For other uses, see Yellow fever (disambiguation) . "American Plague" redirects here. For the rock band, see The American Plague . Not to be confused with malaria . "Yellow plague" redirects here. For the Yellow Plague of Rhos in medieval Wales, see Maelgwn Gwynedd . Viral disease Yellow fever Other names Yellow jack, yellow plague, [1] bronze john [2] A TEM micrograph of yellow fever virus (234,000× magnification) Specialty Infectious disease Symptoms Fever , chills , muscle pain , headache , yellow skin [3] Complications Liver failure , bleeding [3] Usual onset 3–6 days post exposure [3] Duration 3–4 days [3] Causes Yellow fever virus spread by mosquitoes [3] Diagnostic method Blood test [4] Prevention Yellow fever vaccine [3] Treatment Supportive care [3] Frequency ~127,000 severe cases (2013) [3] Deaths 5,100 (2015) [5] Yellow fever is a viral disease of typically short duration . [3] In most cases, symptoms include fever , chills , loss of appetite , nausea , muscle pains particularly in the back, and headaches . [3] Symptoms typically improve within five days. [3] In about 15% of people, within a day of improving the fever comes back, abdominal pain occurs, and liver damage begins causing yellow skin . [3] [6] If this occurs, the risk of bleeding and kidney problems is increased. [3] The disease is caused by yellow fever virus and is spread by the bite of an infected female mosquito . [3] It infects only humans , other primates , and several types of mosquitoes. [3] In cities, it is spread primarily by Aedes aegypti , a type of mosquito found throughout the tropics and subtropics . [3] The virus is an RNA virus of the genus Flavivirus . [7] The disease may be difficult to tell apart from other illnesses, especially in the early stages. [3] To confirm a suspected case, blood-sample testing with polymerase chain reaction is required. [4] A safe and effective vaccine against yellow fever exists, and some countries require vaccinations for travelers. [3] Other efforts to prevent infection include reducing the population of the transmitting mosquitoes. [3] In areas where yellow fever is common, early diagnosis of cases and immunization of large parts of the population are important to prevent outbreaks . [3] Once a person is infected, management is symptomatic; no specific measures are effective against the virus. [3] Death occurs in up to half of those who get severe disease. [3] [8] In 2013, yellow fever resulted in about 127,000 severe infections and 45,000 deaths worldwide, [3] with nearly 90 percent of these occurring in African nations. [4] Nearly a billion people live in an area of the world where the disease is common. [3] It is common in tropical areas of the continents of South America and Africa , but not in Asia . [3] [9] Since the 1980s, the number of cases of yellow fever has been increasing. [3] [10] This is believed to be due to fewer people being immune, more people living in cities, people moving frequently, and changing climate increasing the habitat for mosquitoes. [3] The disease originated in Africa and spread to South America in the 17th century with the Spanish and Portuguese importation of enslaved Africans from sub-Saharan Africa. [1] Since the 17th century, several major outbreaks of the disease have occurred in the Americas, Africa, and Europe. [1] In the 18th and 19th centuries, yellow fever was considered one of the most dangerous infectious diseases ; numerous epidemics swept through major cities of the US and in other parts of the world. [1] In 1927, yellow fever virus was the first human virus to be isolated. [7] [11] Contents 1 Signs and symptoms 2 Cause 2.1 Transmission 3 Pathogenesis 4 Diagnosis 5 Prevention 5.1 Vaccination 5.1.1 Compulsory vaccination 5.2 Vector control 6 Treatment 7 Epidemiology 7.1 Africa 7.2 South America 7.3 Asia 8 History 8.1 Early history 8.2 Causes and transmission 8.3 Current status 9 Research 10 Notes 11 References 12 Further reading 13 External links Signs and symptoms [ edit ] Yellow fever begins after an incubation period of three to six days. [12] Most cases cause only a mild infection with fever, headache, chills, back pain, fatigue, loss of appetite, muscle pain, nausea, and vomiting. [13] In these cases, the infection lasts only three to four days. But in 15% of cases, people enter a second, toxic phase of the disease characterized by recurring fever, this time accompanied by jaundice due to liver damage , as well as abdominal pain. [14] Bleeding in the mouth, nose, the eyes, and the gastrointestinal tract cause vomit containing blood , hence the Spanish name for yellow fever, vómito negro ("black vomit"). [15] There may also be kidney failure, hiccups, and delirium. [16] [17] Among those who develop jaundice, the fatality rate is 20 to 50%, while the overall fatality rate is about 3 to 7.5%. [18] Severe cases may have a mortality greater than 50%. [19] Surviving the infection provides lifelong immunity , [20] and normally results in no permanent organ damage. [21] Cause [ edit ] Yellow fever virus Flavivirus structure and genome Virus classification (unranked): Virus Realm : Riboviria Kingdom: Orthornavirae Phylum: Kitrinoviricota Class: Flasuviricetes Order: Amarillovirales Family: Flaviviridae Genus: Flavivirus Species: Yellow fever virus Yellow fever is caused by yellow fever virus, an enveloped RNA virus 40–50 nm in width, the type species and namesake of the family Flaviviridae . [7] It was the first illness shown to be transmissible by filtered human serum and transmitted by mosquitoes, by American doctor Walter Reed around 1900. [22] The positive- sense , single-stranded RNA is around 11,000 nucleotides long and has a single open reading frame encoding a polyprotein .

