Course Title: Infections of hemolymphatic system - II (Lecture #34)
Instructor: Dr. Mrigendra Rajput, B.Vet. Sc., M.Vet. Sc., Ph.D.
Affiliation: Associate Professor of Microbiology, Richard A. Gillespie College of Veterinary Medicine, Lincoln Memorial University, Harrogate, TN
Credits: PPT adapted from Dr. Ashutosh Verma’s lectures
References and Sources:
* 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.
Learning Objectives:
* List etiological agent(s) and their characteristic features for caseous lymphadenitis, ulcerative lymphangitis, and erysipelas
* Discuss affected host species, epidemiology, and clinical findings of caseous lymphadenitis, ulcerative lymphangitis, and erysipelas
* Discuss diagnosis of caseous lymphadenitis, ulcerative lymphangitis, and erysipelas
* Discuss treatment and control of caseous lymphadenitis, ulcerative lymphangitis, and erysipelas
Overview of Key Pathogens and Core Pathologies
Caseous Lymphadenitis (CL): Primarily affecting sheep and goats, caused by Corynebacterium pseudotuberculosis.
Ulcerative Lymphangitis: Affecting horses and cattle, caused by Corynebacterium pseudotuberculosis.
Erysipelas: Primarily affecting swine and turkeys, caused by Erysipelothrix rhusiopathiae.
General Characteristics of Corynebacterium Species
Morphology and Staining:
* Small, Gram-positive bacteria.
* Non-spore forming.
* Facultative anaerobes.
* Pleomorphic shapes, including coccoid, club, and rod forms.
* In stained smears, they occur singly, in palisades of parallel cells, or in angular clusters resembling "Chinese characters."
Biochemical Characteristics:
* Catalase-positive.
* Most pathogenic members are urease-positive.
* Pathogenic corynebacteria are non-motile.
Growth Requirements:
* Require enriched media for growth.
Ecology and Habitat:
* Many species are commensals on mucous membranes.
* Corynebacterium pseudotuberculosis is specifically noted for its ability to survive for months in the environment.
Infection and Lesions:
* Tissue trauma typically precedes infection establishment. Examples of trauma include cuts, abrasions, shearing wounds, fighting injuries, or thorn/prick injuries.
* Resulting lesions are characterized by suppuration (pus formation).
Summary of Pathogenic Corynebacteria and Host Diseases
C. diphtheriae:
* Host: Humans (Primary) and Horses (Rare).
* Condition: Diphtheria; wound infection (rarely in horses).
* Habitat: Human pharyngeal mucosa.
C. kutscheri:
* Host: Laboratory rodents.
* Condition: Superficial abscesses and caseopurulent foci in liver, lungs, and lymph nodes.
* Habitat: Mucous membranes and environment.
C. pseudotuberculosis (Non-nitrate-reducing biotype):
* Host: Sheep and goats.
* Condition: Caseous lymphadenitis.
* Habitat: Skin, mucous membranes, and environment.
C. pseudotuberculosis (Nitrate-reducing biotype):
* Host: Horses and cattle.
* Condition: Ulcerative lymphangitis and abscesses.
* Habitat: Environment.
C. renale group (Type I: C. renale; Type II: C. pilosum; Type III: C. cystitidis):
* Host: Cattle, sheep, and goats.
* Condition: Cystitis, pyelonephritis (Type I, III); Ulcerative (enzootic) balanoposthitis in sheep/goats (Type I); Severe cystitis (Type III).
* Habitat: Lower Urinary Genital Tract (LUGT) of cows and bulls, prepuce.
Definition: A chronic, contagious bacterial disease manifesting as abscesses of peripheral and/or internal lymph nodes and organs.
Etiological Agent:Corynebacterium pseudotuberculosis (specifically the non-nitrate-reducing biotype).
Microscopic/Cultural Characteristics:
* Small white colonies.
* Late $\beta$-hemolysis (weak).
* CAMP Test: Demonstrates synergistic hemolysis when C. pseudotuberculosis (drawn horizontally) is crossed against Rhodococcus equi.
Economic Impact:
* Significant endemic infection in sheep/goat regions worldwide, including North America.
* Losses due to condemnation of infected carcasses and devaluation of hides.
Epidemiology:
* Entry: Penetration of skin or mucous membranes. Most common through injuries from shearing, tagging, tail docking, castration, or environmental trauma.
* Transmission: Contact with purulent material draining from active lesions. Bacteria can also be inhaled or ingested.
* Survival: Can survive on fomites (bedding/wood) for 2 months and in soil for 8 months. Survival is enhanced by organic material, shade, and moisture.
* Incubation: Varied period of 1 to 3 months, leading to encapsulated abscesses.
Pathogenesis:
* Facultative intracellular pathogen (survives/replicates in phagocytes).
* Virulence Factors: Cell wall lipids and an exotoxin called Phospholipase D (PLD).
* PLD Function: Leukotoxic; damages endothelial cells to promote spread from initial site to regional lymph nodes and viscera.
