Tale of The Microbes

Tale of the Microbes
Rawa Muhsin
Table of Contents
Gastrointestinal Bacteria
Respiratory Bacteria
12
UTIs and STDs
23
Skin and Soft Tissue Infections
34
Febrile and Systemic Infections
44
CSF and Nervous System Infections
54
Treatments
59
Letter of apology from the clans of Staphylococcus and Streptococcus
Dear Sir,
On behalf of the Staphylococcus and Streptococcus families, I would like to express my
hearty gratitude for your generous invitation to your Tale of the Microbes. I offer
my sincere apologies on behalf of the two families for not being able to seize this
invaluable opportunity to meet with the other bacteria. We are very busy at these
times with important meetings that will decide future policies between the two
families. We also thought we would unnecessarily occupy a large amount of space in
your tale. We thus recommend that we be read about in other resources. I myself,
however, have sponsored one of the bacteria in the tale as a form of apology on my
side.
Yours sincerely,
Staphylococcus aureus
CEO of the Staphylococcus Corporation for Quality Infections
Gastrointestinal Bacteria
Clostridium difficile
Campylobacter jejuni
Listeria monocytogenes
Salmonella Typhi
Shigella dysenteriae
Helicobacter pylori
Vibrio cholerae
10
Other Yersinia
11
Escherichia coli
24
Bacillus cereus
36
Clostridium difficile
The clan of Clostridium difficile were always
looking for acceptance among the ruthless
bacteria in the human intestine. They had
to tolerate injustice from their neighbors.
They could only find habitats in about 4%
of adults and half of 1-year-old children.
ascended the pulpit to deliver a heart-
The organisms thus started proliferating
touching sermon. O sons of the difficile
like
clan! This is the day you have been
enterotoxins, the A
awaiting. We have endured injustice for
cytotoxin that destroys intestinal cells and
decades. This is our golden chance to take
elicits
over! Proliferate o thee and release thy
addition
toxins!
secretion) and the
mad,
an
and
releasing
two
toxin (which is a
inflammatory
to
their
causing
response,
excessive
in
fluid
B toxin (another
They were accumulating a great degree of

rage inside them and were looking for the
slightest chance to turn the tables. And
there came the day, where the tablets of
clindamycin bombarded the bowel. One
of the youngsters of Clostridium difficile
shouted as loud as he could to inform his
clan about the unbelievable joy. They all
watched with tears of happiness as the
merciless torpedoes smashed the colonies
of the other bacteria, while not their clan
because they had resistance to it.
It was a true scene of tragedy. Mutilated
bacteria running for their lives, nascent
organisms crying for their mothers, houses
destroyed, misery overshadowing their
hearts. One of the elders of the difficile clan
The epic of Clostridium difficiles fight for control
cytotoxin).
The
end
result
was
the
construction of the Great Wall of China,
When they indeed diagnosed it, they

prescribed metronidazole for it.
Rob and Elene lived with their 4-year-old
the pseudomembrane, composed of mucin
Johny who was attending kindergarten.
from goblet cells, fibrin from the blood,
As the difficile clan were celebrating their
inflammatory
triumph, tablets of metronidazole started
cells,
and
necrotic
cell
debris.
ruining their party. They were seen

running away from their gathering place,
They just thought this was their dream
with the drugs following and crushing
coming true. It didnt cross their minds
them.
that
recovered
maybe
this
is
causing
some
The
other
floral
sufficiently
to
bacteria
had
re-establish
disturbance to the human in whom they
themselves. And thus was the lamentable
are living! So the guy had went to the
difficile clan once again to be pushed under
hospital because of diarrhea. As he told
oppression and silencing, with no hope for
the physician that the diarrhea started
another success in the near future.
after taking the drug, antibiotic-associated

diarrhea (AAD) was suspected. Since
Clostridium difficile is responsible for about
a quarter of cases of AAD, ELISA was
performed for detecting the enterotoxins.
Rob had t o travel to Mozambique for a
business trip. When he arrived there, he
visited a restaurant with three of his
coworkers and ate there. In the same week,
he started feeling cramps in his abdomen
and a diarrhea that was kind of bloody. He
couldn't sleep easily because of fever and
headache. His muscles were all in pain. He
soon arranged an appointment with a
physician.
The physician ordered him to go to a
certain lab and get a stool sample tested.
The lab folks did an initial smear from the
sample and saw slender organisms with
spiral windings. Based on Rob's history
and symptoms, and the sight of spiral
As the results turned positive, clindamycin

was discontinued, fluid replacement was
given. They still didnt know yet whether
the
disease
had
reached
pseudomembranous colitis or not. So they
organisms,
traveler's
they
started
suspecting
diarrhea
and
pseudoappendicitis from Campylobacter.

They incubated it on a blood agar in a
microaerophilic, canaphilic condition for
performed endoscopy to confirm this.
two days. Later, they confirmed their
After Johny was discharged from the
She then started to have pain all over her
diagnosis by urease and oxidase tests on
hospital, his mother took him back home,
joints. When Rob came back from the trip
the culture.
with a kind of a sallow face. What she
and learned about what had happened, he
didn't know was that in the start of the
decided to take her to the hospital. But it
As the lab folks were busy looking for
illness Johny had contaminated several
was too late. The disease had become so
Campy, the physician had put Rob on
articles in the home. She had sliced a piece
advanced that it actually affected her
fluid and electrolyte replacement. Since
of raw meat on a surface in the kitchen few
pregnancy and it led to a septic abortion.
Rob had visited the physician in a slightly
days back, and later prepared salad on the
The physician could do nothing but to
advanced stage of the disease, when the
same surface without disinfecting it first.
advise them to pasteurize milk and its
lab report came back as Campylobacter
After taking Johny back home from the
products
jejuni, the physician decided to also put
hospital, she herself started showing some
disinfect surfaces on which raw meat was
him on ciprofloxacin.
signs and symptoms of GI upset. She just
handled before using them for other food
couldn't bear going back to the hospital
items. In return for his heartly advice, he
again so she just ignored it.
received a silencing punch from angry
Back home, his wife and little Johny were

living happily waiting for his return. One
before
using
them
and
to
Rob.
of the kids in the kindergarten had

recently developed signs of abdominal
Few months later, little Johny started to
pain and diarrhea and had spread the
feel weakness in his feet. He began
infection to many of the other children,
developing paralysis in his feet that
including little Johny. Johny didn't just
gradually progressed upwards. Rob and
develop the usual symptoms but rather
Elene decided to take him to a neurologist.
progressed to bacteremia. After taking
A diagnosis of GuillainBarr syndrome
him to the hospital, he was put on
due to Campylobacter was made and
electrolyte and fluid replacement. When
Johny was put on the specific antibodies
then lab reported Campylobacter fetus, he

was also placed on ampicillin.
It is important to disinfect surfaces on which raw meat
for the disease.
is handled before using them for other items.
Listeria monocytogenes
Jack had just returned home tired from a
tough work day. He opened the fridge and
rolled out a big bottle of milk. He was so
fond of milk that he swallowed the whole
bottle in no more than a minute. What he
didn't know was that an occult gram +ve
rod, Listeria monocytogenes, was thriving in
his fridge at the set temperature of 4 C. In
fact this organism is so ubiquitous that it is
found in around a third of ground meat
and poultry, and even in 10% of normal
The clever macrophages watched with a
showed small colonies with narrow beta
smirk Look who's coming. Huh. and
hemolysis.
they started phagocytosing them. To their

surprise, however, Listeria elaborated a
listeriolysin O that allowed them to
escape the phagosome and enter the
cytosol of the macrophage (by lysing the
phospholipids of the phagosome), making
fun of the macrophages in their turn
Loserssssssss!. So now they prevented
their destruction and started to proliferate
and spread from cell to cell.
humans as flora.
Because the Listeria were present in such a
big
number
(over
million),
the
listeriolysin O was enough to cause

damage to the intestine with symptoms of
gastroenteritis, and a flu-like syndrome.
Had Jack left them alone, they would have
invaded the blood, caused sepsis, and
potentially led to a meningoencephalitis.
However,
Milk is one of the sources that harbor Listeria.
Jack
quickly
rushed
to
physician as soon as he got the GI upset.
So, an avalanche of Listeria particles were
The physician asked him to get a lab
swarming down Jack's gut with the milk.
analysis for his stool. Blood culture
The adventures of Listeria in the body
Streptococcus was excluded because the

colonies
were
catalase
+ve.
Corynebacterium was excluded because the

microbes had some tumbling motility
under the microscope. They had to be
Listeria.
Jack
ampicillin.
was
thus
prescribed
Salmonella Typhi
yummy food, the organisms entered his
It was around 11:30 PM in a hot sunny

summer day when Parker was walking
around in the stores. He was feeling
hungry so he decided to drop by a nearby
restaurant. He didnt feel as comfortable as
he wanted in the restaurant and didnt see
gut and invaded the intestinal cells,

resisting destruction by phagocytes on the
way. Then they gained access to the blood
to result in the fever. Parker arranged an
appointment with his physician. From the
symptoms and the maculopapular rash on
the abdomen (only in 30% of cases), the
a lot of customers there.
physician strongly suspected typhoid, as

A few weeks passed by and Parker started
developing
fever,
chills,
sweating,
well as other conditions. He thus ordered a

lab test for the blood and stool.
weakness and diarrhea. He also noted the

appearance of pink spots on his belly (rose
spots). He hoped the symptoms would
disappear but they persisted and the fever
became
more
intense.
What
was
happening was that some of the restaurant

folks had recently recovered from typhoid
and thus were in the convalescent state
where they still had organisms in the stool.
Without any special direction from the

physician the lab team prepared blood and
MacConkey cultures. The MacConkey
culture showed the growth of colonies and
the biochemical patterns confirmed the
presence of Salmonella. They then did
serotyping by a slide agglutination test to
determine the exact serovar, which turned
out to be Salmonella Typhi. The lab folks
Because of poor hygiene, various utensils

were contaminated by the organisms and
this resulted in contamination of the food
presented to Parker. As he was eating the
didnt do the Widal test because it looks

for antibodies against O and H antigens
but these antibodies may be from previous
infections or the test may even give false
positive results due to other antigens.
inhabited his bladder and cause reinfection from there.
So Parkers brother arrived at the city with
his 10-year-old son, Peter, and paid Parker
If you are wondering why the Typhi up
a visit. He told him with enthusiasm how
there is not in italic, this is because it is a
he
serovar not a species name. Its full name is:

Salmonella enterica enterica Typhi
had
indeed
taken
the
Salmonella
vaccine. As Parker went to work the next

morning, his brother took Peter for a walk
Other serovars causing typhoid fever include
in the stores. Peter asked for a hamburger
Choleraesuis, Paratyphi A, and Paratyphi B.
as they went by a small fast food trailer.

His father bought it for him but he himself
After a few days Parker received a phone

call from his brother who was planning to
travel to Parkers city along with his son
The rose spots are actually very small (few millimeters).
for a vacation. Parker advised him to take
Three black outlines have been drawn above to encircle
the
a number of the small pink spots.
As the physician received the report, he

placed Parker on a fluoroquinolone and
asked him to take it even if he thinks he
has recovered, so as to eradicate the
infection and lessen the shorten the carrier
state. He also noted that he may need a
cholecystectomy if the organisms have
oral
attenuated
vaccine
against
Salmonella before travelling.

