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CATEGORY	HIGH-YIELD FACTS
Risk Factors	Unvaccinated or incompletely vaccinated status is the whole story. Children and young adults in communities with low coverage, people born in countries without a routine rubella program, international travelers, migrants, healthcare personnel, military recruits and university students in crowded housing. Late winter and early spring clustering. For congenital disease: a pregnant woman with no documented immunity, most dangerously in the first trimester.
Etiology	Rubella virus, an enveloped positive-sense single-stranded RNA virus, genus Rubivirus, family Matonaviridae (reclassified out of Togaviridae). Humans are the only reservoir. Spread by respiratory droplets and direct contact with nasopharyngeal secretions, and transplacentally during maternal viremia.
Patient Presentation	A child or young adult who is well enough to be at the clinic rather than in bed, with low-grade fever and a pink rash that started on the face and moved down, plus sore lumps behind the ears. In adolescent and adult women the chief complaint is often joint pain in the hands and wrists as the rash fades. Around a quarter to a half of infections cause no rash at all. In the newborn: failed hearing screen, a murmur, cataract, or purpura at birth.
Classic Physical Exam	Tender postauricular, suboccipital and posterior cervical lymphadenopathy, often preceding the rash by up to a week. Fine pink maculopapular exanthem, non-confluent, face to trunk to extremities within 24 hours, clearing in the same order by day 3 with no desquamation. Forchheimer spots (pinpoint palatal petechiae) in about 20 percent. Mild conjunctivitis without photophobia. The patient does not look toxic.
Key Diagnostic Results	Positive rubella IgM drawn at least 5 days after rash onset, or a $\geq 4\times$ rise in IgG on paired sera 2 to 3 weeks apart. RT-PCR of a throat or nasopharyngeal swab from 2 days before to 4 days after rash onset. Low IgG avidity indicates infection within about 3 months. Congenital disease: infant IgM, infant IgG that persists past 6 to 12 months, or RT-PCR of nasopharynx, urine or lens aspirate. Support: leukopenia, thrombocytopenia, atypical lymphocytes.
Management	No antiviral. Supportive care with paracetamol, and an NSAID for arthritis. Droplet precautions and isolation until 7 days after rash onset, plus notification to public health. Susceptible exposed pregnant woman: serology and gestational-age counselling, not vaccine. Prevention is the testable point: two doses of live attenuated measles-mumps-rubella or measles-rubella vaccine, and postpartum vaccination before discharge for a seronegative mother.
Keywords	three-day measles, German measles, tender postauricular nodes, suboccipital lymphadenopathy, Forchheimer spots, craniocaudal spread, non-confluent pink rash, arthritis in a young woman, blueberry muffin baby, patent ductus arteriosus, peripheral pulmonary artery stenosis, salt and pepper retinopathy, congenital cataract, sensorineural deafness, celery stalk metaphysis, first trimester, no immunity documented

01 Pathophysiology

Rubella is inhaled as a droplet and replicates first in the nasopharyngeal epithelium, then drains into the lymphoid tissue immediately behind it. That anatomy is the reason the exam keeps describing the same three node groups. The postauricular, suboccipital and posterior cervical nodes are the regional drainage basin of the posterior scalp and nasopharynx, so they enlarge and become tender while the virus is still confined locally. This is why lymphadenopathy precedes the rash by up to a week and is the single most useful physical finding: it is present before there is anything to see on the skin.

After roughly 5 to 7 days of local replication a primary viremia carries virus to the reticuloendothelial system, and a secondary viremia seeds the skin, the synovium and, in a pregnant patient, the placenta. Peak shedding from the nasopharynx occurs around the time the rash appears, which is why the contagious window runs from about 7 days before to 7 days after rash onset. Exposure history in a vignette is usually placed inside that window on purpose.

