Bacti- 1St Exam

Front 1

how many of 1400 human diseases are zootic?

Back 1

60%

Front 2

factors determining spread of disease

Back 2

density of population
contact
transmission

Front 3

what are the 3 kingdoms/superkingdoms?

Back 3

bacteria
eukarya
archaea

Front 4

bacillus

Back 4

straight rod
2-5um long, 0.5-1um wide

Front 5

coccus

Back 5

sphere
1um diameter

Front 6

vibrio

Back 6

curved rod
2um long x 0,5um wide

Front 7

spirochete

Back 7

spiral shaped rod
up to 20um long x 0.1-0.2um wide
collection of vibrios

Front 8

bacterial taxonomy is concerned with...

Back 8

classification
nomenclature
identification

Front 9

bacterial classification are artificial in order to...

Back 9

1. speed up the identification process
2. id bacteria using a limited # of characteristics

Front 10

bacterial nomenclature involves use of...

Back 10

1. binomial system to assign a genus and species
2. specific conventions for naming

Front 11

bacterial identification is normally based on...

Back 11

1. morphological, biochemical, and serological "traits"
2. nucleic acid profile (DNA/RNA)

Front 12

division of cell in one plane produces

Back 12

diplococci
streptococci

Front 13

division of cell in 2 planes produces

Back 13

tetrads

Front 14

division of cell in 3 planes produces

Back 14

sarcinae

Front 15

division in multiple planes produces

Back 15

staphylococci

Front 16

features of a typical procaryotic cell

Back 16

- cytoplasm
- nucleoid body with DNA
- plasmid
- ribosome
- fimbrae
- flagella
- inclusion
- capsule
- cell wall
- cytoplasmic membrane

Front 17

what is the process of endospore formation?

Back 17

sporogenesis

Front 18

what color do endospores stain?

Back 18

uncolored

Front 19

sporogenesis

Back 19

1. septum forms btw 2 pockets of DNA
2. 2 membranes form around forespore with peptidoglycan btw them
3. endospore coat surround peptidoglycan
4. release of free endospore

Front 20

what is a major component in the cell wall of a gram + bacteria?

Back 20

peptidoglycan

Front 21

what is peptidoglycan made of?

Back 21

- carbohydrate "backbone" with amino acid linkages
- multiple layers thickness

Front 22

what is interspersed btw the peptidoglycan chains?

Back 22

1. wall trichoic acid
2. lipteichoic acid

Front 23

how is a gram - cell wall different than a gram + cell wall?

Back 23

- gram - cell wall only has one layer of peptidoglycan
- gram - has an outer membrane

Front 24

4 components of peptidoglycan network

Back 24

1. G = N-acetyl-D-glucosamine
2. M = N-acetyl-D-muramic acid
3. transpeptidase
4. M-G linkage

Front 25

purpose and drug targeting transpeptidase

Back 25

- helps retain rigidity
- link btw amino acids (tetrapeptides)
- penicillin target

Front 26

drug targeting M-G linkage

Back 26

lysozyme target

Front 27

action of lysozyme or penicillin on cell wall

Back 27

1. cytoplasmic membrane blebbing
2. hypotonic environment
3. membrane fragments due to lysis

Front 28

mycolic acids are...

Back 28

- acid fast bacteria
- family of alpha substituted beta-OH fatty acids

Front 29

mycolic acids are found in...

Back 29

Corynebacterium
Nocarddia
Mycobacterium

Front 30

are mycolic acids gram + or -?

Back 30

gram + but without teichoic acid

Front 31

stain color of mycolic acid

Back 31

red cells- imparts resistance to acid decolorization

Front 32

mycolic acid linkages

Back 32

- linked to muramic acid (lipids) via phosphodiester links
- linked to arabinogalactans by glycolipid linkages

Front 33

components of gram + cell membrane

Back 33

- lipid bilayer
- peptidoglycan

Front 34

components of gram - cell membrane

Back 34

- lipid bilayer
- peptidoglycan
- porins
- lipid + LPS

Front 35

components of acid fast cell membrane

Back 35

- lipid bilayer
- peptidoglycan
- arabinogalactan
- mycolic acid
- porins
- acyl lipids
- LAM

Front 36

are acid fast cells more resistant to AB than gram +/- cells?

Back 36

yes

Front 37

what is a flagella?

Back 37

- filamentous appendages (2-20um) composed of flagellin monomers
- allow for motility
- "H" antigens can be detected with specific antibodies

Front 38

what is a glycocalyx?

Back 38

- capsule layer (slime) composed of carbohydrates or glycoproteins
- not necessary for growth but inhibits phagocytosis and AB uptake
- very antigenic and "K" antigens can be detected with specific antibodies

Front 39

how does the glycocalyx protect a pathogen?

Back 39

inhibits phagocytosis by macrophage

Front 40

what is a pili?

Back 40

- filamentous appendages (0.5-2um) composed of pilin monomers
- highly antigenic and antibodies can be used for sero-diagnosis

Front 41

what are they two types of pili?

Back 41

1. fimbrae- allow for adhesion
2. specialized sex pili- allow for transfer of DNA btw a donor and a recipient

Front 42

average range in size of bacteria

Back 42

0.5-2 microns overall
(there are exceptions)

Front 43

virulence determinants in pathogens

Back 43

- pili
- flagellae
- capsules

Front 44

what do spores do?

Back 44

they are highly resistanct bodies- permit long term survival

Front 45

some target sites for antibodies

Back 45

- both intracellular and cell envelope components
- enyzmes
- ribosomes
- peptidoglycans
- mycolic acids

Front 46

what color are gram + bacteria?

Back 46

blue/purple

Front 47

what color are gram - bacteria?

Back 47

red/pink

Front 48

why are gram +/- different colors?

Back 48

b/c their cells walls differ in their ability to retain the crystal violet/iodine complex

Front 49

if a bacteria is facultatively anaerobic- under what atmospheric conditions can it grow?

Back 49

in the presence AND in the absence of oxygen

Front 50

what are the steps to solving a case?

