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Infectious Diseases Prepared  by DR.SHERIF REDA Prof. of Pediatrics AL- AZHAR UNIVERSITY CAIRO  -  EGYPT
Introduction
I.        Meningitis II.       Encephalitis III.      Poliomyelitis IV.      Mumps V.       Tetanus Neonatorum VI.      Pertussis
I.      Meningitis The meninges are membranes that cover and protect the brain and spinal cord. There are 3 layers known as the: Dura mater is the tough outer membrane Arachnoid mater is the thin, delicate, web-like membrane Pia mater is the innermost membrane The arachnoid & pia mater are together known the as leptomeninges       Inflammation of the leptomeninges, caused by Bacteria Viruses                           Or rarely,   Fungi The term ASEPTIC MENINGITIS refers principally to viral meningitis, but a similar picture may be seen with: Other infectious organisms (Lyme disease, syphilis, tuberculosis)  Parameningeal infections (brain abscess, epidural abscess, venous sinus empyema)  Chemical exposure (nonsteroidal anti-inflammatory drug, IV immunoglobulin)  Autoimmune disorders 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.
Cont. Bacterial Causes of Meningitis NB:   Viral meningitis is caused principally by entero-viruses, including coxsackieviruses, echoviruses, and, in unvaccinated individuals, polioviruses Mumps virus is a common cause of viral meningitis in unvaccinated children
Cont. Mode of infection: Bacterial meningitis is most commonly results from hematogenous dissemination of microorganisms from a distant site of infection Clinical Manifestations: The onset of acute bacterial meningitis has two predominant patterns:  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.  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.
Cont. 1)  Non specific findings: Fever, anorexia, poor feeding, myalgia, arthralgia, tachycardia, hypotension and various cutaneous signs such as petechiae, purpura or an erythematous macular rush.  2)  Signs of meningeal irritation: ,[object Object]
Kernig’s sign: flexion of the hip 90 degrees with subsequent pain with extension of the leg.
Brudzinski sign: involuntary flexion of the knees and hips after passive flexion of the neck while supine.3)  Symptoms and Signs of increased ICP:  1- Headache and vomiting 		 2- Bulging fontanel or widening of the sutures 3- Cranial neuropathies.		 4- Hypertension with bradycardia 5- Apnea or hyperventilation, stupor and coma. 4)  Seizures:  (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
Cont. Diagnosis: Lumbar puncture for CSF analysis should be performed when bacterial meningitis is suspected: 1- Microorganisms on gram stain and culture. 	 2- Neutrophilpleocytosis (300 - 2000/mm3).  3- Elevated protein (100 - 500mg/dL)			 4- Reduced glucose concentration (< 50% of serum glucose) 5- Physical manifestations (Turbid with elevated pressure,100 - 300 mm H2O). Normal CSF shows: Normal pressure (50 - 80 mm H2O), leucocytes (< 5/mm3), proteins (20 -45 mg/dl) and glucose (75 % of serum glucose)
Cont. Treatment:      A)Initial Antibiotic Therapy: ,[object Object],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.  Duration of antibiotic therapy:  At least for 7-14 days I.V.      B)  Corticosteroids:   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.    C)  Supportive and symptomatic therapy:     - Good evaluation and monitoring are essential.     -Correction of dehydration and electrolyte disturbances and proper nutrition.     -Control of seizures   - Management of neurological complications
Cont. Prevention:  Vaccination and antibiotic prophylaxis of susceptible at – risk contacts: Close contact: 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). Meningococcal quadrivalent Vaccine:  Avaccine is recommended for high-risk children older than 2yr.  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).
II.    Encephalitis ,[object Object]
  Organisms cause encephalitis by one of two mechanisms: direct infection of the brain parenchyma   an apparent immune-mediated response in the CNS that usually begins several days after the appearance of extraneural manifestations of the infection ,[object Object],Etiology: ,[object Object]
  The most common viral causes of encephalitis are the arboviruses (St. Louis, LaCrosse, California, West Nile encephalitis viruses), enteroviruses, and herpesviruses.
