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I. RESPIRATORY INFECTIONS
SMALLPOX
(VARIOLA)
INTRODUCTION
An acute infectious disease caused by variola virus, and clinicall characterized
by a sudden onset of fever,headache, backache, vomiting and sometimes
convulsions, especially in children. On the third day of fever, a typical
rash appears which is centrifugal in distribution and passes through successive
stages of macule, papule, vesicle, pustule, and scab with subsequent scarring.
Previously, it was one of the greatest killer disease.
SMALL POX IN HISTORY
In 1967, WHO began an intensified worldwide campaign to eradicate
smallpox, based on the technique of surveillance and containment. The last
known case of smallpox in India occurred on 24th May 1975. India was
declared smallpox free on 5th July 1975. The eradication of smallpox was
confirmed in April 1977 by an international commission.
The World Health Assembly confirmed the global eradication of smallpox in
May 1980. All countries have discontinued routine vaccination against
smallpox.
However WHO maintains a reserve stock of smallpox vaccine and vaccination
needles - sufficient to protect more than 200 million people, should an
emergency arise
Case definition for notification of smallpox under
the International Health Regulations, 200
 An individual of any age presenting with acute onset of fever , malaise,
and severe prostration with headache and backache occurring 2-4 days
before onset of rash
 Subsequent development of a maculopapula rash starting on the face
and forearms then spreading to the trunk and legs,and round well
Vesicles, and
 Later pustules, which may become umbilicated or confluent
 Lesions that appear at the same stage of development
(i.e. all are vesicles or all are pustules) on any given part of
the body (e.g. the face or arm)
 No alternative diagnosis explaining the illness
 Laboratory confirmation.
Smallpox eradication surveillance
Despite the absence of smallpox, surveillance of "rumours" continues
in order to sustain public confidence in the eradication of the disease.
However, the final chapter of the smallpox story remains to be written, as the
smallpox virus has not been completely destroyed. Stocks are still held at
government research centres in the Russian Federation and at the United
States.
No known treatment is effective for smallpox. Medical management of
smallpox is mainly supportive. Supportive care in patients with symptomatic
smallpox consists of the following:
 The patient should be isolated until all scabs have fallen off (about 3-4
wk after rash onset) to prevent transmission of the variola virus to
nonimmune persons.
CHICKEN POX
Chickenpox or varicella is an acute, highly infectious disease caused by varicella-
zoster (V-Z) virus. It is characterized by vesicular rash that may be accompanied by
fever and malaise.
EPIDEMIOLOGY
It is worldwide in distribution and occurs in both epidemic and endemic forms.
Chickenpox and herpes zoster are now regarded as different host responses to
the same aetiological agent. Inoculation of zoster vesicle fluid into children
produces chickenpox, and children who have recovered from zoster virus related
infection are resistant to varicella
In India, during the year 2013, about 28,090 cases of chickenpox were reported
with 61 deaths. The case fatality rate was about 0.21 per cent. Kerala reported the
highest number of cases (12,168) and West Bengal reported the maximum number
of deaths (68) due to chickenpox
Epidemiological determinants
Agent factors
(a) AGENT :
The causative agent of chickenpox, V-Z virus is also called "Human (alpha) herpes
virus 3". Primary infection causes chickenpox.
(b) SOURCE OF INFECTION:
The virus occurs in the oropharypgeal secretions and lesions of skin
and mucosa. Rarely the source of infection may be a patient with herpes zoster.
(c) INFECTIVITY:
The period of communicability of patients with varicella is estimated to range from
1 to 2 days before the appearance of rash, and 4 to 5 days thereafter. The virus tends
to die out before the pustular stage
Host factors
(a) AGE :
Chickenpox occurs primarily among children under 10 years of age.
Few persons escape infection until adulthood. The disease can be
severe in normal adults.
(b)IMMUNITY:
One attack gives durable immunity; second attacks are rare. The
acquisition of maternal antibody protects the infant during the first few
mont
(c) PREGNANCY
Infection during pregnancy presents a risk for the foetus leading to
congenital varicella syndrome.
