Animal Viruses and Humans, a Narrow Divide: How Lethal

Zoonotic Viruses Spill Over and Threaten Us

Visit the link below to download the full version of this book:
https://cheaptodownload.com/product/animal-viruses-and-humans-a-narrow-divide-ho
w-lethal-zoonotic-viruses-spill-over-and-threaten-us-full-pdf-docx-download/
First Paul Dry Books Edition, 2018
Paul Dry Books, Inc.
Philadelphia, Pennsylvania
www.pauldrybooks.com
Copyright © 2018 Warren A. Andiman
All rights reserved
Printed in the United States of America
ISBN 978-1-58988-122-8
eISBN 978-1-58988-330-7
 To my wife, Marie,
and my daughters, Sarah and Alexis,
whom I love and greatly admire
for their intelligence and selfless devotion
to their fellow human beings.
They have always encouraged me
to do my best work
and taught me to seek after
my better self.
 CONTENTS

Preface

1 Millions of Tiny Crowns Wreak Havoc in Two Kingdoms (Or Never

Wipe a Camel’s Nose)
MERS (Middle East Respiratory Syndrome)

2 It’s a Good Thing Pigs Don’t Fly

Swine Influenza

3 National Parks Can Be Hazardous to Your Health

Hantavirus

4 Prairie Dogs Make Lousy Pets

Monkeypox

5 A Civet? What’s a Civet?

SARS (Severe Acute Respiratory Syndrome)

6 Miniature Masters of a Million Microenvironments

Viruses Rule!

7 It’s Restraining Bats and Dogs

Rabies

8 Behold the Earth … One Mighty Blood Spot

Ebola Virus Disease

9 A Witchy Brew of Bat Spats, Horse Froth, and Womb Drips

Nipah and Hendra Viruses

Concluding Remarks

Acknowledgments
Everybody knows that pestilences have a way of recurring in the world; yet somehow we
find it hard to believe in ones that crash down on our heads from a blue sky.
Albert Camus, The Plague

That human health and Earth’s health are intertwined can sound like a truism—more of a
bumper sticker or poetic truth than scientific fact. Yet a growing body of research suggests
that disrupted ecologies may indeed produce more disease.
Brandon Keim, Anthropocene Magazine, December 14, 2016

All is flux, nothing stays still.

