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Currently important pathogenic Listeria species affecting animals and birds (review)
https://doi.org/10.29326/2304-196X-2024-13-4-307-313
Abstract
Listeriosis is one of the most severe gastrointestinal diseases in the world. Listeria affect different groups of animals and birds. The pathogen has been detected in meat, milk, fish and fish products. The disease shows spring and autumn seasonality. It has been reliably established that Listeria monocytogenes is ubiquitous in the environment. Listeria monocytogenes is a facultative intracellular pathogen. Infection with Listeria monocytogenes causes an invasive disease in animals and humans, which is transmitted via the fecal-oral route from an animal to a human, from a mother to a fetus. The pathogenesis of Listeria infection has been well studied. The gastrointestinal tract is the site of the pathogenic Listeria species transit and spread. The infection incubation period is 20–30 days in animals and humans. The clinical course in different animal species, including birds, has a number of specific features. Listeria can cross the intestinal, placental and blood-brain barriers. The manifestations of listeriosis include encephalitis, meningitis, gastritis, meningoencephalitis, mastitis, abortions, endometritis, etc. Pathogenic Listeria species show hemolytic activity which non-pathogenic species (except Listeria seeligeri) lack. The review presents the up-to-date information on the classification of Listeria, the pathogenicity factors of Listeria monocytogenes as the major pathogen, the mechanisms of Listeria infection development in different animal species.
For citations:
Shastin P.N. Currently important pathogenic Listeria species affecting animals and birds (review). Veterinary Science Today. 2024;13(4):307-313. https://doi.org/10.29326/2304-196X-2024-13-4-307-313
INTRODUCTION
Microorganisms of the genus Listeria belong to the family Listeriaceae, the order Bacillales, the class Bacilli and the phylum Firmicutes. Listeria is a grampositive bacterium genetically related to Clostridium, Enterococcus, Staphylococcus, Streptococcus and Bacillus. Listeria spp. are facultative anaerobic rods with a size of 0.4 × 1–1.5 μm, which do not form spores, have no capsule and are motile at 10-25 °C [1]. Listeria spp. are isolated from various environmental sources such as soil, water, wastewater, animal and human feces, food products. A number of researchers have found that the natural habitat of the bacterium is a decaying plant substrate. Transmission occurs through the fecal-oral route. In rural areas, ruminants are the main vectors of Listeria [2-4]. The genus Listeria is currently represented by the following species: L. monocytogenes, L. innocua, L. ivanovii (formerly known as L. monocytogenes serotype 5), L. farberi, L. seeligeri, L. welshimeri, L. ilorinensis, L. rocourtiae, L. weihenstephanensis, L. marthii, L. grandensis, L. riparia, L. cossartiae, L. fleischmannii, L. portnoy, L. rustica, L. immobilis, L. booriae, L. thailandensis, L. goaensis, L. costaricensis, L. floridensis, L. aquatica, L. grayi, L. valentina, L. newyorkensis, L. swaminathanii, L. cornellensis [5]. Two species, L. ivanovii and L. monocytogenes, are pathogenic for humans and animals [6]. The official discovery of Listeria was in 1924, when a group of researchers (E. G. D. Murray, R. A. Webb, M. B. R. Swann) in Cambridge, England, isolated L. monocytogenes as the etiological agent of a septicemic disease affecting rabbits and guinea pigs [7]. The first case of human listeriosis was reported in Denmark in 1929. L. ivanovii was first isolated from lambs in Bulgaria in 1955 [8]. Cases of L. ivanovii infection are rare; the bacteria of this species are mainly isolated from abortions and neonatal septicemias in sheep and cattle [9-11]. Although L. seeligeri is a non-pathogenic Listeria species, one human case of infection with this bacterium has been reported [12][13].
Listeria spp. are widespread in nature, they have been isolated from more than 90 animal species, as well as from plants and a broad range of food products. These bacteria can persist in the animal body for a long time. Suppressing the growth of Listeria in the ready-to-eat products is still a challenge. The examination of the biological and environmental characteristics of Listeria is aimed at the prevention of Listeria infection and the control of this important food pathogen.
The novelty of the study is the systematization of the up-to-date data on the biological properties and classification of Listeria. The specific features of listeriosis in livestock and poultry are presented.
The work was carried out using analytical research methods and the RSCI, Scopus, Web of Science, Library Genesis, Sci-Hub, Google Scholar, PubMed, Cyberleninka databases.
The purpose of the review was to analyze and systematize current knowledge about pathogenic Listeria species, the classification of Listeria, the mechanism of the disease development and characteristic features of Listeria infection in different animal and bird species.
