Bacterial Infections Flashcards
What bacteria causes TB
Mycobacterium Tuberculosis
Pathogenesis of TB
M.tuberculosis is inhaled and lodge into the alveoli of the lungs, it is then phagocytized and spreads to adjacent tissues by the mobile macrophages.
Within the macrophage it is able to under go rapid replication and prevent digestion.
The increase in numbers will eventually result in the destruction of the macrophage — the bacilli now enters into surrounding tissues and may spread lymphatically
What are the 2 types of pulmonary TB
Primary and Secondary
P = Previously unexposed people ( results in localized chronic inflammation ) These organism may be dormant for many years
S = Re-activation of organisms in previously infected person, associated with compromised host defence
Symptoms of Secondary pulmonary TB?
Fever,Malaise,Weight loss and night sweats
What is Miliary Tuberculosis
Diffuse dissemination through vascular system
Granuloma vs Granulation Tissue
Granuloma - Collection of lymphocytes,histocytes and MN giant cells (A granuloma is a special type of chronic inflammation)
Granulation Tissue - Granulation tissue is a collection of small, microscopic blood vessels and a connective tissue. Its main function is to facilitate wound healing.
How do oral TB lesions occur?
Direct Inoculation - Organisms in sputum implanted in defects in mucosal barrier + Hematogenous deposition
Indirect - spread from lungs
What are the oral manifestations of TB
Oral ulcers ( dorsum of tongue common )
Mandibular swelling due to intrabony involvement
- tuberculous osteomyelitis
Non-healing extraction sockets
Areas of mucosal granularity and granulomatous gingivitis
Diffuse zones of inflammation
Leukoplakia-type lesion
Clinical features of TB ulcer
Chronic, non-healing ulcer painless indurate
often presents with cervical lymphadenopathy
How do we diagnosis TB ( skin test )
Purified protein derivative skin test
- cell-mediated hypersensitivity reaction to tubercular antigen. Only after 2-4 weeks after intial exposure
TB incisional biopsy - methods
Histology - Granulomatous inflammation with caseous necrosis and langerhans giant cells
Ziehl Neelsen stains acid and alcohol fast bacilli
Treatment of TB
Multi-Agent therapy
- 8 weeks pyrazinamide,isoniazid,rifampicin, ethambutol
- 16 weeks isoniazid, rifampicin
Vaccine for TB
BCG - Bacillus Calmette Guerin Vaccine
What is Mycobacterium Bovis infections
Drinking unpasteurized,contaminated milk from infected cows
- Results in enlargement of oropharyngeal lymphoid tissues and cervical lymph nodes
Note - may calcify lymph nodes resulting in sialoliths
Further diagnosis for TB
chest radiograph and CT scan will show characteristic lung involvement. Tuberculous osteomyelitis and calcifed lymph nodes
Which bacteria causes syphilis?
Treponema Pallidum ( Gram negative spirochete )
Pathogenesis of Syphilis
Infection is usually transmitted as an STD, but even kissing can transmit the organism if oral lesions are present as they are highly infectious. Syphilis can be transmitted via blood products or tansplacental
N.B syphilis is highly contagious during the first 2 stages
What are the different stages of syphilis
Primary - Initial area of infection called chancre is where the organism first contacts - lesions appear in weeks.
Secondary - The spirochetes spread throughout the body resulitng in secondary syphilis of which lesions appear in months.
Tertiary - The spirochete remain localized in areas for many years ( latent stage ) and form a gumma.
Congenital Syphilis - A congenital variant is seen as result of the spirochetes crossing the placenta
Describe the clinical features of a chancre
A chancres is a solitary painless papule
- Develops a central cleans-based ulcer
- It may also develop into a vascular proliferation resembling a pyogenic granuloma
- It is highly infectious
when treated - heals with 2 weeks ( little to no scarring )
Untreated - heals within 3 - 8 weeks
Primary syphilis symptoms?
Chancre of-course - rapid replication
Regional lymphadenopathy, may be bilateral ( systemic spread occuring )
Secondary syphilis symptoms?
2-6 months after initial infection
due to haematogenous spread
= Painless lymphadenopathy
= Malaise and muscoluskeletal pain
= Fever and weight loss
Patchy alopecia
Maculpapular rash
- Painless
- Diffuse - painless maculopapular cutaneous rash which affects palmer and plantar areas
Mucous Patches
- Focal areas of sensitive red-whitish mucosa
Ulcers
-snail-track ulcers
Spilt Papules
- Elevated lesions of crease of commissure
Condylomata lata
- cauliflower-like papillary lesions
- usually anogenital regions
- Typically multiple
Lues Maligna ( immune crompromised )
- explosive form of secondary infections
Symptoms of tertiary syphilis
Generally effects on vascular system due to arteritis
- Left ventricular hypertrophy
- Aortic regurgitation
- Congestive heart failure
CNS effects
- Tabes dorsalis ( degeneration of posterior roots of the spinal cord )
- General paralysis
Ocular lesions
- Iritis
- Retinitis
Saddle nose deformitiy
- Destruction of nasal cartilage
Gumma
- Scattered foci of granulomatous inflammation
- Chronic non healing ulcer
Interstitial glossitis
- Tongue becomes large , lobulate and irregular
Luetic glossitis
- Diffuse atrophy and loss of dorsal papillae
Explain Transmission of Congenital Syphilis
Syphilis is infectious during Primary and Secondary
stages.
