Colds and common viral illness Flashcards
General Data:
Our patient is B.A., a 7/M from Tayabas, Quezon who consulted at
your clinic due to sneezing.
History of Present Illness
The patient was apparently well until…
2 months PTA à patient was noted to have episodes of nasal
congestion and rhinorrhea associated with nasal itching and
sneezing. The mother noted that the patient had more severe
episodes of nasal congestion during the night. These episodes
would occur four days a week and due to the severe nasal
congestion, would sometimes awaken the patient from sleep. The
patient was brought to a local clinic where he was advised nasal
decongestants with temporarily relief of symptoms.
1 month PTA à persistence of symptoms was noted, this time
with more frequent episodes of sneezing when the patient was at
playing in the playground in his school. His teacher noted that he
would have difficulty completing tasks due to frequent bouts of
sneezing. Persistence of symptoms prompted consult.
Ancillary History
Birth and Maternal History: delivered via cesarian section with
unremarkable course
Past Medical History: (+) history of episodes of rhinorrhea during
infancy (+) history of atopic dermatitis
Family Medical History: (+) maternal history of bronchial asthma
(+) food allergy in older sibling
Nutritional History: breastfed for one week only then shifted to
formula feeding
Personal/Social History: lives with both parents, has a pet dog
PHYSICAL EXAMINATION
General Survey
Awake, comfortable, not in cardiorespiratory distress
Anthropometrics
Weight =22 kgs, height =110 cm
Vital signs
BP 110/80 HR 92 bpm RR 22 bpm T 36.5C O2 sats (room air) =
100%
Skin
(-) rashes
Head and Neck
Pink conjunctivae, anicteric sclerae, bluish infraorbital skin folds,
(+) nasal congestion, (-) nasal deviation, (-) cervical
lymphadenopathies, chapped lips, moist mucus membranes (+)
transverse nasal crease
Anterior rhinoscopy: clear nasal secretions, (+) edematous, boggy,
and bluish mucous membranes with no erythema/purulent
discharge (+)swollen turbinates
Chest and Lungs
Equal chest expansion, (-) retractions, clear breath sounds,
Cardiac
Adynamic precordium, distinct heart sounds, normal rate and
regular rhythm, no murmurs
Abdomen
Flat, normoactive bowel sounds, (-) masses/tenderness, (-)
hepatomegaly, intact Traube’s space
Extremities
Full and equal pulses, (-) edema/cyanosis/clubbing, CRT 2s
(1) What is your primary working impression?
Primary Working Impression
Allergic Rhinitis, Severe Persistent
Basis for Diagnosis
Basis for Diagnosis
(1) History
7/M with chief complaint of sneezing
2 months PTA of nasal congestion and rhinorrhea
associated with nasal itching and sneezing
Episodes of nasal congestion more severe during the
night.
Symptoms present four days a week and awaken the
patient from sleep
Nasal decongestants afforded temporarily relief of
symptoms
(+) interference with sleep and school
Presence of Risk Factors for AR
o (+) delivered via cesarian section
o (+) history of episodes of rhinorrhea during
infancy
o (+) history of atopic dermatitis
o Family history of atopy (maternal history of
bronchial asthma (+) food allergy in older
sibling)
o NOTE: Other risk factors for AR: IgE >100
IU/mL before age 6 years
(2) Physical Examination
bluish infraorbital skin folds à Dennie Morgan skin
folds
(+) nasal congestion
(-) nasal deviation
Anterior rhinoscopy: clear nasal secretions, (+)
edematous, boggy, and bluish mucous membranes
with no erythema/purulent discharge (+)swollen
turbinates
Chapped lips
(+) transverse nasal crease
Note:
The diagnosis of AR is based on recurrent symptoms of
sneezing, rhinorrhea, nasal itching, and congestion that
occur most often in the absence of an upper
respiratory tract infection or structural abnormalities.
Evaluation of AR calls for a thorough history including
details of the patient’s environment and diet; family
history of allergic conditions such as AR, eczema, and
asthma; physical examination; and laboratory
evaluation. The history and laboratory findings provide
clues to the identity of provoking factors.
(2) What are your differential diagnosis for this case?
(1) Non-allergic rhinitis secondary to
structural/mechanical factors
Deviated
septum/septal
wall anomalies,
Hypertrophic
turbinates
Adenoidal
hypertrophy
Nasal tumors
Rule IN:
(+) recurrent
episodes of nasal
congestion
(+) episodes of
sneezing,
rhinorrhea
LESS LIKELY:
Anterior
rhinoscopy/
speculum
examination
revealed no
anatomic
abnormalities or
nasal
masses/tumors
(-) septal deviation
(2) What are your differential diagnosis for this case?
INFECTION
Infectious
Rhinitis
RULE IN:
(+) nasal congestion
(+) episodes of
sneezing,
rhinorrhea
LESS LIKELY:
(-) purulent
discharge on
anterior
rhinoscopy
(+) chronic history
(+) prominent
personal and
family history of
atopy
(2) What are your differential diagnosis for this case?
(3) Nonallergic inflammatory rhinitis with eosinophils
(NARES)
RULE IN:
(+) nasal congestion
(+) episodes of
sneezing, rhinorrhea
LESS LIKELY
(+) prominent
personal and
family history of
atopy
Also patients do
not have elevated
IgE (see labs)
(2) What are your differential diagnosis for this case?
