DR BILKIS DISORDERS OF LOWER RESPIRATORY TRACT- 2021.pptx

A lecture about lower respiratory tract infections affecting children

1. DISORDERS OF LOWER RESPIRATORY TRACT PROF BILKISU ILAH PAEDIATRIC PULMONOLOGIST 1

2. OUTLINE INTRODUCTION PNEUMONIA BRONCHIOLITIS MEASLES 2

3. INTRODUCTION Inflammation of the airways/pulmonary tissue, due to microorganisms (viral or bacterial infection) below the level of the larynx. 3

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5. LOWER RESPIRATORY TRACT DISORDERS IN CHILDREN Croup Tracheobronchitis Bronchitis Bronchiolitis Bronchial asthma Pneumonia Tuberculosis 5

6. 6 PNEUMONIA

7. OUTLINE INTRODUCTION DEFINITION EPIDEMIOLOGY AETIOLOGY TYPES/ CLASSIFICATIONS PATHOGENESIS & PATHOLOGY CLINICAL FEATURES INVESTIGATIONS TREATMENT COMPLICATIONS PROGNOSIS 7

8. LEARNING OBJECTIVES After completing this lecture, the students should be able to: 1. Discuss the major pathogens of childhood pneumonia, according to age 2. Recognize the Clinical features of children who have pneumonia 3. Outline the antibiotic regimens used to treat pneumonia in children. 4. Describe the radiographic and laboratory findings in pneumonia 5. Identify preventive measures using 5 levels of prevention 8

9. INTRODUCTION Pneumonia is a global leading cause of morbidity and mortality in under fives children killing 900,000 every year. In Nigeria, 142,000 to 160,000 die annually. Accounts for 15% of under 5 mortality. Highest cause of mortality after neonatal period. 9

10. DEFINITION Pneumonia is the inflammation of lung parenchyma due to pathogenic micro-organisms such as bacteria, viruses and fungi. Clinically, it is defined as a condition typically associated with fever, respiratory symptoms, and evidence of parenchymal involvement, either by physical examination or the presence of infiltrates on chest radiograph. 10

11. EPIDEMIOLOGY Morbidity & mortality is higher in infants and toddlers than older children. Nigeria’s mortality is highest in Africa and 2 nd highest in the world. Peaks in rainy season & harmattan in Nigeria. Commoner in boys than girls. 11

12. Important risk factors for childhood pneumonia (Nigeria) malnutrition (weight–for–age z<–2)- (23%) low birth weight (≤2500 g) (12%) non–exclusive breastfeeding (87%) solid fuel use (74%) crowding (7 or more persons sharing the same household). 12

13. OTHER RISK FACTORS Zinc deficiency Measles Poor hygiene PROM Sepsis Mechanical ventilation Endotracheal intubation GERD Tracheoseophageal fistula Vitamin A deficiency CHD with large shunt Mother’s education Mother’s experience as care giver Day care Out door pollution Passive smoking Pre existing lung disease Neurological diseases interfering with mucus clearance 13

14. CLASSIFICATION Based on origin Community acquired, hospital acquired ( nosocomial ), ventilator associated, aspiration, pneumonia in immunocompromised . Based on pattern of involvement/ anatomic Lobar/ segmental, broncho -pneumonia, interstitial pneumonia. Based on infecting organism Bacterial, viral, chlamydia , mycoplasma , fungal, pneumocystis jerovici . 14

15. CLASSIFICATION Contd Based on actual infecting organism Pneumococcal, streptococcal, staphylococcal, Influenza, tuberculous. Based on duration Acute (<2wks) or chronic (commonly fungal or mycobacterial ). Based on severity Non severe or severe pneumonia 15

16. AETIOLOGICAL AGENTS Bacteria Streptococcus pneumoniae , Haemophilus influenzae , Staphylococcus aureus & pyogenes , Streptococcus pyogenes , Bordetella pertusis , non typhoidal salmonella, non typeable H influenza, G- ve ( Klebsiella , Pseudomonas, Proteus). Viruses - : RSV, parainfluenzae viruses 1–3, influenza A & B, human metapneumovirus , adenovirus, coronavirus , bocavirus , rhinovirus, measles virus. 16

