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Bacteriology > Gram Negative Pyogens (Neisseria, H. Influenzae, Bordatella) > Flashcards

Gram Negative Pyogens (Neisseria, H. Influenzae, Bordatella) Flashcards

1
Q

What are the four fastidious gram negative pyogens?

A

1) Neisseria gonorrheae
2) Neisseria meningitidis
3) Haemophilus influenzae
4) Bordetella pertussis

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2
Q

What are the two pathogenic species of Neisseria?

A

1) N. gonorrhoeae
2) N. meningitides

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3
Q

Gram negative organisms cause disease primarily through their production of _____ and the resulting host _____

A

Gram negative organisms cause disease primarily through their production of ENDOTOXINS and the resulting host IMMUNE RESPONSE

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4
Q

Species of Neisseria are differentiated by their ability to _______

A

Use specific sugars for energy

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5
Q

What sugars and pH indicator are placed into a broth to help differentiate N. gonorrheae and N. meningitidis in the lab?

A

Sugars: Glucose, maltose, sucrose, and lactose

pH indicator: Phenol red

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6
Q

What sugars do N. gonorrheae and N. meningitidis ferment (use for energy)?

A

N. gonorrheae: ONLY glucose

N. meningitidis: Glucose AND maltose

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7
Q

What are the two main structural differences between N. gonorrheae and N. meningitidis?

A

Encapsulation and amount of pili

N. gonorrheae: NO capsule, A LOT of pili

N. meningitidis: Thick CAPSULE, some pili (not as many as gonorrheae)

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8
Q

How does Neisseria appear upon gram staining?

A

Gram negative

Non-motile

Diplococci

Usually in pairs

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9
Q

T/F: Neisseria is capable of surviving for long periods in the external environment

A

FALSE

This is why it must be transmitted by close or intimate contact. It dries out in the environment

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10
Q

Neisseria attach to _____ of mucosal surfaces via their pili and outer membrane surface proteins

A

Non-ciliated columnar epithelium

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11
Q

T/F Both pathogenic species of Neisseria are phagocytosed as a part of their life cycle inside the host

A

FALSE

N. gonorrheae: Actively phagocytosed by PMNs → Remains localized → Generates pus

N. meningitidis: EVADES phagocytosis (capsule) → Enters blood stream → Sepsis

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12
Q

What is the lab test that differentiates Neisseria for other organisms? How does it work?

A

Oxidase Test

1) Oxidase reagent placed on filter paper
2) Bacteria rubbed on top
3) Oxidase positive → Purple-blue (Neisseria!)
4) Oxidase negative → no color change

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13
Q

What species of Neisseria is responsible for the STI gonorrhea?

A

N. gonorrheae

Duh

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14
Q

What virulence factor of N. gonorrheae mediates attachment to other cells (sticking to a spermatozoa and moving up the female reproductive tract, e.g.)?

A

Pilin and Opa protein

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15
Q

N. gonorrheae has 3 proteins that strip _____ from transferrin, lactoferrin, and hemoglobin that is used for survival of the organism

A

Iron

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16
Q

What virulence factor of N. gonorrheae is an endotoxin with high activity that generates the pus characteristic of infection?

A

LipoOLIGOsaccharide

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17
Q

What virulence factor of N. gonorrheae is found on mucosal surfaces and protects the organism?

A

IgA1 Protease

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18
Q

What virulence factor of N. gonorrheae lends it its resistance to penicillin or other Beta-lactams?

A

Beta-lactamase

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19
Q

Neisseria gonorrheae forms micro-colonies by attaching their pilito the microvilli of epithelial cells. After formation of the micro-colony, they exhibit _____, where the pili actively extend, grab another cell, and retract, moving the micro-colony across the cell surface.

