FEVER WITH

RASH IN
CHILDREN
Moderator: Dr. P S Suman Babu
Presenter: Dr Amulya K R
Dept of dermatology,
RIMS
INTRODUCTION
 Fever with exanthem is common in childhood and a cause of
anxiety among parents. Many of them are benign viral
exanthems without much clinical significance.
 However, a physician must be aware of the distinguishing
features of the serious illnesses which may be associated
with major complications with substantial morbidity and
mortality.
 There are a large number of infectious and noninfectious
conditions presenting as exanthematous fevers.
COMMON CAUSES OF FEVER WITH RASH
IN A CHILD
Infectious Causes

 Viral infections- Measles, rubella, varicella, HHV-6, HHV-7, EBV, coxsackie,

dengue, chikungunya

 Bacterial infections- Staphylococcus aureus, Group A streptococcus, Neisseria

meningitidis, Listeria monocytogenes, Bartonella quintana, Borrelia,
Leptospira

 Rickettsial infections (diseases)- R. prowazekki (Epidemic typhus), R. typhi

(Murine typhus), R. tsutsugamushi (Scrub typhus), R. conorii (Indian tick
typhus), R. rickettsii (Rocky mountain spotted fever), R. akari (rickettsial pox),
Coxiella burnetti (Q fever), Rickettsia quintana (Trench fever)
Noninfectious Causes

 Collagen vascular diseases- SLE, juvenile dermatomyosistis, KD,

HSP, polyarteritis nodosa, Wegener’s granulomatosis

 Drug hypersensitivity rash- SJS, toxic epidermal necrolysis, acute

generalized exanthematous pustulosis, drug reaction with
eosinophilia and systemic symptoms (DRESS) syndrome
 Rubelliform Morbilliform Scarlitiniform
• Maculopapular • Maculopapular • Pinpoint
• Discrete • Confluent papules in a
diffuse
erythematous
background
VIRAL EXANTHEMS

Duke’s disease, is a nonexistent entity now

because the original descriptions for this disease
were actually overlapping with other classical
exanthems.
MEASLES (SYN: FIRST
DISEASE, RUBEOLA)
 Causative virus - Paramyxovirus, genus Morbillivirus, single-
stranded enveloped RNA virus.
 Most infectious communicable diseases - 76% of household
exposures of susceptible persons lead to measles
 Transmission- direct exposure to an infected individual, but MV
can survive for hours in respiratory droplets
 Most infectious from 4 to 5 days before the appearance of the
rash to 4 days after the onset of rash.
 Incubation period- 7-14 days
 Clinical features: Prodrome of 1–7 days presenting with coryza,
conjunctivitis, cough, and high-grade rising fever
 Erythematous, blanching maculopapular rash usually begins
behind the ears and anterior hairline and rapidly progresses to
profuse coalescence involving the neck, trunk, and extremities in
that order within 2–4 days .
 Koplik’s spots- punctate bluewhite lesions surrounded by erythema on buccal mucosa against
second molar, appear on 2–4 days of fever
 Herman’s spot- pinpoint raised lesions against the red background of deeply congested pharynx for
6–7 days.
 Characteristic multinucleated giant cells present in the lymph nodes, known as Warthin–Finkeldey
cells, and syncytial giant cells in the epidermis.
 Complications
 The most common complication of measles infection is otitis media.
 Other complications- Hecht giant cell pneumonia, croup, diarrhea, Measles keratoconjunctivitis
 Pregnant women with measles are at increased risk for maternal death, spontaneous abortion,
intrauterine fetal death, and low birth-weight infants.
 Central nervous system complications include acute disseminated encephalomyelitis (ADEM),
measles inclusion body encephalitis (MIBE), and subacute sclerosing panencephalitis (SSPE)

Treatment
 Treatment of measles is supportive. Rest, hydration, nutritional support, anticough preparations, and
respiratory isolation are necessary.
 Intravenous or aerosolized ribavirin - severely ill or immunocompromised children.
 Vitamin A administration - decrease morbidity and complications due to severe measles.
 Immune serum globulin administration - should commence within 6 days of exposure.
 MR vaccine- Given in two doses, at 9–12 months and 16–24 months
 The MMR vaccine is typically given in private sectors. Given at 9 months, 12–15 months, and
between 4–5 years.
RUBELLA
(SYN: THIRD DISEASE,
GERMAN MEASLES)
 Caused by Rubella virus, a togavirus that is enveloped and has a single-stranded RNA
genome
 Transmitted by the respiratory route and replicates in the nasopharynx and lymph nodes.
 Incubation period: 15–21 days
 Contagious typically for about 1 week before he/she develops a rash and for about 1 week
thereafter
 The virus has teratogenic properties and is capable of crossing the placenta and infecting the
fetus, where it stops the cells from developing or destroying them
 A prodrome of fever, headache, malaise, cough, and sore throat
 Light pink macules, and papules begin usually on the first day
on cheeks in a butterfly pattern and spreads to retroauricular
area and then spread caudally to trunk and extremities.
 There is always cervical and occipital lymphadenopathy.
 An enanthem of rose-pink pinpoint petechiae (Forchheimer
spots) may be seen on the soft palate and uvula

