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1
James, Shelhamer, ed. Respiratory disease in the immunosuppressed host. J.B. Lippincott, 1991.
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2
Nestlé Nutrition Workshop (64th 2009 Sydney, N.S.W.). Microbial host-interaction: Tolerance versus allergy. Edited by Brandtzaeg Per, Isolauri Erika, Prescott Susan L, and Nestlé Nutrition Institute. Nestec, 2009.
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3
International Symposium on Pyelonephritis (4th 1986 Göteborg, Sweden). Host-parasite interactions in urinary tract infections: Proceedings of the Fourth International Symposium on Pyelonephritis held in Göteborg, Sweden, 23-25 June 1986. University of Chicago Press, 1989.
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4
W, Donachie, Griffiths E. 1940-, Stephen J, and Society for General Microbiology, eds. Bacterial infections of respiratory and gastrointestinal mucosae. Published for the Society for General Microbiology by IRL Press, 1988.
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5
Kimpen, Jan L. L., and Octavio Ramilo. Microbe-Host Interface in Respiratory Tract Infections. Taylor & Francis Group, 2004.
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6
Kimpen, Jan L. L., and Octavio Ramilo. Microbe-Host Interface in Respiratory Tract Infections. Taylor & Francis Group, 2004.
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7
Jan L. L. Kimpen (Editor) and Octavio Ramilo (Editor), eds. The Microbe-Host Interface in Respiratory Tract Infections. CRC, 2004.
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8
Ali, Ased, and Rob Pickard. Infection of the lower urinary tract. Edited by Neil Sheerin. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0176_update_001.
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Lower urinary tract infection is common, distressing, and when recurrent can have a significant impact on quality of life. The normally sterile urinary tract is the site of an ongoing but complex interplay between an evolving pathogen and a highly developed host immune defence system. The development of an active infection generally requires either greater virulence in the pathogen or deficient host immune defence. Nonetheless, even where infection has occurred, the interplay between pathogen and host continues, influencing the extent and level of invasion as well as the duration of infection and extent of tissue damage caused.Asymptomatic bacteriuria is discussed, with implications for treatment (usually not). The risk factors, diagnosis and management of simple cystitis are discussed, with a discussion of approaches to managing recurrent infections. Urethritis requires consideration of sexually transmitted infections and co-infections. Prostatitis requires more prolonged antibiotic treatment.
9
Storey, Elsdon. The Expanded Polyglutamine Tract Spinocerebellar Ataxias. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0013.
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The spinocerebellar ataxias are dominantly-inherited neurodegenerative disorders whose major clinical feature is incoordination. Although 32 have been described to date, those characterized by (CAG)n repeat expansions resulting in elongated polyglutamine tracts in their respective host proteins (SCAs 1, 2, 3, 6, 7, 17, and in part 8) are the most common and have been subject to the most detailed investigation of their pathogenic mechanisms. All are characterized by polyglutamine tract aggregates, toxicity of which was initially thought to be their pathogenic mechanism. However, recent research has emphasised the importance of host protein context, and the disease-specific mechanisms that this implies.
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Grabe, Magnus, and Björn Wullt. Urinary tract infection. Edited by Rob Pickard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0004.
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Infections of the urinary tract are among the most frequent infections encountered in the community and hospital environments. They range from harmless self-curing cystitis to severe pyelonephritis with life-threatening sepsis. Urinary tract infections are often recurrent. Host defence is crucial to control the infection but can also be deleterious in terms of scar formation. Early diagnosis, determination of severity, evaluation of possible risk factors, and assumption of possible pathogen are essential aspects to initiate efficient treatment. Urine culture with antibiotic sensitivity testing is the most important tool to confirm a suspected clinical diagnosis and direct treatment. Patients with urological disease are particularly susceptible to urinary tract infections, and healthcare-associated urinary infections are observed in approximately 10% of hospitalized urological patients. In view of the worsening resistance pattern of common urinary pathogens against available antimicrobial agents, it is important to comply with recommended treatment regimens.
11
(Editor), Edward H. Kass, and Catharina Svanborg Eden (Editor), eds. Host-Parasite Interaction in Urinary Tract Infections (Studies in Infectious Diseases Research). University Of Chicago Press, 1989.