17. AETIOLOGICAL AGENTS Contd Fungal Aspergillus spp , Candida spp , Cryptococcus. Others Mycoplasma pneumoniae , Chlamydia pneumoniae , Pneumocystis jiroveci , Legionnella pneumophilia , Mycobacterium tuberculosis. 17

18. AGES AND PATHOGENS 3 wk to 3 mo Gram – ve , gram + ve ( S.pneumoniae , S. Aureus , grp B streptococcus), Chlamydia trachomatis , Respiratory syncytial virus, Parainfluenza , Bordetella pertussis 3 mo to age 4 y RSV, Parainfluenza , Human metapneumovirus , Influenza, Rhinovirus, S pneumoniae , Bocavirus , Corona virus Mycoplasma pneumoniae , Staph pyogenes , grp A streptococcus, Staph aureus , H influenza 5 y through adolescence Mycoplasma pneumoniae, Chlamydia pneumoniae, Streptococcus pneumoniae, Mycobacterium tuberculosis 18

19. PULMONARY DEFENSE MECHANISMS Normal pulmonary host defence system consists of multiple mechanical barriers, including saliva, nasal hair, the mucociliary apparatus, the epiglottis, and the cough reflex. Humoral immunity , including secretory IgA and serum IgG, complement play roles in microbial killing. Phagocytic cells , including polymorphonuclear cells and alveolar macrophages, play important roles, Cell med iated immunity is important in the defence against certain pathogens, especially viral agents and other intracellular organisms. 19

20. PATHOGENESIS Typically follows an URTI, as LRT is usually sterile . Organisms are transmitted by droplet spread directly from close personal contact or indirectly by contaminated fomites. Following initial colonization of the nasopharynx, organisms may be inhaled , leading to a pulmonary focus of infection; less commonly, bacteraemia results from the initial upper airway colonization, with subsequent seeding of the lung parenchyma. 20

21. PATHOLOGY Changes occur in respiratory bronchioles and alveoli. Exudation of fibrin, inflammatory cells & organisms --- solid exudative reaction. Destructive necrosis of alveolar walls. Confluent involvement of lobar segment (lobar Pneumonia) or patches throughout lobe/lung ( broncho Pneumonia). Red hepatisation. Grey hepatisation. Normal alveolar architecture restored with removal of dead blood cells & fibrinous exudates. 21

22. PATHOPHYSIOLOGY Inflammatory debris narrows airway. Increase airway resistance. Partial/total occlusion of small airways. Resultant atelectasis , hyperinflation, increased work of breathing and wheezing. Increased alveolar diffusion barrier causes significant ventilation perfusion mismatch and intra pulmonary shunt. Increase pulmonary vascular resistance and myocardial oxygen consumption cause heart failure. 22

23. HISTORY Acute onset. Fever, cough, breathlessness, anorexia. Chest pain in older children with lobar Pneumonia. With extensive consolidation, hypoxia present with restlessness and cyanosis. Lower lobe Pneumonia can present with abdominal pain. Infants- diarrhoea, vomiting 23

24. RELEVANT HISTORY QUESTIONS Host related factors- age, immunisation status, Breastfeeding, etc Environmental factors- house hold air pollution e.g. firewood, smoking, over crowding, season etc Co-morbidities- SCA, HIV, GERD, heart disease. 24

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26. EXAMINATION Ill and anxious, restless, toxic, febrile, may be cyanosed. Or dehydrated. Tachycardia. Tachypnoea, retractions (intercostal, subcostal , suprasternal ), wheezing, nasal flaring, and grunting. Tachypnoea (≥60 bpm <2 mths , ≥50 bpm at 2-12 months, ≥40 bpm at 1-5 years, ≥30 bpm for ≥5 years. Subtracting 10 if the child is febrile) is the most sensitive and specific sign of pneumonia. 26

27. EXAMINATION Contd Few children may not exhibit tachypnoea Increased work of breathing (retractions, flaring, grunting) and decreased oxygen saturation (<95%) also are predictive of LRTI. Grunting may be a sign of imminent respiratory failure. 27