A

Twitching motility

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20
Q

T/F Women have a higher incidence of acquiring N. gonorrheae infectioTns from sexual contact

A

TRUE

The vagina and cervix have an 80% chance of infection after exposure, while the male urethra has only a 20% risk of infection after exposure

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21
Q

The majority of N. gonorrheae cases occur in 15-29 year olds, and is associated with _____ and _____

A

Sexual activity

Lack of condom use

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22
Q

What are the non-genital sites of N. gonorrheae infection?

A

Oropharynx, rectum, conjunctiva

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23
Q

T/F N. gonorrheae in non-genital and genital sites of juveniles/childres is a sign of sexual abuse.

A

TRUE

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24
Q

When infected with N. gonorrheae, males present with _____ 2 to 3 days after the sexual encounter with _____ and _____

A

Acute urethritis w/ severe dysuria and purulent dischagre

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25
Q

T/F: Most females infected with N. gonorrheae present with a cervicitis and/or urethritis.

A

FALSE

Most females infected with N. gonorrheae are asymptomatic

Females presenting with symptoms typically do have cervicitis and/or urethritis though

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26
Q

Why is there no effective vaccine against N. gonorrheae?

A

N. gonorrheae undergoes antigenic drift, changing their pili and outer membrane proteins (Opa) to avoid immune eradication

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27
Q

Neonates who acquire gonorrhea from infected mothers often present with _____. Tx?

A

Neonatal ophthalmia

Tx: Abx eye drops

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28
Q

A very small percentage of N. gonorrheae infections lead to bacteremia. What are the two characteristic features of the disseminated infection?

A

1) Painful hemorrhagic lesions on the hands
2) Septic arthritis (usually knees - can culture from pus of infected joints)

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29
Q

How can N. gonorrheae cause an ectopic pregnancy (a life threatening condition)?

A

Untreated → ascends female GU → to fallopian tubes → Inflammation damages tubal cilia → Egg isn’t pushed along normally → Egg trapped and fertilized ectopically

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30
Q

What are the symptoms of Gonorrhea?

A

2-7 Days after exposure:

Burning/itching during urination w/ thick yellowish discharge from penis or vagina

Polyuria/Increased frequency

Swelling/redness of urethral opening

Vulvar itching/burning/pain

Etc

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31
Q

What is the special agar used to culture N. gonorrheae? What components of the agar select against other organisms?

A

Thayer-Martin VCN Agar (Chocolate agar)

  • Vancomycin selects against G(+) organisms
  • Colistin selects against G(-) organisms
  • Nystatin selects against fungi

After other organisms are selected against, oxidase reagent is added to see if N. gonorrheae is there

32
Q

What test that is not a culture looks for the presence of both N. gonorrheae and Chlamydia DNA? It has largely replaced VCN/Chocolate agar

A

Nucleic acid amplification test (NAAT)

33
Q

What is the treatment of N. gonorrheae infxn? What organism is treated at the same time?

A

IM Ceftriaxone + Oral azithromycin or oral doxycycline

Azithromycin treats Chlamydia also

34
Q

What is the morphologic feature of N. meningitidis that distinguishes it from N. gonorrheae?

A

Presence of polysaccharide capsule.

Virtually indistinguishable on media/Gram staining

35
Q

What serogroup of N. meningitidis causes the majority of meningococcal disease? What forms the basis of meningococcal serogrouping in addition to group specific immunity?

A

Group D

Polysaccharide capsule tested for serogrouping and is the basis for group specific immunity

36
Q

What is the exception to the rule that meningococcal capsule serogroups confer specific immunity? Why?

A

Group B

Its sialic acid polymer is recognized as “self”, resulting in little immunity to Group B meningococci and little autoimmune damage

37
Q

There is an inverse correlation between _____ and meningococcal disease

A

Humoral immunity

High incidence in kids < 2 y/o: Immature immune systems

Decreases in incidence as they acquire antibodies thru vaccination

Small increase in incidence at about 20 y/o: Need booster/in close proximity to those without vaccination

38
Q

T/F: N. meningitidis only causes disease in a specific age group

A

FALSE

N. meningitidis causes can seriously infect humans of all ages

39
Q

How is N. meningitidis transmitted?

