Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Joseph Nasr, M.D.[2]; Guillermo Rodriguez Nava, M.D. [3]; Yamuna Kondapally, M.B.B.S[4];

• Classical descriptions: Reports of measles predate the Common Era; the first scientific description of the disease and its distinction from smallpox is attributed to the Persian physician Ibn Razi (Rhazes) (860-932A.D.) in a book entitled “Smallpox and Measles” (in Arabic: Kitab fi al-jadari wa-al-hasbah).
• 18th-19th century milestones: A Scottish physician, Francis Home, demonstrated in 1757 that measles was caused by an infectious agent present in the blood of patients.
• Virus isolation (modern era): In 1954, the measles virus was isolated from an 11-year-old boy from the US, David Edmonston, and adapted and propagated on a chick embryo tissue culture in Boston, Massachusetts, by John F. Enders and Thomas C. Peebles. The Edmonston isolation was the seed for vaccine development^[1].

• Pre-Vaccine Disease Burden (U.S.): Before the measles vaccine, nearly all children contracted the virus by age 15; annually, approximately 549,00 reported cases and 495 deaths; around 48,000 hospitalizations, 7,000 seizures, and about 1,000 permanent disabilities from encephalitis (brain damage or deafness)^[2].
• First U.S. licensure (1963): The Edmonston B live-attenuated vaccine (Rubeovax, Merck) was licensed in 1963; later withdrawn in 1975 due to reactogenicity. It was further attenuated to yield Edmonston-Enders (Moraten) and Edmonston-Zagreb (EZ) strains^[1].
• Inactivated vaccine (1963): Licensed in parallel with Edmonston B, but withdrawn in 1967 due to lack of protection. Recipients often developed atypical measles if exposed to wild-type virus^[3].
• Schwarz strain (1965): Introduced as a further-attenuated vaccine; no longer used in the United States^[1].

• Edmonston-Enders strain (1968): Licensed as a further-attenuated vaccine; caused fewer reactions than Edmonston B^[1].
• Current U.S. use: Only the Edmonston-Enders strain (Moraten) remains in use, incorporated into MMR or MMRV (ProQuad). No single-antigen measles vaccine is available in the U.S^[1].

• Formulation: Vaccines are prepared in chick embryo fibroblast cultures; supplied as freeze-dried powder with stabilizers (human albumin, neomycin, sorbitol, gelatin).

• Additional strains (Global): The Schwarz strain (derived from Edmonston A; genetically identical to Moraten) is a component of MMR (Priorix®, GSK), licensed in 1997 and used in >100 countries. AIK-C (Japan) is licensed as mono- and MR-combination vaccine in Japan, Vietnam, and Iran^[1][4].
• Non-Edmonston Strains: Leningrad-4, Shanghai-191, Chang-47, CAM-70 have been licensed/used regionally (Russia, China, South Africa)^[4].
• Effectiveness & Safety (summary): Dose-1 Effectiveness ≈ 84% (12mo) and 92.5% (≥ 12mo); ~94% after two doses; serious adverse events are rare across licensed strains^[5].

• U.S. elimination (2000): Endemic transmission ceased in 2000 (definition: ≥12 months without endemic transmission with robust surveillance)^[6].
• Americas certification: Region of the Americas declared measles-free on September 27, 2016.

• Ongoing importations: Despite elimination, U.S. cases continue annually due to importations and spread in under-vaccinated communities; frequent sources have included England, France, Germany, India, Philippines, among others^{[7][8][9][10]}.
• Current resurgence: By May 30, 2025, there were 1,088 confirmed U.S. cases and 3 deaths; ~96% were unvaccinated/unknown vaccination status, and 12% were hospitalized. If transmission continues for >12 months, the U.S. will lose its measles elimination status^[10].

• Receptor biology: Measles virus recognizes CD46, SLAM/CD150, and nectin-4. Wild-type virus primarily uses CD150 (lymphocytes) and nectin-4 (epithelial cells), while vaccine strains use CD46. Discovery of SLAM and nectin-4 in 2010–2011 clarified lymphocyte tropism and epithelial exit/transmission^{[11][12][13][14]}.
• Mechanism of immune suppression: Wild-type MeV preferentially infects CD150^hi memory T cells and also infects naïve and memory B cells, leading to depletion and reshaping of preexisting immunity. This immune amnesia diminishes antibody repertoires and alters B-cell diversity, persisting for 5–12 months post-infection^{[15][16][17][18][19][20][21][22]}.
• Loss of prior vaccine protection: Children with prior measles may lose protective antibody levels to other vaccines, e.g., tetanus, highlighting the broad impact of immune amnesia^[23].
• Innate immune amnesia: MeV also induces apoptosis in MAIT cells, weakening first-line mucosal defenses and further increasing vulnerability to secondary infections^[24].

• Contrast with vaccine strains: Attenuated measles vaccines do not cause immune amnesia. Instead, they induce trained immunity, with epigenetic reprogramming of γδ T cells that enhances non-specific defenses against other pathogens^{[25][26][27][28][29][30]}.

• Genotype history: WHO has defined 24 genotypes (based on the 450-bp N-gene window). Since 2018, global circulation has been limited to B3, D4, D8, and H1. As of 2024–2025, B3, D8, and H1 are the dominant strains in ongoing outbreaks^[31].
• Surface glycoproteins: The hemagglutinin (H) and fusion (F) proteins—major neutralizing antibody targets—have remained antigenically stable for decades. A key immunodominant epitope on H overlaps the SLAM-binding domain, which means mutations that escape neutralization often also reduce receptor binding and viral fitness^[32][33][34].
• Vaccine cross-protection: Current vaccines, all derived from genotype A (Edmonston lineage), still provide robust protection against these circulating wild-type genotypes^[33].
• Monoclonal antibody monitoring: A D4.2 sub genotype has shown reduced binding by some neutralizing monoclonals at major H epitopes, but clinical vaccine escape has not been documented. Ongoing sequencing is monitoring such variants^[35].
• Genomic surveillance advances: Low-cost Nanopore full-genome sequencing is increasingly used to track transmission chains and to watch for potential vaccine-escape variants^[36].

