Fever with Rashes

1
 Trigger
Daniel, 11 years old boy presented to hospital with fever
for 4 days associated with chills & rigors, headache,
nausea, vomiting for 3 times and myalgia. He also
complained of right hypochondriac pain, loss of appetite
and bloody watery stool (bright red) for one time only.
His neighbors had hx of dengue infection last week. On
day 7th of fever, maculopapular rash was noted on his
limbs.

2
Physical examinations
General He was conscious, alert but weak with IV
drip of normal saline and has dry lips
Vital signs PR = 84 bpm
BP = 93/59 mmHg
BMI = 16.2
Eyes Polycythemia
Oral Gum bleeding
Abdomen Abdomen soft and non-tender
No hepatomegaly or splenomegaly
Other systems No significant findings
Rashes Maculopapular rash starting from lower
limbs. Blanching.
3
 Type of rashes
• Macule, papule, and maculopapular
• Purpura, petechiae, ecchymoses
• Vesicular, bulla
• Urticaria
• Erythema multiforme
• Erythema nodosum

4
 Macules Papules
Circumscribed, flat, discoloured, not Circumscribed, solid, elevated; if
palpable, erythematous or purpuric; if elevated, flat top and >1cm, it is
>1cm, it is called patch called plaques

Maculopapular rash
=> Measles, Rubella, Roseola infantum (6th disease),
Erythema infectosum (5th disease), Kawasaki disease, Scarlet
fever, Epstein-Barr virus infection
5
 Purpura Petechiae Ecchymoses
• Caused by vasculitis or defects Purpuric macules <2- Bruises that are
in clotting factors 3mm >10mm
• Purpura fulminans (large Due to extravasation of Rare in infection
confluent purpuric patches, blood from capillaries, Consider trauma
subsequently undergo necrosis often appears over a and child abuse
and scar formations) and short time
symmetrical peripheral Lesion that blanches
gangrene are associated with are not extravascular
benign infections (varicella or blood
S. pyogenes)
• Palpable purpura (Small vessel
vasculitis) – meningococcus,
staphylococcus, gonococcus

Petechiae and purpuric rash

=> Enterovirus, Meningococcal infection, Henoch-Schonlein Purpura,
Thrombocytopenia, Congenital rubella, Congenital cytomegalovirus
6
7
 Vesicle, bullae
• Due to disturbance of cohesion of epidermal cells or
components of a basement membrane zone associated with
influx of fluids into or beneath the site of disturbance
• Rapidly evolve into erosions, ulcers or crusts
• Most are benign, others are rapidly progressive and life
threatening

8
 Vesicles (<1cm)
Solitary – Lesions of streptococcal • Staphylococcal scalded skin syndrome
blistering dactylitis
Localised – staphylococcus
bullous impetigo
Grouped or clustered – HSV
infection
Arranged linearly – Shingles
(VZV)
Generalised – Chickenpox (VZV)
Bullae (>1cm)
(SSSS)
• Due to thermal injury or
hypersensitivity response to insect bite
are identical to that of bullous impetigo
• Haemorrhagic bulla
- May accompany gram negative
septicaemia
- Nisseria meningitides
- Necrotising soft tissue infection due
to Strep. pyogenes
9
 Urticaria
• Common problem
• Sudden onset of
circumscribed
erythematous,
oedematous papules or
plaques often showing
central clearance
• Papular urticarial is a
reaction to arthropod bite
• 50% associated with
infection – Strep pyogenes
is most common
• Viral URTI and GIT
infection are the primary
infectious trigger of acute
urticarial in children
Erythema multiforme
Numerous manifestations in
the skin from erythematous
macules, papules, vesicles,
bullae, or urticarial plaques to
patches of confluent
erythema
Diagnosis is established by
finding target lesions (iris or
bullseye)
HSV, Steven Johnson
syndrome
Erythema nodosom
Sudden appearance of
tender erythematous 1-
10cm nodules usually
extensor of the legs
Lesions can develop on
calves, thighs, trunk,
upper limbs, head and
neck
• Group A strep
• Tuberculosis
• Yersinia
• Bartonella (Cat
scratch disease)
• Behchet, SLE, IBD
• Sarcoidosis

10
Urticaria

Erythema nodosum

Erythema multiforme
11
12
 Aetiology
• Caused by single stranded RNA paramyxovirus with one antigenic
type
• Humans are the only natural host
• Spread systemically during a brief, low-titre primary viraemia
• Secondary viraemia (5-7days) occurs as virus-infected monocyte
travel to other organs
• Virus is present in respiratory secretion, blood, and urine
• Transmitted via droplets or airborne and is highly contagious
• Infected person are contagious 5 days before the onset of rash
to 4 days after
• The virus remains active and contagious in the air or infected
surfaces up to 2 hours

13
 Epidemiology
• Endemic in areas where vaccination is not available
• Reported about 1 million deaths annually
• In Malaysia, in 1982, the incidence rate was 65.62 per 100,000 pop.
while in 1998, it dropped to 5.87 per 100,000 pop.
• Most young infants are protected by transplacental maternal
antibodies until the end of their first year

14
 Clinical manifestation
• Divided into four phases:- Incubation, prodromal, exanthematous,
and recovery
• Incubation period is 8-12 days from exposure to symptom onset
with a mean of 14 days from exposure to rash onset
• The prodromal period (3 days) includes cough, coryza, conjunctivitis,
and Koplik spots (pathognomonic; last 12-24 hours)
• The first sign of infection will be a high fever (40.0 C – 40.5 C)
accompanied by classic symptoms of cough, coryza, conjunctivitis
and Koplik spots

Koplik spots
15
• After several days (2-4 days), rash started on the face and upper
neck, which spread downwards
• The rash lasted for 5-6 days before fading in the same pattern
• It can be petechial or haemorrhagic (black measles) and undergoes
desquamation and brownish discolouration when it fades
• Otitis media, pneumonia, and diarrhea are more common in infants
while involvement of liver in adults
• *the conjunctiva may reveal a characteristic transverse line of
inflammation along the eyelid margin (Stimson line)

16
 Investigations
• Routine lab findings are nonspecific. Leukopenia is
characteristics
• Serology test for IgM that appear within 1-2 days of rash and
persists for 12 months in unimmunized person confirms the
diagnosis
• IgM antibodies may be present only transiently in immunized
patient

17
 Differential diagnosis
• Rubella
• Roseola
• Enterovirus/adenovirus infection
• Infectious mononucleosis
• Toxoplasmosis
• Scarlet fever
• Kawasaki disease
• Drug rash

