Bk Polyoma Virus
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The document discusses BK polyomavirus, which is a double-stranded DNA virus that can cause BK virus nephropathy (BKVN) in transplant recipients. It is transmitted through multiple routes and reactivates due to immunosuppression after transplantation. BKVN diagnosis involves detecting viral DNA in plasma/urine and identifying viral inclusions on allograft biopsy. While prevention is important, no treatment has proven fully effective against established BKVN. Common approaches include decreasing immunosuppression and off-label use of antivirals like cidofovir or IV immunoglobulin.
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2. Major arboviruses described include yellow fever, dengue, West Nile, Japanese encephalitis, Zika, and chikungunya viruses. Symptoms range from mild fever and rash to severe encephalitis or hemorrhagic fever
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Reduction of immunosuppression is the primary treatment for BK virus-associated nephropathy (BKVAN) in kidney transplant recipients. Other potential adjunctive therapies include cidofovir, leflunomide, intravenous immunoglobulin, and quinolone antibiotics, but large retrospective studies found that only reduction of immunosuppression was not associated with high risk of graft failure. The optimal treatment strategies for BKVAN continue to be evaluated.
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- HPV's role in causing cervical cancer and other cancers and its transmission and symptoms. Treatment involves vaccination and screening but not a cure for the virus itself.
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H P V
This document discusses human papillomavirus (HPV), including its structure, types, life cycle, and role in cervical cancer. Key points include:
- HPV is a small, non-enveloped virus with circular double-stranded DNA. Over 100 types exist, with about 30 causing genital infections.
- Types are classified as low, intermediate, or high risk based on cancer-causing potential. High-risk HPV 16 and 18 cause most cervical cancers.
- HPV spreads through sexual contact and can cause genital warts or remain asymptomatic. Persistent infection can lead to cervical pre-cancer.
- The virus infects epithelial cells and hijacks the host cell cycle to replicate.
Human Papilloma Virus
This document discusses Human Papilloma Virus (HPV) and cervical cancer. It describes the different types of HPV and their association with cervical lesions and cancer. It provides information on HPV vaccination, including efficacy against cervical lesions, safety, and recommendations for vaccination of girls ages 9-13.
How to Make Awesome SlideShares: Tips & Tricks
Turbocharge your online presence with SlideShare. We provide the best tips and tricks for succeeding on SlideShare. Get ideas for what to upload, tips for designing your deck and more.
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kidney transplantation infection
This document discusses infection following renal transplantation. It covers four main categories of exposures that can lead to post-transplant infection: donor-derived, recipient-derived, nosocomial, and community. It then discusses the timeline of various infections, highlighting that CMV and opportunistic infections are most common in the first 6 months. BK virus is also reviewed in depth, including its virology, risk factors for BK virus nephropathy, diagnosis, clinical management and treatment through immunosuppression modification. Cytomegalovirus infection is also summarized, covering terminology, risk factors, diagnostic methods including histopathology, viral culture, serology and molecular assays to detect viral load.
Dng hbv -kidney disease
This document provides an overview of hepatitis B virus (HBV)-associated kidney diseases. It begins with a brief history of HBV discovery. It then describes the structure and life cycle of HBV. The genomic structure contains 4 open reading frames that encode 7 viral proteins. The life cycle involves attachment, entry, replication of DNA in the nucleus, and secretion of complete or empty particles. Genotypes differ in disease severity and treatment response. HBV is transmitted perinatally, sexually, or through blood exposure. Chronic infection can lead to cirrhosis or liver cancer. Renal involvement includes membranous nephropathy, MPGN, and polyarteritis nodosa due to immune complex deposition. Oral antiviral
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This document provides an overview of hepadnaviruses, including hepatitis B virus (HBV). It discusses the history and discovery of HBV in the 1960s. HBV was found to be a major cause of chronic liver disease worldwide. Animal models including woodchucks, ducks, and chimpanzees were later discovered to have hepatitis viruses closely related to HBV and helped advance research. HBV and related viruses share similarities in genome organization and replication and comprise the Hepadnaviridae family.
Chronic hepatitis b
This document discusses chronic hepatitis B infection. It covers the epidemiology of chronic hepatitis B, including that approximately 400 million people are chronically infected worldwide. It also discusses the hepatitis B virus particle, noting it has a 3.2 kb DNA genome that encodes four overlapping genes. Regarding diagnosis, it emphasizes the importance of optimal HBV screening and diagnosis using markers such as HBsAg, HBeAg, anti-HBe and HBV DNA levels.
