Types Morphology Epidemiology Virulence Factors Diseases Prevention/ Treatment

Yersinia enterolytica: forms envelope/
outer membrane
Yersinia pestis: forms protein
polysaccharide capsule
Yersinia spp.
Not a member of the
Enterobacteriaceae family
Pesudomonas
areuginosa
Family Enterobacteriaceae, genus
Escherichia, species E. coli
Escherichia coli
Gram (-) rod or coccobacillus
Bipolar staining: "safety pin"
appearance
Facultative anaerobe
Indole (-), catalase (+), urease (-)
Will not ferment sucrose, rhamnose,
2) Inhalation of infectious droplets
cellubiose
Grows best at 22-55 C but also
grows at 4 C
Gram (-) baccilus
Most common flat colonies with
spreading borders, B hemolysis,
green pigment
Sweet, grape-like fruity odor
Cytocrome oxidase (+) and non-
fermenters
3 colony types (rough, smooth,
mucoid) depending on where
isolated
motile with single, polar flagella
(unlike proteus but like legionella)
Obligate aerobes (can grow
anaerobically iff Arginine or nitrate
source)
Minimal nutritional requirements -
can grow in distilled water
Optimal temperature growth is 37 C
(but can grow from 4-42 C)
Gram (-) bacillus with outer
envelope
All other Enterobacteriace features
O antigens used for strain typing,
e.g. O157 : H7
1) Invasion gene product: uptake into
Ubiquitous
Zoonotic: most common vectors are rodents:
rats, ground squirrels, rabbits, mice, prairie
dogs, cats, ect.
Can be transmitted by:
1) fleas, Xenopsylla cheopsis, that feed on an
infected animal and then bite humans
3) direct contact on open wound on skin
Increased Risk with:
1) over crowding, poor sanitation, poor personal
hygiene
2) Native Americans, hunters, hikers/campers,
veterinarians
3) Cold climates: Y. enterolytica. Warm/cool
damp climates: Y pestis
Ubiquitous - soil, water, plants, hospital sinks Infections involve: 1) attachment and
and respiratory equipment, swimming pools,
raw vegetables
Two forms: bioflim or planktonic
Low incidence of normal human colonization: 2) Local invasion: elastase, pyocyanin
opportunistic pathogen of humans and horses. (interfere with function of nasal cilia and
Almost never causes disease in
immunocompetent host
Cause wide range of diseases: primary focus of
infection is LU - major cause of morbidity and 3) Dissemination: LPS and exototins
mortality in CF
Also cause soft tissue infections (esp after
burns) bacteremia, ear and eye infections and
systemic infections
Part of the normal flora of the GIT: opportunistic 1) Adhesins: colonize GTU or GIT
pathogen
Increased risk of disease with: hospitalization,
poor personal hygiene, travel to countries with
poorly developed sanitary practices, sub-
optimal immune defences
Public hygiene systems in developed nations
play a significant role in the relative rarity of E.
coli infections
epithelia cells and macrophages of PP
2) Anti phagocytic factors: a) capsular
Ag; b) Type III protein secretion system
3) Plasminogen activator protease:
degrades C3a and C3b
4) Fribrinolysin
5) Iron absorbance factor: independent
of siderophores
6) Various exotoxins and endotoxins:
lipid A part of LPS
7) Protein YopJ: blocks 2 critical cellular
signaling pathways and therefore
induces cell death
colonization, 2) local invasion, 3)
disseminated systemic disease
1) Attachment and colonization: a)
opportunistic fimbria/ pili, b) alginate
slime/polysaccharide capsule (anchors
bacteria to host cell, protect from host
immunity. Increase expression if host
has COPD or CF)
disrupts respiratory epithelium), ABC
resistance
Toxigenesis: Exotoxin A: same
mechanism of action as Diptheriae toxin
despite voiding or peistalsis
2) Exotoxins
3) H and K antigens - relative
importance/ presence of these factors
depends on genetics of the strain + site
of infection + condition of host
Yersinia pestis disease
Yersinia enterolytica diseases
prevention:
Common cause of food borne
1) Plague vaccine (develop only
gastroenteritis in: Sandinavia,
partial immunity)
Europe and colder parts of NA
Major sources of contamination
are: refrigerated milk products,
cold meat (Porl), water 2) Quarantine
contaminated with feces, blood
products
Animal hosts include: rodents,
rabbits, pigs, sheep, cattle, horses, 3) Rodent control
domestic pets
4) Prophylactic ABCs to prevent
high bactermia: plague is toxigenic
Yersinia entrolytica gastroenteritis/ 5) Proper sanitation/ personal
Yersinosis hygiene
Bubonic plague
Pneumonic plauge
Septicemic plague
One of the most difficult bacterial
Bacterial Keratitis
infections to treat and control:
UTI's 1) Many ABC resistance strategies
GIT infections 2) Ubiquitous
3) Most patients with infection are
Swimmer's Ear
immunocompromised
4) Colonization of surfaces as a
Bactermia biofilm makes them impervious to
many ABCs
5) Inappropriate use of ABCs
permits their overgrowth and
Hot tub folliculitis
promotes the development of ABC
resistant strains
Ecthyma gangernosum
Prevent by good personal and
Either:
public hygiene
1) Endogenous infections: in
good BBQ practices are key in the
persons with poor personal
summer
hygiene and debilitated defences
2) Exogenous infections: from
contaminated food or water: ABC terapy is not indicated
gastroenteritis, neonatal meningitis

