Transcript File - International Nursing Symposium

Donald McLaren, MD
Seventh International Symposium in Continuing
Nursing Education/March 2014
Goals of talk
 To highlight measles as a still very important major
cause of under 5 mortality in the developing world
and discuss diagnosis, complications and treatment
 To discuss clinical features, diagnosis, complications
and treatment of various childhood exanthems
 To point out some other childhood diseases which may
present with a rash which you should not miss because
they are potentially fatal if not treated early
Definitions
 Exanthem – widespread rash – from Greek
“a breaking out.” A generalized cutaneous eruption
associated with a systemic illness
 Morbilliform rash – rash that looks like measles.
 Macule – discolored area on skin not raised above the
service
 Papule – raised solid lesion on skin without visible
fluid – varies in size but < 5mm
 Vesicle – small elevation of epidermis containing
serous fluid < 5 mm
 Petechiae – very small red spot on skin due to
hemorrhage – does not blanch to pressure
 Childhood exanthems initially named by number from
first to sixth in 1905 - measles, scarlet fever, rubella,
4th never existed, erythema infectiosum, and roseola
infantum.
 Many other causes of exanthems in children.
Measles (Rubeola)
 Prior to vaccine 90% acquired measles by 15 yoa
 With high rates of immunization, age in epidemics in
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U.S shifted downwards to 6 months of age
Still major cause of mortality in developing world.
In 2000, 31-39.9 million got measles with 733,000 –
777,000 deaths (5th in < 5 mortality)
By 2011 mortality dropped by 71% (WHO)
1990-2008 decreased from 7% to 1% of < 5 mortality!
Van dan Ent M.M.V.X., Brown, DW, Hoekstra, J, Christie A, Cochi SL. Measles Mortality Reduction Contributes Substantially
to Reduction of All Cause Mortality Among Children Less than Five Years of Age, 1990-2008. JID 2011:204 (Supplement 1)
Epidemiology
 1990-2008 decreased from 7% to 1% of < 5 mortality!
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Van dan Ent M.M.V.X., Brown, DW, Hoekstra, J, Christie A, Cochi SL. Measles Mortality Reduction Contributes Substantially
to Reduction of All Cause Mortality Among Children Less than Five Years of Age, 1990-2008. JID 2011:204 (Supplement 1)
 Goal of 95% reduction over 2000 by 2015 and
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elimination in 5 WHO regions by 2020
Africa – 2001-8 vaccination rate 57-73%
SE Asia – 2000-2008 46% reduction in measles deaths
> 70% decreased mortality 2000-2007. 197,000 in 2007
85% measles mortality now in Africa, SE Asia
Measles epidemiology
 Highly contagious – 75% attack rate if exposed
 U.S. pre-vaccine: 500,000-4,000,000 cases/year;
48,000 hospitalized; 1000 chronically disabled; 500
deaths – No longer endemic.
 2001-2011 63 cases/year reported – most 220. 88%
import (travel) related and 66-85% of unvaccinated or
unknown status.
 Outbreak = 3 or more cases linked in time and place
Incidence of global measles 2004
http://dualibra.com/wpcontent/uploads/2012/04/037800~1/Part%207.%20Infectious%20Diseases/Section%2015.%20Infections%20Due%20to%20RNA%20
Viruses/185.htm
http://www.who.int/immunization/monitoring_surveillance/burden/vpd/surveillance_t
ype/active/big_measlesreportedcases6months_PDF.pdf
http://en.wikipedia.org/wiki/Measles
Hunter’s Tropical Medicine and Emerging Infectious Diseases
http://en.wikipedia.org/wiki/Measles
Clinical Manifestations of Classic
measles
 Incubation period: asymptomatic 8-10(6-19) days
 Prodrome: Fever, malaise, anorexia
 Followed by the 3 Cs. Conjunctivitis, coryza,
cough – photophobia. 2-3 days. Fever as high as 400
 Koplick spots (pathognomonic) often appear 48 hours
before rash. 1-2 mm whitish or gray elevations on
erythematous base in buccal mucosa and other parts of
mouth like “grains of salt on a red background”
http://www.atsu.edu/faculty/chamberlain/Rubeola.htm
 Exanthem: Maculopapular blanching rash
 Starts on face then moves downward and outward
 Often become confluent.
 Usually spares palms/soles - Occasionally petechial
 Lymphadenopathy, high fever, respiratory signs,
pharyngitis, nonpurulent conjunctivitis.
