Download Bacteriology Chart Review

Gram Positive Cocci
Treatment
Staphylococcus aureus
Characteristics
Gram + cocci in clusters,immotile
human skin and nares,body walls off
infection w/a fibrinous barrier; S.
aureus causes pus formation.
Staphylococcus epidermidis
Gram + cocci in clusters, human skin
(always),
Staphylococcus saprophyticus
Streptococcus pyogenes
(Group A, -hemolytic)
Gram + cocci in clusters,
skin/genitourinary tract
Gram + cocci in chains, catalase neg.,
Group A causes most strep disease,
asymptomatic carriers, causes
suppurative infections.
Streptococcus agalactiae
(Group B, -hemolytic)
Gram + cocci in chains, catalase neg.,
lower GI tract & female genital tract.
Viridans Streptococci
(-hemolytic)
Gram + cocci in chains, catalase neg.,
oral cavity (up to 60% of normal oral
flora)
Gram + cocci, low pathogenicity,
normal flora of human gut, very hardy.
Enterococcus faecalis
(-hemolytic, non-hemolytic)
Streptococcus pneumoniae
(“the pneumococcus”)
Gram +, encapsulated, lancet shaped
cocci in pairs, usually community
acquired, sporadic.
Transmitted by droplet nuclei or
aspiration by carrier. Facultative
anaerobes, -hemolytic.
Associated Disease(s)
Invasive: suppurative skin infections: minor trauma 
pimples ,carbuncles, impetigo; major osteomyelitis,
fasciitis, cellulitis.
hematogenous inf., nosocomial infection.
Toxinoses: Food Poisoning (enterotoxin), exfoliative
skin disease (Ritter’s disease of newborns), TSS
Pathogenesis
Multifactorial; secrete 4 hemolysins that lyse cells; hemolysin lyses cell similar to pore form. by complement,
also:coagulase +, exfoliatin. Protein A is a surface
molecule that binds IgG to camouflage the bacterium.
Also able to respond to env. w/signal molecule.
Opportunistic infections, large number of nosocomial
infections: bacteremia, endocarditis, endophthalmitis,
osteomyelitis (following surgery), infections of
indwelling foreign devices, neonatal necrotizing
enterocoloitis.
Infections outside of hospital, causes 20% of all
urinary tract infections in young women.
Suppurative: Pharyngitis, Scarlet Fever, erysipelas,
streptococcal pyoderma (impetigo).
Non-suppurative: Acute Rheumatic Fever, Acute
Glomerulonephritis.
Coagulase negative
Puerperal sepsis (after childbirth) , neonatal meningitis
(early onset w/50% mortality or late onset w/20%
fatality)
dental caries, subacute bacterial endocarditis (on preexisting heart valve lesions),enter bloodstream via
decayed teeth or following oral surgery.
subacute bacterial endocarditis, female urinary tract
infections, peritoneal abscess, bacteremia (from above
foci).
Pneumonia (Lobar and Bronchopneumonia, most
common cause of meningitis in adults, most common
cause of otitis media and sinusitis in children, can cause
septicemia, esp. in the very old or very young.
(Immunity to reinfection is type-specific against
capsule.)
Treatment
penicillin
vancomycin
[erythromycin]
(Many strains are
multi-abx resistant.
and make lactamase)
Coagulase negative
Surface molecules confer adherence to tissues and
resistance to phagocytosis.
M-protein(prevents phag.), Protein F (adherencefibronectin), Fc receptor (like Prt.A), C5a peptidase, etc.
Secreted exotoxins: erythrogenic toxin, Streptolysin S,
Streptolysin O, Streptokinase, DNAse.
Capsular polysaccharide (prevent phag.), Hemolysin (like
streptolysin S), IgA receptor (camouflage), Fibronectin
binding protein (adherence).
Very sensitive to
penicillin.
If patient is allergic,
give erythromycin.
Antibiotic resistance to every known antibiotic due to
conjugal transfer of antibiotic resistance genes within and
across species
Capsule confers path: inhibits phagocytosis by inhibiting
alt.pathway, must be present for virulence. Capsule also
stimulates production of type-specific opsonic Ab that
results in killing by PMNs. No toxins involved in path. 85
different serotypes.
???
penicillin
vancomycin
chloramphenicol
penicillin
penicillin
amoxicillin
cephalosporins
vancomycin
Vaccine for people at
risk available.
Gram Positive Rods
Organism
Listeria monocytogenes
(see HO, lots of details for this
one)
Bacillus anthracis
Bacillus cereus
Corynebacterium diphtheriae
“Diphtheroids”
Characteristics
Gram+, non-encapsulatedrod w/a
characteristic “tumbling” motility,
facultative intracellular parasite, grows
under many conditions, found nearly
everywhere, transmitted through
improperly pasteurized milk/products,
oral-fecal contamination of any source
(ie- H20 contamination, vegetable
fertilized w/manure, meat, etc).
Disease(s)
Listeriosis is disease. Rarely causes disease but when it
does is severe esp to fetus, newborn, pregnant women
and the immuno- compromised. 70-90% fatality if
untreated, 30-50% fatality w/treatment depending on
status of host and clinical signs. Can be carried in GI
tract or female genital to lead to disease. Is able to enter
a wide variety of cells where it can survive and multiply.
Immunity to re-inf w/ survivors. Septicemia, meningitis,
abscesses, granulomas, lymphadenitis. Lead cause of
meningitis in CA/renal tp patients
Pathogenesis
Extracellular product listeriolysin O is responsible for
pathogenicity- a cytolysin that specifically dissolves the
endosomal membrane so that it evades the major antibacterial activity of the cell, this way the org. can also get
into cytoplasm. Cell surface virulence includes Internalin
for attachment and invasion and Act A for directional
actin polym. of host cell’s actin. Actin polym. allows
bacteria to move in cytoplasm and is required for cell-cell
spread, also makes it resistant to humoral immunity.