Ocular tb
This document discusses ocular tuberculosis. It begins with an introduction to tuberculosis as a systemic disease caused by Mycobacterium tuberculosis. It then covers the clinical criteria for systemic TB disease and laboratory diagnostic criteria. It discusses the pathophysiology, transmission, and pathogenesis of TB infection. The document outlines various clinical presentations of ocular TB including anterior uveitis, intermediate uveitis, posterior segment manifestations, neuro-ophthalmic manifestations, adnexal involvement, and drug-related ocular toxicity. Investigations for diagnosing ocular TB such as the Mantoux test, chest imaging, and ocular exams are also summarized.
Cytopathic Effects Of Viral Infections
The document discusses various viral infections and their cytopathic effects, including BK virus, respiratory syncytial virus, cytomegalovirus, and herpes virus. It notes that BK virus can be detected on histology of renal biopsies by its presence in tubular cells as multinucleated cells. Screening of urine specimens can reveal subtle cytopathic changes from BK virus and immunostaining is used to identify the virus in renal biopsies. Clinical problems where viral cytopathic effects are relevant include kidney transplants, bone marrow transplants, HIV/AIDS, liver issues, and various cancers.
Viral Hepatitis
Viral hepatitis is a systemic disease with primary inflammation of the liver by any one of a heterogeneous group of hepatotropic viruses.
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This thesis examines the effects of immunosuppressive drugs tacrolimus (TAC) and sirolimus (SIR) on BK polyomavirus (BKPyV) replication and host cells in vitro. The study finds that treatment with clinically relevant levels of SIR leads to downregulation of host cell processes like DNA replication and metabolism, reducing intracellular viral replication. In contrast, TAC treatment upregulates these host cell processes and may stimulate intracellular viral replication. SIR inhibits mTORC1 signaling pathways in host cells, while TAC activates them. This research provides insight into how immunosuppressive drugs influence BKPyV replication and could help optimize treatment of transplant patients experiencing viral replication.
Catheter Associated Urinary Tract Infection (CAUTI)
Catheter Associated Urinary Tract Infection (CAUTI)Philippine Hospital Infection Contol Nurses Associaton (PHICNA) Inc.
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This document outlines a proposed collaborative project between researchers at NUST in Pakistan and UCSD in the US to study Hepatitis B virus (HBV) genotypes and their association with Hepatocellular Carcinoma (HCC) in Pakistan. The objectives are to characterize HBV genotypes, identify virus mutations that increase risk of HCC, and study the role of cellular editing enzymes and HBx protein. The project will involve sample collection from hospitals, genotyping, sequencing, and in vitro studies over 3 years. The researchers have facilities and expertise to conduct molecular and clinical analyses of HBV in Pakistan where genotype D is prevalent and HBV infection is a major health problem.
Hepatitis
This document discusses viral hepatitis, caused by hepatitis viruses A, B, C, D, E, and G. It provides information on the structure, transmission, clinical features, diagnosis, and prevention of each type of viral hepatitis. Hepatitis A virus is enterically transmitted while hepatitis B, C, and D are typically transmitted parenterally. Hepatitis B and C can cause chronic infection and lead to cirrhosis or liver cancer, while hepatitis A and E do not typically cause chronic infection. Diagnosis involves testing for viral markers and antibodies. Prevention strategies include vaccination, blood donor screening, and risk behavior modification.
Candiduria
A 34-week preterm male infant was admitted to the NICU for respiratory support. During his hospital stay he developed sepsis and his antibiotic was changed. A urine culture then showed Candida albicans. The infant also had rising BUN and creatinine levels and yeast cells were found in his urine analysis. An ultrasound showed a hyperechoic lesion in the left renal pelvis with mild hydronephrosis. Risk factors for candiduria in infants include prematurity, catheterization, impaired immune system, prolonged antibiotic therapy, and underlying diseases. Diagnosis involves urine culture and microscopy to identify yeast cells. Treatment depends on the severity and location of infection.
Cytomegalovirus infection in kidny transplantation
HCMV infection is a frequent complication of kidney transplantation, especially in the period 1 to 4 months after transplantation. Overall incidences of HCMV infection and disease during the first 100 days post-transplantation, 60% and 25% respectively, when no HCMV prophylaxis or pre-emptive therapy is given. HCMV infection is an independent risk-factor for kidney graft rejection and associated with high morbidity and mortality rates .
