. In recent
years, trade embargoes or travel restrictions have been
replaced with sensitive early warning surveillance, rapid
verification procedures, and international response networks as well as epidemic preparedness through stockpiles of essential medicines [39, 40]. However, studies
have proven that if implemented within 2 weeks of cases,
travel restrictions are 99% effective in conjunction withborder restrictions that prevent the entry of infectedtravelers. Additionally, a 90% restriction on longdistance flights can lead to delays in the epidemic peakthat range from a few days to a few weeks [41–44].
These developments affect all elements of the infectious
disease chain: hosts, agents, and vectors [45]. Moreover,
we must not ignore the fact that outbreaks are themselves associated with significant costs in terms of lost
trade and tourism revenue. Therefore, a fear of
economic penalties and social stigma can arise and cansometimes lead authorities to underreport data inepidemics, hence risking serious public healthconsequences.
Changes in environment/ecological changes

Global environmental changes are due to human modifications to the environment [46]. National, regional, andglobal environmental threats to human health according
to the World Health Organization (WHO) include “climate change, stratospheric ozone depletion, changes inecosystems due to loss of biodiversity, changes in hydrological systems and the supplies of fresh water, landdegradation, urbanization, and stresses on foodproducing systems” [47].
Changes in the environment, including food-handlingpractices, agriculture, and changes in water ecosystems,
seem to increase the chance of contact with a reservoir
host encountering microorganisms previously unknown
to humans. Anthropogenic changes alter the environment by increasing the risk of transmission of pathogens
unfamiliar to humans [48].
It has been established that there is a relationship between infectious disease outbreaks and changes in theenvironment, including climate change events [49].
Ecological changes are one of the most important driversof (re)emerging infectious diseases, specifically agricultural development, climate changes, food-handling practices, changes in water ecosystems, deforestation, andreforestation [48, 50, 51].
Climate change results in differences in weather conditions and patterns of extreme weather events. Spatiotemporal changes in climate affect the reproduction,
development, survival, and livability of pathogens, hosts,
and their interaction with human beings. Dramatic andPage 3 of 12

unforeseen changes in weather conditions have profoundeffects on many infectious diseases. Extreme weather
events and meteorological hazards make it more complicated to predict the implications for disease pathogens,hosts, and transmission [52–54]. The United Nations
High Commissioner of Refugees (UNHCR) estimatesthat an average of 22.5 million people have been displaced by weather-related events or climate since 2008[55]. The literature on climate variations and infectious
diseases demonstrates that climate-sensitive diseases, i.e.,
vector-borne and food/water-borne diseases, are vastly
affected by climate variability and climate change [56,57]. Vector-borne diseases (VBDs) are the most climate
sensitive. They have several climate drivers [58], causing
over 700,000 deaths annually, accounting for more than
17% of all infectious diseases and having the highest burden in tropical and subtropical areas, particularly affecting the most deprived populations [59]. Some examples
of VBDs of significance to humans and animals are malaria, schistosomiasis, dengue, chikungunya, and Lyme
disease [60–62]. Improving infrastructure and disease
surveillance systems worldwide and funding healthobservatories would help to better detect and attributethe effects of climate change on VBD (re)emergence[60–62]. The burden of food- and water-borne diseases(FWBDs) is found in some parts of developing countries
and areas where food and water hygiene are inadequate.
For example, in Africa, FWBDs account for 91 million
illnesses, resulting in 137,000 deaths, annually [63].
Important causes of food-borne diseases are noroviruses,
Campylobacter spp., and nontyphoidal Salmonella, while
those of water-borne diseases remain diarrheal diseases,
such as cholera, Shigella, and poliomyelitis. Additionally,
food-handling practices have been associated with SARS
and H5N1 outbreaks [48]. Proper water, sanitation, andhygiene interventions can significantly reduce FWBDs[63].
Agricultural development is a factor and the mosttypical way humans alter and interpose themselves into
the environment [64, 65]. It is the world’s single mostsignificant driver of global environmental change and is
key to attaining Sustainable Development Goal (SDG)
2, which aims to end hunger, achieve food security andimproved nutrition, and promote sustainable agriculture [66, 67]. The expansion and intensification ofagriculture come with massive habitat conversion, increasing use of agricultural inputs such as antibiotic
growth promoters and pesticides, and contamination
with animal waste [68]. Several studies have linked agricultural land use or land use change with infectious disease risks. Significant associations were identified for
malaria, spotted fever group rickettsioses, hookworm,
scrub typhus, Schistosoma japonicum, and Trichuris
trichiura.

Sabin et al. Journal of Physiological Anthropology(2020) 39:29

On the other hand, agricultural practices were
implicated in the pandemic influenza outbreak, Nipah,
and West Nile transmission [48]. Exposure to livestock
could result in 2–4 times the risk of infection with
vector-borne, bacterial, or zoonotic diseases [69]. To
withstand the future viability of agriculture, sustainable
practices are required to meet rising human needs while
contributing to the resilience and sustainability oflandscapes, biospheres, and the Earth system [67]. It has
also been shown that deforestation and reforestation can
influence the emergence of some pathogens. For
example, reforestation has been linked to Lyme disease
outbreaks [56, 70].
Human-wild animal interface

Approximately three-fourths of human EIDs are causedby zoonotic pathogens [71]. However, according to theWHO, humans coexist with animals in a variety of ways,
either by hunting [72] or by living as domestic animals[73]. The interface among humans, animals, and the environment we share can be a source of diseases impacting public health [74]. However, in most cases, reported
causes for and drivers of the apparent trends in disease
emergence are lacking in intense evidence-based
research. However, there is circumstantial evidence tosuggest that novel epidemics and disease syndromes are
the results of changing agroecology and human behavior
and movements, intensifying interfaces with certain
wildlife species and climate change [6, 75]. Although noclear evidence has been presented to date, hunting has
been associated with zoonotic diseases [72]. With modern ways of life, however, this hypothesis became obsolete with the low spillover from wild animals to humans.
The possible reason was that when people lived as
hunter-gatherers, they were always on the move, and it
became difficult for microbes to keep up with their human hosts. Once people started living as farmers, they
began residing in more significant numbers in the sameplace and were in daily contact with their accumulating
feces for extended periods [76]. Other evidence has
shown that bushmeat is an essential source of protein
and income in Africa despite its link with numerous
EIDs, such as Ebola and Marburg [7]. The increased demand and commercialization of these types of meat have
exposed people to pathogens and thus facilitated thegeographic spread of the diseases [77]. All the aspects
highlighted above have created conditions highly amenable for the spillover of microbes into the human
ecosystem.
Moreover, the domestication of wild animals has
narrowed the gap between wild animals and humans.
Evidence has shown that domesticated animals that werelong ago associated with humans are the ones at thecenter of those that favor parasite/pathogen transmission

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not only to humans but also to all other domesticatedanimals [78]. It has been revealed not only that humans
are victims of the domestication of wild animals but alsothat the reverse is true. An example is that the occurrence of Taenia tapeworms in humans predated thedevelopment of agriculture, animal husbandry, and domestication of cattle or swine, and later, it accompanied
early human dispersion out of Africa. Swine and cattle
are thought to have acquired infections with Taenia species during their early domestication [79]. Thus far, it is
not possible to stop human-animal interconnections.
However, it is possible to reduce the negative impact of
the human-wild animal interface, which contributes tothe emergence of infectious diseases, by responding before the occurrence of spillover events, epidemics oreven pandemics [80]. For example, people should be educated to stop harvesting bushmeat, especially by avoiding nonhuman primates; future zoonotic spillover eventsshould be prevented through culturally appropriate education, and disease spread should be avoided throughbetter disease surveillance [81, 82].
Antimicrobial resistance

The resistance of microbes (viruses, bacteria, parasites,
and fungi) to antimicrobials has contributed to the reemergence of many diseases that were no longer considered a public health problem [83], narrowing the rangeof antimicrobial drugs and representing a global publichealth concern [84–86]. It has been estimated that approximately 700,000 annual deaths worldwide are a result of antimicrobial resistance (AMR) [87], which posesa problem to achieve the United Nations SDGs [88] andmight reduce the gross domestic product by approximately 3.8% by 2050 [89].
It has been shown that AMR is the consequence of
microbial adaptation and genetic changes that allow
them to bypass the human immune system, infecthuman cells, and spread disease. These microbes canemerge and spread rapidly and become resistant to multiple antimicrobials at the same time [90–94] by developing mechanisms to exchange or incorporate new
genetic material into their genomes, exchanging virtually
any stretch of DNA or RNA [95]. Sometimes, even doctors prescribe inappropriate antimicrobials (i.e., an antimicrobial is not needed at all, or they prescribe thewrong drug or wrong dose) [96], or physicians prescribe
drugs with the wrong prescription doses or antibiotics
with an incorrect duration of treatment [97]. This practice contributes to the growth and spread of microbial
resistance [98] and can be responsible for nosocomial infections in hospitals. For instance, more than 90% of
Staphylococcus aureus species were resistant to penicillin
and beta-lactam antibiotics in hospitals in the UnitedStates (US) and were responsible for approximately 19,

