Gram Positive Cocci
Treatment
Staphylococcus aureus
Staphylococcus epidermidis
Staphylococcus saprophyticus
Streptococcus pyogenes
(Group A, -hemolytic)
Streptococcus agalactiae
(Group B, -hemolytic)
Viridans Streptococci
(-hemolytic)
Enterococcus faecalis
(-hemolytic, non-hemolytic)
Streptococcus pneumoniae
(“the pneumococcus”)
Characteristics
Gram + cocci in clusters,immotile human
skin and nares,body walls off infection w/a
fibrinous barrier; S. aureus causes pus
formation.
Gram + cocci in clusters, human skin
(always),
Gram + cocci in clusters, skin/genitourinary Infections outside of hospital, causes 20% of all urinary tract
tract
Gram + cocci in chains, catalase neg., Group
A causes most strep disease, asymptomatic
carriers, causes suppurative infections.
Gram + cocci in chains, catalase neg., lower Puerperal sepsis (after childbirth) , neonatal meningitis (early
GI tract & female genital tract.
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.
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) Pathogenesis Treatment
Invasive: suppurative skin infections: minor trauma  pimples penicillin
,carbuncles, impetigo; major osteomyelitis, fasciitis, cellulitis.
Multifactorial; secrete 4 hemolysins that lyse cells; -hemolysin
lyses cell similar to pore form. by complement, also:coagulase +, vancomycin
hematogenous inf., nosocomial infection. exfoliatin. Protein A is a surface molecule that binds IgG to
camouflage the bacterium. Also able to respond to env. w/signal
molecule. [erythromycin]
Toxinoses: Food Poisoning (enterotoxin), exfoliative skin
disease (Ritter’s disease of newborns), TSS
(Many strains are multi-
abx resistant.
and make -lactamase)
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
infections in young women.
Suppurative: Pharyngitis, Scarlet Fever, erysipelas, streptococcal Surface molecules confer adherence to tissues and resistance to Very sensitive to penicillin.
pyoderma (impetigo). phagocytosis.
If patient is allergic, give
Non-suppurative: Acute Rheumatic Fever, Acute M-protein(prevents phag.), Protein F (adherence-fibronectin), Fc erythromycin.
Glomerulonephritis. receptor (like Prt.A), C5a peptidase, etc. Secreted exotoxins:
erythrogenic toxin, Streptolysin S, Streptolysin O, Streptokinase,
DNAse.
penicillin
Capsular polysaccharide (prevent phag.), Hemolysin (like
onset w/50% mortality or late onset w/20% fatality) streptolysin S), IgA receptor (camouflage), Fibronectin binding vancomycin
protein (adherence).
chloramphenicol
dental caries, subacute bacterial endocarditis (on pre-existing penicillin
heart valve lesions),enter bloodstream via decayed teeth or
following oral surgery.
subacute bacterial endocarditis, female urinary tract infections, Antibiotic resistance to every known antibiotic due to conjugal ???
peritoneal abscess, bacteremia (from above foci). transfer of antibiotic resistance genes within and across species
penicillin
Pneumonia (Lobar and Bronchopneumonia, most common Capsule confers path: inhibits phagocytosis by inhibiting alt.pathway,
cause of meningitis in adults, most common cause of otitis must be present for virulence. Capsule also stimulates production of amoxicillin
media and sinusitis in children, can cause septicemia, esp. in type-specific opsonic Ab that results in killing by PMNs. No toxins
the very old or very young. (Immunity to reinfection is type- involved in path. 85 different serotypes.
specific against capsule.) cephalosporins
vancomycin
 Vaccine for people at risk
available.

