Download H. influenzae

Acute Bacterial Meningitis Beyond the Neonatal Period
Etiology
The most common cause of bacterial meningitis in children 1 mo
to 12 yr of age in the USA is Neisseria meningitidis. Bacterial
meningitis
caused
by
Streptococcus
pneumoniae
and
Haemophilus influenzae type b has become much less common in
developed
countries
since
the
introduction
of
universal
immunization against these pathogens beginning at 2 mo of
ageInfection caused by S. pneumoniae or H. influenzae type b
must be considered in incompletely vaccinated individuals or
those in developing countries. Those with certain underlying
immunologic (HIV infection, IgG subclass deficiency) or anatomic
(splenic dysfunction, cochlear defects or implants) disorders also
may be at increased risk of infectioncausedbythesebacteria.
Alterations of host defense due to anatomic defects or immune
deficits also increase the risk of meningitis from less common
pathogens such as Pseudomonas aeruginosa, Staphylococcus
aureus, coagulase-negative staphylococci, Salmonella spp., and
Listeria monocytogenes .
Epidemiology
A major risk factor for meningitis is the lack of immunity to
specific pathogens associated with young age. Additional risks
include recent colonization with pathogenic bacteria, close
contact (household, daycare centers, college dormitories,
military barracks) with individuals having invasive disease
caused by N. meningitidis and H. influenzae type b, crowding,
poverty, black or Native American race, and male gender. The
mode of transmission is probably person-to-person contact
through respiratory tract secretions or droplets. The risk of
meningitis is increased among infants and young children with
occult bacteremia; the odds ratio is greater for meningococcus
(85 times) and H. influenzae type b (12 times) relative to that
for pneumococcus.
Specific host defense defects due to altered immunoglobulin
production in response to encapsulated pathogens may be
responsible for the increased risk of bacterial meningitis in
Native Americans and Eskimos. Defects of the complement
system
(C5-C8)
have
been
associated
with
recurrent
meningococcal infection, and defects of the properdin system
have been associated with a significant risk of lethal
meningococcal
disease.
Splenic
dysfunction
(sickle
cell
anemia) or asplenia (due to trauma, or congenital defect) is
associated with an increased risk of pneumococcal, H.
influenzae type b (to some extent), and, rarely, meningococcal
sepsis and meningitis. T-lymphocyte defects (congenital or
acquired
by
chemotherapy,
AIDS,
or
malignancy)
are
associated with an increased risk of L. monocytogenes
infections of the CNS.
Congenital or acquired CSF leak across a mucocutaneous
barrier, such as cranial or midline facial defects (cribriform
plate) and middle ear (stapedial foot plate) or inner ear fistulas
(oval window, internal auditory canal, cochlear aqueduct), or
CSF leakage through a rupture of the meninges due to a basal
skull fracture into the cribriform plate or paranasal sinus, is
associated with an increased risk of pneumococcal meningitis.
Lumbosacral
dermal
sinus
and
meningomyelocele
are
associated with staphylococcal and gram-negative enteric
bacterial meningitis. CSF shunt infections increase the risk of
meningitis due to staphylococci (especially coagulase-negative
species) and other low virulence bacteria that typically colonize
the skin.
Pathology and Pathophysiology
A meningeal purulent exudate of varying thickness may be
distributed around the cerebral veins, venous sinuses,
convexity of the brain, and cerebellum and in the sulci, sylvian
fissures, basal cisterns, and spinal cord. Ventriculitis with
bacteria and inflammatory cells in ventricular fluid may be
present (more often in neonates), as may subdural effusions
and, rarely, empyema. Cerebral infarction, resulting from
vascular occlusion due to inflammation, vasospasm, and
thrombosis, is a frequent sequela. Infarct size ranges from
microscopic to involvement of an entire hemisphere.
Inflammation of spinal nerves and roots produces meningeal
signs, and inflammation of the cranial nerves produces cranial
neuropathies of optic, oculomotor, facial, and auditory nerves.
