Oral infections Flashcards
(104 cards)
1
Q
What are the global figures from WHO 2018 on HIV?
A
- People living with HIV 37.9 million - about 0.8-0.9% of 15-49 year olds
- Newly infected with HIV is 1.7 million
- AIDs mortality is 770000
- Since the beginning of the epidemic 75 million people have been infected and 32 million people have died
- Most cases are seen in Africa
2
Q
What is the HIV virus and how does it work?
A
HIV is a retrovirus. It is a single stranded RNA virus with a reverse transcriptase gene. It is spread by body fluids, mainly by unprotected sex or IV drug use. HIV damages the immune and nervous system. The cellular receptor for HIV is the CD4 molecule. It is found on T helper cells, monocytes and dendritic cells. Cells most affected are CD4 ‘helper’ T cells. Damage causes severe immunodeficiency. There is a broad spectrum of illnesses related to level of immunodeficiency. AIDs occurs with CD4 cell counts <200/UL (normal is >600/UL).
3
Q
What are the symptoms when you are first exposed to HIV virus and how do they change as it progresses to AIDS?
A
When exposed to the virus we may get something called acute seroconversion illness. It may not be noticed as it may feel like a normal cold/flu. There may be rash, temperature, lymph nodes – non-specific. You can be asymptomatic for many years and only when CD4 count starts dropping do symptoms develop. This is why early testing is very important. There will be persistent generalised lymphadenopathy PGL, then AIDs related complex ARC which is when symptoms are mild: pyrexia, diarrhoea, weight loss, fatigue/malaise. Then there will be progression to AIDS: opportunistic infections, Kaposi’s sarcoma and CD4 T cells <200/UL.
4
Q
After how much time are you positive for the HIV antibody and progress to AIDS?
A
You get infected and CD4 count is normal. You will be positive to HIV antibody after about 3 months. You are well for 8-10 years and then the count starts dropping and you become unwell (AIDs).
5
Q
What is the diagnosis of HIV based on?
A
- History and clinical features
- General lab investigations - lymphopenia, CD4 count reduced, CD4/8 ratio reduced
- HIV testing (after counselling) - HIV antibodies, HIV antigens
6
Q
What are the HIV oral manifestations?
A
- Group 1 lesions (strongly associated with HIV infection)
- Group 2 lesions (less commonly associated with HIV)
- Group 3 lesions (possibly associated with HIV infection)
7
Q
What are the group 1 lesions in HIV?
A
- Candidosis - erythematous/pseudomembraneous
- Hairy leukoplakia
- HIV associated periodontal disease
- Kaposi’s sarcoma
- Non-Hodgkin’s lymphoma
8
Q
What is erythematous and pseudomembranous candidosis?
A
Erythematous candidosis will be painful on the roof of mouth and tongue. It is seen with dentures. Pseudomembranous candidosis is white patches.
9
Q
What is the treatment of candida infections?
A
Topical: - Miconazole - oral gel - Nystatin - suspension Systemic: - Fluconazole - Itraconazole - Voriconazole
10
Q
What is hairy leukoplakia and the treatment?
A
Lesions are bilateral but can start as unilateral and corrugated. It is not premalignant. The cause is EBV. It generally does not require treatment, it may regress with acyclovir but it usually returns on stopping therapy.
11
Q
What are the types of HIV associated periodontal disease?
A
- Linear gingival erythema ( red line around teeth - gingival margin)
- Necrotising ulcerative gingivitis NUG
- Necrotising ulcerative periodontitis NUP
- Necrotising ulcerative stomatitis NUS
12
Q
What are the causes of HIV associated periodontal disease?
A
- Spirochaetes
- Fusiform bacteria
- Anaerobic rods (similar to ANUG and cancrum oris)
- In linear gingival erytema candida may also play a role
13
Q
What is the management of HIV associated periodontal disease?