It is noteworthy that two nontyphoidal
cousins of Salmonella Typhi, who are
Salmonella Enteriditis and Salmonella
Typhimurium, are common causes of selflimiting gastroenteritis.
didnt eat one. After a few days, Peter

started
developing
profuse
watery
diarrhea. He gradually noticed pain and

difficulty in defecating (tenesmus) and his
stools basically turned into a mucoid
material with blood and pus (dysentery).
What happened was that the hamburger
trailer guy was recovering from bacillary
dysentery and thus had the organisms in
the stool. He inadvertently contaminated
some of the hamburgers with his hands
and Peter got infected when he ate one of
those hamburgers. The organisms entered
the terminal ileum and colon where they
were taken up by the M cells (overlying

Peyers patches). Beneath these cells they
saw the macrophages running towards
them. You talking to me? remarked one
of the Shigella with a muscular physique.
The hasty macrophages didnt heed the
remark and proceeded to ingest the
sneering bacteria the evil eyes.
As Shigella got into the phagosomes, they
adroitly lyzed it and induced apoptosis of
the naive macrophages. They then reentered the intestinal epithelial cells from
their
basolateral
side
(retrograde
transport). As they got in, they released

their Shiga toxin which went straight to
the ribosome to inhibit the 23S rRNA,
The pathogenesis of shigellosis
thus inhibiting protein synthesis and

killing the cells.
demonstrated Shigella. This was further
prescribed for Peter. The physician also
confirmed by growth on Hektoen enteric
advised Parker and Peters father to
When fever came in and the dysentery
agar. The specific serovar of Shigella
maintain good hygiene as the disease
worsened, Peter was taken to the hospital.
dysenteriae was identified by a slide
frequently involves other family members
He was immediately placed on fluid
agglutination test.
living in the same house since only around
replacement. Stool and blood samples

were taken for analysis. The MacConkey
culture
and
the
biochemical
pattern
200 organisms are enough to cause an

Antibiotic sensitivity showed they were
infection (i.e. it has a low infectious dose).
sensitive to ciprofloxacin so this was
Helicobacter pylori
swim
This whacky bacterium seems to be so

widespread. In areas of poor hygiene,
people start to contract the infection in
their childhood. By the time of adulthood,
almost 100% have the bacterium in their
tummy. In more industrialized countries,
however, only around half of older adults
around
smilingly
with
its
the acid. When these cells are gone, the
lophotricus flagella, binding to stomach
acid shoves its way down the wall. This
cells. The reason for this resistance to acid
results in an acute gastritis that can
is that H. pylori makes urease which
progress to chronic gastritis. In turn, the
breaks down urea present within the
disease can progress to chronic atrophic
stomach into CO2 and ammonia. This
gastritis (a precursor for adenocarcinoma
ammonia seems to provide a sort of a
of stomach) or to peptic ulcer in stomach
protective environment for H. pylori to
or duodenal wall.
thrive in.
have the infection.
Common sites of peptic ulcer.
What Helicobacter does in its free time
When the patient visits a physician for

epigastric pain and discomfort, and the
This bacterium makes fun of the stomach
The ammonia, along with the vacuolizing
physician comes to suspect H. pylori, he
as
its
toxin (VacA), produced by H. pylori itself,
sends the patient to the lab to test for the
powerful weapon of destruction, the
destroy those cells in the stomach that
bacterium. The clever lab folks ask the
acid, to kill it, but H. pylori just
make mucus, which is essential to protect
patient to inhale and swallow radioactive
responds with a yawn and continues to
the stomach wall from the eroding effect of
the
angry
stomach
unleashes
13C-labeled urea. The H. pylori, on seeing

the radioactive urea come down the
stomach, shout Yey! Colorful food! and
start breaking it down to radioactive
13CO2 and ammonia. The patient then
belches out the radioactive CO2 and this is
detected by an external device. A final
confirmation is done by looking for antiHelicobacter antibodies in the serum.
Vibrio cholerae
achlorhydria, you would be much more
The non-cholera strains of Vibrio are

found in seafood. Since they are found in
the sea, they must be tolerating high NaCl
concentrations, say up to 10%. So, you
would
get
infected
parahemolyticus
if
with
you
Vibrio
ingested
crustacean that wasn't cooked well. It will

cause a self-limiting GI upset that doesn't
need antibiotics. The other strains can also
The patient may be adventurous and ask

for an endoscopy (he wants to try one
enter through wounds and cause soft
the sample in microaerobic conditions

(5% both CO2 and O2) on an enriched
medium. When they take a smear, they see
pink spiral organisms on the slide.
physician, he puts the patient on a triple

regimen of omperazole, amoxicillin, and
clarithromycin for two weeks, followed by
six weeks of omeprazole alone. If this fails,
intestine, they will attach by their pili to

the lining epithelial cells. Since you
showed sympathy by providing such a
beautiful alkaline medium, they won't
invade your epithelial cells, but rather
produce their AB toxin, the cholera toxin.
The produced cAMP will activate protein
channels that will result in loss of
Regarding Vibrio cholera O1 strain, you

contract it feco-orally, through ingestion
of contaminated food or water. Since the
bacterium doesn't like the smell of acid,
electrolytes (like Cl-) from the cell. Since

water will be paranoid at the sight of its
osmotic companions leaving the cell, it will
rush behind them.
you need a high infectious dose, around

108 particles, so that some of them will
When the lab report comes back to the
Once they reach the proximal small
kinase, which will in turn activate the
tissue infections and septicemia.
before his death) and so they take a biopsy

from the ulcerated area and they culture
hospitable to V. cholera.
sacrifice their lives to protect the others

who will move by their single polar
flaggelum past the stomach and reach the
small intestine, their dreamland. It would
be
logical,
then,
that
if
you
had
The result is a profuse diarrhea that will

manifest
as
rice-water
stool.
The
laboratory staff are already suspecting

cholera from the stool specimen (especially
if there has been a known epidemic or
endemic) and will thus straight away
he goes for the quadruple therapy, adding
culture it on its favorite medium, the
one more antibiotic.
alkaline peptone water and further select
10
it on TCBS agar. Plus, when they prepare
months even after the symptoms have
a smear out of it, they will see these pink
disappeared.
Other Yersinia
The brother-in-laws of Yersinia pestis are
comma-shaped structures on the slide. Just
Yersinia
for fun, they want to identify the exact
enterocolitica
and
Yersinia
pseudotuberculosis. They are acquired by
strain by bombarding it with specific
ingesting
antibodies, in an agglutination test.
contaminated
meat.
They
penetrate the ileum (causing ulcerative

lesions there) and take a trip inside the
macrophages to the mesenteric lymph
nodes, causing necrotic lesions of Peyers
Vibrio cholerae on TCBS agar
While the lab staff were busy confirming

their suspicion, the physician has already
Mechanism of action of cholera toxin
patches on the road, and mesenteric

lymphadenopathy. They obviously should
present with some diarrhea, abdominal
pain, and fever. Diagnosis is same as
Yersinia pestis and ciprofloxacin is good
enough for treatment.
started fluid and electrolyte replacement.

This has to be done. When the positive lab
report comes back, you decide to put the
patient on doxycycline to reduce the
period of infection. However, the patient
can continue to shed the bacterium for
11
Respiratory Bacteria
Mycobacterium tuberculosis
13
Non-TB Mycobacteria
15
Mycoplasma pneumoniae
16
Bordetella pertussis
18
Haemophilus influenzae
19
Legionella pneumophila
20
Nocardia asteroides
21
Coxiella burnetii
22
Moraxella catarrhalis
22
Chlamydia pneumoniae
33
Bacillus anthracis
35
Pseudomonas aeruginosa
27
Yersinia pestis
37
12
Mycobacterium tuberculosis
Larry's
Larry has been filling out application
actually had TB but he was hiding it from
forms for various job offers for the past
his teammates. He was thus spreading the
couple of weeks. Yesterday he received a
particles of Mycobacterium tuberculosis in
phone call from one of the companies
his respiratory droplets into the air.
telling him that he has been accepted to be
Through continuous exposure, Larry got a
interviewed. He passes the interview and
large amount of the pathogens in his
gets employed in the company. On his first
lungs. When M. tuberculosis enters the
day of work, he meets his 5 teammates
lungs, the macrophages quickly ingest it,
who welcome him warmly to the team.
thinking that it is just another easy prey.
One of them, Frank, is also relatively new
Once Mycobacterium enters the phagosome,
in the team and seems to cough very
however, it prevents the formation of the
often.
phagolysosome
coughing
teammate,
and
Frank,
continues
to
proliferate inside the macrophage.

About a month from his first day of work,
Larry develops a mild chest discomfort
The infected macrophage dials 911 to tell
and cough that go away after a few days.
other macrophages to come to his rescue
Months go by and Larry notices he has
by releasing MAF (macrophage-activating
What happens is that in each focus of
been having this chronic cough that is
factor). When a large amount of particles
infection, there is a large cluster of
getting progressively worse. When he
accumulate in a macrophage, they cause
macrophages and lymphocytes packed
starts to notice blood in his sputum, he
its rupture and are released to the
together (called a tubercle) with a central
decides to see a physician. So let's leave
surrounding. Some may get into contact
area
Larry for now and go behind the scenes to
with T cells to induce memory T cell
undergoes
see what happened.
formation.
then
cavitation of cavern formation). When the
ingested by other macrophages to repeat
macrophages see they can't control the
the same process.
infection, they call fibroblasts to just
These
particles
are
TB granuloma
of
liquefactive
caseation
necrosis
(thus
there
that
is
13
basically fibrose the area and restrict the
the slide can be. So it retains the pink stain
the this injected antigen of M. tuberculosis.
movement of the pathogens. This whole
of carbolfuscin. So the lab guy sees pink
This means that you were someday
thing is called a granuloma, by the way.
slender rods on the slide on a blue
exposed to M. tuberculosis. This, however,
background.
M.
doesn't tell you whether right now you
granulomas
tuberculosis in mind. He does a PCR test
have TB or not, so the lab guy adroitly
throughout your lungs. After months or
and within 8 hours he gets a poisitive
skips this test.
years, 10% of patients get a reactivation of
result for M. tuberculosis.
Thus
you
get
multiple
So
now
he
has
the infection (as did our patient Larry)
Culturing the organism takes 2-8 weeks, so
mostly due to immune suppression. More
the lab guy decides to tell the physician
granulomas form and the organism even
that Larry indeed has TB so that the
spreads to other parts of body (like GUT
physician starts treatment. He, however,
causing UTI, and CNS causing meningitis,
also starts a culture of the organism on
both of which Larry got). So let's go back
Lowenstein-Jensen agar (has high lipid
to Larry.
content and is good for M. tuberculosis).

The benefit of this culture is to do drug
From the chronic history and signs and
sensitivity tests on the organism to
symptoms, the physician puts TB on his
determine which anti-TB drugs are most
differential diagnosis and asks Larry to get
effective for this particular strain since
a sputum analysis at the lab. The lab guy

reads the physician's note asking for TB
tests, so he prepares a smear from the
sputum and stains it with Ziehl-Nielson.
This stain is good for Mycobacterium
because it has such a thick wall (full of
mycolic acid) that it cannot be decolorized
by acid alcohol while everything else on
Tuberculin test (Mantoux procedure)
There is a tuberculin skin test wherein you

inject purified protein derivative (PPD) of
M. tuberculosis into skin. If within 2 to 3
days reddening and induration occur, it
resistance can easily develop. So after

around a month you send the physician
another report containing the results of
your sensitivity testing. The physician thus
checks to see if he should modify his
treatment plan.
means you have memory T cells against
14
better
from
compliance
him
(this
is
directly-
called
NonNon-TB Mycobacteria
There are even whackier relatives of M.
tuberculosis that are brave enough only
observed therapy or
when immunity is down. M. avium and M.
DOT).
intercellulare
are
two
such
non-TB
Mycobacteria that cause mycobacteriosis

Larry
is
have
about
kid
to
commonly in AIDS patients.
soon.
Since he now knows

how troublesome this
infection
is,
he
decides to vaccinate
his baby as soon it
goes past one week
of age with the BCG
(Bacille
Anti-TB drugs
Larry thus continues to receive multiple

drugs in a regimen of 6 to 9 months.
Calmette-
Guerin) vaccine. This

reduces the risk of serious complication by
Granuloma of M. avium intracellulare infection without

any caseation (similar to that of sarcoidosis)
80%.
Initially he takes daily dosing but later on
One problem with these organisms is that
twice weekly. Larry seems to be a little lax
they may be present as part of normal
about taking his medications so his
flora. So when you identify them in a
physician decides to refer him to a TB
specimen, you cannot easily tell whether
center so that they can put him under a
they caused an infection, or where just
program of observation to encourage
peaceful
flora,
or
even
where
poor
laboratory contaminants. In fact, they are
15
the culprits of an infection in only about

10% of all the times in which they are
isolated. All that is needed to be done is to
surgically reset the lesion and put the
patient on combination chemotherapy
(choosing drugs like isoniazid, rifampicin,
or ethambutol) depending on the specific
pneumo
oniae
Mycoplasma pneum
Tom was visiting the local grocery store to
started destroying the cells resulting in a

diffuse patchy bronchopneumonia.
buy some cabbage. As he was looking

through the rows for cabbage, a guy who
was coming in the opposite direction
sneezed in his face. Tom controlled his
anger and didnt say anything about it.
species involved.
After a few days, Tom developed a
relentless headache with fever, chills, ear
pain and weakness. He then started a dry
cough. When he started developing a skin
rash (erythema multiforme) and getting
weak
(hemolytic
anemia
by
cold
Erythema multiforme in atypical pneumoniae
agglutinins), he arranged a visit to his

physician. What had happened was that
The physician asked for an X-ray, which
the guy who sneezed in his face had
demonstrated the bronchopneumonia. He
atypical
was
then sent Tom to the lab for an analysis.
spreading Mycoplasma pneumoniae in his
The lab did culturing for the sputum but
respiratory droplets.
nothing turned up in the first few days.
pneumonia,
and
thus
They could hardly see anything from the