Increased intracranial pressure (ICP) also produces oculomotor
nerve palsy due to the presence of temporal lobe compression
of the nerve during tentorial herniation. Abducens nerve palsy
may be a nonlocalizing sign of elevated ICP.
Increased ICP is due to cell death (cytotoxic cerebral edema),
cytokine-induced increased capillary vascular permeability
(vasogenic
cerebral
edema),
hydrostatic
pressure
(interstitial
and,
possibly,
cerebral
increased
edema)
after
obstructed reabsorption of CSF in the arachnoid villus or
obstruction of the flow of fluid from the ventricles. The
syndrome of inappropriate antidiuretic hormone secretion
(SIADH) may produce excessive water retention and potentially
increase the risk of elevated ICP.
Hydrocephalus can occur as an acute complication of
bacterial meningitis. It most often takes the form of a
communicating
hydrocephalus
Less
often,
obstructive
hydrocephalus develops.
Raised CSF protein levels are due in part to increased
vascular permeability of the blood-brain barrier and the loss of
albumin-rich fluid from the capillaries and veins traversing the
subdural space. Continued transudation may result in subdural
effusions, usually found in the later phase of acute bacterial
meningitis. Hypoglycorrhachia (reduced CSF glucose levels)
is due to decreased glucose transport by the cerebral tissue.
Damage to the cerebral cortex may be due to the focal or
diffuse effects of vascular occlusion (infarction, necrosis, lactic
acidosis),
hypoxia,
bacterial
invasion
(cerebritis),
toxic
encephalopathy (bacterial toxins), elevated ICP, ventriculitis,
and transudation (subdural effusions). These pathologic factors
result in the clinical manifestations of impaired consciousness,
seizures, cranial nerve deficits, motor and sensory deficits, and
later psychomotor retardation.
Clinical Manifestations
The onset of acute meningitis has 2 predominant patterns. The
more dramatic and, fortunately, less common presentation is
sudden onset with rapidly progressive manifestations of shock,
purpura, disseminated intravascular coagulation (DIC), and
reduced levels of consciousness often resulting in progression
to coma or death within 24 hr. More often, meningitis is
preceded by several days of fever accompanied by upper
respiratory tract or gastrointestinal symptoms, followed by
nonspecific signs of CNS infection such as increasing lethargy
and irritability.
The signs and symptoms of meningitis are related to the
nonspecific findings associated with a systemic infection and to
manifestations of meningeal irritation. Nonspecific findings
include fever, anorexia and poor feeding, headache, symptoms
of upper respiratory tract infection, myalgias, arthralgias,
tachycardia, hypotension, and various cutaneous signs, such as
petechiae, purpura, or an erythematous macular rash.
Meningeal irritation is manifested as nuchal rigidity, back pain,
Kernig sign (flexion of the hip 90 degrees with subsequent
pain with extension of the leg), and Brudzinski sign
(involuntary flexion of the knees and hips after passive flexion
of the neck while supine). In some children, particularly in
those younger than 12-18 mo, Kernig and Brudzinski signs are
not consistently present. fever, headache, and nuchal rigidity
are present in only 40% of adults with bacterial meningitis.
Increased ICP is suggested by headache, emesis, bulging
fontanel or diastasis (widening) of the sutures, oculomotor
(anisocoria, ptosis) or abducens nerve paralysis, hypertension
with bradycardia, apnea or hyperventilation, decorticate or
decerebrate posturing, stupor, coma, or signs of herniation.
Papilledema is uncommon in uncomplicated meningitis and
should suggest a more chronic process, such as the presence
of an intracranial abscess, subdural empyema, or occlusion of
a dural venous sinus. Focal neurologic signs usually are due to
vascular occlusion. Cranial neuropathies of the ocular,
oculomotor, abducens, facial, and auditory nerves may also be
due to focal inflammation. Overall, about 10-20% of children
with bacterial meningitis have focal neurologic signs.
