[go: up one dir, main page]

0% found this document useful (0 votes)
47 views28 pages

Wa0003.

Diphtheria is an acute bacterial infection caused by Corynebacterium diphtheriae, primarily affecting children but increasingly seen in adolescents and adults. It spreads through respiratory droplets, leading to symptoms such as sore throat, fever, and the formation of a pseudomembrane in the throat. Diagnosis is clinical, and treatment involves antibiotics and diphtheria antitoxin, with prevention through vaccination being crucial.

Uploaded by

Kato Caleb
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
0% found this document useful (0 votes)
47 views28 pages

Wa0003.

Diphtheria is an acute bacterial infection caused by Corynebacterium diphtheriae, primarily affecting children but increasingly seen in adolescents and adults. It spreads through respiratory droplets, leading to symptoms such as sore throat, fever, and the formation of a pseudomembrane in the throat. Diagnosis is clinical, and treatment involves antibiotics and diphtheria antitoxin, with prevention through vaccination being crucial.

Uploaded by

Kato Caleb
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
You are on page 1/ 28

DIPHTHERIA

PRESENTATION BY KATENDE ROBERTA NAMAKULA


OUTLINE
• Introduction
• Epidemiology
• Pathophysiology
• Cause/risk factors
• Clinical presentation
• Diagnosis
• Differential diagnosis
• Management
• Complications
• Prognosis
INTRODUCTION
Diphtheria in Greek means leather

First described by Hippocrates in 5th centaury BC

An acute bacterial infection caused by an aerobic gram positive bacteria


called Corynebacterium diphtheria.
Its spread through droplet infection and mainly occurs in the
nasopharynx. The bacteria produce a toxin which is responsible for the
systemic effects.
Incubation period is 2-7 days.
EPIDEMIOLOGY
• Diphtheria has been primarily a disease of childhood affecting
populations less than 12 years but recently there was a shift to
adolescents and adults(40years above)

• There's no racial or sex predilection

• Morbidity and mortality rates have dropped significantly due to


vaccine introduction since 1920s
TRANSMISSION
Transmission usually occurs person to person via respiratory droplets
alternatively via exposure to infected skin lesion

Infected patients and asymptomatic carriers can transmit Diphtheria via


respiratory droplets, nasopharyngeal secretions and rarely fomites.

In cutaneous disease, contact with wound exudates may result in the


transmission of the disease to the skin.
PATHOPHYSIOLOGY
• C. diphtheria adheres to the mucosal epithelial cells where the
exotoxin released by the endosomes causes a localized inflammatory
reaction followed by tissue destruction and necrosis

• Local tissue destruction enables the toxin to be carried lymphatically


and hematologically to other parts of the body such as the heart,
kidneys and nervous system.
RISK FACTORS
• Incomplete or absent immunization
• Low herd immunity
• Travelling to endemic areas or regions with current epidemics
• Immunocompromised states, this can be pharmacologic, disease states like
HIV
• Low socioeconomic status
• Poor health care system infrastructure
• Overcrowding like in military barracks, homeless shelters
• Pets (domestic animals like cats) can act as reservoirs for human infection
CLINICAL PRESENTATION
The different clinical types of diphtheria;
➢Pharyngeal diphtheria
➢Laryngeal diphtheria
➢Other rare types like nasal, cutaneous, conjunctival, vulvovaginal
diphtheria
CLINICAL PRESENTATION
Initially symptoms are nonspecific resembling typical viral URTI
• Low grade fever and chills
• Malaise, weakness and prostration
• Headache
➢Pharyngeal diphtheria
• Sore throat
• Cervical lymphadenopathy(bull neck)
CLINICAL PRESENTATION

• Pseudo membrane formation in respiratory tract aka


Pseudomembranous tonsillitis (grey, tough and very sticky
membranes) removal of this membrane leaves a raw bleeding area
• Dysphagia
➢Nasal diphtheria
• unilateral offensive Serosanguinous/seropurulent nasal discharge
CLINICAL PRESENTATION CONTINUED
➢Laryngeal diphtheria
• Dyspnea
• Respiratory stridor
• Wheezing
• Cough
• Hoarseness