• 2019 global surge: Reported measles cases increased from 132,490 (2016) to 869,770 (2019), fueled by major outbreaks in the Democratic Republic of Congo, Madagascar, Samoa, Ukraine, and Brazil. NEJM highlights vaccine hesitancy as a central driver, alongside inequitable access^[7].
• Pandemic shock: COVID-19 pandemic disruptions pushed global MCV1 coverage down to 81%—the lowest since 2008. By 2022–2023, coverage had only partially recovered to 83%, leaving large immunity gaps^[37].
• 2024–2025 outbreaks:
  • Global scale: In 2024, WHO confirmed 395,521 laboratory-confirmed cases worldwide, and another 16,147 in the first two months of 2025. Over half of reported patients were hospitalized, indicating an underestimation of the true burden^[38].
  • Europe: Recorded its highest measles case count in more than 25 years in 2024, accounting for ~20% of global cases^[38].
  • United States: As of May 30, 2025, there were 1,088 confirmed cases and 3 deaths; ~96% were in unvaccinated or unknown-status individuals, and 12% required hospitalization. NEJM warns that if continuous transmission persists for >12 months, the U.S. will lose its elimination status^[2].
• Policy headwinds: NEJM notes that U.S. withdrawal of financial support from WHO (≈19% of its budget) and Gavi (≈13%) threatens global measles control and domestic health security.

• 1987 – Vitamin A policy: WHO/UNICEF issued a landmark statement on vitamin A supplementation for measles, based on trial evidence that supplementation reduced complications and mortality^[39].
• 1998 – Measles Partnership: The Measles Partnership (later Measles & Rubella Initiative) was established by WHO, UNICEF, CDC, UN Foundation, and the American Red Cross to accelerate global control^[6].
• 2000 – Two-dose policy: WHO adopted the two-dose measles vaccination schedule for all children, to achieve and sustain elimination^[6].
• 2012 – Global Vaccine Action Plan (GVAP): Set measles elimination goals across all WHO regions by 2020 (not achieved)^[6].
• 2017 – WHO “Immunization Agenda 2030” (IA2030): Established elimination targets through 2030^[6].
• 2025 – Policy headwinds: According to the New England Journal of Medicine (NEJM), U.S. withdrawal of support from WHO (≈19% of its budget) and Gavi (≈13%), which undermines global measles control capacity and threatens U.S. health security^[40].

• Pre-vaccine burden (United States)^[41]:
  • Before the introduction of a live measles vaccine in 1963, nearly all children contracted measles by age 15.
  • Each year: an average of 549,000 reported cases and 495 deaths, though the true annual burden was closer to 3–4 million infections.
  • Of reported cases, ~48,000 were hospitalized, 7,000 experienced seizures, and ~1,000 developed chronic disability from measles encephalitis.
• Dramatic reduction after vaccination^[6]:
  • Vaccine introduction and scale-up led to a >99% decline in U.S. measles cases compared with the pre-vaccine era.
  • Measles was declared eliminated in the U.S. in 2000, defined as the absence of endemic transmission for ≥12 months with high-quality surveillance.
• Global control milestones:
  • The WHO Expanded Programme on Immunization (EPI) adopted measles vaccine in 1977, marking it as a global public health priority.
  • The Region of the Americas was declared measles-free by PAHO/WHO on September 27, 2016.
• Persistent global burden:
  • Measles remains a leading cause of vaccine-preventable childhood death globally despite progress^[6].
  • In 2024, WHO confirmed 395,521 laboratory-confirmed cases worldwide, with another 16,147 cases in the first 2 months of 2025^[38].
  • Over 50% of reported patients were hospitalized, meaning the true burden is substantially undercounted.
• Importations and outbreaks in the U.S.^[42][43]:
  • Between 2000–2013, the U.S. recorded 37–220 cases annually, largely due to importations from measles-endemic regions and spread in under-vaccinated communities.
  • In recent years, importations often originated from England, France, Germany, India, and the Philippines.
  • By May 30, 2025, the U.S. had 1,088 confirmed cases and 3 deaths, with 96% of cases in un/unknown-vaccinated individuals and 12% hospitalized. If transmission persists beyond 12 months, the U.S. will lose its elimination status.

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Measles
Measles virus electron micrograph
Virus classification
Group: Group V ((-)ssRNA) Order: Mononegavirales Family: Paramyxoviridae Subfamily: Paramyxovirinae Genus: Morbillivirus Species: Measles virus

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In Chief: Joseph Nasr, M.D.[2]

Measles virus (MeV) is a single-stranded, negative-sense, enveloped RNA virus of the genus Morbillivirus within the family Paramyxoviridae. Humans are the natural hosts of the virus; no animal reservoirs are known to exist.

Measles is highly contagious (R₀ ≈ 12–18) and spreads readily where vaccination coverage has fallen^[1].

Persons with measles typically transmit the virus from ~4 days before to ~4 days after rash onset^[1].

• Syndrome. After an incubation of 10–14 days (range 7–23), illness begins with fever and the “3 Cs” (cough, coryza, conjunctivitis); Koplik spots may precede the maculopapular rash by 1–2 days^[1].
• Systemic nature & complications. Because measles is systemic, complications (≈30% of cases) include diarrhea, pneumonia, otitis media, conjunctivitis; pneumonitis/giant-cell pneumonia occur mainly in immunosuppressed persons and young children^[2].
• Encephalitis spectrum. Acute post-infectious encephalitis (days 0–7), measles-inclusion body encephalitis (1–6 months), and SSPE (years later) are rare but serious^[3].
• Immune amnesia (clinical impact). Temporary B- and T-cell memory depletion increases susceptibility to secondary infections for months after recovery^[4].

Additional properties: One antigenic type (epidemiologically); 100–200 nm; inactivated by heat, light, acidic pH, ether, trypsin; short environmental survival (<2 h); transmitted via respiratory secretions/aerosols.

