Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
685 Cards in this Set
- Front
- Back
5 Viral Respiratory Diseases of Horses
|
1. Equine Influenza
2. EHV (Rhinopneumonitis) 3. EVA 4. Equine Adenovirus 5. Equine Rhinovirus |
|
Transmission of EI
|
aerosol
|
|
Envelope in EI contains...
|
Contains Neuroanimnase and Hemmagglutin
|
|
Rare sequele to EI
|
Cardiomyopathy
|
|
Why do you always have to update vaccines with EI?
|
Antigenic Shift
|
|
EI: more severe in young or old?
|
Young
|
|
Diagnosis of EI
|
1. Virus Isolation
2. FA or ELISA 3. Serology (4 fold incr.) |
|
common sequele to EI
|
Post Viral Allergic Pneumonitis: chronic pneumonitis, COPD, bact. and guttural pouch infections, bronchitis and pneumonia
|
|
How often do you vaccinate against EI?
|
Every 3-4 months
Intranasal Booster 2-4 wks before show because if only 10 days or less then could have transiet dz. |
|
Transmission of EHV
|
Inhalation or Ingestion
|
|
MC age for EHV
|
Weanling
|
|
Stain of EHV that can cause abortion and CNS signs
|
EHV 1
|
|
Dx of EHV
|
Serology
Virus Isolation FA Stain (note: ELISA can't disting. between EHV 1 & 4 |
|
When to vaccinate pregnant mares against EHV?
|
5,7, 9 months gestation
|
|
How often to vaccinate foals against EHV?
|
Every 3 months
|
|
EVA is most prevelent in this breed?
|
Standardbreds
|
|
Transmission of EVA
|
Respiratory Secretions and Venereally
|
|
Carriers of EVA
|
Stallions
|
|
CS are febrile, serous nasal discharge that may become purulent, leukopenia, pharyngeal lymphoid hyperplasia, abortions and CNS signs
|
EHV
|
|
CS are acute onset of fever, coughing and nasal discharge
|
EI
|
|
CS are fever, limb edema and stiffness, palpebral edema, rhinitis, conjunctivitis, urticaria, papular eruptions on muc mem., abortions
|
EVA
|
|
What 3 things do you worry about in an overweight horse?
|
1. Lipidosis
2. Laminitis 3. Arthritis |
|
What 3 things do you worry about in an underweight horse?
|
1. Not enough feed
2. Parasites 3. Teeth |
|
where do teeth get sharp on the maxilla?
on the mandible? |
buccal surface on the maxilla and lingual surface on the mandible
(on the top the teeth are sharp on the cheek side and on the bottom the teeth are sharp on the tongue side) |
|
EHV-1 Causes
|
CNS
Rhinopneumonitis Abortion |
|
EHV-2 causes
|
nothing
|
|
EHV-3 causes
|
Coital Exanthema
|
|
EHV-4 causes
|
Respiratory probs
|
|
Exuberant Granulation Tissue aka
|
proud flesh
|
|
cause of proud flesh?
|
poor wound management
|
|
An inflammatory response involving the DORSAL lamina of the hoof
|
Laminitis
|
|
4 Causes of Laminitis
(endotoxemia) |
Carb overload
Retained Placenta Corticosteroids Excessive Work or Stress |
|
Stance with Laminitis
|
Sawhorse Stance: rear limbs are placed under body
|
|
With Laminitis, where is the positive hoof test at?
|
The Toe
|
|
MC place for laminitis to occur?
|
Forelimbs (toe pain)
|
|
Chronic CS of Laminitis?
|
Feet Cool to the Touch
No digital pulse Dropped Sole Diverging Hoof Growth Lines Rotation on P3 |
|
Dx of Laminitis?
|
Rads showing rotation of P3
Nerve Block that shows improvement |
|
Nerve Block to Dx Laminitis?
|
Palmar Digital Nerve Block
|
|
Tx/pain relief for acute laminitis?
|
Bute, Banamin
|
|
Frog Support used with Acute Laminitis?
(3) |
Styrofoam
Lily pads Heart Bar Shoe |
|
Way to reduce stress on lamina with laminitis
|
Wedge pad heel that reduces the pull of the DDF
|
|
Vasodialators used with Laminitis?
|
Acetylpromazine
Nitroglycerin Patches Trental Domperidone |
|
Why is heparin used to treat laminitis?
|
Activates reticuloendothelial system
Decreases clotting in foot microvasculure |
|
Used to reduce inflammation in laminitis?
|
NSAIDS
DMSO |
|
General Treatment for Acute Laminitis?
|
Pain Meds, Frog Support, Heels that reduce strain on DDF, Vasodialators, Heparin, Anti-inflammatories
|
|
Surgical Treatment for Chronic Laminitis?
|
1. Dorsal Hoof Wall Resection
2. Full thickness hoof wall resection 3. DDF Tenotomy 4. Inferior Check Ligament Desmotomy |
|
Dorsal Hoof Wall Resection
|
remove toe and reshape hoof parallel to P3
|
|
Full thickness hoof wall resection
|
drain necrotic debris, allows for new hoof growth
|
|
DDF Tenotomy
|
For pasture soundness only
|
|
Inferior Check Ligament Desmotomy
|
Reduces the pull of the DDF
Allows for an athletic career |
|
MC cause of lameness
|
Subsolar Abcess
|
|
cause of subsolar abcess
|
1. Puncture wounds at the frog
2. Puncture wounds at the white line from gravel |
|
where do puncture wounds at the frog drain?
|
At the heel between the sensitive and insensitive frog
|
|
where do puncture wounds at the white line drain?
|
At the coronary band
|
|
Tx of Subsolar Abcesses?
|
Estab. Ventral Drainage
Maintain Drainage with Epson Salt and Ichthammol Antibiotics in foals |
|
Mares repro barriers
|
1. Vulva lips
2. Vestibular Sphincter: vulvovestibular junction 3. Cervix |
|
Normal Vulvar Conformation
|
The dorsal commisure of the vulva should be even or tightly below the bony floor of the pelvis
|
|
pustules or ulcerations on the labia of mares or the penis of stallions
|
Equine Coital Exanthema
EHV-3 |
|
safe to breed horse with Coital Exanthema when?
|
3 weeks after lesions go away
|
|
Treat Melanoma (small nodules that can metastisize) of the vulva with?
|
Cimetidine
|
|
Treat ACC (granulomatous or plaquelike lesions, rarely metastisizes)
|
Surgery
Cryosurgery |
|
MC psuedohermaphrodite?
|
Male Psuedohemaphrodite: Hypoplastic testicles, elongated rudimentary vulva with penile homologue instead of clitorus, XX, male behav
|
|
Location of Persistant Hymen?
|
Vulvovestibular Junction
|
|
Tx of Persistant Hymen?
|
should be broken down to allow fluid to exit, can breed 2-3 wks later
|
|
First Degree Perineal Laceration
|
Laceration thru the dorsal vulvular commisure and mucosa of the vestibule
|
|
Tx for Primary Perineal Laceration
|
Caslicks
|
|
Second Degree Perineal Laceration
|
Laceration thru the dorsal vulvular commisure, vestibular mucosa, submucosa, muscular layer
|
|
Third Degree Perineal Laceration
|
Laceration thru the rectal floor, vestibular ceiling, and anal sphincter
|
|
Vericose Veins in the Mare?
|
Chronic slow loss of blood from the vulva late in gestation
|
|
Tx for vericose veins in the mare?
|
Can be surgically ligated
|
|
Cause of urine pooling?
|
During estrus, the cervix relaxes and uterine tone decreases so urine pooling can occur
|
|
Urine Pooling can cause these 3 things?
|
1. Endometritis
2. Vaginitis 3. Cervicitis |
|
Treatment for urine pooling?
|
Flush large volumes of saline or antibiotics before cover, Caslicks, or surg correction with a urethral extension
|
|
Pneumovagina
|
Asending infection can result in endometritis
|
|
Uterine Infection
|
Desending infection
|
|
Benign Portions of mesonephric tubules may be a rare cause of secondary infections
|
Gartner's ducts
|
|
Dx degnerative uterine disease
|
Endometrial biopsy
|
|
Seen on endometrial biopsy with degen uterine dz
|
1. Glandular degen
2. lymphatic abnorm 3. endometrial atrophy 4. endometrial cysts |
|
Uterine Neoplasm (rare)
|
Leiomyoma
|
|
Caused by contamination after breakdown in uterine defense mechanisms due to breeding, examination, and poor perineal conformation
|
Endometritis
|
|
Uterine Defense Mechanisms
|
1. Uterine Contraction
2. Phagocytosis by neutrophils 3. Repro anatomy barriers (vulva, vestib sphincter, cervix) |
|
MC cause of endometritis
|
Streptococcus zooepidemicus
|
|
Absolute prognostic indicator of active inflammation
|
Presence of neutrophils in the lumen when doing endometrial cytological eval.
|
|
Seen on ultrasound with Endometritis
|
Demonstration of uterine fluid by ultrasound (7-12 days after ovulation)
|
|
Tx of Endometritis?
|
Lavage enhanced by Oxytocin
Antibiotic therapy |
|
Reportable venereally transmitted bacterial endometritis
|
Contagious Equine Metritis
|
|
Etiology of CEM
|
Taylorella equigenitalis
|
|
Asymptomatic carrier of CEM
|
Stallion
|
|
Discharge with CEM
|
Copious Grey Exudate for short duration
|
|
CEM is localized in the mare where?
|
the Clitorus
|
|
Media to grow CEM
|
Chocolate Agar
|
|
Tx for CEM
|
Scrub clitorus with chlorhex then pack with nitrofurazone or chlor hex ointment
|
|
Cervix location during Diestrus
|
Closed and lies in the middle of the cranial face of the vagina with a round rosette appearance
|
|
Cervix location during Estrus
|
Softens and opens, dropping toward the vaginal floor as it relaxes
|
|
when are pregnancy losses the greatest in the mare?
|
before day 35 (before the embryo enters the uterus)
|
|
Pediculosis aka
|
Lice
|
|
Sucking Louse found on the mane, tail, and distal legs
|
Haematopinus asini
|
|
Biting louse found on the dorsolateral trunk
|
Damalinia equi
|
|
Season that lice is most common?
|
Winter
|
|
Dx lice
|
acetate tape
|
|
Psoroptic aka
|
Mange
|
|
Body Mange
|
Psorpties equi
|
|
Otitis Externa
|
Psoptes caniculi or hippotis
|
|
Quarantine how long with psoroptic mange?
|
7-12 wks
|
|
Tx for psoroptic mange and sarcoptic mange
|
Ivermectin
|
|
Don't use this in the horse for mange because it causes depression, ataxia, and progressive large intestinal impaction
|
Amitraz
|
|
Rare, reportable mange in horses that has been eradicated?
