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Respiratory and GI Tract Infections

The Common Cold. Causative OrganismsRhinoviruses Coronavirusesviruses also responsible for more severe illnessesadenoviruses, coxsackieviruses, echoviruses, influenza

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Respiratory and GI Tract Infections

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    1. Respiratory and GI Tract Infections Mark Pallen

    2. The Common Cold Causative Organisms Rhinoviruses Coronaviruses viruses also responsible for more severe illnesses adenoviruses, coxsackieviruses, echoviruses, influenza & parainfluenza viruses, RSV, enteroviruses Many cases unknown cause Clinical features rhinorrhoea, sore throat, sneezing, cough management Self-limiting Avoid aspirin in children (risk of Reye’s syndrome) Avoid antibiotics

    3. Sore Throat Clinical features: pharyngitis ± tonsillitis Causative organisms mostly viral bacterial causes: Streptococcus pyogenes (a.k.a. Group A beta-haemolytic streptococci) Less commonly: Corynebacterium diphtheriae, Group C and G beta-haemolytic streptococci, Arcanobacterium haemolyticum, Fusobacterium necrophorum

    4. Streptococcal pharyngitis Diagnosis: Throat swab Plate out on Blood agar Beta-haemolysis (complete haemolysis) Lancefield grouping of capsular antigen Rapid diagnostic tests with fluorescent antibody or latex agglutination

    5. Streptococcal pharyngitis Management Oral Penicillin V for 10 days (to prevent Rheumatic Fever) Can cause serious wound infections, so... Isolate patients in hospital Health workers should stay off work, and MUST STAY OUT of the operating theatre!

    6. Streptococcal pharyngitis Complications Paratonsillar abscess (quinsy) Scarlet Fever fine, red, raised rash on trunk & extremities, feels like coarse sandpaper Sequelae Rheumatic Fever or Glomerulonephritis diagnosis: anti-streptolysin O (ASO) antibody titres

    7. Diphtheria Acute toxin-mediated disease caused by Corynebacterium diphtheriae Gram-positive aerobic bacillus Incubation period 2-5 days Typically involves pharynx and tonsils leathery adherent membrane, which can cause respiratory obstruction Toxin effects Myocarditis Neuropathy

    8. Diphtheria Management Diphtheria is a medical emergency! Urgent need for antiserum ± tracheostomy Seek expert advice immediately you suspect it! Do NOT WAIT for bacteriological confirmation Antibiotic treatment Erythromycin Diphtheria is a public health emergency! Contact Public Health authorities immediately you suspect it! Notifiable disease Need for contact tracing, prophylaxis Prevention: routine childhood vaccination (+ adult boosters?)

    9. Glandular Fever a.k.a. “infectious mononucleosis” Caused by Epstein-Bar virus Spread by kissing (incubtaion period ~ 1 month) Clinical features Fever, malaise, sore throat, cervical lymphadenopathy Rarely, splenomegaly, splenic rupture, haemolytic uraemia Ampicillin and amoxycillin rash Diagnosis: Serology Traditionally, detection of heterophil antibodies (agglutinate sheep erythrocytes): Paul Bunnell or monospot tests More specific anti-EBV antibodies can now be detected

    10. Otitis Media & Sinusitis Local spread of organisms from URT , e.g. Streptococcus pneumoniae Haemophilus influenzae viruses probably commonly involved Clinical features Fever, local pain, dizziness, deafness Treatment Short course of co-amoxiclav Surgery, e.g. insert grommets

    11. Acute Epiglottitis Infective emergency Caused by Haemophilus influenzae capsular type B (Hib) Now very rare due to Hib vaccine program Can lead to acute respiratory obstruction Patients must be intubated (± tracheostomy) DO NOT attempt to take throat swabs DO NOT attempt to have a “look/see” Diagnosis take blood cultures H. influenzae requires rich medium (e.g. lysed blood or chocolate agar) Requires X and V growth factors on nutrient agar Management Intravenous cefotaxime or ceftriaxone Isolate the patient Prevention Hib vaccine

    12. Croup & Bronchiolitis RSV & flu/paraflu viruses Clinical Features: cold-like symptoms progress to harsh barking cough, worse at night, or when agitated wheeze in bronchiolitis can progress to respiratory obstruction or exhaustion, requiring hospitalisation Diagnosis Immunofluoresence or PCR on nasopharyngeal aspirate Management Supportive, e.g. intubation, oxygen, assisted ventilation in severe or high-risk cases, nebulised ribavirin (for RSV) Epidemiology Annual epidemics of RSV in winter months

    13. Pertussis “whooping cough” Caused by Bordetella pertussis a fastidious Gram-negative rod Clinical Features Catarrhal stage for ~2 weeks Paroxysmal stage for 2-6 weeks or longer Convalescent stage Sequelae weight loss, surgical emphysema, brain damage Diagnosis Lymphocytosis Culture of B. pertussis from pernasal swab Management erythromycin in catarrhal stage TOO LATE in paroxysmal stage! BUT still prevents infectivity Supportive treatment for paroxysms Prevention Vaccination as part of DTP x3

    14. Acute LRTI Various clinical syndromes Bronchopneumonia Diffuse patchy consolidation S. pneumoniae, H. influenzae Lobar pneumonia Typically S. pneumoniae Interstitial pneumonia Characteristically viral Lung abscess Atypical pneumonia