Complications:
 Arthralgia and arthritis
 Encephalitis, orchitis, neuritis, thrombocytopenia, and late
progressive panencephalitis
 Infection during the first trimester of pregnancy runs the
highest risk of causing congenital rubella syndrome
• Congenital heart defects (patent ductus arteriosus, peripheral
pulmonary artery stenosis, ventricular septal defects, atrial septal
defects)
• Auditory (sensorineural hearing impairment)
• Ophthalmologic (cataracts, pigmentary retinopathy,
microphthalmos, chorioretinitis)
• Neurologic (microcephaly, cerebral calcifications,
meningoencephalitis, behavioral disorders, mental retardation)
• Hematologic (thrombocytopenia, hemolytic anemia,
petechiae/purpura, dermal erythropoiesis causing “blueberry
muffin” rash)
• Neonatal manifestations (low birth weight, interstitial pneumonitis,
radiolucent bone disease leading to “celery stalking” of long bone
metaphyses, hepatosplenomegaly)
• Delayed onset of insulin-dependent diabetes and thyroid disease.
ERYTHEMA INFECTIOSUM
(EI)
(SYN: FIFTH DISEASE)
 Causative agent: Human parvovirus B19
 School-going children between 4 and 10 years
 The disease spreads via droplet infection by saliva, sputum, or nasal discharge
 The incubation period is 4–15 days
 Disease loses infectivity with the appearance of rash.
 Cutaneous and rheumatologic findings develop only after the production of enough antibodies
against parvovirus B19. Hence, the skin manifestations are thought to be due to multisystem
immune complex deposition.
 A prodrome of low-grade fever, malaise, myalgia, pharyngitis,
nausea, diarrhea, or arthralgia
 Characteristic rash described as “slapped cheek appearance”-
macular or occasionally plaque of bright erythema involving the
cheeks. Sparing of periorbital areas, the nasal bridge, and perioral
area (circumoral pallor)
 The rash on cheeks gradually fades in a span of 4–5 days, followed
by another characteristic eruption of lacy, reticular generalized rash,
which occasionally may be pruritic, and involves the trunk and
extensor extremities. This lasts for about 5–9 days and may recur for
the next few weeks to months
Complications:
 In immunocompromised individuals with HIV, congenital immunodeficiencies, acute
leukemia, organ transplants, and lupus erythematosus or in infants, parvovirus B19 can cause
persistent chronic anemia due to lysis of RBC precursors, resulting from active viral
replication.
 The rate of vertical transmission in infants is reported to be 16% if exposed to the infected
mother during the first 20 weeks and 35% if exposed after 20 weeks of gestation.
Treatment:
 Symptomatic
 Aplastic crisis would require fresh blood transfusions.
 Pregnant women with confirmed primary infection due to parvovirus B19 (IgM and rising
titers of IgG) must be carefully followed for fetal complication such as hydrops fetalis
 Intravenous immunoglobulin containing pooled, neutralizing anti-B19 antibody has been
used successfully to prevent complications in immunologically compromised patients
ROSEOLA INFANTUM
(SYN: EXANTHEM SUBITUM, SIXTH
DISEASE,
PSEUDORUBELLA)
 Caused by HHV-6B and HHV-7
 Acquired as a droplet infection, the virus HHV- 6 multiplies in salivary gland and is
secreted in saliva
 Incubation period of 7–14 days
 Clinical features: high-grade fever of 40°C.
 Ulceration or erosions at the uvulopalatal junction.
 On day 5, the hallmark of RI is fever with appearance of generalized erythematous
macules (resembling rubella) on the trunk and neck, but face is usually spared.
Completely clears within the next 2–5 days without any residual change.
 Complications- otitis media, gastroenteritis, eyelid edema, cervical lymphadenopathy,
febrile convulsions, thrombocytopenia, encephalitis, Guillain-Barre syndrome, and
myocarditis.
HAND-FOOT-MOUTH
DISEASE
 Caused by: Coxsackie virus A16 (CAV16) and human enterovirus 71 (HEV71). Other
viruses associated with the syndrome are coxsackie virus A (CVA) 4, 5, 9, and 10 and
coxsackie virus B (CVB) 2 and 5.
 EV71 can also result in severe neurological diseases, such as aseptic meningitis and acute
flaccid paralysis (AFP), and even death
 The incubation period is from 3 to 6 days.
 The disease peculiarly affects children below 10 years of age
 Fecal-oral and oral-oral routes are common modes of transmission than droplet infection.
 A prodrome of fever, malaise, abdominal pain, vomiting,
diarrhea, and anorexia occurs
 Enanthem presenting as painful oral ulcers on the hard palate,
tongue, and buccal mucosa usually precedes the onset of
exanthem.
 It consists of symmetrical erythematous 2–8 mm
maculopapular rash on hands and feet, which soon becomes
vesicular with a typical erythematous halo
 These resolve within 5–10 days. The crust formation ensues
within 8–10 days and heals without scarring
Complications:
 Myocarditis, pneumonia, and meningoencephalitis. Diarrhea
and arthralgia may occur occasionally.
 Infection in the first trimester of pregnancy may result in
spontaneous abortion and intrauterine growth retardation.
 The treatment of HFMD is symptomatic
 Systemic acyclovir 200 mg every 5 hours for 5 days is reported of some benefit, especially
in immunocompromised individuals or those with severe morbidity.
 Pleconaril, a broad-spectrum antiviral drug has demonstrated efficacy in
immunocompromised patients with severe enteroviral infection in the dose of 2.5–5 mg/kg for
7 days
 Rupintrivir (also referred to as AG7088) found to exhibit broad spectrum antiviral activity
VARICELLA (CHICKENPOX)
 VZV is a double-stranded, linear DNA virus
 The incubation period is 14–16 days
 It spreads mainly by respiratory droplets but infection through direct contact may also occur.
 The disease is infectious from 2 days before the onset of rash to 5–6 days after the onset or
until all lesions crust.
 After entry through the mucosa of the upper respiratory tract or oropharynx, the virus
undergoes localized replication along with concurrent replication in regional lymph nodes. The
virus disseminates through blood and lymphatics (primary viremia).
 A secondary phase of viremia occurs after approximately 9 days and persists throughout the
development of skin lesions.
 Granulysin is a recently discovered cytolytic protein of NK-cells and cytotoxic T-
lymphocytes, which is a factor for the prognosis of the clinical course of Varicella
 Prodromal symptoms - older children and adults may have
fever, sore throat, malaise, anorexia, and severe backache for
2–3 days preceding the rash.
 The rash usually starts on the face and scalp and spreads
caudally to extremities
 New lesions occur in crops. Pruritus is common, sometimes
severe.
 Lesions begin as macules that rapidly become papules
followed by characteristic vesicles on an irregular
erythematous base giving rise to “dew drops on a rose
petal” appearance. Turn into pustules, and crust in 2–4 days.
Lesions of different stages are seen in the same area at the
same time.
 Usually 200–300 lesions are seen and more than 500 lesions
indicate severe infection.
 Vesicles can also be present on the mucous membranes
mostly on the palate, and rarely, nose, larynx, pharynx, and
conjunctiva can also be involved, where they rupture easily
and leave behind shallow ulcers
 Tzanck smear from the base of the vesicle reveals multinucleated giant cells and
eosinophilic inclusion bodies.
 Skin lesions show ballooning degeneration of the prickle cell layer with eosinophilic
inclusions and marginated chromatin in nuclei
 Specific antiviral therapy is indicated in infants, older children, and immunocompromised
 Acyclovir inhibits the viral DNA polymerase by acting as a chain terminator, which is the
effective therapy for primary varicella in both healthy and immunosuppressed hosts.
 Valacyclovir, famciclovir, Brivudine, Foscarnet and cidofovir
POSTEXPOSURE PROPHYLAXIS