Heraclitus, c. 540–480 B.C.
 PREFACE

Viruses are obligate intracellular parasites; that is, they can replicate only
within the confines of living animal or plant cells, bacteria included. Once
they gain entry to a cell’s interior, they hijack many of its rich biochemical
offerings and spread by one of three ways: by producing hundreds or
thousands of progeny that bud from the cell’s surface membrane; or by
inducing the fusion of adjoining cells so they can move into neighboring
property as the membranous barrier between cells melts away. Some viruses
completely destroy the cells in which they reproduce and thereby find
sanctuary in the juices between cells or in the blood and lymph, whereupon
they can move to wherever the body’s life blood (literally) carries them.
Thousands of known virus species have evolved since life first appeared
on Earth. They have adapted their parasitic lifestyles to thousands of living
species. Their sole purpose is to reproduce and spread, as is the case for
many higher life forms. As a result, some have developed the capacity to
“jump” from one species to another, thereby expanding their ecological
range in true Darwinian fashion as they continue to mutate and slowly
acclimate to new intracellular milieux.
The arboviruses have found a way to travel among animal species by
hitching a ride inside insects. These highly mobile vectors of disease take a
blood meal from their animal reservoirs—cattle, pigs, birds, bats, monkeys,
etc.—and transmit teeming blood-borne virus herds to other animals. Some
of these animals happen to be humans who find themselves in proximity to
the creatures that passively serve as the source of their infection. In
contrast, some viruses travel directly from animal to animal or from animal
to human being without an insect interloper. (A famous story tells of Joseph
Meister, the boy who acquired rabies from the bite of a dog and who was
cured by Louis Pasteur in 1885; no mosquitoes, ticks, or mites played a
role.) The journey among animals is eased when people, sub-human
mammals, and birds live or work in close quarters. Because vocations,
recreations, and ecological niches vary greatly from place to place, the
kinds of animal vectors and the conditions under which virus transmission
occurs also vary greatly.
The viruses and diseases, the zoonoses, I’ve chosen to write about in this
book are characterized by a direct mode of the spread of infection from
animals to humans, and by the great variety in place of origin and the mix
of animal species involved. These examples are meant to describe only a
small sample of what is already out there but, more menacingly, what is
inevitably on its way, in forms we can only imagine.
HIV, the human immunodeficiency virus, is one of the most recent and,
doubtless, the most terrifying of these zoonoses. Several readers of early
drafts of this book asked why I did not include HIV. My response, perhaps
wrong-headed, was that HIV/AIDS and its history of pestilence and death
were already familiar to many people and that I wanted to expand their
horizons by providing stories of other zoonoses—ones that have already
maimed and killed and that might someday break free, should the right
combination of brief encounters take place.
HIV-induced disease is a paradigm of a series of random animal-to-
human transmission events. There are actually two AIDS viruses, HIV-1
and HIV-2, both members of the lentivirus family, a group of pathogens
shared by monkeys, apes, and human beings. It’s believed that a sequence
of significant cross-species lentivirus transmissions began only in the past
century or two, this despite the fact that Old World simian lentiviruses have
evolved along with their host species for millions of years. There are at
least ten simian immunodeficiency viruses, each related to a different
simian species. SIVcpz, the chimpanzee virus, and SIVgor, the gorilla virus,
are the two candidates that ultimately made their way to humans.
Transmission is thought to have occurred through cutaneous or mucous
membrane exposure to ape blood or other body fluids in the course of
hunting and eating bushmeat.
A number of worthy writers and journalists have covered aspects of
these sorts of events in the last several decades. Much of their focus has
been on the social and environmental conditions that create the settings in
which viruses can easily jump from animals to humans and then, more
ominously, among their human hosts. These writers have sometimes
targeted viruses whose very names are so familiar as to make us stand at
attention: Ebola, avian influenza, and Lassa fever, among others. But as a
physician trained in clinical and diagnostic virology and as a clinician on
the front lines, I felt obliged to introduce readers to the magical and
mysterious world of the viruses themselves: how they look and how their
very structure and molecular make-up allow them to parasitize the cells of
their mammalian and avian hosts so efficiently—and thereafter, to cause
more generalized disease. Having invaded their prey, how do viruses then
take hold of the cells’ complex machinery in order to fulfill their sole raison
d’être, that is, to reproduce promiscuously and to wreak havoc wherever
they can find a home? In addition, I describe some of the physical
manifestations of viral attack. I do this with some trepidation because the
pictures I paint are far from pretty. Many of us get a bit of a kick out of
being scared and even horrified, so I believe there is some value in having
readers understand the consequences of allowing these diseases to cross
international borders and to move uninhibited into our hospitals,
neighborhoods, homes, and bodies. The recent epidemic of Ebola virus
disease has given us a glimpse into the terrors unleashed by these super-
sub-microscopic beasties. Finally, I will briefly revisit some of the lifestyles
and habits that bring members of our own species into intimate contact with
representatives of other species. We not only depend on animals for food,
which brings us close to their very flesh and blood, but we also love
animals, which brings us into contact with their secretions and excretions in
a manner not unlike that of the humans we love and nurture.
As I tell my stories I also take the liberty of conveying some basic
principles of virus disease epidemiology and pathogenesis. Many of these
principles relate to the majority of infectious agents, including bacteria and
fungi, but I have placed them in the text when elements of the story
provided an opportunity for a brief encounter with one of these overarching
principles. There are five basic tenets that explain the behavior of infectious
diseases: i) contact between a microbe and its host does not necessarily
result in infection; ii) the earliest stages of infection do not necessarily
result in clinically apparent illness (that is, some infections are subclinical);
iii) the manifestations of clinical illness can range from very mild to severe;
iv) the clinical expression of disease depends, to a varying extent, on the
host’s immune response to the pathogen; and v) the pathogen and the host
share a geographic locale and an ecological niche, both of which play a role
in determining the host’s susceptibility and the extent of clinical risk.
Finally, I have chosen to assume an informal style in my writing. I am a
physician-scientist who in my daily discourse uses all kinds of polysyllabic
words and arcane phraseology. I have labored to adapt my style to one that
can easily be approached by educated readers, who can, if they wish,
supplement their reading of these chapters with further etymological and
scientific searches. I have made every attempt in these transformations of
language not to distort scientific fact. If by chance I have transgressed in
these attempts, I ask my colleagues and more specialized readers to forgive
me.
I also ask to be forgiven for my tendency to anthropomorphize the
viruses’ appearance and behavior. I worked with these miniature beasties in
the laboratory for thirty-five years, and I’ve cared for patients infected with
them for so long that I have begun to regard them as having motives
(mostly nefarious) and bodies (mostly startlingly beautiful) that seem
almost humanoid, or perhaps even sentient and highly motivated.
 CHAPTER 1

