Gram Positive Cocci

Treatment

Staphylococcus aureus

Characteristics

Associated Disease(s)

Pathogenesis

Invasive: suppurative skin infections: minor trauma pimples

,carbuncles, impetigo; major osteomyelitis, fasciitis, cellulitis.

Gram + cocci in clusters,immotile human

skin and nares,body walls off infection w/a
fibrinous barrier; S. aureus causes pus
hematogenous inf., nosocomial infection.
formation.

Toxinoses: Food Poisoning (enterotoxin), exfoliative skin

disease (Ritters disease of newborns), TSS

Treatment
penicillin

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.

vancomycin
[erythromycin]
(Many strains are multiabx resistant.
and make -lactamase)

Staphylococcus epidermidis

Gram + cocci in clusters, human skin

(always),

Staphylococcus saprophyticus

Gram + cocci in clusters, skin/genitourinary Infections outside of hospital, causes 20% of all urinary tract
tract
infections in young women.

Streptococcus pyogenes
(Group A, -hemolytic)

Opportunistic infections, large number of nosocomial infections: Coagulase negative

bacteremia, endocarditis, endophthalmitis, osteomyelitis
(following surgery), infections of indwelling foreign devices,
neonatal necrotizing enterocoloitis.

Coagulase negative

Suppurative: Pharyngitis, Scarlet Fever, erysipelas, streptococcal Surface molecules confer adherence to tissues and resistance to
pyoderma (impetigo).
phagocytosis.

Gram + cocci in chains, catalase neg., Group

A causes most strep disease, asymptomatic
carriers, causes suppurative infections.
Non-suppurative: Acute Rheumatic Fever, Acute
Glomerulonephritis.

M-protein(prevents phag.), Protein F (adherence-fibronectin), Fc

receptor (like Prt.A), C5a peptidase, etc. Secreted exotoxins:
erythrogenic toxin, Streptolysin S, Streptolysin O, Streptokinase,
DNAse.

Streptococcus agalactiae
(Group B, -hemolytic)

Very sensitive to penicillin.

If patient is allergic, give
erythromycin.

penicillin
Gram + cocci in chains, catalase neg., lower Puerperal sepsis (after childbirth) , neonatal meningitis (early
GI tract & female genital tract.
onset w/50% mortality or late onset w/20% fatality)

Capsular polysaccharide (prevent phag.), Hemolysin (like

streptolysin S), IgA receptor (camouflage), Fibronectin binding
protein (adherence).

vancomycin
chloramphenicol

Viridans Streptococci
(-hemolytic)

Gram + cocci in chains, catalase neg., oral

cavity (up to 60% of normal oral flora)

dental caries, subacute bacterial endocarditis (on pre-existing

heart valve lesions),enter bloodstream via decayed teeth or
following oral surgery.

Gram + cocci, low pathogenicity, normal

flora of human gut, very hardy.

subacute bacterial endocarditis, female urinary tract infections,

peritoneal abscess, bacteremia (from above foci).

penicillin

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.

Antibiotic resistance to every known antibiotic due to conjugal

transfer of antibiotic resistance genes within and across species

???
penicillin

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 typespecific against capsule.)

Capsule confers path: inhibits phagocytosis by inhibiting alt.pathway,

must be present for virulence. Capsule also stimulates production of amoxicillin
type-specific opsonic Ab that results in killing by PMNs. No toxins
involved in path. 85 different serotypes.
cephalosporins
vancomycin

Vaccine for people at risk

available.

Gram Positive Rods

Organism

Characteristics

Disease(s)

Pathogenesis

Treatment
Ampicillin,

Listeria monocytogenes
Gram+, non-encapsulatedrod w/a
characteristic tumbling motility,
facultative intracellular parasite, grows
under many conditions, found nearly
everywhere, transmitted through
improperly pasteurized milk/products, oralfecal contamination of any source (ie- H20
contamination, vegetable fertilized
w/manure, meat, etc).

Listeriosis is disease. Rarely causes disease but when it does is

severe esp to fetus, newborn, pregnant women and the immunocompromised. 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

Extracellular product listeriolysin O is responsible for

pathogenicity- a cytolysin that specifically dissolves the
endosomal membrane so that it evades the major anti- bacterial
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 cells actin. Actin polym. allows bacteria to move in
cytoplasm and is required for cell-cell spread, also makes it
resistant to humoral immunity.

penicillin with an
aminoglycoside,
erythromycin.
Use only pasteurized milk
products b/c of this
bacterium!!!

