Transcript 01. Viruses Causing

Viruses Causing Vesicular
Rash
By: Dr.Mona Badr
Assistant Professor &
Consultant Virologist
College of Medicine & KKUH
Viruses Causing Vesicular Rash
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What is the meaning of vesicular rash?
It is a temporary vesicular eruption on the skin
Vesicle: Is a small circumscribed elevation of the epidermis
containing serious fluid
The two main viruses causing vesicular rash are:
1. Herpes viruses
2. Coxsackie A viruses
Herpes Virus
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The herpesvirus family known to be pathogens for human:
1. Herpes simplex virus type 1
2. Herpes simplex virus type 2
3. Varicella / zoster VZ
4. Cytomegalovirus CMV
5. Epstein Barr virus EBV
6. Human Herpes virus type 6
7. Human Herpes virus type 7
8. Human Herpes virus type 8
Herpes Virus (Continued)
Special Features of Herpes Virus
 Are large in size,
virus.
ds, DNA
, icosahedral, enveloped
 The herpes viruses has the ability to induce latent infection
HSV and VZV
EBV
CMV
macrophage
Nerve cell
B-lymphocyte
lymphocyte and
Electron Microscopy of Herpes Virus
Herpes Viruses (Continued)
 The infection with all herpes virus has very characterized
feature, there are 2 types of presentation:
1. Primary:
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When the virus invade the body for the first time
2. Reactivation (Recurrent):
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When the Latent (Hidden) virus, reactivated
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The predisposing factors of reactivation, if any
situation lead to
decrease the immune
system of the body e.g. diabetes, pregnancy,
menstruation, stress or …. Cancer, AIDS, …
Herpes Virus (Continued)
 Also, some herpes virus has oncogenic potential as
EBV
Burkitt’s lymphoma
B-cell lymphoma
Aplastic Nasopharyngeal carcinoma
Herpes virus 8
Kaposi Sarcoma
Herpes viruses can cause high morbidity and mortality in
immunocompromised patients.
Herpes viruses susceptible to antiviral treatment due
presence of thymidine kinase enzyme in the viruses.
to
Herpes Simplex Virus Type-I Herpes
Simplex Type -II
Pathogenesis and Immunity:
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Both viruses are initially infect and replicate in
mucoepithelial cells and then become latent
(hidden) at trigeminal ganglia (HSV-I), at sacral ganglia
(HSV-II)
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Humoral and cellular immunity are necessary for HSV
infection to be controlled and resolve.
Diseases of HSV1,HSV2
Herpes Virus (Continued)
Herpes Simplex Viruses
Herpes Simplex Virus 1
Herpes Simplex Virus 2
Spread through saliva and
respiratory droplets.
 Spread by sexual contact
Or new born during birth
Usually primary presentation seen in
Usually primary presentation
children 2-4 years.
seen in young
Primary presentation usually
asymptomatic Latency occur in
Primary presentation usually
trigeminal ganglia
adult.
painful. Latency occur in
Sacral ganglia
Herpes Virus (Continued)
A. Primary Infection of HSV1:
 Leasions begin as vesicles, then rapidly become ulcerated
which resolve spontaneously.
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Gingivostomatitis
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Pharyngitis
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Kerato-conjunctivitis
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Herpetic whitlow
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Dendritic ulcer (cornea)
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Herpetic encephalitis
Clinical Syndrome of Herpes Simplex Type-I
A. Primary Presentation:
 Most primary infection are symptomless but disease
can be presented primary as:
1. Gingivostomalitis
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Seen mostly in children from 1-5 years, with 4 days
duration.
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Vesicles inside the mouth and bucal mucosa and on the
gum, fever, sore throat and submandibular lymph nodes
enlarged can be seen.
2. Kerato-conjunctivitis
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Usually in children, due to autoinoculation
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Very severe situation can lead to corneal ulcer.
