Caseous lymphadenitis (CL) is a chronic, contagious disease caused by the bacterium Corynebacterium pseudotuberculosis. CL occurs worldwide. It is a disease of major concern for small ruminant producers in North America. The disease is characterized by abscess formation in or near major lymph nodes (external form), or in the thorax and abdomen (internal form). The internal form of CL can cause ill thrift and respiratory compromise and is a major rule out for the “thin ewe” syndrome. The disease often becomes endemic on farms because it is difficult to eradicate from infected animals, and subclinical shedders maintain environmental contamination. Economic losses arise from condemnation and trim of infected carcasses, decreased leather and wool yield, culling of infected animals, loss of sales of breeding stock, and deaths from internal involvement. Although primarily a disease of sheep and goats, CL occurs sporadically in horses, cattle, camelids, swine, water buffalo, wild ruminants, fowl, and hedgehogs. CL occurs occasionally in people, so appropriate precautions should be taken when handling infected animals and purulent exudate from lesions.
Etiology and Pathogenesis
C pseudotuberculosis is a gram-positive, facultative, intracellular coccobacillus. Two biotypes have been identified based on the ability of the bacteria to reduce nitrate: a nitrate-negative group that infects sheep and goats, and a nitrate-positive group that infects horses. Isolates from cattle are a heterogeneous group. All strains produce an exotoxin called phospholipase D that enhances dissemination of the bacteria by damaging endothelial cells and increasing vascular permeability. The bacterium has a second virulence factor, an external lipid coat, that provides protection from hydrolytic enzymes in host phagocytes. Replication of bacteria occurs in the phagocytes, which then rupture and release bacteria. The ongoing process of bacterial replication, followed by attraction and subsequent death of inflammatory cells, forms the characteristic abscesses associated with CL.
Infection occurs after C pseudotuberculosis penetrates the skin or mucous membranes. Most infections occur through contact with purulent exudate from ruptured external or pulmonary abscesses. Skin injuries from shearing, tagging, docking, castration, environmental hazards (eg, splintered wood, metal edges, jutting nails, wire) provide opportunity for establishment of infection. Use of communal sheep dips can spread the disease, because C pseudotuberculosis can survive in dip solutions for up to 24 hr. Because it often results in skin abrasions, shearing immediately before dipping increases the risk of infection. C pseudotuberculosis does not multiply in the environment, but it can survive on hay, straw, and wood for 2 mo, and in soil for 8 mo. Shade and moisture prolong environmental persistence.
CL is a chronic, recurring disease. One to 3 mo after inoculation of the bacteria, an encapsulated abscess slowly forms at the point of entry into the skin or in a nearby lymph node. The infection can spread in blood or lymph to internal lymph nodes and to viscera such as the lungs, kidney, liver, uterus, and brain. Less common sites of involvement include the udder, scrotum, and joints. Initial infection is subclinical in some animals but can also be associated with fever, anorexia, and cellulitis at the infection site. Superficial abscesses eventually rupture and discharge infectious purulent material into the environment. The skin wound heals, leaving a scar. Abscesses tend to recur months to years later.
Sheep and goats differ somewhat in the distribution of abscesses, possibly as a result of management differences. External abscesses around the head and neck occur more commonly in goats, while the visceral form is more common in sheep. Internal abscesses should be considered as a potential diagnosis for “thin ewe” syndrome, in which an adult small ruminant loses condition in the face of adequate nutrition. Congregation at shearing time increases transmission, mainly through coughing by sheep with pulmonary infections. Additionally, clipper blades contaminated with purulent material can infect other sheep during shearing.
The incidence of abscesses steadily increases with age; clinical disease is more prevalent in adults, and up to 40% of animals in a flock can have superficial abscesses.
In sheep, the abscess often has the classically described laminated “onion-ring” appearance in cross section, with concentric fibrous layers separated by inspissated caseous exudate. In goats, the abscesses are less organized, and the exudate is usually soft and pasty.
The presence of an external abscess on a small ruminant is highly suggestive of CL, especially in an endemic herd, but an aspirate from an intact abscess should be submitted for bacteriologic culture for definitive diagnosis. Other pyogenic organisms such as Arcanobacter pyogenes, Staphylococcus aureus, Pasteurella multocida, and anaerobes such as Fusobacterium necrophorum can also cause abscessation. Affected animals should be kept isolated pending culture results. Animals with visceral abscesses pose a greater diagnostic challenge. Radiography and ultrasonography can be useful to detect internal lesions. Culture of a transtracheal aspirate obtained from an animal with pneumonia can help determine if CL is the cause.