Family Enterobacteriaciae
Very diverse genus > 2400 distinct
serotypes
Recent DNA evidence suggests only 2
oxidase (-)
species:
S. typhi
Salmonella
S. paratyphi and S. enteridis are
actually serotypes
Family Enterobacteriacae, Genus
Shigella
4 species:S. flexneri, S. sonnei, S.
boydii, S. dyseteriae
S. sonnei is the most common cause
of shigellosis in the industrialized
world
Shigella
S. flexneri is MC in developing world
Family Vibrioacae, genus Vibrio
Many species: C. parahemolyticus, V.
vulnificus and Vibrio choleara are MC Motile, single polar flagella
cause of human disease
200 serotypes: O1 and O139 cause
Vibrio Cholera
classic cholera
EI Tor (O1) biotype is MC in world
today
Family Bacillaceae, genera bacullus
B. anthracis - anthrax
Baccilus anthracis
B. cereus - gastroenteritis
Baccilus cereus
Gram (-) bacillus
Facultative anaerobe
SOD (+)
Outer membrane: susceptible to
drying
Gram (-) rod
oxidase (-)
Facultative anaerobe
Significant outer membrane
Does not ferment glucose
Gram (-) bacillus, comma shaped
Oxidase (+)
Wide temperature range (18-37)
Most need salt for growth (except V.
cholera)
Gram (+) bacillus. Single or paired
"joined bamboo rod"
culture - "medusa head - long,
serpentine chains"
Colonies - non-hemolytic, sticky
Gram (+) bacillus
S. enteritidis epidemiology: Common in the
environment
Animals are the primary reservoirs for S.
enteritides: livestock, fish, poultry/ birds,
rodents, humans, reptiles (turtles)
Humans most commonly get Salmonellosis
from: undercooked poultry, contaminated
cutting boards, egg salad, undercooked/ raw
eggs
Disease incidence: peaks in warm summer
months. Most common in children and elderly
S. Typhi epidemiology
Humans are the only known animal host
Disease in NA primarily associated with foreign
travel. Spread by food or water contaminated
by infected food handlers
Less frequent exposure than S. enteritidis but
more likely to get disease because only a small
inoculum is needed (S. enteritidis
gastroenteritis needs a very high inoculum)
Humans are the only carriers
Transmission due to fecal-oral route
Very low inoculum (only 10-100 baccili)
Most cases in children 6 months - 10 years
Adule infx: contact with children, or male
homosexuals
Populations at risk: anyone exposed to carrier
e.g. daycare centers, nurseries, nursing homes,
military barracks, prison, poor sanitation
communities
Ubiquitous in marine environment - even if
increased salinity and temp 10-30 C.
Contaminated shellfish/seawater is most
common way to transmit disease
Asymptomatic human carriers
Relatively high infective dose
Most cases in NA are from returning travelers
Primary reservoirs: domestic herbivores (sheep, Capsule - anti-capsular Abs are NOT
goats, cattle, horses)
Three routes of transmission: Inoculation of
skin, inhalation of spores, ingestion of
contaminated food.
Developing countries: endemic, can't affort to
vaccinate livestock
Developed countries: occupational disease and
biological warfare
Ubiqutous distribution
Low mortality compared to B. anthracis
1) Surface antigens a) O Ag (on LPS),
Improved personal and public
b) V 1 Ag (on capsule) c) species S. enteritidis gastroenteritis
hygiene
specific fimbria attach to M cells of PP
2) exotoxin (LPS) - responsible for the
Spread by the 5 "f's": food, fingers,
fevers seen in bacteremic phase of Salmonella induced septicemia
fomites, feces and flies
enteric fever
3) Invasiveness: penetrate into sub-
Proper preparation and storate of
epithelial spaces without a toxin
Enteric fever food: avoid antacids, clean your
mediated process. Rearrange host cell
cutting boards
actin (membrane ruffling)
4) Enterotoxins. 3 types: 1&2) LT/ST
MC'ly symptomatic Tx instead of
like toxins (Like E. coli), 3) Cell
ABC's
associated toxin (verotoxin-like)
S. typhys: oral or parenteral
5) Other: Acid tolerance response
vaccine. 70% effective, transient,
gene, catalase, SOD
frequent side effects.
Same as Enterobacteriaceae in
Attach and invade M cells in PP Shigellosis general: hygiene, removal and
isolation of linens/diapers
Use Type II secretion system to cause ABC used to shorten course and
membrane ruffling (engulf bacteria into control spread but high likelihood
host cell) of ABC resistance
Unlike Salmonella they are
Shiga toxin (only S. dysenteria) disrupts
resistant to St acid (therefore a
protein synthesis
much smaller infective dose)
Can proceed to damage glomerular
epithelial cells (HUS) in susceptible
persons
1) Cholera toxin complex A-B toxin:
Aggressive fluid/ electrolyte
structurally and functionally similar to Cholera
replacement (oral/IV)
head-labile enterotoxin A of E. coli
- B toxin: binding, A toxin: increase
ABC's reduce exotoxin and more
cAMP, cause electrolyte shift, watery
rapidly eliminate organism
diarrhea
No long term human carriers
2) Adhesins
(unlike S. typhi)
Vaccine: limited usefullness, short
3) Mucinase
lived protection
4) Siderophores - sequester iron
5) Neruamidase
6) Hemolysin - increase intracellular Ca,
therefore inc. chloride secretion
Cutaneous anthrax Pennicillin and ciproflaxacin
protective
Toxin: 3 parts that work together:
Protective Ag (binding, anti-phagocytic), Prevention difficult due to long
Inhalation anthrax
lethal factor, edema factor (stim lived spores
adenylyl cyclase)
No person to person transmission
Ingestion anthrax
with inhalation or ingestion antrax
Vaccinations (military), burn/ bury
infected animals
Gastroenteritis: No ABCs. Rapid
Heat stable enterotoxin - causes
consumption of food after heating.
emesis. Found in contaminated, Two types of gastroenteritis:
Proper refrigeration of uneaten
improperly refrigerated rice dishes
portions.
Heat labile enterotoxin - similar to 1) emetic disease - heat stable Panopthalmitis - early, aggressive
enterotoxin of ETEC and Vibro cholera enterotoxin ABCs. Resistance. EMERGENCY!
2) diarrhoeal disease - heat labile
- profuse, watery diarrhea
enterotoxin
Also causes panopthalmitis -
- contaminated meat, vegetables inflammtion of entire eye post-
traumatic injury
Cereolysin - involved in eye damage
Phospholipase C - involved in eye
damage

Small (0.3-0.6 um) filterable unlike
other bactera
Gram (-) bacillus - "S or gull-wing
shaped"
Campylobacter spp.
Motile - single polar flagella
Microaerophilic (reduced O2,
increased CO2) and thermophilic
(42 C)
Slow grower > 2 days
Closely resembles campylobacter
Gram (-) bacillus: gram stain is
variable. Sprial shape in fresh
culture, coccoid in older culture
Flagellated, highly motile "corkskrew Developing countries high colonization,
motion"
Helicobacter pylori
urease (+)
very slow (2-6 day) growth in
complex media
microaerophilic
temp 30-37 C (not 42 like
campylobacter)
Family Bacillaceae Gram (+) bacilli
3 Classes: MC anaerobic
Clostridium spp. Histotoxic: C. perfringen Spore formers
Enterotoxigenic: C. difficile
Paralytic: C. tetani, C. botulinum
Gram (+) "plump, rectangular" rod
non-motile but rapid growth on
Clostridium sheeps blood agar
perfringens
Replicated in 10 min!
#1 bacterial cause of gastroenteritis and
bacterial endocarditis in USA (most
common is C. jejuni
Zoonoses - poultry, birds, cats/dogs, rabbits,
mink, insects, pigs, bulls
Transmitted via raw milk and water
Peak incidence in warm months, young adults
(20-29)
Found in stomach of humans, primates, pigs,
cheetas, dogs, cats, ferrets, mice, rats
Only found in gastric antrum and body
developed countries low colonization
Only <20% of people, regardless of age whi
Resist immune clearance
test + for H. pylori also get PUD
Form of transmission not clear
Ubiquitous: soil, GIT of humans and animals
Ubiquitous: soil, GIT of humans and animals,
contaminated water. MC harmless saprophytes. for most human disease (B-E
C. perfringens need devitalized tissue to grow Spore formation - long term survival in
best
Disease MC after trauma that causes ischemia:
lowered pO2 and pH favors C. perfringens
growth
Necrotic toxin - involved in eye damage
Adhesins, enterotozxin, cytopathic toxin Gastroenteritis: short course, self-
Gastroenteritis
- not well understood limiting, no ABC's unless high risk
prevent with proper preparation
Need high infectious dose - reduced
Guillian Barre syndrome and storage of food, avoid raw
with hypochlorhydria, TUMs, milk
milk, proper water treatment
Guillian Barre syndrome: no
treatment, proper storage of food
Triple theory: proton pump inhibitor
Surviva acidity: Bacterial acid inhibitory
(omeprozle), clarithromycin,
protein. Urease. Heat shock protein. Type B (infective) gastritis
metronidazole, bismuth (dec acid
Flagella. Mucinase/ phospholipase
and 2 ABCs)
Prevention: stop smothing,
Adhesins Peptic ulcer disease (PUD) drinking, moderate pickled and
salt-preserved food consumption
Avoid nitrates (smoked and
Microaerophilic - survive relatively
Gastric adneocarcinoma processed meats, nitrosamines
anaerobic environment of ST
(BBQ, charred meats))
Gastric mucosa-associated
lymphoid type (MALT) B cell Reduce stress
lymphomas
Pro-inflammatory: LPS Eat healthy stufff. Natural shizzle.
Tissue damaging: PAF (platelet agg
factor) hypersecretion of gastric acid
5 toxin specific types: Type A:
proper cleansing of wound,
permanent soil inhabitant, responsible
Simple wound infection debridement of affected tissue,
ABCs, byperbaric O2 chamber
responsible for animal disease)
Anaerobic cellulitis
environment and throat
Toxin formation: alpha toxin - most
tissue damage. Phospholipase C
C. perfringens myonecrosis
activity increases vascular permeability
--> lyse cells
beta toxin: necrotizing enteritis, HTN
C. perfringens food poisoning
(inc chatecholamines)