Seizures (focal or generalized) due to cerebritis, infarction, or
electrolyte disturbances occur in 20-30% of patients with
meningitis. Seizures that occur on presentation or within the
1st 4 days of onset are usually of no prognostic significance.
Seizures that persist after the 4th day of illness and those that
are difficult to treat may be associated with a poor prognosis.
Alterations of mental status are common among patients with
meningitis and may be due to increased ICP, cerebritis, or
hypotension; manifestations include irritability, lethargy, stupor,
obtundation, and coma. Comatose patients have a poor
prognosis. Additional manifestations of meningitis include
photophobia.
Diagnosis
The diagnosis of acute pyogenic meningitis is confirmed by
analysis of the CSF, which typically reveals microorganisms on
Gram stain and culture, a neutrophilicpleocytosis, elevated
protein, and reduced glucose concentrations LP should be
performed
when
bacterial
meningitis
is
suspected.
Contraindications for an immediate LP include (1) evidence of
increased ICP (other than a bulging fontanel), such as 3rd or
6th
cranial
nerve
consciousness,
respiratory
or
palsy
with
hypertension
abnormalitie
(2)
a
depressed
and
severe
level
bradycardia
of
with
cardiopulmonary
compromise requiring prompt resuscitative measures for shock
or in patients in whom positioning for the LP would further
compromise cardiopulmonary function; and (3) infection of the
skin overlying the site of the LP. Thrombocytopenia is a relative
contraindication for LP. If an LP is delayed, empirical antibiotic
therapy should be initiated. CT scanning for evidence of a
brain abscess or increased ICP should not delay therapy. LP
may be performed after increased ICP has been treated or a
brain abscess has been excluded.
Blood cultures should be performed in all patients with
suspected meningitis. Blood cultures reveal the responsible
bacteria in up to 80-90% of cases of meningitis.
Lumbar Puncture
The CSF leukocyte count in bacterial meningitis usually is
elevated to >1,000/mm3 and, typically, there is a neutrophilic
predominance (75-95%). Turbid CSF is present when the CSF
leukocyte count exceeds 200-400/mm3. Normal healthy
neonates may have as many as 30 leukocytes/mm3 (usually
<10), but older children without viral or bacterial meningitis
have <5 leukocytes/mm3 in the CSF; in both age groups there
is a predominance of lymphocytes or monocytes.
A CSF leukocyte count <250/mm3 may be present in as many
as
20%
of
patients
with
acute
bacterial
meningitis;
pleocytosismay be absent in patients with severe overwhelming
sepsis and meningitis and is a poor prognostic sign.
Pleocytosis with a lymphocyte predominance may be present
during the early stage of acute bacterial meningitis; conversely,
neutrophilicpleocytosis may be present in patients in the early
stages of acute viral meningitis. The shift to lymphocyticmonocytic predominance in viral meningitis invariably occurs
within 8 to 24 hr of the initial LP. The Gram stain is positive in
70-90% of patients with untreated bacterial meningitis.
because 25-50% of children being evaluated for bacterial
meningitis are receiving oral antibiotics when their CSF is
obtained. CSF obtained from children with bacterial meningitis,
after the initiation of antibiotics, may be negative on Gram stain
and culture. Pleocytosis with a predominance of neutrophils,
elevated protein level, and a reduced concentration of CSF
glucose usually persist for several days after the administration of
appropriate intravenous antibiotics. Therefore, despite negative
cultures,
the
presumptive
diagnosis
of
bacterial
meningitiscanbemade.
A traumatic LP may complicate the diagnosis of meningitis.
Repeat LP at a higher interspace may produce less
hemorrhagic fluid, but this fluid usually also contains red blood
cells.
Interpretation
of
CSF
leukocytes
and
protein
concentration are affected by LPs that are traumatic, although
the Gram stain, culture, and glucose level may not be
influenced. it is prudent to rely on the bacteriologic results
rather than attempt to interpret the CSF leukocyte and protein
results of a traumatic LP.
