Bacterial Diseases In Horses PDF

BACTERIAL DISEASES IN HORSES  STRANGLES (DISTEMPER) An infectious, contagious disease of equine characterized by abscessation of the lymphoid tissues of the upper respiratory tract Causative Agent: Streptococcus equi, a Gram-positive, capsulated, B- hemolytic, La...

BACTERIAL DISEASES IN HORSES  STRANGLES (DISTEMPER) An infectious, contagious disease of equine characterized by abscessation of the lymphoid tissues of the upper respiratory tract Causative Agent: Streptococcus equi, a Gram-positive, capsulated, B- hemolytic, Lancefield group C coccus which is an obligate parasite and a primary pathogen Highly host-adapted affecting only horses, donkeys and mules Pathogenesis: Highly contagious, produces high morbidity but low mortality in susceptible animals Transmission is via fomites and direct contact with infectious exudates Carrier animal 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 4 weeks outside of the host but under field conditions, do not survive 96 hours Clinical Findings: 1. Incubation period is 3 to 14 days 2. First sign is fever of 39.4 to 41.1’C 3. Mucoid to mucopurulent nasal discharge 4. Depression 5. Submandibular lymphadenopathy 6. Horses with involvement of the retropharyngeal lymph nodes have difficulty in swallowing, inspiratory respiratory noise due to compression of the dorsal pharyngeal wall, and extended head and neck 7. Animals with residual immunity develop atypical or catarrhal form of the disease with mucoid nasal discharge, cough and mild fever METASTATIC STRANGLES (Bastard Strangles) 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 – neutrophilic leukocytosis and hyperfibrinogenemia 3. Endoscopic examination of the upper respiratory tract 4. Ultrasonography of the retropharyngeal area 5. X-ray of the skull to determine retropharyngeal abscessation Treatment: 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 3 to 5% povidone-iodine until discharge ceases 5. NSAIDS to reduce pain and fever and improve appetite 6. Tracheotomy 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  Penicillin 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 Procaine penicillin at 22,000 IU/kg, IM, bid is the antibiotic of choice Untreated guttural pouch infection can lead to persistent guttural pouch empyema Prevention: 1. Post-exposure immunity produced after natural exposure to the disease; local production of antibodies against antiphagocytic M protein 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 Control: 1. Isolate affected animals to be cared for by caretakers wearing protective clothing 2. Clean contaminated equipment with detergent and disinfect with chlorhexidine gluconate or glutaraldehyde 3. Control fly population 4. Farriers, trainers and veterinarians should wear protective clothing 5. New animals should be quarantined for 14 to 21 days; 2 negative nasal swabs should be obtained Horses continue to shed organisms 1 months after recovery; 3 negative nasopharyngeal swabs at intervals of 4 to 7 days, isolation for 1 month Guttural pouch empyema source of infection in prolonged carrier states  TETANUS (LOCKJAW) Caused by specific neurotoxin produced by Clostridium tetani Almost all mammals susceptible, dogs and cats relatively more resistant Birds quite resistant Horses and lambs 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 necrotic tissue 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, glycine Spasms affecting the larynx, diaphragm, and intercostal muscles lead to respiratory failure Clinical Findings: 1. Incubation period averages from 10 to 14 days 2. Localized stiffness of masseter muscles, muscles of the neck, hind limbs 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 “sawhorse” stance 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 42-43’C toward end of fatal attack 9. Mortality is about 80% 10. Convalescent period is about 2-6 weeks; protective immunity does not develop after recovery Diagnosis: 1. Clinical signs and history of recent trauma 2. Demonstration of toxin in serum of affected animal 3. Anaerobic culture and demonstration of bacteria from wound Treatment and Control: 1. In early stages of disease: curariform agents (muscle relaxants), tranquilizers or barbiturate sedatives in conjunction with 300,000 IU of tetanus antitoxin 2. 