Gram (+) rods
obligate anaerobes, spore-forming
Clostridium difficile
Gram strain variable: (-) in old
cultures of fresh wounds, (+) in
fresh culture
long, thin bacillus with "tennis
raquet" morphology
Clostridium tetani
difficult to grow: sensitivy to O2 -
obligate anaerobe. Relatively
inactive metabolically (unlike C.
perfringens)
Gram (+) bacillus, "sausage
shaped"
Strict aerobe
Clostridium
botulinum
Beta hemolytic on sheeps blood
agar
Produces one of the most potent
exotoxins known to humans
Gram (-) diplococci, "coffee bean"
Two main Human pathogens:
appearance
Neisseria spp. 1) N. meningitidis - normal colonizer of Transparent, non-pigmented
nasopharynx or cause disease colonies on chocolated blood agar
2) N. gonorrhoeae - strict pathogen Facultative anaerobe
Can ferment glucose and maltose
AKA meningococci (onlke N. gonorrhoeae which only
ferments glucose)
Neisseria
meningitidis
Termed "the gonococcus"
Need intimate sexual contact. MC in 15-24 year
Gram (-) diplococci
olds.
Fastidious growth in culture: NO
Neisseria
growth with drying (not on toilet Increased risk if female, multiple sex partners,
gonorrhoeae
seat), need humidity and increased blacks, residents of SE USA
CO2
2nd most common STD in the US
(chlamydia is #1)
Can be a normal part of GI flora without causing
disease
MC after broat spectrum ABCs and Proton
pump inhibitors (PPI's)
Ubiquitous - spores last for years in soil,
sewage, feces contaminated soil
Present in GIT of cows, horses, some humans
Tetanospasmin: heat labile neurotoxin
(one of the most potent toxins). Causes
Developed world: low incidence due to
spasdic paralysis. 2 part toxin: B chain
immunization, herd immunity, urbanization.
binds R in neuronal membrane. A chain
Developing world: higher incidence due to rual,
moves to post-synaptic terminals in
agricultural societies, low immunization.
CNS and irriversibly inhibits the
release of GABA and glycine
Ubiquitous - soil, sedaments of lakes and
ponds, and decaying vegetation
Asymptomatically colonize nasopharynx or
cause meningitis, meningococcemia or
pneumonia
Decrease risk of getting disease with breast
feeding and healthy immune system
MC cause of baterial meningitis in infants
through adolescence and in young adults
transferred via close contact with respiratory
droplets (e.g. daycares, military barracks).
Classmates in school not close enough.
MC carriers are asymptomatic adults
Disease MC in dry, cold months
Humans are sole natural carriers
Women are MC'ly asymptomatic carriers
Toxin A (enterotoxin) - inc cytokines
MC causes post-ABC diarrhea and Discontinue ABCs, maintain
neutrophils. Hemorrhagin necrosis in
pseudomembranous colitis fluid/electrolyte balance.
pseudomem. Colitis
Toxin B (cytotoxin) - depolymerize
Difficult to tx because spores are
actin. Marker for more pathogenic
resistant
strains.
Hyaluronidase - inc spread between Prevent by hygiene and prescribe
tissues ABCs with probiotics
Spore formation
Adhesion factor - to colonocytes
Prevention: no natural immunity
Spores - survive adverse conditions Tetanus
unlike many other diseases
Active immunization - tetanous
Tetanolysin
toxoids: booster every 10 years
Part of DPT vaccine. Proper
wound care and umbilical stump
care.
Spore formation - one of the mose
Support! Adequate ventilation,
resistant: hours at 100 C and 10
Food borne botulism "Intoxication" flush GIT - gastric lavage, IV
minutes at 120 C. Also -190 C and
ABCs, trivalent botulinum antitoxin
irradiation
Botulinum toxin: one of the most potent
neurotoxins. Two parts: B - protects Prevention - food preparation. Acid
Infant botulism "infection-
from ST acid. A part - neurotoxin pH (canned fruit is OK) - grow best
intoxication"
specific to irreversible binding to at pH>4.5 (alkaline risky)
cholinergic neurotoxins
Inhibits acetylcholine release at Refrigerate (Can't survive <4C).
presynaptic terminals and therefore, Heave for min 20 min at 80 C.
Wound botulism
flaccid paralysis (opposite Check cans (swollen from gas
tetanospasmin) release)
Don't give honey to infants under 1
Unclassified botulism
years old
Colonization of nasopharynx - pili attach
Meningiococcemia - mild disease Proper hygiene
to con-ciliated columnar cells
Host immunity - need specific Ags Meningiococcemia - marked
Good diet
against capsule and complement sys disease
Bacteria enters host cell and replicates
Polysaccharide vaccine - not for
in phagocytic vacuoles - capsule is also Meningococcal meningitis
children <2. For travelers.
anti-phagocytic
Avoid close contact with infected
LOS expressed
persons
ABCs
Currently no longer use penicillin:
No exotoxin - host damage is from
resistance (beta-lactamase, need
gonococcal induced inflammatory Gonorrhoeae in males
too high dose, change cell surface
response
so ABC can't penetrate cell)
Anti-phagocytic - negatively charged
Gonorrhoeae in females Prevention: safe sex!
capsule. Highly variable structure.
Pili: tissue trophism: non-ciliated
epithelial cells of foreskin, vagina, Disseminated gonorrhoeae
fallopian tube.
LOS - classic endotoxin activity (like
LPS). No strain specific O antigens Opthalmia neonatorum
(unlike LPS)
Fe 2+ binding proteins
IgA protease - destroys IgA
Bata lactamas - degrades penicillin

