Basics of common childhood viral- induced rashes.

1. Spot Diagnosis
Pediatric Viral Exanthems
Infectious Diseases Block
Fatima Farid, Resident Year One

2. Contents
Case Images
Diagnosis Background

3. Case One

4. Source: 100 Cases in Paediatrics

5. Source: 100 Cases in Paediatrics

6. (seen prior to rash)

7. Source: 100 Cases in Paediatrics

8. Measles Infection

9. Measles
• Single- stranded, lipid- enveloped RNA virus. Paramyxoviridae family, Morbillivirus genus.
Hosted only by humans.
• Six major structural proteins, of which two are most important for induction of immunity:
Haemagglutinin (H) and Fusion (F) proteins.
• Measles virus neutralized by antibodies to H protein, and viral proliferation limited by those
against F protein.
• Different genetic forms of measles virus that express various molecular markers. Useful in
evaluation of endemic/ epidemic spread of disease, but have no effect on immune response.
Eight clades (A- H) of 23 different genotypes.

10. Measles
• Portal of entry is through respiratory tract and conjunctivae following contact with droplet
aerosols with suspended virus. Approximately 90% of exposed susceptible individuals
experience measles.
• Patients are infectious 3 days before, till 4- 6 days after onset of rash. Face to face contact is not
necessary, as virus may be suspended in air for as long as one hour after source leaves the room.
Secondary cases from aerosolized virus have been reported from airplanes/ clinics/ hospitals.
• Measles virus causes necrosis of the respiratory tract epithelium with an accompanying
lymphocytic infiltrate. It also produces small- vessel vasculitis on the skin and oral mucous
membranes.

11. Measles
• Four phases of disease:
1. Incubation: Virus migrates to regional lymph nodes. Primary viremia ensues that
disseminates virus to reticuloendothelial system. Secondary viremia then spreads virus to
body surfaces.
2. Prodrome: Epithelial necrosis and giant cell formation in body tissues. Cells are killed by
cell- to- cell plasma membrane fusion associated with viral replication. Viral shedding
begins in prodromal phase.
3. Exanthematous Period: With onset of rash, antibody production begins and viral
replication/ clinical symptoms decline.
4. Recovery.

12. Measles
• Measles virus attaches to specific cell receptors to infect host cells. Initial targets are the
alveolar macrophages, dendritic cells and lymphocytes.
• It first binds to the signaling lymphocyte activating molecule (CD150), subsequently respiratory
cells become infected but do not express CD150.
• The virus enters respiratory epithelium by attachment to PVRL4 receptors expressed on cells on
oral mucosa, nasopharynx, trachea, and lungs. These two receptors account for epitheliotropic
and lymphotropic nature of measles virus.
• Virus also infects CD4+ T cells resulting in suppression of T- helper immune response.

13. Measles
• Histology of rash reveals intra-cellular edema dyskeratosis associated with formation of
epidermal syncytial giant cells with up to 26 nuclei. Viral particles have been identified
inside these giant cells.
• In lymphoreticular tissue, lymphoid hyperplasia is prominent.
• Fusion of infected cells results in multinucleated giant cells: Warthin- Finkeldey giant
cells which are pathognomonic for measles. They have up to 100 nuclei and intra-
cytoplasmic/ intra- nuclear inclusions.

14. Warthin- Finkeldey Giant Cell

15. Measles
• Serious infection characterized by high fever, enanthem, coryza, cough, conjunctivitis and a
prominent exanthem.
• Prodromal phase begins with mild fever, followed by onset of conjunctivitis with photophobia,
coryza, a prominent cough and increasing fever. Symptoms increase in intensity for 2- 4 days
until the first day of rash.
• Koplik spots are the pathognomonic sign of measles, appearing 1- 4 days before onset of rash.
Discrete red lesions with bluish white spots in the center, located over the inner aspect of the
cheeks at the level of the premolars. May spread to involve the gingiva, hard palate and lips.
Can develop in conjunctival folds and vaginal mucosa.

16. Measles
• Exanthem begins on the forehead (around the hairline), behind the ears, and on the upper neck
as a red maculopapular eruption. It then spreads downwards to the torso and extremities,
reaching the palms and soles in 50% of cases. Exanthem frequently becomes confluent on face
and upper trunk.
• With the onset of rash, symptoms begin to subside. Resolution of rash occurs over seven days,
in same order of appearance, leaving residual fine desquamation of skin.
• Of the major symptoms, cough lasts the longest- often up to 10 days.
• In more severe cases, generalized lymphadenopathy may be present- with cervical and occipital
lymph nodes most commonly involved.

