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Transcript
PLAGUE
PLAGUE
Causative Agent
Yersinia pestis
Causative Agent
Yersinia
pestis
Incubation
Period
2-6 days
Incubation Period
2-6 days Period
Infectious
Throughout duration of illness (pneumonic plague is the most important infectious
Infectious
Period
form).
Throughout duration of illness (pneumonic plague is the most important infectious
form).
Transmission
Transmitted from rats by flea bites, by handling infected animal tissues, or airborne
Transmission
by aerosol from animals or humans with pneumonic plague.
Transmitted from rats by flea bites, by handling infected animal tissues, or airborne
by
aerosol from animals or humans with pneumonic plague.
Epidemiology
There are natural foci of plague infection of rodents in many parts of the world.
Epidemiology
Wild rodent plague is present in central, eastern and southern Africa, South
There
are the
natural
foci part
of plague
infection
of rodents
in many
of theInworld.
America,
western
of North
America
and in large
areasparts
of Asia.
some
Wild
rodent between
plague iswild
present
in central,
andresulting
southernin sporadic
Africa, South
areas, contact
and domestic
rats iseastern
common,
cases
America,
the western
part of North
America and in large areas of Asia. In some
of human plague
and occasional
outbreaks.
areas, contact between wild and domestic rats is common, resulting in sporadic cases
of
plague
occasional
In human
Southeast
Asia,and
Myanmar
andoutbreaks.
Vietnam report the highest number of cases.
In
Southeast
Asia, Myanmar and Vietnam report the highest number of cases.
Clinical
Features
Plague should be suspected in anyone with fever and painful lymphadenopathy who
Clinical
has been Features
to an endemic country.
Plague should be suspected in anyone with fever and painful lymphadenopathy who
has
been
an endemic
There
aretothree
principalcountry.
clinical presentations:
 Bubonic plague: initial fever, headache, myalgia followed by painful acute
There
are threelymphadenopathy
principal clinical presentations:
regional
(pathognomonic bubo), typically involving the
fever, regions.
headache,
myalgia
followed
byprogression
painful acute
 Bubonic
inguinal, plague:
axillary initial
or cervical
If left
untreated,
rapid
to
regional
lymphadenopathy
(pathognomonic
bubo),(fatality
typically
the
septicaemia
and secondary plague
pneumonia occurs
50 -involving
60%).
axillary
or occurs
cervicalwhen
regions.
If leftinvades
untreated,
rapid progression
to
 inguinal,
Septicaemic
plague:
Y. pestis
the bloodstream.
It can
septicaemia
and plague
secondary
plaguewithout
pneumonia
occurs lymphadenopathy
(fatality 50 - 60%).(primary
follow bubonic
or occurs
detectable
when Y. pestis
invades
the shock,
bloodstream.
It can
 Septicaemic
septicaemic plague:
plague).occurs
Complications
include
septic
disseminated
follow
bubonic
plague or occurs
without
detectable lymphadenopathy
(primary
intravascular
coagulation,
meningitis
and multiorgan
failure.
plague).
Complications
shock,
 septicaemic
Pneumonic plague:
the least
common butinclude
the mostseptic
dangerous
and disseminated
fatal form of
intravascular
coagulation,
meningitis
and multiorgan
the disease. It
can develop
as a complication
of failure.
septicaemic plague or be
theinhalation
least common
but the most
form
of
 Pneumonic
plague:by
acquired directly
of aerosols
fromdangerous
a human and
or fatal
animal
with
the
disease.plague.
It can The
develop
a complication
of septicaemic
plague orand
be
pneumonic
signsasinclude
severe pneumonia,
fever, dyspnoea
acquired directly by inhalation of aerosols from a human or animal with
pneumonic plague. The signs include severe pneumonia, fever, dyspnoea and
87
87
often haemoptysis. Patients who do not receive treatment within 18 hours of
onset of respiratory symptoms are unlikely to survive.
often haemoptysis. Patients who do not receive treatment within 18 hours of
Investigations
onset of respiratory symptoms are unlikely to survive.
 Blood, bubo aspirate, sputum/throat swab, necropsy material can be sent for
isolation of Y. pestis.
Investigations
 Acute
convalescent
serology for fourfold
rise in titre.
A single
is
Blood,and
bubo
aspirate, sputum/throat
swab, necropsy
material
cantitre
be >1:16
sent for
suggestive.
isolation of Y. pestis.
Informand
the convalescent
laboratory beforehand
so fourfold
that arrangements
can
made
to >1:16
forward
 Acute
serology for
rise in titre.
A be
single
titre
is
samples if necessary to the Department of Pathology, Singapore General
suggestive.
Hospital,
other designated
sites.so that arrangements can be made to forward
 Inform
theorlaboratory
beforehand
samples if necessary to the Department of Pathology, Singapore General
Hospital, or other designated sites.
Notification
A legally notifiable disease in Singapore. Notify Ministry of Health (Form MD 131
or electronically via CD-LENS) not later than 24 hours from the time of diagnosis.
Notification
Call
MOHnotifiable
Communicable
Surveillance
team at:of 98171463
immediately
A legally
disease Diseases
in Singapore.
Notify Ministry
Health (Form
MD 131
on
suspicion.
or electronically
via CD-LENS) not later than 24 hours from the time of diagnosis.
Call MOH Communicable Diseases Surveillance team at: 98171463 immediately
on
suspicion.
Management
All cases must be managed at the Communicable Disease Centre (CDC).
Management
Gentamicin,
chloramphenicol
or tetracycline
are (CDC).
highly effective if
All cases muststreptomycin,
be managed at
the Communicable
Disease Centre
used within hours of presentation.
Gentamicin, streptomycin, chloramphenicol or tetracycline are highly effective if
used
within
hours of presentation.
Infection
Control
 Patients with uncomplicated infection who are promptly treated present no
healthControl
hazard to others.
Infection
Those with
and other infection
signs of who
pneumonia
must be
placed
in strict
 Patients
withcough
uncomplicated
are promptly
treated
present
no
respiratory
health
hazardisolation
to others.for at least 48 hours after the institution of antibiotic
therapywith
or until
the sputum
culture
is negative.
 Those
cough
and other
signs
of pneumonia must be placed in strict
 Bubo
aspirate
and blood
handled
and aerosolization
of
respiratory
isolation
for atmust
leastbe48
hours with
after gloves
the institution
of antibiotic
these
materials
be avoided.
therapy
or until should
the sputum
culture is negative.
Laboratory
workers
must be
alerted
to exercise
standard
 Bubo
aspirate
and blood
must
be handled
with precautions
gloves and although
aerosolization
of
bacteriological
that safeguard against skin contact and aerosolization
these
materials techniques
should be avoided.
should be adequate.
 Laboratory
workers must be alerted to exercise precautions although standard
bacteriological techniques that safeguard against skin contact and aerosolization
should be
adequate.
Prevention
and
Control
 All cases will be isolated at CDC, Tan Tock Seng Hospital.

Case investigations
Prevention
and Controlwill be carried out and contact tracing will be intensified.
 In
event
death,
proper
disposal
the body
important.
Allthe
cases
willofbe
isolated
at CDC,
TanofTock
SengisHospital.
 Cases
and close contacts,
their
personal
Case investigations
will beincluding
carried out
andclothing
contact and
tracing
will bebelongings,
intensified.will
disinfected
insecticide
dusting.of the body is important.
 be
In the
event ofwith
death,
proper disposal
 Cases and close contacts, including their clothing and personal belongings, will
be disinfected with insecticide dusting.
88
88
Anti-flea measures and rodent trapping will be increased at the focus of
transmission.
Anti-flea
and rodent
trapping willwill
be be
increased
focus of
 The
publicmeasures
and the World
Health Organisation
informedatof the
all suspected
transmission.
and
confirmed cases.
be informed
of infestation
all suspected
 The public and
will the
be World
advisedHealth
to stepOrganisation
up measureswill
to prevent
rodent
in
andpremises
confirmed
cases.
the
and
to avoid contact with rodents (either live or dead).
 The public will be advised to step up measures to prevent rodent infestation in
the premises and to avoid contact with rodents (either live or dead).
Chemoprophylaxis
Consider antibiotic prophylaxis for the following:
Chemoprophylaxis
Persons exposed to patients with pneumonic plague.
antibiotic
prophylaxis
following:
Consider
Persons
exposed
to bites for
of the
wild
rodent fleas during an outbreak or to
 tissues/fluids
Persons exposed
patients with pneumonic
of atoplague-infected
animal. plague.
 Persons travelling
exposed to
to highly
bites endemic
of wild area
rodent
fleasduration.
during an outbreak or to
for short
tissues/fluids of a plague-infected animal.
For Persons
to highly
endemic
area for (100mg
short duration.
adults, travelling
doxycycline
is the
best choice
orally bd for 7 days).
Trimethoprim-sulfamethoxazole is a suitable alternative.
For adults, doxycycline is the best choice (100mg orally bd for 7 days).
Trimethoprim-sulfamethoxazole
Indications for vaccine usage is a suitable alternative.
A formalin-killed plague vaccine has been used for the following groups:
Indications
fortovaccine
usage

Travellers
endemic
or hyperendemic areas.
A formalin-killed
plague
been
the following
groups:

Individuals who
mustvaccine
live andhas
work
inused
closefor
contact
with rodents.
Travellers toworkers
endemic
or hyperendemic
areas.
 Laboratory
who
must handle live
cultures of Y. pestis.
Individuals
who must
live and
in close contact
 Military
personnel
deployed
inwork
plague-endemic
areas.with rodents.
 Laboratory workers who must handle live cultures of Y. pestis.
 Military
personnel
deployed
in plague-endemic
This
vaccine is
not routinely
available
in Singapore. areas.

This vaccine is not routinely available in Singapore.
References
1.
Perry RD, Fetherston JD. Yersinia pestis-etiologic agent of plague. Clin Microbiol Rev 1997; 10:35-
2.
1.
CDC (Atlanta). Information on plague. Available at:
Perry RD, Fetherston JD. Yersinia pestis-etiologic agent of plague. Clin Microbiol Rev 1997; 10:35http://www.cdc.gov/ncidod/dvbid/plague/info.htm. Accessed Aug 2010.
66
Plague as a biological weapon: medical & public health management. JAMA 2000; 283:2281-90
CDC (Atlanta). Information on plague. Available at:
http://www.cdc.gov/ncidod/dvbid/plague/info.htm. Accessed Aug 2010.
Plague as a biological weapon: medical & public health management. JAMA 2000; 283:2281-90
66
References
3.
2.
3.
89
89
PNEUMOCOCCAL DISEASE (INVASIVE)
Causative agent PNEUMOCOCCAL DISEASE (INVASIVE)
Streptococcus pneumoniae (also known as pneumococcus)
Causative agent
Streptococcus
pneumoniae (also known as pneumococcus)
Incubation
Period
Not well defined as colonization usually precedes invasive disease; may be as short
Incubation
Period
as 1 to 3 days.
Not well defined as colonization usually precedes invasive disease; may be as short
as
1 to 3 days.
Infectious
Period
Presumably as long as pneumococci are carried in oro-nasal secretions in
Infectious
Period
asymptomatic
individuals (colonization usually lasts weeks to months); with
Presumably
as long as
pneumococci
carried
in oro-nasal
in nonpenicillin treatment,
persons
infectedare
with
susceptible
strainssecretions
are rendered
asymptomatic
individuals
(colonization usually lasts weeks to months); with
infectious
within
24-48 hours.
penicillin treatment, persons infected with susceptible strains are rendered noninfectious
within 24-48 hours.
Transmission
Respiratory droplets and direct contact with respiratory secretions of an infected
Transmission
person (usually requires frequent or prolonged close contact).
Respiratory droplets and direct contact with respiratory secretions of an infected
person
(usually requires frequent or prolonged close contact).
Epidemiology
S. pneumoniae is one of the most common causes of invasive infections such as
Epidemiology
bacteraemia, meningitis and bacteraemic pneumonia, and bacterial mucosal
S.
pneumoniae
is one
of the
causes
of pneumococcal
invasive infections
such 23
as
infections
such as
sinusitis
andmost
otitiscommon
media. Of
the 91
serotypes,
bacteraemia,
and ofbacteraemic
pneumonia, disease
and bacterial
mucosal
account for themeningitis
vast majority
invasive pneumococcal
(IPD) in humans.
infections
such emergence
as sinusitis of
and
otitis media. resistance
Of the 91 to
pneumococcal
serotypes,
23
The worldwide
pneumococcal
antibiotics, including
betaaccount
the vast majority
of invasive
pneumococcal
disease (IPD) has
in humans.
lactams, for
macrolides,
tetracycline,
cotrimoxazole
and fluoroquinolones
been a
The
worldwide
emergence of pneumococcal resistance to antibiotics, including betaconsiderable
concern.
lactams, macrolides, tetracycline, cotrimoxazole and fluoroquinolones has been a
considerable
concern. infection is defined as the isolation of S. pneumoniae from
Invasive
pneumococcal
normally sterile sites such as blood, pleural fluid and cerebrospinal fluid (CSF).
Invasive pneumococcal
infection
is defined
as the isolation
pneumoniae
from
Pneumococcal
pneumonia
is considered
an invasive
disease of
butS.would
be excluded
normally
sterile
sitesfluid
suchcultures
as blood,
andmedia
cerebrospinal
fluid (CSF).
if blood or
pleural
arepleural
sterile.fluid
Otitis
is not considered
an
Pneumococcal
pneumonia
disease
but would
be excluded
invasive disease,
but may is
beconsidered
included ifanS.invasive
pneumoniae
is isolated
from
normally
if
blood
or pleural
fluid cultures are sterile. Otitis media is not considered an
sterile
middle
ear fluid.
invasive disease, but may be included if S. pneumoniae is isolated from normally
sterile
middle ear
In Singapore,
the fluid.
mean annual hospitalisation rate for IPD from 2000-2008 was 8.9
per 100,000 population (about 380 cases per year). A total of 157 deaths from IPD
In Singapore,
mean
hospitalisation
rate under
for IPD
2000-2008
was
8.9
were
reported the
during
thisannual
period,
of which 5 were
thefrom
age of
5 years. In
2009,
per
population
casesOfper
year).
A met
totalthe
of 157
deaths
there100,000
were 251
reported(about
cases 380
of IPD.
these,
124
criteria
for from
IPD. IPD
The
were
reported
during
of which
5 were
thethe
ageelderly
of 5 years.
In 2009,
highest
incidence
ratethis
wasperiod,
in children
< 5 years
of under
age and
aged 65
years
there
were 251
reported serotypes
cases of IPD.
Of these,
124 met
for IPD.
The
and above.
In children,
14, 6B,
23F, 19F,
6A the
andcriteria
19A were
the most
highest
rate wasand
in children
< 5for
years
the elderly
aged
years
commonincidence
strains isolated,
accounted
89%ofofage
all and
invasive
diseases
in 65
children
and
above.old.
In However,
children, serotypes
6B, 23F,
19F, 6Awas
andmore
19A spread
were the
<5 years
in adults,14,
isolate
distribution
outmost
and
common strains isolated, and accounted for 89% of all invasive diseases in children
<5 years old. However, in adults, isolate distribution was more spread out and
90
90
common ones were 14, 3, 6B, 8 and 19F which accounted for 51% of all invasive
diseases. Mean case fatality rates for IPD in single-centre series were 6.1% in
common
onesrising
were 14,
3, 6B,in 8children
and 19F with
whichpneumococcal
accounted formeningitis;
51% of all while
invasive
children but
to 30%
in
diseases.
case fatality rates for IPD in single-centre series were 6.1% in
adults, thisMean
was 21.4%.
children but rising to 30% in children with pneumococcal meningitis; while in
adults,
this was 21.4%.
A pneumococcal
polysaccharide vaccine (23-valent or serotype) has been available
locally since 1988. It was recommended for children >2 years old with risk factors
A pneumococcal
(23-valent or serotype)
available
for
IPD and adultspolysaccharide
>65 years old, vaccine
but its immunogenicity
was fair has
and been
its uptake
was
locally
sinceHowever,
1988. It itwas
recommended
for children
>2 years old
with risk
very
poor.
would
cover 82.8%
of IPD serotypes
in adults.
A factors
highly
for
IPD and adults
>65 years old,
but its vaccine
immunogenicity
was
fairlicensed
and its uptake
immunogenic
pneumococcal
conjugate
(7-valent)
was
locallywas
for
very
poor.
wouldold
cover
82.8%
IPD
serotypes
in adults. A
highly
children
6 However,
weeks to 9it years
since
2002ofbut
became
commercially
available
immunogenic
pneumococcal
vaccine
(7-valent)
was licensed
for
locally only since
late 2005, conjugate
with uptake
primarily
in children
<5years locally
within the
th
children
6
weeks
to
9
years
old
since
2002
but
became
commercially
available
private sector. In November 2009, it became the 10 vaccine-preventable disease to
locally
onlyinsince
late 2005,
with uptake
primarily Programme.
in children <5years within the
be
included
the National
Childhood
Immunization
private sector. In November 2009, it became the 10 th vaccine-preventable disease to
be
included
in the National Childhood Immunization Programme.
Clinical
Features

Typically between 40-50% of children and 20-30% of adults carry
Clinical
Features asymptomatically in their nasopharynx.
pneumococci
Typicallyisbetween
40-50% by
of children
and 20-30%
of adults

Infection
often preceded
a respiratory
viral illness
beforecarry
local disease
pneumococci
asymptomatically
in their
nasopharynx.
(from
congestion
and concentration
of virulent
pneumococci) or invasion

Infection
often preceded
by adisease
respiratory viral illness before local disease
leading toissystemic
or invasive
(from
congestion
and concentration of virulent pneumococci) or invasion

Can infect
any organ.
leading
systemic include
or invasive
disease

Mucosaltoinfections
acute
otitis media, bacterial sinusitis,

Can
infect any organ.
conjunctivitis.

Mucosal
infections
include
acute
otitis media,
bacterial sinusitis,
 Otitis
media
may be
complicated
by mastoiditis
and intracranial
conjunctivitis.
extension with abscess formation.
 Otitis
media
be complicated
by mastoiditis
and intracranial
Sinusitis
maymay
be complicated
by periorbital
or orbital
cellulitis, with
extension
with abscess
formation.
resultant intracranial
extension.
 Sinusitis
mayor
beinvasive
complicated
by periorbital
or orbital
cellulitis, with

Common
deep-seated
infections
include primary
bacteraemia,
resultant
intracranial
extension. pneumonia without bacteraemia is
pneumonia
(with or
without bacteraemia;

Common
deep-seated
or invasive
infections
primary bacteraemia,
not
traditionally
classified
as “invasive”),
andinclude
meningitis.
pneumonia
(with or without
without effusions
bacteraemia
 Pneumonias
may bebacteraemia;
complicatedpneumonia
by parapneumonic
andis
not traditionally
classified as “invasive”), and meningitis.
empyemas.
 Meningitis
Pneumoniasismay
be complicated
by parapneumonic
effusions
and
infrequently
associated
with development
of subdural
empyemas.
empyemas, intracranial abscesses and vasculitic/ thrombotic
 Meningitis
phenomena.is infrequently associated with development of subdural
empyemas,
intracranial
and vasculitic/

Less commonly,
it can
also causeabscesses
osteomyelitis,
pyogenic thrombotic
arthritis,
phenomena.
endocarditis,
myocarditis, pericarditis, bacterial peritonitis, endophthalmitis

Less
commonly, it can also cause osteomyelitis, pyogenic arthritis,
and salpingitis.
endocarditis,
myocarditis,
pericarditis,
peritonitis, endophthalmitis

In some patients
(especially
those who bacterial
are immunocompromised),
and
salpingitis.
pneumococcal infections may be fulminant and present with overwhelming

In
some
patients
(especially
those who are immunocompromised),
sepsis
and
multi-organ
failure.
pneumococcal infections may be fulminant and present with overwhelming
sepsis and multi-organ failure.
91
91
Risk Factors:
Risk
 Factors:
Age (<5 years and >65 years)

Age
(<5
years and >65(though
years) not evident in local series)
Racial
predisposition

Racial
predisposition
(though
evident inheart,
local series)
Chronic illnesses (chronic not
respiratory,
renal and liver disease,

Chronic
illnesses
alcoholism,
diabetes)(chronic respiratory, heart, renal and liver disease,
alcoholism,
diabetes)

Cochlear implants

Cochlear
implants
Cerebrospinal
fluid leaks

Cerebrospinal
leaks asplenia/ splenic dysfunction (including sickle cell
Functional or fluid
anatomic

Functional
disease) or anatomic asplenia/ splenic dysfunction (including sickle cell
disease)

Immunocompromised—either congenital, acquired (e.g. HIV infection) or

Immunocompromised—either
congenital, acquired (e.g. HIV infection) or
iatrogenic
via immunosuppression.
iatrogenic via immunosuppression.
Investigations
Investigations

Microbiological confirmation by culture remains the gold standard for

Microbiological
confirmation
by culture
remains
gold standard
for
diagnosis and allows
for sensitivity
testing as
well as the
subsequent
serotyping;
diagnosis
for blood
sensitivity
as well
subsequent
serotyping;
however and
the allows
yield in
maytesting
be low
for asdifferent
pneumococcal
however the yield
in blood low
may(around
be low
forindifferent
pneumococcal
syndromes—high
in meningitis,
25%)
pneumonia.
syndromes—high
in
meningitis,
low
(around
25%)
in
pneumonia.
 The volume of inoculum (usually blood, uncommonly pleural fluid or
 The
of inoculum
(usually
blood,
pleural positive
fluid or
CSF)volume
is important,
and blood
cultures
(if uncommonly
positive) are usually
CSF)
is
important,
and
blood
cultures
(if
positive)
are
usually
positive
within 18 hours of inoculation
hours
ofagglutination
inoculation testing of infected body fluids (e.g. CSF,

Gramwithin
stains18and
latex

Gram
stains
and
latex
agglutination
testingalways
of infected
body fluids
(e.g.
CSF,
pleural, peritoneal or joint fluid) should
be performed
and
may
be
pleural,
jointstreptococci
fluid) should
always
performed
and may be
helpful, peritoneal
although or
other
may
also be
appear
as Gram-positive
helpful,
streptococci
appear as Gram-positive
diplococcialthough
and latexother
agglutination
testingmay
lacksalso
sensitivity.
diplococci
and latex agglutination
testing lacks sensitivity.

