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Bacteriology/Mycology > Unit 1 > Flashcards

Unit 1 Flashcards

1
Q

three factors that drive whether or not a pathologic agent will cause disease

A
  • susceptible host - conducive environment - pathogen
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2
Q

____ is the ability of an organism to cause disease

A

pathogenicity

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3
Q

____ is the degree of pathology caused by the organism (and is dependent on conditions)

A

virulence

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4
Q

what variety of organism only invades host cells when they can gain a selective advantage in the host

A

facultative intracellular pathogens

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5
Q

list some ways pathogens can be transmitted

A
  • animal vectors - direct contact - fomites - droplets - airborne - fecal-oral
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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)

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7
Q

____ is the ecological community of commensal, symbiotic, and pathogenic microorganisms found in and on all multicellular organisms

A

microbiota

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8
Q

what is the function of flagella and another name for them

A
  • motility - H Antigen
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9
Q

what is the function of Pili/fimbriae and another name for them

A
  • adhesion - F Antigen
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10
Q

Capsules

composition?

function?

A

composition: polysaccharide and water function: antiphagocytic and protects against complement

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11
Q

what is the key ingredient in bacterial cell walls

A

peptidoglycan cross-linked with NAM and NAG

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12
Q

what is the cell wall composition for gram positive bacteria

A

very thick peptidoglycan layer and a thin inner plasma membrane

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13
Q

____ and ____ guide the immune response for gram positive bacteria

A

teichoic and lipoteichoic acids

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14
Q

what is the cell wall composition for gram negative bacteria

A

a sandwich of outer membrane, peptidoglycan, and plasma membrane

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15
Q

what induces inflammation/immune response in gram negative bacteria

A

the Lipid A portion of Lipopolysaccharide

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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

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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

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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

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19
Q

what process does pili/fimbriae

A

adhesion (enhances it)

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20
Q

what process do toxins and exoenzymes affect

A

invasion of tissues (break down barriers that hold host cells together)

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21
Q

what process do capsules affect

A

immune invasion

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22
Q

____ are proteins produced and secreted by bacteria with a specific activity

A

exotoxins

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23
Q

____ are part of the bacterial cell wall that is usually released when the bacterium is lysed (Lipopolysaccharide in gram negatives)

A

endotoxins

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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
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25
Q

a ____ is an organism that grows on and derives nourishment from dead or decaying organic matter (soil)

A

saprophyte

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26
Q

fungi are known as ____ because they require external carbon

A

heterotrophs

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27
Q

what makes up a mold

A

mycelium made of hyphae

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28
Q

molds that have hyphae with septa are:

A

septate

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29
Q

molds that have hyphae without septa are:

A

coenocytic

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30
Q

molds that are pigmented are:

A

dematiaceous

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31
Q

molds that aren’t pigmented are:

A

hyaline

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32
Q

a fungi (usually pathogenic) that is a mold at room temperature and yeast at body temperature is known as a:

A

dimorphic

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33
Q

three components found in the fungal cell wall

A

chitin, glucans, and mannoproteins

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34
Q

two components of the fungal cell membrane

A
  • phospolipid bilayer
  • sterols such as ergosterol, zymosterol (not cholesterol)
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35
Q

spores are fungal reproductive structures that germinate and yield a new ___

A

mycelium

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36
Q

what fungal spore structure is shown?

A

a sporangium filled with sporangiospores

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37
Q

what fungal spore structure is shown?

A

arthrospores

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38
Q

what fungal spore structure is shown?

A

a: macroconidia
b: microconidia

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39
Q

what fungal spore structure is shown?

A

blastospores

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40
Q

what fungal spore structure is shown?

A

chlamydospores

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41
Q

what fungal spore structure is shown?

