Lymphangitis of Horses and Cattle
Also known as Pigeon Fever or Dry Land Distemper
Caused by:
Corynebacterium pseudotuberculosis
A gram-positive, soil-dwelling bacterium
Infection is common and economically important worldwide
Increasing in frequency in North America
Affected Species:
Horses
Cattle
Occasionally camels, alpacas, llamas, and buffalo
Pathogenesis:
Bacteria enter via skin wounds
Transmission via arthropod vectors such as stable flies, horn flies, and house flies
Transmission by contact with contaminated environment
Onset in horses is variable
Peak incidence in horses is during summer and fall, when flying insects are present
Clinical Findings:
General signs (in horses and cattle):
Diffuse or localized swellings
Ventral pitting edema
Ventral midline dermatitis
Painful and mildly pruritic
Associated with alopecia, exudation, crusting, and ulceration
Lameness
Draining abscesses or tracts
Fever
Weight loss
Depression
Abscesses can be large, up to 20 cm in diameter before rupturing
Abscesses take weeks to months to resolve
Nonhealing abscesses or wounds may be concurrently affected with cutaneous habronemiasis (“summer sores”)
Clinical findings in Horses:
Chronic abscesses along lymphatic chains (lymphangitis) on the limbs
Ulcerative lymphangitis (infection of the lower limbs)
Usually manifests as painful inflammation, nodules, and ulcers, especially in the lower limb region
Lameness and edematous swelling can extend up the entire limb
The exudate is odorless, thick, tan, and blood tinged
Usually only one leg is involved
If not treated aggressively, lesions and swelling usually progress and become chronic with relapses
Chronic abscesses in the pectoral region (most common location)
Chronic abscesses in the ventral abdominal region
Chronic abscesses in the preputial or mammary regions
Secondary dissemination to internal organs
Internal infection
Can affect the liver, spleen, kidneys, or lungs
Suggested by a marked or prolonged fever, anorexia, or weight loss
Clinical signs may include weight loss, colic, splinted abdomen, or lethargy
Clinical findings in Cattle:
Most commonly causes cutaneous excoriated granulomas
Large, ulcerative skin lesions resembling infected granulation tissue
Lymphangitis may occur in 2%-5% of cows
Location varies, but is often associated with skin trauma
Healing often occurs without treatment or with limited topical treatment in 2–4 weeks
Abortion and mastitis may also occur
Visceral involvement has been reported but occurs much less commonly than in horses
Clinicopathologic Findings (usually present):
Anemia
Leukocytosis
Neutrophilia
Hyperfibrinogenemia
Increased concentrations of serum amyloid A (SAA)
Hyperglobulinemia (indicative of inflammation)
Diagnosis:
Confirmation by isolation of the bacteria from lesions
Bacterial culture of pus from external abscesses
Samples for culture in horses: Aspirates of abscesses, swabs of purulent exudate beneath crusts, punch biopsies
Abdominal ultrasonographic examination to detect internal infection or abscesses
Clinicopathologic evidence of inflammation
Serologic testing for internal infection
In horses, the synergistic hemolysis inhibition (SHI) test detects IgG to the phospholipase D exotoxin
Useful adjunct for diagnosis of internal infection in the absence of external infection
By itself, serologic testing is not sufficient to diagnose infection
PCR testing of abdominal fluid for C. pseudotuberculosis
Ultrasonography of the abdomen and thorax is useful for detecting internal infection (liver, spleen, kidneys, lungs)
Ultrasonography is also useful for detecting and draining deep abscesses (e.g., in the triceps musculature of horses)
Transtracheal aspirates are required to confirm pneumonia
Differential diagnoses include:
Pyoderma, abscesses, or lymphangitis due to other bacteria (e.g., Staphylococcus aureus, Rhodococcus equi, Streptococcus spp, or Dermatophilus spp)
Dermatophytosis (in cattle or horses)
Sporotrichosis
Equine cryptococcosis
North American blastomycosis
Onchocerciasis
Treatment:
Lancing and drainage of external abscesses
Abscesses are lanced and flushed with dilute antiseptic solutions
Deep abscesses require ultrasonography to guide placement of an indwelling drain
External swellings treated with hot packs, poultices, or hydrotherapy until they rupture or are drained surgically
Longterm antimicrobials
