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Gram-Positive Rods

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Yasmeen Yahya

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Transcript of Gram-Positive Rods

Gram-Positive Rods
Chapter 17
AP. Dr. Said S. AlGhora
*INTRODUCTION
*SPORE-FORMING
GRAM-POSITIVE RODS:
Bacillus
Clostridium
*NON-SPORE-FORMING
GRAM-POSITIVE RODS:
Corynebacterium diphtheriae
Listeria monocytogenes
CHAPTER CONTENT
There are four medically important genera of gram-positive rods:
Bacillus
,
Clostridium
,
Corynebacterium
, and
Listeria
. Bacillus and Clostridium form spores, whereas Corynebacterium and Listeria do not. Members of the genus Bacillus are aerobic, whereas those of the genus Clostridium are anaerobic.
INTRODUCTION
These gram-positive rods can also be distinguished based on their appearance on Gram stain.
Bacillus
and
Clostridium
species are
longer
and
more deeply staining
than Corynebacterium and Listeria species.
Corynebacterium
species are
club-shaped
(i.e., they are thinner on one end than the other). Corynebacterium and
Listeria
species characteristically appear as
V- or L-shaped
rods.
SPORE-FORMING GRAM-POSITIVE RODS
BACILLUS
CLOSTRIDIUM
There are two medically important Bacillus species: Bacillus anthracis and Bacillus cereus.
1. Bacillus anthracis
Hello, I'm B. anthracis.
I'm a Gram Positive rod that can form a spore.
I can live in the soil for years and still be dangerous.
I cause anthrax.
I kill cattle and horses and humans that touch the animals.

I can act in three different ways.
When I get through your skin I make a black scab and fever.
When I'm inhaled I look like flu, but then I suddenly get you in 24 hours.
I get into your gut in uncooked meat.

If you don't take antibiotics, I'm almost always fatal.
Because I kill quickly, I'm sometimes used by armies as a biological weapon
B. anthracis causes anthrax, which is common in animals but rare in humans. Human disease occurs in three main forms:
cutaneous
,
pulmonary
(inhalation), and
gastrointestinal
. In 2001, an outbreak of both inhalation and cutaneous anthrax occurred in the United States. The outbreak was caused by sending spores of the organism through the
mail
. As of this writing, there were 18 cases, of whom 5 died.
Important Properties
B. anthracis is a large gram-positive rod with square ends, frequently found in chains. Its
antiphagocytic capsule
is composed of
D-glutamate
. (This is unique-capsules of other bacteria are polysaccharides.) It is
nonmotile
, whereas other members of the genus are motile. Anthrax toxin is encoded on one plasmid and the polyglutamate capsule is encoded on a different plasmid.
Transmission
Spores of the organism persist in
soil
for years. Humans are most often infected
cutaneously
at the time of trauma to the skin, which allows the spores on animal products, such as hides, bristles, and wool, to enter. Spores can also be inhaled into the respiratory tract. Pulmonary (
inhalation
) anthrax occurs when spores are inhaled into the lungs. Gastrointestinal anthrax occurs when
contaminated meat
is ingested.
Inhalation anthrax is
not communicable from person-to-person
, despite the severity of the infection. After being inhaled into the lung, the organism moves rapidly to the mediastinal lymph nodes, where it causes
hemorrhagic mediastinitis
. Because it leaves the lung so rapidly, it is not transmitted by the respiratory route to others.
Pathogenesis
Pathogenesis is based primarily on the production of
two exotoxins
, collectively known as
anthrax toxin
. The two exotoxins,
edema factor
and
lethal factor
, each consist of two proteins in an A-B subunit configuration. The B, or binding, subunit in each of the two exotoxins is
protective antigen
. The A, or active, subunit has enzymatic activity.
Edema factor
, an exotoxin, is an adenylate cyclase that causes an increase in the intracellular concentration of cyclic AMP. This causes an
outpouring
of fluid from the cell into the extracellular space, which manifests as
edema
. (Note the similarity of action to that of cholera toxin.)
Lethal factor
is a protease that cleaves the phosphokinase that activates the mitogen-activated protein kinase
(MAPK)
signal transduction pathway. This pathway controls the growth of human cells, and cleavage of the phosphokinase
inhibits cell growth
.
Protective antigen
forms
pores
in the human cell membrane that allows edema factor and lethal factor to enter the cell. The name protective antigen refers to the fact that
antibody against this protein protects against disease.
Clinical Findings
The typical lesion of cutaneous anthrax is a
painless ulcer
with a black eschar (
crust, scab
). Local edema is striking. The lesion is called a
malignant pustule
. Untreated cases progress to bacteremia and death.
Pulmonary (inhalation) anthrax, also known as
"woolsorter's disease"

