Infectious diseases


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  • Recovery is complete, and no neurologic signs or sequelae develop. stiffness of the neck and back with positive Kernig's and Brudzinski's signs. Nuchal rigidity in polio is characterized by being present in the supine position and disappears in the prone position. This differentiates it from pyogenic meningitis where it is present in prone position. Paralysis of motor cranial nerve nuclei. Involvement of 9th, 10th, and 12th cranial nerves is the most important. Hence, there is paralysis of tongue, pharynx, and larynx which results in airway obstruction.Involvement of vital centers leads to:Respiratory centers: irregularity of rate, depth and rhythm of respiration.Circulatory center: hypertension and cardiac arrhythmias.Heat regulating center: rapid changes is body temperature.
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  • Infectious diseases

    1. 1.
    2. 2. Infectious Diseases<br />Prepared <br />by<br />DR.SHERIF REDA<br />Prof. of Pediatrics<br />AL- AZHAR UNIVERSITY<br />CAIRO - EGYPT<br />
    3. 3. Introduction<br />
    4. 4. I. Meningitis<br />II. Encephalitis<br />III. Poliomyelitis<br />IV. Mumps<br />V. Tetanus Neonatorum<br />VI. Pertussis<br />
    5. 5. I. Meningitis<br />The meninges are membranes that cover and protect the brain and spinal cord. There are 3 layers known as the:<br />Dura mater is the tough outer membrane<br />Arachnoid mater is the thin, delicate, web-like membrane<br />Pia mater is the innermost membrane<br />The arachnoid & pia mater are together known the as leptomeninges<br /> Inflammation of the leptomeninges, caused by<br />Bacteria<br />Viruses<br /> Or rarely, Fungi<br />The term ASEPTIC MENINGITIS refers principally to viral meningitis, but a similar picture may be seen with:<br />Other infectious organisms (Lyme disease, syphilis, tuberculosis) <br />Parameningeal infections (brain abscess, epidural abscess, venous sinus empyema) <br />Chemical exposure (nonsteroidal anti-inflammatory drug, IV immunoglobulin) <br />Autoimmune disorders<br />Alterations of host defense: (anatomic defects or immune deficits) increase the risk of meningitis from less common pathogens e.g. Pseudomonasaeruginosa, Staphylococcus aureus, Salmonella spp., and L. monocytogenes. <br />
    6. 6. Cont.<br />Bacterial Causes of Meningitis<br />NB: Viral meningitis is caused principally by entero-viruses, including coxsackieviruses, echoviruses, and, in unvaccinated individuals, polioviruses<br />Mumps virus is a common cause of viral meningitis in unvaccinated children<br />
    7. 7. Cont.<br />Mode of infection:<br />Bacterial meningitis is most commonly results from hematogenous dissemination of microorganisms from a distant site of infection<br />Clinical Manifestations:<br />The onset of acute bacterial meningitis has two predominant patterns: <br />The more dramatic and fortunately less common presentation is sudden onset with rapidly progressive manifestations of shock, purpura, DIC, unconsciousness, and frequently resulting in death within 24 hours. <br />More often, meningitis: is preceded by several days of fever with upper respiratory or gastrointestinal symptoms followed by nonspecific signs of CNS infection such as lethargy or irritability.<br />
    8. 8. Cont.<br />1) Non specific findings:<br />Fever, anorexia, poor feeding, myalgia, arthralgia, tachycardia, hypotension and various cutaneous signs such as petechiae, purpura or an erythematous macular rush. <br />2) Signs of meningeal irritation:<br /><ul><li>Nuchal rigidity and back pain
    9. 9. Kernig’s sign: flexion of the hip 90 degrees with subsequent pain with extension of the leg.
