1/25
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced |
---|
No study sessions yet.
An infectious, contagious disease of equine characterized by abscessation of the lymphoid tissues of the upper respiratory tract
Causative Agent: ______, a Gram-positive, capsulated, B-hemolytic, Lancefield group C coccus which is an obligate parasite and a primary pathogen
•Highly host-adapted affecting only___
Pathogenesis:
•Highly contagious, produces high morbidity but low mortality in susceptible animals
•Transmission is via ________with infectious exudates
•_______ is important source of infection and could initiate outbreaks in premises previously free of the disease
Organism is susceptible to dessication, extreme heat and exposure to sunlight
Under favorable conditions, the organism can survive ____ outside of the host but under field conditions, do not survive ___
Strangles (distemper)
Streptococcus equi
horses, donkeys and mules
fomites and direct contact
Carrier animal
4 weeks
96 hours
Clinical Findings Strangles (Distemper)
1.Incubation period is ____
2.First sign is fever of _____
3.Mucoid to mucopurulent nasal discharge
4.Depression
5.Submandibular lymphadenopathy
6.Horses with involvement of the ______ have difficulty in swallowing, inspiratory respiratory noise due to compression of the dorsal pharyngeal wall, and extended head and neck
7.Animals with_______ develop atypical or catarrhal form of the disease with mucoid nasal discharge, cough and mild fever
3 to 14 days
39.4 to 41.1’C
retropharyngeal lymph nodes
residual immunity
Characterized by abscessation in other lymph nodes particularly those in the abdomen and less frequently in the thorax
• Most common cause of brain abscess in horses although it is rare
Diagnosis:
1.Bacterial culture of exudates from abscesses and nasal swab samples
2.CBC – ________
3.Endoscopic examination of the upper respiratory tract
4.Ultrasonography of the retropharyngeal area
5.X-ray of the skull to determine retropharyngeal abscessation
METASTATIC STRANGLES (Bastard Strangles)
neutrophilic leukocytosis and hyperfibrinogenemia
Treatment of METASTATIC STRANGLES (Bastard Strangles)
1.Keep environment warm, dry and dust free
2.Warm compress will facilitate maturation of abscesses
3.Facilitated drainage of mature abscesses will speed up recovery
4.Flush ruptured abscesses with _______ until discharge ceases
5.______ to reduce pain and fever and improve appetite
6._______ for horses with retropharyngeal abscessation and pharyngeal compression
7.Antimicrobial therapy provides temporary relief from fever but delays maturation of abscess; indicated in dyspnea, dysphagia, prolonged high fever and severe lethargy or anorexia
______ during early stage of infection , < 24 hours of onset of fever will arrest abscess formation
Early antimicrobial treatment fails to mount protective immune response rendering horses susceptible to infection after cessation of treatment
______ at 22,000 IU/kg, IM, bid is the antibiotic of choice
Untreated guttural pouch infection can lead to ____________
3 to 5% povidone-iodine
NSAIDS
Tracheotomy
Penicillin
Procaine penicillin
persistent guttural pouch empyema
Prevention:
1.Post-exposure immunity produced after natural exposure to the disease; local production of antibodies against __________
2.Vaccination with IM products that do not induce mucosal immunity
3.Intranasal live attenuated strain to elicit mucosal immunologic response
Side effects: Abscess at site of IM injection, submandibular lymphadenopathy, serous nasal discharge and purpura hemorrhagica
antiphagocytic M protein
Caused by specific neurotoxin produced by ________
Almost all mammals susceptible, dogs and cats relatively more resistant
_______quite resistant
_________ most sensitive of all species
Etiology and Pathogenesis:
•Caused by C. tetani, an anaerobe with terminal, spherical spores, found in the soil and intestinal tracts
•Introduced into the tissue through wounds that provide suitable anaerobic environment
•In lambs, often follows docking or castration
•Spores of the organism unable to grow in normal tissue and circulating blood
•Bacteria remain localized in_________
•Toxin is absorbed by the motor nerves and causes spasmodic, tonic contractions of voluntary muscles by interfering with the release of inhibitory neurotransmitter from presynaptic nerve endings
•Spasms affecting the larynx, diaphragm, and intercostal muscles lead to________
Tetanus (Lockjaw)
Clostridium tetani
Birds
Horses and lambs
necrotic tissue
respiratory failure
Clinical Findings of Tetanus (Lockjaw)
1.Incubation period averages from ______
2.Localized stiffness of masseter muscles, muscles of the neck, hindlimbs and region of the infected wound which become more pronounced
3.Tonic spasms and hyperaesthesia
4.Difficulty in prehension and mastication, hence lockjaw
In horses: ears erect, tail stiff and extended , anterior nares dilated and third eyelid prolapsed; stiffness of the leg muscles causes the animal to assume a ______
5.Sweating is common