Treatment
Ampicillin,
penicillin with an
aminoglycoside,
erythromycin.
Gram +, sporeforming, non motile rod
with characteristic square cut ends
(boxcar), encapsulated, spores can live
in the soil for 30 years, found carried in
GI tract of animals, transmitted by
spores or respiratory droplets.
Anthrax (cutaneous or inhalational).Mostly a disease
of animals or people who work with animals.Cutaneous
enters thru cut on skin, causes a malignant pustule that
is a necrotic black lesion then rapidly disseminates and
causes death very quickly. Inhalational is from
organisms directly to lung that release exo-toxin and
cause pulmonary necrosis, septicemia, meningitis and
death w/in 24h.
Self limiting type of food poisoning. Incubation period
and clinical sx. resemble staph. food poisoning. Can
also cause disseminated, usually fatal, disease in
immuno compromised pts.(usually post-operatively).
Diphtheria. Fever, chills, pharyngitis, cervical
lymphadenitis, massive neck edema (severe cases) and a
thick, closely adherent dirty gray pharyng., tonsillar or
laryng. pseudomembrane
Death due to resp. paralysis or myocarditis. Cutaneous
diphtheria results in an ulcerative lesion w/a dirty gray
pseudomembrane. W/both there can be toxemic
degeneration and death.
Can cause septicemia in rare instances in
immunosuppressed individuals with a high fatality rate.
Exotoxin produces pathogenesis. Toxin is a heat labile
protein composed of 3 components: protective antigen,
lethal or toxic factor and edema factor. Polypeptide
capsule made exclusively of D-glutamic acid gives antiphagocytic activity but does not stimulate protective
antibody
Vaccine (but is only
50% eff)
Penicillin and
tetracycline are
effective only when
given early
Gram+, motile, non encapsulated, beta
hemolytic, exists as a saprophyte in
water and soil, trans. in contaminated
rice or meat dishes
Gram +, non sporeforming, non motile,
vy. distinct (beaded, barred or
clubbed), facultative anaerobes,
obligate parasite of humans, carried in
URT, transmitted by droplet nuclei or
contaminated milk, people can be
carriers.
Same habitat, may have same
morphological and biochemical
properties as C.diphtheriae but they do
not produce exotoxin
Use only pasteurized
milk products b/c of
this bacterium!!!
Secretes enterotoxins
K antigen on surface is anti-phagocytic. Exotoxin is of 2
polypeptide fragments: B fragment is for transport into
cell and A frag ment is toxin for ADP-ribosylation and
inactivation of elongation factor EF-2 which inhibits
protein synthesis. Lysogeny w/ a beta prophage carrying
the tox gene is essential for toxigenicity.
Often have multiple antibiotic resistance, but do not
produce exotoxin
Vaccination prevents
disease
Active disease: give
anti-toxin immediately,
penicillin or eryth
romycin for killing
bacteria.
Gram Positive, Anaerobic, Sporeforming Rods
Organism
Clostridium botulinum
Characteristics
Gram+, anaerobic, spore form- ing,
multiplies in uncooked meat, sausage,
fish and badly canned items, dx. by
animal injection, cultures show
characteristic “light bulb” appearance.
Spores do not produce toxin, only
vegetative form does.
Disease(s)
Botulism. Caused by intoxication w/bacteria. Clinical
sx. 18-36h after ingestion, ptosis, mydriasis, blurred
vision, dysphagia, dysphonia, urinary retention, muscle
weakness (descending), respiratory paralysis. Death can
occur w/in 18h. This results from Ach presynaptic
blockade. Infant Botulism results in floppy infant, may
be cause of SIDS in some cases.
Clostridium tetani
Gram+, anaerobic, spore formi-ing,
found all over the place, typical entry
through wounds (puncture wound or
laceration, but also burns, ulcers, cpd
fx, operative wounds, injection sites of
IVDAs, Dx. is clinical, appear on
culture as gram+ rods w/spore
formation at tip forming a “drumstick”
Clostridium perfringens
Gram+, anaerobic, spore forming,
occur normally in soil and sewage,
normal in human GI, box shaped
organisms with gram stain, positive
blood cultures(for gas gangrene), found
also in feces for other infections
Tetanus. Caused by intoxication, may take several days
to weeks for symptoms to occur. Onset of sx. may be
muscular contractions in the vicinity of the wound
followed by spastic contraction of the masseter muscle
(trismus) resulting in “locked jaw”, generalized rigidity
and severe spasms of the limbs and trunk. Later signs:
risus sardonicus, spasmic contractions of
back(opisthotonus) and of the resp.muscles which may
lead to death.
Gas gangrene. Destroys tissues esp. muscle,Infects poorly
perfused, injured tissues, incubation 6-72h, severe edema,
bronze discoloration, bullous lesions w/dark thin fluid,
then H2 gas production leading to crepitations, ischemia,
shock and death. Most common organism to cause gas
gangrene.
Also: Anaerobic cellulitis, uterine infection, necrotizing
enteritis, food poisoning (self limiting diarrhea).
Clostridium dificile
Gram+, anaerobic, spore forming,
normal commensal of human gut,
results from superinfection following
antibiotic treatment
Pseudomembranous colitis. Diarrhea and toxic
megacolon. Endoscopy shows multiple small
pseudomembranous colon plaques. Milder form is
antibiotic associated diarrhea w/ same clinical findings
but less severe
Pathogenesis
Botulinus toxin causes path. Released by lysis of bacterial
cells in medium. Toxin has two subunits:H-chain causes
receptor mediated endocytosis by host cell, once in cell the
H and L-chain are separated and the L-chain moves by
retrograde transport to the presynaptic terminal where it
prevents fusion of the synaptic vesicles w/the presynaptic
membrane. All toxins are destroyed by boiling at 100C for
10 minutes.