18
 Treatment
• Adequate hydration and antipyretics
• High-dose vitamin A supplementation for 2
days

Complications
• Otitis media
• Interstitial pneumonia
• Giant cell (Hecht) pneumonia
• Encephalomyelitis
• Subacute sclerosing panencephalitis
• Blindness

19
 Prevention
• Live attenuated measles vaccine
• MMR vaccine at 12-15 months and 4-6 years old
• The second dose is to reduce primary vaccine failure rate from <5%
to <1%
• Contraindication for vaccine:
– Immunocompromised or immunosuppressive course of steroids
(>2 mg/kg/day for >14 days)
– Pregnancy or recent administration of Ig (3-11 months, based on
dosage)
– Allergic to neomycin, or have received another live vaccine in
previous month

20
21
 Etiology
• Also known as German measles or 3-day measles
• Caused by a single-stranded RNA virus with a glycolipid envelope
and a member of the togavirus family
• Human are the only natural host
• It invades and disseminate via primary viraemia. A secondary
viraemia ensues after replication
• The virus can be isolated from peripheral blood monocyte, CSF and
urine

22
• In utero infection can lead to congenital rubella syndrome (CRS)
with associated ophthalmologic, cardiac and neurologic
manifestations
• The virus is transmitted via direct or droplet contact with
nasopharyngeal secretions from 7 days before until 14 days after
the rash
• For CRS, it occurs in 100% of pregnancies if infection in the first 11
weeks, 50% if at 11-12 weeks, and 35% if in 13-16 weeks

Epidemiology
• Usually occurs in spring, in every 6-9 years for
unvaccinated populations
• Transplacental antibodies only protective during the first
6 months of life

23
 Clinical manifestations
• Incubation period is 16-18 days (range, 14-21 days)
• Mild catarrhal symptoms of the prodromal phase of rubella may go
unnoticed
• Characteristics signs include retroauricular, posterior cervical, and
posterior occipital lymphadenopathy accompanied by
erythematous, maculopapular, discrete rash
• Rash begins on face and spread downwards, lasting for 3 days and
less prominent than that of measles
• Forchheimer spots (20%) may appear before the rash as rose-
colored spots on the soft palate
• Other manifestations include mild pharyngitis, conjunctivitis,
anorexia, headache, malaise, and low-grade fever
• Polyarthritis, paresthesias and tendinitis may occurs
24
 Forchheimer spots
Maculopapular rashes
25
 Investigations
• Routine lab findings are nonspecific and WBC usually normal
or low
• Serology test for IgM is positive 5 days after symptoms onset
or a fourfold or greater increase in specific IgG in paired acute
and convalescent sera can be detected
• In CRS, IgM is detectable until 3 months old, and a stable or
rising IgG over the first 7-11 months old

26
 Differential diagnosis
• Measles
• Roseola
• Enterovirus/adenovirus infection
• Infectious mononucleosis
• Scarlet fever
• Kawasaki disease
• Drug rash

27
 Treatment Complications
Adequate hydration and • CRS
antipyrexia • Rubella encephalitis

Prevention
• MMR vaccination as of measles
• In post-pubertal females, arthralgia (25%), and
acute arthritis like symptoms (10%) of vaccinated
individuals
• Women are advised to avoid pregnancy after 28
days of vaccination

28
Chicken pox
Varicella Zoster Virus (VZV)
(Ds DNA, Herpesviridae

29
 EPIDEMIOLOGY
1. Peak at 5- 10 years old
2. During winter or spring
3. Human are natural host
4. Mode of entry:
• Inhalation of respiratory droplets from infected host
• Direct contact with vesicles

30
Pathogenesis

31
 Clinical manifestations

Incubation period 14 to 16 days (range of 10 to 21 days after exposure)

Prodromal • Fever
symptoms • Malaise, irritability
• Loss of appetite
• Headache
• URT symptoms (cough and sore throat)
Rashes 1. Rash appear initially as small red papules -> oval, teardrop
vesicles on an erythematous base (contain fluid that change
from clear to cloudy) -> ulcerate, crust and heal.
2. New cops appear for 3 to 4 days
3. Beginning from trunk -> head, face and proximal extremities,
sparing of distal and lower extremities
4. Pruritus is universal and marked
Others • Generalized lympahadenopathy
• Ataxia
• Alopecia
• Vesicles and bullae
32
Patient with pre-existing dermatologic problems, the lesions tend to
appear first and cluster most heavily at the sites of prior skin irritation
(diaper area/ sites of eczematoid dermatitis)

Enanthem (thin-walled vesicles that rapidly rupture to form shallow

ulcers) is commonly seen

33
34
For Shingles (zoster);

1. During pre-eruption phase, there is intense localized and constant

pain (acute neuritis) along a dermatome (thoracic and lumbar
regions).

Papules-- -------------> Vesicles Crusting

2. ---------->
and heal
several days 1 to 7 days

3. Lesions generally are unilateral and do not cross the midline.

Associated with regional lymphadenopathy.

3. In 1/3 of patients, lesions occur outside of primary dermatome,

involving branch of cranial nerve V -> corneal and intraoral lesions
• Cranial nerve VII -> facial paralysis and ear canal vesicles
(Ramsay Hunt Syndrome)

35
unilateral and do not cross the midline

36
Cranial nerve VII -> facial paralysis and ear canal
vesicles (Ramsay Hunt Syndrome)

37
 Investigations

• PCR and genotyping to distinguish vaccine and wild-type strains

of infection
• Immunofluorescence (IF)
- Detection of varicella-specific antigen in vesicular fluid by IF using
monoclonal antibodies or demonstration of fourfold antibody.
• Full Blood Count
- Leukopenia for 3 days then leukocytosis

38
 Managements
• SUPPORTIVE THERAPHY
– Cool compress
– Regular bathing
– Maintain good hygiene
– Oral antihistamines (diphenhydramine, hydroxyzine)
– Non-aspirin antipyeretics (avoid Reye’s syndrome)

• ANTIVIRAL THERAPHY
– Acyclovir/ valacyclovir/ famiclovir
– Early therapy in immunocompromised patient is effective in
preventing severe complications
– As valacyclovir and famiclovir have much greater oral
bioavailability than acyclovir, it is recommended in adults.