(see HO, lots of details for this one)

Vaccine (but is only 50% eff)
Bacillus anthracis

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.

Bacillus cereus

Gram+, motile, non encapsulated, beta

Self limiting type of food poisoning. Incubation period and
hemolytic, exists as a saprophyte in water and clinical sx. resemble staph. food poisoning. Can also cause
soil, trans. in contaminated rice or meat dishes disseminated, usually fatal, disease in immuno compromised
pts.(usually post-operatively).

Corynebacterium diphtheriae

Diphtheroids

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.

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.

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.

Same habitat, may have same morphological Can cause septicemia in rare instances in immunosuppressed
and biochemical properties as C.diphtheriae individuals with a high fatality rate.
but they do not produce exotoxin

Exotoxin produces pathogenesis. Toxin is a heat labile protein

composed of 3 components: protective antigen, lethal or toxic
Penicillin and tetracycline
factor and edema factor. Polypeptide capsule made exclusively of are effective only when
D-glutamic acid gives anti-phagocytic activity but does not
given early
stimulate protective antibody

Secretes enterotoxins

Vaccination prevents disease

K antigen on surface is anti-phagocytic. Exotoxin is of 2
polypeptide fragments: B fragment is for transport into cell and A Active disease: give antifrag ment is toxin for ADP-ribosylation and inactivation of
toxin immediately, penicillin
elongation factor EF-2 which inhibits protein synthesis. Lysogeny or eryth
w/ a beta prophage carrying the tox gene is essential for
toxigenicity.
romycin for killing bacteria.

Often have multiple antibiotic resistance, but do not produce

exotoxin

Gram Positive, Anaerobic, Sporeforming Rods

Organism

Characteristics

Clostridium botulinum

Gram+, anaerobic, spore form- ing,

Botulism. Caused by intoxication w/bacteria. Clinical sx. 18-36h
multiplies in uncooked meat, sausage, fish after ingestion, ptosis, mydriasis, blurred vision, dysphagia,
and badly canned items, dx. by animal
dysphonia, urinary retention, muscle weakness (descending),
injection, cultures show characteristic light respiratory paralysis. Death can occur w/in 18h. This results from
bulb appearance. Spores do not produce Ach presynaptic blockade. Infant Botulism results in floppy
toxin, only vegetative form does.
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

Clostridium dificile

Disease(s)

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.

Pathogenesis

Botulinus toxin causes path. Released by lysis of bacterial cells in Free toxin can be inactivated
medium. Toxin has two subunits:H-chain causes receptor
with a specific antiserum.
mediated endocytosis by host cell, once in cell the H and L-chain Give a polyvalent antitoxin.
are separated and the L-chain moves by retrograde transport to the Do not give penicillin b/c it
presynaptic terminal where it prevents fusion of the synaptic
causes cell lysis and more
vesicles w/the presynaptic membrane. All toxins are destroyed by toxin.
boiling at 100C for 10 minutes.
Immunization @ 2,4,6 mos.
and boosters every 5-10 y.
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
Antitoxin + immune globupresynaptic membrane. Tetanus toxin specifically blocks the
lin given to wounded people
inhibitory neurons of spinal motor neurons preventing release of w/o immun. immediately!
GABA and glycine which results in uninhibited transmission of
excitatory impulses and muscular spasms.

Gas gangrene. Destroys tissues esp. muscle,Infects poorly

perfused, injured tissues, incubation 6-72h, severe edema, bronze
Gram+, anaerobic, spore forming, occur
discoloration, bullous lesions w/dark thin fluid, then H2 gas
normally in soil and sewage, normal in human production leading to crepitations, ischemia, shock and death.
GI, box shaped organisms with gram stain,
Most common organism to cause gas gangrene.
positive blood cultures(for gas gangrene),
found also in feces for other infections
Also: Anaerobic cellulitis, uterine infection, necrotizing enteritis,
food poisoning (self limiting diarrhea).