CLASSIFICATION AND BIOLOGICAL PROPERTIES OF LISTERIA
The bacteria of the genus Listeria are found on all continents. Soft cheeses and milk products, sausages, pastes, salads, smoked fish and, as a rule, ready-to-eat chilled industrially-made products are most often contaminated [14-17]. Listeria is well adapted to survive on the surfaces of the food processing equipment. For example, Listeria tolerates high salt concentrations (> 10%) and relatively low pH values (< 5.0) and is able to reproduce at low temperatures [18][19]. Listeriosis shall be differentiated from rabies, influenza, brucellosis, pasteurellosis, toxoplasmosis.
Pathogenic Listeria species show hemolytic activity which non-pathogenic species (except L. seeligeri) lack. The hemolysin gene (hly) has a key role in cell destruction [20]. The biological characteristics of some species of the genus Listeria are presented in Table 1 [21].
The classification of L. monocytogenes is based on the structure of the somatic (O) and flagellar (H) antigens, and all members of this species are divided into the following serovars: 1/2a, 1/2b, 1/2c, 3a, 3b, 3c, 4a, 4b, 4c, 4d, 4e and 7 [22].
Listeria monocytogenes is a facultative intracellular pathogen. Infection with L. monocytogenes causes an invasive disease in animals and humans, which is transmitted via the fecal-oral route from an animal to a human, from a mother to a fetus [23]. The pathogenicity factors of this bacterium species are shown in Table 2 [21].
Most of the information on the pathogenesis of listeriosis has been obtained on the basis of the interpretation of epidemiological, clinical and histopathological data in experimental infections in animals. The gastrointestinal tract is the main site of the entry and spread of pathogenic Listeria [17]. It is reported that the increased acidity of gastric juice can destroy a significant amount of Listeria. It is well known that Listeria infection incubation period in animals and humans is 20–30 days. Listeria spp. penetrating through the intestinal barrier are carried by lymph and blood to the mesenteric lymph nodes, liver, spleen [24].
An experimental study in mice (intravenous administration) has revealed that L. monocytogenes is rapidly removed from the bloodstream by resident macrophages of the spleen and the liver [25]. The major bacterial load is located in the liver, in which Kupffer cells are active. These macrophages destroy most of the engulfed bacteria. A number of authors believe that Kupffer cells initiate the activation of anti-listerial immunity by inducing the antigen-dependent proliferation of T lymphocytes and cytokine secretion [26]. Also, various scientific papers note the partial survival of Listeria cells after attack by macrophages, which actively grow over the next 2–5 days [27-29]. Listeria cells move by direct passage from hepatocyte to hepatocyte and disseminate in the liver parenchyma without coming into contact with the humoral immune system. The authors conclude that this explains the levelling of the role of antibodies in the antibody-Listeria interaction [30]. L. monocytogenes is a multi-system pathogen that affects a wide variety of animal and human tissues.
Table 1
Biological characteristics of some species of the genus Listeria [21]
|
Characteristics |
L. monocytogenes |
L. innocua |
L. ivanovii |
L. seeligeri |
L. welshimeri |
L. grayi |
|
|
β-hemolysis |
+ |
– |
+ |
+ |
– |
– |
|
|
САМР test (Staphylococcus aureus) |
+ |
– |
– |
+ |
– |
– |
|
|
САМР test (Rhodococcus equi) |
± |
– |
+ |
– |
– |
– |
|
|
Production |
mannitol |
– |
– |
– |
– |
– |
+ |
|
α-methyl-D-mannoside |
+ |
+ |
– |
– |
+ |
+ |
|
|
L-rhamnose |
+ |
d |
– |
– |
d |
± |
|
|
soluble starch |
– |
– |
– |
+ |
|||
|
D-xylose |
– |
– |
+ |
+ |
+ |
– |
|
|
Hippurate hydrolysis |
+ |
+ |
+ |
– |
|||
|
Nitrate reduction |
– |
– |
– |
± |
|||
|
Pathogenicity for mice |
+ |
– |
+ |
– |
– |
– |
|
|
“+” – 90% or more of the strains are positive; “–” – 90% or more of the strains are negative; d – 11–89% of the strains are positive; |
|||||||
Table 2
Pathogenicity factors of Listeria monocytogenes [21]
|
Protein |
Molecular weight, kDa |
Gene |
Function |
|
prfA |
27 |
prfA |
Regulation of virulence gene transcription |
|
Listeriolysin O |
58 |
hly |
Lysis of primary and secondary phagosomes |
|
PlCA (phosphatidylinositol-specific phospholipase C) |
36 |
plcA |
Phagosome lysis |
|
Lecithinase |
33 |
plcB |
Lysis of secondary phagosome |
|
Metalloprotease |
57 |
mpl |
Post-translational modification of lecithinase |
|
ActA |
67 |
actA |
Polymerization of actin |
|
Internalin, inlB |
88.65 |
inlA, inlB |
Induction of phagocytosis |
BOVINE LISTERIOSIS
Cattle account for a greater number of pathogenic Listeria detections reported worldwide [31]. Bovine listeriosis most commonly manifests itself as encephalitis; miscarriages, septicemia with miliary abscesses are also noted. Foodborne transmission is the main mode of infection in cattle, particularly as a result of low-quality silage feeding, drinking of contaminated water. After ingestion, Listeria cells are disseminated via hematogenous spread to the viscera, nervous system and reproductive organs of pregnant cows. Another route of infection is through the abrasions of the skin or the conjunctiva during grazing or via the teats. When the central nervous system is affected, the pathological process localizes in the medulla oblongata and the pons [32][33]. Damage to the respective nerve underlies the characteristic presentation: damage to the fifth cranial nerve (CN V) and the mandibular nerve leads to the inability to drink or eat and, consequently, to further disorders [34]; the sign of damage to CN IX and CN X is excessive salivation due to the swallowing difficulty; CN XII – the protrusion of the tongue; CN VIII – ataxia and circling, facial paralysis, including unilateral drooping of the lip, eyelid, ear; CN VI – strabismus. In advanced stages of the disease, the animal lapses into a coma and dies within a few days. Postmortem cerebral cortex lesions consist of the foci of necrosis infiltrated with neutrophils, macrophages, bacterial cells [35, 36]. Listeriosis shall be differentiated from rabies.