Back 50

1. problem list
2. differential diagnoses for each problem
3. tests

Front 51

how do most pathogens cause pathology?

Back 51

by causing inflammation

Front 52

what evidence must you see to suspect an infectious disease?

Back 52

inflammation

Front 53

is all inflammation caused by micro-organisms?

Back 53

no

Front 54

name 3 different genera of gram + cocci

Back 54

- staphyloccocus
- streptococcus
- enterococcus

Front 55

how many joints are there in a hock?

Back 55

5:
1. tarsocrural
2. prox intertarsal
3. distal intertarsal
4. tarso-metatarsal
5. tarso-calcaneal

Front 56

what 2 things do you measure to determine if inflammation is present?

Back 56

total cell count
protein

Front 57

does coagulase positive relate to pathogenicity?

Back 57

yes
- it differentiates btw non pathogenic and pathogenic staphylococci

Front 58

what type of bacteria are staph?

Back 58

- gram + cocci
- form clusters
- facultatively anaerobic (grow best aerobically)

Front 59

how many types of species of staph are there and how many are of veterinary importance?

Back 59

~35
5 are of veterinary importance

Front 60

which 2 species of staph are most important?

Back 60

S. aureus- humans and dom species (coagulase positive)
S. intermedius- dogs (coagulase positive)

Front 61

how soon do animals get staph colonization after they're born?

Back 61

within hours

Front 62

are staph part of the normal flora (commensals)?

Back 62

yes

Front 63

where are coagulase + staph found?

Back 63

- skin (near mucocutaenous junctions- perineum, external genitalia, bovine udder- moist areas)
- distal nasal passage & external nares
- animal prods
- environment (long lived- promotes spread btw animals)
- transients in GI tract

Front 64

where are coagulase - staph found?

Back 64

- skin (normal flora)
- upper respiratory tract

Front 65

which two species usually don't have coagulase + staph species?

Back 65

dogs and cats

Front 66

how do animal acquire staph infections?

Back 66

endogenous- normal flora
exogenous- from skin of other animals (direct contact or indirect via fomites, soil, air, water) or from environment

Front 67

is interspecies spread imporant in staph infections?

Back 67

very limited- host adapted species are transiently present on another host species

Front 68

what type of pathogens are staph?

Back 68

opportunistic pathogens
- require underlying alteration in host-pathogen interaction

Front 69

are good or bad pathogens commonly isolated from infections?

Back 69

good pathogens

Front 70

do poor pathogens cause a lot of host compromise and require many bacteria numbers (more than good pathogens)?

Back 70

yes

Front 71

are staphs good or bad pathogens?

Back 71

good pathogens

Front 72

what are 3 virulence factors for staph?

Back 72

1. capsule or pseudocapsule (anti-phagocytic properties)
2. exotoxins- cytotoxins/hemolysins
3. intracellular survival

Front 73

is their strain variation in virulence factors?

Back 73

yes

Front 74

how does a capsule protect staph bacteria?

Back 74

- anti-phagocytic properties

Front 75

do both pathogenic and nonpathogenic staph have capsules?

Back 75

no
- only pathogenic staph have capsules

Front 76

what are capsules made of?

Back 76

carbohydrates- highly antigenic

Front 77

what are 2 types of staph exotoxins?

Back 77

haemolysins
leucocidin

Front 78

what do haemolysins do?

Back 78

- cytotoxic and lethal
- assist in id of pathogenic species of staph

Front 79

describe hemolysin alpha

Back 79

produces a clear zone around colonies (complete cell lysis)

Front 80

describe hemolysin beta

Back 80

produces a partial zone around colonies- partial cell lysis
- mutants without beta toxin are < virulent

Front 81

what is leucocidan?

Back 81

exotoxin for staph
- kills phagocytes, PMNs, macrophages (helps evade immune system)

Front 82

how does intracellular survival help staph bacteria?

Back 82

- evade immune system- Ab and intracellular killing
- evade antibiotics
- contributes to chronicity of disease (not all staph)
- helps staph survive in cells

Front 83

how does a glycocalyx help staph bacteria?

Back 83

helps adhere bacteria to implants- impairs AB access

Front 84

what is the predominant pattern of staph infections?

Back 84

suppuration and abscess formation

Front 85

what is suppuration?

Back 85

components of staph cell wall attract many neutrophils to site of infection- leads to pyogenic response

Front 86

what are 3 pyogenic bacteria?

Back 86

1. staphylococci
2. streptococci
3. corynebacteria

Front 87

how is staph different from strep clinically?

Back 87

staph can surive intracellularly (abscesses may be chronic)

Front 88

how does the immune system help in the dev of lesions in staph infections?

Back 88

- type IV hypersensitivity (delayed or cell mediated)- intensifies inflammatory responses while confining them
-. type III hypersensitivity (Ab/Ag complexes)- in canine pyoderma

Front 89

what is the pathogenesis of pus?

Back 89

1. pyogenic bacteria invade tissues and cause vascular dilation and exudation of neutrophiles from blood vessels
2. neutrophils move towards bacteria and may engulf them
3. pathogenic bacteria are antiphagocytic and prod toxins that kills cells
4. enzymes from dead neutrophiles add to tissue destruction
5. partial liquefaction of dead tissues- thick, yellow pus
6. pus is viscous due to large amt of DNA from nuclei of dead cells

Front 90

what happens if pus isn't drained?

Back 90

fibrous capsule will gradually be formed

Front 91

what specific diseases do staph cause?

Back 91

1. pyoderma
2. "greasy pig disease"
3. cystitis, pyelonephritis, prostatitis
4. discospondylitis, osteomyelitis, and septic arthritis
5. mastitis
6. implant infections

Front 92

what is the main cause of pyoderma?

Back 92

S. intermedius
(can also extend into ears to cause otitis externa)

Front 93

why are there different distributions to the lesions of pyoderma?

Back 93

diff dogs had diff underlying causes- diff distribution to their original lesions

Front 94

what is pyoderma called in birds?