The exanthem itself is not a cytopathic lesion. It appears exactly as neutralizing antibody becomes detectable and viremia is being cleared, so the rash is immune-mediated, driven by immune complex deposition and a cell-mediated response in dermal vessels. That mechanism explains its character: sparse, fine, pink, non-confluent, and gone in three days without desquamation. Compare this with measles, where the rash is a more intense endothelial infection and therefore becomes confluent, lasts five or six days, and leaves brownish staining and fine peeling. The same immune complex mechanism deposited in synovium produces the polyarthralgia and polyarthritis of adolescent and adult women, affecting up to 70 percent of them, beginning as the rash fades and resolving over 2 to 4 weeks.

Congenital disease works by a different mechanism, and this is where most of the testable content lives. During maternal viremia the virus infects the placenta and reaches fetal endothelium. Rubella is not primarily lytic in the fetus. Instead it establishes persistent, non-cytolytic infection that inhibits mitosis and causes focal apoptosis and endothelial necrosis. The result is a fetus built from too few cells and supplied by damaged vessels, which is why congenital rubella produces hypoplastic organs, symmetric growth restriction and vascular malformations rather than the destructive necrosis and calcification seen with cytomegalovirus or toxoplasmosis.

Because the injury is a block on cell division, the defect you get is determined by which organ is dividing at the moment of infection. The lens vesicle detaches and completes its critical growth by about week 7, so cataract only occurs when infection happens before that point. The cochlea and organ of Corti differentiate through the first and early second trimester, so deafness has the widest window and is therefore the commonest single defect. The ductus arteriosus and pulmonary arteries depend on endothelium that the virus damages directly, giving the characteristic patent ductus arteriosus and peripheral pulmonary artery stenosis. Marrow suppression with compensatory dermal extramedullary hematopoiesis produces the purple non-blanching papules known as the blueberry muffin rash. Persistent infection also injures pancreatic islets and thyroid, which is why type 1 diabetes and thyroid disease appear years later.

One consequence of persistent infection deserves its own sentence, because it is a classic infection control question: an infant with congenital rubella keeps shedding virus in urine and nasopharyngeal secretions for months, and is treated as infectious until 1 year of age unless two specimens taken a month apart are negative.

02 Classification and Clinical Manifestation

Rubella splits cleanly into acquired (postnatal) infection, which is a benign illness with an important complication profile in adults, and congenital infection, which is the reason the disease is still notifiable.

ACQUIRED RUBELLA BY STAGE

STAGE	TIMING	FEATURES
Incubation	12 to 23 days, average 17	Asymptomatic. Virus replicating in nasopharynx and regional nodes
Lymphadenopathy	Begins up to 7 days before rash, persists 1 to 2 weeks	Tender postauricular, suboccipital and posterior cervical nodes. The earliest reliable sign and the highest-yield exam finding
Prodrome	1 to 5 days before rash	Low-grade fever usually under 38.5 C, malaise, sore throat, headache, mild non-purulent conjunctivitis without photophobia. Frequently absent in young children, who present with rash as the first sign
Exanthem	Day 0 to day 3	Fine pink maculopapular rash beginning on the face, generalizing within 24 hours, non-confluent, clearing in the order it appeared, no desquamation
Enanthem	With the rash	Forchheimer spots: pinpoint petechiae on the soft palate in about 20 percent. Suggestive but not diagnostic, and also seen in scarlet fever
Convalescence	After day 3	Rash gone. Arthralgia and arthritis often begin here, particularly in adolescent and adult women
Subclinical infection	Any time	25 to 50 percent of infections produce no rash, yet the person is fully contagious. This is how a susceptible pregnant contact gets infected by someone who never looked ill

