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196 Cards in this Set
- Front
- Back
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Klebsiellae
shape, gram staining |
rod-shaped
gram negative |
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klebsiellae
most common strains |
k pneumoniae
k oxytoca |
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klebsiellae
sites of 'normal flora' |
GI tract
Skin pharynx important pathogenic reservoirs commonly nosocomial |
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klebsiellae
entry and damage |
diminished host defense
antibiotic use (often resistance to multiple antibiotics) may make extended-spectrum beta lactamase highly virulent capsular type K55 |
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Klebsiellae
syndromes |
respiratory
UTI |
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Klebsiellae
respiratory infection |
contamination of respiratory support equip
middle/older men with impaired systemic/respiratory defenses lobar pneumonia with destructive changes necrosis, inflammation, hemorrhage "currant jelly sputum" |
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Klebsiellae
UTI |
risk factor from Urinary catheters
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Klebsiellae
virulence factors |
K antigen capsule
antiphagocytic inhibits C3 activation antigenically diverse adhesins, siderophores |
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E Coli
gram staining, metabolism, family, spread |
gram negative,
facultative anaerobes, Enterobacteriacae (enterics), fecal-oral spread |
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E coli genetic virulence organization
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'pathogenicity islands'
extrachromosomal plasmids |
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general action of E. Coli, Salmonella, Shigella on host
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actin hijacking
E. Coli/Salmonella are non-cytoplasmic Shigella enters cytoplasm diarrhea--> severe systemic infection |
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E Coli
pathogenicity and antigens |
specific serotypes are more pathogenic
O antigen= polysaccharide component H antigen= flagellar protein K antigen= capsular antigen |
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E Coli
infection regions |
GI (diarrhea/colitis)
UTI Neonatal Meningitis opportunist (bacteremia, pneumonia etc.) |
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Intestinal Infection Types
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Enterotoxogenic (ETEC)
Enterohemorrhagic (EHEC) Enteropathogenic (EPEC) Enteroinvasive (EIEC) ~shigella Enteraggregative (EAEC) |
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ETEC
causes.. |
traveler's diarrhea
infant diarrhea (developing countries) |
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ETEC
infection |
from contaminated food or water
adheres to intestinal epithelium heat labile heat stable toxins |
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ETEC
symptoms |
loss of water and electrolites
afebrile, watery diarrhea (~cholera, less virulent) resolves in a few days |
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ETEC
heat labile toxin |
AB toxin
B forms a ring (binds ganglioside on GI epithelium) A goes in A targets adenylate cyclase related G protein locks it in the active state- cAMP increases dramatically --->causes electrolytes and water to flow out of the cells into lumen |
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EHEC
symptoms |
water diarrhea progressing to
bloody diarrhea painful cramps 30% of cases require hospitalization 5% mortality |
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EHEC
susceptibility |
young children and elderly most susceptible
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EHEC
progression to HUS |
hemolytic uremic syndrome
caused by Stx (shiga-like toxin) damages endothelial cells (kidney and brain) -thrombocytopenia (not enough platelets- used up in endothelial damage) -hemolytic anemia (from being forced through damaged vessels) -renal failure |
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EHEC
spread |
contaminated meat from slaughter
vegetables from poorly cleaned places contaminated water direct contact (fairs) person-to-person day care centers health care workers |
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EHEC
colonization and growth |
resistant to stomach acid- low infectious dose
"attaching and effacing" lesion into GI epithelium causes pedestal formation |
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EHEC
protein mechanisms for infection |
pedestal formation requires Type III secretion (100-300 injectors)
EHEC & EPEC add filamentous appendage to allow injection over more distance Tir is delivered, acts as receptor to Intimin --required for AE lesions |
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EHEC
damage |
stays in GI- no bacteremia
produces Shiga-like toxin =damages endothelial cells (kidney/brain) |
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EHEC
shiga-like toxin specifics |
cleaves rRNA
encoded on lambda-like phage (NO ANTIBIOTIC TREATMENT) toxin only expressed with phage induction hemorrhagic colitis, abdominal pain, bloody diarrhea, few stool leukocytes, not febrile severe effects- see HUS |
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EPEC
infection process |
small intestine
AE lesions on epithelium no Shiga-like toxin |
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EPEC
symptoms |
diarrhea (with mucous)
malaise, vomiting, fever |
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EPEC
susceptibility |
childhood diarrhea (developing countries)
can be life threatening due to dehydration |
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EAEC
virulence |
carried on plasmids (some in chromosomes)
AAF- aggregative adherence fimbriae plasmic causes 'stack-brick' pattern of adherence no heat stable or heat labile toxins |
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EAEC
