Listeriosis

D J SCHNEIDER

GENERAL INTRODUCTION: REGULAR, NON-SPORING, GRAM-POSITIVE RODS

Introduction

Listeriosis, caused by Listeria monocytogenes, is characterized in some livestock species by three distinct syndromes of meningoencephalitis, abortion or stillbirth, and neonatal septicaemia.^{6, 33} Mastitis and keratoconjunctivitis have also been recorded.^{1, 3} While meningoencephalitis occurs most commonly in ruminants, septicaemia is more frequently found in monogastric animals and young ruminants. The disease is rare in humans and, with the exception of its cutaneous form, is often fatal.^{1, 6, 34}

Listeria monocytogenes is widely distributed in nature, but the disease is usually sporadic and its prevalence low.^{24, 32, 34} Listeriosis particularly affects sheep, goats and cattle. Although the first isolation of L. monocytogenes was from a South African gerbil in 1927,²⁶ the disease has only been reported in goats,⁹ sheep²⁴ and chinchillas⁸ in this country. The disease is not of significant economic importance in southern Africa.

Aetiology

Listeria monocytogenes are Gram-positive, non-acid-fast, non-spore-forming, short, rod-shaped bacteria. Five serotypes, designated 1 to 5, and a number of subtypes have been identified.^{6, 23, 25, 34} Serotype 5 (now called Listeria ivanovii²⁹) is commonly isolated abroad from cases of listerial abortion in sheep, but is of low pathogenicity.^{6, 7}

The optimal growth temperature of the organism is between 30 and 37 °C but some growth may occur in the range of 4 to 44 °C. It propagates best at neutral or slightly alkaline pH and is usually killed at a pH below 5,0. The organism is readily cultured on ordinary media under aerobic conditions, but growth is facilitated by an atmosphere containing 10 per cent carbon dioxide.^{5, 14}

Epidemiology

Listeriosis is found throughout the world. It is, however, more common in countries and regions with a cold, temperate temperate climate, such as New Zealand, certain parts of Australia, North America, Europe, and the UK, than in those with a tropical or subtropical climate. In some countries the prevalence of listeriosis has increased during recent years.^{1, 22, 23} Clinical disease occurs particularly during late winter and early spring.^{4, 6, 21, 22, 32}

Sheep, goats and cattle are the livestock species most frequently affected. The morbidity is usually less than 10 per cent, but the mortality rate in those suffering from meningoencephalitis is often 100 per cent.^{6, 31}

Listeria monocytogenes is widely distributed in nature and has been isolated from a wide variety of healthy and diseased mammals and bird species, as well as from soil, water, sewage, mud and silage.^{5, 18, 32} It may also be found on raw vegetables and fruit. A large proportion of healthy sheep and goats are subclinical carriers of L. monocytogenes, excreting organisms in their faeces and milk when stressed.¹⁵ The organism may withstand low temperature pasteurization of milk, and may be found in dairy products in which it constitutes a danger to human health. It tolerates freezing.³⁰

Listeriosis is often associated with the feeding of large quantities of poor quality silage with a pH in excess of ^{5,5.16, 31, 32, 34} Spoilage and a high pH of silage resulting from poor preparation and maintenance result in a growth of the bacteria, particularly in the top and side layers of the silage.^{10, 13, 23} It is also suspected that, apart from nutritional stress, reduced resistance of the animal because of adverse environmental factors may predispose to disease. ^{24, 31, 34} In sheep, cases of listerial meningoencephalitis may occur 30 days after their initial introduction to silage feeding.²³

Encephalitis has been produced experimentally by the inoculation of L. monocytogenes into the dental pulp⁴ and lips of sheep and goats;² in these cases the incubation periods ranged between 14 and 28 days.

The higher prevalence of listerial meningoencephalitis in certain age groups of sheep has been linked to the changing of teeth in early spring.⁴ It is suspected that ingested L. monocytogenes reach the fine dental terminals of the trigeminal nerve and so cause an ascending neuritis and meningoencephalitis.

Pathogenesis

Listeria monocytogenes is an intracellular organism.¹⁵ In the meningoencephalitis syndrome, these organisms are usually present only in the brain.