17. Source: Illustrated Textbook of Paediatrics, 4th Edition

18. Measles
• Inapparent measles infection may occur in individuals with passively acquired antibodies
(infants, vaccinated children, recipients of blood transfusion). Present with mild/ absent rash
and variable other symptoms. Not actively shedding virus, and cannot transmit infection to
contacts.
• Diagnosis:
• Leukopenia with lymphocytes decreased more than neutrophils. Normal CRP/ ESR.
• IgM positive if collected more than 72 hours from onset of rash. Normalizes after one month.
• IgG four fold rise between acute and convalescent period collected 2- 4 weeks apart.
• Viral PCR from blood, urine or respiratory secretions.

19. Measles
• Treatment:
• Supportive care. No role of antivirals or prophylactic antibiotics.
• Two doses of Vitamin A are indicated for all patients with measles. Third age-
appropriate dose is given in cases symptomatic of Vitamin A deficiency.
Age Dose
Less than 6 months 50,000 IU
6- 11 months 100,000 IU
12 months and older 200,000 IU

20. Measles
• Complications are more likely in ages less than one year, overcrowding, malnutrition,
children with hyporetinolemia and immunocompromised states.
Acute Otitis Media
Diarrhea, vomiting,
dehydration.
Reactivation of latent
TB
Encephalitis
Pneumonia (Giant Cell
Pneumonia or
Bacterial). Bronchiolitis
Obliterans.
Acute appendicitis
Retro- pharyngeal
abscess
Subacute Sclerosing
Panencephalitis
Croup, Tracheitis,
Bronchiolitis
Febrile seizures Myocarditis Hemorrhagic Measles

21. Measles
• Encephalitis in an immunocompetent patient develops during the exanthem phase of disease.
More often occurs in adolescents than younger children. Immune- mediated process (not direct
brain damage from virus). Manifests as seizures, lethargy, irritability, and coma. CSF will show
lymphocytic pleocytosis and elevated protein concentrations. Poor prognosis: 15% die, 20- 40%
have long – term complications (mental retardation, motor disabilities and deafness).
• Encephalitis in an immunocompromised patient develops 1- 10 months after disease. Occurs
due to direct effect of virus on brain. Progressive disease and death occurs.

22. Measles
• Subacute Sclerosing Panencephalitis: Chronic complication that develops secondary to infection with
defective measles virus (missing M protein needed for viral replication) that is able to reside within
neuronal cells for long periods of time, along with an immature immune system. Males affected two times
more than females. Insidious onset 7- 13 years after initial infection.
• Phases:
1. Subtle changes in behaviour: irritability, reduced attention span, temper outbursts, poor school
performance. No fever/ headache or other signs of encephalitis.
2. Massive myoclonus: involuntary movements, repetitive myoclonic jerks starting in single muscle
groups, then progressing to entire axial/ appendicular muscles. Consciousness maintained.
3. Choreoathetosis, immobility, dystonia, lead- pipe rigidity. Sensorium deteriorates to dementia,
stupor then coma. No more involuntary movements.
4. Loss of critical centers controlling breathing, heart rate and blood pressure. Death soon ensues.

23. Measles
• Subacute Sclerosing Panencephalitis
• Progression through phases may be acute, subacute or chronic progressive.
• Diagnosis requires documented clinical course with one of the following:
1. Measles antibody in CSF. Normal cell count, but raised IgG and IgM in dilutions 1: 8.
2. Suppression burst pattern on EEG in second phase of disease.
3. Typical histologic findings and/ or isolation of measles virus from brain biopsy (not recommended).
• Clinical trials show benefit of Isoprinosine +/- Interferon. Carbamezapine useful for controlling myoclonic
jerks. Supportive care only. Most children die in 1- 3 years from infection/ loss of autonomic control.

24. Measles
• Prevention: Vaccination. Airborne contact precautions:
• Immunocompetent: 3 days before till 4- 6 days after onset of rash.
• Immunocompromised: Throughout entire period of illness.
• Post- exposure prophylaxis:
• Within 72 hours of exposure: Vaccination.
• Within 6 days of exposure: Immunoglobulin.