Sabin et al. Journal of Physiological Anthropology(2020) 39:29

000 deaths in 1992 [83]. Additionally, between 1989 and
1993, the incidence of vancomycin-resistant enterococci
increased 20-fold in the US, and in 1997, the susceptibility of Staphylococcus aureus to vancomycin decreased inboth the US and Japan [99]. In the European Union(EU), approximately 15–50% of Klebsiella pneumoniae
species are resistant to carbapenems [100]. Previously,
methicillin-resistant Staphylococcus aureus (MRSA) was
associated with severe invasive disease only in hospitals;
however, in the last 20 years, it has been identified in
the community and named community-associated (CA)MRSA [101]. As an example, CA-MRSA pneumonia is
responsible for approximately 75–85% of admitted patients and 20 to 60% of deaths in the intensive care unit
[102]. Currently, extended-spectrum β-lactamase resistance is endemic in hospitals and the community worldwide [103, 104].
Moreover, multidrug-resistant (MDR)-Acinetobacterbaumannii isolates carrying Cefotaxime-M (CTX-M) enzymes are now responsible for nosocomial infections
and among specific populations and accountable forhigh mortality and morbidity [105], as well as cholera
O1 and O139 [106–109]. Additionally, it has beenshown that the prevalence of MDR-TB among new TB
cases increased from 12% in 2009 to 13.7% in 2010 in
the EU. Thus, drug-resistant TB is still a major concern
despite a decrease in TB incidence in subsequent years[110, 111].
The use of antimicrobials as additives in plant agriculture (fruits, vegetables, orchids, etc.) and animals and,more importantly, food-producing animals can lead tothe development of resistant bacteria [112]. Thus, resistant genes in animals can be transferred to humans
through the consumption of food or direct contact withfood-producing animals or through environmental
spread [113–122]. The misuse of antimicrobials, especially in developing countries, is mainly due to theirunregulated supply chain, the availability of over-thecounter drugs [123–126], and self-medication [125,127–131], which is amplified by poverty [131]. Up tohalf of all antibiotics prescribed are misused and neither
needed nor effective [132, 133]. Another situation is thediscontinuation of treatment by patients with a recurrent
infection, which contributes to the development of avirulent and resistant strain of the microbe [130]. All
these factors contribute to genetic selection pressure forthe emergence of MDR bacterial infections in the community. Given the factors that contribute to the rise of
AMR, reducing its risk implies the need to improve inensuring the appropriate use of antibiotics through theenforcement and improvement of legislation on prescribing and dispensing antibiotics. In addition, the useof antibiotics in animal medicine and food production
must be regulated. The government, pharmacists,

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doctors, veterinarians, and agronomists must work together and establish national guidelines for dispensing
and prescribing antimicrobials. Adequate training on theproper prescription of antimicrobials must be given to
health professionals, and the population must be educated on the use of antimicrobials and the threat of
AMR.
Host susceptibility

Human susceptibility may influence the emergence of
infectious diseases through genetic polymorphisms, impaired immune function, malnutrition, AIDS, immunosuppressive conditions, aging, and others. Innate andacquired immune defenses help humans to fight against
infectious diseases. Genetic polymorphisms are potent
natural selective forces for pathogens to induce humandefenses against infection [134–136]. People sufferingfrom hemoglobinopathy S homozygosity develop more
severe Plasmodium falciparum infection than those whohave hemoglobin S heterozygotes [136, 137]. Malnutrition also increases the severity of some infectious diseases. Thus, malnourished children have a higher risk ofdeath from diarrhea, acute respiratory infections, andpossibly malaria [138]. According to the WHO, 26% of
the world’s malnourished children have been affected bypopulation displacements, natural disasters, wars, civil
disturbances, and population growth in the region [139].
Considering immunosuppressive conditions, people who
suffer from HIV/AIDS and cancers have a higher risk ofincreased disease severity. For example, the emergenceof fungi, such as Aspergillus spp., and other opportunistic agents that were previously uncommon or
unrecognized have increased in populations with cancer
chemotherapy, organ, and tissue transplantation, or
those infected with HIV [140]. It has also been shownthat more than 10% of cancers or transplants are either
colonized or infected with vancomycin-resistant enterococci [141].
Behavior changes

Human behavior has been an essential factor in thetransmission of emerging infectious pathogens. Understanding community behavior during epidemics is key toimproving control strategies [142]. Behavior changes areoften linked to culture, which refers to integrated
patterns of human behavior that include the beliefs, language, communications, actions, and organizations of racial, ethnic, religious, or social groups [143]. Many
infectious disease outbreaks sensibly spread because of
these factors. Since the occurrence of HIV/AIDS and
Ebola, for example, stigmatization, discrimination, ignorance, trust, and misinformation have been the root of
the spread of these diseases [144–146].

Sabin et al. Journal of Physiological Anthropology(2020) 39:29

Another situation concerns human behavior changes
related to conflicts. Conflicts of human behavior occur
where people are interconnected, and they result from avariety of attitudes, needs, beliefs, and ways that humans
react to different situations [147]. Conflict situations canpotentiate the (re)emergence and transmission of infectious diseases and are characterized by war or civil strife.
This usually leads to the displacement of large populations, interruption of primary care and immunization
programs, inadequate safe water supply, poor sanitation,and increased exposure to disease vectors [67–69]. According to UNHCR, 70.8 million people around theworld are forcibly displaced, constituting 41.3 million internally displaced people, 25.9 million refugees, and 3.5
million asylum-seekers [70] from Africa to the Middle
East, South Asia, and Europe [148, 149]. Millions ofpeople live in deplorable conditions, and healthcare facilities in host countries are overburdened; these conditions are suitable for the (re)emergence of infectious
diseases [70, 150]. Displaced populations are prone toviral and bacterial respiratory infections, nosocomial
antibiotic-resistant bacterial infections, cholera, cutaneous leishmaniasis, sexually transmitted infections, poliomyelitis, Chagas, schistosomiasis, hepatitis B and C,
meningococcal infections, and VBDs [57, 151–154]. It
would be better to (1) strengthen health systems in all
countries; (2) evaluate the detection, containment, treatment and control of infectious diseases, including theimplementation of surveillance systems; and (3) devise
strategies for epidemics and protect health-supporting
infrastructure and health workers during conflict situations and the aftermath, ultimately striving to achieve
health equity by key policy actors [68, 81, 151, 155, 156].
Factors related to the spread of COVID-19

COVID-19 is caused by a virus officially named severe
acute respiratory syndrome coronavirus-2 (SARS-Cov-2)[157, 158]. It is a new pandemic that started in December 2019 in Wuhan, Hubei Province of China [159–161].
The disease rapidly spread from Wuhan to the rest of
Mainland China and other parts of the world, affecting
at least 216 countries and territories, with 15,745,102
confirmed cases and 639,317 confirmed deaths as of 26
July 2020 [26, 162, 163]. Countries are reacting differently regarding the WHO-recommended preventive
measures (lockdown, test-trace isolation, wearing masks
and wearing them correctly, covering the mouth whencoughing and sneezing, keeping at least one meter of social distance, frequent washing of hands and avoiding
direct contact of the eyes, nose, and mouth [164]), making some countries more affected than others. Therefore,
the variation in the severity, frequency, and amplitude ofthis pandemic is due to the addition of several factors aswell as government policies.