Although the pathway by which bacteria reach the brain is unclear, it is thought that they probably gain entrance to the body through wounds in the mucosa of the oral cavity. They then reach the brain stem via branches of the trigeminal nerve. The unilateral occurrence of micro-abscesses and the perivascular infiltration of lymphocytes, which are largely restricted to the brain stem (pons and medulla oblongata), are supportive of this view.¹⁹

Following ingestion, organisms may also penetrate the intestinal mucosa to produce a clinically inapparent infection, a bacteraemia with localization of bacteria in various organs, or a fatal septicaemia. In pregnant animals, organisms localize particularly in the uterus. Infection early in pregnancy usually causes abortion, while in late pregnancy it results in stillbirth or in lambs which develop fatal septicaemia soon after birth.⁶

Clinical signs

The syndromes of meningoencephalitis, abortion and septicaemia seldom occur together in an outbreak.²³

In livestock, meningoencephalitis occurs most commonly in ruminants. In goats, sheep and calves the course of the disease is usually two to three days, while in adult cattle it ranges from one to two weeks. During the early stages of disease the rectal temperature is elevated, whereas it is normal to subnormal in more advanced cases. Neurological signs vary according to the location and severity of the lesions in the brain stem. Affected animals are depressed, walk in circles and show incoordination, tilting of the head, and evidence of unilateral facial nerve paralysis characterized by drooping of the lips, ears and eyelids, and paralysis of the muscles of the jaw and pharynx which interferes with mastication and swallowing. They often stand for long periods with food hanging from their mouths and drooling saliva. Lethargy frequently progresses to somnolence, which is followed by generalized paralysis and death. Occasional convulsions and paddling movements with the forelimbs may be seen in terminal cases. Impaired respiration may occur as a result of the inflammatory changes in the brain stem.²⁷ A localized myelitis, manifested clinically by paralysis of one limb, has been recorded in lambs, but is more common in adult ruminants.¹¹ Keratoconjunctivitis has been reported in cattle.²⁷

Sporadic abortions as a result of listeriosis are more common in cattle than in sheep and goats, but rarely reach a rate of 15 per cent. Retained placentas, clinical illness and fever are common in cows and ewes after abortion has taken place in advanced pregnancy. Death of the dam due to septicaemia sometimes follows retention of the foetus. Ewes abort 7 to 11 days after infection; they are asymptomatic before they abort.⁷ Aborted foetuses are usually decomposed. Individual animals may abort again during subsequent pregnancies.⁶

Septicaemic listeriosis is the most common form encountered in foetuses and neonates of ruminants, and is sometimes found in monogastric animals. In these cases many organs and tissues are affected.^{6, 7, 12}

Pathology

Examination of aspirated cerebrospinal fluid reveals the presence of inflammatory cells, mainly lymphocytes, and elevated concentrations of protein in animals affected by the meningoencephalitis syndrome. Grossly, the fluid may be turbid. Results obtained from haematological and biochemical blood analyses are not of significant diagnostic value, although metabolic acidosis is often found in affected animals as a result of excessive salivation.

Gross lesions are not normally noticeable in the central nervous system of animals suffering from listerial meningoencephalitis. In a few cases the meninges, particularly ventrally over the brain stem, may be thickened and slightly yellowish or opaque as a result of mononuclear cell infiltration, or it may be congested and oedematous.^{9, 24, 31} Microscopic changes are confined to the white and/or grey matter of the brain stem, particularly the pons and the medulla oblongata, the spinal cord and the meninges. In the early stage, the lesions in the brain tissue consist of small accumulations of lymphocytes and monocytes, and sometimes a few neutrophils, around or in close proximity to blood vessels. In the later stages of the disease extensive perivascular infiltrations of mononuclear cells and micro-abscesses occur in the periventricular grey and/or white matter. The abscesses are characterized by liquefaction of the neuropil and by the presence of Gram-positive, short, rod-shaped bacteria, usually paired, in and around these lesions. Bacteria are not normally discernible in lesions when only perivascular mononuclear cell infiltrations are present in the brain stem.^{21, 24, 33} A meningitis is almost always present, and may be marked. It is characterized by the presence of infiltrations of lymphocytes, macrophages, neutrophils and plasma cells in the meninges over the brain stem, cerebellum, and cranial cervical spinal cord.²¹ Bacteria have also been reported in the foci of inflammation in the proximal parts of the cranial nerves.³³

In aborted foetuses and animals, especially neonate lambs, which have succumbed to the septicaemic disease, lesions are found consistently. Small, yellowish, pin-point, necrotic foci in the liver, small (1 to 3mm in diameter) erosions in the abomasum and staining of the coat by meconium are seen in aborted lambs. The foetus is usually severely autolysed when expelled.

