Infectious Diseases with Rash, Mumps, Whooping Cough (PDF)

Faculty of Medicine Infectious diseases with rash Infectious Diseases Pentru uz intern Este interzisă copierea și distribuirea neautorizată a acestui material.  MEASLES = highly contagious infe...

Faculty of Medicine Infectious diseases with rash Infectious Diseases Pentru uz intern Este interzisă copierea și distribuirea neautorizată a acestui material.  MEASLES = highly contagious infectious disease with exanthem & pathognomonic enanthem (Koplik’s spots) Pentru uz intern Este interzisă copierea și distribuirea neautorizată a acestui material. MEASLES worldwide spread Measles outbreaks every 4-5 years WHO & USA CDC data: - 2022: 9 bil cases of measles worldwide (> 130 000 deaths) - 1st 3 months of 2024: > 56 000 cases in WHO European Region Romanian Public Health Authority: Febr 2023 - 2024: > 23 900 cases of measles (21 deaths) - 2023: 74% all measles cases reported to ECDC - Romania Herd immunity requires at least 95% population fully vaccinated! Romania – 2022: MMR vaccine coverage: 83% population (1st dose); 71% (2nd dose) Este interzisă copierea și distribuirea neautorizată a acestui material.  MEASLES https://www.ecdc.europa.eu/sites/default/files/docume nts/measles-eu-threat-assessment-brief-february- 2024.pdf Este interzisă copierea și distribuirea neautorizată a acestui material. MEASLES – ETIOLOGY & EPIDEMIOLOGY Measles virus – RNA genome, Morbilivirus genus, Paramyxoviridae fam Young children (not vaccinated), possibly adolescents, young adults (rarely elderly) Risk groups for severe forms: - malnourished - immunocompromised - age < 5 years Source of infection: human Transmission route: airborne Infectivity ↑↑: Secondary attack rate > 90% (contagious 4 days < → 4 days > rash appears) Immunity > disease: life-long - newborns & infants (if immune mother): protected during first 4-6-9 months of life (maternal IgG Ab cross placenta in 3rd trimester of pregnancy) Outbreaks: schools, kindergartens, communities, families Este interzisă copierea și distribuirea neautorizată a acestui material. MEASLES - PATHOGENESIS - Invasion of respiratory epithelium → bloodstream spread (primary viremia 2-3 days > infection) to reticulo-endothelial system → replication → dissemination to skin, respiratory tract & other organs (secondary viremia occurs 3-4 days > 1st viremia - lasts for up to 7 days) - peak viremia = prodromal symptoms - multinucleated giant cells with inclusion bodies in nucleus & cytoplasm (Warthin-Finkeldey cells) in respiratory & lymphoid tissues (tonsils) - pathognomonic rash - results from the immunologic reaction between viral Ag and host immune mechanisms (Ab & T-cells), with involvement of capillary walls - immunocompromised hosts – atypical / absent rash Este interzisă copierea și distribuirea neautorizată a acestui material. MEASLES -IMMUNITY Post-infectious immunity – life-long Post-vaccine immunity: durable (years, probably life-long) Vaccination → disease incidence ↓ Following measles (disease), the host experiences significant immune suppression lasting for several weeks – months → ↑↑ susceptibility to other infections → reactivation of TB, bacterial infections Este interzisă copierea și distribuirea neautorizată a acestui material. MEASLES - CLINICAL MANIFESTATIONS Incubation period: - 10 days (for fever) - 14 days (for rash) Prodromal (pre-eruptive) phase – 2-3 days : * general symptoms: malaise, fever, anorexia * triple catarrh: - ocular: conjunctivitis, hyperlacrimation - resp: coryza, nasal discharge, dysphonia, cough - digestive: nausea, vomiting, ± diarrhea * enanthem=Koplik spots: white-grey spots on erythematous background - on the oral mucosa, corresponding to the level of 2nd molars - appear at the end of prodrome - begin to fade when exanthem appears Este interzisă copierea și distribuirea neautorizată a acestui material. MEASLES – CLINICAL MANIFESTATIONS Source of images: Archive of Infectious Exanthem Diseases Clinic I, Tirgu Mures, Romania usually begins on the face (retroauricular region, latero- cervical region) “descends” downwards from “head-to-toes” (spread from face to soles takes ≈ 3 days): - 1st day: neck & face - 2nd day: trunk & upper limbs - 3rd day: lower limbs erythematous maculo-papular rash confluent, especially on the face & neck lasts about 5 days starts to fade in the same order as the appearance (head-to-toe) followed by discoloration, hyperpigmentation (1 more week) Fever persists Duration of uncomplicated illness: 7-10 days Este interzisă copierea și distribuirea neautorizată a acestui material. Este interzisă copierea și distribuirea neautorizată a acestui material.  MEASLES COMPLICATIONS - RESPIRATORY Laryngitis Croup Otitis media, mastoiditis Pneumonia: - bacterial pneumonia - viral - giant cell (Hecht) pneumonia (severe, with respiratory failure) - mixed pneumonia (viral + bacterial superinfections) *bact superinfections: S pneumoniae, S pyogenes, H influenzae, S aureus Este interzisă copierea și distribuirea neautorizată a acestui material.  MEASLES NEUROLOGIC COMPLICATIONS Seizures Encephalitis (acute disseminated post-eruptive encephalitis) - 1‰ cases - demyelinating autoimmmune condition triggered by measles virus - appears several days / weeks > rash; seizures, neurological deficit, fever Inclusion encephalitis – immunocompromised hosts, 2-6 months > infection - direct infection of brain, neurological deterioration, death Subacute sclerosing panencephalitis (SSPE) – 1/10 000 – 1/100 000 cases - chronic degenerative CNS disorder - predominantly in children in their 1st decade of life - appears 5-10 years / initial infection, esp children who had measles in the 1st 2 years of life - findings: deterioration of intellectual function & personality changes - progressive lethal evolution within 1-3 years - no cure Este interzisă copierea și distribuirea neautorizată a acestui material.  