 Improvement within 48 hours with rash disappearing
in same order as appearance
 Darkens to brown color after 3-4 days and fades
followed by fine desquamation. Lasts 7 days.
 Recovery, immunity. Cough up to 2 weeks.
 Fever beyond day 4 of rash means complication
 Immunity lifelong and reinfection rare.
 Contagious 5 days pre-rash to 4 days after rash appears
 Anergy not uncommon for several weeks after measles
(meaning PPD unreliable)
Measles rash
Measles rash
Measles Clinical Course
Hunter’s Tropical Medicine and Emerging Infections Diseases
Other forms of measles
 Modified: Pt. with incompletely protective measles antibody.
Similar but milder symptoms, longer 17-21 day incubation period
 Atypical: Rare - those immunized with killed virus vaccine used
1963-67. Can be very severe with respiratory distress or mild
 Starts with HA, high fever 7-14 days post exposure
 Dry cough, pleuretic chest pain, pulmonary/hilar nodular
lymphadenopathy
 M-P rash 2-3 days later begins on extremities, spreads to trunk
 Involves palms, soles and spares upper chest, neck and head
 May be purpuric, urticarial, hemorrhagic, accentuated in skin folds
Diagnosis
 In context of endemic measles fairly easy with clinical
presentation
 DDx – many other rashes, but symptoms and
progression of rash should usually distinguish
 Where there is low measles prevalence should
diagnose with paired acute/convalescent sera for antimeasles IgM and IgG - at least fourfold increase in IgG.
 IgM present within 3, gone by 30 days post rash
 IgG 7 days post rash – peak in 14 days after rash.
Complications
 Higher in developing countries: 4-10%
 More common in very young and old (< 5; > 20)
 More complications with malnutrition, crowding, low
vitamin A, immunocompromised, pregnancy
 Deaths due to pulmonary (pneumonia and croup) or
CNS complications
 Morbidities include blindness, malnutrition
Pulmonary complications
 Pneumonia, bronchiolitis, LTB (croup), OM
 Measles giant cell pneumonia in those who are
immunocompromised
 5% get bacterial super-infection most commonly from
Staph, Strep, H. flu, or pneumococcus and in one
South African study 85% deaths due to viral or
bacterial lung infection
 Antibiotic prophylaxis MAY decrease incidence of
secondary infection. Needs more study.
Neurologic complications
 Encephalitis 1 / 1000 cases within days of rash. Most recover but
 25% neurodevelopmental sequela; 15% rapidly progressive fatal
 Acute disseminated encephalomyelitis (ADEM)
 Demyelinating disease during recovery phase
 Autoimmune response within 2 wks of infection or vaccine (F, stiff
neck, HA, seizures, mental status changes, paralysis)
 10-20% mortality (frequent residual neurological abnormalities)
 SSPE (Subacute Sclerosing Panencephalitis)
 Fatal progressive degenerative CNS disease 7-10 years post infection
 Increased if measles before age 2 years.
 Risk much less with vaccine < 1/12 (1:1,000,000)
Other complications
 Eye: measles induced keratitis, vitamin A deficiency,
corneal ulceration, 20 herpes simplex or bacterial
infection, herbal remedies in eye can lead to blindness
• GI: Gingivostomatitis, gastroenteritis, D, hepatitis
 Diarrhea, stomatitis often lead to worsening nutritional status
 Marasmus or Kwashiokor
• Cardiac (myocarditis and pericarditis)
• Immune suppression (T cell infection)
• During pregnancy – uncommon – NOT a teratogen. May
have more severe course. Also increased spontaneous
abortion and perinatal mortality.
Treatment
 Antipyretics
 Fluids
 Tx bacterial super-infection, complications
 Vitamin A – WHO vs. U.S. recommendation
 Especially in young < 2 yoa, complicated measles
 Mortality, complications, hospital stay reduced.
 One study showed no OVERALL decreased mortality
but decreased mortality if under age 2
Role of vitamin A
 WHO – 2 doses vitamin A to all children with measles
in communities with recognized vitamin A deficiency
problem and measles related mortality is > 1%.
 Must give within 5 days of rash onset to reduce
morbidity and mortality
 Why does this reduce mortality?
 Most likely damage to epithelial membranes increased
with low vitamin A AND
 Depression of immune response with low vitamin A
Vitamin A continued
 AAP and vitamin A
 Age 6 months to 12 years AND hospitalized OR
 > 6 mo with immunodeficiency, ophthalmological
evidence of vitamin A deficiency, impaired intestinal
absorption, significant malnutrition, immigration
recently from area with high measles mortality.