A
Immediate management: - Removal of necrotic bone and severely involved teeth - Debridement of necrotis tissue - 6% hydrogen peroxide irrigation of pockets/mouthwash - Antibiotics - metronidazole - Oral hygiene instruction Long term: - Periodontal management
14
Q
What is kaposi’s sarcoma?
A
It is caused by HHV8. It can be in the mouth or on the skin. Red lumps/spots are seen and black spots on the roof of the mouth.
15
Q
What is the management of Kaposi’s sarcoma?
A
May include:
- Radiotherapy
- Systemic chemotherapy
- Intra-lesional chemotherapy
- Surgical excision
16
Q
What is non-hodgkin’s lymphoma and the management?
A
It appears as an abnormal growth in the oral cavity. You may not see any specific features. The management is radiotherapy and chemotherapy.
17
Q
What are the group 2 lesions associated with HIV?
A
- Atypical orophrayngeal ulceration - usually severe with atypical presentation
- Idiopathic thrombocytopenia purpura - low platelet count, can result in purpuric patches on the oral mucosa, if platelet count very low (<60000/ml) risk of post extraction bleeding
- Salivary gland disorder - dry mouth, decreased salivary flow rate, swelling of major salivary glands, treatment with salivary stimulants and oral lubricants
- Viral infections other than EBV - cytomegalovirus (severe or atypical oral ulcers), herpes simples (severe secondary herpes), human papillomavirus (multiple warts), herpes (varicella) zoster (severe shingles)
18
Q
What are the group 3 lesions associated with HIV?
A
- Oral bacterial infections other than periodontal disease
- Fungal infections other than candidosis
- Melanotic hyperpigmentation
- Neurological disturbances - trigeminal neuralgia, facial palsy
19
Q
How is HIV prevented?
A
- Male and female condom use - male condoms have >85% protective effect
- Testing and counselling for HIV (also STI and TB) - TB is responsible for nearly 1 in3 HIV associated deaths
- Voluntary medical male circumcision - reduces risk of heterosexually acquired HIV in men by about 60%
- Use of ARVs for prevention - HIV positive person adhering t ART reduces risk of transmission by 96%, pre-exposure prophylaxis PrEP and post-exposure prophylaxis PEP within 72 hours
20
Q
What is the HIV management?
A
- Systemic treatment with anti-retroviral therapy
- Dental care and oral hygiene provided by GDP
- Oral manifestations - treat as per lesion requirements
21
Q
What is the systemic treatment of HIV?
A
Modern combination anti-retroviral therapy. It is often called HAART (highly active anti-retroviral therapy). It is very effective at preventing progression to AIDs. It reduces immunosuppression and associated opportunistic infections and tumours. There can be prophylactic treatment for opportunistic infections. It is provided by HIV clinics, GUM clinics, GMP etc.
22
Q
What should you do if there is a needle stick/occupational exposure?
A
First aid:
- Encourage bleeding under running water
- Apply or scrub with antiseptic then cover wound
- Irrigate exposed eyes, nasal or oral mucosa
- Record details in accident book
Management:
- Report exposure to occupational health, GUM clinic or GMP. They will arrange counselling re post-exposure prophylaxis with AZT and confidential HBV and possible HIV testing
They will also organise a risk assessment, so identification of source patient and clinical and serological evaluation of HIV/HBV status with patients permission
- Follow up - hep B testing, vaccination and treatment, HIV testing, HCV testing.
23
Q
What are the classical signs of acute inflammation?
A
They are diagnostic: - Swelling - Redness - Loss of function - Heat - Pain or tenderness There may also be systemic signs such as pyrexia or malaise as well as regional lymphdenopathy.
24
Q
What is an abscess and how is it detected clinically?
A
An abscess if a pus filled pathological cavity, which can form as part of the inflammatory response to acute infection. Acute exacerbations of chronic inflammation can also occur followed by periods of quiescence. Every abscess should be drained. Clinically, abscess formation can be determined by the presence of fluctuance to gentle palpation. Pressure exerted by 1 finger should be detected by another finger as ‘bounce’. If there is no fluctuance then cellulitis is present which does not need drainage. Two fingers on abscess and palpate between the fingers.
