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FD6 > FD6 PBL > Flashcards

FD6 PBL Flashcards

1
Q

Describe the properties of Listeria monocytogenes

A
  • small
  • motile
  • gram +ve
  • nonsporeforming
  • extremely resistant
  • diphtheroid coccobacillus
  • grows under a wide temp range (4-44 degrees)
  • Ubiquitous saprophyte- lives in plant soil enviro
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2
Q

Why is its ability to grow at 4 degrees important?

A
  • important diagnostic aid
    • cold enrichment method - isolation of the organism from brain tissue but not from placental or fetal tissues
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3
Q

What are the natural reservoirs of L.monocytogenes?

A
  • soil
  • mammalian GI tracts
    • both contaminate vegetation
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4
Q

How does animal-animal transmission of Listeria occur?

A
  • via fecal-oral route
  • through abrasions in the buccal cavity (dry pasture)
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5
Q

When is Listeria most prominent?

A
  • primarily a winter-spring disease of feedlot/ housed ruminants
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6
Q

When do outbreaks of Listeria normally occur after feeding poor-quality silage

A
  • over 10 days after
  • (4-6 weeks)
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7
Q

Which animals to L.monocytogenes affect?

A
  • sheep
  • cattle
  • humans
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8
Q

What is the incubation period of Listeria?

A
  • 3-70 days
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9
Q

What is this? and why

A
  • Listeria
  • small, gram +ve rods
  • sometimes arranged in short chains
  • can be mistaken for strepococci
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10
Q

Which temp is lethal to L.monocytogenes?

A

50 degrees

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11
Q

What pH range will Listeria grow in?

A
  • pH 4-9.6
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12
Q

Does Listeria grow better in aerobic or anaerobic conditions?

A
  • anaerobic
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13
Q

What is the relationship between silage and Listeria?

A
  • listeria can survive up to 3 months in livestock manure
    • silage may become a source of infection if soil containing Listeria is included
  • improperly prepared silage (pH >5.4), prelonged, slow exposure to air (secondary fermentation)- allows organism to multiply
  • high levels of iron
  • poorly stored silage can be contaminated with vermin
  • close grazing with soil ingestion also can be a cause
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14
Q

What is the best way to prevent silage becoming a source of Listeria infection?

A
  • well compacted silage
  • cover immediatley after harvest
  • well wrapped
  • produce intensively fermented silages and store for over 30 days
  • acid additive to wet silages
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15
Q

Why are the advantages of feeding silage?

A
  • faster forage preserving methods
  • high quality
  • lower loss when harvesting, storing and feeding
  • inexpensive to store
  • wide seasonal harvesting window
  • doesnt need to be fed fresh
  • cheaper
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16
Q

How does Listeria reach the brain?

A
  • L.monocytogenes travel by way of circulating blood,
  • enters nerve fibres, primarily trigeminal nerve/ facial nerve and is transported to the brain stem
  • the nuclei 5th and 7th are in the caudal brain stem
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17
Q

What can Listeria cause in general?

A
  • septicemia
  • abortion
  • latent infection
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18
Q

What are the clinical signs in animals with Listeria?

A
  • initially:
    • anorectic
    • depressed
    • dioriented
    • propel themselves into corners
    • lean against walls
    • circling toward affected side
    • facial paralysis, drooping ear
    • deviated muzzle
    • flaccid lip
    • lack of menace response
    • continous salivation
    • paralysis of masticatory muscle
  • terminally affected animals:
    • recumbancy and death
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19
Q

What is the recovery rate in goats/ sheep?

A
  • 30% with prompt, aggressive therapy
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20
Q

Recovery rate of Listeria in cattle?

A
  • 50%
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21
Q

When do Listeric abortions occur?

A
  • last trimester without premonitory signs
  • fetuses normally die in utero
  • rate may reach 20% in flocks
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22
Q

How long can Listeria be shed in milk/ via vagina?

A
  • > 1 month
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23
Q

Where do Listeria infections acquired via ingestion tend to localize?

