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Maculopapular rash

A maculopapular rash is an acute, generalized skin eruption characterized by the presence of both erythematous macules—flat, discolored patches—and papules—small, elevated bumps—without overlying scaling, often blending into larger patches.^[1] This type of rash is one of the most common dermatologic presentations and typically indicates an underlying systemic process rather than a primary skin disorder.^[2] The rash most frequently arises from infectious etiologies, including viral infections such as enteroviruses, Epstein-Barr virus, cytomegalovirus, parvovirus B19, SARS-CoV-2, measles, and rubella,^[3] which often precede the eruption with prodromal symptoms like fever, malaise, and lymphadenopathy.^[1] Bacterial causes, such as secondary syphilis, rickettsial diseases like Rocky Mountain spotted fever, or typhoid fever, can also produce similar eruptions, sometimes accompanied by high fever and organ involvement.^[2] Drug-induced reactions represent another major category, commonly triggered by antibiotics (e.g., beta-lactams, sulfonamides), anticonvulsants, or nonsteroidal anti-inflammatory drugs, typically emerging 5 to 21 days after drug initiation and starting on the trunk before spreading to the extremities.^[1] Less commonly, it may stem from allergic reactions, autoimmune conditions like Still's disease, or hypersensitivity syndromes such as serum sickness.^[2] Clinically, the rash often begins on the trunk and proximal extremities, spreading centrifugally in viral cases or involving the face and distal limbs in drug reactions, with lesions measuring 2 to 10 mm and potentially pruritic or associated with enanthemas (mucosal involvement).^[1] Accompanying symptoms may include fever, headache, myalgias, arthralgias, or gastrointestinal upset, and the eruption usually resolves within 1 to 2 weeks without scarring, though severe cases can lead to desquamation or hyperpigmentation.^[2] Diagnosis relies on a detailed history, physical examination assessing rash morphology and distribution, and targeted investigations such as blood tests for viral serologies, drug history review, or skin biopsy to differentiate infectious from hypersensitivity origins—histopathology often reveals spongiosis and perivascular lymphocytic infiltrates in drug-induced cases versus viral cytopathic effects.^[1] Treatment is primarily supportive and etiology-specific: discontinuing the offending drug for hypersensitivity reactions, antiviral or antibiotic therapy for confirmed infections (e.g., acyclovir for certain viral causes), and symptomatic relief with topical corticosteroids, oral antihistamines, or oatmeal baths to alleviate pruritus.^[2] In uncomplicated cases, the rash is self-limiting, but prompt medical evaluation is essential if accompanied by high fever, respiratory distress, or signs of systemic involvement to rule out life-threatening conditions like toxic epidermal necrolysis or severe infections.^[1]

Definition and Characteristics

Definition

A maculopapular rash is defined as a cutaneous eruption consisting of both macules—flat, nonpalpable areas of skin discoloration typically less than 1 cm in diameter—and papules—small, solid, elevated lesions less than 1 cm in diameter that are palpable.^[4] These lesions often appear erythematous, blending flat and raised components in a distinctive pattern that differentiates the rash from purely macular or papular eruptions.^[5] The term "maculopapular" derives from "maculo-," rooted in the Latin macula meaning spot or blemish, and "papular," from papula referring to a pimple or raised nodule.^[6] Morphologically, the individual lesions in a maculopapular rash are usually 1 to 5 mm in size, though they can vary, and may coalesce to form larger plaques or patches exceeding 1 cm.^[4] The rash is frequently red or pink on lighter skin tones but can present as purple, brown, or violaceous on darker skin, reflecting variations in pigmentation and erythema visibility.^[7] Lesions may be pruritic, causing itching, or asymptomatic, depending on the underlying process, and they typically do not involve blistering or scaling unless secondarily affected.^[8] The term was coined in dermatology to characterize mixed flat and raised skin eruptions, with early descriptions appearing in 19th-century medical literature for infectious exanthems such as those seen in scarlet fever and measles.^[9] These historical accounts highlighted the rash's role in recognizing systemic illnesses, establishing its morphological framework in clinical observation long before modern etiological classifications.^[10]

