Unit 1 Flashcards
1
Q
three factors that drive whether or not a pathologic agent will cause disease
A
- susceptible host - conducive environment - pathogen
2
Q
____ is the ability of an organism to cause disease
A
pathogenicity
3
Q
____ is the degree of pathology caused by the organism (and is dependent on conditions)
A
virulence
4
Q
what variety of organism only invades host cells when they can gain a selective advantage in the host
A
facultative intracellular pathogens
5
Q
list some ways pathogens can be transmitted
A
- animal vectors - direct contact - fomites - droplets - airborne - fecal-oral
6
Q
list the general immune responses to infection in the order that a pathogen meets them
A
physical barriers innate immunity adaptive immunity (humoral and cellular)
7
Q
____ is the ecological community of commensal, symbiotic, and pathogenic microorganisms found in and on all multicellular organisms
A
microbiota
8
Q
what is the function of flagella and another name for them
A
- motility - H Antigen
9
Q
what is the function of Pili/fimbriae and another name for them
A
- adhesion - F Antigen
10
Q
Capsules
composition?
function?
A
composition: polysaccharide and water function: antiphagocytic and protects against complement
11
Q
what is the key ingredient in bacterial cell walls
A
peptidoglycan cross-linked with NAM and NAG
12
Q
what is the cell wall composition for gram positive bacteria
A
very thick peptidoglycan layer and a thin inner plasma membrane
13
Q
____ and ____ guide the immune response for gram positive bacteria
A
teichoic and lipoteichoic acids
14
Q
what is the cell wall composition for gram negative bacteria
A
a sandwich of outer membrane, peptidoglycan, and plasma membrane
15
Q
what induces inflammation/immune response in gram negative bacteria
A
the Lipid A portion of Lipopolysaccharide
16
Q
why are gram negative bacteria more prone to a toxic immune response
A
the Lipid A portion of Lipopolysaccharide isn’t “visible” until the cell lyses, and then acts as an endotoxin and triggers a cytokine storm
17
Q
what is a virulence factor
A
any bacterial factor that enhances a bacterium’s ability to colonize, invade, replicate within, and/or damage the host
18
Q
what is Koch’s postulate
A
that virulence factors are encoded by genes and if these genes are inactivated then the pathogen is less virulent
19
Q
what process does pili/fimbriae
A
adhesion (enhances it)
20
Q
what process do toxins and exoenzymes affect
A
invasion of tissues (break down barriers that hold host cells together)
21
Q
what process do capsules affect
A
immune invasion
22
Q
____ are proteins produced and secreted by bacteria with a specific activity
A
exotoxins
23
Q
____ are part of the bacterial cell wall that is usually released when the bacterium is lysed (Lipopolysaccharide in gram negatives)
A
endotoxins
24
Q
four ways that exotoxins can act as super antigens to cause sepsis and shock
A
- damage cell membrane - disrupt signaling pathways - act of extracellular tissue - cause constant immune stimulation
25
a ____ is an organism that grows on and derives nourishment from dead or decaying organic matter (soil)
saprophyte
26
fungi are known as ____ because they require external carbon
heterotrophs
27
what makes up a mold
mycelium made of hyphae
28
molds that have hyphae with septa are:
septate
29
molds that have hyphae without septa are:
coenocytic
30
molds that are pigmented are:
dematiaceous
31
molds that aren't pigmented are:
hyaline
32
a fungi (usually pathogenic) that is a mold at room temperature and yeast at body temperature is known as a:
dimorphic
33
three components found in the fungal cell wall
chitin, glucans, and mannoproteins
34
two components of the fungal cell membrane
- phospolipid bilayer
- sterols such as ergosterol, zymosterol (not cholesterol)
35
spores are fungal reproductive structures that germinate and yield a new \_\_\_
mycelium
36
what fungal spore structure is shown?
a sporangium filled with sporangiospores
37
what fungal spore structure is shown?
arthrospores
38
what fungal spore structure is shown?
a: macroconidia
b: microconidia
39
what fungal spore structure is shown?
blastospores
40
what fungal spore structure is shown?
chlamydospores
41
what fungal spore structure is shown?
