BDS10035 Oral Infections: Bacterial - PDF

Summary

This document provides information on bacterial infections, focusing on those of the oral cavity. It details the clinical aspects of bacterial infections, including non-plaque related ones like Treponema pallidum and mycobacterial infections within the oral mucosa.

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BDS10035 Oral infections: Bacterial Bacterial infections Aims The aim of this lecture is to detail the clinical aspects of bacterial of non-plaque related bacterial infection of the oral mucosa Objectives Understand the clinical, diagnostic and therapeutic aspects of bacterial infection of the mo...

BDS10035 Oral infections: Bacterial Bacterial infections Aims The aim of this lecture is to detail the clinical aspects of bacterial of non-plaque related bacterial infection of the oral mucosa Objectives Understand the clinical, diagnostic and therapeutic aspects of bacterial infection of the mouth, in particular Treponema pallidum and mycobacterial infection. Have an awareness of the range of other non-plaque related bacterial infections that may rarely arise in the mouth. There are many possible bacterial infections but only few commonly occur • T. pallidum • M. tuberculosis • A. Israelii • • • • • • • • • • • • • Atypical mycobacteria N. gonorroheae S.pyogenes C.diphtheriae C.tetani C.perfringens C.botulinum P.aeruginosa E.coli B.pertussis Rickettsia N.asteroides Others • Relevant bacterial infections: 1. Syphilis 2. Tuberculosis & related disease 3. Actinomycosis Emerging and re-merging infections include both syphilis & tuberculosis I. Bacteria • Tuberculosis • Syphilis • Others II. Viruses • HIV • Viral hepatitis • Others III. Fungi • Candida • Others IV. Prions I. Syphilis • Epidemiological trends: Worldwide rising frequency (significant) Heterosexuals (Men having sex with men) • Causes of change in epidemiology of syphilis : 1. 2. 3. 4. 5. 6. Political change Social/sexual liberalisation/liaisons via the internet Falling frequency of barrier contraception Migration Commercial sex HIV disease Cause (pathogenic bacteria): • Treponema pallidum. • Exclusively human pathogen. • Anaerobic Spirochetes. • Easily transmitted by direct contact (10-30% per contact). • Causes; endarteritis, endarteritis with eventual fibrosis & possible necrosis. Endartritis Clinical consequences & gradual progression if not treated: 1. 2. 3. 4. Primary Secondary Latent Tertiary (+ congenital disease) General manifestation of syphilis 1) Primary syphilis: 1. Arises ~ 10-90 days post-infection (21 days) 2. Oral chancre. 3) Latent syphilis: 3. Regional lymphadenopathy 1. Asymptomatic 2. +ve serological tests for syphilis 2) Secondary syphilis: 1. 2. 3. 4. 5. 6. 7. Arises 6 weeks to 6 months post-infection Multiple maculopapular lesions Mucosal ulceration Generalised lymphadenopathy, fever, malaise Condylomata lata (warty-like areas) Alopecia Asymptomatic or symptomatic (e.g. meningitis) CNS involvement 4) Tertiary syphilis: 1. Develop many years post-infection 2. Gumma formation (palate, tongue, skin, bones, joints, viscera) 3. Cardiovascular disease • Aortitis (ascending > arch > descending) • Gumma of myocardium, pericardium or endocardium • Rare conductive defects 4. Neurosyphilis: • Meningitis (2 months to 2 years post-infection) • Meningo-vascular syphilis (2 months to 20+ years) • General paresis (3 years+) • General paralysis of the insane: • Tabes dorsalis: (5 years+) a) Lightening pain (at right angles to legs) 1. Initially ill-defined personality changes b) Ataxia of lower limbs 2. Progressive impairment of memory, c) Sphincter dysfunction (e.g. bladder) insight & personality d) Loss of proprioception 3. Inappropriate behaviour, dress e) Loss of deep pain sensation 4. Delusions (grandiose uncommon), dementia 5) Congenital syphilis (increase in frequency in heterosexual community) 1. Early features (< 2 years) 2. Late features (> 2 years) 1. 2. 3. 4. 5. 6. 1. 2. 3. 4. 5. 6. 7. 