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310 Cards in this Set
- Front
- Back
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Erysipelothrix:
- morphology - gram stain - atmospheric requirements - motility |
- long gram-positive rods
- facultatively anaerobic - immotile |
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Listeria:
- morphology - gram stain - atmospheric requirements - motility |
- short gram-positive rods
- facultatively anaerobic - motile |
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Erysipelothrix:
- where are they found? |
- TONSILS OF HEALTHY PIGS
- sewage effluent - abattoirs - decaying vegetation and soil - surface slime of fresh and saltwater fish - GIT and mucus membranes of many animals |
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Listeria:
- where are they found? |
- soil
- sewage effluent - decaying vegetation - stream water - asymptomatic enteric carriers (shed in feces) - food: soft cheeses, seafood, meat |
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Erysipelothrix:
- how are they transmitted? |
INGESTION:
- feco-oral - urine-oral - saliva-oral - exogenous or endogenous |
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Listeria:
- how are they transmitted? |
INGESTION:
- feco-oral - urine-oral - saliva-oral - exogenous or endogenous |
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Erysipelothrix:
- virulence factors and function |
- capsule: prevents phagocytosis
- adherence: to endothelial cells - neuraminidase: hemolysis, vascular damage, coagulopathy, and thrombus formation |
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Listeria:
- virulence factors and function |
- listeriolysin O and Ivanolysin
- these allow lysis of cells (e.g RBC) and intracellular survival |
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What are the four syndromes caused by Erisypelothrix rhusiopathiae and species affected?
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1. Septicemia - PIGS and other animals
2. Diamond Skin Disease - pigs 3. Arthritis - other species (e.g. dogs) 4. Endocarditis - other species (e.g. dogs) |
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What are the two syndromes observed in Listeria monocytogenes and the animals in which they occur?
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1. visceral form - neonates and non-ruminants; abortion in ruminants and humans
2. neural form - Circling Disease in ruminants |
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Erysipelothrix and Listeria
- how do you diagnose infections? |
- history, clinical signs, species
- Sample from lesions: joint, blood, aborted fetus, post-mortem - gram/diff-quik: G+ rods; may not be present in chronic disease - culture aerobically (+/- cold enrichment for Listeria) - other tests: histology, PCR, etc. |
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what is the most effective antibiotic against Erysipelothrix and Listeria?
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penicillin
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comment on the use of antibiotics in the treatment of Erysipelothrix and Listeria infections
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- often not effective in chronic cases (because they are disseminated)
- neural Listeriosis not effective - trimethoprim/sunfonamides and rifampin has been used in dogs |
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how do you manage Erysipelothrix and Listeria infections
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- reduce crowding and poor hygiene (Erysipelothrix)
- don't feed poor silage (Listeria) - cull chronically affected animals (Erysipelothrix) - E. rhusiopathiae vaccines in US - live attenuated vaccines for Listeria in other countries |
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comment on septicemia caused by Erysipelothrix rhusiopathiae
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- ALL ANIMALS with E. rhusiopathiae have septicemia
- particularly pathogenic in young pigs - this is severe and usually fatal |
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comment on ARTHRITIS caused by Erysipelothrix rhusiopathiae
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- localization of infection in joints
- pathology is immune related - synovial membrane hyperplasia with pannus formation |
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comment on endocarditis caused by Erysipelothrix rhusiopathiae
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- valvular endocarditis most common in mitral valve
- source of septic emboli |
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what disease of young animals is caused by Listeria monocytogenes? comment on the pathology
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- neonatal septicemia
- liver "milk spots" - placentitis and contamination of amniotic fluid causing fetal infection and late-term abortion in ruminants |
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what causes Circling Disease in ruminants and what is this disease's scientific name?
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- Listeria monocytogenes
- meningoencephalitis |
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Mycobacterium:
- morphology - gram reaction - atmospheric requirements |
- gram positive rods
- strict aerobe |
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Mycobacterium:
- how do they stain with Diff-Quik? - why |
- will stain negatively with Diff-Quik
- this is because they are acid-fast bacteria with a lipid-rich cell wall containing mycolic acids |
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what is the constituent of the Mycobacterium cell wall that makes them "acid fast"?
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mycolic acids (lipid)
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what are the two classifications of Mycobacteria according to where they live?
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1. obligate parasites (M. tuberculosis, M. bovis)
2. saprophytic (M. avium ss paratuberculosis, others) |
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comment on the pathogenicity of
- obligate parasite Mycobacteria - saprophytic Mycobacteria |
- obligate parasites are also obligate pathogens
- saprophytic are opportunistic pathogens or non-pathogenic |
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what are the virulence factors of Mycobacteria and their function
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1. cord factor - inhibits chemotaxis and is leukotoxic
2. glycolipids - (intracellular survival in macrophages) prevents macrophage activation by INF-gamma 3. sulfatides & sulfolipids - (intracellular survival in macrophages) inhibits phagolysozome formation 4. superoxide dismutase - destroys free radicals 5. mycobactrins & exochalins - iron acquisition |
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what are the two major lesions caused by Mycobacteria and where in the body are they usually found?
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1. caseous necrosis in the lungs
2. granulomas in the lymph nodes |
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what is the pathological process by which Mycobacteria can be contagious by coughing?
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casaous necrotic lesions in the lungs rupture into the bronchi. Animal coughs and aerosolizes the bacteria.
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what are histologic characteristics of lymphatic granulomas caused by Mycobacteria?
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- presence of epithelioid cells (giant cells)
- thick fibrous capsule - ncerotic center (+/- calcification) surrounded by granulocytes and lymphocytes |
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Bovine Tuberculosis
- causative agent - reservior - predisposing factors - five routes of infection |
- Mycobacterium bovis
- reservoir: tuberculous animals - predisposing factors: crowding, dirty environment, genetic 1. inhalation of aerosols 2. ingestion of contaminated feed, water, and milk 3. ingestion of sputum 4. wound infection 5. congenital |
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describe the lesions caused by Mycobacterium bovis infection from the following routes:
- inhalation - ingestion of contaminated feed, water, milk - ingestion of sputum - wound infection |
- inhalation: lung lesions (caseous necrosis)
- ingestion of contaminated feed, water, milk: mesenteric lymph node granulomas - ingestion of sputum: GI infection - wound infection: (rare) "Pathologist's wart" |
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Bovine tuberculosis
- Causative agent - comment on incubation period - clinical signs |
- Mycobacterium bovis
- may be "quietly inactive" for long periods of time post-infection - coughing, fatigue, capricious appetite, emaciation, fluctuating body temp - ↓production (weight gain, etc.) - if spread, affects other tissues (e.g. liver, kidney) |
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what are two problems making eradication of Mycobacterium bovis difficult in the US?
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1. a variety of reservoirs exist
2. US-Mexico exchange |
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what are some reservoir hosts for Mycobacterium bovis?
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wild and domestic animals:
- white-tailed deer (US) - badger, ferret (UK) - lynx (Spain) - possum, ferret (NZ) - lion (South Africa) |
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what are the two main ways in which to reduce the public to bovine tuberculosis?
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1. pasteurize milk
2. diagnose, control, and eradicate the dz by tuberculin tests and abattoir surveillance |
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how is an intradermal tuberculin test administered and interpreted in cattle?
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1. inject PPD of M. bovis into caudal tail fold
2. look for hard swelling > 5mm (suspect or reactor) at 72 hours 3. if suspect or reactor, repeat in neck with M. bovis PPD and M. avium on the other side of the neck 4. if M. bovis lesion id > 4mm the size of M avium, cow is a reactor 5. report positive findings |
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how is tuberculosis treated with antiinfectives in humans and companion animals?
