Infectious Disease Exam 1

Front 1

Nutrient agar

Back 1

Basic media for non-fastidious bacteria

Front 2

blood agar

Back 2

enriched media

most pathogenic bacteria

allows for recognition of hemolysis

Front 3

MacConkey agar

Back 3

selective medium

gram (-) bacteria

Front 4

Eosin Methylene Blue (EMB) agar

Back 4

selective medium

gram (-) bacteria

Front 5

Columbia Nalidixic Acid (CNA)

Back 5

selective medium

gram (+) bacteria

Front 6

Chocolate agar

Back 6

for fastidious bacteria

Front 7

Brilliant green agar

Back 7

for salmonella

Front 8

Trypticose Soy Broth

Back 8

general purpose medium

aerobic bacteria

Front 9

Buffered-peptone water

Back 9

non-selective medium to low number of pathogens in environment and feed

Front 10

Selenite broth

Back 10

selective enrichment medium

Salmonella spp

Front 11

Hayflick liquid medium

Back 11

selective enrichment medium

Mycopasma spp

Front 12

UVM medium

Back 12

selective medium

Listeria spp

Front 13

Selective media

Back 13

-contains substances to either:

+enhance growth of particular organisms

+inhibit growth of unwanted organisms

-dyes (eosin, methylene blue), pH, NaCl, antimicrobials, etc

Front 14

GasPak system

Back 14

anaerobic bacteria

-use reducing media containing compounds like sodium thioglycollate

-plates placed in sealable containers utilizing chemicals to provide oxygen-free environment

Front 15

Streak-plate method

Back 15

Front 16

Pour-plate method

Back 16

Front 17

Confirming presence of pathogenic bacteria

(3 ways)

Back 17

-stained smears

-cultural & biochemical characteristics

-detection by immunological & molecular methods

Front 18

Gram stain

Back 18

Widely used

-crystal violet retained by gram (+)

-crystal violet not retained by gram (-)

Front 19

Giemsa stain

Back 19

Dermatophilus congolensis

Rickettsia

Babesia

Anaplasma

Borrellia

Front 20

Ziehl-Neelsen (acid-fast) stain

Back 20

Mycobacterium spp

Actinomycetes

(red=positive)

Front 21

Carbol fuchsin stain

Back 21

Campylobacter

Brachyspira

Fusobacterium

(stain red)

Front 22

Basic criteria for presumptive ID

Back 22

-colonial morphology and color

-presence/absence of hemolysis

-appearance on gram staining/ability to grow on MacConkey

-motility

-reaction to biochemicals (catalase & oxidase test)

Front 23

Biochemical tests

Back 23

-sugar fermentation

-triple sugar iron (TSI)

-sulfide indole motility (SIM)

-urease

Front 24

Particular tests

Back 24

-CAMP reaction

-Coagulase

-Hemagglutination

-Nagler test

Front 25

ID'ing oxygen requirements

Back 25

Front 26

Immunological techniques

Back 26

-fluorescent antibody tests (Leptospira, Clostridium)

-ELISA tests (Clostridium difficile)

-Agglutination tests (Salmonella typing, Taylorella)

Front 27

Phage typing

Back 27

-use of well-characterized lytic phages to ID specific bacteria

-causes lysis of bacteria

-special labs for Salmonella and Staphlyococcus

Front 28

Molecular techniques

Back 28

PCR tests

-Mycrobacterium paratuberculosis

-Mycoplasmsa bovis

-Moraxella differentiation

-Genotyping C. perfringens and C. difficile

-Leptospira

-Salmonella

DNA sequencing

Front 29

Bacteria & Archaea

Back 29

-prokaryotic

-no nuclei

-single chromosome (usually)

-asexual reproduction

-great majority don't cause disease

-archaea often isolated from extreme environments

Front 30

Fungi

Back 30

-eukaryotic

-have cell walls

-molds and yeasts

Front 31

molds

Back 31

-multicellular

-filamentous growth

-sexual and asexual spores

Front 32

Yeast

Back 32

-unicellular

-oval to round

-reproduce by budding

Front 33

protozoa

Back 33

-single-celled eukaryotes

-most capable of locomotion by pseudopodia, cilia, or flagella

-most asexual

Front 34

algae

Back 34

-unicellular/multicellular photosynthetic organisms

-make own food from CO2 and water using energy from sunlight

Front 35

Viruses

Back 35

-smaller than prokaryotes

-not visible by light microscope

-acellular

-obligate intracellular

Front 36

prokaryotic cells

Back 36

-nucleoid not surrounded by nuclear membrane

-usually single chromosome

-no membrane-bound organelles

-minute size

-binary fission

-no cytoskeleton

-ie bacteria

Front 37

eukaryotic cells

Back 37

-nuclear material surrounded by nuclear membrane

->1 chromosome

-membrane-bound organelles

-fairly large

-mitosis/meiosis

-cytoskeleton

-ie fungi, algae, plant, mammalian cells

Front 38

prokaryotic capsule/glycocalyx

Back 38

-gelatinous, sticky substance surrounding cell

-composed of polysaccharides, polypeptides, or both

+made inside cells and extruded onto cell's surface (K-antigen)

Front 39

prokaryotic capsule/glycocalyx

Back 39

-protect bacteria from immune system cells and desiccation

-virulence factor

-numerous pathogenic bacteria (Bacillus antracis, Klebsiella pneumoiae)

Front 40

flagella

Back 40

-mostly gram (-) bacteria

-bacterial movement

-virulence factor

Front 41

flagella

Back 41

3 parts:

-filament (flagellin protein)

-hook

-basal body (bacterium)

-differences in flagella proteins may allow classification of species into serovars

Front 42

fimbriae

Back 42

-for movement & adherence to each other & environment

-up to 100's on the cell

-shorter than flagella

-important function in biofilms

Front 43

Pili (conjugation pili)

Back 43

-transfer of DNA from one cell to another

Front 44

Bacterial cell walls

Back 44

-provide structure and shape

-protect cell from osmotic forces

-assist in attaching to other cells

-resisting antimicrobial drugs

-target for antibiotics

-give bacteria characteristic shapes

-mainly composed of peptidoglycan

Front 45

Gram staining procedure

Back 45

1. slide flooded with crystal violet, then rinsed in water. all cells purple

2. slide flooded in iodine, then rinsed in water. all cells purple

3. slide flooded in ethanol and acetone, then rinsed with water. Gram (+) remain purple, gram (-) colorless

4. slide flooded with safranin, then rinsed with water and blotted dry. Gram (-) pink.

Front 46

Bacterial cytoplasmic membranes

Back 46

-fluid mosaic model controls passage of substances into/out of phospholipid bilayer:

+hydrophilic heads

+hydrophobic hydrocarbon tails

-membrane proteins for recognition, enzymes, receptors, carriers, and channels

Front 47

Plasma membrane function

Back 47

-selectively permeable

-naturally impermeable to most substances

-proteins allow substances to cross membrane

-maintain concentration & electrical gradient

-site of electron transport for respiration

Front 48

Passage of substances from membrane

Back 48

-passive (smaller molecules)

+diffusion

+facilitated diffusion

+osmosis

-active processes

+active transport

+group translocation

Front 49

cytoplasm

Back 49

-water (mostly) + dissolved/suspended substances (ions, carbohydrates, proteins, enzymes, lipids, DNA, RNA, wastes)

-chemical reactions occur

-houses storage granules (lipids, starch, etc)

Front 50

ribosomes

Back 50

-sites of protein synthesis

-prokaryotic ribosomes different than eukaryotic

+50S + 30S

-some antimicrobial drugs target protein synthesis

Front 51

nuclear material

Back 51

-single haploid circular chromosome

-extensively folded with small amounts of protein & RNA

-some 2 circular chromosomes, 1 linear chromosome, plasmid

Front 52

protein secretion systems

Back 52

-mechanisms to transport large molecules through complex membranes and cell walls