susceptibility |
traveller's diarrhea
HIV patients |
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EAEC
symptoms |
inflammatory, watery diarrhea
vomiting, nasea, fever |
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EAEC
special exception |
German outbreak killed people
produced Shiga-toxin |
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UPEC
severity range |
uncomplicated urethritis
cystitis (bladder) pyelonephritis sepsis |
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UPEC
colonization |
Pili are important
bind better under shear stress (urinary tract) |
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UPEC
host defense/damage |
hemolysin
siderophore complement resistance |
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Neonatal Meningitis
bacteria type, gram staining |
E coli can cause it
gram - agent |
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Neonatal Meningitis
infection process |
passed from mother during birth-
ingestion, GI penetration hematogenous spread, BBB penetration |
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Neonatal Meningitis
protein mechanisms |
manipulation of actin induce uptake by endothelium
75% association with K1 capsule identical to capsular polysaccharide from Group B meningococcus |
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Opportunistic E coli infections
|
complement resistance
siderophore production predisposed by: immune impairment, GI trauma, foreign body can cause bacteremia, pneumonia |
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salmonella
gram staining, metabolism, species, normal flora? |
gram negative
facultative anaerobes (related to e. coli) s. enterica (multiple serotypes/biotypes) not normal flora |
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salmonella
syndromes |
localized gastroenteritis
enteric (typhoid) fever sustained bacteremia and vascular infection |
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salmonella
localized gastroenteritis spread |
animals (dairy farm)
contaminated food person to person health care setting organism shed for several weeks after infection |
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salmonella
localized gastroenteritis symptoms |
nausea, vomiting, fever
loose stools with inflammatory cells no blood or mucous self-limiting after 4-10 days |
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salmonella
localized gastroenteritis serotypes |
s. enteriditis
s. typhimurium |
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salmonella
typhoid fever serotypes |
s. typhi
s. paratyphi |
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salmonella
typhoid fever spread |
fecal-oral
often foreign travel only person-to-person (no animal reservoir) seeds gall bladder for continual shedding (typhoid mary) grow well in macrophages macrophage uptake promotes spread/distribution |
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salmonella
typhoid fever symptoms |
slow onset
severe febrile episodes bacteremia with seeding (30% get rose spots on skin) may get GI hemorrahge, pericarditis, liver/spleen abcess, gall bladder mortality 30% if untreated |
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salmonella
bacteremia and vascular infection serotypes |
s. choleraesuis
s. dublin |
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salmonella
bacteremia and vascular infection effects |
occurs when bacteremia is sustained at high titer
atherosclerotic plaques focal abdomina, UG, soft tissue, pneumonia, CNS, bone infections |
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salmonella
(all types) invasion |
taken up by gut epithelium
type III secretion manipulate actin causes membrane 'ruffling' goes back to normal after |
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salmonella
(all types) damage |
inflammatory response (fever)
neutrophils to GI epithelium post infectious Reiter's syndrome joint arhtritis |
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salmonella
(all types) treatment |
10-30% mortality without antibiotics
vaccination is recommended, but low efficacy |
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Shigella
gram staining, shape, metabolism |
gram negative
rods lactose non-fermenters |
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Shigella
species/groups |
s. sonnei (developed countries)
s. flexneri s. boydii s. dysenteriae- (*most virulent, most important historically, common in developing countries) |
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shigella
spread, susceptibility |
most contagious bacterial diarrhea
person-to-person (fecal contamination) spreads quickly within households most cases under 10yrs old |
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shigella
infection process |
ingestion
multiplication in small intestine invades colonic epithelium uptake by M cells lyse phagosome = CYTOPLASMIC PATHOGEN plasmid encodes proteins for host cell exploitation (actin- ~listeria) macrophages die by apoptosis- self-limiting infection to mucosa |
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Shigella
symptoms |
fever
cramping, straining, pain watery diarrhea frequent defecation blood and mucous in stool |
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Shigella
shiga toxin |
produced significantly by s. dysenteriae
AB model toxin 2nd most potent toxin known inactivates 60s ribosome can produce HUS (~EHEC) |
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Shiga
s. dysenteriae complications |
severe dehydration
febrile seizures septicemia/pneumonia keroconjunctivitis arthritis rare in the US |
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Shigella
diagnosis |
descending intestinal infection
organisms die quickly in stool-culture rapidly leukocytes in stool fluid replacement antibiotic treatment shortens course |
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EIEC
|
less virulent shigella
diarrhea, fever, dysentery self-limiting no toxin not common in US |
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Listeria
gram staining, shape |
Gram + (!)
