Fusobacterium necrophorum infections
- Host Animals
- Hosts/Species Affected
- Systems Affected
- Distribution Table
- List of Symptoms/Signs
- Disease Course
- Impact: Economic
- Zoonoses and Food Safety
- Disease Treatment
- Prevention and Control
- Distribution Maps
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PicturesTop of page
IdentityTop of page
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
Pathogen/sTop of page
OverviewTop of page
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 AnimalsTop of page
|Animal name||Context||Life stage||System|
|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 AffectedTop of page
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.
Foot rot, in synergy with other aerobic and/or anaerobic microorganisms (Roberts, 1967a; Biberstein et al., 1968).
Postpartum intrauterine infections (Bekana et al., 1997).
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).
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).
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).
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 AffectedTop of page
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
DistributionTop of page
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 TableTop of page
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||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Cabo Verde||Absent, No presence record(s)|
|Central African Republic||Absent, No presence record(s)|
|Congo, Democratic Republic of the||Absent, No presence record(s)|
|Djibouti||Absent, No presence record(s)|
|Madagascar||Absent, No presence record(s)|
|Mauritius||Absent, No presence record(s)|
|Sudan||Absent, No presence record(s)|
|Georgia||Absent, No presence record(s)|
|India||Present, Serological evidence and/or isolation of the agent|
|Kazakhstan||Absent, No presence record(s)|
|-Sabah||Absent, No presence record(s)|
|Mongolia||Absent, No presence record(s)|
|Philippines||Absent, No presence record(s)|
|Singapore||Absent, No presence record(s)|
|Syria||Absent, No presence record(s)|
|Taiwan||Absent, No presence record(s)|
|Thailand||Absent, No presence record(s)|
|United Arab Emirates||Absent, No presence record(s)|
|Uzbekistan||Absent, No presence record(s)|
|Vietnam||Absent, No presence record(s)|
|Andorra||Present||CAB Abstracts Data Mining|
|Estonia||Absent, No presence record(s)|
|Finland||Absent, No presence record(s)|
|Isle of Man||Present|
|Jersey||Absent, No presence record(s)|
|Latvia||Absent, No presence record(s)|
|Liechtenstein||Absent, No presence record(s)|
|Lithuania||Absent, No presence record(s)|
|Luxembourg||Absent, No presence record(s)|
|Norway||Absent, No presence record(s)|
|Portugal||Absent, No presence record(s)|
|Serbia and Montenegro||Absent, No presence record(s)|
|Slovenia||Absent, No presence record(s)|
|Ukraine||Absent, No presence record(s)|
|Bermuda||Absent, No presence record(s)|
|British Virgin Islands||Absent, No presence record(s)|
|Cayman Islands||Absent, No presence record(s)|
|Costa Rica||Absent, No presence record(s)|
|Curaçao||Absent, No presence record(s)|
|El Salvador||Absent, No presence record(s)|
|Guatemala||Absent, No presence record(s)|
|Haiti||Absent, No presence record(s)|
|Honduras||Absent, No presence record(s)|
|Mexico||Absent, No presence record(s)|
|Panama||Absent, No presence record(s)|
|Saint Kitts and Nevis||Present|
|Saint Vincent and the Grenadines||Present|
|French Polynesia||Present||CAB Abstracts Data Mining|
|New Caledonia||Absent, No presence record(s)|
|Samoa||Absent, No presence record(s)|
|Bolivia||Absent, No presence record(s)|
|Falkland Islands||Absent, No presence record(s)|
|Guyana||Present, Serological evidence and/or isolation of the agent|
PathologyTop of page
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).
DiagnosisTop of page
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/SignsTop of page
|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 CourseTop of page
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.
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).
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.
EpidemiologyTop of page
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: EconomicTop of page
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 SafetyTop of page
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 TreatmentTop of page
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.
Prevention and ControlTop of page
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).
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.
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).
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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