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.
The document discusses bacterial pathogenesis and virulence. It describes three main ways bacteria cause disease: 1) invasiveness through mechanisms like adhesion and toxin production, 2) toxigenesis through exotoxins and endotoxins, and 3) evading host immune responses. Specific virulence factors and pathogenesis mechanisms are discussed for different bacteria like Pseudomonas aeruginosa and Mycobacterium tuberculosis. The host barriers bacteria must overcome include phagocytosis, complement activation, and adaptive immune responses; bacteria have evolved strategies to inhibit or subvert these defenses.
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.
Bacterial Pathogenesis and Virulence FactorsHany Lotfy
The document discusses various aspects of bacterial pathogenesis and infection. It defines key terms like infection, pathogenicity, and virulence. It describes the host susceptibility factors and different types of pathogens. It explains the various routes of bacterial entry into the human body and the patterns of infections. It discusses Koch's postulates and how pathogens are linked to specific diseases. It also summarizes the multistep process bacteria use to cause infection, including acquiring virulence genes, sensing the environment, expressing virulence factors, adhering to and invading tissues, acquiring nutrients, surviving host defenses, and evading the immune system.
Bacteria have several virulence factors that allow them to cause infection by adhering to host cells, invading tissues, competing for nutrients, resisting the immune system, and secreting toxins. The main virulence factors discussed are adhesion through fimbriae and adhesins, invasion through enzymes, competing for iron through siderophores, resisting phagocytosis through capsules and other mechanisms, and damaging tissues through exotoxins and endotoxins. These virulence factors enable bacteria to overcome the host's defenses and cause disease.
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 defines various terminologies related to microbial pathogenicity and infection. It discusses terms like saprophytes, parasites, commensals, pathogens, opportunistic pathogens, infection, colonization, infestation, and more. It also classifies infections based on factors like source, clinical manifestation, epidemiological patterns, and more. Finally, it covers various mechanisms of microbial pathogenicity like adhesion, invasiveness, toxins, inhibition of phagocytosis, and more.
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.
The document discusses bacterial pathogenesis and virulence. It describes three main ways bacteria cause disease: 1) invasiveness through mechanisms like adhesion and toxin production, 2) toxigenesis through exotoxins and endotoxins, and 3) evading host immune responses. Specific virulence factors and pathogenesis mechanisms are discussed for different bacteria like Pseudomonas aeruginosa and Mycobacterium tuberculosis. The host barriers bacteria must overcome include phagocytosis, complement activation, and adaptive immune responses; bacteria have evolved strategies to inhibit or subvert these defenses.
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.
Bacterial Pathogenesis and Virulence FactorsHany Lotfy
The document discusses various aspects of bacterial pathogenesis and infection. It defines key terms like infection, pathogenicity, and virulence. It describes the host susceptibility factors and different types of pathogens. It explains the various routes of bacterial entry into the human body and the patterns of infections. It discusses Koch's postulates and how pathogens are linked to specific diseases. It also summarizes the multistep process bacteria use to cause infection, including acquiring virulence genes, sensing the environment, expressing virulence factors, adhering to and invading tissues, acquiring nutrients, surviving host defenses, and evading the immune system.
Bacteria have several virulence factors that allow them to cause infection by adhering to host cells, invading tissues, competing for nutrients, resisting the immune system, and secreting toxins. The main virulence factors discussed are adhesion through fimbriae and adhesins, invasion through enzymes, competing for iron through siderophores, resisting phagocytosis through capsules and other mechanisms, and damaging tissues through exotoxins and endotoxins. These virulence factors enable bacteria to overcome the host's defenses and cause disease.
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 defines various terminologies related to microbial pathogenicity and infection. It discusses terms like saprophytes, parasites, commensals, pathogens, opportunistic pathogens, infection, colonization, infestation, and more. It also classifies infections based on factors like source, clinical manifestation, epidemiological patterns, and more. Finally, it covers various mechanisms of microbial pathogenicity like adhesion, invasiveness, toxins, inhibition of phagocytosis, and more.
This document discusses host-parasite relationships and the entry of microorganisms into hosts. It defines key terms like host, parasite, pathogen, and explores different types of symbiotic relationships like commensalism, parasitism, and mutualism. Normal flora that benefit hosts are present in various sites like the skin, mouth, respiratory and intestinal tracts. Microorganisms can enter through these areas, especially if barriers are disrupted. Entry is also possible directly through uptake or antigen sampling in mucous membranes.
