Cmmrs 6+7 Gram Positive Rods

Front 1

which of the spore formers are aerobic?

Back 1

Bacillus enjoys
oxygen (so is aerobic), while Clostridium multiply in
an anaerobic environment. In an air tight Closet, if
you will!

Front 2

explain ""malignant pustule"

Back 2

exotoxin
causes localized tissue necrosis, evidenced by a painless
round black lesion with a rim of edema. This lesion is
called a "malignant pustule" because without antibiotic
therapy (penicillin), Bacillus anthracis can continue to
proliferate and disseminate through the bloodstream,
which can cause death. The skin lesion usually resolves
spontaneously in 80-90% of cases, but sometimes
severe skin edema and shock occur.

Front 3

how come woolsorter's disease is not
actually a pneumonia?

Back 3

. The spores are taken up by
macrophages in the lungs and transported to the hilar and
mediastinal lymph nodes where they germinate. Medi-
astinal hemorrhage occurs resulting in mediastinal
widening (enlarged area around and above the heart seen
on chest radiograph and CT scan) and pleural effusions.

Front 4

clinical presentation of GI anthrax?

Back 4

Patients present with
vomiting, abdominal pain, and bloody diarrhea.

Front 5

EF action?

Back 5

) Edema factor (EF) This is the active A subunit
of this exotoxin and is a calmodulin-dependent adeny-
late cyclase. It increases cAMP, which impairs neu-
trophil function and causes massive edema (disrupts
water homeostasis).

Front 6

PA function?

Back 6

Protective antigen (PA) promotes entry of EF
into phagocytic cells (similar to a B subunit of the other A-B toxins)

Front 7

LF function?

Back 7

Lethal factor (LF) is a zinc metalloprotease that
inactivates protein kinase. This toxin stimulates the
macrophage to release tumor necrosis factor a and in-
terleukin-1(3, which contribute to death in anthrax.

Front 8

pXO2 function?

Back 8

A second plasmid, pXO2, encodes three genes neces-
sary for the synthesis of a poly-glutamyl capsule. This
capsule inhibits phagocytosis of the vegetative bacteria.
Both plasmids are critical for bacterial virulence.

Front 9

pXO1 function?

Back 9

carries genes for EF, LF and PA

Front 10

is b.cereus motile? does it have a capsule?

Back 10

Bacillus cereus is different from Bacillus anthracis in
that it is motile, non-encapsulated, and resistant to
penicillin.

Front 11

what toxins are secreted by b.cereus?

Back 11

Bacillus cereus can secrete 2 types of enterotoxins,
which cause different kinds of food poisoning:
1) A heat-labile toxin similar to the enterotoxin of
cholera and the LT from Escherichia coli (see Fig. 2-8)
causes nausea, abdominal pain and diarrhea, lasting
12-24 hours.
2) A heat-stable toxin produces a clinical syndrome
similar to that of Staphylococcus aureus food poisoning,
with a short incubation period followed by severe nau-
sea and vomiting, with limited diarrhea.

Front 12

When a patient is rushed to the hospital with food
poisoning, and examination of the food reveals B.
cereus, what is the best way to respond when your attending orders you to treat the patient with antibiotics?

Back 12

"Be serious, Dr. Goofball." Since the food poisoning is caused by the pre-formed enterotoxin of Bacillus cereus, antibi-
otic therapy will not alter the course of this patient's symptoms.

Front 13

what diseases are clostridium famous for?

Back 13

botulism, tetanus,
gas gangrene, and pseudomembranous colitis.

Clostridium harm their human hosts by secreting ex-
tremely powerful exotoxins and enzymes. Rapid diag-
nosis of a clostridial infection is crucial, or your patient
will die!!!!

Front 14

what happens after someone ingests botulinotoxin? (e.g. from smoked fish, or canned vegetables, which is left open for spores to seed, and then packed into an anaerobic environment)

Back 14

These afebrile patients initially
develop bilateral cranial nerve palsies causing double
vision (diplopia) and difficulty swallowing (dysphagia).
This is followed by general muscle weakness, which
rapidly leads to sudden respiratory paralysis and death.

Front 15

treatment of botulism?

Back 15

Patients must immediately be treated with an anti-
toxin, which can neutralize only the unbound free neu-
rotoxin in the bloodstream. Intubation and ventilatory
support is critical until the respiratory muscles resume
activity.

