Roses (Rosa sp.) are susceptible to a number of pests, diseases and disorders. A large number of the problems affecting roses are seasonal and climatic. Certain varieties of roses are naturally more resistant or immune than others to certain pests and diseases. Cultivation requirements of individual rose species and cultivars, when observed, often assist in the prevention of certain pests, diseases and disorders.

Pests

Insects that affect roses are often considered pests.

• Aphids: (Greenfly) (Order Hemiptera Family Aphididae) Macrosiphum rosae â€" Likely to be found on new shoots and buds, aphids are soft bodied insects 1-2mm long. Often green but occasionally light-brown, and sometimes with wings, they may cover (in a colony) the complete growing tip of the plant. Aphids are most active in spring and summer and multiply at a prodigious rate feeding on the sap of the plant by piercing the plant cells via a proboscis. In large quantities they may seriously retard the growth of the plant and ruin buds. They are particularly damaging to the new shoots with subsequent damage to the emerging leaves which become malformed with much the same appearance as leaf-curl in peaches.
• Two-spotted mite (Spider-mites or Red spider mite) (Order Acari: Family Tetranychidae) Tetranychus urticae â€" Previously known as red-spider mite these arachnids prefer the underside of leaves and are difficult to see with an unaided eye. Evidence of their presence is silvering of leaves where the mites have destroyed individual leaf cells. Fine webbing and eggs on the undersides of leaves is further evidence of the presence of Tetranychus urticae.
• Thrips (Order Thysanoptera) â€" Thrips are slim-winged insects 1mm in length, resembling fine slivers of wood or rice. Preferring light-coloured blooms and often appearing in plague numbers, flowers are often left looking scarred, warped, and lustreless.
• Rose Slugs (Rose Sawflies)- Sawflies are non-stinging wasps (Hymenoptera) in the suborder Symphyta, not flies (Diptera). They lay eggs in plant leaves or stems with a saw-like ovipositor. There are three species that commonly cause damage to wild or cultivated roses: The Bristly Roseslug (Cladius difformis) is found in Europe, Siberia, and many areas of North America. The larvae is pale green, up to 16 millimetres (0.6 in) long, and covered with hairlike bristles all over its body. It looks like a caterpillar but that term strictly speaking only applies to the larvae of moths and butterflies. It skeletonizes the underside of leaves, with several generations per year. The European Roseslug (Endelomyia aethiops) is found in North America as well as Europe. The larvae is more slug-like (but not slimy), up to 13 millimetres (0.5 in), and skeletonizes the upper surface of leaves with only one generation per year. The Curled Roseslug ( Allantus cinctus) larvae is pastel green on the back, marked on the thorax and abdomen with white dots, and up to 19 millimetres (0.7 in) long. It frequently coils up like a snake. After skeletonizing entire leaves except the main veins, it pupates in the pith of canes, with up to two generations per year in North America.
• Caterpillars (Order Lepidoptera) See also List of Lepidoptera that feed on roses â€" The tortryx (tortrix) moth Lozotaenia forsterana is a prominent pest of roses, although not the sole pest. The caterpillars are green, up to 15mm long, and can be found boring into buds or within curled leaves. When disturbed the caterpillars move swiftly, dropping to the ground on a fine thread. Damage is chewn leaves and flowers and buds with "shot holes".
• Curculio beetles (Family Curculionidae)
• Japanese beetles (Popillia japonica) - This species, introduced to North America in 1912, is now an endemic pest in the eastern United States. Adult beetles emerge from the ground in early summer and join into swarms for four to six weeks, devouring blooms and skeletonizing foliage on roses and many other garden plants. Japanese beetles can be partially controlled, albeit slowly, by spreading milky spore bacillus on the lawn areas where the larvae live. The popular pheromone-baited traps may do more harm than good by attracting beetles from a wide area.
• Scale insects (Order Hemiptera)

Cottony cushion scale (Order Hemiptera : Family Coccoidea) Icerya purchasi â€" This scale infests twigs and branches. The mature female is oval in shape, reddish-brown with black hairs, 5 mm long. When mature the insect remains stationary and produces an egg sac in grooves, by extrusion, in the body which encases hundreds of red eggs. The insect causes little damage but produces copious honeydew (frass) that can cause damaging sooty mould.

California red scale (Order Hemiptera : Family Coccoidea) Aonidiella aurantii â€" A hard scale, orange to orange-pink, the female covering being less than 1.5mm across. Often in plague numbers this scale infests upper surfaces of foliage causing yellowing, leaf fall, and twig and branch dieback. Serious infestations can cause plant death.

Rose scale (Order Hemiptera : Family Coccoidea) Aulacaspis rosae â€" Mainly found on the stems and branches of the plant, lack of control will allow the pest to spread to flower stalks and petioles. At this point the plant would be stunted, spindly and with a white, flaky crust of scales on the bark. Female Aulacaspis rosae may live for 1 year and may lay 80 eggs each with several overlapping generations living within milliimetres of the original parent.

• Leaf Cutting Bee (Order Hymenoptera : Family Megachilidae) Megachile spp. â€" Leafcutter bees are 6-16mm long and mostly black with bands of light-coloured hair. They chew pieces from the edges of leaves. The pieces are regular in shape, circular or oval. Damage is not often significant.
• Nematodes (Eelworms)(Order Tylenchida: Family Heteroderidae)

Root-knot nematode Meloidogyne spp.

See - Root-knot nematode - symptoms of Meloidogyne infestation in roses is stunting, slow-growth, pale green leaves and wilting in mild weather.

• Rose chafer (Order Coleoptera : Family Scarabaeidae) Macrodactylus subspinosus â€" The rose chafer is common to North America, and emerges in late May to mid June. These beetles form aggregations and feed upon foliage, buds, flowers, and fruit of roses and other ornamentals.
• Metallic flea-beetles (Order Coleoptera: Family Chrysomelidae) Altica spp. â€" The small, shiny and metallic Altica beetles have thickened hindlegs adapted to jumping, similar to fleas. The insects are 3mm long and chew holes of irregular shapes in young leaves and buds. As the leaves enlarge so do the holes.

Diseases

Fungal, bacterial and viral diseases that affect roses:

Bacterial diseases

• Crown gall rot (Class Alpha Proteobacteria: Family Rhizobiaceae) Agrobacterium rhizogenes â€" This disease is characterized by large lumps at the base of the plant stem or on roots. Galls may appear higher on stems as the disease progresses. Galls are soft compared to surrounding plant tissues. The pathogenic bacteria enter the plant via a wound. If the disease affects the plant whilst it is young the plant may be affected to the degree where it will not produce blooms. All affected plants wilt readily and grow poorly.

