INFECTIOUS DISEASES IV.pptx
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INFECTIOUS DISEASES IV CHILDHOOD VACCINE PREVENTABLE DISEASES DR UGOLEE JERRY INFECTIOUS DISEASES IV • • • • • • • POLIOMYELITIS PERTUSSIS (WHOOPING COUGH) MEASLES MUMPS TETANUS CHICKEN POX DIPHTHERIA PERTUSSIS PERTUSSIS • It is also known as ‘WHOOPING’ cough and ‘the 100 days cough. Pertuss...
INFECTIOUS DISEASES IV CHILDHOOD VACCINE PREVENTABLE DISEASES DR UGOLEE JERRY INFECTIOUS DISEASES IV • • • • • • • POLIOMYELITIS PERTUSSIS (WHOOPING COUGH) MEASLES MUMPS TETANUS CHICKEN POX DIPHTHERIA PERTUSSIS PERTUSSIS • It is also known as ‘WHOOPING’ cough and ‘the 100 days cough. Pertussis literally means ‘intense cough’ • It is an acute respiratory tract infection caused by a fastidious gram negative coccobacillus that is highly infectious and contagious AETIOLOGY • Bordetella Pertussis -the sole cause of epidemic pertussis - usual cause of sporadic pertussis - exclusive for humans and primates PERTUSSIS AETIOLOGY • Bordetella parapertussis - occasional cause of sporadic pertussis - exclusive for humans and primates • Bordetella bronchoseptica - a common animal pathogen - causes human infection commonly in the immunocompromised PERTUSSIS EPIDEMIOLOGY • It occurs worldwide • One of the leading causes of death pre-vaccination era • Peak incidence 1-5 years • Extremely contagious – attack rate of 100% • Infectivity is in the first 4 weeks • Adolescents and adults are major reservoirs of infection • Incubation period 7-10 days PERTUSSIS EPIDEMIOLOGY • Commoner in the raining than dry season • Neither natural infection or vaccination confers complete or lifelong immunity • Protection begins to wane 3-5 years after vaccination • Immunity unmeasurable after 12 years PERTUSSIS PATHOGENESIS • Pertussis spreads through close contact with oral secretions or respiratory droplets. So it’s easily spread through the cough, sneeze especially when people are in close contact. • B pertussis produces many biologically active substances - Pertussis toxin - Filamentous hemagglutin - agglutinogen - pertactin - adenylate cyclase - tracheal toxin • It only colonizes ciliated epithelium PERTUSSIS PATHOGENESIS • The filamentous hemagglutinin, pertactin and agglutinogen are important for attachment of the organism to ciliated epithelium • The pertussis toxin plays a central multiple role in the pathogenesis and responsible for the systemic manifestations -induces cell cytotoxicity -Inhibits neutrophil and monocytes reponse PERTUSSIS CLINICAL FEATURES • Typically divided into 3 stages • Catarrhal [1-2 weeks] • Paroxysmal [ 2-6 weeks] • Convalescent [ ≥ 2 weeks] PERTUSSIS CLINICAL FEATURES Catarrhal stage • Non-specific features • Congestion, rhinorrhea • Sneezing • Lacrimation, conjunctival redness • Low grade fever * infants may have shorter catarrhal stage before progression PERTUSSIS CLINICAL FEATURES Paroxysmal stage • Cough initially dry and intermittent • Inexorable/relentless paroxysms • Machine gun burst of uninterrupted cough • Bulging eyes----- watering • Tongue protruding maximally • Face purple • Congestion of neck and scalp veins PERTUSSIS CLINICAL FEATURES Paroxysmal stage • Whoops at the end of the paroxysm • Post-tussive emesis • Exhaustion *Number and severity of paroxysm progress over days to weeks *In between the cough episodes child appear well Convalescent stage • Frequency, severity and duration of the cough episodes diminishes PERTUSSIS DIAGNOSIS • Diagnosis is mainly clinical and best made at the paroxysmal stage • Suspect in any patient with predominant complaint of persistent cough especially in the absence of -Malaise, myalgia -Fever, rash, -Sore throat, hoarseness, -Tachypnea, wheeze and rales • Physical exam is usually unremarkable -Conjuctival hemorrhages -petechia PERTUSSIS DIAGNOSIS • FBC -Leukocytosis [15,000-100,000 cells/mm3] with absolute lymphocytosis [ in catarrhal stage] • Culture-gold standard for diagnosis - specimen from posterior nasopharynx - Dacron/ Ca-alginate swab is used • Direct Fluorescent antibody staining • PCR • Serology -Antibody test B. pertussis Ag -in acute and convalescent samples - most sensitive for the immunized PERTUSSIS TREATMENT Specific treatment • Macrolides are the drug of choice • Erythromycin 40-50 mg/kg/day for 14 days • Azithromycin 10mg/kg for 5 days • Clarithromycin 15mg/kg for 7 days * Azithromycin is preferred in neonates because of concerns of infantile hypertrophic pyloric stenosis PERTUSSIS COMPLICATIONS • May be respiratory, sequelae of the forceful cough or CNS • Respiratory :Apnea, Bpneumonia, Atelectasis, Bronchiectasis, Emphysema& Otitis media • Sequelae of forceful cough: Epistaxis, Subconjuctival hemorrhages, Intracranial bleeding, Umbilical/inguinal hernias, Rectal prolapse, Lingual frenulum laceration PERTUSSIS COMPLICATIONS Central nervous system • Usually due to hypoxemia or hemorrhages • Convulsions • Intracranial hemorrhages • Encephalopathy PERTUSSIS PREVENTION General health promotion • Universal Immunization of children with pertussis vaccine • Create awareness about pertussis using media and special campaigns • Avoiding overcrowding • Improved housing • Promoting Exclusive breastfeeding • Improved sanitation PERTUSSIS PREVENTION Early diagnosis and prompt treatment • Macrolides for treatment • Train and retrain doctors and health workers to have high index of suspicion and make clinical diagnosis Limitation of disability • Provision of oxygen • Provision of mist by tent • Cautious small volume feeding to limit malnutrition POLIOMYELITIS POLIOMYELITIS • AFP is a clinical syndrome characterised by rapid onset of weakness of the muscles of the limbs, including weakness of the muscles of respiration & swallowing, progressing to maximum severity within several days to weeks( usually <4weeks) • The term ‘flaccid’( relaxed, flabby, or without tone) indicates the absence of spasticity. • Poliomyelitis is the commonest cause of AFP in our environment POLIOMYELITIS • In 1988, the World Health Assembly (WHA) adopted a resolution calling for global eradication of polio by the year 2000. • At d end of 1999, 30 countries world wide remained polio-endemic and intense activity was directed towards polio eradication • Currently polio is still endemic in 3 countries Afghanistan, Pakistan & India. Nigeria was declared polio-free in 2015 but isolated cases have been reported in the North since 2016 POLIOMYELITIS AETIOLOGY • Poliomyelitis is caused by 3 serotypes of poliovirus(PV1,2&3) a neurotropic RNA virus belonging to the picornaviridae genus. An enterovirus that colonize the GIT especially the oropharynx and intestine • It is transmitted by person to person spread through feco-oral & oral-oral routes(oropharyngeal secretions).Most infectious b/w 7-10 days before and after appearance of symptoms but transmission is possible as long as virus remains in saliva • Humans are the only reservoir • Incubation period( period between 1st exposure and 1st symptom):7-14 days(5-35) POLIOMYELITIS AETIOLOGY • Virus can cross placenta during pregnancy, maternal antibodies also cross placenta providing passive immunity • Factors that increase the risk of polio infection or its severity include immuno-compromised status, malnutrition, physical activity just following paralysis, skeletal muscle injury following injections, low socioeconomic status and pregnancy POLIOMYELITIS PATHOPHYSIOLOGY • Exact mechanism of polio virus spreads to the spine and CNS causing damage is poorly understood • Upon ingestion, the virus binds to a poliovirus receptor in the GI and spreads to the tonsilar germinal centres and intestinal lymphoid tissue(peyer’s patches) where it replicates and enters the blood stream causing a transient viremia • It has been postulated that the virus in the blood stream enter the CNS via retrograde axonal ascension and causes apotosis by blocking the anterior horn cells arterial supply • Denervation of skeletal muscle tissue leads to paralysi POLIOMYELITIS CLINICAL FEATURES • Children infected with polio virus