Fusobacterium necrophorum infections

Pictures

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Picture

Title

Caption

Copyright

Pathology

Necrotic stomatitis in a calf: note white necrotic area

Daniel Elad

Pathology

Ruminal necrobacillary lesions.

Daniel Elad

Pathology

Hepatic necrobacillary lesions (cattle): organ surface

Daniel Elad

Pathology

Hepatic necrobacillary lesions (cattle): pyramidal form of lesion indicating the haematogenous distribution of the infecting microorganism

Daniel Elad

Symptoms

Footrot in cattle: interdigital necrosis

Daniel Elad

Symptoms

Footrot in cattle: coronary band inflammation

Daniel Elad

Symptoms - foot

Toe "abscess" (lamellar suppuration). Necrosis of sensitive laminae underlying hard horn of toe region.

John R. Egerton

Pathology

Calf diphtheria: laryngeal granulomatous reaction.

Daniel Elad

Identity

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Preferred Scientific Name

Fusobacterium necrophorum infections

International Common Names

English: bovine interdigital necrobacillosis; bovine liver abscesses; bull nose; bullnose; bull-nose; bumblefoot; calf diphtheria; chronic necrotic pododermatitis; contagious foot rot; foot abscess; foot abscess in cattle; foot rot; footrot; footrot, foot rot, in cattle, bovine interdigital necrobacillosis; foul-in-the-foot; fusobacterium mastitis in cows; heel abscess; hepatic abscesses; hepatic necrobacillosis; infective bulbar necrosis; interdigital infection in goats, foot rot, footrot; interdigital necrobacillosis; interdigital pododermatitis; lamellar suppuration; laminitis, septic, in sheep; laryngeal abscesses, chondritis, in cattle and sheep; laryngitis, necrotic; liver abscesses in cattle; liver, hepatic, abscess in ruminants; malignant foot rot; mastitis; necrobacillosis; necrobacillosis of swine; necrotic dermatitis; necrotic dermatitis of the udder; necrotic laryngitis, calf diphtheria; necrotic rhinitis, bullnose, in young swine; necrotic stomatitis; necrotis rhinitis; oro-pharyngeal necrobacillosis; phlegmona interdigitalis; seborrhea of the udder; septic laminitis; septic laminitis in sheep; stable foot rot; summer mastitis; summer mastitis in cattle; tail tip necrosis in cattle; toe abscess; udder scald, udder-thigh dermatitis, intertrigo; udder scald, udder-thigh dermatitis, intertrigo in ruminants and mares; virulent foot fot

English acronym

VFR

Pathogen/s

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Fusobacterium necrophorum
Trueperella pyogenes

Overview

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Fusobacterium necrophorum is a Gram-negative, non-motile, strictly anaerobic, non-spore-forming microorganism belonging to the family Bacteroidaceae. It has been divided into four biotypes (A, AB, B and C), which differ in phenotypic characteristics and virulence. These biotypes have been reclassified in 1990-1991 as subspecies (Fusobacterium necrophorum subsp. necrophorum for biotype A, Fusobacterium necrophorum subsp. funduliform for biotype B) or species (Fusobacteriumpseudonecrophorum for biotype C). The classification of biotype AB is still unclear.

F. necrophorum is part of the normal microbial flora of the digestive system. Thus, predisposing factors such as high carbohydrate diet, maceration due to prolonged exposure of feet to wet pasture and stress are necessary for the fulfilment of the microbe’s pathogenic potential.

F. necrophorum is involved in a large variety of pathological processes in different animals, among which liver abscesses and foot lesions in ruminants are probably the most important. It is a part of the human oral cavity and involved in its infections.

Host Animals

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Animal name	Context	Life stage
Bos indicus (zebu)
Bos taurus (cattle)	Domesticated host	Cattle and Buffaloes\|All Stages; Cattle and Buffaloes\|Calf; Cattle and Buffaloes\|Cow; Cattle and Buffaloes\|Heifer
Capra hircus (goats)
Lama glama (llamas)	Domesticated host
Lama pacos (alpacas)	Domesticated host
Ovis aries (sheep)	Domesticated host	Sheep and Goats\|All Stages
Sus scrofa (pigs)	Domesticated host	Pigs\|All Stages

Hosts/Species Affected

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Various animal species have been reported to suffer from infections caused by F. necrophorum (Even et al., 1998). Langworth (1977) suggests, however, that reports dealing with the microorganism dating from periods before adequate identification means were available should be considered with reservation.

Cattle

Liver abscesses (Gudmundson et al., 1978; Nagaraja et al., 1996a, 1996b).

Foot rot, in synergy with other aerobic and/or anaerobic microorganisms (Roberts, 1967a; Biberstein et al., 1968).

Mastitis (Aalbaek, 1978; Shinjo, 1983), ‘summer mastitis’ (Madsen et al., 1990; Hirvonen et al., 1994) and udder sores (Rebhun, 1995).

Postpartum intrauterine infections (Bekana et al., 1997).

Abortion (Pattnaik et al., 1994; Otter, 1996).

Oro-pharyngeal necrobacillosis (necrotic stomatitis and calf diphtheria) (Rebhun, 1995; Yeruham et al., 1998).

Abscesses in various organs other than the liver (Simon and Stovell, 1969).

Sheep and goats

Abscesses in liver and lung (Tadayon et al., 1980; Scanlan and Edwards, 1990; Ramos-Vara et al., 1997).

Necrotic arthritis (Angus, 1991).

Predisposing factor to infection with Dichelobacter nodosum, the causative agent of foot-rot in sheep (Martin and Aitken, 2000) and goats (Piriz Duran et al., 1990).

Necrotic stomatitis following secondary infection of Orf lesions (Martin and Aitken, 2000).

Pigs

Stomatitis (Rao et al., 1997; Ramos-Vara et al., 1998).

