1. Pertussis Syndrome By
DR; RIADH ALOBAIDI

2. ETIOLOGY
The pertussis syndrome includes disease caused by Bordetella pertussis) a gram-negative pleomorphic bacillus ( .
Bordetella parapertussis, which causes a similar but milder illness that is not affected by B. pertussis vaccination
Adenoviruses have been associated with the pertussis syndrome.

3. EPIDEMIOLOGY The mean incubation period is7-10 days , range 4-21 days.
Patients are most contagious during the earliest stage the catarrhal stage through first 3 weeks of coughing stage or until the 5th day of the start of effective antibiotic therapy.
The age at risk for the infection is under 5 years.

4. CLINICAL MANIFESTATIONS
Classic pertussis is the syndrome seen in most infants 6-months through school age. The progression of the disease is divided into
The catarrhal stage is marked by nonspecific signs (upper respiratory tract infection as running nose, sneezing and low-grade fever) that last 1 to 2 weeks.
The paroxysmal stage :coughing stage; is the most distinctive classic stage of pertussis. Coughing occurs in paroxysms (fits, episodes) during expiration, causing young children to lose their breath and even apnea followed by high pitch inspiratory sound -whoop

5. Clinical feature con.
The forceful inhalation against a narrowed glottis that follows this paroxysm of cough produces the characteristic whoop. Post-tussive emesis should raise the suspicion of pertussis .Facial congestion and cyanosis may be seen in the attack. This stage lasts 2-6 weeks. Pertussis may produce anoxic brain damage and even encephalopathy.
3. The convalescent stage is marked by gradual resolution of symptoms over 1 to 2 weeks. Coughing becomes less severe, and the paroxysms and whoops slowly disappear. Although the disease typically lasts 6 to 8 weeks, residual cough may persist for months, especially with physical stress or respiratory irritants.

6. Infants below 6 months and neonates may not display the classic pertussis syndrome; the first signs may be episodes of apnea. Young infants are unlikely to have the classic whoop, are more likely to have CNS damage as a result of hypoxia, and are more likely to have secondary bacterial pneumonia. Adolescents and adults with pertussis usually present with a prolonged bronchitic illness that often begins as a nonspecific upper respiratory tract infection, followed by coughing without whoop ,although they may have severe coughing. The cough may persist many weeks to months. Physical examination is nonspecific

7. LABORATORY AND IMAGING STUDIES
Culture of nasopharyngeal swabs on Bordet-Gengou medium.
Direct fluorescent antibody staining of the swab from nasopharynx.
Serological test for anti- pertussis toxin in the blood.
PCR is useful .
Leukocytosis (15,000–100,000 cells/mm3) due to absolute lymphocytosis seen at the end of the catarrhal stage and during the paroxysmal stage.

8. 5. Radiological X-R ; not specific, It may show segmental lung atelectasis to develop during pertussis, especially during the paroxysmal stage. Perihilar infiltrates are common and are similar to what is seen in viral pneumonia. Secondary bacterial pneumonia may develop.

9. DIFFERENTIAL DIAGNOSIS
1. Respiratory viruses such as RSV, parainfluenza virus, and Chlamydia pneumoniae can produce bronchitic illnesses among infants.
2. In older children and young adults, Mycoplasma pneumoniae may produce a prolonged bronchitic illness that is not distinguished easily from pertussis in this age group.

10. TREATMENT
Erythromycin, Clarithromycin, or Azithromycin given early in the course of illness catarrhal stage: eradicates nasopharyngeal carriage of organisms within 3 to 4 days and ameliorates the effects of the infection. Treatment is not effective in the paroxysmal stage but it prevent the infectivity during the first 3 weeks when given to 5 days. When given to neonates younger than 4 weeks old, erythromycin has been rarely associated with pyloric stenosis, but treatment is still recommended because of the seriousness of pertussis at this age. Azithromycin is drug of choice for neonates and clarithromycin can be given for a shorter duration and are associated with fewer gastrointestinal adverse effects. TMP-SMZ may be beneficial as an alternative.

11. COMPLICATIONS Hypoxia Apnoea
Pneumonia : caused by B. pertussis itself or resulting from secondary bacterial infection from S. pneumoniae, Hib, and S. aureus.
seizures, encephalopathy
failure to thrive.
Atelectasis may develop secondary to mucous plugs.

