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):

Escherichia coli:

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


E. coli: encapsulated?

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.


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

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.


Capsular material is identical to ??
Both capsules are ??

Neisseria meningitidis group B capsule

poorly immunogenic in humans due to molecular mimicry


E. coli: EC or IC??

A facultative intracellular pathogen of macrophages and peripheral blood monocytes


E. coli incidence

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


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

The most common Gram-negative agent of ??

invasive disease in the neonate

neonatal meningitis in the US


Prophylaxis for GBS is causing ??

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


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

preterm birth


source of E. coli

isolation and ID ??

mother’s colon

simple to culture and ID


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

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.


Viral etiology causing infection and morbidity in neonates:

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


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

Mycoplasma spp
Ureaplasma urealyticum, U. parvum
Chlamydia trachomatis

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


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

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*


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

premature infants with chronic lung disease.


Mycoplasma, Ureaplasma, Chlamydia:
Pathogenesis/Clinical manifestations -- neonate, infant, young child manifest with:

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


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

Neisseria gonorrhoeae
Chlamydia trachomatis


Haemophilus influenzae, type b:

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).*


Hib virulence factors

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

Lipooligosaccharide (*LOS*) provokes meningeal inflammation.

Peptidoglycan + other wall components enhance meningeal inflammation.


Hib risk factors: SES and immune status

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).


Hib Pathogenesis

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


Hib Clinical manifestations

*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).


Hib Sequelae:

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

Septic arthritis.

Purpura fulminans can occur.


Hib dx

same as any bac meningitis


Hib tx

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)


Hib Prevention:

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

Prophylaxis with antibiotics (NOT vaccine)

Hib polysaccharide conjugate vaccine.

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