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POX VIRUSES
PRESENTED BY:
ARCHANA KUMARI SHAW
ROLL.NO.: 02
M.SC. 1ST YEAR 1ST SEMESTER
Submitted To,
Dr. N. Shivakumar Sir.
GENERAL CHARACTERISTICS OF VIRUSES
Viruses are intracellular organisms, that are made of either
DNA or RNA, they dwell inside the cell & destroys it. Viral
infections are self limiting. They cannot be killed by antibiotics,
this why no medications are given for the treatment instead
medication are given to relieve the symptoms.
They are measured in nm, about 20-300 in dia, they are
obligate intracellular parasites.
Pox virus is the largest and most complex. So, they can be seen
under microscope. They can replicate in the cytoplasm.
They are dsDNA virus. They can grow in chorioallantoic membrane
(CAM) of chick embryo and tissue culture
MORPHLOGY & GENOME
• Enveloped, brick-shaped or ovoid virion, with rounded corners
(250x200x200) nm. The surface membrane displays surface
tubules or surface filaments. Two distinct infectious virus particles
exists: the intracellular mature virus (IMV) and the extracellular
enveloped virus (EEV).
• The genome of the poxvirus is unsegmented and contains a single
molecule of linear double-stranded DNA. The complete genome is
130000-375000 nucleotides long. The genome has a guanine-
cytosine of 35-64 % but only 20 % for entomopoxviruses. The
genome has terminally redundant sequences that have reiterated
inverted terminal sequences which are tandemly repeated. The
genome sequence is repeated at both ends. The double-stranded
DNA is covalently bonded and is cross-linked at both ends.
STRUCTURE OF POX VIRUS
HOST SPECIFICITY
Poxviruses as a group can infect a large number of animals. However,
at the level of individual viruses, even closely related poxviruses
display highly diverse host ranges and virulence. For example, variola
virus, the causative agent of smallpox, is human-specific and highly
virulent only to humans, whereas related cowpox viruses naturally
infect a broad spectrum of animals and only cause relatively mild
disease in humans. The successful replication of poxviruses depends
on their effective manipulation of the host antiviral responses, at the
cellular-, tissue- and species-specific levels, which constitutes a
molecular basis for differences in poxvirus host range and virulence.
A number of poxvirus genes have been identified that possess host
range function in experimental settings, and many of these host range
genes target specific antiviral host pathways.
LIFE CYCLE
• It involves several stages the virus does is to bind to a
receptor on the host cell surface.
• After binding to the receptor, the virus enters the cell where it
uncoats. Uncoating of the virus is a two step process. Firstly
the outer membrane is removed as the particle enters the cell;
secondly the virus particle (without the outer membrane) is
uncoated further to release the core into the cytoplasm.
• The pox viral genes are expressed in two phases. The early
genes are expressed first. These genes encode the non-
structural protein, including proteins necessary for replication
of the viral genome, and are expressed before the genome is
replicated.
Replication is relatively quick taking approximately 12 hours
1. Entry
Intracellular mature virion (IMV) particles bind to unknown receptor(s)
and fuse with the cell membrane. Extracellular enveloped virion (EEV)
particles bind to unknown receptor(s) and are endocytosed into the cell.
2. Initial Uncoating
The viral core particle (CORE) containing the viral genome, the viral DNA-
dependent RNA polymerase, and other enzymes is released into the
cytoplasm.
3. Early Transcription
Early genes (including those coding for immunomodulatory proteins,
enzymes, and replication and transcription factors) are transcribed and
translated immediately upon core particle entry into the cytoplasm of the
cell.
4. Translocation
The viral core particle translocates to the outside of the cell nucleus.
5. Secondary Uncoating
The viral nucleoprotein (NP) complex, which contains the viral genome, is
released. At this point the viral genome is replicated as a concatemer and
transcription and translation of intermediate genes (mainly coding for
transcription factors) occurs.
6. Late Transcription
The viral late genes (coding for structural proteins, enzymes, and
transcription factors) are transcribed and translated.
7. Assembly
Concatemeric intermediates are resolved into linear double-stranded DNA
and packaged with late viral proteins into immature virions (IV).