-gram (-) bacteria (esp) have evolved secretion pathways

Front 53

effector proteins

Back 53

-proteins transported through secretion systems

-includes enzymes (proteases, lipases, cytotoxic/apoptosic proteins)

Front 54

endospores

Back 54

-produced for durability and pathogenicity

-high content of dipicolinic acid and calcium

-resistant to drying, pasteurization, radiation

-ie Bacillus anthracis, Clostridium tetani, Clostridium perfringens

Front 55

biofilms

Back 55

-bacterial populations adherent to each other &/or surfaces

-enclosed in a biopolymer matrix

-immobile form

-complex relationships among numerous microorganisms

Front 56

biofilms

Back 56

-develop extracellular matrix

-allows attachment to substrate

-drug penetration difficult

-microorganisms more harmful as part of a biofilm

Front 57

formation of endospore

Back 57

Front 58

endospore germination

Back 58

-initiated when conditions are favorable

-heat, warm weather, nutrients

Front 59

microbial growth

Back 59

increase in a population of microbes that results in either:

-discrete colony-aggregation of cells arising from a single parent cell

-biofilm-collection of microbes in the surface of a complex community

Front 60

typical microbial growth curve

Back 60

Front 61

binary fission

Back 61

Front 62

generation time

Back 62

time required for bacterial cell to grow and divide

-dependent on chemical and physical conditions

Front 63

obligate aerobes

Back 63

oxygen is essential

Front 64

obligate anaerobes

Back 64

oxygen is deadly

-toxic forms of O2 are highly reactive and excellent oxidizing agents

-resulting oxidation causes irreparable damage to cells

Front 65

ID oxygen requirements

Back 65

Front 66

nitrogen requirements

Back 66

-anabolism often ceases due to insufficient nitrogen

-acquired from organic & inorganic nutrients

-cells recycle nitrogen from amino acids and nucleotides

-nitrogen fixation by certain bacteria essential to life on earth

Front 67

chemical requirements

Back 67

-phosphorus-membrane/cell wall, DNA, RNA, ATP

-sulfur-disulfide bonds of proteins

-trace elements required in small amounts (se)

-growth factors-some amino acids, purines, pyrimidines, NADH, heme

Front 68

effect of temperature on growth

Back 68

-too low, membranes become rigid and fragile

-too high, membranes become too fluid

pathogenic bacteria usually can't grow outside specific temperature range

Front 69

psychrophiles

Back 69

-5C to 20C

Front 70

mesophiles

Back 70

most of the pathogenic bacteria

15C to 45C

Front 71

thermophiles

Back 71

42C to 80C

Front 72

hyperthermophiles

Back 72

polymerases for PCR reactions

67C to 105C

Front 73

pH requirement

Back 73

organisms sensitive to changes in acidity

-H+ and OH- interfere with H-bonding

Front 74

Neutrophiles

Back 74

grow best in narrow range around neutral (7) pH

most pathogens grow best around neutral pH

Front 75

Acidophiles

Back 75

grow best in acidic (<7) pH

-yeast (Candida) and Clostridium difficile

Front 76

physical effects of water

Back 76

-osmotic pressure

-hydrostatic pressure

-microbes require water to dissolve enzymes, nutrients

-most cells die in absence of water

-some have cell walls the retain water (Mycobacterium spp)

-Endospores & cysts-most metabolic activities stop

Front 77

culturing microorganisms

Back 77

-cultivating microorganisms

-inoculum introduced into medium

Front 78

obtaining pure cultures

Back 78

-cells arising from a single progenitor

-aseptic technique prevents contamination of sterile substances/objects

-streak plates

-pour plates

Front 79

colony forming unit

Back 79

-progenitor of cells

Front 80

characteristics of bacterial colonies

Back 80

Front 81

culture media

Back 81

some microorganisms don't require specific nutrients (E. coli), but some do (Haemophilus somni)

-liquid & solid media

Front 82

agar

Back 82

complex polysaccharide

-most microbes can't digest agar

-powdered agar dissolves at 100C

-solidifices at 40C

Front 83

solid media

Back 83

-blood agar

-MacConkey

-Hekton

-CNA

-urease slant

-citrate slant

Front 84

defined media

Back 84

know concentration of each ingredient in media

Front 85

complex media

Back 85

contains variety of nutrients released by partial digestion of yeast, soy, beef, or casein

-exact chemical composition unknown

-blood often added to provide NADH and heme

Front 86

selective media

Back 86

contains substance either to encourage growth of particular organisms or inhibit growth of unwanted organisms

-some dyes (eosin, methylene blue), pH, NaCl, antimicrobials used

Front 87

differential media

Back 87

used to differentiate microorganisms

-visible changes in medium or differences in appearance of colonies

-many media selective & differential

Front 88

transport media

Back 88

used for carrying clinical specimens

-feces, saliva, sputum, blood

-Amie's transport medium + charcoal

Front 89

special culture techniques

Back 89

-low-O2 culture-microaerophiles

-enrichment culture-enhancing growth of less abundant microbes in specimen

-cold enrichment-cold tolerant microbes (Listeria, Vibrio cholerae)

-animal-no growth in liquid media (M. laprae-armadillos; Treponema pallidum-rabbit)

-cell culture-viruses, rickettsias

Front 90

direct method

(measuring microbial reproduction)

Back 90

-serial dilution & viable plate counts

-membrane filtration

-most probable number

-microscopic counts

-electronic counters

Front 91

serial dilution & viable plate count

Back 91

Front 92

membrane filtration

Back 92

-used when population density is low

pic

Front 93

cell counter

Back 93

-no incubation required

pic

Front 94

indirect methods

(measuring population size)

Back 94

-metabolic activity

-turbidity

-dry weight

-genetic methods

Front 95

metabolic activity

Back 95

measure nutrient utilization, waste production, pH

Front 96

turbitidy

Back 96

MacFarland for antimicrobial susceptibility, spectrophotometer

Front 97

dry weight

Back 97

filtered, dried, weighed

Front 98

genetic methods

Back 98

isolate total DNA of microorganism

-perform real-time PCR

-UV spectrophotometry of DNA

-used to estimate number of microbes

Front 99

refrigeration

preserving cultures

Back 99

stores for short periods of time

Front 100

deep-freezing

preserving cultures

Back 100

stores for years

Front 101

lyophilization

preserving cultures

Back 101

stores for decades

Front 102

role of HEPA filters

Back 102

prevents human contamination from specimen

pic

Front 103

tissue & organ specimens

Back 103

-suitable portions placed in individual polyethylene bags/suitable leakproof container

-portions of intestine (tied off) should be packaged separately

Front 104

swab specimens

Back 104

-abscesses

-nasal passages

-pharynx

-tonsil

-eye

-ear

-skin

-vagina/cervix

prevent drying by using suitable transport medium

Front 105

fecal specimen

Back 105

-preferably obtained directly from rectum in manner that avoids contamination

-avoid submission of fresh droppings

-place in leak-proof container and ship immediately

Front 106

milk specimen

Back 106

collected aseptically using sterile screw-capped/stoppered vials (not bags)

-should be refrigerated immediately following collection

-deliver to lab under refrigerated conditions

Front 107

urine specimen

Back 107

collected aseptically

-refrigerated immediately

-avoid free-catch samples

-minimum 5mL urine

Front 108

antrax, plaque, tularemia, foreign diseases

special considerations

Back 108

clearly label all boxes & bags to avoid exposure to lab personnel

Front 109

antrax

special considerations

Back 109

cotton swabs soaked in extruded blood/blood taking from superficial ear vein

-swine-swabs taken from exudates & cut surfaces of hemorrhagic lymph nodes

Front 110

blackleg, malignant edema

special considerations

Back 110

submission of fresh affected tissues

-clostridium rapidly invades tissues after death

-2 impression smears on glass slides

Front 111

clostridial enterotoxemia

special considerations

Back 111

several ounces of fresh intestinal contents or tied-off section of affected intestine

Front 112

Johne's disease

special considerations

Back 112

fecal specimen from live animals

Front 113

Campylobacteriosis

special considerations

Back 113

-semen, preputial washing, fetal stomach contents, cervical mucus obtained aseptically

