Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 3 > Meningitis > Flashcards

Meningitis Flashcards

1
Q

define meningism

A

symptom complex characterised by:

headache, photophobia, vomiting, muscle spams leading to neck rigidity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

causes of meningism

A

meningitis
sub-arachnoid haemorrhage
infection accompanied by bacteraemia
severe influenza

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

infection spread from the frontal and ethmoid sinuses may produce what?

A

abscess in the frontal lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

infection in the middle ear may spread to?

A

temporal lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What feature means that the capillaries of the brain and spinal cord are different to the rest of the vascular system? what does this cause?

A

no fenestrations and intercellular clefts

less diffusion more active transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

describe the five steps of pathogenesis in most cases of meningitis

A
  1. attachment to mucosal epithelial cells
  2. transgression of the mucosal barrier
  3. survival in the blood stream
  4. entry into CSF
  5. production of overt infection in the meninges with or without brain infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Common bacterial causes of meningitis (adults)

A

neisseria meningitis

streptococcus pneumoniae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Common bacterial causes of meningitis (neonates)

A

e. coli

group B strep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Common viral causes of meningitis

A

enteroviruses (echovirusees, parechoviruses, coxsackie A and B, polio)
Mumps
HSV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Less common causes of meningitis

A 
Haemophilus influenzae type b
listeria monocytogenes
mycobacterium tuberculosis
leptospirosis
borrelia burgdorferi (lyme disease)
mycoplasma pneumoniae
cryptococcus neoformans (in AIDS)
HIV
VZV
EBV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what organisms may produce a meningo-encephalitis?

A

enteroviruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is aseptic meningitis?

A

CSF shows excessive # lymphocytes and elevated protein but no organism is cultured

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Causes of non-infective meningitis

A 
Tumour cells in CSF
drugs 
chemicals
sarcoidosis
SLE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

meningeal infection should be considered in every patient with?

A

history of URTI + one of the meningeal symptoms of vomiting, stiff neck, headache, lethargy or clouding of consciousness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

neurological signs of meningitis

A

usually absent or minimal in CN VI, VII, VIII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

associated illness

A

recent skull trauma
alcoholism
DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

CSF microbiology tests

A 
gram stain
differential cell count
antigen detection test
bacterial culture
mycobacterial or fungal culture
PCR for viruses/bacteria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

CSF biochemistry tests

A

glucose

protien

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what will be seen in suspected DIC on blood films?

A

thrombocytopaenia
abdnormal clotting
increased fibrin degradation products

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Appearance of CSF normal

A

clear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Appearance of CSF bacterial

A

usually turbid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Appearance of CSF viral

A

clear to turbid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Appearance of CSF tuberculous meningitis

A

clear to turbid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

CSF cells normal

A

small numbers <5/mm3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

CSF cells bacterial

A

greatly increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

CSF cells viral

A

moderately increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

CSF cells tuberculous meningitis

A

moderate increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

CSF predominant cell type normal

A

lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

CSF predominant cell type bacteral

A

neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

CSF predominant cell type viral

A

lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

CSF predominant cell type tuberculous meningitis

A

lymphocyte or mixed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

CSF glucose normal

A

normal - approx 60% blood level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

CSF glucose bacterial

A

reduced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

CSF glucose viral

A

normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

CSF glucose tuberculous meningitis

A

reduced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

CSF protein normal

A

normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

CSF protein bacterial

A

greatly increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

CSF protein viral

A

moderate increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

CSF protein tuberculous meningitis

A

greatly increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what is essential in order to reduce death rate in bacterial meningitis?

A

early clinical recognition
rapid detection of pathogen
rapid initiation of appropriate bactericidal antimicrobial therapy
early recognition and treatment of sequelae of septicaemia
antibiotic prophylaxis to close contacts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

antibiotics in meningitis

A

benzylpenicillin - meninges must be inflammed, 4hrly high dose
Ceftriaxone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what bacteria causes meningococcal meningitis?

A

neisseria meningitidis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

epidemiology of meningococcal meningitis

A

children and young adults
sporadic in UK
1/2 causes in 1st 3 months of the year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

how can meningococcal meningitis organism be typed?

A

capsular polysaccharide (serogroup) and outer membrane proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what has caused the causes of meningococcal C to decreased?

