Oral Infections Flashcards
Treatment principles of acute infection
General and local
General:
Admission if unwell
Analgesia
Control of infection
Local: Removal of cause Drainage Prevention of spread Restoration of function
Microbial aetiology of dentoalveolar abscesses
FASBENS
Fusobacterium Aneorobic cocci - peptostreptococcus, paryimonas Streptococcus Black pigmented anaerobes Eubacterium Non-pigmented anaerobes Spirochaetes
Periodontal abscess
Pain
Swelling - small, localised, diffuse
Lymphadenopathy and fever may be present
Facial or neck cellulitis v rare
Tooth usually vital
Could be due to pre-existing perio pocket becoming inflamed by foreign body
Or trauma to preiodontium
Or secondary infection of lateral periodontal cyst
Radiolucency lateral aspect of tooth
Multiple perio abscesses in poorly controlled diabetics
Microbial aetiology - same as chronic perio + candida
Treatment - drain and debride
Streptococcal gingivostomatitis
Rare in non-compromised hosts
Most frequently follows tonsilitis
Severe inflammation of gingiva with marked pain
Caused by s.pyogenes - complications fascitis, tissue destruction, rheumatic heart disease, nephritis
Would need to differentiate from drug and viral causes so would need to take samples and send to microbiology to check cause
Treatment - prompt txt wit pencillin
Acute ulcerative gingivitis
Poor OH, smoking, stress
Ulceration and destruction of interdental papilla
Invasion of tissue by microorganisms
Halitosis, bad breath, malaise, lymphadenopathy
Txt - debridement, hygiene
Cancrum oris or noma
Usually preceded by ANUG and a recent deblitating illness e.g. infection:
viral - measles
bacterial - TB, SF
parasitic infection - malaria
use of immunosupressants/malnutrition
F. necropharum, P. intermedia
T vincenti, T. denticola
T. forsythia, a-streptococciTuberculosis
^ incidence in UK, esp among immigrants
Rare in oral cavity - usually secondary to pulmonary TB, cough or cervical lymphadenopathy
Can result in delayed healing after tooth extraction - can cause osteomyelitis
Oral ulceration
Investigation - smear/sample
Biopsy - stained with NZ stain
Culture - Lowenstein Jensen medium - brown colonies = mycobacterium tuberculosis
Serology - PCR, reactive T cells
Txt - Abs for 6 months
Histology will show epithelioid granulomas, caseation
Syphilis
1^ lesion - chancre on lip, tongue, ulcer, local oedema, painless
Smear shows spirochaetes - treponema pallidum
Treponemas are visible only by dark field illumination
Gram - but too thin to be gram stained
Lymphadenopathy
2^ syphilis - 6 weeks after healing of chancre. Snail track ulcers, lyphadenopathy, skin rash
3^ syphilis - recognised by gumma on palette, tongue or tonsil - firm necrotic centre surrounded by inflamed tissue
Leukoplakia on dorsum tongue and increased incidence oral cancer
Congenital syphilis
Hutchinsons incisors
Mulberry molars
Gonorrhoea
Pharynx and any part of mucosa can be affected
Variable appearance - ulceration, oedema, pseudomembranes
Direct examination of smear and or culture necessary to diagnose - Neisseria gonorrhoae
Pink blobs - polymophonuclear lymphocytes, pink dots - gram - diplococci - N. gonorrhoae
On the rise, superbug, developing Ab resistance
Actinomycosis
Large lump/bulge, usually under mandible
Slow growing lump, usually secondary to trauma e.g. broken jaw
Actinomyces israelli, A.oris, A.naeslundii
Smear - gram stain will show + branches filamentous microbes
Histology will show locules of pus surrounded by fibrous septa
Txt - surgical drainage and debridement, Abs 6-8 weeks
Acute bacterial sialadenitis
Ascending infection - mainly parotid
Usually failure of secretion e.g. Sjogrens, gland pathology, sialolithiasis, drugs
Unilateral, firm, red swelling, extreme pain, trismus, possibly febrile, milking duct releases pus
Sampling difficult
Microbial causes - oral streptococci, oral anaerobes, staphylococcus aureus
Txt - amoxicillin, flucloxacillin
Exploration - sialography after resolution, possible surgical exploration
Angular chelitis
Haemtological deficiency - Fe, vit B2, 3, 6, 12
Candida sp., staph aureus - alone or mixed
Treat with miconazole, nystatin or fusidic acid depending on cause
Spread of infection in mandible
Spread of denoalveolar infection governed by site of origin and surrounding tissue planes limited by facial layers and muscle insertions. Position of apices of tooth relative to this will influence clinical presentation
If apex of mandibular molar is above mylohyoid attachment, infection will track laterally above mylohyoid space - sublingually
If apex of mandibular molar is below mylohyoid attachment, infection will track down mylohyoid and present E/O on the skin, under lower border of mandible
If infection tracks laterally, above attachment of buccinator, infections tracks through buccal cortex and abscess in buccal sulcus adjacent to tooth
If infection tracks below attachment of buccinator, would present in the skin of the face above the angle of the mandible
Infections from lower 2/3rd molars can track posteriorly into masticator space or pharyngeal/retropharyngeal space.