Subcutaneous oedema, hydrothorax, ascites, and an enlarged pale or bronze-red, friable liver are generally found in newborn lambs that have died of congenital infection.⁷ The most characteristic microscopic lesion in new-born animals is multifocal necrosis of the liver and, less frequently, of the spleen, lymph nodes, myocardium, lungs, adrenals, gastrointestinal tract and brain. The lesions are infiltrated by mononuclear cells, mainly lymphocytes, and some neutrophils. The organisms are easily demonstrated in tissue sections of affected areas.^{7, 28}

Various degrees of oedema and sometimes greyishwhite, leathery areas of necrosis, 100 to 120mm in diameter, are evident around the cotyledons. Most cotyledons are paler than normal and range from a mottled orange to a pale greyish-pink.⁷ Microscopical lesions in the placenta include severe oedema, infiltration of neutrophils in the chorioallantois, necrotic vasculitis, mineralization of the villous mesenchyme, and numerous Listeria organisms in the chorionic epithelium.⁷

Diagnosis and differential diagnosis

A provisional diagnosis can be based on the clinical signs, epidemiological findings and histopathological examination of organs. Confirmation of the diagnosis requires isolation of L. monocytogenes from affected tissues.⁴

Attempts should be made to culture the organism from the brain stem in cases suffering from the meningoencephalitis syndrome, and from all organs as well as the placenta, faeces, urine, blood and milk in animals which have contracted the septicaemic syndrome. It must be borne in mind that the organisms can be very irregularly distributed in the body, so specimens should be collected from various organs. The exposure of tissues to a temperature of 4 °C for up to two months, known as ‘cold enrichment’, is advisable in order to promote the isolation of L. monocytogenes from tissue specimens.^{4, 29}

The meningoencephalitis syndrome should be clinically differentiated from other neurological conditions in livestock livestock, such as brain abscesses, Coenuris cerebralis infestation, lead poisoning, heartwater, and cerebrocortical necrosis (thiamine deficiency).⁶ Clinically, animals suffering from listeriosis may also be confused with those that are affected by rabies; circling and unilateral facial nerve paralysis are, however, not usually present in rabies, while bellowing and aggressiveness are not usually present in listeriosis. In thrombotic meningoencephalitis caused by Histophilus somni, the course of the disease is short, several young feedlot animals are often affected at once, and the condition is often preceded by respiratory disease.²⁷

The abortion and septicaemic syndromes should be differentiated from other causes of foetal loss and neonatal mortality in sheep, goats and cattle.

Control

Listeria monocytogenes is sensitive in vitro to a wide variety of drugs, including chloramphenicol, streptomycin, oxytetracycline, neomycin, furazolidone, sulphonamide-trimethoprim mixtures, penicillin, fluoroquinolones, erythromycin and rifampicin.³² Penicillin at a dosage of 44 000 IU/kg twice daily for one to two weeks, followed by half that dosage for a further one to two weeks, gives good results in early cases of listeriosis in cattle.²⁷ In general, the prognosis is poor once nervous signs have developed. Good responses are usually obtained from the parenteral administration of high doses of antibiotics in septicaemic cases and in the treatment of uterine infection after abortions. Correction of dehydration, acid-base imbalance and electrolyte disturbances in clinically affected animals is advisable. Intravenous and oral fluid therapy must be continued until affected animals regain their ability to drink. Nonsteroidal analgesic drugs and selenium/vitamin E injections are essential in animals with exertional myopathy resulting from struggling, as is soft bedding to prevent pressure necrosis. ²⁷

Immunity of listeriosis is based on the cell-mediated immune response.¹⁶ Experiments with live vaccines have given promising results in sheep.^{17, 20}

References

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