Gram Positive Rods

Organism Characteristics Disease(s) Pathogenesis Treatment

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, oral-
fecal 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 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
Ampicillin,
Extracellular product listeriolysin O is responsible for
pathogenicity- a cytolysin that specifically dissolves the penicillin with an
endosomal membrane so that it evades the major anti- bacterial aminoglycoside,
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. erythromycin.
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. 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.
Vaccine (but is only 50% eff)
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

Bacillus cereus
Corynebacterium diphtheriae
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).
Diphtheria. Fever, chills, pharyngitis, cervical lymphadenitis,
massive neck edema (severe cases) and a thick, closely
Gram +, non sporeforming, non motile, vy. adherent dirty gray pharyng., tonsillar or laryng.
distinct (beaded, barred or clubbed), pseudomembrane
facultative anaerobes, obligate parasite of
humans, carried in URT, transmitted by
droplet nuclei or contaminated milk, people Death due to resp. paralysis or myocarditis. Cutaneous
can be carriers. diphtheria results in an ulcerative lesion w/a dirty gray
pseudomembrane. W/both there can be toxemic degeneration
and death.
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 anti-
frag 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.

“Diphtheroids” Same habitat, may have same morphological Can cause septicemia in rare instances in immunosuppressed Often have multiple antibiotic resistance, but do not produce
and biochemical properties as C.diphtheriae individuals with a high fatality rate. exotoxin
but they do not produce exotoxin
Gram Positive, Anaerobic, Sporeforming Rods

Organism Characteristics Disease(s) Pathogenesis

Clostridium botulinum Gram+, anaerobic, spore form- ing, Botulism. Caused by intoxication w/bacteria. Clinical sx. 18-36h Botulinus toxin causes path. Released by lysis of bacterial cells in Free toxin can be inactivated
multiplies in uncooked meat, sausage, fish after ingestion, ptosis, mydriasis, blurred vision, dysphagia, medium. Toxin has two subunits:H-chain causes receptor with a specific antiserum.
and badly canned items, dx. by animal dysphonia, urinary retention, muscle weakness (descending), mediated endocytosis by host cell, once in cell the H and L-chain Give a polyvalent antitoxin.
injection, cultures show characteristic “light respiratory paralysis. Death can occur w/in 18h. This results from are separated and the L-chain moves by retrograde transport to the Do not give penicillin b/c it
bulb” appearance. Spores do not produce Ach presynaptic blockade. Infant Botulism results in floppy presynaptic terminal where it prevents fusion of the synaptic causes cell lysis and more
toxin, only vegetative form does. infant, may be cause of SIDS in some cases. 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.
Clostridium tetani Gram+, anaerobic, spore formi-ing, found Tetanus. Caused by intoxication, may take several days to weeks Secretes tetanus toxin which is a dimer similar to botulinus toxin
all over the place, typical entry through for symptoms to occur. Onset of sx. may be muscular (H and L chain) L chain functions as a synaptobrevin on the
wounds (puncture wound or laceration, but contractions in the vicinity of the wound followed by spastic surface of synaptic vesicles that inhibits their fusion with the Antitoxin + immune globu-
also burns, ulcers, cpd fx, operative contraction of the masseter muscle (trismus) resulting in “locked presynaptic membrane. Tetanus toxin specifically blocks the lin given to wounded people
wounds, injection sites of IVDAs, Dx. is jaw”, generalized rigidity and severe spasms of the limbs and inhibitory neurons of spinal motor neurons preventing release of w/o immun. immediately!
clinical, appear on culture as gram+ rods trunk. Later signs: risus sardonicus, spasmic contractions of GABA and glycine which results in uninhibited transmission of
w/spore formation at tip forming a back(opisthotonus) and of the resp.muscles which may lead to excitatory impulses and muscular spasms.
“drumstick” death.
Gas gangrene. Destroys tissues esp. muscle,Infects poorly
perfused, injured tissues, incubation 6-72h, severe edema, bronze
Clostridium perfringens Gram+, anaerobic, spore forming, occur discoloration, bullous lesions w/dark thin fluid, then H2 gas Produces extotoxins. Most important toxin is -toxin which surgical excision of inf.
normally in soil and sewage, normal in human production leading to crepitations, ischemia, shock and death. cleaves lecithin in host cell membranes and is lethal and skin and muscle, limb amp
GI, box shaped organisms with gram stain, Most common organism to cause gas gangrene. necrotizing on injection. Perfringolysin O (similar to strep- utation, hyper-baric O2.
positive blood cultures(for gas gangrene), tolysin O, pore complexes). The combined action of -toxin and Abx to well perfused
found also in feces for other infections streptolysin O may be the cause for the intravascular hemolysis tissues, no time to wait for
Also: Anaerobic cellulitis, uterine infection, necrotizing enteritis, associated w/ infections. b-toxin important in necrosis of cultures! Surg.for bowel in
food poisoning (self limiting diarrhea). necrotizing enteritis. Spores in food germinate & release toxin in enteritis.
food pois.