Back 94

bumble foot

Front 95

what is it called when pyoderma penetrates deep tissues?

Back 95

cellulitis

Front 96

pyoderma is a problem in what 3 species?

Back 96

dogs
horses
rabbits

Front 97

what causes "greasy pig disease"?

Back 97

S. hyicus ss hyicus

Front 98

what is "greasy pig disease"?

Back 98

exudative dermatitis (thick, grayish brown) in piglets (<7 wks)- transmitted on vaginal mucosa and skin of sows thru minor abrasions

Front 99

in what organs does "greasy pig disease" usually become systemic and what is the prognosis?

Back 99

- lung
- LN
- kidney
- brain
- rapidly fatal (24-48hrs) but varies btw groups

Front 100

what causes cystitis, pyelonephritis, and prostatitis?

Back 100

S. intermedius

Front 101

what can cystitis lead to?

Back 101

struvite crystals and calculi due to urease production by bacteria (alkalises urine by prod ammonia)
- may ascend to cause pyelonephritis or prostatitis

Front 102

what causes discospondylitis, septic arthritis and osteomyelitis?

Back 102

S. aureus (horse/human skin, environment)
- infections usually iatrogenic- performance horses given intra-articular injections (direct innoculation)
- also haematogenously from cystitis, dermatitis, endocarditis, dental disease... (dogs and young animals)

Front 103

what causes mastitis?

Back 103

S. aureus
- infections usually endogenous but can go from cow-to-cow (contagious)

Front 104

how does mastitis occur?

Back 104

via teat canal

Front 105

what are the courses of infection in mastitis?

Back 105

- subclinical
- acute suppurative
- gangrenous (alpha hemolysin)
- chronic

Front 106

what are inplant infections caused by?

Back 106

staph coagulase negative species
(catheter, bone hardware)

Front 107

what are 2 characteristics of implants infections?

Back 107

- associated with significant local host compromise
- glycocalyx slime layer

Front 108

why do coagulase + staph cause disease so commonly?

Back 108

- part of normal flora so ready to cause disease
- effective virulence factors
- req little host compromise to cause disease

Front 109

is there long-lived immunity to staph infections?

Back 109

no

Front 110

what disease do coagulase - staph cause?

Back 110

implant infections

Front 111

what disease does S. hyicus ss hyicus cause?

Back 111

"greasy pig disease"
(exudative epidermitis)

Front 112

what diseases do S. intermedius cause?

Back 112

- otitis externa
- pyoderma
- urolithiasis, cystitis
- pyelonephritis, prostatitis

Front 113

what diseases do S. aureus cause?

Back 113

- arthritis and osteomyelitis
- mastitis

Front 114

what must be present to diagnose staph infections?

Back 114

- must be evidence of inflammation and bacteria
- bacteria isolated must have opportunity and be capable of causing disease

Front 115

what tests do we use to diagnose staph infections?

Back 115

- FNA
- culture on blood agar
- catalase test
- coagulase test
- sensitivity testing- esp if recurrent disease or in a compromised host or site

Front 116

are staph catalase + or -?

Back 116

catalase +

Front 117

do some strains of staph have an unpredictable sensitivity pattern?

Back 117

yes

Front 118

how are staph infections treated?

Back 118

- drain pus
- topical administration of mild antiseptics
- oral or topical AB
- APPROPRIATE LENGTH OF TIME

Front 119

inter-species spread of staph is rare, but is of concern in what species?

Back 119

S. aureus- MRSA

Front 120

what AB can be used to treat S. aureus?

Back 120

penicillinase-resistance penicillin (resistance has been recorded)

Front 121

are vaccines effective against staph bacteria?

Back 121

benefits are dubious
- no controlled clinical evaluations

Front 122

what does the gram stain of streptococci look like?

Back 122

- gram + cocci
- in chains (long)

Front 123

what is the oxygen req for strep?

Back 123

facultatively anaerobic

Front 124

how many species of strep are there and how many are of veterinary importance?

Back 124

~37 species
~9 are of veterinary importance

Front 125

what are 3 systems used to classify diff types of strep?

Back 125

1. haemolytic patterns
2. lancefield grouping
3. species level

Front 126

what are they types of haemolytic patterns in strep?

Back 126

1. beta-haemolytic strep: cause most imp diseases in domestic species
2. alpha haemolytic strep: imp in cattle, humans, dogs

Front 127

are non-haemolytic strep pathogenic?

Back 127

no

Front 128

who is in the group C lancefield group?

Back 128

horses

Front 129

who is in the group G lancefield group?

Back 129

dogs

Front 130

most strep infections cause what in horses?

Back 130

lymphadenitis

Front 131

most strep infections cause what in cattle?

Back 131

mastitis

Front 132

is strep catalase + or -?

Back 132

catalase -

Front 133

what are lancefield groups?

Back 133

- correlate to pathogenicity
- based on their C-substance (polysaccharide in cell wall)

Front 134

what species is in group A lancefield group?

Back 134

humans

Front 135

what species is in group B lancefield group?

Back 135

bovine mastitis

Front 136

what species in in group D,E lancefield groups?

Back 136

pigs

Front 137

where are strep bacteria found?

Back 137

- worldwide
-normal flora
- mucous membranes- upper resp tract, lower genitourinary tract, GI tract
- skin
- environment

Front 138

which strep species is part of the normal flora?

Back 138

S. equi ss zooepidemicus

Front 139

what strep species is on carrier animals?

Back 139

S. equi ss equi
- hang out in guttural pouch

Front 140

are strep bacteria fragile and susceptible to dessication?

Back 140

yes
- usually survive only short periods off host species

Front 141

which strep species is an obligate parasite (can't live off host)?

Back 141

s. agalactiae

Front 142

which strep species is environmental?

Back 142

S. uberis (bovine mastitis)
- do not live on host

Front 143

how do animals aquire strep infections?

Back 143

- endogenous infections- resident bacteria
- exogenous infections- environment
- contagious

Front 144

which strep species are resident bacteria?