    10. 10. Brudzinski sign: involuntary flexion of the knees and hips after passive flexion of the neck while supine.</li></ul>3) Symptoms and Signs of increased ICP: <br />1- Headache and vomiting <br />2- Bulging fontanel or widening of the sutures<br />3- Cranial neuropathies. <br />4- Hypertension with bradycardia<br />5- Apnea or hyperventilation, stupor and coma.<br />4) Seizures: <br />(focal or generalized) due to, cerebritis, infarction or electrolyte disturbances. Seizures that occur on presentation or within the first 4 days of onset are usually of no prognostic significance<br />
    11. 11. Cont.<br />Diagnosis:<br />Lumbar puncture for CSF analysis should be performed when bacterial meningitis is suspected:<br />1- Microorganisms on gram stain and culture. <br />2- Neutrophilpleocytosis (300 - 2000/mm3). <br />3- Elevated protein (100 - 500mg/dL) <br />4- Reduced glucose concentration (< 50% of serum glucose)<br />5- Physical manifestations (Turbid with elevated pressure,100 - 300 mm H2O).<br />Normal CSF shows:<br />Normal pressure (50 - 80 mm H2O), leucocytes (< 5/mm3), proteins (20 -45 mg/dl) and glucose (75 % of serum glucose)<br />
    12. 12. Cont.<br />Treatment:<br /> A)Initial Antibiotic Therapy:<br /><ul><li>Vancomycin 60 mg/kg/24hr given every 6 hr in combination</li></ul>With either cefotaxime (200 mg/kg/24hr given every 6 hours) or ceftriaxone (100 mg/kg/24hr single dose or given every 12 hour). Patients allergic to β- Lactam antibiotics can be treated with chloramphenicol, 100 mg/kg/24 hr given every 6 hr. <br />Duration of antibiotic therapy: At least for 7-14 days I.V.<br /> B) Corticosteroids: <br />I.V dexamethasone 0.15 mg/kg/dose given every 6hr for 2 days in the treatment of children older than 6wk with acute bacterial meningitis caused by H. influenzae type b to decrease the permanent auditory nerve damage. <br /> C) Supportive and symptomatic therapy: <br /> - Good evaluation and monitoring are essential. <br /> -Correction of dehydration and electrolyte disturbances and proper nutrition. <br /> -Control of seizures <br />- Management of neurological complications <br />
    13. 13. Cont.<br />Prevention: <br />Vaccination and antibiotic prophylaxis of susceptible at – risk contacts:<br />Close contact:<br />Should be treated with RIFAMPIN 10mg/kg/dose every 12hr, for 2 days (in N. meningitides) and 20mg/kg/24 for 4 days (in H. influenzae type b).<br />Meningococcal quadrivalent Vaccine: <br />Avaccine is recommended for high-risk children older than 2yr. <br />Also Vaccines for H. influenzae type b should be given to all children beginning at 2 mo of age 3 doses (2, 4, 6 months). <br />
    14. 14. II. Encephalitis<br /><ul><li> Encephalitis is an inflammatory process of the brain parenchyma that usually is an acute infectious process, but may be a postinfectious encephalomyelitis, a chronic degenerative disease, or a slow viral infection.
    15. 15. Organisms cause encephalitis by one of two mechanisms: </li></ul>direct infection of the brain parenchyma <br />an apparent immune-mediated response in the CNS that usually begins several days after the appearance of extraneural manifestations of the infection<br /><ul><li> Encephalitis may be diffuse or localized</li></ul>Etiology:<br /><ul><li> Viruses are the principal causes of acute infectious encephalitis.
    16. 16. The most common viral causes of encephalitis are the arboviruses (St. Louis, LaCrosse, California, West Nile encephalitis viruses), enteroviruses, and herpesviruses.
    17. 17. Encephalitis also may result from other types of infection, metabolic, toxic, and neoplastic disorders. </li></li></ul><li>Cont.<br />Clinical Manifestations:<br /><ul><li> Acute infectious encephalitis usually is preceded by a prodrome of several days of nonspecific symptoms, such as cough, sore throat, fever, headache, and abdominal complaints.
    18. 18. The characteristic symptoms of progressive lethargy, behavioral changes, and neurologic deficits, followed.
    19. 19. Seizures are common at presentation.
    20. 20. Children with encephalitis also may have a maculopapular rash and severe complications, such as fulminant coma, transverse myelitis, anterior horn cell disease (polio-like illness), or peripheral neuropathy.
    21. 21. Acute DisseminatedEncephaloMyelitis (ADEM):</li></ul> - Is the abrupt development of multiple neurologic signs related to an inflammatory, demyelinating disorder of the brain and spinal cord. <br /> - Acute disseminated encephalomyelitis follows childhood viral infections, such as measles and chickenpox or vaccinations. <br />
    22. 22. Cont.<br />Laboratory And Imaging Studies:<br /><ul><li> The diagnosis of viral encephalitis is supported by examination of the CSF, which typically shows a lymphocytic pleocytosis, slight elevation in protein content, and normal glucose level. Increased erythrocytes and CSF protein may occur with HSV.