Treatment
The therapeutic approach to patients with presumed bacterial
meningitis depends on the nature of the initial manifestations of
the illness. A child with rapidly progressing disease of less than
24 hr duration, in the absence of increased ICP, should receive
antibiotics as soon as possible after an LP is performed. If
there are signs of increased ICP or focal neurologic findings,
antibiotics should be given without performing an LP and
before obtaining a CT scan. Increased ICP should be treated
simultaneously. Immediate treatment of associated multiple
organ system failure, shock, and acute respiratory distress
syndromeisalsoindicated.
Patients who have a more protracted subacute course and
become ill over a 4-7 day period should also be evaluated for
signs of increased ICP and focal neurologic deficits. Unilateral
headache, papilledema, and other signs of increased ICP
suggest a focal lesion such as a brain or epidural abscess, or
subdural empyema. Under these circumstances, antibiotic
therapy should be initiated before LP and CT scanning. If signs
of increased ICP and/or focal neurologic signs are present, CT
scanning should be performed first to determine the safety of
performing an LP.
Initial Antibiotic Therapy
The initial (empirical) choice of therapy for meningitis in
immunocompetent infants and children is primarily influenced
by the antibiotic susceptibilities of S. pneumoniae. Selected
antibiotics should achieve bactericidal levels in the CSF. In the
USA, 25-50% of strains of S. pneumoniae are currently
resistant to penicillin; Resistance to cefotaxime and ceftriaxone
is also evident in up to 25% of isolates. In contrast, most
strains of N. meningitidis are sensitive to penicillin and
cephalosporins, although rare resistant isolates have been
reported. Approximately 30-40% of isolates of H. influenzae
type b produce β-lactamases and, therefore, are resistant to
ampicillin. These β-lactamase–producing strains are sensitive
to the extended-spectrum cephalosporins.
Based on the substantial rate of resistance of S. pneumoniae
to β-lactam drugs, vancomycin (60 mg/kg/24 hr, given every
6 hr) is recommended as part of initial empirical therapy.
Because of the efficacy of 3rd-generation cephalosporins in
the therapy of meningitis caused by sensitive S. pneumoniae,
N. meningitidis, and H. influenzae type b, cefotaxime
(200 mg/kg/24 hr,
given
every
(100 mg/kg/24 hr
administered
6 hr)
once
or
ceftriaxone
per
day
or
50 mg/kg/dose, given every 12 hr) should also be used in
initial empirical therapy. Patients allergic to β-lactam antibiotics
and >1 mo of age can be treated with chloramphenicol,
100 mg/kg/24 hr, given every 6 hr. Alternatively, patients can
be desensitized to the antibiotic.
If L. monocytogenes infection is suspected, as in young infants
or
those
with
a
T-lymphocyte
deficiency,
ampicillin
(200 mg/kg/24 hr, given every 6 hr) also should also be given
because
cephalosporins
are
inactive
against
L.
monocytogenes. Intravenous trimethoprim-sulfamethoxazole is
an alternative treatment for L. monocytogenes.
If a patient is immunocompromised and gram-negative
bacterial meningitis is suspected, initial therapy might include
ceftazidime and an aminoglycoside.
Duration of Antibiotic Therapy
Therapy for uncomplicated penicillin-sensitive S. pneumoniae
meningitis should be completed with 10 to 14 days with a 3rdgeneration
cephalosporin
or
intravenous
penicillin
(400,000 U/kg/24 hr, given every 4-6 hr). If the isolate is
resistant to penicillin and the 3rd-generation cephalosporin,
therapy should be completed with vancomycin. Intravenous
penicillin (400,000 U/kg/24 hr) for 5-7 days is the treatment of
choice
for
uncomplicated
N.
meningitidis
meningitis.
