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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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No Vomiting (unlike salmonella)
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 Syndromes Other
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 Cholera toxin complex A-B Cholera: Shellfish/seawater is most
toxin: -abrupt onset of watery diarrhea and vomiting common way to transmit (also
Ubiquitous Heat stabile -structurally & functionally passes Hep A)
similar to heat labil -no abdominal cramps, no fever (unlike
High infectious dose enterotoxin A of E. Coli Shigella, Salmonella, Campylobactor) Returning Travellers –
1,000,000 cases/year in world
Rarely seen in Gram A toxin: -can resemble ETEC induced gastroenteritis
stained stool or wound -increase cAMP Aggressive fluid/electrolyte
specimens – there are lots -cause electrolye shift, -Rice Water stools – no protein, speckled with replacement (oral/IV) – don’t
of them but are really small watery diarrhea (can lost 1 mucous, colourless, odourless do too quickly as osmolarity is
L of water/hour) important
Dark field/phase contrast -Severe fluid and electrolye loss
microscopy: characteristic Different A-B to No long term human carriers
darting motility (flagella) Cornybacterium -Hypolovemic shock (unlike S. Typhi)

Direct ELIZA Adhesins -Death

Mucinase

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BACILLACEAE Family
Bacteria Properties Virulence Factors Syndromes Other
Bacillaceae Family Gram (+) Bacillus
Endospore forming –
does under adverse
conditions
-multi-layered coat,
therefore hard to get rid of
B. Anthracis Clinical samples – single Capsule: 1. Cutaneous Anthrax (most common) Developing Countries:
or paired “jointed Anti-capsular Abs are Inoculation of skin (break in skin) – post contact Endemic – can’t vaccinate all
bamboo-rod” NOT protective with infected animals 20% mortality livestock
Normally develop Abs to a Mail carrier
Culture – “Medusa head”; bacterial capsule that will Painless, itchy, necrotic eschars (scabs) Developed Countries:
long, serpentine chains protect you – not anthracis Not contagious Occupational disease
Internal Hemorrhage Biological warfare
Resevoir: Toxin:
Domestic herbivores: 3 parts (need 2): Cutaneous VS Orf Prevention:
sheep, goats, cattle, 1. protective Ag – required Bacillis Anthracus Pox Virus Difficult due to long lived
horses for binding Spore contaminated Infected sheep or spores
2. lethal factor animals/products goats
3. Edema factor – adenyly Painless papule Painless vesicles No person to person
cyclase 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
B. Cereus Heat stable Enterotoxin: 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: 4 types of Tetanus – Generalized, localized, Developed world:
Paralytic (-) when old Survive adverse cephalic, neonatal • Low disease incidence –
(+) when fresh conditions immunization, herd
Clostridium = cloister (of Have to boil for 3 hours Generalized Tetanus immunity, urbanization
nuns), spindle Looks like a tennis • M/C form of tetanus
racquet Tetanospasmin: • Bacterium introduced by trauma to skin Developing world:
Tetani = extreme tension • Heat labile neurotoxin • Animal bites • Higher
• Very sensitive to O2 (one of three most • Infant tetanus can be a
obligate anaerobe potent toxins) S and Sxs: problem (>50% of
• Responsible for the • Exaggerated DTRs (reflexes) neonatal deaths)
• Relatively inactive spastic paralysis • Trismus (lock jaw)
metabolically (unlike • 2 part toxin – post- • Risus Sardonicus (mocking smile) Diagnosis
C. Perfringen) synaptic terminals in
• Drooling • Patient history
CNS; irreversibly • Clinical S and Sxs
inhibits the release of • Opisthotonus (paraspinal muscles arch
GABA and glycine backwards) happens later • Gram stain and culture
not that important (only
Ubiquitous – spores last Neonatal 30% of people with
for years in soil • From improperly cleaned umbilical stupm tetanus are culture (+))
• First sign is difficulty sucking (8-19 days after
Present in GIT of cows, birth) Treatment
horses and some humans • 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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complete recovery
Bacteria Properties Virulence Factors Syndromes Other
Helicobacter pylori Gram stain variable – Survive Acidity: Type B (infective) gastritis) Stress → ↑acidity → ↑ H.
Like Campylobacter changes depending on age -30-50% of people with gastritis have H. Pylori Pylori
of culture -acid inhibitory protein but M/C asymptomatic
In it’s own family Corkscrew motion – highly (blocks release of acid Possibly spread through
motile from parietal cells) S & Sx & Lab Dx dental plague and saliva, but
Urease (+) (alkaline buffer; -Urease -Epigastric pain don’t really know
cloud of ammonia around Flagella -Foul smelling breath
them from breaking down Mucinase/phospholipase -13C urea breath test Increased risk with pickley
urea (enzymes break up -anti H. Pylori Abs (IgG) foods, salted fish and meats,
Very slow growth (2-6 day) stomach lining so it can get -gastroscopy with biopsy smoked meats
in complex media through) -CLO test (+) – Campylobacter-like organ test
Temp 30-37C (not at 42C
like Campylobacter Microaerophilic: Progresses to:
Until early 80s thought that -survive relatively PUD; especially duodenal ulcers
stomach acid was too low anaerobic environment of
to grow – wrong ST S & Sx & Lab Dx
• burning, gnawing upper GI pain 1-3 hours < 20% of people, regardless
Stomach of humans, Tissue Damaging: after meals, of age, who test + for H.
primate, pigs, cheetahs, PAF – hypersecretion of • worse night Pylori also get Peptic Ulcer
dogs, ferrets, mice, rats gastric acid Disease (PUD)
(but they don’t all get
• better eating or antacids (best with protein
gastritis) b/c good buffer)
• Endoscopy
Found in gastric antrum • Urea breath test
and body only (not in • Serology (anti-H. Pylori Abs)
fundus or pyloric region)
Gastric Adenocarcinmo Treatment:
Developed countries – up -sequelae of untreated chronic gastritis
to 45% in adults > 50 yoa 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 No exotoxin: 95% of males get acut symptoms: 2nd most common STD in US
On chocolate blood agar • Host damage is from • gonococcal urethritis Chlamydia is #1
gonococcal induced
Strict pathogen inflammatory response 2-7 day incubation: M/C in 15-24 yoa
• purulent urethral discharge
“the gonococcus” Pili: Increased risk if:
• red/edematous urethral meatus (opening
• Non-ciliated epithelial at end of penis) • Female (50% risk with
fastidious growth – no cells of foreskin, single exposure as
growth with drying vagina, fallopian tube opposed to males with
therefore has to stay moist, >50% of women are asymptomatic or mild
therefore needs intimate
• Highly variable symptoms: 20% risk)
structure; therefore • cervicitis • multiple sex partners
sexual contact
can get gonorrhoea • vaginal discharge
more than once Women are M/C’ly
Gram stain is sensitive and • abnormal vaginal bleeding
asymptomatic carriers – don’t
specific IFF men with • ascending infection
LOS (Lipo Oligo know they have disease until
purulent urethritis – doesn’t • major cause of infertility
Saccharide): try to have kids and find out
work for women
• Classic endotoxin they are infertile because
Disseminated Gonorrhoea scarring has blocked their
For women, must confirm activity (like LPS)
• Rare but M/C in women (1-3%) fallopian tubes.
with culture • No strain specific O
antigens (unlike LPS) • Migratory arthralgias
• Tender papillary lesions -associated with Chlamydia
IgA protease • 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

