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Microbio Block 1 > Neisseria, Haemophilus, & Pasteurella > Flashcards

Neisseria, Haemophilus, & Pasteurella Flashcards

1
Q

Neisseria - how many species, and which ones are human pathogens?

A

10 species in humans, 8 colonize mucosa

Pathogens: N. gonorrhoeae, N. meningitidis

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2
Q

Morphology of Neisseria spp

A

Gram neg diplococci; intracellular in neutrophils

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3
Q

Transmission of Neisseria spp

A

Non-motile = intimate contact for transmission

*Sensitive to drying = can’t be transmitted on dry contaminated toilet seat

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4
Q

Lab diagnosis of Neisseria

A

Grows on chocolate agar (fastidious growth, non-selective) & on selective Thayer Martin agar (abx + chocolate)

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5
Q

Abx on Thayer-Martin agar

A

Vancomycin, colisitin, TMP-lactate; anti-fungals nystatin & anisomycin or amphotericin B

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6
Q

What is chocolate agar?

A

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

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7
Q

Sugars oxidized by Neisseria human pathogens

A 
Gonococci = Glucose
MeninGococci = Maltose + Glucose
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8
Q

N. meningitidis important wall/membrane features

A

PS capsule* (virulence); outer membrane with porin, Opa, Rmp proteins; cytoplasmic membrane pilli

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9
Q

Most important antigens in PS capsule of N. meningitidis

A

A, B, C, W-135, Y*
Many others
No PS capsule in N. gonorrhoeae

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10
Q

Quellung reaction

A

In encapsulated bacteria, capsule swells when specific anti capsular antisera added
*SHNKSS = Strep pneumo, H. flu B, N. meningitidis, Salmonella, Kleb pneumo, GBS

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11
Q

Pilli structure

A

Originate at cytoplasmic membrane; repeating subunits (pillins) with conserved amino end and highly variable carboxyl end (PilC) = antigenic diversity

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12
Q

Pilli function

A

Virulence (attachment to nonciliated epithelial cells, resistance to neutro killing), transfer of genetic material, motility

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13
Q

Virulence of Por proteins

A

Prevent granulation of neutros (phagolysosome fusion), invasion into epithelial cells, resistance to complement-mediated serum killing
PorA,B in mening; only PorB in gonococci

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14
Q

Virulence of Opa proteins

A

Binds epithelial cells to phagocytic cells = cell-cell signaling
Causes localized disease pathogens to appear opaque on culture; advanced disease = transparent

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15
Q

Virulence of Rmp proteins

A

Reduction modifiable proteins; protects surface antigens from bactericidal antibodies

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16
Q

Why are Neisseria strictly human pathogens?

A

Compete with human hosts for iron by binding host transferrin w/ transferrin binding protein
*Different from siderophores made by other bacteria to scavenge Fe

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17
Q

LOS antigen

A

In cell wall of Neisseria, lipid A endotoxin + core oligosaccharide
*Missing the O-ag PS in LPS in most G- bacilli

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18
Q

Lipid A in Neisseria

A

Endotoxin, stimulates release of proinflam cytokines, like TNF-a
Causes acute vascular damage assc with meningococcus

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19
Q

Extracellular virulence factors of Neisseria

A

IgA1 protease - allows colonization on mucosal surfaces

Beta-lactamase - resistance to abx

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20
Q

Neisseria vaccines

A

No vaccine for gonococci

Vaccine available for meningococci (except B)

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21
Q

N. meningitidis colonization

A

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

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22
Q

Diseases caused by N. meningitidis

A

Meningitis, meningococcemia, meningococcal pneumonia

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23
Q

N. meningitidis as a cause of meningitis

A

M/c cause of acute bacterial meningitis in children

Second m/c cause in adults (S. pneumo)

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24
Q

Meningococcemia symptoms

A

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)

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25
Q

Prevalence and complications of meningococcal diseases

A

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

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26
Q

Tumbler test for meningococcal disease

A

If petechiae do not blanch when pressed with a glass, raises concern for meningococcal disease

27
Q

Bacterial latex-ag testing in CSF for N. meningitidis

A

Low sensitivity for diagnosing acute bact men; useful if individual has received prior abx

28
Q

Bacterial latex-ag testing in CSF for N. gonorrhoeae

A

No capsule - test can’t be done

29
Q

Infection control of N. meningitidis

A

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

30
Q

Populations at risk for meningococcal disease

A

Asplenia (SCD, surgical removal)

Terminal complement deficiency (6000x risk)

31
Q

N. meningitidis immunity

A

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

32
Q

2 types of meningococcal vaccines

A

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

33
Q

Who gets meningococcal vaccines?

