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Bacteriology F > Neisseria > Flashcards

Neisseria Flashcards

1
Q

Shape, motility, aerobic/anaerobic

A
  • Kidney shaped diplococci
  • Non motile
  • Mostly aerobic (can grow in anaerobic conditions)
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2
Q

Culture medium used for neisseria

A

Specific: Mueller Hinton medium
Non specific: modified Thayer-Martin or modified chocolate agar.
They are fastidious, require 5% CO2 when incubated and need 48 hours to grow

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3
Q

Mode of transmission of Gonococci:

A

Humans are the only reservoir.
Transmitted by direct contact:
- Sexually
- Congenitally: passage of baby through infected birth canal

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4
Q

Why they can’t be transmitted by fomites?

A

Due to their high autolytic activity outside the host

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5
Q

Virulence factors of Gonococci:

A 
Pili
POR proteins
OPA proteins
LOS
Rmp
IgA1 protease
Capsule
Siderophores
Beta-lactamase
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6
Q

About pili in gonococci:

A

Antiphagocytic, attachment to human mucosal epithelium, variable antigenicity within the same bacterial cell —> different types of pili —> no specific Ab
Strains without pili will not cause disease and can be part of the transient normal flora then swept away

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7
Q

About POR proteins in gonococci:

A

Antigenic
Form pores for nutrient transfer
Less variability than pili, can be within population not in the same bacterial cell
Bacteria can have no por protein, one or two por proteins

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8
Q

About OPA proteins in gonococci:

A

Give opacity to the colonies (same for capsule), when both absent, transparent nonvirulent colonies
Antigenic
One portion within the outer membrane, the rest is exposed to the outside
Adherence of bacteria together (aggregation), adherence of bacteria intracellularly in PMN, adherence to epithelial cells
Non virulent strains: no OPA protein
Gene can be transferred to bacteria by transformation

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9
Q

About LOS in gonococci:

A

Mimic some host cell antigens
Contain sialytransferase which will transport sialic acid from host cell and expose it on LOS
Most endotoxic activity of gonococci is related to LOS

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10
Q

About Rmp in Gonococci:

A

Active only when reduced
Most stable protein, it stabilizes other variable proteins
Participate in formation of pores with por proteins
Kill bactericidal Ab in the serum

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11
Q

About IgA protease:

A

Destruction of local IgA in mucosal surfaces, so no more first line of defense

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12
Q

What’s the function of the capsule?

A

Resists phagocytosis unless Ab are present (the capsule in most cases it’s not present)

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13
Q

What will be expressed when iron supply is limited?

A

Siderophores

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14
Q

Resistance to which antibiotics is developed in gonococci?

A
  • resistance to penicillin (beta lactamase genes are found in the plasmids)
  • resistance to tetracyclins (genes are transferred from streptococci by conjugation)
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15
Q

Target of gonococci

A

Mucosal membrane (Genital tract, rectum, throat, conjunctiva) where they have receptors.

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16
Q

How bacteria penetrate through mucosal surfaces?

A

They will bind to local mucosal cells and go deeper to the sub epithelial layer between cell junctions causing a chronic inflammatory state leading to the formation of pus.

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17
Q

What’s the name of the inflammation of rectum and anus?

A

Proctitis

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18
Q

What happens if the primary infection was in the pharynx or the rectum?

A

The probability of asymptomatic infection and carriage increases

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19
Q

Local effects of gonococci infection in babies

A

Ophthalmia neonatorum

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20
Q

About ophthalmia neonatorum:

A

It’s a purulent conjunctivitis
Appear 2 to 5 days after birth, if not treated within 48 hours it can lead to irreversible blindness
Inflammation and edema are l more severe than with chlamydia (bacteria that giving similar outcome)

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21
Q

How they used to treat babies? Why they stopped doing that?

A

Silver nitrate

It was replaced with antibiotics because of its toxicity

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22
Q

Which prophylaxis is given when the mother is infected?

A

Adding tetracyclines and erythromycin as ointments in the tear sacs of the baby for few days.

