Gram Positive Cocci
Treatment
Characteristics
Staphylococcus aureus
Gram + cocci in clusters,immotile human
Invasive: suppurative skin infections: minor trauma  pimples
skin and nares,body walls off infection w/a ,carbuncles, impetigo; major osteomyelitis, fasciitis, cellulitis.
fibrinous barrier; S. aureus causes pus
formation.
hematogenous inf., nosocomial infection.
Associated Disease(s)
Pathogenesis
Treatment
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.
penicillin
vancomycin
[erythromycin]
Toxinoses: Food Poisoning (enterotoxin), exfoliative skin
disease (Ritter’s disease of newborns), TSS
(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.
Coagulase negative
Streptococcus pyogenes
Gram + cocci in chains, catalase neg.,
Group A causes most strep disease,
asymptomatic carriers, causes suppurative
infections.
Suppurative: Pharyngitis, Scarlet Fever, erysipelas,
streptococcal pyoderma (impetigo).
Surface molecules confer adherence to tissues and resistance to
phagocytosis.
Very sensitive to
penicillin.
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.
If patient is allergic, give
erythromycin.
Capsular polysaccharide (prevent phag.), Hemolysin (like
streptolysin S), IgA receptor (camouflage), Fibronectin binding
protein (adherence).
penicillin
(Group A, -hemolytic)
Streptococcus agalactiae
Opportunistic infections, large number of nosocomial
infections: bacteremia, endocarditis, endophthalmitis,
osteomyelitis (following surgery), infections of indwelling
foreign devices, neonatal necrotizing enterocoloitis.
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)
(Group B, -hemolytic)
Coagulase negative
vancomycin
chloramphenicol
Viridans Streptococci
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).
Gram +, encapsulated, lancet shaped cocci
in pairs, usually community acquired,
sporadic.
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.)
(-hemolytic)
Enterococcus faecalis
penicillin
Antibiotic resistance to every known antibiotic due to conjugal
transfer of antibiotic resistance genes within and across species
???
(-hemolytic, non-hemolytic)
Streptococcus pneumoniae
(“the pneumococcus”)
Transmitted by droplet nuclei or aspiration
by carrier. Facultative anaerobes, hemolytic.
Capsule confers path: inhibits phagocytosis by inhibiting alt.pathway, penicillin
must be present for virulence. Capsule also stimulates production of
type-specific opsonic Ab that results in killing by PMNs. No toxins
amoxicillin
involved in path. 85 different serotypes.
cephalosporins
vancomycin
Vaccine for people at risk
available.
Gram Positive Rods
Organism
Listeria monocytogenes
Characteristics
Disease(s)
Pathogenesis
Treatment
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 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.
Ampicillin,
penicillin with an
aminoglycoside,
erythromycin.
Use only pasteurized milk
products b/c of this
bacterium!!!
(see HO, lots of details for this one)
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.
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.
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 anti-phagocytic activity but does not
stimulate protective antibody
Bacillus cereus
Gram+, motile, non encapsulated, beta
hemolytic, exists as a saprophyte in water and
soil, trans. in contaminated rice or meat
dishes
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).
Secretes enterotoxins
Corynebacterium diphtheriae
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.
Diphtheria. Fever, chills, pharyngitis, cervical lymphadenitis,
massive neck edema (severe cases) and a thick, closely
adherent dirty gray pharyng., tonsillar or laryng.
pseudomembrane
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.
“Diphtheroids”
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
Vaccine (but is only 50%
eff)
Penicillin and tetracycline
are effective only when
given early
Vaccination prevents
disease
Active disease: give antitoxin immediately,
penicillin or eryth
romycin for killing bacteria.
Often have multiple antibiotic resistance, but do not produce
exotoxin
Gram Positive, Anaerobic, Sporeforming Rods
Organism
Characteristics
Disease(s)
Pathogenesis
Clostridium botulinum
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.
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.
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.
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.
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”
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.
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.
Immunization @ 2,4,6 mos.
and boosters every 5-10 y.
Antitoxin + immune globulin given to wounded people
w/o immun. immediately!
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
Also: Anaerobic cellulitis, uterine infection, necrotizing enteritis,
food pois.
food poisoning (self limiting diarrhea).
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
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.
Clostridium dificile
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
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
Gram Negative Coccobacilli
Organism
Bordetella pertussis
Haemophilus influenzae
Characteristics
Disease(s)
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
Pertussis (whooping cough). 4 phases: 1. incubation; 2. catarrhal Attaches (firmly) to ciliated resp.epithelial cells(using FHA,pili
(mild cold-like sx. , mild cough of severity,most infectious phase) and peritactin), secretes toxins to inhibit phago.cells (adenylate
cyclase toxin, pertussis toxin )& inhibit muco-ciliary
defense(tracheal toxin), multiplies and causes local damage,
3. paroxysmal (severe, forceful, spasmodic coughing w/ “whoop” systemic disease results (lymphocytosis, insulin, glycemia) See
following and then vom-iting, complicated by otitis media,
HO for details of toxins.
seizures, apnea, pneumonia); 4. convalescent (less fr. paroxysms,
recovery). 1% death rate, mental retardation and paralysis can
occur.