28. EXAMINATION Contd Central trachea. Diminished chest expansion over affected lobe. Dull percussion note in lobar, may be resonant in BPN. Tactile fremitus increased over affected site. Breath sounds diminished, in early phase bronchial BS. Crepitations (fine or coarse). 28

29. CHEST SIGNS OF LOBAR AND BRONCHOPNEUMONIA SIGN LOBAR BRONCHOPNEUMONIA Chest deformity None None Chest movement Diminished/absent Normal Mediastinal shift None None Vocal fremitus Increased Normal Percussion note Dull Resonant Breath sound Bronchial/vesicular Vesicular Added sound Crepitations Crepitations Vocal resonance Increased Normal 29

30. SEVERITY OF PNEUMONIA Non severe Mild chest in drawing, decreased breath sounds, bronchial BS, crepitations . Severe Cyanosis/ oxygen saturation ≤90%, severe respiratory distress, decreased/absent BS or vocal resonance, danger signs eg inability to BF or drink, lethargy, unconscious, convulsions, complications or co-morbidities e.g. heart failure, SAM, SCA. 30

31. INVESTIGATIONS Useful when available CX Ray Culture or PCR of tracheal secretions. Blood culture, serology Lung puncture Culture of pleural effusion Viral tissue culture Rapid test on nasopharyngeal aspirates by immunoflourescence Antigen detection in urine (bacterial) Lung biopsy 31

32. INDICATIONS FOR CHEST X-RAY Presence of significant chest retractions Failure to respond to initial course of antibiotics after 48 hours Complications e.g. pneumothorax , effusion Progressive symptoms despite antibiotic therapy 32

33. INVESTIGATIONS Contd Supportive investigations Arterial blood gas and pulse oximetry FBC Throat swab MCS Sputum MCS C- reactive protein ESR U/ E,Cr CT scan MRI 33

34. DIFFERENTIAL DIAGNOSIS Bronchiolitis Asthma Bronchitis Heart failure Bronchiectasis Lung abscess Pulmonary oedema Atelectasis from FB or mucous plug Chemical pneumonitis 34

35. PNEUMOCOCCAL PNEUMONIA Streptococcus pneumoniae or pneumococcus accounts for >90%. Highest incidence is in pre-school children. Increased risk of pneumococcal infection - immunocompetent children who have had splenectomy , or physiological splenectomy such as those with sickle cell anaemia, and with nephrotic syndrome. Causes primary lobar Pneumonia in >1 yr. Complications uncommon. 35

36. STAPHYLOCOCCAL PNEUMONIA High morbidity & mortality, serious pneumonia which may follow a bacteraemia or viral illness. Common in infancy, Cystic Fibrosis, malnourished children, immunosuppression or congenital malformation. Lesions are often extensive with bilateral involvement and focal areas arising from haematogenous seeding leading to abscess formation. Pneumatoceles occur in approximately 40%, with associated pneumothorax in 20% and empyema in 60% of patients. 36

37. STAPH PN CONTD Causes tissue destruction Haemolysin—lyses rbc , leukocidin —destroys wbc , staphylokinase —clot dissolution, coagulase —clot formation. Can present with anaemia. Radiological changes usually lag behind the clinical condition. Pneumatoceles can persist for 2–6 months 37

38. GROUP A STREPTOCOCCAL PNEUMONIA This is a rare cause of bacterial pneumonia and usually is secondary to viral infections such as influenza, chicken pox or measles. Presentation is similar to Pneumococcal pneumonia with sudden onset of high fever and pleuritic chest pain. Identification of the organism is for epidemiological purposes only. 38

39. HAEMOPHILUS INFLUENZAE PNEUMONIA This is now a rare cause of pneumonia due to routine vaccination against H. Influenza type b. It affects mainly 1mth-5yrs, with a peak at 3–12 months. 39

40. ATYPICAL PNEUMONIA Mycoplasma or Chlamydia pneumoniae , usually are of school age or older. Present with constitutional symptoms of myalgias , fever, malaise, headache, and gradual development of dry cough later in the illness as other symptoms improve. The chest radiograph often shows infiltrates, which can be bilateral or unilateral, patchy or dense. 40