Urinary pneumococcal
cell wall polysaccharide
(antigen) testing is currently

Urinary
cell result
wall polysaccharide
(antigen) testing
is currently
availablepneumococcal
and a positive
is strongly suggestive
of pneumococcal
available
and a positive
result
is strongly
disease/ pneumonia
in adults,
although
it can suggestive
be positiveofin pneumococcal
the setting of
disease/
pneumonia incarriage
adults, although
can beinpositive
the hence
setting the
of
acute nasopharyngeal
(as often itoccurs
children)in and
acute
nasopharyngeal
carriage
(as
often
occurs
in
children)
and
hence
the
specificity is much poorer in children.
specificity
is much
poorer
in children.tomography, ultrasound, and nuclear or

Imaging (e.g.
X-ray,
computerised

Imaging (e.g.
X-ray,imaging)
computerised
nuclearwith
or
magnetic
resonance
assiststomography,
in localisingultrasound,
infection inand
patients
magnetic
resonance
imaging) and
assists
in localising infection in patients with
appropriate
clinical symptoms
signs
appropriate clinical symptoms and signs
Notification
Notification
A legally notifiable disease in Singapore. Notify Ministry of Health (Form MD 131
A
notifiable
in Singapore.
Notify
of the
Health
MD 131
or legally
electronically
via disease
CD-LENS)
not later than
72 Ministry
hours from
time(Form
of diagnosis.
or electronically via CD-LENS) not later than 72 hours from the time of diagnosis.
Management
Management

Appropriate resuscitation, oxygenation and invasive or supportive care as

Appropriate
invasive or supportive care as
required; the resuscitation,
importance of oxygenation
this cannot beand
overemphasized.
required; the importance of this cannot be overemphasized.
92
92
Initial choice of empirical antibiotics should be guided by local ageappropriate guidelines for respective clinical syndromes (by institution or
college).choice of empirical antibiotics should be guided by local age
Initial

Once confirmed
microbiologically,
appropriate,
targeted antibiotic
treatment
appropriate
guidelines
for respective
clinical syndromes
(by institution
or
should be guided by susceptibility testing after the initial empirical regime.
college).
OncePenicillins
by 1st and appropriate,
2nd generation
cephalosporins)
are the

confirmed(followed
microbiologically,
targeted
antibiotic treatment
preferred
choice
of antimicrobials;
however,
on the regime.
site of
should
be guided
by susceptibility
testing
after thedepending
initial empirical
infection, much
higherbydoses
may
be generation
required, orcephalosporins)
3rd generation are the
 Penicillins
(followed
1st and
2nd
cephalosporins
be used (e.g. meningitis).
preferred
choicemay
of antimicrobials;
however, depending on the site of
 Where
pneumococci
aredoses
resistant
treatment
may be
infection,
much higher
mayto
bebeta-lactams,
required, or 3rd
generation
individualized
cephalosporinswith
mayvancomycin,
be used (e.g. quinolones
meningitis).or tetracyclines as
 appropriate.
Where pneumococci are resistant to beta-lactams, treatment may be

Source
control (e.g.with
drainage
of infections
in closed
spaces like empyemas
or
individualized
vancomycin,
quinolones
or tetracyclines
as
cerebral
abscesses)
are
often
critical
to
success
or
failure
of
antibiotic
appropriate.
treatment.

Source control (e.g. drainage of infections in closed spaces like empyemas or

Adjunct therapies
to betoconsidered
dexamethasone
in
cerebral
abscesses)may
are also
oftenneed
critical
success ore.g.
failure
of antibiotic
pneumococcal meningitis, activated protein C in severe pneumococcal sepsis.
treatment.

Adjunct therapies may also need to be considered e.g. dexamethasone in
pneumococcal meningitis, activated protein C in severe pneumococcal sepsis.
Prevention and Control


All children <2 years old should receive pneumococcal conjugate vaccine as
Prevention
and Control
recommended
under the National Childhood Immunization Program.
 children
Children<2
<1years
year old
primary doses conjugate
at 3 months
and 5 as

All
old should
shouldreceive
receive2pneumococcal
vaccine
months followed
by National
a boosterChildhood
at 1-2 years.
recommended
under the
Immunization Program.
>1 year old should receive 2age
appropriate
of
 Children <1
primary
doses doses
at 3 months
and 5
pneumococcal
conjugate
vaccine
and also
depending on whether they
months
followed
by a booster
at 1-2
years.
have risk >1
factors
 Children
year for
oldIPD.
should receive age appropriate doses of

All adults
≥65 yearsconjugate
old, and vaccine
personsand
2 toalso
64 depending
years with on
riskwhether
factors they
for IPD
pneumococcal
(as above)
should
receive
23-valent pneumococcal polysaccharide vaccine as
have risk
factors
for IPD.
recommended
MOH.

All
adults ≥65 by
years
old, and persons 2 to 64 years with risk factors for IPD

All above)
childhood
vaccinations
should be
notified to the
National Immunisation
(as
should
receive 23-valent
pneumococcal
polysaccharide
vaccine as
Registry, Health
Promotion Board. All post vaccination adverse reactions
recommended
by MOH.
should
also bevaccinations
notified to the
Pharmacovigilance
Health
Sciences

All childhood
should
be notified to theBranch,
National
Immunisation
Authority.
Registry, Health Promotion Board. All post vaccination adverse reactions
should also be notified to the Pharmacovigilance Branch, Health Sciences
Authority.
93
93
References
References
1. O’Brien KL, Wolfson LJ, Watt JP et al. Burden of disease caused by Streptococcus pneumoniae in
2.
1.
3.
2.
4.
3.
5.
4.
6.
5.
7.
6.
8.
7.
8.
children younger than 5 years: global estimates. Lancet 2009; 374:893-902
van
der Poll
Opal SM.
prevention
O’Brien
KL,T,
Wolfson
LJ, Pathogenesis,
Watt JP et al. treatment
Burden ofand
disease
caused of
bypneumococcal
Streptococcuspneumonia.
pneumoniae in
Lancet
374:1543-56
children2009;
younger
than 5 years: global estimates. Lancet 2009; 374:893-902
Lowder
S, Chan
L F, Cutter
J et al. A national
studyand
of the
epidemiology
of pneumococcal
disease
van
Poll T,F Opal
SM. Pathogenesis,
treatment
prevention
of pneumococcal
pneumonia.
among 2009;
hospitalised
patients in Singapore: 1995 to 2004. Singapore Med J 2007; 48:824-9
Lancet
374:1543-56
Chong
MokJ et
YH
Invasive
pneumococcal
disease inofSingapore
children.
Low S, CY,
ChanThoon
F L F,KC,
Cutter
al.etAal.
national
study
of the epidemiology
pneumococcal
disease
Vaccine
2008; 26:3427-31
among hospitalised
patients in Singapore: 1995 to 2004. Singapore Med J 2007; 48:824-9
Hsu LY,
LuiThoon
SW, Lee
et al.
Adult
and peri-pneumococcal
Chong
CY,
KC,JL
Mok
YH
et al.invasive
Invasivepneumococcal
pneumococcaldisease
diseaseprein Singapore
children.
connjugate
vaccine
introduction in a tertiary hospital in Singapore. J Med Microbiol 2009; 58:101-4
Vaccine 2008;
26:3427-31
Musher
Streptococcus
In Mandell
GL, Bennet
JE, Dolin
R (eds).
Principles and
Hsu LY,DM.
Lui SW,
Lee JL et pneumoniae.
al. Adult invasive
pneumococcal
disease
pre- and
peri-pneumococcal
Practice of Infectious
Diseases. 7th
Philadelphia,
Churchill JLivingstone;
2010:2623-42.
connjugate
vaccine introduction
in aed.
tertiary
hospital PA:
in Singapore.
Med Microbiol
2009; 58:101-4
Ministry
of Health.
Vaccination
against pneumococcal
disease.
Bulletin
2010;and
36:
Musher DM.
Streptococcus
pneumoniae.
In Mandell GL,
BennetEpidemiol
JE, DolinNews
R (eds).
Principles
7-15.
Practice of Infectious Diseases. 7th ed. Philadelphia, PA: Churchill Livingstone; 2010:2623-42.
Ministry of
of Health.
Health. Vaccination
Laboratory-based
surveillance
system
of invasive
pneumococcal
diseases
in 36:
Ministry
against
pneumococcal
disease.
Epidemiol
News Bulletin
2010;
Singapore:
a nationwide monitoring of vaccine serotype coverage. Epidemiol News Bulletin
7-15.
2010;36:
40-5.
Ministry of
Health. Laboratory-based surveillance system of invasive pneumococcal diseases in
Singapore: a nationwide monitoring of vaccine serotype coverage. Epidemiol News Bulletin
2010;36: 40-5.
94
94
POLIOMYELITIS
POLIOMYELITIS
Causative Agent
Poliovirus, types 1, 2 and 3
Causative Agent
Poliovirus,
1, 2 and 3
Incubationtypes
Period
7-14 days (Range 5-35 days)
Incubation Period
7-14
days (Range
Infectious
Period5-35 days)
A few days before and after onset of illness.
Infectious Period
A
few days before and after onset of illness.
Transmission
Faeco-oral or respiratory transmission.
Transmission
Faeco-oral or respiratory transmission.
Epidemiology
The last indigenous case of poliomyelitis notified in Singapore was in 1973.
Epidemiology
The
last indigenous
casehave
of poliomyelitis
notified
Singapore
was infrom
1973.estimated
Globally,
polio cases
decreased by
over in
99%
since 1988,
350,000 cases then to 1997 reported cases in 2006. In 2008, only four countries
Globally,
polio cases
haveIndia,
decreased
by Nigeria
over 99%
from
estimated
remain endemic
(northern
northern
and since
border1988,
between
Afghanistan
350,000
cases
then
to
1997
reported
cases
in
2006.
In
2008,
only
four
countries
and Pakistan).
remain endemic (northern India, northern Nigeria and border between Afghanistan
and
Pakistan).
Clinical
Features
 Disease manifestation can range from subclinical infection to severe paralysis
Clinical
Features
and death.

Disease
manifestation
range from
subclinical
paralysis
 The infection
should becan
suspected
in someone
withinfection
a historytoofsevere
an incomplete
and
death.
immunisation against polio or recent travel to an endemic country.

be polio
suspected
in someone
with a history of an incomplete
 The
Threeinfection
forms ofshould
paralytic
may be
seen:
immunisation
against
polio
or
recent
travel
to
an
endemic country.
1. Spinal Paralytic Polio
 Three
forms
of paralytic
may beillness
seen: with fever, muscle pain, headache,
This
is preceded
bypolio
a “minor”
1. Spinal
nausea,Paralytic
vomitingPolio
and stiff neck/back and less frequently, signs of aseptic
This is preceded
by a “minor”
illness
muscle
headache,
meningitis.
The minor
illness lasts
1-3with
daysfever,
followed
by apain,
symptom-free
nausea,
vomiting
and
stiff
neck/back
and
less
frequently,
signs
of
aseptic
period of 1-5 days before the onset of “major” illness of paralysis.
meningitis.
The
minor
illness
lasts
1-3
days
followed
by
a
symptom-free
Paralysis which varies from single muscle involvement to quadriplegia, is
period of
1-5 days and
before
the onset
of with
“major”
of paralysis.
usually
asymmetric
typically
flaccid
loss illness
of tendon
reflexes.
Paralysis
which
varies
from
single
muscle
involvement
to
quadriplegia,
is
There is no accompanying sensory loss.
usually
asymmetric
and
typically
flaccid
with
loss
of
tendon
reflexes.
2. Bulbar Paralytic Polio
There is noofaccompanying
sensory
loss.and larynx resulting in dysphagia,
Paralysis
the soft palate,
pharynx
2. nasal
Bulbarspeech
Paralytic
and Polio
dyspnoea.
Paralysis of the soft palate, pharynx and larynx resulting in dysphagia,
3. Polioencephalitis
nasal speech is
andmanifested
dyspnoea.by confusion and change in sensorium. This is
Encephalitis
3. an
Polioencephalitis
uncommon form of polio seen in infants. Seizures are common and
Encephalitis
manifested
by as
confusion
changeparalysis.
in sensorium. This is
there
may be is
spastic
paralysis
opposedand
to flaccid
an uncommon form of polio seen in infants. Seizures are common and
there may be spastic paralysis as opposed to flaccid paralysis.
95
95
The most common differential diagnoses are those causing acute flaccid
paralysis including transverse myelitis, Guillain-Barré Syndrome, enterovirus
Westcommon
Nile virusdifferential
infections. diagnoses are those causing acute flaccid
 71
Theand
most
paralysis including transverse myelitis, Guillain-Barré Syndrome, enterovirus
Investigations
71 and West Nile virus infections.
 CSF findings consistent with any viral meningitis. CSF protein is minimally
elevated (unlike in Guillain-Barre syndrome).
Investigations
 Polioviruses
usually be
frommeningitis.
the throat CSF
swabprotein
in the first
week of
CSF findingscan
consistent
withisolated
any viral
is minimally
illness
and
stool in
cultures
may remain
positive for several weeks.
elevated
(unlike
Guillain-Barre
syndrome).
 In
the absence
a virusbeisolate,
diagnosis
is confirmed
a four-fold
Polioviruses
canofusually
isolatedthe
from
the throat
swab in thebyfirst
week of
increase
in stool
antibody
titre may
of theremain
acute and
convalescent
sera.
illness and
cultures
positive
for several
weeks.
 In the absence of a virus isolate, the diagnosis is confirmed by a four-fold
Notification
increase in antibody titre of the acute and convalescent sera.
A legally notifiable disease in Singapore. Notify Ministry of Health (Form MD 131
or
electronically via CD-LENS) not later than 72 hours from the time of diagnosis.
Notification
A legally notifiable disease in Singapore. Notify Ministry of Health (Form MD 131
Management
or electronically via CD-LENS) not later than 72 hours from the time of diagnosis.
Refer all confirmed cases to the Communicable Disease Centre (CDC), Tan Tock
Seng Hospital, for isolation and management. Specific anti-viral therapy is not
Management
available.
Management
is therefore
supportive andDisease
symptomatic.
Refer
all confirmed
cases
to the Communicable
Centre (CDC), Tan Tock
Seng Hospital, for isolation and management. Specific anti-viral therapy is not
PreventionManagement
and Controlis therefore supportive and symptomatic.
available.
 Case investigation and contact tracing will be carried out to identify
unrecognised
and unreported cases. Contacts below 12 years old without
Prevention
and Control
complete
immunisation
be referred
the nearest
Polyclinic
School
 Case
investigation
and will
contact
tracing towill
be carried
out toor identify
Health Clinic for
unrecognised
andvaccination.
unreported cases. Contacts below 12 years old without
 complete
All infants
are routinely
as part
of the
immunisation
willvaccinated
be referredagainst
to the poliomyelitis
nearest Polyclinic
or School
Childhood
Immunisation
Programme in Singapore.
Health
Clinic
for vaccination.
Bothinfants
IPV (inactivated
polio vaccinated
vaccine) and
OPV (live,
attenuatedas vaccine)
 All
are routinely
against
poliomyelitis
part of have
the
been used Immunisation
for more thanProgramme
30 years inincontrolling
Childhood
Singapore.paralytic poliomyelitis. IPV
be used
for immunocompromised
children
including
travellers.
 should
Both IPV
(inactivated
polio vaccine) and
OPV and
(live,adults
attenuated
vaccine)
have
 Notify
all
childhood
vaccinations
to
the
National
Immunisation
Registry,
been used for more than 30 years in controlling paralytic poliomyelitis.Health
IPV
Promotion
and post-vaccination
adverse
reactions travellers.
to the
should be usedBoard,
for immunocompromised
children and
adults including
HealthtoSciences
Authority.
 Pharmacovigilance
Notify all childhoodBranch,
vaccinations
the National
Immunisation Registry, Health
Promotion Board, and post-vaccination adverse reactions to the
References
Pharmacovigilance Branch, Health Sciences Authority.