* Cell Wall Lipid: High lipid content allows the organism to resist killing by phagocytes and maintain chronic infection.
* Immune Response: Antibodies against PLD help prevent the spread of infection.
Clinical Signs and Presentations:
* Superficial Form: Involves palpable nodes near skin (intermandibular, parotid, retropharyngeal, cervical, prescapular, prefemoral, and supramammary). More common in goats.
* Visceral Form: Abscesses in internal organs and lymph nodes (lungs, kidney, liver, mesenteric lymph nodes). Associated with chronic weight loss and ill thrift ("Internal CL"). More common in sheep.
* Lesion Character: Purulent material is thick and non-odorous. Chronic lesions show an "onion ring" appearance in cross-section with encapsulated layers. Initial pus is greenish, later becoming putty-colored and caseous.
Diagnosis:
* Based on clinical signs and animal species.
* Direct Gram-stain examination of pus/exudate (shows pleomorphism).
* Definitive diagnosis via culture of active lesions.
* ELISAs to detect antibodies against cell wall antigens or PLD.
Treatment and Control:
* Treatment: Intralesional or systemic antimicrobial therapy; supportive care. Lesions must be isolated until dry/resolved.
* Strict Biosecurity: Elimination of diseased animals, prepurchase serologic screening, and quarantine (1−3 months based on incubation).
* Management: Disinfection of equipment (shearing, tagging), removal of environmental hazards, and vaccination.
Ulcerative Lymphangitis
Etiological Agent: Nitrate-reducing biotype of Corynebacterium pseudotuberculosis.
Host Species: Horses and cattle.
Clinical Presentation:
* Lymphangitis of Lower Limbs: Onset is slow, and condition is chronic. Lymphatic vessels become swollen and firm with nodules forming along the length.
* Edema: Develops in affected limbs; ulcerated nodules exude thick, odorless, greenish, blood-tinged pus.
* "Pigeon Breast" or "Pigeon Fever": Abscessation in the pectoral region (pectoral muscles); abscesses can reach the size of a grapefruit.
Diagnosis: Isolation and identification of C. pseudotuberculosis from lesions.
Treatment: Systemic antibiotic therapy combined with topical treatment, such as iodophor shampoo.
Erysipelas in Swine
Etiological Agent:Erysipelothrix rhusiopathiae.
Agent Characteristics:
* Gram-positive, non-motile, non-spore forming small rods (smooth form) or filaments (rough form).
* Catalase-negative, coagulase-positive.
* Facultative anaerobe.
* Exhibits alpha-hemolysis (greenish) on blood agar.
* Produces H2S along the stab line in Triple Sugar Iron (TSI) agar.
Epidemiology:
* Carried by up to 50% of healthy pigs, primarily in tonsillar tissue.
* Shed in feces and oronasal secretions.
* Infection occurs via ingestion of contaminated feed/water or through skin abrasions.
* The organism survives the stomach environment and remains viable in feces for several months.
* Immunity: Maternal antibodies provide passive immunity for young pigs. Older pigs develop active immunity via exposure.
Clinical Manifestations:
* Acute Form: Septicemia (leads to sudden death, fever) and cutaneous erythema.
* Chronic Form: Arthritis (proliferative, non-suppurative polysynovitis) and vegetative endocarditis.
* Diamond Skin Disease (Urticarial Form): Red to purple rhomboidal (diamond-shaped) patches on skin.
* Pathogenesis of patches: Bacteria in circulation damage vessel endothelium $\rightarrow$ Deposition of antigen-antibody complexes $\rightarrow$ Microthrombi formation $\rightarrow$ Ischemia $\rightarrow$ Necrosis.
Diagnosis:
* Diamond-shaped skin lesions are pathognomonic.
* Bacterial culture from fresh tissues (spleen, kidney, long bones, heart blood), fluid, or blood.
* Identification criteria: Colony morphology (48 h), no growth on MacConkey, negative catalase, positive coagulase, H2S production in TSI.
Treatment and Control:
* Susceptibility: Highly susceptible to beta-lactam antibiotics (Penicillin is the primary recommendation).
* Herd Treatment: Tetracyclines in feed or water.
* Ancillary Care: NSAIDs for fever; Erysipelas antiserum (adjunct, though less available).
* Control: Vaccination is very effective (though stress can cause failure); sanitation, hygiene, and culling clinically ill pigs.
Erysipelas in Other Species
Poultry (Birds):
* Manifests as acute septicemia worldwide.
* Outbreaks are sudden with mortality ranging from less than 1% to 50%.
* Species Affected: Turkeys (most important), chickens, ducks, and geese.
* Key Sign: Dark-colored, swollen snoods in turkeys.
Humans (Erysipeloid):
* Occurs via occupational exposure (veterinarians, butchers, fish handlers, abattoir workers).
* Skin infection leads to erythematous swelling at entry site and ulceration.
* Can progress to systemic septicemia, endocarditis, or arthritis.
* Predisposing Factors: Alcoholism, malignancy, or steroid use.