Clinical Presentation

A maculopapular rash typically manifests as an acute, generalized eruption of discrete erythematous macules and papules, measuring 1 to 4 mm in diameter, without overlying scaling. These lesions are often flat or slightly raised and may coalesce into larger patches over time. The rash commonly begins on the trunk and spreads symmetrically to the proximal extremities, with possible involvement of the face or distal limbs in varying degrees.^[1]^[11]^[12] Patients frequently report mild pruritus or a burning sensation with the rash, though it can be asymptomatic in some instances. Systemic symptoms such as fever and malaise often accompany the eruption, but the rash itself is generally blanching upon diascopy, distinguishing it from purpuric lesions. In acute presentations, the rash evolves rapidly over 48 hours to several days and typically resolves within 3 to 7 days, whereas chronic forms may persist longer.^[13]^[11]^[1] Variations in appearance occur based on skin type and patient age. In lighter skin tones, the lesions appear pink to red, while in darker skin, they may present as hyperpigmented, violaceous, or non-blanching patches. Pediatric cases often feature a more truncal distribution with peripheral spread, whereas adult presentations may show greater involvement of the extremities.^[7]^[14]^[12] The rash's progression varies, with acute forms exhibiting sudden onset and rapid evolution, potentially leading to desquamation upon resolution. In other scenarios, onset is more insidious, with gradual intensification over days to weeks, followed by fading that may leave post-inflammatory hyperpigmentation.^[13]^[11]^[1]

Causes

Infectious Causes

Maculopapular rashes are frequently associated with infectious agents, particularly viruses, which trigger immune responses leading to the characteristic eruption. Viral causes predominate in pediatric and adult populations, often transmitted via respiratory droplets or close contact. For instance, measles (rubeola), caused by the measles virus, has an incubation period of 10-14 days and typically begins with a prodrome of fever, cough, coryza, and conjunctivitis, followed by a maculopapular rash starting on the face and spreading downward. Transmission occurs through airborne spread from respiratory secretions, with higher incidence in unvaccinated children in endemic areas. Rubella, caused by the rubella virus, features a milder maculopapular rash with a 14-21 day incubation period, often accompanied by low-grade fever and lymphadenopathy, and is transmitted similarly via respiratory droplets. Parvovirus B19 infection presents with a "slapped-cheek" erythema followed by a lacy maculopapular rash on the trunk and limbs, with an incubation of 4-21 days, spread through respiratory secretions or blood. Enteroviruses, such as coxsackieviruses, cause summer-associated maculopapular rashes with hand-foot-mouth involvement, transmitted fecal-orally or via respiratory routes, and incubation of 3-6 days. Epstein-Barr virus (EBV) causes a maculopapular rash in 3-15% of infectious mononucleosis cases, often on the trunk and arms, with a 4-6 week incubation period and transmission via respiratory secretions or saliva.^[15] Cytomegalovirus (CMV) can produce a similar diffuse maculopapular eruption in primary infection, especially in immunocompetent adults, with a 3-8 week incubation and spread through bodily fluids.^[16] Human herpesvirus 6 (HHV-6) leads to roseola infantum, featuring high fever followed by a pink maculopapular rash on the trunk in infants, with 5-8 days incubation and respiratory or fecal-oral transmission.^[17] Zika virus, a flavivirus transmitted by Aedes mosquitoes, induces a pruritic maculopapular rash often with arthralgia, following a 3-14 day incubation. Acute HIV seroconversion can manifest as a diffuse maculopapular rash on the trunk and face during the 2-4 week incubation post-exposure, via sexual, bloodborne, or perinatal transmission.^[18] Bacterial causes of maculopapular rashes include spirochetal, rickettsial, and streptococcal infections, often with systemic symptoms. Secondary syphilis, the stage following primary chancre in Treponema pallidum infection, features a symmetric maculopapular rash involving palms and soles, with an overall incubation of 10-90 days (average 21 days) and sexual transmission. Rickettsial infections like Rocky Mountain spotted fever, caused by Rickettsia rickettsii and transmitted by tick bites, evolve from maculopapular to petechial rash starting on extremities after a 2-14 day incubation, with potential for severe vascular involvement. Group A Streptococcus-induced scarlet fever presents with a sandpaper-like maculopapular rash on the trunk and folds, following pharyngitis, with transmission via respiratory droplets and incubation of 2-5 days. Typhoid fever, caused by Salmonella enterica serovar Typhi, features rose-colored maculopapular spots (rose spots) on the trunk and abdomen after the first week of prolonged fever, with fecal-oral transmission, 7-14 day incubation, and higher incidence in areas with poor sanitation.^[19] Mycoplasma pneumoniae infection often presents with a diffuse maculopapular rash in 10-25% of cases, alongside atypical pneumonia, transmitted via respiratory droplets with 2-3 week incubation, common in children and adolescents.^[20] Other microbial causes encompass fungal and parasitic pathogens, typically in immunocompromised or endemic settings. Disseminated histoplasmosis, caused by Histoplasma capsulatum inhalation from soil, can produce maculopapular eruptions in severe cases, with incubation of 3-17 days and higher risk in endemic river valley regions. Parasitic infections like onchocerciasis (river blindness), due to Onchocerca volvulus transmitted by blackfly bites in sub-Saharan Africa and Latin America, may cause pruritic maculopapular rashes as part of dermatitis, with chronic exposure rather than fixed incubation. The underlying mechanism for infectious maculopapular rashes involves immune-mediated cytokine release, such as interferon-gamma and tumor necrosis factor, which induce vascular endothelial changes, perivascular inflammation, and T-cell infiltration, resulting in the flat-topped papules and macules without blistering.