They should receive VZV specific immunoglobulin (VZIG) within 96 hours of exposure.

Acyclovir prophylaxis for 1 week (40–80 mg/kg/day) is effective in aborting or reducing the
severity of the disease if given within 9 days after exposure
 ERUPTIVE PSEUDOANGIOMATOSIS
(SYN: HEMANGIOMA-LIKE EXANTHEM, CHERRY
ANGIOMA-LIKE EXANTHEM)
 Multifactorial viral etiology has been suggested

 Initial prodrome of mild fever, sore throat, or gastrointestinal symptoms.

 The rash erupts as small, discrete cherry angioma-like tiny papules (1–
4 mm) surrounded by a perilesional halo on the face, neck, extremities,
and trunk
 The rash completely blanches on pressure.

 They are asymptomatic or slightly pruritic, and resolve without residual

scarring in a period of 2–18 days in children and 1–3 months in adults.
 Histopathology shows predominantly lymphohistiocytic infiltrate of
varying intensity around the affected vessel.
 The disease is benign, self-resolving yet distinctive, and lasts for a short
duration. Hence, the treatment is not required
GIANOTTI-CROSTI SYNDROME (SYN:
INFANTILE PAPULAR ACRODERMATITIS,
PAPULAR ACRODERMATITIS OF INFANTS,
INFANTILE LICHENOID DERMATITIS)
 GCS is typically a disease of children between the age
group of 1 to 6 years
 Hepatitis B , Epstein-Barr virus
 Other viruses- enteroviruses, parvovirus, parainfluenza
virus, mumps virus, rotavirus, poxvirus, respiratory
syncytial virus, ECHO, hepatitis A virus, hepatitis C
virus, molluscum contagiosum virus, human
immunodeficiency virus, and HHV-6
 Nonviral organisms such as Mycoplasma pneumoniae,
Bartonella henselae, β-hemolytic streptococcus, and
Borrelia burgdorferi.
 History of immunization with oral polio, hepatitis B, and
MMR vaccines.
 Minimal constitutional symptoms of fever and malaise. The commonest type of rash is pink or
red papules, or papulovesicles of 1–10 mm size symmetrically distributed on the extensor
aspect of extremities, face, and buttocks.
 Involvement of trunk, palms, and soles is rare.
 Lymphadenopathy is seen in up to one-third of patients involving mainly cervical and
sometimes axillary and inguinal groups
 Leucocytosis with lymphocytosis, remarkable monocytosis may be present indicating an
active viral infection
 The histologic findings in the vesicular type show mild acanthosis and spongiosis with
intraepidermal vesicle.
 Langerhans cells are present in a significant number inside the vesicle.
 In papular variants, acanthosis, parakeratosis, hyperkeratosis with mixed lymphohistiocytic
perivascular infiltrate, and occasional hemorrhages may be seen.
 The rash resolves within 2–8 weeks without scarring
 Complications include chronic hepatitis, especially in those positive for hepatitis B surface
antigen
ASYMMETRIC PERIFLEXURAL
EXANTHEM
 Disease of young children between 1 and 5 years.
 Parainfluenza 2 and 3, parvovirus B19, and
adenovirus.
 Classically unilateral and presents as a macular-papular
scarlatiniform eruption that starts in one axillary fold, but
it can also begin in other flexures, such as the thigh, flank,
or inguinal fold
 After 10–15 days, the rash may spread to involve the
thorax, the corresponding arm, and the contralateral side
in 70% of cases
 Symptoms disappear on average between 4 and 6 weeks
without recurrences or scars.
PAPULAR PURPURIC GLOVES AND
SOCKS SYNDROME
 Self-limiting febrile dermatosis characterized by edema,
erythema, and purpuric lesions of the hands and feet
 Parvovirus B19. Other viral association of this peculiar rash
includes EBV, CMV, HHV-6, HHV-7, coxsackie B6, measles,
rubella, and hepatitis B
 The incubation period is about 10 days.
 asymptomatic eruption as edema and erythema of hands
and feet, which soon turns out to be purpuric. There is sharp
demarcation at the wrist and ankles signifying the term,
“purpuric socks and gloves”
 The condition usually resolves spontaneously within 1–2
weeks
INFECTIOUS
MONONUCLEOSIS