A

Men C vaccine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

group A strains of meningococcal meningitis are commonly responsible for outbreaks where?

A

indian sub-continent
middle east
sub-saharan Africa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

why are polysaccharides not generally highly immunogenic?

A

similar or identical repeating sugar residues linked together and do not contain a wide variety of epitopes, as proteins usually do

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

for what strains of meningococcal are their vaccines?

A

A + C vaccine = some protection
C = very effective
B = not yet part of UK schedule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what type of organism are meningococcal meningitis?

A

gram negative diploccoi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

where can n. meningitidis be isolated from?

A

blood

petechiae or purpuric skin lesions (occasionally)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

clinical syndromes in meningococcal infection

A

meningitis

fulminant meningococcal septicaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what is fulminant meningococcal septicaemia?

A

characterised by startling suddenness of symptoms causing with rapid deterioration in consciousness, fever, septicaemic shock with renal failure, and disseminated intravascular coagulation (DIC). CSF is sterile with little or no increase in white blood cells (i.e. this syndrome is technically not meningitis), but the outcome is generally worse. FIFTY PERCENT OF THESE PATIENTS DIE WITHIN
THE FIRST 24 HOURS OF ILLNESS. For this reason, antibiotics should be given by the GP prior to hospitalisation. A purpuric rash is characteristic. This is the Waterhouse- Friedrichsen syndrome, where autopsy reveals bilateral adrenal haemorrhages with
adrenal ablation/hypoadrenalism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

why are oly 50% of children with meningococcal disease sent to hospital after the first consultation?

A

non-specific symptoms in first 4-6 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

classic feature of meningococcal disease?

A

purpuric rash

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

describe a purpuric rash

A

does not blanche on pressure

56
Q

describe chronic meningococcaemia

A

uncommon illness that may last weeks or even months with a rash (recurring every 48-72 hours), joint pains, malaise and fever, sometimes complicated by endocarditis.

57
Q

what may be related to chronic meningococcaemi

A

serum complement deficiency

58
Q

treatment of meningococcal meningitis or sepsis

A

early antipoints
GP - parenteral penicillin 3-4 MU
hospital - high dose ceftriaxone prior to LP but after blood cultures
supportive therapy

59
Q

at time of discharge a meningococcal meningitis patient should be given what and why?

A

rifampicin or ciprofloxacin (adults only) to eradicate carriage of N. meningitidis from the nasopharynx

60
Q

poor clinical prognostic factors in meningococcal septicaemia

A

delay in instigation of antibiotic therapy
extremes of age
purpuric lesions
shock with absence of signs of meningitis and hyperpyrexia (rectal temperature > 40)

61
Q

poor laboratory prognostic factors in meningococcal septicaemia

A

presence of DIC
metabolic acidosis
absence of polymorph leucocytosis

62
Q

notification and prophylaxis of meningococcal meningitis

A

all cases notified
all close contacts and the index case before discharge from hospital should recieve chemoprohylaxis with rifampicin or ciprofloxacin

63
Q

what organism causes pneumococcal meningitis?

A

streptococcus pneumoniae

64
Q

what is the most frequent cause of bacterial meningitis in adults?

A

streptococcus pneumoniae

65
Q

what are common predisposing factors for the development of pneumococcal meningitis?

A 
pneumonia
sinusitis
endocarditis
head trauma
alcoholism
splenectomy
66
Q

what type of organism as pneumococci?

A

gram +ve diplococci

alpha haemolytic

67
Q

what is an important virulence factor on pneumocci? why?

A

capsular serotype

antiphagocytic

68
Q

what is the treatment of choice for pneumococci?

A

benzylpenicillin

69
Q

where are penicillin resistant strains of pneumococci developing?

A

South Africa

Spain

70
Q

in what way are pneumococci developing resistance?

A

chromosomal change coding fro different penicillin binding proteins

71
Q

onset of symptoms in pneumococcal meningitis

A

The onset of symptoms is usually acute with
meningitis developing in 1-2 days. Patients
are more likely to have altered conscious
level or focal neurological signs than
those with haemophilus or meningococcal
meningitis. Petechiae can occur although
this is uncommon. Always look for concurrent
infection in the sinuses and ear or the
presence of skull defects, notably fractures.