Spirochete moves through the placenta to the fetus and disseminates systemically. The spirochete interfere with the incisal and cusp growth centres and affect development of these centres
Clinical features of congenital syphilis
Saddle nose deformity
Hutchinsons Triad
High arched palate
Frontal bossing
Hydrocephalus
Saber shin
8th nerve deafness
Oral manifestation of congenital syphilis
Hutchinson Triad
Dental anomalies - Hutchinson incisors and mulberry molars
Ocular Interstitial keratitis - opacified cornea - leads to blindless
Eighth nerve deafness
Describe clinical features of hutchinsons incisors and mulberry molars
Hutchinsons incisors - Straight edge screwdriver. greatest M-D width in mid 1/3 Crown.
Central hypoplastic notch on incisal edge
Diagnosis of Syphilis
Smear biopsy for genital lesions
Incisional Biopsy ( oral lesions )
- Histology
- Histochemistry ( Warthin Starry Stain )
Serology —>
Non specific ( Not highly sensitive tests )
- Venereal Disease Research Laboratory (VDRL)
- Rapid Plasma Reagin
Specific and highly sensitive tests
- Fluorescent Treponemal AntiBody Absorption test
- Treponema Pallidum HemAgglutination assay
- Treponema Pallidum Particle Agglutination assay
Treatment of syphilis
Primary and Secondary - Intramuscular Syphilis ( long-acting benzathine penicillin G )
Tertiary - same treatment but once a week
Pathogenesis of Necrotizing ulcerative gingivitis
Often caused by anaerobic fusiform baci
- Fusobacterium Nucleatum are commonly encountered
- Stress -> induced corticosteriods are thought to alter T4/T8 lymphocyte ratios and may lead to decreased neutrophilic chemotaxis and phagocytic response. Stress induced adrenaline may result in localized ischaemia.
Immunosuppressions, smoking, diabetes, local trauma, poor nutrition .
Clinical appearance of NUG?
- Starts at tips of interdental papillae.
- Blunted or punched out craterlike necrosis.
- Spreads along gingival margins.
- Yellow - grey pseudomembranous covering.
- Surrounding erythema and oedema.
Management of NUG
Manage predisposing factors
- Smoking cessation if necessary
- Oral Hygiene
- Supportive therapy
- Follow - Up
Debridement
- Topical or Local Anaesthetic often required
- Scaling and curettage
Mouth Washes
- Increase therapeutic Response
- Chlorhexidine / Warm saltwater
Adjunctive antimicrobial cover
- Metronidazole and penicillin
Noma/Cancrum Oris
Rapidly progressive necrotising infections
Polymicrobial, opportunistic infection
Pre-disposing Factors
- Poverty
- Malnutrition
- Poor OH
- Poor Sanitation
- Unsafe drinking water
- Proximity to unkempt livestock
- Malignancy
- Immunodeficiency
Actinomycosis pathogenesis?
- Actinomyces Israeli
- Actinomyces viscosus
Bacterial Invasion
Trauma
Periodontal pathology
Surgery
Dental Extraction
- Middle Aged
N.B
Does not spreads via normal tissue planes or lymphatic routes - usually direct extension through tissues.
Clinical Features of Actinomycosis
Discharge yellow flecks - Sulphur granule
Clinical Features of Cervicofacial actinomycosis
- ST of submd, submental, cheek areas
- Entry through area of prior trauma
- Can erode through bone
- Indurated area of fibrosis
- Forms central, softer abscess area
- Small yellow sulphur granules
Other presentations of Actinomycosis
- Abscess of Soft tissues
- Abscess of tonsillar crypts
- Salivary gland involvement
- Actinomycotic osteomyelitis
- Colonization of dentigerous cyst
- Periapical inflammatory lesions
Diagnosis of Actinomycosis
Sulphur granules is a strong clinical presentation
surgical exploration to obtain tissue
Treatment Actinomycosis
Chronic-Fibrosing cases
-Debridement
-Prolonged high doses of antibiotics
-Penicillin/tetracycline/clindamycin
-Couple of weeks to months
Actinomycotic osteomyelitis
- adequate debridement
- subsequemt antibiot treatment