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Human behavior is an essential determinant of thetransmission and spread of COVID-19 because the pandemic is spread by individual movements through large
droplets and contacts, and possibly by aerosols and fomites, from person to person with direct or indirect contact based on the experience with SARS-CoV and
MERS-CoV [165–167]. Self-protection may be the critical determinant for the prevention of COVID-19 [168]from one person to another because when a person
protects himself or herself, he or she also protects
others. Thus, understanding the collective behavior
between and within individual groups would be usefulfor decision-making. Behavioral differences regarding
COVID-19 containment measures such as lockdowns,
social distancing, and the use of facial masks may causesome individuals to be more at risk than others andsome countries to be more affected than others. Community behavior regarding preventive measures is influenced by cultural habits and misinformation. For
example, there was also a great deal of misinformation
and rumors that were widespread among the Chinese
population and abroad with regard to the virus origin[169–172], transmission mode, treatment, prevention,and control measures [173, 174]. In addition, the WHO
also created misinformation at the beginning of the pandemic by restricting the wearing of masks only to sickpeople showing symptoms and those who are caring forpeople with suspected infection [175]. Thus, some countries advised populations to wear masks only in enclosed
spaces such as shops or public transport. Additionally,
misinformation created from social media and websites
with no credible evidence has generated changes in the
behavior of many people, increasing the frequency andspread of COVID-19 locally, regionally, and internationally [176, 177]. In some countries, such as Japan,
Singapore, China, and South Korea, cultural habits—
such as the culture of mask-wearing, minimal personal
contact, improved hand sanitization, and fanciful suggestions that Japanese speakers emit fewer potentially virusladen droplets when talking than do speakers of otherlanguages—have helped to flatten the curve and to limit
the spread of COVID-19 in communities [178, 179]. On
the other hand, in Western countries such as Italy,
Spain, the United States, the United Kingdom, France,and many other countries where the culture of maskwearing is not a habit and where hugging, kissing, shaking hands, spending time together, and engaging in othersocial practices are common, the virus has spreadquickly [180, 181].
Another factor is the lack of transparency from government, and politicization of this outbreak by politicians has created confusion among communities andurged people not to follow prevention and control measures such as early detection, isolation, and treatment ofSabin et al. Journal of Physiological Anthropology(2020) 39:29

cases, contact tracing, and containment measures incommunities to prevent disease transmission within andbetween societies.
Host susceptibility includes aged individuals and otherindividuals with compromised immunity (such as highblood pressure, HIV, kidney diseases, diabetes, and cancers) who face higher risks of COVID-19 [182–184].
Immune-compromised individuals are in a highly
susceptible group, as their host defense is indigent; theirdefenses are already down, which could result in an increasingly poor prognosis for them [182]. Atmospherictemperature variation also plays a role in the spread of
COVID-19. It is known that winter is the flu season incold temperate countries because influenza viruses survive better in cold-dry weather with reduced ultraviolet
light. Reduced innate immunity is due to low levels ofvitamin D and melatonin and to staying indoors frequently during winter, increasing opportunities for thevirus to spread among people [185, 186]. COVID-19
started during winter, and it has been shown that the
local immune response in the nasal passage is reducedin people during cold winter, making them more susceptible to flu-like viruses [186]. This situation may makepeople living in such areas more vulnerable than thoseliving in tropical areas, leading to differences in thespatial distribution of COVID-19 worldwide.
High temperature may be a protective factor, as it can
provoke the evaporation of respiratory droplets, reducing
infectivity [187–189]. African and Asian tropical countries where high temperatures and high relative humidity
are common may be protected from COVID-19 becauseof their negative effect on the spread of the disease. On
the other hand, in Western countries where there are
low temperatures and high humidity, its transmission in
air-conditioned and temperate climatic environments
may be facilitated [187, 189]. Closed areas with low airflow and ventilation have been shown to play a role in
the increasing risk of COVID-19 infection [162], whichmakes developed countries at greater risk than developing countries. For instance, in developing countries,
apart from some places in large cities, most people live
under more natural atmospheric temperatures than dopeople in Western countries, where most houses arebuilt with air-conditioning systems. Living in airconditioned housing in addition to other factors, such as
being older, having respiratory diseases or diabetes, orbeing an immune-compromised person, may increase
the risk of transmission of COVID-19 [190–193].
High population density has also been associated withthe spread of epidemics, including COVID-19 [194]. In
the case of COVID-19, a high number of cases havebeen observed in overcrowded cities in countries such as
China, Japan, India, and the United States. Additionally,
countries with a high proportion of elderly populations,Page 7 of 12

such as Italy and Spain, have a higher risk of severity[181], and this risk increases when young and older
people live together [195].
International travel and trade have facilitated the
spread of COVID-19. In the past, humanity has survived
previous pandemics by infectious agents such as influenza viruses. However, the present one is unprecedented
in its capacity to take advantage of modern globalization,
allowing for the massive transborder spread at a surprising speed [196]. With the current international travel
and trade, it has been quite difficult to contain the
spread of this virus. Countries have tried to impose
travel restrictions and have reduced the exportation ratefrom mainland China, but these restrictions are insufficient to contain the geographic spread. Such measures
have led to discrimination against foreigners [197]. However, travel restrictions cannot be expected to fully apprehend the global expansion of COVID-19 but may
decrease the rate of case exports if enacted during theearly stages of the epidemic. This is because the onset ofsymptoms at the time of arrival is, in most cases, notdetectable as the virus is still under incubation period[198].
Delayed government response, inadequate infrastructures, and lack of biosafety and biosecurity awarenesshave also contributed to the transmission and spread of
COVID-19. Most countries have facilitated the transmission and spread of the disease due to inadequate preventive and/or mitigating strategies. Many countries
failed to prevent the epidemic in the beginning by delaying preventive measures. However, a few countries succeeded in controlling the outbreak by adopting aneffective mitigating strategy. South Korea and othercountries, such as Singapore, Hong Kong, Japan, andGermany, quickly responded after the first case byadopting a strategy involving the testing and isolation ofcases, contact tracing, and quarantining of suspectedcases to suppress the full transmission of the virus incommunities [199]. Additionally, countries that have experienced SARS-like epidemics such as Taiwan, Hong
Kong, and South Korea have successfully prevented the
spread of COVID-19 from China by adopting preventive
measures such as travel bans, closing of borders to nonresidents, and 14-day quarantines [200]. Regarding lockdown measures, in the beginning, some countries
delayed adopting this strategy because they sought toprevent harm to their economy (including some developed and developing countries) and because of poverty,
especially in developing countries, where people areforced to go out as they need to work for their daily
livelihood.
Inadequate infrastructures and equipment and lack ofawareness regarding laboratory biosafety and biosecurity
in certain countries, especially in developing countries,

Sabin et al. Journal of Physiological Anthropology(2020) 39:29

Page 8 of 12

have contributed to the spread of the disease in hospitals. Handling pathogens, especially viruses, may expose
health workers to a high risk of contamination if they
are not well trained. Thus, to prevent nosocomial infections, sufficient training of health workers in the principles and procedures of good laboratory practice (GLP) is
needed. Health workers should be well trained on biohazards and the safe management of biological agents inthe laboratory. Laboratory workers must have sufficientknowledge and experience about how to handle emerging pathogens safely and securely [201, 202]. However,good awareness of GLPs must be reinforced by the availability of adequate equipment and infrastructures. In
many countries, health professionals are working without PPE and are exposed to the infection. Thus, the lackof awareness about COVID-19 preventive measurescause health workers to be exposed and become infected. Additionally, the lack of testing kits, ventilators,
and other equipment is impeding some countries fromadopting an effective testing and tracing strategy andpreventing deaths among severe cases.

Funding
This work was supported by Grants-in-Aid for Scientific Research (KAKENHI
No. JP19K24679) from the Japan Society for the Promotion of Science.

Conclusions
Human activities are still the significant determinants ofthe transmission and spread of (re)emerging infectious
diseases. To date, we are still dealing with the COVID19 pandemic, and it is challenging to predict when it willend. However, it is possible to face the disease or to reduce the risk of its transmission and spread by changing
human behavior and implementing better early warning
systems and effective disease control and prevention.
Thus, effective global surveillance, global political will,
and multidisciplinary collaboration of all stakeholders
will be helpful in responding to any future threats.

