Infections of Oral Cavity and Salivary Glands PDF

Infections of the Oral Cavity and Salivary Glands PROF. JANANIE KOTTAHACHCHI CONSULTANT MICROBIOLOGIST LLOs Describe the clinical presentation, etiology & pathogenesis of infections of oral cavity Outline microbiological basis of diagnosis (including specimen collection & transport), ma...

Infections of the Oral Cavity and Salivary Glands PROF. JANANIE KOTTAHACHCHI CONSULTANT MICROBIOLOGIST LLOs Describe the clinical presentation, etiology & pathogenesis of infections of oral cavity Outline microbiological basis of diagnosis (including specimen collection & transport), management & prevention of infections of the mouth and salivary glands  INFECTIONS OF ORAL CAVITY  Oral thrush – Candidiasis  Herpes gingivo – stomatitis  Herpangina - Coxsackie A virus  Hand – foot – and – mouth disease - Coxsakie A 16  Vincent’s angina  Dentoalveolar infections  Oral candidiasis/ oral thrush Opportunistic infection caused by Candida sp. Seen in people with disturbed host defense mechanisms ◦ Diabetes ◦ HIV Infections ◦ Steroid Therapy ◦ Newborn babies ◦ Denture uses Clinical Features Lesions occur on the buccal mucosa or the hard palate Appear as white adherent patches and may eventually become confluent and form a curd like pseudomembrane Surrounding mucosa is red and sore  Diagnosis Specimen – Scrapings / swabs from the surface lesions Investigations - Gram stain - Culture on Sabouraud’s agar Treatment Topical antifungal agents Nystatin suspensions Miconazole lozenges Clotrimazole  Herpes gingivo – stomatitis A viral infection of the oral mucous membrane caused by Herpes simplex virus Usually, HSV-1 and rarely HSV-2 Commonly reported in children between 6 months to 6 years Clinical features Abrupt onset of symptoms High fever Headache, malaise, anorexia, irritability Bilateral sensitive regional lymphadenopathy Sore mouth lesions Affected mucosa is red and oedematous with numerous coalasing vesicles that rupture rapidly leaving painful ulcers Clinical features… New lesions continue to develop during 3-5 days Ulcers heal in 10-14 days Both movable and non movable oral mucosa are affected Gingival lesions are almost always present, resulting in enlargement, oedematous and painful erosions Clinical features… Patiens experience fever for 1-3 days Cervical lymphadenopathy present Virus remain latent following the primary infection Herpes labialis (cold sore) results as reactivation Pathogenesis Virus targets epithelial cells that cause ballooning degeneration Tzank cells Infected cells fuse and form multinucleated cells Oedema of infected cells leads to formation of intraepithelial vesicles that rupture and develop a purulent exudate Discrete ulceration leads to release of exudate DD Necrotizing ulcerative gingivitis Erythema multiforme Steves-Johnsons Syndrome Apthos stomatitis Herpangina Desquamative gingivitis Early pemphigus Diagnosis Proper clinical history and examination findings Specimens Aspirate from the vesicles Swabs from the lesion Blood for serology Biopsy Tzank cells- from swabs PCR Histology from biopsy Serological investigations- IgM, IgG Isolation of HSV by cell culture Treatment Acyclovir Local application Oral tablets Symptomatic treatment Topical lignocaine  Herpangina An acute febrile illness associated with small vesicular or ulcerative lesions on the posterior oropharyngeal area Tonsils and soft palate Caused by Coxsackievirus A 1-24 It occur during the summer and a without distinctive features Clinical features Abrupt onset of fever, sore throat Anorexia, dysphagia, vomiting, or abdomim pain The pharynx is usually hyperaemic, a characteristic discrete vesicles occur on anterior pillars of the fauces, the uvula, tonsils, or tongue The illness is most frequent in small children Pathogenesis Transmission – from person to person Faeco-oral-usual route Respiratory droplets Contact transmission and formites- E.g. from soft toys Incubation period- 2-10 days Initially replicate at upper respiratory tract and distal small bowel Replicate in the sub mucosal lymph tissues Disseminate to reticulo endothelial system Diagnosis History and clinical examination Specimens-Stools, swabs from lesions, blood for serology RT-PCR Detection of specific antibodies Treatment and prevention Analgesics Adequate fluid intake Rest Prevention by hand washing  Hand foot and mouth disease Caused by Enterovirus 71 and Coxsackievirus A 16 Highly contagious Mainly affects infants and young children Typically occur in small epidemics in nursery schools or kindergartens Clinical features Begin as a common illness and e.g. fever, headache, malaise, conjunctival injection Causes rapidly ulcerating painful red blisters on Throat Tongue Gums Hard palate Inside cheeks Palms and hands Soles and feet Diarrhoea and abdominal pain Four stages of the disease