A

zygospore

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42
Q

list some predisposing factors to fungal invasion

A
  • immunosuppression (stress, steroids, diabetes, autoimmune)
  • prolonged antibiotic therapy
  • immune defects
  • immaturity, aging, malnutrition
  • heavy exposure to spores
  • compromized tissues
  • persistently moist skin
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43
Q

what is the function of the polyene Amphotericin B

A

kills fungi by binding both ergosterol and cholesterol

can cause nephrotoxicity

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44
Q

what is the mechanism of action of the antifungal class: azoles

A

inhibit synthesis of ergosterol, which disrupts the cell membrane

fungistatic (not fungicidal) so it takes prolonged treatment because several generations have to pass

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45
Q

what is the mechanism of action of the antifungal class: allylamines

A

inhibit

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46
Q

allylamines are especially good for treating _____

A

dermatophytes

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47
Q

what drug would you use to treat Candida or Cryptococcus

A

Flucytosine

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48
Q

an _____ is a naturally occuring chemical, whereas an ______ is a naturally occuring or manmade chemical

A

an antibiotic is a naturally occuring chemical, whereas an antimicrobialis a naturally occuring or manmade chemical

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49
Q

four mechanisms of action of antimicrobials

A

1: affect cell wall/membrane integrity
2: interfere with protein synthesis
3: impede DNA repair and replication
4: block metabolic pathways

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50
Q

what is the mechanism of action of β-Lactams

A

they inhibit cell wall synthesis by binding to the enzymes involved in the production or cross-linking of peptidoglycan

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51
Q

three main classes of β-Lactams

A
  • penicillins
  • cephalosporins
  • carbapenems
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52
Q

how often are carbapenems used

A

not often. theyre saved as the last resort antibiotics

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53
Q

which class of β-Lactams is known for being more resistant to β-Lactamases

A

cephalosporins

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54
Q

what is the mechanism of action of glycopeptides

A

inhibit cell wall synthesis (different class than beta lactams though)

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55
Q

what is the mechanism of action of Polymyxins

A

disrupt cell membrane phospholipids by binding the Lipid A region of LPS

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56
Q

what formulation are polymyxins usually given in and why

A

mostly topicals because the systemic form causes nephrotoxicity and neurotoxicity

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57
Q

what are some examples of drug classes that inhibit protein synthesis

A
  • tetracyclines
  • macrolides
  • lincosamides
  • aminoglycosides
  • phenicols
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58
Q

three classes of drugs that affect nucleic acids

A

fluoroquinolones

nitroimidazoles

nitrofurans

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59
Q

two classes of drugs that disrupt the folic acid pathway

A

sulfonamides

trimethoprim

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60
Q

what are some good antibacterials for anaerobes

A

nitroimidazoles

beta-lactams

macrolides

tetracyclines

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61
Q

what are some bad antibacterials for anaerobes

A

aminoglycosides

fluoroquinolones

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62
Q

what would be a good antibacterial for a mycoplasma (no cell wall)

A

tetracyclines

macrolides

lincosamides

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63
Q

what is a good choice of antibacterial for intracellular bacterial

A

tetracyclines

phenicols

macrolides

lincosamides

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64
Q

what drugs would you administer to cover a four-quadrant approach

A

beta-lactam with metranidazole

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65
Q

what is a “four quadrant approach” and when is it important

A

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

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66
Q

what is intrinsic resistance

A

an innate ability to resist through structural or functional characteristics and not through genomic changes (these organisms have never been susceptible)

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67
Q

why dont aminoglycosides work on anaerobes

A

they lack the oxidative metabolism needed to uptake aminoglycosides

68
Q

what are some characteristics/structures of biofilms that help with intrinsic resistance

A
  • electrical charge
  • efflux pumps in the slime
  • slow growing cells at the bottom layer (so theyre hard to kill)
69
Q

four mechanisms of antibiotic resistance

A
  • pump out the drug (efflux pumps)
  • modify/ inactivate the drug (enzymes)
  • modify the drug target
  • inhibit drug uptake (modified cell wall proteins)
70
Q

three methods of acquired resistance

A

mutation of current genes

acquisition of foreign genes

combination of both

71
Q

what is acquired resistance

A

bacteria obtains the ability to resist the activity of a particular agent to which it was previously susceptible