|
Sarcoptic mange
|
|
Chorioptic mange aka
|
Leg Mange
|
|
Quarantine for how long with chorioptic mange
|
10 wks
|
|
Causes pruritis, erythema, alopecia and crust formation along legs
|
Chorioptic mange
|
|
MC breed affected with Chorioptic mange: feathers in fetlock region
|
Draft horses
|
|
Chorioptic: surface mange or deeper?
|
Surface
|
|
Etiology of demodex in horses?
|
Demodex caballi and equi
|
|
Rare mange associated with immunosuppressive conditions or therapies?
|
Demodex
|
|
Trobiculosis aka
|
Chiggers
|
|
Free living larva that normally feed on small rodents: associated with pruitic papules and wheals on horses
|
Chiggers
|
|
Dx Chiggers?
|
Colorful larvae id in the center of a wheal or papule
|
|
More common in cows, but seen in horses that live close to cows
|
Warbles
|
|
Hypodermiasis aka?
|
Warbles
|
|
stage of warbles that penetrate the skin and produce a breathing hole?
|
L3
|
|
CS: SQ nodules and cysts over the dorsal back
|
Warbles
|
|
aka for summer sores
|
Habronemiasis
|
|
Etiology for Habronemiasis
|
Habronema musca
Drashia megastoma |
|
Summer sores life cycle
|
Adults live in the stomach
Eggs and larva are passed in the feces Ingested by maggots of flies Flies deposit larva on horse mouth CS occur when the larva are deposited in other places (prepuce) |
|
Summer sores may cause this reaction
|
Hypersensitivity
|
|
Common findings with habronemia
|
Nonhealing wounds
Proud flesh (exuberant granulation tissue) |
|
Discharge and granules with habronemia?
|
Serosanginous or hemorrhagic
Yellow granules |
|
DX habronemia?
|
id larva on granule exam or tissue biosy
|
|
Onchocerca of nuchal ligament
|
O. gutturosa
|
|
Onchocerca of CT of flexor tendons and suspensory ligaments of the fetlock
|
O. reticulata
|
|
Onchocerca of the funicular portion of the nuchal ligament
|
O. cervicalis
|
|
Intermediate host for Onchocerca
|
Cullucoides gnats
|
|
Onchocerca: hypersensitivity to the microfilaria along the ...
|
the *ventral midline*, face and neck
|
|
ocular lesions with Onchocerca
|
keratitis, uveitis, peripaular choroidal sclerosis
depigmentation of the bulbar conjunctiva |
|
Dx of Onchocerca
|
Micro exam of skin biopsy with an eosinophilic granulomatous reaction to the parasite around the microfilaria
|
|
Oxyuriasis aka
|
Pinworm
|
|
where does pinworm adult female lay her eggs
|
out of the horses anus
|
|
CS of pinworms
|
Rubbing tail on fence posts, trees, etc
|
|
Dfdx of pinworms (4)
|
1. Food allergy
2. culicoides hypersensitivity 3. lice 4. stable vice |
|
Premature/dysmature foal
|
neutropenia
|
|
any sick foal
|
septicemia
|
|
barker foal, hypoxiod ischemic
|
Neonatal maladjustment syndrome
|
|
lymphopenia, decreased IgM, lymphoid hypoplasia
|
Combined immunodeficiency
|
|
COPD aka
|
Heaves
Allergic Airway Disease |
|
COPD signs can appear after this vaccine
|
Flu vax
|
|
COPD: allergy to...
|
spores of hay molds=indoor
pollens in pasture=outdoor |
|
type of dyspnea due to bronchitis from COPD
|
Expiratory dyspnea
|
|
heave line is hypertrophy of these muscles
|
External abdominal oblique
|
|
Seen on TTW with COPD
|
Healthy neutrophils (segs)
lg amnt of mucous (curschmann's spirals) |
|
response to this with suspected COPD means postive dx
|
atropine or glycopyrolate
|
|
TX of COPD
|
Corticosteroids (dex, triamcilinolone, beclamethasone)
Bronchodialtors (brethine, clenbuteral, albuterol) Lasix Hyposens test |
|
Infectious degen disease of the frog that results in black necrotic material in this region
|
Thrush
|
|
Thrush associated with these 3 things..
|
1. filthy stalls
2. failure to clean frog reg. 3. lack of frog pressure |
|
Tx of Thrush?
|
Debride diseased frog
Pick feet daily Coppertox Formalin Mild Antiseptics |
|
Shock aborber between cartilage and cortical bone
|
Subchondral bone
|
|
_________(incr. or decr) PG's and HA's with Arthritis
|
Decreased
|
|
_________(incr. or decr) vol., protein count with Arthritis
|
Increased
|
|
Configuration of collagen fibrils with arthritis
|
Parallel
|
|
Arthritis: inflamm. induces
|
Cytokines, kkinins, PG E, thromboxanes, leukotrienes, and prostacycline
|
|
Synovial fluid analysis with aseptic arthritis
|
total leukocytes: norm or slightly elevated
increased lymphocytes increased protein |
|
Synovial fluid analysis with septic arthritis
|
Predominance of segmented neutrophils
|
|
Pathogneum of septic arthritis
|
Segs greater than 30,000 in synovial fluid
|
|
Seen with septic arthritis on rads
|
osteophytes
subchondral bone reabsorption sclerosis periosteal bone formation |
|
uses 90m-methylene diphosphonate isotope and reflects relative blood flow in tissue
|
Neuclear scintigraphy
|
|
Tx of Arthritis
|
NSAIDS
Corticosteroids HA Antiarthritics like PSGAG's (adequan) joint lavage |
|
Ocular trauma can result in
|
Uveitis
|
|
How much of their body wt shuld foals consume in a day?
|
20-30%
|
|
Uses to assess malnutrition
|
Albumin
Lymphocytes |
|
If foal can't suckle, how do you feed
|
Nasogastric tube
|
|
Why shouldn't you force feed with foals?
|
Aspiration pneumonia
|
|
Onchocerca of the funicular portion of the nuchal ligament
|
O. cervicalis
|
|
Intermediate host for Onchocerca
|
Cullucoides gnats
|
|
Onchocerca: hypersensitivity to the microfilaria along the ...
|
the *ventral midline*, face and neck
|
|
ocular lesions with Onchocerca
|
keratitis, uveitis, peripaular choroidal sclerosis
depigmentation of the bulbar conjunctiva |
|
Dx of Onchocerca
|
Micro exam of skin biopsy with an eosinophilic granulomatous reaction to the parasite around the microfilaria
|
|
Oxyuriasis aka
|
Pinworm
|
|
where does pinworm adult female lay her eggs
|
out of the horses anus
|
|
CS of pinworms
|
Rubbing tail on fence posts, trees, etc
|
|
Dfdx of pinworms (4)
|
1. Food allergy
2. culicoides hypersensitivity 3. lice 4. stable vice |
|
Premature/dysmature foal
|
neutropenia
|
|
any sick foal
|
septicemia
|
|
barker foal, hypoxiod ischemic
|
Neonatal maladjustment syndrome
|
|
lymphopenia, decreased IgM, lymphoid hypoplasia
|
Combined immunodeficiency
|
|
COPD aka
|
Heaves
Allergic Airway Disease |
|
COPD signs can appear after this vaccine
|
Flu vax
|
|
Common condition associated w/ severe straining or tearing of flexor tendons
|
Bowed Tendons
|
|
Causes of Bowed Tendons
|
1.Hyperextension of the fetlock
2.Trauma w/ exercise 3.Muscle fatique w/ exhaustion 4.External trauma 5.Improper bandaging |
|
MC Cause of Bowed Tendons
|
Hyperextension of the fetlock
|
|
3 types of Bowed Tendons
|
1.High bow – w/in carpal sheath
2.Mid bow – between carpal and digital sheaths 3.Low bow – caudal to P1 |
|
MC limbs for bowed tendons
|
forelimbs
|
|
rule outs for bowed tendons
|
Cellulitis and suspensory desmitis
|
|
Immed tx for bowed tendons
|
1.For three days
2.Ice 20 minutes every 6 hours 3.Bute 4.DMSO 5.Stall rest 6.Hydrotherapy 7.Poultice bandages |
|
Follow up therapy for bowed tendons
|
1.U/S 4 days post injury and then every 30 days
2.Stop DMSO and possibly bute 3.Stall rest until heat is gone 4.Support bandages and controlled hacks for 4-8 weeks |
|
Surgical treatments for bowed tendons
|
1.Proximal check ligament desmotomy
2.Tendon splitting 3.Volar ligament transection |
|
Tendon splitting
|
Allows for collagen reconstruction of core tendon- In association w/ proximal check desmotomy
|
|
Volar ligament transection
|
-SDF tendinitis-Restricted movment of SDF through fetlock canal- Notching of sheath over volar annular ligament
|
|
prognosis with bowed tendons
|
20% return to previous level of training
|
|
aka lumpy wool and Strawberry fot rot, cutaneous streptotrichosis, rain rot, rain scald, dew poisoning
|
Dermatophilosis
|
|
Dermatophilosis etiology
|
Dermatophilus congolensis
|
|
Infection of the epidermis characterized by exudative dermatitis w/ scab formation
·Seen in cattle, sheep and goats most commonly (occasionally horses) |
Dermatophilus
|
|
causes of Dermatophilosis
|
Prolonged wetting by rain, high humidity, high temp and flies and ticks can increase it
|
|
Dermatophilosis: how do scabs look?
|
Scabs look raised and circular
|
|
Dermatophilosis: Lumpy wool
|
pyramid-shaped masses of scabs on wool
|
|
Dermatophilosis:· Strawberry foot rot
|
skin from coronet to carpus or hock
|
|
Tx of Dermatophilosis
|
PPG or streptomycin injections
|
|
where is dermatophysis seen?