Fungal diseases

• Black Spot (Class Leotiomycetes: Family Helotiales) Diplocarpon rosae syn. Marssonina rosae â€" Marssonina rosae causes black spots on leaves. The spots, which may be as much as 12mm across, are generally circular and have an irregular edge often with a yellow halo. Leaves frequently turn yellow and fall early. Sometimes new leaves are produced, and these may also become affected. Continual defoliation will cause weakness, dieback or death of the plant. Some very susceptible species may have stems affected with a considerable reduction in plant vigour.

• Powdery Mildew Podosphaera pannosa â€" P. pannosa produces a very fine, powdery coating on the surface of buds and leaves. Significant cases have stems and particularly thorns, infected. Attacks on young leaves and buds will cause deformity with retardation of growth. Infected buds will fail to open. The disease is likely in hot, humid weather, with fungal spores overwintering on the stems and fallen leaves.
• Downy mildew (Class Oomycetes : Family Peronosporaceae) Peronospora sparsa â€" Peronospora causes purple-red to dark-brown spots on the leaves with irregular margins, however, often angular. Stems, petioles and flower stalks can split and spotted with purple marks. Buds, sepals, petals and calyces can be affected and will present purple spots. New growth affected will be deformed. The disease is spread by wind.

• Rust Phragmidium mucronatum â€" Rose rust appears as yellow patches on the surface of leaves, with orange pustules of spores underneath the leaf. The fungus is spread by wind. Affected leaves fall prior to healthy ones and plants may be defoliated in serious infections.

• Anthracnose Sphaceloma rosarum â€" Spots caused by this fungus originate from a point where leaves are water soaked, usually unnoticeable at first, until they turn black with a very distinct defined edge. As the spots enlarge the centre becomes gray and may fall out resulting in a shot-hole appearance. Defoliation may occur but is often not serious.
• Grey mould (Class Leotiomycetes: Family Sclerotiniceae) Botrytis cinerea â€" On roses grey mould is primarily a disease of the flowers and buds, leaves are infrequently attacked. Infected buds rot on the stem and infection may progress down the stem. On petals botrytis cinerea produces pink rings.
• Verticillium wilt (Class Incertae sedis: Family Verticillium) Verticillium dahliae
• Sooty moulds Alternaria spp. â€" Sooty mould appears as black, dry powder on leaves similar to chimney soot. Many sooty moulds grow on the honeydew (frass) produced by sap-sucking insect such as aphids and soft scales. Alternaria does no direct damage to plants but surface cover of leaves will reduce the plants capacity to photosynthesise and may create an unsatisfactory plant appearance.
• Canker Leptosphaeria coniothyrium and Cryptosporella umbrina â€" Cankers present as small yellowish or reddish spots on bark slowly increasing in size. Leptosphaeria coniothyrium turns brown, increases in size, and may eventually girdle the stem. The tissue within the infection begins to dry out and shrink, presenting a shriveled appearance. If the disease infects only part of the stem, growth above the canker will continue. If it girdles the stem, however, growth will cease and the stem will die.

Nematodes, parasitic

Plant-parasitic nematodes include several genera and can be detrimental to plants in different ways - from attacking plants, acting as vectors spreading plant viruses to endoparasites.

Phytoplasma, Virus and viruslike diseases

(And graft-transmissible pathogens [GTP])

• Rose mosaic â€" This disease is caused by a complex or viruses and is characterized by yellow patterns on the leaves. The patterns vary considerably, ranging between all-over fine blotches to patterns of lines in waves. The patterns may appear on a few or many leaves. Plants are infected by this virus at propagation using infected plant material.
• Rose wilt â€" Rose wilt is a complex of viruses and is referred to as dieback in some areas. The disease can be spread by vectors such as aphids. Symptoms are variable and range from stunted growth to curled young leaves. The soft tissue symptoms are more evident in spring and new leaves will reflex towards their own petioles. The affected leaves are brittle and easily fall from the plant. Fully formed leaves will 'wilt' as if the plant were water stressed.
• Rose rosette disease - This disease is caused by a new virus, rose rosette virus, that is transmitted by an eriophyid, rose leaf curl mite (Phyllocoptes fructiplilus), which inhabits the shoot tips and leaf petal bases of roses, as well as by grafting but not by seed or many other common vectors. Rose rosette was initially mistaken for a phytoplasma disease; however, heat and tetracycline treatments did not cure the disease showing that a phytoplasma is not the causal agent. Also called witches’ broom of roses, it is fatal (average lifespan after infection 22 months) in the shrub Rosa multiflora, commonly found wild or as hedges (and considered a noxious weed in some places). It can also infect other rose species, such as garden rose climbers, miniatures, hybrid teas, floribundas, and antique varieties and is capable of killing these as well. Roses are the only plants known to be susceptible. Symptoms include mosaic pattern on the leaves, malformed l eaves and flowers, elongated shoots that are often red, and sometimes thorn proliferation. The distorted growth may be mistaken for herbicide damage. There is no treatment for the disease, and control is limited to controlling the vector and destroying infected plants. It is reported that the causal agent does not survive in the soil, but can survive in root fragments. See also Phyllody.

Environmental disorders

• Frost will destroy fresh growth causing stems and leaves to wilt, turn black and fall away from the plant. Timing pruning to promote growth after the threat of frost is a means to avoid frost damage.
• Salinity will present in roses as limp and light brown leaves with dry leaf margins. Soil may require testing to determine salinity levels. Symptoms will present if salinity is greater than 1200 parts per million.
• Herbicide Damage â€" Overspray or soil leaching of herbicidal sprays can present with several symptoms: :Prolonged exposure to overspray of glyphosate will cause yellow leaves and new leaves will be small and elongated. Hormone weed sprays (e.g. 24-D & 245-T) may cause grotesque new growth with thin twisted leaves and distorted buds. Plants may die in severe cases. Pre-emergent herbicides contacting the plants' root system via the soil will cause yellowing foliage. Effects of soil borne herbicide may take several years to clear.

Miscellaneous diseases and disorders

References

• Common Names of Diseases, The American Phytopathological Society

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Hand, foot and mouth disease (HFMD) is a common infection caused by a group of viruses. It typically begins with a fever and feeling generally unwell. This is followed a day or two later by flat discolored spots or bumps that may blister, on the hands, feet, and mouth, and occasionally buttocks and groin. Signs and symptoms normally appear 3â€"6 days after exposure to the virus. The rash generally goes away on its own in about a week. Fingernail and toenail loss may occur a few weeks later and these then regrow.

The viruses that cause HFMD are spread through close personal contact, through the air from coughing, and the feces of an infected person. Contaminated objects can also spread the disease. Coxsackievirus A16 is the most common cause and Enterovirus 71 is the second-most common cause. Other strains of coxsackievirus and enterovirus can also be responsible. Some people may carry and pass on the virus despite having no symptoms of disease. Other animals are not involved. Diagnosis can often be made based on symptoms. Occasionally throat or stool sample may be tested for the virus.

