Volume 03 Issue 10-2023
24
International Journal of Medical Sciences And Clinical Research
(ISSN
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2771-2265)
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03
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OCLC
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1121105677
Publisher:
Oscar Publishing Services
Servi
ABSTRACT
In this article you will get information about diphtheria, which currently has its place within insfection diseases.
through this article , you will receive the necessary information about what kind of infeskia diphtheria itself is , its
spread, transmission routes and Prevention.
KEYWORDS
Corynebacteriophages, diphtheriae , blood, toxin , infection, pathogenesis.
INTRODUCTION
C. diphtheriae is an aerobic, gram-positive bacillus.
Toxin production (toxigenicity) occurs only when the
bacillus is itself infected (lysogenized) by specific
viruses (corynebacteriophages) carrying the genetic
information for the toxin (tox gene). Diphtheria toxin
causes the local and systemic manifestations of
diphtheria.
C. diphtheriae has four biotypes: gravis, intermedius,
mitis, and belfanti. All biotypes can become toxigenic
and cause severe disease. All isolates of C. diphtheriae
should be tested for toxigenicity.
Pathogenesis. Susceptible persons may acquire
toxigenic diphtheria bacilli in the nasopharynx. The
organism produces a toxin that inhibits cellular protein
synthesis and is responsible for local tissue destruction
and formation of the pseudomembrane that is
characteristic of this disease. The toxin produced at the
site of the membrane is absorbed into the bloodstream
Research Article
PREVENTION OF THE SPREAD OF DIPHTHERIA INFECTION,
PATHOGENESIS AND STATISTICS ON THE WORLD
Submission Date:
October 06, 2023,
Accepted Date:
October 11, 2023,
Published Date:
October 16, 2023
Crossref doi:
https://doi.org/10.37547/ijmscr/Volume03Issue10-05
Jo’rayev Muzaffar G’ulomovich
Andijan State Medical Institute, Uzbekistan
Journal
Website:
https://theusajournals.
com/index.php/ijmscr
Copyright:
Original
content from this work
may be used under the
terms of the creative
commons
attributes
4.0 licence.
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Publisher:
Oscar Publishing Services
Servi
and then distributed to the tissues of the div. The
toxin is responsible for major complications such as
myocarditis, polyneuropathies, and nephritis, and can
also cause thrombocytopenia.
Non-toxin-producing C. diphtheriae strains can cause
mild to severe exudative pharyngitis. Severe cases with
pseudomembranes caused by such strains have been
reported rarely; it is possible that these infections were
caused by toxigenic strains that were not detected
because of inadequate culture sampling. Other
manifestations of nontoxigenic C. diphtheriae
infection include cutaneous lesions, endocarditis,
bacteremia, and septic arthritis.
Clinical Features . The incubation period for diphtheria
is 2 to 5 days, with a range of 1 to 10 days. Disease can
involve almost any mucous membrane. In untreated
people, organisms can be present in discharges and
lesions 2 to 6 weeks after infection. For clinical
purposes, it is convenient to classify diphtheria by
anatomic site: respiratory (pharyngeal, tonsillar,
laryngeal, nasal) and non-respiratory (cutaneous and
other mucus membranes) disease.
Pharyngeal and Tonsillar Diphtheria
The most common sites of diphtheria infection are the
pharynx and the tonsils. Infection at these sites is
usually
associated
with
substantial
systemic
absorption of toxin. The onset of pharyngitis is gradual.
Early symptoms include malaise, sore throat, anorexia,
and low-grade fever (less than 101°F). Within 2 to 3
days, a bluish-white membrane forms and extends,
varying in size from covering a small patch on the
tonsils to covering most of the soft palate. Often by the
time a physician is contacted the membrane is greyish-
green or, if bleeding has occurred, black. There is a
minimal amount of mucosal erythema surrounding the
membrane. The membrane is firmly adherent to the
tissue, and forcible attempts to remove it cause
bleeding. Extensive membrane formation may result in
respiratory obstruction.
