Pediatrics EOR (2026): Infectious Diseases (Smarty PANCE)

What is botulism?

A neuroparalytic illness caused by *Clostridium botulinum* toxin blocking presynaptic acetylcholine release at the neuromuscular junction, producing symmetric descending flaccid paralysis.

What is the most common form of botulism in children?

Infant botulism (intestinal colonization), typically in infants

What is the classic history clue for infant botulism?

Ingestion of honey or exposure to soil/construction dust, though most cases have no identifiable source.

What is the classic clinical presentation of infant botulism?

Constipation first, then poor feeding, weak cry, hypotonia ("floppy baby"), ptosis, sluggish pupils, loss of head control, and descending symmetric flaccid paralysis with intact sensorium and no fever.

How is infant botulism diagnosed?

Detection of botulinum toxin or *C. botulinum* organisms in the stool (mouse bioassay/PCR); EMG may show brief, small, abundant motor unit potentials (BSAP pattern).

What is the treatment for infant botulism?

Human-derived botulism immune globulin IV (BabyBIG) plus supportive care with airway monitoring; antibiotics (especially aminoglycosides) are avoided because bacterial lysis releases more toxin and aminoglycosides potentiate neuromuscular blockade.

Why is honey avoided in infants under 1 year?

Honey may contain *C. botulinum* spores, which can germinate in the immature infant gut lacking protective flora.

What is Group A streptococcal (GAS) infection?

Infection with *Streptococcus pyogenes*, a beta-hemolytic, bacitracin-sensitive gram-positive coccus that causes pharyngitis, impetigo, scarlet fever, cellulitis, and invasive disease in children.

What is the peak age for GAS pharyngitis?

School-age children 5–15 years; it is uncommon under age 3.

What findings suggest GAS pharyngitis rather than viral pharyngitis?

Sudden-onset sore throat, fever, tonsillar exudate, palatal petechiae, tender anterior cervical adenopathy, headache, and abdominal pain — with ABSENCE of cough, coryza, conjunctivitis, hoarseness, and oral ulcers.

What are the Centor/McIsaac criteria components?

Fever >38°C, absence of cough, tender anterior cervical nodes, tonsillar exudate/swelling, plus age points (+1 if 3–14 years, 0 if 15–44, −1 if ≥45).

How is GAS pharyngitis diagnosed in children?

Rapid antigen detection test (RADT); a NEGATIVE RADT in a child must be confirmed with throat culture because of lower sensitivity in pediatrics.

What is the first-line treatment for GAS pharyngitis?

Penicillin V or amoxicillin for 10 days (amoxicillin preferred in children for palatability); a first-generation cephalosporin, azithromycin, or clindamycin for penicillin allergy.

What is scarlet fever?

GAS pharyngitis plus an erythrogenic toxin–mediated sandpaper-like blanching rash beginning on the neck/trunk with circumoral pallor, Pastia lines in skin folds, strawberry tongue, and later desquamation.

Why treat GAS pharyngitis with antibiotics?

To prevent acute rheumatic fever, reduce suppurative complications (peritonsillar abscess, otitis media), shorten symptoms, and decrease transmission; antibiotics do NOT prevent post-streptococcal glomerulonephritis.

When may a child with GAS pharyngitis return to school?

After at least 12–24 hours of appropriate antibiotic therapy and once afebrile.

What is acute rheumatic fever?

A delayed, immune-mediated inflammatory complication of untreated GAS PHARYNGITIS (not skin infection) occurring 2–4 weeks later, affecting the heart, joints, skin, subcutaneous tissue, and CNS.

What is the peak age for acute rheumatic fever?

Children 5–15 years old.

What are the major Jones criteria (mnemonic JONES)?

Joints (migratory polyarthritis), ♥ Carditis, Nodules (subcutaneous), Erythema marginatum, Sydenham chorea.

What are the minor Jones criteria?

Fever, arthralgia, elevated ESR/CRP, and prolonged PR interval on ECG.

How is acute rheumatic fever diagnosed?

Evidence of preceding GAS infection (elevated/rising ASO or anti-DNase B, or positive throat culture/RADT) PLUS 2 major criteria, or 1 major + 2 minor criteria.

What is the most common and most serious manifestation of rheumatic carditis?