41. VIRAL PNEUMONIA Children who have viral LRTIs generally present with URI symptoms, are not highly febrile or toxic, and often have bilateral auscultatory findings. Wheezing is common. Radiographs may show bilateral interstitial infiltrates 41

42. FUNGAL PNEUMONIA Common in immunocompromised . Risk factors- prolonged neutropenia , prolonged IV cannulation esp central line, prolonged antibiotic use. CXR – nodular changes & cavitations. Rx- IV Amphotericin B, Fluconazole , Caspofungin . 42

43. Viral pneumonia caused by RSV Hyperinflation, mild peribronchial cuffing, increased parahilar markings, and patchy lingular opacity (note the loss of the left heart border on the frontal view), likely representing atelectasis 43

44. Pneumococcal pneumonia Rounded area of airspace consolidation in the superior segment of the right lower lobe. A few air bronchograms are seen medially. 44

45. Necrotizing pneumonia Airspace consolidation in the right middle lobe with numerous central cavities. 45

46. Pneumococcal empyema Left lower lobe and lingular consolidation (note loss of the left hemidiaphragm and lower left heart border) with associated large left pleural effusion tracking up laterally. Volume loss on the left also indicates a component of atelectasis . 46

47. COMPLICATIONS Heart failure Pleural effusion/ empyema thoracis Pneumatocoeles Necrotising pneumonia Air leak syndromes ( pneumothorax , pneumomediastinum , subcutaneous emphysema Purulent pericarditis Embolisation (septicaemia, brain abcess , osteomyelitis , meningitis, pyomyositis ) Lung abscess SIADH 47

48. Pleural effusion Sterile parapneumonic effusions in association with bacterial pneumonia is common. With therapy, it resolve without additional intervention. Purulent effusions with resultant empyema can occur. Empyema presents with persistent fever, diminished appetite, fatigue, chest pain, and respiratory distress. 48

49. Lung abscess A lung abscess is a circumscribed, thick walled cavity in the lung which contains purulent material resulting from suppuration and necrosis of the involved lung parenchyma. Streptococcus and anaerobes; S aureus and gram-negative rods also may be involved. Tuberculosis always should be considered. Treatment include Drainage – tube drainage or thoracoscopy; fibrinolytics- urokinase or streptokinase and thoracotomy ±decortication 49

50. Air leak syndromes Pneumatoceles are usually small and thin walled with multiple cystic air-filled cavities which result from alveolar and bronchiolar necrosis. Seen with pneumonia caused by S. aureus and less frequently Group A Streptococcus and H influenzae . Staphylococcal pneumatoceles may be seen early in the illness (several days to one week) and are seen in as many as 85% of patients. Pneumothorax or pyopneumothorax can occur. 50

51. TREATMENT The treatment of bacterial pneumonia can occur either in the community or hospital setting depending on the clinical status of the child. In the community, supportive management includes anti- pyretics and early review by a medical practitioner if there is deterioration or no response to oral antibiotics within 48 hours. 51

52. INDICATIONS FOR ADMISSION Neonates Suspected staph or G- ve PN. Hypoxaemia Dehydration or malnutrition Unable to drink/lethargic/toxic Immunocompromised Complications Poor compliance with therapy Living far from health facility 52

53. TREATMENT contd 1 st line antibiotics in <5yrs are Pennicillins or Cephalosporins and in >5yrs Macrolides may also be considered. Aminoglycosides for G- ves . Severely ill child, place on oxygen. Fluid therapy/feeding. Antipyretic- Paracetamol 10-15mg/kg /dose, 6-8hrly. Treatment is for 5-10 days if no complications. With complications, can be extended to 14 days or more. 53

54. OUTPATIENTS < 2 months- admit and treat as neonatal sepsis (NNS). > 2 months/HIV infected/SCA- 1 ST line high dose oral Amoxycillin (90mg/kg/d in 2 divided doses) x at least 5 days (10 days for HIV infected). Alternative – Amoxycillin Clavulanic acid, Cefpodoxime (10mg/kg/d 2 ⁄doses) or Cefuroxime (20-30mg/kg/d 2/doses) x at least 5 days. 54