Millions of Tiny Crowns Wreak Havoc in Two

Kingdoms (Or Never Wipe a Camel’s Nose)
MERS (MIDDLE EAST RESPIRATORY SYNDROME)

CDC is working closely with the World Health Organization (WHO) and other partners to
better understand the public health risk presented by a recently detected, novel coronavirus.
This virus has been identified in two patients, both previously healthy adults who suffered
severe respiratory illness. The first patient, a man aged 60 years from Saudi Arabia, was
hospitalized in June 2012 and died; the second patient, a man aged 49 years from Qatar
with onset of symptoms in September 2012 was transported to the United Kingdom for
intensive care. He remains hospitalized on life support with both pulmonary and renal
failure.
Morbidity and Mortality Weekly Report, Vol. 61, No. 40, October 12,
2012

In June 2012, a 60-year-old Saudi man was admitted to a hospital in

Jeddah. He complained of week-long symptoms of productive cough, fever,
and shortness of breath. He had no history of chronic diseases affecting his
lungs or kidneys. Examination of his chest X-ray revealed opacities in both
lungs, inflammatory fluids in the tissues surrounding them, and diminished
lung volume. These abnormalities progressed over the next several days
despite treatment with a cocktail of antibacterial, antiviral, and anti-fungal
antibiotics prescribed for him hurriedly even in the absence of a definitive
diagnosis. (There was no test for the agent that infected him.) Initially, three
different pathogenic bacteria were isolated from his lung secretions, but
none was believed to be causing his illness. The patient required
mechanical ventilation to keep his tissue oxygen levels normal. Days later,
quite unexpectedly, his kidneys began to fail; on his eleventh day in the
hospital, he died of progressive pulmonary and renal failure.
Analysis of the man’s sputum by PCR (polymerase chain reaction, the
genetic technique commonly used to analyze and identify the source of
blood at a crime scene, or of semen in a rape victim) revealed that he had
been infected with a coronavirus. Another test proved that the man had
antibody to the virus in his blood, but clearly not enough to quell advancing
disease. To everyone’s surprise, blood samples from 2,400 other Saudis
(“controls”) were found not to contain antibodies to the new virus,
indicating that the poor dead man had been infected with a virus that very
few, if any, of his countrymen had ever been exposed to.
After sufficient quantities of this coronavirus had been grown in cell
culture, exhaustive genetic analysis of the viral genome was undertaken. It
was discovered that the new virus belonged to a lineage called beta
coronaviruses and, oddly, that its closest relatives were coronaviruses that
commonly persist silently in bats. Stranger still, the new virus was more
closely related to bat coronaviruses than to the other coronaviruses already
known to infect humans. This finding suggested strongly that one or more
other animal species, certainly including bats, were the likely reservoir.
Corona is a Latin word meaning “crown,” from the ancient Greek,
korōnē (“garland, wreath”). Each coronavirus particle is surrounded by a
garland of club-shaped projections, creating the appearance of a daisy or a
crown. The projections comprise sugar and protein moieties which together
form the “keys” that latch onto receptors on the host cell’s outer membrane.
This lock and key interaction determines the tissue specificity of the virus.
For example, the cells that bear these coronavirus receptors are found in the
mucous membranes of the nose and trachea, as well as the kidney and some
fibrous tissues. Based on this very specific virus-tissue interaction, it is not
surprising that the Saudi man’s respiratory and urinary tracts were the
systems most dramatically affected and the first to fail.
Transmission electron micrograph of coronavirus particles. Note the crown-like (corona) or halo-like
appearance. Coronaviruses are responsible for SARS, the severe acute respiratory syndrome, and
MERS, the Middle East respiratory syndrome. Content provider Dr. Fred Murphy of the Centers for
Disease Control and Prevention and the Public Health Image Library (PHIL).