bacilli |
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Listeria
spread, susceptibility |
bood-borne outbreaks
often assymptomatic in healthy people high fatality in immunocompromised predilection for pregnant women |
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Listeria
infection process |
induces uptake in gut epithelium (macrophages and M-cells from peyers patches)-CYTOPLASMIC (~shigella)
immune protection phagocytes are killed- bacteria spread can spread to LN's, blood, spleen, liver |
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Listeria
damage during pregnancy |
no systemic exotoxins
bacteremia, meningitis may precipitate labor in pregnant women fetus may get transmission- may be fatal with multiorgan abscesses |
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Listeria
damage to neonates & immunosuppressed |
100X greater risk for AIDS
fever meningitis cerebritis |
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Listeria
pathogenic strategy |
growth within macrophages-
(escape after acidifying phagosome) LLO- pore forming toxin multiplies intracellularly actin comet tails project into new cells -repeat- |
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listeria
host defense |
class I MHC presentation
cytotoxic T Cells kill it ctyoplasmic so avoids other immune response |
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listeria
in pregnancy |
is bad
it can pass through placenta by projections into new cells cellular immunity (cell-mediated) is not too good in the fetus |
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Vibrio
gram staining, shape, motility |
gram -
vibrio shaped (comma) polar flagellae |
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Vibrio
spread |
normal environmental inhabitant
fresh/salt/brackish water fecal-oral spreading bile salt resistant |
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Vibrio
types |
vibrio cholerae (O1 and non-O1)
vibrio vulnificus vibrio parahaemolyticus |
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Vibrio
GI disease |
decreases in stomach acidity predispose
12-17 hr incubation period dehydration/metabolic acidosis rice water stools IgA takes care of it if patient stays hydrated |
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Vibrio
GI virulence factors |
O antigens
Adhesins (allow invasion) cholera enterotoxin (acts like ETEC) binds G-protein, cAMP increases, electrolytes and fluid out |
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Vibrio
Vulnificus/parahemolyticus infection |
invaded ankle wounds
hemorrhagic infections bullous formation antibiotic therapy, surgical debridement can be fatal if untreated |
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vibrio
sepsis syndrome |
raw shellfish consumption
patients with liver disease (no complement or hepatic RES activity) fever, hypotension, cutaneous bullae with hemorrhage, multiorgan fail generalized damage by cytotoxins treat with antibiotics |
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Campylobacter
serotypes and syndromes caused |
c. jejuni- gastroenteritis
c. fetus- systemic infection |
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campylobacter
gram staining, shape, motility |
gram -
bacilli motile |
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Campylobacter
spread |
commensal GI of cattle, sheep, goats, dogs, cats, etc.
