Equine Pathogens Flashcards
What are the bacterial features of Streptococcus equi equi
Causative Agent: Streptococcus equi equi
* Gram (+) cocci
* Very contagious
* Found in all horses
What disease does Strep equi equi cause? How to confirm the diagnosis (samples/tests)?
Diagnosis: Strangles
- Confirm with: LN aspirate/nasal discharge
- Test: C/S, PCR
- If deeper infection (bastard strangles)/before vx: Strep M protein ELISA
What are the 4 types of clinical manifestations of Strep equi equi
- Classic strangles = upper airway infection of mandibular/retropharyngeal abscess
- Bastard strangles
- Purpura hemorrhagic = vasculitis (very severe)
- Immune mediate myositis/Myosin heavy chain myopathy = after vx/agent exposure, severe muscle wasting
o Due to quarter horse genetic mutation in myosin chain
Explain the features of bacterial shedding of strep equi equi
- Silent carriers
o Nasal shedding for 2-3 weeks post recovery (some can be for 6 weeks- rarely they can shed for years)
Reservoir in the guttural pouches with no clinical signs
How are strep equi equi outbreeaks managed
o Quarantine and separate horses with clinical signs, those exposed, and those who weren’t exposed
o Biosecurity – no movement in/out of property + disinfect material
How are persistant shedders of strep equi equi tested for?
o Screen for persistent shedders: 3 weeks after recovery from clinical signs
Guttural pouch endoscopy and lavage for C/S and PCR = best
Or 3 nasopharyngeal washes weekly for C/S and PCR
If persistently positive = treat with local/systemic abx
Horse cleared from quarantine if they have 3 consecutive negative nasopharyngeal swabs
List the common differentials for a filly with pneumonia (tachypnea/increased resp effort)
- Rhodococcus equi
- Klebsiella/E. coli
- Bordatella
- Streptococcus equi zooepidemicus
- Viruses
How should pneumonia in horses be worked up? What samples/tests?
Diagnosis: Pneumonia
* TTW to identify gram stain, C/S, PCR
* Chest U/S, radiographs
* CBC/Chem/SAA
* Arterial blood gas
What are the bacterial features of Rhodococcus equi
Rhodococcus equi
* Gram (+) pleomorphic
* Facultative intracellular
* Virulent and avirulent strains: if virulent they have aa plasmid with VapA virulence protein genes
Where is Rhodococcus equi found
- Located: widely distributed no farms in soil and GI of horses
- Varied prevalence
What is the mortality rate of Rhoococcus equi infection
= 0-30%
What are the risk factors for Rhodococcus equi
- Risk factors
o Large acreage
o Many mares having foals
o Dusty environment
o Transient mares and foals
o Foaling inside
What is the pathogenesis for Rhodococcus equi
o Invade and replicate in macrophages
o Destroy macrophages
o Require VapA for virulence and replication
o If phagocytosed via complement = no killing of bacteria
o If phagocytosed via Ig = bacteria killed
o Form pyogranulomas
Describe how immunity develops for Rhodococcus equi
o Most foals do not develop disease
o Adults resistant
o Per-weaning disease <4 month
What are the clinical signs of Rhodococcus equi
- Clinically
o Can be subclinical for a long time
o Fever/lethargy/decreased appetite/tachypnea/increased resp effort
What are the 4 clinical manifestations of Rhodococcus equi
- Chronic pyogranulomatous pneumonia = most common
- Abdominal disease (enterocolitis/typhlitis/abdominal abscess)
- Non-septic polysynovitis/uveitis (immune mediate)
- Bone/joint disease (osteomyelitis/septic arthritis)
Describe how to treat Rhodococcus equi
o Lots of antimicrobial resistance – do not treat based on U/S findings only
o Treat if they have clinical disease
o If subclinical with abscesses on U/S = monitor (if they begin to show clinical signs = treat)
o If >10cm abscesses = treat (regardless of clinical signs
How is lawsonia intracellularis diagnosed? Main features of the disease? Samples? Tests?
- Signalment and history
o Weanling: 3-13 months (mainly 4-7 months)
o Hypoproteinemia
o Thickened small intestinal loops - Feces for PCR (can have false negatives)
- Serology is less specific but more sensitive
In whaat othere species is lawsonia intracellularis common
- Initially, a pig disease
What are the clinical signs of lawsonia intracellularis
- Clinically
o Depression
o Anorexia
o Weight loss/d+/colic/poor BCS
o Rough hair coat
o Pot bellied
What is the epidemiology of lawsonia intracellularis
- Epidemiology: sporadic cases and can cause outbreaks on breeding farms
What are the classical lesions associated with lawsonia intracellularis? What is an alternative form
o Jejunum/ileum (ileum mainly) with marked thickening and irregular surface
o Hyperplasia of epithelium crypts
- Can have acute presentation = rapid death
o Septicemia and DIC related
List 4 main differentials for Acute colitis/typhlocolitis
- Potomac horse fever
- Salmonella
- Clostridium difficile/perfringens
- Coronavirus
How is Acute colitis/typhlocolitis worked up in horses? What samples/tests are used?