Secretes tetanus toxin which is a dimer similar to botulinus
toxin (H and L chain) L chain functions as a synaptobrevin
on the surface of synaptic vesicles that inhibits their fusion
with the presynaptic membrane. Tetanus toxin specifically
blocks the inhibitory neurons of spinal motor neurons
preventing release of GABA and glycine which results in
uninhibited transmission of excitatory impulses and
muscular spasms.
Produces extotoxins. Most important toxin is -toxin
which cleaves lecithin in host cell membranes and is
lethal and necrotizing on injection. Perfringolysin O
(similar to strep-tolysin O, pore complexes). The
combined action of -toxin and streptolysin O may be
the cause for the intravascular hemolysis associated w/
infections. b-toxin important in necrosis of necrotizing
enteritis. Spores in food germinate & release toxin in
food pois.
Produces two heat labile toxins: A and B. The toxins
are released by vegetative cells and together cause fluid
loss, mucosal damage and necrosis of intestinal mucosa.
Toxin can be id by ELISA.
Free toxin can be
inactivated with a
specific antiserum.
Give a polyvalent
antitoxin. Do not give
penicillin b/c it causes
cell lysis and more
toxin.
Immunization @ 2,4,6
mos. and boosters
every 5-10 y.
Antitoxin + immune
globu-lin given to
wounded people w/o
immun. immediately!
surgical excision of
inf. skin and muscle,
limb amp utation,
hyper-baric O2. Abx
to well perfused
tissues, no time to wait
for cultures! Surg.for
bowel in enteritis.
Stop previous abx tx.
Vancomycin or
metronidazol to stop
inf. Surg-ery for
megacolon
Gram Negative Coccobacilli
Organism
Bordetella pertussis
Haemophilus influenzae
Characteristics
Gram neg, coccobacillus, non motile,
non sporeforming, piliated, LPS,
obligate aerobe, slow growing, hard to
grow, human respiratory tract, no
known animal or environment-al
reservoir, transmitted by respiratory
droplets, highly communicable, mostly
children
Gram neg, coccobacillus, non spore,
non motile, encapsulated and
nonencapsulated strains, fastidious,
facultative anaerobe, requires hemin
and NAD, found in human respiratory
tract, transmitted by respiratory
droplets.
Disease(s)
Pertussis (whooping cough). 4 phases: 1. incubation; 2.
catarrhal (mild cold-like sx. , mild cough of severity,most
infectious phase)
3. paroxysmal (severe, forceful, spasmodic coughing w/
“whoop” following and then vom-iting, complicated by
otitis media, seizures, apnea, pneumonia); 4. convalescent
(less fr. paroxysms, recovery). 1% death rate, mental
retardation and paralysis can occur.
Meningitis, epiglottitis (in kids), not seen often any more
b/c of vaccine, 75% unencapsulated causes otitis media,
sinusitis, bronchopneumonia, 5% encapsulated causes
pneumonia, epiglottitis, bacteremia, meningitis
Most common from 3mos to 4 yr after maternal ab’s have
worn off and T cell response not active. Complications are
severe.
Pathogenesis
Attaches (firmly) to ciliated resp.epithelial cells(using
FHA,pili and peritactin), secretes toxins to inhibit
phago.cells (adenylate cyclase toxin, pertussis toxin )&
inhibit muco-ciliary defense(tracheal toxin), multiplies
and causes local damage, systemic disease results
(lymphocytosis, insulin, glycemia) See HO for details
of toxins.
Characteristics
gram-, diplococci, fastidious, habitat is
human mucosal surfaces, poor
environmental survival, symptomatic &
asymp inf. Spread by respiratory
droplets. Detect by gram st, serum Ag,
culture, clinical dx.
gram- diplococci, fastidious, human
mucosa/poor environ. survival,
sympt/asympt inf.
Spread by sexual contact or perinatal
inf. Gram st of exudate in males can dx.
but for sure culture to confirm from any
source.
Disease(s)
Meningococcal disease: meningitis and/or
septicemia(fever,ha,chills, malaise, wkness, hemorrhagic
skin lesions/petechiae/purpura, DIC, Thrombocytopenia,
leukocytosis, hypotension, septic shock (LPS-A). Can be
epidemic, bacteremia in susceptible people (asplenic pts,
children), carrier state in others
Gonorrhea: Urethritis (males), cervicitis (females), rectal
inf, pharyngeal inf, ophthalmia neonatorum (mother to
infant gonococcal conjunctivitis).
Complications: PID, Disseminated gonococcal infection
(DGI, only 0.5-3% of inf) leading to arthritis, dermatitis,
tenosynovitis(Lover’s heels), fever, often mild systemic
toxicity.
Pathogenesis
Attaches to non-ciliated cells of the nasopharyngeal
mucosa and undergo TRANSCYTOSIS to cross the
basement membrane. Features: Pilus(attachment), IgA1
protease(cleaves IgA), antiphagocytic capsule,
LipidA(septic shock).
Treatment
IV antibiotics, manage
complications,
prophylaxis during
epidemics
Attachment: by a pilus that shows Ag variation to
effectively evade the immune system and by an opacity
protein that also has Ag variation,
Lipooligosaccharide(LOS) toxic also shows Ag
variation, IgA1 protease to evade IgA on mucosal
surfaces, P1 porin shows resistance. Inflammation is
intense, dissemination can occur but not as prone as in
N.meningitidis
Uncomplicated
ceftriaxone +
doxycycline.
