URTI Lecture Notes October 2024 PDF

Upper Respiratory Tract Infections Laura Musson With thanks to Dr Veronica Chorro-Mari Objectives: By the end of this session you should be able to: Know the difference between an upper respiratory tract infection (URTI) and lower respiratory tract infection (LRTI) Discu...

Upper Respiratory Tract Infections Laura Musson With thanks to Dr Veronica Chorro-Mari Objectives: By the end of this session you should be able to: Know the difference between an upper respiratory tract infection (URTI) and lower respiratory tract infection (LRTI) Discuss the pathophysiology and epidemiology of a range of respiratory infections Understand the role of the immune system in RTIs Know appropriate treatment regimens for named RTIs The Respiratory System UPPER LOWER Definitions Upper Respiratory Tract Infections – which affect the nose, nasal passages, sinuses, ear and throat (pharynx and larynx) Lower Respiratory Tract Infections – which affect the airways and lungs (trachea, bronchi, bronchioles and alveoli) Upper Respiratory Tract Infections Anatomy of the Upper Respiratory Tract Natural host defences Saliva – pH, antibodies Sinuses – immunological defence Tonsils – part of lymphatic system Nose hairs & sneezing – filtration Cough reflex & cilia Mucosal layer (mucociliary escalator) Respiratory tract epithelium – secretion on antimicrobial peptides  Figure 18.1 The normal flora of the respiratory tract. Typical causative organisms 1. Streptococcus pneumoniae 2. Haemophilus influenzae Moraxella catarrhalis Staphylococcus aureus Mycoplasma pneumoniae Streptococcus pyogenes RSV Viruses are MAIN Adenovirus causative organisms for URTI’s Influenzae viruses RT defence mechanisms (1) Filtration – Air passes through tortuous channels coated with mucous Only particles < 3 mm reach lungs If filtration anatomy disturbed / damaged → sinusitis, pneumonia Mucosal adherence – Stress disrupts commensal balance → G-ve pneumonias Macrophages in alveoli--- destroys foreign material Bacterial interference – Altered flora → superinfections Secretions – eg. lysosyme RT defence mechanisms (2) Secretory IgA Mucociliary clearance – eg. CF pts., smoking, ciliary dyskinesia → sinusitis, bronchitis Cough reflex – Normal tracheo-bronchial sensitivity Affected by medicines eg. inappropriate OTC Rxing (dextromethorphan) Cells and cell products – Compromised Immune system → opportunistic infections eg. AIDS  Common URTI (1/3) Croup: Common in children, usually caused by parainfluenza virus. Characterized by a barking cough, hoarseness, inspiratory stridor, and respiratory distress. Severe cases may require medical intervention, including corticosteroids or nebulized epinephrine. Epiglottitis: A bacterial infection of the epiglottis, often caused by Haemophilus influenzae type B (Hib) or Streptococcus pneumoniae. Presents with rapid onset of severe sore throat, high fever, difficulty swallowing, and drooling. Can rapidly progress to airway obstruction and respiratory failure if not treated promptly. Pertussis (Whooping Cough): Caused by Bordetella pertussis bacteria. Initial symptoms mimic a common cold but progress to severe, uncontrollable coughing fits (paroxysmal cough), often with a "whooping" sound upon inhalation. Can be life-threatening, especially in infants and young children.  Common URTI (2/3) Adenoiditis: Inflammation of the adenoids, often due to viral or bacterial infections. Symptoms include nasal congestion, mouth breathing, snoring, and chronic or recurrent ear infections. Severe cases may require surgical intervention (adenoidectomy). Pharyngitis (Sore Throat): Can be viral (e.g., common cold, flu) or bacterial (e.g., strep throat). Symptoms include throat pain, difficulty swallowing, and swollen tonsils with or without white patches. Bacterial pharyngitis, particularly strep throat, requires prompt treatment with antibiotics to prevent complications. Common Cold (Viral Rhinitis): Typically caused by rhinoviruses, coronaviruses, or adenoviruses. Mild symptoms include nasal congestion, runny nose, sore throat, cough, and sneezing.  