COMPLICATION SPECTRUM OF ACQUIRED RUBELLA

PATTERN	WHO GETS IT	KEY FEATURES
Uncomplicated	Most children	Three-day rash, mild fever, complete recovery. No treatment beyond comfort measures
Arthralgia and arthritis	Up to 70 percent of adult and adolescent women, uncommon in men and children	Symmetric, small joints of hands and wrists plus knees, starts as the rash fades, self-limited over 2 to 4 weeks. Also follows vaccination in a small minority
Thrombocytopenic purpura	About 1 in 3,000, more often children and girls	Petechiae, epistaxis, gastrointestinal bleeding. Post-infectious and usually self-limited over weeks to months
Encephalitis	About 1 in 6,000, more often adults	Headache, seizures, altered consciousness within a week of the rash. The complication with the highest mortality
Progressive rubella panencephalitis	Very rare, second decade after congenital or acquired infection	Progressive dementia, ataxia, seizures, myoclonus. The rubella counterpart of subacute sclerosing panencephalitis after measles
Myocarditis, hepatitis, Guillain-Barre syndrome	Rare	Reported but not commonly tested

CONGENITAL RUBELLA SYNDROME: DEFECT CATEGORIES

CATEGORY	DEFECTS	NOTE
Category A (cardinal)	Cataracts, congenital glaucoma, congenital heart disease (most often patent ductus arteriosus or peripheral pulmonary artery stenosis), sensorineural hearing loss, pigmentary "salt and pepper" retinopathy	Two Category A findings, or one Category A plus one Category B, meet the probable case definition
Category B (supporting)	Purpura (blueberry muffin lesions), hepatosplenomegaly, jaundice, microcephaly, developmental delay, meningoencephalitis, radiolucent bone disease with "celery stalk" metaphyses	These are the transient and neurologic findings that accompany the cardinal defects
Classic triad	Sensorineural deafness, cataracts, cardiac defects	Deafness is the single commonest defect and may be the only one present
Late-onset and delayed	Type 1 diabetes mellitus, thyroid dysfunction, growth hormone deficiency, late-onset or progressive hearing loss, progressive rubella panencephalitis	Appears in childhood through the second and third decades. A normal newborn examination does not exclude late disease
Congenital rubella infection without syndrome	Laboratory evidence of infection with no compatible defect	Still infectious, still needs isolation precautions and follow-up hearing tests

GESTATIONAL TIMING DETERMINES THE DEFECT

MATERNAL INFECTION	RISK OF DEFECTS	DEFECTS EXPECTED
Before conception	Negligible	None attributable
Under 8 weeks	85 to 90 percent	Full syndrome: cataract, cardiac defects, deafness, growth restriction
9 to 12 weeks	About 50 percent	Deafness and cardiac defects. Cataract becomes unlikely after the lens has formed at roughly week 7
13 to 16 weeks	About 16 to 20 percent	Sensorineural deafness, sometimes retinopathy
17 to 20 weeks	Low	Isolated, often mild sensorineural deafness
After 20 weeks	Minimal	Growth restriction only. Structural defects are not expected

Read the gestational age in the stem before you read anything else. A vignette that gives "6 weeks pregnant" and one that gives "26 weeks pregnant" are asking two different questions with two different correct answers, even when every other word is identical.