The organisms thus entered Toms airways
smear.
and attached to the cells of the trachea,
Mycoplasma doesnt have a cell wall so it
bronchi,
doesnt take the conventional stains easily.
and
bronchioles.
They
then
The
reason
for
this
is
that
When the lab guy couldnt find things like
16
Mycobacterium and other folks, he started
As a precaution, the doctor put Tom on
disease. A good old tetracycline should do
suspecting Mycoplasma.
doxycycline. So the symptoms started
away with it.
going down and the time for the lab revisit

He thus decided to culture it on its special
arrived. When Tom went back to the lab,
Ureaplasma urealyticum, on the other hand,
medium which contains sources of the
the lab guy did another antibody titer test
is the other cause of urethritis in men
sterols that Mycoplasma uniquely have in
and saw that the titer had increased four-
when Neisseria or Chlamydia cannot be
their plasma membranes. Because the
fold (i.e. four-fold difference between
found. In women, it is associated with
colonies appear after around two weeks,
acute and convalescent titers). The minute
endometritis and is found in infants of
the lab guy decided to look for antibodies
colonies with the fried-egg appearance
premature labor and low-birth weight.
against Mycoplasma, and he sure could find
had also showed up on the agar. This
them! He thus sent the preliminary results
confirmed the diagnosis of Mycoplasma
One final Mycoplasma that is always made
back to the physician that this could be
and indicated that no further line of
fun of by his relatives is Mycoplasma
atypical pneumonia but that he will send
management is required.
incognitus.
back the definitive results after two weeks.
They
tease
him
saying
Humans are not even sure whether you

cause disease or not! What a shame!
Since Mycoplasma doesnt have a cell wall, if

you try a cell wall synthesis inhibitor like
penicillin on it, it will probably laugh at you.
Mycoplasma incognitus responds, however,

by stating how he shows up in pneumonia
in AIDS patients but doesnt tell them
There are two troublesome relatives of
whether he is involved or not.
Mycoplasma pneumoniae, who are the floral

Mycoplasma hominis, and Ureaplasma
urealyticum.
Mycoplasma
hominis
is
associated with post-partum and postabortal fever (found in the blood of 10% of
such patients) and pelvic inflammatory
Fried egg colonies of Mycoplasma pneumoniae
17
James was having guests at his home. His
daughter,
Kate,
was
playing
in
the
guestroom. One of the guests seemed to

cough frequently. After around one to
three weeks, little Kate began to have a
runny nose with fever and reddening and
swelling of her conjunctiva. She then
developed a dry cough which gradually
became worse and was often following by
a whooping sound.
guest had recently acquired Bordetella

pertussis pathogens. Since these never
negotiate or compromise their honor to
agree with carrier status, they caused him
pertussis but not as severe as it occurs in
He
was thus spreading
the
organisms in aerosols. Kate had inhaled

some of those and Bordetella attached to the
ciliated epithelial cells of her bronchi by
their filamentous haemagglutinin (FHA)
and pertussis toxin (Ptx).
on the surface of Bordetella and would
(remember they are pompous) but only
fluoresce if they were present, and they
secrete their pertussis toxin and their
did! Since he was a newbie, he also wanted
tracheal cytotoxin, both of which will
to do a third confirmatory test by detecting
result in cell death and an inflammatory
specific antibodies in Kate's serum (which
response, leading to the manifestations.
form two weeks after the onset of the

disease).
Kate's father decided to take her to the

physician. The physician listened carefully
to the sound after the coughs and
exclaimed silently I hear a whoop!
Bordetella!!! and sent them to the lab (with
What happened was that the coughing
infants.
They don't like to invade the cells
a note asking the lab to pay special

attention to finding Bordetella). The lab lad
Clinical Note: The inflammatory cells, mainly

lymphocytes, can reach such a high number
(~50,000 cells/micL), called a leukemoid
reaction, that can scare the pediatrician like
mad. Why? Because one of the differential
diagnoses will be LEUKEMIA due to the high
lymphocyte count. Which type of leukemia?
Acute lymphoblastic leukemia is the
leukemia of children.
took a nasopharyngeal swab with some

show-off technique and cultured it on a
medium that contained blood and charcoal
The physician received the lab report and
(to disinhibit the growth of Bordetella)
decided to put Kate on a macrolide for
while keeping in mind that this was a late
eradicating the infection, and to her family
stage of the disease and the organism may
as chemoprophylaxis. He also noted that
be difficult to demonstrate.
during the convalescent period she may

prone to ear and chest infections, and
Since he knew it would take three to four
seizures.
days for the pinpoint colonies to appear,

he proceeded to an immunofluorescence
test that would target the agglutinogens
18
Haemophilus influenzae
Note: This bacterium is sponsored by
Staphylococcus
aureus.
StaphAU
and Neisseria, it used the old trick of IgA
They could also demonstrate antigens on
protease to overcome the local defense
the
forces of secretory IgA.
agglutination reaction.
Later on she developed signs of upper
As the lab results came back, Katie was put
respiratory tract infection, like epiglottitis,
on ceftriaxone. Mary decided to vaccinate
sinusitis, and otitis media. It was even
her other child, now 6 months old, when
about
she becomes near 2 years old with an Hib
bronchopneumonia. As the bacterium got
vaccine to try avoiding this scenario
into the blood, meningitis and arthritis set
happening again.
capsule
by
antibodies
in
an
Golden infections like never before.*

Parker had been a heavy smoker for years.
One day he developed a viral infection of
his upper respiratory tract. The seeminglymild infection became superinfected by
long-term occult enemy in carrier state that
was waiting for a chance to break free, the
dreadful
Haemophilus
influenzae.
This
caused an acute exacerbation of his

chronic bronchitis. As Parker was walking
down the road on his way to his
physician's office, he was sneezing all the
way through.
to
go
down
and
cause
in and so Mary rushed her to the hospital.

The lab people took a pharyngeal swab
and a blood and CSF sample. As they
cultured it on chocolate agar, the organism
happily grew. This is because it loves
two growth factors found in blood, X
factor (or hemin) needed for synthesis of
heme derivatives, and V factor (or NAD)
At the same time Mary and her 2-year-old
for redox reactions.
Katie were out shopping, and as they

passed by Parker, little Katie inhaled some
of the respiratory droplets containing H.
influenzae. It established itself on her
upper respiratory tract. Since it had
graduated the same year as Streptococcus
The lab folks were, however, scared when

they could culture it from the CSF and
blood samples. Suspecting Haemophilus
from the child's age and its growth on
chocolate
agar,
they
demonstrated
swelling of the capsule by Quellung test.
Result
of
Quellung
test
(though
this
slide
is
Streptococcus pneumoniae). The large pink spaces

around the cells are the swollen capsules.
19
* Staphylococcus aureus can make NAD in

plentiful amounts and secrete it into the
medium on which they grow. Since
normal blood agar doesn't contain enough
NAD, Haemophilus can grow readily on
blood agar if S. aureus colonies are also
present. This is known as the satellite
phenomenon.
Jack and Schwartz where on their way to a
dinner invitation from their boss. They
with a lysosome, thus thwarting its

digestion and multiplying within that
protected
rotected environment.
were impressed by the big dinner hall,

with all the meticulously-matched colors,
and the colorful food. They also noticed a
large number of huge air conditioners in
the room. After around ten days, Schwartz
developed a sharp chest pain along with
vomiting, watery diarrhea, and dizziness.
Jack, on the other hand, only developed a
fever. Later it became known that many
other attendants at the dinner had also
The reason why Jack and others only

developed a fever (called Pontiac fever),
was that they were relatively healthy,
immunocompetent
fever
would go
individuals.
away
Their
spontaneously
within a week. Schwartz, however, got

symptoms
of
Legionnaire's
disease
because he had cardiopulmonary disease

and thus was immune-compromised.
developed fever.
Schwartz arranged an appointment with
What was happening was that Legionella
pneumophila was being spread in aerosols
from the big air conditioners. This is
because it has a thing for damp biotopes
Satellite phenomenon on blood agar. The small
colonies are those of Haemophilus surrounding the big
(including whirlpools, water systems, etc)
continuous mass which represents the colonies of
and the water has to reach around 70 oC to
Staphylococcus.
destory them. It entered the lungs of the

people, and was phagocytosed by their
macrophages. The organism, however,
prevented the fusion of the phagosome
his physician. The physician learned about

the history of the dinner and the other
members getting fever. He ordered an Xray, on which he noted multiple areas of
necrosis.. He also demonstrated certain
abnormal
neurological
findings
from
Schwartz. He thus ordered a lab test for

Schwartz' sputum. The clever lab guy
prepared an initial smear and could hardly
see a few gram -ve rods. He then re-read
the history in the note from the physician
20
and
said
to
himself
Could
it
be
Llll.....Legionella?
Nocardia asteroides
decolorization. They also notice that the
Jane was running back home as the

sandstorm was encompassing the region.
He thus decided to do a urinary antigen

test for Leginella, and it returned positive!
He found antigens in the sputum by direct
fluorescence, and also found antibodies
against Legionella by indirect fluorescence.
As a final confirmatory test, he decided to
culture it on buffered charcoal yeast
extract containing L-cysteine, iron, and
alpha-ketoglutarate.
As
the
colonies
appeared after around four days, he

became absolutely sure this was Legionella
She had inhaled a lot of dust. Months after

the incident, Jane starts to have several
manifestations
of
chest
with urination and has started feeling

dizzy lately. She thus decides to visit her
physician. What had happened was that
Nocardia was present in the inhaled dust
it
caused
primary
pneumonia
followed by metastasis to the kidneys and

the brain.
and sent the results back to the physician.
prescribed a macrolide for Schwartz and

told him not to worry about spreading the
infection to other people because that is
not possible with this bacterium.
slowly. A diagnosis of Nocardiosis is

made.
On receiving the report, the physician
wants
to
know
why
Nocardia
had
metastasized to the brain and kidneys. He

asks Jane if she has any other illnesses or is
taking any medications. She tells him that
she
is
receiving
medications
for
rheumatoid arthritis. So the physician puts

Jane on sulfamethoxazole to contorl the
infection and sends her to a surgeon for
The physician asks for a chest X-ray. He

When the physician received the report, he
agar in aerobic conditions but rather
infection.
Furthermore, she's been having problems
and
organism can grow on standard nutrient
draining the lesions.
notices multiple cavitations. He screams

inside himself Could it be TB?! So he
sends Jane to the lab for a specimen
analysis. They see that there is pus without
any specific granules inside. They do a
smear and see gram positive rods. They
find that these are not acid-fast (thus not
TB, yey) but are weakly acid-fast when
sulfuric acid alcohol is used instead for
Nocardia saying Cheeeeeze! for the microscope
21
Coxiella burnetii
infected by inhaling infected dust in his
55-year-old Simon, who was living in the

countryside, was getting worried about
some of his cows getting sick lately. He
was taking care of them all the time. He
then started noticing that he himself began
developing
chest
pain,
cough,
and
dyspnea. He tried to ignore the condition

until it got worse and he started getting
weak at which time he decided to visit a
barnyard. This is possible since the

organism is so whacky that it can resist
heat and desiccation for long periods
outside the body. The organism entered
his respiratory tract and initiated an
interstitial pneumonitis. They also baffled
the macrophages when they thanked them
for providing such a breath-taking acidic
condition in their phagolysosomes for free.
Moraxella
Moraxella catarrhalis
Moraxella catarrhalis is the poor ignored
outlier in the corner who strives to a get a
place in the microbial community. It
changed its name from Branhamella to
Moraxella, but that didnt make any
difference. It always tries to boast of how it
is present in the upper respiratory tract
and can cause infections in the nearby
locations (like sinusitis up there, otitis
media near there, pneumonia down there,
local physician.
When he ignored it, the organism got the
chance to disseminate to his heart, causing
endocarditis, and other organs like the
liver causing granulomatous hepatitis.
The physician noticed how worried Simon
acute exacerbation of chronic bronchitis

not so down there, etc). It tries to impress
its fellow microbes by how it can make
brand new penicillinases. Naa, say the
other microbes, that is old school pal.
was about his sick cows. He also knew that

recently a number of Q fever cases were
Moraxella lacunata used to be active in
diagnosed with similar symptoms. He thus
the eye infection business but now its
asked Simon to get a lab test. The lab folks
getting old and has largely retired from it.
looked for the antibodies against Coxiella,