 EBV, a member of the γ-herpesviruses, is the etiologic agent of IM

 Peaks in incidence are observed in individuals 1–6 and 14–20 years of age

 Transmission: Direct contact with an infected person’s saliva, such as through kissing or sharing
toothbrushes and cups
 Incubation period: 4 to 7 weeks.

Pathogenesis:
 EBV infects the B-cells in the oropharyngeal epithelium and affects the entire reticular endothelial system,
that is, liver, spleen, and peripheral lymph nodes via circulating B-cells
 Natural killer cells and predominantly CD8+ cytotoxic T-cells control proliferating B-lymphocytes infected
with EBV.
 The T-lymphocyte cellular response decides the clinical presentation of EBV infection. A rapid and efficient
T-cell response results in control of the primary EBV infection and lifelong suppression of EBV. Ineffective
T-cell response may cause uncontrolled B-cell proliferation, resulting in B-lymphocyte malignancies such as
B-cell lymphomas
 Triad of fever, pharyngitis, and lymphadenopathy (especially cervical)

 Fever, lymphadenopathy, rash, and periorbital edema are the early signs
of IM.
 Exanthematous rash is of two kinds.

 First is a transient, asymptomatic faint maculopapular rash occurring

directly due to the viral infection and is seen in early course of the disease
(within 24–48 hours)
 The other type follows after administration of antibiotics, commonly β-
lactams, viz., ampicillin or amoxicillin, eruption is profuse, often pruritic,
and lasts longer affecting the trunk and upper extremities
 Bilateral, transient upper eyelid edema (Hoagland sign)

 Bilateral tender posterior cervical lymphadenopathy is a common

presentation of IM
 Splenomegaly may occur after the first week, often with tenderness
Complications:
 Splenic rupture is an unusual but potentially life-threatening complication in 1% of patients

 Gastrointestinal -mesenteric adenitis, acalculous cholecystitis, pancreatitis

 CNS - meningoencephalitis, transverse myelitis, aseptic meningitis, cranial nerve palsies, especially
facial nerve, and Guillain-Barre syndrome
 Renal complications - glomerulonephritis

 Lymphocytosis with atypical lymphocytes in peripheral blood (>10%) is helpful in the diagnosis.

 Mononucleosis is a constant feature on peripheral smear.

 Monospot test, a latex agglutination test detects
heterophile antibodies against EBV. It may not be
positive until 2–6 weeks after initial symptoms.
 False-negative results are seen in children below 2
years and false positive in toxoplasmosis, rubella,
lymphoma, and leukemias.
 A short course of corticosteroids (1 mg/kg/day for 3
days, gradually tapered over 2 weeks) should be
reserved for the patients with mononucleosis induced
hemolytic anemia, CNS involvement, severe tonsillar
enlargement, thrombocytopenia, and myocarditis
KAWASAKI DISEASE
(MUCOCUTANEOUS
LYMPH NODE SYNDROME)
 Acute febrile illness characterized by self-limiting multisystem vasculitis of unknown etiology
occurring in infants and children.
 Children with KD are younger than 5 years of age

 There is a genetic predisposition to the development of KD. Polymorphisms of the IgG receptor can
increase the susceptibility of children to KD and increase the risk of developing coronary artery
aneurysm
 An infective cause was also suggested for the incidence of KD. Virus could have been inhaled and later
engulfed by tissue macrophages activation of the innate immune response. Further activation of the
adaptive immune responses antigen specific T-lymphocytes and plasma cell activation.
 The presence of the infection in coronary tissue secretion of multiple growth factors such as vascular
endothelial growth factors, tumor necrosis factor-α (TNF-α), and metalloproteinase 9 destruction of
the intima, and fragmentation of the internal and external elastic lamina of the coronary artery
development of a coronary artery aneurysm
 ACUTE FEBRILE PHASE (1–11 DAYS):