72
Q

what is a plasmid

A

a circle of DNA that can move between cells

73
Q

what is a transposon

A

small piece of DNA that moves back and forth between chromosomes and plasmids

74
Q

how can bacteriophages enable horizontal gene transfer

A

they attack bacteria and can carry DNA from germ to germ

75
Q

what are the three methods of horizontal gene transfer

A

transduction (movement via phages)

conjugation (germs connect directly)

transformation (genes released from nearby and picked up by another germ)

76
Q

what are some ways to avoid the judicious use of antibacterials

A
  • culture and sensitivity (low budget? gram stain)
  • avoid combination therapy unless indicated
  • identify compliance issues
  • prevent in-house infections
77
Q

four common ailments/procedures that dont call for antimicrobials

A
  • feline lower urinary tract disease
  • spay/neuter
  • feline upper respiratory disease (usually viral)
  • kennel cough (self-limiting)
78
Q

what can you do instead of medicated milk replacer

A

adequate colostrum within 24 hours

husbandry and management

79
Q

what can you do instead of using antibiotics for neonatal scours

A

rehydrate only unless systemic

colostrum management

hygiene & cleanliness

reduce stress

regulate traffic flow

vaccination protocols

80
Q

what can you do instead of using antibiotics for mastitis

A

culture samples with high somatic cell count (number of neutrophils in the milk)

dont treat if about to cull or dry off

MANAGEMENT

81
Q

How can you prevent bovine respiratory disease

A

wean/castrate/dehorn at least 30 days prior to shipping (stress)

parasite treatment

vaccinate

biosecurity

82
Q

four instances where a four quadrant approach would be indicated

A

pilonephritis (kidney infection)

prostatitis

pneumonia

sepsis

83
Q

Ringworm

disease name:

location on host body:

zoonotic?

A

Ringworm

disease name: dermatophytosis

location on host body: keratinized structures (hair, skin, nails)

zoonotic? YES, can jump species

84
Q

how is dermatophytosis (ringworm) diagnosed and treated

A

diagnosed suggestively with Wood’s lamp (UV) and definitively with a DTM culture.

treated with topical therapy

85
Q

Dermatomycosis

what pathogen:

predisposing factors:

effect of overgrowth:

A

Dermatomycosis

what pathogen: Malassezia pachydermatis

predisposing factors: immunosupression (normally is present in small numbers)

effect of overgrowth: dermatitis and otitis

86
Q

Aspergillosis

species affected:

contracted by:

other:

A

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
Q

histoplasmosis

form:

found (environment and geographical):

symptoms:

A

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
Q

list two important pyogenic (induce pus formation) bacteria

A

Saphylococcus,

Streptococcus

89
Q

Staphylococci

Morphology:

arrangement:

oxygen needs:

behavior:

A

Staphylococci

Morphology: gram positive cocci

arrangement: clusters

oxygen needs: most are facultative anaerobes

behavior: opportunistic, colonize nasal cavity, nasopharynx, skin, and mucous membranes

90
Q

what is the main pathogen that causes abscesses, mastitis, dermatitis, and “bumble foot”

A

Staphylococcus aureus

91
Q

what is the main pathogen that causes canine and feline pyoderma

A

Staphylococcus pseudintermedius

92
Q

three main virulence factors of staphylococcus aureus

A
  • secreted factors (toxins, enzymes, and invasins)
  • membrane-bound factors (adhesins)
  • capsule/slime layer
93
Q

Streptococci

Morphology:

arrangement:

oxygen needs:

behavior:

other:

A

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
Q

list some bacteria that belong in the group Enterobacteriaceae

A

Escherichia coli

Salmonella

Yersinia (plague)

Enterobacter

95
Q

many Enterobacteriaceae are considered Coliforms. what does this mean?

