DR (MRS) M.B. FETUGA1 PERTUSSIS (WHOOPING COUGH).

22
DR (MRS) M.B. FETUGA 1 PERTUSSIS (WHOOPING COUGH)

Transcript of DR (MRS) M.B. FETUGA1 PERTUSSIS (WHOOPING COUGH).

Page 1: DR (MRS) M.B. FETUGA1 PERTUSSIS (WHOOPING COUGH).

DR (MRS) M.B. FETUGA 1

PERTUSSIS

(WHOOPING COUGH)

Page 2: DR (MRS) M.B. FETUGA1 PERTUSSIS (WHOOPING COUGH).

DR (MRS) M.B. FETUGA 2

Introduction

• Occurs worldwide (pertussis –intensive cough)• Pertussis is one of the major causes of childhood

mortality in the developing world.• It is an acute infectious disease caused by the

bacterium Bordetella pertussis. This organism is the sole cause of endemic pertussis.

• Bordetella parapertussis is an occasional cause of pertussis.

• Mycoplasma, the influenza virus, respiratory syncytial virus and the enteroviruses are not causes of pertussis although they also cause protracted cough

Page 3: DR (MRS) M.B. FETUGA1 PERTUSSIS (WHOOPING COUGH).

DR (MRS) M.B. FETUGA 3

Bordetella pertussis

• B. pertussis is a small aerobic gram-negative coccobacillus.

• It produces multiple antigenic and biologically active products, including pertussis toxin, filamentous hemagglutinin, agglutinogens, adenylate cyclase, pertactin, and tracheal cytotoxin.

Page 4: DR (MRS) M.B. FETUGA1 PERTUSSIS (WHOOPING COUGH).

DR (MRS) M.B. FETUGA 4

Bordetella pertussis

• These products are responsible for the adherence of the organism to the epithelial linings and the clinical features of pertussis disease.

• Immune response to one or more produces immunity to subsequent clinical illness.

• Unlike previous reports, more recent evidence suggests that neither vaccination nor natural infection confers permanent immunity.

Page 5: DR (MRS) M.B. FETUGA1 PERTUSSIS (WHOOPING COUGH).

DR (MRS) M.B. FETUGA 5

Occurrence of Pertussis

• Pertussis is a human disease with no animal or insect source or vector.

• Transmission most commonly occurs by the respiratory route through contact with respiratory droplets, or by contact with airborne droplets of respiratory secretions.

• A silent carrier state is thought to exist, but is infrequent, transient in duration, and probably of little importance in maintaining pertussis organisms in the community.

Page 6: DR (MRS) M.B. FETUGA1 PERTUSSIS (WHOOPING COUGH).

DR (MRS) M.B. FETUGA 6

Occurrence of Pertussis

• No intrauterine acquired protection hence occurs even 1st month of life i.e any age after birth

• Severity of disease ↓ with ↑ age• Attack rate is 80-100%

Page 7: DR (MRS) M.B. FETUGA1 PERTUSSIS (WHOOPING COUGH).

DR (MRS) M.B. FETUGA 7

Communicability & Infectivity

• Pertussis is highly communicable.• Secondary attack rates of 80% among

susceptible household contacts. • Persons with pertussis are most

infectious during the catarrhal period and the first 2 weeks after cough onset (i.e., approximately 21 days).

Page 8: DR (MRS) M.B. FETUGA1 PERTUSSIS (WHOOPING COUGH).

DR (MRS) M.B. FETUGA 8

Pathogenesis of Pertussis

• Pertussis is primarily a toxin-mediated disease.

• The bacteria attach to the respiratory cilia, produce toxins that paralyze the cilia, and cause inflammation of the respiratory tract, which interferes with the clearing of pulmonary secretions.

• Pertussis antigens appear to allow the organism to evade host defenses. Despite remarkable lymphocytosis, chemotaxis is impaired.

Page 9: DR (MRS) M.B. FETUGA1 PERTUSSIS (WHOOPING COUGH).

DR (MRS) M.B. FETUGA 9

Clinical Features (1)

• IP of pertussis is usually 7–10 days, with a range of 4–21 days, and rarely may be as long as 42 days.

• Catarrhal stage-1st stage (1-2/52) insidious onset of coryza (runny nose),

sneezing, low-grade fever, and a mild, occasional cough, similar to the common cold.

Cough gradually becomes more severe.

Page 10: DR (MRS) M.B. FETUGA1 PERTUSSIS (WHOOPING COUGH).

DR (MRS) M.B. FETUGA 10

Clinical Features (2)

• Paroxysmal stage- 2nd stage; begins after the catarrhal stage.

• Paroxysms of numerous, rapid coughs. At the end of the paroxysm, a long inspiratory effort is accompanied by a characteristic high-pitched whoop as air is inhaled forcefully thro narrow bronchial tree.

• Infants younger than 3 months do not whoop.

• Cyanosis & apnea may occur in very young children.

Page 11: DR (MRS) M.B. FETUGA1 PERTUSSIS (WHOOPING COUGH).

DR (MRS) M.B. FETUGA 11

Clinical Features (3)

• Convulsion may occur due to hypoxia or intracerebral hemorrhage

• Vomiting and exhaustion commonly follow the bout of cough.