39
 Varicella-zoster Vaccination
S.C-Live attenuated Varicella Vaccine.

Indications Contraindications
• In all children • Pregnant
- 12mnths – 12 y/o (single dose) • Patients receiving high dose systemic
- >12 y/o (2 doses > 4 wks apart) immunosuppression therapy.
• Patients with malignancy especially
• Non immune susceptible health haematological malignancies or blood
care worker who regularly come in dyscrasias.
contact with VZV infection • Hypersensitivity to neomycin.
• Children in remission from
leukemia for ≥ 1 yr, have .700/ml
circulating lymphocytes may
receive vaccine under paeditrician
supervision (2 doses)
• Asymptomatic/mildly symptomatic
children with HIV (with CD4% >
15%) : 2 doses a 3 mths interval

40 Paediatric protocols 3rd ed.

 Fever
Injection site
Papulovesicular reactions (pain &
eruptions erythema, allergic
reaction to gelatin)

Side effects
of
vaccination

Headache
Paresthesia

Fatigue

41
42
Chickenpox Clinical Diagnosis Flowchart

43
 DDX

Eczema herpeticum or Kaposi

varicelliform eruption (caused by
HSV)
- An extensive cutaneous vesicular
eruption that arise from pre-
existing skin disease

44
 Complications
• Secondary infection of skin lesions by streptococci or
staphylococci. May lead to toxic shock syndrome or
necrotising fasciitis
• Reye syndrome (so avoid use aspirin)
• Neurology => post-infectious encephalopathy, cerebellar
ataxia, nystagmus, tremor, transverse myelitis, optic
neuritis
• Immunocompromised => haemorrhagic lesions,
pneumonitis, hepatitis, DIC

45
 Prognosis

1. Primary varicella resolves spontaneously

2. Mortality rate higher in person > 20 years old and
immunocompromised
3. Scarring is more common is zoster because of
involvement of deepest layer of skin

46
 Congenital Varicella Syndrome
• When pregnant women contract chickenpox early in pregnancy, 25%
may become infected.
• Foetus infected at 6–12 week of gestation appear to have maximal
interruption with limb development
• The virus may select tissues that are in a rapid developmental stage,
such as the limb buds, result in 1 or more shortened and malformed
extremities.
• Foetus infected at 16–20 week POG may have eye and brain
involvement such as cataracts, microcephaly
• Severe form of neonatal varicella may develop in newborn’s mother
with varicella occurring 5 days before or 2 days after delivery – as
maternal Ab not develop yet and virus can cross placenta.

47
48
• Characteristic cutaneous lesion is called a cicatrix, a zigzag
scarring, in a dermatomal distribution associated with
atrophy of the affected limb.
• Infants should treated as soon as possible with VZIG or IV
immunoglobulin

VZIG
v Passive immunity within 96 hours of exposure for
susceptible individuals at increased risk for severe illness
(Immunocompromised, newborn’s mothers with varicella
before or after delivery, premature infants, <1 yr, adults
without evidence of immunity, pregnant women)

49
Hand, Foot & Mouth Disease
(HFMD)
Enteroviruses (coxsackie virus, echovirus, poliovirus)
Family picornaviridae
(small, non-enveloped, single-stranded RNA virus)

50
1. Mild, contagious viral infection common in young
children characterized by sores in mouth and rash on
palms and soles of feet.
2. < 5 years old
3. MOT = person to person (nose and throat discharge,
saliva, fluid from blisters, stools
4. Most contagious in first week of illness.
5. HFMD not transmit by pets or animals

Ministry of health HFMD Guidelines

51
 Pathogenesis

Invasion of
skin and Widespread
Viremia Lesions forms
mucous apoptosis
membrane

52
 Clinical manifestations

Incubation 1. 3-7 days

period 2. Most contagious in 1st week
Prodromal • low-grade fever
symptoms • malaise
• sore throat
• poor appetite (anorexia)
• vomiting (EV-71)

53
Rashes • Within 1-2 days, oral lesions and soon skin lesions
appear
• Characteristics: shallow, yellow ulcers surrounded by
red halos
• Macular lesions appear on the labial and buccal
mucosal surfaces, gingivae, tongue, soft palate, uvula,
anterior tonsillar pillars
• Evolve rapidly to form small, thick-walled, gray vesicles
on an erythematous base of palate and mucosal
surface (slivers, pruritic/ asymptomatic)
• Cutaneous lesions begin as erythematous macules
(palmar aspect of the hands and fingers/ plantar
surface of the feet and toes/ interdigital surfaces)

Neurological involvement (ET-71)

(polio-like syndrome, aseptic meningitis, encephalitis,
encephalomyelitiis, acute cerebellar ataxia)

54
55
56
 Investigations
• Not always necessary
• Obtain samples from cutaneous lesion, mucosal lesion/ stool
samples for culture and immunoassay
• Oral specimen (highest isolation rate)
• Two swab collections are recommended
• Polymerase Chain Reaction (PCR)

57
 Managements

1. Recover in 7 to 10 days with minimal or no medical intervention

2. No specific treatment
3. Medication: relief the symptoms (fever and aches)
4. Supportive management & symptomatic treatment
1. Adequate hydration
2. Antipyretics (acetaminophen/ paracetamol)
3. Analgesia (acetaminophen/ ibuprofen)
4. Salt water rinse (soothe the mouth and throat)
5. Criteria for admission
• Unable to tolerate oral feeds
• Toxic-looking
• Persistent hyperpyrexia (>38 ̊C for > 48 hrs)
• Neurologic and cardiac complications

58
 Prevention
• No vaccine available
• Preventive measures
– Wash hands with soap and water often after changing
diaper/ using toilet
– Avoid touching eyes, nose, mouth with unwashed hands
– Clean and disinfect frequently touched surfaces (toys,
doorknobs)
– Avoid close contact (hugging, kissing, sharing utensils or
cups with infected person)

59
 Complications

• Rare
• Enterovirus 71 (EV71) may associated with neurological
complications such as aseptic meningitis, encephalitis,
increase drowsiness, seizures.
• Cardiac complications – myocarditis (low BP, low pulse
volume, arrhythmia, murmurs, displaced apex beat)

60
 Fifth Disease or
Erythema Infectiosum
Parvovirus B19
(ssDNA, parvoviridae)

61
Pathogenesis

62
 Clinical manifestations
Transmission Respiratory secretions and blood product transfusion
Incubation 4 -14 days
period
Prodromal • Low grade fever, malaise, myalgia , headache
symptoms • Pharyngitis
• Mild conjunctivitis
Rashes • Slapped cheek rash with circumoral pallor (pale ring
around mouth)
• 1-4 days later, maculopapular (truncal rash) appear
• As the rash fades and central clearing takes place, the
lacy, reticulated rash develop, lasted 2-40 days.
• Rash may be pruritic, does not desquamate and may
recur with exercise, bathing, rubbing or stress.