Pathogenic mechanisms of microbes of medical importanceJoyce Mwatonoka
The document summarizes the pathogenic mechanisms of microbes that are medically important. It discusses key terms and outlines various mechanisms including adherence, invasion, evasion of host defenses, and toxigenesis. Specifically, it describes how bacteria adhere to host cells using adhesins and receptors. It also explains how they invade tissues using invasins like hyaluronidase and collagenase. Bacteria can evade host defenses by inhibiting phagocytosis and surviving inside phagocytes. Some vary antigens to avoid immune responses. Toxins including exotoxins and endotoxins are also discussed.
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.
Viral infections can occur at the cellular, individual, and community levels. At the cellular level, viral infection may cause cytocidal effects, cellular proliferation, or steady state infection through various mechanisms of cellular injury. Inclusion bodies are virus-specific intracellular masses that can be seen in infected cells under microscopy. Viral infections may be classified as inapparent, apparent acute, subacute, or chronic, and some viruses like herpes can cause latent infections. Viruses enter the body through routes like respiratory, alimentary, skin, genital, conjunctival, or congenital transmission. The host mounts non-specific responses like age, hormones, malnutrition, fever, and interferons as well as specific humoral
The document discusses host and virus interaction, including the stages of viral infection and types of virus-cell interaction. It provides details on:
1. The stages of viral infection include primary infection of cells at the site of entry, viremia where the virus enters the bloodstream, and secondary infection of other organs.
2. Virus-cell interaction can be cytocidal, causing cell death, or non-cytocidal where cells survive infection. Persistent and latent infections allow long-term virus maintenance in cells.
3. Common sites of viral entry into the host include respiratory, urogenital, ocular, and skin routes, which viruses access by exploiting breaches in barriers.
This document provides an overview of bacterial pathogenesis. It discusses Koch's postulates, virulence factors, types of infections, mechanisms of pathogenesis including transmission, adherence, invasion, inflammation and toxin production. Key points covered include the definition of a pathogen and virulence, examples of virulence factors for common bacteria, how bacteria adhere and invade host tissues, and the role of exotoxins and endotoxins in disease.
This document discusses bacterial adhesion, invasion, and colonization. It describes how bacteria initially adhere to host surfaces through transient association with mucus, weak association with carbohydrates, or strong association with proteins. This adhesion allows bacteria to colonize sites like the nasal cavity or intestines. The document then examines two mechanisms of bacterial invasion - the zipper mechanism where engagement of bacterial and host proteins triggers strengthening of cell contacts, and the trigger mechanism where bacteria activate host signaling to induce membrane ruffling and bacterial uptake. Specific examples of Listeria and Salmonella invasion are provided. The document concludes with details on Salmonella colonization in the intestines facilitated by its ability to use tetrathionate as an electron acceptor.
This document defines key terminology related to microbial pathogenicity and discusses various concepts including:
1. It classifies microbes as saprophytes, parasites, commensals, and pathogens.
2. It describes the infection process and different types of infections such as primary, secondary, and nosocomial.
3. It explains mechanisms of microbial pathogenicity including routes of transmission, infective dose, evasion of host defenses, adhesion, invasion, and the role of toxins and pathogenicity islands.
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.
This document summarizes bacterial toxins. It describes two main types - endotoxins and exotoxins. Endotoxins are lipopolysaccharides associated with the cell walls of gram-negative bacteria. They are heat-stable and can cause fever, shock, and death. Exotoxins are heat-labile protein toxins secreted by bacteria, including diphtheria toxin, staphylococcal enterotoxins, and streptococcal toxins. Many exotoxins have an A/B subunit structure and act intracellularly through enzymatic activity. They can cause illnesses like toxic shock syndrome. Bacterial toxins are major virulence factors that damage host cells through various mechanisms.
Viruses are small infectious agents that can only replicate inside living host cells. They contain either DNA or RNA and have a variety of shapes, sizes, and structures. Viruses infect all types of organisms from plants and animals to bacteria and archaea. They lack cellular machinery like ribosomes and must hijack host cell mechanisms to produce new viral particles. The replication cycle involves a virus attaching to and entering a host cell, releasing its genetic material, making copies of itself using host cell resources, assembling new viral particles, and exiting to infect new host cells.
The document discusses normal flora, which are microorganisms that inhabit healthy humans without causing harm. Normal flora are found on skin and mucous membranes but not inside organs. The skin and mucous membranes harbor both resident and transient flora. The document then describes characteristics, types, roles, and locations of normal flora in different parts of the body including skin, oral cavity, respiratory tract, digestive tract, and urogenital tract. Common genera of normal flora are discussed for each location.