The measles virus has two envelope glycoproteins on the viral surface – hemagglutinin (H) and membrane fusion protein (F). These proteins are responsible for host cell binding and invasion. Three receptors for the H protein have been identified to date: complement regulatory molecule CD46, the signaling lymphocyte activation molecule (SLAM) and the cell adhesion molecule Nectin-4.^[5]

• Entry receptors (H protein). CD46, SLAM/CD150^[10], and nectin-4 are the three recognized receptors; CD150 (immune cells) and nectin-4 (epithelium) were identified in 2010–2011.
• Wild-type vs vaccine strains. Wild-type MeV primarily uses CD150^[11], whereas vaccine strains mainly use CD46 (attenuation-associated shift).
• Cellular targeting in humans. CD150^hi memory T cells are preferential targets; CD150⁺ memory B cells and naïve B cells are also susceptible^[12].
• Pathogenesis timeline: NEJM’s figure aligns incubation, contagious window (Day −4 to +4), MeV viremia, and immune-cell targets (CD150⁺ lymphocytes).

• Entry & fusion. H binds receptor (CD150 or nectin-4), F mediates membrane fusion → nucleocapsid release.
• Early spread & shedding. After initial respiratory/lymphoid infection, systemic viremia follows; patients are typically infectious Day −4 to +4 around rash appearance^[1].

• Immune amnesia. During acute infection and for ≈5–12 months after resolution, measles can cause diminished pre-existing antibody repertoires and alter B-cell diversity, mechanistically explaining elevated post-measles morbidity/mortality from other infections.
• Vaccine does not cause amnesia; potential trained immunity. The appendix notes that measles vaccine strains do not cause adaptive or innate immune amnesia and summarizes evidence that MMR can induce “trained immunity” (innate immune reprogramming, including γδ T cells).

The measles virus evolved from the formerly widespread rinderpest virus, which infects cattle.^[13] Sequence analysis has suggested that the two viruses most probably diverged in the 11th and 12th centuries, though the periods as early as the 5th century fall within the 95% confidence interval of these calculations.^[13]

Other analysis has suggested that the divergence may be even older because of the technique’s tendency to underestimate ages when strong purifying selection is in action.^[14] There is some linguistic evidence for an earlier origin within the seventh century.^[15][16] The current epidemic strain evolved at the beginning of the 20th century—most probably between 1908 and 1943.^[17]

Virology (brief). Measles virus (MV/MeV) is an enveloped, non-segmented, negative-sense RNA virus (Paramyxoviridae, Morbillivirus). It measures ~100–200 nm; two envelope glycoproteins drive entry: F (fusion) for membrane merger and H (hemagglutinin) for receptor binding. There is functionally one antigenic type in circulation; documented H changes have not translated into loss of vaccine effectiveness. MV is rapidly inactivated by heat, light, acidic pH, ether, and trypsin and survives <2 h in air/on surfaces.

Genotyping framework. For molecular surveillance, 24 MeV genotypes are recognized using the 450-bp N-gene window (“N-450”). Since 2018, genotypes B3, D4, D8, and H1 have been identified in global surveillance, with B3, D8, and H1 dominating 2024–2025 outbreaks^[18].

(WHO defines 8 clades (A–H) with numbered subtypes (e.g., A1, D2); the genotyping scheme was introduced in 1998 and extended in 2002–2003; N-450 is the minimum sequence required for genotyping)

Antigenic stability (why vaccines still work). The surface glycoproteins H and F have largely retained their antigenic structure for decades; H-specific antibodies are major contributors to protection. A conserved immunodominant epitope on H overlaps the SLAM-binding site, so escape mutations tend to impair receptor binding/fitness rather than propagate^[10][11][12].

Vaccine lineage & breadth. All currently used measles vaccines descend from genotype A (Edmonston lineage) and remain protective against circulating wild-type strains; the main text also reiterates that the vaccine is highly effective against all circulating genotypes^[10][11][12].

Watch items (surveillance). Sub-genotype D4.2 has shown reduced binding to several monoclonal antibodies targeting major H epitopes; while clinical vaccine escape has not been shown, NEJM flags this as requiring close monitoring^[19].

Elimination status notes. The predominant genotypes differ across regions and depend on whether endemic circulation persists. (indigenous transmission was interrupted in the United States and Australia by 2000 and in the Americas by 2002.)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Guillermo Rodriguez Nava, M.D. [2]; Vidit Bhargava, M.B.B.S [3]

Measles is a disease characterized by the classical clinical triad of cough, coryza and conjunctivitis. In most cases the presentation is classical and the diagnosis can be sufficiently made clinically. However, in a few cases certain other diagnostic possibilities must be kept in mind. These include other viral exanthams such as erythema infectiosum, other maculopapular rashes etc. Also, in areas where killed vaccines are used, the probability of atypical measles with fever, conjunctivitis, pneumonitis and rash must be kept in mind. It is worthwhile to consider Kawasaki’s disease, rubella, dengue, systemic lupus erythematosus and serum sickness while considering the diagnosis of measles.

The following table summarizes the most commonly confused conditions with measles:

The following table is a list of differential diagnosis oral lesions presenting similar to measles:

Disease	Presentation	Risk Factors	Diagnosis	Affected Organ Systems	Important features	Picture
Coxsackie virus	Fever Sores in the mouth Rash with blisters Aches	Pregnancy immunodeficiency	History and Physical exam Throat swabs Swabs from the lesion Tzanck test	Oral cavity Skin	Symptomatic treatment
Chicken pox	Conjunctival symptoms Catarrhal symptoms Characteristic spots on the trunk appearing in two or three waves Itching	Pregnancy Premature infants born to susceptible mothers All infants born at less than 28 weeks gestation or who weigh ≤1000 grams Immunocompromised	History and physical exam PCR to detect VZV in skin lesions (vesicles, scabs, maculopapular lesions)	Oral cavity Skin	Sodium bicarbonate in baths or antihistamines for itching Paracetamol (acetaminophen) for fever Prednisolone is contraindicated
Measles	Fever Rash Cough Coryza (runny nose) Conjunctivitis (pink eye) Malaise Koplick spots in mouth	Unvaccinated individuals[2][3] Crowded and/or unsanitary conditions Traveling to less developed and developing countries Immunocompromized Winter and spring seasons Born after 1956 and never fully vaccinated Health care workers	History and examination PCR for Measles-specific IgM antibody PCR for Measles RNA	Oral cavity Skin Respiratory tract Eyes Throat	Caused by Morbillivirus Primary site of infection is the respiratory epithelium of the nasopharynx Transmitted in respiratory secretions, via aerosol droplets containing virus particles
Herpangina	Sudden fever Sore throat and dysphagia– These can occur several hours(up to 24 hours), before the appearance of the enanthem. Vomiting Abdominal pain Myalgia Headache Pharyngeal lesions	Attendance at a kindergarten/child care center Contact with herpangina cases Residence in rural areas Overcrowding Poor hygiene Low socioeconomic status	Clincial diagnosis Pharyngeal viral and bacterial cultures can be taken to exclude HSV infection and streptococcal pharyngitis.	Skin Oral Cavity	Characteristic enanthem- Punctate macule which evolve over a period of 24 hours to 2-4mm erythematous papules which vesiculate, and then centrally ulcerate. The lesions are usually small in number, and evolve rapidly. The lesions are seen more commonly on the soft palate and uvula. The lesions can also be seen on the tonsils, posterior pharyngeal wall and the buccal mucosa.
Primary herpetic gingivoestomatitis[4]	Pin-head vesicles rupture to form painful irregular ulcerations covered by yellow-grey membrane Severe pain Submandibular lymphadenopathy Halitosis It involves buccal mucosa, tongue, posterior pharynx, and gingival and palatal mucosa	Direct contact HIV infection	Tzanck test demonstrates multinucleated epithelial giant cells[5] Viral culture is the gold standard for diagnosis Direct immunofluorescence	Oral cavity Mucous membranes	Ulcers are common on lips, gums, throat, front of tongue, inside of the cheeks and roof of the mouth Treatment is with antiviral agents such as Valacyclovir and Famciclovir

Koplik spots must be differentiated from other diseases causing oral lesions such as leukoplakia and herpes simplex virus infection.

