Oral Manifestations of Bacterial Infections

Question 1

Necrotizing Ulcerative Gingivitis (NUG/ANUG)

Answer 1

Painful, erythematous gingiva with necrosis of the interdental papillae (Yellow/red fibrin in the interdental papillae and blunting)

Etiology: Fusiform bacillus and the spirochete Borrelia vincentii

Clinical features: foul odor, metallic taste, possible fever and lymphadenopathy

Question 2

Txt of NUG

Answer 2

Metronidazole** used for the treatment of NUG (anti-bact)

Prescribe and re-evaluate in 2 weeks and then f/u with OHI

Question 3

Streptococcal tonsillitis and pharyngitis

Answer 3

Streptococcal sore throat (Strep throat)

Etiology: Group A, b hemolytic streptococci

Transmission: person-to-person contact with infectious nasal or oral secretions

Tested by rapid chair side tests for Strep and wait to see before prescribing
Antibiotics

Clinical Presentation:

• Sudden onset sore throat
• Fever
• Dysphagia
• Erythema of the oropharynx and tonsils
• Tonsillar hyperplasia with exudate
• Cervical lymphadenopathy

Question 4

Prominent sign in BACTERIAL tonsilitis

Answer 4

neutrophil filled yellow pus on the tonsils

Question 5

xt of Strep

Answer 5

Most cases are self-limiting; resolve within 4 days

Goal: Prevention of complications
- Sensitive to penicillin, cephalosporins (more expensive), erythromycin (patients allergic to penicillin)

Question 6

Complications of Strep Infection

Answer 6

> Scarlet fever:
- Systemic infection with group A, β-hemolytic
streptococci
- Organisms produce an erythrogenic toxin that
attacks blood vessels and produces a skin rash
- Strawberry Tongue

> Rheumatic fever
- An acute, immunologically mediated, multisystem
inflammatory disease that occurs a few weeks
following an episode of streptococcal sore throat
- Acute carditis may progress to chronic rheumatic
heart disease

> Post streptococcal glomerulonephritis
- An immunologically mediated inflammatory disease
of glomeruli that follows streptococcal infection of
the pharynx or skin (impetigo)

Question 7

Noma (Cancrum oris, Gangrenous stomatitis)

Answer 7

rapidly progressive, destructive, opportunistic infection caused by components of the oral microflora that become pathogenic during periods of compromised immune status

Key players: Fusobacterium and Prevotella*

Typically affects children (1-10 years) or adults with major debilitating disease or HIV

Question 8

Risk Factors for Noma

Answer 8

• Significantly compromised systemic health
• Immunodeficiency including AIDS
• Severe malnutrition
• Poor oral hygiene
• Pre-existing bacterial infections (ANUG)

Question 9

Txt of Noma

Answer 9

• Debridement of gross necrotic tissue
• Antibiotics: penicillin, metronidazole
• Reconstruction after healing

Question 10

Actinomycosis

Answer 10

• Bacterial Infection caused by Actinomyces israelii
• May be acute or chronic
• Slowly spreading lesion associated with fibrosis
• Organism typically enters tissue through an area of prior trauma

Clinical Presentation:
> Indurated “woody” area of fibrosis
> Draining abscess with characteristic “sulfur granules” (yellow colored colonies)
> usually does not involve lymphatics
> does not spread along usual fascial planes
> Feels firm, leathery, woody, fibrotic, and exudes sulfur granules

Question 11

Diagnosis of Actinomycosis

Answer 11

-Culture
> Clinical features with “sulfur granules”

-Biopsy
> shows bacterial colonies surrounded by neutrophils
“island of bacteria in a sea of neutrophils”

Question 12

Txt of Actinomycosis

Answer 12

Antibiotic therapy with penicillin or amoxicillin– prolonged high dose

Abscess drainage

Excision of the sinus tracts

Question 13

Cat scratch disease

Answer 13

Comes from contact with cat

Begins in the skin and involves the adjacent lymph nodes

Etiology: Bartonella henselae enters skin through a cat scratch or bite

Begins as a papule or pustule that develops along the scratch line

Lymp node enlargement follows about 3 weeks later

Question 14

Diagnosis Cat Scratch Disease

Answer 14

Contact with a cat

Indirect fluorescent antibody assay (serological) for detecting antibodies to Bartonella henselae

