Enterococcosis: Introduction - The Merck Veterinary Manual

Enterococcosis: Introduction

The application of new bacteriologic techniques, especially DNA-DNA and DNA-rRNA hybridization has led to the reclassification of Lancefield group D streptococci as Enterococcus spp . (For a discussion of diseases caused by the Lancefield antigenic serogroup C and other Streptococci spp, see streptococcosis, Streptococcosis: Introduction.)

Enterococcus spp in avian species are worldwide in distribution. Enterococci are ubiquitous in nature and commonly found in various poultry environments. Enterococcus spp are considered normal microflora of the intestinal tract of poultry and other birds. A high percentage of ready-to-eat poultry products are contaminated with Enterococcus spp ; however, no resultant food poisoning in humans has been reported.

Etiology and Epidemiology:

The genus Enterococcus is composed of gram-positive, spherical bacteria occurring singly, in pairs, or in short chains, which are nonmotile, non- sporeforming, facultative anaerobes. They are catalase-negative and ferment sugars, usually to lactic acid. Common avian isolates can be differentiated by their ability to ferment mannitol, sorbitol, and L-arabinose and by their growth on MacConkey agar without crystal violet or salt. (Other types of MacConkey agar inhibit Enterococcus and may provide false-negative results.) Enterococcus spp isolated from avian species and associated with disease include E faecalis , E faecium , E durans , E avium , and E hirae . E faecalis affects birds of all ages; it is a serious disease occurring in embryos and young chicks from fecal-contaminated eggs. E faecium is a cause of mortality in ducklings.

Enterococci are transmitted most commonly via oral and aerosol routes. However, transmission can occur through skin injuries, especially in caged layers. Aerosol transmission of E faecalis results in acute septicemia in chickens. Concurrent enteric infections or any condition compromising the intestinal villous epithelium, allowing penetration of resident enterococci, can result in septicemia, bacterial endocarditis, or both. Incubation periods range from 1 day to several weeks, with 5-21 days most common. Endocarditis can occur when a septicemic enterococcal infection progresses to a subacute or chronic stage. Enterococcus spp have been associated with brain necrosis and encephalomalacia in young chickens. Some enterococci, however, have been demonstrated to have a beneficial effect on growth and feed efficiency and are being studied as potential probiotics.

Clinical Findings:

Enterococcus spp in poultry can result in 2 distinct clinical forms of disease, acute and subacute/chronic. In the acute form, clinical signs are related to septicemia and include depression, lethargy, lassitude, pale combs and wattles, ruffled feathers, diarrhea, fine head tremors, and decrease or cessation of egg production. Often, only dead birds are found. In the subacute/chronic form, depression, loss of body weight, lameness, and head tremors may be observed. Body temperature is elevated in birds with persistent bacteremia. Clinically affected birds eventually die if not treated. Egg transmission or fecal contamination of hatching eggs results in late embryo mortality and an increased number of chicks or poults unable to “pip” or penetrate through the shell at hatch.

Lesions:

Gross lesions of enterococci infection in acute disease include splenomegaly, hepatomegaly (with or without foci), enlarged kidneys, and congestion of subcutaneous tissue. Omphalitis or enlarged yolk sacs may be seen in chicks or poults infected at hatching. Hepatomegaly, splenic necrosis, fibrinous pericarditis, perihepatitis, and airsacculitis are observed in ducks infected with E faecium . Lesions of chronic enterococcal infections include fibrinous arthritis and/or tenosynovitis, osteomyelitis, fibrinous pericarditis and perihepatitis, necrotic myocarditis, and valvular vegetative endocarditis similar to that observed with Streptococcus zooepidemicus infection (see streptococcosis, Streptococcosis: Introduction). Additional gross lesions associated with valvular endocarditis include an enlarged, pale, flaccid heart; pale to hemorrhagic areas in the myocardium; infarcts in the liver, spleen, or heart; and, less commonly, infarcts in the lung, kidney, and brain.

On microscopic examination, the liver has dilated sinusoids congested with RBC and increased heterophils. Splenomegaly is characterized by congestion and hyperplasia of cells in the mononuclear phagocytic system. Valvular lesions consist primarily of fibrin with bacteria, heterophils, macrophages, and fibroblasts. Other microscopic lesions related to endocarditis include cerebral vasculitis and infarcts, leptomeningitis, glomerulonephritis, and thrombosed pulmonary vessels. Focal granulomas can be found in virtually any tissue as a result of septic emboli. Aggregates of bacteria are present throughout necrotic areas with a zone of heterophils just within the necrotic border, a characteristic feature of the lesion. Gram-positive bacterial colonies are readily observed in thrombosed vessels and within necrotic foci.

Diagnosis:

Demonstration of bacteria typical of enterococci in blood or impression smears of affected heart valves or lesions from birds with typical clinical signs will provide a presumptive diagnosis of enterococcosis. Isolation of Enterococcus spp (without fecal contamination) from typical lesions will confirm the diagnosis. Enterococci are easily isolated on blood agar or more specific differential media, which should help differentiate species. Fermentation of mannitol, sorbitol, and arabinose, and growth on MacConkey agar (without crystal violet or salt) can also aid in differentiating enterococci from Streptococcus spp . Preferred tissues for culture include liver, spleen, blood, yolk, embryo fluids, or any suspected lesion. Diagnosis of bacterial endocarditis is based on valvular vegetations with secondary infarcts of myocardium, liver, or spleen. In suspected cases, it is important to culture lesions to establish a definitive diagnosis and rule out other bacteria.

Differential diagnosis includes other bacterial septicemic diseases, eg, staphylococcosis, streptococcosis, colibacillosis, pasteurellosis, and erysipelas.

Treatment and Prevention:

Treatment includes use of antibiotics such as penicillin, erythromycin, novobiocin, oxytetracycline, chlortetracycline, or tetracycline in acute and subacute infections. Clinically affected birds respond well early in the course of the disease. As the disease progresses within a flock, treatment efficacy decreases. Antibacterial sensitivity should be performed on bacterial isolates in any clinical cases of enterococcosis before treatment begins. There is no treatment for poultry with bacterial endocarditis.

Prevention and control requires reducing stress and preventing immunosuppressive diseases and conditions. Proper cleaning and disinfection can reduce environmental enterococcal resident flora to minimize external exposure.