Enterobacteriacea Family

Orange – not bolded on slides

Regular writing – bolded on slides (looked silly with most of the chart bolded)
Other colours – bolded stuff with colour to make it look nicer
Bacteria Properties Virulence Factors Syndromes Other
Escherichia Coli Gram (-) bacillus -Adhesions (needs to stick Endogenous (opportunistic): ABC therapy is not indicated
Opportunistic Outer envelope as lots of motion in Poor hygiene/immune
0157:H7 Citochrome oxidase (-) GTU/GIT) Pneumonia,
Catalase (+) -H and K antigens UTIs
(variation – doesn’t stay E. Coli = 80% of community acquired
the same) Very common infection – 10-20% of women
Exotoxins will have =>1 in life
Ascending infection = anus → vagina →
ureters → kidneys
Special adhesions are used to attach to
uroepithelium (attach to mannose) – resist
flushing

Sx
Pyelonephritis – severe dysuria, urgency,
increased frequency, incomplete voiding,
fever, loin pain, (+) KI punch

Septicaemia
most commonly caused by E. coli (45%)

Exogenous (external pathogen):

Contaminated food or water

Gastroenteritis – see separate chart

Neonatal meningitis
E.Coli and Group B Strep are most common
causes
E. Coli have K1 capsular Ags – get anti K1
Abs from mother through breast feeding. 50-
70% babies are exposed but don’t get b/c of
mother’s Abs

Gastroenteritis
M/C E. Coli infection in healthy people

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ETEC/VTEC – EIEC – EPEC – EAggEc – DAEC – EHEC - Enterohemorrhagic HUS – Hemolytic
Enterotoxigenic Enteroinvasive Enteropathogenic Enteroaggregative Diffuseaggregative Uremic Syndroms

Traveller’s diarrhea Scant, bloody Common cause of Persistent watery Watery diarrhea M/C strain causing disease in M/C cause of acute
Infant diarrhea stool that is infant diarrhea diarrhea Last longer b/c developed nations renal failure in
Exotoxins leukocyte (+) Non-bloody stool – Lasts longer b/c aggregates Cause of “Hamburger children – destruction
ST a/ST b: heat watery aggregates together Bacteria are disease” And HUS of renal glomeruli
stable, stimulate Fever Fever embedded in cell (Hemolytic Uremic Bloody diarrhea
guanylyl cyclase membrane of Syndrome) Stool culture (+) for E.
LT I/ LT II: heat Progress to elongated microvilli Very low inoculation is Coli
labile, stimulate colonic ulceration needed (100 bacilli) Hemolytic anemia
adenylyl cyclase Virulence Factor: Thrombocytopenia –
(like Cholera toxin) Similar to Shigella Hemolysin platelets in low
Watery diarrhea number
(*vs bloody*) Sx
Rare Vomiting Bloody diarrhea b/c
hemoragic
No fever
Can progress to HUS
Spread via beef or other
meat, feces contaminated
water

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Bacteria Properties Virulence Factors Syndromes Other
Salmonella Gram (-) bacillus Surface Antigens: Salmonellosis – same syndrome whether Spread by 5 Fs:
Outer membrane – -Species specific fimbria enteritidis or typhi Food, Fingers, Fomites,
susceptible to drying – attach to M cells of Peyer’s Feces, Flies
need moist surface patches – membrane S. Enteritidis Gastroenteritis -avoid antacids – b/c stomach
ruffling: get in w/o -6-48 hrs after ingestion of contaminated food acid will kill them if properly
S. Enteritidis: disrupting cell membrane or water high
-Poultry, birds, reptiles -non-bloody diarrhea -clean cutting boards
-Undercooked poultry, Invasiveness: -fever
contaminated cutting -Penetrate into sub- -in and out quickly
boards, egg salad, epithelial spaces w/o a
undercooked/raw eggs toxin mediated process Septicemia
-High inoculum needed -Rearrange host cell actin -10% of patients develop arthritis,
(membrane ruffling) osteomyelitis and endocarditis
S. Typhi:
-Foreign Travel Entertoxins: Enteric Fever = Typhoid Fever
-Spread by food or water -LT/ST like toxins (like E. -M/C spread is by food handlers infected
contaminated by infected Coli) -Unlike other salmonellosis, bacteria pass
food handlers -cell associated toxin directly through intestinal walls
-Only small inoculum is (verotoxin like) -low inoculum
needed -heat labile **This is not Typhus**
-stabile toxins S & Sx
-increasing remittent fever (comes and goes)
-Rose coloured spots on abdomen – self
limiting, but only in 50% of Pxs)

S. Typhi Pathogenisis
-replicate in GB
-back into the intestine to cause increased
inflammation
-1-3% become chronic carriers
Shigella Gram (-) rod M cells in Peyer’s patches, Causes Shigellosis Fecal-oral transmission
Kiosho Shiga Significant outer membrane ruffling (like S. Flexneri – developing nations
Enterobacteriacae membrane salmonella) S. Sonnei – industrialized (milder) Resistant to stomach acid
Related to E. Coli Does not ferment glucose (unlike Salmonella) – why it
(DDX: E. Coli will ferment Shiga exotoxin – disrupt GI symptoms are caused by Shiga toxin only needs a small dose
gluose) protein synthesis Presents initially:
-profuse watery diarrhea High likelihood of ABC
Very low inoculum (10-100 Can proceed to damage -fever resistance
bacilli) glomerular epithelial cells
(HUS) - like E. Coli EHEC Proceeds to:
-abundant blood and pus in stool
-tenesmus – cramping in lower abdominal;
persistent ineffectual spasms; wanting to go
but can’t