MEASLES OTHER COMPLICATIONS gastrointestinal complications – diarrhea (+ dehydration) exacerbation / reactivation of tuberculosis (TB) transient hepatitis (↑liver enzymes) disseminated intravascular coagulation keratitis (malnourished, vit A deficiency) deafness thrombocytopenia Este interzisă copierea și distribuirea neautorizată a acestui material. MEASLES IN PECULIAR SITUATIONS Immunocompromised hosts: - rash: absent or atypical (since rash = result of interaction between T-cells, Ab and viral Ag) - giant cell pneumonia - encephalitis Pregnancy - measles virus – not teratogenic itself - more severe forms of disease in pregnant & parturient women - risk of miscarriage & premature delivery Neonates: “congenital measles” - rash: present at birth or appears in the first 10 days of life - infection acquired from non-immune mother who developed measles around delivery date - may be severe, mortality approaches 30% Este interzisă copierea și distribuirea neautorizată a acestui material.  MEASLES – POSITIVE DG Epidemiologic data: previously non-immunized, infectious contact 10 days < onset Clinical data: fever, triple catarrh, characteristic exanthem & enanthem Lab dg: WBC – normal / low (leukocytosis – bacterial superinfection) - serologic tests – most often used: anti-measles virus IgM Ab titer: ↑↑ in paired sera (acute & convalescent samples) - become detectable > 3rd day of rash - measles virus Ag detection – immunofluorescence – respir secretions - measles virus RNA detection (PCR): pharyngeal swab, respir secretions - detectable from onset, useful in partially vaccinated pts Este interzisă copierea și distribuirea neautorizată a acestui material. MEASLES -DDx Kawasaki disease Scarlet fever Infectious mononucleosis Toxoplasmosis Rash due to drug allergy Mycoplasma pneumoniae infection Este interzisă copierea și distribuirea neautorizată a acestui material. MEASLES TREATMENT no etiologic treatment (antiviral) therapy: largely supportive & symptomatic (NSAIDs, +- oxygen inhalation, IV fluids) Isolation ( quiet, well ventilated) Skin care Oral and nasal hygiene antibiotics in case of bacterial superinfection (otitis media, pneumonia) encephalitis - supportive care, therapy for increased intracranial pressure (depletion) (Isoprinosine attempted for SSPE) Este interzisă copierea și distribuirea neautorizată a acestui material.  MEASLES PROPHYLAXIS Anti-measles vaccine – live attenuated vaccine - induces seroconversion in 95% recipients - Immunity > vaccination: probably lifelong - included in a combination vaccine: measles–mumps-rubella (MMR) - 1st dose: adm to children age 12-15 months - 2nd dose: school-age children (age 5-6 years-old) - 10% healthy vaccine recipients develop high fever 5-7 days > vaccination, accompanied by a transient rash Contraindications: pregnancy, immune suppression (live attenuated virus), history of anaphylaxis to egg protein / neomicin Este interzisă copierea și distribuirea neautorizată a acestui material. RUBELLA (“German measles”) Pentru uz intern Este interzisă copierea și distribuirea neautorizată a acestui material. RUBELLA - ETIOLOGY & EPIDEMIOLOGY Rubella virus – RNA, Togaviridae fam highest incidence: spring most common age - children 5 - 9 years infectivity: moderate (compared to measles / varicella): attack rate: 40-80% Transmission: airborne (resp secretions droplets from infected pts, incl those with subclinical illness) → contagiousness: 7 days before – 7 days after onset of rash (highest while rash is erupting) vertical (maternal infection during pregnancy) → congenital rubella pts excrete the virus for months / years, despite presence of Ab Este interzisă copierea și distribuirea neautorizată a acestui material.  RUBELLA PATHOGENESIS > respiratory transmission: the virus replicates in the nasopharyngeal mucosa & regional lymph nodes - viremia: 5-7 days after exposure → spread to the tissues - placenta & fetus infected via hematogenous spread during viremia Este interzisă copierea și distribuirea neautorizată a acestui material. POST-NATAL RUBELLA - CLINICAL MANIFESTATIONS usually mild disease (in children – milder than in adults) up to 50% cases – subclinical incubation: 12-23 days (average: 18 days) prodrome phase – adults: fever, malaise, anorexia (several days) major sign: adenopathy - may appear 7 days < rash and last 2-6 weeks > - micropolyadenopathy (< 1 cm diameter): Retroauricular Posterior cervical Suboccipital Can be generalized Este interzisă copierea și distribuirea neautorizată a acestui material. POST-NATAL RUBELLA - CLINICAL MANIFESTATIONS Exanthem: maculopapular, not confluent, erythematous (pink) - begins on the face and spreads downwards on the body - transient – may disappear in 2-3 days, or even several hours - may be absent in some cases - may be accompanied by mild coryza, conjunctivitis Enanthem: petechial lesions on the soft palate (Forschheimer spots) +/- splenomegaly Este interzisă copierea și distribuirea neautorizată a acestui material.  POST-NATAL RUBELLA COMPLICATIONS arthritis / arthralgia – the most common complication → up to 1/3 adult female pts - fingers, wrists & knees - occurs at the appearance of rash / soon afterwards hemorrhagic manifestations - approx 1 / 3000 cases - more often in children than adults - secondary to thrombocytopenia & vascular damage, probably immunologically mediated → purpura encephalitis - uncommon (1 / 5000 cases) - more frequent in adults than children - mortality 20 - 50% 24 Este interzisă copierea și distribuirea neautorizată a acestui material. CONGENITAL RUBELLA - Transplacental spread to fetus: - Chronic fetal infection - Compromised fetal oxygenation - Disruption of normal organogenesis - Permanent organ defects: - Impaired mitosis - Cellular necrosis - Chromosomal breakage Consequences: - premature delivery - fetal death - birth defects Este interzisă copierea și distribuirea neautorizată a acestui material. CONGENITAL RUBELLA The earlier the infection during pregnancy - the more severe the illness first 2 months: 40-60% fetal risk - multiple congenital defects - and/or spontaneous abortion 3rd month: 30-35% risk - single defect: deafness / congenital heart defects 4th month:10 % risk - single congenital defect up to the 20th week of gestation: occasional fetal damage Gregg syndrome: - Cataract - Deafness - Cardiac birth defects - CNS malformations Este interzisă copierea și distribuirea neautorizată a acestui material.  