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Pertussis

Pertussis. Dr. Rezai MS Pediatrics infectious disease sub specialist. ETIOLOY. Bordetella pertussis Bordetella parapertussis is an occasional cause Exclusive pathogens of humans and some primates. B. bronchiseptica is a common animal pathogen. Protracted coughing. Mycoplasma

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Pertussis

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  1. Pertussis Dr. Rezai MS Pediatrics infectious disease sub specialist

  2. ETIOLOY • Bordetella pertussis • Bordetella parapertussis is an occasional cause • Exclusive pathogens of humans and some primates. • B. bronchiseptica is a common animal pathogen.

  3. Protracted coughing • Mycoplasma • Parainfluenza or influenza viruses • Enteroviruses • Respiratory syncytial virus • Adenoviruses.

  4. EPIDEMIOLOY • 60 million cases of pertussis each year • >500,000 deaths. • Widespread use of pertussis vaccine led to a >99% decline in cases. • Pertussis is increasingly endemic.

  5. EPIDEMIOLOY • Approximately 60% of cases are in adolescents and adults. • Infants have the highest morbidity • Pertussis is extremely contagious attack rates as high as 100%

  6. EPIDEMIOLOY • Chronic carriage by humans is not documented. • After intense exposure as in households, the rate of subclinical infection is as high as 80% in fully immunized or previously infected individuals.

  7. EPIDEMIOLOY • Neither natural disease nor vaccination provides complete or lifelong immunity against reinfection or disease. • Protection against typical disease wane 3-5 yr after vaccination unmeasurable after 12 yr

  8. PATHOGENES • B.ordetella organisms are tiny, fastidious, gramnegative coccobacilli that only colonize ciliated epithelium. • Only B. pertussis expresses pertussis toxin (PT), the major virulence protein. • (PT), histamine sensitivity, insulin secretion, leukocyte dysfunction

  9. PATHOGENES • PT causes lymphocytosis immediately • Tracheal cytotoxin, adenylate cyclase, and PT appear to inhibit clearance of organisms. • Tracheal cytotoxin, dermonecrotic factor, and adenylate cyclase are postulated to be predominantly responsible for the local epithelial damage that produces respiratory symptoms and facilitates absorption of PT.

  10. CLINICAL MANIFESTATION 3stages • Catarrhal • paroxysmal • convalescent

  11. CLINICAL MANIFESTATION • incubation period ranging from 3-12 days • catarrhal stage (1-2 wk) begins insidiously congestion and rhinorrhea, lacrimation low-grade fever sneezing conjunctival suffusion

  12. CLINICAL MANIFESTATION • paroxysmal stage (2-6 wk). • The cough begins as a dry, intermittent, irritative hack and evolves into the inexorable paroxysms that are the hallmark of pertussis. • anxious aura, whoop follows after caugh • Post-tussive emesis is common

  13. CLINICAL MANIFESTATION • At the peak of the paroxysmal stage, patients may have more than 1 episode hourly.

  14. CLINICAL MANIFESTATION • Convalescent stage (≥2 wk) • The number, severity, and duration of episodes diminish.

  15. CLINICAL MANIFESTATION • Infants <3 mo of age • Do not display classical stages. • Cough (expiratory grunt) may not be prominent. • Whoop infrequently occurs in infants <3 mo • Cyanosis can follow a coughing paroxysm • Apnea may be the only symptom. • Apnea can occur without a cough

  16. CLINICAL MANIFESTATION • Paradoxically, in infants, cough and whooping may become louder and more classic in convalescence. • Convalescence includes intermittent paroxysmal coughing throughout the 1st year of life, including "exacerbations" with subsequent respiratory illnesses; these are not due to recurrent infection or reactivation of B.pertussis.

  17. CLINICAL MANIFESTATION • Immunized children have foreshortening of all stages of pertussis. • Signs of lower respiratory tract disease are not expected unless complicating secondary bacterial pneumonia is present. • Conjunctival hemorrhages and petechiae on the upper body are common.

  18. DIAGNOSIS • Clinical suspect • Leukocytosis (15,000-100,000 cells/mm3) due to absolute lymphocytosis is characteristic in the catarrhal stage. • Lymphocytes are of T- and B-cell origin and are normal small cells, rather than the large atypical lymphocytes seen with viral infections.

  19. DIAGNOSIS • Eosinophilia is not a manifestation of pertussis. • A severe course and death are correlated with extreme leukocytosis (median peak white blood cell count fatal vs nonfatal cases, 94 vs 18 x 109 cells/L) and thrombocytosis (median peak platelet count fatal vs nonfatal cases, 782 vs 556 x 109/L)

  20. DIAGNOSIS • Mild hyperinsulinemia and reduced glycemic response to epinephrine • Hypoglycemia is reported only occasionally. • Parenchymal consolidation suggests secondary bacterial infection. • Pneumothorax, pneumomediastinum, and air in soft tissues can be seen occasionally.

  21. DIAGNOSIS • Isolation of B. pertussis in culture remains the gold standard for diagnosis. • deep nasopharyngeal aspiration or by use of a flexible swab, preferably a dacron or calcium alginate swab, held in the posterior nasopharynx for 15-30 sec (or until coughing).

  22. A 1.0% casamino acid liquid is acceptable for holding a specimen up to 2 hr; Stainer-Scholte broth or Regan-Lowe semisolid transport medium is used for longer periods, up to 4 days.

  23. Direct testing of nasopharyngeal secretions by DFA is a rapid test • PCR to test nasopharyngeal wash specimens • Less than 10% of any of these test results are positive in partially or remotely immunized individuals tested in the paroxysmal stage.

