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Books on the topic 'Endemic disease'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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1

Sun, Dianjun, ed. Endemic Disease in China. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-2529-8.

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2

Queen, H. L. Chronic mercury toxicity: New hope against an endemic disease. Colorado Springs, Colo: Queen and Co. Health Communications, 1988.

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3

Queen, H. L. Chronic mercury toxicity: New hope against an endemic disease. Colorado Springs, Colo: Queen and Company Health Communications, 1988.

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4

Winter, Lieven de. Political corruption in the Belgian partitocracy: (still) an endemic disease. Badia Fiesolana, Italy: European University Institute, 2000.

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5

Dieleman, Maria Areke. Triggering meaningful change: Human resource management and health worker performance in an AIDS-endemic setting. Amsterdam: Kit Publishers, 2010.

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6

Tkacz, Borys M. Association of an endemic mountain pine beetle population with lodgepole pine infected by Armillaria root disease in Utah. Ogden, UT: U.S. Dept. of Agriculture, Forest Service, Intermountain Research Station, 1985.

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7

Tkacz, Borys M. Association of an endemic mountain pine beetle population with lodgepole pine infected by Armillaria root disease in Utah. Ogden, UT: U.S. Dept. of Agriculture, Forest Service, Intermountain Research Station, 1985.

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8

Tkacz, Borys M. Association of an endemic mountain pine beetle population with lodgepole pine infected by Armillaria root disease in Utah. Ogden, UT: U.S. Dept. of Agriculture, Forest Service, Intermountain Research Station, 1985.

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9

Global Roadmap for Improving the Tools to Control Foot-and-Mouth Disease in Endemic Settings (2006 Agra, India). Global Roadmap for Improving the Tools to Control Foot-and-Mouth Disease in Endemic Settings: Report of a workshop held at Agra, India, 29 November-1 December 2006, and subsequent roadmap outputs. Nairobi, Kenya: International Livestock Research Institute, 2007.

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10

Global Roadmap for Improving the Tools to Control Foot-and-Mouth Disease in Endemic Settings (2006 Agra, India). Global Roadmap for Improving the Tools to Control Foot-and-Mouth Disease in Endemic Settings: Report of a workshop held at Agra, India, 29 November-1 December 2006, and subsequent roadmap outputs. Nairobi, Kenya: International Livestock Research Institute, 2007.

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11

Crompton, D. W. T. (David William Thomasson), 1937-, Daumerie Denis, Peters Patricia, Savioli Lorenzo, and World Health Organization, eds. Working to overcome the global impact of neglected tropical diseases: First WHO report on neglected tropical diseases. Geneva, Switzerland: World Health Organization, 2010.

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12

Zupanič-Slavec, Zvonka. Endemski sifilis: Škrljevska bolezen na Slovenskem : razvoj in širjenje bolezni po naših krajih v prvi polovici 19. stoletja = Endemic syphilis : skrljevo disease among Slovenians : the development and spreading of the disease in the first half of the 19th century. Ljubljana: Inštitut za zgodovino medicine Medicinske fakultete, 2001.

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13

Endemic areas of tropical infections. 2nd ed. Toronto: Huber, 1988.

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14

Montero, Darío Novoa. Miocardiopatía crónica endémica rural venezolana: Chagásica? Mérida, Venezuela: Gobernación del Estado Mérida, Consejo de Publicaciones, 1985.

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15

Homei, Aya. Chapter 4 Endemic Mycoses and Allergies: Diseases of Social Change. Basingstoke: Springer Nature, 2013.

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16

Zinsser, Hans. Rats, lice, and history: Being a study in biography, which, after twelve preliminary chapters indispensable for the preparation of the lay reader, deals with the life history of typhus fever ... New York, NY: Black Dog & Leventhal Publishers, 1996.

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17

Zinsser, Hans. Rats, lice and history: A study in biography. New Brunswick, N.J: AldineTransaction, 2007.

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18

Rats, lice, & history: Being a study in biography, which, after twelve preliminary chapters indispensable for the preparation of the lay reader, deals with the life history of typhus fever ... London: Papermac, 1985.

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19

Zinsser, Hans. Rats, lice, and history. New Brunswick: Transaction Publishers, 2008.

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20

Schettler, Gotthard, ed. Endemic Diseases and Risk Factors for Atherosclerosis in the Far East. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-83358-8.

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21

1932-, Dunn John T., ed. Towards the eradication of endemic goiter, cretinism, and iodine deficiency: Proceedings of the V Meeting of the PAHO/WHO Technical Group on Endemic Goiter, Cretinism, and Iodine Deficiency. Washington, D.C., U.S.A: Pan American Health Organization, Pan American Sanitary Bureau, 1986.

