This presentation contains slides describing normal microbial flora of human body, significance of normal flora, distribution of normal flora, immune response to infection, source and transmission of infective agents, stages of infection
This document discusses various aspects of infectious diseases including definitions, classification, transmission, and pathogenic mechanisms. It defines infection as the lodgement and multiplication of an infectious agent in the body. Infections are classified as endogenous or exogenous depending on the source, and as acute, chronic, latent, or atypical depending on clinical manifestations. Microbes can be transmitted via contact, airborne droplets, ingestion, inoculation, transplacentally, or through iatrogenic means. Pathogenicity is determined by microbial adhesion, invasiveness, antiphagocytic factors, and toxins. Exotoxins are often heat-labile proteins that can be converted to toxoids.
The document discusses specific and non-specific immune responses and immune disorders. It begins by defining specific and non-specific immunity, with non-specific immunity involving innate barriers and responses that protect against all antigens. Specific immunity provides targeted protection against specific pathogens through antibodies and T-cells. The document also examines four types of hypersensitivity reactions (allergies) and common immune disorders, providing examples to illustrate immune system functions and what can go wrong.
The document discusses the immune system and different types of immunity. It describes innate immunity, which provides non-specific protection, and adaptive immunity, which provides antigen-specific protection through B cells and T cells. It then focuses on the differences between active and passive immunity. Active immunity develops through exposure to an antigen and results in immunological memory, while passive immunity involves the transfer of ready-made antibodies without memory. Active immunity can be acquired naturally through infection or artificially through vaccination.
Host pathogen interactions - This presentation is about the Host pathogen interaction played between bacteria virus and the human body and it also explains about the different protein and enzymes secreted by pathogens to cause infection and diseases in human like the release of endotoxin and exotoxin.
The document discusses the normal microbial flora that inhabit healthy humans. It is divided into resident and transient flora. The resident flora consists of microorganisms regularly found in a given area, while the transient flora inhabits areas temporarily. The four major phyla that make up most of the human microbiota are Actinobacteria, Firmicutes, Proteobacteria, and Bacteroidetes. The normal flora varies across body sites like skin, mouth, respiratory and GI tracts. Maintaining the balance of the normal flora is important for health.
1. Innate immunity provides the first line of defense against pathogens and includes anatomical barriers, inflammation, phagocytosis, and antimicrobial proteins/peptides.
2. Adaptive immunity develops over time upon exposure to specific pathogens and provides enhanced protection through antibody production and immunological memory.
3. The major categories of innate immunity defenses are anatomical barriers, inflammation, phagocytosis, microbial antagonism by normal flora, and antimicrobial substances in tissues. Adaptive immunity involves B cells, T cells, and production of antibodies.
This document discusses various aspects of infectious diseases including definitions, classification, transmission, and pathogenic mechanisms. It defines infection as the lodgement and multiplication of an infectious agent in the body. Infections are classified as endogenous or exogenous depending on the source, and as acute, chronic, latent, or atypical depending on clinical manifestations. Microbes can be transmitted via contact, airborne droplets, ingestion, inoculation, transplacentally, or through iatrogenic means. Pathogenicity is determined by microbial adhesion, invasiveness, antiphagocytic factors, and toxins. Exotoxins are often heat-labile proteins that can be converted to toxoids.
The document discusses specific and non-specific immune responses and immune disorders. It begins by defining specific and non-specific immunity, with non-specific immunity involving innate barriers and responses that protect against all antigens. Specific immunity provides targeted protection against specific pathogens through antibodies and T-cells. The document also examines four types of hypersensitivity reactions (allergies) and common immune disorders, providing examples to illustrate immune system functions and what can go wrong.
The document discusses the immune system and different types of immunity. It describes innate immunity, which provides non-specific protection, and adaptive immunity, which provides antigen-specific protection through B cells and T cells. It then focuses on the differences between active and passive immunity. Active immunity develops through exposure to an antigen and results in immunological memory, while passive immunity involves the transfer of ready-made antibodies without memory. Active immunity can be acquired naturally through infection or artificially through vaccination.
Host pathogen interactions - This presentation is about the Host pathogen interaction played between bacteria virus and the human body and it also explains about the different protein and enzymes secreted by pathogens to cause infection and diseases in human like the release of endotoxin and exotoxin.
The document discusses the normal microbial flora that inhabit healthy humans. It is divided into resident and transient flora. The resident flora consists of microorganisms regularly found in a given area, while the transient flora inhabits areas temporarily. The four major phyla that make up most of the human microbiota are Actinobacteria, Firmicutes, Proteobacteria, and Bacteroidetes. The normal flora varies across body sites like skin, mouth, respiratory and GI tracts. Maintaining the balance of the normal flora is important for health.
1. Innate immunity provides the first line of defense against pathogens and includes anatomical barriers, inflammation, phagocytosis, and antimicrobial proteins/peptides.
2. Adaptive immunity develops over time upon exposure to specific pathogens and provides enhanced protection through antibody production and immunological memory.
3. The major categories of innate immunity defenses are anatomical barriers, inflammation, phagocytosis, microbial antagonism by normal flora, and antimicrobial substances in tissues. Adaptive immunity involves B cells, T cells, and production of antibodies.