Handwashing may prevent spread and those infected should not go to work, daycare, or school. No antiviral medication or vaccine is available, but development efforts are underway. Most cases require no specific treatment. Simple pain medication such as ibuprofen or numbing mouth gel may be used. Occasionally intravenous fluids are given to children who are unable to drink enough. Rarely viral meningitis or encephalitis may complicate the disease.

HFMD occurs in all areas of the world. It often occurs in small outbreaks in nursery schools or kindergartens. Large outbreaks have been occurring in Asia since 1997. It usually occurs during the spring, summer, and fall months. Typically it occurs in children less than five years old, but can occasionally occur in adults. HFMD should not be confused with foot-and-mouth disease (also known as hoof-and-mouth disease) which mostly affects livestock.

Signs and symptoms

Common constitutional signs and symptoms of the HFMD include fever, nausea, vomiting, feeling tired, generalized discomfort, loss of appetite, and irritability in infants and toddlers. Skin lesions frequently develop in the form of a rash of flat discolored spots and bumps which may be followed by vesicular sores with blisters on palms of the hands, soles of the feet, buttocks, and sometimes on the lips. The rash is rarely itchy for children, but can be extremely itchy for adults. Painful facial ulcers, blisters, or lesions may also develop in or around the nose or mouth. HFMD usually resolves on its own after 7â€"10 days.

Cause

The viruses that cause the disease are of the Picornaviridae family. Coxsackievirus A16 is the most common cause of HFMD. Enterovirus 71 (EV-71) is the second-most common cause. Many other strains of coxsackievirus and enterovirus can also be responsible.

Transmission

HFMD is highly contagious and is transmitted by nasopharyngeal secretions such as saliva or nasal mucus, by direct contact, or by fecal-oral transmission.

Diagnosis

A diagnosis usually can be made by the presenting signs and symptoms alone. If the diagnosis is unclear, a throat swab or stool specimen may be taken to identify the virus by culture. The common incubation period (the time between infection and onset of symptoms) ranges from three to six days.

Prevention

Preventive measures include avoiding direct contact with infected individuals (including keeping infected children home from school), proper cleaning of shared utensils, disinfecting contaminated surfaces, and proper hand hygiene. These measures have been shown to be effective in decreasing the transmission of the viruses responsible for HFMD.

Vaccine

A vaccine known as the EV71 vaccine is available to prevent HFMD in China as of December 2015. No vaccine is currently available in the United States.

Treatment

Medications are usually not needed as hand, foot and mouth disease is a viral disease that typically gets better on its own. Currently, there is no specific curative treatment for hand, foot and mouth disease. Disease management typically focuses on achieving symptomatic relief. Pain from the sores may be eased with the use of analgesic medications. Infection in older children, adolescents, and adults is typically mild and lasts approximately 1 week, but may occasionally run a longer course. Fever reducers and lukewarm baths can help decrease body temperature.

A minority of individuals with hand, foot and mouth disease may require hospital admission due to complications such as inflammation of the brain, inflammation of the meninges, or acute flaccid paralysis. Non-neurologic complications such as inflammation of the heart, fluid in the lungs, or bleeding into the lungs may also occur.

Complications

Complications from the viral infections that cause HFMD are rare, but require immediate medical treatment if present. HFMD infections caused by Enterovirus 71 tend to be more severe and are more likely to have neurologic or cardiac complications including death than infections caused by Coxsackievirus A16. Viral or aseptic meningitis can occur with HFMD in rare cases and is characterized by fever, headache, stiff neck, or back pain. The condition is usually mild and clears without treatment; however, hospitalization for a short time may be needed. Other serious complications of HFMD include encephalitis (swelling of the brain), or flaccid paralysis in rare circumstances.

Fingernail and toenail loss have been reported in children 4â€"8 weeks after having HFMD. The relationship between HFMD and the reported nail loss is unclear; however, it is temporary and nail growth resumes without treatment.

Epidemiology

Hand, foot and mouth disease most commonly occurs in children under the age of 10 and tends to occur in outbreaks during the spring, summer, and fall seasons. HFMD is most commonly caused by infection with Coxsackievirus A16.

Major outbreaks

• In 1998, there was an outbreak in Taiwan, affecting mainly children. There were 405 severe complications, and 78 children died. The total number of cases in that epidemic is estimated to have been 1.5 million.
• In 2008 an outbreak in China, beginning in March in Fuyang, Anhui, led to 25,000 infections, and 42 deaths, by May 13. Similar outbreaks were reported in Singapore (more than 2,600 cases as of April 20, 2008), Vietnam (2,300 cases, 11 deaths), Mongolia (1,600 cases), and Brunei (1053 cases from Juneâ€"August 2008)
• In 2009 17 children died in an outbreak during March and April 2009 in China's eastern Shandong Province, and 18 children died in the neighboring Henan Province. Out of 115,000 reported cases in China from January to April, 773 were severe and 50 were fatal.
• In 2010 in China, an outbreak occurred in southern China's Guangxi Autonomous Region as well as Guangdong, Henan, Hebei and Shandong provinces. Until March 70,756 children were infected and 40 died from the disease. By June, the peak season for the disease, 537 had died.
• The World Health Organization reporting between January to October 2011 (1,340,259) states the number of cases in China had dropped by approx 300,000 from 2010 (1,654,866) cases, with new cases peaking in June. There were 437 deaths, down from 2010 (537 deaths).
• In December 2011, the California Department of Public Health identified a strong form of the virus, coxsackievirus A6 (CVA6), where nail loss in children is common.
• In 2012 in Alabama, United States there was an outbreak of an unusual type of the disease. It occurred in a season when it is not usually seen and affected teenagers and older adults. There were some hospitalizations due to the disease but no reported deaths.
• In 2012 in Cambodia, 52 of 59 reviewed cases of children reportedly dead (as of July 9, 2012) due to a mysterious disease were diagnosed to be caused by a virulent form of HFMD. Although a significant degree of uncertainty exists with reference to the diagnosis, the WHO report states, "Based on the latest laboratory results, a significant proportion of the samples tested positive for enterovirus 71 (EV-71), which causes hand foot and mouth disease (HFMD). The EV-71 virus has been known to generally cause severe complications amongst some patients."
• HFMD infected 1,520,274 people with up to 431 deaths reported at the end of July in 2012 in China.
• The governorate of Daraa in Syria reported over 200 cases of HFMD there in early 2015. These were due to the central Syrian government denying the region water chlorination.

History

HFMD cases were first described in New Zealand in 1957.

Research

Novel antiviral agents to prevent and treat infection with the viruses responsible for HFMD are currently under development. Preliminary studies have shown inhibitors of the EV-71 viral capsid to have potent antiviral activity.

References

External links

Media related to Hand, foot and mouth disease at Wikimedia Commons News related to Highly contagious Hand, foot and mouth disease killing China's children at Wikinews

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The Centers for Disease Control and Prevention (CDC) is the leading national public health institute of the United States. The CDC is a United States federal agency under the Department of Health and Human Services, headquartered near Atlanta, Georgia.