 High-grade fever (102–104°F), highly irritable child, bilateral

conjunctivitis, and rashes. Lips become erythematous, fissured
and may bleed
 Oral mucosa and tongue is swollen and erythematous with
prominent papillae (strawberry tongue)
 Conjunctivitis is typically bilateral, bulbar, and non-purulent

 A polymorphic non-vesicular rash may affect the trunk,

extremities, and face
 Tender lymphadenitis of cervical and less commonly of
axillary and inguinal groups is often noticed.
 Hepatic dysfunction, myocarditis, aseptic meningitis and
pericarditis may occur in this phase
SUBACUTE PHASE (11–21 DAYS):

 Fever gradually resolves

 Thrombocytosis ensues and the platelet counts are quite
high
 Desquamation of finger and toe tips begin
 Coronary aneurysms may occur at this stage and the child
may have a risk of sudden death.
CONVALESCENT PHASE (21–60 DAYS):

 All physical signs of the disease start receding and acute phase reactants begin to normalize.

After 60 days, the child enters the chronic phase

of the disease. It is of importance for those who
demonstrate cardiac complications. The coronary
dilatation or aneurysm persists indefinitely and
may have a risk of rupture in adulthood. Hence, a
regular follow-up is a must in such patients.
 KD is a self-limiting disease and completely resolves within 2–6 weeks
 Mild-to-moderate normochromic anemia, leucocytosis, and increase in acute phase reactants
such as ESR, C-reactive protein (CRP), and α-1 antitrypsin. Platelet counts are remarkably
raised in the subacute phase
 Echocardiogram is must to demonstrate the coronary aneurysm. It is ideally done on the first
visit, at 1–3 weeks and 1 month, and then every year thereafter
 Histopathology: In the early stages of KD vasculitis, edema of endothelial cells with nuclear
degeneration is seen, along with edema and mild inflammatory changes in the adventitial
layer.
 At 1–2 months following the onset of illness, inflammatory cells begin to disappear and
fibrous connective tissue, consisting of collagen and elastic fibers, begins to form within the
structure of the vessel wall.
Diagnostic criteria for KD put forth by the American heart
association are as follows:
1. High grade, persistent fever unresponsive to antibiotics >5 days.
2. Bilateral non purulent conjunctivitis.
3. One or more mucous membrane changes: Diffuse injection of oral and pharyngeal mucosa,
erythema, or fissuring of the lips, strawberry tongue
4. Acute non purulent cervical lymphadenopathy (>1.5 cm in at least one node).
5. Polymorphic non vesicular rashes.
6. One or more of the extremity changes: Erythema of palms and/or soles, indurative edema of
hands and/or feet, membranous desquamation of the fingertips.
(Criterion 1 plus any 4 of 2–6, after exclusion of alternative clinical diagnosis, is diagnostic of
KD.)
 Hospitalization is necessary.
 A full dose of intravenous immunoglobulin (IVIG) at 2 g/kg is the mainstay of the treatment.
It is to be administered within 10 days of illness and intravenous infusion should be given
slowly over 10–12 hours
 Aspirin should be added to the therapy in the doses of 80–100 mg/ kg/day until 36 hours of
disappearance of fever, followed by 3–5 mg/kg/day until the platelet count and ESR returns to
normal or longer in the children with coronary lesion.
 Infliximab or abciximab, cyclophosphamide, ulinastatin, and plasma exchange are reserved for
refractory KD.
 Cyclosporine A and methotrexate been used as a third line of treatment in some cases of KD
CHIKUNGUNYA
 Chikungunya virus (CHIKV) is a RNA virus belonging to the family Togaviridae

 CHIKV is most commonly transmitted to humans through the bite of an infected mosquito, specifically
mosquitoes of the Aedes genus, which usually bite during daylight (dawn and dusk)
 Vertical maternal-fetal transmission of CHIKV has been observed