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12
Jacobs, Samantha E., Catherine B. Small, and Thomas J. Walsh. Fungal diseases of the respiratory tract. 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/9780198755388.003.0030.
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Fungal respiratory infections are important causes of morbidity and mortality in immunocompromised patients. Invasive aspergillosis remains the most common invasive fungal infection whereas other filamentous fungi, such as Fusarium spp., Mucorales, and Scedosporium spp., are increasing in frequency, particularly in neutropenic hosts. Endemic mycoses, including those due to Histoplasma capsulatum, Coccidioides spp., and Talaromyces marneffei, are increasingly prevalent in patients with cell-mediated immunodeficiencies in respective geographic regions. Culture remains the gold standard of diagnosis but has limited sensitivity and often requires invasive procedures. Non-invasive diagnostic tests, including the serum sandwich enzyme immunoassay for the detection of galactomannan, the (1→3)-β-D-glucan assay, and molecular amplification methods have been developed to facilitate early and accurate diagnosis. Successful therapy depends upon early initiation of antifungal agents and reversal of immunosuppression. Lipid formulations of amphotericin B and newer generation triazoles including voriconazole, posaconazole, and isavuconazole have expanded the ability to treat multi-drug resistant pathogens more effectively and with less toxicity.
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Urinary Tract Infections - the Imbalance Between the Pathogen Virulence and the Host Defense [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.91541.
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Jarzembowski, Tomas, Agnieszka Daca, and Maria Alicja Dębska-Ślizień, eds. Urinary Tract Infection - The Result of the Strength of the Pathogen, or the Weakness of the Host. InTech, 2018. http://dx.doi.org/10.5772/intechopen.68271.
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Papaioannou, Vasilios, Ioannis Pneumatikos, Ibrahim A. Janahi, and Robert Naeije. Urinary Tract Infection - the Result of the Strength of the Pathogen, or the Weakness of the Host. DI Press, 2022.
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16
Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Prebiotics and probiotics in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0027.
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Probiotics are live, non-pathogenic commensal microorganisms with beneficial effects on the host organism; they improve and/or maintain intestinal flora balance by suppressing and displacing harmful bacteria. Prebiotics are nondigestible food components that stimulate growth or activity of these beneficial intestinal bacteria. Such microorganisms form an integral part of the intestinal mucosal defence system and are important for the development and maturation of the infant#amp;#x2019;s gastrointestinal tract. Maternal ingestion of probiotics and prebiotics from dietary sources during pregnancy, or by the infant at weaning, may enhance the development and maturation of the neonatal gastrointestinal tract. Probiotic foods may also help control insulin resistance and the development of gestational diabetes.
17
Sohn, Woon-Mok, and Jong-Yil Chai. Anisakiosis (Anisakidosis). Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0070.
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The term ‘anisakiosis (anisakidosis)’ or ‘anisakiasis’ collectively defines human infections caused by larval anisakids belonging to the nematode family Anisakidae or Raphidascarididae. Anisakis simplex, Anisakis physeteris, and Pseudoteranova decipiens are the three major species causing human anisakiosis. Various kinds of marine fish and cephalopods serve as the second intermediate hosts and the infection source. Ingestion of viable anisakid larvae in the fillet or viscera of these hosts is the primary cause of infection. The parasite does not develop further in humans as they are an accidental host. Clinical anisakiosis develops after the penetration of anisakid larvae into the mucosal wall of the alimentary tract, most frequently the stomach and the small intestine. The affected sites undergo erosion, ulceration, swelling, inflammation, and granuloma formation around the worm. The patients may suffer from acute abdominal pain, indigestion, nausea, vomiting, and in some instances, allergic hypersensitive reactions. Symptoms in gastric anisakiosis often resemble those seen in peptic ulcer or gastric cancer, and symptoms in intestinal anisakiosis resemble those of appendicitis or peritonitis. Treatments include removal of larval worms using a gastroendoscopic clipper or surgical resection of the mucosal tissue surrounding the worm. No confirmed effective anthelmintic drug has been introduced, though albendazole and ivermectin have been tried in vivo and in vitro. Prevention of human anisakiosis can be achieved by careful examination of fish fillet followed by removal of the worms in the restaurant or household kitchen. Immediate freezing of fish and cephalopods just after catching them on fishing boats was reported helpful for prevention of anisakiosis. It is noteworthy that anisakiosis is often associated with strong allergic and hypersensitivity reactions, with symptoms ranging from isolated angioedema to urticaria and life threatening anaphylactic shock.