03 Diagnostic Workup

TEST	PURPOSE	WHEN TO ORDER
Rubella IgM, serum enzyme immunoassay	Best initial test for acute acquired infection	Draw at least 5 days after rash onset, when over 90 percent of true cases are positive. On the day of rash only about half are positive, so repeat a negative result
Paired rubella IgG, acute and convalescent	Confirms acute infection by a $\geq 4\times$ rise in titer	Second sample 2 to 3 weeks after the first. Use when IgM is equivocal, negative but drawn early, or when a false positive is suspected
Rubella IgG avidity index	Separates recent from remote infection	Positive or equivocal IgM in a pregnant patient. Low avidity indicates infection within roughly the last 3 months, high avidity indicates past infection or vaccination
RT-PCR, throat or nasopharyngeal swab	Most accurate confirmation. Detects viral RNA and permits genotyping for outbreak tracing	From 2 days before to 4 days after rash onset, ideally within the first 3 days. Urine and oral fluid are acceptable alternatives
Viral culture	Historical reference standard	Reference laboratory and outbreak investigation only. Too slow for clinical decisions
Rubella IgG alone	Documents immunity, not acute infection	Preconception counselling, first prenatal visit, healthcare personnel onboarding, after exposure in a person with no vaccination record
Infant serum IgM	Best initial test for congenital rubella syndrome	Any newborn with compatible defects. IgM does not cross the placenta, so a positive result is the infant's own. Repeat at 1 month if negative and suspicion is high
Serial infant IgG titers	Confirms congenital infection when IgM is negative	Maternal IgG decays with a half-life of about 30 days and should be gone by 6 to 12 months. IgG that persists or rises past that point is the infant's own antibody
RT-PCR of infant nasopharynx, urine, cerebrospinal fluid, lens aspirate	Confirms congenital infection, genotypes the virus, and defines infectivity	At diagnosis, and repeated to document clearance before relaxing isolation
Amniotic fluid RT-PCR	Confirms fetal infection after confirmed maternal infection	Only after 21 weeks gestation and at least 6 weeks after maternal infection. Sensitivity falls below 86 percent when drawn earlier
Serial fetal ultrasound	Detects growth restriction, cardiac defects, microcephaly, hepatosplenomegaly	Throughout pregnancy after confirmed maternal infection. A normal scan does not exclude deafness
Complete blood count	Supportive only, never diagnostic	Leukopenia, thrombocytopenia and atypical lymphocytes are common and are distractors, not answers
Newborn hearing screen and formal audiology	Detects the commonest defect	At birth and repeated through childhood in any infant with congenital infection, because hearing loss can be late-onset

Start from the principle that rubella cannot be diagnosed clinically with enough confidence to act on. The rash is nonspecific, half of infections have no rash at all, and the consequence of a missed case is a congenital infection in someone else's pregnancy. Every suspected case therefore gets laboratory confirmation, and every suspected case is notified to public health.

The best initial test in acquired disease is serum rubella IgM, because it is fast, widely available, and positive in over 90 percent of true cases when the sample is drawn at least 5 days after rash onset. The timing is the tested detail: on the day the rash appears only around half of true cases are IgM positive, so a negative IgM drawn on day 0 or day 1 does not exclude rubella and the correct next step is to repeat it, not to abandon the diagnosis. IgM remains detectable for up to about 3 months.

The most accurate confirmation is detection of viral RNA by RT-PCR from a throat or nasopharyngeal swab, which also yields the genotype that public health laboratories need to link cases and prove elimination has not been lost. Its own timing constraint mirrors the biology: RNA is detectable from about 2 days before to 4 days after rash onset and the yield is best in the first 3 days, so the swab is collected at the same visit as the serology rather than later. Where PCR is unavailable, a $\geq 4\times$ rise in IgG between acute and convalescent sera taken 2 to 3 weeks apart is an accepted confirmation.

The order of testing changes in pregnancy, and this is where questions get built. A pregnant woman who has been exposed and has no documented immunity gets IgG and IgM immediately. Detectable IgG with negative IgM in a sample drawn shortly after exposure means pre-existing immunity and reassurance. Negative IgG means she is susceptible, so serology is repeated in 2 to 3 weeks to catch seroconversion. Isolated positive IgM in an asymptomatic pregnant woman is the trap: false positives arise from rheumatoid factor, heterophile antibodies, parvovirus B19, Epstein-Barr virus and cytomegalovirus, and IgM can persist from a remote infection. The correct next step there is IgG avidity testing or repeat testing by a different assay format, not counselling on the basis of a single positive IgM. Low avidity supports infection within the last 3 months; high avidity effectively excludes recent primary infection.

In the newborn, infant IgM is the best initial test because maternal IgM does not cross the placenta, so anything detected belongs to the baby. When it is negative and suspicion persists, follow serial IgG: transplacental maternal IgG falls with a half-life near 30 days and should be undetectable by 6 to 12 months, so persistent or rising IgG past that point confirms congenital infection. RT-PCR of nasopharyngeal secretions, urine, cerebrospinal fluid or a lens aspirate confirms the diagnosis and, just as importantly, tells you whether the infant is still shedding and therefore still a hazard to susceptible pregnant contacts.

