Fastidious Gram Neg Rods Flashcards
HACEK Organisms
-Haemophilus
-Aggregatibacter
-Cardiobacterium / Capnocytophage
-Eikenella
-Kingella
-Normal flora of oral cavity
-Need CO2 to grow
-Can be isolated from blood cultures
-Endocarditis
Haemophilus characteristics
-Small pleomorphic GNR
-Nonmotile
-Facultative anaerobe
-Ox+
-Cat+
-Comprise 10% of NRF
-Need X (hemin) and V (NAD) Factors
-Satellitism = growth around hemolytic Staph, Strep, or Neisseria colony bc these produce NAD
H. flu virulence factors
1) Capsule
2) IgA Protease
3) Fimbriae
4) LPS and OMP
H flu capsule
-Six serotypes (a, b, c, d, e, f) based on capsule polysaccharides
-Hib most invasive prior to vaccine
–b capsule consists of ribose, ribitol, PRP
–only subtype to NOT adhere to epis, which is why is goes systemic instead
-children have Ig from their mom until 6 months of age and then are susceptible to infection until ~ 6 years of age
H flu other antigens
-IgA protease that breaks down secretory IgA on mucosal surfaces of the resp tract
-Adherence (fimbriae) to epi cells
-LPS blocks sweeping motion or resp cillia
H flu invasive disease
-Caused by encapsulated strains
-Septicemia, meningitis, arthritis, epiglottitis, tracheitis, and pneumonia
-Post-vaccine, encapsulated c and f most likely to cause disease
1) Meningitis and bacteremia, mostly in < 6 years of age
–Inhalation->lymph nodes->bloodstream->meninges
2) Epiglottitis -> rapid onset, acute inflammation and edema -> tracheostomy needed to unobstruct airway
–Examination of the larynx can cause spasm that obstructs airway
3) Tracheitis after viral resp infection -> thick secretions after 2-7 days of mild symptoms
4) Septic arthritis - fever, pain, swelling
5) Sepsis - typically in children with no / nonfunctioning spleen
H flu noninvasive disease
-Nonencapsulated strains
-Spread via respiratory close proximity
-Conjunctivitis, sinusitis, otitis media
-Can cause pneumonia in older patients and meningitis in immunocompromised
-COPD patients prone to infection
H aegyptius
Similar to H flu but causes pinkeye
H influenzae aegyptius
Brazilian purpuric fever (BPF)
-conjunctivitis, high fever, vomiting, rash, septicemia, shock, death
-70% mortality rate w/in 48 hours
H flu invasive disease treatment
-AmpR due to plasmid
-3rd gen ceph (cefotaxime, ceftriaxone) treatment of choice
-Antibiotics cause the bacteria to lyse and secrete LPS
-“Violent immune response” that destroys neurons
-Give steroids after antibiotics
H ducreyi
-Strict human pathogen
-Chancroid Genital Ulcer Disease
-Infects mucosal epi, genital and nongential skin, regional lymph nodes
-“soft chancre”
-4-14 day incubation period then lesion with irregular edge, pus, and draining lymph nodes (buboes)
-treat w/ erythromycin, azithro, ceftriaxone, or cipro
H paraflu
Rare endocarditis 1 month after dental procedure
Haemophilus culture
1) Choc
2) Choc w/ bacitracin if resp specimen
3) Choc w/ IsoVitaleX if H aegyptius or H ducreyi
–add Vanc for H ducreyi bc resistant
–hold 4-7 days
Haemophilus ID
1) X/V factor requirements
–H flu / H haemo +/+
–H parai / H paraheamo =/+
–A. aphro =/=
–H ducreyi +/=
2) Porphyrin rxn
–convert ALA into porphyrins
–add Kovacs
–red / UV light = +
Aggregatibacter aphrophilus
-endocarditits
-found in dental plaque
-fever, heart murmur, CHF, embolism
-convex, granular colonies, yellow, opaque at center
Aggregatibacter actinomycetomcomitans
-Infection through animal bites (cattle, sheep, pig, horse)
-six serotypes
-peridontitis
–destruction of alveolar bone
-collagenase & leukotoxin
-colonies are star shaped after 48 hours
-X/V =/=
-Urease =
-3rd gen ceph, quinolones, chloram, tet
Cardiobacterium hominis
-pleomorphic, nonmotile, fastidious, GNR
-normal flora of mouth, nose, throat, GI tract
-Endocarditis after dental procedures
-large vegetations and no fever
-most likely to infect aortic valve
-gram stain looks like rosettes
-colonies pit agar
Eikenella corrodens
-mouth and gut flora
-Infectious due to trauma like bites or hitting someone in the mouth
-opportunistic
-meningitis, empyema, pneumonia, osteomyelitis, arthritis, postop tissue infection, IV drug user cellulitis (licking needle before use)
-ox+, nonmotile, cat=, yellow
-Pit agar fuzzy zone around them
-smells like bleach
Kingella
-GVCB w/ squared ends in pairs and chains (resist decolorization)
-nonmotile, ox+, cat=
-Colonize upper resp tract - tonsils
-Can grow on MTM -> use cat to differentiate between Kingella and Neisseria
-K. kingea spready corroding colony OR smooth convex B-hemo colony
-Osteoarthritis in children < 3
-Endocarditis in older children / adults
Capnocytophaga
-Normal oral flora
-Septicemia in neutropenic patients, endocarditis, juevenile periodontitis
-Fastidous, facultative anaerobe, thin fusiform GNR
-Gliding motility
-Yellow adherent colonies with moist spreading
_C canimorsus / C cyodegmi -> life threatening after dog or cat bite
-Resistant to aminoglycosides
Pasteurella
-Zoonotic -> animal bites especially cats
–do not close wound
-Cutaneous infection can become systemic
–spread to joints, bones
-GNCB w/ bipolar staining, nonmotile, facultative anaerobic
-Cat+ / ox+
-Colonies become mucoid (capsule) w/ brown/green halo
-NOT facultative intracellular
-treat with pen or doxy
Brucella
-cat B select agent
-Undulant Fever
-High risk - vets, hunters, lab workers, meat packers
-Acquired through aerosol, percutaneous, or oral route
–no lesion
–spreads to mphages, invades blood and organs
–direct contact with animals or milk products
-Rare sex or breast feeding transmission
Brucella stages
1) Acute
–fever, malaise, headache, myalgia, back pain
–w/in 8 weeks of exposure
2) Subchronic
–undulating fevers (normal in morning, high at night), arthritis, testes inflammation
–< 1 year after exposure
3) Chronic
–> 1 year after exposure
–depression, arthritis, chronic fatigue
Brucella characteristics
-small GNR
-aerobic
-nonmotile
-unencapsulated
-smooth, raised, translucent colonies on BAP
-obligate/facultative intracellular
-Ox+ / cat+ / urease +
- H2S+ using lead acetate
-BSL3!!!!!!
-2% of cases are from lab (most common lab acquired infection)