Valvulitis — the MITRAL valve is most commonly affected (mitral regurgitation acutely, mitral stenosis chronically); carditis is the only manifestation causing permanent damage.

What is the treatment for acute rheumatic fever?

Penicillin (or amoxicillin) to eradicate GAS, anti-inflammatory therapy with high-dose aspirin (or corticosteroids for severe carditis), and supportive care for heart failure.

What is secondary prophylaxis for acute rheumatic fever?

Long-term intramuscular benzathine penicillin G every 4 weeks (or oral penicillin V) — duration depends on carditis and valve disease, often 10 years or until age 21–40.

What is Sydenham chorea?

A late neurologic manifestation of ARF (up to 1–8 months after infection) with involuntary purposeless movements, emotional lability, and milkmaid's grip; it is a stand-alone major criterion diagnostic of ARF.

What is Group B streptococcal (GBS) infection?

Infection with *Streptococcus agalactiae*, a beta-hemolytic gram-positive coccus that is the leading cause of neonatal sepsis, pneumonia, and meningitis, acquired from maternal genital tract colonization.

When is maternal GBS screening performed?

Rectovaginal culture at 36 0/7 to 37 6/7 weeks gestation.

What are the indications for intrapartum antibiotic prophylaxis (IAP)?

Positive GBS screen, GBS bacteriuria in current pregnancy, previous infant with invasive GBS disease, or unknown status with

What is the intrapartum prophylaxis of choice for GBS?

IV penicillin G (ampicillin alternative), given at least 4 hours before delivery; cefazolin, clindamycin, or vancomycin for penicillin allergy depending on severity and susceptibility.

What distinguishes early-onset from late-onset GBS disease?

Early-onset: 0–6 days of life, vertical transmission, presents with sepsis, pneumonia, and respiratory distress. Late-onset: 7 days to 3 months, presents with bacteremia and MENINGITIS.

What is the empiric treatment of neonatal GBS disease?

Ampicillin plus gentamicin empirically; once GBS confirmed, penicillin G — treat 10 days for bacteremia and 14–21 days for meningitis.

Does intrapartum prophylaxis prevent late-onset GBS disease?

No — IAP prevents early-onset disease only.

What is pertussis?

A highly contagious respiratory infection caused by *Bordetella pertussis*, a gram-negative coccobacillus, characterized by paroxysmal coughing ("whooping cough") that can be life-threatening in infants.

What are the three stages of pertussis?

Catarrhal (1–2 weeks, URI symptoms, MOST contagious), paroxysmal (2–6 weeks, coughing fits with inspiratory whoop and post-tussive emesis), and convalescent (weeks to months of gradually resolving cough).

How does pertussis present differently in young infants?

Infants

What laboratory finding is characteristic of pertussis in infants and young children?

Marked lymphocytosis (absolute lymphocyte count often >10,000/µL); extreme leukocytosis (>50,000) predicts severe disease and death.

How is pertussis diagnosed?

Nasopharyngeal PCR is the test of choice (most sensitive in first 3–4 weeks); culture is specific but slow; serology is useful in later disease.

What is the treatment for pertussis?

Macrolides — azithromycin is preferred in infants

Who should receive pertussis post-exposure prophylaxis?

All household and close contacts regardless of immunization status, using the same macrolide regimen as treatment.

How is pertussis prevented in newborns?

Maternal Tdap during EVERY pregnancy at 27–36 weeks gestation, DTaP series in infants beginning at 2 months, and "cocooning" of close contacts.

What are congenital (TORCH) infections?

A group of vertically transmitted maternal infections — Toxoplasmosis, Other (syphilis, varicella, parvovirus B19, HIV, Zika), Rubella, CMV, and HSV — that cause overlapping patterns of fetal loss, growth restriction, and multi-organ neonatal disease.

What is the MOST COMMON congenital infection in the United States?

Congenital cytomegalovirus (CMV).

What is the classic triad of congenital toxoplasmosis?

Chorioretinitis, DIFFUSE intracranial calcifications, and hydrocephalus (associated with maternal exposure to cat feces or undercooked meat).

What findings suggest congenital CMV?