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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 Virulence Factors Syndromes Other
Bordetella Spp Gram (-) Bordetella Pertussis (whooping cough) Pertussis vaccine now found
Very small bacilli (rodlike) to only last for 10 years.
Want people to pay to get
Fastidious (picky) growth booster, but only a mild
Needs humidity, disease in adults.
specialized media
(charcoal, blood, NAD-
enriched)

Haemophilus also needs


chocolate agar

Bordetella Pertussis Bacteria is best isolated Pertussis toxin: Whooping Cough (4 stages) Reportable Disease
using nasopharyngeal • Increase adenylate 1. Incubation – 7-10 days, sub-clinical (no
aspirates during catarrhal cyclase Sxs), increasing # of bacteria M/C in developing countries
stage • cAMP – respiratory in children < 1yoa
secretions/mucous 2. Catarrhal – 2 weeks, looks like common
Culture – difficult because cold, rhinorrhea. Most infectious stage. Spread by infectious droplets
need humidity, 35C, 7days, Tracheal Cytotoxin: Peak number of bacteria
specialized agar. Only • Part of the PG layer No long term immunity
50% of infected people are
• Cause ciliostatis and
culture (+) “protection” in developed
then damage to 3. Paroxysmal stage – 1-2 weeks, dry non- countries due to DPT vaccine
ciliated epithelial cells productive, repetitive “whooping” cough.
• Causes cough 40-50 coughs/day causing damage and no environmental or animal
• Can’t repair damaged exhaustion reservoir known
cells due to DNA
interference 4. Convalescent Stage – 2-4 weeks. Treatment and Prevention:
• Increase IL-1 causes Cough resolves but can have secondary ABCs are of limited use
fever complications. (disease is not recognized
until peak of infectiousness
Filamentous Haemagglutin Hard to DDX because looks like a cold in has passed.) ABCs are
and other adhesions: Catarrhal stage which is when it should be meant for when bacteria is
• Intracellular survival treated because damage isn’t done yet and is actively dividing.
protects against highest bacterial count.
clearance by humoral DPT vaccine – 2, 4, 6, 15
immunity Usually DX at Paroxysmal stage when months and 4-6 years
bacteria have moved into the cells.
Used to use whole cell
Coughing can collapse lung, cause hernia vaccine (DTwP) – caused
side effects

No use acllular B. Pertussis


(DTaP) which causes “fewer

16
side effects”