1.
Chew SK. Certification of poliomyelitis eradication in the World Health Organisation Western
Pacific Region. Epidemiological News Bulletin 1997; 23:70-1
References
2.
WHO. Poliomyelitis 2008. Available at http://www.who.int/mediacentre/factsheets/fs114/en/index.html.
1. Accessed
Chew SK.
Certification
of poliomyelitis eradication in the World Health Organisation Western
August
2010.
Pacific Wild
Region.
Epidemiological
NewsaBulletin
3. WHO.
poliovirus
isolation from
Nigerian1997;
child23:70-1
with acute flaccid paralysis seeking medical
2.
WHO.
Poliomyelitis
2008.
Available
at
http://www.who.int/mediacentre/factsheets/fs114/en/index.html.
care in Singapore. Weekly Epidemiological Record 2006; 81:285-6.
2010.Cutter J et al. Evaluation on the effectiveness of the National Childhood
4. Accessed
Liew F, August
Ang LW,
3. WHO.
Wild poliovirus
isolation
from a 1982-2007.
Nigerian child
with
acute
flaccid
paralysis
seeking
medical
Immunisation
Programme
in Singapore,
Ann
Acad
Med
Singapore
2010;
39:532-41.
care in Singapore. Weekly Epidemiological Record 2006; 81:285-6.
4. Liew F, Ang LW, Cutter J et al. Evaluation on the effectiveness of the National Childhood
Immunisation Programme in Singapore, 1982-2007. Ann Acad Med Singapore 2010; 39:532-41.
96
96
RABIES
RABIES
Causative Agent
Rabies virus
Causative Agent
Rabies
virusPeriod
Incubation
20 - 90 days (range 4 days - 19 years)
Incubation Period
20 - 90 daysPeriod
(range 4 days - 19 years)
Infectious
Throughout duration of clinical illness
Infectious Period
Throughout
duration of clinical illness
Transmission
From saliva of infected animals via bites. Rarely, contamination of mucous
Transmission
membranes by infectious material, aerosol transmission and organ transplantation.
From saliva of infected animals via bites. Rarely, contamination of mucous
membranes by infectious material, aerosol transmission and organ transplantation.
Epidemiology
Although reservoir is present in many mammalian species, dog bites account for the
Epidemiology
majority of human infections. Rabies has not been reported locally since 1953. but
Although
reservoir in
is present
in many
mammalian
species,
dog bites
account
for the
remains prevalent
many parts
of the
region and
the world.
Recent
decrease
in
majority
of
human
infections.
Rabies
has
not
been
reported
locally
since
1953.
human rabies cases has been due to improved post-exposure treatment as wellbut
as
remains
prevalent
in inmany
parts
of the via
region
the world.ofRecent
decrease in
elimination
of rabies
animal
reservoirs
oraland
immunisation
wildlife.
human rabies cases has been due to improved post-exposure treatment as well as
elimination
of rabies in animal reservoirs via oral immunisation of wildlife.
Clinical Features
 The first symptoms of rabies usually begin when the virus enters the CNS. A
Clinical
Featuresprodrome of 2-10 days includes fever, malaise, fatigue, anorexia,
non-specific
 cough,
The firstsore
symptoms
of rabies usually
begin when
the virus
enters the The
CNS.
A
throat, abdominal
pain, nausea,
vomiting
or diarrhoea.
first
of
2-10
days
includes
fever,
malaise,
fatigue,
anorexia,
non-specific
prodrome
rabies-specific symptom is pain or paraesthesia referred to the site of the
cough, sore throat, abdominal pain, nausea, vomiting or diarrhoea. The first
exposure.
rabies-specific
symptom
is pain
or paraesthesia
to the
site rabies)
of the
 The
acute neurological
period
manifests
as either a referred
hyperactive
(furious
exposure.
in
80% or a paralytic (dumb rabies) form in 20%. Autonomic instability is often
manifests
as either aand
hyperactive
(furious rabies)
 prominent
The acute neurological
period
(hyperthermia,
salivation,
hypertension
tachycardia).
in 80%
or a paralytic
(dumb
in 20%.
Autonomic
instability
is often
 The
neurological
phase
lasts rabies)
2-7 daysform
before
development
of coma
then death.
prominent (hyperthermia, salivation, hypertension and tachycardia).
 The neurological phase lasts 2-7 days before development of coma then death.
Investigations
No tests are available to diagnose human rabies during the incubation period.
Investigations
No tests
areof
available
diagnose
human rabies
during
the incubation period.
After
onset
clinical to
disease,
diagnostic
methods
include:
 Direct fluorescent antibody staining of skin biopsy from nape of neck (50%).
AfterRabies
onset of
clinical disease,
diagnostic
methods
include:

neutralising
antibodies
in serum
or CSF.
 Rabies
Direct fluorescent
antibody
stainingCSF,
of skin
biopsy
from nape
of neck (low).
(50%).

virus isolation
from saliva,
urine
and tracheal
secretions
 Rabies
Rabies RT-PCR
neutralising
antibodies
serum
ortissue.
CSF.

in saliva,
CSF,inurine
and
 Cortical
Rabies virus

brainisolation
biopsy. from saliva, CSF, urine and tracheal secretions (low).
 Rabies
RT-PCR
in saliva,
CSF,
urineoverseas
and tissue.
 Specimens may
need to
be sent
for tests.
 Cortical brain biopsy.
 Specimens may need to be sent overseas for tests.
97
97

Post-mortem brain examination for Negri bodies and fluorescent staining
for rabies antibodies.
 Post-mortem brain examination for Negri bodies and fluorescent staining
for rabies antibodies.
Notification
Notify all suspected and confirmed cases immediately. Call MOH Communicable
Notification
Diseases Surveillance team at 98171463 and the Agri-Food and Veterinary
Notify all of
suspected
and
confirmed
casesinvestigation.
immediately. Call MOH Communicable
Authority
Singapore
(AVA)
for further
Diseases Surveillance team at 98171463 and the Agri-Food and Veterinary
Authority of Singapore (AVA) for further investigation.
Management
 There is no specific treatment for clinical human rabies. Intensive supportive
Management
care in the ICU is often used although mortality is virtually 100%.

is no
treatment
for clinical
rabies. byIntensive
supportive
 There
Standard
andspecific
respiratory
precautions
shouldhuman
be observed
healthcare
workers
care
in
the
ICU
is
often
used
although
mortality
is
virtually
100%.
caring for such patients. Pre-exposure immunisation of medical staff is
 generally
Standard and
precautions
should
observedisbynot
healthcare
workers
not respiratory
required. Routine
delivery
of be
healthcare
an indication
of
caring
for
such
patients.
Pre-exposure
immunisation
of
medical
is
post-exposure prophylaxis unless the healthcare worker is reasonably staff
certain
generally
not
required.
Routine
delivery
of
healthcare
is
not
an
indication
of
that he or she was bitten or mucous membranes or non-intact skin was exposed
post-exposure
prophylaxis
unless
the healthcare
worker is reasonably certain
to
potentially infectious
saliva
or neural
tissue.
that he or she was bitten or mucous membranes or non-intact skin was exposed
to potentially
infectious saliva or neural tissue.
Prevention
and Control
 In rabies-free Singapore, the AVA exercises strict control on importation and
Prevention
andofControl
quarantine
dogs, cats and wild animals and intensive control of stray dog and
 In
rabies-free
cat population.Singapore, the AVA exercises strict control on importation and
quarantine
and wild
animals suspected
and intensive
controlrabies,
of stray
dog and
 In
the case of
of dogs,
humancats
exposure
to animals
of having
immediate
cat
population.
attempts should be made to identify, capture or kill the animal involved. The
 In
the case ofAVA,
humanwill
exposure
animals
of having
rabies,forimmediate
veterinarian,
removetothe
brain suspected
of the animal
to examine
presence
attempts
shouldantigen
be made
to identify, capture or kill the animal involved. The
of rabies virus
by immunofluorescence.
veterinarian, AVA, will remove the brain of the animal to examine for presence
of rabies virus
antigen by immunofluorescence.
Pre-Exposure
Vaccination
 For travellers visiting rabies endemic countries (Central and South America,
Pre-Exposure
Vaccination
Africa, Indian
subcontinent and Southeast Asia), pre-exposure vaccination may
 be
For recommended
travellers visiting
rabies endemic
countries
(Central
and South
America,
depending
on intended
activity,
duration
of stay,
local
Africa,
Indian
subcontinent
and
Southeast
Asia),
pre-exposure
vaccination
incidence of rabies and availability of appropriate anti-rabies biologicals. may
be recommended
depending
onsimplifies
intended but
activity,
duration
of the
stay,
 Pre-exposure
vaccination
greatly
does not
eliminate
needlocal
for
incidence of rabies
and availability of appropriate anti-rabies biologicals.
post-exposure
treatment.
 Pre-exposure
Pre-exposure vaccination
butgiven
doeson
notdays
eliminate
the 21
need

vaccination greatly
consistssimplifies
of 3 doses
0, 7 and
or for
28
post-exposure
treatment.
days.
 The
Pre-exposure
vaccination
3 doses is
given
days 0, 7 virus
and 21vaccine
or 28

human diploid
cell consists
vaccine of(HDCV)
an on
inactivated
days.
available in Singapore.
 The human diploid cell vaccine (HDCV) is an inactivated virus vaccine
available inTreatment
Singapore.
Post-Exposure
 The most effective mechanism of protection against rabies is to wash and flush
Post-Exposure
Treatment
a wound or
point of contact with soap and water, followed by application of
 ethanol,
The mosttincture
effective
mechanism
of protection
or aqueous
solution
of iodine.against rabies is to wash and flush
a wound or point of contact with soap and water, followed by application of
ethanol, tincture or aqueous solution of iodine.
98
98
Suturing should be postponed and where indicated, anti-tetanus toxoid and
antimicrobials should be administered.
 Suturing
should and
be postponed
and where
Rabies vaccine
immunoglobulin
shouldindicated,
be given anti-tetanus
as soon as toxoid
possibleand
if
antimicrobials
should
be administered.
indicated (see table
below).
Post-exposure vaccination consists of 5 doses given
 on
Rabies
immunoglobulin
be given keeps
as soon
as possible
if
daysvaccine
0, 3, 7, and
14 and
28. Tan Tockshould
Seng Hospital,
a stock
of rabies
indicatedand
(see
table rabies
below).immunoglobulin.
Post-exposure vaccination consists of 5 doses given
vaccine
human
on days 0, 3, 7, 14 and 28. Tan Tock Seng Hospital, keeps a stock of rabies
vaccine
and human rabies
immunoglobulin.
Guide
for Post-Exposure
Treatment

Guide for Post-Exposure
Type of contactTreatment
with a suspect
Category
Category
I
I
II
II
III
III
a
a
b
cb
c
or confirmed rabid domestic
a
or
wild
animal,with
or animal
Type
of contact
a suspect
unavailable
observation
or
confirmedfor
rabid
domestic
or
wild a animal,
or animal
Touching
or feeding
of
unavailable
for observation
animals.
Licks on intact
skin. of
Touching
or feeding
Nibbling of uncovered skin.
animals.
Minoron
scratches
or abrasion
Licks
intact skin.
without bleeding.
Nibbling
of uncovered skin.
Licks on
broken or
skin.
Minor
scratches
abrasion
without bleeding.
Licks on broken skin.
Single or multiple transdermal
bites or scratches.
Contamination
of mucous
Single
or multiple
transdermal
membrane
with saliva (i.e.
bites or scratches.
licks).
Contamination
of mucous
membrane with saliva (i.e.
licks).
Recommended treatment
Recommended
None, if reliabletreatment
case history is
available.
None, if reliable case history is
Administer vaccine immediately. b
available.
Stop treatment if animal remains healthy
throughout an
observation
period bc of 10
Administer
vaccine
immediately.
days or
if animal
is euthanised
and
Stop
treatment
if animal
remains
healthy
found to be an
negative
for rabies
byc of 10
throughout
observation
period
appropriate
laboratory
techniques.
days
or if animal
is euthanised
and
Administer
immunoglobulin
found
to be rabies
negative
for rabies by and
vaccine immediately
Stop treatment if
appropriate
laboratoryb. techniques.
animal remains
healthy
throughout an
Administer
rabies
immunoglobulin
and
b 10 days or if the
observation
period c of
vaccine immediately
. Stop treatment if
is euthanised
andthroughout
found to bean
animal remains
healthy
c appropriate
negative
for period
rabies by
observation
of 10 days or if the
laboratory
techniques.and found to be
animal
is euthanised
negative for rabies by appropriate
techniques.
Source: Rabies pre- and post-exposurelaboratory
prophylaxis
in humans (revised 15 June
2010). Dept of Neglected Tropical Diseases. Neglected Zoonotic Diseases team.
WHO, Geneva.
to rodents, rabbits
and hares
seldom, (revised
if ever, requires
Source:
Rabies Exposure
pre- and post-exposure
prophylaxis
in humans
15 June
specific
anti-rabies
treatment.
2010). Dept
of Neglected
Tropical Diseases. Neglected Zoonotic Diseases team.
If an apparently
healthy dog
or cat inrabbits
or from
low-risk
area ifis ever,
placed
under
WHO,
Geneva. Exposure
to rodents,
anda hares
seldom,
requires
observation,
it may treatment.
be justified to delay specific treatment.
specific anti-rabies
This
period applies
onlyintoordogs
cats. Except
the case
of
If an observation
apparently healthy
dog or cat
fromand
a low-risk
area isinplaced
under
threatened
species,
other specific
domestictreatment.
and wild animals suspected as
observation,oritendangered
may be justified
to delay
rabid
should be period
euthanised
their
tissues
using
This observation
appliesand
only
to dogs
andexamined
cats. Except
in appropriate
the case of
laboratory techniques.
threatened
or endangered species, other domestic and wild animals suspected as
rabid should be euthanised and their tissues examined using appropriate
laboratory techniques.
99
99
References
1.
2.
3.
4.
5.
6.
Rupprecht CE, Hanlon CA, Hemachudha T. Rabies re-examined. Lancet Infect Dis. 2002; 2:327-43
Whitley RJ, Gnann JW. Viral encephalitis: familiar infections and emerging pathogens. Lancet
2002; 359:507-13
WHO Rabies Fact Sheet No 99 December 2008. Available at
http://www.who.int/mediacentre/factsheets/fs099/en/index.html. Accessed August 2010
Committee on Epidemic Diseases. An imported case of human rabies in Singapore. Epidemiological
News Bulletin 1999; 25:71
Warrell MJ, Warrell DA. Rabies and other Lyssavirus diseases. Lancet 2004; 363:959-69
CDC (Atlanta). Human Rabies Prevention. Recommendations of the Advisory Committee on
Immunization Practices 2008
100
RUBELLA
Causative Agent
Rubella virus
RUBELLA
Causative Agent
Incubation Period
Rubella virus
2 - 3 weeks
Incubation Period
Infectious Period
2 - 3 weeks
Few days before until seven days after onset of rash. Infants with congenital rubella
syndrome may shed the virus from their body secretions for 1 year or more after
Infectious Period
birth.
Few days before until seven days after onset of rash. Infants with congenital rubella
syndrome may shed the virus from their body secretions for 1 year or more after
Transmission
birth.
Respiratory droplets and direct contact with nasopharyngeal secretions.
Transmission
Epidemiology
Respiratory droplets and direct contact with nasopharyngeal secretions.
Rubella immunisation was introduced in Nov 1976 for female primary school
leavers at 11+ years of age. However as rubella outbreaks continued to occur in
Epidemiology
susceptible populations especially national servicemen (NS men), the vaccination
Rubella immunisation was introduced in Nov 1976 for female primary school
was extended to cover male primary school leavers in 1982. NS men were also
leavers at 11+ years of age. However as rubella outbreaks continued to occur in
routinely vaccinated to eliminate rubella in army camps. The programme was further
susceptible populations especially national servicemen (NS men), the vaccination
expanded to include children 1-2 years of age using the trivalent measles, mumps,
was extended to cover male primary school leavers in 1982. NS men were also
rubella (MMR) vaccine in Jan 1990. The 2nd dose of MMR was introduced in 1997
routinely vaccinated to eliminate rubella in army camps. The programme was further
for secondary and junior college students in a catch-up measles vaccination
expanded to include children 1-2 years of age using the trivalent measles, mumps,
programme and to all primary school leavers in 1998. Since 2008, the 2nd dose of
rubella (MMR) vaccine in Jan 1990. The 2nd dose of MMR was introduced in 1997
MMR vaccine is now given at 6-7 years of age (primary 1) under the revised
for secondary and junior college students in a catch-up measles vaccination
National Childhood Immunisation Programme.
programme and to all primary school leavers in 1998. Since 2008, the 2nd dose of
MMRrubella
vaccine
is now peaked
given atin 6-7
agenotifications.
(primary 1) With
underthe
thecatch-up
revised
The
incidence
1996years
withof487
National vaccination
Childhood Immunisation
measles
program, the Programme.
number of rubella cases has gradually declined
from 10.9 cases per 100,000 population in 1999 to 3.6 per 100,000 in 2009. The
The rubella incidence peaked in 1996 with 487 notifications. With the catch-up
incidence of congenital rubella is about 0-2 cases per year since 1995.
measles vaccination program, the number of rubella cases has gradually declined
from 10.9 cases per 100,000 population in 1999 to 3.6 per 100,000 in 2009. The
incidence
of congenitalstudy
rubella
about 0-2
cases perinyear
since
In a serosurveillance
ofisrubella
conducted
1998,
it 1995.
was found that the
overall immunity of the population to rubella was 80.2% with the lowest immunity
in the 10-14 year age group (65.5%). Another survey in 2004 showed that 15.8% of
In a serosurveillance study of rubella conducted in 1998, it was found that the
women aged 18 to 44 years were non-immune to rubella (a relatively high level
overall immunity of the population to rubella was 80.2% with the lowest immunity
compared to women of reproductive age in other developed countries).
in the 10-14 year age group (65.5%). Another survey in 2004 showed that 15.8% of
women aged 18 to 44 years were non-immune to rubella (a relatively high level
It is important to ensure that at least 95% of the children are immunised at 1-2 years
compared to women of reproductive age in other developed countries).
of age. Congenital rubella can only be completely eliminated if every woman in the
It is important to ensure that at least 95% of the children are immunised at 1-2 years
of age. Congenital rubella can only be completely eliminated if every woman in the
101
101
15-44 year age group is immunised against the disease. Women should be advised to
be vaccinated before they are married and prior to conception.
15-44 year age group is immunised against the disease. Women should be advised to
be
vaccinated
before they are married and prior to conception.
Clinical
Features
 Many cases are subclinical.
Clinical
Features
 Infection
usually starts with a mild prodrome and appearance of tender
 Many
casespost-auricular
are subclinical.
occipital,
and cervical lymphadenopathy which precedes the
 appearance
Infection usually
starts with a mild prodrome and appearance of tender
of the rash.
occipital, post-auricular
and cervical
lymphadenopathy
precedes
the
 Prodromal
symptoms include
low grade
fever, headache,which
malaise,
anorexia,
appearance
of the rash.
mild
conjunctivitis,
coryza, sore throat, cough and lymphadenopathy. The
 Prodromal
symptoms
include
low grade
malaise, anorexia,
symptoms last
1 - 5 days
and subside
rapidlyfever,
after headache,
the rash appears.
mildenanthem
conjunctivitis,
coryza,
sore throat,
and
lymphadenopathy.
 An
consisting
of reddish
spots oncough
the soft
palate
may be observedThe
in
symptoms
last period
1 - 5 days
and
rapidly
appears.
the
prodromal
or on
thesubside
first day
of theafter
rashthe
butrash
is not
diagnostic.
An enanthem
consisting
reddish spots ondirection
the soft and
palate
may be
observed
 The
rash progresses
in aofcephalo-caudal
usually
subsides
in in3
the prodromal
or the
on the
first
daythe
of the
rashisbut
is not diagnostic.
days.
By theperiod
end of
first
day,
body
covered
with red, discrete
 maculopapules.
The rash progresses
in athird
cephalo-caudal
andwithout
usuallyany
subsides
By the
day, the rashdirection
disappears
stainingin or3
days. By the end of the first day, the body is covered with red, discrete
desquamation.
maculopapules.
Byslightly
the third
day, the rash disappears without any staining or
 The
spleen may be
enlarged.
desquamation.
 Fever
if present is usually low grade and lasts 1 - 3 days.
The spleen maysuch
be slightly
enlarged.and arthritis, which are more common in
 Complications
as arthralgia
 adults,
Fever ifclear
present
is usually
lowdays.
gradeEncephalitis
and lasts 1 -and
3 days.
in about
5 - 10
thrombocytopaenia are rare
 complications.
Complications such as arthralgia and arthritis, which are more common in
adults,
clear
aboutinfection
5 - 10 days.
and thrombocytopaenia
are rare
 The
risk
of in
foetal
and Encephalitis
congenital anomalies
depends on stage
of
complications.
pregnancy at which infection occurs (lower risk after 20 weeks).
 The risk of foetal infection and congenital anomalies depends on stage of
pregnancy
at which
infection occurs (lower risk after 20 weeks).
Differential
diagnoses
include:
 Exanthem subitum (Roseola infantum)
Differential
diagnoses
include:
 Drug
rash
Exanthem mononucleosis
subitum (Roseola infantum)
 Infectious
 Drug
rash infections
Enteroviral
 Infectious
mononucleosis
Mild measles
 Enteroviral
Scarlet feverinfections
 Mild measles
 Scarlet fever
Investigations
 Indicate on the request form a brief clinical history, as the assays used for
Investigations
immunity screening and for diagnosing recent infection may differ.
 Indicate
on the
request form
brief clinical ahistory,
the in
assays
used for
Rubella can
be diagnosed
by ademonstrating
fourfoldasrise
IgG antibody
immunity
screening
diagnosingsamples
recent infection
may differ.
titres between
acute and for
convalescent
and by detecting
rubella-specific
 IgM
Rubella
can be diagnosed by demonstrating a fourfold rise in IgG antibody
antibody.
between acute
convalescent
samples
and bybydetecting
 titres
Rubella-specific
IgMand
antibody
is usually
detectable
five daysrubella-specific
after onset of
IgM
antibody.
illness
and remains detectable for at least one month but commonly for two
 Rubella-specific
IgM antibody is usually detectable by five days after onset of
months.
illness and remains detectable for at least one month but commonly for two
months.
102
102
 Caution is advised in interpretation of rubella IgM antibody tests since false
positive results are not uncommon. They may arise during other virus infections
 Caution
is advised
interpretation
of rubella
IgM antibody tests since false
such as those
due to in
parvovirus
B19, CMV
or EBV.
positive results are not uncommon. They may arise during other virus infections
such as those due to parvovirus B19, CMV or EBV.
Notification
A legally notifiable disease in Singapore. Notify Ministry of Health (Form MD 131
Notification
or electronically via CD-LENS) not later than 72 hours from the time of diagnosis.
A legally notifiable disease in Singapore. Notify Ministry of Health (Form MD 131
or electronically via CD-LENS) not later than 72 hours from the time of diagnosis.
Management
 Patient is managed symptomatically.
Management

