Neisseria, Haemophilus, & Pasteurella Flashcards
Neisseria - how many species, and which ones are human pathogens?
10 species in humans, 8 colonize mucosa
Pathogens: N. gonorrhoeae, N. meningitidis
Morphology of Neisseria spp
Gram neg diplococci; intracellular in neutrophils
Transmission of Neisseria spp
Non-motile = intimate contact for transmission
*Sensitive to drying = can’t be transmitted on dry contaminated toilet seat
Lab diagnosis of Neisseria
Grows on chocolate agar (fastidious growth, non-selective) & on selective Thayer Martin agar (abx + chocolate)
Abx on Thayer-Martin agar
Vancomycin, colisitin, TMP-lactate; anti-fungals nystatin & anisomycin or amphotericin B
What is chocolate agar?
Heated blood agar = deactivates enzymes that degrade NAD (f V), which is needed with hemin (f X) for fastidious growth of bacteria
Grows Haemophilus, Neisseria, Tularemia
Sugars oxidized by Neisseria human pathogens
Gonococci = Glucose MeninGococci = Maltose + Glucose
N. meningitidis important wall/membrane features
PS capsule* (virulence); outer membrane with porin, Opa, Rmp proteins; cytoplasmic membrane pilli
Most important antigens in PS capsule of N. meningitidis
A, B, C, W-135, Y*
Many others
No PS capsule in N. gonorrhoeae
Quellung reaction
In encapsulated bacteria, capsule swells when specific anti capsular antisera added
*SHNKSS = Strep pneumo, H. flu B, N. meningitidis, Salmonella, Kleb pneumo, GBS
Pilli structure
Originate at cytoplasmic membrane; repeating subunits (pillins) with conserved amino end and highly variable carboxyl end (PilC) = antigenic diversity
Pilli function
Virulence (attachment to nonciliated epithelial cells, resistance to neutro killing), transfer of genetic material, motility
Virulence of Por proteins
Prevent granulation of neutros (phagolysosome fusion), invasion into epithelial cells, resistance to complement-mediated serum killing
PorA,B in mening; only PorB in gonococci
Virulence of Opa proteins
Binds epithelial cells to phagocytic cells = cell-cell signaling
Causes localized disease pathogens to appear opaque on culture; advanced disease = transparent
Virulence of Rmp proteins
Reduction modifiable proteins; protects surface antigens from bactericidal antibodies
Why are Neisseria strictly human pathogens?
Compete with human hosts for iron by binding host transferrin w/ transferrin binding protein
*Different from siderophores made by other bacteria to scavenge Fe
LOS antigen
In cell wall of Neisseria, lipid A endotoxin + core oligosaccharide
*Missing the O-ag PS in LPS in most G- bacilli
Lipid A in Neisseria
Endotoxin, stimulates release of proinflam cytokines, like TNF-a
Causes acute vascular damage assc with meningococcus
Extracellular virulence factors of Neisseria
IgA1 protease - allows colonization on mucosal surfaces
Beta-lactamase - resistance to abx
Neisseria vaccines
No vaccine for gonococci
Vaccine available for meningococci (except B)
N. meningitidis colonization
Humans are only natural carriers; asymptomatic in 1-40% (young, crowded)
Disease more common in dry/cold months bc crowding
Carriage transient - cleared with specific IgG
Diseases caused by N. meningitidis
Meningitis, meningococcemia, meningococcal pneumonia
N. meningitidis as a cause of meningitis
M/c cause of acute bacterial meningitis in children
Second m/c cause in adults (S. pneumo)
Meningococcemia symptoms
Preceded by pharyngeal infection
Multiorgan failure w bacteremia, small blood vessel thrombosis, petechiae on trunk & lower extremities coalesce to form hemorrhagic lesions