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- treatment lasts for ~6 to 9 months with one set of antimicrobials:
- e.g. isoniazid in combination with ethambutil, pyrazinamide, and/or rifampin - switch to a different combination and monitor for ~ 3 years |
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comment on vaccination for mycobacterium bovis
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- BCG (bacillus Calmette Guerin) vaccine given orally to humans in anticipaton of exposure
- not routine in US and not in animals |
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Johne's disease:
- causative agent - comment on incubation - transmission |
- Mycobacterium avium ss paratuberculosis
- ingestion of feed and water contaminated with Jone's-positive feces; subclinical carriers are important - long incubation time: juvenile/neonatal exposure; dz seen in 2-3 yr, but not older than 5 |
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Johne's disease
- causative agent - clinical signs - what species are mainly affected |
- Mycobacterium avium ss paratuberculosis
- progressive, persistent granulomatous enteritis and severe, chronic diarrhea leading to emaciation and death - ruminants are affected |
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Johne's disease
- causative agent - describe the typical lesions seen in the disease |
- Mycobacterium avium ss paratuberculosis
- thickened and sclerotic intestinal wall - infiltration of intestinal wall with EPITHELIOID cells - locally enlarged lymph nodes - intracellular clumps of bacteria - rarely, infection seen in udder, uterus, genitalis of bulls |
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what two histological tests could you perform of an intestinal biopsy to presumptively diagnose Johne's disease?
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(Mycobacterium avium ss paratuberculosis)
- H&E stain reveals accumulation of macrophages and epithelioid cells in the intestinal villi - Acid-fast stain will reveal masses of pink rods inside of macrophages |
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what are eight tests in the diagnosis of Johne's disease?
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(Mycobacterium avium ss paratuberculosis)
1. history & clinical signs 2. acid-fast stain of fecal smears (not very sensitive) 3. rectal scrapings and biposy 4. fecal culture 5. intradermal (Johinin test) - unreliable 6. DNA probes 7. Serology 8. Immunity tests to IFN-γ |
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why is treatment of Johne's disease in farm animals not an option?
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(Mycobacterium avium ss paratuberculosis)
- cost - low efficacy - reservoirs - antibiotic resistance |
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what are some ways to control Johne's disease?
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(Mycobacterium avium ss paratuberculosis)
- problematic - cull infected animals - test and cull sub-clinical animals - hygiene and husbandry (young animals) - vaccines not recommended due to cross-reaction with Tb test |
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what is a specific disease of dogs caused by opportunistic infection of Mycobacteria?
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canine leproid granuloma syndrome
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canine leproid granuloma syndrome
- causative agent - transmission - lesions - diagnosis - treatment |
- unidentified Mycobacteria
- biting insects are a mechanical vector - nodular granulomatous lesions on the head and ears that may ulcerate before spontaneous resolution - Dx: cytology (Diff-Quik) or histology (acid-fast) - Tx: lesions tend to 'self cure'. If refractory, treat with a combination of rifampicin and clarithromycin |
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an obese cat presents for a chronic, infection of the inguinal fat pad and a thickened patch of chronically inflamed, hairless skin with drainage tracts and focal purplish areas might have what disease? Causative agent?
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Panniculitis syndrome
(Mycobacterium smegmatic, fortuitum, chelonae) |
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panniculitis syndrome
- causative agent - lesions in cat - lesions in dog - how do they get infected? |
- a complex of Mycobacterium smegmatis, fortuitum, and chelonae
- granulomatous inflammation and necrosis of the inguinal fat pad in obese cats - lesion in subcutis of chest wall in dogs - follows trauma that penetrates fatty tissues and deposits dirt in the wound (note that these are saprophytes) |
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what Mycobacteria of clinical importance are obligate pathogens?
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- M. bovis
- (M. tuberculosis) |
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comment on how the treatment of canine leproid granuloma syndrome differs from panniculitis syndrome
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- canine leproid granuloma syndrome self-cures most of the time
- panniculitis syndrome almost never self cure and requires surgical debridement, and antibiotics |
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what are antibiotics used to treat panniculitis syndrome
- initially - for refractory cases |
- initially: doxycycline and fluoroquinolones (e.g. ciprofloxacin)
- refractory: clarithromycin, moxifloacin, gatifloxacin |
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the Family of bacteria that includes the genera Escherichia, Yersinia, and Klebsiella
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Enterobacteriaceae
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what seven genera of Family Enterobacteriaceae are of veterinary importance?
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1. Escherichia
2. Salmonella 3. Klebsiella 4. Proteus 5. Yersinia 6. Enterobacter 7. Serratia |
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Enterobacteriaceae
- morphology - gram reaction - atmospheric requirements - oxidase test |
- gram negative rods
- facultatively anaerobic - oxidase negative |
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E. coli
- morphology - gram reaction - atmospheric requirements - oxidase test - lactose fermentation |
- gram negative rods
- facultatively anaerobic - oxidase negative - lactose positive |
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Salmonella
- morphology - gram reaction - atmospheric requirements - oxidase test - lactose fermentation |
- gram negative rods
- facultatively anaerobic - oxidase negative - lactose negative |
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Klebsiella:
- morphology - gram reaction - atmospheric requirements - oxidase test - lactose fermentation |
- gram negative rods
- facultatively anaerobic - oxidase negative - lactose positive |
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Enterobacter:
- morphology - gram reaction - atmospheric requirements - oxidase test - lactose fermentation |
- gram negative rods
- facultatively anaerobic - oxidase negative - lactose positive |
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Proteus:
- morphology - gram reaction - atmospheric requirements - oxidase test - lactose fermentation |
- gram negative rods
- facultatively anaerobic - oxidase negative - lactose negative |
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Yersinia:
- morphology - gram reaction - atmospheric requirements - oxidase test - lactose fermentation |
- gram negative rods
- facultatively anaerobic - oxidase negative - lactose negative |
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E. coli:
- where are they found? |
- normal flora of the Gi tract
- found in the environment (i.e. "coliform counts") |
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comment on the source of E. coli infection in
- enteric infection - non-entric infection - canine pyometra |
- enteritis: exogenous
- non-enteric: endogenous - canine pyometra: ascending transient infection in the vagina |
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of the six Enterobacteriaceae genera that we have discussed:
- which are considered good pathogens? - which are considered intermediate-to-poor pathogens? |
- good: E. coli, Salmonella
- intermediate/poor: Klebsiella, Proteus, Yersinia, Enterobacter |
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what are the virulence factors and function of non-enteric infectious E. coli strains?
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1. fimbriae or adhesions - attachment
2. capsule - avoid phagocytosis 3. O somatic antigens - avoid phagocytosis 4. lemolysins (leukotoxins) - cellular toxicity 5. endotoxin - systemic effects |
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E. coli canine pyometra in dogs
- given the strong immunity of the female repro tract, why would this disease develop? |
- prolonged exposure to progesterone enables E. coli to adhere more effectively; causes secondary endometrial hyerplasia, leading to fluid accumulation in the uterus; and does not allow the uterus to evacuate
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E. coli canine pyometra in dogs
- why could PU/PD develop? - what other sequalae could occur as a result of this ascending infection? |
- endotoxin interferes with ADH secretion, so renal medullary washout occurs
- cystitis can develop - bacteremia can lead to immune complex glomerulonephritis - mild interstitial and tubular nephritis is also common |
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E. coli canine pyometra in dogs
- what is the best way to reverse the acute renal failure resulting from this disease? |
clear up the pyometra and remove the source of the bacterial toxin/antigen
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what is the most common causative agent of cystitis in dogs?
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E. coli
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E. coli mastitis
- common host species - source of infection - when is infection most frequently seen - major virulence factor for the infection - why can it be gangrenous and deadly? |
- cow and sow are most commonly infected
- common source is fecal contamination of the udder/mammae - infection most prevalent during periparturient period and times of milk production, when host compromise is at its worst - pili mediate the attachment - it can be gangrenous and deadly if endotoxin is absorbed into the system |
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what is an economically important disease of fowl involving E. coli?
- route of infection - clinical signs |
- colibacillosis of birds
- infection by GI or respiratory tracts, especially from dirty envirnments 1. septicemia 2. air sacculitis 3. coligranulomas (Hjarre's disease) 4. serositis, synovitis, etc. (septicemia) 5. egg infections |
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what type of E. coli cause infectious diarrhea?
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ETEC (enterotoxigenic E. coli)
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for a case of neonatal colibacillosis, how could you prove that E. coli was causing this diesase?
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1. isolate from the feces
2. determine if that particular strain is capable of causing that disease |
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Neonatal colibacillosis:
- causative agent - virulence factors and their function |
- ETEC (enterotoxigenic E. Coli)
- Pili - attachment (required for dz) - cytoTONIC enterotoxin |
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If pili are required for causing E. coli enteritis infections, why don't all E. coli with pili cause this disease?