6.Generalized spasms disturb circulation and respiration resulting to increased heart rate, rapid breathing and congestion of mucous membranes
7.Sheep, goats and pigs fall to the ground and exhibit opisthotonus
8.Temperature remains slightly above normal but may rise to ______ toward end of fatal attack
9.Mortality is about ____
10.Convalescent period is about _______; protective immunity does not develop after recovery
10 to 14 days
“sawhorse” stance
42-43’C
80%
2-6 weeks
Diagnosis of Lockjaw
1.Clinical signs and history of recent trauma
2.Demonstration of toxin in ____ of affected animal
3.Anaerobic culture and demonstration of bacteria from wound
serum
Treatment and Control of Lockjaw
1.In early stages of disease: _______ (muscle relaxants), tranquilizers or barbiturate sedatives in conjunction with 300,000 IU of ______
2.%0,000 IU of ________ into the subarachnoid space thru the cisterna magna
3.Draining and cleaning of wounds and administering ___________
4.Place in quiet, darkened stall box with feeding and watering devices
5.Sling for horses with difficulty in standing or rising
curariform agents
tetanus antitoxin
tetanus antitoxin
penicillin or broad spectrum antibiotics
Prevention of Lockjaw
1.Active immunization with _______; wound after immunization, another toxoid
2.If not previously immunized, give ______ of tetanus antitoxin which provides protection for 2 weeks
3.Toxoid given simultaneously with antitoxin and repeated in _______
4._______ toxoid booster
5.Mares vaccinated during _______ week of pregnancy
6.Foals at _____ weeks of age; in high risk foals, given antitoxin immediately after birth then __________ then given toxoid
tetanus toxoid
1,500-3,000 IU
30 days
Yearly
last
5-8
every 2-3 weeks until 3 months old
________
• Rare in horses but fatal
• Caused by toxins produced by _______
• _________ acts on the peripheral nervous system by preventing transmission of the nervous impulses
• Found in soil and decaying plant or animal matter
• Adult horses and foals less than________ affected
Clinical Signs
Foals
1. Impaired suckling
2. Inability to swallow
3. Decreased eyelid and tail tone and dilated pupils
4. Respiratory paralysis
Adults
1. Many of same signs seen in foals
2. Eventual muscle weakness, tremors and collapse
3. Respiratory paralysis which causes death
Botulism
Clostridium botulinum
Botulinum toxin
8 mos. old
Treatment of botulism
1. ________
Prevention
1. Vaccine recommended for endemic areas
Polyvalent equine antitoxin
Contagious Equine Metritis
•Caused by _____
• Transmission through direct breeding , AI and contact with contaminated items
Clinical Signs
1. Highly contagious, often asymptomatic though affected mares show mucoid vaginal discharge
2. Infertility or abortion in mares, no clinical signs in stallions
Infertility can last for ______ breeding cycles
Treatment
1. __________
Prevention
1. Clearance of stallion
Stallion allowed to undergo test breeding to negative mares
3. Process takes _____to declare stallion negative
4. Average to clear stallion takes ___
5. Good hygiene practices
Contagious Equine Metritis
Taylorella equigenitalis
one or more
Topical and systemic antibiotics
35 days
6-8 weeks
Tyzzer’s Disease
• Rare disease caused by ________
• Characterized by severe and peracute hepatitis affecting foals ______
• Foals infected by ingestion of spores from _______
• Following colonization of _____ it infects the liver causing _____
Clinical Signs
1. Foals simply found dead
2. Weakness, lethargy, anorexia, dehydration, pyrexia, diarrhea, tachycardia, tachypnea and icterus
3. Seizures, coma and death may rapidly ensue
• Prognosis for foals poor and most affected foals found dead
Clostridium (Bacillus) piliforme
1 to 6 weeks old
feces or environment
intestinal tract,
severe hepatic necrosis
Treatment of Tyzzer’s disease
1. IV fluids
2. Anti-inflammatories
3. Antibiotics such as ampicillin and gentamycin
4. Parenteral nutrition
•Pneumonia in Foals
• Caused by _______ in foals
• Also causes ulcerative enterocolitis, colonic-mesenteric lymphadenopathy, immune-mediated synovitis and uveitis, osteomyelitis, pyogranulomatous dermatitis, brain abscess, immune mediated anemia and septic arthritis
• Inhalation of _______ most important route for pneumonic infection in foals
• Facultative intracellular parasites of _______
Clinical Signs
1. Most common is suppurative bronchopneumonia with extensive abscess formation and suppurative lymphadenitis
2. Early signs include slight increase in respiratory rate and mild fever
3. More commonly __________ (105-106’F or 40-41’C)
4. Intestinal manifestations characterized by granulomatous or suppurative inflammation of Peyer’s patches and mesenteric or colonic lymph nodes
Rhodococcus equi
contaminated dust
monocytes and macrophages
acute respiratory distress and high fever
Treatment of Pneumonia in foals
1. Administration of _______ (25 mg/kg PO every 8 hours) and ______ (5 mg/kg PO every 12 hours)
Costly and labor intensive and can result to diarrhea and hyperthermia in treated foals