18
Heyns, Chris. Tuberculosis and parasitic infestations involving the urogenital system. Edited by Rob Pickard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0006.
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Urogenital tuberculosis is caused by Mycobacterium tuberculosis, which evokes a granulomatous tissue reaction leading to caseous necrosis, fibrosis, and eventual calcification. It most commonly presents as cystitis with sterile pyuria but can show many other symptoms and signs requiring a high index of suspicion to make the diagnosis. Schistosomiasis (Bilharzia) affecting the urinary tract is caused by the flatworm Schistosoma haematobium. Humans are infested by contact with fresh water harbouring the intermediate snail host. Echinococcosis (hydatid disease), is caused by the tapeworm Echinococcus granulosis or multilocularis. Human infection results from close contact with the parasite host (usually dogs and sheep). Filariasis, caused by the roundworm Wuchereria bancrofti, is transmitted by mosquito bite
19
Jex, Aaron R., Rachel M. Chalmers, Huw V. Smith, Giovanni Widmer, Vincent McDonald, and Robin B. Gasser. Cryptosporidiosis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0053.
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Cryptosporidium species represent a genus of parasitic protozoa (Apicomplexa) that are transmitted via the faecal-oral route and commonly infect the epithelial tissues of the gastric or intestinal (or sometimes the respiratory) tract of many vertebrates, including humans. Infection occurs following the ingestion of viable and resistant oocysts, through direct host-to-host contact or in contaminated food, drinking or recreational water. Infection can be transmitted via anthroponotic (human-to-human, human-to-animal) or zoonotic (animal-to-human or animal-to-animal) pathways, depending upon the species of Cryptosporidium. Although infection can be asymptomatic, common symptoms of disease (cryptosporidiosis) include diarrhoea, colic (abdominal pain), nausea or vomiting, dehydration and/or fever. In humans, cryptosporidial infection in immunocompetent patients is usually short-lived (days to weeks) and eliminated following the stimulation of an effective immune response. However, infection in immunodeficient individuals (e.g., those with HIV/AIDS) can be chronic and fatal (in the absence of immunotherapy), as there are few effective anti-cryptosporidial drugs and no vaccines available. The present chapter provides an account of the history, taxonomy and biology, genomics and genetics of Cryptosporidium, the epidemiology, pathogenesis, treatment and control of cryptosporidiosis and the advances in tools for the identification and characterisation of Cryptosporidium species and the diagnosis of cryptosporidiosis.
20
Cooke, Graham. Viral infection. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0308.
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Viral infection includes any clinical illness caused by a pathogenic virus. Acute viral infections are amongst the most common illnesses of humans and range from minor upper respiratory tract infections to viral haemorrhagic fever. The principles in diagnosing acute viral infection are, first, recognize the syndrome, then identify key features that might suggest a specific diagnosis, and, finally, consider laboratory investigations to elucidate the specific causative agent. The host–pathogen response determines different outcomes for specific viral infections. After infection with some viruses (e.g. measles virus, rubella virus) protective immunity develops, there is no latency or chronic carriage, and reinfection is prevented. Another group of viruses, in the presence of inadequate immune response, can cause chronic infection (e.g. hepatitis B and C viruses). This chapter reviews the clinical features, diagnosis, and management of acute viral infections in immunocompetent individuals.
21
Young, Raymond. Infection in the Patient with Sickle Cell Anemia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0060.
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This chapter provides a brief overview of the clinical manifestations of and management strategies for infectious complications in the immunocompromised sickle cell disease patient. The chapter discusses infections in various organ systems, including the respiratory tract, central nervous system, bone, hematopoietic cell lineage, and blood-borne infections. Differentiating infections from noninfectious processes that often have similar presentations in the sickle cell patient may at times be difficult, and clinicians managing sickle cell patients should be keenly aware of this fact. This chapter discusses the common bacterial pathogens associated with infection and a notable viral agent known to profoundly worsen anemia in the sickle cell host, parvovirus B19. Additionally, fundamental antimicrobial regimens and primary and secondary prophylactic strategies are included in this concise summary prepared for clinicians involved in the acute care management of the sickle cell patient.