- Potomac horse fever
- Salmonella
- Clostridium difficile/perfringens
- Coronavirus
Diagnosis: Acute colitis/typhlocolitis
- PCR for the above organisms/toxins of the organisms
o Use blood or feces for the potomac horse fever PCR - Culture – salmonella (5 consecutive fecal culture)
- Clostridium culture/toxin assays
What are the causative agents of potomac horse fever? what are the bacterial features? Where is it located? When is it common?
Causative Agent: Neorickettsia risticii or findlayensis
* Obligate intracellular gram (-) cocci
* Located: freshwater streams/rivers/irrigated pastures
* When (AB): late July to October
What is the pathogenesis of potomac horse fever
- Pathogenesis
o Trematode pathogen
o Trematode infects snails/aquatic insects
o Horse accidentally eats snail/aquatic insects
o Bacteria are released from the trematode in the GI
o Invade colon/cecal epithelium and tissue macrophages
o Pro-inflammatory reaction
Increase vascular permeability/neutrophil infiltration/tissue damage and inflammation
Bacteria translocation in the blood can infect monocytes
What are the clinical signs of potomac horse fever
- Clinically: 1-3 weeks after infection
o Acute depression/anorexia
o Decreased gut sounds
o D+ in 60% within 1-2 days
o Some get toxemia/laminitis - CBC = transient leukopenia with leukocytosis after
How to treat potomac horse fever
- Tx: IV oxytetracycline
o If give early (within 24h) = rapid recovery
What are the bacterial features of clostridium perfringens
Causative Agent: C. perfringens.
* Gram (+) anaerobic spore forming bacilli
* Very pathogenic
What is the main ddx for Injection site abscess/myositis
- Clostridium perfringens
- Other Clostridia spp.
Diagnosis: Injection site abscess/myositis
How is Injection site abscess/myositis worked up? Test? Sample?
- U/S
- Aspirate fluid for C/S and gram stain
What causes Injection site abscess/myositis? Where is it common?
- Caused: flunixin (or dexamethasone) given IM
o Injecting a non-abx product + tissue necrosis - Common in the neck
How to treat Injection site abscess/myositis
- Tx: slash neck and add drains + systemic abx
How is botulism diaagnosed in horses? Samples? Test?
- Clinical signs and history
- Detect toxin
o Sample: serum/feces/GI content/suspected feed material/carcasses contaminating feed material
o Test: ELISA/RIA/PCR (PCR detects toxin gene)
Mouse inoculation test – treat mouse with botulism and sample/suspect = best way to diagnose (but mice are less sensitive than horses = can have false negatives)
o Difficult to detect because horses are very susceptible to the toxin = there is a very low amount to detect
What are 3 ways botulism can infect a horse
o Forage poisoning = most common
Contaminated food
o Toxic infectious botulism = shaker foals
Ingest spores which sporulate in GI
1-3mo old
o Wound botulism = rare
How is botulism pervented
- Prevent: vaccine against botulism type B = fully protective
o For endemic areas
o 4-6 weeks before foaling
What are the clinical signs of tetanus
- Clinically
o Increased tonus of masticatory muscles/spastic paralysis
o Stiff gait
o Protruding 3rd eyelid
o Startled by noise
How to confirm tetanus diagnosis
- Confirm via clinical signs – fairly pathognomonic
What is the pathogenesis of tetanus
o 2 exotoxins
Tetanolysin = local tissue damage that increases anaerobic infection
Tetanospasmin
* Neurologic signs
* Diffuses locally and then enter blood stream
* Attach to peripheral nerve terminals
* Retrograde transport to CNS
* Cross synaptic cleft and irreversibly bind pre-synaptic inhibitory interneurons
How to prevent tetanus
- Prevent: vaccine is protective
What is the causative agent of pigeon fever
Corynebacterium pseudotuberculosis
What are the bacterial features of Corynebacterium pseudotuberculosis
Causative Agent: Corynebacterium pseudotuberculosis
* Gram (+) pleomorphic rod, intracellular
* Facultative anaerobe
Where is Corynebacterium pseudotuberculosis found
- Located: soil
o Worldwide
What are the clinical signs of Corynebacterium pseudotuberculosis
- Clinically: swelling in pectorals, at the end of summer
What is the pathogenesis of Corynebacterium pseudotuberculosis
- Pathogenesis
o Abrasion/wound/insect
o Wrm/dry months
o Bacteria phagocytosed and continue to replicate intracellularly
How to treat Corynebacterium pseudotuberculosis
- Tx:
o Wit for abscess to mature then establish drainage/lavage
o Don’t contaminate environment with pus
o Strict biosecurity and fly control
How is pigeon fever diagnosed? Samples? Treat?
Diagnosis: Pigeon fever
* U/S
* Aspiration for C/S
* +/- serology
o Synergistic hemolysis inhibition test
What are 3 clinical presentations of Corynebacterium pseudotuberculosis
- External abscesses = mainly
o Good prognosis once drainage is established - Internal abscesses – less common
o Moorer difficult to treat – death if no tx - Ulcerative lymphangitis
o Rare
o Lymphangitis f hind legs lymphatic pathways
o Very difficult to treat