 Single dose (6-12 mo 100,000; > 12 mo 200,000 IU)
 Repeat day 2 and 28 if evidence vitamin A deficiency
http://www.measlesrubellainitiative.org/wp-content/uploads/2013/06/Treating-Measles-in-Children1.pdf
http://www.measlesrubellainitiative.org/wp-content/uploads/2013/06/TreatingMeasles-in-Children1.pdf
Prevention
 Vaccine beginning at 12 months of age
 As early as 6 months if travelling to endemic area
 But must give 2 doses after age 1
 Many foreign countries give at 9 months
 MMR vs. MMRV (Slightly greater risk of seizure with
MMRV with first dose only)
 Very effective – 95% if 1st vaccine at age 12 moa
 Second dose at least 28 days later (ACIP) and for sure
by school entry at 4-6 years of age
Prevention if exposed
 Measles vaccine within 3 days of exposure
 Immune globulin if can’t get vaccine, or 3-6 days after
exposure, or < 12 months old in household
 SE vaccine: Fever (5-15%) or transient rash (5%) 1-2
weeks later; NO autism association
 If refuse vaccine – exclude from setting for 3 weeks
after onset of rash of last measles case
Scarlet Fever or Scarlatina
 Diffuse erythematous eruption usually associated with
strep pharyngitis and following it by 12-48 hours
 Due to delayed – type skin reactivity to pyogenic exotoxin
from Group A (B and C) streptococci
 Rash:
 diffuse blanching erythema
 Numerous small 1-2 mm papular elevations giving rise to
sandpaper feel to skin
 Starts head/neck with circumoral pallor , strawberry tongue
 Extends to trunk then extremities
 Ultimately desquamates.
 Most marked at skin folds of inguinal, axillary,
antecubital and abdominal areas, pressure points.
 Pastia’s lines – petechia in antecubital fossa and
axillary folds.
 Treatment – antibiotics: Penicillin, Amoxicillin or
Ampicillin, erythromycin, cephalosporins
 Isolate till 24 hours after antibiotics started
Rubella (“German Measles”)
 Three day measles. Initially thought to be measles or
scarlet fever variant.
 Described 1750s in Germany
 Named rubella in 1866
 Interest increased when Australian eye doctor described
teratogenic effects on the eye in 1941
 Prior to good vaccine up to 12 million cases in 1964-65
with 20,000 CRS (Congenital rubella syndrome) cases
 Pre-vaccine (1969) 58 cases/100,000. 1983 ↓ to 0.5 /
100,000. Eliminated from U.S. (2004); Americas (2010)
Clinical Course of Rubella
 Incubation 14-18 days (12-23) after inhalation of
particulate aerosols
 Contagious 1-2 wks before clinical recognition
 Viral shedding decreases with appearance of rash
but contagious till a week after rash
 Re-infection possible but rarely leads to CRS
 “Rubella is a mild disease with clinical features
that are neither distinctive nor diagnostic.”
Hartley
AH and Rasmussen JE. “Infections Exanthems.” Pediatrics in Review accessed online a
http://pedsinreview.aappublications.org/content/9/10/321
Signs/symptoms
 Usually mild and often asymptomatic
 Acute onset M-P rash - few systemic symptoms
 Rash erythematous, nonpruritic, discrete
 Low grade fever, lymphadenopathy concurrently or 1-5
days prior to rash
 Lymphadenopathy – posterior cervical, posterior
auricular, suboccipital
 Spreads face to trunk, extremities – fading on face by
day 2
 Generalized within 24 hours, gone within 3 days (1-8)
without peeling or scaling. Much more rapid than
measles; does not darken or coalesce
 Teens, adults – more likely to be more symptomatic
with fever, systemic complaints. Arthralgias, arthritis
in 70% lasting up to a month – knees, wrists, fingers
 Complications more common in adults –
postinfectious encephalitis (1 in 6000 within week):
immune mediated and good prognosis OR progressive
rubella panencephalitis (rare and devastating)
Congenital Rubella Syndrome
 Real concern with Rubella is CRS – hearing loss, MR,
CV defects, ocular defects
 CRS highly variable but any organ system can be
effected. Can manifest throughout life.
