Block 4 Flashcards
Actinomyces overview
Gram pos or neg?
what do they look like?
describe?
what do they require?
are the motile?
Gram pos., club shaped rods with filamentous branching,
facultative/strict anaerobe, capnophilic (requires CO2), non-motile
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?
Sulphur granules
Actinomyces overview
what animals usually get these?
where?
why?
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
Actinomyces overview
if an infection is growing from within an organism, it is called?
endogenous
Actinomyces overview
are both mammals and humans affected?
Affects mammals and humans
Actinomyces overview
what about the Virulence factors?
- Virulence factors: not well understood
Actinomyces overview
what about the Pathogenesis?
example?
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
Actinomyces overview
can it spread via blood or lymphatics?
Can also spread via blood or lymphatics
Actinobacillus lignieresi
what is it?
who gets it?
Dx?
DDx?
Tx?
-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
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?+
Pyogranulomatous osteomyelitis AKA Lumpy jaw in cattle
Actinomyces bovis
Pyogranulomatous osteomyelitis AKA Lumpy jaw in cattle
Transmission?
Predisposing factor?
- Transmission: bacteria enters via penetrating wounds such as course hay or stick puncturing the oral mucosa
- Predisposing factor: trauma to the oral mucosa
Actinomyces bovis
Pyogranulomatous osteomyelitis AKA Lumpy jaw in cattle
CS?
Dx?
Tx?
Prevention?
- 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
Dermatophilus overview
is it Commensal?
Gram + or -
describe
can it ever be zoonotic?
- Gram pos., filamentous branching, aerobic so attracted to skin and is an obligate skin pathogen, also can be zoonotic
*Not commensal
Dermatophilus overview
How does it reproduce?
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
Dermatophilus overview
how is it transmitted?
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
Dermatophilus overview
predisposing factors?
Predisposing factors (all break down skin protective layers): persistently wet skin, humidity, high temperatures, ectoparasites
Dermatophilus overview
Pathogenesis?
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
Dermatophilus overview
where is it more more prevelent?
who gets it?
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
Dermatophilus overview
what does an acute infection look like?
chronic infection?
Acute infections: lesions heal spontaneously in 2-3 weeks
* Chronic infections: invasion of epithelium, scabs, proliferation and release of motile zoospores
Dermatophilus overview
what is necessary for it to occur?
what happens to cattle/goats/horses?
sheep?
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
Dermatophilus congolensis
zoonotic?
what result?
yes
Can see significant morbidity and mortality in endemic areas
* Mortality mostly seen with secondary infections
Dermatophilus congolensis
Pathogenesis?
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!
Dermatophilus congolensis
CS?
Dx?
Tx?
Prevention?
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
Truperella
gram + or-
describe
Gram pos., pleomorphic, facultative
anaerobic, capnophilic, non-motile
Truperella
is it commensal?
where is it found?
yes
Found in the environment or on mucosa
of GI tract/resp. tract/urogenital tract of
cattle and swine
Truperella
who gets it and what does it cause?
what does it work synergistically with?
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
Truperella
hemolytic toxin that kills
neutrophils and macrophages, also
dermatonecrotic and fatal for lab
animals
what is it?
Pyolysin
Truperella
Truperella pyogenes- Summer mastitis
what is it?
who gets it?
when does it occur?
how does it occur? hint what 3 bacteria…
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
Truperella
Truperella pyogenes- Summer mastitis
transmission?
cs?
- 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
Truperella
Truperella pyogenes- Summer mastitis
Dx?
Tx?
Prevention?
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
Actinobaculum suis
gram + or -
describe
who gets it (gender specifically)
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
Actinobaculum suis
transmission
speed of development?
result?
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
Actinobaculum suis
cs?
prevention?
CS: anorexia, arching up back, dysuria, hematuria (painful urination, blood in urine)
Prevention: artificial insemination
REVIEW QUESTION:
What are the 3 acid fast partial
bacteria?
corynebacterium
rhodococcus
nocardia
Anaerobes overview
what is required to grow?
example?
where can they be found?
