Mycobacteriumpart2

Description:	Quiz Two
Category:	Veterinary
Created by:	Alva Jackson on 2009-10-23

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 infmalignant 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/ woundsinfectionToxinSynaptic 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 musclesabdominal 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 carcassesoutbreaks(Ingestion of preformed toxin)	C. botulinum(neurotoxic
Toxininhibition 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 damcorticosteroids 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 exotoxinsrapid death	C. chauvoei(histotoxic
Braxy (abomasitis)	C. septicum(histotoxic
Sheep	C. septicum(histotoxic
Anorexia, depression, feverrapid 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 productionSubcutaneous crepitation, clinical signs of toxemia	C. perfringensType A(histotoxic
Necrotizing lethal alpha toxin (has lecithinase activityopalescence 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 hemorrhagicbloody 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 autolysispulpy/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 parasitesexotoxins of C. novyihepatic 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