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A number sign (#) is used with this entry because pachyonychia congenita-4 (PC4) is caused by heterozygous mutation in the KRT6B gene (148042) on chromosome 12q13. Description Pachyonychia congenita (PC) is an autosomal dominant genodermatosis with the main clinical features of hypertrophic nail dystrophy, painful and highly debilitating plantar keratoderma, oral leukokeratosis, and a variety of epidermal cysts. Although the condition had previously been subdivided clinically into Jadassohn-Lewandowsky PC type 1 and Jackson-Lawler PC type 2, patients with PC were later found to have a mixed constellation of both types, leading to a classification of PC based on genotype (summary by Sybert, 2010; Eliason et al., 2012; McLean et al., 2011). For a discussion of genetic heterogeneity of pachyonychia congenita, see 167200. Historical Classification of Pachyonychia Congenita Gorlin et al. (1976) suggested that 2 distinct syndromes are subsumed under the designation pachyonychia congenita.
Pachyonychia congenita (PC) is a rare genodermatosis predominantly featuring painful palmoplantar keratoderma, thickened nails, cysts and whitish oral mucosa. Epidemiology The prevalence is not known but approximately 1000 patients have been registered to date worldwide. Clinical description PC presents clinically as a spectrum of conditions. PC onset is variable with most cases manifesting soon after birth, others becoming clinically apparent only in late childhood and rarely in adulthood. The first signs of the disease usually are thickened nails or neonatal teeth.
Pachyonychia congenita (PC) is a rare inherited condition that primarily affects the nails and skin. The fingernails and toenails may be thickened and abnormally shaped . Affected people can also develop painful calluses and blisters on the soles of their feet and less frequently on the palms of their hands ( palmoplantar keratoderma ). Additional features include white patches on the tongue and inside of the mouth (leukokeratosis); bumps around the elbows, knees, and waistline (follicular hyperkeratosis); and cysts of various types including steatocystoma. Features may vary among affected people depending on their specific mutation.
For a phenotypic description and a discussion of genetic heterogeneity of pachyonychia congenita, see 167200. Inheritance Chong-Hai and Rajagopalan (1977) suggested autosomal recessive inheritance of pachyonychia congenita in a 4-year-old Malaysian girl with first-cousin parents, although they recognized new dominant mutation as a possibility. See also Sivasundram et al. (1985). INHERITANCE - Autosomal recessive HEAD & NECK Mouth - No oral leukoplakia SKIN, NAILS, & HAIR Skin - Horny papules (face, leg, buttocks) - No palmoplantar hyperkeratosis - No hyperhidrosis Nails - Episodic inflammatory swelling of nail bed - Recurrent shedding of nails - Hard,thickened nails (pachyonychia) - Subungual hyperkeratosis MISCELLANEOUS - See also pachyonychia congenita, type 3 (PC1, 167200 ) ▲ Close
A number sign (#) is used with this entry because pachyonychia congenita-3 (PC3) is caused by heterozygous mutation in the keratin-6a gene (KRT6A; 148041) on chromosome 12q13. Description Pachyonychia congenita (PC) is an autosomal dominant genodermatosis with the main clinical features of hypertrophic nail dystrophy, painful and highly debilitating plantar keratoderma, oral leukokeratosis, and a variety of epidermal cysts. Although the condition had previously been subdivided clinically into Jadassohn-Lewandowsky PC type 1 and Jackson-Lawler PC type 2, patients with PC were later found to have a mixed constellation of both types, leading to a classification of PC based on genotype (summary by Sybert, 2010; Eliason et al., 2012; McLean et al., 2011). For a discussion of genetic heterogeneity of pachyonychia congenita, see 167200. Historical Classification of Pachyonychia Congenita Gorlin et al. (1976) suggested that 2 distinct syndromes are subsumed under the designation pachyonychia congenita.