Q fever is usually acquired by inhaling infected dust in
as per the physicians request, and they
barns.
sure did find them. The physician on
What had happened was that Coxiella

burnetii had infected his cows. He then got
receiving
the
report
prescribed
doxycycline for Simon.
22
Urinary Tract Infections &

Sexually-transmitted Diseases
Urinary Tract Infections
Escherichia coli
24
27
Proteus
28
Other UTI Whackos
29
Sexually-transmitted Diseases
Treponema pallidum
29
Neisseria gonorrhoeae
31
Chlamydia trachomatis
32
23
Escherichia coli
Pam got married a few weeks ago. She
recently developed dysuria and a burning
sensation during voiding. She decided to
visit her physician. What had happened
was
that
Escherichia
uropathogenic
coli
from
her
strains
colon
of
had
colonized her periurethral region and

eventually reached the urethra during
intercourse. These uropathogenic strains
have P fimbriae, or pili, that allow them to
attach to the lining cells of the lower
urinary tract and establish themselves.
The progress of UTI caused by Escherichia coli
They had then started destroying cells,
sent Pam to the lab for a urinalysis. The
resulting in an inflammatory response,
lab lass gave her a sterile container and
leading to the signs and symptoms. Since
told her to collect a urine sample in it.
the most common cause of a UTI is

How uropathogenic Escherichia coli reach the urethra
Escherichia coli, the physician already had it
She carefully told Pam to let a small initial
at the top of her differential diagnoses. She
amount of urine pass then collect the
24
sample from mid-stream. This should be
So Pam headed back home with the
O157:H7 strain).
strain The organism entered his
done so that if other non-pathogenic
medications. On the way she passed by
large
Escherichia coli strains are present on the
her parents house so she thought Why
destruction of intestinal cells by its Shiga-
mucosa, they will be flushed, and if there
not pay a visit? She went in and saw her
like toxin or verotoxin, without itself
are real pathogenic Escherichia coli strains
8-year-old brother, Potter, lying on the
invading
in the urine causing the infection, they will
couch with a sallow expression and sweat
inflammatory response. This resulted in
remain even in the mid-stream sample.
all over his face. She asked what had
the copious bloody diarrhea.

d
The problem
happened. Her mother replied that he
was that the organism had entered the
The lab lass then cultured the sample on
developed this copious bloody diarrhea
blood and started causing hemolytic
blood and MacConkey. The biochemical
yesterday or so and now he
is having
uremic syndrome (HUS). This is basically
pattern established presence of Escherichia
fever. Pam exclaimed Why havent you
the development of thrombosis on sites of
taken him to the hospital? Lets go now.
blood vessel walls where bacterial antigens
coli
beyond
doubt.
But
was
it
When she saw it was more than 100,000

bacteria/ml of the urine, she became
confident it was an infection (whereas
around 1,000 indicates contamination and
10,000 is doubtful). She then did antibiotic
sensitivity testing and saw it was highly
sensitive to cephalosporins. She wrote all
the
and
started
cells
or
causing
causing
an
have been deposited. This results in
contamination or a real infection? She thus

measured the bacterial count in the urine.
intestine
There are five important strains of Escherichia

coli causing intestinal infections:
1. Enterotoxigenic (ETEC) (discussed here)
2. Enterohemorrhagic (EHEC) (discussed here)
3. Enteropathogenic (EPEC): watery diarrhea in
newborn babies by Shiga-like toxin
4. Enteroinvasive (EIEC): dysentery-like bloody
diarrhea with fever
5. Enteroadhesive (EAEC): travelers diarrhea,
and persistent diarrhea in children and in AIDS
thrombocytopenia
RBCs
when
thrombosed
and
going
areas
destruction
through
of
these
(
(microangiopathic
hemolytic anemia).
anemia It can end with acute
renal failure if not cared for.
In the hospital, Potter was placed on fluid
resuscitation and a stool sample was sent
to the lab for analysis. An initial blood
that and sent it back to the physician.

What was happening was that Potter had
picture showed thrombocytopenia and the
When the physician received the report,
eaten contaminated food outside the home
presence of schistocytes (damaged RBCs).
she prescribed cefotaxime for Pam and
and it contained the enterohemorrhagic
The MacConkey culture of the stool
told her not to worry about it.
strain of Escherichia coli (specifically the
sample
and
the
biochemical
tests
25
the
LT toxin (which elevates cAMP) to cause a
enterohemorrhagic strain of Escherchia coli.
net loss of chloride and water from the
supported
They
didnt
diagnosis
have
gene
of
probes
for
intestinal cells into the lumen and decrease
confirmation of this so they just depended
in the reabsorption of sodium, resulting in
on these basic findings.
the watery diarrhea.
The hospital staff made sure not to give
He was thus placed on fluid replacement
antibiotics
to
and
exacerbate
the
supportive
therapy.
Potter
because
HUS
but
it
can
provided
Eventually
monitored
to
see
if
he
Enterobacteriaceae family (which includes

Escherichia, Yersinia, Salmonella, etc.) are
serologically typed by their O antigen (cell
wall antigen on their LPS). The H antigen is
only present on flagella and the K antigen on
capsules. Common pathogenicity factors in
these bacteria include colonizing factors,
invasins, endotoxins, and exotoxins.
needs
antibiotics or not.
the
symptoms calmed down and Potter was

taken home after a few days. When they
distance travel.
After about a week, Potters uncle started
developing significant watery diarrhea.
At the hospital, he was diagnosed with
travelers
diarrhea
caused
by
the
enterotoxigenic strain of Escherichia coli.

The organism had entered his gut with
contaminated food. It had attached itself
using its pili to the intestinal mucosal cells.
intestine to bring about their pathogenic effect
day Potters uncle arrived from a long-
How various strains of Escherichia coli act in the
arrived at home, the evening of the same
It then elaborated its heat-stable ST toxin

(which elevates cGMP) and its heat-labile
26
Tom is 72 years old. Recently he started
having difficulty in urination. The dysuria
progressed until he could barely pass
urine any longer. His daughter, Kate,
decided to take him to the hospital along
with her child, Spike, who has been having
cough, chest pain, and dyspnea recently.
At
the
hospital,
catheter
These findings confirmed Pseudomonas
When within the next months Spike
aeruginosa
Since
continued to develop lung infections plus
Pseudomonas frequently shows resistance
problems elsewhere, further investigations
to many antibiotics, the lab folks also did
led to a diagnosis of cystic fibrosis.
an
antibiotic
beyond
doubt.
sensitivity
testing
to
determine which antibiotics they should
As for Tom, after a few days he started to
recommend
have symptoms characteristic of a UTI.
to
the
physician.
Aminopenicillins, aminoglycosides, and
Laboratory
quinolones were good candidates.
Pseudomonas infection. Pseudomonas is the
investigations
confirmed
type of organism that likes moist milieus,
was
such as toilets, inhalers, cosmetics, infected
administered for Tom. As for Spike, they
patients or carriers, etc., and had probably
took a swab to determine the infectious
entered Tom's urinary tract along with the
agent responsible for his pneumonia.
catheter.
When the lab staff incubated the specimen
As
Pseudomonas
entered,
it
attached itself to the lining epithelial cells
on blood agar, they saw colonies that
of the urinary tract by its pili. If there is
looked like a pellicle on the surface of the
cilia on the surface, they wouldn't be able
medium. This is because Pseudomonas
to expel Pseudomonas easily because of its
loves free O2 like crazy so it wants to be
slime layer. So it can infect just about any
near the air as much as possible. There was
mucosal surface in the body.
also a diffuse green coloration throughout

the plate (green metallic sheen due to
As
pyocyanin produced by the organism) and
they
began
to
get
excited,
Pseudomonas secreted their cytotoxin
a fruity odor. Their biochemical pattern
(which forms pores in the membrane of
allowed their definitive diagnosis.
the cells), exotoxin A (which inhibits

Airway in normal subject and in cystic fibrosis.
protein synthesis), and exoenzyme S
27
(which inactivates G
proteins
and
cytoskeletal
This
causes
an
inflammatory
infection
untreated,
If
is
hospitals. Generally people in hospitals

are
colonized
by
gram
-ve
bacteria
(including Proteus). So whenever there is a
response leading to
UTI.
Besides being present as intestinal flora,

Proteus species can cause UTIs primarily in
proteins).
the
Proteus
the
left
the
organisms can invade the bloodstream
crack, a break, anything in the skin or

mucus membranes, which allows access to
the inside of the body, these organisms
will make sure they dont miss the chance
and jump straight into the body.
causing bacteremia. Complications from

there include secondary infections of bone,
joints, lungs, heart, CNS, etc.
Two nephews of Pseudomonas aeruginosa,

who are Stenotrophomonas maltophilia
and Burkholderia cepacia, also wander
around in hospitals annoying the patients.
They also take courses on drug resistance
every once in a while.
So our poor patient was administered to
The characteristic swarming of Proteus cultures
the hospital. A catheter was administered

because he had low urine output. After a
What could it have been? It could have
few weeks he develops a UTI. You do lab
been due to Proteus. This is because Proteus
analysis and find out it was Proteus
makes urease, which converts urea to
mirabilis which had entered through the
ammonia, which alkalinizes the urine and
trauma caused by the catheter. Simply give
increases
him penicillin and bye-bye him. After
magnesium phosphate stones. Likewise
months or years, the guy develops flank
there
pain and dysuria. Investigations indicate
commonly found in chronic care facilities.
stone formation.
This one may need a cephalosporin.
is
the
risk
Proteus
of
vulgaris
developing
which
is
28
Other UTI Whackos
Treponema pallidum
Expanding your scope of criminals when it
Bob was living a very unhealthy life, being
comes to a UTI in a hospital setting,
indulgent in his desires. He recently had
consider these in your list:
unprotected intercourse with a prostitute.
Klebsiella oxytoca and Klebsiella
What he didn't know was that the
pneumoniae
cause
prostitute had syphilis, and so Treponema
necrotizing lobar pneumonia in
pallidum had entered through a skin crack
COPD
into his genitalia. The organism cannot
-->
patients,
also
alcoholics,
and
diabetics
survive for more than few minutes
Enterobacter --> also lung infection
outside the body and thus needs such a
Serratia marcescens --> also lung
direct transmission. Three weeks after the
infection
incident, he developed a painless hard
The chancre is caused by coagulative

necrosis of the local tissue which results
from ischaemia because of infection of
small blood vessels by the organism.
Nerve fibers are also destroyed so there is
no pain. Bob didn't even pay it attention
and left it to disappear by itself, and it
did. Hence the first stage ended.
ulcer (called chancre) on his genitalia.
Palmar rash of second stage of syphilis
The helical spirochete, however, was not

gone. It was swimming through the blood
and lymph throughout the body until after
around 6 months it began the second stage
Syphilitic chancre of the lip
of the war, by causing red maculopapular

rash on Bob's palms and soles, and moist
29
flat papules in his anogential region
with a prostitute. The physician thus noted
As the physician received the report, he
(called condyloma lata), armpits, and
in the paper he sent to the lab that they
decided to put Bob on penicillin. Bob,
mouth. Bob almost decided to visit a
should test for syphilis. The lab guy knew
however, told him that he had allergy to
physician but again ignored the idea. He
that Treponema is too slender to detect
penicillin, so the physician changed it to
was happy when these lesions also went
easily by staining, and he didn't like using
erythromycin.
away. Didn't I tell you to just ignore
darkfield
'em? he whispered to himself.
undulating movements. He thus decided
It's worth noting that syphilis can also be
to use serology for diagnosis!
transmitted through the placenta to the
microscopy
to
detect
its
After several years, however, Bob turned

out to be in those 40% of the patients who
would progress to the tertiary stage. The
organism had infected the vasa vasorum of
the aorta, causing weakness of its wall and
leading to aneurysm; they had caused
granulomatous lesions (gummas) in his
liver and bones; and they also had affected
fetus beginning from around the 10th week