Pathogenesis
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.
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
Treatment
Erythromycin for active
disease.
Vaccination to prevent
disease. Vaccine can
cause some se’s but is safe
and prevents epidemics.
Capsule is antiphagocytic major virulence factor (PRP polymer,
Vaccination
most adults have anti- PRP Ab), pili may have a role in
attachment, LPS, outer membrane proteins, IgA protease
(specific role not yet established)
For active disease give
cephalospor-ins,
ampicillin +
Most common from 3mos to 4 yr after maternal ab’s have worn off
chloramphenicol.
and T cell response not active. Complications are severe.
Gram Negative Cocci
Name
Characteristics
Disease(s)
Pathogenesis
Treatment
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
undergo TRANSCYTOSIS to cross the basement membrane.
Features: Pilus(attachment), IgA1 protease(cleaves IgA),
antiphagocytic capsule, LipidA(septic shock).
IV antibiotics, manage
complications,
prophylaxis during
epidemics
Neisseria gonorrheae
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).
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.
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(Lover’s heels), fever, often mild systemic toxicity.
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
Brucella melitensis
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 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
Ususally combo tx
w/tetracycline and
streptomycin or rifampin;
or co-trimoxazole, vacc
for cattle but not people.
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
start asap, for pneumonic,
give streptomycin,
tetracycline(good
prophylactic) or
chloramphenicol for
meningitis. Reduces
mortality if started vy
early, vaccine available.
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
same as above
(and suis and abortus)
Francisella tularensis
Pasteurella multocida
Adults, exudative pharyngitis, Reiter syndrome and erythema
nodosum in pts. w/HLA B-27 marker
tetracycline,
chloramphenicol, cotrimoxazole, and
gentamicin
Gram Negative Rods (Nosocomial)
Name
Characteristics
Escherichia coli
Gram - rods, facultative anaerobes, ferment Meningitis of newborn
Meningitis of newborn: Strains w/K1 poly-saccharide,forms a
lactose, found in human colon, vagina,
capsule that is poorly immunogenic(like N.meningitidis).Mom
urethra. Transmitted during birth in
w/ E.coli K1(carrier)confers risk to the newborn
neonatal meningitis, travels from urethra in Uropathogenic:UTI(cystitis or pyelonephritis) Untreated
pyelonephritis
is
a
chronic
infection
that
can
last
for
many
months.
UTI and pyelonephritis.
Cystitis:Have “common pili” that allow binding to D-mannose
on bladder epithelial surfacesecrete 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)
(extraintestinal infections)
Disease(s)
Pathogenesis
Treatment
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
(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 (fecaloral).
Infant diarrhea: Enteropathogenic E.coli (EPEC). Chronic
Attachment by EPEC: 3 stages; 1st nonintimate adherence to the
diarrhea of children, can cause dehydration and malnutrition. Non- epithelial cell surface by pili. 2nd is induction of microvilli
inflammatory enteritis w/ watery diarrhea w/o fecal leukocytes.
effacement (flattening out). 3rd is intimate adherence and host
cell cytoskeletal rearrangement by intimin, a bacterial adhesin
Traveler’s diarrhea (dehydrating diarrhea): Enterotoxigenic E.coli encoded by the eaeA gene.
(ETEC). Non-inflammatory enteritis (as for infant diarrhea)
E.coli O157:H7 is probably from acquisition of the Shiga toxin
gene by EPEC (maybe via bacteriophage), transforming it into
Hemolytic Uremic Syndrome, blood and non bloody diarrhea:
Enterohemorrhagic E.coli (EHEC). Diarrhea is dysenteric w/fecal EHEC
leukocytes. HUS is hemolytic anemia, renal failure w/ uremia,
thrombocytopenia and neurological sx. (E.coli 0157:H7)
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.
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.
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
Combination antibiotic
chemotherapy
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
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.
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
Erythromycin (or newer
analogs), and rifampin,
only bacteriostatic Host
immune system must kill
maybe by cytotoxic T
cells?
Pontiac Fever: Febrile illness w/o pneumonia, mild and non-fatal
Gram Negative Rods (Enteric)
Organism
Characteristics
Associated Disease(s)
Pathogenesis
Treatment
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
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.
Raising pH of stomach encourages infection.
Replace fluids &
electrolytes po or iv,
tetracycline  duration,
vaccine under dev. Tx. is
very effective & easy to
give.
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.
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
Campylobacter jejuni
gram-,curved,spiral or comma shaped rods, Common cause of diarrhea.
motile, micro-aerophilic, worldwide
zoonosis in GI tract of dom. animals, trans
Acute enteritis: diarrhea, malaise, fever, abd. pain. Range of
by cont food/water, common, est
diarrhea from loose to watery to bloody. Ususally self limiting,
2Mcases/yr in US
bacteremia rare, dx. by stool culture.
