Week 10 Flashcards
Neisseria gonorrhoeae
GNDC
-Gonococcus” or “GC” common names
-humans only host
-susceptible to lack of water (humidity) not found in the environment
-STI
-can pass mom to baby
-always a pathogen
-can cause acute pyogenic infections of vaginal, ureteral and oral epithelium
-short incubation period (2-7 days)
Gonorrhea in Males VS Women
Men
-in urethra; acute urethritis in 7 days of exposure
-purulent discharge and dysuria can lead to permanent sterility
Females
-endocervix
-discharge, dysuria and lower abdominal pain
-50% asymptomatic
-can lead to joint infections when asymp - gonococcal cervicitis - PID
-can cause sterility, ectopic pregnancy, perihepatitis (Fitz-Hugh-Curtis)
-GC 2ndary to clap trachomatis
What is Disseminated gonococcal infection
-if untreated can go to other parts of the body
-rash - dermatitis
-purulent arthritis - joint fluid culture
-endocarditis and meningitis
When disseminated it is related to the AHU strain. the GC isolate needs arginine, hypoxanthine, uracil
-meningitis in CSF
NG infections
Anorectal
Oropharyngeal
Anorectal- asymp or non specific can be discharge, rectal pain or bloody stools
Oropharyngeal- pharyngitis
-if the swab is positive then the culture will also be positive. But the swabs have to be specifically requested
All tests have to be specifically requested because throat and rectal swabs are not routinely tested for GC
What types of eye infections can you get from NG or otherwise known as GC
Ophthalmia neonatorum (newborns)
-can cause blindness
◦ Antimicrobial eyedrops (erythromycin) legally required to give
-Ocular infections (conjunctivitis) in adults
-rare in lab via eye splashes
-eye samples are not usually cultured for GC but only on request or history
What are some virulence factors for GC
-Receptors for host transferrin, capsule, IgA protease
-Pili (fimbriae) 5 types - attach, inhibit phagocytosis, exchange genetic material
-Virulent with pili 2 types in culture
-Non Virulent types 3-5
-Lipid A
-Lipooligosaccharide (LOS)
-beta lactamase enzyme
-Endo toxin - causes damage to tissues and starts inflammatory response
-Cell membrane proteins: Outer membrane protein (POR) which protect against host inflammatory response
Protein II - facilitate adherence to phagocytic and epithelial cells
Laboratory Diagnosis: Specimens for Culture for GC
Specimen of choice
Female: endocervix
Male: urethra
Endocervix swab
Urethra
Anal/rectal swab
Pharynx/throat swab
Joint fluid-Not usually from Blood culture
◦ GC inhibited by sodium polyanethol
sulfonate (anticoagulant in BC
media)
Laboratory Detection of N. gonorrhoeae
PCR based techniques
NAAT (Nucleic Acid Ampli Test )
-more sensitive than culture which detects live and dead organisms
-earlier detection- repeat if neg
-only in some regions
-combined with Clap test
-urine, urethra, cervical, and vaginal
-urine less sensitive in women
-NO AST
In men
-Mic for male urethral swabs ONLY - quick TAT and follow up with culture or NAAT
-grams need to be confirmed with culture or pcr
-Culture
specific but has a lower sensitivty than NAAT
-AST
-ANY SITE
-false neg if collected too soon
Specimen Collection for GC
-use dacron or rayon swabs because cotton and CA alginate are inhibitory
-collect the purulent discharge right on the swab and transport media should have charcoal in it to reduce toxicity
-if no discharge, swab anterior urethra and rotate
-rectal swab
-fluid collected by syringe
-Specimens for NAAT – first catch urine –transferred into specific transport media
-Swab –own transport container
-GC sensitive to drying and temp changes
-best to direct plate, incubate BEFORE transport in CO2 or use a special transport system to get to lab in 6 hours
-delays and temp changes can decrease GC recovery
JEMBEC plate
for GC
* Contains selective media
* CO2 atmosphere is produced
* Collection at Dr’s office
-use swab and cross streak with loop
What type of plates does GC need
-most fastidious of the Neisseria
-Selective & Non selective
Selective - modified Thayer-Martin (MTM), Martin-Lewis (ML), New
York City (NYC), or GC-Lect
Non selective
Chocolate agar
◦ Requires cysteine – found in chocolate (non-selective & enriched media)
Requires 3-7% CO2 (capnophiles) and humidity - more CO2
What is NYC agar
-transparent medium lysed horse blood, serum and yeast dialysate
Antibiotics
* Colistin-kills Gram -ve except Neissaria and not very active against Proteus
* Vancomycin - kills gram pos
* Amphotericin B - inhibits yeast/fungus
* Trimethoprim lactate (inhibit swarming of Proteus species)
What is Modified Thayer Martin (MTM) agar
-Chocolate agar base + enrichment (yeast extract)
-Colistin
➢Inhibits saprophytic Neisseria & GNB
➢Some GC and N. meningitidis susceptible
-Nystatin (inhibit yeast)
-Vancomycin (inhibit GPs) Trimethoprim lactate
Direct Examination (Microscopy) on male or female samples for GC
