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Similar to MMP seminar presentation on aetiopathogenesis of respiratory tract infections.pptx
MMP seminar presentation on aetiopathogenesis of respiratory tract infections.pptx
- 1. A SEMINAR PRESENTATION ON ETIOLOGY ANDPATHOGENESIS OF RESPIRATORY TRACT INFECTIONS ONYEMA CHIIDIMMA OGUCHI 19051145007 DEPARTMENT OF MEDICINE AND SURGERY FACULTY OF CLINICAL SCIENCES UNIVERSITY OF CALABAR, CALABAR
- 2. Outline Introduction Classificationof Respiratory tract infections Upper respiratory tract infections Etiology Pathogenesis Clinical manifestations Prevention and Treatment Lower respiratory tract infections Etiology Pathogenesis Clinical manifestations Prevention and Treatment Conclusion
- 3. Introduction Respiratory tractinfections refers to any of a number of infectious diseases involving the respiratory tract.
- 4. Classification of RTIs Infections of the respiratory tract are classified into their symptomatology and anatomic involvement. Upper an lower respiratory tract infections
- 5. Upper Respiratory TractsInfections (URTIs) URTIs involve structures at or above the vocal cords (nasal cavity, sinues, pharynx and/or larynx. URTIs are common cold, influenza, COVID19, sinusitis, otitis media, pharyngitis, laryngitis, epiglottitis, laryngotracheitis (croup), pertussis and infectious mononucleosis. Organisms gain entry to the respiratory tract by inhalation of droplets and invade the mucosa. Epithelial destruction may ensue along redness, edema, haemorrhage and sometimes exudate.
- 6. Common Cold Etiology Mainly caused by viruses Rhinovirus is most common cause Other viruses are: Respiratory syncytial virus, parainfluenza viruses and adenoviruses Pathogenesis Virus introduced into RT by aerosol, contact with saliva or other respiratory secretions from an infected individual Act by direct invasion of epithelial cells of the respiratory mucosa. Destruction and sloughing of these cells or loss of ciliary activity depends on specific organisms involved. Increase in leukocyte infiltration and nasal secretions and Large amounts of protein and immunoglobin is secreted. This suggest that cytokines and immune mechanisms may be responsible for some of the clinical manifestations of common cold. Clinical manifestations (gradual onset) Nasal congestion, nasal discharge, sneezing, sore throat and cough. Fever is rare Prevention and treatment Treatment is mainly symptomatic (Use of decongestants, antipyretics, fluids and bed rest Restrict activities to prevent spread, practice good hand washing technique
- 7. Influenza Etiology Influenzavirus Pathogenesis Same as common cold Clinical manifestation (abrupt onset) High fever, chills, myalgias, sore throat and dry cough Prevention and treatment Supportive care and antiviral therapy in severe cases. Vaccination for prevention
- 8. COVID-19 Etiology SARS-CoV-2 Pathogenesis Not fully elucidated, however, it involves the attachment, entry and replication of the virus in the host cells. Entry is gain through the reaction with angiotensin-converting enzyme 2 receptor with the virus spike proteins. The overproduction of highly inflammatory cytokines leads to an increase in respiratory distress syndrome, coagulopathy and multi-organ failure Clinical manifestation Fever, cough, shortness of breath, loss of smell and/or taste Prevention and treatment Supportive care In severe cases, antiviral therapy (remdesivir) and glucocorticoids (dexamethasone) Vaccination for prevention
- 9. Sinusitis (acute inflammatorycondition of paranasal sinuses) Etiology Acute sinusitis mostly follow a common cold infection of viral origin Vasomotor and allergic rhinitis can cause sinusitis Infection of maxillary sinuses may follow dental extraction Extension of infections from the roots of the upper teeth Common bacterial agents that can cause sinusitis (Streptococcus pneumonia, Haemophilus influenza and Moraxella catarrhalis) Pathogenesis Viruses/bacteria impair ciliary activity of the epithelial lining of the sinuses Increased mucous secretions, leading to obstruction of the paranasal sinusal ostia which impedes drainage. Bacterial can multiple in the sinus cavities, converting the mucus to mucopurulent exudates The pus irritates the mucosal lining causing more edema, epithelial destruction and ostial obstruction. It can become chronic and lead to mucosal thickening Clinical manifestation Pain, Sensation of pressure, tenderness over affected sinuses, malaise and low grade fever. Purulent nasal discharge Prevention and treatment Supportive care Anti-microbial therapy (Beta-lactamase resistance antibiotic e,g amoxicillin-clavulanate or a cephalosporin)
