Micro 4 part 1 and 2 Flashcards
Stroptococcal Pharyngitis Symptoms
inflammation of pharynx, tonsils, uvula with exudate, cervical lymphadenopathy, fever
What percentage of pharyngitis is due to Group A streptococci?
30%
How is group A streptococci diagnosed?
family/social history, rapid antigen detection (fale negative), bacterial culture (slow)
What does bacterial culture of group A streptococci show?
gram + cocci that grow in chains, beta-hemolyitc, bacitracin-sensitive, react with Lancefield group-a antiserum
What are group A streptococci toxins? Effect of each toxin?
streptokinase (tissue lysis); streptodornase (digests DNA); hyaluronidase (digests connective tissue; pyrogenic toxin (fever, super antigen, toxic shock); erythrogenic toxin (skin rash)
Steptolysin O
Group A strep - not virulence but used for identification. highly antigenic, inducing short-lived IgM
What are complications of group A strep?
tonsillitis, peritonsillar abscess, Ludwig’s angina (no airway because floor of mouth swollen - die), middle ear infections, meningitis, mastoiditis, scarlet fever, rheumatic fever
Scarlet Fever
due to exotoxin encoded by bacteriophage that carries gene for the erythrogenic toxin. skin rash and strawberry tongue
What is prevention for group A strep?
no vaccine, prophylactic antibiotics for patients with post-strep diseases, treatments for carriers NOT recommended, tonsillectomy reduces risk of future infection
Treatment of group A strep?
no essential (self-limiting) - use systemic penicillin G, amoxicillin, erythromycin, cephalosporins if needed - drug resistance not a problem
Rheumatic fever etiology
post-strep condition (3 weeks later) - autoimmune condition with fever, polyarthritis, and inflammation of the heart leading to permanent deformations
At risk groups for rheumatic fever
children 6-15
Rheumatic fever diagnosis
clinical features (triad of fever, polyarthritis, inflammation of heart) with IgM anti-streptolysin O antibody - no bacteremia
Rheumatic fever pathogenesis
autoimmune
Which types of strep are more likely to be associated with rheumatic fever?
M protein 3 and 5
What is a complication of rheumatic fever carditis?
fibrosis/calcification of endocardium with permanent valve distortion (will need antibiotics at times of likely bacteremia)
Treatment of Rheumatic fever
anti-inflammatory drugs (aspirin/steroids) - no antibacterial therapy indicated. sometimes replacement of heart valves
Rheumatic fever prevention
aggressive anti-bacterial therapy in the event of later strep infections
Dental Caries etiology
infection of viridian’s streptococci - alpha hemolytic and optochin resistant
What is the pathogenesis of dental caries?
produce high molecular weight carbohydrates that form biofilm on tooth surfaces - break down sugars to make acid that demineralizes enamel and dentin
Diagnosis of dental caries
6-monthly dental exams show early demineralization - lab testing doesn’t help because bacteria are part of normal flora in 100% of people
Virulence factors of dental caries
extracellular polysaccharides and acid (decalcifies)
Prevention of dental caries
optimal flouride concentration of drinking water during dental enamel formation - topical fluorides to tooth surfaces, low sugar diet
Complications of dental caries
pulpitis (inflammation of dental pulp tissue where the blood vessels, nerves, and connective tissue are), abscesses, cellulitis
treatment of dental caries
dental treatment to remove decalcified tissue - acute abscesses can be treated temporarily with penicillin, erythromycin, cephalosporins - dental extraction most effective
Endocarditis etiology
previous rheumatic fever leads to turbulent blood flow - any stick bacteria attach and replicate - continuous damage and persistent infection
Which bacteria normal cause endocarditis?
viridans streptococci (staph aureaus in drug users/infected IV)
Diagnosis of endocarditis
variable clinical features, cardiac exam. satellite infectious foci (splinter hemorrhages) under fingernails and conjunctiva - blood culture positive for causative organisms
Endocarditis treatment
prolonged antibiotics, replacement of heart valves
Endocarditis prevention
antibiotic coverage of dental treatment, cath, at-risk patients (prophylactic)
Periodontal disease
chronic inflammation in oral tissues that are in contact with dental plaque (early = gingivitis)
What is the pathogenesis of periodontal disease?
over years, gingiva detach from tooth creating a pocket where microorganisms proliferate - becomes deeper, alveolar bone is destroyed, mature plaque becomes calcified - eventually teeth become loose and bye
What organism is responsible for periodontal disease?