The genital form of listeriosis in cows presents as abortions in the last trimester of gestation. In case of fetal infection, newborn animals develop meningitis and subsequently die [37].
The authors also note the seasonality of bovine listeriosis, with the number of cases increasing in winter and spring and decreasing in summer [32].
PORCINE LISTERIOSIS
In pigs (the young ones), listeriosis most often manifests itself as septicemia and is less common than in other animal species. Encephalitis and miscarriages are rarely reported [38]. Hepatic necrosis is a characteristic morphological feature of listerial septicemia in newborn piglets [39, 40]. The first case of listeriosis in piglets was reported in Russia in 1936 by T. P. Slabospitsky, who named the pathogen L. suis [41]. In sows, L. monocytogenes localizes in the tonsils, from where it then enters the gastrointestinal tract. Porcine listeriosis cases are more frequently detected in winter and spring. The symptoms of central nervous system disturbance in young animals with listerial encephalitis are incoordination, weakness and apathy, followed by death. Meningoencephalitis in pigs is characterized by a sudden decrease in appetite, neurological disorders (trembling, partial paralysis, urinary incontinence, seizures), elevated body temperature [42]. Histopathological examination reveals severe monocytic infiltration, many blood vessels show perivascular constriction [43][44]. The largest outbreak of listerial meningoencephalitis in pigs was reported in India, in which 27 of 75 pigs died [45].
OVINE LISTERIOSIS
Ovine listeriosis is caused by L. monocytogenes serotypes 1/2 and 3, as well as by L. ivanovii. Ovine listeriosis (circling disease) was first reported in New Zealand in 1929. The frequency of infection in sheep is higher (up to 30%) than in cattle (up to 15%). Ovine listeriosis manifests itself as encephalitis, gastrointestinal septicemia with hepatitis, splenitis, pneumonitis and abortions more commonly occurring in the last trimester of gestation. Encephalitis is the most common form of listeriosis diagnosed in sheep [46]. Lambs aged 5 weeks may develop septicemia, older lambs develop encephalitis. Listeria infection in adult sheep presents as a central nervous system disorder (meningoencephalitis), refusal to eat or drink, elevated temperature, teeth grinding, paralysis of the muscles of mastication, excessive salivation caused by the inability to swallow due to damage to the cranial nerve, circling movements (circling disease). In advanced stages, muscular incoordination develops, which is followed by the animal’s inability to walk; death occurs within 2–3 days after the onset of the first symptoms. Histological examination reveals microgranulomas and microabscesses in the brainstem. Listerial encephalitis in sheep is most common in late autumn, winter and early spring. After hematogenous spread to the uterus, L. monocytogenes is detected within 48 hours in the fetus and the amniotic fluid. Initially, pregnant ewes develop purulent metritis. The clinical symptoms resolve after the abortion, and the ewes begin to feel much better. Morbidity in ewes ranges from 1 to 20%, with mortality of lambs being high. Septicemia is most frequent in newborn lambs and follows 2–3 days after oral infection. It is characterized by high temperature, loss of appetite, diarrhea. Death may occur as a result of extensive liver damage, pneumonia; the mortality rate is much lower for the septicemic form of listeriosis than for the encephalitic one. The factors contributing to the pathogenicity of Listeria are overcrowding, stress and feed quality [47, 48].
Listeria ivanovii is a recognized etiological agent of abortions in sheep [48]. Ovine listeriosis cases caused by L. ivanovii and characterized by abortions make up 8%. Factors predisposing to infection with L. ivanovii are the same as for L. monocytogenes and include stress, decreased immunity, feeding of poor-quality feed, contact with infected animals, etc. [49][50].
