GI Infections 1: Teeth, Gingivae, Jaws, Mouth, Tongue, and Parotids

Question 1

Dental caries

Gingivitis

Acute Necrotizing Ulcerative Gingitivits

Cinvent’s Angina

and Periodontal Disease

can all spread to cause…?

Answer 1

Cardiovascular disease

Ludwig’s Angina - sublingual space infection

Vincent’s angina - infection of the oropharynx

Endocarditis

Osteomylitis - destruction of jaw

Head and Neck Abscesses

Rhinosinusitis

Otitis Media

Question 2

Define dental caries.

What does this often cause in children? (Caries are the number one cause)

What is the most common etiology causing dental caries?

What are 4 other etiologies that can lead to dental caries?

Answer 2

Dental caries: damage to surface of tooth (enamel and/or dentin)

Most common cause of tooth loss in children

Mutans group of Streptococcus (S.mutans, S.sobrinus) - most common cause of tooth decay

Lactobacillus casei

Actinomyces sp.

Bifido-bacterium

low pH tolerant Streptococcus sp.

Question 3

Describe the role of biofilm in the pathogenesis of dental caries.

What do you call an old hardened biofilm?

Answer 3

Bacteria form a biofilm on the surface of your teeth. Under this biofilm the bacteria gobble up the sucrose you eat, but as fermenters they digest this to lactic acid. This lactic acid decreases the pH (less than or equal to 5.5) which then demineralizes tooth enamel causing damage and cavitation. Caries can penetrate into the dentin and pulp then killing the tooth.

No punch line, its tartar

Question 4

What virulence factors help make biofilms and cause dental caries?

Answer 4

Adhesins - bind tooth

Acidogenicity - make acid

Aciduricity - survive low pH

EPS - extracellular polysaccharide, helps stay at surface of tooth

intracellular polysaccharides - storage helps increase length of time pH is low in the mouth

Question 5

Define periodontal disease.

List 5 periodontal diseases.

Answer 5

Periodontal disease: infection/inflammation of the structures surrounding the teeth (gingiva, periodontal ligament, and alveolar bone)

1. Gingivitis
2. Acute necrotizing ulcerative gingivitis (trench mouth) - WWI couldn’t brush teeth, very infected, very rare in US
3. Vincent’s angina - oropharynx infection
4. Chronic periodontitis - progressed gingivitis, gums inflamed and damage to periodontal ligament, loosening of tooth, and alveolar bone is lost, occurs over years
5. Aggressive periodontitis - happens quickly

Question 6

What is the most common cause of tooth loss in children?

What is the most common cause of tooth loss in adults?

Answer 6

Dental caries

Periodontitis

Question 7

Who gets gingivitis?

How many microbes are typically involved in periodontal disease?

Answer 7

Almost everyone gets gingivitis

Polymicrobial process: 10-20 organisms involved in periodontal disease, typically more gram negative anaerobes and spirochetes

chance of periodontal disease affected by organisms in plaque

Question 8

Which 3 organisms are the most likely to cause periodontal disease?

How are organisms divided in reference to their risk of causing periodontal disease? Which type of organisms are typically found in each group?

Answer 8

Red Complex (High risk): Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola (gram negative anaerobes and spirochetes

Orange complex (moderate)

Yellow complex (low risk): typically streptococcus

Question 9

Which 3 organisms are responsible for aggressive periodontitis?

Answer 9

Aggressive periodontitis:

Aggregatibacter actinomycetemcomitans

Eikenella corrodens with Fusobacterium nucleatum

Question 10

Where does biofilm accumulate in the case of gingivitis?

What virulence factors are responsible for gingivitis?

Describe the symptoms of gingivitis?

Answer 10

Biofilm in gingival crevice. More plaque on tooth = more likely gingivitis will occur.

hemolysins and proteases

inflammation: redness, swelling, bleeding with trauma, but no pain

Question 11

What lifestyle factors lead to Acute Necrotizing Ulcerative Gingivitis?

How many microbes are involved?

What are the symptoms?

Answer 11

Poor oral hygiene, immunosuppressive, and extreme stress, rare in the United States.

Polymicrobial

Symptoms

fever, malaise

Lymphadenopathy, usually cervical

halitosis

painful and inflamed gingiva with necrotic gray/black ulceration of interdental papillae that bleed easily

gray pseudomembrane convers lesions and is easy to remove

Question 12

What is Vincent’s angina?

What are the associated symptoms?

Answer 12

Extension of trench mouth (acute necrotizing ulcerative gingivitis) into the oropharynx.