Many pcnase
producing strains, tx
for chlamydia too, tx
for sexual partner, no
vax, use a condom
Capsule is antiphagocytic major virulence factor (PRP
polymer, most adults have anti- PRP Ab), pili may have
a role in attachment, LPS, outer membrane proteins, IgA
protease (specific role not yet established)
Treatment
Erythromycin for
active disease.
Vaccination to prevent
disease. Vaccine can
cause some se’s but is
safe and prevents
epidemics.
Vaccination
For active disease give
cephalospor-ins,
ampicillin +
chloramphenicol.
Gram Negative Cocci
Name
Neisseria meningitidis
Neisseria gonorrheae
Gram Negative Rods (Enteric)
Organism
Vibrio cholerae
Characteristics
gram-,curved rod, single polar
flagellum(motile), endemic, epidemic,
pandemic, trans in contaminated
food/H20 (fecal-oral trans),lives in
brackish water/shellfish, human is
transitory habitat.
Associated Disease(s)
Cholera: Inf. is asymptomatic to acute in nature, can be
spread by asymp people, early signs: vomiting, cramps,
then PROFUSE secretory diarrhea (rice water stools),
massive fluid loss of 10L/day leads to dehydration,
electrolyte deficiency and hypovolemic shock. W/o tx.
60% fat., w/tx. only 1% fat.
Pathogenesis
Raising pH of stomach encourages infection.
1)colonization: ingestion, gastric acid barrier,
attachment to sm.bowel (microvilli)
2) cholera toxin: ADP ribosylates G prt. to “turn on”
adenylate cyclase, loss of salt and H20 by diffusion into
lumen, loss of bicarb can lead to acidosis.
Treatment
Replace fluids &
electrolytes po or iv,
tetracycline 
duration, vaccine
under dev. Tx. is very
effective & easy to
give.
Vibrio parahaemolyticus
Halophilic (salt loving), marine habitat
(coastal waters)
Seawater
gram-,curved,spiral or comma shaped
rods, motile, micro-aerophilic,
worldwide zoonosis in GI tract of dom.
animals, trans by cont food/water,
common, est 2Mcases/yr in US
Food poisoning: undercooked seafood, causes secretory
diarrhea
Septicemia in compromised host, cellulitis in healthy host
Common cause of diarrhea.
Acute enteritis: diarrhea, malaise, fever, abd. pain. Range
of diarrhea from loose to watery to bloody. Ususally self
limiting, bacteremia rare, dx. by stool culture.
Pathogenic mechanisms uncertain
Fluid and electro-lyte
replacement,
antibiotics may be
indicated(bloody
stool), usually no tx is
necessary.
Campylobacter fetus
Helicobacter pylori
fairly rare
gram-,spiral rods, motile, produce
urease, habitate the gastric epithelium
Salmonella enterica
(serotypes referred to as if they are
species)
Gram- rods, motile, facultative
intracellular, usually aquired by
contaminated food or animals esp.
poultry meat or eggs, infections are
typically animal associated, fecal oral
transmission as well.
Gram - rods, motile, facultative
intracellular, infects only man, get from
people who are chronic carriers and
excreters (Typhoid Mary) a condition
that occurs in 1-3% of untreated cases.
Fecal oral transmission
Shigella
(dysenteriae, flexneri, boydii or
sonnei)
Gram- rods, not normal flora,
facultative intracellular,motile
exclusive to primates, vy few needed to
infect, evade host def like gastric acid,
fecal-oral transmission: The Four F’s:
food, fingers, feces, flies. Only person
to person.
Virulence: motility, urease, cytotoxin, exact cause of
inflammation is unknown, infection remains for life if
not treated.
Invades epithelial cells by contact w/ micro-villi of host,
then bact cell assembles invasomes (invasion organelles)
which triggers host cell memb. ruffling, the bact then
shed their invasomes followed by host cell uptake.
Salmonella can turn on and off genes according to if
they are in a host cell or not, PhoQ is a sensor molecule
(ex: low pH inside a phagolysosome) that regulates
genes for transcriptional regulation and turns off other
genes. Pag C is essential for resistance to killing by
macrophages.
S. typhi first invades small bowel epithelial cells or M
cells in Peyer’s patches trans-cytosis across epithelial
cellsendocytosis by lamina propria M. Bact survive
in “spacious phagosomes” and reach systemic
circulation via thoracic duct reticuloendo-thelial
system (phagocytes in liver, spleen and bone marrow).
Gall bladder inf leads to the chronic carrier state. Inf
dose is large.
Intracellular, 1st invades M cells of gut lymphoid
follicles, kill resident macrophages invade intestinal
epith cells on basolateral surface, then spread cell-cell.
Use host cell’s actin to rocket from cell-cell (like
Listeria), express IcsA protein. Invasion plasmid is
essential for pathogenicity. Secrete shiga toxin, causes
endothelial damage. Expression of proteins is temp.
controlled.
triple tx: pepto,
metronidazole,
amoxicillin.
Antibiotics not
recommended for
uncomplicated
enterocolitis,
ceftriaxone for sepsis.
Prevent w/ public
health measures (ie
restaurant safety) no
vaccine available
Salmonella typhi
Systemic disease in immunocompromised host
Gastritis/ulcers: thought to be cause of much gastritis and
predisp to stomach CA, abx. tx. against clears up ulcers
and gastritis.