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23
Q

Local infection caused by gonococci in males:

A

Gonococcal urethritis

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24
Q

What’s the incubation period?

A

2-7 days

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25
Q

Manifestations of gonococcal urethritis:

A

Symptoms are: frequent urination, dysuria, hematuria and an important pyuria.

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26
Q

How can we differentiate between gonococcal urethritis and other urethritis?

A

We can differentiate gonococcal urethritis from other types by the yellow and creamy color of discharge.

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27
Q

What happens if it is left untreated?

A

If remained untreated, it can cause urethral stricture and carriage.

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28
Q

Local infection of gonococci in females:

A

Cervicitis that can progress to urethra and vagina.
It may also progress to fallopian tubes causing salpingitis which can lead to strictures. 20% of women who have become sterile. From fallopian tubes it can progress to peritoneal cavity closing peritonitis and infect capsule of the liver leading to Fitz-Hugh-Curtis syndrome.

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29
Q

What’s pelvic inflammatory disease?

A

Abscess and pus in nearly all genital organs especially ovaries

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30
Q

Systemic infections caused by gonococci:

A
  • Skin lesions ( erythematous papules, to pustular and hemorrhagic
  • Septic arthritis
  • Endocarditis
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31
Q

Where skin lesions could be found?

A

In the extremities not in the face or the trunk

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32
Q

What are the manifestations of septic arthritis?

A

It is marked by erythema and swelling of the ankle, knee or wrist?

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33
Q

When gonococci can lead to meningitis?

A

After a bacteremia

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34
Q

From where the specimen can be taken? Can bacteria be found in skin lesions or joints?

A

The specimen is taken from pus or from blood in the case of bacteremia.
It’s difficult to find bacteria in skin lesions or joints.

35
Q

Why serology is not useful in the case of gonococcal antibodies?

A

Because of antigenic variability and because antibodies developed late in the infection.

36
Q

Why it is difficult to culture bacteria from skin lesions?

A

Since they might be present in low amounts and because they are very sensitive

37
Q

Which test is helpful in diagnosis?

A

Genetic probes, they give results within few hours.

38
Q

What’s the results of the oxidase test?

A

Oxidase positive

39
Q

What was the DOC in the past used to treat gonococcal infections and why it is not anymore used?

A

Penicillin G, resistance against it was acquired from Haemophilus species by conjugation and production of beta lactamase was encoded plasmids

40
Q

How resistance to tetracyclines was acquired by gonococci?

A

It was acquired from Streptococcus species by conjugation. Resistance genes was coded by plasmids then transfered to bacterial chromosome by transposones

41
Q

What’s the drug of choice used now for treatment of gonococcal infections?

A

IM injection of ceftriaxone with tetracycline

42
Q

Is there any vaccine?

A

No vaccine

43
Q

In which body part we can find Neisseria Meningitidis?

A

In the nasopharynx as part of our normal flora in 5 to 30% of the population

44
Q

What is the sign of the development of an epidemic of neisseria meningitides?

A

We see that the carrier rate has increased to 80% or more.

45
Q

Which speculations explain how members of the normal flora change to bacteria causing an invasive disease?

A

Long exposure to sunlight

46
Q

What increases carrier rate? How bacteria are transmitted?

A

Crowding

Transmission of the bacteria is from person to person by respiratory tract secretions

47
Q

Who are the reservoir?

A

Humans

48
Q

What is the difference between Ag of meningococci and those of gonococci?

A

Antigens of meningococci are much more stable than those of gonococci.

49
Q

How many capsular strains we have? What are the major types?

A

20

A, B, C, Y and W-125

50
Q

What are the major factors that are responsible for meningococcal disease?

A

The pili
Capsule
Endotoxic activity of LOS

51
Q

What is the function of pili?

A

Colonizing the nasopharynx

52
Q

What is the function of the capsule?

A

Inhibits phagocytosis

It’s ability for a systemic spread

53
Q

Which receptors do they attack?

