an epidemiological study of listeriosis in dairy cattle

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The infection of the host’s cell begins with internalisation of the bacterium either by host derived phagocytosis in the case of macrophages or by pathogen induced phagocytosis in the case of non-phagocytic cells (Dramsi and others 1996). In the process of entry two surface proteins which take part in the induced internalisation of L. monocytogenes by nonprofessional phagocytic cells have been identified. These are internalin, and a p60 extracellular protein which are regulated by genes called inlA and inlB, and iap respectively (Sheehan and others 1994). InlA has been shown to initiate entry into enterocyte like cell lines by binding to the host cell E- cadherin receptors, while inlB is required for entry into hepatocytes and some epithelial cell lines. The receptor for inlB is not known but it is suggested that phosphoinositic (PI)-3 kinase is required for L. monocytogenes uptake triggered by inlB (Dramsi and others 1997). In recent years 5 more internalin proteins of unknown functions have been identified. These are internalin C (inlC), C2 (inlC2), D (inlD), E (inlE) and F (inlF) (Dramsi and others 1997) and actin polymerase regulated by ActA has recently been identified as being involved in the entry process by interacting with heparin sulfate- proteoglycan receptor (Kuhn and Goebel 1997). The studies have shown that strains lacking these genes failed to enter or adhere to cells (Sheen and others 1994). Following internalisation, Listeria are trapped within a phagosome where they produce haemolysin or listeriolysin O, a pore forming thiol-activated cell product and phospholipase C which together break up the phagosomal membrane so that the Listeria are released and enter the cell cytoplasm. Listeria then multiply using host cell nutrients. The production of Listeriolysin O and Phospholipase C is respectively regulated by genes called hlyA and plcA. (Sheehan and others 1994). Experimental studies have shown that strains lacking these genes were not able to multiply within the cell (Portnoy and others 1988, Goebel and others 1988, Camilli and others 1991). The strategy for survival in a host’s cell is believed to be a major virulence determinant of L. 19
monocytogenes and a prerequisite to successful infection by this bacterium (Dramsi and others 1996). After escape from the phagosome L. monocytogenes utilises cytoplasmic nutrients to sustain its growth within the cell. During the process of multiplication, actin, a product of actA gene, is produced. This enables the bacterium to move within the cell. While moving freely the bacterium makes contact with the macrophage membrane generating a pseudopod organelle. This is then taken up by an adjacent cell. The life cycle continues in this newly infected cell (Tilney and Portnoy, 1989, Tilney and Tilney 1993, Southwick and Purich 1996). d) Resistance: Having briefly explained virulence and its determinants the following is a brief description of mechanisms of resistance of the host to L. monocytogenes which involves elements that deal with the organism at each stage of infection. Within first hours of the internalisation around 90% of invading listeria are killed by phagocytes. The recruitment of inflammatory cells such as neutrophils is also induced by interleukin 1 produced by infected macrophages. Neutrophils play an important role by limiting L. monocytogenes access to host’s cells and aborting cell to cell spread by lysing infected cells. Macrophages activated by phagocytosing L. monocytogenes release interleukin-1, tumor necrosis factor-α and interleukin 12. TNF-α and IL-12 then stimulate natural killer cells to produce interferon-γ. INFγ and IL-1 are necessary for macrophages to express MHC class II molecules and for enhanced listeriocidal activity. The activated macrophages inhibit the release of the organism from the phagosome. Macrophage activation and the destruction of L. monocytogenes enable listeria specific antigens to be presented to T cells which together with the IL-12 production promote the induction of T helper 1 cells and CD8+ T cells resulting in a protective effect. L. monocytogenes remaining in the endocytic compartment will be presented through the MHC class II 20
Page 1 and 2: AN EPIDEMIOLOGICAL STUDY OF LISTERI
Page 3 and 4: In the second part of the study a l
Page 5 and 6: I would like to thank to Metin Oztu
Page 7 and 8: DECLARATION I declare that apart fr
Page 9 and 10: 2. 2. Materials and Methods 47 2. 2
Page 11 and 12: 4. 4. Discussion 125 CHAPTER 5 A pi
Page 13 and 14: CHAPTER 1 LIST OF TABLES AND FIGURE
Page 15 and 16: Table 3. 11. The relationship betwe
Page 17 and 18: CHAPTER 5 Table 5. 1. Date of visit
Page 19 and 20: Figure 6. 4. The monthly faecal exc
Page 21 and 22: Listeralla hepatolytica. In the sam
Page 23 and 24: Listeriolysin O (Fernandaz-Garayzab
Page 25 and 26: L. monocytogenes was the only recog
Page 27 and 28: Table 1. 2. Serovar distribution of
Page 29 and 30: Serotyping is based on the identifi
Page 31 and 32: electrophoresis. Different strains
Page 33 and 34: and others (1995) came to the concl
Page 35 and 36: animals suggests that L. monocytoge
Page 37: Immunity reducing Septicaemia facto
Page 41 and 42: a variable number of cases of encep
Page 43 and 44: The relationship between age and Li
Page 45 and 46: a reservoir from which it spreads t
Page 47 and 48: 1. 8. Clinical signs and pathology
Page 49 and 50: is seldom clinical illness in the d