|
·In horses it is seen on the rump, limbs and face
|
|
Bacterial pneumonia in foals: common primary
|
Primary – Streptococcus zooepidemicus and Rhodococcus equi
|
|
Bacterial pneumonia in foals
Secondary to sepsis |
E coli, Actinobacillus equuli & suis, Klebsiella pneumonia, and Salmonella
|
|
Bacterial pneumonia in foals
Secondary to virus |
Influenza, EAV, EHV-1,2,4, or Rhino
|
|
Bacterial pneumonia in foals
Others often seen in combination with above organisms are |
Pasteurella multocida and Bordetella bronchiseptica
|
|
bacterial pneumonia of the foal caused by
|
overcrowding, poor housing, transportation, rough handling, inadequate nutrition, dehydration, poor ventilation, FPT, poor vaccination of mare
|
|
Clinical signs of bacterial pneumonia of the foal
|
a.Fever – early
b.Resp rate > 30 bpm c.Flared nostrils, exaggerated rib movement and abdominal effort d.Exercise intolerance, cyanosis, weakness and reluctnce to move – esp R. equi infection e.Mucopurulent nasal discharge f.Coughing – exacerbated by exercise or restraint g.Auscultation shows increased bronchial and tracheal sounds, esp in cranioventral lungs h.R. equi foals may show nonseptic synovitis, D+ and uveitis |
|
Rhodococcus equi
|
8-10 weeks old, when passive immunity declines
|
|
Two clinical forms of Rhodococcus equi
|
a.Subacute – diffuse miliary pyogranulomatous pneumonia, usually die w/in days
b.Chronic – pneumonia, compromised resp fxn and untrhiftiness |
|
Inflammation of the pleural surface w/ exudation into the pleural space
|
Pleuritis/pleuropneumonia
|
|
Horses are ...more prone or less prone... to pleural fluid accumulation b/c arterial supply to pleura is from sytemic circulation (not pulmonary circulation)
|
more prone
|
|
Pleuritis/pleuropneumonia
In the horse (not other spp), it is... |
secondary to pneumonia or pulmonary abscesses
|
|
Pleuritis/pleuropneumonia MC secondary to...
|
Streptococcus
|
|
most common Pleuritis/pleuropneumonia in horses recently transported
|
Bacteroides
|
|
Clinical signs with Pleuritis/pleuropneumonia
|
·Clinical signs
a.Fever, ADR b.Nasal discharge – mucopurulent to serohemorrhagic c.May see halitosis, wt loss and edema and pleural pain d.Dyspnea, Tachypnea e.O may complain of low grade colic or laminitis signs f.Auscultation – can hear all but bronchial sounds |
|
best prognostic indicator for Pleuritis/pleuropneumonia
|
ODOR – , can detect putrid smell (anaerobic bactreial infection)
|
|
Dx of Pleuritis/pleuropneumonia
|
Thoracocentresis for cell cont, cytology, protein, Gram stain, bacterial culture and senstivity, aneaerobic bacterial culture and mycoplasmal isolation
|
|
Tx of Pleuritis/pleuropneumonia
|
antimicrobial therapy and drains
|
|
Etiology of Tuberculosis in horses
|
Mycobacterium avium, bovis or tuberculosis
|
|
how is tb in horses spread?
|
Ingestion and inhalation, hematogenous spread causing acute miliary tuberculosis in lung or specific organ involvement w/ nodular lesions
|
|
Nutritional D+ in foals caused by
|
Caused by overfeeding milk or sudden intro of grain or roughage, or ingestion of sand, dirt or wood
|
|
Gastroduodenal ulcers in foals caused by
|
a. High grain diet or severe malnutrition
b. May be other causes including stress, NSAIDs, infectious agents |
|
Clinical signs of Gastroduodenal ulcers
|
Clinical signs are bruxism (grinding teeth), ptyalism, low volume D+, colic and anorexia, lie in dorsal recumbancy
|
|
tx of Gastroduodenal ulcers
|
- H2 blockers (Cimetidine & Ranitidine)
- antacids (Aluminum hydroxide) - Sucralfate - proton pump inhibitor Omeprazole - Prostaglandin E analog Misoprostel - Metoclopromide – stimulate GI motility and enhance gastric empyting - Bethanechol – cholinergic agonist |
|
cause of septicemia in foals
|
Caused by bacteria through the blood stream from resp, GI, umbilicus, placenta or locatlized infection (jt ill, navel ill, pneumonia, encephalitis)
|
|
MC cause of septicemia in foals
|
E. coli
|
|
Clincial signs with septicemia in foals
|
a.ADR – depression, lethargy
b.Petechial and echymotic hemorrhaging in MM and ears c.Shock or coma d.Pneumonia, D+, ecepthalitis, uveitis, septic arthritis e.Owner will think mare stepped on her foal f.Neutropenia most often with toxic changes |
|
Dx of septicemia in foals
|
IgG of < 800
|
|
Tx of septicemia in foals
|
colostrum IV if less than 12 hours old, Ab therapy
|
|
Parturition problems in the mare Number one cause is
|
presentation problem
|
|
Causes of prolonged gestation are:
|
a. Draft breeds
b. Mule crosses c. Fescue |
|
sequela of dystocia in a mare
|
a. Laminitis
b. Retained placenta c. Metritis |
|
fatal problem in older mares
|
ruptured middle uterine artery
|
|
low calcium
|
Eclampsia
|
|
indications for induction on partuition in the mare
|
a.Owner conventince
b.Prolonged gestation c.Urterine atony d.Periparturent colic e.Impending prepubic tendon rupture f.Problem mare (steps on foal) g.Preparturent leakage of colostrum h.Nurse mare – used for colostrum only |
|
guidelines for induction of partuition in the mare
|
a.Foal is in correct PPP
b.Gestation over 320 days c.Full mammary development d.Cevix is dilated at least 3-4 findgers e.DO NOT induce if the mare has a systemic dz, there is a foul smelling discharge, or will have an abortion |
|
DOC for induction of partuition in the mare
|
Oxytocin
|
|
watch for this during partuition in the mare
|
‘red bag’ or premature placental separation
|
|
Moldy sweet clover – contains
|
dicurmarol which inhibits blood clotting
|
|
botulism occurs with
|
large round bales and ensilted forage w/ inadequate storage
|
|
tall fescue toxicity
|
N. coenophialum causes prolonged gestation, thickened placenta, abortion and agalacia
|
|
red clover toxin and CS
|
slaframine, slobbering (black spots on leaves and stems)
|
|
blister beetle toxin and CS
|
cantharidine, contaminate of alfalfa hay; causes D+, colic and synchronous diaphragmatic flutter
|
|
problem with Corn grain mold: Fusarium moniliforma
|
leukoencephalomalacia
|
|
Corn and CSM
|
aflotoxins w/ Aspergillus
|
|
Ionophores
|
Monensin and Lasaocid, mixing errors w/ cattle feed; D+, colitis and death
|
|
can produce bilateral panophthalmitis in foals w/ pneumonia
|
Rhodococcus equi
|
|
exophthalmos and blindness from frontal sinus and retrobulbar inflammation
|
Cryptococcus neoformans
|
|
retrobulbar abscess and orbital cellulits and exophthalmos
|
Steptococcus equi
|
|
caused by infecton of adjacent paranasal and nasal sinus cavities or guttoral pouch inflammation
|
Orbital cellulitis
|
|
Habronemiasis or onchocerciasis cause this ocular prob
|
Marginal blepharitis
|
|
Moraxellaacute conjunctivits w/ ocular disharge and superficial keratitis
|
pink eye
|
|
EHV-2 causes
|
keratoconjunctivits
|
|
transmitted to conjunctival sac by Musca fly
|
Thelazia lacrymalis
|
|
Loss of corneal epithelium accompanied by stromal cellular infilatrates and stromal edema
|
Infectious keratitis
|
|
·Most frequent eye problem of the horse
·Group of diseases involving the inner coats of the eye |
Uveitis
|
|
classic cause of uveitis
|
Classic cause is Coliform or mycoplasma-associated omphalophlebitis, septicemia and infectious arthritis
|
|
hyperreactivity to any exciting stimulus via prostaglandins
|
recurrent uveitis
|
|
Signs of recurrent uveitis:
|
a.Hyperemia
b.Aqueous flare, keratic ppts, and synechia c.Changes in the pupil |
|
Clostridial myositis
|
Clostridial chauvoei, septicum and perfringens
|
|
TX: Clostridial myositis
|
PPG:
aggressive, high doses of PPG & wound drainage to induce an aerobic environment |
|
transmission of Clostridial myositis
|
Direct inoculation or sporulation in muscle necrosis and anaerobic environment (severe wounds)
|
|
CS of Clostridial myositis
|
a.Life threatening situation
b.Fever, ADR, injected membranes c.Signs of septic shock d.Painful and edematous at site of infection |
|
Moderate to severe muscle contusion w/ susequent calcification
|
Fibrotic myopathy (ossifying myositis)
|
|
MC area for Fibrotic myopathy
|
semitendiosus (and semimembranosus or biceps femoris)
|
|
Show characteristic gait deficit at a walk with fibrotic myopathy
|
protraction of the hindlimb followed by a brief period of retraction before the stance phase
|
|
will palpate this with fibrotic myopathy
|
Will palpate a firm, nonpainful mass at the musculotendinous junction
|
|
fibrotic myopathy Does not improve w/
|
local anesthesia or NSAIDs
|
|
tx of acute fibrotic myopathy
|
systemic and topical antiinflammatories
|
|
tx of chronic fibrotic myopathy
|
sx tx w/ semitendinosus tenotomy
|
|
Most common muscle disorder of horses
|
Exertional phabdomylolysis
|
|
AKA tying up, Monday morning sickness
|
Exertional phabdomylolysis
|
|
causes of Exertional phabdomylolysis
|
·Possible etiologies include electrolyte imbalances, hypothyroidism, Vit E/sel def
·Fillies and horses on high nutritional planes are most commonly affected ·Occur w/ exercise |
|
clin path with Exertional phabdomylolysis
|
increased CK and AST
|
|
Increased tissue pressure w/in an osteofascial compartment – compromising local circulation and function
|
Compartment syndrome
|
|
compartments syndrome most commonly caused by
|
hypotension and poor positioning during anesthesia
|
|
always check this part of placenta after birth
|
· Always check placenta (chorioallantois) after a birth to ensure it is intact (can fill with water to check)
|
|
Clinical signs of Retained Placenta:
|
a.Toxic metritis
b.Septicemia c.Toxemia d.Laminitis e.Death |
|
MC tx of retained placenta
|
oxytocin
|
|
other tx of retained placenta
|
a.Oxytocin – most common and best tx
b.Fill chorioallantois w/ warm saline to stretch receptors and allow endogenous release of oxytocin c.Sytemic and local Abs d.Uterine lavage e.Exercise f.Prophylactic measures of laminitis (Banamine, pack feet) |
|
Chronic end stage renal disease causes anemia how?
|
decrease in erythropoietin production
|
|
causes Aplastic anemia and bone marrow depression, defect in blood forming organs or is idiopathic
|
Estrogens (Estradiol, estrone, estriol, Zeranol, Diethylstilbestrol DES)
|
|
how does Congenital methemoglobinemia cause anemia
|
lack of methmoglobne reductase causing cyanosis b/c iron is not kept in reduced state
|
|
how does Nitrate toxicity cause anemia
|
– acquired methemoglobinemia causing cyanosis b/c iron is not kept in reduced state
|
|
how does Benzocaine toxicity cause anemia
|
acquired methemoglobinemia causing cyanosis b/c iron is not kept in reduced state
|
|
how does Acetemenophen toxicity cause anemia
|
overwelms hexose monophosphate pathway where glutathione reductase is needed to protect the RBC from oxidants (Heinz body formation – denatured Hb)
|
|
other causes of anemia in horses
|
·Thyroid hormones
·Pituitary hormones ·adrenocrotical hormones ·Hypothryodisim ·Hypoadrenocortisism – Addisons |
|
Variable flexion of fetlock at birth
May walk on dorsal surface |
Congenital fetlock flexural deformities
|
|
MC area for Congenital fetlock flexural deformities
|
forelimbs
|
|
conservative tx for Congenital fetlock flexural deformities
|
-Splints to force weight bearing on toe
– may correct in a few days -Oxytetracycline – binds Ca in the muscle -Casts or splints may be dangerous |
|
surgical tx for Congenital fetlock flexural deformities
|
-Inferior check ligament desmotomy
-Deep digital flexor tenotomy -Superficial flexor tenotomy |
|
occurs with Acquired fetlock flexural deformities
|
Normal at birth, then develops...
