Block 4 Flashcards

Question 1

Q

Actinomyces overview

Gram pos or neg?
what do they look like?
describe?
what do they require?
are the motile?

Answer

A

Gram pos., club shaped rods with filamentous branching,
facultative/strict anaerobe, capnophilic (requires CO2), non-motile

Question 2

Q

Actinomyces overview

(bacteria surrounded by macrophages and
neutrophils) are formed and in chronic progressive infections the outer
zone of lesion has granulomatous characteristics

what is this?

Answer

A

Sulphur granules

Question 3

Q

Actinomyces overview

what animals usually get these?
where?
why?

Answer

A

Commensal of the oral cavity (mucosa and tooth surface) and mostly
cause infection in cattle when there is a break in the mucosa- therefore,
infections are typically endogenous

Question 4

Q

Actinomyces overview

if an infection is growing from within an organism, it is called?

Answer

A

endogenous

Question 5

Q

Actinomyces overview

are both mammals and humans affected?

Answer

A

Affects mammals and humans

Question 6

Q

Actinomyces overview

what about the Virulence factors?

Answer

A

Virulence factors: not well understood

Question 7

Q

Actinomyces overview

what about the Pathogenesis?
example?

Answer

A

Pathogenesis: Actinomyces has an affinity for bone
* There is a break or disruption of the oral mucosa barrier which allows the
bacteria to directly spread into the bone and can cause bone lysing in
chronic infections

Question 8

Q

Actinomyces overview

can it spread via blood or lymphatics?

Answer

A

Can also spread via blood or lymphatics

Question 9

Q

Actinobacillus lignieresi

what is it?
who gets it?
Dx?
DDx?
Tx?

Answer

A

-Wooden/timber tongue
-affects ruminants and horses but mostly cattle
-found in nasppharynx , enters through breaks in the mucosa and forms granulomas
-DX drooling, face swelling, histology, microscopic granules
-actinomyces bovis–lumpy jaw
-must catch early
difficult surgery
-cautious use of iodine treatments due to toxicity

Question 10

Q

Actinomyces bovis

Chronic and progressive granulomatous abscess that extends to the mandible, maxilla, and other bony tissue
of the head
* Eventually normal bone gets replaces by porous bone with sinus tracts containing pus

what is it?+

Answer

A

Pyogranulomatous osteomyelitis AKA Lumpy jaw in cattle

Question 11

Q

Actinomyces bovis

Pyogranulomatous osteomyelitis AKA Lumpy jaw in cattle
Transmission?
Predisposing factor?

Answer

A

Transmission: bacteria enters via penetrating wounds such as course hay or stick puncturing the oral mucosa
Predisposing factor: trauma to the oral mucosa

Question 12

Q

Actinomyces bovis

Pyogranulomatous osteomyelitis AKA Lumpy jaw in cattle
CS?
Dx?
Tx?
Prevention?

Answer

A

CS: facial swelling and distortion, draining of purulent exudate from fistulous tracts, loose teeth, dyspnea due to
swelling into the nasal cavity
Dx: culture purulent material (capnophilic), examine crushed sulfur granules under the microscope from
unopened lesions, rads to see degree of bone destruction
Tx: very long antibiotic treatment (3-12 mo.) with high doses of penicillin, surgical removal/excision if lesions are
small, generally euthanasia is the best option
Antibiotic treatment typically fails due to the microcolonies being walled off- hard for the antibiotics to reach the bacteria
Prevention: decrease risk of potential mechanical injury, remove foreign bodies

*Actin on my mandible

Question 13

Q

Dermatophilus overview

is it Commensal?
Gram + or -
describe
can it ever be zoonotic?

Answer

A

Gram pos., filamentous branching, aerobic so attracted to skin and is an obligate skin pathogen, also can be zoonotic

*Not commensal

Question 14

Q

Dermatophilus overview

How does it reproduce?

Answer

A

Reproduce by motile asexual zoospores, the filamentous hyphae will germinate
* Hyphae separate and appear like train tracks, then they produce coccoid fragments that become motile zoospores

Question 15

Q

Dermatophilus overview

how is it transmitted?