Risk factor for swine dysentery: Diets rich in soluble non-starch polysaccharide and/or resistant starch might cause an increase in the number of F. necrophorum in the digestive tract and facilitate the colonization of the intestine by Serpulina hyodysenteriae, the causative agent of swine dysentery (Durmic et al., 1998).

Foot-rot following infection of hoof cracks (Dewey, 1999).

F. necrophorum found by McKay and Carter (1953a; 1953b) in cases of atrophic rhinitis and considered to possibly be the causative agent of this syndrome, are probably only secondary invaders (Langworth, 1977).

Horses

Gangrenous dermatitis, greasy heals, quittor, intestinal ulceration, paraceacal abscess and necrotic pneumonia (Simon and Stovell, 1969; Trevillian et al., 1998).

Other animals

F. necrophorum was the most frequently isolated anaerobe from various organs of dogs, horses, cats, exotic animals (wallabies), pigs and ruminants (Smith et al., 1984; Jang and Hirsh, 1994). Infections in various other animals, including birds and reptiles have been reviewed (Simon and Stovell, 1969). F. necrophorum may cause oropharyngeal necrobacillosis in rabbits (Seps et al., 1998) and be involved in mastitis in camels (El Jakee, 1998).

Human infection

F. necrophorum may be isolated from faecal material (Ohtani, 1970), the oral cavity and the female genital tract (Gorbach and Bartlett, 1974). It may be involved in infections of the oropharynx (Oleske et al., 1976; Seidenfeld et al., 1982; Henry et al., 1983; Rams et al., 1991; Uematsu and Hoshino, 1992). Bacteremia and metastasization to various organs may be eventual complications (Gorbach and Bartlett, 1974; Vogel and Boyer, 1980; Islam and Shneerson, 1980; Seidenfeld et al., 1982; Kleinman and Flowers, 1984; Moreno et al., 1989; Pace-Balzan et al., 1991). F. necrophorum LPS was found to enhance the growth of Bacteroidesintermedius, thus possibly serving as a risk factor for periodontitis (Price and McCallum, 1986; 1987).

Systems Affected

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bone, foot diseases and lameness in large ruminants
bone, foot diseases and lameness in pigs
bone, foot diseases and lameness in small ruminants
mammary gland diseases of large ruminants
mammary gland diseases of pigs
mammary gland diseases of small ruminants
multisystemic diseases of large ruminants
multisystemic diseases of pigs
multisystemic diseases of small ruminants
respiratory diseases of large ruminants
respiratory diseases of pigs
respiratory diseases of small ruminants
skin and ocular diseases of large ruminants
skin and ocular diseases of pigs

Distribution

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Fusobacterium necrophorum is probably present in most countries worldwide (Biberstein and Hirsch, 1979) but the number of reports dealing with its specific geographical distribution is very limited.

Distribution Table

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The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Last updated: 10 Jan 2020