63
 maculopapular (truncal rash)

Slapped cheek rash

lacy, reticulated rash

64
1. Children with shortened erythrocyte life span (eg; sickle cell)
may develop transient aplastic crisis.

2. They may have;

• Fever, lethargy, malaise, pallor, headache
• GI symptoms and respiratory symptoms
• Reticulocyte counts are extremely low
• Haemoglobin low than normal
• Transient neutropenia and thrombocytopenia

65
 Measles

Scarlet
Rubella
fever
Differential
diagnosis

Kawasaki
SLE
disease

66
 Investigations
 FBC & differential count
◦ Thrombocytopenia, Lymphopenia, neutropenia, reticulocytopenia
 B19-specific IgM
◦ +ve: Indicates current or recent infection
◦ False –ve: In immunocompromised patients
 B19-specific IgG
◦ +ve: Indicates immunity, usu. appears 2 weeks after infection & persists
for life
• Polymerase chain reaction (PCR)
◦ For the specific detection of parvovirus B19

67
 Managements
• No specific therapy
• Supportive care: maintain
adequate hydration, antipyretic
• Transfusion: for transient aplastic
crisis, intrauterine transfusion for
hydrops fetalis a/w fetal
parvovirus B19 infection
• IV immunoglobulin: for
immunocompromised person,
person with severe anaemia or
chronic infection
Prevention
• No vaccine
• Good handwashing and
hygiene
• No need absenteeism from
school because children are
not infectious by the time
rash is present
• Antenatal screening

68
 Complications Prognosis
• Parvovirus B19 is not
• Prognosis is excellent
teratogenic but in utero
• 2 - 9% = < 5y/o
infection lead to foetal HF,
• 15 – 35% = 5 – 18 y/o
hydrops foetalis and foetal
• 30 – 60% = adults
death

• Fatalities associated with

transient aplastic crisis is rare

69
Herpes Simplex
Virus
(HSV)

70
 Introduction
Herpes Simplex Virus
dsDNA of herpes family

HSV-1 HSV-2

Acquired Mainly transmitted by Exclusively Infection in

Infections in or
during oral to oral contact to sexually the genital
around the
childhood, cause infection in or transmitted or anal area
mouth, CNS &
and around the mouth (oral (genital
eyes
infection is herpes) herpes)
lifelong

Both oral herpes infections and genital herpes infections are mostly asymptomatic but can
cause mild symptoms or painful blisters or ulcers at the site of infection.
71
 Epidemiology
International
• HSV is well distributed worldwide

Mortality/Morbidity
• The mortality rate associated with
herpes simplex infections is related
to 3 situations: perinatal infection,
encephalitis and infection in the
immunocompromised host.
Race
• Seroprevalence of HSV-2 antibodies
in 45% of blacks, 22% of Mexican-
Americans, and 17% of whites
72
Gender

• Seropositivity to antibodies to HSV-2 is more common in

women (25%) than in men

Age

• HSV-1 infections transmitted via saliva are common in children,

although primary herpes gingivostomatitis can be observed at
any age.
• HSV-2 infections are clustered perinatally (from a maternal
episode at delivery) and primarily once sexual activity begins.
• HSV-2 genital infections in children can be an indication of
sexual abuse.
• Increased age (after onset of sexual activity) and total number
of sexual partners are independent factors associated with 73
 Pathophysiology
HSV (both types 1 and 2) belongs to the family Herpesviridae and to the
subfamily Alphaherpesvirinae. It is a double-stranded DNA virus characterized
by the following unique biological properties:

Virus latency
maintained in the Reinfection can occur
• Virus infect the with exposure to the
mucosal surfaces & ganglia by immunity
other type
enter cutaneous system, undergoes
neuron periodic reactivation or even a second
• Migrate along axon and replication strain of the same
to sensory ganglia type.
triggered by events
• As virus replicate it
destroy epithelial 74
cell
 Mode of Transmission
• Sexual contact
• Child birth
• Any contact of open sores
• Sharing bodily fluid (ex: healthcare worker stabbed by needle
from a HSV-infected patient)

75
 Clinical Features
1. Mostly asymptomatic
2. Gingivostomatitis Most common form of primary HSV illness
in
children
• May persist for up to 2 weeks
• Occurs from 10 months to 3 years of age
• Vesicular lesions on lips, gums and
anterior surfaces of the tongue and hard
palate → often progress to extensive,
painful ulceration with bleeding
• High fever, malaise, fetid breath
• Cervical lymphadenopathy
• Eating and drinking are painful, so can
lead to dehydrated

76
3. Skin manifestation 1. Mucocutaneous junctions and damaged skin
particularly prone to infection
i. Cold sores = recurrent HSV1 lesions on the
lip margin
ii. Eczema herpeticum
• Cutaneous HSV infection in person with underlying
skin disorder (e.g. atopic dermatitis)
• Wide-spread vesicular lesions develop on
eczematous skin.
• May be complicated by secondary bacterial
infection → septicaemia

2. Herpetic skin lesions are painful and

characteristically begin as:
a. Erythematous papules
b. Quickly progress to characteristically grouped, 2-
4mm, fluid-filled vesicles on an erythematous base
c. Within several days, vesicles become pustular,
rupture and encrust.
• The characteristic grouped vesicles distinguish HSV
from chickenpox. 77
 3. Herpetic whitlows
• Painful erythematous, oedematous white
pustules on the site of broken skin on the
fingers.
• Spread by auto-inoculation from
gingivostomatitis, in children who suck their
thumbs, bite their nails, and in infected
adults kissing their children’s fingers.
• In sexually active adolescents, HSV2 may be
the cause.