 Vaccine effective; goal of immunization to prevent CRS
(25% transient arthralgia; 10% arthritis after vaccine)
 Rubella still a big deal in third world
Congenital rubella syndrome
 Highest risk first 10 weeks of gestation – Unlikely if
after 18-20 weeks. 80% risk first trimester
 Consider in any birth if rubella during pregnancy or
any infant with IGR or other findings c/w CRS
 Children can shed virus after CRS at least a year
 Dx of rubella unnecessary except when CRS suspected.
Cord blood IgM or persistence of IgG beyond 1st year of
life (normally disappears at 3-6 weeks)
Erythema Infectiosum or Fifth
disease
 Mild febrile disease with rash: caused by Parvovirus
B19 infection
 Five forms of B19 infections which also causes
 Arthropathy
 Non-immune hydrops fetalis with Intrauterine fetal
death or miscarriage
 Transient aplastic crisis in chronic hemolytic disorders
 Chronic pure RBC aplasia in the immunocompromised
Signs/symptoms
 Incubation period 4-14 days – biphasic illness
 25% asymptomatic, 50% flu like symptoms, 25%
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classic presentation including rash.
First week viremia with non-specific flu like illness
(fever, malaise, myalgia, coryza, HA, pruritis)
Can have low platelets, Hgb, or leukopenia
Next week rash and/or arthralgia
In adults less characteristic - can be confused with
rubella
 Fifth disease outbreaks among school age children
 Nonspecific prodromal symptoms (Fever, coryza, HA,
N, D)
 2-5 days later classic erythematous malar rash
(slapped cheek appearance)relative circumoral pallor
 Followed by reticulated (lacelike) rash on trunk,
extremities
 Viremia has resolved and child feels well by time rash
appears (rash felt to be immune mediated)
 Typical feature is recrudescence of rash to
nonspecific stimuli (i.e. Δ Temp, sunlight exposure,
exercise, emotional stress) resolving within weeksmonths or rarely years.
 Can also be associated with morbilliform rash,
confluent or even vesicular rash
 No treatment
 If normal immune system – not contagious after rash no need to isolate
 Infectious – close contact, large droplets, blood
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transfusion
Household transmission in 50%
Risk of fetal death with maternal infection 2-5 %
Rarely if ever causes congenital anomalies
If get when pregnant – weekly US. May need Hct via
umbilical vein and transfusions and other treatment
and intrauterine treatment of pleural effusion, ascites
Roseola Infantum
 Exanthem subitum, pseudorubella, sixth disease
 Caused most often by herpes virus 6 (HHV-6)
 2/3 have a + serology to HHV-6 by age 1 year
 Viremia precedes rash; antibody forms at time of rash.
 Peak incidence 7-13 months. 90% occur at < 2 years
 Occurs year round
 Incubation 9-10 days. Virus believed to be shed for life.
Clinical presentation
 3-5 days fever often over 400 which resolves abruptly with
appearance of the rash (or within 24 hours)
 Irritability – otherwise active, alert, appears well
 Other symptoms
 Bulging fontanelle often leads to LP
 Lymphadenopathy 98%
 erythematous TMs 93%
 irritability 92%
 Nagayama spots (uvulopalatoglossal junctional macules or
ulcers, papules, purpuric rash) 87%
 Anorexia 80%, URTI 25%, D 15%, cough 11%, convulsions 4%
 As fever goes away, blanching M, MP, occasionally
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vesicular nonpruritic rash starting on neck, trunk and
spreading to face and extremities. Persists 1-2 days and
often confused with drug allergy
Lab: Relative neutropenia; Low platelets; mild atypical
lymphocytosis. (nadir 3000 day 3-6)
Usually benign and self limited. Seizures 0-6% of
time, aseptic meningitis, encephalitis and TTP.
NO recommendation for exclusion from child care.
Sporadic cases not contagious. Contagious prior to
rash and can return to school once fever gone.
Can be fatal in immunocompromised
http://www.mayoclinic.com/health/medical/IM03111
Chicken Pox - Epidemiology
 Pre-1995 CDC estimated about 4,000,000 cases; 11,000
admissions; 100 deaths / year
 Since vaccine – fewer cases, complications, admissions,
deaths
 Prior to vaccine >95% immune by age 20 and only 2%
of adults susceptible
 More serious with increasing age (and < 1 yo). In past
adults > 20 represented 5% of cases but 55% of deaths.
 In U.S. > 92% vaccinated - 90% decreased incidence
 Powerful herd immunity effect as rate has gone down
in unvaccinated adults.
