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micro_db > Micro 9-Neisseria > Flashcards

Micro 9-Neisseria Flashcards

1
Q

Most Neisseria species are pathogenic. True/False

A

False.
•Most Neisseria spp. are normal flora of the upper respiratory tract (“commensal”)
• important pathogenic species are N. gonorrhoeae, N. meningitidis

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2
Q

Niesseria are Gram negative or positive?

A

negative

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3
Q

describe the shape of Neisseria

A

diplococci, kidney bean or coffee bean-shaped

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4
Q

Neisseriae typically are intracellular or extracellular

A

intracellular

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5
Q

Neisseria are aerobic or anaerobic?

A

Aerobic but require addition CO2 to enhance growth

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6
Q

describe the requirement for the growth of pathogenic Neisseria?

A

Pathogenic species are fastidious (i.e., they dry out very easily & die quickly when the environmental temperature drops) and require enriched media (chocolate agar) to grow (especially N. gonorrhoeae)

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7
Q

Site of colonization of Neisseria?

A
  • Commensal Neisseria species colonize the nasopharynx & oropharynx (e.g., N mucosa, N. subflava)
  • These species contribute to immunity against N. meningitidis by leading to the production of cross-reacting antibodies
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8
Q

What is the clinical significance of N meningitidis?

A
  • A common cause of community-acquired sepsis and/or meningitis
  • Associated with outbreaks and epidemics
  • Asymptomatic carriage in the nasopharynx is common, transient
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9
Q

invasive meningococcal infection is caused by strains possessing?

A

capsule

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10
Q

The incubation period of meningococcal meningitis typically is …

A

1-10 days

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11
Q

common modes of transmission of meningococcus?

A

aerosols, droplets

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12
Q

crowding is a risk factor for meningococcal infection. True/False

A

True
other environmental risk factors are:
•Travel to endemic areas
•Seasonal (dry season in African meningitis belt)

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13
Q

which patient factors predispose to invasive meningococcal infection?

A 
•Underlying conditions
–Splenectomy/hyposplenism
–HIV
–Complement (MAC-membrane attack complex) 
	or properdin deficiency
•Young age
•Acute viral respiratory infection
•Extreme fatigue
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14
Q

which serogroups of meningococcus cause most invasive disease?

A

serogroups A, B, C, W135 and Y

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15
Q

group B capsule is highly immunogenic. True/False

A

False.

Group A and C have a highly immunogenic capsule; Group B capsule is poorly immunogenic

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16
Q

what is the significance of pilli and fimbriae of meningococci?

A

help to colonize nasopharynx with adhesins and capsule

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17
Q

what is the significance of the polysaccharide capsule?

A

prevent phagocytosis

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18
Q

endotoxin of meningococci is composed of lipopolysaccharide or lipooligosaccharide?

A

lipopolysaccharide (the only bacteria with this). Part of the immunogenic outer membrane protein located behind the capsule.

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19
Q

what are the clinical features of meningococcal meningitis?

A

–Headache, fever, stiff neck, photophobia, vomiting

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20
Q

what are the clinical features of meningococcemia?

A

–Presents as sepsis
–Characteristic rash
–May occur with or without meningitis

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21
Q

outer membrane protein can be released by living bacteria. True/False.

A

True.

OMP blebs released from a living organism, and LOS from dead organisms. The only bacteria that can do this

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22
Q

what are the effects of endotoxin on the host organism?

A

–Increased vascular permeability
–Pathological vasoconstriction and vasodilatation
–Loss of thromboresistance, and activation of the coagulation system leading to DIC
–Damage to blood vessel walls leads to profound shock
•Damage to small blood vessels leads to skin lesions (rash) and thrombosis
–Myocardial dysfunction

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23
Q

meningococcemia can lead to gangrene of digits. True/False

A

True

24
Q

what are the complications of invasive Meningococcal disease?