2 main pathogenic spp:
H. influenzae - encapsulated
Heaemophilius spp.
H. ducreyi - non-encapsulated
Non-encapsulated strains: colonize
both upper and lower respiratory
tracts (cause sinusitis, OM, bronchitis, membranes of humans and animals
pneumonia)
Encapsulated strains (serotype b) -
can become systemic (meningitis,
epiglottitis, cellulitis). Vaccine is
against this strain only
3 human pathogens:
Most notorious is Bordatella pertussis
(whooping cough)
Bordatella Spp.
Family Treponema, order
Spirochaetalis
1 species cause human disease (strict
M/C strict anaerobes
human pathogen):
Treponema pallidum Treponema pallidum (2 subspecies)
Treponema pertue
2 separate genera: 1) Chlamydia:
Chlamidia trachomatis
2) Chlamydophila: C. psittaci (from
birds), C. pneumonia
Chlamydia
Small, gram (-) coccobacillus
(pleomorphic)
Fastidious growth requirements: X
factor (hematin) and V factor (NAD).
Chocolate agar (heated sheeps
blood)
non-spore formers, non-motile
obligate parasites on mucous
Gram (-), very small bacili (rodlike)
strict aerobes
oxidase (+)
Fastidious growth - humiditiy,
specialized media. (Charcoal, blood,
NAD-enriched)
Small, thin, coiled spirochetes -
can't visualize via Gram stain and
light microscopy
Fastidious growth - only in cultured very labile, susceptible to drying - only spread
rabbit epithelial cells, doubling time with direct contact of warm, moist infectious
30 hours
Motile - "corkskrew motility" via thin
fibrils at both ends
VERY small Gram (-) bacillus with:
Virus-like properties - filterable and gains access through minute abrasions or
obligate intracelular parasites
Bacteria-like properties - inner/ outer
membranes, bacterial ribosomes,
contain DNA, RNA and LPS
Unlike other bacteria there is no
PG layer, therefore no Gram stain
Unique growth cell cycle within host clinical signs and symptoms due to direct
cell - EBs (elementary body) and
RBs (reticylite body)
Primarily a pediatric problem (<5 yo). Since the serotype and virlence and trophism.
vaccine in 1987, now a pediatric problem in the Invasive disease MC HiB. Anti-
developing world.
Also increased risk in elderly (esp with COPD,
smokers, alcoholism, altered mental state,
hospitalized)
Can only cause disease in humans -
reportable disease
> 1 million deaths per year. Most common in
developing countries in children < 1 year old.
Spread by infectious droplets.
Increased incidence in older individuals -
waning immunity
No long term imminity - can get disease more vasoconstriction of peripheral blood
than once
"protection" in developed countries due to DPT
vaccine
Humans are the only reservoir of disease:
increased risk if 20-35, urban areas, drug user, host cell. High lipid to escape cell
prostitution, lo SES
3rd most common STD in the USA
lesions
Contagious only during primary stage and rash
of secondary stage - not highly contagious (only
30% chance after single sexual contact)
Active genital lesions increase risk of HIV
infection
Only affects humans
lacerations
Limited tissue trophism
Strains causing LGV (lymphoma granuloma
venereum) can cause systemic infections by
entering lymphatic system
destruction of cells during replication and host
inflammatory response
No long term immunity - re-infection leads to
vigorous inflammatory response
Leading cause of preventable blindness in
developing countries
most commonly in children due to poor hygiene
Spread by droplets, hands, contaminated
clothing, eye make-up, flies
Can get from toilet seat - EB is resistant to the
environment!
Capsule (PRP capsule). Determines
Conjugated HiB vaccine (purified
PRP). 2 types.
phagocytic. Anti-Hib capsule Abs
determines severity of disease.
Pili - damage respiratory ciliated H. Ducreyi: Treatment with ABCs.
epithelium Safe sex!
LPS - responsible for mengitis
Pertussis toxin - increase Adenylate
cyclase. cAMP respiratory secretions/ Mostly supportive (hydration,
mucous. Binds ciliated epithelium and Whooping cough control secretions, maintenance of
kills NK cells, monocytes, airway)
macrophages, neutrophils
ABCs are of limited use (disease is
Adenylate cyclase toxin (cyclosin) -
not recognized until peak of
increase cAMP
infectiousness has passed)
Tracheal cytotoxin - part of the PG
layer. Cause ciliostasis and then
Erythromycin is ABC of choice
damage to ciliated epithelial cells -
cough - IL-1 = fever
Dermonecrotic toxin - heat labile,
Prevention - DPT vaccine. 2, 4, 6,
vessels, hemorrhage, localized 15 months and 4-6 years.
ischemia
Filamentous haemagglutin and other
Used to use whole cell vaccine
adhesins: attachment to ciliated
(DTwP) but now use acellular B.
epithelial cells and PMNs. Intracellular
pertussis (DTaP) - "fever side
survival protects against clearance by
effects"
humoral immunity
LPS - two types, lipid A and lipid X
Outer Membrane - proteins adhere to High dose penicillin - maintain in
Syphilis = pig lover!! blood for a few days since it
immunity. divides every 33 hours
Prevention: hygiene (spirochetes
Hyaluronidase - spreads through tissue destroyed by soap and water,
temp >42 and drying)
LPS - similar to gram (-) LPS Safe sex practices
EB: major outer membrane proteins
Treatment MC also have
tightly cross-linked: extracellular Trachoma disease
presumptive TX for gonorrhea
survival and initiation of infection
Reticulate body: Less cross linking so
Prevetion: hygiene: hand/face
more fragile, adapted for intracellular Trachoma inclusion conjunctivitis
washing
growth; metabolically active
Inclusion body: Phagosome with
accumulated RBs: high amount of Chlamydia urogenital infections Practice safe sex
glycogen, therefore stain with iodine
Reactive arthritis (Reiter's
syndrome)
Lymphogranuloma vererum
Chlamydiophilia pneumonia
Chlamydophila psittace
 Runyon classification depending
>70 spp, many associated with
on growth characteristics and
disease in humans
pigments produced with light
Acid fast (fungus like), weakly Gram
M. tuberculosis - TB
(+) bacillus
Mycobacterium
M. bovis obligate aerobe
fastidious, slow growth - one of the
M. leprae - leprosy slowest dividing microorganisms
(need ABCs for long time)
M. avium Complex - assoc with AIDS
M. Gordonae (won't talk about)
Treatment: "Denver protocol" -
Cause of more fatalities worldwide than any Contains much mycolic acid in its cell
multi-drug cocktail for >3-6
other infectious disease (humans are the only wall - acid fast, resist drying, TB
months. Quarantine. Problem:
known carrier) detergents, acids/bases
MDR-TB
MC'ly person-person transmission via infectious Protein polypeptides on cell surface -
Prevention: Diet/ robust immune
aerosolized particles - very small inoculum immongenic, source of PPD for
system
needed Mantoux test
Inhaled to terminal airways --> resist BCG vaccine - not as effective in
Increased risk if immunocompromised,
killing by phagosome/lysosome fusion adults, not used in
Mycobacterium homeless, substance abuse, elderly, chemo,
and evade humoral immunity b/c of immunocompromised, give false
tuberculosis tavelers, first nation persons
intracellular growth (+) later on
Spread to LN and into bloodstream to
other tissues
No known toxin: tissue destruction is
due primarily to host immune response
form tubercles - develop into caseous
granulomas
Ghon complex - initial lung lesion and
locally enlarged LNs
Rare in US, common in India, Brazel, Myanmar,
Similar to M. tuberculosis but: Indonesia, Bangladesh. MC in men and Capsule Tuberculoid (paudibacillary) Emptional support
children.
Can not be articicially cultured (need Armadillos are naturally infected and provide Preference for lower temperatures -
Mycobacterium Lepromatous (Multibacillary) ABC for years
live mice or armadillos) reservoir limits infection to skin and nasopharynx
leprae
Grow in globi bundles (encapsulated Spread via respiratory route or contact with Intracellular survival - in Histiocytes and Surgery and grafts, physical
globs of rods in tissues) break in skin Schwann cells therapy
Hot wax baths

Similar to M. tuberculosis but only

Ubiquitous in water and soil MAC disease ABCs
case opportunistic infections
Mycobacterium
avium intracellulare MC'ly disease in HIV/ AIDS patients
complex but can cause disease in birds and
pigs
Also can cause lymphadenitis in
children

Many different spp Gram (-) spirochete, spiral shaped
Larger than other spirochetes and
Borrelia burgoderferi
more complex nutrition required
Microaerophilic
Internal flagella
Borrelia spp.
Contain cholesterol in cell wall
(unlike other bacteria)
Gram (-), very thin, tightly coiled
2 main:
spirochete
L. biflexa - free living, non pathogenic obligate aerobe
L. interrogenes - human pathogen - minimal nutrition requirements:
leptospirosis LCFA, vitamin B1 and B12
Leptospira spp
Survive moist, slightly alkaline
environment for many days (up to 6
weeks in urine soaked soil).
Susceptible to drying, detergents,
heat (50 C), salt water
Internal periplasmic flagella (like
other spirochetes)
Many spp Originally thought to be viruses
Human pathogen is Rickettsia ricketsii
(cause Rocky Mountain Spotted Small bacteria
Fever)
Rickettsia spp. Structurally similar to Gram (-)
bacteria (min PG layer, LPS,
MC in children and in summer months
sysceptible to ABCs, need O2, have
metabolic enzymes)
No flagella, weakly adherent slime
capsule
Cause relapsing fever and Lyme disease
Dormant in glial cells Lyme disease Avoid potential tick infested areas
(Boreellia burgodorferi). Need ticks as vestors
Spirochetes release neurotoxins that
MC vector borne disease in USA (no person to Light colored clothing, tuck pants
affect pre and post-synaptic Neruoborelliosis
person spread) into socks and shirts into pants
membranes
vector: deer tick (Ioxdes scapularis/ Ioxdes
Autoimmunity?? Insect repellants
pacificus)
Reservoir: white footed mouse or white tailed
Check and remove ticks
deer
MC in Northern temperate zone esp New York Treatment: ABCs, vaccine not very
Sate effective
Increased risk in grassy, wooded areas and mid
May-mid August
One of the fastest growing infectious diseases
in the world
Can mimic signs and symptoms of MANY
diseases!
Zoonotic - rodent (rat) and domestic animal Spirochetes enters via contaminated
Leptospirosis
(dog) reservoirs urine: entry to broken skin and mucosa
Humans are accidental hosts: MC'ly acquire
Unknown mechanism of tissue damage
disease via contact with infected urine
Replicate in endothelium lining of
Increased risk in tropical areas and in men
capillaries (affect meninges, LV, KI) and
(farmers, veterinarians, back-packers, hunters)
interfere with blood flow
Need arthropod vectors - hard ticks (dog tick or
Must be exposed to tick >24 hours Rocky Mountain Spotted Fever Treatment: aggressive ABCs
wood tick) - Dermacentor
Inc when outdoors, miliatry activity in endemic Multiply in skin site first, then affect Control: same as other tick borne
areas other organs diseases
Weak endotoxin, host immunity plays
no role in pathology - survive within
Almost impossible to get rid of
phagocytes, tissue damage due to
ticks (can survive up to 4 years
multiplication in vascular epithelium and
without feeding)
causing leakage - leads to dec
perfusion and organ failure
Worst prognosis if elderly, males, G6PD
deficiency
 Nausea/
Microbe System Condition Signs and Symptoms Vomiting Fever Diarrhea DDX and Lab Dx
Need a large infective dose, ingest contaminated food product. 4-6 day
Yersinia entrolytica gastroenteritis/ incubation. Right sided abdominal pain. Lasts for 1-2 weeks. Can progress to
1 Yersinia enterolytica GI Yes Watery or bloody
Yersinosis perforation of ilum and skin rash (erythema nodosum). Can get mesenteric
adenitis in children (mimics acute signs of appendicitis)
Black plague 2 types: Urban: affects
Get bitten by infected flea, 2-6 days later get high fever, chills. Not large but humans and can cause 3 types of
painful buboes in groin, axilla, neck. Prostration with rapid, thready pulse, plague. Rats are the main reservoir,
2 Yersinia pestis Circulatory Bubonic plague delerium. Bubonic purperea: vasculitis of superficial blood vessels cause High rat flea (Xeopsylla cheopsis) is main
bleeding into skin - black death. Can spread to blood then to lungs. Fatal vector. 2) Sylvatic (Woodland):
within days (75% mortality) disease of wild rodents found
everywhere but Australia
Hematogenous spread from infected buboes or aerosols from infected
3 Yersinia pestis Respiratory Pneumonic plauge person. Only 2-3 day incubation. Fever, malaise, hemoptysis, dyspnea. Highly Yes
virulent, rapidly fatal form of bronchopneumonia (90% mortality)
Direct deposit of bacteria into open wound or orifice. Most common in
4 Yersinia pestis CNS Septicemic plague
children. Rapidly fatal meningitis before buboes form.
Especially tricuspid valve. Increased risk with IV drug users and prosthetic HT
5 Pseudomonas Circulatory Endocarditis
valves
6 Pseudomonas CNS CNS infections meningitis, brain abscesses
Especially fibrocartilaginous joints of axial skeleton. Most comon pathogen in
7 Pseudomonas Skeletal Bone and joint infections
osteochondritis after puncture wound to the foot.

