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Maxillo-Facial Path > Bacterial Infections > Flashcards

Bacterial Infections Flashcards

1
Q

What bacteria causes TB

A

Mycobacterium Tuberculosis

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2
Q

Pathogenesis of TB

A

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

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3
Q

What are the 2 types of pulmonary TB

A

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

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4
Q

Symptoms of Secondary pulmonary TB?

A

Fever,Malaise,Weight loss and night sweats

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5
Q

What is Miliary Tuberculosis

A

Diffuse dissemination through vascular system

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6
Q

Granuloma vs Granulation Tissue

A

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.

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7
Q

How do oral TB lesions occur?

A

Direct Inoculation - Organisms in sputum implanted in defects in mucosal barrier + Hematogenous deposition
Indirect - spread from lungs

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8
Q

What are the oral manifestations of TB

A

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

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9
Q

Clinical features of TB ulcer

A

Chronic, non-healing ulcer painless indurate

often presents with cervical lymphadenopathy

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10
Q

How do we diagnosis TB ( skin test )

A

Purified protein derivative skin test
- cell-mediated hypersensitivity reaction to tubercular antigen. Only after 2-4 weeks after intial exposure

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11
Q

TB incisional biopsy - methods

A

Histology - Granulomatous inflammation with caseous necrosis and langerhans giant cells

Ziehl Neelsen stains acid and alcohol fast bacilli

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12
Q

Treatment of TB

A

Multi-Agent therapy
- 8 weeks pyrazinamide,isoniazid,rifampicin, ethambutol
- 16 weeks isoniazid, rifampicin

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13
Q

Vaccine for TB

A

BCG - Bacillus Calmette Guerin Vaccine

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14
Q

What is Mycobacterium Bovis infections

A

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

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15
Q

Further diagnosis for TB

A

chest radiograph and CT scan will show characteristic lung involvement. Tuberculous osteomyelitis and calcifed lymph nodes

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16
Q

Which bacteria causes syphilis?

A

Treponema Pallidum ( Gram negative spirochete )

17
Q

Pathogenesis of Syphilis

A

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

18
Q

What are the different stages of syphilis

A

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

19
Q

Describe the clinical features of a chancre

A

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

20
Q

Primary syphilis symptoms?

A

Chancre of-course - rapid replication
Regional lymphadenopathy, may be bilateral ( systemic spread occuring )

21
Q

Secondary syphilis symptoms?

A

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

22
Q

Symptoms of tertiary syphilis

A

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

23
Q

Explain Transmission of Congenital Syphilis

A

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

24
Q

Clinical features of congenital syphilis

A

Saddle nose deformity
Hutchinsons Triad
High arched palate
Frontal bossing
Hydrocephalus
Saber shin
8th nerve deafness

25
Q

Oral manifestation of congenital syphilis

A

Hutchinson Triad
Dental anomalies - Hutchinson incisors and mulberry molars
Ocular Interstitial keratitis - opacified cornea - leads to blindless
Eighth nerve deafness

26
Q

Describe clinical features of hutchinsons incisors and mulberry molars

A

Hutchinsons incisors - Straight edge screwdriver. greatest M-D width in mid 1/3 Crown.
Central hypoplastic notch on incisal edge

27
Q

Diagnosis of Syphilis

A

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

28
Q

Treatment of syphilis

A

Primary and Secondary - Intramuscular Syphilis ( long-acting benzathine penicillin G )

Tertiary - same treatment but once a week

29
Q

Pathogenesis of Necrotizing ulcerative gingivitis

A

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 .

30
Q

Clinical appearance of NUG?

A
  • Starts at tips of interdental papillae.
  • Blunted or punched out craterlike necrosis.
  • Spreads along gingival margins.
  • Yellow - grey pseudomembranous covering.
  • Surrounding erythema and oedema.
31
Q

Management of NUG

A

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

32
Q

Noma/Cancrum Oris

A

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

33
Q

Actinomycosis pathogenesis?

A
  • 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.

34
Q

Clinical Features of Actinomycosis

A

Discharge yellow flecks - Sulphur granule

35
Q

Clinical Features of Cervicofacial actinomycosis

A
  • 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
36
Q

Other presentations of Actinomycosis

A
  • Abscess of Soft tissues
  • Abscess of tonsillar crypts
  • Salivary gland involvement
  • Actinomycotic osteomyelitis
  • Colonization of dentigerous cyst
  • Periapical inflammatory lesions
37
Q

Diagnosis of Actinomycosis

A

Sulphur granules is a strong clinical presentation
surgical exploration to obtain tissue

38
Q

Treatment Actinomycosis

A

Chronic-Fibrosing cases
-Debridement
-Prolonged high doses of antibiotics
-Penicillin/tetracycline/clindamycin
-Couple of weeks to months

Actinomycotic osteomyelitis
- adequate debridement
- subsequemt antibiot treatment

Maxillo-Facial Path (9 decks)

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