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1. Measles_Polio disease for mbbs students
- 1. A 2 year-oldgirl presents an unrelenting fever of with 4 day history of low grade fever, a dry cough, nasal congestion and rash. What are the differential diagnosis? Case Study
- 2. Measles Acute viral infectioncharacterized by a final stage with a maculopapular rash erupting successively over the neck and face, trunk, arms, and legs, and accompanied by a high fever
- 3. Epidemiology RNA virusof the genus Morbillivirus in the family Paramyxoviridae. Measles is endemic throughout the world but commoner from Oct to Mar Droplet transmission during the Catarrhal stage. It is highly contagious (Attack rate of ~ 90%)
- 5. Pathology Epithelium •Necrosis •Serous exudate •Proliferation ofmononuclear cells and a few polymorphonuclear cells occur around capillaries •Notable around sebaceous glands and hair follicles GI •Koplik Spots •General inflammatory reaction extending to lymphoid tissue
- 6. Pathology Respiratory system • HetchGiant Cell Pneumonia/Interstitial Pneumonia • Bacteria Pneumonia • Laryngitis/Croup/Bronchitis: General inflammatory Reaction CNS • Encephalomyelitis: perivascular demyelinization occurs in areas of the brain and spinal cord • In subacute sclerosing panencephalitis (SSPE), there may be degeneration of the cortex and white matter with intranuclear and intracytoplasmic inclusion bodies Lymphoid Tissue •Hyperplasia and Multinucleated (Warthin-Finkeldey reticuloendothelial giant cells)
- 7.
- 8. Three clinical stages: 1.Incubation stage (10 -12 days) 2. Prodromal stage with an enanthem (Koplik spots) and mild symptoms 3. Exanthematous stage - maculopapular rash accompanied by high fever Clinical Manifestations
- 9. Prodromal phase • Usuallylasts 3-5 days and is characterized by: • Fever • Dry cough • Coryza • Conjunctivitis • Symptoms precede Koplik spots by 2-3 days • Grayish white dots, usually as small as grains of sand, that have slight, reddish areolae • Tend to occur opposite the lower molars but may spread irregularly over the rest of the buccal mucosa. • Appear and disappear rapidly, usually within 12-18 hr
- 10.
- 11. Prodromal phase • Temperaturerises abruptly as the rash appears and often reaches 40°C or higher • Coryza, fever, and cough are increasingly severe up to the time the rash has covered the body • Occasionally, this phase may be severe with sudden high fever, sometimes with convulsions, pneumonia • Other features of panmucositis • Otitis media • Bronchopneumonia • Gastrointestinal symptoms such as diarrhea and vomiting
- 12. Exanthematous Phase • Startsas faint macules on ipper parts of the neck, behind the ears, along the hairline and behind cheeks • Evolves from macules to papules and rapidly spreads to entire face, neck, upper arms, upper chest • By 2nd-3rd day, it begins to fade on the face in the same sequence • Pruritus is not prominent • Severity of the disease is directly related to the extent and confluence of the rash
- 16. Variants • In severecases • the rash is confluent, the skin is completely covered, including the palms and soles with swollen face. • confluent rash with petechiae, and there may be extensive ecchymoses (Atypical Measles) • Papular (Less macular) • Hemorrhagic • Absent • Received IgG • HIV infection • Young infants
- 17. Diagnosis Diagnosis is mostlyclinical in this environment •Immunology •Microbiology •Histology
- 18. Diagnosis • Immunology • IgMis detectable for 1month after illness • Testing of acute and convalescent sera demonstrates the diagnostic seroconversion or fourfold increase in titer • Microbiology • Tissue culture in human embryonic or rhesus monkey kidney cells • Histology • During the prodromal stage multinucleated giant cells can be demonstrated in smears of the nasal mucosa
- 19. Diagnosis • Low WBCwith relative lymphocytosis • CSF of patients with measles encephalitis usually shows an increase in protein and a small increase in lymphocytes. The glucose level is normal
- 20. Differential Diagnosis • Rubella •Roseola infantum (human herpesvirus 6) • Erythema Infectiosum • Scarlet fever • Meningococcemia • Drug rashes • Infections resulting from echovirus, coxsackievirus, adenovirus • Rickettsial diseases • Infectious mononucleosis • Toxoplasmosis • Kawasaki disease
- 21.
