Quiz Two
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| Cell walls rich in complex lipids containing mycolic acid | Mycobacterium
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| Pathogens grow slow, colonies visible after several weeks | Mycobacterium
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| Resistant to chemical disinfectants but susceptible to heat treatment ( pasteurization ) | Mycobacterium
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| Multiply intracellularly & cause granulamatous infections | Mycobacterium
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| Major diseases: Tuberculosis (TB), Johne’s disease and Feline leprosy | Mycobacterium
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| Some produce carotenoid pigments | Mycobacterium
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| Acid-fast (Z-N) positive rods | Mycobacterium
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| Complex egg-enriched media required for growth of pathogenic species | Mycobacterium
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| Aerobic, non-motile, non-spore-forming | Mycobacterium
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| Includes obligate pathogens, opportunistic pathogens & saprophytes | Mycobacterium
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| Gram- positive, filamentous rodsStrict aerobes | Mycobacterium
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| Facultative or obligate intracellular parasitesVery slow growing (up to 2 months) | Mycobacterium
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| Non- encapsulatedNon –spore-forming | Mycobacterium
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| Grows only within infected animals. | Mycobacterium
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| causes granulomatous lesions referred to as tubercles.Inhaled or ingested | Mycobacterium
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| Replicate within host cells, initiating an inflammatory cascade | Mycobacterium
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| The surrounding tissues necrotizesEpithelial cells surround the lesion, walling it off.Eventually, connective tissue encompasses the lesions impairing organ function | Mycobacterium
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| Causative agent of classic tuberculosis | Mycobacterium bovis
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| Also infects pigs, dogs, cats, horses, sheep, and primates | Mycobacterium bovis
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| Was responsible for about 20% of human TB infections | Mycobacterium bovis
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| “Eradicated” from US pigs in 1976. | Mycobacterium bovis
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| Inhibited by glycerol | Mycobacterium bovis
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| Primary culture requires 3-4 weeks | Mycobacterium bovis
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| Short, plump rods in tissues; large filaments from culture | Mycobacterium bovis
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| Does not grow at 25oC (optimal temp. is 37 C).Is killed by sunlight | Mycobacterium bovis
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| Exposure is via inhalation or ingestion of infected flakes. | Mycobacterium bovis
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| The organism disseminates via the lymph and lodges in the spleen and liver. Localized lesions of the lymph nodes of the head and lungs are also observed | Mycobacterium bovis
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| Progression is slow and requires several years before clinical signs become apparent | Mycobacterium bovis
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| Progression leads to:. Coughing. Emaciation. Dyspena. Increased respiration. Nodules on organs | Mycobacterium bovis
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| All cattle must be tested prior to interstate shipment | Mycobacterium bovis
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| About 4 weeks after infection, animals develop a cell- mediated immunity | Mycobacterium bovis
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| DTH response to detect reactors:. Tuberculin test | Mycobacterium bovis
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| Positive reaction is characterized by a hard or edematous swelling | Mycobacterium bovis
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| Animal are slaughtered and necropsied | Mycobacterium bovis
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| Infection is confirmed by culture | Mycobacterium bovis
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| natural reservoirs- captive elk, deer and bison are infected at a high rate | Mycobacterium bovis
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| PCR based diagnostic testing offers increased specificity & speed of detecting active infections | Mycobacterium bovis
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| Mycobacterium bovis Specimens suitable for lab | include lymph nodes, tissue lesions, aspirates and milk
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| Identification criteria Mycobacterium bovis | Growth rate; positive ZN-staining of bacilli; biochemical profile;analytical & molecular techniques
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| Mycobacterium bovis | Treatment and vaccination are inappropriate in control programs for cattle
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| are major obstacles in eradication programs in some countries | Wildlife reservoirs (badgers & possums)
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| Very stable in soil | M. avium complex
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| Colonies appear in 10-14 days on egg yolk medium. | M. avium complex
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| Causes classic tuberculosis in most avian species except psittacines | M. avium complex
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| A serious problem in immunocompromised humans | M. avium complex
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| Exposure is via ingestion of fecal materia | M. avium complex
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| Cadavers may infect predators and raptors | M. avium complex
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| Poultry: occurs most often in free-range adult birds | M. avium complex
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| Weight loss Ruffled feathers Nodular lesions of marrow, spleen and liver | M. avium complex
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| Rare cases in cats, dogs and horses have been reported | M. avium complex
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| Pigs infected thru ingestion of uncooked swill | M. avium complex
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| World- wide distribution, especially in the great lakes region of the US | Mycobacterium avium subsp. paratuberculosis
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| Requires an exogenous source of mycobactin for growth in vitro | Mycobacterium avium subsp. paratuberculosis
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| Slow growth (2-3 months). | Mycobacterium avium subsp. paratuberculosis
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| Yields short, plump rods. | Mycobacterium avium subsp. paratuberculosis
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| Strongly acid-fast | Mycobacterium avium subsp. paratuberculosis
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| Causative agent of Johne’s disease, a chronic enteritis of cattle and wild ruminants | Mycobacterium avium subsp. paratuberculosis
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| Animals ingest materials contaminated with infected feces (usually young animals during suckling) | Mycobacterium avium subsp. paratuberculosis
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| The organism penetrates the ileum and colon | Mycobacterium avium subsp. paratuberculosis
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| Macrophages ingest the organism, but no phagolysosome fusion occurs | Mycobacterium avium subsp. paratuberculosis
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| Thickening of the intestinal wall due to epithelial cell proliferation | Mycobacterium avium subsp. paratuberculosis
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| Emaciation despite normal appetite | Mycobacterium avium subsp. paratuberculosis
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| Swelling of regional lymph nodes | Mycobacterium avium subsp. paratuberculosis
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| Coats becomes dry and rough | Mycobacterium avium subsp. paratuberculosis
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| Main clinical feature is diarrhea, initially intermittent but becoming persistent and profuse | Mycobacterium avium subsp. paratuberculosis
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| Mucosa is usually thickened and folded into transverse corrugations | Mycobacterium avium subsp. paratuberculosis
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| Mesenteric & ileocecal lymph nodes are enlarged & edematous | Mycobacterium avium subsp. paratuberculosis
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| Fresh fecal samples are usually submitted | Mycobacterium avium subsp. paratuberculosis
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| Animals with clinical signs should be isolated and if confirmed should be slaughtered. | Mycobacterium avium subsp. paratuberculosis
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| Causative agent of feline leprosy | Mycobacterium lepraemurium
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| Causes granulomatous lesions of cats | Mycobacterium lepraemurium
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| Transmitted by bites from rats & cats | Mycobacterium lepraemurium
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| Nodular lesions involving subcutaneous tissues, may be solitary or multiple and usually confined to the head region or the limbs | Mycobacterium lepraemurium
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| Nodules are fleshy and freely movable, tend to ulcerate | Mycobacterium lepraemurium
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| Surgical excision of lesions is the preferred treatment | Mycobacterium lepraemurium
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| Does not infect other domestic animals or humans | Mycobacterium lepraemurium
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| Gram negative Aerobic (obligate)Rod shaped | Pseudomonas
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| Motile (one or morepolar flagella | Pseudomonas
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| Non-spore formingMost species produce pigmentsHighly resistant to disinfectants | Pseudomonas
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| Water Soil, common on plants, fruits and vegetablesMoist environment Skin, Burn tissues Mucus membrane | Pseudomonas aeruginosa
