(1) Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. Septic shock is persisting hypotension requiring vasopressors and elevated lactate levels despite fluid resuscitation. Organ dysfunction is identified as an acute change in total SOFA score ≥2 points due to infection.
(2) Laboratory diagnosis of sepsis involves blood cultures, biomarkers like PCT, CRP, lactate, cytokines and invasive fungal biomarkers like galactomannan and beta-D-glucan. Hematological parameters and newer techniques like MALDI-TOF and multiplex PCR are also used. Blood cultures remain the gold standard but are often culture negative
This document provides information about hepatitis C virus (HCV) including its structure, genome, genotypes, epidemiology, transmission, pathogenesis, diagnosis, and management. It discusses:
- HCV has a single-stranded RNA genome within the Flaviviridae family. It exists as different genotypes that determine treatment response.
- HCV is a major cause of liver disease worldwide, with transmission primarily through blood exposure. Diagnosis involves antibody and RNA testing.
- Treatment aims to eradicate HCV and involves pegylated interferon and ribavirin combinations. Response is monitored via viral load decline. Adverse effects require monitoring and management. New direct-acting antivirals are improving treatment outcomes.
SEPSIS IS MOST FATAL DISEASE WORLD WIDE. EARLY DETECTION OR PREDICTION OF SEPSIS IS A CHALLENGE
SEPSIS BIOMARKERS ARE OUR WEAPON TO EARLY DETECT SEPSIS. WE HAVE TO UNDERSTAND IT WELL
This document discusses cytokine storm syndrome in patients with COVID-19. It defines cytokine storm as an uncontrolled release of inflammatory cytokines that can lead to organ damage. COVID-19 is proposed to progress through four stages, with stage II involving an excessive immune response and cytokine release. Cytokine storm is associated with acute respiratory distress syndrome and multi-organ failure in COVID-19 patients. The document outlines treatments for cytokine storm including immunomodulators, anticoagulants, antivirals, and extracorporeal therapies.
This document discusses sepsis markers that can be used for the diagnosis, assessment, and prognosis of sepsis. It describes several commonly used markers including lactate, C-reactive protein (CRP), and procalcitonin (PCT). Lactate levels indicate tissue hypoperfusion and are prognostic, with higher lactate clearance associated with lower mortality. CRP is an acute phase protein that rises within hours of infection but can remain elevated. PCT rises more quickly than CRP and correlates better with sepsis severity and outcome. Newer markers like presepsin and heparin-binding protein show promise as early markers of sepsis. No single marker is perfect and combinations may provide better diagnosis and guidance of sepsis management and
This document provides information on skin and soft tissue infections (SSTIs). It discusses the difference between uncomplicated and complicated SSTIs, giving examples of each. It also provides short notes on specific SSTIs including impetigo, bullous impetigo, erysipelas, and cellulitis. The document further discusses the typical bacterial causes of various SSTIs and treatment approaches.
This document discusses the potential utility of biomarkers for diagnosing and prognosing sepsis. It begins by explaining why improving diagnostic and prognostic tools for sepsis is important, as it is a leading cause of death in ICU patients. It then discusses how early detection and treatment are paramount but current detection strategies are limited. The document introduces the biomarker paradigm for sepsis, where biomarkers can identify inflammation, coagulation, tissue damage and repair processes to better stratify severity and prognosticate outcomes. Several candidate biomarkers are discussed, such as procalcitonin, cytokines, chemokines, and pentraxin 3. The document considers how biomarkers may help with diagnosis, prognostication, and identifying high-risk patients and treatment response. It concludes the future
Tumor markers can play roles in early detection, diagnosis, prognosis, monitoring treatment response, and detecting recurrence of certain cancers. This document discusses various tumor markers including their reference ranges, associated cancers, clinical applications, and methods of detection. Key points covered include the roles of AFP for liver cancer screening, CEA and CA19-9 for colorectal cancer monitoring, PSA for prostate cancer screening and follow up, and CA125 for ovarian cancer treatment assessment and recurrence detection. The document also provides recommendations for optimal use of tumor marker tests.
This document provides information about hepatitis C virus (HCV) including its structure, genome, genotypes, epidemiology, transmission, pathogenesis, diagnosis, and management. It discusses:
- HCV has a single-stranded RNA genome within the Flaviviridae family. It exists as different genotypes that determine treatment response.
- HCV is a major cause of liver disease worldwide, with transmission primarily through blood exposure. Diagnosis involves antibody and RNA testing.
- Treatment aims to eradicate HCV and involves pegylated interferon and ribavirin combinations. Response is monitored via viral load decline. Adverse effects require monitoring and management. New direct-acting antivirals are improving treatment outcomes.
SEPSIS IS MOST FATAL DISEASE WORLD WIDE. EARLY DETECTION OR PREDICTION OF SEPSIS IS A CHALLENGE
SEPSIS BIOMARKERS ARE OUR WEAPON TO EARLY DETECT SEPSIS. WE HAVE TO UNDERSTAND IT WELL
This document discusses cytokine storm syndrome in patients with COVID-19. It defines cytokine storm as an uncontrolled release of inflammatory cytokines that can lead to organ damage. COVID-19 is proposed to progress through four stages, with stage II involving an excessive immune response and cytokine release. Cytokine storm is associated with acute respiratory distress syndrome and multi-organ failure in COVID-19 patients. The document outlines treatments for cytokine storm including immunomodulators, anticoagulants, antivirals, and extracorporeal therapies.
This document discusses sepsis markers that can be used for the diagnosis, assessment, and prognosis of sepsis. It describes several commonly used markers including lactate, C-reactive protein (CRP), and procalcitonin (PCT). Lactate levels indicate tissue hypoperfusion and are prognostic, with higher lactate clearance associated with lower mortality. CRP is an acute phase protein that rises within hours of infection but can remain elevated. PCT rises more quickly than CRP and correlates better with sepsis severity and outcome. Newer markers like presepsin and heparin-binding protein show promise as early markers of sepsis. No single marker is perfect and combinations may provide better diagnosis and guidance of sepsis management and
This document provides information on skin and soft tissue infections (SSTIs). It discusses the difference between uncomplicated and complicated SSTIs, giving examples of each. It also provides short notes on specific SSTIs including impetigo, bullous impetigo, erysipelas, and cellulitis. The document further discusses the typical bacterial causes of various SSTIs and treatment approaches.