Its main goal is to protect public health and safety through the control and prevention of disease, injury, and disability in the US and internationally. The CDC focuses national attention on developing and applying disease control and prevention. It especially focuses its attention on infectious disease, food borne pathogens, environmental health, occupational safety and health, health promotion, injury prevention and educational activities designed to improve the health of United States citizens. In addition, the CDC researches and provides information on non-infectious diseases such as obesity and diabetes and is a founding member of the International Association of National Public Health Institutes.

History

The Communicable Disease Center was founded July 1, 1946, as the successor to the World War II Malaria Control in War Areas program of the Office of National Defense Malaria Control Activities.

Preceding its founding, organizations with global influence in malaria control were the Malaria Commission of the League of Nations and the Rockefeller Foundation. The Rockefeller Foundation greatly supported malaria control, sought to have the governments take over some of its efforts, and collaborated with the agency.

The new agency was a branch of the U.S. Public Health Service and Atlanta was chosen as the location because malaria was endemic in the Southern United States. The agency changed names (see infobox on top) before adopting the name Communicable Disease Center in 1946. Offices were located on the sixth floor of the Volunteer Building on Peachtree Street.

With a budget at the time of about $1 million, 59 percent of its personnel were engaged in mosquito abatement and habitat control with the objective of control and eradication of malaria in the United States (see National Malaria Eradication Program).

Among its 369 employees, the main jobs at CDC were originally entomology and engineering. In CDC's initial years, more than six and a half million homes were sprayed, mostly with DDT. In 1946, there were only seven medical officers on duty and an early organization chart was drawn, somewhat fancifully, in the shape of a mosquito. Under Joseph Walter Mountin, the CDC continued to advocate for public health issues and pushed to extend its responsibilities to many other communicable diseases.

In 1947, the CDC made a token payment of $10 to Emory University for 15 acres (61,000 m²) of land on Clifton Road in DeKalb County, still the home of CDC headquarters today. CDC employees collected the money to make the purchase. The benefactor behind the “gift” was Robert W. Woodruff, chairman of the board of The Coca-Cola Company. Woodruff had a long-time interest in malaria control, which had been a problem in areas where he went hunting. The same year, the PHS transferred its San Francisco based plague laboratory into the CDC as the Epidemiology Division, and a new Veterinary Diseases Division was established. An Epidemic Intelligence Service (EIS) was established in 1951, originally due to biological warfare concerns arising from the Korean War; it evolved into two-year postgraduate training program in epidemiology, and a prototype for Field Epidemiology Training Programs (FETP), now found in numerous countries, reflecting CDC's influence in promoting this mod el internationally.

The mission of CDC expanded beyond its original focus on malaria to include sexually transmitted diseases when the Venereal Disease Division of the U.S. Public Health Service (PHS) was transferred to the CDC in 1957. Shortly thereafter, Tuberculosis Control was transferred (in 1960) to the CDC from PHS, and then in 1963 the Immunization program was established.

It became the National Communicable Disease Center (NCDC) effective July 1, 1967. The organization was renamed the Center for Disease Control (CDC) on June 24, 1970, and Centers for Disease Control effective October 14, 1980. An act of the United States Congress appended the words "and Prevention" to the name effective October 27, 1992. However, Congress directed that the initialism CDC be retained because of its name recognition.

Currently the CDC focus has broadened to include chronic diseases, disabilities, injury control, workplace hazards, environmental health threats, and terrorism preparedness. CDC combats emerging diseases and other health risks, including birth defects, West Nile virus, obesity, avian, swine, and pandemic flu, E. coli, and bioterrorism, to name a few. The organization would also prove to be an important factor in preventing the abuse of penicillin. In May 1994 the CDC admitted having sent several biological warfare agents to the Iraqi government from 1984 through 1989, including Botulinum toxin, West Nile virus, Yersinia pestis and Dengue fever virus.

On April 21, 2005, then-CDC Director Julie Gerberding, formally announced the reorganization of CDC to "confront the challenges of 21st-century health threats". The four Coordinating Centers â€" established under the G. W. Bush Administration and Gerberding â€" "diminished the influence of national centers under [their] umbrella", and were ordered cut under the Obama Administration in 2009.

The CDC's Biosafety Level 4 laboratories are among the few that exist in the world, as well as one of only two official repositories of smallpox in the world. The second smallpox store resides at the State Research Center of Virology and Biotechnology VECTOR in the Russian Federation.

The CDC revealed in 2014 that it had discovered several misplaced smallpox samples and also that lab workers had potentially been infected with anthrax.

Organization

The CDC is organized into "Centers, Institutes, and Offices" (CIOs) which allow it to be responsive and effective in its interface with public health concerns. Each organizational unit implements the agency's response in a particular area of expertise. Within "Offices" are Centers, Divisions, and Branches.

CIOs are

• CDC Washington Office
• Center for Global Health
• National Institute for Occupational Safety and Health
• Office for State, Tribal, Local and Territorial Support
• Office of Equal Employment Opportunity
• Office of Infectious Diseases
  • National Center for Emerging and Zoonotic Infectious Diseases
    • Division of High-Consequence Pathogens and Pathology (DHCPP)
      • Viral Special Pathogens Branch (VSPB)
  • National Center for HIV/AIDS, Viral Hepatitis, STD, and TB Prevention
  • National Center for Immunization and Respiratory Diseases
• Office of Minority Health and Health Equity
• Office of Noncommunicable Diseases, Injury and Environmental Health
  • National Center for Chronic Disease Prevention and Health Promotion
  • National Center for Environmental Health/Agency for Toxic Substances and Disease Registry
  • National Center for Injury Prevention and Control
  • National Center on Birth Defects and Developmental Disabilities
• Office of Public Health Preparedness and Response
  • Division of Emergency Operations
    • Emergency Operations Center (EOC)
• Office of Public Health Science Services
  • Center for Surveillance, Epidemiology and Laboratory Services
  • National Center for Health Statistics
• Office of the Associate Director for Communication
• Office of the Associate Director for Policy
• Office of the Associate Director for Science
• Office of the Chief of Staff
• Office of the Chief Operating Officer

Global Health

The CDC partners with many international organizations such as the World Health Organization (WHO) and global divisions include: Division of Global HIV & TB (DGHT), Division of Parasitic Diseases and Malaria (DPDM), Division of Global Health Protection (DGHP), and Global Immunization Division (GID).

The CDC is integral in working with WHO in establishing the International Health Regulations (IHR), that is binding on 194 member countries, through the Global Disease Detection Program (GDD) and the WHO and CDC Global Surveillance Systems

Budget and workforce

CDC’s Fiscal Year 2014 budget was $6.9 billion.

As of 2008, staff numbered approximately 15,000 (including 6,000 contractors and 840 Commissioned Corps officers) in 170 occupations. Eighty percent have earned bachelor's degrees or higher; almost half have advanced degrees (a master's degree or a doctorate such as a PhD, D.O., or M.D.). CDC job titles include engineer, entomologist, epidemiologist, biologist, physician, veterinarian, behaviorial scientist, nurse, medical technologist, economist, public health advisor, health communicator, toxicologist, chemist, computer scientist, and statistician.

