B Y : M A N I S H A S H A R M A
N U R S I N G T U T O R
CHICKENPOX & SMALLPOX
CHICKENPOX
DEFINITION AND INTRODUCTION
 Chickenpox, also known as varicella, is a
highly contagious disease caused by the
initial infection with varicella zoster virus (VZV). The
disease results in a characteristic skin rash that
forms small, itchy blisters, which eventually scab
over. It usually starts on the chest, back, and face. It
then spreads to the rest of the body. Other symptoms
may include fever, tiredness, and headaches.
Symptoms usually last five to seven days.
EPIDEMIOLOGY
 Chickenpox is primarily a disease of children, with most
cases occurring during the winter and spring, most likely
due to school contact. Chickenpox occurs in all parts of
the world. In 2013 there were 140 million cases of
chickenpox and shingles worldwide. Before routine
immunization the number of cases occurring each year
was similar to the number of people born. In 2015
chickenpox resulted in 6,400 deaths globally – down
from 8,900 in 1990. Death occurs in about 1 per 60,000
cases. Chickenpox was not separated from smallpox until
the late 19th century. In 1888 its connection
to shingles was determined. The first documented use of
the term chicken pox was in 1658.
MODE OF TRASMISSION
 Chickenpox is an airborne disease which spreads
easily from one person to the next through the
coughs and sneezes of an infected person. It may be
spread from one to two days before the rash appears
until all lesions have crusted over. It may also spread
through contact with the blisters. Those
with shingles may spread chickenpox to those who
are not immune through contact with the blisters.
CLINICAL MANIFESTATIONS
 In children, the first sign is the rash or the spots in the
oral cavity. The rash begins as small red dots on the face,
scalp, torso, upper arms and legs; progressing over 10–12
hours to small bumps, blisters and pustules; followed
by umbilication and the formation of scabs.
 At the blister stage, intense itching is usually present.
Blisters may also occur on the palms, soles, and genital
area. Commonly, visible evidence of the disease develops
in the oral cavity and tonsil areas in the form of small
ulcers which can be painful or itchy or both; this
enanthem (internal rash) can precede the exanthem
(external rash) by 1 to 3 days or can be concurrent.
CONTINUE
 These symptoms of chickenpox appear 10 to 21 days after
exposure to a contagious person. Adults may have a more
widespread rash and longer fever, and they are more
likely to experience complications, such as
varicella pneumonia.
 The early (prodromal) symptoms in adolescents and
adults are nausea, loss of appetite, aching muscles, and
headache. This is followed by the characteristic rash or
oral sores, malaise, and a low-grade fever that signal the
presence of the disease. Oral manifestations of the
disease not uncommonly may precede the external rash.
CONTINUE
 During pregnancy the dangers to the fetus
associated with a primary VZV infection are greater
in the first six months. In the third trimester, the
mother is more likely to have severe
symptoms. Varicella infection in pregnant women
could lead to spread via the placenta and infection of
the fetus. If infection occurs during the first 28
weeks of gestation, this can lead to fetal varicella
syndrome (also known as congenital varicella
syndrome). Effects on the fetus can range in severity
from underdeveloped toes and fingers to severe anal
and bladder malformation.
CONTINUE
• Possible problems include:
 Damage to brain:
• Encephalitis, microcephaly, hydrocephaly, aplasia of brain
 Damage to the eye:
• Optic stalk, optic cup, and
lens vesicles, microphthalmia, cataracts, chorioretinitis, optic
atrophy
 Other neurological disorder:
• Damage to cervical and lumbosacral spinal cord, motor/sensory
deficits, absent deep tendon reflexes
 Damage to body:
• Hypoplasia of upper/lower extremities, anal and
bladder sphincter dysfunction
 Skin disorders:
• Skin lesions, hypopigmentation
PATHOPHYSIOLOGY
 Exposure to VZV in a healthy child initiates the
production of host IgG, IgM, and IgA antibodies; IgG
antibodies persist for life and confer immunity. Cell-
mediated immune responses are also important in
limiting the scope and the duration of primary varicella
infection. After primary infection, VZV is hypothesized to
spread from mucosal and epidermal lesions to
local sensory nerves. VZV then remains latent in
the dorsal ganglion cells of the sensory nerves.
Reactivation of VZV results in the clinically distinct
syndrome of herpes zoster (i.e., shingles), postherapuetic
neuralgia.