  Encephalitis also may result from other types of infection, metabolic, toxic, and neoplastic disorders. ,[object Object]
  The characteristic symptoms of progressive lethargy, behavioral changes, and neurologic deficits, followed.
Seizures are common at presentation.
  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.
  Acute DisseminatedEncephaloMyelitis (ADEM):    - Is the abrupt development of multiple neurologic signs related to an inflammatory, demyelinating disorder of the brain and spinal cord.      - Acute disseminated encephalomyelitis follows childhood viral infections, such as measles and chickenpox or vaccinations.
Cont. Laboratory And Imaging Studies: ,[object Object]
 The CSF occasionally may be normal.
Neuroimaging studies (CT, MRI) may be normal or may show diffuse cerebral swelling of the parenchyma or focal abnormalities.
 The EEG is the definitive test and shows diffuse, slow wave activity, although focal changes may be present.
Brain biopsy may be appropriate for patients with severe encephalopathy who show no clinical improvement if the diagnosis remains obscure.,[object Object]
 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.
 IV acyclovir is the treatment of choice for HSV infections.
 ADEM has been treated with high-dose IV corticosteroids.,[object Object]
 There is no cross immunity between the three types of the virus. Most extensive epidemics of the disease are due to type 1.
 The polioviruses can retain activity for several days at room temperature, and can be stored indefinitely frozen at -20°C.
 They are rapidly inactivated by heat (>56°C), formaldehyde, chlorination, and ultraviolet light.
  Humans are the only known reservoir for the polioviruses.,[object Object]
Cont. Clinical Manifestations: 1-  Unapparent infection, which occurs in 90-95% of cases and causes no disease and no sequelae. 2-  Abortive poliomyelitis occursin about 5% of patients (nonspecific influenza-like syndrome). The illness is short-lived (up to 2-3 days).  3-  Nonparalytic poliomyelitis: 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: ,[object Object]
 Generalized muscle pain and tenderness.
Tripod sign. The patient can sit only with hands thrown far behind for support.

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Infectious diseases

  • 1.
  • 2. Infectious Diseases Prepared by DR.SHERIF REDA Prof. of Pediatrics AL- AZHAR UNIVERSITY CAIRO - EGYPT
  • 4. I. Meningitis II. Encephalitis III. Poliomyelitis IV. Mumps V. Tetanus Neonatorum VI. Pertussis
  • 5. I. Meningitis The meninges are membranes that cover and protect the brain and spinal cord. There are 3 layers known as the: Dura mater is the tough outer membrane Arachnoid mater is the thin, delicate, web-like membrane Pia mater is the innermost membrane The arachnoid & pia mater are together known the as leptomeninges Inflammation of the leptomeninges, caused by Bacteria Viruses Or rarely, Fungi The term ASEPTIC MENINGITIS refers principally to viral meningitis, but a similar picture may be seen with: Other infectious organisms (Lyme disease, syphilis, tuberculosis) Parameningeal infections (brain abscess, epidural abscess, venous sinus empyema) Chemical exposure (nonsteroidal anti-inflammatory drug, IV immunoglobulin) Autoimmune disorders 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.
  • 6. Cont. Bacterial Causes of Meningitis NB: Viral meningitis is caused principally by entero-viruses, including coxsackieviruses, echoviruses, and, in unvaccinated individuals, polioviruses Mumps virus is a common cause of viral meningitis in unvaccinated children
  • 7. Cont. Mode of infection: Bacterial meningitis is most commonly results from hematogenous dissemination of microorganisms from a distant site of infection Clinical Manifestations: The onset of acute bacterial meningitis has two predominant patterns: 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. 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.
  • 8.
  • 9. Kernig’s sign: flexion of the hip 90 degrees with subsequent pain with extension of the leg.