As a preventive measure, vaccination with live attenuated strains of L. monocytogenes takes place. For example, in Germany and Greece, immunization of sheep with an attenuated vaccine based on serovars 1/2a and 4b reduced the incidence of listeriosis and abortions as compared with the control group. The results of field tests showed that the immunized ewes delivered more lambs free from Listeria (92.4 vs 69.7%) and of higher birth weight (2.2 vs 1.8 kg) than lambs from the control unvaccinated ewes. Besides, L. monocytogenes was not isolated from the milk samples from the vaccinated ewes, in contrast to the control group, in which Listeria was detected in 31.9% of milk samples [47].
In the event of an outbreak, several strains of the same or different Listeria serotypes may be isolated. DNA fingerprinting, phage typing, pyrolysis mass spectrometry are used as additional diagnostic methods to confirm the diagnosis [51].
CAPRINE LISTERIOSIS
Clinical listeriosis in goats is similar to that in sheep and manifests itself as septicemia, abortion, encephalitis [52]. The mechanism of the disease development is as follows: pathogenic Listeria penetrates into the goat body through the gastrointestinal tract, which leads to a transient bacteremia and further spread to the central nervous system, viscera, as well as to the placenta. Depression, decreased appetite and milk yield, diarrhea, elevated body temperature (41 °C) are the first signs of septicemia. In pregnant does, L. monocytogenes penetrates through the placenta into the fetus and subsequently causes late miscarriages [53].
A number of researchers note that meningoencephalitis is the most frequently reported form of listeriosis in goats. Early signs of listerial encephalitis in goats are excessive salivation, ear droop, tongue protrusion, absence of rumination [54]. Some researchers also point out that goats are more susceptible to listeriosis than sheep [52]. For example, during an outbreak of listeriosis in Iraq, the morbidity (30.0 vs 16.7%) and mortality (21.2 vs 14.9%) were higher in goats than in sheep [55]. Listeria isolations from goats are more frequent in winter and spring.
AVIAN LISTERIOSIS
Avian listeriosis was first reported in 1935 [56]. Wild ducks, turkeys, pheasants, geese are asymptomatic carriers of Listeria. Birds become Listeria-infected orally by pecking feces, soil, carcasses. Listeriosis is much less common in birds than in sheep, goats and cattle [57-59]. Listeriosis in birds can also develop as a secondary infection associated with viral diseases, as well as with salmonellosis, coccidiosis, worm infections, tick-borne encephalitis, lymphocytosis, enteritis and others that contribute to a decrease in immunity [60]. One of the distinguishing features of avian listeriosis is septicemia characterized by focal necrosis of viscera, particularly the liver and the spleen. At the same time, a number of authors note cardiac lesions such as vascular occlusion, pericarditis and increased amounts of pericardial fluid. The septicemic form of listeriosis produces the following conditions: splenomegaly, peritonitis, nephritis, ulcers in the ileum and caecum, necrosis of the oviduct, generalized pulmonary edema, conjunctivitis, enteritis. In acute cases of the septicemic form of listeriosis, all internal organs are affected. Birds show practically no overt clinical signs other than emaciation and die on days 5–9 of the disease [59][61].
Listerial meningoencephalitis is far less common in birds. It is characterized by the disturbances of the central nervous system such as incoordination, tremors, torticollis, dropped wings, unilateral or bilateral toe paralysis [62], which later lead to death. Necropsy reveals congestion and necrotic foci in the brain [63][64].
Chicken embryos and young chickens are the most susceptible to listeriosis [61][65][66]. In day-old chicks, Listeria is most frequently detected in the caecum, liver, spleen and cloacal swab samples [63].
Thus, the incubation period of listeriosis depends on the overall clinical picture. In animals and birds, the infection occurs in the septicemic, encephalitic, abortive forms. Pathogenic Listeria species are important etiological agents of animal and bird diseases that lead to severe consequences and economic damage [67]. To date, listeriosis remains an urgent issue and does not receive sufficient coverage in the public space.
CONCLUSION
Listeria spp. are distributed globally in a wide variety of domestic and wild animals, as well as in humans, and possess a zoonotic potential.
The analysis of scientific publications has made it possible to summarize data on the mechanisms and routes of transmission, pathogenicity factors of Listeria, their serological diversity, localization in the body of susceptible animals, the forms of listeriosis in cattle, pigs, sheep, goats and birds.
References
1. Collins M. D., Wallbanks S., Lane D. J., Shah J., Nietupski R., Smida J., et al. Phylogenetic analysis of the genus Listeria based on reverse transcriptase sequencing of 16S rRNA. International Journal of Systematic and Evolutionary Microbiology. 1991; 41 (2): 240–246. https://doi.org/10.1099/00207713-41-2-240
2. Fenlon D. R., Ryser E. T., Marth E. H. Listeria monocytogenes in the natural environment. In: Listeria, Listeriosis and Food Safety. Ed. by E. T. Ryser, E. H. Marth. 2nd ed. New York: Marcel Dekker Inc.; 1999; 21–37.
