L. monocytogenes is a ubiquitous, facultative pathogen that is a small, gram-positive, non spore-forming, catalase-positive, facultative anaerobic, motile rod sometimes arranged in short chains. Flagella are produced at room temperatures, but not at 37ēC. It can grow in refrigeration temperatures (4ēC - also known as cold enrichment) which is why this bacterium can cause severe food-borne infections. Sources of L. monocytogenes include soil, mammalian gastrointestinal tract, vegetation and silage.
Listeriosis affects all ages and sexes, but animals less than three years of age are more commonly prone to clinical disease than older animals. The bacterial disease is seen clinically in animals as one of four forms and is more common during the winter or spring months. Adult animals usually get the encephalitis form, while neonates often get the septicemic or visceral form of the disease. Cattle and sheep can also get the abortion form of the disease if there is an intra-uterine infection of the fetus. The fourth form of the disease is ophthalmitis associated with bacterial contamination of the cornea from the feed source. Some lactating ruminants may also have clinical mastitis associated with listeriosis.
The septicemic/visceral form in young animals is due to ingestion of the bacterium and primarily affects the gastrointestinal tract. Bacteria are usually found in the intestinal epithelial cells and specialized epithelial cells covering the Peyer's patches. Infection may be inapparent or may progress to bacteremia resulting in fatal septicemia.
Abortion is caused by placentitis resulting in fetal death and abortion. Some infections by Listeria sp. may result in fetal infection leading to stillbirths, neonatal death, or possible viable carriers of the bacteria. Listerial abortion rarely occurs with the encephalitis form of the disease.
The ophthalmic form is often associated with silage feeding and corneal contamination by the bacterium while eating. Ocular involvement may also consist of exposure keratitis if the animal has the encephalitis form with CN VII dysfunction resulting in inability of the animal to blink properly.
Mastitis caused by L. monocytogenes is rare but may occur. L. monocytogenes does not readily invade the udder. If mastitis occurs, the animal may have prolonged shedding of the bacteria in the milk.
Adult ruminants may also have the visceral form of the infection, but not have clinical disease. The bacterium is generally in the distal intestinal tract and most cases are too mild to be recognized clinically. Animals may commonly be asymptomatic intestinal carriers and shed the organism in significant numbers.
Infection by L. monocytogenes has been reported to be increasing in incidence and may be as high as 52% in farm animals, but overt clinical disease is considered to be rare. The disease is diagnosed clinically by the history and presenting signs with a failure of response to thiamine therapy. The most common treatment is oxytetracycline or penicillin G. Therapy works best in animals treated early in the disease process. Sheep and goats usually have an acute form of listeriosis and death occurs in 4-48 hours. Recovery is rare. Cattle, on the contrary, have a more chronic disease with survival for 4-14 days and potential spontaneous recovery with lasting brain damage.
A definitive diagnosis can only be made postmortem by histopathology of the pontomedullary region of the brainstem and by bacterial culture. Usually there are no gross lesions seen in the brain at necropsy. The characteristic microscopic lesions include multifocal asymmetrical microabscesses and mononuclear cell meningoencephalitis (thus, the name L. monocytogenes) in the brainstem, anterior spinal cord and, occasionally, cerebellum. Peroxidase-antiperoxidase test, a more accurate diagnostic tool than histopathology, is used to detect degraded bacterial proteins as well as intact bacteria in formalin-fixed tissue.
L. monocytogenes is transmitted from animal to animal through fecal oral routes, usually via manure contamination of the pasture or silage with the microorganism. Animal to human transmission is either directly through contact with infected animals or indirectly via milk, cheese, meat, eggs, or vegetables. The bacterium is inactivated with pasteurization; however, contamination of the pasteurized product with raw product has been reported as a source of infection.
Listeriosis in humans is seen primarily in pregnant women, newborns, elderly, and immunosuppressed (e.g. transplant recipients or AIDS patients). It has been reported that as many as 5-10% of humans may be asymptomatic carriers, harboring Listeria sp. in their feces or vagina. Disease in adult humans is commonly of the encephalitic or septicemic/visceral form.
Prevention is the key to listeriosis. In the livestock industry, feeding of spoiled silage and other rotten vegetation should be avoided and any sick animals should be isolated from the healthy animals. Good hygiene and sanitation on the farm is also important.
Whenever possible, people at risk for listeriosis ( see above) should avoid the consumption of those foods most frequently linked to listeriosis. Those at risk also need to adhere strictly to the food label directions for storage and "use by" information. It is virtually impossible to provide Listeria-free food products because L. monocytogenes infects many animal species with many infections being inapparent, and because the bacterium can survive and grow at refrigeration temperature levels.
Other means of prevention include thoroughly washing raw vegetables, thoroughly cooking raw meats, proper hygiene during food preparation, and consuming only pasteurized dairy products. Humans at risk should also avoid contact with animals that have aborted as well as with aborted materials (placenta and fetuses) on the farm.
Finally, livestock and crop producers can help control the spread of L. monocytogenes by avoiding the use of untreated manure on vegetable crops.
-by Andrea Starkey, Class of 2005
-edited by Dr. Ingeborg Langohr, ADDL
References
-
Arumugaswamy R and LF Gibson: 1999. Listeria in Zoo Animals and Rivers. Australian Veterinary Journal. 77(12): 819-820
-
Cooper, J and RD Walker: 1998. Microbial Food Borne Pathogens: Listeriosis. Veterinary Clinics of North America: Food Animal Practice. 14(1): 113-125.
-
George LW: 2002. Listeriosis. In Smith, Bradford P. large Animal Internal Medicine. 3rd edition, Mosby, Philadelphia, :A 946-949.
-
Finley MR and SR Dennis: 1999. Listeriosis (Circling Disease, Silage Sickness). In Howard & Smith Current Veterinary Therapy 4: Food Animal Practice. Saunders. Philadelphia, PA 396-400.
-
Rebhun, William C: 1995. Listeriosis. In Diseases of Dairy Cattle. Lippincott Williams & Wilkins. Philadelphia, PA 121: 410-413.
-
Ryser ET and EH Marth: 1991. Listeriosis in Animals. Listeria, Listeriosis, & Food Safety. Marcel Dekker. New York, NY 33-43.
-
Todar K: 2003. Listeria monocytogenes and Listeriosis. Todar's Online Textbook of Bacteriology. University of Wisconsin-Madison, Department of Bacteriology. http://textbookofbacteriology.net/Listeria.html
-
Whitlock RH: 1999. Brain Stem Diseases of Cattle: Listeriosis. Howard & Smith Current Veterinary Therapy 4: Food Animal Practice. Saunders. Philadelphia, PA. 663-665.
-
Working Group on Zoonoses. Zoonotic Pathogens: Health Risks from Listeria. Vederal Veterinary Office Magazine. June 2002: 14-15.
-
Washington State Department of Health. Listeriosis. October 2002: 1-5.