25. Case Two

26. Five year old previously healthy girl
seen in clinic with one week history
of low grade fever, runny nose and
malaise. No other complaints.
Recent infectious exposure with
URTI. Unremarkable remainder of
history.
Vital signs normal. Suboccipital and
postauricular lymph nodes palpable.
Throat mildly congested. Small red
lesions noted over hard palate. Rash
over face. Systemic exam normal.
(lesions seen with rash)

28. Rubella Infection

29. Rubella
• Rubella is also known as German Measles or Three Day Measles.
• Single- stranded, lipid- enveloped RNA virus. Member of Togaviridae family, genus
Rubivirus. Humans are the only known hosts.
• Following infection, virus replicates in respiratory epithelium and then spreads to
regional lymph nodes. Viremia then occurs, along with viral shedding from
nasopharynx approximately 10 days after infection.
• Period of communicability is from 5 days before to 6 days after onset of rash.

30. Rubella
• Post- natal infection with rubella is a mild disease not easily discernable from other viral infections.
• Phases:
1. Incubation:- 14- 21 days.
2. Prodrome: Low grade fever, headache, malaise, conjunctivitis +/- pain, lymphadenopathy
(suboccipital, post- auricular, anterior cervical lymph nodes).
3. Exanthem: Small irregular pink macules starting on face/ neck then spreading centrifugally (away
from center of body) to involve torso and extremities. Forchheimer spots (tiny, rose- coloured lesions
in the oropharynx)/ soft palate petechial hemorrhage that coincide with rash onset. Rash fades from
face as it spreads to the rest of the body (whole body may not be involved at any one time).
4. Recovery: Rash lasts for three days and resolves without desquamation.

31. Rubella
• Diagnosis:
• Leukopenia, neutropenia and mild thrombocytopenia may occur.
• Rubella IgM antibody detection.
• Treatment: Supportive care only. Prevented by vaccination and contact precautions.
• Complications
Thrombocytopenia
Post- infectious Encephalitis following Acute
Rubella
Arthritis Progressive Rubella Panencephalitis

32. Rubella
• Complications:
• Thrombocytopenia. Develops two weeks after onset of rash. Petechiae, epistaxis, GI bleeding,
hematuria. Self- limited.
• Arthritis. Mostly in older females. Begins one week after rash, affecting mainly small joints of the
hand. Self- limited.
• Post- infectious Encephalitis following Acute Rubella. Appears within seven days of rash. Fever may
recrudesce along with headache, seizures, confusion, coma, focal neurological signs and ataxia. CSF
may be normal, or have mild mononuclear pleocytosis/ raised protein concentration. Virus is rarely
isolated in CSF. Most patients recover completely, but 20% develop long term neurologic sequelae.
• Progressive Rubella Panencephalitis (PRP). Identical presentation and course to SSPE. Virus will be
isolated from brain tissue. Death occurs 2- 5 years after onset.

33. Case Three

34. Five year old previously healthy
girl seen in clinic with irritability
and trouble feeding due to pain.
Child also has fever and rash for
three days. Attending nursery.
Remainder history unremarkable.
Vital signs normal. Oropharynx
inflamed with scattered vesicles.
Painful blisters and pustules
noted on hands mainly, few on
feet. Rest systemic exam normal.

36. Enterovirus Infection

37. Enterovirus Infection
• Enterovirus infection (single- stranded, non- enveloped RNA virus with several
subtypes). Common infection, peaks in summer/ fall. Tropism to target organ is
determined by infection serotype.
• HFMD is most commonly caused by Coxsackie A16 virus. Atypical cases (more severe
in presentation) occur secondary to Coxsackie A6 virus. Epidemics with involvement of
CNS/ CVS occur with Enterovirus 71 infection.
• Transmission is respiratory, feco- oral, vertical/ via breastfeeding and also from fomites.