CONGENITAL RUBELLA CLINICAL MANIFESTATIONS Low birth weight Cataract or glaucoma Thrombocytopenic purpura Retinopathy Hepatosplenomegaly Patent ductus arterious Bone lesions (radiolucent bone disease) Pulmonary stenosis Large anterior fontanelle Meningoencephalitis Behavioral disorders Generalized lymphadenopathy Mental retardation Hemolytic anemia Microcephaly Deafness Spastic diplegia Este interzisă copierea și distribuirea neautorizată a acestui material. Este interzisă copierea și distribuirea neautorizată a acestui material. Gregg syndrome (congenital rubella): - Cataract - Deafness - Cardiac birth defects - CNS malformations Este interzisă copierea și distribuirea neautorizată a acestui material. RUBELLA – POSITIVE DG Clinically difficult (usually a mild disease, nonspecific symptoms) Routine laboratory tests - not helpful for dg (leukopenia, atypical lymphocytes) Lab dg of rubella - most often serological (Ab) - Hemagglutination –inhibition (HAI) / ELISA techniques IgM – acute infection IgG – previous infection or vaccination In pregnancy: IgG avidity test: can establish the date of infection as less than 3 months (low avidity – primary recent infection in the previous 3 months) Este interzisă copierea și distribuirea neautorizată a acestui material. RUBELLA - DDx Scarlet fever Measles Infectious mononucleosis Toxoplasmosis Roseola infantum Erythema infectiosum Enterovirus infections Este interzisă copierea și distribuirea neautorizată a acestui material. RUBELLA - TREATMENT & PROPHYLAXIS No etiologic therapy (antiviral) Symptomatic treatment (fever, arthralgia) Anti-rubella vaccination - seroconversion rate of approx 95% - part of MMR (measles-mumps-rubella) vaccine – live attenuated vaccine - contraindicated in - immunocompromised hosts - pregnant women (avoid pregnancy 1 month > vaccination) - however, no cases of congenital rubella were reported after inadvertent adm of vaccine during pregnancy (not motif for termination of pregnancy) Este interzisă copierea și distribuirea neautorizată a acestui material. ENTEROVIRUS INFECTIONS Pentru uz intern Este interzisă copierea și distribuirea neautorizată a acestui material. ENTEROVIRUS INFECTIONS RNA genome, Picornaviridae fam no lipidic envelope → resistant to acid environment (gastric HCl) → able to replicate inside the digestive tract – “entero”virus > 100 serotypes enteroviruses: Poliovirus – 3 serotypes (1-3: Brunhilde, Lansing, Leon) Coxsackievirus: - group A: → flaccid paralysis in suckling mice - group B: – spastic paralysis in mice Echovirus (Enteric Cytopathic Human Orphan virus): cytopathic effect (cell cultures), no disease in mice Enterovirus serotypes 68-71 - enterovirus 70 – acute hemorrhagic conjunctivitis outbreaks - enterovirus 71 – paralytic disease Este interzisă copierea și distribuirea neautorizată a acestui material. ENTEROVIRUS INFECTIONS - EPIDEMIOLOGY worldwide distribution, endemic-epidemic pattern seasonality: temperate climate – warm season (tropical reg – all year round) ¾ cases – children risk factors: overcrowding, poor hygiene, potential nosocomial transmission Source of infection: human – pts with symptomatic / asymptomatic infection 50% all enterovirus inf / 90% poliovirus inf – asymptomatic Infectivity: high Susceptibility: universal Immunity: serotype-specific (infection with other serotypes is possible) - IgM Ab appear 1-3 days > infectious contact, last for 2-3 months - IgG Ab initially appear about 10 days > infectious contact, persist life-long Este interzisă copierea și distribuirea neautorizată a acestui material. ENTEROVIRUS INFECTIONS - EPIDEMIOLOGY Transmission route: - enterovirus particles – found in faeces / oro-pharynx - direct route: ◦ fecal-oral (contaminated hands) ◦ airborne - via respiratory droplets as enterovirus can be found in the patient’s stool and pharynx. - indirect route – via contaminated objects or water (including swimming pools) - enterovirus detected in vesicular fluid (hand-foot-and-mouth disease) - mother-to-child transmission (last week of pregnancy) – reported - direct inoculation of conjunctiva (contaminated hands / fomites) → acute hemorrhagic conjunctivitis Este interzisă copierea și distribuirea neautorizată a acestui material. ENTEROVIRUS INFECTIONS - PATHOGENESIS Entry gate – digestive / upper respiratory (oropharynx) tract ↓ Replication (in submucosal lymphoid structures at entry gate) ↓ bloodstream dissemination Minor viremia ← immune mechanisms → inapparent forms (50% cases) ↓ Replication in RES structures (liver, spleen, bone marrow) ↓ bloodstream dissemination Major viremia → clinical manifestations Este interzisă copierea și distribuirea neautorizată a acestui material. ENTEROVIRUS INFECTIONS - CLINICAL MANIFESTATIONS Incubation: average 7 days (2-14 days) Poliovirus – flaccid paralysis Coxsackie & ECHOvirus – wide range of diseases: - herpangina - hand-foot-and-mouth disease - infectious gastroenteritis: fever, vomiting, diarrheic stools, +/- dehydration - central nervous system infections: - aseptic meningitis (most frequent cause of clear CSF meningitis in young pts) - encephalitis - paralytic disease - Guillain-Barre syndrome Este interzisă copierea și distribuirea neautorizată a acestui material. ENTEROVIRUS INFECTIONS - CLINICAL MANIFESTATIONS Coxsackie & ECHOvirus – wide range of diseases: - febrile exanthem – non-specific – mimics allergy / measles, rubella, scarlet fever, purpura - non-specific febrile illness flu-like (“summer flu”) – spontaneous resolution (3-7 days) - acute hemorrhagic conjunctivitis: initially unilateral, then bilateral, 7-10 days duration - myocarditis / pericarditis (50% viral myopericarditis): arrhythmia, cardiac failure, dyspnea, thoracic pain, pericardial friction rub → sequelae (1/3 cases), potentially fatal Este interzisă copierea și distribuirea neautorizată a acestui material. ENTEROVIRUS INFECTIONS - CLINICAL MANIFESTATIONS - resp tract infections: coryza, croup (laryngo-trachea- bronchitis), bronchiolitis, pneumonia (interstitial / patchy – X-ray) - pleurodinia Bornholm: clinical picture of pleuritis, but negative X-ray – actually myositis - generalized neonatal disease (acquired from mother – last week of pregnancy / 1st month > delivery): hepatitis, myocarditis, encephalitis, ARDS, potentially fatal - other: acute nephritis, acute arthritis, parotitis, orchitis, polymyositis, acute pancreatitis Este interzisă copierea și distribuirea neautorizată a acestui material. ENTEROVIRUS INFECTIONS - CLINICAL MANIFESTATIONS Herpangina: - most often: Coxsackievirus A - possible: Coxsackie B, Echoviruses - acute onset - fever, malaise, myalgia, headache - Sore throat, odynophagia - +/- vomiting - characteristic enanthem: ◦ 2-4 mm φ vesicles on erythematous base → subsequent ulcerations ◦ on the soft palate, uvula, tonsillary