Continent/Country/Region	Distribution	Reference	Notes
Africa
Algeria	Present	OIE Handistatus (2005)
Benin	Present	OIE Handistatus (2005)
Cabo Verde	Absent, No presence record(s)	OIE Handistatus (2005)
Central African Republic	Absent, No presence record(s)	OIE Handistatus (2005)
Congo, Democratic Republic of the	Absent, No presence record(s)	OIE Handistatus (2005)
Côte d'Ivoire	Present	OIE Handistatus (2005)
Djibouti	Absent, No presence record(s)	OIE Handistatus (2005)
Eritrea	Present	OIE Handistatus (2005)
Ethiopia	Present	OIE Handistatus (2005)
Guinea	Present	OIE Handistatus (2005)
Kenya	Present	OIE Handistatus (2005)
Libya	Present	OIE Handistatus (2005)
Madagascar	Absent, No presence record(s)	OIE Handistatus (2005)
Mauritius	Absent, No presence record(s)	OIE Handistatus (2005)
Morocco	Present	OIE Handistatus (2005)
Namibia	Present	OIE Handistatus (2005)
Nigeria	Present	OIE Handistatus (2005)
Seychelles	Present	OIE Handistatus (2005)
South Africa	Present	OIE Handistatus (2005)
Sudan	Absent, No presence record(s)	OIE Handistatus (2005)
Tanzania	Present	OIE Handistatus (2005)
Togo	Present	OIE Handistatus (2005)
Zimbabwe	Present	OIE Handistatus (2005)
Asia
Bahrain	Present	OIE Handistatus (2005)
Bhutan	Present	OIE Handistatus (2005)
Brunei	Present	OIE Handistatus (2005)
Georgia	Absent, No presence record(s)	OIE Handistatus (2005)
India	Present, Serological evidence and/or isolation of the agent	OIE Handistatus (2005)
Indonesia	Present	OIE Handistatus (2005)
Iraq	Present	OIE Handistatus (2005)
Israel	Present	OIE Handistatus (2005)
Jordan	Present	OIE Handistatus (2005)
Kazakhstan	Absent, No presence record(s)	OIE Handistatus (2005)
Kuwait	Present	OIE Handistatus (2005)
Malaysia
-Sabah	Absent, No presence record(s)	OIE Handistatus (2005)
Mongolia	Absent, No presence record(s)	OIE Handistatus (2005)
North Korea	Present	OIE Handistatus (2005)
Philippines	Absent, No presence record(s)	OIE Handistatus (2005)
Saudi Arabia	Present	OIE Handistatus (2005)
Singapore	Absent, No presence record(s)	OIE Handistatus (2005)
Syria	Absent, No presence record(s)	OIE Handistatus (2005)
Taiwan	Absent, No presence record(s)	OIE Handistatus (2005)
Thailand	Absent, No presence record(s)	OIE Handistatus (2005)
United Arab Emirates	Absent, No presence record(s)	OIE Handistatus (2005)
Uzbekistan	Absent, No presence record(s)	OIE Handistatus (2005)
Vietnam	Absent, No presence record(s)	OIE Handistatus (2005)
Europe
Andorra	Present	OIE Handistatus (2005)	CAB Abstracts Data Mining
Croatia	Present	OIE Handistatus (2005)
Cyprus	Present	OIE Handistatus (2005)
Estonia	Absent, No presence record(s)	OIE Handistatus (2005)
Finland	Absent, No presence record(s)	OIE Handistatus (2005)
France	Present	OIE Handistatus (2005)
Germany	Present	OIE Handistatus (2005)
Hungary	Present	OIE Handistatus (2005)
Ireland	Present	OIE Handistatus (2005)
Isle of Man	Present	OIE Handistatus (2005)
Jersey	Absent, No presence record(s)	OIE Handistatus (2005)
Latvia	Absent, No presence record(s)	OIE Handistatus (2005)
Liechtenstein	Absent, No presence record(s)	OIE Handistatus (2005)
Lithuania	Absent, No presence record(s)	OIE Handistatus (2005)
Luxembourg	Absent, No presence record(s)	OIE Handistatus (2005)
Malta	Present	OIE Handistatus (2005)
Netherlands	Present	OIE Handistatus (2005)
North Macedonia	Present	OIE Handistatus (2005)
Norway	Absent, No presence record(s)	OIE Handistatus (2005)
Portugal	Absent, No presence record(s)	OIE Handistatus (2005)
Serbia and Montenegro	Absent, No presence record(s)	OIE Handistatus (2005)
Slovenia	Absent, No presence record(s)	OIE Handistatus (2005)
Spain	Present	OIE Handistatus (2005)
Ukraine	Absent, No presence record(s)	OIE Handistatus (2005)
United Kingdom	Present	OIE Handistatus (2005)
-Northern Ireland	Present	OIE Handistatus (2005)
North America
Barbados	Present	OIE Handistatus (2005)
Bermuda	Absent, No presence record(s)	OIE Handistatus (2005)
British Virgin Islands	Absent, No presence record(s)	OIE Handistatus (2005)
Canada	Present	OIE Handistatus (2005)
Cayman Islands	Absent, No presence record(s)	OIE Handistatus (2005)
Costa Rica	Absent, No presence record(s)	OIE Handistatus (2005)
Cuba	Present	OIE Handistatus (2005)
Curaçao	Absent, No presence record(s)	OIE Handistatus (2005)
Dominica	Present	OIE Handistatus (2005)
El Salvador	Absent, No presence record(s)	OIE Handistatus (2005)
Guatemala	Absent, No presence record(s)	OIE Handistatus (2005)
Haiti	Absent, No presence record(s)	OIE Handistatus (2005)
Honduras	Absent, No presence record(s)	OIE Handistatus (2005)
Jamaica	Present	OIE Handistatus (2005)
Martinique	Present	OIE Handistatus (2005)
Mexico	Absent, No presence record(s)	OIE Handistatus (2005)
Panama	Absent, No presence record(s)	OIE Handistatus (2005)
Saint Kitts and Nevis	Present	OIE Handistatus (2005)
Saint Vincent and the Grenadines	Present	OIE Handistatus (2005)
United States	Present	OIE Handistatus (2005)
Oceania
French Polynesia	Present	OIE Handistatus (2005)	CAB Abstracts Data Mining
New Caledonia	Absent, No presence record(s)	OIE Handistatus (2005)
New Zealand	Present	OIE Handistatus (2005)
Samoa	Absent, No presence record(s)	OIE Handistatus (2005)
South America
Argentina	Present	OIE Handistatus (2005)
Bolivia	Absent, No presence record(s)	OIE Handistatus (2005)
Brazil	Present	OIE Handistatus (2005)
Chile	Present	OIE Handistatus (2005)
Falkland Islands	Absent, No presence record(s)	OIE Handistatus (2005)
Guyana	Present, Serological evidence and/or isolation of the agent	OIE Handistatus (2005)
Paraguay	Present	OIE Handistatus (2005)
Peru	Present	OIE Handistatus (2005)
Uruguay	Present	OIE Handistatus (2005)

Pathology

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Hepatic abscesses

Hepatic abscesses have great importance from the clinical as well as the economic point of view. Certain strains of F. necrophorum subsp. necrophorum, having adequate virulence factors, reach the liver from ruminal lesions (see Pictures) through the portal circulation. Other, less virulent strains and F. necrophorum subsp. funduliforme require the presence of other microorganisms to be able to reach the liver (Berg and Scanlan, 1982; Lechtenberg et al., 1988). The severity of the hepatic lesions is related to the virulence of the invading microbe: F. necrophorum subsp. necrophorum causes more extensive damage than F. necrophorum subsp. funduliforme (Lechtenberg et al., 1988).

The number and dimension of the hepatic lesions vary. Small and large, sometimes coalesced, lesions may be present at the same time (see Pictures).

The histopathologic aspects of typical hepatic lesions were described by Lechtenberg et al. (1988). They consist of a necrotic centre, surrounded by a phagocytic zone of damaged hepatocytes, giant cells and phagocytes containing bacteria, which may be found also in the next, transitional, layer with immature fibroblasts and collagen strands and, at the periphery, a connective capsule of mature collagen with elastic fibres and undamaged neutrophils. Bile duct proliferation and neovascularization were observed in portal triads (branches of portal vein, hepatic artery and bile ductule) in the proximity of the capsule. Fibrosis, resulting in an aspect similar to that of porcine liver and calcification of older lesions were often observed.

Foot rot and abscesses

Caseous interdigital necrosis (see Pictures) and swelling around the coronary band (see Pictures) characterize this clinical form of necrobacillosis. The infection may spread and cause arthritis. Lameness is the principal clinical sign associated with foot rot. In addition, a typical foetid odour emanates from the lesion. Pyrexia, and a decrease in milk yield and food intake often accompanies the infection (Berry, 2001).