Legg-Calvé-Perthes disease is a bone disorder that affects the hips. Usually, only one hip is involved, but in about 10 percent of cases, both hips are affected. Legg-Calvé-Perthes disease begins in childhood, typically between ages 4 and 8, and affects boys more frequently than girls. In this condition, the upper end of the thigh bone, known as the femoral head, breaks down. As a result, the femoral head is no longer round and does not move easily in the hip socket, which leads to hip pain, limping, and restricted leg movement. The bone eventually begins to heal itself through a normal process called bone remodeling, by which old bone is removed and new bone is created to replace it.

A rare disorder characterized by uni- or bilateral avascular necrosis (AVN) of the femoral head in children. Epidemiology Reported annual incidences vary greatly, from 1/250,000 in Hong Kong and 1/18,000 in the UK, to 1/3,500 in the Faroe Islands. Legg-Calvé-Perthes disease (LCPD) affects children between 2 and 12 years of age, but it is more prevalent among children of 5-6 years, and more common in boys. Clinical description The initial symptoms are usually a limping gait, pain in the hip, thigh or knee, and a reduced range of hip motion. Later in the disease course, leg length discrepancy, as well as atrophy of musculature around the hip can be observed.

Osteochondrosis that results in death and fracture located in hip joint This article needs additional citations for verification . Please help improve this article by adding citations to reliable sources . Unsourced material may be challenged and removed. Find sources: "Legg–Calvé–Perthes disease" – news · newspapers · books · scholar · JSTOR ( July 2014 ) ( Learn how and when to remove this template message ) Legg–Calvé–Perthes syndrome Other names Perthes disease or Legg–Perthes disease Radiograph of a person with Legg–Calvé–Perthes disease Pronunciation / ˈ l ɛ ɡ k æ l ˈ v eɪ ˈ p ɜːr t iː z , k ɑː l -, - t ɪ z / Specialty Orthopedics Symptoms Pain in the hip, knee, ankle (hip pathology can refer pain to a normal knee or ankle), or groin. Usual onset 4 to 8 years Causes Artery of the ligmentum teres femoris being constricted or even blocked too early Diagnostic method X-Ray Treatment Orthotics Frequency 1/1200 Legg–Calvé–Perthes disease ( LCPD ), is a childhood hip disorder initiated by a disruption of blood flow to the head of the femur. Due to the lack of blood flow, the bone dies ( osteonecrosis or avascular necrosis ) and stops growing.

A number sign (#) is used with this entry because of evidence that Legg-Calve-Perthes disease (LCPD), a form of avascular necrosis of the femoral head (ANFH; see 608805) in growing children, is caused by heterozygous mutation in the COL2A1 (120140) on chromosome 12q13. Description Legg-Calve-Perthes disease is characterized by loss of circulation to the femoral head, resulting in avascular necrosis in a growing child. Clinical pictures of the disease vary, depending on the phase of disease progression through ischemia, revascularization, fracture and collapse, and repair and remodeling of the bone. The disease occurs more frequently in boys, and most patients tend to be shorter than their peers. Both familial and isolated cases of LCPD have been reported (summary by Chen et al., 2004).