Men
Yes do a gram
-male urethral swab is diagnostic , many PMN, GNDC most being intracellular
Women
No gram because female samples are not predictive of GC other orgs in the sample look similar and youll need a culture to diagnose
grams from pharyngeal swabs are not recommended as other neisseria can be present you need to do a culture
Identification after incubation for GC
PRESUMPTIVE
-grow on selective and non selective
-size variation
-small, tan/gray translucent
-need to check for atleast 3 days because of slow growth
-do oxidase test
-on the last day checking flood the plate with oxidase reagent and subculture the positives
Methods for Identification
CULTURE-BASED for GC
ID test - Carbohydrate utilization
Need to use 2 types of tests with 2 diff principles to confirm
Conventional: (acid production)
◦ Sugars (Carbohydrates)
Chromogenic Substrate: (enzyme production)
◦ BactiCard, GonoChek
Multitest: (enzyme + biochemicals)
◦ Rapid NH
Immunoassay: (Monoclonal antibodies)
◦ GonogenII
Vitek NH card, MALDI-ToF
◦ CHO utilization
◦ *note dextrose=glucose
◦ GC uses Glucose ONLY
◦ (does not use maltose, lactose, sucrose)
how is the bacticard read
- Commercial test for the detection of preformed enzymes of Neisseria spp and Moraxella catarrhalis
. - IB: for M. catarrhalis
- BGAL: N. lactamica
- PRO: N. gonorrhoeae
- GLUT: N. meningitidis
- Limitation –must be done from
selective media
-needs a heavy inoculum
how is the Gonogen ™ II read
-needs heavy suspension
-GC is gonogen POS
-monoclonal antibody based colorimetric test
-Confirmatory identification of Neisseria gonorrhoeae.
-< 7 minutes to run
-Does not require isolated, viable or fresh cultures.
-red dot for a positive reaction = eliminates agglutination, guesswork
Susceptibility Testing for GC
-beta lactamase testing done to predict penicillin resistance
-to detect PPNG (penicillinase-producing Neisseria gonorrhoeae)
-org sent to public health for disk diffusion with specialized agar and MIC methods
YES AST - BLAC
Treatment and Prevention of GC
- contact tracing needed because you can be asymp and penicillin resistance can be seen
-safe sex, education
-report to public health
-now resistance to penicillin
Neisseria meningitidis what is it
“meningococcus” common name
-ONLY FOUND IN HUMANS
-carriers oro- or nasopharynx
-transient carriage
-anogenital flora of some people
What is the clinical significance of Neisseria meningitidis
-direct contact with carrier, exposure to infectious secretions
-carried on respiratory ducts with the primary focus of infection being on nasopharynx
-strains A-C, X, Y , W135 are associated with disease and outbreaks mostly in Canada
-Fulminant meningococcemia
(sepsis) or meningitis; meningococcemia may occur without
meningitis
report to PHL
What is the clinical significance to Neisseria meningitidis
-Meningitis -leading cause of fatal bacterial meningitis
-Can disseminate to joints, lungs, and heart valves
Septicemia (meningococcemia)
◦ Incidence highest in school-age children, adolescents and young adults
-◦ Purpura (hemorrhaging of blood into skin) with petechial rash, tachycardia, hypotension, gangrene, DIC, septic shock or hemorrhage in adrenal glands known as Waterhouse Friderichsen syndrome
What are some virulence factors for Neisseria meningitidis
-State of host is important
-PILI - needed as first step in colonization
-Capsule
types A-C can cause epidemics, Y causes pneumonia
-B is most common in Canada
-C was common until there was a vaccine
-W135 causes severe invasive disease in people older than 30
-IgA1 protease
-Lipooligosaccharide (LOS)- released after multiplication and autolysis; cause many toxic signs of systemic meningococcal disease
What is the specimen collection like for Neisseria meningitidis
-direct gram stain - NOT good for nasopharyngeal
-Intracellular and extracellular
GNDC
◦ inside or outside the PMNs
Use cytocentrifugation of CSF
(cerebrospinal fluid) to enhance
detection
What type of culture is used for Neisseria meningitidis
- same as GC but less fastidious and will grow on BA
-needs increased CO2 and humidity
-best at body temp
◦ Gray, transparent, smooth, round, convex
◦ 1-1.5 mm @ 24hrs incubation
◦ Mucoid with capsule
Identification and AST Neisseria meningitidis
GNDC
-Oxidase positive
Bacticard= GLUT +
-gonogen -neg
-acid from carb metabolism = GLU/Malt
-serology must be done
-work must be done in a BSC if isolated from invasive sample
-treatment failure is rare
-AST not usually done
-send to PHL for broth and agar
Note that Neisseria lactamica
G+M+L+ (can use ONPG)
Treatment and Prevention
Neisseria meningitidis
-vaccine with 1 dose+booster
-group B if high risk
-Contacts of primary disease
receive prophylactic antibiotic
therapy (chemoprophylaxis), or a
vaccine (immunoprophylaxis)
depending on risk level.