A

Respiratory droplets or direct contact with nasopharyngeal secretions

40
Q

After colonizing the _____, N. meningitidis invades the _____. If the patient does not have protective antibodies (not vaccinated), the organism may then get into the _____ and disseminate

A

1) Colonization of nasopharynx
2) Invasion of epithelial lining
3) No vaccination/Abs: Gets into the bloodstreat and disseminates to tissues (Meninges)

41
Q

N. meningitidis can shed its outer membrane, releasing blebs/vesicles that are rich in _____. What are the consequences of this?

A

Rich in LOS (endotoxin)

If released throughout the body, the endotoxins generate a huge cytokine response that cause a lot of problems (micro-clots, shock, e.g.)

42
Q

Meningococcemia presents as ______ that develop within 1-2 days

A

Flu-like symptoms (fatigue, vomiting, cold hands/feet, chills, severe myalgia, joint pain, pain in chest/abdomen, rapid breathing, diarrhea)

43
Q

What is the characteristic physical findings in late stage disseminated meningococcemia?

A
  • DARK PURPLE RASH that may be seen all over the body (vs. GC’s rash appearing only on the hands)
    • Appears as a trasient macular/papular rash on upper chest and face
  • Purpura from EARLY DIC COAGULATION due to septicemia forming grey-black areas on infarction
    • Progression leads rapid enlargement of lesions → ISCHEMIC NECROSIS AND GANGRENE
      • Ischemia can be focal or within entire extremity (amputate)
44
Q

Bilateral infection by N. meningitidis and necrosis of adrenal glands causing a lethal adrenal insufficiency (5-15% of pts with meningococcemia) is known as _____

A

Waterhouse-Friedrichsen Syndrome

45
Q

_____ is a medical emergency characterized by the sudden onset of fever, headdace, stiff neck, nausea, vomiting, photophobia, altered mental status due to N. meningitidis infection. How is diagnosis accomplished?

A

Meningitis

Diagnosed by lumbar puncture of purulent CSF for gram staining

46
Q

Which polyvalent meningitis vaccine is very effective in young adults, is non-conjugated, and is a freeze dried mixture?

A

MENOMUNE - MPSV4

47
Q

Which polyvalent meningitis vaccine is administered to patients who can’t make antibodies to N. meningitidis capsule, and is composed of 4 serogroups conjugated to diphtheria toxoid?

A

MENACTRA - MCV4

48
Q

Exposure prophylaxis of meningococcal meningitis is administered within 24 hours of close contact w/ infected individuals and includes _____ + _____ +/- _____

A

Oral rifampin and ciprofloxacin + parenteral ceftriaxone +/- booster shot

49
Q

The presence/absence of a _____ determines the spectrum of disease caused by H. influenzae

A

Capsule

50
Q

What diseases are caused by encapsulated/non-encapsulated H. influenzae?

A
  • Encapsulated: Meningitis, epiglottitis, cellulitis, conjunctivitis (aegyptius)
  • Non-encapsulated: Otitis media, bronchitis/bronchopneumonia
51
Q

How is H. influenzae transmitted?

A

Respiratory/droplet inhalation

52
Q

How is infection by H. influenzae prevented?

A
  • PRP conjugate vaccine
  • Rifampicin prophylaxis
53
Q

What two factors are required to grow H. influenzae in the lab? What agar has these factors?

A
  • Hemin (Factor X) + NADH (Factor Y)
  • Chocolate agar contains RBC that, when lysed, release both of these factors.
54
Q

What is the major pathogenic serotype of H. influenzae? What diseases can it cause?

A
  • Encapsulated HiB
    • Meningitis - Requires dissemination into bloodstream
      • Sx similar to those of other meningitides but with fewer petechial lesions
    • Cellulitis - local invasion of skin
    • Epiglottitis - obstructs air flow, may need cricothyrotomy
55
Q

Post infectious sequelae of HiB occur in 1/10 infected infants. What are some of them?