22
Limaye, Ajit P., and Lynne Strasfeld. Introduction. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199938568.003.0200.
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Chapter 2 focuses on the solid organ transplantation (SOT). The Solid organ transplantation (SOT) is undertaken to restore organ function for patients with failing or end-stage disease of the liver, heart, lung, kidneys, and/or pancreas or to re-establish function in patients with short gut or other disorders of the intestinal tract. Organ transplantation requires lifelong maintenance immune suppression to prevent organ rejection. Infection can be related to donor transmission, reactivation from latency in the recipient, or acquisition de novo post-transplant. The evaluation of suspected infection in SOT recipients is guided by the clinical presentation, with likelihood shaped by prophylaxis strategies, host factors, and exposure history. Prompt evaluation is critical, often requiring multimodality imaging, microbiologic testing with cultures and molecular diagnostics, and invasive diagnostics or biopsy. The chapter concludes that, through use of biomarkers and indicators of pathogen-specific immune competence as well as better laboratory assessment of overall immune competence, a more granular identification of those SOT recipients at highest risk for infection will allow for optimization of prophylaxis and other infection prevention strategies.
23
Pozio, Edoardo. Trichinellosis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0068.
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Trichinellosis is caused by nematodes of the genus Trichinella. These zoonotic parasites show a cosmopolitan distribution in all the continents, but Antarctica. They circulate in nature by synanthropic-domestic and sylvatic cycles. Today, eight species and four genotypes are recognized, all of which infect mammals, including humans, one species also infects birds, and two other species infect also reptiles.Parasites of the genus Trichinella are unusual among the other nematodes in that the worm undergoes a complete developmental cycle, from larva to adult to larva, in the body of a single host, which has a profound influence on the epidemiology of trichinellosis. When the cycle is complete, the muscles of the infected animal contain a reservoir of larvae, capable of long-term survival. Humans and other hosts become infected by ingesting muscle tissuescontaining viable larvae.The symptoms associated with trichinellosis vary with the severity of infection, i.e. the number of viable larvae ingested, and the time after infection. The capacity of the worm population to undergo massive multiplication in the body is a major determinant. Progression of disease follows the biological development of the parasite. Symptoms are associated first with the gastrointestinal tract, as the worms invade and establish in the small intestine, become more general as the body responds immunologically, and finally focus on the muscles as the larvae penetrate the muscle cells and develop there. Although Trichinella worms cause pathological changes directly by mechanical damage, most of the clinical features of trichinellosis are immunopathological in origin and can be related to the capacity of the parasite to induce allergic responses.The main source of human infection is raw or under-cooked meat products from pig, wild boar, bear, walrus, and horses, but meat products from other animals have been implicated. In humans, the diagnosis of infection is made by immunological tests or by direct examination of muscle biopsies using microscopy or by recovery of larvae after artificial digestion. Treatment requires both the use of anthelmintic drugs to kill the parasite itself and symptomatic treatment to minimize inflammatory responses.Both pre-slaughter prevention and post-slaughter control can be used to prevent Trichinella infections in animals. The first involves pig management control as well as continuous surveillance programmes. Meat inspection is a successful post-slaughter strategy. However, a continuous consumer education is of great importance in countries where meat inspection is not mandatory.
24
Thomas, Daniel Rh. Other bacterial diseasesPasteurellosis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0021.