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
Anaerobes overview
gram + are called?
gram - are called?
There are gram pos. spore forming and gram neg. non-spore forming species
Anaerobes overview
When sending bacterial samples to the lab for testing, what must you use?
When sending bacterial samples to the lab for testing, you must use anaerobic
transport conditions
Anaerobes overview
characteristics of infections?
origin?
examples?
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
Clostridium overview
gram + or -?
describe?
what relevence Epsilon toxin?
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
Clostridium overview
where found?
where located in animals?
what happens to the bacteria?
what sort of animals have a higher number of bacteria?
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
Clostridium overview
what is Caillas anthracis
is it contagious?
how transmitted
bioterrorism relevance?
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
Clostridium overview
NEUROtoxic clostridia:
what is it?
NEUROtoxic clostridia: C. tetani and C. botulinum affect neuromuscular function
Clostridium overview
HISTOtoxic clostridia:
what is it?
HISTOtoxic clostridia: C. chauvoei, C. septicum, C. novyi, C. haemolyticum, cause localized lesion in the
muscle and liver
Clostridium overview
ENTEROtoxic clostridia:
what is it?
ENTEROtoxic clostridia: C. perfringens and C. difficile target the intestinal lining first and interfere with
protein synthesis
Clostridium overview
Predisposing factor?
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
Clostridium tetani
? is a severe and potentially fatal intoxication with a NEUROtoxic clostridia causing SPASTIC
PARALYSIS
Tetanus
Clostridium tetani
where is it found?
who is most susceptible?
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
Clostridium tetani
transmission?
Transmission: wound gets contaminated with endospores from the environment
Clostridium tetani
toxins?
MOA?
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
Clostridium tetani
toxin spreads FROM the regional motor nerve in the limb TO other parts of the body
(dogs & cats)
what is this called?
Ascending tetanus
*all dogs go to heaven
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
Descending tetanus
Clostridium tetani
where do spasms start?
IP?
CS?
spasms start near head
IP: 5-10 days
* CS: stiffness in the head/neck, localized spasms, altered HR and resp. rate, dysphagia
*difficulty swallowing
Clostridium tetani
Dx?
what relevance immunity?
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
Clostridium tetani
**know all 6 Tx- what are they?
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
Clostridium tetani
Prevention & control?
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
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?
Botulism
Clostridium botulinum
where found?
who gets it?
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
Clostridium botulinum
Transmission?
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?)
Clostridium botulinum
Toxin?
MOA?
result?
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
Clostridium botulinum
what effect aquatic birds?
Aquatic birds: Type E, consume toxins from the same source (like maggots containing toxins), will see
protrusion of 3rd eyelid
Clostridium botulinum
what effect humans
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…
Clostridium botulinum
IP?
CS?
IP: 3-17 days after ingestion of toxin
* CS: dilated pupils (1st CS), dry mucous membranes, decreased salivation, tongue flaccidity, dysphagia,
abdominal breathing
Clostridium botulinum
Dx- 2 ways, what are they?
Dx: 2 ways to confirm
* Toxins in serum of animal
* Toxins in food/stomach contents of animal
Clostridium botulinum
Tx?
Prevention and control?
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
Clostridium chauvoei
is a severe exogenous infection by HISTOtoxic clostridia, causing necrotizing myositis
* 100% fatality
what is it called?
Blackleg
Clostridium chauvoei
where found?
susceptible species?
Bacteria is found throughout the environment
* Susceptible species: mainly young cattle (3 mo. to 2 years) and sheep of any age
Clostridium chauvoei
Transmission & pathogenesis
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
Clostridium chauvoei
CS?
Tx?
Prevention?
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
Clostridium novyi & Clostridium hemolyticum
an exogenous, necrotizing, wound infection caused by HISTOtoxic
clostridia
is called?
Malignant edema or Gas gangrene
Clostridium novyi & Clostridium hemolyticum
who gets it?
predisposing factors?
prevention?
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
Clostridium novyi & Clostridium hemolyticum
* Exogenous
* Gas gangrene
* Big head in rams
what is it and is it extrovert or introvert?
C. novyi Type A
extrovert
Clostridium novyi & Clostridium hemolyticum
Endogenous
* Black disease (infectious necrotic
hepatitis)
* Predisposing factor: fluke
damage
what is it and is it extrovert or introvert?
C. novyi Type B
introvert
Clostridium novyi & Clostridium hemolyticum
Endogenous (GI commensal)
* Liver damage (lots of blood)
* Bacillary hemoglbinuria
* Mainly affects cattle and sheep
what is it?
C. hemolyticum
Clostridium
? is a HISTOtoxic
clostridia from either an exogenous or
endogenous infection
* Braxy: abomasitis of sheep caused by exotoxins of
C. septicum
* Exogenous: via wounds
* Endogenous: dormant spores present in the
muscle
Clostridium septicum
Malignant edema or Braxy
Clostridium
Clostridium septicum
Predisposing/risk factors:
Predisposing/risk factors: IM injections, shearing,
docking, lambing, traumatic parturition,
castration
* Local exotoxins cause inflammation and myositis
that ultimately results in edema and necrosis
Clostridium
Clostridium septicum
Diagnosis, treatment, control ?
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)
Clostridium perfringens
bacteria with biotypes A-E based on their
toxins is called?
ENTEROtocxic bacteria
Clostridium perfringens
ENTEROtocxic bacteria
* 4 major toxins?
how produced?
- 4 major toxins: Alpha, Beta, Iota, Epsilon
- Alpha is produced by ALL C. perfringens strains
- Enterotoxin: produced by ALL C. perfringens strains
Clostridium perfringens
ENTEROtocxic bacteria
where are the 4 found?
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)
Clostridium perfringens
ENTEROtocxic bacteria
Predisposing factors:
Predisposing factors: STRESS
* Literally anything that may result in change to the gut
microbiota
* Examples: inappropriate husbandry, sudden diet changes,
temp changes, poor ventilation
Clostridium perfringens
ENTEROtocxic bacteria
C. perfringens causes…
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
enterotoxaemia caused by costridium perfringes type B and C
This is the disease: lamb dysentery
what is the C.perfringens type?
what is the host?
B
lambs less than 3 wks
enterotoxaemia caused by costridium perfringes type B and C
This is the disease: calf enterotoxaemia
what is the C.perfringens type?
what is the host?
B and C
well-fed calves less than 1 month
enterotoxaemia caused by costridium perfringes type B and C
This is the disease: pig enterotoxaemia
what is the C.perfringens type?
what is the host?
C
newborn piglets
enterotoxaemia caused by costridium perfringes type B and C
This is the disease: foal enterotoxaemia
what is the C.perfringens type?
what is the host?
B
foals less than 1 week
enterotoxaemia caused by costridium perfringes type B and C
This is the disease: struck
what is the C.perfringens type?
what is the host?
C
adult sheep
enterotoxaemia caused by costridium perfringes type B and C
This is the disease: goat enterotoxaemia
what is the C.perfringens type?
what is the host?
C
adult goats
4 steps
Virulence factors and pathogenesis Step 1
Rapid mucus-associated
proliferation
–>?
–> sialidases remove sialic acid from cells–> ?
resulting in binding sites for other clostridial
toxins and enzymes
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
Virulence factors and pathogenesis Step 2
Toxin production (alpha
perfringolysin O)–>?
Toxin production (alpha
perfringolysin O) –> influx
neutrofiles, …
Virulence factors and pathogenesis Step 3
Epithelial sloughing and capillary
congestion–>?