38. Enterovirus Infection
• Pathogenesis: Viral replication occurs in pharynx and regional lymphoid tissue (tonsils, Peyer patches and
regional lymph nodes). Followed by minor viremia to spread virus to distant reticuloendothelial system (liver,
spleen, bone marrow and distant lymph nodes). Infection may be stopped here to produce only subclinical
presentation. May progress to major viremia to target organs (CNS, CVS, lungs, liver, kidneys, muscles, joints,
skin).
• Commonly implicated organisms in HFMD:
1. Coxsackie A16
2. Enterovirus 71
3. Coxsackie A5, 6, 7, 9, 10
4. Coxsackie B2, 5
5. Echovirus

39. Hand- Foot- and- Mouth Disease
• HFMD has a distinctive rash. Child is mildly ill +/- low grade fever.
• Oropharynx is inflamed and contains scattered vesicles on the tongue, buccal mucosa, posterior
pharynx, palate, gingiva, and/ or lips. The lesions may ulcerate, leaving 4- 8 mm shallow lesions
with surrounding erythema. Maculopapular, vesicular, and/ or pustular lesions may occur on
hands and fingers, feet and buttocks/ groin. Hands are more commonly involved than the feet.
• Lesions on the hands and feet are tender, 3- 7 mm vesicles occurring more commonly on dorsal
surfaces but frequently also on palms and soles. Vesicles resolve within one week. Buttock
lesions do not progress to vesiculation.

40. Hand- Foot- and- Mouth Disease
• Atypical HFMD presents with severe disease including fever, generalized rash (face,
proximal extremities, trunk, hands, feet, buttocks), pain, dehydration, desquamation of
palms and soles, and onychomadesis (nail shedding).
• Diagnosis: Clinical features and viral RT- PCR.
• Treatment: Supportive care only. Prevention: Hygiene and environmental sanitation.

41. Non- Polio Enterovirus Infection
1. Non- specific febrile illness (abrupt onset of fever 38.5- 40 C with malaise/ irritability/ non- specific
complaints). Lasts 4- 7 days. FBC normal, may have transient neutropenia.
2. Skin rashes: Macular, maculopapular, urticarial, vesicular, petechial eruptions (blanching).
3. Hand- Foot- and- Mouth Disease
4. Herpangina (sudden onset of fever, sore throat, dysphagia and lesions in posterior pharynx). Start as 1-
2 mm then grow to 3- 4 mm over 2- 3 days, surrounded by erythematous ring. 1- >15 lesions present.
Resolves in 7 days. May result in meningitis. Less severe than Herpetic Gingivostomatitis.
5. Respiratory manifestations: Coryza, sore throat, asthma exacerbation, pneumonia, bronchiolitis, croup,
otitis media, pharyngotonsillitis. Pleurodynia (Bornholm disease- myositis of chest and abdominal wall
muscles: malaise/ myalgia/ headaches followed by sudden onset of fever and spasmodic/ pleuritic chest
pain).

42. Non- Polio Enterovirus Infection
• Acute Hemorrhagic Conjuncitivitis: Enterovirus 70 and Coxsackie A24/A24 variant. Sudden onset severe eye pain with
photophobia, blurred vision, lacrimation, conjunctival erythema and congestion, lid edema, preauricular lymphadenopathy
and subconjunctival hemorrhage/ superficial punctate keratitis.
• Uveitis, chorioretinitis, uveoretinitis, optic neuritis and unilateral acute idiopathic maculopathy.
• Myocarditis, pericarditis.
• Acute/ chronic gastritis, intussusception, sporadic hepatitis, pancreatitis and chronic intestinal inflammation in cases of
hypogammaglobinemia.
• Viral meningitis, encephalitis, Guillaine- Barre Syndrome, Transverse Myelitis, cerebellar ataxia, opsoclonus- myoclonus
syndrome, benign intracranial hypertension, rhomboencephalitis, axonal polyneuropathy, Miller- Fisher Syndrome, ADEM,
peripheral neuritis, optic neuritis, sudden hearing loss, tinnitus, vestibular neuritis, cranial nerve dysfunction.
• Myositis, arthritis.

43. Case Four

44. Eight year old previously healthy
girl seen in ED with fever,
pruritus and painful rash with
swelling of hands and feet.
Child is febrile. Systemic exam
normal aside for oral lesions and
rash as shown.

46. Parvovirus B19 Infection

47. Parvovirus B19
• Small single- stranded DNA virus. Member of genus Erythrovirus. Only one known serotype.
• Common infection world-wide. Peak in late winter/ spring seasons. Transmission is via large
droplets (respiratory) from nasopharyngeal viral shedding, and can also occur via blood/ blood
products.
• Parvovirus B19 targets erythroid precursor cells near the pro-normoblast stage producing cell
lysis, leading to progressive depletion of erythroid precursors and transient arrest of
erythropoiesis. Viral receptors are also present on endothelial and myocardial cells.
• Exanthem and arthritis are post- infectious phenomena (immune- mediated), whereas aplastic
crisis is directly due to viral effect.

