10 and 11 Diphtheria_Pertussis_tetanus.ppt

Common tropical diseases that affect population in under develop countries

1. MEDICAL SURGICAL NURSING I
NURS 313
Lecturer:AbdulrahmanSalihuKombo, PhD, RN
Class-Undergraduate 300l Class
TOPIC-
February, 2023
AbouHajara

2. OUTLINE :
Introduction
Epidemiology
Pathogenesis
Clinical manifestation
Diagnosis
Treatment
Prevention
Complication
Introduction
Epidemiology
Etiology
Pathogenesis
Clinical manifestation
Diagnosis
Treatment
Prevention
Complication

3. Diphtheria (Corynebacteriumdiphtheriae)
DiphtheraisGreek word for leather
Bull-neck appearance of diphtheritic cervical lymphadenopathy

4. INTRODUCTION
AnacutetoxicinfectioncausedbyCorynebacteriumdiphtheriaeandrarelytoxigenic
strainsofCorynebacteriumulcerans
aerobic,nonencapsulated,non–spore-forming,mostlynonmotile,pleomorphic,gram-
positivebacilli
DifferentiationofC.diphtheriaefromC.ulceransisbasedonureaseactivity,C.
ulceransisurease-positive
FourC.diphtheriaebiotypes-mitis,intermedius,belfanti,gravis;differentiatedby
colonialmorphology,hemolysis,andfermentationreactions

5. INTRODUCTION
Diphtheritictoxinproductionoccursonlyafteracquisitionofa
lysogenicCorynebacteriophagebyeitherC.diphtheriaeorC.ulcerans,which
encodesthediphtheritictoxingeneandconfersdiphtheria-producingpotentialon
thesestrains
Demonstrationofdiphtheritictoxinproductionorpotentialfortoxinproductionby
anisolateisnecessarytoconfirmdisease
Theformerisdoneinvitrousingtheagarimmunoprecipitintechnique(Elektest)or
invivowiththetoxinneutralizationtestinguineapigs,thelatterbypolymerasechain
reactiontestingforcarriageofthetoxingene
Toxinislethalinhumanbeingsinanamount130μg/kgBW

6. EPIDEMIOLOGY
Transmission: airborne respiratory droplets, direct contact with respiratory secretions of symptomatic individuals,
or exudates from infected skin lesions
Asymptomatic respiratory tract carriage is important in transmission. Where diphtheria is endemic, 3-5% of
healthy individuals can carry toxigenic organisms
Skin infection and skin carriage are silent reservoirs and organisms can remain viable in dust or on fomites for up to
6months
Transmission through contaminated milk and an infected food handler has been documented

7. EPIDEMIOLOGY
Children aged 1-5yrs are commonly infected
A herd immunity of 70% is required to prevent epidemics
Contaminated objects like thermometers, cups, spoons, toys and pencils can spread the disease
Overcrowding, poor sanitation and hygiene, illiteracy, urban migration and close contacts can lead to outbreak

8. PATHOGENESIS
Within the first few days of respiratory tract infection , a dense necrotic coagulum of organisms,
epithelial cells, fibrin, leukocytes and erythrocytes forms, advances, and becomes a gray-brown, leather-
like adherentpseudomembrane. Removal is difficult and reveals a bleeding edematous submucosa
The major virulence of the organism lies in its ability to produce the potent 62-kd polypeptide exotoxin, which inhibits protein
synthesis and causes local tissue necrosis
Entry into nose or mouth
The organism remains in the superficial layers of skin lesions or respiratory tract mucosa, inducing local inflammatory reaction

9. Presentation
Local effect of diphtheritic toxin:
Paralysis of the palate and hypopharynx
Pneumonia
Systemic effects (Toxin absorption ):
kidney tubule necrosis
hypoglycemia
myocarditis and/or demyelination of nerves
Myocarditis:10-14 days
Demyelination of nerves: 3-7 weeks

10. Presentation
Influenced by the anatomic site of infection, the immune status of the host and the
production and systemic distribution of toxin
Incubation period: 1-6 days
Classification (location):
nasal
pharyngeal
tonsillar
laryngeal or laryngotracheal
skin, eye or genitalia

11. CLINICAL MANIFESTATIONS
Nasaldiphtheria:Infectionoftheanteriornares-morecommonamong
infants,causesserosanguineous,purulent,erosiverhinitiswithmembrane
formation
Shallowulcerationoftheexternalnaresandupperlipischaracteristic
Unilateralnasaldischargeisquitepathognomicofnasaldiphtheria
Accuratediagnosisofnasaldiphtheriadelayed-paucityofsystemicsignsand
symptoms