Most common cause of bacterial

8 Pseudomonas
keratitis and neonatal opthalmia.
Increased risk iff
immunocompromised, contaminated
Unilateral, acutely painful, photophobic, intensely injected eye. Decreased
eye drops (contacts), hypoxic damage
Eye Bacterial Keratitis visual acuity. Profuse tearing, thick ropey mucopurulent discharge.
from prolonged contact wearing,
Edematous cornea and eyelid
corneal trauma, eye operations. Can
lead to blindness. Most common
bacteria is S. aureus unless contact
wearer, then P. aeruginosa.

9 Pseudomonas Urinary UTI's 3rd leading cause of nosocomial UTIs. Prolonged indwelling catheters.
Any part of the tract. Eg. Perirectal, pediatric diarrhea, gasteroenteritis,
10 Pseudomonas GI GIT infections
necrotizing enteritis
Can get chronic supporitive OM,
Initial pruritis and fullness in ear. Increased pain/tenderness on palpation. malignant otitis externa or Swimmer's
11 Pseudomonas Ear Swimmer's Ear Otorrhea (?), Possible hearing loss (mild erythema and edema of external ear (acute diffuse otitis externa).
auditory canal. Dull injected TM with displaced COL). No systemic signs. Weber test: laterlize to affected side.
Rinne test: AC>BC.
Primarily nosocomial. Increased risk if immunocompromised. Similar clinical
12 Pseudomonas Systemic Bactermia
presentation as other bacteremias but with higher mortality.
After breakdown in skin integrity (burns, trauma, cuts, dermatitis). High
13 Pseudomonas Skin Hot tub folliculitis
moisture conditions or immunocompromised.
Pathognomic Pseudomonas skin infection. Erythematous vessels become
14 Pseudomonas Skin Ecthyma gangernosum hemorrhagic, necrotic and ulcerated with a fruity odor. Can have rapid
necrosis to adjacent tissue (potentially fatal)
Most commonly caused by E. coli and
group B strep. Most isolated strains
15 Escherichia coli CNS Neonatal Meningitis Colonization of infants with E. coli is common but rarely leads to disease
from babies have K1 capsular Ags
(maternal anti-K1 Abs are protective).
E. coli is most common cause of
Usually results from spread from GIT or GTU. Increased mortality if
16 Escherichia coli Systemic Septicemia enterobacterial septicemia (45%),
immunocompromised or due to complication of intestinal perforation.
then K. pnemonia
Very common infection: 10-20% of all
women will have at least 1 in their
lifetime. Spread is from GTU:
ascending infection. Virulence factors:
Cystitis: dysuria, urgency, increased frequency, incomplete voiding.
special adhesins are used to attach to
17 Escherichia coli Urinary UTI's Pyelonephritis: same as cystitis but more severe and with fever, loin pain and
uroepithelium and resist flushing durin
(+) KI punch.
micturation (decrease attachment with
D-mannose, blueberry & cranberry
juice). Lab dx: pyuria, hematuria,
bacteriuria.
Gastroenteritis (6 types) - most
common E coli infection in normally
healthy persons. Exotoxins: St a/ST b:
Most important cause of traveler's diarrhea and infant diarrhea (in developing
Gastroenteritis - Enterotoxigenic Cramps, nausea, heat stable, stimulate guanylyl
18 Escherichia coli GI countries). Symptoms take 3-4 days to resolve. Symptoms similar to cholera Low grade Watery
(ETEC/ VTEC) vomiting (rare) cyclase. LT1/ LT 11: heat labile,
but much milder.
stimulate adenylyl cyclase. Induce
fluid and electrolyte loss: watery
diarrhea
 Initial watery
diarrhea
Variable onset (1-4 days). Intense abdominal cramps. Can progress to progressing to
19 Escherichia coli GI Enteroinvasive (EIEC) Yes Bacteria invade and destroy tissue.
colonic ulceration and more severe sequelae. Similar disease to Shigella scant, bloody stool
that is leukocyte
(+)
Bacteria adhere to plasma membrane
of mucosal epithelial cells and destroy
20 Escherichia coli GI Enteropathogenic (EPEC) Yes Yes Non-bloody stool
adjacent microvilli. Common cause of
infant diarrhea.
Cause persistant diarrhea in
Persistent, watery
developing countries. Subset of EPEC
21 Escherichia coli GI Enteroaggregative (EAggEC) Yes Low grade diarrhea
that can form aggregates on surfaces
(dehydration risk)
that they colonize.
Most common strain causing disease
3-4 day incubation. Severe abdominal pain. Most commonly self-limiting in 4- Initial non-bloody in developed nations. Cause of
10 days but can progress to HUS (hemolytic uremic syndrome). Spread via: No fever or just diarrhea "Hamburger disease" and HUS
22 Escherichia coli GI Enterohemorrhagic (EHEC) Yes
undercooked beef or other meat, feces contaminated water, unpasteurized low grade progresses to (Walkerton). Virulence factor:
milk, fruit juices, raw veggies/fruit. bloody diarrhea hemolysin. Very low inoculation is
needed (100 bacilli)
Wattery diarrhea Bacteria are embedded in cell
23 Escherichia coli GI Diffuseaffregative (DAEC)
(infants 1-5) membrane of elongated microvilli.
Abdominal pain. Irritability, lethargy or seizures. HTN, pallor. Anuria or
Most common cause of acute renal
oliguria. Acute renal failure - destruction of renal glomeruli. Potentially fatal
failure in children. Lab dx: stool
24 Escherichia coli Urinary HUS sequelae of gastroenteritis in 10% of children. Spread: person to person. Vomiting Bloody diarrhea
culture (+) for E coli O157 : H7,
Handwashing is important and child must be isolated until 2 consecutive (-)
hemolytic anemia, thrombocytopenia
stool cultures.
Occurs 6-48 hours after ingestion of contaminated food or water. Abdominal
Non-bloody
25 Salmonella enteritidis GI S. enteritidis gastroenteritis cramps, h/a, myalgia. Most commonly self limiting (2 days to 1 week). Low Yes Yes Most common type of Salmonellosis
diarrhea
mortality but increased risk with elderly and children.
Most commonly due to S. typhi and S.
Salmonella typhi / Salmonella Symptomology similar to other Gram (-) septicemia: 10% of patients develop paratyphi but also seen with S.
26 Systemic Salmonella induced septicemia
paratyphi arthritis, osteomyelitis, and endocarditis enteritidis. Increased risk with AIDS,
geriatrics and pediatrics.

