MCB 405: PRINCIPLE OF

EPIDERMOLOGY
VIRAL AIRBORNE DISEASES
Because air does not support virus
growth, any virus that is airborne must
have originated from a living source.
When humans are the source of the
airborne virus, it’s usually propelled from
the respiratory tract by coughing,
sneezing, or vocalizing.
Chickenpox (Varicella) and Shingles (Herpes
Zoster)
Chickenpox (varicella) is a highly contagious skin
disease primarily of children 2 to 7 years of age.

Humans are the reservoir and the source for this virus,
which is acquired by droplet inhalation into the
respiratory system.
The virus is highly infectious with secondary infection
rates in susceptible household contacts of 65% to
86%.
In the pre-vaccine era, about 4 million cases of
chickenpox occurred annually in the United States,
resulting in approximately 11,000 hospitalizations and
100 deaths.
The causative agent is the enveloped, DNA varicella-
zoster virus (VZV), a member of the family
Herpesviridae.
The virus produces at least six glycoproteins that play
a role in viral attachment to specific receptors on
respiratory epithelial cells.
Their recognition by the human immune system
results in humoral and cellular immunity.

Following an incubation period of 10 to 23 days,

small vesicles erupt on the face or upper trunk, fill
with pus, rupture, and become covered by scabs.
Healing of the vesicles occurs in about 10 days.
During this time intense itching often occurs.
Laboratory confirmation of varicella virus is by detection
of 1varicella-zoster immunoglobulin M (IgM) antibody;
2
detection of VZV, 3demonstration of VZV antigen by
direct fluorescent antibody and by 4polymerase chain
reaction in clinical specimens or a 5significant rise in
serum IgG antibody level to VZV.

Laboratory confirmation is recommended, though, to

confirm the diagnosis of severe or unusual cases of
chickenpox.

As the incidence of chickenpox continues to decline due

to vaccination, fewer cases are seen clinically, resulting
in the likelihood of misdiagnosis.
Chickenpox can be prevented or the infection
shortened with an attenuated varicella vaccine
(Varivax) or the drug acyclovir (Zovirax or Valtrex).

It should be noted that Valtrex (valacyclovir) is an

orally administered prodrug of Zovirax or acyclovir.
Valtrex is the valyl ester of acyclovir and is rapidly
hydrolyzed to acyclovir in the body.
Individuals who recover from chickenpox are
subsequently immune to this disease; however, they
are not free of the virus, as viral DNA resides in a
dormant (latent) state within the nuclei of cranial
nerves and sensory neurons in the dorsal root ganglia.
This viral DNA is maintained in infected cells but
virions cannot be detected.
When the infected person becomes
immunocompromised by such factors as age,
neoplastic diseases, organ transplants, AIDS, or
psychological or physiological stress, the viruses may
become activated.
They migrate down sensory nerves, initiate viral
replication, and produce painful vesicles because of
sensory nerve damage. This syndrome is called
postherpetic neuralgia.
To manage the intense pain, corticosteroids or the
drug gabapentin (Neurontin) can be prescribed. The
reactivated form of chickenpox is called shingles
(herpes zoster).
Most cases occur in people over 50 years of age.
Except for the pain of postherpetic neuralgia,
shingles does not require specific therapy; however,
in immunocompromised individuals, acyclovir,
valacyclovir, vidarabine (Vira-A), or famciclovir
(Famvir) are recommended.
Influenza (Flu)
Influenza or the flu, is a respiratory system disease
caused by negative-strand RNA viruses that belong to
the family Orthomyxoviridae.
There are four groups: influenza A, influenza B,
influenza C, and Thogoto viruses. They contain 7 to 8
segments of linear RNA, with a genome length between
12,000 to 15,000 nucleotides.
The enveloped virion can be spherical (50–120 nm in
diameter) or filamentous (200–300 nm long, 20 nm in
diameter).
Influenza A infections are responsible for the majority
of clinical influenza cases, with influenza B accounting
for approximately 3% of flu Disease.
Influenza A infections usually peak in the winter and
involve 10% or more of the population, with rates as
high as 50 to 75% in school-age children.
Influenza A viruses are widely distributed, infect a
variety of mammal and bird hosts, and are further
classified into subtypes (or strains) based on their
membrane surface glycoproteins, hemagglutinin
(HA), and neuraminidase (NA).
HA and NA function in viral attachment and virulence.
There are 16 HA and 9 NA antigenic forms known;
they can recombine to produce various HA/NA
subtypes of influenza.
All subtype combinations infect birds.
Influenza A viruses having H1, H2, and H3 HA
antigens, along with N1 and N2 NA antigens, are
predominant in nature, infecting humans since the
early 1900s.
H1N1 viruses appeared in 1918 and were replaced in
1957 by H2N2 subtypes as the predominant subtype.
The H2N2 viruses were subsequently replaced by
H3N2 as the principle subtypes in 1968.