Gingivostomatitis Primary HSV-I
Dendritic ulcer (corneal ulcer) can be primary
or reactivation can lead to blindness
Clinical Syndrome of Herpes Simplex Type-I (Continued)
3. Herpetic Whitlow
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Is an infection of the finger, or infection at any site of the
body.
The virus can enter through cut or abrasion in the skin.
Herpetic whitlow usually occur in nurses, physician and
dentists
4. Acute herpetic encephalitis
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The disease can occur at any age can be primary or
reactivation
Very rare presentation of HSV-I usually limited to one
lobe.
Started as acute fever, headache, mental confusion and lack
of coordination.
Can lead to severe morbidity and mortality
5. Disseminated herpesVery rare disseminated vesicular
lesions on skin and internal
Herpetic Whitlow
Herpes Virus (Continued)
A. Latent Infection OF HSV- I:
 From the primary lesion virus travels through nerves and
then remain latent in trigeminal ganglia (HSV 1)
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Virus persist for life time
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Recurrent occur if immunity
 Cold sore:
nose and
vesicless at mucocutaneous function of
mouth
 Dendritic ulcer
Virus reach the cornea via ophthalmic branch of Trigeminal
nerve very serious conditions can lead to blindness
Cold Sore 2nd Presentation of HSV-I
Dendritic ulcer (corneal ulcer) can be primary
or reactivation can lead to blindness
Herpes Virus (Continued)
B. Primary infection of HSV-2:
 Genital herpes, Vesiculo
ulcerative Leasion
associated with fever and lymphadenopathy.
 I.P. one week after sexual contact
 Lesion on the external genitalia as on penis,
vulva and also in the cervix which is very
painful.
 HSV II proctitis
homosexual
lession on the anus in
 Associated with fever and
lymphadenopathy
HSV2 on Penis
HSV2 on Vulva
Herpes Virus (Continued)
B.Primary infection of HSV-2:
 Neonatal herpes: can occur with great risk (50%) if mother
have the primary presentation around time of delivery when
there is no maternal antibody is present to protect the baby. If
mother has recurrent herpes the transmission (8%). The
affected infants have jaundice, hepatosplenomegaly,
thrombocytopenia and large vesicular lesions on the skin with
high fatality rate. To avoid neonatal infection we do
Caesarean section.
 Meningitis: as a complication of genital HSV2
Herpes Virus (Continued)
Latent Infection OF HSV- 2:
 From the primary lesion virus travel to be latent in sacral
ganglia.
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Virus persist for life time
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Recurrent occur if immunity
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Recurrent HSV2 are shorter and less severe than primary
Herpes Virus (Continued)
Treatment and Prevention
Acyclovir is used for treatment of serious lesions as herpetic
encephalitis, immunocompromised patient, dendritic ulcer,
neonatal herpes, primary genital herpes.
Prevention
Avoid contact with infected cases, droplet or vesicular lesion.
Avoid venereal transmission
Caesarian section
contact with birth canal.
sex education.
to prevent transmission to baby during
Herpes Simplex Type-I and Type-II
Laboratory Diagnosis
Viral detection
1) Culture
Specimen:
Vesicular
fluid
infected
cell
become enlarged and
produce multinucleated
giant cell (appear after 13 days)
2) Direct
immunofluorescent:detect
the virus directly from
scraping of base vesicle.
Antibody
detection
Serum IgM Ab is diagnostic
of Acute infection.
Serum IgG Ab is diagnostic of
pat infection.
Neonatal herpes diagnosed
by the detection of
Ab
IgM
from the serum of the
baby.
Herpes Virus (Continued)
Varicella-Zoster
These are two distinct (different) diseases caused by the same virus.
Primary Presentation
Varicella - Chickenpox
2nd Presentation Or Reactivation
Herpes Zoster
Herpes Vesicles Chickenpox
Herpes Virus (Continued)
Primary presentation:(ckickenpox)
 This is a high infectious disease of children, occur in Epidemic
with seasonal variation late winter and early spring with 21
days I.P.