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This document provides a history of the discovery of hepatitis B virus (HBV). HBV was originally identified in the 1960s and associated with serum hepatitis. It was found to be a unique DNA virus that replicates via reverse transcription of an RNA intermediate. Several related hepatitis viruses were later discovered in other species. These viruses were classified in the Hepadnaviridae family based on their small genomes and novel replication strategy. HBV itself exists as different genotypes that tend to have distinct geographic distributions. The structure of the HBV virion is described, consisting of an inner core containing the viral DNA, surrounded by envelope proteins that are acquired from host cells.
CR-BSI
Catheter-related bloodstream infections (CR-BSI) are common, costly infections associated with central venous catheters. According to the document, CR-BSI occur in approximately 80,000 ICU patients per year in the US, costing $45,000 per episode and $2.3 billion annually. The median rate of CR-BSI in ICUs ranges from 1.8 to 5.2 per 1000 catheter days. Biofilm formation on intravascular catheters allows pathogens to survive and persist despite host defenses and antimicrobial treatment.
Hepatitis viruses - A,B & C
This talks about the HAV, HBV and HCV , intro, properties, epidemiology and transmission, pathogenesis , clinical findings , laboratory diagnosis, and prevention
Hepatitis B virus
Hepatitis B virus is a double-stranded DNA virus that causes hepatitis B disease. It is able to establish chronic infections and has been shown to integrate into host DNA. The virus primarily infects liver cells and establishes lifelong infections in around 5% of adults and up to 90% of infants infected. While vaccination has been effective at reducing new infections, chronic hepatitis B remains an important global public health issue.
Occult hepatitis B virus infection
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This document discusses a case of Kaposi sarcoma involving the small intestine. CT and endoscopy showed jejunal thickening and lymphadenopathy. Biopsy showed spindle cell proliferation and immunohistochemical staining was positive for HHV-8, indicating Kaposi sarcoma. Kaposi sarcoma commonly involves the GI tract in AIDS patients and can cause bleeding, pain, weight loss, nausea or diarrhea. Treatment involves antiretroviral therapy and radiation or chemotherapy.
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Focal Glomerulosclerosis
Focal segmental glomerulosclerosis (FSGS) is a pattern of kidney injury with segmental scarring of glomeruli. There are primary and secondary causes, with primary FSGS characterized by diffuse foot process effacement and nephrotic syndrome. Histologically, FSGS shows segmental glomerular scarring involving some but not all glomeruli, with foot process effacement on electron microscopy. Variants include collapsing, tip, and cellular variants seen on light microscopy. Secondary FSGS occurs due to adaptations from primary glomerular disease and shows focal global scarring with compensatory hypertrophy.
MPGN/MCGN
This document discusses several types of glomerular diseases that present with a membranoproliferative pattern of injury on histology, including membranoproliferative glomerulonephritis (MPGN) types I, II, and III, cryoglobulin-associated glomerulonephritis, lupus nephritis class IV, and thrombotic microangiopathies (both acute and chronic). It provides details on the etiology, clinical features, histopathology, immunofluorescence, and electron microscopy findings of each condition.
Membranous GN
Membranous Nephropathy and Lupus Nephritis Class V involve thickening of the peripheral capillary loops with basement membrane 'spikes' and 'craters' visible on staining. Immunofluorescence shows deposition of IgG and C3 along the peripheral capillary loops. Electron microscopy reveals extensive foot process effacement and subepithelial electron-dense deposits that vary in appearance based on disease stage. The glomerular basement membrane may be attenuated or thickened. Lupus Nephritis Class V additionally shows mesangial expansion and a 'full house' immunofluorescence pattern with proliferative features sometimes present.
Nodular GN
Nodular glomerulosclerosis (GN) can be caused by long-standing diabetes mellitus, monoclonal immunoglobulin deposition disease, amyloidosis, or healed immune complex glomerulonephritides. Histologically, it is characterized by nodular mesangial expansion and thickening of peripheral capillary loops. Idiopathic nodular GN is a diagnosis of exclusion when no underlying cause is identified.
Tubulointerstitial diseases
1. Acute tubular necrosis is characterized by low epithelial lining, single cell necrosis, and casts in tubule lumens. Regenerative changes include nucleomegaly and mitosis. Ethylene glycol poisoning causes tubule swelling and vacuolization with oxalate crystals.