zygospore
42
list some predisposing factors to fungal invasion
- immunosuppression (stress, steroids, diabetes, autoimmune)
- prolonged antibiotic therapy
- immune defects
- immaturity, aging, malnutrition
- heavy exposure to spores
- compromized tissues
- persistently moist skin
43
what is the function of the polyene **Amphotericin B**
kills fungi by binding both ergosterol and cholesterol
can cause nephrotoxicity
44
what is the mechanism of action of the antifungal class: **azoles**
inhibit synthesis of ergosterol, which disrupts the cell membrane
fungistatic (not fungicidal) so it takes prolonged treatment because several generations have to pass
45
what is the mechanism of action of the antifungal class: **allylamines**
inhibit
46
allylamines are especially good for treating \_\_\_\_\_
dermatophytes
47
what drug would you use to treat Candida or Cryptococcus
Flucytosine
48
an _____ is a naturally occuring chemical, whereas an ______ is a naturally occuring _or_ manmade chemical
an **_antibiotic_** is a naturally occuring chemical, whereas an **_antimicrobial_**is a naturally occuring _or_ manmade chemical
49
four mechanisms of action of antimicrobials
1: affect cell wall/membrane integrity
2: interfere with protein synthesis
3: impede DNA repair and replication
4: block metabolic pathways
50
what is the mechanism of action of β-Lactams
they **inhibit cell wall synthesis** by binding to the enzymes involved in the production or cross-linking of peptidoglycan
51
three main classes of β-Lactams
- penicillins
- cephalosporins
- carbapenems
52
how often are carbapenems used
not often. theyre saved as the last resort antibiotics
53
which class of β-Lactams is known for being more resistant to **β-Lactamases**
cephalosporins
54
what is the mechanism of action of glycopeptides
inhibit cell wall synthesis (different class than beta lactams though)
55
what is the mechanism of action of **Polymyxins**
disrupt cell membrane phospholipids by binding the Lipid A region of LPS
56
what formulation are polymyxins usually given in and why
mostly topicals because the systemic form causes nephrotoxicity and neurotoxicity
57
what are some examples of drug classes that inhibit protein synthesis
- tetracyclines
- macrolides
- lincosamides
- aminoglycosides
- phenicols
58
three classes of drugs that affect nucleic acids
fluoroquinolones
nitroimidazoles
nitrofurans
59
two classes of drugs that disrupt the folic acid pathway
sulfonamides
trimethoprim
60
what are some good antibacterials for anaerobes
nitroimidazoles
beta-lactams
macrolides
tetracyclines
61
what are some bad antibacterials for anaerobes
aminoglycosides
fluoroquinolones
62
what would be a good antibacterial for a mycoplasma (no cell wall)
tetracyclines
macrolides
lincosamides
63
what is a good choice of antibacterial for intracellular bacterial
tetracyclines
phenicols
macrolides
lincosamides
64
what drugs would you administer to cover a four-quadrant approach
beta-lactam with metranidazole
65
what is a "four quadrant approach" and when is it important
a four quadrant approach affects gram positives, gram negatives, aerobic, and anaerobic organisms
important is critical situations where you cant wait for a culture result
66
what is **intrinsic resistance**
an innate ability to resist through structural or functional characteristics and not through genomic changes (these organisms have never been susceptible)
67
why dont aminoglycosides work on anaerobes
they lack the oxidative metabolism needed to uptake aminoglycosides
68
what are some characteristics/structures of biofilms that help with intrinsic resistance
- electrical charge
- efflux pumps in the slime
- slow growing cells at the bottom layer (so theyre hard to kill)
69
four mechanisms of antibiotic resistance
- pump out the drug (efflux pumps)
- modify/ inactivate the drug (enzymes)
- modify the drug target
- inhibit drug uptake (modified cell wall proteins)
70
three methods of acquired resistance
mutation of current genes
acquisition of foreign genes
combination of both
71
what is acquired resistance
bacteria obtains the ability to resist the activity of a particular agent to which it was previously susceptible
72
what is a plasmid
a circle of DNA that can move between cells
73
what is a transposon
small piece of DNA that moves back and forth between chromosomes and plasmids
74
how can bacteriophages enable horizontal gene transfer
they attack bacteria and can carry DNA from germ to germ
75
what are the three methods of horizontal gene transfer
transduction (movement via phages)
conjugation (germs connect directly)
transformation (genes released from nearby and picked up by another germ)
76
what are some ways to avoid the judicious use of antibacterials
- culture and sensitivity (low budget? gram stain)
- avoid combination therapy unless indicated
- identify compliance issues
- prevent in-house infections
77
four common ailments/procedures that dont call for antimicrobials
- feline lower urinary tract disease
- spay/neuter
- feline upper respiratory disease (usually viral)
- kennel cough (self-limiting)
78
what can you do instead of medicated milk replacer
adequate colostrum within 24 hours
husbandry and management
79
what can you do instead of using antibiotics for neonatal scours
rehydrate only unless systemic
colostrum management
hygiene & cleanliness
reduce stress
regulate traffic flow
vaccination protocols
80
what can you do instead of using antibiotics for mastitis
culture samples with high somatic cell count (number of neutrophils in the milk)
dont treat if about to cull or dry off
MANAGEMENT
81
How can you prevent bovine respiratory disease
wean/castrate/dehorn at least 30 days prior to shipping (stress)
parasite treatment
vaccinate
biosecurity
82
four instances where a four quadrant approach would be indicated
pilonephritis (kidney infection)
prostatitis
pneumonia
sepsis
83
**Ringworm**
disease name:
location on host body:
zoonotic?