Acute enterocolitis: Most common disease syndrome of
salmonella, follows 6-8 hr incub-ation, most pts. have
nausea, vomiting, diarrhea. Fever and abd cramping also
common, inf involves small bowel and colon (different site
from shigella), Fecal PMN’s are present, dx. by stool
culture for enteric pathogens, death is rare. Infections can
spread beyond intestinal mucosa to produce bacter-emia
and seed distant tissues that can result in later focal
infections (osteomyelitis in sickle cell pts. occurs w/
increased frequency)
Typhoid fever (enteric fever): Incubation 1-3 weeks,
gradual onset of fever, abd pain and hepatosplenomegaly,
duration usually 4 weeks w/o tx. Dx. by culture of blood,
bone marrow and stool. bone marrow gives the highest
yield of organisms b/c it is a systemic infection of
mononuclear phagocytes. Death may occur despite use of
antibiotics b/c of the fatal comp-lication of intestinal
perforation and peritonitis
Vibrio vulnificus
Campylobacter jejuni
Shigellosis: suspect in any diarrhea lasting > 48 hours.
Abd cramps, may have fever. Stools have PMN’s, blood,
mucous. 1wk is avg. time. Dx. by stool culture, produce
disease at very low inoculation.
Ceftriaxone (1st ),
ampicillin or cotrimoxazole if not
severe. Prevent by
public health
measures. Killed and
live -attenuated
vaccine available.
Gram Negative Rods (Nosocomial)
Name
Escherichia coli
(extraintestinal infections)
Characteristics
Gram - rods, facultative anaerobes,
ferment lactose, found in human colon,
vagina, urethra. Transmitted during
birth in neonatal meningitis, travels
from urethra in UTI and pyelonephritis.
Disease(s)
Meningitis of newborn
Uropathogenic:UTI(cystitis or pyelonephritis) Untreated
pyelonephritis is a chronic infection that can last for many
months.
(Different strains of E.coli have acquired traits that allow
them to be infective to these regions)
Escherichia coli
(enteric pathogens)
Gram - rods, facultative anaerobes,
ferment lactose, enterotoxigenic E.coli
are not usually part of the normal flora
of the human gut. Enterotoxigenic
strains are found in parts of the world
w/ poor sanitation and can also be in
food (fecal-oral).
Infant diarrhea: Enteropathogenic E.coli (EPEC).
Chronic diarrhea of children, can cause dehydration and
malnutrition. Non-inflammatory enteritis w/ watery
diarrhea w/o fecal leukocytes.
Traveler’s diarrhea (dehydrating diarrhea):
Enterotoxigenic E.coli (ETEC). Non-inflammatory enteritis
(as for infant diarrhea)
Hemolytic Uremic Syndrome, blood and non bloody
diarrhea: Enterohemorrhagic E.coli (EHEC). Diarrhea is
dysenteric w/fecal leukocytes. HUS is hemolytic anemia,
renal failure w/ uremia, thrombocytopenia and neurological
sx. (E.coli 0157:H7)
Dysentery:Enteroinvasive E.coli (EIEC), similar to
shigellosis, fecal leukocytes present.
Very rare in healthy people, causes life threat-ening and
fatal infections in burn pts, Cystic fibrosis, and
immunocompromised pts. Also a common cause of
surgical wound infection. Causes rapid tissue destruction
and/or sepsis, foci of infection on man made devices
(indwelling catheters, prosthetic heart valves, prosthetic
joints) is very difficult to cure.
Legionnaires’ Disease: Pneumonia, often severe and
fatal;Stage 1:mild illness (flu like), Stage 2:moderately
serious pneumonia, non remitting fever, bradycardia, chest
pain, hemoptysis, cxr:diffuse or lobar infiltrate, Stage
3:Severe multilobar pneumonia, resp failure,
disorientation, liver abnormalities, hyponatremia and
hypophosphatemia.
Pontiac Fever: Febrile illness w/o pneumonia, mild and
non-fatal
Pseudomonas aeruginosa
gram- rod, obligate aerobe,ubiquitous
in environment, not found in GI tract of
healthy people, an opportunistic
infection and a common nosocomial
pathogen.
Legionella pneumophila
gram- aerobic, tough to stain,
flagellated,intracellular path, catalase+,
oxidase+, gelatinase+, -lactamase+,
lots of branched chain fatty acids,
transmitted by aerosolization of
contaminated water, reservoir is aquatic
unicellular organisms, humans are
accid-ental hosts
(See HO, lots of info for this one)
Pathogenesis
Meningitis of newborn: Strains w/K1 polysaccharide,forms a capsule that is poorly
immunogenic(like N.meningitidis).Mom w/ E.coli
K1(carrier)confers risk to the newborn
Cystitis:Have “common pili” that allow binding to Dmannose on bladder epithelial surfacesecrete
hemolysin,a cytotoxic prt. that damages bladder &
causes sx.of cystitis.
Pyelonephritis:Bind to renal epithelium by a Pap
pilus:binds to ,1-4 digalactoside (only on renal epith),
has PapG adhesin only on tip, (very small), also secretes
hemolysin.
Attachment by EPEC: 3 stages; 1st nonintimate
adherence to the epithelial cell surface by pili. 2nd is
induction of microvilli effacement (flattening out). 3rd
is intimate adherence and host cell cytoskeletal
rearrangement by intimin, a bacterial adhesin encoded
by the eaeA gene.