8. 9. Fulminant, disseminated infection. Mucocutaneous disease. Osteochondritis Anaemia Hepatosplenomegaly CNS involvement Frontal bossing Saddle deformity of nose 8th nerve deafness Interstitial keratitis Dental anomalies Periostitis Osteochondritis Paroxysmal cold haemoglobinuria. Neurosyphilis Oral manifestations of primary syphilis: 1. Chancre: •Single or multiple areas of ulceration at the site of acquisition. •Upper lip (males),Lower lips (females). •Site: Tongue, gingivae, fauces •Lasts 3 to 10 weeks. •Usually heal spontaneously. •Serology may be negative. •Responds rapidly to therapy. •May be prolonged in patients with HIV disease. 2. Local lymphadenopathy. Orofacial manifestations of secondary syphilis: 1. Mucous patches: • Painless, grey erosions/ulcers. • Coalesce to produce serpiginous “snail track” ulcers. • Fauces, soft palate, buccal mucosae, rarely in gingiva. 2. 3. 4. 5. 6. 7. Macular syphilides (often undetected). Papular syphilides Nodular disease (may occur on the lip) Lymphadenopathy Syphilitic sialadenitis (very rare!) In HIV disease lesions can be prolonged Deep plasma cell infiltrates Oral manifestations of tertiary syphilis 1. Gumma formation: • Site: Hard palate, tongue, rarely at soft palate & gingiva. • Fistula formation. 3ry syphilis Granuloma 3ry syphilis Langhans-type giant cells 2. Syphilitic Leukoplakia: • Rare. • More common in males • Associated with tobacco • Risk of OSCC (Possible interaction with tobacco/alcohol/HPV) • Observed by Hutchinson in London in the 19th Century Syphilitic leukoplakia 2. 3. 4. 5. Osteomyelitis Arterial erosion Trigeminal neuropathy Acute syphilitic meningitis causes cranial neuropathies (III, VI, VII and VIII) 6. Argyll-Robertson pupils: Light near dissociation do not react to light, but respond to accommodation/convergence. 7. Expressionless face, lip tremor (in general paralysis of insane). 8. Neuropathy (butterfly area of face (Hitzig zones) in tabes dorsalis. Orofacial manifestations of congenital syphilis • Early orofacial manifestations: 1. Condylomata lata at mucocutaneous junctions 2. Radiating scars (rhagades) at angle of mouth, nose eyes 3. Mucosal ulceration (severe) • Late orofacial manifestations: 1. Dental anomalies 2. Skeletal anomalies 3. Neurological disease • Dental features of congenital syphilis 1. Permanent incisors “screw-driver” ”Hutchinson’s teeth” • Maxillary > mandibular. 2. First molars “Mulberry teeth” • Loss of mesio-distal convexity / Bud-shaped Influence of HIV upon syphilis • Prolonged primary disease (?) • Enhanced progression to secondary disease (?) • Prolonged, atypical and/or more severe secondary disease (?) • Rapid progression to neurosyphilis (?) • False negative serological tests (?) • Variable response to therapy (?) • Increased risk of hypersensitivity to therapy (?) • Diagnosis of syphilis: 1. Direct methods (i.e. to detect T. pallidum) • Dark ground illumination microscopy of “wet preparation” for primary & secondary disease (now historical). • Direct fluorescent antibody testing or PCR –not widely available & not routine done. 2. Serology (the main method of diagnosis) • Screening tests (non-specific to T. Pallidum) e.g. Enzyme immunoassay) (EIA) or Chemiluminescence immunoassay (CLIA) – that point towards but do not confirm syphilis. • Specific tests (specific to T. Pallidum): TPPA • The rapid plasma reagin (RPR) test determines the titre of anti-TP antibodies & thus determines disease activity & response to therapy. • Treatment of syphilis: 1. 2. 3. 4. Penicillin (e.g. IM benzathine penicillin) Ceftriaxone (cephalosporin) Azithromycin Tetracycline • Resistance to these therapies can arise • Variable response in HIV disease? Conclusions on syphilis 1. 2. 3. 4. 