This document discusses pathogenicity and virulence of microbes. It defines key terms like pathogenicity, infectiousness, infection, disease, and discusses the relationship between microbes and their hosts. It describes different types of pathogens like primary/obligate and opportunistic pathogens. It also discusses factors that determine pathogenicity like the microbial species, host species, and environment. It provides examples of opportunistic pathogens like E. coli and S. aureus. Finally, it defines virulence and describes how microbes can be attenuated to produce vaccines.
This document discusses bacteriophages (phages), viruses that infect bacteria. It covers the composition and structure of phages, how they infect host cells through adsorption and nucleic acid injection, and their multiplication cycles of either the lytic or lysogenic pathways. The document also discusses phage typing, which uses specific phages to identify and differentiate bacterial pathogens, and applications of phages in areas like diagnostics, therapeutics, biocontrol, and more.
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.
The document defines key terms related to bacterial pathogenicity and mechanisms by which bacteria cause disease. It discusses how bacteria penetrate host defenses through adherence, capsules, and enzymes. It also describes the role of toxins, including exotoxins and endotoxins, in bacterial pathogenesis. The summary provides an overview of the main points covered in the document.
Virology is the study of viruses and their relationship with hosts. Viruses are acellular organisms that can only replicate inside host cells. They have nucleic acid genomes and use host cell machinery to assemble new viral particles. Viruses come in a variety of shapes and sizes, and some have envelopes derived from host cell membranes. They enter host cells, express their genes, replicate their genomes, assemble new viral particles, and exit host cells to infect new targets. Viruses are cultivated using various methods including cell cultures, embryonated eggs, and animal models to study viral replication and pathogenesis.
The document discusses key concepts related to host-pathogen relationships and the occurrence and spread of infectious diseases. It defines important terms like infection, disease, colonization, and defines the roles of the host and pathogen. It describes the chain of infection and factors that influence a host's resistance or susceptibility to disease. It also outlines common routes of entry for pathogens, signs and symptoms for different types of infections, and ways that pathogens can spread within the body and between hosts through different modes of transmission.
A short yet comprehensive presentation on bacterial genetics, an important microbiology topic for BDS 2nd, MBBS 2nd and MD/MS /MDS 1st . Made using CP Baveja's Textbook of Microbiology. Meant as an introduction and overview with stress on some key areas.
Topics covered: Basic Principles, Synthesis of Protein, Extra Chromosomal Genetic Material, Bacterial Variation , Gene Transfer, Genetic Mechanisms of Drug Resistance, Genetic Engineering, DNA Probes, Polymerase Chain Reaction, Genetically Modified Organisms and Gene Therapy.
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.
Anti-microbial resistance has become a world health issue today. Therefore it is imperative to know about the methods of acquiring resistance and ways to deal with the situation and prevent resistance.
The seminar is about this article: Containment of a Methicillin-resistant Staphylococcus aureus outbreak in a Neonatal Intensive Care Unit.
I described
This document discusses host-parasite relationships and the entry of microorganisms into hosts. It defines key terms like host, parasite, pathogen, and explores different types of symbiotic relationships like commensalism, parasitism, and mutualism. Normal flora that benefit hosts are present in various sites like the skin, mouth, respiratory and intestinal tracts. Microorganisms can enter through these areas, especially if barriers are disrupted. Entry is also possible directly through uptake or antigen sampling in mucous membranes.
Pathogenic mechanisms of microbes of medical importanceJoyce Mwatonoka
The document summarizes the pathogenic mechanisms of microbes that are medically important. It discusses key terms and outlines various mechanisms including adherence, invasion, evasion of host defenses, and toxigenesis. Specifically, it describes how bacteria adhere to host cells using adhesins and receptors. It also explains how they invade tissues using invasins like hyaluronidase and collagenase. Bacteria can evade host defenses by inhibiting phagocytosis and surviving inside phagocytes. Some vary antigens to avoid immune responses. Toxins including exotoxins and endotoxins are also discussed.
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.
Viral infections can occur at the cellular, individual, and community levels. At the cellular level, viral infection may cause cytocidal effects, cellular proliferation, or steady state infection through various mechanisms of cellular injury. Inclusion bodies are virus-specific intracellular masses that can be seen in infected cells under microscopy. Viral infections may be classified as inapparent, apparent acute, subacute, or chronic, and some viruses like herpes can cause latent infections. Viruses enter the body through routes like respiratory, alimentary, skin, genital, conjunctival, or congenital transmission. The host mounts non-specific responses like age, hormones, malnutrition, fever, and interferons as well as specific humoral
The document discusses host and virus interaction, including the stages of viral infection and types of virus-cell interaction. It provides details on:
1. The stages of viral infection include primary infection of cells at the site of entry, viremia where the virus enters the bloodstream, and secondary infection of other organs.