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because the pili have adherence factors for specific receptor types in the GI tract. The same is true for other diseases such as pyometra, mastitis, and septicemia
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comment on the enterotoxin in ETEC infections:
- pathophysiology - types of toxins and their function |
it is cytoTONIC:
- do not damage intestinal walls - do not cause inflammation - heat labile toxin - ↑intracellular cGMP - heat stable toxin: ↑intracellular cAMP - both of these toxins cause a net chloride excretion and loss of electrolytes, causing hypersecretory diarrhea |
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what is the common name for neonatal colibaccilosis of calves? why is it called this?
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- "White Scours"
- called "White" because there is no blood in the diarrhea. - there is no blood because ETEC produce cytoTONIC enterotoxin which causes hypersecretory diarrhea, but does not damage the epithelium |
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what is a common ETEC disease in piglets?
- virulence factors - host factors - environmental factors |
pre-weaning disease of piglets
- VF: pili, enterotoxin, numbers (exposure) - HF: receptors to bind pili are only in the GI lumen for the first week of life; the piglets need adequate antibodies from colostrum and milk - EF: overcrowding, wet/dirty environment, cold weather, high numbers of bacteria |
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what are the four major types of E. coli that cause enteric disease?
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1. ETEC - enterotoxigenic
2. EPEC/AAEC - enteropathogenic 3. EHEC - enterohemorrhagic 4. NTEC - necrotoxigenic |
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what are the three basic types of E. coli that produce cytotoxic enterotoxins? What type produces cytotonic enterotoxins?
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CYTOTOXIC:
1. EPEC/AAEC - enteropathogenic 2. EHEC - enterhemorrhagic 3. NTEC - necrotoxigenic CYTOTONIC: - ETEC - enterotoxigenic |
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in what three ways do EPEC/AAEC E. coli cause disease?
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(enteropathogenic)
1. initiate adherence to epithelial cells 2. efface micro villi (attaching and effacing lesions) 3. diarrhea due to malabsorption |
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in what three ways do EHEC E. coli cause disease?
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(enterohemorrhagic)
1. attaching and effacing lesions 2. microvillus destruction 3. Shiga-like toxin - hemorrhage and edema (clinical signs similar to Salmonella) |
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in what two ways to NTEC E. coli cause disease?
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1. intestinal colonization
2. cytotoxic necrotizing factors damage enterocyte cytosleketon |
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which type of E. Coli is a rule-out for Salmonellosis?
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EHEC (enterohemorrhagic)
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what types of E. coli cause post-weaning diarrhea in piglets and calves? why? how is this disease controlled?
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- the endoTOXIC ones: ETEC, EHEC, and/or EPEC
- these diseases occur as a result of waning maternal antibodies - disease is controlled through good management practices to control numbers of bacteria. They need to develop immunity to these bugs |
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what is a major rule-out for an enterohemorrhagic E. coli infection?
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Salmonellosis
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edema disease of pigs
- causative agent - which pigs are most at risk? - clinical signs - pathogenesis |
- caused by a hemolytic but NOT invasive E. coli
- disease of thriving weaner or grower pigs (6-14 wk) - edema, especially of the subcutis on the head. Edema of the EYELIDS. - edema of the greater curvature of the stomach (post-mortem) - CNS signs, e.g. staggering gait - caused by Shiga-like toxin (aka ANGIOTOXIN aka vasotoxin) absorbed into the bloodstream |
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what type of E. coli is the infamous O:157;H:7?
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EHEC (enterohemorrhagic)
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practically, how are enteric E. coli infections diagnosed in farm animals? How are they treated?
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- they are diagnosed empircally by signalment (e.g. age) and clinical signs
- they are treated by supportive therapy such as electrolytes and fluids, and adequate nutrition. Antibiotic use is very controversial |
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If you really wanted to, how would you get a definitive diagnosis for an enteric E. coli disease?
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- collect a large amount of feces and send it for analysis
- FI Ab or ELISA for pili - ELISA for enterotoxins - Bioassays or DNA probes - Multiplex PCR for pili and enterotoxin genes |
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how is a non-enteric E. coli infection diagnosed?
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- collect a sample from a sterile site
- make sure that the E. coli you isolate is capable of producing the disease |
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how are non-enteric Enterobacteriaceae infections treated? which antibiotics would you use for empirical therapy? What are some ancillary therapies?
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- susceptibility testing must be performed because there is widespread resistance. Also, resistance plasmids (R factors) are readily transferred among members of this family.
- aminoglycosides, fluoroquinolones, third-generation cephalosporins, trimethoprim/sulfonamides - surgery/drainage/debridement, fluid therapy, anti-endotoxin therapies |
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what are the best ways to control Enterobacteriaceae infections?
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GOOD MANAGEMENT
- strengthen the host (colostrum) - decrease exposure (cleanliness) - vaccines available (e.g. anti-pili vaccines for cows and pigs) |
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comment on interpretation of the presence of Salmonella in a fecal culture of a patient with diarrhea.
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- it is not normal flora
- it can cause enteritis/dysentery - a positive culture suggestive of disease, but the animals may be shedders, so it is just SUGGESTIVE, not a definitive diagnosis |
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what is the most common species of Salmonella of veterinary importance. How are strains differentiated? What is this differentiation based upon?
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- Salmonella enterica ss enterica
- strains are differentiated by serovars - serovars are based upon O, H, and Vi antigens |
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what is is the pathogenesis of enteric Salmonellosis?
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- adhesion to M cells in the lower ileum and large intestine
- invade these cells ("ruffling") and multiply - bacteria released into the lamina propria - diarrhea caused by a number of virulence factors (enterotoxins, cytotoxins, endotoxin, inflammation) |
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what are the virulence factors of Salmonella?
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1. adhesion to M cells of the lower ileum and large intestine
2. intracellular survival and multiplication 3. enterotoxins 4. cytotoxins that cause enteric cell death 5. endotoxin 6. inflammation (causes release of prostaglandins and ↑cAMP) |
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what is the typical disease cause by a virulent enteric Salmonella infection?
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- hemorrhage and fibrin in intestinal exudate due to exo- and endotoxins
- hypersecretory component due to prostaglandin release - bloody, hypersecretory diarrhea |
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how do Salmonella induce a carrier state in an animal?
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- phagocytosed and live inside macrophages
- macrophages localize in lymph nodes and spleen - intermittent shedding in the feces - can last for weeks or years |
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why can a feco-oral transmission of Salmonella lead to septicemia and subsequent localization into non-GI organs?
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- Salmonella can live intracellularly inside macrophages
- when these infected macrophages become blood-borne, they can cause disease in other places such as joints, lungs, osteomyelitis, etc. |
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what are seven bacteria involved in canine bacterial cystitis?
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1. E. coli
2. Proteus 3. Klebsiella 4. Pseudomonas aerugnosa 5. Staphylococcus intermedius/pseudintermedius 6. Streptococcus canis 7. Enterococcus |
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for a bacterial cystitis infection, why would you only culture the bacteria aerobically?
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because anaerobes don't cause bacterial cystitis
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Klebsiella:
- sources - transmission - virulence factors |
- they are saprophytes and commensals in the GIT. They love wood shavings.
- they are transmitted by inoculation into sterile sites (e.g. inhaled, ascend into bladder) - VF: pili, capsule, hemolysin, endotoxin |
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name six diseases commonly associated with Klebsiella infection
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1. pneumonia (secondary)
2. CYSTITIS 3. mastitis 4. equine endometritis 5. navel ill/septicemia 6. nosocomial infections |
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why are Klebsiella associated with nosocomial infections?
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because they have broad antibiotic resistance
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how would you diagnose and treat a suspected Klebsiella infection?
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- isolate from a sterile site
- sensitivity testing (a/b resistance) - treat accordingly |
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what is a common Klebsiella species that causes cystitis in dogs?
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Klebsiella pneumoniae
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what is a common Proteus species that causes cystitis in dogs?
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Proteus mirabilis
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Proteus:
- sources - transmission - virulence factors |
- they are ubiquitous in the environment and transient in the GIT
- transmitted by inoculation into sterile sites (e.g. ascend into the bladder, invade external ear) - VF: pili, hemolysin, endotoxin, MOTILITY, UREASE |
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what are five diseases commonly associated with Proteus infection?