Oro-pharygeal necrobacillosis: necrotic stomatitis and calf diphtheria

Necrotic stomatitis (see Pictures) is characterized by cheek swellings, salivation, foetid odour from the mouth and feed residues hanging from the mouth (Radostits et al., 2000). Cough, dyspnea, fever, salivation, nasal discharge and foetid odour are the principal clinical signs of calf diphtheria (Rebhun, 1995). Calf diphtheria may be lethal if untreated, due to the development of toxaemia, pneumonic dissemination (Tan et al., 1996) or asphyxia. The laryngeal lesions may be covered by granulation tissue (see Pictures), causing respiratory difficulties and cough (Smith, 1996).

Diagnosis

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The presumptive diagnosis of the various forms of necrobacillosis is often based on the clinical characteristics of the lesion (Biberstein and Hirsch, 1969). Hepatic necrobacillosis is often diagnosed only at slaughter (Nagaraja et al., 1996b). Gram- or Giemsa-stained slides from necrotic material sampled from the periphery of the lesion may reveal typical filamentous microorganisms (see Pictures). Methods for the isolation of F. necrophorum, on enriched (Emery et al., 1985) or selective media (Fales and Theresa, 1972a) have been described. Antibiotics, especially from the aminoglycoside group, may be added to the medium. Several authors (Garcia et al., 1971; Fales and Theresa, 1972b) developed fluorescent antibody techniques. F. necrophorum may be differentiated from other species of the genus by its ability to produce propionic acid from lactate and indol (Langworth, 1977). Morphological and biochemical characteristics of the isolate provide the final identification but gas-chromatographical analysis of fatty acids may be necessary in some cases. Commercial kits are available.

ELISA was able to detect specific increases in ant-F. necrophorum IgG but not IgM in cattle with liver abscesses, thus making it a candidate for the diagnosis of hepatic necrobacillosis (Kaneyama et al., 1992; Kanoe et al., 1996).

[The table summarizes signs across a range of conditions.]

List of Symptoms/Signs

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Sign	Life Stages	Type
Cardiovascular Signs / Peripheral venous distention, jugular distention		Sign
Cardiovascular Signs / Tachycardia, rapid pulse, high heart rate		Sign
Digestive Signs / Abdominal distention		Sign
Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed	Other\|Not known	Sign
Digestive Signs / Congestion oral mucous membranes, erythema, redness oral mucosa		Sign
Digestive Signs / Diarrhoea		Sign
Digestive Signs / Difficulty in prehending or chewing food	Other\|Not known	Sign
Digestive Signs / Dysphagia, difficulty swallowing	Other\|Not known	Sign
Digestive Signs / Excessive salivation, frothing at the mouth, ptyalism	Other\|Not known	Sign
Digestive Signs / Oral mucosal ulcers, vesicles, plaques, pustules, erosions, tears	Other\|Not known	Sign
Digestive Signs / Rumen hypomotility or atony, decreased rate, motility, strength		Sign
Digestive Signs / Tongue protrusion	Other\|Not known	Sign
Digestive Signs / Tongue ulcers, vesicles, erosions, sores, blisters, cuts, tears	Other\|Not known	Sign
General Signs / Ataxia, incoordination, staggering, falling		Sign
General Signs / Cyanosis, blue skin or membranes		Sign
General Signs / Cyanosis, blue skin or membranes		Sign
General Signs / Cyanosis, blue skin or membranes		Sign
General Signs / Dysmetria, hypermetria, hypometria		Sign
General Signs / Fever, pyrexia, hyperthermia	Other\|Not known	Sign
General Signs / Forefoot swelling, mass front foot, feet	Other\|Not known	Sign
General Signs / Forelimb lameness, stiffness, limping fore leg	Other\|Not known	Sign
General Signs / Forelimb swelling, mass in fore leg joint and / or non-joint area	Other\|Not known	Sign
General Signs / Generalized lameness or stiffness, limping	Other\|Not known	Sign
General Signs / Generalized weakness, paresis, paralysis		Sign
General Signs / Generalized weakness, paresis, paralysis		Sign
General Signs / Head, face, ears, jaw, nose, nasal, swelling, mass	Other\|Not known	Sign
General Signs / Hindfoot swelling, mass rear foot, feet	Other\|Not known	Sign
General Signs / Hindlimb lameness, stiffness, limping hind leg	Other\|Not known	Sign
General Signs / Hindlimb swelling, mass in hind leg joint and / or non-joint area	Other\|Not known	Sign
General Signs / Icterus, jaundice		Sign
General Signs / Lack of growth or weight gain, retarded, stunted growth	Other\|Not known	Sign
General Signs / Laryngeal, tracheal, pharyngeal swelling, mass larynx, trachea, pharynx	Other\|Not known	Sign
General Signs / Lymphadenopathy, swelling, mass or enlarged lymph nodes		Sign
General Signs / Mammary gland swelling, mass, hypertrophy udder, gynecomastia		Sign
General Signs / Oral cavity, tongue swelling, mass in mouth	Other\|Not known	Sign
General Signs / Reluctant to move, refusal to move	Other\|Not known	Sign
General Signs / Stiffness or extended neck	Other\|Not known	Sign
General Signs / Sudden death, found dead		Sign
General Signs / Swelling skin or subcutaneous, mass, lump, nodule		Sign
General Signs / Swelling skin or subcutaneous, mass, lump, nodule		Sign
General Signs / Swelling, mass tail		Sign
General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift	Other\|Not known	Sign
General Signs / Weight loss	Other\|Not known	Sign
Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless	Other\|Not known	Sign
Nervous Signs / Head pressing		Sign
Ophthalmology Signs / Blindness		Sign
Pain / Discomfort Signs / Forefoot pain, front foot	Other\|Not known	Sign
Pain / Discomfort Signs / Hindfoot pain, rear foot	Other\|Not known	Sign
Pain / Discomfort Signs / Mouth, oral mucosal or tongue pain	Other\|Not known	Sign
Pain / Discomfort Signs / Pain mammary gland, udder		Sign
Pain / Discomfort Signs / Pain on external abdominal pressure	Other\|Not known	Sign
Pain / Discomfort Signs / Pain, pharynx, larynx, trachea	Other\|Not known	Sign
Pain / Discomfort Signs / Pain, tail, anus, perineum		Sign
Pain / Discomfort Signs / Skin pain	Other\|Not known	Sign
Reproductive Signs / Agalactia, decreased, absent milk production	Other\|Not known	Sign
Reproductive Signs / Edema of mammary gland, udder		Sign
Reproductive Signs / Firm mammary gland, hard udder		Sign
Reproductive Signs / Mastitis, abnormal milk	Other\|Not known	Sign
Reproductive Signs / Warm mammary gland, hot, heat, udder		Sign
Respiratory Signs / Abnormal breath odor, foul odor mouth	Other\|Not known	Sign
Respiratory Signs / Abnormal breathing sounds of the upper airway, airflow obstruction, stertor, snoring	Other\|Not known	Sign
Respiratory Signs / Coughing, coughs	Other\|Not known	Sign
Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping	Other\|Not known	Sign
Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea	Other\|Not known	Sign
Respiratory Signs / Purulent nasal discharge	Other\|Not known	Sign
Skin / Integumentary Signs / Alopecia, thinning, shedding, easily epilated, loss of, hair		Sign
Skin / Integumentary Signs / Defective growth of nail, claw, hoof	Other\|Not known	Sign
Skin / Integumentary Signs / Foul odor skin, smell	Other\|Not known	Sign
Skin / Integumentary Signs / Moist skin, hair or feathers	Other\|Not known	Sign
Skin / Integumentary Signs / Nail, claw, hoof, abscess, ulcer, under-run	Other\|Not known	Sign
Skin / Integumentary Signs / Oily skin, hair or feathers, greasy		Sign
Skin / Integumentary Signs / Purulent discharge skin		Sign
Skin / Integumentary Signs / Purulent discharge skin		Sign
Skin / Integumentary Signs / Skin crusts, scabs		Sign
Skin / Integumentary Signs / Skin crusts, scabs		Sign
Skin / Integumentary Signs / Skin edema		Sign
Skin / Integumentary Signs / Skin erythema, inflammation, redness	Other\|Not known	Sign
Skin / Integumentary Signs / Skin fistula, sinus	Other\|Not known	Sign
Skin / Integumentary Signs / Skin necrosis, sloughing, gangrene		Sign
Skin / Integumentary Signs / Skin necrosis, sloughing, gangrene		Sign
Skin / Integumentary Signs / Skin necrosis, sloughing, gangrene		Sign
Skin / Integumentary Signs / Skin ulcer, erosion, excoriation	Other\|Not known	Sign