References
1. World Health Organization. Division of emerging other communicablediseases surveillance control emerging infectious diseases. Geneva: World
Health Organization; 1997.
2. Mackey TK, Liang BA. Lessons from SARS and H1N1/A: employing a WHOWTO forum to promote optimal economic-public health pandemic
response. J Public Health Policy. 2012;33:119–30.
3. Woolhouse ME, Taylor LH, Haydon DT. Population biology of multihost
pathogens. Science. 2001;292:1109–12.
4. Slingenbergh JI, Gilbert M, de Balogh KI, Wint W. Ecological sources ofzoonotic diseases. Rev Sci Tech. 2004;23:467–84.
5. Heymann DL, Dixon M. Infections at the animal/human interface: shifting
the paradigm from emergency response to prevention at source. Curr Top
Microbiol Immunol. 2013;366:207–15.
6. Jones BA, Grace D, Kock R, Alonso S, Rushton J, Said MY, et al. Zoonosis
emergence linked to agricultural intensification and environmental change.
Proc Natl Acad Sci U S A. 2013;110:8399–404.
7. Jones KE, Patel NG, Levy MA, Storeygard A, Balk D, Gittleman JL, et al.
Global trends in emerging infectious diseases. Nature. 2008;451:990–3.
8. Murphy FA. Emerging zoonoses: the challenge for public health andbiodefense. Prev Vet Med. 2008;86:216–23.
9. Taylor LH, Latham SM, Woolhouse ME. Risk factors for human disease
emergence. Philos Trans R Soc Lond Ser B Biol Sci. 2001;356:983–9.
10. Barry L. A national food-safety initiative : report to the president may 1997.
Washington, DC: National Academies Press; 1998.
11. Marwick C. Investigators present latest findings on Hong Kong 'bird flu' to
the FDA. JAMA. 1998;279:643–4.
12. Centers for Disease Control Prevention. Outbreak of West Nile-like viral
encephalitis--New York, 1999. MMWR Morb Mortal Wkly Rep. 1999;48:845.
13. Rezza G, Nicoletti L, Angelini R, Romi R, Finarelli AC, Panning M, et al.
Infection with chikungunya virus in Italy: an outbreak in a temperate region.
Lancet. 2007;370:1840–6.
14. van der Hoek W, Dijkstra F, Schimmer B, Schneeberger PM, Vellema P,
Wijkmans C, et al. Q fever in the Netherlands: an update on theepidemiology and control measures. Euro Surveill. 2010;15:19520.
15. van der Hoek W, Morroy G, Renders NH, Wever PC, Hermans MH, Leenders
AC, et al. Epidemic Q fever in humans in the Netherlands. Adv Exp Med
Biol. 2012;984:329–64.
16. Severe acute respiratory syndrome (SARS). Wkly Epidemiol Rec. 2003;78:
81–3.
17. Pugliese A, Beltramo T, Torre D. Emerging and re-emerging viral infections
in Europe. Cell Biochem Funct. 2007;25:1–13.

Abbreviations
AIDS: Acquired immunodeficiency syndrome; AMR: Antimicrobial resistance;
CA-MRSA: Community-associated methicillin-resistant Staphylococcus aureus;
CDC: Centers for Disease Control and Prevention; COVID-19: Coronavirus
disease 2019; CTX-M: Cefotaxime-M; DRC: The Democratic Republic of theCongo; EIDs: Emerging infectious diseases; EVD: Ebola virus disease;
FWBDs: Food- and water-borne diseases; HIV: Human immunodeficiency
virus; MARS: Middle East respiratory syndrome; MDR: Multidrug-resistant;
MRSA: Methicillin-resistant Staphylococcus aureus; SARS: Severe acuterespiratory syndrome; SDGs: Sustainable Development Goals;
TB: Tuberculosis; EU: European Union; UK: United Kingdom of Great Britain
and Northern Ireland; UNHCR: The Office of the United Nations HighCommissioner for Refugees; US: The United States; VBDs: Vector-borne
diseases; WHO: World Health Organization
Acknowledgements
Not applicable.
Authors’ contributions
NSS and TY participated in the design of the study; NSS, ASC, and SVS
searched the literature, selected the reviewed articles, and wrote the draft ofthe manuscript. HA, HI, and TN also contributed to the design of the study
and wrote the manuscript. All authors approved the final version of themanuscript.

Availability of data and materials
Not applicable.
Ethics approval and consent to participate
Not applicable.
Consent for publication
Not applicable.
Competing interests
The authors declare that they have no competing interests.
Author details
1
Department of International Health and Medical Anthropology, Institute ofTropical Medicine, Nagasaki University, 1-12-4 Sakamoto, Nagasaki 852-8523,
Japan. 2Graduate School of Biomedical Sciences, Nagasaki University,
Nagasaki, Japan. 3Leading Program, Graduate School of Biomedical Sciences,
Nagasaki University, Nagasaki, Japan. 4Department of Human Science, Facultyof Design, Kyushu University, Fukuoka, Japan. 5Department of Public Health,Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki,
Japan.
Received: 21 May 2020 Accepted: 16 September 2020

Sabin et al. Journal of Physiological Anthropology(2020) 39:29

18. Snell NJ. Novel and re-emerging respiratory infections. Expert Rev AntiInfect Ther. 2004;2:405–12.
19. World Health Organization. Middle East respiratory syndrome
coronavirus (MERS-CoV). 2019. https://www.who.int/en/news-room/factsheets/detail/middle-east-respiratory-syndrome-coronavirus-(mers-cov).
Accessed 26 Jul 2020.
20. World Health Organization. Influenza (avian and other zoonotic). 2018.
https://www.who.int/news-room/fact-sheets/detail/influenza-(avian-andother-zoonotic) . Accessed 26 Jul 2020.
21. Fouchier RA, Schneeberger PM, Rozendaal FW, Broekman JM, Kemink SA,
Munster V, et al. Avian influenza A virus (H7N7) associated with human
conjunctivitis and a fatal case of acute respiratory distress syndrome. Proc
Natl Acad Sci U S A. 2004;101:1356–61.
22. Avian influenza A/(H7N2) outbreak in the United Kingdom. Euro Surveill.
2007;12:E070531.2.
23. Gao R, Cao B, Hu Y, Feng Z, Wang D, Hu W, et al. Human infection with anovel avian-origin influenza A (H7N9) virus. N Engl J Med. 2013;368:1888–97.
24. World Health Organization. Ebola situation report. 2016. https://apps.who.
int/ebola/current-situation/ebola-situation-report-16-march-2016. Accessed
26 Jul 2020.
25. World Health Organization. Ebola virus disease? Democratic republic of theCongo. 2020. https://www.who.int/csr/don/12-March-2020-ebola-drc/en/.
Accessed 16 Jul 2020.
26. World Health Organization. Coronavirus disease (COVID-2019) situation
reports. 2020. https://www.who.int/emergencies/diseases/novelcoronavirus-2019/situation-reports. Accessed 26 Jul 2020.
27. Wolfe ND, Dunavan CP, Diamond J. Origins of major human infectious
diseases. Nature. 2007;447:279–83.
28. Snieszko SF. The effects of environmental stress on outbreaks of infectious
diseases of fishes. J Fish Biol. 1974;6:197–208.
29. Lederberg J, Hamburg MA, Smolinski MS. Microbial threats to health:emergence, detection, and response. Washington, DC: National Academies
Press; 2003.
30. Chareonsook O, Foy HM, Teeraratkul A, Silarug N. Changing epidemiology
of dengue hemorrhagic fever in Thailand. Epidemiol Infect. 1999;122:161–6.
31. Frieden TR, Tappero JW, Dowell SF, Hien NT, Guillaume FD, Aceng JR. Safercountries through global health security. Lancet. 2014;383:764–6.
32. World Health Organization. Globalization and infectious diseases: a reviewof the linkages. 2004. https://www.who.int/tdr/publications/documents/seb_
topic3.pdf. Accessed 26 Jul 2020.
33. Oshitani H. Globalization and emerging infectious diseases. Nihon Rinsho.
2016;74:1956–61.
34. Vignier N, Bouchaud O. Travel, migration and emerging infectious diseases.
EJIFCC. 2018;29:175–9.
35. Delisle E, Rousseau C, Broche B, Leparc-Goffart I, L'Ambert G, Cochet A, et al.
Chikungunya outbreak in Montpellier, France, September to October 2014.
Euro Surveill. 2015;20:21108.
36. Jacob E. Coronavirus: trois premiers cas confirmes en France, deux d'entre
eux vont bien. 2020. https://www.lefigaro.fr/sciences/coronavirus-troispremiers-cas-confirmes-en-france-20200124. Accessed 26 Jul 2020.
37. Marchand E, Prat C, Jeannin C, Lafont E, Bergmann T, Flusin O, et al.
Autochthonous case of dengue in France, October 2013. Euro Surveill. 2013;
18:20661.
38. van den Berg T. The role of the legal and illegal trade of live birds andavian products in the spread of avian influenza. Rev Sci Tech. 2009;28:
93–111.
39. World Health Organization. International health regulations (2005). 2016.
https://www.who.int/ihr/publications/9789241580496/en/. Accessed 26 Jul
2020.
40. World Trade Organization. WTO agreements & public health: a joint study
by the WHO and the WTO Secretariat. 2002. https://www.wto.org/english/
res_e/booksp_e/who_wto_e.pdf. Accessed 26 Jul 2020.
41. Chinazzi M, Davis JT, Ajelli M, Gioannini C, Litvinova M, Merler S, et al. The
effect of travel restrictions on the spread of the 2019 novel coronavirus(COVID-19) outbreak. Science. 2020;368:395–400.
42. Ferguson NM, Cummings DA, Fraser C, Cajka JC, Cooley PC, Burke DS.
Strategies for mitigating an influenza pandemic. Nature. 2006;442:448–52.
43. Mateus AL, Otete HE, Beck CR, Dolan GP, Nguyen-Van-Tam JS.
Effectiveness of travel restrictions in the rapid containment of human
influenza: a systematic review. Bull World Health Organ.
2014;92:868–0D.

