Chapter 14: Pathogenesis of Infectious Diseases: Chapter 14: Pathogenesis of Infectious Diseases Group 1 BSN II-B Slide 2: Pathogenesis -the steps or mechanisms involved in the development of a disease. Pathogenicity -the ability to cause disease. Infectious Diseases -diseases that are caused by pathogenic microorganisms such as bacteria, viruses, parasites or fungi. Infection -colonization by a pathogen(according to microbiologists) Why Infection does not always occur?: Why Infection does not always occur? The microbe may land at an anatomic site where it is unable to multiply. Many pathogens must attach to specific receptor sites before they are able to multiply and cause damage. If they land at a site where such receptors are absent, they are unable to cause disease. Antibacterial factors that destroy or inhibit the growth of bacteria may be present at the site where a pathogen lands Slide 4: The indigenous microflora of that site may inhibit growth of the foreign microbe by occupying space and using up available nutrients. The indigenous microflora at the site may produce anti-bacterial factors that destroy newly arrived pathogen. The individual’s nutritional and overall health status often influences the outcome of the pathogen-host encounter. Slide 5: The person may be immune to a particular pathogen. Phagocytic WBCs present in the blood and other tissues may engulf and destroy the pathogen before it has an opportunity to multiply, invade and cause disease. Four Periods in the Course of Infectious Disease: Four Periods in the Course of Infectious Disease Incubation period the time that elapses between arrival of the pathogen and the onset of symptoms. Prodromal period the time during which the patient feels “out of sorts”, but is not yet experiencing actual symptoms of the disease. Slide 7: Period of illness - the time during which the patient experiences the typical symptoms associated with that particular disease. Convalescent period - time during which the patient recovers . Localized vs Systemic Infections: Localized vs Systemic Infections Once an infectous process is initiated, the disease may remain localized to one site or it may spread. Pimples, boils, and abscesses are examples of localized infections . When the infection has spread throughout the body, it is referred to as systemic or generalized infection. Acute, Subacute and Chronic Diseases: Acute, Subacute and Chronic Diseases Acute disease - has a rapid onset, usually followed by a relatively rapid recovery. Chronic disease - has an insidious(slow) onset and lasts a long time. Subacute disease - come on more suddenly than chronic disease, but less suddenly than an acute disease. Symptoms vs Signs of a disease: Symptoms vs Signs of a disease A symptom of a disease is defined as some evidence of a disease that is experienced or perceived by the patient; something that is subjective. It may be symptomatic or asymptomatic. A sign of a disease is defined as some type of objective evidence of a disease. Latent Infections: Latent Infections - an infectious disease that may go from being symptomatic to be asymptomatic and then some time later go back to becoming symptomatic. Primary vs Secondary Infections: Primary vs Secondary Infections One infectious disease may commonly follow another, in which case the first disease is referred to as a primary infection and the second disease is referred to as a secondary infection. Steps in the Pathogenesis of Infectious Diseases: Steps in the Pathogenesis of Infectious Diseases . Entry of the pathogen into the body. Attachment of the pathogen to some tissues within the body. Multiplication of the pathogen. Invasion or spread of the pathogen. Evasion of host defenses. Damage to host tissues Virulence: Virulence Virulence is a measure or degree of pathogenicity. Different species or even different strains of the same species vary in their ability to cause disease; thus, some are more virulent than others. Some strains of a particular species may be virulent, whereas other strains of the same species are avirulent. Slide 15: Virulent - capable of causing disease Avirulent - not capable of causing disease Slide 16: VIRULENT FACTORS - properties of pathogens that allow them to escape various host defense mechanisms and cause disease. Attachment: Receptor and Integrin- molecules on the surface of a host cell that a pathogen is