-refrigerated & delivered to lab within 5-6 hours of collections

-OR frozen as soon as collected with dry ice and shipped in insulated container with adequate amount of dry ice

Front 114

Brucellosis

special considerations

Back 114

placenta, stomach content of aborted fetus, mammary lymph nodes, milk samples preferred

-shipped under refrigerated conditions

Front 115

Listeriosis

special considerations

Back 115

submit brain stem sample and indicate Listeria is suspected

Front 116

fungal isolations

Back 116

take up to 3 week before reported out

-collect samples aseptically before antifungal therapy

Front 117

fungal specimens

Back 117

-superficial mycoses-hair & skin scrapings from edge of active lesions

+submit in small paper envelope

+saprophytic fungi will proliferate rapidly and overgrow ringworm fungi in sealed container

-deep-seated mycoses-tissues & organs as for bacteriology

Front 118

drug

Back 118

chemical that affects physiology in any manner

Front 119

antimicrobial agent

Back 119

-drug that treat infections

-kill or inhibit growth of susceptible microorganisms

Front 120

Paul Erlich

Back 120

-"magic bullets"

-arsenic compounds that killed Treponema pallidum (causative agent of syphillus)

Front 121

Gerhard Domgak

Back 121

-Prontosil red for Streptococi infections

-Converted to sulfanilamide in body by liver

Front 122

Alexander Fleming

Back 122

-Penicillin released from Penicillium sp.

Front 123

Selman Wkasma

Back 123

-Antimicrobial agents produced naturally by organisms

-Other antibiotics-streptomycin

Front 124

Selective toxicity

Back 124

more toxic to pathogen than host

-based on differences of biochemical, structural, or metabolic pathways between bacteria and eukaryotes

Front 125

Bactericidal

Back 125

drugs that kill bacteria

Front 126

bacteriostatic

Back 126

drugs that inhibit bacterial pathogenity

Front 127

Ratio of drugs available

Back 127

Antibacterial>antifungal>antiviral

Front 128

Inhibition of cell wall synthesis

Back 128

-prevent cross-linkage of NAM subunits in peptidoglycan layer

-prevent bacteria from increasing amount of peptidoglycan

Front 129

Beta-lactams

Back 129

-functional groups are beta-lactam rings

-bind to enzymes that cross-link NAM subunits

-Penicillins

Cephalosporins

Front 130

Beta-lactams: affect existing peptidoglycan layer?

Back 130

-NO!

-bacteria have weakened cell walls and eventually lyse due to increased osmotic pressure inside cell

Front 131

Vancomycin & cycloserine mechanism

Back 131

-interfere with particular bridges that link NAM subunits

-many gram (+)

Front 132

Bacitracin mechanism

Back 132

-blocks secretion of NAG and NAM from cytoplasm

Front 133

Isoniazid and ethambutol mechanism

Back 133

-disrupt mycolic acid formation in mycobacterial species

Front 134

Semi-synthetic beta-lactam derivative benefits

Back 134

-more stable in acidic environments (stomach)

-more readily absorbed

-less susceptible to deactivation

-more active against more types of bacteria

Front 135

monobactams vs synthetics/semisynthetics (amoxicillin, ampicillin)

Back 135

monobactams-effective ONLY against aerobic gram (-)

synthetics-more effective on gram (+)

Front 136

Inhibition of protein synthesis

Back 136

-prokaryotic ribosomes 70S (30S & 50S)

-eukaryotic ribosomes 80S (40S & 60S)

+mitochondria contain 70S-drugs can be more toxic with more adverse effects

-drugs selectively target translation

Front 137

different mechanisms of inhibiting protein synthesis

Back 137

Front 138

Aminoglycosides

Back 138

-used topically-not absorbed well orally

-little activity against anaerobes

-amikacin, kanamycin, neomycin, tobramycin, spectionomycin

Front 139

tetracyclines

Back 139

-block docking site of mRNA

-large spectrum

-shouldn't be used in pregnant animals

-textracycline, doxycycline, minocycline

Front 140

chloramphenicols

Back 140

-binds and blocks binding site of amino acids

-chloramphenicol, florfenicol

Front 141

macrolides

Back 141

-bind to 50S subunit, blocking proper mRNA movement through ribosome, stopping synthesis

-enytromycin, axithromycin, claritromysin, tylosin

-mainly affect gram (+) cocci and intracellular pathogens

Front 142

disruption of cytoplasmic membrane

Back 142

-form channel through cytoplasmic membrane and damage integrity

Front 143

polymyxin

Back 143

-disrupts cytoplasmic membranes of gram (-)

-toxic to kidneys

Front 144

amphotericin b

Back 144

-attaches to ergosterol in fungal membranes

-bacteria lack sterols, so not susceptible

Front 145

inhibition of nucleic acid synthesis

Back 145

-block DNA replication or mRNA transcription

-often affect eukaryotic & prokaryotic cells

-limited clinical use-except quinolones and fluoroquinalones

Front 146

quinolones and fluroquinolones

Back 146

-act against prokaryotic DNA gyrase and topoisomerase IV

Front 147

rifampin

Back 147

-inhibit RNA polymerase during transcription

Front 148

reverse transcriptase inhibitors

Back 148

-acts against enzyme of retroviruses

-don't harm mammalians because they lack reverse transcriptase

Front 149

inhibition of metabolic pathways

Back 149

-effective when metabolic processes of pathogen & host differ

Front 150

sulfonamides

Back 150

-structural analogs

Front 151

heavy metals

Back 151

-inactivate enzymes

Front 152

clinical considerations

Back 152

-ideal antimicrobial agent

-spectrum of action

-efficacy

-routes of administration

-safety & side effects

Front 153

ideal antimicrobial agent

Back 153

-readily available

-inexpensive

-chemically stable

-easily administered

-nontoxic & nonallergenic

-selectively toxic against wide range of pathogens

Front 154

spectrum of action

Back 154

-number of different pathogens a drug acts against

-narrow-spectrum effective against few organisms

-best to perform antimicrobial susceptibility test before starting treatment

Front 155

broad-spectrum

Back 155

-effective against many organisms

-may allow for secondary or superinfections to develop

-killing of normal flora reduces microbial antagonism

Front 156

efficacy

Back 156

ascertained by

-diffusion susceptibility test

-minimum inhibitory concentration (MIC) test

-minimum bactericidal concentration test

Front 157

minimum inhibitory concentration teset

Back 157

-lowest concentration of antimicrobial that prevents visible growth of microorganisms in a broth dilution susceptibility test

Front 158

Susceptible

Back 158

an infection due to the isolate may be treated in body sites with the recommended dosage

Front 159

resistant

Back 159

isolates are not inhibited by the usual achievable concentration of a drug and not reliable in treatment

Front 160

intermediate

Back 160

infection due to isolate may be treated in body sites where high dosage of the drug can be used

Front 161

no interpretation

Back 161

no interpretative criteria established yet

Front 162

routes of administration

Back 162

-topical-external infections

-oral-no needles

-IM-via needle into muscle

-IV-via needle into bloodstream

must know how antimicrobial agent will be distributed to infected tissues

Front 163

toxicity

Back 163

-cause of many adverse reactions poorly understood

-may be toxic to kidneys, liver, or nerves

-pregnant animals need extra consideration

Front 164

allergies

Back 164

-rare, but may be life-threatening

-anaphylactic shock

Front 165

disruption of normal microbiota

Back 165

-may result in secondary infections

-overgrowth of normal flora causes superinfections

-greatest concern in hospitalized animals

Front 166

resistance to drugs

Back 166

-some pathogens naturally resistant

acquired in 2 ways:

-new mutations of chromosomal genes

-acquisition of R-plasmids via transformation, transduction, and conjugation

Front 167

mechanisms of resistance

Back 167

-produce enzyme that destroys or deactivate drug

-slow or prevent entry of drug into cell

-alter target of drug so it bind less effectively

-alter their metabolic chemistry

-pump drug out of cell before it can act

-biofilms retard drug diffusion and slow metabolic rate

-Mycobacterium tuberculosis produces MfpA protein, binds DNA gyrase depriving fluoroquinolones