Page 9 of 12

44. Wood JG, Zamani N, MacIntyre CR. Effects of internal border control on
spread of pandemic influenza. 2010. https://www.nc.cdc.gov/eid/article/13/
7/06-0740_article. Accessed 26 Jul 2020.
45. Torner N. Risky trade: infectious disease in the era of global trade. J
Epidemiol Community Health. 2007;61:926.
46. Hautier Y, Tilman D, Isbell F, Seabloom EW, Borer ET, Reich PB. Plant
ecology. Anthropogenic environmental changes affect ecosystem stability
via biodiversity. Science. 2015;348:336–40.
47. World Health Organization. Global environmental change. 2020. https://www.who.int/globalchange/environment/en/. Accessed 26 Jul 2020.
48. National Academy of Sciences. Infectious disease emergence: microbial
evolution and co-adaptation. England: National Academies Press; 2009.
49. Nava A, Shimabukuro JS, Chmura AA, Luz SLB. The impact of global
environmental changes on infectious disease emergence with a focus on
risks for Brazil. ILAR J. 2017;58:393–400.
50. Morens DM, Fauci AS. Emerging infectious diseases: threats to humanhealth and global stability. PLoS Pathog. 2013;9:e1003467.
51. Morse SS. Factors and determinants of disease emergence. Rev Sci Tech.
2004;23:443–51.
52. Galvani AP, Bauch CT, Anand M, Singer BH, Levin SA. Human-environment
interactions in population and ecosystem health. Proc Natl Acad Sci U S A.
2016;113:14502–6.
53. Semenza JC, Ebi KL. Climate change impact on migration, travel, travel
destinations and the tourism industry. J Travel Med. 2019;26:taz026.
54. Wu X, Lu Y, Zhou S, Chen L, Xu B. Impact of climate change on humaninfectious diseases: empirical evidence and human adaptation. Environ Int.
2016;86:14–23.
55. UNHCR. Environment, disasters and climate change. 2020. http://www.
unhcr.org/environment-disasters-and-climate-change.html. Accessed 26 Jul
2020.
56. Barbour AG, Fish D. The biological and social phenomenon of Lyme
disease. Science. 1993;260:1610–6.
57. Cisse G, Alves MJ, Confalonieri U. Climate-sensitive infectious diseases.
In: UNEP, editor. The adaptation gap report 2018. Nairobi: UNEP; 2018.
p. 49–59.
58. McIntyre KM, Setzkorn C, Hepworth PJ, Morand S, Morse AP, Baylis M.
Systematic assessment of the climate sensitivity of important human anddomestic animals pathogens in Europe. Sci Rep. 2017;7:7134.
59. World Health Organization. Vector-borne diseases. Geneva: World HealthOrganization; 2020.
60. Caminade C, McIntyre KM, Jones AE. Impact of recent and future climatechange on vector-borne diseases. Ann N Y Acad Sci. 2019;1436:157–73.
61. Choi SY, Kim JH, Kim J. World outbreak trend of infectious diseases withsurveillance. J Bacteriol. 2019;49:141–51.
62. Ciota AT, Keyel AC. The role of temperature in transmission of zoonotic
arboviruses. Viruses. 2019;11:1013.
63. Cissé G. Food-borne and water-borne diseases under climate change inlow- and middle-income countries: further efforts needed for reducing
environmental health exposure risks. Acta Trop. 2019;194:181–8.
64. Fenollar F, Mediannikov O. Emerging infectious diseases in Africa in the 21st
century. New Microbes New Infect. 2018;26:S10–8.
65. Morse SS. Factors in the emergence of infectious diseases. Emerg Infect Dis.
1995;1:7–15.
66. Department of Economic Social Affairs Disability. Envision2030: 17 goals totransform the world for persons with disabilities. 2020. https://www.un.org/
development/desa/disabilities/envision2030.html. Accessed 26 Jul 2020.
67. Rockström J, Williams J, Daily G, Noble A, Matthews N, Gordon L, et al.
Sustainable intensification of agriculture for human prosperity and global
sustainability. Ambio. 2017;46:4–17.
68. Rohr JR, Barrett CB, Civitello DJ, Craft ME, Delius B, DeLeo GA, et al.
Emerging human infectious diseases and the links to global foodproduction. Nat Sustain. 2019;2:445–56.
69. Shah HA, Huxley P, Elmes J, Murray KA. Agricultural land-uses consistently
exacerbate infectious disease risks in Southeast Asia. Nat Commun. 2019;10:4299.
70. Mayer JD. Geography, ecology and emerging infectious diseases. Soc Sci
Med. 2000;50:937–52.
71. Morse SS, Schluederberg A. From the national institute of allergy andinfectious diseases, the fogarty international center of the national institutesof health, and the rockefeller university. Emerging viruses: the evolution ofviruses and viral diseases. J Infect Dis. 1990;162:1–7.

Sabin et al. Journal of Physiological Anthropology(2020) 39:29

72. Wolfe ND, Daszak P, Kilpatrick AM, Burke DS. Bushmeat hunting,deforestation, and prediction of zoonotic disease. Emerg Infect Dis.
2005;11:6.
73. Domestic animals and infectious diseases of man. J Am Med Assoc. 1902;
XXXVIII:1520–1.
74. World Health Organization. Animal–human interface for health. https://www.who.int/myanmar/activities/animal%2D%2Dhuman-interface-forhealth. Accessed 26 Jul 2020.
75. Roche B, Guégan JF. Ecosystem dynamics, biological diversity and emerging
infectious diseases. C R Biol. 2011;334:385–92.
76. Knobler S, Mahmoud A, Lemon S, Pray L. The impact of globalization on
infectious disease emergence and control exploring the consequences andopportunities workshop summary. Washington, DC: National Academies
Press; 2006.
77. Kurpiers LA, Schulte-Herbrüggen B, Ejotre I, Reeder DM. Bushmeat andemerging infectious diseases: lessons from africa. In: Angelici FM, editor.
Problematic wildlife: a cross-disciplinary approach. Cham: Springer
International Publishing; 2016. p. 507–51.
78. Morand S, McIntyre KM, Baylis M. Domesticated animals and humaninfectious diseases of zoonotic origins: domestication time matters. InfectGenet Evol. 2014;24:76–81.
79. Hoberg EP, Alkire NL, de Queiroz A, Jones A. Out of Africa: origins of the
Taenia tapeworms in humans. Proc Biol Sci. 2001;268:781–7.
80. Childs JE, Gordon ER. Surveillance and control of zoonotic agents prior todisease detection in humans. Mt Sinai J Med. 2009;76:421–8.
81. Angeletti S, Ceccarelli G, Vita S, Dicuonzo G, Lopalco M, Dedej E, et al.
Unusual microorganisms and antimicrobial resistances in a group of Syrian
migrants: sentinel surveillance data from an asylum seekers centre in Italy.
Travel Med Infect Dis. 2016;14:115–22.
82. Kilonzo C, Stopka TJ, Chomel B. Illegal animal and (bush) meat tradeassociated risk of spread of viral infections. In: Singh SK, editor. Viral
infections and global change chapter: 10 Illegal animal and (bush) meat
trade associated risk of spread of viral infection. Hoboken: Wiley; 2013. p.
179–94.
83. Institute of Medicine. Forum on emerging infections. In: Harrison PF,
Lederberg J, editors. Antimicrobial resistance: issues and options.
Washington, DC: The National Academies Press; 1998. p. 128.
84. Boucher HW, Talbot GH, Bradley JS, Edwards JE, Gilbert D, Rice LB, et al. Badbugs, no drugs: no ESKAPE! an update from the infectious diseases societyof America. Clin Infect Dis. 2009;48:1–12.
85. Spellberg B, Guidos R, Gilbert D, Bradley J, Boucher HW, Scheld WM, et al.
The epidemic of antibiotic-resistant infections: a call to action for the
medical community from the infectious diseases society of America. Clin
Infect Dis. 2008;46:155–64.
86. Taubes G. The bacteria fight back. Science. 2008;321:356–61.
87. Review on Antimicrobial Resistance. Tackling drug-resistant infections
globally: final report and recommendations. Review on Antimicrobial
Resistance; 2016.
88. United Nations Interagency Coordination Group on Antimicrobial
Resistance. AMR framework for action supported by the IACG. Working
document. Geneva: United Nations Interagency Coordination Group on
Antimicrobial Resistance; 2017.
89. World Bank. Drug-resistant infections: a threat to our economic future(discussion draft). Washington, DC: World Bank; 2016.
90. Centers for Disease Control and Prevention (CDC). Notes from the field:
New Delhi metallo-beta-lactamase-producing Escherichia coli associatedwith endoscopic retrograde cholangiopancreatography - Illinois, 2013.
MMWR Morb Mortal Wkly Rep. 2014;62:1051.
91. Centers for Disease Control and Prevention (CDC). Notes from the field:
hospital outbreak of carbapenem-resistant Klebsiella pneumoniae producing
New Delhi metallo-beta-lactamase--Denver, Colorado, 2012. MMWR Morb
Mortal Wkly Rep. 2013;62:108.
92. Centers for Disease Control and Prevention (CDC). Carbapenem-resistant
Klebsiella pneumoniae associated with a long-term care facility—West
Virginia, 2009-2011. MMWR Morb Mortal Wkly Rep. 2011;60:1418–20.
93. Doi Y, Paterson DL. Carbapenemase-producing Enterobacteriaceae. Semin
Respir Crit Care Med. 2015;36:74–84.
94. McGann P, Hang J, Clifford RJ, Yang Y, Kwak YI, Kuschner RA, et al.
Complete sequence of a novel 178-kilobase plasmid carrying bla(NDM-1) ina Providencia stuartii strain isolated in Afghanistan. Antimicrob Agents
Chemother. 2012;56:1673–9.

