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Libros sobre el tema "Bacterial kidney disease (Fish disease)"

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Publicado: 4 de junio de 2021
Última modificación: 17 de febrero de 2022

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1

Moffitt, Christine A. FDA approved registration of erythromycin for treatment of bacterial kidney disease (BKD) in juvenile and adult chinook salmon: Annual report, reporting period: year 1, 10 March 1989 - 9 March 1990. Portland, OR: U.S. Dept. of Energy, Bonneville Power Administration, Division of Fish and Wildlife, 1991.

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2

O'Connor, Glenda. Use of ELISA for monitoring bacterial kidney disease in naturally spawning chinook salmon. Salem, Or: Oregon Dept. of Fish and Wildlife, 2006.

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3

Kaattari, S. L. Development of a vaccine for bacterial kidney disease in salmon: Final report. Portland, Or: U.S. Dept. of Energy, Bonneville Power Administration, Division of Fish & Wildlife, 1991.

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4

Bruno, David W. Bacterial kidney disease. Aberdeen: Department of Agriculture and Fisheries for Scotland, Marine Laboratory, 1988.

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5

A, Austin D., ed. Bacterial fish pathogens: Disease in farmed and wild fish. 2a ed. New York: E. Horwood, 1993.

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6

A, Austin D., ed. Bacterial fish pathogens: Disease in farmed and wild fish. Chichester: E. Horwood, 1987.

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7

Bullock, G. L. Bacterial kidney disease of salmonid fishes caused by Renibacterium salmoninarum. Washington, D.C: U.S. Dept. of the Interior, Fish and Wildlife Service, Research and Development, 1988.

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8

Stephen, Kaattari, United States. Bonneville Power Administration. Division of Fish and Wildlife. y Oregon State University. Dept. of Microbiology., eds. Development of a vaccine for bacterial kidney disease in salmon: Annual report FY 1984. Portland, Or: U.S. Dept. of Energy, Bonneville Power Administration, Division of Fish & Wildlife, 1985.

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9

Bruno, D. W. Bacterial Kidney Disease (Aquaculture Information Series: 3. 1988). The Stationery Office Books (Agencies), 1988.

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10

Austin, D. A. y B. Austin. Bacterial Fish Pathogens: Disease of Farmed and Wild Fish. Springer, 2010.

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11

Austin, Dawn A. y Brian Austin. Bacterial Fish Pathogens: Disease of Farmed and Wild Fish. Springer, 2018.

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12

Bacterial Fish Pathogens: Disease of Farmed and Wild Fish. Brian Austin, 2012.

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13

Austin, Dawn A. y Brian Austin. Bacterial Fish Pathogens: Disease of Farmed and Wild Fish. Springer, 2016.

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14

Austin, Dawn A. y Brian Austin. Bacterial Fish Pathogens: Disease of Farmed and Wild Fish. Springer, 2012.

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15

Winearls, Christopher G. Kidney disease-focused features on examination. Editado por Christopher G. Winearls. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0005.

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Examination depends on the context and clinical presentation and the emphasis will be different too. Tell-tale signs are often unnoticed in the general examination of the eyes (lecithin cholesterol acyltransferase deficiency, Fabry disease, corneal calcification), the skin (vasculitis, Anderson–Fabry disease), the optic fundus (haemorrhages and exudates, papilloedema), and the hands (nail patella syndrome, splinter haemorrhages of systemic lupus erythematosus, and subacute bacterial endocarditis). Many of these are illustrated. The regular review of patients on dialysis or with a kidney transplant is also considered.
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16

Bacterial Fish Pathogens: Disease of Farmed and Wild Fish (Springer Praxis Books / Environmental Sciences). 4a ed. Springer, 2007.

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17

Bacterial Fish Pathogens: Disease of Farmed and Wild Fish (Springer Praxis Books / Aquaculture and Fisheries). 3a ed. Springer, 1999.

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18

Holt, Richard Allen. Cytophaga psychrophila, the causative agent of bacterial cold-water disease in salmonid fish. 1987.

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19

Mesa, Matthew G. Ecological influence of bacterial kidney disease on juvenile spring chinook salmon: Effects on predator avoidance ability, smoltification, and physiological responses to stress. 1999.

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20

Morgan, Marina. Other bacterial diseasesStreptococcosis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0023.