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VIBRIOACAE FAMILY
200 Serotypes:
EI Tor (named after camp on the way to Meca) biotype is M/C in world today
Bacteria Properties Virulence Factors
Vibrioacae Family Gram (-) bacillus
Comma shaped
Motile – single polar
flagella
Wide Temp Range –
18-37°C
Most need salt for growth
(exception is V. Cholera)
Vibrio Cholera Survives salt water
Ubiquitous Heat stabile
High infectious dose
Rarely seen in Gram
stained stool or wound
specimens – there are lots
of them but are really small
Dark field/phase contrast
microscopy: characteristic
darting motility (flagella)
Direct ELIZA
Cholera toxin complex A-B
toxin:
-structurally & functionally
similar to heat labil
enterotoxin A of E. Coli
A toxin:
-increase cAMP
-cause electrolye shift,
watery diarrhea (can lost 1
L of water/hour)
Different A-B to
Cornybacterium
Adhesins
Mucinase
No Vomiting (unlike salmonella)
Syndromes
Cholera:
-abrupt onset of watery diarrhea and vomiting
-no abdominal cramps, no fever (unlike
Shigella, Salmonella, Campylobactor)
-can resemble ETEC induced gastroenteritis
-Rice Water stools – no protein, speckled with
mucous, colourless, odourless
-Severe fluid and electrolye loss
-Hypolovemic shock
-Death
Other
Shellfish/seawater is most
common way to transmit (also
passes Hep A)
Returning Travellers –
1,000,000 cases/year in world
Aggressive fluid/electrolyte
replacement (oral/IV) – don’t
do too quickly as osmolarity is
important
No long term human carriers
(unlike S. Typhi)
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 BACILLACEAE Family
Bacteria Properties
Bacillaceae Family Gram (+) Bacillus
Endospore forming –
does under adverse
conditions
-multi-layered coat,
therefore hard to get rid of
B. Anthracis Clinical samples – single
or paired “jointed
bamboo-rod”
Culture – “Medusa head”;
long, serpentine chains
Resevoir:
Domestic herbivores:
sheep, goats, cattle,
horses
B. Cereus
Virulence Factors
Capsule:
Anti-capsular Abs are
NOT protective
Normally develop Abs to a
bacterial capsule that will
protect you – not anthracis
Toxin:
3 parts (need 2):
1. protective Ag – required
for binding
2. lethal factor
3. Edema factor – adenyly
cyclase
Heat stable Enterotoxin:
Syndromes Other
1. Cutaneous Anthrax (most common) Developing Countries:
Inoculation of skin (break in skin) – post contact Endemic – can’t vaccinate all
with infected animals 20% mortality livestock
Mail carrier
Painless, itchy, necrotic eschars (scabs) Developed Countries:
Not contagious Occupational disease
Internal Hemorrhage Biological warfare
Cutaneous VS Orf Prevention:
Bacillis Anthracus Pox Virus Difficult due to long lived
Spore contaminated Infected sheep or spores
animals/products goats
Painless papule Painless vesicles No person to person
Necrotic eschar- Red weeping transmission with inhalation
gelatinous edema nodules or ingestion anthrax
Potentially fatal (20%) Benign-self limiting
2. Inhalation Anthrax
Inhalation of spores/wool – “Woolsorter’s
disease”; 95% mortality
-prolonged latency
Initial disease goes away
Comes back in
Second stage:
-massive enlargement of mediastinal LNs (on
sternum),
Hemorrhagic Meningitis Sxs M/C than pulmonary
Sxs
*no person to person transmission b/c no cough
3. Ingestion Anthrax
Ingestions of Contaminated Food – 100%
mortality
IFF Upper GI:
Oral/esophogeal ulcers, edema, sepsis, regional
lymphadenopathy-dysphagia
IFF Lower GI:
n/v, malaise, systemic S & Sx, bloody diarrhea
2 types of Gastroentertitis: Low mortality compared to B.
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Cereal! -causes emesis Anthracis
-found in improperly 1. Emetic disease (vomiting)
refrigerated rice dishes -heat stable enterotoxin Exam Q:
-15 min to 4 hr incubation (quick incubation What would happen if you
Heat Labile Enterotoxin: therefore pre-formed toxin) heated rice?
-similar to enterotoxin of -no fever
ETEC and V. Cholera -no diarrhea Treatment/Prevention:
-causes profuse, watery
diarrhea 2. Diarrhoeal disease Gastroenteritis:
-found in contaminated -heat labile enterotoxin -rapid consumption of food
meat, vegetables, sauces -bloody diarrhea after eating
-no fever -proper refrigeration of
Cereolysin: uneaten portions
Eye damage Also causes panopthalmitis (entire eye inflamed; no ABCs – is already a toxin
recall contact lens wearers with pseudomonas) when in the food
Phoepholipase C:
Eye damage Panopthalmitis Panopthalmitis:
-post traumatic Early, aggressive ABCs
Necrotic Toxin: -Rapid (<48 hrs)
Eye damage
Clostridium Spp. Gram (+) bacilli
*M/C’ly anaerobic
*Spore formers
C. Perfringen Gram (+) 5 toxin specific types: Wound/soft tissue infections Lots in wounds and times of
Histotoxic Plump, rectangular rod Type A: war and car accidents etc.
(Sausage) Permanent soil inhabitant, Anaerobic cellulites (as with Strep):
responsible for most If mm doesn’t respons to
Non-motile but rapid human disease • organism spread through subcutaneous stimulus = gas gangrene
growth on sheep’s blood tissue (myonecrosis)
agar (divide in 15-18mins) Spore Formation • spares fascia and deep muscle
• superficial skin discoloration and skin If does respond = still
Ubiquitous – Toxin Formation: necrosis cellulites (take skin of to test
opportunistic: Alpha toxin: mm and see)
• gas forms – develop suppurative myositis –
Soil, GIT of animals and Most tissue damage –
foul smelling discharge
humans, contaminated increase vascular Food Poisoning M/C:
water permeability (lyse cells) • no muscle necrosis, no systemic Ss and Sxs 1. Campylobacter
(DDX from myonecrosis) 2. Salmonella
Disease M/C after trauma 3. Staph Aureus
that causes ischemia: 4. C. Perfringens
-Needs devitalized tissue Myonecrosis (Gas Gangrene)
(more acidic) • Rapid worsening of cellulites
-Favours lowered pO2 • Rapid onset of intense pain
and pH • Extensive muscle necrosis (blue black,
edematous, does not bleed or contract on
stimulation)
• Toxic delirium