A number sign (#) is used with this entry because of evidence that pachyonychia congenita-2 (PC2) is caused by heterozygous mutation in the KRT17 gene (148069) on chromosome 17q21. Description Pachyonychia congenita (PC) is an autosomal dominant genodermatosis with the main clinical features of hypertrophic nail dystrophy, painful and highly debilitating plantar keratoderma, oral leukokeratosis, and a variety of epidermal cysts. Although the condition had previously been subdivided clinically into Jadassohn-Lewandowsky PC type 1 and Jackson-Lawler PC type 2, patients with PC were later found to have a mixed constellation of both types, leading to a classification of PC based on genotype (summary by Sybert, 2010; Eliason et al., 2012; McLean et al., 2011). For a discussion of genetic heterogeneity of pachyonychia congenita, see 167200. Historical Classification of Pachyonychia Congenita Gorlin et al. (1976) suggested that 2 distinct syndromes are subsumed under the designation pachyonychia congenita.
A number sign (#) is used with this entry because pachyonychia congenita-1 (PC1) is caused by heterozygous mutation in the keratin-16 gene (KRT16; 148067) on chromosome 17q21. Description Pachyonychia congenita (PC) is an autosomal dominant genodermatosis with the main clinical features of hypertrophic nail dystrophy, painful and highly debilitating plantar keratoderma, oral leukokeratosis, and a variety of epidermal cysts. Although the condition had previously been subdivided clinically into Jadassohn-Lewandowsky PC type 1 and Jackson-Lawler PC type 2, patients with PC were later found to have a mixed constellation of both types, leading to a classification of PC based on genotype (summary by Sybert, 2010; Eliason et al., 2012; McLean et al., 2011). Historical Classification of Pachyonychia Congenita Gorlin et al. (1976) suggested that 2 distinct syndromes are subsumed under the designation pachyonychia congenita. PC type 1, the Jadassohn-Lewandowsky type, shows oral leukokeratosis.
Human African Trypanosomiasis (HAT), also called sleeping sickness, is a vector-borne parasitic disease caused by a protozoa of the Trypanosoma genus transmitted by the bite of a tsetse fly (genus Glossina ), that is found under its chronic form (average duration of 3 years) in western and central Africa (in case of the T. brucei gambiense sub-species), and under its acute form (lasting from few weeks to 6 months) in eastern and southern Africa (in case of the T. brucei rhodesiense sub-species). HAT comprises an initial hemo-lymphatic stage characterized by fever, weakness, musculoskeletal pain, anemia, and lymphadenopathy, along with dermatologic, cardiac and endocrine complications or hepatosplenomegaly, followed by a meningo-encephalitic stage characterized by neurologic involvement (sleep disturbances, psychiatric disorders, seizures) that progresses, in the absence of treatment, towards a fatal meningoencephalitis.
A study by Iwatsuki et al. detected Epstein-Barr virus (EBV) positive T-cells in the perivascular infiltration on biopsy in 28/29 patients tested. Antibody titers to EBV were measured in 14 of these patients and only five had abnormal antibody patterns consistent with chronic active EBV infection. [6] Treatment [ edit ] Antiviral treatment has been tried with some success in a small number of patients. [7] See also [ edit ] List of cutaneous conditions Epstein-Barr virus References [ edit ] ^ Bazin, E (1862). ... Feb, 42(2 Pt 1) (2): 208–13. doi : 10.1016/s0190-9622(00)90127-0 . PMID 10642674 . ^ James, William D.; Berger, Timothy G.; et al. (2006). Andrews' Diseases of the Skin: clinical Dermatology . Saunders Elsevier. ISBN 0-7216-2921-0 . ^ Rezk SA, Zhao X, Weiss LM (September 2018).
A rare photodermatosis characterized by the development of pruritic or painful vesicles in a photodistributed pattern in response to sunlight exposure. The lesions heal with permanent varioliform scarring. Ocular involvement, deformities of ears and nose, or contractures of the fingers may occasionally be observed. Systemic signs and symptoms are absent. The condition typically occurs in childhood and regresses spontaneously in adolescence or young adulthood.