pillars, posterior pharyngeal wall Acute lymphonodular pharyngitis: variety of herpangina – small yellow nodules on palate, uvula, no ulcerations Este interzisă copierea și distribuirea neautorizată a acestui material. ENTEROVIRUS INFECTIONS - CLINICAL MANIFESTATIONS Hand-foot-and-mouth disease: - most often Coxsackievirus A16, possible other enteroviruses as well - fever - vesicles and ulcerations in the oral cavity, sometimes perioral papules - skin lesions: erythematous papules / clear vesicles surrounded by erythema, distributed characteristically on the hand, feet, sometimes gluteal regions (etiologic agent can be detected inside vesicular fluid) Este interzisă copierea și distribuirea neautorizată a acestui material. Hand-foot-and-mouth disease Este interzisă copierea și distribuirea neautorizată a acestui material. Hand-foot-and-mouth disease Este interzisă copierea și distribuirea neautorizată a acestui material. ENTEROVIRUS INFECTIONS – LAB DG Serologic tests: Ab are serotype-specific: - Anti-enterovirus IgM Ab: appear 1-3 days > contact, persist 1-3 months - Anti-enterovirus IgG Ab - appear > 10 days > infective contact, with lifelong duration Detection of enterovirus from: blood, stool, CSF, naso-pharyngeal / tissue samples, vesicle fluid (skin lesions) by: - PCR – detects viral RNA - isolation of virus on cell cultures (monkey kidney cells / human embryonic fibroblasts / human rhabdomyosarcoma lines) – rarely done → cytopathic effect (pyknosis) - inoculation of suckling mice (rarely done): Coxsackievirus – pathogenic effect Este interzisă copierea și distribuirea neautorizată a acestui material. ENTEROVIRUS INFECTIONS – TREATMENT & PROPHYLAXIS No etiologic treatment (antiviral) so far No available vaccine (except: anti-poliomyelitis) Iv Ig – in severe forms, immunocompromised hosts (agammaglobulinemia) - newborns with severe generalized neonatal disease - Guillain-Barre sy Symptomatic - supportive therapy anti-inflammatory medication CNS infections (meningitis / encephalitis): glucocorticoids, depletion, neuronal trophic medication, group B vitamins General preventive measures: isolation (home / hospital), hand washing, hygiene Enteric precautions: for about 1 week > onset of the disease Este interzisă copierea și distribuirea neautorizată a acestui material. SCARLET FEVER = acute infectious disease caused by group A beta-hemolytic streptococcus (GABHS), characterized by: fever enanthem + characteristic exanthem, followed by desquamation Pentru uz intern Este interzisă copierea și distribuirea neautorizată a acestui material.  SCARLET FEVER ETIOLOGIC AGENT Group A beta-hemolytic Streptococcus (GAS / GABHS) = Streptococcus pyogenes - sporulated, gram-positive cocci, arranged in pairs or short chains - produces complete (beta) hemolysis around the colonies on blood-containing media - extracellular products: toxins & enzymes ✓ streptolysin O (strong antigen – induce Ab production: ASLO – not protective) and S ✓ streptokinase (role in fibrinolysis) ✓ exotoxins A, B and C (erythrotoxin) - cell membranes distruction - responsible for the rash - highly immunogenic → antitoxin Ab (maximum 3 episodes of scarlet fever) Este interzisă copierea și distribuirea neautorizată a acestui material.  SCARLET FEVER ETIOLOGIC AGENT GABHS cell structure: - Capsule (Ag) – anti-phagocytic role → pharyngeal colonization (carriers) - Cell wall (Ag): protein C (polysaccharide) → 20 Lancefield groups (A-V, excluding E, I, J) protein M: type-specific, through its structural variability (> 130 serotypes) → major virulence factor! → C & M proteins – similar to components of human tissue (cardiac, synovial, kidney) – post-streptococcal disease (immuno-allergic) - Cytoplasm proteins – role of cross-reactive Ag Este interzisă copierea și distribuirea neautorizată a acestui material.  SCARLET FEVER EPIDEMIOLOGY Worldwide spread (↑ temperate climate – cold season) Age group: 4-12 years (rare in infants & elderly) Source of infection: - patients with pharyngitis / scarlet fever - pharyngeal carriers of GABHS Transmission route - airborne – entry gate: pharyngeal mucosa - direct / indirect contact: recently contaminated objects (saliva) - digestive (contaminated milk) - cutaneous – rare – “wound” scarlet fever Este interzisă copierea și distribuirea neautorizată a acestui material.  SCARLET FEVER EPIDEMIOLOGY Infectivity: 2-3 days after initiation of adequate antibiotic therapy GABHS carriers retain this status indefinitely Susceptibility: universal Immunity: - anti-erythrogenic toxin Ab (antibodies) – toxin-type- specific - solid &lasting → maximum 3 episodes of scarlet fever, but: - any number of streptococcal infections (Ab are directed anti-exotoxin A, B, C, but do not destroy the bacteria itself) Este interzisă copierea și distribuirea neautorizată a acestui material.  SCARLET FEVER PATHOGENESIS GABHS remains at the entry gate – produces inflammation → pharyngitis - releases its toxins and enzymes Erythrogenic exotoxin disseminates by bloodstream, produces: ✓ exanthem followed by desquamation ✓ fever ✓ digestive and neurological manifestations (toxic sy) ✓ hypertoxic forms (marked toxemia → streptococcal toxic shock; toxic complications - hepatitis, myocarditis, nephritis) Este interzisă copierea și distribuirea neautorizată a acestui material.  SCARLET FEVER PATHOGENESIS Toxic syndrome Septic syndrome: caused by GABHS infection itself (ability to spread in the neighboring tissues, causing local / systemic septic complications) Immuno-allergic syndrome: result of the cross-reactive antibodies against streptococcal Ag ( 14-21 days after the acute illness) - post-streptococcal diseases specific antitoxic immunity: eritrogen antitoxin (14-21 days > acute illness) Este interzisă copierea și distribuirea neautorizată a acestui material. SCARLET FEVER – CLINICAL MANIFESTATIONS Incubation: 1-10 days (average 3-6 days) Onset : ✓ typically sudden, even brutal ✓ 38-40 ⁰ C fever ✓ dysphagia ✓ headache ✓ abdominal pain, vomiting ✓ agitation or delirium in hypertoxic forms Physical examination: ✓ pharyngotonsillar hyperemia ✓ regional angulo-mandibular lymphadenopathy (prolonged persistance) ✓ white, coated tongue Este interzisă copierea și distribuirea neautorizată a acestui material.  