PEDIATRIC INFECTIONS
DISEASES
Pediatric Exanthems
Dr. JOHN SRAGOWICZ
2008
PA-C, MPAS
History
Detailed history:
Recent travel
Woodland exposure
Drug ingestion
ILL contacts
Medical history
History
Rash details: macular, papular, petecchia
blister, vesicular, reticulate
Distribution: acral, palmoplantar, unilateral, truncal
Direction of spread: centripetal, centrifugal,
cephalocaudal
Pruritus
Relationship of rash and fever
Oral or topical therapies
Physical Examination
Identify primary lesion and presence of secondary
lesions
Thorough physical examination essential to
accurate diagnosis
Etiology: Viral, Bacterial, Rickettsial,
Fungal, Drug-induced
Laboratory Data
Serologic tests not often helpful in acute
setting
Aspirates, scrapings and pustular fluid may
be obtained
The exanthematous diseases of childhood were named according to the
order in which they were reported:
First disease: Measles (Rubeola)
Second disease: Scarlet fever
Third disease: German measles (rubella)
Fourth disease: Duke’s Filatow disease (possible a scarlet fever variant)
Fifth disease: Erythema infecciosum
Sixth disease: Roseola, Erythema subitum
Rubella (German measles)
Etiology: Is a Togavirus, a single stranded RNA virus
Transmission:
• Humans are the only host.
• via infected respiratory droplets, where it replicates in the respiratory tract, and
viremia follows 5-7 days
• Infected patients shed the virus 7 days prior to the exanthem to 7 days after.
• They are contagious during the exanthem period
• Transplacental transmission during viremia (first 16 weeks of pregnancy)
deafness, cataracts, heart problems, and CNS abnormalities
• Late winter – early spring
• Incubation period: 14-21 days
Rubella (German measles)
Prodomal symptoms:
Uncommon in children, mainly in Adolescents:
Low fever, HA/malaise 1- 4 days, mild pharyngitis,
Lymphadenopathy: Post-auricular, occipital
Forschheimer’s spots – petechiae papules on soft palate before rash
Exanthem:
Eruption generalized within 24-48 hours
Fine Pink (erythematous) maculopapules with discrete lesions
Start in face/neck progressing in a cephalocaudal fashion
By 3rd day: Rash starts to fade in 3 days, signaling end of the viremia
Rash on face disappeared
Only extremities are involved
Rash may disappear by end of 3rd day
No desquamation
Milder, more evanescent rash
Others signs:
Often transient polyarthralgia, polyarthritis, more in teens
Rubella (German measles)
LAB: Isolation from nasopharinx
Serologic studies: presence of anti-rubella-specific IGM (pregnancy)
Elisa: rise of IgG antibody
Treatment: Supportive
Prevention: MMR Vaccine 12-15 months
4-6 years
Not indicated in pregnant women.
Avoid pregnancy for 3 months after vaccination
Rubeola (Measles-First Disease)
Highly contagious disease characterized by enanthem and exanthem
Etiology:
Paramyxovirus virus, an RNA virus
Rare in developing countries due to universal immunization
Happens in Third world countries where can be fatal to malnourished children
Transmission:
Humans are the natural host and reservoir of the virus.
Spread by respiratory droplets, primary replication of the virus occurs in the respiratory
epithelial cells, where it replicates, later spreading to to the local lymphnodes, and then to
the blood, resulting in a viremia
Incubation period: 10-21 days with average of 14 days
Late winter – early spring
Rubeola (measles)
Prodrome: high fever (104F), malaise, anorexia followed by URI sx
Three C’s: cough, coryza, conjunctivitis (exsudative, photophobia)
Exanthem:
Appearance of macular-papular (confluent) rash on or about 3th febrile day
(coincides with peak of fever)
Rash first of face/neck (hairline) with a cephalocaudal progression; fades in 5days
Mild desquamation and brown staining of skin follow the rash
Enanthem:
Koplic Spots: White-Gray dots on erythematous buccal mucosa
Seen 2 days before and 2 days after the rash appears
Appears at: buccal mucosa opposite the lower molars
Measles – United States, 1950-2002
Cases (thousands)
900
800
Vaccine Licensed
700
600
500
400
300
200
100
0
1950
1960
1970
1980
1990
2000
Measles – United States, 1980-2002
30000
25000
Cases
20000
15000
10000
5000
0
1980
1985
1990
1995
2000
Measles with Bronchopneumonia
Koplick spots
LAB:
-Nasopharinx culture
-CBC: leukopenia and lymphocytosis
-Rise in measles specific-antibody titers (IgM)
-CSF in suspected encephalitis: Increased protein, Normal glucose
Predominance of lymphocytes
TX:
Supportive
MMR vaccine 12-15 months, 4-6 years. Current vaccine 95% effective,
Immunoglobulin (up to 6 days after exposure)
Complications:
Otitis media
Pneumonia: Interstitial Pneumonitis
BCP 2ary to bacterial infection
Encephalitis 1/1000 cases
KAWASAKY DISEASE
Is a febrile mucocutaneous lymph node syndrome.
Systemic vasculitis with devastating cardiac sequelae
Etiology:
The exact cause is unknown.
It is an immune-mediated disorder in a genetically predisposed child
Epidemiology:
