Pathogenicity, Virulence, Infection, Epidemiology Host Microbes Severe to One
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Pathogenicity, Virulence, Infection, Epidemiology Host Microbes severe To one Parasitism Unilateral benefit benefit harm Commensalism Mutualism Shelter and food Reciprocal benefit both none partial complete dependency Human microbiota Bacteria, Archea, Fungi and Protozoa colonize our body surfaces: skin, mucous membranes of upper respiratory tract, digestive tract, lower urethra, vagina • the ratio of microbial-to-human cells is 3:1 (American Academy of Microbiology FAQ: Human Microbiome January 2014) Human microbiota Resident Transient Throughout the life Remain hours - of the human months How microbiota become opportunistic pathogens: • Immune suppression (AIDS, transplantation, cancer treatment, …) • Changes in the normal microbiota ( ATB treatment) • Introduction of normal microbiota species into an unusual site of the body (surgery, invasive medical devices,…) © 2012 Ottman, Smidt, de Vos and Belzer Impact of microbiota on our health Pathogenicity • Pathogenicity – treat of the microbial species - ability to cause disease • Virulence – degree of the pathogenicity • Virulence factors – mechanisms that promote the growth in the host at the expense of the host’s tissues e.g. Surface molecules for attachment to the tissue, extracellular enzymes, toxins Pathogens Primary Opportunistic – cause disease in healthy – cause disease when the host host’s defenses are (Influenza virus, donkey cough, compromised or when morbilli virus, Salmonella they become established Typhi) in a part of the body that is not natural to them. (Enetrococcus faecalis, E. coli, Candida albicans) Factors That Weaken Host Defenses and Increase Susceptibility to Infection • Old age and extreme youth (infancy, prematurity) • Genetic defects in immunity and acquired defects in immunity (AIDS) • Surgery and organ transplants • Organic disease: cancer, liver malfunction, diabetes • Chemotherapy/immunosuppressive drugs • Physical and mental stress • Other infections 1. Contamination Colonization by Loss Allergy Infiltration 2. Infection microbiota Source of infection: Exogenous – outside the host body, from environment, another person, animal Endogenous – already on the host body Ports of entry Ports of entry • Skin – wands, bites, abrasions, nicks • Conjunctiva • The gastrointestinal tract – food, drink, anus (STD) • The respiratory portals – nasal and oral cavity • The urogenital portals – urinary infections, Sexualy Transmmited Disease • Transplacental infection, during delivery Infection Host Pathogen • Sensitivity or resistance on the • Pathogenicity of the species species level • Virulence of the strain • Level of unspecific and specific • Infection dosage immune defense Cure, immunity 2. Infection Entrenchment 3. Disease Carrier state Virulence factors 1. Ability to enter the host body adhesion – attach to surfaces penetration – break through the tissue 1. Ability to growth inside a host body 2. Ability to spread inside a host body 3. Ability to escape from host’s immune defense Attachment (Adhesion) Surface structures (adhesins): • Fimbriae, flagella, capsules • Glycoproteins, or lipoproteins (ligand) – binds to specific cell receptors • Biofilm (web of bacteria and polysaccharides) Penetration and spreading Kinds of penetration direct Bites, broken skin or mucus, lytic enzymes Through phagocytosis Invasins (Shigella, Listeria, Yersinia), crinkling of the cell surface (Salmonella) From destroyed cells viruses Spreading in the host body Byblood HVB By lymph plague Alongside the neurons Rabies, herpes simplex per continuitatem (from cell to cell) Shigella, donkey cough Mechanisms of escaping host immune defense Avoiding Phagocytosis • Capsule, M protein, covering by the host own molecules Surviving phagocytosis • Prevent the fusion of the phagosome with lysosome vesicles • Producing leukocidin that kills the phagocytes • Blocking the oxidative burst and other processes in the phagosome • Escape from phagosome Antigen variability Blocking of complement activation Producing molecules that weak the immune response Toxigenicity • Damage caused directly by microbes Exotoxin Endotoxin secreted outside the Part of the microbe’s cell, microbe’s cell release after the cell’s death Enzymes, low molecules with LPS – lipid A, teichoic acids pharmacologic effect Exotoxins Secreted enzymes Hyaluronidase, colagenase, hemolysins, coagulases, kinases, neurotoxins Botulinum toxin, tetanospasmine Inhibitors of Shiga toxin, diphtheria toxin protheosynthesis Super-antigens TSST, pyrogenic toxins enterotoxins choleragen Toxins modifying cell Bordetella toxin, Anthrax signalization A-B toxin