 Second dose vaccine recommended since 2006
 Secondary attack rate in family > 90% in susceptible
individuals
 By contact with aerosolized NP secretions or direct
contact with vesicle fluid from skin lesion
Clinical presentation
 Incubation 14-16 days (10-21)
 Prodrome: fever, malaise, pharyngitis, loss of appetite
 Generalized pruritic vesicular rash within 24 hours -
successive crops of rash over several days
 Macules-papules–vesicles - pustular -- crusted
papules.
 Lesions in different varying stages on face, trunk,
extremities is hallmark of disease
Clinical
 New lesions stop developing within 4 days
 Most fully crusted in normal host within 6 days
 Crusts fall off within 1-2 weeks leaving area of
hypopigmentation temporarily
 Infective 48 hours prior to rash till all skin lesions
crusted
 Can be reinfected but unusual
 20% with one vaccine develop Chicken Pox if exposed
(breakthrough disease)
 Milder and atypical – fewer lesions and less fever if one
gets varicella after one dose vaccine
 Fewer complications
Complications
 Those at increased risk – adults, very young, pregnant
women, immunocompromised
 Complications – not a benign disease
 GAS soft tissue infection, cellulitis, myositis, fasciitis,
toxic shock
 Encephalitis, Reyes, transverse myelitis, etc.
 Acute cerebellar ataxia (complete recovery)
 Pneumonia – major cause M/M in adults – not common
since vaccine – treat with acyclovir as high mortality
Complications
 Elevated ALT/AST common but hepatitis rare except in
those with immune compromise
 Immune compromised – including HIV, on steroids or
TNF antagonists - more likely to get crops of vesicles for
weeks, need hospitalization, disseminated varicella,
large hemorrhagic skin lesions, pneumonia, widespread
disease with DIC
Treatment
 Treatment – usually none except symptomatic for
pruritis, fever, cut fingernails
 Avoid ASA as associated with Reyes syndrome
 Acyclovir (needs 10X levels as for HSV) not usually
recommended for mild case – modest effects
 But safe and fewer lesions, reduced timing of new
lesions and quicker healing and crusting
Treat with Acyclovir recommended
 Treat
 > 12 yoa
 Secondary household cases (more severe)
 Chronic cutaneous or cardiopulmonary disorders
 Those on intermittent or inhaled steroids
 Those on chronic salicylates
 Disseminated disease with pneumonia or encephalitis
Acyclovir
 In adult studies didn’t show much help. Some evidence
suggests it helps outcome in varicella pneumonia.
 UpToDate recommends if can get within 24 hours of
infection
 For immunocompromised or if complications serious
give IV – otherwise 20 mg/kg/dose po 4-5 times/day
for 5 days- 800 mg for adults
 Can cause GI Side Effects and HA
Varicella in pregnancy
 Varicella more severe in pregnant women
 Mother to child transmission of VZ in utero,
perinatally, or postnatally
 Varicella pneumonia more common in pregnancy so
recommend acyclovir in pregnant women with
varicella – appears to lower mortality from varicella
pneumonia (Class B drug in pregnancy)
Congenital varicella
 Congenital varicella syndrome – cutaneous scars, IGR,
neurological, ocular and limb abnormalities.
 Newborn – Congenital varicella syndrome – most
when mothers infected 8-20 weeks. Risk small: 2% <
20 weeks and 1% < 13 weeks. (0.4-2 %)
 Risk congenital varicella syndrome estimated with
PCR of fetal blood or amniotic fluid + US for fetal
abnormality
 If pregnant woman exposed, test serologically and give
post exposure prophylaxis within 96 hours with
VariZIG (up to 10 days)
Neonatal varicella
 Neonatal varicella is serious illness - up to 30% mortality.
 At risk if mother had VZV within 2 weeks of delivery and
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worst if within 5 days of delivery
If maternal VZV 21 days or more before delivery baby has
passive IgG and should be ok.
Often disseminated with pneumonia, hepatitis,
meningoencephalitis
VariZIG within first day may ameliorate – VariZIG prolongs
incubation period
If infant gets it after 10 days of age usually mild
Acyclovir for newborn in severe disease
Rocky Mountain Spotted Fever
 Not like others mentioned but can be fatal if missed.