04 Management and Treatment

SETTING	FIRST-LINE MANAGEMENT	NOTES AND CAUTIONS
Acquired rubella, child	Supportive only. Paracetamol 10 to 15 mg/kg per dose orally every 4 to 6 hours, maximum 5 doses in 24 hours. Fluids and rest	No antiviral exists. Avoid aspirin in children because of Reye syndrome
Acquired rubella, adult	Paracetamol 500 to 1000 mg every 6 hours, maximum 4 g in 24 hours	Illness is self-limited within about a week
Rubella arthritis	Ibuprofen 400 to 600 mg orally every 6 to 8 hours with food, or naproxen 250 to 500 mg twice daily, continued 2 to 4 weeks as needed	Self-limited. No disease-modifying agent and no steroid course is indicated
Thrombocytopenic purpura	Observation. Corticosteroids or intravenous immunoglobulin only for clinically significant bleeding	Resolves over weeks to months in most children
Encephalitis	Supportive intensive care, seizure control, airway protection	No proven antiviral therapy. Highest case fatality of the acquired complications
Infection control, acquired case	Droplet precautions. Isolate and exclude from work, school and childcare until 7 days after rash onset	Notify public health, generally within 24 hours. Contagious from 7 days before rash onset, so contact tracing reaches backwards
Infection control, infant with congenital infection	Contact and droplet precautions. Treat as infectious until 1 year of age, or until two specimens taken 1 month apart are negative	Caregivers, including healthcare personnel, need documented rubella immunity. Keep susceptible pregnant contacts away
Susceptible exposed person, not pregnant	Offer measles-mumps-rubella vaccine, and exclude from work or school from day 7 to day 23 after exposure if a case develops in the setting	Post-exposure vaccine does not reliably prevent illness from this exposure, but it protects against the next one
Susceptible exposed pregnant woman	Serology now and repeated in 2 to 3 weeks. Counselling anchored to gestational age. Serial ultrasound. Amniotic fluid RT-PCR after 21 weeks if confirmation is needed	Vaccine is contraindicated in pregnancy. Immunoglobulin 0.55 mL/kg intramuscularly may be considered only when termination is not an option, and it does not reliably prevent fetal infection
Infant with congenital rubella syndrome	Multidisciplinary care: early cataract surgery, hearing amplification or cochlear implantation, repair of patent ductus arteriosus or pulmonary stenosis, developmental and early intervention services	Lifelong follow-up for late-onset diabetes, thyroid disease and progressive hearing loss
Prevention, routine childhood	Live attenuated measles-mumps-rubella vaccine, subcutaneous. Dose 1 at 12 to 15 months, dose 2 at 4 to 6 years. Programs using a measles-rubella schedule give dose 1 at 9 months and dose 2 at 18 months with campaign catch-up	Minimum interval between doses 28 days. One dose produces about 95 percent seroconversion with lifelong protection
Prevention, adults without evidence of immunity	One dose of measles-mumps-rubella. Two doses for healthcare personnel, students in post-secondary education and international travelers	Evidence of immunity means documented vaccination, positive serology, or laboratory-confirmed past disease. Self-reported past rubella does not count
Seronegative woman identified in pregnancy	Vaccinate postpartum before hospital discharge, ideally together with the Tdap dose	The commonest missed step in the whole topic. Breastfeeding is not a contraindication

Acute care. There is nothing to treat. Acquired rubella in a child is fever control, fluids and reassurance, and the illness is over in about a week. In an adult, the part that lingers is joint disease, and it is managed with a non-steroidal anti-inflammatory drug for 2 to 4 weeks. If a stem describes a young woman with a symmetric polyarthritis of the hands and wrists that began days after a transient rash, the answer is not rheumatoid arthritis and not a rheumatology referral. It is supportive treatment and reassurance that this resolves.