begins with nonspecific respiratory tract symptoms resembling influenza, especially a dry cough and substernal pressure. This rapidly progresses to
hemorrhagic mediastinitis
, bloody pleural effusions, septic shock, and death. Although the lungs are infected, the classic features and x-ray picture of pneumonia are not present. Mediastinal widening seen on chest x-ray is an important diagnostic criterion. Hemorrhagic mediastinitis and
hemorrhagic meningitis
are severe life-threatening complications.
The symptoms of gastrointestinal anthrax include vomiting, abdominal pain, and bloody diarrhea.
Laboratory Diagnosis
Smears show large, gram-positive rods in chains.
Spores
are usually
not seen
in smears of exudate because spores form when nutrients are insufficient, and nutrients are plentiful in infected tissue.
Nonhemolytic colonies
form on blood agar aerobically.
In case of a bioterror attack, rapid diagnosis can be performed in special laboratories using polymerase chain reaction
(PCR)-based assays
. Another rapid diagnostic procedure is the
direct fluorescent antibody test
that detects antigens of the organism in the lesion. Serologic tests, such as an
ELISA
test for antibodies, require acute and convalescent serum samples and can only be used to make a diagnosis retrospectively.
Ciprofloxacin
is the drug of choice. Doxycycline is an alternative drug. No resistant strains have been isolated clinically.
Treatment
Prevention
Ciprofloxacin or doxycycline was used as prophylaxis in those exposed during the outbreak in the United States in 2001. People at high risk can be immunized with
cell-free vaccine containing purified protective antigen
as immunogen. The vaccine is weakly immunogenic, and six doses of vaccine over an 18-month period are given. Annual boosters are also given to maintain protection. Incinerating animals that die of anthrax, rather than burying them, will prevent the soil from becoming contaminated with spores
2. Bacillus cereus
Hello.
My name is B. cereus.
I'm a Gram Positive rod and I can form spores if I want.

I love rice!
Rice is one of my favourite places to live, especially if it's been reheated over and over.
You can get food poisoning from me that will give you diarrhea and vomiting.
I use a special toxin to make you sick.
B. cereus causes
food poisoning
.
Spores on grains such as rice survive steaming and rapid frying. The spores germinate
when rice is kept warm for many hours
(e.g., reheated fried rice). The portal of entry is the gastrointestinal tract.
Transmission
Pathogenesis
B. cereus produces
two enterotoxins
. The mode of action of one of the enterotoxins is the same as that of cholera toxin; i.e., it adds adenosine diphosphate-ribose, a process called
ADP-ribosylation
, to a G protein, which stimulates adenylate cyclase and leads to an increased concentration of cyclic adenosine monophosphate (AMP) within the enterocyte. The mode of action of the other enterotoxin resembles that of staphylococcal enterotoxin; i.e., it is a
superantigen
.
Clinical Findings
There are two syndromes:

(1) one has a
short
incubation period (4 hours) and consists primarily of nausea and vomiting,
similar to staphylococcal
food poisoning;

(2) the other has a
long
incubation period (18 hours) and features watery, nonbloody diarrhea,
resembling clostridial
gastroenteritis.
Laboratory diagnosis is not usually done.

Only symptomatic treatment is given.

