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mariam kavtaria

on 7 October 2018

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Transcript of DIPHTHERIA


C. diphtheriae is transmitted via the
aerosol route during close contact
There are no reservoirs other than humans.
Before the vaccine the disease was seen primarily
in children and nonimmune young adults.

Is the primary
virulence factor
The toxin is produced in the pseudomembranous lesion and is taken up into the bloodstream, through which it is distributed to all organ systems.
Toxin causes ADP ribosylation of elongation factor 2 and thus leads to
irreversible inhibition of protein synthesis
The result is the death of the cell.

Punched-out ulcerative lesions
- most commonly on the extremities
or pseudomembrane formation
The diagnosis requires cultivation of C. diphtheriae from lesions
Nonhealing or enlarging skin ulcers -
may be associated with a preexisting wound or eczema, psoriasis, and venous stasis
The lesions rarely exceed 5 cm.

Airway obstruction
- Pseudomembranes may
slough and obstruct the Airways
Children are particularly prone to obstruction because of their small airways

Mariam Kavtaria
The incubation period is 2–5 days
The clinical diagnosis is based on the constellation of :
Sore throat
Adherent tonsillar, pharyngeal, or nasal
Low-grade fever

Diagnosis requires the
isolation of C. diphtheriae
The Centers for Disease Control and Prevention (CDC) recognizes:
Confirmed respiratory diphtheria
- laboratory proven
Probable diphtheria
- clinically compatible but not laboratory proven

The systemic manifestations stem from the effects of diphtheria toxin:
- result of neurotoxicity
Cardiac arrhythmias
congestive heart failure
due to
"bull-neck" diphtheria - massive edema of the submandibular and paratracheal region characterized by foul breath, thick speech, and stridorous breathing.

Respiratory diphtheria should be suspected in patients with
sore throat
pharyngeal exudates
should raise suspiction of diphtheria.
Once a clinical diagnosis of diphtheria is made,
diphtheria antitoxin
should be administered as soon as possible.
Laboratory diagnosis :
of C. diphtheriae from the site of infection
demonstration of lesions with characteristic histopathology
Throat samples should be submitted to the laboratory for culture with the notation that diphtheria is being considered
Patients in whom cutaneous diphtheria is identified should have the nasopharynx cultured for C. diphtheriae.
Respiratory diphtheria remains a notifiable disease in the United States, whereas cutaneous diphtheria is not.

Eradication of C. diphtheriae
should be documented
after antimicrobial therapy is complete.
repeat throat culture 2 weeks later
If the organism is not eradicated after a 14-day course of erythromycin or penicillin,
an additional 10-day course
followed by repeat culture is recommended.
Treatment of Cutaneous diphtheria is the same as for respiratory disease.
Individuals infected with toxigenic strains should receive antitoxin.

Risk factors for death:
Bull-neck diphtheria;
Ventricular tachycardia;
Atrial fibrillation;
Complete heart block;
Age >60 years or <6 months;
Pseudomembrane elongation
Laryngeal, tracheal, or bronchial involvement


toxoids and
acellular pertussis
vaccine - 5 recommended doses for children up to the 7:
2mo, 4mo, 6mo, 15mo, 18mo, 4-6y
Adults receive a
single dose of Tdap

Continue with
Td every 10 years

Intervals <10 years for:
health care workers,
adults who have contact with infants,
adults not previously vaccinated for pertussis.

Contacts of diphtheria cases should undergo
throat culture
to determine whether they are carriers
Antimicrobial prophylaxis should given to

all close contacts
, even those who are culture-negative.
The options are:
7–10 days of
oral erythromycin
One dose of
IM benzathine penicillin G

Contacts with uncertain immunization status should receive the
diphtheria toxoid vaccine.
- as the booster for adults who have not received an acellular pertussis vaccine.
Carriers of C. diphtheriae in the community should be treated and vaccinated when identified

Causes a
Produces diphtheria toxin and dermonecrotic toxin.