12. 7. The force of the paroxysm may rupture alveoli and produce pneumomediastinum, pneumothorax, or interstitial or subcutaneous emphysema;
8. epistaxis; and retinal and subconjunctival hemorrhages, hernia
9. Otitis media and sinusitis may occur.
Infants <4 mo of age account for 90% of cases of fatal pertussis

13. PREVENTION
Active immunity can be induced with acellular pertussis vaccine, given in combination with the toxoids of tetanus and diphtheria (DTaP). Pertussis vaccine has an efficacy of 70% to 90%; efficacy declines with fewer vaccinations.
Compared with older, whole cell pertussis vaccines, acellular vaccines have fewer adverse effects and local reactions .
Patient who have pertussis produce life long immunity.

14. Erythromycin is effective in preventing disease in contacts exposed to pertussis. Close contacts younger than 7 years old who have received four doses of vaccine should receive a booster dose of DTaP, unless a booster dose has been given within the preceding 3 years. They also should be given a macrolide antibiotic. Close contacts older than age 7 should receive prophylactic macrolide antibiotic for 10 to 14 days, but not the vaccine.

15. Diphtheria

16. Etiology Corynebacterium diphtheriae
aerobic, nonencapsulated, non– spore-forming, mostly nonmotile, pleomorphic, gram-positive bacillus
Three biotypes (i.e., mitis, gravis, and intermedius), each capable of causing diphtheria

17. Clinical Manifestations
The manifestations of C. diphtheriae infection are influenced by the anatomic site of infection, the immune status of the host, and the production and systemic distribution of toxin.

18. RESPIRATORY TRACT DIPHTHERIA
the primary focus of infection was the tonsils or pharynx in 94%, with the nose and larynx being the next two most common sites. After an average incubation period of 2–4 days, local signs and symptoms of inflammation develop.
In tonsiller and pharyngeal diphtheria, sore throat is a universal early symptom, fever is not characteristic of the disease but only half of patients have fever, other symptoms ;dysphagia, stridor, hoarseness, malaise, or headache. Mild pharyngeal injection is followed by unilateral or bilateral tonsiller membrane formation, which extends variably to affect the uvula, soft palate, posterior pharynx, and glottic areas with oedema and obstruction of air way.

19. a gray-brown adherent tonsiller pseudomembrane will be formed
a gray-brown adherent tonsiller pseudomembrane will be formed. Removal is difficult and reveals a bleeding edematous submucosa. Paralysis of the palate and hypopharynx is an early local effect of the toxin
Underlying soft tissue edema and enlarged lymph nodes can cause a bull-neck appearance

20. complications
TOXIC CARDIOMYOPATHY: occurs in approximately 10–25% of patients with diphtheria and is responsible for 50–60% of deaths
The evidence of cardiac toxicity characteristically occurs in the 2nd–3rd wk of illness as pharyngeal disease improves includes; carditis; tachycardia, dysrhythmia, heart block, heart failure, cardiomyopathy.

21. 2. TOXIC NEUROPATHY: Acutely or 2–3 wk after onset of oropharyngeal inflammation, local paralysis of the soft palate occur commonly. Weakness of the pharyngeal, laryngeal, and facial nerves may follow, causing a nasal quality in the voice, difficulty in swallowing, and risk of death due to aspiration. Cranial neuropathies characteristically occur in the 5th wk

22. Diagnosis
Swab specimens for culture should be obtained from the nose and throat and any other mucocutaneous lesion

23. Treatment Specific antitoxin is the mainstay of therapy
Equine diphtheria antitoxin is the available for treatment .It combat the free toxin only.
Antitoxin is administered as a single empirical dose of 20,000–120,000 IU based on the degree of toxicity, site and size of the membrane, and duration of illness
Antibiotics penicillin or erythromycin can be used for patients and as preventive for contacts

24. Antimicrobial therapy is indicated to halt toxin production, treat localized infection, and prevent transmission of the organisms to contacts. C. diphtheriae is usually sensitive to various agents including penicillins, erythromycin, clindamycin, rifampin, and tetracycline