Non-Infectious Causes

Non-infectious causes of maculopapular rash encompass a range of hypersensitivity reactions, autoimmune disorders, paraneoplastic syndromes, and idiopathic or environmental triggers that lead to erythematous, flat-topped papules and macules on the skin. These etiologies often present with systemic symptoms and require differentiation from infectious mimics based on history and timing. Unlike microbial causes, non-infectious rashes typically arise from extrinsic or internal dysregulations without pathogen involvement. Drug-related maculopapular rashes, also known as morbilliform or exanthematous eruptions, are among the most frequent non-infectious triggers, accounting for a significant portion of cutaneous adverse drug reactions. They commonly occur 7 to 14 days after initial exposure to the offending agent, presenting as symmetric, measles-like eruptions starting on the trunk and spreading to extremities. Antibiotics such as beta-lactams (e.g., amoxicillin) and sulfonamides are frequent culprits, alongside anticonvulsants like phenytoin, lamotrigine, and carbamazepine, as well as non-steroidal anti-inflammatory drugs (NSAIDs). These reactions often manifest as type IV delayed hypersensitivity, with histological features including lymphocytic infiltration. Fixed drug eruptions, a variant, recur at the same sites with each exposure, appearing as round, erythematous patches that may blister. Serum sickness-like reactions, another drug-induced form, can produce maculopapular rashes with arthralgias and fever, typically 1 to 3 weeks post-exposure to drugs like cefaclor or bupropion. Autoimmune conditions can also precipitate maculopapular rashes through immune-mediated inflammation. Adult-onset Still's disease features an evanescent, salmon-pink maculopapular eruption on the trunk and proximal limbs, coinciding with fever spikes and resolving between episodes. Dermatomyositis may present with pruritic, violaceous maculopapular lesions in a heliotrope distribution around the eyes or on knuckles (Gottron's papules), often with proximal muscle weakness. These rashes reflect underlying systemic autoimmunity, with histological evidence of interface dermatitis. Contact dermatitis, while primarily localized, can overlap with diffuse maculopapular patterns in severe allergic responses to topical agents. Other non-infectious etiologies include paraneoplastic syndromes associated with malignancies, such as lymphomas, where generalized maculopapular rashes may precede diagnosis by weeks or months as an immune-mediated response. Idiopathic conditions like pityriasis rosea typically begin with a solitary herald patch—a larger oval lesion—followed by a widespread maculopapular eruption on the trunk, oriented along skin tension lines (Christmas tree pattern). Environmental factors, such as photoallergic reactions from topical agents combined with UV exposure, can induce pruritic maculopapular rashes 1 to 14 days after sensitization. Risk factors for non-infectious maculopapular rashes include a personal or family history of atopy, which heightens susceptibility to hypersensitivity reactions, though delayed T-cell mediated types are less directly linked than IgE-mediated ones. Genetic polymorphisms in drug metabolism (e.g., HLA alleles) increase vulnerability to specific agents like anticonvulsants. Temporal correlation with drug initiation or environmental exposure remains crucial for identification, with prior sensitization shortening latency to 1 to 4 days upon re-exposure.