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| Intestinal tract of both humans and animalsOpportunistic organism | Pseudomonas aeruginosa
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| Gram negativeAerobic - obligate | Pseudomonas aeruginosa
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| Survives & multiplies over a wide temperature range, 20 - 42 oC | Pseudomonas aeruginosa
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| Survives high salt content | Pseudomonas aeruginosa
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| Characterized by the production of diffusible pigmentation | Pseudomonas aeruginosa
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| Pigment production is seen most clearly in nutrient agar | Pseudomonas aeruginosa
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| Causes opportunistic infections in variety of animal species | Pseudomonas aeruginosa
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| Pseudomonas aeruginosa Mastitis, metritis, pneumonia, dermatitis, enteritis | Cattle
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| Pseudomonas aeruginosa Metritis, Otitis media, pneumonia | Sheep
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| Pseudomonas aeruginosa Respiratory infections | Pigs
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| Pseudomonas aeruginosa Genital tract infections, pneumonia, ulcerative keratitis | Horses
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| Pseudomonas aeruginosa Otitis externa, Cystitis, Pneumonia, ulcerative keratitis | Dogs and Cats
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| Pseudomonas aeruginosa Haemorrhagic pneumonia, septicemia | Mink
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| Pseudomonas aeruginosa Necrotic stomatitis | Reptiles
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| Pseudomonas aeruginosa Specimens for lab. exam | Pus, respiratory aspirates, mid-stream urine, milk (mastitis), ear swabs
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| Colony morphology (large and flat with serrated edges) and characteristic fruity, grape-like odor | Pseudomonas aeruginosa
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| lactose-negative; pale colonies on MacConkey; oxidase-positive; TSI (unchanged | Pseudomonas aeruginosa
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| Extremely resistant to many antibiotics & susceptibility testing should be done before treatment | Pseudomonas aeruginosa
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| Combination of gentamycin or tobramycin with carbenicillin or ticaricillin may be effective | Pseudomonas aeruginosa
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| Vaccines: Polyvalent or autogenous inactivated bacterins; polyvalent exotoxin A-polysaccharide | Pseudomonas aeruginosa
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| BURKHOLDERIA Sp. of importance | Burkholderia mallei
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| Causes Glanders in horses and solipeds (Mules and donkeys) and carnivores | Burkholderia mallei
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| Highly contagious disease of horses | Burkholderia mallei
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| Can be a fatal disease in horses | Burkholderia mallei
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| Sheep, Cattle, Swine, Birds are resistant | Burkholderia mallei
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| Humans – Seldom occurs. Sporadic | Burkholderia mallei
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| No naturally acquired cases in US in almost 60 years | Burkholderia mallei
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| Glanders | Burkholderia mallei
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| Characterized by formation of nodules and ulcers in the respiratory tract or on the skin | Burkholderia mallei
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| Humans and carnivores are susceptible | Burkholderia mallei
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| Eradicated from most developed countries | Burkholderia mallei
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| Transmission: ingestion of food or water contaminated by nasal discharges of infected animals and less by inhalation or thru skin abrasions | Burkholderia mallei
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| In zoos and circuses, carnivores have contracted as a consequence of eating meat from infected solipeds | Glanders
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| Acute septicemic form of the disease glanders Characterized by | fever, mucopurulent discharge and respiratory signs. Death within a few weeks
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| (more common): presents as nasal, pulmonary and cutaneous forms | glanders Chronic form
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| ulcerative nodules on the nasal septum & lower part of the turbinates with purulent, blood-stained nasal discharge & regional lymphadenopathy (ulcers usually heals leaving star-shaped scars | glanders nasal form
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| characterized by lymphangitis (nodules along the lymphatic vessels of the limbs) with development of ulcers containing yellowish pus. Death after several months or may recover & shed organisms from the respiratory tract or skin | Cutaneous form (“farcy”)
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| Burkholderia mallei Specimens for lab | discharge from lesions, blood for serology & must be processed in a biohazard cabinet
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| Grows on media containing 1% glycerol | Burkholderia mallei
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| Will grow on MacConkey (2 to 3 days incubation) | Burkholderia mallei
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| Colony characteristics ( white and smooth becoming granular and brown with age) | Burkholderia mallei
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| Comparatively unreactive biochemically and non-motile | Burkholderia mallei
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| Serology: CF and Agglutination tests | Burkholderia mallei
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| Mallein test: effective field test for confirmation and for screening in-contact animals | Burkholderia mallei
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| A test and slaughter policy enforced in countries where the disease is exotic | Burkholderia mallei
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| Antibiotic therapy is inappropriate (subclinical carriers) | Burkholderia mallei
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| Effective cleaning and disinfection (Formalin 1.5% or Iodophor 2% with contact time of 2 hrs.) | Burkholderia mallei
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| Causes Melioidosis in many animal species | Burkholderia pseudomallei
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| Endemic in tropical and subtropical regions of Southeastern Asia and Australia | Burkholderia pseudomallei
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| Transmission: Ingestion, inhalation or skin contamination from environmental sources | Burkholderia pseudomallei
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| Stress factors or immunosuppression may predispose to clinical disease | Burkholderia pseudomallei
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| Abscesses develop in many organs including lungs, spleen, liver, joints and CNS | Burkholderia pseudomallei
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| Chronic, debilitating, progressive disease | Burkholderia pseudomallei
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| Horses: mimics glanders (“pseudoglanders”) | Burkholderia pseudomallei
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| Gross pathological lesions may aid diagnosis | Burkholderia pseudomallei
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| Specimens for lab.: pus from abscesses, affected tissues & blood for serology (biohazard cabinet for processing) | Burkholderia pseudomallei
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| FA test to demonstrate organism in tissue smears (only in reference labs.) | Burkholderia pseudomallei
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| Colony morphology (Smooth and mucoid to rough and dull becoming yellowish-brown with age) with characteristic musty odor | Burkholderia pseudomallei
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| Treatment is expensive and unreliable (relapses when therapy is discontinued) | Burkholderia pseudomallei
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| Vaccines being developed in some countries | Burkholderia pseudomallei
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| MORAXELLA Species of veterinary importance | Moraxella bovis
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| Causative agent of Infectious bovine keratoconjunctivitis (“pinkeye”) | Moraxella bovis
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| Important ocular disease of cattle and occurs worldwide | Moraxella bovis
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| Short, plump gram-negative rods, usually in pairs | Moraxella bovis
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| Optimal growth in enriched media (growth enhanced by the addition of serum to media) | Moraxella bovis
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| Aerobic, non-motileUsually catalase- and oxidase-positive | Moraxella bovis
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| Unreactive with sugar substrates | Moraxella bovis
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| Virulent strains are fimbriated and hemolytic | Moraxella bovis
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| Susceptible for desiccation | Moraxella bovis
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| Found on mucus membranes of carrier cattle | Moraxella bovis
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| Highly contagious disease, usually in animals under 2 years of age | Infectious bovine keratoconjunctivitis (IBK)
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| Economic loss due to decreased weight gain in beef breeds, loss of milk production, disruption of breeding programs & treatment costs | Infectious bovine keratoconjunctivitis (IBK)
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| Transmission: direct contact, aerosols, thru flies acting as vectors | Infectious bovine keratoconjunctivitis (IBK)
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| Virulence attributed to the fimbriae, which allow adherence of the organism to the cornea | Moraxella bovis
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| Initially manifests as blepharoplasm, conjunctivitis and lacrimation | Infectious bovine keratoconjunctivitis (IBK)
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| Progresses to keratitis, corneal ulceration, opacity and abscessation, leading sometimes to panophthalmitis and permanent blindness | Infectious bovine keratoconjunctivitis (IBK)
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| Can be unilateral or bilateral | Infectious bovine keratoconjunctivitis (IBK)