This document discusses various concepts related to bacterial infection and virulence factors. It begins by defining key terms like infection, disease, signs and symptoms. It then describes the different types of hosts and modes of transmission of infectious agents. It discusses the concepts of reservoirs, carriers and zoonotic infections. The major sections cover the epidemiology of infections, modes of transmission including direct and indirect, and routes of entry of pathogens. The last section provides details on various bacterial virulence factors that enhance pathogenicity like adherence factors, invasion factors, toxins and mechanisms of biofilm formation.
Immunology (Innate and adaptive immune systems) (ANTIGENS (Ag)) Amany Elsayed
The document provides an overview of immunology and the immune system. It defines key terms like immunity, the immune system, and immune response. It describes the two main branches of the immune system: innate (natural) immunity and adaptive (acquired) immunity. The innate system provides non-specific resistance and is the body's first line of defense. The adaptive system provides antigen-specific immunity and develops memory to enhance the response. The document also outlines the major cells involved in the immune response, including lymphocytes, granulocytes, monocytes, macrophages and dendritic cells. It discusses the functions of phagocytic cells in phagocytosis and intracellular/extracellular killing of pathogens.
1. Microbial pathogens must gain access to the host, adhere to tissues, and evade host defenses in order to cause disease. Common entry points include mucous membranes of the respiratory, gastrointestinal, and genital tracts.
2. Once inside the host, pathogens must adhere using adhesins and penetrate host defenses using mechanisms like capsules, cell wall components, and enzymes to damage tissues. They may also produce toxins or utilize host nutrients.
3. Viruses evade immunity by growing inside host cells and causing cytopathic effects that disrupt cell functions or directly damage cells. Eukaryotic pathogens like fungi and protozoa can also invade tissues and cause disease.
The document summarizes key aspects of innate immunity. It discusses physical barriers like skin and mucous membranes, as well as cells and proteins involved in innate immunity. Cells discussed include phagocytes like macrophages and neutrophils, which kill microbes via phagocytosis and release of enzymes, reactive oxygen species, and nitric oxide. Proteins of the complement system and acute phase proteins are also summarized. The roles of fever, interferons, and tumor necrosis factors in the innate immune response are briefly described.
Mechanism of bacterial pathogenesis and virulenceMeher Rizvi
This document discusses bacterial virulence factors and mechanisms of pathogenesis. It defines key terms like pathogens, opportunistic pathogens, virulence, and colonization. It then describes several virulence factors like adhesins, pili, capsules, toxins, enzymes, and plasmids that allow bacteria to adhere to and invade host cells, evade the immune system, and cause damage. Methods of acquiring new virulence genes like plasmids, bacteriophages, and horizontal gene transfer are also summarized.
Macrophages are tissue-resident immune cells that differentiate from circulating monocytes. They perform important functions in innate and adaptive immunity such as phagocytosis of pathogens and cellular debris, antigen presentation, and secretion of inflammatory signals. Macrophages exist in different types defined by their activation mechanisms and secretory profiles, including classically activated M1 macrophages which promote inflammation and alternatively activated M2 macrophages which suppress inflammation. They play roles in tissue homeostasis, repair, and immune regulation through their phagocytic, secretory, and adaptive functions.
Central tolerance refers to deletion of self-reactive T and B cells in the thymus and bone marrow during maturation. T cells that recognize self antigens undergo apoptosis in the thymus. Peripheral tolerance uses backup mechanisms like clonal deletion through activation-induced cell death, clonal anergy from lack of co-stimulation, and suppression by regulatory T cells. These mechanisms help prevent autoimmune disease by silencing self-reactive cells that escape central tolerance.
Streptococcus pyogenes is a Gram-positive bacterium that can cause a variety of infections in humans. It commonly colonizes the throat and skin. It produces toxins and enzymes that contribute to its virulence and ability to cause disease. S. pyogenes can cause suppurative infections like pharyngitis, impetigo, and necrotizing fasciitis. It can also cause non-suppurative sequelae after infection like acute rheumatic fever and glomerulonephritis. Diagnosis involves culturing samples on blood agar and testing for sensitivity to bacitracin. Treatment involves antibiotics like penicillin. Prevention focuses on proper treatment of streptococcal infections to reduce risk of
The document summarizes the humoral immune response. It involves B cells producing antibodies that destroy extracellular microorganisms and prevent spread of intracellular infections. The process begins when a bacterium is phagocytosed by an antigen presenting cell. The antigen is processed and displayed on the cell surface. This activates helper T cells, which trigger B cell activation and antibody production. The antibodies then bind to antigens on microorganisms, marking them for destruction by immune cells and complement proteins.
This document discusses bacterial virulence factors. It defines virulence as the ability of an infectious agent to cause disease. Virulence factors help bacteria invade hosts, cause disease, and evade host defenses. These include attachment via adhesins, colonization, invasiveness through toxins/enzymes, and inhibition of phagocytosis. Specific virulence factors that promote these abilities include pili/fimbriae, adhesins, biofilms, hyaluronidase, coagulase, streptokinase, toxins like neurotoxins and enterotoxins, enzymes, and mechanisms to avoid or survive phagocytes.
This document provides an overview of the innate immune system, including its components and functions. It discusses:
1) The major components of innate immunity include anatomical barriers, cellular responses like phagocytosis, and soluble proteins. Innate immunity provides the initial response to pathogens and stimulates adaptive immunity.