may take any of the following known clinical courses of the disease • In 90-95% of cases, an inapparent infection showing no symptoms at all and developing no sequelae • In 5% of cases, develop Abortive polio developing nonspecific influenza-like symptoms, occur 1-2 weeks after infection. The illness is short-lived(2-3 days) • Examination may be normal or reveal a non-specific pharyngitis, abd or muscular tenderness & weakness • Recovery is complete & no neurologic signs or sequelae POLIOMYELITIS CLINICAL FEATURES • In 1% of cases develop Non-paralytic polio • Some signs of abortive polio present but headache, nausea & vomiting more intense • Soreness & stiffness of the posterior muscles of the neck, trunk & limbs • Fleeting paralysis of d bladder & constipation is frequent • Nuchal & spinal rigidity are d basis for the diagnosis POLIOMYELITIS CLINICAL FEATURES • In less than 1% of cases they develop Paralytic polio • There are 3 types: Spinal polio -79% of paralytic cases Bulbospinal polio – 19% of paralytic cases Bulbar polio – 2% of paralytic cases Polio encephalitis- rare, usually restricted to infants POLIOMYELITIS CLINICAL FEATURES Distinguishing features of Paralytic polio: • Fever at onset • Rapid progression of paralysis within 24-48hrs • Asymmetrical distribution of limb paralysis affecting proximal limb muscle > distal • Preservation of sensory nerve function • Residual paralysis after 60 days POLIOMYELITIS CLINICAL FEATURES Spinal paralytic polio • May occur as 2nd phase of a biphasic illness • Severe muscle pain is usually present • Examination findings show that the distribution of paralysis is spotty with single muscles, multiple muscles or group of muscles been involved in any pattern • Asymmetric flaccid paralysis or paresis occurs within 12days • Involvement of only one leg common followed by involvement of one arm. Sensation is intact POLIOMYELITIS CLINICAL FEATURES Bulbar poliomyelitis • Dominance of dysfunction of the cranial nerves & medullary centre • There is a nasal twang to the child's voice or cry • Inability to swallow smoothly, resulting in accumulation of saliva in the pharynx and an absence of an effective cough reflex • Nasal regurgitation of saliva & fluids as a result of palatal paralysis may lead to aspiration • Hypertension & other autonomic disturbances are common. Occasionally hypotension, shock, irregular or failed respiratory effort POLIOMYELITIS CLINICAL FEATURES Polio encephalitis • A rare form of the disease • Higher centres of d brain severely involved • Seizures, coma & spastic paralysis with ↑ reflexes may be observed • Irritability ,disorientation, drowsiness &coarse tremors • Hypoxia & hypercapnia caused by inadequate ventilation due to respiratory insufficiency POLIOMYELITIS DIAGNOSIS • Paralytic poliomyelitis may be clinically suspected in children with an acute flaccid paralysis in one or more limbs with diminished or absent tendon reflexes with no sensory or cognitive loss • Laboratory diagnosis is usually based on the recovery of poliovirus from a stool sample or pharyngeal swab • CSF analysis shows lymphocytosis with elevated CSF protein • PCR amplification issued to determine the wild type strain POLIOMYELITIS TREATMENT • There is no cure for polio but there are supportive treatments • Antibiotics to prevent infections in weakened muscles, Analgesics for pain, moderate exercise and nutritious diet • Long term rehabilitation including occupational therapy, physical therapy, braces, corrective shoes, orthopaedic surgery POLIOMYELITIS PROGNOSIS • Patients with spinal polio, if the affected nerve cells are completely destroyed, paralysis will be permanent; if not, the loss of function is temporary and recovery may following 4-6 weeks • Half of the patients with spinal polio recover fully, one-quarter recover with some disability and the other quarter with severe disability • Bulbar polio often causes death if respiratory support is not provided from suffocation or aspiration pneumonia TETANUS TETANUS INTRODUCTION • Tetanus is an acute, spastic paralytic disease caused by spores of the bacterium Clostridium tetani. • It remains an important public health problem in many parts of the world, but especially in low-income countries or districts, where immunization coverage is low, and unclean birth practices are common. TETANUS EPIDEMIOLOGY • Tetanus is predominantly a disease of underdeveloped countries. It is common in areas where soil is cultivated, in rural areas, in warm climates, during hamathan months, and among males. • In countries without a comprehensive immunization program, tetanus predominantly develops in neonates and young children. • WHO estimated that in 2002, there were 213,000 tetanus deaths, 198,000 of them in children younger than 5 years. TETANUS EPIDEMIOLOGY • No overall gender predilection has been reported, except to the extent that males may have more soil exposure in some cultures. • In developing countries, women have an increased immunity where tetanus toxoid is administered to women of childbearing age to prevent neonatal tetanus. • Majority of childhood cases in the US have occurred in unimmunised children whose parents objected to immunization. TETANUS RISK FACTORS • Most non-neonatal cases of Tetanus are associated with traumatic injury-a penetrating wound by dirty object eg nail, splinters, glass etc • Illicit drug injections • Contaminated sutures • Animal bites, abscesses, body piercings burns, fractures etc • Rarely, there may be no history of trauma • Neonatal cases are associated with poor cord care TETANUS AETIOLOGY • Tetanus is caused by Clostridium tetani, a motile, spore forming (terminally located spores), gram +ve, obligate anaerobe. • The spores are found everywhere in the environment, particularly in soil, ash, intestinal tracts/feces of animals and humans, and on the surfaces of skin and rusty tools like nails, needles, barbed wire, etc. • The spores are very resistant to heat and most antiseptics and can survive for years. • Vegetative cells are killed by antibiotics, autoclaving, and standard disinfectants TETANUS AETIOLOGY • C. Tetani is not tissue invasive, it produces illness through the effects of a toxintetanospasmin • Tetanospasmin is the second most poisonous substance known(only surpassed in potency by botilinum toxin) TETANUS PATHOPHYSIOLOGY • When wounds are infected with clostridium tetani, the spores germinate, multiply and produce the toxins at the injury site. Anaerobic conditions in necrotic tissues encourage this. • Clostridium tetani produces 2 toxins- tetanolysin, tetanospasmin. • Tetanolysin locally damages the tissues surrounding the infection while tetanospasmin is responsible for the spasms in tetanus. TETANUS PATHOPHYSIOLOGY • The toxins bind at the neuromuscular junction (gangliosides on the membrane of nerve terminals), entering the nerves by endocytosis. • They undergo retrograde transport to the cell body, first in the motor neurons, later in sensory and autonomic nerves • From there they diffuse and enter other neurones, even the spinal inhibitory interneurons • The light chain cleaves synaptobrevin thereby preventing the release of neurotransmitters in the cell. Thus the inhibition of antagonist muscles are blocked. • The affected muscles contract maximally and cannot relax. • The autonomic nervous system is also affected in tetanus Neuromuscular junction TETANUS CLINICAL FEATURES Tetanus may be categorized into the following 4 clinical types: • Generalized tetanus • Localized tetanus • Cephalic tetanus • Neonatal tetanus TETANUS CLINICAL FEATURES • Generalized tetanus follows an incubation period typically of 2-14 days, but may be as long as months after injury. • Clinical features includes nuchal rigidity, jaw lock and dysphagia which are early complaints and may produce a scornful smile (risus sardonicus) resulting from facial muscle spasm. TETANUS CLINICAL FEATURES • As generalized tetanus progresses, the child develops generalized muscle rigidity with intermittent reflex spasms in response to stimuli (eg, noise, touch). During these episodes, patients have an intact sensorium and feel severe pain • Tonic contractions cause opisthotonos from a flexion and adduction of the arms, clenching of the fists, and extension of the lower extremities TETANUS CLINICAL FEATURES • Sudden painful muscle spasms often triggered by sudden noises, light and touch • Laryngeal and airway muscle spasms can lead to airway obstruction and asphyxiation • Fever may result from substantial metabolic consumption by spastic muscles • Autonomic effects include tarchycardia, dysryhthmias, sweating and changes in blood pressure. TETANUS NEONATAL TETANUS • The Infection usually results from umbilical cord contamination during unsanitary delivery, cutting of the umbilical cord with rusted contaminated sharps and the cultural practise of coating the umbilical cord with Vaseline, cow dung and toothpaste, coupled with a lack of maternal immunization. • At the end of the first week, infected infants become irritable, feed poorly, and develop rigidity with spasms. • Neonatal tetanus has a very poor prognosis • Symptoms include muscle spasms, which are often preceded by the newborn’s inability to suck or breastfeed, and excessive crying. TETANUS LOCALISED TETANUS • Patients with localized tetanus present with persistent rigidity in the muscle group close to the injury site. The muscular rigidity is caused by a dysfunction in the interneurons that inhibit the alpha motor neurons of the affected muscles. No further central nervous system (CNS) involvement occurs in this form, and mortality is very low. TETANUS CEPHALIC TETANUS • Cephalic tetanus is uncommon and usually occurs after head trauma or otitis media. • Patients with this form present with cranial nerve (CN) palsies. • The infection may be localized or may become generalized. TETANUS DIAGNOSIS • Diagnosis is usually clinical. • There is usually a history of a contaminated wound followed by jaw stiffness, stiffness of neck or other muscles , dysphagia and subsequent spams with minimal stimuli with an intact sensorium is suggestive • An important diagnostic tool is the spatula test. Here the oropharynx is touched with a spatula. In a normal patient, the gag reflex is elicited. A positive test as seen in tetanus results when the patients develops a reflex spasm and bites the spatula TETANUS DIAGNOSIS • No laboratory test exists for diagnosis of tetanus • The organism is rarely isolated from wound sites and may be cultured in individuals without the disease • Ancillary investigations to rule out differentials or comorbidities may include CSF analysis, serum electrolytes urea and creatnine, Ca+,Mg+& Phosp TETANUS DIFFERENTIAL DIAGNOSIS • Meningitis • Dental abscess • Phenothiazine toxicity • Strychnine poisoning TETANUS TREATMENT PRINCIPLES OF MANAGEMENT • Eradication of clostridium tetani • Neutralization of circulating tetanus toxin • Proper wound care • Sedation and seizure control • Supportive care • Prevention of recurrence TETANUS TREATMENT Eradication of clostridium tetani • Antimicrobials are used to decrease vegetative forms of clostridium tetani in the wound. • Metronidazole is effective against clostridium and is also associated with lower mortality • Erythromycin and tetracycline (in persons older than 8yrs) have also been used. • Antibiotics- penicillin G is no longer the drug of choice as it is a known antagonist of GABA TETANUS TREATMENT Neutralization of circulating toxins • Passive immunization with human tetanus immunoglobulin(TIG) shortens the course and may lessen the severity • TIG 500 units by IM or IV as soon as possible; in addition tetanus toxoid should be administered by IM injection at a separate site, given as soon as possible to neutralise circulating toxins before they bind to muscles • Doses as high as 3000-6000units may be administered TETANUS TREATMENT Neutralization of circulating toxins • Passive immunization with human tetanus immunoglobulin(TIG) shortens the course and may lessen the severity • TIG 500 units by