Uncomplicated H. influenzae type b meningitis should be
treated for 7-10 days. Patients who receive intravenous or oral
antibiotics before LP and who do not have an identifiable
pathogen but do have evidence of an acute bacterial infection
on the basis of their CSF profile should continue to receive
therapy with ceftriaxone or cefotaxime for 7-10 days. If focal
signs are present or the child does not respond to treatment, a
parameningeal focus may be present and a CT or MRI scan
should be performed.
A routine repeat LP is not indicated in patients with
uncomplicated
meningitis
due
to
antibiotic-sensitive
S.
pneumoniae, N. meningitidis, or H. influenzae type b. Repeat
examination of CSF is indicated in some neonates, in patients
with gram-negative bacillary meningitis, or in infection caused
by a β-lactam–resistant S. pneumoniae. The CSF should be
sterile within 24-48 hr of initiation of appropriate antibiotic
therapy.
Meningitis due to Escherichia coli or P. aeruginosa requires
therapy with a 3rd-generation cephalosporin active against the
isolate in vitro. Most isolates of E. coli are sensitive to
cefotaxime or ceftriaxone, and most isolates of P. aeruginosa
are sensitive to ceftazidime. Gram-negative bacillary meningitis
should be treated for 3 wk or for at least 2 wk after CSF
sterilization, which may occur after 2-10 days of treatment.
Side effects of antibiotic therapy of meningitis include phlebitis,
drug fever, rash, emesis, oral candidiasis, and diarrhea.
Ceftriaxone may cause reversible gallbladder pseudolithiasis,
detectable by abdominal ultrasonography. This is usually
asymptomatic but may be associated with emesis and upper
right quadrant pain.
Corticosteroids
the use of intravenous dexamethasone, 0.15 mg/kg/dose given
every 6 hr for 2 days, in the treatment of children older than
6 wk with acute bacterial meningitis caused by H. influenzae
type b. corticosteroid recipients have a shorter duration of
fever, lower CSF protein and lactate levels, and a reduction in
sensorineural hearing loss. Early treatment of adults with
bacterial meningitis, especially those with pneumococcal
meningitis, resultsinimprovedoutcome.
Corticosteroids appear to have maximum benefit if given 1-2 hr
before antibiotics are initiated. They also may be effective if
given concurrently with or soon after the 1st dose of antibiotics.
Complications
bleeding,
of
corticosteroids
hypertension,
include
hyperglycemia,
gastrointestinal
leukocytosis,
and
rebound fever after the last dose.
Glycerol
Glycerol increases plasma osmolality, reducing CNS edema
and enhancing cerebral circulation. glycerol appeared to reduce
the incidence of severe neurologic sequelae, including
blindness, hydrocephalus requiring shunt placement, severe
psychomotor retardation, quadriparesis, and quadriplegia, in
children with bacterial meningitis. Because it is safe,
inexpensive,
available,
easy
to
store,
and
has
oral
administration, it may be helpful in resource-poor areas;
Supportive Care
Repeated medical and neurologic assessments of patients with
bacterial meningitis are essential to identify early signs of
cardiovascular, CNS, and metabolic complications. Pulse rate,
blood pressure, and respiratory rate should be monitored
frequently. Neurologic assessment, including pupillary reflexes,
level of consciousness, motor strength, cranial nerve signs, and
evaluation for seizures, should be made frequently in the 1st
72 hr, when the risk of neurologic complications is greatest.
Important laboratory studies include an assessment of blood
urea nitrogen; serum sodium, chloride, potassium, and
bicarbonate levels; urine output and specific gravity; complete
blood and platelet counts; and, in the presence of petechiae,
purpura, or abnormal bleeding, measures of coagulation
function (fibrinogen, prothrombin, and partial thromboplastin
times).