*Waterhouse-Friderichsen syndrome (bilateral adrenal destruction)
Prevalence and complications of meningococcal diseases
1000-1200 people/y in US
W/o abx -> almost 100% fatal; w abx, 10-15% fatal
If survive: 11-19% lose limbs (thrombosis, necrosis), CNS problems (toxins and inflam), deaf, mental impairment, seizures or strokes
Tumbler test for meningococcal disease
If petechiae do not blanch when pressed with a glass, raises concern for meningococcal disease
Bacterial latex-ag testing in CSF for N. meningitidis
Low sensitivity for diagnosing acute bact men; useful if individual has received prior abx
Bacterial latex-ag testing in CSF for N. gonorrhoeae
No capsule - test can’t be done
Infection control of N. meningitidis
Transmitted by resp droplets/saliva
*Droplet precautions for first 24h abx
Chemoprophylaxis: given to close contacts with exposure to secretions w/in 24h identified; rifampin, cipro, ceftriaxone
Populations at risk for meningococcal disease
Asplenia (SCD, surgical removal)
Terminal complement deficiency (6000x risk)
N. meningitidis immunity
Passive for 6 mos of life d/t maternal Abs
Acquired d/t colonization with N. men or bact w cross-rx Ags (non-encapsulated Neisseria, E. coli K1 Ag, etc.)
Vaccine
2 types of meningococcal vaccines
Meningococcal PS vaccine MPSV4 - over 55 yoa
Men conjugate vaccine MCV4 - younger than 55, stronger immune response
Both cover A, C, Y, W-135, *NOT B
Who gets meningococcal vaccines?
Routine: 11-12 and booster at 16
High risk routine: children >2 mos w asplenia or term comp def, booster 5 y later for unvacc college freshman in dorms, travel/ residence in high-risk area, science/lab techs with routine exposure, unvacc military
*During outbreaks for high risk groups
Where is the meningococcal belt?
26 countries in sub-Saharan Africa, from Senegal to Ethiopia
Men B vaccine
Recommended for individuals
How is N. gonorrhoeae transmitted?
1’: sexual contact
Major reservoir in infected asymptomatic person
W -> M, 20% chance
M -> W, 50% chance
Clinical presentation of gonococcal disease in men
25% asymptomatic
Purulent urethral discharge 2-5d post-infxn
Rare complications: epididymitis, prostatitis, peri-urethral abscesses
Clinical presentation of gonococcal disease in women
50% asymptomatic
Vaginal discharge, dysuria, abd pain
Complications in 10-20%: salpingitis, tubo-ovarian abscesses, PID, infertility
Dx of gonococcal disease
Gram stain of discharge
NAAT: 4 hours rapid test of urine (M,W), cerv/vag (W), urethral (M); no info about abx resistance w/ NAAT
Tx and abx resistance of gonococcal disease
2007: quinolones no longer recommended (resistance in Asia -> HI -> US); 2009: ceph-resistant in Japan
Ceftriaxone IM x1 (+ azithro for Chlamydia; no oral bc resistance concerns); contact all sexual exposures in past 2m for evaluation/tx
Differences in meningococcal and gonococcal treatment regimens
Essentially the same: 3rd gen cephalosporin (usually ceftriaxone)
Men: 2gm IV every 12 h
Gono: 250 mg IM x1
Gonococcal ophthalmia neonatorum
¼ of infants with untreated mothers -> corneal ulceration, permanent blindness
*Universal prophylaxis at birth
Prevalence and symptoms of disseminated gonococcal infection
1-3% infected individuals
Skin papules -> hemorrhagic pustules, typically on extremities
Septic gonococcal arthritis
Two presentations: 1) pustular skin lesions, tenosynovitis (knees, wrists, ankles, fingers), arthralgia w/o purulent arthritis; OR 2) purulent arthritis w/o skin lesions
STD = synovitis, tenosynovitis, dermatitis
Typical arthritis of gonococcal disease