complex mix of anaerobic organisms
Diphtheria etiology
infection of the pharyngeal mucous membrane causing necrosis and membrane with respiratory obstruction
Virulence factor of diphtheria
diphtheria toxin (encoded by bacteriophage) - causes systemic muscle paralysis (including myocarditis and death)
Transmission of diptheria
air-borne droplets
Diagnosis fo diphtheria
growth of corynebacterium diphtheria on tellurite plates (gram + rods with clubbed end and internal beads) - labs = toxin or toxin gene
Diphtheria treatment and prevention
treatment: antitoxin (penicillin and erythromycin also help) prevention: diphtheria vaccine (toxoid)
Impetigo organism and site
mixture of streptococci and staphylococci on the surface of skin
Diagnosis of impetigo
clinical appearance and history - smears from pus may show gram + cocci in clumps or chains
Bullous impetigo is associated with what?
staph aureus due to exfoliatin
Treatment of mild impetigo
mupirocin ointment topically - OTC antibiotic creams less likely to be effective
Treatment of severe cases of impetigo
penicillinase-resistant penicillins (nafcillin or oxacillin) or amoxicillin with penicllinase-inhibitor, or cephalosporin
Prevention of impetigo
cover lesions and discard dressings appropriately, isolate children, no sharing shit, wash hands
How does impetigo appear?
yellow crusted skin lesions - near nostrils typically - can spread across face and appear on trunk and limbs - more common in children - ver contagious
Infected piercings/catheters etiology
entry site of foreign materials can be infected by biofilms that contain large numbers of bacteria (typically start with attachment of low-grade pathogens from the normal skin flora that stick to the foreign material
Which organism most often appears in infected piercings/catheters? Virulence factor?
staphylococcus epidermidis (attaches to nylon and plastic) - has biofilm to protect organisms from immune system
Diagnosis of infected piercing/catheter?
clincial features - lab = gram + cocci growing in clumps, catalase positive, coagulase negative, non-hemolytic
Treatment of infected piercings/catheters?
remove infected device
Prevention of infected piercings/catheters?
change all indwelling cathers, IV lines on a regular schedule - use gold or surgical stainless steel for decorative piercings - no plastic
Scabies bug
sarcoptes scabei (mite) - burrows into skin and lays eggs
Transmission of scabies
personal contact or fomites
Scabies diagnosis
clinical findings, observation of mites in skin scrapings
Scabies prevention
hygiene - change clothes and don’t share gross shit
Treatment for scabies
steroids for itching and permethrin to kill mites
Skin abscess etiology
localized collection of pus - can be deep or superficial, infected or sterile
furunculitis
abscess - superficial sweat gland or follicle infection
carbuncle
abscess - multiple abscesses fused sub-cutaneously
acne
abscess - mixed infection involving increased susceptibility of the skin to infection - small abscesses and superficial inflammation of the surface and sebaceous glands
Organism responsible for skin abscesses
staph aureus (propionobacterium acnes for acne - anaerobic)
Diagnosis of skin abscesses
clinical appearance and history - smears from pus show mixed bacterial population including some gram + shit - coagulase positive and beta hemolytic - DNAse positive, salt resistant
Treatment of skin abscesses
drain (remove all dead tissue),, mupirocin ointment for mild cases, systemic antibiotics if sever case (nafcillin or oxacillin)
Prevention of skin abscesses
public health measures - remove carriers fro ICUs, operating rooms and newborn nurseries
Scalded skin syndrome
widespread exfoliation due to a localized infection by staph aureus - exfoliation toxin causes separation between epidermal cells - usually seen in newborns
Toxic Shock syndrome
systemic immune reaction to the super-antigen toxic shock syndrome toxin or streptococcal toxic shock syndrome toxin
Erysipelas/cellulitis/necrotizing fasciitis etiology
infections beneath the surface of the skin that spread in a diffuse manner
Erysipelas
superficial
Cellulitis
deep and associated with lymphadenopathy, fever, bacteremia
Necrotizing fasciitis
starts as minor skin infection which becomes rapidly extensive - spreading through the subcutaneous fascia with widespread necrosis and gangrene of extremities
What organism is responsible for erysipelas/cellulitis/necrotizing fasciitis?
S. pyogenes
Which bacteria is termed “flesh eating bacteria”? What do that have that enables this?
necrotizing fasciitis - potent protease enzyme
Diagnosis of Erysipelas/cellulitis/necrotizing fasciitis
clinical features - cultures often negative - streptococcal therefore assumed
Treatment for erysipelas/cellultis
penicillin or cephalosporin
Treatment for necrotizing fasciitis
rapid surgical internvention, including amputation of affected limb
Surgical site infection - cause, what are symptoms similar to, and treatment
casue: staph/strep. similar to cellulitis. treatment: local excision and drainage