2. Virus-cell interaction can be cytocidal, causing cell death, or non-cytocidal where cells survive infection. Persistent and latent infections allow long-term virus maintenance in cells.
3. Common sites of viral entry into the host include respiratory, urogenital, ocular, and skin routes, which viruses access by exploiting breaches in barriers.
This document provides an overview of bacterial pathogenesis. It discusses Koch's postulates, virulence factors, types of infections, mechanisms of pathogenesis including transmission, adherence, invasion, inflammation and toxin production. Key points covered include the definition of a pathogen and virulence, examples of virulence factors for common bacteria, how bacteria adhere and invade host tissues, and the role of exotoxins and endotoxins in disease.
This document discusses bacterial adhesion, invasion, and colonization. It describes how bacteria initially adhere to host surfaces through transient association with mucus, weak association with carbohydrates, or strong association with proteins. This adhesion allows bacteria to colonize sites like the nasal cavity or intestines. The document then examines two mechanisms of bacterial invasion - the zipper mechanism where engagement of bacterial and host proteins triggers strengthening of cell contacts, and the trigger mechanism where bacteria activate host signaling to induce membrane ruffling and bacterial uptake. Specific examples of Listeria and Salmonella invasion are provided. The document concludes with details on Salmonella colonization in the intestines facilitated by its ability to use tetrathionate as an electron acceptor.
This document defines key terminology related to microbial pathogenicity and discusses various concepts including:
1. It classifies microbes as saprophytes, parasites, commensals, and pathogens.
2. It describes the infection process and different types of infections such as primary, secondary, and nosocomial.
3. It explains mechanisms of microbial pathogenicity including routes of transmission, infective dose, evasion of host defenses, adhesion, invasion, and the role of toxins and pathogenicity islands.
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.
This document summarizes bacterial toxins. It describes two main types - endotoxins and exotoxins. Endotoxins are lipopolysaccharides associated with the cell walls of gram-negative bacteria. They are heat-stable and can cause fever, shock, and death. Exotoxins are heat-labile protein toxins secreted by bacteria, including diphtheria toxin, staphylococcal enterotoxins, and streptococcal toxins. Many exotoxins have an A/B subunit structure and act intracellularly through enzymatic activity. They can cause illnesses like toxic shock syndrome. Bacterial toxins are major virulence factors that damage host cells through various mechanisms.
Viruses are small infectious agents that can only replicate inside living host cells. They contain either DNA or RNA and have a variety of shapes, sizes, and structures. Viruses infect all types of organisms from plants and animals to bacteria and archaea. They lack cellular machinery like ribosomes and must hijack host cell mechanisms to produce new viral particles. The replication cycle involves a virus attaching to and entering a host cell, releasing its genetic material, making copies of itself using host cell resources, assembling new viral particles, and exiting to infect new host cells.
The document discusses normal flora, which are microorganisms that inhabit healthy humans without causing harm. Normal flora are found on skin and mucous membranes but not inside organs. The skin and mucous membranes harbor both resident and transient flora. The document then describes characteristics, types, roles, and locations of normal flora in different parts of the body including skin, oral cavity, respiratory tract, digestive tract, and urogenital tract. Common genera of normal flora are discussed for each location.
This document discusses pathogenicity and virulence of microbes. It defines key terms like pathogenicity, infectiousness, infection, disease, and discusses the relationship between microbes and their hosts. It describes different types of pathogens like primary/obligate and opportunistic pathogens. It also discusses factors that determine pathogenicity like the microbial species, host species, and environment. It provides examples of opportunistic pathogens like E. coli and S. aureus. Finally, it defines virulence and describes how microbes can be attenuated to produce vaccines.
This document discusses bacteriophages (phages), viruses that infect bacteria. It covers the composition and structure of phages, how they infect host cells through adsorption and nucleic acid injection, and their multiplication cycles of either the lytic or lysogenic pathways. The document also discusses phage typing, which uses specific phages to identify and differentiate bacterial pathogens, and applications of phages in areas like diagnostics, therapeutics, biocontrol, and more.
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.
The document defines key terms related to bacterial pathogenicity and mechanisms by which bacteria cause disease. It discusses how bacteria penetrate host defenses through adherence, capsules, and enzymes. It also describes the role of toxins, including exotoxins and endotoxins, in bacterial pathogenesis. The summary provides an overview of the main points covered in the document.