3. Kampelmacher E. H., van Noorle Jansen L. M. Listeriosis in humans and animals in the Netherlands (1958–1977). Zentralblatt für Bakteriologie. A: Medizinische Mikrobiologie, Infektionskrankheiten und Parasitologie. 1980; 246 (2): 211–227. https://pubmed.ncbi.nlm.nih.gov/6775441
4. McCarthy S. A. Listeria in the environment. In: Foodborne Listeriosis. Ed. by A. L. Miller, J. L. Smith, G. A. Somkuti. New York: Elsevier; 1990; 25–29.
5. Je H. J., Kim U. I., Koo O. K. A comprehensive systematic review and meta-analysis of Listeria monocytogenes prevalence in food products in South Korea. International Journal of Food Microbiology. 2024; 415:110655. https://doi.org/10.1016/j.ijfoodmicro.2024.110655
6. Cruza P. E. H. Bacterias patógenas emergentes transmisibles por los alimentos. In: Aspectos Higiénicos de los Alimentos Microbiológicamente Seguros. Ed. by B. S. Pérez. Real Academia Nacional de Farmacia; 2010; 147–179. https://dialnet.unirioja.es/servlet/libro?codigo=785064 (in Spanish)
7. Murray E. G. D., Webb R. A., Swann M. B. R. A disease of rabbits characterised by a large mononuclear leucocytosis, caused by a hitherto undescribed bacillus Bacterium monocytogenes (n. sp.). The Journal of Pathology and Bacteriology. 1926; 29 (4): 407–439. https://doi.org/10.1002/path.1700290409
8. Ivanov I. Untersuchungen über die Listeriose der Schafe in Bulgarien. Monatshefte für Veterinärmedizin. 1962; 17: 729–736. (in German)
9. Alexander A. V., Walker R. L., Johnson B. J., Charlton B. R., Woods L. W. Bovine abortions attributable to Listeria ivanovii: Four cases (1988–1990). Journal of the American Veterinary Medical Association. 1992; 200 (5): 711– 714. https://doi.org/10.2460/javma.1992.200.05.711
10. Chand P., Sadana J. R. Outbreak of Listeria ivanovii abortion in sheep in India. Veterinary Record. 1999; 145 (3): 83–84. https://doi.org/10.1136/vr.145.3.83
11. Dennis S. M. Perinatal lamb mortality in Western Australia. 6. Listeric infection. Australian Veterinary Journal. 1975; 51 (2): 75–79. https://doi.org/10.1111/j.1751-0813.1975.tb09409.x
12. Rocourt J., Grimont P. A. D. Notes: Listeria welshimeri sp. nov. and Listeria seeligeri sp. nov. International Journal of Systematic and Evolutionary Microbiology. 1983; 33 (4): 866–869. https://doi.org/10.1099/00207713-334-866
13. Rocourt J., Hof H., Schrettenbrunner A., Malinverni R., Bille J. Méningite purulente aiguë à Listeria seeligeri chez un adulte immunocompétent = Acute purulent Listeria seelingeri meningitis in an immunocompetent adult. Schweizerische medizinische Wochenschrift. 1986; 116 (8): 248–251. https:// pubmed.ncbi.nlm.nih.gov/3082004 (in French)
14. Farber J. M., Peterkin P. I. Listeria monocytogenes, a food-borne pathogen. Microbiological Reviews. 1991; 55 (3): 476–511. https://doi.org/10.1128/mr.55.3.476-511.1991
15. Rocourt J. Risk factors for listeriosis. Food Control. 1996; 7 (4–5): 195–202. https://doi.org/10.1016/S0956-7135(96)00035-7
16. Norton D. M., Braden C. R. Foodborne Listeriosis. In: Listeria, Listeriosis and Food Safety. Ed. by E. T. Ryser, E. H. Marth. 3rd ed. New York: CRC Press; 2007; 305–356. https://doi.org/10.1201/9781420015188
17. Shastin P. N., Yakimova E. A., Supova A. V., Savinov V. A., Ezhova E. G., Khabarova A. V., Laishevtsev A. I. Antibiotic resistance and phage sensitivity of topical listeriosis pathogens. Agrarian science. 2024; (3): 50–56. https:// doi.org/10.32634/0869-8155-2024-380-3-50-56 (in Russ.)
18. McLauchlin J., Greenwood M. H., Pini P. N. The occurrence of Listeria monocytogenes in cheese from a manufacturer associated with a case of listeriosis. International Journal of Food Microbiology. 1990; 10 (3–4): 255–262. https://doi.org/10.1016/0168-1605(90)90073-E
19. Lou Y., Yousef A. E. Characteristics of Listeria monocytogenes important to food processors. In: Listeria, Listeriosis, and Food Safety. Ed. by E. T. Ryser, E. H. Marth. 2nd ed. New York: Marcel Dekker Inc.; 1999; 131–224.
