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)
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
serious in immunocompromised patients.
4. • Basic pathological lesions :
Cutaneous/ mucocutaneous vesicles (2-4 mm)
surrounded 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
14. 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.
17. 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.
18. Infant with intrauterine infection
• Have
skin vesicles
chorioretinitis
kerato-conjunctivitis
microcephaly that are present at delivery.
19. 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
20.
21. • 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.
22. 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)
23. • HSV IgM are unreliable & 4 fold rise of IgG
between acute & convalescent serum samples
is useful only in retrospect.
24. • Evaluation of neonate
Include
• 1.culture of lesions as well as eye & mouth swab
• 2.PCR of both CSF & blood
25. 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.
26. 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)
27. 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.
28. 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.