A

•Mortality approaches 100% in untreated meningococcal meningitis
–10- 15% mortality if treated
–Long-term neurological complications in some survivors
•Septicemia: Also very high mortality (100%)
•Disseminated intravascular coagulation
•Multi-organ failure
•Bilateral adrenal hemorrhage (Waterhouse-Friderichsen syndrome)

25
Q

which antibiotics are empirical given in suspected meningococcal meningitis?

A

3rd-generation cephalosporin e.g., CEFTRIAXONE or cefotaxime
DO NOT DELAY giving appropriate antibiotics

26
Q

rash in meningococcemia is blanching or non-blanching?

A

non-blanching

27
Q

In invasive meningococcal diseases what samples need to be collected for diagnosis?

A

1) Blood cultures
2) CSF cultures
3) skin scrapings if there is rash
4) CSF PCR

28
Q

what reaction is used to differentiate N. Meningitidis and N. gonorrheae?

A

Maltose fermentation.

N. meningitidis is maltose positive, whereas N Gonorrheae is negative

29
Q

what are the measures to prevent meningococcal disease at the population level?

A

• Vaccines (conjugate vaccines)
–Serogroup C conjugate vaccine (MenC)
•Part of Irish immunization schedule since 2000
– Serogroup B conjugate vaccine (MenB)
•New to Irish immunization schedule since Oct 2016
– Serogroup A conjugate vaccine (MenAfriVac®)
•Population-level vaccination programme in Africa
– Quadrivalent (MenACWY) conjugate vaccine
•Indicated for travel (e.g. Hajj, sub-Saharan Africa)
•Part of UK immunisation schedule since 2015
Saudi Arabia: pilgrims – Haj
•Very large outbreaks of meningococcal disease in pilgrims in the 1980s and again in the 1990s
•Certification of vaccination is required by the authorities since 1988
•Saudi Arabia Ministry of Health issued specific requirements in 2000
•The current general recommendation for Hajj and Umrah: quadrivalent ACW135Y

MenAfriVac in the meningitis belt
•1996–1997: more than 250,000 cases, >25,000 deaths
•MenAfriVac® introduced 2010
•By June 2015, over 220 million people aged 1-29 vaccinated
•2014: 11,908 suspected cases reported from the 19 countries implementing enhanced surveillance

Epidemic meningococcal disease in the African Meningitis Belt
•NW Nigeria 2013 and 2014, an outbreak of IMD with a new serogroup C strain
•Niger 2014/2015 Dry Season, serogroup C outbreak, >8500 cases, and 550 deaths
•Before these outbreaks, the most recent outbreak of serogroup C infection in the Meningitis Belt was in 1979 in Burkina Faso

30
Q

what are the indications of antibiotic prophylaxis of meningococcal infection?

A

•Underlying risk: Long-term antibiotic prophylaxis
e.g., splenectomy/hyposplenism, (?? complement deficiency, HIV)
•Contacts of a case: Once-off prophylaxis
–Close contact” network
–Healthcare workers (certain circumstances)
Ciprofloxacin or rifampin are used

31
Q

what are the contact precautions to a patient with a meningococcal disease?

A

– Droplet precautions (in addition to standard precautions)
– Patient placement: ≥1m from other patients (single room ideally) for the first 24 hours of antibiotics
– Surgical mask when droplet exposure is likely i.e., within 1m of patient, suctioning, intubation, autopsy etc

32
Q

Gonorrhea is the most common sexually transmitted disease. True/False?

A

False

It is the second one (the first one is syphilis)

33
Q

N. gonorrheae can affect animals. True/False

A

False.

Only humans

34
Q

mode of transmission of N gonorrheae?

A

sexual transmission, cause infection of mucous membranes, reinfection is common due to lack of protective immunity.

35
Q

what immune defect leads to an increased risk of disseminated N. gonorrheae infection?

A

complement deficiency

36
Q

what factors help to attach N. gonorrheae to mucous membranes?

A

Pilli/fimbriae
OMPs including Lipooligosaccharides
Urethral epithelial cells contain re3ceptors for LOS

37
Q

what is the role of IgA proteases produced by N. gonorrheae?