Required for ulcerative lymphangitis, limb infection, and internal infection
Minimum of 1 month duration or as directed by follow-up ultrasonography
The organism is susceptible to many commonly administered antimicrobials
Antimicrobial treatment of uncomplicated external abscesses may prolong the disease by delaying abscess maturation
Fly control
Systemic administration of phenylbutazone or flunixin meglumine relieves pain and swelling
General supportive and nursing care is indicated
If treatment is successful, swelling gradually recedes over days or weeks
Prevention:
Isolation of infected animals
Comprehensive fly control including insect growth regulators
Good sanitation
A conditionally licensed bacterin or toxoid is currently available for horses
Prognosis/Outcome:
In cattle, healing often occurs without treatment or with limited topical treatment in 2–4 weeks
If not treated aggressively, the disease in horses is often chronic
Severe or untreated lymphangitis cases often become chronic, leading to fibrosis and induration of the leg
Internal infection in horses has a 30%–40% mortality rate, even with appropriate treatment
Caseous Lymphadenitis (CL) of Sheep and Goats
Also Known As: (Not explicitly mentioned as having other common names like the Horse/Cattle Lymphangitis sources did, but the context refers to it solely as Caseous Lymphadenitis)
Caused By: Corynebacterium pseudotuberculosis
Gram-positive, facultative, intracellular coccobacillus
Soil-dwelling bacterium (Implied by hardy environmental survival and contamination from environment)
Two biotypes identified:
Nitrate-negative (infects sheep and goats)
Nitrate-positive (infects horses)
Produces phospholipase D exotoxin
Enhances dissemination by damaging endothelial cells
Has external lipid coat virulence factor
Provides protection from phagocyte enzymes
Affected Species:
Sheep
Goats
(C. pseudotuberculosis isolates from cattle are heterogeneous)
Pathogenesis:
Bacteria penetrate skin or mucous membranes
Most common entry: Skin injury (shearing, tagging, tail docking, castration, environmental hazards)
Transmission:
Contact with purulent material from draining lesions (most common source)
Inhalation or ingestion (less common)
Contamination of environment (draining lesions, nasal discharge/coughing from internal form)
Bacteria are hardy in environment
Survive on fomites (bedding, wood) for 2 months
Survive in soil for 8 months
Movement to lymph nodes via regional lymphatics
Establishment in lymph nodes and viscera
Bacteria replicate in phagocytes, which rupture
Ongoing replication and cell death forms abscesses
Incubation period: 1–3 months
Culminates in encapsulated abscesses
Clinical Findings:
Chronic, infectious disease
Characterized by abscess formation
Purulent material is thick and nonodorous
Lesions increase with age
Forms of the Disease:
External (Peripheral) Form:
Abscesses in region of peripheral lymph nodes (single or multiple)
More common in goats
Common sites: submandibular, parotid, prescapular, prefemoral
Less common: supramammary, inguinal, ectopic locations
If untreated, lesions mature into open, draining abscesses
Purulent material consistency: soft/pasty (goats), thick/caseous (sheep)
Skin heals with scarring after draining
Recurrence is common (often months later)
Internal Form:
Abscesses within internal organs and lymph nodes
More common in sheep ("thin ewe syndrome")
Typically manifests as chronic weight loss and ill thrift
Presence of other signs depends on organs involved
Lung abscessation is common
Signs: chronic ill thrift, cough, purulent nasal discharge, fever, tachypnea, increased lung sounds
Diagnosis:
Physical examination (especially for external abscesses)
Bacterial Culture:
Definitive diagnosis
Culture of purulent material from an intact abscess
Culture of transtracheal aspirate (for internal form/pneumonia)
Isolate animals pending culture results (differentiates from other pyogenic organisms)
Serologic Testing:
Synergistic Hemolysin Inhibition (SHI) test
Detects antibodies against phospholipase D exotoxin
Available at many labs
Results interpreted with caution (consider history, active infection, vaccination)
Positive titers indicate: past resolved infection, recent exposure, recent vaccination, or active/developing lesions
Correlation between high titer and active/developing abscesses varies
