![Nervous system
• HSV encephalitis [rare]
• HSV meningitis
• Transverse myelitis [rare]
• Sacral autonomic dysfunction
• Guillian Barre syndrome [rare]
• Bell’s palsy [rare]](https://image.slidesharecdn.com/herpesvirusandvaricella-221203063807-e3f4f814/75/Herpes-Virus-and-Varicella-19-2048.jpg)
![Visceral
• HSV esophagitis
• Tracheobronchitis & Pneumonitis
• Hepatitis [uncommon]
• Disseminated HSV infection](https://image.slidesharecdn.com/herpesvirusandvaricella-221203063807-e3f4f814/75/Herpes-Virus-and-Varicella-20-2048.jpg)
Uploaded byDr. Rakesh Prasad Sah
Herpes Virus and Varicella
HSV are DNA viruses that establish latent infections in hosts. There are 8 human herpesviruses including HSV-1, HSV-2, VZV, CMV, EBV, and HHV-6/7/8. HSV-1 typically causes oral lesions while HSV-2 typically causes genital lesions. VZV causes chickenpox during primary infection and shingles during reactivation from latency in nerve ganglia. These viruses are diagnosed via microscopy, antigen/DNA detection, virus isolation, and serology. Antivirals like acyclovir are used to treat infections while vaccination can prevent chickenpox and shingles.
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Herpes Virus and Varicella
- 1. Dr. Rakesh PrasadSah Assistant Professor, Microbiology HERPESVIRUSES
- 2. Introduction + GeneralProperties • Large family of DNA viruses ds in animals including human beings. • Latin word “herpin” “to creep” referring to latent, re-occuring infections • possess a unique property of: – Establishing latent or persistent/lytic infections in their hosts – Undergo periodic reactivation. – immunocompromised
- 3. Classification Subfamily Scientific nameCommon name Acronym Alphaherpesvirinae Human herpesvirus 1 Herpes simplex virus type 1 HSV-1 Human herpesvirus 2 Herpes simplex virus type 2 HSV-2 Human herpesvirus 3 Varicella-zoster virus VZV Betaherpesvirinae Human herpesvirus 5 cytomegalovirus HCMV Human herpesvirus 6 -------------- HHV-6 Human herpesvirus 7 -------------- HHV-7 Gammaherpesvirin ae Human herpesvirus 4 Epstein-Barr virus EBV Human herpesvirus 8 Kaposi’s Sarcoma associated virus HHV-8
- 4. Infecting Humans • HerpesSimplex virus 1 and 2 • Varicella Zoster Viruses • Cytomegalovirus virus • Epstein Barr virus • Human Herpes viruses 6, 7. • Kaposi's Sarcoma associated Viruses
- 5. Morphology • 100-200nm indiameter, spherical in shape with icosahedral capsid composed of 162 capsomeres. • Is double stranded DNA virus surrounded by lipid envelope containing glycoprotein peplomers.
- 6. • Enveloped -lipoprotein in nature • Lipid part is derived from the nuclear membrane. • Protein part- Virus coded glycoprotein spikes, about 8 nm long are inserted into the lipid part. • Between capsid and envelope “Tegument” multiply in nuclei of infected cells produce Cowdry type A intranuclear inclusion bodies..
- 7. Herpes Simplex Virus •Herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) are distinguished by two main criteria – Antigenicity – Location of lesions. • HSV-1: above the waist (Oral & Occular), primarily in adults – Acute gingivostomatitis – Pharyngotonsilitis – Recurrent herpes labialis(cold sores), – Keratoconjunctivitis(keratitis), – Encephalitis – Eczema herpeticum – Dendritic keratitis
- 8. • HSV-2: belowthe waist (Genital infections) – Genital Herpes (Penis, urthra, cervix, vulva, vagina) – Neonatal herpes vertical transmission from mother to newborn. – Aseptic meningitis • Humans are the natural hosts of both.
- 9. Differences between HSV1and HSV2
- 10. Differences between HSV1and HSV2
- 11. Transmission • Occurs abraded skin or mucosa from any site but more commonly by: – HSV 1: transmitted primarily in saliva or direct skin contact. – HSV 2: transmitted by sexual contact or rarely by vertical mode (from mother to foetus) • Oral (Kissing)–genital sexual activity (genito-oral sex): HSV-1 infections of the genitals and HSV-2 lesions in the oral cavity. • HSV-2 infections has markedly increase comparatively.