Club foot Upright pastern Knuckling fetlock |
|
causes of Acquired fetlock flexural deformities
|
1. 2° to lamenessa. Foot abscess
b. OCD c. Trauma 2. Improper nutrition Excess energy intake b. Imbalance tendon to bone growth (grows too fast) |
|
Club foot at 5 months old due to:
|
Growth at distal metacarpal physis
Deep flexor tendon – MCIII to P3 or Inferior check ligament |
|
Fetlock knuckling at 6-18 months old due to:
|
Growth at distal radial physis
Superficial flexor tendon (P1 & P2) -Radius to P1 & P2 -Superior check ligament |
|
Degrees of severity of Acquired fetlock flexural deformities
|
Stage I – hoof < 90°
Stage II – hoof > 90° |
|
shoeing treatment for Club foot
|
a.Shorten heel and extend toe
b.Reverse wedge shoe pad c.Increase tension on deep flexor tendon |
|
shoeing treatment for Fetlock knuckling
|
Elevate the heel
b.Wedge pad c.Reduces tension on deep flexor tendon d.Increases tension on SDF |
|
sx tx for Club foot
|
inferior check ligament desmotomy
|
|
origin and insertion for inferior check ligament
|
Origin in palmar carpal fascia
Insertion is mide deep flexor tendon |
|
tx for Fetlock knuckling is
|
Superior check ligament desmotomy
|
|
origin and insertion of Superior check ligament
|
Origin is caudal radius
Insertion is superificial flexor tendon |
|
salvage procedure: Acquired fetlock flexural deformities
|
Superficial flexor tenotomy
|
|
prognosis with club foot
|
good
|
|
prognosis with knuckling
|
fair to guarded
|
|
with this condition Newborns rock back on bulbs of heels so that sole of foot does not bear weight
|
Flexor tendon weakness in foals
|
|
Flexor tendon weakness in foals MC in which limbs
|
hindlimbs
|
|
tx for flexor tendon weakness
|
1.Rasp heels to remove fulcrum
2.Extended heel glue shoe 3.Cast and other support is NOT INDICATED b/c foal hoof wall is very thin |
|
MC area for Angular limb deformities
|
Most common in distal radial physis (metaphysis & epiphysis, not diaphysis)
|
|
area for valgus? varus?
|
Carpal valgus
Fetlock varus |
|
causes of angular limb deformities
|
1.Premature birth – weak supporting structures or hypoplasia of carpal tarsal bones
2.Fetal malposition 3.Dysplasia a.Epiphysis b.Metaphysis – most common c.Diaphysis 4.Trauma |
|
Weak collateral support
|
-PE shows switching between varus and valgus deformity
-Easy to manipulate joints into correct position -Rads show normal osseous structures |
|
Hypoplasia of carpal bones
|
-Angular deformity
-First 2 weeks of life of limbs -Cannot be straightened out w/ manipulation -Rads show lack of carpal bone development -Axis lines cross the joint |
|
Epiphyseal dysplasia
|
-Angular deformity
-Defect cannot be corrected w/ manipulation -2° to metaphyseal dysplasia or cupboidal bone hypoplasia -Rads show abonormal shaped epiphysis and axis lines across the epiphysis |
|
Metaphyseal dysplasia
|
-Most common cause of angular deformites
-Can not correct w/ manipulation -Rads show axis lines cross the physis & widening and roughening of physis on convex side |
|
Weak collateral support tx
|
Stall or small paddock turnout No external coaptaiton needed
|
|
Hypoplasia of carpal bones tx
|
-External stabilization w/:
a.Tube casts or splints b.Wt bearing w/ foot exposed c.Prevents flexor tendon laxity d.Limbs are kept straight until cuboidal bones ossify e.Fair prognosis if caught before bones start to collapse |
|
Epiphyseal tx
|
-Tube cases if seen early enough
-Periosteal stripping -Guarded prognosis |
|
Metaphyseal dysplasia tx
|
-Medical tx
a.Confinement and time of 30 days in a small paddock b.Usually considerable improvement c.Splints and tube casts (not used anymore) to correct minor problems, labor intensive |
|
staples or screw and wire to slow growth on convex side, needs general anesthesia; is the most aggressive tx, can accomplish more changes in less time; hardware must come out when leg is straight
|
Transphyseal bridging
|
|
hemicircumferential transection and periosteal elevation on concave side of leg, easy to do in the field; no implant to remove
|
Periosteal stripping –
|
|
remove wedge of bone to correct angle after growth plate closure, rare
|
Wedge osteotomy
|
|
Glandular, lymphatic or endometrial atrophy
|
Degenerative Uterine dz
|
|
neoplastic ovarian diseases
|
granulosa theca cell tumors, teratoma, adenocarcinomas
|
|
Most common ovarian neoplasm
|
granulosa theca cell tumors
|
|
granulosa cell tumors produce
|
testosterone causing masculine behavior
|
|
appearance of granulosa cell tumors on ultrasound
|
honey comb
|
|
·Germ cell origin
·See bone, skin, teeth, cartilage and hair ·Contralateral ovary may be normal and so she may be ovulating normally ·MAY HAVE NORMAL FERTILITY |
teratoma
|
|
·Nonsecretory
·Orginate from epithelial tissue and are located on surface of ovulatory fossa ·Wt loss, colic, recurring abdominal fluid |
Adenocarcinoma
|
|
·Rarely pathological
·Common – may be confused w/ ovarian tumors ·Occurs w/ excessive amount of hemorrhage after ovulation ·Can have normal ovarian cyclic activity ·Will shrink over time |
Ovarian hematomas
|
|
Sequela of FNA of ovarian cysts
|
Ovarian abscesses
|
|
Follicular and luteal cysts that are normally found in the bovine ...
|
DO NOT exist in the horse
|
|
Mares can have multiple preovulatory follicles, ovarian hematomas or prolonged estrus cystles during the breeding season, but are not
|
true ‘cystic’ conditions
|
|
normally a mare ovulate ____ follicle during each estrous cycle
|
one
|
|
If there is multiple ovulations, the mare should be bred....
|
12-24 hours before the ovulation of the most promising follicle
|
|
Most common cause of abortion in mares
|
twinning
|
|
prevention of twins
|
pinching via U/S before day 35 (before establishment of endometrial cups)
|
|
causes prolonged gestation, dystocia , thickened placentas, and agalactia
|
fescue
|
|
Needed from ovaries to maintain pregnancy for first 50 days of gestation
|
progesterone
|
|
Hydroallantois
|
excessive accumulation of fluid in allantoic cavity
|
|
Hydraamnios
|
excessive accumulation of fluid in amniotic cavity is rare (one case reported)
|
|
most common causing brain damage in foal
|
Hydroallantois
|
|
viral causes of abortion in mares
|
a.Equine herpes virus
b.EVA – equine arteritis virus |
|
diseases causing decreased progesterone cause abortion such as..
|
Glucocorticoid administration
babesiosis, colic, navicular dz, weaning a baby |
|
bacterial causes of abortion
|
a.Leptospirosis – serovar pomona most commonly involved
b.Bacterial placentitis – transcervical, hematogenous, intrauterine |
|
mycotic causes of abortion in mares
|
Aspergillus, Absidia, Mucor
|
|
Inflammation disruption of suspensory ligament esp in TB & SB
|
Suspensory desmitis
|
|
MC sites for Suspensory desmitis
|
Most common sites:
1.Proximal to sesamoids 2.Attachment to MCIII |
|
Suspensory desmitis caused by
|
Caused by:
1.Trauma associated w/ exercise 2.Callous from enlarged splints |
|
CS of Suspensory desmitis
|
Mild pain on palpation
Marked enlargment of ligament Usually a lameness prior to injury |
|
tx for suspensory desmitis
|
Conservative Tx same as above w/ Bowed tendons except longer healing timeSx tx is ligament splitting
|
|
which flexor tendon is lacerated?
-toe up -fetlock slightly dropped -when toe is held down, fetlock is lose to normal |
DDF tendon
|
|
which flexor tendon is lacerated?
-fetlock dropped in weight bearing -toe is normal on ground |
SDF tendon
|
|
which flexor tendon is lacerated?
-toe is raised -fetlock on or close to ground -when toe is held down, fetlock is close to the ground |
DDF & SDF tendon
|
|
which flexor tendon is lacerated?