2) Innate immune cells recognize pathogens through pattern recognition receptors (PRRs) that bind pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). Major PRR families include Toll-like receptors, NOD-like receptors, RIG-I-like receptors, and C-type lectin receptors.
3) Defects in PRR signaling pathways can increase
This document outlines the objectives, introduction, and conclusion of a student paper on virulence factors of bacteria. It discusses how virulence factors help bacteria colonize hosts, evade the immune system, and cause damage. The objectives are to understand how virulence factors promote colonization and damage, differentiate between endotoxins and exotoxins, and identify factors that induce autoimmune disease. Key virulence factors and their mechanisms are briefly mentioned.
This document discusses bacterial pathogenesis and infection. It covers several key topics:
1) Normal flora are microorganisms that normally live in or on the human body without causing disease. Opportunistic pathogens are normal flora that can cause disease under certain conditions if the host's immunity is compromised.
2) Bacterial infection is determined by factors of both the bacterium and host. The number and virulence of bacteria as well as the host's innate and acquired immunity impact whether infection occurs.
3) Bacterial pathogenicity is influenced by virulence factors like toxins, invasiveness, and the portal of entry. Virulence refers to an organism's ability to cause disease and is determined by its inv
The document discusses the normal microbial flora that inhabit healthy humans. It describes the different microorganisms typically found colonizing various body sites like the skin, respiratory tract, gastrointestinal tract, and genitourinary tract. The flora varies between sites and helps protect against pathogens by competing for resources and binding sites. While important for health, the normal flora can sometimes cause disease if defenses are compromised or microbes reach abnormal body sites. Key resident skin bacteria include Staphylococcus epidermidis and propionibacteria. The mouth harbors streptococci and actinomyces. The GI tract contains large numbers of lactobacilli and bifidobacteria in the small intestine and numerous anaerobes
The document discusses viral pathogenesis and genetics. It describes the cycle of viral infection as entry into host cells, primary replication at the infection site, spread within the host, and shedding/transmission. It also discusses the effects of viruses on cells and the host organism. The genetic principles of viruses are explained as mutation, selection, and recombination, which impact viral evolution, management, and experimental study.
Normal flora are microorganisms that reside harmlessly in various areas of the human body. The document discusses the normal flora found in different body sites like skin, respiratory tract, gastrointestinal tract, and urogenital tract. Key organisms that commonly constitute normal flora include Staphylococcus epidermidis and Propionibacterium acnes on the skin, Streptococcus salivarius and Streptococcus mutans in the mouth, Lactobacillus species and Bifidobacterium species in the gastrointestinal tract, and Lactobacillus acidophilus in the vagina. Normal flora play important roles like protecting the host from pathogens and aiding nutrient absorption.
This document defines and discusses antigens from several perspectives:
1) It provides a brief history of the term "antigen" and its definition as a substance that stimulates antibody production.
2) It classifies antigens based on their immunogenicity as complete or incomplete antigens.
3) It categorizes antigens based on their origin as exogenous, endogenous, autoantigens, isoantigens, or heterophile antigens.
4) It lists 10 properties that determine an antigen's ability to stimulate an immune response, including foreignness, size, chemical nature, and specificity.
5) It briefly discusses superantigens and common tests used to detect antigens.
T-Cell Activation
• Concept of immune response
• T cell-mediated immune response
• B cell-mediated immune response
I. Concept of immune response
• A collective and coordinated response to the introduction of foreign substances in an individual mediated by the cells and molecules in the immune system.
II. T cell-mediated immune response
• Cell-mediated immunity is the arm of the adaptive immune response whose role is to combat infection of intracellular pathogens, such as intracellular bacteria (mycobacteria, listeria monocytogens), viruses, protozoa, etc.
This document discusses the mechanisms of bacterial pathogenesis. It defines key terms like commensal, opportunistic pathogen, pathogen, virulence, infection, and portal of entry. It describes bacterial virulence factors such as capsules, adhesins, invasiveness, exoenzymes, and toxins. It also discusses concepts like infecting dose, clinical manifestations, and the evolution of infection.
Cytokines are small secreted proteins that mediate and regulate immunity, inflammation, and hematopoiesis. They are produced in response to an immune stimulus and act as signaling molecules between cells during immune responses. There are several main classes of cytokines, including interleukins, interferons, tumor necrosis factors, growth factors, colony stimulating factors, and chemokines. Cytokines bind to specific cell surface receptors and influence cellular processes like proliferation, differentiation, and activation.
This document summarizes opportunistic fungal infections that predominantly affect immunocompromised individuals. The most common opportunistic fungi are Candida, Aspergillus, Cryptococcus, and Pneumocystis. Candida normally exists as part of the human microbiome but can cause infections in immunocompromised patients. Aspergillus is ubiquitous in the environment and can cause infections through inhalation of spores. Cryptococcus primarily infects the lungs and central nervous system of those with advanced HIV/AIDS. Diagnosis involves microscopy, culture, and serological testing of samples from infected sites.