12. Tonsillarandpharyngealdiphtheria:
sorethroatistheuniversalearlysymptom
Onlyhalfofpatientshavefeverandfewerhavedysphagia,hoarseness,
malaise,orheadache
Mildpharyngealinjection unilateralorbilateraltonsillarmembrane
formationextendtoinvolvetheuvula,softpalate,posteriororopharynx,
hypopharynx,orglotticareas
Underlyingsofttissueedemaandenlargedlymphnodes:bull-neck
appearance

14. Laryngeal diphtheria: At significant risk for suffocation because of local soft tissue edema and airway obstruction
by the diphtheritic membrane
Classic cutaneous diphtheria is an indolent, nonprogressive infection characterized by a superficial, ecthymic,
nonhealing ulcer with a gray-brown membrane

15. Infection at Other Sites:
ear(otitis externa), the eye (purulent and ulcerative conjunctivitis), the genital tract (purulent and ulcerative
vulvovaginitis) and sporadic cases of pyogenic arthritis

16. Diagnosis
Clinical features
Culture: from the nose and throat and any other mucocutaneouslesion. A portion of membraneshould be removed
and submitted for culture along with underlying exudate
Elektest: rapid diagnosis (16-24 hrs)
Enzyme immunossay
PCR for A or B portion of the toxic gene “tox”
Hypoglycemia, glycosuria, BUN, or abnormal ECG for liver, kidney and heart involvement
Differential diagnosis:
1.Common cold
2.Congenital syphilis snuffle
3.Sinusitis
4.Adenoiditis and foreign body in nose
5.Streptococcal pharyngitis, Infectious mononucleosis
6..

17. TREATMENT
1.Antitoxin:
Mainstay of therapy
Neutralizes only free toxin, efficacy diminishes with elapsed time
Antitoxin is administered as a single empirical dose of 20,000-120,000U based on the degree of toxicity, site and size of the membrane,
and duration of illness
2.Antimicrobial therapy
Halt toxin production, treat localized infection and prevent transmission of the organism to contacts
erythromycin(40-50mg/kg/day 6hrly [PO] or [IV]), aqueous crystalline penicillin G(100,000-150,000U/kg/day 6hrly IV or [IM]),
or procaine penicillin (25,000-50,000U/kg/day 12hrly IM) for 14 days

18. Elimination of the organism should be documented by negative results of at least 2 successive cultures of specimens
from the nose and throat (or skin) obtained 24hr apart after completion of therapy
Prognosis:depends on the virulence of the organism (subspecies gravis), patient age, immunization status, site of
infection and speed of administration of the antitoxin
The case fatality rate of almost 10% for respiratory tract diphtheria
At recovery, administration of diphtheria toxoid is indicated to complete the primary series or booster doses of
immunization, because not all patients develop antibodies to diphtheritic toxin after infection

19. PREVENTION
Asymptomatic Case Contacts:
Antimicrobial prophylaxis -erythromycin(40-50mg/kg/day divided qid PO for 10 days) or a singleinjection of benzathine penicillin G
(600,000U IM for patients <30kg, 1,200,000U IM for patients ≥30kg)
Diphtheria toxoid vaccine-to immunized individuals who have not received a booster dose within 5yr. Children who have not received
their 4th dose should be vaccinated. Those who have received fewer than 3 doses of diphtheria toxoid or who have uncertain immunization
status are immunized with an age-appropriate preparation on a primary schedule
Asymptomatic Carriers:
Same+Repeat cultures are performed about 2wk after completion of therapy. if results are positive, an additional 10-day course of oral
erythromycin should be given and follow-up cultures performed
VACCINE

20. COMPLICATIONS
1.Respiratory tract obstruction by pseudomembranes: bronchoscopyor intubation and mechanical ventilation
2.Toxic Cardiomyopathy:
-in 10-25%of patients
-responsible for 50-60%of deaths
-the risk for significant complications correlates directly with the extent and severity of exudativelocal oropharyngealdisease as well as
delay in administration of antitoxin
-Tachycardiaout of proportion to fever
-prolonged PR interval and changes in the ST-T wave
-Elevation of the serum aspartateaminotransferaseconcentration closely parallels the severity of myonecrosis

21. Complication contn…
3.Toxic Neuropathy:
Acutely or 2-3wk after: hypoesthesia and soft palate paralysis
Afterwards weakness of the posterior pharyngeal, laryngeal, and facial nerves : anasal qualityin the voice, difficulty in swallowing and
risk for aspiration
Cranial neuropathies(5th wk): oculomotorand ciliaryparalysis-strabismus, blurred vision, or difficulty with accommodation
Symmetric polyneuropathy(10 days to 3mo): motor deficits with diminished deep tendon reflexes
Monitoring for paralysis of the diaphragm muscle
Recovery from the neuritis is often slow but usually complete. Corticosteroids are not recommended.