Diagnosis

History and Physical Examination

The evaluation of a maculopapular rash commences with a comprehensive patient history to elucidate potential triggers and associated features. Clinicians should inquire about the onset and progression of the rash, including its initial location and evolution over time, as acute onset within days often points to infectious or drug-related causes, while subacute or chronic development may suggest autoimmune or neoplastic etiologies. Recent exposures are critical, encompassing travel to regions with endemic infections, initiation of new medications (prescription, over-the-counter, or supplements), close contacts with individuals exhibiting similar symptoms, and potential environmental factors such as pets, hobbies, or occupational hazards. Vaccination status, particularly for measles, rubella, and varicella, should be assessed to identify susceptibility to vaccine-preventable exanthems.^[21]^[12]^[22] Associated symptoms provide further diagnostic clues and help gauge severity. Fever, arthralgias, myalgias, lymphadenopathy, or gastrointestinal complaints may accompany infectious causes, whereas pruritus is more indicative of hypersensitivity reactions like drug eruptions. Family history of similar rashes, atopy, or autoimmune disorders can highlight genetic predispositions, and a sexual history is relevant for sexually transmitted infections such as syphilis. In pediatric patients, details on prodromal symptoms like cough or coryza are particularly useful for viral differentials.^[21]^[12]^[23] The physical examination focuses on meticulous skin inspection and systemic assessment to characterize the rash and detect extracutaneous involvement. Vital signs, including temperature, are evaluated to identify systemic illness, as fever often accompanies infectious maculopapular eruptions. Lesions are inspected for distribution patterns—such as centripetal spread from trunk to extremities in many viral exanthems or acral involvement (palms and soles) in secondary syphilis—and palpated for induration, tenderness, or scaling. Standard rash evaluation includes assessing lesion size (typically 2-10 mm), color (erythematous), blanching (to distinguish vascular components), and arrangement (discrete or confluent). Dermoscopy may be employed to further assess blanching or other features. Lymph nodes, mucous membranes, and general appearance are examined for enlargement, ulceration, or toxicity.^[21]^[12]^[23] Red flags warrant urgent evaluation and may indicate life-threatening conditions. These include mucosal involvement (e.g., oral erosions suggesting Stevens-Johnson syndrome), rapid progression or confluence of lesions implying vasculitis or toxic epidermal necrolysis, petechiae with fever raising concern for meningococcemia, and signs of hemodynamic instability or neurologic compromise. A toxic appearance or non-blanching purpura further heightens suspicion for bacterial sepsis or thrombotic disorders.^[21]^[12]^[23]

Diagnostic Tests

Diagnostic tests for maculopapular rash are selected based on the patient's history and physical examination findings to identify underlying infectious, allergic, autoimmune, or other causes. These tests are typically reserved for cases where the etiology remains unclear after initial assessment, atypical presentations, or persistent symptoms, as many maculopapular rashes resolve spontaneously without extensive investigation.^[21] Blood tests form the cornerstone of laboratory evaluation. A complete blood count (CBC) is often performed to detect eosinophilia, which suggests an allergic or drug-induced etiology, or leukocytosis and thrombocytopenia indicative of infection.^[21] Serologic testing targets specific pathogens; for example, IgM antibodies for rubella virus confirm acute infection in patients with compatible rash and exposure history.^[24] Similarly, polymerase chain reaction (PCR) assays detect viral DNA, such as parvovirus B19 in cases of slapped cheek-like rashes extending to maculopapular patterns, particularly in pregnant patients or those with joint symptoms; for suspected COVID-19 associated with recent respiratory symptoms, SARS-CoV-2 PCR or antigen testing is indicated.^[25]^[26] For autoimmune disorders like systemic lupus erythematosus, antinuclear antibody (ANA) testing is indicated if photosensitivity or multi-system involvement is present, with a positive titer supporting further specific autoantibody evaluation.^[27] In suspected drug reactions, liver and kidney function tests assess for organ involvement, as elevations may signal severe hypersensitivity syndromes like DRESS (drug reaction with eosinophilia and systemic symptoms).^[28] Skin biopsy is recommended for atypical, persistent, or non-resolving maculopapular rashes to provide histopathological confirmation. In drug-induced cases, it often reveals interface dermatitis with vacuolar degeneration of the basal layer and perivascular lymphocytic infiltrates.^[29] For infectious etiologies, biopsies may show perivascular infiltrates with atypical lymphocytes or focal spongiosis, aiding differentiation from viral exanthems.^[30] Direct immunofluorescence can further identify immune complex deposits in certain autoimmune rashes. Additional specialized tests are employed based on clinical suspicion. Patch testing identifies contact allergens in cases suggestive of delayed hypersensitivity, though it is less useful for systemic drug reactions.^[31] For rashes involving palms and soles raising concern for syphilis, rapid plasma reagin (RPR) or Venereal Disease Research Laboratory (VDRL) tests screen for treponemal infection, with darkfield microscopy confirming spirochetes in lesion exudates if available.^[32] Imaging studies, such as computed tomography (CT), are rarely needed but may evaluate systemic involvement in malignancy-associated rashes, like paraneoplastic dermatoses linked to underlying tumors.^[33] Guidelines emphasize tailoring tests to historical clues, such as travel, medications, or exposures, to avoid unnecessary procedures while prioritizing rapid testing for life-threatening causes like meningococcemia or severe drug reactions.^[21]