72
Q

treatment of pneumococcal meningitis

A

high dose ceftriaxone

73
Q

complications of pneumococcal meningitis

A 
death - 30-50% 
loss of hearing
cranial nerve defects
hemiparesis
hydrocephalus
seizures
74
Q

what drug may reduce the complications of pneumococcal meningitis?

A

dexamethasone

75
Q

prevention of pneumococcal meningitis

A

pneumococcal vaccine - 23 common polysaccharide capsular serotypes
recommended > 65 yrs

<65 - splenectomy, DM, chronic renal disease, Cardio-resp disease, HIV

<2yrs conjugate vaccine - Prevenar, 7 common polysaccharide

76
Q

what is a common presentation of haemophilus influenzae meningitis?

A

young child

URTI followed by rapid deterioration

77
Q

signs of haemophilus influenzae meningitis

A

Antecedent symptoms of upper respiratory
tract infection and an associated otitis
media/pharyngitis are common. There are
often few signs of meningitis, with fever and
lethargy/drowsiness being more common.
Petechial spots are rare. Nuchal rigidity is
often absent. In late disease, seizures and
coma may occur. Rapid fulminant disease or a
syndrome characterised by an insidious onset
(similar to TB meningitis) may occur.

78
Q

what type of organism is haemophilus influenzae?

A

pleomorphic

mixture of gram -ve cocci and bacilli

79
Q

haemophilus influenzae with a polysaccharide capsule is often associated with what infection?

A

meningitis
epiglottitis
arthritis

80
Q

haemophilus influenzae without a polysaccharide capsule is often associated with what infection?

A

oro-pharyngeal commensals

exacerbations of COPD in adults

81
Q

why is blind therapy with amoxycillin or ampicillin no longer recommended for haemophilus influenzae?

A

10-15% produce b-lactamase

82
Q

dexamethasone has been shown to cause what in haemophilus influenzae meningitis infected patients?

A

improve survival

reduce long-term neurological sequelae

83
Q

what prophylaxis should be given to close contacts of haemophilus influenzae meningitis patients?

A

rifampicin

84
Q

describe the haemophilus influenzae b vaccine

A

The type b polysaccharide capsule is not very
immunogenic in young children unless linked
(conjugated) to a carrier protein. A variety
of suitable carrier proteins (eg, diphtheria
or tetanus toxoids, group B meningococcal
outer membrane proteins) may be used. The
conjugate Hib vaccine was introduced in 1993
in the UK and is recommended for all infants
from two months of age. Three doses should
be given, with an interval of one month
between doses.

85
Q

what type of organism is listeria monocytogenes?

A

gram +ve bacillis

86
Q

what age group are especially vulnerable to listeria monocytogenes meningitis?

A

neonates

87
Q

to cover listeria, the initial management of meningitis in adults over the age of 55 should include what?

A

IV ampicillin

88
Q

who is most likely to have tuberculous meningitis in the UK?

A

elderly men or alcoholics

89
Q

describe the clinical features of tuberculous meningitis

A

Meningitis follows rupture of a subependymal
tubercle into the subarachnoid space. In
childhood, it is usually an early post-primary
event associated with either miliary TB or
pleural effusion. In adults, at least threequarters
will have clinical evidence of
extrameningeal tuberculosis. TBM should be
considered in any patient with meningism
and low grade fever who has active extrameningeal
tuberculosis. It usually presents
subacutely with lethargy, chronic headache
and change in mentation. It may present
occasionally with an acute and severe
meningitis with unconsciousness.

90
Q

describe the investigations in tuberculous meningits

A

The CSF white cell response is mixed or
lymphocytic in nature. Only 30-40% of initial
CSF examinations are positive for acid and
alcohol fast bacilli (AAFB) on Ziehl-Neelsen
stain, but many more cases are subsequently
proven on culture. Note, that in general,
culture is a much more sensitive technique
than microscopy. The importance of repeated
lumbar punctures cannot be over-emphasised
in achieving better microbiological diagnosis.
TBM should always be considered as a
possible diagnosis if the CSF glucose is
reduced and Gram stain and conventional
culture are negative, especially in the
absence of any previous antibiotic therapy.
Chest x-ray (showing miliary TB) or CT head
scan (showing tuberculoma) may be helpful in
the diagnosis. PCR can now be used to detect
mycobacterial DNA in CSF and is available in
certain reference laboratories. Liquid culture
systems allow M.tuberculosis to grow in
10-14 days.

