Bacterial Infections of the Mouth and Pharynx Flashcards
streptococcal pharyngitis
sore throat. inflammation of pharynx, tonsils, uvula, cervical lymphadenopathy and fever. not possible to clinically identify each cause reliably. 30% due to group A strep
streptococcal pharyngitis diagnosis
group A strep origin suggested by family or social history. rapid antigen detection assays can work, but are prone to false negatives. bacterial culture shows it. beta hemolytic, bacitracin sensitive and react with lancefield group A antiserum
streptococcal pharyngitis reservoir
carriers, in the pharynx and skin. transmission is by contact or saliva
group A streptococci toxins
streptokinase (tissue lysis), streptodornase (digests DNA), hyaluronidase (digests connective tissue), pyrogenic toxin (fever, super antigen, toxic shock), erythrogenic toxin (skin rash)
streptolysin O
highly antigenic, inducing short lived IgM antibody which can be diagnostically useful
complications of streptococcal pharyngitis
tonsillitis -> peritonsillar abcess -> ludwig’s angina
middle ear infections, mastoiditis, meningitis, scarlet fever, rheumatic fever
scarlet fever
due to exotoxin encoded by bacteriophage that carries gene for the erythrogenic toxin. skin rash and tongue rash (strawberry tongue)
streptococcal pharyngitis treatment
systemic penicillin G, amoxicillin, erythromycin, cephalosporins
rheumatic fever etiology
post-streptococcal condition. 3 weeks after resolution of sore throat, get fever, polyarthritis, inflammation of heart leading to permanent deformations. recurrences common
rheumatic fever diagnosis
clinical features plus presence of IgM anti-streptolysin O antibody. heart lesions and inflamed joints are sterile. no bacteremia
rheumatic fever pathogenic
auto immune. certain M-protein types are more likely to be associated with rheumatic fever (M3, M5). some HLA types are more common in patients. carditis can resolve with fibrosis of endocardium, or calcification with permanent valve distortion
rheumatic fever treatment and prevention
anti inflamm drugs. no antibacterial therapy needed. replace heart valves if needed. aggressive anti bacterial therapy in the event of later strep infections
dental carries etiology
infection of streptococci viridans. alpha hemolytic. optochin resistant. organisms produce high molecular weight carbohydrates that form biofilm on tooth surfaces. break down sugars to make acid that demineralizes enamel and dentin
dental carries diagnosis
dental exam shows early demineralization. lab testing not informative since bacteria are part of normal mouth flora for 100% of people
strep viridans virulence factors
extracellular polysaccharides. acids.
prevention of dental carries
optimal fluoride concentration of drinking water during dental enamel formation. low sugar diet, and topical fluorides
dental carries complications
pulpitis, abcesses, cellulitis. bacteremia and endocarditis may follow dental treatment of susceptible patients.
dental carries treatment
remove decalcified tissue. acute abscesses can be treated temporarily with penicillin, erythromycin, or cephalosporins. dental extraction is more effective.
endocarditis etiology
previous rheumatic fever causes distortion of endothelium in the heart that leads to turbulent blood flow. sticky bacteria can come into contact with this distorted layer and attach and replicate. infection can be very persistent. . heart vegetations can be foci of infection and metastatic abcesses. valves are gradually destroyed. antibiotics do not penetrate these vegetation. usually caused by viridans. can be staph aureus in druggies
endocarditis diagnosis
cardiac exam. satellite infectious foci under fingernails and in conjunctiva due to release of infected material into circulation. blood culture may be positive for organisms
endocarditis treatment
prolonged antibiotics and replace heart valve (carries risk of new valve being infected)
peridontal disease
chronic inflammation in oral tissues that are in contact with dental plaque. early stage is gingivitis, and is reversible if dental hygiene is improved. gingiva can detach and create a pocket where microorganisms proliferate. as pocket becomes deeper, alveolar bone is destroyed and mature plaque becomes calcified, causing teeth to loosen and fall out. no specific microorganism is responsible. treat with improved dental hygiene or surgery
diptheria etiology
infection of pharyngeal mucous membrane causes necrosis and membrane covering pharynx. release of toxins causes systemic muscle paralysis including myocarditis and death in 10-20% of people. mostly childhood disease
diptheria virulence factor
diptheria toxin encoded by bacteriophage
diptheria transmission
airborne droplets
diptheria diagnosis
growth of corynebacterium diptheria on tellurite plates. appearance of gram positive rods with clubbed end and internal beads. lab cultures are confirmed to produce toxin by antibody tests or toxin gene on PCR. smears not useful since there are non-pathogenic strains
diptheria treatment
antitoxin given ASAP. penicillin or erythromycin helps resolution
diptheria prevention
vaccine. DTaP includes diptheria toxoid. required for all NYS children in school