Epithelial sloughing and capillary
congestion –> haemorrhages,
increased vascular permeability, …
Virulence factors and pathogenesis Step 4
Intestinal necrosis–>?
resulting in systemic circulation, shock,
rapid death
Intestinal necrosis –> absorption of
inflammatory cytokines and toxins
–>into systemic circulation, shock,
rapid death
Necrotic Enteritis in Poultry
what is it?
how does it occur?
what sort of poultry affected?
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
Necrotic Enteritis in Poultry
predisposing factors?
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
Necrotic Enteritis in Poultry
Clinical signs
Clinical signs
- Acute, dark diarrhea
- Increasing flock mortality
- Ruffled feathers, lethargy, inappetence
Necrotic Enteritis in Poultry
what kind of disease is this and how do you get it?
Foodborne disease (consumption of chicken meat!)
Clostridium perfringens
is caused by C. perfingens type B (toxins Alpha, Beta,
Epsilon) mostly effecting lambs that are less than 3 weeks of age
* Abdominal distention, pain, blood stained feces, necrotic intestines, sudden death
what is it?
Lamb dysentery
Clostridium perfringens
Lamb dysentery
Predisposing factors?
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)
Clostridium perfringens
is caused by C. perfingens type D and affects lambs
between 3-10 weeks of age
what is it?
Pulpy kidney disease or Overeating disease
Clostridium perfringens
Pulpy kidney disease or Overeating disease
Predisposing factors?
toxins?
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
Clostridium perfringens
Pulpy kidney disease or Overeating disease
Pathogenesis?
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
Clostridium perfringens
Pulpy kidney disease or Overeating disease
CS?
post-mortem findings?
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
Clostridium perfringens
Pulpy kidney disease or Overeating disease
* Dx?
- 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
Clostridium perfringens
Pulpy kidney disease or Overeating disease
Tx?
Prevention and control?
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
Clostridium difficile
what is bacteria that causes sometimes fatal enterocolitis in man species of animals and humans?
Enterotoxic
*commensal
*horses
Clostridium difficile
what is the primary cause?
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
Clostridium difficile
Predisposing factors?
antibiotic treatment and/or hospitalization (especially long term), old age, clindamycin in horses is a significant risk factor
Clostridium difficile
transmission
fecal-oral route and infection occurs die to dysbiosis (imbalance of microbial homeostasis)
Clostridium difficile
toxins?
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
Clostridium difficile
Dx?
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
Clostridium difficile
Tx
- 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)
Clostridium spp.
Clostridium spiroforme
what is it?
ENTEROtoxemia and explosive diarrhea disease of
rabbits between 4-8 weeks old
Clostridium spp.
Clostridium spiroforme
Commensal bacteria that produced what ?
what result?
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
Clostridium spp.
what 3 antibiotics are contraindicated in rabbits? why?
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)
Clostridium spp.
Clostridium piliforme
gram + or -
what does it cause, to who? how does it present?
Gram neg. clostridium causing Tyzzer’s disease
of many species
* Lab animals: acute fatal diarrhea with
associated focal liver necrosis
Clostridium spp.
Clostridium piliforme
Predisposing factors?
CS?
Tx?
Prevention?
Predisposing factors: poor sanitation, stress
* CS: watery diarrhea, anorexia, dehydration,
lethargy, death
* Tx: oxytetracycline
* Prevention: disinfection and decontamination
of the lab animal cages
Fusobacterium necrophorum
gram + or -
describe
Gram neg. and NON-spore forming bacteria that can be involved in a wide range of anaerobic and
mixed bacterial infections
Fusobacterium necrophorum
common names?
where found?
does it work synergistically? with what?
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
Fusobacterium necrophorum
transmission?
Cs?
Dx?
Transmission: a break in mucosal or epithelial barriers allow for entrance of the bacteria
* CS: extensive pus and necrosis
* Dx: CS, PCR, anaerobic culture
Fusobacterium necrophorum
tx?
prevention?
do genetics play a role?
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