50,000 IU of tetanus antitoxin into the subarachnoid space thru the cisterna magna 3. Draining and cleaning of wounds and administering penicillin or broad spectrum antibiotics 4. Place in quiet, darkened stall box with feeding and watering devices 5. Sling for horses with difficulty in standing or rising Prevention 1. Active immunization with tetanus toxoid; wound after immunization, another toxoid 2. If not previously immunized, give 1,500-3,000 IU of tetanus antitoxin which provides protection for 2 weeks 3. Toxoid given simultaneously with antitoxin and repeated in 30 days 4. Yearly toxoid booster 5. Mares vaccinated during last week of pregnancy 6. Foals at 5-8 weeks of age; in high risk foals, given antotoxin immediately after birth then every 2-3 weeks until 3 months old then given toxoid  BOTULISM Rare in horses but fatal Caused by toxins produced by Clostridium botulinum Botulinum toxin 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 8 mos. old 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 Treatment 1. Polyvalent equine antitoxin Prevention 1. Vaccine recommended for endemic areas  CONTAGIOUS EQUINE METRITIS Caused by Taylorella equigenitalis 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 one or more breeding cycles Treatment 1. Topical and systemic antibiotics Prevention 1. Clearance of stallion  Stallion allowed to undergo test breeding to negative mares Process takes 35 days to declare stallion negative Average to clear stallion takes 6-8 weeks 2. Good hygiene practices TYZZER’S DISEASE Rare disease caused by Clostridium (Bacillus) piliforme Characterized by severe and peracute hepatitis affecting foals 1 to 6 weeks old Foals infected by ingestion of spores from feces or environment Following colonization of intestinal tract, it infects the liver causing severe hepatic necrosis 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 Treatment 1. IV fluids 2. Anti-inflammatories 3. Antibiotics such as ampicillin and gentamycin 4. Parenteral nutrition  SUPPURATIVE BRONCHOPNEUMONIA Caused by Rhodococcus equi 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 contaminated dust most important route for pneumonic infection in foals Facultative intracellular parasites of monocytes and macrophages 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 acute respiratory distress and high fever (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 Treatment 1. Administration of erythromycin (25 mg/kg PO every 8 hours) and rifampin (5 mg/kg PO every 12 hours) ❖Costly and labor intensive and can result to diarrhea and hyperthermia in treated foals  Azithromycin (10 mg/kg PO every 24 hrs. for first 5 days then every other day and Clarithromycin (7.5 mg/kg PO every 12 hrs.) Used in combination with rifampin Doxycycline (10 mg/kg PO every 12 hrs.) Prevention 1. Husbandry – stocking density, proper ventilation, dust control 2. Passive immunity – transfusion of hyperimmuned plasma 1L during first 24 hrs. and 25 days later 3. Chemoprophylaxis – development of superinfections, bacterial resistance and antimicrobial-induced colitis  LYME DISEASE Caused by Borrelia burgdorferi 2-year enzootic dual infection with Anaplasma phagocytophilum cycle involving Ixodes ticks and mammals (deer and white-footed mouse) Ticks must be attached to mammal for at least 24 hrs. 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 Treatment 1. Tetracycline - 6.6 mg/kg IV every 24 hrs. for 1 week before treatment with doxycycline 2. Doxycycline – 10 mg/kg PO every 12 hrs. for 1 month 3. Ceftiofur – 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  LEPTOSPIROSIS Caused by highly invasive Leptospira 1. Leptospira interrogans serovar Pomona type kennewicki – North America (skunk most common maintenance host) 2. Leptospira kirschneri serovar Grippotyphosa strain duster – Western Europe 3. Leptospira kirschneri serovar Grippotyphosa strain moskva – Eastern Europe 4. L. interrogans serovar Bratislava – host-adapted serovar of the horse Clinical Syndrome 1. Reproductive Tract L. interrogans serovar Pomona 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 L. Pomona Ever and acute renal failure; tubulointerstitial nephritis and pyuria without visible bacteria 3. Recurrent Uveitis L. interrogans serovar Pomona Most common is equine recurrent uveitis (ERU) and immune- mediated keratitis IgG and IgA 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; Appaloosas genetically predisposed ERU most common cause of blindness in horses Treatment 1. Systemic administration of antimicrobials; fever and acute renal failure: penicillin, ampicillin,cephalosporin, enrofloxacin,  tetracycline and doxycycline 2. Fluid therapy 3. Corticosteroid and cyclosporine – temporary relief 4. Vitrectomy – inoculation of gentamycin lavage Prevention 1. Acutely infected horses isolated for 14 to 16 weeks 2. Urine detected by FAT 3. Limiting exposure to stagnant water and potential maintenance hosts 4. Vaccination  SALMONELLA AND NOSOCOMIAL INFECTION Salmonella enterica subspp. Enterica serotype Typhimurium, Newport, Anatum and Agona Clinical Signs 1. Enterocolitis 2. Diarrhea 3. Fever 4. Leukopenia Danger of fecal shedding Treatment 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  Have A Wonderful Day!