Legg-Calve-Perthes disease (LCPD) occurs when blood supply to the ball of the thighbone in the hip (femoral head) is disrupted. Without an adequate blood supply, the bone cells die. LCPD usually occurs in children between the ages of 4 and 10. Early symptoms may include limping; pain in the hip, thigh or knee; and reduced range of hip motion. Later in the disease course, there may be leg length discrepancy (one leg longer than the other) and wasting of the muscles around the hip. The condition can last for several years before new bone formation (re-ossification) and eventual healing occurs.

A tropical disease mainly found in latin America and transmitted by triatomine insects (mostly Triatoma infestans and Rhodnius prolixus and Panstrongylus megistus ) harboring the hemoflagellate protozoan parasite Trypanosoma cruzi . The disease is characterized by an acute phase which is either asymptomatic or manifest with fever, inflammation at the inoculation site (inoculation chancre or chagoma), unilateral palpebral edema called the Romaña sign (when the triatomine bite occurs near the eye), enlarged lymph nodes, and splenomegaly. The chronic phase is lifelong and development of chagasic cardiomyopathy (30%; complex arrhythmias, heart failure, and thromboembolic events), digestive (10%; megaoesophagus and megacolon), neurological (10%; stroke, peripheral neuropathy and autonomic dysfunction), or mixed alterations (10%) may be observed. These can all lead to high morbidity and mortality rates.