Sensorineural hearing loss (most common sequela), PERIVENTRICULAR intracranial calcifications, microcephaly, petechial "blueberry muffin" rash, hepatosplenomegaly, and jaundice; treat symptomatic infants with valganciclovir.

What is the classic triad of congenital rubella syndrome?

Sensorineural deafness, cataracts, and cardiac defects (patent ductus arteriosus and peripheral pulmonary artery stenosis), with "blueberry muffin" rash.

What findings suggest congenital syphilis?

Snuffles (rhinitis), maculopapular rash involving palms and soles, hepatosplenomegaly, and long-bone metaphyseal lucencies; late findings include Hutchinson teeth, saddle nose, and saber shins — treat with penicillin G.

What are the findings of congenital varicella syndrome?

Cicatricial limb scarring in a dermatomal pattern, limb hypoplasia, cortical atrophy, and chorioretinitis after maternal varicella in the first 20 weeks.

What does congenital parvovirus B19 cause?

Fetal anemia leading to nonimmune hydrops fetalis and intrauterine fetal demise.

How is neonatal HSV acquired and how does it present?

Usually intrapartum from maternal genital lesions; presents in three forms — skin/eye/mouth (SEM), CNS disease (seizures, lethargy at 2–3 weeks), and disseminated disease (sepsis-like, hepatitis, DIC); treat with high-dose IV acyclovir.

What is fever in the infant?

A rectal temperature ≥38.0°C (100.4°F) in an infant ≤60 days of age, which is a medical emergency because immature immunity and unreliable exam make serious bacterial infection difficult to exclude clinically.

What is the ONLY acceptable way to measure temperature in a young infant?

Rectal temperature — axillary, temporal, and tympanic measurements are unreliable in this age group.

What are the most common pathogens causing serious bacterial infection in febrile neonates?

*E. coli* (most common overall, especially UTI), Group B *Streptococcus*, and *Listeria monocytogenes*; HSV must also be considered.

What is the most common serious bacterial infection in febrile infants?

Urinary tract infection.

What is the standard workup for a febrile infant ≤28 days old?

Full sepsis evaluation — CBC with differential, blood culture, inflammatory markers (procalcitonin, CRP), catheterized urinalysis and urine culture, and lumbar puncture with CSF studies; admit and give empiric parenteral antibiotics.

What is the empiric antibiotic regimen for a febrile neonate ≤28 days?

Ampicillin plus either gentamicin or cefotaxime/ceftazidime; add IV acyclovir if HSV is suspected (maternal lesions, vesicles, seizures, hypothermia, transaminitis, CSF pleocytosis).

How does management differ for a well-appearing febrile infant 29–60 days old?

Risk stratification using inflammatory markers (procalcitonin, CRP, ANC) may permit omission of LP and outpatient management with close follow-up if all markers are normal and urinalysis is negative; any ill appearance mandates full evaluation and admission.

What is fever without a source?

Acute fever (

What age group is classically considered for "fever without a source" risk stratification?

Infants and young children 3–36 months of age.

What is occult bacteremia and how has its epidemiology changed?

Bacteremia in a well-appearing febrile child without an identifiable focus; its incidence has fallen dramatically since routine *H. influenzae* type b and pneumococcal conjugate vaccination — most fever without a source is now viral.

What is the most important diagnostic test in a well-appearing, fully immunized child 3–36 months with fever without a source?

Urinalysis and urine culture — UTI is the most common occult serious bacterial infection, especially in girls

What features increase concern for serious bacterial infection in fever without a source?

Ill or toxic appearance, temperature ≥39°C, incomplete immunization, immunocompromise, prolonged fever, and abnormal inflammatory markers.

What is the management of a well-appearing, fully immunized 3–36 month old with fever without a source?

Urinalysis/urine culture as indicated, antipyretics for comfort, and close outpatient follow-up in 24–48 hours; routine empiric antibiotics and reflexive blood cultures are NOT recommended.

What is fever of unknown origin (FUO) in children?

Fever >38.0–38.3°C documented on multiple occasions for at least 8–14 days (definitions vary) without an identified cause after an initial thorough history, physical examination, and preliminary evaluation.

What are the three broad categories of pediatric FUO?

Infectious (most common in children), autoimmune/inflammatory (e.g., systemic JIA, IBD, Kawasaki disease), and malignancy (leukemia, lymphoma, neuroblastoma).