TREPONEMA Family
Bacteria Properties Virulence Factors Syndromes Other
Treponema Pallidum Small Motile – corkscrew motility 3 different Subspecies Cause:
Thin via thin fibrils at both ends, Syphillus, Bjel, and Pinta
Coiled spirochetes but no flagella
Can’t usually visualize via
gram stain and light Strict Human Pathogen
microscopy

Only in cultured rabbit


epithelial cells
Treponema Pallidum Humans are the only Outer membrane: Syphilis 3rd M/C bacterial STD in the
subspecies pallidum reservoir of disease • Proteins to adhere to Primary: USA
host cell – covers itself • Small papule – painless, hard chancre
Susceptible to drying (like with host cell protein (VS H. Ducreyi) 1. Chlamydia
niesseria), therefore can’t • Painless, regional lymphadenopathy- 2. Gonorrhoea
get from toilet seat Very labile 3. Syphilis
buboes
• Very infectious
Contagious only during
primary stage and rash of • Heals spontaneously within 2 months Syphilis Treatment and
secondary stage without scarring prevention:
Secondary: • Hygiene (spirochetes
Syphilis lab diagnosis: • Flu-like syndrome destroyed by soap and
• No gram stain b/c too • Localized lymphadenopathy water, temperature >42C
small • Diffuse, non-pruritic maculopapular rash – and drying
• Use silver or wide spread even on palms • Safe sex practices
fluorescent stains • Very infectious (kissing)
• Resolves slowly in weeks to months
• Non-specific tests: Tertiary (Lues/Leutic):
• VDRL (Venereal • After 3-40 years of latent syphilis
Disease Research o Long latent people where not
Laboratory test) and contagious. Causing tumors but
RPR don’t know until see S & Sx later
• Indicate current active on
disease • Gummmas – rubbery tumor
• Can effect many organ systems:
• Specific tests: o Neurosyphilis
• FTA (fluorescent o Cardiosyphilis
Tremanemal A?) and • Painless or deep burrowing pain
TPHA (MHA-TP)
• Indicate past infection Congenital Syphilis (vertical transmission)
• Infected mother infects fetus

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• 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

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• 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)

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• Transmitted via inhaled dried bird
excrement, urine and respiratory
secretions
• Non-productive cough
• Commonly progresses to CNS
• 5% mortality

Bacteria Properties Virulence Factors Syndromes Other


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 Evade humoral immunity Pulmonary TB On the rise in North America
worldwide than any other because intracellular Primary Infection: – 1 new person infected every
infectious disease growth • Only 5% get active TB within 2 years of second
exposure
M/C’ly person to person Tissue destruction is due • Ghon complex – initial lung lesion and “TB is the master
transmission via infectious primarily to host immune locally enlarged LNs impersonator”
aerosolized particles response
Insidious onset Treatment:
Very small inoculum Form tubercles – body • Malaise/listlessness • Problem – MDR-TB
needed reacts to contain bacteria
• Night sweats
by enclosing in small, Prevention:
Immunocompromised have fibrous granulomas • Low grade fever
• Diet/robust immune
increased risk containing epithelial cells • Unexplained weight loss
system
and Giant (Langehan) cells • Progressive fatigue
• Only 5% of all vaccine
Sputum Sample: – develop to larger necrotic preventable deaths are
• Acid fast bacillus or caseous granulomas CXR:
due to TB
• Fluorescent stain Cavitations in one or more upper lobes of lung
• Fastidious culture
Miliary TB
requirements
• No pulmonary sign

20
• PCR • Effects the liver and others
• Tubercle resembles millet seed
Skin test (Mantoux test):
• Wait 48 hours and
measure induration/
erythema

M. Leprae Similar structure to M. Capsule Tuberculoid (Paucibacillary)


tuberculosis but: • Pauca = few
Preference for lower • Not infectious
Can not be artificially temperatures – limits • <5 cutaneous macular lesions with
cultured (need live mice or infection to skin and hypopigmented centers
armadillos) and grow in nasopharynx
• will react to skin test – lepromin
Globi bundles
(encapsulated globs of Intracellular survival – in
Lepromatous (Multibacillary)
rods in tissues) Histiocytes and Schwann
cells • Highly infectious
Armadillos are naturally • Most destructive – disfiguring skin/bone,
infected and provide a cartilage lesions (“Leonine faces”)
natural reservoir for • Anhidrosis (deficiency or absence of
disease sweating)
• Not reactive to skin test (Leprumanin test)
Spread via respiratory
route or contact with break • >5 skin lesions
in skin • tend to get with weak cellular immunity but
strong humoral immunity
M. avium Complex Similar to tuberculosis but Begins as mild pulmonary disease and spread Over half the people in USA
MAC only causes opportunistic to local lymph nodes and then quickly to every with HIV/AIDs also have MAC
infections organ
Increased risk in elderly
• Disease in HIV/AIDs Pulmonary disease is similar to TB: women in lingual of lung –
patients • Usually GIT tract involvement Lady Windermere Syndrome
• Lymphadenitis in • Usually fatal within months
children
• Ubiquitous in water No person to person spread via aerosolized
droplet

Mostly obtained by ingestion

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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

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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


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

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 (+)

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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