Symptoms

Fever

swelling of low face and neck

difficulty with speech or swallowing

membranous pharyngitis

painful ulcers on gingivae, buccal mucosa, and pharynx with hyperemic patches and edema

Question 13

How does gingivitis progress to periodontitis?

What virulence factor causes destruction of periodontal ligament?

What leads to alveolar bone resorption?

Answer 13

Plaque spreads down root surface, inflammation causes detachment of gingiva leading to pocket formation

Collagenases - destroy periodontal ligament

Inflammation causes alveolar bone resorption

Question 14

What is prescribed for trench mouth and Vincent’s angina?

Answer 14

Debridment, oral penicillin, and metronidazole

Question 15

What are 4 types of periapical tissue and jaw infections?

Answer 15

Dentoalveolar abscess - infection that results in a small pocket of infection

Periodontal abscess

Ludwig’s angina - sublingual

Osteomyelitis of the jaw

Question 16

What is the difference in location between periodontal and dentoalveolar abscesses? What is the difference in symptoms?What is their etiology?

What are the general symptoms of both abscesses in these locations?

Answer 16

periodontal - abscess along tooth root, starts as periodontitis, will likely also see redness and receding of gum line, polymicrobial

dentoalveolar - abscess forms at the end of the tooth root, starts as caries going through enamel then dentin then the nerve root, can extend and show itself in gums along the tooth, polymicrobial especially anaerobes

Symptoms of abscesses

pain in and around affected tooth

swelling of face over abscess

tapping the affected tooth causes pain

Question 17

What is the plan of care for patients with periodontal/dentoalveolar abscesses?

Answer 17

Radiographs and refer to dentist

Typically remove tooth, rooth canal, and I&D

Question 18

What is Ludwig’s angina?

What organisms cause Ludwig’s?

What are predisposing factors for Ludwig’s angina?

Answer 18

What?

Cellulitis of sublingual/submylohyoid space

Organisms

Streptococcus, Bacteroides, Fusobacterium, Staph aureus

Predisposing factors:

caries or recent dental treatment,

sickle cell or immunocompromised

trauma or tongue piercing

can occur in children without any cause

Question 19

What are the symptoms of Ludwig’s angina?

What is the principal concern with Ludwig’s angina?

Answer 19

Symptoms

severely ill/ fever, appears toxic

dysphagia (difficulty swallowing), drooling

Bad breath (more common with anaerobic organisms)

trismus (lock jaw, tetanus with no swelling under the jaw)

sitting upright (can’t breath lying down)

dysphonia (change in voice)

swelling and erythema of neck under chin

TTP of floor of mouth

Pain on movement of tongue, tongue is moved up and backward

What is the concern?

Acute airway closure at any moment, this is rapidly fatal without treatment

Question 20

How is Ludwig’s angina diagnosed?

How is it treated?

How is this prevented?

Answer 20

DX: clinically, CT, blood cultures

RX: airway management, abx, I&D if abx fail, nutrition and hydration

Prevention: good oral hygeine

Question 21

What is stomatitis?

What are the 3 most common causes of stomatitis?

Answer 21

Stomatitis: inflammation of the mucosal surfaces of the mouth and tongue. Gingivostomatitis is also common with HSV (affecting gingival structures)

Most common infectious causes: HSV 1 (80% of infections) and 2 and Candida albicans (germ tubes)

Question 22

What is the incubation period of oral herpes?

What is the duration of oral herpes?

What are the primary manifestations of herpes?

Where do recurrences of oral herpes typicall present?

Answer 22

Incubation: 2-12 days

Duration: 2-3 weeks

Primary manifestations:

fever, malaise, muscle aches, irritability

Pain, burning, itching of infection site with clusters of blisters

Blister breakdown form small shallow gray ulcers on a red base

Very painful sores may occur on lips, gums, anterior tongue, insides of cheeks, throat, and roof of mouth

Cervical lymphadenopathy

Recurrance not as severe and not usually in the mouth but on exterior

Question 23

What population is oral herpes most commonly seen in?

What are the causes of oral herpes?

Describe the 3 stages of oral herpes.

Where do recurrences occur?

Is asymptomatic shedding infectious?

Answer 23

usually seen in children (60% infected by 15)

HSV1 causes about 80% - contant with infected saliva, mucous membranes or skin

HSV2 causes about 20% - oral sex

1. primary infection - oral sores and fever (or asymptomatic)

2. Latency - chills in nerves

3. Recurrence - during times of stress, new sores

Recurrences inside the mouth are uncommon, typically seen on the lips and face

Asymptomatic shedding is infectious

Question 24

How is oral herpes diagnosed?

How is oral herpes treated?