4. Herpes of eyes • May cause:

i. Blepharitis
ii. Conjunctivitis
• If extend to involve the cornea→ dendritic
ulceration → corneal scarring→loss of
vision

• Herpetic lesions near/involving the eye

requires ophthalmic investigation of the
cornea by slit lamp examination 78
5. Central Nervous System i. Neonatal HSV infection
• 70-85% is caused by HSV-2.
Infection • Acquired from the mother:
a. Shortly before delivery (ascending
infection) or
b. During passage through the birth canal at
delivery
• May be:
a. Focal, affecting the skin or eyes or
encephalitis or
b. Widely disseminated (involving multiple
organ systems , most notably the liver and
lungs)
• Morbidity and mortality high.

ii. Infection in immunocompromised

• May be severe
• Cutaneous lesions may spread to involve
adjacent sites → oesophagitis, proctitis
• Complications: pneumonia, disseminated
infections

79
 Investigations
1. Diagnosis made clinically
2. Viral culture
• Specimens obtained from any skin vesicle,nasopharynx, eyes,
urine, blood, CSF, stool, or rectum.
3. PCR Assay
• Higher sensitivity than culture.
• Detecting HSV DNA in blood, urine and CSF

80
 Treatment & Management
1. Oral famciclovir and valacyclovir
– To reduce severity and duration of symptoms in primary
cases.
– To reduce recurrences.
2. Intravenous acyclovir therapy
– For infants, persons with eczema and person with
immunodeficiency which are at increased risk for
disseminated and severe HSV disease.
3. Local hygiene and sitz bath may relieve discomfort
4. Use condom for protection against sexual transmission of HSV

81
Dengue

82
 Introduction
i. Dengue is the most common arthropod-borne viral(arboviral)
illness in humans.

ii. Cause by Dengue virus (DENV)

• Single -stranded RNA virus (+ssRNA)
• With an icosahedral nucleocapsid
• Covered by a lipid envelope
• Family : Flaviviridae
• Genus : Flavivirus
• Vector: Mosquitoes (genus Aedes).
• Female mosquitoes’ biting activity is early in the morning and at
dusk

83
iii. There are four serotypes of dengue virus (Den 1, Den 2,
Den 3, Den 4) that can be distinguished serologically.

iv. While infection by one serotype produces life-long

immunity against reinfection by that same serotype, there is
only temporary and partial protection against other serotypes.

v. The incubation period of dengue varies from 3-10 days with

an average of 4-6 days (WHO, 1997, level 6; Kabra et al, 1999,
level 8).

84
85
86
Dengue fever

87
 Febrile phase
High grade fever for 2 -
7 days with > 2 of the
following manifestations:
• facial flushing
• skin erythema
• frontal and retro-orbital headache
• myalgia
• arthralgia
• frontal and retro-orbital headache
• chills
• anorexia, nausea and vomiting
• Some have sore throat, conjunctival
injection, injected pharynx
• haemorrhagic manifestations
(petechiae)
• leukopenia
• Enlarged and tender liver, suggestiv
e of DHF
Critical phase
Occur at late febrile phase (3rd day of fever)or a
round defervescence (3rd-5th day of
illlness, up to 7th day.
• There is rapid drop in temp with increasing
capillary permeability.
• Thus, patient may become better if minima
l plasma leaks occurs OR worsen if a critical
volume of plasma is lost.
• Lasts about 24-48 hours
Can recover spontaneously, or after a short
period of fluid or electrolyte therapy
• In more severe forms of plasma leakage →
→ sweat, become restless, have cool extre
mities and prolonged capillary refill time
• Increase in pulse rate and diastolic blood pr
essure, pulse pressure narrows
88
89
 Recovery phase
• After 24-48 hours of defervescence, plasma leakage stops
• Reabsorption of extravascular fluid
• General well being improves, appetite returns, GI symptoms ab
ate, haemodynamic status stabilises and diuresis
• May have a classical rash of “islands-of-white-in-a-sea-of-red”
• May experience generalised pruritus
• Observe for complication for at least 2 days after recovery from
fever as a life threatening complications occur during this time.

90
 Clinical features
• High fever of acute onset of 3 days or more
• Altered sensorium
• Shock in an afebrile patient who had fever over
the previous 3-5 days
• Petechial rash
• Epistaxis or gum bleeding
• Backache or retro-orbital pain (in older children)
• Convulsion or headache
• Haemorrhagic manifestations
• Loose stools or diarrhoea
• Hepatomegaly
• Nausea and anorexia

91
Maculopapular rash &
petechiae 92
 Tourniquet test

1. Inflating a blood pressure cuff to a point mid-way between

the systolic and diastolic pressures for five minutes.

2. A test is considered positive when 10 or more petechiae per

2.5 cm2 (1 inch’) are observed.

3. In DHF, the test usually gives a definite positive result (i.e.

>20 petechiae).

4. The test may be negative or mildly positive during the phase

of profound shock.
93
 Severe Dengue
Dengue haemorrhagic fever (DHF)
• DHF with no shock
• DHF with shock (DSS) which can be further
graded into: -
1. DHF with compensated shock
• Signs of shock - tachycardia out of proportion
to body temperature, decreased tissue
perfusion as evidenced by cool extremities,
increased capillary refill time, narrowing of
pulse pressure, weak distal pulses, oliguria
and altered conscious level.
• Systolic pressure within the normal range
Dengue shock syndrome (DSS)
• Inadequate perfusion of the t/s lead to
increased anaerobic glycolysis and
lactic acidosis.
• If hypovolaemia not corrected
promptly, patient will progress to a
refractory shock state.
• Prolonged shock lead to massive
bleeding, DIC, multi-organ failure.

2. DHF with decompensated shock

• Signs of shock – tachycardia, cool extremities,
increased capillary refill time, weak or absent
pulses, oliguria and altered conscious level.
• Systolic hypotension 94
In more severe cases…

• Skin: Cold peripheries, pallor, prolonged

capillary refill time (>2 secs)
• CVS: Narrow pulse pressure (↑ diastolic
pressure), ↑ pulse rate
• CNS: Lethargy, restless, altered conscious level
• GIT: Abdominal pain, persistent vomiting
• RS: Tachypnea
• Renal: ↓ urine output

95
Diagnostic Criteria

96
97
Investigations

98
Disease Full Blood Count WCC: Normal in early febrile phase BUT decreased rapidly as
Monitoring disease progress
HCT: Rising HCT is a marker for plasma leakage
– Help to differentiate btw DF & DHF.
• Masked in patients with concurrent significant bleeding and
those receiving early fluid replacement
PLT: Normal in early febrile phase BUT decreased rapidly as
disease progress

