CHAPTER 39 Glanders
Glanders is one of the oldest recorded plagues among perissodactyls (odd-toed ungulates) and may have been originally described by early Greek and Roman writers.1 Three forms of glanders are generally recognized: cutaneous (farcy), nasal, and pulmonary. Pulmonary glanders is an extension of the nasal form. The common etiology of these diseases was first demonstrated by Viborg at the end of the eighteenth century.1 The etiologic agent, now known as Burkholderia mallei, was isolated in 1882 by German and French scientists.2 The mallein test for diagnosis of glanders was developed in 1890.2
By the second half of the nineteenth century, glanders was widespread in horses in North America, and a major epidemic of disease occurred in association with movement of horses during and after the Civil War.2,3 During World War I, B. mallei was used as a biologic warfare agent against the horses of the Allied forces, and currently it is considered significant as a potential agent of bioterrorism today (category B, U.S. Centers for Disease Control and Prevention).4,5 Disease caused by B. mallei must be reported to the World Organization for Animal Health (formerly the Office International des Epizooties [OIE]) in Paris.
ETIOLOGY
Burkholderia mallei (formerly Pseudomonas, Bacillus, Pfeiferella, Loefflerella, Malleomyces, Actinobacillus, Corynebacterium, and Mycobacterium) is a short, rod-shaped, gram-negative, aerobic, facultative intracellular, nonmotile and non–spore-forming bacterium. The organisms survive outside the host for varying times depending on many factors. Relatively little is known about virulence factors of B. mallei. Capsular polysaccharide is essential for virulence in hamsters and mice.6 An acapsular mutant of B. mallei failed to induce disease in experimentally infected horses.7 Disease caused by B. mallei must be reported to the World Organization for Animal Health.
EPIDEMIOLOGY AND PATHOGENESIS
Glanders is restricted geographically to Eastern Europe, Asia, and North Africa and is considered endemic in countries such as Iraq, Turkey, Pakistan, India, Mongolia, and China,8–12 where reported outbreaks appear to be increasing in the last 10 to 20 years. Reports of recent outbreaks in Brazil and the United Arab Emirates have appeared in the veterinary literature13 and on the OIE website. Glanders has been eradicated from Europe, Australia, and North America by a rigorous policy of culling animals that are positive by complement fixation test, serum agglutination test, or the mallein test (see Diagnosis). An accidental human infection occurred in a laboratory worker in 2000,14 but there have been no naturally occurring cases of glanders in North America for more than 60 years. The last case in animals in the United States was in 1942.
Burkholderia mallei is a host-adapted pathogen that does not persist in the environment outside of its equine host.7 The organisms are thought to gain entrance through mucous membranes; common water and feed are likely the main source of infection. The disease can be spread by subclinically infected horses. Poor sanitation, crowding, and immunosuppression from parasitism are considered risk factors. The incubation period varies from a few days to several months. Some workers have suggested that the disease is more severe in donkeys and mules than in horses.9 The disease has been the target of eradication efforts for many decades because of its clinical effects in Equidae and its public health implications.
CLINICAL FINDINGS
In the cutaneous form of glanders, also known as farcy, nodules develop into crater-shaped ulcers with exudation (Fig. 39-1). The subcutaneous tissues and lymph nodes are affected. Lymphatic vessels become swollen and corded with development of “farcy buds,” swellings that enlarge, ulcerate, and drain.
In horses with the nasal form of glanders, small nodules on the nasal septum develop into ulcers called stellate (starlike) scars (Fig. 39-2), with a purulent unilateral or bilateral discharge (Fig. 39-3). These lesions degenerate into deep ulcers with raised, irregular borders that may ultimately obstruct the oropharynx, resulting in extreme dyspnea. There is an accumulation of necrotic cells with kayorrhectic nuclei.9 Submaxillary and other lymph nodes are enlarged and edematous. There may be severe congestion of the spleen and liver. Orchitis may be present (Fig. 39-4).