    23. 23. The CSF occasionally may be normal.
    24. 24. Neuroimaging studies (CT, MRI) may be normal or may show diffuse cerebral swelling of the parenchyma or focal abnormalities.
    25. 25. The EEG is the definitive test and shows diffuse, slow wave activity, although focal changes may be present.
    26. 26. Brain biopsy may be appropriate for patients with severe encephalopathy who show no clinical improvement if the diagnosis remains obscure.</li></li></ul><li>Cont.<br />Treatment:<br /><ul><li> With the exception of HSV and HIV, there is no specific therapy for viral encephalitis.
    27. 27. Management is supportive and frequently requires ICU admission, which allows aggressive therapy for seizures, timely detection of electrolyte abnormalities, and, when necessary, airway monitoring and protection and reduction of increased intracranial pressure.
    28. 28. IV acyclovir is the treatment of choice for HSV infections.
    29. 29. ADEM has been treated with high-dose IV corticosteroids.</li></li></ul><li>III. Poliomyelitis<br />Etiology:<br /><ul><li> The polioviruses are non-enveloped, RNA viruses belonging to the Picornaviridae family,</li></ul> the genus Enterovirus.<br /><ul><li> It includes three antigenically distinct serotypes (types 1, 2, and 3).
    30. 30. There is no cross immunity between the three types of the virus. Most extensive epidemics of the disease are due to type 1.
    31. 31. The polioviruses can retain activity for several days at room temperature, and can be stored indefinitely frozen at -20°C.
    32. 32. They are rapidly inactivated by heat (>56°C), formaldehyde, chlorination, and ultraviolet light.
    33. 33. Humans are the only known reservoir for the polioviruses.</li></li></ul><li>Cont.<br />Incubation Period:<br />7-14 days<br />Mode of Infection:<br />Feco-oral mainly<br />Pathogenesis:<br />- Poliovirus gain entry through the gastrointestinal tract, multiplies in the alimentary tract (in Peyer's patches) and in lymph nodes of the intestine.<br />- Virus will invade the CNS along the peripheral nerves.<br />
    34. 34. Cont.<br />Clinical Manifestations:<br />1- Unapparent infection, which occurs in 90-95% of cases and causes no disease and no sequelae.<br />2- Abortive poliomyelitis occursin about 5% of patients (nonspecific influenza-like syndrome). The illness is short-lived (up to 2-3 days). <br />3- Nonparalytic poliomyelitis:<br />In about 1% of infected patients, the signs of abortive poliomyelitis are present but headache, nausea and vomiting are more intense. In addition there is the following:<br /><ul><li> Signs of meningeal irritation.
    35. 35. Generalized muscle pain and tenderness.
    36. 36. Tripod sign. The patient can sit only with hands thrown far behind for support.
    37. 37. Head-drop sign: If you place the hands under the patient's shoulders and raise the trunk, the head drops back to the bed instead of following the plane of the trunk as normally occurs.</li></ul>NB: Nonparalytic polio may be followed by complete recovery or may progress to paralysis. <br />Characteristics of <br /> Polio paralysis<br />Asymmetrical<br />Purely motor<br />Sensation intact<br />Affects group of muscle<br />4- Paralytic poliomyelitis: <br /> Paralysis develops in about 0.1% of persons infected <br />with poliovirus causing:-<br /><ul><li>Spinal Paralytic Poliomyelitis
    38. 38. Bulbar Poliomyelitis
    39. 39. Polioencephalitis