Human infectious disease Chagas disease Other names American trypanosomiasis Photomicrograph of Giemsa -stained Trypanosoma cruzi Pronunciation / ˈ tʃ ɑː ɡ ə s / , Portuguese pronunciation: [ˈʃaɡɐs] Specialty Infectious disease Symptoms Fever, large lymph nodes, headache [1] Complications Heart failure , enlarged esophagus , enlarged colon [1] Causes Trypanosoma cruzi spread by kissing bugs [1] Diagnostic method Finding the parasite, its DNA, or antibodies in the blood [2] Prevention Eliminating kissing bugs and avoiding their bites [1] Medication Benznidazole , nifurtimox [1] Frequency 6.2 million (2017) [3] Deaths 7,900 (2017) [4] Chagas disease , also known as American trypanosomiasis , is a tropical parasitic disease caused by Trypanosoma cruzi . [1] It is spread mostly by insects known as Triatominae , or "kissing bugs". [1] The symptoms change over the course of the infection. In the early stage, symptoms are typically either not present or mild, and may include fever, swollen lymph nodes , headaches, or swelling at the site of the bite. [1] After four to eight weeks, untreated individuals enter the chronic phase of disease, which in most cases does not result in further symptoms. [2] [5] Up to 45% of people with chronic infection develop heart disease 10–30 years after the initial illness, which can lead to heart failure . [2] Digestive complications, including an enlarged esophagus or an enlarged colon , may also occur in up to 21% of people, and up to 10% of people may experience nerve damage. [2] T. cruzi is commonly spread to humans and other mammals by the bite of a kissing bug. [6] The disease may also be spread through blood transfusion , organ transplantation , eating food contaminated with the parasites, and vertical transmission (from a mother to her baby). [1] Diagnosis of early disease is by finding the parasite in the blood using a microscope or detecting its DNA by polymerase chain reaction . [5] Chronic disease is diagnosed by finding antibodies for T. cruzi in the blood. [7] It affects more than 150 types of animals. [8] Prevention focuses on eliminating kissing bugs and avoiding their bites. [1] This may involve the use of insecticides or bed-nets . [9] Other preventive efforts include screening blood used for transfusions. [1] As of 2019 [update] , a vaccine has not been developed. [1] Early infections are treatable with the medications benznidazole or nifurtimox , which usually cure the disease if given shortly after the person is infected, but become less effective the longer a person has had Chagas disease. [1] When used in chronic disease, medication may delay or prevent the development of end–stage symptoms. [1] Benznidazole and nifurtimox often cause side effects, including skin disorders, digestive system irritation, and neurological symptoms, which can result in treatment being discontinued. [1] [2] As of 2019 [update] , new drugs for Chagas disease are under development, and experimental vaccines have been studied in animal models. [10] [11] It is estimated that 6.2 million people, mostly in Mexico, Central America and South America, have Chagas disease as of 2017, [1] [3] resulting in an estimated 7,900 deaths. [4] Most people with the disease are poor, [12] and most do not realize they are infected. [13] Large-scale population migrations have carried Chagas disease to new regions, which now include the United States and many European countries. [1] The disease was first described in 1909 by Brazilian physician Carlos Chagas , after whom it is named. [1] Chagas disease is classified as a neglected tropical disease . [14] Contents 1 Signs and symptoms 2 Cause 2.1 Transmission 3 Pathophysiology 4 Diagnosis 5 Prevention 6 Management 6.1 Complications 7 Epidemiology 7.1 Non-endemic countries 8 History 9 Research 9.1 Treatments 9.2 Diagnostic tests 10 See also 11 References 12 External links Signs and symptoms [ edit ] An acute Chagas disease infection with swelling of the right eye (Romaña's sign) Chagas disease occurs in two stages: an acute stage, which develops one to two weeks after the insect bite, and a chronic stage, which develops over many years. [2] [5] [15] The acute stage is often symptom-free. [2] When present, the symptoms are typically minor and not specific to any particular disease. [5] Signs and symptoms include fever, malaise , headache, and enlargement of the liver , spleen , and lymph nodes . [1] [2] [5] Rarely, people develop a swollen nodule at the site of infection, which is called "Romaña's sign" if it is on the eyelid, or a "chagoma" if it is elsewhere on the skin. [5] [16] In rare cases (less than 1–5%), infected individuals develop severe acute disease, which can cause life-threatening fluid accumulation around the heart , or inflammation of the heart or brain and surrounding tissues . [2] The acute phase typically lasts four to eight weeks and resolves without treatment. [2] Unless treated with antiparasitic drugs , individuals remain chronically infected with T. cruzi after recovering from the acute phase. [2] Most chronic infections are asymptomatic, which is referred to as indeterminate chronic Chagas disease. [2] However, over decades with chronic Chagas disease, 30–40% of people develop organ dysfunction ( determinate chronic Chagas disease), which most often affects the heart or digestive system . [2] [5] The most common manifestation is heart disease , which occurs in 14–45% of people with chronic Chagas disease. [2] People with Chagas heart disease often experience heart palpitations and sometimes fainting due to irregular heart function. [17] By electrocardiogram , people with Chagas heart disease most frequently have arrhythmias . [17] As the disease progresses, the heart's ventricles become enlarged ( dilated cardiomyopathy ), which reduces its ability to pump blood. [17] In many cases the first sign of Chagas heart disease is heart failure , thromboembolism , or chest pain associated with abnormalities in the microvasculature . [17] Also common in chronic Chagas disease is damage to the digestive system, particularly enlargement of the esophagus or colon , which affects 10–21% of people. [2] Those with enlarged esophagus often experience pain ( odynophagia ) or trouble swallowing ( dysphagia ), acid reflux , cough, and weight loss. [2] Individuals with enlarged colon often experience constipation , which can lead to severe blockage of the intestine or its blood supply . [2] Up to 10% of chronically infected individuals develop nerve damage that can result in numbness and altered reflexes or movement. [2] While chronic disease typically develops over decades, some individuals with Chagas disease (less than 10%) progress to heart damage directly after acute disease. [17] Signs and symptoms differ for people infected with T. cruzi through less common routes. People infected through ingestion of parasites tend to develop severe disease within