- 10. Otitis media Etiology Most common causes (Streptococcus pneumonia, Haemophilus influenza and beta-lactamase producing Moraxella catarrhalis) Pathogenesis Acute otitis commonly follows an URTI extending from the nasopharynx via the Eustachian tube to the middle ear. This is exacerbated by vigorous nose blowing during common cold, sudden change in air pressure and perforation of the tympanic membrane. The presence of purulent exudate in the middle ear may lead to a spread of infection to the inner ear and mastoids or even meninges Clinical manifestation Severe ear ache, fever, vomiting Prevention and treatment Amoxicillin, amoxicillin-clavulanate, second and third generation cephalosporins, tetracyclines and other Macrolides
- 11. Acute Tonsillopharyngitis (Strepthroat) Etiology Inflammation of pharynx involving lymphoid tissues of the posterior pharynx and lateral pharyngeal bands Bacterial, viral, fungal or non-infectious causes (Smoking) Most common cause are viruses(rhinoviruse, type A coxsackievirus, adenovirus, herpes simplex virus. It’s a common symptom for Epstein-Barr virus and cytomegalovirus) Bacteria (Group A beta-haemolytic streptococcus (GAS)(Streptococcus pyogenes) associated with pharyngitis and tonsilities, Corynebacterium diphtheria, Mycoplasma pneumonia) Fungal (Candida albicans which causes oral candidiasis/thrush, can involve the pharynx, leading to inflammation and pain Pathogenesis Viral pathogens invade the mucosal cells of nasopharynx and oral cavity, resulting in edema and hyperemia of mucous membrane and tonsils Bacteria (GAS): invade the mucosa of URT, GAS has surface M protein (anti-phagocytic), secretes extracelluar proteins e.g haemolysins O and S, Dnase, NADase, streptokinase and pyrogenic toxin which causes immune reaction. In diphtheria, a potent bacterial exotoxin inhibits protein synthesis by ADP ribosylation of elongation factor 2 (EF-2) which causes local inflammation and cell necrosis Clinical manifestation Red, sore, scratchy throat. Inflammatory exudate may cover tonsils, there may be fever, malaise, myalgia or headache Treatment and prevention Viral infection: Supportive care Antibiotics (e.g penicillin G, amoxicillin, macrolides) for patients with confirmed GAS infection Vaccination (diphtheria toxoid)
- 12. Laryngitis Etiology Rhinovirus Streptococcus pneumonia Haemoplius influenzae Pathogenesis Similar to common cold and pharyngitis Clinical manifestation Hoarseness of voice Barking cough Prevention and treatment Supportive care (hydration, air humidification) Vocal rest
- 13. Epiglottitis and Laryngotracheitis Etiology Haemophilus influenza type b (Hib) (most common) Streptococcus pneumonia Streptococcus pyogenes (epiglottitis) Croup is mainly viral (para influenza virus most common) Pathogenesis Infection leads to rapid progressive erythema and swelling of epiglottis and bacteremia In croup, viral infection begins in the nasopharynx and moves to larynx and trachea. Inflammation and edema involves the epithelium, mucosa and submucosa of the subglottis which can lead to airway obstruction. Clinical manifestation Acute onset, sore throat, hoarseness, drooling, stridor, dyspnea, dysphagia within a few hours to severe respiratory distress, cherry-red epiglottis Prevention and treatment Antibiotics (e.g. cefotaxime, ampicillin/sulbactam), Glucocortcoids (e.g. dexamethasone) Airway management in epiglottis Oxygen therapy Vaccination with Hib vaccine
- 14. Pertussis Etiology Bordetellapertussis Pathogenesis Toxin mediated disease Bacteria attach to cilia of respiratory epithelial cells via a protein on pili called filamentous haemagglutinin Toxin inactivates Gi via ADP ribosylation causing a rise in cAMP and downstream cAMP-dependent protein kinase activity leading to inflammation which interferes with clearance of pulmonary secretions Pertussis antigens allow evasion of host defenses Clinical manifestation Fever is rare, paroxysms of whooping cough Rhinorrhae Myalgias and sore throat (rare) Prevention and treatment Antibiotics (e.g Azithromycin) vaccination