If infection occurs in early pregnancy, the patient should be referred to a
 Patient
is managed
gynaecologist
or ansymptomatically.
infectious disease physician who can provide advice and
 If
infection
occurs
in early risks
pregnancy,
the patient
should beandreferred
to a
counselling on the possible
of congenital
malformation
appropriate
gynaecologist
anpoint
infectious
disease physician who can provide advice and
management atorthat
in pregnancy.
on be
theisolated
possiblefrom
risks
of congenital
malformation
and precautions)
appropriate
 counselling
Patients should
non-immune
persons
(with droplet
management
at
that
point
in
pregnancy.
for seven days after onset of rash.
 Patients should be isolated from non-immune persons (with droplet precautions)
for seven
days
after onset of rash.
Prevention
and
Control
 Combined measles/ mumps/rubella (MMR) vaccine is given to all pre-school
Prevention
Control
childrenand
at the
age 12-15 months and primary school entrants at the age of 6-7
 years
Combined
measles/
mumps/rubella
(MMR) vaccine
is given Programme
to all pre-school
as part
of the
National Childhood
Immunisation
(see
children at2).
the age 12-15 months and primary school entrants at the age of 6-7
Appendix
part of the
National
Childhood
(see
 years
Rubellaasvaccination
is also
routinely
offeredImmunisation
at polyclinicsProgramme
to non-immune
Appendix
2). and mothers who have just delivered their first babies.
married women
 Rubella
vaccination
is alsoatroutinely
at polyclinics
to non-immune
All unimmunised
children
nurseries,offered
kindergartens
and schools
where an
married
and mothers
who
have just delivered their first babies.
outbreakwomen
is occurring
should be
immunised.
 All
at nurseries,
kindergartens
schools
where
an
The unimmunised
vaccine shouldchildren
be avoided
in pregnancy
and womenand
who
received
rubella
outbreakshould
is occurring
shouldtobe
immunised.
vaccine
be advised
avoid
pregnancy for one month after vaccination.
 The vaccine
be avoided
in pregnancycongenital
and women
who received
rubella
observedshould
risk for
vaccine-associated
rubella
is zero but
the
vaccine
should
beasadvised
avoid
pregnancy
one month
after vaccination.
theoretical
risk is
high asto2%.
The
currentlyfor
recognised
theoretical
risk does
The
observed automatic
risk for vaccine-associated
congenital ifrubella
is zerohasbutbeen
the
not mandate
termination of pregnancy
a woman
theoretical
riskvaccinated
is as highwith
as 2%.
Thevaccine.
currently recognised theoretical risk does
inadvertently
rubella
mandate automatic
termination
pregnancy
a woman
has been
 not
All childhood
immunisations
should beofnotified
to theifNational
Immunisation
inadvertently
vaccinated
withBoard.
rubella Post-vaccination
vaccine.
Registry, Health
Promotion
adverse reactions should
 All
should be notified
the National
alsochildhood
be notifiedimmunisations
to the Pharmacovigilance
Branch, to
Health
Sciences Immunisation
Authority.
Registry, Health Promotion Board. Post-vaccination adverse reactions should
also be notified to the Pharmacovigilance Branch, Health Sciences Authority.
References
1.
Committee on Epidemic Disease. Serosurveillance of rubella in Singapore. Epidemiological News
2.
1.
Ang LW, Chua LT, James L et al. Epidemiological surveillance and control of rubella in Singapore,
Committee on Epidemic Disease. Serosurveillance of rubella in Singapore. Epidemiological News
1991-2007. Ann Acad Med Singapore 2010; 39; 95-101
Bulletin 2001; 27:1-3
Ang LW, Chua LT, James L et al. Epidemiological surveillance and control of rubella in Singapore,
1991-2007. Ann Acad Med Singapore 2010; 39; 95-101
Bulletin 2001; 27:1-3
References
2.
103
103
SEVERE ACUTE RESPIRATORY SYNDROME
(SARS)
SEVERE ACUTE RESPIRATORY SYNDROME
(SARS)
Causative Agent
SARS-associated coronavirus (SARS-CoV)
Causative Agent
SARS-associated
coronavirus (SARS-CoV)
Incubation
Period
Typically 2-7 days but may be prolonged up to 10-14 days
Incubation Period
Typically 2-7
days but may be prolonged up to 10-14 days
Infectious
Period
Throughout the symptomatic phase of the disease.
Infectious Period
Throughout
the may
symptomatic
phaseviral
of the
disease.in the stool for up to 6 weeks after
Although there
be persistent
shedding
recovery from clinical illness, transmission of the disease has not been documented
Although
there maynor
be convalescent
persistent viral
shedding in the stool for up to 6 weeks after
from asymptomatic
individuals.
recovery from clinical illness, transmission of the disease has not been documented
from asymptomatic nor convalescent individuals.
Transmission
Respiratory droplets and less often by direct contact with objects contaminated by
Transmission
respiratory
secretions. Oral-faecal and airborne transmission may occur under
Respiratory
droplets and less often by direct contact with objects contaminated by
special
circumstances.
respiratory secretions. Oral-faecal and airborne transmission may occur under
special
circumstances.
Epidemiology
The first outbreak of this new infectious disease occurred in Guangdong, China in
Epidemiology
November 2002, but soon spread to several Asian countries and Canada by March
The
outbreak
of this
newoninfectious
occurred in
China in
2003, although
twoGuangdong,
cases attributed
to
2003.first
The
outbreak
ended
5th July disease
November
2002,
but
soon
spread
to several
Asian countries
and Canada
by March
laboratory transmission were reported
from
Singapore
and
Taiwan
in
September
and
2003, although
twooutbreak
cases attributed
to
2003.
The 2003,
outbreak
ended onAnother
5th Julylaboratory
December
respectively.
associated
occurred in
laboratory
transmission
were
reported
from
Singapore
and
Taiwan
in
September
and
China in April 2004.
December 2003, respectively. Another laboratory associated outbreak occurred in
The
majority
transmission occurred in hospitals and other institutional healthcare
China
in Aprilof2004.
settings.
The majority of transmission occurred in hospitals and other institutional healthcare
settings.
By the end of the worldwide outbreak in July 2003, a total of 8096 cases were
reported, with 774 deaths and a case-fatality rate of 9.6 percent.
By the end of the worldwide outbreak in July 2003, a total of 8096 cases were
reported, March
with 774
deaths
a case-fatality
ratecases,
of 9.6with
percent.
Between
and
May and
2003,
a total of 238
33 deaths, were reported
in Singapore. 41% of the cases were healthcare workers, and 68% were females. The
Betweenage
March
Maycases
2003,
a total
of 238
with 33 deaths, were reported
median
of alland
SARS
was
36 (range
4 tocases,
90) years.
in Singapore. 41% of the cases were healthcare workers, and 68% were females. The
median age of all SARS cases was 36 (range 4 to 90) years.
104
104
Clinical Features
 The clinical presentation is non-specific and resembles other influenza-like
Clinical
Features
illnesses.
clinical presentation
non-specific
influenza-like
 The prodrome
is prolongedis lasting
from 3and
to 7resembles
days and other
is characterised
by
illnesses.
fever,
malaise, headache and myalgia. Respiratory symptoms and diarrhoea, if
 present,
The prodrome
is occur
prolonged
from
to 7 of
days
and is characterised by
typically
a few lasting
days after
the3onset
fever.
malaise,
headache
and
myalgia.
Respiratory
diarrhoea, if
 fever,
Physical
examination
is not
helpful
except
as a gaugesymptoms
of severityand
of illness.
present, typically
occur vary
a fewfrom
daysmild
after infection
the onset (80%)
of fever.
 Clinical
manifestations
to severe disease (20%)
 with
Physical
examination
not death.
helpful except as a gauge of severity of illness.
respiratory
failureisand
 Death
Clinical
manifestations
vary
from mild infection
(80%)
to multiorgan
severe disease
(20%)
is usually caused by combination
of respiratory
and
failure.
with
respiratory
failure
and
death.
 The clinical course is marked by deterioration in the second week of illness and
 Death
is usually
caused
by combination
of respiratory
and multiorgan
failure.and
recovery
by the third
week
in the majority
of cases. Children
have a shorter
 The
clinical
is marked by deterioration in the second week of illness and
milder
coursecourse
of illness.
byevidence
the third at
week
in the
of cases.
Children have a shorter and
 recovery
There is no
present
of majority
intra-partum
infection.
milder course of illness.
 There is no evidence at present of intra-partum infection.
Investigations
 Chest X-ray. This may be normal early in the course of the disease. However,
Investigations
the more distinct radiographic features include:
 Chesta predominantly
X-ray. This may
be normal
early inofthe
course of
the disease. However,
peripheral
location
air-space
opacity;
distinctfrom
radiographic
include:
the more
progression
unifocal features
to multifocal
or bilateral lung involvement
 aduring
predominantly
location of air-space opacity;
treatment;peripheral
and
progression
from unifocal
to multifocal
bilateral
lung involvement
 lack
of cavitation,
lymphadenopathy
andorpleural
effusion.
during treatment; and
lack of cavitation, lymphadenopathy and pleural effusion.
Case Definitions
 At the time of and in the immediate aftermath of the SARS epidemic, both the
CaseWorld
Definitions
Health Organization (WHO) and the US CDC issued case definitions for
 At
the time of and in the immediate aftermath of the SARS epidemic, both the
SARS.
Health
Organization
(WHO)
and the
US CDCifissued
caseindefinitions
for
 World
According
to the
WHO, a case
of SARS
is notifiable
it occurs
an individual
SARS.
with laboratory confirmation of infection who either meets the clinical case
 According
to has
the WHO,
case
SARS iswith
notifiable
if it occurs
in an individual
definition or
workeda in
a of
laboratory
live SARS
coronavirus
or with
with
laboratory
confirmation
infection
who either meets the clinical case
clinical
specimens
infected withofSARS
coronavirus.
has definition
worked inused
a laboratory
withincludes:
live SARS coronavirus or with
 definition
The clinicalorcase
by the WHO
clinical
specimens
infected
with SARSfever;
coronavirus.
 A history
of fever
or documented
and
 The One
clinical
case definition
by the
WHO includes:
or more
symptomsused
of lower
respiratory
tract illness (cough, difficulty
 A
history
of
fever
or
documented
fever;
in breathing, shortness of breath); and and
One or more symptoms
oflung
lowerinfiltrates
respiratory
tract illness
difficulty
 Radiographic
evidence of
consistent
with(cough,
pneumonia
or
in breathing,
shortness
of syndrome
breath); and
acute
respiratory
distress
(ARDS) or autopsy findings consistent
 with
Radiographic
evidence
of lung infiltrates
consistent
with
pneumonia
or
the pathology
of pneumonia
or ARDS
without an
identifiable
cause;
acute
and respiratory distress syndrome (ARDS) or autopsy findings consistent
the pathology
of pneumonia
or ARDS
 with
No alternative
diagnosis
fully explaining
thewithout
illness.an identifiable cause;
and
 Laboratory
diagnostic tests that are required include one or both of the
 No alternative diagnosis fully explaining the illness.
following:
 Laboratory diagnostic tests that are required include one or both of the
following:
105
105
Detection of virus (reverse transcriptase PCR) assay detecting viral RNA
present in two separate samples, or virus culture from any clinical
 specimen.
Detection of
virustwo
(reverse
transcriptase
PCR) from
assayeither
detecting
RNA
These
samples
can be obtained
two viral
separate
present
in nasopharyngeal
two separate samples,
or virus
culture
sites (e.g.
and stool)
or from
the from
same any
site,clinical
but at different
specimen.
two samples
can be obtained
from
either two separate
times (e.g. These
sequential
nasopharyngeal
aspirates);
and/or
(e.g. nasopharyngeal
andinstool)
or from
same
site,negative
but at different
 sites
Detection
of antibody (a rise
antibody
titre,the
either
from
to
times
(e.g.
nasopharyngeal
and/or immunosorbent
positive
or sequential
at least a four-fold
increase)aspirates);
by enzyme-linked
 assay
Detection
of antibody
(a rise in antibody titre,
either
from negative to
(ELISA)
and/or immunofluorescent
assay
(IFA).
positive
at leastsensitive
a four-fold
by enzyme-linked
immunosorbent
 These
areorhighly
andincrease)
specific but
positive only from
the second
assay
(ELISA)
immunofluorescent assay (IFA).
week of
illness and/or
onwards.
 These are highly sensitive and specific but positive only from the second
week of illness onwards.
Notification
A legally notifiable disease in Singapore. Notify Ministry of Health (Form MD 131
Notification
or electronically via CD-LENS) not later than 24 hours from the time of diagnosis.
A legallyMOH
notifiable
disease inon
Singapore.
Notify
Health (Form MD
131
Notify
immediately
suspicion.
CallMinistry
MOH of
Communicable
Diseases
or electronically
Surveillance
teamvia
at:CD-LENS)
98171463 not later than 24 hours from the time of diagnosis.
Notify MOH immediately on suspicion. Call MOH Communicable Diseases
Surveillance team at: 98171463
Management
 All suspected and probable/confirmed cases of SARS will be isolated and
Management
treated at the Communicable Disease Centre (CDC).
 Symptomatic
All suspectedand
andsupportive
probable/confirmed
of SARS will be isolated and
treatment forcases
all cases.
treated at the
Communicable
Diseaseduring
Centrethe
(CDC).
 Ribavirin
which
was used initially
pandemic has been shown to be
 ineffective
Symptomatic
treatment
for all cases.
in and
vitrosupportive
towards SARS
coronavirus
and is associated with significant
 toxicities.
Ribavirin which was used initially during the pandemic has been shown to be
ineffective
in vitro
towards SARS
coronavirus
significant
 Some
centres
recommend
a short
courseandofis associated
moderate with
to high
dose
toxicities.
corticosteroids.
 Some
centres
a short using
course
of moderate
dose
There may
be arecommend
role for treatment
protease
inhibitor to
likehigh
lopinavir,
corticosteroids.
immunoglobulins and interferon based on prior experience.
 There may be a role for treatment using protease inhibitor like lopinavir,
immunoglobulins
and interferon based on prior experience.
Infection
Control
 Patients with SARS should ideally be nursed in negative pressure isolation
Infection
rooms.Control
 Patients
with
SARSand
should
ideally
nursed
in negative
Respiratory
(droplet
airborne)
andbe
contact
precautions
are pressure
required. isolation
 rooms.
Procedures which may aerosolize the virus (viz. nebulizer therapy) should be
 avoided
Respiratory
(droplet and airborne) and contact precautions are required.
if possible.
 Movement
Procedures of
which
may(viz.
aerosolize
nebulizer
therapy)
should be
patients
for scansthe
or virus
other (viz.
procedures)
within
the hospital
avoided
if
possible.
should be kept to a minimum.
 Movement of patients (viz. for scans or other procedures) within the hospital
should be
kept
to a minimum.
Prevention
and
Control
 Public health measures to limit transmission include:
Prevention
and Control
 Shortening
the time from symptom-onset to isolation of patients (viz. early
 Public
health
measures to limit transmission include:
case
detection)
Shorteningcontact
the time
from symptom-onset to isolation of patients (viz. early
 Effective
tracing
case detection)
 Effective contact tracing