Clostridium dificile Gram+, anaerobic, spore forming, normal Pseudomembranous colitis. Diarrhea and toxic megacolon. Produces two heat labile toxins: A and B. The toxins are released Stop previous abx tx.
commensal of human gut, results from Endoscopy shows multiple small pseudomembranous colon by vegetative cells and together cause fluid loss, mucosal damage Vancomycin or
superinfection following antibiotic treatment plaques. Milder form is antibiotic associated diarrhea w/ same and necrosis of intestinal mucosa. Toxin can be id by ELISA. metronidazol to stop inf.
clinical findings but less severe Surg-ery for megacolon

Gram Negative Coccobacilli

Organism Characteristics
Gram neg, coccobacillus, non motile, non
Bordetella pertussis
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, recovery). 1% death rate, mental retardation and paralysis can
mostly children
Haemophilus influenzae 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.
Gram Negative Cocci
Name Characteristics
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.
gram- diplococci, fastidious, human
mucosa/poor environ. survival,
Neisseria gonorrheae sympt/asympt inf.
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.
Gram Negative Rods (Zoonotic)
Name Characteristics
Brucella melitensis
gram- nonmotile coccobacilli, aerobic (may
(and suis and abortus) 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) Pathogenesis Treatment
Pertussis (whooping cough). 4 phases: 1. incubation; 2. catarrhal Erythromycin for active
(mild cold-like sx. , mild cough of severity,most infectious phase)
Attaches (firmly) to ciliated resp.epithelial cells(using FHA,pili disease.
and peritactin), secretes toxins to inhibit phago.cells (adenylate
3. paroxysmal (severe, forceful, spasmodic coughing w/ “whoop” cyclase toxin, pertussis toxin )& inhibit muco-ciliary
following and then vom-iting, complicated by otitis media, defense(tracheal toxin), multiplies and causes local damage, Vaccination to prevent
seizures, apnea, pneumonia); 4. convalescent (less fr. paroxysms, systemic disease results (lymphocytosis, insulin, glycemia) See disease. Vaccine can cause
HO for details of toxins. some se’s but is safe and
occur. prevents epidemics.
Meningitis, epiglottitis (in kids), not seen often any more b/c of
Vaccination
vaccine, 75% unencapsulated causes otitis media, sinusitis,
bronchopneumonia, 5% encapsulated causes pneumonia, Capsule is antiphagocytic major virulence factor (PRP polymer,
epiglottitis, bacteremia, meningitis most adults have anti- PRP Ab), pili may have a role in
attachment, LPS, outer membrane proteins, IgA protease For active disease give
(specific role not yet established) 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.
Disease(s) Pathogenesis Treatment
Meningococcal disease: meningitis and/or Attaches to non-ciliated cells of the nasopharyngeal mucosa and IV antibiotics, manage
septicemia(fever,ha,chills, malaise, wkness, hemorrhagic skin undergo TRANSCYTOSIS to cross the basement membrane. complications, prophylaxis
lesions/petechiae/purpura, DIC, Thrombocytopenia, leukocytosis, Features: Pilus(attachment), IgA1 protease(cleaves IgA), during epidemics
hypotension, septic shock (LPS-A). Can be epidemic, bacteremia antiphagocytic capsule, LipidA(septic shock).
in susceptible people (asplenic pts, children), carrier state in others
Gonorrhea: Urethritis (males), cervicitis (females), rectal inf, Uncomplicated ceftriaxone
pharyngeal inf, ophthalmia neonatorum (mother to infant + doxycycline.
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 Many pcnase producing
variation, IgA1 protease to evade IgA on mucosal surfaces, P1 strains, tx for chlamydia
porin shows resistance. Inflammation is intense, dissemination too, tx for sexual partner,
can occur but not as prone as in N.meningitidis no vax, use a condom
Disease(s) Pathogenesis Treatment
Brucellosis: Undulating fevers (daily cycling), night sweats, Enter through alimentary tract, conjunctivae, or skin and are Ususally combo tx
malaise, chills, weakness, myalgia, HA. May have enlaged spleen engulfed by PMN’s that carry bact to the lymphatics, there they w/tetracycline and
and liver, vertebral spondylitis, bacteremia (20%) and epididymitis enter mononuclear cells and multiply w/in by inh. of streptomycin or rifampin;
Neurological sx. may occur as may endocarditis. Causes chronic phagolysosomal fusion, cells die, bact are released into blood or co-trimoxazole, vacc for
illness w/ an acute onset. and go to reticuloendo-thelial system, cause granulomatous cattle but not people.
lesions
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 In flea gut at lower temps and low Ca the bact can multiply but start asap, for pneumonic,
nodes causing a very painful swelling (bubo) high fever, malaise, does not secrete toxins. In host @ 37 and incr Ca, chaperone give streptomycin,
then bacteria spread to liver, spleen and lungs. DIC can occur. prts allow the translocation of YOPS (virulence factors) out of tetracycline(good
Secondary pneumonia leads trans. by respiratory the cell. Two cytotoxins are also secreted into the host cell as prophylactic) or
droplets.Pneumonic form from resp drops is very conta-gious and well as YopM that binds to human a-thrombin and is thought to chloramphenicol for
100% fatal w/o tx. Septicemic plague is caused by bite but no bubo produce the hemorrhagic lesion Killing fleas w/insecticide and meningitis. Reduces
forms and pt presents w/fever and dies of bacteremia since hard to quarantining victims is effective for prevention mortality if started vy
dx. all very fatal! early, vaccine available.