48. Parvovirus B19
• Erythema infectiosum, also known as Fifth Disease is a benign self- limited condition.
• Phases:
1. Incubation: 4- 28 days.
2. Prodrome: Low grade fever, headache, mild upper respiratory tract infection.
3. Exanthem: Hallmark three stage rash:
1. Slapped cheek appearance: erythematous facial flushing.
2. Diffuse macular erythema spread down from face to trunk and proximal extremities.
3. Lacy reticulated rash appearance by central clearing of macular lesions. More prominent on
extensor surfaces, sparing palms and soles.

49. Parvovirus B19
• Older children may complain of pruritus. Atypical rashes/ petechiae may occur. Rash resolves
spontaneously without desquamation, but may wax/ wane over the next 1- 3 weeks. It can recur with
exposure to sunlight, heat, exercise and stress.
• Also known to cause transient aplastic crisis in patients of chronic hemolysis/ rapid RBC turnover,.
Patient is much more ill (fever, pallor, malaise tachycardia, lethargy), and rarely has rash. Parvovirus can
also produce variable degree of joint involvement. Myocarditis may occur.
• Atypical presentations:
• Vasculitis causing petechial/ purpuric lesions.
• Papular purpuric “gloves and stocks” syndrome (PPGSS): Fever, pruritus, plus painful edema and
erythema localized to distal extremities (in a distinct gloves and stock appearance). Followed by acral
petechiae and oral lesions. Self- limited, resolves in a few weeks.

50. Parvovirus B19
• Diagnosis: Clinical mainly. IgG/ IgM serology with viral PCR can be used.
• Treatment: Symptomatic only.
• Complications:
Arthritis, arthralgia Aseptic meningitis, encephalitis
Infection- induced HLH Stroke (SCD with aplastic crisis)
Thrombocytopenic purpura Peripheral neuropathy

51. Case Five

52. Source: 100 Cases in Paediatrics

53. Source: 100 Cases in Paediatrics

54. Source: 100 Cases in Paediatrics

56. One year old previously healthy
boy seen in ED with high grade
fever, crying and inability to feed
due to severe oral ulceration/
pain.
Child is febrile at 40 C,
dehydrated. Ulcers noted. Rest
systemic exam normal.

58. Herpes Simplex Infection

59. Herpes Simplex Infection
• Double- stranded DNA virus. Only human host. No seasonal preference.
• Transmission is via mucocutaneous membranes. No documented infection from fomites.
• Primary infections occur in individuals who have not been previously infected with HSV-1 or 2.
Infection more severe.
• Non- primary first infections occur in those previously infected with one type, and currently
infected with the second type. Less severe features.
• Virus harbors itself in regional sensory ganglia to establish latent infection. Then can re-
activate intermittently to produce recurrent infection.

60. Herpes Simplex Infection
• All infected individuals harbor latent infection and experience recurrent infections, which may be
asymptomatic. All are periodically contagious, which explains high disease prevalence.
• Both HSV-1 and 2 are equally capable of causing both initial infection at any anatomic site but differ in their
capacity to cause recurrent infections. HSV-1 has a greater propensity to cause oral infections, HSV-2 for
recurrent genital infections.
• Pathogenesis: Virus replicates at site of entry resulting in cell death producing an inflammatory response which
manifests as the characteristic herpetic vesicles and ulcers. Virus replicates in sensory neurons and has intra-
neuronal transport to nerve endings to produce infections. Nerves that do not allow replication become the sites
of latent infection (viral genome persists within neuronal nucleus in a largely metabolically inactive state).
Reactivation again leads to intra- neuronal transport and infection at cutaneous end. Hematogenous spread
occurs in immunocompromised, neonates and children with eczema.

61. Herpes Simplex Infection
• Classic infections manifest a small 2- 4 mm vesicle surrounded by an erythematous base for a few days, then progress to become shallow,
minimally erythematous ulcers. Vesicular phase persists longer when keratinized epithelium is involved, and is briefer when mucous
membranes are the source of infection.
• Manifestations:
1. Herpes gingivostomatitis.
2. Fever blisters/ cold sores: Most common manifestation of recurrent HSV- 1 infection.
3. Herpes whitlow.
4. Herpes gladiatorum/ scrum pox.
5. Eczema herpeticum: May be life- threatening if progress to disseminated infection. Also in conditions like pemphigus, burns, laser
skin resurfacing, Darier disease.
6. Genital herpes.
7. Ocular infection. Dendritic/ geographic corneal ulcers.
8. HSV Encephalitis (specifically expressive aphasia, hallucinations, anosmia, memory loss). Most common cause of recurrent aseptic
meningitis (Mollaret Meningitis).