8. Release
IVs mature into IMVs via an undescribed mechanism which may include
processing of the IV through the Golgi apparatus. The IMVs are transported
to the periphery of the cell where they are released in one of three ways.
IMVs released via cell lysis remain IMVs. Alternatively, IMVs can bud
through to the cell surface, picking up a viral envelope from the cell plasma
membrane. Lastly the IMV can bud through the plasma membrane picking
up an envelope and becoming an EEV.
• The late genes are expressed after the genome has been
replicated and encode the structural proteins to make the virus
particle.
• Poxviruses are unique among DNA viruses in that they replicate
in the cytoplasm of the cell rather than in the nucleus. In order
to replicate, poxviruses produce a variety of specialized proteins
not produced by other DNA viruses, the most important of which
is a viral-associated DNA-dependent RNA polymerase.
• IMV consists of a single lipoprotein membrane, while the EEV is
surrounded by two membrane layers
• The IMV is the most abundant infectious form and is thought to
be responsible for spread between hosts and the EEV is thought
to be important for long range dissemination within the host
organism.
 MONKEYPOX: was first isolated from monkeys in 1958, but it was
not until 1970 that it was associated with human disease. The
pathogenesis and clinical features for monkeypox is the same as for
smallpox. The main differences are a greater degree of
lymphadenopathy and a lower capacity for case-to-case spread. Most
cases occur in unvaccinated children. The mortality in human
monkeypox is appreciable, being in the order of 10%. The
management of human monkeypox is the same as for smallpox. Human
monkeypox has not been detected outside West Africa. Although
monkeypox was first isolated from monkeys, there is no evidence
that African monkeys act as the reservoir. The most likely candidate
for reservoir is the African squirrel. One important difference
between human monkeypox is the lower capacity for human
spread. The main difference between symptoms of smallpox and
monkeypox is that monkeypox causes lymph nodes to swell
(lymphadenopathy) while smallpox does not.
 SYMPTOMS: The incubation period (time
from infection to symptoms) for monkeypox
is usually 7−14 days but can range from
5−21 days. The illness begins with: Fever,
Headache, Muscle aches, Backache,
Swollen lymph nodes, Chills, Exhaustion.
Within 1 to 3 days (sometimes longer) after
the appearance of fever, the patient develops
a rash, often beginning on the face then
spreading to other parts of the body. Lesions
progress through the following stages before
falling off: Macules, Papules, Vesicles,
Pustules, Scabs
The illness typically lasts for 2−4 weeks.
 PREVENTION: Avoid contact with animals
that could harbor the virus & Practice good
hand hygiene after contact with infected
animals or humans
 VACCINIA (SMALLPOX): Vaccination with
vaccinia was associated with certain
risks. Complications ranged from mild
reactions and fatal encephalitis. The
overall incidence of complications was
around 1/800 although the more severe
forms occurred only in 15 per million
vaccinees. Recent interest has focused
on the possible usage of vaccinia as a
vector for immunization against other
viruses. It is possible that certain
changes can be made to the vaccinia
genome which makes it less likely to
develop side effects.
 Cidofovir and Brincidofovir have been
shown to be effective against the virus
that causes smallpox.
By 4th day, the early
rash
By 6th day, the rash
becomes pustules
After 3 weeks, the
scabs fall off.
 COWPOX: Cowpox is a viral skin infection caused by the cowpox or catpox virus.
This is a member of the orthopoxvirus family, which includes the variola virus
that causes smallpox. Cowpox is similar to but much milder than the highly
contagious and sometimes deadly smallpox disease. This process can take up to
12 weeks with the following skin findings over that period:
 SIGNS AND SYMPTOMS: Days 1-6 (after infection): the site
of infection appears as an inflamed macule (flat red lesion). Days 7-12: the
inflamed lesion becomes raised (papular), then develops into a blister-like sore
(vesicle). Days 13-20: the vesicle becomes filled with blood and pus and
eventually ulcerates. Other lesions may develop close by. Weeks 3-6: the
ulcerated wound turns into a deep-seated, hard, black crusty sore (eschar)
which is surrounded by redness and swelling. Weeks 6-12: the eschar begins to
flake and slough and the lesion heals, often leaving a scar behind.
 Other generalised symptoms are fever, tiredness, vomiting, and sore throat.