No specific means of prevention. Rice should not be kept warm for long periods.

There are four medically important species:
Clostridium tetani
,
Clostridium botulinum
,
Clostridium perfringens
(which causes either gas gangrene or food poisoning), and
Clostridium difficile
. All clostridia are
anaerobic
, spore-forming, gram-positive rods
1. Clostridium tetani
2. Clostridium botulinum
3. Clostridium perfringens
4. Clostridium difficile
Hello, my name is C. tetani.
I am a gram Positive rod bacteria.
I'm anaerobic, but I can make spores.
I live in the soil and my spores get into your cuts.

Then I use a toxin that moves up into your central nervous system (your spine and brain).
The toxin makes your muscle contract, or spasm.
You can get lockjaw in your face or a smiling spasm called risus sardonicus.
I also get into your back, arms and breathing muscles.

Most people have vaccines that stop me getting into them.
Transmission
Spores are widespread in
soil
. The portal of entry is usually a
wound site
, e.g., where a nail penetrates the foot, but the spores can also be introduced during "skin-popping," a technique used by drug addicts to inject drugs into the skin. Germination of spores is favored by necrotic tissue and poor blood supply in the wound.
Neonatal tetanus
, in which the organism enters through a
contaminated umbilicus
or circumcision wound, is a major problem in some developing countries.
Tetanus toxin (
tetanospasmin
) is an exotoxin produced by vegetative cells at the wound site. This polypeptide toxin is carried intra-axonally (
retrograde
) to the central nervous system, where it binds to ganglioside receptors and
blocks release of inhibitory mediators
(e.g., glycine) at spinal synapses.
Tetanus
toxin and
botulinum
toxin are among the
most toxic substances known
. They are proteases that cleave the proteins involved in mediator release.
Pathogenesis
Tetanus toxin has one antigenic type, unlike botulinum toxin, which has eight. There is therefore only
one antigenic type
of tetanus toxoid in the vaccine against tetanus.
Clinical Findings
Tetanus is characterized by strong muscle spasms (
spastic paralysis, tetany
). Specific clinical features include
lockjaw
(
trismus
) due to rigid contraction of the jaw muscles, which prevents the mouth from opening; a characteristic grimace known as
risus sardonicus
; and exaggerated reflexes.
Opisthotonos
, a pronounced arching of the back due to spasm of the strong extensor muscles of the back, is often seen. Respiratory failure ensues. A high mortality rate is associated with this disease. Note that in tetanus, spastic paralysis (strong muscle contractions) occurs, whereas in
botulism
,
flaccid paralysis
(weak or absent muscle contractions) occurs.
Laboratory Diagnosis
There is no microbiologic or serologic diagnosis. Organisms are rarely isolated from the wound site. C. tetani produces a
terminal spore
, i.e., a spore at the end of the rod. This gives the organism the characteristic appearance of a "
tennis racket
."
Tetanus immune globulin
is used to neutralize the toxin. The role of antibiotics is uncertain.
Treatment
Prevention
Tetanus is prevented by
immunization
with tetanus toxoid (formaldehyde-treated toxin) in childhood and every 10 years thereafter.
Tetanus toxoid
is usually given to children in combination with diphtheria toxoid and the acellular pertussis vaccine (
DTaP
).
When trauma occurs, the wound should be cleaned and debrided and
tetanus toxoid booster
should be given. If the wound is grossly contaminated,tetanus immune globulin, as well as the toxoid booster, should be given and penicillin administered. Tetanus immune globulin (tetanus antitoxin) is made in humans to avoid
serum sickness
reactions that occur when antitoxin made in horses is used. The administration of both immune globulins and tetanus toxoid (at
different sites
in the body) is an example of passive-active immunity.
Hello, I'm C. botulinum.
I'm Gram Positive and rod shaped.
I make spores.
I live in soil and in foods like cans of beans.
I can live in them for a very long time, even if they get cooked.
I secrete botulin toxin which is carried to your nerves.