-toe is raised -fetlock in on the ground -when toe is held down, fetlock is on the ground |
Suspensory, DDF, SDF tendon
|
|
mc area for Laceration of extensor tendons
|
proximal dorsal cannon bone
|
|
mc area in forelimb Laceration of extensor tendons
|
common digital extensor tendon
|
|
mc area in hindlimb Laceration of extensor tendons
|
Long digital extensor tendon
|
|
tx of forelimb Laceration of extensor tendons
|
-Check for joint involvment by performing arthrocentesis away from the wound
-Debride -BS Abs -Appropriate bandaging and support -External coaptation for 3-4 weeks |
|
tx of hindlimb Laceration of extensor tendons
|
-Check for joint involvment by performing arthrocentesis away from the wound
-Debride -BS Abs -Appropriate bandaging and support no external copitation |
|
can occur in young foals at pasture than have been ran until fatiqued
|
Common digital extensor tendon rupture
|
|
tx of Common digital extensor tendon rupture
|
Stall rest for 2-3 weeks
Splinting of carpus Sx NOT indicated Lateral digital extensor tendon will take over fxn of common |
|
Caused by:
1.Too much work too young 2.Common injury in training horses (TB, QH) |
Bucked shins
|
|
gait with Bucked shins
|
Shortened anterior phase of stride
|
|
leg affected with Bucked shins
|
Inside leg more severely affected – left leg in TB
|
|
Bucked shins rads show
|
Show doral thickening of MCIII
Deep palpation of anterior MCIII will exhibit pain |
|
Medical tx
Bucked shins |
1.Rest for 60 days
2.Poultice 3.NSAIDs 4.Pin firing & blistering |
|
sx tx
Bucked shins |
1.For dorsal cortical fx
2.Bucked shin the 2nd time 3.Osteostixis- Drill holes into cortex of cannon bone-Multiple fxs- Cast recovery 4.Intracortical internal fixation – compression lag screw across fx 5.Stall confinement for 60 days/30 days of handwalking 6.Follow up rads in 60 days |
|
Epistaxis during intense exercise in racehorses and polo ponies (not endurance horses)
|
EIPH – exercise induced pulmonary hemorrhage
|
|
what happens to cause EIPH
|
Pulmonary capillary rupture when capillary blood pressure increases during strenuous exercise
|
|
heart abnorm noted with EIPH
|
Atrial fibrillation
|
|
tx for EIPH
|
Lasix
Rest? Vit C? Nitroglycerine? Rest for 3-6 mos? Change environ?Bronchodilators don’t work |
|
etiology of epm
|
Sarcocystic neurona
|
|
host for epm
|
possum
|
|
Signalment
epm |
Usually occurs in young (1-6 years) in eastern US
|
|
cs of epm
|
Multfocal, asymmetric, UMN & LMN dz
Can mimic any neurologic syndrome |
|
dx of epm
|
1.Definitive dx only at necropsy
2.Serum Western blot – limited value 3.CSF Western blot or PCR – interpreted as meaning the horse has EPM, but horse may be normal |
|
tx of epm
|
1.Folic acid inhibitors – sulfa + pyrimethamine – synergistic drugs for 1-3 months
2.Diclazuril – anticoccidial drug kills the organism 3.Nitrazonxanide (NTE) 4.Totrazarul 5.Ponazuril 6.Folic acid – b/c using folic acid inhibitors causes anemia and doesn’t affect efficacy of drugs 7.Strongid C – daily wormer 8.NSAIDs w/ DMSO and bute may be helpful |
|
Anatomy of horse esophagus is
|
cranial 2/3 skeletal muscle
|
|
4 layer of esophagus –
|
adventitia
muscularis submucosa mucosa |
|
cs of choke
|
Anxiety
Stretching of head & neck Repeated swallowing Food and water at nostrils |
|
tx choke
|
Heavy sedation to drop head (xylazine, ace)
Water lavage w/ stomach tube and pump If lavage doesn’t work, use general anesthesia w/ cuffed tube & oxytocin and sx remove Ab for aspiration pneumonia Esophagotomy for difficult obstructions or perforations – ID carotid and LRLN, incise next to obstruction, open healing, feed via stomach tube |
|
cs of gi ulcers
|
a.Most are not apparent
b.Bruxism c.Ptyalism d.Inappetence e.Colic signs – dorsal recumbency |
|
most common layer for ulcers in adult horses
|
Nonglandular mucosal ulcers:
Squamous mucosa adjacent to the margo plicatus |
|
Ulcers are caused by:
|
a.Secondary to D+
b.Seconarday to Pneumonia c.NSAIDs use |
|
tx for ulcers
|
H2 antagonist therapy
|
|
layer of LPS is responsible for the pathophysiologic effects of endotoxin in mammals
|
Lipid A,
|
|
Endotoxemia - Septic shock
|
a.C/V collapse
b.Inadequate perfusion to vital tissues c.Ileus d.Multisytem organ failure |
|
the component for the pathogenicity of Gram negative enterbacteria
|
One of the cell walls of Gram-negative bacteria consists of LPS (lipopolysaccharid)
|
|
Abnormal arytenoid cartilage function due to atropy of intrinsic muscles (dorsal cricoarytenoid muscle) of larynx b/c of the tortuous and unusual course of the left recurrent laryngeal nerve
|
Laryngeal hemiplegia - Roarer
|
|
cs w/ Laryngeal hemiplegia
|
exercise intolerance or audible respiratory noise
|
|
dx of
|
endoscopic exam – evaluate larynx at rest and during strenuous exercise
|
|
see on endoscope w/ LH
|
a.There will be no artytenoid cartilage abduction
b.Slap test can assist in dx |
|
Normal Cardiac arrhythmias
|
·P wave is normally split
·Wandering atrial pacemaker – P wave will look morphologically different each time; due to large SA node causing a shift in conduction ·QRS is predominantly negative ·T wave is extremely variable – most T wave changes have little significance ·Normal arrythmias: a. 1° AV block b. 2° AV block c. Sinus arrhtyhmia |
|
·Tall spiked T wave
·Dimishished P wave and atrial standstill ·AV block ·Surpraventricular tachcardia |
Hyperkalemia
|
|
·Speeding and slowing of heart w/ respiration
·High vagal tone and increased HR should abolish this arrhythmia |
Sinus Arrhythmia
|
|
1° AV block
|
·Conductio delay causing a prolonged P-R interval
·High vagal tone in the resting horses and not w/ cardiac pathology |
|
2° AV Block
|
·Electrical activity is inermittently completely blocked at the AV node
·Common in horses ·NORMAL – homeostatic mechanism to control blood pressure ·Atropine or glycopyrollate can be used to R/O pathology in these horses b/c it will go away w/ parasympatholytic agents ·Mobitz type I – most common, w/ progressvely lengthening P-R interval in the beats preceding the block ·Mobitz type II w/ a fixed P-R interval is less common but also normal |
|
Most common clinically significant arrhythmia in the horse
|
Atrial fibrillation
|
|
Atrial fibrillation Characterized by
|
wavy baseline known as ‘F’ waves
|
|
tx Atrial fibrillation
|
Quinidine
|
|
Side effects of quinidine
|
vasodilation and hypotension
|
|
Advanced 2° or 3° AV block
|
a.Atropine and glycopyrrolate – parasympathlytic (anticholinergics)
b.Dopamine – sypthomimetic c.Na bicarb – hyperkalemia, insulin, and dextrose d.Ca may have a cardioprotective effect in yperkalemia – Ca gluconate |
|
·No conduction through AV node; atrium and ventricles are completely dissociated
·Will see promenent jugular pulses |
3° AV block
|
|
AV block is occurring for prolonged P-R periods or present at high heart rates
|
Advanced 2° AV block
|
|
P waves occur earlier than normal
|
Atrial premature depolarizations (APDs)
|
|
most rectal tears occur
|
Most tear occur dorsally, apporx. 12 inches cranial to anus in pertoneal cavity
|
|
4 grades of rectal tears
|
Grade 1: mucosa and submucosa
Grade 2: muscular layer, intact mucosa Grade 3: All tissue except serosa (3a) or mesorectum (3b) Grade 4: all layers |
|
Immediate tx of rectal tears
|
Sedate
Epidural Atropine Tamponage Broad Abs, NSAIDs Refer immediately |
|
Tx of Grade 3 rectal tears
|
Colostomy
Rectal liner Suturing tear intrarectum Empyting of colon via enterotomy and daily lavage of tear |
|
Empyema & Mycosis
|
Accumulation of pus within the pouch cavity
|
|
Empyema & Mycosis:Chronic sequella
|
URT infections, esp Strangles (Strep.)
|
|
cs w/ Empyema
|
Mucopurulent discharge most evident when head is lowered
Unilateral Non-odorous Dyspnea and dysphagia from collapse of the nasopharynx Chondroid – inspissated exudate, may cause outward distension |
|
dx of Empyema
|
Endoscope or catheter placement will show stream of discharge from gp opening
X-ray will see fluid line |
|
tx of Empyema
|
Daily irrigation w/ Isotonic saline through catheter
Feed & water on ground to establish drainage |
|
Guttural pouch Mycosis
|
Fungal dz of gutteral pouch roof, can affect internal carotid
|
|
cs gutteral pouch mycosis
|
Epistasix not associated w/ exercise is most common sign by erosion of int carotid in medial compartment
Neuro signs:Dysphagia Pain on deglutition Parotid pain Head tilt Abnormal resp noise Laryngeal hemiplegia (R sided – rare) Facial paralysis Horner’s syndrome |
|
gutteral pouch mycosis
unilat or bilat |
unilat
|
|
tx of gutteral pouch mycosis
|
Amphotericin B
Itroconizole Enilconazole Sx ligation of internal carotid artery |
|
Reported in young horses (Standardbred and TWH)
Cause unknown – Mycobacteria paratuberculosis? Often compared to Crohn’s dz in people |
Chronic D+/granulomatous enteritis
|
|
Lesions involving the small intestine with Chronic D+/granulomatous enteritis
|
Affected bowel is thickened w/ mononuclear cells
Villus atrophy common (malabsorption)PLE |
|
Loss of dopamine negative feedback causes Pars intermedia pituitary adenoma, causing excess cortisol production by adrenal cortex via Ý POMC, a precursor to ACTH and b-endorphin.
|
Equine Cushings Dz
|
|
increased Temp
what kind of colic? |
anterior enteritis, Colitis
|
|
increased pulse
what kind of colic? |
Ischemia, obstruction, displacement
|
|
increased gastric reflux
what kind of colic? |
anterior enteritis
|
|
MC NSAIDS used in equine vet med
|
a. Banamine
b. Phenylbutazone c. Dipyrone d. Ketoprofen |
|
MOA of NSAIDS
|
· Inhibit cyclooxygenase enzyme-mediated production of eicosanoids form arachidonic acid in the cell membrane
|
|
Side effects from NSAIDS
|
a.GI ulceration
b.Protein loss c.Abdominal pain d.Endotoxemia e.Ulceration of the right dorsal colon – phenylbutazone f.Paplillary necrosis – renal toxicity from phenylbutazone |
|
Anti-ulcer meds
· H2 antagonists |
Cimetindine – Tagamet
|
|
Anti-ulcer meds
· Proton pump inhibitors |
Omeprazole – Prolosec
|
|
Anti-ulcer meds
· PGE2 |
Misoprostol
|
|
Anti-ulcer meds
Cytoprotective agents |
Sucrafalate
|
|
H 2 Blocker MOA
|
Blocks histamine stimulated gastric acid secretion
|
|
ulcer tx
|
Tagamet + antibiotic
if only use tagament: Ulcers will come back after medication is stopped b/c H. pyloric bacteria |
|
Uses of H 2 Blocker
|
gastric ulcer tx, chronic gastritis, reflux exophogitis, prophylactically prior to mast cell removal
|
|
Examples of H2 Blockers
|
Ranitidine (Zantac)
Fomotidine (Pepcid) Nizatidine (Axid) Cimetidine (Tagamet) |
|
MOA of proton pump inhib
|
· Blocks ALL acid producers b/c blocks protone pump, blocks 100%, gastric acid is completely inhibited
|
|
what is PGE1 used for?