Disease	Presentation	Risk Factors	Diagnosis	Affected Organ Systems	Important features	Picture
Diseases predominantly affecting the oral cavity
Oral Candidiasis	Dysphagia or odynophagia White patches on the mouth and tongue	Newborn babies Denture users Poorly controlled diabetes As a side effect of medication, most commonly having taken antibiotics. Inhaled corticosteroids for the treatment of lung conditions (e.g, asthma or COPD) may also result in oral candidiasis which may be reduced by regularly rinsing the mouth with water after taking the medication. People with poor nutrition, specifically vitamin A, iron and folate deficiencies. People with an immune deficiency (e.g. as a result of AIDS/HIV or chemotherapy treatment). Women undergoing hormonal changes, like pregnancy or those on birth control pills. Organ transplantation patients	Clinical diagnosis Confirmatory tests rarely needed	Localized candidiasis Oral and esophageal candidasis Candida vulvovaginitis Chronic mucocutaneous candidiasis Invasive candidasis Candidaemia Candida endocarditis Candida osteoarticular disease	Oral candidiaisis is a benign self limiting disease unless accompanied by immunosuppression.
Herpes simplex oral lesions	Fever Sore throat Painful ulcers	Stress Recent URTI Female sex	Physical examination Viral culture Tzanck smear	Orofacial Infection Anogenital Infection Ocular Infection Herpes Encephalitis Neonatal Herpes Herpetic Whitlow Herpes Gladiatorum	The symptoms of primary HSV infection generally resolve within two weeks
Aphthous ulcers	Painful, red spot or bump that develops into an open ulcer	Being a female Between the ages of 10-40 Family history of aphthous ulcers	Physical examination Diagnosis of exclusion	Oral cavity	Self-limiting , Pain decreases in 7 to 10 days, with complete healing in 1 to 3 weeks
Squamous cell carcinoma	Non healing ulcer, nodule, indurated plaque or mass May involve skin, lips, inside the mouth, throat or esophagus	Chronic sun or UV exposure Fair skin Elderly age (>45 yrs) Male sex Smoking	Physical exam Biopsy	Oral Cavity Floor of mouth Lateral tongue Throat Esophagus	Malignant Can spread to TMJ Some times associated with leukoplakia
Leukoplakia	White leathery spots on the mucous membranes of the tongue and inside of the mouth Lateral borders of tongue	Atypical Tobacco use Chronic irritation Immunodeficiency Bloodroot (sanguinaria)	Physical exam Diagnosis of exclusion Biopsy	Vulvar lesions occur independent of oral lesions	Associated with HIV Persistant white spots Benign but can progress to carcinoma after almost 10 years Oral proliferative verrucous leukoplakia is an aggressive sub type with multiple lesions and higher conversion to warts or carcinoma[6]
Melanoma	A lesion with ABCD Asymmetry Border irregularity Color variation Diameter changes Bleeding from the lesion	UV radiations Genetic predisposition Old age Male gender Family or personal history of melanoma Multiple benign or atypical nevi	ABCD characteristics Bleeding or ulceration may show malignancy Serum LDH may be elevated in case of malignancy Biopsy	Can metastasize All UV radiation or sun exposed areas can be effected independently 1-2 to hundreds of granules	Neural crest cell derivative Development begins with disruption of nevus growth control Progression involves MAPK/ERK pathway N-RAS or BRAF oncogene also involved
Fordyce spots	Rice-like granules or spots Small, painless, raised, pale, red or white 1 to 3 mm in diameter	Greasy skin types Some rheumatic disorders Hereditary nonpolyposis colorectal cancer Lower gingiva (gums) Vestibular mucosa	Physical exam Small keratin-filled pseudocysts May be seen on incidental mucosal biopsy Biopsy not done for them primarily	Oral cavity Vermilion border of the lips Oral mucosa of the upper lip Buccal mucosa in the commissural region often bilaterally Genitals	Benign neoplasms with sebaceous features Visible sebaceous glands No surrounding mucosal change Several adjacent glands may coalesce into a larger cauliflower-like cluster
Burning mouth syndrome	Burning or tingling on the lips, tongue, or entire mouth	Nutritional deficiencies Chronic anxiety or depression Diabetes type 2 Menopause Oral thrush or dry mouth, or damaged nerves transmitting taste Female gender Menopause	Presentation Physical exam	Oral cavity	Pain typically is low in the morning and builds up over the day Low dosages of benzodiazepines, tricyclic antidepressants or anticonvulsants may be effective
Torus palatinus	Bony growth on midline of the hard palate Nodular mass covered with normal mucosa	Genetic predisposition Autosomal dominant	Physical exam Types Flat tori Spindle tori Nodular tori Lobular tori	Hard palate	More common in Asian and Inuit populations Twice more common in females Repeated trauma can cause bleeding Surgery may be required in symptomatic
Diseases involving oral cavity and other organ systems
Behcet’s disease	Painful mouth sores Acne like skin lesions Headache, fever, poor balance, disorientation Abdominal pain, diarrhea or bleeding Uveitis Joint swelling and joint pain Genital sores wit pain and scaring Aneurysms	Over active immune system	Physical examination	Mouth Genitals GIT Eye Joints Skin Vascular system Brain	Outbreaks of exaggerated inflammation Affects smaller blood vessels
Crohn’s disease	Chronic, episodic diarrhea or constipation Abdominal pain Vomiting Weight loss or weight gain	Smoking Whites and European Jews Hormonal contraception Diets high in microparticles, sweet, fatty or refined foods Industrialized country	Typical history and symptoms Skip lesions on biopsy Anti-Saccharomyces cerevisiae antibodies (ASCA) Anti-neutrophil cytoplasmic antibodies (ANCA)	Eyes Joints Skin	May lead to Obstructions Abscesses Free perforation Hemorrhage
Agranulocytosis	Fever or chills Frequent infections Unusual redness, pain, or swelling around a wound Mouth ulcers Abdominal pain Burning sensation when urinating Sore throat	Medications[7] Cytotoxic chemotherapy Hematologic malignancies Autoimmune disorders	Neutropenia <100 cells per micro litre Eosinopenia Basopenia	Oral cavity Skin GIT Urinary system Conjunctiva	Immunocompromization Types Drug-induced Malignant Autoimmune
Syphilis[8]	Chancre Regional lymphadenopathy	Multiple sexual partners Illicit drug use Unprotected sex Men who have sex with men Residence in highly prevalent areas HIV infection Presence of other STIs Previous history of STIs Intravenous drug use	Darkfield microscopy Non treponemal tests like VDRL and RPR test) Treponemal testsFTA-ABS tests, (TP-PA) assay, enzyme immunoassays, and chemiluminescence immunoassays)	Oral cavity Penis Cervix Labia Anal canal Rectum CNS CVS	Primary syphilis Chancre Secondary syphilis Condylomata lata Latent syphilis Asymptomatic Tertiary syphilis Gummas Neurosyphilis
Coxsackie virus	Fever Sores in the mouth Rash with blisters Aches	Pregnancy immunodeficiency	History and Physical exam Throat swabs Swabs from the lesion Tzanck test	Oral cavity Skin	Symptomatic treatment
Chicken pox	Conjunctival symptoms Catarrhal symptoms Characteristic spots on the trunk appearing in two or three waves Itching	Pregnancy Premature infants born to susceptible mothers All infants born at less than 28 weeks gestation or who weigh ≤1000 grams Immunocompromised	History and physical exam PCR to detect VZV in skin lesions (vesicles, scabs, maculopapular lesions)	Oral cavity Skin	Sodium bicarbonate in baths or antihistamines for itching Paracetamol (acetaminophen) for fever Prednisolone is contraindicated
Measles	Fever Rash Cough Coryza (runny nose) Conjunctivitis (pink eye) Malaise Koplick spots in mouth	Unvaccinated individuals[2][3] Crowded and/or unsanitary conditions Traveling to less developed and developing countries Immunocompromized Winter and spring seasons Born after 1956 and never fully vaccinated Health care workers	History and examination PCR for Measles-specific IgM antibody PCR for Measles RNA	Oral cavity Skin Respiratory tract Eyes Throat	Caused by Morbillivirus Primary site of infection is the respiratory epithelium of the nasopharynx Transmitted in respiratory secretions, via aerosol droplets containing virus particles

References

1. ↑ “Epidemiology and Prevention of Vaccine-Preventable Diseases”.
2. ↑ ^{2.0 2.1} Feikin DR, Lezotte DC, Hamman RF, Salmon DA, Chen RT, Hoffman RE (2000). “Individual and community risks of measles and pertussis associated with personal exemptions to immunization”. JAMA. 284 (24): 3145–50. PMID 11135778.CS1 maint: Multiple names: authors list (link)
3. ↑ ^{3.0 3.1} Ratnam S, West R, Gadag V, Williams B, Oates E (1996). “Immunity against measles in school-aged children: implications for measles revaccination strategies”. Can J Public Health. 87 (6): 407–10. PMID 9009400.CS1 maint: Multiple names: authors list (link)
4. ↑ Kolokotronis, A.; Doumas, S. (2006). “Herpes simplex virus infection, with particular reference to the progression and complications of primary herpetic gingivostomatitis”. Clinical Microbiology and Infection. 12 (3): 202–211. doi:10.1111/j.1469-0691.2005.01336.x. ISSN 1198-743X.
5. ↑ Chauvin PJ, Ajar AH (2002). “Acute herpetic gingivostomatitis in adults: a review of 13 cases, including diagnosis and management”. J Can Dent Assoc. 68 (4): 247–51. PMID 12626280.
6. ↑ Ann M. Gillenwater, Nadarajah Vigneswaran, Hanadi Fatani, Pierre Saintigny & Adel K. El-Naggar (2013). “Proliferative verrucous leukoplakia (PVL): a review of an elusive pathologic entity!”. Advances in anatomic pathology. 20 (6): 416–423. doi:10.1097/PAP.0b013e3182a92df1. PMID 24113312. Unknown parameter |month= ignored (help)CS1 maint: Multiple names: authors list (link)
7. ↑ Andrès E, Zimmer J, Affenberger S, Federici L, Alt M, Maloisel F. (2006). “Idiosyncratic drug-induced agranulocytosis: Update of an old disorder”. Eur J Intern Med. 17 (8): 529–35. Text “pmid 17142169” ignored (help)CS1 maint: Multiple names: authors list (link)
8. ↑ title=”By Internet Archive Book Images [No restrictions], via Wikimedia Commons” href=”https://commons.wikimedia.org/wiki/File:A_manual_of_syphilis_and_the_venereal_diseases%2C_(1900)_(14595882378).jpg“
9. ↑ “Dermatology Atlas”.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Joseph Nasr, M.D.[2] ;Guillermo Rodriguez Nava, M.D. [3];

