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Table II: Occupational health Management Strategy for Infectious Diseases in HCWs

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Viruses Causing Vesicular Rash By: Dr.Mona Badr Assistant Professor & Consultant Virologist College of Medicine & KKUH – PowerPoint PPT presentation

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Title: Table II: Occupational health Management Strategy for Infectious Diseases in HCWs


1
Viruses Causing Vesicular Rash
By Dr.Mona Badr
Assistant Professor Consultant Virologist
College of Medicine KKUH
2
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

3
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

4
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

5

6

Electron Microscopy of Herpes Virus
7
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,

8
Herpes Virus (Continued)
  • Also, some herpes virus has oncogenic potential
    as
  • HSV 2 Cervical carcinoma ??
  • 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.

9
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),
  • Sacral ganglia(HSV-11).
  • Humoral and cellular immunity are necessary for
    HSV infection to be controlled and resolve.

10

Disease syndrome of HSV1,HSV2
11
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
  • To newborn 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

12
Herpes Virus (Continued)
  • Primary Infection of HSV1
  • Lesions begin as vesicles, then rapidly become
    ulcerated which resolve spontaneously.
  • Gingivo -stomatitis
  • Pharyngitis
  • Kerato-conjunctivitis
  • Herpetic whitlow
  • Dendritic ulcer (cornea)
  • Herpetic encephalitis

13
Clinical Syndrome of Herpes Simplex Type-I
  • Primary Presentation
  • Usually primary infection are symptomless but
    disease can be presented primary as
  • Gingivostomalitis (cold sore)
  • 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.

14

Gingivostomatitis Primary HSV-I
15

Dendritic ulcer (corneal ulcer) can be primary or
reactivation can lead to blindness
16
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 herpes
  • Very rare disseminated vesicular lesions on skin
    and internal organs.

17

Herpetic Whitlow
18
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

19

Cold Sore 2nd Presentation of HSV-I
20

Dendritic ulcer (corneal ulcer) can be primary or
reactivation can lead to blindness
21
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

22

HSV2 on Penis
23

HSV2 on Vulva
24
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

25
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

26
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.

27
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.
  • Direct immunofluorescent
  • detect the virus directly from scraping of base
    of the vesicle.

Neonatal herpes diagnosed by the detection of
IgM Ab from the serum of the baby.
28
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
29

Herpes Vesicles Chickenpox
30
Herpes Virus (Continued)
  • Primary presentation
  • This is a high infectious disease of children,
    occur asEpidemic 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.

31

Chickenpox
32

Chickenpox
33

Chickenpox
34

Dark Skin
Light Skin
35

Chickenpox
36
  • 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.

37
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.

38
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39

Herpetic Zoster on trunk
40

Herpetic Zoster
41

Herpetic Zoster
42

Herpetic Zoster in immunocompromized dessiminated
43
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,and now is giving
    for children but not routienly.
  • Varicella-Zoster immunoglobulin can be given to
    protect immunosuppressed patient within 3 days of
    exposure is protective.

44
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.

45
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.

46
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
47
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

48
Herpangina caused by Coxsackivirus A
49
Hand foot and mouth diseases
50
Hand foot and mouth diseases
51
Hand foot and mouth diseases
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