Listeriosis in Animals

Listeria monocytogenes is the most common cause of listeriosis in domestic animals, and multiple serotypes have been documented; additionally, other pathogenic species of Listeria have been documented. Listeria are small, motile, gram-positive, non–spore-forming, catalase-positive, diphtheroid coccobacilli and facultative anaerobes that grow in a wide temperature range (4–44°C [39–111°F]). This organism can be resistant to detergents and sanitizers and can persist in cold, damp environments for years.

Listeria's ability to grow at 4°C is an important diagnostic aid for isolating the organism from brain tissue or for finding listeria when other organisms are present; the process of isolating the organism in colder-than-normal culture environments is called cold enrichment. Listeria can sometimes be isolated from culture without cold enrichment, and other methods of enrichment are also used.

Primary isolation is enhanced under microaerophilic conditions. L monocytogenes is a ubiquitous saprophyte that lives in a plant-soil environment. It has been isolated from at least 42 species of domestic and wild mammals and 29 species of birds, as well as fish, crustaceans, insects, sewage, water, silage and other feedstuffs, milk, cheese, meconium, feces, and soil (1).

The natural reservoirs of L monocytogenes appear to be soil and mammalian GI tracts, both of which contaminate vegetation. Grazing animals ingest the organism and further contaminate vegetation and soil. Animal-to-animal transmission appears to primarily occur via the fecal-oral route; research does not suggest that other routes are significant in maintenance of the pathogen (1).

Listeriosis occurs most often in winter and spring in temperate and cooler climates or in warmer temperatures when animals are concentrated near contaminated, wet sources. Listeriosis has been historically associated with silage feeding; the less acidic pH of spoiled silage enhances multiplication of L monocytogenes. Outbreaks are reported to occur after feeding poor-quality silage. Removing or changing silage in feed rations often stops the spread of listeriosis; however, feeding the same silage months later could result in new cases.

A 2025 meta-analysis of listeriosis in ruminants suggested that the link between silage feeding and listeriosis might not be as direct as was once considered (2). Other sources of infection include feed bunks with moist, feces-contaminated feed, rotting round bales, decaying weed feeders, other moist feces-contaminated feed, or contamination from excretions (eg, feces, milk, urine, or oculonasal secretions) of infected animals.

Listeria monocytogenes lives as a saprophyte in the soil, persists for years in cold damp environments associated with animal contamination, and remains capable of invasive disease in a wide variety of animals. Listeria infections are most commonly associated with rhombencephalitis, septicemia, abortion, and latent infection, and less commonly with cardiac or ocular manifestations.

Exposure is often oral; host cell invasion is accomplished by multiple virulence factors associated with cell invasion and immune evasion. In neurological listeriosis of ruminants, the organism likely travels via axonal migration along the cranial nerves (most commonly the trigeminal nerve) to the brainstem and can spread to other regions in the brain, likely by intracerebral axonal migration. Microabscesses in the brain are an important feature of listeriosis. Diffuse meningitis and meningoencephalitis are rarely reported in ruminants. Listeria crosses tissue barriers such as the GI tract, placenta, and blood-brain barrier. This ability to cross barriers and invade tissues also results in septicemic, cardiac, and reproductive forms of disease.

Various manifestations of listeriosis occur in all susceptible species and are associated with characteristic clinical syndromes:

• rhombencephalitis in adult ruminants and occasionally camelids

• abortion and perinatal death in many species

• septicemia in neonatal ruminants and monogastric animals (and occasionally camelids)

• septicemia with myocardial or hepatic necrosis (or both) in poultry

Cardiac signs in camelids and primary ocular signs ("silage eye") in ruminants are less commonly reported.

Septicemic or visceral listeriosis is most common in monogastric animals, including pigs, dogs, cats, domestic and wild rabbits, and many other small mammals. These animals may play a role in transmission of L monocytogenes. This form of disease also occurs in young ruminants before the rumen is functional. Although rare, septicemia has been reported in older domestic ruminants and deer. The septicemic form affects organs other than the brain; the principal lesion is focal hepatic necrosis.

The uterus of all domestic animals, especially ruminants, is susceptible to infection with L monocytogenes at all stages of pregnancy, which can result in placentitis, fetal infection and death, abortion, stillbirths, neonatal deaths, metritis, and possibly viable carriers. Metritis has little or no effect on subsequent reproduction; however, Listeria can be shed for 1 month or longer via the vagina and milk.

