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Mycobacteriumpart2
Quiz Two
| Question | Answer |
|---|---|
| Cell walls rich in complex lipids containing mycolic acid | Mycobacterium |
| Pathogens grow slow, colonies visible after several weeks | Mycobacterium |
| Resistant to chemical disinfectants but susceptible to heat treatment ( pasteurization ) | Mycobacterium |
| Multiply intracellularly & cause granulamatous infections | Mycobacterium |
| Major diseases: Tuberculosis (TB), Johne’s disease and Feline leprosy | Mycobacterium |
| Some produce carotenoid pigments | Mycobacterium |
| Acid-fast (Z-N) positive rods | Mycobacterium |
| Complex egg-enriched media required for growth of pathogenic species | Mycobacterium |
| Aerobic, non-motile, non-spore-forming | Mycobacterium |
| Includes obligate pathogens, opportunistic pathogens & saprophytes | Mycobacterium |
| Gram- positive, filamentous rodsStrict aerobes | Mycobacterium |
| Facultative or obligate intracellular parasitesVery slow growing (up to 2 months) | Mycobacterium |
| Non- encapsulatedNon –spore-forming | Mycobacterium |
| Grows only within infected animals. | Mycobacterium |
| causes granulomatous lesions referred to as tubercles.Inhaled or ingested | Mycobacterium |
| Replicate within host cells, initiating an inflammatory cascade | Mycobacterium |
| The surrounding tissues necrotizesEpithelial cells surround the lesion, walling it off.Eventually, connective tissue encompasses the lesions impairing organ function | Mycobacterium |
| Causative agent of classic tuberculosis | Mycobacterium bovis |
| Also infects pigs, dogs, cats, horses, sheep, and primates | Mycobacterium bovis |
| Was responsible for about 20% of human TB infections | Mycobacterium bovis |
| “Eradicated” from US pigs in 1976. | Mycobacterium bovis |
| Inhibited by glycerol | Mycobacterium bovis |
| Primary culture requires 3-4 weeks | Mycobacterium bovis |
| Short, plump rods in tissues; large filaments from culture | Mycobacterium bovis |
| Does not grow at 25oC (optimal temp. is 37 C).Is killed by sunlight | Mycobacterium bovis |
| Exposure is via inhalation or ingestion of infected flakes. | Mycobacterium bovis |
| 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 |
| Progression is slow and requires several years before clinical signs become apparent | Mycobacterium bovis |
| Progression leads to:. Coughing. Emaciation. Dyspena. Increased respiration. Nodules on organs | Mycobacterium bovis |
| All cattle must be tested prior to interstate shipment | Mycobacterium bovis |
| About 4 weeks after infection, animals develop a cell- mediated immunity | Mycobacterium bovis |
| DTH response to detect reactors:. Tuberculin test | Mycobacterium bovis |
| Positive reaction is characterized by a hard or edematous swelling | Mycobacterium bovis |
| Animal are slaughtered and necropsied | Mycobacterium bovis |
| Infection is confirmed by culture | Mycobacterium bovis |
| natural reservoirs- captive elk, deer and bison are infected at a high rate | Mycobacterium bovis |
| PCR based diagnostic testing offers increased specificity & speed of detecting active infections | Mycobacterium bovis |
| Mycobacterium bovis Specimens suitable for lab | include lymph nodes, tissue lesions, aspirates and milk |
| Identification criteria Mycobacterium bovis | Growth rate; positive ZN-staining of bacilli; biochemical profile;analytical & molecular techniques |
| Mycobacterium bovis | Treatment and vaccination are inappropriate in control programs for cattle |
| are major obstacles in eradication programs in some countries | Wildlife reservoirs (badgers & possums) |
| Very stable in soil | M. avium complex |
| Colonies appear in 10-14 days on egg yolk medium. | M. avium complex |
| Causes classic tuberculosis in most avian species except psittacines | M. avium complex |
| A serious problem in immunocompromised humans | M. avium complex |
| Exposure is via ingestion of fecal materia | M. avium complex |
| Cadavers may infect predators and raptors | M. avium complex |
| Poultry: occurs most often in free-range adult birds | M. avium complex |
| Weight loss Ruffled feathers Nodular lesions of marrow, spleen and liver | M. avium complex |
| Rare cases in cats, dogs and horses have been reported | M. avium complex |
| Pigs infected thru ingestion of uncooked swill | M. avium complex |
| World- wide distribution, especially in the great lakes region of the US | Mycobacterium avium subsp. paratuberculosis |