A
  • in intestinal wall
  • results in prolonged fecal excretion
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24
Q

Describe the virulence and infectivity of Listeria

A
  • L.monocytogenes ingested
  • may survive the stomach enviro and enter intestine where it penetrates the intestinal ep cells
  • the organism is taken up by macrophages and non-phagocytic cells
    • L.monocytogenes surface protein interalin required for the uptake by non-phagocytic cells (binds to receptors on host cells)
  • bacterium initially located in vacuole after uptake
  • L.monocytogenes secrete listeriolysin O protein (breaks down vacuole wall and enables bacteria to escape into cytoplasm)
  • L.monocytogenes replicate in cytoplasm
  • then transported around the body by blood, most being inactivated with reaching liver/ spleen
  • L.monocytogenes able to utilise actin molecules of the host to propel the bacteria into neighbouring host cells
  • cross blood-brain barrier and placental barrier
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25
Q

In listeric encephalitis, where are microcropic lesions confined to?

A
  • pons
  • medulla oblongata
  • anterior spinal cord
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26
Q

What lesions would be found in an animal with septicemic listeriosis?

A
  • small necrotic foci in any organ, esp liver
  • haemorrhagic gastroenteritis
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27
Q

What could be seen in aborted fetuses? (Listeria)

A
  • slight to marked autolysis
  • clear to blood-tinged fluid in the serous cavities
  • numeroud small necrotic foci in the liver (esp right half)
  • necrotic foci may be found in lungs/spleen
  • shallow erosions, 1-3mm, may be present in abomasal mucosa
  • autolytic changes may mask these lesions
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28
Q

Describe the placental lesions seen in Listeria

A
  • severr diffuse necrotizing and supprative placentitis ofboth the cotyledons and the inter cotyledonary
  • aborted foetus - multiple 1mm yellow/ white foci in many organs, large numbers in liver
    • these foci are areas of acute necrotising hepatitis in which the gram +ve listeria microbes are numerous
    • these lesions identical to campylobacteriosis and brucellosis (except the trophoblasts)
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29
Q

What are the differential diagnosis of Listeria?

A
  • toxaemia (last 4 wks of pregnancy)
  • brain abscesses
  • peripheral vestibular lesions (middle ear infections)
  • Gid (tapeworm cyst in brain)
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30
Q

How do you test for Listeria?

A
  • isolate L.monocytogenes from the placenta, foetus or uterine discharges after an abortion
    • blood/ CSF can be cultured in animals with septicaemia/ encephalitis
    • at necropsy, the liver, kidneys and spleen can be cultured in septicaemic animals/ pons, medulla with encephalitis
    • L.monocytogenes isolated from nasal discharges, urine, faeces or milk
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31
Q

How is Listeria cultured?

A
  • samples directly plated on blood agar and simultaneously cultured with a cold enrichment procedure
  • growth may take 3 months
  • use biochemical tests to identify colonies
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32
Q

What is the difference in CSF in an animal with Listeria?

A
  • increased protein content and mild pleocytosis composed of large mononuclear cells
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33
Q

How can Listeriosis be differentiated from pregnancy toxemia or ketosis in cattle?

A
  • careful clinical examination
  • CSF changes
  • 3-OH butyrate concs well below 3mmol/L
  • and facial/ ear paralysis absent in preg toxaemia and ketosis
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34
Q

What tests are used to identify presence of Listeria?

A
  • use rabbit polyclonal anti-Listeria antiserum
  • peroxidase-antiperoxidase technique
  • ELISAs
  • immunoflurescence
  • immunochromatography
  • immunomagnetic separation
  • PCR
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35
Q

Why isnt serology used for diagnosis?

A
  • many healthy animals have high Listeria titers
36
Q

What is the human risk of Listeriosis?

A
  • aborted foetuses and necropsy of septicemic animals- greatest hazard
  • L.monocytogenes confined to brain
  • people have developed fatal meningitis, septicemia, and papular exanthema on arms
  • pregnant women:
    • danger to foetus
    • possible abortion
    • stillbirth
    • infection of neonates
  • most infections are caused by eating the bacteria in food, or by aerosol/ direct contact
  • spread indirectly via milk, cheese, meat, eggs, or veg
37
Q

How do you treat Listeriosis?

A
  • need early, aggressive antibiotic treatment
    • penicillin (drug of choice)
    • ceftiofur
    • erythromycin
    • trimethoprim/sulfonamide
  • high doses - difficult in achieving minimum bactericidal concs in brain
  • in heavily pregnant ewes - propylene glycol and rehydration therapies
  • poor prognosis in sheep
  • treatment only initated if not recumbent
38
Q

What dosage of penicillin G should be given?