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| Cattle with very little eye pigmentation are more severely affected | Infectious bovine keratoconjunctivitis (IBK)
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| Hereford and Holstein, Shorthorn cattle very susceptible - because they lack pigment around the eyes. Angus are less affected. Zebu and Brahma are apparently not affected) | Infectious bovine keratoconjunctivitis (IBK)
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| Jersey cattle are highly susceptible to Pinkeye. Prominence of their eyes may expose them to more intense sun light | Infectious bovine keratoconjunctivitis (IBK)
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| High solar radiation is a predisposing factor | Infectious bovine keratoconjunctivitis (IBK)
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| Lower incidence in dairy breeds compared to beef herds | Infectious bovine keratoconjunctivitis (IBK)
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| Lacrimal secretion is most suitable for lab. exam. & must be processed promptly (extreme susceptibility to desiccation | Infectious bovine keratoconjunctivitis (IBK)
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| Specimens should be cultured in blood agar and MacConkey agar ( 48 to 72 hrs) | Infectious bovine keratoconjunctivitis (IBK)
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| Round, small, shiny, friable, colonies after 48 hrs. Colonies of virulent strains are surrounded by a zone of complete hemolysis & embedded in the agar | Moraxella bovis
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| No growth on MacConkey agar | Moraxella bovis
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| Cultures of virulent strains agglutinate in saline | Moraxella bovis
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| Smears from colonies reveal short, plump, gram-negative rods, usually in pairsCatalase- and oxidase- positive | Moraxella bovis
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| Antimicrobial therapy subconjunctivally or topically early in the disease | Infectious bovine keratoconjunctivitis (IBK)
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| Vitamin A supplementation may be benificial | Infectious bovine keratoconjunctivitis (IBK)
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| Prophylactic use of intramuscular oxytetracycline for animals at risk | Infectious bovine keratoconjunctivitis (IBK)
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| Fimbriae: Aid in the attachment to the Corneal epithelium | Moraxella bovis
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| Enzymes: Break down the junctions between corneal epithelial cells - initiate inflammatory response | Moraxella bovis
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| Infection range from sub-clinical carrier to acute fatal septicemia | Salmonella Sp
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| Salmonella in poultry | Salmonella gallinarum and Salmonella pullorum
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| Salmonella in pigs | Salmonella choleraesuis
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| Non-host-specific Salmonella | Salmonella typhimurium
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| Salmonella in dogs and cattle | Salmonella dublin
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| Carnivores are innately resistant to | salmonellosis
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| Often localize in the mucosa of the ileum, cecum and colon & in the mesenteric lymph nodes | Salmonella
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| Clinical disease: Animals under stress may develop clinical disease from sub-clinical and latent infections | Salmonella
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| Stress factors: Intercurrent infections; Transportation; Overcrowding; Pregnancy; Extreme ambient temperatures; Water deprivation; Oral antimicrobial therapy; Sudden changes in the diet | Salmonella
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| Other factors: # of organisms ingested, virulence of serotype or strain and susceptibility of the host (immunological status; genetic make-up; age) | Salmonella
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| In most animal species, both enteric and septicemic forms do occur | Salmonella
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| causes enteric and septicemic salmonellosis in many animal species | Salmonella typhimurium
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| Abortion in farm animals without clinical signs do occur | Salmonella
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| Terminal dry gangrene and bone lesions are common manifestations in chronic infections in calves | Salmonella dublin
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| many animal species (enterocolitis & septicemia) & humans (food poisoning) | Salmonella typhimurium
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| Cattle (many disease conditions) & Sheep, horses & dogs (enterocolitis & septicemia) | Salmonella dublin
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| Pigs (enterocolitis & septicemia) | Salmonella choleraesuis
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| Chicks (Pullorum disease --- bacillary whit diarrhea) | Salmonella pullorum
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| Adult birds Fowl typhoid) | Salmonella gallinarum
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| Turkeys (Arizona or paracolon infection) | Salmonella arizonae
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| Poultry (subclinical) & humans (food poisoning) | Salmonella enteritiditis
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| Sheep (abortion) | Salmonella brandenburg
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| Sub-clinical fecal excretors/all ages: probable outcome of most infections --- small numbers & intermittently | Salmonella dublin
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| Latent carriers/all ages: present in gall bladder with no excretions | Salmonella dublin
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| Acute or chronic enteric disease/all age: Enterocolitis with foul-smelling diarrhea containing blood, mucus & epithelial shreds or casts | Salmonella dublin
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| Septicemia/all ages: potentially fatal disease with fever & depression. Diarrhea or dysentery may be present. Dramatic drop in milk production in dairy cows; meningitis or pneumionia | Salmonella dublin
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| Abortion: Common cause in some European countries with no clinical signs | Salmonella dublin
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| Joint ill/calves: may follow septicemia or umbilical infection | Salmonella dublin
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| Osteomyelitis/young animals: often involve cervical vertebrae or bones of the distal | Salmonella dublin
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| Terminal dry gangrene/calves: Disseminated intravascular coagulation due to endotoxemia results in local ischemia & gangrene of distal parts of hind limbs, ears & tail | Salmonella dublin
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| Poultry constitute an important animal reservoir for | Salmonella
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| A very wide variety of serotypes have been isolated from chickens, turkeys, ducks, and other species of domestic poultry | Salmonella
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| can infect ovaries of hens and be transmitted thru eggs ( vertical transmission) | S. gallinarum, S. pullorum and S. enteritidis
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| non-host-adapted (Paratyphoids) --- often sub-clinical in laying hens | S. enteritidis & S. typhimurium
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| disease (Bacillary white diarrhea) World-wide in its distribution, National schemes (NPIP-National Poultry Improvement Plan) have reduced the incidence of this disease in the U.S. | S. pullorum
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| in the yolks A proportion of eggs laid by adults with infected ovaries contain | S. pullorum
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| can survive in the litter for several months | S. pullorum
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| All turkey and chicken breeder flocks are tested for the presence of infection. Use agglutination test | S. pullorum
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| infects young chicks andTurkey poults up to 2 – 3 weeks of age | Pullorum disease
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| The mortality rate is very high | S. pullorum
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| Birds are depressed, huddle under heat source, anorexic | S. pullorum
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| whitish fecal pasting around their vents | S. pullorum
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| Whitish nodes through out the lungs | S. pullorum
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| Necrotic lesions in liver and spleen | S. pullorum
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| The cycle of infection from the hen to the chick (vertical transmission), as occurs in pullorum disease, can also take place with | S. gallinarum
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| It is more usual, however, for fowl typhoid to develop as | a disease of varying severity among growing birds and adult stock
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| Common route of infection is by ingestion | S. gallinarum
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| The severity of outbreaks can vary from acute with high mortality rates to chronic infection | Fowl typhoid
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| When the disease occurs in young chicks the symptoms are indistinguishable from pullorum disease | Fowl Typhoid
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| Mortality rate can go up to 50% or more | Fowl Typhoid
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| Diarrhea with greenish colored feces, purple discoloration of comb and wattles | Fowl Typhoid
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| Diagnosis: Culture liver, spleen, and heart blood | Fowl Typhoid
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| is a name given to infections of poultry by non-host adapted salmonella | Paratyphoid
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| Day-old antibiotic injection is practiced in many hatcheries | Gentamycin and Spectinomycin
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|
||||
| are the most common causes of bovine Salmonellosis | Salmonella dublin and Salmonella typhimurium
🗑
|
||||
| Affect cattle of all ages, disease may be acute or chronic. Calves are more susceptible to infection than adults | Salmonellosis
🗑
|
||||
| Adult cattle infected with this may act as symptom less carriers, excrete the organism intermittently in the feces | S. dublin
🗑
|
||||