Eye complaints such as conjunctivitis, periorbital swelling and corneal
involvement.
PREVENTION: There is no cure but the disease is self-limiting.
The human immune response after being infected is sufficient to
control the infections on its own. The lesions heal by themselves
within 6-12 weeks.
 Parapoxviruses: are widespread in sheep, goats and cattle and
relatively unimportant but common human infections occur.
Infections in sheep and goats as orf. Infection occurs via small
cuts and abrasions in all hosts and is usually localized. Although
the lesions are similar to the early lesions of cowpox and vaccinia,
true macrovesicles do not form. In humans, lesions usually occur
on the hand but may be transferred to the face.
 The laboratory diagnosis is usually made by EM. The virus may also
be isolated in human, bovine but such investigations are not part of
routine diagnostic virology. Parapoxvirus infections occur
worldwide, and are of considerable importance. The lesions are
surprisingly painless. Idoxuridine had occasionally been prescribed
for treatment. Prevention of human infection is difficult.
Reasonable precautions should be undertaken when handling
infected animals.
SORE MOUTH IN
SHEEP
DAIRYMAIDS HANDS
AFTER GETTING
INFECTION
MILKER’S NODULES
 MOLLUSCUM CONTAGIOSUM: is a specifically human disease of worldwide
distribution. The incubation period varies from 1 week to 6 months. The lesion
begins as a small papule and gradually grows into a discrete, waxy, smooth,
dome-shaped, pearly or flesh-coloured nodule. Usually 1-20 lesions but
occasionally they may be present in hundreds. In children, the lesions are
found on the trunk and the proximal extremities. In adults they tend to occur
on the trunk, pubic area and thighs. Individual lesions persist for about 2
months, but the disease usually lasts 6 to 9 months. Constitutional disturbance
is rare. The disease occurs world-wide and is spread by direct contact or
fomites. In general it tends to occur in children. The disease by may
transmitted from skin to skin after sexual intercourse.
 A diagnosis can usually be made on clinical appearance alone. The diagnosis can
be supported by EM. Unlike other poxviruses, molluscum have not been
demonstrated to grow in cell culture. Infection is usually benign and painless,
with spontaneous recovery in most cases. Where treatment is required for
cosmetic reasons, various procedures are available such as curettage,
cryotherapy with liquid nitrogen, silver nitrate etc., which are routinely used
for the removal of warts.
Typical molluscum bumps,
the early apperance &
dimple in the center of the
bumps.
Typical molluscum lesions
on the torso of a child
approx. 3-5 mm in
diameter.
Less typical appearance
numerous lesions on
face.
 Tanapox: It comes from the
genus Yatapoxvirus, is a poxvirus
infection first recognized in 1957 in
the Tana River area of Kenya. The
distribution of the virus and the real
extent of the human infection and
incubation period is not known. The
virus produces a mild febrile illness
with one or two skin lesions. The
virus does not grow in CAM but will
grow in a variety of cell lines.
 Most patients show a mild pre-
eruptive fever; lasts 3-4 days,
severe headaches & backaches, and
often itching. Skin lesions usually
heal on their own after 5 to 6
weeks.
• Host Defenses: The first line of defense is unbroken skin. The initial
response after infection involves interferon and inflammation. Cell-
mediated and humoral responses to viral antigens are important for
recovery and subsequent immunity. The immune response to antigens
on the membrane of naturally released virions is particularly important.
• Epidemiology: With smallpox now eradicated, all natural human poxvirus
infections except molluscum are zoonoses and are geographically
restricted, except for molluscum and parapox infections. Despite their
names, the reservoir hosts of cowpox and monkeypox viruses are not
known with certainty.
• Signs and symptoms are: Skin eruption, Skin spots, Fever, Swollen
lymph gland, Rash, Muscle pain, Malaise, Headache, Body aches &
Vomiting.
• Diseases: Human monkeypox, vaccinia, cowpox,
parapoxvirus infections (orf, milker’s nodules), tanapox,
molluscum contagiosum.
• Etiologic Agents: Monkeypox, vaccinia, cowpox, parapox,
tanapox, and molluscum contagiosum viruses.