 Transmitted by respiratory droplet and direct contact, patients are
contagious before and during symptoms.
 Fever, vesicular rash started on trunk, then extremities, face and
even Scalp.
 Recovery is the rule without scar formation.
 Solid immunity develop after chickenpox
 The disease is very severe in adult and immunocopromized
patient.
 Complication: are rare as encephalitis, pneumonia may seen in
adult, disseminated disease in immunocompromized patient.
Chickenpox
Chickenpox
Chickenpox
Dark Skin
Light Skin
Chickenpox
 Congenital varicella
Limb – hypoplasia, muscular atrophy and cerebral
retardation very rare complication can occur in baby
born to mother infected with varicella early in
pregnancy.
 Peri-natal varicella (neonatal)
If mother develop chickenpox within 7 days before
delivery there is no maternal antibody and the baby
is liable to develop severe disease.
Herpes Virus (Continued)
2nd Presentation of Chickenpox (Zoster):
 Zoster means belt
 Viral DNA is present in dorsal root ganglia during latency for
years.
 Zoster result as reactivation of latent varicella (chickenpox)
usually as sporadic cases occur in old adult Or
immunocompromised patients.
 Virus affect sensory nerve and ganglia leading to severe pain of
area of skin supplied with this nerve.
 Followed by appearance of very painful vesicles .
 Uni-lateral, usually in the trunk, less common cranial, thoracic
 Disseminated zoster can be seen in immunocompromized patient.
Herpetic Zoster on trunk
Herpetic Zoster
Herpetic Zoster
Herpetic Zoster in immunocompromized dessiminated
Herpes Virus (Continued)
Laboratory Diagnosis
Virus isolation from vesicles on cell culture
CPE.
 Detection of IgM or rising titer of IgG.
Prophylaxis
Vaccine: live attenuated varicella vaccine given to high risk
group patient e.g. hospitalized patient exposed to varicella. To be
given as wide scale still under studies.
Varicella-Zoster immunoglobulin can be given to protect
immunosuppressed patient within 3 days of exposure is protective.
Herpes Virus (Continued)
Treatment
 Acyclovir
Interferon
are used in immunocompromised children with
varicella.
Also used for adult developing complication as
encephalitis or adult with reactivation as
Zoster.
Viruses Causing Vesicular Rash
Herpangina and Hand,
Foot and Mouth Disease
These are two diseases caused by
Coxsackie A viruses
 Coxsackie A virus is one of the picornaviridae family
 Small, RNA virus
 Stable at acid pH
 Both disease are transmitted mainly by Fecal oral route and rarely
by aerosol droplet
 Incubation period from 3-7 days.
Viruses Causing Vesicular Rash Herpangina and Hand,
Foot and Mouth Disease (Continued)
Herpangina
Hand, foot & Mouth Dis.
Fever,
Cervical
lymphadenopathy, sore
throat and multiple small
vesicles on the tonsils,
pharynx and soft palate.
These vesicles become
ulcers later on.
Multiple small vesicles and ulcers
seen on the
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Tongue, and buccal mucosa.
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Palm of the hands
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Plantar of the foot
vesicles become ulcers
Both are self-limiting diseases with complete recovery.
No vaccine available
No specific treatment
Diagnosed by virus isolation in tissue culture.
Complication Aseptic meningitis
also
Laboratory Diagnosis of Coxsackie Viruses
 Control: by improving the standard of hygiene.
 No vaccine available.
 Diagnosis:
Culture:
Specimen from: Stool, CSF, Vesicular
fluid and eye secretion, throat swab
Some enterivorus fail to grow in tissue
culture only in newborn mice.
Some enterovirus can gro on several tissue culture
few days neutralization.
CPE after
Serology:
By ELISA
PCR
to detect IgM, IgG and neutrilization
detect RNA test for identification
Herpangina caused by Coxsackivirus A
Hand foot and mouth diseases
Hand foot and mouth diseases
Hand foot and mouth diseases