*Unprotected healthcare worker
*Household contact
*Airline passenger
*Shared food, cigarettes, etc.
Moraxella catarrhalis what is it
-found in RT of children and old people
-PATHOGEN causing otitis media, sinusitis , Bronchopneumonia, endocarditis, meningitis, LRTI in old people with COPD
-Bacteremia 2nd to pneumonia in
immunocompromised
What are some virulence factors for Moraxella catarhhalis
Pili - adherence to pharyngeal epithelial cell
-Presence of intracellular GNDC in respiratory specimens (sputum) may
be possible infection with M. catarrhalis
Laboratory Identification of Moraxella catarhhalis
-less fastidious than GC or meningococci
-NON SPORE FORMING NON MOTILE
-growth on BA or CHOC strict AEROBE but grows more at CO2
-grey -creamy white and raised
-FRIABLE can push like a hockey puck
-Oxidase and catalase positive
-No acid production (glucose,
maltose, lactose, sucrose
negative)
-DNase positive
-Tributyrin hydrolysis positive SAME AS BactiCard Neisseria- first well
AST
-chromogenic cephalosporin method to detect βlactamase (e.g. cefinase)
Genus Haemophilus
blood lover
Pathogenic
◦ Haemophilus influenzae
◦ H. ducreyi
Non-pathogenic or opportunistic
◦ H. parainfluenzae
◦ H. hemolyticus
◦ H. parahemolyticus
◦ H. aphrophilus
◦ Aggregatibacter sp.
General Characteristics of Genus Haemophilus
always look at CHOC plate to see if difference between the types
-GNB, pleomorphic, coccobacilli
◦ Small coccobacilli (direct smears of clinical specimen)
◦ Thin GNB (picking of colonies)
-non motile, non spore forming
-facultative ANO2
-Ferments carbs
-reduce nitrates to nitrites
- oxidase +, catalase +
-require X factor (hemin or hematin), V factor (nicotinamide adenine
dinucleotide [NAD]), or both
-sensitive to drying and cold
What is Haemophilus influenzae
-found in NF of resp tract of humans and animals
-Non-typeable (no capsule)
-serotypes by CAPSULAR AG
-◦ *Type b most virulent (HiB) – once leading cause of meningitis
Nonencapsulated strains vs
Encapsulated strains
Nonencapsulated strains
- Otitis media
- Conjunctivitis
- Bacteremia
- Pneumonia (LRTI)
- Meningitis (immunocompromised,
elderly)
Encapsulated strains
- Meningitis
- Between 3mos-6yrs: type b
- Septicemia
- Osteomyelitis
- Cellulitis in children (neck/face)
- Septic arthritis
- Pneumonia
- Epiglottitis (peak: 2-4 yrs)
- Bacteremia
Vaccine for H. influenzae type b works very well
Virulence Factors of Haemophilus influenzae
-Capsule but not all H flu has one
IgA protease
◦ Only produced by H. flu
◦ Cleave secretory IgA
Adherence by fimbriae
◦ found in nonencapsulated strains (more localized infections)
Outer membrane protein (OMP)
LPS – paralyzing effect on cilia in respiratory epithelials
B-lactamase
Cellulitis in children in Haemophilus influenzae
-deep infection of the skin, with
(systemic) symptoms such as fever and chills
-redness increases as infection spreads
What is Haemophilus parainfluenzae
-always treated as NF
-found in oral cavity
-low pathogenicity
-if there is disease itll be endocarditis but first there will be no symptoms but they will start later
-first symptom will be a month AFTER dental procedure
-MITRAL VALVE primary site of infection
Haemophilus ducreyi what is it
- HUMAN PATHOGEN
-CHANCROID - a VD
-4-14 day incubation period
◦ Highly communicable genital ulcer disease; can infect non-genital skin
◦ Lesion (soft chancre) that resembles a syphilitic chancre (hard chancre)
◦ Painful, pus forming; associated with swelling of lymph nodes in the inguinal area (buboes)
Haemophilus: Identification
-facultative anaerobe
-CHOC mostly used for incubation
-Chocolate agar with bacitracin used for selective medium also known as Haemophilus selective agar (HSA)
- Blood agar with Staph streak (CO2)- satelliting colonies