    15. Pneumococcal pneumonia Diagnosis Blood cultures ± sputum Strept. pneumoniae a.k. a. the pneumococcus Seen on Gram stain Grows on blood agar Draughtman’s colonies Bile soluble Optochin-sensitive Treatment Traditionally benzylpenicillin Risk of resistance means blind therapy with cefotaxime or ceftriaxone Prevention Polyvalent pneumococcal vaccine Offered to those at risk Elderly (>65) splenectomised patients Diabetics, alcoholics, CSF leak, COAD

    16. Atypical Pneumonia Caused by Mycoplasma pneumoniae (unusual bacterium) Legionella pneumophila (fastidious GNR) Chlamydia psittaci, C. pneumoniae Empirical treatment of all community-acquired pneumonia should include erythromycin to cover “atypicals” Diagnosis antigen detection & culture for L. pneumophila Serology ± PCR for all “atypicals”

    17. Influenza Epidemiology Yearly epidemics in winter months antigenic drift: point-mutational changes Intermittent worldwide pandemics with increased morbidity and mortality antigenic shift: recombination in birds, pigs totally new antigen types Rates of infection highest among children Severity increased greatly among elderly, those with medical conditions

    18. Influenza Two types (A and B) and many subtypes Type and subtype related to surface antigens (hemagglutinin and neuraminidase) Immunity decreases likelihood and severity of disease Immunity to one type or subtype offers little to no immunity to others

    19. Influenza Clinical features Abrupt onset fever, myalgias, headache, malaise, sore throat, rhinitis, nonproductive cough Complications viral pneumonia and/or bacterial superinfection typically S. pneumoniae Hospitalisation and Death greatest among elderly Antiviral agents shorten or prevent disease traditional amantadine (A) neuraminidase inhibitors oseltamivir (A and B) and zanamivir (A and B) Influenza vaccination > 65 years old Others at risk of complications Health care staff?

    20. Tuberculosis natural history & clinical features Caused by Mycobacterium tuberculosis Primary infection asymptomatic or non-specific symptoms: fever, malaise, weight loss, night sweats Inhalation of tubercle bacilli leads to lung infection Ingestion of tubercle bacilli tonsils & cervical nodes small bowel with mesenteric nodes Direct implantation into skin 

    21. Progressive Primary Infection local erosion by primary focus pleural cavity = pleurisy pericardium = pericarditis bronchus = tuberculous bronchopneumonia (highly infectious) disseminated infection miliary tuberculosis multiple discrete granulomas resembling millet seeds metastatic infection tuberculous meningitis bone & joint kidney uterus/testis 

    22. Post-Primary Infection as a result of reactivation of latent infection latent period between primary infection and reactivation can be several decades certain factors predispose to reactivation: immunosuppression, e.g. AIDS, cytotoxics malnutrition alcoholism diabetes old age 

    23. Diagnosis Clinical features Constitutional Fever, Malaise, Weight loss, Night sweats Focal Cough, Haemoptysis, Chest pain Radiological features Patchy opacities mainly in the upper zone cavitation, calcification, hilar shadowing diffuse nodular shadowing in miliary TB

    24. Lab Diagnosis Specimens large multiple specimens in sterile containers pulmonary TB early morning sputum specimens (x3) gastric washings bronchoscopy specimens a single negative sample does not rule out tuberculosis extra-pulmonary TB EMUs, LNs, BM, CSF unfixed! special risk to lab staff Category 3 pathogens In sealed leak-proof container Danger of Infection label In plastic bag

    25. Diagnosis Microscopy stain poorly with the Gram-stain Acid-fast bacilli (AFBs) rely on Acid-fast staining Ziehl-Neelsen stain

    26. Diagnosis Culture Lowenstein-jensen slopes M. tuberculosis grows after 4-6 weeks, rough buff an tough, breadcrumb-like colonies Kirschner’s broth

    27. Tuberculin Testing Mantoux test, Heaf test Purified protein derivative (PPD) delayed type (Type IV) hypersensitivity Positive Induration not erythema past or present infection or previous BCG vaccination Negative no previous infection or vaccination

    28. Tuberculosis Treatment Multi-drug regimens used prevent the emergence of resistance during therapy & more effective Initial Phase: 3 drugs for 2 months Continuation Phase: 2 drugs for 4-7 months Seek expert advice from chest physician! compliance problems & drug toxicity common repeated consultations risk of resistance

    29. Prevention of tuberculosis Eradicate poverty Control TB in cattle Early diagnosis & treatment of cases Side-room isolation of open “smear-positive” cases in hospital Selective screening with CXR Follow up of contacts of cases TUBERCULOSIS IS A NOTIFIABLE DISEASE Notification of the Public Health authorities is a legal requirement!! Immunisation with BCG traditionally at 11-13 years at birth in at risk infants

    30. Two new interlocking problems Effect of HIV pandemic on TB Greatest public health disaster since the bubonic plague... Evil synergy between TB and HIV infection Reactivation rates much higher in HIV-positives 10% lifetime risk of reactivation in HIV-negatives 8% annual risk in HIV-positives TB more aggressive in HIV-positives Emergence of multi-resistant TB In many areas, eg NYC, Nepal, Florida, multi-resistant strains have emerged, resistant to most, if not all, anti-TB drugs several outbreaks of multi-resistant TB in the USA, often centred on HIV-positive patients Medical & prison staff have caught fatal untreatable tuberculosis!

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