- 22. Differential Diagnosis Incubation Period Infectivity RashFeatures Measles (1st ) 8-12 4 days before 4 days after Rash Maculopapula r from the face Koplik spots Grp A Strept (2nd ) 2 - 5 Variable Can be colonized Papular Sand paper rash Sore throat Strawberry tongue Rubella (3rd ) 14 - 21 7 days before 7 days after Maculopapula r High grade fever Enlarged nodes (Occipita Parvovirus E. Infectiosum (5th ) 4 - 14 No isolation needed Slapped cheek Human Herpes Virus 6 Roseola Infantum (6th ) 10 Unclear Maculopapula r High grad fever Fever disappears with Rash
- 23. Treatment Treatment is supportive •Bed rest • Antipyretics • Manage symptoms (photophobia, cough etc) • Maintenance of an adequate fluid intake • Vitamin A • Manage complications
- 24. Respiratory tract complications 1.Bacterial superinfection • Pneumococcus, • group A Streptococcus, • Staphylococcus aureus, • Haemophilus influenzae type b 2. Interstitial pneumonia (giant cell pneumonia) 3. Laryngitis, tracheitis, and bronchitis are common 4. Reactivation TB
- 25. Cardiovascular Complications • Nomaof the cheeks • Gangrene elsewhere appears to be secondary to • Purpura fulminans • Disseminated intravascular coagulation • Transient ECG changes may be relatively common • Myocarditis is an infrequent serious complication
- 26. Neurologic complications •Direct Invasionof the brain particularly in Immunosuppressed patients •Post Infectious Immunologically mediated Encephalitis that occurs later is predominantly demyelinating •Sub acute Encephalitis (particularly in Immunosuppressed patients •Sub acute Sclerosing Panencephalitis •Others include: Guillain-Barré syndrome, Hemiplegia, Cerebral thrombophlebitis, Retrobulbar neuritis (Rare)
- 27. Prognosis • Deaths areprimarily due to pneumonia or secondary bacterial infections • In developing countries measles frequently occurs in infants; possibly because of concomitant malnutrition, the disease is very severe in these locations and has a high mortality.
- 28. Prevention Isolation precautions, especiallyin hospitals and other institutions, should be maintained from the 7th day after exposure until 5 days after the rash has appeared.
- 29. Post Exposure Prophylaxis Passiveimmunization with immune globulin is effective for prevention within 5 days of exposure Eligibility •Susceptible household and hospital contacts who are younger than 12months of age or pregnant •Infants 6 mo of age or younger born to nonimmune mothers should receive immune globulin Regimen •I.M. Immune globulin (0.25 mL/kg; maximum: 15 mL) within 5 days of exposure
- 30.
- 31. Definition Acute flaccid paralysiscaused the polio virus WHO “Any child <15yrs with Acute Flaccid Paralysis or any person with paralytic illness at any age when polio is suspected”
- 32. What?: RNA Virus.Picornaviridae family, in the genus Enterovirus. 3 serotypes (P1, P2, P3 ) Survives in water for 3mths and in faeces for 6mths. Inactivated by heat, formaldehyde, Chlorine, UV light. How? : Faeces & pharyngeal secretions of infected persons. Excreted 2wks b4 paralysis and several weeks after Who? : Young children and adolescents in developing countries while adults are more commonly affected with increased disease severity and deaths in developed countries Sex: Male : Female 3:1 Where?: Nigeria, Afghanistan, Pakistan Epidemiology of Polio
- 33. Pathogenesis of PolioVirus Infection
- 35. Pathology • Neuronal inflammationand destruction • Anterior horn cells (Spinal Cord) • Cranial nerve nuclei (Medulla oblongata) • Cerebellum • Substantia Nigra
- 36. Risk Factors • Unimmunizedstatus, especially if <5 years • Immune deficiency • Poverty and low socioeconomic class • Poor sanitation and hygiene
- 37.