-wont see in ANO2 unless another org provides the V factor
X and V factor requirements of Haemophilus
X factor : hemoglobin degradation products hemin and hematin (X=unknown)
V factor : nicotinamide adenine dinucleotide (NAD) or coenzyme I (V=vitamin)
-both factors are present in CHOC which is why its the medium of choice
-we use horse/rabbit blood instead of sheep because Sheep RBCs release NADase which can inactivate NAD in the medium therefore no V factor
V factor also produced by
◦ some bacteria e.g. Staphylococcus aureus - hence satelliting in BA
◦ Some Yeasts
H flu needs both X and V
PARA needs only V
Ducreyi needs X
XV test
done on TSA agar or BHI plate
-look for cloud of growth
-if there is growth it is positive
-streak with 0.5McF and make a CHOC PURITY PLATE
disks
x
v
xv
ALA Porphyrin test
-test looks for the ability of the organism to convert substrate δ-aminolevulinic acid (ALA) to porphyrin, an intermediate in synthesis of X factor
◦ Porphyrin detected by UV light with 360nm wavelength (Wood’s lamp) –
fluoresces reddish-orange
◦ No fluorescence – Negative test
◦ i.e. X factor not synthesized
H. influenzae :
ALA Negative (X factor required)
as it cannot synthesize heme
H. parainfluenzae
ALA Positive (X factor not required)
H. flu: Laboratory Diagnosis
-direct gram stain then culture
-GNCB
-WEAK oxidase and catalase positive
-Requires both X and V
Direct Antigen Test
◦ antisera for direct detection of H. flu antigen in clinical specimens e.g. CSF
◦ Not considered very sensitive and specific – false positive results after vaccination
on CHOC
-Small, translucent, tan, moist, smooth
-“mousy” or “bleach-like” odor
Treatment for Haemophilus
-Amplicillin - because there was penicillin resistance because of beta lactamase production
-Beta lactamase on H flu (not para because its NF) using Nitrocefin or
acidometric methods
- Negative beta-lactamase does not rule out penicillin resistance by other
mechanisms
Fastidious Gram Negative Bacilli
Bordetella
-Bordetella pertussis – in humans only- causes pertussis, “whooping cough”
-B. parapertussis – both humans and lambs, may cause mild pertussis
-Small GNCB, nonmotile (except B. bronchiseptica), non-spore forming
-obligate aerobe - growth at body temp
-Grow well on ordinary media except B. pertussis
Bordetella pertussis
Habitat and virulence factors
-HUMANS ONLY host
-Affinity for ciliated epithelium of the respiratory tract = nasopharynx
Virulence
pertussis toxin and hemolysin; and has a capsule =Causative agent of pertussis (“whooping cough”)
Bordetella pertussis: Pathogenesis
-very contagious through respiratory droplets during the incubation period
Classic pertussis has 3 stages
Stage I: Catarrhal or Prodromal (1-2 weeks) - Cough, cold, low-grade fever
Stage II: Paroxysmal (2-4 weeks)
◦ Severe and spasmodic cough with “whoop”; absolute and lymphocytosis
Stage III: Convalescent (1-3 weeks or more)- Cough slowly subsides
Complications: Bronchopneumonia, acute encephalopathy, asphyxia followed by death
Pertussis: Prevalence in Canada
-declined since vaccination but there are still spikes every year
-part of DPT vaccine
-adults are harder to diagnose
Culture Media Pertussis
-special media for growth – unsaturated fatty acids, metal ions
toxic
Bordet-Gengou (B-G) medium with potato, glycerol, blood – made selective by adding methicillin or cephalexin- medium must be used in <5days
Regan-Lowe – horse blood, charcoal, antibiotics – lasts for 8 weeks
-incubate 35 aerobically with moisture
-on RL the colonies are shiny like mercury droplets and then turn white grey as they age
on BG agar they are hemolytic
Identification of B pertussis
Gram stain, motility, pigment, oxidase, urease
B. pertussis : small GNCB hard to stain, non-motile, oxidase
positive, urease negative.