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Pasteurellosis is a zoonosis that occurs worldwide, caused by bacteria of the genus Pasteurella, and other related organisms. Pasteurellosis reported in humans is most frequently caused by the species Pasteurella multocida. In humans, cutaneous infection is most common, but more severe outcomes have been reported, particularly in those with underlying chronic disease. Infection in animals is usually subclinical, but may give rise to a range of clinical symptoms, depending on the host species. Disease in animals usually occurs as a consequence of stress such as overcrowding, chilling, transportation, or as a result of a concurrent infection. In animals, pasteurellosis is known as: shipping fever or pneumonia, transport or transit fever, stockyard pneumonia, bovine pneumonic pasteurellosis, haemorrhagic septicaemia, or avian, bird or fowl cholera. The pasteurella bacterium is commonly present in the mouth and gastrointestinal tract of a wide range of mammals. Transmission to humans occurs after bites, scratches, or licks from infected animals, most frequently from dogs or cats, although infection has been associated with other animals including: cows, pigs, hamsters and rabbits. However, not all patients report a history of direct animal contact. Infection may be prevented through the avoidance of animal bites and the prompt hygienic care of wounds. Health professionals should be aware of the risk of pasterurellosis in immunocompromised patients exposed to companion animals.
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Weiss, Louis M. Microsporidiosis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0056.
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The class or order Microsporidia was elevated in to the phylum Microspora by Sprague and Vavra (1997) and Sprague and Becnel (1998) subsequently suggested that the term Microsporidia instead be used for the phylum name. Miicrosporidia, i.e. Nosema bombycis, were first described about 150 years ago as the cause of the disease pebrine in silkworms. In 1922, there were descriptions of gram-positive spores consistent with microspordiosis in the brain of rabbits that were being used for investigations on poliomyelitis (Wright and Craighead 1922). From 1923 to 1926, Levaditi and colleagues studied the organisms seen by Wright and Craighead, which they named Encephalitozoon cuniculi, recognizing them as Microsporidia and demonstrating their lack of host specificity by transmitting infections from rabbits to mice, rats and dogs (Levaditi et al. 1923). Microsporidia were clearly confirmed of being a cause of human disease in 1959 (Matsubayashi et al. 1959), when they were isolated from the cerebrospinal fluid of a 9 year old boy with encephalitis with seizures, coma, and fever lasting about 25 days. Bergquist et al. (1984) reported a 2 year old child with encephalitis and seizures who had Encephalitozoon spores in urine and Margileth et al. (1973) isolated the microsporidium Anncaliia (Nosema) connori from a 4 month old athymic male infant who died with severe diarrhoea and malabsorption. Microsporidia can produce a wide range of clinical diseases. A diarrhoeal syndrome associated with microsporidiosis and HIV infection was reported by Desportes et al. (1985) and the number of articles describing human disease increased rapidly after 1990. In addition to gastrointestinal tract involvement, it has been recognized that Microsporidia can infect virtually any organ system; and patients with encephalitis, ocular infection, sinusitis, myositis, and disseminated infection are well described in the literature.
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Bowman, Dwight D. Zoonotic hookworm infections. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0069.
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Hookworms on occasion cause creeping lesions in the superficial layers of the human skin that have been designated as cutaneous larva migrans for the purpose of contrasting the condition with visceral larva migrans. Currently, the disease is presenting most commonly to physicians specializing in tropical or travel medicine in patients who have just visited a tropical beach and are presenting with serpiginous tracks in their skin. The serpiginous tracts can persist for week, and are often pruritic, may be associated with accompanying bulla, and can rarely lead to secondary sequelae. The larval are likely to penetrate ultimately to deeper tissues, where they may be persisting in the tissues of humans in the same fashion as they would within the tissues of any other vertebrate paratenic host.Most hookworm larvae are capable of penetrating the skin and causing lesions that are similar to cutaneous larvae migrans. However, the geographic distribution of cases still seems to suggest that only one species, A. braziliense, is the offending species. The other species appear to spend less time in the skin of the human host, and if they do cause lesions, they appear to produce lesions that are more vesicular or that cause disease of a markedly shorter duration. It seems that the development of improved molecular methods will ultimately lead to the means of more carefully discrimination the geographical location of the offending species and may someday be able to identify specific larvae from lesions.There are other manifestations of zoonotic hookworm infection. These include the infection of the human intestinal tract with the adults of the canine/feline hookworm Ancylostoma ceylanicum; the induction of cases of eosinophilic colitis in people with the canine hookworm, Ancylostoma caninum; suspected cases of ocular larva migrans due to hookworm larvae, and the rare case of cutaneous larva migrans due to hookworm species that are only rarely associated with human infections.