Monkeypox

Monkeypox
Human monkeypox lesions
Classification and external resources
Specialty infectious disease
ICD-10 B04
ICD-9-CM 059.01

Monkeypox is an infectious disease caused by the monkeypox virus. The disease was first identified in laboratory monkeys, hence its name, but in its natural state it seems to infect rodents more often than primates. The disease is indigenous to Central and West Africa. An outbreak that occurred in the United States in 2003 was traced to a pet store where imported Gambian pouched rats were sold.[1]

Monkeypox virus is a zoonotic viral disease that occurs primarily in remote villages of Central and West Africa in proximity to tropical rainforests where there is more frequent contact with infected animals. Monkeypox is usually transmitted to humans from rodents, pets, and primates through contact with the animal's blood or through a bite. Human monkeypox can be difficult to distinguish clinically from smallpox (to which it is closely related) and chickenpox (to which it is not).[2]

Epidemiology

Monkeypox virus
Virus classification
Group: Group I (dsDNA)
Order: Unassigned
Family: Poxviridae
Subfamily: Chordopoxvirinae
Genus: Orthopoxvirus
Type species
Vaccinia virus
Species

Monkeypox virus

In addition to monkeys, reservoirs for the virus are found in Gambian pouched rats (Cricetomys gambianus), dormice (Graphiurus sp.) and African squirrels (Heliosciurus, and Funisciurus). The use of these animals as food may be an important source of transmission to humans.

Monkeypox as a disease in humans was first associated with an illness in the Democratic Republic of the Congo (formerly Zaire), in the town of Basankusu, Équateur Province, in 1970.[3] A second outbreak of human illness was identified in DRC/Zaire in 1996–1997. In 2003, a small outbreak of human monkeypox in the United States occurred among owners of pet prairie dogs.[4] The outbreak originated from Villa Park, Illinois, outside of Chicago, when an exotic animal dealer kept young prairie dogs in close proximity to an infected Gambian pouched rat (Cricetomys gambianus) recently imported from Accra, Ghana. Seventy-one people were reportedly infected, of which there were no fatalities.

A second African focus of infection has been discovered in Sudan. No infected patients died.[5]

Monkeypox virus

Monkeypox virus causes the disease in both humans and animals. It was first identified in 1958 as a pathogen of crab-eating macaque monkeys (Macaca fascicularis) being used as laboratory animals. The crab-eating macaque is often used for neurological experiments. Monkeypox virus is an Orthopoxvirus, a genus of the family Poxviridae that contains other viral species that target mammals. The virus is found mainly in tropical rainforest regions of central and West Africa.

The virus was first discovered in monkeys (hence the name) in 1958, and in humans in 1970. Between 1970 and 1986, over 400 cases in humans were reported. Small viral outbreaks with a death rate in the range of 10% and a secondary human to human infection rate of about the same amount occur routinely in equatorial Central and West Africa.[6] The primary route of infection is thought to be contact with the infected animals or their bodily fluids.[6] The first reported outbreak in the United States occurred in 2003 in the midwestern states of Illinois, Indiana, and Wisconsin, with one occurrence in New Jersey. The outbreak was traced to a prairie dogs infected from an imported Gambian pouch rat. No deaths occurred.

The virus can spread both from animal to human and from human to human. Infection from animal to human can occur via an animal bite or by direct contact with an infected animal’s bodily fluids. The virus can spread from human to human by both respiratory (airborne) contact and contact with infected person's bodily fluids. Risk factors for transmission include sharing a bed, room, or using the same utensils as an infected patient. Increased transmission risk associated with factors involving introduction of virus to the oral mucosa.[7] Incubation period is 10–14 days. Prodromal symptoms include swelling of lymph nodes, muscle pain, headache, fever, prior to the emergence of the rash.The rash is usually only present on the trunk but has the capacity to spread to the palms and soles of the feet, occurring in a centrifugal distribution. The initial macular lesions exhibit a papular, then vesicular and pustular appearance.[7]

Morbidity and mortality

Symptoms and course

In humans, monkeypox is similar to smallpox, although it is often milder. Vaccination against smallpox is assumed to provide protection against human monkeypox infection considering they are closely related viruses and the vaccine protects animals from experimental lethal monkeypox challenge.[8] This has not been conclusively demonstrated in humans because routine smallpox vaccination was discontinued following the apparent eradication of smallpox and due to safety concerns with the vaccine. Limited person-to-person spread of infection has been reported in disease-endemic areas in Africa. Case-fatality ratios in Africa have ranged from 1% to 10%.[9]

Prevention and treatment

Currently, there is no proven, safe treatment for monkeypox. Smallpox vaccine has been reported to reduce the risk of monkeypox among previously vaccinated persons in Africa. The decrease in immunity to poxviruses in exposed populations is a factor in the prevalence of monkeypox. It is attributed both to waning cross-protective immunity among those vaccinated before 1980 when mass smallpox vaccinations were discontinued, and to the gradually increasing proportion of unvaccinated individuals.[7] The United States Centers for Disease Control and Prevention (CDC) recommends that persons investigating monkeypox outbreaks and involved in caring for infected individuals or animals should receive a smallpox vaccination to protect against monkeypox. Persons who have had close or intimate contact with individuals or animals confirmed to have monkeypox should also be vaccinated. The people who have been infected can be vaccinated up to 14 days after exposure. CDC does not recommend preexposure vaccination for unexposed veterinarians, veterinary staff, or animal control officers, unless such persons are involved in field investigations.