5. Infective syphilis is re-emerging Congenital disease may be on the increase. Oral manifestations are variable, but can arise at any stage. HIV (perhaps) may modify the clinical course of syphilis. Oral health care staff may be the first to witness oral disease of syphilis and/or HIV Other treponemal infections Pinta Yaws • T. carateum • Central and South America • Probable non-sexual (direct or indirect) transmission, young adults affected • No congenital form • Penicillin • T.pertenue • S.East Asia, Africa, W.Pacific, S.America, Caribbean • Non-sexual transmission (direct contact with exudate or via utensils etc). • Children usually affected • No congenital form • Penicillin, tetracycline, erythromycin Orofacial aspects: • Initially subcutaneous granulomatous lesions of face, trunk or leg. • Later papules then pigmented plaques that depigment and cause skin atrophy. • No oral lesions • Orofacial aspects: • primary disease; cf syphilis, papules/ulcer at site of infection. • Later secondary granulomas of skin, axillae, groin, peri-orally. • Gummatous destruction after a long (eg 5 yrs) • Bone thickening about nose in secondary and tertiary disease causes facial appearance “Goundou” • Destruction of palate causes nasal collapse “saddle-nose” Other spirochete infections 1. Acute necrotising gingivitis 2. Lyme disease: • Borellia burgdorferi • Transmitted by Ixodid ticks • Initial disease 7-10 days after bite – erythema, migrans, headache, myalgia, malaise, pyrexia, lymphadenopathy • Second stage – weeks/months later meningo-encaphalitis, cranial or peripheral neuropathies and/or myocarditis • Third stage - recurring arthritis • Diagnosis: detection of organism, antibodies to Borellia burgdorferi • Therapy: penicillin or tetracycline • Orofacial manifestations - Facial palsy II. Tuberculosis Epidemiology: • Tuberculosis incidence is 9,000,000 new cases/year. • Approximately 2 million deaths per year (the most common cause of death from a single infective agent). • Two billion people are infected with M. tuberculosis worldwide. • ~30% of the 40 million estimated HIV+ individuals are infected with tuberculosis worldwide. • 450,000 cases of multidrug-resistant TB (MDR-TB) per year occur. •10% are extensively drug-resistant forms. Aetiology/pathogenesis 1. Infection by M. tuberculosis complex family species & principally M. tuberculosis. 2. M. tuberculosis interacts with macrophages and dendritic cells leading to TNF-α production and activation of T-cells. 3. Results into a Th-1 type immune reaction which includes IFN-γ secretion. 4. Effective immune response results in isolation of bacilli. 5. Granuloma formation. 6. Oral tuberculosis is a consequence of inoculation of bacilli to oral mucosa. Type of tuberculosis General Clinical features of TB Pulmonary tuberculosis Primary disease Cough (non productive or productive) Hemoptysis Malaise Phlyctenular conjunctivitis Erythema nodosum Fever Weight loss Pulmonary tuberculosis Post primary disease Miliary tuberculosis Cough Chest pain Anorexia Weight loss Hemoptysis Dyspnea Malaise Fever Sputum mixed with blood Miliary TB affecting lungs Fever Weight loss Symptoms specific to the organs infected. Anorexia Possible tachycardia. Fatigue. Cachexia in late stage TB Reported oral manifestations Salivary gland (49 Patients) Ulceration (27 Patients) Other lesions (31 patients) Parotid (45) Submandibular gland (4) Tongue (15), Buccal mucosa (2), Lips (2), Gingiva (2), Generalized ulceration (2), Floor of the mouth (1), Commissures (1), Lingual phrenum (1) Osteomyelitis (8) Swelling (9: tongue, lip, palate, buccal mucosa, uvula, tonsils) Lymph node (5) Gingival enlargement (2) Alveolar bone loss (2) TMJ dysfunction (2) Tuberculomas (2) Granular lesion (1) Tuberculosis - diagnosis 1. Tuberculin skin test (TST) 2. Chest radiology 3. Microscopy (biopsy & stain of tissue for acid fast bacilli identification) 4. Culture (Gold standard) 5. Nucleic acid amplification tests (NAATs) (includes PCR) 6. INF-γ assays 7. Drug susceptibility testing New VS Old Diagnostic methods INF-γ more accurate than TST NAATs higher specificity and sensitivity comparing to microscopy (100% vs 95-98%-87.5%vs20-60%) New vaccines such as the MVA85A (viral based vaccine expressing 