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1. cystitis
2. otitis externa 3. prostatitis 4. diarrhea 5. would infections |
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how would you diagnose and treat a suspected Proteus infection?
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- with care - may need repeated cultures
- not as resistant to antibiotics as other Enterobacteriaceae |
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a dog presents for bacterial cystitis. The lab results of a sterile cystocentesis come back with a significant count of Yersinia pestis. What do you do next?
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take another sample because Y. pestis does not cause bladder infections (you stuffed up!)
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Yersinia:
- sources - transmission - virulence factors (species differences) |
- come from intestinal tracts of many animals; Y. pestis comes from the flea-rodent-flea cycle.
- transmission is feco-oral; or with Y. pestis, flea bites, ingestion of fleas or infected animals, or contact with infected secretions - VF: facultative intracellular parasite (live and multiply in macrophages), endotoxin, motile (except Y. pestis), adhesins/invasins, capsule (Y. pestis) |
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what are three species of Yersinia of veterinary importance and what diseases do they cause (host species)?
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1. Y. pestis - plague (humans, cats, rarely dogs and other spp.)
2. Y. pseudotuberculosis - enteritis, sporadic abortion, septicemia (ruminants, birds, lab animals) 3. Y. enterocolitica - enteritis (humans, dogs, cats) |
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Plague (e.g. The Black Death)
- causative agent - species affected - in what three forms does this disease exist - where is this bug prevalent in the US? |
- Yersinia pestis
- humans, cats, and rarely dogs and other spp. - 3 forms: bubonic (lymph nodes), septicemic, pneumonic - in the Western states: AZ, NM, UT, CO, CA, OR |
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Yersinia
- diagnosis - clinical signs - definitive diagnosis |
- diagnose with care because it is zoonotic and Y. pestis is highly virulent
- clinical signs (in cats): fever, swollen lymph nodes, severe depression - for definitive Dx, send to specialized labs, where they can use bipolar staining |
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what is the fancy name for endotoxin?
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lipopolysaccharide (LPS)
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when is endotoxin released into the body?
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upon bacterial death or during proliferation/multiplication
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when does endotoxin cause the clinical syndrome of endotoxemia?
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when it is freely circulating in the blood
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what are the three structureal domains of endotoxin from outside to inside?
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1. polar polysaccharide (O-region; O-side chains)
2. Core acidic polysaccharide region 3. Lipid A region: there is a hydrophilic region and a hydrophobic region |
|
|
comment on the function of and immune response to the O-region of LPS
|
- these are sugars that project into the aqueous extracellular milieu
- high antigenic variability specific for each bacterial strain |
|
|
comment on the function of and the immune response to the Core acidic polysaccharide region of LPS
|
- connects the O-region to Lipid A
- low antigenic variability, so this is a good target for antibodies |
|
|
comment on the function of and effects of the hydrophilic and hydrophobic regions of Lipid A
|
hydrophilic: anchors LPS to the bacterial outer membrane and mediates most of the toxic effects of endotoxin
hydrophobic: highly conserved, but variation in number, length, saturation, and position confers degree of toxicity |
|
|
describe the six-step process leading to death/recovery from endotoxemia
|
1. physical barriers are breached
2. initial contact of LPS with blood 3. macrophage activation and dependent processes 4. neutrophil activation and dependent processes 5. clinically apparent circulatory insufficiency and organ damage 6. death or recovery |
|
|
Given that the average horse has over 2 grams of endotoxin in the cecum and ventral colon, and that it only takes 1 μg of endotoxin to kill a horse, why do we not see clinical signs of endotoxemia all of the time?
|
- because physical barriers must be breached (e.g. integument, mucosa, or lymphatics)
- intestinal mucosal cells and mucus are an efficient barrier - small amounts that make it past the mucosa are destryoed by liver Kupffer cells, so the Kupffer cells must be saturated to produce a reaction |
|
|
what are some examples of host compromise leading to endotoxemia?
|
1. bacterial enteritis (e.g. Salmonella)
2. bowel ischemia (e.g. torsion, infarcts) 3. bowel inflammation 4. trauma to the bowel 5. grain overload 6. pleuropneumonia 7. wound infections 8. placentitis/metritis 9. septicemia 10. omphalitis |
|
|
what are the two immunologic responses produced when the blood is initially exposed to LPS?
|
1. anti-LPS antibody - clears it out
2. binding to LPS-binding protein (LBP) - causes badness |
|
|
when endotoxin binds to LBP, what happens next in the process of septic shock?
|
- the LPS-LBS complex binds with CD14 receptors in macrophages
- macrophage signalling pathways are activated, and after about 30 minutes, the macrophages will be activated |
|
|
when macrophages have been activated by the LPS-LBP complex, what two things do the macrophages do?
|
1. production of thromboxane A2 and subsequent vasoconstriction and platelet aggregation
2. secretion of TNF-α, IL-1, and IL-6, leading to fever and an amplification of the inflammatory response |
|
|
after macrophages have released TNF-α and IL-1 into the bloodstream after binding with LPS-LBP complex, how does the inflammatory response change?
|
after about 1 hour, PMNs will be activated and will ahdere and marginate to endothelial cells
|
|
|
in endotoxemia, when PMNs have been activated by TNF-α and IL-1 to adhere and marginate to vascular endothelium, what would a CBC look like?
|
leukopenia
|
|
|
what happens to macrophages 24 hours after exposure to LPS-LBS complex? What would you see on a CBC?
|
they release cytokines such as GM-CSF and IL-8, which upregulate the production of circulating neutrophils. You would see leukocytosis in a CBC.
|
|
|
In an endotoxemia inflammatory response, what are the four main effects of PMN activation by macrophages?
|
1. ↑activates complement
2. ↑vascular permeabiliity and ↑damage to vascular endothelium 3. release of factors that induce platelet aggregation and adhesion 4. ↑nitric oxide, causing vasodilation |
|
|
in endotoxemia, what circulatory disturbances occur after widespread PMN activation?
|
1. vascular leakage - hypovolemic shock
2. coagulation and thromboembolism - DIC |
|
|
what are the three general methods to combat endotoxemia?
|
1. reduce movement into circulation
2. neutralize endotoxin 3. adjunctive therapies |
|
|
in the treatment of endotoxemia, what can be done to reduce movement of endotoxin into the circulation?
|
1. remove necrotic intestine
2. drain/debride local infections and treat with antibiotics |
|
|
in the treatment of endotoxemia, what is a common way to neutralize the effects of endotoxin using the immune system? How does this work?
|
- neutralizing antibodies
- they bind to the core region and/or to Lipid A to block interaction with macrophages |
|
|
what drugs can be administered to neutralize endotoxin? why is this problematic?
|
- polymyxin B - nephrotoxic
- synthetic peptides under development |
|
|
Pseudomonas:
- morphology - gram reaction - atmospheric requirements - oxidase reaction |
- gram negative rods
- obligate aerobe - oxidase positive |
|
|
what is an important way to distinguish a Pseudomonas infection from an E. coli infection?
|
Pseudomonas is oxidase positive, whereas E. coli is oxidase negative
|
|
|
what Pseudomonas species is of veterinary importance?