- 15. Lower respiratory tractinfections Infections of the LRTIs include bronchitis, bronchiolitis and pneumonia It is usually severe or fatal. Bacteria are the most common cause, although viruses, mycoplasma, rickettsiae and fungi can also cause LRTIs Organisms enter distal airway by inhalation, aspiration or by haematogenous seeding. Pathogens mutiples in epithelium causing inflammation, increased mucus secretion and impaired mucociliary function. Other lung function may be affected In severe bronchiolitis, inflammation and necrosis of the epithelium may block small airways leading to air way obstruction
- 16. Bronchitis and Bronchiolitis Etiology Bronchitis and bronchiolitis involve inflammation of the bronchial tree. Bronchitis precedes a URTI such as influenza, pertussis (influenza A & B, parainfluenza, respiratory syncytial virus Chronic bronchitis with persistent cough and sputum production is caused by combination of environmental factors (smoking) and bacteria infection (Haemophilus influenza and streptococcus pneumoniae) Bronchiolitis is a viral respiratory disease of infants. It is caused primarily by respiratory syncytial virus. Other viruses are : parainfluenza viruses, influenza irus and adenoviruses Pathogenesis Infected bronchial tree leads to hyperemia of mucosa, mucosa is edematous and produces copious bronchial secretions. The damage to the mucosa can be loss of mucociliary function, destruction of respiratory epithelium Necrosis of respiratory epithelium with eventual sloughing Thickened bronchial walls Exudate is made up of necrotic material and respiratory secretions and the narrowing of the bronchial lumen leading to airway obstruction. Areas of air trapping and atelectasis develop and may lead to respiratory failure Clinical manifestations Symptoms of URTIs with a cough is typical, mucopurulent sputum and moderate temperature elevation in Bronchitis Coryza and cough precedes bronchiolitis, fever is common, deepening cough, increased respiratory rate, retractions of chest wall, nase flaring and grunting, wheezing, absence of breath sounds, respiratory failure and death Prevention and treatment RSV treated with ribavirin. In chronic bronchitis, corticosteroids and bronchodialotors can be used
- 17. Pneumonia Pneumonia isan inflammation of the lung parenchyma Lobar pneumonia denotes an alveolar process involving an entire lobe of the lung Bronchopneumonia describes an alveolar process occurring in a distribution that is patchy without filling an entire lobe
- 18. Etiology Numerous factors,including environmental contaminants and autoimmune diseases, as well as infection, may cause pneumonia. Pneumonias occurring in usually healthy persons not confined to an institution are classified as community- acquired pneumonias. Infections arise while a patient is hospitalized or living in an institution such as a nursing home are called hospital- acquired or nosocomial pneumonias. Etiologic pathogens associated with community-acquired and hospital-acquired pneumonias are somewhat different. However, many organisms can cause both types of infections.
- 19. Bacterial pneumonias Streptococcuspneumoniae is the most common agent of community-acquired acute bacterial pneumonia Pneumonias caused by other streptococci are uncommon. Streptococcus pyogenes pneumonia is often associated with a hemorrhagic pneumonitis and empyema Community-acquired pneumonias caused by Staphylococcus aureus are also uncommon and usually occur after influenza or from staphylococcal bacteremia. Infections due to Haemophilus influenzae and Klebsiella pneumoniae are more common among patients who have chronic obstructive lung disease or alcoholism. most common agents of nosocomial pneumonias are aerobic gram-negative bacilli that rarely cause pneumonia in healthy individuals. Pseudomonas aeruginosa, Escherichia coli, Enterobacter, Citrobacter, Proteus, MRSA and Klebsiella species are often identified
- 20. Aspiration pneumonias Aspirationpneumonia from anaerobic organisms usually occurs in patients with periodontal disease or depressed consciousness. It can cause lung abscess The bacteria involved are usually part the oral flora and cultures generally show a mixed bacterial growth. Actinomyces, Bacteroides, Peptostreptococcus, Veilonella, Propionibacterium, Eubacterium, and Fusobacterium spp are often isolated.