Animals can become carriers and shed Listeria in the feces, birthing fluids during abortion, milk in lactating animals, or other bodily secretions. Infections acquired via ingestion tend to localize in the intestinal wall and result in prolonged fecal excretion. It has been postulated that contaminated silage results in latent infections, often approaching 100% of the exposed herd or flock; however, clinical signs of listeriosis are evident in only a few animals.

Cardiac signs of listeriosis are reported in some animals, including poultry, camelids, and humans. Myocardial necrosis is a key finding of listeriosis in poultry. Mural and valvular endocarditis associated with Listeria infection are reported in camelids.

Clinical signs of listeriosis vary according to the organs affected. In neurological listeriosis of ruminants, clinical signs depend on which cranial nerves are damaged and the location and extent of rhombencephalitis. The most common neurological signs are asymmetric and include the following:

• trigeminal and facial nerve paralysis

• ipsilateral weakness

• circling

• dysphagia

• systemic signs of illness, including depression and recumbency

The most common clinical signs are due to lesions in cranial nerves V, VII, and VIII; however, lesions or clinical signs referable to cranial nerves III-–XII are reported. Additionally, lesions in the reticular activating system and damage to long tracts likely contribute to clinical signs of depression and weakness (see images of listeriosis in goats with facial paralysis, excessive salivation, and cranial nerve deficits).

Severe dehydration, metabolic acidosis, and electrolyte abnormalities may be present secondary to dysphagia and ptyalism. Ocular damage can result from inability to blink and/or lack of lacrimation secondary to cranial nerve V and VII dysfunction.

Listeriosis, facial paralysis, goat

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Neurological listeriosis in a goat with facial paralysis due to damage to the facial and trigeminal nerves.

Courtesy of Dr. Thomas Lane.

Listeriosis, salivation, goat

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Goat with listeriosis showing profuse salivation due to damage to the facial and trigeminal nerves.

Courtesy of Dr. Philip Scott.

Listeriosis, cranial nerve deficits, cow

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Depression, head turn, ear droop, tongue protruding, and enophthalmos in a dairy heifer with clinical signs of neurological listeriosis. The patient was unable to blink but was able to retract the globe and allow the nictitating membrane to pass over the cornea during menace response tests

Courtesy of Dr. Sarah Depenbrock.

The neurological form of listeriosis affects all ages and sexes of animals and is usually sporadic but sometimes occurs as an epidemic. Neurological listeriosis can recur on the same premises in successive years. Usually, only a small percentage of the herd or flock is clinically affected in an outbreak; however, in exceptional circumstances, the percentage can be large.

The course of neurological listeriosis in sheep and goats can be rapid; in severe cases, death can occur 24–48 hours after onset of clinical signs. In cattle, the disease course is typically less acute. The recovery rate is highly variable; some animals do recover with treatment.

Initially, affected animals are anorectic, depressed, and disoriented. They may propel themselves into corners, lean against stationary objects, or circle toward the affected side. Facial paralysis with a drooping ear, deviated muzzle, flaccid lip, and lowered eyelid often develops on the affected side; lack of a menace response and continuous ptyalism are also characteristic. Food material often becomes impacted in the cheek because of paresis or paralysis of the muscles used for mastication. Terminally affected animals fall and when unable to rise, lie on the same side. (See video of abnormal palpebral reflex, neurological listeriosis.)

Abnormal palpebral reflex and ...

video

Neurological listeriosis also occurs in camelids, although less frequently, with clinical signs similar to those in ruminants.

Listeriosis is relatively uncommon in pigs, with encephalitis occurring in older pigs and septicemia in those < 1 month old; it has a rapid fatal course in swine.

Reproductive signs caused by Listeria usually include abortion in the last trimester without prior clinical signs; however, it can occur at any stage of gestation. Fetuses usually die in utero; however, stillbirths and neonatal deaths also occur. The abortion rate is highly variable, with an average of approximately 13% across reports in the literature (2). Fatal septicemia of the dam secondary to metritis is rare. Encephalitis and abortion do not usually occur simultaneously in the same herd or flock.

In affected animals, the placenta shows evidence of placentitis, including necrotic, friable, dark red cotyledons, and thick, opaque intercotyledonary regions that have a brown exudate. Aborted fetuses can be autolyzed or not and can have small necrotic foci in the liver and/or lung. (See Abortion in Large Animals.)

