Bacterial Infections of the Mouth and Pharynx Flashcards
0
Q
What is the classification of Group A strep?
A
- cocci
- gram +
- catalase negative
- beta-hemolytic
- bactracin sensitive
1
Q
What are the microbial causes of pharyngitis?
A
Viruses: EBV, Adenoviruses, Herpes Simplex 1, Coxsachie virus
Fungi: Candida albicans
Bacteria: Strep pyogenes, Corynebacterium diphtheriae, Neisseria gonorrhoeae, Hemophilis influenzae
2
Q
What are the virulence factors of Group A Strep?
A
- Structural Pili
- Streptokinase- tissue lysis
- Streptodornase- digests DNA
- hyaluronidase- digests connective tissue
- Pyrogenic toxin- fever, super antigen, toxic shock
- Erythrognic toxin- skin rash
3
Q
What is the etiology of streptococcal pharyngitis?
A
- sore throat common complaint of children and adults
- examination shows inflammation of pharynx, tonsils, uvula with exudate, cervical lymphadenopathy, and fever
- can be caused by a variety of viruses, fungi and bacteria
- clinically it is not possible to identify each reliably, but Hepes simplex, Coxsackie or Candida infection
- 30% of pharyngitis is due to group A strep
4
Q
What is the reservoir and transmission of Group A strep?
A
Carriers or infected patients have direct contact with a susceptible person and then they contract the disease.
-Transmission is by contact or saliva
5
Q
How do you diagnose a Group A strep infection?
A
- suggested by family or social history
- rapid office tests with antibody assays (quick but not 100% sensitive)
- swab- culture- gram positive cocci growing in chains, beta- hemolytic, bacitracin sensitive and react with Lancefield Group A antiserum- accurate but slow
- not direct examination of smear
- do not use antibiotics until diagnosis is confirmed
6
Q
How do you treat Group A strep infection?
A
- no essential as infection is self-limiting but antibiotics can shorten symptoms by 16 hours and reduce complications
- sensitive to Penicillin G, amoxicillin, erythromycin, or cephalosporins
- drug resistance is not a serious problem
- patients with a history of rheumatic fever need special attention
7
Q
What are the complications of streptococcal pharyngitis?
A
- Tonsillitis- peritonsillar absecess- Ludwig’s angina (under tongue)
- Middle ear infections (also caused by S. pneumoniae or H. influenzae)
- Nastoiditis
- Meningitis (also caused by N. menginitides and S. pneumoniae)
- Scarlet fever- due to exotoxin encoded by bacteriophage that carries gene for erythrogenic toxin. Skin rash and tongue rash (Strawberry tongue)
- Rheumatic fever
8
Q
How do you recognize Scarlet Fever?
A
skin rash and stawberry tongue
9
Q
How do you prevent Group A strep infections?
A
- no vaccines despite many potent antigens
- prophylactic antibiotic for patients who have had post-streptococcal diseases
- treatment of carriers is not recommended
- tonsillectomy reduces the risk of future infections in some studies
10
Q
What is the etiology of Rheumatic Fever
A
- a post-strep condition that arises about 3 weeks after resolution of a sore throat caused by some strains of Group A strep
- an autoimmune condition with fever, polyarthritis and inflammation of heart leading to permanent deformations.
- recurrences are common
- patients may need future prophylatic antibiotics for dentistry and minor surgical procedures
11
Q
What is the clinical presentation of rheumatic fever?
A
- fever
- polyarthritis
- heart murmur
- at risk groups are children aged 6-15
- duration can be several weeks or months
- case fatality 2-5%
12
Q
How is rheumatic fever diagnosed?
A
- clinical features plus presence of IgM anti-streptolysin O antibody
- heart lesions and inflamed joints are sterile- no bactemia
- Aschoff body
13
Q
What is the pathogenesis of Rheumatic fever?
A
- presumably auto-immune
- certain M protein types of Strep (M5, M3, M13) are more likely to be associated
- certain HLA types also more common
- reduction in prevalence
- carditis can resolve with fibrosis of endocardium or calcification often with permanent valve distortion= life-long risk of endocarditis and be need to be given antibiotics at times likely of bacteremia
14
Q
How do you treat rheumatic fever?
A
- anti-inflammatory drugs (aspirin/steroids)
- no antibacterial therapy
- later replacement of heart valves may be necessary
- to prevent future recurrence treat with aggressive anti-bacterial therapy in the event of later strep infections
15
Q
What is the etiology of dental carries?
