CORYNEBACTERIUM AND LISTERIA

(NON-SPORE-FORMING RODS)
Both of these gram-positive rods
infect patients in the pediatric age
group.
 Corynebacterium diphtheriae
• Corynebacterium diphtheriae is the pathogen
responsible for diphtheria. It colonizes the
pharynx, forming a grayish pseudomembrane
composed of fibrin, leukocytes,necrotic epithelial
cells, and Corynebacterium diphtheriae cells.
• From this site, the bacteria release a powerful
exotoxin into the bloodstream, which specifically
damages heart and neural cells by interfering
with protein synthesis.
• While working in the pediatric emergency room, you see
a child with a sore throat and fever. There is a dark
inflammatory exudate on the child's pharynx, which
appears darker and thicker than that of strep throat.
• Although you may feel the urge to scrape off this tightly
adherent pseudomembrane, you must resist this
temptation,because bleeding will occur and the systemic
absorption of the lethal exotoxin will be enhanced.
• Being the brightest medical student in the pediatric
emergency room, you immediately recognize.
• Immediately send the throat and nasopharynx swabs for
culture on potassium tellurite agar and Loeffler's
coagulated blood serum media.
• However , these culture results will not be ready for
days!!! You may try a Gram stain of a specimen from the
pseudomembrane,but gram-positive rods are not always
seen.
• Since there is no time to loaf with diphtheria, it is often
best to proceed rapidly to treatment via the following 3-
step method.
1) Antitoxin:
• The diphtheria antitoxin only inactivates circulating toxin, which has not yet target
tissue, so this must be administered quickly to prevent damage to the heart and
nervous system.
2) Penicillin or erythromycin:
Either antibiotic will kill the bacteria, preventing further exotoxin
release and rendering the patient non-contagious.
3) DPT vaccine:
The child must receive the DPT vaccine, as infection by Corynebacterium diphtheriae
does not always result in immunity to future infection by this organism. The DPT vaccine
stands for:
D = Diphtheria;
P = Pertussis (Whooping Cough); and
T = Tetanus.
The diphtheria portion contains formalin inactivated diphtheria toxin.
• Now that therapy has been administered, we can sit
back, relax, and confirm our clinical suspicion of
diphtheria.
• On the potassium-tellurite plate, colonies of
Corynebacterium diphtheriae become gray to black
within 24 hours.
• With Loeffler's coagulated blood serum, incubation
for 12 hours followed by staining with methylene
blue will reveal rod-shaped pleomorphic bacteria.
• Fortunately for nonimmunized children, not all
Corynebacterium diphtheriae secrete this exotoxin.
• Just as Group A beta-hemolytic streptococci must
first be lysogenized by a temperate bacteriophage
to produce the erythrogenic toxin that causes
scarlet fever,Corynebacterium diphtheriae first
must be lysogenized by a temperate bacteriophage
which codes for the diphtheria exotoxin.
• This powerful exotoxin contains two subunits. The B subunit
binds to target cells and allows the A subunit to enter the cell.
Once inside the cell, the A subunit blocks protein synthesis by
inactivating elongation factor( EF2), which is involved in
translation of eucaryotic mRNA into proteins .
• Notice an interesting comparison: Anti-ribosomal antibiotics
are specifically designed to inhibit protein synthesis in
bacterial (procaryotic) cells. Similarly, this exotoxin specifically
inhibits protein synthesis in humans (eucaryotes). Thus this
exotoxin can be considered a "human antibiotic,"because its
damage to heart and neural cells can be lethal.
 LISTERIA MONOCYTOGENES

• Listeria monocytogenes, a grampositive motile rod, actually has

endotoxin!
• is a common cause of meningitis in 2 particular groups.
• The first group is neonates, who contract this organism from
their asymptomatic mothers during delivery. Listeria
monocytogenes is the third most common cause of neonatal
meningitis, following only group B streptococci and Escherichia
coli.
• The second group of patients at risk for Listeria meningitis is
immunosuppressed patients,such as those with cancer, renal
transplants, or AIDS. The mortality rate for meningitis in this
second group is extremely high.
• You may wonder why this organism invades
neonates and certain immunosuppressed patients
but not an immune competent host. The main
reason is that Listeria monocytogenes is a resistant
fellow, able to hide out and survive within certain
immune cells, such as macrophages and neutrophils
that can phagocytose, or engulf, foreign objects such
as bacteria. Since they can survive either outside or
within cells, Listeria monocytogenes is called a
facultative intracellular organism.
• However, in immune competent hosts, the
immune system can release factors that
activate the macrophage, so that these cells
can now destroy the "vagrant" bacteria within
them. Immunologists refer to this immune
system-mediated method of destroying
Listeria as cell-mediated immunity.
• However,neonates (up to 3 months of age) and
immuno suppressed patients are unable to
activate their phagocytic cells, thus allowing
Listeria monocytogenes to flourish and infect the
meninges.
• Since pregnancy may also depress cell-mediated
immunity, Listeria monocytogenes can infect
pregnant women as well, who may develop
meningitis or remain asymptomatic carriers.
• When meningitis develops in a patient who is at high risk
for Listeria monocytogenes, it is important to treat it
empirically with antibiotics that will cover this bacterium.
• After a lumbar puncture confirms that this is a bacterial
meningitis (cerebrospinal fluid analysis reveals a high
number of neutrophils, a high protein level, a low glucose,
and the Gram stain of the cerebrospinal fluid may
demonstrate gram-positive rods), we must add either
ampicillin or trimethoprim-sulfamethoxazole to the
antibiotic regimen. These are 2 antibiotics that cover
Listeria monocytogenes.