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 • Much damage due to alpha toxin and gas
bubbles (bubble pack material crepitis –
cracking sound from gas bubbles)
• Debridement and examination of underlying
muscle tissue
• Fast growth of culture of sheep’s blood agar
• Nagler’s reaction
• Gram(+) rods in tissue specimens with no
leukocytes

Food Poisoning
• Ingest meat – refrigeration and re-heating
destroys entertoxins
• Large infection dose
• Abdominal cramps
• Watery diarrhea
• No fever
• No N/V
• Looks similar to salmonella
C. Difficile Toxin A (Entertoxin): Range of Problems: Can be normal part of GI
Enterotoxigenic • Hemorrhagic necrosis • Mild Diarhea flora W/O causing disease
in pseudo • Colitis
membranous colitis • Life threatening pseudo membranous colitis M/C causes post-ABC
diarrhea and pseudo
• Prolonged diarrhea (signs of dehydration)
Hyaluronidase: membranous colitis (also
• Increase spread caused by Staph Aureus)
Pseudo Membranous colitis
between tissues • is confirmed by biopsy – multiple, raised M/C ly after broad spectrum
white/yellow exudative plaques adhering to ABCs
colonic mucosa
• in vitro cytotoxicity assay in culture cells Treatment:
• immunoassay for C. Difficile toxins A and B • Discontinue ABCs
(look for toxins using Direct ELISA); best • Maintina fluid/electrolyte
way to diagnose balands
• Sigmoidoscopy • Avoid drug therapies that
• Fecal leukocytes decrease intestinal
motility

Prevent By:
• Prescribe ABCs with
probiotics (separate by
8hrs)

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C. Tetani Gram stain variable Spores:
Paralytic (-) when old Survive adverse
(+) when fresh conditions
Clostridium = cloister (of Have to boil for 3 hours
nuns), spindle Looks like a tennis
racquet Tetanospasmin:
Tetani = extreme tension • Heat labile neurotoxin
• Very sensitive to O2 (one of three most
obligate anaerobe potent toxins)
• Responsible for the
• Relatively inactive spastic paralysis
metabolically (unlike • 2 part toxin – post-
C. Perfringen) synaptic terminals in
CNS; irreversibly
inhibits the release of
GABA and glycine
Ubiquitous – spores last
for years in soil
Present in GIT of cows,
horses and some humans
4 types of Tetanus – Generalized, localized, Developed world:
cephalic, neonatal • Low disease incidence –
immunization, herd
Generalized Tetanus immunity, urbanization
• M/C form of tetanus
• Bacterium introduced by trauma to skin Developing world:
• Animal bites • Higher
• Infant tetanus can be a
S and Sxs: problem (>50% of
• Exaggerated DTRs (reflexes) neonatal deaths)
• Trismus (lock jaw)
• Risus Sardonicus (mocking smile) Diagnosis
• Drooling • Patient history
• Clinical S and Sxs
• Opisthotonus (paraspinal muscles arch
backwards) happens later • Gram stain and culture
not that important (only
Neonatal 30% of people with
• From improperly cleaned umbilical stupm tetanus are culture (+))
• First sign is difficulty sucking (8-19 days after
birth) Treatment
• Tetanospasmin binds
irreversibly and therefore,
can only treat symptoms
until nerve terminals
regenerate
• Passive immunization –
bind free tetanospasmin
Prevention
• No natural immunity
unlike many other
disease
• Active immunization –
tetanus toxoids: booster
every 10 years
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C. Botilinum Gran (+) bacillus Spore Formation: Intoxication (toxin, not bacteria)– Food borne Too much Mg can mimic
Paralytic Sausage shaped One of the most resistant: botulism botulism
• Heat (hrs at 100C and Inadequate sterilization of food (home canned
Produces one of the most 10 mins at 120C) foods – beans, asparagus b/c low acidity, Diagnosis:
potent exotoxins known to preserved fish) Clinical signs and symptoms
humans – lethal dose < • Cold (down to -190C) are paramount
1ug • Irradiation S and Sx
• 2-72 hour incubation Prevention:
Ubiquitous – soil, VERY RESISTENT • No GI distress unlike other food poisonings • Acid pH (canned fruit is
sediments of lakes and • No fever ok) – grow best at
ponds Botulinum Toxin pH>4.5
• One of the most
• Clear sensorium (thinking) – completely
• Refrigerate (can’t survive
aware
potent known <4C)
neurotoxins • Dilated, fixed pupils when eye is exposed to
• Heat for minimum 20 min
• Cholinergic neurons light source - bilateral
at 80C
• Dry, fuzzy tongue – Furry tongue, red, dry
• Inhibits acetylcholine
• Bilateral descending weakness of neck, face,
• No honey to infants <
release at presynaptic 1yoa
throat • Check cans –
terminals and
• Respiratory paralysis – mortality (32-40%)
therefore flaccid contaminated ones might
paralysis (opposite to be swollen from gas
tetanospasmin) (don’t No permanent immunity – can get repeated released by bacterial
get excitatory signal) occurrences enzymes)
Infant Botulism – Infection Intoxication
• Honey contaminated with spores
• M/C form of botulism in USA
• M/C in 1-6 months old because caused by
bacteria growing and producing neurotoxin in
infant GIT; infant GIT doesn’t have as many
competitive bowel microbes

S and Sx
• Non-specific
• Floppy baby

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 CAMPYLOBACTERACAE Family
Bacteria Properties Virulence Factors Syndromes Other
Campylobacter Gran (-) bacillus Zoonoses: birds
“S or gull-wing shaped” Raw milk and water
Peak incidence in young
Small (0.3-0.6um) adults (20-29 yoa)
Filterable unlike other
bacteria – will go through a
filter, other bacteria are too
big

Motile
Single polar flagella

Microaerophilic reduced
O2, increased CO2)

Thermophilic (42°C)(needs
higher temp than others)