A
  • 44,000 U/kg body wt, IM, daily for 1-2 weeks
  • +fluid and electrolytes
39
Q

How is silage made?

A
  • silage must be made from plant material with a suitable moisture content (50-60%)
  • undegoes anerobic fermentation, which starts about 48 hrs after silo is filled and converts sugars to acids
  • completed after 2 wks
40
Q

How are sweet and sour silages made?

A
  • Sour:
    • when silage is closely packed- the suppy of oxygen is limited and acid fermentation casues decomp of the carbs into acetic, butyric, lactic acids
  • Sweet:
    • if silage is unchaffed and loosely packed/ silo is built gradually, oxidation proceeds more rapidly and temp rises
    • if the mass is compressed when the temp is 60-71 degrees, fermentation stops
41
Q

Outline the steps of silage making?

A
  • Pre-sealing-
    • enables some resp and some dry matter loss
  • Fermentation-
    • occurs over a few weeks,
    • pH drops
    • more DM loss
    • hemicellulose broken down
    • aerobic resp stops
  • Infiltration-
    • some oxygen filtration
    • limited micriobial resp
    • CHOs lost
  • Emptying
42
Q

What type of silageis least conductive to listeria growth?

A
  • silage that is compacted (anaerobic fermentation)
  • pH of under 4.5
  • has no incorporated soil
43
Q

Optimum conditions for listeria?

A
  • temp: 1-45 degrees/ optimum = 30-37
  • pH - 4.5- 9.6
  • anerobic and microaerobic conditions
44
Q

How should the diet of a pregnant ewe be managed?

A
  • in late pregnancy ewe appetite reduces by 30% due to lambs taking up more space
    • increase nutrient density
  • good quality silage supplies most nutrients needed but a source of DUP
  • ewes with twins - BCS 3.3 by lambing
  • ewes with single - BCS 2.8+ by lambing
  • floor feeding - good so they have access to enough feed
45
Q

What does Campylobacter result in?

A
  • late abortion/ stillbirths
  • easily spread by poor hygiene
  • bacteria commonly found in sheep dung or abortion material
46
Q

How does Toxoplasma result in abortion?

A
  • parasite
  • spread by infected cats defecating on sheeps feed
  • parasite uses sheep as an intermediate host and causes them to abort in late pregnancy or absorb the foetus if infected early in pregnancy
47
Q

What is the result of Enzootic abortion (EAE)?

A
  • caused by the bacteria Chlamydophila abortus
  • abortion occurs in last 2-3 wks of pregnancy
  • once infected ewe carries bacteria for life
48
Q

Sheep gestation period?

A
  • 152 days
49
Q

When does the majority of foetal growth occur?

A
  • final 60 days
  • from day 100-150 growth of placenta has finished
50
Q

Why were there no gross lesions present in the brain of the sheep at autopsy?

A
  • rare
  • when lesions do occur - in caudal brainstem
51
Q
A
52
Q

What is the difference between gross pathology and histopathology?

A
  • histopathology:
    • microscopic examination of various forms of tissue
    • examination of a biopsy or surgical specimen by a pathologist, after the specimen has been processed and histological sections have been placed onto glass slides
  • Gross pathology
    • macroscopic manifestations of disease in organs, tissues and body cavities
53
Q

How do you age a lamb foetus?

A
  • crown-anus length (50-100 days)
  • brain weight, long bone length and number of appendicular ossification centres
54
Q

What biosecurity measures can be taken to reduce Listeria spread between sheep?

A
  • do not feed silage, if you do make sure it is high quality, not rotten, and without soil contamination or prolonged air exposure
  • remove left over silage after feeding
  • any sick animals isolated
  • affected sheep treated with antimicrobials
  • recumbent animals - euthanised
55
Q

What biosecurity measures can be taken to reduce the risk of transmission of Listeria to humans?

A
  • movement of livestock bedding waste from pens to secondary store, and storage under conditions conducive for increased temp
  • dont use untreated manure on crops
  • wash raw veg, thoroughly cooking meat, hygiene, consume only pasteurized products
  • gloves
56
Q

What is encephalitis?

A
  • inflammation of brain
57
Q

Which animals is Listeria ivanovii specific to?

A
  • ruminants
58
Q

What is autolysis?

A
  • the destruction of cells and tissues by their own enzymes
59
Q

What % of CO2 enhances Listeria growth?

A
  • 10%
60
Q

What are the clinical signs of Listeria in cattle?

A
  • mainly listeria monocytogenes
  • septicaemia- visceral listeriosis
  • neural listeriosis - circling disease
  • abortion
  • iritis
  • not eating
  • drooping etc
  • much more pronounced facial paralysis and go off their food a lot more than sheep
  • third eyelid prolapse
  • drooping tongue
61
Q

What is this?

A
  • multifocal bacterial encephalitis
    • perivascular cuffing
    • inflam cells around vessels in brain
    • may see microabcesses
  • to confirm 100% Listeria either:
    • immunohistochemistry with Listeria antibody
    • insitu PCR
62
Q

What is this?

A
  • Perivascular cuffing
63
Q

What are these?

A
  • Listeria monocytogenes
    • not always in huge numbers
64
Q

What can be seen here? when would this be seen?

A
  • granulomatous encephalitis- sheep
    • seen in chronic cases
65
Q

What samples would you collect for diagnosis in sheep?

A
  • visceral form - liver, kidney, spleen
  • abortion - placenta, foetal abomasal contents, uterine discharge and afterbirth
66
Q

On farm risk factors for Listeria?

A
  • biosecurity
  • rodents
  • previous infections on farm
  • poor silage making/ storage facilities
67
Q

How to prevent silage conducting Listeria?

A
  • discard spoiled silage
  • clean feed troughs daily
  • avoid soil/ manure contamination of feed troughs from tractor wheels
  • discard refusals
  • clean water troughs regularly
  • repaire punctured wrapped bales
  • inside of silage bale warm - take it out, cold shock, kick starts the listeria
  • use additives
  • silage clamps rolled continously
  • silage clamps must be sheeted to prevent entry of air
  • use block cutter
  • cut across a narrow silage face
68
Q

Listeria Vaccines?

A
  • none licensed in UK
  • only autogenous vaccines
  • experimental live attenuated vaccine (concern about zoonoses)
69
Q

If Listeria is inhaled, what does it cause?

A
  • abortion
  • latent infection
  • septicaemia
70
Q

Listeria that is ingested and gains entry to tissue:

A
  • localise in intestinal wall, medulla oblongata and placents
  • causes encephalitis via minute wounds in bucal mucosa
71
Q

Which animals does Listeric encephalitis affect?

A
  • sheep
  • cattle
  • goats
  • pigs
  • (adult ruminants)
72
Q

What animals does Septicaemic listeriosis affect?

A
  • dogs
  • cat
  • pigs
  • rabbits
  • young ruminants- rumen not functional yet
  • (neonatal ruminants, monogastric animals, poultry)
73
Q

What causes the miliary yellow-white foci in the foetal liver?

A
  • due to necrosis, pus filled, containing listeria bacterium
  • liver susceptible- blood supply
74
Q

What doesnt silage supply?

A
  • calcium
  • protein
75
Q

What type of silage has increased chance of spreading listeriosis?

A
  • maize silage
76
Q

What BCS should ewes be at lambing?

A
  • 3-3.5
77
Q

What is the minimum % protein that should be fed?

A
  • 18%
78
Q

Does Listeria have flagella?

A
  • has Pentrichous flagella at room temp
79
Q

How long after infection does encephalitis occur?

A
  • 10 days - 3 weeks
80
Q

How do L.monocytogenes travel in blood?

A
  • via monocytes, macrophages and granulocytes
81
Q

What is a Gitter cell?

A
  • microglia that transforms into macrophages
82
Q

What are glial nodules?

A
  • aggregates of reactive astrocytes
83
Q

What is Torticollis?

A
  • head tilts to 1 side
84
Q

What happens to the uterus of infected animals?

A
  • normally becomes infected at all stages of pregnancy causing:
    • placentitis
    • metritis
    • still births
    • abortions
    • potential carrier via vertical transmission
85
Q

What localised infections occur from Listeria in cows and sheep?

A
  • cattle - chronic/ acute mastitis
  • sheep - opthalmitis
86
Q
A

FD6 (15 decks)

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