• Clinical Manifestations: Monkeypox—generalized pustular
rash, lymphadenopathy, fever; 11% case fatality rate.
Vaccinia and cowpox—localized pustular skin lesions,
slight fever. Orf, milker’s nodules, and tanapox—localized
nodular skin lesions. Molluscum contagiosum—multiple
chronic skin nodules.
• Laboratory Diagnosis: All poxvirus diseases: electron microscopic
demonstration of characteristic virions. Monkeypox, vaccinia, and
cowpox viruses can be isolated on chorioallantoic membrane and
produce characteristic lesions. Parapox viruses have a distinctive
morphology and can be isolated in tissue culture. Tanapox—electron
microscopy, clinical signs, and epidemiology. Molluscum
contagiosum—electron microscopy and biopsy of lesion.
• Treatment: Symptomatic. Else vaccination for 4-7 days after the
exposure likely offers some protection from the disease or may
modify the severity of disease.
• Prevention and Control: Human monkeypox—vaccination with vaccinia
virus is protective but is not used. Vaccinia, cowpox, parapoxvirus
infections—avoidance of contact with infectious animals. Tanapox—
avoidance of enzootic areas. Molluscum contagiosum—avoidance of
physical contact with cases.
POXVIRUS PATHOGENESIS
• Poxviruses are a highly successful family of pathogens, with variola
virus, the causative agent of smallpox, being the most notable
member. Poxviruses are unique among animal viruses in several
respects.
• First, owing to the cytoplasmic site of virus replication, the virus
encodes many enzymes required either for macromolecular
precursor pool regulation or for biosynthetic processes.
• Second, these viruses have a very complex morphogenesis, which
involves the de novo synthesis of virus-specific membranes and
inclusion bodies.
• Third, and perhaps most surprising of all, the genomes of these
viruses encode many proteins which interact with host processes
at both the cellular and systemic levels.
• Poxvirus infections, in general, are acute, with no strong evidence
for latent, persistent, or chronic infections. They can be localized
or systemic. The host response to infection is progressive and
multifactorial.
• Pathology: Monkeypox, vaccinia, and cowpox—vesiculopustular
skin lesions; parapoxvirus infections—proliferative skin lesions;
tanapox—thickening of epidermis, with characteristic inclusion
bodies; molluscum contagiosum—hyperplasia of epidermis with
large cells containing“molluscum bodies.”
Pox virus

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Pox virus

  • 1. POX VIRUSES PRESENTED BY: ARCHANA KUMARI SHAW ROLL.NO.: 02 M.SC. 1ST YEAR 1ST SEMESTER Submitted To, Dr. N. Shivakumar Sir.
  • 2. GENERAL CHARACTERISTICS OF VIRUSES Viruses are intracellular organisms, that are made of either DNA or RNA, they dwell inside the cell & destroys it. Viral infections are self limiting. They cannot be killed by antibiotics, this why no medications are given for the treatment instead medication are given to relieve the symptoms. They are measured in nm, about 20-300 in dia, they are obligate intracellular parasites. Pox virus is the largest and most complex. So, they can be seen under microscope. They can replicate in the cytoplasm. They are dsDNA virus. They can grow in chorioallantoic membrane (CAM) of chick embryo and tissue culture
  • 3.
  • 4. MORPHLOGY & GENOME • Enveloped, brick-shaped or ovoid virion, with rounded corners (250x200x200) nm. The surface membrane displays surface tubules or surface filaments. Two distinct infectious virus particles exists: the intracellular mature virus (IMV) and the extracellular enveloped virus (EEV). • The genome of the poxvirus is unsegmented and contains a single molecule of linear double-stranded DNA. The complete genome is 130000-375000 nucleotides long. The genome has a guanine- cytosine of 35-64 % but only 20 % for entomopoxviruses. The genome has terminally redundant sequences that have reiterated inverted terminal sequences which are tandemly repeated. The genome sequence is repeated at both ends. The double-stranded DNA is covalently bonded and is cross-linked at both ends.