Page 51 and 52: Bacterial culture is widely used fo
Page 53 and 54: Differential diagnosis: Listerial m
Page 55 and 56: Since elimination of L. monocytogen
Page 57 and 58: first description, it was only 1980
Page 59 and 60: and meat products have resulted in
Page 61 and 62: infectious dose for the infection i
Page 63 and 64: a longitudinal study involving five
Page 65 and 66: in Britain. In this part of the stu
Page 67 and 68: groups were excluded from analysis.
Page 69 and 70: The proportions of farms with cases
Page 71 and 72: Table 2. 3. The proportion of anima
Page 73 and 74: percentage 50 45 40 35 30 25 20 15
Page 75 and 76: Milking cows (%) Rep. heifers (%) D
Page 77 and 78: Abortion 274 (57.8%) 28 (21.9%) Ner
Page 79 and 80: with others (Kanuk and Berenson 197
Page 81 and 82: occurred in replacement heifers and
Page 83 and 84: CHAPTER 3 The relationship between
Page 85 and 86: (ii) Cases in milking cows: Farms r
Page 87 and 88: To assess the relationship between
Page 89 and 90:
) Duration of housing: If animals w
Page 91 and 92:
d) Presence of moles: Farmers were
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listeriosis. Maize silage feeding a
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found between the duration of feedi
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a) Type of housing : Housing animal
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Herd sizes n Y N OR P value x Y N O
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of disease. Similarly storing feed
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a) Type of forages: Feeding maize s
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) Use of bedding: Using straw beddi
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) Source of forages: Home made gras
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1.29-18.22) whereas straw bedding i
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100 2 34 2.33 0.01 X 2 22 3.35 0.01
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a) Dung disposal: Storage of manure
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vaccination against Leptospirosis +
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suppression of the growth of Lister
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1989, Sargison 1993). It is also po
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L. monocytogenes has been isolated
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association (Kirkwood 1988, Thrusfi
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The predictor variables that met ou
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Forage feeding Maize silage Hay Str
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indoor feeding fed ad libitum on th
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cases of Listeriosis in sheep 2.9 1
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and controlling moles in fields wer
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Cases of Listeriosis in beef cattle
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This model was similar to the Model
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Table 4. 9. The multivariate relati
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5) Nervous signs: Cases of Listerio
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feeders, maize silage feeding in ri
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A contradictory finding was made ab
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selective enrichment broth, at refr
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growth of some strains of Listeria
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5. 2. 2. Bacteriology : a) Culture
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culturing negative LSEB (1/10w/v) s
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6) Sugar tests: Listeria are capabl
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uffered saline (PBS), pH 7.2, centr
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Investigation of non-specific bindi
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and 0.94 for L. monocytogenes (17/1
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Detection limit of the method: A si
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Relationship between housing, silag
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5 13 3 3 1 3 1 1 1 6 14 1 4 5 3 1 0
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Table 5. 11. The relationship betwe
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frequency of isolation of L. monocy
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CHAPTER 6 A study of the dynamic of
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There were no sample size calculati
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4 of the farms had their silage ana
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a) Faecal samples: Faecal samples w
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• • • 1 5 9 6. 2. 5. Sample p
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A total of 944 isolates of L. monoc
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UK), 0.5μM DNA primer, 1 unit Supe
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entered and left the herd over the
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Table 6. 7. Monthly frequency of ex
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Table 6. 8. The relationship betwee
