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1. Welcome to seminar on HSV, CMV, TOXOPLASMA Infection Presenter: Dr.Sadia Fahmida (MD phase A) Dr.Tanjina Sultana(MD phase A) Dr.Ferdous Fatema (MD phase A)

2. HSV INFECTION

3. HSV is a double stranded virus belong to Human herpes virus family . Human is the only host. Set up latent infection following primary infection. Reactivation more likely to take place during periods of immunosuppression. Both primary infection & reactivation are likely to be more s erious in immunocompromised patients.

4. Basic pathological lesions : Cutaneous/ mucocutaneous vesicles (2-4 mm) s urrounded by erythematous base and shallow ulcer.

5. Transmission : direct contact with active lesion On skin or mucous membrane Or asymptomatic viral shedding from saliva , semen,Or cervical secretion

6. Type 1.HSV 1 2.HSV 2

7. P athogenesis virus replicate in skin or mucus membrane Migrates up the neuron by retrograde axonal flow Becomes latent in sensory ganglion cell

8. Virus can be reactivated from latent state by inducer Migrates down the neuron & replicates in skin causing lesions.

9. site Ds by HSV 1 Ds by HSV 2 skin Vesicular lesion above the waist Below the waist mouth gingivostomatitis rare eye keratoconjunctivitis rare CNS Encehalitis ( temporal lobe) High mortality & severe neurological sequele . Meningitis.(self limited ) Few sequele . Dissemination to viscera In immunocompromised pt yes rare Neonate rare Skin lesion ,disseminated infection,encephalitis Usual site of latency Cranial sensory ganglia Lumber,sacral sensory ganglia.

10. Features(HSV 1) 1.gingivostomatitis

11. Herpes Labialis (cold sore)

12. Herpetic Whitlow

13. Encephalitis Characterized by necrotic lesion in frontal & temporal lobe. Fever,headache,vomiting,seizures & altered mental status are typical features. Expressive aphasia,changes in speech ,focal seizues (indicate injury to frontal or temporal cortex). The untreated infection progresses to coma & death in 75 % cases.

14. Eczema herpeticum (Kaposi varicelliform eruption)

15. Features(HSV 2) Genital herpes Neonatal herpes

16. Perinatal infections Transmission from mother to child occur in 50% cases With a primary attack at term It may be acquired in utero during birth process. The most common portal of entry : conjunctiva, mucosal epithelium of nose & mouth break or abrasion in skin.

17. Infant with intrauterine infection Have skin vesicles chorioretinitis kerato -conjunctivitis microcephaly that are present at delivery.

18. Infant infected during delivery Present with 1 of the following 3 patterns: 1.Ds localized to skin,eye , mouth(SEM) : (5-11) days 2.encephalitis with/ without SEM :(8-7)days 3.Disseminated infection :(5-11) days involve brain , lung,liver,heart

19. Serious neonatal infection occur when mother Is experiencing primary infection than recurrent. 1.Amount of virus produced during primary infection is greater than secondary infection. 2.Mother previously infected can pass IgG across the placenta which protect neonate from disseminated infection.

20. Diagnosis Confirmation can be made from : 1.smears of lesion : Tzanck smear( multinucleated giant cell) 2.vesicular fluid 3.tissue biopsy These include : 1.culture of virus 2.electronic microscopic visualization 3.serology ( complement fixation test)

21. HSV IgM are unreliable & 4 fold rise of IgG between acute & convalescent serum samples is useful only in retrospect.

22. Evaluation of neonate Include 1.culture of lesions as well as eye & mouth swab 2.PCR of both CSF & blood

23. Lab findings HSV meningoencephalitis CSF : increase leucocytes Increase protein Glucose normal or reduced RBC may be present HSV encephalitis (beyond the neonatal period) EEG & MRI show temporal lobe abnormalities HSV encephalitis (neonatal period) Tends to be more global & not limited to temporal lobe. Disseminated infection Elevated liver enzymes Thrombocytopenia Abnormal coagulation.

24. Treatment Neonatal herpes Acyclovir IV (60 mg/kg/day) (Skin , Eye,mouth ) treated for 14 days (CNS) 21 days Suppressive therapy following Neonatal herpes with CNS involvement Acy (PO) 300 mg/meter square for 6 month after IV therapy. HSV encephalitis Acy (IV) 10 mg/kg 14 -21 days HSV gingivostomatitis Acy (PO) 15 mg/kg/dose 5 times 7 days Genital herpes Acy ( po )

25. Prognosis Most HSV infections are self limiting, last few days to 2-3 wks , & Heal without scarring. Some HSV infection can be severe & may have grave consequences without promt antiviral therapy. Life threatening condition include neonatal herpes, Herpes encephalitis.

26. Prevention Avoid contact with contaminated secretion. Good hygienic practices include: handwashing & use of gloves. Cesarean section is recommended who have genital lesions. Circumcision reduces risk of infection by HSV-2. Infant receive anticipatory acyclovir therapyfor at least 2 wk if signs develop or if surface cultures beyond 12-24 hr Of life are positive. No vaccine against HSV 1 or HSV 2.