bile salt resistant |
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Campylobacter
c. jejuni virulence |
relatively common
flagellae= motility, burrow through mucous enterotoxins ~e. coli cytotoxins |
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campylobacter
c. jejuni symptoms |
12-24 hr fever, myalgia, malaise, cramps, diarrhea
post infectious- Guillain barre treat with antibiotic |
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campylobacter
c. fetus |
invades portal circulation
spreads only with impaired defense bacteremia, meningitis S-layer proteins = armor treat with antibiotics |
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Helicobacter
gram staining, shape, environmental niche, spread |
gram negative
spirochetes human GI only fecal/gastric- oral |
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helicobacter
virulence factors |
persist and survive in mucosa
(protects from acid and host immune) adhesins urease production (converts urea--> CO2 to create pH neutral) CagA (cytotoxin) virulence island= peptic ulcer disease VacA (cytotoxin) = immunosuppressive |
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helicobacter
disease progression |
indefinite infection
low grade gastritis Peptic ulcer disease (with increased gastric acid secretion) gastric cancer (MALT lymphoma) non-ulcer dyspepsia |
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helicobacter
potential protective fxn |
GERD is somewhat staved off by H. Pylori CagA+
treatment of H pylori with PUD increases GERD risk (which increases esophageal cancer risk...) inverse relationship with childhood asthma |
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Clostridia
gram staining, shape, metabolism |
gram negative
rods anaerobic spore-forming |
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clostridia
oxygen |
dont make catalase--
so oxygen is toxic usually dont make superoxide dismutase spores are resistant to oxygen |
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clostridia
spread/habitat |
soil (spores)
also in GI of humans/animals |
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clostridia
pathogenesis |
neurotoxins (very potent)
tetanus(c. tetani), botulinum tissue damaging toxins c. perfringens -->muslce, soft tissue lysis c. difficile --> colon ulceration other food poisoning toxins- self limiting |
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clostridium botulinum
|
spores are common in nature
honey only infect infants as spores- no live bacteria may ingest just toxin |
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c. botulinum toxin
|
inhibits nerve conduction
acts at cholinergic synapses of peripheral nerves (inactivates Synaptobrevin- blocks Ach release) -->flaccid paralysis inability to breathe (paralyzed diaphragm, occluded airway by glottis) A and B subunits- disulfide bridge carried on bacteriophage |
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c. botulinum
shape, types |
large rod (botulus= sausage)
not invasive 7 types (A-G based on toxin antigenicity) A, B, E common human strains |
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botulism poisoning
how does it occur |
toxin ingested with food
germination/growth of bacteria in food 80C for 10 min inactivates toxin need anaerobic environment to grow |
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botulism poisoning
symptoms |
double vision
difficulty swallowing weakness, flaccid paralysis |
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wound botulism
|
germination/growth of c. botulinum in wound
uncommon A & B types |
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botulism treatment
|
pump stomach
give polyvalent antitoxin respiratory support 20% mortality even with treatment |
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c. tetani
encounter/colonization |
spores in soil
enter via wound- stay in that area anaerobic conditions promote growth |
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c. tetani
toxin |
tetanospasmin
related to botulism acts on inhibitory nerves from brain stem- prevents GABA release (zinc-dependent protease--inactivates synaptobrevin) --> prolonged rigid contraction paralysis spasmodic obstruction of airway/respiratory muscles are danger |
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c. tetani
shape, metabolism, motility, gram staining |
gram positive
rod spore former motile |
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c. tetani
reservoirs |
soil- wound infection from soil (ex splinter)
colon |
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c. tetani
infection |
puncture wound
burn at birth presence of facultative anaerobes days-weeks incubation 'lock-jaw' minor reflex may cause spasm begins to involve other muscle groups (arched back-opisthotonus; rigid smile- risus sardonicus) untreated mortality 50% |
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c. tetani
treatment |
antitoxin- neutralize toxin
avoid stimulation (quiet, dark) maintain airway drugs may be require to block nerve transmition |
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c. tetani
immunization |
toxoid is used in DPT
boosters needed at 10 yr intervals |
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c. perfringens
encounter |
soil
intestines (humans, animals) contaminated food |
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c. perfringens
multiplication/spread |
grows well in anaerobic environ (necrotic tissue)
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c. perfringens
toxins |
lecithinase a-toxin
kills adjacent tissue--> anaerobic = gangrene (may require surgical removal can also cause sudden lysis of most RBCs can be fatal can also cause food poising from ingested toxin |