- sources - transmission - five virulence factors and their function |
- Pseudomonas aeruginosa
- sources: soil, water, found in feces, skin, mucus membranes of normal animals; can survive in "weird places" such as old disinfectants, soap, medical equipment (e.g. endoscope), "sterile" water for injection - transmitted secondary to compromised host tissues as an opportunistic pathogen VIRULENCE FACTORS 1. pili (adhesion; requires damage to epithelium) 2. endotoxins and hemolysins (A, S, and T; kills cells, especially phagocytes) 3. biofilm production (colonization, antibiotic resistance) 4. procyanins and fluoroscein - kills cells and damages tissues 5. Collagenase and elastase - breaks down collagen (e.g. melting ulcers) and damages BVs, skin, etc. |
|
|
what diseases are commonly found as a result of Pseudomonas aeruginosa infection in:
- dogs - horses - sheep - cows - farmed mink and chinchillas - snakes - all species |
- dogs - otitis externa, recurrent cystitis
- horses - chronic endometritis - sheep - "green wool" - cows - mastitis secondary to antibiotic therapy - farmed mink and chinchillas - abscesses, pneumonia/septicemia - snakes - necrotic stomatitis - all species - abscesses (ESPECIALLY CORNEAL), septicemia in severely compromised patients, wound infections (ESPECIALLY BURNS) |
|
|
what bacterial infection is of patricular concern in burn patients?
|
Pseudomonas aeruginosa
|
|
|
why is interpretation of isolation of Pseudomonas from an infection problematic?
|
because it is a poor pathogen that requires significant host compromise to cause disease.
|
|
|
how are Pseudomonas infections treated?
|
- they have widespread antimicrobial resistance
- MUST do susceptibility testing - resolve underlying host compromise (e.g. Sx/debridement, drying out, Dx underlying disease) |
|
|
why is Pseudomonas aeruginosa so good at infecting burn wounds
|
- significant host compromise is present
- they thrive in most envornments - they have widespread resistance to antimicrobials |
|
|
list five bacteria that may be involved in superinfections?
|
1. Pseudomonas aeruginosa
2. Enterococcus spp. 3. Nocardia spp. 4. Klebsiella pneumoniae 5. Bacillus cereus |
|
|
what is a superinfection and what causes them?
|
An extremely difficult-to-treat infection of weakly pathogenic, but highly resistant bacteria (can be mixed infections), usually caused secondarily to treatment of an underlying disease or predisposing factor with antibiotics without addressing the underlying host compromise. This will disrupt the normal flora and the underlying host compromise will allow for these infections to persist.
|
|
|
how are Pseudomonas infections controlled?
|
- they are not because they are caused by a variety of different factors related to host compromise.
- correctly Dx disease, get rid of underlying conditions, to prevent superinfections |
|
|
why can the use of "broad spectrum" antibiotics in the treatment of infections such as mastitis, without treating the underlying condition worsen the condition?
|
because highly resistant, opportunistic pathogens such as Pseudomonas aeruginosa can lead to superinfections.
|
|
|
Pasteurella:
- gram reaction and morphology - oxidase reaction - common species of veterinary importance |
- gram negative coccobacilli
- oxidase positive - Pasturella multocida |
|
|
Mannheimia:
- gram reaction and morphology - oxidase reaction - common species of veterinary importance |
- gram negative coccobacilli
- oxidase positive - Mannheimia haemolytica |
|
|
Name ten diseases (and host species) are associated with infection of Pasteurella multocida?
|
1. hemorrhagic septicemia (ruminants)
2. Shipping Fever (bronchopneumonia) (ruminants) 3. mastitis (cattle and sheep) 4. Fowl cholera (poultry) 5. atrophic rhinits (swine) 6. pneumonia (swine, rabbits) 7. snuffles (rabbits) 8. septicemia (rabbits) 9. local infections; bite wound infections (cats, dogs, humans) 10. respiratory infection (dogs and cats) |
|
|
where is the most common site of Pasteurella and Mannheimia infections?
|
respiratory tract
|
|
|
Pasteurella multocida:
- sources - transmission |
- normal flora of the URT of many mammals; in birds, it is not normal flora
- transmission are usually endogenous, following stressful events such as shipping or secondary infection |
|
|
Hemorrhagic Septicemia
- causative agent - hosts - clinical signs |
- Pasteurella multocida
- ruminants - blood in cavities, enteritis, edema, septicemia, pneumonia |
|
|
Fowl Cholera
- causative agent - hosts - clinical signs |
- Pasteurella multocida
- chickens, turkeys, ducks, geese - overwhelming bacteremia/septicemia, depression, inappetence, diarrhea, swollen wattles, cellulitis, pleuropneumonia, air sacculitis, "swollen head syndrome" - chronic infection of air sacs and mucus membranes (colds) RECALL: P. multocida is not normal flora in birds |
|
|
Atrophic Rhinitis
- causative agent - host - clinical signs |
- Pasturella multocida in combination with Bordatella bronchiseptica
- swine - atrophy and deviation of the snout, destruction of nasal turbinate bones, bloody and serous nasal discharge |
|
|
Snuffles
- causative agent - host - clinical signs |
- Pasturella multocida
- rabbits - mucopurulent discharge of the external nares and conjunctiva, pneumonia, fever, respiratory distress, ear infection, septicemia |
|
|
what are some compromising factors that allow opportunity for Pasteurella multocida infection?
|
- stress (e.g. shipping)
- viral or mycoplasma infection - bite wounds - inclement weather - wounds RECALL: mostly endogenous infections in mammals; pathogenic in birds |
|
|
Pasturella multocida: virulence factors and their function
|
- capsule made of hyaluronic acid - antiphagocytic
- endotoxin - pili - adherence - siderophores - iron acquisition - dermonecrotoxin (in some strains) - hyaluronidase - aids dissemination out of capsule - neuraminidase - aids colonization |
|
|
how is Pasteurella infection diagnosed and treated?
|
- sterile sampling technique - abscess material, tracheal wash, blood
- ID and treat with antibiotics such as penicillin, tetracyclines, sulfonamides |
|
|
Mannheimia haemolytica:
- species affected - specific diseases |
- ruminants
- shipping fever, pneumonia, septicemia, mastitis in sheep (bluebag) |
|
|
Mannhemia haemolytica virulence factors and their function
|
- capsule - antiphagocytic
- endotoxin - RTX leukotoxin - specific for lysing bovine WBCs |
|
|
Francisella:
- gram stain and morphology - atmospheric requirements - oxidase reaction - bacterial species of veterinary importance - most common hosts |
- gram negative coccobacilli
- obligate aerobe - oxidase positive - Francisella tularensis - cats, sheep, wildlife (arthropod vector); affects lagomorph, possums, beavers |
|
|
what is the causative agent of the human disease Rabbit Fever?
|
Francisella tularensis
|
|
|
why is Francisella tularensis a health concern for humans?
|
Because it is zoonotic and can be used as a bioterrorism agent
|
|
|
Francisella tularensis virulence factors
|
- facultative intracellular pathogen
- capsule - LPS (not an endotoxin) |
|
|
what is the general relationship between the the ability of a pathogen to cause disease, with regards to numbers, virulence, and host resistance (in equation format)
|
Disease = (number x virulence) / resistance of host
|
|
|
what type of immune response is needed to clear a Francisella tularensis infection? Why?
|
A Th-1 type response because it is an intracellular pathogen
|
|
|
what is the general disease caused by Francisella tularensis? what type of immunity fights these infections?
|
- tularemia
- CMI |
|
|
what lesions do Fransicella tulermia produce in humans?
|
- granuloma tumors
|
|
|
Actinobacillus
- gram stain and morphology - atmospheric requirements - where are they found? |
- gram-negative coccobacilli
- facultative anaerobes - obligate parasite of mucosal surfaces, especially the oral cavity |
|
|
name four Actinobacillus species of veterinary importance and the species they infect
|
1. A. lignieresii - ruminants, pigs, humans, others
2. A. pleuropneumoniae - pigs 3. A. suis - pigs, horses (rare) 4. A. equuli - horses, pigs, others (rare) |
|
|
which species of Actinobacillus is absolutely specific for pigs?
|
A. pleuropneumoniae
|
|
|
what specific diseases are caused by Actinobacillus lignieresii?
|
1. wooden tongue
2. granuloma tumors |
|
|
what disease is caused by Actinobacillus pleuropneumoniae? Species affected?
|
pleuropneumonia in pigs
|
|
|
which bacteria causes "wooden tongue"?
|
Actinobacillus lignierseii
|
|
|
what diseases are caused by Actinobacillus suis? Comment on the age of the pigs in these diseases
|
1. septicemia (piglets 1-8 wk)
2. systemic lesions - petechiae and edema (piglets 1-8 wk) 3. pneumonia (older pigs) |
|
|
What diseases are caused by Actinobacillus equuli?
|
1. septicemia ("sleepy foal disease")
2. abortion (adult horses) 3. endocarditis (adult horses) 4. pneumonia (adult horses) 5. bite wounds (humans) |
|
|
what disease is caused by Avibacterium paragallinarum?
