Properties Pathogenesis

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Herpes simplex virus Enveloped double stranded DNA viruses ( HSV-1 : cold sore ; HSV-2 : genital herpes ) Spread by contact, as the virus is shed in saliva, tears, genital and other secretions. During the primary infection, HSV spreads locally and a short-lived viraemia occurs, whereby the virus is disseminated in the body. Spread to the to craniospinal ganglia occurs. The virus then establishes latency in the craniospinal ganglia. Reactivation - It is well known that many triggers can provoke a recurrence. These include physical or psychological stress, infection; especially pneumococcal and meningococcal, fever, irradiation; including sunlight, and menstruation.

Clinical manifestatio n (1)

  Acute Gingivostomatitis  Acute gingivostomatitis is the commonest manifestation of primary herpetic infection.  The patient experiences pain and bleeding of the gums. 1 - 8 mm ulcers with necrotic bases are present. Neck glands are commonly enlarged accompanied by fever.  Herpes labialis (cold sore)  Following primary infection, 45% of orally infected individuals will experience reactivation..  Herpes labialis (cold sore) is a recurrence of oral HSV.  A prodrome of tingling, warmth or itching at the site usually heralds the recurrence. About 12 hours later, redness appears followed by papules and then vesicles.  Ocular herpes HSV causes a broad spectrum of ocular disease, ranging from mild superficial lesions involving the external eye, to severe sight-threatening diseases of the inner eye. Diseases caused include the following: Primary HSV keratitis – dendritic ulcers  Recurrent HSV keratitis  HSV conjunctivitis  Iridocyclitis, chorioretinitis and cataract  Genital herpes  Genital lesions may be primary, recurrent or initial.  Many sites can be involved which includes the penis, vagina, cervix, anus, vulva, bladder, the sacral nerve routes, the spinal and the meninges.  The lesions of genital herpes are particularly prone to secondary bacterial infection eg. S.aureus, Streptococcus, Trichomonas and Candida Albicans.  Dysuria is a common complaint, in severe cases, there may be urinary retention.  Local sensory nerves may be involved leading to the development of a radiculitis @ meningitis

Clinical manifestatio n (2)

Herpes simplex virus Clinical manifestatio n (3)  Herpes simplex encephalitis  Neonatal – there is global involvement and the brain is almost liquefied.V.  Other cutaneous manifestations include :  eczema herpeticum which is potentially a serious disease that occurs in patients with eczema. It is available in a number of formulations: I. The mortality rate is high (70%) without treatment. Many organs other than the skin may be involved e. It usually takes only 1 . It is possible that many of these cases arise from reactivation of virus.  “zosteriform herpes simplex".g.5 days for a result to be available. The widespread vesicular resembles that of chickenpox. (HSV infection in normal and immunocompromised patients)  Oral (treatment and long term suppression of mucocutaneous herpes and prophylaxis of HSV in immunocompromised patients) Clinical manifestatio n (4) Other manifestatio n Lab dx management .  Focal disease – the temporal lobe is most commonly affected. This form of the disease appears in children and adults.  Serology  Not that useful in the acute phase because it takes 1-2 weeks for before antibodies appear after used routinely for the diagnosis of herpes simple encephalitis  Virus Isolation  HSV-1 and HSV-2 are among the easiest viruses to cultivate.  Premature rupturing of the membranes is a well recognized risk factor.  Neonatal herpes simplex  The baby is usually infected perinatally during passage through the birth canal. Used to document to recent infection.rapid result but cannot distinguish between HSV and VZV  Immunofluorescence of skin scrappings . lungs.  Disseminated herpes simplex are much more likely to occur in immunocompromised individuals.  Direct Detection  Electron microscopy of vesicle fluid .  Acyclovir – this the drug of choice for most situations at present. and CNS. The mortality rate approaches 100%. This is a rare presentation of herpes simplex where HSV lesions appear in a dermatomal distribution similar to herpes zoster.can distinguish between HSV and VZV  PCR .  It is of utmost importance to make a diagnosis of HSE early. It is general practice that IV acyclovir is given in all cases of suspected HSE before laboratory results are available. liver.  Infected from other sources such as oral lesions from the mother or a herpetic whitlow in a nurse.  Herpetic whitlow which arise from implantation of the virus into the skin and typically affect the fingers. spleen.

 These agents are highly toxic and is suitable for topical use for opthalmic infection only .g.  Other older agents – e. trifluorothymidine. idoxuridine. Vidarabine (ara-A). more expensive than acyclovir. Cream (HSV infection of the skin and mucous membranes)  Ophthalmic ointment  Famciclovir and valacyclovir – oral only.

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