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22

Studart, Studart Guilherme. Climatologia, epidemias e endemias do Ceará. Fortaleza: Fundação Waldemar Alcântara, 1997.

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23

International, Thyroid Symposium (1984 Budapest Hungary). Treatment of endemic and sporadic Goitre: International thryoid symposium, October 18-21, 1984, Budapest. Stuttgart: Schattauer, 1985.

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24

Freitas, Celso Arcoverde de. Histórias da peste e de outras endemias. [Rio de Janeiro]: Programa de Educação Continuada da Escola Nacional de Saúde Pública, 1988.

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25

Freitas, Celso Arcoverde de. Histórias da peste e de outras endemias. [Rio de Janeiro]: Programa de Educação Continuada da Escola Nacional de Saúde Pública, 1988.

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26

National Workshop on the Control of Iodine Deficiency Disorders (IDD) (2nd 1985 Arusha, Tanzania). Towards the eradication of endemic goitre, cretinism, and iodine deficiency in Tanzania: Proceedings of the Second National Workshop on the Control of Iodine Deficiency Disorders (IDD), held at the Arusha International Conference Centre, November 18-20th, 1985. Dar es Salaam: TFNC, 1988.

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27

Williams, Carroll B. Incidence and effects of endemic populations of forest pests in young mixed-conifer forests of the Sierra Nevada. Berkeley, Calif: Pacific Southwest Research Station, 1992.

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28

Alvarez, Elías Delgado. Bocio endémico en Asturias: 10 años de profilaxis con sal yodada. [Oviedo]: Universidad de Oviedo, 1996.

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29

editor, Márquez Morfín Lourdes, Centro de Investigaciones y Estudios Superiores en Antropología Social (Mexico), Instituto de Investigaciones Dr. José María Luis Mora, Escuela Nacional de Antropología e Historia (Mexico), and Universidad Nacional Autónoma de México. Instituto de Investigaciones Históricas, eds. El miedo a morir: Endemias, epidemias y pandemias en México : análisis de larga duración. México, D.F: CIESAS, 2013.

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30

Edward, Hutson J., and Fraser Henry, eds. Observations on the changes of the air and the concomitant epidemical diseases in the island of Barbados, 1752-1758. Kingston, Jamaica: University of the West Indies Press, 2011.

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31

Bleiker, K. P. Mountain pine beetle range expansion: Assessing the threat to Canada's boreal forest by evaluating the endemic niche : final report. Victoria, B.C: Pacific Forestry Centre, 2011.

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32

Sacks, Oliver W. The island of the colorblind: And, Cycad island. New York: A.A. Knopf, 1997.

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33

Sacks, Oliver W. The island of the colorblind: And, Cycad island. New York: A.A. Knopf, 1997.

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34

Sacks, Oliver W. The island of the colour-blind: And, Cycad Island. London: Picador, 1997.

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35

Sun, Dianjun. Endemic Disease in China. Springer, 2019.

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36

K, Barraclough Rosemary, ed. Current topics in avian disease research: Understanding endemic and invasive diseases. Washington, D.C: American Ornithologists' Union, 2006.

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37

Radović, Milan, and Adalbert Schiller. Balkan endemic nephropathy. Edited by Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0090_update_001.

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Balkan endemic nephropathy (BEN) is a chronic, slowly progressive tubulointerstitial nephritis, with familial clustering, occurring in several endemic rural regions in countries of the Balkan Peninsula. BEN is characterized by anaemia, tubular proteinuria, renal shrinkage, and slowly declining glomerular filtration rate (GFR). Up to one-third of patients may also develop upper urothelial tumours. The aetiology of BEN is unclear; chronic exposure to aristolochic acid and a polygenic predisposition are the most likely contributing factors. The major pathological characteristics of BEN are symmetrically shrunken, smooth-shaped kidneys, with interstitial fibrosis, mild interstitial inflammation, and tubular atrophy. Diagnosis is usually based upon positive family history of BEN, past or current residence in endemic regions, tubular proteinuria, tubular dysfunctions (such as urine acidification defects, salt wasting, and impaired excretion of ammonia, uric acid, and phosphate), scant urinary sediment, bilateral and symmetrically reduced kidney size, accompanied by severe anaemia, disproportionate to the degree of GFR reduction. There is no specific therapy for BEN; patients should therefore be treated as all patients with chronic kidney disease, in general. The use of distant water supplies or moving to another residence area should be advised to affected families. Careful evaluation for urothelial cancers is mandatory in patients with haematuria.
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38

Emerging And Endemic Pathogens Advances In Surveillance Detection And Identification. Springer, 2010.

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39

Cleverley, Joanne. The imaging of fungal disease. Edited by Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum, and Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0041.