In addition to its Atlanta headquarters, the CDC has other locations in the United States and Puerto Rico. Those locations include Anchorage; Cleveland; Cincinnati; Fort Collins; Hyattsville; Morgantown; Pittsburgh; Research Triangle Park; San Juan, Puerto Rico; Spokane, Washington; Detroit; and Washington, D.C. The CDC also conducts the Behavioral Risk Factor Surveillance System, the world’s largest, on-going telephone health survey system.

The CDC offers grants that help many organizations each year bring health, safety and awareness to surrounding communities throughout the entire United States. As a government-run department, the Centers for Disease Control and Prevention awards over 85 percent of its annual budget through these grants to accomplish its ultimate goal of disease control and quality health for all.

The CDC operates the Public Health Associate Program (PHAP), a two-year paid fellowship for recent college graduates to work in public health agencies all over the United States. PHAP was founded in 2007 and currently has 159 associates in 34 states.

Directors

The President of the United States appoints the director of the CDC and the appointment does not require Senate confirmation. The director serves at the pleasure of the President and may be fired at any time.

Sixteen directors have served the CDC or its predecessor agencies.

• Louis L. Williams Jr., MD (1942â€"1943)
• Mark D. Hollis, ScD (1944â€"1946)
• Raymond A. Vonderlehr, MD (1947â€"1951)
• Justin M. Andrews, ScD (1952â€"1953)
• Theodore J. Bauer, MD (1953â€"1956)
• Robert J. Anderson, MD, MPH (1956â€"1960)
• Clarence A. Smith, MD, MPH (1960â€"1962)
• James L. Goddard, MD, MPH (1962â€"1966)
• David J. Sencer, MD, MPH (1966â€"1977)
• William H. Foege, MD, MPH (1977â€"1983)
• James O. Mason, MD, MPH (1983â€"1989)
• William L. Roper, MD, MPH (1990â€"1993)
• David Satcher, MD, PhD (1993â€"1998)
• Jeffrey P. Koplan, MD, MPH (1998â€"2002)
• Julie Gerberding, MD, MPH (2002â€"2008)
• Thomas R. Frieden, MD, MPH (2009â€"Jan 2017)
• Anne Schuchat, MD (RADM, USPHS)

Data and survey systems

• CDC Scientific Data, Surveillance, Health Statistics, and Laboratory Information.
• Behavioral Risk Factor Surveillance System.
• Mortality Medical Data System.
• Abortion statistics in the United States

Diseases

Influenza

The CDC has launched campaigns targeting the transmission of influenza, including the H1N1 swine flu. The CDC has launched websites including [flu.gov] to educate people in proper hygiene.

Other infectious diseases

The CDC's website (see below) has information on other infectious diseases, including smallpox, measles, and others. The CDC runs a program that protects the public from rare and dangerous substances such as anthrax and the Ebola virus. The program, called the Select Agents Program, calls for inspections of labs in the U.S. that work with dangerous pathogens.

During the 2014 Ebola outbreak in West Africa, the CDC helped coordinate the return of two infected American aid workers for treatment at Emory University Hospital, the home of a special unit to handle highly infectious diseases.

As a response to the 2014 Ebola outbreak, the U.S. House of Representatives proposed and passed a Continuing Appropriations Resolution to allocate up to $30,000,000 towards CDCP's efforts to fight the virus.

Non-infectious diseases

The CDC also works on non-infectious diseases, including chronic diseases caused by obesity, physical inactivity and tobacco-use.

Antibiotic resistance

The CDC implemented their National Action Plan for Combating Antibiotic Resistant Bacteria as a measure against the spread of antibiotic resistance in the United States. This initiative has a budget of $161 million and includes the development of the Antibiotic Resistance Lab Network.

Epidemic Intelligence Service

The Epidemic Intelligence Service (EIS) provides "Boots-on-the-ground disease detectives," which investigate public health problems.

Epidemiologic Assistance

Within the EIS, the Epidemiologic Assistance (Epi-Aids) provides short-term epidemiologic assistance when asked by a governmental body.

Foundation

The CDC Foundation operates independently from CDC as a private, nonprofit 501(c)(3) organization incorporated in the State of Georgia. The creation of the Foundation was authorized by section 399F of the Public Health Service Act to support the mission of CDC in partnership with the private sector, including organizations, foundations, businesses, educational groups, and individuals.

Popular culture and controversies

Historically, the CDC has been relatively free of political manipulation.

Tuskegee Study of Untreated Syphilis in the Negro Male

For 15 years, the CDC had direct oversight over the Tuskegee syphilis experiment. In the study, which lasted from 1932 to 1972, a group of African American men (nearly 400 of whom had syphilis) were studied to learn more about the disease. Notably, the disease was left untreated in the research subjects and they never gave their informed consent to serve as research subjects. The Tuskegee Study was initiated in 1932 by the Public Health Service. The CDC took over the study in 1957.

The CDC's response to the AIDS crisis in the 1980s has been criticized for promoting some public health policies that harmed HIV+ people and for providing ineffective public education. The agency's response to the 2001 anthrax attacks was also criticized for ineffective communication with other public health agencies and with the public.

CDC zombie apocalypse outreach campaign

On May 16, 2011, the Centers for Disease Control and Prevention's blog published an article instructing the public on what to do to prepare for a zombie invasion. While the article did not claim that such a scenario was possible, it did use the popular culture appeal as a means of urging citizens to prepare for all potential hazards, such as earthquakes, tornadoes, and floods.

According to David Daigle, the Associate Director for Communications, Public Health Preparedness and Response, the idea arose when his team was discussing their upcoming hurricane information campaign and Daigle mused that "we say pretty much the same things every year, in the same way, and I just wonder how many people are paying attention." A social media employee mentioned that the subject of zombies had come up a lot on Twitter when she had been tweeting about the Fukushima Daiichi nuclear disaster and radiation. The team realized that a campaign like this would most likely reach a different audience from the one that normally pays attention to hurricane preparedness warnings and went to work on the zombie campaign, launching it right before hurricane season began. "The whole idea was, if you're prepared for a zombie apocalypse, you're prepared for pretty much anything," said Daigle.

Once the blog article became popular, the CDC announced an open contest for YouTube submissions of the most creative and effective videos covering preparedness for a zombie apocalypse (or apocalypse of any kind), to be judged by the "CDC Zombie Task Force". Submissions were open until October 11, 2011. They also released a zombie themed graphic novella available on their website. Zombie-themed educational materials for teachers are available on the site.

Gun violence

One area of current partisan dispute related to CDC funding is studying gun violence. The 1996 Dickey Amendment states "none of the funds made available for injury prevention and control at the Centers for Disease Control and Prevention may be used to advocate or promote gun control". Advocates for gun control oppose the amendment and have tried to overturn it.