25
How is an abscess diagnosed?
Diagnosis of an acute dentoalveolar abscess is usually solely by clinical means. Radiographs do not typically show any change in the periapical tissues. This is because it takes approximately 10 days for sufficient bone loss to occur to be detectable on an intra-oral film. The earliest radiological sign is widening of the periodontal ligament space.
26
Where does the pus from an abscess track?
Pus from an acute dentoalveolar abscess takes the track of least resistance through the cancellous bone and points on the nearest epithelial surface. This is usually on the buccal aspect of the maxillary or mandibular alveolus where the overlying bone is thinnest, but can be palatally/lingually.
27
What are the general measures for an acute infection?
- Admission if unwell
- Analgesia
- Control of infection
Patients that are toxic (systemically unwell with malaise, pyrexia, tachycardia or hypotension) should be admitted to hospital. These patients need intravenous antibiotics as well as surgical drainage. NSAIDs will help with pain relief and have an anti-pyrexial effect. Antibiotics are given blindly in the first instance as it is not practical to wait for the results of culture and sensitivity testing. Typically amoxicillin and metronidazole are used in combination and changes made only in the face of microbiological results.
28
What are the local measures for an acute infection?
- Removal of the cause
- Drainage
- Prevention of spread
- Restoration of function
29
How do you remove the cause of acute infection?
The most important principle in management of infections, sometimes this is all that needs to be done. However, it can be easier to institute drainage and prevent spread in the acute phase. Examples include extraction of non-vital or hopelessly mobile teeth, removal of sequestrae (dead bone), foreign bodies or salivary calculi.
30
How is an abscess drained?
Reddening, fluctuance and a point of maximum tenderness indicate pus formation. Pus should be drained and a surgical incision leaves less scarring than spontaneous draining, particularly through the skin. Antibiotics are not a substitute for drainage. There needs to be adequate anaesthesia with 2% lignocaine with adrenaline injected into the overlying mucosa, not into the abscess cavity. Horizontal incision parallel to the occlusal surface of the teeth 1-2cm in length. Consider local anatomy such as the mental nerve. Use a no.11 blade held backwards with an upward sweep. Open the abscess cavity with artery forceps (Hilton's method). Hot salt water mouthwashes will encourage any remaining pus to drain.
31
What is done when incising the abscess is not sufficient to drain it?
Incising an abscess cavity to drain it is almost always sufficient for intra-oral abscesses. However, when pus has to pass through several tissue planes in order to escape, for example in deep neck abscesses, a drain can be inserted into the abscess cavity which is exteriorized into the mouth or onto the skin surface (sometimes both: through and through).
32
How is spread prevented?
This is achieved by drainage, use of antimicrobials and rest. Rest is difficult in the orofacial region but trismus when present achieves this naturally.
33
How do we restore function?
Review the patient after the acute phase to ensure that things have settled and function has been restored. Sometimes trismus can persist and need treatment e.g. Therabite.
34
What is the microbial aetiology of dentoalveolar abscesses?
- Black pigmented anaerobes
- Fusobacterium
- Anaerobic cocci (peptostreptococcus, parvimonas)
- Streptococcus
- Non-pigmented anaerobes
- Eubacterium
- Spirochaetes
35
What are the periodontal abscess symptoms?
- Pain
- Swelling – small localised to diffuse
- Lymphadenopathy and fever may be present
- Facial or neck cellulitis
36
What are the causes of periodontal abscesses?
The tooth is usually vital.
- Pre-existing periodontal pockets that become occluded - foreign body
- Trauma to the periodontium
- Secondary infection of lateral periodontal cyst
37
What is seen radiographically for a periodontal abscess and what is the treatment?
There will be radiolucency on the lateral aspect of the root. Multiple periodontal abscesses will be seen in poorly controlled diabetic patients. The microbial aetiology is the same as chronic periodontitis and candida. Treatment is to drain and debride.