91
Q

treatment for tuberculous meningitis

A

as for pulmonary TB

92
Q

prognosis of tuberculous meningitis

A 
Extremes of age, duration of symptoms
(illness greater than 2 months) and the
presence of a neurological deficit are
poor prognostic markers in TBM. Resistant
organisms lead to a poor response and
increasing the drug dosage may not be
effective.
93
Q

leptospirosis and lyme disease are caused by what?

A

spirochaetes

94
Q

leptospirosis and lyme disease may cauase?

A

apparent aseptic meningitis

95
Q

what is leptospirosis caused by and how is it transmitted?

A

leptospira interrogans

animal urine

96
Q

leptospirosis is associated with what occupations?

A

farmers
abattoir workers
watersports
exposure to rats, dogs or cattle

97
Q

leptospirosis presents with?

A

septicaemic illness with fever, rigors, myalgia, vomiting, conjunctival effusion and meningism

followed by rash and hepato-renal damage

98
Q

how is diagnosis of leptospirosis made?

A

serology

99
Q

what cases lyme disease and how is it spread?

A

borrelia burgdorferi

ticks - ixodes species from an animal reservoir e.g. rodents or deer

100
Q

clinical presentation of lyme disease

A

erythema chronicum migrans

some may later develop neurological symptoms incl meningitis and peripheral or cranial (esp VII) neuropathes

101
Q

how is diagnosis of lyme disease made?

A

serology

102
Q

when in the year is viral meningitis most common?

A

late summer

early autum

103
Q

most common causes of viral meningitis

A

enterovirus esp echovirus and coxsackie

104
Q

in immunocompromised patients persistent infection with enterovirus may cause what?

A

chronic enteroviral meningitis

meningoencephalitis

105
Q

important causes of viral meingitis

A 
mumps
polio
HSV2
VZV during reactivation with or without rash
EBV - seroconversion illness HIV
106
Q

clinical presentation of viral meningitis

A

Most patients have a non-specific prodromal
illness, followed by rapid onset of headache,
photophobia, low grade fever and a stiff
neck. Patients are usually lucid and alert. If
encephalitis is also present, then lethargy,
confusion, seizures and focal neurological
signs occur. With enteroviral meningitis, a
rash may be present which, if petechial, may
resemble menincococcaemia. With mumps
meningitis, 50% do not have detectable
parotitis

107
Q

investigations in viral meningitis

A

PCR of CSF for enteroviruses, herpes
simplex, mumps and other viruses is now the
investigation of choice because it is much
more sensitive and rapid than culture. The
CSF in viral meningitis shows a lymphocytosis
with normal CSF glucose. Enteroviruses can
also be detected in throat swabs (in viral
transport medium) and from faeces, and
although their presence here does not prove
causation, testing by PCR is appropriate.
Testing for HIV should be considered,
remembering that the initial screening test
may be negative if the symptoms are part of
a seroconversion illness.

108
Q

treatment of viral meningitis

A

enterovirus + parechoviruses - usualy recover in 72 hrs
chronic infection - IV IG
HSV - aciclovir, initially IV

109
Q

prognosis of viral meningitis

A

most make complete recovery with no long-term sequelae

mumps - deafness, orchitis, testicular atrophy

110
Q

prevention of viral meningitis

A

MMR

Hand hygiene

111
Q

cause of fungal meningitis

A

cryptococal meningitis

112
Q

what yeast is the most important cause of meningitis in patients with HIV?

A

cryptococcus neoformans

113
Q

other than HIV, crytococcus neoformans may rarely cause fungal meningitis in patients with?

A

diabetes
lymphoma
those receiving immunosuppressive drugs

114
Q

where is cryptococcus neoformans found?

A

bird droppings esp pigeons

115
Q

microbiology of cryptococcus neoformans

A

The organism is a yeast which has a
polysaccharide capsule, the capsule being
visualised as a clear zone around the yeast
cell on staining with India ink. Investigation
by Gram stain shows yeast cells which are
indistinguishable from Candida sp. CSF
examination with Indian ink may demonstrate
the capsule (not present in Candida sp.), but
artefacts are easily mis-identified as capsular
yeasts, and this test should not be relied
upon in the absence of a Gram stain showing
typical yeast cells. Measurement of CSF and
serum cryptococcal polysaccharide antigen
is an important means of diagnosis, but C
neoformans grows readily on culture.