Disease Course

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Hepatic abscesses

Since the initial study of McFadyean in 1890, the bacteriological aspects of bovine liver abscesses have been the focus of much research (Scanlan and Hathcock, 1983; Nagaraja et al., 1996a). Infections have been experimentally reproduced in cattle by introducing F. necrophorum through the portal (Scanlan and Berg, 1983; Nakajima et al., 1986; Itabisashi et al., 1987; Lechtenberg and Nagaraja, 1991; Tan et al., 1994d) or ruminal (Takeuchi et al., 1984) veins.

Risk factors

The origin of F. necrophorum causing liver abscesses is the rumen. This was confirmed by comparing rRNA genes of hepatic, ruminal wall and ruminal content isolates. Matching hybridization patterns were found between the first two but not the third group of isolates (Sanjeevkumar et al., 1997).

Improper feeding practices, such as high energy or low roughage contents, sudden dietary changes, irregular feeding and letting animals hunger, act as predisposing factors to ruminal necrobacillosis by two mechanisms.

Firstly, an increase in lactic acid produced from starch by the ruminal microflora can cause ruminal acidosis and subsequent lesions to the organ’s wall (Nagaraja et al., 1996a). Foreign bodies, especially hair, may aggravate these lesions (Nagaraja et al., 1996b). This phenomenon was not observed in sheep, probably due to differences between hair and wool (Fell et al., 1972).

Secondly, accumulation of lactate in the rumen, being the base source of energy for F. necrophorum, triggers an increase in the microbe’s population: feeding a high-grain diet causes a tenfold increase of the number of F. necrophorum in the rumen (Tan et al., 1994c).

In addition to management risk factors, certain breeds such as Holstein cows are more predisposed to hepatic necrobacillosis, possibly due to different feeding habits (Hicks et al., 1990) and more intensive grooming, a typical characteristic of this breed (Nagaraja et al., 1996b).

The damaged ruminal wall and the elevated number of F. necrophorum lead to ruminal abscesses that may metastase through the portal circulation to the liver (Nagaraja et al., 1996a). F. necrophorum virulence factors play an important role in this phase of the infection. F. necrophorum subsp. funduliforme, which lacks many of these factors, only rarely invades, without the synergistic action of other microorganisms, the ruminal wall and subsequently the liver. To successfully colonize the liver, a highly oxidized organ, F. necrophorum has to cope with the phagocytes present in the organ and create the anaerobic environment necessary for its proliferation.

This is achieved by the following virulence factors of the microbe. Protection from phagocytosis by the lipopolysaccharide and possibly the capsule and destruction of phagocytes by the leucotoxin. Direct and indirect hepatic tissue damage by toxins and hypoxia (a result of haemolysis and intravascular coagulation), respectively. Synergistic aerobic microorganisms play an important role in creating anaerobiosis, especially for F. necrophorum biotypes that lack the appropriate virulence factors to do so by themselves.