Enteroviral infection causes 4 stages of disease Stage 1 Development of oral ulcer and vesicular rash Stage 2 CNS involvement- aseptic meningitis, encephalitis Stage 3 Cardiopulmonary failure, pulmonary oedema or haemorrhage, LVF Stage 4 Convalescence Pathogenesis Transmits through direct contact with mucus or faeces of an infected person Nasal discharges, saliva, equipment and toys Incubation period- 4-6 days Most contagious during 1st week of illness High risk groups-children in nurseries, pre schools, crowded and unsanitary environments Usually mild and self-limiting Rarely it can occasionally cause complications affecting the central nervous system, heart, or lungs Complications Due to Coxsackie A 16- milder course Myocarditis with intractable shock, death Enterovirus 71- more severe infection Meningitis, encephalitis, neurogenic pulmonary oedema Diagnosis History and clinical examination Specimens-Swabs from lesions, CSF, blood for serology RT-PCR Detection of specific antibodies Treatment and prevention Most patients do not require admission Symptomatic treatment, adequate hydration and rest Maintain personal hygiene Isolate the patient Hand washing Do not share personal items  Vincent’s angina A progressive painful infection with ulceration, swelling and sloughing off of dead tissue from the mouth and throat due to the spread of infection from the gums Was common in the first world war - was known as trench mouth Other names- Acute necrotizing ulcerative gingivitis (ANUG) Caused by Treponema vincentii Fusobacterium necrophorum Common in young patients with Poor oral hygiene Smoking Clinical features Characterized by presence of grayish membrane and foul odour of breath Abrupt onset of Gingival pain and bleeding Foul metallic taste, halitosis Salivation Enlarged, tender cervical lymph nodes Fever, malaise, anorexia Oral examination reveals punched-out, ragged gingival ulceration Pharyngeal mucosa is also inflamed Diagnosis Specimens- Throat swabs Investigations Culture and ABST May need anaerobic culture Treatment Hydrogen peroxide mouth wash Debridement Antibiotics - penicillins  Dentoalveolar infections Pyogenic infections associated with teeth and surrounding supportive structures such as periodontium and alveolar bone Originate in the tooth or its supporting structures and can spread to the surrounding tissues Infections can also affect the gums, causing gingivitis, which can later cause periodontal disease Clinical presentation The clinical presentation depends on the Virulence of the causative organism Local and systemic defense mechanisms of the host Anatomical features of the region Depending on the interaction of above it result An abscess localized to the tooth Diffuse cellulitis that spread along fascial planes A mixture of both Clinical features Bitter taste in the mouth Breath odor General discomfort, uneasiness, or ill-feeling Fever Pain when chewing Sensitivity of the teeth to hot or cold Swelling of the gum over the infected tooth Swollen lymph nodes of the neck Dentoalveolar abscess Develops by the extension of the initial carious lesion into dentine and spread of bacteria to the pulp via the dental tubule The pulp responds to infection by Rapid acute inflammation involving the whole pulp which quickly become necrosed Development of chronic localized abscess with most of pulp remaining viable Pathogenesis Organisms further enter by Traumatic tooth fracture or pathological exposure due to tooth wear Traumatic exposure due to dental treatment Through periodontal membrane and accessory root canals  Sequelae Abscess remain localized at the root apex Develop into acute or chronic abscess Develop into a focal osteomyelitis Spread into the surrounding tissues and even cause sinus formation Haematogenous and lymphatic spread to distant areas also may occur Ludwig’s angina-spreading, bilateral infection of the sublingual and submandibular spaces Microbiology Infections usually are polymicrobial Strict anaerobes are predominant Streptococcus anginosus group Actinomyces spp. Peptostreptococcus spp. Porphyromonas spp. Prevotella spp. Fusobacterium spp. Diagnosis Specimens- Pus collected by needle aspiration or by incision, swabs Transport closing the container tightly maintaining anaerobic conditions Culture anaerobically Management Draining pus Removing the source of infection Antibiotics Penicillin V Erythromycin Metronidazole Periodontal abscess Caused by an acute or chronic destructive process in the periodontium, resulting in localized collection of pus Formed by occlusion or trauma to the orifice of a periodontal pocket, leading to extension of infection from the pocket into the supporting tissues Results from impaction of food or compression of the pocket wall by orthodontic tooth movement Cervicofacial actinomycosis An endogenous granulomatous