Anaerobic Gram Negative Rods

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Widespread in the mucous membranes, gingiva and gut.

Opportunists (except for those causing foot rot), disease results from extension of normal flora (obligate and facultative anerobic microorganisms) into a compromised site. e.g. contamination of a wound with nearby flora or inoculation with teeth or instruments.

Trauma, vascular breakdown and concurrent infection with facultative anaerobes help to establish anaerobic conditions that allow anaerobes to proliferate.

Signs of an anaerobic infection

fight wound

necrotic, gangrenous, suppurative lesion

foul smelling discharges

presence of gas in tissues or lesion

abscesses and other infections around the mouth

Cat bite abscess

Common anaerobic pathogens: Bacteriodes, prevotella, and prophyromonas often with P multocida and streptococcus.

Treatment: surgical drainage is often sufficient. If there are systemic signs of infection then antimicrobials are indicated, amoxycillin being the first choice then amoxycillin-clavulanic acid.

Gingivitis

Agents:

Porphyromonas gingivalis

Bacteroides asaccharolyticus

Fusobacterium nucleatum

Actinomyces viscosus

Aodontolyticus

Sample collection

Containers should contain very little if any space of O2 e.g. a syringe with the air dispelled, or swabs.bronchial brushes in anaerobic transport media is ideal.

Diagnosis

Direct examination of sample, isolation by culture (although time consuming and difficult).

Treatment

Drainage

Antimicorbials

- penicillin, amoxycillin, tetracyclines, metronidazole, clindamycin.

Necrotic liver abscesses

secondary to rumenitis

fusobacterium necrophorum + other anaerobes + Trueperella pyogenes

Csx rare, often found at slaughter

manage by diet to reduce rumenitis,

Calf diphtheria

Necrotic pharyngitis/laryngitis in calves <3months old. Due to infection with F necrophorum. If untreated necrotizing pneumonia results.

Tx: sulphonamides or tetracycline.

Infectious foot conditions of cattle

Bovine interdigital dermatitis: fusobacterium necrophorum, Dichelobacter nodosus and spirochaetes implicated. A benign condition with superficial lesions limited to interdigital skin.

Bovine interdigital necrobacillosis: due to F necrophorum, severe necrotizing condition of interdigital skin, characterized by foetid odour, may extend deeper and include joints. Predisposing factors include trauma, prolonged wetting and nutritional deficiencies. Treat with parental antibiotics such as long acting tetracycline, or daily penicillin. Prevention by reducing risk of trauma so having appropriate non-slip flooring in dairy, paths without little stones, and reduce faecal contamination of paths e.g. wash dairy flooring after milking.

Infectious foot conditions of sheep

Ovine interdigital dermatitis: F necrophorum, benign strains of D nodosus, supercial interdigital inflammation, caused primarily by F necrophroum, mild condition.

Ovine footrot: Dichelobacter nodosus must be present to occur, often involvement with F necrophorum too. The severity of lesions depend on the virulence of the D nodosus strain.

Ovine foot rot

D nodosus is the primary agent: it is a strict parasite that spreads from sheep to sheep and can survive in the environment for up to 7 days.

F necrophorum is always present in the soil, faeces and on pasture, it aids penetration of D nodosus, but cannot cause foot rot on its own. Trueperella pyogenes may also be invovled in damaging the skin assiting invasion by D nodosus.

Infection of hoof by D nodosus --> inflammation of skin-horn junction --> progressive under-running/rotting of the soft horn, extending outwards to the hard horn --> lameness, weight loss (from reduced ability to walk and graze + pain)

Under favourable environmental conditions (wet) D nodosus can be rapidly transmitted.

Benign strains of D nodosus have poor keratolytic activity, limited separation of horn from underlying matrix and lameness rapidly regresses after topical treatment or the onset of dry weather.

Strains of high virulence area able to cause extensive separation of the horn from the underlying matrix from the heel to the sole and toe. There is a foul smelling necrotic exudate. Lameness is severe and persistent, usually involving more than one foot.

D nodosus virulence factors: pili for adherence to interdigital epidermis that is damaged by proteases secreted by F necrophorum.

D nodosus can survive in soft horn for years, so chronic carriers are important source of re-emergence of disease.

In warm wet pasture there is rapid spread, disease resolves when conditions become drier, but once they become wet again the chronic carriers will be able to spread D nodosus to other sheep.

Diagnosis: visual inspection, but scoring not 100% reliable, culture is not often down due to the fastidious nature of the organism. Can take a deep swab from the soft horn area and examine smear for characteristic morphology, and/or do a gelatin gel and zymography tests with differentiate virulent stains from benign strains, however this takes 1-5 weeks to complete.

Control and Eradication

Combination approach of

foot paring

antibiotics (penicillin)

vaccine

footbaths in formalin, or zinc-sulphate

clean pastures (spelled for at least a week)

culling

quarantine of incoming sheep

Control options

Immediate slaughter of affected sheep at an abattoir, if the sheep are aged, or at a high slaughter value compared to replacements. The property will be cleared from D nodosus in 7 days.

Control, then slaughter after shearing and/or weaning

Summer eradication program: possible if the prevalence is less than 5%. Must have good control during the spring leading up to summer, using foot baths and vaccinating. All sheep must have feet pared and examined, cull chronic carriers, run all sheep through a foot bath, turn on to clean pasture, repeat in 4-6 weeks. Property will not be clean until next spring.