 Rickettsial rickettsii
 U.S., Canada, Mexico, Central America and South
America (Bolivia, Argentina, Brazil and Columbia)
 In one group of patients, 4533 cases: 25% hospitalized,
0.5% death
 Bite of tick – most 5-7 (2-14) days prior to illness
Clinical
 Initially nonspecific: fever, HA, malaise, myalgias,
arthralgias, abd. HA, abd. pain can be severe.
 88-90% get rash (10% don’t – RM Spotless Fever)
often does not start though till 2-3 day of illness
 Blanching erythematous rash with macules becoming
petechial over time (varies)
 Begins on ankles heels, extremeties and goes inward
 On palms and soles characteristic
 Can be atypical or absent
Treatment
 No reliable early test and treatment needs to be begin
in first 5 days or mortality higher so treat on suspicion
 Doxycycline in adults AND children.
 UpToDate recommends chloroamphenicol for
pregnant women
 Doxycycline: 100 po bid for most > 45 kg.
 2.2 mg/kg/dose twice daily for children.
 For critically ill 200 mg po bid for 72 hours
 Treat 5-7 days – 3 days past last fever.
http://sitemaker.umich.edu/mc5/rocky_mountain_spotted_fever
 Other less dangerous Rickettsia cause spotted fevers in
other countries – fever, headache, intense myalgia and
often rash.
 Clinical features to diagnose. Similar rash to RMSF
 Doxycycline for all – 100 twice daily. (children 2.2
mg/kg/dose every 12 hours)
Other Exanthems - Dengue
 Rash begins towards end of febrile period and 2-5 days
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after symptoms appear in 50% of cases
Confluent erythematous macular rash
Extremities with scattered well circumscribed areas
of sparing (“sea of red with islands of normal skin)”
Tends to cover the body but spares the face – may
involve the palms and soles.
+ tourniquet test or few spontaneous petechiae.
http://www.emedicinehealth.com/dengue_fever/page2_em.htm
Other exanthems – drug eruption
 Exanthematous, morbilliform, M-P drug eruption
 Symmetric macules, small papules 5-14 days after initiating
drug or even after drug stopped
 Sooner within 1-2 days if previously exposed
 Occurs 2% of drug exposures; 2nd only to urticarial reactions
 Tend to involve trunk, proximal extremities – or whole body
 Can itch or produce low grade fever. Resolved 7-14 days.
 Tx: D/C meds - “treating through” sometimes indicated
 Treatment for rash – topical steroids, oral antihistamines
Other exanthems – enteroviruses
 Non-polio Enteroviruses and Parechovirus viral rashes
 Ubiquitous viruses – fecal-oral spread
 Coxackieviruses A and B, echoviruses, enteroviruses
 90% asymptomatic or undifferentiated febrile illness
 10-15 million symptomatic infections / year in the U.S.
 If not hand foot and mouth disease not distinctive –
mimic other exanthems and can be morbilliform
Enterovirus
 Especially the echoviruses cause a M-P nonspecific rash.
 Often in multiple household members
 Mild Fever 24-36 hours – disappears with appearance of
discrete, nonpruritic salmon-pink macules, papules < 1
cm on face and upper chest (sometimes face, proximal
extremities).
 No need to isolate
Other rashes - meningococcemia
 Meningococcemia – mentioned so as to not miss
 Fatal if missed
 > 50% of time begins with petechial 1-2 mm rash
 Trunk and lower portion of body
 Can begin with M-P rash resembling rubella for 1-2 days
 15-25% get purpura fulminans – severe complication.
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Painful
Acute onset cutaneous hemorrhage and necrosis
Watch out for petechiae or hemorrhage with pain
Other exanthems - typhoid
 Rash usually in second week of illness
 Called "rose spots"
 Faint salmon colored macules
 On trunk, abdomen
http://pathmicro.med.sc.edu/infectious%20disease/typhoid%20spots.jpg
Other exanthems
 Infectious mononucleosis
 10-15% get pink-red maculopapular rash
 If given Ampicillin 80-90% develop bright red
morbilliform rash
 HIV
 Secondary syphilis
 Leptospirosis
 Many others with similar appearance.
Summary
 Measles is still a very important disease in the
developing world with considerable morbidity and
mortality. Giving Vitamin A may lower mortality.
 Most childhood exanthems recognized by progression
of rash, other S/S rather than just a characteristic rash
 Be very wary of petechiae as they indicate a serious
infection such as RMSF and meningococcemia.
References
 Albrecht MA. “Clinical features of varicella-zoster virus infection:
Chickenpox.” UpToDate accessed 12/24/2013.
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