Front 16

presentation of tetanus?

Back 16

Clinically, the patient with tetanus presents
with severe muscle spasms, especially in the muscles of
the jaw (this is called trismus, or lockjaw). The af-
fected patient exhibits a grotesque grinning expression,
called risus sardonicus, which is due to spasm of the
facial muscles. Mortality is high once the stage of lock-
jaw has been reached.

Front 17

which 3 types of patients will come to the clinic with skin wounds?

Back 17

1) Patients who were immunized as a child and re-
ceived periodic boosters but the last shot was more
than 10 years ago. These patients are given another
booster.
2) Patients who have never been immunized. Not
only do these patients need a booster, but they should
also receive preformed antibodies to the tetanus toxin
called human tetanus immune globulins.
3) Patients who come to the hospital having already
developed tetanus. The big picture is to clear the toxin
and the toxin-producing bacteria and to keep the pa-
tient alive until the toxin has cleared.

Front 18

5 steps of tetanus treatment?

Back 18

a) Neutralize circulating toxin with human
tetanus immune globulins.
b) Give an immunization booster to stimulate the
patient's own immune system to develop anti-
tetanus toxin antibodies.
c) Clean the wound, excising any devitalized tis-
sue, to remove any remaining source of Clostridium
tetani.
d) Antibiotics (penicillin) may help to clear the
remaining toxin-producing bacteria.
e) Provide intensive supportive therapy until the
toxin is cleared. Muscle relaxants may have to be
administered, and the patient may have to be placed
on a ventilator.

Front 19

describe the 2 types of manifestations of infections by clostridium perfringens?

Back 19

1) Cellulitis/wound infection: Necrotic skin is
exposed to Clostridium perfringens, which grows and
damages local tissue. Palpation reveals a moist, spongy,
crackling consistency to the skin due to pockets of gas;
this is called crepitus.
2) Clostridial myonecrosis: Clostridium perfrin-
gens, inoculated with trauma into muscle, secretes exo-
toxins that destroy adjacent muscle. These anaerobic
bacteria release other enzymes that ferment carbohy-
drates, resulting in gas formation. A computerized to-
mogram (CT) scan reveals pockets of gas within the
muscles and subcutaneous tissue. As the enzymes degrade the muscles, a thin, blackish fluid exudes from
the skin.
Clostridial myonecrosis is fatal unless identified and
treated very early. Hyperbaric oxygen, antibiotics (such
as penicillin), and removal of necrotic tissue can be life-
saving.

Front 20

how do the gas pockets arise in gas gangrene?

Back 20

due to fermentation of carbohydrates by the anaerobic clostridium perfringens

Front 21

in which cases can we see infections by c. difficile?

Back 21

Clostridium difficile is the
pathogen responsible for antibiotic-associated pseudo-
membranous colitis (diarrhea), which can follow the use
of broad spectrum antibiotics (such as ampicillin, clin-
damycin, and the cephalosporins). These antibiotics can
wipe out part of the normal intestinal flora, allowing the
pathogenic Clostridium difficile that is sometimes pre-
sent to superinfect the colon. Once Clostridium difficile
grows in abundance, it then releases its exotoxins.
Toxin A causes diarrhea, and Toxin B is cytotoxic to the
colonic cells. This disease is characterized by severe di-
arrhea, abdominal cramping, and fever.

Front 22

what will we see in colonoscopic examination of a patient with c.difficile infection?


what usually causes this infection?

Back 22

Examination by colonoscopy can reveal red inflamed
mucosa and areas of white exudate called pseudo-
membranes on the surface of the large intestine.
Necrosis of the mucosal surface occurs underneath the
pseudomembranes.

this infection typically occurs due to ATB treatment, which wipes out much of the normal flora, giving c.difficile, if present, an advantage to proliferate and create this pseudomembranous enterocolitis!

Front 23

what is the b.anthracis capsule composed of?

Back 23

gamma-D-glutamic acid polymers

Front 24

which plasmids are required by b.anthracis for its pathogenicity?

Back 24

both pXO1 and 2! (toxins and capsule)

Front 25

which is the only clostridium without flagellum (H antigen)?

Back 25

c.perfringens

Front 26

which toxins are produced by b.cereus?