Cardiac forms of Listeria in poultry are associated with sepsis, and affected birds may become lethargic prior to death. Clinical signs of endocarditis associated with Listeria in camelids can include weakness, respiratory signs, fever, and murmurs.

Lesions in Listeriosis

In the neurological form of Listeria, there are few gross lesions except for some congestion of meninges or reddening of the brainstem. Lesion location and chronicity support neuronal travel of listeria to the brainstem and spread from the brainstem to other parts of the brain; the location and extent of spread varies among cases. Histopathological lesions can be found in all cranial nerve nuclei located in the brainstem (nuclei for cranial nerves III–XII), brainstem, upper cervical spinal cord, midbrain, thalamus, hippocampus, basal nuclei, cerebral cortex, and cerebellum.

In septicemic listeriosis, small necrotic foci can be found in any organ, especially the liver. In calves that die at < 3 weeks old, in addition to focal hepatic necrosis, marked hemorrhagic gastroenteritis frequently occurs.

Gross findings in aborted fetuses typically include slight to marked autolysis, clear to blood-tinged fluid in serous cavities, and numerous small necrotic foci in the liver. Necrotic foci can be found in other viscera (eg, lung and spleen). Shallow erosions, 1–3 mm in diameter, may be evident in abomasal mucosa; however, autolytic changes can mask these lesions. Gram-stained smears of abomasal contents reveal numerous gram-positive, pleomorphic coccobacilli (see photomicrograph of postmortem brainstem samples).

Listeria monocytogenes, brainstem, postmortem specimen, phot...

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Tissue smear of postmortem brainstem samples from an animal with listeriosis. Note the presence of large numbers of the gram-positive bacterium Listeria monocytogenes. Gram stain, high power.

Courtesy of Dr. John Prescott.

• Clinical signs

• CSF analysis

• Culture, immunofluorescence assay, or PCR assay

Antemortem diagnosis of neurological listeriosis can be supported by findings of CSF analysis. Samples of lumbosacral CSF can be collected using local anesthesia. In cases of listeriosis, the CSF has an increased protein concentration and a mild pleocytosis composed of large mononuclear cells; species-specific reference intervals should be used.

Listeriosis is confirmed by isolation and identification of L monocytogenes via culture, PCR assay, or other molecular testing of CSF. In septicemic listeriosis, blood cultures or PCR assay can be used to confirm the diagnosis. In abortive listeriosis, placenta and fetal tissues can by analyzed by culture or molecular techniques such as PCR assay. Immunofluorescence assay is also available for tissue testing.

Many different diseases can result in neurological signs in ruminants; listeriosis should be strongly suspected when depression and cranial nerve deficits are present, especially when deficits are asymmetric. Other lesions, such as otitis, brain abscesses, or parasite migrations, can result in unilateral or asymmetric neurological disease and should also be considered. Other causes of depression and recumbency should be considered, including rabies virus, thromboembolic meningoencephalitis, other causes of encephalitis, polioencephalomalacia, and other causes of systemic illness, such as ketosis or sepsis; however, these diseases are less likely to present with asymmetric neurological deficits.

Animals with mass lesions in the brain (eg, brain abscesses, otitis, or parasite migrations in the CNS) can develop overlapping or similar asymmetric neurological deficits (such as circling) and proprioceptive deficits; however, unless the lesion happens to affect cranial nerves or their nuclei, these animals should not have cranial nerve deficits. Vestibular disease is not uncommon in growing ruminants; these animals may show ipsilateral spontaneous nystagmus or strabismus, but typically they remain bright and alert without trigeminal nerve dysfunction. These diseases can be further differentiated antemortem using CSF analysis (eg, cytological evaluation, protein concentration, culture, and molecular diagnostics, such as PCR assay) or advanced imaging (eg, CT or MRI) in cases where substantial investment in antemortem diagnostics is feasible and desired.

Specimens of choice for postmortem diagnosis are brain tissue from animals with CNS involvement, aborted placenta and fetus from abortion cases, and affected tissues such as the liver in septicemic listeriosis. L monocytogenes has been isolated from blood, spinal fluid, nasal discharge, urine, feces, placenta, fetuses, and milk of clinically affected ruminants. Serological analysis is not used routinely for diagnosis because many healthy animals have been exposed to Listeria and thus have high titers.

• Administration of parenteral antimicrobial therapy

• Supportive care

Recovery from listeriosis depends on early, aggressive antimicrobial treatment. The prognosis for recovery after treatment is worse for animals that are more severely affected, such as those that are down and unable to rise.