A subunit – acting inside the cell A B B B B B subunit – binding the receptor on the cell surface and transport A subunit into the cell Endotoxine Effect of endotoxin Septic Schock Fever Inflamation Hypotension – dilatation of vessels Disseminated blood coagulation Haemorrhaging – capillary leak syndrome Diarhea Loss of function of internal organs Damage caused by immune defense • Damage caused by the inflammation (edema, scars, fibrous non function tissue) • Damage caused by specific immune defense, (hypersensitivity) 1. Allergy 2. Cytotoxic – Antibody dependent 3. Immune complexes 4. Cells-mediated memory response – Antibody independent The stages of infectious diseases Signs and Symptoms Sign – objective evidence as noticed by observer Symptom – subjective evidence as sensed by patient Common signs and symptoms of Infectious Diseases Signs Symptoms Fever Chills Septicemia Pain, ache, soreness, irritation Microbes in tissue fluids Nausea Skin eruptions Malaise, fatigue Leukocytosis Chest tightness Leukopenia Itching Swollen lymph nodes Headache Abscesses Abdominal scamps Tachycardia (increased heart rate) Anorexia (lack of appetite) Antibodies in serum Sore throat Patterns of infection • Due to extension primary local systemic focal secondary mixed • Due to duration Fulminant Subacute (hours) (months) Acute (days, weeks) Chronic (years) Chronic disease Manifest (with symptoms) Persistent (can prove the infective agent) inapparent Latent (inactive infective agent, can’t prove) Portals of exit Modes of disease transmission Modeof transmission Disease spread include Contact transmission Direct contact e.g. handshaking, kissing, Cutaneous anthrax, genital warts, sexual intercourse, bites gonorrhea, rabies, staphylococcal infections Indirect contact e.g. drinking glasses, Common cold, enterovirus inf., influenza, toothbrushes, toys, punctures measles, Q ever, pneumonia, tetanus Droplet transmission e.g. droplets from Whooping cough, streptococcal pharyngitis sneezing Vehicle transmission Airborne e.g. dust particle Chickenpox, histoplasmosis, influenza, measles, tuberculosis Waterborne e.g., streams, swimming pools Campylobacter inf., cholera, Giardiosis Food borne e.g., poultry, seafood… Botulism, hepatitis A, listeriosis, typhoid fever Vector transmission Mechanical e.g., (on insect bodies) flies Trachoma, Chagas disease Biological e.g., lice, mites, mosquitoes, ticks Lyme disease, malaria, yellow fever Sources of infectious diseases Anthroponosis Zoonosis - Human to Human - Directly - Human to animal - By vector Human carrier Animal reservoir 1. Biological vector vector 2. Mechanical vector man reservoir Common zoonoses Disease Causative agent Animal reservoir Bacterial Anthrax Bacillus antharacis Domestic livestock Brucellosis Brucella melitensis Cow, goat, swine, dogs Lyme disease Borrelia burgdorferi Deer Salmonellosis Salmonella enterica Domestic livestock, birds Typhus Rickettsia prowazeki Rodents Viral Rabies Lyssa virus Bats, foxes, dogs Yellow fever Flavi virus Monkeys Avian Influenza Inlfuenza virus Birds (ducks) Tick-born encephalitis Flavi virus Rodents Fungal Trichophyton sp., Ringworm Microsporum sp., Domestic animals Epidermophyton sp. Protozoan Malaria Plasmodium spp. Monkeys Toxoplasmosis Toxoplasma gondii Cats, other animals Helminthic Tapeworm Infestation Dipylidium caninum Dogs Fasciola Infestation Fasciola hepatica Sheep, cattle Communicable disease – pathogen comes from another host Contagious disease – communicable disease that spreads easily from host to host (influenza, measles) Non-communicable disease – not transmitted from host to host. (opportunistic endogenous infections, tetanus) Nosocomial infections • Infections acquired as a result of a hospital stay • Tendency to drug-resistance Presence of microorganism Iatrogenic infections –in hospital subset environment of nosocomial infections (invasive devices e.g. catheters, surgery) NosocomialNosocomial infection Transmission of infection pathogens between Immunocompromised staff and patients and patients among the patients Epidemiology • Study of the frequency and distribution of disease and other health-related factors in defined human populations Prevalence - 100 = % Incidence - = ratio Patterns of infectious disease occurrence • Descriptive epidemiology - tabulation data concerning a disease, identify index case (the first case) • Analytical epidemiology – analyzing data from descriptive epidemiology to determinate the probable cause, mode of transmission, possible prevention (often retrospective) • Experimental epidemiology – testing hypothesis resulting from an analytical study Factors influencing the decrease in infectious diseases in the twentieth century Decrease in infectious diseases .