• Leading vaccine-preventable killer of children. Measles remains a leading cause of vaccine-preventable childhood mortality worldwide.
• Steep global resurgence since 2019. After a historic low of 132,490 reported cases in 2016, global measles reports surged to 869,770 in 2019, driven by large outbreaks in the DRC, Madagascar, Samoa, Ukraine, and Brazil, with vaccine hesitancy cited as a major driver; in 2019 the WHO listed vaccine hesitancy among the top 10 global health challenges^[1][2][3].
• Pandemic shock to coverage. Routine immunization disruptions during Covid-19 pushed MCV1 coverage to 81% (lowest since 2008), with only partial recovery to 83% in 2022–2023; coverage is lowest in low-income countries (64%) and 86% in middle-income countries^[4].
• Current case burden (2024–2025). All WHO regions have reported increases since 2024; 395,521 laboratory-confirmed cases were reported in 2024 and 16,147 in the first 2 months of 2025; >50% of reported patients were hospitalized, implying substantial under-ascertainment^[5][6].

• European region, 2024. The WHO European Region recorded its highest measles case count in >25 years in 2024, accounting for ~20% of global cases^[5].

Historical mortality reductions (Measles Initiative) according to the World Health Organization (WHO). Global measles deaths fell ~60% (from ~873,000 in 1999 to ~345,000 in 2005). In Africa, deaths declined ~75% (from ~506,000 to ~126,000 in 5 years).

• Importations sustain outbreaks in elimination settings. Countries with interrupted endemic transmission (e.g., United States, elimination declared 2000) still see outbreaks seeded by imported cases, with spread in undervaccinated pockets^[7][2].
• Global elimination setbacks. Since 2019, no WHO region has achieved and sustained measles elimination^[7].

• Sub-national heterogeneity (U.S. example). County-level analyses in 37 U.S. states showed MMR coverage <95% in 990/1501 counties and <74% in 70 counties, identifying large susceptible clusters^[8].
• Infants. Maternal antibody waning earlier than in past decades leaves most infants seronegative by 6 months, amplifying risk during periods of community transmission^{[9][10][11][12]}.
• Adolescents/young adults. Immunity gaps are documented among persons ~13–30 years (and some >40 years) who received the standard two-dose schedule in childhood; these gaps account for some adult cases during outbreaks in well-vaccinated countries^[10][13][14].

• Hospitalization share as severity proxy. In 2024–2025, >50% of reported cases required hospitalization, which the NEJM authors note implies undercounting of true infections^[5].
• Complications and fatality gradients (context for demographic risk and setting): case-fatality 1–3/1000 in high-income settings vs 9–16/1000 in middle-/low-income settings; up to 180/1000 in humanitarian crises^[15][16][17].

• 2019 surge and 2024 peak. >100,000 European cases in 2019 amid global resurgence; in 2024, the region reached the highest burden in >25 years (~20% of global cases)^[1][5].

• In the decade prior to the licensure of live measles vaccine in 1963, an average of 549,000 measles cases and 495 measles deaths were reported annually.^[18]
• Almost every American was affected by measles during their lifetime; it is estimated that 3–4 million measles cases occurred each year.
• Following implementation of the one dose measles vaccine program, there was significant reduction in the reported incidence in the United States by 1988 resulting in decline in measles-related hospitalizations and death.
• During 1989–1991, a resurgence of measles occurred when over 55,000 cases and 123 deaths were reported.
• The epidemiology during the resurgence was characterized mainly by cases in unvaccinated preschool-age children who had not been vaccinated on time with one dose of measles vaccine.
• Outbreaks were reported among highly vaccinated school-age children who received one dose of measles-containing vaccine.
• In 1989, a second-dose vaccination schedule was recommended by the Advisory Committee on Immunization Practices (ACIP), the American Academy of Pediatrics (AAP), and the American Academy of Family Physicians (AAFP).
• In 1998, the ACIP recommended that states ensure second dose coverage of children in all grades by 2001.
• Following the resurgence, improved implementation of the timely administration of the first dose of MMR vaccine and increased implementation of two doses among school-age children led to a dramatic decline in measles cases.
• In 2000, endemic measles was declared “eliminated” from the United States.

• Elimination and ongoing importations. The U.S. declared elimination in 2000; present-day cases reflect importations and spread within undervaccinated communities^[7][2].

• In 2017, a measles outbreak began in Minnesota among the Somali American community. The number of cases of measles in Minnesota by May 2017 exceeded the annual rate in the entire United States in 2016.