 The incubation period is usually 2–3 days

 Characterized by fever, severe arthralgia, constitutional symptoms, and rash lasting for a period of 1–7
days
 Fever rises abruptly, often as high as 39–40°C. This acute phase lasts for 2–3 days. The temperature may
remit and recur after a gap of 4–10 days, resulting in “biphasic or saddleback” fever.
 Headache, retrobulbar pain, sore throat, and conjunctival redness may occur. The arthralgias are
polyarticular, migratory, and predominantly affect the small joints of hands, wrists, ankles, and feet.
CUTANEOUS LESIONS OBSERVED IN CHIKUNGUNYA
 Leucopenia and relative lymphocytosis may occur. The ESR is significantly elevated. C
reactive protein is positive in few patients
 There are three specific tests for diagnosis of CHIK infection, virus isolation, reverse
transcriptase PCR (RT-PCR) test, and serological tests to identify CHIKV specific antibodies.
 The disease is self-limiting and subsides spontaneously with time. There is no specific
treatment for CHIK.
DENGUE
 Dengue is caused by four distinct types of Dengue viruses (DEN 1, 2, 3, and 4). They are
RNA viruses that belong to the genus Flavivirus and the family Flaviviridae.
 Dengue is transmitted by mosquitoes, the most important being Aedes aegypti.
 It presents mainly in three forms: Dengue fever (DF), Dengue hemorrhagic fever (DHF), and
Dengue shock syndrome (DSS).
 Dengue fever is characterized by biphasic fever, myalgia, arthralgia, headache, retrobulbar
pain, and rash.
 DHF is a lethal complication that occurs during convalescence, while recovering from fever,
typically after 3–4 days of illness. It is characterized by marked thrombocytopenia,
hemorrhagic manifestations in terms of hematemesis, bleeding from gums and nose, melena,
purpura, ecchymoses
 DSS is a severe form of DHF leading to an acute circulatory failure (restlessness, cool
extremities, capillary refill time >2 s, tachycardia) and death
 The generalized rash starts peripherally on the hands and feet, spread to arms and trunk, usually spares
palms and soles and subsides without any desquamation

 NS1 antigen detection- Detected within the first 1-7 days after onset of symptoms. The NS1 glycoprotein
is not exclusive of Dengue and these kits may cross-react with other flaviviruses like Zika.
 IgM is detectable 6–7 days after the onset of the illness
 There is no specific antiviral treatment for DF. Adequate and appropriate supportive care
alleviates symptoms of DF
 Cutaneous lesions do not require any specific treatment. They usually resolve spontaneously
with the subsidence of acute infection. They do not leave behind any residual sequelae.
 Dengvaxia (CYD-TDV)- First dengue vaccine licensed in 2015.
 Target Age Group: 9-45 years old
 Dosage: 3 doses administered at 6-month intervals.
 Higher risk of severe dengue in seronegative individuals (those who have not had a prior
dengue infection).
 Due to the increased risk of serious infection in the previously seronegative population, the
WHO recommends this vaccine only in individuals with previous, confirmed dengue infection
BACTERIAL INFECTIONS
 Staphylococcal infections in children range from
furuncles, carbuncles, folliculitis, bullous impetigo (which
may or may not be associated with fever) to TSS and
SSSS (which are associated with high temperatures)
 TSS is an acute multisystem disease characterized by high
fever, vomiting, diarrhea, conjunctival congestion,
strawberry tongue and diffuse, dark, and sunburn-like
rash. This is accompanied by altered sensorium,
disseminated intravascular coagulation, and hypotension.
Symptoms resolve by 7-10 days, associated with
desquamation of palms and soles
 SSSS affecting predominantly children below 5 years consists of a scarlatiniform erythema
transforming into a wrinkled paper appearance with peeling of large sheets of epidermis.
Healing occurs within 10-15 days without scarring
 SCARLET FEVER
 Group A streptococcal infection

 Rash is typically diffuse, erythematous, blanchable, and

finely papular(like sandpaper), starting from the neck and
spreading to trunk and extremities with sparing of face.
 Strawberry tongue- the prominent papillae are initially
covered by a white coating giving a “white strawberry”
appearance to the tongue. This coating desquamates in a
few days giving rise to the typical “red strawberry”
tongue
 Pastia lines(Thompson sign): pink or red lines formed of
confluent petechiae in the skin creases particularly of
antecubital fossa
 Rash fades with desquamation after 3-4 days

 Penicillin or amoxicillin is the first-line treatment. If the

affected person has an allergy to penicillin, a first-
generation cephalosporin, clindamycin, or erythromycin
can be used
 Meningococcemia
 Meningococcemia is characterized mainly by fever with petechiae, but other
transient lesions resembling a viral maculopapular rash may also be seen.
 The petechiae are often raised with a "smudged" appearance involving trunk
and extremities.
 Gangrenous hemorrhagic areas resembling purpura fulminans are seen in
fulminant meningococcemia which is also associated with adrenal hemorrhage,
hypotension, multiorgan failure (MOF) with or without meningitis
 Lumbar puncture - An increased number of white cells are seen under the
microscope, with meningitis confirmed when the leukocyte count in the CSF is
> 5 cells/µL
 Microscopy (a Gram stain showing Gram-negative diplococci), culture
and polymerase chain reaction (PCR) for meningococcus will confirm the
diagnosis.
 Penicillin is the drug of choice. Third-generation cephalosporins are a suitable
alternative.
 The Indian Academy of Pediatrics recommends the Meningococcal ACWY
Vaccine for children 9 months to 2 years old, with two doses three months
apart. For children above 2 years old, a single dose is recommended
 Leptospirosis
 Rats are the most common source of the disease worldwide
 Infection is usually transmitted by direct contact with the urine of an
infected animal or by contact with a urine-contaminated environment
 Leptospirosis encompass a wide spectrum ranging from asymptomatic
infection at one extreme to MOF at the other.
 Symptomatic children present with a biphasic pattern, beginning with
abrupt onset of high fever with chills, headache, severe tenderness over
lower half of the body, conjunctival suffusion, hepatosplenomegaly (HSM),
and generalized lymphadenopathy (LAD).
 After a brief period of well-being, the second phase occurs characterized
by a transient (<24 hours) rash in 10% of cases.
 The rash may be urticarial, petechial-purpurial or desquamating type.
 Meningitis and uveitis may occur in this phase