55. INPATIENTS < 2 months- admit and trt as NNS. > 2 months/HIV infected/SCA- 1 ST line IV Amoxycillin (150mg/kg/d in 3 divided doses) and IV/IM Genticin (5-7.5mg/kg daily) at least 5 days. Alternative for >2months– IV Ceftriaxone (50-100mg/kg/d 12-24hrs) OR IV Cefotaxime (100-200mg/kg/d 4 ⁄doses) OR IV/IM Genticin (5-7.5mg/kg daily) with IV Cloxacillin (100-200mg/kg/d in 4/doses) OR IV Cefuroxime (150mg/kg/d 3/doses) and IV/IM Genticin at least 5 days. 55

56. INPATIENTS contd Alternative HIV/SCA– IV Ceftriaxone (50-100mg/kg/d 12-24hrs) OR IV Cefotaxime (100-200mg/kg/d 4 ⁄doses) OR IV Cefuroxime (150mg/kg/d 3/doses) and IV/IM Genticin , at least 5 days SCA, 10 days HIV HIV infected- Add high dose Co- trimoxazole 20mg/kg/day of Trimethoprim in 4/doses x at least 10 days. SCA pts- Erythromycin (60-100mg/kg/day in 4 divided doses) x at least 5 days or alternatively Azithromycin (10mg/kg/day) x3 days. 56

57. RECURRENT PNEUMONIA Defined as > one radiographically confirmed episode in a year or > three episodes in a lifetime (with clinical or radiographic resolution between episodes). Causes include anatomic lesions such as vascular rings, cysts, and pulmonary sequestration; cystic fibrosis, TEF, CHD with large shunt, GERD and aspiration; and immunologic disorders such as HIV infection, chronic granulomatous disease and hypogammaglobulinemia . 57

58. PROGNOSIS Overall mortality is 5% in community-acquired pneumonia (CAP) managed in hospital, and 30% in nosocomial pneumonia and CAP requiring intensive care. 58

59. PREVENTION 5 levels of prevention. General health promotion and education- good hand and respiratory hygiene, improved housing and ventilation, reduce overcrowding & indoor air pollution, EBF. Specific protection- improve nutrition and micronutrients supplementation, immunisation, Treatment. Limiting disability. Rehabilitation. 59

60. National Integrated Pneumonia Control Strategy & Implementation Plan Involves 10+ interventions from protection, to prevention, diagnosis and treatment. Protection-- breastfeeding, nutrition and clean cooking to improve household air quality. Prevention-- hygiene practices, clean and safe delivery, postnatal care and immunization. Diagnosis and treatment-- caregiver awareness of the benefits of protection, prevention, and recognition of danger signs, access to health services, and coverage of essential medicines (e.g., Amox DT) at appropriate points of care. 60

61. KEY PRODUCTS FOR PNEUMONIA CONTROL

62. 62 BRONCHIOLITIS

63. OUTLINE INTRODUCTION AND EPIDEMIOLOGY AETIOLOGY RISK FACTORS PATHOGENESIS PATHOLOGY PATHOPHYSIOLOGY HISTORY EXAMINATION INVESTIGATIONS DDX TREATMENT PREVENTION PROGNOSIS 63

64. INTRODUCTION Bronchiolitis results from inflammatory obstruction of the smaller airways. A leading cause of LRTI and hospitalization in children less than 1 year of age worldwide. Usually a mild disease, but some children especially Infants with pre-existing risk factors may be predisposed to a severe form of the disease, requiring hospital admission and ventilatory support in the ICU. Host anatomic and immunologic factors seem to play a significant role in the severity of the clinical syndrome. 64

65. EPIDEMIOLOGY Acute infection of toddlers (<2yrs). Commoner in males. Common in winter and spring- temperate. Rainy and harmattan season in tropics. 65

66. AETIOLOGY Paramyxoviruses - respiratory syncitial virus (RSV), and parainfluenza virus account for >70% of cases. Human metapneumo virus. Bocavirus . Mycoplasma and Chlamydia pneumoniae . Adenovirus. 66

67. RISK FACTORS Age : < 2yr affected, peak 2-10 months. Gender: M>F, 1.5:1. Breast feeding: more in children not EBF. Early exposure: day care, creche , over crowding, older siblings. Seasonal factors: rainy and harmattan season. Winter and spring in temperate regions. Others: black infants- parainfluenza type III. Pre-existing disease-Prematurity, bronchopulmonary dysplasia (BPD), congenital heart diseases (CHD) and immunodeficiency. 67

