Week 1 - URTI, Oral lesions, Influenza, Salivary glands Flashcards
(42 cards)
Outline upper respiratory tract infections (URTIs).
- Rhinitis, Tonsilitis, Pharyngitis, Epiglottitis, Laryngitis, Sinusitis.
- Strong primary pathogens (e.g. diphtheria) in normal/secondary pathogens (streptococcus) in weak.
- Contact is the most important risk factor - crowding, school, kindergarten, travel, congregations (unhygienic situations, transmitted through aerosols).
- Influenced by many factors - immunity, nutrition, age, smoking, carrier states e.g. GABHS.
Identify common pathogens of URTIs.
- Nasopharynx - Rhinovirus (30-50%), parainfluenza viruses, RSV, adenovirus, coronavirus and influenza viruses.
- Oropharynx (usually bacteria) - Group A Strep, corynebacterium, EBV, adenoviruses.
- Epiglottis - H. influenzae.
- Larynx-trachea - Parainfluenza, S. aureus.
- Bronchi - Influenza virus, Strep pneumoniae, H. influenzae.
Provide an overview of pathogen microbiology:
• Characteristics of microbe promoting infection.
• Host defences preventing infection.
• Pathogenesis.
Characteristics of microbe promoting infection:
• Selective survival (microbe has strong preference for certain sites).
• High virulence organisms (infect normal healthy respiratory tract/evade defences).
• Low virulence organisms (secondary infections occur when host defences are weak).
• Factors affecting virulence: adhesion, invasiveness, toxigenicity, plasmids, bacterial products, appendages, infecting dose, route of infection, communicability.
Host defences preventing infection:
• Physical barriers: nasal hairs, cilia, cough & sneeze reflexes, bronchial mucus.
• Immunological barriers: tonsils, lymph nodes, antibodies, alveolar macrophages.
• Normal flora of upper respiratory tract (prevent pathogens from binding).
Pathogenesis:
• Organism enters respiratory tract, evades host defences and causes irritation/inflammation to respiratory mucosa.
Outline the common cold (rhinitis): • Aetiology. • Transmission. • Incubation period. • Clinical features. • Complications.
• Most common, seasonal, self-limiting.
Aetiology:
• Rhinovirus most common cause (>100 serotypes).
• Others - influenza, parainfluenza, corona (SARS), adenovirus and RSV.
Transmission:
• Highly contagious, droplets spread by sneezing, coughing or hand contact with the nose, eyes or face (hygiene measures required for prevention).
Incubation period:
• Incubation 2-4 days followed by sneezing, coughing and malaise for 3-6 days.
• Usually resolves by day 7 (with or without treatment) - treatment does not make much difference - maintaining good health and nutrition is important rather then taking antibiotics. Antibiotics prevent secondary infection).
Clinical features:
• Headache, nasal congestion, scratchy throat, clear watery rhinorrhoea. After 2-3 days, nasal discharge is thicker, cloudy and yellowish.
• Acute serous inflammation, catarrhal - excess mucous (catarrhal inflammation).
• Secondary bacterial infection common - suppurative (pus).
Complications: • Sinusitis. • Pharyngitis. • Tonsilitis. • Otitis media. • Septicaemia. • Nasal polyps - inflammatory (allergy) - long term complication usually seen in hypersensitivity/allergic people (inflammatory tissue accumulates under the mucosa - polyps).
Outline pharyngitis:
• Aetiology.
• Clinical features.
• Centor criteria.
• Inflammation of the pharynx (sore throat).
Aetiology:
• GAS Strep. pyogenes.
• Virus - rhinovirus, adenovirus, EBV etc.
Clinical features:
• Pain, headache, fever, myalgia, arthralgia (no cough).
• Bacteria - yellow white exudates on throat.
Centor criteria:
• 0 (unlikely) to 4 (likely).
• Fever, anterior lymphadenopathy, tonsilar exudate, no cough (each worth 1 point on the Centor criteria).
Sputum culture/microscopy:
• Gram positive streptococci in chains.
Outline epiglottitis:
• Aetiology.
• Clinical features.
• Complications.
• Inflammation of the epiglottis.
Aetiology:
• H. influenzae B.
• Can be due to strep.
Clinical features:
• Typically affects children, not common due to vaccine.
• Fever, dysphagia, drooling, hoarseness, stridor (severe distress in breathing).
Complications
• Inflammation can cause complete obstruction → urgent endotracheal intubation.
• Thumbprint sign on X-ray
Outline sinusitis.
- Inflammation of sinuses, most commonly paranasal ducts (maxillary sinusitis). Can occur in frontal sinus. Inflammation, pus formation.
- Chronic rhinosinusitis (CRS) - paranasal, >12 weeks. 3 types - associated with polyps, not associated with polyps and allergic (+/- polyps, allergic).