 Severe cases are usually treated with intravenous benzylpenicillin. Less

severe cases are treated with oral antibiotics such as doxycycline or
amoxicillin
 Lyme disease
 Lyme disease is an infectious disease caused by Borrelia
burgdorferi, which is spread by ticks.
 Erythema migrans, an annular rash, is typical of Lyme
disease.
 It may be uniformly erythematous or may take the form of a
target lesion with necrosis and vesicles in the center.
 Axilla, periumbilical area, thigh, and groin are the usual sites.
 The rash enlarges to average 15 cm with a sharply demarcated
peripheral reddish band about 1-2 cm wide and resolves
without treatment in 4 weeks
 For patients older than 8 years of age with early, localized
disease, doxycycline is recommended for 10 days. Patients
under the age of 8 should receive amoxicillin or cefuroxime
for 14 days to avoid the potential for tooth staining caused by
tetracycline use in young children.
RICKETTSIAL INFECTIONS
 Rickettsial disease encompasses a group of diseases caused by the microorganisms, rickettsiae.
 Common rickettsial diseases in India: Scrub typhus, spotted fever, Indian tick typhus,
rickettsial pox
 Fever, rash, headache, lymphadenopathy
 The rash is macular or maculopapular, ocassionally petechial
 Typical painless eschar with erythematous rim
 Doxycycline is the drug of choice. Chloramphenicol may be used as an alternative. Supportive
therapy with electrolyte and fluid maintenance are also essential to the management of patients
with rickettsial diseases, particularly if there are signs of low blood pressure, electrolyte
disturbances, and blood coagulation (clotting) problems (DIC).
ROCKY MOUNTAIN SPOTTED
FEVER
• Onset gradual or abrupt, starting about 2–8 days after a
tick bite
• Fever, headache, confusion, aching muscles,
gastrointestinal symptoms
• Rash from day 2–3, consisting of of small red blotches on
wrists and ankles that become widespread and sometimes
blister
• 20% of cases do not develop rash (spotless rocky mountain
spotted fever)
 RICKETTSIALPOX
• Irregular fluctuating fever occurs and lasts for < 1 week
• Headache, chills, aching muscles, runny nose, sore throat,
nausea and vomiting, abdominal pain
• Red raised spot develops at site of mite bite, later forming a
dry scab (eschar)
• Rash distributed on the face, neck, trunk and extremities, and
is easily confused with rash of varicella (chickenpox)
 BOUTONNEUSE FEVER
• Fever, headache, malaise, aching muscles
• A characteristic rash that may start as small petechiae and
later develop into larger purpura
• Rash appears on days 3–5 of illness, spreading from the
extremities to the trunk, neck, face, palms and soles within 36
hours
• Rash is spotty and blotchy and may persist for 2–3 weeks
SCRUB TYPHUS
• Orientia tsutsugamushi
• Transmitted by the bite of infected chiggers (larval mites),
not by adult ticks
• Generalised swelling of the lymph nodes is common
• Fever and headache
• Maculopapular Rash occur 1–3 weeks after a mite bite and
is a dry scab-like lesion (eschar)
• Rash usually only around the trunk and has a short duration
MACULOPAPULAR DRUG
RASH
 AKA exanthematous drug eruption or morbilliform drug eruption
 Most common type of drug hypersensitivity reaction
 Usually starts within 7-10 days of drug intake
 Diffuse and symmetrical eruption of erythematous macules and small papules
 Antibiotics: Beta lactams, sulphonamides, fluoroquinolones, tetracyclines
 Anticonvulsants: phenytoin, carbamazepine
 NSAIDs, allopurinol
Maculopapular drug eruption Maculopapular viral exanthem

Eruption starts 7-10 days after Varying days after onset of fever

Starts in the trunk, upper Cephalocaudal distribution

extremities and progresses
caudally
T-cell mediated delayed type of Exanthem occurs as a result of
hypersensitivity reaction perivascular inflammatory reaction
to the virus
Low to moderate grade fever High grade fever- erythema
infectiosum, roseola infantum
Low grade fever-measles, rubella,
EBV, CMV

Lesions are pruritic Lesions are non pruritic

Raised eosinophil counts and Lymphocytosis or lymphopenia,

deranged liver function test atypical lymphocytes,
thrombocytopenia
Histopathology- Focal spongiosis, Superficial perivascular infiltrate of
occasional necrotic keratinocytes, lymphocytes without associated
superficial and deep perivascular epidermal changes
lymphocytes and eosinophils
ACUTE GENERALIZED
EXANTHEMATOUS
PUSTULOSIS
 Acute onset of fever with generalized scarlatiniform
erythema and many small, sterile, non-follicular pustules
 Drug history
 Evolution- 5-7 days
 Resolves by desquamation over a few days
DRUG RASH WITH
EOSINOPHILIA AND
SYSTEMIC SYMPTOMS
 Onset 2-8 weeks after starting the responsible medicine.
 A high fever of 38–40 C is usually noticed first. This is quickly
followed by a widespread skin rash.
 Characteristics of the rash are diverse.