  • 6. HOST SPECIFICITY Poxviruses as a group can infect a large number of animals. However, at the level of individual viruses, even closely related poxviruses display highly diverse host ranges and virulence. For example, variola virus, the causative agent of smallpox, is human-specific and highly virulent only to humans, whereas related cowpox viruses naturally infect a broad spectrum of animals and only cause relatively mild disease in humans. The successful replication of poxviruses depends on their effective manipulation of the host antiviral responses, at the cellular-, tissue- and species-specific levels, which constitutes a molecular basis for differences in poxvirus host range and virulence. A number of poxvirus genes have been identified that possess host range function in experimental settings, and many of these host range genes target specific antiviral host pathways.
  • 7. LIFE CYCLE • It involves several stages the virus does is to bind to a receptor on the host cell surface. • After binding to the receptor, the virus enters the cell where it uncoats. Uncoating of the virus is a two step process. Firstly the outer membrane is removed as the particle enters the cell; secondly the virus particle (without the outer membrane) is uncoated further to release the core into the cytoplasm. • The pox viral genes are expressed in two phases. The early genes are expressed first. These genes encode the non- structural protein, including proteins necessary for replication of the viral genome, and are expressed before the genome is replicated.
  • 8. Replication is relatively quick taking approximately 12 hours 1. Entry Intracellular mature virion (IMV) particles bind to unknown receptor(s) and fuse with the cell membrane. Extracellular enveloped virion (EEV) particles bind to unknown receptor(s) and are endocytosed into the cell. 2. Initial Uncoating The viral core particle (CORE) containing the viral genome, the viral DNA- dependent RNA polymerase, and other enzymes is released into the cytoplasm. 3. Early Transcription Early genes (including those coding for immunomodulatory proteins, enzymes, and replication and transcription factors) are transcribed and translated immediately upon core particle entry into the cytoplasm of the cell. 4. Translocation The viral core particle translocates to the outside of the cell nucleus. 5. Secondary Uncoating The viral nucleoprotein (NP) complex, which contains the viral genome, is released. At this point the viral genome is replicated as a concatemer and transcription and translation of intermediate genes (mainly coding for transcription factors) occurs. 6. Late Transcription The viral late genes (coding for structural proteins, enzymes, and transcription factors) are transcribed and translated. 7. Assembly Concatemeric intermediates are resolved into linear double-stranded DNA and packaged with late viral proteins into immature virions (IV). 8. Release IVs mature into IMVs via an undescribed mechanism which may include processing of the IV through the Golgi apparatus. The IMVs are transported to the periphery of the cell where they are released in one of three ways. IMVs released via cell lysis remain IMVs. Alternatively, IMVs can bud through to the cell surface, picking up a viral envelope from the cell plasma membrane. Lastly the IMV can bud through the plasma membrane picking up an envelope and becoming an EEV.
  • 9. • The late genes are expressed after the genome has been replicated and encode the structural proteins to make the virus particle. • Poxviruses are unique among DNA viruses in that they replicate in the cytoplasm of the cell rather than in the nucleus. In order to replicate, poxviruses produce a variety of specialized proteins not produced by other DNA viruses, the most important of which is a viral-associated DNA-dependent RNA polymerase. • IMV consists of a single lipoprotein membrane, while the EEV is surrounded by two membrane layers • The IMV is the most abundant infectious form and is thought to be responsible for spread between hosts and the EEV is thought to be important for long range dissemination within the host organism.
  • 10.  MONKEYPOX: was first isolated from monkeys in 1958, but it was not until 1970 that it was associated with human disease. The pathogenesis and clinical features for monkeypox is the same as for smallpox. The main differences are a greater degree of lymphadenopathy and a lower capacity for case-to-case spread. Most cases occur in unvaccinated children. The mortality in human monkeypox is appreciable, being in the order of 10%. The management of human monkeypox is the same as for smallpox. Human monkeypox has not been detected outside West Africa. Although monkeypox was first isolated from monkeys, there is no evidence that African monkeys act as the reservoir. The most likely candidate for reservoir is the African squirrel. One important difference between human monkeypox is the lower capacity for human spread. The main difference between symptoms of smallpox and monkeypox is that monkeypox causes lymph nodes to swell (lymphadenopathy) while smallpox does not.