ELISA for IgM antibodies to the organism

Negative results for other causes of lymphadenopathy
Lymph node biopsy

Question 15

Txt of Cat Scratch Disease

Answer 15

Self-limiting; usually resolves within 4 months

Aspiration of node if suppurative

Antibiotics reserved for prolonged or severe cases
(Azithromycin or erythromycin)

Question 16

Syphilis

Answer 16

Etiology: Treponema pallidum (spirochete)
Transmission: Direct contact; sexual or mother-to-fetus

Three Stages
1. Primary - infectious
Chancre ( yellow ulcer with red rolled border
- found on genitalia and tongue most
frequently)
Regional lymphadenopathy
2. Secondary – infectious
skin rash (palms and soles of feet)
oral lesions
mucous patches (gelatinous, mucoid
form that cannot be wiped off)
3. Tertiary – NOT infectious
Gumma (granulomatous inflammation)
CNS involvement

Question 17

Microscopic Identification of Spirochetes

Answer 17

Silver stain or Darkfield

Question 18

Serologic Tests for Syphilis

Answer 18

> Reagin

- VDRL – Venereal Disease Research Laboratory
- RPR – Rapid plasma reagin
- Complement fixation tests – Wassermann
- Tests for reagin are sensitive but not specific
- Many false positives

> Antitreponemal antibodies
- TPI
- FTA-ABS
- These tests are more specific than reagin tests
- Tests become positive at the time of the
development of the first lesion and remain positive
for life

Question 19

Mechanism of Syphilis

Answer 19

Intracellular pathogen

Rapid dissemination through the endothelium

Immune evasion to antibodies

Bacteria reside in tissues quiescently

Bacteria reactivation (mechanism unknown)

Question 20

Congenital Syphilis

Answer 20

• crosses the placental barrier
• any tissue can be infected
• children who survive may show abnormal tooth development such as Hutchinson’s incisors, Mulberry molars
• preventable if mother is treated early for her syphilis infection - txt with pencillin

Question 21

Hutchinson triad

Answer 21

deafness, keratitis, tooth defects

Question 22

Tuberculosis

Answer 22

Etiology: Mycobacterium tuberculosis

Oral lesions

Secondary infection from pulmonary lesions

Scrofula
Involvement of cervical lymph nodes from drinking contaminated milk (M. bovis)

Question 23

Clinical Features

Answer 23

Primary TB: usually asymptomatic
Secondary TB: fever, malaise, night sweats, weight loss, productive cough
Progressive TB: wasting syndrome

Question 24

Oral Manifestations of TB

Answer 24

Chronic, non-healing, progressively enlarging, indurated ulcers

Mimics a malignancy
(SCC or deep fungal)

Nodular granulomatous proliferations

Usually painless

Question 25

Diagnosis of Oral TB

Answer 25

Biopsy showing lymphocytic infiltrate, granulomas, and necrosis

Biopsy - acid fast bacilli (AFB) stain shows presence of bacilli

Question 26

Txt of Oral TB

Answer 26

Multiagent therapy for several months: isoniazid, rifampin, pyrazinamide, ethambutol

Prevention: BCG vaccine worldwide, restricted in US due to controversial effectiveness

Question 27

Osteomyelitis

Answer 27

Inflammation of bone and bone marrow

Acute osteomyelitis- extension of periapical abscess, bacteremia, may not be seen on x-ray

Chronic osteomyelitis- long-standing inflammation of bone, Paget disease, bone irradiation, x-ray shows diffuse and irregular radiolucency with focal radiopacities

Question 28

Txt of Osteomyelitis

Answer 28

• Drainage of area
• Debridement
• Appropriate systemic antibiotics
• Hyperbaric oxygen