Monoarticular, migratory, asymmetric; swollen joint, painful, red
Fitz-Hugh-Curtis syndrome
Adhesions bt liver capsule and parietal peritoneum = RUQ pain
Fibrosis of hepatic capsule in females, d/t gonorrhea or chlamydia
Morphology of Haemophilus
Small pleomorphic gram neg bacilli (coccobacillus); facultative anaerobes, fastidious growth requiring fV (NAD) or fX (Hemin), nonmotile
Structure of Haemophilus
Cell wall with LPS
PS capsule with 6 antigenic serotypes (A-F)
Virulence factors of Haemophilus
PS capsule (avoid phago) Colonization by pilus, adhesions, IgA protease LPS, cell wall components impair ciliary function -> damaged resp epithelium
Other species of Haemophilus and their diseases
H. parainfluenzae & non-encapsulated H. influenzae -> upper resp tract in almost everyone w/in few mos of life
Local spread -> OM, sinusitis, bronchitis, pneumonia
Disseminated dz (rare): usually in non-vacc, d/t encapsulated H. flu type B
H. flu type B vaccine
Uses PRP (found on PS capsule) conjugated to protein Given b/t 2-18 mos
Transmission of Haemophilus
Resp droplets; droplet precautions for 24h of abx for kids w/ pneumonia d/t H. spp; standard precautions for adults
Droplet precautions if epiglottis/ meningitis
Progression of dz in Haemophilus
Nasopharynx infxn -> bacteremia -> metastases to meninges (low mortality w treatment), and rarely: epiglottitis, cellulitis (cheek/ periorbital), arthritis (single large jt)
Dx of Haemophilus
NEVER CULTURE EPIGLOTTIS
Culture: 1-2 mm opaque colonies; satellite phenomenon
*Alert lab if suspect H. ducreyi (STI)
Satellite test
Streak S. aureus -> lyses RBCs, releasing NAD for Haemophilus sp.
H. flu will only grow around S. aureus on blood agar
Tx of Haemophilus
Broad-spectrum ceph in severe disease
Less severe: ampicillin (30% strains resistant, check culture)
Chemoprophylaxis in kids at high risk to eliminate carriage: rifampin
H. ducreyi disease
STI primarily in Africa, Asia, with cycles in US
Buboes, chancroid ulcer
Buboes & chancroid
Classic for H. decreyi
Buboes: inguinal lymphadenopathy, may suppurate
Chancroid ulcer: ragged w/ raised edges, sharply demarcated without induration; purulent, dirty/gray base; base is friable
Morphology of Pasteurella sp.
Small, facultative anaerobes, G- coccobacilli, bipolar staining
Location and transmission of Pasteurella
Normal commensal in oropharynx of healthy animals; transmission by direct contact with saliva of animals (bite, scratch, lick, share food)
Most common species of Pasteurella and animals hosting them
P. multocida - m/c; cats, dogs
P. canis - dogs
Others assc with animal bites but less common
3 clinical presentations of Pasteurella
M/c: local cellulitis/ lymphadenitis after bite or scratch
Exacerbation of chronic resp dz if underlying lung dz; ? reflects colonization or oropharynx -> aspiration of oral secretions -> consolidated pneumonia; RARE
Systemic infxn in immunocompromised pts (esp underlying liver dz) -> fulminant dz w fever, rigors, vom, shock, coagulopathy; RARE
Most common presentation of Pasteurella infection
Following animal bite/scratch -> rapid inflam (1-2 h) w excruciating pain at lesion
Septic phlegmon (diffuse inflam w purulent exudate), mod-high fever +/- n/v, HA, diarrhea
Can develop septic arthritis (more common in jt replacements)
Dx & tx of Pasteurella
Grows well on blood agar, chocolate agar, poorly on MAC and other G- rod-selective media
“Mouse-like” odor
Tx: susc to many abx (not semisynthetic pens, 1st g ceph, or AGs), penicillin is DOC (often amox/clav acid; may use more broad spectrum)