    40. 40. Paralytic Poliomyelitis with Ventilatory Insufficiency</li></li></ul><li>Cont.<br />Diagnosis:<br />Isolation and identification of poliovirus in the stool.<br />CSF changes in polio are nonspecific.<br />Differential Diagnosis:<br /><ul><li>Nonparalytic Polio: </li></ul>- Meningitis: T.B, pyogenic meningitis and aseptic meningitis.<br />- Meningism: pneumonia, typhoid fever. <br /><ul><li> Paralytic Polio:</li></ul>1. Infectious polyneuritis (Guillian-Barre' syndrome): <br /> a- Symmetrical L.M.N. paralysis. <br /> b- Sensory changes are present.<br /> c- Cytoalbuminous dissociation in C.S.F. <br />2. Post diphtheritic polyneuritis: bilateral symmetrical L.M.N. paralysis.<br />3. Acute transverse myelitis: sensory changes with a level together with paralysis of the bladder and rectum.<br />4. Acute traumatic sciatic neuritis<br />
    41. 41. Cont.<br />Complications:<br /><ul><li> Respiratory failure
    42. 42. Heart failure and hypertension
    43. 43. Urinary tract infection, urine retention and calculi
    44. 44. Pneumonia and deformities in the thoracic cage</li></ul>Treatment:<br />Prevention:<br /><ul><li> No specific antiviral agents for treating polio
    45. 45. Supportive management </li></ul> - During the acute stage:<br /> a- Strict bed rest with minimal handling; I.M injection should be avoided <br /> b- Neutral position of the limbs <br /> c- Analgesics and proper feeding<br /> d- Mechanical ventilation in case of severe respiratory failure<br /> e- Other supportive measures <br />
    46. 46. IV. Mumps (Epidemic Parotitis)<br />Mumpsis an acute, contagious disease that causes painful swelling of the salivary glands.<br />Etiology: <br />Mumps virus is a Paramyxovirus. Humans are the only host. <br />Mode of Transmission:<br />Droplet.<br />Incubation Period:<br />2-3 weeks.<br />Contagiousness: - Contagious one day before to 9 days after start of parotitis. <br /> - Transplacental immunity gives protection for 6 months. <br /> - The active disease gives life long immunity. <br />
    47. 47. Cont.<br />Clinical Manifestations:<br /><ul><li>Prodromal period short period (1-2 days) of fever, headache, vomiting, neck pain, and pain behind the ears on chewing or swallowing.
    48. 48. Salivary gland enlargement: usually involves the parotid gland, but the submandibular and sublingual glands may be occasionally affected.</li></ul>The parotid gland enlargement is characterized by: <br /><ul><li> Being somewhat painful and tender.
    49. 49. Obliterating the angle of the mandible.
    50. 50. The opening of Stensen duct (parotid duct) is commonly pointed and red.
    51. 51. Swelling subsides in 3-7 days.
    52. 52. Involvement may be unilateral at onset but becomes bilateral later.
    53. 53. Parotitis may be preceded or accompanied by ear pain on the ipsilateral side</li></li></ul><li>Cont.<br />Laboratory Diagnosis:<br />Non specific findings:<br /><ul><li>Leukopenia with relative lymphocytosis
    54. 54. Increased serum amylase. </li></ul>Serologic testing: <br />is usually a more convenient and available mode of diagnosis.<br /><ul><li> A significant increase in serum mumps immunoglobulin G (IgG) antibody between acute and convalescent serum specimens establish the diagnosis.
    55. 55. EIA for mumps IgM antibody is used to identify recent infection.</li></ul>Complications:<br />1- Neurological Complications: Meningoencephalitis, aseptic meningitis, encephalitis, Guillian-Barre syndrome and transient facial palsy.<br />2- Orchitis and epididymitis:<br /><ul><li> Usually occurs at the end of first week of illness.
    56. 56. Unilateral, bilateral affection occurs in 3% of cases.
    57. 57. Testes are red, swollen, painful and tender.