Treatment and Management

Symptomatic Relief

Symptomatic relief for maculopapular rash focuses on alleviating itching (pruritus), discomfort, and associated symptoms like fever or pain, without addressing the underlying cause. Topical therapies are often the first line for mild cases, including calamine lotion applied several times daily to soothe irritated skin and reduce itching. Low-potency hydrocortisone cream (1%) can also be used sparingly on unaffected areas to decrease inflammation and pruritus, but it should be avoided on areas suspected of infection to prevent worsening bacterial spread.^[34] Oral medications provide additional relief for more persistent symptoms. Antihistamines such as diphenhydramine (25-50 mg every 6 hours in adults) are commonly recommended to manage pruritus, particularly when the rash has an allergic component. For fever or mild pain accompanying the rash, acetaminophen can be administered at standard doses (e.g., 500-1000 mg every 4-6 hours in adults, not exceeding 4000 mg daily) to provide comfort without anti-inflammatory effects that might complicate viral etiologies.^[12]^[35] Supportive care measures enhance overall comfort and promote skin healing. Cool compresses applied for 15-30 minutes several times a day, along with oatmeal baths or baking soda soaks, help calm inflamed skin and reduce itching. Wearing loose, breathable clothing minimizes friction on the rash, while maintaining hydration and encouraging rest supports the body's recovery, especially in viral cases. In children, aspirin must be strictly avoided due to the risk of Reye's syndrome when used during viral illnesses that may present with maculopapular rashes.^[36]^[37]

Cause-Specific Interventions

For infectious causes of maculopapular rash, treatment targets the underlying pathogen to promote resolution. In cases of varicella-zoster virus infection, particularly severe presentations, intravenous acyclovir at 10 mg/kg every 8 hours for 7-10 days is recommended, especially in immunocompromised individuals or those at high risk for complications.^[38] For secondary syphilis, which often manifests with a symmetric maculopapular eruption on the trunk and extremities, a single intramuscular dose of benzathine penicillin G 2.4 million units remains the first-line therapy, effectively eradicating Treponema pallidum and resolving the rash.^[39] Contagious etiologies such as measles require supportive isolation measures, with patients excluded from contact until 4 days after rash onset to prevent transmission, alongside post-exposure prophylaxis using measles-mumps-rubella (MMR) vaccine within 72 hours of exposure for susceptible individuals without contraindications.^[40]^[41] Non-infectious maculopapular rashes necessitate etiology-specific strategies focused on removing triggers or modulating immune responses. Drug-induced eruptions, a common non-infectious cause, are primarily managed by immediate discontinuation of the offending agent, which typically leads to rash resolution within 1-2 weeks, though desensitization protocols may be employed under specialist supervision to allow continued use of essential medications like antibiotics in select cases.^[31]^[42] For autoimmune conditions such as dermatomyositis, which can present with a pruritic maculopapular rash on sun-exposed areas, high-dose corticosteroids (e.g., prednisone 1 mg/kg/day) serve as initial therapy, often combined with steroid-sparing immunosuppressants like methotrexate or azathioprine for long-term control of both cutaneous and muscular symptoms.^[43]^[44] Professional guidelines emphasize tailored interventions and vigilant monitoring. The Infectious Diseases Society of America (IDSA) endorses MMR vaccination or intramuscular immunoglobulin for measles post-exposure prophylaxis in high-risk groups, while consultation with an allergist is advised for suspected drug reactions to guide desensitization or alternative therapies.^[41] Follow-up evaluation, typically 2-4 weeks after initiating cause-specific treatment such as antibiotics, is essential to confirm rash resolution and assess for recurrence or complications, with serial serologic testing recommended for infections like syphilis.^[39]^[8]