38
What is streptococcal gingivostomatitis?
Streptococcal gingivostomatitis is rare in non-compromised hosts and it most frequently follows tonsillitis. There is severe inflammation of the gingivae with marked pain. It is caused by s.pyogenes. the complications are fasciitis, tissue destruction, rheumatic heart disease, nephritis etc. Differentiate from drug and viral causes. The treatment is prompt treatment with penicillin.
39
What is acute ulcerative gingivitis?
Acute ulcerative gingivitis is due to poor OH, smoking, stress. It is ulceration and destruction of interdental papilla due to invasion of tissue. There will be halitosis, bad taste, malaise, lymphadenopathy. Treatment is debridement and hygiene.
40
What is cancrum oris?
Cancrum oris or Noma is usually preceded by ANUG and recent debilitating illness. It is categorised by WHO as a necrotising ulcerative stomatitis. It is a rapid spreading destructive disease where there are gangrenous lesions destroying soft and hard tissues of the face.
41
What is the cause of cancrum oris?
- Infection - viral e.g. measles, bacterial e.g. TB, scarlet fever or parasitic infection e.g. malaria
- Immune suppressive drugs/disease
- Malnutrition
- F.necrophorum, P.intermedia, T.vincentii, T.denticola, T.forsynthia, alpha-streptococci
42
What is TB?
Tuberculosis has increasing incidence in the UK particularly among immigrants. It is rare in the oral cavity and is usually secondary to pulmonary TB. There will be a cough or cervical lymphadenopathy. It can result in delayed healing after tooth extraction – secondary osteomyelitis. There may be oral ulceration.
43
What are the investigations for TB?
- Biopsy - Ziehl Neelson
- Culture - 4-6 weeks
- Serology, PCR, reactive T cells
44
What is the treatment and histology of TB?
Treatment is antibiotics for around 6 months. When looking at TB histologically there will be epithelioid granulomas which is inflammation. It is a collection of immune cells called macrophages and acts to wall off substances perceived as foreign but unable to eliminate. There is caseation.
45
What is syphilis and the types?
In syphilis the primary lesion may be a chancre on lip or tongue, ulcer, local oedema, painless. Smear shows spirochaetes. There will be lymphadenopathy. Secondary syphilis is approximately 6 weeks after healing. There will be snail track ulcers, lymphadenopathy and skin rash. Tertiary syphilis is now rarely seen in the western world. There will be a gumma (tissue nodule) on palate, tongue or tonsil. It has a firm, necrotic centre surrounded by inflamed tissue. There will be leukoplakia on dorsum of tongue and increased incidence of oral cancer.
In congenital syphilis you may see Hutchinson’s incisors or mulberry molars (abnormal cusps).
46
What is gonorrhoea?
In gonorrhoea the pharynx and any part of the oral mucosa can be affected. There can be pain and lymphadenopathy. It can have a variable appearance: ulceration, oedema, pseudomembranes. Direct examination of a smear and/or culture is necessary to diagnose Neisseria gonorrhoeae. There will be gram negative diplococci.
47
What is actinomycosis, the histology and treatment?
Actinomycosis is caused by actinomyces israelii, A.oris, A.naeslundii. Histologically there will be locules of pus surrounded by fibrous septa. Treatment is surgical drainage and debridement. Antibiotics for 6-8 weeks.
48
What is the cause and treatment of acute bacterial sialadenitis?
Acute bacterial sialadenitis is an ascending infection mainly parotid. It is a calcified mass or sialolith forms within salivary gland. It is usually a failure of secretion: Sjogren’s syndrome, gland pathology, sialolithiasis, drugs. There will be unilateral, firm, red swelling, extreme pain, trismus, possibly febrile, milking duct releases pus. Sampling is difficult. The microbial causes are oral streptococci, oral anaerobes, staphylococcus aureus. The treatment is amoxicillin, flucloxacillin. Exploration is sialography after resolution, possibly surgical exploration.