Syphilis triggers the formation of two types
of antibodies:
1. Antibodies that are directed against
antigens of Treponema itself (detected by
the tests below)
2.
Antibodies
against
cardiolipin,
a
mitochondrial phospholipid; since these
antibodies may also form in SLE, a false
positive syphilis may get reported
neurological signs and finally decided it
The serological tests available for syphilis

are:
may be a good time to give the physician a
FTA-ABS (fluorescent Treponemal antibodyabsorption)
visit.
TPHA (T. pallidum haemagglutination)
Bob recalled his history of the genital
from abortion, to stillbirth, to birth with

symptoms of secondary syphilis.
There are non-syphilitic diseases with even

whackier names, caused by other
Treponema:
1. Bejel: in hot, arid areas like Africa
the blood supply of the brain causing CNS

degeneration. Bob was getting all kinds of
of gestation. The result could be anything
MHA-TP (microhaemagglutination
pallidum)
for
2. Yaws: in humid, tropical areas

3. Pinta: in America and others
T.
ulcer, the rash, the papules, and his current

symptoms. The physician also managed to
make him admit he had had illict relations
30
with gonorrhea from another partner.
So Bob changed his life for the better and

became more responsible. The prostitute,
however, continued her life as she was.
She recently had intercourse with a man
and as days went by she started noticing
some greenish-yellow discharge from her
cervix. She also noticed that she had
Neisseria
gonorrhea
prostitutes
thus
cervix
and
entered
the
Then they progressed up to the uterus and

the tubes, and finally entered the blood.
established
themselves by using their pili and opacity
From
protein (OMPII) to attach to the lining
bleeding, then pelvic pain, then the fever
epithelial
an
and joint pain, the gynecologist put
inflammatory response and development
gonorrhea at the top of her differential
of the symptoms.
diagnoses. She sent the patient to the lab
cells.
This
resulted
in
the
history
of
the
discharge,
for a specimen analysis. Blood and cervical
bleeding even in between her menses.
specimens were taken. An initial smear

from the cervical discharge demonstrated
Since she could bear the symptoms (which
gram -ve
ve diplococci. This, however, is not
were not so severe), the disease progressed
significant in a female because normally
further to involve the uterus, and from
there is a lot of floral microbes in the
there the ovarian tubes. The inflammatory
vagina. Besides regular blood cultures,
response ended in fibrosis and scarring of
they also cultured the cervical sample on
the tubes, resulting in infertility. As the

causative
agent
got
into
the
bacteremia resulted in fever (by their lipooligosaccharide),
joint pain,
Thayer-Martin
Martin agar (chocolate agar with
blood,
A small pustule on the hand in disseminated gonorrhea
inhibitors of other bacteria) and the

colonies of Neisseria showed up.
and she
would notice small pustules on her skin
As secretory IgA1 came to the scene, they
during her menses. She now couldnt bear
rushed toward the bacteria with all their
Since the blood sample also demonstrated
all this and decided to visit a gynecologist.
might and power, and as they were about
the presence of Neisseria, this was alarming
to bind to them, the bacteria released their
and indicated dissemination into blood.
secret weapon, the IgA protease, to see the
Of course it wouldnt
wouldn make sense to try
naive IgA1 shatter in front of their eyes.
and determine whether this is Neisseria
What was happening was that the man

who had intercourse with her was infected
gonorrhoeae
or
Neisseria
meningitidis
31
because
the
latter
doesnt
cause
gonorrhoeae. But if you find Neisseria in a
will need assisted reproductive techniques

if she ever wants to have a baby.
So, the prostitute repented from her
blood sample, then it may make sense to

determine which one it is.
previous life, and became committed to a

Other infections caused by Neisseria
gonorrhoeae:
1. Rectal infection in homosexuals:
constipation, difficulty in defecation, and anal
discharge
2. Pharyngitis from oral-genital contact:
purulent pharyngeal exudate
3. Ophthalmia neonatorum: eye infection of
newborn from mothers infected cervix; acute
conjunctivitis can end with blindness; treat
with erythromycin
chocolate agar allows growth of many others as well
As the gynecologist received back the

report, she told her patient she will
prescribe her a single IM injection of
ceftriaxone. No, objected the patient
stating that she doesnt like injections. So
the doctor changed it to a single oral dose
of ciprofloxacin. Since other investigations
demonstrated
tubal
scarring,
the
gynecologist told her patient that she

cannot get pregnant in a natural way and
more meaningful life with clear goals set in

her mind. The guy who previously
transmitted the gonorrhea to her, however,
continued in his way. In fact, when he
developed the gonorrhea, he later on
developed a more mucoid, less purulent
discharge from his genitalia. This was
basically
non-gonococcal
urethritis
caused by Chlamydia, as it often occurs
Notice how Thayer-Martin medium only allows growth

of Neisseria (hard to notice at this size) while standard
By the way, the guy who transmitted the
sequentially
gonorrhea to her, had himself developed a
gonorrhea.
(or
simultaneously) with
yellow discharge from his genitalia. When

the smear for this discharge showed gram
The interesting thing, though, is that while
-ve
he developed that discharge, he also
diplococci,
they
immediately
even
developed purulence in his eyes. It was
having to culture because the flora in
logical for the physician to conclude an
vagina do not exist in male genitalia.
inclusion conjunctivitis also caused by
prescribed
ceftriaxone
without
Chlamydia (serotypes D-K).

So he still continued with his life style, and
he recently had intercourse with another
woman. This time he developed transient
32
papules on his genitalia. He hoped they
commitment to make positive changes in
transmitted to him by the fly) and
would go away and they did. Few months
his life and also decided to visit a
lymphogranuloma venereum (caused by
went by and he noticed the development
physician. He complained about his eye
serotypes L1-L3).
of many bumps in his inguinal and
and his inguinal region. The physician
perirectal regions (lymphadenopathy). He
noted all the large masses in his inguinal
The physician had already put him on
now started thinking about correcting his
region as well as the groove sign (which is
Azithromycin even before receiving the
life and making positive changes in it. As
due to the inguinal ligament standing out
report, as he suspected Chlamydia infection
he was in deep thinking at a hill overlying
among the swollen lymph nodes). So he
from the history. When the report came
a river, a fly from out of the blue bumped
sent the him to the lab for analysis of his
back, he was happy that he was right.
into his right eye. He became outrageous
conjunctival pus as well as a specimen
and started chasing it like mad.
from the lymph nodes.
As it is common throughout the sexuallytransmitted diseases, any infant born to an
The lab guy removed the exudate from the
infected mother can get the chance for eye
conjunctiva and then took a scrap of
infection. It is thus a good habit to give the
exfoliate from the infected epithelial cells.
baby an eye drop of erythromycin because
Since it was almost too obvious that it was
this works well for syphilis, gonorrhea,
Chlamydia
playing
nasty,
microscopic
and trachoma.
examination of the sample using direct

fluorescent antibody staining was used to
Chlamydia pneumoniae is another whacky
demonstrate the cytoplasmic inclusions of
Chlamydia that can cause infection of the
Chlamydia in the epithelial cells. PCR
respiratory tract anywhere from the top to
demonstrated the presence of the baterial
the bottom. In fact it takes a good portion
After this incident, he started noticing pus
genome in the urine. These findings lead
of the shares of community-acquired
in his eyes. Urghhhhhh. I cant stand all
to the conclusion that the guy had two
respiratory infections and often gets
this. This must be a sign for me to stop. he
Chlamydia infections at the same time:
knocked off by blindly giving the patient
said
trachoma
doxycycline.
Cases of trachoma
to
himself.
He
made
firm
(caused
by
serotypes
A-C,
33
Skin and Soft Tissue Infections
Bacillus anthracis
35
Clostridium perfringens
36
Yersinia pestis
37
Mycobacterium leprae
39
Bacteroides fragilis
40
Actinomycetes
41
Francisella tularensis
42
Pasteurella multocida
42
Propionibacterium
43
Lactobacilli
43
Bartonella henselae
43
Other Haemophili
43
32
34
Bacillus anthracis
Mike was visiting his grandfather in the
countryside with his parents. He was
thrilled at learning how to cycle on his
brand new bicycle. Initially he could go as
far as a few meters only. He then decided
on trying further. He was inadvertently
heading toward a car so he made such a
sharp turn that he fell on the ground and
injured his forearm. He stood up, looked
around, brushed his arm, and went on
The physician noted the carbuncle on his
physician
forearm and from the history suspected
decided to put Mike on ciprofloxacin.
after
receiving
the
report
malignant pustule (cutaneous anthrax).

He sent them to the lab so that a specimen
Mike's grandfather, Pete, raised sheep and
could be taken from it. An initial smear
other animals for a living. Recently he had
showed blunt-ended gram +ve rods that
developed fever and some difficulty in
didn't show spores often. This is because
breathing that were progressively getting
spores are not needed in the comfortable
worse. After visiting the physician and
body conditions. They form later when
having a lab specimen analysis, he was
they have been outside the body for a
diagnosed
while.
(woolsorter's disease) due to Bacillus
with
inhalational
anthrax
anthracis. The bacilli (and their spores) had
training.
entered his respiratory tract with the

animal hides and wool. They then used
Behind the scenes, the spores of Bacillus
their edema factor and lethal toxin to cause
anthracis had entered the wound with the
a progressive hemorrhagic lymphadenitis
soil. After germination, the bacilli used
that caused the shortness of breath and
their protective antigen to allow their

edema factor and lethal toxin to get into
other symptoms.
Examples of malignant pustule (cutaneous anthrax)
the local cells to cause edema and

destruction. Within two to three days, a
The incubated blood agar showed large,
painless black ugly mass developed on
mucoid (due to capsule), grayish colonies
Mike's forearm. He was so scared that he
with no hemolysis around them. Their
went with his dad to a physician.
border was irregular and medusa hairlike. Diagnosis of Bacillus anthracis was
confirmed by immunofluorescence. The
So Pete was put on a combination of

ciprofloxacin, rifampin, and vancomycin.
On hearing the term 'inhalational anthrax',
Pete
exclaimed
and
related
to
the
physician how some years ago he had

heard about the head of a Mafia group
who had died of this disease after
35
receiving a letter inoculated with this

organism. Pete was so scared that he
decided to tell his neighbors to receive the
cell-free vaccine and to get prophylaxis
with ciprofloxacin after they handle a lot
of wool.
Jack was driving at 150 km/hr down a
found a suitable anaerobic climate to

germinate into vegetative cells.
straight road in a semi-desert area. He was

in one of his most relaxed moments in life.
This comfort was disrupted when he saw a
camel crossing the road. He made such a
sharp turn that the car flipped over and he
got several severe and open wounds on
his body. Several hours passed by until
somebody else driving through the same
road saw the car and called emergency. An
ambulance arrived from a nearby city and
Jack was driven to the hospital.
Letter tainted with B. anthracis
The cousin of Bacillus anthracis is Bacillus

cereus. It has no capsule (so it has rough
colonies) and can only cause one type of
infection (which can also be caused B.
anthracis) which is food poisoning through
an enterotoxin leading to diarrhea and
vomitting.
They noticed he had a big necrotic ulcer

on his thigh. When they pressed on it they
could feel a crinkling sensation (or
crepitation). This indicated formation of
gas under there. They were afraid of gas
gangrene and the possibility of shock and
renal failure. They were in fact right. The
soil had spores of Clostridium perfringens
in it. When Jack got the injuries there, the
spores entered one of the deep injuries and
Gas gangrene (myonecrosis) caused by Clostridium

perfringens
They then elaborated their alpha toxins (a

phospholipase C) to start destroying the
cell membranes of local tissue cells. Since
they are anaerobic chaps and can only use
fermentation to acquire energy, their use
of glucose and further metabolism of the
resultant pyruvate produced CO2 which
was the gas that resulted in the crepitation
under the skin. Their hyaluronidase and
other tissue destroyers allowed them to
break through the ground substance and
eventually get into blood. So now there
36
was the risk of causing shock and
learned
intravascular hemolysis. But Jack hadnt
management steps were accurate.
that
their
preliminary
yet reached this stage.
Yersinia pestis
It was a soothing evening in the year 1348.
Edward had just returned home worried
and afraid of news about the plague
everybody was talking about. It had
Other infections caused by Clostridium perfringens:

1. Diarrhea by enterotoxin acting in ileum
2. Enteritis necroticans with high mortality
3. Anaerobic cellulitis: fasciitis and gas formation,
but no muscle involvement and no toxemia
4. Endometritis: gangrene of uterus and toxemia
due to incomplete or non-sterile abortion
already spread among people of nearby

villages. In the next morning, he was out
in the store when he noticed that his friend
started spitting out bloody sputum. He
had also developed blue bumps on his arm
(buboes).
Jack was immediately placed on high
the anaerobic bacteria) because there was
of the
sputum
had
contaminated Edwards store and he later
doses of cephalosporins and hyperbaric

oxygen was applied to his lesions (to kill
Some
had to clean it up.

