In this article, we will discuss Short Note on Herpes Simplex Infection. So, let’s get started.
Herpes Simplex Infection
Causative organisms are HSV-1 and HSV-2, both of which cause primary and secondary as well as acute and latent infections.
Both viruses replicate in the skin and mucous membranes at the site of entry (oropharynx and genitals) and produce infective virions, which induce vesicular lesions. The virions then spread to sensory neurons that innervate the primary sites.
Virus is transported along axons to neuronal cell bodies where the virus establishes latent infection and is not immunologically recognized. In an immunocompetent individual, infection resolves in a few days, but the virus remains dormant in nerve cells. Reactivation occurs repeatedly when the virus travels from neurons to skin and mucous membranes.
Clinical Manifestations
Oral herpes can be caused by HSV-1 or HSV-2 infection. In primary herpetic gingivostomatitis, the typical clear lesions are the first to develop followed by ulcers. The infection, often initially on the lips, spreads to all parts of the mouth and pharynx.
Reactivation from the trigeminal ganglia can result in what are known as cold sores. Intraepithelial vesicles (due to intracellular oedema and ballooning of cells) are formed, which burst and crust, and can lead to superficial ulceration.
Gingivostomatitis encountered in children is usually caused by HSV-1. It is a vesicular eruption extending from tongue to retropharynx causing cervical lymphadenopathy.
Swollen, erythematous HSV lesions of fingers or palm (herpetic whitlow) occur in infants and occasionally, in healthcare workers.
Herpes keratitis is an infection of the eye primarily caused by HSV-1. It can be recurrent and may lead to blindness.
Herpes gladiatorum is contracted by wrestlers. It spreads by direct contact from skin lesions on one wrestler to his/her opponent, and usually appears in the head and neck region (which are frequent sites of contact in wrestling holds).
Genital herpes (Fig. 9.20) is usually the result of HSV-2 with about 10% of cases being the result of HSV-1. Primary infection is often asymptomatic, but sometimes, painful lesions can develop on glans or shaft of the penis in men and on vulva, vagina, cervix, and perianal region of women. HSV-2 can be transmitted to neonates during passage through birth canal of infected mothers. HSV-2 disease in the neonate can vary from being mild to severe with generalized lymphadenopathy, splenomegaly, and necrotic foci throughout the lungs, liver, adrenals and central nervous system.
Eczema herpeticum is characterized by confluent, pustular, or haemorrhagic blisters, often with bacterial superinfection and viral dissemination to internal viscera.
Herpes bronchopneumonia can result from insertion of an airway through oral herpes lesions.
Herpes hepatitis can cause liver failure.
HSV can be a cause of inflammation of rectum and anus (proctitis).
HSV encephalitis due to HSV-1 infection is the most common sporadic viral encephalitis.
HSV meningitis is the result of HSV-2 infection and usually resolves spontaneously.
Morphology
- Morphologic hallmark of HSV infection is large pink-to-purple intranuclear (Cowdry type A) inclusions, whichpush nuclear chromatin to periphery.
- There is mild increase in cellular size along with formation of multinucleated syncytial cells that also have inclusions.