MC spread is by food handlers

infected with S. typhi (typhoid fever) or
S. paratyphi (paratyphoid fever).
Non-specific systemic symptoms (H/A, malaise, myalgias, and anorexia).
Bacteria pass directly through
Salmonella typhi / Salmonella Rose coloured spots on abdomen (erythematous, maculopapular, blances Increasing,
27 Systemic Enteric fever intestinal walls. Enter thoracic duct
paratyphi with pressure, only 50% of patients). Complications: GI lesions, Toxemia, remittent
and then blood stream to replicated in
meningitis, osteomyelitis, endocarditis. 1-3% become chronic carries.
Sp, LV, bone marrow and GB. Back
into the intestine to cause increased
inflammation. This is NOT typhus.

GI symptoms are caused by Shiga toxin. Enterotoxic, neurotoxic and

Bacteremia rare. Infection self-limited.
28 Shigella GI Shigellosis cytotoxic. 1-3 day incumation. Fever and diarrhea proceeds to tenesmus, None Yes Profuse watery
5% can asymptomatically carry.
abdundant blood and pus in stool.
Cam resemble ETEC induced
2-3 day incubation. Abrupt onset of watery diarrhea and vomiting. Rice water gastroenteritis. Lab Dx: rarely seen in
stools. Severe fluid and electrolyte loss.Hypovolemic shock leads to cardiac Fram stained stool or wound
29 Vibrio cholera GI Cholera Yes None Watery, rice water
arrhythmia, renal failure, muscle cramps. 60% mortality iff untreated, self specimens. Dark field/ phase contrast
limiting within a week. No abdominal cramps or fever. microscopy: characteristing darting
motility.
Painless papule. Ulcer surrounded by vesicles - necrotic eschar - Direct contact with spore
gelatinous edema. MC arms, hands, face, neck. Potentially fatal - 20% contaminated animals/producers.
30 Bacillus anthracis Skin Cutaneous anthrax
mortality (could spread to blood/lymph) . Internal hemorrhage, myalgia, fever, Look at px history: wool worker? Gm
H/A, n/v. (+) bacillus in lesions, no neutrophils.
Carried by alveolar macrophages to mediastinal LN - prolonged latency. Initial
disease: fever/chills, dyspnea, cough, H/A, vomiting, chest/ab pain. Second
No person to person disease
31 Bacillus anthracis Systemic Inhalation anthrax stage: rapidly worsening fever, pulmonary edema, massive enlargement of
transmission. 87% mortality.
mediastinal LNs, shick/death within 3 days. Hemorrhagic meningitis Sx's MC
than pulmonary Sx's.
IFF upper GI: ulcers, edema, sepsis, regional lymphadenopathy - dysphagia.
32 Bacillus anthracis GI Ingestion anthrax Extremely rare. 100% mortality.
IFF lower GI: n/v, malaise, systemic s's and sx's, bloody diarrhea
 Contaminated rice, not refrigerated. 15 min-4hr incubation. Self limiting >24
33 Bacillus cereus GI Emetic disease Yes No No
hrs.
Contaminated meat, veggies, sauces. 8-12 hr incubation in GIT. Self limiting
34 Bacillus cereus GI Diarrheal disease Nausea No Bloody diarrhea
<24 hrs
Post-traumatic, penetrating eye injury or hematogenous spread. Pain, H/A,
35 Bacillus cereus Eye Bacillus cereus panopthalmitis drowziness, swelling. Muddy grey iris, turbid aqueos humor, precipitate on Yes
posterior surface of cornea. Rapid <48 progressive loss of light perception
2-11 day incubation. Foul smelling, watery diarrhea progressing to profuse
36 Campylobacter jejuni GI Gastroenteritis bloody diarrhea. Resolution in 3 days - 3 weeks. Residual histological Yes Watery --> bloody
damage to mucosa of jejuni, ileum and colon.
Many causes. Also immunizations,
Idiopathic, peripheral polyneuritis 1-3 weeks after mild above conidition. pregnancy, URI, EBV, CMV,
Progressive, symmetric pain and weakness in extremities - might ascend to Hodgkin's lymphoma. Autoimmune
37 Campylobacter jejuni Neural Guillian Barre syndrome
trunk, face, thorax. Self limiting (few weeks to months) with complete link: cross reactivity with
recovery. glycosphingolipids on surface of
neural tissue

30-50% of people with gastritis have

Epigastric pain, abdominal tenderness, bloating, nausea, anorxia, dyspepsia. H. pylori but most commonly
38 Helicobacter pylori GI Type B (infective) gastritis Epigastric tenderness on percussion, foul smelling breath, hematemesis Nausea asymptomatic. Lab Dx: 13C urea
(coffee grounds) breath test, anti-H. pylori Abs (IgG),
gastroscopy with biopsy, CLO test (+(
Expecially dodenal ulcers. Burning, gnawing upper GI pain 1-3 hours after Endoscopy, urea breath test, serology
39 Helicobacter pylori GI Peptic ulcer disease (PUD)
meals. < night, > eating or > antacids. Anemia, epigastric tenderness. (anti-H. pylori Abs)
Sequelae of untreated chronic gastritis. Classifies as a class I carcinogen. Nausea,
40 Helicobacter pylori GI Gastric adneocarcinoma Fatigue, weight loss, low grade fever, night pain. Epigastric/abdominal mass. sometimes Low grade
Hemoccult (+) stools, anemia. vomiting
Chronic H. pylori infection assoc with
Gastric mucosa-associated lymphoid B-cell lymphoma. No evidence that
41 Helicobacter pylori Systemic Dysphagia, dyspepsia, weight loss, GI bleeding - hematemesis.
type (MALT) B cell lymphomas eradicating H. pylori prevents the
progression of gastritis to carcinomas
42 Clostridium perfringens Skin Simple wound infection MC, no clinical consequences
Trauma and favourable conditions. Organism spread through subQ tissue -
spares fascia and deep muscles. Pain, redness, inflammation, superficial skin
43 Clostridium perfringens Skin Anaerobic cellulitis discoloration and skin necrosis. Gas forms develop suppurative myostitis -
foul smelling discharge. No muscle necrosis, no systemic signs and
symptoms.
Rapid worsening of cellulitis. Trauma and 1 week incubation. Rapid onset of
intense pain, extensive muscle necrosis (blue black, edematous, does not Fast growth of culture on sheep's
bleed or contract on stimulation), toxic delerium. Progress to shock, renal blood agar. Nagler's reaction on egg
44 Clostridium perfringens Skin C. perfringens myonecrosis
failur, death within 48hrs if untreated. Much damage due to alpha toxin and yolk agar. Gram (+) rods in tissue
gas bubbles. MC in areas of poor blood supply. Need to perform debridement specimens with no leukocytes.
and examine inderlying tissue.
Ingest meat (refrigerating and re-heating destroys enterotoxins) Large
45 Clostridium perfringens GI C. perfringens food poisoning infective dose. Short incubation: 8-24 hrs. Abdominal cramps. Self limiting > None None Watery
24 hrs.
Pseudomem colitis confirmed by
biopsy - multiple, raised white/yellow
exudative plaques adhering to colonic
Range from mild diarrhea to colitis to potentially life-threatining Prolonged
46 Clostridium difficile GI Pseydomembranous colitis mucosa. In vitro cytotoxicity assay in
pseudomembranous colitis. (dehydration)
culture cells. Immunoassay for C.
difficile toxins A and B.
Sigmoidoscopy. Fecal leukocytes.
Patient history. Clinical S's and Sx's.
MC form of tetanus. Bacterium introduced by trauma to skin: rusty nail, animal Gram stain culture not that important
bites. 3 Early signs: 3 day-2 week incubation. Muscle stiffness/ ridigity, diagnostically - only 30% of people
exaggerated DTRs (deep tendon reflexes). Trismus (lockjaw), risus sardonius with tetanus are culture (+).
(rye smile), drooling, dysphagia, diaphoresis, irritabiliey. Later signs: Treatment: tetanospasmin binds
opisthotonus (backward arching), flexion of arms, extension of lower irreversible and therefore, can only
47 Clostridium tetani Musculoskeletal Tetanus
extremitis. Complications: HTN/hypotension, tachycardia, pneumonia, treat symptoms until nerve terminals
dehydration, bone fractures, meningitis, Rh incompatibility. Other forms: 1) regenerate. Either penicillin high
localized (to point of infection, less common than generalized), 2) Cephalic doses or tetracycline, or passive
(rare but poor prognosis, from improperly cleaned umbilical stump), 3) immunization - bind free
Neonatal - first sign, difficulty sucking 8-10 days after birth. tetanospasmin and decrease
progression of disease.
 Inadequate sterilization of food: home canned foods, preserved fish. 2h-72
Clinical signs and symptoms
hour incubation. No GI distress - unlike other food poisonings, Dilated, fixed
No fever - clear paramount. Patient history. Culture
48 Clostridium botulism Musculoskeletal Food borne botulism "Intoxication" pupils; dry/ "furry" tongue. Bilateral descending weakness - of neck, face,
sensorium stool/food for toxin (only > 60%
throat. Respiratory paralysis (mortality 32-40%.) No permanent immunity - can
specificy).
get repeated occurances. MC complete recovery in months to years.