Liver Function Test • Greater elevation of AST (2-3x) as compared to ALT

• Degree of elevation of liver enzymes are higher with DHF
compared to DF.
Diagnostic Test Dengue serology • Haemagglutination-Inhibition Titers- Gold standard BUT
tests for research purpose
• Dengue IgM Test- Significantly higher in primary infection.
Once the IgM is detectable, it rises quickly and peaks at
about 2 weeks after the onset of the symptoms, and it
wanes to undetectable levels by 60 days
• Indirect IgG ELISA Test- Detected 100% after day 7 of onset
of fever in both primary and secondary infection.
• Dengue Rapid Test- Qualitative detection of dengue
IgM/IgG. Could be used when ELISA facilities not available
1. Other flavivirus –Japanese Encephalitis 2. Non-flavivirus- Malaria,Leptospirosis,Toxoplasmosis,Syphilis
3.Connective tissue diseases - Rheumatoid Arthritis
99
 Con’t Diagnostic Test
Virus isolation • Most definitive test.
• Useful in the early phase of illness.
• Blood collected before day 5 of illness (before
formation of neutralizing antibodies)
• Takes up to 2 weeks and expensive.
Polymerase chain • Useful in <5 days of illness
reaction • Sensitivity 100% in the first 5 days of illness.
• Only available in few centers
• Expensive
• Requires special storage temperature and
short transportation time
NS1 Antigen • NS1 antigen – hallmark of flavivirus infecting
mammalian cells (dengue,yellow fever,West Nile
virus infection)
• High concentration during the early phase of
disease.
• Not useful in the convalescence phase.
100
Managements

101
a) Priorities during first encounter are:

1 - Establish whether patient has dengue

2 - Determine phase of illness
3 - Recognise warning signs and/or the presence of severe
dengue if present.

• Most patients with DF and DHF can be managed without

hospitalization if
1. No warning signs or evidence of abnormal bleeding
2. Oral intake and urine output are satisfactory
3. Caregiver is educated regarding fever control and avoiding
NSAID agents

102
 b) Indication for Hospitalization

• Presence of warning signs.

• Infants.
• Children with co-morbid factors (diabetes, renal failure,
immune compromised state, hemoglobinopathies and
obesity).
• Social factors - living far from health facilities, transport
issues.

103
c) Major priorities of managing hospitalized patient

The THREE major priorities of managing hospitalized patient with dengue in

the critical phase are:
A - Replacement of plasma losses.
B - Early recognition and treatment of hemorrhage.
C - Prevention of fluid overload.

Fluid therapy in a patient with dengue shock has two parts: initial, rapid
1. Initial - NS/ Ringers lactate at 5-7ml/kg over 1-2 hours
2. Rapid fluid boluses - to reverse shock followed by titrated fluid volumes to
match ongoing losses
a) Replacement fluids – NS 0.9% (10-20ml/kg or 20ml/kg)
b) Maintenance fluid – 5% D ½ NS +/- KCl

• fluid boluses to reverse shock followed by titrated fluid volumes to match

ongoing losses.
• However, for a patient who has warning signs of plasma leakage but is not
yet in shock, the initial fluid boluses may not be necessary.

104
d) Monitoring

Clinical parameters: Laboratory parameters

• Temperature • Haemoglobin/haematocrit
• Oral fluid intake (4-6hrly depend to
• Urine output severity)
• Hydration status • Total white cell (TWC)
• Haemodynamic count , platelet count, BUSE,
creatinine, dengue Serology

105
VOLUME REPLACEMENT FLOWCHART FOR PATIENTS WITH SEVERE
DENGUE AND COMPENSATED SHOCK

106
e) Discharge of Children with Dengue

• Afebrile for 24 hours without antipyretics.

• Good appetite, clinically improved condition.
• Adequate urine output.
• Stable hematocrit level.
• At least 48 hours since recovery from shock.
• No respiratory distress.
• Platelet count greater than 50,000 cells/μL.

107
 Complications of DHF/DSS
Primary complications
• Gastrointestinal bleeding (Hongsiriwon, 2002, level 3)
• Liver failure ( Lum et al, 1993, level 3)
• Dengue encephalopathy (Solomon et al, 2000; Pancharoen et al,
2001, level 3)
• Acute renal failure

Secondary Complications
• Respiratory failure secondary to massive pleural effusion and gross
ascites (Soni et al, 2001, level 3)
• Acute pulmonary oedema (Soni et al, 2001, level 3)
• Acute respiratory distress syndrome (Soni et al, 2001,level 3)
• Nosocomial infection

108
KAWASAKI
DISEASE

109
 Definition
• KD is vasculitis of unknown etiology that is characterized by
multisystem involvement and inflammation of small to
medium sized arteries with resulting aneurysm formation
• Also known as Kawasaki syndrome (mucocutaneous LN
syndrome
• Main cause of acquired heart disease in kids
• No known cause (virus suspected)

110
 Pathology
• Generalized systemic vasculitis involving blood vessels
throughout the body
• Edema of the tunica media and lead to influx of neutrophils
and cause destruction of internal elastic lamina
• Eventually cause fibroblastic proliferation (fibrosis)

111
 Epidemiology
• Second most common vasculitis of childhood
• The highest frequency is in Japan
• Most commonly occur in children younger than 5 years of age
• Peak incidence between 2 to 3 years
• Rare in children older than 7 years
• Seasonal variability with peak between February and May, but
the disease occur throughout the year

112
 Clinical manifestations
1. Acute : fever with conjunctivitis, cracked lip and strawberry tongue,
cervical lymphadenopathy, mucocutaneus sign, giant coronary
artery aneurysms

2. Subacute : defervescene, desquamation of skin (fingers and toes),

thrombocytosis, coronary artery aneurysms

3. Convalescent : normalization of acute inflammatory markers (ESR

returns to normal usu. 6 to 8 weeks after onset of illness), beau
lines of fingernails also appear

113
114
115
 Diagnostic criteria
• Fever more than 5 days
• Bilateral non purulent conjunctivitis
• Changes in extremities (edema/erythema of extremities,
desquamation of finger and toes)
• Mucosal changes of oropharynx (strawberry tongue, injected
pharynx, dry fissured lip)
• Cervical lymphadenopathy
• Polymorphous rash (mostly hand and feet)

116
 Differential diagnosis

INFECTIOUS INFLAMMATORY HYPERSENSITIVITY

• Viral infection • Juvenile • Drug reaction
(measles, rubella, idiopathic • SJS (erythema
adenovirus, EBV) arthritis multiforme)
• Staphylococcal • Polyarteritis
scaled skin nodosa
syndrome
• Scarlet fever
• Leptospirosis
• Meningococcemia
• Roseola infantum

117
 Laboratory and imaging studies
• Blood and urine culture (TRO infection)
• CXR
• Inflammatory markers (ESR & CRP)
• Platelet count (may be inappropriately low or normal)
• Lumbar puncture (to exclude infection and reveal pleocytosis)
• Hepatobiliary function test (may be abnormal)
• 2D ECG (to monitor development of coronary artery
aneurysms usu at acute phase
• Coronary angiography (pts who develop coronary artery
abnormalities)