**Ringworm**
disease name: _dermatophytosis_
location on host body: _keratinized structures (hair, skin, nails)_
zoonotic? _YES, can jump species_
84
how is dermatophytosis (ringworm) diagnosed and treated
diagnosed suggestively with Wood's lamp (UV) and definitively with a DTM culture.
treated with topical therapy
85
**Dermatomycosis**
what pathogen:
predisposing factors:
effect of overgrowth:
**Dermatomycosis**
what pathogen: *_Malassezia pachydermatis_*
predisposing factors: _immunosupression (normally is present in small numbers)_
effect of overgrowth: _dermatitis and otitis_
86
**Aspergillosis**
species affected:
contracted by:
other:
**Aspergillosis**
species affected: _birds, horses (guttural pouch mycosis), dogs (nasal aspergillosis), cattle (placentitis/abortion)_
contracted by: _usually inhalation of spores_
other: _factors into otitis, abortion, mastitis, and systemic disease_
87
**histoplasmosis**
form:
found (environment and geographical):
symptoms:
**histoplasmosis**
form: _dimorphic, soil saprophyte and yeast in body_
found (environment and geographical): _soil in areas with bird and bat feces. Mississippi and Ohio River Valley_
symptoms: _granulomatous lung lesions and possible disseminated disease_
88
list two important pyogenic (induce pus formation) bacteria
Saphylococcus,
Streptococcus
89
**Staphylococci**
Morphology:
arrangement:
oxygen needs:
behavior:
**Staphylococci**
Morphology: _gram positive cocci_
arrangement: _clusters_
oxygen needs: _most are facultative anaerobes_
behavior: _opportunistic, colonize nasal cavity, nasopharynx, skin, and mucous membranes_
90
what is the main pathogen that causes abscesses, mastitis, dermatitis, and "bumble foot"
Staphylococcus aureus
91
what is the main pathogen that causes canine and feline pyoderma
Staphylococcus pseudintermedius
92
three main virulence factors of staphylococcus aureus
- secreted factors (toxins, enzymes, and invasins)
- membrane-bound factors (adhesins)
- capsule/slime layer
93
**Streptococci**
Morphology:
arrangement:
oxygen needs:
behavior:
other:
**Streptococci**
Morphology: _gram positive cocci_
arrangement: _chains_
oxygen needs: _facultative anaerobes_
behavior: _commensal organisms of the upper respiratory mucosa and lower urogenital mucosa_
other: _most have capsule_
94
list some bacteria that belong in the group **Enterobacteriaceae**
Escherichia coli
Salmonella
Yersinia (plague)
Enterobacter
95
many Enterobacteriaceae are considered **Coliforms.** what does this mean?
they are **gram-negative rods, non-spore forming, and ferment lactose** and are found in large numbers in feces of warm-blooded animals
96
**Escherichia coli**
morphology:
predisposed individuals:
general symptoms:
symptoms in freshly weaned pigs:
**Escherichia coli**
morphology: _enterobacteriaceae so gram-negative rods_
predisposed individuals: _young animals without established immune system_
general symptoms: _neonatal sepsis and diarrhea, UTI from fecal contamination_
symptoms in freshly weaned pigs: _conjunctivits and ciguatoxin (bloody eyes)_
97
**Clostridium**
morphology:
large, spore-forming, gram-positive rods
98
list two main endospore forming bacterium
bacillus and clostridium
99
list the four types of exotoxin driven disease caused by clostridia
- Neurotoxic (tetanus and botulism)
- histotoxic (blackleg, bacillary hemoglobinuria)
- enteropathogenic (clostridial enterocolitis)
- atypical (Tyzzer's Disease)
100
what makes Mycobacterium hard to kill and stain
their cell wall is lipid rich
101
**Mycobacterium**
symptoms:
treatment issue:
zoonitic?