Gram+, anaerobic, spore forming, normal

Pseudomembranous colitis. Diarrhea and toxic megacolon.
commensal of human gut, results from
Endoscopy shows multiple small pseudomembranous colon
superinfection following antibiotic treatment plaques. Milder form is antibiotic associated diarrhea w/ same
clinical findings but less severe

Gram Negative Coccobacilli

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 streptolysin 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.

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.

Produces two heat labile toxins: A and B. The toxins are released Stop previous abx tx.
by vegetative cells and together cause fluid loss, mucosal damage Vancomycin or
and necrosis of intestinal mucosa. Toxin can be id by ELISA.
metronidazol to stop inf.
Surg-ery for megacolon

Organism

Characteristics

Disease(s)
Pertussis (whooping cough). 4 phases: 1. incubation; 2. catarrhal
(mild cold-like sx. , mild cough of severity,most infectious phase)

Bordetella pertussis

Haemophilus influenzae

Gram neg, coccobacillus, non motile, non

sporeforming, piliated, LPS, obligate aerobe,
slow growing, hard to grow, human
3. paroxysmal (severe, forceful, spasmodic coughing w/ whoop
respiratory tract, no known animal or
following and then vom-iting, complicated by otitis media,
environment-al reservoir, transmitted by
seizures, apnea, pneumonia); 4. convalescent (less fr. paroxysms,
respiratory droplets, highly communicable, recovery). 1% death rate, mental retardation and paralysis can
mostly children
occur.

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.

Pathogenesis

Treatment
Erythromycin for active

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.

disease.
Vaccination to prevent
disease. Vaccine can cause
some ses but is safe and
prevents epidemics.

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

Vaccination
Capsule is antiphagocytic major virulence factor (PRP polymer,
most adults have anti- PRP Ab), pili may have a role in
For active disease give
attachment, LPS, outer membrane proteins, IgA protease
cephalospor-ins, ampicillin
(specific role not yet established)
+ chloramphenicol.
Most common from 3mos to 4 yr after maternal abs have worn off
and T cell response not active. Complications are severe.

Gram Negative Cocci

Name

Characteristics

Disease(s)

Pathogenesis

Neisseria meningitidis

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.

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

Attaches to non-ciliated cells of the nasopharyngeal mucosa and IV antibiotics, manage

undergo TRANSCYTOSIS to cross the basement membrane.
complications, prophylaxis
Features: Pilus(attachment), IgA1 protease(cleaves IgA),
during epidemics
antiphagocytic capsule, LipidA(septic shock).

gram- diplococci, fastidious, human

mucosa/poor environ. survival,
sympt/asympt inf.

Gonorrhea: Urethritis (males), cervicitis (females), rectal inf,

pharyngeal inf, ophthalmia neonatorum (mother to infant
gonococcal conjunctivitis).

Neisseria gonorrheae

Spread by sexual contact or perinatal inf.

Complications: PID, Disseminated gonococcal infection (DGI,
Gram st of exudate in males can dx. but for only 0.5-3% of inf) leading to arthritis, dermatitis,
sure culture to confirm from any source.
tenosynovitis(Lovers heels), fever, often mild systemic toxicity.

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

Treatment

Uncomplicated ceftriaxone
+ doxycycline.
Many pcnase producing
strains, tx for chlamydia
too, tx for sexual partner,
no vax, use a condom

Gram Negative Rods (Zoonotic)

Name

Characteristics

Disease(s)

Pathogenesis

Treatment

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

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.

Enter through alimentary tract, conjunctivae, or skin and are

engulfed by PMNs 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

Ususally combo tx
w/tetracycline and
streptomycin or rifampin;
or co-trimoxazole, vacc for
cattle but not people.

Brucella melitensis
(and suis and abortus)

Francisella tularensis

Pasteurella multocida

Yersinia pestis

gram- bacillus, short non-motile, non-spore

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

Yersinia pseudotuberculosis

Does not display bipolar staining, more

motile at 22C but not at 37C, reservoir in
wild and domesticated animals and fowl.