I cause botulism.
Your muscles get very weak and floppy, especially your respiratory muscles.
You may not be able to see, swallow or even breath.
Transmission
Spores, widespread in soil, contaminate vegetables and meats. When these foods are canned or vacuum-packed without adequate sterilization, spores survive and germinate in the anaerobic environment. Toxin is produced within the
canned food
and ingested preformed. The highest-risk foods are (1)
alkaline vegetables
such as green beans, peppers, and mushrooms and (2)
smoked fish
. The toxin is relatively
heat-labile
; it is inactivated by boiling for several minutes. Thus, disease can be prevented by sufficient cooking.
Pathogenesis
Botulinum toxin is absorbed from the gut and carried via the blood to peripheral nerve synapses, where it
blocks release of acetylcholine
. It is a protease that cleaves the proteins involved in acetylcholine release. The toxin is a polypeptide encoded by a lysogenic phage. Along with tetanus toxin, it is among the most toxic substances known.
There are
eight immunologic types
of toxin; types A, B, and E are the most common in human illness.
Botox
is a commercial preparation of exotoxin
A
used to remove wrinkles on the face. Minute amounts of the toxin are effective in the treatment of certain spasmodic muscle disorders such as
torticollis
,
"writer's cramp,"
and
blepharospasm
.
Clinical Findings
Descending weakness
and paralysis, including diplopia, dysphagia, and respiratory muscle failure, are seen. No fever is present.
In contrast, Guillain-Barré syndrome
is an
ascending paralysis

Two special clinical forms occur:
(1) wound botulism, in which spores contaminate a wound, germinate, and produce toxin at the site;
(2) infant botulism, in which the organisms grow in the gut and produce the toxin there. Ingestion of
honey
containing the organism is implicated in transmission of infant botulism. Affected infants develop weakness or paralysis and may need respiratory support but usually recover spontaneously.
In the United States, infant botulism accounts for about half of the cases of botulism, and wound botulism is associated with
drug abuse
, especially skin-popping with black tar heroin.
Laboratory Diagnosis
The organism is usually not cultured. Botulinum toxin is demonstrable in uneaten food and the patient's serum by
mouse protection tests
. Mice are inoculated with a sample of the clinical specimen and will die unless protected by antitoxin.
Treatment
Trivalent antitoxin
(types A, B, and E) is given, along with respiratory support. The antitoxin is made in horses, and serum sickness occurs in about 15% of antiserum recipients.
Prevention
Proper sterilization
of all canned and vacuum-packed foods is essential. Food must be
adequately cooked
to inactivate the toxin. Swollen cans must be discarded (clostridial proteolytic enzymes form gas, which swells cans).
Hello
My name is C. perfringens.
I'm a Gram Positive rod and anaerobic.
I live in soil and can make spores to survive to for a long time.

I can cause myonecrosis, or "gas gangrene".
I get into your muscles in wounds and make toxins.
As I eat away at your muscles, I let off gases that build up between them.

When I am "type A", I can cause food poisoning.
I live in undercooked meat and make spores in your gut.
I make an enterotoxin that gives you cramping and diarrhoea.

My "type C" form causes "necrotising enteritis".
You have to eat undercooked pork with me in it.
You also have to eat alot of foods like sweet potatoes, which have a chemical called trypsin inhibitor in them.
When they are together, I can make my B-toxin and eat away at your bowels
Hello, my name is C. difficile.
I'm an anaerobic, Gram Positive rod that can make spores.
I live in your digestive tract.

I cause pseudomembranous colitis.
Sometimes if you take broad spectrum antibiotics (especially clindamycin and the cephalosporins) you kill off your friendly bacteria.
That leaves lots of room for me.
I make toxins that cause very bad inflammation.
You get diarrhea, abdominal pain and a fever.

I covered myself in a white membrane like coating that can be seen on the inside of your intestines.
Transmission
Spores are located in the soil and can contaminate food. ; vegetative cells are members of the normal flora of the colon and vagina.