Disease of young children, mainly boys
Most of patients (80%) are less than 5 years of age, average 2-3 years
If child is older than 5 years old doubt the diagnosis
Most common in Asians than whites, and least in blacks
Most common in winter. Suspect of cases during spring months
Pathogenesis:
An unknown superantigen result in heavy cytokine release, being
responsible for the multiple clinical findings.
Clinical Features:
Acute phase: Last 7-14 days.
Presence of 4/5 of the following:
Fever- 104F/39C averaging 5-10 days. Can persist up to 4 weeks
Conjunctivitis- Dry eyes with dilated vessels (bulbar). Non purulent, non
edema, non tearing, bilateral.
Changes in oral mucosa: red strawberry tongue, pharyngeal erythema,
dry red and cracked lip
Extremity changes: edema hand/feet, erythema of palms/ sole precedes
desquamation of fingers on palm and soles.
The rash is erythematous, maculo-papular or morbiliform, scarlatiniform,
non vesicular, affecting the groin and perineum .
occurs on the trunk 3 days after fever. Also over buttocks
Cervical lymphadenopathy: At least 1 node measuring 1.5 cms . The node
is unilateral, nontender / nonsuppurative
Subacute Phase:
From day 14 to 25:
- Decrease of fever.
-Arthralgias occurs involving large and small joints.
-Giant and painless skin desquamation occurs around day 14, in the fingertips,
palms, soles, perineal areas (groin)!!!
Convalescent Phase:
Begins in day 21-60:
- In this phase, coronary artery aneurysms are detected by Echo
- Arthritis may persist, but other Sx subside.
- Beau Line in fingernails
- Observe signs of cardiac insufficiency: Fatigue, chest pain, DOE
- Control with weekly ECG.
LAB:
WBC: elevated with left shift. Greater than 20.000 in 50% of cases
ESR:
Increased. Often greater than 40/50mm or more
CRP:
Elevated, above 3mg/dL
Albumin 3g/dL or less
Platelet count: Increase after the 1st week of illness.
U/A: 10 wbc/hpf, Pyuria, proteinuria
Elevation of alanine aminotransferase
ECG: acute phase- prolonged PR interval, Flat T waves, ST changes
CX-Ray: May show dilated heart during acute phase
ECHO: Detection of aneurysm. Strict ECHO follow-up.
DD: Scarlet- Throat CX Positive, Increase ASO Titer
Measles- Increase IgG, IgM Titer
EBV, TOXO, CMV- Saliva, U/A, Titers
TX:
Bed Rest until 72 hours without fever
IVIG: Intravenous Immunoglobulin- 2g/kg one time over 10 hs
Repeat to patients who fail to response the first shot.
Aspirin:
80-100 mg/kg/d in divided dosis, for 10 days, or until child 48 hours afebrile
3-10 mg/kg/d for 6-8 weeks after fever resolves or until platelets count returns to normal
Descontinue if patient has varicella or Influenza
Steroids: controversial
Complications: coronary artery dilatation and aneurysms
VARICELLA-ZOSTER (CHICKEN-POX)
Highly contagious disease caused by Varicella-zoster virus: member of herpes virus family,
a double-stranded DNA viruses causing varicella as a primary infection, or a recurrent
infection (Shingles).
Humans are the only source of infection
Transmission:
Contact with respiratory secretions, lesion fluid, airborne spread
Primary infection occurs in the nasopharinx through droplet inoculation.
Local replication starts in the nasopharinx, causing viremia and dissemination by
circulating mononuclear cells
Epidemiology:
Varicella affects the preschool and school children (5-10 years)
Seen more during late winter and early spring
Transplacental transmission- newborn can develop varicella if mother
contracted the disease 5 days before delivery
Incubation period: 10-21 days, average 12-14 days
Clinical Features:
Disease is preceded by fever, malaise, and URI symptoms.
Skin Eruption:
Centripetal distribution (lesions more on torso than face/extremities)
Lesions can be seen on scalp and mucous membranes
Lesions go through several stages: Papules, Vesicles, Pustules, Crust
Classic Lesion: vesicle surrounded by erythema described as a “dew
drop on a rose petal”
Different types of lesions can be seen together in the same area.
Eruption last 5-7 days
Infectivity:
Most contagious: 1-2 days before and 7 days after the onset of rash.
Lesions are infected until they have turned into dried crust
Lab: Tzanc test:
+ presence of multinucleated giant cells, with epithelial cell degeneration.
Viral culture from a new vesicle
TX:
Acyclovir 80mg/kg/d in 4/5 doses in immunocompromised patients .
NEVER give ASPIRIN due to the association with REYE Syndrome.
Active Immunization:
Varivax: 1 dose between 1-13 y, 2 doses after 13 y with 1-2 months apart.
Is contraindicated in persons with hypersensitivity to gelatin or neomycin.
Passive Immunization:
Varicella-Zoster Immune globulin (VZIG):
Immunocompromised children
Neonates whose mothers get varicella 5 days or less before delivery or within 48 hours after
delivery
Complications: 2ary Skin infection, Cellulitis, abscesses ( Staph, strept ), BCP
fever, soreness on site of injection, varicella rash
Varicella-zoster virus