While some patients may recover at this point without
treatment, others may develop severe disease. The
patient may appear quite toxic, but the fever is usually
not high. Patients with severe disease may develop
marked edema of the submandibular areas and the
anterior neck along with lymphadenopathy, giving a
characteristic “bull neck” appearan
ce. If enough toxin
is absorbed, the patient can develop severe
prostration, pallor, rapid pulse, stupor, and coma.
Death can occur within 6 to 10 days.
Laryngeal Diphtheria
Laryngeal diphtheria can be either an extension of the
pharyngeal form or can involve only this site.
Symptoms include fever, hoarseness, and a barking
cough. The membrane can lead to airway obstruction,
coma, and death.
Anterior Nasal Diphtheria
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The onset of anterior nasal diphtheria looks much like
the common cold and is usually characterized by a
mucopurulent nasal discharge that may become blood-
tinged. A white membrane usually forms on the nasal
septum. The disease is usually fairly mild because of
apparent poor systemic absorption of toxin from this
location, and it can be terminated rapidly by diphtheria
antitoxin and antibiotic therapy.
Cutaneous Diphtheria
Skin infections may be manifested by a scaling rash or
by ulcers with clearly demarcated edges and an
overlying membrane, but any chronic skin lesion may
harbor C. diphtheriae along with other organisms.
Cutaneous diphtheria is quite common in the tropics
and is probably responsible for the high levels of
natural immunity found in these populations. Infection
with toxigenic strains appears to result less frequently
in systemic complications with cutaneous compared to
other forms of diphtheria. C. diphtheriae isolated from
cutaneous cases in the United States typically has been
nontoxigenic, although recently a number of imported
toxigenic cutaneous cases have been identified.
Complications
Most complications of diphtheria, including death, are
caused by effects of the toxin. The severity of the
disease and complications are generally related to the
extent of local disease. The toxin, when absorbed,
affects organs and tissues distant from the site of
invasion. The most frequent complications of
diphtheria are myocarditis and neuritis.
Myocarditis may present as abnormal cardiac rhythms
and can occur early in the course of the illness or weeks
later. Myocarditis can lead to heart failure and, if it
occurs early, it is often fatal.
Neuritis most often affects motor nerves and usually
resolves completely. Paralysis of the soft palate is most
frequent during the third week of illness. Paralysis of
eye muscles, limbs, and the diaphragm can occur after
the fifth week. Secondary pneumonia and respiratory
failure may result from diaphragmatic paralysis.
Other complications include otitis media and
respiratory insufficiency due to airway obstruction,
especially in infants.
The estimated overall case fatality ratio for diphtheria
is 5% to 10%.
Laboratory Testing
Diagnosis of respiratory diphtheria is usually made
based on clinical presentation because it is imperative
to begin presumptive therapy quickly. Non-respiratory
diphtheria, such as cutaneous diphtheria, may not be
clinically suspected and therefore diagnosis is typically
based on the laboratory finding.
Confirmatory testing for diphtheria includes culture to
identify the bacterial species and the Elek test to
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confirm diphtheria toxin production. Capacity for
diphtheria culture may be available at public health or
commercial laboratories. CDC’s Pertussis and
Diphtheria Laboratory routinely performs culture to
confirm C. diphtheriae and is currently the only
laboratory in the United States that tests for toxin
production. It is critical to take a swab of the affected
area, especially any ulcerations or pseudomembranes.
The organism can be cultured on common laboratory
media; culture on a selective medium containing
tellurite allows for distinguishing C. diphtheriae and C.
ulcerans from other Corynebacterium species that
normally inhabit the nasopharynx and skin (e.g.,
diphtheroids). However, further biochemical tests are
required to fully identify an isolate as C. diphtheriae. If
C. diphtheriae or C. ulcerans are isolated, they must be
tested for toxin production.