This document discusses the potential utility of biomarkers for diagnosing and prognosing sepsis. It begins by explaining why improving diagnostic and prognostic tools for sepsis is important, as it is a leading cause of death in ICU patients. It then discusses how early detection and treatment are paramount but current detection strategies are limited. The document introduces the biomarker paradigm for sepsis, where biomarkers can identify inflammation, coagulation, tissue damage and repair processes to better stratify severity and prognosticate outcomes. Several candidate biomarkers are discussed, such as procalcitonin, cytokines, chemokines, and pentraxin 3. The document considers how biomarkers may help with diagnosis, prognostication, and identifying high-risk patients and treatment response. It concludes the future
Tumor markers can play roles in early detection, diagnosis, prognosis, monitoring treatment response, and detecting recurrence of certain cancers. This document discusses various tumor markers including their reference ranges, associated cancers, clinical applications, and methods of detection. Key points covered include the roles of AFP for liver cancer screening, CEA and CA19-9 for colorectal cancer monitoring, PSA for prostate cancer screening and follow up, and CA125 for ovarian cancer treatment assessment and recurrence detection. The document also provides recommendations for optimal use of tumor marker tests.
This document discusses septic shock, its definitions, signs, symptoms, causes, risk factors, pathophysiology, management, and treatment. It defines septic shock as persisting hypotension requiring vasopressors to maintain blood pressure and a serum lactate above 2 mmol/L despite fluid resuscitation. Management involves early antibiotic therapy, source control, fluid resuscitation, vasopressor support, and organ support. The key goals are starting appropriate antibiotics quickly, resuscitating from shock, identifying and treating the infection source, and maintaining organ function.
The complement system is an important part of the innate immune system that activates through three pathways - classical, lectin, and alternative. Activation leads to the formation of C3 and C5 convertases that generate inflammatory molecules like C3a and C5a, and opsonins like C3b that promote phagocytosis. It ultimately forms the membrane attack complex that lyses target cells. Complement is tightly regulated to prevent damage to host cells and excessive inflammation. Deficiencies in complement components can increase risk of certain infections.
The document discusses the pathophysiology of sepsis and multiple organ dysfunction syndrome (MODS). It defines sepsis, SIRS, severe sepsis, and septic shock. Mediators of the septic response include pro-inflammatory and anti-inflammatory factors. Sepsis can lead to organ injury and failure through mechanisms like ischemia, apoptosis, leukocyte-mediated tissue damage, and cytopathic hypoxia. Therapies aim to optimize organ perfusion, control infection, and support dysfunctional organs. Experimental therapies target modulating the host inflammatory response but many past attempts showed little benefit. Evidence-based guidelines incorporate best practices for early recognition, resuscitation, and management of sepsis patients.
This document summarizes various skin and soft tissue infections, including their causes, symptoms, and treatments. Erysipelas is a streptococcal infection of the skin that causes a painful, erythematous rash. Impetigo is a contagious superficial infection commonly caused by streptococci or staphylococci in children. Folliculitis is a bacterial infection of hair follicles that causes papules and pustules. Boils are deeper hair follicle infections forming tender, red swellings. Carbuncles are clusters of interconnected boils. Cellulitis is a spreading bacterial skin infection beneath the skin. Necrotizing fasciitis is a severe infection of the fascia requiring aggressive
This document discusses new approaches to diagnosing and monitoring sepsis, focusing on biomarkers and molecular diagnostics. It describes some limitations of conventional detection methods for sepsis and introduces the biomarker paradigm for earlier detection. Several candidate biomarkers are examined that are linked to inflammation, coagulation, tissue damage and repair during sepsis. Biomarkers discussed in more detail include C-reactive protein, procalcitonin, presepsin, and their clinical significance for diagnosis, prognosis, and monitoring treatment response. The use of biomarker panels and ROC curve analysis to improve diagnostic accuracy is also covered.
This document discusses opportunistic infections that can occur in patients with AIDS/HIV. It begins by providing background on the HIV epidemic in India. It then describes the structure and life cycle of HIV. The document outlines the typical stages of HIV disease progression from acute infection to chronic infection to AIDS. It discusses how HIV evades the immune system and establishes a chronic infection. Finally, it provides details on common opportunistic infections caused by fungi, bacteria, viruses and protozoa that patients with advanced HIV/AIDS face, such as Pneumocystis pneumonia, toxoplasmosis and cryptosporidiosis.
This document discusses sepsis and septic shock. It defines severe sepsis as acute organ dysfunction caused by infection, and septic shock as sepsis with hypotension refractory to fluid resuscitation requiring vasopressors. Common infection sites include the respiratory tract, intra-abdominal space, and urinary tract. Gram-positive and gram-negative bacteria, as well as fungi, can cause sepsis. The pathophysiology involves an initial inflammatory response that can lead to organ damage and dysfunction if not controlled. Complications include disseminated intravascular coagulation, acute respiratory distress syndrome, and acute renal failure. Treatment involves identifying and treating the infection source along with early, targeted antimicrobial therapy and organ support.
Sepsis biomarkers an update by Dr Puneet JainPuneet Jain
sepsis biomarkers play a crucial role in decision making and management of sepsis cases. these biomarkers can be diagnostic, prognostic or theranostic. CRP and Procalcitonin are most widely used and studied biomarkers.
various cutaneous lymphomas though having low incidence but need to be diagnosed accurately. they can be mimiced by many non neoplastic conditions of skin. so discussing both T and B cell lymphomas
Serum sickness is an immune-mediated disease caused by antigen-antibody immune complexes depositing in vessel walls. It was first discovered in 1905 in children treated with horse antiserum who developed arthritis, rash and fever 8-13 days later. Key characteristics include fever, rash, arthritis occurring 1-3 weeks after exposure to a foreign protein. Laboratory tests may show elevated inflammatory markers and detection of circulating immune complexes. Treatment focuses on removing the antigen, reducing inflammation and promoting clearance of immune complexes.
The recent definition, concept and terminologies of septic shock, surviving sepsis campaign, management techniques, SOFA score. Also includes antibiotics and supportive modalities.
This document provides guidelines for the management of sepsis and septic shock. It outlines criteria for diagnosing sepsis, severe sepsis, and septic shock. It recommends initial resuscitation efforts within 3 hours that include measuring lactate, obtaining blood cultures, administering antibiotics and fluids. The guidelines recommend targeting a mean arterial pressure of 65 mmHg with vasopressors as needed, and normalizing lactate if initially elevated. Source control through drainage or removal of infection sites is also advised within 12 hours of diagnosis if possible.
