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mariam kavtaria

on 6 April 2017

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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 occur on the extremities
or pseudomembrane formation
The diagnosis requires cultivation of C. diphtheriae from lesions
Nonhealing or enlarging skin ulcers, which may be associated with a preexisting wound or dermatoses such as eczema, psoriasis, and venous stasis disease.
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:
1. Confirmed respiratory diphtheria - laboratory proven
2. 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 myocarditis.
"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
Pseudomembrane should raise suspiction of diphtheria.
Once a clinical diagnosis of diphtheria is made,
diphtheria antitoxin
should be administered as soon as possible.
Laboratory diagnosis :
culture of C. diphtheriae from the site of infection
or 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
is recommended.
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 - is the recommended for children up to the age of 7
Adults receive a single dose of Tdap
Continue with Td every 10 years
Intervals <10 years for Tdap vaccination of health care workers, adults anticipating contact with infants, and 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 who have an uncertain immunization status should receive the diphtheria toxoid vaccine.
- as the booster vaccine for adults who have not recently received an acellular pertussis vaccine.
Carriers of C. diphtheriae in the community should be treated and vaccinated when identified

Causes a diphtherialike illness
Produces diphtheria toxin and dermonecrotic toxin.

The organism causes
exudative pharyngitis
among individuals exposed to cattle.
cutaneous disease
has also been reported.
In contrast to diphtheria, C. ulcerans infection is considered a
Pigs 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
appear to be the first-line agents

Infections are rare and are reported almost exclusively from Australia.
Causes suppurative
granulomatous lymphadenitis
Eosinophilic pneumonia
syndrome among individuals who handle horses, cattle, goats, and deer or who drink unpasteurized milk.
The organism is an 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

The predominant syndrome is
, which 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
Effective therapy involves
removal of the source of infection
, be it a catheter, a prosthetic joint, or a prosthetic valve.

Urease-positive nondiphtherial Corynebacterium
Is an opportunistic cause of sepsis and urinary tract infection.
This organism is the cause of a severe urinary tract syndrome -
alkaline-encrusted cystitis
a chronic bladder infection with deposition of ammonium magnesium phosphate on the walls of ulcerating lesions in the bladder.

Obstructive uropathy
has been reported in renal transplant recipients.
C. urealyticum has been associated with pneumonia, peritonitis, endocarditis, osteomyelitis, and wound infection.
It is resistant to most antibiotics except
, which has been used successfully in the treatment of severe infections.

Related to the corynebacteria.
Gram-positive coccobacilli

cause of
Tuberculosis-like infections
in humans.
Infections in cattle, sheep, and swine
The organisms vary in length; appear as spherical to long, curved, clubbed rods; and produce large, irregular mucoid colonies.
intracellular pathogen of macrophages
, R. equi can cause granulomatous necrosis and caseation.
Disease manifests as nodular cavitary pneumonia of the upper lobe—a picture similar to that seen in 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.
A 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
Hoarseness suggests laryngeal diphtheria
Large pseudomembranes are associated with severe disease and a poor prognosis.
Characteristic findings of diphtheria
C. diphtheriae is a:
Nonsporulating bacillus.
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 are 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 and 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 -
raised levels of protein
without pleocytosis
Diphtheria neuropathy is a
noninflammatory demyelinating disorder
mediated by the exotoxin.
Gradual improvement
is the rule 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 antitoxin
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
to complete 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)
The dermatologic presentation is coral-red fluorescence.
this fluorescent microbe has been associated with
in patients with hematologic malignancy.
treatment: topical erythromycin, clarithromycin, clindamycin
More severe infections may require oral macrolide therapy.
C. minutissimum - Common 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,
A. pyogenes is a 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
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