**Mycobacterium**
symptoms: _chronic granulomatous lesions (macrophages)_
treatment issue: _multidrug resistance_
zoonitic? _YES, especially bovine tuberculosis_
102
**Rickettsiales**
oxygen requirements:
obligate intracellular
103
what is the tissue target of **Rickettsiaceae**
vascular endothelium
104
what is the tissue target of **Anaplasma**
erethrocytes, platelets, and leukocytes
105
what is the tissue target of **Ehrlichia**
leukocytes
106
what is the tissue target of **Neorickettsia**
leukocytes
107
what is sepsis
sepsis occurs when an infection triggers the systemic inflammatory response system (SIRS) and the body is unable to maintain a physiological normal and leads to DIC and death
infection + SIRS = sepsis
108
list some common presenting clinical signs of sepsis
bounding to weak pulses,
brick red mucous membranes (dog),
pale mm (cat),
fever (dogs) or hypothermia (cats),
tachypnea,
hypotension,
lethargy
109
what lab abnormalities are common for an animal in sepsis
anemia (esp cats),
elevated hematocrit,
left shift and toxic change,
thrombocytopenia,
hyperlactemia,
clotting disorders
110
disease of what system is most likey to result in sudden death
cardiovascular
111
list some common bacterial causes of sudden death
anthrax, clostridial disease, anaplasmosis, salmonella, Leptospirosis, MRSA, Streptococcus equi, acute pneumonia
112
list some common viral causes of sudden death
Classical and African swine fever, distemper
113
list some common toxin-driven causes of sudden death
bracken fern, sweet clover, lead, blister beetles
114
list some common trauma causes of sudden death
lightnight strike, bloat, colic
115
**Bacillus anthracis**
morphology:
longevity:
oxygen requirements:
**Bacillus anthracis**
morphology: gram-positive spore-forming saprophyte
longevity: spores remain viable in soil for 50 years
oxygen requirements: facultative anaerobic
116
what are the presenting clinical signs of a _ruminant_ with anthrax
peracute:
acute:
peracute/acute:
what are the presenting clinical signs of a _ruminant_ with anthrax
peracute: SUDDEN DEATH
acute: high fever, weakness, convulsions, death
peracute/acute: tachycardia, tachypnea, melena, bloody milk
117
presenting clinical signs of a _horse_ with anthrax
rapidly developing subcutaneous edema, fever, severe colic, bloody diarrhea, death in 2-3 days
118
presenting clinical signs of a _dog_ with anthrax
pharyngeal edema, gastroenteritis
119
describe the lesions found during an anthrax necropsy
"blackberry jam" spleen, hemorrhages of skin and lymph nodes, bloody discharge from orifices, failure of blood to clot, delayed or incomplete rigor mortis
120
list three virulence factors of anthrax
capsule (inhibits phagocytosis)
tripartitie exotoxin
host macrophages (release toxic contents when they explode)
121
what cell recognizes and engulfs anthrax spores in the host
macrophages
122
describe how Tripartite Exotoxin of Anthrax works
- **protective antigen** forms a hole for entry of other toxins
- **edema factor** causes fluid release and edema
- **lethal factor** inhibits cytokine release
123
list some techniques helpful for diagnosing anthrax
paying attention to the time of year
blood smears allowed to grow
culture
PCR
124
what should you do for necropsy of a suspected anthrax case
collect blood with needle and syringe from ear or tail vein
do not send ears
if animal is already open, collect spleen (otherwise leave carcass closed so vegetative cells will die eithout sporulating)
125
how is anthrax treated
prevented
treated with penicillin, tetracyclines, and quarantine
prevented by live vaccination
126
Anthrax zoonosis
most common transmission route:
highest mortality rate route:
Anthrax zoonosis
most common transmission route: _cutaneous (from contacting an infected carcass)_
highest mortality rate route: _inhalation_
127
list four clostridial agents and the disease they cause that are associated with toxemia induced fatality
Blackleg: Clostridium chauvoei
Bacillary Hemoglobinuria: Clostridium haemolyticum
Malignant Edema: Clostridium septicum
Hemorrhagic bowel: Clostridium perfringens A
128
**Feline Infectious Anemia**
pathogen:
signalment:
signs:
transmission:
**Feline Infectious Anemia**
pathogen: Mycoplasma haemofelis
signalment: outdoor males
signs: weakness, pallor, tachypnea, tachycardia, collapse
transmission: fleas and bite wounds (blood contact)
129
**Mycoplasma haemofelis**
appearance on blood smear
epicellular, small gram-negative rods on the periphery of RBC
130
why might a cat come up positive on PCR for FIA but their blood smear was clear
FIA is cyclical anemia, the pathogen is at lowest when RBC number is lowest
131
how is FIA treated
supportive care (oxygen and transfusion), doxycycline, and enrofloxacin/marbofloxacin
will not be completely eliminated
132
is FIA zoonotic?
