Smallpox pathophysiology: Difference between revisions
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* At the 14th day [[pustules]] loose liquid content and become crusted | * At the 14th day [[pustules]] loose liquid content and become crusted | ||
* At the 3rd week, most crusts will separate (palms and soles last) | * At the 3rd week, most crusts will separate (palms and soles last) | ||
This form of [[smallpox]] is typical of an [[immunocompetent]] patient, whose [[immune system]] is able to inhibit [[viral replication]]. | |||
===Flat-type Smallpox=== | ===Flat-type Smallpox=== | ||
Revision as of 22:58, 9 July 2014
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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]
- Physical contact
- Contact with infected body fluids
- Contact with infected objects
- Air through aerosolized particles
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]
- Asymptomatic respiratory mucosa infection
- Viral replication within respiratory epithelium
- Transient primary asymptomatic viraemia
- Virus enters macrophages and spreads to lymph nodes and reticuloendothelial system, where it replicates during 4 - 14 days
- Exuberant secondary viraemia, leading to symptom onset
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]
- Initial hypopigmented macules
- Macules progress into papules and subsequently to vesicles
- Vesicles become pustules
- At the 14th day pustules loose liquid content and become crusted
- At the 3rd week, most crusts will separate (palms and soles last)
This form of smallpox is typical of an immunocompetent patient, whose immune system is able to inhibit viral replication.
Flat-type Smallpox
Hemorrhagic-type smallpox
Microscopic Pathology
The typical skin vesicles observed in smallpox occur following:[8]
- Viral infection of the epidermal cell
- Cells in malpighian layer enter balloon degeneration due to formation of vacuoles
- Cytoplasmic enlargement leads to loss of nuclear material
- Destruction of upper and middle layers of stratum spinosum
- Formation of vesicle, with high viral index
On the other hand, in the infected mucosal 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 through the oropharynx.[9]
References
- ↑ "Smallpox disease overview".
- ↑ Cecil, Russell (2012). Goldman's Cecil medicine. Philadelphia: Elsevier/Saunders. ISBN 1437716040.
- ↑ 3.0 3.1 "Smallpox and its Eradication" (PDF).
- ↑ 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.
- ↑ 5.0 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.
- ↑ Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.
- ↑ Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.
- ↑ Cecil, Russell (2012). Goldman's Cecil medicine. Philadelphia: Elsevier/Saunders. ISBN 1437716040.
- ↑ Cecil, Russell (2012). Goldman's Cecil medicine. Philadelphia: Elsevier/Saunders. ISBN 1437716040.