1. HIV can cause a variety of hematological manifestations including anemia, leukopenia, thrombocytopenia, and coagulation disorders due to bone marrow infiltration and effects on hematopoietic progenitor cells.
2. The bone marrow in HIV/AIDS commonly shows hypercellularity, dysplasia of the erythroid and myeloid lineages, plasmacytosis, and lymphoid aggregates. Opportunistic infections also frequently involve the bone marrow.
3. HIV is associated with increased risk of aggressive B-cell lymphomas such as diffuse large B-cell lymphoma. Lymphomas in HIV often involve extranodal sites and the bone marrow.
Cellulitis and soft tissue infections can be either purulent (containing pus) or non-purulent. Common non-purulent soft tissue infections include cellulitis, necrotizing fasciitis, and erysipelas. Cellulitis presents as expanding erythema with signs of inflammation and no pus or well-defined edges. Necrotizing fasciitis is a rapidly spreading infection of the skin and soft tissue including fascia. Risk factors include diabetes, immunosuppression, and obesity. Surgical inspection and debridement are often needed for severe non-purulent infections. Purulent infections include furuncles, carbuncles, and abscesses. Treatment involves incision and
This document provides an overview of IgG4-Related disease including its epidemiology, pathogenesis, clinical presentation, diagnostic criteria, and organ involvement. Some key points include:
- It predominantly affects men aged 50-70 years.
- Pathogenesis involves IgG4-positive plasma cells and T-helper type 2 immune responses leading to fibrosis and organ swelling.
- Diagnosis requires specific histological findings and elevated serum IgG4 levels.
- It can affect many organs including lacrimal glands, salivary glands, lungs, pancreas, kidney, and lymph nodes, causing swelling.
The document discusses biomarkers for diagnosing and monitoring sepsis. It describes fungal biomarkers like galactomannan (GM) and beta-D-glucan (BG) which detect components of fungal cell walls. GM detects Aspergillus species while BG detects a wider range of fungi. Studies show variable accuracy for both biomarkers. Combining GM and BG tests may improve specificity without affecting sensitivity. Neither detects zygomycetes fungi.
Sepsis is a life-threatening condition caused by the body's response to an infection. It can progress to septic shock, which has a high mortality rate. The initial management of sepsis involves rapid fluid resuscitation, administration of broad-spectrum antibiotics within 1 hour, and measuring serum lactate levels and obtaining blood cultures. Implementation of a code sepsis protocol can improve compliance with treatment guidelines and reduce mortality rates by facilitating early goal-directed therapy. De-escalation of antimicrobial therapy based on the patient's clinical response is important to prevent overuse of antibiotics.
1. Neuroendocrine tumors (NETs) are increasing in incidence and are often metastatic at diagnosis. They originate from neuroendocrine cells and secrete hormones.
2. Somatostatin analogues are first-line treatment for symptomatic control in NETs but resistance can develop. Chemotherapy has limited efficacy except in high-grade tumors.
3. Emerging biomarkers and molecular targeted therapies such as inhibitors of angiogenesis are improving outcomes beyond traditional approaches.
Sepsis in surgical patients and its biomarkers.pptxsamrat277229
The document discusses sepsis in surgical patients and biomarkers for diagnosis. It defines sepsis and outlines the Surviving Sepsis Campaign guidelines for treatment, including early antibiotic therapy, source control, and hemodynamic support. Biomarkers like lactate, C-reactive protein, and procalcitonin are described as potential diagnostic tools, though each has limitations. Procalcitonin in particular increases significantly in response to bacterial infection and can help differentiate between infectious and non-infectious causes of inflammation. The document concludes that while biomarkers show promise in rapid sepsis diagnosis and treatment monitoring, further research is still needed.
This document discusses septic shock, its definitions, signs, symptoms, causes, risk factors, pathophysiology, management, and treatment. It defines septic shock as persisting hypotension requiring vasopressors to maintain blood pressure and a serum lactate above 2 mmol/L despite fluid resuscitation. Management involves early antibiotic therapy, source control, fluid resuscitation, vasopressor support, and organ support. The key goals are starting appropriate antibiotics quickly, resuscitating from shock, identifying and treating the infection source, and maintaining organ function.
The complement system is an important part of the innate immune system that activates through three pathways - classical, lectin, and alternative. Activation leads to the formation of C3 and C5 convertases that generate inflammatory molecules like C3a and C5a, and opsonins like C3b that promote phagocytosis. It ultimately forms the membrane attack complex that lyses target cells. Complement is tightly regulated to prevent damage to host cells and excessive inflammation. Deficiencies in complement components can increase risk of certain infections.
The document discusses the pathophysiology of sepsis and multiple organ dysfunction syndrome (MODS). It defines sepsis, SIRS, severe sepsis, and septic shock. Mediators of the septic response include pro-inflammatory and anti-inflammatory factors. Sepsis can lead to organ injury and failure through mechanisms like ischemia, apoptosis, leukocyte-mediated tissue damage, and cytopathic hypoxia. Therapies aim to optimize organ perfusion, control infection, and support dysfunctional organs. Experimental therapies target modulating the host inflammatory response but many past attempts showed little benefit. Evidence-based guidelines incorporate best practices for early recognition, resuscitation, and management of sepsis patients.
This document summarizes various skin and soft tissue infections, including their causes, symptoms, and treatments. Erysipelas is a streptococcal infection of the skin that causes a painful, erythematous rash. Impetigo is a contagious superficial infection commonly caused by streptococci or staphylococci in children. Folliculitis is a bacterial infection of hair follicles that causes papules and pustules. Boils are deeper hair follicle infections forming tender, red swellings. Carbuncles are clusters of interconnected boils. Cellulitis is a spreading bacterial skin infection beneath the skin. Necrotizing fasciitis is a severe infection of the fascia requiring aggressive
This document discusses new approaches to diagnosing and monitoring sepsis, focusing on biomarkers and molecular diagnostics. It describes some limitations of conventional detection methods for sepsis and introduces the biomarker paradigm for earlier detection. Several candidate biomarkers are examined that are linked to inflammation, coagulation, tissue damage and repair during sepsis. Biomarkers discussed in more detail include C-reactive protein, procalcitonin, presepsin, and their clinical significance for diagnosis, prognosis, and monitoring treatment response. The use of biomarker panels and ROC curve analysis to improve diagnostic accuracy is also covered.