IM or IV as soon as possible; in addition tetanus toxoid should be administered by IM injection at a separate site, given as soon as possible to neutralise TETANUS TREATMENT Proper Wound Care • It is recommended that at least 2cm of normal viable tissue around the wound margin be excised • Abscesses should be incised and drained • Because of the risk of releasing tetanospasmin into the blood stream, wound manipulation is delayed until several hours after administration of antitoxin TETANUS TREATMENT Sedation and Seizure Control • Diazepam is the most frequently studied and used drug; it reduces anxiety, produces sedation and relaxes muscles. Dose required is 1-10mg/kg/day; up to 600mg/day. Lorazepam is an effective alternative. • Phenobarbital can be used to prolong the effects of diazepam. It can also provide sedation and muscle relaxation. • Chlorpromazine is an alternative anticonvulsant for controlling spams • Other agents used for spasm control include baclofen, dantrolene TETANUS TREATMENT Supportive Care • Patients are best managed in ICU/emergency unit • Nursing in a dark quiet environment is required to avoid reflex spasms • Unnecessary procedures and manipulations are avoided • Adequate hydration, maintenance of electrolyte balance, urinary catheterization and treatment of intercurrent infection and anaemia if present • Cardiorespiratory monitoring, suctioning of airway • Nutritional support commonly via NG-tube feeds Prevention Levels of prevent ion Level 1 General health promotion Creating awareness, safety precautions to avoid injury, avoiding animal bites, hygiene. Level 2 Specific protection Immunization, chlorhexidine cord care, good antenatal care and delivery practices. Level 3 Early diagnosis & prompt good history, physical treatment examination and treatment Level 4 Limitation of disability Good supportive care to avoid pressure ulcers, calorie & electrolyte imbalance. Level 5 Rehabilitation Clutches in cases of amputation, ambulation Prevention Tetanus toxoid schedule for women. Dose When to give Protection level (%) Duration of protection TT 1 At first contact/ as early as possible in pregnancy 0 0 TT 2 At least 4wks after TT 1 80 3 years TT 3 At least 6 months after TT 2/ subsequent pregnancy 95 5 years TT 4 At least 1 year after TT 3/ subsequent pregnancy 99 10 years TT 5 At least 1 year after TT 4/ subsequent pregnancy For life TETANUS PROGNOSIS • Recovery in tetanus occur when synapses in the spinal cord regenerate. • The prognosis is dependent on incubation period, the time from spore inoculation to first symptom(onset period), and the time from first symptom to first tetanic spasm. • In general, shorter intervals indicate more severe tetanus and a poorer prognosis TETANUS PROGNOSIS • A high risk of mortality is associated with: • Short incubation period • Early onset of convulsions • Delay in treatment • Contaminated lesions of the head and the face • Neonatal tetanus MEASLES MEASLES INTRODUCTION • Measles also known as Rubeola is a highly contagious childhood infection caused by a virus once very common but now almost always prevented by vaccination • Death rates from measles have fallen worldwide and endemic outbreaks have been interrupted especially in areas with good vaccine coverage, still globally more than 100,000 under 5year children die yearly from complications of measles infection • There has been a noted occurrence in infants as early as 6months of age and a resurgence among preschool children attributed to fast waning maternal antibodies in infants of mothers who never experienced the wild-type measles infection in childhood MEASLES AETIOLOGY • The measles virus is a single-stranded, lipid enveloped RNA virus of the genus Morbillivirus with the family Paramyxoviridae • Humans are the only natural host to the highly contagious virus that is said to infect 90% of nonimmune contacted household members • The virus has 6 structural proteins but two, the hemagglutinin(H protein) and Fusion protein(F protein) are important in the