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MSII Micro Unit 2 > Bacterial Infections of the Mouth and Pharynx > Flashcards

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
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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

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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
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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
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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

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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
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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
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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
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8
Q

How do you recognize Scarlet Fever?

A

skin rash and stawberry tongue

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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
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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
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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%
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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
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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
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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
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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
Q

How do you treat endocarditis?

A
  • prolonged antibiotics

- replacement of heart valves carries the risk of new valve becoming infected

25
Q

How do you prevent endocarditis?

A
  • 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
Q

What is the etiology of periodontal disease?

A
  • 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
Q

What is the etiology of Diptheria?

A
  • 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
Q

What is the virulence factor in Diptheria?

A

-Diptheria toxin, encoded by bacteriophage

29
Q

How is diptheria transmitted?

A

-air borne droplets, can be direct contact

30
Q

How is Diphtheria diagnosed?

A
  • 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
Q

How is Diphtheria treated?

A
  • Antitoxin (equine)
  • Penicillin or erythromycin helps resolution
  • mechanical ventilation as needed
32
Q

How can Diphtheria be prevented?

A
  • Diphtheria vaccine
  • DTap includes diphtheria toxoids
  • boosters after 1 year, 5 years
  • boosters for adults when traveling to endemic areas

MSII Micro Unit 2 (7 decks)

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