Area of beta hemolysis surrounded by an area of alpha
hemolysis for colonies of Clostridium perfringens on
blood agar
suspicion of gas gangrene. They remved

the dead tissue by surgical debridement
then a specimen was taken from it to
prepare a smear. The smear showed
different organisms including gram +ve
spore-forming rods. Culturing on blood at
anaerobic conditions demonstrated the
rapidly-growing colonies with double
zone of hemolysis. So their suspicion of
Buboes of bubonic plague
gas gangrene was confirmed and they
37
What had happened was that Yersinia
dizziness
some
occurs today (which is rare and sporadic),
pestis, the culprit of the plague, had spread
showed signs of throat infection (palgue
the physician suspects Yersinia from the
through
pharyngitis); and some showed the typical
buboes on the guys skin. He sends him to
bubonic course of the plague.
the lab, and a blood sample or a buboe
sputum
of
infected
people,
through people touching infected rats,
(plague
meningitis);
and among rats by rat flea. Edwards
sample cultured on MacConkey or even
friend had acquired the infection when he
blood agar will show colonies. From the
had removed a dead rat from the road. At
biochemical
that time Yersinia entered through a crack
diagnosed. If not enough, anti-Yersinia
in his skin. They entered phagocytes of the
antibodies can be detected in serum.
pattern,
Yersinia
can
be
skin and resisted destruction and caused

the hemorrhagically-altered, blue, swollen
The patient is then placed on streptomycin
lymph nodes (buboes) to appear. Then
and supportive therapy is given as needed.
they
Aggressive management is essential if
entered
septicemia,
blood,
and
from
resulting
there
in
entered
there is septicemia.
various organs, including the lungs, to

cause a secondary pulmonary plague.
Edward got the infection by aerogenic
transmission from the infected sputum of
his
pal
and
developed
primary
pulmonary plague. Thus after a few days,

he himself started noticing blood in his
sputum. He was very scared. He also
noticed that many people of the town had
started getting sick. Some of them showed
signs of neck stiffness, vomiting, and
Yersinia pestis can be acquired by touching a rat

infected with it.
A lot of the town people died from the

plague, and within a few years the plague
actually killed around 1/3rd the total
population of Europe. If the same infection
38
Mycobacterium leprae
A nephew of M. tuberculosis is M. leprae.
This organism is very similar to M.
tuberculosis in shape and pathogenesis;
after all, they are nephews. Back in the
middle ages, lepers were isolated in
leprosy houses to prevent spread of the
The
sad
part,
though,
was
that
if
The organism is so pompous that you
somebody merely had a fungal infection in
cannot really culture it on anything.
those days, they would still consider him a
Maybe if you are whacky enough you can
leper and he would also be put in those
get footpads of mice or armadillos and
leprosy houses where he would get the real
grow the bacteria there. When the leper
leprosy within 2-20 years (incubation
visit a physician with the characteristic
period)! Too bad.
lesions, the physician requests a lab

analysis. The lab folk carefully takes a
disease. This is because this organism

spreads by long-term contact between the
infected persons's skin and the skin of a
healthy person. So, for example, if the
infected person had crackles in his hand
which contained exudate, and the healthy
person had some minor cut in his skin, the
organism would spread through hand
contact.
As M. leprae enters the skin, it initiates
specimen and prepares a smear. Ziehl-
granulomatous inflammation just like M.
Nielson stain shows pink slender rods.
mainly
This makes it almost certain that this is M.
involve the mucocutaneous tissues (like
leprae. So the lab guy ignores the PCR test
tuberculosis.
nose)
and
The
granulomas
peripheral
nerves.
The
and writes the report telling the physician
tuberculoid form of the disease includes
that it is indeed leprosy. The physician
large spots (maculae) on the skin of nose,
puts the patient on multiple drug therapy
outer ears, and testes along with patches of
(choosing from dapsone, rifampin, and
anesthesia
clofazamine) for a long time.
(from
neuritis).
The
lepromatous form is slowly progressing

and causes severe disfigurement of the
M. leprae continues to infect around 11
body.
million people worldwide, found mainly

in developing countries. BCG, the same
vaccine used for TB, is also effective
against this pathogen.
A leper hospital
Tuberculoid (left) and lepromatous (right) leprosy
39
Bacteroides fragilis
Clark recently developed mid-abdominal
pain. The pain gradually started localizing
to the lower right side of his abdomen.
When the pain turned unbearable, he
rushed to his physician. The physician
diagnosed a perforated appendicitis and
sent him to a fellow surgeon. The surgeon
fever and malaise. What had happened
anaerobic blood cultures.

cultures The aerobic
was that Bacteroides fragilis and a number
culture returned E. coli and many others.
of other bacteria, all of which normally

colonize the colon, had gained access to
After a few days, the slower anaerobic
the peritnoeum through the perforated
culture demonstrated mainly Bacteroides
appenditis to form an abdominal abscess
fragilis,, as well as a few other street
and from there gained access to the blood
rappers like Prevotella, Porphyromonas, and
causing bacteremia.
Fusobacterium The lab folk even did

Fusobacterium.
sensitivity testing for all the bacteria, and
performed the appendectomy and asked

for
some
general
antibiotics
to
be
prescribed for Clark.
Clark thus went back to his physician. The
he saw that for the anaerobes they had
physician was afraid of an abdominal
become resistant to ampicillin-sulbactam,

ampicillin
abscess so he sent him for a CT scan (>95%
imipenem
imipenem-cilastin,
and clindamycin. They
accuracy for diagnosis). The scan returned
were, however, sensitive to metronidazole
a positive result. As Clark was showing
and cefoxitin.
cefoxitin
signs of bacteremia, the physician sent him

to the lab for blood analysis.
When the physician received the report

back, he directed
direct Clark to the surgeon for
Appendicitis can end with perforated appendix which

provides fertile ground for abdominal abscess
The lab folks received the physicians
draining the abscess

ab
and prescribed him
request for finding the culprits of an
metronidazole. He also wrote a note to the
abdominal abscess. They took the blood
surgeon telling him Didnt your seniors
sample and did an initial smear to see all
teach you to put your post-op patients on
kinds of whacky organisms having a party
cefoxitin to prevent abdominal abscesses
with the polymorphs, throwing debris at
or did the hospital run out of

o it?
each other. The shrewd lab lad then

A few weeks later, however, Clark started
decided to prepare both aerobic and
developing intense abdominal pain with
40
Actinomycetes
45-year-old Bob comes in to your clinic
complaining of a lump in his mouth. As
he opens his mouth at your request, you
strive to hold yourself from showing facial
signs of disgust at what you see: dead
rotten things that are supposed to be teeth,
sitting in a neighborhood of pus and
mucosal lesions. You control yourself and
direct your attention to the lump. You
notice it is a red, hard, and non-tender
swelling that has ruptured to release pus.
You think to yourself what's happening
receive the lab report, you decide to put
could be actinomycosis due to poor oral
Bob on penicillin G to control the
hygiene and a recent tooth extraction.
infection. As for the current lesion, you
Since actinomycetes is normal flora in the
direct him to a surgeon for debridement
mouth, those conditions allowed it to enter
and drainage. Finally you advise him to
the soft tissue beneath the mucosa and
visit a dentist to maintain good oral
proliferate in an anaerobic condition.
hygiene from now on.
They elicited the inflammatory response

that caused the swelling and eventually
underwent rupture with release of pus.
The yellow granules were small colonies of
Actinomycetes surrounded by leukocytes.
The pus interestingly contains yellow

granules.
You send Bob to the lab for specimen

analysis. The lab guy takes an initial smear
and sees purple rods having branches. He
is almost sure this is Actinomycetes. Just for
fun, however, he decides to culture it as
well. He does so in anaerobic, canaphilic
conditions on blood agar. In the first few
days he doesn't see any colonies. He
whispers to himself This must be the
stage of the microscopic colonies.
After two weeks, white colonies appear. I
Actinomycosis of tongue due to poor oral hygiene
knew it! he whispers fervently. After you
41
Francisella tularensis
Little Tom was looking through the wind
ows of their car with a smile on his face as
they were driving to their picnic site. After
settling in the place, he notices a small
rabbit near some trees; he goes towards it
and tries to play with it. The apparently
pacific rabbit gets intimidated when little
Tommy touches its ears. The red-eyed
rabbit turns angry like mad and sticks its
claws in Tom's palms. Baargghhhhh!
screams little Tom.
their long-awaited picnic and thus simply

clean the wound and dress it up from their
first aid kit. Few weeks later, Tom is
getting scared of a ulcer at the site of
wound and notices painful bumps (tender
lymphadenopathy) under his skin. His
parents take him to a physician. From the
history and symptoms, the physician
suspects tularemia. If it is left as it is, there
is the risk of septicemia (typhoidal
tularemia), and spread to the liver and
spleen. So he sends Tom to the lab for a
specimen analysis.
Little Bobby liked to play with his puppy.
One day as he was playing outside, he fell
on the ground and injured his leg. The
scratch was relatively small and didn't
need much attention. As was its habit, the
puppy would lick Bobby's leg often. The
day after the incident, Bobby started to
develop a painful ulcer on his leg. What
happened was that Pasteurella multocida
entered Bobby's skin with the dog's saliva.
This organism can also be transmitted by a
bite or scratch, whether from a dog, a cat,
or other animals.
The lab folks do

a
smear
and
notice
pink
coccoid
rods.
They
confirm
the diagnosis of
Francisella
tularensis by finding specific antibodies
Tularemia involving the thumb
against it in Tom's serum. When the report

comes back, the physician prescribes
His parents rush to him to see what
streptomycin for Tom, and tells him not to
happened. They don't want to mess up
mess with rabbits any more.
As his parents took him to the hospital, the

physician noted the acute cellulitis and
from the history put Pasteurella multocida in
his differential diagnosis. In the lab a
smear was prepared from the ulcer
specimen
and
it
showed
gram
-ve
coccobacilli that also exhibited bipolar

staining.
Further
tests
Pasteurella
multocida
and
confirmed
Bobby
was
prescribed penicillin.
42
Propionibacterium
Lactobacilli
You know how ugly zits can develop on
Trichomonas vaginalis, the protozoan that
the face. Actually, the acne bacteria, or
causes vaginal infections, has a long
Propionibacterium, are normally present
history of hatred against the pacific
on the skin and can only contribute to acne
lactobacilli. The reason is that these
when certain conditions are met. So
bacteria make the vaginal pH acidic while
bombarding them with antibiotics isnt a
the protozoan doesn't like that.
which can look like Kaposi's sarcoma

