BACTERIAL DISEASES IN HORSES

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26 Terms

1
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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

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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

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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

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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

  1. ______ during early stage of infection , <  24 hours of onset of fever will arrest abscess formation

  2. Early antimicrobial treatment fails to mount protective immune response rendering horses susceptible to infection  after cessation of treatment

  3. ______ at 22,000 IU/kg, IM, bid is the antibiotic of choice

  4. Untreated guttural pouch infection can lead to ____________

  • 3 to 5% povidone-iodine

  • NSAIDS

  • Tracheotomy

  • Penicillin

  • Procaine penicillin

  • persistent guttural pouch empyema

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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

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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

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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

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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

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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

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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

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________

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

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Treatment of botulism

   1. ________

Prevention

   1. Vaccine recommended for endemic areas

  • Polyvalent equine antitoxin

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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

  1. 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

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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

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Treatment of Tyzzer’s disease

   1. IV fluids

   2. Anti-inflammatories

   3. Antibiotics such as ampicillin and gentamycin

   4. Parenteral nutrition

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•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

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Treatment of Pneumonia in foals

   1. Administration of _______ (25 mg/kg PO every 8 hours) and ______ (5 mg/kg PO every 12 hours)

  1. Costly and labor intensive and can result to diarrhea and hyperthermia in treated foals

    1. ______ (10 mg/kg PO every 24 hrs. for first 5 days then every other day and ______ (7.5 mg/kg PO every 12 hrs.)

    2. Used in combination with rifampin

    3. _______(10 mg/kg PO every 12 hrs.)

  • erythromycin

  • rifampin

  • Azithromycin

  • Clarithromycin

  • Doxycycline

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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

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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.

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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

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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

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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

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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

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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

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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

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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