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Viruses Causing Vesicular Rash By: Dr.Mona Badr Assistant Professor & Consultant Virologist College of Medicine & KKUH 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: 1. Herpes viruses 2. Coxsackie A viruses Herpes Virus 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: 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) 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: 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. 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. Gingivostomatitis Pharyngitis Kerato-conjunctivitis Herpetic whitlow Dendritic ulcer (cornea) 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 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 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) Virus persist for life time 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. Virus persist for life time Recurrent occur if immunity 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 Tongue, and buccal mucosa. Palm of the hands 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