Answer

A

Transmission: contact via infected animals or indirect contact by arthropod mechanical vectors
* Can also infect humans by direct contact (rare) so be sure to wear gloves and use antibacterial soap

Question 16

Q

Dermatophilus overview

predisposing factors?

Answer

A

Predisposing factors (all break down skin protective layers): persistently wet skin, humidity, high temperatures, ectoparasites

Question 17

Q

Dermatophilus overview

Pathogenesis?

Answer

A

Pathogenesis: normal protective layer of skin barriers have to be weakened or deficient and then the bacteria will breach the
skin given the opportunity
* Once zoospores germinate to produce the hyphae, the hyphae will penetrate down into the epidermis and then spread in all
directions which results in a sever inflammatory response with scab and crust formation, epidermal abscesses, and hyperkeratosis

Question 18

Q

Dermatophilus overview

where is it more more prevelent?
who gets it?

Answer

A

More prevalent in the tropics (commonly seen here at St. Kitts) but is seen worldwide in cattle, sheep, goats, horses and
sometimes pigs, dogs, and cats

Question 19

Q

Dermatophilus overview

what does an acute infection look like?
chronic infection?

Answer

A

Acute infections: lesions heal spontaneously in 2-3 weeks
* Chronic infections: invasion of epithelium, scabs, proliferation and release of motile zoospores

Question 20

Q

Dermatophilus overview

what is necessary for it to occur?
what happens to cattle/goats/horses?
sheep?

Answer

A

Moisture is key

Cattle/goats/horses get dermatophilosis or cutaneous streptothricosis, horses also get rain rot or mud fever, **sheep get lumpy
wool **or strawberry foot rot

Question 21

Q

Dermatophilus congolensis

zoonotic?
what result?

Answer

A

yes
Can see significant morbidity and mortality in endemic areas
* Mortality mostly seen with secondary infections

Question 22

Q

Dermatophilus congolensis

Pathogenesis?

Answer

A

Pathogenesis: exudative epidermatitis with scab formation (dermatophilosis)
* First, bacteria will colonize in the hair follicles and penetrate the layers of the skin
* Next, there is an inflammatory response that causes keratinization followed by scab and crust formation
* Lastly, the cutaneous keratinization will form wart-like lesions and the hair will matte together
*shit poor freaking horse!

Question 23

Q

Dermatophilus congolensis

CS?
Dx?
Tx?
Prevention?

Answer

A

CS: epidermal abscesses, hyperkeratosis, scab formation
* Dx: appearance of lesions (very recognizable), histo or stained smears of scabs, cytology of fresh crust stained
with Giemsa
* Tx: injectable antibiotics primarily used
* Can use topicals to help prevent secondary infections, but they are not very effective against D. congolensis
* Q. Why are injectable AB indicated versus topical? Topicals wouldn’t reach all skin legions past epidermis
* Prevention: isolate and treat infected animals, shelter from rain, decrease scratch hazards in the grazing area,
reduce tick infestation
* Can do prophylactic treatment in endemic regions but antimicrobial resistance needs to be considered

Question 24

Q

Truperella

gram + or-
describe

Answer

A

Gram pos., pleomorphic, facultative
anaerobic, capnophilic, non-motile

Question 25

Q

Truperella

is it commensal?
where is it found?

Answer

A

yes
Found in the environment or on mucosa
of GI tract/resp. tract/urogenital tract of
cattle and swine

Question 26

Q

Truperella

who gets it and what does it cause?
what does it work synergistically with?

Answer

A

Opportunistic bacteria in cattle, sheep
and swine and causes suppurative
infections of any type in any location
(infections can lead to bacteremia)
* Commonly works synergistically with
Fusobacterium necrophorum

Question 27

Q

Truperella

hemolytic toxin that kills
neutrophils and macrophages, also
dermatonecrotic and fatal for lab
animals

what is it?

Question 28

Q

Truperella

Truperella pyogenes- Summer mastitis
what is it?
who gets it?
when does it occur?
how does it occur? hint what 3 bacteria…

Answer

A

Mastitis of non-lactating cows and heifers during the summer
months
* Works synergistically with: Peptostreptococcus indolicu and
Streptococcus dysgalactiae
* All 3 bacteria work together to cause Summer mastitis

Question 29

Q

Truperella

Truperella pyogenes- Summer mastitis
transmission?
cs?

Answer

A

Transmission: Hydrotea irritans (head fly)
CS: swollen/hard/painful/hot udder quarter with enlarged
teat (on teat ends)
Rice grain like clots and green to yellow pus will be secreted from
the udder

Question 30

Q

Truperella

Truperella pyogenes- Summer mastitis
Dx?
Tx?
Prevention?

Answer

A

CS: swollen/hard/painful/hot udder quarter with enlarged
teat
* Rice grain like clots and green to yellow pus will be secreted from
the udder
* Dx: gram stain smear of purulent material, necropsy, culture
* Tx: penicillin, but possibility of resistance
* Prevention: no vaccine, prevent the primary cause, vector
control

Question 31

Q

Actinobaculum suis

gram + or -
describe
who gets it (gender specifically)

Answer

A

Gram pos., rods, anaerobe,
non-motile

**Commensal **of the preputial diverticulum of boars, but NOT found
as a commensal in sows * So, causes problems in the sows but not the boars

Question 32

Q

Actinobaculum suis

transmission
speed of development?
result?

Answer

A

Transmission: only during coitus
* Disease develops quickly
* Porcine cystitis (UTI) and pyelonephritis in 3-4 weeks following coitus, and is potentially fatal due to renal failure

Question 33

Q

Actinobaculum suis

cs?
prevention?

Answer

A

CS: anorexia, arching up back, dysuria, hematuria (painful urination, blood in urine)
Prevention: artificial insemination

Question 34

Q

REVIEW QUESTION:
What are the 3 acid fast partial
bacteria?

Answer

A

corynebacterium
rhodococcus
nocardia

Question 35

Q

Anaerobes overview

what is required to grow?
example?
where can they be found?

Answer

A

Require anaerobic conditions to grow, an example of this is necrotized tissue
* Can be found in small amount in the GI tract (typically cecum, colon, and
rectum) of mammals

Question 36

Q

Anaerobes overview

gram + are called?
gram - are called?

Answer

A

There are gram pos. spore forming and gram neg. non-spore forming species

Question 37

Q

Anaerobes overview

When sending bacterial samples to the lab for testing, what must you use?

Answer

A

When sending bacterial samples to the lab for testing, you must use anaerobic
transport conditions

Question 38

Q

Anaerobes overview

characteristics of infections?
origin?
examples?

Answer

A

Infections are usually localized, oral and GI tract associated, and extend from
mucosal surfaces
* Commonly from endogenous origin
* Can see bacterial dissemination and a secondary localization
* Infections can include: abscesses, wound infections, aspiration pneumonia,
intra-abdominal infections, bacteremia, enteric infection, toxemia
* Mixed bacterial infection and synergistic relationships can occur

Question 39

Q

Clostridium overview

gram + or -?
describe?
what relevence Epsilon toxin?

Answer

A

Very large gram pos. rods, anaerobic, flagella for motility (except C. perfringens), rapid multiplication,
endospore forming, toxin producing
* C. perfringens produces Epsilon toxin, which is one of the most lethal and can be used as a bioterrorism agent

Question 40

Q

Clostridium overview

where found?
where located in animals?
what happens to the bacteria?
what sort of animals have a higher number of bacteria?

Answer

A

Found throughout the soil and can be seen in the GI tract of animals and humans
* Ultimately bacteria ends up in the feces
* Higher numbers of bacteria are found in carnivores

Question 41

Q

Clostridium overview

what is Caillas anthracis
is it contagious?
how transmitted
bioterrorism relevance?

Answer

A

Humans (wool sorters disease)
pulmonary-inhalation of spores and can take 2 months to manifest, rare but deadly

bioterrorism attacks in the US wen turning spores into powder form
not contagious

Question 42

Q

Clostridium overview

NEUROtoxic clostridia:
what is it?

Answer

A

NEUROtoxic clostridia: C. tetani and C. botulinum affect neuromuscular function

Question 43

Q

Clostridium overview

HISTOtoxic clostridia:
what is it?

Answer

A

HISTOtoxic clostridia: C. chauvoei, C. septicum, C. novyi, C. haemolyticum, cause localized lesion in the
muscle and liver

Question 44

Q

Clostridium overview

ENTEROtoxic clostridia:
what is it?

Answer

A

ENTEROtoxic clostridia: C. perfringens and C. difficile target the intestinal lining first and interfere with
protein synthesis

Question 45

Q

Clostridium overview

Predisposing factor?

Answer

A

Predisposing factor: necrotic tissue (the more necrotic tissue the higher chance of Clostridium spread)
* Vicious circle of necrotic tissue providing the environment for Clostridium growth, and then Clostridium producing
toxins that cause more necrosis

Question 46

Q

Clostridium tetani

? is a severe and potentially fatal intoxication with a NEUROtoxic clostridia causing SPASTIC
PARALYSIS

Question 47

Q

Clostridium tetani

where is it found?
who is most susceptible?

Answer

A

Found in the soil (usually the source of infection) or in the feces in low numbers
* Horses are the most susceptible species followed by humans and other species of animals

Question 48

Q

Clostridium tetani

transmission?

Answer

A

Transmission: wound gets contaminated with endospores from the environment

Question 49

Q

Clostridium tetani

toxins?
MOA?

Answer

A

Toxins: tetanospasmin (neurotoxin) and tetanolysin (tissue destruction and necrosis)
* MOA: tetanospasmin block neurotransmitters resulting in continuous stimulation or spastic paralysis
* There is irreversible binding of the toxin of the receptor and GABA cannot do its job of inhibition
*inhibition is stopped

Question 50

Q

Clostridium tetani

toxin spreads FROM the regional motor nerve in the limb TO other parts of the body
(dogs & cats)

what is this called?

Answer

A

Ascending tetanus

*all dogs go to heaven

Question 51

Q

Clostridium tetani

toxin in the blood stream spread FROM the head/neck TO other parts of the body
(horses & humans), and more commonly results in death
what is this called

Answer

A

Descending tetanus

Question 52

Q

Clostridium tetani

where do spasms start?
IP?
CS?

Answer

A

spasms start near head
IP: 5-10 days
* CS: stiffness in the head/neck, localized spasms, altered HR and resp. rate, dysphagia
*difficulty swallowing

Question 53

Q

Clostridium tetani

Dx?
what relevance immunity?

Answer

A

Dx: CS and look for wound/portal of entry
* Latent tetanus: wound site of infection is already healed
* Not beneficial to culture and toxins in serum or tissue is very challenging to find
* IMPORTANT: animals that recover are not necessarily immune because the toxin could have been in an
amount too low to reach the threshold to stimulate antibodies

Question 54

Q

Clostridium tetani

**know all 6 Tx- what are they?

Answer

A

Antitoxin: administered quickly to neutralize unbound toxin, quick but short term protection
* Anti-tetanus serum: passive immunization, gives a boost
* Toxoid: inactive vaccine to promote an immune response, based on TOXIN and not the bacteria
* Penicillin: give in large doses to kill bacteria that are producing toxins
* Surgical debridement and flush with peroxide (makes the wound an aerobic environment)
* Supportive care: reduce stimuli (put in a dark/quiet area), sedatives, muscle relaxants

Question 55

Q

Clostridium tetani

Prevention & control?

Answer

A

Prevention & control: vaccine in the key! Tetanus is a 100% preventable disease
* Toxoid immunization, prophylactic treatment post exposure with a toxoid booster, wound management, aseptic surgical
techniques and sterilization of surgical equipment
* Rapid case ID, surveillance and promote awareness

Question 56

Q

Clostridium botulinum

is a severe and potentially fatal intoxication by INGESTION (food) of pre-formed NEUROtoxins
causing FLACCID PARALYSIS
* Toxin type determines species from the wide group of neurotoxic clostridia (types A-G)

what is this called?

Question 57

Q

Clostridium botulinum

where found?
who gets it?

Answer

A

Found in rotting carcasses, decaying vegetation and contaminated canned foods due to germination
of endospores and growth of vegetative cells

Many animals species along with humans are all susceptible for botulism

Question 58

Q

Clostridium botulinum

Transmission?

Answer

A

bacteria is growing on food and producing toxins, animals then consumes food containing
TOXINS which are absorbed into the GI tract resulting in bacteremia
*stays on neuromusculas juction (sp?)

Question 59

Q

Clostridium botulinum

Toxin?
MOA?
result?

Answer

A

Toxin:** botulinum toxin is the most powerful exotoxin** (a very tiny amount can kill a human)
* MOA: the toxin blocks ACH release from vesicle, AKA the excitatory neurotransmitter is blocked with results in
flaccid paralysis
* Death due to paralysis of respiratory muscles

Question 60

Q

Clostridium botulinum

what effect aquatic birds?

Answer

A

Aquatic birds: Type E, consume toxins from the same source (like maggots containing toxins), will see
protrusion of 3rd eyelid

Question 61

Q

Clostridium botulinum

what effect humans

Answer

A

Humans: foodborne (rare but fatal, ingestion of toxins that have been formed in contaminated food),
wound/needles, infant (honey on pacifier, most common), inhalation (rare, unnatural so bioterrorism?)

**btw.. the honey comment is bullshit. My german nanny used to do it all the time. Also, Timmy had GI issues and I put caro syrup in every bottle (although I did replace the syrup often). just sayin…

Question 62

Q

Clostridium botulinum

IP?
CS?

Answer

A

IP: 3-17 days after ingestion of toxin
* CS: dilated pupils (1st CS), dry mucous membranes, decreased salivation, tongue flaccidity, dysphagia,
abdominal breathing

Question 63

Q

Clostridium botulinum

Dx- 2 ways, what are they?

Answer

A

Dx: 2 ways to confirm
* Toxins in serum of animal
* Toxins in food/stomach contents of animal

Question 64

Q

Clostridium botulinum

Tx?
Prevention and control?

Answer

A

Tx: depends on the stage/degree of infection
* Prevention & control: toxoid vaccination of cattle in endemic regions, don’t feed/eat food that is
suspected to have clostridium bacteria, prepare and preserve food accordingly

Answer 62

A

Bacteria is found throughout the environment
* Susceptible species: mainly young cattle (3 mo. to 2 years) and sheep of any age

Answer 63

A

exogenous infection of a wound (anaerobic environment), bacteria will
geminate and multiple thus producing toxins that cause tissue destruction
* Fermentation of the muscle glycogen will accumulate gas with a distinctive smell
* Bacteremia and toxemia will result in death within 24 hours
* Targets muscles with large mass: limbs, back, neck

Answer 64

A

CS: febrile (fever), emphysematous swelling (condition causing shortness of breath) and crepitation (crackling or rattling sound) due to gas accumulation, lameness, potentially see
lesion on myocardium and diaphragm (post-mortem)
* Tx: no treatment, the disease process is too fast
* Prevention: vaccination

Answer 65

A

Malignant edema or Gas gangrene

Answer 66

A

Many species are susceptible including sheep, horses, and cattle
* Predisposing factors: deep/traumatic anaerobic wound
* Prevention: surgically remove necrotizing missle tissue and promote drainage, can give penicillin prophylactically

Answer 67

A

C. novyi Type A
extrovert

Answer 68

A

C. novyi Type B
introvert

Answer 69

A

C. hemolyticum

Answer 70

A

Clostridium septicum
Malignant edema or Braxy

Answer 71

A

Predisposing/risk factors: IM injections, shearing,
docking, lambing, traumatic parturition,
castration
* Local exotoxins cause inflammation and myositis
that ultimately results in edema and necrosis

Answer 72

A

Dx: **direct fluorescent antibody
staining **test
* Anaerobic culture is not
necessarily rewarding and it
takes a significant amount of
time
* Tx: can use penicillin if caught
early enough
* Prevention & control: routine
vaccination with a
multicomponent toxoid (one
vaccine for several
bacteria/diseases)

Answer 73

A

ENTEROtocxic bacteria

Answer 74

A

4 major toxins: Alpha, Beta, Iota, Epsilon
Alpha is produced by ALL C. perfringens strains
Enterotoxin: produced by ALL C. perfringens strains

Answer 75

A

Found in the soil, feces, and GI tract (commensal) (in small numbers) of
animals and humans
* Types B, C, D: can survive in the soil as spores
* Type A: more likely to survive in the gut (especially of
carnivores)

Answer 76

A

Predisposing factors: STRESS
* Literally anything that may result in change to the gut
microbiota
* Examples: inappropriate husbandry, sudden diet changes,
temp changes, poor ventilation

Answer 77

A

C. perfringens causes necrotizing
hemorrhagic enteritis in many animal
species and can result in sudden death
without signs

Hemorrhagic so we see a lot of blood in the
intestines

Answer 78

A

B
lambs less than 3 wks

Answer 79

A

B and C
well-fed calves less than 1 month

Answer 80

A

C
newborn piglets

Answer 81

A

B
foals less than 1 week

Answer 82

A

C
adult sheep

Answer 83

A

C
adult goats

Answer 84

A

Rapid mucus-associated
proliferation
–> mucin degrading enzymes –>
break down mucus
–> sialidases remove sialic acid from
cells _-> epithelial cells easier to reach
à binding sites for other clostridial
toxins and enzymes
–>binding sites for other clostridial
toxins and enzymes

Answer 85

A

Toxin production (alpha
perfringolysin O) –> influx
neutrofiles, …

Answer 86

A

Epithelial sloughing and capillary
congestion –> haemorrhages,
increased vascular permeability, …

Answer 87

A

Intestinal necrosis –> absorption of
inflammatory cytokines and toxins
–>into systemic circulation, shock,
rapid death

Answer 88

A

C. perfringens types and and c –> toxins damage small intestine and liver (NetB pore-forming toxin)

opportunistic pathogen found in healthy gut flora of chickens

broilers 2-6 weeks old

Answer 89

A

Predisposing factors:
- High dietary amounts of animal by-products (fish meal), wheat, barley, oats (~NSP)
- Mycotoxin contamination à harm gut integrity à favorable pathogen environment
- Coccidiosis (Eimeria spp.) à leakage of plasma proteins by damage to epithelial cells + enhanced
mucus production in intestine

Answer 90

A

Clinical signs
- Acute, dark diarrhea
- Increasing flock mortality
- Ruffled feathers, lethargy, inappetence

Answer 91

A

Foodborne disease (consumption of chicken meat!)

Answer 92

A

Lamb dysentery

Answer 93

A

Predisposing factors: remember the intestinal system is not fully developed in
neonatal lambs
* Low proteolytic activity in the neonatal intestine
* Presence of trypsin INHIBITORS in the colostrum & low levels of pancreatic secretion (not
enough trypsin pro-enzyme)
* Decreased trypsin means decreased digestion of Beta toxins
* Immature intestinal microbiota
* Dietary influences in older lambs
* Abrupt change in diet to a rich diet like a spring pasture
* The lambs will overeat/gorge on this energy rich diet which will decreases intestinal
motility (hypomotility)

Answer 94

A

Pulpy kidney disease or Overeating disease

Answer 95

A

Predisposing factors: overeating or goring on a high grain diet or rich pasture
* Toxins: Epsilon toxin is produced and activated by proteolytic enzymes resulting in toxemia

Answer 96

A

lambs ingest a massive amount of food which allows ”carry over” of food into the intestines
along with a massive amount of starch and sugar
* Bacteria love sugar and this is a good substrate for bacterial proliferation

Answer 97

A

CS: (these are unique)
* Focal symmetrical encephalomalacia: dullness, convulsions, terminal coma
* Hyperglycemia and glycosuria (increased sugar content in blood and urine)
Post-mortem findings:
* Fluid distended intestines with petechial hemorrhage of the serosa
* Rapid kidney autolysis: pulpy cortical softening

Answer 98

A

CS such as sudden death (in unvaccinated animals) and/or post-mortem findings
Microscopy of stained intestinal fluids
Anaerobic culture to determine biotype, but not commonly done
Toxin detection in intestinal content

Answer 99

A

Tx:
* Hyperimmune serum when applicable
* Antimicrobials are usually not of much use and can cause more dysbiosis of the normal microbiota
* Prevention & control: vaccine is key!
* Routine vaccination of the toxoid in farm animals
* Avoid predisposing factors such as sudden diet changes or overeating

Answer 100

A

Enterotoxic

*commensal
*horses

Answer 101

A

primary cause of hospica acquired enterocolitis of humans who have received antibiotics or chemo
*neonates are resisitance but can carry toxogenic strains

Endospores are widespread and should be found in low numbers in a normal gut microbiota

Answer 102

A

antibiotic treatment and/or hospitalization (especially long term), old age, clindamycin in horses is a significant risk factor

Answer 103

A

fecal-oral route and infection occurs die to dysbiosis (imbalance of microbial homeostasis)

Answer 104

A

2 toxins usually work synergistically and increase the amount of damage:
-tox A enterotoxin- mainly causes diarrhea and some mucosal tissue damage
-tox b cytotoxin affects the intestinal cell lining

Answer 105

A

anaerobic culture but bacteria is sensitive and needs a selective media, direct toxin detection (tissue culture assay, ELISA, agglutination) * Gold standard test: tissue culture assay with specific antibody naturalizations for Tox
B

Answer 106

A

Tx: supportive care, stop antibiotics if possible, give probiotics, avoid anti-diarrhea meds (want to continue
getting rid of toxins), fecal microbial transplant (healthy stool transplanted into sick patients GI)

Answer 107

A

ENTEROtoxemia and explosive diarrhea disease of
rabbits between 4-8 weeks old

Answer 108

A

Commensal bacteria that produced Iota toxin but
typically causes problems following owners
medicating with “left over” antibiotics
* Causes fluid distention with hemorrhage of the
intestines and serosal surface

Answer 109

A

Antibiotics contraindicated in rabbits: lincomycin,
clindamycin, erythromycin
* These antibiotics can induce clostridial enterotoxemia
due to their selective effect of gram pos. bacteria
(basically they suppress the normal gut microbiota)

Answer 110

A

Gram neg. clostridium causing Tyzzer’s disease
of many species
* Lab animals: acute fatal diarrhea with
associated focal liver necrosis

Answer 111

A

Predisposing factors: poor sanitation, stress
* CS: watery diarrhea, anorexia, dehydration,
lethargy, death
* Tx: oxytetracycline
* Prevention: disinfection and decontamination
of the lab animal cages

Answer 112

A

Gram neg. and NON-spore forming bacteria that can be involved in a wide range of anaerobic and
mixed bacterial infections

Answer 113

A

Foot rot, Necrotic laryngitis, liver abscess

F. necrophorum is found as a commensal in the respiratory, GI and genital tracts of many animals and
also found in the environment
In severe infections, you will commonly see F. necrophorum, Trueperella pyogenes(also commensal) and Dichelobacter nodus
working synergistically

Answer 114

A

Transmission: a break in mucosal or epithelial barriers allow for entrance of the bacteria
* CS: extensive pus and necrosis
* Dx: CS, PCR, anaerobic culture

Answer 115

A

Tx: remove necrotic tissue, dip in antiseptic foot bath, antimicrobials
* Penicillin, metronidazole (targets anaerobic bacteria), clindamycin, chloramphenicol
* Not effective: aminoglycosides and sulfonamides
* Prevention: keep feet dry, avoid mechanical injury, vaccinate (sheep, cattle)

genetics play a role

Brainscape's Knowledge GenomeTM

Block 4 Flashcards

Brainscape's Knowledge Genome^TM