| can survive in feces for 2-4 months. Pastures, food, and water may become contaminated from feces of carrier animals or aborted fetuses and fetal membranes | S. dublin
🗑
|
||||
| is a non-host-adapted Salmonella Occurs in 2-6 week old calves | Salmonella typhimurium
🗑
|
||||
| Infection of cattle may originate from disease in another animal species or from cattle | Salmonella typhimurium
🗑
|
||||
| Pathogenesis is similar to infection with S. dublin except that the development of chronic carriers over a period of several years does not occur frequently | Salmonella typhimurium
🗑
|
||||
| Fever, diarrhea with brown or greenish-brown feces with blood sometimes | Salmonella typhimurium
🗑
|
||||
| Sometimes arthritis, pneumonia, encephalitis may be evident | Salmonella typhimurium
🗑
|
||||
| Adult cattle: go off their milk, run high temperature. Blood may appear in the feces and followed by a stinking which may contain shreds of mucus membrane | Salmonellosis
🗑
|
||||
| The cow becomes very weak and rapidly goes down and may die in 1 to 5 days | Salmonellosis
🗑
|
||||
| If death does not occur, diarrhea, emaciation may continue for sometime before recovery finally ensues | Salmonellosis
🗑
|
||||
| If the cow is pregnant abortion may occur | Salmonellosis
🗑
|
||||
| Human infection results through consumption of raw or improperly pasteurized milk, milk products or contaminated beef | Salmonellosis
🗑
|
||||
| Salmonellosis in pigs | S. choleraesuis and non-host adapted types
🗑
|
||||
| is the most common type in the US and causes necrotic enteritis | Salmonella choleraesuis
🗑
|
||||
| Sudden onset of high fever, depression and recumbency & die within 48 hrs | Salmonellosis in pigs
🗑
|
||||
| Survivors develop persistent diarrhea, arthritis, meningitis or pneumonia | Salmonellosis in pigs
🗑
|
||||
| Characteristic bluish discoloration of the ears and snout (clinical D/D from Classical Swine Fever) | Salmonellosis in pigs Septicemic form
🗑
|
||||
| is also an important cause of disease in pigs (enterocolitis and septicemia) | S. typhimurium
🗑
|
||||
| have been isolated from both diseased animals and from mesenteric lymph glands, intestinal tracts and other sites in the carcasses of apparently healthy animals at slaughter. | Less frequently a wide variety of other non-host adapted Salmonella types
🗑
|
||||
| Salmonella in swine - a source for | humans
🗑
|
||||
| In the US the most common types Salmonella infection in Horses | S. typhimurium, S. enteritidis, S. newport, and S. heidelberg
🗑
|
||||
| Young animals are particularly susceptible Salmonella infection in | Horses
🗑
|
||||
| Stress apparently has a major role in the initiation of clinical disease and predisposing factors including surgery, passing nasogastric tubes, concurrent illness | Salmonella infection in Horses
🗑
|
||||
| High temperature, colic pains are frequently the first symptoms followed by diarrhea | Salmonella infection in Horses
🗑
|
||||
| can be found in the feces of many normal dogs | Salmonella
🗑
|
||||
| intermittent diarrhea is all that one might expect in infected adults | Salmonella infection in Dogs
🗑
|
||||
| Many different types can be seen in dogs | Salmonella
🗑
|
||||
| Puppies are more susceptible | Salmonella
🗑
|
||||
| Adults rarely develop septicemia | Salmonella infection in Dogs
🗑
|
||||
| Many different types of Salmonella have been isolated | in Cats
🗑
|
||||
| Salmonella infection in Cats usually occurs | eating usually contaminated food, wild rats and mice and contact with feces of other animals
🗑
|
||||
| Kittens are more susceptible than adults | Salmonella infection
🗑
|
||||
| may be carriers of Salmonella without showing symptoms | Cats
🗑
|
||||
| acute or sub-acute outbreaks of enteritis with or without septicemia may occur | in kittens with Salmonella infection
🗑
|
||||
| intermittent diarrhea, vomiting may occur sometimes | In adult cats with Salmonella infection
🗑
|
||||
| Many types have been isolated from sheep | Salmonella
🗑
|
||||
| Salmonella infection in Sheep Most common in some countries | S. typhimurium
🗑
|
||||
| in Sheep Raised temperature in most cases scouring is usually present, passing of blood in feces is occasionally noted | Salmonella infection in Sheep
🗑
|
||||
| In acute Salmonellosis, a severe watery putrid diarrhea occurs and a high proportion die | Salmonella infection in Sheep
🗑
|
||||
| In some cases persistent scouring of greenish or yellowish paint like material with a foul smell is the striking symptom | Salmonella infection in Sheep
🗑
|
||||
| Overcrowding sheep | Salmonella infection in Sheep
🗑
|
||||
| Pregnant animals may die of septicemia before aborting. Aborted fetus and placenta -highly contaminated | Salmonella infection in Sheep
🗑
|
||||
| Rearing turtles for sale in contaminated stagnant water particularly where a heavy sewage contamination exists has led to a high level of | Salmonella
🗑
|
||||
| In some establishments in the USA, 25-50% of these animals were found to be actively excreting Salmonella | Turtles
🗑
|
||||
| In 1975 the interstate shipment of turtles was | banned in US
🗑
|
||||
| is the commonest Salmonella found in captive birds | S. typhimurium
🗑
|
||||
| Infection is particularly frequent in canaries. Captive birds are at particular risk of being exposed because surplus feed tends to attract rodents and wild birds | Salmonella
🗑
|
||||
| Homing pigeons very frequently suffer from | Salmonellosis
🗑
|
||||
| In large cities wild pigeons may theoretically pose a risk to humans contracting | Salmonella
🗑
|
||||
| Salmonella source of human infection | Pet turtles and iguanas
🗑
|
||||
| Epidemic due to intact and disinfected grade A eggs | Salmonella enteritidis
🗑
|
||||
| Infects the ovaries of healthy hens & contaminates the eggs before the shells are formed | Salmonella enteritidis
🗑
|
||||
| What is being done to reduce S. enteritidis outbreaks | Some states require refrigeration of eggs from the producer to the consumer
🗑
|
||||
| Pleomorphic, Gram- negative short rods | Actinobacillus
🗑
|
||||
| Non- motile. Oxidase- and urease- positive | Actinobacillus
🗑
|
||||
| Facultative anaerobe. Good growth on MacConkey agar (except A. pleuropneumoniae | Actinobacillus
🗑
|
||||
| No gas production from sugar fermentation | Actinobacillus
🗑
|
||||
| Commensals on mucus membranes --- particularly in the upper respiratory tract and oral cavity | Actinobacillus
🗑
|
||||
| Cannot survive for long in the enviornment | Actinobacillus
🗑
|
||||
| Carrier animals play a major role in transmission | Actinobacillus
🗑
|
||||
| Exhibit some host specificity | Actinobacillus
🗑
|
||||
| Mainly pathogens of farm animals | Actinobacillus
🗑
|
||||
| Purulent infections usually involving soft tissuesWide range of diseases in domestic animalsWorldwide distribution | Actinobacillus
🗑
|
||||
| Buccal membrane of cattle and sheepFirst isolated from cattle and sheep in 1902 | Actinobacillus lignieresii
🗑
|
||||
| Small rods on blood agar; prefers serum, 10% CO2 | Actinobacillus lignieresii
🗑
|
||||
| 6 serotypes exist with geographical distribution | Actinobacillus lignieresii
🗑
|
||||
| Causative agent of Actinobacillosis in cattle (“timber or wooden tongue”) | Actinobacillus lignieresii
🗑
|
||||
| Causative agent of Cutaneous Actinobacillosis of sheep (doesn’t involve tongue) | Actinobacillus lignieresii
🗑
|
||||
| Chronic granulomatous lesions of the soft tissue of face and jaw (most often manifest clinically in cattle as induration of the tongue (“wooden tongue” (“Timber tongue”). | Actinobacillus lignieresii
🗑
|
||||
| Potentially important lesions occur in the oesophageal groove and the retropharyngeal lymph nodes | Actinobacillus lignieresii
🗑
|
||||
| Organism enters via wounds in the buccal epithelium, usually in conjunction with penetration of foreign material | Actinobacillus lignieresii
🗑
|
||||
| usually a sporadic disease, herd outbreaks of limited extent can occur | Bovine actinobacillosis
🗑
|
||||
| difficulty in swallowing and drool saliva | Animals with “wooden tongue”
🗑
|
||||
| may be found on the head, thorax, flanks and upper limbs | Lesions of cutaneous actinobacillosis
🗑
|
||||
| Gm-ve rods in smears from exudates, pyogranulomatous foci in tissue sections | Actinobacillus lignieresii
🗑
|
||||
| Small, sticky, non-hemolytic colonies on blood agar | Actinobacillus lignieresii
🗑
|
||||
| Sodium iodide parenterally or Potassium iodide orally is effective | Actinobacillus lignieresii
🗑
|
||||
| Potentiated sulfonamides or a combination of penicillin/streptomycin are usually effective | Actinobacillus lignieresii
🗑
|
||||
| Rough feed or pasture should be avoided | Actinobacillus lignieresii
🗑
|
||||
| presents as granulomatous lesions mainly on the head without tongue involvement | Cutaneous actinobacillosis of sheep
🗑
|
||||
| Granulomatous mastitis in sows, bite wound in dogs and glossitis in horse have been attributed to infection with | A. lignieresii
🗑
|
||||
| Intestinal and tonsils of horses | Actinobacillus equuli
🗑
|
||||
| Grows readily on normal media; usually non- hemolytic | Actinobacillus equuli
🗑
|
||||
| Colony type on blood agar --- Forms smooth, very sticky (cohesive) colonies, Liquid cultures become very viscous | Actinobacillus equuli
🗑
|
||||
| Grows on MacConkey agar | Actinobacillus equuli
🗑
|
||||
| Causative agent of a septic polyarthritis called “ sleepy foal disease” --- an acute, potentially fatal septicemia of newborn foals | Actinobacillus equuli
🗑
|
||||
| Occasionally produces septicemia, nephritis or abortion in adult horses | Actinobacillus equuli
🗑
|
||||
| Organisms are found in the reproductive and intestinal tracts of mares | Actinobacillus equuli
🗑
|
||||
| Foals can be infected in utero and after birth via the umbilicus. Affected foals are febrile and recumbent. Death usually occurs in 1 to 2 days. Foals which recover may develop polyarthritis, nephritis, enteritis or pneumonia | Actinobacillus equuli
🗑
|
||||
| Foals dying within 24 hrs. of birth have petechiation of serosal surfaces and enteritis | Actinobacillus equuli
🗑
|
||||
| Meningoencephalitis can be detected histologically | Actinobacillus equuli
🗑
|
||||
| Foals which survive for 1 to 3 days have typical pin-point suppurative foci in the kidneys | Actinobacillus equuli
🗑
|
||||
| Specimens cultured on blood agar (sticky colonies with variable hemolysis) and MacConkey agar (lactose-fermenting colonies | Actinobacillus equuli
🗑
|
||||
| Antimicrobial therapy beneficial if disease is detected early: tetracycline, streptomycin and ampicillin are effective | Actinobacillus equuli
🗑
|
||||
| Supportive treatment: blood transfusion & bottle-feeding with colostrum | Actinobacillus equuli
🗑
|
||||
| Nocommercial vaccines available | Actinobacillus equuli
🗑
|
||||
| Not considered normal flora & worldwide distribution | Actinobacillus suis
🗑
|
||||
| Grows as sticky, adherent colonies, with complete hemolysis on sheep blood agar | Actinobacillus suis
🗑
|
||||
| Grows well on MacConkey agar | Actinobacillus suis
🗑
|
||||
| In young (<3 months) pigs causes a rapidly progressing septicema and endocarditis. These cases are usually fatal (mortality may be up to 50% in some litters) | Actinobacillus suis
🗑
|
||||
| Clinical signs: Fever, respiratory distress, prostration and paddling of the forelimbs | Actinobacillus suis
🗑
|
||||
| Petechial and ecchymotic hemorrhages occur in many organs and evidence of interstitial pneumonia, pleuritis, meningoencephalitis, myocarditis and arthritis | Actinobacillus suis