20. Cossart P., Mengaud J. Listeria monocytogenes. A model system for the molecular study of intracellular parasitism. Molecular Biology & Medicine. 1989; 6 (5): 463–474. https://pubmed.ncbi.nlm.nih.gov/2516599
21. Tartakovsky I. S., Maleev V. V., Ermolaeva S. A. Listeria: Role in human infectious pathology and laboratory diagnostics. Moscow: Meditsina dlya vsekh; 2002. 200 p. (in Russ.)
22. Bakulov I. A., Vasiliev D. A., Kovaleva N. E., Egorova I. Yu., Selyaninov Yu. O. Listeria and listeriosis: monograph. 2nd ed., corrected and supplemented. Ulyanovsk: Ulyanovsk State Agrarian University named after P. A. Stolypin; 2016. 334 p. (in Russ.)
23. Torres K., Sierra S., Poutou R., Carrascal-Camacho A., Mercado M. Patogénesis de Listeria monocytogenes, microorganismo zoonótico emergente. Revista MVZ Córdoba. 2005; 10 (1): 511–543. (in Spanish)
24. Marco A. J., Prats N., Ramos J. A., Briones V., Blanco M., Dominguez L., Domingo M. A microbiological, histopathological and immunohistological study of the intragastric inoculation of Listeria monocytogenes in mice. Journal of Comparative Pathology. 1992; 107 (1): 1–9. https://doi.org/10.1016/0021-9975(92)90090-H
25. Cousens L. P., Wing E. J. Innate defenses in the liver during Listeria infection. Immunological Reviews. 2000; 174 (1): 150–159. https://doi.org/10.1034/j.1600-0528.2002.017407.x
26. Gregory S. H., Wing E. J. Accessory function of Kupffer cells in the antigen-specific blastogenic response of an L3T4+ T-lymphocyte clone to Listeria monocytogenes. Infection and Immunity. 1990; 58 (7): 2313–2319. https://doi.org/10.1128/iai.58.7.2313-2319.1990
27. Lepay D. A., Nathan C. F., Steinman R. M., Murray H. W., Cohn Z. A. Murine Kupffer cells. Mononuclear phagocytes deficient in the generation of reactive oxygen intermediates. Journal of Experimental Medicine. 1985; 161 (5): 1079–1096. https://doi.org/10.1084/jem.161.5.1079
28. Mandel T. E., Cheers C. Resistance and susceptibility of mice to bacterial infection: histopathology of listeriosis in resistant and susceptible strains. Infection and Immunity. 1980; 30 (3): 851–861. https://doi.org/10.1128/iai.30.3.851-861.1980
29. De Chastellier C., Berche P. Fate of Listeria monocytogenes in murine macrophages: evidence for simultaneous killing and survival of intracellular bacteria. Infection and Immunity. 1994; 62 (2): 543–553. https://doi.org/10.1128/iai.62.2.543-553.1994
30. Portnoy D. A. Innate immunity to a facultative intracellular bacterial pathogen. Current Opinion in Immunology. 1992; 4 (1): 20–24. https://doi.org/10.1016/0952-7915(92)90118-x
31. Terentjeva M., Šteingolde Ž., Meistere I., Elferts D., Avsejenko J., Streikiša M., et al. Prevalence, genetic diversity and factors associated with distribution of Listeria monocytogenes and other Listeria spp. in cattle farms in Latvia. Pathogens. 2021; 10 (7):851. https://doi.org/10.3390/pathogens10070851
32. Nightingale K. K., Schukken Y. H., Nightingale C. R., Fortes E. D., Ho A. J., Her Z., et al. Ecology and transmission of Listeria monocytogenes infecting ruminants and in the farm environment. Applied and Environmental Microbiology. 2004; 70 (8): 4458–4467. https://doi.org/10.1128/aem.70.8.4458-4467.2004
33. Hilliard A., Leong D., O’Callaghan A., Culligan E. P., Morgan C. A., DeLappe N., et al. Genomic characterization of Listeria monocytogenes isolates associated with clinical listeriosis and the food production environment in Ireland. Genes. 2018; 9 (3):171. https://doi.org/10.3390/genes9030171
34. Demaître N., Van Damme I., De Zutter L., Geeraerd A. H., Rasschaert G., De Reu K. Occurrence, distribution and diversity of Listeria monocytogenes contamination on beef and pig carcasses after slaughter.Meat Science. 2020; 169:108177. https://doi.org/10.1016/j.meatsci.2020.108177
35. Aiyedun J. O., Olatoye O. I., Oludairo O. O., Adesope A. O., Ogundijo O. Occurrence, antimicrobial susceptibility and biofilm production in Listeria monocytogenes isolated from pork and other meat processing items at OkoOba abattoir, Lagos State, Nigeria. Sahel Journal of Veterinary Sciences. 2020; 17 (4): 24–30. https://saheljvs.org/index.php/saheljvs/article/view/111/37