The H1N1 subtype reappeared in 1977 and co-

circulates today with H2N1, H3N2, H5N2, H7N2,
H7N3, H7N7, H9N2, H10N7, and H5N1 viruses.
Measles (Rubeola)
Measles [rubeola: Latin rubeus, red] is a highly contagious
skin disease that is endemic throughout most of the world.
It is a negative strand, enveloped RNA virus, in the genus
Morbillivirus and the family Paramyxoviridae.
The measles virus is monotypic, with a small variations at
the epitope level. The variations are based on genetic
variability in the virus genes.
Such variations, however, have no effect on protective
function since a measles infection still provides a lifelong
immunity against re-infection.
The virus enters the body through the respiratory tract or
the conjunctiva of the eyes.

The receptor for the measles virus is the complement

regulator CD46, also known as membrane cofactor protein.
The incubation period is usually 10 to 21 days, and
the first symptoms begin about the tenth day with a
nasal discharge, cough, fever, headache, and
conjunctivitis.
Within 3 to 5 days skin eruptions occur as faintly pink
maculopapular lesions that are at first discrete, but
gradually become confluent.
The rash normally lasts about 5 to 10 days. Lesions
of the oral cavity include the diagnostically useful
bright-red Koplik’s spots with a bluish-white speck in
the center of each.
Very infrequently a progressive degeneration of the
central nervous system called subacute sclerosing
panencephalitis occurs. No specific treatment is
available for measles.
The use of attenuated measles vaccine
(Attenuvax) or in combination (MMR vaccine;
measles, mumps, rubella) is recommended for all
children.
Since public health immunization programs began
in 1963, there has been near eradication of
measles in the United States.
In less well-developed countries, however, the
morbidity and mortality in young children from
measles infection remain high.
It has been estimated that measles infects 50
million people and kills about 4 million a year
worldwide.
Mumps
Mumps is an acute, generalized disease that occurs
primarily in school-age children. Occasional outbreaks
occur in non-immunized populations. The mumps virus
is a member of the genus Rubulavirus in the family
Paramyxoviridae.
This virus is a pleomorphic, enveloped virus that
contains a helical nucleocapsid containing negative-
strand RNA. The virus is transmitted in saliva and
respiratory droplets. The portal of entry is the
respiratory tract.
Mumps is about as contagious as influenza and
rubella, but less so than measles or chickenpox.
The virus replicates in the nasopharynx and lymph nodes of
an infected person. Viral transmission is airborne or through
direct contact with contaminated droplets or saliva.
The most prominent manifestations of mumps are swelling
and tenderness of the salivary (parotid) glands 16 to 18
days after infection of the host by the virus. The swelling
usually lasts for 1 to 2 weeks and is accompanied by a low-
grade fever.
Severe complications of mumps are rare, however,
meningitis and inflammation of the epididymis and testes
(orchitis) can be important complications associated with
this disease—especially in the postpubescent male. Therapy
of mumps is limited to symptomatic and supportive
measures.
A live, attenuated mumps virus vaccine is available. It
usually is given as part of the trivalent MMR vaccine.
Smallpox (Variola)
Smallpox (variola) is a highly contagious illness of
humans caused by the orthopoxvirus. Characteristic
symptoms of infection include acute onset of fever
101°F (38.3°C) followed by a rash that features firm,
deep-seated vesicles or pustules in the same stage of
development without other apparent cause. The variola
virus belongs to the family Poxviridae, which includes
vaccinia (cowpox and also the smallpox vaccine virus),
monkey-pox virus, and molluscum contagiosum virus.
Humans are the only natural hosts of variola. The virion
is large, brick shaped, and contains a dumbell-shaped
core. Interestingly, the size of the smallpox virus (300 by
250 to 200 nm) is slightly larger than that of some of the
smallest bacteria—for example, Chlamydia.
The genome inside the core consists of a single,
linear molecule of double-stranded DNA and
replicates in the host cell’s cytoplasm.
Smallpox was once one of the most prevalent of all
diseases. It was a universally dreaded scourge for
more than 3 millennia, with case fatality rates of 20 to
50%.
The first immunizations Since the advent of
immunization with the vaccinia virus, and because of
concerted efforts by the World Health Organization,
smallpox has been eradicated throughout the world—
the greatest public health achievement ever. (The last
case from a natural infection occurred in Somalia in
1977.)
Eradication was possible because smallpox has obvious
clinical features, virtually no asymptomatic carriers, only
human hosts as reservoirs, and a short period of
infectivity (3 to 4 weeks).
The disease was successfully eliminated by a global
immunization effort to prevent the spread of smallpox
until no new cases developed.
There are two clinical forms of smallpox. Disease caused
by Variola major is more severe and the most
common form of smallpox, with a more extensive rash
and higher fever.
This form of smallpox had an overall fatality rate of
about 33%; with significant morbidity in those who did
not die. Variola minor is a less common form of
smallpox, with much less severe disease and death rates
of 1% or less.
Yellow Fever
Yellow fever is less lethal than other viral diseases caused by
a flavivirus, and no longer occurs in the developed countries,
but it remains a public health problem in Africa and South
America, causing over 200,000 infections and 30,000 deaths
each year.
In addition it is a potential bio-weapon. Yellow fever was first
identified by Benjamin Rush, who catalogued its signs and
symptoms in attempt to discover its cause and cure.
Yellow fever holds the distinction as the first human disease
found to be caused by a virus (Walter Reed discovered this
in 1901).
It also provided the first confirmation (by Carlos Juan Finley)
that an insect could transmit a virus.
The disease received its first name, yellow jack, because
jaundice is a prominent sign in severe cases.
The jaundice is due to the deposition of bile pigments in
the skin and mucous membranes because of liver
damage.
The disease is spread through a population in two
epidemiological patterns.
In the urban cycle, human to-human transmission is by
Aedes aegypti mosquitoes.
In the sylvatic cycle the mosquitoes transmit the virus
between monkeys and from monkeys to humans
(sylvatic means in the woods or affecting wild animals).

