Bacterial infections of Mouth and Pharynx Flashcards
what does a sore throat usually show upon exam?
inflammation of pharynx, tonsils, uvula with exudate, cervical lymphadenopathy and fever
what are the most common causes of sore throat? what are other alternatives?
virus is most common
also caused by bacteria- strep. pyogenes, c. diphtheria, n gonorrhoeae and h influenzae
what percent of pharyngitis is due to group A strep?
30% (streptococcus pyogenes)
how is group A strep tested? what are the limitations of the test?
rapid antigen detection- prone to false negatives (not sensitive)
can also culture
what are the defining characteristics of group A strep?
gram positive cocci that grow in chains
beta- hemolytic, bacitracin sensitive and react with lancefield group A antiserum
what is the reservoir of group A strep. how is it transmitted?
carriers have it in pharynx and skin. transmitted by contact or saliva
what are the toxins of group A strep?
streptokinase (tissue lysis), streptodornase (digests DNA), hyaluronidase (digests CT), pyrogenic toxin (fever and toxic shock) and erythrogenic toxin (rash)
what is streptolysin and how is it useful?
a substance associated with group A strep that produces hemolysis on blood agar. induces short lived IgM antibody that is diagnostically useful
what physical virulence factor does group A strep have?
pilli
what are some complications of streptococcal pharyngitis?
tonsillitis, middle ear infection, mastoiditis, meningitis, scarlet fever and rheumatic fever
how does mastoiditis arise in strep pharyngitis? meningitis?
an ear infection travels upward into the mastoid air cells. can go from there to the meninges
what is the cause of scarlet fever? what are the clinical manifestations?
exotoxin from a bacteriophage of group A strep
skin and tongue rash (strawberry tongue)
how is strep throat prevented?
prophylactic antibiotics for patients who have had post strep diseases or tonsillectomy may reduce the risk of future infections
what is the treatment for group A strep?
penicillin, amoxicillin, erythromycin or cephalosporins (little resistance). not essential because infection is self limiting
what is the progression of rheumatic fever? what is it caused by?
arises 3 weeks after resolution of strep throat with fever, polyarthritis and inflammation of the heart. autoimmune
how is rheumatic fever diagnosed?
fever, polyarthritis and heart murmur plus IgM anti streptolysin O antibody. heart lesions and joints are sterile
how does carditis from rheumatic fever resolve?
fibrosis of the endocardium or calcification. often has permanent valve distortion with life long risk of endocarditis (give prophylaxis to prevent)
what is the treatment for rheumatic fever?
anti inflammatory drugs with replacement of heart valves if necessary
how is rheumatic fever prevented?
if there is a prior history, aggressive antibacterial therapy should be given if there is another strep throat infection
what bacteria causes dental carries? what identifies them?
streptococcus viridans. alpha hemolytic and optochin resistant
what is the biofilm produced on teeth? how do they cause cavities?
bacteria produce carbohydrates that form biofilm. produce acids that demineralize enamel and dentin
what are complications of dental caries?
pulpitis, abscesses and cellulitis
how are dental caries treated?
decalcified tissue is removed and acute abscess are treated temporarily with penicillin, erythromycin or cephalosporins
what is the usual cause of endocarditis? what other organisms can cause it?
usually viridans streptococci. IV drug users and pts with infected IV lines may contract s aureus. alternatively the HACEK group of gram negative rods
how is diagnosis of endocarditis confirmed? what clinical features may be present?
confirmed by cardiac exam. may cause splinter hemorrhages under fingernails and in conjunctiva. blood culture may be positive
how is endocarditis treated?
prolonged antibiotics. replacement of valves may be necessary but the new valve may become infected
how is endocarditis prevented?
antibiotic coverage of dental treatment and catheterization in at risk patients
what is peridontal disease? what is the early stage?
chronic inflammation in oral tissues that are in contact with dental plaque. early stage is gingivitis (reversible)
what occurs with prolonged gingivitis?
gingiva detach from the tooth creating a pocket where alveolar bone is destroyed. mature plaque is calcified and teeth are eventually lost
what organism is responsible for peridontal disease?
not a single microorganism- complex mix of anerobic organisms
what is the treatment of peridontal disease?
improvement in dental hygine including regular dental scaling to remove calcified plaque. peridontal surgurey can reduce pockets
what is the etiology of diphtheria infection?
infection of pharyngeal mucous membrane causing necrosis and “membrane” with respiratory obstruction
what does the diphtheria toxin cause?
causes systemic muscle paralysis- may lead to myocarditis and death (encoded by bacteriophage)
how is diphtheria transmitted?
air borne droplets
how is diphtheria diagnosed?
by growth of the bacteria on tellurite plates (have to order specially). gram positive rods with clubbed end and internal beads. confirmed to produce toxin by antibody tests or contain toxin gene by PCR
how is diphtheria treated?
with antitoxin (asap). penicillin or erythromycin helps with resolution
how is diphtheria prevented?
with a vaccine inlcuding toxoid. required for all school children