Prognosis and Complications

Prognosis

The prognosis of maculopapular rash varies depending on the underlying cause, patient age, and immune status, but most cases are self-limiting and resolve without long-term sequelae. Viral-induced maculopapular rashes, common in children, typically resolve within 1 to 2 weeks without scarring, often accompanied by mild systemic symptoms that subside concurrently.^[12]^[45] For instance, the rash in measles lasts 5 to 6 days following its onset, with full recovery expected in uncomplicated cases.^[40] In contrast, maculopapular rashes associated with autoimmune disorders, such as systemic lupus erythematosus, tend to be chronic or relapsing, potentially persisting for months or recurring with disease flares, though they do not typically impact overall life expectancy when limited to cutaneous involvement.^[46] Drug-induced maculopapular eruptions, the most frequent non-infectious type, generally resolve within 7 to 14 days after discontinuation of the offending agent, with over 90% of hypersensitivity reactions presenting in this form achieving complete resolution upon cause removal.^[8]^[12] Prognosis is more favorable in pediatric patients with infectious etiologies, where symptoms are often milder and self-resolve without intervention, compared to adults or immunocompromised individuals. In patients with HIV or other immunosuppressive conditions, maculopapular rashes may signal disease progression or opportunistic infections, leading to prolonged courses or increased risk of complications that worsen outcomes.^[47]^[48] Recurrence rates are low for acute infectious causes following acquired immunity, as seen in post-viral exanthems, but remain high for drug allergies if re-exposure to the causative medication occurs without prior avoidance strategies.^[49] Overall, more than 90% of maculopapular rashes resolve fully with identification and elimination of the trigger, and mortality is rare except in cases linked to severe complications like encephalitis in measles.^[12]^[50]

Complications

Maculopapular rashes can predispose the skin to secondary bacterial infections, such as impetigo, particularly when the integrity of the skin barrier is compromised by scratching or excoriation.^[51] This occurs as bacteria like Staphylococcus aureus or Streptococcus pyogenes colonize disrupted areas, leading to superficial crusting and potential spread if untreated.^[52] Post-inflammatory hyperpigmentation is a common sequela, manifesting as tan to brown macules at sites of resolved inflammation due to excess melanin production in response to the rash.^[53] This pigmentary change is more pronounced in individuals with darker skin tones and typically fades over months but may persist longer without intervention.^[54] In severe cases, such as those evolving into more extensive cutaneous reactions, scarring can result from deeper dermal involvement or secondary ulceration.^[55] Systemic complications vary by etiology; for instance, measles-associated maculopapular rashes carry risks of encephalitis in approximately 1 per 1,000 cases, often leading to permanent neurological sequelae, and pneumonia in up to 1 in 20 children, which is the leading cause of measles-related mortality in young patients.^[56] Drug-induced maculopapular eruptions rarely progress to severe forms like Stevens-Johnson syndrome, with an overall incidence of such reactions estimated at less than 1% but potentially higher in susceptible individuals exposed to culprit medications like antibiotics or anticonvulsants.^[57] Cause-specific risks include Guillain-Barré syndrome following Zika virus infection, where epidemiological data show a temporal association with increased incidence during outbreaks, affecting up to 97% of cases with preceding viral symptoms.^[58] In serum sickness-like reactions, renal involvement such as acute kidney injury can occur in severe or recurrent episodes due to immune complex deposition, though this is uncommon in isolated incidents.^[59] Early intervention, including prompt identification and management of the underlying cause, mitigates these risks; vaccination against measles, for example, prevents up to 97% of complications by averting infection altogether.^[60] While most maculopapular rashes resolve without long-term issues, these potential complications underscore the importance of monitoring, especially in high-risk etiologies.

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Apr 17, 2024 · If there are no contraindications to vaccination, MMR vaccine can be given as post- exposure prophylaxis to people who lack evidence of ...
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The morbilliform rash is characteristic of a drug eruption and consistent with use of a sulfonamide medication. Morbilliform rash is the most common drug ...Missing: etymology | Show results with:etymology<|separator|>
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Rest; Increased fluid intake (to prevent dehydration); Cool baths with baking soda or Aveeno (to relieve itching). Children should not scratch the blisters, as ...Missing: relief | Show results with:relief
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... serum sickness. However, repeat exposure to a causative agent leading to multiple episodes of serum sickness has caused renal failure and death in animal models ...
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Jan 17, 2025 · Two doses of the MMR vaccine are recommended by doctors as the best way to protect against measles, mumps, and rubella.