Back 144

S. equi ss zooepidemicus
S. agalactiae

Front 145

which strep species are aquired from the environment?

Back 145

S. uberis

Front 146

which strep species are contagious?

Back 146

S. equi ss equi- transmitted by inhalations (aerosol droplets)
S. agalactiae- tranmitted during milking

Front 147

where do neonatal strep infections come from?

Back 147

maternal in origin

Front 148

can strep infections be transmitted indirectly by hands/fomites?

Back 148

yes

Front 149

how do strep virulence factors protect the bacteria?

Back 149

- avoid phagocytosis
- kill phagocytes

Front 150

can strep species survive intracellularly?

Back 150

no

Front 151

what are the virulence factors for strep?

Back 151

1. M protein (major factor)
2. capsules
3. hemolysins

Front 152

how does the M protein work?

Back 152

- ineffective opsonization: anti-phagocytic properties thru interference with effective deposition of complement
- reduces hemotaxis
- allows adherence to epithelial cells (S equi ss equi)
- induces Ab production which are protective- type specific immunity (imp in vaccines)

Front 153

where is M protein?

Back 153

a cell wall protein

Front 154

loss of M protein causes what?

Back 154

- loss of virulence
- change in colony type from rough to smoth

Front 155

are capsules present in every strep species?

Back 155

no

Front 156

what is alpha hemolysis in strep?

Back 156

- incomplete hemolysis
- zone of green around colonies
- most commensal streptococci
- cause less dz than beta hemolysis

Front 157

what is beta hemolysis in strep?

Back 157

- complete hemolysis
- result of action of streptolysins- destroy RBCs
- clear clarity around colony
- sensitive to penicillin
- most pathogenic

Front 158

how do capsules protect strep bacteria?

Back 158

avoid phagocytosis

Front 159

what is gamma hemolysis in strep?

Back 159

- non hemolytic
- little/no clearing around colonies
- most are non pathogenic

Front 160

are strep exotoxins well understood?

Back 160

no

Front 161

what do you see in strep infections clinically?

Back 161

suppuration and abscess formation- pyogenic bacteria

Front 162

are strep infections acute or chronic?

Back 162

acute
- cleared with production of protective antibodies (w/i 7-14 days)

Front 163

pathogenesis of strep?

Back 163

1. change in host/parasite interaction creating opportunity
2. invasion by potential pathogens that are part of normal flora- avoid host defenses and cause tissue damage
3. disease

Front 164

what do type III hypersensitivity reactions in strep cause?

Back 164

- causes disease to become chronic
- rheumatic fever
- purpura haemorrhagica
- glomerlulonephritis

Front 165

what is the normal gram stain for strep with abscesses and why?

Back 165

gram - b/c walls have been damaged by lytic enzymes released by phagocytes

Front 166

what is purpura haemorrhagica?

Back 166

- diffuse swelling of legs due to leakage of fluid from damaged blood vessels (edema)
- severe cases- sloughing of skin and exudation due to intravascular thrombosis and necrosis

Front 167

what species does strep cause most diseases in?

Back 167

horses

Front 168

what are diseases caused by strep?

Back 168

1. strangles
2. mastitis
3. pneumonia
4. neonatal septicemia
5. necrotising fasciitis
6. endometritis, endocarditis, arthritis (horses)

Front 169

what causes strangles and is it contagious?

Back 169

S. equi ss equi
yes

Front 170

what are characteristics of strangles?

Back 170

- worldwide
- young horses
- high morbidity
- low mortality

Front 171

what are signs of strangles?

Back 171

- fever
- nasal discharge
- anorexia
- abscess formation

Front 172

what are some complications from strangles?

Back 172

- guttural pouch empyema
- "bastard strangles"- metastatic spread
- purpura haemorrhagica

Front 173

what other species is strangles (as cervical lymphadenitis) seen in?

Back 173

- pigs
- cats

Front 174

is reinfection of strangles common in horses?

Back 174

no- very rare

Front 175

is strangles a notifiable disease?

Back 175

yes

Front 176

what strep species cause mastitis?

Back 176

S. agalacatiae
S. dysgalactiae
S. uberis

Front 177

do strep species need to be differentiated in mastitis and why?

Back 177

yes
- control measures are different

Front 178

what strep species cause pneumonia?

Back 178

S. pneumoniae- humans
S. zooepidemicus- horses
S. canis- dogs/cats
S. equisimilis- pigs

Front 179

what is required for pneumonia?

Back 179

predisposing factors (stressors)

Front 180

who is susceptible for neonatal septicemia?

Back 180

- foals
- piglets
- puppies
- kittens

Front 181

what is the source of infection for neonatal septicemia?

Back 181

mother
- normal flora of vagina/mouth
(mucus membranes)

Front 182

where does neonatal septicemia go in the body?

Back 182

- joints
- kidneys
- heart (endocarditis)
- meningitis

Front 183

what causes necrotising fasciitis in dogs/cats and humans?

Back 183

- group G (S. canis)- dogs/cats
- group A (S pyogenes)- humans

Front 184

what is necrotising fasciitis?

Back 184

flesh eating bacteria

Front 185

define infectious

Back 185

caused by a micro-organism

Front 186

define contagious

Back 186

infection capable of being transmitted from animal to animal

Front 187

where in the respiratory tract is it considered sterile?

Back 187

"sterile" after the larynx

Front 188

how does the host get rid of strep infections?

Back 188

antibody mediated immunity

Front 189

what is antibody mediated immunity?

Back 189

- strep are killed by antibody (opsonization) with phagocytosis or complemented-mediated killing
- antibody is serotype specific
- immunity is mostly long lived (not for vaxed animals)
- in cattle with mastitis, no useful immunity will develop (need to treat to cure)

Front 190

how do you diagnose a strep infection if it's part of the normal flora?

Back 190

- only significant if it has been isolated from a normally sterile site
- shows inflammation

Front 191

how do you diagnose a strep infections if the bacteria only exists in carriers or diseased animals?

Back 191

- isolationg even from a normal flora site is considered significant
- has to have clinical signs

Front 192

how do you treat strep infections?

Back 192

1. ancillary therapy- drain abscess, nursing care, anti-inflammatory agents
2. antibiotics- B hemolytic strep sensitive to penicillin

Front 193

what AB are B hemolytic strep species resistant to?

Back 193

- fluoroquinolones
- aminoglycosides
- tetracyclines

Front 194

what AB are A hemolytic strep species and enterococci resistant to?

Back 194

broader resistance than B hemolytic strep including penicillin

Front 195

how do you treat strangles?

Back 195

1. drain abscess
2. nursing care
3. no AB unless- very early (fever only), life threatening, "bastard" strangles

Front 196

how long can strep survive in the environment?

Back 196

weeks to month in dry, dusty conditions

Front 197

what kills most strep species?

Back 197

disinfectants

Front 198

how long should isolation/quarantine procedures be taken with strep?

Back 198

until free of organism- negative culture
(3-6 wks with strangles)

Front 199

how do you control strangles?

Back 199

- isolate infected animals
- use sep tact, brushes, rugs, feed, water bins...
- use different boots, clothes
- monitor temp of horses and isolate any febrile horse

Front 200

who is the vaccine for strangles for?

Back 200

horses
pigs

Front 201

what is the vaccine for strangles?

Back 201

- whole cell bacterin
- live avirulent vaccines (intranasal- US, in lip- UK)
- M protein (experimental)

Front 202

what is the controversy with live vaccines for strangles?

Back 202

- induction of disease
- induction of purpura

Front 203

what is the advantage with live vaccines?

Back 203

induces better immunity

Front 204

what does the gram stain for enterococci look like?

Back 204

gram + cocci

Front 205

where are enterococci found?

Back 205

normal flora of GI tract of animals

Front 206

are enterococci good or bad pathogens?

Back 206

bad pathogens
- not as virulent

Front 207

how does enterococci cause infections?

Back 207

- nosocomial and community acquired infections in compromised patients
- infections due to widespread antimicrobial resistance (vancomycin resistant enterococci- VRE)

Front 208

what are some characteristics of enterococci?

Back 208

- increasingly recognized in vet medicine (animals with prior antimicrobial theraphy)
- SUPERINFECTIONS

Front 209

what are micrococcus species and where is it found?

Back 209

- gram + cocci
- normal flora of skin
- NEVER pathogenic (common contaminants)

Front 210

what are peptococcus and peptostreptococcus?

Back 210

- gram + cocci
- strict anaerobes

Front 211

what are the 5 gram + cocci?

Back 211

1. staphylococci
2. streptococci
3. enterococci
4. micrococcus spp.
5. peptococcus and peptostreptococcus

Front 212

what are characteristics of gram + rods?

Back 212

- less freq isolated (but imp diseases)
- "tend" to cause syndromes
- more definitive diagnosis is required (morphology is very helpful)

Front 213

what is the gram stain for bacillus?

Back 213

- gram + rods
- large, blunt ended rods
- spores

Front 214

what is the most important bacillus species?

Back 214

bacillus anthracis

Front 215

what are some characteristics of bacillus?

Back 215

- spore forming (aerobic conds)
- capsulated (in vivo)
- facultatively anaerobic
- common lab contaminants
rarely involved in disease
- ubiquitous

Front 216

what are the spore forming gram + rods?

Back 216

- bacillus
- clostridia

Front 217

what bacillus species causes mastitis in cattle?

Back 217

B. cereus

Front 218

where does bacillus anthracis come from?

Back 218

- soil (saprophytes)- source for ruminants
- animals or animal products- source for humans/carnivores

Front 219

what kind of soil does bacillus anthrasis reside in?

Back 219

- alkaline pH
- rich in calcium and nitrate
- "Anthrax Belts"
- spores come to surface during heavy rain after drought
- source for ruminants

Front 220

where is bacillus anthracis endemic?

Back 220

- Africa
- Asia
- South Europe
- Australia
- South America

Front 221

where have there been outbreaks of bacillus anthracis in the US?

Back 221

- CA, Nebraska
- OK, SD
- TX, MN
- Gulf Coast
- Mississippi River delta

Front 222

how do animals aquire bacillus anthracis infections?

Back 222

1. ingestion of spores- primary route for herbs and carns (invade mm thru breaks in epithelium)
2. thru scratches or wounds- most common in humans
3. mechanical transmission- with biting insects
4. inhalation- rare, humans

Front 223

what was the first bacterium shown to be the cause of disease and by whom?

Back 223

bacillus anthracis by Robert Kock in 1877

Front 224

what kind of pathogen is bacillus anthracis?

Back 224

obligate pathogen

Front 225

what are the 2 virulence factors required for bacillus anthracis?

Back 225

1. capsule
2. exotoxin
* encoded by plasmids
* if present then B anthracis is an obligate pathogen in susceptible species

Front 226

what does the capsule do for bacillus anthracis?

Back 226

- confers resistance to phagocytosis
- Ab to capsule is not protective
- now have newer vaccines which induce protective anti-capsule antibodies

Front 227

what are the 3 components of the toxin for bacillus anthracis?

Back 227

1. protective antigen
2. edema factor
3. lethal factor

Front 228

what does the protective antigen do in bacillus anthracis?

Back 228

gets other 2 toxins inside cells

Front 229

what does the edema factor do in bacillus anthracis?

Back 229

- adenylate cyclase
- causes fluid and electrolytes to be released from cells
- decreases phagocytosis by PMNs

Front 230

what does the lethal factor do in bacillus anthracis?

Back 230

- causes massive IL-1 release from macrophages
- resultant inflammatory cascade is cause of death

Front 231

what specific diseases does B. anthracis cause?

Back 231

- anthrax in cattle, pigs, horses, goats, dogs, cats
- anthrax in humans

Front 232

different species have different susceptibility to what in bacillus anthracis?

Back 232

- infection
- toxins
*different clinical signs are observed in different species

Front 233

what is the most susceptible species to anthrax?

Back 233

ruminants
- relatively few spores req to cause disease

Front 234

describe the pathogenesis of anthrax in cattle

Back 234

1. enters thru abrasions in mm
2. build up toxin
3. invades bloodstream and causes septicemia
4. lethal factor comes into play
(initially stays localized and causes little edema- rel resistant to edema factor)

Front 235

what are the signs of anthrax in cattle?

Back 235

- tarry blood from body orifices (failure to clot)
- absence of rigor mortis
- sudden death (most common presenting sign in ruminants)

Front 236

what species are least susceptible to anthrax?

Back 236

- pigs
- dogs
- cats

Front 237

describe the pathogenesis of anthrax in pigs, dogs, cats

Back 237

- many spores req to cause disease
1. enter thru abrasions in mm
2a. rarely get build up of toxin and invades bloodstream
2b. usually stays in area and causes local edema (relatively susceptible to EF)

Front 238

what are the signs of anthrax in pigs, dogs, cats?

Back 238

- longer clinical course
- edema factor has greater role than in cattle
- localized edema in pharyngeal region (#1 area invaded)
- may get asphyxiation due to pharyngeal swelling

Front 239

describe anthrax in horses and goats

Back 239

- less susceptible
- signs depend on method of transmission

Front 240

what are signs of anthrax in horses and goats?

Back 240

- severe disease- colic septicemia (due to ingestion)
- mild disease- local edema (due to local inoculation)

Front 241

what are the 3 forms of anthrax in humans?

Back 241

1. cutaneous form "malignant carbuncle"
2. pulmonary form- "woolsorter's disease)
3. intestinal form

Front 242

describe the cutaneous form of anthrax in humans

Back 242

- most common (also in horses, pigs, rabbits)
- skin lesions marked by black eschar
- responds to therapy
- usually not fatal

Front 243

describe the pulmonary form of anthrax in humans

Back 243

- due to inhalation of lots of spores
- develop septicemia
- rapidly fatal if untreated
- postal workers

Front 244

describe the pulmonary form of anthrax in humans

Back 244

- ingestion
- uncommon in western world

Front 245

what specific diseases does bacillus cause?

Back 245

gangrenous mastitis (B. cereus)

Front 246

describe gangrenous mastitis

Back 246

- opportunistic infection
- commonly seen in treated cows (superinfection)

Front 247

what are signs of gangrenous mastitis?

Back 247

- milk is typically "port wine" color
- cows very sick and usually die
- can cause abortion...

Front 248

do you do a post mortem if you suspect anthrax?

Back 248

no

Front 249

how do you diagnose bacillus anthracis?

Back 249

- clinical signs
- blood sample
- gram/capsule stain

Front 250

what is a presumptive diagnosis for bacillus anthracis?

Back 250

encapsulated gram + rods with typical signs of anthrax

Front 251

is bacillus anthracis a notificable disease?

Back 251

yes

Front 252

what do you do if you want to confirm bacillua anthracis?

Back 252

let experts do it (FAT and culture)

Front 253

how do you treat bacillus anthracis?

Back 253

QUICKLY
- antibiotics
- antiserum (if available)

Front 254

what antibiotics do you use to treat bacillus anthracis?

Back 254

- penicillin & streptomycin
(both in ruminants)
- tetracyclines, fluoroquinolones
**other spp are more resistant to AB (esp. B. cereus)

Front 255

how do you control bacillus anthracis?

Back 255

YOU DON'T
- quarantine
- disinfection/disposal
- vaccination
- bury deep (>6.5ft) with 6" of quick lime underneatha dn on top of carcass
- incinerate carcasses (best but difficult in large outbreaks)

Front 256

is anthrax a zoonotic infection?

Back 256

yes

Front 257

what does a gram stain look like for clostrdium?

Back 257

- gram + rods
- spores

Front 258

describe clostridium

Back 258

- strict anaerobes
- motile
- gas producing
- endospore forming

Front 259

what AB is clostridia sensitive to?

Back 259

penicillin

Front 260

where does clostridia live?

Back 260

- soil
- GI tract- animals and humans
- freshwater and marine sediment

Front 261

how can clostridia survive?

Back 261

as spores or vegetative bacteria

Front 262

what is the virulence factor for clostridia?

Back 262

exotoxins

Front 263

what diseases are neurotoxic?

Back 263

- botulism
- tetanus

Front 264

what diseases are histotoxic?

Back 264

- malignant oedema/gas gangrene
- black disease
- black leg

Front 265

what diseases are entertoxemic?

Back 265

- enterotoxemia (C. perfringens)
- enteritis

Front 266

what is the pathogenesis of c. tetani

Back 266

1. predisposing factor that created an anaerobic environment in the host (deep penetrating wound with minimal trauma)
2. introduction of spores of c. tetani
3. germinated and produced toxins
4. toxins transported within axons of peripheral motor/sensory fibers to CNS
5. toxin has a high affinity for spinal cord (acts centrally rather than locally)
6. neurotoxin acts specifically on inhibitory synapses- prevent release of glycine and GABA from inhibitory interneuron's in brain/spinal cord
7. lack of inhibition leads to over-excitation of motor neurons that manifests as increased muscle tone, ridigity, spasm
8. spastic paralysis

Front 267

what is the exotoxin in c. tetani?

Back 267

tetanospasmin

Front 268

are clinical signs for c. tetani the same in all species?

Back 268

- yes and no
- muscle rigidity but extent of clinical signs is different

Front 269

why are there diff clinical signs for c. tetani between species?

Back 269

b/c resistance is related to the inability of the toxin to penetrate and bind nervous tissue
(if inject toxin directly into spinal cord, signs same in all species)

Front 270

which species are highly susceptible to c. tetani?

Back 270

- HORSES (most)
- guinea pigs
- humans
- mouse
- rabbies

Front 271

which species are less susceptible to c. tetani?