Yersinia pseudotuberculosis
Yersinia enterocolitica
Does not display bipolar staining, more Mesenteric adenitis and pseudoappendicitis syndrome, usually a On entry the bact bind to integrin receptors on the host cell with ampicillin,
motile at 22C but not at 37C, reservoir in sporadic infection invasin proteins on their surface, this allows them to be chloramphenicol,
wild and domesticated animals and fowl. phagocytosed. tetracycline, or
aminoglycosides
Diarrhea in children: acute self-limiting gastroenteritis,
enterocolitis and lymphadenitis
Does not display bipolar staining, in same as above tetracycline,
contaminated food and water, mostly milk chloramphenicol, co-
and meat Adults, exudative pharyngitis, Reiter syndrome and erythema trimoxazole, and
nodosum in pts. w/HLA B-27 marker gentamicin

Gram Negative Rods (Nosocomial)

Name Characteristics Disease(s) Pathogenesis Treatment

Escherichia coli
(extraintestinal infections)
Gram - rods, facultative anaerobes, ferment
lactose, found in human colon, vagina,
urethra. Transmitted during birth in neonatal pyelonephritis is a chronic infection that can last for many months.
meningitis, travels from urethra in UTI and
pyelonephritis.
Meningitis of newborn
Uropathogenic:UTI(cystitis or pyelonephritis) Untreated
(Different strains of E.coli have acquired traits that allow them to
be infective to these regions)
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
Cystitis:Have “common pili” that allow binding to D-mannose
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.
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. Non- epithelial cell surface by pili. 2nd is induction of microvilli traveler’s diarrhea, co-
Gram - 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