A year and a half after the first unfortunate Saudi man died, a forty-
three-year-old countryman of his, also from the Jeddah region, went to the
hospital, complaining of shortness of breath. This followed a week-long
illness characterized by runny nose, cough, and malaise. The patient owned
a herd of nine camels. The camels were housed about forty-five miles south
of Jeddah, where he and a group of friends visited the animals every day.
Coincidentally, the men noticed that four of the camels had runny noses and
that one was being treated by their sick friend, who had been gently
applying a medicinal salve to the camel’s nostrils. This kind man developed
irremediable lung disease and died two weeks after being admitted to the
hospital.
The patient’s eighteen-year-old daughter developed an upper respiratory
infection some time during her father’s hospital stay, but she recovered fully
after three days. None of the dead man’s friends got sick. There’s an
important principle at work here—inoculum size: that is, the density of
pathogenic virus particles in a particular body fluid which later find a
welcome home in one or more of the body’s portals of entry—for example,
nose, mouth, throat, urethra, rectum, damaged skin, or conjunctiva. The
dead man who tended to his sick camel’s URI by direct contact with the
animal’s nasal discharge was clearly put at greater risk than his buddies by
having handled the camel’s mucus, a slimy inoculum later found to be
teeming with virus. His friends merely visited the camels, and his daughter
only lived in the same house with him. One can easily imagine that a
simple, unconscious movement of the dead man’s mucus-contaminated
finger from the camel’s nose to his own transferred as many as thousands or
millions of virus particles from one juicy home to another. Remember,
viruses are very, very, very small. (One lusty sneeze laden with influenza or
common cold viruses can easily contaminate half an auditorium or most of
an airplane cabin, as thousands of viruses seek a welcoming human landing
platform.)
The disease caused by this camel (or bat) coronavirus was given the
name Middle East Respiratory Syndrome, or MERS. (It bore some
resemblance to an earlier disease with a similar acronymic name, Severe
Acute Respiratory Syndrome, or SARS, one with a more alarming and
widespread influence. See chapter 5.) Exhaustive genomic analysis of nasal
fluid collected from the drippy-nosed camel and from the patient on four
different hospital days showed that the RNA of all five samples were
identical. In contrast, no virus was found in the nose of the dead man’s
daughter and none was found in the milk, urine, or feces of any of the
camels. In this particular illness cluster, the MERS virus, like many other
coronaviruses known to us, appeared to share a proclivity for infecting cells
of the respiratory tract. When the structure of the camel coronavirus RNA
was compared to dozens of other coronavirus RNAs in the GenBank
database, it was found to be closely related to coronavirus isolates from
Riyadh, Munich, Abu Dhabi, England, France, Jordan, the United Arab
Emirates, and Qatar. Coronaviruses in this branch of the coronavirus family
tree were already widely dispersed in parts of Europe and the Middle East,
yet no serious outbreaks occurred. It was a mere handful of fatal respiratory
illnesses in these Saudi men, a few others, and several camels, that brought
MERS to the world’s attention. During the following year, about eighty
cases of MERS were identified; a little more than half of those afflicted
died, for a case fatality rate of fifty-six percent. Based on extensive
understanding of the MERS coronavirus, that is, MERS-CoV, and its
molecular structure and behavior in vitro, we now know that it spreads from
animals to humans, but also among humans in very close contact with one
another, within households, for example, or in hospital settings, as with
other respiratory and gastrointestinal viruses. Most of the patients identified
have had underlying diseases such as diabetes or end-stage kidney disease,
suggesting that the MERS coronavirus takes advantage of people with some
degree of immune compromise. And some minority of the patients appear
to have been “super shedders,” each one secreting and then transmitting the
infection to more than a half-dozen of their close contacts.
The early months of 2014 were characterized by a continuous ebb in the
number of confirmed MERS cases that came to light. No more than twenty
or thirty samples of respiratory secretions were received each day by the
Jeddah Regional Laboratory. The Jeddah Laboratory is a reference facility
governed by the Saudi Ministry of Health and does preliminary and
confirmatory testing for MERS-CoV for laboratories throughout the
kingdom of Saudi Arabia. Infections consistent with MERS-CoV were
springing up all over, but most were focused on Jeddah. The third week of
March 2014 saw an abrupt increase in samples submitted, which continued
to escalate through most of April. The reference lab began receiving
somewhere between 200 and 400 respiratory specimens a day, and, as
before, the majority came from patients living in and around Jeddah. As the
outbreak advanced, the lab served not only as a diagnostic facility but also
as the hub of a detailed epidemiologic investigation for which the submitted
specimens served as source material. The specimens allowed investigators
to follow webs of transmission and, perhaps, would yield some clues about
the virus’s virulence. The scientists also believed they might discover new
sources or a greater frequency of animal to human, that is, zoonotic
transmissions, and maybe even instances of nosocomial transmission, that
is, spread from person to person within the hospital setting. Of the more
than 6,200 samples that were tested in Jeddah between January and the end