• Morbilliform eruption affects 80% of cases, with

varying morphology including targetoid lesions, blisters
and pustules
• Erythroderma or exfoliative dermatitis (involving > 90% body
surface area) may follow in about 10%
• Facial swelling affects 30%
• Mucosal involvement affects 25% (lips, mouth,
throat, genitalia)
SYSTEMIC SYMPTOMS

• Enlarged lymph nodes

• Haematological disorders: raised white count , eosinophilia (in 30% this is > 2.0 x
109/L), atypical lymphocytes , thrombocytopenia , anaemia,
• Liver enlargement, hepatitis and rarely hepatic necrosis with liver failure.
• Kidneys -mild interstitial nephritis. Renal failure is rare.
• Inflammation of the heart (myocarditis) or pericarditis causing chest pain, breathlessness, and lowered
blood pressure
• Lung involvement -interstitial pneumonitis, pleuritis, pneumonia and acute respiratory distress
syndrome
• Neurological - meningitis and encephalitis, polyneuritis, causing headache, seizures, coma, and palsies
• Gastrointestinal symptoms: gastroenteritis, pancreatitis, bleeding and dehydration. In severe cases,
acute colitis and pancreatitis can occur, and chronic enteropathy may follow.
• Endocrine abnormalities: thyroiditis and diabetes
• Myositis
• Uveitis.
 Systemic corticosteroids (eg, prednisone) are generally used in the more severe cases of drug
hypersensitivity syndrome with significant exfoliative dermatitis
 Ciclosporin has been reported to be an alternative and effective treatment for drug
hypersensitivity syndrome.
 SJS/ TEN
 Stevens-Johnson syndrome (SJS) is a serious
mucocutaneous illness with systemic symptoms
characterized by the presence of flat, atypical target lesions,
epidermal detachment comprising less than 10% of the
total body surface area (BSA) and involvement of two or
more mucosal sites.
 TEN is a life-threatening condition characterized by high
fever associated with widespread (involving more than
30% of BSA) confluent erythema followed by necrolysis.
 An epidermal involvement between 10-30% of BSA has
been referred to as SJS-TEN overlap.
 Anticonvulsants, especially carbamazepine and phenytoin,
are most frequently implicated in causing SJS and TEN.
Other drugs include antibiotics like sulphonamides,
penicillins, and fluoroquinolones as well as NSAIDs
SERUM SICKNESS-LIKE
CUTANEOUS ERUPTIONS
 Begins with erythema on the sides of the fingers, hands, and toes and progress to a widespread
morbilliform or urticarial eruption. Multiorgan involvement, fever, arthralgia, and arthritis are
common.
CONNECTIVE TISSUE
DISORDERS
Disease Mucocutaneous lesions Associated clinical
features
Systemic lupus Malar rash Insidious onset fever
erythematosus Photosensitive rash Arthritis
Discoid rash Serositis
Erosions on palatal and nasal Hematological
mucosa abnormalities
Livedo reticularis HSM
Raynauds phenomenon Neuropsychiatric features
Alopecia Lupus nephritis
Juvenile Periorbital violaeous heliotrope rash Insidious onset fever
dermatomyositis Gottron papules over metacarpals, Proximal myopathy
knees, elbows Dysphagia
Periorbital edema Constipation
Cardiac conduction defects
VASCULITIS
Disease Mucocutaneous lesions Associated clinical
features
Leukocytoclastic vasculitis Erythematous macules Fever myalgia, arthritis,
replaced later by palpable abdominal pain
purpura 7-21 days after
onset of drug therapy
Polyarteritis nodosa Linear erythema with Fever, weight loss,
edema, palpable, painful abdominal pain,
nodules along the course hypertension, hematuria,
of affected arteries stroke, myocarditis,
arthritis
Henoch Schoenlein Initially maculopapular Arthritis, hematemesis,
purpura blanchable rash melaena, intussusception,
Later palpable purpura nephritis
occurring in crops over
dependent areas below
waist, eyelids, lips, dorsum
of hands and feet
Wegener’s granulomatosis Palpable purpuric nodules Chronic sinusitis,
DIAGNOSTIC
APPROACH TO
FEVER WITH
RASH
HISTORY
Age Season
 Roseola infantum- pre-school children:  Enterovirus- summer and autumn
3-36 months  Measles- spring
 Measles, rubella, varicella- 3 years of age
 Meningococcemia- winter and early
or less spring
 Kawasaki disease- below 5 years of age
 Lyme disease and rickettsial infection-
summer
HISTORY TAKING
 Onset
 Duration and type of fever
 Evolution of rash
 Sequence of distribution of rash
 Blanching or non blanching
 Associated symptoms
 Presence of similar rash in close contacts
 Any contact with infection or travel abroad
 Recent intake of medicines
 Incubation period
 Measles-10-14 days Varicella – 1st day
Scarlet fever- 2nd day
 Varicella- 14-18 days
Small pox- 3rd day
 Rubella-18-21 days Measles – 4th day
 Enterovirus-4-7 days Typhus – 5th day
Dengue – 6th day
Typhoid – 7th day

( Very Sick Patients Must

Take Double Tablets)
Based on type of
rash