Jaypee Brothers Publishers. 2007. pp. 347–. ISBN 978-81-8061-996-0 . ^ Leonard J. Deftos (1 January 1998). ... Rowman & Littlefield Publishers. pp. 73–. ISBN 978-0-7591-2332-8 . ^ Vasan; R.S. (1 January 1998). ... Biochemistry and Function of Sterols . CRC Press. pp. 26–27. ISBN 978-0-8493-7674-0 . ^ Michael Crocetti; Michael A. ... Lippincott Williams & Wilkins. pp. 564–. ISBN 978-0-7817-3770-8 . ^ W. Steven Pray (2006). ... Elsevier Health Sciences. pp. 1281–. ISBN 978-0-323-08678-3 . ^ Guy I. Benrubi (28 March 2012).
Hagerstown, MD: Lippincott Williams & Wilkins. p. 1150. ISBN 0-7817-2655-7 . Retrieved 2008-06-16 . ^ a b c d e f Scalea TM (2005). ... Boca Raton: CRC. pp. 26–32. ISBN 978-0-8493-8138-6 . Retrieved 2008-07-06 . ^ a b Porth, Carol (2007). ... Hagerstown, MD: Lippincott Williams & Wilkins. p. 838. ISBN 978-0-7817-7087-3 . Retrieved 2008-07-03 . ^ Pitkänen A, McIntosh TK (2006). ... Neurotrauma: New Insights Into Pathology and Treatment . Elsevier. pp. 13–19. ISBN 978-0-444-53017-2 . Retrieved 2008-06-10 . ^ a b Granacher RP (2007). ... Neuroscience . 101 (2): 289–95. doi : 10.1016/S0306-4522(00)00380-8 . PMID 11074152 . S2CID 20457228 . ^ Sauaia A, Moore FA, Moore EE, et al.
Lippincott Williams & Wilkins. pp. 254–256. ISBN 0-7817-3905-5 . ^ a b c d e f g h i Smith, Melanie N. (2006-05-10). ... Cambridge University Press . p. 77. ISBN 1-900151-51-0 . ^ Papadakis, Maxine A.; Stephen J. ... McGraw-Hill Professional. p. 60. ISBN 0-07-145892-1 . ^ a b Bosze, Peter; David M. ... Informa Health Care. p. 66. ISBN 963-00-7356-0 . ^ "Cervical Polyps" (PDF) .
Lippincott Williams & Wilkins. pp. 2199–. ISBN 978-0-7817-5777-5 . ^ Andres Kanner; Steven C. Schachter (28 July 2010). Psychiatric Controversies in Epilepsy . Elsevier. pp. 54–. ISBN 978-0-08-055959-9 . ^ Michael R. Trimble; Bettina Schmitz (9 June 2011). ... Oxford University Press. pp. 147–. ISBN 978-0-19-970699-0 .
Glycogen storage disease type 0 (also known as GSD 0) is a condition caused by the body's inability to form a complex sugar called glycogen, which is a major source of stored energy in the body. GSD 0 has two types: in muscle GSD 0, glycogen formation in the muscles is impaired, and in liver GSD 0, glycogen formation in the liver is impaired. The signs and symptoms of muscle GSD 0 typically begin in early childhood. ... Because some people with muscle GSD 0 die from sudden cardiac arrest early in life before a diagnosis is made and many with liver GSD 0 have mild signs and symptoms, it is thought that GSD 0 may be underdiagnosed. Causes Mutations in the GYS1 gene cause muscle GSD 0, and mutations in the GYS2 gene cause liver GSD 0.
A number sign (#) is used with this entry because of evidence that liver glycogen storage disease-0 (GSD0A) is caused by homozygous or compound heterozygous mutation in the GYS2 gene (138571), which encodes glycogen synthase-2, on chromosome 12p12. ... Mapping Orho et al. (1998) established linkage of glycogen storage disease 0 to intragenic and flanking polymorphic markers of the GYS2 gene on chromosome 12p12.2. Molecular Genetics In affected members of 5 families with liver glycogen storage disease 0, Orho et al. (1998) identified homozygous or compound heterozygous mutations in the GYS2 gene (138571.0001-138571.0008) Inheritance - Autosomal recessive Neuro - Seizures Lab - Glycogen synthetase deficiency Metabolic - Neonatal hypoglycemia - Fasting hypoglycemia - Fasting hyperketonemia - Hyperglycemia and hyperlactatemia with feeding ▲ Close
A genetically inherited anomaly of glycogen metabolism and a form of glycogen storage disease (GSD) characterized by fasting hypoglycemia. This is not a glycogenosis, strictly speaking, as the enzyme deficiency decreases glycogen reserves. Epidemiology It is an extremely rare disease; about 20 cases have been reported in the literature so far. Clinical description It commonly appears in infancy or in early childhood. Patients present with morning fatigue and fasting hypoglycemia (without hepatomegaly) associated with hyperketonemia but without hyperalaninemia or hyperlactacidemia.