49
What is angular cheilitis?
Angular cheilitis can be due to haematological deficiency. The bacterial/fungal causes are candida sp, staph aureus, strep pyogenes alone or mixed. Treat with miconazole, nystatin or fusidic acid depending on cause.
50
What does the spread of dentoalveolar infections depend on?
The spread of dentoalveolar infections is governed by the site of origin and the surrounding tissue planes that are limited by fascial layers and muscle insertions. The position of the apices of the originating tooth relative to muscles and fascia will influence the clinical presentation. The abscess forms at the apex and then tracks through bone. In the mandible there are muscle attachments which are the buccinator and the mylohyoid. Whether the apex is above or below these muscle attachments affects the direction of tracking.
51
What are the layers of fascia in the neck?
The neck is surrounded by multiple layers of fascia of which the deep cervical fascia is the most important. These fascial layers continue superiorly and split around various structures to form tissue spaces. Fascial planes and tissue spaces are an anatomical framework for understanding how infection can spread.
52
What are the three separate parts to the deep cervical fascia?
- The investing layer
- The visceral layer
- The prevertebral layer
53
How does infection spread from a mandibular tooth?
How infection spreads from a mandibular tooth depends on the relation of the tooth to the insertion of 2 muscles: buccinator and mylohyoid. Buccinator attaches to the lateral buccal cortex of the mandible, adjacent to the molar teeth and mylohyoid attaches to the mylohyoid ridge which is on the medial (lingual) cortex. Abscesses that track laterally above buccinator point in the mouth. Those below buccinator point onto the facial skin. Abscesses that track medially above mylohyoid point in the sublingual space. Those below mylohyoid point into the submandibular space.
54
Where can infection from lower 2nd and 3rd molars spread?
Infection from lower 2nd and 3rd molars can also track posteriorly into either the masticator space or the parapharyngeal/retropharyngeal spaces. A sub-masseteric abscess causes profound trismus and the patient will not be able to open their mouth. Spread into the parapharyngeal and/or retropharyngeal spaces is dangerous due to possible airway compromise and tracking of pus into the chest via the retropharyngeal space.
55
Where can infection from maxillary teeth spread to?
Most maxillary dental abscesses track buccally, as the bone is thinnest here, to point in the mouth, but abscesses arising from upper lateral incisors and palatal roots of 1st molars can point laterally. The relationship between the tooth apices and the levator anguli oris and buccinator muscles determines whether the abscess points in the oral cavity or on the skin of the cheek. The apex of the upper canine tooth can occasionally be situated above the origin of levator anguli oris and infection can therefore present at the medial canthus of the eye, deep to levator labii superioris.
56
What are deep neck space infections?
These are rare but most are dental in origin, typically from mandibular 2nd/3rd molars as their apices are often below the mylohyoid muscle. Presenting features include:
- Fever
- Pain
- Sore throat
- Difficult or painful swallowing (dysphagia, odynophagia)
- Trismus
57
What is the management of a deep neck space infection?
The same principles of management of intra-oral abscesses apply, namely general and local measures, but broadly speaking the mainstays are:
- Airway management
- Intravenous antibiotics
- Surgical drainage
58
What are the complications of orofacial infection?
Cavernous sinus thrombosis.
59
What is cavernous sinus thrombosis?
The cavernous sinus is a venous sinus that surrounds the pituitary gland. It receives blood from the orbits, skull vault and cerebral hemispheres. At the medial canthus of the eye there is communication between the facial and ophthalmic veins. Infection from an upper anterior tooth can, very rarely, drain into the cavernous sinus causing venous thrombosis.
60
What are the symptoms of cavernous sinus thrombosis?
- Opthalmoplegia (no eye movements)
- Ptosis (drooping upper lid)
- Proptosis (bulging eye)
- Chemosis (red eye)
61
When are antibiotics indicated?