A

cleave mucosal IgA helping to colonize mucous membranes

38
Q

what are the major contributors to the spread of the infection?

A

asymptomatic infection and antibiotic resistance

39
Q

routes of acquisition of N. gonorrheae?

A 
-Sexual Acquisition
•Mucous membranes of the lower genital tract, e.g. cervix, urethra 
•Rectum 
•Pharynx
•Disseminated infection (uncommon)

-Perinatal Acquisition
•Conjunctivitis (ophthalmia neonatorum)
•Disseminated infection (uncommon)

40
Q

what are the presentations of perinatal infection with N. gonorrheae?

A
  • Conjunctivitis (ophthalmia neonatorum)

* Disseminated infection (uncommon)

41
Q

what is the incubation period of N. gonorrheae?

A

2-7 days

42
Q

clinical manifestations of gonorrhea in males?

A
  • Urethritis
  • Epididymitis
  • Typically asymptomatic
43
Q

clinical manifestations of gonorrhea in females?

A

• Cervicitis (often asymptomatic)
• Progresses to pelvic inflammatory disease (PID) in 15%
Epididymitis or salpingitis are most likely to occur with untreated/ inadequately treated infection

44
Q

what is the common complication of untreated gonorrhea in a female?

A

-PID (pelvic inflammatory disease):
Salpingitis/ PID may lead to scarring of the Fallopian tubes which can lead to
tubal infertility
increased risk of ectopic pregnancy
Risk of tubal infertility in women increases with the number of episodes of PID
In developing countries, gonococcal PID is a frequent cause of female hospital admissions with abdominal pain and is a major cause of childlessness

45
Q

what is the typical clinical manifestation of disseminated gonorrhea?

A

Tenosynovitis
arthralgias
skin lesions (pustules)
cause septic arthritis, oral lesions.

46
Q

risk of untreated gonorrheal infection during pregnancy?

A
  • Untreated gonococcal infection in pregnancy increases the risk of preterm delivery and chorioamnionitis
  • The principal issue is the risk of transmission to the baby around the time of delivery, resulting in neonatal gonococcal infection
47
Q

the most common presentation of neonatal gonococcal infection?

A

•Ophthalmia neonatorum, purulent conjunctivitis, is by far the most common presentation
–Typically, in newborn infant (median 48h, up to 7 days)
Also can lead to disseminated infection/ septic arthritis may occur (uncommon)

48
Q

do gonorrhea treatment require laboratory confirmation or can be treated empirically?

A

can be treated empirically (ceftriaxone), but make sure to cover also chlamydia with azithromycin

49
Q

what agar is used to isolate N. gonorrheae?

A

NYC agar (New York City)

50
Q

which body sites are used to take a swab to diagnose gonorrhea?

A

urethral
cervical
rectal
pharyngeal

51
Q

do public health authorities need to be notified in diagnosed gonorrhea?

A

Yes.

Also, a partner needs to be notified

52
Q

treatment of anogenital or pharyngeal N. gonorrheae infection?

A

• Empiric therapy for anogenital/ pharyngeal gonorrhea
– Single-dose intramuscular CEFTRIAXONE
PLUS
– Single-dose oral AZITHROMYCIN
N.B Test of cure, using NAAT/PCR, should be performed two weeks later

53
Q

treatment of disseminated gonorrhea?

A

– 1-week treatment (initially with intravenous CEFTRIAXONE)

– It may be possible to rationalize once culture results are available

54
Q

what is the management of neonatal gonococcal infection?

A

Hospitalization and intravenous antibiotics
•Prophylaxis: In countries or populations with high risk or incidence, eye drops instilled in the eyes of newborn infants as prophylaxis
•The best way of preventing neonatal infection is to treat pregnant mums who have gonorrhea

55
Q

there is an effective vaccine against N. gonorrheae infection.true/False.

A

False.

No vaccine

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