This document discusses opportunistic infections that can occur in patients with AIDS/HIV. It begins by providing background on the HIV epidemic in India. It then describes the structure and life cycle of HIV. The document outlines the typical stages of HIV disease progression from acute infection to chronic infection to AIDS. It discusses how HIV evades the immune system and establishes a chronic infection. Finally, it provides details on common opportunistic infections caused by fungi, bacteria, viruses and protozoa that patients with advanced HIV/AIDS face, such as Pneumocystis pneumonia, toxoplasmosis and cryptosporidiosis.
This document discusses sepsis and septic shock. It defines severe sepsis as acute organ dysfunction caused by infection, and septic shock as sepsis with hypotension refractory to fluid resuscitation requiring vasopressors. Common infection sites include the respiratory tract, intra-abdominal space, and urinary tract. Gram-positive and gram-negative bacteria, as well as fungi, can cause sepsis. The pathophysiology involves an initial inflammatory response that can lead to organ damage and dysfunction if not controlled. Complications include disseminated intravascular coagulation, acute respiratory distress syndrome, and acute renal failure. Treatment involves identifying and treating the infection source along with early, targeted antimicrobial therapy and organ support.
Sepsis biomarkers an update by Dr Puneet JainPuneet Jain
sepsis biomarkers play a crucial role in decision making and management of sepsis cases. these biomarkers can be diagnostic, prognostic or theranostic. CRP and Procalcitonin are most widely used and studied biomarkers.
various cutaneous lymphomas though having low incidence but need to be diagnosed accurately. they can be mimiced by many non neoplastic conditions of skin. so discussing both T and B cell lymphomas
Serum sickness is an immune-mediated disease caused by antigen-antibody immune complexes depositing in vessel walls. It was first discovered in 1905 in children treated with horse antiserum who developed arthritis, rash and fever 8-13 days later. Key characteristics include fever, rash, arthritis occurring 1-3 weeks after exposure to a foreign protein. Laboratory tests may show elevated inflammatory markers and detection of circulating immune complexes. Treatment focuses on removing the antigen, reducing inflammation and promoting clearance of immune complexes.
The recent definition, concept and terminologies of septic shock, surviving sepsis campaign, management techniques, SOFA score. Also includes antibiotics and supportive modalities.
This document provides guidelines for the management of sepsis and septic shock. It outlines criteria for diagnosing sepsis, severe sepsis, and septic shock. It recommends initial resuscitation efforts within 3 hours that include measuring lactate, obtaining blood cultures, administering antibiotics and fluids. The guidelines recommend targeting a mean arterial pressure of 65 mmHg with vasopressors as needed, and normalizing lactate if initially elevated. Source control through drainage or removal of infection sites is also advised within 12 hours of diagnosis if possible.
1. HIV can cause a variety of hematological manifestations including anemia, leukopenia, thrombocytopenia, and coagulation disorders due to bone marrow infiltration and effects on hematopoietic progenitor cells.
2. The bone marrow in HIV/AIDS commonly shows hypercellularity, dysplasia of the erythroid and myeloid lineages, plasmacytosis, and lymphoid aggregates. Opportunistic infections also frequently involve the bone marrow.
3. HIV is associated with increased risk of aggressive B-cell lymphomas such as diffuse large B-cell lymphoma. Lymphomas in HIV often involve extranodal sites and the bone marrow.
Cellulitis and soft tissue infections can be either purulent (containing pus) or non-purulent. Common non-purulent soft tissue infections include cellulitis, necrotizing fasciitis, and erysipelas. Cellulitis presents as expanding erythema with signs of inflammation and no pus or well-defined edges. Necrotizing fasciitis is a rapidly spreading infection of the skin and soft tissue including fascia. Risk factors include diabetes, immunosuppression, and obesity. Surgical inspection and debridement are often needed for severe non-purulent infections. Purulent infections include furuncles, carbuncles, and abscesses. Treatment involves incision and
This document provides an overview of IgG4-Related disease including its epidemiology, pathogenesis, clinical presentation, diagnostic criteria, and organ involvement. Some key points include:
- It predominantly affects men aged 50-70 years.
- Pathogenesis involves IgG4-positive plasma cells and T-helper type 2 immune responses leading to fibrosis and organ swelling.
- Diagnosis requires specific histological findings and elevated serum IgG4 levels.
- It can affect many organs including lacrimal glands, salivary glands, lungs, pancreas, kidney, and lymph nodes, causing swelling.
The document discusses biomarkers for diagnosing and monitoring sepsis. It describes fungal biomarkers like galactomannan (GM) and beta-D-glucan (BG) which detect components of fungal cell walls. GM detects Aspergillus species while BG detects a wider range of fungi. Studies show variable accuracy for both biomarkers. Combining GM and BG tests may improve specificity without affecting sensitivity. Neither detects zygomycetes fungi.
Sepsis is a life-threatening condition caused by the body's response to an infection. It can progress to septic shock, which has a high mortality rate. The initial management of sepsis involves rapid fluid resuscitation, administration of broad-spectrum antibiotics within 1 hour, and measuring serum lactate levels and obtaining blood cultures. Implementation of a code sepsis protocol can improve compliance with treatment guidelines and reduce mortality rates by facilitating early goal-directed therapy. De-escalation of antimicrobial therapy based on the patient's clinical response is important to prevent overuse of antibiotics.
1. Neuroendocrine tumors (NETs) are increasing in incidence and are often metastatic at diagnosis. They originate from neuroendocrine cells and secrete hormones.
2. Somatostatin analogues are first-line treatment for symptomatic control in NETs but resistance can develop. Chemotherapy has limited efficacy except in high-grade tumors.
3. Emerging biomarkers and molecular targeted therapies such as inhibitors of angiogenesis are improving outcomes beyond traditional approaches.
Sepsis in surgical patients and its biomarkers.pptxsamrat277229
The document discusses sepsis in surgical patients and biomarkers for diagnosis. It defines sepsis and outlines the Surviving Sepsis Campaign guidelines for treatment, including early antibiotic therapy, source control, and hemodynamic support. Biomarkers like lactate, C-reactive protein, and procalcitonin are described as potential diagnostic tools, though each has limitations. Procalcitonin in particular increases significantly in response to bacterial infection and can help differentiate between infectious and non-infectious causes of inflammation. The document concludes that while biomarkers show promise in rapid sepsis diagnosis and treatment monitoring, further research is still needed.