Environmental factors
Chickenpox shows a seasonal trend in temperate settings and in most tropical
settings, with peak incidence during winter and spring, or in coolest, driest
months in the tropics.
Transmission
Chickenpox is transmitted from person to person by droplet infection and by
droplet nuclei. Most patients are infected by "face-to-face" (personal) contact.
The portal of entry of the virus is the upper respiratory tract or the
conjunctiva.
Incubation period
Usually 14 to 16 days, although extremes as wide as 10 to 21 days.
CLINICAL FEATURES
(A) PRE-ERUPTIVE STAGE :
Onset is sudden with mild or moderate fever, pain in the back,
shivering and malaise. This stage is very brief, lasting about 24 hours
(B) ERUPTIVE STAGE : In children the rash is often the first sign. It
comes on the day the fever starts. The distinctive features of the rash are :
(a) Distribution.:
The rash is symmetrical. It first appears on the trunk where it is abundant, and
then comes on the face, arms and legs where it is less abundant. Mucosal
surfaces (e.g., buccal, pharyngeal) are generally involved.
(b) Rapid evolution :
The rash advances quickly through the stages of macule, papule, vesicle and
scthe vesicles filled with clear fluid and looking like "dew-drops" on the skin.
They are superficial in site, with easily ruptured walls and surrounded by an
area of inflammation.
(c) Pleomorphism :
A characteristic feature of the rash in chickenpox is its pleomorphism, that is,
all stages of the rash (papules, vesicles and crusts) may be seen
simultaneously at one time, in the same area.
(d) Fever
The fever does not run high but shows exacerbations with each fresh crop of
eruption.
LABORATORY DIAGNOSIS
 Detecting VZV DNA using polymerase chain reaetion (PCR)
 Isolating VZV in cell culture from vesicular fluid, crusts, saliva,
cerebrospinal fluid or other specimens.
 Direct immunofluorescence
 Detection of VZV-specific serum lgM antibody
Prevention
1. VARICELLA-ZOSTER IMMUNOGLOBULIN (VZIG)
Varicella-Zoster Immunoglobulin (VZIG) given within 72 hours of exposure
has been recommended for prevention of chickenpox in exposed susceptible
individuals particularly in immunosuppressed persons.
VZIG is given by intramuscular injection in a dose of 12.5 units/kg body
weight up to a maximum of 625 units, with a repeat dose in 3 weeks,
2. VACCINE
A live attenuated varicella virus vaccine is safe and currently recommended
for children between 12-18 months of age who have not had chickenpox.
Monovalent vaccine can be administered following one or two dose schedule
(0.5 ml) each by subcutaneous injection. A 2 dose schedule is
recommended for all persons aged 2 13 years.
When 2 doses(bivalent) are administered, the minimum interval between
doses is either 6 weeks or 3 months for children (12 months to 12 years of age
inclusive), and 4 or 6 weeks for adolescents and adults (13 years of age and
older).
Combination vaccines (MMRV) can be administered to children from 9
months to 12 years. If 2 doses of MMRV are used, the minimum interval
between doses should be 4 weeks. It is preferred that the 2nd dose be
administered 6 weeks to 3 months after the first dose or at 4-6 years of age.
COMPLICATIONS
 haemorrhages (varicella haemorrhagical),
 pneumonia,
 encephalitis,
 acute cerebellar ataxia and
 Reye's syndrome (acute encephalopathy associated with fatty
degeneration of the viscera especially liver)
 Maternal varicella during pregnancy may cause,
 foetal wastage and birth defects such as cutaneous scars,
atrophied limbs, microcephaly and low birth weight,
 cataract, microphthalmia, chorioretinitis, deafness
 Secondary bacterial infections, particularly with group A
{3-haemolytic streptococci and staphylococcus aureus are common.
 Cellulitis,
 erysipelas,
 epiglottitis,
 osteomyelitis,
 scarlet fever and rarely meningitis are observed.
 Pitted scars
 acute retinal necrosis and progressive outer retinal necrosis, both of
which occur with increased frequency among AIDS patients.