62. Herpes Simplex Infection
• Herpes Gingivostomatitis: 7- 14 days untreated. Lymphadenopathy may persist for weeks.
• 6 months- 5 years of age affected.
• Sudden onset, pain in mouth, drooling, refusal to eat/ drink, fever 40- 40.6 C. Gums are markedly
swollen ad vesicles develop throughout the oral cavity (gums, lips, tongue, palate, tonsils, pharynx,
peri-oral skin).
• During initial phase of illness, there may be a tonsillar exudate.
• Vesicles remain for a few days before progressing to form shallow indurated ulcers that may be covered
with a yellow- gray membrane.
• Tender submandibular, submaxillary and cervical lymphadenopathy is common.
• Breath may be foul due to overgrowth of anaerobic oral bacteria.

63. Herpes Simplex Infection
• Fever blisters/ Herpes Labialis: Most commonly occurs along vermillion border of lip (may also
occur on cheeks, nose, chin and oral mucosa) Older patients can report burning, tingling, itching
or pain 3- 6 hours before lesions develop. Lesions begin as small groups of erythematous
papules progressing over a few hours to small thin walled vesicles. Vesicles then dry and form
shallow ulcers or become pustules. Heals without scarring within 6- 10 days.
• Cutaneous herpes infections present secondary to trauma usually. Multiple discrete lesions
involving a larger surface area. Grouped erythematous lesions that progress to vesicles,
pustules, ulcers and crusts, then heal without scarring in 6- 10 days.
• Herpes Whitlow: Toddlers who suck fingers while experiencing HSV-1 oral infection. Persist
for 10 days, recovery in 20 days. Even recurrent infections are painful.

64. Herpes Simplex Infection
• Diagnosis: PCR. Viral culture by rupturing vesicle and vigorously rubbing base of
lesion to collect fluid and cells. Mucocutaneous infections produce moderate polymorph
leukocytosis.
• Treatment: Oral/ IV/ topical Acyclovir. Prevention: Hygiene/ contact precaution with
lesions.

65. Case Six

66. One year old previously
healthy boy presented with
fever, headache and malaise
for two days followed by
severe intense pruritic rash
on head and spreading to the
trunk.
Child is febrile at 39 C. Rash
as in image. Rest
examination normal.

67. One year old post- BMT on
immunosuppressive therapy
presented with fever and
skin rash.
Child is febrile at 39 C. Rash
as in image. Rest
examination normal.

68. Varicella Zoster Infection

69. Varicella Zoster Virus
• Neurotropic human herpes virus. Primary infection (chicken pox) is followed by life- long latent infection
in sensory ganglion neurons (reactivation leads to shingles).
• Droplet transmission. Susceptible persons may acquire varicella after close/ direct contact with patients
having herpes zoster. Exposure to varicella in a previously infected child will increase immunity against
VZV and reduce possibility of developing shingles.
• Contagious 1- 2 days before onset to rash until vesicles are crusted (3- 7 days after onset of rash).
• Pathophysiology: Virus replicates in local lymphoid tissue, then spreads to RES by primary viremia (10-
21 days). Secondary viremia spreads to produce widespread cutaneous lesions (3- 7 days). In
immunocompromised hosts, defects especially in cell- mediated immunity results in continued viral
replication and organ damage.

70. Varicella Zoster Infection
• Phases: (Unvaccinated)
• Incubation: 14- 16 days after exposure.
• Prodrome: Fever, malaise, anorexia, headache, abdominal pain (24- 48 hours).
• Exanthem: Starts on face/ scalp/ trunk. Intensely pruritic, erythematous macules that evolve through the
papular stage to form clear, fluid- filled vesicles. Clouding and umbilication of lesions begins in 24- 48
hours. While the initial lesions are crusting, new crops form on the trunk and extremities (the
simultaneous presence of lesions in various stages of evolution is characteristic of varicella). Rash is
predominantly central/ centripetal with greatest concentration on trunk. Ulcerative lesions may be
present on mucosa/ eyelids/ vagina. Average number of lesions is 300 (< 10 to > 1, 500). Hypo/
hyperpigmentation persists for days to weeks in children, but scarring is rare unless secondary infection
occurs .
• Recovery.