Answer 24

Clinical presentation, culture, serology, Tzanck (multinucleated giant cell) test positive

Usually self-limiting, antiviral can be given for severe outbreaks but this will not cure

Question 25

Describe the three types of candidiasis manifestations of the mouth.

Answer 25

3 types of candidiasis 1. **_Pseudomembranous_** (thrush) - acute creamy, white plaques with mucosal and yeast cells and neutrophils hard to remove, and leaves inflammed painful base when removed, sometimes bleeding 2. **_Erythematous_** (red) - acute/chronic red areas of varying sizes can occur on any part of oral mucosa If on tongue it is fiery red and shiny with depapillation probem for denture wearers 3. **_Hyperplastic_** (leukoplakia) - chronic \*can results in cancer\* individual lesion of cheek near comminsure, at angles of mouth, or on the tongue descrete, raised lesions homogenous or speckled areas does not rub off

Question 26

Where is candidia albicans obtained? Who is more likely a carrier, men or women? What are predisposing factors that could increase liklihood of disease?

Answer 26

Common flora (50%) - acquired from birth canal, saliva, etc. carriers higher in women than men predisposing factors usually present to cause disease _predisposing factors:_ infants and neonates patking abx or steroids or drugs that cause dry mouth polyendocrine disorders or immune dysfunction smokers denture wearers

Question 27

What characteristics help candida cause infection? Describe the pathogenesis of Thrush. Of Erythematous candidosis. Of Hyperplastic candidiasis

Answer 27

_Virulence factors_ ability to produce **biofilms** **germ tubes** - helps yeast penetrate tissue **Thrush** - overgrowth of fungus, pseudomembrane forms made of keratin, bacteria, yeast, and necrotic tissue (infants also typically have diaper rash) **Erythematous candidosis**- inflammation due to overgrowth, no pseudomembrane but can follow pseudomembrane type, de novo in AIDS patients, prolonged drug use, dentures increase risk **Hyperplastic (leukoplakia)** - marked hyperplasia of parakeratinized layer with candidal hyphae invading at right angles into the layer, can become malignant

Question 28

How is candidiasis diagnosed? How is candidiasis treated?

Answer 28

_Diagnosis_ swab lesions for culture, scrapping can be stained for yeast cells biopsy hyperplasia _Treatment_ antifingal agents hyperplastic may require surgery if malignant

Question 29

What is oral hairy leukoplakia? What populations of patients is this most common? What is the etiological agent that causes this? Describe the pathogenesis of oral hairy leukoplakia? How is this diagnosed?

Answer 29

White growth on lateral borders of tongue Populations: immunocompromised/patients with malignant tumors/organ transplant recipients. 4% of IV drug users and homosexual males with HIV. Most common in HIV infected homosexual males. Etiology: Epstein Barr virus, usually in I/C Pathogenesis: latent EBV infection, immune suppression, replication in oral mucosa, resulting in benign thickening of mucosa and hyperproliferation of epithelial cells Diagnosed: clinical picture, looking for Cowdry type A inclusions in scraping Treatment: rarely treat unless HIV+, ART therapy. podophyllum resin and antiviral agent

Question 30

What is angular cheilitis? What organisms typically cause this? What populations is this common in and why?

Answer 30

**Angular Cheilitis** (angular stomatitis or perleche) inflammation of the angles of the mouth _Etiology_ usually **candida** albicans (red inflammation) **yellow** crusting typically indiciative of **Staph a**. _Common populations_ **elderly** (sagging facial muscles and ill fitting dentures), **children** (suck on their digits), and people with **riboflavin** or **iron deficiency** (anemia)

Question 31

How is angular cheilitis diagnosed? How is angular cheilitis treated? How can you prevent angular cheilitis?

Answer 31

_Diagnosis_ Usually clinical Swab and culture _Treatment_ Antifungal (candida, red inflammation) or antibacterial (staph a, yellow crusting) agent Hydrocortizone if chronic _Prevention_ Proper nutrition Proper fitting dentures

Question 32

Why is mumps less common recently? Who gets it when they do? What is mumps? What are some serious complications? What etiological agent causes mumps? What is the incubation period? Describe the transmission? When is the infectious period? Where is this common?