68. PATHOGENESIS Viral infection of upper airway following inhalation of infected droplets or inoculation of nostrils or conjunctivae from contaminated hands. Infection of distal bronchi & bronchioles leads to mucous hyper secretion, necrosis of the epithelium and submucosal inflammatory oedema. Submucosal collagen & elastic tissue are preserved. Intraluminal plugs of cellular debris & fibrin clots. 68

69. PATHOLOGY Peribronchial infiltration by mononuclear cells. Alveoli are spared except those adjoining the inflammed bronchioles. Extensive destruction of resp epith , pulmonary parenchymal necrosis and hyaline membrane formation. RSV provoke cellular and immune responses with consequent cellular injury. Eosinophils degranulate and release eosinophil cationic protein which is cytotoxic to airway epithelium RSV invades bronchioles 69

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71. PATHOPHYSIOLOGY Peripheral airway of infants and toddlers are narrow, hence has propensity for airway obstruction. Increased airway resistance from inflammatory oedema, mucous plugs and epithelial debris. Air trapping beyond site of obstruction causes hyper inflation (ball valve obstruction). Increased functional residual capacity accounts for difficulty in breathing and prolonged expiratory phase. 71

72. PATHOPHYSIOLOGY Contd Increased work of breathing from uneven distribution of resistance & decrease lung compliance. Complete (check valve) obstruction in some bronchioles. Absorption of trapped air leads to multiple but patchy atelectasis . With increase resistance to airflow, volume of dead space, work of breathing and RR also increase. Hypercapnoea , hypoxaemia and ventilation perfusion mismatch. IgE antibody release may be related to wheezing 72

73. HISTORY Usually <2yrs Wet season + ve hx of an older contact with URTI. Prodromal symptoms of clear rhinorrhoea , nasal congestion, sneezing & cough with mild fever <7 days. Sudden onset wheezing, breathlessness. Episodic or paroxysmal cough. Irritability and poor feeding. 73

74. HISTORY Contd Cough & wheezing in younger infants may not be prominent but may have apnoea. Other systemic manifestations usually absent Symptoms disappear in 1-3days or may be protracted, severe symptoms may be seen within 1 st 3-4 days 74

75. EXAMINATION Cyanosis may be present, pyrexia, irritability /lethargy, dehydration. Tachypnoea, chest retractions, grunting. Hyperinflation of chest. Expiratory polyphonic rhonchi, fine inspiratory crepitations . Near silent chest-imminent respiratory failure. Tachycardia. Hepatomegaly or splenomegaly from hyper inflation. Co morbid condition- otitis media (20%), 75

76. NATURAL HISTORY 1 st 48-72hrs- severe resp distress, risk of resp failure or metabolic acidosis. 1-2wks- gradual resolution of symptoms. Risk of death- cong hrt ds , congenital or acquired chronic resp ds ( laryngo - or tracheomalacia , BPD, bronchiectasis), neonates. Adenovirus aetiology can lead to obliterative bronchiolitis. 76

77. INVESTIGATIONS Neither laboratory tests or radiological exams are usually indicated for the routine workup of infants with bronchiolitis. 77

78. INVESTIGATIONS CXR PA view- peri bronchial thickening, features of hyper inflation (horizontal splaying of ribs, flattened diaphragm, relative microcardia ). Increased bronchovascular markings, interstitial streaks radiating from hilar area. Patchy/segmental opacities may suggest atelectasis &/ bacterial consolidation. CXR lat view- Hyperinflation with increased AP diameter. 78

79. INVESTIGATIONS Contd Virus may be demonstrated by antigen detection tests-enzyme immunoassay, immunoflorescence ; PCR; culture. Blood culture in cases of superimposed bacterial pneumonia (Staph aureus or Staph epidermidis ). Blood gas analysis. Pulse oximetry – oxygen sat <92% , place on oxygen. U/ E,Cr - metabolic acidosis FBC, diff- non specific, may be normal. Diagnosis mainly clinical especially in a previously healthy child with a 1 st wheeze during an outbreak . 79