SHINGLES
 After a chickenpox infection, the virus remains
dormant in the body's nerve tissues for about 50
years. This, however, does not mean that VZV cannot
be contracted later in life. The immune
system usually keeps the virus at bay, however it can
still manifest itself at any given age between 1 and
60, causing a different form of the viral infection
called shingles (also known as herpes zoster)
Shingles affects one in five adults infected with
chickenpox as children, especially those who are
immune-suppressed, particularly from cancer, HIV,
or other conditions.
DIAGNOSTIC EVALUATION
 The diagnosis of chickenpox is primarily based on
the signs and symptoms, with typical early
symptoms followed by a characteristic rash.
Confirmation of the diagnosis is by examination of
the fluid within the vesicles of the rash, or by testing
blood for evidence of an acute immunologic
response.
 Vesicular fluid can be examined with a Tzanck
smear, or by testing for direct fluorescent antibody.
CONTINUE
 Blood tests can be used to identify a response to
acute infection (IgM) or previous infection and
subsequent immunity (IgG).
 Prenatal diagnosis of fetal varicella infection can
be performed using ultrasound, though a delay of 5
weeks following primary maternal infection is
advised. A PCR (DNA) test of the mother's amniotic
fluid can also be performed
TREATMENT
 Treatment mainly consists of easing the symptoms. As a
protective measure, people are usually required to stay at
home while they are infectious to avoid spreading the
disease to others. Cutting the nails short or
wearing gloves may prevent scratching and minimize the
risk of secondary infections. Calamine lotion a topical ,
and one of the most commonly used interventions it has
an excellent safety profile. It is important to maintain
good hygiene and daily cleaning of skin with warm water
to avoid secondary bacterial infection. Scratching may
also increase the risk of secondary infection.
CONTINUE
 In children: Aciclovir by mouth is started within 24 hours
of rash onset, it decreases symptoms by one day but has no
effect on complication rates. Use of aciclovir therefore is not
currently recommended for individuals with normal immune
function.
 Infection in otherwise healthy adults tends to be more
severe. Antiviral drugs Aciclovir etc is generally advised,
as long as it is started within 24–48 hours from rash onset.
Adults are more often prescribed antiviral medication, as it is
effective in reducing the severity of the condition and the
likelihood of developing complications. Adults are advised to
increase water intake. Painkillers such as paracetamol are
recommended. Antihistamines relieve itching and may be
used in cases where the itching prevents sleep, because they
also act as a sedative.
PREVENTION
 Hygiene measures
The spread of chickenpox can be prevented by
isolating affected individuals. Contagion is by
exposure to respiratory droplets, or direct contact
with lesions, within a period lasting from three days
before the onset of the rash, to four days after the
onset of the rash. The chickenpox virus is susceptible
to disinfectants, notably chlorine bleach (i.e., sodium
hypochlorite). Like all enveloped viruses, it is
sensitive to drying, heat and detergents.
SMALLPOX
DEFINITION & INTRODUCTION
 Smallpox was an infectious disease caused by one
of two virus variants, Variola major and Variola
minor. The agent of variola virus belongs to the
genus Orthopoxvirus. The last naturally occurring
case was diagnosed in October 1977, and the World
Health Organization (WHO) certified the global
eradication of the disease in 1980. The risk of
death after contracting the disease was about 30%,
with higher rates among babies. Often those who
survived had extensive scarring of their skin, and
some were left blind.
Man with facial scarring and blindness due to smallpox
HISTORIC EPIDEMIOLOGY
 The origin of smallpox is unknown; however, the
earliest evidence of the disease dates to the 3rd
century BCE in Egyptian mummies. The disease
historically occurred in outbreaks. In 18th-century
Europe, it is estimated that 400,000 people died
from the disease per year, and that one-third of all
cases of blindness were due to smallpox. Smallpox is
estimated to have killed up to 300 million people in
the 20th century and around 500 million people in
the last 100 years of its existence.
CLASSIFICATION
 There were two forms of the smallpox virus:
 Variola major was the severe and most common
form, with a more extensive rash and higher fever. It
could result in confluent smallpox, which had a high
death rate of about 30%.
 Variola minor was a less common presentation,
causing less severe disease, typically discrete
smallpox, with historical death rates of 1% or
less. Subclinical (asymptomatic) infections
with Variola virus were noted but were not common.
CONTINUE
 In addition, a form called variola sine
eruptione (smallpox without rash) was seen
generally in vaccinated persons. This form was
marked by a fever that occurred after the
usual incubation period and could be confirmed only
by antibody studies or, rarely, by viral culture.
 In addition, there were two very rare and fulminating
types of smallpox, the malignant and hemorrhagic
forms, which were usually fatal.