  • 11.  SYMPTOMS: The incubation period (time from infection to symptoms) for monkeypox is usually 7−14 days but can range from 5−21 days. The illness begins with: Fever, Headache, Muscle aches, Backache, Swollen lymph nodes, Chills, Exhaustion. Within 1 to 3 days (sometimes longer) after the appearance of fever, the patient develops a rash, often beginning on the face then spreading to other parts of the body. Lesions progress through the following stages before falling off: Macules, Papules, Vesicles, Pustules, Scabs The illness typically lasts for 2−4 weeks.  PREVENTION: Avoid contact with animals that could harbor the virus & Practice good hand hygiene after contact with infected animals or humans
  • 12.  VACCINIA (SMALLPOX): Vaccination with vaccinia was associated with certain risks. Complications ranged from mild reactions and fatal encephalitis. The overall incidence of complications was around 1/800 although the more severe forms occurred only in 15 per million vaccinees. Recent interest has focused on the possible usage of vaccinia as a vector for immunization against other viruses. It is possible that certain changes can be made to the vaccinia genome which makes it less likely to develop side effects.  Cidofovir and Brincidofovir have been shown to be effective against the virus that causes smallpox. By 4th day, the early rash By 6th day, the rash becomes pustules After 3 weeks, the scabs fall off.
  • 13.  COWPOX: Cowpox is a viral skin infection caused by the cowpox or catpox virus. This is a member of the orthopoxvirus family, which includes the variola virus that causes smallpox. Cowpox is similar to but much milder than the highly contagious and sometimes deadly smallpox disease. This process can take up to 12 weeks with the following skin findings over that period:  SIGNS AND SYMPTOMS: Days 1-6 (after infection): the site of infection appears as an inflamed macule (flat red lesion). Days 7-12: the inflamed lesion becomes raised (papular), then develops into a blister-like sore (vesicle). Days 13-20: the vesicle becomes filled with blood and pus and eventually ulcerates. Other lesions may develop close by. Weeks 3-6: the ulcerated wound turns into a deep-seated, hard, black crusty sore (eschar) which is surrounded by redness and swelling. Weeks 6-12: the eschar begins to flake and slough and the lesion heals, often leaving a scar behind.  Other generalised symptoms are fever, tiredness, vomiting, and sore throat. Eye complaints such as conjunctivitis, periorbital swelling and corneal involvement.
  • 14. PREVENTION: There is no cure but the disease is self-limiting. The human immune response after being infected is sufficient to control the infections on its own. The lesions heal by themselves within 6-12 weeks.
  • 15.  Parapoxviruses: are widespread in sheep, goats and cattle and relatively unimportant but common human infections occur. Infections in sheep and goats as orf. Infection occurs via small cuts and abrasions in all hosts and is usually localized. Although the lesions are similar to the early lesions of cowpox and vaccinia, true macrovesicles do not form. In humans, lesions usually occur on the hand but may be transferred to the face.  The laboratory diagnosis is usually made by EM. The virus may also be isolated in human, bovine but such investigations are not part of routine diagnostic virology. Parapoxvirus infections occur worldwide, and are of considerable importance. The lesions are surprisingly painless. Idoxuridine had occasionally been prescribed for treatment. Prevention of human infection is difficult. Reasonable precautions should be undertaken when handling infected animals.
  • 16. SORE MOUTH IN SHEEP DAIRYMAIDS HANDS AFTER GETTING INFECTION MILKER’S NODULES
  • 17.  MOLLUSCUM CONTAGIOSUM: is a specifically human disease of worldwide distribution. The incubation period varies from 1 week to 6 months. The lesion begins as a small papule and gradually grows into a discrete, waxy, smooth, dome-shaped, pearly or flesh-coloured nodule. Usually 1-20 lesions but occasionally they may be present in hundreds. In children, the lesions are found on the trunk and the proximal extremities. In adults they tend to occur on the trunk, pubic area and thighs. Individual lesions persist for about 2 months, but the disease usually lasts 6 to 9 months. Constitutional disturbance is rare. The disease occurs world-wide and is spread by direct contact or fomites. In general it tends to occur in children. The disease by may transmitted from skin to skin after sexual intercourse.  A diagnosis can usually be made on clinical appearance alone. The diagnosis can be supported by EM. Unlike other poxviruses, molluscum have not been demonstrated to grow in cell culture. Infection is usually benign and painless, with spontaneous recovery in most cases. Where treatment is required for cosmetic reasons, various procedures are available such as curettage, cryotherapy with liquid nitrogen, silver nitrate etc., which are routinely used for the removal of warts.