🗑
|
||||
| An unusual form of the infection in mature pigs has been reported with skin lesions resembling those of swine erysipelas (important for D/D) | Actinobacillus suis
🗑
|
||||
| In older pigs is associated with focal necrotizing pneumonia and with subcutaneous abscesses in the neck, shoulder and flank | Actinobacillus suis
🗑
|
||||
| More rarely, causes a suppurative arthritis in the joints, similar to A.equuli | A. suis
🗑
|
||||
| Sticky, hemolytic colonies on blood agar | Actinobacillus suis
🗑
|
||||
| Pink, lactose-fermenting colonies on MacConkey agar | Actinobacillus suis
🗑
|
||||
| Treatment following antibiotic sensitivity testing: Usually susceptible to ampicillin, carbenicillin, potentiated sulfonamides and tetracyclines | Actinobacillus suis
🗑
|
||||
| No commercial vaccines available | Actinobacillus suis
🗑
|
||||
| Upper respiratory tract of pigs; not a commensalWorldwide distribution (12 serotypes with different geographic distribution & virulence) | Actinobacillus pleuropneumoniae
🗑
|
||||
| Grows as a short, pleomorphic rod; most give complete hemolysis | Actinobacillus pleuropneumoniae
🗑
|
||||
| CAMP test with S. aureus --- CAMP- positiveCapsules present on virulent strains | Actinobacillus pleuropneumoniae
🗑
|
||||
| A major cause of highly contagious pleuropneumonia in predominantly younger pigs ( < 6 months of age), in the U.S., Asia, and Europe | Actinobacillus pleuropneumoniae
🗑
|
||||
| The disease is often fatalSubclinical infection is common | Actinobacillus pleuropneumoniae
🗑
|
||||
| Stress plays a role in induction of disease (concurrent infection with P. multocida and mycoplamas can exacerbate the condition) | Actinobacillus pleuropneumoniae
🗑
|
||||
| Spread is via respiratory route between pigs in close contact. Exposure is via inhalation | Actinobacillus pleuropneumoniae
🗑
|
||||
| Animals show anorexia, fever, and lung hemorrhages in progressing cases | Actinobacillus pleuropneumoniae
🗑
|
||||
| Fibrinous pleurisy is observed | Actinobacillus pleuropneumoniae
🗑
|
||||
| Blood-stained froth may be found in the trachea and bronchi | Actinobacillus pleuropneumoniae
🗑
|
||||
| animals are anorexic, show respiratory distress due to pleurisy. Poor weight gain with lung lesions seen at slaughter | Actinobacillus pleuropneumoniae Chronic
🗑
|
||||
| : high fever, anorexia, ataxia, and cyanosis. Animals may tremble & have difficulty in swallowing. Blood from nose & mouth & death can occur in 24 hrs | Actinobacillus pleuropneumoniae Acute
🗑
|
||||
| sudden death occurs within 8 hours. Bloody froth is usually observed at the mouth. Animals quickly becomes prostrate. Is similar to endotoxic shock | Actinobacillus pleuropneumoniae Peracute
🗑
|
||||
| Blood agar --- small colonies surrounded by clear hemolysisNo growth on MacConkey agarPositive CAMP test | Actinobacillus pleuropneumoniae
🗑
|
||||
| Twelve serotypes have been identified. | Actinobacillus pleuropneumoniae
🗑
|
||||
| Vaccines exist, but protection is serotype- specific. Vaccines do not block infection but severity greatly decreased | Actinobacillus pleuropneumoniae
🗑
|
||||
| Polyvalent bacterins may induce protective immunity but fail to prevent transmission or development of a carrier state | Actinobacillus pleuropneumoniae
🗑
|
||||
| Enterobacteriaceae gram | Gram-negative rods
🗑
|
||||
| Enterobacteriaceae oxidase and catalase | Oxidase-negative, Catalase-positive
🗑
|
||||
| Facultative anaerobes | Enterobacteriaceae
🗑
|
||||
| Ferment glucose, reduce nitrate to nitrite | Enterobacteriaceae
🗑
|
||||
| Most are motile by peritrichous flagella | Enterobacteriaceae
🗑
|
||||
| Enteric bacteria which tolerate bile salts in MacConkey agar | Enterobacteriaceae
🗑
|
||||
| Variety of clinical infections | Enterobacteriaceae
🗑
|
||||
| E. coli Salmonella Yersenia | Major enteric and systemic pathogens
🗑
|
||||
| Proteus Enterobacter Klebsiella | Opportunistic pathogens
🗑
|
||||
| Found in the intestinal tract of animals and humans | Enterobacteriaceae
🗑
|
||||
| Contaminate vegetation, soil and water | Enterobacteriaceae
🗑
|
||||
| Major pathogens | E. coli, Salmonella sp. and Yersinia sp
🗑
|
||||
| are involved in localized infections in diverse anatomical locations | Opportunistic pathogens
🗑
|
||||
| Gram-negative, short rods | E. coli
🗑
|
||||
| Most strains are motile by peritrichous flagella | E. coli
🗑
|
||||
| Often fimbriate | E. coli
🗑
|
||||
| A capsule is often present --- mucoid | E. coli
🗑
|
||||
| Grows well on a variety of media at 37 oC | E. coli
🗑
|
||||
| Characteristic growth on EMB (metallic sheen | E. coli
🗑
|
||||
| non-spore-forming | E. coli
🗑
|
||||
| Ferments lactose (pink colonies in MacConkey agar | E. coli
🗑
|
||||
| E. coli are serotyped on the basis of | lipopolysaccharide
🗑
|
||||
| lipopolysaccharide | “O” (Somatic), “H” (Flagellar) and “K” (Capsular
🗑
|
||||
| possesses non-flagellar appendages called pilli | E. coli
🗑
|
||||
| pilli Important types | K88 or F4, K99 or F5, and 987P or F6
🗑
|
||||
| are almost always associated with isolates from swine | K88 and 987P
🗑
|
||||
| associated with isolates from cattle, sheep, swine | K99
🗑
|
||||
| Occurs due to the colonization of the intestinal tract from environmental sources, shortly after birth | Colibacillosis in mammals
🗑
|
||||
| Colibacillosis as a primary infection | by shell penetration, inhalation in the hatchery & occurs during the first few days of age
🗑
|
||||
| Colibacillosis as a secondary infection | complicating agent during the growing period
🗑
|
||||
| Occurs due to the colonization of the intestinal tract from environmental sources, shortly after birth | Colibacillosis in mammals
🗑
|
||||
| the mechanism of pathogenesis Based on | (1) Tissue localization of E.coli and (2) Biological activity of E.coli toxin
🗑
|
||||
| Enterotoxigenic E.coli (ETEC) | strain that causes Enteric colibacillosis and Enterotoxemic colibacillosis
🗑
|
||||
| strain that cause Local invasive colibacillosis | Enteropathogenic E.coli (EPEC)
🗑
|
||||
| strain that cause Septicemic colibacillosis | Enteroinvasive E.coli (EIEC)
🗑
|
||||
| strain that cause Hemorrhagic Uremic Syndrome (HUS) in children | Enterohemorrhagic E.coli (EHEC)
🗑
|
||||
| Causes diarrhea in animals 2 weeks to 1 month of age | Enteric colibacillosis caused by (ETEC
🗑
|
||||
| Produce Enterotoxins (Exotoxins): 1. Heat-labile (LT) type (Immunogenic) and 2. Heat-stable (ST) type (Non-immunogenic) | Enteric colibacillosis caused by (ETEC
🗑
|
||||
| Produce Pilus antigens (K antigens), important for adherence & colonization | Enteric colibacillosis caused by (ETEC
🗑
|
||||
| Causes Neonatal diarrhea in animals less than 1 week of age | Enterotoxemic colibacillosis caused by (ETEC
🗑
|
||||
| Produce Enterotoxins (Exotoxins): 1. Heat-labile (LT) type (Immunogenic) and 2. Heat-stable (ST) type (Non-immunogenic | Enterotoxemic colibacillosis caused by (ETEC
🗑
|
||||
| Produce pilus antigens (K antigens | Enterotoxemic colibacillosis caused by (ETEC
🗑
|
||||
| K antigens involved in Neonatal diarrhea | K88 (piglets) and K99 (calves Enterotoxemic colibacillosis caused by (ETEC
🗑
|
||||
| There is absorption of toxins | Enterotoxemic colibacillosis caused by (ETEC
🗑
|
||||
| Causes Local invasive colibacillosis | Enteropathogenic Colibacillosis caused by (EPEC
🗑
|
||||
| Local invasion and destruction of intestinal epithelium by E.coli ( invade beyond epithelium to the lamina propria | Enteropathogenic Colibacillosis caused by (EPEC
🗑
|
||||
| Not enterotoxigenic (do not produce enterotoxins) and do not become bacteremic or septicemic (do not produce endotoxin) | Enteropathogenic Colibacillosis caused by (EPEC
🗑
|
||||
| Diarrhea is associated with colonization, attachment and destruction of microvilli | Enteropathogenic Colibacillosis caused by (EPEC
🗑
|
||||
| Mechanism of invasion not known | Enteropathogenic Colibacillosis caused by (EPEC
🗑
|
||||
| Associated with bacteremia or septicemia | Septicemic colibacillosis (Colisepticemia) caused by (EIEC
🗑
|
||||
| Endotoxin-mediated | Septicemic colibacillosis (Colisepticemia) caused by (EIEC
🗑
|
||||
| May or may not have diarrhea or intestinal lesions | Septicemic colibacillosis (Colisepticemia) caused by (EIEC
🗑
|
||||
| Enters thru respiratory or intestinal tract | Septicemic colibacillosis (Colisepticemia) caused by (EIEC
🗑
|
||||
| Multiply in blood or tissue | Septicemic colibacillosis (Colisepticemia) caused by (EIEC
🗑
|
||||
| Fibrinopurulent systemic lesions in different organs such as pericardium, liver and heart | Septicemic colibacillosis (Colisepticemia) caused by (EIEC
🗑
|
||||
| are present in E. coli similar to many other Gram- negative bacteria | Endotoxins
🗑
|
||||
| They are part of the outer layer of the cell wall. Embedded in the outer membrane of the cell | Endotoxins
🗑
|
||||
| It is a complex phospholipids-polysaccharide-protein macromolecule | Endotoxins
🗑
|
||||
| are released in soluble form during bacterial growth and liberated when bacteria lyse | Endotoxins
🗑
|
||||
| They are less toxic than exotoxins | Endotoxins
🗑
|
||||
| Causes leucopenia, hypotension | Endotoxins
🗑
|
||||
| Complement activation | Endotoxins
🗑
|
||||
| Intravascular coagulation | Endotoxins
🗑
|
||||
| Death | Endotoxins
🗑
|
||||
| also produce EXOTOXINS | Certain strains of E. coli (ETEC
🗑
|
||||
| Certain strains of E. coli (ETEC) also produce EXOTOXINS | Two types Heat-labile and Heat-stable exotoxin
🗑
|
||||
| Large immunogenic portion | Heat labile type
🗑
|
||||
| Non-immunogenic | Heat stable type
🗑
|
||||
| These exotoxins are produced in the intestines | ENTEROTOXINS
🗑
|
||||
| They attach to different receptors on the intestinal epithelium | ENTEROTOXINS
🗑
|
||||
| ENTEROTOXINS | activate adenylate cyclase which results in increased cAMP
🗑
|
||||
| The increased cAMP causes | hyper secretion of water and chlorides into the gut lumen resulting in fluid loss
🗑
|
||||
| Very soon after birth a neonate ingests | E. coli
🗑
|
||||
| may inhibit the sudden and abnormal rate of multiplication of these organisms in the intestines | Colostrum
🗑
|
||||
| should receive 50 ml to 80 ml (or 5% body weight) colostrum/kg body weight within the first 12 hours of birth. Repeat 18 to 20 hours | Calves
🗑
|
||||
| can be frozen for several months, with almost no deterioration | Colostrum
🗑
|
||||
| Thaw in lukewarm water before you use frozen | Colostrum
🗑
|
||||
| Occurs in calves under 2 weeks but has been seen in calves up to a month old | Enteric colibacillosis (ETEC): E.coli with K99 pili
🗑
|
||||
| Typically occurs in calves 4 to 5 days old | Septicemic colibacillosis or colisepticemia (EIEC
🗑
|
||||
| Excess fluid in the intestineDiarrhea for several daysMucus present | Enteric colibacillosis (ETEC): E.coli with K99 pili
🗑
|
||||
| Septicemic colibacillosis or colisepticemia | (EIEC E. coli infections in Cattle
🗑
|
||||
| there is no scouring. In most acute cases there may be no temperature as the septicemia is overwhelming | acute colisepticemia
🗑
|
||||
| is associated with cases of acute mastitis in bovine | E. coli
🗑
|
||||
| Usually associated with poor sanitation | Bovine Mastitis
🗑
|
||||
| One or more quarters of the udder become swollen and painful | Bovine Mastitis
🗑
|
||||
| High temperature, 103 to 108 | Bovine Mastitis
🗑
|
||||