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c. perfringens
gram stain, shape, metabolism, generation time, motility, unique feature |
gram +
rod spore former highly invasive obligate anaerobe grows fast (7 min at shortest) non-motile produces capsule (other clostridia dont) |
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c. perfringens
reservoir/transmission |
in soil (only type A)
intestinal flora of vertebrates (all types) ingestion leads too food poisoning (enterotoxin) usually- contamination of wounds or other necrotic tissue |
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c. perfringens
toxins |
6 types (A-F) -->12 toxins
a-toxin = phospholipase hydrolizes lecithin & sphingomyelin leading to cell lysis q-toxin= streptolysin-O related pore-forming toxin oxygen labile, causes cell lyses enterotoxin, extracellular degradative enzymes (multiples) |
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c. perfringens
gas gangrene |
often a mixed infection
penetrating wound predisposes surgery, abortion, burns, cancer, neutropenia hours-weeks incubation period edema necrosis with blisters inflamm cells absent (toxins) systemic sweating, tachycardia, shock 100% mortality in 48 hours untreated treatment = antibiotics, oxygen, surgical removal of affected tissue |
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c. perfringens
anaerobic cellulitis |
local infection
less serious producing gas- may tear connective tissue spreads along fascial planes -->more serious antibiotics and drainage for treatment |
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c. perfringens
food poisoning |
3rd most common cause
contaminated meat requires a large dose 24 hr incubation watery diarrhea/cramping self-limiting |
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c. difficile
general |
antibiotic-associated diarrhea
pseudomembranous colitis |
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c. difficile
encounter |
soil
GI objects/hands in hospitals toxogenic strains less common especially in outpatients predisposed by- elderly, underlying disease, reduced intestinal motility |
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c. difficile
multiplication/spread |
colonization normal
kept in check by other bacteria after antibiotic treatments opportunistic multiplication |
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c. difficile
toxins |
two related
inactivate GTP-binding protins of Rho family (glycosylate) dsitribute throughout gut lumen toxin A- damages enterocytes loss of epithelial integrity fluid secretion/inflammation acts as neutrophil chemoattractant (-->pseudomembrane) Toxin B- 10fold more potent, but similar to A |
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c. difficile
diagnosis/treatment |
confirm detection of cytotoxins in stool
enzyme immunoassay discontinue antibiotics treat with metronidazole/vancomycin |
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corynebacterium diphtheria
encounter |
throat is only known reservoir
asymptomatic carriers infections in children colonizes pharyngeal epithelium |
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c. diphtheria
damage |
diphtheria toxin
pseudomembrane local edema may cause paralysis of muscle groups damage to cardiac tissues may cause neurologic impairment (usually reversible over a few months) |
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c. diphtheria
gram staining, spore?, shape, metabolism, motility |
gram +
no spores rods facultative anaerobe non-motile |
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c. diphtheria
toxin |
only when infected with bacteriophage
AB toxin blocks protein syntehsis by ADP ribosylation of EF2 (~pseudomonas aeruginosa) |
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Diphtheria
disease/symptoms |
children
2-4 day incubation pharyngitis, fever, malaise pseudomembrane in throat (cell debris from tissue damage) 'bull neck' systemic (heart/neuro) effects from toxin absorption |
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C. Diphtheria
diagnosis/treatment/prevention |
vaccine-
to toxoid (D of DTaP) isolation of organism to confirm diagnosis antitoxin/antibiotic (antitoxin produced in horses) |
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bordetella pertussis
gram, shape, contagious?, disease |
gram-
rod highly contageous (close contact) whooping cough |
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bordetella pertussis
clinical stages |
1-catarrhal phase (7-14 days)
cold- URI, cough, most infectious 2-paroxysmal phase (2-4 weeks) 'whoop', low-grade/no fever, lymphocytosis 3-convalescent phase- (weeks-month) +/- seizures, chronic cough improves |
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bordetella pertussis
encounter, entry/colonization |
sick humans
cough-->aerosol (90% household rate) colonizes ciliated epithelium remains localized local inflamm- coughing, fever (catarrhal phase) |
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bordetella pertussis
damage |
most effects are toxin mediated
ciliated cells extruded mucus build up superinfection by other pathogens= potential complication cough reflex increases= whoop paroxysms--> cerebral hypoxia, apnea, small brain hemorrhage, encephalopathy |
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bordetella pertussis
virulence factors |
adhesins-
sugars integrins filamentous hemaglutinin pili |
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bordetella pertussis
pertussis toxin |
adhesin and toxin
AB toxin (A1B5) diarrhea of the throat A subunit binds GTPase Gi to continually activate adenylate cyclase--> high cAMP -increase resp secretions -hyperstim cough reflex -lymphocytes stop adhering to wall= lymphocytosis -diminished chemotaxis/oxidative killing by neutrophils |