(enteric pathogens)
cell cytoskeletal rearrangement by intimin, a bacterial adhesin duration of sx.
lactose, enterotoxigenic E.coli are not Traveler’s diarrhea (dehydrating diarrhea): Enterotoxigenic E.coli encoded by the eaeA gene.
usually part of the normal flora of the human (ETEC). Non-inflammatory enteritis (as for infant diarrhea) Only eat cooked food and
gut. Enterotoxigenic strains are found in boiled water in certain
parts of the world w/ poor sanitation and can E.coli O157:H7 is probably from acquisition of the Shiga toxin countries, prophy-lactic
also be in food (fecal-oral). Hemolytic Uremic Syndrome, blood and non bloody diarrhea: gene by EPEC (maybe via bacteriophage), transforming it into Pepto Bismol or
Enterohemorrhagic E.coli (EHEC). Diarrhea is dysenteric w/fecal EHEC doxycycline may be
leukocytes. HUS is hemolytic anemia, renal failure w/ uremia, preventive.
thrombocytopenia and neurological sx. (E.coli 0157:H7)

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.
gram- aerobic, tough to stain,
flagellated,intracellular path, catalase+,
oxidase+, gelatinase+, -lactamase+, lots of pneumonia, resp failure, disorientation, liver abnormalities,
branched chain fatty acids, transmitted by
aerosolization of contaminated water,
reservoir is aquatic unicellular organisms,
humans are accid-ental hosts
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
hyponatremia and hypophosphatemia.
Pontiac Fever: Febrile illness w/o pneumonia, mild and non-fatal
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/pmn’s, M, & fibrin, many intra and Erythromycin (or newer
extra cellular bacteria in M (inside vacuoles) and pmn’s. analogs), and rifampin,
Multiplies intra cellularly in alveolar M and monocytes until only bacteriostatic Host
host cell destroyed, enters by “coiling phagocytosis” mediated immune system must kill
by complement rec. on phagocyte and C3 component on bact maybe by cytotoxic T
called Major Outer Membrane Protein, inh fusion of phagosome cells?
w/host cell lysosomes, inhibits acidification of phagosome.needs
Fe