|
Coryza (acute rhinits) of birds
|
|
|
how and why does Actinobacillus cause Wooden Tongue? What are complications associated with this disease?
|
trauma, such as rough silage, may perforate the tongue, allowing an opportunistic infection. When the lesions on the tongue ulcerate, they may spread to internal organs and the skin.
|
|
|
Actinobacillus lignieresii virulence factors. Immune response
|
- LPS
- endotoxin (RTX toxin) - dissemination - immune response: CMI |
|
|
Actinobacillus pleuropneumoniae virulence factors. Immune response
|
- toxins (RTX toxins)
- LPS - capsule - immune response is antibodies to RTX toxins, capsule, and somatic antigens |
|
|
Actinobacillus suis virulence factors. Immune response
|
- toxins (RTX toxin)
- LPS - immune response is antibodies |
|
|
Actinobacillus equuli virulence factors. Immune response
|
- toxins (RTX)
- LPS - immune response is antibodies |
|
|
Actinobacillus gallinarum virulence factors. Immune response
|
- toxins
- LPS - immune response is antibodies |
|
|
what makes pigs most susceptible to Actinobacillus pleuropneumoniae? How is this controlled?
|
- stress such as overcrowding, previous infection
- closed herds (all-in all-out) is a good way to control this disease |
|
|
in general, what does RTX toxin do? Comment on species differences.
|
lyses blood cells. RTX toxin is highly specific to its host.
|
|
|
Actinobacillus equuli:
- where in the body are they found primarily? - who is the most important host of an infection with this bacteria? |
- resides primary in the tonsils and reproductive tract of horses
- most important infection is in foals |
|
|
how do foals acquire "sleepy foal disease?" What organism causes this disease? Prognosis?
|
- acquired in utero or at birth
- Actinobacillus equuli - grave prognosis |
|
|
what vaccines exist for Actinobacillus? What is the best?
|
- live attenuated is the best, but not available
- bacterins (inadequate because antibodies to capsule are serotype-specific) |
|
|
how would you treat Actinobacillus infections with antimicrobials?
|
- A. lignieresii is not treated with antibiotics; it is treated with sodium iodide
- susceptibility testing needed - ampicillin, cephalosporins, tetracycline, aminoglycosides |
|
|
Haemophilus:
- gram stain and morphology - atmospheric requirements - oxidase test - where are they found? |
- gram-negative coccobacilli
- facultative anaerobe - oxidase positive - obligate parasite of mucosal surfaces |
|
|
name the Haemophilus species of veterinary importance and the host species they commonly infect
|
H. parasuis: pigs
|
|
|
what diseases are caused by Haemophilus parasuis and in which species do they occur?
|
(all pigs)
- Glasser's disease (polyserositis) - pneumonia |
|
|
what diseases are associated with Haemophilus somni infection?
|
1. pneumonia
2. TME (thrombotic meningoencephalitis) 3. arthritis 4. abortion 5. myocarditis 6. septicemia |
|
|
which two bacterial genera used to be classified under Haemophilus, but are now in different genera?
|
1. Avibacterium
2. Histophilus |
|
|
what causes Fowl Coryza? What are their preferred hosts? What are clinical signs of this disease?
|
- Avibacterium paragallinarium
- chickens are primary host - inflammation of turbinates, sinus epithelium, and air sacs |
|
|
Avibacterium paragallinarium major virulence factors. Host immune response?
|
- capsule
- LOS (lipooligosaccharide) - Antibody mediated immunity |
|
|
what are come compromizing factors that may predispose chickens to fowl coryza due to Avibacterium paragallanarium infection?
|
- viral or mycoplasma infection
- stress of being in a commercial environment - not seen in backyard farms or pet chickens |
|
|
what is LOS in bacteria? Which three bacterial genera of veterinary importance have it?
|
- lipooligosaccharide - endotoxin similar to LPS, but lower molecular weight O-region
- Avibacterium, Histophilus, and Moraxella |
|
|
what type of vaccinations are most effective against Avibacterium paragallinarium?
|
bacterins
|
|
|
Glasser's disease:
- scientific name of this disease - causative agent - who gets this disease? - clinical signs |
- polyserositis
- Haemophilus parasuis - young pigs mostly get this disease - fibrinous inflammation of serous surfaces such as pleura, joints, PERICARDIUM; cyanosis, especially in the ears, where they can turn purple and fall off |
|
|
Haemophilus parasuis major virulence factors. Type of immunity to infections?
|
1. capsule
2. LOS - antibody mediated immunity |
|
|
Haemophilus somni major virulence factors. What type of immunity to infections?
|
1. LOS
2. Immunoglobulin binding protein 3. biofilm 4. INTRACELLULAR SURVIVAL - antibody mediated immunity and CMI |
|
|
name two species of Bordatella of veterinary importance and the hosts they infect
|
1. B. bronchiseptica - dogs, cats, pigs, humans, others
2. B. avium - birds |
|
|
Bordatella bronchiseptica virulence factors. What type of immunity to infections?
|
1. pili
2. hemaglutinin 3. toxins 4. LPS 5. flagella (motility) - antibody mediated immunity |
|
|
Bordatella avium virulence factors. Immune response by the host?
|
1. pili
2. hemaglutinin 3. toxins 4. LPS 5. flagella (motility) - antibody mediated immunity |
|
|
what is the causative agent of bovine pinkeye?
|
Moraxella bovis
|
|
|
Moraxella bovis virulence factors. Common disease? Immune response by the host?
|
1. pili
2. hemolysin 3. toxins 4. capsule 5. LOS - causes bovine pinkeye - antibody mediated immunity |
|
|
what species do Histophilus somni specifically infect? Why are they so host-specific?
|
bovines and sheep. They are host specific because the bacterial transferrin used to acquire iron from the host is host-specific
|
|
|
Histophilus somni:
- where are they found? - how do they cause disease? - compromising factors |
- normal flora of the genital and respiratory tracts
- they cause disease by becoming bacteremic; stress and viral infection are required - STRESS, viral infection, previous infection, infection with a particularly virulent strain |
|
|
what is special about Histophilus somni toxins? How does this affect immunity and vaccination?
|
- there is a phase variation in the IgG binding proteins on the cytotoxin
- this is a method to evade the immune system and there are no effective vaccinations yet |
|
|
Name the Histophilus species of veterinary importance and the hosts they commonly infect
|
H. somni: cattle and sheep ONLY
|
|
|
Bordatella:
- gram stain and morphology - oxidase reaction - atmospheric requirements - where is it found? - how it is it transmitted? |
- gram-negative coccobacilli
- oxidase positive - obligate aerobe - obligate parasite of the URT of mammals - transmitted by aerosol |
|
|
what specific diseases does Bordatella bronchiseptica cause and what are the host species for these diseases?
|
1. Kennel cough (tracheobronchitis) - dogs
2. pneumonia - dogs, young pigs, cats 3. atrophic rhinitis - pigs (occurs synergistically with Pasteurella multocida) 4. systemic infections - humans |
|
|
what two bacteria are involved in swine atrophic rhinitis?
|
1. Bordatella bronchiseptica
2. Pasteurella multocida |
|
|
how does Bordatella bronchiseptica cause tracheobronchitis?
|
- bacteria attach to cilia of the respiratory tract
- toxins kill the ciliated cells - these cells detach and accumulate with mucus to cause a chronic cough |
|
|
what are some compromising factors that may predispose a dog to kennel cough?
|
- being in a kennel (duh)
- viral infection such as distemper or parainfluenza - inclement weather |
|
|
what are the most effective vaccinations for Bordatella bronchiseptica? why?
|
- live attenuated intranasal vaccines are most effective
- this is because the vaccine stimulates IgA mucosal immunity |
|
|
how is Bordatella bronchiseptica treated with antibiotics?
|
- mild cases not usually treated
- tetracyclines, erythromycin; also aminoglycosides, sulfa drugs |
|
|
what disease is caused by Bordatella avium?