A
- an infection of Viridans streptococci- bacteria are of no particular Lancefield Group, alpha hemolytic, optochin resistant
- organisms produce high molecular weight carbohydrates that form biofilm of tooth surfaces leading to dental plaque
- also break down sugars to make acid that demineralizes enamel and dentin
16
Q
How are dental caries diagnosed?
A
- 6 month dental exams show early demineralization
- lab testing is not informative since the bacterial are part of the normal flora of the mouth of 100% of people
17
Q
What are the virulence factors of viridans strep>
A
- extracellular polysaccharides
- acids
18
Q
How do you prevent dental caries?
A
- optimal fluoride concentration of drinking water during dental enamel formation
- topical fluorides to tooth surfaces
- low-sugar diet
19
Q
What are the complications of dental caries?
A
- pulpitis, abcesses, and cellulitis
- bacteremia and endocarditis may follow dental treatment of susceptible patients
20
Q
Which dental procedures produce S. viridans bacteremia?
A
- Extraction of 4 first premolars- 51%
- extraction (single)- 38.5
- polishing teeth- 24.5
- placing bands - 10
- adjusting bands- 0
21
Q
How do you treat dental caries?
A
- dental treatment to remove decalcified tissue
- acute abscesses can be treated temporarily with penicillin, erythromycin or cephalosporins, but dental extraction is more effective
22
Q
What is the etiology of endocarditis?
A
- previous rheumatic fever causes distortion of endothelium in the heart leads to turbulent blood flow
- any sticky bacteria that come into contact with a distorted endothelium can attach and replicate
- infection can be very persistent
- damage to heart may be continuous
- valves are particularly susceptible
- heart “vegetations” can be foci of infection and of metastatic abscesses. Valves are gradually destroyed. Antibiotics do not penetrate the vegetations
- usually caused by strep viridans
- in drug abuses or infected IV line S. aureus can be the cause, or alternatively the HACEK group of gram neg rods can be involved
23
Q
How is endocarditis diagnosed?
A
- variable clinical features, confirmed by cardiac exam
- satellite infections foci (splinter hemorrhages) under fingernails and in conjunctiva due to release of infected material into the circulation
- blood culture may be positive for causative organisms
24
How do you treat endocarditis?
- prolonged antibiotics
| - replacement of heart valves carries the risk of new valve becoming infected
25
How do you prevent endocarditis?
- antibiotic coverage of dental treatment, catheterization etc. in at risk patients
- bacteremia should be prevented by prophylactic antibiotics at the time of dental treatment, following the current guidelines of the American Heart Association
26
What is the etiology of periodontal disease?
- chronic inflammation in oral tissues that are in contact with the dental plaque
- early stage is termed gingivitis and is reversible if dental hygiene is improved
- over a period of years the gingiva detach from the tooth creating pocket where the microorganisms proliferate
- as the pocket becomes deeper alveolar bone is destroyed and mature plaque becomes calcified
- eventually teeth loosen and are lost
- no specific microorganism is responsible, but rather a complex mix of anerobic organisms- these organisms are present in small numbers in all people
- treatment is improved by dental hygiene, including regular dental scaling to remove calcified plaque. Periodontal surgery can reduce or eliminate pockets
27
What is the etiology of Diptheria?
- infection of pharyngeal mucous membrane by Corynebacterium diphtheria that causes necrosis and pseudomembrane with respiratory obstruction
- release of toxin causes systemic muscle paralysis including myocarditis and death in 10-20% of cases
- mostly a childhood condition
- strains may be toxigenic or not (diptheroids)
- bacteria inhabit skin and mucous membrane, carriage may be asymptomatic
- spread by respiratory droplets, direct contact
28
What is the virulence factor in Diptheria?
-Diptheria toxin, encoded by bacteriophage
29
How is diptheria transmitted?
-air borne droplets, can be direct contact
30
How is Diphtheria diagnosed?
- growth of Corynebacterium diphtheria on fellurite plate
- appearance of Gram positive rods with clubbed end and internal beads
- lab cultures confirmed to produce toxin by antibody tests or to have the toxin gene by PCR
- examination of smears is not useful because of the existence of non-pathogenic Corynebacteria (diphtheroids)
31
How is Diphtheria treated?
- Antitoxin (equine)
- Penicillin or erythromycin helps resolution
- mechanical ventilation as needed
32
How can Diphtheria be prevented?
- Diphtheria vaccine
- DTap includes diphtheria toxoids
- boosters after 1 year, 5 years
- boosters for adults when traveling to endemic areas