(4) Vasomotor rhinitis
Vasomotor
rhinitis/
Perennial nonallergic
rhinitis
RULE IN:
Chronic history of
symptoms
(+) nasal
congestion
(+) episodes of
sneezing,
rhinorrhea
LESS LIKELY:
No excessive
responsiveness of
nasal mucosal to
physical stimuli
(2) What are your differential diagnosis for this case?
(5) Rhinitis medicamentosa
RULE IN:
Chronic history
of symptoms
(+) nasal
congestion
(+) episodes of
sneezing,
rhinorrhea
LESS LIKELY:
No history of
overuse of topical
vasoconstrictors
(2) What are your differential diagnosis for this case?
Other Less Likely Differentials for AR in this case
hormonal rhinitis (associated with
pregnancy or hypothyroidism)
neoplasms
vasculitides
granulomatous
disorders/inflammatory/immunologic
conditions (Wegener granulomatosis,
Sarcoidosis, Midline granuloma, Systemic
lupus erythematosus, Sjögren
syndrome, Nasal polyposis)
drug induced (NSAIDs, anti-hypertensives,
ASA)
What is your plan of management for this patient?
What are the differentials for colds?
What is allergic rhinitis?
Etiopathogenesis:
- Inflammatory disorder of the nasal mucosa
- Repeated intranasal introduction of allergens cause
“priming” – more brisk response with lesser
provocation
- Exposure to allergen à inc IgE production à allergic
response characterized by degranulation of mast cells
and release of inflammatory mediators (histamine,
PG2) à infiltrate nasal mucosa
What are the classification of allergic rhinitis?
Intermittent:
<4 days/week OR < 4weeks at a time
Persistent:
≥4days/week AND ≥4 weeks at a time
MILD:
ALL of the following:
normal sleep
normal daily activities
normal work and school
no troublesome symptoms
MODERATE TO SEVERE:
abnormal sleep
impairment of daily activities, sport and leisure
impaired work or school
troublesome symptoms
How to avoid allergic rhinitis?
Protective factors
1. Early exposure to dogs and cats
2. Prolonged breastfeeding
3. Early introduction to wheat, rye, oats, barley, fish, eggs
What are the risk factors of allergic rhinitis?
Risk factors:
1. Family hx of atopy
2. High serum IgE levels before 6 yo >100 IU/mL
3. Maternal smoking
4. Cesarean section
5. >3 episodes rhinorrhea in the 1st year of life
What are the clinical manifestations of allergic rhinitis?
CM:
1. Sneezing, rhinorrhea, nasal obstruction
2. Itching of the nose, palate, pharynx and ears
3. Itching, redness, and tearing of the eyes
4. Allergic salute – upward rubbing of nose to relieve
itching and blockage
5. Transverse nasal crease
6. Allergic gape – continuous open-mouth breathing
7. Chapped lips, dental malocclusion
8. Allergic shiners – dark circles under eyes
9. Clear nasal secretions
10. Edematous, boggy, bluish mucus membrane and
swollen turbinates
11. Headaches, fatigue, limits daily activities, interferes
with sleep, impaired cognitive functioning and learning
What are the diagnostics?
Dx:
1. Skin test – to avoid false (-): monteleukast should be
withheld for 1 d, sedating antihistamines x 3-4d, nonsedating
antihistamines x 5-7d
2. Serum IgE – indications:
a. Dermatographism or extensive dermatitis
b. Intake of meds that interferes with mast cell
degranulation
c. High risk for anaphylaxis
d. Uncooperative px
3. Nasal smears – presence of eosinophils
Management of allergic rhinitis
- Mild intermittent – oral or intranasal antihistamine or
intranasal glucocorticoids
a. May add LTRA if with asthma
b. May add decongestant - Moderate-severe or persistent AR – intranasal
glucocorticoids
a. May add oral or intranasal antihistamine
(2nd gen > 1st gen)
b. May add LTRA instead of antihistamine if
with asthma
c. Intranasal chromones
d. Add intraocular antihistamines/chromones
for ocular sx
Antihistamines:
1st Gen: Chlorpheniramine - reduces sneezing rhinorrhea, ocular symptoms
2nd Gen: Cetirizine, loratadine, desloratadine, levocetirizine, fexofenadine - preferred over 1st gen antihistamine due to less sedation
Decongestants:
Cetirizine + pseudoephedrine: oral decongestants; not favored due to irritabilty, insomnia, link with infant mortality
Chlorpheniramine maleate + phenylephrine HCl: oral decongestatnt
Anticholinergics: Ipratropium bromide- relief of rhinorrhea; may cause epistaxis, nasal dryness; nasal spray not locally available
Leukotriene receptors: montelukast- modest effect on rhinorrhea and nasal blockage
Intranasal corticosteroids:
Fluticasone furoate/proprionate
Mometasone
Triamcinolone
-most effective therapy for severe, persistent AR
-may cause nasal irritation, epistaxis, monitor growth of patients
How do we monitor patients with persistent rhinitis?