Page 10 of 12

95. Ochman H, Moran NA. Genes lost and genes found: evolution of bacterial
pathogenesis and symbiosis. Science. 2001;292:1096–9.
96. Usluer G, Ozgunes I, Leblebicioglu H. A multicenter point-prevalence study:
antimicrobial prescription frequencies in hospitalized patients in Turkey.
Ann Clin Microbiol Antimicrob. 2005;4:16.
97. Saleh N, Awada S, Awwad R, Jibai S, Arfoul C, Zaiter L, et al. Evaluation of
antibiotic prescription in the Lebanese community: a pilot study. Infect Ecol
Epidemiol. 2015;5:27094.
98. Neu HC. The crisis in antibiotic resistance. Science. 1992;257:1064–73.
99. Cohen ML. Changing patterns of infectious disease. Nature. 2000;406:762–7.
100. European Centre for Disease Prevention Control. Antimicrobial resistancesurveillance in Europe 2015. Annual report of the European antimicrobial
resistance surveillance network (EARS-Net). Stockholm: ECDC. p. 2015.
101. Nakou A, Woodhead M, Torres A. MRSA as a cause of community-acquired
pneumonia. Eur Respir J. 2009;34:1013–4.
102. Vardakas KZ, Matthaiou DK, Falagas ME. Incidence, characteristics andoutcomes of patients with severe community acquired-MRSA pneumonia.
Eur Respir J. 2009;34:1148–58.
103. Livermore DM, Canton R, Gniadkowski M, Nordmann P, Rossolini GM, Arlet
G, et al. CTX-M: changing the face of ESBLs in Europe. J Antimicrob
Chemother. 2007;59:165–74.
104. Queenan AM, Bush K. Carbapenemases: the versatile beta-lactamases. Clin
Microbiol Rev. 2007;20:440–58 table of contents.
105. Peleg AY, Seifert H, Paterson DL. Acinetobacter baumannii: emergence of a
successful pathogen. Clin Microbiol Rev. 2008;21:538–82.
106. Basu A, Garg P, Datta S, Chakraborty S, Bhattacharya T, Khan A, et al. Vibrio
cholerae O139 in Calcutta, 1992-1998: incidence, antibiograms, andgenotypes. Emerg Infect Dis. 2000;6:139–47.
107. Faruque SM, Abdul Alim AR, Rahman MM, Siddique AK, Sack RB, Albert MJ.
Clonal relationships among classical Vibrio cholerae O1 strains isolated
between 1961 and 1992 in Bangladesh. J Clin Microbiol. 1993;31:2513–6.
108. Mukhopadhyay AK, Garg S, Mitra R, Basu A, Rajendran K, Dutta D, et al.
Temporal shifts in traits of Vibrio cholerae strains isolated from hospitalized
patients in Calcutta: a 3-year (1993 to 1995) analysis. J Clin Microbiol. 1996;
34:2537–43.
109. Sharma C, Maiti S, Mukhopadhyay AK, Basu A, Basu I, Nair GB, et al. Uniqueorganization of the CTX genetic element in Vibrio cholerae O139 strains
which reemerged in Calcutta, India, in September 1996. J Clin Microbiol.
1997;35:3348–50.
110. European Centre for Disease PC. Tuberculosis surveillance and monitoring inEurope 2012. 2020. https://www.ecdc.europa.eu/en/publications-data/
tuberculosis-surveillance-and-monitoring-europe-2012. Accessed 26 Jul 2020.
111. Loddenkemper R, Sotgiu G, Mitnick CD. Cost of tuberculosis in the era ofmultidrug resistance: will it become unaffordable? Eur Respir J. 2012;40:9–11.
112. Vidaver AK. Uses of antimicrobials in plant agriculture. Clin Infect Dis. 2002;
34:S107–10.
113. Aarestrup F. Sustainable farming: get pigs off antibiotics. Nature. 2012;486:
465–6.
114. Addis Z, Kebede N, Worku Z, Gezahegn H, Yirsaw A, Kassa T. Prevalence andantimicrobial resistance of Salmonella isolated from lactating cows and incontact humans in dairy farms of Addis Ababa: a cross sectional study. BMC
Infect Dis. 2011;11:222.
115. Doyle ME. Multidrug-resistant pathogens in the food supply. Foodborne
Pathog Dis. 2015;12:261–79.
116. Fortini D, Fashae K, Garcia-Fernandez A, Villa L, Carattoli A. Plasmidmediated quinolone resistance and beta-lactamases in Escherichia coli fromhealthy animals from Nigeria. J Antimicrob Chemother. 2011;66:1269–72.
117. Kikuvi GM, Ombui JN, Mitema ES. Serotypes and antimicrobial resistanceprofiles of Salmonella isolates from pigs at slaughter in Kenya. J Infect Dev
Ctries. 2010;4:243–8.
118. Mezali L, Hamdi TM. Prevalence and antimicrobial resistance of Salmonella
isolated from meat and meat products in Algiers (Algeria). Foodborne
Pathog Dis. 2012;9:522–9.
119. Mitema ES, Kikuvi GM, Wegener HC, Stohr K. An assessment of antimicrobial
consumption in food producing animals in Kenya. J Vet Pharmacol Ther.
2001;24:385–90.
120. Simango C, Rukure G. Potential sources of Campylobacter species in thehomes of farmworkers in Zimbabwe. J Trop Med Hyg. 1991;94:388–92.
121. Wall B, Mateus A, Marshall L, Pfeiffer D, Lubroth J, Ormel H, et al. Drivers,
dynamics and epidemiology of antimicrobial resistance in animal
production. Rome: Food and Agriculture Organization; 2016.