E.coli O157:H7 is probably from acquisition of the
Shiga toxin gene by EPEC (maybe via bacteriophage),
transforming it into EHEC
Antibiotic resistance is very common and tends to
develop during the course of therapy, so two antibiotics
are always used. Multifactorial virulence: secretes a
slime that inh. WBC activities, secretes hemolysins and
proteolysins that damage cells and tissues, also secretes
exotoxin A (m.a. is the same as diphtheria toxin
w/inhibition of prt synthesis
Lung: alveoli filled w/pmn’s, M, & fibrin, many intra
and extra cellular bacteria in M (inside vacuoles) and
pmn’s. Multiplies intra cellularly in alveolar M and
monocytes until host cell destroyed, enters by “coiling
phagocytosis” mediated by complement rec. on
phagocyte and C3 component on bact called Major
Outer Membrane Protein, inh fusion of phagosome
w/host cell lysosomes, inhibits acidification of
phagosome.needs Fe
Treatment
Rehydration is
effective for traveler’s
diarrhea, cotrimoxazole can
shorten duration of sx.
Only eat cooked food
and boiled water in
certain countries,
prophy-lactic Pepto
Bismol or doxycycline
may be preventive.
Combination
antibiotic
chemotherapy
Erythromycin (or
newer analogs), and
rifampin, only
bacteriostatic Host
immune system must
kill maybe by
cytotoxic T cells?
Gram Negative Rods (Zoonotic)
Name
Brucella melitensis
(and suis and abortus)
Francisella tularensis
Pasteurella multocida
Yersinia pestis
Yersinia pseudotuberculosis
Yersinia enterocolitica
Characteristics
gram- nonmotile coccobacilli, aerobic
(may require CO2 for growth), all are
pathogenic in their natural host,
pasteuriz-ation kills, people in close
contact w/animals are most likely to be
infected
Disease(s)
Brucellosis: Undulating fevers (daily cycling), night
sweats, malaise, chills, weakness, myalgia, HA. May have
enlaged spleen and liver, vertebral spondylitis, bacteremia
(20%) and epididymitis Neurological sx. may occur as may
endocarditis. Causes chronic illness w/ an acute onset.
Pathogenesis
Enter through alimentary tract, conjunctivae, or skin and
are engulfed by PMN’s that carry bact to the lymphatics,
there they enter mononuclear cells and multiply w/in by
inh. of phagolysosomal fusion, cells die, bact are
released into blood and go to reticuloendo-thelial
system, cause granulomatous lesions
Treatment
Ususally combo tx
w/tetracycline and
streptomycin or
rifampin; or cotrimoxazole, vacc for
cattle but not people.
gram- bacillus, short non-motile, nonspore forming, tends to stain bipolar
(“safety pin”), rats are the primary
reservoir and trans. is by the bite of
their fleas, bact multiply in flea gut and
cause flea to regurgitate onto next
animal, also can be spread by people
via respiratory droplets.
Plague: Bubonic form is by bacteria spreading to regional
lymph nodes causing a very painful swelling (bubo) high
fever, malaise, then bacteria spread to liver, spleen and
lungs. DIC can occur. Secondary pneumonia leads trans.
by respiratory droplets.Pneumonic form from resp drops is
very conta-gious and 100% fatal w/o tx. Septicemic plague
is caused by bite but no bubo forms and pt presents w/fever
and dies of bacteremia since hard to dx. all very fatal!
In flea gut at lower temps and low Ca the bact can
multiply but does not secrete toxins. In host @ 37 and
incr Ca, chaperone prts allow the translocation of YOPS
(virulence factors) out of the cell. Two cytotoxins are
also secreted into the host cell as well as YopM that
binds to human a-thrombin and is thought to produce
the hemorrhagic lesion Killing fleas w/insecticide and
quarantining victims is effective for prevention
Does not display bipolar staining, more
motile at 22C but not at 37C, reservoir
in wild and domesticated animals and
fowl.
Does not display bipolar staining, in
contaminated food and water, mostly
milk and meat
Mesenteric adenitis and pseudoappendicitis syndrome,
usually a sporadic infection
On entry the bact bind to integrin receptors on the host
cell with invasin proteins on their surface, this allows
them to be phagocytosed.
Diarrhea in children: acute self-limiting gastroenteritis,
enterocolitis and lymphadenitis
Adults, exudative pharyngitis, Reiter syndrome and
erythema nodosum in pts. w/HLA B-27 marker
same as above
start asap, for
pneumonic, give
streptomycin,
tetracycline(good
prophylactic) or
chloramphenicol for
meningitis. Reduces
mortality if started vy
early, vaccine
available.
ampicillin,
chloramphenicol,
tetracycline, or
aminoglycosides
tetracycline,
chloramphenicol, cotrimoxazole, and
gentamicin
Obligate Intracellular Parasites
Name
Chlamydia trachomatis
Characteristics
only grows in eukaryotic cells,
developmental cycle with two growth
forms, spread by sexual contact,
peripartum or close personal contact
Chlamydia psittaci
only grows in eukaryotic cells,
developmental cycle with two growth
forms, aerosol spread, zoonosis (in
certain birds)
obligate intracellular of vascular
endothelium, trans by tick bite,
southeast and south central US
Rickettsia rickettsii
Rickettsia prowazekii
Rickettsia typhi
Rickettsia tsutsugamushi
Coxiella burnetii
obligate intracellular of vascular
endothelium, trans by human louse
(close personal contact), unsanitary
cond, military campaigns
obligate intracellular of vascular
endothelium, trans by the rat flea, in
urban and suburban dep on rodent
expos.
obligate intracellular of vascular
endothelium, trans by chiggers (larval
mites), humans are accidental hosts
(usually rodents)
obligate intracellular pathogen, in
urine,feces, milk and birth products of
cattle, sheep and goats, trans by
inhalation of contaminated aerosols
Disease(s)
Genitourinary tract infection:cervicitis, non gonococcal
urethritis, PID, neonatal ophthalm-orrhea and pneumonia,
lymphogranuloma venereum, Trachoma (ocular inf),
chronic sequelae: tubal infertility, ectopic preg-nancy,
blindness.