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bordetella pertussis
other toxins (besides pertussis) |
adenylate cyclase toxin
also increases cAMP- binds calmodulin dermonecrotic toxin- tracheal cytotoxin- peptidoglycan fragment causes IL1 release--> extrusion of ciliated cells |
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bordetella pertussis
virulence factor regulation |
1- sensor BvgS = kinase
2- BvgA- regulated by BvgS influences FHA and pertussis toxin production |
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bordetella pertussis
treatment |
1- catarrhal phase-> antibiotic
2-paroxysmal phase- less bacteria, (effects from toxin) but antibiotic may help 2-supportive care to treat toxin damage *treat close contacts |
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bordetella pertussis
vaccine |
DPT (whole killed B pertussis)
had adverse rxns DTaP and Tdap use purified proteins for vaccination |
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mycoplasma pneumonia
|
atypical pneumonia
walking pneumonia nonlobar, patchy bulture negative |
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mycoplasma pneumoniae
general |
lacks murein wall
very small membranes contain sterols |
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oplasma pneumoniae
encounter- infection |
human reservoir
droplets from coughing moderately contageous attaches via P1 adhesive protein slow growing (2-3 week incubation) remains in URT |
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oplasma pneumoniae
spread, damage |
5-10% turn into tracheobronchitis or pneumonia
not tissue invasive (only resp mucosa) not destructive blocks ciliary action (leading to cough) causes sloughing of ciliated epithelium) elicits mononuclear inflitrate |
|
|
oplasma pneumoniae
diagnosis and treatment |
usually self-limited and not diagnosed
difficult to culture clinical picture suspicion not effected by cell wall antibiotics- treat with tetracycline, erythromycins |
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Legionella Pneumophila
risk factors, incubation |
community acquired pneumonia
increased incidence with central air age, smoking, COPD, immunosuppression predispose people 2-10 day incubation period can be nosocomial (25%) |
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Legionella Pneumophila
gram stain, shape, cell type infection |
gram -
bacillus infects amoebae-- accidentally infected human lung macrophages |
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Legionella Pneumophila
encounter/entry |
inhaled from aerosol
(live in protozoa in the water) never acquired from another person only infects susceptible people grow in macrophages (C3 helps) |
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Legionella Pneumophila
modification of living environment |
in macrophage phagosome-
isolates it (removes markers) pH neutral hijacks vesicles in transit ER-->Golgi uses type IV secretion to modify (DOT) |
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Legionella Pneumophila
replication |
within the phagosome
exponential phase= nonvirulent post-exponential= virulent (resistant to biocide, antibiotic, cytotoxic, osmotic) induced by AA starvation |
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Legionella Pneumophila
damage |
elicits vigorous immune response
microabscesses (infiltrate on chest x-ray) LPS contributes in inflammation |
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Legionella Pneumophila
host response |
IFN-gamma activates macrophages
downregulates transferrin receptor (suppressing growth) antibodies help neutrophil uptake |
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Legionella Pneumophila
diagnosis/treatment |
clinical suspicion
chest x-ray alveolar, unilateral slow culture treat with erythromycin, tetracycline, quinolones, macrolides |
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Brucella
gram, shape, special product, location of growth species |
gram -
rod makes urease intracellular b. abortus, b. suis, b. melitensis |
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brucella
general disease |
usually animal pathogens
people working with animals greatest risk causes granulomatous disease (brucellosis) |
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brucella
symptoms |
fever
headache anorexia granulomas lasts weeks-2years |
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brucella
encounter/spread |
unpasteurized dairy
skin/mucous membrane penetration disseminate to lymph nodes then to RES |
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brucella
growth/virulence |
can grow in unactivated macrophages
uses type IV secretion to promote formation of replicative vacuole (like legionella pneumophila) |
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brucella
chronic infection |
can survive in macrophages
gives undulant fever arthritis, epididymitis, orhcitis can persist for years in bone, joints, liver, spleen, kidney may form granulomas activation of macrophages by TH1 cells thought to play major role antibodies minor |
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brucella
diagnosis/treatment |
requires isolation
slow to culture antibiotics to penetrate macrophages can act in acid, intracellular multiple use, extended time (often relapses) treatment resembles TB treatment (bc slow growing intracellular) |
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chlamydia
two morphologic stages |
elementary body (EB) = compact infectious form in extrecellular environ
attaches to epithelium and induces phagocytosis Reticulate body- metabolically active modifies vesicle through type III (~EHEC/Salmonella) uses host for things they can't make- ex// ATP vesicle= inclusion bodies as nutrients are used up- reconverts to EBs |