Virology is the study of viruses and their relationship with hosts. Viruses are acellular organisms that can only replicate inside host cells. They have nucleic acid genomes and use host cell machinery to assemble new viral particles. Viruses come in a variety of shapes and sizes, and some have envelopes derived from host cell membranes. They enter host cells, express their genes, replicate their genomes, assemble new viral particles, and exit host cells to infect new targets. Viruses are cultivated using various methods including cell cultures, embryonated eggs, and animal models to study viral replication and pathogenesis.
The document discusses key concepts related to host-pathogen relationships and the occurrence and spread of infectious diseases. It defines important terms like infection, disease, colonization, and defines the roles of the host and pathogen. It describes the chain of infection and factors that influence a host's resistance or susceptibility to disease. It also outlines common routes of entry for pathogens, signs and symptoms for different types of infections, and ways that pathogens can spread within the body and between hosts through different modes of transmission.
A short yet comprehensive presentation on bacterial genetics, an important microbiology topic for BDS 2nd, MBBS 2nd and MD/MS /MDS 1st . Made using CP Baveja's Textbook of Microbiology. Meant as an introduction and overview with stress on some key areas.
Topics covered: Basic Principles, Synthesis of Protein, Extra Chromosomal Genetic Material, Bacterial Variation , Gene Transfer, Genetic Mechanisms of Drug Resistance, Genetic Engineering, DNA Probes, Polymerase Chain Reaction, Genetically Modified Organisms and Gene Therapy.
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.
Anti-microbial resistance has become a world health issue today. Therefore it is imperative to know about the methods of acquiring resistance and ways to deal with the situation and prevent resistance.
The seminar is about this article: Containment of a Methicillin-resistant Staphylococcus aureus outbreak in a Neonatal Intensive Care Unit.
I described
This document provides an overview of advancements in vaccinology. It discusses the concept and types of vaccines including live attenuated, inactivated, toxoid, subunit, conjugate, DNA, and recombinant vaccines. It describes the process of designing vaccines including determining antigens, conducting pre-clinical and clinical trials. New approaches like reverse vaccinology and edible vaccines are also summarized. Reverse vaccinology uses genomic sequencing to predict vaccine candidates while edible vaccines aim to induce mucosal immunity by expressing antigens in edible plants. The document outlines the development of several vaccines including the first successful meningococcal B vaccine which was developed using reverse vaccinology.
This document discusses the classification and typing of bacteria. It begins by explaining that bacteria can be grouped using phenotypic typing schemes utilized by clinicians, which examine bacterial morphology, staining properties, oxygen requirements, and biochemical tests. It also notes the importance of identifying the environmental reservoir and transmission means for clinicians. The document then provides details on various classification schemes for bacteria, including based on shape, staining, oxygen requirements, temperature tolerance, and structure. It focuses on the Gram stain technique and discusses characteristics of Gram-positive and Gram-negative bacteria.
This document provides an overview of antimicrobial resistance. It begins by defining drug resistance as the unresponsiveness of microorganisms to antimicrobial agents. It then discusses the history of resistance, noting that Fleming warned of this danger in 1945. The document outlines the different types of resistance, including natural/primary resistance that microbes innately possess and acquired resistance that develops from use of antimicrobials over time. Microbes can develop resistance through mutation of genetic material or acquisition of new genes. The mechanisms of resistance include drug tolerance, drug destruction, changes to target sites, and altered membrane permeability. Cross-resistance between related drugs is also explained. The document concludes by discussing ways to prevent resistance, including prudent antimicrobial use and
Streptococci and enterococci are Gram-positive cocci that are classified based on hemolytic patterns, Lancefield antigens, and biochemical characteristics. Medically important species include Streptococcus pyogenes (Group A), S. agalactiae (Group B), S. pneumoniae, and Enterococcus faecalis. These bacteria commonly colonize humans and can cause diseases like pneumonia, meningitis, toxic shock syndrome, and endocarditis. Laboratory identification involves culturing specimens on blood agar to observe hemolysis and performing tests like bile solubility and optochin sensitivity.
This document provides information about malaria vaccines. It discusses the context of malaria globally and the need for a vaccine. Several potential vaccine candidates target different stages of the malaria parasite's lifecycle, including sporozoites, infected hepatocytes, and erythrocytic stages. Developing an effective vaccine is challenging due to the parasite's diversity and complexity. The most promising current candidate is RTS,S, which provides some protection against malaria in clinical trials but is not fully effective.