|
·Prevents NSAID-induced gastric ulcers
|
|
DMSO MOA
|
·Scavenge hydroxyl radicals generated by neutrophils during inflammation and reperfusion
|
|
use DMSO to treat?
|
·Tx endotoxemia and cerebral edema
|
|
why no greater than a 10 percent solution should be administered at a relatively slow rate with DMSO
|
Hemolysis
|
|
Wear on teeth from cribbing is where?
|
·Excessive wear on rostral margin of upper central incisors
|
|
Dental bud is split during development, usually with incisors
|
Supernumerary teeth
|
|
brachygnathia, the upper jaw is longer than the lower jaw
|
Parrot mouth
|
|
prognathia, the lower jaw is longer than the upper jaw
|
Sow mouth/monkey mouth
|
|
·Maxilla is wider than the mandible
·Sharp edges on buccal of upper and lingual of lower |
Shear mouth
|
|
aka for First premolar
|
wolf tooth
|
|
Removal of dental caps
|
deciduous teeth of premolars that can impede the eruption of underlying permanent tooth
|
|
Preanesthesia in a horse
|
a.withold food for 12 hours (not water)
b.Mineral oil 6 hours before sx c.Atropine or Isoproterenol only when anesthesia used will induce bradycardia (atropine will cause ileus) d.Sedate with Xylazine or Detomidine |
|
Anesthesia in a horse
|
a.Induction agents – GG, Thiopental, Ketamine, Telazol, Profofol
b.Inhalation – Halothane (more potent and more lipid soluble, but more myocardial depression), Isoflurane (peripheral vasodilation), Sevoflurane |
|
Blood pressure during anesthesia
|
ideal MAP is 60-90
|
|
Apnea: anesthesia complication
|
·Early induction period of anesthetic b/c high plasma protein concentration
·Too deep anesthesia ·Doxapram can be used as a respiratory stimulant that also initiates relase of endogenous epinephrine and causes an inr HR and BP |
|
When does hypoxemia occur?
|
Is when PaO2 is less than 60 (should be > 90)
|
|
what do you treat hypoxemia with?
|
a.Dobutamie infusion – increases oxygen delivery to tissue
b.Clenbuterol - b2 agonist c.minimizing time in dorsal recumbency |
|
Neuropathies during surgeries caused by
|
a.improper positioning during anesthesia
b.malignant hyperthermia c.prolonged sx d.excessive anesthetic depth e.low PaO2, ß BP or acidosis |
|
Neuropathies during surgeries prevented by
|
a.maintaining light anesthesia and c/v fxns
b.avoid excessed preanesthetic especially phenothiazines c.Adequate padding d.Support of upper front and hind legs e.Balanced electrolytes and Ca gluconate (maintain muscle contraction) f.Dobutamine, dopamine or ephedrine to maintain adequate BP g.Don’t put horse under until surgeon is ready h.Dantrolene – muscle relaxation i.Diazepam – muscle relaxation j.Na bicarb – correct metabolic acidosis |
|
what can be used for standing sedation in horses?
|
·ace + (Xylazine &/or Butorphanol, Meperidine, Pentazocine &/or xylazine)
·Xylazine + (Butorphanol, Pentazocine) ·Detomidine + Butorphanol |
|
Intercoccygeal Epidural
|
·Lidocaine (5-10 mL) –fast & short
·Xylazine in saline – slow & long ·Lidocaine + Xylazine w/ saline – fast and long |
|
Lumbosacral or suarachnoid epidural
|
·Detomidine in saline &/or morphine
·Butorphanol + lidocaine |
|
Injectable anesthetics
|
·Thiopental – long, rough recovery
·GG/Thiopental – better muscle relaxation, poor analgesia ·Xylazine/Ketamine – (xylazine 5 min before ketamine), smooth induction and recovery, inadequate muscle relaxation ·xylazine/Ketamine/Butorphanol – give w/ xylazine, improved analgesia ·Xylazine/Ketamine/Diazepam – improved muscle relaxation ·GG/Xylazine/Ketamine – narcosis, analgesia & muscle relaxation, smooth recovery, reverse w/ yohimbine, tolazoline, atipamezole ·Detomidine/Ketamine – recovery depends on duration of anesthesia ·GG/Detomidine/Ketamine – same as triple drip above, but recovery slightly longer ·Xylazine/Telazol – relatively smooth recovery & may require more than one attempt ·Detomidine/Telazol – same as above ·Propofol – short term, rapid redistribution and hepatic metabolism ·Profofol/GG – lasts longer |
|
why vasoconstriction with laminitis
|
increased cortisol, incr. catecholamine vasoactivity and insulin antagonism, coritsol ties up insulin receptors needed for vasodilation, causing chronic vasoconstriction
|
|
ADH antagonism from excess cortisol or decr ADH secretion from posterior pituitary due to expansion of intermediate lube into posterior pituitary
|
Diabetes Insipidus
|
|
initiating insulin insensitivity
|
Diabetes Mellitus
|
|
behavior change in older horses can be caused by...
|
beta endorphin in CSF
|
|
cause of hirutism
|
thermo dysfxn by tumor pressure on hypothalamus, or incr androgens by adrenal cortex
|
|
TOC for Equine Cushings
|
TRH stim –
CD have incr cortisol w/ TRH |
|
DOC for Equine Cushings
|
Dopamine agonist (Pergolide medylate)
|
|
autosomal recessive microdeletion of 5 basepairs of DNA-PKcs in Arabian foals
Cell receptors on T cells and Ig on B cells don’t mature Signs are pneumonia and profound lymphopenia ß IgG even with colostrum intake at 100 days old Hypoplasia of all lymphoid tissue |
Equine CIDs (SCIDs)
|
|
Fairly severe colic signs followed by depression and mild pain
|
Anterior Enteritis
|
|
seen with Anterior Enteritis
|
NG reflux (orange brown)
Tap has high protein and low WBC Tap is yellow serosanguinousDepression, fever Rectal multiple loops of SI, thickness of wall on U/S |
|
Potomac horse fever aka
|
Equine monocytic ehrlishiosis
|
|
Potomac horse fever etiology
|
Ehrlichia risticii
|
|
CS with Potomac horse fever
|
Fever, leukopenia, explosive D+
|
|
Vax protocol for Potomac horse fever
|
Two vaccinations 3-4 weeks apart in spring followed by a booster in the fall in high risk areas
|
|
Most common form of thoracic tumor
|
Lymphosarcoma
|
|
CS with lymphosarcoma
|
Clinical signs are inappetance, wt loss, vetral edema, dyspnea, pleural effusion and distension of jugular veins
Coughing when mediastinal mass was compressing the major bronchi and trachea |
|
What signs will the horse show w/ peritonitis?
|
Colic
Brick red MM |
|
What is the bloodwork like of a horse w/ peritonitis?
|
Acidotic – accumulation of lactic acid
Increased Fibrinogen Leukopenia w/ L shift |
|
What does the tap fluid look like with peritonitis?
|
Huge buffy coat
Bright, cloudy yellow Acute – segs Chronic MÆ Sepsis – degenerative segs |
|
What is the tx of peritonitis?
|
Banamine for analgesia
Correct fluid, protein, C/V, electrolytes to tx endotoxic shock Usually can’t wait for blood culture, so give broad spectrum Ab (Penicillin, Gentamycin, Metranidazole) Only do lavage if not responding to Ab Warn owners this is a long term therapy |
|
Who are most likely to get uroperitoneum
|
colts
|
|
What is the tap look like in uroperitoneum
|
CREA will be twice that of blood
|
|
What are PE findings and bloodwork of uroperitoneum
|
Distension of ventral abdomen
Electrolytes change, decr Na, incr K Could have cardiac arrythmia |
|
What is the tx of uroperitoneum
|
Give NaCl & glucose
If ECG is abnormal, give bolus of glucose Drain abdomen before surgery |
|
prevents erection in stallion
|
Stallion ring scar
|
|
Abscesses could indicate what in a stallion
|
bastard strangles (strep)
|
|
eval penis on stallion BSE for....
|
scars, adhesions, lacerations, Squamous Cell Carcinoma, Sarcoids, Cutaneous habronema, & melanoma
|
|
history of little ejaculate or loose heads
|
have impaction of ampulla
|
|
tx of impaction of ampulla
|
Tx is to milk ampulla toward urethra, strip and repeat ejaculate
|
|
location of the epididymus in the stallion
|
dorsomedial side of testicle
|
|
how do testicles lay in a horse?
in a bull? |
horizontal in a horse
vertical in a bull |
|
to evaluate sperm in a stallion...
|
Collect twice, one hour apart. Evaluate 2nd ejaculate.
|
|
daily sperm output
|
collect for 5-7 days, 3 days that are the same in a row
|
|
to get a mare pregnant...
|
begin on 2nd day of estrus and breed every other day
|
|
to get a mare pregnant should have ____ progressively motile sperm
|
Need 500 x 106 progressively motile sperm
|
|
morphologically normal sperm?
|
Should have 75% morphologically normal sperm
|
|
3 cultures taken from stallion
|
1.Sinus of urethra
2.Urethral opening both pre and post ejaculate (especially in aged stallions)- Pseudomonas aeroginosus- CEM – cutaneous equine metritris in chocolate agar |
|
Inflammation of blood vessels
|
Peripheral vascular dz – vasculitis
|
|
causes of vasculitis
|
a.EIAv
b.Equine granulocytic ehrlichiosis c.Equine viral arteritis d.Purpura hemorrhagica – immune mediated cutaneous vasculaitis; involved w/ Steptococcus, influenza, or EHV; febrile, ventral edema |
|
Toxin secreted by Clostridium tetani in soil heavily contaminated w/ feces
|
tetanus
|
|
incubation for tetanus
|
2-4 weeks
|
|
3 Toxins secreted by Clostridium tetani
|
1.Tetanolysin – increases tissue necrosis
2.Tetanospasmin – binds to nerves & inhibits the inhibitory interneurons in ventral horn of spinal cord 3.Nonspasmogenic toxin overstimulation of sympathetic nervous system |
|
CS of tetanus
|
Prolapse of 3rd eyelid (DDx HYPP)
Stiff gait initially Sawhorse stance Flared nostrils, lips retraced, erect ears (Sardonic expression) |
|
Tx of tetanus
|
Non sitmulating environment – dark stall, ears plugged w/ mineral oil soaked cotton
Sedate w/ Ace at 4-6 hour intervals Sedate w/ Chloral hydrate, valuim, sodium pentobarbital Muscle relaxantes in combo w/ sedatives – GG IV drip, Methocarbamol Slings or deep bedding Penicillin to tx originating wound infection Antitoxin at high doses Parenteral nutrition and IV electrolytes |
|
prognosis for tetanus
|
Good if:
1. Horse can drink 2. Remain standing 3. Survive more than one week |
|
is the vax for tetanus against the organism or the toxin?