C. Jejuni Gastroenteritis: 3 most common ways to get

Need high infectious dose (need reduced with diarrhea:
hypochlorhydria (elderly; parietal cells get 1. Campylobacter Jejuni
hammered), TUMs (buffered; many elderly 2. Enterotoxigenic E. Coli
given to get Ca – not good system b/c Cl to 3. Rhodovirus
bind Ca & if lowered HCL via TUMs won’t
work), milk
#1 bacterial cause of
2-11 day incubation gastroenteritis and
foul smelling, watery diarrhea progressing to endocarditis in USA
profuse bloody diarrhea.
No vomiting
Resolutiong in 3 days to 3 weeks Treatment/Prevention :
Residual histological damage (effect Gastroenteritis:
absorption) -prevent with proper
preparation and storage of
Guillain Barre Syndrome: food
-idiopathic, peripheral polyneuritis 1-3 weeks -avoid raw milk
after the mild condition proper water treatment
-progressive, symmetric pain and weakness in
extremities – might ascend to trunk, face, Guillain Barre Syndrome:
thorax No treatment
-attack myelin of nerves, get symmetrical
weakness
-auto-immune link
-self-limiting (few weeks to months) with

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Bacteria Properties
Helicobacter pylori Gram stain variable –
Like Campylobacter changes depending on age
of culture
In it’s own family Corkscrew motion – highly
motile
Urease (+) (alkaline buffer;
cloud of ammonia around
them from breaking down
urea
Very slow growth (2-6 day)
in complex media
Temp 30-37C (not at 42C
like Campylobacter
Until early 80s thought that
stomach acid was too low
to grow – wrong
Stomach of humans,
primate, pigs, cheetahs,
dogs, ferrets, mice, rats
(but they don’t all get
gastritis)
Found in gastric antrum
and body only (not in
fundus or pyloric region)
Developed countries – up
to 45% in adults > 50 yoa
Virulence Factors
Survive Acidity:
-acid inhibitory protein
(blocks release of acid
from parietal cells)
-Urease
Flagella
Mucinase/phospholipase
(enzymes break up
stomach lining so it can get
through)
Microaerophilic:
-survive relatively
anaerobic environment of
ST
Tissue Damaging:
PAF – hypersecretion of
gastric acid
complete recovery
Syndromes Other
Type B (infective) gastritis) Stress → ↑acidity → ↑ H.
-30-50% of people with gastritis have H. Pylori Pylori
but M/C asymptomatic
Possibly spread through
S & Sx & Lab Dx dental plague and saliva, but
-Epigastric pain don’t really know
-Foul smelling breath
-13C urea breath test Increased risk with pickley
-anti H. Pylori Abs (IgG) foods, salted fish and meats,
-gastroscopy with biopsy smoked meats
-CLO test (+) – Campylobacter-like organ test
Progresses to:
PUD; especially duodenal ulcers
S & Sx & Lab Dx
• burning, gnawing upper GI pain 1-3 hours < 20% of people, regardless
after meals, of age, who test + for H.
• worse night Pylori also get Peptic Ulcer
Disease (PUD)
• better eating or antacids (best with protein
b/c good buffer)
• Endoscopy
• Urea breath test
• Serology (anti-H. Pylori Abs)
Gastric Adenocarcinmo Treatment:
-sequelae of untreated chronic gastritis
classified as a Class I carcinogen Gastric mucosa-associated
lymphoid type (MALT) B cell
S & Sx lymphomas
• Fatigue
• Weight loss Triple Therapy:
• Low grade fever Proton pump inhibitor
(omeprazole), clarithromycin,
• Night pain
metronidazole, bismuth
• Hemoccult (+) stools
• Anemia 2 week course gets rid of
90% of H. Pylori
M/C cancer in the world behind Lung
Gastric mucosa-associated lymphoid type
(MALT) B cell lymphomas
Rare
No evidence that eradicating H. Pylori
prevents progression of gastritis to
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 carcinomas

NEISSERIACEAE Family
Bacteria Properties Virulence Factors Syndromes Other
Neisseria Spp Gram(-) diplococci
“coffee bean”

transparent, non-
pigmented colonies on
chocolate blood agar (heat
treated blood agar)
N. Meningitidis Normal colonizer of Pili – needed to attach to Asymptomatically colonize nasopharynx or Meningitis Causes:
nasopharynx or cause non-ciliated columnar cells cause meningitis, meningococcemia or 1. N. Meningitides
disease (opportunistic) pneumonia 2. H. influenza
Bacteria enters host cell 3. S. pneumonia
and replicates in M/C cause of bacterial meningitis in infants
phagocytic vacules through adolescence and in young adults
Capsule is also anti-
phagocytic Transferred via close contact with respiratory
droplets (day cares, military barracks)
LOS expressed?
Meningococcemia (Mild disease)
• Arthritis
• Petechial skin rashes (little red dots)

Meningicoccemia (marked disease)

• URI then 1-3 day incubation
• Small petechial rash on trunk and lower
extremities that can coalesce to form
larger bullae (due to thrombosis of small
blood vessels)

Meningococcal meningitis
• 2nd most common cause of adult bacterial
meningitis
• 1st is strep pneumonia
• rapid onset of fever, nuchal rigidity,
blinding headache
• high number of organisms
• Gram (-) diplococci in PMNs

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N. Gonorrhoeae Gram(-) diplococci
On chocolate blood agar
Strict pathogen
“the gonococcus”
fastidious growth – no
growth with drying
therefore has to stay moist,
therefore needs intimate
sexual contact
Gram stain is sensitive and
specific IFF men with
purulent urethritis – doesn’t
work for women
For women, must confirm
with culture
No exotoxin:
• Host damage is from
gonococcal induced
inflammatory response
Pili:
• Non-ciliated epithelial
cells of foreskin,
vagina, fallopian tube
• Highly variable
structure; therefore
can get gonorrhoea
more than once
LOS (Lipo Oligo
Saccharide):
• Classic endotoxin
activity (like LPS)
• No strain specific O
antigens (unlike LPS)
IgA protease
95% of males get acut symptoms: 2nd most common STD in US
• gonococcal urethritis Chlamydia is #1
2-7 day incubation: M/C in 15-24 yoa
• purulent urethral discharge
Increased risk if:
• red/edematous urethral meatus (opening
at end of penis) • Female (50% risk with
single exposure as
opposed to males with
>50% of women are asymptomatic or mild
symptoms: 20% risk)
• cervicitis • multiple sex partners
• vaginal discharge
Women are M/C’ly
• abnormal vaginal bleeding
asymptomatic carriers – don’t
• ascending infection
know they have disease until
• major cause of infertility
try to have kids and find out
they are infertile because
Disseminated Gonorrhoea scarring has blocked their
• Rare but M/C in women (1-3%) fallopian tubes.
• Migratory arthralgias
• Tender papillary lesions -associated with Chlamydia
• Rash on the extremeties
• Arthritis – M/C ly mono articular knee in -stays on foreskin, therefore
less risk is circumsized
females
Penicillin resistant – beta-
N. Gonorrhoea is the #1 cause of purulent
lactamase, need too high
(pussy) arthritis in young adults
dose, change cell surface so
ABC can’t penetrate cell
Opthalmia Neonatorum
• Caused by N. gonorrhoea of C.
trachomatis
• Purulent conjunctivitis in newborns
infected during vaginal delivery
• Sticky discharge
• Edema / inflammation
*know what bacteria effect the eyes*
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Bacteria Properties Virulence Factors Syndromes Other
Haemophilus Spp Small 1st to have whole genome
= “blood loving” Gram (-) sequenced
Coccobacillus
(pleomorphic)