Monitoring for Persistent rhinitis (review after 2-4 weeks)
- If improved: continue tx for 1 mo
- Failure:
§ Review dx, compliance, infections
§ Inc. intranasal steroid dose
§ Add antihistamine if w/ itch/sneeze
§ Add ipratropium if w/ rhinorrhea
§ Add intranasal decongestant if with
blockage
§ Give short term oral steroids if with severe
nasal & ocular sx
§ If persistent failure: surgical referral
3. Avoidance of allergens
4. Immunotherapy – recalcitrant sx
What are the complications of rhinitis?
Complications:
1. Allergic conjunctivitis
2. Chronic sinusitis
- Sinusitis of triad asthma – asthma, sinusitis, with nasal
polyps: poorly responsive to tx
3. Asthma
4. Postnasal drip (PND)
5. Eustachian tube dysfunction, middle ear effusion, otitis
media, OSA
Case
General Data:
Our patient is J.K., a 3/F from Pandacan, Manila who was brought
in by his mother at your clinic with a chief complaint of fever and
rashes.
History of Present Illness
The patient was apparently well until…
Seven days prior to consult – the patient was noted to have nonproductive
cough associated with runny nose. The patient was
given cough syrup with no apparent relief of symptoms. She also
described the patient’s eyes to be somewhat reddish and watery
but with no discharge. The patient was afebrile and had good
appetite and activity, hence no consult was done.
Three days prior to consult – the patient was noted to have
persistence of symptoms this time associated with high grade, nonremitting
fever (Tmax 40C) associated with a diffuse reddish rash
that was noted by the mother to begin at the forehead and face.
The patient was brought to a local health center where she was
given Paracetamol and advised increased oral fluid intake. There
was noted temporary relief of fever.
Two days prior to consult – there was persistence of high-grade
fever; however, the rash became blotchy and progressed to the
trunk and extremities. She had good appetite and activity and the
mother opted to observe the patient at home and continue
Paracetamol. However, on the day of consult, due to persistence of
the rash and fever, the mother opted to bring the patient to you for
opinion, hence this consult.
Review of Systems
(-) increased sleeping time (-) dyspnea (-) diarrhea
(+) good urine output
(-) weight loss (-) diaphoresis (-)
constipation
(-) seizures (-) abdominal pain (-) jaundice
Birth and Maternal History
The patient was born full term via normal delivery at home to a 30
year old G2P1 (1001) mother assisted by a midwife with no fetomaternal
complications. Her mother had regular pre-natal checkup
c/o local health center with no maternal history of illnesses,
smoking, alcohol or illicit drug exposure during the pregnancy. At
birth, the patient had good suck and activity.
Past Medical History
The patient had no history of bronchial asthma, allergy to food or
medications or primary tuberculosis. There were no history of
previous hospitalizations or surgery.
Family Medical History
The patient had an elder brother with similar illness about 2
weeks ago. There is family history of hypertension and diabetes
on the mother side. There is no history of bronchial asthma,
pulmonary tuberculosis or other illnesses in the family.
Developmental History
Rides tricycle, knows age and sex, copies cross, imitates circle,
says 3-word sentences
Immunization History
The patient was given BCG x 1 dose, OPV x 3 doses, Hepatitis B x 2
doses, DPT x 3 doses and oral rotavirus vaccine c/o the local
health center. No other immunizations were given.
Nutritional History
The patient was exclusively breastfed from birth until six months
and then started on complementary feeding. Presently, the
patient eats table foods and prefers meat and vegetables.
Personal/Social History
The patient is the younger of two siblings. Her mother is a 24 year
old sales clerk while her father is a 30 year old pedicab driver. The
patient lives with her parents, sibling and her aunt in a singlestorey
house in Pandacan. The family’s source of water is boiled
water from a deep well.
PHYSICAL EXAMINATION
General Survey
Awake, comfortable, not in cardiorespiratory distress
Anthropometrics
Weight = 17 kgs (z-score=2), height = 95 cms (z-score=1), head
circumference = 50 cm (z-score=1)
Vital signs
BP 90/60 HR 100 bpm RR 30 bpm T 38.0C O2 sats (room air) = 99%
Skin
(+) diffuse erythematous, generalized maculopapular rash
Head and Neck
Pink conjunctivae, anicteric sclerae, (-) nasal congestion, (-) eye
redness/discharge, (+) bluish red spots on buccal mucosa, (-)
cervical lymphadenopathies
Otoscopy: intact tympanic membrane, (-) TM bulging
Chest and Lungs
Equal chest expansion, clear breath sounds, (-) retractions
Cardiac
Adynamic precordium, distinct heart sounds, normal rate and
rhythm, no murmurs
Abdomen
Flat, normoactive bowel sounds, (-)
masses/tenderness/organomegaly
Extremities
Full and equal pulses, (-) edema/cyanosis/clubbing
Neurologic Exam
Awake, pupils 3 mm bilaterally briskly reactive to light, (+) intact
gross extraocular movements, (-) gross facial asymmetry, (+) can
swallow, tongue appears midline, good muscle tone, (-)
wasting/hyponia, intact deep tendon reflexes, (-) Babinski, (-)
clonus
Laboratory Examination Results
Complete Blood Count
Date Normal*
WBC 4 x109/L
RBC 3.1x109/L
Hgb 120 g/L
Hct 0.420%
MCV 80fL
MCH 30 pg
MCHC 360g/L
RDW 14.0
Platelets 350x109/L
Neut% 0.7
Lymph% 0.3
Mono% 0.0
Eo% 0.0
Baso% 0.0
Measles IgM: Elevated
(3) What is your primary working impression?