Neonatal chickenpox
 Delivery within one week before or after
the onset of maternal varicella – often
severe

Congenital varicella syndrome
 25% of fetuses infected – not always
significant
 6-20 weeks gestation – 2% VZV
embryopathy
 Affect limbs, eyes, skin, and brain

Progressive varicella – visceral organ
involvement
HERPES ZOSTER – SHINGLES
Is an acute vesico-pustular eruption that occurs in a dermatomal distribution.
Etiology: Varicella-zoster virus, an Herpesvirus
Incubation period: 1-3 weeks
Pathogenesis:
- HZ is the localized recurrence of a VZ virus infection
- There is a past history of varicella
- The virus is reactivated after lying dormant in a sensory dorsal root ganglion
- Precipitating factors include: - Lowered host immunity
- Radiation/chemo therapy
- Physical trauma or emotional stress
- Poor nutrition, fatigue
- An infant may develop HZ if mother had varicella during pregnancy
CLINICAL FEATURES :
Skin Lesions:
-First SX: Elevated rash group vesicles on an erythematous base that form blisters, and
later they form scabs resembling Varicella.
Blisters disappear in 2 weeks, but pain can continue.
- Eruption is preceded by severe pain, itching, redness, tingling , hyperesthesia
-In severe cases, rash can leave permanent scars, long standing pain
(post-herpetic neuralgia, numbness, and skin discoloration).
- Linear distribution
- Site: Along one or two dermatomes supplied by a spinal or cranial nerve
Most common Involved Dermatomes:
- Those supplied by thoracic spinal nerves (thorax) T-3/L-2
- Ophthalmic Branch of the Trigeminal nerve (forehead)
LAB: Tzank smear
Treatment: Acyclovir , Valaclovir
2Y girl with HZ on C-4/C-5 dermatome
8 months with HZ on C-5/C-6 dermatome
Neurocutaneous pathway on
the trunk
HZ in the T-1 dermatome
HERPES SIMPLEX
Caused by the Herpes-virus hominis, which consists of 2 related viruses:
Herpes simplex virus type 1 (HSV-1) / Herpes simplex virus type-2 (HSV-2)
produce infections involving mucocutaneous surfaces, the CNS.
Epidemiology:
Seen in children/adolescents of all ages
Spread through Direct Mucocutaneous contact ( potential exposure to HSV from sexual or
other close contact (kissing, sharing of glasses, etc)
Transmission result from:
contact with persons with active ulcerative lesions
persons without clinical manifestations of infection who are shedding HSV
Pathogenesis:
Exposure to HSV at mucosal surfaces or abraded skin sites permits entry of the virus and
initiation of its replication in cells of the epidermis and dermis.
On entry into the neuronal cell, the virus is transported to the nerve cell bodies in ganglia,
where the virus remains dormant in a sensory ganglion and dorsal root ganglia
Latent virus may be reactivated and viral replication cycle occurs in ganglia and contiguous
neural tissue.
Virus then spreads to other mucosal skin surfaces through centrifugal migration of
infectious virions via peripheral sensory nerves.
Stimuli that have been observed to be associated with the reactivation of latent HSV have
included stress, menstruation, and exposure to ultraviolet light.
Clinical features:
Herpetic Gingivostomatitis (herpes labialis):
•Caused by HSV-1.
•MC form of HSV primary infection in children
•Most common age: 1-3 years of age
•Infection of the pharynx usually results in exsudative or ulcerative
lesions of the posterior pharynx and/or tonsillar pillars.
•Lesions begins as vesicles, forming Ulcers (painful, bleed easy)
•Fever very high lasting from 2 to 7 days
•Sites: Lesions involve the hard and soft palate, lip, gums and facial area
Lesions of the tongue, buccal mucosa, or gingiva may occur later
in the course in one-third of case
•Cervical lymphadenopathy
•Inability to eat or drink, malaise, myalgias, irritability, Foul breath
•Self limited illness, resolves in 5-7 days
Herpetic Dermatitis:
•Caused by HSV-1
•Herpetic Whitlow
HSV infection of the finger—may occur as a complication by inoculation of virus through a
break in the epidermal surface or by direct introduction of virus into the hand through
occupational or some other type of exposure.
Signs and symptoms include the abrupt onset of edema, erythema, and localized tenderness
of the infected finger. V esicular or pustular lesions on the fingertip. Fever, lymphadenitis,
epitrochlear and axillary lymphadenopathy
•Herpes Gladiatorum
HSV may infect almost any area of skin.
Mucocutaneous HSV infections of the thorax, ears, face, and hands have been described
among wrestlers.
Transmission of these infections is facilitated by trauma to the skin sustained during
wrestling.
Herpetic Vulvovaginitis:
Caused by HSV-2
Genital herpes is characterized by fever, headache, malaise, and myalgias.
Pain, itching, dysuria, vaginal and urethral discharge, and tender inguinal lymphadenopathy
are the predominant local symptoms.
Lesions may be present in varying stages, including vesicles,
pustules, or painful erythematous ulcers.
The cervix and urethra are involved in >80% of women with first-episode infections.
May result from sexual abuse
LAB:
Molecular techniques are the gold standard.
Tzanck test (Giemsa): + test: presence of multinucleated giant cells, degeneration of
epithelial cells
HSV infection is best confirmed in the lab by isolation of the virus in tissue culture or by
demonstration of HSV antigens or DNA in scrapings from lesions.
Spin-amplified culture with subsequent staining for HSV antigen has shortened the time