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Many pyogenic (β -haemolytic) streptococci of clinical significance have animal connections. In the last edition of this book two species of streptococci were considered of major zoonotic interest, namely Streptococcus suis and S. zooepidemicus. Since then, numerous sporadic zoonoses due to other streptococci have been reported, and a newly recognized fish pathogen with zoonotic potential termed S. iniae has emerged. Changes in nomenclature make the terminology confusing. For example, the organism known as S. zooepidemicus — now termed S. dysgalactiae subsp. zooepidemicus — still causes pharyngitis in humans, complicated rarely by glomerulonephritis after ingestion of unpasteurized milk. Pigs remain the primary hosts of S. suis with human disease mainly affecting those who have contact with pigs or handle pork.Once a sporadic disease, several major epidemics associated with high mortality have been reported in China. The major change in reports of zoonotic streptococcal infections has been the emergence of severe skin and soft tissue infections, and an increasing prevalence of toxic shock, especially due to S. suis (Tang et al. 2006), group C (Keiser 1992) and group G β -haemolytic streptococci (Barnham et al. 2002). Penicillin remains the mainstay of treatment for most infections, although some strains of group C and G streptococci are tolerant (minimum bactericidal concentration difficult or impossible to achieve in vivo) (Portnoy et al. 1981; Rolston and LeFrock 1984) and occasionally strains with increased minimum inhibitory concentrations (MIC) for penicillin are reported.Agents preventing exotoxin formation, such as clindamycin and occasionally human intravenous immunoglobulin, may be used in overwhelming infection where circulating exotoxins need to be neutralized in order to damp down the massive release of cytokines generated by their production (Darenberg et al. 2003). Prevention of human disease focuses on maintaining good hygienic practice when dealing with live animals or handling raw meat or fish products, covering skin lesions, thorough cooking of meats and pasteurization of milk.
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21

Birtles, Richard. Other bacterial diseasesAnaplasmosis, ehrlichiosis and neorickettsiosis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0020.

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In 2001, taxonomic reorganization of the bacterial genera Anaplasma, Ehrlichia, Cowdria and Neorickettsia resulted in the transfer of numerous species between these taxa, and the renaming of the transferred species to reflect their new taxonomic position (Dumler et al. 2001). Among the members of these genera, there are four species of established zoonotic importance, which are therefore the subject of this chapter. Two of these species were affected by the changes outlined above.Although these four species possess markedly different ecologies, they share the fundamental biological character of being obligate intracellular bacteria that reside within vacuoles of eukaryotic cells. This lifestyle underlies their fastidious nature in the laboratory and hence our limited knowledge of their biology and pathogenicity. Nonetheless, despite this shortfall, all four are associated with diseases of established or emerging importance: E. chaffeensis provokes human monocytic ehrlichiosis (HME), E. ewingii causes human ewingii ehrlichiosis (HEE), A. phagocytophilum causes human granulocytic anaplasmosis (HGA), N. sennetsu is the agent of sennetsu neorickettsiosis.The first three pathogens are transmitted by hard (ixodid) ticks and are encountered across the temperate zones of the northern hemisphere (and maybe beyond), although the vast majority of human infections caused by them are currently reported in the USA. There, HME and HGA are second only to Lyme disease (caused by Borrelia burgdorferi) in terms of public health significance. Furthermore, given that there is evidence of increasing population sizes and changing distributions for ixodid species (Scharlemann et al. 2008), it is not unreasonable to predict that the infections they transmit will present an increased medical burden in the future. N. sennetsu remains an enigmatic pathogen; case reports remain scarce, but serological surveys suggest high levels of exposure. The widespread consumption of raw fish across east Asia presents specific infection risks to this region, and an increased awareness that sennetsu neorickettsiosis is among the infections that can be acquired from this source is required before its public health importance can be accurately assessed.
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22

Cárdenas, Andrés y Pere Ginès. The patient with hepatorenal syndrome. Editado por Giuseppe Remuzzi. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0169_update_001.