This study analyzed blood cultures from neonatal intensive care unit patients from 1997 to 2001 in Tripoli Medical Center, Libya. A total of 1431 blood culture sets from 1092 patients were positive for bacterial growth in 801 sets, representing 648 cases of neonatal bacteraemia. The most common causative agents were members of the Enterobacteriaceae family including Serratia, Klebsiella, and Enterobacter species as well as coagulase-negative and positive Staphylococci. Antibiotic susceptibility testing found high levels of resistance among the most frequent pathogens, though resistance to newer antibiotics like aztreonam and imipenem was less common. Resistance in Staphylococcus to anti-stap
1. The document discusses the classification and mechanisms of action of various antibiotics. It begins by defining antibiotics and explaining their selective toxicity towards bacteria.
2. The document then covers various classifications of antibiotics including by chemical structure and mechanism of action. The main mechanisms discussed are inhibition of cell wall synthesis, protein synthesis, and DNA/RNA synthesis.
3. Specific antibiotic classes are then described in more detail, including beta-lactams, glycopeptides, macrolides, lincosamides, streptogramins, aminoglycosides, tetracyclines, oxazolidinones, quinolones, metronidazole, rifampin, sulfonamides, and tri
The document discusses several key points:
1) It questions the common belief that childhood exposure to measles provides immunity and that avoiding it threatens health.
2) It suggests that genetically modified foods and agricultural chemicals may promote disease more than genetics.
3) It warns that mandatory vaccinations could require Americans to accept poor and chronic health. Overall, the document casts doubt on mainstream views of health, immunity, and the role of vaccines and industrialized foods.
This document discusses human parasite vaccines. It begins by explaining what vaccines do in stimulating the host's protective immune response. Developing effective parasite vaccines faces challenges including not fully understanding the parasite's life cycle and which stages elicit a protective immune response. Effective vaccines must produce long-lasting protection without boosting and be low-cost, stable, and safe. Progress has been limited for parasite vaccines due to parasites' ability to evade the immune system, uncertainty regarding which antigens stimulate protection, and differences between animal models and human immune responses. Major human parasitic diseases discussed include malaria, African sleeping sickness, Chagas disease, leishmaniasis, intestinal protozoa, schistosomiasis, onchocerciasis
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.
The document discusses the need for a malaria vaccine and challenges in developing one. It provides details on various vaccine candidates and approaches, including pre-erythrocytic (preventing infection of liver), asexual blood stage (preventing growth in red blood cells), and sexual stage (blocking transmission) vaccines. Top candidates mentioned are RTS,S/AS02, which has undergone phase 3 trials, and SPf66, the first to undergo field testing. Developing an effective and durable malaria vaccine faces difficulties due to the parasite's complex life cycle and ability to evade the immune system.
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.
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
Babesiosis, caused by infection with intra erythrocytic parasites of the genus Babesia, is one of the most common infections of free living animals worldwide and is gaining increasing interest as an emerging zoonosis in humans. this is a detailed study on this ......considering all the facts such as definition , management, parthenogenesis, diagnosis, treatment, prevention , etc
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principles of antimicrobial therapy (1).pptxogadatv
This document discusses principles of antimicrobial therapy. It begins by classifying antimicrobials based on their source, mechanism of action, and spectrum. Narrow, extended, and broad spectrum antimicrobials are defined. The document emphasizes selecting the appropriate antimicrobial based on infection type, patient factors, and culture/susceptibility results. It stresses dosing antimicrobials based on pharmacodynamic principles like concentration-dependent killing. Adverse effects like resistance and superinfection are also addressed. The goal of therapy is to optimize treatment for each patient while limiting antimicrobial use to avoid harm and resistance.
This document discusses principles of antimicrobial therapy. It begins by classifying antimicrobials based on their source, mechanism of action, and spectrum. Narrow, extended, and broad spectrum antimicrobials are defined. The document emphasizes selecting the appropriate antimicrobial based on the infecting organism, patient factors, and pharmacokinetic properties. It stresses starting empiric therapy and then narrowing based on culture results. Monitoring treatment response and adjusting for toxicity or resistance is also highlighted. The goal of antimicrobial use is effective treatment of infection while limiting emergence of resistance.
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Contains slides describing essential elements for bacterial growth, bacterial growth curve, mechanism of energy production and metabolism, principle of in-vitro bacterial culture
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.
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- Video recording of this lecture in English language: https://youtu.be/Pt1nA32sdHQ
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1. PATHOGENESIS I
Bacterial virulence factors
MBBS Program
Dr. Tarek Mahbub Khan
MBBS, M.Phil (virology)
Assistant Professor
14/1/2018 1Dr. Traek/SSMC/2016
2. TLO
• Definition of some terminologies
• Koch’s postulates
• Stages of Bacterial pathogenesis
• Definition of bacterial virulence
• Explanation f bacterial virulence
• Description of bacterial virulence factors
14/1/2018 2Dr. Traek/SSMC/2016
3. DEFINITION
• PATHOGEN:
– A microorganism capable of causing disease.