Sub-masseteric abscess - profound trismus
Spread to pharyngeal/retropharyngeal space - dangerous due to airway compromise and tracking of pus into chest via retropharyngeal space
Spread of infection in maxilla
Most maxillary abscesses point bucally in the mouth as bone is thinnest here
Roots of some lateral incisors and palatal roots of 6’s can point palatally
Infection can track superiorly in the roots of upper premolars and molars into maxillary sinus
Relationship between apices and levator anguli oris and buccinator determines whether abscess points in oral cavity or skin of cheek
Apex of upper canines can be situated above origin of levator anguli oris and infection can present at medial canthus of eye, deep to levator labii superioris
Deep neck space infection
Rare, but most dental in origin Typically from mandibular 2/3rd molars as apices lie below mylohyoid muscle. Presenting features: Fever Pain Sore throat Difficult or painful swallowing Trismus
Mgt: General and local management Airway management IV Abs Surgical drainage
Complications of orofacial infection
Cavernous sinus thrombosis
Cavernous sinus - venous sinus that surrounds pituitary gland in brain. At medial canthus of eye there is communication between facial vein and opthalmic veins. Infection from upper anterior tooth can drain into cavernous sinus causing venous thrombosis
V v rare
Presenting symptoms: Opthalmoplegia (no eye movement) Ptosis (drooping upper eyelid) Proptosis (bulging eye) Chemosis (red eye)
When Abs are indicated:
When systemic symptoms - fever, malaise
Spreading infections
Chronic infection despite drainage e.g. actinomycosis
Immuno or medically compromised
Conditions difficult to resolve without or that speed up recovery e.g. osteomyelitis, ANUG
Local measures first - Abs rarely first line
Selection of anti-microbial agent
Must be aimed at microorganism present
Must achieve 4-8x MIC in blood
Must be present long enough to adequately reach site
Selection of agent:
Broad spectrum agents - acitve against gram + and -
Associated with rise in c.difficile
Care when prescribing to elderly and GI disease
Empirical use - amoxcicillin, pen V, metro and eryhromycin
Why Abs fail
Agent doesnt reach site - inadequate drainage, poor blood supply, presence of foreign body, inadequate duration
Impaired defences - immunocompromised
Inapropriate agent - resistance
Poor patient compliance
Herpesvirus classification
a-herpes viruses:
Herpes simplex type 1 - HHV1
Herpes simplex type 2 - HHV2
Varicella-zoster virus - HHV3
b-herpesviruses:
Cytomegalovirus (HCMV) - HHV5
Human herpesvirus 6 - HHV6
Human herpesvirus 7 - HHV7
y-herpesviruses
Epstein Barr virus - HHV4
Human herpesvirus 8 - HHV8
Herpes simplex virus
enveloped, DNA virus, highly cytolyitc, infects via heparin sulohate
Type 1 - skin and oral mucosa mucous mmebranes
Type 2 - associated with genital mucosa
Trasmitted via droplet spread or intimate contact
Virus enters trigeminal sensory neurones
Migrates to ganglion via retrograde axonal flow
Latency - 50% cases lie dormant
30% cases reactivated
Migrates to peripheral nerve endings
Virus shed
Reactivation caused by - stress, UV light, immunosupression
Human papillomavirus (HPV)
Circular HPV dsDNA
Capsid L1 and L2 - give protection and bind to host cell receptors
>100 types
v small, 9 genes
HPV16 and HPV18 associated w/carcinogenesis - cervical, oropharynx and anal
HPV6 and HPV11 with warts
Infects basal keratinocytes - can only enter is damage to epithelium/micro-abrasions to gain access to basal layer
Cell entry via L1 and cell surface integrins and proteoglycans
DNA enters nucleaus and replicates
As keratinocytes differetiate, HPV assembled and shed at surface
HPV eliminated
If HPV DNA integrated into chromosomes - expression of E6/E7 viral proteins - drive carcinogenesis
Oral lesions include: Squamous cell papilloma/verruca vulgaris Focal epithelial hyperplasia - excision, imiquimod 5 5 cream Dysplasia/SCC
C albicans
Pathogenic/virulence factors:
Polymorphic - yeast, pseudohyphae, hyphae
Yeast commensal, hyphae pathogenic
pathogenic/virulence factors:
Agglutinin-like-sequence (ALS) - hyphal wall protein (hwp1), b-glucan - cell adhesion molecules
Yeast to hyphal transition - pH>7. Serum/environment can drive this transition.