Sabin et al. Journal of Physiological Anthropology(2020) 39:29

122. Witte W. Medical consequences of antibiotic use in agriculture. Science.
1998;279:996–7.
123. Byarugaba DK. A view on antimicrobial resistance in developing countries
and responsible risk factors. Int J Antimicrob Agents. 2004;24:105–10.
124. Laxminarayan R, Duse A, Wattal C, Zaidi AK, Wertheim HF, Sumpradit N,
et al. Antibiotic resistance-the need for global solutions. Lancet Infect Dis.
2013;13:1057–98.
125. Okeke IN, Klugman KP, Bhutta ZA, Duse AG, Jenkins P, O'Brien TF, et al.
Antimicrobial resistance in developing countries. Part II: strategies forcontainment. Lancet Infect Dis. 2005;5:568–80.
126. World Health Organization. Assessing non-prescription and inappropriate
use of antibiotics: report on survey. 2019. https://apps.who.int/iris/bitstream/
handle/10665/312306/9789289054089-eng.pdf?sequence=1&isAllowed=y.
Accessed 26 Jul 2020.
127. Alliance for the Prudent Use of Antibiotics. Executive summary: selectfindings, conclusions, and policy recommendations. Clin Infect Dis. 2005;41:
S224–7.
128. Goossens H, Ferech M, Vander Stichele R, Elseviers M. Outpatient antibiotic
use in Europe and association with resistance: a cross-national databasestudy. Lancet. 2005;365:579–87.
129. Kunin CM. Resistance to antimicrobial drugs—a world wide calamity. Ann
Intern Med. 1993;118:557–61.
130. Okeke IN, Lamikanra A, Edelman R. Socioeconomic and behavioral factors
leading to acquired bacterial resistance to antibiotics in developing
countries. Emerg Infect Dis. 1999;5:18–27.
131. Okeke IN, Laxminarayan R, Bhutta ZA, Duse AG, Jenkins P, O'Brien TF, et al.
Antimicrobial resistance in developing countries. Part I: recent trends andcurrent status. Lancet Infect Dis. 2005;5:481–93.
132. Fridkin S, Baggs J, Fagan R, Magill S, Pollack LA, Malpiedi P, et al. Vital signs:
improving antibiotic use among hospitalized patients. MMWR Morb Mortal
Wkly Rep. 2014;63:194–200.
133. Marston HD, Dixon DM, Knisely JM, Palmore TN, Fauci AS. Antimicrobial
resistance. JAMA. 2016;316:1193–204.
134. Hill AV. The immunogenetics of human infectious diseases. Annu Rev
Immunol. 1998;16:593–617.
135. Lederberg JJBS. Haldane (1949) on infectious disease and evolution.
Genetics. 1999;153:1–3.
136. Weatherall DJ. The genetics of common diseases: the implications of
population variability. CIBA Found Symp. 1996;197:300–8 discussion 8-11.
137. Weatherall DJ. Host genetics and infectious disease. Parasitology. 1996;112:
S23–9.
138. Rice AL, Sacco L, Hyder A, Black RE. Malnutrition as an underlying cause ofchildhood deaths associated with infectious diseases in developing
countries. Bull World Health Organ. 2000;78:1207–21.
139. World Health Organization. Fifty-third world health assembly, provisional
agenda item 12.4, A53/7. Infant and young child nutrition, Report by the
director-general. 2000. https://apps.who.int/gb/archive/pdf_files/WHA53/ea7.
pdf. Accessed 26 Jul 2020.
140. Dixon DM, McNeil MM, Cohen ML, Gellin BG, La Montagne JR. Fungal
infections: a growing threat. Public Health Rep. 1996;111:226–35.
141. Morris JG Jr, Potter M. Emergence of new pathogens as a function ofchanges in host susceptibility. Emerg Infect Dis. 1997;3:435–41.
142. Yan QL, Tang SY, Xiao YN. Impact of individual behaviour change on the
spread of emerging infectious diseases. Stat Med. 2018;37:948–69.
143. Rockville. Improving cultural competence. 2020. https://store.samhsa.gov/
sites/default/files/d7/priv/sma14-4849.pdf. Accessed 26 Jul 2020.
144. Mawar N, Saha S, Pandit A, Mahajan U. The third phase of HIV pandemic:
social consequences of HIV/AIDS stigma & discrimination & future needs.
Indian J Med Res. 2005;122:471–84.
145. Vinck P, Pham PN, Bindu KK, Bedford J, Nilles EJ. Institutional trust andmisinformation in the response to the 2018–19 Ebola outbreak in NorthKivu, DR Congo: a population-based survey. Lancet Infect Dis. 2019;19:529–
36.
146. Yin W, Couzin O. HIV-related stigma and discrimination in China. In: Wu Z,
Wang Y, Detels R, Bulterys M, McGoogan JM, editors. HIV/AIDS in China:
epidemiology, prevention and treatment. Singapore: Springer; 2020. p. 515–
41.
147. Agnieszka R, Jan OA. Conflicts of human behavior in organizations and theinfluence of human factor on innovation. IOSR J Bus Manag. 2016;18:35–41.
148. Bloom DE, Cadarette D. Infectious disease threats in the twenty-first century:
strengthening the global response. Front Immunol. 2019;10:549.

Page 11 of 12149. Gayer M, Legros D, Formenty P, Connolly MA. Conflict and emerging
infectious diseases. Emerg Infect Dis. 2007;13:1625–31.
150. Sharara SL, Kanj SS. War and infectious diseases: challenges of the Syrian
civil war. PLoS Pathog. 2014;10:e1004438.
151. Abbas M, Aloudat T, Bartolomei J, Carballo M, Durieux-Paillard S, Gabus L,
et al. Migrant and refugee populations: a public health and policy
perspective on a continuing global crisis. Antimicrob Resist Infect Control.
2018;7:113.
152. Heywood AE, Castelli F, Greenaway C. Migration health: highlights from
inaugural international society of travel medicine (ISTM) conference on
migration health. Curr Infect Dis Rep. 2019;21:48.
153. Seedat F, Hargreaves S, Nellums LB, Ouyang J, Brown M, Friedland JS. How
effective are approaches to migrant screening for infectious diseases in
Europe? A systematic review. Lancet Infect Dis. 2018;18:NIMe259–71.
154. UNHCR. Figures at a glance. 2020. http://www.unhcr.org/figures-at-a-glance.
html. Accessed 26 Jul 2020.
155. Nimer NA. A review on emerging and reemerging of infectious diseases in
Jordan: the aftermath of the Syrian crises. Can J Infect Dis Med Microbiol.
2018;2018:8679174.
156. Ozaras R, Leblebicioglu H, Sunbul M, Tabak F, Balkan II, Yemisen M, et al.
The Syrian conflict and infectious diseases. Expert Rev Anti-Infect Ther. 2016;
14:547–55.
157. Centers for Disease Control Prevention. Coronavirus disease 2019 (COVID2019). 2020. https://www.cdc.gov/coronavirus/2019-ncov/cdcresponse/
about-COVID-19.html. Accessed 1 Sep 2020.
158. World Health Organization. Naming the coronavirus disease (COVID-19) andthe virus that causes it. 2020. https://www.who.int/emergencies/diseases/
novel-coronavirus-2019/technical-guidance/naming-the-coronavirus-disease(covid-2019)-and-the-virus-that-causes-it. Accessed 17 Aug 2020.
159. Gorbalenya AE, Baker SC, Baric RS, de Groot RJ, Drosten C, Gulyaeva AA,
et al. Severe acute respiratory syndrome-related coronavirus: the species
and its viruses—a statement of the Coronavirus Study Group. bioRxiv. 2020.
https://doi.org/10.1101/2020.02.07.937862.
160. Lu H, Stratton CW, Tang YW. Outbreak of pneumonia of unknown etiology
in Wuhan, China: the mystery and the miracle. J Med Virol. 2020;92:401–2.
161. World Health Organization. WHO director-general's remarks at the media
briefing on 2019-nCoV on 11 February 2020. 2020. https://www.who.int/dg/
speeches/detail/who-director-general-s-remarks-at-the-media-briefing-on-2
019-ncov-on-11-february-2020. Accessed 26 Jul 2020.
162. Novel Coronavirus Pneumonia Emergency Response Epidemiology Team.
The epidemiological characteristics of an outbreak of 2019 novel
coronavirus diseases (COVID-19)—China, 2020. China CDC Wkly. 2020;2:113–
22.
163. World Health Organization. WHO Coronavirus disease (COVID-19)
dashboard. 2020. https://covid19.who.int/. Accessed 26 Jul 2020.
164. World Health Organization. Home care for patients with COVID-19
presenting with mild symptoms and management of their contacts. 2020.
https://www.who.int/publications/i/item/home-care-for-patients-withsuspected-novel-coronavirus-(ncov)-infection-presenting-with-mildsymptoms-and-management-of-contacts. Accessed 26 Jul 2020.
165. Hui DS, Azhar EI, Kim YJ, Memish ZA, Oh MD, Zumla A. Middle East
respiratory syndrome coronavirus: risk factors and determinants of primary,household, and nosocomial transmission. Lancet Infect Dis. 2018;18:e217–
27.
166. Peiris JSM, Guan Y, Yuen KY. Severe acute respiratory syndrome. Nat Med.
2004;10:S88–97.
167. Riou J, Althaus CL. Pattern of early human-to-human transmission of Wuhan
2019 novel coronavirus (2019-nCoV), December 2019 to January 2020. Euro
Surveill. 2020;25:2000058.
168. Wang Y, Wu W, Cheng Z, Tan X, Yang Z, Zeng X, et al. Super-factors
associated with transmission of occupational COVID-19 infection among
healthcare staff in Wuhan, China. J Hosp Infect. 2020;106:25–34.
169. Li X, Zai J, Zhao Q, Nie Q, Li Y, Foley BT, et al. Evolutionary history, potential
intermediate animal host, and cross-species analyses of SARS-CoV-2. J Med
Virol. 2020;92:602–11.
170. Liu P, Jiang J-Z, Wan X-F, Hua Y, Wang X, Hou F, et al. Are pangolins theintermediate host of the 2019 novel coronavirus (2019-nCoV)? bioRxiv. 2020.
https://doi.org/10.1101/2020.02.18.954628.
171. Lu R, Zhao X, Li J, Niu P, Yang B, Wu H, et al. Genomic characterisation andepidemiology of 2019 novel coronavirus: implications for virus origins andreceptor binding. Lancet. 2020;395:565–74.