71. Varicella Zoster Infection
• Varicelliform rash: (wild type VZV, vaccine strain VZV, insect bite/ coxsackie virus).
• 0- 42 days post- vaccination: reflects exposure to varicella before vaccination could
provide protection (especially day 0- 14).
• 14- 42 days post- vaccination: exposure/ infection before protection or vaccine-
associated rash.
• Break- through varicella: Wild- type virus infection after 42 days of immunization.
Atypical, predominantly maculopapular rash. Less severe, less contagious and of shorter
duration. Still considered infectious till vesicles crust over.

72. Varicella Zoster Infection
• Complications:
1. Secondary bacterial infection of skin (Group A Streptococcus, Staph aureus).
2. Encephalitis and cerebellar ataxia: 2- 6 days after onset of rash/ incubation period/ after resolution of rash. Complete
recovery within 24- 72 hours.
3. Pneumonia: 1- 6 days after onset of rash.
4. Progressive varicella: visceral involvement, coagulopathy, severe hemorrhage, continued vesicular lesion formation
beyond 7 days. Risk highest in infants with congenital cellular immune deficiency, post- organ transplant and
malignancy (especially if on chemotherapy/ steroids with absolute lymphocyte count < 500 cells/uL).
5. Herpes Zoster: Vesicular lesions clustered within one or two dermatomes. Minimal pain in children, with spontaneous
resolution in 1- 2 weeks. Severe presentation in immunocompromised children.
6. Hepatitis, nephritic/ nephrotic syndromes, HUS, arthritis, pericarditis, myocarditis, pancreatitis, orchitis, acute retinal
necrosis.

73. Varicella Zoster Infection
• Diagnosis: Direct fluorescence assay of vesicle fluid (fast). PCR (more sensitive). IgG four fold
rise over 2- 3 weeks.
• Treatment: Supportive.
• Five days oral Acyclovir therapy: chronic cutaneous/ pulmonary disorders, short term,
intermittent aerosolized corticosteroid therapy, long term salicylate therapy.
• IV Acyclovir: disseminated infection, and immunocompromised patients. Continue for 7- 10
days or until no new lesions appeared for 48 hours.
• IV Foscarnet for HIV patients resistant to Acyclovir therapy.
• Shingles treated with oral Acyclovir for 5- 7 days. IV for immunocompromised.

74. Case Seven

75. One year old presented with three
days history of high grade fever,
followed by generalized body rash
which appeared with normalization of
fever. Remainder of history
unremarkable.
Normal vitals and systemic physical
examination aside for nasal discharge,
congested throat and rash.

76. Roseola Infantum

77. Roseola Infantum
• Human Herpes Virus 6 and 7 cause roseola infantum/ exanthema subitem/ sixth disease.
• Double- stranded DNA virus.
• Transmission: Droplet and vertical (transplacental, chromosomal integration- virus integrated at telomere
end of human chromosome).
• Pathogenesis: Cytopathic effect with latency in monocytes and macrophages. May cause infection post-
hematopoietic stem cell transplantation.
• Abrupt onset of fever and fussiness lasting for 72 hours, followed by defervescence and appearance of a
rose coloured, non- pruritic 2- 3 mm morbilliform rash on the trunk. Rash lasts for 1- 3 days, but is often
described as evanescent and may only be visible for a few hours.

78. Roseola Infection
• Associated with mild injection of pharynx/ palpebral conjunctivae/ tympanic membranes, runny
nose, GI upset and enlarged sub- occipital lymph nodes. Nagayama spots have been reported
(spots at uvulopalatoglossal junction).
• Diagnosis: Leukopenia mainly. May have thrombocytopenia, atypical lymphocytes or deranged
LFT. PCR.
• Treatment: Supportive only.
• Complications: Febrile seizures. Viral reactivation 2- 4 weeks after HCST causing fever, rash,
GVHD of variable severities. PALE (post- transplant acute limbic encephalitis) with HHV6
especially after cord blood stem cell transplantation (short term memory dysfunction, confusion,
insomnia, seizures).

79. References
• Nelson Textbook of Pediatrics, 20th Edition.
• Oxford Handbook of Paediatrics, 2nd Edition.
• Illustrated Textbook of Paediatrics, 4th Edition.

80. Thank You