    58. 58. Absolute infertility due to bilateral atrophy is rare but partial impairment is common.</li></ul>3- Oophoritis:<br />Present as lower abdominal pain and tenderness. It does not affect fertility.<br /> 4- Acute pancreatitis: Should be suspected if there is high fever, nausea, vomiting and severe epigastric pain. (Serum amylase and lipase are increased).<br />
    59. 59. Cont.<br />Differential Diagnosis:<br />Acute Purulent (suppurative) parotitis, usually caused by Staphylococcus aureus, is unilateral, extremely tender, and associated with an elevated white blood cell count, and may have purulent drainage from the Stensen duct.<br />Other viral parotitis e.g.parainfluenza 1 and 3, influenza A, cytomegalovirus, Epstein-Barr virus, enteroviruses, lymphocytic choriomeningitis virus, and HIV<br />Cervical lymphadenitis. <br />Other noninfectious causes of parotid swelling include obstruction of the Stensen duct, collagen vascular diseases such as Sjögren syndrome, systemic lupus erythematosis, and tumors. <br />Prevention:<br />MMR vaccine<br />Treatment:<br />Non specific therapy, <br />only supportive management. <br />
    60. 60. Tetanus is an acute toxemic illness caused by Clostridium tetani infections at a laceration or skin break, burns, puerperal infections, umbilical stump infections (tetanus neonatorum), and surgical sites (due to contaminated sutures, dressings, or plaster). 1<br />Tetanus is an acute toxemic illness caused by Clostridium tetani infections at a laceration or skin break, burns, puerperal infections, umbilical stump infections (tetanus neonatorum), and surgical sites (due to contaminated sutures, dressings, or plaster). 1<br />Tetanus is an acute toxemic illness caused by Clostridium tetani infections at a laceration or skin break, burns, puerperal infections, umbilical stump infections (tetanus neonatorum), and surgical sites (due to contaminated sutures, dressings, or plaster). 1<br />Tetanus is an acute toxemic illness caused by Clostridium tetani infections at a laceration or skin break, burns, puerperal infections, umbilical stump infections (tetanus neonatorum), and surgical sites (due to contaminated sutures, dressings, or plaster). 1<br />V. Tetanus Neonatorum<br />Tetanus, historically called lockjaw, <br /> is an acute, spastic paralytic illness caused by the neurotoxin produced by:<br />Clostridium Tetani,<br /> a motile, gram-positive, spore-forming obligate anaerobe whose natural habitat worldwide is soil, dust, and the alimentary tracts of various animals<br />Incubation Period:<br />3-14 days<br />Route of Entry:<br />is through the umbilicus by using contaminated scissors or dressing.<br />Neonatal tetanus (tetanus neonatorum):<br /> The infantile form of generalized tetanus, typically manifests within 3–12 days of birth as progressive difficulty in feeding (sucking and swallowing), associated hunger, and crying.<br />
    61. 61. Cont.<br />Clinical Manifestations:<br /><ul><li> Tetanus may be either generalized, which is more common, or localized.
    62. 62. In generalized tetanus:</li></ul>the presenting symptom in 50 % of cases is trismus (masseter muscle spasm, or lockjaw).<br /><ul><li> The so-called sardonic smile of tetanus (risussardonicus) results from intractable spasms of facial and buccal muscles.
    63. 63. When the paralysis extends to abdominal, lumbar, hip, and thigh muscles, the patient may assume an arched posture of extreme hyperextension of the body, or opisthotonos
    64. 64. Laryngeal and respiratory muscle spasm can lead to airway obstruction and asphyxiation.
    65. 65. Fever, occasionally as high as 40°C, is common because of the substantial metabolic energy consumed by spastic muscles</li></li></ul><li>Cont.<br />Treatment:<br />The goals of therapy are: <br /><ul><li>EradicateC. Tetani
    66. 66. Neutralize its toxin
    67. 67. Provide supportive care</li></ul>- General treatment:<br /><ul><li> Patients should be managed in an intensive care setting in a quiet darkened room, utilizing suction , oxygen, cardiac and respiratory monitors, a ventilator, and tracheostomy equipment.
    68. 68. Sedation and muscle relaxation should be instituted, usually with diazepam ( 0.1 to 0.2 mg/kg IV ,q 4 to 6 h).
    69. 69. Maintenance of adequate nutrition, hydration, skin care, and excretory functions is of outmost importance. Patients must be immunized with tetanus toxoid to prevent further disease. </li></li></ul><li>Cont.<br />- Specific treatment: <br /><ul><li> Tetanus immune globulin of human origin (TIG), 3000-6000 units IM.
    70. 70. If TIG is not available, antitetanic serum (antitoxin) 100,000 units.
    71. 71. Penicillin (100,000 U/kg/day divided every 4–6 hr IV for 10–14 days), the antibiotic of choice.