induction of immunity and serve as biomarkers in the differentiation of types MEASLES PATHOPHYSIOLOGY •Spread is by contact with cough and sneeze droplets via personal contact or through direct contact with secretions which remain viable for up to 1hour in droplets suspended in the air after the source leaves the room •Patients are infectious from 3days before the appearance of the rash till 4-6days after its onset •Measles is primarily an infection of the respiratory tract, once it enters the respiratory tract epithelium, its H protein binds to host receptors on nucleated immune cells and the F protein facilitates viral entry and there is subsequent translation and replication of the virus MEASLES PATHOPHYSIOLOGY • Measles infection causes necrosis of the respiratory epithelium and lymphocytic infiltrates • Infected mucosal and dermal cell experience intracellular oedema and dysketratosis resulting in the formation of giant multinucleated cells that may fuse together forming WarthinFinkeldey giant cells pathognomonic for measles • Measles occurs over 4 phases  Incubation phase  Prodromal phase  Exanthematous phase  Recovery phase MEASLES CLINICAL FEATURES • Measles is characterized by 3 C’s(cough, coryza and conjunctivitis) with fever and an exanthem (maculopapular rash) • After a symptom free incubation period of 10-14 days, the prodromal phase begins with a fever of increasing intensity and the 3 C’s. • 1-4 days prior to the onset of the exanthematous phase, an enathem (Koplik’s spots) appears briefly as small white spots seen on the buccal mucosa, inside the cheeks opposite the molar, may involve the hard palate and is a pathognomonic sign of measles MEASLES CLINICAL FEATURES • The exanthematous phase begins with the appearance of a rash 2-4 days after the prodromal symptoms and lasts for up to 8-10 days • The typical rash is a red maculopapular eruption that begins on the forehead(along the hairline) spreading behind the ears, face, neck, torso the to the extremities(centrifugal distribution) • It is commonly itchy • The rash is said to ‘stain’ or change color becoming darker before disappearing • Overall the recovery phase may last up to 3weeks with the desquamation of the rash and resolution of cough MEASLES DIAGNOSIS • Diagnosis is typically clinical with a history of fever, malaise and the 3C’s or the observation of Koplik’s spots on examination • Laboratory findings may include leucopenia with a relative lymphocytosis on FBC and occasional neutropenia. ESR and C-reactive protein are normal in the absence of secondary bacterial infection • Confirmatory laboratory investigation involves identification of IgM antibodies in serum or the viral particles by PCR. MEASLES DIFFRENTIAL DIAGNOSIS • Rubella • Erythema Infectiosum • Kawasaki disease • Drug eruptions • Dengue fever • Scarlet fever MEASLES COMPLICATIONS • Measles complications are largely attributed to the pathogenic effect of the virus to the respiratory tract and the child's immune system • Pneumonia / Croup • Otitis media • Diarrhoea and vomiting • Myocarditis • Subacute Sclerosing Parencephalitis (SSPE) • Keratitis MEASLES TREATMENT • There is no specific anti-viral treatment, medications are generally aimed at treating superinfections, maintaining good hydration and fever &pain relief • Very young children and malnourished patients are also given Vitamin A and zinc supplements as an immunomodulator and to decrease the risk of keratitis & night blindness • Humidified oxygen therapy • Prophylactic antibacterial antibiotics is not indicated MEASLES PREVENTION • Mothers who are immune pass antibodies to their babies in utero, these protect the child till about 9months of age when they must waned out • WHO currently recommends that in developing countries, 2 doses be given at 6 & 9 months of age • At 12months and between 4-6years of age it is also recommended that the child receives booster doses as part of a three-part MMR vaccine • The claims of an association between measles vaccine and autism is false.