Once inside a person the virus spreads to local lymph

nodes and multiplies; from this site it moves to the liver,
spleen, kidneys, and heart,where it can persist for days.
Yellow fever has an abrupt onset after an incubation
period of 3 to 6 days, and usually includes fever,
prostration, headache, sensitivity to light, low-back pain,
extremity pain, epigastric pain, anorexia, and vomiting.
The illness can progress to liver and renal failure, and
hemorrhagic symptoms and signs caused by
thrombocytopenia (low platelet count) and abnormal
clotting and coagulation can occur.
The fatality rate of severe yellow fever is approximately
20%.
Diagnosis of yellow fever is made by culture of virus
from blood or tissue specimens or by identification of
viral antigen or nucleic acid in tissues using
immunohistochemistry (IHC), ELISA antigen capture, or
PCR.
There is no specific treatment for yellow fever. An
active immunity to yellow fever results from initial
infection or from vaccines containing the attenuated
yellow fever 17D strain or the Dakar strain virus.
Prevention and control of this disease involves
vaccination and control of the insect vector.
Hepatitis B (serum hepatitis) is caused by the hepatitis
B virus (HBV), an enveloped, double-stranded circular
DNA virus of complex structure. HBV is classified as an
Orthohepadnavirus within the family Hepadnaviridae.

Serum from individuals infected with hepatitis B contains

three distinct antigenic particles: a spherical 22 nm
particle, a 42 nm spherical particle (containing DNA and
DNA polymerase) called the Dane particle, and tubular
or filamentous particles that vary in length.