- When systemic symptoms are present e.g. fever, malaise, nausea etc
- 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, sialadenitis
Local measures first as antibiotics are usually not the first line of treatment.
62
How are antimicrobials used?
- Must be aimed at the organism(s) present
- Dose must achieve 4-8 times MIC in blood – keep up to date with BNF
- Must be present long enough to penetrate adequately to the site but not too long
63
How do you select the antimicrobial agent?
- Broad spectrum agent - associated with a rise in C.difficile disease, care in prescribing in elderly and GI disease, including proton pump inhibitors and reflux disease
- Empirical use - main drugs are amoxicillin, pen V, metronidazole and erythromycin, clindamycin, co-amoxiclav, clarithromycin no advantages
- Do not prescribe for pulpitis, prevention of dry socket unless in difficult extractions in immunocompromised
64
Why do antibiotics fail?
- Agent does not reach the site due to inadequate drainage, poor blood supply, presence of a foreign body, inadequate duration
- Impaired defences - immunocompromised (bacteriostatic agent used)
- Inappropriate agent - resistance, inherent, acquired (mutation, plasmids)
- Poor patient compliance
65
What are the viral infections of oral importance?
- Herpes viruses:
- Simplex 1 and 2
- Varicella zoster
- Cytomegalovirus
- Epstein barr
- Coxsackie viruses
- Measles
- HPV
66
What is herpes simplex virus?
It is an enveloped DNA virus which is highly cytolytic and infects via heparan sulphate. Type 1 is associated with skin and oral mucous membranes and type 2 is associated with genital mucosa. It is transmitted via droplet spread or intimate contact. 90-100% of individuals have antibodies to herpes simplex.
67
How does type 1 herpes simplex infect the body and get reactivated?
The virus enters the trigeminal sensory neurones and migrates to the ganglion by retrograde axonal flow. There is then latency. In 50% of cases it lies dormant and in 30% it is reactivated. It migrates to peripheral nerve endings and the virus is shed. Reactivation can be caused by UV, stress, illness and immunosuppression.
68
What is the primary infection of herpes simplex?
Primary gingivostomatitis which is seen in children and young adults. It has an incubation period of 5 days and there is healing within 10-14 days. Many cases are subclinical and asymptomatic.
69
What are the signs and symptoms of primary gingivostomatitis?
- Malaise and fever
- Vesicles which ulcerate
- Secondary infection - longer time to heal
- Erythematous gingivitis can be the differential diagnosis
- Extra-oral lesions - often seen when immunocompromised
70
How is the diagnosis made of herpes simplex virus?
It is made on clinical features. Patients have a rising antibody titre to herpes simplex.
71
What is the pathogenesis of herpes?
The herpes virus replicates in epithelial cells. It causes epithelial cell destruction and ballooning degeneration of cells. This results in intra-epithelial vesicles.
72
What is the secondary herpes infection and the clinical features?
Herpes labialis which is a cold sore. It occurs in 30% of patients. The clinical features are prodromal tingling, vesicles at the muco-cutaneous junction. They ulcerate and crust over and last 7-10 days.
73
What is the main difficulty in diagnosing herpes labialis and the treatment?
The main difficulty is differentiating from erythema multiforme. The treatment is effective in the prodromal stage. It can be acyclovir cream (Zovirax) and penciclovir.
74
What is varicella zoster?
Herpes (varicella) zoster virus is type 3 herpes virus. The primary infection is chicken pox. The secondary lesion is known as shingles. It most commonly affects one of the divisions of the trigeminal nucleus.
75
What are the three phases of varicella zoster?
Pre-herpetic neuralgia:
- Pain in the affected division, may mimic dental pain
Rash:
- Unilateral vesicles, ophthalmic, maxillary, mandibular
- Ulcers (mucosa), crusting lesions (skin)
- Lasts 2-3 weeks
Post-herpetic neuralgia:
- Burning pain affects 10-20%
- More common in the elderly
76
What is the management of varicella zoster?