Other bacterial species, especially Arcanobacter pyogenes, Staphylococcus aureus, Escherichia coli and several other enterobacteria increase the infectivity of F. necrophorum. The influence of such bacteria may, however, vary with different strains of F. necrophorum (Roberts, 1967a, 1967b; Smith et al., 1989, 1990, 1991a, 1991b).

Since A. pyogenes is the most frequent bacterium associated with F. necrophorum infections, the infective synergism between the two microorganisms has been investigated and proven in mice (Takeuchi et al., 1983) as well as cattle (Lechtenberg et al., 1993). Apparently the mechanism of this synergism was the reduction of tissue oxidative potential by the aerobic A. pyogenes on one hand, and its protection from host defenses by fusobacterial leucotoxin, on the other.

In liver abscesses, F. necrophorum may be isolated in pure culture (Berg and Scanlan, 1982; Lechtenberg et al., 1988) (especially subsp. necrophorum) or in mixed culture (especially subsp. funduliforme), with one or more of the bacterial species mentioned above, Bacteroides spp., or Clostridium spp. (Newsom, 1938; Madin, 1949; Calkins and Scrivner, 1967; Calkins and Dewey, 1968; Simon and Stovell, 1971; Kanoe et al., 1979; Berg and Scanlan, 1982; Kanoe et al., 1986; Lechtenberg et al., 1988).

F. necrophorum from hepatic necrobacillary abscesses may disseminate in some cases, through the posterior vena cava, and cause pulmonary thromboembolism and abscesses leading to pulmonary haemorrhages and haemoptysis (Gudmundson et al., 1978). This condition is often lethal.

Foot rot (interdigital necrobacillosis, foul-in-the-foot, interdigital pododermatitis, phlegmona interdigitalis)

Since F. necrophorum may be isolated from the feet of healthy animals (Emery et al., 1985), predisposing factors such as trauma and maceration are assumed to play an important role in the development of clinical disease (Berry, 2001).

In cattle, foot rot is caused by the synergistic activity of F. necrophorum, Bacteroides melaninogenicus and/or Dichelobacter nodosus. (Edgerton and Laing, 1979; Weaver, 1986). Although several attempts to reproduce the syndrome experimentally by injecting the microorganism into the digital artery (Flint and Jenson, 1951) or the interdigital skin (Gupta et al., 1964) were unsuccessful, Clark et al. (1985) were able to induce typical lesions by the subcutaneous inoculation of F. necrophorum alone. Only leucotoxin-producing strains were able to cause foot abscesses in cattle following experimental subcutaneous inoculation of F. necrophorum (Emery et al., 1985).

A severe form of foot-rot, named ‘super foot-rot’, possibly caused by penicillin-resistant strains of F. necrophorum in conjunction with other bacteria has been reported (personal communication of Dr Chuck Guard, reported by Rebhun, 1995).

If left untreated, the infection may spread and cause more deep-seated pathologic processes such as arthritis and teno-synovitis (Stokka et al., 2001).

In sheep, foot rot is caused primarily by D. nodosum. F. necrophorum, however, acts as a predisposing factor for this type of foot rot (Martin and Aitken, 2000). Lambs of infected mothers have been found to be at high contagion risk (McCoy et al., 1997).

Oro-pharyngeal necrobacillosis: necrotic stomatitis and calf diphtheria

Because F. necrophorum may be part of the natural microflora of the upper respiratory tract, it is considered a secondary invader of primary lesions caused by other microorganisms, trauma, chemical substances or allergens (Jensen et al., 1980; 1981; Panciera et al., 1989) and stress (Badura et al., 1992).

Necrotic stomatitis is considered a sequel to traumatic mucosal lesions. Calves up to 3 months of age are the most frequently afflicted (Radostits et al., 2000).

Calf diphtheria (necrotic laryngitis, laryngeal necrobacillosis) is characterized by necrotic lesions of the pharynx and/or larynx, of calves primarily up to 2 years of age (Mackey, 1968). Cases are usually sporadic and occur especially under bad hygienic conditions (Smith, 1996). The infection may spread through the use of contaminated utensils or under crowded conditions (Rebhun, 1995).

Bovine virus diarrhea infection and the resulting reduction in the efficiency of the immune system, was suggested to be a possible predisposing factor for severe F. necrophorum infections (Daniel et al., 1995).

Mastitis

F. necrophorum has been reported to be present in cases of bovine mastitis, usually in conjunction with other microorganisms such as A. pyogenes (Shinjo, 1983), but occasionally alone (McGillivery et al., 1984). Its significance in the pathogenesis of the syndrome is, however, not clear, since it has been isolated from healthy udders as well (Tan et al., 1996). Strains of Fusobacterium necrophorum isolated from cases of mastitis usually belong to subsp. funduliforme (Aalbæk, 1978).

A special clinical entity, ‘summer mastitis’ (Madsen et al., 1992) is an acute, suppurative udder infection, observed primarily in cattle on pasture. The fly Hydrotea irritans (Fallén), endemic in Northern Europe (Hillerton, 1987), has been reported to act as a vector in the transmission of the microorganism.

Epidemiology

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F. necrophorum is part of the normal flora of the digestive system of various animals and humans (Langworth, 1977; Scanlan and Hathcock, 1983). F. necrophorum was recovered from the oral cavity of clinically healthy cows, especially during the pasture period (Madsen et al., 1992).