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.
Raising pH of stomach encourages infection.
Cholera: Inf. is asymptomatic to acute in nature, can be spread by Replace fluids &
asymp people, early signs: vomiting, cramps, then PROFUSE 1)colonization: ingestion, gastric acid barrier, attachment to electrolytes po or iv,
secretory diarrhea (rice water stools), massive fluid loss of 10L/day sm.bowel (microvilli) tetracycline  duration,
leads to dehydration, electrolyte deficiency and hypovolemic vaccine under dev. Tx. is
shock. W/o tx. 60% fat., w/tx. only 1% fat. very effective & easy to
2) cholera toxin: ADP ribosylates G prt. to “turn on” adenylate give.
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)
Vibrio vulnificus Seawater
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
Campylobacter fetus fairly rare
Helicobacter pylori gram-,spiral rods, motile, produce urease,
habitate the gastric epithelium
Salmonella enterica
Gram- rods, motile, facultative intracellular,
(serotypes referred to as if they are usually aquired by contaminated food or
species) animals esp. poultry meat or eggs, infections
are typically animal associated, fecal oral
transmission as well.
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
Shigella Gram- rods, not normal flora, facultative
intracellular,motile exclusive to primates, vy
few needed to infect, evade host def like
(dysenteriae, flexneri, boydii or sonnei) gastric acid, fecal-oral transmission: The
Four F’s:
food, fingers, feces, flies. Only person to
person.
Obligate Intracellular Parasites
Food poisoning: undercooked seafood, causes secretory diarrhea
Septicemia in compromised host, cellulitis in healthy host
Common cause of diarrhea.
Pathogenic mechanisms uncertain Fluid and electro-lyte
replacement, antibiotics
may be indicated(bloody
stool), usually no tx is
necessary.
Systemic disease in immunocompromised host
Gastritis/ulcers: thought to be cause of much gastritis and predisp Virulence: motility, urease, cytotoxin, exact cause of triple tx: pepto,
to stomach CA, abx. tx. against clears up ulcers and gastritis. inflammation is unknown, infection remains for life if not metronidazole,
treated. amoxicillin.
Acute enterocolitis: Most common disease syndrome of Invades epithelial cells by contact w/ micro-villi of host, then Antibiotics not
salmonella, follows 6-8 hr incub-ation, most pts. have nausea, bact cell assembles invasomes (invasion organelles) which recommended for
vomiting, diarrhea. Fever and abd cramping also common, inf triggers host cell memb. ruffling, the bact then shed their uncomplicated
involves small bowel and colon (different site from shigella), Fecal invasomes followed by host cell uptake. Salmonella can turn on enterocolitis, ceftriaxone
PMN’s are present, dx. by stool culture for enteric pathogens, death and off genes according to if they are in a host cell or not, PhoQ for sepsis. Prevent w/
is rare. Infections can spread beyond intestinal mucosa to produce is a sensor molecule (ex: low pH inside a phagolysosome) that public health measures (ie
bacter-emia and seed distant tissues that can result in later focal regulates genes for transcriptional regulation and turns off other restaurant safety) no
infections (osteomyelitis in sickle cell pts. occurs w/ increased genes. Pag C is essential for resistance to killing by vaccine available
frequency) macrophages.
Typhoid fever (enteric fever): Incubation 1-3 weeks, gradual onset S. typhi first invades small bowel epithelial cells or M cells in Ceftriaxone (1st ),
of fever, abd pain and hepatosplenomegaly, duration usually 4 Peyer’s patches trans-cytosis across epithelial ampicillin or co-
weeks w/o tx. Dx. by culture of blood, bone marrow and stool. cellsendocytosis by lamina propria M. Bact survive in trimoxazole if not severe.
bone marrow gives the highest yield of organisms b/c it is a “spacious phagosomes” and reach systemic circulation via Prevent by public health
systemic infection of mononuclear phagocytes. Death may occur thoracic duct reticuloendo-thelial system (phagocytes in liver, measures. Killed and live
despite use of antibiotics b/c of the fatal comp-lication of intestinal spleen and bone marrow). Gall bladder inf leads to the chronic -attenuated vaccine
perforation and peritonitis carrier state. Inf dose is large. available.
Shigellosis: suspect in any diarrhea lasting > 48 hours. Abd cramps, Intracellular, 1st invades M cells of gut lymphoid follicles, kill
may have fever. Stools have PMN’s, 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 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.
Name Characteristics Disease(s) Pathogenesis Treatment

Chlamydia trachomatis only grows in eukaryotic cells, Genitourinary tract infection:cervicitis, non gonococcal urethritis, (Dx: serology, culture, PCR, direct hybridization, LCR w/ urine) Tetracycline or
developmental cycle with two growth forms, PID, neonatal ophthalm-orrhea and pneumonia, lymphogranuloma doxycycline,
spread by sexual contact, peripartum or venereum, Trachoma (ocular inf), chronic sequelae: tubal erythromycin,
close personal contact infertility, ectopic preg-nancy, blindness. azithromycin, atypical
pneum-onia d/dx

Chlamydia psittaci only grows in eukaryotic cells, Psittacosis: fever, respiratory symptoms, systemic infection Tetracycline
developmental cycle with two growth forms,
aerosol spread, zoonosis (in certain birds)

Rickettsia rickettsii obligate intracellular of vascular
endothelium, trans by tick bite, southeast
and south central US
Rickettsia prowazekii obligate intracellular of vascular
endothelium, trans by human louse (close
personal contact), unsanitary cond, military trunk.
campaigns
Rocky Mountain Spotted Fever: Affects vascular endothelium (Dx. by serology, isolation, direct immunofluorescence) Chloramphenicol,
(vasculitis), multi-system presentation w/fever, myalgias, HA, rash tetracyline, rifampin,
on palms/soles 3-5 days post fever, serious compl: gangrene, renal ciprofloxacin
failure, neurological involvement, DIC in very severe cases.
Chloramphenicol &
tetracycline.
Epidemic Typhus: vasculitis leading to intense HA, chills,fever, (Dx. by serology, clinical hx)
myalgia (w/o eshcar), rash begins in axillary folds and the upper
Control human body louse
and sanitation

Rickettsia typhi obligate intracellular of vascular Endemic Typhus: HA, myalgia and fever, a rash occurs in 60-80% same as other typhus
endothelium, trans by the rat flea, in urban of cases and is central in distribution
and suburban dep on rodent expos.