The organism causes
exudative pharyngitis
in individuals exposed to cattle.
cutaneous disease
has also been reported.
In contrast to diphtheria, C. ulcerans infection is considered a
have been identified as a source of human infection;
Person-to-person transmission has not been established


Antitoxin and antibiotics
should be initiated
Investigation in close contacts to determine the need for antimicrobial prophylaxis and vaccination
- the first-line agents

Infections are rare and are reported almost exclusively from

Causes suppurative
granulomatous lymphadenitis
Eosinophilic pneumonia
- among individuals who handle
horses, cattle, goats, and deer
or who drink
unpasteurized milk
Important veterinary pathogen but is rarely a human pathogen.
Successful treatment with
erythromycin or tetracycline
has been reported, with surgery also performed when indicated

Important opportunistic pathogen among

neutropenic patients

sepsis -
can occur in conjunction with
endocarditis, meningitis, osteomyelitis, or epidural abscess
Risk factors are:
hematologic malignancy
prolonged hospitalization,
Exposure to multiple antibiotics
Skin disruption.
C. jeikeium can become the part of normal flora in hospitalized patients.

It is resistant to most antibiotics tested
except for vancomycin.
Effective therapy involves
removal of the source of infection
, be it a catheter, a prosthetic joint, or a prosthetic valve.

Urease-positive nondiphtherial Corynebacterium
opportunistic cause of
sepsis and urinary tract infection
severe urinary tract syndrome -
alkaline-encrusted cystitis
a chronic bladder infection
Deposition of ammonium magnesium phosphate
on the walls of the bladder.

Related to the corynebacteria.
Gram-positive coccobacilli

The organisms vary in length; appear as
spherical to long, curved, clubbed rods;
produce large, irregular mucoid colonies.
Infections in
cattle, sheep, and swine
cause of
Tuberculosis-like infections
in humans.
intracellular pathogen of macrophages
, R. equi can cause granulomatous necrosis and caseation.
Nodular cavitary pneumonia
of the upper lobe—a picture similar to tuberculosis
Most patients are
Subcutaneous nodular lesions have also been identified.
Infection is treated with
macrolides, clindamycin, rifampin, trimethoprim-sulfamethoxazole, tigecycline, and linezolid
The organism is susceptible to vancomycin
Diphtheria Toxin
formalinization of toxin resulted in the production of
diphtheria toxoid
, which is:
Highly immunogenic.
Immunization with diphtheria toxoid

Elicits antibodies
Neutralizes the toxin
Prevents manifestations of diphtheria
Mucosal ulcers with a
In advanced diphtheria the pseudomembranes
turn gray/green as necrosis progresses
Mucosal ulcers
toxin-induced necrosis
of the epithelium plus edema, hyperemia, and vascular congestion of the submucosa.
fibrinosuppurative exudate
from the ulcer develops into the pseudomembrane.
The pseudomembrane in diphtheria is
tightly adherent to the underlying tissues
Attempts to dislodge the membrane
causes bleeding
suggests laryngeal diphtheria
Large pseudomembranes are associated with severe disease and a poor prognosis.
Characteristic findings of diphtheria
C. diphtheriae is a:
Club-shaped bacillary appearance
Forms clusters that look like Chinese characters.
(tox–) or
(tox+) strains.
Toxigenic strains
produce toxin
that causes systemic toxicity, myocarditis, and polyneuropathy
nasopharyngeal and skin infection caused by
Corynebacterium diphtheriae
The development of
diphtheria antitoxin and diphtheria toxoid vaccine
led to the near-elimination of diphtheria in Western countries
Diphtheria is still common in countries where mass immunization programs are not enforced.
Respiratory Diphtheria

Carriers = individuals who have positive cultures for C. diphtheriae but lack pseudomembranes
Pseudomembranes in severe cases may extend from the pharynx into medium bronchi.
Sloughing of membranes may result in
fatal airway obstruction
Cutaneous Diphtheria
was seen in 22% and
neuropathy in 5% of patients.