The real acute management is containment, and this is where "next best step" questions live. Place the patient on droplet precautions, isolate until 7 days after rash onset, and notify public health. Because the contagious period begins 7 days before the rash, the contact list reaches back a full week, and it must be screened for two groups above all others: pregnant women without documented immunity and susceptible healthcare personnel. Susceptible contacts are excluded from day 7 through day 23 after exposure, which is the incubation window plus a margin.

The pregnant patient. If a pregnant woman is exposed or develops a compatible rash, the next best step is always serology, never vaccine and never immunoglobulin as a reflex. Document IgG and IgM, repeat in 2 to 3 weeks if she is susceptible, and use avidity testing to resolve an isolated positive IgM. Once infection is confirmed, counselling is driven entirely by gestational age using the timing table above: before 8 weeks the risk of defects is 85 to 90 percent, by 13 to 16 weeks it is around one in five and is mostly deafness, and after 20 weeks structural defects are not expected. Options are discussed within the framework of local law, and continued pregnancies get serial ultrasound and a newborn evaluation regardless of how normal the scans look, because deafness is not visible on ultrasound.

Immunoglobulin at 0.55 mL/kg intramuscularly is a narrow, second-line consideration: it may reduce maternal symptoms, it has not been shown to prevent fetal infection or congenital rubella syndrome, and infants have been born with the syndrome to mothers who received it. It is reserved for a susceptible woman who has been exposed and for whom termination is not an option.

Prevention, which is the actual answer to most questions. The vaccine is live attenuated, and every rule follows from that. Two doses of measles-mumps-rubella at 12 to 15 months and 4 to 6 years, given subcutaneously, with a minimum interval of 28 days when catching up. A single dose seroconverts about 95 percent of recipients and protection is lifelong. Adults born after routine vaccination began who lack evidence of immunity get one dose, or two if they are healthcare personnel, students in post-secondary education, or international travelers.

Contraindications worth memorizing: pregnancy, with conception avoided for 28 days afterwards; severe immunodeficiency, including high-dose corticosteroid therapy and advanced untreated human immunodeficiency virus infection; anaphylaxis to neomycin or gelatin; and recent receipt of immunoglobulin or blood products, which requires deferring the vaccine by 3 to 11 months depending on the product. Note carefully what is not a contraindication: breastfeeding, egg allergy, a household contact who is pregnant, and a household contact who is immunocompromised. Vaccine virus is not transmitted from a vaccinated person to others, which is why vaccinating the household is the correct way to protect a susceptible pregnant woman.

Inadvertent vaccination in early pregnancy, or conception within 28 days of a dose, is a scenario written to see whether you overreact. No case of congenital rubella syndrome has been attributed to the vaccine strain in decades of surveillance. The answer is counselling and reassurance with continued routine prenatal care, not termination.

NEXT BEST STEP, CONDENSED Rash plus tender postauricular nodes, patient not pregnant: send IgM and a throat swab for RT-PCR, isolate 7 days, notify public health. Pregnant and exposed: serology first. Pregnant and non-immune on booking bloods: vaccinate postpartum before discharge. Newborn with cataract and a murmur: infant IgM plus RT-PCR, contact isolation, audiology.