- Acyclovir 800mg 5x daily 7 days
- Valaciclovir 1g 3x daily 7 days
- Famiciclovir 250mg 3x daily 7 days
- Analgesics and other supportive measures
- Referral to ophthalmology if eye involved
- Post-herpetic neuralgia - treat pain with neuropathic pain drugs, gabapentin, antidepressants
77
What is herpetic whitlow?
It is a herpes infection of the fingers.
78
What does epstein Barr virus (HV4) cause?
- Infectious mononucleosis (glandular fever) - affects tonsils, petechiae on soft palate, cervical lymphadenopathy
- Burkitt's lymphoma
- Nasopharyngeal carcinoma
- Hairy leukoplakia
79
What is oral hairy leukoplakia?
It is corrugated white patches with lots of white lines which are not continuous which are seen bilaterally on the lateral borders of the tongue. They are seen in 25% of HIV infected patients. It can occur in non-HIV patients. The diagnosis is based on the demonstration of EBV in tissues.
80
What is cytomegalovirus and the pathogenesis?
It is HV5 and it rarely causes problems in healthy subjects. The rare appearances are glandular fever like illness (no lymphadenopathy) and salivary gland swelling. The pathogenesis is inclusion bodies which are dormant in lymphocytes and there is interference with MHC1 presentation.
81
How does cytomegalovirus present in the immunocompromised?
- Large ragged oral mucosal ulcers
- Salivary gland swelling
- Retinitis
In new borns it can be life threatening.
82
What are coxsackie viruses and what do they cause?
Types 4, 5, 10 and 16 cause the most problems. It causes herpangina and hand, foot and mouth disease.
83
What is herpangina?
It is caused by CVA4 and is usually a trivial, mild, febrile illness. It affects young children and adults. There are vesicles and ulcers on the soft palate, usually towards the back of the mouth. It lasts a few days. There is usually no treatment. Can use analgesic mouthwash e.g. difflam.
84
What is hand, foot and mouth disease?
It is caused by CVA16. It is similar to herpangina with mild systemic upset. There will be rashes, vesicles on palms of hands and soles of feet. There are intraoral ulcers and vesicles.
85
What is measles?
It is caused by paramyxovirus. The person will be systemically unwell. There will be Koplik's spots which are white papules on the buccal and palatal mucosa during the prodromal phase. There can be a skin rash and long term effects.
86
What is human papilloma virus?
There are over 40 types of virus. It is a DNA virus of just 9 genes. It only infects keratinocytes. It gets into basal cells by attaching into integrins and it integrates its genome into the host genome which allows it to replicate. The high risk oncogenic subtypes are HPV 16 and 18. They can cause cervical, oropharynx and anal cancer.
87
What are the main oral lesions caused by HPV?
- Squamous cell papilloma/veruca vulgaris
- Condyloma accuminatum - genital warts in the mouth
- Focal epithelial hyperplasia (HPV13, common in small native communities and HIV infection, treatment is excision and imiquimod 5% cream)
- Dysplasia/SCC - controversial
88
What are the oral fungal infections?
- Aspergillosis
- Blastomycosis
- Candidosis
- Coccidiodomycosis
- Cryptococcosis
- Histoplasmosis
- Rhinosporidiosis
89
What are the candida species?
- C.albicans
- C.tropicalis
- C.krusei
- C.glabrata
- C.dubliniensis
90
What are the predisposing factors for candidosis?
- Prosthesis - no exfoliation
- Low saliva, no flow, reduces soluble defences - low ph, induced by high sugar diet
- Antibiotics - reduced bacterial competition
- Immunosuppression: reduced cellular defence (very young/old, diabetes, corticosteroids including steroid inhalers, malignancy, HIV, immunosuppressive therapy)
91
What are the pathogenic/virulence factors that allow tissue invasion and pathogenesis?