| Milk production falls rapidly and may cease | Bovine Mastitis
🗑
|
||||
| Vaccines usually contains E.coli, Streptococcus sp. & Staphylococcus sp | Bovine Mastitis
🗑
|
||||
| Pigs are susceptible to disease during the first 14 weeks or so after birth | E. coli
🗑
|
||||
| E. coli infection in Pigs Various names have been given to these conditions according to | age, symptoms and lesions
🗑
|
||||
| 1 to 12 days of age | Neonatal colibacillosis/Piglet scours
🗑
|
||||
| Diarrhea, dehydration with high mortality - 70% | Neonatal colibacillosis/Piglet scours
🗑
|
||||
| Edema disease | (Post-weaning colibacillosis E. coli enterotoxemia (ETEC
🗑
|
||||
| Occurs at about 1 week after weaning | Edema disease (Post-weaning colibacillosis) E. coli enterotoxemia (ETEC
🗑
|
||||
| An acute, highly fatal neurological disorder | Edema disease (Post-weaning colibacillosis) E. coli enterotoxemia (ETEC
🗑
|
||||
| The disease is dependent upon colonization of small intestine by E. coli that produces a toxin | Edema disease (Post-weaning colibacillosis) E. coli enterotoxemia (ETEC
🗑
|
||||
| staggering gait, muscular tremors & spasms, edema of eyelids, subcutaneous sub-serosal edema | Edema disease (Post-weaning colibacillosis) E. coli enterotoxemia (ETEC
🗑
|
||||
| All edema producing E. coli produce hemolysin and have K88 pili antigens | Edema disease (Post-weaning colibacillosis) E. coli enterotoxemia (ETEC
🗑
|
||||
| Toxin causes arterial degeneration and increased vascular permeability | Edema disease (Post-weaning colibacillosis) E. coli enterotoxemia (ETEC
🗑
|
||||
| Yolk sac of embryos is the center of infection | E.coli infection in Poultry
🗑
|
||||
| Occurs in all types and age groups of poultry | E. coli infection
🗑
|
||||
| Associated with dusty litter | Airsacculitis
🗑
|
||||
| Navel infection | Omphalitis
🗑
|
||||
| A variety of syndromes from which E. coli has been isolated | Enteritis Coligranuloma Synovitis arthritis
🗑
|
||||
| A new disease of racing greyhounds ” caused by O157:H7 strain | Alabama Rot
🗑
|
||||
| Lactose fermenter, non hemolytic | Enterobacter
🗑
|
||||
| Found widely in nature | Enterobacter
🗑
|
||||
| is the species of veterinary importance | Enterobacter aerogenes
🗑
|
||||
| They are opportunistic pathogens | Enterobacter
🗑
|
||||
| can be associated with mastitis in cows and sows | Enterobacter aerogenes
🗑
|
||||
| Lactose fermenter, non hemolytic | Klebsiella
🗑
|
||||
| Opportunistic pathogen Has a large polysaccharide capsule | Klebsiella
🗑
|
||||
| Associated with mastitis in cattle, cervicitis and endometritis in mares | Klebsiella
🗑
|
||||
| pneumonia in calves and foals and urinary tract infections in dogs | Klebsiella
🗑
|
||||
| Lactose non-fermenter | Proteus
🗑
|
||||
| Motile, characteristic swarming on blood agar and non- hemolytic | Proteus
🗑
|
||||
| Hydrolyze urea. Deaminate phenylalanine and produce H2S | Proteus
🗑
|
||||
| Otitis externa in dogs | Proteus
🗑
|
||||
| are the species of veterinary importance | Proteus mirabilis and Proteus vulgaris
🗑
|
||||
| in dogs and horses Urinary tract infections are frequently caused by | Proteus
🗑
|
||||
| Gram negative rods, oxidase negative | Klebsiella
🗑
|
||||
| Blood agar: Large, wet mucoid, whitish-grey | Klebsiella
🗑
|
||||
| MacConkey agar: Pink, slimy coalescing, not surrounded by red haze (D/D: E.coli | Klebsiella
🗑
|
||||
| Metritis and cervicitis in mares | K. pneumoniae
🗑
|
||||
| Pneumonia and suppurative lesions in calves and foals; Mastitis in cows on wood shavings and sawdust; Urinary tract infections in dogs | Klebsiella
🗑
|
||||
| Treatment: Amoxicillin-Clavulanate, enrofloxacin, tetracycline, trimethoprim-sulfonamide | Klebsiella
🗑
|
||||
| Susceptibility test recommended | Klebsiella
🗑
|
||||
| Gram negative coccobacilli, non-hemolytic, slow growth in MacConkey | Yersenia
🗑
|
||||
| are important human and animal pathogens | Y. enterocolitica, Y. pestis and Y. pseudotuberculosis
🗑
|
||||
| causes enteric red-mouth of fish & infection usually results in hemorrhagic septicemia | Y. ruckeri
🗑
|
||||
| causative agent of human plague. (Cats are infected most frequently than other domestic animals --- source of infection to humans | Y. pestis
🗑
|
||||
| human enteric pathogen | Y. enterocolitica
🗑
|
||||
| enteric (wild & domestic animals & septicemic (cage birds & laboratory rodents | Y. pseudotuberculosis
🗑
|
||||
| Enterobacteriaceae gram | Gram-negative rods
🗑
|
||||
| Enterobacteriaceae oxidase and catalase | Oxidase-negative, Catalase-positive
🗑
|
||||
| Facultative anaerobes | Enterobacteriaceae
🗑
|
||||
| Ferment glucose, reduce nitrate to nitrite | Enterobacteriaceae
🗑
|
||||
| Most are motile by peritrichous flagella | Enterobacteriaceae
🗑
|
||||
| Enteric bacteria which tolerate bile salts in MacConkey agar | Enterobacteriaceae
🗑
|
||||
| Variety of clinical infections | Enterobacteriaceae
🗑
|
||||
| E. coli Salmonella Yersenia | Major enteric and systemic pathogens
🗑
|
||||
| Proteus Enterobacter Klebsiella | Opportunistic pathogens
🗑
|
||||
| Found in the intestinal tract of animals and humans | Enterobacteriaceae
🗑
|
||||
| Contaminate vegetation, soil and water | Enterobacteriaceae
🗑
|
||||
| Major pathogens | E. coli, Salmonella sp. and Yersinia sp
🗑
|
||||
| are involved in localized infections in diverse anatomical locations | Opportunistic pathogens
🗑
|
||||
| Gram-negative, short rods | E. coli
🗑
|
||||
| Most strains are motile by peritrichous flagella | E. coli
🗑
|
||||
| Often fimbriate | E. coli
🗑
|
||||
| A capsule is often present --- mucoid | E. coli
🗑
|
||||
| Grows well on a variety of media at 37 oC | E. coli
🗑
|
||||
| Characteristic growth on EMB (metallic sheen | E. coli
🗑
|
||||
| non-spore-forming | E. coli
🗑
|
||||
| Ferments lactose (pink colonies in MacConkey agar | E. coli
🗑
|
||||
| E. coli are serotyped on the basis of | lipopolysaccharide
🗑
|
||||
| lipopolysaccharide | “O” (Somatic), “H” (Flagellar) and “K” (Capsular
🗑
|
||||
| possesses non-flagellar appendages called pilli | E. coli
🗑
|
||||
| pilli Important types | K88 or F4, K99 or F5, and 987P or F6
🗑
|
||||
| are almost always associated with isolates from swine | K88 and 987P
🗑
|
||||
| associated with isolates from cattle, sheep, swine | K99
🗑
|
||||
| Occurs due to the colonization of the intestinal tract from environmental sources, shortly after birth | Colibacillosis in mammals
🗑
|
||||
| Colibacillosis as a primary infection | by shell penetration, inhalation in the hatchery & occurs during the first few days of age
🗑
|
||||
| Colibacillosis as a secondary infection | complicating agent during the growing period
🗑
|
||||
| Occurs due to the colonization of the intestinal tract from environmental sources, shortly after birth | Colibacillosis in mammals
🗑
|
||||
| the mechanism of pathogenesis Based on | (1) Tissue localization of E.coli and (2) Biological activity of E.coli toxin
🗑
|
||||
| Enterotoxigenic E.coli (ETEC) | strain that causes Enteric colibacillosis and Enterotoxemic colibacillosis
🗑
|
||||
| strain that cause Local invasive colibacillosis | Enteropathogenic E.coli (EPEC)
🗑
|
||||
| strain that cause Septicemic colibacillosis | Enteroinvasive E.coli (EIEC)
🗑
|
||||
| strain that cause Hemorrhagic Uremic Syndrome (HUS) in children | Enterohemorrhagic E.coli (EHEC)
🗑
|
||||
| Causes diarrhea in animals 2 weeks to 1 month of age | Enteric colibacillosis caused by (ETEC
🗑
|
||||
| Produce Enterotoxins (Exotoxins): 1. Heat-labile (LT) type (Immunogenic) and 2. Heat-stable (ST) type (Non-immunogenic) | Enteric colibacillosis caused by (ETEC
🗑
|
||||
| Produce Pilus antigens (K antigens), important for adherence & colonization | Enteric colibacillosis caused by (ETEC
🗑
|
||||
| Causes Neonatal diarrhea in animals less than 1 week of age | Enterotoxemic colibacillosis caused by (ETEC
🗑
|
||||
| Produce Enterotoxins (Exotoxins): 1. Heat-labile (LT) type (Immunogenic) and 2. Heat-stable (ST) type (Non-immunogenic | Enterotoxemic colibacillosis caused by (ETEC
🗑
|
||||
| Produce pilus antigens (K antigens | Enterotoxemic colibacillosis caused by (ETEC
🗑
|
||||
| K antigens involved in Neonatal diarrhea | K88 (piglets) and K99 (calves Enterotoxemic colibacillosis caused by (ETEC
🗑
|
||||
| There is absorption of toxins | Enterotoxemic colibacillosis caused by (ETEC
🗑
|
||||
| Causes Local invasive colibacillosis | Enteropathogenic Colibacillosis caused by (EPEC
🗑
|
||||
| Local invasion and destruction of intestinal epithelium by E.coli ( invade beyond epithelium to the lamina propria | Enteropathogenic Colibacillosis caused by (EPEC
🗑
|
||||
| Not enterotoxigenic (do not produce enterotoxins) and do not become bacteremic or septicemic (do not produce endotoxin) | Enteropathogenic Colibacillosis caused by (EPEC
🗑
|
||||
| Diarrhea is associated with colonization, attachment and destruction of microvilli | Enteropathogenic Colibacillosis caused by (EPEC
🗑
|
||||
| Mechanism of invasion not known | Enteropathogenic Colibacillosis caused by (EPEC
🗑
|
||||
| Associated with bacteremia or septicemia | Septicemic colibacillosis (Colisepticemia) caused by (EIEC
🗑
|
||||
| Endotoxin-mediated | Septicemic colibacillosis (Colisepticemia) caused by (EIEC
🗑
|
||||
| May or may not have diarrhea or intestinal lesions | Septicemic colibacillosis (Colisepticemia) caused by (EIEC
🗑
|
||||
| Enters thru respiratory or intestinal tract | Septicemic colibacillosis (Colisepticemia) caused by (EIEC
🗑
|
||||
| Multiply in blood or tissue | Septicemic colibacillosis (Colisepticemia) caused by (EIEC
🗑
|
||||
| Fibrinopurulent systemic lesions in different organs such as pericardium, liver and heart | Septicemic colibacillosis (Colisepticemia) caused by (EIEC
🗑
|
||||
| are present in E. coli similar to many other Gram- negative bacteria | Endotoxins
🗑
|
||||
| They are part of the outer layer of the cell wall. Embedded in the outer membrane of the cell | Endotoxins
🗑
|
||||
| It is a complex phospholipids-polysaccharide-protein macromolecule | Endotoxins
🗑
|
||||
| are released in soluble form during bacterial growth and liberated when bacteria lyse | Endotoxins
🗑
|
||||
| They are less toxic than exotoxins | Endotoxins
🗑
|
||||
| Causes leucopenia, hypotension | Endotoxins
🗑
|
||||
| Complement activation | Endotoxins
🗑
|
||||
| Intravascular coagulation | Endotoxins
🗑
|
||||
| Death | Endotoxins
🗑
|
||||
| also produce EXOTOXINS | Certain strains of E. coli (ETEC
🗑
|
||||
| Certain strains of E. coli (ETEC) also produce EXOTOXINS | Two types Heat-labile and Heat-stable exotoxin
🗑
|
||||
| Large immunogenic portion | Heat labile type
🗑
|
||||
| Non-immunogenic | Heat stable type
🗑
|
||||
| These exotoxins are produced in the intestines | ENTEROTOXINS
🗑
|
||||
| They attach to different receptors on the intestinal epithelium | ENTEROTOXINS
🗑
|
||||
| ENTEROTOXINS | activate adenylate cyclase which results in increased cAMP
🗑
|
||||
| The increased cAMP causes | hyper secretion of water and chlorides into the gut lumen resulting in fluid loss
🗑
|
||||
| Very soon after birth a neonate ingests | E. coli
🗑
|
||||
| may inhibit the sudden and abnormal rate of multiplication of these organisms in the intestines | Colostrum
🗑
|
||||
| should receive 50 ml to 80 ml (or 5% body weight) colostrum/kg body weight within the first 12 hours of birth. Repeat 18 to 20 hours | Calves
🗑
|
||||
| can be frozen for several months, with almost no deterioration | Colostrum