A

they are gram-negative rods, non-spore forming, and ferment lactose and are found in large numbers in feces of warm-blooded animals

96
Q

Escherichia coli

morphology:

predisposed individuals:

general symptoms:

symptoms in freshly weaned pigs:

A

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
Q

Clostridium

morphology:

A

large, spore-forming, gram-positive rods

98
Q

list two main endospore forming bacterium

A

bacillus and clostridium

99
Q

list the four types of exotoxin driven disease caused by clostridia

A
  • Neurotoxic (tetanus and botulism)
  • histotoxic (blackleg, bacillary hemoglobinuria)
  • enteropathogenic (clostridial enterocolitis)
  • atypical (Tyzzer’s Disease)
100
Q

what makes Mycobacterium hard to kill and stain

A

their cell wall is lipid rich

101
Q

Mycobacterium

symptoms:

treatment issue:

zoonitic?

A

Mycobacterium

symptoms: chronic granulomatous lesions (macrophages)

treatment issue: multidrug resistance

zoonitic? YES, especially bovine tuberculosis

102
Q

Rickettsiales

oxygen requirements:

A

obligate intracellular

103
Q

what is the tissue target of Rickettsiaceae

A

vascular endothelium

104
Q

what is the tissue target of Anaplasma

A

erethrocytes, platelets, and leukocytes

105
Q

what is the tissue target of Ehrlichia

A

leukocytes

106
Q

what is the tissue target of Neorickettsia

A

leukocytes

107
Q

what is sepsis

A

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
Q

list some common presenting clinical signs of sepsis

A

bounding to weak pulses,

brick red mucous membranes (dog),

pale mm (cat),

fever (dogs) or hypothermia (cats),

tachypnea,

hypotension,

lethargy

109
Q

what lab abnormalities are common for an animal in sepsis

A

anemia (esp cats),

elevated hematocrit,

left shift and toxic change,

thrombocytopenia,

hyperlactemia,

clotting disorders

110
Q

disease of what system is most likey to result in sudden death

A

cardiovascular

111
Q

list some common bacterial causes of sudden death

A

anthrax, clostridial disease, anaplasmosis, salmonella, Leptospirosis, MRSA, Streptococcus equi, acute pneumonia

112
Q

list some common viral causes of sudden death

A

Classical and African swine fever, distemper

113
Q

list some common toxin-driven causes of sudden death

A

bracken fern, sweet clover, lead, blister beetles

114
Q

list some common trauma causes of sudden death

A

lightnight strike, bloat, colic

115
Q

Bacillus anthracis

morphology:

longevity:

oxygen requirements:

A

Bacillus anthracis

morphology: gram-positive spore-forming saprophyte
longevity: spores remain viable in soil for 50 years

oxygen requirements: facultative anaerobic

116
Q

what are the presenting clinical signs of a ruminant with anthrax

peracute:

acute:

peracute/acute:

A

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
Q

presenting clinical signs of a horse with anthrax

A

rapidly developing subcutaneous edema, fever, severe colic, bloody diarrhea, death in 2-3 days

118
Q

presenting clinical signs of a dog with anthrax

A

pharyngeal edema, gastroenteritis

119
Q

describe the lesions found during an anthrax necropsy

A

“blackberry jam” spleen, hemorrhages of skin and lymph nodes, bloody discharge from orifices, failure of blood to clot, delayed or incomplete rigor mortis

120
Q

list three virulence factors of anthrax

A

capsule (inhibits phagocytosis)

tripartitie exotoxin

host macrophages (release toxic contents when they explode)

121
Q

what cell recognizes and engulfs anthrax spores in the host

A

macrophages

122
Q

describe how Tripartite Exotoxin of Anthrax works

A
  • protective antigen forms a hole for entry of other toxins
  • edema factor causes fluid release and edema
  • lethal factor inhibits cytokine release
123
Q

list some techniques helpful for diagnosing anthrax

A

paying attention to the time of year

blood smears allowed to grow

culture

PCR

124
Q

what should you do for necropsy of a suspected anthrax case

A

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
Q

how is anthrax treated

prevented

A

treated with penicillin, tetracyclines, and quarantine

prevented by live vaccination

126
Q

Anthrax zoonosis

most common transmission route:

highest mortality rate route:

A

Anthrax zoonosis

most common transmission route: cutaneous (from contacting an infected carcass)

highest mortality rate route: inhalation

127
Q

list four clostridial agents and the disease they cause that are associated with toxemia induced fatality

A

Blackleg: Clostridium chauvoei

Bacillary Hemoglobinuria: Clostridium haemolyticum

Malignant Edema: Clostridium septicum

Hemorrhagic bowel: Clostridium perfringens A

128
Q

Feline Infectious Anemia

pathogen:

signalment:

signs:

transmission:

A

Feline Infectious Anemia

pathogen: Mycoplasma haemofelis
signalment: outdoor males
signs: weakness, pallor, tachypnea, tachycardia, collapse
transmission: fleas and bite wounds (blood contact)

129
Q

Mycoplasma haemofelis

appearance on blood smear

A

epicellular, small gram-negative rods on the periphery of RBC

130
Q

why might a cat come up positive on PCR for FIA but their blood smear was clear

A

FIA is cyclical anemia, the pathogen is at lowest when RBC number is lowest

131
Q

how is FIA treated

A

supportive care (oxygen and transfusion), doxycycline, and enrofloxacin/marbofloxacin

will not be completely eliminated

132
Q

is FIA zoonotic?

A

rarely. usually it is species specific

133
Q

cat scratch fever

pathogen:

signalment:

transmission:

symptoms:

zoonotic?

A

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
Q

Bovine anaplasmosis

pathogen:

symptoms:

transmission:

A

Bovine anaplasmosis

pathogen: Anaplasma marginale
symptoms: progressive anemia due to extravascular destruction of erythrocytes
transmission: ticks or used needles

135
Q

anaplasma marginale

morphology:

how it causes disease:

A

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
Q

does anaplasmosis cause hemoglobinuria?

does babesia?

A

does anaplasmosis cause hemoglobinuria? NO

does babesia? YES

137
Q

Anaplasmosis

diagnosis:

Treatment:

prevention:

A

Anaplasmosis

diagnosis: cELISA is gold standard. blood smear

Treatment: tetracycline or Imidocarb

prevention: vector control and good hygiene

138
Q

Canine Cyclic Thrombocytopenia

pathogen:

action:

transmission:

A

Canine Cyclic Thrombocytopenia

pathogen: Anaplasma platys
action: infects platelets and cause thrombocytopenia
transmission: tick vector

139
Q

Bacillary Hemoglobinuria

pathogen:

primary sign:

A

Bacillary Hemoglobinuria

pathogen: Clostridium haemolyticum

primary sign: intravascular hemolysis causes hemoglobinuria (“red wine urine”)

140
Q

Rocky Mountain Spotted Fever

pathogen:

role of ticks:

clinical signs:

A

Rocky Mountain Spotted Fever

pathogen: Rickettsia rickettsii

role of ticks: vector AND reservoir (must be attached for 5-20 hours)

clinical signs: vasculitis

141
Q

rocky mountain spotted fever

diagnosis:

treatment:

zoonotic:

A

rocky mountain spotted fever

diagnosis: paired sera taken 10-14 days apart (ELISA)
treatment: doxycycline
zoonotic: yes but from ticks not dogs

142
Q

describe the Ehrlichia spp. life cycle

A
  • 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
Q

Canine Monocytic Ehrlichiosis

pathogen:

vector:

treatment:

A

Canine Monocytic Ehrlichiosis

pathogen: Ehrlichia canis
vector: brown dog tick
treatment: doxycycline for 3 weeks

144
Q

Ehrlichia acute phase symptoms

A

fever, anorexia, occulonasal discharge, lymphadenopathy, limb edema, possible nerve deficits, thrombocytopenia