Front 168

multiple resistance

Back 168

-pathogen can acquire resistance to more than 1 drug

-common when R-plasmids are exchanged

-develop in animal hospitals

+constant use of drugs eliminates sensitive cells

-superbugs

Front 169

cross resistance

Back 169

resistance to structurally similar drugs at the same time

Front 170

limiting antibacterial resistance

Back 170

-effective surveillance systems for collection of data at local & national level

-treatment based on susceptibility test results

-strict adherence to drug withdrawal periods in food-producing animals

-maintain high concentration of drug in patient for sufficient time

-use only when necessary

-use in combination

Front 171

synergism

Back 171

two agents enhancing the individual effects of drugs

Front 172

Trueperella (Arcanobacterium) pyogenes pathogenicity

Back 172

opportunistic causing suppurative lesions

-hemolytic toxin pyolysin causes pus formation

-neurominidases, extracellular matrix proteins, and fibria

-proteases

Front 173

Trueperella (Arcanobacterium) pyogenes

species

Back 173

cattle, pigs, sheep

Front 174

Trueperella (Arcanobacterium) pyogenes

affected area

Back 174

any organ system

-bovine pneumonia

-hepatitis

-osteomyelitis

-peritonitis

-cerebral abscesses

-lymphadenitis

-mastitis

Front 175

Trueperella (Arcanobacterium) pyogenes

appearance on culture

Back 175

-small hemolytic colonies in BAP

-typical pleomorphic cell morphology in gram stain

Front 176

Trueperella (Arcanobacterium) pyogenes

treatment

Back 176

-based on antimicrobial susceptibility test

-resistance to macrolides and tetracyclines

-feedlot cattle receive sub-therapeutic doses of tylosin (macrolide) as prophylaxis against liver abscessation

-no vaccine

Front 177

Actinomyces bovis

disease

Back 177

bovine actinomycosis-lumpy jaw

-assumed to invade following trauma

Front 178

Actinomyces bovis

affected area

Back 178

-mandible

-maxilla less common

causes chronic osteomyletis

-min involvement with regional lymph nodes

-swelling painful

-fistulous tracts

Front 179

Actinomyces bovis

diagnosis

Back 179

-advanced cases-distinctive clinical signs

-radiography

-bacterial culture

Front 180

Actinomyces bovis

culture appearance

Back 180

-filamentous branching

-non acid-fast (purple)

Front 181

Actinomyces bovis

treatment

Back 181

-small lesions: surgery

-adv cases: surgery unrewarding

prolonged therapy with penicillins

sodium iodine-IV multiple times

Front 182

Actinomyces viscosis

disease

Back 182

canine actinomycosis

-A. canis and A. hordeovulnaris also isolated in similar conditions

Front 183

Actinomyces viscosis

affected area

Back 183

extensive fibrovascular proliferation on the peritoneal and pleural surfaces

-with sanguinopurulent exudate

Front 184

Back 184

Actinomyces viscosis

gross apperance

Front 185

Actinomyces viscosis

diagnosis

Back 185

bacterial culture

Front 186

Actinomyces viscosis

treatment

Back 186

penicillins

Front 187

Nocardia sp

characteristics

Back 187

-gram (+)

-aerobic

-inhabitant of soils rich in organic matter

-opportunistic infections

Front 188

Nocardia sp

smear characteristics

Back 188

-smears: long, slender, branching filaments

+partial acid-fast

+gram staining (+)

Front 189

Nocardia sp

pathogenesis

Back 189

-assc with immunosuppression or heavy challenge

-usual mode of infection: inhalation

+may occur by skin wounds and teat canal

-supreoxide disnutase, catalase, and thick peptidoglycan confer resistance

Front 190

Nocardia sp

culture characteristics

Back 190

-culture: produce aerial filaments

+may have spores

+white, powdery, odorless, firmly adherent to agar

-grow in Sabouraud agar

Front 191

Nocardia sp

sequencing

Back 191

-16S rRNA DNA sequencing

Front 192

Nocardia asteroides

common name

Back 192

Canine nocardiosiis

Front 193

Nocardia asteroides

affected systems

Back 193

-pulmonary

-cutaneous

-CNS

Front 194

Nocardia asteroides

pulmonary

Back 194

-develop from inhalation

-not typically seen

-mostly in dry, warm climates

Front 195

Nocardia asteroides

cutaneous

Back 195

-result from intro of bacteria into wounds

-may produce mycetoma

Front 196

Nocardia asteroides

CNS

Back 196

-result from spread of bacteria in blood

-meningitis in humans-inhfalation to blood

Front 197

Nocardia asteroides

tx + control

Back 197

-tx less effective than for canine actinomycosis

+intrinsically resistant

-susceptibility using broth microdilution

-amikacin, imipenem-cilastatin, TMX usually effective

-prevention-avoiding exposure to bacteria in soil

Front 198

Bovine nocaridal mastitis

characteristics

Back 198

-chronic bovine mastitis

-usually sporadic cases

-diffuse or multifocal fibrosis

-white clots intermittently in milk

-systemic reactions may be induced during early lactation

Front 199

Bovine nocaridal mastitis

tx

Back 199

-difficult to treat

-dry-cow therapy with neomycin could be effective

Front 200

Bovine nocardiosis

common name + distribution

Back 200

bovine farcy

-limited to tropical areas

-Mycobacterium spp also isolated

Front 201

Bovine nocardiosis

systems affected

Back 201

chronic infection of superficial lymphatic vessels and lymph nodes

+thickened and cord-like

-nodules on the medial aspects of legs and on neck

Front 202

Actinobaculum suis

common name/disease

Back 202

porcine cystitis and pyelonephritis

Front 203

Actinobaculum suis

pathogenecity

Back 203

-causes cystitis and pyelonephritis in breeding pigs (mostly female)

-ascending infection

Front 204

Actinobaculum suis

predisposing conditions

Back 204

-mating

-trauma to urogenital tract

-presence of other organisms

-water restriction

Front 205

Actinobaculum suis

presentation

Back 205

-sudden death with or without clinical signs

-hematuria, azotemia

-mild fever

-painful urination

-arching of back

Front 206

Actinobaculum suis

diagnosis

Back 206

-gram stain (+)

-culture

-PCR

-immunofluoresence

Front 207

Actinobaculum suis

tx

Back 207

penicillin

ampicillin

Front 208

Dermatophilus congolensis

smear characteristics

Back 208

-gram (+)

-filamentous

-branching

-produces motile coccal zoospores

Front 209

Dermatophilus congolensis

predisposing factors + pathogenesis

Back 209

-maybe present in skin of healthy animals

-trauma and persistent wet conditions

-when activated, zoospores produce germ tubes and invade epidermis

-cyclical pattern or invasion/regeneration of epidermis, serous exudation and microabscess formation lead to raised scab-like crusts

Front 210

Dermatophilus congolensis

virulance factors

Back 210

-phospholipases

-proteolytic enzymes

-ceramidase

Front 211

Dermatophilus congolensis

dx

Back 211

-clinical picture

-scab material & skin in formalin

-smears from undersurface of scabs for Giemsa

-cultured on BAP

+small, yellowish, hemolytic colonies

-no growth in Sabouraud agar

-16S DNA sequencing

Front 212

Dermatophilus congolensis

clinical picture

Back 212

-dorsal areas of animals

+prolonged rainfall

+warm environment

-early lesions appear as papules

-serous exudate and inflammation produces adherent scabs

Front 213

Dermatophilus congolensis

tx

Back 213

-localized lesions can resolve spontaneously

-systemic long-acting oxytetracycline or penicillin/streptomycine

-topical tx ineffective

Front 214

Nocardioform placentitis

causative agents

Back 214

Crossiella equi

Amycolatopsis spp

Front 215

Nocardioform placentitis

pathogenesis

Back 215

gram (+) filamentous branching bacteria

-causes brown mucoid placentitis

-sporadic

Front 216

Nocardioform placentitis

clinical signs

Back 216

-premature udder development/lactation

-vulvar discharge

<1/2 mares exhibit signs

Front 217

Nocardioform placentitis

dx

Back 217

-ultrasound exam

Front 218

Nocardioform placentitis

outcomes

Back 218

-abortion

-premature foal

-term, but compromised foal

-normal foal

mare clears infection rapidly, rebreeds normally, not at increased risk of subsequent abortion