Glycogen storage disease type 0, liver (liver GSD 0), a form of glycogen storage disease (GSD), is a rare abnormality of glycogen metabolism (how the body uses and stores glycogen, the storage form of glucose). Unlike other types of GSD, liver GSD 0 does not involve excessive or abnormal glycogen storage, and causes moderately decreased glycogen stores in the liver. ... This condition differs from another form of GSD 0 which chiefly affects the muscles and heart ( Glycogen storage disease type 0, muscle ) and is thought to be caused by mutations in the GYS1 gene.
Examples of treatment options for breast atrophy, depending on the situation/when appropriate, can include estrogens, antiandrogens , and proper nutrition or weight gain . [ citation needed ] See also [ edit ] Mammoplasia Micromastia References [ edit ] ^ a b c Prem Puri; Michael E. Höllwarth (28 May 2009). Pediatric Surgery: Diagnosis and Management . ... Cambridge University Press. pp. 1–. ISBN 978-0-521-88159-3 . ^ Ricardo Azziz (3 July 2007). ... Springer Science & Business Media. pp. 20–. ISBN 978-0-387-69248-7 . ^ Susan Scott Ricci; Terri Kyle (2009). ... Lippincott Williams & Wilkins. pp. 213 –. ISBN 978-0-7817-8055-1 . ^ J.P. Lavery; J.S. ... Lippincott Williams & Wilkins. pp. 558–. ISBN 978-0-7817-3894-1 . ^ Cynthia Feucht; Donald E.
Glycogen storage disease type 0 Glycogen storage disease type 0 has defect in glycogen synthase Specialty Medical genetics Glycogen storage disease type 0 is a disease characterized by a deficiency in the glycogen synthase enzyme (GSY). ... Serum electrolytes calculate the anion gap to determine presence of metabolic acidosis ; typically, patients with glycogen-storage disease type 0 (GSD-0) have an anion gap in the reference range and no acidosis. ... In patients with glycogen-storage disease type 0, hyperlipidemia is absent or mild and proportional to the degree of fasting. ... In patients with glycogen-storage disease type 0, urine ketones findings are positive, and urine-reducing substance findings are negative. ... The identification of asymptomatic and oligosymptomatic siblings in several glycogen-storage disease type 0 families has suggested that glycogen-storage disease type 0 is underdiagnosed. [2] Mortality/Morbidity [ edit ] The major morbidity is a risk of fasting hypoglycemia, which can vary in severity and frequency.