• NON-PATHOGEN:
– A microorganism that does not cause disease.
• OPORTUNISTIC PATHOGEN:
– An organism capable of causing disease when host
resistance is impaired.
• INFECTION:
– Multiplication of infectious (pathogenic) agent within the
body.
4. • COMUNICABLE DISEASE:
– Diseases that are directly transmitted from host to host.
– Not all infectious diseases are communicable.
• ENDEMIC:
– Infections that are constantly present at low level in a define
population. (e.g., Malaria is endemic in hill-tracts)
• EPIDEMIC:
– Disease that occurs in more frequent pattern. (e.g., Cholera is
endemic in India)
• PANDEMIC:
– Infections that are distributed worldwide. (e.g., Swine-flu was
pandemic in the world in 2009)
DEFINITION
5. • In 1884, Robert Koch proposed a
series of postulates that have been
applied broadly to link many specific
bacterial species with particular
diseases. These are Koch’s postulates.
• Microbial genes are related to their
virulence factors. Molecular diagnosis
established the genetic relation ship
of infectious diseases through
Molecular Koch’s Postulates
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KOCH’S POSTULATES
6. 1. Microorganism should be found in all cases of the disease in
question, and its distribution in the body should be in
accordance with lesions observed.
2. The microorganism should be grown in pure culture for
several generations.
3. When such a pure culture is inoculated into susceptible
animal species, the typical disease must result.
4. The microorganism must again be isolated from the lesions
of such experimentally produced disease
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KOCH’S POSTULATES
7. • Phenotype or property under investigation should be related
with a pathogenic strain of a species and not with non-
pathogenic strains.
• Inactivation of the gene/genes related to virulence factors
should lead to measurable decrease in pathogenicity.
• Reversion or replacement of mutated gene with wild type
gene should lead to restoration of pathogenicity or virulence.
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MOLECULAR KOCH’S POSTULATES
8. • Some microorganisms do not grow in pure culture however
they have animal model to grow. Example: Treponema
pallidum, Mycobacterium leprae.
• Some microorganism do not have animal model to grow
though can readily be cultured in vitro. Example: Neisseria
gonorrhoeae.
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LIMITATION OF KOCH’S POSTULATES
9. • Detection of rise of specific antibody titer.
• Molecular detection of microbial gene by PCR,
hybridization or other related molecular tests.
• Demonstration of pathogenicity in in-vitro model.
Example: Escherichia coli induced diarrhea in in-vitro
cell culture.
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ADJUNCT OF KOCH’S POSTULATES
10. • Analysis of infection and diseases.
• Classification of bacteria into pathogens, non-pathogens
or opportunistic pathogens.
• Laboratory application in infectious disease diagnosis
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APPLICATION OF KOCH’S POSTULATES
11. 1. Transmission from the source of infection into the portal of
entry.
2. Evasion of primary host defense.
3. Adherence to mucous membrane.
4. Colonization by growth of the bacteria at the site of
adherence.