• Patient usually appears normal between attacks.

Page 12: DR (MRS) M.B. FETUGA1 PERTUSSIS (WHOOPING COUGH).

DR (MRS) M.B. FETUGA 12

Clinical Features (4)

• Paroxysmal attacks occur more frequently at night and increase in frequency during the first 1 or 2 weeks of this stage.

• It remains at the same level for 2 to 3 weeks, and then gradually decrease.

• The paroxysmal stage usually lasts for about 6 weeks but may persist for up to 10 weeks.

Page 13: DR (MRS) M.B. FETUGA1 PERTUSSIS (WHOOPING COUGH).

DR (MRS) M.B. FETUGA 13

Clinical Features (5)

• Convalescent stage-3rd stage; recovery is gradual.

• The cough becomes less paroxysmal and disappears in 2 to 3 weeks.

• However, paroxysms often recur with subsequent viral respiratory infections for many months after the onset of pertussis.

Page 14: DR (MRS) M.B. FETUGA1 PERTUSSIS (WHOOPING COUGH).

DR (MRS) M.B. FETUGA 14

Complications

• Secondary bacterial pneumonia. • Dehydration.• Otitis media.• Severe malnutrition.• Pnemothorax and subcutaneous emphysema.• Epistaxis.• Umbilical and inguinal hernias.• Rectal prolapse.• Subconjuctival haemorrhage.• Seizures and encephalopathy.

Page 15: DR (MRS) M.B. FETUGA1 PERTUSSIS (WHOOPING COUGH).

DR (MRS) M.B. FETUGA 15

Differential Diagnoses

• FB aspiration.• Bronchiolitis.• Adenoviral respiratory infection.• Chlamydial respiratory infection.• Mycoplasma respiratory infection.• TB

Page 16: DR (MRS) M.B. FETUGA1 PERTUSSIS (WHOOPING COUGH).

DR (MRS) M.B. FETUGA 16

Laboratory Diagnosis

• FBC - leukocytosis with an absolute lymphocytosis (effect of one of the pertussis toxins).

• CXR may be NORMAL. It may also show perihilar infiltrates with variable degrees of atelectasis.

• Isolation of B. pertussis by culture. Direct plating of specimens from the posterior nasopharynx on Bordet-Gengou medium is most successful during the catarrhal stage.

Page 17: DR (MRS) M.B. FETUGA1 PERTUSSIS (WHOOPING COUGH).

DR (MRS) M.B. FETUGA 17

Laboratory Diagnosis

• Bordet-Gengou agar (glycerine-potato-bld) + penicillin to inhibit growth of other organisms

Page 18: DR (MRS) M.B. FETUGA1 PERTUSSIS (WHOOPING COUGH).

DR (MRS) M.B. FETUGA 18

Serological Diagnosis

• Polymerase chain reaction (PCR) testing of nasopharyngeal swabs is a rapid, sensitive, and specific method for diagnosing pertussis.

• Direct fluorescent antibody (DFA) testing of nasopharyngeal specimens.

• Serological testing has proven useful in clinical studies, but is not yet standardized. Due to lack of association between antibody levels and immunity to pertussis, results of serologic testing are difficult to interpret.

Page 19: DR (MRS) M.B. FETUGA1 PERTUSSIS (WHOOPING COUGH).

DR (MRS) M.B. FETUGA 19

Management of Pertussis

• The medical management of pertussis cases is primarily supportive.

• Maintenance of adequate fluid and caloric balance. Small frequent feeds are preferred.

• Steam inhalation may improve breathing by making the respiratory secretions less viscid.

Page 20: DR (MRS) M.B. FETUGA1 PERTUSSIS (WHOOPING COUGH).

DR (MRS) M.B. FETUGA 20

Drug treatment of Pertussis

• Antibiotics do not usually alter the course of the disease but if given early (within 2/52 of whoop) may shorten duration of paroxysmal stage.

• This therapy eradicates the organism from respiratory secretions, thereby decreasing communicability.

• Erythromycin (40mg/kg in divided doses administered orally for 14 days) is the drug of choice.

• Azithromycin (oral daily doses of 10-12 mg/kg in for a total of 5 days) & Clarithromycin (15-20 mg/kg/day in 2 divided doses orally) are also useful.

Page 21: DR (MRS) M.B. FETUGA1 PERTUSSIS (WHOOPING COUGH).

DR (MRS) M.B. FETUGA 21

Prevention of Pertussis

• Active immunization is quite effective• The use of the triple vaccine DPT is recommended at

6,10 and 14 weeks of life in Nigeria. (killed B.pertussis)• In most developing countries, the whole cell pertussis

vaccine is still in use whereas in the developed world, the acellular pertussis vaccine is widely used.

• Booster doses of pertussis vaccine may also be given at school entry.

• Un-immunized contacts of pertussis cases should be given prophylactic erythromycin for 10 days.

Page 22: DR (MRS) M.B. FETUGA1 PERTUSSIS (WHOOPING COUGH).

DR (MRS) M.B. FETUGA 22

Prevention of Pertussis

• Adverse reactions to pertussis vaccine• Fever, (convulsions, encephalitis – further

doses C.I