of April 2014, ninety-three percent were received after March 26. But of
that number, only 168 samples, or three percent, contained MERS-CoV.
This may appear to be a shockingly small number, but with diseases like
MERS, which has no unique clinical presentation (coughs, colds,
pneumonia, and fevers are ubiquitous), and which is bound to cause
exaggerated fretfulness in specific populations at risk, doctors are obliged to
submit many more specimens for analysis than are expected to be positive.
After all, as healthcare workers, we do not want to miss any bona fide
infections, especially potentially fatal ones, which are most likely to
respond to intervention in their early stages.
 Half the positive samples came from King Fahd Hospital, a clear signal
of nosocomial spread. KFH serves many of the expatriates who flock to the
city to find employment. Quite logically, there were more samples taken
from contacts of patients identified in Jeddah, the outbreak’s epicenter, than
from contacts traced to other parts of the country. Not surprisingly, the
secretions from asymptomatic close contacts of patients carried lower titers
of virus than those from symptomatic patients themselves, because persons
who find their way to doctors’ offices or hospitals are more likely to be
symptomatic and symptomatic patients are more likely to be carrying
greater amounts of virus. Viral load usually correlates with degree of illness
and a greater likelihood of infectiousness, and hence, transmissibility.
The genomes of a representative number of virus isolates from the
Jeddah outbreak were fully sequenced. That is, every genetic signature in
the chain of sequences that constitute the complete genetic code of each
virus isolate was identified. They showed that all the Jeddah viruses
clustered in a single small genetic family, or clade. In contrast, the viruses
from Riyadh were a bit more genetically diverse. One clade from the
Riyadh family of viruses showed internal similarities that suggested person-
to-person transmission. One person carried the Riyadh MERS virus back to
Indiana, in the United States, and a few other carriers exported the virus to
the Netherlands. Only one coronavirus isolate collected in Riyadh was
similar to those that clustered in Jeddah. The patient who carried this viral
isolate had visited his hospitalized son in King Fahd Hospital in Jeddah
before returning to his home in Riyadh, but there were no reports of further
family household spread.
When subjected to the most detailed forms of genetic analysis, MERS-
CoV isolates collected from camels in Taif, Jeddah, and Qatar were found
to resemble closely human isolates from Riyadh and Bisha. Taif is southeast
of Jeddah and Qatar is on the eastern edge of the Arabian Peninsula. I
present these seemingly obscure geographic details to illustrate how
efficiently respiratory and gastrointestinal viruses cross both domestic and
international borders. A virus that likely leaked from the nose of a camel in
Saudi Arabia traveled, with minor variations, through that country and soon
found its way to the American Midwest and the Netherlands and Greece.
We now know that MERS-CoV was widely distributed in camels
throughout Arabia at least since late 2013.
 Luckily, although small clusters of MERS cases occurred in both
hemispheres, the disease never spread widely; there has been no epidemic.
Isolated bits of data suggest that the titers of virus in respiratory secretions
did not rise significantly in the course of human-to-human transmission, as
sometimes happens when viruses slowly adapt as they pass from host to
host. Also, unlike influenza virus, the MERS-CoV virus outer coat did not
change very much as it moved from person to person, lending credence to
the idea that specific antibodies raised in the course of one infection might
also protect the host against subsequent infection by a closely related virus,
increasing the levels of “herd immunity” in the general population.
The broader coronavirus family of viruses infects many animal species.
Among the targets are humans, dogs, cats, cattle, rabbits, turkeys, and
chickens, in which each coronavirus affects, primarily, parts of the
respiratory tract. Pigs are pummeled in the GI tract and central nervous
system, mice in the liver, and rats in the tear ducts and lymph glands of the
head and neck. Coronavirus particles have been seen by electron
microscopy in human feces, and some of these strains are related to calf
diarrhea virus, providing compelling evidence of likely spread between
ungulates and people. This interspecies spread is further supported by the
fact that the first human coronavirus was isolated from a schoolboy
suffering from a URI in 1965. The morphology of this early isolate closely
resembled the avian infectious bronchitis viruses. Despite compelling
evidence of animal-to-human transmission, it is not clear whether the
converse holds true: can human coronaviruses spread to and infect animals
of other species?
Coronaviruses spread disease throughout the world, and we believe that
the great majority of healthy adults have at some time survived infection,
beginning in early childhood. Nevertheless, coronavirus infections are less
common than those caused by rhinoviruses (the “common cold virus”) and
influenza viruses, but they always skulk somewhere among the marauders
that can be found in the throats, windpipes, and lungs of sneezing, coughing
humans during the winter and spring. Also, the clinical manifestations
produced by these multiple respiratory pathogens are indistinguishable. As
with influenza and rhinoviruses, coronaviruses are also known to be
responsible for some acute exacerbations in patients with asthma and
COPD. When coronaviruses infect cells of the tracheal mucosa,
degenerative changes are observed in the cilia, those gentle, waving,
feathery cellular appendages that clear the mucus from our noses and
airways.