Definition of sepsis and septic shock.
The new definition of sepsis 2016 conference.
SIRS, SOFA, QSOFA
Most common pathogen causing sepsis.
Pathogenesis and pathophysiology of sepsis
Biomarkers for detection of sepsis and septic shock
Preseason, sCD14 Subtype marker
Comparison of Procalcitonin and CRP with presepsin.
Mechanism of presepsin detection.
Management of sepsis.
Sepsis is a major cause of death worldwide, and early diagnosis and treatment are important for improving outcomes. Biomarkers that can objectively identify sepsis are ideal for diagnosis and prognosis. Procalcitonin and C-reactive protein are two biomarkers that have been studied extensively in sepsis. Procalcitonin levels rise more specifically with bacterial infection compared to viral infections and can help guide antibiotic therapy and determine when antibiotics can be de-escalated or stopped. Newer biomarkers continue to be investigated including presepsin, cell-free DNA, and markers of immunosuppression, but procalcitonin remains the most widely used biomarker in clinical practice for diagnosing and managing sepsis.
This document summarizes information about sepsis in surgical patients, biomarkers for sepsis detection, and the Surviving Sepsis Campaign 2021 guidelines. It discusses definitions of sepsis, SIRS criteria, qSOFA and SOFA scores. Key points include the importance of early source control, the role of lactate and C-reactive protein as biomarkers, and the need for a multidisciplinary approach involving surgeons, infectious disease specialists and others to determine the best source control strategy for each patient.
Approach to Sepsis & Septic Shock in Emergency Medicine.AngelGovekar
Sepsis and septic shock result from a dysregulated host response to infection. Sepsis criteria include suspected or proven infection and an increase in the SOFA score of 2 or more, while septic shock requires sepsis with vasopressor need to maintain blood pressure and elevated lactate. Treatment involves early recognition, source control with antibiotics, initial fluid boluses of 1-2L for hypotension or elevated lactate, vasopressors if needed, and lactate clearance-guided resuscitation.
Septic shock, updated presentation, including latest guidelines from Intensive care societies and how to approach to the diagnosis with few notes about Early Goal Directed Therapy and role of steroids
Procalcitonin is an excellent biomarker for antibiotic use in bacterial infections alone. POCT guided PCT levels can help decide whether to add antibiotics or not in opd settings for respiratory tract infection.
Sepsis – pathophysiology and managementVidhi Singh
- Sepsis is a systemic inflammatory response caused by infection that can progress to severe sepsis and septic shock. Severe sepsis is defined as sepsis with organ dysfunction, while septic shock involves hypotension refractory to fluid resuscitation along with lactate levels over 2 mmol/L despite fluid resuscitation.
- The pathophysiology involves an initial infection that triggers a systemic inflammatory response and release of cytokines and mediators, leading to endothelial damage, coagulation abnormalities, hypotension, and ultimately multiple organ dysfunction if not treated.
- Treatment involves early goal-directed therapy within 3-6 hours including antibiotics, fluid resuscitation, vasopressors, inotropes, and measures to optimize
This document discusses new diagnostic tests for sepsis. It describes current definitions for sepsis, severe sepsis, septic shock, and SIRS. It then summarizes several new molecular diagnostic techniques that can more rapidly identify pathogens causing bloodstream infections compared to traditional blood culture methods. These include techniques like PCR, fluorescence in situ hybridization, and multiplex assays that can detect bacteria and fungi directly from blood within a few hours rather than the days required for standard culture. This allows for earlier targeted antibiotic treatment which is associated with better outcomes for sepsis patients.
This document provides guidelines for treating sepsis, septic shock, and surviving sepsis. It defines terms like SIRS, sepsis, severe sepsis, and septic shock. The key pathophysiology of organ injury in sepsis is described. Treatment protocols like the Sepsis Six and Surviving Sepsis Campaign aim to rapidly identify and treat sepsis patients. Initial resuscitation focuses on fluid administration, vasopressors, inotropes, and lactate normalization. Antimicrobial therapy within 1 hour is critical. Source control through drainage or surgery may be needed. Overall the document provides clinical definitions and guidelines for diagnosis and management of sepsis.
Sepsis is a clinical syndrome caused by a dysregulated host response to infection that can lead to organ dysfunction and death. It ranges from systemic inflammatory response syndrome (SIRS) to sepsis, severe sepsis, septic shock, and multiple organ dysfunction syndrome (MODS). The leading causes are respiratory, intra-abdominal, and urinary infections from gram-negative bacteria like E. coli. Treatment involves early diagnosis, source control, broad-spectrum antibiotics, fluid resuscitation, vasopressors like norepinephrine for hypotension, and organ support. Despite aggressive treatment, sepsis mortality remains high and is associated with the number and duration of organ dysfunctions.
This document discusses sepsis and septic shock and provides guidelines for management. It defines sepsis as a systemic inflammatory response to infection and outlines the sepsis spectrum from sepsis to septic shock. It describes the typical host immune response and how an uncontrolled response can lead to systemic effects. Clinical presentation, diagnosis, bacteriology, and management including initial resuscitation, antimicrobial therapy and treatment duration are covered. Treatment aims to rapidly identify and treat the infection while stabilizing the patient and preventing further progression along the sepsis spectrum.
Severe sepsis and septic shock :evaluation and managementMd Shahid Iqubal
Sepsis and septic shock are life-threatening medical emergencies caused by dysregulated host response to infection leading to organ dysfunction. Management involves immediate evaluation and treatment, initial fluid resuscitation, early goal directed therapy including antibiotics and source control. Vasopressors, corticosteroids, glucose control, ventilation and DVT prophylaxis are also important supportive therapies to treat sepsis and prevent complications. The goal is to treat the infection and reverse the associated organ dysfunction.
The document discusses sepsis and septic shock. It defines shock and classifies different types including cardiogenic, hypovolemic, anaphylactic, septic, and neurogenic shock. It describes the systemic inflammatory response syndrome (SIRS) criteria. Non-infective processes like trauma or surgery can also cause SIRS. Investigations for sepsis may include blood cultures, imaging, and biomarkers like procalcitonin. Positive findings include leukocytosis/leukopenia, thrombocytopenia, organ dysfunction, hyperglycemia, and hyperlactatemia. Early goal-directed resuscitation including antibiotics, fluid resuscitation, and inotropes can improve outcomes in septic shock.