80. DDX Asthma Pertusis Pneumonia Cystic fibrosis Foreign body Aspiration of food/milk GERD Heart failure Adenoidal hypertrophy Croup 80

81. INDICATIONS FOR ADMISSION Low oxygen saturation (<92%) Moderate-to-severe respiratory distress Dehydration Apnoea Children with pre-existing risk factors should be carefully assessed and admitted if necessary. 81

82. TREATMENT No specific treatment for viral bronchiolitis, and the mainstay of therapy is supportive care. 82

83. TREATMENT Supportive 1Oxygen- humidified. 2 Antipyretics to ameliorate fever & reduce oxygen requirement 3 Adequate hydration and feeds Antimicrobial therapy 1 Macrolide for Mycoplasma . 2 Ribavarin for high risk infants- neonates, CHD, chronic lung disease. 3 Routine antibiotics- not recommended, except in superimposed bacterial pneumonia. 83

84. TREATMENT Contd Other measures 1 Saline nasal decongestant/ nebulised 3% hypertonic saline- infants are obligate nasal breathers. Benefit is in decreased respiratory distress and enhance oral intake. Suction of secretions. 2 Bronchodilators- controversial. Trial of 2 doses, if no response stop. β2 agonist e.g Salbutamol and anti-cholinergic e.g Ipratopium bromide. 84

85. TREATMENT Contd 3 Nebulised Adrenaline- not recommended. 4 Cough mixtures- not recommended. 5 Steroid therapy- not recommended. 6 Sedatives- to be avoided. 7 Montelukast - not recommended. 8 DNAse - not recommended. 85

86. PREVENTION Immunisation- active -RSV, PIV 1-3. Passive- Palivizumab - RSV. Palivizumab for preterm infants with a gestational age of ≤35 weeks and birth age ≤6 months; children ≤2 years with BPD; children ≤2 years with congenital heart disease. Prevention of child to child transmission- hand washing, excusing staff or children with ARI from work or school. 86

87. COURSE AND PROGNOSIS Average duration of illness 12 days Viral bronchiolitis, especially in the case of severe form, may correlate with an increased incidence of recurrent wheezing in pre-schooled children and with asthma at school age. Most recover without complications. Adenovirus serotypes may develop bronchiectasis (not common in Nigeria). 87

88. 88 MEASLES

89. INTRODUCTION A.k.a Rubeola . Highly contagious acute viral illness. Near universal infection of childhood in pre vaccination era. Frequent and often fatal in developing countries. 89

90. MEASLES VIRUS Paramyxovirus (RNA), genus Morbillivirus - spherical in appearance. 100~150nm in diameter., with an outer envelope composed of M-protein, H-protein, F-protein. One antigenic type Detected from blood, nasal and pharyngeal secretions. Rapidly inactivated by heat and light. 3 types of antibodies are produced after infection 1 complement combining antibody 2 hemagglutinin inhibiting antibody 3 neutralizing antibody 90

91. EPIDEMIOLOGY Reservoir- Human. Transmission- Respiratory/ Airborne. Temporal pattern- Peak in late winter and spring, dry season. Age- 6 months to 5 years old. Communicability- 4-7 days before to 4-6 days after onset of rash. Susceptibility of population. 1 All age groups are susceptible; 90% of contact persons acquire the disease. 2 Permanent immunity acquired after disease. 91

92. PATHOGENESIS Respiratory transmission of virus Replication in nasopharynx and regional lymph nodes Primary viraemia 2-3 days after exposure Secondary viraemia 5-7 days after exposure with spread to tissues

93. PATHOLOGY Causes necrosis of the respiratory tract epithelium and an accompanying lymphocytic infiltrate. Produces a small vessel vasculitis on the skin and on the oral mucous membranes. Histology of the rash and exanthem reveals intracellular oedema and dyskeratosis associated with formation of epidermal syncytial giant cells. Fusion of infected cells results in multinucleated giant cells, Warthin-Finkeldey giant cells that are pathognomonic for measle . 93

94. CLINICAL FEATURES Incubation period 10-12 days (6-18) Prodrome (2-4 days) Fever, step wise increase Photophobia Cough, Coryza , and/or Conjunctivitis (the three “C’s) Enanthem ( Koplik spots)- pathognomonic sign, appears 1 to 4 days prior to the onset of the rash . First appear as discrete red lesions with bluish white spots in the center on the inner aspects of the cheeks at the level of the premolars. May spread to involve the lips, hard palate, and gingiva . They also may occur in conjunctival folds and in the vaginal mucosa. Koplik spots have been reported in 50–70% of measles cases. Transient prodromal rashes.