Fastidious growth
requirements:
X factor (hematin) and V
factor (NAD)
Chocolate agar

Obligate parasites on
mucous membranes of
humans and animals

H. influenzae Chocolate Agar Non-encapsulated strains Pneumonia 25-80% of us have non-

– colonize both upper encapsulated form in us all
Conjugated HiB vaccine and lower respiratory Meningitis the time
(purified PRP) tracts • Same S and Sx as other bacterial meningitis
• But more insidious onet and increased risk of Primarily a paediatric
Encapsulated strains neurological sequelae problem (< 2yoa at very
(serotype b) – can • Used to be most common cause of meningitis high risk) b/c can’t block
become systemic before vaccine capsule

Capsule: • Lots of kids get, but few die

Invasive disease is
M/C’ly due to H. Epiglottitis
influenzae type b (“Hib” • Medical emergency (can’t breath( Vaccine will not stop OM,
infection) • M/C in boys 2-4 yoa OS or pneumonia b/c
• Dysphagia caused by non-
Pili: • Drooling encapsulated strains and
Damage respiratory, • Muffled voice vaccine works against
ciliated epithelium capsule
• Minimal cough
LPS: • Severs dyspnea Vaccine works against
Responsible for • Don’t want to swab when extremely inflamed – meningitis
meningitis painful

Otitis Media/Sinusitis
M/C caused by:
1. H. influenzae
2. S. Pneumonia
3. Moraxella catarrhalis

14
H. Ducreyi Small Can cause an STD – M/Cly in developing world Perhaps isn’t Haemophillus
Gram (-) – wrongly named?
Coccobacillus • Causes chancroid (soft chancre)
• Unlike primary syphilis which causes hard
Non-encapsulated chancre
Aka Ducreyi bacillus Chancroid Primary syphilis
H. Ducreyi Treponema pallidum
Soft, purulent, painful Hard, non-purulent, non-
ulcer on genitalia painful ulcer (genitalia,
anus, mouth)
M/C in males, Both sexes
uncircumcised, tropical
& sub-tropical
Females M/C 20-35 yoa
asymptomatis
5-7 day incubation 3 week incubation
Progress to painful Painless buboes
buboes, phimosis
(can’t retract foreskin),
urethral stricture
Gram(-) coccobacillur Poor Gram stain:
Dark field microscopy
(spiral rods, thin, tightly
coiled), non-specific
tests (VRDL, RPR),
specific tests (FTA-Abs,
TPHA)

15
Bacteria Properties
Bordetella Spp Gram (-)
Very small bacilli (rodlike)
Fastidious (picky) growth
Needs humidity,
specialized media
(charcoal, blood, NAD-
enriched)
Haemophilus also needs
chocolate agar
Bordetella Pertussis Bacteria is best isolated
using nasopharyngeal
aspirates during catarrhal
stage
Culture – difficult because
need humidity, 35C, 7days,
specialized agar. Only
50% of infected people are
culture (+)
Virulence Factors
Pertussis toxin:
• Increase adenylate
cyclase
• cAMP – respiratory
secretions/mucous
Tracheal Cytotoxin:
• Part of the PG layer
• Cause ciliostatis and
then damage to
ciliated epithelial cells
• Causes cough
• Can’t repair damaged
cells due to DNA
interference
• Increase IL-1 causes
fever
Filamentous Haemagglutin
and other adhesions:
• Intracellular survival
protects against
clearance by humoral
immunity
Syndromes
Bordetella Pertussis (whooping cough)
Whooping Cough (4 stages)
1. Incubation – 7-10 days, sub-clinical (no
Sxs), increasing # of bacteria
2. Catarrhal – 2 weeks, looks like common
cold, rhinorrhea. Most infectious stage.
Peak number of bacteria
3. Paroxysmal stage – 1-2 weeks, dry non-
productive, repetitive “whooping” cough.
40-50 coughs/day causing damage and
exhaustion
4. Convalescent Stage – 2-4 weeks.
Cough resolves but can have secondary
complications.
Hard to DDX because looks like a cold in
Catarrhal stage which is when it should be
treated because damage isn’t done yet and is
highest bacterial count.
Usually DX at Paroxysmal stage when
bacteria have moved into the cells.
Coughing can collapse lung, cause hernia
Other
Pertussis vaccine now found
to only last for 10 years.
Want people to pay to get
booster, but only a mild
disease in adults.
Reportable Disease
M/C in developing countries
in children < 1yoa
Spread by infectious droplets
No long term immunity
“protection” in developed
countries due to DPT vaccine
no environmental or animal
reservoir known
Treatment and Prevention:
ABCs are of limited use
(disease is not recognized
until peak of infectiousness
has passed.) ABCs are
meant for when bacteria is
actively dividing.
DPT vaccine – 2, 4, 6, 15
months and 4-6 years
Used to use whole cell
vaccine (DTwP) – caused
side effects
No use acllular B. Pertussis
(DTaP) which causes “fewer
16