Consumption of honey contaminated with spores. MC form of Botulism in the

USA. MC in 1-6 months because infant GIT doesn't have as many
competitive bowel microbes. Can resemble SIDS iff rapid onset. Non-specific
49 Clostridium botulism Musculoskeletal Infant botulism "infection-intoxication"
signs: constipation, weak cry, failure to thrive, weak sucking. Floppy baby:
acude flaccid paralysis (head, fact, throat), descent to extremities/trunk.
Death reom respiratory paralysis (low 1-2% mortality)
Very rare, little evidence of clinical infection. Limited paralysis. Same sx's of
50 Clostridium botulism Musculoskeletal Wound botulism food borne botulism but long incubation (1-4 days) and no abdominal pain or
constipation
People over 1 year who have had symptoms of botulism but no documented
51 Clostridium botulism Musculoskeletal Unclassified botulism
vehicle of transmission. DDX is important.
52 Neisseria meningitis Meningiococcemia - mild disease Persistent (few days to weeks). Arthritis. Petechial skin rashes. Pharyngitis. Low grade
URI infection 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). Iff untreated can progress to DIC or hammorhage into
53 Neisseria meningitis Systemic Meningiococcemia - marked disease Rapid onset
adrenal glands (Waterhous-Friderichsen syndrome). Sequelae: none or large
areas of necrosis. Deafness. Mortality 100% if untreated, 25% if treated.
Occurs with or without meningitis
N. mengintidis is 2nd MC cause of adult bacterial meningitis. Triad: fever, Clinical signs and symptoms and CSF
54 Neisseria meningitis Systemic Meningococcal meningitis nuchal rigidity, blinding HA. Neurological sequelae (hearing deficits, In children Fever analysis. High number of Gram (-)
arthritis, memory loss) low compared to H. influenzae or S. pneumonia diplococci in PMNs.
Clinical signs similar to Chlamydia.
95% of men get acute symptoms. MC'ly gonococcal urethritis. Infection
Gram stain: sensitive and specific iff
usually restricted to mucous of penis. 2-7 day incubation - purulent urethral
55 Neisseria gonorrhoeae Reproductive Gonorrhoeae in males men with purulent urethritis. Oxidase
discharge, red/ edematous urethral meatus, itching, burning, dysuria,
(+), Gram (-) diplococci on chocolate
urgency. Can progress to peri-urethral abcesses, prostatitis, epididymitis.
blood agar. Genetic probes: PCR.
>50% of women are asymptomatic or mild symtoms. Infection site MC'ly
cervix (cervicitis). 2-7 day incubation. Vaginal discharge or abnormal vaginal
bleeding, dysuria, urgency, swollen painful abdomen (RUQ). If untreated an
56 Neisseria gonorrhoeae Reproductive Gonorrhoeae in females
ascending infection can develop. Major cause of infertility iff chronic.
Secondary: Fitz Hughe Curtis syndrome: periphepatitis (affects liver -
symptomatic gonorrhea)
Rare but MC in women (1-3%). Systemic symptoms or complex syndrome
with fever, migratory arthralgias, tender papillary lesions/ rash on extremities.
57 Neisseria gonorrhoeae Reproductive Disseminated gonorrhoeae Fever
Arthritis: MC'ly mono-articular - knee in females. N. gonorrhoeae is the #1
cause of purulent arthritis in young adults
MC'ly caused by N. gonorrhoeae or C. trachomatis. 2-5 days after vaginal
birth. Purulent conjunctivitis in newborns infected during vaginal delivery.
58 Neisseria gonorrhoeae Eye Opthalmia neonatorum
Sticky discharge, edema/ inflammation. Can lead to scarring and blindness.
Reason why newborns get eye drops of 1% sulver nitrate.
Same signs and symptoms as other bacterial meningitis - but more insidious Gram stain of CSF. Chocolate agar
59 Haemophilius influenzae Systemic Menigitis onset and increased risk of neurological sequelae. Used to be MC pediatric culture. Agglutination reaction to PRP
meningitis, before Hib vaccine capsule in CSF and urine.
Medical emergency, MC'ly in boys 2-4 yo. Dysphagia, drooling, muffled voice,
60 Haemophilius influenzae Respiratory Epiglottitis High "Thumb sign" on lateral X-ray of neck
minimal cough. Severe dyspnea.
61 Haemophilius influenzae Skin Cellulitis Reddish/ blue patch on cheek or peri-orbital Yes Gram stain of blood
62 Haemophilius influenzae Skeletal Arthritis Monoarticular. Large joint. Gram stain of blood
63 Haemophilius influenzae Respiratory Otitis media / Sinusitis Three MC causes: H. influenzae, S. pneumonia, Moraxella catarrhalis. In children Unexplained Gram stain of blood
Might be secondary to influenzae virus damage to respiratory epithelium.
64 Haemophilius influenzae Respiratory Pneumonia Gram stain of blood
Secondary bacterial infection is more life-threatening than primary.
STD, most common to developing world. Unlike primary syphilis which causes
hard chancre. Sof, purulent, painful ulcer (genitalia). MC males,
65 Haemophilus ducreyi Reproductive Chancroid
uncircumcised, tropical & sub-tropical (female MC asymptomatic). 5-7 day
incubation. Progress to painful buboes, phimosis, urethral stricture.
Bacteria are best isolated using
Incubation: 7-10 days, sub-clinical. Catarral phase: 2 weeks, looks like nasopharyngeal aspirates during
common cold: rhinorrhea, sneezing, low grade fever, anorexia, malaise (most catarrhal stage. Culture: difficult
infectious stage). Paroxymal stage: 1-2 weeks, dry non-productive repetitive humitidy, 35 C, 7 days, specialized
66 Bordatella pertussis Respiratory Whooping cough
"whooping" cough. Cough ends in vomiting and exhaustion. Convalescent agar (only 50% of infected people are
stage: 2-4 weeks. Cough resolves, secondary complications: aspiration culture (+). Throat swabs not as good
pneumonia, seizures, encephalopathy. - need synthetic fiber swabs. PCR.
Lymphocytosis (not specific)