2. Acute interstitial nephritis shows interstitial inflammation with lymphocytes and macrophages invading tubules. Chronic interstitial nephritis displays tubular atrophy, fibrosis and hyaline casts.
3. Granulomatous interstitial nephritis is defined by granulomas that can be non-necrotizing or necrotizing. Causes include drugs, sarcoidosis
Minimal Light Microscopic Changes
The document summarizes the light microscopic, immunofluorescence, and electron microscopic findings for several different kidney diseases:
1. Minimal change disease shows normal or mildly expanded glomeruli and mesangium on light microscopy. Immunofluorescence may show fine IgG deposits in podocytes. Electron microscopy shows diffuse foot process effacement without deposits.
2. IgA nephropathy shows normal or minimally expanded glomeruli and mesangium on light microscopy. Immunofluorescence shows dominant mesangial IgA with C3 deposits. Electron microscopy shows normal epithelial cells and mesangial deposits.
3. Class I lupus nephritis shows normal findings on light microscopy. Immunofluorescence is positive
Crescentic GN
This document discusses the histopathological features of several types of crescentic glomerulonephritis (GN), including anti-glomerular basement membrane (GBM) disease, pauci-immune GN, immune complex-mediated GN, lupus nephritis class IV, IgA nephropathy, and post infectious GN. Key findings include fibrinoid necrosis, crescent formation, immune complex deposition patterns on immunofluorescence, and electron-dense deposits, effacement of foot processes, and basement membrane abnormalities on electron microscopy. The diseases are distinguished by their pathogenic mechanisms and specific immune staining and ultrastructural characteristics.
Diffuse Proliferative GN
Diffuse proliferative glomerulonephritis (GN) involves over 50% of glomeruli showing endocapillary or extracapillary proliferation. It is commonly seen in immune complex diseases like lupus nephritis and post-infectious GN. Histopathology shows proliferative changes, neutrophils, cellular crescents in some glomeruli, and C3-dominant immune complex deposition. Electron microscopy reveals foot process effacement, thickened basement membranes, and subepithelial immune complex deposits. Lupus nephritis class IV has similar features but with full house immune complex deposition and possible membranoproliferative changes. IgA nephropathy shows mes
Mesangial proliferative GN
The document discusses several glomerular diseases characterized by a mesangioproliferative pattern of injury including mesangial proliferative GN, lupus nephritis class II, IgA nephropathy, resolving post-infectious GN, fibrillary GN, immunotactoid glomerulopathy, early diabetic glomerulosclerosis, and minimal change disease. For each disease, the document describes histopathological findings on light microscopy, immunofluorescence, and electron microscopy.
Focalproliferative Glomerulonephritis
Focal proliferative glomerulonephritis involves segmental or global endocapillary or extracapillary proliferative changes in less than 50% of glomeruli. It can be pauci-immune associated with ANCA or immune complex-mediated such as lupus nephritis class III or IgA nephropathy. Lupus nephritis class III shows segmental or global endocapillary proliferation, expanded mesangium, irregular capillary loops, intraluminal thrombi, and full house immunofluorescence staining. IgA nephropathy demonstrates mesangial hypercellularity, expansion, and segmental endocapillary proliferation or crescents, with dominant mes
Basement Membrane Abnormalities
1. Glomerular basement membrane (GBM) abnormalities are inherited disorders of basement membrane collagens that are X-linked in about 80% of cases and cause thin GBMs seen in up to 9% of the general population.
2. Thin GBMs are caused by genetic defects in collagen type IV, including genes COL4A5 and COL4A6 (X-linked) in 80% of cases and COL4A3 and COL4A4 (autosomal) in the remaining 20% of cases.
3. Patients with thin GBMs are usually asymptomatic but may have microscopic hematuria, while those with Alport's syndrome caused by the same genetic defects may also have sensor
Humoral Immunity
- Naive B cells express IgM and IgD antibodies on their surface that recognize antigens. Upon activation, a single B cell can produce up to 10^12 antibody molecules per day through plasma cell differentiation.
- Repeated antigen exposure leads to affinity maturation through somatic hypermutation in germinal centers, increasing antibody affinity over time. Helper T cells are required for isotype switching and affinity maturation.