| Requires an exogenous source of mycobactin for growth in vitro | Mycobacterium avium subsp. paratuberculosis |
| Slow growth (2-3 months). | Mycobacterium avium subsp. paratuberculosis |
| Yields short, plump rods. | Mycobacterium avium subsp. paratuberculosis |
| Strongly acid-fast | Mycobacterium avium subsp. paratuberculosis |
| Causative agent of Johne’s disease, a chronic enteritis of cattle and wild ruminants | Mycobacterium avium subsp. paratuberculosis |
| Animals ingest materials contaminated with infected feces (usually young animals during suckling) | Mycobacterium avium subsp. paratuberculosis |
| The organism penetrates the ileum and colon | Mycobacterium avium subsp. paratuberculosis |
| Macrophages ingest the organism, but no phagolysosome fusion occurs | Mycobacterium avium subsp. paratuberculosis |
| Thickening of the intestinal wall due to epithelial cell proliferation | Mycobacterium avium subsp. paratuberculosis |
| Emaciation despite normal appetite | Mycobacterium avium subsp. paratuberculosis |
| Swelling of regional lymph nodes | Mycobacterium avium subsp. paratuberculosis |
| Coats becomes dry and rough | Mycobacterium avium subsp. paratuberculosis |
| Main clinical feature is diarrhea, initially intermittent but becoming persistent and profuse | Mycobacterium avium subsp. paratuberculosis |
| Mucosa is usually thickened and folded into transverse corrugations | Mycobacterium avium subsp. paratuberculosis |
| Mesenteric & ileocecal lymph nodes are enlarged & edematous | Mycobacterium avium subsp. paratuberculosis |
| Fresh fecal samples are usually submitted | Mycobacterium avium subsp. paratuberculosis |
| Animals with clinical signs should be isolated and if confirmed should be slaughtered. | Mycobacterium avium subsp. paratuberculosis |
| Causative agent of feline leprosy | Mycobacterium lepraemurium |
| Causes granulomatous lesions of cats | Mycobacterium lepraemurium |
| Transmitted by bites from rats & cats | Mycobacterium lepraemurium |
| Nodular lesions involving subcutaneous tissues, may be solitary or multiple and usually confined to the head region or the limbs | Mycobacterium lepraemurium |
| Nodules are fleshy and freely movable, tend to ulcerate | Mycobacterium lepraemurium |
| Surgical excision of lesions is the preferred treatment | Mycobacterium lepraemurium |
| Does not infect other domestic animals or humans | Mycobacterium lepraemurium |
| Gram negative Aerobic (obligate)Rod shaped | Pseudomonas |
| Motile (one or morepolar flagella | Pseudomonas |
| Non-spore formingMost species produce pigmentsHighly resistant to disinfectants | Pseudomonas |
| Water Soil, common on plants, fruits and vegetablesMoist environment Skin, Burn tissues Mucus membrane | Pseudomonas aeruginosa |
| Intestinal tract of both humans and animalsOpportunistic organism | Pseudomonas aeruginosa |
| Gram negativeAerobic - obligate | Pseudomonas aeruginosa |
| Survives & multiplies over a wide temperature range, 20 - 42 oC | Pseudomonas aeruginosa |
| Survives high salt content | Pseudomonas aeruginosa |
| Characterized by the production of diffusible pigmentation | Pseudomonas aeruginosa |
| Pigment production is seen most clearly in nutrient agar | Pseudomonas aeruginosa |
| Causes opportunistic infections in variety of animal species | Pseudomonas aeruginosa |
| Pseudomonas aeruginosa Mastitis, metritis, pneumonia, dermatitis, enteritis | Cattle |
| Pseudomonas aeruginosa Metritis, Otitis media, pneumonia | Sheep |
| Pseudomonas aeruginosa Respiratory infections | Pigs |
| Pseudomonas aeruginosa Genital tract infections, pneumonia, ulcerative keratitis | Horses |
| Pseudomonas aeruginosa Otitis externa, Cystitis, Pneumonia, ulcerative keratitis | Dogs and Cats |
| Pseudomonas aeruginosa Haemorrhagic pneumonia, septicemia | Mink |
| Pseudomonas aeruginosa Necrotic stomatitis | Reptiles |
| Pseudomonas aeruginosa Specimens for lab. exam | Pus, respiratory aspirates, mid-stream urine, milk (mastitis), ear swabs |
| Colony morphology (large and flat with serrated edges) and characteristic fruity, grape-like odor | Pseudomonas aeruginosa |
| lactose-negative; pale colonies on MacConkey; oxidase-positive; TSI (unchanged | Pseudomonas aeruginosa |
| Extremely resistant to many antibiotics & susceptibility testing should be done before treatment | Pseudomonas aeruginosa |
| Combination of gentamycin or tobramycin with carbenicillin or ticaricillin may be effective | Pseudomonas aeruginosa |