- 21. Atypical pneumonias Mycoplasmapneumonia (most common) Legionella species, including L pneumophila Chlamydia spp noted to cause pneumonitis are C trachomatis, C psittaci and C pneumoniae. Chlamydia trachomatis causes pneumonia in neonates and young infants. C psittaci is a known cause for occupational pneumonitis in bird handlers such as turkey farmers. Coxiella burnetii the rickettsia responsible for Q fever, is acquired by inhalation of aerosols from infected animal placentas and feces. Pneumonitis is one of the major manifestations of this systemic infection Viral pneumonias are rare in healthy adults. A serious complication following influenza virus infection is a secondary bacterial pneumonia, particularly staphylococcal pneumonia. Respiratory syncytial virus can cause serious pneumonia among infants as well as outbreaks among institutionalized adults. Adenoviruses may also cause pneumonia, serotypes 1,2,3,7 and 7a have been associated with a severe, fatal pneumonia in infants.
- 22. Other pneumonias and immunosuppression Cytomegalovirus is well known for causing congenital infections in neonates, as well as the mononucleosis-like illness seen in adults. However, among its manifestations in immunocompromised individuals is a severe and often fatal pneumonitis. Herpes simplex virus also causes a pneumonia in this population. Giant-cell pneumonia is a serious complication of measles and has been found in children with immunodeficiency disorders or underlying cancers who receive live attenuated measles vaccine. Actinomyces and Nocardia spp can cause pneumonitis, particularly in immunocompromised hosts. Cryptococcus neoformans, Blastomyces dermatitidis, Coccidioides immitis, Histoplasma capsulatum, Aspergillus and Candida spp, are responsible for pneumonias in severely ill or immunosuppressed patients and neonates Pneumocystis jiroveci produces a life-threatening pneumonia among patients immunosuppressed by acquired immune deficiency syndrome (AIDS), hematologic cancers, or medical therapy. It is the most common cause of pneumonia among patients with AIDS when the CD4 cell counts drop below 200/mm .
- 23. Pathogenesis and ClinicalManifestations Infectious agents gain access to the lower respiratory tract by the inhalation of aerosolized material, by aspiration of upper airway flora, or by hematogenous seeding. Bacteria reproducing in the alveoli stimulate local macrophages and immune response is initiated. In lobar pneumonia, acute congestion stage (engorgement of the capillaries and recruitment of neutrophils into the lung parenchyma, then red hepatization where there is flow of RBCs from the capillaries into the alveolar space), Grey hepatization (large numbers of dead and dying neutrophils and degenerating RBCs) and Resolution (arrival of anti-bodies) Virulence factor in strep pneumonia, H influenza and kleb pneumonia is capsular polysaccharide. IgA protease (degrades IgA) allowing S. pneumonia and H influenza to attach and colonize the mucosal surfaces Pseudomonas toxin inhibits protein synthesis by ADP ribosylation of elongation factor 2 The major symptoms of pneumonia are cough, chest pain, fever, shortness of breath and sputum production, tachycardia, Headache, confusion, abdominal pain, nausea, vomiting and diarrhea may be present.
- 24. Prevention and Treatment Antibiotics should be used for the bacterial cause of pneumonia (Macrolides or fluoroquinolones for L pneunophila, M pneumonia and S pneumonia) and Anti-fungals for fungal causes (Voriconazole with or without caspofungin or amphotericin B with flucytosine in Aspergillus infection) The pneumococcal vaccine should be given to patients at high risk for developing pneumococcal infections, including asplenic patients, the elderly and any patients immunocompromised Yearly influenza vaccinations should also be provided In AIDS patients, trimethoprim/sulfamethoxazole, aerosolized pentamidine or other antimicrobials can be given for prophylaxis of Pneumocystis jiroveci infection
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