Front 219

Back 219

Trueperella (Arcanobacterium) pyogenes

Front 220

Back 220

Actinomyces bovis

Front 221

Back 221

Nocardia asteroides

canine nocardiosis

Front 222

Back 222

Dermatophilus congolensis

Front 223

Back 223

Nocardioform placentitis

Crossiella equi

Amycolatopsis spp

Front 224

Diseases associated with Staphylococcal sp

Back 224

infections of dogs and cats, S. intermedius(S. pseudointermedius)
staphylococcal mastitis, S. aureus
exudative epidermitis–S. hyicus
Omphalitis– S. aureus
Botryomycosis– S. aureus
Tick Pyemia– S. aureus
Methicillin resistant Staphylococcal infections

Front 225

Causative agent of Staphylococcal infections in dogs and cats

Back 225

S. intermedius(S. pseudointermedius)

Front 226

Staphylococal infections of cats and dogs are

Back 226

opportunistic pathogens

Front 227

staphylococcal diseases of cats and dogs cause

Back 227

suppurative conditions: dermatitis, pyoderma, otitis externa, endometritis, cystitis, osteomyelitis and wound infections

Front 228

symptoms of staphylococcal diseases of cats and dogs

Back 228

fever, pain, loss of appetite, itching, pus filled lesions such as pyoderma

Front 229

who is more susceptible to staphylococcal diseases of cats and dogs and why

Back 229

younger and older dogs due to weak immune system

Front 230

staphylococcal diseases of cats and dogs; cystitis cases signs and symptoms

Back 230

often urination, urinalysis may indicate increased protein and hemoglobin

Front 231

staphylococcal diseases of cats and dogs; diagnosis

Back 231

clinical signs
gram staining of clinical specimen
culture and/or biopsy

Front 232

When obtaining specimen for bacteriological culters one must

Back 232

–avoid superficial contamination
–special swab protected by a sterile otoscope for otic specimens
–skin shaved and disinfected for blood specimens
–urine collected by cystocentesis, catherter or midstream(clean catch)
–swabs should be kept in transport media, kept cold and submitted to lab ASAP

Front 233

staphylococcal diseases of cats and dogs: Tx

Back 233

–stop itching and scratching for skin diseases
–topical therapy may be ineffective in uncomplicated superficial infections(combinations of silver sulfadiazine, mupiracin, fusidic act etc)
–susceptible to antimicrobials including beta lactams though some multi resistance strains(MRS) detected
–for urinary infections drugs excreted by urine should be chosen for up to 2 weeks

Front 234

Staphylococcal mastitis

Back 234

common form of mastitis worldwide caused by S. aureus
–can be subclinical, chronic, and acute
–necrosis due to alpha toxins

Front 235

transmission of Staphylococcal mastitis

Back 235

contaminated hands and milking equipment

Front 236

what could cause systemic reaction and be lethal in staphylococcal mastitis

Back 236

peracute and gangrenous forms

Front 237

symptom of gangrenous form of staphylococcal mastits

Back 237

effected quarter is cold, dark and eventually sloughs

Front 238

Staphylococcal mastitis Tx

Back 238

–Cephalosporins, cloxacillin, erythromycin, penicillin
–if susceptible penicillin can be combined with novobiocin, pirliycin, tylosine or tilmicosin

Front 239

Staphylococcal mastitis Tx concerns

Back 239

–Antimicrobials administered by parenteral or intrammamary routes
–difficult to treat with success rate up to 60%
–intrammamary route advised: parenteral could be used during acute mastitis
–culture and susceptibility should be done

Front 240

Desirable characteristic of antimicrobials to treat mastitis

Back 240

–low MIC for pathogen
–high distribution and availability in mammary tissue
–low serum protein binding activity
–long half life

Front 241

control plan for mastitis

Back 241

–properly maintain of milking equipment
–hygienic milking practices
–post–milking teat disinfection
–antibiotic therapy for clinical cases and for dry cows
–culling of persistently infected cows

Front 242

Exudative epidermitis

Back 242

caused by S. hyicus in suckling and weaned pigs

Front 243

characteristics of exudative epidermitis

Back 243

widespread sebaceous secretion and exudation on skin surface and highly contagious

Front 244

symptoms of exudative epidermitis

Back 244

anorexic, depressed, febrile and non prutic dermatitis with greasy exudate

Front 245

Mobidity/mortality of exudative epidermitis

Back 245

20–100%/can reach 90% in litters

Front 246

S. hyicus can be isolated from

Back 246

healthy pigs' vaginal mucosa and skin

Front 247

Exudatie epidermitis transmission

Back 247

via minor abrasions on the skin

Front 248

exudative epidermitis predisposing factors/major virulence factor

Back 248

weaning/ exfoliative toxin

Front 249

exudative epidermitis diagnosis

Back 249

clinical: high mortality rate in oung pigs with exudative, non prutic skin lesions
laboratory: isolation and identification of S. hycus by culture

Front 250

Tx of exudative epidermitis

Back 250

early systemic antibiotic combined with topical antiseptics and/or antibiotics

Front 251

control of exudative epidermitis

Back 251

–strict isolation of infected pigs
–cleaning and disinfecting of contaminated buildings
–sows should be washed prior to farrowing with antiseptic soap

Front 252

S. aureus infections in poultry

Back 252

omphalitis– infection of yolk sac can be seen in young chicks
–skin injuries may cause localized abscesses like on the foot(bubblefoot)
–may also cause invasive infections in bones, joints, tendon sheaths, and sternal bursa

Front 253

omphalitis causes

Back 253

decreased weight gain and egg production and mortality

Front 254

S. aureus infections in poultry diagnosis

Back 254

E. coli and Pasteurela multocida may cause similar lesions in poultry so identification by culture

Front 255

S. aureus infections in poultry Tx

Back 255

AST must be performed due to common drug resistance

Front 256

S. aureus infections in poultry prevention

Back 256

–proper management to reduce injury and immunosuppression
–elimination of wood splinters, protruding wires of cages and fighting
–good litter management and hatchery management

Front 257

Botryomycosis

Back 257

–a chronic, suppurative condition often caused by S. aureus
–can occur within a few week of castration of horses due to infection of spermatic cord(schirrhous cord)
–can also happen in mammary tissues of sows, composed of fibrous tissue and pus

Front 258

Tick pyemia

Back 258

characterized by either septicemia and rapid death or by localized abscesses in many organs

Front 259

predisposing factor for tick pyemia

Back 259

Anaplasma phagocytophilum transmitted by ticks

Front 260

confirmatory test for tick pyemia

Back 260

microscopic identification of S. aureus in pus and isolation

Front 261

tick pyemia Tx

Back 261

–limited value
–prophylactic Tx of lambs can be initiated at age week 1

Front 262

most MRS strains are

Back 262

coagulase positive

Front 263

MRS Tx

Back 263

– limited options
–antimicrobial susceptibility must be performed
–vancomycin often the only drug of choice as well as oxazolidiones like Linezolid but never be used as a single agent to Tx MRSA infections

Front 264

Diseases/important species of Streptococcus spp

Back 264

–Strangles–S equi subsp equi
–Purpura hemorrhagca
–S. zooepidemicus and S.equisimilis
–S. canis
–Bovine streptococcal mastitis
–S. suis
–enterococcus spp

Front 265

Strangles

Back 265

–a febrile disease, with abscessation of lymph nodes, commonly in young horses that's highly contagious disease of horses
reportable disease