  24. DIAGNOSIS • Serologic tests in acute and convalescent samples are the most sensitive tests in immunized individuals and are useful epidemiologically. • (lgG) antibody to pertussis toxin elevated >2 standard deviations above the mean of the immunized population indicates recent infection.

  25. DIAGNOSIS • IgA and IgM pertussis antibody tests are not reliable methods for diagnosis.

  26. DIAGNOSIS • Adenoviral infections are usually distinguishable by associated features, such as fever, sore throat, and conjunctivitis. • Mycoplasma and B. pertussis in young adults can be difficult to distinguish on clinical grounds.

  27. DIAGNOSIS • Chlamydia trachomatis • B. pertussis is not associated with staccato cough (breath with every cough), purulent conjunctivitis, tachypnea, rales or wheezes

  28. TREATMEN • Goals of therapy are to limit the number of paroxysms,to observe the severity of the cough, to provide assistance when necessary • Infants <3 mo of age are admitted to hospital almost without exception • 3-6 mo unless witnessed paroxysms are not severe, and those of any age if significant complications occur.

  29. Typical paroxysms that are not life threatening • Duration <45 sec • Red but not blue color change • Tachycardia, bradycardia (not <60 beats/min in infants) • Oxygen desaturation that spontaneously resolves at the end of the paroxysm • Whooping or strength for self-rescue at the end of paroxysm • self-expectorated mucus plug • post-tussive exhaustion but not unresponsiveness.

  30. TREATMEN • Mist by tent can be useful in some infants with thick, tenacious secretions and excessively irritable airways. • Large volume feedings are avoided. • Portable oxygen, monitoring, or suction apparatus should not be needed at home.

  31. Hospital discharge • If over a 48-hr period disease severity is unchanged or diminished • No intervention is required during paroxysms, • Nutrition is adequate, no complication has occurred • Parents are adequately prepared for care at home.

  32. Antibiotics • given when pertussis is suspected or confirmed primarily to limit the spread of infection and secondarily for possible clinical benefit. • A 7- to 10-fold relative risk for infantile hypertrophic pyloric stenosis (IHPS) has been reported in neonates treated with orally administered erythromycin. • Azithromycin is the preferred agent for use in neonates.

  33. Antibiotics

  34. Antibiotics

  35. Adjunct Therapies • Corticosteroids clinical use is not warranted. • Beneficial effect of beta2-adrenergic is not documented

  36. Isolation • Respiratory isolation with use of masks by all health care personnel entering the room. • Children and staff with pertussis in child-care facilities or schools should be excluded until macrolide prophylaxis has been taken for 5 days.

  37. Care of Household and Other Close Contacts. • A macrolide agent should be given promptly to all household contacts and other close contacts, such as those in daycare, regardless of age, history of immunization, or symptoms • Children <7 yr of age who received a 3rd dose >6 mo before exposure or a 4th dose ≥3 yr before exposure should receive a booster dose.

  38. Care of Household and Other Close Contacts • Individuals ≥9 yr should be given a booster if they have not previously received Tdap and >2 yr have passed since receipt of a diphtheria containing vaccine • Coughing health care workers, with or without known exposure to pertussis, should be promptly evaluated for pertussis

  39. COMPLICATION • Infants <6 mo of age have excessive mortality and morbidity • Infants <4 mo of age account for 90% of cases of fatal pertussis. • Preterm birth and young maternal age are significantly associated with fatal pertussis.

  40. COMPLICATION • Progressive pulmonary hypertension or hemorrhage (especially in very young infants) and secondary bacterial pneumonia are usual causes of death. mortality rate of >80%. • otitis media • pneumonia(S. aureus, S. pneumoniae) • Seizure

  41. COMPLICATION • Seizures are usually a result of hypoxemia, but hyponatremia from excessive secretion of antidiuretic hormone during pneumonia can occur. • infants with apnea raises the possibility of a primary effect of PT on the CNS.

  42. COMPLICATION • Conjunctival and scleral hemorrhages petechiae on the upper body, epistaxis • Hemorrhage in the central nervous system (CNS) and retina • Pneumothorax and subcutaneous emphysema, and umbilical • Inguinal hernias.

  43. COMPLICATION • Children ≤2 yr may have abnormal pulmonary function into adulthood. • Laceration of the lingual frenulum is not uncommon.

  44. PREVENTION • 2, 4, and 6 mo of age. • Booster:15-18 mo, 4-6 yr • A 5th dose is not necessary if the 4th dose in the series is administered on or after the 4th birthday. • The preferred age for Tdap vaccination is 11-12 yr

  45. Tetanus

  46. Tetanus(Clostridium tetani) lockjaw • C. tetani is not a tissue-invasive organism and instead causes illness through the effects of a single toxin, tetanospasmin • The human lethal dose of tetanus toxin is estimated to be 10-5 mg/kg.

  47. EPIDEMIOLOG • Tetanus occurs worldwide and is endemic in approximately 90 developing countries. • The most common form, neonatal (or umbilical) tetanus, kills approximately 500,000 infants each year, with about 80% of deaths in just 12 tropical Asian and African countries. • It occurs because the mother was not immunized.

  48. maternal tetanus that results from postpartum, postabortal, or postsurgical wound infection with C.tetani. • Most non-neonatal cases of tetanus are associated with a traumatic injury, often a penetrating wound inflicted by a dirty object such as a nail, splinter, fragment of glass, or unsterile injection. • Tetanus occurring after illicit drug injection is becoming more common. (quinine)

  49. PATHOGENESIS • Toxin is released after vegetative bacterial cell death and lysis. • Tetanus toxin binds at the neuromuscular junction and enters the motor nerve by endocytosis, after which it undergoes retrograde axonal transport to the cytoplasm of the a motoneuron.

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