needed to identify HSV to <24 h.
PCR is being used for the detection of HSV DNA
TX: Supportive therapy: antipyretics, diet (cold drinks, soft diet, popsicles
Acyclovir, Valacyclovir, Famciclovir (act on viral replication, causing
chain termination of the viral DNA
topical vidarabine, and cidofovir
Idoxuridine ophtalmic drops when lesions are near the eye
Roseola
It is an acute infection of infants characterized by a rash that appears after 3-4 days of high
fever
AKA: exanthem subitum, roseola subitum, sixth Ds
Etiology: Human herpes virus 6 or 7, double stranded DNA virus
Self-limited benign disease
Epidemiology: Affects 6 months to 36 months infants. Peak 6-7 months
Incubation period 7-15 days
Transmission: Saliva, airbone
Lab: Serology: Anti-HHV-6 IgM, Anti-HHV-7 IgM
Polymerase chain reaction of HHV-6 DNA
Complication: Febrile seizures during the prodromal stage
TX: Supportive
Clinical features:
Incubation period 7-15 days
Sudden onset of fever lasting 1-6 days, average of 4 days ( high as 40.0 C)
Infant looks well
Mild irritability despite fevers
Exam: reveal cervical adenopathy (posterior cervical & occipital)
tonsillar, pharyngeal and TM erythematous
1/3 with diarrhea & vomiting
Bulging anterior fontanel in 26% of patients
Rash:
Appears after Temp. drops suddenly on 4th – 5th day (defervescence)
Rarely rash appears before fever has subsided completely
Diffuse blanching pink morbiliform maculopapules rash
Distribution on Trunk, Neck, Extremities, spares the face
It last hours to 2-3 days
Clears without any pigmentation or desquamation
Nagayama spots: erythematous papules on the soft palate and uvula
ROSEOLA
Erythema infectiosum (fifth disease)
Etiology:
Human Parvovirus B-19
Smallest human DNA virus (single strand of DNA)
Epidemiology:
Occurs in all children age, most common on school age children
Rare in African-American children
Common in late winter and early spring
When rash appears, child is not contagious.
Transmission: Respiratory secretions
Transplacental (higher risk at second trimester)
Lab: Serology for IgM andIgGantibodies via radiommunoassy or Elisa.
IgM is present at time of rash and lasts 2-3 months. IgG once present lasts several
years and confers future immunity
Complications: Arthralgyas, Fetal hydrops in pregnants,
anemia with low Reticulocytes ( aplastic crises)
TX: Supportive
Clinical features:
Incubation period: 4 - 18 days
Primarily children between 3 to 15 years of age
Mild prodrome: Fever, coryza, malaise are minimal for 3 days before rash
Arthralgias, arthritis in about 10%.
Three stages of Rash:
1- Slapped cheek appearance (1-4 days)
2- Erythematous papular eruption over upper and lower extremities spreading to trunk,
assuming a lacy evanescent reticular appearance as it fades (lasts 4 days)
3- Evanescent stage: Rash typically resolves in 5-10 days although may
wax & wane for weeks or months.
Is precipitated by: Hot showers, vigorous exercise, sunlight
4-Papular Purpuric Gloves and Socks syndrome (only hands and feet affected)
Parvovirus B-19, usually teenagers, lasts 7-14 days. Fever, rash and arthralgias.
Rash is contagious at the time of eruption, presenting acral painful or pruritic palpable
purpura mainly at ankle and wrists. Also presents symmetric swelling of digits,and oral
petecchia and erosions, pharingeal erythema and edematous lips.
Hand, Foot and Mouth Disease
Etiology: Coxsackie-virus A -16, A-5, A-6, A-10 & B-3
Epidemiology: Highly contagious, airborne spread
Bi-modal: late summer, and early fall
Children < 5 yrs (1-4 years)
Clinical features:
Incubation: Up to 7 days
Malaise, fever, lymphadenopathy
Vesicular lesions in Mouth, Hand, Feet, Buttocks lasting 7-10 days
Rash:
Mouth lesions: Oval gray-yellowish vesicles( ulcers) with erythematous
borders in palate, tongue, lips, buccal mucosa, buttocks
Painful causing anorexia, dehydration
Skin lesions: Gray-White/Erythematous macules, papules, vesicles
on the hands, feet , soles, buttocks
Distributed bilaterally and symmetrically
Lab: Viral culture from vesicle, Nasopharinx
TX: Supportive care, self-limited within 2 weeks.
B19
MUMPS-PAROTITIS
Systemic ds. characterized by swelling of the salivary glands specially the
parotid gland
Etiology: Is caused by a Paramyxovirus, an RNA
Bacterial cases 2ary to Staphylococcus. (suppurative parotitis)
Epidemiology: 5-15 years. Declined due to the MMR.
Mumps Ds. gives lifelong immunity
Pathogenesis:
- Humans are the only natural hosts for this virus
- Acquired by direct contact with saliva or resp. dropplets of infected person
-
Virus enters through the mouth and nostrils, replicating in the URT and lymphanodes,
later the viremia spreads to salivary glands. Also gonads, pancreas, meninges
Clinical Signs:
Incubation of 16-21 days
Contagiosity:
1-3 days before, to 7 days after the onset of parotid swelling
Children return to school, 10 days after onset of parotid swelling
Starts with fever, headache, malaise.
Onset of mumps is pain and non-erythematous swelling in front and below the ear
obscuring the mandibular ramus (ear displaced outward, upward)
Swelling starts with one ear and then progresses to the other ear
Often submaxillar and sublingual glands are also swollen
Low grade fever and intense parotid pain when chewing
Inflammation of the opening of Stensen duct in mouth
Complications:
Meningitis: Most frequent. Asseptic meningitis
Pancreatitis: mild inflammation is present