_______
MUMPS
An acute infectious disease caused by an RNA virus classified as
genus Rubulavirus of the family paramyxoviridae which has a predilection for
glandular and nervous tissues. Clinically, the disease is recognized by
nonsuppurative enlargement and tenderness of one or both the parotid glands.
Agent factors
(a)AGENT :
The causative agent, Myxovirus parotiditis is a RNA virus of the
myxovirus family. The virus can be grown readily in chick embryo or tissue
culture. There is only one serotype.
(b) SOURCE OF INFECTION :
Both clinical and subclinical cases. Subclinical cases which account for
30-40 per cent of all cases appear to be responsible for maintaining the cycle
of infection. The virus can be isolated from the saliva or from swabs taken
from the surface of Stenson's duct. Virus has also been found in the blood,
urine, human milk and on occasion in the CSF.
(c)PERIOD OF COMMUNICABILITY :
Usually 4-6 days before the onset of symptoms and a week or more
thereafter. The period of maximum infectivity is just before and at the onset of
parotitis.
Host factors
(a)AGE AND SEX :
Mumps is the most frequent cause of parotitis in children in the age
group 5-9 years.
(b)IMMUNITY:
One attack, clinical or subclinical, is assumed to induce lifelong
immunity. There is only one antigenic type of mumps virus, and it does
not exhibit significant antigenic variation.
Most infants below the age of 6 months are immune because
of maternal antibodies.
Environmental factors
Mumps is largely an endemic disease. Cases occur throughout the year, but
the peak incidence is in winter and spring. Epidemics are often associated
with overcrowding.
Mode of transmission
The disease is spread mainly by droplet infection and after direct contact with
an infected person.
Incubation period
Varies from 2 to 4 weeks, usually 14-18 days
CLICAL FEATURES
 pain and swelling in either one or both the parotid glands but may also
involve the sublingual and submandibular glands.
 Complaint of "ear ache" on the affected side prior to the onset of
swelling.
 pain and stiffness on opening the mouth before the swelling of the
gland is evident.
 Mumps may also affect the testes, pancreas, CNS, ovaries, prostate,
etc.
In severe cases, there may be fever,headache and other constitutional
symptoms which may last from 3-5 days.
The swelling subsides slowly over 1-2 weeks.
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  • 1. I. RESPIRATORY INFECTIONS SMALLPOX (VARIOLA) INTRODUCTION An acute infectious disease caused by variola virus, and clinicall characterized by a sudden onset of fever,headache, backache, vomiting and sometimes convulsions, especially in children. On the third day of fever, a typical rash appears which is centrifugal in distribution and passes through successive stages of macule, papule, vesicle, pustule, and scab with subsequent scarring. Previously, it was one of the greatest killer disease. SMALL POX IN HISTORY In 1967, WHO began an intensified worldwide campaign to eradicate smallpox, based on the technique of surveillance and containment. The last known case of smallpox in India occurred on 24th May 1975. India was declared smallpox free on 5th July 1975. The eradication of smallpox was confirmed in April 1977 by an international commission. The World Health Assembly confirmed the global eradication of smallpox in May 1980. All countries have discontinued routine vaccination against smallpox. However WHO maintains a reserve stock of smallpox vaccine and vaccination needles - sufficient to protect more than 200 million people, should an emergency arise Case definition for notification of smallpox under the International Health Regulations, 200  An individual of any age presenting with acute onset of fever , malaise, and severe prostration with headache and backache occurring 2-4 days before onset of rash  Subsequent development of a maculopapula rash starting on the face and forearms then spreading to the trunk and legs,and round well
  • 2. Vesicles, and  Later pustules, which may become umbilicated or confluent  Lesions that appear at the same stage of development (i.e. all are vesicles or all are pustules) on any given part of the body (e.g. the face or arm)  No alternative diagnosis explaining the illness  Laboratory confirmation. Smallpox eradication surveillance Despite the absence of smallpox, surveillance of "rumours" continues in order to sustain public confidence in the eradication of the disease. However, the final chapter of the smallpox story remains to be written, as the smallpox virus has not been completely destroyed. Stocks are still held at government research centres in the Russian Federation and at the United States. No known treatment is effective for smallpox. Medical management of smallpox is mainly supportive. Supportive care in patients with symptomatic smallpox consists of the following:  The patient should be isolated until all scabs have fallen off (about 3-4 wk after rash onset) to prevent transmission of the variola virus to nonimmune persons.