This document discusses sepsis markers and their clinical use. It summarizes several biomarkers that show potential for diagnosing and monitoring sepsis, including procalcitonin (PCT), C-reactive protein (CRP), and soluble CD14 subtype (sCD14-ST). sCD14-ST shows diagnostic value in distinguishing infection from SIRS and sepsis from severe sepsis. Studies found sCD14-ST levels correlated with severity of illness and organ dysfunction in sepsis patients. The document reviews several clinical trials and studies that evaluated these biomarkers for diagnosing and predicting outcomes in sepsis, abdominal infections, febrile neutropenia, and burns.
Sepsis is a life-threatening condition caused by a dysregulated immune response to infection that can lead to organ dysfunction. It is a major public health challenge worldwide with high mortality rates. The pathophysiology of sepsis involves an initial hyperinflammatory state followed by immune suppression that increases susceptibility to secondary infections. Biomarkers such as C-reactive protein and procalcitonin can help diagnose sepsis and evaluate severity, but an ideal biomarker has yet to be identified. Treatment of sepsis involves both resuscitative strategies and infection control according to surviving sepsis guidelines, and focuses on the complex pathophysiology of the condition.
The document provides information on sepsis epidemiology, pathogenesis, diagnosis, management and prognosis. Some key points:
- Sepsis cases and deaths are increasing worldwide, with the highest incidence among Black males, older adults, and in winter months. Regional disparities exist with most cases in low-income countries.
- Common infectious organisms include gram-positive bacteria and opportunistic fungi/viruses in immunocompromised patients. Culture-negative sepsis occurs in around half of cases.
- Sepsis diagnosis is based on life-threatening organ dysfunction caused by infection, as indicated by a SOFA score ≥2. Septic shock requires vasopressors to maintain blood pressure.
- Management
This document discusses sepsis, including definitions, pathophysiology, clinical features, diagnosis, and management. It defines sepsis as a life-threatening condition caused by a dysregulated immune response to infection leading to organ dysfunction. The pathophysiology involves a dysregulated inflammatory response and coagulation system. Signs and symptoms may include altered vital signs and organ dysfunction. Diagnosis involves identifying infection source through cultures and biomarkers. Treatment involves prompt antibiotics, fluid resuscitation, and supportive care based on Surviving Sepsis Campaign guidelines.
This document defines sepsis, SIRS, severe sepsis, septic shock, and MODS. It outlines the progression from SIRS to sepsis to septic shock and MODS if left untreated. Key signs and symptoms of each condition are provided. The pathophysiology of the systemic inflammatory response and multiple organ dysfunction syndrome is described. Treatment recommendations for sepsis include early antibiotics, fluid resuscitation, and vasopressors. Preventing secondary insults and providing organ support are important for managing MODS. Scoring systems can help predict outcomes of critically ill sepsis patients.
Debunking Nutrition Myths: Separating Fact from Fiction"AlexandraDiaz101
In a world overflowing with diet trends and conflicting nutrition advice, it’s easy to get lost in misinformation. This article cuts through the noise to debunk common nutrition myths that may be sabotaging your health goals. From the truth about carbohydrates and fats to the real effects of sugar and artificial sweeteners, we break down what science actually says. Equip yourself with knowledge to make informed decisions about your diet, and learn how to navigate the complexities of modern nutrition with confidence. Say goodbye to food confusion and hello to a healthier you!
Spontaneous Bacterial Peritonitis - Pathogenesis , Clinical Features & Manage...Jim Jacob Roy
In this presentation , SBP ( spontaneous bacterial peritonitis ) , which is a common complication in patients with cirrhosis and ascites is described in detail.
The reference for this presentation is Sleisenger and Fordtran's Gastrointestinal and Liver Disease Textbook ( 11th edition ).
Osvaldo Bernardo Muchanga-GASTROINTESTINAL INFECTIONS AND GASTRITIS-2024.pdfOsvaldo Bernardo Muchanga
GASTROINTESTINAL INFECTIONS AND GASTRITIS
Osvaldo Bernardo Muchanga
Gastrointestinal Infections
GASTROINTESTINAL INFECTIONS result from the ingestion of pathogens that cause infections at the level of this tract, generally being transmitted by food, water and hands contaminated by microorganisms such as E. coli, Salmonella, Shigella, Vibrio cholerae, Campylobacter, Staphylococcus, Rotavirus among others that are generally contained in feces, thus configuring a FECAL-ORAL type of transmission.
Among the factors that lead to the occurrence of gastrointestinal infections are the hygienic and sanitary deficiencies that characterize our markets and other places where raw or cooked food is sold, poor environmental sanitation in communities, deficiencies in water treatment (or in the process of its plumbing), risky hygienic-sanitary habits (not washing hands after major and/or minor needs), among others.
These are generally consequences (signs and symptoms) resulting from gastrointestinal infections: diarrhea, vomiting, fever and malaise, among others.
The treatment consists of replacing lost liquids and electrolytes (drinking drinking water and other recommended liquids, including consumption of juicy fruits such as papayas, apples, pears, among others that contain water in their composition).
To prevent this, it is necessary to promote health education, improve the hygienic-sanitary conditions of markets and communities in general as a way of promoting, preserving and prolonging PUBLIC HEALTH.
Gastritis and Gastric Health
Gastric Health is one of the most relevant concerns in human health, with gastrointestinal infections being among the main illnesses that affect humans.
Among gastric problems, we have GASTRITIS AND GASTRIC ULCERS as the main public health problems. Gastritis and gastric ulcers normally result from inflammation and corrosion of the walls of the stomach (gastric mucosa) and are generally associated (caused) by the bacterium Helicobacter pylor, which, according to the literature, this bacterium settles on these walls (of the stomach) and starts to release urease that ends up altering the normal pH of the stomach (acid), which leads to inflammation and corrosion of the mucous membranes and consequent gastritis or ulcers, respectively.
In addition to bacterial infections, gastritis and gastric ulcers are associated with several factors, with emphasis on prolonged fasting, chemical substances including drugs, alcohol, foods with strong seasonings including chilli, which ends up causing inflammation of the stomach walls and/or corrosion. of the same, resulting in the appearance of wounds and consequent gastritis or ulcers, respectively.
Among patients with gastritis and/or ulcers, one of the dilemmas is associated with the foods to consume in order to minimize the sensation of pain and discomfort.