Epididymoorchitis: Adolescents, young adults. Develops 4-10 days within
the onset of the parotid swelling (testicular pain/swelling)
LAB:
Uncomplicated Parotitis: Leukopenia with lymphocytosis
Suppurative parotitis/orchitis: leukocytosis
Pancreas Involvement: Hyperamilasemia / Hyperlipasemia
Meningitis: CSF pleocytosis (mainly mononuclear)
Body fluid isolation of mumps virus in tissue culture
TX:
Rest, Bland diet, Buccal hygiene, Atb if suppurative parotitis, MMR, Tylenol/Motrin.
INFECTIOUS MONONUCLEOSIS
Lymphoproliferative self-limited disease caused by the Epstein-Barr virus.
Etiology: EBV, a DNA virus, belongs to the Herpes group virus
Epidemiology:
Occurs in all age groups, predominates in adolescents (intimacy period)
and young adults. Mild cases can be seen in children
Incubation: 30-50 days
EBV spreads via respiratory droplets, coughing, kissing
Pathophysiology:
EBV replicates in oropharingeal epithelium
Selective infection of B-lymphocytes occurs, resulting in proliferation of
cells in tonsils, lymph nodes, spleen
Clinical Features:
Incubation period of 30-50 days
Low grade fever, sore throat, coryza, malaise,
Exsudative pharyngitis (50%) with palatal petecchia
Associated GABS pharingytis (25%)
Cervical Lymphadenopathy- Enlarged, usually nontender
Hepatomegaly
Splenomegaly: moderate enlargement (50%)
Skin rash: Seen in 10-15%. Increase to 40% if penicillin derivatives is used
Morbiliform or scarlanitiform.
CNS features: Encephalitis, asseptic meningitis, Guillain-Barre syndrome
Classic illness is characterized by:
fatigue, low grade fever, malaise, tonsillopharyngitis (often exsudative)
adenopathy, HSplenomegaly (may persist for months)
LAB:
CBC:
> 10% of atypical lymphocytes (greater than 50% lymphocytes), Leukocytosis
Liver enzymes: Mild hepatitis is found, jaundice is rare
EBV serology:
Elisa (Monospot): rapid slide agglutinin test for heterophile antibodies:
Often negative in children under 5 years old
Detects 90% of cases in adolescents
Anti-VCA IgG/IgM (viral capsid antigen) recent/past infection
EBNA: Ebstein Barr Nuclear Antigen- positive means no latent infection
1st antibody: IgM VCA- positive 2-3 week of infection. Wanes in 2-4 weeks
2nd antibody: IgG VCA- positive in 2nd to 4th week of infection
3rd antibody: EA- Present during EBV replication.
4th antibody: EBNA- Presence coincides with recovery. Rises beyond 6 weeks
Complications:
Dehydration (due to severe pharyngitis)
- Streptococcal pharyngitis: 25% G-A strep infection
- Atb induced rash: morbiliforme. After use of ampicillin or amoxicillin
-Splenic rupture  hemorrhage  shock death. Rupture occurs
between 4th /21th day after onset of symptoms.
- Chronic fatigue syndrome
- Hepatitis frequently accompanies IM. High liver enzymes, hepatomegaly
TX:
Supportive care (fluids, acetoaminophen, rest)
Prednisone 1mg/kg/d bid. Reduce swelling of spleen, lymphnodes,
airway obstruction
No contact sports until 6 weeks have passed after resolution of Sx
Return to full activity average 1month, fatigue may persist for 3-4 months
-
ROCKY MOUNTAIN SPOTTED FEVER (RMSF)
Etiology: Is Rickettsia rickettsii, transmitted by those vectors:
- Dog tick: Dermacentor variabilis
(east)
- Wood tick: Dermacentor andersoni (west)
- Lone star tick: Amblyomma americanum (southwest)
Epidemiology: Endemic in Southeastern, Central, Rocky mountain states.
More common in children (5-9y), and in the summer
Pathophysiology:
Transmitted mainly by a tick bite, airborne droplets
Incubation period; 2-14 days, average 7 days
After exposure:
Rickettsia multiply in the endothelial lining and smooth muscle cells of blood vessels.
- Disseminates via bloodstream, producing a generalized vasculitis associated with a
centripetal petecchial rash and fever
-
Clinical features:
Incubation period: 1 week
Tick must attach and feed for 4-6 hours to transmit disease.
Abrupt or gradual onset of fever, more than 40-C, not responding to meds
Abrupt onset of Headache: intense, frontal, retrobulbar
Myalgia (calf or thigh), abdominal pain, confusion, photophobia, vomiting
Rash:
Usually appears by 2nd or 3rd day after fever onset.
Rash is small, irregular, erythematous macules that blanch, becoming maculopapular and
petecchial ( rose to purpuric) spreading centrally
Starts from wrists, ankles. (periphery)
Whitin hours spreads centrally from extremities toward trunk, neck, face.
Can appear in palms and soles and scrotum
Can progress to necrosis of toes, ears, scrotum, nose, fingers.
Also: CNS, Cardiac, Pulmonary, GI, Ocular symptoms
Prognosis:
Improvement in 24-36 hours
Defervescence in 2-3 days
Majority improve in less than 1 week if treated early.
TX:
Supportive care ( avoid tick areas, pants inside boots, repellants, gloves
hydration support, Platelets for thrombocytopenia
Doxycycline: 2.2mg/kg BID PO 1 day. Then qd for 7-10days
Tetracycline: 25-50mg/kg/d PO qd or 20-30mg/kg/d IV
Chloramfenicol is an alternate drug
LAB:
CBC: WBC normal or low first 4 days. Later, leukocytosis, ↑ band count
anemia, thrombocytopenia ( consumptive coagulopathy)
CMP, LFT: abnormal, DIC screen, CXR, ABG, EKG, Echo, Lytes: Hyponatremia
CSF: Clear, with/ without ↑ protein. Pleiocytosis and ↑ protein in 1/3 of cases
ELISA: sensitive and accurate, but it takes about 6 days (seroconversion)
IFA: Indirect Fluorescent antibody- sensitivity 94-100%, specificity 100%
IHA: Indirect Hemagglutination: sensitivity 91-100%, specificity 99%