(caused
by
human
herpes
virus
8).
Bartonella henselae can be demonstrated by

silver stain, and the infections are treated
with broad-spectrum antibiotics.
good idea. Rather balancing diet and

hormonal status under supervision of an
The lactobacilli aren't that peaceful either.
experienced nutritionist is better. These
In fact, they have been found guilty of
folks can also cause endocarditis and
assisting the criminals who cause tooth
infections of plastic implants.
decay in the mouth. It is possible, then,

that Trichomonas doesn't just harbor a
Cat scratch disease
personal hatred against them.
Bartonella henselae
Other Haemophil
Haemophilii
Bartonella henselae is transmitted by a
Two colleagues of Haemophilus influenzae
scratch from a cat. It causes necrotizing
had gone different paths. Haemophilus
lesions at the scratch site with local
ducreyi took its PhD in causing a tropical
lymphadenopathy and fever.
venereal soft chancre and in being

difficult to culture except on special media.
The composition of an acne
In AIDS patients, Bartonella henselae is
Haemophilus aegyptius, on the other
associated with a vascular proliferative
hand, got its master's degree in causing
disorder called bacillary angiomatosis,
purulent conjunctivitis in Egypt.
43
Febrile and Systemic Infections
Brucella melitensis
45
Corynebacterium diphtheriae
46
Rickettsia rickettsii
47
Rickettsia prowazekii
48
Borrelia burgdorferi
49
Leptospira interrogans
50
Bartonella quintana
51
Borrelia recurrentis
51
Chlamydia psittaci
51
Ehrlichia
52
Spirillium minus
53
44
Brucella melitensis
Jubayr had been working in an abattoir
(place where animals are slaughtered) for
over 10 years. On a seemingly-regular
shiny day, they received a whole new set
of animals from a new farm. After a few
weeks, Jubyar began having fever and
chills particularly in the evening. These
and
other
non-specific
constitutional
symptoms made him very depressed since

he was working hard all day, and when he
would return home he couldn't take some
The symptoms then started following an
symptoms, so he wrote a note to the lab
undulant course; there would be fever for
regarding that so that they keep the
a few days, followed by days of no fever,
culture for up to a month before declaring
followed by recurrence. Jubayr decided to
them negative. The lab guy decided to take
visit his physician. What had happened
a bone marrow specimen (most sensitive
was that Brucella melitensis was present
specimen) and culture on blood agar as
in the new set of animals. Jubayr got
well as brucella agar under aerobic
infected as the organisms entered cuts in
conditions. Blood agar cannot be trusted
his skin and he even inhaled some of
here since a period of up to a month is
them.
needed
These
organisms
can
also
be
before
declaring
it
negative.
contracted by eating products of infected
Diagnosis of brucellosis was confirmed by
animals.
agglutination tests.
As the organisms enter the local tissue,
they spread through the lymph nodes and
decided to put Jubayr on combination
blood to the reticuloendothelial system.
therapy of doxycycline and gentamicin for
They localize intracellularly and multiply
a month and a half to prevent relapse and
there, causing formation of granulomas.
avoid complications. He was careful to
Whenever they enter the blood, they cause
inform Jubayr that he doesn't need to
the signs and symptoms of the disease
isolate himself from people as the disease
rest.
through
releasing
LPS,
creating
an
is not communicable.
undulant pattern of symptoms (undulant

fever).
An abattoir showing cattle carcasses
The physician had reasonable suspicion of

brucellosis from Jubayr's job and his
45
the
Richard was speaking with an old friend
spreading the organism in aerosols.
convalescent
period
and
was
mouth (say Aaaa) so that he can take a

look at his pharynx. He noticed this thick,
in the market. As they were discussing life
grayish,, adherent exudate. He already
issues, the old friend mentioned that he
established his suspicion of diphtheria
had just recently recovered from an illness
from this, but he had to send Richard to
that had reached to the point of involving
the lab for analysis. So the lab folk took a
his heart. After five days from the
pharyngeal swab from Richard and did an
encounter, Richard started developing a
initial smear to see gram +ve organisms
sore throat, which he thought was trivial
arranged in V and Y patterns. He was

ALMOST sure this is Corynebacterium
and ignored it. As days went by, however,

the
sore
developed
throat
became
low-grade
worse,
fever,
Diphtheria pseudomembrane
he
and
prominent bumps in his neck (cervical

lymphadenopathy).
What happened was that his old friend
had recently recovered from complicated
diphtheria that involved the heart (where
it can cause cardiac conduction defects
and myocarditis) and can even involve the
cranial nerves causing paralysis of palate
and eyes. The bacteria had reached down
from pharynx to lower airways almost
increasing risk of suffocation. Since his
friend had recovered recently, he was in
diphtheriae But, he had to make sure.

diphtheriae.
Richard thus got the bacteria through

inhaling the aerosols. The organisms
established themselves in his throat and
started releasing the diphtheria toxin. This
is an exotoxin (of A and B subunits) that
enters the cells and stops elongation factor
(EF-2) thus inhibiting protein synthesis
and resulting in cell death. This initiates an
inflammatory response that results in the
formation of a pseudomembrane (the gray
stuff).
Corynebacterium diphtheria under the microscope; note

the V and
nd Y patterns of arrangement;
arrangement the terminal
purple round structure are polyphosphates, not spores
He thus arranged a visit to his physician.

The physician asked Richard to open his
46
He thus cultured the sample on Loeffler
The physician thus received the report
slant
or
back confirming his initial suspicion. He
modified Tinsdale medium. Within 1 to 2
placed Richard on penicillin to eradicate
days, the results of the culture turned
the infection and a single dose of horse
positive for Corynebacterium diphtheriae.
serum
The ginger lab guy did a final confirmation
circulating toxins. He also advised him to
of his diagnosis by an ELISA test, looking
vaccinate his children (with the DPT or
for
diphtheria-pertussis-tetanus
and
cystine-tellurite
antibodies
against
agar
Corynebacterium
diphtheriae and he sure found them.
antitoxin
to
neutralize
free
vaccine)
starting from infancy, then giving booster

doses every ten years, so that they have a
lower risk of developing the infection that
their father developed.
Cowdry was on a trip going around
different countries in the US. In one of the
countries he went hiking for the day. It
was a hot summer day when he felt a
pinch in his leg while climbing the
mountain. About a week after the incident,
after he had returned home, he started
developing a high fever with malaise, and
a macular spotty rash on his skin with
some areas showing frank hemorrhage. He
quickly arranged a visit to his doctor.
Rash in rocky mountain spotted fever

Colonies of Corynebacterium diphtheriae on cysteinetellurite agar
What had happened was that the pinch

was a dog tick taking a bite at Cowdrys
47
leg. The tick injected Rickettsia rickettsii into
hemorrhages that were responsible for the
Cowdrys body. The ticks are a good
rash.
Amy was living in northeast Africa with
vector of these organisms and can even

pass
them
down
to
their
progeny
Rickettsia prowazekii
her husband and two kids. She was
The
doctor
started
suspecting
rocky
transovarially to keep the infection source
mountain spotted fever from the history
going for years.
of the travel and the spotty rash on his

skin. He thus sent him to the lab for an
analysis. When the lab folk noticed the
doctors suspicion of Rickettsia, he said to
himself I know that Rickettsia are obligate
intracellular bacteria and can only be
grown in cell cultures and hen embryo
pregnant in her fifth month. They were

recently displaced from their village and
had to reside in concentration camps
along with fifty other families. About a
week after they had gotten there, a lot of
people including Amy started developing
an intense fever, chills, and headache that
would overall lead them to prostration
and stupor.
yolk sacs, so why should I not just look for

the antibodies? Why bother? So he just
did
serological
test
looking
for
antibodies against Rickettsia, and he sure

found them. The reason for their obligate
Dog tick, the vector of Rickettsia rickettsii
intracellularity
So
the
organisms
circulation
and
entered
started
into
the
entering
is their
leaky
plasma
membrane through which nutrients and

coenzymes can pass.
endothelial cells of blood vessels in a

manner like phagocytosis. Inside the cells
The enthusiastic doctor received the report
Typhus often occurs in displaced people in
they would mobilize the actin filaments in
telling him it is Rickettsia rickettsii. He thus
concentration camps
order to form bridges that would get them
put Cowdry on doxycycline.
to adjacent cells, leaving the first infected

cell dead. In this way, they started causing
What had happened was that Rickettsia

prowazekii had spread through the body
48
louse among different individuals in the
setting in which it occurred (displaced
camp. When the louse takes a bite on the
crowd of people), the team suspected
skin, it also places the organisms on the
typhus, caused by Rickettsia prowzekii.
Borrelia burgdorferi
Spook lived in a very dirty apartment. It
harbored all kinds of whacky organisms.
skin along with its feces. The person
There were ticks all over the place. He had
reflexly scratches the site of the bite
They thus went straight to serological
causing the organisms to enter the body.
tests to demonstrate antibodies produced

against
the
organism.
When
they
identified the bacterium, they started

giving the affected patients antibiotics like
doxycycline. Since Amy was pregnant,
however, she was instead prescribed
chloramphenicol. The team also reassured
developed so many infections before that

he had become tolerant to many of them.
One day he brought a new friend of his,
Spikes, to see his apartment and convince
him that he wasn't rich. Spikes could only
stay there for around 10 minutes then
rushed out with the excuse that he had
something important to do.
the people that the epidemic shouldnt last

long since the bacterium eventually also
kills the body louse that transmits it; so
much for helping out a bacterium.
Body louse, vector of Rickettsia prowazekii
the incident. Some of the younger patients

recovered. Older individuals retained the
infection and were starting to show
signs
and
chest
development of a red circle with a clear

center on his arm (erythema chronicum
migrans) and soon developed fever. After
About two weeks passed over the start of
neurological
After a few weeks, Spikes noticed the
pain
(myocarditis). A health team was called to

the region. From the pattern of the disease,
a few weeks, he began having joint pain,

vomiting, stiff neck, and headache, and
chest pain. What had happened was that
the ticks in Spook's apartment were
harboring Borrelia burgdorferi inside them
and one of those ticks had bitten Spikes
when he was in the apartment.
the location (northeast Africa), and the
49
Pete was goin g for a picnic near some
green hills with his wife and two kids.
There they used up all the water they had
taken with them. They then had to use
his physician. The physician ordered a lab

test for his blood and CSF. From the
culture, elveated IgM, and seeing the
bacterium in the blood, diagnosis of
leptospirosis was made.
from the water of a river near them. His

wife and kids refused to drink from the
water while Pete himself didn't mind.
About a week later, Pete developed a
fever. Leptospira had entered the water
when it was contiaminated with animal
urine so Pete got infected when he drank
Erythema chronicum migrans
The organism caused the local lesion, then

spread to the joints causing arthritis, to the
CNS causing meningitis, and to the heart
causing carditis. Spikes immediately set an
appointment with his physician. After a
diagnosis of Lyme disease was made, the
physician informed Spikes that if he had
waited for another few months, the disease
could have progressed to chronic arthritis
and even progressive CNS disease. He
thus put Spikes on antibiotics.
the water.

became alert as he knew this was the
second stage of the disease since there is a
mortality rate of 10% at this stage. He
decided to hospitalize Pete and put him on
IV penicillin G as well as supportive
therapy for the complications.
As the week passed by, the fever

went down a little bit, but Pete then
started to notice yellow coloration
in his eyes along with vomiting,
stiff neck, and urinary problems.
The organism had caused vasculitis
in different organs such as the liver
(causing centrilobular necrosis),
the kidneys (causing nephritis),
and the CNS (causing meningitis).
He arranged an appointment with
Transmission and pathology of leptospirosis
50
Bartonella
It was December 1914. Potter was forced to
enroll in the army. He just despised it; he
didn't want to die young. After a few days
in his camp, he and many other soldiers
developed fever, maculopapular rash, and
called it Rickettsia quintana. Later they

placed it in the genus Rochalimaea, and
finally
reclassified
it
as
Bartonella
quintana. A broad-spectrum antibiotic

(like a tetracycline) is good enough for
treatment.
headache. This was creatively called

trench fever. The symptoms would recur
Chlamydia psittaci
Arthur recently turned 75 years old. He
was still engaged in good acts and helping
people for their needs. He liked to also
take care of an animal; he thus decided to
buy a parrot. About a few days after
buying the parrot, he suddenly started
developing a dry cough with fever. He
every 4 or 5 days until he recovered after a
few months.
This organism is transmitted by body
contrary he started noticing prominence
louse (just like Bartonella quintana) and
of his abdomen. He thus arranged a visit
causes relapsing fever, which is now rare
to his physician.
hoped it would a mild infection, but to the
in developed countries. The organism can

be demonstrated in blood, and the patient
is prescribed penicillin.
After the physician welcomed him and

they talked a little about Arthurs life and
how everything was going, he told the
doctor that recently he bought a parrot and
now that a few days have passed, he has
started to get fever with dry cough, and
Pediculus humanus, human body louse
So many years later the human body louse

was shown to be the vector of the
causative agent. Since they initially found
rickettsia-like agents in the lice, they first
prominence of his abdomen. The physician

performed some physical examinations
and
noticed
hepatosplenomegaly.
He
suspected a zoonosis from the history and

the
symptoms,
and
was
afraid
of
51
complications because of Arthurs old age.
went by and Arthur got much better. Just
He thus prescribed a number of wide-
for record keeping, they took another
spectrum
(including
serum sample to measure the antibody
doxycycline) as a precautionary step and
titers and see if there is a rise. They noticed
sent Arthur for lab investigations.
that the antibody titer Chlamydia psittaci
antibiotics
had risen fourfold.
This
confirmed
diagnosis
of
psittacosis.
It
turned out
that
Arthur
had
Ehrlichia
A patient enters your clinic with a recent
fever and muscle aches, and asks you with
a straight face Doctor, what do I have?
You give him a straight-face look back and
remark How on earth am I supposed to
know? It could ANYthing. You write him
a list of regular lab tests to give you an
initial idea. From the blood film, you
notice a decrease in white cell and platelet
counts. That still doesnt tell you much.
obviously inhaled
dust
contaminated
with the feces of
the parrot, which
was a carrier for
Psittacosis is transmitted by inhaling dust contaminated with bird droppings.
Chlamydia psittaci.
Ehrlichias morula in a neutrophil (left) and a monocyte
(right); what an insult
A few days went by and no standard

culture turned positive for any significant
After so many days of trying all kinds of
pathogen. Since psittacosis (or ornithosis)
lab tests trying to find the causative agent,
was one of the differential diagnoses,
finally the serology of Ehrlichia chafeensis
serum antibody titers were measured for
turns positive. Whewww!, sighs the
it in the initial lab visit. So a few more days
52
poor lab guy to himself. When you receive

the report, you learn that the patient had
human monocytic ehrlichiosis (HME)
acquired from a tick bite and prescribe
Spirillum minus
In the dark alleys of town nowhere, there
existed a savage rat with two red eyes and
a spiral unculturable organism inhabiting
him doxycycline. And here is my 25th
its body, Spirillum minus. A warrior and
doxycyline prescription this week..., you
master of ancient arts, Sodoku, decides to
remark to yourself.
rid the town of the evil of this stinking rat.