Campylobacter fetus
fairly rare
Systemic disease in immunocompromised host
Helicobacter pylori
gram-,spiral rods, motile, produce urease,
habitate the gastric epithelium
Salmonella enterica
Pathogenic mechanisms uncertain
Fluid and electro-lyte
replacement, antibiotics
may be indicated(bloody
stool), usually no tx is
necessary.
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
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)
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
Salmonella typhi
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
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.
Ceftriaxone (1st ),
ampicillin or cotrimoxazole if not severe.
Prevent by public health
measures. Killed and live
-attenuated vaccine
available.
Shigella
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:
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.
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.
(serotypes referred to as if they are
species)
(dysenteriae, flexneri, boydii or
sonnei)
food, fingers, feces, flies. Only person to
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.
Pathogenesis
Tetracycline or
doxycycline,
erythromycin,
azithromycin, atypical
pneum-onia d/dx
Chlamydia psittaci
only grows in eukaryotic cells,
developmental cycle with two growth
forms, aerosol spread, zoonosis (in certain
birds)
Psittacosis: fever, respiratory symptoms, systemic infection
Tetracycline
Rickettsia rickettsii
obligate intracellular of vascular
endothelium, trans by tick bite, southeast
and south central US
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.
Chloramphenicol,
tetracyline, rifampin,
ciprofloxacin
Rickettsia prowazekii
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
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
urine,feces, milk and birth products of
cattle, sheep and goats, trans by inhalation
of contaminated aerosols
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.
Tetracycline
Dx. by serology and
history
Mycoplasma (Wall-less Cells)
Name
Characteristics
Disease(s)
Pathogenesis
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, PMN’s; malaise, cough may
persist for 2-6 weeks, tracheobronchitis is most common
complication.
(Dx. by culture, serology with rising titers, complement fixation Erythromycin or
is the gold standard serology)
tetracycline
Treatment
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 Therapies are being
of bacteria, dissem-ination is mediated by the spirochete’s
developed
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
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)
Has the capacity to undergo antigenic variation of Variable
Major Protein (VMP), periods of illness and wellness alternate
as bact goes through antigenic repertoire
Leptospira interrogans
(as above for spirochetes) rare in US, often Acute febrile illness, sometimes fatal systemic illness marked by
in developing nations
hepatic invovement in fatal cases.
Treponema pallidum
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
Dx. by blood smear and
serology
an uncommon infection
(this one has a lot too)
Contains a lipopolysaccharide like material (LLS) in the outer
membrane
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
lymph nodes, then disseminate to liver, spleen & bone marrow
communicable at this stage), lesions heal.
via circulation, bact exit through tight junctions of endothelial
cells sets up chronic inflammatory response.
2: bact in circulation (septicemia) go to lymph nodes and
tissues:fever, HA, lymphaden-opathy, generalized rash
[Congenital syphilis: Thru placenta 18th week, damage depends
(palms/soles), mucous patches in oral cavity, condylomata
on stage of disease in mom/# of treponemes. Ususally
(commun-icable lesions), alopecia. Also hepatoslpen-omegaly,
nephritis, periostitis. Latency: 2 stage may occur again. AIDS pts miscarriage or stillbirth. 1Sx. can present up to age 2. Mucous
membrane lesions, osteochondritis, anemia, organomegaly,
have higher rate of recur, rapidly progr CNS involvement.
CNS 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.
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)
Pathogenesis
Treatment
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: 1TB: exudative response, bacteria are phagocytized
by PMN’s but remain inside the cytoplasm, followed by formation 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
Chronic asymptomatic infections: bact. enter and multiply
inside macrophages and never escape. Unknown cues cause
multiplication of bacteria and release from macrophages.
4 drug regimen:
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
Survival: resistance to oxidative killing, inhibition of
phagosome-lysosome fusion, resistance to lysosomal enzymes.
INH, rifampin,
pyrazinamide, ethambutol
(last 2 for only 1st 3 mo)
give for 9mos, 12 mos in
Reactivation TB: from caseous lesion can be-come active,
liquefaction, spread through lung, fever,cough, malaise, wt.loss,
night sweats
AIDS is a common cause of reactivation by mechanisms
unknown.
AIDS pts
Miliary TB when bacteria disseminates (AIDS)
Also: stress, overcrowding, age, silicosis
Combination tx. b/c of
MDR.
Best treatment is prevention.
Exact pathogenesis unknown.
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.
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
Lepromatous leprosy:More contagious. CMI lost or  allowing
CMI), + in tuberculoid pts/neg. in lepromatous pts. In reversal
spread of bacteria.Sx:diffuse thickening of skin: eyebrow alopecia, rxn Mitsuda goes from neg to + (DTH). Pts w/ HLA-DR 2,3
enlarged earlobes, broadening of nose, swelling of fingers,
tend to get tuberculoid form, HLA-DQ 1 assoc w/ lepromatous
hypopigmentation.
form.
Reversal Reaction(lepromatoustuberculoid)
Erythema Nodosum Leprosum (systemic)
Lucio’s reaction(hemorrhagic infarcts)
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
lepro-matous form or if
organism is resistant to
dapsone. Tx. is for at least
2 yr. Give dapsone for
close family contacts,
vaccine being researched.