Yeast to hyphal transition and growth is essential for virulence and pathogenesis. Yeast forms bind to the epithelium. If there is an environmental change hyphae start to form which express ALS3. The hyphae start to invade using SAPs. As they penetrate, the hyphae secrete candidalysin – a pore forming toxin that binds to the epithelial membrane and kills human cells and also initiates an immune response. There are proteases called secreted aspartyl proteases SAP (allows penetration through cells) candida secrete SAP from the tip to clear a path for the candida to pass through to go deeper into tissues. There will be lots of yeast forms on top and hyphae moving down into epithelium. This leads to cytolysis and inflammation.
92
What are the types of sap?
- Sap 1-3 - needed for mucosal infection
- Sap 1-3 - degrade complement
- Sap 4-6 - contribute to systemic infection
Used to invade between/through epithelial cells.
93
What is the classification of candida infections?
Acute forms:
- Acute pseudomembraneous candidosis (thrush)
- Acute atrophic candidosis (antibiotic sore mouth)
Chronic forms:
- Chronic atrophic candidosis (denture stomatitis)
- Chronic hyperplastic candidosis (candidal leukoplakia)
- Chronic mucocutaneous candidosis (various: inherited syndromes)
Candida-associated lesions:
- Median rhomboid glossitis
- Angular cheilitis
HIV related candidosis
94
What is acute pseudomembraneous candidosis?
It is creamy thick, white plaques consisting of a thick biofilm of yeast and hyphal forms. It is easily rubbed off. It is not seen in healthy patients so investigate what the systemic cause is.
95
What is HIV related candidosis?
It is erythematous candidosis and there are red patches.
96
What is the cause of acute atrophic candidosis?
- Prolonged corticosteroid or antibiotic therapy
| - Bacterial flora altered, allows candida to flourish
97
What is the treatment and management of acute atrophic candidosis?
The treatment is to reduce antibiotic use if possible. The management is to confirm diagnosis using swabs or oral rinse +/- MC+S. Investigate and treat underlying cause. Treat with antifungal agents. Topical:
- Miconazole oral gel (interfere with warfarin - any ending in azole)
- Nystatin suspension
- Amphotericin B (only available in hospital pharmacies)
Systemic:
- Fluconazole
- Itraconazole
98
What is denture related candidosis?
The palate is protected from saliva and it is caused by poor denture hygiene. The treatment is to improve denture hygiene:
- Leave out at night
- Clean denture and soak in Milton or Corsodyl
Antifungals:
- Nystatin +/- miconazole gel to fitting surface tds
- 2-3 weeks
99
What is median rhomboid glossitis?
It is an erythematous area on the dorsum of the tongue which is depapillated. There may sometimes be a matching lesion on the palate. There is epithelial proliferation and candida in the epithelium. It is not premalignant. Diagnosis is usually on the clinical grounds.
100
What is angular cheilitis?
It is due to reduced vertical dimension and drooling of saliva. It can also be due to haematological deficiency: iron, B12, folate deficiency, Crohn's disease.
In some cases it is associated with staph aureus. It may be due to undiagnosed type II diabetes. The treatment is to address the underlying cause and miconazole cream or fusidic acid depending on the cause.
101
What is chronic hyperplastic candidosis?
There can be a white or red/white patch which is nodular. It can't be rubbed off. It is seen in labial commissures or tongue. It is premalignant 'candida leukoplakia'. There is an up to 25% risk of malignant change. The diagnosis is by biopsy.
102
What is the aetiology of chronic hyperplastic candidosis?
- Usually candida risk factors
- Smoking
- Not clear if candida cause the lesion or invade a pre-existing lesion
- Some lesions regress following antifungal therapy
103
How is chronic hyperplastic candidosis diagnosed?
The biopsy will establish diagnosis. Assess the degree of dysplasia and risk of malignant transformation.
104
What is the treatment of chronic hyperplastic candidosis?
Systemic antifungals 7-14 days fluconazole or amphotericin B. Also smoking cessation. If no improvement and high risk of malignant transformation then excise.