Camels and humans have had an intimate and historically critical

relationship going back at least fifteen centuries. Arab Bedouins have
shaped their armies and nourished their people, supported by the virtues of
their camel herds. The rise of the Islamic empires of the Middle East could
not have succeeded without the foundations built upon the camel’s back. So
it’s not at all surprising that some present-day Arabs continue to revere and
love their camels to such a degree that they are apt to wipe a camel’s nose
and apply soothing salves much as any good parent does for a child with a
sore, runny nose.
With concern growing about the probable spread of MERS throughout
the Arabian Peninsula and beyond, the World Health Organization updated
its guidelines and cautioned locals and international visitors to the kingdom
to practice general hygienic measures, which included the recommendation
to wash hands regularly before and after touching animals and particularly
to avoid all contact with sick animals. Travelers were also warned to avoid
consumption of raw and undercooked animal products. To provide greater
specificity, WHO reminded persons at high risk for MERS—those with
diabetes, kidney disease, and chronic lung disease—to avoid all contact
with camels, to refrain from eating camel meat, and most especially, to
eschew drinking raw camel milk and raw camel urine. It was advised that
camel milk be boiled before drinking.
But why camel urine? For more than a thousand years, the health and
beauty benefits of camel urine have been applauded in many Middle
Eastern countries. In some Islamic nations various facial creams, hair oils,
cosmetics, and aphrodisiacs have included camel urine as an essential
ingredient. On occasion, it’s also been promoted as a nostrum for certain
cancer patients. Its proponents claim that camel urine is sterile and free of
toxins and can be stored at room temperature for up to two weeks “without
being corrupted.”
According to some religious scholars, the health benefits of camel urine
can be traced back to a verse in the Hadith, a Muslim holy book. The legend
describes the healing benefits that camel urine afforded to members of a
certain tribe who were ill-suited to the climate in Medina. On the advice of
a prophet, they drank camel urine and became healthy.
 The WHO admonition against contact with camel urine in any form has
now been echoed by the Saudi agricultural ministry, a precedent in a
country where camels are integral to the culture and are both lauded and
revered.
Despite the MERS virus’s relatively low transmission rate, two family
clusters of MERS infection have been meticulously recorded in the medical
literature, one occurred in Riyadh and the other in London. The English
cluster originated in a UK resident who had recently returned from an eight-
day sojourn in Saudi Arabia, during which time he made pilgrimage to
Mecca and Medina. The traveler reported no known contacts with persons
afflicted by serious respiratory illnesses, but within days of returning to the
UK, the man’s condition deteriorated rapidly and he received every
conceivable form of intensive care, including the most up-to-date
modalities of respiratory support. An initial viral culture revealed the
presence of influenza A, but another, collected a week later, contained the
MERS coronavirus. Among twenty household contacts of the index patient
(a term used to identify the first person in a cluster shown to be definitely
infected), six developed respiratory infections, but the MERS virus was
isolated from only two. The two had also visited the index patient in the
hospital, and like the index case, both had also been infected with a second
respiratory virus, para-influenza. One of the two had cancer and was
receiving chemotherapeutic agents likely to have damaged his immune
system. Despite heroic efforts, the traveler’s illness progressed and he died
on the eleventh hospital day. One of the MERS carriers, a woman who had
direct contact with the hospitalized index case for a total of two and a half
hours, survived, following nine days of a flu-like illness. The cancer patient
also survived.
Intensive public health efforts were launched to identify and study all the
close contacts of the dead man. Six persons among his seventeen household
and healthcare contacts and hospital visitors developed colds and coughs,
but none had MERS virus in respiratory samples. Similarly, among the
twenty-five close contacts of the woman with the “flu,” three developed
self-limited respiratory illnesses, and none was found to have the MERS
virus in samples taken from their respiratory tracts. Clearly, this particular
virus strain in its original incarnation was not easily transmitted from
person to person and did not acquire that particular characteristic in its
subsequent travels. The degree to which a virus is transmitted person-to-