SCARLET FEVER CLINICAL MANIFESTATIONS Steptococcal pharyngitis: erythematous pharyngitis: intense pharyngo-tonsillar congestion erythematous exsudative pharyngitis: marked edema and erythema of the tonsils, with white-grey exsudate in their crypts (purulent deposits) pseudomembranous pharyngitis: false membranes on the tonsils necrotizing ulcerative Henoch pharyngitis: ulcers caused by tissue necrosis , local bleeding, systemic hematogenous dissemination; deeply altered general status, intensely fetid halitosis; severe/lethal gangrenous pharyngitis: coinfection with anaerobes, poor prognosis Este interzisă copierea și distribuirea neautorizată a acestui material.  SCARLET FEVER CLINICAL MANIFESTATIONS Tongue cycle: day 1: white, coated tongue days 2-3: desquamation starts from the tip and lateral margins of the tongue progressing to its base, suggesting a lingual "V“ days 4-5: pathognomonic aspect: “strawberry tongue" (proeminent lingual papillae due to desquamation) subsequently the re-epithelization gives the tongue the aspect of a lacquered, glossy mucosa - "cat tongue" (day 7-8) gradually fades until days 10-12, when it normalizes Este interzisă copierea și distribuirea neautorizată a acestui material.  SCARLET FEVER CLINICAL MANIFESTATIONS The phase of illness Begins 24-48 hours > onset Exanthem: -initially on the chest -extending in 24 hours on the trunk and limbs, where is more expressed proximally; -it does NOT appear on the face, palms and soles -diffuse erythema with congestive micropapules (rough skin – “goosebumps”) Este interzisă copierea și distribuirea neautorizată a acestui material.  SCARLET FEVER CLINICAL MANIFESTATIONS The phase of illness Facies: characteristic: Filatov’s mask (clown mask). - slapped: contrasting perioral pallor + flushed cheeks, red lips Pastia-Grozovici’s lines: = haemorrhagic lines at the bending folds (result of microbleeds due to capillary fragility secondary to erythrotoxin effect) Este interzisă copierea și distribuirea neautorizată a acestui material.  SCARLET FEVER CLINICAL MANIFESTATIONS The phase of illness: - fever and symptoms from the onset period persist - in the absence of antibacterial therapy: ✓ cardio-circulatory manifestations (tachycardia, hypotension), ✓ liver impairment (jaundice, hepatomegaly), ✓ kidney impairment (focal nephritis) ✓ neuro-psychological (meningismus, agitation, delirium) manifestations – toxic mechanism Este interzisă copierea și distribuirea neautorizată a acestui material.  SCARLET FEVER CLINICAL MANIFESTATIONS The desquamation period: occurs 1-2 weeks after onset last 2-3 weeks aspect & intensity of desquamation - significantly influenced by early start of antibiotics Squamae: ✓ classically: glove flaps on fingers & toes ✓ fine desquamation on trunk & face ✓ very mild after correct antibiotic therapy Este interzisă copierea și distribuirea neautorizată a acestui material.  SCARLET FEVER CLINICAL FORMS depending on the severity of the disease: average, common form: previously described benign forms: abortive, oligosymptomatic, forms without rash severe, malignant forms: ❖ toxic form: hyperpyrexia, cyanotic / hemorrhagic exanthema, hypotension, tachycardia, circulatory failure, oligo-anuria, shock, possibly fatal ❖ septic form: necrotizing ulcerative pharyngitis, painful cervical lymphadenitis, adenophlegmons, sepsis ❖ toxico-septic form 61 Este interzisă copierea și distribuirea neautorizată a acestui material.  SCARLET FEVER CLINICAL FORMS depending on the aspect of the rash miliary scarlet fever: rash covered by microvesicles haemorrhagic / purpuric scarlet fever: haemorrhagic exanthem cyanotic or livid exanthem: in severe, hypertoxic forms depending on the entrance gate: pharyngeal entry gate wounds (traumatic / surgical) scarlet fever Este interzisă copierea și distribuirea neautorizată a acestui material.  SCARLET FEVER COMPLICATIONS 1. toxic: appear early (1st week of illness) Myocarditis Nephritis Hepatitis 2. septic: during 2nd week of illness – local / systemic peritonsillar: abscess, phlegmon, adenophlegmon, ENT (sinusitis, otitis, mastoiditis) by spread towards CNS through the cribriform plate of ethmoid bone: thrombosis of cavernous sinus, meningitis, brain abscess by hematogenous dissemination: infective endocarditis, bronchopneumonia, abscesses (hepatic, cerebral, pulmonary), septic arthritis, meningitis 63 Este interzisă copierea și distribuirea neautorizată a acestui material.  SCARLET FEVER COMPLICATIONS 3. immuno-allergic: 3-4 weeks (1-2 months) after the acute disease rheumatic fever rheumatic carditis → valvulopathy Schonlein-Henoch purpura Chorea Sydenham erythema nodosum acute diffuse poststreptococcal glomerulonephritis Este interzisă copierea și distribuirea neautorizată a acestui material.  SCARLET FEVER POSITIVE DG clinical data (fever, dysphagia, characteristic exanthem & enanthem, digestive and nervous manifestations) epidemiologic data (contact with patients with scarlet fever / streptococcal pharyngitis, or carriers of GAS) laboratory data: Detection of GAS from throat swab ( cultivation on blood agar or immunofluorescence) detection of GAS antigen by rapid tests of latex agglutination; sensitivity lower than cultural techniques (70%) serological diagnosis; late: positive ASLO titer (anti-streptolysine O antibody) – after 2-3 weeks from onset nonspecific tests: leukocytosis with granulocytosis, ↑ ESR, CRP & fibrinogen Este interzisă copierea și distribuirea neautorizată a acestui material.  SCARLET FEVER DDx Measles Rubella Enterovirus infections Kawasaki disease Erythroderma Allergic rash pre-eruptive rash of chickenpox Este interzisă copierea și distribuirea neautorizată a acestui material. Differential diagnosis: Kawasaki disease  SCARLET FEVER TREATMENT In Romania - hospitalization Symptomatic treatment: anti-pyretics: acetaminophen analgesics oral disinfectants Pathogenic treatment common forms: NSAIDs (Ibuprofen) 3-5 days severe, toxic forms: ✓ emergency: glucocorticoids (hydrocortisone hemisuccinate 15 -30 mg/kg/day) ✓ standard iv Ig (0.3-0.4 mg / kg / day) Este interzisă copierea și distribuirea neautorizată a acestui material.  SCARLET FEVER TREATMENT Etiologic treatment ✓ Penicillin G iv 50 000 - 100 000 IU / kg / day in children, 2-6 million IU / day in adults, 7-10 days ✓ Alternatively: Penicillin V, (oral, before food), q 6 hours ✓ allergy to Penicillin: generation I/ II cephalosporins 7 days, or macrolides (erythromycin, clarithromycin, azithromycin) or clindamycin for 10 days ✓ ulceronecrotic and gangrenous forms: Clindamycin or Penicillin G + Metronidazole – to cover anaerobic bacteria 69 Este interzisă copierea și distribuirea neautorizată a acestui material.  