This document discusses innate immunity and the body's first lines of defense against infection. It describes how the epithelial surfaces provide mechanical, chemical and microbiological barriers. Phagocytes like macrophages and neutrophils play a key role by recognizing, ingesting and destroying pathogens. These cells use mechanisms like phagocytosis and generation of toxic molecules to kill invading microbes. However, some pathogens have evolved ways to avoid destruction by innate immune defenses.
This document discusses various concepts related to bacterial infection and virulence factors. It begins by defining key terms like infection, disease, signs and symptoms. It then describes the different types of hosts and modes of transmission of infectious agents. It discusses the concepts of reservoirs, carriers and zoonotic infections. The major sections cover the epidemiology of infections, modes of transmission including direct and indirect, and routes of entry of pathogens. The last section provides details on various bacterial virulence factors that enhance pathogenicity like adherence factors, invasion factors, toxins and mechanisms of biofilm formation.
Immunology (Innate and adaptive immune systems) (ANTIGENS (Ag)) Amany Elsayed
The document provides an overview of immunology and the immune system. It defines key terms like immunity, the immune system, and immune response. It describes the two main branches of the immune system: innate (natural) immunity and adaptive (acquired) immunity. The innate system provides non-specific resistance and is the body's first line of defense. The adaptive system provides antigen-specific immunity and develops memory to enhance the response. The document also outlines the major cells involved in the immune response, including lymphocytes, granulocytes, monocytes, macrophages and dendritic cells. It discusses the functions of phagocytic cells in phagocytosis and intracellular/extracellular killing of pathogens.
1. Microbial pathogens must gain access to the host, adhere to tissues, and evade host defenses in order to cause disease. Common entry points include mucous membranes of the respiratory, gastrointestinal, and genital tracts.
2. Once inside the host, pathogens must adhere using adhesins and penetrate host defenses using mechanisms like capsules, cell wall components, and enzymes to damage tissues. They may also produce toxins or utilize host nutrients.
3. Viruses evade immunity by growing inside host cells and causing cytopathic effects that disrupt cell functions or directly damage cells. Eukaryotic pathogens like fungi and protozoa can also invade tissues and cause disease.
The document summarizes key aspects of innate immunity. It discusses physical barriers like skin and mucous membranes, as well as cells and proteins involved in innate immunity. Cells discussed include phagocytes like macrophages and neutrophils, which kill microbes via phagocytosis and release of enzymes, reactive oxygen species, and nitric oxide. Proteins of the complement system and acute phase proteins are also summarized. The roles of fever, interferons, and tumor necrosis factors in the innate immune response are briefly described.
Mechanism of bacterial pathogenesis and virulenceMeher Rizvi
This document discusses bacterial virulence factors and mechanisms of pathogenesis. It defines key terms like pathogens, opportunistic pathogens, virulence, and colonization. It then describes several virulence factors like adhesins, pili, capsules, toxins, enzymes, and plasmids that allow bacteria to adhere to and invade host cells, evade the immune system, and cause damage. Methods of acquiring new virulence genes like plasmids, bacteriophages, and horizontal gene transfer are also summarized.
Macrophages are tissue-resident immune cells that differentiate from circulating monocytes. They perform important functions in innate and adaptive immunity such as phagocytosis of pathogens and cellular debris, antigen presentation, and secretion of inflammatory signals. Macrophages exist in different types defined by their activation mechanisms and secretory profiles, including classically activated M1 macrophages which promote inflammation and alternatively activated M2 macrophages which suppress inflammation. They play roles in tissue homeostasis, repair, and immune regulation through their phagocytic, secretory, and adaptive functions.
Central tolerance refers to deletion of self-reactive T and B cells in the thymus and bone marrow during maturation. T cells that recognize self antigens undergo apoptosis in the thymus. Peripheral tolerance uses backup mechanisms like clonal deletion through activation-induced cell death, clonal anergy from lack of co-stimulation, and suppression by regulatory T cells. These mechanisms help prevent autoimmune disease by silencing self-reactive cells that escape central tolerance.
Streptococcus pyogenes is a Gram-positive bacterium that can cause a variety of infections in humans. It commonly colonizes the throat and skin. It produces toxins and enzymes that contribute to its virulence and ability to cause disease. S. pyogenes can cause suppurative infections like pharyngitis, impetigo, and necrotizing fasciitis. It can also cause non-suppurative sequelae after infection like acute rheumatic fever and glomerulonephritis. Diagnosis involves culturing samples on blood agar and testing for sensitivity to bacitracin. Treatment involves antibiotics like penicillin. Prevention focuses on proper treatment of streptococcal infections to reduce risk of
The document summarizes the humoral immune response. It involves B cells producing antibodies that destroy extracellular microorganisms and prevent spread of intracellular infections. The process begins when a bacterium is phagocytosed by an antigen presenting cell. The antigen is processed and displayed on the cell surface. This activates helper T cells, which trigger B cell activation and antibody production. The antibodies then bind to antigens on microorganisms, marking them for destruction by immune cells and complement proteins.
This document discusses bacterial virulence factors. It defines virulence as the ability of an infectious agent to cause disease. Virulence factors help bacteria invade hosts, cause disease, and evade host defenses. These include attachment via adhesins, colonization, invasiveness through toxins/enzymes, and inhibition of phagocytosis. Specific virulence factors that promote these abilities include pili/fimbriae, adhesins, biofilms, hyaluronidase, coagulase, streptokinase, toxins like neurotoxins and enterotoxins, enzymes, and mechanisms to avoid or survive phagocytes.