The mortality rate was
7% with myocarditis
2% among patients without myocardial manifestations.
The median time to death in hospitalized patients was 4.5 days.
Neurologic manifestations appears during the 1st or 2nd week of illness
1. Begins with
dysphagia and nasal dysarthria

2. Progresses to:
Weakness of the tongue and facial numbness
Blurred vision
due to paralysis of cilliary Muscles (accommodation), intact light reflex.
May be followed by respiratory muscle weakness requiring
artificial ventilation.
Several weeks later - a
generalized sensorimotor polyneuropathy
may appear, with prominent autonomic manifestations (hypotension).
Findings on lumbar puncture -
elevated protein
without pleocytosis
Diphtheria neuropathy is a
noninflammatory demyelinating disorder
mediated by the exotoxin.
Gradual improvement
- in patients who survive the acute phase.
Other complications include:
pneumonia, renal failure, encephalitis, cerebral infarction, and pulmonary embolism.
Serum sickness can result from treatment with diphtheria antitoxin
Late manifestations of diphtheria:
- Arrhythmias and dilated cardiomyopathy
Outbreak in the
Kyrgyz Republic in 1995
C. pseudodiphtheriticum,
a nontoxigenic organism, is a common component of the normal throat flora and does not pose a significant risk.
Administration of
is critical in the management of respiratory diphtheria.
Reduces the extent of local disease
Reduces the risk of complications - myocarditis and neuropathy.
Reduces the mortality risk
cannot neutralize cell-bound toxin
, that's why prompt initiation is important.
Patients who are allergic require
before a full dose of antitoxin is administered.

Penicillin G

IM until the patient can swallow comfortably, then
oral penicillin V
- a 14-day course

- until the patient can swallow comfortably.
Alternative agents for patients
who are allergic to penicillin or cannot take erythromycin
Cutaneous diphtheria has a low mortality rate and is rarely associated with myocarditis or peripheral neuropathy.
Interval between disease development and antitoxin administration is important predictor of fatal outcome
Prophylaxis of Contacts
C. Ulcerans
C. pseudotuberculosis (ovis)
C. Jeikeium (Group JK)
C. Urealyticum (Group D2)
this fluorescent microbe - The dermatologic presentation is
has been associated with
in patients with hematologic malignancy.
topical erythromycin, clarithromycin, clindamycin
More severe infections may require
oral macrolide
C. minutissimum - Cause of Erythrasma
Cutaneous infection with
reddish-brown, macular, scaly, pruritic patches
An agent that caused wound infections in
U.S. soldiers in the South Pacific during World War II
Commensal of the
human nasopharynx and skin
Cause of
pharyngitis and chronic skin ulcers
Pharyngitis is associated with a
scarlatiniform rash
in half of cases;
Primarily affects teenagers,
Has also been reported as a cause of
bacteremia, soft tissue infection, osteomyelitis, and cavitary pneumonia
, in the setting of underlying
diabetes mellitus
The organism is susceptible to
beta-lactams, macrolides, fluoroquinolones, clindamycin, vancomycin, and doxycycline
. .
Arcanobacterium Haemolyticum
Actinomyces Pyogenes
A cause of
seasonal leg ulcers
in humans in
rural Thailand,
pathogen of cattle, sheep, goats, and pigs.
Human cases of
sepsis, endocarditis, septic arthritis, pneumonia, meningitis, and empyema
have been reported.
Is susceptible to
beta-lactams, tetracycline, aminoglycosides, and fluoroquinolones
Harrison's Principles of Internal Medicine - 18th edition
Obstructive uropathy
has been reported in renal transplant recipients.
C. urealyticum has been associated with pneumonia, peritonitis, endocarditis, osteomyelitis, and wound infection.
Resistant to most antibiotics
except vancomycin
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