disease Most common in cervicofacial region Causative organism is Actinomyces israelii- a commensal present in dental plaques, carious dentine and calculus Trauma to jaws, tooth extraction and teeth with gangrenous pulps may precipitate infection Predominantly younger people are affected Clinical features Acute, subacute or chronic forms History of trauma, such as tooth extraction or blow to the jaw Localised or diffuse swelling may progress to discharging sinus if do not treat Pain, multiple discharging sinuses, trismus, pyrexia, fibrosis around the swelling and presence of infected teeth Submandibular region is most commonly affected Diagnosis Specimens- fluid by aspiration or by an incision Gram stain – Suphur granules Culture anaerobically Management Acute lesions Remove associated dental focus Incision and drainage of abscess Antibiotic for 2-3 weeks- Penicillin is the drug of choice Subacute lesions Surgical intervention Antibiotics for 5-6 weeks Erythromycin, tetracycline or clindamycin- if hypersensitive to penicillin  INFECTIONS OF THE SALIVARY GLANDS Also known as sialadentitis Majority are viral infections and also may be due to bacterial and fungal infections Parotid glands are more commonly infected than submandibular glands Accessory salivary glands are very rarely infected Mainly seen in adults Initiation and progression depends on the virulence of the organisms and the host resistance Viral infections-Mumps The most common viral cause of infections of salivary glands, a non suppurative acute sialadentitis Occurs due to Mumps virus- a systemic illness that infect children most Transmitted via direct contact with saliva and by droplet spread Incubation period- 14-18 days Virus replicate in salivary duct epithelial cells leading to periductal oedema and infiltrate The virus shed in saliva and spread into bloodstream causing viraemia Saliva is infectious during prodromal period and upto 2 weeks of onset of clinical symptoms Viral infections-Mumps… Clinical features Pyrexia, sore throat and ear ache Pain on salivation and chewing Majority of infections are bilateral Reddening at the opening of parotid duct Increased in gland size May displace ipsilateral pinna Low salivary flow rate leading to halitosis Complications-Mumps Orchitis, testicular atrophy, and sterility in about 20% of young men Oopharitis in 5% of females Aseptic meningitis Pancreatitis Myocarditis, thyroiditis and nephritis Sensorineural hearing loss Usually permanent Majority is unilateral Other viral infections HIV CMV Parainfluenza types 2 and 3 Echo virus Coxsackie virus Bacterial infections Also known as acute suppurative parotitis Mostly seen in adults with salivary gland abnomalities and other predisposing factors Predisposing factors Drugs reduce salivary flow- diuretics Salivary gland abnormalities-calculus, mucus plug, strictures Dehydration Sjoren’s syndrome- an autoimmune condition Aetiological agents Alpha haemolytic streptococci Staphylococcus aureus Haemophilus spp. Bacteroides spp. Anaerobic streptococci Clinical features Fever with chills Unilateral or bilateral swelling of parotid glands Swelling may extend to pre and post auricular area Purulent salivary secretions at the duct orifice Recurrent bouts of acute infection followed by remission leading to fibrosis Diagnosis Specimens- pus aspirated by a catheter attached to a syringe, collect to a swab milking the duct Culture and ABST Treatment Parenteral antibiotic therapy guided by ABST-Penicillins Surgical drainage of pus Encourage salivation by increased fluid intake and by sialagogues e.g. lemon juice Oral hygiene Complications Extension of oedema to neck leading to respiratory obstruction Cellulitis of face and neck Osteomyelitis of adjacent facial bones Sepsis and death Fungal infections Caused by Actinomyces israelii Endogenous infection from mouth  Diagnosis of infections of salivary glands Clinical history Examination Laboratory investigations IgM, IgG antibody detection- mumps Serum amylase – increase in mumps Fine needle biopsy if suspecting a tumor is contributing to the infection autoimmune conditions, including Sjögren’s disease Imaging tests Ultrasound scan CT scan MRI scan Salivary endoscopy -sialoendoscopy Sialography - injecting a dye that appear on X-rays Treatment of infections of salivary glands Generally resolve on its own, without medication If the infection is bacterial, antibiotics are recommend Abscess may require draining Blockages in the glands may require additional treatment E.g. massaging the area to remove a salivary gland stone Some patients may need surgery to repair kinks or narrowed ducts If an autoimmune condition is suspected, additional treatment may be needed Prevention Less alcohol Avoid tobacco products Maintaining good oral hygiene Have a dental cleaning every 6 months Avoid dehydration