| Vaccines: Polyvalent or autogenous inactivated bacterins; polyvalent exotoxin A-polysaccharide | Pseudomonas aeruginosa |
| BURKHOLDERIA Sp. of importance | Burkholderia mallei |
| Causes Glanders in horses and solipeds (Mules and donkeys) and carnivores | Burkholderia mallei |
| Highly contagious disease of horses | Burkholderia mallei |
| Can be a fatal disease in horses | Burkholderia mallei |
| Sheep, Cattle, Swine, Birds are resistant | Burkholderia mallei |
| Humans – Seldom occurs. Sporadic | Burkholderia mallei |
| No naturally acquired cases in US in almost 60 years | Burkholderia mallei |
| Glanders | Burkholderia mallei |
| Characterized by formation of nodules and ulcers in the respiratory tract or on the skin | Burkholderia mallei |
| Humans and carnivores are susceptible | Burkholderia mallei |
| Eradicated from most developed countries | Burkholderia mallei |
| Transmission: ingestion of food or water contaminated by nasal discharges of infected animals and less by inhalation or thru skin abrasions | Burkholderia mallei |
| In zoos and circuses, carnivores have contracted as a consequence of eating meat from infected solipeds | Glanders |
| Acute septicemic form of the disease glanders Characterized by | fever, mucopurulent discharge and respiratory signs. Death within a few weeks |
| (more common): presents as nasal, pulmonary and cutaneous forms | glanders Chronic form |
| 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 |
| 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”) |
| Burkholderia mallei Specimens for lab | discharge from lesions, blood for serology & must be processed in a biohazard cabinet |
| Grows on media containing 1% glycerol | Burkholderia mallei |
| Will grow on MacConkey (2 to 3 days incubation) | Burkholderia mallei |
| Colony characteristics ( white and smooth becoming granular and brown with age) | Burkholderia mallei |
| Comparatively unreactive biochemically and non-motile | Burkholderia mallei |
| Serology: CF and Agglutination tests | Burkholderia mallei |
| Mallein test: effective field test for confirmation and for screening in-contact animals | Burkholderia mallei |
| A test and slaughter policy enforced in countries where the disease is exotic | Burkholderia mallei |
| Antibiotic therapy is inappropriate (subclinical carriers) | Burkholderia mallei |
| Effective cleaning and disinfection (Formalin 1.5% or Iodophor 2% with contact time of 2 hrs.) | Burkholderia mallei |
| Causes Melioidosis in many animal species | Burkholderia pseudomallei |
| Endemic in tropical and subtropical regions of Southeastern Asia and Australia | Burkholderia pseudomallei |
| Transmission: Ingestion, inhalation or skin contamination from environmental sources | Burkholderia pseudomallei |
| Stress factors or immunosuppression may predispose to clinical disease | Burkholderia pseudomallei |
| Abscesses develop in many organs including lungs, spleen, liver, joints and CNS | Burkholderia pseudomallei |
| Chronic, debilitating, progressive disease | Burkholderia pseudomallei |
| Horses: mimics glanders (“pseudoglanders”) | Burkholderia pseudomallei |
| Gross pathological lesions may aid diagnosis | Burkholderia pseudomallei |
| Specimens for lab.: pus from abscesses, affected tissues & blood for serology (biohazard cabinet for processing) | Burkholderia pseudomallei |
| FA test to demonstrate organism in tissue smears (only in reference labs.) | Burkholderia pseudomallei |
| Colony morphology (Smooth and mucoid to rough and dull becoming yellowish-brown with age) with characteristic musty odor | Burkholderia pseudomallei |
| Treatment is expensive and unreliable (relapses when therapy is discontinued) | Burkholderia pseudomallei |
| Vaccines being developed in some countries | Burkholderia pseudomallei |
| MORAXELLA Species of veterinary importance | Moraxella bovis |
| Causative agent of Infectious bovine keratoconjunctivitis (“pinkeye”) | Moraxella bovis |
| Important ocular disease of cattle and occurs worldwide | Moraxella bovis |
| Short, plump gram-negative rods, usually in pairs | Moraxella bovis |
| Optimal growth in enriched media (growth enhanced by the addition of serum to media) | Moraxella bovis |
| Aerobic, non-motileUsually catalase- and oxidase-positive | Moraxella bovis |
| Unreactive with sugar substrates | Moraxella bovis |
| Virulent strains are fimbriated and hemolytic | Moraxella bovis |
| Susceptible for desiccation | Moraxella bovis |
| Found on mucus membranes of carrier cattle | Moraxella bovis |