The American Medical Association, the American Psychological Association and the American Academy of Pediatrics sent a letter to the leaders of the Senate Appropriations Committee in 2013 asking them "to support at least $10 million within the Centers for Disease Control and Prevention (CDC) in FY 2014 along with sufficient new funding at the National Institutes of Health to support research into the causes and prevention of gun violence. Furthermore, we urge Members to oppose any efforts to reduce, eliminate, or condition CDC funding related to gun violence prevention research." Congress maintained the ban in subsequent budgets.

Publications

• CDC publications
• State of CDC report
• CDC Programs in Brief
• Morbidity and Mortality Weekly Report
• Emerging Infectious Diseases (monthly journal)
• Preventing Chronic Disease
• Vital statistics

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Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy (TSE) of mule deer, white-tailed deer, elk (or "wapiti"), and moose ("elk" in Europe). As of 2016, CWD had only been found in members of the deer family. First recognized as a clinical "wasting" syndrome in 1967 in mule deer in a wildlife research facility in northern Colorado, USA, it was identified as a TSE in 1978 and has spread to free-ranging and captive populations in 23 US states and two Canadian provinces. CWD is typified by chronic weight loss leading to death. No relationship is known between CWD and any other TSE of animals or people.

Although reports in the popular press have been made of humans being affected by CWD, a study by the Centers for Disease Control and Prevention suggests, "[m]ore epidemiologic and laboratory studies are needed to monitor the possibility of such transmissions." The epidemiological study further concluded, "[a]s a precaution, hunters should avoid eating deer and elk tissues known to harbor the CWD agent (e.g., brain, spinal cord, eyes, spleen, tonsils, lymph nodes) from areas where CWD has been identified."

Clinical signs

Most cases of CWD occur in adult animals; the youngest animal diagnosed with natural CWD was 17 months. The disease is progressive and always fatal. The first signs are difficulties in movement. The most obvious and consistent clinical sign of CWD is weight loss over time. Behavioral changes also occur in the majority of cases, including decreased interactions with other animals, listlessness, lowering of the head, tremors, repetitive walking in set patterns, and nervousness. Excessive salivation and grinding of the teeth also are observed. Most deer show increased drinking and urination; the increased drinking and salivation may contribute to the spread of the disease.

Causative agent

The agent responsible for CWD (and other TSEs, such as scrapie and bovine spongiform encephalopathy) is PRNP which is highly conserved among mammals and has been found and sequenced in deer. It is a prion, an abnormal form of a normal protein, known as prion protein (PrP), most commonly found in the central nervous system (CNS), and is capable of spreading to the peripheral nervous system (PNS), thus infecting meat, or muscle, of deer and elk. The abnormal PrP infects the host animal by promoting conversion of normal cellular prion protein (PrP^C) to the abnormal prion form (PrP^res or PrP^d). The build-up of PrP^d in the brain is associated with widespread neurodegeneration.

Diagnosis

Diagnosis is based on post mortem examination (necropsy) and testing; examination of the dead body is not definitive as many animals die early in the course of the disease and conditions found are non-specific; general signs of poor health and Aspiration pneumonia, which may be the actual cause of death, are common. On microscopic examination, lesions of CWD in the central nervous system resemble those of other TSEs. In addition, scientists use immunohistochemistry to test brain, lymph, and neuroendocrine tissues for the presence of the abnormal prion protein to diagnose CWD; positive IHC findings in the obex is considered the gold standard.

As of 2015 there were no commercially feasible diagnostic tests that could be used on live animals. It is possible to run a bioassay, taking fluids from cervids suspected of infection and incubating them in transgenic mice that express the cervid prion protein, to determine if the cervid is infected, but there are ethical issues with this and it is not scalable.

Epidemiology

The origin and mode of transmission of the prions causing CWD is unknown, but recent research indicates that prions can be excreted by deer and elk, and are transmitted by eating grass growing in contaminated soil. Animals born in captivity and those born in the wild have been affected with the disease. Based on epidemiology, transmission of CWD is thought to be lateral (from animal to animal). Maternal transmission may occur, although it appears to be relatively unimportant in maintaining epidemics. An infected deer's saliva is able to spread the CWD prions. Exposure between animals is associated with sharing food and water sources contaminated with CWD prions shed by diseased deer.

The disease was first identified in 1967 in a closed herd of captive mule deer in contiguous portions of northeastern Colorado. In 1980, the disease was determined to be a TSE. It was first identified in wild elk and mules in 1981 in Colorado and Wyoming, and in farmed elk in 1997.

In May 2001, CWD was also found in free-ranging deer in the southwestern corner of Nebraska (adjacent to Colorado and Wyoming) and later in additional areas in western Nebraska. The limited area of northern Colorado, southern Wyoming, and western Nebraska in which free-ranging deer, moose, and/or elk positive for CWD have been found is referred to as the endemic area. The area in 2006 has expanded to six states, including parts of eastern Utah, southwestern South Dakota, and northwestern Kansas. Also, areas not contiguous (to the endemic area) areas in central Utah and central Nebraska have been found. The limits of the affected areas are not well defined, since the disease is at a low incidence and the amount of sampling may not be adequate to detect it. In 2002, CWD was detected in wild deer in south-central Wisconsin and northern Illinois and in an isolated area of southern New Mexico. In 2005, it was found in wild white-tailed deer in New York and in Hampshire County, West Vir ginia. In 2008, the first confirmed case of CWD in Michigan was discovered in an infected deer on an enclosed deer-breeding facility. It is also found in the Canadian provinces of Alberta and Saskatchewan.

In February 2011, the Maryland Department of Natural Resources reported the first confirmed case of the disease in that state. The affected animal was a white-tailed deer killed by a hunter.

CWD has also been diagnosed in farmed elk and deer herds in a number of states and in two Canadian provinces. The first positive farmed elk herd in the United States was detected in 1997 in South Dakota. Since then, additional positive elk herds and farmed white-tailed deer herds have been found in South Dakota (7), Nebraska (4), Colorado (10), Oklahoma (1), Kansas (1), Minnesota (3), Montana (1), Wisconsin (6) and New York (2). As of fall of 2006, four positive elk herds in Colorado and a positive white-tailed deer herd in Wisconsin remain under state quarantine. All of the other herds have been depopulated or have been slaughtered and tested, and the quarantine has been lifted from one herd that underwent rigorous surveillance with no further evidence of disease. CWD also has been found in farmed elk in the Canadian provinces of Saskatchewan and Alberta. A retrospective study also showed mule deer exported from Denver to the Toronto Zoo in the 1980s were affected. In June 2015, the disease was detected in a male white-tailed deer on a breeding ranch in Medina County, Texas. State officials euthanized 34 deer in an effort to contain a possible outbreak.

