Family – Poxviridae
Genome -large, double-stranded DNA viruses.
They affect both vertebrate and invertebrate animals
The pox viruses include the following genera which are important for humans:
o Orthopox virus: smallpox, alastrim, vaccinia, cowpox, monkeypox, camelpox, buffalopox
o Parapox virus: orf, pseudocowpox (syn. pseudovaccinia or milker's nodules), sealpox, bovine papular stomatitis, deer pox
o Molluscipox virus: molluscum contagiosum
o Yatapox virus: tanapox, yabapox
The most common are vaccinia (seen on Indian subcontinent) and molluscum contagiousum, but monkeypox infections are rising (seen in west and central African rainforest countries).
Camelpox is a disease of camels caused by a virus of the family Poxviridae, subfamily Chordopoxvirinae, and the genus Orthopoxvirus. It causes skin lesions and a generalized infection. Approximately 25% of young camels that become infected will die from the disease, while infection in older camels is generally more mild.
Poxviruses are brick-shaped (240 nm by 300 nm) and have a complex internal structure including a double-stranded DNA genome (130–260 kb) and associated enzymes. Naturally released virions have an additional outer membrane not found on infective virions extracted artificially from infected cells. Parapoxviruses have a characteristic morphology.
Poxvirus replication takes place in cytoplasmic inclusions. Infecting virions are partly uncoated by cellular enzymes and then fully uncoated by viral enzymes released from the virion core. The viral DNA is not infectious per se, and other core enzymes (including a DNA-dependent RNA polymerase) play essential roles in the replication cycle. The replication cycle can be divided into functions controlled by early (prereplicative) gene products and those controlled by late (postreplicative) gene products. Most virions (80 to 90 percent) remain within cells and therefore lack the outer envelope found on naturally released virions.
Pathogenesis: Small Pox
o Other name: red Plague
o Smallpox localized in small blood vessels of the skin and in the mouth and throat.
o V. major produces a more serious disease and has an overall mortality rate of 30–35%.
o V. minor causes a milder form of disease (also known as alastrim, cottonpox, milkpox, whitepox, and Cuban itch) which kills about 1% of its victims.
o Long-term complications of V. major infection include characteristic scars, commonly on the face, which occur in 65–85% of survivors.
Smallpox is believed to have emerged in human populations about 10,000 BC.
The earliest physical evidence of it is probably the pustular rash on the mummified body of Pharaoh Ramses V of Egypt. The disease killed an estimated 400,000 Europeans annually during the closing years of the 18th century (including five reigning monarchs), and was responsible for a third of all blindness. Of all those infected, 20–60%—and over 80% of infected children—died from the disease. Smallpox was responsible for an estimated 300–500 million deaths during the 20th century. As recently as 1967, the World Health Organization (WHO) estimated that 15 million people contracted the disease and that two million died in that year
After vaccination campaigns throughout the 19th and 20th centuries, the WHO certified the eradication of smallpox in 1979. Smallpox is one of two infectious diseases to have been eradicated, the other being rinderpest, which was declared eradicated in 2011.
o The incubation period is around 12 days.
o In the initial growth phase the virus seems to move from cell to cell, but around the 12th day, lysis of many infected cells occurs and the virus is found in the bloodstream in large numbers @(this is called viremia), and a second wave of multiplication occurs in the spleen, bone marrow, and lymph nodes.
o Smallpox virus preferentially attacks skin cells, causing the characteristic pimples (@macules) associated with the disease.
o A rash develops on the skin 24 to 48 hours after lesions on the mucous membranes appear.
o Typically the macules first appear on the forehead, then rapidly spread to the whole face, proximal portions of extremities, the trunk, and lastly to distal portions of extremities. The process takes no more than 24 to 36 hours, after which no new lesions appear
o Virus invades through broken skin, replicates at the site of inoculation, and causes dermal hyperplasia and leukocyte infiltration.
o With cowpox, and to a lesser extent with parapox, there is limited lymphatic spread; this causes lymphadenopathy and elicits an immune response.
o The lesion of molluscum is circumscribed by a connective tissue capsule, and the dermis, although distorted, is not usually broken.
o Some poxviruses express an epidermal growth factor and host range genes which play a role in pathogenesis and cell tropism.
Human monkeypox is usually acquired via the respiratory tract, and during a 12-day incubation period viremia distributes infection to internal organs, which are damaged by virus infection. Spread to the skin initiates the clinical phase, and the lesions progress through the classic stages of macule to papule to vesicle to pustule to crust. Lymphadenopathy, usually involving the cervical and inguinal areas, is often marked.
o It is transmitted from one person to another primarily through prolonged face-to-face contact with an infected person, usually within a distance of 6 feet (1.8 m), but can also be spread through direct contact with infected bodily fluids or contaminated objects (fomites) such as bedding or clothing.
o Smallpox is highly contagious, but generally spreads more slowly and less widely than some other viral diseases, perhaps because transmission requires close contact and occurs after the onset of the rash.
o The clinical definition of smallpox is an illness with acute onset of fever greater than 101 °F (38.3 °C) followed by a rash characterized by firm, deep seated vesicles or pustules in the same stage of development without other apparent cause.
o If a clinical case is observed, smallpox is confirmed using laboratory tests.
o Guarnieri bodies are readily identified in skin biopsies stained with hematoxylin and eosin, and appear as pink blobs.
o They are found in virtually all poxvirus infections but the absence of Guarnieri bodies cannot be used to rule out smallpox.
o The diagnosis of an orthopoxvirus infection can also be made rapidly by electron microscopic examination of pustular fluid or scabs.
o However, all orthopoxviruses exhibit identical brick-shaped virions by electron microscopy.
Chickenpox was commonly confused with smallpox in the immediate post-eradication era. Chickenpox and smallpox can be distinguished by several methods. Unlike smallpox, chickenpox does not usually affect the palms and soles. Additionally, chickenpox pustules are of varying size due to variations in the timing of pustule eruption: smallpox pustules are all very nearly the same size since the viral effect progresses more uniformly.
o Smallpox vaccination within three days of exposure will prevent or significantly lessen the severity of smallpox symptoms in the vast majority of people.
o Vaccination four to seven days after exposure can offer some protection from disease or may modify the severity of disease.
o Other than vaccination, treatment of smallpox is primarily supportive, such as wound care and infection control, fluid therapy, and possible ventilator assistance.
o People with semi-confluent and confluent types of smallpox may have therapeutic issues similar to patients with extensive skin burns.
o No drug is currently approved for the treatment of smallpox.
o However, antiviral treatments have improved since the last large smallpox epidemics, and studies suggest that the antiviral drug cidofovir might be useful as a therapeutic agent. The drug must be administered intravenously, however, and may cause serious kidney toxicity.
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