  • 10. Brudzinski sign: involuntary flexion of the knees and hips after passive flexion of the neck while supine.3) Symptoms and Signs of increased ICP: 1- Headache and vomiting 2- Bulging fontanel or widening of the sutures 3- Cranial neuropathies. 4- Hypertension with bradycardia 5- Apnea or hyperventilation, stupor and coma. 4) Seizures: (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
  • 11. Cont. Diagnosis: Lumbar puncture for CSF analysis should be performed when bacterial meningitis is suspected: 1- Microorganisms on gram stain and culture. 2- Neutrophilpleocytosis (300 - 2000/mm3). 3- Elevated protein (100 - 500mg/dL) 4- Reduced glucose concentration (< 50% of serum glucose) 5- Physical manifestations (Turbid with elevated pressure,100 - 300 mm H2O). Normal CSF shows: Normal pressure (50 - 80 mm H2O), leucocytes (< 5/mm3), proteins (20 -45 mg/dl) and glucose (75 % of serum glucose)
  • 12.
  • 13. Cont. Prevention: Vaccination and antibiotic prophylaxis of susceptible at – risk contacts: Close contact: 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). Meningococcal quadrivalent Vaccine: Avaccine is recommended for high-risk children older than 2yr. 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).
  • 14.
  • 15.
  • 16. The most common viral causes of encephalitis are the arboviruses (St. Louis, LaCrosse, California, West Nile encephalitis viruses), enteroviruses, and herpesviruses.
  • 17.
  • 18. The characteristic symptoms of progressive lethargy, behavioral changes, and neurologic deficits, followed.
  • 19. Seizures are common at presentation.
  • 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. Acute DisseminatedEncephaloMyelitis (ADEM): - Is the abrupt development of multiple neurologic signs related to an inflammatory, demyelinating disorder of the brain and spinal cord. - Acute disseminated encephalomyelitis follows childhood viral infections, such as measles and chickenpox or vaccinations.
  • 22.
  • 23. The CSF occasionally may be normal.
  • 24. Neuroimaging studies (CT, MRI) may be normal or may show diffuse cerebral swelling of the parenchyma or focal abnormalities.
  • 25. The EEG is the definitive test and shows diffuse, slow wave activity, although focal changes may be present.
  • 26.
  • 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. IV acyclovir is the treatment of choice for HSV infections.
  • 29.
  • 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. The polioviruses can retain activity for several days at room temperature, and can be stored indefinitely frozen at -20°C.
  • 32. They are rapidly inactivated by heat (>56°C), formaldehyde, chlorination, and ultraviolet light.
  • 33.
  • 34.
  • 35. Generalized muscle pain and tenderness.
  • 36. Tripod sign. The patient can sit only with hands thrown far behind for support.
  • 37.
  • 40.
  • 41.
  • 42. Heart failure and hypertension
  • 43. Urinary tract infection, urine retention and calculi
  • 44.
  • 45. Supportive management - During the acute stage: a- Strict bed rest with minimal handling; I.M injection should be avoided b- Neutral position of the limbs c- Analgesics and proper feeding d- Mechanical ventilation in case of severe respiratory failure e- Other supportive measures
  • 46. IV. Mumps (Epidemic Parotitis) Mumpsis an acute, contagious disease that causes painful swelling of the salivary glands. Etiology: Mumps virus is a Paramyxovirus. Humans are the only host. Mode of Transmission: Droplet. Incubation Period: 2-3 weeks. Contagiousness: - Contagious one day before to 9 days after start of parotitis. - Transplacental immunity gives protection for 6 months. - The active disease gives life long immunity.
  • 47.
  • 48.
  • 49. Obliterating the angle of the mandible.
  • 50. The opening of Stensen duct (parotid duct) is commonly pointed and red.
  • 51. Swelling subsides in 3-7 days.
  • 52. Involvement may be unilateral at onset but becomes bilateral later.
  • 53.
  • 54.
  • 55.
  • 56. Unilateral, bilateral affection occurs in 3% of cases.
  • 57. Testes are red, swollen, painful and tender.
  • 58. Absolute infertility due to bilateral atrophy is rare but partial impairment is common.3- Oophoritis: Present as lower abdominal pain and tenderness. It does not affect fertility. 4- Acute pancreatitis: Should be suspected if there is high fever, nausea, vomiting and severe epigastric pain. (Serum amylase and lipase are increased).