Back 26

Heat Labile and Heat Stable toxins!

Front 27

treatment protocol for diptheria?

Back 27

1) antitoxins
2) ATB
3) vaccination

Front 28

why do not all c.diptheriae secrete the dangerous exotoxin?

Back 28

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 diph-
theria exotoxin.

Front 29

Mechanism of toxicity of the diptheria toxin?

Back 29

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

BASICALLY, THIS MAKES THE TOXIN A HUMAN ANTIBIOTIC!

Front 30

How come listeria causes meningitis in neonates, but not normal immunocompentent adults?

how come pregnant women can be infected?

Back 30

in immune competent
hosts, the immune system can release factors that acti-
vate the macrophage, so that these cells can now destroy
the "vagrant" bacteria within them. Immunologists re-
fer to this immune system-mediated method of destroy-
ing Listeria as cell-mediated immunity.


Since pregnancy may also de-
press cell-mediated immunity, Listeria monocytogenes
can infect pregnant women as well, who may develop
meningitis or remain asymptomatic carriers.

Front 31

how do we diagnose and treat listeria infections?

Back 31

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 ei-
ther ampicillin or trimethoprim-sulfamethoxazole
to the antibiotic regimen. These are 2 antibiotics that
cover Listeria monocytogenes.

Front 32

are all clostridia anaerobes?

Back 32

yes

Front 33

is clostridium difficile part of normal flora?

Back 33

yes

Front 34

which antibiotics to use if a c-difficile infection is so severe that we cant simply wait for the normal flora to reproliferate?

Back 34

METRO AND VAN!
metronidazole and vancomycin

Front 35

prevention of nosocomial c-diff infections?

Back 35

limitation of broad spectrum ATB usage.

also, isolation of symptomatic patients!

Front 36

are listeria facultative intracellular?

Back 36

yes

Front 37

how come listeria can go directly from cell to cell without going extracellularily?

Back 37

the actin polymerase surf board :)

Front 38

can listeria grow in the cold?

transmission?

Back 38

yes! cheeses and deli-meats and unpasteurized dairy,

it is transmitted by food, or by vertical transmission from the placenta to fetus!

Front 39

who is affected by listeriosis?

Back 39

pregnant women and neonates. fetuses can aquire the infection thru placenta and this leads to the very dangerous disease granulomatosis infantiseptica (very high mortality - sepsis, necrotic granulomas). alternatively, neonates can contract listeria thru childbirth (meningitis, septicemia)

Front 40

how does the diptheria toxin work?

how is c.diptheria transmitted?

how will a pharynx w/ diptheria look?

treatment of diptheria

Back 40

by inhibition of proteosynthesis (by blocking peptide elongation)

transmission; respiratory droplets

presentation: dirty grey pseudomemb. in pharynx, will bleed if scraped on

treatment: antitox and erthromycin

Front 41

how to differentiate d-diphteria from other corynebacteria (diptheroids)?

Back 41

ELEK test, where antitoxin is on a test plate - toxigenic strains will precipitate the antitoxin

Front 42

treatment of diptheria?

what does tthe diphteria toxin do?

Back 42

1) antitoxin (the toxin attacks CNS and heart, and works by inhibition of proteosynthesis - EF2 inhibition)
2) erythromycin and penicillin
3) DPT vaccine

Front 43

yes frank may brush sally list's legs

Back 43

yersinia
franciscella
mycobacterium tb
brucella
salmonella
listeria
legionella

Front 44

presentation of pontiac fever?

Back 44

Like influenza, this disease in-
volves headache, muscle aches, and fatigue, followed
by fever and chills. Pontiac fever strikes suddenly and
completely resolves in less than one week.

Front 45

presentation of legionnaire's disease?

treatment?

Back 45

Patients develop very
high fevers and a severe pneumonia.
Legionella pneumophila is one of the most common
causes of community acquired pneumonia and is esti-
mated to be diagnosed correctly in only 3% of cases! It
should be suspected in all patients who have pneumo-
nia who are over 50 years of age and especially if they
are smokers or if the sputum gram stain reveals neu-
trophils and very few organisms. (Legionella is so small
it is hard to see on gram stain.)
Treat with erythromycin because this organism has
a beta-lactamase making it resistant to penicillins.
Then attempt to determine the source of Legionella. Is
the air conditioning system contaminated?