Answer 32

Benign viral parotitis - **Mumps** Was common but now **rare** due to **MMR vaccine** (given at 1 year) Primarily childhood infection with 60% occuring in children \<15 Disease of the **salivary glands** with occassional serious complications including: **aseptic meningitis**, **oophoritis**, **epididymoorchitis** _Etiology_ **Paramyxovirus** - RNA virus _Incubation period_ 14-25 days _Transmission_ airborne with infected droplet nuclei or saliva, or direct person to person contact very contagious no carrier state is known _Infectious period_ 3 days before symptoms to 9 days after symptoms _Location and setting_ World wide, more common in winter-spring months but can occur year round

Question 33

Describe the typical manifestations of Mumps

Answer 33

Presentation **Usually asymptomatic**(can still spread): maybe low respiratory infection in presechool kids _Prodrome_: myalgia, headache, anorexia, malaise, low fever _Parotitis_ (can be unilateral or bilateral): **swollen** and **tender salivary glands** with **earache** (30-40% of patients) Typically symptoms occur within first 2 days, first sign earache then tenderness of angle of jaw Symptoms typically decrease after a week and gone by 10d

Question 34

How often is parotitis absent in individuals with CNS complications with a Mumps infection? How often is CNS infection with mumps symptomatic versus asymptomatic? What are some more severe complications of a CNS complication with a Mumps infection? What populations are at higher risk of CNS complications with mumps?

Answer 34

_Aseptic meningitis as a complication of Mumps_ **-Parotitis** may be **absent** in **50%** of cases that infect CNS **-asymptomatic** aseptic meningitis in **40-50%** of mumps cases **-symptomatic** CNS infections in **10%** of mumps cases - can result in severe **encephalitis** (rare but fatal in 1.4% of those cases), permanent **sequelae** in 25% and 1% **die** - adults and boys are at higher risk of CNS complication

Question 35

Describe the symptoms of orchitis. Which population of mumps infected people is this most common in? How long do symptoms last? Are there any permenent effects? How common is oophoritis among females with mumps? Does this have any lasting effects.

Answer 35

_Orchitis_ **Testicular swelling**, **tenderness**, **nausea**, **vomiting**, and **fever** Most common complication in **postpubertal males** Pain and swelling may subside in a **week**, but **tenderness** may last for **weeks**. Sterility is rare. _Oophoritis_ Ovarian inflammation in **5%** of **postpubertal females** **No evidence** that this can cause **impaired fertility**

Question 36

What is a rare but permanent complication of Mumps? How does mumps affect the fetus during the 3 trimesters of pregnancy?

Answer 36

Deafness occurs about 1 in 15000, usually unilateral, sudden onset but damage is permanent 1st trimester can result in fetal death 2nd and 3rd not typically major problem

Question 37

How is Mumps transmitted? Where does it replicate? When does viremia occur and by what mechanism are tissues infected during viremia? What tissues does the virus go after?

Answer 37

- **airborne** transmission/**direct contact** with infected droplets - Replicates in **nasopharynx** and **regional lymph nodes** - **Viremia 12-25 days later** multiple tissues infected during viremia - **hemagglutinin-neuraminidase** of virus binds to trisaccharide (**alpha2,3-linked sialic acid**) on host cells - Tropisms for **glandular tissue** and **CNS** meninges, salivary glands, testes, ovaries, pancreas, kidneys, thyroid, eyes, mammary glands

Question 38

How is mumps diagnosed?

Answer 38

_Diagnosis_ Clinically obvious - jelly feel salivary glands with **no warmth** Isolate virus from salive, urine, and CSF Serology: EIA for IgM and IgG IgM positive: first few days (acute case) IgM: requires 2 samples 2 weeks apart

Question 39

How is mumps treated? How is mumps prevented?

Answer 39

_Treatment_ Treat the **symptoms** _Prevention_ **MMR** vaccine (**live attenuated** vaccine - so no preggos or I/C) 95% develop immune response to single dose given at 12-15 months again at 4-6 years with those that did not respond to primary dose (typically just do this to everyone because testing is expensive)

Question 40

How does bacterial parotitis present? What etiological agent causes this? Describe the pathogenesis

Answer 40

Acute Bacterial Parotitis _Presents as:_ **swelling** of **salivary glands** pain **worse with chewing** skin is **erythematous** and **_warm_** (not mumps) can massage out **purulent saliva** _Etiology_ **Staphylococcus aureus** _Pathogenesis_ Flow of saliva is affected Bacteria enter duct, ascend to gland, causing inflammation and pain

Question 41

Who is most likely affected by bacterial parotitis?

Answer 41

_Epidemiology_ Elderly- meds that affect flow of saliva dehydrated chronically ill post-op dry mouth

Question 42

How is bacterial parotitis diagnosed? How is it treated? How can it be prevented?

Answer 42

_Diagnosis_ **Clinical** - skin is erythematous and warm, can massage out purulent material Gram stain and culture _Treatment_ **IV abx** - staphylococcus aureus **rehydrate** may need **surgery** _Prevention_ **hydration** of chronically ill, elderly, and post-op patients