Rickettsia tsutsugamushi obligate intracellular of vascular
endothelium, trans by chiggers (larval
mites), humans are accidental hosts (usually
rodents)
Coxiella burnetii obligate intracellular pathogen, in
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
contaminated aerosols
Scrub Typhus: Bite site ulcerates and forms a black crust called an same as other typhus
eschar, regional lymphadenopathy next 4-5 days, fever, HA and
myalgia, rash occurs on the trunk and spreads to extremities, may
be CNS symptoms
Tetracycline
Q fever: Typically an acute self-limiting febrile
Dx. by serology and
may cause atypical or rapidly progressive pneumonia. “Chronic” history
inf can result in endocarditis or hepatitis w/ a “donut granuloma” of
a fibrin ring around a central lipid vacuole.

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.
Erythromycin or
Atypical pneumonia: a prolonged “flu” or bronchitis, cxr shows (Dx. by culture, serology with rising titers, complement fixation tetracycline
lower lobe bronchial pneumonia, PMN’s; malaise, cough may is the gold standard serology)
persist for 2-6 weeks, tracheobronchitis is most common
complication. 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
mycoplasm
Mycoplasma hominis same as above, colonization rates 0-31%
Spirochetes (Flexible, thin walled cells)
Name Characteristics
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.
Borrelia hermsii (as above for spirochetes), predominantly
found the western US, most often at
elevations above 5000 ft.
Leptospira interrogans (as above for spirochetes) rare in US, often
in developing nations
Treponema pallidum
spirochete characteristics, stains well with
(this one has a lot too) Silver stain. obligate parasite of humans,
does not appear in nature or in animals. Can
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
routes, endogenous activation of latent
disease may also occur
Tetracycline (10% resist)
or postpartum fever/abortion/chorioamnionitis(?) or erythromycin
Pyelonephritis, PID, salpingitis, postabortal/ postpartum fever, may Tetracycline
contribute to nongonococcal urethritis
Disease(s) Pathogenesis Treatment
Lyme disease: Chronic infection, disseminates to many organs. Hallmarks of Lyme disease are dissemin-ation and persistence of Therapies are being
Erythema migrans (EM) is most distinctive feature (60%). Early bacteria, dissem-ination is mediated by the spirochete’s ability to developed
disease shows localized EM, disseminated lympho-cytoma invade endothelial intercellular junctions, relative low amounts
(swelling ear or nipple), arthritis attacks, migratory of outer membrane spanning proteins is possibly a factor in
musculoskeletal and joint pain, chronic meningitis, heart problems, ability of bacteria to cause chronic disease.
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)
Has the capacity to undergo antigenic variation of Variable Dx. by blood smear and
Major Protein (VMP), periods of illness and wellness alternate serology
an uncommon infection as bact goes through antigenic repertoire
Acute febrile illness, sometimes fatal systemic illness marked by Contains a lipopolysaccharide like material (LLS) in the outer
hepatic invovement in fatal cases. membrane
Syphilis: 1: appearance of painless, indurated, well circumscribed Enter through abraded skin or mucous membranes, attach by Dx: Hx. of pt, can mimic
ulcer (chancre) and regional lymphadenopathy (disease is their tips to host cells and colonize, w/in hours organisms go to other diseases. Dark-field
lymph nodes, then disseminate to liver, spleen & bone marrow microscopy.
communicable at this stage), lesions heal.
via circulation, bact exit through tight junctions of endothelial
cells sets up chronic inflammatory response.
VDRL or RPR serology
tests, 30% may show false
(palms/soles), mucous patches in oral cavity, condylomata [Congenital syphilis: Thru placenta 18th week, damage depends neg, false + w/autoimmune
(commun-icable lesions), alopecia. Also hepatoslpen-omegaly, on stage of disease in mom/# of treponemes. Ususally diseases (SLE).
nephritis, periostitis. Latency: 2 stage may occur again. AIDS pts miscarriage or stillbirth. 1Sx. can present up to age 2. Mucous
have higher rate of recur, rapidly progr CNS involvement. membrane lesions, osteochondritis, anemia, organomegaly, CNS
Tx: penicillin or
disease. Late sx: keratitis, 8th nerve deaf., abn 2nd tooth dvlp
doxycycline, tetracycline,
(raspberry molars), abn long bones (sabre shins), perf nasal
3 (or late stage): anywhere from months to >50 years. erythromycin. Educate,
septum, gummas.]
neurosyphilis from treponemes in CNS, CV (aneurysm, aortic cond-oms, screening.
endocarditis), benign gummas.
Mycobacteria (Acid fast, aerobic rods, facultative intracellular)