- 38. Abortive poliomyelitis (5%) •Influenza like symptoms 1-2 weeks later • Lasts only for 2-3 days • Clinical examination unremarkable • Complete recovery
- 39. Non paralytic poliomyelitis(1%) •Initial minor illness-headache, nausea, vomiting, soreness and stiffness of neck muscles, fleeting paralysis of bladder and constipation •Short symptom free interlude between major and mild illness
- 40. Non paralytic poliomyelitis •Nuchal and spinal rigidity are hallmark • Tripod sign • Kernigs sign • Head drop • Reflexes usually normal • Changes in reflex indicate impending paralysis
- 41.
- 42. Paralytic poliomyelitis -Spinal • Spotty paralysis • Asymmetric flaccid paralysis • One leg most common followed by one arm • Absent DTRs • No sensory deficits • Bowel and bladder dysfunction • Paralysis is complete by 3days
- 43. Paralytic Poliomyelitis -Spinal Recovery •Starts after several weeks but usually within 6 months •Recovery may continue for as long as 18 months •Sequelae - Atrophy, deformity
- 44. Paralytic poliomyelitis-Bulbar Vital centersin medulla being involved with ascending paralysis and autonomic disturbances • Nasal twang to voice • Nasal regurgitation of food • Inability to swallow and pooling of oral secretions • Palatal and tongue involvement • Vocal cord palsy • Recovery is variable
- 45. Paralytic Poliomyelitis-Encephalitis Involvement ofhigher centers •Seizures •Coma •Spastic paralysis •Peripheral & cranial nerve palsies •Respiratory paralysis-due to variety of possibilities
- 47. Complications • Urinary TractInfection • Atelectasis & Pneumonia • Skin ulcers • Traumatic injuries to affected limb(s) • Myocarditis • Respiratory muscle involvement and death • Post poliomyelitis syndrome
- 48. Diagnosis 1. Clinical presentation 2.Laboratory findings • Microbiology: Virus recovery from stool, throat washing, blood. Virus recovery from stool is essential to diagnosis • CSF: Leukocytosis, Increased protein, Normal glucose. • PCR amplification of poliovirus RNA from CSF • Immunologic: Positive IgM is diagnostic. Demonstration of a four fold rise in IgG
- 49. Time course ofpoliovirus infection
- 50. Differential diagnosis • Guillain-Barresyndrome • Transverse Myelitis • Spinal cord compression • Tuberculosis (Spinal) • Non polio enteroviruses • Polymyositis & Viral myositis • Botulism
- 51. Polio GBS TraumaticNeuritis Transverse Myelitis Etiology Polio type 1,2,3 viruses Immunologic Trauma Unknown-multiple viruses Fever at onset High at onset of paralysis Not common Before during or after paralysis Rarely present Flaccid paralysis Acute asymmetric, (proximal muscles) Acute symmetrical, (distal muscles) Acute asymmetrical (only one limb) Acute symmetrical involving Lower limbs CNS involvement Only Bulbar involvement May Occur Absent Absent Respiratory insufficiency Only Bulbar involvement In severe cases Absent Absent Autonomic nervous system Plus Rare May be present May be present CSF High WBC’s; Normal to Slightly elevated protein < 10 WBC’s; High Protein Normal Normal Count; Normal to Slightly elevated protein EMG (@ 3 weeks) Abnormal Normal Normal Normal Sequelae (3 - 12mths) Severe asymmetrical atrophy Variable Variable Yes
- 52. Treatment - Abortive •Analgesics & sedatives • Bed rest • Nutrition • Avoid exertion & IM injections
- 53. Treatment-non paralytic • Hotpacks & hot tub baths • Firm bed • Foot board or splint • Gentle physical therapy
- 54. Treatment-Paralytic • Care ofbowel & bladder • Increased fluid intake • Care of airway & secretions • Monitor vital signs • Ventilation • Tracheostomy
- 55. Complications • Hypertension • Hypercalcemiaand nephrolithiasis • Myocarditis • Respiratory embarrassment
- 56. Prognosis • Complete recoveryin abortive & non paralytic polio • 60% mortality in bulbar polio & 5% in spinal polio • Conditions that enhance paralysis • Male sex • Pregnancy • Tonsillectomy: a risk factor for bulbar paralysis • Intramuscular injections or trauma
- 57. Prevention • Hygiene • Vaccination •Inactivated Polio Vaccine (IPV) • Oral Polio Vaccine (OPV) WHO Four Prong Strategy to eradicate Polio 1.Routine Immunization 2.National Immunization Days (NIDs) 3.Acute Flaccid Paralysis Surveillance 4.Mopping up Immunization