Species that have been affected with CWD include elk, mule deer, white-tailed deer, black-tailed deer, and moose. Other ruminant species, including wild ruminants and domestic cattle, sheep, and goats, have been housed in wildlife facilities in direct or indirect contact with CWD-affected deer and elk, with no evidence of disease transmission. However, experimental transmission of CWD into other ruminants by intracranial inoculation does result in disease, suggesting only a weak molecular species barrier exists. Research is ongoing to further explore the possibility of transmission of CWD to other species.

By April 2016 CWD had been found in captive animals in South Korea; the disease arrived there with live elk that were imported for farming in the late 1990s.

Europe

In 2016, the first case of CWD in Europe was from the Nordfjella free ranging reindeer in Southern Norway. Scientists surveyed the diseased female reindeer until the reindeer died and used the carcass to isolate the prions. The main origin of CWD to Norway is still unknown, whereas importation of infected deer was the contamination source in South Korea. Norway has strict legislation and rules not allowing importation of live animals and cervids into the country. Norway has had a scrapie surveillance program since 1997; while no reports of scrapie within the range of Nordfjella reindeer sup population have been identified, sheep are herded through that region and are a potential source of infection.

In each of May and June, infected wild moose were found around 300 km north from the first case, in Selbu. By the end of August, a fourth case had been confirmed in a wild reindeer shot in the same area as the first case in March.

Transmission pathways

Direct transmission

CWD may be directly transmitted via contact with infected animals, their bodily tissues, and their bodily fluids. Transmission may result from contact with both clinically affected and infected, but asymptomatic, cervids.

Recent research on Rocky Mountain elk found that with CWD-infected dams, many sub-clinical, there was a high rate (80%) of maternal-to-offspring transmission of CWD prions, regardless of gestational period. While not dispositive relative to disease development in the fetus, this does suggest that maternal transmission may be yet another important route of direct CWD transmission.

Experimental transmission

In addition to the cervid species in which CWD is known to naturally occur, Black-tailed deer and European red deer have been clinically demonstrated to be naturally susceptible to CWD. Other cervid species, including reindeer and caribou, are also suspected to be naturally vulnerable to this disease. Many other non-cervid mammalian species have been experimentally infected with CWD, either orally or via intracerebral inoculation. These species include monkeys, sheep, cattle, prairie voles, mice, and ferrets.

An experimental case study of oral transmission of CWD to reindeer shows certain reindeer breeds may be susceptible to CWD while other sub-populations may be protective against CWD in free ranging populations. None of the reindeer in the study showed symptoms of CWD potentially signifying resistance to different CWD strains.

Indirect/environmental transmission

Environmental transmission has been linked to contact with infected bodily fluids and tissues, as well as contact with contaminated environments. Once in the environment, CWD prions may remain infectious for many years. Thus, decomposition of diseased carcasses, infected "gut piles" from hunters who field dress their cervid harvests, as well as the urine, saliva, feces, and antler velvet of infected individuals that are deposited in the environment, all have the potential to create infectious environmental reservoirs of CWD.

One avian scavenger, the American crow, was recently evaluated as a potential vector for CWD. As CWD prions remain viable after passing through the bird's digestive tract, crows represent a possible mechanism for the creation of environmental reservoirs of CWD. Additionally, the crows' extensive geographic range presents ample opportunities for them to come in contact with CWD. This coupled with the population density and longevity of communal roosting sites in both urban and rural locations suggests that the fecal deposits at roosting sites may represent a CWD environmental reservoir. Conservative estimates for crows' fecal deposits at one winter roosting site for one winter season ranged from 391,552 - 599,032 kg.

CWD prions adhere to tightly to soil surface particles and the ground itself becomes a source of infection and may be a major route of transmission due to frequent ground contact when cervids graze.

The potential for human exposure to CWD

As of 2013 there was no evidence of transmission to humans from cervids, nor by eating cervids, but both channels remain a subject of public health surveillance and research.

Research

Research is focused on better ways to monitor disease in the wild, live animal diagnostic tests, developing vaccines, better ways to dispose of animals who died from the disease and to decontaminate the environment, where prions can persist in soils, and better ways to monitor the food supply.

References

External links

• This entry incorporates public domain text originally from the Animal and Plant Health Inspection Service, APHIS.
• Chronic Wasting Disease Alliance
• "Chronic Wasting Disease (CWD) of Deer and Elk". Canadian Food Inspection Agency. 2006-10-03. Archived from the original on September 25, 2006. Retrieved October 23, 2006. 
• Elk Research Institute
• United States Geological Survey
• United States Department of Agriculture
• Colorado Division of Wildlife
• Illinois Department of Natural Resources
• Minnesota Department of Natural Resources
• Nebraska Game and Parks Commission
• New York State Department of Environmental Conservation
• Wisconsin Department of Natural Resources
• Wyoming Game and Fish
• Wildlife Disease Information Node Chronic Wasting Disease Factsheet and resources
• A case of chronic wasting disease in a captive red deer (Cervus elaphus)

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Osgoodâ€"Schlatter disease (OSD), also known as apophysitis of the tibial tubercle, is an inflammation of the patellar ligament at the tibial tuberosity. It is characterized by a painful bump just below the knee and is most often seen in young adolescents. Risk factors include overuse (especially in sports involving running, jumping and quick changes of direction) and adolescent growth spurts.

The condition is named after Robert Bayley Osgood (1873â€"1956), an American orthopedic surgeon and Carl B. Schlatter, (1864â€"1934), a Swiss surgeon who described the condition independently in 1903.

Signs and symptoms

Osgoodâ€"Schlatter disease causes pain in the front lower part of the knee. This is usually at the ligament-bone junction of the patellar ligament and the tibial tuberosity. The tibial tuberosity is a slight elevation of bone on the anterior and proximal portion of the tibia. The patellar tendon attaches the anterior quadriceps muscles to the tibia via the knee cap.

Intense knee pain is usually the presenting symptom that occurs during activities such as running, jumping, squatting, and especially ascending or descending stairs and during kneeling. The pain is worse with acute knee impact. The pain can be reproduced by extending the knee against resistance, stressing the quadriceps, or striking the knee. Pain is initially mild and intermittent. In the acute phase, the pain is severe and continuous in nature. Impact of the affected area can be very painful. Bilateral symptoms are observed in 20â€"30% of patients.

Diagnosis

Diagnosis is made based on signs and symptoms.

Ultrasonography

This test can see various warning signs that predict if OSD might occur. Ultrasonography can detect if there is any swelling within the tissue as well as cartilage swelling. Ultrasonography's main goal is to identify OSD in the early stage rather than later on. It has unique features such as detection of an increase of swelling within the tibia or the cartilage surrounding the area and can also see if there is any new bone starting to build up around the tibial tuberosity.

Types

OSD may result in an avulsion fracture, with the tibial tuberosity separating from the tibia (usually remaining connected to a tendon or ligament). This injury is uncommon because there are mechanisms that prevent strong muscles from doing damage. The fracture on the tibial tuberosity can be a complete or incomplete break.