Patients should initially receive nothing by mouth. If a patient is
judged to be normovolemic, with normal blood pressure,
intravenous fluid administration should be restricted to one half
to two thirds of maintenance, or 800-1,000 mL/m2/24 hr, until
it can be established that increased ICP or SIADH is not
present. Fluid administration may be returned to normal
(1,500-1,700 mL/m2/24 hr) when serum sodium levels are
normal. Fluid restriction is not appropriate in the presence of
systemic hypotension because reduced blood pressure may
result in reduced cerebral perfusion pressure and CNS
ischemia. Therefore, shock must be treated aggressively to
prevent brain and other organ dysfunction (acute tubular
necrosis, acute respiratory distress syndrome). Patients with
shock, a markedly elevated ICP, coma, and refractory seizures
require intensive monitoring with central arterial and venous
access and frequent vital signs, necessitating admission to a
pediatric intensive care unit. Patients with septic shock may
require fluid resuscitation and therapy with vasoactive agents
such as dopamine and epinephrine. The goal of such therapy
in patients with meningitis is to avoid excessive increases in
ICP without compromising blood flow and oxygen delivery to
vital organs.
Neurologic
complications
include
increased
ICP
with
subsequent herniation, seizures, and an enlarging head
circumference due to a subdural effusion or hydrocephalus.
Signs of increased ICP should be treated emergently with
endotracheal intubation and hyperventilation (to maintain the
pCO2 at approximately 25 mm Hg). In addition, intravenous
furosemide (Lasix, 1 mg/kg) and mannitol (0.5-1.0 g/kg)
osmotherapy may reduce ICP (Chapter 63). Furosemide
reduces brain swelling by venodilation and diuresis without
increasing
intracranial
blood
volume,
whereas
mannitol
produces an osmolar gradient between the brain and plasma,
thus shifting fluid from the CNS to the plasma, with subsequent
excretion during an osmotic diuresis.
Seizures are common during the course of bacterial
meningitis. Immediate therapy for seizures includes intravenous
diazepam
(0.1-0.2 mg/kg/dose)
or
lorazepam
(0.05-
0.10 mg/kg/dose), and careful attention paid to the risk of
respiratory suppression. Serum glucose, calcium, and sodium
levels should be monitored. After immediate management of
seizures, patients should receive phenytoin (15-20 mg/kg
loading dose, 5 mg/kg/24 hr maintenance) to reduce the
likelihood of recurrence. Phenytoin is preferred to phenobarbital
because it produces less CNS depression and permits
assessment of a patient's level of consciousness. Serum
phenytoin levels should be monitored to maintain them in the
therapeutic range (10-20 ?g/mL).
Complications
During the treatment of meningitis, acute CNS complications
can include seizures, increased ICP, cranial nerve palsies,
stroke, cerebral or cerebellar herniation, and thrombosis of the
dural venous sinuses.
Collections of fluid in the subdural space develop in 10-30% of
patients with meningitis and are asymptomatic in 85-90% of
patients. Subdural effusions are especially common in
infants. Symptomatic subdural effusions may result in a bulging
fontanel, diastasis of sutures, enlarging head circumference,
emesis, seizures, fever, and abnormal results of cranial
transillumination. CT or MRI scanning confirms the presence of
a subdural effusion. In the presence of increased ICP or a
depressed level of consciousness, symptomatic subdural
effusion should be treated by aspiration through the open
fontanel Fever alone is not an indication for aspiration.
SIADH occurs in some patients with meningitis, resulting in
hyponatremia and reduced serum osmolality. This may
exacerbate cerebral edema or result in hyponatremic seizures
Fever associated with bacterial meningitis usually resolves
within 5-7 days of the onset of therapy. Prolonged fever (>10
days) is noted in about 10% of patients. Prolonged fever is
usually due to intercurrent viral infection, nosocomial or
secondary
bacterial
infection,
thrombophlebitis,
or
drug
reaction. Secondary fever refers to the recrudescence of
elevated temperature after an afebrile interval. Nosocomial
infections are especially important to consider in the evaluation
of these patients. Pericarditis or arthritis may occur in patients
being treated for meningitis, especially that caused by N.
meningitidis. Involvement of these sites may result either from
bacterial dissemination or from immune complex deposition. In
general, infectious pericarditis or arthritis occurs earlier in the
course of treatment than does immune-mediated disease.