This document provides an overview of the innate immune system, including its components and functions. It discusses:
1) The major components of innate immunity include anatomical barriers, cellular responses like phagocytosis, and soluble proteins. Innate immunity provides the initial response to pathogens and stimulates adaptive immunity.
2) Innate immune cells recognize pathogens through pattern recognition receptors (PRRs) that bind pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). Major PRR families include Toll-like receptors, NOD-like receptors, RIG-I-like receptors, and C-type lectin receptors.
3) Defects in PRR signaling pathways can increase
This document outlines the objectives, introduction, and conclusion of a student paper on virulence factors of bacteria. It discusses how virulence factors help bacteria colonize hosts, evade the immune system, and cause damage. The objectives are to understand how virulence factors promote colonization and damage, differentiate between endotoxins and exotoxins, and identify factors that induce autoimmune disease. Key virulence factors and their mechanisms are briefly mentioned.
This document discusses bacterial pathogenesis and infection. It covers several key topics:
1) Normal flora are microorganisms that normally live in or on the human body without causing disease. Opportunistic pathogens are normal flora that can cause disease under certain conditions if the host's immunity is compromised.
2) Bacterial infection is determined by factors of both the bacterium and host. The number and virulence of bacteria as well as the host's innate and acquired immunity impact whether infection occurs.
3) Bacterial pathogenicity is influenced by virulence factors like toxins, invasiveness, and the portal of entry. Virulence refers to an organism's ability to cause disease and is determined by its inv
The document discusses the normal microbial flora that inhabit healthy humans. It describes the different microorganisms typically found colonizing various body sites like the skin, respiratory tract, gastrointestinal tract, and genitourinary tract. The flora varies between sites and helps protect against pathogens by competing for resources and binding sites. While important for health, the normal flora can sometimes cause disease if defenses are compromised or microbes reach abnormal body sites. Key resident skin bacteria include Staphylococcus epidermidis and propionibacteria. The mouth harbors streptococci and actinomyces. The GI tract contains large numbers of lactobacilli and bifidobacteria in the small intestine and numerous anaerobes
The document discusses viral pathogenesis and genetics. It describes the cycle of viral infection as entry into host cells, primary replication at the infection site, spread within the host, and shedding/transmission. It also discusses the effects of viruses on cells and the host organism. The genetic principles of viruses are explained as mutation, selection, and recombination, which impact viral evolution, management, and experimental study.
Normal flora are microorganisms that reside harmlessly in various areas of the human body. The document discusses the normal flora found in different body sites like skin, respiratory tract, gastrointestinal tract, and urogenital tract. Key organisms that commonly constitute normal flora include Staphylococcus epidermidis and Propionibacterium acnes on the skin, Streptococcus salivarius and Streptococcus mutans in the mouth, Lactobacillus species and Bifidobacterium species in the gastrointestinal tract, and Lactobacillus acidophilus in the vagina. Normal flora play important roles like protecting the host from pathogens and aiding nutrient absorption.
This document defines and discusses antigens from several perspectives:
1) It provides a brief history of the term "antigen" and its definition as a substance that stimulates antibody production.
2) It classifies antigens based on their immunogenicity as complete or incomplete antigens.
3) It categorizes antigens based on their origin as exogenous, endogenous, autoantigens, isoantigens, or heterophile antigens.
4) It lists 10 properties that determine an antigen's ability to stimulate an immune response, including foreignness, size, chemical nature, and specificity.
5) It briefly discusses superantigens and common tests used to detect antigens.
T-Cell Activation
• Concept of immune response
• T cell-mediated immune response
• B cell-mediated immune response
I. Concept of immune response
• A collective and coordinated response to the introduction of foreign substances in an individual mediated by the cells and molecules in the immune system.
II. T cell-mediated immune response
• Cell-mediated immunity is the arm of the adaptive immune response whose role is to combat infection of intracellular pathogens, such as intracellular bacteria (mycobacteria, listeria monocytogens), viruses, protozoa, etc.
This document discusses the mechanisms of bacterial pathogenesis. It defines key terms like commensal, opportunistic pathogen, pathogen, virulence, infection, and portal of entry. It describes bacterial virulence factors such as capsules, adhesins, invasiveness, exoenzymes, and toxins. It also discusses concepts like infecting dose, clinical manifestations, and the evolution of infection.
Cytokines are small secreted proteins that mediate and regulate immunity, inflammation, and hematopoiesis. They are produced in response to an immune stimulus and act as signaling molecules between cells during immune responses. There are several main classes of cytokines, including interleukins, interferons, tumor necrosis factors, growth factors, colony stimulating factors, and chemokines. Cytokines bind to specific cell surface receptors and influence cellular processes like proliferation, differentiation, and activation.
This document summarizes opportunistic fungal infections that predominantly affect immunocompromised individuals. The most common opportunistic fungi are Candida, Aspergillus, Cryptococcus, and Pneumocystis. Candida normally exists as part of the human microbiome but can cause infections in immunocompromised patients. Aspergillus is ubiquitous in the environment and can cause infections through inhalation of spores. Cryptococcus primarily infects the lungs and central nervous system of those with advanced HIV/AIDS. Diagnosis involves microscopy, culture, and serological testing of samples from infected sites.