36. McLauchlin J., Grant K. A., Amar C. F. L. Human foodborne listeriosis in England and Wales, 1981 to 2015. Epidemiology and Infection. 2020; 148:e54. https://doi.org/10.1017/s0950268820000473
37. Al S., Disli H. B., Hizlisoy H., Ertas Onmaz N., Yildirim Y., Gonulalan Z. Prevalence and molecular characterization of Listeria monocytogenes isolated from wastewater of cattle slaughterhouses in Turkey. Journal of Applied Microbiology. 2022; 132 (2): 1518–1525. https://doi.org/10.1111/jam.15261
38. Blenden D. C. Latency in listeriosis: a review and assessment. Canadian Journal of Public Health. 1974; 65 (3): 198–201. https://pubmed.ncbi.nlm.nih.gov/4840130
39. Szatalowicz F. T., Blenden D. C., Khan M. S. Occurrence of Listeria antibodies in select occupational groups. Canadian Journal of Public Health. 1970; 61 (5): 402–406. https://pubmed.ncbi.nlm.nih.gov/4991114
40. Morin D. E. Brainstem and cranial nerve abnormalities: listeriosis, otitis media/interna, and pituitary abscess syndrome. Veterinary Clinics of North America: Food Animal Practice. 2004; 20 (2): 243–273. https://doi.org/10.1016/j.cvfa.2004.02.007
41. Yatusevich A., Maximovich V., Semyonov V. Listeriosis: veterinary and human medical problem. Animal Husbandry of Russia. 2015; (12): 29–32. https://elibrary.ru/vlnpjf (in Russ.)
42. Stein H., Stessl B., Brunthaler R., Loncaric I., Weissenböck H., Ruczizka U., et al. Listeriosis in fattening pigs caused by poor quality silage – a case report. BMC Veterinary Research. 2018; 14:362. https://doi.org/10.1186/s12917-018-1687-6
43. Lopez A., Bildfell R. Neonatal porcine listeriosis. Canadian Veterinary Journal. 1989; 30 (10): 828–829. https://pubmed.ncbi.nlm.nih.gov/17423443
44. Moreno L. Z., Paixão R., Gobbi D. D., Raimundo D. C., Ferreira T. P., Hofer E., et al. Characterization of atypical Listeria innocua isolated from swine slaughterhouses and meat markets. Research in Microbiology. 2012; 163 (4): 268–271. https://doi.org/10.1016/j.resmic.2012.02.004
45. Rajkhowa S., Neher S., Pegu S. R., Sarma D. K. Bacterial diseases of pigs in India: A review. Indian Journal of Comparative Microbiology, Immunology and Infectious Diseases. 2018; 39 (2si): 29–37. https://doi.org/10.5958/0974-0147.2018.00014.4
46. Isom L. L., Khambatta Z. S., Moluf J. L., Akers D. F., Martin S. E. Filament formation in Listeria monocytogenes. Journal of Food Protection. 1995; 58 (9): 1031–1033. https://doi.org/10.4315/0362-028X-58.9.1031
47. Linde K., Fthenakis G. C., Lippmann R., Kinne J., Abraham A. The efficacy of a live Listeria monocytogenes combined serotype 12a and serotype 4b vaccine. Vaccine. 1995; 13 (10): 923–926. https://doi.org/10.1016/0264410X(95)00010-X
48. Braun U., Stehle C., Ehrensperger E. Clinical findings and treatment of listeriosis in 67 sheep and goats. Veterinary Record. 2002; 150 (2): 38–42. https://doi.org/10.1136/vr.150.2.38
49. Dunnett E., Florea L., Thurston L., Floyd T., Collins R., Otter A. Deaths of weaned lambs with visceral Listeria ivanovii infections. Veterinary Record Case Reports. 2020; 8 (4):e001254. https://doi.org/10.1136/vetreccr-2020-001254
50. Gonzalez-Zorn B., Suarez M. Listeria y listeriosis. Profesión Veterinaria. 2009; 16 (71): 58–67. (in Spanish)
51. Keelara S., Malik S. V. S., Nayakvadi S., Das S., Barbuddhe S. B. Isolation and characterization of Listeria spp. from organized and migratory sheep flocks in India. Advances in Animal and Veterinary Sciences. 2015; 3 (6): 325–331. http://dx.doi.org/10.14737/journal.aavs/2015/3.6.325.331
52. Johnson G. C., Maddox C. W., Fales W. H., Wolff W. A., Randle R. F., Ramos J. A., et al. Epidemiologic evaluation of encephalitic listeriosis in goats. Journal of the American Veterinary Medical Association. 1996; 208 (10): 1695–1699. https://doi.org/10.2460/javma.1996.208.10.1695