Gas gangrene is associated with
war wounds
, automobile and motorcycle accidents, and septic abortions (endometritis).

The heat-resistant spores survive cooking and germinate. The organisms grow to large numbers in reheated foods, especially
meat dishes
.
Gas gangrene
(myonecrosis, necrotizing fasciitis)
Organisms grow in traumatized tissue (especially muscle) and produce a variety of toxins. The most important is
alpha toxin
(
lecithinase
), which damages cell membranes, including those of erythrocytes, resulting in hemolysis. Degradative enzymes produce gas in tissues.
Pain, edema, and cellulitis occur in the wound area.
Crepitation
indicates the presence of gas in tissues. Hemolysis and jaundice are common, as are blood-tinged exudates. Shock and death can ensue. Mortality rates are high.
C. perfringens is a member of the normal flora in the colon but
not
in the
small bowel
, where the enterotoxin acts to cause diarrhea. The mode of action of the enterotoxin is the same as that of the enterotoxin of S. aureus; i.e., it acts as a
superantigen
.
Food Poisoning
The disease has an
8 to 16
hour incubation period and is characterized by watery diarrhea with cramps and little vomiting. It resolves in 24 hours.
Diagnosis
This is not usually done. There is no assay for the toxin. Large numbers of the organisms can be isolated from uneaten food.
In case of food poisioning,,
In case of gas gangrene,,
Smears of tissue and exudate samples show large gram-positive rods. Spores are not usually seen because they are formed primarily under nutritionally deficient conditions. The organisms are
cultured anaerobically
and then identified by
sugar fermentation reactions
and organic acid production.
C. perfringens
colonies exhibit a
double zone of hemolysis
on blood agar.
Egg yolk
agar is used to demonstrate the presence of the
lecithinase
. Serologic tests are not useful.
Treatment
Penicillin G is the antibiotic of choice. Wounds should be debrided.
Food Poisoning
Symptomatic treatment is given; no antimicrobial drugs are administered.
Gas Gangrene
Prevention
Food should be adequately cooked to kill the organism.

Wounds should be cleaned and debrided. Penicillin may be given for prophylaxis. There is no vaccine.
C. difficile is the most common nosocomial cause of diarrhea.
Transmission
The organism is carried in the
gastrointestinal tract
in approximately 3% of the general population and up to 30% of hospitalized patients.
Most people are not colonized
, which explains why most people who take antibiotics do not get
pseudomembranous colitis
. It is transmitted by the
fecal-oral route
. The hands of hospital personnel are important intermediaries.
Pathogenesis
Antibiotics suppress drug-sensitive members of the normal flora, allowing C. difficile to multiply and produce exotoxins A and B. Both exotoxin A and exotoxin B are enzymes that glucosylate (add glucose to) a G protein called
Rho GTPase
. The main effect of exotoxin B in particular is to cause depolymerization of actin, resulting in a
loss of cytoskeletal integrity
,
apoptosis
, and
death of the enterocytes
.
Clindamycin
was the
first
antibiotic to be recognized as a cause of pseudomembranous colitis, but many antibiotics are known to cause this disease. At present,
second and third-generation cephalosporins
are the most common causes because they are so frequently used. Ampicillin and fluoroquinolones are also commonly implicated. In addition to antibiotics,
cancer chemotherapy
also predisposes to pseudomembranous colitis. C. difficile rarely invades the intestinal mucosa.
Clinical Findings
C. difficile causes diarrhea associated with pseudomembranes (
yellow-white plaques
) on the colonic mucosa. The diarrhea is usually not bloody, and neutrophils are found in the stool in about half of the cases.
Fever and abdominal cramping often occur. The pseudomembranes are visualized by sigmoidoscopy. Toxic megacolon can occur, and surgical resection of the colon may be necessary. Pseudomembranous colitis can be distinguished from the transient diarrhea that occurs as a side effect of many oral antibiotics by testing for the presence of the
toxin in the stool
.
In 2005, a new, more virulent strain of C. difficile emerged. This new strain causes more severe disease, is more likely to cause recurrences, and responds less well to metronidazole than the previous strain. The strain is also characterized by resistance to quinolones. It is thought that the widespread use of quinolones for diarrheal disease may have selected for this new strain.
Laboratory Diagnosis
The presence of exotoxins in a filtrate of the patient's stool specimen is the basis of the laboratory diagnosis. There are two types of tests usually used to detect the exotoxins. One is an enzyme-linked immunosorbent assay (
ELISA
) using known antibody to the exotoxins. The ELISA tests are rapid but are less sensitive than the cytotoxicity test.
In the
cytotoxicity test
, human cells in culture are exposed to the exotoxin in the stool filtrate and the death of the cells is observed. This test is more sensitive and specific but requires 24–48 hours' incubation time. To distinguish between cytotoxicity caused by the exotoxins and cytotoxicity caused by a virus possibly present in the patient's stool, antibody against the exotoxins is used to neutralize the cytotoxic effect.
The causative antibiotic should be withdrawn.
Oral
metronidazole
or
vancomycin
should be given and fluids replaced.
Fidaxomycin
(Dificid) is used both in the treatment of pseudomembranous colitis and in preventing relapses of this disease. It is effective in life-threatening cases.
Treatment
Prevention
There are no preventive vaccines or drugs. Antibiotics should be prescribed only when necessary.
NON-SPORE-FORMING GRAM-POSITIVE RODS
There are two important pathogens in this group: Corynebacterium diphtheriae and Listeria monocytogenes .
LISTERIA MONOCYTOGENES
CORYNEBACTERIUM DIPHTHERIAE
Hello.
My name is C. diphtheriae.
I'm a Gram Positive rod bacteria that can't form any spores.
I have an irregular shape.
I used to live in lots of places
Now I mostly live where people don't have vaccines for me.