If antibiotic therapy was started prior to specimen
collection from a suspected diphtheria case, and
culture was negative for C. diphtheriae, two sources of
evidence can help support presumptive diagnosis:
1.
a positive polymerase chain reaction (PCR) test
for diphtheria tox gene;
2.
isolation of C. diphtheriae from cultures of
specimens from close contacts.
Medical Management
Diphtheria Antitoxin
Diphtheria antitoxin, produced in horses, has been
used for treatment of respiratory diphtheria in the
United States since the 1890s. It typically is not
administered in cases of non-respiratory diphtheria
and it is not indicated for prophylaxis of diphtheria
patient contacts. Diphtheria antitoxin is available only
from CDC, through an Investigational New Drug (IND)
protocol. Diphtheria antitoxin does not neutralize
toxin that is already fixed to tissues, but it will
neutralize circulating toxin and prevent progression of
disease.
After a provisional clinical diagnosis of respiratory
diphtheria is made, appropriate specimens should be
obtained for culture and the patient placed in isolation.
Persons with suspected diphtheria should be promptly
given diphtheria antitoxin and antibiotics in adequate
dosage, without waiting for laboratory confirmation.
Respiratory support and airway maintenance should
also be provided as needed. Consultation on the use of
and access to diphtheria antitoxin is available through
t
he duty officer at CDC’s Emergency Operations Center
at 770-488-7100.
Antibiotics
In addition to diphtheria antitoxin, patients with
respiratory diphtheria should also be treated with
antibiotics. The disease is usually no longer contagious
48 hours after antibiotics have been given. Elimination
of the organism should be documented by two
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consecutive negative cultures taken 24 hours apart,
with the first specimen collected 24 hours after
therapy is completed.
Preventive Measures
Diphtheria disease might not confer immunity.
Unvaccinated or incompletely vaccinated persons
recovering from diphtheria should begin or complete
active immunization with diphtheria toxoid during
convalescence.
Vaccination history of close contacts of diphtheria
patients should also be assessed: if vaccination history
is incomplete or unknown, the contact should receive
a dose of diphtheria toxoid-containing vaccine
immediately, and the vaccination series should be
completed according recommendations from the
Advisory Committee on Immunization Practices (ACIP).
If the contact is up-to-date according to ACIP
recommendations but the last dose was more than 5
years ago, a diphtheria toxoid-containing vaccine
should be immediately administered. In addition, close
contacts should receive a single intramuscular dose of
benzathine penicillin G or a 7- to 10-day course of oral
erythromycin. Benzathine penicillin G should be given
to contacts for whom surveillance cannot be
maintained for 7 to 10 days. Contacts should be closely
monitored and begin diphtheria antitoxin treatment at
the first signs of illness.
Secular Trends in the United States
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During the 1920s, 100,000 to 200,000 cases of
diphtheria (140 to 150 cases per 100,000 population)
and 13,000 to 15,000 deaths were reported each year.
After diphtheria toxoid-containing vaccines became
available in the 1940s, the number of cases gradually
declined to about 19,000 in 1945 (15 cases per 100,000
population). A more rapid decrease began with
implementation of a universal childhood vaccination
program which included diphtheria toxoid-containing
vaccines beginning in the late 1940s.
From 1996 through 2018, 14 cases of diphtheria were
reported in the United States, an average of less than 1
per year. One fatal case occurred in a 63-year-old male
returning to the United States from a country with
endemic diphtheria disease.
Within the United States, coverage with diphtheria
toxoid childhood vaccines (DTaP) has been
consistently high. Among children born during 2016
–
2017, 93.3% had received at least 3 doses of DTaP
vaccine by age 24 months, and 80.6% had received at
least 4 doses of DTaP vaccine by age 24 months.
Coverage with the adolescent and adult diphtheria
toxoid vaccines (Tdap or Td) is variable: Tdap coverage
among adolescents age 13 through 17 years reached
90.2% in 2019.
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