| Highly contagious disease, usually in animals under 2 years of age | Infectious bovine keratoconjunctivitis (IBK) |
| Economic loss due to decreased weight gain in beef breeds, loss of milk production, disruption of breeding programs & treatment costs | Infectious bovine keratoconjunctivitis (IBK) |
| Transmission: direct contact, aerosols, thru flies acting as vectors | Infectious bovine keratoconjunctivitis (IBK) |
| Virulence attributed to the fimbriae, which allow adherence of the organism to the cornea | Moraxella bovis |
| Initially manifests as blepharoplasm, conjunctivitis and lacrimation | Infectious bovine keratoconjunctivitis (IBK) |
| Progresses to keratitis, corneal ulceration, opacity and abscessation, leading sometimes to panophthalmitis and permanent blindness | Infectious bovine keratoconjunctivitis (IBK) |
| Can be unilateral or bilateral | Infectious bovine keratoconjunctivitis (IBK) |
| Cattle with very little eye pigmentation are more severely affected | Infectious bovine keratoconjunctivitis (IBK) |
| 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) |
| Jersey cattle are highly susceptible to Pinkeye. Prominence of their eyes may expose them to more intense sun light | Infectious bovine keratoconjunctivitis (IBK) |
| High solar radiation is a predisposing factor | Infectious bovine keratoconjunctivitis (IBK) |
| Lower incidence in dairy breeds compared to beef herds | Infectious bovine keratoconjunctivitis (IBK) |
| Lacrimal secretion is most suitable for lab. exam. & must be processed promptly (extreme susceptibility to desiccation | Infectious bovine keratoconjunctivitis (IBK) |
| Specimens should be cultured in blood agar and MacConkey agar ( 48 to 72 hrs) | Infectious bovine keratoconjunctivitis (IBK) |
| 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 |
| No growth on MacConkey agar | Moraxella bovis |
| Cultures of virulent strains agglutinate in saline | Moraxella bovis |
| Smears from colonies reveal short, plump, gram-negative rods, usually in pairsCatalase- and oxidase- positive | Moraxella bovis |
| Antimicrobial therapy subconjunctivally or topically early in the disease | Infectious bovine keratoconjunctivitis (IBK) |
| Vitamin A supplementation may be benificial | Infectious bovine keratoconjunctivitis (IBK) |
| Prophylactic use of intramuscular oxytetracycline for animals at risk | Infectious bovine keratoconjunctivitis (IBK) |
| Fimbriae: Aid in the attachment to the Corneal epithelium | Moraxella bovis |
| Enzymes: Break down the junctions between corneal epithelial cells - initiate inflammatory response | Moraxella bovis |
| Infection range from sub-clinical carrier to acute fatal septicemia | Salmonella Sp |
| Salmonella in poultry | Salmonella gallinarum and Salmonella pullorum |
| Salmonella in pigs | Salmonella choleraesuis |
| Non-host-specific Salmonella | Salmonella typhimurium |
| Salmonella in dogs and cattle | Salmonella dublin |
| Carnivores are innately resistant to | salmonellosis |
| Often localize in the mucosa of the ileum, cecum and colon & in the mesenteric lymph nodes | Salmonella |
| Clinical disease: Animals under stress may develop clinical disease from sub-clinical and latent infections | Salmonella |
| Stress factors: Intercurrent infections; Transportation; Overcrowding; Pregnancy; Extreme ambient temperatures; Water deprivation; Oral antimicrobial therapy; Sudden changes in the diet | Salmonella |
| Other factors: # of organisms ingested, virulence of serotype or strain and susceptibility of the host (immunological status; genetic make-up; age) | Salmonella |
| In most animal species, both enteric and septicemic forms do occur | Salmonella |
| causes enteric and septicemic salmonellosis in many animal species | Salmonella typhimurium |
| Abortion in farm animals without clinical signs do occur | Salmonella |
| Terminal dry gangrene and bone lesions are common manifestations in chronic infections in calves | Salmonella dublin |
| many animal species (enterocolitis & septicemia) & humans (food poisoning) | Salmonella typhimurium |
| Cattle (many disease conditions) & Sheep, horses & dogs (enterocolitis & septicemia) | Salmonella dublin |
| Pigs (enterocolitis & septicemia) | Salmonella choleraesuis |
| Chicks (Pullorum disease --- bacillary whit diarrhea) | Salmonella pullorum |
| Adult birds Fowl typhoid) | Salmonella gallinarum |
| Turkeys (Arizona or paracolon infection) | Salmonella arizonae |
| Poultry (subclinical) & humans (food poisoning) | Salmonella enteritiditis |