- 12. Pathogenesis Entry by skinor mucous membrane Multiplies locally Vesicle formation Virus spreds to draining lymph nodes lymphadenitis Ulcerate heal with residual scarring Settles within neuron of ganglia; Trigeminal (HSV-1) and sacral (HSV-2) Travels to sensory root ganglia Herpesvirus DNA integrated into host cell genome. Reactivation • Cold •Fever •Pneumonia •Surgery •Stress Latency
- 13. Pathogenesis Entry by skinor mucous membrane Multiplies locally Vesicle formation Virus spreds to draining lymph nodes lymphadenitis Ulcerate heal with residual scarring Settles within neuron of ganglia; Trigeminal (HSV-1) and sacral (HSV-2) Travels to sensory root ganglia Herpesvirus DNA integrated into host cell genome. Reactivation • Cold •Fever •Pneumonia •Surgery •Stress Latency
- 14. Clinical features • Cutaneousinfection • Mucosal • Opthalmic • Nervous system • Visceral • Genital • Neonatal • Infections in immunocompromised
- 15. Cutaneous infection • Infectsthrough abraded skin and causes various cutaneous lesions – Face – Buttocks: In infants as napkin rash • Febrile blisters (herpes febrilis) – Fever due to other cause provocate HSV to cause recurrent blisters. • Herpetic whitlow : Lesions +nt on fingers of Doctors , Dentists & Nurses • Herpes gladiatorum : lesions +nt on body of Wrestlers /rugby • Eczema herpeticum: • Caused by HSV-1 in patients with chronic eczema
- 16. Mucosal lesions • Oral-facialmucosal lesions most common manifestations of HSV infections. • Most common affected site Buccal mucosa • Most frequent lesions – Gingivostomatits – Pharyngitis • Recurrent herpes labialis – Painful vesicular near lips • Other lesions – Ulcerative stomatitis – Tonsillitis – Vesicular lesions on eyerlids – Many cases asymptomatic predispose to secondary bacterial infections.
- 17. Other infective Syndromesof HSV • Opthalmic lesions • CNS lesions • Visceral • Genital • Congenital
- 18. Opthalmic lesions 1. AcuteKerato conjuctivitis 2. Corneal ulcers and blindness 3. Follicular conjuctivitis with vesicle formation on lids 4. Dendritic keratitis 5. Acute necrotising retinitis 6. Choreoretinitis 5 4 3 3 2 1 6
- 19. Nervous system • HSVencephalitis [rare] • HSV meningitis • Transverse myelitis [rare] • Sacral autonomic dysfunction • Guillian Barre syndrome [rare] • Bell’s palsy [rare]
- 20. Visceral • HSV esophagitis •Tracheobronchitis & Pneumonitis • Hepatitis [uncommon] • Disseminated HSV infection
- 21. Genital herpes • Lesion •In males : on penis / in urethra • In females : cervix , vagina, vulva & perineum • Inguinal lymphadenopathy in both • In homosexuals : rectal / perineal lesions
- 22. Congenital/Neonatal Herpes • Neonatalherpes : rare • Lesions confined to eyes , mouth & skin / Disseminated disease • Clinical features- Babies are almost always symptomatic and presenting •One of the three forms Local lesions involving skin, eye and mouth •Encephalitis •Disseminated disease involving multiple organs,including the CNS-Neonate has the highest frequency of visceral infections.
- 23. LAB DIAGNOSIS • Microscopy •Ag / DNA detection • Virus isolation • Serology Specimens • Vesicle Fluid • Skin Swab • Saliva • Corneal Scrapings • Brain Biopsy • CSF
- 24. Microscopy Direct Examination OfSmear 1. Toludine Blue: Multi-nucleated giant cells with faceted nuclei homogenously stained “ground glass” chromatin (Tzanck Cells) +nt in positive smears.