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(MA) mean age, (n) number, (R) rang
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frequency of excretion (P
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There was no evidence from this far
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) Environmental samples: Both L. in
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monocytogenes. By April the proport
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A total of 211 milking cows were ex
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100 % 90 80 70 60 50 40 30 20 10 0
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The number of new cases each month
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monocytogenes was also isolated fro
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Table 6. 18 The isolates, their ori
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Table 6. 19. The distribution of th
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On farm C pattern 1 was detected in
Page 217 and 218:
Figure 6. 8. The repeatability of R
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Figure 6. 10. The distribution of s
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Figure 6. 12a. The RAPD pattern obt
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1988, Husu 1990) and from zero to a
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experimentally been shown that ther
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periods. However, on farms B and E
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A large number of L. monocytogenes
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Figure 6. 13. Animal-environment cy
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Some important farming practices we
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chance finding of L. monocytogenes
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Asahi, O., Hosoda, T. and Akuyama,
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Bourry, A. and Poutrel, B. (1996) B
Page 241 and 242:
Chakraborty, T., Ebel, F., Wehland,
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delGarso, L. and Wallop, W. (1975)
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Eveland, W.C. (1963) Demonstration
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Fraser, J.A. and Sperber, W.H. (198
Page 249 and 250:
Golden, D.A, Beuchat, L.R. and Brac
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humans. In Miller, A.J.,. Smith, J.
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Jones, F.S. and Little, R.B. (1934)
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Listeria innocua by oral inoculatio
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Low, J.C. and Donachie, W.A. (1997)
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McBride, M.E. and Girard, K.F. (196
Page 261 and 262:
Nieman, R.E. and Lorber, B. (1980)
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Peters, M., Pohlenz, J., Jaton, K.,
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Bakteriologie, Mikrobiologie und Hy
Page 267 and 268:
Seeliger, H.P.R. (1981) Apathogenic
Page 269 and 270:
Tilney, L.G. and Portnoy, D.A. (198
Page 271 and 272:
Walker, J.K., Morgan, J.H., McLauch
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APPENDIX 3 PREPARATION OF BACTERIOL
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Cool to 50 0 C Mix Solution A with
Page 277 and 278:
Phosphate buffered saline (PBS; 10x
Page 279 and 280:
APPENDIX 2 THE OVERALL RESULTS OF U
Page 281 and 282:
Grass silage Y N OR (95% CL) p Valu
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storage Y N OR (95% CL) p Value cla
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source home made 38 182 0.6 (0.1-16
Page 287 and 288:
source home made 34 345 0.8 (0.3-2.
Page 289 and 290:
source barley 27 251 0.93(0.6-1.6)
Page 291 and 292:
source potatoes 2 11 1.4 (0.-7.7) 0
Page 293 and 294:
in a covered barn 73 595 0.8 (0.4-1
Page 295 and 296:
sawdust 0 16 0.0 (0.0-2.73) 0.3 str
Page 297 and 298:
APPENDIX 5 THE QUESTIONNAIRE AND TH
Page 299 and 300:
Abbreviations: 1 first blood sampli
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B 113 1 114 1 115 1 116 1 117 1 118
Page 303 and 304:
B 104 1 104 2 104 3 105 1 105 2 105
Page 305 and 306:
B 20 1 20 2 20 3 21 1 21 2 21 3 19
Page 307 and 308:
0.169 1.157 1.134 1.467 1.356 0.145
Page 309 and 310:
Plate 4 Layout and ODs B 73 1 73 2
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UNIVERSITY OF BRISTOL LISTERIOSIS I
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PART C : HERD SIZE :--BETWEEN JULY
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(please circle one for each) 3. Wha
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etween which months were your milki
Page 320 and 321:
not stored beneath the slats compos
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STUDY OF LISTERIOSIS IN DAIRY CATTL
Page 324 and 325:
STUDY OF LISTERIOSIS IN DAIRY CATTL
Page 326 and 327:
Now I would like to get some detail
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Root crops : ______________________
Page 330 and 331:
In this section I will be asking qu
Page 332 and 333:
33. Which days of the week bulk tan
Page 334 and 335:
-what was used to treat? -what was
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an epidemiological study of listeriosis in dairy cattle

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