Sources of environmental contamination are:

Faeces: faecal excretion of F. necrophorum subsp. necrophorum by animals is limited, but disturbances in the balance between the components of the digestive bacterial flora have been found to lead to its increase. Thus, carbohydrate-rich diets or antibacterial treatment with drugs such as aminoglycosides (to which F. necrophorum, like other anaerobes, is intrinsically resistant), might increase the environmental contamination with the microbe and may be considered risk factors for infection (Smith and Thornton, 1993a; 1993b).

Animals suffering from foot-rot (Radostits et al., 2000).

Insects, especially the fly Hydrotea irritans (Fallén), endemic in Northern Europe (Hillerton, 1987) might act as a vector for the pathogen in "summer mastitis" (Madsen et al., 1991; Chirico et al., 1997).

The survival period of F. necrophorum in the environment might vary under different conditions but may be as long as 10 months (Stokka et al., 2001).

Impact: Economic

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Liver abscesses, foot rot and calf diphtheria are probably the most important clinical entities caused by F. necrophorum, from the economic point of view (Langworth, 1977). The damages, in addition to treatment costs, result from:

Condemnation of livers with abscesses caused by F. necrophorum (Montgomery, 1992).

Decrease in feed efficiency of the afflicted animals. Results of surveys assessing the latter, however, differ: some authors (Wieser et al., 1966; Harman et al., 1989) found no such effect, whereas others (Brink et al., 1990) reported a significant decrease in daily gain and feed efficiency (11% and 9.7%, respectively) in affected cattle. Brown et al. (1975), after grouping afflicted cattle by severity of the lesions, found that only the group suffering from the most extensive hepatic damage showed a decrease in feed intake, weight gain, feed efficiency and carcass weight.

Decrease in milk production, as a direct result of mastitis, or indirectly due to decreased feed intake and general conditions in cases of oro-pharyngeal necrobacillosis and foot rot (Berry, 2001).

Foot rot limits the mobility of the animals and thus their ability to feed, especially on pasture. Lambs with foot rot weighed an average 3.23 kg less than healthy ones (McCoy et al., 1997).

Prepartum losses caused by pregnancy toxaemia and mismothering by recumbent ewes (Harwood et al., 1997).

Zoonoses and Food Safety

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Although it was suggested that animals are the source of the original colonization of the human gastrointestinal tract with F. necrophorum, a hypothesis difficult to test, the only true zoonotic aspects of F. necrophorum are (rare) bite wound infections (Biberstein and Hirsch, 1969).

Disease Treatment

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Tylosin, clindamycin (Cook and Cutler, 1995), tilmicosin (Merrill et al., 1998), florfenicol (Cosgrove et al., 1999), erythromycin and oxytetracycline (Autef et al., 1998) were found to be effective in the treatment of bovine pododermatitis. In an extensive study of in-vitro susceptibility, F. necrophorum subsp. necrophorum and F. necrophorum subsp. funduliforme were found to be susceptible to penicillins, tetracyclines, lincosamides and macrolides but not aminoglycosides (which have generally no activity upon anaerobic bacteria), ionophores (except narasin) and peptides. Minimal inhibitory concentrations [MICs] for clindamycin and lincomycin were significantly lower for F. necrophorum subsp. necrophorum than F. necrophorum subsp. funduliforme. Feed additives used to prevent necrobacillosis (bacitracin, chlortetracycline, oxytetracycline, tylosin and virginiamycin) were inhibitory (Lechtenberg et al., 1998).

About half the human isolates were found to be resistant to beta-lactam antibiotics (Appelbaum et al., 1990).

Penicillin G is the drug of choice in most F. necrophorum infections (Hirvonen et al., 1994; Bateman, 2000; Menzies, 2000; Friendship, 2000). Ceftiofur is the drug of choice in lactating cows since it is a zero milk-withdrawal-period drug. Alternative drugs are oxytetracycline and trimethoprim-sulfadoxine in cattle (Bateman, 2000), ampicillin and long-acting oxytetracycline in small ruminants (Menzies, 2000) and tetracyclines and sulfonamides in pigs (Friendship, 2000). Animals with a predominant Gram-positive enteric microflora (such as rabbits) should be treated with metronidazole, chloramphenicol or tetracyclines (Burgmann, 2000) since narrow-spectrum anti-Gram-positive antibiotics (such as penicillin) could induce harmful changes in the microbial balance in the digestive system.

Although susceptible to most antibacterial drugs, the frequent concomitant involvement of other, more resistant microorganisms in the infections and the necrotic tissue of the lesion, might lead to therapeutic failure (Jang and Hirsh, 1994).

Drug are therapies listed in the Table (from Prescott, 2000a; 2000b; 2000c; Bishop, 2001).

Withdrawal periods may vary according to preparations and country policies. Consequently, the relevant documentations should be consulted for information on this topic.

In addition to antibacterial drugs, antiseptic baths with solutions containing 10% zinc sulfate, 10% CuSO₄ or 2-5% formaldehyde are suggested foot-rot treatments (Rebhun, 1995; Berry, 2001).

Prevention and Control

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Liver abscesses

Adequate hygienic conditions, balanced diets and a rational use of therapeutic antibacterial drugs are the principal tools to limit F. necrophorum infections. Feed additives which inhibit the growth of the microorganism in the digestive system have been shown to decrease its shedding (Nagaraja et al., 1999a, 1999b; Coe et al., 1999).

Vaccination

The presence of liver abscesses in various stages of pathologic development indicates that natural immunity to F. necrophorum is weak since it does not prevent new foci of infection (Nagaraja et al., 1996b). Nevertheless, great efforts have been made to develop a vaccine able to prevent hepatic necrobacillosis in animals at risk (Garcia et al., 1975b; Abe et al., 1976; 1978; Conlon et al., 1977; Garcia and McKay, 1978). The first report of an attempt to use toxoids to vaccinate animals against hepatic necrobacillosis was published in 1974 (Garcia et al., 1974). Various vaccination protocols were used in farm and laboratory animals. Among the potential immunogens tested were bacterins (Roberts, 1970; Abe et al., 1976; Cameron and Fuls, 1977; Conlon et al., 1977), cytoplasmic toxoids (Garcia et al., 1974; 1975b; Garcia and McKay, 1978), culture supernates (Clark et al., 1986), endotoxin (Garcia et al., 1974; 1975b; Abe et al., 1976; Cameron and Fuls, 1977; Conlon et al., 1977), leucotoxin (Roberts, 1970; Garcia et al., 1974; Emery and Vaughan, 1986; Emery et al., 1986a, 1986b), and combined bacterin/leucotoxoid preparations (Terhaar et al., 1996).