SCARLET FEVER OUTPATIENT MONITORING Follow up – up to 3 months clinical and laboratory examination ✓urinalysis ✓ASLO ✓CRP ✓fibrinogen - to detect possible poststreptococcal complications Este interzisă copierea și distribuirea neautorizată a acestui material. WHOOPING COUGH Este interzisă copierea și distribuirea neautorizată a acestui material. Definition Acute contagious infectious disease Several weeks of evolution Paroxysmal spasmodic cough + noisy inhalation Etiology: Bordetella pertussis Bordetella parapertussis (no pertussis toxin, milder disease) Este interzisă copierea și distribuirea neautorizată a acestui material. Etiology Bordetella pertussis: small, aerobic, Gram-negative cocco-bacillus belongs to genus Bordetella Slow-growing, fastidious microorganism cultivated on Bordet-Gengou medium (agar + blood + glycerol + potato), or Regan Lowe medium (selective medium) whooping cough = = toxin-mediated disease Este interzisă copierea și distribuirea neautorizată a acestui material.  Virulence factors: pertussis toxin (pertussigen): A-B type toxin (A: active, ADP-ribosylates a G protein in target cells, B: binding) lymphocytosis-promoting factor (mitogenic) blocks the action of neutrophils, macrophages, natural killer cells adhesin – bacterial binding to cilliated resp cells hypoglycemiant effect – neurotoxin histamine-sensitizing factor antigenic, with immunizing effect (Ab) component of acellular pertussis vaccines Este interzisă copierea și distribuirea neautorizată a acestui material.  Biologically active products of the bacillus – virulence factors: endotoxin: lipopolysaccharide (LPS) adenylat cyclase toxin: activation of cAMP antiphagocytic, anti-inflammatory haemolytic Tracheal cytotoxin respiratory epithelial damage Dermonecrotic toxin respiratory epithelial damage Este interzisă copierea și distribuirea neautorizată a acestui material. Virulence factors: fimbriae: adhesins (attachment to ciliated epithelial cells) agglutinogens, stimulate the production of antibodies (Ab), component of acellular pertussis vaccines filamentous hemagglutinin: adhesion antigenic, with immunizing effect (Ab), component of acellular pertussis vaccines pertactin: outer membrane protein adhesion enhances protective immunity (Ab), component of acellular pertussis vaccines Este interzisă copierea și distribuirea neautorizată a acestui material.  Specific antibodies: agglutinins complement-fixating antibodies appear after the 2nd week of illness Susceptibility to antibiotics: Erythromycin Clarithromycin Azithromycin Cotrimoxazole (TMP-SMX) Este interzisă copierea și distribuirea neautorizată a acestui material. Epidemiology worldwide spread Maximum incidence: winter and spring Morbidity and mortality have dramatically decreased since the initiation of immunization 2023-2024: significant increase in pertussis incidence in Europe WHO - 2022: 84% TDaP vaccine coverage worldwide Romania – 2023: TDaP vaccine coverage in 14 y.o. children: 78% Este interzisă copierea și distribuirea neautorizată a acestui material.  Source: ECDC https://www.ecdc.europa.eu/sites/default/files/documents/Increaseinpertussis casesinthe EU-EES- May2024 Este interzisă copierea și distribuirea neautorizată a acestui material. Epidemiology Pertussis is most often seen in preschool and school-age children Source of infection: sick persons, including those with mild / atypical forms Transmission: directly, through airborne droplets rarely: through contaminated objects Contagiousness: 7 days after infectious contact until 3 weeks following onset reduced to 10 days in case of antibiotic therapy Highest contagiousness: during the catarrhal phase (attack rate - 90 % among unimmunized family contacts) Este interzisă copierea și distribuirea neautorizată a acestui material. EPIDEMIOLOGY Susceptibility: general, including neonates (maternal Ab do not cross placenta in sufficient quantities) – Rec: anti-pertussis vaccination during each pregnancy in order to increase passive transfer of Ab from mother-to-infant) - specific antibodies: appear after 2 weeks > onset Immunity after disease – long (4-20 years), but not lifelong Infection is possible with another type of Bordetella (ex B. parapertussis) Immunity after vaccination: 10-12 years - longer in case of whole-cell vaccines (more side effects) than > acellular vaccines Adolescents and adults can have milder diseases but transmit the infection to household contacts (susceptible infants and children, who can develop severe disease) Este interzisă copierea și distribuirea neautorizată a acestui material.  PATHOGENESIS 2 phases (stages) of cough: - Bronchogenic cough: local inflammation, irritation of vagal nerve terminations with initiation of cough - Neurogenic cough: a cortical site of cough stimulation appears – cough is triggered by various sensory stimuli: noise, strong light, touch (ex. medical examination) Bordetella pertussis is not an invasive microorganism - attaches to the ciliated epithelial cells (nasopharynx, tracheo-bronchial mucosa) & releases exotoxins (afterwards dispersed throughout the host organism): - systemic manifestations (ex. lymphocytosis) - result of toxin activity Neurologic events (seizures, encephalitis) - influenced by: hypoxic factors (paroxysmal cough with apnea) toxic factors hemorrhagic factors Este interzisă copierea și distribuirea neautorizată a acestui material.  