I get into your throat and airway and make them swell up.
The swelling forms a covering, so you can't breath.
I give off toxins that hurt your heart and nerves.
Corynebacteria are gram-positive rods that appear
club-shaped
(wider at one end) and are arranged in palisades or in V- or L-shaped formations. The rods have a beaded appearance. The beads consist of granules of highly polymerized polyphosphate, a storage mechanism for high-energy phosphate bonds. The granules stain
metachromatically
; i.e., a dye that stains the rest of the cell blue will stain the granules
red
.
C. diphtheriae causes diphtheria. Other Corynebacterium species (diphtheroids) are implicated in opportunistic infections.
Transmission
Humans are the only natural host of C. diphtheriae. Both toxigenic and nontoxigenic organisms reside in the upper respiratory tract and are transmitted by
airborne droplets
. The organism can also infect the skin at the site of a preexisting
skin lesion
. This occurs primarily in the tropics but can occur worldwide in indigent persons with poor skin hygiene.
Pathogenesis
Although
exotoxin
production is essential for pathogenesis,
invasiveness
is also necessary because the organism must first establish and maintain itself in the throat. Diphtheria toxin inhibits protein synthesis by
ADP-ribosylation
of elongation factor 2 (
EF-2
). The toxin affects all eukaryotic cells regardless of tissue type but has no effect on the analogous factor in prokaryotic cells.
The toxin is a single polypeptide with two functional domains. One domain mediates binding of the toxin to glycoprotein receptors on the cell membrane. The other domain possesses enzymatic activity that cleaves nicotinamide from nicotinamide adenine dinucleotide (NAD) and transfers the remaining ADP-ribose to EF-2, thereby
inactivating
it.
The DNA that codes for diphtheria toxin is part of the genetic material of a
temperate bacteriophage
. During the lysogenic phase of viral growth, the DNA of this virus integrates into the bacterial chromosome and the toxin is synthesized. C. diphtheriae cells that are not lysogenized by this phage do not produce exotoxin and are nonpathogenic.
The host response to C. diphtheriae consists of:
1.
Local inflammation
in the throat, with a fibrinous exudate that forms the tough, adherent,
gray pseudomembrane
characteristic of the disease
2.
Antibody
that can neutralize exotoxin activity by blocking the interaction of fragment B with the receptors, thereby preventing entry into the cell. The immune status of a person can be assessed by
Schick's test
. The test is performed by intradermal injection of 0.1 mL of purified standardized toxin. If the patient has no antitoxin, the toxin will cause inflammation at the site 4–7 days later. If no inflammation occurs, antitoxin is present and the patient is immune. The test is rarely performed in the United States except under special epidemiologic circumstances.
Clinical Findings
Although diphtheria is rare in the United States, physicians should be aware of its most prominent sign, the thick, gray,
adherent pseudomembrane
over the tonsils and throat. The other aspects are nonspecific: fever, sore throat, and cervical adenopathy.
There are three prominent complications:
1. Extension of the membrane into the larynx and trachea, causing
airway obstruction
2.
Myocarditis
accompanied by arrhythmias and circulatory collapse
3. Nerve weakness or
paralysis
, especially of the cranial nerves. Paralysis of the muscles of the soft palate and pharynx can lead to regurgitation of fluids through the nose. Peripheral neuritis affecting the muscles of the extremities also occurs.
Cutaneous diphtheria causes
ulcerating skin
lesions covered by a gray membrane. These lesions are often indolent and often do not invade surrounding tissue. Systemic symptoms rarely occur. In the United States, cutaneous diphtheria occurs primarily in the indigent.
Laboratory Diagnosis
Laboratory diagnosis involves both isolating the organism and
demonstrating toxin production
. It should be emphasized that the decision to treat with antitoxin is a clinical one and cannot wait for the laboratory results. A
throat swab
should be cultured on
Löffler's medium
, a
tellurite plate
, and a
blood agar
plate. The tellurite plate contains a tellurium salt that is reduced to elemental tellurium within the organism.
The typical