Psittacosis: fever, respiratory symptoms, systemic
infection
Pathogenesis
(Dx: serology, culture, PCR, direct hybridization, LCR
w/ urine)
Treatment
Tetracycline or
doxycycline,
erythromycin,
azithromycin, atypical
pneum-onia d/dx
Tetracycline
Rocky Mountain Spotted Fever: Affects vascular
endothelium (vasculitis), multi-system presentation
w/fever, myalgias, HA, rash on palms/soles 3-5 days post
fever, serious compl: gangrene, renal failure, neurological
involvement, DIC in very severe cases.
Epidemic Typhus: vasculitis leading to intense HA,
chills,fever, myalgia (w/o eshcar), rash begins in axillary
folds and the upper trunk.
(Dx. by serology, isolation, direct immunofluorescence)
Chloramphenicol,
tetracyline, rifampin,
ciprofloxacin
(Dx. by serology, clinical hx)
Chloramphenicol &
tetracycline.
Control human body
louse and  sanitation
same as other typhus
Endemic Typhus: HA, myalgia and fever, a rash occurs in
60-80% of cases and is central in distribution
Scrub Typhus: Bite site ulcerates and forms a black crust
called an eschar, regional lymphadenopathy next 4-5 days,
fever, HA and myalgia, rash occurs on the trunk and
spreads to extremities, may be CNS symptoms
Q fever: Typically an acute self-limiting febrile
illness:HA,fever,chills,fatigue,myalgia; rash almost never
occurs, may cause atypical or rapidly progressive
pneumonia. “Chronic” inf can result in endocarditis or
hepatitis w/ a “donut granuloma” of a fibrin ring around a
central lipid vacuole.
same as other typhus
Tetracycline
Dx. by serology and
history
Mycoplasma (Wall-less Cells)
Name
Mycoplasma pneumoniae
Ureaplasma urealyticum
Mycoplasma hominis
Characteristics
no cell wall, require sterols for growth,
many commensal mucosal species, 1020% of pneumonias, 50% of summer
pneumonias, school children and young
adults.
no cell wall, require sterols for growth,
able to metabolise urea (have urease),
genital mycoplasm
same as above, colonization rates 031%
Disease(s)
Atypical pneumonia: a prolonged “flu” or bronchitis, cxr
shows lower lobe bronchial pneumonia,  PMN’s; malaise,
cough may persist for 2-6 weeks, tracheobronchitis is most
common complication.
Pathogenesis
(Dx. by culture, serology with rising titers, complement
fixation is the gold standard serology)
Treatment
Erythromycin or
tetracycline
resistant to penicillin
b/c lacks cell wall
Tetracycline (10%
resist) or erythromycin
Nongonococcal urethritis: can progress to
prostatitis/epididymitis, or postpartum
fever/abortion/chorioamnionitis(?)
Pyelonephritis, PID, salpingitis, postabortal/ postpartum
fever, may contribute to nongonococcal urethritis
Tetracycline
Spirochetes (Flexible, thin walled cells)
Name
Borrelia burgdorferi
Borrelia hermsii
Leptospira interrogans
Treponema pallidum
(this one has a lot too)
Characteristics
highly motile(by endo-flagella in
periplasmic space), cork-screw shaped
(spirochete), must use darkfield
microscope, does not have LPS.
Worldwide, spread by bite of Ixodes
tick,it winters in the fur of deer and
feeds on the white-footed mouse, inf in
mouse skin is major reservoir of bact.
Most common in mid west and
northeast US.
(as above for spirochetes),
predominantly found the western US,
most often at elevations above 5000 ft.
Disease(s)
Lyme disease: Chronic infection, disseminates to many
organs. Erythema migrans (EM) is most distinctive feature
(60%). Early disease shows localized EM, disseminated
lympho-cytoma (swelling ear or nipple), arthritis attacks,
migratory musculoskeletal and joint pain, chronic
meningitis, heart problems, severe malaise and fatigue.
Chronic disease on skin shows ACA. Musculoskeletal
recurrent oligoarthritis or chronic arthritis, chronic
parenchymal brain inf. Chronicity defined by >1yr of joint
infection. Assoc w/HLA-DR-4.
Relapsing fever (alternating periods of fever and illness
alternate with periods of wellness)
an uncommon infection
(as above for spirochetes) rare in US,
often in developing nations
spirochete characteristics, stains well
with Silver stain. obligate parasite of
humans, does not appear in nature or in
animals. Can be sexually trans-mitted
or congenital, trans. is greatest during
1 or 2 stage, exogenous routes,
endogenous activation of latent disease
may also occur
Acute febrile illness, sometimes fatal systemic illness
marked by hepatic invovement in fatal cases.
Syphilis: 1: appearance of painless, indurated, well
circumscribed ulcer (chancre) and regional
lymphadenopathy (disease is communicable at this stage),
lesions heal.
2: bact in circulation (septicemia) go to lymph nodes and
tissues:fever, HA, lymphaden-opathy, generalized rash
(palms/soles), mucous patches in oral cavity, condylomata
(commun-icable lesions), alopecia. Also hepatoslpenomegaly, nephritis, periostitis. Latency: 2 stage may occur
again. AIDS pts have higher rate of recur, rapidly progr
CNS involvement.
3 (or late stage): anywhere from months to >50 years.
neurosyphilis from treponemes in CNS, CV (aneurysm,
aortic endocarditis), benign gummas.
Pathogenesis
Hallmarks of Lyme disease are dissemin-ation and
persistence of bacteria, dissem-ination is mediated by
the spirochete’s ability to invade endothelial
intercellular junctions, relative low amounts of outer
membrane spanning proteins is possibly a factor in
ability of bacteria to cause chronic disease.