116
Q

clinical features of cryptococcal meningitis

A

Most commonly, there is a subacute onset of
symptoms with low grade fever, headache,
nausea, lethargy, confusion and abdominal
pain. Meningism is less common, although
it can develop quickly as the condition
progresses.

117
Q

treatment of cryptococcal meningitis

A

parenteral amphotericin

sometimes combination with flucytosine

118
Q

prevention of cryptococcal meningitis

A

Long term chemoprophylaxis with fluconazole is now given to patients with HIV infection following an episode of cryptococcal meningitis (secondary prophylaxis).

119
Q

how does neonatal meningitis differ from adult?

A 
1. The symptoms and signs are usually nonspecific
or not well
localised.
2. The bacteria commonly involved are
group B streptococci, E. coli and L.
monocytogenes as well as enteroviruses
and parechoviruses. Predisposing
conditions include low birth weight,
prolonged rupture of membranes and
maternal diabetes mellitus.
120
Q

incidence of neonatal meningitis in UK

A

1/2,500 births

121
Q

most common causes of neonatal meningitis

A

group b strep
e. coli
listeria monocytogenes

122
Q

group b strep are commensals where?

A

female genital tract

123
Q

what type of organism are e. coli?

A

lactose fermenting gram -ve baccili

124
Q

where is e coli found?

A

GIT

125
Q

what strains of e. coli are commonly responsible for neonatal meningitis?

A

capsulate K1

126
Q

e. coli is usually sensitive to what antibiotic?

A

cefotaxime

127
Q

group b strep are commonly sensitive to what antibiotics?

A

benzylpenicillin

amoxycillin

128
Q

in pregnant women what does listeria monocytogenes cause?

A

febrile flu-like bacteraemic illness

129
Q

in pregnancy what may listeria monocytogenes cause?

A

abortion

neonatal sepsis

130
Q

what is the treatment of choice for listeria monocytogenes?

A

ampicillin and gentamicin for 3 weeks or longer

131
Q

clinical features of early onset neonatal meningitis

A

within 3 days of birth and associated with prematurity or a difficult or prolonged birth. Marked respiratory distress, bacteraemia and a high mortality (50%) are typical. The organism has usually been acquired at birth from the mother’s genital tract.

132
Q

clinical features of late onset neonatal meningitis

A

more than one week after birth. The infection is typified by bacteraemia and meningitis but pulmonary involvement is rare. Mortality is 10-20%. The organism may have been spread by cross-infection from other mothers, babies or healthcare workers.

133
Q

diagnosis of bacterial neonatal meningitis

A

Neonatal CSF and blood cultures are central to making the diagnosis. Maternal blood cultures and cultures of specimens from the genital tract may also be helpful.

134
Q

diagnosis of viral neonatal meningitis

A

CSF, EDTA blood, faeces and nasopharyngeal secretions

135
Q

treatment of neonatal meningitis

A

Parenteral ampicillin (to cover group B streptococci and Listeria) and gentamicin or cefotaxime (to cover the gram negative bacilli) are used in combination, until the causative organism is identified. IVIG may be appropriate for enteroviruses or parechoviruses.

136
Q

prognosis of neonatal meningitis

A

Neonatal meningitis is associated with a high mortality (up to 50%) and neurological and developmental sequelae (in about 33% of the patients). Early and appropriate treatment is therefore essential.

137
Q

prevention of neonatal meningitis

A

Chemoprophylaxis to prevent neonatal Group B strep infection is given to high risk mothers during labour - usually amoxicillin or co-amoxiclav. Significant risk factors for Group B neonatal infection include preterm delivery (<37wks), a prolonged interval between membrane rupture and delivery (>18hrs), a previous infant with Group B streptococcal disease, and intrapartum fever. Screening for Group B Strep in pregnancy is recommended in the USA, but the disease is more common there and in the UK, intrapartum prophylaxis of high risk deliveries is considered sufficient.

Source isolation of neonates with enterovirus or parechovirus, if necessary by cohorting during an outbreak, and strict attention to hand hygiene are essential to prevent spread. IVIG may be appropriate for neonatal contacts.

Year 3 (164 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions