lecture #32

Introduction and Learning Objectives

• This lecture, titled "Infection of Musculoskeletal System - III," is the 32nd lecture in the series delivered by Dr. Dipak Kathayat, Assistant Professor of Microbiology at the Richard A. Gillespie College of Veterinary Medicine, Lincoln Memorial University.
• The material is sourced from several authoritative texts, including:     * Veterinary Microbiology and Microbial Diseases (Quinn et al., 2nd ed.)     * Veterinary Microbiology (Songer and Post)     * Clinical Veterinary Microbiology (Markey et al., 2nd ed.)     * Infectious Diseases of the Dog and Cat (Greene, 4th ed.)     * Veterinary Microbiology (Hirsh et al., 2nd ed.)     * Veterinary Microbiology (McVey et al., 4th ed.)
• The primary goals of this session include:     * Explaining the importance of mixed infections caused by opportunistic anaerobic non-spore forming Gram-negative bacteria.     * Listing the different bacterial genera involved in these infections.     * Differentiating the morphological features of $F. necrophorum$ and $D. nodosus$.     * Describing the virulence factors and functions of both $F. necrophorum$ and $D. nodosus$.     * Explaining the synergistic interaction of $Fusobacterium necrophorum$ with $Trueperella (Arcanobacterium) pyogenes$ and $Dichelobacter nodosus$ in ruminant foot lesions.     * Describing etiologies, clinical findings, diagnosis, treatment, and control strategies for bovine footrot and infectious footrot in sheep.

Bovine Footrot Overview

• Synonyms: This condition is also known as:     * Infectious bovine pododermatitis     * Interdigital phlegmon     * Interdigital necrobacillosis     * Foul in the foot
• Key Points and Etiology:     * The primary etiology is $Fusobacterium necrophorum$, specifically biotypes A and AB.     * Other organisms can facilitate the infection process.
• Epidemiology:     * Cattle of all ages are susceptible to the disease.     * The primary source of infection is the feet of already infected animals.     * Transmission rates are highest during wet and humid environmental conditions.
• Pathogenesis:     * Injury to the interdigital skin serves as the portal of entry.     * Precursors to injury include the maceration of skin by water, feces, and urine.     * $Fusobacterium necrophorum$ is the major cause and can survive in moist soil or as a saprophyte in feces, making environmental control difficult.
• Secondary and Involved Organisms:     * $Dichelobacter nodosus$     * $Staphylococcus aureus$     * $Escherichia coli$     * $Trueperella pyogenes$     * $Bacteroides melaninogenicus$

Microbiological Differentiation of Non-Spore Forming Gram-Negative Anaerobes

• Morphological Features:     * $Dichelobacter nodosus$: Characterized as thick, straight, or slightly curved rods. They can be up to $6\,\mu m$ in length and possess a distinct bulge at one or both ends.     * $Fusobacterium necrophorum$: Exhibits irregular staining and appears as long, non-branching filamentous forms.
• Colonial Appearance:     * Generally, these anaerobes produce a fetid or putrid odor due to the production of volatile fatty acids.     * $Dichelobacter nodosus$: Colonies from virulent ovine footrot lesions typically show a dark central zone, a pale granular middle zone, and a spreading irregular periphery with a "ground glass" appearance.     * $Fusobacterium necrophorum$: Colonies are described as grey, round, and shiny.

Virulence Factors of Pathogenic Anaerobes

$Fusobacterium necrophorum$ Virulence Factors

• Leukotoxin:     * At low concentrations, it induces apoptosis.     * At high concentrations, it lyses bovine leukocytes.     * It is cytotoxic for ruminant hepatocytes and moderately toxic for equine neutrophils.
• Haemagglutinin: Responsible for adherence to the ruminal epithelium.
• Haemolysin: Damages erythrocytes, leading to impaired oxygen transport, which helps maintain the required anaerobic environment.
• Dermonecrotic Toxin: Contributes to tissue necrosis (necrotizing activity associated with lipopolysaccharide endotoxin).

$Dichelobacter nodosus$ Virulence Factors

• Type IV Fimbriae:     * Essential for disease production.     * Enables twitching motility.     * Responsible for adherence to host cells.
• Serine Proteases:     * Responsible for the lysis of collagen.     * Degrades host proteins including fibronectin, elastin, and other hoof-specific proteins.

Synergistic Interactions in Ruminant Foot Lesions

• Synergy occurs when two or more bacterial species interact to produce lesions that an individual organism cannot cause on its own.
• $T. pyogenes$ and $F. necrophorum$:     * $T. pyogenes$ produces a heat-labile factor that stimulates the replication of $F. necrophorum$.     * $F. necrophorum$ produces a leukotoxin that aids the survival of $T. pyogenes$ by inhibiting leukocytes.
• $D. nodosus$ and $F. necrophorum$:     * $F. necrophorum$ facilitates the invasion of tissue by $D. nodosus$.     * $D. nodosus$ elaborates a growth factor that further stimulates $F. necrophorum$.

Clinical Findings in Bovine Footrot

• Incubation Period: Typically about one week ($7\,\text{days}$).
• Affected Limbs:     * Can affect fore- or hindlimbs; however, hindlimbs are more commonly affected.     * It is rare for more than one foot to be involved simultaneously in mature cows.
• Primary Signs:     * Sudden onset of lameness and fever.     * Swelling and erythema (redness) of the soft tissues in the interdigital space and the adjacent coronary band.     * A typical fissuring, necrotic lesion appears in the skin at the top of the interdigital cleft.     * Claws are markedly separated due to inflammatory edema distributed uniformly between the digits.
• Progression and Severity:     * Extreme pain leads to increasing lameness; animals may become reluctant to bear weight.     * Interdigital skin becomes discolored, then fragments with exudate production.     * Progression to tissue sloughing as necrosis advances.     * Production of a characteristic foul odor.
• Systemic Effects:     * Significant drop in milk production (yield may not recover during the current lactation).     * Severe weight loss and anorexia.     * Secondary invaders may infect open lesions if left unchecked.

Treatment and Control of Bovine Footrot

• Diagnosis: Primarily based on clinical findings; bacterial culture may be performed for confirmation.
• Medical Treatment:     * Rapid recovery is common if treated early.     * Penicillin G administered intramuscularly (IM) for $3\,\text{days}$ provides good results.     * Treatment should begin immediately upon observation of signs.     * Local treatment is essential for longstanding (chronic) cases.
• Preventive Measures:     * Footbaths: Preventive use of footbaths containing antiseptic and astringent solutions (e.g., copper sulfate or zinc sulfate).     * Environment: Avoidance of abrasive underfoot conditions.     * Supplements: High levels of zinc fed as a supplement can improve epidermal resistance to bacterial invasion.     * Vaccination: Vaccines targeting $F. necrophorum$ provide approximately $60\%$ protection.

Infectious Footrot in Sheep (Ovine Footrot)

• Etiology:     * $Dichelobacter nodosus$ is the essential, primary causal pathogen.     * $F. necrophorum$ acts as an aid, helping $D. nodosus$ invade the foot and contributing to the inflammatory reaction.
• Pathogenesis and Transmission:     * The source of $D. nodosus$ is discharge from active or chronically infected sheep.     * The organism is fragile in the environment, surviving for only a few days outside the host.     * Infection is typically introduced to a flock via a "carrier sheep."
• Susceptibility:     * All ages of sheep are susceptible.     * The Merino breed is specifically noted as the most susceptible breed.     * Goats are susceptible, but sheep are the principal affected species.     * Arid and semiarid areas rarely see the disease; it thrives in wet and warm conditions.
• Diagnosis and Treatment:     * Clinical Diagnosis: Based on visual inspection of the foot.     * Topical Treatment: Bactericides applied via footbaths.     * Parenteral Treatment: Parenteral antibiotics are used to treat virulent strains of footrot.     * Vaccination: Options include multivalent, autogenous mono-, or bivalent vaccines.     * Control Strategy: Destocking of flocks may be necessary if they are affected by virulent footrot.