TREPONEMA Family
Bacteria Properties
Treponema Pallidum Small
Thin
Coiled spirochetes
Can’t usually visualize via
gram stain and light
microscopy
Only in cultured rabbit
epithelial cells
Treponema Pallidum Humans are the only
subspecies pallidum reservoir of disease
Susceptible to drying (like
niesseria), therefore can’t
get from toilet seat
Contagious only during
primary stage and rash of
secondary stage
Syphilis lab diagnosis:
• No gram stain b/c too
small
• Use silver or
fluorescent stains
• Non-specific tests:
• VDRL (Venereal
Disease Research
Laboratory test) and
RPR
• Indicate current active
disease
• Specific tests:
• FTA (fluorescent
Tremanemal A?) and
TPHA (MHA-TP)
• Indicate past infection
Virulence Factors
Motile – corkscrew motility
via thin fibrils at both ends,
but no flagella
Outer membrane:
• Proteins to adhere to
host cell – covers itself
with host cell protein
Very labile
side effects”
Syndromes Other
3 different Subspecies Cause:
Syphillus, Bjel, and Pinta
Strict Human Pathogen
Syphilis 3rd M/C bacterial STD in the
Primary: USA
• Small papule – painless, hard chancre
(VS H. Ducreyi) 1. Chlamydia
• Painless, regional lymphadenopathy- 2. Gonorrhoea
3. Syphilis
buboes
• Very infectious
• Heals spontaneously within 2 months Syphilis Treatment and
without scarring prevention:
Secondary: • Hygiene (spirochetes
• Flu-like syndrome destroyed by soap and
• Localized lymphadenopathy water, temperature >42C
• Diffuse, non-pruritic maculopapular rash – and drying
wide spread even on palms • Safe sex practices
• Very infectious (kissing)
• Resolves slowly in weeks to months
Tertiary (Lues/Leutic):
• After 3-40 years of latent syphilis
o Long latent people where not
contagious. Causing tumors but
don’t know until see S & Sx later
on
• Gummmas – rubbery tumor
• Can effect many organ systems:
o Neurosyphilis
o Cardiosyphilis
• Painless or deep burrowing pain
Congenital Syphilis (vertical transmission)
• Infected mother infects fetus
17
 • Only primary ad • Born appearing well then several weeks
secondary stage or up to 2 years later get snuffles (bloody
syphilis can be found nasal discharge), widespread
in tests desquamating maculopapular rash

CHLAMYDIA Family
Bacteria Properties Virulence Factors Syndromes Other
Chlamydophila VERY Small • Gains access through Chlamydia growth cycle: Can get from toilet seat
C. Psittaci Gram (-) (very weak minute abrasions or Elementary body:
C. pneumonia though) laverations Adapted for extracellular survival and initiation Chlamydia Urogenital
C. Trachomatis Bacillus of infection (resistant to environment) Infections
• Limited tissue tropism Currently M/C bacterial STD
Virus like properties Reticulate Body: in USA
Adapted for intracellular growth; metabolically
Unlike other bacteria there
• Strains causing LGV
active (growth phase) Women:
can cause systemic
is not PG layer, therefore • Termed Chlamydia (the
no Gram stain infections by entering Inclusion Body: Clap)
lymphatic system High amount of glycogen, therefore stain with • M/C asymptomatic (80%)
Unique growth cycle within iodine. • Pain/cramping in lower
host cell – EBs and RBs • Clinical signs and
symptoms due to abdomen
Trachoma
direct destruction of • Dyspaerunia
• Leading cause of preventable blindness in
cells during replication • Bleeding between
developing countries
ad host inflammatory menses
• M/C in children
response
• Poor hygiene Men
• No long term immunity • M/Cly spread by droplets, hands, • Termed NGU (non
contaminated clothing, eye make-up, flies gonoccocal urethritis)
• M/Cly symptomatic (75%)
• Could decrease by 50% if had enough • Yellow clear discharge
water to wash just once per day
• Pain, tenderness of
genitals
• Must have specific attachment to
• Reactive arthritis (Reiter’s
conjunctiva
syndrome)
• Resist flushing from tears – sticks to eye
• Begins as conjunctivitis Reactive Arthritis (Reiter’s
• Inflamed eyelids cause entropion syndrome)
(eyelashes chronically irritate cornea • Seronegative
cause ulceration spondyloarthropathy
• M/C in young men (20-
Trachoma inclusion conjunctivitis 40yoa)
Adult: • That are HLA-B27
M/Cly 18-30 yoa and sexually active positive
Genital infection 1st and then unilateral • C. Trachomatis in M/C
mucopurulent discharge in eye bacterial pathogen

18
 • Unexplained diarrhea
Neonatal: • Superficial lesions on
Bilateral, intense papillary conjunctivitis with palms/sole/oral mucosa
lid swelling
“Can’t see, can’t pee,
Lymphogranuloma venereum (LGV)
can’t dance with me”
• M/C in Africa, Asia, South America
• M/C in male homosexuals Treatment:
• M/C also have
Initial lesion: presumptive Tx for
• Small painless papule on penis, urethra, Gonorrhea
glans, scrotum and vaginal wall (similar to
Syphilis but not a chancre) Prevention:
• Hygiene (hand/face
2nd Stage: washing)
• inflammation and swelling in LNs (buboes) • Practise safe sex
– painful, can rupture and drain
spontaneously
• systemic
• can get proctitis in men and women
C. Trachomatis Lab Dx:
Need adequate sample of
infected cells (specimen of
pus/discharge is
inappropriate) – b/c
bacteria are intracellular so
do scraping

Culture:
• most specific method
• only infects certain cell
lines
• formation of inclusion
bodies (key to
recognizing)
C. pheumonia Human pathogen that can cause atypical
pneumonia (mild/persistent cough and
malaise that might progress to lobar
pneumonia)

Potential link to atherosclerosis, MS,

Alzheimer’s?
C. psittaci Causes psittacosis
• Biggest risk from psittacine birds (parrots,
macawsm parakeets, cockatiels)

