Viruses Causing Vesicular Rash

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Viruses Causing Vesicular Rash
By Dr.Mona Badr
Assistant Professor Consultant Virologist
College of Medicine KKUH
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Viruses Causing Vesicular Rash

• 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
• Herpes viruses
• Coxsackie A viruses

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Herpes Virus

• The herpesvirus family known to be pathogens
  for human
• Herpes simplex virus type 1
• Herpes simplex virus type 2
• Varicella / zoster VZ
• Cytomegalovirus CMV
• Epstein Barr virus EBV
• Human Herpes virus type 6
• Human Herpes virus type 7
• Human Herpes virus type 8

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Herpes Virus (Continued)
Special Features of Herpes Virus

• Are large in size, ds, DNA , icosahedral,
  enveloped virus.
• The herpes viruses has the ability to induce
  latent infection
• HSV and VZV Nerve cell
• EBV B-lymphocyte
• CMV lymphocyte and
  
  macrophage

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Electron Microscopy of Herpes Virus
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Herpes Viruses (Continued)

• The infection with all herpes virus has very
  characterized feature, there are 2 types of
  presentation
• Primary
• When the virus invade the body for the first time
• Reactivation (Recurrent)
• When the Latent (Hidden) virus, reactivated
• 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,

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Herpes Virus (Continued)

• Also, some herpes virus has oncogenic potential
  as
• EBV Burkitts 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 to presence of thymidine kinase enzyme in
  the viruses.

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Herpes Simplex Virus Type-I Herpes Simplex Type
-II

• Pathogenesis and Immunity
• 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)
• Humoral and cellular immunity are necessary for
  HSV infection to be controlled and resolve.

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Diseases of HSV1,HSV2
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Herpes Virus (Continued)
Herpes Simplex Viruses

• Herpes Simplex Virus 1
• Spread through saliva and
• respiratory droplets.

• Herpes Simplex Virus 2
• Spread by sexual contact Or new born during
  birth
• Usually primary presentation seen in young adult.
• Primary presentation usually painful. Latency
  occur in Sacral ganglia

• Usually primary presentation seen in children 2-4
  years.
• Primary presentation usually asymptomatic
  Latency occur in trigeminal ganglia

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Herpes Virus (Continued)

• Primary Infection of HSV1
• Leasions begin as vesicles, then rapidly become
  ulcerated which resolve spontaneously.
• Gingivostomatitis
• Pharyngitis
• Kerato-conjunctivitis
• Herpetic whitlow
• Dendritic ulcer (cornea)
• Herpetic encephalitis

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Clinical Syndrome of Herpes Simplex Type-I

• Primary Presentation
• Most primary infection are symptomless but
  disease can be presented primary as
• Gingivostomalitis
• Seen mostly in children from 1-5 years, with 4
  days duration.
• Vesicles inside the mouth and bucal mucosa and
  on the gum, fever, sore throat and submandibular
  lymph nodes enlarged can be seen.
• Kerato-conjunctivitis
• Usually in children, due to autoinoculation
• Very severe situation can lead to corneal ulcer.
  

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Gingivostomatitis Primary HSV-I
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Dendritic ulcer (corneal ulcer) can be primary or
reactivation can lead to blindness
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Clinical Syndrome of Herpes Simplex Type-I
(Continued)

• Herpetic Whitlow
• 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
• Acute herpetic encephalitis
• 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
• Disseminated herpesVery rare disseminated
  vesicular lesions on skin and internal

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Herpetic Whitlow
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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)
• Virus persist for life time
• Recurrent occur if immunity
• Cold sore vesicless at mucocutaneous function of
  nose and mouth
• Dendritic ulcer
• Virus reach the cornea via ophthalmic branch of
  Trigeminal nerve very serious conditions can
  lead to blindness

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Cold Sore 2nd Presentation of HSV-I
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Dendritic ulcer (corneal ulcer) can be primary or
reactivation can lead to blindness
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Herpes Virus (Continued)

• 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 lession on the anus in
  homosexual
• Associated with fever and lymphadenopathy

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HSV2 on Penis
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HSV2 on Vulva
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Herpes Virus (Continued)

• 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

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Herpes Virus (Continued)

• Latent Infection OF HSV- 2
• From the primary lesion virus travel to be latent
  in sacral ganglia.
• Virus persist for life time
• Recurrent occur if immunity
• Recurrent HSV2 are shorter and less severe than
  primary

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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 sex
  education.
• Caesarian section to prevent transmission
  to baby during contact with birth canal.

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Herpes Simplex Type-I and Type-II
Laboratory Diagnosis
Viral detection
Antibody detection

1. Culture

Specimen Vesicular fluid infected cell become
enlarged and produce multinucleated giant cell
(appear after 1-3 days)

• Serum IgM Ab is diagnostic of Acute infection.
• Serum IgG Ab is diagnostic of pat infection.

1. Direct immunofluorescentdetect the virus
   directly from scraping of base vesicle.

Neonatal herpes diagnosed by the detection of
IgM Ab from the serum of the baby.
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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
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Herpes Vesicles Chickenpox
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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.

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Chickenpox
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Chickenpox
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Chickenpox
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Dark Skin
Light Skin
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Chickenpox
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• 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.

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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.

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Herpetic Zoster on trunk
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Herpetic Zoster
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Herpetic Zoster
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Herpetic Zoster in immunocompromized dessiminated
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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.

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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.

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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.

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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
• Tongue, and buccal mucosa.
• Palm of the hands
• Plantar of the foot also 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
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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 CPE after few days neutralization.
• Serology
• By ELISA to detect IgM, IgG and neutrilization
• PCR detect RNA test for identification

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Herpangina caused by Coxsackivirus A
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Hand foot and mouth diseases
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Hand foot and mouth diseases
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Hand foot and mouth diseases