Mesenteric adenitis and pseudoappendicitis syndrome, usually a

sporadic infection

On entry the bact bind to integrin receptors on the host cell with ampicillin,
invasin proteins on their surface, this allows them to be
chloramphenicol,
phagocytosed.
tetracycline, or
aminoglycosides

Yersinia enterocolitica

Does not display bipolar staining, in

contaminated food and water, mostly milk
and meat

Diarrhea in children: acute self-limiting gastroenteritis,

enterocolitis and lymphadenitis

start asap, for pneumonic,

give streptomycin,
tetracycline(good
prophylactic) or
chloramphenicol for
meningitis. Reduces
mortality if started vy
early, vaccine available.

same as above

tetracycline,
chloramphenicol, cotrimoxazole, and
gentamicin

Disease(s)

Pathogenesis

Treatment

Meningitis of newborn

Meningitis of newborn: Strains w/K1 poly-saccharide,forms a

capsule that is poorly immunogenic(like N.meningitidis).Mom
w/ E.coli K1(carrier)confers risk to the newborn

Adults, exudative pharyngitis, Reiter syndrome and erythema

nodosum in pts. w/HLA B-27 marker

Gram Negative Rods (Nosocomial)

Name
Escherichia coli
(extraintestinal infections)

Characteristics

Gram - rods, facultative anaerobes, ferment

lactose, found in human colon, vagina,
Uropathogenic:UTI(cystitis or pyelonephritis) Untreated
urethra. Transmitted during birth in neonatal pyelonephritis is a chronic infection that can last for many months.
meningitis, travels from urethra in UTI and
Cystitis:Have common pili that allow binding to D-mannose
pyelonephritis.
on bladder epithelial surfacesecrete hemolysin,a cytotoxic prt.
(Different strains of E.coli have acquired traits that allow them to
that damages bladder & causes sx.of cystitis.
be infective to these regions)
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.

Escherichia coli

Infant diarrhea: Enteropathogenic E.coli (EPEC). Chronic diarrhea Attachment by EPEC: 3 stages; 1st nonintimate adherence to the Rehydration is effective for
of children, can cause dehydration and malnutrition. Nonepithelial cell surface by pili. 2nd is induction of microvilli
travelers diarrhea, coGram - rods, facultative anaerobes, ferment inflammatory enteritis w/ watery diarrhea w/o fecal leukocytes.
effacement (flattening out). 3rd is intimate adherence and host trimoxazole can shorten

cell cytoskeletal rearrangement by intimin, a bacterial adhesin

(enteric pathogens)

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 (fecaloral).

Travelers 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)

duration of sx.

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

Only eat cooked food and

boiled water in certain
countries, prophy-lactic
Pepto Bismol or
doxycycline may be
preventive.

Dysentery:Enteroinvasive E.coli (EIEC), similar to shigellosis,

fecal leukocytes present.

Pseudomonas aeruginosa

Legionella pneumophila

(See HO, lots of info for this one)

gram- rod, obligate aerobe,ubiquitous in

environment, not found in GI tract of
healthy people, an opportunistic infection
and a common nosocomial pathogen.

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,
gram- aerobic, tough to stain,
non remitting fever, bradycardia, chest pain, hemoptysis,
flagellated,intracellular path, catalase+,
cxr:diffuse or lobar infiltrate, Stage 3:Severe multilobar
oxidase+, gelatinase+, -lactamase+, lots of pneumonia, resp failure, disorientation, liver abnormalities,
branched chain fatty acids, transmitted by hyponatremia and hypophosphatemia.
aerosolization of contaminated water,
reservoir is aquatic unicellular organisms,
Pontiac Fever: Febrile illness w/o pneumonia, mild and non-fatal
humans are accid-ental hosts

Antibiotic resistance is very common and tends to develop

Combination antibiotic
during the course of therapy, so two antibiotics are always used. chemotherapy
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/pmns, M, & fibrin, many intra and

extra cellular bacteria in M (inside vacuoles) and pmns.
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

Erythromycin (or newer

analogs), and rifampin,
only bacteriostatic Host
immune system must kill
maybe by cytotoxic T
cells?

Pathogenesis

Treatment

Gram Negative Rods (Enteric)

Organism

Characteristics

Associated Disease(s)

Raising pH of stomach encourages infection.

Vibrio cholerae

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.

Cholera: Inf. is asymptomatic to acute in nature, can be spread by

asymp people, early signs: vomiting, cramps, then PROFUSE
1)colonization: ingestion, gastric acid barrier, attachment to
secretory diarrhea (rice water stools), massive fluid loss of 10L/day sm.bowel (microvilli)
leads to dehydration, electrolyte deficiency and hypovolemic
shock. W/o tx. 60% fat., w/tx. only 1% fat.
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.