A
  • Blindness
  • Deafness
  • Obstructive hydrocephalus
  • Mental retardation
  • Poor reading/language skills
56
Q

What drug is used as to prevent HiB infection in immune & non-immune household members?

A

Rifampicin

57
Q

What H. influenzae biotype causes conjunctivitis?

A

Aegyptius

58
Q

If trapped in specific locations, nonencapsulated H. influenzae causes local disease such as _____ and _____

A
  • Otitis media
  • Bronchopneumonia/Bronchitis
59
Q

What is the major virulence factor of H. influenzae?

A

Capsule

60
Q

What virulence factor of H. influenzae functions in attachment?

A

Outer membrane proteins/Pili

61
Q

What virulence factor of H. influenzae is an endotoxin that causes ciliary stasis in respiratory epithelium and endotoxin shock?

A

Lipo-oligosaccharide

62
Q

What virulence factor of H. influenzae protects the organism at mucosal sites?

A

IgA-ase

63
Q

The PRP vaccine most effective against HiB is a Type B capsular antigen containing what three components?

A
  • Pentose sugars
  • Ribose
  • Ribitol phosphate
64
Q

What gram negative pyogenic organism causes whooping cough?

A

Bordatella pertussis

65
Q

What vaccine is administered to provide immunity against Whooping Cough (B. pertussis)

A

DTaP

aP = acellular pertussis

66
Q

Attachment of B. pertussis to cilia of respiratory epithelium is mediated by _____, _____, and _____

A
  • Pili
  • Filamentous hemagluttinin
  • Pertactin
67
Q

After attachment of B. pertussis to respiratory epithelium cilia, what two chemicals are made that injure the ciliated epithelium? Additional injury is from the peptidoglycan fragments of what toxin?

A
  • Pertussis toxin
  • Adenylate cyclase
  • Additional injury: Tracheal cytotoxin (TCT)
68
Q

After damage from the toxins and adenylate cyclase of B. pertussis, the mucosa is _____ and pertussis toxin _____

A
  • Mucosa is denuded without protective cilia
  • Pertussis toxin enters the bloodstream to act systemically
69
Q

The first stage of B. pertussis infection is characterized by _____ and _____.

A
  • Attachment to respiratory epithelium
  • Cold like symptoms (slight cough, runny nose, low grade fever)
70
Q

In the first stage of B. pertussis infection, the organism is slightly _____, and is responsive to _____

A
  • Slightly infectious
  • Responsive to abx (azithromycin)
71
Q

What stage of B. pertussis infection is highly infectious, with the bacteria being expelled to the environment via a productive cough that produces thick mucus?

A

Second (Catarrhal/Commuicable) stage

72
Q

The death of epithelial cells in the second/catarrhal stage of B. pertussis infection increases risk of _____

A

Secondary infection

73
Q

What stage of B. pertussis infection produces the characteristic “whooping” cough?

A

Third / Paroxysmal Stage

74
Q

T/F The second stage of B. pertussis infection is susceptible to abx (azithromycin)

A

TRUE

75
Q

What are the caracteristic features of the third stage of B. pertussis infection?

A
  • Whooping cough
  • Leukocytosis
  • Hypoglycemia
  • Unresponsive to abx
    • Danger to infant posed by inability to clear secretions and maintain nutrition
76
Q

What stage of B. pertussis infection is characterized by a diminished cough, a hypoglycemic state, and a lymphocyte count that returns to normal?

A

Fourth/Convalescent stage

77
Q

What are the consequences of the Fourth/Convalescent stage of B. pertussis infection?

A
  • Secondary bronchopneumonia
  • Acute encephalopathy
    • Convulsions/Brain damage
  • Generation of protective immunity

Bacteriology (19 decks)

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