Sabin et al. Journal of Physiological Anthropology(2020) 39:29

172. Zhou P, Yang XL, Wang XG, Hu B, Zhang L, Zhang W, et al. A pneumonia
outbreak associated with a new coronavirus of probable bat origin. Nature.
2020;579:270–3.
173. U. S. Food and Drug Administration. FDA warns consumers about thedangerous and potentially life-threatening side effects of miracle mineralsolution. 2020. Accessed 10 Mar 2020.
174. The New York Times. Surge of virus misinformation stumps Facebook andTwitter. 2020. Accessed 10 Mar 2020.
175. BBC News Singapore. Coronavirus: why some countries wear face masks
and others don’t. 2020. https://www.bbc.com/news/world-52015486.
Accessed 26 Jul 2020.
176. Mian A, Khan S. Coronavirus: the spread of misinformation. BMC Med. 2020;
18:89.
177. Ren SY, Gao RD, Chen YL. Fear can be more harmful than the severe acuterespiratory syndrome coronavirus 2 in controlling the corona virus disease2019 epidemic. World J Clin Cases. 2020;8:652–7.
178. Grace H. Japan may have beaten coronavirus without lockdowns or mass
testing. But how? 2020. https://time.com/5842139/japan-beat-coronavirustesting-lockdowns/. Accessed 26 Jul 2020.
179. Hasan Muhammad B, Mizanur R, Mohammad Tareq H. The COVID-19
pandemic: why are some countries more successful than others? 2020.
https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3575251. Accessed 26
Jul 2020.
180. Alex W. How Spain’s coronavirus outbreak got so bad so fast—and how
Spaniards are trying to cope. 2020. https://www.vox.com/2020/3/20/211
83315/coronavirus-spain-outbreak-cases-tests. Accessed 27 Jul 2020.
181. Sara B. 5 reasons the coronavirus hit Italy so hard. 2020. https://theconversation.com/5-reasons-the-coronavirus-hit-italy-so-hard-134636.
Accessed 27 Jul 2020.
182. Raghupathi V. An empirical investigation of chronic diseases: a visualization
approach to medicare in the United States. Int J Healthc Manag. 2019;12:
327–39.
183. Young BE, Ong SWX, Kalimuddin S, Low JG, Tan SY, Loh J, et al.
Epidemiologic features and clinical course of patients infected with SARSCoV-2 in Singapore. JAMA. 2020;323:1488–94.
184. Zhou F, Yu T, Du R, Fan G, Liu Y, Liu Z, et al. Clinical course and risk factors
for mortality of adult inpatients with COVID-19 in Wuhan, China: aretrospective cohort study. Lancet. 2020;395:1054–62.
185. Lowen AC, Mubareka S, Steel J, Palese P. Influenza virus transmission isdependent on relative humidity and temperature. PLoS Pathog. 2007;3:1470–6.
186. Harvard Health Publishing. Out in the cold. 2010. https://www.health.
harvard.edu/staying-healthy/out-in-the-cold. Accessed 27 Jul 2020.
187. Woodward A. High temperatures and muggy weather might make the newcoronavirus less contagious, a group of experts says. 2020. https://www.
businessinsider.in/science/news/high-temperatures-and-muggy-weathermight-make-the-new-coronavirus-less-contagious-a-group-of-experts-says/
articleshow/74697538.cms. Accessed 27 Jul 2020.
188. Bannister-Tyrrell M, Meyer A, Faverjon C, Cameron A. Preliminary evidence
that higher temperatures are associated with lower incidence of COVID-19,
for cases reported globally up to 29th February 2020. medRxiv. 2020.
https://doi.org/10.1101/2020.03.18.20036731.
189. Chan KH, Peiris JS, Lam SY, Poon LL, Yuen KY, Seto WH. The effects oftemperature and relative humidity on the viability of the SARS coronavirus.
Adv Virol. 2011;2011:734690.
190. Boldog P, Tekeli T, Vizi Z, Dénes A, Bartha FA, Röst G. Risk assessment ofnovel coronavirus COVID-19 outbreaks outside China. J Clin Med. 2020;9:571.
191. Booth TF, Kournikakis B, Bastien N, Ho J, Kobasa D, Stadnyk L, et al.
Detection of airborne severe acute respiratory syndrome (SARS) coronavirus
and environmental contamination in SARS outbreak units. J Infect Dis. 2005;
191:1472–7.
192. Donnelly CA, Ghani AC, Leung GM, Hedley AJ, Fraser C, Riley S, et al.
Epidemiological determinants of spread of causal agent of severe acuterespiratory syndrome in Hong Kong. Lancet. 2003;361:1761–6.
193. Ijaz MK, Brunner AH, Sattar SA, Nair RC, Johnson-Lussenburg CM. Survival
characteristics of airborne human coronavirus 229E. J Gen Virol. 1985;66:2743–8.
194. Mangen MJ, Nielen M, Burrell AM. Simulated effect of pig-population
density on epidemic size and choice of control strategy for classical swine
fever epidemics in The Netherlands. Prev Vet Med. 2002;56:141–63.

Page 12 of 12

195. Camilo R. As the number of elderly people with coronavirus varies between
countries. 2020. https://www.nexojornal.com.br/expresso/2020/03/18/Comoo-número-de-idosos-comcoronavírus-varia-entre-países. Accessed 27 Jul
2020.
196. Mas-Coma S, Jones MK, Marty AM. COVID-19 and globalization. One Health.
2020;9:100132.
197. Zhai Y, Du X. Mental health care for international Chinese students affectedby the COVID-19 outbreak. Lancet Psychiatry. 2020;7:e22.
198. St John RK, King A, de Jong D, Bodie-Collins M, Squires SG, Tam TW. Borderscreening for SARS. Emerg Infect Dis. 2005;11:6–10.
199. Jason B. How South Korea reined in the outbreak without shutting
everything down. 2020. https://www.npr.org/sections/goatsandsoda/2020/
03/26/821688981/how-south-korea-reigned-in-the-outbreak-withoutshutting-everything-down. Accessed 27 Jul 2020.
200. Shibani M, Simon D. How the U.S. can defeat coronavirus: Heed Asia’s
lessons from past epidemics. 2020. https://www.washingtonpost.com/
world/asia_pacific/how-the-us-can-defeat-coronavirus-heed-asias-lessonsfrom-epidemics-past/2020/03/18/9aa7916a-67a5-11ea-b199-3a9799c54512_
story.html. Accessed 27 Jul 2020.
201. Artika IM, Ma'roef CN. Laboratory biosafety for handling emerging viruses.
Asian Pac J Trop Biomed. 2017;7:483–91.
202. Peng H, Bilal M, Iqbal HMN. Improved biosafety and biosecurity measures
and/or strategies to tackle laboratory-acquired infections and related risks.
Int J Environ Res Public Health. 2018;15:2697.

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