• NB . Respiratory failure is eminent due to airway obstruction or aspiration


of pseudomembrane
➢Cutaneous diphtheria often develops at a site of previous trauma and its
characterized by indolent non healing ulcers covered by a gray membrane
PSEUDOMEMBRANE COVERING
BULL NECK APPERANCE
BULL NECK APPEARNCE
DIFFFERENTIAL DIAGNOSES
➢Laryngeal diphtheria(other causes of stridor)
• Angioedema
• Epiglottitis
• Peritonsillar abscess
• Retropharyngeal abscess
• Viral croup
• Foreign body aspiration
DIFFERENTIAL DIAGNOSIS
Pharyngeal diphtheria
• Follicular tonsilitis
• Infectious mononucleosis
• Vincent's angina
• Pharyngitis
Others
• Oropharyngeal/esophageal candidiasis
• myocarditis
• Infective endocarditis
DIAGNOSIS
The diagnosis is mainly clinical
Carefully examine the child’s nose and
throat and look for a grey, adherent
membrane. Great care is needed when
examining the throat, as the examination
may precipitate complete obstruction
of the airway. A child with pharyngeal diphtheria may have an
obviously swollen neck, termed a ‘bull neck’.
INVESTIGATIONS
• Culture from throat swab
Other investigations
• Gram stain shows club shaped , non encapsulated non motile bacilli found
in clusters
• CBC
• Serum antibodies to diphtheria toxin
• Serum troponin levels
• Chest and soft tissue neck radiography/ULTRASONOGRAPY
• Echocardiography may reveal valvular vegetations
• ECG
TREATMENT
• Treatment should be initiated before the confirmatory tests due to
high risk of mortality
• Prompt isolation of all access to limit number of possible contacts
• Secure airway for patients with impending airway compromise(severe
chest indrawing and restlessness) with tracheostomy or intubation.
• Close monitoring of cardiac activity to detect any abnormal rhythms
• Circulatory access with two large bore cannulas in toxic looking
patients for resuscitation
• Initiate prompt antibiotic coverage with erythromycin or penicillin
TREATMENT CONTINUED
• Child: procaine benzylpenicillin 50,000 IU/kg per
• day IM once daily until patient can swallow
• When patient is able to swallow
• ‰Give Penicillin V 250 mg every 6 hours per day to
• complete 14 days.
• Child 1-6 years: 125 mg 6 hourly
• Child< 1 years: 12.5 mg/kg every 6 hours
• In case of penicillin allergy
• ‰Erythromycin 500 mg every 6 hours for 14 days
• Child: 50 mg/kg every 6 hours
NOTE
• Erythromycin is a first line agent in infants more than 6months old
there for infants less than 6months old azithromycin is a preferred
option.
TREATMENT CONTINUED
• Diphtheria antitoxin, a horse derived hyperimmune antiserum that
neutralizes the circulating toxins
Dosage IM or 20000-120000iu single dose, however an initial
intradermal test to detect hypersensitivity should be done
• Repeat throat cultures two weeks after treatment
➢Supportive care;
• Give paracetamol if child has fever,
• Encourage child to eat and drink. If there's any difficulty feeding a
nasogastric tube should be placed
PREVENTION
➢Immunization with the diphtheria, tetanus, and acellular
pertussis(DTaP) vaccine .Three doses given at 6, 10 and 14 weeks
➢Booster vaccines are required as childhood immunity wanes off, CDC
recommends Tdap at least every 10years to maintain immunity.
➢Monitor close contacts for 7 days and give prophylactic antibiotics;
single dose benzathine penicillin IM
Less than 10years; 600000IU
More than 10years;1.2MIU
PREVENTION CONTINUED

➢Verify their immunization status, complete if needed

➢Give a booster dose if last dose was more than a year before
COMPLICATIONS
Respiratory complications
▪ Airway obstruction by the bull neck
▪ Lung collapse due aspiration of detached membranes
▪ Bronchopneumonia
Cardiac complications
• Toxic myocarditis
• Cardiogenic shock
• Heart block
COMPLICATIONS
Nervous system complications
▪ palatal paralysis (nasal tone, food regurgitation)
▪ Ocular paralysis(ptosis, squint)
▪ Pharyngeal and laryngeal paralysis(dysphagia, dysphonia)
▪ Generalized paralysis
▪ Phrenic nerve paralysis(respiratory failure)
PROGNOSIS

• Recovery from myocarditis and neuropathy is slow but complete

• Mortality varies from 3-25% mainly related to myocarditis or


respiratory failure
REFFERENCES
• Nelson Textbook of Pediatrics 21st Edition
• WHO Pocket Handbook 2013
• Medscape 2024
• UCG 2023 PUBLICATION

You might also like