- Characterised by fever, pain, nasal discharge, hyposmia/anosmia.
- Requires long term antibiotic treatment and potential surgical treatment.
- Usually mixed microbial flora, especially normal inhabitants of nasal cavity.
- Often follows rhinitis - impairment of sinus drainage by inflammatory mucosal oedema
- Build up of microbes within sinuses → damage and inflammation.
Outline diphtheria: • Epidemiology. • Aetiology. • Transmission. • Clinical features. • Complications. • Prevention.
Epidemiology:
• Rare in developed countries. Not common because of vaccination but there is lack of vaccination in developing countries because of different belief systems.
Aetiology:
• Corynebacterium diphtheria.
• Gram +ve, pleomorphic bacilli (each one looks different - Chinese letter pattern).
• Exotoxin AB (activity and binding).
Transmission:
• Contact, aerosol spread, primary pathogen.
Clinical features:
• High fever, SOB, sore throat, cough, hoarse voice, nausea and vomiting. Neck lymphadenopathy, bull neck.
• Mucosal necrosis with fibrinopurulent exudate (pseudomembrane) - formation of pseudomembrane (thick pus sticking on the surface of the ulcerated mucosa - over pharynx and tonsils).
Complications (due to systemic spread of exotoxin):
• Aspiration of pseudomembrane and airway obstruction, spread of exotoxin, myocarditis, heart failure, peripheral neuritis.
• Cutaneous diphtheria - non healing ulcer.
Prevention:
• Vaccination - DPT (diphtheria, pertussis, tetanus).
Outline EBV - infectious mononucleosis (glandular fever): • Aetiology. • Transmission. • Incubation period. • Clinical features. • Pathogenesis. • Diagnosis. • Prognosis. • Complications.
Aetiology:
• Epstein- Barr virus (EBV).
• Herpes gp (10% by CMV - infectious mononucleosis occasionally caused by CMV - spread through saliva).
Transmission:
• Youth, close contact, saliva (kiss).
Incubation period:
• Incubation 1-2 months.
Clinical features:
• Adolescents and young adults.
• URTI (fever, sore throat, fatigue, malaise) + lymphadenopathy, splenomegaly, hepatitis.
• Enlarged spleen* - easy rupture - youth death* (may die with minor trauma).
Pathogenesis:
• EBV infect epithelium and B lymphocytes.
• EBV specific CD8+ T cells - defense (atypical lymphocytes) - protective mechanism - seen in peripheral blood smear - diagnosis is looking at atypical lymphocytes in peripheral blood.
• Viruses which enter upper respiratory tract → taken up by B lymphocytes → starts multiplying within B lymphocytes → infected B cells continue to divide and attack other organs.
• CD8 T lymphocytes - seen in peripheral blood - activated T lymphocytes (atypical, protective) kill infected B lymphocytes.
Diagnosis:
• Lymphocytosis with atypical lymphocytes (peripheral smear).
• Serology - heterophile antibody (monospot test).
• Monospot +ve (heterophile Ab) and rising titer of EBV antibody.
• Monospot - abnormal B lymphocytes produce many antibodies which are not normally seen e.g. heterophile Ab - specific to RBCs.
• Blood chemistry - altered liver enzymes.
Prognosis:
• Self limited (4-6 weeks then heals).
Complications:
• Hepatitis.
• Spleen rupture.
• Organ failure - fatal (e.g. meningitis).
Outline coxsackie virus.
- RNA virus. Enterovirus group. Faeco-oral, 2-6 day incubation.
- Coxsackievirus A: herpangina, hand, foot and mouth disease.
- Herpangina - fever, sore throat, oral, tiny papulovesicles → ulcers.
- Hand, foot and mouth disease - fever, sore throat, dysphagia, oral, tiny papulovesicles, erythematous halo.
• Coxsackievirus B: myocarditis, pericarditis.
- Myocarditis - fever, chest pain or asymptomatic → ventricular fibrillation (serious condition, can cause death due to VF).
- Bornholm disorder: intercostal myositis. DDx - MI, pulm, embolism etc.
- Coxsackie A - typically produce small blister-like lesions - hand, foot and mouth disease. Oral lesions also called herpangina.
- Coxsackie B - myocarditis, pericarditis.
Describe aphthous ulcers (canker sores).
- Common, young age (<20yo), self-limited (few days/weeks).
- Painful, superficial ulcers of unknown aetiology.
- Covered by thin exudate, surrounded by hyperemia.
- Associated with stress, autoimmune IBD and other disorders.
- Sugar as a therapy - sugar on top and keep it there → causes hyperosmolar absorption of all the inflammatory fluid → healing/relief of ulcer.
Describe pyogenic granuloma.
- Inflammatory - granulation tissue.