Thrombocytosis, eosinophilia, and anemia may develop during
therapy for meningitis. Anemia may be due to hemolysis or
bone marrow suppression. DIC is most often associated with
the rapidly progressive pattern of presentation and is noted
most commonly in patients with shock and purpura. The
combination of endotoxemia and severe hypotension initiates
the
coagulation
cascade;
the
coexistence
of
ongoing
thrombosis may produce symmetric peripheral gangrene.
Prognosis
Appropriate antibiotic therapy and supportive care have
reduced the mortality of bacterial meningitis after the neonatal
period to <10%. The highest mortality rates are observed with
pneumococcal
meningitis.
Severe
neurodevelopmental
sequelae may occur in 10-20% of patients recovering from
bacterial meningitis, and as many as 50% have some, albeit
subtle, neurobehavioral morbidity. The prognosis is poorest
among infants younger than 6 mo and in those with high
concentrations of bacteria/bacterial products in their CSF.
Those with seizures occurring more than 4 days into therapy or
with coma or focal neurologic signs on presentation have an
increased risk of long-term sequelae. There does not appear
to be a correlation between duration of symptoms before
diagnosis of meningitis and outcome.
The most common neurologic sequelae include hearing loss,
mental retardation, recurrent seizures, delay in acquisition of
language,
visual
impairment,
and
behavioral
problems.
Sensorineural hearing loss is the most common sequela of
bacterial meningitis and, usually, is already present at the time
of initial presentation. Frequent reassessment on an outpatient
basis is indicated for patients who have a hearing deficit.
Prevention
Vaccination and antibiotic prophylaxis of susceptible at-risk
contacts represent the 2 available means of reducing the
likelihood of bacterial meningitis.
Neisseria meningitidis
Chemoprophylaxis is recommended for all close contacts of
patients with meningococcal meningitis regardless of age or
immunization status. Close contacts should be treated with
rifampin 10 mg/kg/dose every 12 hr (maximum dose of
600 mg) for 2 days as soon as possible after identification of a
case of suspected meningococcal meningitis or sepsis. Close
contacts include household, daycare center, and nursery school
contacts and health care workers who have direct exposure to
oral secretions (mouth-to-mouth resuscitation, suctioning,
intubation).
Meningococcal vaccine is recommended for high-risk children
older than 2 yr. High-risk patients include those with anatomic
or functional asplenia or deficiencies of terminal complement
proteins. Use of meningococcal vaccine should be considered
for college freshmen, especially those who live in dormitories,
Haemophilus influenzae Type B
Rifampin prophylaxis should be given to all household contacts
of patients with invasive disease caused by H. influenzae type
b, if any close family member younger than 48 mo has not
been fully immunized or if an immunocompromised person, of
any age, resides in the household. Family members should
receive rifampin prophylaxis immediately after the diagnosis is
suspected in the index case
The dose of rifampin is 20 mg/kg/24 hr (maximum dose of
600 mg) given once each day for 4 days.
Although each vaccine elicits different profiles of antibody
response in infants immunized at 2-6 mo of age, all result in
protective levels of antibody with efficacy rates against invasive
infections ranging from 70-100%. All children should be
immunized with H. influenzae type b conjugate vaccine
beginning at 2 mo of age
Streptococcus Pneumoniae
Routine administration of conjugate vaccine against S.
pneumoniae is recommended for children younger than 2 yr of
age. The initial dose is given at about 2 mo of age. Children
who are at high risk of invasive pneumococcal infections,
including those with functional or anatomic asplenia and those
with underlying immunodeficiency (such as infection with HIV,
primary
immunodeficiency,
and
those
receiving
immunosuppressive therapy) should also receive the vaccine.