22. Whooping cough: whooping sound made when gasping for air after a fit of coughing
Cough of 100 days
PERTUSSIS (WHOOPING COUGH)

23. INTRODUCTION
A highly contagious acute bacterial infection caused by the bacilli Bordetella pertussis
Currently worldwide prevalence is diminished due to active immunization
However it remains a public health problem among older children and adults
It continues to be an important respiratory disease afflicting unvaccinated infants and previously vaccinated
children and adults (waning immunity)

24. EPIDEMIOLOGY
Transmission: through the respiratory route in the form of droplet infection
Adolescents and adults are the reservoir. No animal or insect reservoir
A highly communicable disease. SAR 80% among households contacts
In the catarrhal stage and 2 weeks after the onset of cough

25. ETIOLOGY
Bordetella pertussis –aerobic gram-negative coccobacilli
Produces toxinsnamely pertussis toxin, filamentous hemagglutinin, hemolysin, adenylate cyclase toxin,
dermonecrotic toxin and tracheal cytotoxin-responsible for clinical features (toxin mediated disease) and the
immunity

26. PATHOGENESIS
-This exudatepredisposes to atelectasis, cough, cyanosis and pneumonia -Organism causes local tissue damage and systemic effects
mediated through its toxin
The organism get attached to the respiratory cilia and toxin causes paralysis of cilia
muocopurulent-sanguineous exudateforms in the respiratory tract

27. CLINICAL MANIFESTATIONS
Incubation period: 7-10 days
Infection lasts for 6 weeks –10 weeks
Stage I (catarrhal stage; 1-2 weeks):insidious onset of coryza, sneezing, low grade fever and occasional cough
Stage II (paroxysmal cough stage; 1-6 weeks): due to difficulty in expelling the thick mucous form the
tracheobronchial tree
At the end of paroxysm long inspiratory effort is followed by a whoop
In between episodes child look well. During episode of cough the child may become cyanosed, followed by
vomiting, exhaustion and seizures

28. CLINICAL MANIFESTATIONS
Cough increase for next 2-3 weeks and decreases over next 10 weeks
Absence of whoop and/or post-tussive vomiting does not rule out clinical diagnosis of pertussis
paroxysmal cough>2 weeks with or without whoop and/or post-tussive vomiting is the hallmark feature of
pertussis
Stage III (convalecence stage): period of gradual recovery even up to 6 months

29. COMPLICATIONS
1.Secondary pneumonia (1 in 5) and apneicspells (50%; neonates and infant<6 months of age)
2.Neurological complications: seizures (1 in 100) and encephalopathy (1 in 300) due to the toxin or hypoxia or
cerebral hemorrhage
3.Otitismedia, anorexia and dehydration, rib frcture, pneumothorax, subdural hematoma, hernia and rectal prolapse
Differential diagnosis:
1. B. parapertussis, adenovirus, mycoplasmapneumonia, and chlamydiatrachomatis
2. Foreign body aspiration, endobronchialtuberculosis and a mass pressing on the airway

30. DIAGNOSIS
1.Suspected on the basis of history and clinical examination and is confirmed by culture, genomics or serology
2.Elevated WBC count with lymphocytosis. The absolute lymphocyte count of ≥20,000 is highly suggestive
3.Culture: gold standard specially in the catarrhal stage. A saline nasal swab or swab from the posterior pharynx is
preferred and the swab should be taken using dacronor calcium alginate and has to be plated on to the selective
medium

31. DIAGNOSIS
However culture are not recommended in clinical practice as the yield is poor because of previous vaccination,
antibiotic use, diluted specimen and faulty collection and transportation of specimen.
4.PCR: most sensitive to diagnose; can be done even after antibiotic exposure. It should always be used in addition
with cultures
5.Direct fluorescent antibody testing: low sensitivity and variable specifity

32. TREATMENT
1.Avoidance of irritants, smoke, noise and other cough promoting factors
2.Antibiotics: effective only if started early in the course of illness. Erythromycin(40-50mg/kg/day 6hrly orally
for 2 weeksor Azithromycin10 mg/kg for 5 days in children<6 months and for children>6 months 10 mg/kg on
day 1, followed by 5mg/kg from day2-5 or Clarithromycin15 mg/kg 12 hrly for 7 days
3.Supplemental oxygen, hydration, cough mixtures and bronchodilators (in individual cases)

33. PREVENTION
All household contacts should be given erythromycin for 2 weeks
Children <7 years of age not completed the four primary dose should complete the same at the earliest
Children <7 years of age completed primary vaccination but not received the booster in the last 3 years have to be
given a single booster dose
VACCINE

34. THANKS A MILLION