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The imaging of fungal infection is diverse and often non-specific with multiple abnormalities commonly identified, frequently with more than one organ involved. By correlating the clinical information, which should include patient immune status, pre-existing chronic disease, and potential exposure to endemic fungi, and using this information with an awareness of the radiographic findings of fungal infection, a potential diagnosis can be ascertained. In this chapter, the imaging of fungal infection is discussed, concentrating on the various imaging modalities available, their role, and the major organs involved, highlighting any distinguishing radiographic findings, which may help in the search for a definitive diagnosis.
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40

Schofield, C. J. American trypanosomosis (Chagas disease). Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0050.

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American trypanosomosis is due to infection with Trypanosoma cruzi (Protozoa, Kinetoplastidae). This is a widespread parasite of small mammals and marsupials throughout most of the Americas, roughly from the Great Lakes of North America (approx. 42 ° N) to southern Argentina (approx. 46 ° S). It is mainly transmitted by blood-sucking bugs of the subfamily Triatominae (Hemiptera, Reduviidae) which are widespread in the Americas, but rare in the Old World. Except in some research laboratories, and infected immigrants from Latin America, T.cruzi has not been reported from the Old World, although closely-related trypanosome species are commonly found in Old and New World bats.Human infection with T.cruzi is generally known as Chagas disease, taking the name of Brasilian clinician Carlos Justiniano das Chagas who first described it from patients in central Brasil (Chagas 1909). Chagas isolated and described the parasite, correctly deduced most of its life-cycle and clinical symptoms associated with the infection, identified the insect vectors and some of the reservoir hosts, and also trialed initial attempts to control it. He was nominated at least twice for the Nobel prize in medicine (Coutinho and Dias 2000; Lewinsohn 2003).Although difficult to treat, Chagas disease can be controlled by measures to halt transmission, primarily by eliminating domestic populations of the insect vectors, together with serological screening to avoid transmission by blood donation from infected donors. Since 1991, a series of multinational initiatives have used this approach to halt transmission over vast regions of the areas previously endemic for the human infection. Estimated prevalence of the human infection has declined from the 1990 estimate of 16–18 million people infected, to the current estimate of just over 7 million infected (OPS 2006; Schofield & Kabayo 2008). Prevalence is expected to decline further, and control strategies are now being adjusted to develop a sustainable system of disease surveillance, focal vector control, and specific treatment for any new cases (Schofield et al. 2006; WHO 2007). Guidance for diagnosis and treatment is also required for non-endemic countries, where recent years have seen increasing migration from Latin America such that cases of chronic Chagas disease have now been reported from amongst Latin American migrants in Europe, USA and Canada, and Japan, together with some congenital cases and transmission from infected blood donors and by organ transplant.
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41

Good Laboratory Practice Training Manual For The Trainee A Tool For Training And Promoting Good Laboratory Practice Glp Concepts In Disease Endemic Countries. World Health Organization, 2010.

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42

Good Laboratory Practice Training Manual For The Trainer A Tool For Training And Promoting Good Laboratory Pracice Glp Concepts In Disease Endemic Countries. Who, 2010.

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43

Moriuchi, Hiroyuki. Human T-cell Lymphotropic Virus. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190604813.003.0010.

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Human T-cell lymphotropic virus type 1 (HTLV-1), a human retrovirus that infects an estimated 10–20 million people worldwide, has endemic foci in Japan, West and Central Africa, the Caribbean, Central and South America, and Melanesia. Also, it is the etiological agent of a lymphoproliferative malignancy, adult T-cell leukemia/lymphoma (ATLL), as well as chronic inflammatory diseases such as HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). HTLV-1 can be transmitted vertically, sexually, or by blood-borne transmission. ATLL occurs in approximately 5% of carriers who are infected during early childhood, and primary prevention is the only strategy likely to reduce this fatal disease. Children born to carrier mothers acquire the virus predominantly from breastfeeding. In endemic areas, mother-to-child transmission (MTCT) can be significantly reduced by screening pregnant women for the HTLV-1 antibody, followed by replacing breastfeeding with exclusive formula feeding. Indications for serological screening and recommendations for prevention of perinatal transmission are reviewed in this chapter.
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44

Budke, Christine M., Hélène Carabin, and Paul R. Torgerson. Health impact assessment and burden of zoonotic diseases. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0004.