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chlamydia pneumoniae
disease |
pharyngitis, bronchitis, pneumonia
transmitted through aerosols presence in atherosclerotic lesions presumably seed from respiratory infection |
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clamydia trachomatis
disease |
sexually transmitted
urogenital tract infections may also cause Trachoma- eye epithelial infection (mediated by flies) 45% of the time presents with gonorrhea may turn invasive--> lymphogranuloma venerium genital infection turns to systemic |
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chlamydia psittici
disease |
transmitted in aerosol-
generated by infected birds |
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clamydia trachomatis
in women |
PID, vaginal discharge, cervicitis, fever
untreated may scar fallopian tubes infertility, tubo-ovarian abscess, ectopic pregnancy pre-term labor and spontaneous abortion are a risk for pregnant women |
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clamydia trachomatis
in men |
urethritis- watery discharge
pain on urination prostatitis epididymitis proctitis (gay) |
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clamydia trachomatis
fetus/newborn |
purulent conjunctivits
mild pneumonia present 3-6 weeks even though acquired at birth rarely have long term consequences |
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clamydia trachomatis
diagnosis/treatment |
clinical suspician
DFA(fluorescent Ab)/ DNA probe test treat with antibiotics |
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Reiter's syndrom
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triggered by a variety of antigens (incl. chlamydia)
--arthritis --dermatitis --conjunctivitis |
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chlamydia pneumoniae disease
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community acquired pneumonia
mostly young adults/elderly pharyngitis, bronchitis, atypical pneumonia (~mycoplasma) culture is slow |
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chlamydia pneumoniae
atherosclerosis |
increased risk of symptomatic CAD
inflammation cause by colonization maybe? antibiotic trials haven't shown benefit |
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chlamydia psittaci
|
zoonotic pneumonia
most from contact with birds fevers, headache, rash, chest x-ray with patchy infiltrates |
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chlamydia (all kinds)
treatment |
doxycycline
or erythromycin or azythromycin (1 dose) |
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Rickettsiae
spore? where do they live? what is the reservoir? |
intracellular- endothelial
no spore depend on arthropod vectors for transmission btw humans |
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rickettsiae
general infection strategy |
induce endothelial uptake
escape from phagosome use actin for motility/transfer ~listeria/shigella |
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Rickettsiae
damage |
hemorrages in BV's
spots on skin can have serious consequences in the brain rocky mountain spotted fever can result in sepsis- multi organ failure |
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rickettsiae
diagnosis/treatment |
vasculitic rash (palpable purpura)
treat presumptively tetra/doxycyline may need IV antibiotics/supportive care |
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Coxiella burnetti
encounter |
atypical rickettsiae
hardy spore-like form can be infected via tick bite concentrations high in placental tissue- arerosol transmission during birth |
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coxiella burnetti
replication/spread |
lives in phagocytes
grows in phagolysosome only metabolically active at the low pH |
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coxiella burnetti
damage/ treatment |
varies widely
self-limiting flu like pneumonia chronic fever endocarditis common in chronic Q fever treat with tetracycline endocarditis requires cirpo also |
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mycobacterium tuberculosis
gram, shape, unique general features |
no gram stain = acid fast
aerobic slow-growing rod waxy coat |
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mycobacterium tuberculosis
pathogenesis factors |
slow growth- effects treatment
cell envelope- thick wax protect, limid bacteriocidal mechanisms, and antibiotics must be able to pass through pores RD1- secretion system (~Type III) spontaneously lost = BCG vaccine |
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mycobacterium tuberculosis
encounter |
brief encounters are low risk
close contacts can get infected droplet nuclei during active disease |
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mycobacterium tuberculosis
entry |
once in alveoli, ingested by macrophages
survives as intracellular pathogen arrests normal phagosome maturation- stays a vacuole pH neutral may spread to other sites- upper lobes most oxygenated and best |
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mycobacterium tuberculosis
infection outcomes |
stable control- 90% of immunocompetent have 'latent disease'
10% of immunocompetent (and higher immunosuppressed) get primary disease genetic factors play a role 'lubeck disaster' |
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directly observed therapy (DOT)
|
to prevent Multi drug resistant TB
(50% incidence for relapse) long course- and patients usually feel better early on |
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mycobacterium tuberculosis
reactivation disease |
if latent TB carrier becomes immunodeficient (stress, illness, etc.)