- Young age, pregnancy (AKA pregnancy tumour - very common).
- May regress or heal as fibroma or osteoma (may regress if primary infection cleared or heal as a fibroma or bone formation within healed scar tissue - osteoma).
- Looks like a tumour but it is excess granulation tissue due to chronic irritation, tooth caries, gingivitis → produces something similar to a tumour.
Describe fibroma.
- Nodular swelling of fibrous tissue - scar tissue.
- Chronic irritation - common on buccal mucosa, along bite lines (continuous damage by sharp teeth → produces swelling → fibrous scar tissue → healing scar). Reaction to chronic irritation - reactive connective tissue hyperplasia.
- Firm nodule of scar tissue.
Outline oral cancers.
- Head and neck 6th most common cancer in the world.
- Male (4%), female (2%) of all cancers are oral.
- Squamous cell carcinoma 95% of cases.
- 95% occur after 40 years of age (~60y).
- Location: Lips, tongue, floor of mouth, oropharynx (HPV).
- Aetiology: Tobacco (commonest - usually secondary to smoking), alcohol, HPV, sunlight (UV radiation - lips). Sunlight etiology in lip cancers, HPV becoming more common - also involved in cervical cancer.
Describe the pathogenesis of oral cancers.
- From precursor lesions (leuko/erythroplakia).
- Injury → hyperplasia → metaplasia → dysplasia (erythro/leuko) → carcinoma in situ (CIS) → carcinoma.
- HPV-16 → loss of E1, E2 tumor suppressor genes (commonest strain of HPV - loss of E1 and E2 tumor suppressor genes leading to cancer).
- Spread: cervical lymph nodes (stages) - spreads to cervical lymph nodes and then to distant organs.
- Cancer starts from precursor lesion - injury due to any aetiology (e.g. smoking, HPV etc.) → initial damage causes hyperplasia → metaplasia (change to thick keratinized epithelium) → dysplasia (irregularity of cell division) → CIS → carcinoma.
Differentiate between leukoplakia and erythroplakia.
Leukoplakia:
• Asymptomatic, chronic, painless, white (excess keratin forms white plaque).
• Tobacco, irritation, infection, EBV, HIV.
• Thick keratinised epidermis, less vascular submucosa.
• Microscopy - 10% dysplasia/cancer (plenty of inflammatory cells within).
• Cannot be scraped off.
Erythroplakia:
• Asymptomatic, chronic, red (loss of keratin).
• Tobacco, alcohol.
• Thin dysplastic epidermis with vascular submucosa.
• Microscopy - 90% dysplasia/cancer (chances of cancer greater).
- Important in oral lesions because represent early stage of malignancy (precursor to cancer caused by aetiology factors). But not all white/red patches are pre-malignant (any inflammation can also produce red patch. Chronic irritation can cause white patch).
- Usually leukoplakia → erythroplakia → cancer (SCC). Sometimes straight to cancer (neither plakia) or erythroplakia → cancer. (Not every patch goes through leukoplakia/erythroplakia. Some cancers can start without either plakia).
- White patch = more keratin.
- Red patch = more inflammation.
Describe the pathogenesis of oral dysplasia and cancer.
- Normal mucosa exposed to irritation/injury e.g. tobacco, HPV.
- Hyperplasia (thickening).
- Excess keratin cells start becoming irregular because of mutation.
- Leukoplakia with irregularities.
- Starts producing erythroplakia (initially it is mixed leuko and erythroplakia (speckled) but then it becomes malignant erythroplakia).
- Malignant.
Metaplasia - normal epithelium becomes keratinised.
Dysplasia - irregularity of cell division (basement membrane intact, stage 0 cancer or CIS). When it starts spreading → cancer.
Describe the morphology of oral squamous cell carcinoma.
Gross:
• May arise anywhere in oral cavity but the most common locations are the ventral surface of the tongue, floor of the mouth, lower lip, soft palate and gingiva.
• In early stages, these cancers appear as raised, firm, pearly plaques or as irregular, roughened or verrucous mucosal thickenings. Either pattern may be superimposed on a background of leukoplakia or erythroplakia.
• As these lesions enlarge they typically form ulcerated and protruding masses that have irregular and indurated or rolled borders.
Microscopy:
• Pleomorphic cells in clusters (no uniformity, very irregular, infiltrate, cause damage to own blood vessels (haemorrhage), inflammatory cells).
• Keratin pearls (keratin formation within nodules of cancer cells).
• Areas of inflammation, some necrosis and haemorrhage.
• Malignant cells form large nodules, inflammatory cells inbetween.
Clinical features:
• Patches inside mouth (leukoplakia, erythroplakia may become malignant).
• Bleeding in mouth.
• Difficulty or pain when swallowing.
• Lymph node involvement in 50% of tongue and 60% floor of mouth SCC at diagnosis.