🗑
|
||||
| Thaw in lukewarm water before you use frozen | Colostrum
🗑
|
||||
| Occurs in calves under 2 weeks but has been seen in calves up to a month old | Enteric colibacillosis (ETEC): E.coli with K99 pili
🗑
|
||||
| Typically occurs in calves 4 to 5 days old | Septicemic colibacillosis or colisepticemia (EIEC
🗑
|
||||
| Excess fluid in the intestineDiarrhea for several daysMucus present | Enteric colibacillosis (ETEC): E.coli with K99 pili
🗑
|
||||
| Septicemic colibacillosis or colisepticemia | (EIEC E. coli infections in Cattle
🗑
|
||||
| there is no scouring. In most acute cases there may be no temperature as the septicemia is overwhelming | acute colisepticemia
🗑
|
||||
| is associated with cases of acute mastitis in bovine | E. coli
🗑
|
||||
| Usually associated with poor sanitation | Bovine Mastitis
🗑
|
||||
| One or more quarters of the udder become swollen and painful | Bovine Mastitis
🗑
|
||||
| High temperature, 103 to 108 | Bovine Mastitis
🗑
|
||||
| Milk production falls rapidly and may cease | Bovine Mastitis
🗑
|
||||
| Vaccines usually contains E.coli, Streptococcus sp. & Staphylococcus sp | Bovine Mastitis
🗑
|
||||
| Pigs are susceptible to disease during the first 14 weeks or so after birth | E. coli
🗑
|
||||
| E. coli infection in Pigs Various names have been given to these conditions according to | age, symptoms and lesions
🗑
|
||||
| 1 to 12 days of age | Neonatal colibacillosis/Piglet scours
🗑
|
||||
| Diarrhea, dehydration with high mortality - 70% | Neonatal colibacillosis/Piglet scours
🗑
|
||||
| Edema disease | (Post-weaning colibacillosis E. coli enterotoxemia (ETEC
🗑
|
||||
| Occurs at about 1 week after weaning | Edema disease (Post-weaning colibacillosis) E. coli enterotoxemia (ETEC
🗑
|
||||
| An acute, highly fatal neurological disorder | Edema disease (Post-weaning colibacillosis) E. coli enterotoxemia (ETEC
🗑
|
||||
| The disease is dependent upon colonization of small intestine by E. coli that produces a toxin | Edema disease (Post-weaning colibacillosis) E. coli enterotoxemia (ETEC
🗑
|
||||
| staggering gait, muscular tremors & spasms, edema of eyelids, subcutaneous sub-serosal edema | Edema disease (Post-weaning colibacillosis) E. coli enterotoxemia (ETEC
🗑
|
||||
| All edema producing E. coli produce hemolysin and have K88 pili antigens | Edema disease (Post-weaning colibacillosis) E. coli enterotoxemia (ETEC
🗑
|
||||
| Toxin causes arterial degeneration and increased vascular permeability | Edema disease (Post-weaning colibacillosis) E. coli enterotoxemia (ETEC
🗑
|
||||
| Yolk sac of embryos is the center of infection | E.coli infection in Poultry
🗑
|
||||
| Occurs in all types and age groups of poultry | E. coli infection
🗑
|
||||
| Associated with dusty litter | Airsacculitis
🗑
|
||||
| Navel infection | Omphalitis
🗑
|
||||
| A variety of syndromes from which E. coli has been isolated | Enteritis Coligranuloma Synovitis arthritis
🗑
|
||||
| A new disease of racing greyhounds ” caused by O157:H7 strain | Alabama Rot
🗑
|
||||
| Lactose fermenter, non hemolytic | Enterobacter
🗑
|
||||
| Found widely in nature | Enterobacter
🗑
|
||||
| is the species of veterinary importance | Enterobacter aerogenes
🗑
|
||||
| They are opportunistic pathogens | Enterobacter
🗑
|
||||
| can be associated with mastitis in cows and sows | Enterobacter aerogenes
🗑
|
||||
| Lactose fermenter, non hemolytic | Klebsiella
🗑
|
||||
| Opportunistic pathogen Has a large polysaccharide capsule | Klebsiella
🗑
|
||||
| Associated with mastitis in cattle, cervicitis and endometritis in mares | Klebsiella
🗑
|
||||
| pneumonia in calves and foals and urinary tract infections in dogs | Klebsiella
🗑
|
||||
| Lactose non-fermenter | Proteus
🗑
|
||||
| Motile, characteristic swarming on blood agar and non- hemolytic | Proteus
🗑
|
||||
| Hydrolyze urea. Deaminate phenylalanine and produce H2S | Proteus
🗑
|
||||
| Otitis externa in dogs | Proteus
🗑
|
||||
| are the species of veterinary importance | Proteus mirabilis and Proteus vulgaris
🗑
|
||||
| in dogs and horses Urinary tract infections are frequently caused by | Proteus
🗑
|
||||
| Gram negative rods, oxidase negative | Klebsiella
🗑
|
||||
| Blood agar: Large, wet mucoid, whitish-grey | Klebsiella
🗑
|
||||
| MacConkey agar: Pink, slimy coalescing, not surrounded by red haze (D/D: E.coli | Klebsiella
🗑
|
||||
| Metritis and cervicitis in mares | K. pneumoniae
🗑
|
||||
| Pneumonia and suppurative lesions in calves and foals; Mastitis in cows on wood shavings and sawdust; Urinary tract infections in dogs | Klebsiella
🗑
|
||||
| Treatment: Amoxicillin-Clavulanate, enrofloxacin, tetracycline, trimethoprim-sulfonamide | Klebsiella
🗑
|
||||
| Susceptibility test recommended | Klebsiella
🗑
|
||||
| Gram negative coccobacilli, non-hemolytic, slow growth in MacConkey | Yersenia
🗑
|
||||
| are important human and animal pathogens | Y. enterocolitica, Y. pestis and Y. pseudotuberculosis
🗑
|
||||
| causes enteric red-mouth of fish & infection usually results in hemorrhagic septicemia | Y. ruckeri
🗑
|
||||
| causative agent of human plague. (Cats are infected most frequently than other domestic animals --- source of infection to humans | Y. pestis
🗑
|
||||
| human enteric pathogen | Y. enterocolitica
🗑
|
||||
| enteric (wild & domestic animals & septicemic (cage birds & laboratory rodents | Y. pseudotuberculosis
🗑
|
||||
|
🗑
|
|||||
| Large, Gram-positive rods | Clostridium
🗑
|
||||
| Produce endospores | Clostridium
🗑
|
||||
| Anaerobic | Clostridium
🗑
|
||||
| Catalase-negative, oxidase-negative | Clostridium
🗑
|
||||
| Enriched media required for growth | Clostridium
🗑
|
||||
| Motile (except C. perfringens | Clostridium
🗑
|
||||
| Present in soil & alimentary tracts of animals & in feces | Clostridium
🗑
|
||||
| Neurotoxic Clostridia | Clostridium tetani Clostridium botulinum (types A - G)
🗑
|
||||
| Causative agent of tetanus | Clostridium tetani
🗑
|
||||
| Straight, slender, anaerobic, Gm +ve rod with special terminal endospores, giving characteristic “drumstick” appearance | Clostridium tetani
🗑
|
||||
| Endospores resistant to chemicals & boiling but killed by autoclaving at 121 deg. C for 15 mins | Clostridium tetani
🗑
|
||||
| Has swarming growth & hemolytic on blood agar | Clostridium tetani
🗑
|
||||
| Ten serologic types based on flagellar antigens | Clostridium tetani
🗑
|
||||
| Cross-neutralizing antibodies to neurotoxins between all serotypes | Clostridium tetani
🗑
|
||||
| Infection occurs by entry of endospores into traumatized tissues (abrasions & wounds | Clostridium tetani
🗑
|
||||
| Mode of action is by synaptic inhibition | Clostridium tetani
🗑
|
||||
| Incubation period is 5 to 7 days, may extend to 3 weeks | Clostridium tetani
🗑
|
||||
| Clinical effects of neurotoxins are similar in all domestic animals | Clostridium tetani
🗑
|
||||
| Nature & severity of clinical signs are dependent on anatomical site of the replicating bacteria, amount of toxin produced & species susceptibility | Clostridium tetani
🗑
|
||||
| Clinical signs include stiffness, localized spasms, altered facial expression, spasm of mastigatory muscles (“lock jaw”), generalized muscle stiffness (“saw-horse”) stance, especially in horses | Clostridium tetani
🗑
|
||||
| Recovered animals are not necessarily immune (toxin concentration that induce clinical disease is usually below threshold required to stimulate production of neutralizing antibodies | Clostridium tetani
🗑
|
||||
| Serious & fatal disease | Botulism
🗑
|
||||
| cause most outbreaks in domestic animals | C. botulinum types C and D
🗑
|
||||
| Inactivated by boiling for 20mins | C. botulinum
🗑
|
||||
| Gm +ve rod with sub-terminal endospores | C. botulinum
🗑
|
||||
| Occurs most commonly in waterfowl, cattle, horses, sheep, mink, poultry & farmed fish | C. botulinum
🗑
|
||||
| Pigs & dogs are relatively resistant & rare in domestic cats | C. botulinum
🗑
|
||||
| Poor quality baled silage & silage or hay containing rodent carcasses have been linked to outbreaks in horses & ruminants | C. botulinum
🗑
|
||||
| the most potent biological toxin known Neurotoxins of | C. botulinum
🗑
|
||||
| C. botulinum Mode of action is by | inhibition of neuro-muscular transmission
🗑
|
||||
| Botulism Clinical signs | Develops 3 to 17 days after ingestion of toxin in all species of animals
🗑
|
||||
| Acute disease of cattle & sheep caused by | C. chauvoei Blackleg
🗑
|
||||
| bomasitis in sheep caused by | C. septicum Braxy
🗑
|
||||
| Manifests as cellulitis with minimal gas gangrene & gas formation | Malignant edema
🗑
|
||||
| Acute disease affecting sheep & occasionally cattle, caused by C. novyi type B | Infectious necrotic hepatitis
🗑
|
||||
| Occurs primarily in cattle & occasionally in sheep, caused by C. haemolyticum | Bacillary hemogl
🗑
|
||||
| Neuro disorder in newborn foals under 2 months, due to stress in dam, high level of corticosteroids in milk, high mortality | Shaker foal symptom
🗑
|
||||
| Cattle & Sheep: Gangrenous cellulitis & myositis caused by exotoxins, leading to rapid death | Blackleg
🗑
|
||||
| Large muscle masses of limbs, back & neck are frequently affected | Blackleg
🗑
|
||||
| Manifests as cellulitis with minimal gas gangrene & gas formation | Malignant edema
🗑
|
||||
| Clinical features of toxemia are similar to malignant edema | Gas gangrene
🗑
|
||||
| Hemoglobinuria: major clinical feature as a result of extensive red cell destruction | Bacillary hemogl
🗑
|
||||
| Histotoxic clostridia Vaccination | Adjuvanted bacterin & toxoid is most effective
🗑
|
||||
| is the causative agent of Gas gangrene in human & domestic animals | C. perfringens type A
🗑
|
||||
| C. perfringens type B | Lamb dysentery
🗑
|
||||
| Many animals die suddenly & high susceptibility of this group is attributed to the absence of microbial competition and the low proteolytic activity in the neonatal intestine | C. perfringens type B
🗑
|
||||
| Occurs in sheep at pasture, usually manifests as sudden death | perfringens type C
🗑
|
||||
| Sudden death in goats & feedlot cattle | Clostridia
🗑
|
||||
| Necrotic enteritis in chickens | Enteropathogenic & Enterotoxaemia-producing Clostridia
🗑
|
||||
| Haemorrhagic enteritis in neonatal pigs | Enteropathogenic & Enterotoxaemia-producing Clostridia
🗑
|
||||
| Neuro disorder in newborn foals under 2 months, due to stress in dam, high level of corticosteroids in milk, high mortality | Shaker foal symptom
🗑
|
||||
| Gram + rods (large)Endospores | Clostridium
🗑
|
||||
| CAT –Oxidase –Enriched media required | Clostridium
🗑
|
||||
| Strict AnaerobeMotile (except perfringes)Exotoxins toxemia | Clostridium
🗑
|
||||
| Present in soil, alimentary tract and fecesExogenous infmalignant edema & gas gangreneEndogenous inf: dormant spores in muscle and liver | Clostridium
🗑
|
||||
| Tetanus Terminal endospores (“drumstick”) | C. tetani(neurotoxic
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|
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| All animals Same clinical effects of neurotoxins | C. tetani(neurotoxic
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|
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| Lock Jaw (spasm-masticatory mm); Saw Horse stance (esp horses)/generalized muscle stiffness, altered facial expression, arched back.Tx: antitoxin(passive immunity) + toxiod + penicillin | C. tetani(neurotoxic
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|