05 Differential Diagnosis and Distractors

ACQUIRED RUBELLA AGAINST ITS LOOK-ALIKES

DIFFERENTIAL	WHY IT IS SIMILAR	KEY DISCRIMINATOR
Measles (rubeola)	Febrile maculopapular rash spreading from face downward in an unvaccinated patient	Measles brings high fever to 40 C, a toxic-looking patient, and the three C's of cough, coryza and conjunctivitis with photophobia, plus Koplik spots. Its rash becomes confluent, lasts 5 to 6 days and leaves brownish staining with fine desquamation. Rubella has minimal fever, a well-appearing patient, no cough, a non-confluent rash gone in 3 days, and tender postauricular nodes
Roseola infantum (human herpesvirus 6)	Pink maculopapular rash in a young child	The sequence is reversed. Three to five days of high fever that then breaks, and the rash appears as the fever disappears, starting on the trunk and spreading outward. Rubella has fever and rash together, and starts on the face
Erythema infectiosum (parvovirus B19)	Facial rash plus arthralgia in a young woman, and a risk to pregnancy	Bright confluent "slapped cheek" erythema with circumoral pallor, then a lacy reticular rash on the extremities that waxes and wanes for weeks. Parvovirus causes hydrops fetalis and aplastic crisis, not cataract or deafness. No postauricular nodes
Scarlet fever	Sore throat, fever, generalized rash, palatal petechiae	Sandpaper texture, accentuated in flexures as Pastia lines, circumoral pallor, strawberry tongue, exudative pharyngitis, and coarse desquamation of hands and feet in convalescence. Positive rapid streptococcal test. Rubella has a soft velvety rash and no desquamation
Infectious mononucleosis (Epstein-Barr virus)	Posterior cervical lymphadenopathy, sore throat, malaise, and a rash	Nodes are posterior cervical but not postauricular or suboccipital, plus exudative tonsillitis, splenomegaly and marked fatigue lasting weeks. Rash usually appears only after aminopenicillin exposure. Atypical lymphocytosis with a positive heterophile antibody test
Enteroviral exanthem	Nonspecific febrile maculopapular rash in summer and autumn	Seasonal clustering, often with herpangina, hand-foot-and-mouth lesions or aseptic meningitis. No prominent postauricular adenopathy, and serology for rubella is negative
Drug eruption	Generalized morbilliform rash	Pruritus is prominent, onset follows a new drug by about a week, and there is no true prodrome or regional lymphadenopathy. Eosinophilia may be present
Dengue	Fever with a generalized rash and myalgia in an endemic setting	High fever, retro-orbital pain, severe myalgia, leukopenia with progressive thrombocytopenia and rising hematocrit. Rash is confluent with islands of sparing. Positive NS1 antigen
Zika virus	Mild febrile rash illness with a congenital syndrome	Prominent non-purulent conjunctivitis and arthralgia with rash, and its congenital syndrome centers on severe microcephaly with cortical malformations, not cataract, deafness and patent ductus arteriosus
Kawasaki disease	Rash, fever, cervical lymphadenopathy in a child	Fever for at least 5 days that does not respond to antipyretics, bilateral non-exudative conjunctival injection, oral mucosal changes, extremity swelling then periungual peeling, and a single large cervical node. Markedly raised inflammatory markers

CONGENITAL RUBELLA SYNDROME AGAINST THE OTHER CONGENITAL INFECTIONS

DIFFERENTIAL	WHY IT IS SIMILAR	KEY DISCRIMINATOR
Congenital cytomegalovirus	Sensorineural deafness, growth restriction, hepatosplenomegaly, thrombocytopenia and a blueberry muffin rash	Cytomegalovirus gives periventricular calcifications with microcephaly, and the diagnosis is urine or saliva polymerase chain reaction within the first 3 weeks of life. It has no cataract and no patent ductus arteriosus, and it is treatable with valganciclovir for symptomatic disease. Rubella is a vascular and hypoplastic picture, not a calcifying one
Congenital toxoplasmosis	Chorioretinitis, intracranial calcifications, jaundice, hepatosplenomegaly	Toxoplasmosis gives diffuse scattered intracranial calcifications with hydrocephalus and a dense chorioretinitis. Rubella gives a fine pigmentary "salt and pepper" retinopathy that does not impair vision, plus cataract and cardiac lesions
Congenital syphilis	Snuffles, hepatosplenomegaly, jaundice, rash, bone changes	Syphilis gives a desquamating palmoplantar rash, copious nasal discharge, metaphysitis and periostitis with Wimberger sign, and later Hutchinson teeth and saber shins. Positive non-treponemal and treponemal serology, and it responds to penicillin
Congenital varicella syndrome	Limb and eye abnormalities after first-half-of-pregnancy infection	Cicatricial skin scarring in a dermatomal pattern with limb hypoplasia is the signature. Rubella does not scar the skin and does not cause limb hypoplasia
Congenital Zika syndrome	Microcephaly, ocular findings, arthrogryposis	Severe microcephaly with overlapping sutures, subcortical calcifications and macular scarring dominate. No cardiac lesion and no cataract
Neuroblastoma or congenital leukemia	Blueberry muffin rash	The blueberry muffin appearance is dermal extramedullary hematopoiesis and is not unique to rubella. A mass, marked hepatomegaly, or an abnormal blood film points away from infection
Isolated congenital heart disease	Patent ductus arteriosus or pulmonary stenosis in a newborn	Rubella pairs the cardiac lesion with deafness, cataract or growth restriction, and with a mother who has no documented immunity. An isolated lesion in a term infant of an immune mother is not rubella