Foot deformities were first observed between ages two and ten years, were moderately or severely disabling, and required surgery in 6% (1/18) to 11% (3/28) of cases (Table 2). Table 2. Occurrence of Manifestations of CMT4C by Study View in own window Study Finding Study (Total Patients) Azzedine et al [2006] (28) Colomer et al [2006] (14) Senderek et al [2003] (18) Houlden et al [2009] (6) Baets et al [2011] (9) Laššuthová et al [2011] (16) Yger et al [2012] (14) Fischer et al [2012] (6) Cumulative Data Age at onset 1 st symptoms 2-10 4-39 Infancy-12 1-16 <1 1-12 1-12 ND 1-16 Neuropathy 2-10 Infancy-12 1-16 <1 2-50 2-50 2-25 1-50 Age at (last) exam (yrs) 5-45 8-45 11-56 8-42 ND ND 8-59 5-59 Foot deformity Pes cavus 20/28 14/14 1 8/18 Yes ND 13/15 12/14 ND Pes planus 7/28 4/18 Yes ND no no ND Pes valgus 1/28 ND ND ND no 3/14 ND Other No Hammer toes 8/18 Small feet ND Hammer toes no ND Total 28/28 14/14 13/18 2 6/6 1 7/9 14/15 14/14 ND 96/104 (92%) Age at onset (yrs) 2-10 No data 2-12 ND ND ND 1,12 3 ND 1-12 Surgery 3/28 None 1/13 No ND 9/14 4/14 ND 17/69 (24%) Spine deformity Total 27/28 5/14 4 11/18 4 6/6 6/9 10/12 12/12 5/6 82/105 (78%) Age at onset (yrs) 2-10 4 4-12 5 ND 2, 6, 7, 12 6 ND 7-15 ND 2-15 Surgery 7 7 + 6 8 = 13/27 1/14 1/11 3/6 3/6 ND 1/12 ND 22/76 (29%) ND = not done or not documented 1. ... Additional Clinical Findings in CMT4C by Study View in own window Clinical Finding Study (Total Patients) Azzedine et al [2006] (28) Colomer et al [2006] (14) Senderek et al [2003] (18) Houlden et al [2009] (6) Baets et al [2011] (9) Laššuthová et al [2011] (16) Yger et al [2012] (14) Cumulative Data Hypoacusis 5/280/14 2/18 0/6 0/9 0/15 8/13 15/103 Deafness 0/28 5/14 1/18 2/6 1/9 3/15 0/13 12/103 Nystagmus 0/280/14 2/18 0/6 2/9 0/15 0/13 4/103 Pupillary light reflexes 0/28 3/14 0/18 1/6 0/9 0/15 14/13 4/20 Other pupillary disturbances -- -- -- Asymmetric size 1/6 -- -- -- 1/6 Lingual fasciculation -- 3/14 -- -- -- -- -- 3/14 Tongue atrophy and/or weakness -- -- -- 1/6 -- -- 2/13 3/19 Facial paresis 1/28 -- -- 1/6 1/9 -- 4/13 7/56 Facial weakness -- -- -- 1/6 -- -- -- 1/6 Head tremor -- 2/14 -- -- -- -- -- 2/14 Vocal cord involvement -- -- -- -- -- -- 1/13 1/13 Total patients w/cranial nerve involvement 5/28 9/14 5/14 1 4/6 -- -- 10/13 33/73 Respiratory insufficiency or hypoventilation 7/28 2 -- 2/18 -- 1/9 -- -- 10/55 Sensory ataxia 1/28 2/14 -- -- -- -- -- >3/42 3 Diabetes mellitus -- -- 1/18 -- -- -- -- 1/18 Romberg sign -- 2/14 -- -- -- -- -- 2/14 1. 14 of 18 patients were examined for cranial nerve involvement. 2. ... Genotype-Phenotype Correlations Significant intrafamilial variability in the disease course makes it difficult to identify genotype-phenotype correlations [Kessali et al 1997, Gabreëls-Festen et al 1999, Senderek et al 2003, Azzedine et al 2005a, Azzedine et al 2005b, Azzedine et al 2006]. In 28 individuals with CMT4C, Azzedine et al [2006] found no correlation between the nature and the position of the pathogenic variant, disease duration, and the stage of disability.
A number sign (#) is used with this entry because Charcot-Marie-Tooth (CMT) disease type 4C is caused by homozygous or compound heterozygous mutation in the SH3TC2 gene (608206). Mild mononeuropathy of the median nerve (MNMN; 613353) is a less severe allelic disorder caused by heterozygous mutation in the SH3TC2 gene. For a phenotypic description and a discussion of genetic heterogeneity of autosomal recessive demyelinating Charcot-Marie-Tooth disease, see CMT4A (214400). Clinical Features Kessali et al. (1997) reported 2 large consanguineous Algerian families with autosomal recessive demyelinating CMT. Mean age at onset was 5.2 years (range 2 to 10 years). All patients had foot deformities and scoliosis, often requiring surgery.