These and other experiments indicated the following.

The immunogenicity of culture supernatant was higher than whole-cell cultures (Saginala et al., 1996), possibly due to the higher content in toxins reported by Fifis et al. (1996)

A single dose of inactivated culture or cellular material was unable to confer a significant protection in mice and rabbits (Beveridge, 1934; Roberts, 1970; Cameron and Fuls, 1977; Conlon et al., 1977, Smith et al., 1984), but repeated inoculations with a bacterin (Abe et al., 1976; 1978) or with a cytoplasmic toxoid (Garcia and McKay, 1978) or homologous lipopolysaccharide (Garcia et al., 1975b) did so.

Delayed-type hypersensitivity could be experimentally induced in mice by injecting them intraperitoneally with live F. necrophorum (Inoue et al., 1994).

Experimental leukotoxoid vaccines induced a dose-dependant humoral response and partial protection against experimental infection in cattle. Antileucotoxin antibody levels were significantly higher in animals without hepatic lesions (Saginala et al., 1996; 1997).

No protection to artificial re-infection of cured mice could be induced (Smith and Wallace, 1992).

Garcia et al. (1974) found that sonicated whole-cell preparations had no protective effect, whereas cytoplasmic toxoid reduced the incidence of hepatic necrobacillosis in feedlot cattle, from 35% to 10%.

In mice, endotoxin and outer membrane proteins were protective against non-pathogenic strains only, whereas gel-filtered culture supernates containing endotoxin and having toxigenic activity conferred protection. Not all mouse strains were found to be equally susceptible (Conlon et al., 1977; Abe et al., 1978; Emery and Vaughan, 1986).

Generally, vaccination experiments showed, in the best case, a reduction in the infection’s incidence and the severity of the lesions, but complete protection could thus far not be achieved (Tan et al., 1996).

A couple of commercial vaccines, based on bacterins, are available for the prevention of foot rot (see Table).

Antimicrobial feed additives

Tylosin (Nagaraja et al., 1999a) and virginiamycin (Coe et al., 1999) reduce the number of F. necrophorum in the rumen of high-concentrate-fed cattle. Virginiamycin does so by direct action on the microbe and indirectly, by lowering the lactate concentration, a prime source of its energy, in animals on such diet (Coe et al., 1999). The incidence of F. necrophorum subsp. necrophorum in liver abscesses of tylosin-fed cattle, in pure culture (but not in mixed infections with A. pyogenes), was lower than in animals that were not fed the antibiotic. Resistance did not seem to be induced by prolonged feeding with the drug (Nagaraja et al., 1999b).

It is of interest that virginiamycin-resistant enterococci have been found to be resistant to quinipristin-dalfopristin, a ‘last ditch’ drug used to treat human infections caused by vancomycin-resistant strains (VRE) of these microorganisms (Prescott, 2000d). The emergence of VRE might be related to the use of another feed additive: avoparcin.

Bacitracin was reported to be less effective in reducing liver abscesses than other approved antibiotic feed additives (chlortetracycline, oxytetracycline, tylosin and virginiamycin (Nagaraja et al., 1996b). F. necrophorum was found to be resistant to other feed additives such as avoparcin and monensin (Lechtenberg et al., 1998).

Authorization for the use of bacitracin, tylosin, virginiamycin and spiramycin in the European Union has been revoked as of July 1999 (Shyrock, 2000).

Foot-rot

Adequate hygienic conditions, removal of potential causes of trauma and maceration, isolation and rapid treatment of infected animals by antibacterial drugs and antiseptic foot baths are the suggested means to prevent infection and limit its spread (Rebhun, 1995; Berry, 2001).

Experiments aimed at the immunization of cattle and sheep against foot-rot (Glenn et al., 1985; Clark et al., 1986; Emery et al., 1986b) induced partial protection. Several commercial vaccines based on bacterins are available. Vaccination may be less cost effective than the above-mentioned alternatives (Salman et al., 1988).

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Vogel LC; Boyer KM, 1980. Metastatic complications of Fusobacterium necrophorum sepsis: two cases of Lemierre's postanginal septicemia. American Journal of Disabled Children, 134(4):358.

Warner JF; Fales WH; Sutherland RC; Teresa GW, 1975. Endotoxin from Fusobacterium necrophorum of bovine hepatic abscess origin. American Journal of Veterinary Research, 36(7):1015-1019.

Weaver AD, 1986. Interdigital necrobacillosis. In: Chandler EA, Bedford PGC, Sutton JB, eds. Bovine Surgery and Lameness. Oxford, UK: Blackwell Scientific Publication.

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Wieser MF; Preston TR; Macdearmid A; Rowland AC, 1966. Intensive beef production. 8. The effect of chlortetracycline on growth, feed utilization and incidence of liver abscesses in barley beef cattle. Animal Production, 8(3):411-423.

Yamaguchi M; Kanoe M; Kai K; Okada Y, 1999. Actin degradation concomitant with Fusobacterium necrophorum subsp. necrophorum adhesion to bovine portal cells. Microbios, 98(390):87-94; 17 ref.

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Distribution References

OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (dataset for 2004)., Paris, France: Office International des Epizooties.

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Fusobacterium necrophorum infections

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