rarely. usually it is species specific
133
**cat scratch fever**
pathogen:
signalment:
transmission:
symptoms:
zoonotic?
**cat scratch fever**
pathogen: Bartonella henselae
signalment: shelter kittens, especially young or immunosupressed
transmission: fleas
symptoms: lymphadenopathy and contributes to endocarditis
zoonotic? yes, but self limiting
134
**Bovine anaplasmosis**
pathogen:
symptoms:
transmission:
**Bovine anaplasmosis**
pathogen: Anaplasma marginale
symptoms: progressive anemia due to extravascular destruction of erythrocytes
transmission: ticks or used needles
135
**anaplasma marginale**
morphology:
how it causes disease:
**anaplasma marginale**
morphology: gram-negative obligate intraerythrocytic cocci
how it causes disease: the erythrocytes get coated in antibodies that are phagocytosed by macrophages in the spleen and liver
136
does anaplasmosis cause hemoglobinuria?
does babesia?
does anaplasmosis cause hemoglobinuria? **NO**
does babesia? **YES**
137
Anaplasmosis
diagnosis:
Treatment:
prevention:
Anaplasmosis
diagnosis: cELISA is gold standard. blood smear
Treatment: tetracycline or Imidocarb
prevention: vector control and good hygiene
138
**Canine Cyclic Thrombocytopenia**
pathogen:
action:
transmission:
**Canine Cyclic Thrombocytopenia**
pathogen: Anaplasma platys
action: infects platelets and cause thrombocytopenia
transmission: tick vector
139
**Bacillary Hemoglobinuria**
pathogen:
primary sign:
**Bacillary Hemoglobinuria**
pathogen: Clostridium haemolyticum
primary sign: intravascular hemolysis causes hemoglobinuria ("red wine urine")
140
**Rocky Mountain Spotted Fever**
pathogen:
role of ticks:
clinical signs:
**Rocky Mountain Spotted Fever**
pathogen: Rickettsia rickettsii
role of ticks: vector AND reservoir (must be attached for 5-20 hours)
clinical signs: vasculitis
141
**rocky mountain spotted fever**
diagnosis:
treatment:
zoonotic:
**rocky mountain spotted fever**
diagnosis: paired sera taken 10-14 days apart (ELISA)
treatment: doxycycline
zoonotic: yes but from ticks not dogs
142
describe the Ehrlichia spp. life cycle
- taken into a leukocyte
- it envades lysosomes through inhibition of phagosome-lysosome fusion and undergoes binary fission to replicate
- clusters of bacteria form morulae (like a lil pouch of bacteria)
- exit and spread through lysis and cytoplasmic projections
143
**Canine Monocytic Ehrlichiosis**
pathogen:
vector:
treatment:
**Canine Monocytic Ehrlichiosis**
pathogen: Ehrlichia canis
vector: brown dog tick
treatment: doxycycline for 3 weeks
144
Ehrlichia acute phase symptoms
fever, anorexia, occulonasal discharge, lymphadenopathy, limb edema, possible nerve deficits, thrombocytopenia
145
Ehrlichia chronic phase symptoms
splenomegaly, renal failure, pneumonitis, uveitis, meningitis, severe thrombocytopenia, pancytopenia, severe weight loss
146
four diseases tested for by the SNAP 4Dx Plus
Heartworm (Dirofilaria immitis)
Lyme Disease (Borrelia burgdorferi)
Ehrlichiosis (E. canis and E. ewingii)
Anaplasma
147
**Canine Granulocytic Ehrlichiosis**
pathogen:
vector:
symptoms:
treatment:
**Canine Granulocytic Ehrlichiosis**
pathogen: Ehrlichia ewingii
vector: lone star tick
symptoms: polyarthritis, lameness, joint swelling, stiff gait
treatment: doxycycline
148
**Equine Granulocytic Ehrlichiosis**
pathogen:
vector:
symptoms:
**Equine Granulocytic Ehrlichiosis**
pathogen: Anaplasma phagocytophilum