53. Kennedy S., Passler T., Stockler J., Bayne J. Risk factors associated with outcome in goats with encephalitic listeriosis: A retrospective study of 36 cases from 2008 to 2021. Journal of Veterinary Internal Medicine. 2023; 37 (3): 1271–1277. https://doi.org/10.1111/jvim.16704
54. Fentahun T., Fresebehat A. Listeriosis in small ruminants: A review. Advances in Biological Research. 2012; 6 (6): 202–209. https://core.ac.uk/download/pdf/199937204.pdf
55. Yousif Y. A., Joshi B. P., Ali H. A. Ovine and caprine listeric encephalitis in Iraq. Tropical Animal Health and Production. 1984; 16: 27–28. https://doi.org/10.1007/BF02248925
56. Seastone C. V. Pathogenic organisms of the genus Listerella. Journal of Experimental Medicine. 1935; 62 (2): 203–212. https://doi.org/10.1084/jem.62.2.203
57. Gray M. L. Listeriosis in fowls – a review. Avian Diseases. 1958; 2 (3): 296–314. https://doi.org/10.2307/1587530
58. Crespo R., Garner M. M., Hopkins S. G., Shah D. H. Outbreak of Listeria monocytogenes in an urban poultry flock. BMC Veterinary Research. 2013; 9:204. https://doi.org/10.1186/1746-6148-9-204
59. McLauchlin J., Aird H., Amar C., Barker C., Dallman T., Elviss N., et al. Listeria monocytogenes in cooked chicken: detection of an outbreak in the United Kingdom (2016 to 2017) and analysis of L. monocytogenes from unrelated monitoring of foods (2013 to 2017). Journal of Food Protection. 2020; 83 (12): 2041–2052. https://doi.org/10.4315/jfp-20-188
60. Cummins T. J., Orme I. M., Smith R. E. Reduced in vivo nonspecific resistance to Listeria monocytogenes infection during avian retrovirusinduced immunosuppression. Avian Diseases. 1988; 32 (4): 663–667. https://doi.org/10.2307/1590981
61. Tavakkoli H., Rahmani M., Ghanbarpoor R., Kheirandish R. Induced systemic listeriosis in Alectoris chukar chicks: clinical, histopathological and microbiological findings. British Poultry Science. 2015; 56 (6): 651–657. https://doi.org/10.1080/00071668.2015.1113505
62. Barnes H. J. Miscellaneous and sporadic bacterial infections. In: Diseases of Poultry. Ed. by Y. M. Saif. 11th ed. Ames: Iowa State Press; 2003; 845–862.
63. Bailey J. S., Fletcher D. L., Cox N. A. Recovery and Serotype Distribution of Listeria monocytogenes from broiler chickens in the Southeastern United States. Journal of Food Protection. 1989; 52 (3): 148–150. https://doi.org/10.4315/0362-028X-52.3.148
64. Cooper G., Charlton B., Bickford A., Cardona C., Barton J., Channing-Santiago S., Walker R. Listeriosis in California broiler chickens. Journal of Veterinary Diagnostic Investigation. 1992; 4 (3): 343–345. https://doi.org/10.1177/104063879200400322
65. Avery S. M., Buncic S. Differences in pathogenicity for chick embryos and growth kinetics at 37 °C between clinical and meat isolates of Listeria monocytogenes previously stored at 4 °C. International Journal of Food Microbiology. 1997; 34 (3): 319–327. https://doi.org/10.1016/s01681605(96)01191-9
66. Rothrock M. J. Jr., Davis M. L., Locatelli A., Bodie A., McIntosh T. G., Donaldson J. R., Ricke S. C. Listeria occurrence in poultry flocks: Detection and potential implications. Frontiers in Veterinary Science. 2017; 4:125. https://doi.org/10.3389/fvets.2017.00125
67. Ryser E. T. Listeria. In: Foodborne Infections and Intoxications. Ed. by J. Glenn Morris, D. J. Vugia. 5th ed. Academic Press; 2021; Chapter 11: 201–220. https://doi.org/10.1016/B978-0-12-819519-2.00028-1
About the Author
P. N. Shastin
Federal Scientific Centre VIEV
Russian Federation
Russian Federation
Pavel N. Shastin, Cand. Sci. (Veterinary Medicine), Senior Researcher, Laboratory for Diagnostics and Control of Antibiotic Resistance of Pathogens of the Most Clinically Significant Infectious Animal Diseases
24/1 Ryazansky Prospekt, Moscow 109428
Review
For citations:
Shastin P.N. Currently important pathogenic Listeria species affecting animals and birds (review). Veterinary Science Today. 2024;13(4):307-313. https://doi.org/10.29326/2304-196X-2024-13-4-307-313
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