| Sheep (abortion) | Salmonella brandenburg |
| Sub-clinical fecal excretors/all ages: probable outcome of most infections --- small numbers & intermittently | Salmonella dublin |
| Latent carriers/all ages: present in gall bladder with no excretions | Salmonella dublin |
| Acute or chronic enteric disease/all age: Enterocolitis with foul-smelling diarrhea containing blood, mucus & epithelial shreds or casts | Salmonella dublin |
| 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 |
| Abortion: Common cause in some European countries with no clinical signs | Salmonella dublin |
| Joint ill/calves: may follow septicemia or umbilical infection | Salmonella dublin |
| Osteomyelitis/young animals: often involve cervical vertebrae or bones of the distal | Salmonella dublin |
| 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 |
| Poultry constitute an important animal reservoir for | Salmonella |
| A very wide variety of serotypes have been isolated from chickens, turkeys, ducks, and other species of domestic poultry | Salmonella |
| can infect ovaries of hens and be transmitted thru eggs ( vertical transmission) | S. gallinarum, S. pullorum and S. enteritidis |
| non-host-adapted (Paratyphoids) --- often sub-clinical in laying hens | S. enteritidis & S. typhimurium |
| 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 |
| in the yolks A proportion of eggs laid by adults with infected ovaries contain | S. pullorum |
| can survive in the litter for several months | S. pullorum |
| All turkey and chicken breeder flocks are tested for the presence of infection. Use agglutination test | S. pullorum |
| infects young chicks andTurkey poults up to 2 – 3 weeks of age | Pullorum disease |
| The mortality rate is very high | S. pullorum |
| Birds are depressed, huddle under heat source, anorexic | S. pullorum |
| whitish fecal pasting around their vents | S. pullorum |
| Whitish nodes through out the lungs | S. pullorum |
| Necrotic lesions in liver and spleen | S. pullorum |
| The cycle of infection from the hen to the chick (vertical transmission), as occurs in pullorum disease, can also take place with | S. gallinarum |
| It is more usual, however, for fowl typhoid to develop as | a disease of varying severity among growing birds and adult stock |
| Common route of infection is by ingestion | S. gallinarum |
| The severity of outbreaks can vary from acute with high mortality rates to chronic infection | Fowl typhoid |
| When the disease occurs in young chicks the symptoms are indistinguishable from pullorum disease | Fowl Typhoid |
| Mortality rate can go up to 50% or more | Fowl Typhoid |
| Diarrhea with greenish colored feces, purple discoloration of comb and wattles | Fowl Typhoid |
| Diagnosis: Culture liver, spleen, and heart blood | Fowl Typhoid |
| is a name given to infections of poultry by non-host adapted salmonella | Paratyphoid |
| Day-old antibiotic injection is practiced in many hatcheries | Gentamycin and Spectinomycin |
| 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 |
| All animals Same clinical effects of neurotoxins | C. tetani(neurotoxic |
| 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 |
| Endospores enter abrasions/ woundsinfectionToxinSynaptic inhibition mode of actionSeverity: site of bact., amt of toxin, spp susceptibility | C. tetani(neurotoxic |
| Only killed by autoclavingBA: swarming/hemolyticFlagellar Ag’s: 10 serotypesD/D: strychnine poisoningRecovered animals not immune | C. tetani(neurotoxic |
| Most potent biological toxin known | C. botulinum(neurotoxic |
| Botulism Subterminal endospores | C. botulinum(neurotoxic |
| 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 |
| Cattle, Waterfowl, HorsesSheep, mink, poultry farmed fishPigs/dogs/cats:rare/resistantPoor quality silage w/rodent carcassesoutbreaks(Ingestion of preformed toxin) | C. botulinum(neurotoxic |
| Toxininhibition of neuromuscular transmission | mode of actionTx: antiserum(neutralizes unbound toxin) |
| Inactivated by boiling 20min.Type C&D-most outbreaksTypes may be geographically restricted | C. botulinum(neurotoxic |
| Foals <2months(neurological dz) | Shaker-foal Syndrome |
| Stress on damcorticosteroids in milk | Shaker-foal Syndrome |
| Botulinum type B | Shaker-foal Syndrome |
| Vacc dam: passive transfer of neutralizing antitoxins | Shaker-foal Syndrome |
| 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 |
| 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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