    72. 72. Erythromycin and tetracycline (for persons >8 yr of age) are alternatives for penicillin-allergic patients. </li></ul>Prevention:<br />Tetanus is an entirely preventable disease<br /><ul><li>Active immunization should begin in early infancy with combined diphtheria toxoid-tetanus toxoid-acellularpertussis (DTaP) vaccine at 2, 4, and 6 mo of age, with a booster at 4–6 yr of age and at 10 yr intervals thereafter throughout adult life (Td or TdaP)
    73. 73. Immunization of women with tetanus toxoid prevents neonatal tetanus.</li></li></ul><li>Cont.<br />
    74. 74. VI. Pertussis(Whooping cough)<br />Pertussis is an acute respiratory tract infection. The term pertussis(intense cough) is preferable to whooping cough because most infected individuals do not develop whoop<br />Etiology:<br />Bordetellapertussis, is a highly communicable, vaccine-preventable disease, a gram-negative coccobacillus, lasting for many weeks and typically afflicts children with severe coughing, whooping, and posttussive vomiting. <br />Droplet infection<br />Mode of Transmission:<br />Incubation period:<br />3-12 days<br />is from one week before to three weeks after <br />the onset of symptoms. <br />The period of infectivity:<br />
    75. 75. Cont.<br />Clinical manifestations:<br /> Any age can be affected but mostly in the first few years of life. Lack of transplacental immunity makes the newborn susceptible<br />Manifestations are divided into 3 stages:<br />A- Catarrhal stage (1-2 weeks):<br />B- Paroxysmal stage (2-6 weeks):<br /><ul><li> Repetitive series of severe cough during a single expiration followed by a sudden deep inspiratory whoop (forceful inspiratory gasp).
    76. 76. During the attack chin and chest are held forward, tongue protrudes maximally, eyes bulge, and face becomes purple or cyanosed.
    77. 77. Vomiting commonly follows the paroxysm, may lead to PEM and alkalosis which decreases ionized calcium with manifestations of tetany (normocalcemic).
    78. 78. Between attacks the child does not appear ill and chest signs are minimal.
    79. 79. The typical paroxysms and whoop are usually absent in infants and are replaced by attacks of apnea and cyanosis. The infant many die during an attack.</li></ul>C- Convalescent stage (1-2 weeks):<br />
    80. 80. Cont.<br />Diagnosis:<br /><ul><li>Pertussis should be suspected in any individual who has pure complaint of cough, especially if the followings are absent; fever, malaise or myalgia, exanthem or enanthem, sore throat, hoarseness, tachypnea, wheeze and rales.
    81. 81. Paroxysms of cough > 14 days with post-tussive vomiting or whoop.
    82. 82. Apnea or cyanosis is a clue in infants < 3 months of age.
    83. 83. B. pertussis is an occasional cause of sudden infant death.
    84. 84. History of contact may be positive.
    85. 85. WBC count reveals leukocytosis (>20,000/mm3) with predominating lymphocytosis.
    86. 86. Isolation of the organism is only possible during the early phase of the disease by culture of nasopharyngeal swab </li></ul>Differential Diagnosis:<br />(1) Bordetellaparapertussis<br />(2) Mediastinallymphadenopathy, compressing trachea<br />(3) Foreign body in the larynx or trachea <br />(4) Bronchiolitis, bronchitis, bronchial asthma and conditions causing postnasal discharge<br />
    87. 87. Cont.<br />Complications:<br />1- Respiratory:<br /> - Commonest one is pneumonia. <br />- Otitis media and sinusitis. <br /> - Atelectasis (due to mucus plug), bronchiectasis.<br /> - Forceful paroxysm  emphysema, ruptured alveoli pneumothorax, pneumomediastinum<br />and rupture of the diaphragm. <br /> - Dissemination of previously existing primary tuberculosis. <br />2- Gastro-Intestinal:<br /> - Severe and prolonged vomiting may lead to malnutrition, dehydration, alkalosis and tetany. <br /> - Hernias and rectal prolapse. <br />3- Nervous:<br /> - Convulsions due to cerebral anoxia during paroxysms (common in infants). <br /> - Tetany and intracranial hemorrhages. <br />4- Hemorrhagic:<br /> - Hemorrhage is usually mechanical in origin <br /> (epistaxis, subconjunctival, hemoptysis, intraventricular and subarachnoid). <br />
    88. 88. Cont.<br />Prevention:<br />- Active immunization (DTaP) at 2, 4, 6, 18 mo plus booster dose at school entrance.<br /><ul><li> All contacts should be given Erythromycin 40 mg/kg /day divided 6 hourly for </li></ul> 10-14 days + Booster DTaP if the age of the contact is less than 6 years. <br />- Isolation of patients and household contacts for 5 days after starting erythromycin.<br />Treatment:<br /><ul><li> Symptomatic treatment: </li></ul>- General supportive measures, bed rest, soft diet and warm fluids. <br />- Anti-tussives for spasmodic cough. <br /><ul><li> Specific treatment: Erythromycin 40 mg/kg for 14 days.</li></li></ul><li>
    89. 89. Dr.SHERIF REDA<br />