145
Q

Ehrlichia chronic phase symptoms

A

splenomegaly, renal failure, pneumonitis, uveitis, meningitis, severe thrombocytopenia, pancytopenia, severe weight loss

146
Q

four diseases tested for by the SNAP 4Dx Plus

A

Heartworm (Dirofilaria immitis)

Lyme Disease (Borrelia burgdorferi)

Ehrlichiosis (E. canis and E. ewingii)

Anaplasma

147
Q

Canine Granulocytic Ehrlichiosis

pathogen:

vector:

symptoms:

treatment:

A

Canine Granulocytic Ehrlichiosis

pathogen: Ehrlichia ewingii
vector: lone star tick
symptoms: polyarthritis, lameness, joint swelling, stiff gait
treatment: doxycycline

148
Q

Equine Granulocytic Ehrlichiosis

pathogen:

vector:

symptoms:

A

Equine Granulocytic Ehrlichiosis

pathogen: Anaplasma phagocytophilum
vector: Ixodes ticks
symptoms: necrotizing vasculitis, fever, anorexia, depression, limb edema, petechiation, icterus

149
Q

how is Equine Granulocytic Ehrlichiosis

detected:

treated:

A

how is Equine Granulocytic Ehrlichiosis

detected: PCR, IFA
treated: oxytetracycline and tick control

150
Q

Equine Monocytic Ehrlichiosis (Potomac Horse Fever)

pathogen:

causes:

vector:

A

Equine Monocytic Ehrlichiosis (Potomac Horse Fever)

pathogen: Neorickettsia risticii
causes: acute enterocolitis
vector: trematodes

151
Q

Tularemia

Pathogen:

zoonosis:

vector:

easily confused with:

A

Tularemia

Pathogen: Francisella tularensis

zoonosis: very very. most common in sheep, cats, and rabbits
vector: ticks

easily confused with: plague, pseudotuberculosis, pneumonia

152
Q

Francisella tularensis

morphology:

infects:

which subspecies is worse:

A

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
Q

three ways Tularemia can be transmitted and their resulting forms

A
  • aerosol transmission: pneumonic form
  • direct contact: ulceroglandular or occuloglandular forms
  • ingestion: oropharyngeal or typhoidal form
154
Q

four steps of Tularemia pathogenesis

A
  • local ulcerative lesion
  • local lymphadenopathy
  • transient bacteremia
  • spread to lymph nodes, liver, spleen, bone marrow, and sometimes lung
155
Q

Tularemia

diagnosis:

treatment:

A

Tularemia

diagnosis: culture, 4-fold increase in antibody titers, lymph node aspirate/biopsy
treatment: isolation, tetracycline, streptomycin, gentamicin, fluoroquinolones

156
Q

Plague

pathogen:

morphology:

zoonosis:

transmission:

A

Plague

pathogen: Yersinia pestis
morphology: small gram-negative coccobacillus
zoonosis: yes. rodents, humans, cats, and dogs
transmission: fleas

157
Q

three forms of plague

A

bubonic form

septicemic form

pneumonic form

158
Q

plague

diagnosis:

treatment:

A

plague

diagnosis: lymph node aspirates, biopsies
treatment: aminoglycosides and tetracyclines for three weeks

159
Q

Glanders

pathogen:

zoonosis:

transmission:

pathogenesis:

A

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
Q

Melioidosis

pathogen:

morphology:

species affected:

pathogenicity:

A

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
Q

signs of right-sided heart failure

A

ascites, GI congestion (causes anorexia, GI distress, and weight loss), liver congestion

162
Q

signs of left sided heart failure

A

decreased cardiac output

pulmonary congestion

163
Q

definition of endocarditis

A

inflammation of the inner layer of the heart (endocardium)

164
Q

what are the steps that lead to vegetative lesions of the heart and what are they composed of

A

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
Q
A

Bacteriology/Mycology (1 decks)

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