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Numerous zoonotic diseases cause morbidity, mortality and productivity losses in both humans and animal populations. Recent studies suggest that these diseases can produce large societal impacts in endemic areas. Estimates of monetary impact and disease burden provide essential, evidence-based data for conducting cost-benefit and cost-utility analyses that can contribute to securing political will and financial and technical resources. To evaluate burden, monetary and non-monetary impacts of zoonoses on human health, agriculture and society should be comprehensively considered. This chapter reviews the framework used to assess the health impact and burden of zoonoses and the data needed to estimate the extent of the problem for societies. Case studies are presented to illustrate the use of burden of disease assessment for the zoonotic diseases cystic echinococcosis, Taenia solium cysticercosis, brucellosis and rabies.
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45

Thompson, Loyd, and William H. Deaderick. The Endemic Diseases Of The Southern States. Kessinger Publishing, LLC, 2007.

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46

Thompson, Loyd, and William H. Deaderick. The Endemic Diseases Of The Southern States. Kessinger Publishing, LLC, 2007.

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47

Tunnicliffe, Georgia, and Matthew Wise. Pulmonary fungal infections. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199657742.003.0007.

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Pulmonary fungal infections remain relatively uncommon, although they are increasingly diagnosed as a consequence of a growing population of immunocompromised individuals, foreign travel, and improved diagnostic tools. Groups who were not previously thought to be at significant risk of invasive disease are also being recognized. The increasing incidence of fungal lung disease as a consequence of changing patient demographics means that clinicians will encounter cases in outpatient clinics, medical admission departments, and the intensive care unit with increasing frequency. As international travel increases, so too will presentations of endemic mycoses to respiratory physicians practising in the United Kingdom. Many fungi, such as Aspergillus species, are ubiquitous and can cause a spectrum of pulmonary disorders from colonization, leading to hypersensitivity reactions, to invasive disease with high mortality rates. This chapter considers commonly encountered fungi and how diseases associated with them may present.
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48

Ogunbambi, Olabambo, and Yusuf I. Patel. Parasitic infection. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0105.

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Parasitic infections remain prevalent, particularly in the developing world. However, increasing global travel poses a risk of contracting parasitic infections while travelling through endemic areas and therefore all medical practitioners should remain aware of parasitic infections and investigate for them when appropriate. Increased understanding of the relationship of parasites with the immune system has led to some progress with therapeutics but this still lags behind other infectious diseases. In this chapter we outline the musculoskeletal manifestations of parasitic infection and updated therapeutic approaches to these infections. The burden of disease may change with increasing use of potent biologic immunosuppressants and global travel, as seen in HIV-related immunosuppression, but as yet no significant increased incidence of parasitic infection has been reported within 'rheumatic diseases' cohorts around the world.
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49

Reaching a Billion - Fifth progress report on the London Declaration on NTDs: Ending Neglected Tropical Diseases: A gateway to Universal Health Coverage. Uniting to Combat NTDs, 2017.

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50

Burdmann, Emmanuel A., and Vivekanad Jha. Rickettsiosis. Edited by Vivekanand Jha. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0193.

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Rickettsiae are obligate intracellular bacteria transmitted by arthropods to a vertebrate host. Clinically relevant rickettsioses have a similar clinical pattern, manifesting as an acute febrile disease accompanied by headache, articular and muscle pain, and malaise.Epidemic typhus is a worldwide distributed disease caused by the Rickettsia prowazekii, with a human louse as a vector. Data on epidemic typhus-related renal injury is extremely scarce.Murine typhus is caused by the Rickettsia typhi and has a rodent flea as the vector. It is one of the most frequent rickettsioses, and is usually a self-limited febrile illness. Proteinuria, haematuria, elevations in serum creatinine (SCr) and/or blood urea nitrogen (BUN) and AKI have been reported. The real frequency of renal involvement in murine typhus is unknown. Renal abnormalities recover after the infectious disease resolution.Scrub typhus, caused by the Orientia tsutsugamushi, has the Leptotrombidium mite larva as vector. It is endemic in the Tsutsugamushi triangle delimited by Japan, Australia, India, and Siberia. It can manifest either as a self-limiting disease or as a severe, life-threatening multiorgan illness. Early administration of adequate antibiotics is essential to prevent adverse outcomes. Proteinuria, haematuria, and acute kidney injury (AKI) are frequent.Tick-borne rickettsioses are caused by bacteria from the spotted fever group and have ticks as vectors. Rocky Mountain spotted fever (RMSF) is caused by Rickettsia rickettsii. It is the most severe of the spotted fever rickettsial diseases, causing significant morbidity and lethality. RMSF occurs in North, Central, and South America. Renal impairment is frequent in severe forms of RMSF. Mediterranean spotted fever is caused by Rickettsia conorii, and is endemic in the Mediterranean area. It is usually a benign disease, but may have a severe course, clinically similar to RMSF. Haematuria, proteinuria, increased serum creatinine, and AKI may occur. Japanese spotted fever is caused by Rickettsia japonica. Lethal cases are reported yearly and AKI has occurred in the context of multiple organ failure.
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