  • 3. CHICKEN POX Chickenpox or varicella is an acute, highly infectious disease caused by varicella- zoster (V-Z) virus. It is characterized by vesicular rash that may be accompanied by fever and malaise. EPIDEMIOLOGY It is worldwide in distribution and occurs in both epidemic and endemic forms. Chickenpox and herpes zoster are now regarded as different host responses to the same aetiological agent. Inoculation of zoster vesicle fluid into children produces chickenpox, and children who have recovered from zoster virus related infection are resistant to varicella In India, during the year 2013, about 28,090 cases of chickenpox were reported with 61 deaths. The case fatality rate was about 0.21 per cent. Kerala reported the highest number of cases (12,168) and West Bengal reported the maximum number of deaths (68) due to chickenpox Epidemiological determinants Agent factors (a) AGENT : The causative agent of chickenpox, V-Z virus is also called "Human (alpha) herpes virus 3". Primary infection causes chickenpox. (b) SOURCE OF INFECTION: The virus occurs in the oropharypgeal secretions and lesions of skin and mucosa. Rarely the source of infection may be a patient with herpes zoster. (c) INFECTIVITY: The period of communicability of patients with varicella is estimated to range from 1 to 2 days before the appearance of rash, and 4 to 5 days thereafter. The virus tends to die out before the pustular stage
  • 4. Host factors (a) AGE : Chickenpox occurs primarily among children under 10 years of age. Few persons escape infection until adulthood. The disease can be severe in normal adults. (b)IMMUNITY: One attack gives durable immunity; second attacks are rare. The acquisition of maternal antibody protects the infant during the first few mont (c) PREGNANCY Infection during pregnancy presents a risk for the foetus leading to congenital varicella syndrome. Environmental factors Chickenpox shows a seasonal trend in temperate settings and in most tropical settings, with peak incidence during winter and spring, or in coolest, driest months in the tropics. Transmission Chickenpox is transmitted from person to person by droplet infection and by droplet nuclei. Most patients are infected by "face-to-face" (personal) contact. The portal of entry of the virus is the upper respiratory tract or the conjunctiva. Incubation period Usually 14 to 16 days, although extremes as wide as 10 to 21 days. CLINICAL FEATURES (A) PRE-ERUPTIVE STAGE : Onset is sudden with mild or moderate fever, pain in the back, shivering and malaise. This stage is very brief, lasting about 24 hours
  • 5. (B) ERUPTIVE STAGE : In children the rash is often the first sign. It comes on the day the fever starts. The distinctive features of the rash are : (a) Distribution.: The rash is symmetrical. It first appears on the trunk where it is abundant, and then comes on the face, arms and legs where it is less abundant. Mucosal surfaces (e.g., buccal, pharyngeal) are generally involved. (b) Rapid evolution : The rash advances quickly through the stages of macule, papule, vesicle and scthe vesicles filled with clear fluid and looking like "dew-drops" on the skin. They are superficial in site, with easily ruptured walls and surrounded by an area of inflammation. (c) Pleomorphism : A characteristic feature of the rash in chickenpox is its pleomorphism, that is, all stages of the rash (papules, vesicles and crusts) may be seen simultaneously at one time, in the same area. (d) Fever The fever does not run high but shows exacerbations with each fresh crop of eruption. LABORATORY DIAGNOSIS  Detecting VZV DNA using polymerase chain reaetion (PCR)  Isolating VZV in cell culture from vesicular fluid, crusts, saliva, cerebrospinal fluid or other specimens.  Direct immunofluorescence  Detection of VZV-specific serum lgM antibody Prevention 1. VARICELLA-ZOSTER IMMUNOGLOBULIN (VZIG) Varicella-Zoster Immunoglobulin (VZIG) given within 72 hours of exposure has been recommended for prevention of chickenpox in exposed susceptible individuals particularly in immunosuppressed persons.