able to recognize and attach to. Adhesin and Ligand- molecules on the surface of a pathogen that is able to bond to a particular receptor. Slide 17: Obligate Intracellular Pathogens - pathogens that must live within host cells to survive and multiply. Facultative Intracellular Pathogens: Facultative Intracellular Pathogens Pathogens that are capable of both an intracellular and extracellular existence They are also able to survive within phagocytes Intracellular Survival Mechanisms: Intracellular Survival Mechanisms 2 most important phagocytes in the body or “Professional Phagocytes”: - Macrophages & neutrophils Once phagocytized, most pathogens are destroyed within the phagocytes, however, certain pathogens are able to survive and multiply within phagocytes after being ingested. Slide 20: Some pathogens has a cell wall that resist digestion -> myobacterial cell walls contain waxes that protect the organism from digestion. Others prevent fusion of lysosomes with phagocytic vacuole. - Other pathogens produce phospho lipases that destroy the phagosome membrane that prevents lysosome-phagosome fusion. Slide 21: Encapsulated bacteria that gain access to the blood stream or tissues are protected from phagocytosis, they are able to multiply, invade, and cause disease Non-encapsulated bacteria are phagocytized and killed. Flagella : Flagella Considered virulence factors because flagella enable flagellated bacteria to invade aqueous areas of the body which unflagellated bacteria are unable to reach. Enable bacteria to avoid phagocytosis. Exoenzymes: Exoenzymes Are produced by pathogens Enables pathogens to evade host defense mechanisms, invade, or cause damage to body tissues Exoenzymes include necrotizing enzymes, coagulase, kinases, hyaluronidase, collagenase, hemolysins and lecithinase. Necrotizing Enzymes: Necrotizing Enzymes - Exoenzymes that destroy tissues Coagulase: Coagulase Binds to prothrombin, forming a complex called staphylothrombin In the body, coagulase enables S. Aureus to clot plasma and form a sticky coat fibrin around themselves for protection from phagocytes, antibodies, and other host defense mechanisms Kinases: Kinases Opposite effect of coagulase Are enzymes that dissolves clots; pathogens that produce kinases are able to escape from clots. Hyaluronidase: Hyaluronidase -called “spreading factor” - Enables pathogens to spread through connective tissues by breaking down hyaluronic acid (a polysaccharide that holds tissue cells together.) Collagenase: Collagenase -breaks down collagen (supportive protein found in tendons, cartilage, bones. -enables pathogens to invade tissues Hemolysins: Hemolysins -with a source of iron enzymes that cause damage to the host red blood cells -provides pathogens Lecithinase: Lecithinase -breaks down phospholipids called lecithin -is destructive to cell membranes of red blood cells and other tissues TOXINS: TOXINS -poisonous substances released by pathogens that enables them to damage the host. -2 major types: 1.) endotoxins - integral parts of the cell wall of gram negative bacteria. Can cause adverse physiological effects such as fever and shock. ***Septic shock-results from gram negative sepsis. Slide 32: 2.) exotoxins - toxins produced within cells and then released from the cells. -poisonous proteins secreted by a variety of pathogens. neurotoxins - affects central nervous system. Enterotoxins - toxins affecting GI tract. Exoliative Toxins- causes the epidermal layers of skin to slough away. Slide 33: d.) Leukocidins - Toxins that destroy WBC Mechanisms by Which Pathogens Escape Immune Responses: Mechanisms by Which Pathogens Escape Immune Responses Antigenic Variation Pathogens that are able to periodically change their surface antigens. By the time that the host has produced antibodies in response to pathogen’s surface antigens, those antigens are shed and new ones appear in their place. Slide 35: b) Camouflage and Molecular Mimicry Camouflage: pathogens are able to conceal their foreign nature by coating themselves with host proteins. Molecular Mimicry: pathogen’s surface antigens closely resemble host antigens and are not recognized being foreign C) Destruction of Antibodies Pathogens that produce an enzyme that destroys IgA antibodies These pathogens are capable of destroying some of the antibodies that the host’s immune system has produced in an attempt to destroy them.