06 Traps and High-Yield Pearls

The single most common way to lose a rubella question is to answer measles. Both are unvaccinated patients with a maculopapular rash spreading from the face down, and the stem is written so that the two look alike until you read the details that were placed there on purpose. Three things separate them and all three appear in almost every rubella vignette: the patient is well-appearing with a low-grade fever rather than toxic with a fever near 40 C, the rash is non-confluent and gone by day 3 rather than confluent for 5 or 6 days with brownish staining, and there is tender postauricular and suboccipital lymphadenopathy rather than cough, coryza, photophobic conjunctivitis and Koplik spots. If the stem never mentions the nodes and does mention cough and conjunctivitis, you are being asked about measles.

The second trap is vaccinating the wrong person at the wrong time. A pregnant woman who is found to be rubella non-immune on her booking bloods is not vaccinated during pregnancy, because this is a live attenuated vaccine. The correct answer is postpartum vaccination before hospital discharge, and it is the step most often forgotten, which is exactly why it is written into questions. The mirror-image trap is over-reacting to an inadvertent dose given just before or during early pregnancy: no case of congenital rubella syndrome has been attributed to the vaccine strain, so the answer there is counselling and routine prenatal care.

Third, serology timing decides the answer more often than serology itself. A negative IgM drawn on the day the rash appeared is not a negative result, because only about half of true cases are positive that early. The next best step is to repeat testing after day 5, or to send an acute and convalescent IgG pair looking for a $\geq 4\times$ rise. Running the other way, an isolated positive IgM in an asymptomatic pregnant woman is more likely a false positive from rheumatoid factor or cross-reacting viral antibody than a true infection, and the correct next step is IgG avidity testing or confirmation on a different assay, not counselling about termination. Getting a woman to a decision on the strength of one unconfirmed IgM is the mistake the question is testing for.

Fourth, gestational age is not background detail. It is usually the variable the question turns on. Under 8 weeks the risk of defects is 85 to 90 percent and the full syndrome is on the table. By 13 to 16 weeks the risk is roughly one in five and it is essentially deafness. After 20 weeks structural defects are not expected. Two vignettes with identical wording and different gestational ages have different correct answers.

Fifth, know which congenital infection you are looking at from the calcification pattern and the eye. Rubella is cataract plus patent ductus arteriosus or peripheral pulmonary artery stenosis plus deafness, with a salt and pepper retinopathy and no calcifications. Cytomegalovirus is periventricular calcifications with microcephaly and deafness, no cataract. Toxoplasmosis is diffuse scattered calcifications with hydrocephalus and chorioretinitis. The blueberry muffin rash belongs to none of them exclusively and is never the discriminator.

Finally, remember that a congenitally infected infant is a public health problem, not just a patient. Shedding continues for months, so the infant is treated as infectious until 1 year of age unless two specimens a month apart are negative, and every caregiver needs documented immunity. A question that ends with a pregnant nursery nurse or a pregnant relative visiting the baby is asking about isolation and immunity documentation, not about treatment.

The core competency being tested across this topic is recognizing a mild illness whose importance lies entirely outside the patient in front of you: identifying rubella from lymphadenopathy and rash character rather than severity, confirming it with correctly timed serology or polymerase chain reaction, translating gestational age into fetal risk, and knowing that the intervention that matters is vaccination given to the right person at the right moment.

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