Name Characteristics Disease(s) Pathogenesis Treatment

Facultative,intracellular, obligate aerobe,
Mycobacterium tuberculosis
slightly bent rods, slow growing, four
unique surface layers,trans. by respiratory
droplets, acid-fast (red) bacilli, dry
(see HO for sure, this one has a lot of
cauliflower like colonies
detail!)
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
Tuberculosis: 1TB: exudative response, bacteria are phagocytized Chronic asymptomatic infections: bact. enter and multiply inside 4 drug regimen:
by PMN’s 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.
INH, rifampin,
necrosis). Ghon complex is hilar lymph node granuloma, caseous
pyrazinamide, ethambutol
lesions can heal w/fibrosis. Humoral immunity makes dormant but
Survival: resistance to oxidative killing, inhibition of (last 2 for only 1st 3 mo)
doesn’t elim.bact
phagosome-lysosome fusion, resistance to lysosomal enzymes.
give for 9mos, 12 mos in
Reactivation TB: from caseous lesion can be-come active,
AIDS is a common cause of reactivation by mechanisms
liquefaction, spread through lung, fever,cough, malaise, wt.loss, AIDS pts
unknown.
night sweats
Combination tx. b/c of
Also: stress, overcrowding, age, silicosis
Miliary TB when bacteria disseminates (AIDS) MDR.

Best treatment is prevention.

Check w/cxr and

Exact pathogenesis unknown.

sputum culture.

Mycobacterium bovis same characteristics as M.TB, caused by
infected dairy products, eradicated by
pasteurization
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
Tuberculosis in cattle. In man enters through GI, infects lymph
nodes (scrofula), can also infect vertebrae and joints, collapse of
vertebrae (Pott’s disease)
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, lymphocytes and macro-phages (competent CMI), + in
enlarged earlobes, broadening of nose, swelling of fingers,
Disease is pretty much eradicated in the US due to source of BCG vaccine, no
pasteurization. longer used, only 70%
effective
M. leprae is an intracellular pathogen. The clinical sx. correlate Dapsone + rifampin for the
with the immune response to the pathogen. Tuberculoid pts have tuberculoid form.
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
dapsone. Tx. is for at least
tuberculoid pts/neg. in lepromatous pts. In reversal rxn Mitsuda 2 yr. Give dapsone for
incubation of 1-20 years, hard to contract. hypopigmentation. goes from neg to + (DTH). Pts w/ HLA-DR 2,3 tend to get close family contacts,
Must have prolonged contact. Found in tuberculoid form, HLA-DQ 1 assoc w/ lepromatous form. vaccine being researched.
human skin and nerves.
Reversal Reaction(lepromatoustuberculoid)

Erythema Nodosum Leprosum (systemic)

Lucio’s reaction(hemorrhagic infarcts)