Front 266

transmission of strangles

Back 266

via purulent exudates or discharging absesses
–sales, shows, race–tracks increase the risk

Front 267

Strangles:Clinical signs

Back 267

–incubation period 3–6 days
–high fever, depression, and anorexia followed by oculonasal discharge which becomes purulent
–lymph nodes are swollen and painful characteristically submandibular lymph nodes are effected and eventually rupture discharging purulent highly infectious material
–guttural pouch empyema common
–most horses become immune with reinfection occurring in some horses

Front 268

Strangles Morbidity/mortality

Back 268

–up to 100%/less than 5%
–death due to complications

Front 269

Strangles– diagnosis

Back 269

–clinical signs and history of recent exposure to suspect animal
–must be differentiated from S. zooepidemicus and S. equisimilis for causing similar problems
–culture and PCR(tests are very sensitive to detect)
–colonies are beta hemolytic slightly mucoid
sugar fermentation tests help to differentiate

Front 270

Strangles Tx

Back 270

–Penicillin to in contact animals
–antimicrobial therapy is controversial for infected horses and limited if abscesses have formed
–carriers may be treated with local antibiotic treatment of guttural pouch
–ruptured abscesses should be flushed with 3–5%povidine–iodine solutions
–anti–inflammatory drugs for pain and fever

Front 271

Strangles– Control

Back 271

–isolation of suspected and infected horses
– isolated for 2 weeks when first introduced or when returning to property
–guttural pouch should be examined and tested by PCR to detect carriers
–live attenuated vaccines though may cause infections and side effects
–predisposing factors such as overcrowding should be avoided
–buildings and equipments should be cleaed following outbreaks

Front 272

Back 272

Purpura hemorrhagica

Front 273

Back 273

Strangles

Front 274

Purpura hemorrhagica

Back 274

immune mediated disease that may occur due to strangles
type 3 immune mediated vasculitis by damaging blood vessels leading to edema of head, ventral abdomen and libs and petechial hemorrhages of mucous membranes

Front 275

Tx of purpura hemorrhagica

Back 275

–dampening the immune response and removing the inciting cause
–started on dexamethasone to suppress the immune reaction
–then put on antibiotics to eliminate any underlying respiratory infections

Front 276

Back 276

Ascending placentitis associated with S. zooepidemicus and S. equisimilis being number 1 reason in horses

Front 277

S. zooepidemicus and S. equisimilis

Back 277

–mucosal commensals, opportunistic pathogens
–causes abortion, respiratory infections and suppurative conditions in horses, cattle, sheep and pigs

Front 278

strangles like syndromes in horses reported in

Back 278

S. zooepidemicus and S. equisimilis cases

Front 279

Differentiation of S. zooepidemicus and S. equisimilis

Back 279

–beta hemolytic colonies
– sugar fermentation tests and PCR
–must be differentiated from S. equi

Front 280

Tx of S. zooepidemicus and S. equisimilis

Back 280

–in early phase susceptible to beta lactams
–in early detection of placentitis tx could be effective
–no vaccines available

Front 281

Back 281

S. canis

Front 282

Back 282

S. canis

Front 283

S. canis

Back 283

–opportunistic pathogen causing neonatal septicemia, suppurative conditions(otitis externa, pneumonia, pleuritis, dermatitis, myositis, nephritis) and toxic shock syndrome in carnivores
–severe infections in puppies and kittens

Front 284

S. canis infections diagnosis

Back 284

–gram staining of exudate may reveal streptococci in chain
–culture of affected tissure reveals the presence of S. canis

Front 285

Tx of S. canis

Back 285

–usually susceptible to beta–lactams but Tx may not always be successful
–draining and flushing the abscesses hasten recovery
–dose could be higher than normally recommended because organisms could be harbored in the tonsillar crypts and pus
–cats with diskospondylitis may require up to 6 months of antimicrobial, usually starting with a parenteral injection then subsequent oral meds

Front 286

Bovine streptococcal mastitis

Back 286

three kinds
S. agalactiae
S. dysgalatiae
S. uberis

Front 287

S. agalactiae

Back 287

bovine streptococcal mastitis which colonizes milk ducts and produces intermittent acute infections

Front 288

S. dysgalatiae

Back 288

bovine streptococcal mastitis which is found in the buccal cavity, genitalia and skin and causes acute mastitis

Front 289

S. uberis

Back 289

bovine streptococcal mastitis which is a normal inhabitant of skin tonsils and vaginal mucosa, a major causative agent of mastitis usually without systemic signs.

Front 290

Bovine streptococcal mastitis diagnosis

Back 290

–clinical sins–inflammation of mammary tissue and clots in milk
–milk samples should be sent to lab for culture

Front 291

differentiation of mastitis causing streptococci

Back 291

by CAMP test and sugar fermentation tests
PCR also available

Front 292

Tx of bovine streptococcal mastitis

Back 292

susceptible antimicrobials following culture–tx success is high especially for S. agalactiae
for environmental streptococci dry season therapy

Front 293

bovine streptococcal mastitis control

Back 293

–milking hygiene
– biosecurity to limit reintroduction
–avoid cross–suckling in calves
–avoid any nutritional deficency
–minimize teat sealants prepartum
–cows that are refractory to tx should be culled

Front 294

S. suis is recognized as

Back 294

significant losses to pig industry

Front 295

S. suis Lancefiled group D

Back 295

–at least 35 serotypes with varying virulence
–serotype 2 is the most prevalent serotype

Front 296

S. suis is associated with

Back 296

–meningitis, arthritis, septicemia and bronchopneumonia of all ages
–sporadically can cause endocarditis, neonatal deaths and abortions
–respiratory cases are in conjunction with Mycoplasma spp and Pasteurella spp

Front 297

S. suis pathogenesis

Back 297

–capsule and an opacity factor are both essential pathogenic factors
–strains positive for suilysin, extracellular factor(EF), and muramidase released protein(MRP) are mose virulent
–adhesions such as fibronectin–binding protein are other factors
–hyaluronidase may facilitate local spread

Front 298

S. suis Tx

Back 298

–most strains susceptible to beta–lactams
–prophylactic long–acting penicillins can be given by injection to sows 1 week before farrowing and piglets during first 2 weeks of life

Front 299

S. suis control

Back 299

–bacteria tend to be endemic in a herd and eradication is not feasible
–improved husbandry needed
–vaccine are available but may not be effected mostly due to serotype differences

Front 300

Enterococcus species

Back 300

can cause opportunistic infections such as UTI and otitis in dogs, mastitis in cattle with E. faecalis most frequently isolated

Front 301

Enterococcus species identification

Back 301

–forms short chains and pairs and lacks a capsule
–previously classified with group D streptococci and reclassified as a separate genus

Front 302

enterococcus species are found in

Back 302

the human colon though rarely pathogenic at this site and can cause disease if introduced into other parts of body

Front 303

Tx of enterococcus species

Back 303

intrinsically resistant to many antimicrobials so difficult to treat making it a possible major health concern in humans

Front 304

Enterococcus spp differ from streptocci by

Back 304

–not sensitive to bile salts so will grow on MacConkey Agar
– some are motile

Front 305

prevention of enterococcus spp

Back 305

–difficult in health care setting
–patients often have weakened immune systems

Front 306

Back 306

Enterococcus

Front 307

Back 307

gram stain of purulent exudate of staphylococcal infections of dogs and cats

Front 308

Back 308

bubblefoot from omphalitis

Front 309

Back 309

omphalitis

Front 310

Back 310

Staphylococcal infections in dogs and cats

Front 311

Back 311

Staphylococcal infections in dogs and cats

Front 312

Back 312

Staphylococcal mastitis

Front 313

Corynebacterium spp morphology

Back 313

–small, pleomorphic, gram +
–in stained smears appear Chinese letter characters
–relatively slow growth in lab media

Front 314

Differentiating factors of corynebacterium spp

Back 314

–most are catalase +, oxidase –,
–non spore forming
–pathogenic bacteria are non motile
–cause pyogenic infections