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)

Food poisoning: undercooked seafood, causes secretory diarrhea

Vibrio vulnificus

Seawater

Septicemia in compromised host, cellulitis in healthy host

Common cause of diarrhea.

Campylobacter jejuni

gram-,curved,spiral or comma shaped rods,

motile, micro-aerophilic, worldwide
Acute enteritis: diarrhea, malaise, fever, abd. pain. Range of
zoonosis in GI tract of dom. animals, trans diarrhea from loose to watery to bloody. Ususally self limiting,
by cont food/water, common, est 2Mcases/yr bacteremia rare, dx. by stool culture.
in US

Pathogenic mechanisms uncertain

Fluid and electro-lyte

replacement, antibiotics
may be indicated(bloody
stool), usually no tx is
necessary.

Campylobacter fetus

fairly rare

Systemic disease in immunocompromised host

Helicobacter pylori

gram-,spiral rods, motile, produce urease,

habitate the gastric epithelium

Gastritis/ulcers: thought to be cause of much gastritis and predisp

to stomach CA, abx. tx. against clears up ulcers and gastritis.

Virulence: motility, urease, cytotoxin, exact cause of

inflammation is unknown, infection remains for life if not
treated.

triple tx: pepto,

metronidazole,
amoxicillin.

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.

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
PMNs 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)

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.

Antibiotics not
recommended for
uncomplicated
enterocolitis, ceftriaxone
for sepsis. Prevent w/
public health measures (ie
restaurant safety) no
vaccine available

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

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

S. typhi first invades small bowel epithelial cells or M cells in

Peyers patches trans-cytosis across epithelial
cellsendocytosis 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.

Ceftriaxone (1st ),
ampicillin or cotrimoxazole if not severe.
Prevent by public health
measures. Killed and live
-attenuated vaccine
available.

Salmonella enterica
(serotypes referred to as if they are
species)

Salmonella typhi

Shigella

Gram- rods, not normal flora, facultative

intracellular,motile exclusive to primates, vy
Shigellosis: suspect in any diarrhea lasting > 48 hours. Abd cramps, Intracellular, 1st invades M cells of gut lymphoid follicles, kill
few needed to infect, evade host def like
(dysenteriae, flexneri, boydii or sonnei) gastric acid, fecal-oral transmission: The
may have fever. Stools have PMNs, blood, mucous. 1wk is avg.
resident macrophages invade intestinal epith cells on basolateral
time. Dx. by stool culture, produce disease at very low inoculation. surface, then spread cell-cell. Use host cells actin to rocket from
Four Fs:
cell-cell (like Listeria), express IcsA protein. Invasion plasmid is
essential for pathogenicity. Secrete shiga toxin, causes
food, fingers, feces, flies. Only person to
endothelial damage. Expression of proteins is temp. controlled.
person.

Obligate Intracellular Parasites

Name

Characteristics

Disease(s)

Chlamydia trachomatis

only grows in eukaryotic cells,

developmental cycle with two growth forms,
spread by sexual contact, peripartum or
close personal contact

Genitourinary tract infection:cervicitis, non gonococcal urethritis, (Dx: serology, culture, PCR, direct hybridization, LCR w/ urine)
PID, neonatal ophthalm-orrhea and pneumonia, lymphogranuloma
venereum, Trachoma (ocular inf), chronic sequelae: tubal
infertility, ectopic preg-nancy, blindness.

Chlamydia psittaci

only grows in eukaryotic cells,

Psittacosis: fever, respiratory symptoms, systemic infection
developmental cycle with two growth forms,
aerosol spread, zoonosis (in certain birds)

Tetracycline

Rickettsia rickettsii

obligate intracellular of vascular

endothelium, trans by tick bite, southeast
and south central US

Chloramphenicol,
tetracyline, rifampin,
ciprofloxacin

Rickettsia prowazekii

Pathogenesis

Rocky Mountain Spotted Fever: Affects vascular endothelium

(Dx. by serology, isolation, direct immunofluorescence)
(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.

obligate intracellular of vascular

Epidemic Typhus: vasculitis leading to intense HA, chills,fever,
endothelium, trans by human louse (close
myalgia (w/o eshcar), rash begins in axillary folds and the upper
personal contact), unsanitary cond, military trunk.
campaigns

(Dx. by serology, clinical hx)

Treatment

Tetracycline or
doxycycline,
erythromycin,
azithromycin, atypical
pneum-onia d/dx

Chloramphenicol &
tetracycline.
Control human body louse
and sanitation

Rickettsia typhi

obligate intracellular of vascular

endothelium, trans by the rat flea, in urban
and suburban dep on rodent expos.