Treatment
Therapies are being
developed
Has the capacity to undergo antigenic variation of
Variable Major Protein (VMP), periods of illness and
wellness alternate as bact goes through antigenic
repertoire
Contains a lipopolysaccharide like material (LLS) in the
outer membrane
Enter through abraded skin or mucous membranes,
attach by their tips to host cells and colonize, w/in hours
organisms go to lymph nodes, then disseminate to liver,
spleen & bone marrow via circulation, bact exit through
tight junctions of endothelial cells sets up chronic
inflammatory response.
[Congenital syphilis: Thru placenta 18th week, damage
depends on stage of disease in mom/# of treponemes.
Ususally miscarriage or stillbirth. 1Sx. can present up
to age 2. Mucous membrane lesions, osteochondritis,
anemia, organomegaly, CNS disease. Late sx: keratitis,
8th nerve deaf., abn 2nd tooth dvlp (raspberry molars),
abn long bones (sabre shins), perf nasal septum,
gummas.]
Dx. by blood smear
and serology
Dx: Hx. of pt, can
mimic other diseases.
Dark-field
microscopy.
VDRL or RPR
serology tests, 30%
may show false neg,
false + w/autoimmune
diseases (SLE).
Tx: penicillin or
doxycycline,
tetracycline,
erythromycin.
Educate, cond-oms,
screening.
Mycobacteria (Acid fast, aerobic rods, facultative intracellular)
Name
Mycobacterium tuberculosis
Characteristics
Facultative,intracellular, obligate
aerobe, slightly bent rods, slow
growing, four unique surface
layers,trans. by respiratory droplets,
acid-fast (red) bacilli, dry cauliflower
like colonies
Positive PPD: documents infection but
not state of TB
Negative TB: doesn’t say much pt. may
be anergic (AIDS), have to re-test if
still suspected
Disease(s)
Tuberculosis: 1TB: exudative response, bacteria are
phagocytized by PMN’s but remain inside the cytoplasm,
followed by form-ation of a productive lesion w/granuloma
and tubercule resulting(caseous necrosis). Ghon complex is
hilar lymph node granuloma, caseous lesions can heal
w/fibrosis. Humoral immunity makes dormant but doesn’t
elim.bact
Reactivation TB: from caseous lesion can be-come active,
liquefaction, spread through lung, fever,cough, malaise,
wt.loss, night sweats
Miliary TB when bacteria disseminates (AIDS)
Mycobacterium bovis
same characteristics as M.TB, caused
by infected dairy products, eradicated
by pasteurization
Tuberculosis in cattle. In man enters through GI, infects
lymph nodes (scrofula), can also infect vertebrae and
joints, collapse of vertebrae (Pott’s disease)
Mycobacterium leprae
Acid-fast rods, aerobic, facultative
intracellular,cannot be cultured in vitro,
very slow growing, optimal growth at
less than body temperature, carried on
armadillos (low body temp), also trans
by nasopharyngeal secretions or contact
of skin wounds w/bacilli in the soil.
Very long incubation of 1-20 years,
hard to contract. Must have prolonged
contact. Found in human skin and
nerves.
Tuberculoid leprosy: Annular lesions in extremities
(cooler) w/ red, raised border. Red area has most bact.
Lesioned areas have  sensitivity. Destructive
lesions.Damage to fingers can occur b/c of sensation.
CMI is effective at stemming spread of bacteria.
Lepromatous leprosy:More contagious. CMI lost or 
allowing spread of bacteria.Sx:diffuse thickening of skin:
eyebrow alopecia, enlarged earlobes, broadening of nose,
swelling of fingers, hypopigmentation.
Reversal Reaction(lepromatoustuberculoid)
Erythema Nodosum Leprosum (systemic)
Lucio’s reaction(hemorrhagic infarcts)
(see HO for sure, this one has a lot
of detail!)
Pathogenesis
Chronic asymptomatic infections: bact. enter and
multiply inside macrophages and never escape.
Unknown cues cause multiplication of bacteria and
release from macrophages.
Survival: resistance to oxidative killing, inhibition of
phagosome-lysosome fusion, resistance to lysosomal
enzymes.
AIDS is a common cause of reactivation by mechanisms
unknown.
Also: stress, overcrowding, age, silicosis
Best treatment is prevention.
Exact pathogenesis unknown.
Disease is pretty much eradicated in the US due to
pasteurization.
M. leprae is an intracellular pathogen. The clinical sx.
correlate with the immune response to the pathogen.
Tuberculoid pts have good CMI, lepromatous pts have
decr CMI and their disease is disseminated. CMI is
assessed by skin testing: Fernandez rxn, Mitsuda
rxn:characterized by presence of granulomas, org.
lymphocytes and macro-phages (competent CMI), + in
tuberculoid pts/neg. in lepromatous pts. In reversal rxn
Mitsuda goes from neg to + (DTH). Pts w/ HLA-DR 2,3
tend to get tuberculoid form, HLA-DQ 1 assoc w/
lepromatous form.
Treatment
4 drug regimen:
INH, rifampin,
pyrazinamide,
ethambutol (last 2 for
only 1st 3 mo)
give for 9mos, 12 mos
in AIDS pts
Combination tx. b/c of
MDR.
Check w/cxr and
sputum culture.
source of BCG
vaccine, no longer
used, only 70%
effective
Dapsone + rifampin
for the tuberculoid
form. Clofazimine is
added for lepromatous form or if
organism is resistant
to dapsone. Tx. is for
at least 2 yr. Give
dapsone for close
family contacts,
vaccine being
researched.