Primary Working Impression
Measles Virus Infection
Basis for Diagnosis
(3) History
3/F, apparently well, presenting with fever and rash
(+) viral prodrome à 4 days prior to onset of rash,
noted to have cough, coryza and conjunctivitis
High grade fever associated with erythematous,
maculopapular rash proceeding in a cephalocaudal
pattern
No other systemic symptoms
No history of vaccination with measles
Exposure to a sibling with similar illness 2 weeks
(apparently infectious at this time)
(4) Physical Examination
(+) fever
(+) conjunctivitis
(+) Koplik spot - pathognomonic
(+) diffuse, generalized, maculopapular rash
(5) Laboratory Examination
Neutropenia, with lymphocytes decreased more
Serologic test: (+) measles antibody
(4) What are your differential diagnosis for this case?
(6) Exanthematous viral infections
a. Rubella
Rule in:
(+) fever
(+) generalized erythematous macupapular rash
Rule out:
a prodrome of low-grade fever, sore throat, red eyes
with or without eye pain, headache, malaise, anorexia,
and lymphadenopathy more characteristic of rubella
pattern of rash different from this case: rash fades
from the face as it extends to the rest of the body so
that the whole body may not be involved at any 1 time
Suboccipital, postauricular, and anterior cervical lymph
nodes more prominent
b. Adenovirus
Rule in:
(+) fever and coryza (Primary infections in infants are
frequently associated with fever and respiratory
symptoms), conjunctivitis=Pharyngoconjunctival fever
Rule out:
Adenovirus respiratory infections are associated with a
significant incidence of diarrhea which is not present in
this case
c. Enterovirus
Rule in:
Fever associated with rash
Nonspecific fever illness is a common manifestation
Rule out:
mild conjunctivitis, mild pharyngeal injection and
ulcers in the pharynx more prominent, also usually
present with symptoms of meningitis
d. Roseola
Rule in:
Fever associated with rash
Rule out:
Characteristic pattern of fever not seen (usually rash
follows onset of the fever on the 3rd day of illness)
(7) Exanthematous bacterial infection
a. Mycoplasma
Rule in:
fever and rash
common in pre-school and school aged
Rule out:
lesions
b. Group A streptococcus
Rule in:
Fever and rash
Rule out:
Usually with pharyngitis
c. Toxic shock syndrome
Rule in:
Sudden onset of fever and erythematous rash
Rule out:
No predisposing factors (skin and wound infections, tampon
use, vaginal infections and packing, post-infectious bacterial
URTI)
Does not meet criteria for TSS: no hypotension
d. SSSS
Rule in:
Present with fever and a diffuse maculopapular rash
Rule out:
Often associated with purulent rhinitis (not present)
(8) Exanthematous immune mediated illness
a. Kawasaki disease
Rule in:
(+) Fever of at least 5 days
(+) rash
Nonpurulent conjunctivitis
Rule out:
Other diagnostic criteria lacking: unilateral cervical
lymphadenopathies, mucous membrane abnormalities,
extremity changes (erythema/ desquamation
characteristic thrombocytosis of Kawasaki syndrome is
absent in measles
Other less likely differentials*:
(9) Drug eruptions
a. SJS/TEN
Rule in:
(+) diffuse erythematous rash
Rule out:
(-) history of drug exposure
(antibiotics/anticonvulsant/steroids)
Usually present with bullous lesions
Rash characterized as poorly defined macules with purpuric
center coalescing to form blisters
(5) What is your plan of management for this patient?
a. Diagnostic Tests/Labs
For this case:
The diagnosis of measles is based on clinical and
epidemiologic findings. In the absence of a recognized
measles outbreak, confirmation of the clinical
diagnosis is recommended.
Laboratory findings in the acute phase include
reduction in the total white blood cell count, with
lymphocytes decreased more than neutrophils.
Serologic confirmation is most conveniently made by
identification of immunoglobulin M (IgM) antibody in
serum. IgM antibody appears 1–2 days after the onset
of the rash and remains detectable for about
Other labs:
In measles not complicated by bacterial infection, the
erythrocyte sedimentation rate and C-reactive protein
levels are normal.
Serologic confirmation may also be made by
demonstration of a 4-fold rise in IgG antibodies in
acute and convalescent specimens taken 2–4 wk later.
Viral isolation from blood, urine, or respiratory
secretions can be accomplished by culture at the
Centers for Disease Control and Prevention (CDC) or
local or state laboratories.
Molecular detection by polymerase chain reaction is
possible but is a research tool.
b. Management
b.1. Goals of Management:
Management of measles is supportive. Maintenance of
hydration, oxygenation, and comfort are goals of
therapy.
b.2. Pharmacologic Management
Antipyretics for comfort and fever control
b.3. Non-pharmacologic management
Oral fluids
Eye care
Nutrition
b.4. Anticipatory care
Developmental surveillance
Dental health care
Avoidance of injury
Child protection vs maltreatment
Immunization
Proper nutrition
Others*:
Vitamin A supplementation
Oxygen support (For patients with respiratory tract
involvement, airway humidification and supplemental
oxygen may be of benefit while respiratory failure due
to pneumonia may require ventilatory support_
How do we give Vitamin A in measles?
- Children 6 mo to 2 yr of age hospitalized with measles
and its complications (e.g., croup, pneumonia, and
diarrhea). - Children >6 mo of age with measles who are not
already receiving vitamin A supplementation and who
have any of the following risk factors: - Immunodeficiency
- clinical evidence of vitamin A deficiency
- impaired intestinal absorption
- moderate to severe malnutrition
- recent immigration from areas where high
mortality rates attributed to measles have
been observed
Single dose of 200,000 IU orally for children ≥1 yr of
age (100,000 IU for children 6 mo to 1 yr of age)
* The dose should be repeated the next day and again
4 wk later for children with ophthalmologic evidence
of vitamin A deficiency
- What are possible complications for this case?
Otitis media
Measles pneumonia – Giant cell pneumonia
Dehydration
Subacute Sclerosing Panencephalitis
How can we prevent measles?
- How can this illness be prevented?
Vaccination with measles vaccine
Administration of measles vaccine to children, adolescents and
adults with incomplete or no vaccination using the monovalent or
trivalent vaccine (contains measles, mumps and rubella). A
tetravalent vaccine, MMRV (contains measles, mumps, rubella
and varicella) may be used for infants 12 months to 12 years of
age
Indications:
o For those who have not received any dose of the measles
vaccine, they should receive 2 doses 1 month apart
o For those who have received 1 dose of measles vaccine at 12
months of age or older, administer the second dose
o For those with unknown history of measles vaccination, give
measles vaccine for 2 doses 1 month apart
o Children 6 months to 11 months of age should receive measles
vaccine and followed by 1 dose administered on or after the first
birthday, preferably between 12-15 months of age, then another
dose at least 1 month after and usually given at 4-6 years
o In outbreak areas, where measles involves infants <12 months
of age and have ongoing risk of exposure, measles vaccine can be
given as early as 6 months
o Individuals exposed to measles should receive measles vaccine
(monovalent or trivalent vaccine) within 72 hours of exposure
What is the etiology of measles? other name for measles?
Rubeola
Etiology:
- Paramyxovirus
- Humans are the only host of measles virus
- Prolonged immunosuppression x 2-3 yrs
- Most infectious virus (r knot 12-18)
What is the epidemiology of measles?
- The status of vaccine coverage is important in the
epidemiology of measles - High measles vaccination coverage early in life are
essential to maintain the endemic spread (>90% at 12-
15mos, and >95% 2 dose coverage in school age) - Outbreaks due to lower coverage rates of vaccination
due to personal belief - Indicator of weakness of immunization program
(geographic) - Risk for complicated disease:
a. <5 yo, >20yo
b. Malnourished
c. Insufficient vit A
d. Weak immune system (AIDS)
How is measles transmitted?
Transmission:
- Respiratory tract/conjunctiva after contact with large
droplets or small droplet aerosols
- Virus viable in droplet for 1h, and 2h on surfaces
- 90% of exposed individuals are susceptible to measles
What are the phases of measles?
4 Phases:
1. Incubation period – measles migrates to regional LN
primary viremia to RES à secondary viremia to body
surfaces
2. Prodromal illness – epithelial cell necrosis and giant
cell formation in tissues. Cell death via viral replication,
viral shedding begins.
3. Exanthematous phase – onset of rash. Ab production.
Viral replication & sx subside. Immunosuppression of
Th1.
4. Recovery phase
Incubation period of measles?
Period of communicability: 3 days before until 4-6 day after onset
of rash
Incubation period: 8-12 days (1-2w)
What are the clinical manifestations of measles?
CM
1. Prodromal phase – fever, conjunctivitis, coryza, cough,
photophobia
- Koplik spots – pathognomonic. Grayish white dots with
red border opposite lower molars. Enanthem.
a. appear 1-4 days before rash
b. also at lips, hard palate, and gingiva
2. exanthematous phase – after 1-4 days from onset of
sx, usually at height of fever
- rash: MP begins at forehead which spreads downward
to torso, ext., palms, soles (craniocaudal
dissemination/ centrifugal distribution)
- x7-10d days and fade in the same pattern leaving
fine/branny desquamation
3. recovery – cough lasts longest x 10d
How is measles diagnosed?
Dx:
Always clinical
1. CBC: dec WBC, dec lym<neu
2. Serum measles IgM – (+)1-2d after rash until 1 mo
3. Measkes PCR(+)
4. Warthin-Finkelday giant cells – fusion of infected cells
5. Virus C/S (nasopharynx, urine)
What are the complications of measles?
Complications:
Highest M&M at 5yo (esp <1 yo) and >2 yo
1. PN – most common cause of death (giant cell PN) or
bacterial superinfection (S.pneumonia, S.aureus, HiB)
2. AOM – most common complication
3. Croup, tracheitis, bronchiolitis
4. Febrile sz
5. Encephalitis
6. Subacute sclerosing panecephalitis (SSPE)
- 1-10mos after infection (immunocompromised)
- Sz, myoclonus, stupor, coma
- Nearly always fatal
- Secondary to persistent infection with an altered
measles virus in intracellular CNS
- After 7-13 yrs, attack CNS à inflammation à cell
death à neurodegenerative process
- Risk factors:
a. 20% measles <2yo
b. 75% measles <4yo
- S/Sx:
a. Stage I: behavioral changes, irritability, dec
attention, temper outbursts
b. Stage II: massive myoclonus
c. Stage III: choreoathetosis, immobility,
dystonia, lead pipe rigidity, dec. sensorium,
coma
Dx:
a. S/Sx + CSF measles Ab
b. EEG: suppression-burst episodes
c. Biopsy – show evidence of astrogliosis,
neuronal loss, degeneration of dendrites,
demyelination, neurofibrillary tangles, and
infiltration of inflammatory cells
- Tx: supportive
- Death in 1-3 yrs
7. Hemorrhagic/black measles – hemorrhagic skin
eruptions, fatal
8. Bronchiolitis obliterans – final common PW to an
obliterative outcome
What is the management of measles? how do we prevent measles?
Mgt
1. Supportive
2. Vitamin A – for all pxs
200,000 IU OD x 2 d >12mo
100,000 IU 6-11mo
50,000 IU <6mo
Prevention
- Viral shedding = 7 days after exposure to 4-6 d after
onset of rash
1. Standard and airborne precautions
2. Isolation
3. MMR/measles vax @ 9mos, then at 12-15mos, then 4-
6yo
- Protective of SSPE
- AE: fever, rash (rare) – 6-12d after vax
- PEP if within 72h after exposure
4. IVIG – 0.25ml/kg within 6d after exposure for <6mo,
pregnant, immunocomp
What is the cause of mumps and transmission?
CH 248: MUMPS
- Rubulavirus
Transmission:
- Respiratory droplets
Period of communicability: 1-2 days before to 5 days after
parotid swelling
Incubation period: 16-18 d (12-25d)(2-3w)
What is the pathophysiology of mumps?
Patho
- Virus targets the salivary glands, CNS, pancreas, testes
> thyroid, ovaries, heart, kidneys, liver, joint synovia –>
viral replication at epithelium of URT –> LN spread to
tissues –> necrosis of infected cells and lymphocytic
inflammatory infiltrate
What are the clinical manifestations of mumps?
CM:
1. 1-2 days prodrome of fever, headache, vomiting,
myalgia, then parotitis
2. Parotid swelling and tenderness, peaks in 3d then
gradually subsides over 7d, bilateral (70%)
3. Angle of jaw obscured as swelling ensues and earlobe
lifted upward and outward
4. Edema over the sternum due to lymphatic obstruction
How is mumps diagnosed?
Dx:
Usually clinical
1. CBC – leukopenia with relative lymphocytosis
2. Mumps IgM, IgG
3. Viral culture – gold standard, buccal/oral swab
4. Immunofluorescence – detect viral Ag
5. RT-PCR – samples URT secretions, urine, CSF during
acute phase
6. Elev Serum amylase
What is the management of mumps?
Supportive – antipyretics, pain relief, adequate
hydration
What are the complications of mumps?
Complications
1. Meningitis w/ or w/o encephalitis – most commonly
manifests 5d after parotitis. Sx resolve in 7d
2. Orchitis – 30-40% of postpubertal males. Begins within
days after onset of parotitis, HG fever, chills, exquisite
testicular pain and swelling, B (30%). Sterility is rare
3. Pancreatitis, myocarditis, PN, optic neuritis,
conjunctivitis, nephritis, thrombocytopenia
prevention: MMR vaccine
What is Rubella?
- German Measles/3-day measles
- Togavirus
- Usually pre-school and school-age children
- Epidemiology relative to Rubella vax
What is the pathophysiology of Rubella?
- Virus replicates in the respiratory epithelium then to
regional LN (10-17d) - Viral shedding = 10d after infection to 2 weeks after
rash onset - in fetus: causes tissue necrosis due to vascular
insufficiency, reduced cellular multiplication time,
chromosomal breaks, and production of protein
inhibitor causing mitotic arrests - Chronicity – most distinctive feature. Virus persists
until postpartum
How is rubella transmitted and period of communicability?
Transmission:
- Droplet, respiratory, stool, urine, cervical
- transplacental
Period of communicability: 5 days before to 6 days after rash
onset
Incubation period: 14-21d (2-3wks)
What are the risk factors of rubella?
Risk factor:
1. Pregnant women – most impt for congenital defects
- 1st 8 weeks AOG – most severe and widespread defects
a. <11 wks -90% risk
b. 11-12 wks – 33%
c. 13-14 wks – 11%
d. 15-16 wks -24 %
e. >16 wks – uncommon
- Thus, early infection (1-12 wks) higher risk of
congenital defects and higher risk to fetus
- Pregnant woman develops mononucleosis-like illness
What are the clinical manifestations of rubella?
CM:
1. Prodrome – LG fever (dec in T on D3-4 when rashes
appear), sore throat, red eyes+pain, headache, flu-like
sx, LNE
2. Suboccipital, postauricular, anterior cervical LNE
- Begins 24h before rash & remains for 1 wk
3. Rash – pink macules that spread centrifugally (from
face, neck à torso and ext, discrete x3d. resolves
without desquamation
4. Forchheimer spots – tiny, rose colored spots at soft
palate. Appear at same time as rash
5. No photophobia
How is rubella diagnosed?
Dx:
1. CBC – dec WBC, dec neu, plt
2. Rubella IgM, IgG – 4x increase is diagnostic, taken
before 3 mos old
3. C/S – can be done until 1 yr of illness (nasopharyngeal
swab, conjunctival scrapings, urine, CSF_
4. PCR (+)
5. CSF – encephalitis with inc protein and cell count
What are the complications of Rubella?
Complications
1. Thrombocytopenia
2. Arthritis – after 1 week, fingers
3. Encephalitis – most serious
4. Progressive Rubella Panencephalitis (PRP)– like SSPE
5. GBS, myocarditis, neuritis
What is congenital rubella syndrome?
Congenital Rubella Syndrome (CRS)
CM:
1. Hearing loss/sensorineural deafness – single most
common sx in infants, most common sx
2. IUGR
3. Salt and pepper retinopathy – most common eye sx
4. Cataract – most serious eye sx
5. microphthalmos
6. PDA – most freq heart defect
7. CV: PAS, valvular pulmonic stenosis
8. Interstitial pneumonitis
9. Blueberry muffin rash
10. Meningoencephalitis
11. Psychomotor retardation, MR, speech and language
delay
12. Death
Tx:
1. Supportive
2. IVIG, CS – for severe, non-remitting thrombocytopenia
3. Hearing screening – for early intervention of CRS
Prevention
1. Isolation x7d after rash onset
2. Standard & droplet prec
3. CRS: contact precaution until 1yo (viral secretion in
respiratory secretions)
4. Rubella IgG -for pregnant women; repeated at 2wks, 6
wks
5. MMR/MMRV vax - @12-15mo (#1), then @4-6yo (#2)
- CI: severe immunocomp, pregnancy
- AE: fever, rash
What is roseola infantum? other name?
Enanthem subitum/6th disease
- Human Herpesvirus (HHV)6B, 7
What is the epidemiology of roseola?
Epid:
- Peak age @6-9mos following loss of maternal Ab,
usually <3yo
- Sporadic, (-)seasonal predilection, (-)contact exposure
Transmission:
- Saliva, respiratory droplets
- Vertical transmission = transplacental infection and
chromosomal integration
Communicability: unknown
Incubation period: 9-10d
What are the clinical manifestations of Roseola?
CM
1. Fever – HG (>39.7C) x 3-5d, abrupt, usually acutely
resolves after 72h (“crisis”) or gradually fades over the
day “lysis” coincident with appearance of rash
2. Rash – blanching, MP, faint, pink, nonpruritic on trunk
x 1-3d, evanescent spreading to face and ext.
(centripetal)
3. Pharyngeal injection, palpebral conjunctiva, TM
4. Bulging of anterior fontanelle
5. Suboccipital LNE
6. Nagayama spots – ulcers at uvulopalatal junction
7. Fussiness, irritability
8. Colds, congestion
9. GI sx
10. Encephalopathy, convulsions
Mean duration = 6d (3d fever + 3d rash)
How do we diagnose roseola?
Dx:
Mainly clinical = 3d fever with blanching MP rash in nontoxic 6-
10mo child
1. CBC – dec WBC, lym, neu, plt
2. Elev serum transaminase
3. MRI – hyperintense T2 images at amygdala,
hippocampus, uncus
4. Viral C/S – gold standard
5. PCR
what are the complications of roseola?
Complication
1. Convulsion – most common, peak at 12-15mo
2. Encephalitis, cerebellitis
3. Hepatitis
4. Myocarditis
5. Developmental abN, autism
Tx: supportive
Prognosis: self-limited with complete recovery
What is erythema infectiosum?
- Fifth disease
- Parvovirus B19, bocavirus
- 5-15yo
Transmission:
- Respiratory route via large droplet, blood, blood
products
What is the pathophysiology of erythema infectiosum?
Patho:
- Viral tropism to erythroid cells à dec plt and neu
- Biphasic illness
a. After inoculation, at 7-11d = viremia & viral
shedding. Fever, malaise.
b. @17-18d = rash, arthralgia
Period of communicability of erythema infectiosum?
Communicability = before onset of the rash until after the onset
of rash
Incubation period = 4-28d (ave 16-17d)
What are the clinical manifestations of erythema infectiosum?
CM
1. Benign, self-limited
2. Prodrome – LG fever, headache, URTI
3. Rash = 3 stages:
a. Slapped cheek appearance – erythematous,
facial flushing
b. Rash spread to trunk, ext, diffuse macular
erythema
c. Lacy, reticulated rash, macular, with central
clearing, esp extensors. Sparing palms and
soles. Wax and wane X 1-3w
- Atypical skin eruption: papular-purpuric “gloves &
socks” syndrome (PPGSS), then fever, pruritus, painful
edema & erythema localized to distal extremities,
followed by acral petechiae & oral lesions
How is erythema infectiosum diagnosed?
Mainly clinical
1. CBC – WOF for low Hgb in aplastic crisis
2. Low reticulocyte count
3. B19 IgM – (+) for 6-8wks, recent/acute infection
4. PCR – detectable for 4 months
Management of erythema infectiosum?
Supportive
What are the complications of erythema infectiosum?Epid
- Lifetime risk for zoster 20-30%, >45yo 75%
Complication:
1. Arthralgia, arthritis
2. Transient aplastic crisis – fever (-)rash. Chronic
hemolysis, rapid RBC turnover, severe anemia
3. In pregnant women = miscarriage, intrauterine death
(<5%), hydrops fetalis, bone lesions
a. Most sn period = 2nd trimester
b. No tx
Prevention:
1. Isolation not necessary, rash is postinfectious
What is the epidemiology of Varicella?
Epid
- Lifetime risk for zoster 20-30%, >45yo 75%
- Lifelong latent infection
– > dorsal/sensory ganglia
Period of communicability of varicella?
communicability: 1-2d before rash until vesicles are crusted
usually 3-7d after rash onset
Incubation period: 10-21d (1-3w)
Transmission
- Airborne spread, direct contact with secretions (oral
and skin)
What is the pathophysiology of varicella?
Patho
- Virus inoculated in the URT and tonsillar lymphoid
tissue –> viremia spreads to the RES–> infection in
lungs, liver, brain, etc (chickenpox) –> virus transported
retrogradely through sensory axons to the dorsal root
ganglia of SC –> latent infection (herpes zoster)
What are the clinical manifestations of varicella?
- Chickenpox
- Sx start 14-16d after exposure
- Fever (37.8-41.1C)
- Anorexia, headache
- Mild abdominal pain
- Rash – intensely pruritic erythematous macules to
papules to vesicles at scalp, face, trunk. Simultaneous
presence of lesions at various stages of evolution.
Central/centripetal distribution (most at trunk,
prox.ext)
- Ulcerative mucosal lesions (oropharynx, vagina)
- Complications:
a. Secondary bacterial infection – skin, PN,
sepsis, arthritis
b. Encephalitis & cerebellar ataxia – highest
morbidity <5yo or >20yo
§ Begins 2-6d after rash
c. Meningitis
d. Reye syndrome
e. GN - Herpes zoster
- Vesicular lesions clustered within 1-2 adjacent
dermatomes with pain, hyperesthesia, pruritus, LG
fever
- Usually 1-2 weeks, milder in children
- Complic: Postherpetic neuralgia - Neonatal varicella
- High mortality rate
- Mom with VZV 5 days before delivery to 2 days
afterward are at risk for severe varicella
a. Transmission: transplacental from maternal
viremia.
b. Mom has not yet developed significant Ab
response, infant receives large viral load
w/o maternal Ab
- Mom with VZV >5 days prior to delivery
a. Attenuated infection due to maternal Ab
b. Esp after 30 weeks AOG
a. Rash – 2d to 2nd week of life
b. PN, hepatitis, encephalitis - Congenital/Fetal varicella syndrome (CVS)
- Mom with VZV during 1st half of pregnancy (8th-20th
week)
- <13wks AOG (0.4%)
13-20wks AOG (2%)
- Virus spreads to all fetal organs hematogenously
a. Rash – cicatricial skin scarring, dermatomal
distribution
b. Limb hypoplasia
c. CNS: microcephaly, cortical & SC atrophy,
sz, MR, encephalitis, cerebral calcifications
d. Eye: chorioretinitis, microphthalmia,
cataract, optic atrophy, nystagmus, Horner
syndrome (ptosis, miosis, enophthalmos)
e. Renal: hydroureter, hydronephrosis
f. ANS: neurogenic bladder, swallowing
dysfunction, aspiration PN
g. LBW, PT, IUGR
h. 30% die within first 4 mos
i. High risk to develop zoster in first 2 yrs
j. Pneumonitis
- Dx: PCR
How is varicella diagnosed?
- CBC – dec WBC during 1st 72h of rash, then
lymphocytosis - Elev LFT
- PCR – most sn (fetal blood and amniotic fluid)
- VZV IgG – after 2-3 weeks for chickenpox
a. for CVS, @>7mos or VZV zoster @1yo - cranial UTZ – for CVS, cortical atrophy, dilated
ventricles
What is the management of varicella?
Mgt:
1. Acyclovir – 20mkdose q6h x 5d for:
a. Nonpregnant >12yo
b. On CS tx, ASA
c. Most effective if started within 24h of rash
onset until 72h
d. For herpes zoster – 10mkdose q8 if with
lesions
e. For neonatal varicella
f. Not indicated for CVS, but may be used to
stop progression of eye ds or tx shingles
(first 2 yrs of life)
g. For mother if diagnosed during pregnancy
2. Famciclovir, valacyclovir
3. VZIG or IVIG – severe (PN, hepa, dec plt).
- Given w/in 72-96h of exposure of mother
4. Supportive
5. VarizIg + Acyclovir – for pregnant, immunocomp,
infants after exposure
a. NB of mom with varicella 5 days before to 2
days after delivery
b. PT infant <28wks AOG
What is the prognosis of varicella?
Prognosis:
Death due to PN, CNS, secondary infection, hemorrhage in infants
and adults