  • 18. Typical molluscum bumps, the early apperance & dimple in the center of the bumps. Typical molluscum lesions on the torso of a child approx. 3-5 mm in diameter. Less typical appearance numerous lesions on face.
  • 19.  Tanapox: It comes from the genus Yatapoxvirus, is a poxvirus infection first recognized in 1957 in the Tana River area of Kenya. The distribution of the virus and the real extent of the human infection and incubation period is not known. The virus produces a mild febrile illness with one or two skin lesions. The virus does not grow in CAM but will grow in a variety of cell lines.  Most patients show a mild pre- eruptive fever; lasts 3-4 days, severe headaches & backaches, and often itching. Skin lesions usually heal on their own after 5 to 6 weeks.
  • 20. • Host Defenses: The first line of defense is unbroken skin. The initial response after infection involves interferon and inflammation. Cell- mediated and humoral responses to viral antigens are important for recovery and subsequent immunity. The immune response to antigens on the membrane of naturally released virions is particularly important. • Epidemiology: With smallpox now eradicated, all natural human poxvirus infections except molluscum are zoonoses and are geographically restricted, except for molluscum and parapox infections. Despite their names, the reservoir hosts of cowpox and monkeypox viruses are not known with certainty. • Signs and symptoms are: Skin eruption, Skin spots, Fever, Swollen lymph gland, Rash, Muscle pain, Malaise, Headache, Body aches & Vomiting.
  • 21. • Diseases: Human monkeypox, vaccinia, cowpox, parapoxvirus infections (orf, milker’s nodules), tanapox, molluscum contagiosum. • Etiologic Agents: Monkeypox, vaccinia, cowpox, parapox, tanapox, and molluscum contagiosum viruses. • Clinical Manifestations: Monkeypox—generalized pustular rash, lymphadenopathy, fever; 11% case fatality rate. Vaccinia and cowpox—localized pustular skin lesions, slight fever. Orf, milker’s nodules, and tanapox—localized nodular skin lesions. Molluscum contagiosum—multiple chronic skin nodules.
  • 22. • Laboratory Diagnosis: All poxvirus diseases: electron microscopic demonstration of characteristic virions. Monkeypox, vaccinia, and cowpox viruses can be isolated on chorioallantoic membrane and produce characteristic lesions. Parapox viruses have a distinctive morphology and can be isolated in tissue culture. Tanapox—electron microscopy, clinical signs, and epidemiology. Molluscum contagiosum—electron microscopy and biopsy of lesion. • Treatment: Symptomatic. Else vaccination for 4-7 days after the exposure likely offers some protection from the disease or may modify the severity of disease. • Prevention and Control: Human monkeypox—vaccination with vaccinia virus is protective but is not used. Vaccinia, cowpox, parapoxvirus infections—avoidance of contact with infectious animals. Tanapox— avoidance of enzootic areas. Molluscum contagiosum—avoidance of physical contact with cases.
  • 23. POXVIRUS PATHOGENESIS • Poxviruses are a highly successful family of pathogens, with variola virus, the causative agent of smallpox, being the most notable member. Poxviruses are unique among animal viruses in several respects. • First, owing to the cytoplasmic site of virus replication, the virus encodes many enzymes required either for macromolecular precursor pool regulation or for biosynthetic processes. • Second, these viruses have a very complex morphogenesis, which involves the de novo synthesis of virus-specific membranes and inclusion bodies.
  • 24.
  • 25. • Third, and perhaps most surprising of all, the genomes of these viruses encode many proteins which interact with host processes at both the cellular and systemic levels. • Poxvirus infections, in general, are acute, with no strong evidence for latent, persistent, or chronic infections. They can be localized or systemic. The host response to infection is progressive and multifactorial. • Pathology: Monkeypox, vaccinia, and cowpox—vesiculopustular skin lesions; parapoxvirus infections—proliferative skin lesions; tanapox—thickening of epidermis, with characteristic inclusion bodies; molluscum contagiosum—hyperplasia of epidermis with large cells containing“molluscum bodies.”