Back 271

- dogs
- cats
- cattle
- pigs
- sheep
- goats

Front 272

which species are extremely resistant to c. tetani?

Back 272

- birds
- cold-blooded animals

Front 273

what are signs of c. tetani?

Back 273

- convulsive contractions of voluntary muscles
- extensor rigidity ("sawhorse stance")- stiff gait, tail held erect
- protrusion of 3rd eyelid and enopthalmus (extraocular muscle hypertonicity)
- death due to spasm of muscles involved in respiration

Front 274

what is the parasympathetic involvement of c. tetani?

Back 274

- increase temp (excess muscular activity) -> increase HR (or decrease) -> increase RR -> increase salivation (parasympathetic involvement

Front 275

what are signs of c. tetani in dogs and cats

Back 275

- localized tetanus
- extensor rigidity in one body part (leg)
* can be more difficult to diagnose in cats/dogs with single limb affected

Front 276

what is c. tetani associated with in piglets and lambs?

Back 276

- castration
- shearing
- docking
- vaccinating
- injections

Front 277

what is c. tetani associated with in cattle?

Back 277

- genital tract post-parturition
- post-castration

Front 278

how is neonatal tetanus transmitted?

Back 278

via umbilical cord
(death in all species, including humans)

Front 279

how does the host get rid of infections of c. tetani?

Back 279

- natural immunity
- acquired immunity

Front 280

describe natural immunity of c. tetani

Back 280

host variation in susceptibility

Front 281

describe aquired immunity of c. tetani

Back 281

- passive- antitoxin administered to neutralize unbound toxin (horses/humans)
- active- toxoid (essential for horses) (also sheep, cattle, people)

Front 282

how do you diagnose c. tetani?

Back 282

- no good methods
- FNA and culture (hard b/c can't always find wound and bacterial numbers are low)
- serum tests- looking for Ab to exotoxin (rarely used)
** usually based on history of recent wound and clinical signs

Front 283

what is the treatment for c. tetani?

Back 283

- clean wound and debride
- antibiotics- penicillin G, metronidazole
- antitoxin (equine)- can cause anaphylaxis in SA
- sedatives
*difficult to treat in horses

Front 284

when should tetanus toxoid be given?

Back 284

- any horse with pentrating wound if not recently vaccinated
- pregnant mares often vaccinated with toxoid 4-6wks before foaling
- vaccination with toxoid givent o foals at 3-4mos of age, repeated 3-6 wks later
* protective titres within 14 days, last 1-5yrs
* boosters common (every 1-2yrs)

Front 285

where does c. botulinum come from?

Back 285

- soil, silage
- GI tract- animals/humans (can contaminate feed inside dead animals)
- freshwater and marine sediment

Front 286

what happens do c. botulinum under appropriate physical conditions?

Back 286

spores germinate and vegetative bacteria produce an exotoxin that is released upon bacterial cell lysis

Front 287

how do c. botulinum suvive?

Back 287

as spores or vegetative bacteria

Front 288

what is the pathogenesis of c. botulinum?

Back 288

1. germinate and produce toxin (soil, rotting vegetation, carcasses)
2. animals ingests preformed toxin and absorbed into bloodstream (or infects wounds)
3. transport to neurons via blood stream
4. circulating toxin reaches susceptible nerve endings and binds at the neuromuscular junctions or nerve-nerve junctions (cholinergic junctions of peripheral nerves)
5. toxin acts presynaptically and blocks acetylcholine release (binding of toxin is irreversible, once toxin enters cell, antitoxin can't reach it)
6. failure to cause a nerve action potential
7. flaccid paralysis, respiratory depression, possible vascular thrombus formation
8. respiratory failure cause of death

Front 289

which toxin is one of the most powerful toxins known?

Back 289

botulism toxin
- only tiny amts required to cause death

Front 290

how does the bacteria release the exotoxin in c. botulinum and what activates it?

Back 290

- releases the exotoxin as an inactive protoxin
- requires activation by enzymes (protein rish/rotting food provides these enzymes)

Front 291

how is the toxin acquired in c. botulinum?

Back 291

1. ingestion- pre-formed toxin in food, then absorption from GIT into bloodstream (most common)
2. multiplication of bacteria in wounds (rare)
3. colonization of GIT- produce toxin locally (infants- foals/humans)

Front 292

are all species susceptible to c. botulinum?

Back 292

species are susceptible to different types of botulinum neurotoxin

Front 293

what will you see clinically in c. botulinum?

Back 293

- severity depends on amt of toxin ingested (less severe = general weakness, muscle fasciculation, buckling, dysphagis, paralysis of tongue)
- incubation period is usually <6 days
- progressive, ascending, symmetrical flaccid paralysis
- generalized lower motor neuron disease
- weak and unable to stand

Front 294

what are signs of autonomic dysfunction in c. botulinum?

Back 294

- constipation
- urinary retention
- decreased salivation and lacrimation
- dilated pupils
- dysphagia
- colic

Front 295

what is c. botulinum called in birds?

Back 295

- chickens, water fowl
- "limber neck"
- birds willb e seen with their heads or necks dragging the ground

Front 296

what are the risks and signs of c. botulinum in cattle/sheep?

Back 296

- eating spoiled silage or feed contaminated with dead animals
- cattle grazing pastures deficient in phosphorous (cows eat bones/pica/to get phosphorus and ingest preformed toxin)
- recumbent, drooling
- dysphagis, rumenal atony
- laboured breathing

Front 297

what is the prevalence of c. botulinum in cats/lions?

Back 297

- cats are resistant to the effects of botulinum toxin
- reported occasionally in lions

Front 298

how is c. botulinum diagnosed?

Back 298

- normal PM grossly and histologically
- made by typical clinical signs
- demonstration of toxin (toxin specific ELISA, PCR on bacteria, mouse bioassays)
- need to do while acute disease present

Front 299

how is c. botulinum treated?

Back 299

- antibiotics have no value
- antitoxin may help if given early in disease (must be type specific)
- supportive- turn animal, help eat, respiratory support

Front 300

how is c. botulinum controlled?