Secreted aspartyl proteases - tissue invasion by degrading protein at tip of hyphae
Candidalysin - pore forming toxin, tissue damage
Yeast form - binding to oral keratinocyte. In ceratin environments, hyphal form evelops, binding to diff host receptors causing c. albicans to penetrate within epithelium via SAPs
Production candidalysin - further damage to epithelium
Herpes simplex/primary herpetic gingivostomatitis
Signs and symptoms
Pathogenesis
Management
Primary herpetic gingivostomatitis
Child/younf adults
Incubation period 5 days
Heal within 10-14
Signs and symptoms: Many cases subclinical so asymptomatic Malaie and fever Vesicles which ulcerate Secondary bacterial infections Erythematous gingivitis Extra-cricum oral lesion
Dx - made on clinical appearance. Serum should show rising Ab titre to herpes simplex (IgM)
Pathogenesis - herpes virus replicates in epithelial cells, causes epithelial cell desreucton and ‘ballooning’ degeneration of cells
Results in intra-epithlial vesicles
Mgt - supportive - fluids, analgesics, soft diet, chx
Medical - acyclovir 500tdscan go. Effective if started early.
Herpes labialis
Cold sore
30% cases
Cln features - prodormal tingling, vesciles at mucocutaneous junction of lip, con occur IO, ulcerateand crust over 7 - 10 days
Dx - main doffoculty differentiating from erythema multiforme
Txt - acyclovr rea, effectve in prodromal stage, penciclovir cream
Herpes (varicella) zowster
HHV3 1^ infection - chicken pox 2^ - shingled 3 phases: pre-herpetic neuralgia rash - unilateral vesicles associated with division of nerve affected Ulcers Post-herpetic neuralgia - burning pain
Mgt - acyclovir 800mg 5x daily. 7 days
should be started within 72 hours rash onset
analgesics and other supportive measures
referral to ophthalm if eye involved
post herpetic neuralg - neuro pain drugs e.g. gabapentin/antiepressants
Epstein Barr HP4
Infectious mononucleosis:
fever and malaise
enlarged tonsils
patechiae on soft palate
cervical lymphadenopathy
Burkitts lyphoma
Nasopharyngeal carcinoma
Hairy leukoplakia - corruated white patches, bilateral borders of tongue, seen in 25% HIV+ pt's. Can occur in non-HIV - immunocompromised, long term steroids
Diagnosis - demonstration of EBV in tissueCytomegalovirus
HV5
Rarely cause problems in healthy subjects
In immunocompromised - large ragged oral mucosal ulcers, salivary gland swelling, retinitis
Life threatening in newborns
Predisposing factors to fungal infections
prosthesis
low saliva
Abs
immuno-supression
Classification of candida infections
Acute, chronic, associated, HIV
ACUTE:
Acute pseudomembranous candidosis (thrush)
Acute atrophic/erythematous candidosis (Ab sore mouth)
CHRONIC:
Chronic hyperplastic candidosis (candidal leukoplakia)
Chronic atrophic candidosis (denture stomatitis)
Chronic mucocutaneous candidosis (various - inherited syndromes)
CANDIDA ASSOCIATED:
Median rhomboid glossitis
Angular chelitis
HIV RELATED:
Prolonged pseudomembranous or erythematous forms
Acute pseudomembranous candidosis
Creamy, thick, white plaques - thick biofilm of yeast and hyphal forms
Easily rubbed off - bleeding base
Erythematous/atrophic candidosis - HIV
Long standing, erythematous lesions
Acute atrophic candidosis
Site
Cause
Txt
Red, painful lesions
Most commonly dorsum of tongue
Causes: prolonged corticosteroid or Ab therapy
Bacterial flora altered, candida allowed to thrive
Treatment - reduce Ab use if possible
Management of candidosis
Confirm diagnosis - swab or oral rinse
Investigate and treat underlying cause
Treat with anti-fungals
Topical - miconazole gel, nystatin suspension, amphotericin B (hosp only)
Systemic - fluconazole, itraconazole
Careful warfarin interactions - miconazole/ketoconazole inhibit cytochrome P450 enzymes - heightening anti-coag effect of warfarin - bleeding risk - internal bleeding or prolonged after injury
Denture related candidosis
Palate protected from saliva
Poor denture hygiene
Txt - improve denture hygiene, leave out at night, clean denture and soak in Miltons (hypochlorite only for acrylic)/Sterodent, rinse before reinserting
Antifungals - nystatin +/- miconazole gel to fitting surface tds 2-3 weeks
Median rhomboid glossitis
Erythematous area on dorsum tongue - epithelial proliferation and candida within epithelium
Not premalignant
Diagnosis usually on clinical grounds
Typically matching lesion on palate
Angular chelitis
Soreness and fissuring at corners of mouth
Associated factors:
Reduced OVD
Haematological deficienies -
B12, Fe, folate
Drooling of saliva
Sysemic disease e.g. Crohn’s
Most candida related, some staph aureus related
Txt - address underlying cause, miconazole cream (candida) or fusidic acid (staph au)
Chronic hyperplastic candidosis
White or red/white patch, nodular
CANT be rubbed off
Labial comissures or lateral tongue
Premalignant - candidal leukoplakia - up to 25% risk premalignant change
Diagnosis by biopsy
Aetiology:
Usual candida risk factors
Smoking
Not clear if candida cause lesion or invade pre-existing lesion
Some lesions regress following anti fungal therapy
Mgt - biopsy - needed to assess degree dysplasia and risk of malignant trans
Txt - systemic antifunagls, 7-14 days fluconazole or amphotericin B
Smoking cessation
If not improvement and high risk malignant change, may need to excise