|
Turkey coryza
|
|
|
Turkey coryza
- causative agent - transmission - pathogenesis - clinical signs |
- Brodatella avium
- highly contagious; transmitted by dust - destroys the ciliated epithelium - mucus accumulation, coughing, conjunctivitis, facial and wattle swelling, eyelids swollen closed, nasal discharge, rales |
|
|
Turkey coryza
- causative agent - clinical signs |
- Bordatella avium
- inflammation → mucus accumulation - conjunctivitis, facial and wattle swelling, eyelids swollen closed, nasal discharge, rales |
|
|
what are the two major types of immunity that protect birds from Turkey coryza (Bordatella avium)?
|
- mucosal IgA to prevent colonization
- antibodies against toxins |
|
|
what type of vaccines are given to protect against Bordatella avium?
|
- live, attenuated are the best
- bacterins are protective against disease |
|
|
what is the fancy name for bovine pinkeye? what is the causative agent? clinical signs? epidemiology?
|
- infectious bovine keratoconjuctivitis (IBK)
- Moraxella bovis - conjuctivitis, keratitis, corneal ulceration - usually affects > 5% of the herd |
|
|
Moraxella bovis
- common disease - where is it found? - how is it transmitted? - what is required for the bacteria to cause disease? - predisposing factors |
- bovine pinkeye (infectious bovine keratoconjuctivitis; IBK)
- normal flora of the URT - transmitted by fomites or dust - attachment and colonization required for infection - predisposing factors: flies, sunlight, breed, irritation, prior infection |
|
|
which type of cattle are most susceptible to infectious bovine keratoconjuctivitis?
|
those with "hooded" eyelids
|
|
|
comment on the immunity to Moraxella bovis
|
(bovine pinkeye)
- Ig to pili, but strain specific - IgA highest in lacrimal secretions, but may not prevent dz - Ig to toxins may reduce or prevent dz |
|
|
comment on vaccinations for Moraxella bovis?
|
(bovine pinkeye)
- only vaccinate of herd outbreak - use strain isolated from herd - only bacterins are available - may take up to 4 weeks to work |
|
|
what are some preventative measures to be taken to manage bovine pinkeye
|
(Moraxella bovis)
- fly control - good animal management |
|
|
how is bovine pinkeye treated?
|
- obtain susceptibility test
- M. bovis is susceptible to a wide range of drugs |
|
|
how is Actinobacillus lignieresii most commonly treated?
|
with sodium or potassium iodide IV or in local lesions (unless going to slaughter)
|
|
|
Brucella:
- gram stain and morphology - atmospheric requirements - oxidase reaction - motility |
- gram negative coccobacilli
- obligate aerobes - oxidase positive - immotile |
|
|
Brucella virulence factors. Host immunity?
|
- INTRACELLULAR PATHOGEN
- LPS - proteins (heat shock proteins, porins, SOD) - host immunity: CMI |
|
|
Name four Brucella species of veterinary importance and their principal hosts (and other hosts)
|
1. B. abortus - horse, cattle (pig, dog, sheep, goat)
2. B. suis - pig, cattle (horse, dog) 3. B. canis - dog 4. B. melitensis - sheep, goat (dog, cattle) ALL ARE ZOONOTIC |
|
|
why is Brucella melitensis zoonosis a major concern?
|
because it can be used as a bioterrorism agent
|
|
|
comment on the severity of disease caused by Brucella LPS
|
Brucells LPS is not an endotoxin
|
|
|
Brucella
- sources - transmission |
- reservoir animals, carriers, newly-infected animals
- ingestion (placenta, uterine fluids, milk (and cheese), urine); exposure of infected mucous membranes; venereal; congenital |
|
|
what is the pathogenesis of disease caused by Brucella abortus infection?
|
1. bacteria penetrate mucous membranes
2. they localize in regional lymph nodes 3. become intracellular by phagocytosis 4. bacteremia 5. dissemination to udder, uterus, and reticuloendotheilal system, genital tract of males 6. proliferate best in sites with erythritol, i.e. the placenta 7. necrosis of placenta; edematous fetus |
|
|
comment on the immune response to Brucella abortus. What do lesions look like?
|
- Ig immunity is ineffective; in fact, they may help the bacteria become intracellular
- CMI is the most effective response - granulomatous lesions |
|
|
comment on vaccination for Brucella abortus
|
- attenuated, live strain (CMI)
- normal vaccination protocol - can use to interrupt outbreaks |
|
|
Brucella abortus control and treatment measures
|
- test and slaughter
- test market cattle - vaccinate - hygiene - treatment not indicated for food animals; cull |
|
|
how is Brucella canis transmitted?
|
- ingestion
- venereal |
|
|
what are the clinical signs of Brucella canis disease in bitches? Dogs?
|
BITCHES
- abortion in last trimester - lymphadenitis and splenitis - infertility - sick or stillborn puppies DOGS - epididymitis - scrotal dermatitis - (unilateral) testicular atrophy |
|
|
what are the two ways in which Brucella canis outbreaks are controlled in canines?
|
1. euthanasia (test and cull)
2. neuter and long-term antibiotic therapy |
|
|
what is the most virulent species of Brucella for humans?
|
B. melitensis
|
|
|
what is the common site of cilinical signs in males with Brucella infection?
|
scrotum, epididymis, testes
|
|
|
besides abortion and infection of the balls (in males), what other clinical signs are associated with Brucella suis infection?
|
metritis, spondylitis, lameness, and paralysis
|
|
|
which two antibiotics are most commonly used in humans with Brucella infection?
|
tetracyclines, gentamycin
|
|
|
what are the three Camphylobacter species of veterinary importance and the hosts they infect?
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1. C. jejuni - calves, sheep, dogs, foals, humans
2. C. fetus venerealis - cattle 3. C. fetus fetus - sheep, cattle |
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which Camphylobacter species of veterinary importance has motility?
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C. jejuni
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Camphylobacter jejuni virulence factors. Host immunity?
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1. LPS
2. toxins 3. motility 4. adhesins 5. proteins - antibody mediated immunity |
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Camphylobacter fetus ss venerealis & fetus virulence factors. Host immunity?
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1. slime layer
2. LPS 3. adhesins - antibody mediated immunity |
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Camphylobacter:
- gram stain and morphology - oxidase test - atmospheric requirements |
- gram negative curved rods
- oxidase positive - microaerophilic |
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Camphylobacter jejuni
- sources - transmission - infectivity |
- flora of intestinal tracts of domestic and wild animals
- oral transmission - highly infectious |
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what specific diseases are associated with Camphylobacter jejuni infection and in what species do they occur?
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1. Enteritis (bloody diarrhea) - calves, sheep, dogs, cats, foals, humans
2. bovine mastitis 3. abortions in sheep 4. infectious hepatitis in chickens |
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what is the pathogenesis of diesase caused by Camphylobacter jejuni infection?
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- bacteria penetrate the intestinal mucosa and infect the enterocytes
- attachment - motility allows them to bore through tissues - INTRACELLULAR PATHOGEN in phagocytes |
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what is the most common way in which Camphylobacter fetus ss venerealis is transmitted? who are the carriers?
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- venereal transmission
- young bulls are transient carriers - older bulls may be permanent carriers |
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how does Camphylobacter fetus ss venerealis cause disease?
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- transmitted venereally from infected bulls
- colonize and ascend up the female repro tract - can cause placentitis and metritis, leading to abortion |
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comment on Camphylobacter fetus ss venerealis vaccination and control
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- vaccination is effective for therapy and prophylaxis
- AI is preventative measure |
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why does Camphylobacter fetus ss fetus cause such a high abortion rate in sheep?
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because it is an enzootic (endemic) infection
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how is Camphylobacter fetus ss fetus transmitted?
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ingestion, NOT VENEREAL
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what types of lesions are caused by Camphylobacter fetus ss fetus infection
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- placental edema
- systemic fetal changes - mid to late term abortion |
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which Camphylobacter species are most virulent in humans? What type of infections occur?
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- C. jejuni - severe enteritis
- C. fetus ss fetus - causes severe systemic infections |
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how are Camphlyobacter infections treated and controlled?
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- antimicrobials are usually not used in food animals
- supportive care for enteritis - AI - remove aborted materials - cull carrier bulls - bacterins eliminate bull carrier stare for C. fetus ss venerealis |
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Helicobacter
- gram stain and morphology - host species - common diseases |
- gram negative curved rods
- dogs, cats, pigs, humans, rodents (i.e. the monogastrics) - enteritis, ulcers, hepatitis |
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how are Helicobacter infections treated?