106
106
 Quarantine of exposed persons
 Surveillance of fever clusters and atypical pneumonia cases
 combination
Quarantineof
ofclinical
exposedand
persons
 A
relevant epidemiological features should raise
suspicions
Surveillance
of
fever
clusters
atypical
cases
of SARS. However, it isand
quite
likelypneumonia
that a de novo
case will be
 missed
A combination
of
clinical
and
relevant
epidemiological
features
should
raise
initially, and success of current preventive policies will be
gauged
by the
suspicions
of SARS. However,
size of the consequent
outbreak.it is quite likely that a de novo case will be
missed are
initially,
and success
of current
preventive
policies
bestage.
gauged by the
 Efforts
underway
to prepare
a vaccine
but are still
at anwill
early
size of the consequent outbreak.
 Efforts are underway to prepare a vaccine but are still at an early stage.
References
1. SARS Reference. http://www.sarsreference.com. Accessed Aug 2010
2. CDC (Atlanta) http://www.cdc.gov/ncidod/sars. Accessed Aug 2010
References
3. SARS
WHO http://www.who.int/csr/sars/en/index.html.
Accessed Aug
Aug 2010
2010
1.
Reference. http://www.sarsreference.com. Accessed
4. CDC
Peiris (Atlanta)
JS, Yuenhttp://www.cdc.gov/ncidod/sars.
KY, et al. The severe acute respiratory
syndrome.
N Engl J Med 2003; 349: 2431-41
2.
Accessed
Aug 2010
5.
JA, Low DE, Hefland RF. Combining clinical
and epidemiologic
features for early
3. Jernigan
WHO http://www.who.int/csr/sars/en/index.html.
Accessed
Aug 2010
of SARS.
Dis
2004;
10: 327-33
4. recognition
Peiris JS, Yuen
KY, etEmerg
al. TheInfect
severe
acute
respiratory
syndrome. N Engl J Med 2003; 349: 2431-41
6.
G, Choo
P, Leo YS
al. SARS clinical
transmission
and hospital containment.
Emerg
5. Gopalakrishna
Jernigan JA, Low
DE, Hefland
RF. et
Combining
and epidemiologic
features for early
Infect
Dis. 2004;
10:395-400
recognition
of SARS.
Emerg Infect Dis 2004; 10: 327-33
7. Gopalakrishna
Lim PL, KurupG,
A,Choo
Gopalakrishna
Laboratory-acquired
acute
respiratory Emerg
syndrome.
6.
P, Leo YSGetetal.al.SARS
transmission andsevere
hospital
containment.
N
EngDis.
J Med.
2004;
350:1740-5
Infect
2004;
10:395-400
8.
definitions
forGopalakrishna
the 4 diseases G
requiring
notification to WHOsevere
in allacute
circumstances
under
the IHR
7. Case
Lim PL,
Kurup A,
et al. Laboratory-acquired
respiratory
syndrome.
(2005).
Rec 2009; 84:52
N
Eng JWkly
Med. Epidemiol
2004; 350:1740-5
9.
Pharmacologic
of SARS:notification
current knowledge
recommendations.
Annthe
Acad
8. Tai
CaseDY.
definitions
for the 4treatment
diseases requiring
to WHOand
in all
circumstances under
IHR
Med
Singapore.
2007;36:438-43.
(2005).
Wkly Epidemiol
Rec 2009; 84:52
10. Tai
Stockman
L.J., Bellamy R.,
Garnerof
P.SARS:
SARS:current
systematic
review of
effects. PLoS
9.
DY. Pharmacologic
treatment
knowledge
andtreatment
recommendations.
Ann Acad
Med 3.
e343.2006
Med
Singapore.
2007;36:438-43.
11. Stockman
Goh KT, Cutter
J, Heng BH
et al. Epidemiology
and control
of SARS
in Singapore.
Acad Med
10.
L.J., Bellamy
R., Garner
P. SARS: systematic
review
of treatment
effects.Ann
PLoS
Singapore
2006;35:301-6.
Med
3. e343.2006
11. Goh KT, Cutter J, Heng BH et al. Epidemiology and control of SARS in Singapore. Ann Acad Med
Singapore 2006;35:301-6.
107
107
SEXUALLY-TRANSMITTED INFECTIONS
Causative AgentsSEXUALLY-TRANSMITTED INFECTIONS
In 2009, the top 5 sexually-transmitted infections (STIs) diagnosed in Singapore
Causative
Agentstrachomatis (infection of the urethra, cervix, pharynx and rectum),
were:
Chlamydia
In 2009, the
top 5 sexually-transmitted
infections
(STIs)
diagnosed
in Singapore
Neisseria
gonorrhoeae
(infection of the urethra,
cervix,
pharynx
and rectum),
nonwere:
Chlamydia
trachomatis
of the urethra,
cervix, pharynx
gonococcal
urethritis
(NGU),(infection
herpes simplex
virus (HSV):
types 1 and rectum),
2 (anoNeisseria
gonorrhoeae
(infection
of the urethra,
cervix, (ano-genital
pharynx and warts).
rectum),Other
nongenital herpes),
and human
papilloma
virus (HPV)
gonococcal
urethritis
herpespallidum
simplex (syphilis),
virus (HSV):
types 1 andvaginalis
2 (anoimportant STIs
are (NGU),
Treponema
Trichomonas
genital herpes), and human
humanimmunodeficiency
papilloma virus virus
(HPV)
(ano-genital
(trichomoniasis),
infection
(HIV). warts). Other
important STIs are Treponema pallidum (syphilis), Trichomonas vaginalis
(trichomoniasis),
and human immunodeficiency virus infection (HIV).
Incubation Period
Chlamydia
:
5 - 14 days
Incubation Period
Gonorrhoea
:
3 - 5 days
Chlamydia herpes
Ano-genital
:
25 - 14 days
Gonorrhoea warts
3 -65months
days (mean 3 months)
Ano-genital
:
1Ano-genital herpes
2 - -14
Syphilis
:
10
90days
days (mean 21 days)
Ano-genital warts
6 months
Trichomoniasis
:
a1-few
days (mean 3 months)
Syphilis
:
10 - 90ofdays
(mean
days)
HIV
mean
1 month
to 21
acute
HIV infection,
Trichomoniasis
:
amean
few of
days
5 to 8 years to AIDS if untreated
HIV
:
mean of 1 month to acute HIV infection,
mean
of 5 to 8 years to AIDS if untreated
Infectious Period
Gonorrhoea, chlamydia
:
active infection, symptomatic or asymptomatic
Infectious
Ano-genitalPeriod
herpes
:
presence of vesicles and erosions; asymptomatic
Gonorrhoea, chlamydia
:
active shedding
infection, is
symptomatic
or asymptomatic
viral
also an important
route of
Ano-genital herpes
:
presence
of vesicles and erosions; asymptomatic
transmission
viral
is also
an important
Ano-genital warts
:
highershedding
with presence
of active
lesions; route of
transmissioninfections common
subclinical
Ano-genital
warts
:
higher
presence
of active stages
lesions;
Syphilis
during with
primary
and secondary
subclinical
infections
commonor asymptomatic
Trichomoniasis
:
active
infection,
symptomatic
Syphilis
during primary
stagesif untreated
HIV
infection
:
infectious
from and
earlysecondary
on till demise
Trichomoniasis
:
active infection, symptomatic or asymptomatic
HIV infection
:
infectious from early on till demise if untreated
Clinical
Features
STI may present with:
Clinical
Features
 genital
discharges (gonorrhoea, chlamydia, trichomoniasis)
STI
presentulcers
with: (herpes, syphilis)
 may
ano-genital
 ano-genital
genital discharges
(gonorrhoea,
chlamydia,
trichomoniasis)
growths
(warts, molluscum
contagiosum)
ano-genital
ulcersscabies)
(herpes, syphilis)
 rashes
(syphilis,
 ano-genital
growths (warts,
contagiosum)
pelvic inflammatory
diseasemolluscum
(gonorrhoea,
chlamydia)
 rashes
(syphilis, scabies)
epididymo-orchitis
(gonorrhoea, chlamydia)
pelvicinfection
inflammatory
diseasein(gonorrhoea,
 HIV
may present
several wayschlamydia)
depending on the organ systems
 affected
epididymo-orchitis
(see chapter(gonorrhoea,
on HIV). chlamydia)
 HIV infection may present in several ways depending on the organ systems
affected (see chapter on HIV).
108
108
Many STIs may be asymptomatic and can be detected only if the appropriate
laboratory screening tests are performed (see references).
Many STIs may be asymptomatic and can be detected only if the appropriate
laboratory
screening
tests are
Investigations
and Guide
to performed
Diagnosis (see references).
 Ano-genital Herpes (First episode/ Recurrent)
Investigations
Guideor
to erosions
Diagnosisin the ano-genital area (may be severe with
 Typicaland
vesicles
 Ano-genital
Herpes (First episode/ Recurrent)
initial episode).
 Typical
vesicles
or isolation,
erosions in
the immunofluorescence
ano-genital area (may(DIF),
be severe
Confirmed
by viral
direct
PCR, with
EIA
initial
episode). serological test against glycoprotein gG1 (HSV-1) & gG2
or
type-specific
 (HSV-2)
ConfirmedforbyHSV
viral (serology
isolation, is
direct
(DIF),
PCR, as
EIA
not immunofluorescence
useful for first episode
infection
it
or type-specific
test for
against
glycoprotein
gG1 following
(HSV-1) &a gG2
takes
between 6serological
and 8 weeks
serological
detection
first
(HSV-2) for HSV (serology is not useful for first episode infection as it
episode).
takes between 6 and 8 weeks for serological detection following a first
episode).
 Chlamydia
Genital Infection—(A laboratory diagnosed infectious disease)
 Nucleic acid amplification test (NAAT) (e.g. PCR) positive for C.
diagnosed
 Chlamydia
Genital
Infection—(A
trachomatis
from
ano-genital laboratory
specimen or
urine; or infectious disease)
Nucleic detection
acid amplification
(NAAT) for
(e.g.
positive
foranoC.
 Antigen
(e.g. EIA, test
IF) positive
C. PCR)
trachomatis
from
trachomatis
from ano-genital specimen or urine; or
genital specimen.
 Antigen
detection
EIA,
IF)aspositive
for distinguish
C. trachomatis
from
anoChlamydia
serology(e.g.
is not
useful
it does not
between
past
or
genital
specimen.
current infection; there is also cross-reactivity with other chlamydial
 species.
Chlamydia serology is not useful as it does not distinguish between past or
current infection; there is also cross-reactivity with other chlamydial
species.
 Gonorrhoea
 Purulent genital discharge (associated with dysuria in males), history of
 Gonorrhoea
recent unprotected sexual intercourse; or
Purulent genitalsmear
discharge
dysuria with
in males),
history of
 Gram-stained
from(associated
genital with
discharges
Gram-negative
recent unprotected
sexualorintercourse; or
intracellular
diplococci;
 Positive
Gram-stained
frommedia
genital
with
culture smear
on selective
for N.discharges
gonorrhoeae;
or Gram-negative
intracellular
diplococci;
or
 Urine nucleic acid amplification test (NAAT) (e.g. PCR) positive for N.
 Positive
culture on selective media for N. gonorrhoeae; or
gonorrhoeae.
 Urine
nucleic
acid amplification
(NAAT)
PCR)&positive
for N.
Gonorrhoea
serology
is not useful test
due to
lack of (e.g.
sensitivity
specificity.
gonorrhoeae.
 Gonorrhoea serology
not useful due to lack of sensitivity & specificity.
 Non-Gonococcal
Urethritisis(NGU)
 Mucopurulent or whitish discharge from urethra associated with dysuria or
 Non-Gonococcal
Urethritis (NGU)
urethral discomfort/itch
in males, history of recent unprotected sexual
 intercourse;
Mucopurulent
or or whitish discharge from urethra associated with dysuria or
urethral discomfort/itch
in males,
history
of count
recent(5unprotected
sexual
 Gram-stained
smear showing
increased
pus cell
or more WBC
per
intercourse;
or
high-power field) in absence of Gram-negative intracellular diplococci; or
Gram-stained
increased
pus urine
cell count
 Visible
threadssmear
in theshowing
first glass
of a 2 glass
test. (5 or more WBC per
high-power field) in absence of Gram-negative intracellular diplococci; or
 VisibleSyphilis
threads in the first glass of a 2 glass urine test.
 Infectious
 Presence of primary chancre usually solitary, indurated, non-tender (but the
 Infectious
Syphilis
ulcer may
also be atypical), inguinal lymphadenopathy; or
 Presence of primary chancre usually solitary, indurated, non-tender (but the
ulcer may also be atypical), inguinal lymphadenopathy; or
109
109

Presence of clinical features of secondary syphilis e.g. rash especially on
palms and soles, ano-genital patches and growths, generalized
 Presence
of clinicalpatchy
features
secondary
syphilis
lymphadenopathy,
hairofloss;
confirmed
by: e.g. rash especially on
palms and
soles, dark-field
ano-genitalmicroscopic
patches examination
and growths,
generalized
 Positive
of exudate
from
lymphadenopathy,
patchy
hair
loss;
confirmed
by:
primary or secondary ano-genital lesions for spirochaetes; or
Positive dark-field
 Reactive
blood testsmicroscopic
for syphilis:examination of exudate from
primary or secondary
ano-genital
lesions for spirochaetes; or
1. Non-specific
treponemal
tests (RPR/VDRL)
 Specific
Reactivetreponemal
blood tests tests
for syphilis:
2.
(TPPA/TPHA, LIA, Syphilis EIA)
1. Non-specific treponemal tests (RPR/VDRL)
2. Syphilis
Specific treponemal tests (TPPA/TPHA, LIA, Syphilis EIA)
Non-Infectious
 Presence of clinical features of tertiary syphilis (viz. cardiovascular
Non-Infectious
Syphilis
syphilis, central
nervous system syphilis); or
 Asymptomatic
Presence of clinical
of tertiary
syphilis
(viz. cardiovascular
infectionfeatures
with reactive
blood tests
for syphilis
syphilis,
central nervous
system
syphilis);
or
 Note
- persistence
of reactive
serology
in patients
with treated syphilis may
 be
Asymptomatic
with scar
reactive blood tests for syphilis
indicative ofinfection
a serological
 Note - persistence of reactive serology in patients with treated syphilis may
be indicative
of a serological scar
Congenital
Syphilis
 Presence of clinical features of active disease (e.g. muco-cutaneous signs,
Congenital
Syphilishepatosplenomegaly) and confirmed by reactive blood tests
bone changes,
 for
Presence
of clinical features of active disease (e.g. muco-cutaneous signs,
syphilis.
bone
changes,
hepatosplenomegaly)
by reactive
 Asymptomatic infection
in infant bornand
to confirmed
infected mother
with: blood tests
for syphilis.
 Detectable LIA IgM in infant; or
 Asymptomatic
infection in titre
infant
to fourfold
infected or
mother
with:
 RPR/VDRL
inborn
infant
greater
than in mother;
 or
Detectable LIA IgM in infant; or
titre in
infant
fourfold
 RPR/VDRL titres
show
serial
rise; oror greater than in mother;
or
 Reactive
CSF-VDRL or abnormal CSF FEME in infant.
 RPR/VDRL titres show serial rise; or
 Reactive CSF-VDRL or abnormal CSF FEME in infant.
Trichomoniasis
 Diagnosed by direct wet-mount microscopy and culture. Serology is not
Trichomoniasis
useful.
 Diagnosed by direct wet-mount microscopy and culture. Serology is not
useful. There are no clear guidelines for screening with serology.
Mycoplasma:

There
clearasguidelines
for screening
with serology.
Mycoplasma:
Candida:
Serology
is are
not no
useful
it is not indicative
of a genital
cause/disease.







 Candida: Serology is not useful as it is not indicative of a genital cause/disease.
Management
 All patients with a STI should be screened for syphilis, hepatitis B and HIV
Management
infection.
All patients
with
a STIrecommended
should be screened
for syphilis,
B and HIV
 Patients
should
receive
antimicrobials
in thehepatitis
correct dosages
(see
infection.
references).
Test-of-cure is important to assess treatment efficacy particularly
 for
Patients
should and
receive
recommended antimicrobials in the correct dosages (see
gonorrhoea
syphilis.
references). Test-of-cure is important to assess treatment efficacy particularly
for gonorrhoea and syphilis.
110
110






Chlamydia:
 Doxycycline 100mg bid x 7days (avoid if pregnant)
Chlamydia:
Erythromycin 500mg qid x 7 days
 Doxycycline
bid x 7days
Erythromycin100mg
ethylsuccinate
800 (avoid
mg qidifx pregnant)
7days
 Azithromycin
Erythromycin 500mg
x 7(useful
days if adherence is an anticipated problem)
1gm x 1qid
dose
 Erythromycin ethylsuccinate 800 mg qid x 7days
Gonorrhoea:
Azithromycin 1gm x 1 dose (useful if adherence is an anticipated problem)
 All patients with gonorrhoea should be given concurrent treatment for
Gonorrhoea:
chlamydia.
All patients with are
gonorrhoea
should bedue
given
concurrent
treatment
 Fluoroquinolones
not recommended
to high
prevalence
(80%) for
of
chlamydia.in N. gonorrhoeae.
resistance
Fluoroquinolones
not recommended
due to high
of
 Repeat
smears andarecultures
should be performed
onprevalence
or around (80%)
the 14th
resistance in N.day.
gonorrhoeae.
post-treatment
Repeat
smears
culturesallergy,
should IM
be performed
on orcan
around
the 14th
 For
those
withand
penicillin
spectinomycin
be used.
Or
post-treatment
day. testing and desensitization. Specialist consultation
consider
allergy
 recommended.
For those with penicillin allergy, IM spectinomycin can be used. Or
consider allergy
testing and desensitization. Specialist consultation
 Uncomplicated
(pharynx/urethra/rectum/cervix):
recommended.
 IM Ceftriaxone 250mg x 1 dose; or
(pharynx/urethra/rectum/cervix):
 Uncomplicated
 Cefixime
400mg x 1 dose
IM Ceftriaxone
250mg Infections
x 1 dose; or
 Severe orDisseminated
Gonococcal
(DGI):
 IV
Cefixime
400mg 1-2g
x 1 dose
Ceftriaxone
daily. Duration depending on site of
 Severe or Disseminated
Gonococcal
infection and
response Infections (DGI):
 IV Ceftriaxone 1-2g daily. Duration depending on site of
infection and response
Syphilis:
 Cases of syphilis should be treated with intramuscular benzathine penicillin.
Syphilis:
They should have serological tests repeated at 3 months, and then every 6
 months
Cases offor
syphilis
should
be treated
intramuscularshould
benzathine
2 years.
Suspected
caseswith
of neurosyphilis
have penicillin.
a lumbar
They should
have serological tests repeated at 3 months, and then every 6
puncture
performed.
months
2 years.
Suspected
of neurosyphilis
have asyphilis,
lumbar
 For
late for
latent
syphilis,
syphiliscases
of unknown
duration,should
congenital
puncture performed.
neurosyphilis
or syphilis in pregnancy, the treatment recommendations are
 different
For late latent
syphilis,
syphilis
of should
unknown
and relevant
expert
advice
be duration,
sought. congenital syphilis,
neurosyphilis
or syphilisSyphilis:
in pregnancy, the treatment recommendations are
 Primary
and Secondary
different and relevant
expert advice
should
be million
sought. units x 1 dose. (Some
IM Benzathine
Penicillin
G 2.4
 Primary and Secondary
authoritiesSyphilis:
use 2 doses for secondary syphilis); or
IM Aqueous
Benzathine
Penicillin
G 2.4 million
units units
x 1 dose.
 IM
Procaine
Penicillin
G 600,000
daily(Some
x 10
authorities use 2 doses for secondary syphilis); or
days
IM Aqueous
 Penicillinallergic
patients: Procaine Penicillin G 600,000 units daily x 10
days
 Doxycycline 100mg bid x 14 days; or
 Penicillinallergic
patients: 500mg qid x 14 days; or
Erythromycin
Doxycycline 100mg
x 14
days;
or
 Azithromycin
500mgbid
daily
x 10
days
 Erythromycin 500mg qid x 14 days; or
 Azithromycin 500mg daily x 10 days
111
111
Cases of first-episode genital herpes should be treated with acyclovir or related
medications. Recurrent genital herpes may be treated with either episodic or
 Cases
of first-episode
genital herpes
should be treated with acyclovir or related
suppressive
anti-viral regimens
(see references).
medications. warts
Recurrent
herpes
may be or
treated
with either
or
 Ano-genital
can genital
be treated
medically
surgically;
they episodic
should be
suppressive
anti-viral
regimens
(see
references).
followed up till all visible warts are cleared. Regular PAP smears are
 Ano-genital
can be
treated medically or surgically; they should be
recommendedwarts
for female
patients.
followed
up till all visible
warts
aremetronidazole
cleared. Regular
PAP smears are
 Cases
of trichomoniasis
are treated
with
(see references).
recommended for female patients.
 Cases of trichomoniasis are treated with metronidazole (see references).
Notification
 Chlamydia, gonorrhoea, syphilis (infectious, non-infectious and congenital),
Notification
NGU, genital herpes (first episode and recurrent) should be notified to the DSC
 clinic
Chlamydia,
syphilis
andCD-LENS.
congenital),
by fax gonorrhoea,
(62994335) using
form(infectious,
MD 131 ornon-infectious
electronically via
NGU, genital
herpeson
(first
recurrent)
should
be notified to the DSC
 Provide
information
typeepisode
of HSVand
detected
where
available.
clinic bynotifications
fax (62994335)
using form
MDherpes
131 orare
electronically
via CD-LENS.
 Repeat
of recurrent
genital
not necessary.
Provide
information
on typeand
of HSV
detected
whereneed
available.
 The
name,
NRIC, address
telephone
number
not be completed, but
 initials,
Repeat notifications
of recurrent
genital
herpes arestatus
not necessary.
sex, date of birth,
ethnicity
and residential
should be provided.
 The name, NRIC, address and telephone number need not be completed, but
initials, and
sex, Control
date of birth, ethnicity and residential status should be provided.
Prevention
 Patients with STI should be given information about their current infection.
Prevention
and future
Control

To prevent
infections, information on safer sex should be given too e.g.
 correct
Patientsand
withconsistent
STI should
be given
condom
use.information about their current infection.
 To
prevent
future infections, tracing
information
onbe
safer
sex should
be givenand
too treat
e.g.
Partner
management/contact
should
conducted
to diagnose
correct andinconsistent
condom
use. complications and further transmission.
infections
sex partners,
to prevent
 Partner
management/contact
should
be conducted
to diagnose
andB treat
Antenatal
mothers should betracing
routinely
screened
for syphilis,
hepatitis
and
infections
in sex partners, to prevent complications and further transmission.
HIV infection.
 Antenatal
should
be routinely
syphilis,
hepatitis
and
Hepatitis Bmothers
vaccination
should
be givenscreened
to thosefor
who
are negative
forBHBV
HIV
infection.
markers.
 Hepatitis
B vaccination
should
be givenwith
to those
whoeducational
are negative
for HBV
Brothel-based
sex workers
are provided
STI/HIV
information
markers.
and taught negotiation skills to achieve 100% condom use; they are screened
 Brothel-based
sex workers
are provided
with STI/HIV
routinely for syphilis,
gonorrhoea,
chlamydia,
HIV andeducational
hepatitis Binformation
infections.
and
taughtSTI/HIV
negotiation
skills toforachieve
condom
use; they
are screened
Targeted
education
at risk100%
groups
e.g. youth,
MSM,
military
routinely
gonorrhoea,
HIV and hepatitis
personnel,for
andsyphilis,
clients of
sex workerschlamydia,
should be conducted
regularly.B infections.
STI/HIV
education
for early
at risk
groups e.g.
MSM, military
 Targeted
Patients are
encouraged
to seek
treatment,
not toyouth,
self-medicate
and to
personnel,
and
clients ofmedications.
sex workers should be conducted regularly.
complete all
prescribed
 Patients
are encouraged
to seek may
earlyresult
treatment,
to self-medicate
and to
Self-medication
with antibiotics
in the not
emergence
of drug-resistant
complete
all
prescribed
medications.
strains. Medical practitioners should not dispense antibiotic chemoprophylaxis
 as
Self-medication
antibiotics
may result
in thethis
emergence
drug-resistant
there is no onewith
universally
effective
antibiotic,
may alsoofresult
in a false
strains.
should not dispense antibiotic chemoprophylaxis
sense ofMedical
security practitioners
and may be dangerous.
as there is no one universally effective antibiotic, this may also result in a false
sense of security and may be dangerous.