After a bloody 2-hour fight, the rat takes a
whacky
feature
of
both
Ehrlichia
chafeensis and its sister-in-law Anaplasma

phagocytophilum
[which causes human
granulocytic anaplasmosis (HGA)] is that
bite at Sodoku's leg, and Sodoku responds

by pressing his spear down the rat's head.
As Sodoku returns home with his triumph,
he develops a fever. End of story.
they make an absolute straightforward

insult to the leukocytes by trying to claim
legitimate right of inhabitation inside them
within cytoplasmic vacuoles, causing the
appearance of inclusions called morulae.
They are reminiscent of the state of Israel
(only that you cant use doxycycline for
eradicating that).
Spirillum minus under some super-magnification
Oh, and Sodoku is the name of the disease.
53
CSF and Nervous System Infections
Neisseria meningitidis
55
Clostridium tetani
56
Clostridium botulinum
58
54
Samuel was living with his parents and
two brothers in a modest hut in Senegal.
He did different kinds of jobs for a living,
such as sometimes working as a laborer.
He was recently accepted as a laborer in
organisms established themselves on his
that they will cause shock and circulatory
nasopharynx. They were laughing at the
collapse by their lipo-oligosaccharides
capsule
and also cause hemorrhagic rash on the
prevented them from being phagocytosed.
skin. This stage results in death of the
They also released their IgA protease to
patient within 2 days. Thats why Samuel
silence the nearby secretory IgA1.
rushed to the hospital as soon as possible.
macrophages
because
their
the construction of a building along with a

large number of other laborers. After about
four days from starting the job, he
developed fever. Then he noticed his neck
was getting stiff, he started vomiting, and
his eyes became sensitive to bright light.
As he was living in Senegal (part of the
African meningitis bell), he
became
scared this might be meningitis and

rushed to the hospital.
Skin rash in meningococcal septicemia caused by

Samuel
was
indeed
right
about
his
concern. What had happened was that one

of the other laborers was a carrier for
Neisseria meningitidis in his throat (about
10% of the population are carriers). As he
was talking with Samuel on the first day of
work, Samuel unknowingly inhaled some
of the infected respiratory droplets. The
They
then
started
invading
the
nasopharynx to get to the blood; this

resulted in the fever. As they crossed the
blood-brain barrier, the inflammatory
response resulted in the meningitis. Had
The areas highlighted in orange comprise the African
Samuel ignored this, the organisms would
meningitis bell
have proceeded to cause a fulminant

meningococcal septicemia, which means
55
The hospital staff had gotten used to
Samuel was thus prescribed ceftriaxone
diagnosing and treating cases of Neisseria
for himself and prophylactic ceftriaxone
meningitidis and would make the diagnosis
for his family members. He was also
just by seeing the patient. But because
advised that if he has small siblings, they
there was a staff of visiting doctors from
should receive the MCV4 tetravalent
outside the country to monitor the quality
vaccine conjugated with diphtheria toxoid.
of health practice in the city, the hospital
Clostridium tetani
Little Sally was visiting the house of one of
her relatives with her mother. When they
got there, she rushed to their garden and
started playing with the butterflies on the
flowers. She incidentally injured her arm
with a splinter but didnt want to make
staff had to perform all the standard tests
There is a good-intentioned imposter that
to reach a legitimate diagnosis. So they
can be confused for Neisseria because of
took a CSF sample by lumbar puncture
its shape. They call him Acinetobacter and
and also took a blood sample. They saw
it has been wondering around in hospitals
the gram -ve diplococci in the initial
trying
smear. They didnt want to use Thayer-
patients. If you are ever doubtful, check its
Martin in this case because normally there
oxidase
isnt flora in blood or CSF.
(Neisserias is positive), plus it cannot
its
luck
and
it
on
immunodeficient
should
be
negative
ferment sugars (while Neisseria can).
her mommy angry so she kept quiet about

it. Four days later, little Sally started
noticing spasm at the site of the injury. As
time went by, she started developing
spasm
in other
parts of her
body,
including her jaw (lockjaw), as well as

difficulty in swallowing (due to spasm).
What happened was that spores of
So they just used good old chocolate agar
Clostridium tetani were present in the
to grow the polite Neisseria. Just to pretend
garden and Sally had been only partially
to be smart, they did sugar fermentation
vaccinated against tetanus because of her
tests to show that the Neisseria could

ferment both glucose and maltose thus it
was Neisseria meningitidis and not a
disseminated
infection
of
Neisseria
gonorrhoeae (which cant ferment maltose).

The specific serovar of meningitidis was
parents negligence. When the splinter

injured her arm, the spores of the bacillus
entered beneath her skin and germinated.
The vegetative organisms then released
their A-B toxin, called tetanospasmin or
tetanus toxin, which entered the local
then identified by slide agglutination.
56
neurons and went even further retrograde

within the neuron. It also gained access to
distant neurons by migrating through
blood. It is basically a protease that cleaves
a protein called synaptobrevin, and this
basically prevents the release of inhibitory
neurotransmitters
like
GABA
thus
preventing relaxation of muscles.

Clostridium tetani has the shape of a tennis racquet
She alarmed her mom about it so she was
because of its single terminal spore.
taken to the hospital. The features were

They then took a blood sample and
very characteristic of tetanus so she was

antitoxin
injected it into a mouse to notice whether
(because human hyperimmune globulin
the features of tetanus will be produced or
wasnt available) and an endotracheal tube
not (mouse neutralization test). A casual
was inserted to secure her breathing. She
smear showed racquet-shaped gram +ve
was also given sedatives to relieve her
organisms (because of terminal spores).
anxiety, muscle relaxants to release the
They didnt have PCR to multiply the gene
spasm, and penicillin to kill the bacteria.
of the toxin in the bacterium and then
immediately
given
horse
detect it. They really didnt care because

they saw that the symptoms gradually
disappeared after institution of therapy.
Sallys mother was advised to give more
attention to fully vaccinating her other
Mechanism of action of tetanus toxin
children with the DPT vaccine to avoid

having to go through this again.
57
Clostridium botulinum
vesicles with the neuronal membrane. As a

result, acetylcholine cannot be released.
Jeremys relatives from the countryside
Consequently, this inhibits the signals for
had arranged a trip to the city to visit him
muscle contraction.
and his family; it was around the evening

when they arrived. They had brought
As they got to the hospital, suspicion of
many things with them, including a pot of
botulism was quite reasonable from the
honey from one of their nearby farms.
symptoms and Jeremy was straightaway
Jeremy just loved honey. He started eating
given polyvalent antitoxins to neutralize
from it as soon as he took it to the kitchen.
the free circulating toxins. An endotracheal
The next morning, he noticed he couldnt
tube was also instituted to support his
focus his vision on things. He couldnt
ventilation. The staff also commended his
enjoy eating his breakfast because he
early visit to the hospital because death
found it difficult to swallow the food.
from respiratory failure can occur in 15%

of patients if not treated. Just for the
He had no fever, but he just noticed
records, a serum sample was taken and
getting weaker and weaker. He asked his
injected into a mouse to see whether it will
older son to take him to the hospital. What
result
was happening was that botulinum toxin,
in
botulism
or
not
(mouse
neutralization test).
produced by Clostridium botulinum, was

present in the honey. So Jeremy got an
Mechanism of action of botulinum toxin
intoxication (not an infection) by eating

from the honey. As the toxin got into the
intestine, it was absorbed into the blood
where it spread around the body, gaining
access to cholinergic neurons.
As the toxin got in the neurons, it cleaved

some protein receptors on the surface of
the
acetylcholine
vesicles
inside
Clostridium botulinum can also cause:

1. Infant botulism: feeding problems with
poor muscle from contaminated formulas
such as honey containing the spores
2. Wound botulism
the
neuron. This prevented the fusion of these
58
Treatments
Penicillin
Pseudomonas aeruginosa (aminopenicillin)
Proteus mirabilis
Treponema pallidum
Actinomycetes (penicillin G)
Doxycycline
Ciprofloxacin
Vibrio cholerae
Mycoplasma pneumoniae
Salmonella Typhi
Mycoplasma hominis
Coxiella burnetii
Other Yersinia
Chlamydia pneumoniae
Brucella melitensis
Listeria monocytogenes (ampicillin)
Macrolide
Chlamydia trachomatis (azithromycin)
Helicobacter pylori (triple regimen of
Chlamydia psittaci
omeprazole, amoxicillin, and clarithromycin)
Ehrlichia
Bacillus anthracis (combination of
Clostridium tetani
Campylobacter fetus (ampicillin)
Others
ciprofloxacin, rifampin, and vancomycin)
Cephalosporin
Mycobacterium leprae (dapsone, rifampin, or
Haemophilus influenza
clofazamine)
Escherichia coli (cefotaxime)
Mycobacterium tuberculosis and non-TB
Proteus vulgaris
Mycobacteria (see page 15)
Clostridium difficile (metronidazole or
vancomycin)
Bacteroides fragilis (cefoxitin)

Nocardia asteroides (sulfamethoxazole)

Yersinia pestis (streptomycin)
Francisella tularensis (streptomycin)
Rickettsia prowazekii (chloramphenicol)
59

Tale of The Microbes

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Tale of The Microbes

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Tale of the Microbes

UTIs and STDs

Skin and Soft Tissue Infections

Febrile and Systemic Infections

CSF and Nervous System Infections

Letter of apology from the clans of Staphylococcus and Streptococcus

ascended the pulpit to deliver a heart-

The organisms thus started proliferating

touching sermon. O sons of the difficile

clan! This is the day you have been

awaiting. We have endured injustice for

cytotoxin that destroys intestinal cells and

decades. This is our golden chance to take

over! Proliferate o thee and release thy

secretion) and the

They were accumulating a great degree of

construction of the Great Wall of China,

When they indeed diagnosed it, they

Rob and Elene lived with their 4-year-old

the pseudomembrane, composed of mucin

Johny who was attending kindergarten.

from goblet cells, fibrin from the blood,

As the difficile clan were celebrating their

triumph, tablets of metronidazole started

ruining their party. They were seen

They just thought this was their dream

with the drugs following and crushing

coming true. It didnt cross their minds

disturbance to the human in whom they

themselves. And thus was the lamentable

are living! So the guy had went to the

difficile clan once again to be pushed under

hospital because of diarrhea. As he told

oppression and silencing, with no hope for

the physician that the diarrhea started

another success in the near future.

after taking the drug, antibiotic-associated

As the results turned positive, clindamycin

pseudomembranous colitis or not. So they

pseudoappendicitis from Campylobacter.

performed endoscopy to confirm this.

two days. Later, they confirmed their

After Johny was discharged from the

She then started to have pain all over her

diagnosis by urease and oxidase tests on

hospital, his mother took him back home,

joints. When Rob came back from the trip

with a kind of a sallow face. What she

and learned about what had happened, he

didn't know was that in the start of the

decided to take her to the hospital. But it

As the lab folks were busy looking for

illness Johny had contaminated several

was too late. The disease had become so

Campy, the physician had put Rob on

articles in the home. She had sliced a piece

advanced that it actually affected her

fluid and electrolyte replacement. Since

of raw meat on a surface in the kitchen few

pregnancy and it led to a septic abortion.

Rob had visited the physician in a slightly

days back, and later prepared salad on the

The physician could do nothing but to