CLINICAL MANIFESTATIONS prolonged coughing illness clinical manifestations vary by age incubation period: average 7-10 days (5-21 days) Catarrhal phase: 1-2 weeks - clinically indistinguishable from the common cold: high contagiossness coryza non-specific cough hyperemic conjunctiva mild fever At the end of the catarrhal stage the cough becomes mainly nocturnal, spastic, accompanied by vomiting Este interzisă copierea și distribuirea neautorizată a acestui material. CLINICAL MANIFESTATIONS Paroxysmal phase: 2-6 weeks Paroxysmal episode consist of: aura (the child anticipates the episode) sudden inhalation followed by (5-10) spasmodic cough bursts expiratory pause (congested, cyanotic face) deep prolonged high-pitched wheezing inhalation (whoop) there may be several cycles of prolonged inspiration and cough bursts sputum expectoration - difficult: thick, sticky mucus, accompanied by vomiting During paroxysmal episode, the patient’s face is congested, cyanotic, eyes are bulging, injected, neck veins are distended Ulceration of lingual frenulum can appear Cough – not influenced by symptomatic cough-suppressant therapy Este interzisă copierea și distribuirea neautorizată a acestui material. CLINICAL MANIFESTATIONS Convalescent phase: gradual resolution of coughing episodes can last for 1-3 months For the next 6 months the symptoms can recur during other acute viral respiratory illnesses Clinical forms: Based on the number of paroxysmal episodes / 24 hours: mild form: 4-6 episodes medium form: 10-30 episodes severe form: 30-40 episodes, bloated face with periorbital edema Este interzisă copierea și distribuirea neautorizată a acestui material.  COMPLICATIONS & SEQUELAE Complications: Mechanical (pressure ↑ during cough attacks): intracerebral, conjuctival, pulmonary bleeding, epistaxis rectal prolapse, umbilical or inguinal hernia pneumothorax, subcutaneous emphysema, atelectasis - Superinfection: pneumonia (Streptococcus pneumoniae, Haemophilus influenzae), otitis media - B. pertussis pneumonia - Encephalitis: severe in infants, appears in weeks 3-4 of illness, with seizures - Weight loss Sequelae: - bronchiectasis - pulmonary emphysema > encephalitis: cognitive impairment, motor deficits Este interzisă copierea și distribuirea neautorizată a acestui material.  DIAGNOSIS Epidemiological data: - ongoing outbreak - absence / incomplete previous immunization, - infectious contact Clinical data Laboratory findings: leukocytosis 20-50.000/mm3 lymphocytosis (60-80%) normal ESR Characteristic chest X-ray image: hilar and basal infiltrates in the cardiophrenic angle, Gotche triangle or „heart in flame / fuzzy heart”. Este interzisă copierea și distribuirea neautorizată a acestui material. DIAGNOSIS Bordetella pertussis cultivation from naso-pharyngeal secretions (during catarrhal phase & beginning of paroxysmal phase) - cultivation on Bordet-Gengou / Regan Lowe medium Direct fluorescent antibody (DFA) test: detects B pertussis Ag from naso-pharyngeal secretions RT-PCR - detects bacterial DNA in naso-pharyngeal secretions - more sensitive than culture, rapid result Serologic tests: serum anti-toxin antibodies -enzyme immunoassays: IgA, IgG (paired sera, 2-4 fold increase) Este interzisă copierea și distribuirea neautorizată a acestui material. DIFFERENTIAL DIAGNOSIS - DDx During catarrhal stage: influenza, measles, adenovirosis, other viral respiratory infections During paroxysmal stage: - pertussis-like syndrome: adenoviruses, respiratory syncytial virus, parainfluenza viruses Chlamydia trachomatis (newborn – vertical transmission) - laryngeal spasm - intralaryngeal / intrabronchial foreign body Prolonged cough in adults: Mycoplasma pneumoniae, Chlamydophila pneumoniae infections ACE inhibitors Asthma bronchiale Mediastinal compression Este interzisă copierea și distribuirea neautorizată a acestui material. PROGNOSIS - severe in children younger than 2 years old WHO – case-fatality ratio – 4% in infants < 12 months - 1% in children age 1-4 y.o. Este interzisă copierea și distribuirea neautorizată a acestui material.  TREATMENT Early treatment of pertussis can improve evolution (initiated during the first 1 - 2 weeks, during catarrhal stage, before cough paroxysms occur) Isolation at home / hospital (min 48 hours from start of antibiotics, 3 weeks if untreated) ICU – severe cases (newborns, infants) Peaceful, quiet environment – not to trigger paroxysms Diet: fractioned meals in reduced amounts postural drainage, aspiration of respiratory secretions oxygen therapy / mechanic ventillation Beta-adrenergic agonists (salbutamol) & glucocorticoids – advocated by some – not very effective iv Ig – severe cases Symptomatic treatment – cough tranquilizers & mucolytics – not effective Pathogenic Encephalitis: cerebral edema control, anticonvulsants Este interzisă copierea și distribuirea neautorizată a acestui material. TREATMENT Antimicrobial therapy: Clarithromycin 15 mg/kg/day (divided in 2 doses/day) 7 days Azithromycin 10 mg/kg/day qid 3 days Erythromycin 40-50 mg/kg/day 7 days Cotrimoxazole (TMP-SMX -8+40 mg/kg/day) 7 days Este interzisă copierea și distribuirea neautorizată a acestui material. PREVENTION Notify Public Health Authorities Antibiotic prophylaxis for contacts: macrolides / co-trimoxazole 7 days Immunization: TdaP vaccine (combinated anti-diphtheria, tetanus & pertussis) - acellular pertussis vaccine (DTaP) has replaced whole-cell pertussis vaccine (fewer side effects) Anti-pertussis vaccine: - 2 months / 4 months / 12-18 months / 4-6 years Booster vaccinations for general population every 10 years Vaccination – rec for: Infants healthcare professionals – booster vaccinations Pregnancy – booster vaccinations – during each pregnancy – in the 3rd trimester Este interzisă copierea și distribuirea neautorizată a acestui material.  MUMPS (EPIDEMIC PAROTITIS) Este interzisă copierea și distribuirea neautorizată a acestui material. Definition acute viral infection inflammation of one or both parotid glands +/- involvement of other salivary glands / CNS / pancreas / genital organs usually benign & self-limited disease 1:3 cases subclinical adults: higher severity than in children Este interzisă copierea și distribuirea neautorizată a acestui material. Etiologic agent mumps virus Paramyxovirus genus, Paramyxoviridae (same fam as measles v & RSV) Before widespread vaccination: – highest incidence was in winter & spring, with epidemics every 2-5 years - 50% of children aged 4-6 years & 90% of children aged 14- 15 years had positive serology for mumps (previous infection) 1 episode of mumps usually confers lifelong immunity long-term immunity - also associated with vaccination (probably life-long) Este interzisă copierea și distribuirea neautorizată a acestui material. Epidemiology & Pathogenesis Transmission: direct contact with saliva airborne fomites mumps virus – isolated from saliva 7 days < onset → 9 days > clinical onset contagiousness – highest 1-2-3 days < onset → several days(3) > onset enters through the nasal or oral mucosa more prolonged & closer contact is needed to transmit mumps than either measles or varicella viral replication in upper respiratory