The in vitro susceptibility of L monocytogenesisolates to a variety of drugs used in human and veterinary medicine has been reported (3, 1). Drugs commonly used in veterinary medicine with reports of Listeria susceptibility include penicillin, ampicillin, oxytetracycline, erythromycin, florfenicol, and trimethoprim/sulfonamide. Antimicrobial resistance of Listeria isolates from animals has been reported to most classes of antimicrobial drugs used commonly in veterinary medicine. Susceptibility testing of clinical samples can guide antimicrobial therapy.

No antimicrobial drugs are labeled for the treatment of listeriosis in ruminants in the US.

The use of approved antimicrobials for the extralabel indication of listeriosis is allowable in the US as long as it is within a valid veterinary-client-patient relationship and done in accordance with the Animal Medicinal Drug Use Clarification Act. Outside of the US, extralabel antimicrobial use for listeriosis should be performed in accordance with regional laws and regulations.

Antimicrobial drug concentrations in the CNS of animals with listeriosis is not well described; however, presumably the inflammation associated with CNS disease provides increased access of antimicrobial drugs across the damaged blood-brain barrier compared to access in healthy animals, for which drug tissue distribution is more commonly published.

Extralabel high dosage of penicillin was historically considered the drug of choice for neurological listeriosis in ruminants. However, for many reasons (eg, drug residue avoidance, ability to obtain the drug, and need for IM dosing every 12 hours), some veterinarians prefer to use other antimicrobial drugs.

Initiation of therapy with antimicrobials that can be administered IV is desirable, particularly in cases with evidence of poor tissue perfusion. Water-soluble forms of penicillin (such as potassium penicillin), have been recommended at dosages between 22,000 and 44,000 U/kg, IV, every 6 hours. Later in the course of treatment, penicillin therapy can be switched to penicillin procaine G at a dosage of 22,000–44,000 U/kg, IM, every 12–24 hours (procaine penicillin G cannot be administered IV) (4, 5, 6).

Common alternatives to penicillin treatment include oxytetracycline and florfenicol. Both are lipid-soluble drugs with some ability to cross the blood-brain barrier; however, florfenicol has particularly high lipid solubility compared to the other drugs discussed. IV oxytetracycline has also been used at the label dose of 10 mg/kg, IV, every 24 hours for initial therapy, followed by 20 mg/kg, SC, every 48 hours (both within label dose, route, and frequency) once tissue perfusion has improved (5, 7).

Injectable florfenicol, at bovine label doses and routes, has also been used to treat the neurological form of listeriosis in ruminants. Duration of antimicrobial therapy is guided by patient response to treatment. Clinical signs may indicate that duration of therapy should extend past the duration of use specified by the label. Careful attention should be paid to antimicrobial drug selection for each case on the basis of signalment, intended use, and any comorbidities. For example, florfenicol is typically not administered to animals being used for milk production because of label instructions not to use in dairy cattle ≥ 20 months old and the risk of very prolonged milk residues.

Contraindications to specific antimicrobial therapy should be considered. Renal damage can result from treatment with potentially nephrotoxic drugs such as oxytetracycline in dehydrated or hypovolemic animals or animals with existing renal disease;fluid therapy prior to or in combination with other treatments, especially oxytetracycline therapy, might be warranted. Any extralabel drug use (deviation in species, production class, age, indication, dose, route, volume injected, frequency, or duration of therapy) requires provision of a scientifically based and sufficiently extended withdrawal interval for any animal products originating from treated animals.

Anti-inflammatory treatment is often indicated. Either NSAIDs such as flunixin meglumine (1.1–2.2 mg/kg, IV, every 24 hours [8]) or steroids such as dexamethasone (0.1–0.5 mg/kg, IM or IV, every 24 hours [4]) may be used. These drugs should not be used in combination in ruminants.Treatment of animals with infectious disease with steroids is controversial; it may increase shedding of Listeria, and pregnant ruminants may abort after dexamethasone treatment (depending on the species and stage of gestation). Contraindications to anti-inflammatory drugs should be considered, such as in animals with evidence of renal disease, dehydration, hypovolemia, or suspicion of abomasal ulcers. Fluid therapy may be indicated prior to or concurrently with anti-inflammatory treatment.