three weeks of consumption, with symptoms including fever, vomiting , shortness of breath , cough , and pain in the chest, abdomen , and muscles . [2] Those infected congenitally typically have few to no symptoms, but can have mild non-specific symptoms, or severe symptoms such as jaundice , respiratory distress , and heart problems. [2] People infected through organ transplant or blood transfusion tend to have symptoms similar to those of vector-borne disease, but the symptoms may not manifest for anywhere from a week to five months. [2] Chronically infected individuals who become immunosuppressed due to HIV infection can suffer particularly severe and distinct disease, most commonly characterized by inflammation in the brain and surrounding tissue or brain abscesses . [5] Symptoms vary widely based on the size and location of brain abscesses, but typically include fever, headaches, seizures, loss of sensation, or other neurological issues that indicate particular sites of nervous system damage. [18] Occasionally, these individuals also experience acute heart inflammation, skin lesions, and disease of the stomach, intestine, or peritoneum . [5] Cause [ edit ] Life cycle and transmission of T. cruzi Chagas disease is caused by infection with the protozoan parasite T. cruzi , which is typically introduced into humans through the bite of triatomine bugs, also called "kissing bugs". [5] At the bite site, motile T. cruzi forms called trypomastigotes invade various host cells. [6] Inside a host cell, the parasite transforms into a replicative form called an amastigote, which undergoes several rounds of replication. [6] The replicated amastigotes transform back into trypomastigotes, which burst the host cell and are released into the bloodstream. [2] Trypomastigotes then disseminate throughout the body to various tissues, where they invade cells and replicate. [2] Over many years, cycles of parasite replication and immune response can severely damage these tissues, particularly the heart and digestive tract. [2] Transmission [ edit ] Triatoma infestans , a common vector of T. cruzi [19] T. cruzi can be transmitted by various triatomine bugs in the genera Triatoma , Panstrongylus , and Rhodnius . [2] The primary vectors for human infection are the species of triatomine bugs that inhabit human dwellings, namely Triatoma infestans , Rhodnius prolixus , Triatoma dimidiata and Panstrongylus megistus . [19] These insects are known by a number of local names, including vinchuca in Argentina, Bolivia, Chile and Paraguay, barbeiro (the barber ) in Brazil, pito in Colombia, chinche in Central America, and chipo in Venezuela. [20] The bugs tend to feed at night, preferring moist surfaces near the eyes or mouth. [15] [19] A triatomine bug can become infected with T. cruzi when it feeds on an infected host. [15] T. cruzi replicates in the insect's intestinal tract and is shed in the bug's feces. [15] When an infected triatomine feeds, it pierces the skin and takes in a blood meal , defecating at the same time to make room for the new meal. [15] The bite is typically painless, but causes itching. [15] Scratching at the bite introduces the T. cruzi -laden feces into the bite wound, initiating infection. [15] In addition to classical vector spread, Chagas disease can be transmitted through food or drink contaminated with triatomine insects or their feces. [21] Since heating or drying kills the parasites, drinks and especially fruit juices are the most frequent source of infection. [21] This route of transmission has been implicated in several outbreaks, where it led to unusually severe symptoms, likely due to infection with a higher parasite load than from the bite of a triatomine bug. [7] [21] T. cruzi can also be transmitted independent of the triatomine bug during blood transfusion, following organ transplantation, or across the placenta during pregnancy. [2] Transfusion with the blood of an infected donor infects the recipient 10–25% of the time. [2] To prevent this, blood donations are screened for T. cruzi in many countries with endemic Chagas disease, as well as the United States. [7] Similarly, transplantation of solid organs from an infected donor can transmit T. cruzi to the recipient. [2] This is especially true for heart transplant, which transmits T. cruzi 75–100% of the time, and less so for transplantation of the liver (0–29%) or a kidney (0–19%). [2] An infected mother can also pass T. cruzi to her child through the placenta; this occurs in up to 15% of births by infected mothers. [22] As of 2019, 22.5% of new infections occurred through congenital transmission. [23] Pathophysiology [ edit ] Large scale anatomy of a heart damaged by chronic Chagas disease In the acute phase of the disease, signs and symptoms are caused directly by the replication of T. cruzi and the immune system 's response to it. [2] During this phase, T. cruzi can be found in various tissues throughout the body and circulating in the blood. [2] During the initial weeks of infection, parasite replication is brought under control by production of antibodies and activation of the host's inflammatory response , particularly cells that target intracellular pathogens such as NK cells and macrophages , driven by inflammation-signaling molecules like TNF-α and IFN-γ . [2] During chronic Chagas disease, long-term organ damage develops over years due to continued replication of the parasite and damage from the immune system. Early in the course of the disease, T. cruzi is found frequently in the striated muscle fibers of the heart. [24] As disease progresses, the heart becomes generally enlarged, with substantial regions of cardiac muscle fiber replaced by scar tissue and fat . [24] Areas of active inflammation are scattered throughout the heart, with each housing inflammatory immune cells, typically macrophages and T cells . [24] Late in the disease, parasites are rarely detected in the heart, and may be present at only very low levels. [24] In the heart, colon, and esophagus, chronic disease also leads to a massive loss of nerve endings . [17] In the heart, this may contribute to arrythmias and other cardiac dysfunction. [17] In the colon and esophagus, loss of nervous system control is the major driver of organ dysfunction. [17] Loss of nerves impairs the movement of food through the digestive tract, which can lead to blockage of the esophagus or colon and restriction of their blood supply. [17] Diagnosis [ edit ] T. cruzi trypomastigotes seen in a blood smear The presence of T. cruzi is diagnostic of Chagas disease. During the acute phase of infection, it can be detected by microscopic examination of fresh anticoagulated blood, or its buffy coat , for motile parasites; or by preparation of thin and thick blood smears stained with Giemsa , for direct visualization of parasites. [5] [7] Blood smear examination detects parasites in 34–85% of cases.