Endemic Typhus: HA, myalgia and fever, a rash occurs in 60-80%

of cases and is central in distribution

same as other typhus

Rickettsia tsutsugamushi

obligate intracellular of vascular

endothelium, trans by chiggers (larval
mites), humans are accidental hosts (usually
rodents)

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

same as other typhus

Coxiella burnetii

obligate intracellular pathogen, in

Q fever: Typically an acute self-limiting febrile
urine,feces, milk and birth products of cattle, illness:HA,fever,chills,fatigue,myalgia; rash almost never occurs,
sheep and goats, trans by inhalation of
may cause atypical or rapidly progressive pneumonia. Chronic
contaminated aerosols
inf can result in endocarditis or hepatitis w/ a donut granuloma of
a fibrin ring around a central lipid vacuole.

Tetracycline
Dx. by serology and
history

Mycoplasma (Wall-less Cells)

Name

Characteristics

Disease(s)

Pathogenesis

Treatment

Mycoplasma pneumoniae

no cell wall, require sterols for growth,

many commensal mucosal species, 10-20%
of pneumonias, 50% of summer
pneumonias, school children and young
adults.

Atypical pneumonia: a prolonged flu or bronchitis, cxr shows

lower lobe bronchial pneumonia, PMNs; malaise, cough may
persist for 2-6 weeks, tracheobronchitis is most common
complication.

(Dx. by culture, serology with rising titers, complement fixation tetracycline

is the gold standard serology)

Erythromycin or

resistant to penicillin b/c

lacks cell wall

Ureaplasma urealyticum

no cell wall, require sterols for growth, able Nongonococcal urethritis: can progress to prostatitis/epididymitis,
to metabolise urea (have urease), genital
or postpartum fever/abortion/chorioamnionitis(?)
mycoplasm

Tetracycline (10% resist)

or erythromycin

Mycoplasma hominis

same as above, colonization rates 0-31%

Tetracycline

Pyelonephritis, PID, salpingitis, postabortal/ postpartum fever, may

contribute to nongonococcal urethritis

Spirochetes (Flexible, thin walled cells)

Name

Characteristics

Disease(s)

Pathogenesis

Borrelia burgdorferi

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.

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.

Hallmarks of Lyme disease are dissemin-ation and persistence of Therapies are being
bacteria, dissem-ination is mediated by the spirochetes ability to developed
invade endothelial intercellular junctions, relative low amounts
of outer membrane spanning proteins is possibly a factor in
ability of bacteria to cause chronic disease.

Borrelia hermsii

(as above for spirochetes), predominantly

found the western US, most often at
elevations above 5000 ft.

Relapsing fever (alternating periods of fever and illness alternate

with periods of wellness)
an uncommon infection

Has the capacity to undergo antigenic variation of Variable

Major Protein (VMP), periods of illness and wellness alternate
as bact goes through antigenic repertoire

Acute febrile illness, sometimes fatal systemic illness marked by

hepatic invovement in fatal cases.