vector: Ixodes ticks
symptoms: necrotizing vasculitis, fever, anorexia, depression, limb edema, petechiation, icterus
149
how is Equine Granulocytic Ehrlichiosis
detected:
treated:
how is Equine Granulocytic Ehrlichiosis
detected: PCR, IFA
treated: oxytetracycline and tick control
150
Equine Monocytic Ehrlichiosis (Potomac Horse Fever)
pathogen:
causes:
vector:
Equine Monocytic Ehrlichiosis (Potomac Horse Fever)
pathogen: Neorickettsia risticii
causes: acute enterocolitis
vector: trematodes
151
**Tularemia**
Pathogen:
zoonosis:
vector:
easily confused with:
**Tularemia**
Pathogen: Francisella tularensis
zoonosis: very very. most common in sheep, cats, and rabbits
vector: ticks
easily confused with: plague, pseudotuberculosis, pneumonia
152
Francisella tularensis
morphology:
infects:
which subspecies is worse:
Francisella tularensis
morphology: gram-negative facultative intracellular coccobacillus
infects: macrophages
which subspecies is worse: Type A is highly virulent and found in NA only
153
three ways Tularemia can be transmitted and their resulting forms
- aerosol transmission: pneumonic form
- direct contact: ulceroglandular or occuloglandular forms
- ingestion: oropharyngeal or typhoidal form
154
four steps of Tularemia pathogenesis
- local ulcerative lesion
- local lymphadenopathy
- transient bacteremia
- spread to lymph nodes, liver, spleen, bone marrow, and sometimes lung
155
Tularemia
diagnosis:
treatment:
Tularemia
diagnosis: culture, 4-fold increase in antibody titers, lymph node aspirate/biopsy
treatment: isolation, tetracycline, streptomycin, gentamicin, fluoroquinolones
156
**Plague**
pathogen:
morphology:
zoonosis:
transmission:
**Plague**
pathogen: Yersinia pestis
morphology: small gram-negative coccobacillus
zoonosis: yes. rodents, humans, cats, and dogs
transmission: fleas
157
three forms of plague
bubonic form
septicemic form
pneumonic form
158
plague
diagnosis:
treatment:
plague
diagnosis: lymph node aspirates, biopsies
treatment: aminoglycosides and tetracyclines for three weeks
159
**Glanders**
pathogen:
zoonosis:
transmission:
pathogenesis:
**Glanders**
pathogen: Burkholderia mallei
zoonosis: yes. mostly equids but also cats and humans
transmission: ingestion of food or water contaminated with nasal discharges
pathogenesis: ulcerative nodules in nasal cavity, respiratory tract, lungs, and skin resulting in septicemia
160
**Melioidosis**
pathogen:
morphology:
species affected:
pathogenicity:
**Melioidosis**
pathogen: Burkholderia pseudomallei
morphology: motile gram-negative facultative anaerobe
species affected: sheep goats and pigs but zoonotic through mastitic milk
pathogenicity: suppurative or caseous lesions of lungs, liver, spleen, lymph nodes, or SQ tissue
161
signs of right-sided heart failure
ascites, GI congestion (causes anorexia, GI distress, and weight loss), liver congestion
162
signs of left sided heart failure
decreased cardiac output
pulmonary congestion
163
definition of endocarditis
inflammation of the inner layer of the heart (endocardium)
164
what are the steps that lead to vegetative lesions of the heart and what are they composed of
microbial colonization of the heart valves because of the turbulence there. microbes expose underlying collagen. platelets aggregate on collagen. coagulation cascade is activated.
vegetative lesions are aggregates of platelets, fibrin, blood, and bacteria
165