What are the most common infectious causes of pediatric FUO?

Epstein–Barr virus, CMV, cat-scratch disease (*Bartonella henselae*), osteomyelitis, urinary tract infection, tuberculosis, and endemic zoonoses.

What historical clues are essential in evaluating pediatric FUO?

Travel, animal and tick exposures, unpasteurized foods, sick contacts, tuberculosis exposure, medications (drug fever), family history of periodic fever, and ethnic background.

What is the initial laboratory evaluation for pediatric FUO?

CBC with differential and smear, ESR/CRP, blood and urine cultures, comprehensive metabolic panel with LFTs, LDH and uric acid, EBV/CMV serologies, HIV testing, tuberculin skin test or IGRA, and chest radiograph.

What is the general management approach to pediatric FUO?

Serial reassessment with a stepwise, hypothesis-driven workup; avoid empiric antibiotics or steroids in a stable child because they obscure the diagnosis. Most pediatric FUO resolves without a diagnosis or represents an atypical presentation of a common disease.

What are pediatric fungal infections?

Infections caused by yeasts, dermatophytes, or dimorphic fungi, ranging from superficial skin and mucosal disease in healthy children to invasive disease in neonates and immunocompromised hosts.

What is oral thrush and how is it treated?

*Candida albicans* infection of the oral mucosa causing adherent white plaques that DO NOT scrape off easily (leaving erythema/bleeding when removed); treat with oral nystatin suspension or fluconazole.

What causes Candida diaper dermatitis and how is it distinguished from irritant dermatitis?

*Candida albicans*; it produces beefy-red confluent plaques with SATELLITE lesions and INVOLVES the skin folds, whereas irritant dermatitis SPARES the creases; treat with topical nystatin or clotrimazole.

What is tinea capitis and how is it treated?

Dermatophyte infection of the scalp (usually *Trichophyton tonsurans*) causing scaly patches with alopecia, black dots, and occipital adenopathy; it requires ORAL griseofulvin or terbinafine — topical therapy is inadequate.

What is a kerion?

A boggy, tender, inflammatory mass of the scalp representing a hypersensitivity reaction to tinea capitis; it is often mistaken for a bacterial abscess but requires systemic antifungal therapy.

What is tinea corporis and how is it treated?

Dermatophyte infection of the body causing annular, scaly plaques with raised borders and central clearing ("ringworm"); treat with topical antifungals such as clotrimazole or terbinafine.

What is tinea versicolor?

Superficial infection with *Malassezia* species causing hypopigmented or hyperpigmented scaly macules on the trunk, most common in adolescents; KOH prep shows a "spaghetti and meatballs" pattern; treat with topical selenium sulfide or ketoconazole.

What is pinworm infection (enterobiasis)?

Intestinal infection with the nematode *Enterobius vermicularis*, the most common helminth infection in U.S. children, spread by the fecal–oral route.

What is the classic presentation of pinworm infection?

Nocturnal perianal pruritus causing sleep disturbance and irritability; girls may develop vulvovaginitis and secondary excoriation or bacterial infection.

Why does perianal itching occur at night with pinworms?

The gravid female worm migrates out of the anus at night to deposit eggs on the perianal skin.

How is pinworm infection diagnosed?

The "tape test" — transparent adhesive tape pressed to the perianal skin in the early morning before bathing or defecation, examined microscopically for characteristic ova; stool O&P is usually negative.

What is the treatment for pinworm infection?

Albendazole, mebendazole, or pyrantel pamoate as a single dose, REPEATED in 2 weeks to kill newly hatched worms.

Why should household contacts be treated for pinworms?

Reinfection and asymptomatic carriage are common; simultaneous treatment of all household members plus laundering of bedding and clothing prevents recurrence.

What is pediatric sepsis?

Life-threatening organ dysfunction caused by a dysregulated host response to infection; septic shock is sepsis with cardiovascular dysfunction requiring vasoactive support or with persistent hypoperfusion despite fluid resuscitation.

How does pediatric septic shock differ from adult septic shock?

Children most often present with COLD shock (low cardiac output, high SVR — cool extremities, delayed capillary refill, narrow pulse pressure), whereas adults typically show warm vasodilated shock; children compensate with tachycardia, and HYPOTENSION IS A LATE AND OMINOUS SIGN.

