Viruses Causing Vesicular Rash By Dr Mona Badr

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

Viruses Causing Vesicular Rash Ø Ø 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 Ø The herpesvirus family known to be pathogens for human: 1. 2. 3. 4. 5. 6. 7. 8. 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

Herpes Virus (Continued) Special Features of Herpes Virus Ø Are large in size, ds, DNA, icosahedral, enveloped virus. Ø The herpes viruses has the ability to induce latent infection HSV and VZV Nerve cell EBV B-lymphocyte CMV lymphocyte and macrophage

Electron Microscopy of Herpes Virus

Herpes Viruses (Continued) Ø The infection with all herpes virus has very characterized feature, there are 2 types of presentation: 1. Primary § When the virus invade the body for the first time 2. 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, …

Herpes Virus (Continued) Ø Also, some herpes virus has oncogenic potential as HSV 2 Cervical carcinoma ? ? EBV Burkitt’s lymphoma B-cell lymphoma Aplastic Nasopharyngeal carcinoma Herpes virus 8 Kaposi Sarcoma ØHerpes viruses can cause high morbidity and mortality in immunocompromised patients. ØHerpes viruses susceptible to antiviral treatment due to presence of thymidine kinase enzyme in the viruses.

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.

Disease syndrome of HSV 1, HSV 2

Herpes Virus (Continued) Herpes Simplex Viruses Herpes Simplex Virus 1 Herpes Simplex Virus 2 §Spread through saliva and § Spread by sexual contact Or respiratory droplets. To newborn during birth. §Usually primary presentation seen in children 2 -4 years. §Usually primary presentation seen in young adult. §Primary presentation usually asymptomatic painful. §Latency occur in trigeminal §Latency occur in Sacral ganglia

Herpes Virus (Continued) A. Primary Infection of HSV 1: Ø Lesions begin as vesicles, then rapidly become ulcerated which resolve spontaneously. § Gingivo -stomatitis § Pharyngitis § Kerato-conjunctivitis § Herpetic whitlow § Dendritic ulcer (cornea) § Herpetic encephalitis

Clinical Syndrome of Herpes Simplex Type-I A. Primary Presentation: Ø Usually primary infection are symptomless but disease can be presented primary as: 1. 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. 2. Kerato-conjunctivitis § Usually in children, due to autoinoculation § 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 § § § 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 § 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 herpes § Very rare disseminated vesicular lesions on skin and internal organs.

Herpetic Whitlow

Herpes Virus (Continued) A. Latent Infection OF HSV- I: Ø 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: § Dendritic ulcer vesicless at mucocutaneous function of nose and mouth Virus reach the cornea via ophthalmic branch of Trigeminal nerve very serious conditions can lead to blindness

Cold Sore 2 nd 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: Ø 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 § Associated with fever and lymphadenopathy lession on the anus in homosexual

HSV 2 on Penis

HSV 2 on Vulva

Herpes Virus (Continued) B. Primary infection of HSV-2: Ø 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. Ø Meningitis: as a complication of genital HSV 2

Herpes Virus (Continued) Latent Infection OF HSV- 2: Ø From the primary lesion virus travel to be latent in sacral ganglia. § Virus persist for life time § Recurrent occur if immunity § Recurrent HSV 2 are shorter and less severe than primary

yng osion Herpes Virus (Continued) Treatment and Prevention ØAcyclovir is used for treatment of serious lesions as herpetic encephalitis, immunocompromised patient, dendritic ulcer, neonatal herpes, primary genital herpes. Prevention ØAvoid contact with infected cases, droplet or vesicular lesion. ØAvoid venereal transmission ØCaesarian section contact with birth canal. sex education.

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 of the vesicle. Antibody detection §Serum Ig. M Ab is diagnostic of Acute infection. §Serum Ig. G Ab is diagnostic of pat infection. Neonatal herpes diagnosed by the detection of Ig. M Ab 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 2 nd Presentation Or Reactivation Herpes Zoster

Herpes Vesicles Chickenpox

Herpes Virus (Continued) Primary presentation: Ø This is a high infectious disease of children, occur as. Epidemic with seasonal variation (late winter and early spring )with 21 days I. P. Ø Transmitted by respiratory droplet and direct contact, patients are contagious before and during symptoms. Ø Fever, vesicular rash started on trunk, then extremities, face and even Scalp. Ø Recovery is the rule without scar formation. Ø Solid immunity develop after chickenpox !! Ø The disease is very severe in adult and immunocopromized patient. Ø 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) 2 nd Presentation of Chickenpox (Zoster): Ø Zoster means belt Ø Viral DNA is present in dorsal root ganglia during latency for years. Ø Zoster result as reactivation of latent varicella (chickenpox) usually as sporadic cases occur in old adult Or immunocompromised patients. Ø Virus affect sensory nerve and ganglia leading to severe pain of area of skin supplied with this nerve. Ø Followed by appearance of very painful vesicles. Ø Uni-lateral, usually in the trunk, less common cranial, thoracic Ø 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 ØVirus isolation from vesicles on cell culture CPE. Ø Detection of Ig. M or rising titer of Ig. G. Prophylaxis ØVaccine: 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. ØVaricella-Zoster immunoglobulin can be given to protect immunosuppressed patient within 3 days of exposure is protective.

Herpes Virus (Continued) Treatment Ø 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 Ø Coxsackie A virus is one of the picornaviridae family Ø Small, RNA virus Ø Stable at acid p. H Ø Both disease are transmitted mainly by Fecal oral route and rarely by aerosol droplet Ø 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 § 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

Laboratory Diagnosis of Coxsackie Viruses Ø Control: by improving the standard of hygiene. Ø No vaccine available. Ø 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 Ig. M, Ig. G 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