A synergistic hemolysin inhibition test is available at the University of California, Davis Diagnostic Laboratory. This test detects antibodies to the phospholipase D exotoxin. Titer results must be evaluated in light of the herd history, presence or absence of clinical disease, and history of CL vaccination. Titers of 1:8 and higher are considered indicative of infection, and titers of 1:256 and higher are correlated with internal abscessation. However, serologic testing will not differentiate a vaccinated animal from a naturally infected animal. False-negative results can occur if testing is done in the first 2 wk after exposure before the animal has seroconverted. Also, animals with chronic, walled-off abscesses can have a false-negative result. When the status of an animal with a positive titer is in doubt, the titer should be repeated in 2–4 wk. If the titer is rising and clinical signs of abscesses are noted, then CL can be assumed to be the cause. Colostral titers usually disappear by 3–6 mo of age, so serologic testing of lambs or kids <6 mo old should be interpreted with caution.
Treatment and Control
Once a diagnosis of CL has been established, owner education stressing the persistent, recurrent nature of the disease is necessary. The most practical approach for commercial animals infected with CL is to cull them from the herd. However, animals with draining abscesses should not be sent through sale barns until draining has ceased and the wound has healed. Treatment of individual animals should be undertaken with the understanding that CL is not considered a “curable” disease. Animals with economic or emotional value are treated mainly for esthetic reasons and to limit their infectivity to the rest of the herd or flock. Whenever possible, an intact abscess should be surgically removed. Alternatively, external abscesses can be lanced and drained, and the abscess cavity lavaged with dilute iodine solution. The purulent material should be collected into a disposable container and incinerated. The surgeon should wear disposable gloves to avoid inadvertent self-inoculation. The treated animal should be isolated from other small ruminants until the wound is healed.
The efficacy of systemic antimicrobial therapy is controversial. Because most treatments will be extra-label, a client-patient-veterinary relationship is necessary. Although C pseudotuberculosis is susceptible to penicillin in vitro, treatment is not necessarily effective in vivo because the antibiotic cannot penetrate into the abscesses well. Longterm (4–6 wk) penicillin (22,000 IU/kg, IM, bid) and rifampin (10–20 mg/kg, PO, sid) has been used to treat the internal form of CL with limited success. The practice of injecting abscesses with formalin should be strongly discouraged because the FDA has zero tolerance for extra-label use of a potent carcinogen in a food-producing animal.
Commercial CL vaccines are currently licensed for use in sheep. Vaccination of young replacement stock reduces the incidence and prevalence of CL within a flock, but it will not prevent all new infections or cure infected animals. Currently, all contain phospholipase D toxoid, and some also contain killed whole bacterial cells. The vaccine is available as a monovalent bacterin and as a polyvalent preparation combined with Clostridium tetani and C perfringens type D. The initial dose is given SC in the axillary space after colostral immunity has waned (~3 mo of age) and should be repeated in 4 wk. Colostral immunity can be improved by administering a booster to pregnant ewes and does 1 mo before lambing/kidding. Annual boosters are recommended. Evidence suggests that increasing the frequency of vaccination to every 4–6 mo may be of benefit in flocks in which exposure is high (eg, housed in confinement for part of the year). These vaccines should be used with caution in potentially infected sheep, because adverse reactions (eg, lameness, lethargy) are sometimes reported.
Extralabel use of the vaccine in goats is associated with poorer efficacy and more adverse reactions (eg, decreased milk production, fever, malaise, ataxia, ventral edema, and occasionally death). However, some success using the commercial CL vaccine in goats has been reported. Anecdotal successes have been reported with the use of autogenous CL vaccines in sheep and goats.
An effective control program is necessary once CL is confirmed in the herd or flock to reduce the disease incidence. Infected animals should be culled right away or, alternatively, housed separately from the uninfected “clean” animals in a separate area. The presence of infected asymptomatic animals in the “clean” herd or flock limits the success of this approach, and is one reason why eradication of CL is difficult. Lambs and kids from infected dams can be raised on pasteurized colostrum and milk away from infected animals. Vaccination of the young replacement stock should be considered, and older infected animals should be gradually culled as economics allow. Once the disease is at a low prevalence rate, vaccination should be stopped and all seropositive unvaccinated animals culled. Replacement animals should be purchased from producers with good CL prevention programs whenever possible. Purchase of animals with unknown histories from sale barns is strongly discouraged. Only seronegative animals, and those with no evidence or scars or abscesses near lymph nodes, should be allowed into the clean herd or flock.
Producers should remove hazardous items (barbed wire, exposed nails, rough feeders) from the environment to decrease injury and potential CL transmission. Producers should also purchase their own shearing equipment and dip solutions, and not share it with other flocks. Older animals and those with abscesses should be shorn last, and equipment should be disinfected after contamination by exudate. Shearers should arrive at the flock with clean hands and wearing clean footwear and clothing. All items that come in contact with animals from different flocks should be sterilized, replaced, or thoroughly cleaned between flocks.
Last full review/revision July 2011 by Lisa H. Williamson