85A antigen) are under development in order to achieve better levels of protection than BCG (protection 0-80% for pulmonary TB). Tuberculosis therapy: A) First line anti-TB agents • Isoniazid (H), Rifampicin (R), Pyrazinamide (Z), Ethambutol (E) • Most common regimens: • Initial Phase: 2 months HRZE daily • Continuation phase: 4 months HR daily B) Second line anti-TB agents • Streptomycin, • Aminoglycosides (Kanamycin, Amikacin, Capreomycin) • Thionamides (Ethionamide, Prothionamide) • Fluoroquinolones: (Ofloxacin, Ciprofloxacin) • Cycloserine • Para-aminosalicylic acids • TB caused by drug-susceptible M. tuberculosis strains can be cured in 95% of cases. • All patients with recently reported oral tuberculosis had cure. Recent data concerning Tuberculosis • Patients with MDR-TB and extensively drug resistant TB (XDR-TB) cases have been detected all over the world & particularly in China and Former Soviet Union Countries. • MDR-TB is a result of inappropriate treatment or lack of compliance to therapy. • Signs and symptoms do not differ from drug susceptible TB. • MDR-TB has 50% less favorable treatment outcomes & the cost of second line therapy is higher and have higher toxicity. Oral manifestations of Mycobacteria other than TB (MOTT): 1) M. avium: • Oral ulceration. • Addisonian pigmentation. 2) M. leprae : • Nodules (lepromas) of palate, tongue which may ulcerate & scar. • Mucosal infiltrations • Cranial nerves V, VII neuropathies • Loss of taste III. Actinomycosis • Typically A.isrealii • Often associated with dental trauma (e.g. extractions) • Adulthood usually. • Cervicofacial manifestations: 1. Cutaneous swelling with possible sinus formation. 2. Typically at angle of mandible. 3. Occasional lymphadenopathy. • Diagnosis: 1. Sulphur granules macroscopically within pus 2. Gram positive filaments within sulphur granules 3. Actinomyces cultured • Therapy: 1. Drainage 2. Penicillins or tetracyclines Other bacterial infections affecting the mouth 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. N. meningitidis: petechiae, Herpes labialis, VII palsy H. Influenzae: cellulitis, ulceration S. pyogenes: peritonsilar abscess, cellulitis, raspberry tongue, petechiae C. diphtheriae: faucial membrane, palatal palsy Cl. tetani: Trismus, risus sardonicus. Cl. perfringens (C.welchii): gas gangrene Cl. botulinum: xerostomia, parotitis, muscle weakness P.aeruginosa: ulceration P.mallei (glanders): ulceration P.pseudomallei: melioidosis, accesses, parotitis E. coli: ulceration, occasional commensal B.pertussis: palatal petechiae, lingual frenal ulceration Brucella: cervical lymphadenopathy M.pneumoniae: VII palsy, erythema multiforme Rickettsia rickettsiae: petechiae, facial gangrene R. akari: vesicles Bacterial infections – summary 1. Syphilis is an increasingly common infection in which oral manifestations commonly arise. 2. Tuberculosis remains a world wide health problem reflecting societal poverty. 3. Actinomycosis, although uncommon, can arise following invasive dental treatment and give rise to orofacial features. 4. A spectrum of other bacterial infections may, very rarely, affected the mouth and allied structures. References & further readings • Odell E.W. Cawson’s Essentials of Oral Pathology and Oral Medicine. 9th Edition. Elsevier, 2017 pp 242-244 • Robinson M et al. Soames’ and Southam’s Oral Pathology. 5th edition. Oxford University Press, 2018 pp 26-28 • O’Bryne P et al, Syphilis. BMJ. 2019 Jun 28;365:l4159. doi: 10.1136/bmj.l4159. Bacterial infections Aims The aim of this lecture is to detail the clinical aspects of bacterial of non-plaque related bacterial infection of the oral mucosa Objectives Understand the clinical, diagnostic and therapeutic aspects of bacterial infection of the mouth, in particular Treponema pallidum and mycobacterial infection. Have an awareness of the range of other non-plaque related bacterial infections that may rarely arise in the mouth.

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