Supportive therapy is required for animals having difficulty eating, drinking, or moving about. Fluid therapy with attention to electrolyte deficiencies and acid-base status is often indicated, particularly in animals that have been off feed or are dysphagic. Dysphagic ruminants can lose saliva continuously, which can result in metabolic acidosis due to loss of salivary bicarbonate; additionally, fluid deficits can result in increased lactate production, which can contribute to metabolic acidosis. Provision of soft, palatable feed in small, easily prehended pieces can be helpful for dysphagic animals. Easy access to food and water directly next to recumbent animals or animals with limited mobility is needed.

For animals that cannot eat because of severe dysphagia, some nutrition can be provided via soaked pelleted feeds administered by ruminal intubation. A rumenostomy can be performed for longer-term feeding of animals physically incapable of eating. Regular provision of clean, deep, soft bedding is necessary for recumbent animals to limit damage secondary to recumbency.

Additional medications or treatments for comorbidities might be necessary. Animals with abnormal rumen function (which can occur for a variety of reasons associated with listeriosis, including neurological dysfunction, systemic illness, and dysphagia) should receive thiamine supplementation to treat or prevent concurrent thiamine deficiency and subsequent polioencephalomalacia. Additionally, polioencephalomalacia is a common differential diagnosis for ruminants with central neurological signs, and thus thiamine treatment is often initiated as part of initial empirical therapy for the neurologically abnormal ruminant. Eye lubrication and treatment for ocular damage secondary to inability to blink might also be necessary.

Clinical progress of treated animals is variable. In general, animals treated early in the course of disease respond more favorably and more rapidly; recumbent and severely affected animals have a worse prognosis for recovery and generally require a longer course of treatment.

Affected animals should be segregated. Prevention should focus on feed management and hygiene. If silage is being fed, further feeding of silage temporally associated with disease onset should be avoided. Improperly ensiled or spoiled silage should be avoided. Silage with a more acidic pH discourages multiplication of L monocytogenes; published methods are available to manage silage pH. For more information on properly ensiling ruminant feeds, please consult your local extension specialist and the peer-reviewed ruminant nutrition literature.

Regardless of silage feeding, old, wet, or decomposing feed should not be fed and should be regularly removed from feeders. Wooden feeders with decomposing vegetation should be avoided. Fecal contamination of feed and water should be avoided.

Vaccination for Listeria in animals has been studied; the potential benefit of any vaccination should be weighed against the costs or risks, especially given the often sporadic nature of listeriosis in animals. No veterinary vaccines are approved for prevention of listeriosis in the US.

All materials from suspected clinical cases of listeriosis carry the risk of zoonotic infection and should be handled with caution. Aborted fetuses, necropsy of septicemic animals, and handling of infected tissues present the greatest hazards. Humans have developed fatal meningitis, sepsis, and papular exanthema on the arms after handling aborted material. Pregnant animals and women should be protected from infection because of danger to the animal, woman, and fetus, with possible abortion, stillbirth, and infection of neonates. Most human cases involve older patients, pregnant women, or immunocompromised people. Milk from affected animals should not be consumed.

L monocytogenes can be isolated from milk of mastitic, aborting, and apparently healthy cows. Excretion in milk is usually intermittent but can persist for many months.Infected milk can remain hazardous after pasteurization because the organism can survive certain forms of pasteurization. Listeria has also been isolated from milk and cheeses from sheep and goats.

• Listeriosis fact sheet. The Center for Food Security and Public Health.

• Bandelj P, Jamnikar-Ciglenecki U, Ocepek M, Blagus R, Vengust M. Risk factors associated with fecal shedding of Listeria monocytogenes by dairy cows and calves. J Vet Intern Med. 2018 Sep;32(5):1773-1779.

• Oevermann A, Di Palma S, Doherr MG, Abril C, Zurbriggen A, Vandevelde M. Neuropathogenesis of naturally occurring encephalitis caused by Listeria monocytogenes in ruminants. Brain Pathol. 2010;20(2):378-390.

• Bagatella S, Tavares-Gomes L, Oevermannet A. Listeria monocytogenes at the interface between ruminants and humans: a comparative pathology and pathogenesis review. Vet Pathol. 2021;59(2):186-210.

• McLane MJ, Schlipf JW Jr, Margiocco ML, Gelberg H. Listeria associated mural and valvular endocarditis in an alpaca. J Vet Cardiol. 2008;10(2):141-145.

• Smith MC, Sherman DM. Goat Medicine. 3rd ed. Wiley-Blackwell; 2022.

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