MODE OF TRANSMISSION
 Transmission occurred through inhalation
of airborne Variola virus, usually droplets expressed
from the oral, nasal, or pharyngeal mucosa of an
infected person. It was transmitted from one person
to another primarily through prolonged face-to-face
contact with an infected person, usually, within a
distance of 1.8 m (6 feet), but could also be spread
through direct contact with infected bodily fluids or
fomites such as bedding or clothing. Rarely,
smallpox was spread by virus carried in the air in
enclosed settings such as buildings, buses, and
trains.
CLINICAL MANIFESTATIONS
 The initial symptoms were similar to other viral
diseases that are still extant, such as:
• Influenza
• Common cold
• Fever of at least 101 °F
• Muscle pain
• Malaise
• Headache
• Fatigue
CONTINUE
 Digestive symptoms such as
• Nausea
• Vomiting
• Backache
 The early prodromal stage usually lasted 2–4 days.
By days 12–15, the first visible lesions – small
reddish spots called enanthem – appeared on
mucous membranes of the mouth, tongue, palate,
and throat, and the temperature fell to near-normal.
These lesions rapidly enlarged and ruptured,
releasing large amounts of virus into the saliva
PATHOGENESIS
 Smallpox virus tended to attack skin cells, causing
the characteristic pimples, or macules, associated
with the disease. A rash developed on the skin 24 to
48 hours after lesions on the mucous membranes
appeared. Typically the macules first appeared on
the forehead, then rapidly spread to the whole
face, proximal portions of extremities, the trunk, and
lastly to distal portions of extremities. The process
took no more than 24 to 36 hours, after which no
new lesions appeared.
PATHOPHYSIOLOGY
 Once inhaled, the variola virus invaded the mucus
membranes of the mouth, throat, and respiratory
tract. From there, it migrated to regional lymph
nodes and began to multiply. In the initial growth
phase, the virus seemed to move from cell to cell, but
by around the 12th day, widespread lysis of infected
cells occurred and the virus could be found in the
bloodstream in large numbers, a condition known
as viremia. This resulted in the second wave of
multiplication in the spleen, bone marrow, and
lymph nodes.
TREATMENT
 Treatment of smallpox is primarily supportive, such
as wound care and infection control, fluid therapy,
and possible ventilator assistance. Flat and
hemorrhagic types of smallpox are treated with the
same therapies used to treat shock, such as fluid
resuscitation.
 Tecovirimat, the first drug approved for treatment of
smallpox. Antiviral treatments have improved since
the last large smallpox epidemics, and studies
suggest that the antiviral drug cidofovir might be
useful as a therapeutic agent
THANK YOU

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Chickenpox and smallpox

  • 1. B Y : M A N I S H A S H A R M A N U R S I N G T U T O R CHICKENPOX & SMALLPOX
  • 3. DEFINITION AND INTRODUCTION  Chickenpox, also known as varicella, is a highly contagious disease caused by the initial infection with varicella zoster virus (VZV). The disease results in a characteristic skin rash that forms small, itchy blisters, which eventually scab over. It usually starts on the chest, back, and face. It then spreads to the rest of the body. Other symptoms may include fever, tiredness, and headaches. Symptoms usually last five to seven days.
  • 4. EPIDEMIOLOGY  Chickenpox is primarily a disease of children, with most cases occurring during the winter and spring, most likely due to school contact. Chickenpox occurs in all parts of the world. In 2013 there were 140 million cases of chickenpox and shingles worldwide. Before routine immunization the number of cases occurring each year was similar to the number of people born. In 2015 chickenpox resulted in 6,400 deaths globally – down from 8,900 in 1990. Death occurs in about 1 per 60,000 cases. Chickenpox was not separated from smallpox until the late 19th century. In 1888 its connection to shingles was determined. The first documented use of the term chicken pox was in 1658.
  • 5. MODE OF TRASMISSION  Chickenpox is an airborne disease which spreads easily from one person to the next through the coughs and sneezes of an infected person. It may be spread from one to two days before the rash appears until all lesions have crusted over. It may also spread through contact with the blisters. Those with shingles may spread chickenpox to those who are not immune through contact with the blisters.
  • 6. CLINICAL MANIFESTATIONS  In children, the first sign is the rash or the spots in the oral cavity. The rash begins as small red dots on the face, scalp, torso, upper arms and legs; progressing over 10–12 hours to small bumps, blisters and pustules; followed by umbilication and the formation of scabs.  At the blister stage, intense itching is usually present. Blisters may also occur on the palms, soles, and genital area. Commonly, visible evidence of the disease develops in the oral cavity and tonsil areas in the form of small ulcers which can be painful or itchy or both; this enanthem (internal rash) can precede the exanthem (external rash) by 1 to 3 days or can be concurrent.