gray-black color
of tellurium in the colony is a telltale diagnostic criterion. If C. diphtheriae is recovered from the cultures, either animal inoculation or an antibody-based gel diffusion precipitin test is performed to document toxin production. A
PCR assay
for the presence of the toxin gene in the organism isolated from the patient can also be used.
Smears of the throat swab should be stained with both
Gram stain
and
methylene blue
. Although the diagnosis of diphtheria cannot be made by examination of the smear, the finding of many tapered, pleomorphic gram-positive rods can be suggestive. The methylene blue stain is excellent for revealing the typical
metachromatic granules
.
The treatment of choice is
antitoxin
, which should be given immediately on the basis of clinical impression because there is a delay in laboratory diagnostic procedures. The function of antitoxin is to neutralize unbound toxin in the blood.
Treatment with
penicillin G
or erythromycin is also recommended, but neither is a substitute for antitoxin.
Treatment
Prevention
Diphtheria is very rare in the United States because children are immunized with
diphtheria toxoid
(usually given as a combination of diphtheria toxoid, tetanus toxoid, and acellular pertussis vaccine, often abbreviated as
DTaP
). Diphtheria toxoid is prepared by treating the exotoxin with formaldehyde. This treatment inactivates the toxic effect but leaves the antigenicity intact.
Immunization consists of three doses given at 2, 4, and 6 months of age, with boosters at 1 and 6 years of age. Because immunity wanes, a booster every 10 years is recommended. Immunization does not prevent nasopharyngeal carriage of the organism.
Hello hello.
I'm known as L. monocytogenes.
I'm a Gram Positive rod bacteria that can't form any spores.
I live in many meats, vegetables and dairy products.
My favorite foods are fancy soft cheeses, pate, coleslaw and sliced meats.