112
112
References
1.
DSC clinic website: http://www.dsc-sexualhealth.com.sg. Accessed Dec 2010.
References
2. STI Management Guidelines - Department of STI Control, National Skin Centre, 2007
3.
Clinical
Guidelines on genital Accessed
ulcers Dec
& 2010.
discharges, May
1. MOH
DSC clinic
website:Practice
http://www.dsc-sexualhealth.com.sg.
Accessed
2010.
2. http://www.moh.gov.sg/mohcorp/publications.aspx?id=22326.
STI Management Guidelines - Department of STI Control, National
Skin Dec
Centre,
2007
3.
MOH Clinical Practice Guidelines on genital ulcers & discharges,
http://www.moh.gov.sg/mohcorp/publications.aspx?id=22326. Accessed Dec 2010.
113
113
May
2009:
2009:
SHIGELLOSIS (BACILLARY DYSENTERY)
Causative AgentsSHIGELLOSIS (BACILLARY DYSENTERY)
Shigella sonnei, S. flexneri, S. boydii and S. dysenteriae.
Causative Agents
Shigella
sonnei,
S. flexneri, S. boydii and S. dysenteriae.
Incubation
Period
Usually 1 - 3 days. Up to 1 week for S. dysenteriae type 1
Incubation Period
Usually 1 -Period
3 days. Up to 1 week for S. dysenteriae type 1
Infectious
Throughout duration of acute illness and until the organism is no longer present in
Infectious
Periodwithin 4 weeks after illness.
the
stool, usually
Throughout duration of acute illness and until the organism is no longer present in
the stool, usually within 4 weeks after illness.
Transmission
 Direct or indirect faecal-oral transmission from a symptomatic person or shortTransmission
term asymptomatic carrier. Also via faecally-contaminated water, milk or food.
 Transmission
Direct or indirect
faecal-oral
transmission
from a symptomatic person or shortby house
flies has
also been documented.
termfew
asymptomatic
Alsocan
viacause
faecally-contaminated
water,
milk or food.
 As
as 10-100 carrier.
organisms
infection, enabling
person-to-person
Transmissionwhere
by house
flies conditions
has also been
transmission
hygiene
aredocumented.
compromised.
As few as have
10-100
organisms
can cause men;
infection,
person-to-person
 Outbreaks
occurred
in homosexual
underenabling
conditions
of crowding;
transmission
where hygiene
are compromised.
and
where personal
hygieneconditions
is poor such
as in day care centres, jails, mental
 institutions
Outbreaks have
occurredrefugee
in homosexual
and crowded
camps. men; under conditions of crowding;
and where personal hygiene is poor such as in day care centres, jails, mental
institutions and crowded refugee camps.
Epidemiology
Endemic throughout the world with the greatest burden of disease occurring in
Epidemiology
developing
countries afflicting children less than five years of age particularly. S.
Endemic
throughout
world of
with
the greatest
burden countries.
of disease occurring in
sonnei
accounts
for thethe
majority
shigellosis
in developed
developing countries afflicting children less than five years of age particularly. S.
sonnei
accountsa for
of shigellosis
developedwere
countries.
In
Singapore,
totaltheofmajority
29 sporadic
cases of in
shigellosis
reported in 2008, as
compared to 13 cases in 2007. The serotypes involved were Shigella sonnei
In Singapore,
a total
of 29 sporadic
cases
shigellosis
reported
in 2008,
as
(75.9%),
Shigella
dysenteriae
(13.8%),
and of
Shigella
boydiiwere
(10.3%).
Of the
reported
compared
to 13local
cases
in 2007.
The serotypes
involved
cases,
17 were
residents
comprising
12 indigenous
andwere
five Shigella
imported sonnei
cases.
(75.9%),
Shigella
dysenteriae (13.8%),
and Shigella
boydiilocally.
(10.3%).
the reported
There
were
two non-residents
that acquired
the infection
TheOfremaining
10
cases, comprised
17 were local
comprising
12 indigenous
andmedical
five imported
cases.
cases
oneresidents
tourist and
nine foreigners
seeking
treatment
in
There were The
two non-residents
acquired
the the
infection
locally.
remaining(1),
10
Singapore.
five imported that
cases
acquired
infection
fromThe
Bangladesh
cases comprised
oneKong
tourist
foreigners
seeking medical treatment in
Cambodia
(1), Hong
(1), and
Indianine
(1) and
Nepal (1).
Singapore. The five imported cases acquired the infection from Bangladesh (1),
Cambodia
Hong Kong
(1), India
(1) and Nepal (1).(esp. in Asia), nalidixic acid,
Increasing (1),
antibiotic
resistance
to flouroquinolones
TMP/SMX, ampicillin and tetracycline, has been reported.
Increasing antibiotic resistance to flouroquinolones (esp. in Asia), nalidixic acid,
TMP/SMX,
ampicillin
and tetracycline,
been reported.
S.
dysenteriae
type 1 (SD1)
serotype is has
responsible
for epidemics and for the most
severe clinical illness of Shigella species. Only SD1 elaborates true Shiga toxin—a
S. dysenteriae
1 (SD1)that
serotype
is responsible
epidemicsUremic
and forSyndrome
the most
neurotoxin
andtype
enterotoxin
is associated
with thefor
Haemolytic
severe clinical illness of Shigella species. Only SD1 elaborates true Shiga toxin—a
neurotoxin and enterotoxin that is associated with the Haemolytic Uremic Syndrome
114
114
(HUS). All Shigella species secrete enterotoxins responsible for the watery
diarrhoea.
(HUS). All Shigella species secrete enterotoxins responsible for the watery
diarrhoea.Features
Clinical
Causes a spectrum of illness from watery diarrhoea to classical dysentery.
Clinical Features
Causes
a spectrum
of illnessseverity
from watery
to classical
dysentery.
The spectrum
of disease
variesdiarrhoea
according
to the host’s
immunity and
serogroup of the infecting organism. S. sonnei commonly causes mild disease, which
The
spectrum
severity varies
to the
host’s
immunity
and
may be
limited of
to disease
watery diarrhoea,
while according
S. dysenteriae
or S.
flexneri
commonly
serogroup
of the infecting
organism.
S. sonneihealthy
commonly
mild disease,
which
causes dysenteric
symptoms.
In a normal
host,causes
the course
of disease
is
may
be limited
to watery
diarrhoea,
S. dysenteriae
S. untreated.
flexneri commonly
generally
self-limited,
lasting
no morewhile
than seven
days whenorleft
causes dysenteric symptoms. In a normal healthy host, the course of disease is
generally self-limited, lasting no more than seven days when left untreated.
 Diarrhoea: Sudden onset; initial voluminous watery stool (small intestine
phase); subsequently containing blood and mucus (colonic phase); fluid
 depletion
Diarrhoea:typically
Sudden uncommon.
onset; initial voluminous watery stool (small intestine
 phase);
Fever subsequently containing blood and mucus (colonic phase); fluid
typically uncommon.
 depletion
Nausea. Occasionally
vomiting
 Fever
Abdominal cramps
 Nausea.
Occasionally
Tenesmus
(common) vomiting
Abdominal
cramps
 Stools
usually
contain blood and mucous (dysentery)
 Tenesmus
(common)
Painful rectal
examination by proctoscopy and the rectum may be hyperaemic
 Stools
usually contain blood and mucous (dysentery)
or ulcerated.
 Painful rectal examination by proctoscopy and the rectum may be hyperaemic
or ulcerated.
Complications
 Intestinal:
Complications
 Proctitis/rectal prolapse
 Intestinal:
 Toxic megacolon
 Proctitis/rectal
prolapse
Intestinal obstruction
 Toxic
megacolon
Colonic
perforation
 Intestinal
obstruction
Protein losing
enteropathy
 Colonic perforation
 Systemic:
Protein losing
enteropathy
 Reactive
arthritis:
May follow after S. flexneri infection. Can be seen
 Systemic:alone or in association with conjunctivitis and urethritis (formerly
 Reactive
May followHLA-B27
after S. flexneri
infection. Can be seen
known as arthritis:
Reiter’s syndrome).
associated.
alone or in association
with inconjunctivitis
and urethritis
 Haemolytic-uremic
syndrome
Shiga toxin producing
strains.(formerly
known as Reiter’s
syndrome).
HLA-B27
associated.
 Neurological
(seizure,
headache,
encephalopathy,
lethargy, confusion)
 Haemolytic-uremic syndrome in Shiga toxin producing strains.
 Neurological (seizure, headache, encephalopathy, lethargy, confusion)
Investigations
 Stool leukocytes and culture (select portion with blood or mucus) or rectal swab
Investigations
(if the patient is unable to provide a stool specimen). Shigella is a fastidious
 Stool
leukocytes
and culture
(select
portion with
blood or
mucus) or rectal
swab
organism;
and requires
prompt
handling.
Antibiotics
susceptibility
testing
is
(if
the patient
is unable to provide a stool specimen). Shigella is a fastidious
needed
for all specimens.
organism; and requires prompt handling. Antibiotics susceptibility testing is
needed for all specimens.
115
115

Blood cultures are usually negative

Blood cultures are usually negative
Notification
If two or more cases are recognised in an institution, this should be reported to the
Notification
Ministry of Health (Form MD 131 or electronically via CD-LENS). Shigellosis is no
If two aornotifiable
more cases
are recognised in an institution, this should be reported to the
longer
disease.
Ministry of Health (Form MD 131 or electronically via CD-LENS). Shigellosis is no
longer
a notifiable disease.
Management
 Mild infections are usually self-limited and most patients recover without
Management
antibiotic treatment.
Mild infections
are usually
patients
without
 Anyone
whose stool
cultures self-limited
are positiveand
for most
Shigella
shouldrecover
be treated
for
antibiotic
treatment.
public
health
reasons.
 Antibiotics
Anyone whose
stool
positive
for Shigella
should be
treated for
shorten
thecultures
durationare
of fever,
diarrhoea
and shedding
of Shigella
in
public
stool. health reasons.
 Antibiotics
shorten the
duration of fever, diarrhoea and shedding of Shigella in
Treatment regimens
include:
stool. Ciprofloxacin 500 mg bd x 5 days (Recommended)
 Treatment
regimens include:
 Azithromycin
500 mg day1, then 250mg daily x 4 days (Alternative)
 Ciprofloxacin
x 5 for
days
(Recommended)
IV Ceftriaxone500
1-2mg
gmbd
daily
hospitalized
patients
 Azithromycin
500make
mg day1,
then 250mg
x 4 days
 Anti-diarrhoeal
agents can
the illness
worse daily
and should
be (Alternative)
avoided.
 IV Ceftriaxone 1-2 gm daily for hospitalized patients
 Anti-diarrhoeal
Infection
control agents can make the illness worse and should be avoided.
Contact precautions should be observed when nursing a patient with shigellosis.
Infection
control
This involves
strict hand-washing before and after handling the patient as well as
Contact precautions
be observed
nursing
a patient
withhandling
shigellosis.
wearing
of personal should
protective
garments when
e.g. plastic
aprons.
Proper
and
This involves
strict
before
and after
handling
patient
as well
as
disposal
of stool
is hand-washing
important as the
organism
is present
in the
large
amounts
in the
wearing
stool. of personal protective garments e.g. plastic aprons. Proper handling and
disposal of stool is important as the organism is present in large amounts in the
stool.
Food handlers infected with Shigella must be treated with antibiotics and should not
be involved in preparation of food as long as their stool cultures are positive;
Food handlers
infected
Shigellagenerally
must be requires
treated with
antibiotics
andofshould
not
conversion
of the
stool with
to negative
at least
48 hours
antibiotic
be
involved
in preparation
food
as long
as their
stool
cultures
are positive;
treatment.
Health
care and dayofcare
centre
workers
should
always
be treated
as well.
conversion of the stool to negative generally requires at least 48 hours of antibiotic
treatment.
care and day care centre workers should always be treated as well.
PreventionHealth
and Control
 The Ministry of Health will carry out epidemiological investigations to trace the
Prevention
and
Control
source of
infection
when an outbreak is suspected.
The Ministry
Health
will carry
outscreened
epidemiological
investigations
to trace
 Contacts
and of
food
handlers
will be
for Shigella
and those found
tothe
be
source ofwill
infection
when an outbreak is suspected.
infected
be treated.
 Contacts
and food of
handlers
willand
be screened
for Shigella
and those
to be
A high standard
personal
food hygiene
is important
in found
preventing
infected
will be treated.
transmission.
 A high standard of personal and food hygiene is important in preventing
transmission.
116
116
References
1. Thielman NM, Guerrant RL. Acute infectious diarrhoea. N Engl J Med 2004; 350:38-47
References
2.
Christopher PR, David KV, John SM et al. Antibiotic therapy for Shigella dysentery. Cochrane
Database Syst
2010RL.
AugAcute
4;(8):CD006784.
AvailableNat:
1. Thielman
NM,Rev.
Guerrant
infectious diarrhoea.
Engl J Med 2004; 350:38-47
http://info.onlinelibrary.wiley.com/userfiles/ccoch/file/CD006784.pdf.
Accessed
Dec Cochrane
2010.
2. Christopher PR, David KV, John SM et al. Antibiotic therapy for Shigella
dysentery.
Database Syst Rev. 2010 Aug 4;(8):CD006784. Available at:
http://info.onlinelibrary.wiley.com/userfiles/ccoch/file/CD006784.pdf. Accessed Dec 2010.
117
117
SMALLPOX
SMALLPOX
Causative Agent
Variola virus, a species of Orthopoxvirus
Causative Agent
Variola
virus,
a species of Orthopoxvirus
Incubation
Period
12-14 days (range 7-17 days)
Incubation Period
12-14
days Period
(range 7-17 days)
Infectious
From fever onset (usually 2–4 days before rash) until last scab has separated; about
Infectious
Period
three
weeks.
From fever onset (usually 2–4 days before rash) until last scab has separated; about
three
weeks.
Transmission
Aerosols/droplets from nasopharyngeal lesions and contact with contaminated
Transmission
articles.
Aerosols/droplets from nasopharyngeal lesions and contact with contaminated
articles.
Epidemiology
Last naturally acquired human case in the world occurred in Somalia in 1977; global
Epidemiology
eradication was certified two years later.
Last naturally acquired human case in the world occurred in Somalia in 1977; global
eradication
two
years major
later. and the variola minor.
There are atwas
leastcertified
2 strains,
variola
There
are at least
2 strains,
variola
major
andwith
the variola
minor.rate up to 30-50% in
 Variola
major:
the more
severe
form
case fatality
susceptible populations.
major: the
more
severe
form
with with
case more
fatalitydiminutive
rate up topox
30-50%
in
 Variola minor:
milder
form
of the
disease
lesions;
susceptible
case fatalitypopulations.
rate of 1-2% in susceptible populations.
 Variola minor: milder form of the disease with more diminutive pox lesions;
case Features
fatality rate of 1-2% in susceptible populations.
Clinical
 Characteristic rash appears 2-4 days after non-specific, flu-like prodrome (fever
Clinical
Features
and headache).
Characteristic rash
after of
non-specific,
prodrome
(fever
 Maculopapular
rashappears
begins2-4
ondays
mucosa
mouth andflu-like
pharynx,
face, hands,
and
headache).
forearms
and spreads to legs and centrally to trunk; lesions are more
 Maculopapular
rashface
begins
on mucosathan
of mouth
and pharynx,
face, hands,
predominant on the
and extremities
on the trunk
(centrifugal).
forearmsprogress
and spreads
to legs onand
lesions
are more
 Lesions
synchronously
any centrally
given parttoof trunk;
the body
from macules
to
predominant
on thetoface
and extremities
thanscabs.
on the trunk (centrifugal).
papules
to vesicles
pustules
and to crusty
 Two
Lesions
any given
partbeen
of the
body from macules to
rareprogress
forms ofsynchronously
invariably fatalonsmallpox
have
reported:
papules
to
vesicles
to
pustules
and
to
crusty
scabs.
 Purpura variolosa or hemorrhagic type smallpox
 Two
raretype
forms
of invariably fatal smallpox have been reported:
 Flat
smallpox
 Purpura variolosa or hemorrhagic type smallpox
 Flatdiagnosis
type smallpox
Differential
 Chickenpox, monkeypox, disseminated herpes zoster.
Differential

Clues todiagnosis
distinguish smallpox from chickenpox:
 Chickenpox,
disseminatedinherpes
zoster.of development
Smallpoxmonkeypox,
lesions are synchronous
their stage
 Clues to distinguish smallpox from chickenpox:
 Smallpox lesions are synchronous in their stage of development
118
118
Smallpox has many more lesions on the face and extremities than trunk
(centrifugal spread)
are more common
on the
palms
soles
 Smallpox lesions
has many
lesions on
faceand
and
extremities than trunk
 (centrifugal
Smallpox lesions
are more deeply imbedded in the dermis compared with
spread)
the superficial
lesions
of chickenpox
 Smallpox
lesions
are more
common on palms and soles
 Smallpox lesions are more deeply imbedded in the dermis compared with
Investigations
the superficial lesions of chickenpox
 Electron microscopy, PCR, viral isolation (culture of pharyngeal swab or
lesions).
Investigations
 Guarnieri
bodies on Giemsa
modified
silver(culture
stain. of pharyngeal swab or
Electron microscopy,
PCR,orviral
isolation
lesions).
Management

Guarnieri bodies on Giemsa or modified silver stain.

Supportive care.

Antibiotics may be used for secondary bacterial infection.
Management

Supportive care.
Prophylaxis

Antibiotics may be used for secondary bacterial infection.
Vaccination within 3 days of exposure may significantly ameliorate or prevent
smallpox. Vaccination 4 to 7 days after exposure likely still offers some protection
Prophylaxis
or modification
of disease
severity.
Vaccination
within
3 days
of exposure may significantly ameliorate or prevent
smallpox. Vaccination 4 to 7 days after exposure likely still offers some protection
Notification
or
modification of disease severity.
Notify MOH immediately on suspicion. Call MOH Communicable Diseases
Surveillance
Notification team at: 98171463
Notify MOH immediately on suspicion. Call MOH Communicable Diseases
Isolation
Precautions
Surveillance
team at: 98171463
 Airborne and contact precautions. Isolate patients in negative pressure isolation
room.Precautions
Isolation
 Patients
be considered
infectious
all scabs
separate
and should
be
Airborneshould
and contact
precautions.
Isolateuntil
patients
in negative
pressure
isolation
isolated during this period.
room.
 Droplet
airborne
precaution
for a minimum
17 days
following
exposure
Patients and
should
be considered
infectious
until allofscabs
separate
and should
be
for
all
persons
in
direct
contact
with
the
index
case.
isolated during this period.
 Droplet and airborne precaution for a minimum of 17 days following exposure
for all persons in direct contact with the index case.