• During 2001–2011, 911 measles cases were reported. ^[18]
• The median number of measles cases reported per year was 62 (range: 37–220 cases/year).
• Measles incidence has continuously remained below one case per million since 1997. The majority of measles cases were unvaccinated (65%) or had unknown vaccination status (20%).
• Of the 911 reported measles cases, 372 (40%) were importations (on average 34 importations/year), 239 (26%) were epidemiologically linked to these importations, 190 (21%) either had virologic evidence of importation or had been linked to those cases with virologic evidence of importation, and 110 (12%) had unknown source (unknown source cases represent cases where epidemiologic- or virologic-link to an imported case was not detected0
• The highest incidence of measles cases in recent years occurred in 2008 (0.48 cases/million) and 2011 (0.72 cases/million):
  • The epidemiology of measles in 2008 was characterized by (1) a high proportion (95%) of cases among U.S. residents who were unvaccinated or who had unknown vaccination status, most of whom were U.S. school-age children whose parents had religious or philosophical objections to vaccination, and (2) more spread from imported cases than other years.
  • In 2011, 220 measles cases were reported, the highest number of reported measles cases since 1996; 80 (36%) were importations, 144 (65%) were unvaccinated, and 47 (21%) had unknown vaccination status. Most of the importations were the result of unvaccinated U.S. travelers who had traveled to measles endemic countries, mainly Western Europe and India.
• Although measles elimination has been achieved in the United States, importation of measles will continue to occur as measles remains endemic in many other parts of the world.

• 2025 situation (as of May 30). 1,088 confirmed cases and 3 deaths; ~96% unvaccinated/unknown status; ~12% hospitalized; current counts are ~4× the 2024 total; loss of U.S. elimination status is possible if transmission persists >12 months^[20].
• Domestic determinants. Misinformation (e.g., now-disproven autism claims) and vaccine hesitancy contribute to under-vaccination; modeling suggests that a 10% drop in MMR could yield ~11.1 million U.S. measles cases over 25 years^[21][22].

• Routine immunization commonly at ~12–18 months as part of MMR; importation-linked outbreaks still occur when pockets of susceptibility exist; Japan experienced a notable 2007 surge; broad MMR eradication proposals have circulated but are not prioritized before global polio eradication.

• Regional initiatives to eliminate rubella by 2010; as of 2006, endemic measles still reported in Bolivia, Brazil, Colombia, Guatemala, Mexico, Peru, Venezuela; immunization campaigns ongoing (e.g., Dominican Republic)^[23].
• The Americas were formally declared free of endemic rubella and congenital rubella syndrome (CRS) in April 2015, and PAHO notes the region has maintained rubella/CRS elimination in subsequent years (despite measles flare-ups)^[24].

• Programmatic setbacks (e.g., early-2000s northern Nigeria) with vaccine refusals led to large outbreaks and child deaths^[25].
• In developing countries, measles remains common. Unvaccinated populations are at risk for the disease.
• After vaccination rates dropped in northern Nigeria in the early 2000s due to religious and political objections, the number of cases rose significantly, and hundreds of children died.^[25]
• A 2005 measles outbreak in Indiana was attributed to children whose parents refused vaccination.^[26]
• 2016→2019 global surge (major LMIC impact). Reported measles cases climbed to 869,770 in 2019 (highest since 1996), with deaths up ~50% from 2016 to ~207,500 in 2019; large outbreaks were concentrated in countries with chronic under-immunization and health-system gaps (DRC, Madagascar, Samoa, Ukraine, others)^[4][27].

• DRC, 2019–2020: “World’s worst measles epidemic” with >6,000 deaths by Jan 2020; drivers included low coverage, malnutrition, weak systems, other epidemics, access insecurity^[28].
• Madagascar, 2018–2019: explosive nationwide epidemic; >100,000 cases over first 6 months^[29][30].
• Pacific (Samoa et al.), 2019: severe outbreaks with emergency declarations; extremely low MMR coverage preceded the surge^[31].
• WHO Europe spillover affecting lower-income settings (2019): Regional spike, majority of cases in Ukraine early 2019 (vaccine gaps)^[32].

• Pandemic shock and recovery lag in LMICs. First-dose measles coverage (MCV1) fell to ~81% (2021) and only partly recovered to ~83% (2022), below 2019’s 86%; WHO estimates ~35.2 million additional children at risk from service disruptions^[4][33].
• Ongoing high burden post-COVID. CDC estimates ~10.3 million infections in 2023 and outbreaks in every region; LMICs bear disproportionate morbidity/mortality^[34].
• Surveillance & lab capacity improvements relevant to LMICs.
  • Field confirmation: Rapid diagnostic tests (RDTs) for measles IgM (capillary blood/oral fluid) facilitate real-time confirmation where EIA/RT-PCR capacity is limited. Genes can be amplified from dried IgM-positive RDTs to support genotyping. (Appendix section “Measles diagnostic and genotypes monitoring”)^[35][36].
  • Genomic surveillance: 24 genotypes (N-450 window) remain the basis for global tracking; since 2018, B3, D4, D8, H1 are identified, with B3/D8/H1 dominating 2024–2025 outbreaks; Nanopore enables low-cost near-full genomes for chain tracking in resource-limited labs^[37][38].
  • Antigenic stability & vaccine breadth: Despite genotype diversity, H and F have remained antigenically stable for decades; H-specific antibodies dominate protection; vaccine lineage (genotype A) continues to protect across circulating genotypes^{[39][40][41][42]}.
• Programmatic shifts & evidence relevant to LMIC policy.
  • Early-age vaccination discussions: WHO technical consultations and multiple studies examine <9-month dosing (maternal antibody interference vs. outbreak control), waning dynamics, and boost strategies — critically relevant for LMIC settings with high infant exposure risk^[43][44][45].
  • Vitamin A in severe measles (still pertinent in LMICs): WHO clinical guidance and evidence syntheses reaffirm adjunct vitamin A for complicated measles (malnutrition, eye complications), reflecting persistent LMIC risk profiles^[46][47][48].
• Financing headwinds (program risk). Recent reporting raised concerns about potential U.S. cuts to Gavi; Gavi stated no official termination notice had been received, but any reduction would jeopardize LMIC immunization^[49].