Type I: A small fragment is displaced proximally and does not require surgery.

Type II: The articular surface of the tibia remains intact and the fracture occurs at the junction where the secondary center of ossification and the proximal tibial epiphysis come together (may or may not require surgery).

Type III: Complete fracture (through articular surface) including high chance of meniscal damage. This type of fracture usually requires surgery.

Differential diagnosis

Sinding-Larsen and Johansson syndrome, is an analogous condition involving the patellar tendon and the lower margin of the patella bone, instead of the upper margin of the tibia. Sever's disease is an analogous condition affecting the achille's tendon attachment to the heel.

Prevention

One of the main ways to prevent OSD is to check the participant's flexibility in their quadriceps and hamstrings. Lack of flexibility in these muscles can be direct risk indicator for OSD. Muscles can shorten, which can cause pain but this is not permanent. Stretches can help reduce shortening of the muscles. The main stretches for prevention of OSD focus on the hamstrings and quadriceps.

Treatment

Treatment is generally conservative with rest, ice, and specific exercises being recommended. Simple pain killers may be used if required such as acetaminophen (paracetamol) or ibuprofen. Typically symptoms resolve as the growth plate closes. Physiotherapy is generally recommended once the initial symptoms have improved to prevent recurrence. Surgery may rarely be used in those who have stopped growing yet still have symptoms.

Physiotherapy

Recommended efforts include exercises to improve the strength of the quadriceps, hamstring and gastrocnemius muscles.

Bracing or use of an orthopedic cast to enforce joint immobilization is rarely required and does not necessarily give quicker resolution. Sometimes, however, bracing may give comfort and help reduce pain as it reduces strain on the tibial tubercle.

Surgery

Surgical excision may rarely be required in skeletally mature patients. In chronic cases that are refractory to conservative treatment, surgical intervention yields good results, particularly for patients with bony or cartilaginous ossicles. Excision of these ossicles produces resolution of symptoms and return to activity in several weeks. After surgery, it is common for lack of blood flow to below the knees and to the feet. This may cause the loss of circulation to the area, but will be back to normal again shortly. A high pain may come and go every once in a while, due to the lack of blood flow. If this happens, sitting down will help the pain decrease. Removal of all loose intratendinous ossicles associated with prominent tibial tubercles is the procedure of choice, both from the functional and the cosmetic point of view.

Rehabilitation

Rehabilitation focuses on muscle strengthening, gait training, and pain control to restore knee function. Nonsurgical treatments for less severe symptoms include: exercises for strength, stretches to increase range of motion, ice packs, knee tape, knee braces, anti-inflammatory agents, and electrical stimulation to control inflammation and pain. Quadriceps and hamstring exercises prescribed by rehabilitation experts restore flexibility and muscle strength.

Education and knowledge on stretches and exercises is important. Exercises should lack pain and increase gradually with intensity. The patient is given strict guidelines on how to perform exercises at home to avoid more injury. Exercises can include leg raises, squats, and wall stretches to increase quadriceps and hamstring strength. This helps to avoid pain, stress, and tight muscles that lead to further injury that oppose healing. Knee orthotics such as patella straps and knee sleeves help decrease force traction and prevent painful tibia contact by restricting unnecessary movement, providing support, and also adding compression to the area of pain.

Prognosis

The condition is usually self-limiting and is caused by stress on the patellar tendon that attaches the quadriceps muscle at the front of the thigh to the tibial tuberosity. Following an adolescent growth spurt, repeated stress from contraction of the quadriceps is transmitted through the patellar tendon to the immature tibial tuberosity. This can cause multiple subacute avulsion fractures along with inflammation of the tendon, leading to excess bone growth in the tuberosity and producing a visible lump which can be very painful, especially when hit. Activities such as kneeling may also irritate the tendon.

The syndrome may develop without trauma or other apparent cause; however, some studies report up to 50% of patients relate a history of precipitating trauma. Several authors have tried to identify the actual underlying etiology and risk factors that predispose Osgoodâ€"Schlatter disease and postulated various theories. However, currently it is widely accepted that Osgoodâ€"Schlatter disease is a traction apophysitis of the proximal tibial tubercle at the insertion of the patellar tendon caused by repetitive micro-trauma. In other words, Osgoodâ€"Schlatter disease is an overuse injury and closely related to the physical activity of the child. It was shown that children who actively participate in sports are affected more frequently as compared with non-participants. In a retrospective study of adolescents, old athletes actively participating in sports showed a frequency of 21% reporting the syndrome compared with only 4.5% of age-matched nonathletic controls.

The symptoms usually resolve with treatment but may recur for 12â€"24 months before complete resolution at skeletal maturity, when the tibial epiphysis fuses. In some cases the symptoms do not resolve until the patient is fully grown. In approximately 10% of patients the symptoms continue unabated into adulthood, despite all conservative measures.

Long-term implications

OSD occurs from the combined effects of tibial tuberosity immaturity and quadriceps tightness. There is a possibility of migration of the ossicle or fragmentation in Osgood-Schlatter patients. The implications of OSD and the ossification of the tubercle can lead to functional limitations and pain for patients into adulthood.

Of people admitted with OSD, about half were children who were between the ages of 1 and 17. In addition, in 2014, a case study of 261 patients was observed over 12 to 24 months. 237 of these patients responded well to sport restriction and non-steroid anti-inflammatory agents, which resulted in recovery to normal athletic activity.

Epidemiology

Osgoodâ€"Schlatter disease generally occurs in boys and girls aged 9â€"16 coinciding with periods of growth spurts. It occurs more frequently in boys than in girls, with reports of a male-to-female ratio ranging from 3:1 to as high as 7:1. It has been suggested that difference is related to a greater participation by boys in sports and risk activities than by girls.

Society and culture

Paul Scholes is a sportsman who has recovered from this condition whilst Mick Bennett took up cycling as a means of treatment. The French tennis player, Gaël Monfils wears patella bands in an attempt to combat the condition. Liverpool F.C. captain Jordan Henderson is also said to require regular treatment for his condition.

References

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The following is a list of aquarium diseases. Aquarium fish are often susceptible to numerous diseases, due to the artificially limited and concentrated environment. New fish can sometimes introduce diseases to aquaria, and these can be difficult to diagnose and treat. Most fish diseases are also aggravated when the fish is stressed.

Common aquarium diseases include the following:

Freshwater

Saltwater

• Cryptocaryon (marine ick)
• Marine Velvet or Coral Reef Fish Disease
• Anemonefish Disease

Both

Uncategorized

• Myxobacteriosis
• Ichthyobodo (costia)

Quarantine

The goal of quarantine is to prevent problems in the main tank due to sickness. A quarantine tank should be used before to introduce any newly acquired animals in the main tank and to treat fish that are already sick. By doing this, the aquarist can avoid the spread of the disease and make it easier to treat the fish.

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