Common URTI (3/3) Influenza (Flu): Caused by influenza viruses (types A, B, and rarely C). Symptoms include sudden onset of high fever, chills, headache, muscle aches, fatigue, dry cough, and sore throat. Can lead to severe complications such as pneumonia, especially in high-risk individuals. Sinusitis (Sinus Infection): Often follows a viral upper respiratory infection or allergies. Symptoms include facial pain or pressure, nasal congestion, headache, and post-nasal drip. Can be bacterial in origin (bacterial sinusitis) requiring antibiotics in some cases. Strep Throat (Streptococcal Pharyngitis): Caused by Group A Streptococcus (Streptococcus pyogenes). Symptoms include severe sore throat, difficulty swallowing, fever, and swollen tonsils with white patches. Can lead to complications such as rheumatic fever or post-streptococcal glomerulonephritis if untreated. Bronchitis: Upper and mostly a lower RTI (trachea affected: URTI) Inflammation of the bronchial tubes, often viral in origin. Symptoms include persistent cough, sometimes with sputum production, chest discomfort, and low-grade fever. Bacterial bronchitis may occur in some cases, requiring antibiotics.  Pathogenesis Most common cause of URTI is viral There are 2 types of infection: Type Examples Consequences Restricte Common cold viruses Local spread d to Influenza Local (mucosal) defences important adaptive surface Streptococci in throat (immune) response sometimes too late to be Chlamydia important in recovery (conjunctivitis) Short incubation period (days) Diptheria Bordetella Pertusis Candida albicans (thrush) Spread Measles, mumps, rubella Little or no lesion at entry site through EBV,CMV Microbe spreads through body, returns to body Chlamydophila psittaci surface for final multiplication & shedding e.g. Q fever salivary gland (mumps, EBV, CMV), respiratory Cryptococcosis tract (measles) Adaptive immune response important in recovery  Pathogenesis: 2 groups of microbes Type Requirement Examples Professional Adhesion to normal mucosa (in Respiratory viruses (influenza, rhinoviruses) invaders spite of mucociliary system) Streptococcus pyrogenes (throat) (infect Mycoplasma pneumoniae healthy Ability to interfere with cilia Chlamydia (psittacosis, chlamidial respiratory conjunctivitis & pneumonia, trachoma) tract) Ability to resist destruction in Bordetella pertussis, M.pneumoniae, Strep. alveolar macrophage Pneumoniae (pneumolysin) Ability to damage local (mucosal, Legionella, Mycobacterium tuberculosis submucosal) tissues Corynebacterium diptheriae (toxin), Strep. Pneumoniae (pneumolysin) Secondary Initial infection and damage by Staphylococcus aureus, Strep.pneumoniae, invaders respiratory virus (e.g. influenza pneumonia complicating influenza (infect when virus) host Local defenses impaired (e.g. cystic Staph. Aureus, Pseudomonas defences fibrosis) impaired) Chronic bronchitis, local foreign Haemophilus influenzae, Strep. Pneumoniae body or tumor Pneumocystis jiroveci, cytomegalovirus, Depressed immune responses (e.g. M.tuberculosis AIDS, neoplastic disease) Strep.pneumoniae, Staph. Aureus, H.influenzae Depressed resistance (e.g. elderly,  Virulence factors For bacteria to cause infection they must colonise, multiply to a substantial bacterial load, evade chemical and mechanical immunity Virulence factor examples: Pili (adhesins)-bordetella pertussis Capsule- strept pneumoniae, H. influenzae (help evade macrophages phagocytosis) M proteins- S.pyogenes (prevent phagocytosis) Toxin production- staphylococcus aureus + streptococcus pyogenes Figure 18.2 The respiratory tract as a continuum. Figure 18.5 Common cold viruses and their mechanisms of attachment.  