||||
| Endospores enter abrasions/ woundsinfectionToxinSynaptic inhibition mode of actionSeverity: site of bact., amt of toxin, spp susceptibility | C. tetani(neurotoxic
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|
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| Only killed by autoclavingBA: swarming/hemolyticFlagellar Ag’s: 10 serotypesD/D: strychnine poisoningRecovered animals not immune | C. tetani(neurotoxic
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|
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| Most potent biological toxin known | C. botulinum(neurotoxic
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|
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| Botulism Subterminal endospores | C. botulinum(neurotoxic
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|
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| Dilatd pupils, dry mucus memb, decreased salivation, tongue flaccidity, dysphagia, paralysis of resp musclesabdominal breathing, paralysis neck muscles (“limberneck”), straddled stance.Fatal | C. botulinum(neurotoxic
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|
||||
| Cattle, Waterfowl, HorsesSheep, mink, poultry farmed fishPigs/dogs/cats:rare/resistantPoor quality silage w/rodent carcassesoutbreaks(Ingestion of preformed toxin) | C. botulinum(neurotoxic
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|
||||
| Toxininhibition of neuromuscular transmission | mode of actionTx: antiserum(neutralizes unbound toxin)
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|
||||
| Inactivated by boiling 20min.Type C&D-most outbreaksTypes may be geographically restricted | C. botulinum(neurotoxic
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|
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| Foals <2months(neurological dz) | Shaker-foal Syndrome
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|
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| Stress on damcorticosteroids in milk | Shaker-foal Syndrome
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|
||||
| Botulinum type B | Shaker-foal Syndrome
🗑
|
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| Vacc dam: passive transfer of neutralizing antitoxins | Shaker-foal Syndrome
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|
||||
| Shaker-foal Syndrome | C. botulinum(neurotoxic
🗑
|
||||
| Blackleg | C. chauvoei(histotoxic
🗑
|
||||
| Cattle: 3months-2 years | endogenous infectionSheep: any age,exogenous infection
🗑
|
||||
| Gangrenous cellulites and myositis due to exotoxinsrapid death | C. chauvoei(histotoxic
🗑
|
||||
| Braxy (abomasitis) | C. septicum(histotoxic
🗑
|
||||
| Sheep | C. septicum(histotoxic
🗑
|
||||
| Anorexia, depression, feverrapid death | C. septicum(histotoxic
🗑
|
||||
| Winter ingestion of frozen herbage | C. septicum(histotoxic
🗑
|
||||
| Malignant Edema | C. septicum(histotoxic
🗑
|
||||
| cellulitis w/minimal gas gangrene | Malignant Edema
🗑
|
||||
| Tissue swelling (edema),Coldness, discoloration of overlying skin, depression, prostration (due to toxemia) | Malignant Edema
🗑
|
||||
| Rapid death w/extensive lesions | Malignant Edema
🗑
|
||||
| Gas Gangrene | C. perfringensType A(histotoxic
🗑
|
||||
| Humans/Domestic animals | C. perfringensType A(histotoxic
🗑
|
||||
| Gas productionSubcutaneous crepitation, clinical signs of toxemia | C. perfringensType A(histotoxic
🗑
|
||||
| Necrotizing lethal alpha toxin (has lecithinase activityopalescence on yolk agar | Nagler Rxn)
🗑
|
||||
| Anaerobic culture on BA: circular, flat, grey colonies/ double hemolysis+CAMP w/S. agalactiae | C. perfringensType A(histotoxic
🗑
|
||||
| Food poisoning | C. perfringensType A(histotoxic
🗑
|
||||
| Necrotizing enterocolitis | C. perfringensType A(histotoxic
🗑
|
||||
| Necrotic enteritis | C. perfringensType A(histotoxic
🗑
|
||||
| Canine hemorrhagic gastroenteritis | C. perfringensType A(histotoxic
🗑
|
||||
| Necrotizing enterocolitis Pigs |
🗑
|
||||
| Necrotic enteritis Chickens |
🗑
|
||||
| Canine hemorrhagic gastroenteritis Dogs |
🗑
|
||||
| Lamb dysentery Hemorrhagic enteritis | C. perfringens Type B
🗑
|
||||
| 1 week old-high mortalityCalves/Foals | C. perfringens Type B
🗑
|
||||
| (All Clostridium produce immunologically distinct exotoxins) | C. perfringens Type B
🗑
|
||||
| Sudden death: absence of microbial competition/low proteolytic activity in neonatal intestine | C. perfringens Type B
🗑
|
||||
| Struck(acute enterotoxemia- specific geog. regions) | C. perfringens Type C
🗑
|
||||
| Adult Sheep+Goats, feedlot cattle, chickens, neonatal pigs | C. perfringens Type C
🗑
|
||||
| Sudden death on pasture;Gut is hemorrhagicbloody diarrhea | C. perfringens Type C
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|
||||
| Pulpy Kidney Dz | C. perfringens Type D
🗑
|
||||
| Sheep | C. perfringens Type D
🗑
|
||||
| Over-eating disease-high grain diet/succulent pasture- worldwide | C. perfringens Type D
🗑
|
||||
| Hyperglycemia Glycosuria Symmetrical hemorrhagic lesions in basal ganglia and midbrain | C. perfringens Type D
🗑
|
||||
| PM: Kidney autolysispulpy/cortical softening | C. perfringens Type D
🗑
|
||||
| Enteritis | C. perfringens Type E
🗑
|
||||
| Rabbits Hemorrhagic in calves | C. perfringens Type E
🗑
|
||||
| Young rams C. novyi Type A | Big Head
🗑
|
||||
| Infection of head wounds due to fighting possible rapid death | C. novyi Type A Big Head
🗑
|
||||
| Necrotizing lethal alpha toxin | C. novyi Type A:Big Head
🗑
|
||||
| SheepCattle (+/-) C. novyi Type Type B | Black Disease(Infectious necrotic hepatitis)
🗑
|
||||
| Dark skin discoloration due to SQ venus congestion | C. novyi Type B Black Disease(Infectious necrotic hepatitis)
🗑
|
||||
| Liver damage by migrating parasitesexotoxins of C. novyihepatic necrosis | C. novyi Type B: Black Disease(Infectious necrotic hepatitis)
🗑
|
||||
| Bacillary hemoglobinuria | C.haemolyticum
🗑
|
||||
| CattleSheep (+/-) | C.haemolyticum
🗑
|
||||
| Extensive RBC destruction & liver lesions | C.haemolyticum
🗑
|
||||
| Tyzzer’s disease | C. piliformeGram –Spore forming/filamentousIntracellular pathogen
🗑
|
||||
| Foals< 6 weeksMice | C. piliformeGram –Spore forming/filamentousIntracellular pathogen
🗑
|
||||
| Severe hepatic necrosis and enteritis | C. piliformeGram –Spore forming/filamentousIntracellular pathogen
🗑
|
||||
| Chronic diarrhea Hemorrhagic enterocolitis | C. difficile
🗑
|
||||
| Dogs Newborn foals | C. difficile
🗑
|
||||
| Quail dz Rabbits | C. colinumC. spiroforme
🗑
|
||||
| Diarrhea in neonates. K88: swine; K99: cattle | Enterotoxic E. coli
🗑
|
||||
| Do not invade tissue; heat labile or stable; exotoxins are absorbed | > more cAMP
🗑
|
||||
| cause septicemia and bacteremia in neonatal animals | enteroinvasive E. coli (EIEC
🗑
|
||||
| Penetrate epithelium, endotoxins cause damage | Enteroinvasive E. coli
🗑
|
||||
| Edema disease in pigs. O157:H7 in greyhounds and humans (Hemolytic uremia) | Enterohemorrhagic E. coli
🗑
|
||||
| Attach to microvilli and cause effacement or destruction; NOT invasive. (NO enterotoxins) | Enteropathogenic E. coli
🗑
|
||||
| a short gram-negative rod with petritrouchous flagella | Escherichia coli
🗑
|
||||
| It is motile and non spore-forming and ferments lactose and glucose | Escherichia coli
🗑
|
||||
| gives E. coli a metallic green appearance | EMB agar
🗑
|
||||
| Somatic/Lipopolysaccharide | O
🗑
|
||||
| Flagella | H
🗑
|
||||
| Capsular | K
🗑
|
||||
| Pili/Fimbrae | F
🗑
|
||||
| almost always associated with pigs | K88 (also called F4) and 987p (also called F6)
🗑
|
||||
| Diarrhea in calves is often caused by | K99
🗑
|
||||
| All enterotoxins are | exotoxins.
🗑
|
||||
| The virulence factors of enterotoxic E. coli are | exotoxins and pili antigens
🗑
|
||||
| The exotoxins are absorbed into the | epithelial cells.
🗑
|
||||
| cause effacement or degeneration of microvili without entering the cell | Enteropathogenic E.
🗑
|
||||
| cause septicemia and bacteremia in neonatal animals | enteroinvasive E. coli
🗑
|
||||
| Acute colisepticemia | usually does NOT cause diarrhea or fever
🗑
|
||||
| Bovine mastitis | caused by E. coli rapidly reduces milk production
🗑
|
||||
| causes 70% of pyometra cases in bitches | Escherichia coli
🗑
|
||||
| Pigs are quite susceptible until they are about 14 weeks old | E coli
🗑
|
||||
| Post-weaning colibacillosis in pigs is almost always caused by | K88
🗑
|
||||
| Edema disease in pigs is caused by | EHEC or VTEC
🗑
|
||||
| The symptoms are muscle tremors, staggering gait, facial edema (especially eyelids) and posterior paralysis before death | Edema disease
🗑
|
||||
| Birds of any age can get acute septicemia caused by | E coli
🗑
|
||||
| Arthritis may develop in poultry after | septicemic infection
🗑
|
||||
| can cause E. coli poisoning in humans | Raw hamburgers
🗑
|
||||
| Hemolytic uremia syndrome in humans is caused by | O157:H7
🗑
|
||||
| Greyhounds can get “Alabama rot” which is caused by | E. coli O:157:H7
🗑
|
||||
| Bacteremia in humans is occasionally caused by | Enterobacter cloacae
🗑
|
||||
| Mastitis can be caused by | Enterobacter aerogenes
🗑
|
||||
| is normally found in the soil | Citrobacter
🗑
|
||||
| has a large capsule, is not hemolytic and can cause mastitis in cattle, cervicitis and metritis in mares, and urinary tract infections | Klebsiella
🗑
|
||||
| does not ferment lactose, is highly motile and non-hemolytic | Proteus
🗑
|
||||
| frequently causes urinary tract infections in cats and dogs | Proteus
🗑
|
||||
| causes bubonic plague | Yersenia pestus
🗑
|
||||
| Salmonella Typhiurium | No host preference
🗑
|
||||
| Salmonella Choleraesuis | pigs
🗑
|
||||
| Salmonella Pullorum | poultry
🗑
|
||||
| Salmonella Gallinarum | poultry
🗑
|
||||
| Salmonella Enteritidis | No host preference
🗑
|
||||
| Salmonella Dublin | cattle and humans
🗑
|
||||
| Salmonella Typhi | Humans
🗑
|
||||
| describes salmonella infections caused by non-host-adapted serotypes | Paratyphoid
🗑
|
||||
| flagellar antigen is referred to as | H-O variation
🗑
|
||||
| The differences in capsule thickness (quantitative antigenic changes involving Vi antigens) are called | V-W variants
🗑
|
||||
| A strain changes from smooth to rough (S-R variation) when there is gradually lost to expose the core polysaccharide | O antigen
🗑
|
||||
| is destroyed by boiling | flagellar antigen
🗑
|
||||
| Typhoid fever is caused by | human-adapted serovar
🗑
|
||||
| are non-motile and paratyphoids are motile | Pullorum and Gallinarum
🗑
|
||||
| causes bacillary white diarrhea in poultry | Salmonella Pullorum
🗑
|
||||
| Fowl typhoid is caused by | Salmonella Gallinarum
🗑
|
||||
| Organism identification is the only way to distinguish fowl typhoid from | pullorum
🗑
|
||||
| produces green diarrhea and the wattles and combs have a purple discoloration | Fowl typhoid
🗑
|
||||
| is usually caused by Salmonella Dublin and Salmonella Typhimurium | Bovine salmonellosis
🗑
|
||||
| Calves 2-6 weeks are most susceptible | Salmonella Typhimurium
🗑
|
||||
| is more likely to produce the carrier state in cattle | Salmonella Dublin
🗑
|
||||
| Cattle with fever, diarrhea (brown or green, sometimes bloody) and sometimes get arthritis, pneumonia, or encephalitis | salmonellosis
🗑
|
||||
| is the most common serovar in pigs | Salmonella Choleraesuis
🗑
|
||||
| are often carriers of salmonella | Turtles
🗑
|
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