Charcot-Marie-Tooth disease type 4C (CMT4C) is a subtype of Charcot-Marie-Tooth type 4 characterized by childhood or adolescent-onset of a relatively mild, demyelinating sensorimotor neuropathy that contrasts with a severe, rapidly progressing, early-onset scoliosis, and the typical CMT phenotype (i.e. distal muscle weakness and atrophy, sensory loss, and often foot deformity). A wide spectrum of nerve conduction velocities are observed and cranial nerve involvement and kyphoscoliosis have also been reported.
John Wiley and Sons. p. 719 . ISBN 978-0-470-57712-7 . ^ Becker, Judith V.; Stinson, Jill D. (2008). ... John Wiley & Sons . pp. 522 . ISBN 978-0-470-25721-0 . ^ Money 1986 , p. 290 . ^ Money 1986 , p. 34 . ^ Money, J. (1984). ... Prometheus Books . p. 147. ISBN 978-0-87975-277-4 . ^ Wilson, Glen Daniel (1987). ... Taylor and Francis. pp. 107–11 . ISBN 978-0-7099-3698-5 . ^ Kaufman, F (1997). ... Washington Square Press. ISBN 978-0-87140-840-2 . Further reading [ edit ] Love, B (1992).
Console and Classify: The French Psychiatric Profession in the Nineteenth Century . University of Chicago Press. ISBN 0-226-30161-3 . ^ a b Eigen, Joel Peter (January 1991). ... Cambridge: Cambridge University Press. ISBN 0-521-43736-9 . ^ Valverde, Mariana (1998-10-28). ... American Psychiatric Society. 2000. p. xxv. ISBN 0-89042-025-4 . ^ Berrios's note states: "Monomania was a diagnosis invented by Esquirol which achieved certain popularity, particularly in forensic psychiatry. ... Cambridge University Press. pp. 426, 447, 453 n. 50. ISBN 0-521-43736-9 . External links [ edit ] Van Zuylen, Marina (2005). ... Ithaca, New York: Cornell University Press. ISBN 978-0-8014-4298-8 . Find out more on Wikipedia's Sister projects Media from Commons Definitions from Wiktionary Data from Wikidata
Clin Dermatol . 19 (1): 69–71. doi : 10.1016/S0738-081X(00)00215-7 . PMID 11369491 . ^ "Drugs that call for extra caution. ... New York: Simon Schuster. p. 56. ISBN 978-0-684-87309-1 . ^ M.d. Kamath, Bob (30 May 2007). ... Kendall Hunt Publishing. p. 25. ISBN 978-0-7872-8701-6 . ^ Ashton CH (2002).
While diarrhea is common in people with SARS, the fecal–oral route does not appear to be a common mode of transmission. [9] The basic reproduction number of SARS-CoV, R 0 , ranges from 2 to 4 depending on different analyses. ... Tested substances, include ribavirin , lopinavir , ritonavir , type I interferon , that have thus far shown no conclusive contribution to the disease's course. [21] Administration of corticosteroids , is recommended by the British Thoracic Society / British Infection Society / Health Protection Agency in patients with severe disease and O2 saturation of <90%. [22] People with SARS-CoV must be isolated, preferably in negative-pressure rooms , with complete barrier nursing precautions taken for any necessary contact with these patients, to limit the chances of medical personnel becoming infected. [10] In certain cases, natural ventilation by opening doors and windows is documented to help decreasing indoor concentration of virus particles. [23] Some of the more serious damage caused by SARS may be due to the body's own immune system reacting in what is known as cytokine storm . [24] Vaccine [ edit ] See also: Economics of vaccines and COVID-19 vaccine As of 2020, there is no cure or protective vaccine for SARS that has been shown to be both safe and effective in humans. [25] [26] According to research papers published in 2005 and 2006, the identification and development of novel vaccines and medicines to treat SARS was a priority for governments and public health agencies around the world. [27] [28] [29] In early 2004, an early clinical trial on volunteers was planned. [30] A major researcher's 2016 request, however, demonstrated that no field-ready SARS vaccine had been completed because likely market-driven priorities had ended funding. [14] Prognosis [ edit ] Several