LA: latex agglutination-sensitivity 71-94%, specificity 99%
PCR by DNA: takes 48 hours.
Weil-Felix: 3-5 minutes. Poor specificity and insensitive. Titer 1:160 suspect
SCARLET FEVER
Etiology: Group A Beta-hemolytic streptococcus strain (Streptococcus pyogenes) that
produces erythrotoxigenic toxins
Epidemiology: Occur in children between 2-10 years old
Most cases seen in winter and early spring
Pathogenesis: Oropharinx is the portal of entry to airborne droplets where it replicates.
Complications: Acute glomerulonephritis, Rheumatic fever
LAB: CBC, Rapid strept antigen test, Throath Cx, Dick test not in use
Treatment: Supportive, rest
Oral or IM Penicillin or derivatives
Erythromycin / Clindamycin if allergic to Penicillin
Clinical Features:
Incubation period: 2- 4 days. Average 1- 7 days
Prodomal symptoms: fever, sore throat, malaise, myalgia, HA, abd. Pain
Mouth:
Pharinx, tonsils are beefy red, and may have exsudate
Hemorrhagic spots on anterior pillar of tonsils and palate (petecchia)
Large, tender anterior cervical nodes
Tongue: white coat with edematous red papilla. The coat desquamate and
reveals a swollen, red and a strawberry aspect of tongue
Face: Malar flush with Circumoral pallor present
Pastia line’s: Deep red non blanching lesions in the antecubital area
RASH:
Starts 12-48 hours after onset of fever.
fine maculopapular, sandpaper texture, on erythematous background.
Affect neck, axilla, shoulders, most prominent in trunk, groin
Blanches when pressure is applied.
Skin desquamates within 7-21 days from onset of illness, starting with hands.
PERTUSSIS- WHOOPING COUGH
Is a life threatening infection in very young infants
Etiology: Bordetella pertussis, a gram negative
Epidemiology:
Disease of young infants, children, and adolescents
Infection via respiratory droplets, direct contact with nasal secretions
Pathophysiology:
Replicates only in association with ciliated epithelium, causing congestion, inflammation of
the bronchi
LAB:
Culture of Bordetella by nasopharyngeal culture is the standard test.
Direct immunofluorescent assay of nasopharyngeal secretions
TX:
Isolation, Supportive (hydration, sucction secretions, humidified oxygen)
Erythromycin for 14 days. 50mg/kg/d divided 4 doses , Zythromax
Corticoids is questionable.
Prevention: Immunization DTaP (fade after 5-10 y), Boostrix/Adacel (10-18 y)
Clinical features: Incubation period of 7-14 days (4-21 days)
3 stages:
Catarrhal:
Last 1-2 weeks
URI symptoms, low grade or absent fever, mild cough, coryza
Highly communicable during this stage and the first 3 weeks after cough
Paroxysmal:
Last 2- 6 weeks
Salvo of paroxysmal cough ending with an inspiratory whoop through narrowed glottis
during the forceful inspiratory phase with accumulation of a thick airway secretion
Presence: petecchia, subconjuntival hemorrhage, cyanosis, eyelid edema
Convalescent:
Last 1-3 weeks
Cough lessens and disappears or cough can persist for several weeks
Lung auscultation is normal, unless atelectasis or pneumonia occurred
Complications: Pneumonia (90%), atelectasis, subcutaneous emphysema
LYME DISEASE
Etiology: spirochete Borrelia burgdorferi transmitted by a deer tick, Ixodes
dammini. Deer tick is flat, small, 8 legs, male is black, female is red/black.
According to a specialized California laboratory, 20% of patients with Lyme are coinfected with Anaplasma, Babesia or Erlichia
Epidemiology: Affect people from all ages, 1/3 are children, adolescent.
late spring/early summer months in Northeast, North Central, Pacific states
Pathophysiology:
Borrelia is injected into the skin with the saliva of the deer tick.
Then migrate within the skin, forming a rash (erythema chronicum migrans).
Rash starts as red macule or papule and expands to an annular lesion up to 30 cm
in diameter with partial central clearing.
Then the spirochete is spread hematogeneously to heart, joints and CNS.
Complications: Chronic arthritis in 10% (pauciarticular)
Clinical Features:
Stage I- Localized Ds:
May begin within hours to several weeks after infection.
Rash (erythema chronicum migrans) starts as red macule or papule, and 8 days
after the tick bite, it expands to an annular lesion up to 30 cm in diameter with
partial central clearing. Can be painful, burning, fever, regional adenopathy
Stage II-Disseminated Ds:
Occurs weeks to months following the tick bite
Characterized by neurologic and cardiac involvement .
Malaise, high fever, myalgias, headache
Neurologic signs (aseptic meningitis, Bell’s palsy , Guillain-Barre like Ds.
Arthritis affecting large joints (knee).
Joint fluid mainly neutrophil. WBC up to 110.000 cells
Cardiac signs ( AV block mc) pericarditis, miocarditis
Stage IIICan develop within a few weeks to 2 years following infection
Most common symptom is arthritis, intermittent, lasting several days to weeks
Late Lyme disease can affect central nervous system
Patients may have memory loss, fatigue and polyneuropathy
LAB: Lyme Titer:
ELISA- develops 3-4 weeks after infection begins
Western blot Test: More specific test, confirmatory test.
Negative western blot and a positive Elisa: no Lyme Ds.
Western Blot positive test: confirms a positive Elisa result
Skin biopsy: positive direct immunofluorescence provides a rapid test
IgG/IgM Titers will remain elevated for months/years, after the treatment.
TX: Amoxicillin 250mg tid for 30 days for under 8/9 years old