Influenza (types A, B, C) Virus replication A/Gs: H, N Mode of transmission: by droplet inhalation + contact Antigenic variation: drift vs. shift 1918: Spanish ‘flu (H1N1) 1957: Asian ‘flu (H2N2) 1968: Hong Kong ‘flu (H3N2) 1977: Russian ‘flu (H1N1) 1997: (H5N1) 2004: Avian ‘flu (H5N1) 2008: ? Swine ‘flu 2019: Covid 19 Treatment- FLU Vaccination remains the most efficient mechanism at preventing influenza Treatment should be within 48 hours symptoms Neuraminidase inhibitors- limits severity of infection of all strains of flu (oseltamivir (oral)and zanamivir (dry powder inhalation)- interfere with release of progeny viruses from host cell Amantadine- M2 ion channel inhibitors- blocks uncoating of the virus intracellularly in the host cell (only effective against Inf.A- CNS S/E and resistance)  URTI- bacterial causative organisms Streptococcus pyogenes – (group A strept) Most common (pharingitis) but can lead to complications treat with penicillin Streptococcus pnemoniae- sinusitis, pneumonias, otitis media, can also exacerbate chronic respiratory conditions. Treat with penicillin- check always local guidelines for resistance Haemophilus influenzae- children mainly sinusitis, and otitis media (not influenza!)- Hib vaccine introduction reduced incidence of these severe infections Staphylococcus aureus- mainly associated with skin and soft tissue infections, but can cause sinusitis and otitis media in predisposed patients with risk factors (eg immunocompromised, nasal colonisation) treat with flucloxacillin Moraxella catarrhalis - sinusitis and otitis media (children and adults with underlying resp conditions such as CF) Bordetella pertussis – Whopping cough (severe coughing fits, vaccination has reduced significantly the incidence of pertussis)  Bacterial infections Streptococcus pyrogenes URTI’s Streptococcus pnemoniae Tonsillitis Sinusitus Haemophilus influenzae Otitis Media Pharyngitis Staphylococcus aureus Laryngitis Moraxella catarrhalis (LRTI’s –CAP + HAP) Complications of Strep.pyogenes (pus-producing) Otitis media, sinusitis, mastoiditis Scarlet fever – red tongue Rheumatic fever➔myocarditis/pericarditis Rheumatic heart disease – repeated attacks affect heart valves Acute glomerulonephritis Medicines advice https://www.medicinesforchildren.org.uk /advice-guides/giving-medicines/how-to- give-medicines-tablets/ https://www.e- lfh.org.uk/programmes/kidzmed/ Investigations for URTI Not normally necessary for URTI Except if suspect Strep.pyrogenes; Throat swab Antibiotic treatment- where bacterial infection highly suspected Phenoxymethylpenicillin Tonsillitis Pen allergy- clarithromycin Phenoxymethylpenicillin Sinusitis Pen allergy-clarithromycin Or doxycycline (C/I -children) Otitis Media Amoxicillin Pen allergy- clarithromycin MUMPs Viral Infection (family: paramyxoviridae) Extremely contagious Droplet entry—colonises nasopharynx Viraemia-----tissues and organs (CNS- meningitis, encephalitis) Kidney, has preference for PAROTID SALIVARY GLANDS (causes swelling, ear ache, trismus (spasms of chewing muscles) Males- (adolescence-orchitis, epididymitis) Generally self limiting MUMPS An ‘ancient’ disease Figure 18.17 The pathogenesis of mumps.  (ie. worse for adult!) Figure 18.19 Clinical consequences of mumps virus invasion of different body tissues. SSPE: subacute sclerosing panencaphalitis Respiratory route – direct spread; NO carriers = exanthem Prodromal period (enanthem in mouth) maculopapular paramyxovirus Summary: You should now be able to: Discuss the pathophysiology and epidemiology of a range of both respiratory infections and other infections spread by droplet transmission Understand the role of the immune system in RTIs Appreciate the clinical importance of non-RTI spread by droplet transmission eg. mumps & measles Know appropriate treatment regimens for named RTIs  tombstone%2520cartoon ABUSE THEM AND WE’LL LOSE THEM