118
 Treatment and management
• IVIG is the mainstray of the therapy (2g/kg over 12 hours)
• Aspirin given in anti inflammatory doses (80 to 100
mg/kg/day every 6 hours)
• Once fever resolved, aspirin is reduced to anti thrombotic
doses (3 to 5 mg/kg/day in single dose given through
subacute and convalescent phases)
• F/up ECG to the resolution of coronary artery aneurysm
• Corticosteroid (rarely used but have role during acute phase if
acute carditis appeared)
• If platelet continue to increase, anti platelet aggregation
agents is given to reduce thrombosis

119
 Complications
• Coronary artery thrombosis
• Peripheral artery aneurysm
• Myocardial infarction
• Myopericarditis
• Heart failure
• Hydrops of GB
• Aseptic meningitis
• Arthritis

Prognosis
IVIG reduces the prevalence of coronary
artery disease from 20% to 25%
KD has excellent prognosis

120
Scarlet Fever

54
 Definition
• Is an erythematous eruption that is associated with a
febrile illness.
• It may occur with streptococcal pharyngitis due to infection of
= group A beta-haemolytic streptococci = (GABHS)

• Scarlet fever and streptococcal toxic shock syndrome are systemic

responses to circulating bacterial toxins.

55
56
 What causes scarlet fever…??
Streptococcus pyogenes
• Gram -positive cocci
• In chains.
• Beta- haemolytic (complete haemolysis)
• Able to survive extremes of temperature and humidity,
which allows spread by fomites.
• Normal flora of the nasopharynx
• Infectivity: pharyngitis, skin infections (including erysipelas
pyoderma and cellulitis), pneumonia, bacteraemia, and
lymphadenitis.

57
 Virulence
Antigenic components
Capsular polysaccharide (c-
substance)
Cell wall peptidoglycan
Lipoteichoic acid (LTA)
Surface proteins
M protein
Fimbrial proteins
Fibronectin-binding proteins
(e.g. Protein F)

Secretory product
Cell-bound
streptokinase.

58
 1
3 4
2

59
 Pathophysiology
• The circulating toxin, produced by GABHS and often referred to as
erythemogenic or erythrogenic toxin (was
discovered by Dick and Dick in 1924) Pathognomonic
rash as a consequence of local production of inflammatory
mediators and alteration of the cutaneous cytokine milieu.

• This results in a sparse inflammatory response and dilatation of

blood vessels, leading to the characteristic scarlet colour of the
rash.

60127
 Source of infection
• Tonsils and pharynx (most commonly)
• Wound infections of the skin and soft tissue (pyoderma) or
burns
• Surgical wounds (i.e., surgical scarlet fever)
• Upper respiratory tract infections.
• Uterus (i.e., puerperal scarlet fever)
• Food-borne outbreaks

Route of transmission
• Person-to-person spread
• Respiratory droplets is the most common mode of
transmission
61128
 Scarlet fever

• Incubation period = 2–5 days

• Duration: ranges from 12 hours to 7 days
• Predominantly occurs in children aged 1-10 years, though
it can also occur in older children and adults.

62
 History taking

• Its emergence tends to be abrupt, usually heralded by

sudden onset of fever associated with sore throat,
headache, chills, nausea, myalgias, and malaise.

• Young children may also present with vomiting, abdominal

pain, and seizure

• The characteristic rash appears 12-48 hours after the onset

of fever, first on the neck and then extending to the trunk
and extremities.

63
 Physical Examination
• The patient usually appears moderately ill.
• Fever may be present.
• The patient may have tachycardia.
• Tender anterior cervical lymphadenopathy may be
present.
• The mucous membranes usually are bright red,
and scattered petechiae and small red papular
lesions on the soft palate are often present.
• On day 1 or 2, the tongue is heavily coated with a
white membrane through which edematous red
papillae protrude (classic appearance of white
strawberry tongue).
• By day 4 or 5, the white membrane sloughs off,
revealing a shiny red tongue with prominent
papillae (red strawberry tongue).
• Red, edematous, exudative tonsils are typically
observed if the infection originates in this area.
64
 Clinical feature
Prodrome
• Infection is spread by respiratory secretions and droplets, or
by self-infection from nasal carriage.
• During the incubation period, the child may have fever, vomiting, and
abdominal pain.

Exanthematous phase
• ‘sandpaper-like’ diffuse rash (in the neck and chest)
• With perioral pallor spreading to the flexor creases.
• The pharynx is erythematous and there may be exudative tonsillitis,
palatal petechiae, uvular edema, and strawberry tongue.

Other features :
• Tender anterior cervical lymphadenopathy.

65132
Sandpaper-like’ diffuse rash
66
 Perioral pallor
Strawberry tongue

Exudative tonsillitis
Uvular oedema
Palatal petechiae
67
• Capillary fragility is increased, and rupture may occur.
• Often, transverse areas of hyperpigmentation with linear arrays of
petechiae in the axillary, antecubital, and inguinal areas (Pastia lines,
or the Pastia sign) can be observed.
• These arrays may persist for 1-2 days after resolution of the
generalized rash.
• Followed by fine desquamation…

68
 Differential diagnosis

• Abortion Complications • Pediatric Pneumonia

• Drug Eruptions • Pediatric Rubella
• Erythema Infectiosum
• Pityriasis Rosea
• Exfoliative Dermatitis
• Recurrent toxin-mediated
• Infectious Mononucleosis
perineal erythema
• Kawasaki Disease
• Staphylococcal Scalded Skin
• Measles
Syndrome
• Pediatric Erythema Toxicum
• Toxic Shock Syndrome
• Pediatric Pharyngitis
• Viral exanthem 69
 Diagnosis and Investigations

• The diagnosis is mostly based on the clinical

presentation.
• However, leucocytosis with left shift presentation and
possibly eosinophilia a few weeks after convalescence on
a standard blood test and urine tests are part of a
complete medical workup.

70137
Throat or nasal • Culture and growth of the organism in a symptomatic
swab individual
• Note also asymptomatic carriage common
Serum • Anti-streptolysin O (ASO)
• Anti-dnase B titres
• Anti-hyaluronidase
• Anti-fibrinolysin
one or both may rise in acute infection
CBC • Commonly reveals a leukocytosis.
• The white blood cell (WBC) count may be > 12,000-16,000/μL
• Differential count of up to 95% polymorphonuclear lymphocytes.
• During the second week, eosinophilia, as high as 20%, can
develop.
Urinalysis and • May reveal changes associated with complications of scarlet fever.
LFT • Haemolytic anaemia can occur
• Mild albuminuria and haematuria may be present early in the
disease.

