The virus occupies a peculiar stage in life. It cannot reproduce or replicate itself unless it infects another cell. Viruses are categorized by the type of nucleic acid within its core, either DNA or RNA viruses. Many viruses have the unique ability to remain dormant in the infected host for many years, often a lifetime. One classic example is the Varicella zoster virus, the cause of chicken pox. After the usual childhood infection, the virus can remain dormant in the nervous system. During periods of stress or immunocompromised states, reactivation of the virus can occur and the result is shingles.
Enterovirus (Coxsackie, Polio, Echovirus)
Erythema infectiosum (Fifth Disease)
Herpes Simplex Virus
Herpes Zoster (Shingles)
Human Herpes Virus Type 6
HTLV-1 (Human T-cell Lymphotropic Virus)
Mononucleosis (Infectious Mononucleosis)
Parvovirus (Parvovirus B19)
SARS (Severe Acute Respiratory Syndrome)
Shingles (Herpes Zoster)
Verruca Vulgaris (Warts)
West Nile Virus
CLINICAL VARIANTS CHARACTERIZATION GENERAL VARIANTS ADENOVIRUS Fatal Disseminated Adenovirus Infections in Immunocompromised Patients
Teresa Tram N. Pham, MD, James L. Burchette, Jr, HT(ASCP), and Laura P. Hale, MD, PhD
Am J Clin Pathol 2003;120:575-583 Abstract quote
Adenovirus has emerged as an important pathogen in immunocompromised patients, in whom disseminated disease occurs frequently and is associated with a high mortality rate.
In a retrospective review of 1,847 consecutive autopsies, we identified 84 cases where adenovirus infection was suspected clinically. Adenovirus infection was confirmed at autopsy in 8 (10%) of 84 cases; all were immunocompromised patients. Six (75%) of these cases had disseminated adenovirus infection that contributed to death. Pathologic findings attributed to adenovirus infection included pneumonia with or without intra-alveolar hemorrhage, hepatic necrosis, enterocolitis with or without mucosal hemorrhage, epicardial hemorrhage, and ulcerations of the larynx, trachea, and ileum.
This work shows that severe and fatal adenovirus infections are not infrequent, particularly in the immunocompromised population. Both clinicians and pathologists must become aware of the pathogenicity of adenovirus in this patient population, including its potential for causing life-threatening hemorrhage.
- Monkeypox virus: histologic, immunohistochemical and electron-microscopic findings.
Marshfield Clinic, Marshfield, WI, USA.
J Cutan Pathol. 2005 Jan;32(1):28-34. Abstract quote
Background: Human monkeypox, an emerging viral zoonosis first recognized in Africa, has recently emerged in the mid-western US. Initially, it presents with skin eruptions and fevers with diaphoresis and rigors. Clinically, the skin lesions progress from papules to vesiculopustules to resolving eschars.
Methods: Three cutaneous biopsy specimens from two patients with polymerase chain reaction (PCR)-proven monkeypox were available for review. The histologic, immunohistochemical and electron-microscopic features were identified.
Results: The clinical progression of lesions is mirrored histologically with ballooning degeneration of basal keratinocytes and spongiosis of a mildly acanthotic epidermis progressing to full thickness necrosis of a markedly acanthotic epidermis containing few viable keratinocytes. A lichenoid-mixed inflammatory cell infiltrate is present, which exhibits progressive exocytosis with the keratinocyte necrosis. Inflammation of the superficial and deep vascular plexes, eccrine units and follicles is also present. Viral cytopathic effect is manifest by multinucleated syncytial keratinocytes. Immunohistochemically, viral antigen is detected within keratinocytes of the lesional epidermis, follicular and eccrine epithelium and few dermal mononuclear cells. Electron microscopy reveals virions at various stages of assembly within the keratinocyte cytoplasm.
Conclusions: The histologic differential diagnosis includes herpes simplex virus, varicella and other pox viruses, such as smallpox. The first one may be differentiated histologically, immunohistochemically and electron microscopically. The last two may be differentiated using PCR assay for the monkeypox extracellular-envelope virus protein gene.
Tropical dermatology: viral tropical diseases.
Lupi O, Tyring SK.
Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
J Am Acad Dermatol. 2003 Dec;49(6):979-1000; quiz 1000-2. Abstract quote
Viruses are important pathogens in tropical areas; most of them, especially the tropical hemorrhagic fevers, produce mucocutaneous manifestations. More than any other kind of pathogen, viruses have the possibility for being widespread, since they have a greater probability of mutation than do bacteria, can cross species barriers easily, and infect both human beings and animals in habitats with a great biodiversity.
Tropical habitats also have been subject to major ecologic changes in the last few decades, exposing humans to direct contact with these viruses and allowing hemorrhagic fevers due to new emergent viruses such as flaviviruses, filoviruses, arenaviruses, and hantaviruses to become major threats to public health. The collapse of eradication programs in many countries, as well as population increases and ecologic modifications, have led to the spread of dengue and yellow fever to large portions of the world owing to the dissemination of vectors, especially mosquitoes, with broad ecologic ranges. Viruses previously restricted to some geographic areas, such as Rift Valley fever, Crimean-Congo hemorrhagic fever, West Nile fever, and monkeypox are now affecting new countries and populations. Other viruses such as herpes B infection often affect travelers and animal handlers in most parts of the world.
Dermatologic lesions occur in all these diseases and can facilitate a rapid diagnosis, leading to control of the virus and helping prevent possible outbreaks.
Henry JB. Clinical Diagnosis and Management by Laboratory Methods. Twentieth Edition. WB Saunders. 2001.
Rosai J. Ackerman's Surgical Pathology. Ninth Edition. Mosby 2004.
Sternberg S. Diagnostic Surgical Pathology. Fourth Edition. Lipincott Williams and Wilkins 2004.
Robbins Pathologic Basis of Disease. Seventh Edition. WB Saunders 2005.
DeMay RM. The Art and Science of Cytopathology. Volume 1 and 2. ASCP Press. 1996.
Weedon D. Weedon's Skin Pathology Second Edition. Churchill Livingstone. 2002
Fitzpatrick's Dermatology in General Medicine. 6th Edition. McGraw-Hill. 2003.
Weiss SW and Goldblum JR. Enzinger and Weiss's Soft Tissue Tumors. Fourth Edition. Mosby 2001.
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Last Updated September 13, 2005
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