References
1.
Henderson DA, Inglesby TV et al. Smallpox as a biological weapon: medical and public health
management. Working group on Civilian Biodefense. JAMA 1999; 281: 2127-37
References
2. Committee on Epidemic Diseases. Clinical guidelines on anthrax, botulism, plague and smallpox.
1. Epidemiological
Henderson DA, Inglesby
TV et2001;
al. Smallpox
News Bulletin.
27:61-68as a biological weapon: medical and public health
management.(Atlanta),
Working group on
Civilian Biodefense.
JAMA 1999;
281: 2127-37
3. CDC
Smallpox
overview.
2004.
Available
from
2. http://emergency.cdc.gov/agent/smallpox/overview/disease-facts.asp.
Committee on Epidemic Diseases. Clinical guidelines on anthrax, botulism,
and smallpox.
Accessedplague
Dec 2010.
Epidemiological
Bulletin.
2001;from
27:61-68
4. WHO.
Smallpox.News
2010.
Available
http://www.who.int/mediacentre/factsheets/smallpox/en.
3. CDC
Smallpox
overview.
2004.
Available
from
Accessed Dec(Atlanta),
2010.
http://emergency.cdc.gov/agent/smallpox/overview/disease-facts.asp. Accessed Dec 2010.
4. WHO. Smallpox. 2010. Available from http://www.who.int/mediacentre/factsheets/smallpox/en.
Accessed Dec 2010.
119
119
TUBERCULOSIS (TB)
TUBERCULOSIS (TB)
Causative Agent
Mycobacterium tuberculosis (rarely M. bovis).
Causative Agent
Mycobacterium
tuberculosis (rarely M. bovis).
Incubation Period
Weeks to years
Incubation Period
Weeks
years
Initial toinfection
usually goes unnoticed—latent TB infection (LTBI).
Approximately 10% of those with LTBI will eventually progress to active disease,
Initial
unnoticed—latent
TB following
infection infection.
(LTBI).
and halfinfection
will dousually
so in goes
the first
2 to 3 years
Approximately
10%
of
those
with
LTBI
will
eventually
progress
to
active
disease,
Immunocompromised patients (e.g. HIV infection, diabetes mellitus) are at higher
and for
half
will do
so TB.
in the first 2 to 3 years following infection.
risk
developing
active
Immunocompromised patients (e.g. HIV infection, diabetes mellitus) are at higher
risk
for developing
Infectious
Period active TB.
Sputum bacteriologically positive, drug-susceptible pulmonary TB is considered
Infectious Period
non-infectious
after two weeks of effective therapy. (Multi-drug resistant TB may
Sputuma bacteriologically
positive,therapy
drug-susceptible
TB is considered
require
longer period of effective
before casespulmonary
become non-infectious).
non-infectious after two weeks of effective therapy. (Multi-drug resistant TB may
require
a longer period
of effective
therapyTB)
before
cases
become non-infectious).
Non-pulmonary
TB (except
for laryngeal
is not
infectious.
.
Non-pulmonary TB (except for laryngeal TB) is not infectious.
Transmission
.Airborne. Rarely through unpasteurized milk (M. bovis).
Transmission
Airborne.
Rarely through unpasteurized milk (M. bovis).
Epidemiology
 The TB incidence in the local Singapore population (i.e. citizens and permanent
Epidemiology
residents) rose for the first time in ten years to 40 per 100,000 in 2008 and 39
 per
The 100,000
TB incidence
in thePrior
localtoSingapore
and permanent
in 2009.
this, the population
TB rate of(i.e.
thecitizens
local population
had
residents)steadily
rose forfrom
the first
time
in ten years
to 40
perper
100,000
in 2008
and TB
39
declined
57 per
100,000
in 1998
to 35
100,000
in 2007.
per
100,000
in
2009.
Prior
to
this,
the
TB
rate
of
the
local
population
had
continued to be a disease of older males. The TB incidence rate among Malays
declined
from
57 per
in 1998
35 per 100,000 in 2007. TB
remainedsteadily
the highest
among
the100,000
three main
ethnictogroups.
continued
to
be
a
disease
of
older
males.
The
TB
incidence
rateextrapulmonary
among Malays
 The majority (83.6%) had pulmonary TB. The two commonest
remained
the
highest
among
the
three
main
ethnic
groups.
sites were the pleura and the lymphatic system.

(83.6%)
had pulmonary
TB. Theintwo
commonest
 The
The majority
number of
TB cases
among foreigners
Singapore
has extrapulmonary
increased since
sites
were
the
pleura
and
the
lymphatic
system.
2005. In 2009, long-term immigration pass holders comprised 20.8% and short term
The number
of TB
casesofamong
foreigners
in in
Singapore
has increased since
pass holders
21.9%
all notified
TB cases
the country.
2005.
In
2009,
long-term
immigration
pass
holders
comprised
and short In 2009, the proportion of primary drug resistance among new20.8%
pulmonary
TB
term
pass
holders
21.9%
of
all
notified
TB
cases
in
the
country.
cases in Singapore residents examined was 6.6%. Streptomycin resistance was
 In
the proportion
of primary
drug
resistance
among newresistant
pulmonary
TB
the2009,
most commonly
encountered.
The
proportion
of multi-drug
(MDR)
cases
in
Singapore
residents
examined
was
6.6%.
Streptomycin
resistance
was
tuberculosis among new pulmonary TB cases in Singapore residents examined
the most
commonly
encountered.
multi-drug
resistant
has
remained
very low,
at 0.3%.The
Theproportion
MDRTB of
rate
is, however,
10 or(MDR)
more
tuberculosis
pulmonary
TB cases
in Singapore
residents
examined
times higher among
among new
foreigners
reported
with TB
in Singapore,
i.e. 3%
among
has remained very low, at 0.3%. The MDRTB rate is, however, 10 or more
times higher among foreigners reported with TB in Singapore, i.e. 3% among
120
120
Indonesians and those from the People’s Republic of China, 4% among
Vietnamese and 6% among Burmese.
Indonesians and those from the People’s Republic of China, 4% among
Vietnamese
and 6% among Burmese.
Clinical
Features
 Pulmonary TB: Common symptoms are prolonged cough (> 3 weeks), chest
Clinical
pain Features
and haemoptysis. Patients with miliary TB may have minimal respiratory
 Pulmonary
TB:present
Common
are prolonged cough (> 3 weeks), chest
symptoms and
withsymptoms
systemic complaints.
pain
and
haemoptysis.
Patients
with
miliary
TB may
have minimal
 Extrapulmonary TB: Lymphadenitis (especially
cervical),
pleuralrespiratory
effusion,
symptoms
and
present
with
systemic
complaints.
osteomyelitis, meningitis or gastrointestinal involvement.

TB:associated
Lymphadenitis
cervical),
 Extrapulmonary
Patients often have
fever, (especially
night sweats,
loss of pleural
appetite,effusion,
loss of
osteomyelitis,
meningitis
or
gastrointestinal
involvement.
weight and fatigue.

oftenforhave
fever, night
sweats, loss
lossoral
of
 Patients
Risk factors
HIVassociated
and examination
for physical
signsofofappetite,
HIV (e.g.
weight
and
fatigue.
candidiasis) should be sought.
 Risk factors for HIV and examination for physical signs of HIV (e.g. oral
candidiasis) should be sought.
Investigations
 Chest X-Ray. All persons with chest X-ray findings suggestive of TB should
Investigations
have sputum specimens submitted for microbiological examination.

X-Ray.
persons
with
X-ray findings
suggestive
TB should
 Chest
Acid fast
bacilliAll
(AFB)
smear
andchest
TB culture
of sputum
and otherofpathological
have
sputum
specimens
submitted
for
microbiological
examination.
specimens such as pleural fluid, CSF, urine and pus. All patients suspected of
 Acid
bacilli (AFB)
TB culture
sputum
and other
pathological
havingfastpulmonary
TB smear
shouldand
have
at leastoftwo,
preferably
three,
sputum
specimens such
as
pleural
fluid,
CSF,
urine
and
pus.
All
patients
suspected
of
obtained for microscopic examination and TB culture (with drug
having
pulmonary
TB
should
have
at
least
two,
preferably
three,
sputum
susceptibility testing), with at least one early morning specimen where possible.
specimens
obtained
for microscopic
examination
TB culture
(with
 Nucleic
acid
amplification
tests (NAATs)
do notand
obviate
the need
fordrug
TB
susceptibility
testing),
with
at
least
one
early
morning
specimen
where
possible.
culture as these tests do not provide information on the drug susceptibility
 Nucleic
amplification
(NAATs)
do not obviate
the for
need
for TB
pattern ofacid
the organism.
The tests
NAATs
are not sufficiently
sensitive
a negative
culture
these TB
testsindo
not provide sputum
information
on the drug susceptibility
result toas
exclude
smear-negative
samples
of theshould
organism.
The NAATs
arepatients.
not sufficiently sensitive for a negative
 pattern
HIV testing
be performed
for all
result
to
exclude
TB
in
smear-negative
sputum
samples
 Screening for diabetes mellitus is strongly recommended.
 HIV testing should be performed for all patients.
 Screening for diabetes mellitus is strongly recommended.
Notification
 Healthcare providers are required to notify suspected and confirmed cases to the
Notification
Director, TB Control Unit, c/o STEP Registry (Form MD 532 or electronically
 via
Healthcare
providers
CD-LENS)
withinare
72 required
hours. to notify suspected and confirmed cases to the
Director, TB
Control Unit,
STEP
Registry
MD or
532via
or CD-LENS,
electronically
 Attending
physicians
shouldc/oalso
submit
Form(Form
MD 117,
to
via CD-LENS)
72 hours.
update
treatmentwithin
progress
and changes at each visit, preferably monthly until a
 Attending
physicians
should also submit Form MD 117, or via CD-LENS, to
final outcome
is reached.
update treatment progress and changes at each visit, preferably monthly until a
final outcome is reached.
Management
 Any physician treating a patient for TB is assuming an important public health
Management
responsibility; he must not only prescribe an appropriate regimen but also be
 Any physician treating a patient for TB is assuming an important public health
responsibility; he must not only prescribe an appropriate regimen but also be
121
121
capable of assessing adherence of the patient to the regimen, and addressing
poor adherence when it occurs.
of assessing
the patient
regimen, drugs:
and addressing
 capable
Initial drug
therapy foradherence
new casesofshould
consisttoofthe
4 first-line
isoniazid
poor adherence
whenpyrazinamide
it occurs.
(INH),
rifampicin,
and ethambutol or streptomycin. Initiating
 treatment
Initial drugusing
therapy
for new cases
should consist
of not
4 first-line
drugs:
isoniazid
a quinolone
as a first-line
drug is
a standard
practice.
In
(INH), rifampicin,
pyrazinamide TB
and cases,
ethambutol
or streptomycin.
Initiating
uncomplicated,
drug-susceptible
6 months
of drug therapy
is
treatment using
a quinolone
as a first-line
is as
notthis
a standard
practice.
In
sufficient.
Monotherapy
should
never bedrug
given
will generate
druguncomplicated,
drug-susceptible
TB cases,
6 months
of regimen.
drug therapy is
resistant
TB. A single
drug should never
be added
to a failing
sufficient.
should
never
be given
as this
drug The
treating Monotherapy
physician should
be alert
to the
TB culture
andwill
druggenerate
susceptibility
resistant
TB. Amay
single
should
never
to a There
failingshould
regimen.
results which
takedrug
several
weeks
to be
be added
available.
be an index
 The
treating physician
should be alert
to the TB culture
drug susceptibility
of suspicion
for the possibility
of drug-resistant
TB and
in patients
who were
results which
may take
weeks to be
available.
There
should of
be MDRTB
an index
previously
treated,
whoseveral
fail treatment,
who
are known
contacts
of
suspicion
for
the
possibility
of
drug-resistant
TB
in
patients
who
were
cases, or who come from countries with high prevalence of TB drug resistance.
previously treated,
who of
failadverse
treatment,
who and
are prolonged
known contacts
 Non-adherence
because
reactions
therapyofisMDRTB
a major
cases, or who
come from countries
with hightreatment
prevalence
of TBand
drug
resistance.
problem.
Non-adherence
leads to possible
failure
acquired
drug
 resistance.
Non-adherence because of adverse reactions and prolonged therapy is a major
problem. observed
Non-adherence
to possible
treatment for
failure
and patients,
acquired as
drug
 Directly
therapyleads
(DOT)
is recommended
all TB
it
resistance.
allows for closer monitoring, thus ensuring adherence to treatment, preventing
 Directly
observedoftherapy
(DOT) isDOT
recommended
foratall
it
the development
drug resistance.
is available
theTB
TBpatients,
Control as
Unit
allows
closer
monitoring, thus ensuring adherence to treatment, preventing
(TBCU)for
and
polyclinics.
of be
drug
resistance.
DOT isleave
available
the TB
Unit
 the
All development
patients should
issued
with medical
for atatleast
two Control
weeks, after
(TBCU)
andmay
polyclinics.
which they
be considered non-infectious.
 All
patientsappointments
should be issued
withbemedical
leave for
at least
two intervals
weeks, after
Follow-up
should
at no longer
than
monthly
for
which they
be considered
non-infectious.
patients
on may
TB treatment.
Patients
should be asked about clinical response to
 treatment,
Follow-up adherence
appointments
should be
no longer
for
to therapy
andat any
adversethan
drugmonthly
effects, intervals
particularly
patients onPatients
TB treatment.
Patients
should be suggestive
asked aboutofclinical
response
to
hepatitis.
with signs
or symptoms
hepatitis
such as
treatment,nausea,
adherence
to appetite,
therapy abdominal
and any adverse
drugteaeffects,
particularly
jaundice,
loss of
discomfort,
coloured
urine and
hepatitis.
Patientsshould
with be
signs
or symptoms
suggestive
of hepatitis
easy fatiguability
further
evaluated with
liver function
studies.such as
jaundice,
nausea,
loss
of
appetite,
abdominal
discomfort,
tea
coloured
and
 Response to treatment is best monitored bacteriologically with repeaturine
sputum
easy fatiguability
be further
with of
liver
functionphase)
studies.
examination
at theshould
very least
at twoevaluated
months (end
intensive
and at the
 Response
to treatment
bestdomonitored
with repeat
end of treatment.
Those iswho
not convertbacteriologically
their sputum cultures
at two sputum
months
examination
at the veryofleast
at twoduration
monthsbeyond
(end ofsix
intensive
may
require extension
treatment
months.phase) and at the
of treatment.
who do not
convert
their sputumresponse,
cultures atand
two adverse
months
 end
A record
of allThose
medications
given,
bacteriological
may require
extension
of treatment
duration
beyond six months.
reactions
should
be maintained
for all
patients.
 Sputum
A record
of all medications
given, bacteriological
adverse
smear-positive
cases, relapsed
cases and thoseresponse,
with riskand
factors
for
reactions
should
maintained
for alltopatients.
drug-resistant
TBbeshould
be referred
the TBCU.
 Non-compliance
Sputum smear-positive
cases, relapsed
and those
with risk
factorscases
for
to TB treatment
should cases
be detected
promptly,
and these
drug-resistant
TB
should
be
referred
to
the
TBCU.
should be referred to TBCU.
 Non-compliance to TB treatment should be detected promptly, and these cases
should be
referred
to TBCU.
Prevention
and
Control
 In an endemic area, BCG vaccination at birth helps to reduce the incidence of
Prevention
Control
miliary and
TB and
TB meningitis in childhood.
 In an endemic area, BCG vaccination at birth helps to reduce the incidence of
miliary TB and TB meningitis in childhood.
122
122
Early recognition and early appropriate treatment of TB cases. Suspect TB in
any person with unexplained cough for three or more weeks.
 In
Early
recognition
and early
appropriate
treatment
of TB cases. Suspect
hospitals
and other
institutions,
isolation
of smear-positive
patients TB
for in
at
any
person
with
unexplained
cough
for
three
or
more
weeks.
least 2 weeks after initiation of appropriate drug therapy will help reduce
 transmission.
In hospitals and other institutions, isolation of smear-positive patients for at
2 weeks
after
initiation
of appropriate
drug bacteriologically
therapy will helppositive)
reduce
 least
Screening
of close
contacts
of infectious
(i.e. sputum
transmission.
TB cases for latent TB infection (LTBI) and preventive therapy. This is
 Screening
contacts
of infectious
performed of
byclose
the TBCU
Contact
Clinic. (i.e. sputum bacteriologically positive)
TB caseso forThe
latent
TB infection
(LTBI)test
andis the
preventive
This
is
tuberculin
skin (Mantoux)
standardtherapy.
method of
LTBI
performed byscreening.
the TBCU Contact
Criteria Clinic.
for a positive reaction depend on the patient’s
o The
tuberculin
skin
test is the standard method of LTBI
health
status and
TB(Mantoux)
risk.
for a positive
dependshould
on thebepatient’s
o screening.
All screenedCriteria
close contacts
found reaction
to have LTBI
offered
health
status
and
TB
risk.
treatment, regardless of age and BCG vaccination status. Before
o All
screened
close contacts
found
LTBI
should
be history,
offered
initiating
treatment,
active TB
musttobehave
ruled
out by
patient
treatment,
regardless of
age
andX-ray.
BCG vaccination status. Before
physical examination,
and
chest
initiating treatment,
active
TB must
ruledfor
outLTBI.
by patient
o Isoniazid
(INH) is the
treatment
of be
choice
Forhistory,
adults,
physical
examination,
and chest
the
recommended
duration
ofX-ray.
treatment is at least six, and
o Isoniazid
is the treatment of choice for LTBI. For adults,
preferably,(INH)
nine months.
the recommended duration of treatment is at least six, and
preferably, nine months.
Air Travel
 According to WHO guidelines, people with infectious or potentially infectious
Air Travel
TB should not travel by commercial air transportation on a flight of any
 According
to WHO
infectiousinfection
or potentially
infectious
duration, until
there isguidelines,
no longer people
a risk ofwith
transmitting
to others.
TB should should
not travel
by all
commercial
air infectious
transportation
on a flight
of any
 Physicians
inform
patients with
or potentially
infectious
duration,
untilpose
therea isrisk
no of
longer
a risktoofothers,
transmitting
infection
to that
others.
TB
that they
infection
and advise
them
they must
 Physicians
should
with infectious
infectious
not travel by
any inform
public all
air patients
transportation
as long or
as potentially
they are considered
TB
that they
pose a riskinfectious.
of infection to others, and advise them that they must
infectious
or potentially
not travel by any public air transportation as long as they are considered
infectious or potentially infectious.
References