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Guillermo Rodriguez Nava, M.D. [2]

Measles is a disease with very low incidence in the developed world. Lack of vaccination against measles is one of the biggest risk factors that predisposes measles spread. In developed countries like USA, most cases are attributed to unvaccinated or incompletely vaccinated travelers from other parts of the world. Primary vaccine failure occurs in approximately 5% of individuals vaccinated with a single dose of vaccine at 12 months of age or older and also predisposes an individual to the risk of developing measles.^[1]

• Unvaccinated individuals: a retrospective cohort study showed that children who have philosophical and religious exemptions from immunization were 22.2 times (95% confidence interval [CI], 15.9-31.1) more likely to acquire measles.^[2]
• Limited vaccination: incomplete doses of the vaccine; up to 35% children vaccinated with only 1 dose of MMR vaccine do not have protective antibodies.^[3]
• Living in crowded and/or unsanitary conditions such as prisons and college dorm rooms
• Traveling to less developed and developing countries where measles is common
• Weakened immune system even if vaccinated
• Winter and spring seasons
• Born after 1956 and never fully vaccinated since.
• Health care workers

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Guillermo Rodriguez Nava, M.D. [2]; Vidit Bhargava, M.B.B.S [3]

Measles spreads through the air by breathing, coughing or sneezing. It is so contagious that any child who is exposed to it and is not immune will probably get the disease. The virus lives in the mucus in the nose and throat of the infected person. When that person sneezes or coughs, droplets spray into the air. The virus can live on infected surfaces for up to 2 hours and spreads so easily that people who are not immune will probably get it when they come close to someone who is infected. Measles is a disease of humans.

Complications with measles are relatively common, ranging from relatively mild and less serious diarrhea, to pneumonia and encephalitis (subacute sclerosing panencephalitis – SSPE). Complications are usually more severe amongst adults who catch the virus.

Measles itself is unpleasant, but the complications are dangerous. Six to 20 percent of the people who get the disease will get an ear infection, diarrhea, or even pneumonia. One out of 1000 people with measles will develop inflammation of the brain, and about one out of 1000 will die.

• The incubation period usually lasts 10 days (with a range from 7 to 18 days) from exposure to the onset of fever.
• The disease is characterised by prodromal fever, conjunctivitis, coryza, cough and the presence of Koplik spots (reddish spots with a white centre) on the buccal mucosa.
• A characteristic red rash appears on the third to seventh day beginning on the face, becoming generalized and lasting 4-7 days.
• The rash is caused by an allergic response due to the union of sensitized lymphoid cells and measles antibody with the virus in the skin.
• A similar reaction occurs in the epithelium, leading to conjunctivitis, stomatitis, pneumonitis and acute inflammation of the gastrointestinal tract.
• This allergic reaction clears the virus and is followed by a period of anergy during which many immune responses are greatly diminished.
• This immuno-suppression, which may last for many weeks, results in increased susceptibility to other infections such as those caused by pneumococcus.
• The three major causes contributing to the high case-fatality rate are pneumonia, diarrhea and croup.^[1]

Complications with measles are relatively common. In industrialized countries, complications occur in around 10-15% of cases, ranging from relatively mild and less serious diarrhea, to pneumonia and encephalitis (subacute sclerosing panencephalitis – SSPE). The frequency of complications in developing countries is less well known. At least three-quarters of cases in developing countries can be expected to have at least one complication and some have multiple systems involvement. Complications are usually more severe amongst adults who catch the virus. SSPE is a very rare, but fatal degenerative disease of the central nervous system that results from a measles virus infection acquired earlier in life. The first signs of SSPE may be changes in personality, a gradual onset of mental deterioration and myoclonia (muscle spasms or jerks). The diagnosis of SSPE is based on signs and symptoms and on test results, such as typical changes observed in electroencephalographs, an elevated anti-measles antibody (IgG) in the serum and cerebrospinal fluid, and typical histologic findings in brain biopsy tissue. There are reports of remission and some treatments are available; however, the average survival is one to two years. There is no evidence that measles vaccine can cause SSPE.

The fatality rate from measles for otherwise healthy people in developed countries is low: approximately 1 death per thousand cases. In underdeveloped nations with high rates of malnutrition and poor healthcare, fatality rates of 10 percent are common. In immunocompromised patients, the fatality rate is approximately 30 percent.

Serious Complications^[2]

• Diarrhea
• Ear infections
• Pneumonia
• Encephalitis
• Seizures
• Death

Approximately 20% of reported measles cases experience one or more complications. These complications are more common among children under 5 years of age and adults over 20 years old. Measles causes ear infections in nearly one out of every 10 children who get it. As many as one out of 20 children with measles gets pneumonia, and about one child in every 1,000 who get measles will develop encephalitis. (This is an inflammation of the brain that can lead to convulsions, and can leave your child deaf or mentally retarded.) For every 1,000 children who get measles, one or two will die from it. Measles can also make a pregnant woman have a miscarriage, give birth prematurely, or have a low-birth-weight baby. In developing countries, where malnutrition and vitamin A deficiency are prevalent, measles has been known to kill as many as one out of four people. It is the leading cause of blindness among African children. Measles kills almost 1 million children in the world each year.

Measles can also lead to life-long disabilities, including blindness, brain damage and deafness. Low vitamin A status has been associated with a higher rate of complications and a higher death rate, as it has similar pathological effects on epithelia and the immune system.

Measles itself is unpleasant, but the complications are dangerous. Six to 20 percent of the people who get the disease will get an ear infection, diarrhea, or even pneumonia. One out of 1000 people with measles will develop inflammation of the brain, and about one out of 1000 will die.

Most measles deaths (98%) occur in developing countries, where vitamin A deficiency is common. The case fatality rates in developing countries are normally estimated to be 3-5%, but may reach 10-30% in some situations. This compares with 0.1% in many industrialised countries. Through synergy with measles infection, vitamin A deficiency contributes to the estimated 1 million childhood deaths from measles every year. Half of the childhood corneal blindness in developing countries is attributable to vitamin A deficiency, and half to measles infection.^[1]

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