Pineoblastoma is a rare, malignant type of supratentorial primitive neuroectodermal tumor (sPNET), found mainly in children (less than 10% of cases are reported in adults), and located in the pineal region of the brain but that can metastasize along the neuroaxis. As it is the most aggressive of the pineal parenchymal tumors, it is usually associated with a poor prognosis.

Pineoblastoma is a type of cancerous ( malignant ) tumor that grows in a part of the brain known as the pineal gland . It occurs mainly in children. Symptoms of pineoblastoma include a buildup of fluid around the brain (hydrocephalus), headaches, nausea, and difficulty with eye movement. Without treatment, pineoblastomas can cause weakness and difficulty controlling movement. The long term outcome depends on the age at diagnosis, the size of the tumor, and if the tumor has spread outside the brain ( metastasized ). The cause of pineoblastoma is unknown, but specific inherited genetic variants in two genes, RB1 and DICER1 can increase the risk for a pineoblastoma.

A rare mycosis characterized by an acute form mostly occurring in children and young adults presenting with fever, weight loss, lymph node enlargement, hepatosplenomegaly, and bone marrow dysfunction, versus a chronic form which usually involves the lungs and mucosae of the upper respiratory tract, skin, lymph nodes, and adrenal glands, but may affect any part of the body. The most common sequelae are chronic respiratory insufficiency and Addison's disease. The infectious agent, Paracoccidioides brasiliensis , is a fungus limited to Latin America.

Infectious bovine keratoconjunctivitis ( IBK ), also known as pinkeye , New Forest eye or blight , [1] is a veterinary infection of cattle caused by Moraxella bovis , a Gram-negative, β-haemolytic, aerobic , rod-shaped bacterium . It is spread by direct contact or by flies serving as vectors . It is the most common ocular disease of cattle (mostly beef). IBK is similar to human pink eye and causes severe infection of the conjunctiva , edema , corneal opacity , and ulceration . This disease is highly contagious and occurs worldwide. Younger animals are more susceptible, but recovery with minimal damage is usual, if they are treated early. Contents 1 Cause 2 Predisposing factors 3 Clinical signs and diagnosis 4 Treatment and control 5 Vaccination 6 References 7 External links Cause [ edit ] Moraxella bovis is a Gram-negative rod-shaped aerobe .

Description Focal epithelial hyperplasia is a benign hyperplasia of the oral mucosa induced by human papillomavirus (HPV) (Premoli-De-Percoco et al., 1993). Clinical Features Premoli-De-Percoco et al. (1993) demonstrated a familial aggregation of oral FEH in a Venezuelan family. DNA sequences of HPV were demonstrated in the affected individuals. HPV13 and HPV32 have been demonstrated as etiologic agents; HPV13 was demonstrated in this kindred. (See 226400 and 305350 for possible examples of skin disorders (epidermodysplasia verruciformis) due to genetic susceptibility to HPV.) In 2 of 4 sibs born of Mexican-American parents of Navajo and Comanche Native American lineage, Mealey et al. (1993) described FEH in association with leukocyte adhesion deficiency (116920).