A

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

34
Q

Where is the meningococcal belt?

A

26 countries in sub-Saharan Africa, from Senegal to Ethiopia

35
Q

Men B vaccine

A

Recommended for individuals

36
Q

How is N. gonorrhoeae transmitted?

A

1’: sexual contact
Major reservoir in infected asymptomatic person
W -> M, 20% chance
M -> W, 50% chance

37
Q

Clinical presentation of gonococcal disease in men

A

25% asymptomatic
Purulent urethral discharge 2-5d post-infxn
Rare complications: epididymitis, prostatitis, peri-urethral abscesses

38
Q

Clinical presentation of gonococcal disease in women

A

50% asymptomatic
Vaginal discharge, dysuria, abd pain
Complications in 10-20%: salpingitis, tubo-ovarian abscesses, PID, infertility

39
Q

Dx of gonococcal disease

A

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

40
Q

Tx and abx resistance of gonococcal disease

A

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

41
Q

Differences in meningococcal and gonococcal treatment regimens

A

Essentially the same: 3rd gen cephalosporin (usually ceftriaxone)
Men: 2gm IV every 12 h
Gono: 250 mg IM x1

42
Q

Gonococcal ophthalmia neonatorum

A

¼ of infants with untreated mothers -> corneal ulceration, permanent blindness
*Universal prophylaxis at birth

43
Q

Prevalence and symptoms of disseminated gonococcal infection

A

1-3% infected individuals

Skin papules -> hemorrhagic pustules, typically on extremities

44
Q

Septic gonococcal arthritis

A

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

45
Q

Typical arthritis of gonococcal disease

A

Monoarticular, migratory, asymmetric; swollen joint, painful, red

46
Q

Fitz-Hugh-Curtis syndrome

A

Adhesions bt liver capsule and parietal peritoneum = RUQ pain
Fibrosis of hepatic capsule in females, d/t gonorrhea or chlamydia

47
Q

Morphology of Haemophilus

A

Small pleomorphic gram neg bacilli (coccobacillus); facultative anaerobes, fastidious growth requiring fV (NAD) or fX (Hemin), nonmotile

48
Q

Structure of Haemophilus

A

Cell wall with LPS

PS capsule with 6 antigenic serotypes (A-F)

49
Q

Virulence factors of Haemophilus

A 
PS capsule (avoid phago)
Colonization by pilus, adhesions, IgA protease
LPS, cell wall components impair ciliary function -> damaged resp epithelium
50
Q

Other species of Haemophilus and their diseases

A

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

51
Q

H. flu type B vaccine

A 
Uses PRP (found on PS capsule) conjugated to protein
Given b/t 2-18 mos
52
Q

Transmission of Haemophilus

A

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

53
Q

Progression of dz in Haemophilus

A

Nasopharynx infxn -> bacteremia -> metastases to meninges (low mortality w treatment), and rarely: epiglottitis, cellulitis (cheek/ periorbital), arthritis (single large jt)

54
Q

Dx of Haemophilus

A

NEVER CULTURE EPIGLOTTIS
Culture: 1-2 mm opaque colonies; satellite phenomenon
*Alert lab if suspect H. ducreyi (STI)

55
Q

Satellite test

A

Streak S. aureus -> lyses RBCs, releasing NAD for Haemophilus sp.
H. flu will only grow around S. aureus on blood agar

56
Q

Tx of Haemophilus

A

Broad-spectrum ceph in severe disease
Less severe: ampicillin (30% strains resistant, check culture)
Chemoprophylaxis in kids at high risk to eliminate carriage: rifampin

57
Q

H. ducreyi disease

A

STI primarily in Africa, Asia, with cycles in US

Buboes, chancroid ulcer

58
Q

Buboes & chancroid

A

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

59
Q

Morphology of Pasteurella sp.

A

Small, facultative anaerobes, G- coccobacilli, bipolar staining

60
Q

Location and transmission of Pasteurella

A

Normal commensal in oropharynx of healthy animals; transmission by direct contact with saliva of animals (bite, scratch, lick, share food)

61
Q

Most common species of Pasteurella and animals hosting them

A

P. multocida - m/c; cats, dogs
P. canis - dogs
Others assc with animal bites but less common

62
Q

3 clinical presentations of Pasteurella

A

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

63
Q

Most common presentation of Pasteurella infection

A

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)

64
Q

Dx & tx of Pasteurella

A

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)

Microbio Block 1 (14 decks)

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