Back 300

- vaccine- toxoid not routine for most species, need to use correct "type"
- management- prevent access to pre-formed toxin (spoiled silage, drinking water contaminated with dead animals)

Front 301

why is it not a good idea to give tetanus antitoxin to mares in the US?

Back 301

associated with Theiler's disease

Front 302

what is a major symptom of histoxic clostridia?

Back 302

gas pockets in muscle

Front 303

who and where does gas gangrene effect?

Back 303

- any species/age
- any tissue can be involved, but main tissues are muscle, liver, udder, intestine

Front 304

what histotoxic clostridia species is most often isolated (70%)?

Back 304

C. perfringens

Front 305

what causes infections of histotoxic clostridia?

Back 305

- wounds/trauma- anaerobic conditions
- management procedures- castration, injections, sx, dental procedures

Front 306

how does histotoxic clostridia cause disease?

Back 306

1. spores enter wound/latent in tissue
2. germination of spores if conditions are right (anaerobic)
3. exotoxins cause muscle necrosis and destruction of white cells, allowing more replication of bacteria
4. gas and collagenase cause further muscle damage
5. exotoxins absorbed into circulation causing widespread damage to endothelial and blood cells, liver, muscle

Front 307

how is histotoxic clostridia diagnosed?

Back 307

- quickly!
- history and clinical signs
- visualization of organisms in tissue (FNA)
- culture (take time, don't delay txt)
- fluorescent Ab test- on impression smears for confirmation

Front 308

how is histotoxic clostridia treated?

Back 308

- debridement (most important)
- penicillin (all clostridia are sensitive)- big doses
- antitoxin- value?
- oxygen therapy- intranasal, S/A, hyperbaric oxygen chamber

Front 309

what are 2 other names for gas gangrene?

Back 309

- myonecrosis
- malignant edema

Front 310

what are clinical signs of histotoxic clostridia?

Back 310

- febrile
- increased HR, RR
- depression
- crepitus
- discharge/pus from abscess

Front 311

what clostridia species causes black disease?

Back 311

c. novvi type B

Front 312

what is the role of the metacerariae in black disease?

Back 312

- liver fluke helps move c. novvi from GIT to the liver
- creates a trail of liver necrosis that is perfect home for an oxygen hating anaerobe

Front 313

how does c. novyi cause black disease?

Back 313

1. conds in liver allow it to germinate and multiply, produce exotoxin, enters circulation
2. exotoxin causes:
- increased capillary permeability (edema)
- damage to muscles including heart
- congestion of SQ vessels
- hemolysis (can be marked)
- death

Front 314

how is black disease diagnosed?

Back 314

- history & clinical signs
- PM- blood stained serous fluid in pericardium/pleural/peritoneal cavities, blood stained froth from nostrils, SQ edema and blackening of skin, swollen liver (areas of necrosis), presence of mature liver flukes
- impression smear of cut surface shows gram + rods
- fluorescent Ab test on liver samples

Front 315

what are risk factors for enterotoxemic clostridia?

Back 315

- lambs, calves, sheep, goats- overeating
- seen in feedlots when feeding rich grains
- lambs suckling heavily lactating ewes feeding on lush grass

Front 316

how does overeating cause disease?

Back 316

- overeating leads to gut stasis
- allows migration of c. perfringens type D from LI to SI- multiplication
- lil damage in gut (more in adults)
- bacteria releases epison prototoxin (exotoxin)- activated by trypsin and chymotrypsin in SI
- SI has receptors on enterocytes that allow toxin absorption
- large amts of activated epsilon toxin absorbed into circulation (increase capillary permeability- brain edema and necrosis, damage/necrosis to capillaries/renal cortex in kidney
- death due to convulsions, hypovolaemia, edema of lungs, fliud in body cavities

Front 317

overeating disease is also called what?

Back 317

pulpy kidney due to necrosis of renal cortex in kidney

Front 318

what species of enterotoxemic clostridia causes disease?

Back 318

C. perfringens type D

Front 319

what exotoxin is released from c perfringens type d?

Back 319

epsilon prototoxin

Front 320

what activates epsilon prototoxin?

Back 320

activated by trypsin and chymotrypsin in SI

Front 321

how is c. perfringens type d diagnosed?

Back 321

- history, clinical signs
- PM- large numbers of clostridia in upper SI
- samples must be taken quickly after death
- id epsilon toxin in SI contexts or serum (ELISA)

Front 322

how is black disease and overeating treated?

Back 322

- penicillin and antitoxin
- supportive
- sudden death
- rarely economical in sheep

Front 323

how are histotoxic clostridia infections controlled?

Back 323

- combined vaccines
- management- multi-use preparations, poor hygiene

Front 324

how are enterotoxemic clostridia controlled?

Back 324

- vax with toxoid against epislon toxin (short lived vaccine)
- vax ewes before lambing
- vax lamb at 1-2 mos, booster in 4 wks
- management- control things that cause gut stasis, contro liver fluke, multi-use preparations, poor hygiene

Front 325

what species of clostridia produce dysentery and enteritis?

Back 325

- c. perfringens (primarily)
- c. difficile

Front 326

what are signs of dysentery and enteritis?

Back 326

- diarrhea
- severe- hemorrhagic- dehydration, hypovolemia, toxemia, depression, dark/dry mm

Front 327

who is more susceptible to dysentery and enteritis?

Back 327

- young animals
(foals, calves, lambs, piglets)
- adults
(dogs, horses)

Front 328

are dysentery and enteritis pathognomonic?

Back 328

no

Front 329

how are dysentery and enteritis diagnosed?

Back 329

- clinical signs- not pathognomonic
- isolation of bacteria- no good
- fecal smears- dubious
- fecal enterotoxin immunodetection (best!)

Front 330

how are dysentery and enteritis treated?

Back 330

- treat acute disease- ampicillin, metronidazole, erythromycin
- may treat mild/chronic disease with AB
- tetracyclines are not useful
- supportive therapy!