This document discusses innate immunity and the body's first lines of defense against infection. It describes how the epithelial surfaces provide mechanical, chemical and microbiological barriers. Phagocytes like macrophages and neutrophils play a key role by recognizing, ingesting and destroying pathogens. These cells use mechanisms like phagocytosis and generation of toxic molecules to kill invading microbes. However, some pathogens have evolved ways to avoid destruction by innate immune defenses.
This document summarizes immunity to microbes, including both innate and adaptive immunity. It discusses extracellular bacteria that can replicate outside of cells, such as Staphylococcus aureus and Streptococcus pneumoniae, and the innate immune response of complement activation and phagocytosis. Intracellular bacteria like Mycobacterium tuberculosis that can survive inside cells require a cell-mediated adaptive immune response. The document also covers topics like adaptive humoral and cellular immunity, superantigen activation of T cells, mechanisms of bacterial evasion of the immune system, and the roles of macrophages and cytokines in responses to intracellular microbes.
- Mycobacterium tuberculosis causes tuberculosis and infects around 1.7 million people annually, causing over 9 million new cases and 1.7 million deaths per year. An estimated 500,000 people are infected with multidrug resistant strains.
- Risk of infection and disease is highest among socioeconomically disadvantaged people with poor housing and nutrition. Tuberculosis is transmitted via respiratory aerosols from people with active, untreated tuberculosis.
- Laboratory diagnosis involves microscopy, culture, and molecular techniques using sputum, gastric washings, urine, tissues or other clinical samples. Staining methods like Ziehl-Neelsen identify acid-fast bacilli. Culturing is needed for species identification and drug
Malaria is a disease caused by Plasmodium parasites transmitted through the bites of infected Anopheles mosquitoes. It is a major global health issue affecting millions each year, with most cases and deaths occurring in sub-Saharan Africa. The parasites complete part of their life cycle in the liver and red blood cells of the human host. Malaria prevention focuses on reducing human-mosquito contact through vector control measures like insecticide-treated bed nets and indoor residual spraying.
This document provides an overview of immunology concepts and terminology. It begins with definitions of key terms like antigen, antibody, innate immunity and acquired immunity. It then describes in more detail:
- The cells and organs involved in the immune system like B cells, T cells, lymph nodes, spleen.
- Types of immunity like natural, artificial, active, passive.
- Mechanisms of innate immunity like epithelial barriers, mucus, cilia, antimicrobial peptides, inflammation, fever.
- Antigen-antibody reactions like precipitation, agglutination, complement fixation, neutralization.
- Structure and properties of antibodies like IgG, IgM, IgA classes.
So
The document summarizes the key differences between innate and adaptive immunity. Innate immunity is present from birth and provides non-specific resistance to pathogens. It involves anatomical barriers, phagocytes, complement proteins, cytokines and other cellular components. Adaptive immunity is acquired during life and provides pathogen-specific resistance through T cells, B cells, antibodies, immunological memory and specificity. Dendritic cells, macrophages, complement pathways and cytokines act as bridges between the innate and adaptive immune systems.
This document discusses bacterial pathogenicity and virulence factors. It begins with defining key terms like pathogenesis, virulence, and types of bacterial pathogens. It then covers various requirements for bacterial pathogenicity like adhesion, invasion, multiplication, and tissue destruction. The document discusses several virulence factors like capsules, cell wall proteins, cytotoxins, fimbriae, biofilms, and exotoxins that allow bacteria to evade host defenses and cause disease. It also covers concepts like quorum sensing, bacterial secretion systems, and mechanisms of bacterial infection and colonization.
Dennis M. Mondah presented a seminar topic on multi drug resistant tuberculosis under the guidance of Dr. Prof Ramalingappa, Chairman of the Department of Microbiology at Davangere University. The presentation covered the microbiology, pathogenesis, diagnosis and treatment of tuberculosis, with a focus on drug resistant forms of the disease. It discussed how mutations in genes like inhA, kasA, ndh and rpoB can lead to resistance to first line drugs like isoniazid and rifampicin. Diagnosis of multi drug resistant tuberculosis involves drug susceptibility testing, while treatment follows WHO guidelines using at least four effective drugs over an 18-24 month period. The development of drug resistance poses a challenge for
The document discusses three pathogenic gram-positive bacilli: Corynebacterium, Listeria monocytogenes, and Erysipelothrix rhusopathiae. Corynebacterium includes the species C. diphtheriae, which causes respiratory diphtheria, and C. urealyticum, which can cause urinary tract infections. L. monocytogenes is an intracellular pathogen that can cause listeriosis, especially in immunocompromised individuals. E. rhusopathiae causes erysipeloid skin lesions in those exposed through meat/fish handling and can potentially spread systemically.
The document discusses innate immunity, which is the first line of defense against infection. It has no memory and acts quickly through physical, chemical, and biological barriers as well as cellular and soluble components. Pattern recognition receptors recognize pathogen associated molecular patterns to initiate innate immune responses without prior exposure. Phagocytic cells play a key role through mechanisms like phagocytosis, respiratory burst, and degranulation to destroy pathogens intracellularly or extracellularly. Inflammation is induced as a secondary response to aid in pathogen elimination and tissue repair.