  • 6. VZIG is given by intramuscular injection in a dose of 12.5 units/kg body weight up to a maximum of 625 units, with a repeat dose in 3 weeks, 2. VACCINE A live attenuated varicella virus vaccine is safe and currently recommended for children between 12-18 months of age who have not had chickenpox. Monovalent vaccine can be administered following one or two dose schedule (0.5 ml) each by subcutaneous injection. A 2 dose schedule is recommended for all persons aged 2 13 years. When 2 doses(bivalent) are administered, the minimum interval between doses is either 6 weeks or 3 months for children (12 months to 12 years of age inclusive), and 4 or 6 weeks for adolescents and adults (13 years of age and older). Combination vaccines (MMRV) can be administered to children from 9 months to 12 years. If 2 doses of MMRV are used, the minimum interval between doses should be 4 weeks. It is preferred that the 2nd dose be administered 6 weeks to 3 months after the first dose or at 4-6 years of age. COMPLICATIONS  haemorrhages (varicella haemorrhagical),  pneumonia,  encephalitis,  acute cerebellar ataxia and  Reye's syndrome (acute encephalopathy associated with fatty degeneration of the viscera especially liver)  Maternal varicella during pregnancy may cause,  foetal wastage and birth defects such as cutaneous scars, atrophied limbs, microcephaly and low birth weight,  cataract, microphthalmia, chorioretinitis, deafness
  • 7.  Secondary bacterial infections, particularly with group A {3-haemolytic streptococci and staphylococcus aureus are common.  Cellulitis,  erysipelas,  epiglottitis,  osteomyelitis,  scarlet fever and rarely meningitis are observed.  Pitted scars  acute retinal necrosis and progressive outer retinal necrosis, both of which occur with increased frequency among AIDS patients. _______ MUMPS An acute infectious disease caused by an RNA virus classified as genus Rubulavirus of the family paramyxoviridae which has a predilection for glandular and nervous tissues. Clinically, the disease is recognized by nonsuppurative enlargement and tenderness of one or both the parotid glands. Agent factors (a)AGENT : The causative agent, Myxovirus parotiditis is a RNA virus of the myxovirus family. The virus can be grown readily in chick embryo or tissue culture. There is only one serotype. (b) SOURCE OF INFECTION : Both clinical and subclinical cases. Subclinical cases which account for 30-40 per cent of all cases appear to be responsible for maintaining the cycle of infection. The virus can be isolated from the saliva or from swabs taken from the surface of Stenson's duct. Virus has also been found in the blood, urine, human milk and on occasion in the CSF. (c)PERIOD OF COMMUNICABILITY : Usually 4-6 days before the onset of symptoms and a week or more thereafter. The period of maximum infectivity is just before and at the onset of parotitis.
  • 8. Host factors (a)AGE AND SEX : Mumps is the most frequent cause of parotitis in children in the age group 5-9 years. (b)IMMUNITY: One attack, clinical or subclinical, is assumed to induce lifelong immunity. There is only one antigenic type of mumps virus, and it does not exhibit significant antigenic variation. Most infants below the age of 6 months are immune because of maternal antibodies. Environmental factors Mumps is largely an endemic disease. Cases occur throughout the year, but the peak incidence is in winter and spring. Epidemics are often associated with overcrowding. Mode of transmission The disease is spread mainly by droplet infection and after direct contact with an infected person. Incubation period Varies from 2 to 4 weeks, usually 14-18 days CLICAL FEATURES  pain and swelling in either one or both the parotid glands but may also involve the sublingual and submandibular glands.  Complaint of "ear ache" on the affected side prior to the onset of swelling.  pain and stiffness on opening the mouth before the swelling of the gland is evident.  Mumps may also affect the testes, pancreas, CNS, ovaries, prostate, etc. In severe cases, there may be fever,headache and other constitutional symptoms which may last from 3-5 days. The swelling subsides slowly over 1-2 weeks.