Describe verrucous carcinoma.
- Warty, exophytic, white → ‘cauliflower’ like cancer.
- Buccal mucosa, vestibule, gingiva.
- Males > females; >60 years, tobacco and HPV infection (same aetiology).
- Papillary hyperkeratosis over dysplastic epithelial overgrowth.
- Low grade/well differentiated.
- No/rare metastasis.
- Wide excision is adequate (curative, good prognosis).
- Hard keratin producing tumor. Type of carcinoma - becomes more whitish instead of becoming red. Normal keratin production although it is an infiltrating cancer.
- Low grade cancer, well differentiated. Marked hyperkeratosis continuing without much infiltration.
Describe hairy leukoplakia.
- EBV virus - immunocompromised - AIDS.
- White patches of fluffy hairy hyperkeratotic thickenings.
- Lateral side of tongue more common (uni or bilateral),
- Some times with candidiasis also.
- Microscopy: acanthosis and balloon cells (loaded with EBV virus).
- Leukoplakia like patch. Hairy because appears irregular rough surface - usually due to EBV virus infection in an immunocompromised host e.g. AIDS patient. White patch can be due to inflammation, chronic infection, candida infection.
- Whenever you see white plaque → must take biopsy. Could be simple inflammation/infection or malignancy. Clinically you cannot tell the difference - red or white patch with/without symptoms → better to take biopsy
Summary of oral cancers.
• Normal → hyperplasia/hyperkeratosis → mild/moderate dysplasia (leukoplakia) → severe dysplasia/CIS (erythroplakia) → SCC.
- White lesion, symptomatic = hyperkeratosis.
- White lesion, asymptomatic = dysplasia.
- Gradual irregularity of cells (dysplasia).
- Leukoplakia → erythroplakia → cancer.
- Important to take biopsy.
Describe the differences in the oral epithelium.
Parakeratinised: • Less keratin with nuclei. • Long dermal papilla. • Buccal, lips, soft palate. • Mobile area, less trauma.
Absorptive:
• Flexible, more mucous.
• Under surface tongue, floor of mouth.
• Mobile, more blood vessels, minor salivary glands.
Keratinised: • Flat, thick keratin, no nuclei. • Short dermal papilla. • Gingiva and hard palate. • Fixed area, exposed to trauma.
Outline influenza.
- Globally, over 4 million cases, 200,000 hospitalisations and 40,000 deaths per year (commonest acute respiratory infection, presents like an URTI).
- Several types (influenza A, B & C) with each having a variety of strains; new strains each year (new vaccine each year). Type A and B most common.
- Only infection where a new vaccine has to be created every year. Beginning of cycle involves identification of strains and development of vaccine. Not 100% effective because there are so many strains and many new strains appearing - prevents from 40-80% of influenza attacks.
- More severe in susceptible population e.g. aged, young, pregnant, immunosuppressed, diabetes, chronic disease etc.
- Incubation 1-5 days; contagious 24 hours before to 7 days after symptoms. Person to person spread - crowd, school, aged care etc.
- Clinical: Mild URTI to high fever, exhaustion, malaise, sore throat, chills, headache, muscle aches and dry cough. Abdominal pain and diarrhoea especially in children.
- Diagnosis: Nasopharyngeal swab for a rapid antigen test or PCR serum antibodies later (usually develop later).
- Evolution - pandemics. Due to antigen variation → influenza spreads → spreads beyond borders with travel of people → pandemics (global attacks).
Identify the different types of influenza and describe its pathogenesis.
- Orthomyxovirus, single-stranded RNA virus.
- Bound by a nucleoprotein that determines the virus type.
- Type A, B and C (many strains, also many substrains).
- ~500 surface molecules of haemagglutinin (“H”).
- ~100 surface molecules of neuraminidase (“N”).
- A (H1N1) and A (H3N2).
- B Yamagatta, B Victoria etc. (named according to the place they were identified e.g. Brisbane).
- C rare - vaccine A and B only (vaccines developed based on the most common strains in a given population).
- Trivalent (2A and 1B).
- Quadrivalent (2A and 2B).
- Type A has many surface antigens - need to remember H and N antigen e.g. H1N1 - type of haemagglutinin and type of neuraminidase.
- Haemagglutinin (H) attaches virus to cell surface - virus enters cell.
- Neuraminidase (N) acts to release virus from cell surface - virus leaves cell.
Pathogenesis:
- Virus is transmitted via respiratory droplets (has incubation period of 1-5 days, is contagious 24 hours before and up to 4 days after the start of symptoms).
- Virus invades respiratory epithelial cells via the haemagglutinin (H) glycoprotein.
- Virus replicates in cells, triggers inflammation & causes damage to cells.
- Virus leaves cells via neuraminidase (N) glycoprotein.