|
the toxin
|
|
tetnus antitoxin can cause this liver dz
|
highly fatal liver dz called Theiler’s dz
|
|
avoid using tetnus antitoxin if
|
vaccinated or older than 2
|
|
Cervical Vertebral stenosis/malformation/malarticulation
|
aka wobblers
|
|
cervical vertebral instability (dynamic) at C3-4 in weanlings
|
1. CVI
|
|
CSS
|
cervical static stenosis at C5-6 in older horses
|
|
Vertebral instability with wobblers leads to...
|
soft tissue (muscle and ligament) hypertrophy causing spinal cord compression
|
|
causes of wobblers
|
a.overfeeding
b.diet imbalances esp of Ca Ph, Co & Zn c.osteochondrosis involving the epiphyseal plate or articular process d.heredity – but osteochondrosisi is an inherited condition, and wobblers is a form of osteochondrosis) |
|
common signalment for wobblers
|
Young TB or TWH males when training begins
|
|
most obvious gait abnorm with wobblers
|
in hindlimbs
|
|
tx for wobblers is usually
|
euthanasia
|
|
most common equine arbovirus and most mild
|
WEE
|
|
reportable EE
100% mortality |
EEE
|
|
% mortality with VEE
|
60%
|
|
transmission of EE
|
Reservoir – birds and small mammals (VEE)
Vector – very specific spp. Of mosquitos |
|
highest incidence of EE in what months?
|
Highest incidence in August and September – important for vaccination schedule
|
|
pathology seen with EE
|
CSF pleocytosis of small mononuclear cells w/ a slight increase in protein (esp in WNV)
Gross lesions of edema &hemorrhage w/ EEE |
|
CS with EE
|
altered consciousness
CN dysfxn Ataxia Fever |
|
Dx of EE
|
Viral isolation from cold brain
High titer |
|
Ddx with EE
|
Moldy corn
Rabies EPM Trauma |
|
Tx EE
|
Good nursing care – NSAIDs, IV DMSO; seizure meds; forced feeding
Dex is controversial in viral dzs but ma decrease viral inflammation |
|
Zoonosis of EE
|
Horse is dead end host for EEE and WEE
Horses act as sentinels for humans VEE horse is NOT dead end host |
|
etiology of lyme's disease
|
Borrelia burgdorfere (a spirochette)
|
|
vector for lymes disease
|
Ixodes scapularis (deer tick)
|
|
CS for lymes disease
|
Fever
Anorexia Intermittent (shifting leg) lameness |
|
seen with stage I lymes dz
|
Erythema chronicum migrans (ECM) rash
Flu-like symptoms Fatique Fever/chills Headache |
|
seen with stage II lymes dz
|
Neurological signs
Cardiac signs (AV block)Arthritis |
|
seen with stage III lymes dz
|
CNS signs
Chronic arthritis |
|
tx for lymes dz
|
Tetracycline
|
|
MC tick born dz in US
|
Lymes dz
|
|
most common pemphigus in the horse
|
Pemphigous folliaceous
|
|
Where does pemphigous folliaceous occur?
|
In below the stratum corneum (subcorneal) or in the stratum granulosum (intragranular) of epidermis
|
|
first CS with Pemphigous folliaceous
|
Depigmentation, Pustules, crusts or erosions On face and ears (periocularly and around the mouth) Fever/anorexia in cat & horse
|
|
second CS seen with Pemphigous folliaceous
|
Generalized seborrhea
Coalescing papules Folliculitis |
|
third CS seen with Pemphigous folliaceous
|
Footpad Hyperkeratosis
|
|
what do you see on cytology/impression smear with pemphigus folliacus
|
Neutrophils & acantholytic cells with possible eosinophils – but not dx
|
|
ANA test with pemphigus folliacus
pos or neg |
Negative
|
|
seen on skin biopsy with pemphigus folliacus
|
Most Dx
Subcorneal or intragranular pustular dermatitis with acantholytic cells |
|
seen on direct EF with pemphigus folliacus
|
Intercellular staining within the epidermis(looks like a fishnet)
|
|
Seizures: abnorm motor or sensory impairment
|
motor
|
|
seizures due to...
|
Episodes of impariment or loss of consciousness or abnormal motor impariment due to paroxysmal cerebral dysrhythmia
|
|
extracranial causes of seizures...
|
1. hypoglycemia
2. hyperglycemia 3. renal disease 4. hyperlipidemia 5. hyperkalemia 6. hypocalcemia 7. hyperthermia 8. infectious agents 9. toxicosis 10. neoplasia 11. hydrocephalus 12. cardiac arrhythmias |
|
see with lactation tetany (hypocalcemai)
|
see violent respirations w/ thumps, muscle fibrillation, tetanic convulsions
|
|
see hyperkalemia with...
|
HYPP, ruptured bladder in foal
|
|
see hyperlipidemia in...
|
stressed ponies & minis
|
|
hyperthermia causes...
|
swelling of the brain
|
|
infectious agents causing seizures
|
tetanus; botulism
|
|
toxicosis causing seizures
|
Strychnine, lead, arsenic, organophosphates
|
|
neoplasia causing seizures
|
a.Pituitary adenoma – uncommon cause of seizures
b.LSA c.Cholesteatoma – cholesterol granuloma plugs up ventricle causing blindness b/c pressure on optic chiasm |
|
Intracranial causes of seizures...
|
1. viruses
2. bacterial meningitis 3. cerebral abcesses 4. verminous encephalitis 5. EPM 6. Fungal encephalitis 7. head trauma 8. vascular accidents 9. idiopathic epilepsy |
|
viruses that cause intracranial causes of seizures
|
Togaviruses (EEE, WEE, VEE), rabies
|
|
seen with bacterial meningitis
|
foals, uveitis, incr fibrinogen, incr WBC, discolored iris, pus in anterior chamber
|
|
cause of Cerebral abscesses
|
strangles or trauma
|
|
tx Verminous encephalitis with?
|
larvacidal anthelmintis
|
|
common cause of seizures
|
head trauma
|
|
vascular accident causing intracranial cause of seizure
|
Neonatal Maladjusment Syndrome – hypoxic ischemic encephalopathy due to dystocia; ‘dummy foal’
|
|
tx Idiopathic epilepsy with
|
tx w/ Phenobarbital or Diphenylhydantoin
|
|
idiopathic epilepsy in arab foals...
|
Egyptian lineage, self limiting; tx for acute seizures w/ Valium
|
|
most common botulism
|
Clostridium botulinum Type B
|
|
route of infection with botulism
|
1.Ingestion – preformed toxin in forage/silage, usually type C & D
2.Wound – rare 3.Toxicoinfectious – ‘Shaker Foal Syndrome’; spores ingested, cause gastric ulcers |
|
pathogenesis of botulism
|
Toxin binds to neuromuscular jxns causing pralysisi of cholinergic nerve fibers by blocking release of Ach
|
|
CS with botulism
|
Afebrile progressive muscular paralysis
Weakness, restlessness, incoordination Inability to rise, shaking as rising (‘shaker foal’) Sternal recumbancy w/ head at flanks Dysphagia often first sign Decreased tongue and tail tone |
|
DX of botulism
|
Toxin in feces, serum or tissue
Tentative dx by finding toxin in feed |
|
Tx of botulism
|
1.Antiserum – from Upenn, very expensive
2.Restrict movement 3.Ventilation and O2 tx 4.Abs – avoid ones that potentiate neuromuscular weakness – Ags, Tetracycline, & procaine penicillin 5.IV penicillin is recommended 6.DON’T use metranidazole 7.Avoid edpson salt 8.DON’T use parasympathomimetic drugs (Neostimine) b/c may increase mortality |
|
prevention of botulism
|
Vaccinate pregnant mares during last part of pregnancy to prevent shaker foals
|
|
tx with spinal cord trauma
|
1.Corticosteroids or NSAIDs – Solu-delta cortef is very helpful in tx of human spinal trauma victims
2.Very high DMSO 3.Mannitol – expensive – may cause brain edema via hypertonicity 4.Bute 5.Sx tx – initial decompression or later decompression after callus formation 6.Euthanasia – if paralysis |
|
MC spinal cord trauma area
|
C1-C2 broken dens most common
|
|
common history with spinal cord trauma
|
Peracute onset & nonprogressive
Signs depend on level of injury (T2-S2 involve hind limbs only) |
|
General Overall Vaccination Schedule
|
Give all vaccines initally at 2 injections 4 weeks apart and then booster annually
|
|
Encephalities & PHF
how often do you booster? |
booster twice a year
|
|
EHV-1
how often do you booster? |
booster every 3 months
|
|
Rabies
how often do you booster? |
needs only one initial shot
|
|
Strangles
how often do you booster? |
initially give 3 injections at 3 week intervals, foals at 1 year old, and then no annual booster is necessary
|
|
General Overall Vaccination Schedule
|
Give all vaccines initally at 2 injections 4 weeks apart and then booster annually
|
|
Encephalities & PHF
how often do you booster? |
booster twice a year
|
|
EHV-1
how often do you booster? |
booster every 3 months
|
|
Rabies
how often do you booster? |
needs only one initial shot
|
|
Strangles
how often do you booster? |
initially give 3 injections at 3 week intervals, foals at 1 year old, and then no annual booster is necessary
|
|
Gram positive spore forming anaerobic bacteria
|
Tetanus
|
|
Pathogen of Tetanus
|
Extensive tissue damage or deep penetrating wound causes exotoxins to travel w/in the motor neurons to the CNS where it inhibits postsynaptic inhibitory impulses in the spinal cord
|
|
CS with tetanus
|
‘lockjaw’ – tonic spasms and hyperesthesia; sawhorse stance
|
|
Vax protocol: tetanus
Foal in high risk area |
give antitoxin after birth and then give toxoid every 2-3 months until 3 months old
|
|
Vax protocol:tetanus
foal |
vaccinate w/ antitoxin at 5-8 weeks old and then booster at 3 months old
|
|
Vax protocol:tetanus
Mare |
during last 4-6 weeks before birth
|
|
Vax protocol: tetanus
Adults |
give toxoid annually
|
|
Vax protocol: tetanus
Adults w/ extensive wound or deep penetrating wound that is up to date on tetanus shot |
another injection of toxoid to increase Ab
|
|
Vax protocol: tetanus
Adults w/ wounds that is NOT up to date on tetanus |
1500 IU of antitoxin and toxoid simultaneously in different IM arease and repeated in 30 days
|
|
associated w/ administering antitoxin in horses over 2 years old; hepatic failure (heptoencephalopathy)
|
· Theilers disease
|
|
Sleeping sicknesses
|
Viral Equine Encepthalopathies
|
|
etiology
· EEE, WEE, VEE |
arbovirus
|
|
EEE, WEE, VEE transmitted by
|
transmitted by hematophgous insects (mosquitos)
|
|
dead end host for EEE, WEE, VEE
|
horse
|
|
highest mortality rate of Viral Equine Encepthalopathies
|
EEE
|
|
Vaccination protocol for EEE, WEE, VEE:
foal |
give between 2-6 months old at 4-6 week intervals
|
|
Vaccination protocol for EEE, WEE, VEE:
adult |
booster twice a year in endemic areas
|
|
Common in racetracks, show grounds, sale barns and breeding farms
|
Influenza
|
|
Vaccination protocol:
Influenza |
a. Foals and adults should be boostered every 3-4 months with IN (intranasal)
b. Booster 2-4 weeks before anticipated exposure (show, sale) c. Avoid vaccinating w/in 10 days of competitiion b/c vaccine may cause transient disease |
|
3 syndromes with EHV-1
|
a.Abortion – vasculitis causes placental detachment and hypoxia to the fetus
b.Respiratory c.Neurological – rectal incontinence, urinary incontinence, loss of tail tone, dog sitting, posterior paralysis |
|
most common cause of respiratory dz outbreaks in horses in KY
|
· EHV-4
|
|
· Causes a vasculitis via the leukocytes – can remain latent
|
EHV-1
|
|
EHV-1 is spread how
|
· Spread via nasal secretions and aborted fetuses and remains active in environment for 14 days in on horse hairs for 42 days
|
|
EHV-1 Vax: labeled for use in pregnant mares at 5,7, and 9 months gestation
|
Killed - Pneumobort
|
|
Recovering EHV horses quarantine for how long?