1.
Ministry of Health. Communicable Diseases Surveillance in Singapore 2009.
1.
3.
2.
2003; 52RR(11):
1-77.
Ministry
of Health.
Communicable Diseases Surveillance in Singapore 2009.
Small
PM, Fujiwara
PI. Management
of tuberculosis
in the United
States. N MMWR
Engl J Med
2001; 345:
US Centers
for Disease
Control and Prevention.
Treatment
of tuberculosis.
Recomm
Rep
189-200.
2003; 52RR(11): 1-77.
Tuberculosis
Coalition
for
Technical
Assistance.
International
Standards
of
Tuberculosis
Care
Small PM, Fujiwara PI. Management of tuberculosis in the United States. N Engl J Med 2001; 345:
(ISTC), second edition.. The Hague, Tuberculosis Coalitions for Technical Assistance, 2009.
189-200.
Ministry
of Health.
pulmonaryInternational
tuberculosisStandards
in Singapore,
2000 to 2006.
Tuberculosis
CoalitionMultidrug-resistant
for Technical Assistance.
of Tuberculosis
Care
Epidemiological
News Bulletin
2007;Tuberculosis
33:50-5. Coalitions for Technical Assistance, 2009.
(ISTC), second edition..
The Hague,
Fern
RH, Brian
HN, Amiesha
SP. Identification
and management
of latent
tuberculosis
infection.
Ministry
of Health.
Multidrug-resistant
pulmonary
tuberculosis
in Singapore,
2000
to 2006.
American
FamilyNews
Physician,
May
15 2009.
Available at:
Epidemiological
Bulletin
2007;
33:50-5.
http://www.aafp.org/afp/2009/0515/p879.html#afp20090515p879-b14.
Accessed
Dec
2010.
Fern RH, Brian HN, Amiesha SP. Identification and management of latent tuberculosis infection. rd
World
Health
Organization.
Tuberculosis
air travel–Guidelines
for prevention and Control, 3
American
Family
Physician, May
15 2009.and
Available
at:
edition
2008.
http://www.aafp.org/afp/2009/0515/p879.html#afp20090515p879-b14.
Accessed Dec 2010.
2. US Centers for Disease Control and Prevention. Treatment of tuberculosis. MMWR Recomm Rep
References
4.
3.
5.
4.
6.
5.
6.
7.
7.
World Health Organization. Tuberculosis and air travel–Guidelines for prevention and Control, 3rd
edition 2008.
123
123
TULAREMIA
Causative Agent
TULAREMIA
Francisella tularensis
Causative Agent
Incubation tularensis
Period
Francisella
3 - 5 days (range 1 to 14 days)
Incubation Period
Infectious
Period1 to 14 days)
3
- 5 days (range
No human-to-human transmission
Infectious Period
Transmission
No human-to-human transmission
Humans can become incidentally infected through diverse routes of exposures: bites
of
infective arthropods (primarily ticks and mosquitoes); handling infectious animal
Transmission
tissue or can
fluids;
ingestion
of contaminated
water, diverse
or inadequately
meat
of
Humans
become
incidentally
infected through
routes of cooked
exposures:
bites
infected
animals;
and (primarily
inhalationticks
of and
dustmosquitoes);
from contaminated
soil. Laboratory
of
infective
arthropods
handling infectious
animal
infections
occuringestion
throughofaccidental
inoculation
by inhaling
aerosolized
tissue
or fluids;
contaminated
water, or or
inadequately
cooked
meat of
organisms.animals; and inhalation of dust from contaminated soil. Laboratory
infected
infections occur through accidental inoculation or by inhaling aerosolized
Inoculation or inhalation of as few as 10 organisms is needed to cause disease and is
organisms.
one of the most infectious pathogenic bacteria known.
Inoculation or inhalation of as few as 10 organisms is needed to cause disease and is
The of
primary
concern
for intentional
by the organism is through inhalation
one
the most
infectious
pathogenicinfection
bacteria known.
after aerosol dissemination of bacteria.
The primary concern for intentional infection by the organism is through inhalation
Epidemiology
after
aerosol dissemination of bacteria.
The majority of infections in humans and animals are caused by the two species: F.
tularensis
subspecies tularensis (most virulent) and F. tularensis subspecies
Epidemiology
holarctica
andofrarely
subspecies
philomiragia
and novicida.
The
majority
infections
in humans
and animals
are caused by the two species: F.
tularensis subspecies tularensis (most virulent) and F. tularensis subspecies
The diseaseand
occurs
throughout
much
North America and Eurasia. F.
holarctica
rarelynaturally
subspecies
philomiragia
andofnovicida.
tularensis is found in widely diverse animal hosts and habitats and can be recovered
water, soil,
and vegetation.
A variety
of small
mammals,
from
contaminated
The disease
occurs naturally
throughout
much of North
America
and Eurasia.
F.
andhabitats
hares, and
are natural
reservoirs
including
mice,
water rats,
squirrels,
animal rabbits,
hosts and
can be recovered
tularensis voles,
is found
in widely
diverse
of infection.
from
contaminated water, soil, and vegetation. A variety of small mammals,
including voles, mice, water rats, squirrels, rabbits, and hares, are natural reservoirs
Tularemia
of infection.is almost entirely a rural disease, though exposure in urban or suburban
settings does occur. Certain activities, such as hunting, trapping, butchering, and
with transmission
risk.though exposure in urban or suburban
farming, areisassociated
Tularemia
almost entirely
a rural disease,
settings does occur. Certain activities, such as hunting, trapping, butchering, and
The agent
tularemia
is transmission
not indigenous
arefor
associated
with
risk.in Singapore. Bioterrorism should be
farming,
suspected should this disease be diagnosed in Singapore in persons without a
relevant
travel
The
agent
for history.
tularemia is not indigenous in Singapore. Bioterrorism should be
suspected should this disease be diagnosed in Singapore in persons without a
relevant travel history.
124
124
Clinical Features
 Clinical forms vary in presentation and severity depending on virulence of the
Clinical
Features
infecting
organism, dose and site of inoculation.
 Clinical forms vary in presentation and severity depending on virulence of the
infecting
organism,
dose and site of inoculation.
 Main
forms
of disease:
Pneumonia:
 Main forms
of disease:
Pleuropneumonitis
with hilar lymphadenitis (through airborne or
Pneumonia:
haematogenous routes).
Pleuropneumonitis
with
lymphadenitis
(through
airborne
or
 Occurs
more often in
thehilar
elderly
and has a higher
mortality
rate.
haematogenous
routes).of tularemic pneumonia include patchy
 Radiographic
features
 unilateral
Occurs more
often in infiltrates,
the elderlylobar
and has
a higher mortality
rate.
or bilateral
or segmental
opacities,
hilar
 adenopathy,
Radiographicpleural
features
of tularemic
pneumonia
include
patchy a
effusions,
cavitary
lesions and
occasionally
unilateral
or bilateral infiltrates, lobar or segmental opacities, hilar
miliary
pattern.
adenopathy,
pleural effusions, cavitary lesions and occasionally a
Ulceroglandular
(60-80%):
miliary pattern.
 Patients
typically present with fever and a single erythematous
Ulceroglandular
(60-80%):lesion with a central eschar accompanied by tender
papuloulcerative
 regional
Patients typically
present with fever and a single erythematous
lymphadenopathy.
papuloulcerative
lesionrecent
with ahandling
central eschar
accompanied
by tender
 Patients
usually report
of an animal,
an animal
bite
regional lymphadenopathy.
(especially
cat bites), or exposure to potential vectors, particularly
 ticks.
Patients usually report recent handling of an animal, an animal bite
(especially
cat bites), or exposure to potential vectors, particularly
Oculoglandular
(1-2%):
ticks.
 Chemosis
/conjunctivitis with regional lymphadenitis (through
Oculoglandular
(1-2%):
inoculation
of conjunctiva).
 Chemosis
/conjunctivitis with regional lymphadenitis (through
Oropharyngeal
(1-4%):
inoculationpharyngitis/tonsillitis
of conjunctiva).
 Exudative
with cervical adenitis (through
Oropharyngeal
(1-4%):
inoculation
of oropharyngeal mucosa).
Exudative should
pharyngitis/tonsillitis
with
cervical
adenitis
(through
 Diagnosis
be considered in
patients
with
pharyngitis
inoculation oftooropharyngeal
unresponsive
penicillin. mucosa).
 Diagnosis
Glandular
(3-15%):should be considered in patients with pharyngitis
 unresponsive
Enlargement to
of penicillin.
a single or multiple lymph nodes without an
Glandularidentifiable
(3-15%): skin lesion.

Enlargement of a single or multiple lymph nodes without an
Typhoidal:
identifiable tularemia
skin lesion.with or without pneumonia is an uncommon
 Typhoidal
Typhoidal:
presentation.
Typhoidalillness
tularemia
with or without
pneumonia is an uncommon
 Systemic
with non-localizing
fever.
presentation.
 ofSystemic
withabrupt,
non-localizing
fever.
 Onset
illness isillness
usually
with fever
(38°- 40°C), headache, chills,
coryza and sore throat. Pulse-temperature dissociation has been noted in as
 Onset
illness
is usually abrupt, with fever (38°- 40°C), headache, chills,
many asof42%
of patients.
dissociation
hastightness
been noted
in as
sore throat.
Pulse-temperature
frequently
 coryza
A dry orand
slightly
productive
cough and substernal
pain or
many as
42%
patients.
occur
with
or of
without
objective signs of pneumonia, such as purulent sputum,
 dyspnoea,
A dry or slightly
productive
cough
substernal pain or tightness frequently
or haemoptysis.
tachypnoea,
pleuritic
pain,and
occur with or without objective signs of pneumonia, such as purulent sputum,
dyspnoea, tachypnoea, pleuritic pain, or haemoptysis.
125
125
Nausea, vomiting, and diarrhoea sometimes occur. Sweats, fever and chills,
progressive weakness, malaise, anorexia, and weight loss characterize the
 Nausea,
vomiting,
illness. and diarrhoea sometimes occur. Sweats, fever and chills,
continuing
malaise,
anorexia, and
weight loss characterize
the
progressive
 Any
form of weakness,
tularemia may
be complicated
by hematogenous
spread, resulting
illness.
continuing
in secondary
pleuro-pneumonia, sepsis and rarely, meningitis.
 Any form of tularemia may be complicated by hematogenous spread, resulting
in secondary pleuro-pneumonia, sepsis and rarely, meningitis.
Investigations
The laboratory needs to be notified for special diagnostic and safety procedures.
Investigations
 Direct examination of secretions, exudates and biopsy specimens using Gram
The stain,
laboratory
to be notified
fororspecial
diagnostic and
safety procedures.
directneeds
fluorescent
antibody
immunochemical
stains.
 Culture
Direct examination
of secretions,
exudates
and biopsy
specimens
usingsputum
Gram
of F. tularensis
from clinical
specimens
(pharyngeal
washings,
stain,
direct
fluorescent
antibody or immunochemical stains.
or fasting
gastric
aspirates).
 Serology
Culture ofwith
F. tularensis
clinicalofspecimens
(pharyngeal
washings,
sputum
a fourfold from
titre change
serum antibodies
against
F. tularensis.
or fasting gastric aspirates).
 Serology with a fourfold titre change of serum antibodies against F. tularensis.
Management
In contained casualty setting:
Management
Drugs of choice:
In contained
casualty setting:
 IM streptomycin
1gm 12 hourly for 10 days; or
Drugs
choice:gentamicin 5mg/kg once daily for 10 days
 of IV/IM
 IM streptomycin 1gm 12 hourly for 10 days; or
Alternatives:
 IV
IV/IM
gentamicin
daily
10 days;
days or
doxycycline
1005mg/kg
mg 12 once
hourly
for for
14-21
Alternatives:
 IV ciprofloxacin 400 mg 12 hourly for 10 days
 IV doxycycline 100 mg 12 hourly for 14-21 days; or
 casualty
IV ciprofloxacin
In mass
setting: 400 mg 12 hourly for 10 days
Drugs of choice:
In mass
setting:
 casualty
Doxycycline
100 mg orally 12 hourly for 14-21 days; or
Drugs
choice:
 of Ciprofloxacin
500 mg orally 12 hourly for 10 days
 Doxycycline 100 mg orally 12 hourly for 14-21 days; or
 Ciprofloxacin 500 mg orally 12 hourly for 10 days
Chemoprophylaxis
Exposed persons can be prophylactically treated with 14 days of oral doxycycline or
Chemoprophylaxis
ciprofloxacin. If unexplained fever or flu-like illness develops within 14 days of
canasbeforprophylactically
treated with 14 days of oral doxycycline or
Exposed
exposure,persons
then treat
infection.
ciprofloxacin. If unexplained fever or flu-like illness develops within 14 days of
exposure, then treat as for infection.
Notification
Notify MOH immediately on suspicion. Call MOH Communicable Diseases
Notification
Surveillance team at: 98171463
Notify MOH immediately on suspicion. Call MOH Communicable Diseases
Surveillance
team at: 98171463
Vaccine
Currently no vaccine is available locally. In the United States, a live attenuated
Vaccine
vaccine has been used by laboratory staff working routinely with the bacterium.
Currently no vaccine is available locally. In the United States, a live attenuated
vaccine has been used by laboratory staff working routinely with the bacterium.

126
126
Isolation Precautions
Standard precautions are recommended. Respiratory isolation is not necessary given
Isolation
lack ofPrecautions
human-to-human transmission. Bodies of patients who die of tularemia
the
are standard
recommended.
Respiratory
isolation
is notlikely
necessary
given
Standard
should
beprecautions
handled using
precautions.
Autopsy
procedures
to produce
lack
of
human-to-human
transmission.
Bodies
of
patients
who
die
of
tularemia
the
aerosols or droplets should be avoided.
should be handled using standard precautions. Autopsy procedures likely to produce
aerosols or droplets should be avoided.
References
1.
Dennis DT, Ingleshy TV, Henderson DA et al. Tularemia as a biological weapon: medical and
2.
1.
3.
Ellis J, Oyston
PC, Green
M, et al. Tularemia.
Microbiol
2002;15:631-46
Dennis
DT, Ingleshy
TV, Henderson
DA et al. Clin
Tularemia
as a Rev.
biological
weapon: medical and
CDC (Atlanta)
informational
website:
http://www.bt.cdc.gov/agent/tularemia.
Accessed Dec 2010.
public
health management.
JAMA.
2001;
285:2763-73
Ellis J, Oyston PC, Green M, et al. Tularemia. Clin Microbiol Rev. 2002;15:631-46
CDC (Atlanta) informational website: http://www.bt.cdc.gov/agent/tularemia. Accessed Dec 2010.
public health management. JAMA. 2001; 285:2763-73
References
2.
3.
127
127
TYPHOID AND PARATYPHOID FEVER
Causative Agents TYPHOID AND PARATYPHOID FEVER
Salmonella typhi (Typhoid fever)
Salmonella
paratyphi A, B and C (Paratyphoid fever).
Causative Agents
Salmonella typhi (Typhoid fever)
Salmonella paratyphi
Incubation
Period A, B and C (Paratyphoid fever).
1 - 3 weeks
Incubation Period
1 - 3 weeksPeriod
Infectious
During acute infection and until stool and urine clearance.
Infectious Period
During acute infection and until stool and urine clearance.
Transmission
Faeco-oral route through contaminated food or water. Transmission through sexual
Transmission
contact,
especially among men who have sex with men have been documented.
Faeco-oral
through
contaminated
foodthe
or water.
through
sexual
There
is noroute
animal
reservoir
so ultimately
diseaseTransmission
always involves
human-tocontact,spread.
especially among men who have sex with men have been documented.
human
There is no animal reservoir so ultimately the disease always involves human-tohuman spread.
Epidemiology
During the period 2005-2009, there were 349 reported cases of typhoid (94%
Epidemiology
imported)
and 139 reported cases of paratyphoid (88.5% imported). The disease is
During the
period 2005-2009,
were
349 reported cases of typhoid (94%
endemic
in Southeast
Asia and thethere
Indian
subcontinent.
imported) and 139 reported cases of paratyphoid (88.5% imported). The disease is
endemic Features
in Southeast Asia and the Indian subcontinent.
Clinical
 Typhoid fever
Clinical
 Features
1st week of illness: Rising, “stepwise” fever, bacteraemia and diarrhoea
 Typhoid
(78%fever
of children) or constipation (more frequent in adults).
st
week
“stepwise”
fever,
weekof
ofillness:
illness: Rising,
Abdominal
pain and
rashbacteraemia
(rose spots) and diarrhoea
 21nd
rd
of children)
constipation (more frequent
in adults).
week
of illness:orHepatosplenomegaly,
intestinal
bleeding and
 3(78%
 perforation
2nd week of illness: Abdominal pain and rash (rose spots)
 3rd week of illness: Hepatosplenomegaly, intestinal bleeding and
perforation(rare if diagnosed and treated early)
 Complications
 Intestinal haemorrhage or perforation
(rare if diagnosed and treated early)
 Complications
Toxic myocarditis
Intestinal haemorrhage
perforation
 Confusion,
convulsions,orencephalitis
Toxic myocarditis
 Haemolytic
anaemia (especially in G6PD deficiency)
Confusion,
convulsions, encephalitis
 Renal
failure
Haemolyticinanaemia
(especially
in G6PD deficiency)
 Abscesses
liver, spleen,
bone etc.
 Renal failure
 Abscesses
in liver, spleen, bone etc.
 Paratyphoid
fever
 Maybe clinically mild or asymptomatic
 Paratyphoid fever
 Maybe clinically mild or asymptomatic
128
128

Nausea, vomiting, fever, diarrhoea, and cramping—usually occur within 8
to 72 hours of ingesting contaminated food or water
 Nausea,
fever, diarrhoea,
and cramping—usually
occur within 8
Less thanvomiting,
5% of non-typhoidal
salmonella
gastroenteritis develop
to
72 hours of
ingesting
contaminated
food or manifestations
water
bacteraemia
and
may result
in extra-intestinal
including
 endocarditis,
Less than 5%mycotic
of non-typhoidal
gastroenteritis develop
aneurysmsalmonella
and osteomyelitis.
bacteraemia and may result in extra-intestinal manifestations including
endocarditis, mycotic aneurysm and osteomyelitis.
Investigations
 Blood test frequently show anaemia, elevated hepatic transaminases and either
Investigations
leucopoenia or leucocytosis.

testoffrequently
elevated
hepatic transaminases and either
 Blood
Isolation
organism show
is the anaemia,
gold standard
for diagnosis.
leucopoenia
or
leucocytosis.
 Blood culture usually positive for 1st two weeks only.
 Stool
Isolation
organism
the goldfrom
standard
4thdiagnosis.
weeks.

andof
urine
cultureispositive
2 nd tofor

culture
positive for
1st two
weeks
only.
 Blood
The yield
fromusually
bone marrow
culture
is
high
and
is usually positive even after
 Stool
and urine
positive from 2 nd to 4th weeks.
antibiotics
have culture
been initiated.
 The
The Widal
yield from
marrowin culture
is high
is usually
positive
evenforafter

test isbone
unreliable
itself, but
may and
provide
additional
support
the
antibiotics
have
been
initiated.
diagnosis when the clinical picture is suggestive.
 The Widal test is unreliable in itself, but may provide additional support for the
diagnosis when the clinical picture is suggestive.
Notification
A legally notifiable disease in Singapore. Notify Ministry of Health (Form MD 131
Notification
or electronically via CD-LENS) not later than 24 hours from the time of diagnosis.
A legally notifiable disease in Singapore. Notify Ministry of Health (Form MD 131
or electronically via CD-LENS) not later than 24 hours from the time of diagnosis.
Management
Typhoid
Management
 Patients should be hospitalised during antibiotic treatment.
Typhoid

Rehydration and other supportive care.
 Current
Patients drugs
shouldofbechoice:
hospitalised during antibiotic treatment.

 Rehydration
and
other
supportive
 PO Ciprofloxacin 500
mg bd care.
x 7-10 days (if sensitive to ciprofloxacin and
 Current
drugs
of
choice:
nalidixic acid)
 PO
Ciprofloxacin
500once
mg daily
bd x 7-10
daysdays
(if sensitive to ciprofloxacin and
IV Ceftriaxone
2-3g
x 10-14
nalidixic acid)
 Alternative: PO Azithromycin 1g once then 500mg once daily x 5-7 days
 IV
Ceftriaxone 2-3g once daily x 10-14 days
N.B. 70-90 % of isolates in some parts of Nepal, India and Vietnam are
 Alternative:
Azithromycin
nalidixic acidPO
resistant
strains. 1g once then 500mg once daily x 5-7 days

N.B.
70-90
%
of
isolates
some parts
of Nepal,
are
 Dexamethasone 3mg/kg thenin1mg/kg
6 hourly
x 8 India
dosesand
forVietnam
severe typhoid
nalidixic
acid
resistant
strains.
fever (as suggested by delirium, shock and altered mental status) decreases
 Dexamethasone
3mg/kg then 1mg/kg 6 hourly x 8 doses for severe typhoid
mortality.
fever
(as
suggested
bynewer
delirium,
shock (10-25%
and altered
status) decreases
 Relapse rate 1-6% with
antibiotics
withmental
chloramphenicol)
mortality.
 One to four percent of adults become chronic carriers despite antibiotics.
 Follow-up
Relapse ratestool
1-6%
with newer
antibioticsstool
(10-25%
with after
chloramphenicol)

evaluation
to document
clearance
treatment:
 One Three
to fourconsecutive
percent of adults
antibiotics.
stool become
sampleschronic
taken atcarriers
weeklydespite
intervals
no sooner than
 Follow-up
stoolafter
evaluation
to document
stool treatment.
clearance after treatment:
two weeks
completion
of antibiotic
 Three consecutive stool samples taken at weekly intervals no sooner than
two weeks after completion of antibiotic treatment.
129
129
Chronic carriers (positive stool samples after 6 months): give prolonged
course of ciprofloxacin (750 bd orally for 1 month) and perform abdominal
 ultrasound;
Chronic carriers
(positive stool
after if6 gallstones
months): give
prolonged
cholecystectomy
maysamples
be necessary
are present
and
course
of
ciprofloxacin
(750
bd
orally
for
1
month)
and
perform
abdominal
prolonged antibiotic treatment fails.
ultrasound; cholecystectomy may be necessary if gallstones are present and
prolonged
antibiotic treatment fails.
Prevention
and Control
 Public health measures: education on good personal and food hygiene.
Prevention
and Control

Vaccination
for travellers: (see section on travel vaccination in Appendix 3).
Public health
measures:
education
on good personal
and food
hygiene. for
 Follow
up stool
examinations
recommended
for all cases
and mandatory
 Vaccination
for travellers: (see section on travel vaccination in Appendix 3).
food handlers.
 Follow
up stoolrequire
examinations
recommended
for (three
all cases
and mandatory
for
Food handlers
further stool
examination
consecutive
daily stool
food
handlers.
samples) at three and six months post treatment.
 Carriers
Food handlers
require further
stooland
examination
(threenot
consecutive
daily
stool
(convalescent,
temporary
chronic) must
work as food
handlers.
samples) at three and six months post treatment.
 Carriers (convalescent, temporary and chronic) must not work as food handlers.
References

1.
Teoh YL, Goh KT, Neo KS et al. A nationwide outbreak of coconut-associated paratyphoid A fever
2.
1.
3.
Parry
CM,Goh
HienKT,
TT,Neo
Dougan
et A
al.nationwide
Typhoid fever.
N Engl
Med 2002; 347: 1770-82.
Teoh YL,
KS etGal.
outbreak
of Jcoconut-associated
paratyphoid A fever
Slinger
R, Desjardins
McCarthy
AE1997;
et al.26:544-8.
Suboptimal clinical response to ciprofloxacin in
in Singapore.
Ann AcadM,Med
Singapore
patients
with
enteric
fever due
spp. N
with
reduced
susceptibility: a
Parry
CM,
Hien
TT, Dougan
G ettoal.Salmonella
Typhoid fever.
Engl
J Med fluoroquinolone
2002; 347: 1770-82.
case
series.
BMC InfectM,
DisMcCarthy
2004; 20:4-36.
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