The viral genome is 3.2 kb in length, consisting of four

partially overlapping, open-reading frames that encode
viral proteins.
Viral replication takes place in hepatocytes. The infecting virus
encases its double-shelled Dane particles within membrane
envelopes coated with hepatitis B surface antigen (HBsAg).
The inner nucleocapsid core antigen (HBcAg) encloses a single
molecule of double-stranded HBV DNA and an active DNA
polymerase.
HBsAg in body fluids is (1) an indicator of hepatitis B infection,
(2) used in the large-scale screening of blood for the hepatitis B
virus, and (3) the basis for the first vaccine for human use
developed by recombinant DNA technology.
Diagnosis of HBV is made by detection of HBsAg in unimmunized
individuals or HBcAg antibody, or detection of HBV nucleic acid
by PCR. The hepatitis B virus is normally transmitted through
blood or other body fluids (saliva, sweat, semen, breast milk,
urine, feces) and body-fluid-contaminated equipment (including
shared intravenous needles). The virus can also pass through the
placenta to the fetus of an infected mother.
Hepatitis A
Hepatitis A (infectious hepatitis) usually is transmitted
by fecal oral contamination of food, drink, or shellfish
that live in contaminated water and contain the virus in
their digestive system.
The disease is caused by the hepatitis A virus (HAV) of
the genus Hepatovirus in the family Picornaviridae.
The hepatitis A virus is an icosahedral, linear, positive-
strand RNA virus that lacks an envelope.
Once in the digestive system, the viruses multiply
within the intestinal epithelium.
Usually only mild intestinal symptoms result.
Occasionally viremia (the presence of viruses in the
blood) occurs and the viruses may spread to the liver.
The viruses reproduce in the liver, enter the bile, and are released
into the small intestine. This explains why feces are so infectious.
Symptoms last from 2 to 20 days and include anorexia, general
malaise, nausea, diarrhea, fever, and chills. If the liver becomes
infected, jaundice ensues. Laboratory diagnosis is by detection of
anti-hepatitis A antibody.
The number of new cases has been dramatically reduced since
the introduction of the hepatitis A vaccine in the 1990s.
Fortunately the mortality rate is low (less than 1%), and
infections in children are usually asymptomatic.
Control of infection is by simple hygienic measures, the sanitary
disposal of excreta, and the killed HAV vaccine (Havrix).
This vaccine is recommended for travelers going to regions with
high evidence rates of hepatitis A.
Poliomyelitis
Poliomyelitis [Greek polios, gray, and myelos, marrow
or spinal cord], polio, or infantile paralysis is caused by
the poliovirus, a member of the family Picornaviridae.
The poliovirus is a naked, positive-strand RNA virus
with three different serotypes—P1, P2, and P3.
The virus is very stable, especially at acidic pH, and
can remain infectious for relatively long periods in food
and water—its main routes of transmission.
The average incubation period is 6 to 20 days. Once
ingested, the virus multiplies in the mucosa of the
throat and/or small intestine.
From these sites the virus invades the tonsils and
lymph nodes of the neck and terminal portion of the
small intestine.
Generally, there are either no symptoms or a brief
illness characterized by fever, headache, sore throat,
vomiting, and loss of appetite. The virus sometimes
enters the bloodstream and causes a viremia.
In most cases (more than 99%), the viremia is
transient and clinical disease does not result.
In the minority of cases (less than 1%), the viremia
persists and the virus enters the central nervous
system and causes paralytic polio.
The virus has a high affinity for anterior horn motor
nerve cells of the spinal cord.
Once inside these cells, it multiplies and destroys the
cells; this results in motor and muscle paralysis.
Lassa Fever
Lassa fever is an acute illness caused by a negative-stand
RNA virus in the family Arenaviridae. The illness was
discovered in 1969 in Nigeria, West Africa. Lassa fever can
be mild and has no observable symptoms in about 80% of
people infected.
Lassa virus appears to be harbored by Old World rats and
mice (family Muridae, subfamily Murinae).These rodents
become chronically infected with arenaviruses, yet the
viruses do not appear to cause disease in their hosts.
The viruses are shed by infected rodents in urine or feces.
Lassa virus can be transmitted from person to person;
airborne and contact transmissions have been reported. No
vaccine is yet available to prevent Lassa fever. However,
ribavirin has been approved for use as a preventative
therapy.
Lymphocytic Choriomeningitis
Lymphocytic choriomeningitis (LCM) is another rodent-borne viral
infection caused by the lymphocytic choriomeningitis virus
(LCMV), a negative-strand RNA virus. LCMV is a member of the
family Arenaviridae and often presents as aseptic meningitis,
encephalitis, or meningoencephalitis.
Asymptomatic infection or mild febrile illnesses are also common
clinical manifestations of LCMV. Infection in utero may result in
spontaneous abortion, congenital hydrocephalus and
chorioretinitis, and mental retardation. LCMV is known to be
transmissible through organ transplantation. Recently, the death
of three organ transplant patients prompted an investigation by
the Rhode Island Department of Health, the Massachusetts
Department of Public Health, the CDC, the New England Organ
Bank, and the transplant centers involved. The three deceased
patients and one other living patient received organs from a
common donor. The CDC confirmed that all four patients were
infected with LCMV.
Rabies
Rabies [Latin rabere, rage or madness] is caused by a
number of different strains of highly neurotropic
viruses. Most belong to a single serotype in the genus
Lyssa virus [Greek lyssa, rage or rabies], family
Rhabdoviridae.
The bullet-shaped virion contains a negative-strand
RNA genome. Rabies has been the object of human
fascination, torment, and fear since the disease was
first recognized.
Improvements in prevention during the past 50 years
have led to almost complete elimination of
indigenously acquired rabies in the United States
where rabies is primarily a disease of feral animals.
Most wild animals can become infected with rabies, but
susceptibility varies according to species. Foxes,
coyotes, and wolves are the most susceptible;
intermediate are skunks, raccoons, insectivorous bats,
and bobcats; while opossums are quite resistant.
Worldwide, almost all cases of human rabies are
attributed to dog bites. In developing countries where
canine rabies is still endemic, rabies accounts for up to
40,000 deaths per year.
Occasionally, other domestic animals are responsible
for transmission of rabies to humans. It should be
noted, however, that not all rabid animals exhibit signs
of agitation and aggression (known as furious rabies).
In fact, paralysis (dumb rabies) is the more common
sign exhibited by rabid animals.
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