This film, produced by INCEF for distribution in communities prone to infection, describes the nature of the illness and how best to confront it.

2003 U.S. outbreak

In May, 2003, a young child became ill with fever and rash after being bitten by a prairie dog purchased at a local swap meet near Milwaukee, Wisconsin.[10] In total, 71 cases of monkeypox were reported through June 20, 2003. All cases were traced to Gambian rats imported by a Texas exotic animal distributor, from Accra, Ghana in April, 2003. No deaths resulted.[11] Electron microscopy and serologic studies were used to confirm that the disease was human monkeypox.

Patients typically experienced prodromal symptoms of fever, headaches, muscle aches, chills, and drenching sweats. Roughly one-third of patients had nonproductive coughs. This prodromal phase was followed 1–10 days later by the development of a papular rash that typically progressed through stages of vesiculation, pustulation, umbilication, and crusting. In some patients, early lesions had become ulcerated. Rash distribution and lesions occurred on head, trunk, and extremities; many of the patients had initial and satellite lesions on palms, soles, and extremities. Rashes were generalized in some patients. After onset of the rash, patients generally manifested rash lesions in different stages. All patients reported direct or close contact with prairie dogs, later found to be infected with the monkeypox virus.[12]

See also

References

  1. "Update: Multistate Outbreak of Monkeypox - Illinois, Indiana, Kansas, Missouri, Ohio, and Wisconsin, 2003". Cdc.gov. Retrieved 2013-03-22.
  2. Jezek Z, Szczeniowski M, Paluku KM, Mutombo M, Grab B (1988). "Human monkeypox: confusion with chickenpox". Acta Trop. 45 (4): 297–307. PMID 2907258.
  3. Ladnyj ID, Ziegler P, Kima E. "A human infection caused by monkeypox virus in Basankusu Territory, Democratic Republic of the Congo". Bull World Health Organ. 46: 593–7. PMC 2480792Freely accessible. PMID 4340218.
  4. "What You Should Know About Monkeypox" (PDF). Fact Sheet. Centers for disease control and prevention. 2003-06-12. Retrieved 2008-03-21.
  5. Damon IK, Roth CE, Chowdhary V (2006). "Discovery of monkeypox in Sudan". N. Engl. J. Med. 355 (9): 962–3. PMID 16943415. doi:10.1056/NEJMc060792.
  6. 1 2 Meyer, H.; Mathilde Perrichot; Markus Stemmler; Petra Emmerich; Herbert Schmitz; Francis Varaine; Robert Shungu; Florimond Tshioko; Pierre Formenty (2002). "Outbreaks of Disease Suspected of Being Due to Human Monkeypox Virus Infection in the Democratic Republic of Congo in 2001". Journal of Clinical Microbiology. American Society for Microbiology. 40 (8): 2919–2921. PMC 120683Freely accessible. PMID 12149352. doi:10.1128/JCM.40.8.2919-2921.2002.
  7. 1 2 3 Kantele A, Chickering K, Vapalahti O, Rimoin AW (2016). "Emerging diseases—the monkeypox epidemic in the Democratic Republic of the Congo". Clinical Microbiology and Infection. 22 (8): 658–659.
  8. Marriott KA, Parkinson CV, Morefield SI, Davenport R, Nichols R, Monath TP (2008). "Clonal vaccinia virus grown in cell culture fully protects monkeys from lethal monkeypox challenge". Vaccine. 26 (4): 581–8. PMID 18077063. doi:10.1016/j.vaccine.2007.10.063.
  9. Hutin YJ, Williams RJ, Malfait P, et al. (2001). "Outbreak of human monkeypox, Democratic Republic of Congo, 1996 to 1997". Emerging Infect. Dis. 7 (3): 434–8. PMC 2631782Freely accessible. PMID 11384521. doi:10.3201/eid0703.010311.
  10. Anderson MG, Frenkel LD, Homann S, and Guffey J. (2003), "A case of severe monkeypox virus disease in an American child: emerging infections and changing professional values"; Pediatr Infect Dis J;22(12): 1093–1096; discussion 1096–1098.
  11. "Medscape Monkeypox Review". Bcbsma.medscape.com. Retrieved 2013-03-22.
  12. Centers for Disease Control (CDC), Morbidity and Mortality Weekly Report. Atlanta, Georgia. (MMWR) July 11, 2003. (52) 27; 642-646.
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