This document discusses vaccine delivery systems, including uptake of antigens, single shot vaccines, and mucosal and transdermal delivery. It defines vaccines as biological preparations that improve immunity, and outlines the history from Edward Jenner's smallpox vaccine to modern vaccines. Traditional vaccines include killed and live attenuated versions for bacteria and viruses. Single shot vaccines aim to replace boosters with encapsulated antigens. Mucosal surfaces are a major entry point for pathogens, and mucosal vaccines aim to induce protective immunity at sites of entry using emulsions, strips, liposomes or nanoparticles. The skin is also a vaccine delivery site due to its size and accessibility, using technologies like microneedles or electroporation to enhance permeation
This document provides an overview of microbiology and the antibiotic meropenem. It discusses microbiology topics like pathogens, disease, and antibiotics. It then focuses on meropenem, describing it as a broad-spectrum carbapenem antibiotic. Details are provided on its mechanism of action, pharmacokinetics, therapeutic uses, dosing and administration for various bacterial infections and pathogens. Adverse effects and drug interactions are also summarized.
Tuberculosis is caused by the bacterium Mycobacterium tuberculosis. It primarily affects the lungs but can spread to other organs. TB is transmitted through inhaling respiratory droplets from infected individuals. Most people who are exposed will contain the infection without symptoms, but some will develop active progressive disease. The immune response involves macrophages and T cells forming granulomas to wall off the bacteria. Diagnosis involves tuberculin skin testing and sputum examination. Treatment requires a multi-drug regimen over several months to eliminate the infection.
The normal human skin is colonized by many bacteria that live harmlessly in communities known as the skin microbiome. The resident bacteria include propionibacterium species in hair follicles, and aerobic cocci and coryneforms on the surface. Staphylococcus aureus and propionibacteria can produce free fatty acids from skin lipids. Impetigo is a common skin infection caused by S. aureus or streptococci, occurring as non-bullous or bullous types. Bullous impetigo is caused by exfoliative toxins that disrupt skin adhesion molecules.
Drugs affecting gastrointestinal function: Drugs for Constipation & Diarrhoea...jhabarola
The innate immune system provides the first line of defense against pathogens. It recognizes pathogens through pattern recognition receptors (PRRs) that detect pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). The main PRRs are Toll-like receptors, NOD-like receptors, RIG-I-like receptors, and lectins. Recognition of PAMPs/DAMPs by PRRs activates innate immune responses like phagocytosis, inflammation, and antigen presentation. Innate immunity has no immunological memory and acts through physical, chemical, and cellular barriers against pathogens in a nonspecific manner.
Basic immunology from the dermatologic point of viewAhmed Amer
The document discusses the immune system, focusing on innate immunity and the skin's role in protection. It describes how the skin provides a mechanical barrier and uses the immune system for protection through skin-associated lymphoid tissues. The innate immune system includes physical barriers and pattern recognition receptors that recognize pathogens. Toll-like receptors are a type of pattern recognition receptor that recognize pathogen-associated molecular patterns and trigger cytokine production and adaptive immunity.
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This lecture presentation contains description of arbovirus particularly detailing Dengue virus infections. Lecture outlined general characteristics of Arbovirus, classification of Arboviruses, salient features of Dengue virus, dengue pathogenesis, clinical course, laboratory diagnosis, complications of secondary dengue and some recent aspect of dengue vaccine preparation.
This powerpoint contains slides describing types of hepatitis viruses, pathogenesis, clinical course, laboratory diagnosis, treatment and prevention against hepatitis viruses. This presentation is intended to use by medical students, nurses, paramedics in the learning on virology. The slided could also be resource materials for the academicians.
This presentation contains 53 power point slides. These slides have description between virus and host cell interactions including concept of permissive and non-permissive infection, latent infection and host immune response to viral infection. Slides are designed for medical students, nurses, academicians who are teaching virology and microbiology in medical universities, schools or college.
This presentation contains 45 slides on general virology comprises of topics on viral classification, transmission, pathogenesis, viral cytopathic effect, stages of viral infections, antiviral drugs and viral vaccines. It also have a slide noting an outline of laboratory diagnosis of viral infection. This power point presentation was designed for medical students, nurses and academicians teaching virology and microbiology in medical universities, schools or colleges.
The document discusses the history of virology research from the late 19th century to present day. Some of the key events summarized include:
- In 1892, Iwanowski discovered an infectious agent that could pass through porcelain filters.
- In 1898, Loeffler and Frosch concluded that the foot-and-mouth disease agent was smaller than bacteria and must replicate.
- Advances in tissue culture and electron microscopy in the 1900s allowed visualization and growth of viruses outside of host cells.
- Discovery of plant, insect, bacterial, and oncogenic viruses followed. Twort and d'Herelle proved bacterial viruses.
- Methods of virus purification, structure determination, and growth in eggs and
This presentation is on basic virology on Enterovirus diseases. Viruses includes Coxsackie virus, entero virus 71, rota virus, polio virus. Slides are suitable for medical students and medical graduate.