19

Bacteria Properties
Mycobacterium Spp. Acid Fast
M. tuberculosis Gram (+)
M. Leprae Bacillus
M. avium Complex
M. Gordonae One of the slower dividing
microorganisms – 12-24
hours
Mycolic acid in its cell wall
Acid fast
Resist drying, detergents,
acids/bases
Source of PPD for
Mantoux test
Looks kinda like a fungus
in culture
M. tuberculosis Cause of more fatalities
worldwide than any other
infectious disease
M/C’ly person to person
transmission via infectious
aerosolized particles
Very small inoculum
needed
Immunocompromised have
increased risk
Sputum Sample:
• Acid fast bacillus
• Fluorescent stain
• Fastidious culture
requirements
Virulence Factors
Evade humoral immunity
because intracellular
growth
Tissue destruction is due
primarily to host immune
response
Form tubercles – body
reacts to contain bacteria
by enclosing in small,
fibrous granulomas
containing epithelial cells
and Giant (Langehan) cells
– develop to larger necrotic
or caseous granulomas
• Transmitted via inhaled dried bird
excrement, urine and respiratory
secretions
• Non-productive cough
• Commonly progresses to CNS
• 5% mortality
Syndromes Other
Pulmonary TB On the rise in North America
Primary Infection: – 1 new person infected every
• Only 5% get active TB within 2 years of second
exposure
• Ghon complex – initial lung lesion and “TB is the master
locally enlarged LNs impersonator”
Insidious onset Treatment:
• Malaise/listlessness • Problem – MDR-TB
• Night sweats
Prevention:
• Low grade fever
• Diet/robust immune
• Unexplained weight loss
system
• Progressive fatigue
• Only 5% of all vaccine
preventable deaths are
CXR:
due to TB
Cavitations in one or more upper lobes of lung
Miliary TB
• No pulmonary sign
20
 • PCR
Skin test (Mantoux test):
• Wait 48 hours and
measure induration/
erythema
M. Leprae Similar structure to M.
tuberculosis but:
Can not be artificially
cultured (need live mice or
armadillos) and grow in
Globi bundles
(encapsulated globs of
rods in tissues)
Armadillos are naturally
infected and provide a
natural reservoir for
disease
Spread via respiratory
route or contact with break
in skin
M. avium Complex Similar to tuberculosis but
MAC only causes opportunistic
infections
• Disease in HIV/AIDs
patients
• Lymphadenitis in
children
• Ubiquitous in water
Capsule
Preference for lower
temperatures – limits
infection to skin and
nasopharynx
Intracellular survival – in
Histiocytes and Schwann
cells
• Effects the liver and others
• Tubercle resembles millet seed
Tuberculoid (Paucibacillary)
• Pauca = few
• Not infectious
• <5 cutaneous macular lesions with
hypopigmented centers
• will react to skin test – lepromin
Lepromatous (Multibacillary)
• Highly infectious
• Most destructive – disfiguring skin/bone,
cartilage lesions (“Leonine faces”)
• Anhidrosis (deficiency or absence of
sweating)
• Not reactive to skin test (Leprumanin test)
• >5 skin lesions
• tend to get with weak cellular immunity but
strong humoral immunity
Begins as mild pulmonary disease and spread Over half the people in USA
to local lymph nodes and then quickly to every with HIV/AIDs also have MAC
organ
Increased risk in elderly
Pulmonary disease is similar to TB: women in lingual of lung –
• Usually GIT tract involvement Lady Windermere Syndrome
• Usually fatal within months
No person to person spread via aerosolized
droplet
Mostly obtained by ingestion
21
Bacteria Properties Virulence Factors Syndromes Other
Borrelia Spp. Gram (-)
Spirochete
Larger than other
spirochetes and more
complex

Many species cause

relapsing fever and Lyme
disease (Borellia
burgdorferi) – need ticks
as vectors

B. burgdorferi M/C vector borne disease Lyme Disease

in USA Stage One (of 3):
Erythema migrans rash “bull’s eye lesions”
No person to person
spread Diagnosis:
• Clinical signs and Sxs and patient history
Vector: • Culture and IFA stain of biopsy of initial
deer tick (Ioxdes rash
scapularis/Ioxdes • Indirect ELISA
pacificus)

Resevoir:
White footed mouse or
white tailed deer

Increased risk in grassy,

wooded areas

22
Bacteria Properties Virulence Factors Syndromes Other
Leptospira Spp Spirochete Spirochete enters via Zoonotic – rodent and
contaminated urine – entry domestic dog reservoirs
Minimal nutrition to broken skin and mucosa
requirements (LCFA, M/C’ly acquire disease via
vitamin B1 and B12) Replicate in endothelium contact with infected urine
lining of capillaries
Survive in moist, slightly
alkaline environment for Significant cause of KI
many days failure
L. interrogenes Human pathogen

Leptospirosis
No skin lesion at site of entry (unlike Lyme
disease)

• Septic Phase
o Abrupt onset fever, severe H/A,
severe myalgia (esp. calf and
back), nausea
o Lasts 1 week
• Immune Phase
o 2 days asymptomatic, then
aseptic meningitis with severe
H/A, N/V, myalgia
• Weil’s disease (icteric = jaundice)
o KI failure (M/C cause of death)

Lab Dx
Too small for light microscope and Gram stain

23
Bacteria Properties Virulence Factors Syndromes Other
Rickettsia Spp Energy parasite – like Tick bite – must be Need arthropod vectors –
Chlamydia needs energy exposed to tick for >24hrs hard ticks like dog tick
from host (Dermacenter variabili)
Tissue damage due to
Small bacteria multiplication in vascular Need tick like Lyme Disease
Similar to Gram (-) bacteria epithelium damaging cells
causing leakage … organ
No flagella failure
R. ricketsii Rocky Mountain Spotted Fever RMSF Lad Dx:
Painless tick bite leaves no mwar (very low DFA (Direct Flourescent Ab)
inoculum <10 organisms) stain

1 week incubation Prevention

5 days later
rash – diffuse, maculopapular rash, M/C
spread from extremities to trunk (including
palms and soles)
Almost impossible to get rid of
ticks – can surviv up to 4
years without feeding

Typhoid Typhus
Salmonella typhi Rickettsia ricketsii
Transmitted by Transmitted from
contaminated milk, infected rodents to
water, food humans by bites of
ticks, lice, fleas or
mites
Rash
Blanching Erythema
chronicum migrans
Faint macuopapular Maculopapular
rosy spots over skin eschar formation.
of abdomen and
chest
Not on face, soles,
palms

24
 FUNGUS
Hard to treat because are eukaryotes therefore look like us and any treatment will also effect us – serious side effects.