  • 7. CONTINUE  These symptoms of chickenpox appear 10 to 21 days after exposure to a contagious person. Adults may have a more widespread rash and longer fever, and they are more likely to experience complications, such as varicella pneumonia.  The early (prodromal) symptoms in adolescents and adults are nausea, loss of appetite, aching muscles, and headache. This is followed by the characteristic rash or oral sores, malaise, and a low-grade fever that signal the presence of the disease. Oral manifestations of the disease not uncommonly may precede the external rash.
  • 8. CONTINUE  During pregnancy the dangers to the fetus associated with a primary VZV infection are greater in the first six months. In the third trimester, the mother is more likely to have severe symptoms. Varicella infection in pregnant women could lead to spread via the placenta and infection of the fetus. If infection occurs during the first 28 weeks of gestation, this can lead to fetal varicella syndrome (also known as congenital varicella syndrome). Effects on the fetus can range in severity from underdeveloped toes and fingers to severe anal and bladder malformation.
  • 9. CONTINUE • Possible problems include:  Damage to brain: • Encephalitis, microcephaly, hydrocephaly, aplasia of brain  Damage to the eye: • Optic stalk, optic cup, and lens vesicles, microphthalmia, cataracts, chorioretinitis, optic atrophy  Other neurological disorder: • Damage to cervical and lumbosacral spinal cord, motor/sensory deficits, absent deep tendon reflexes  Damage to body: • Hypoplasia of upper/lower extremities, anal and bladder sphincter dysfunction  Skin disorders: • Skin lesions, hypopigmentation
  • 10. PATHOPHYSIOLOGY  Exposure to VZV in a healthy child initiates the production of host IgG, IgM, and IgA antibodies; IgG antibodies persist for life and confer immunity. Cell- mediated immune responses are also important in limiting the scope and the duration of primary varicella infection. After primary infection, VZV is hypothesized to spread from mucosal and epidermal lesions to local sensory nerves. VZV then remains latent in the dorsal ganglion cells of the sensory nerves. Reactivation of VZV results in the clinically distinct syndrome of herpes zoster (i.e., shingles), postherapuetic neuralgia.
  • 11. SHINGLES  After a chickenpox infection, the virus remains dormant in the body's nerve tissues for about 50 years. This, however, does not mean that VZV cannot be contracted later in life. The immune system usually keeps the virus at bay, however it can still manifest itself at any given age between 1 and 60, causing a different form of the viral infection called shingles (also known as herpes zoster) Shingles affects one in five adults infected with chickenpox as children, especially those who are immune-suppressed, particularly from cancer, HIV, or other conditions.
  • 12. DIAGNOSTIC EVALUATION  The diagnosis of chickenpox is primarily based on the signs and symptoms, with typical early symptoms followed by a characteristic rash. Confirmation of the diagnosis is by examination of the fluid within the vesicles of the rash, or by testing blood for evidence of an acute immunologic response.  Vesicular fluid can be examined with a Tzanck smear, or by testing for direct fluorescent antibody.
  • 13. CONTINUE  Blood tests can be used to identify a response to acute infection (IgM) or previous infection and subsequent immunity (IgG).  Prenatal diagnosis of fetal varicella infection can be performed using ultrasound, though a delay of 5 weeks following primary maternal infection is advised. A PCR (DNA) test of the mother's amniotic fluid can also be performed
  • 14. TREATMENT  Treatment mainly consists of easing the symptoms. As a protective measure, people are usually required to stay at home while they are infectious to avoid spreading the disease to others. Cutting the nails short or wearing gloves may prevent scratching and minimize the risk of secondary infections. Calamine lotion a topical , and one of the most commonly used interventions it has an excellent safety profile. It is important to maintain good hygiene and daily cleaning of skin with warm water to avoid secondary bacterial infection. Scratching may also increase the risk of secondary infection.
  • 15. CONTINUE  In children: Aciclovir by mouth is started within 24 hours of rash onset, it decreases symptoms by one day but has no effect on complication rates. Use of aciclovir therefore is not currently recommended for individuals with normal immune function.  Infection in otherwise healthy adults tends to be more severe. Antiviral drugs Aciclovir etc is generally advised, as long as it is started within 24–48 hours from rash onset. Adults are more often prescribed antiviral medication, as it is effective in reducing the severity of the condition and the likelihood of developing complications. Adults are advised to increase water intake. Painkillers such as paracetamol are recommended. Antihistamines relieve itching and may be used in cases where the itching prevents sleep, because they also act as a sedative.