Editor's Notes
- #20 1.Koplik spots are pathognomonic for measles. 2. The rashes of rubella and of enteroviral and adenoviral infections tend to be less striking than that of measles, as do the degree of fever and severity of illness. 3.The rash of roseola infantum appears as the fever disappears, whereas in measles it appears concomitantly. 4. Although cough is present in many rickettsial infections, the rash usually spares the face, which is characteristically involved in measles. 5.The absence of administration of a drug in the history usually serves to exclude serum sickness or drug rashes. 6. Meningococcemia may be accompanied by a rash that is somewhat similar to that of measles, but cough and conjunctivitis are usually absent. 7. In acute meningococcemia the rash is characteristically petechial and purpuric. 8.The diffuse, finely papular rash of scarlet fever has a "goose flesh" texture on an erythematous base and is relatively easy to differentiate from the maculopapular rash of measles.
- #21 1.Koplik spots are pathognomonic for measles. 2. The rashes of rubella and of enteroviral and adenoviral infections tend to be less striking than that of measles, as do the degree of fever and severity of illness. 3.The rash of roseola infantum appears as the fever disappears, whereas in measles it appears concomitantly. 4. Although cough is present in many rickettsial infections, the rash usually spares the face, which is characteristically involved in measles. 5.The absence of administration of a drug in the history usually serves to exclude serum sickness or drug rashes. 6. Meningococcemia may be accompanied by a rash that is somewhat similar to that of measles, but cough and conjunctivitis are usually absent. 7. In acute meningococcemia the rash is characteristically petechial and purpuric. 8.The diffuse, finely papular rash of scarlet fever has a "goose flesh" texture on an erythematous base and is relatively easy to differentiate from the maculopapular rash of measles.
- #22 1.Koplik spots are pathognomonic for measles. 2. The rashes of rubella and of enteroviral and adenoviral infections tend to be less striking than that of measles, as do the degree of fever and severity of illness. 3.The rash of roseola infantum appears as the fever disappears, whereas in measles it appears concomitantly. 4. Although cough is present in many rickettsial infections, the rash usually spares the face, which is characteristically involved in measles. 5.The absence of administration of a drug in the history usually serves to exclude serum sickness or drug rashes. 6. Meningococcemia may be accompanied by a rash that is somewhat similar to that of measles, but cough and conjunctivitis are usually absent. 7. In acute meningococcemia the rash is characteristically petechial and purpuric. 8.The diffuse, finely papular rash of scarlet fever has a "goose flesh" texture on an erythematous base and is relatively easy to differentiate from the maculopapular rash of measles.
- #33 Pathogenesis of Poliovirus Infection (1) Pathogenesis of poliovirus infection is composed of 4 stages:Digestive stage: The virus enters by the oral route. It starts to replicate in the oropharyngeal and the intestinal mucosa from 1 to 3 days after penetration in the digestive tract. As a consequence of multiplication, the virus begins to appear in the throat and in the feces. Lymphatic stage: The spread of the virus to deep regional lymph nodes gives rise to an early, transient "minor" viremia, which spreads the virus to nodes, bone marrow, and the liver.Viremia stage: Further replication of the virus systemic reticuloendothelial tissues leads to a more sustained viremia, which coincides with the onset of clinical symptoms. Neural stage: If it has the ability to pass the blood-brain barrier, it can rapidily invade, via this route (lymph and blood) the CNS. There, it infects preferentially motoneurones of the anterior horn. Key messages : Pathogenesis of poliovirus infection is composed of 4 stages.Reference:Crainic R. Ann Inst Pasteur/Actual 1995;6:75-85