95. CLINICAL FEATURES Contd Eruption phase/ Rash ~14 days after exposure (7-21 days) Maculopapular , spreads from behind the ear→along hairline→face→neck→chest→back→abdomen→limbs→hand and feet ( palm,sole ). May become confluent. Lasts 5-6 days and fades in order of appearance. Temperature rise continuously and accompanied with the toxic symptoms. Convalescent stage Desquamation, lasts 10-14 days. 95

96. CLINICAL CASE DEFINITION Generalized rash lasting > 3 days, and Temperature >38.3◦C (101 F), and Cough, coryza , or conjunctivitis

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101. INAPPARENT/SUB CLINICAL MEASLES In individuals with passively acquired antibody, such as infants or recipients of blood products. The rash may be indistinct, brief or rarely, entirely absent. Some individuals who have received vaccine when exposed to measles may develop a rash but few other symptoms. Persons with inapparent or subclinical measles do not shed measles virus and do not transmit infection to household contacts. 101

102. ATYPICAL MEASLES Children who had received the original formalin-inactivated measles vaccine at times developed a more severe form of disease. Patients had onset of high fever and headache followed by the appearance of a maculopapular rash on the extremities that become petechael and purpuric and progressed in a centripetal direction. Frequently complicated by pneumonia and pleural effusion. Thought to be caused by development of circulating immune complexes that formed due to an abnormal immune response to the vaccine. 102

103. ATYPICAL MEASLES TYPES Mild Severe- shock Haemorrhagic measles 103

104. INVESTIGATIONS Isolation of measles virus from a clinical specimen (e.g., nasopharynx , urine) Significant rise in measles IgG by any standard serologic assay (e.g., EIA, HA) Positive serologic test for measles IgM antibody Serum Ab measurement- complement combining antibody; hemagglutinin inhibiting antibody; neutralizing antibody. Multinucleated giant cells are detected in nasopharyax mucosa secretions. FBC- leucopenia, lymphocytes lower than neutrophils . ESR, CRP- normal unless complicated by bacteria.

105. COMPLICATIONS Respiratory Pneumonia- (bronchiolitis obliterans ), o titis media, l aryngitis , tracheitis , croup, reactivation of dormant Tuberculosis, emphysema, subcutaneous emphysema, sinusitis, mastoditis Neurologic complications Febrile convulsions, encephalitis and SSPE GIT/Nutritional Diarrhoea, Malnutrition, Cancrum oris , Herpes stomatitis , mesenteric lymphadenitis Cardiac Myocarditis Eyes Bacterial conjunctivitis, Vit A eye changes Death

106. DIFFERENTIAL DIAGNOSIS Rubella (German measles). Roseola infantum (infant subitum , exanthem subitum , sixth disease) Drug rashes. Mycoplasma pneumoniae and group A streptococcus ( Scarlet fever ) . Kawasaki disease.

107. TREATMENT Supportive- oxygen, hydration, rest, antipyretic. Antibiotics Ventilatory support Antiviral not recommended, except in immunocompromised children. Vitamin A. 50 000 IU for infants aged <6 months 100 000 IU for infants aged 6–11 months 200 000 IU for children aged ≥12 months Day 1,2 and 14 Eye/ gutt antibiotics- Chloramphenicol , Ofloxacin Calamine lotion

108. PREVENTION 5 levels of prevention. Patients shed measles virus from 7 days after exposure to 4–6 days after the onset of rash. Exposure of susceptible individuals to measles patients should be avoided during this period. In hospitals, standard and airborne precautions should be observed for this period. Immunocompromised patients with measles will shed for the duration of the illness, and isolation should be maintained throughout. 108

109. 109 QUESTIONS?

110. CONCLUSIONS 110