B. parapertussis : oxidase negative,
non-motile, urease positive in 18 hours
B. bronchiseptica (rarely a human pathogen): oxidase positive, motile,
urease positive in 4 hours
Specimens/Laboratory Diagnosis for B pertussis
◦ Nasopharyngeal swab
◦ Nasopharyngeal aspirate
-done by PCR or DFA (Direct fluorescent antibody) Test
Bordetella AG in the specimen plus Specific AB with fluorescent label : Fluorescence – Positive test
Advantages - quick and detects non viable orgs
DIS- can cross react with other bordetellae, false neg can occur ahrd to read due to non specific fluorescence
Treatment of B pertussis
-Erythromycin or azithromycin
-prophylaxis for contacts
no standard treatment
-use vaccines but a failure to maintain the booster schedule can cause outbreaks. Adults can become colonized and contribute to source
Brucella where is it found
Zoonotic in people
B. abortus – in cattle
B. melitensis – in sheep, goats
B. suis – in pigs
B. canis – in dogs
Brucellosis what is it
transmission
-extremely infectious;
-level 3 for cultivation
◦eating contaminated meat
◦ Through skin, mucous membranes by contact with infected animal/ carcass
◦ Inhalation
How to reduce
-mandatory pasteurization of dairy products,
-immunization of cattle
Brucellosis
(Undulant fever, Malta fever)
Pathogenesis
◦ Obligate intracellular parasites; survive in phagocytes
◦ Circulated throughout the body by cells of the RE system
Phases: acute, chronic, convalescent
◦ Chronic recurring fever (undulant fever), chills, headache, malaise, weight loss, anorexia – organisms intermittently in blood
◦ Complications: osteomyelitis, endocarditis, lung lesions,
meningoencephalitis
Laboratory Diagnosis of Brucellosis
-Class III safety cabinet – sent to a reference lab (PHL)
-Blood – specimen of choice- during febrile period of acute illness multiple samples
◦ Automated culture systems or bi-phasic Castaneda bottle used
Other specimens: lymph node aspirate, joint fluid, urine, CSF,
liver/spleen biopsies
Brucellosis Culture
-CO2 incubation for 3 weeks at 35
-enriched media BA, CHOC best on Brucella agar-enriched with casein
-NO GROWTH ON MAC
-convex colonies
-NH
-serology with blood
-Strict aerobes, capnophilic
-some have affinity for placenta
(erythritol)
-GNCB (faintly staining)
▪ Catalase, oxidase, urea pos
▪ Nitrate to nitrites
▪ Potential bioterrorism agent
▪ Reportable to MOH
Francisella
found where
transmission
Habitat: Many wild animals, mainly
rabbits, rodents, beavers,
Francisella tularensis –
◦ human pathogenic species causing tularemia
Transmission
-low effective dose
-handling dead infected animals like rabbit
-insect vectors deerflies, ticks
-eat infected carnivores
-hunters at risk
Small pleomorphic GNB
Tularemia
Virulence Factors and Symptoms
can turn typhoidal
Virulence factors:
◦ Capsule
◦ invasive, can invade intact skin
◦ Intracellular, survives in RE cells
Symptoms:
◦ Granulomatous lesions in many organs
◦ High fever, headache
◦ Lymphadenopathy
◦ Ulcerative lesion at the site of invasion
◦ Heals poorly
◦ Pneumonia, rhabdomyolysis
◦ High mortality rate without treatment
Tularemia: Biosafety
Level 2 pathogen for clinical specimens
Level 3 for handling cultures
Preventing aerosols is important
Lab Diagnosis
Francisella
-Strict aerobe, no growth on MacConkey
-Needs a special medium,
cystine-glucose with thiamine, or charcoalyeast extract medium
(Legionella medium)
- 2-4 days, to 2 wks to grow
Identification and Treatment Francisella
Identification
◦ Small pleomorphic gncb
◦ catalase weak positive
◦ oxidase negative
◦ Serological identification from
blood specimens
◦ Direct fluorescent antibody tests