Front 315

Back 315

chinese letter characters of corynebacterium spp

Front 316

corynebacteriu spp pathogenesis and pathogenicity

Back 316

–opportunistic pathogens
–pyrogenic organisms(with the exception of C. Bovis which can be isolated from teat canal of healthy cattle)

Front 317

C. presudotuberculosis can surviv and replicate in

Back 317

phagocytes

Front 318

virulence in C. presudotuberculosis is linked to

Back 318

–cell wall lipid and an exotoxin(phospholipase D(PLD)) and Corynebacteial secreted protease 40(CP40)

Front 319

what may enhance survival and multiplication of corynebacterium spp

Back 319

PLD

Front 320

CP40 induces

Back 320

strong immune response which may provide protection

Front 321

What do C. pseudotuberculosis and C. ulcerans produce

Back 321

diphtheria–toxin which the presence of in milk may have public implications

Front 322

C.renale group are

Back 322

–urinary tract pathogens and produce urease
–also posses fimbriae for attachment to urogenital mucosa

Front 323

Diagnositc procedures of Corynebacterium spp

Back 323

–animals species affected and clinical signs may suggest a specific infection
–suitable specimens for the lab: pus, exudate, affected tissue, midstream urine
–direct examination of gram stained smears may reveal corynebacteria
–culture media: blood agar, McConkey and CNA incubated up to 5 days at 37C

Front 324

Corynebacterium spp identifying diagnostic procedures

Back 324

–colonial characteristics
– presence of hemolysis
–absence of growth in McConkey, presences of growth in BAP and CNA
–typical corynebacterium polymorphism on gram stain
–biochemical tests

Front 325

Caseous lymphadenitis is

Back 325

a chronic suppurative condition of sheep, goat, and rarely cattle caused by C. pseudotuberculosis with organisms surviving in the environment for several months

Front 326

Caseous lymphadenitis transmission route

Back 326

–skin wounds, arthropod bites, or dips
–ruptured abscesses
–hematogenous spread causes abscesses in internal lymph nodes

Front 327

caseous lymphadenitis clinical signs

Back 327

–abscessation and enlargement of superficial and internal lymph nodes
–goats usually develop superficial, subcutaneous abscesses usually in the head and neck
–ill–thrift and pneumonia may be present
–visceral form may not be detected antemortem

Front 328

Back 328

caseous lymphadenitis

Front 329

incubation period of caseous lymphadenitis

Back 329

around 3 months

Front 330

Caseous lymphadenitis diagnosis

Back 330

–clinical (or postmortem) findings
–smears from lesions by gram stain
–isolation and identification of bacteria via submitted swabs to lab
–serological diagnosis:ELISA (individual and flock screen)
–interferon–gamma test as flock screen

Front 331

Caseous lymphadenitis: Tx

Back 331

susceptible to many antimicrobials but therapy is usually ineffective due to intracellular survival ability of bacteria and inability of drugs to penetrate into abscesses

Front 332

caseous lymphadenitis: control

Back 332

–import animals from countries/states/flocks free of caseous lymphadenitis
–animals should be subjected to pre–importation screening tests such as ELISA
–imported animals should be quarantines up to 3 months
–infected animals should be slaughtered
–contaminated buildings and equipment should be disinfected
–vaccines available

Front 333

ulcerative lymphangitis is/caused by

Back 333

– slow and chronic either lymphangitis of lower limbs or abscessation of pectoral region(also called pigeon fever)
–C. pseudotuberculosis in horses and rarely in cattle
–prevalent in fall and early winter

Front 334

ulcerative lymphangitis is transmited by

Back 334

skin wounds, arthropod bites or contact of infected animals

Front 335

Back 335

ulcerative lymphangitis

Front 336

Back 336

ulcerative lymphangitis

Front 337

ulcerative lymphangitis clinical signs

Back 337

–lymphatic vessels swollen and firm with nodules forming along their length
–edema develops in affected limbs and ulcerated nodules exude a thick odorless, greenish blood–tinged pus

Front 338

ulcerative lymphangitis diagnosis

Back 338

based on isolation and identification in the lab

Front 339

Tx and control of ulcerative lymphangitis

Back 339

–systemic antimicrobials may be combined with topical Tx
– affected animals should be isolated and contaminated areas disinfected

Front 340

Bovine pyelonephritis causative agent

Back 340

C. renale– which may be isolated from healthy cattle vulva, vagina and prepuce

Front 341

Bovine pyelonephritis acquired by

Back 341

stress of parturition and short urethra in cow may predispose to infection

Front 342

Back 342

Bovine pyelonephritis
–ascending infection from bladder to ureters can result in pyelonephritis with chronic infections possibly leading to extensive renal damage

Front 343

Bovine pyelonephritis: clinical signs

Back 343

–fever, anorexia and decreased milk production
–restlessness and kicking in the abdomen may indicate renal pain
–dysuria and blood tinged urine are present
–clinical signs may suggest UTI
–red blood cells and protein are present in the urine
– thickened ureter and enlarged kidneys may be detected by renal palpation and or ultrasonography: unilateral
–culture of C. renale frome urine is confirmatory

Front 344

Bovine pyelonephritis: Tx

Back 344

–antimicrobial tx based on susceptibility test, should start early for at least 3 weeks
–penicillin is usually good choice for high excretion in urine

Front 345

Ulcerative balanoposthitis

Back 345

–caused by C. renale
–characterized by ulceration around prepucial orifice with a brownish crust developing over the lesion
–similar lesion may happen on the vulva of ewes
–castrated sheep more prone
–untreated cases may progress to total occlusion of preputial orifice

Front 346

C. renale may cause mucosal irritation and ulceration by

Back 346

hydrolyizing urea into ammonia

Front 347

predisposing factor of Ulverative balanoposthitis

Back 347

high urea level in the urine due to high protein intake

Front 348

Back 348

ulcerative balanoposthitis

Front 349

rhodococcus equi morphology

Back 349

–gram positive rods or cocci
–salmon–pink, mucoid, non–hemolytic colonies
–aerobic, non motile
–CAMP test positive
–major respiratory pathogen of foals

Front 350

Back 350

Rhodococcus equi

Front 351

Rhodococcus equi– suppurative bronchopneumonia epidemiology

Back 351

–one of the most common causes of pneumonia in folas
–generally acquired by inhalation of dust
–may be present in high number in horse feces
–environmental influences–dry weather, poorgrass coverage
–high foal density
–only young foals susceptible

Front 352

Rhodococcus equi– suppurative bronchopneumonia pathogenesis

Back 352

–ability to survive and multiply in macrophage
–virulence is principally associated with a large??(not on slide)
–encodes several proteins most important VapA
–only equine isolates have VapA gene
–capsular polysaccharides, mycolic acids and exoenzymes

Front 353

Rhodococcus equi– suppurative bronchopneumonia clinical signs

Back 353

–usually less than 4 weeks old foals
–sudden onset of fever
–anorexia
–signs of bronchopneumonia
–could be insidious in 2–4 month old foals
–coughing, dyspnea, weight loss, exercise intolerance
–loud, moist rales on auscultation

Front 354

Back 354

Rhodococcus equi– suppurative bronchopneumonia

Front 355

Rhodococcus equi– suppurative bronchopneumonia: diagnosis

Back 355

–differentiating lower respiratory trac infections problematic
–WBC, fibronegen, radiography, ultrasonography,
–bacterial culture from tracheobronchial aspirate
–salmon color mucoid colonies on BAP, CAMP test
–PCR tests

Front 356

Rhodococcus equi– suppurative bronchopneumonia: Tx

Back 356

–combination of oral rifampin and a macrolide for up to 10 weeks
–severely affected foals have poor prognosis
–response to therapy monitored by radiography/ultrsonagrophy and plasma fibrinogen
–supportive therapy: rehydration and bronchodilatotory agents or expectorants