- 25. 2. Geimsa Stain: Cowdry Type A Intranuclear Inclusion Bodies 3. If Staining : Viral Ag in scraping from base of lesions & tissue stained by immunofluorescent staining. 4. Fluroscent Ab Test : On brain biopsy in encephalitis
- 26. Virus isolation • Tissueculture: human diploid fibroblasts, Hep-2 cells, Vero cells and Chorioallantoic membrane. • CPE : Swollen, rounded cells (1-5 days) observed for 2 wks • Some HSV 2 strains – syncytium formation (fusion of infected cells) • Confirmed by IF staining of infected cell culture or by neutralization test.
- 27. Serology • Useful inprimary infection • IgM Ab • Rise in titre • CFT, Neutralization , IF, ELISA , RIA • Other PCR – HSV DNA in CSF
- 28. Chemotherapy • Idoxuridine usedtopically in eye and skin • infections – first successful antiviral • agent. • • Acyclovir : treatment of choice • –shortens the duration of the lesions • –reduces the extent of shedding of the virus • • Other Drugs – Valaciclovir, Famiciclovir, • • Orally effective • Valacyclovirand famciclovir: genital herpes and in the suppression of recurrences. • • Foscarnet.
- 29. Prevention • Avoiding contactwith the vesicular lesion or ulcer. • Abstain from oral sex. • Use condom to prevent genital herpes. • Cesarean section is recommended for women who are at term and who have genital lesions or positive viral cultures. • Can be treated with antiviral drugs. • Can be prevented by immunization.
- 30. Varicella Zoster Virus(VZV) • VZV produces vesicular eruptions (rashes) on skin and mucous membranes in the form of – Varicella (Chicken Pox) primary infection of non-immune person – Herpes Zoster (Shingles) reactivation of virus +nt in the latent stage • Virus is reactivated when the fall in immunity levels is unable to contain it • Culture – human fibroblast , human amnion , HeLa cells • CPE: Similar to HSV but slow & less marked Contact with either Zoster Chicken Pox Chicken Pox not Zoster or
- 31. • Chickenpox causesmorbidity and mortality which is more in: – Adolescents – Adults – Immunocompromised • Can be treated with antiviral drugs. • Can be prevented by immunization.
- 32. Varicella (chicken pox) •Characterized by generalized diffuse bilateral vesicular rashes following primary infection usually affecting children • Highly infectious disease characterized by vesicular rash mostly on trunk. • Can occur at any age • Infections occurring in childhood are milder • Commonest childhood exanthemata • Infections occurring in adulthood are more serious • The source is a chicken pox or herpes zoster patient
- 33. Pathogenicity POE respiratorytract or conjunctiva Virus enters blood stream and lymphatic system (primary viremia) Reticulo-endothelial system (RES) Secondary viremia Skin ( produces rashes) Respiratory tract (Shed through resp secretions) Neurones (undergoes latency) Incubation period is 7-23 days
- 34. After primary infection,virus migrates along sensory nerve fibres Doral root ganglia and cranial nerve ganglia Latent Reactivation in elderly or immunocompromised Migration along nerves Herpes zoster or shingles
- 35. Clinical Manifestations ofChickenpox Rashes • Initially, buccal lesions may appear, which may go unnoticed • The rash in varicella evolutes rapidly (over 48 hours) through the stages of maculepapulevesiclepustulescab • The rash appears in crops therefore, lesions of varying age can be seen in the same patient • The rash first appears on trunk, and spreads centrifugally • Fever appears with each crop of rashes.