What is the earliest and most sensitive vital sign abnormality in pediatric sepsis?

Tachycardia (with tachypnea); altered mental status and prolonged capillary refill are key perfusion clues.

What are the components of the first hour ("golden hour") sepsis bundle in children?

Obtain blood cultures and lactate, give broad-spectrum IV/IO antibiotics within 1 hour, administer rapid isotonic crystalloid boluses (20 mL/kg, up to 40–60 mL/kg titrated to perfusion), and start vasoactive agents if fluid-refractory.

What is the first-line vasoactive agent in fluid-refractory pediatric septic shock?

Epinephrine (preferred for cold shock); norepinephrine is preferred for warm/vasodilated shock. Dopamine is a second-line option.

What must be considered in a child with fluid- and catecholamine-refractory shock?

Adrenal insufficiency — give stress-dose hydrocortisone; also evaluate for obstructive causes such as tamponade or pneumothorax.

What is multisystem inflammatory syndrome in children (MIS-C)?

A hyperinflammatory, post-infectious syndrome occurring 2–6 weeks after SARS-CoV-2 infection, characterized by fever, multiorgan involvement, elevated inflammatory markers, and no alternative diagnosis.

What is the typical age and presentation of MIS-C?

School-age children (median 8–9 years) with persistent fever, prominent GASTROINTESTINAL symptoms (abdominal pain, vomiting, diarrhea), rash, conjunctivitis, mucocutaneous changes, and shock.

How does MIS-C differ from Kawasaki disease?

MIS-C occurs in older children, has more prominent GI symptoms, more frequent myocardial dysfunction and shock, and characteristic LYMPHOPENIA, THROMBOCYTOPENIA, and markedly elevated ferritin, BNP, and troponin; Kawasaki disease typically affects children

What laboratory findings support MIS-C?

Markedly elevated CRP, ESR, ferritin, D-dimer, procalcitonin, BNP/NT-proBNP, and troponin, with lymphopenia, thrombocytopenia, hypoalbuminemia, and hyponatremia; positive SARS-CoV-2 PCR, antigen, serology, or known exposure is required.

What cardiac complications occur in MIS-C?

Ventricular dysfunction, myocarditis, arrhythmias, valvular regurgitation, and coronary artery dilation/aneurysms — echocardiography is mandatory.

What is the treatment for MIS-C?

IVIG plus systemic glucocorticoids, with biologics (anakinra, infliximab) for refractory disease; low-dose aspirin for coronary/thrombotic risk and supportive ICU care for shock.

What are pediatric sexually transmitted infections?

Infections transmitted through sexual contact, seen in sexually active adolescents and — importantly — as a red flag for SEXUAL ABUSE in prepubertal children.

Which STIs in a prepubertal child are diagnostic of sexual abuse until proven otherwise?

Gonorrhea, syphilis, chlamydia (beyond the perinatal period), HIV (non-perinatal), and *Trichomonas* — all require mandatory reporting and child protective services involvement.

What is the current treatment for uncomplicated gonorrhea in adolescents?

Ceftriaxone 500 mg IM as a single dose (1 g if ≥150 kg); treat for chlamydia with doxycycline 100 mg BID x 7 days if chlamydia is not excluded.

What is the treatment for chlamydia in adolescents?

Doxycycline 100 mg twice daily for 7 days (azithromycin 1 g single dose is an alternative, and is preferred in pregnancy).

What causes neonatal conjunctivitis and how is the timing distinguished?

Chemical (silver nitrate) within 24 hours; GONOCOCCAL at 2–5 days (purulent, sight-threatening — treat with IM/IV ceftriaxone); CHLAMYDIAL at 5–14 days (treat with ORAL erythromycin, which also prevents chlamydial pneumonia at 4–12 weeks).

Who should be screened for STIs in pediatrics?

All sexually active adolescent females and males who have sex with males should be screened annually for chlamydia and gonorrhea; HIV screening is recommended at least once for all adolescents 15–18 years.

What causes trichomoniasis and how is it treated?

*Trichomonas vaginalis*, presenting with frothy, malodorous yellow-green discharge and a "strawberry cervix"; treat with metronidazole (7-day course preferred in women).