Amoxicillin 500mg tid for 30 days if over 9 years old
Doxycycline 100mg bid for 30 days if over 9 years old
Eythromycin 30mg/kg/day for 30 days
Patients with only a rash: treat for 14 days
Severe arthritis or carditis: Ceftriaxone or PCN IV 14-21 days
GONOCOCCAL INFECTION
Etiology: Neisseria gonorrhea, G- diplococcus
Epidemiology: Seen in the following groups of children:
Newborn infants: acquired from the infected maternal vaginal canal
Prepubertal children: as a result of sexual abuse
Adolescents: as a result of sexual abuse or voluntary sexual activity
Males: 15/19 20/24 years
Female: 15/19 years
Incubation period is 2-7 days
LAB:
Gram stain: G – intracellular paired organisms
Culture in Thayer-Martin medium or chocolate agar of specimens taken
from the eyes, vagina, cervix, penis, anus, throat
STD panel: HIV, Chlamydia, Syphilis, Trichomonas
Synovial fluid culture is positive in 50% with Gonococcal Bacteremia
Clinical features:
Newborn: Ophtalmia neonatorum.
Appear 2-5 days after delivery. Bilateral discharge that becomes muco-purulent
with/without streaks of blood. Conjunctiva and Lid is edematous. Corneal ulcer,
blindness if not treated early
Sexually abused children:
copious purulent discharge from vagina/penis. other sites: Rectum, throat
Disseminated gonococcal infection: Is a gonococcal bacteremia.
Cervical motion tenderness:
Characteristic on pelvic examination in patients with ascending cervical infection
Urethritis:
Copious mucoid purulent discharge after exposure, often bloodstained
Micturition is painful, associated with urine retention.
The persistent inflammation predisposes to a urethral stricture.
Proctitis may be present in homosexuals
Complications:
Blindness, meningitis, Inf. endocarditis, osteomyelitis, PID
Arthritis-Dermatitis syndrome:
Seen in > 90% of cases
May be migratory
Associated pain/ swelling of big joints (knees, ankles, wrists, elbows),
Tenosynovitis
Rash:
In Disseminated Gonococcal Infection cases: 50-75% of cases.
petecchial or pustural lesions appear on distal extremity, 3-21 days after
exposure, together with arthralgias, septic arthritis, fever, chills, malaise
Tx:
Neonate:
Hospitalize after cultures: blood, spinal fluid, eye, urine.
Ophtalmia neonatorum
Ceftriaxone single dose 25/50mg/kg IV-IM up to 125mg given once
Eye care: sterile saline irrigation at frequent intervals
Prophylaxis: 1% silver nitrate or 0,5% erythromycin ointment
Non-disseminated:
Ceftriaxone single dose of 125mg IM and
Erythromycin or Zythromax for prepubertal children.
Doxycyclin or Zythromax for children older than 8 years old (presumption of
having Chlamydia)
Disseminated gonococcal infection:
Hospitalize
Ceftriaxone 25/50mg/kg IV-IM daily/7 days
Cefotaxime 50-100 mg IV-IM in two doses for 7 days.
Continue for 14 days if meningitis is present
Erythromycin, Zythromax, Doxycyclin, PO (presumption of having Chlamydia)
Intracellular diplococci
Urethritis
Gonococcal rash
SYPHILIS
Etiology: Treponema pallidum, a spirochete
Epidemiology:
Occurs in sexually active adolescents and adults
May result from sexual abuse in children
Spread: sexual contact with ulcerative lesions of skin/ mucous membrane from
one infected individual to another non infected individual
LAB:
Non treponemal antibody test: VDRL, RPR: rapid plasma reagin
Treponemal antibody test:
Confirmatory test of diagnosis of syphilis infection. Once infected, stays +
FTA-ABS (fluorescent treponemal antibody)+ MHA-TP (microagglutination assay
for antibody to treponema pallidum
CSF: neurosyphilis- mononuclear pleocytosis, ↑ protein, normal glucose
Dark-Field microscopy of smears from skin/ mucous membranes lesions
X-R: Long Bones- metaphyseal osteochondritis and/or diaphyseal periostitis
Chest: fluffy difuse infiltration in pneumonia alba
Clinical Feature:
Incubation period: 3 weeks (range 10-90 days)
Primary Stage: Chancre-Primary Syphilis
Last 1-6 weeks.
Solitary, painless, indurated, ulcerated lesion on genitalia
This lesion represents the site of inoculation
Painless inguinal adenopathy
Secondary Stage: Secondary Syphilis
Last 2-10 weeks
Flu-like illness: fever, malaise, myalgia, HA, Arthralgias, adenopathy
Moth eaten Alopecia in beard, scalp, eyelashes
mucous patches: on tongue, mouth, look superficial erosions, but papules can be
seen. Are round, oval, serpiginous in outline and red color or covered with a
greyish membrane. Serpiginous lesions are called snail track ulcers.
Rash: Erythematous maculopapular squamous lesions on torso, palms, soles
Condyloma Lata: whitish, moist, anal condyloma lata lesions are highly infectious
wart like lesions distributed mainly in the anogenital area
Subclinical latent stage:
Diagnosed by presence of reactive sorologic test. Lasts 1-40 years
Late stage (Tertiary Syphilis):
seen in 1/3 of patients many years after the 1ary/2ary stage.
Gummas or granulomatous lesions develop subcutaneously, expand and
ulcerate in the skin. They can also appear in the liver, bones, brain, etc…
cutaneous, visceral, CV, CNS (neurosyphilis, gummatous lesions) death
TX:
Syphilis less than 1 year duration:
Benzathine penicillin G: 50,000 U/kg IM in a single dose. Up to 2,400.000 U
Erythromycin 50mg/kg PO QID, 2 weeks
Tetracycline 500mg PO QID, 2 weeks in patients over 9 years old
Doxycycline 100mg PO BID for 2 weeks in patients over 9 years old
Syphilis greater than 1 year duration:
Benzathine Penicillin G 50,000 U/kg IM weekly, for 3 consecutives weeks
