Page 187 - Concise Pathology for Exam Preparation ( PDFDrive )

172 SECTION I General Pathology

Parvovirus B19

Produces erythema infectiosum (fifth disease), which typically manifests with a confluent
maculopapular rash, usually beginning on the cheeks (giving a ‘slapped-face’ appearance)
and extending centripetally to involve trunk.

Viral Haemorrhagic Fevers
• These are systemic infections characterized by fever and haemorrhages. They are caused
by enveloped RNA viruses belonging to four different families: arena virus, filo virus,
bunya virus and flavivirus.
• The viruses survive in animals and are transmitted by insects. Humans are infected
when they come in contact with infected hosts and vectors.
• Manifestations vary from a mild illness (fever, myalgias, headache, rash, neutropenia
and thrombocytopenia) to life-threatening disease (haemodynamic disturbances and
shock; Flowchart 7.3).

Virus enters bloodstream by bite of an insect/
mucous membrane exposure

Endothelial cell dysfunction

Increased vascular permeability

Widespread haemorrhage and necrosis

Disseminated intravascular coagulation
FLOWCHART 7.3. Pathogenesis of viral haemorrhagic diseases.

Herpes Virus
Herpes viruses are large encapsulated viruses having a double-stranded DNA genome.
They cause acute infection followed by latent infection in which the viruses persist in a
noninfectious form with periodic reactivation. There are nine types of human herpes vi-
ruses, belonging to three subgroups defined by the type of cell most frequently infected
and site of latency (Table 7.5):
• a-Group viruses: Herpes simplex virus-1 (HSV-1), HSV-2 and varicella zoster virus
(VZV)
• b-Lymphotropic viruses: CMV, human herpes virus-6 (which causes exanthem subi-
tum, also known as roseola infantum and sixth disease—a benign rash of infants) and
human herpes virus-7 (which is not yet associated with a specific disease)
• g-Group viruses: EBV and KSHV/HHV-8 (Table 7.5)—the cause of Kaposi sarcoma

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 la-
tent infection and is not immunologically recognized. In an immunocompetent indi-
vidual, 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.

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