◦ Immunohistochemical staining
◦ PCR
◦ Streptomycin
Legionella
habitat
and pathogenicity
L. pneumophila causes most diseases
Habitat:
-found in nature
-aquatic environement , AC, plumbing, water cooling tower
Pathogenicity: Legionnaire’s disease
-◦ Inhibits destruction by phagocytes
Clinical Significance, Treatment
Legionella
Subacute illness – asymptomatic
Pontiac fever: fever, cough, no lung involvement
Legionnaire’s disease: high fever with pneumonia, cough with lung involvement , sporadic/epidemic, nosocomial
Extrapulmonary: bacteremia, pericarditis, cellulitis, GI/liver abscess
Laboratory Diagnosis of Legionella
erology –Serum Antibody detection
◦ 2 blood samples –initial & 4-6 weeks after
◦ IFA test -Seroconversion (increase in titre)
Direct examination
◦ DFA: not very useful, replace with PCR
Lower Respiratory Tract PCR & Culture
◦ If PCR (Real time PCR) positive, then cultured
Urine antigen test
◦ Only 1 serotype, but effective for that one
◦ acute phase sample preferred
class 2 path- sputum , bronch washings, urine .
No transport medium -inhibitory
-vortex and centrifuge
Culture for Legionella
◦ Dies very quickly so process immediately
◦ NG on ordinary media
◦ BCYE agar – buffered charcoal, yeast extract
◦ BCYE agar with antibiotics as a selective medium
-O2 incubation at 35 for 3-4 days
-colonies are smooth GLASS SHINE, and FLUORESCE blue white in UV light
-can grow between 25-43
AROBIC
MOTILE
SLENDER GNB
OXIDASE AND CATALASE POSITIVE
HACEK group and
Capnocytophaga sp
-Haemophilus aphrophilus (now called Aggregatibacter
aphrophilus)
-Aggregatibacter actinomycetemcomitans
-Cardiobacterium hominis
-Eikenella corrodens
-Kingella kingae
What are the HACEK orgs
-NF HUMAN oropharyngeal, urogenital flora
-associated with endocarditis, bacteremia, and polymicrobic
wound infections
-Slow growers; NG on MAC
-cultures can take over 2 weeks
-need enriched media
-hemin enhances recovery in culture
Haemophilus aphrophilus/paraphrophilus
fastidious
-Dental plaque, gingival scrapings
-Endocarditis; periodontal disease in teens
- V factor dependent/independent
- Small GNCB, yellow colonies opaque centre,
catalase negative
Aggregatibacter actinomycetemcomitans
-related to Haemophilus; small GNCB
-Colonies stick to agar; old colonies look like stars
Nitrate positive; negative for oxidase, catalase and urea
Cardiobacterium hominis
-Infects diseased heart valves, endocarditis
-History of dental work preceding endocarditis
-Isolated from blood cultures
- aerobic and anaerobic, (CO2 enhances growth)
-Gram variable, retains crystal violet at poles of cell; GNB
-Cells pleomorphic: “tear-drop”, “dumbbell” , “lollipop” shapes; rosette clusters or picket fence formations
Oxidase positive, negative for catalase, nitrate, urea
Eikenella corrodens
fight bite
-human bites, dental and periodontal infection, root canals, mixwed wound
Eikenella corrodens
-Facultative anaerobe, capnophile
-Pits (corrodes) agar; “bleach smell“; produce yellow pigment after extended growth
-NH
-Slender GNB or GNCB
-No carbohydrate utilization
-Oxidase positive; negative for catalase and urea
Kingella species
PLUMP GNB/GNCB in pairs and short chains
-Facultative anaerobe, NG on MAC
-B-hemolytic; pits agar
-Oxidase positive
-Negative for catalase and urea
-Osteoarthritis in children <4
-endocarditis in teens and adults
-related to poor oral hygiene
Capnocytophaga species
NORMAL ORAL FLORA
-associated also with bite wounds and oral cavities
-Gram-negative fusiform bacilli
-Gliding motility
-growth on BA and CHOC not MAC
-Colonies yellowish-tan; film around
colony
-juvenile periodontitis
-sepsis in immunosuppressed and pt with no spleen