Contains a lipopolysaccharide like material (LLS) in the outer

membrane

Leptospira interrogans

(as above for spirochetes) rare in US, often

in developing nations

Treponema pallidum

Syphilis: 1: appearance of painless, indurated, well circumscribed Enter through abraded skin or mucous membranes, attach by
their tips to host cells and colonize, w/in hours organisms go to
ulcer (chancre) and regional lymphadenopathy (disease is
spirochete characteristics, stains well with
lymph nodes, then disseminate to liver, spleen & bone marrow
communicable at this stage), lesions heal.
Silver stain. obligate parasite of humans,
via circulation, bact exit through tight junctions of endothelial
does not appear in nature or in animals. Can
cells sets up chronic inflammatory response.
be sexually trans-mitted or congenital, trans. 2: bact in circulation (septicemia) go to lymph nodes and
is greatest during 1 or 2 stage, exogenous tissues:fever, HA, lymphaden-opathy, generalized rash
[Congenital syphilis: Thru placenta 18th week, damage depends
routes, endogenous activation of latent
(palms/soles), mucous patches in oral cavity, condylomata
on stage of disease in mom/# of treponemes. Ususally
disease may also occur
(commun-icable lesions), alopecia. Also hepatoslpen-omegaly,
nephritis, periostitis. Latency: 2 stage may occur again. AIDS pts miscarriage or stillbirth. 1Sx. can present up to age 2. Mucous
membrane lesions, osteochondritis, anemia, organomegaly, CNS
have higher rate of recur, rapidly progr CNS involvement.
disease. Late sx: keratitis, 8th nerve deaf., abn 2nd tooth dvlp
(raspberry molars), abn long bones (sabre shins), perf nasal
3 (or late stage): anywhere from months to >50 years.
septum, gummas.]
neurosyphilis from treponemes in CNS, CV (aneurysm, aortic
endocarditis), benign gummas.

(this one has a lot too)

Treatment

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
(see HO for sure, this one has a lot of
detail!)

Characteristics

Disease(s)

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

Tuberculosis: 1TB: exudative response, bacteria are phagocytized Chronic asymptomatic infections: bact. enter and multiply inside
by PMNs but remain inside the cytoplasm, followed by form-ation macrophages and never escape. Unknown cues cause
of a productive lesion w/granuloma and tubercule resulting(caseous multiplication of bacteria and release from macrophages.
necrosis). Ghon complex is hilar lymph node granuloma, caseous
lesions can heal w/fibrosis. Humoral immunity makes dormant but
Survival: resistance to oxidative killing, inhibition of
doesnt elim.bact
phagosome-lysosome fusion, resistance to lysosomal enzymes.

Positive PPD: documents infection but not

state of TB
Negative TB: doesnt say much pt. may be
anergic (AIDS), have to re-test if still
suspected

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)

Pathogenesis

Treatment
4 drug regimen:
INH, rifampin,
pyrazinamide, ethambutol
(last 2 for only 1st 3 mo)
give for 9mos, 12 mos in

AIDS is a common cause of reactivation by mechanisms

unknown.

AIDS pts

Also: stress, overcrowding, age, silicosis

Combination tx. b/c of

MDR.

Best treatment is prevention.

Exact pathogenesis unknown.

Disease is pretty much eradicated in the US due to

pasteurization.

Check w/cxr and

sputum culture.

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 (Potts disease)

source of BCG vaccine, no

longer used, only 70%
effective

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

Tuberculoid leprosy: Annular lesions in extremities (cooler) w/ red,

raised border. Red area has most bact. Lesioned areas have
M. leprae is an intracellular pathogen. The clinical sx. correlate Dapsone + rifampin for the
sensitivity. Destructive lesions.Damage to fingers can occur b/c of
with the immune response to the pathogen. Tuberculoid pts have tuberculoid form.
sensation. CMI is effective at stemming spread of bacteria.
good CMI, lepromatous pts have decr CMI and their disease is Clofazimine is added for
disseminated. CMI is assessed by skin testing: Fernandez rxn,
lepro-matous form or if
Mitsuda rxn:characterized by presence of granulomas, org.
organism is resistant to
Lepromatous leprosy:More contagious. CMI lost or allowing
dapsone. Tx. is for at least
spread of bacteria.Sx:diffuse thickening of skin: eyebrow alopecia, lymphocytes and macro-phages (competent CMI), + in
tuberculoid pts/neg. in lepromatous pts. In reversal rxn Mitsuda 2 yr. Give dapsone for
enlarged earlobes, broadening of nose, swelling of fingers,

incubation of 1-20 years, hard to contract.

Must have prolonged contact. Found in
human skin and nerves.

hypopigmentation.
Reversal Reaction(lepromatoustuberculoid)
Erythema Nodosum Leprosum (systemic)
Lucios reaction(hemorrhagic infarcts)

goes from neg to + (DTH). Pts w/ HLA-DR 2,3 tend to get

tuberculoid form, HLA-DQ 1 assoc w/ lepromatous form.

close family contacts,

vaccine being researched.