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Since our release of the PGx capabilities in VarSeq, we’ve had a few months to gather some insights from various use cases. Some users approach PGx workflows by means of array genotyping or what seems to be a growing trend of adding the star allele calling to the existing NGS pipeline for whole genome data. Luckily, both approaches are supported with the VarSeq software platform. The genotyping method being used will also dictate what the scope of the tertiary analysis will be. For example, are your PGx reports a standalone pipeline or would your lab’s goal be to handle a dual-purpose workflow and report on PGx + Diagnostic findings.
The purpose of this webcast is to:
Discuss and demonstrate the approaches with array and NGS genotyping methods for star allele calling to prep for downstream analysis.
Following genotyping, explore alternative tertiary workflow concepts in VarSeq to handle PGx reporting.
Moreover, we will include insights users will need to consider when validating their PGx workflow for all possible star alleles and options you have for automating your PGx analysis for large number of samples. Please join us for a session dedicated to the application of star allele genotyping and subsequent PGx workflows in our VarSeq software.
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2. Definitions
Sepsis is defined as life-threatening organ dysfunction caused by a
dysregulated host response to infection
Septic shock is defined as persisting hypotension requiring vasopressors to
maintain MAP ≥65 mm Hg and having a serum lactate level >2 mmol/L
(18mg/dL) despite adequate volume resuscitation
Organ dysfunction can be identified as an acute change in total SOFA score
≥2 points consequent to the infection
Surviving sepsis campaign 2018 updates
3. SOFA Score
Mendonça, A & Vincent, Jean-Louis & Suter, Peter & Moreno, Rui & Dearden, N & Antonelli, Massimo & Takala, Jukka & Sprung, Charles & Cantraine, F. (2000). Acute renal failure in the ICU:
Risk factors and outcome evaluated by the SOFA score. Intensive care medicine. 26. 915-21. 10.1007/s001340051281.
5. Epidemiology
• In 2017, an estimated 48·9 million incident cases of sepsis were
recorded worldwide and 11 million sepsis-related deaths were
reported, representing 19·7% of all global deaths
• Study found that the sepsis death rate is 213 per 1,00,000 people
in India, 206 in Pakistan, 183 in Nepal, 136 in Bangladesh, 109 in
Bhutan, 69 in Sri Lanka and 27 in Maldives and 285 in Afghanistan
Rudd KE, Johnson SC, Agesa KM, et al. Global, regional, and national sepsis incidence and mortality, 1990-2017:
analysis for the Global Burden of Disease Study. Lancet. 2020;395(10219):200-211. doi:10.1016/S0140-
6736(19)32989-7
6. Pathophysiology of sepsis
Bhan C, Dipankar P, Chakraborty P, Sarangi PP. Role of cellular events in the pathophysiology of sepsis. Inflamm Res.
2016;65(11):853-868. doi:10.1007/s00011-016-0970-x
7. • Infection and the subsequent interaction of pathogen motifs
with various receptors present on immune cells activate a
cascade of inflammatory events that aim at removing the
pathogen and restoration of normalcy.
• If the host responses fail to contain the infection, there is a
systemic spread of infection that further leads to progression
of inflammatory changes in a dysregulated manner.
• Thus, excessive inflammatory and anti-inflammatory
responses culminate in irreversible tissue damages, multi-
organ failure, and death
Outline of sepsis development
8.
9. Overview of cellular changes occurring during sepsis
• Entry and recognition of PAMPs by PRRs upregulation of adhesion
molecules, cytokines, and ROS productions.
• These responses, when succeed in clearing the pathogens
upregulation of anti-inflammatory responses and ultimately resolution
and restoration of tissue homeostasis
• Failure of innate & adaptive responses to contain the ongoing infection
locally systemic spread of infection hyperinflamm.immune
response
• To regulate the hyperinflammatory immune cell activities, body’s
immunoregulatory responses are activated at a higher magnitude
ultimately leading to a loss of balance between inflammatory and anti-
inflammatory response and generalized immunosuppressive stage
• Different phenotypic and molecular changes take place in the immune
cells as sepsis progresses from a hyperinflammatory to an
immunosuppressive stage
• Thus, a host response that is designed to protect against pathogen causes
tissue-damaging events leading to multiorgan system failure and death.
10. Lab diagnosis of sepsis
Direct
Blood culture:
Gold standard
Methods :
• Conventional
• Automated
• MALDI-TOF
• Multiplex real
time PCR
Indirect
Biomarkers :
• Procalcitonin
• CRP
• Endotoxin
Activity Assays
• Cytokines – IL-
10,IL-6 etc
Invasive fungal
biomarkers :
• Galactomannan
• Beta-D-Glucan
Hematological parameters
• White blood count:
• > 12,000/mm3 or
• < 4,000/mm3 or
• > 10% immature forms
• Neutrophil lymphocyte
ratio > 5
• Platelet count <
80,000/mm3
11. Blood culture
• Gold standard
• Atleast 2 sets - Aerobic and Anaerobic
• Obtained prior to initiation of anti-micobial therapy
• Automated Blood cultures are preferred over conventional
• In presence of intra vascular catheters (> 48 hrs)- one blood
culture set from cath. Alongwith periph.bld cult. To rule out
CRBSI
• Differential time to positivity i.e flashing of blood collected
from cath.2 hrs before periph.bld cult.sample is useful in
diag.of CRBSI
• Disadvtgs.: 30-50% of sepsis patients are culture negative
• Time to diag.sepsis is long
12. MALDI-TOF
• Quick detection of pathogen from blood culture
• MALDI Sepsityper –Bruker Daltronics and VITEK MS blood culture (bioMerieux)
• Advtgs. :
• ID is avail.after culture within 20 min.
• Very low cost per test
• Problems encountered :
• Polymicrobial infections cannot be diagnosed
• Currently overnight incubation of blood culture broth on solid media is required prior
to MALDI-TOF MS analysis
• AST not possible
• Set up cost is very high
13. Multiplex real time PCR
• FilmArray (Biofire Dx/bioMérieux) Blood Culture Identification
Panel
• It tests for 24 bacterial and yeast pathogens plus 3 antibiotic
resistance markers.
• Verigene (Nanosphere) BC-GP and BC-GN assays that use
Gold/Ag nanoparticle probes and micro-array for detection of
bacterial pathogens and several resistance markers
14. Biomarkers
WHO defn: Any substance, structure, or process that can be measured in the
body or its products and influence or predict the incidence of outcome or
disease
• Ideal charact.of biomarkers:
• Short half life – rapid incr.with onset of sepsis and rapid decr.