Monomorphic or Dimorphic depending on species – more are Di

Dimorphic means are a different structure in the environment to in the body because of change in temperature

Filamentous:
• Molds
• M/C at lower temperature and free living

Unicellular
• Yeasts
• M/C at higher temperature and when parasitizing tissue (in you)

Fungal Disease Classification:

1. Superficial
⇒ Infect only outermost layers of skin and hair
⇒ eg - Black and white piedre, tinea versicolor, tinea nigra
2. Cutaneous
⇒ Most tineas
⇒ Most infectious disease – ring worm
3. Submucotaneous
4. Systemic
⇒ Invade internal organ M/C’ly from lung foci of infection
 Histoplasmosis, blastomycosis, coccidioidomycoses

25
Fungal Type Properties Virulence Factors Syndromes Other
Superficial Mycoses Outermost, non-living Tinea (pityriasis) versicolor (bran like) Tinea = worm/moth like
layer of skin (survive by • Malassezia furfur
diffusion) • Non-itchy hypo-pigmented lesions on
upper torso, arms, abdomen
No immune reaction • Dandruff like
because no blood or
• Concentrate near sebaceous gland 0
langerhan cells
axilla
Primarily cosmetic issues • “spaghetti and meatballs” organism
only after KOH preparation
• Wood’s lamp (+) (will fluoresce)

Tinea Nigra
• Found in soil
• Macular lesions on palms and soles
• Dark pigmented yeast cells
Piedra = more than 2
colours
Black Piedra
• Black under microscope
• Dark, hard nodules
• Hairs of scalp, moustache, beard
• Direct or sexual contact
• Gritty feeling when combing hair
• Alopecia possible
• Really notice under microscope

White Piedra
• Soft, pasty white
• Direct contact only

Cutaneous Mycoses From showers Tinea Cruris – Jock itch

Tinea Pedis – Athletes foot
2nd M/C disease in adults
Contagious – wear gloved
Deeper layers
Mistakenly termed
Evoke inflammatory dermatophytes (thought
immune response was by plants, but isn’t)

Clinical diseases are Further names according to

termed tineas (worm like what part of the body they
lesions) are found

Wood’s lamp (+)

26
Subcutaneus Mycoses Fascia, muscle, bone

M/C’ly due to tissue

trauma

Difficult to treat –
debridement (cutting out),
amputation
Systemic Mycoses M/C’ly develop mild Monomorphic – cryptococcus Strict pathogens
acute/ asymptomatic lung neoformans and
infections Or Opportunistic pathogens
Dimorphic – thermal dimorphism
Also can develop chronic Mycotic agents
disease or sub-clinical • Cause disease in healthy humans
(latent)
Respiratory tract as initial foci of infection
Histoplasma Saprobic phase Inhale Primary Histoplasmosis KOH gets rid of
capsulatum • In N2 rich soil (farms) • 10 day incubation “background” noise (other
Convert to yeast form and • Flu like cells)
Parasitic phase replicate in macrophages • Acute, self-limiting, influenza like illness
• In macrophages of • Some residual calcified lesions
Carried by lymphatics
RES • Not contagious
Lab Dx • Overly aggressive immune response
M/C found in “Histo” belt • Mediastinal fibrosis
Microscopy:
Grows in soil rich in • 10% KOH prep with Silver or • Ocular histoplasmosis syndrome is a
nitrogen Glemsa stain possible comlication

Also in areas of a lot of Serological: Ocular Histoplasmosis Syndrome

bird (starling/ chicken) • Skin tests • Serious retinal condition
and bat excrement • Too many false (+) • Leading cause of blindness in 20-40
yoa
Inhale Cultures:
• “histo spots” bilaterally – little black
Slow growing (1-2 weeks) and
spots
Convert to yeast form spores are infectious
and replicate in
o yeast travels through blood
macrophages vessels to eyes
• M/C’ly no visual loss
Carried by lymphatics
Histoplasmomis
• Progressive – disseminated via
lymphatics – increased risk if impaired
CMI
• TB-like iff chronic

27
 o Fever, night sweats, weight
loss with destructive (caseating
necrosis) lung lesions

Blastomyces Endemic areas overlap Lab Dx Blastomycosis Know all TB like illnesses
Dermatides those of histoplasmosis Skin test and serology (Gilchrists disease, Chicago Disease)
• Too many false (+)
Unknown reservoir – Acute
unlike H capsulatum it is Microscopy • Bronchopneumonia
rarely cultured from soil • Biopsy/ histology of KOH • Drenching sweats

Dust clouds at
prepped tissue sample • No residual calcified lesions (unlike
construction sites or crop Histoplasmosis)
Culture • Not contagious even if they cough
dust during farming • On selective Sabourand agar
Inhale condia (sexual Chronic
phase of fungi) • TB or cancer like
Replicate in Blastomycosis skin lesions
macrophages • Slowly expanding ulcerative or
verrucous (wart like) lesions
Carried by lymphatics or • Face, nose, mouth
blood
Coccidiodes immitis Dimorphic Saprobic Form Coccidiodomycosis
(San Joaquin Valley fever, desert
37C, tissue, rheumatism, Posada – Wernicke disease)
multinucleated spherule
“sporangia” Inhalation of conidia
• M/C’ly asymptomatic
endemic in soils of hot • 40% mild, febrile to moderately severe
dry, semi-arid areas respiratory disease
• not contagious
extensively spread via
• erthyema nodosum with arthralgia (pain
dusty storms
in joints)
Parasitic Form
M/C’ly in males 25-55
Dx:
yoa
Skin test antigens
• Use for skin test 2-4 weeks after
symptoms
• Coccidiodin – cell free culture of
mycellum growth
• Spherulin – cell free culture of spherule
phase
CXR
“Egg shell” lesions
Tissue biopsy

28
• Staining and microscopy for spherules
Culture
• Caution – infections; leading cause of
lab acquired infections

29