Primary: small papule - painless, hard chancre. Painless, regional

Microscopy: no Gram stain, use silver
lymphadenopathy (buboes). Very infectious. Heals spontaneously within 2
stain and fluorescent stains. Non-
months without scarring. Secondary: flu-like syndrome. Painless, localized
specific tests: VDRL (veneral disease
lumphadenopathy. Diffuse, non-pruritic maculpapular rash, includes soles,
research lab) and RPR (rapid plasma
palms. Very infecious (kissing). Tertiary (Lues/Leutic): after 3-40 years of
reagin) (+4-6 weeks after infection -
67 Treponema pallidum Reproductive Syphilis latent syphilis. Gummas (flat rubbery tumors anywhere in body - ulcerate and
indicates current active disease but
heal by scarring). Affect many organ systems: neurosyphilis, cardiosyphilis.
false positive). Specific tests: FTA-
Painless or deep burrowing pain. Congenital: infected mother infects fetus.
Abs (fluroscent treponema Ab) and
1) Intra-uterine death; 2) Congenital abnormalities 3) Born appearing well
MHA-TP (micro haemoglotunin for
then several weeks or up to 2 years later: snuffles, widespread desquamating
Treponema) - indicate past infection
maculopapular rash. (Risk if mother is in primary or secondary syphilis)
 Must have spscific attachment to conjuctiva - resist flushing from tears.
68 Chlamydia trachomatis Eye Trachoma disease Begins as conjunctivits. Entropian - eyelashes chronically irritate cornea
causing ulceration
Adult. Most common 18-30. Genital infection 1st then unilateral mucopurulent
discharge in eye. Neonatal: infected mother and vaginal birth. Bilateral,
69 Chlamydia trachomatis Eye Trachoma inclusion conjunctivitis
intense papillary conjunctivitis with lid swelling, chemosis, and mucopurulent
discharge
Women: termed Chlamydia (the drip?) Most commonly asymptomatic (80%)
but risk of intertility, miscarriage, ectopic pregnancy. Can cause urethritis,
conjunctivits, perihepatitis (pain in RUQ). Pain/ cramping in lower abdomen,
70 Chlamydia trachomatis Reproductive Chlamydia urogenital infections dyspaerunia, bleeding between menses. Men: NGU (non gonoccocal Currently MC bacterial STD in USA.
urethritis). MC symptomatic (75%) - yellow clear discharge, pain/ tenderness
of genitals. Ractive arthritis (Reiter's syndrome) - can't see, can't pee, can't
dance with me!

Seronegative (Rh-) spondyloarthropathy. MC in young men (20-40 years) that

are HLA-B27 positiv. C. trachomatis is MC bacterial pathogen. Unexplained Clear yellow discharge (gonorrhea is
71 Chlamydia trachomatis Reproductive Reactive arthritis (Reiter's syndrome) Low grade Unexplained
diarrhea, low grade fever. 2-4 weeks later conjunctivits, superficial lesions on yellow/purulent)
palms/ sole/ oral mucosa, asymptomatic polyarthritis, urethritis

Also termed LGC. MC in Africa, Asia,

South America (male homosexuals).
Need adequeate sample of infected
Reportable STD. Initial lesion: small painless papule on penis, urethra,
cells (specimen of pus/ discharge is
glans, scrodtum, vaginal wall. 2nd stage: buboes --> painful, can rupture and
72 Chlamydia trachomatis Reproductive Lymphogranuloma vererum inapproptirate since they are in the
drain spontaneously. Systemic. Mimics IBS. Can get proctitis in men and
cells). Culture: most specific method,
women.
only infects certain cell lines;
formation of inclusion bodies. DFA
(direct fluorescent) staining. PCR.
TWAR isovar. Human pathogen that can cause atypical pneumonia (mild,
persistent cough/ malaise that might progress to lobar pneumonia). Potential Difficult: PCR,
73 Chlamydophila Respiratory Chlamydiophilia pneumonia
link to atherosclerosis, CAD, MS, asthma, Alzheimer's disease? MC in adults. Microimmunoflorescence
Spread via respiratory droplets.
Cause psittacosis. Biggest risk from psittacine birds (parrots, mascaws, Rare person to person spread (non-
parakeets, cockatiels) Transmitted via inhaled dried bird excrement, urine and productive cough). DX: serology: 4x
74 Chlamydophila Respiratory Chlamydophila psittace respiratory secretions. Non-productive cough., rales, mucous plug can block increase in Ab titre. Prevention:
bronchi. Commonly progesses to CNS(encephalitis, convulsions, coma, control and quarantine domestic and
death) imported birds.
CXR: cavitations in one or more upper
lobes of lung. Sputum sample: acid
"TB is the master impersonator." Primary infection (only 5% get active TB
fast bacillus. Fastidious growth
within 2 years): insidious onset: malaise/ listlessness, night sweats, low grade
requirements, PCR.. Skin test
fever, unexplained weight loss and progressive fatigue. Productive purulent
75 Mycobacterium tuberculosis Respiratory TB Low grade (Mantoux test) - intradermal injection,
cough progressing to hemoptysis, dyspnea. Apical rales, cyanosis.
wait 48 hours and measure induration/
Secondary TB (reactivation): haematogenous spread anywhere: miliaty TB
erythema (type IV hypersensitivity).
(no pulmonary signs). Destroys tissues - liver, adrenals...
Doesn't tell whether TB is active or
not.
3-6 year incubation. Strong cellular response, weat humoral. Not infectious.
76 Mycobacterium leprae Skin Tuberculoid (paudibacillary) <5 cutaneous macular lesions with hypopigmented centers. Some nerve Will react to skin test - lepromin
enlargement and damage.
3-10 year infection. Weak cellular response, strong humoral. Relatively highly
infectious. Most destructive - disfiguring skin/bone, cartilage lesions ("leonine
77 Mycobacterium leprae Skin / Neural Lepromatous (Multibacillary) Not reactive to skin test
face") Diffuse nerve involvement. Erythema nodosum present and >5 kin
lesions
Opportunistic infection. Begins as mild pulmonary disease: spreads to local
lymph nodes and then quickly to every organ. AIDS px: fever, sweats, weight Sputum cultures: acid fast bacilli. CBC
Mycobacterium avium
78 Respiratory MAC diseases loss, fatigue, diarrhea, SOB. Pulmonary disease is similar to TB: usually GIT with diff: AIDS diagnosis, anemia,
intracellulare complex
involvement, usually fatal within months. No person to person spread via neutropenia.
aerosolized droplets.
Unlike othr Borrelia diseases - non relapsing. Tick bite - must stay attached
for >48 hrs. 7-30 day incubation. Stage 1: erythema migrans rash "bull's eye
lesion". Annular rash with central clearing (40-60% don't get this!) Painless, Clinical signs and symptoms and
non-infectious, H/A, myalgia, lymphadenopathy. Resolves 1-2 months. Stage patient history. Culture and IFA stain
79 Borrelia burgdorferi Skin / Neural Lyme disease 2: iff untreated develop into neurologic signs (meningitis, Bell's palsy, etc.), of biopsy of initial rash (30% don't get
conjunctivitis or cardiac dysfunction. Stage 3: 2 months to 2 years after stage rash and cross-reactivity with
1: migratory arthralgias/arthritis (knees, large joint, TMJ), encephalitis. Treponema). Indirect ELISA. PCR.
Resolves in months, years or never. )Can manifest as popliteal cyst. ) If
neurologic symptoms: neruoborelliosis.
Range from mild, febrile disease to LV/KI failure (Wei's disease iff
icteric) No skin lesion at site of entry. Septic phase: aprupt onset fever, HA,
myalgia, nausea, lasts 1 week. Immune phase - two days asymptomatic, then Too small for light microscope and
80 Leptospira interrogenes Skin / Eye / Liver Leptospirosis
aseptic meningitis with severe HA, NV, myalgia. Weil's disease (icteric) - Gram stain. Microscopic agglutination.
jaundice, scleral and conjunctival hemmorhages and KI failure (MC cause of
death)

Painless tick bite leaves no mark (very low inoculum - <10 organisms) 1 week DDX with Typhoid. (Typhus is
incubation - rapid fever, severe HA, nausea. 5 days later: rash - diffuse, Rickettsia). DFA stain of skin biopsy.
81 Rickettsia Skin / Systemic Rocky Mountain Spotted Fever maculopapular rash, MC spread from trunk to extremities (inclusing palms IFA stain for LPS. Complement
and soles). Respiratory symptoms. Iff untreated spread to CNS (confusion), fixation tests, (+) iff <4x increase in Ab
SP, GIT, LV. Encephalitis, DIC, shock, death (up to 20% mortality) titer.