Front 357

Rhodococcus equi– suppurative bronchopneumonia: control

Back 357

–vaccines not available
–screening of foals twice a week clinical examination
–prevention of dust ihalation
–limit the foal density
–limited time spent indoor
–foaling at pasture may reduce the occurence
–passive immunization–hyperimmune plasma
–chemoprophylaxis–conflicting evidence and danger or resistance
–development of active immunization highly needed(aka vaccine)

Front 358

Symbiosis

Back 358

"live together"

Front 359

mutualism

Back 359

benefits mammal

benefits bacteria

Front 360

commensalism

Back 360

benefits bacteria

neither harms/benefits mammal

Front 361

parasitism

Back 361

benefits bacteria

harms mammal

Front 362

resident microbiata

Back 362

"normal flora"

"indigenous microbiota"

not normally causing disease

-resident

-transiet

Front 363

resident microbiota

Back 363

-part of the normal microbiota throughout life

-mostly commensal

Front 364

transient microbiota

Back 364

-remain in body for short period

-found in same regions as resident

-cannot persist in body

-competition from other microorganisms

-elimination by body's defense cells

Front 365

acquisition of normal microbiota

Back 365

-development in womb free of microorganisms

-microbiota begin to develop during birthing process

-much resident microbiota established during first months of life

-communities tend to be host-specific or organ-specific

-normal microflora primes the immune system

Front 366

Opportunistic pathogens

Back 366

-normal microbiota that cause disease under certain circumstances

-introduction into unusual site

-immune suppression

-changes in relative abundance may allow opportunity for member to thrive and cause disease

Front 367

reservoirs of infectious disease

Back 367

-most pathogens cannot survive for long period outside of their host

-sites where pathogens are maintained as a source of infection

-3 types

+infected animals

+carriers

+nonliving reservoir

Front 368

infected animal

Back 368

transmit disease by excretions

-aerosol

-direct

-feed

-venereal

Front 369

carriers

Back 369

-infected individual who are asymptomatic but infective to others

-some eventually develop illness, others never get sick

-healthy carriers may have defensive systems that protect them

Front 370

nonliving reservoirs

Back 370

-soil

-food

-water

contaminated often by feces or urine

Front 371

zoonoses

Back 371

-diseases naturally spread from animal host to humans

Front 372

acquisition of zoonoses

Back 372

-direct contact with animal/waste

-eating animals

-bloodsucking arthropods

humans usually dead-end host

Front 373

contamination

Back 373

the mere presence of microbes in/on the body

Front 374

infection

Back 374

when organism evades body's external defenses, multiplies, and becomes established in the body

Front 375

portals of entry

Back 375

-sites where pathogens enter body

-skin

-ear

-mucous membranes

-placenta

-parenteral route

Front 376

portals of exit

Back 376

-where we obtain specimens

-ear

-blood

-skin

-urine

-feces

-semen/vaginal excretions

-eye tears

-nose secretions

-saliva

-milk

Front 377

pathogen

Back 377

infectious biological agent causing disease to its host

-must find appropriate niche

-must compete with normal microflora

-must evade/overcome host defese

Front 378

pathogenisis

Back 378

-express proteins, adhesins, and other virulence factors to cause disease

Front 379

virulence genes

Back 379

many encoded within mobile genetic elements

-plasmid

-bacteria phage

-composon

some encoded in bacterial chromosome

Front 380

antibiotic resistance genes

Back 380

carried in plasmids

-makes other bacteria resistant to AB

Front 381

adhesion in infection

Back 381

-process by which microorganisms attach themselves to other cells

-required to successfully establish colonies in host

Front 382

Back 382

adhesion of pathogens to host cells

Front 383

adhesion factors

Back 383

-specialized structures

-attachment proteins

Front 384

role of adhesion

Back 384

-attachment proteins help in adhesion

-changing/blocking ligand or its receptor can prevent infection

-inability to make attachment proteins/adhesins renders microorganisms avirulent

-some bacterial pathogens attach to each other to form a biofilm

Front 385

attachment proteins

Back 385

-found on viruses and many bacteria

-viral/bacterial ligands bind host cell receptors

Front 386

virulence factors

Back 386

-adhesion factors

-biofilms

-extracellular enzymes

-toxins

-antiphagocytic factors

Front 387

pathogenicity

Back 387

ability of microorganism to cause disease

Front 388

virulence

Back 388

degree of pathogenicity

Front 389

virulence factors

extracellular enzymes

Back 389

-secreted by pathogen

-dissolve structural chemicals in body

-help pathogen maintain infection, invade, and avoid body defenses

Front 390

Back 390

extracellular enzymes

Front 391

Back 391

toxins

Front 392

virulence factors

toxins

Back 392

chemicals that harm tissues or trigger host immune responses that cause damage

-endotoxins

-exotoxins

Front 393

toxemia

Back 393

toxins in bloodstream that are carried beyond site of infection

Front 394

virulence factors

antiphagocytic factors

Back 394

prevent phagocytosis by the host's phagocytic cells

-bacterial capsule

+composed of chemicals not recognized as foreign

+slippery-difficult to engulf

-antiphagocytic chemicals

+prevent fusion of lysosome and phagocytic vesicles

+leukocidins directly destroy phagocytic WBCs

Front 395

infection

Back 395

the invasion of the host by a pathogen

Front 396

disease

Back 396

results if the invading pathogen alters normal bodily functions

-aka morbidity

Front 397

Back 397

stages of infectious disease

Front 398

symptom

Back 398

subjective characteristics of disease felt only by patient

Front 399

sign

Back 399

objective manifestations of disease observed/measured by others

Front 400

syndrome

Back 400

symptoms & signs that characterize disease/abnormal condition

Front 401

asymptomatic/subclinical

Back 401

lack symptoms, but may still have signs of infection

Front 402

acute diseases

Back 402

relatively sudden onset of symptoms that are usually severe

Front 403

chronic disease

Back 403

disease that persists for a long time. A chronic disease is one lasting 3 months or more

Front 404

subacute

Back 404

poorly defined state between acute and chronic

Front 405

latent disease

Back 405

remaining in an inactive or hidden phase

Front 406

communicable disease

Back 406

illness caused by an infectious agent or its toxins that occurs through the direct or indirect transmission of the infectious agent or its products from an infected individual or via an animal, vector or the inanimate environment to a susceptible animal or human host

Front 407

contageous disease

Back 407

An infectious disease that is spread through contact with infected individuals

Front 408

principal challenge of host response

Back 408

detection of pathogen & mounting a rapid defensive response

Front 409

innate immunity

Back 409

-external physical barriers

-internal protective cells

Front 410

external physical barriers

Back 410

-skin

-mucous membranes

Front 411

internal protective cells

Back 411

-macrophages

-neutrophils

-anti-microbial peptides

-interferons, complement inactivating pathogens

Front 412

Back 412

inflammation

Front 413

adaptive immunity

Back 413

acquired immunity against unique species of pathogens by highly specialized immune cells

Front 414

5 attributes of adaptive immunity

Back 414

-specificity

-inducibility

-clonality

-unresponsivesness to self

-memory

Front 415

4 functions of antiboides

Back 415

-neutralization

-opsonization

-oxidation

-agglutination

Front 416

Back 416

cellular immune response

Front 417

etiology

Back 417

-study of the cause of disease

Front 418

germ theory of disease

Back 418

disease caused by infections of pathogenic microorganisms

Front 419

Koch's postulates

Back 419

-suspected agent must be present in every case of the disease

-agent must be isolated and grown in pure culture

-cultured agent must cause disease when it is inoculated in a healthy, susceptible experimental host

-same agent must be reisolated from the diseased experimental host

Front 420

exceptions to Koch's postulates

Back 420

-some pathogens can't be cultured in lab

-disease caused by combo of pathogens & other cofactors

-ethical considerations prevent applying Koch's postulates to pathogens that require a human host

Front 421

difficulties in satisfying Koch's postulates

Back 421

-disease can be caused by more than 1 pathogen

-pathogens that are ignored as potential causes of disease