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RESPIRATORY TRACT INFECTIONS Donna Duckworth ID Class March 1, 2004 GOALS General Principles of Pathogenesis of Respiratory Tract Infection Host Defenses in the URT, LRT Agents of Infection in URT, LRT Pathogenesis of Diphtheria Prevention and Treatment of Diphtheria Pathogenesis of Whooping Cough Prevention and Treatment of Whooping Cough Host Defenses in the Respiratory Tract Upper Tract Lower Temperature Mucosal Surface Washing IgA Inflammation may bring phagocytes Lower Tract Ciliated Epithelium Phagocytes General Principles Encounter Entry Spread Multiplication Evasion of Host Defenses Damage Transmission Agents of Upper Respiratory Tract Infections Common cold (rhinitis) Many viruses; rhino, corona, adeno, influenza Streptococcus pyogenes Corynebacteria diphtheriae Neisseria gonorrhoea Many viruses Haemophilus influenzae Bordetella pertussis Many viruses Pharyngitis and laryngotracheitis Epiglottitis Bronchitis Systemic Diseases that Begin in the URT Measles Mumps Smallpox Influenza Meningitis Sinusitis Middle Ear Infection Pneumonia Agents of Lower Respiratory Tract Infections Legionairre’s Disease; Legionella pneumophila Tuberculosis: Mycobacterium tuberculosis Pneumonia Bacteria Streptococcus pneumoniae Mycoplasma pneumoniae Staphylococcus aureus Almost ANY other Influenza Measles Many others Viruses Fungi Many Diphtheria Symptoms Sore throat Low grade fever Swollen lymph glands (Bull neck) Trachael obstruction due to pseudomembrane Heart and kidney damage Corynebacteria diphtheriae C. diphtheriae Pathogenesis of Diphtheria Encounter – Corynebacterium diphtheriae encountered only from other people (carriers) Entry – respiratory droplets; organism colonizes pharynx Spread Multiplication – iron likely a factor Evasion of host immune response – adhesins; toxin may kill phagocytes contributing to pseudomembrane Damage – inflammation; circulating toxin Transmission – aerosolized droplets; fomites Action of Diphtheria Toxin B binds to HB (heparin binding) receptor Entire molecule is endocytosed A released into cytoplasm Acts as enzyme to ADP-ribosylate EF2 NAD and EF2 are substrates ADPribose added to diphthamide residue in EF2 Protein synthesis stops and cells die Diphtheria Toxin Synthesis of Diphtheria Toxin Structural gene for toxin is part of genome of beta bacteriophage Phage causes lysogenic conversion First proven by finding mutant phage that produced CRM Toxin synthesized as a single polypeptide chain Low iron concentration induces synthesis Treatment and Prevention of Diphtheria Treatment Horse anti-toxin Antibiotics Prevention DPT vaccine Symptoms of Whooping Cough Fever Malaise Anorexia Rhinorrhea Sneezing Lacrimation Conjunctivitis Leukocytosis Dry cough Paroxysmal cough (violent cough followed by inspiratory "whoop― or vomiting,cyanosis, seizures Pathogenesis of Whooping Cough Encounter – Bordetella pertussis --from other people Entry – respiratory droplets Spread – none Multiplication – is highly fastidious; may enter phagocytes by self initiation and multiply there Evasion of host defenses – adheres primarily via the FHA (filamentous haemagglutinen); prevents normal phagocytosis Damage – variety of toxins Transmission – cough, aerosolization of droplets Bordetella pertussis Virulence Factors of Bordetella Pertussis Adhesins FHA Pertussis toxin Pertactin Fimbriae Toxins Pertussis toxin (lymphocytosis-promoting toxin) Adenylate cyclase toxin Tracheal cytotoxin Lethal toxin (dermonecrotic toxin) Virulence Factors of Bordetella Pertussis Adhesins FHA Pertussis toxin Pertactin Fimbriae Pertussis toxin (lymphocytosis-promoting toxin) Adenylate cyclase toxin Tracheal cytotoxin Lethal toxin (dermonecrotic toxin) Endotoxin Toxins Pertussis Toxin 105 KD protein; 6 subunits S1 – ADP ribosylase S2 – binds to glycolipid on ciliated epithelial cells S3 – binds to glycolipid on phagocytes S4 (2) S5 Activity of S1 Subunit of PT Transfers the ADP ribosyl moiety of NAD to the membrane-bound regulatory protein Gi Gi protein is inactivated and cannot perform its normal function to inhibit adenylate cyclase. The conversion of ATP to cyclic AMP cannot be stopped and intracellular levels of cAMP increase Results of PT Activity disrupt cellular function decrease their phagocytic activities such as chemotaxis, engulfment, the oxidative burst, and bacteridcidal killing lymphocytosis and alteration of hormonal activities that are regulated by cAMP increased insulin production (resulting in hypoglycemia) increased sensitivity to histamine (resulting in increased capillary permeability, hypotension and shock). Treatment and Prevention of Whooping Cough Treatment Erythromycin Prevention Vaccination Whole cell vaccine – not used anymore Subunit vaccine ASSIGNMENT http://medinfo.ufl.edu/year2/mmid/ bms5300/cases/index.html Do Case 19 before Wednesday Do Case 20 before next exam Streptococcal Infections -- Goals Differentiate between different kinds of Streptococci Know why Strep throat is so important to diagnose Know pathogenesis of rheumatic fever Know difference between rheumatic fever and endocarditis Know how to prevent rheumatic fever and endocarditis Staphylococcus aureus Streptococcus pyogenes Streptococcal Pathogens Streptococcus pneumoniae – pneumoniae, otitis media, sinusitis, meningitis Streptococcus pyogenes (Group A) – pharyngitis, rheumatic fever, glomerular nephritis, impetigo, TSLS Streptococcus agalactiae (Group B) – neonatal meningitis Viridans Streptococci -- endocarditis Major Virulence Factors of Streptococci S. pneumoniae – capsule S. pyogenes – M protein Viridans Streptococci -- adhesins? Why Care About Diagnosing Streptococcal Infections? Viridans Streptococci – normal flora; opportunists, not overt pathogens Streptococcus pyogenes – can cause rheumatic fever if not treated Streptococcus pneumoniae – causes many very serious diseases; looks like viridans Streptococci on BAP; has antibiotic “issues” Differentiation of Streptococci Hemolysis Alpha – viridans and pneumoniae Beta – pyogenes and agalactiae Group CHO A – pyogenes B -- agalactiae Antibiotic sensitivity bacitracin optichin Beta Hemolysis Alpha Hemolysis Bacitracin (A) disc Optichin (P) disc Pathogenesis of Rheumatic Fever Encounter -- carriers of S. pyogenes Entry – droplets; colonizes pharynx Spread – NO! Multiplication Evasion of Host Defenses—adhesin, M protein Damage – inflammation (in pharynx) cross reacting antibody (heart valve) Transmission Pathogenesis of Endocarditis Encounter --endogenous Entry – transient bacteremia Spread -- hematogenous Multiplication -Evasion of Host Defenses -Damage – mechanical interference with heart valve Transmission Prevention Rheumatic Fever Diagnose Strep throat Treat with penicillin 10 days Endocarditis Prophylaxis with penicillin for anyone with damaged heart valves before dental, other procedures
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