tract epithelium → viremia → infection of glandular tissues and/or CNS Este interzisă copierea și distribuirea neautorizată a acestui material. Clinical manifestations incubation: 14-24 days (average 18 days) prodromal symptoms – nonspecific, include: Low-grade fever Anorexia Malaise Headache Myalgia Este interzisă copierea și distribuirea neautorizată a acestui material. The phase of illness: Within 1 day: otalgia, tenderness at palpation of the ipsilateral parotid region Parotitis - initially unilateral → may become bilateral The opening of Stensen’s (Stenon’s) duct is frequently edematous and erythematous. Trismus may result from parotitis → difficult pronunciation & mastication submaxillary & sublingual glands – involved less often than the parotid (almost never involved alone) Este interzisă copierea și distribuirea neautorizată a acestui material. Clinical manifestations The phase of illness: Epididymo-orchitis – the most common extrasalivary manifestation in adult male pts Appears in 20-30% of post-pubertal men with mumps Bilateral involvement - in 1/6 pts with orchitis Gonadal involvement may precede parotitis, may appear 1 week > onset, or it can occur as the only manifestation of mumps Este interzisă copierea și distribuirea neautorizată a acestui material. Epididymo-orchitis Onset - abrupt temperature 39-41 C chills headache vomiting testicular pain Genital examination reveals: warmth swelling tenderness of the involved testicle erythema of the scrotum Testicular atrophy – ½ cases of orchitis, but infertility is rare Oophoritis - 5% of postpubertal women with mumps Pain in the lower abdomen Fever, vomiting Este interzisă copierea și distribuirea neautorizată a acestui material. Clinical manifestations The phase of illness Pancreatitis manifests with: epigastric pain tenderness fever nausea, vomiting Laboratory dg of mumps pancreatitis - difficult: ↑↑ serum amylase level can be associated with either parotitis / pancreatitis (isoenzymes test – pancreatic / salivary) Favorable evolution Este interzisă copierea și distribuirea neautorizată a acestui material. Clinical manifestations The phase of illness: Central nervous system (CNS) involvement - the most common extrasalivary manifestation Aseptic meningitis: - meningeal symptoms may occur before, during, after, or in the absence of parotitis (similar to all other manifestations of mumps) - onset: average 4 days > parotitis, but may occur as early as 1 week < or as late as 2 weeks > parotitis Typical clinical features associated with viral meningitis are present: Headache Vomiting Fever Nuchal rigidity Este interzisă copierea și distribuirea neautorizată a acestui material. Clinical manifestations Aseptic meningitis – CSF exam: clear containing 1000-2000 cells/mm3 predominantly lymphocytes 20-25% patients have a polymorphonuclear leukocyte predominance (CSF), within the first 24 h, followed by lymphocytic predominance CSF protein levels: normal to mildly elevated Low CSF glucose level is reported in 6-30% of the patients, more common than in other viral meningitis Rarely - encephalitis Este interzisă copierea și distribuirea neautorizată a acestui material.  Other CNS conditions (occasional): Cerebellar ataxia Facial palsy Transverse myelitis Guillain-Barre syndrome Aqueductal stenosis leading to hydrocephalus Deafness Other clinical manifestations Migratory polyarthritis Thyroiditis Mastitis Hepatitis Thrombocytopenia Prostatitis Myocarditis: ECG changes Este interzisă copierea și distribuirea neautorizată a acestui material.  Diagnosis In most cases – dg based on epidemiologic data + parotid swelling & tenderness + mild / moderate constitutional symptoms WBC: normal / mild leukopenia with relative lymphocytosis - when meningitis, orchitis, or pancreatitis: leukocytosis + left shift deviation Serum amylase level is elevated due to parotitis (may remain abnormal for 2-3 weeks) Laboratory confirmation: - PCR - detects mumps virus RNA in throat swabs, saliva, CSF - Serologic dg – serum IgM Ab anti-mumps virus Este interzisă copierea și distribuirea neautorizată a acestui material.  ETIOLOGY COMMENTS Systemic infections Rare in countries with good vaccination programs Parotitis Mumps DDX Coxsackie virus infection Most often in children, young adults HIV positive-children without antiretroviral therapy HIV infection (bilateral parotitis) Parainfluenza virus type 3 infection Acute respiratory tract symptoms Influenza A virus infection Seasonal; Acute respiratory tract symptoms Regional adenopathy, conjunctivitis, unusual cause for Cat-scratch disease (Bartonella henselae) parotitis Epstein-Barr virus infection Unusual but described Systemic Noninfectious Causes Sarcoidosis Additional manifestations of disease likely Syὄgren, s syndrome Additional manifestations of disease likely Uremia Additional manifestations of disease likely Diabetes mellitus Additional manifestations of disease likely Drugs Thiouracil, Phenylbutazone Unilateral Parotitis Ductal obstruction due to lithiasis or Unilateral, gradual onset, suppurative strictures Parotid cyst Unilateral, gradual onset Parotid tumor Unilateral, gradual onset Acute Suppurative Parotitis Este interzisă copierea și distribuirea neautorizată a acestui material.  DDx - Acute suppurative (septic) parotitis Bacterial etiology: Staphylococcus aureus, Streptococcus, anaerobic bacteria, Gram-negative Local inflammatory signs: erythema, edema, pain, increased local temperature purulent secretions on the opening of Stensen’s duct at parotid palpation Este interzisă copierea și distribuirea neautorizată a acestui material. Therapy No etiologic therapy mumps parotitis – symptomatic & supportive measures analgesics apply warm or cold dressings on the parotid area to reduce pain orchitis – local cold dressing, iv fluids – pts with meningitis / pancreatitis with persistent vomiting Este interzisă copierea și distribuirea neautorizată a acestui material. Prevention Live attenuated mumps vaccine: 95% seroconversion rate – Ab (IgM , followed by IgG) confer long-term post-vaccine protection part of the measles-mumps-rubella (MMR) vaccine – doses: - at the age of 12-15 months - at the age of 4-12 years live attenuated virus vaccine – contraindicated in: Pregnancy Persons with a severe febrile illness Immunocompromised hosts Este interzisă copierea și distribuirea neautorizată a acestui material.