- Engagement of complement receptors and toll-like receptors enhances B cell activation and antibody production. Activated B cells also upregulate costimulators to amplify helper T cell responses.
Introduction to Renal Pathology
This document provides guidance on sampling, allocating, and fixing renal biopsy tissue for light microscopy, immunofluorescence, and electron microscopy evaluation. It discusses obtaining adequate sample sizes from different renal regions and dividing tissue between fixatives. Common stains used for light microscopy like H&E, PAS, trichrome, and silver stains are also described. Normal renal histology of the glomerulus, interstitium, tubules, and vessels is outlined.
Intro Immune
The document provides an overview of the immune system, including:
- Innate immunity acts as the first line of defense through barriers like skin and mucous membranes. Adaptive immunity responds later with targeted responses.
- Adaptive immunity includes humoral immunity from B cells producing antibodies and cellular immunity from T cells killing infected cells.
- Lymphocytes circulate and are concentrated in lymphoid tissues like lymph nodes and spleen to scan for pathogens using antigen presenting cells. Memory lymphocytes provide faster responses upon reexposure.
Nephrotic Syndrome
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Screening
1. Early detection of renal disease is important through screening methods like urine and blood tests as most early renal failures are asymptomatic.
2. High risk groups for renal disease include those with diabetes, hypertension, cardiovascular disease, urinary tract infections, and a family history of kidney disease. These groups should be regularly screened.
3. Screening allows for early treatment and measures to slow disease progression, reducing complications and allowing time for education and vascular access planning for renal replacement therapy if needed. Benefits of early detection include better outcomes.
Dry Weight Dr Rosna
This document discusses dry weight, which is the ideal post-dialysis weight that allows a patient to maintain normal blood pressure without medication until their next dialysis session. It explains that extracellular volume overload is a main cause of hypertension in dialysis patients. Achieving the correct dry weight through clinical assessment and trial and error allows blood pressure to be controlled in most patients. Dry weight can be difficult to determine accurately and must be regularly adjusted as patient factors like appetite and nutrition change over time.
Bartter’S And Gittleman’S Syndromes
The document summarizes Bartter's and Gitelman's syndromes, which are inherited tubular defects characterized by low potassium levels and metabolic alkalosis. Bartter's syndrome involves defects in sodium reabsorption in the thick ascending limb of the loop of Henle, while Gitelman's syndrome involves a primary defect in the thiazide-sensitive sodium-chloride cotransporter in the distal convoluted tubule. Both conditions result in activation of the renin-angiotensin-aldosterone system and loss of potassium and hydrogen ions in the urine. Gitelman's syndrome generally presents later in life and has a more mild phenotype. Treatment aims to block prostaglandin E2 and al
Mycophenolate Mofetil in Primary Glomerulonephritis
This document reports on a study examining the use of mycophenolate mofetil (MMF) for treating primary glomerulonephritis. Four patients with focal segmental glomerulosclerosis (FSGS) or membranous nephropathy received MMF for at least 6 months. Results showed reduced urine protein levels and improved or stable kidney function in most patients, suggesting MMF may be useful for treating these conditions. However, larger randomized controlled trials are still needed to validate MMF's efficacy.
Mycophenolate Mofetil In Relapsing Lupus Nephritis
This study examined the use of mycophenolate mofetil (MMF) for treating relapsing lupus nephritis in 6 patients who had not responded well to previous treatments including cyclophosphamide. The patients were given MMF for an average of 14 months. Their proteinuria decreased on average from 1.62 g/24 hours to 0.86 g/24 hours. Serum albumin and eGFR levels improved. Two patients experienced temporary side effects of diarrhea and nausea. The study concluded that MMF is an effective therapy for relapsing lupus nephritis and is generally well tolerated.
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Mycophenolate Mofetil in Primary Glomerulonephritis
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There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
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Bk Polyoma Virus
- 1. BK Polyoma Virus Dr Goh Ching Yan
- 9. Decoy cells
- 12. Type I: An amorphous ground-glass variant “ Ground-glass” appearance of nucleus
- 13. Type II: granular variant surrounded by a “halo”
- 14. Type III: a finely granular variant without halo
- 15. Type II/III hybrid: Intranuclear vesicles
- 16. Type IV: a vesicular variant with clumped, irregular chromatin
- 18. Screening Algorithm Clin J Am Soc Nephrol 1: 374–379, 2006
- 29. THANK YOU