  • 16. PREVENTION  Hygiene measures The spread of chickenpox can be prevented by isolating affected individuals. Contagion is by exposure to respiratory droplets, or direct contact with lesions, within a period lasting from three days before the onset of the rash, to four days after the onset of the rash. The chickenpox virus is susceptible to disinfectants, notably chlorine bleach (i.e., sodium hypochlorite). Like all enveloped viruses, it is sensitive to drying, heat and detergents.
  • 18. DEFINITION & INTRODUCTION  Smallpox was an infectious disease caused by one of two virus variants, Variola major and Variola minor. The agent of variola virus belongs to the genus Orthopoxvirus. The last naturally occurring case was diagnosed in October 1977, and the World Health Organization (WHO) certified the global eradication of the disease in 1980. The risk of death after contracting the disease was about 30%, with higher rates among babies. Often those who survived had extensive scarring of their skin, and some were left blind.
  • 19. Man with facial scarring and blindness due to smallpox
  • 20. HISTORIC EPIDEMIOLOGY  The origin of smallpox is unknown; however, the earliest evidence of the disease dates to the 3rd century BCE in Egyptian mummies. The disease historically occurred in outbreaks. In 18th-century Europe, it is estimated that 400,000 people died from the disease per year, and that one-third of all cases of blindness were due to smallpox. Smallpox is estimated to have killed up to 300 million people in the 20th century and around 500 million people in the last 100 years of its existence.
  • 21. CLASSIFICATION  There were two forms of the smallpox virus:  Variola major was the severe and most common form, with a more extensive rash and higher fever. It could result in confluent smallpox, which had a high death rate of about 30%.  Variola minor was a less common presentation, causing less severe disease, typically discrete smallpox, with historical death rates of 1% or less. Subclinical (asymptomatic) infections with Variola virus were noted but were not common.
  • 22. CONTINUE  In addition, a form called variola sine eruptione (smallpox without rash) was seen generally in vaccinated persons. This form was marked by a fever that occurred after the usual incubation period and could be confirmed only by antibody studies or, rarely, by viral culture.  In addition, there were two very rare and fulminating types of smallpox, the malignant and hemorrhagic forms, which were usually fatal.
  • 23. MODE OF TRANSMISSION  Transmission occurred through inhalation of airborne Variola virus, usually droplets expressed from the oral, nasal, or pharyngeal mucosa of an infected person. It was transmitted from one person to another primarily through prolonged face-to-face contact with an infected person, usually, within a distance of 1.8 m (6 feet), but could also be spread through direct contact with infected bodily fluids or fomites such as bedding or clothing. Rarely, smallpox was spread by virus carried in the air in enclosed settings such as buildings, buses, and trains.
  • 24. CLINICAL MANIFESTATIONS  The initial symptoms were similar to other viral diseases that are still extant, such as: • Influenza • Common cold • Fever of at least 101 °F • Muscle pain • Malaise • Headache • Fatigue
  • 25. CONTINUE  Digestive symptoms such as • Nausea • Vomiting • Backache  The early prodromal stage usually lasted 2–4 days. By days 12–15, the first visible lesions – small reddish spots called enanthem – appeared on mucous membranes of the mouth, tongue, palate, and throat, and the temperature fell to near-normal. These lesions rapidly enlarged and ruptured, releasing large amounts of virus into the saliva
  • 26. PATHOGENESIS  Smallpox virus tended to attack skin cells, causing the characteristic pimples, or macules, associated with the disease. A rash developed on the skin 24 to 48 hours after lesions on the mucous membranes appeared. Typically the macules first appeared on the forehead, then rapidly spread to the whole face, proximal portions of extremities, the trunk, and lastly to distal portions of extremities. The process took no more than 24 to 36 hours, after which no new lesions appeared.
  • 27. PATHOPHYSIOLOGY  Once inhaled, the variola virus invaded the mucus membranes of the mouth, throat, and respiratory tract. From there, it migrated to regional lymph nodes and began to multiply. In the initial growth phase, the virus seemed to move from cell to cell, but by around the 12th day, widespread lysis of infected cells occurred and the virus could be found in the bloodstream in large numbers, a condition known as viremia. This resulted in the second wave of multiplication in the spleen, bone marrow, and lymph nodes.
  • 28. TREATMENT  Treatment of smallpox is primarily supportive, such as wound care and infection control, fluid therapy, and possible ventilator assistance. Flat and hemorrhagic types of smallpox are treated with the same therapies used to treat shock, such as fluid resuscitation.  Tecovirimat, the first drug approved for treatment of smallpox. Antiviral treatments have improved since the last large smallpox epidemics, and studies suggest that the antiviral drug cidofovir might be useful as a therapeutic agent