This document describes the structures and components of bacterial cells. It discusses the essential structures like the cell wall, plasma membrane, ribosomes, and nucleoid as well as nonessential structures like capsules, flagella, and pili. The cell wall is composed of peptidoglycans, teichoic acids, and lipopolysaccharides. Gram-positive and gram-negative bacteria differ in their cell wall composition, affecting how they stain. Other structures like plasmids, capsules, and spores are described along with their functions. The roles of bacterial structure in laboratory identification through staining methods like gram and acid-fast staining are also summarized.
This document discusses the morphology and structures of bacterial cells. It begins by outlining the learning objectives which are to describe different bacterial shapes and arrangements, basic bacterial cell structures and their functions, staining characteristics based on structures, and how structure relates to laboratory identification. It then details the various bacterial cell components such as the cell wall, plasma membrane, ribosomes, and other internal structures. It explains how these structures determine staining properties and relates morphology to identification. The document uses diagrams to illustrate the different bacterial forms, components, and arrangements.
Contents of this presentation is targeted towards undergraduate medical students who have started their general Microbiology. Slides of this presentation shall also provide critical thinking to correlate basic Medical Microbiology with clinical aspect. Contents includes morphology of bacteria, cell wall structure of bacteria, accessory organs like flagellum, capsule, spore, plasmid etc. Also discuss the role of antibiotics over different structure of bacteria and staining characters of gram positive, gram negative or acid fast bacteria.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
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Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
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.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
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1. PATHOGENESIS II:
HOST DEFENSE AND PAHOGENICITY
OF THE MICROBES
Dr. Tarek Mahbub Khan
MBBS, M.Phil (virology)
Assistant professor
2. TLO
• Outline of host defense against infectious disease
• Define normal flora
• Distribution of normal flora
• Protective function and clinical significance of normal flora
• Stages of bacterial pathogenesis
• Mode of transmission
• Routes of transmission
7. INFLAMMATORY RESPONSE
• PYOGENIC RESPONSE (Result in formation of pus)
– Pathogens are pyogenic
– Extracellular
– Mediated by complements, PMN, antibody
– Usually acute
• GRANULOMATOUS RESPONSE (Formation of granuloma)
– Pathogens are intracellular
– Macrophage and helper T cells are the components
– Usually chronic
12. PROCESS OF PHAGOCYTOSIS
• MIGRATION
– Mediated by IL-8, C5a, Killikrein
– Adhesion is mediated by interactions between PMN cells
with selectin protein of endothelium and integrin of PMN
cells with ICAM
• INGESTION
– Formation of phagosome
– Mediated by IgG, C3b (opsonization)
• KILLING
13. NORMAL FLORA: role in host defense
Normal flora is the term used to describe the various bacteria
and fungi that are permanent residents of certain body sites,
especially the skin, oropharynx, colon, and vagina
14. COMMENSALS
Commensals are organisms that derive benefit from
another host but do not damage that host.
The normal flora are often referred as commensals.
15. SIGNIFICANCE OF THE NORMAL FLORA
• May produce disease in the following conditions:
– In immunocompromised patient
– When organisms travel to an unusual site
• Colonization resistance:
– Occupy receptors of other pathogenic bacteria and
thereby limits infection
• Some has metabolic function:
– Synthesis of vitamin B12 and vitamin K
16. NORMAL FLORA OF DIFFERENT BODY SITES
• SKIN
– Staphylococcus epidermidis, propionibacterium acnes,
Candida albicans
• RESPIRATORY TRACT
– NOSE: Staphylococcus aureus
– THROAT: Viridans streptococci, Neisseria species
– MOUTH: Eikenella corodens, Bacteroides
17. • INTESTINAL TRACT
– The small intestine usually contains small numbers of
streptococci, lactobacilli, and yeasts, particularly C.
albicans.
– Escherichia coli
• GENITOURINARY TRACT
– Group B Streptococci
– Candida Albicans
NORMAL FLORA OF DIFFERENT BODY SITES
18. TYPES OF BACTERIAL INFECTIONS
• TWO major mechanisms:
– Toxin mediated
• Exotoxin
• Endotoxin
– Invasion and inflammation
19. STAGES OF BACTERIAL PATHOGENESIS
1. Transmission into the portal of entry.
2. Evasion of primary host defence
3. Adherence
4. Colonization
20. 5. Disease :by toxin production or invasion
6. Host responses
7. Progression or resolution of infection
STAGES OF BACTERIAL PATHOGENESIS
21.
22. SUMMARY
• Host defense is mediated through innate and acquired arm of
the immune system
• Intracellular pathogens are controlled by macrophage and T
cells mediated response
• Extracellular pathogens are controlled by complement
activation, antibody
• Infection may be pyogenic or granulomatous in type
• Bacterial disease may be toxin mediated or invasive
23. • Normal flora are the permanent resident of certain body sites
• They have protective function but some time may produce
disease when patient becomes immunocompromised
• Transmission may occurs through respiratory, gastrointestinal,
skin or genitourinary routes
• Vertical transmission occurs from mother to the offspring
through placental route, vaginal route or breast milk
SUMMARY
24. REFERENCE
• Warren Levinson. Review of Medical Microbiology and
Immunology, 11th edition (2010). Appleton and Lange.
• Geo. F. Brooks, Karen C. Carroll, Janet S. Butel, Stephen A.
Morse, Timothy A. Mietzner. Medical Microbiology, 25th
edition (2010). Appleton & Lange.