  • 59. Cont. Differential Diagnosis: 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. Other viral parotitis e.g.parainfluenza 1 and 3, influenza A, cytomegalovirus, Epstein-Barr virus, enteroviruses, lymphocytic choriomeningitis virus, and HIV Cervical lymphadenitis. Other noninfectious causes of parotid swelling include obstruction of the Stensen duct, collagen vascular diseases such as Sjögren syndrome, systemic lupus erythematosis, and tumors. Prevention: MMR vaccine Treatment: Non specific therapy, only supportive management.
  • 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 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 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 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 V. Tetanus Neonatorum Tetanus, historically called lockjaw, is an acute, spastic paralytic illness caused by the neurotoxin produced by: Clostridium Tetani, a motile, gram-positive, spore-forming obligate anaerobe whose natural habitat worldwide is soil, dust, and the alimentary tracts of various animals Incubation Period: 3-14 days Route of Entry: is through the umbilicus by using contaminated scissors or dressing. Neonatal tetanus (tetanus neonatorum): 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.
  • 61.
  • 62.
  • 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. Laryngeal and respiratory muscle spasm can lead to airway obstruction and asphyxiation.
  • 65.
  • 67.
  • 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.
  • 70. If TIG is not available, antitetanic serum (antitoxin) 100,000 units.
  • 71. Penicillin (100,000 U/kg/day divided every 4–6 hr IV for 10–14 days), the antibiotic of choice.
  • 72.
  • 73.
  • 74. VI. Pertussis(Whooping cough) 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 Etiology: 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. Droplet infection Mode of Transmission: Incubation period: 3-12 days is from one week before to three weeks after the onset of symptoms. The period of infectivity:
  • 75.
  • 76. During the attack chin and chest are held forward, tongue protrudes maximally, eyes bulge, and face becomes purple or cyanosed.
  • 77. Vomiting commonly follows the paroxysm, may lead to PEM and alkalosis which decreases ionized calcium with manifestations of tetany (normocalcemic).
  • 78. Between attacks the child does not appear ill and chest signs are minimal.
  • 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.C- Convalescent stage (1-2 weeks):
  • 80.
  • 81. Paroxysms of cough > 14 days with post-tussive vomiting or whoop.
  • 82. Apnea or cyanosis is a clue in infants < 3 months of age.
  • 83. B. pertussis is an occasional cause of sudden infant death.
  • 84. History of contact may be positive.
  • 85. WBC count reveals leukocytosis (>20,000/mm3) with predominating lymphocytosis.
  • 86. Isolation of the organism is only possible during the early phase of the disease by culture of nasopharyngeal swab Differential Diagnosis: (1) Bordetellaparapertussis (2) Mediastinallymphadenopathy, compressing trachea (3) Foreign body in the larynx or trachea (4) Bronchiolitis, bronchitis, bronchial asthma and conditions causing postnasal discharge
  • 87. Cont. Complications: 1- Respiratory: - Commonest one is pneumonia. - Otitis media and sinusitis. - Atelectasis (due to mucus plug), bronchiectasis. - Forceful paroxysm  emphysema, ruptured alveoli pneumothorax, pneumomediastinum and rupture of the diaphragm. - Dissemination of previously existing primary tuberculosis. 2- Gastro-Intestinal: - Severe and prolonged vomiting may lead to malnutrition, dehydration, alkalosis and tetany. - Hernias and rectal prolapse. 3- Nervous: - Convulsions due to cerebral anoxia during paroxysms (common in infants). - Tetany and intracranial hemorrhages. 4- Hemorrhagic: - Hemorrhage is usually mechanical in origin (epistaxis, subconjunctival, hemoptysis, intraventricular and subarachnoid).
  • 88.

Editor's Notes

  1. Recovery is complete, and no neurologic signs or sequelae develop. stiffness of the neck and back with positive Kernig&apos;s and Brudzinski&apos;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.
  2. T