71
 Treatments
1. Antibiotics

• Penicillin V (or amoxicillin) remains the drug of choice

(documented cases of penicillin-resistant GAS infections
still do not exist).
• A first-generation cephalosporin may be an effective
alternative, as long as the patient does not have any
documented anaphylactic reactions to penicillin.
• If this is the case, clindamycin or erythromycin may be
considered as an alternative.
• However, some strains of group A streptococci may not be
susceptible to macrolides.
**Hence, a culture and sensitivity test have to be carried
out to select for suitable antibiotics.

• A 10 - 14-day course of treatment is usually

recommended, and clinical improvement should be noted
after 24-48 hours of antibiotic initiation.
73
2. Topical cream
• Emollients - moisturising
treatments applied directly to the
skin to reduce water loss and
cover it with a protective film

3. Epsom salt
• Chemically known as
heptahydrate epsomite
• Extensively used for cleansing
purpose

74
 Prevention
• Hand hygiene and proper maintenance
of environmental hygiene should be
highly reinforced.

• Children with scarlet fever should not

return to school or day-care until they
have completed 24 hours of antibiotic
therapy and are clinically improving.

• Follow-up evaluation

75
 Complications
Suppurative
Peritonsillar abscess
Otitis media and/or mastoiditis
Ethmoiditis
Retropharyngeal abscess
Sinusitis
Bronchopneumonia
Meningitis
Septicemia, osteomyelitis, and septic arthritis

Immune-mediated sequelae
Acute glomerulonephritis (post-streptococcal )
Rheumatic fever
76142
 Prognosis
• Most patients recover fully after 4-5 days, with
resolution of skin symptoms over several weeks.
• However, attacks may recur.

77
Meningococcal
Disease

144
 Meningococcal
• Causative agents => Neiserria menigitidis.
• Meningococci are gram-negative aerobic cocci
• Many serogroups. Common in human disease (serogroups A, B, C,
W135 and Y)
• Increase number of cases during winter and spring
• Most cases are sporadically in < 2y/o
• Diseases caused by meningococci
 90% - meningitis and septicemia
 Others – infections of lungs, joints, respiratory passage, GIT, eye,
pericardium and endocardium

145
 Clinical manifestations
Meningitis of Meningococcal Fulminant
meningococcemia septicemia meningococcemia
symptoms
• Headache • Fever • Waterhouse-
• Fever • Rash Friderichsen syndrome
• Vomit • Tachycardia (adrenal haemorrrhage)
• Photophobia • Hypotension
• Lethargy • Cool extremities
• Neck stiffness
• Kernig and Brudzinki
signs

• Sepsis with multiple

organ failure
• Shock
• DIC 146
 Rashes

Hemorrhagic petechial and purpura

Initially maculopapular on
trunk or legs
147
148
 Investigations
1. Gram stain and culture
• Neisseria are small, gm-negative cocci
2. Latex agglutination – rapid diagnosis of N. meningtidis in blood, CSF,
synovial fluid and urine. (But still need to confirmed with culture)
3. Full blood count
4. Serum electrolytes
5. Serum glucose
6. Lumbar puncture
7. CSF studies
8. CT & MRI of the brain

149
 Differential diagnoses
● Encephalitis
● Rheumatic diseases
● Brain abscess
● Vasculitis

150
 Treatment
● Antibiotics
– For newborn – cefotaxime/ceftriaxone + ampicillin
with/without gentamicin
– For others – ceftriaxone/cefotaxime + vancomycin
● Dexamethasone as adjunctive therapy
● Hydration if needed

151
 Complications
● Subdural effusions
● DIC
● Coma
● Herniation
● Septic arthritis
● purulent pericarditis

152
Salmonella

153
 Salmonella infection

Salmonella gastroenteritis
● Incubation period 6-72 hours
● Presented with abdominal pain, nausea, vomiting, and loose
watery stools.
● Usually resolve spontaneously in 2-7 days
Typhoid fever
● Caused by salmonella typhi & paratyphi
● Incubation period 3-60 days, symptoms usually occur in 1-2 weeks
● can be presented with abdominal pain, malaise, myalgia, headache,
cough, diarrhea, constipation
154
 Clinical presentation
Salmonella gastroenteritis
● Signs of dehydration, such as delayed capillary refill, sunken eyes, dry
mucous membranes, or tachycardia.
● May have tenderness to palpation on abdominal examination, which
sometimes can be difficult to differentiate from appendicitis.
● Rectal examination may reveal heme-positive stools, gross blood, or
mucoid stools.
Typhoid fever
● Typical finding is bradycardia
● Hepatosplenomegaly may be found on examination
● May present with rose spots; these spots are blanching pink papules most
commonly found on the anterior thorax. They usually fade about 3-4 days
after appearance, are 2-4 mm in diameter, and occur in groups of 5-20.
155
156
 Investigations
● Full blood count
● Culture
● Stool examination
● Serum electrolyte
● Serologic tests

157
 Treatment
Salmonella gastroenteritis
● If caused by non-typhoidal salmonella, no need anti-miCrobial therapy
● Monitor hydration status, IV therapy to correct electrolyte imbalance
● Recommended antibiotics for individuals with high risk for invasive
disease include ampicillin, amoxicillin, and TMP-SMZ
● If there are multidrug resistance, use cefotaxime or ceftriaxone

Invasive salmonella disease (bacteremia, extraintestinal manifestaion)

● Broad spectrum cephalosporin (cefotaxime and ceftriaxone) until
susceptibilities are available, use narrow therapy agents (ampicillin,
amoxicillin)
● 14 days course for patients with bacteremia
● For salmonella meningitis, ceftriaxone/cefotaxime recommended for 4
weeks or longer 158
Typhoid fever
● Initial therapy with ceftriaxone is recommended due to widespread
resistance. If susceptible, chloramphenicol, ampicillin, or TMP-SMZ
may be used. Duration of therapy should be 14 days
● In severe infection, parenteral therapy is indicated
● Use antipyretics with caution or not at all because they may cause
precipitous drops in temperature and shock. Fever may last 5-7
days, even with appropriate therapy
● A short course of high dose-corticosteroids may be involved in
treatment of patients with life-threatening neurologic
complications of enteric fever
● High-dose ampicillin or high-dose amoxicillin plus probenecid for 4-
6 weeks has cured many chronic carriers. Ciprofloxacin is the drug
of choice for adult carriers
● Relapse is common (≤15%), and patients must be re-treated
159
Thank you

160