Other agents of Neonatal Meningitis and/or Encephalitis

Question 1

Escherichia coli:

Answer 1

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

Question 2

E. coli: encapsulated?

Answer 2

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.

Question 3

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

Answer 3

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.

Question 4

Capsular material is identical to ??

Both capsules are ??

Answer 4

Neisseria meningitidis group B capsule

poorly immunogenic in humans due to molecular mimicry

Question 5

E. coli: EC or IC??

Answer 5

A facultative intracellular pathogen of macrophages and peripheral blood monocytes

Question 6

E. coli incidence

Answer 6

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

Question 7

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

The most common Gram-negative agent of ??

Answer 7

invasive disease in the neonate

neonatal meningitis in the US

Question 8

Prophylaxis for GBS is causing ??

Answer 8

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

Question 9

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

Answer 9

preterm birth

Question 10

source of E. coli

isolation and ID ??

Answer 10

mother’s colon

simple to culture and ID

Question 11

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

Answer 11

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.

Question 12

Viral etiology causing infection and morbidity in neonates:

Answer 12

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

Question 13

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

Answer 13

Mycoplasma spp
Ureaplasma urealyticum, U. parvum
Chlamydia trachomatis

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

Question 14

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

Answer 14

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

Question 15

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

Answer 15

premature infants with chronic lung disease.

Question 16

Mycoplasma, Ureaplasma, Chlamydia:

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

Answer 16

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

Question 17

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

Answer 17

Neisseria gonorrhoeae

Chlamydia trachomatis

Question 18

Haemophilus influenzae, type b:

Answer 18

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).

Question 19

Hib virulence factors

Answer 19

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

Lipooligosaccharide (LOS) provokes meningeal inflammation.

Peptidoglycan + other wall components enhance meningeal inflammation.

Question 20

Hib risk factors: SES and immune status

Answer 20

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).

Question 21

Hib Pathogenesis

Answer 21

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

Question 22

Hib Clinical manifestations

Answer 22

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).

Question 23

Hib Sequelae:

Answer 23

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

Septic arthritis.

Purpura fulminans can occur.

Question 24

Hib dx

Answer 24

same as any bac meningitis

Question 25

Hib tx

Answer 25

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)

Question 26

Hib Prevention:

Answer 26

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

Prophylaxis with antibiotics (NOT vaccine)

Hib polysaccharide conjugate vaccine.