consequent reports from China on some recovered SARS patients showed severe long-time sequelae . ... As a result of quarantine procedures, some of the post-SARS patients have been documented as suffering from post-traumatic stress disorder (PTSD) and major depressive disorder . [31] [32] Epidemiology [ edit ] Main article: 2002–2004 SARS outbreak SARS was a relatively rare disease; at the end of the epidemic in June 2003, the incidence was 8,422 cases with a case fatality rate (CFR) of 11%. [4] The case fatality rate (CFR) ranges from 0% to 50% depending on the age group of the patient. [9] Patients under 24 were least likely to die (less than 1%); those 65 and older were most likely to die (over 55%). [33] As with MERS and COVID-19 , SARS resulted in significantly more deaths of males than females. 2003 Probable cases of SARS – worldwide Probable cases of SARS by country or region, 1 November 2002 – 31 July 2003 [34] Country or region Cases Deaths Fatality (%) China [a] 5,327 349 6.6 Hong Kong 1,755 299 17.0 Taiwan [b] 346 73 [35] [36] 21.1 Canada 251 43 17.1 Singapore 238 33 13.9 Vietnam 63 5 7.9 United States 27 00 Philippines 14 2 14.3 Thailand 9 2 22.2 Germany 9 00 Mongolia 9 00 France 7 1 14.3 Australia 6 00 Malaysia 5 2 40.0 Sweden 5 00 United Kingdom 4 00 Italy 4 00 Brazil 3 00 India 3 00 South Korea 3 00 Indonesia 2 00 South Africa 1 1 100.0 Colombia 1 00 Kuwait 1 00 Ireland 1 00 Macao 1 00 New Zealand 1 00 Romania 1 00 Russia 1 00 Spain 1 00 Switzerland 1 00 Total excluding China [a] 2,769 454 16.4 Total (29 territories) 8,096 774 9.6 ^ a b Figures for China exclude Hong Kong and Macau, which are reported separately by the WHO . ^ After 11 July 2003, 325 Taiwanese cases were 'discarded'. ... CNN. 10 April 2003. Archived from the original on 28 November 2007 . Retrieved 3 April 2007 . ^ Fong K (16 August 2013).
Overview Severe acute respiratory syndrome (SARS) is a contagious and sometimes fatal respiratory illness. severe acute respiratory syndrome (SARS) first appeared in China in November 2002. Within a few months, SARS spread worldwide, carried by unsuspecting travelers. SARS showed how quickly infection can spread in a highly mobile and interconnected world. On the other hand, a collaborative international effort allowed health experts to quickly contain the spread of the disease. There has been no known transmission of SARS anywhere in the world since 2004.
A rare pulmonary disease induced by SARS-CoV coronavirus infection, with a reported incubation period varying from 2 to 7 days. Patients present flu-like symptoms, including fever, malaise, myalgia, headache, diarrhoea, and rigors. Dry, nonproductive, cough and dyspnea are frequently reported. Severe cases evolve rapidly, progressing to respiratory distress and failure, requiring intensive care. Mortality rate is 10%. The disease appeared in 2002 in southern China, subsequently spreading in 2003 to 26 countries. Reported human-to-human transmission occurred in Toronto (Canada), Hong Kong Special Administrative Region of China, Chinese Taipei, Singapore, and Hanoi (Viet Nam).
See also [ edit ] List of cutaneous conditions References [ edit ] ^ "Hereditary leiomyomatosis and renal cell cancer | Genetic and Rare Diseases Information Center (GARD) – an NCATS Program" . rarediseases.info.nih.gov . Retrieved 28 April 2019 . ^ a b Freedberg, et al. (2003). Fitzpatrick's Dermatology in General Medicine . (6th ed.). Page 1033. McGraw-Hill. ISBN 0-07-138076-0 . External links [ edit ] Classification D ICD - 10 : C64 OMIM : 150800 External resources Orphanet : 523 This Dermal and subcutaneous growths article is a stub .
. ^ "Deaths in the district of Inveresk and Musselburgh in the County of Edinburgh" . Statutory Deaths 689/00 0032 . ScotlandsPeople . Retrieved 11 April 2015 . External links [ edit ] Classification D ICD-O : 8011/0, 8011/3 Wikimedia Commons has media related to Epithelioma .