A

Receptors for meningococcal pili present on the non-ciliated columnar cells of the nasopharynx

54
Q

What is responsible for the severe reaction associated with men in google disease?

A

The continuous hyperproduction of endotoxin.

55
Q

Where do bacteria colonize?

A

The nasopharynx

56
Q

Which Ab they evade and how?

A

IgA1 Ab

With IgA1 protease

57
Q

How do they cross the mucosa to enter the bloodstream?

A

Via phagocytic vacuoles of non-ciliated cells.

58
Q

What are the 2 ways of invasion of the meninges from the throat?

A
  • directly

- through the bloodstream

59
Q

Symptoms of meningitis:

A
  • Piercing headache
  • Vomiting
  • High fever which can reach 41
  • Stiff neck and back
60
Q

What is the result of the LOS endotoxic activity?

A

Thrombosis of vessels of the brain and meninges.

61
Q

Because of the piercing headache in meningitis:

A

The presence of a purulent exudate in the brain

62
Q

How endotoxic shock is caused?

A

LOS is a highly active in meningococci than in gonococci.
There is also an overproduction of bacterial surface proteins and an excessive production of fibrin split products that will cause the endotoxic shock.

63
Q

Why bactericidal Ab don’t have an effect on these bacteria?

A

Because of the capsule

64
Q

Which age group do not suffer from neisserial meningitis?

A

Children less than two years of age.

65
Q

What is the fatality rate if untreated?

A

100%

66
Q

How changes the fatality rate when it is treated?

A

It decreases to 10-15%

67
Q

Pathogenesis of meningococcal septicemia:

A

Bacteria will multiply in the bloodstream releasing their endotoxin leading to vascular necrosis and hemorrhage in skin (Petechial rash).
In severe cases there will be a vascular necrosis leading to adrenal insufficiency (Waterhouse Friderischen syndrome) along with shock, DIC, multiple organ failure and possibly death

68
Q

Which type of rashes do we see and where?

A

petechial and maculopapular rash (similar to lesions caused by gonococci)
On extremities and exterior surfaces

69
Q

What is meningococcemia?

A

Meningococcal septicemia

70
Q

Does the fatality rate decreases after treatment?

A

Even if treated it has a high fatality rate

71
Q

Steps done in diagnosis of neisseria meningitides:

A

No time for culture so blood staining or CSF specimen by lumbar puncture.

72
Q

Which type of sequelae individuals might have in case of meningitis or meningococcemia?

A

Neurological sequelae

73
Q

Drug of choice for neisseria meningitidis:

A

Penicillin G (If allergic to penicillin shift to ceftriaxone)

74
Q

Vaccine for neisseria meningitidis:

A

It’s a killed vaccine made of polysaccharides of the capsule of A, C, Y and W125.

75
Q

Where moraxella can be found in the body?

A

Part of the normal flora in the URT

We can have along with moraxella, gonococci and meningococci (as part of nasopharyngeal carriage or part of the disease)

76
Q

What causes moraxella in elderly people with background diseases?

A

In elderly people with chronic pulmonary or heart disease it can cause bronchitis or bronchopneumonia (lower respiratory tract infections that can develop into pneumonia)

77
Q

What does it cause in healthy people?

A

Sinusitis, otitis and URT infections (infection is confined to the upper area)

78
Q

They are a cause of which disease principally?

A

Non specific flu symptoms

78
Q

Where does it colonize?

A

The nasopharynx

79
Q

How does it cause disease after colonization?

A

Spreads to contiguous mucosal surfaces, releases endotoxins and stimulates inflammatory response.

79
Q

Which sugar it doesn’t use?

A

Lactose, glucose and sucrose

81
Q

Treatment for moraxella

A

It can develop resistance against beta lactam, so we do not give penicillin we give an alternative or synergistic treatment

83
Q

About acinetobacter:

A

They are found in hospitals where they are opportunistic causing nosocomial diseases

84
Q

About kingella

A

Cause bacteremia, Bone diseases and endocarditis in persons with background heart problems

Bacteriology F (16 decks)

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