caseous necrotic lesions can liquefy and discharge-- spreading |
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mycobacterium tuberculosis
damage |
immune mediated
cytokines release by macrophages IL1--> fever TNF--> weight loss |
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mycobacterium tuberculosis
diagnosis |
AFB staining of sputum (fast, insensitive)
culture (slow, definitive) PPD test (tests immune response, not disease) may have false positive with previous BCG vaccination may have false negative with immunocompromised patients |
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mycobacterium tuberculosis
treatment |
isoniazid
rifampin pyrazinamide ethambutol careful to avoid resistance heterogeneity of population- growing/dormant, intra/extracellular etc. |
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mycobacterium leprae
growth, gram stain, culture, disease |
leprosy/Hansen's diases
rapid- m. fortuitum skin/nail infections after foot baths, sternal wounds after surgery slow- m. avium intermediate- m. marinum fish tank granuloma uncultivable in vitro gram+ AND acid fast |
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mycobacterium leprae
pathology (2 types) |
tuberculoid-
few bacteria, abundant lymphocytes with well formed granulomas lepromatous numerous bacteria, few lymphocytes, without well-formed granuloma |
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mycobacterium leprae
m. avium (most common) |
= slow growing
chronic pulmonary disease no person-person spread environmental organisms |
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pseudomona aeruginosa
gram staining, metabolism, typical infection reservoir |
gram -
aerobe hospital acquired opportunist |
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pseudomonas auruginosa 3 virulence factors
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1- metabolic diversity
just needs moisture, can survive in disinfectant, distilled water, rubber stoppers, resistance to drying 2- membrane has relatively small pores and has multi-drug pumps 3-versatility in pathogenicity plants, nematodes, insects, secretes toxins, degredative enzymes, and type III toxin secretion despite this- generally self-limiting in healthy individuals |
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pseudomonas auruginosa
encounter/colonization |
soil/water
may be found on humans (stool, auditory canal) hot tubs, contact lens solution, shoes colonization in hospital approaches 50% |
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pseudomonas auruginosa
introduction to host |
skin/mucous membrane disruption
medical devices pili produced- help colonize epithelia single polar flagella |
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pseudomonas auruginosa
damage |
PROTEASES: elastase, alkaline protease, lylendopeptidase
MEMBRANE DAMAGE: cytotoxin, phospholipase C INTRACELLULAR TOXINS: exotoxin A (~diphtheria), exotoxins S,T, U LPS: endotoxin |
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pseudomonas auruginosa
disease manifestation |
CF- lower respiratory tract-->COPD
Otitis externa- swimmers ear Dermatitis- Hot tub Endocarditis - (IV drug use) Keratitis- (contact lens solution) Bone/joint infections- drug uses, sneaker osteomyelitis, diabetic foot infections |
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pseudomonas auruginosa
nosocomial |
bacteremia (IV cath)
pneumonia UTI wound infections |
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pseudomonas auruginosa
diagnosis/treatment |
culture- grows readily
antibiotics |