- 38. Infectivity • Infectivity ismaximum is early stages of disease, when the virus is present in large numbers in the upper respiratory tract. • The buccal lesions and vesicular fluid is rich in virus, and is infectious • The person is considered to be infectious during two days before the onset and till five days after the onset of lesions. • Scabs have very low infectivity
- 39. Varicella (Chickenpox) inadults • It causes a more serious illness in adults • The rash is more severe • The rash may become hemorrhagic, and bullous lesions can appear • Lesions can become secondarily infected • Fatal pneumonia can develop • Other systemic manifestations like myocarditis, nephritis, meningitis and encephalitis can occur
- 40. Reye’s syndrome • Occurswhen salicylates are prescribed during chicken pox or flu, especially to young children • Swelling of brain and liver • Symptoms – Confusion – Seizures and – Loss of consciousness
- 41. Chicken pox duringpregnancy 1. Disease is more severe in pregnant women 2. Prognosis of foetus depends on the period of gestation during which the mother develops varicella: i.e. whether the infection develops in the first half of the pregnancy OR in the second half of pregnancy
- 42. Maternal varicella infirst half of pregnancy • Foetal infection is usually asymptomatic • Some develop foetal varicella syndrome, which manifests as: – Cicatrising skin lesions (heal by scar formation) – Hypoplasia of limbs – Chorioretinitis – CNS lesions • Some carry latent varicella infection Chorioretinitis Hypoplasia of limbs
- 43. Maternal varicella insecond half of pregnancy • If mother’s rash began more than week before delivery mother develops antibodies, which usually pass on to the foetus foetus usually escapes infection. • If mother’s rash began within a week before delivery only the virus passes transplacentally and not the antibodies neonatal varicella develops in the newborn
- 44. Maternal varicella insecond half of pregnancy Mother Antibodies Passes to Foetus Within week of delivery Viruses passes transplacentally not Abs Began >1 week before delivery Escape from infection Neonatal Varicella Varicella rashes in Pregnant mother
- 45. Neonatal varicella • Disseminateddisease with high risk of pneumonia and encephalitis
- 46. Herpes zoster (shingles) Herpein= Creep Zoster = girdle
- 47. • Chickenpox is ds of childhood • Zooster ds of old age >60yrs (occurs in people had chickenpox several years earlier). • Virus remain latent in the sensory ganglia. • Virus usually held in check by the residual immunity. • Reactivation by some precipitating stimulus. • Reactivation is associated with inflammation of the nerve neuritic pain very severe.
- 48. Pathogenesis Typically a diseaseof late adulthood Due to reactivation of latent VZV in the ganglia VZV replicates & migrates along sensory nerve rash on the dermatome supplied by that nerve Pain due to inflammation of the nerve
- 49. • Rash issimilar to varicella, but is limited in distribution to the area supplied by that nerve • Pain starts a few days before the appearance of rash, stays during the rash, and can persists for months after the disappearance of rash
- 50. Complications • Disseminated herpeszoster (especially in HIV patients) • Herpes zoster ophthalmicus (ophthalmic nerve involvement) • Ramsay Hunt syndrome (herpes zoster oticus): facial nerve palsy + vesicles in external auditory canal
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- 53. Laboratory diagnosis • Specimens –Vesicular lesions – Scabs – Maculopapular lesions • Cytopathology – Giemsa staining (scrapings from ulcer base) Tzanck smear multinucleated gaint cells. • Virus isolation – Various cell line produces CPE diffuse rounding and ballooning of infected cells
- 54. • VSZ-specific methods –Specific Ag detection by direct immunofluoroscence staining. – Specific IgM and IgG Ab detection by ELISA. – PCR detecting VZV-specific genes.
- 55. Laboratory diagnosis • Tzancksmear from the base of vesicles shows multi- nucleated giant cells and type A intranuclear inclusion bodies • Electron microscopy • Immunofluorescence microscopy • Virus isolation • ELISA • PCR
- 56. Treatment • Specific treatmentis given only in the immunodeficient, elderly or those with disseminated disease • Acyclovir, famciclovir and valacyclovir
- 57. Prophylaxis • Active: Liveattenuated vaccine is available • Passive: Varicella Zoster Immunoglobulin (VZIg) is usually given to newborns of infected mothers
- 58. Human herpes 6(HHV-6) – Infects T cells by binding to CD46 receptor – Has two variants 6A and 6B. – Transmission infected oral secretions – Sixth disease also called as exanthem subitum or roseola infantum characterized by high grade fever and skin rashes. – In older age HHV-6 associated with mononucleosis-like syndrome.
- 59. Human herpesvirus 7 •HHV-7 shows tropism for T cells • Transmitted by oral secretions; mainly children • Associated with – Fever – Seizures – Respiratory or GIT symptoms – Pityriais rosea. Human herpesvirus 8 • Causes malignancy called Kaposi sarcoma in HIV-infected individuals.
- 60.