Repeat titer in 2–4 weeks if status uncertain
Rising titer + clinical signs = CL assumed
False negatives possible: within first 2 weeks post-exposure, chronic walled-off abscesses
Colostrum-derived titers in young (< 6 months) require caution
Not sufficient alone for diagnosis of active cases if abscesses not accessible
Other Tools (especially for internal form):
Radiography and ultrasonography (detect lesions)
Exclusion of other causes of chronic weight loss (Johne's disease, parasitism, poor dentition)
Economic Losses:
Death
Condemnation and trimming of infected carcasses
Hide and wool loss
Loss of sales for breeding animals
Premature culling
Major concern for small ruminant producers in North America
Zoonotic Potential:
Care should be taken when handling infected animals or purulent exudate
Treatment:
CL is not considered a curable disease
Treatment mainly for aesthetic reasons and limiting infectivity (animals with genetic/emotional value)
Options:
Lancing and draining of external abscesses
Cavity lavage with dilute iodine solution
Isolate animal until lesion stops draining and heals
Carefully collect and dispose of drainage material
High recurrence rates
Surgical excision of intact accessible abscesses
More expensive
Undetected abscesses often present
High recurrence rates
Formalin injection of lesions (strongly discouraged - FDA bans extra-label use of potent carcinogens in food animals)
Antimicrobials (extra-label use, strict adherence to guidelines/VCPR mandatory)
Intralesional and/or Systemic
Longterm procaine penicillin G and rifampin successful in some cases
Penicillin alone unlikely to penetrate capsule
Highly lipid-soluble tulathromycin may help internal cases
Studies show efficacy of SC and/or intralesional tulathromycin in resolving lesions without lancing
Effective concentrations achieved within walled-off abscesses after single SC dose of tulathromycin
Intralesional oxytetracycline eliminated bacterial growth in tissue cages in one study
IM oxytetracycline did not eliminate growth in tissue cages in one study
Recurrence remains a problem despite efficacy
Cannot be considered curative
Acceptable alternative when culling is not an option
Supportive care
Owner education stressing persistent, recurrent nature
Control and Prevention:
Focus on strict biosecurity measures
Goals: Eliminate CL from herd/flock, decrease new cases
Measures:
Elimination of diseased animals (Culling)
Best way to eliminate CL from herd/flock
Cull immediately if possible
Animals with draining abscesses should not be sent through sale barns
Dividing herds/flocks into clean and infected groups
Eliminating older/less genetically valuable animals over time
Isolation of infected animals
Until lesions are dry and/or resolved
If immediate removal is not possible
Vaccination
Commercial CL vaccines licensed for sheep and goats
Use only in species labeled (adverse reactions reported in goats given sheep vaccine)
Rigid adherence to schedules can decrease prevalence/incidence
Efficacy not 100%
Will not clear infected animals
Consider for young replacement animals
Stop vaccination in clean herds/flocks (no history)
Gradually cull older infected animals as economics allow
Cull seropositive unvaccinated animals once prevalence is low
Disinfection
Shearing equipment and other instruments between animals
Dilute bleach and chlorhexidine effective on hard surfaces/fomites (after cleaning organic material)
Shearers understanding hazards and vector potential
Dipping-tank solutions kept fresh
Environment Modification:
Removal of hazards (barbed wire, exposed nails, rough feeders) to decrease injury and transmission from fomites
Prevention of Introduction of New Animals
Common way CL is introduced/reintroduced
Clinically normal animals can be incubating
Hazardous to buy from unknown histories
Prepurchase examination for lesions/scars
Serologic screening for CL
Quarantine before introduction
Only seronegative animals with no evidence of present/past lesions allowed
Raising young from infected dams on pasteurized milk away from infected animals (limited success)
Prognosis:
Chronic disease
Challenging to eliminate within an individual animal or herd
Not considered a curable disease
Recurrence is common
Internal form is difficult to definitively diagnose antemortem
Internal form serves as a reservoir of infective animals
Economic losses include death.