Smallpox pathophysiology: Difference between revisions

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====B-type, or Guarnieri bodies====
====B-type, or Guarnieri bodies====
* Areas of active [[viral replication]]
* Areas of active [[viral replication]]
 
* Present in [[infections]] by all poxviruses
* Present in [[infections]] by all [[poxviruses]]
* Appear as [[basophilic]] bodies near the [[nucleus]] on hematoxylin and eosin-stained samples
 
* On hematoxylin and eosin-stained samples appear as [[basophilic]] bodies near the [[nucleus]]
* Evident at [[epithelial cells]] underlying [[vesicles]] and [[pustules]]
* Evident at [[epithelial cells]] underlying [[vesicles]] and [[pustules]]



Revision as of 23:55, 9 July 2014

Smallpox Microchapters

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Overview

Historical Perspective

Eradication
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Causes

Differentiating Smallpox from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Criteria

History and Symptoms

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Laboratory Findings

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]

Overview

Transmission

Smallpox virus is transmitted by:[1]

Genetics

Pathogenesis

The smallpox virus commonly enters the body through the upper respiratory tract, invading the oropharyngeal and respiratory mucosa.[2] Other possible ports of entry include: skin, conjunctivae as well as through the placenta.[3] Although the viral scabs may contain life viruses, they are commonly contained within thickened material, which limits transmissibility.

Once in the respiratory mucosa, the infection commonly progresses as:[4][3][5]

During secondary viraemia the virus infects mucous cells of the pharynx and mouth, and endothelium of the capillaries of the dermis, causing skin scabs. Other organs with high viral loads include:[5]

Before development of the rash, the first lesions appear on the oropharyngeal mucosa, at which time the virus is released through the mucosal secretions, making that patient infectious.

Skin lesions develop due to migration of macrophages to the infected areas of the dermis, leading to edema and necrosis. With the influx of more polymorphonuclear cells, skin pustules will develop.[4]

The immune system responds to the viremia with activation of lymphocytes T and B and concomitant production of:[5]

  • Neutralizing antibodies, during first week of disease, remaining for many years
  • Hemagglutination-inhibition antibodies, by the 16th day of infection, beginning to decrease after 1 year
  • Complement-fixation antibodies, by the 18th day of infection, beginning to decrease after 1 year
  • Memory T cells, remaining for 50 years

Death by smallpox was commonly due to toxemia, following:[4]

Associated Conditions

Gross Pathology

Depending on the status of the patient's immune system, there may be identified 3 forms of smallpox:[6]

Ordinary Smallpox

Characterized by the following progression of lesions:[7]

This form of smallpox is typical of an immunocompetent patient, whose immune system is able to inhibit viral replication.

Flat-type Smallpox

Characterized by the following progression of lesions:[8]

  • Delayed appearance of macules
  • Slow progression of the lesions, usually with flat and soft appearance
  • Possible slough of skin sections

Most cases are fatal with presence of severe toxemia. This form of smallpox is typical of patients with weak cellular immune response to the virus.

Hemorrhagic-type smallpox

Characterized by the following progression of lesions:[9]

This rare form of smallpox is typical of patients with severely compromised immune response, in which there is intense viral replication in the bone marrow and spleen It is also associated with intense toxemia.

Microscopic Pathology

The typical skin vesicles observed in smallpox occur following:[10]

On the other hand, in the infected mucous surfaces, the viral proliferation and absence of the stratum corneum lead to the formation of ulcers. These ultimately lead to the release of greater loads of virus to the oropharynx.[11]

Histopathology

Poxviruses are characterized by cytoplasmic inclusions, however, these do not identify specifically the smallpox virus on a biopsy. There are 2 types of inclusion bodies:[12]

A-type

Typical of some viruses of the:

  • Genus Orthopoxvirus:
  • Cowpox virus
  • Ectromelia virus
  • Genus Avipoxvirus

B-type, or Guarnieri bodies

References

  1. "Smallpox disease overview".
  2. Cecil, Russell (2012). Goldman's Cecil medicine. Philadelphia: Elsevier/Saunders. ISBN 1437716040.
  3. 3.0 3.1 "Smallpox and its Eradication" (PDF).
  4. 4.0 4.1 4.2 Moore, Zack S; Seward, Jane F; Lane, J Michael (2006). "Smallpox". The Lancet. 367 (9508): 425–435. doi:10.1016/S0140-6736(06)68143-9. ISSN 0140-6736.
  5. 5.0 5.1 5.2 Breman, Joel G.; Henderson, D.A. (2002). "Diagnosis and Management of Smallpox". New England Journal of Medicine. 346 (17): 1300–1308. doi:10.1056/NEJMra020025. ISSN 0028-4793.
  6. Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.
  7. Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.
  8. Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.
  9. Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.
  10. Cecil, Russell (2012). Goldman's Cecil medicine. Philadelphia: Elsevier/Saunders. ISBN 1437716040.
  11. Cecil, Russell (2012). Goldman's Cecil medicine. Philadelphia: Elsevier/Saunders. ISBN 1437716040.
  12. Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.

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