|
4 wks
|
|
is it neccessary to vaccinate non-pregnant horses for EHV-1?
|
only if they are close to broodmares
vax every 3-6 mon |
|
when to vax horse against rabies?
|
only in endemic areas
|
|
Causes behavior change from aggressiveness to depression; colic, lameness may be complaint
|
Rabies
|
|
vax protocol: rabies:
for foal |
3 months of age, one shot
|
|
vax protocol: rabies:
for adult |
annually w/ 2 mL IM w/ killed
|
|
type of paralysis with rabies
|
Causes progressive ascending paralysis
|
|
etiology of strangles
|
Streptococcus equi spp equi
|
|
type of strep with strangles
|
beta hemolytic
|
|
Clinical findings with strangles
|
· Fever, thick mucopurulent nasal discharge, swelling and absessation of head LNs
|
|
how long can recovered horses spread strangles
|
· Recovered horses can spread for up to 4 months
|
|
Vaccination protocol for strangles for foals only on endemic farms with IN (intranasal)
|
a. M protein or bacterin – 3 doses 3 weeks apart then at 1 years old
b. Enzyme extract – 2 injections 3 weeks apart then at 1 years old |
|
can develop after vaccination of horses previously sensitized to streptococcual antigens
|
Purpura hemorrhagica (edema)
|
|
why don't vax adult horse for strangles?
|
risk of Purpura hemorrhagica (edema)
|
|
vax protocol for PHF
|
Two vaccinations 3-4 weeks apart in spring followed by a booster in the fall in high risk areas
|
|
etiology of EVA
|
togavirus
|
|
transmission of EVA
|
Aerosol transmission of nasal secretions and venereally through infected semen
|
|
CS with EVA
|
Edema – scrotal, preputial, hindlimb, nasal and ocular discharge, and abortion
|
|
vax protocol with EVA
|
a.Vaccinate Seronegative mares 3 weeks before being bred to a positive stallion w/ attenuated live virus
b.Vaccinated horses are then seropositive and subject to export restrictions |
|
Shaker foal syndrome etiology
|
Clostridium botulinum
|
|
pathophys of Botulism
|
Germinate in ulcerated areas of GI tract and produce exotoxins that block Ach release at neuromuscular jxns
|
|
CS of Botulism
|
· Signs are foals that tremble and become paretic, may cause respiratory paralysis
|
|
vax protocol for botulism
|
a. Mares – 3 times every month w/ last dose 4 weeks before parturition
b. Foals are protected by ingesting colostrum |
|
etiology of anthrax
|
· Bacillus anthracis
|
|
edema with anthrax
|
· Ventral edema – die w/in 2-4 days
|
|
vax protocol with anthrax
|
a.Avirulent noncapsulated spore vaccine on annual basis in endemic arease and face of outbreak to reduce losses
b.Vacicnate 4 weeks before warm, dry summer months and the booster 3 weeks later c.Given SQ d.Do not give Ab after vaccination |
|
etiology of ascarids in horses
|
Parascaris equorum
|
|
where do they hatch and develop
|
Hatch in small intestins and migrate through liver then to the lungs (coughed and swallowed) and then develop in smallintestines
|
|
CS with ascarids
|
Pot belly, respiratory signs
|
|
can ascarids cause colic?
|
yes it is an Ascarid-induced colic when they cause an impaction
|
|
deworming foals for ascarids
|
· Start foals at 2 months old, then worm every 2 months
· If heavy burden is expected, use slow-acting compounds to prevent intestinal obstruction or rupture |
|
Most pathogenic of all endoparasites
|
Large and small strongyles
|
|
which is most damaging Strongyle?
|
Large (Strongylus vulgaris)
|
|
why?
|
b/c L migrate extensively through intestine vasculature – their prevelence has almost been eliminated b/c of anthelmintics
|
|
what CS do small strongyles cause?
|
cause Wt loss, D+ and colic
|
|
life cycle of small strongyle
|
a. ingestion of L3 on grass, develop into adult in the cecum and colon.
b. Molt from EL3 à LL3 à L4 in mucose and submucosa of cecum and colon forming a fibrous cyst for 30-60 days c. L4 emerge (can take up to 2.5 years) causes an intense inflammatory reaction d. This is called Larvae Cyathostomiasis – chronic D+, severe wt loss, protein losing enteropathy |
|
have developed a resistance to benzimidazole wormers
|
Cyathostomes
|
|
tx for strongyles
|
Moxidectin (Quest)
|
|
what stage of strongyles does moxidectin kill?
|
LL3 and L4 w/ a single dose
|
|
another tx for strongyles that will get 90% of EL3
|
Double dose of Fendbendazole (Panacur) for 5
|
|
etiology of bots
|
Gastrophilus fly larva
|
|
where do bots live in the horse?
|
· Inhabit stomach and large intestine
|
|
how horse infected with bots
|
· Adult flies lay eggs (nits) on horse hair
· Horse licks the eggs and they hatch and burrow in horse’s tongue, then migrate to the stomach and attach to the epithelium for several months |
|
tx of bots
|
· Ivermectin effectively removes bots
· Give 1 month after nits are seen on horses legs and repeat after the last frost kills the adult flies |
|
D+ and unthriftiness in suckling foals
|
Strongyloids westeri
|
|
transmission of Strongyloids westeri
|
via mare’s milk
|
|
when to treat for Strongyloids westeri
|
· Tx mares 12 ours after birth
· Foals at 3 weeks old |
|
· Adult females create perineal irritation while laying eggs around anus
· Affected horses lose hair form the tail and rump during scratching attempts |
pinworms
|
|
tapeworms of horse
|
Anoplocephala maga and perfoliata
|
|
intermediate host for horse tapeworm
|
mite
|
|
how horse infected with tapeworms?
|
· Horse ingests mite and tapeworm emerge and attached to mucosa in distal small intestine and proximal large intestine
· Grow to egg-laying adults in intestine |
|
type of floatation to dx tapeworms?
|
· Sedimentation techniques are more reliable than floatation b/c ova do not easily rise in solution
|
|
tx for tapeworms in horses?
|
Strongid (Pyrantel pamoate) at high doses is very effective
|
|
how to "clean pastures" for parasite control?
|
physical removal of feces one to two times a week
|
|
rotation: parasite control
|
a. Slow rotation – use only one class of drugs over one year; reduces chance of resistance in small strongyles
b. Fast rotation – alternating different classes of wormers w/in one year |
|
when to worm?
|
a. Worm when egg producing adult strogyles peak
b. North – spring and early summer and a botacide in the fall after a frost c. Cannot seasonally worm in the south b/c the climate favor prolonged periods of strongyle transmission d. Young horses (< 1 ½ years old) should be wormed in fixed intervals for ascarid control |
|
acessment of deworming program?
|
a. Assess 2 weeks after deworming via fecal floatation
b. < 10 % of herd should have ova – if more could have a resistance problem, or did not deworm properly c. If failure is detected, then use a modified McMaster or Wisconsin technique to assess d. Strongyle should be < 100 eggs/gram |
|
how long should you test after deworming?
|
2 wks
|
|
strongyles should be under ___eggs per gram
|
100
|
|
Excessive Flexion on Hindlimbs
|
Stringhalt
|
|
dropped elbow: which nerve is damaged?
|
Radial N Paralysis
|
|
where is the pain seen on hoof testers with laminitis?
|
sole
|
|
Gait of horse with laminitis
|
short strides
place feet down quickly |
|
Etiology of Thrush
|
Fusobacterium necrophorum
|
|
Obel Grade 1
|
Foot Discomfort without pain
A short, stilted gait at a trot No lameness |
|
Obel Grade 2
|
Some discomfort and lameness as seen by a stilted gait at the walk
Forefeet are lifted without difficulty |
|
Obel Grade 3
|
Reluctance to move
Resists lifting of forefeet |
|
Obel Grade 4
|
Horse does not move his feet without being forced
|
|
Lamintis can be a sequele to these diseases
|
Endometritis
Salmonella Colitis X |
|
P3 rotates in how many days after onset of acute laminitis
|
3-4 days
|
|
Used for pain relief with laminitis
|
Phenylbutazone
Flunixin Meglumine Aspirin |
|
Tx used to restore digital blood flow with laminitis
|
Ace
Phenoxybenzamine Isoxsuprine Hydrochloride DMSO Sodium Heparin Nitroglycerine |
|
Tx for chronic laminitis
|
D-I Methionine
Hoof Wall Resection |