• High sensitivity,high specificity
• Discriminate etiology of sepsis
• Level should not increase with assoc.co-morbidities
• Provide clinicians time to intervene for treatment
• Guide for starting and stopping antibiotics
• Standardized values
• Accurately predict severity of disease
• Help in prognostication
• Test should be easily doable
• Cost effective
• Short turn around time
• Sample requirement small
15. Procalcitonin
• PCT 116 amino acid pro-hormone synth.prim.by C-cells of
thyroid gland
• Seum levels in healthy persons < 0.05 ng/ml
• In systemic inflamm . particul . Bact .infectns it is produced in
a number of other tissues and released into circulation where
its level increases upto 1000 times
16. Limitations of PCT
Falsely raised Falsely low
Neonates < 48 hrs Early course of infection
Major trauma Localized infectns
Surg . Intervention Subacute endocarditis
Severe burns
Treatment with drugs stimul. Release of
pro-inflamm.cytokines
Invasive fung.infections
Ac.plasm.falcip.malaria
Severe cardiogenic shock
Severe liver cirrhosis/viral hepatitis
Small cell lung ca/med.ca thyroid
17. Lactate
• Sepsis may progress rapidly to septic shock that is associated with
decreased delivery of oxygen and nutrients into peripheral tissues.
• Lactate levels serve as an endpoint for resuscitation in patients with
sepsis and septic shock as part of the sepsis bundle
• Limitations :
• Elevated lactate levels can be seen in a wide variety of conditions,
such as cardiac arrest, trauma, seizure or excessive muscle activity
• Elevated levels of lactate are not considered specific for either the
diagnosis of sepsis, or predicting mortality
18. C - Reactive protein
• Synthesized prim.in liver hepatocytes
• Disc in 1930 by Tillet and Francis
• Elevated in inflamm.condns.such as Rhuematoid
arthritis,cardiovasc.dis,infection
• IL-6 is main inducer ,IL-1 enhances effect
• Limitations :
• It is sensitive but not very specific
• Levels rise within 6-24 hrs and remain elevated for 3-5 days
19. Endotoxin activity assays
• Principle : Endotoxin binds to Anti-endotoxin antibodies (IgM)
• It is delivered to neutrophils via complement receptors
• In presence of zymosan and luminol,neutrophils undergo a
respiratory burst accompanied by light emission
• Light produced is quantified by chemiluminometer
• Intensity is proportional to amount of endotoxin
• It is a predictor of mortality in critically ill patients
EAA Level Interpretation
<0.4 Low
0.4-0.6 Intermediate
>0.6 High
20. Cytokines
• Cytokines are regulators produced by the host immune
system in response to an infection or injury which have a role
in the complex pathophysiology of sepsis
• IL-6 levels are increased in patients with infectious
complications
• Studies have shown that IL-6 and IL-10 levels are correlated
with the mortality rate in septic patients
• IL-8 has been used to predict the severity of sepsis in
pediatric patients, although the utility of IL-8 has not been
confirmed in adults
• None of the cytokine markers has been proven to be more
sensitive or specific than PCT or CRP
21. Galactomannan
• Galactomannan is polysaccharide antigen that exists prim.in cell
wall of Aspergillus sp.
• GM is released in blood and other body fluids even in early stages
• Remains for 1-8 weeks
• Detection of GM antigen by ELISA is considered a
diag.microb.criterion for invasive fungal infections by EORTC/MSG
22. Galactomannan
• Galactomannan in serum and/or BAL fluid is a criterion to
classify patiens with Inv.Asp. By EORTC/MSG in 2008
• Serum galac.index ≥ 0.5 in 2 separate serum samples or ≥ 1 in
single serum sample
• BAL fluid galac.index ≥ 1 in 2 aliquots of single BAL fluid
sample
• Bio Rad Platelia Aspergillus EIA is the FDA approved assay
• Limitations :
• False positive with :
• piperacillin/tazobactam
• Fluids containing sod.gluc
• Infectns with histoplasma,paecilomyces,geotrichum
27. Other markers
• TNF alpha
• CD 64
• Soluble form of urokinase –type plasminogen activator
receptor (suPAR)
• Soluble trigging receptor expressed on myeloid cells-1 (Strem-
1)
• D-dimer
• Proadrenomedullin (ProADM)
• Myocardial Biomarkers—troponin, natriuretic peptides and
myoglobin
28. Hour-1 Surviving sepsis campaign Bundle of care
• Measure lactate level.Re-measure within 2-4 hrs if initial
lactate > 2 mmol/L
• Obtain blood cultures prior to administration of antibiotics
• Administer broad- spectrum antibiotics
• Begin rapid administration of 30ml/kg crystalloid for
hypotension or lactate ≥4 mmol/L
• Apply vasopressors if the patient is hypotensive during or
after fluid resuscitation to maintain MAP≥65 mmHg
Fig. 3 Overview of cellular changes occurring during sepsis: Entry and recognition of PAMPs by PRRs expressed on innate immune cells induce a cascade of inflammatory responses, including upregulation of adhesion molecules, cytokines, and ROS productions. These responses, when succeed in clearing the pathogens, there is upregulation of anti-inflammatory responses and ultimately resolution and restoration of tissue homeostasis (upper panel). However, if the innate and adaptive responses fail to contain the ongoing infection locally, the infection spreads systemically triggering a hyperinflammatory innate and adaptive immune response against infection. Further progression of infection and spread of the dysfunctional and altered cellular responses, including changed surface receptor expressions, inappropriate inflammatory mediator secretion, and untimely apoptosis of certain immune cells, lead to the development of sepsis (middle panel). To regulate the hyperinflammatory immune cell activities, body’s immunoregulatory responses are activated at a higher magnitude ultimately leading to a loss of balance between inflammatory and anti-inflammatory response and generalized immunosuppressive stage (bottom Panel). As described in the figure, different phenotypic and molecular changes take place in the immune cells as sepsis progresses from a hyperinflammatory to an immunosuppressive stage. Thus, a host response that is designed to protect against pathogen causes tissue-damaging events leading to multiorgan system failure and death. PE proteolytic enzymes, ADCC antibody-dependent cell-mediated cytotoxicity, iDCs immature dendritic cells (other abbreviations are described in the text)