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- bismuth subsalicycylate and antibiotics
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Arcobacter
- gram stain and morphology - atmospheric requirements - species infected - common diseases |
- gram negative curved rods
- microaerophilic (aerotolerant) - infect livestock and dogs - cause enteritis, late-term abortions, and low-grade mastitis |
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Lawsonia intracellularis
- gram stain and morphology - common hosts - common disease - major virulence factor |
- gram negative rods
- infect pigs and hamsters - cause proliferative enteritis - intracelluar pathogens |
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Leptospira:
- gram stain and morphology - atmospheric requirements |
- gram-negative sprirochetes with hooks on the ends
- strict aerobe |
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Leptospira
- sources - transmission |
- reservoir in renal tubules (asymptomatic); after excretion: freshwater, soil, mud
- bacteria enter the host through a wound or through the mucous membrane, especially from exposure to CONTAMINATED URINE. Transplacental; milk; semen |
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Leptospira virulence factors. Host immunity?
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1. LPS
2. sphingomyelinase (a hemolysin) 3. toxins 4. motility - antibody mediated immunity |
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what are six diseases of vertebrates associated with Leptospira infection?
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1. abortion
2. infertility 3. febrile jaundice 4. agalactia 5. hemoglobinuria 6. premature birth |
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which domestic species are particularly susceptible to Leptospira infections?
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- horses
- cattle - dogs - pigs - rodents |
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Leptospirosis in dogs:
- three forms of the disease - diseases |
- hemorrhagic, icteric, uremic
- kidney failure, severe liver disease |
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what is the general pathogenesis of Leptospirosis?
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1. bacteria enter through a wound or mucous membranes
2. enter the bloodstream 3. replicate in the liver 4. migration to other organs such as repro tract, lungs, KIDNEY, brain, eye 5. cause vasculitis in small vessels, hemorrhage, and fluid leakage through toxins or cytokines 6. can induce a carrier state in the renal tubules |
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how does Leptospirosis cause jaundice?
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bile duct occlusion
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how is Leptospirosis controlled and treated?
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- need to know local serovars
- vaccination: q 6 mos in swine, q 12 mos in dogs and cats - bacterin and a/b's are effective in outbreaks - PREVENT EXPOSURE |
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In which what organ systems do Leptospira commonly cause disease in
- dogs? - bovines? - pigs? - horses? |
- dogs: kidney, liver
- bovines, pigs, horses: uterus/placenta (abortion), kidney, liver |
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why is Leptospirosis a public health concern?
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it is zoonotic, especially to children, and people can be infected by swimming in contaminated waters
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what are the four spirochete genera of veterinary importance in Family Spirochetales?
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1. Treponema
2. Borrelia 3. Brachyspira 4. Leptospira |
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Treponema
- gram stain and morphology - common host species - atmospheric requirements |
- gram-negative spirochetes
- cattle, sheep, rabbits - anaerobes |
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What diseases are associated with Treponema infection in
- Cattle? - Sheep? - Rabbits? |
- cattle: bovine papillomatous digital dermatitis (heel warts or hairy footwarts)
- Sheep: Ovine footrot (contagious ovine digital dermatitis) - Rabbits: syphillis |
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what causes heel warts in dairy cows? What do the lesions look like?
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- Treponema
- moist, painful, strawberry-like lesions in the skin or chronic wart-like raised lesions - ulceration of the skin on the heel results in lamemess |
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Borrelia burgdorferi
- gram stain and morphology - atmospheric requirements - major vector - major reservoir |
- gram negative spirochetes
- aerobic - vector: Ixodes ticks - reservoir: small rodents |
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Borrelia burgdorferi:
- main species affected - virulence factors - Host immune response |
- humans, dogs, horses, cattle
- LPS, motility, proteins (phase variation of surface antigens) - antibody mediated immunity |
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Infection with Borrelia burgdorferi is associated with which diseases/clinical signs in
- humans? - dogs? - horses? - cattle? |
- humans: Lyme disease
- dogs: Lyme disease: fever, swollen lymph nodes, front-leg lameness with infectious arthritis, CNS, myocarditis - horses: muscle soreness, lameness, uveitis, arthritis, encephalitis, in utero infections → abortion or sick foals - cattle: lameness, fever, loss of appetite, in utero → abortion |
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what is the basic pathogenesis of Lyme disease?
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1. tick bite and infection
2. LPS inflammatory response 3. IL-1: rever, rash, arthopathy, antibody synthesis (this may halt infection) 4. infection can continue and continued inflammation and/or autoimmune responses will ensue |
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what drug is used to treat Lyme disease?
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doxycycline
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how does hemolysis relate to Moraxella infections?
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non-hemolytic strains do not cause disease
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which antibiotics are used to treat Brucella infections?
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tetracycline combined with streptomycin or gentamicin
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Brachyspira:
- gram stain and morphology - atmospheric requirements - two species of veterinary importance |
- gram negative spirochetes
- obligate anaerobes - B. hyodysenteriae and B. pilosicoli |
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Brachyspira hyodysenteriae:
- susceptible species - disease - virulence factors |
- pigs
- swine dysentery: diarrhea with mucus and blood - hemolysin, invades goblet cells, flagella |
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Brachyspira pilosicoli:
- susceptible species - disease |
- pigs
- intestinal spirochetosis: mucoid diarrhea |
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what bacteria causes acute and chronic swine dysentery? What is the pathogenesis of the disease?
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- Brachyspira hyodysenteriae
- infection of the intestinal mucosa - proliferation in the crypts and invasion of the GOBLET CELLS - excessive production of mucus - leukocyte infiltration - explosive, projectile, garden hose-variety, bloody diarrhea due to edema and in later stage infections, ulcerative necrotizing colitis |
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how do spirochetes divide?
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transverse binary fission
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name seven bacteria genera/types capable of causing pleuritis
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1. enterobacteriaceae (e.g. E. coli, Klebsiella, Proteus, Enterobacter)
2. Pasturella spp. 3. Actinomyces 4. Nocardia 5. Streptococci 6. Staphylococci 7. NSF mixed infection |
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what is SIRS?
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Systemic Inflammatory Response Syndrome - similar to endotoxemia
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what is MOD?
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multiple organ dysfunction
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NSF bacteria:
- gram stain and morphology - atmospheric requirements - requirements to grow |
- a mix of G+ and G- bacteria of many species
- obligate anaerobes (with varying degrees of aerotolerance) - requires low oxygen tension, a low redox potential, sometimes a low pH (e.g. necrotic tissue) |
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on a bacterial smear, what is a morphological clue that you may be dealing with an NSF infection?
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fusiform rods
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NSF bacteria
- sources - benign function in the body - how they become pathogenic |
- normal flora of skin; mucous membranes of the URT, GI, urogential tract
- they are the "bouncers", limiting the growth of other bacteria - they can cause disease by overgrowing or being inoculated into sterile sites (opportunistic infections) |
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what are some predisposing factors that allow normally benign NSF bacteria to become pathogenic?
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- decreased immunity (e.g. dz, chemotherapy)
- prior use of a/b (esp. narrow spectrum aerobic) - inoculation (e.g. trauma, aspiration into lungs) - prior infection that caused tissue damage |
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where and what type of tissue compromise is required for NSF to cause disease?
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- near sites where they are normal flora
- need necrotic tissue because they are anaerobes |
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NSF bacteria virulence factors
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- oxygen tolerance
- enzymes (e.g. proteases) - endotoxin - capsule - synergy between microbes (they work as a team) |
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what are three common clinical presentations of a lesion that might cause you to suspect an NSF infection?
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- foul smell
- production of gas - black discoloration at the site |
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name common diseases associated with NSF infection
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- cat fight abscess
- periodontal disease → tooth root abscess - pleuropneumonia - pyothroax - pyometra - osteomyelitis secondary to fracture - ovine footrot - otitis externa - cystitis - superficial pyoderma - endometritis (horses) |
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how are NSF infections treated?
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- drainage/debridement
- copious lavage - +/- empirical antibiotics (don't use animoglycosides or quinolones becuase they are not effective against anaerobes) - nursing support |