Tetracycline 500mg PO QID, 4 weeks in patients over 9 years old
Doxycycline 100mg PO BID, 4 weeks in patients over 9 years old
NeuroSyphilis:
Aqueous Penicillin G 200,000/300,000 U/kg/d. Not exceed 24 million units day
divided in q4 or q6 for 10-14 days
All cases should be reported to the health department
CONGENITAL SYPHILIS
Intrauterine infection by fetus from a mother infected with Treponema Pallidum
Etiology: Treponema pallidum, a spirochete
Epidemiology:
Associated with lack of prenatal care, and illicit drug use
Lab: Non-treponemal test on cord blood: VDRL, RPR
Confirmatory test: treponemal test FTA-ABS
Darkfield microscopy of skin/membranes lesion
X-ray of long bones
CSF fluid exam: Pleocytosis, ↑ protein, VDRL +
Complications: Stillbirth, Blindness, Deformities (saber shin, saddle nose)
TX: Aqueous crystalline penicillin G: 100,000/150.000 U/kg/d IV 2/3X, 14d
Procaine penicillin G: 50,000 U/kg IM daily, 10-14 days
3 weeks tx, if CNS is involved
Clinical features:
Early congenital Syphilis < 2 years of age
Clinical signs absent or minimal
Rhinitis (snuffles): mucopurulent , profuse discharge
May result in rhagades or fissures around mouth
Cutaneous eruptions: Erythematous macules or papules, or papulosquamous
lesions, round or oval in shape. Lesions fade to coppery brown color.
Vesicobullous hemorrhagic lesions, palmo-plantar scaling
Late congenital Syphilis > 2 years of age
Interstitial keratitis: appears between 6-14 years, corneal opacity, pain,
photophobia, lacrimation
Hutchinson teeth: notching of biting surface of upper central incisors
8th nerve deafness
Saber shins
Higoumenaki sign (unilateral tickening of inner clavicle)
Syphilitic arthritis (8-15 years)
Gummas in bones
Meningococcemia
Gram negative diplococcus
Colonization of nasopharynx 2-30%
Disseminated into blood stream – inflammatory reaction and endotoxin
production leads to organ necrosis
Fever and occult bacteremia to sepsis and death
Often presents with malaise, pharyngitis, fever
Prompt hospitalization, blood and CSF culture
Penicillin G (ceftriaxone and cefotaxime)
Mortality 8-13%
Complications: Tissue necrosis and gangrene,
meningitis, purpura fulminans
JUAN SRAGOWICZ PA-C, MPAS
Meningitis
Viral - 80% due to enterovirus,
most common in summer or fall,
spontaneous remission and no sequelae
Clinical
Bacterial –
Sudden onset and rapidly progressive with shock, purpura, disseminated
intravascular coagulation
fever, poor feeding,
signs of increased intracranial pressure – meningeal irritation, nuchal
rigidity, headache, emesis, bulging faontanel, diastasis (widening of the
sutures), occulomotor paraslysis, back pain (Kernigs and Brudzinski
signs)
Seizures in 30% of patients, alterations in consciousness
Dx: CSF analysis and culture (blood cx often positive)
WBC
Protein
Glucose
Normal
Age dependent
20-45
>50% of serum
Acute
bacterial
Elevated
Increased
Decreased
Partially
treated
Nl or increased
Increased
Nl or decreased
Viral
Increased,
rarely >1000
Mild elevation
Treatment:
Start antibiotics after lumbar puncture (signs of shock start immediately)
Empiric therapy – ceftriaxone or cefotaxime
+/- vancomycin until culture and sensitivities prove
Strep pneumonia - if uncomplicated Penicillin or cephalosporins 10/14 d.
N. meningitidis 5-7 days iv PCN
Partially treated - cx neg. Third generation cephalosporin for 7-10 days
Corticosteroids – Rapidly killing of bacteria by antibiotics can release toxic
products – massive inflamation
Corticosteroids (Dexamethasone) esp H. influenzae
Prognosis:
Mortality 1-8%
Severe neurodevelopmental sequelae 10-20%
50% with some subtle neurobehavioral morbidity
Complications:
SIADH – hyponatremia
Stroke
Seizures
Cerebellar or cerebral herniation
Mental retardation
Language delay
Behavioral problem
Visual impairment
Cranial nerve palsy
sensorineural hearing loss
Prevention
Neisseria meningitidis:
Chemoprophylaxis for all close contacts (household, day care, hospital workers in
contact with body secretions):
Rifampim
Vaccination – not all serotypes, poor response children<2 yrs
H. influenzae vaccination
Prevnar – Streptococcus pneumoniae
Influenza

Viral infection causing a broad range of respiratory symptoms

Animal reservoir: Antigenic drift – minor changes
Antigenic shift – major changes

Annual spread from Asia to N. America

Novel (serologically distinct) virus enters the population, have potential for pandemic
(1918 flu killed >20 million)

More often - small yearly variations in the antigenic
composition causing localized epidemics

Mortality primarily in elderly and chronically ill
Influenza

High attack rate - 30%

Clinically
 Predominatly respiratory:
Coryza, conjuntivitis, pharyngitis, cough
Fever, malaise, headache, myalgia

Complications: Secondary bacterial otitis media and pneumonia

Less common: acute myositis, myocarditis
Diagnosis: Influenza A+B test
Viral Culture

Treatment
 Oseltamivir, Zanamivir – prophylaxis and treatment if given in first 48 hrs

Fluids and rest, no salicylates
Influenza

Vaccination
 Children 6 months or older in chronic care facilities with pulmonary or
cardiovascular disease

Asthma

Chronic metabolic disease (diabetes)

Renal dysfunction

Hemoglobinopathies (sickle cell)

Immunosuppressed

On long term aspirin therapy

Pregnant women in 2nd or 3rd trimester during season

Health care workers who may transmit the illness to a high risk population