Other agents of Neonatal Meningitis and/or Encephalitis Flashcards Preview

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Flashcards in Other agents of Neonatal Meningitis and/or Encephalitis Deck (26)
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1
Q

Escherichia coli:

A

Gram-negative rod
An enteric bacteria and a coliform.
Oxidase negative

2
Q

E. coli: encapsulated?

A

YES; exopolysaccharide

Many (Over 200) serotypes of various K antigens exist.

The important virulence factor for strains causing meningitis is the K1 antigen/sialic acid residues. K1 also refers to a specific capsular serotype.

Confers serum resistance to Escherichia coli and resistance to killing by neutrophils (antiphagocytic).

K1 antigen is highly associated with severe disease and higher incidence of neurological sequelae.

3
Q

All strains of E. coli isolated from extraintestinal infections sites in humans are now designated as ??

A

extraintestinal pathogenic E. coli (ExPEC):

  • clonal and possess specific virulence factors necessary to cause disease at various non-intestinal sites
  • cause the majority of urinary tract infections (UTIs) in humans.
4
Q

Capsular material is identical to ??

Both capsules are ??

A

Neisseria meningitidis group B capsule

poorly immunogenic in humans due to molecular mimicry

5
Q

E. coli: EC or IC??

A

A facultative intracellular pathogen of macrophages and peripheral blood monocytes

6
Q

E. coli incidence

A

Incidence in the US is high (3→4,000 cases/y of invasive neonatal disease [sepsis, meningitis, neonatal enterocolitis]

7
Q

E. coli:
2nd most common agent of ??

The most common Gram-negative agent of ??

A

invasive disease in the neonate

neonatal meningitis in the US

8
Q

Prophylaxis for GBS is causing ??

A

increasing incidence of invasive disease by Gram-negative bacteria and especially E. coli K1

9
Q

There is strong association between vaginal colonization by E. coli K1→??

A

preterm birth

10
Q

source of E. coli

isolation and ID ??

A

mother’s colon

simple to culture and ID

11
Q

Additional bac etiologic agents of blood/systemic infections in the neonate (Besides S. agalactiae, L. monocytogenes, E. coli K1:

A

G- agents:

Klebsiella pneumoniae (encapsulated; K1 or K2 serotypes) causes early and late neonatal sepsis in premature infants (simple to culture and identify)

Pseudomonas aeruginosa & Klebsiella pneumoniae (VLBW infants)

G+ agents: Staphylococcus epidermidis
(CoNS) causes early neonatal sepsis and meningitis.

12
Q

Viral etiology causing infection and morbidity in neonates:

A

Cytomegalovirus [CMV],

Herpes simplex virus [HSV]) -

Human Human herpes virus-6 and –7. (HHV-6 and HHV-7)

non-polio-enterovirus infections - Neonatal sepsis (viremia).

Human papilloma virus and laryngeal warts.

Lymphocytic choriomeningitis virus

13
Q

Additional etiologic agents of organ/tissue specific infections in the neonate:

A

Mycoplasma spp
Ureaplasma urealyticum, U. parvum
Chlamydia trachomatis

closely associated with vertical transmission/during parturition, mother is often asymptomatic, newborn is not

14
Q

Ureaplasma urealyticum, U. parvum infection of the child occurs via

A

ingestion of infected amniotic fluid after agent ascends from the vaginal canal.

intrauterine bacteremia after crossing the placenta from mother’s blood.

aspiration during passage through birth canal

15
Q

Ureaplsama urealyticum, U. parvum produces respiratory infections from perinatal period → 3-y-o-age, esp. in ??

A

premature infants with chronic lung disease.

16
Q

Mycoplasma, Ureaplasma, Chlamydia:

Pathogenesis/Clinical manifestations – neonate, infant, young child manifest with:

A

bronchiolitis.
respiratory distress (pneumonia, ARDS).
cough and wheeze.

17
Q

Additional etiologic agents of organ/tissue specific infections in the neonate: eye infections

A

Neisseria gonorrhoeae

Chlamydia trachomatis

18
Q

Haemophilus influenzae, type b:

A

Gram-negative, non-motile, coccobacilli/pleomorphic rod.
Fastidious growth requirements

Meningitis is the most common and serious manifestation of systemic infection due to H. influenzae, type b (Hib).

19
Q

Hib virulence factors

A

Exopolysaccharide/Capsule (Type b, polyribose phosphate; PRP) is antiphagocytic.

Lipooligosaccharide (LOS) provokes meningeal inflammation.

Peptidoglycan + other wall components enhance meningeal inflammation.

20
Q

Hib risk factors: SES and immune status

A
SES factors:
Presence of siblings.
Crowded households.
Parental smoking.
Short duration of breast-feeding.

Persons with humoral immunodeficiencies:
Persons with IgA deficiencies
Alaskan natives and Native Americans (deficient in IgG2, IgG4).

21
Q

Hib Pathogenesis

A

In unvaccinated children: window of infection is >6 mo-age → @6-y-o-age

In vaccinated children: if child seroconverts, there is NO window of infection

22
Q

Hib Clinical manifestations

A

Meningitis:
insidious onset (important clues for diagnosis, unusual for bacterial meningitis)

Several days of mild illness (e.g., URI or ear infection – Antecedent symptoms common)
followed by deterioration (common s/s of meningitis).

23
Q

Hib Sequelae:

A

Risk (33→50%) of permanent neurologic damage, commonly hearing loss.

Septic arthritis.

Purpura fulminans can occur.

24
Q

Hib dx

A

same as any bac meningitis

25
Q

Hib tx

A

ceftriaxone + dexamethasone or other corticosteroids

Dexamethasone or other corticosteroids must be given 15 min BEFORE (or at??) start antibiotic treatment.

Use of dexamethasone in non-Hib meningitis is controversial except with S. pneumoniae meningitis in persons >17-y-o-age (i.e. use in only S. pneumo and Hib)

26
Q

Hib Prevention:

A

Prophylaxis - to decrease:
carriage rate.
incidence of disease.

Prophylaxis with antibiotics (NOT vaccine)

Hib polysaccharide conjugate vaccine.

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