______ (10 mg/kg PO every 24 hrs. for first 5 days then every other day and ______ (7.5 mg/kg PO every 12 hrs.)
Used in combination with rifampin
_______(10 mg/kg PO every 12 hrs.)
erythromycin
rifampin
Azithromycin
Clarithromycin
Doxycycline
Prevention of Pneumonia in Foals
1. ______– stocking density, proper ventilation, dust control
2. _______ – transfusion of hyperimmuned plasma 1L during first 24 hrs. and 25 days later
3. _________ – development of superinfections, bacterial resistance and antimicrobial-induced colitis
Husbandry
Passive immunity
Chemoprophylaxis
Lyme Disease
• Caused by _________
• 2-year enzootic dual infection with ________ cycle involving Ixodes ticks and mammals (deer and white-footed mouse)
• Ticks must be attached to mammal for at least ________
Clinical Signs
1. Low-grade fever
2. Stiffness and lameness in more than one limb
3. Muscle tenderness, hyperaesthesia, swollen joints
4. Lethargy and behavioral changes
Borrelia burgdorferi
Anaplasma phagocytophilum
24 hrs.
Treatment of Lyme Ds.
1. _______ - 6.6 mg/kg IV every 24 hrs. for 1 week before treatment with doxycycline
2. _______ – 10 mg/kg PO every 12 hrs. for 1 month
3. ________- – 2-4 mg/kg IV or IM every 12 hrs.
Prevention
1. Preventing tick exposure or prolonged attachment
2. Early antimicrobial treatment after exposure
3. Vaccination
Tetracycline
Doxycycline
Ceftiofur
Leptospirosis
• Caused by highly invasive Leptospira
1.____________ – North America (skunk most common maintenance host)
2.__________– Western Europe
3.___________ – Eastern Europe
4__________ – host-adapted serovar of the horse
Leptospira interrogans serovar Pomona type kennewki
Leptospira kirschneri serovar Grippotyphosa strain duster
Leptospira kirschneri serovar Grippotyphosa strain moskva
.L. interrogans serovar Bratislava
Clinical Syndrome of Leptospirosis
1. Reproductive Tract
________
•Responsible for most Leptospira abortions but serovars Grippotyphosa and Hardjo has also been reported
•Abortion after 9 months, infected fetuses carry Leptospira in placenta, umbilical cord, kidney and liver
•Aborting mares shed the organism in their urine for 2-3 months
•May develop uveitis weeks later
2. Acute Renal Failure
____
•Ever and acute renal failure; tubulointerstitial nephritis and pyuria without visible bacteria
L. interrogans serovar Pomona
L. Pomona
Clinical Syndrome of Leptospirosis
3. Recurrent Uveitis
L. interrogans serovar Pomona
•Most common is ___________
•_________ against Leptospira antigens cross-reacting with tissues of the lens, cornea and retina
•Live Leptospira organisms in the uveal tissue, aqueous and vitreous fluid of horses with recurrent uveitis
•Genetic factors in recurrent uveitis; ________genetically predisposed
•ERU most common cause of blindness in horses
equine recurrent uveitis (ERU) and immune-mediated keratitis
IgG and IgA
Appaloosas
Treatment of leptospirosis
1.Systemic administration of antimicrobials; fever and acute renal failure: ________
2.Fluid therapy
3._________ – temporary relief
4.______ – inoculation of gentamycin lavage
penicillin, ampicillin,cephalosporin, enrofloxacin, tetracycline and doxycycline
Corticosteroid and cyclosporine
Vitrectomy
Prevention of Leptospirosis
1.Acutely infected horses isolated for _________
2.Urine detected by ______
3.Limiting exposure to stagnant water and potential maintenance hosts
4.Vaccination
14 to 16 weeks
FAT
Salmonella and Nosocomial Infections
_______________
Clinical Signs
1. Enterocolitis
2. Diarrhea
3. Fever
4. Leukopenia
• Danger of fecal shedding
Treatment
1. Antimicrobial treatment
Prevention
1. Cleaning and disinfecting of horse facilities
2.Temporarily close, empty wards and institute thorough and intensive cleaning and disinfecting procedures
3.Strict traffic of humans and animals
4.Adequate ventilation and distance between cases
Salmonella enterica subspp. Enterica serotype Typhimurium, Newport, Anatum and Agona