5. Disease symptoms caused by bacterial toxin or invasion.
6. Host immune response during steps 3,4,5
7. Progression or resolution of the disease.
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STAGES OF BACTERIAL PATHOGENESIS
14. MODES OF TRANSMISSION
(Human to human)
Direct contact Gonorrhea
No direct contact
(flies, flea, fomites, food)
Dysentery
Vertical Congenital syphilis
Blood born Syphilis, hepatitis B, AIDS
15. VERTICAL TRANSMISSION
(Infected mother to the offsprings)
Transplacental Treponema pallidum
Listeria monocytogenes
Toxoplasma gondii
Cytomegalovirus
Within birth canal Streptococcus agalactiae
Escherichia coli
Neisseria gonorrhoeae
Herpes simplex
Breast milk Staphylococcus aureus
Cytomegalovirus
17. BACTERIAL VIRULENCE
• Define as a quantitative measurement of bacterial
pathogenicity
• It is measured by amount of bacteria required to
cause disease
• Virulence of an organism is determined by its ability
to produce various virulence factors
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18. • LD50 (50% lethal dose): Referred as number of
bacteria required to kill half (50%) of the host
• ID50 (50% infectious dose): Referred as number of
bacteria required to cause infection in half (50%) of
the host
• Infectious dose varies among the pathogenic bacteria
BACTERIAL VIRULENCE
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22. ADHERENCE
• The first step in bacterial pathogenicity
• Occurs by an interaction between bacterial surface
structures (ligand) and host cell receptor
• ADHERENCE FACTORS:
– Pili or fibriae
– Capsule or glycocalyx
– Teichoic acid of gram positive bacteria
– Adhesin
• Antibody against these adherence factors will
prevent bacterial entry into the host cell
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24. • Invasive FACTORS are:
• Enzymes
– Coagulase
– Collagenase and hyaluronidase
– Immunoglobulin A protease: degrades IgA
• Antiphagocytic factors
– Leukocidin :destroy neutrophils, macrophages
– Capsule: prevents adherence of phagocytic cells
– M protein of Group A streptococci: Antiphagocytic
– Protein A of Staphylococcus: Binds IgG thereby block
complement activation
INVASION
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25. • EXOTOXIN
– Are polypeptides secreted from gram positive bacteria
– Secreted by a ‘secretion system’ present in the bacteria
– Some are secreted extracellularly, some in between cells
– Among SIX secretion system, type III is more in virulence
• ENDOTOXIN
– Lipopolysaccharide
– Cell wall of gram negative bacteria
– It is not secreted, but released after death of bacteria
TOXINS
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26. EXOTOXIN ENDOTOXIN
Polypeptide Lipopolysaccharide
From gram positive bacteria From gram negative bacteria
Gene located in the plasmid or
bacteriophage
Gene located in the bacterial
chromosome
Induce antibody (antitoxin) Poorly antigenic
Toxoid (inactive toxin) used as
vaccine
No vaccine production is
possible
Usually destroyed at 600C Stable at 1000C for an hour
DIFFERENCES BETWEEN EXOTOXIN
AND ENDOTOXIN
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27. • Structurally all exotoxins have two sub-units:
– Sub-unit A: A sub-unit acts as enzyme that catalyzes
different activities
– Sub-unit B: This sub-unit binds with membrane receptor of
the target cell
• Sub-unit A causes ADP-ribosylation: adds ADP-ribose
to a target protein and exerts different function
14/1/2018 Dr. Traek/SSMC/2016 27
MECHANISM OF ACTIONS OF
EXOTOXIN
30. 14/1/2018 Dr. Traek/SSMC/2016 30
VASCULAR EVENTS OF ENDOTOXIN
Initial arteriolar and venular constriction
Peripheral vasodilatation and increase vascular permeability
Decrease venous return, low cardiac output and stagnant microcirculation
Peripheral vasoconstriction, shock and impaired organ perfusion
31. • Gene clusters in a region of chromosome.
• These genes are not capable of self replication.
• Encode different virulence factors.
• Determines different pathogenic strains in a
particular species.
• EXAMPLES OF THE BACTERIA:
– Escherichia coli, Salmonella, Shigella
– Streptococcus pneumoniae
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PATHOGENECITY ISLANDS
32. • More thick in the gram positive bacteria
• Can produce shock due to vascular changes
• There effect is similar as lipopolysaccharide in gram
negative bacteria:
– Peripheral vasodilatation
– Decrease venous return
– Lower cardiac output
– Shock and impaired organ perfusion
PEPTIDOGLYCAN
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33. • Some bacteria grow inside PMN, macrophages or in
monocytes
• They survive by several mechanism:
– Avoid entry into phagolysosome
– Prevent phagososme-lysososme fusion
– Acquire resistance to lysosomal activity
• EXAMPLE: Mycobacterium tuberculosis, Brucella
species, Listeria species
INTRACELLULAR SURVIVAL
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34. • Bacterial surface proteins are antigenic
• One Species of bacteria may have different antigenic
type (serotypes)
– EXAMPLES: 2000 different types of Salmonella
• Microorganism has the ability to make frequent shift
of their antigens
– EXAMPLE: Borrelia recurrentis, Neisseria gonorrhoeae
ANTIGENIC HETEROGENEITY
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35. BACTERIA AND VIRULENCE FACTORS
Corynebacteria diphtheriae
• –May only have 1 virulence mechanism
• –diphtheria toxin
Staphylococcus aureus
• –Express many virulence factors
• –Adhesins, degradative enzymes, toxins, catalase, coagulase
• –Produce spectrum of disease
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36. Mycobacterium tuberculosis
• –able to inhibit phagolysosome fusion and promote the
development of a granuloma
• –viable bacteria may reside inside the infected person
Neisseria gonorrhoeae
• –Vary the structure of surface antigen
• –Produce protease to degrade IgA
BACTERIA AND VIRULENCE FACTORS
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37. • 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.
REFERENCES
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