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Hepatorenal syndrome (HRS) is a dreaded and common complication of patients with end-stage liver disease. The syndrome is characterized by functional renal failure due to renal vasoconstriction in the absence of underlying kidney pathology. The pathogenesis of HRS is the result of an extreme underfilling of the arterial circulation secondary to an arterial vasodilation located in the splanchnic circulation. This phenomenon triggers a compensatory response with activation of vasoconstrictor systems leading to intense renal vasoconstriction.Besides HRS, there are several other causes of renal failure in patients with cirrhosis including those secondary to bacterial infections, hypovolaemia, nephrotoxicity, and intrinsic renal disease. Thus, the diagnosis of HRS is based on established diagnostic criteria aimed at excluding non-functional causes of renal failure.The prognosis of patients with HRS is poor, especially in those who have a rapidly progressive course. Liver transplantation is the best option in suitable candidates, but it is not always applicable due to the short survival expectancy of listed candidates.Pharmacological therapies based on the use of vasoconstrictor drugs to reverse splanchnic vasodilation are the standard first line of therapy. The vasopressin analogue terlipressin is the best proven. Transjugular intrahepatic portosystemic shunts may be helpful in limited circumstances. Prevention of HRS can be attained with the use of albumin infusion in patients with spontaneous bacterial peritonitis, with norfloxacin in patients very advanced liver disease and with N-acetylcysteine in those with severe acute alcoholic hepatitis.
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23

Eastwood, John, Cathy Corbishley y John Grange. Mycobacterial infections. Editado por Vivekanand Jha. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0197.

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Mycobacterium leprae, the causative agent of leprosy, is one of over a hundred species of Mycobacteria. The many other species are environmental saprophytes, present particularly in free and piped water sources, and some species are causes of opportunist disease in humans, especially in those who are immune compromised.In 2009, world-wide notifications of leprosy amounted to 244,796 new cases, a significant fall compared with 514,718 in 2003. Elimination of leprosy as a public health problem, defined as a prevalence of registered cases of under 1 per 10,000 population, has been achieved in many countries where leprosy was once highly endemic, and most others are close to reaching this stage.Direct bacterial invasion of the kidney is rare in leprosy but renal amyloidosis and various forms of glomerulonephritis are common, especially those with multibacillary forms of the disease.Renal disease due to environmental mycobacteria is very rare but as these bacteria are frequently present as contaminants of the lower urethra and external genitalia, care is required to distinguish disease from contamination of urine samples.The risk of generalized disease due to environmental mycobacteria is increased by any form of immune compromise including renal failure and post-renal transplant immunosuppression.
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24

Barsoum, Rashad S. Schistosomiasis. Editado por Vivekanand Jha. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0194_update_001.

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The urinary system is the primary target of Schistosoma haematobium infection, which leads to granuloma formation in the lower urinary tract that heals with fibrosis and calcification. While the early lesions may be associated with distressing acute or subacute symptoms, it is the late lesions that constitute the main clinical impact of schistosomiasis. The latter include chronic cystitis, ureteric fibrosis, ureterovesical obstruction or reflux which may lead to chronic pyelonephritis. Secondary bacterial infection and bladder cancer are the main secondary sequelae of urinary schistosomiasis.The kidneys are also a secondary target of S. mansoni infection, attributed to the systemic immune response to the parasite. Specific immune complexes are responsible for early, often asymptomatic, possibly reversible, mesangioproliferative lesions which are categorized as ‘class I’. Subsequent classes (II–VI) display different histopathology, more serious clinical disease, and confounding pathogenic factors. Class II lesions are encountered in patients with concomitant salmonellosis; they are typically exudative and associated with acute-onset nephrotic syndrome. Classes III (mesangiocapillary glomerulonephritis) and IV (focal segmental sclerosis) are progressive forms of glomerular disease associated with significant hepatic pathology. They are usually associated with immunoglobulin A deposits which seem to have a significant pathogenic role. Class V (amyloidosis) occurs with long-standing active infection with either S. haematobium or S. mansoni. Class VI is seen in patients with concomitant HCV infection, where the pathology is a mix of schistosomal and cryoglobulinaemic lesions, as well as amyloidosis which seems to be accelerated by the confounded pathogenesis.Early schistosomal lesions, particularly those of the lower urinary tract, respond to antiparasitic treatment. Late urological lesions may need surgery or endoscopic interventions. As a rule, glomerular lesions do not respond to treatment with the exception of class II where dual antiparasitic and antibiotic therapy is usually curative. Patients with end-stage kidney disease may constitute specific, yet not insurmountable technical and logistic problems in dialysis or transplantation. Recurrence after transplantation is rare.
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