Pediatrics Pertussis and Pertussis syndrome Zhi-min Chen Dept. Pediatric Pulmonology, Children’s Hospital Zhejiang University School of Medicine.

Presentation on theme: "Pediatrics Pertussis and Pertussis syndrome Zhi-min Chen Dept. Pediatric Pulmonology, Children’s Hospital Zhejiang University School of Medicine."— Presentation transcript:

1 Pediatrics Pertussis and Pertussis syndrome Zhi-min Chen Dept. Pediatric Pulmonology, Children’s Hospital Zhejiang University School of Medicine

2 Definition  Pertussis (whooping cough)  caused by Bordetella pertussis,  The pertussis syndrome  includes disease caused by Bordetella pertussis and certain other infectious agents

3 Etiology  Bordetella pertussis  Gram-negative  Other infectious agents  Bordetella parapertussis  Adenovirus  Dual infection (of above)  Other common pathogens of protracted cough: mycoplasma, chlamydia, RSV, parainfluenza virus

4 Epidemiology  Infect only humans and transmitted person to person by coughing  Most contagious during the earliest stage  The peak incidence <4 m  The annual rate--100 to 200/100,000, higher in developing countries

5 Clinical manifestation  The mean incubation period is 6 days.  The progression of pertussis  Catarrhal stage  Paroxysmal stage  Convalescent stage

6 Clinical manifestation  Catarrhal stage  nonspecific signs Injection increased nasal secretions low-grade fever  last 1 to 2 weeks

7 Clinical manifestation  The paroxysmal stage  approximately 2 to 4 weeks.  as catarrhal symptoms wane, coughing begins first as a dry, intermittent, irritative hack;  then evolve into coughing in paroxysms during expiration, causing young children to lose their breath (machine-gun burst of uninterrupted coughs).

8 Clinical manifestation  The paroxysmal stage  After the most insignificant startle from a draught, light, sound, sucking or stretching, a well- appearing young infant begins to choke, gasp, and flail extremities, eyes watering and bulging, face reddened or purple, tongue protruding maximally until at the seeming last moment of consciousness.  Characteristic whoop follows this paroxysm of cough (the forceful inhalation against a narrowed glottis).  Others: post-tussive emesis, conjunctival hemorrages and petechiae on the upper body

9 Clinical manifestation  The Convalescent stage  gradual resolution of symptoms over 1 to 2 weeks.  residual cough may persist for months, especially with physical stress or respiratory irritants

10 Clinical manifestation  Young infants may not display the classic pertussis syndrome:  the first signs may be episodes of apnea  unlikely to have the classic whoop  more likely to have CNS damage as a result of hypoxia  more likely to have secondary bacterial pneumonia.

11 LABORATORY STUDIES  The diagnosis depends on isolation of B. pertussis  Culture of nasopharyngeal swabs  Direct fluorescent antibody staining  Serologic tests are not useful for diagnosis of acute infection.  Leucocytosis (20,000~ 50,000/mm 3 ) with lymphocytosis is characteristic beyond the neonatal age

12 IMAGING STUDIES  NOT specific  Segmental lung atelectasis  not unusual during pertussis, especially during the paroxysmal stage.  Perihilar infiltrates  common and similar to what is seen in viral pneumonia.

13 Diagnosis and differential diagnosis  the diagnosis based on recognition of the pattern of illness is quite accurate  Respiratory viruses such as RSV, parainfluenza virus, and C. pneumoniae among infants and M. pneumoniae in older children may produce a bronchitic illness that is not distinguished easily from pertussis.

14 Complications  Major complications:hypoxia, apnea, pneumonia, seizures, encephalopathy, and malnutrition.  The most frequent complication is pneumonia caused by B. pertussis itself or resulting from secondary bacterial infection from S. pneumoniae, Hib, and S. aureus.

15 Complications  Other complications  atelectasis, pneumomediastinum, pneumothorax, or interstitial or subcutaneous emphysema; epistaxis; hernias; and retinal and subconjunctival hemorrhages, otitis media and sinusitis.

16 Goal of therapy  Limit the number of paroxysms  Observe the severity of cough to provide assistance when necessary  Maximize nutrition, rest, and recovery without sequelae

17 Treatment  Erythromycin  given early, eradicates nasopharyngeal carriage of organisms within 3 to 4 days and ameliorates the effects of the infection.  not effective in the paroxysmal stage.  Azithromycin and clarithromycin  TMP-SMZ  Pertussis-specific immunoglobulin ( effective)

18 PREVENTION  Active immunization  acellular pertussis vaccine, given in combination with the toxoids of tetanus and diphtheria (DTaP with an efficacy of 70% to 90%;  Compared with older, whole cell pertussis vaccines, acellular vaccines have fewer adverse effects and local reactions.

19 PREVENTION  Erythromycin and other macrolides  effective in preventing disease in contacts exposed to pertussis.

20 PREVENTION  Close contact <7y  should be given a macrolide antibiotic.  should receive a booster dose of DTaP, unless a booster dose has been given within the preceding 3 years.  Close contact > 7y  prophylactic macrolide antibiotic for 10 to 14 days  NOT the vaccine.

21 Thank you for your attention