I am especially dangerous for babies, the elderly and those without a good immune system.
In these people I cause listeriosis, made up of bacteraemia and meningitis.
In pregnant women I cause granulomatosis infantiseptica.
The fetus becomes infected and sometimes dies.
L. monocytogenes causes
meningitis
and
sepsis
in
newborns
,
pregnant women
, and
immunosuppressed adults
. It also causes outbreaks of febrile gastroenteritis.
L. monocytogenes is a small gram-positive rod arranged in
V- or L-shaped
formations similar to corynebacteria. The organism exhibits an unusual
tumbling movement
that distinguishes it from the corynebacteria, which are nonmotile. Colonies on a blood agar plate produce a narrow zone of
beta-hemolysis
that resembles the hemolysis of some streptococci.
Listeria grows well at cold temperatures, so storage of contaminated food in the
refrigerator
can
increase the risk
of gastroenteritis. This paradoxical growth in the cold is called
"cold enhancement."
Pathogenesis
Listeria infections occur primarily in two clinical settings: (1) in the
fetus
or
newborn
as a result of transmission across the placenta or during delivery; and (2) in
pregnant women
and
immunosuppressed
adults, especially renal transplant patients. (Note that pregnant women have reduced cell-mediated immunity during the third trimester.)
The organism is distributed worldwide in animals, plants, and soil. From these reservoirs, it is transmitted to humans primarily by
ingestion of unpasteurized milk
products,
undercooked meat
, and
raw vegetables
. Contact with domestic farm animals and their feces is also an important source. In the United States, listeriosis is primarily a food-borne disease associated with eating unpasteurized cheese and delicatessen meats.
The pathogenesis of Listeria depends on the organism's
ability to invade and survive within cells
. Invasion of cells is mediated by
internalin
made by Listeria and
E-cadherin
on the surface of human cells. The ability of Listeria to pass the placenta, enter the meninges, and invade the gastrointestinal tract depends on the interaction of internalin and E-cadherin on those tissues.
Upon entering the cell, the organism produces
listeriolysin
, which allows it to escape from the phagosome into the cytoplasm, thereby escaping destruction in the phagosome. Because Listeria preferentially grows intracellularly, cell-mediated immunity is a more important host defense than humoral immunity. Suppression of cell-mediated immunity predisposes to Listeria infections.
L. monocytogenes can move from cell to cell by means of
actin rockets
, a filament of actin that contracts and propels the bacteria through the membrane of one human cell and into another.
Clinical Findings
Infection during pregnancy can cause
abortion
, premature delivery, or
sepsis
during the peripartum period. Newborns infected at the time of delivery can have
acute meningitis
1–4 weeks later. The bacteria reach the meninges via the bloodstream (bacteremia). The infected mother either is asymptomatic or has an influenza-like illness. L. monocytogenes infections in immunocompromised adults can be either sepsis or meningitis.
Gastroenteritis caused by L. monocytogenes is characterized by
watery diarrhea
, fever, headache, myalgias, and abdominal cramps but little vomiting. Outbreaks are usually caused by contaminated dairy products, but undercooked meats such as chicken and hot dogs have also been involved.
Laboratory Diagnosis
Laboratory diagnosis is made primarily by
Gram stain and culture
. The appearance of gram-positive rods resembling diphtheroids and the formation of small,
gray colonies
with a narrow zone of
beta-hemolysis
on a blood agar plate suggest the presence of Listeria. The isolation of Listeria is confirmed by the presence of
motile organisms
, which differentiate them from the nonmotile corynebacteria. Identification of the organism as L. monocytogenes is made by s
ugar fermentation tests
.
Treatment
trimethoprim-sulfamethoxazole
Prevention is difficult because there is no immunization. Limiting the exposure of pregnant women and immunosuppressed patients to potential sources such as farm animals, unpasteurized milk products, and raw vegetables is recommended. Trimethoprim-sulfamethoxazole given to immunocompromised patients to prevent Pneumocystis pneumonia can also prevent listeriosis.
Prevention
Self-Assessment Questions
This envelope contained anthrax that was mailed to Senator Patrick Leahy in 2001.
Courtesy of the Federal Bureau of
Investigation
THANK YOU
Yasmeen Y. Sarraj
That's enough for today
See you next time..
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