Glanders is a contagious, acute or chronic, usually fatal disease of Equidae caused by Burkholderia mallei and characterized by serial development of ulcerating nodules that are most commonly found in the upper respiratory tract, lungs, and skin.
Glanders is one of the oldest diseases known and once was prevalent worldwide.
It has now been eradicated or effectively controlled in many countries, including the USA.
Glanders is one of the oldest diseases known and once was prevalent worldwide.
It has now been eradicated or effectively controlled in many countries, including the USA.
Etiology
Burkholderia mallei, a clonal gram-negative facultative intracellular obligate pathogen, is present in nasal exudates and discharges from ulcerated skin of infected animals.
Glanders is commonly contracted by ingesting food or water contaminated with nasal discharges of infected animals.
Glanders is commonly contracted by ingesting food or water contaminated with nasal discharges of infected animals.
Clinical Findings
Septicemia,
High fever (as high as 106°F [41°C]),
weight loss, and, subsequently,a thick, mucopurulent nasal discharge and respiratory signs.
Death occurs within a few days.
The chronic disease is common in horses and is seen as a debilitating condition with nodular or ulcerative lesions of the skin and internal nares. Infected animals may live for years and continue to disseminate the organism. In some, the infection may be latent and persist for long periods.
High fever (as high as 106°F [41°C]),
weight loss, and, subsequently,a thick, mucopurulent nasal discharge and respiratory signs.
Death occurs within a few days.
The chronic disease is common in horses and is seen as a debilitating condition with nodular or ulcerative lesions of the skin and internal nares. Infected animals may live for years and continue to disseminate the organism. In some, the infection may be latent and persist for long periods.
Nasal, pulmonary, and cutaneous forms
In the nasal form, nodules develop in the mucosa of the nasal septum and lower parts of the turbinates.
The nodules degenerate into deep ulcers with raised irregular borders. Characteristic star-shaped cicatrices remain after the ulcers heal. In the early stage, the submaxillary lymph nodes are enlarged and edematous and later become adherent to the skin or deeper tissues.
In the nasal form, nodules develop in the mucosa of the nasal septum and lower parts of the turbinates.
The nodules degenerate into deep ulcers with raised irregular borders. Characteristic star-shaped cicatrices remain after the ulcers heal. In the early stage, the submaxillary lymph nodes are enlarged and edematous and later become adherent to the skin or deeper tissues.
In the pulmonary form, small, tubercle-like nodules, which have caseous or calcified centers surrounded by inflammatory zones, are found in the lungs. If the disease process is extensive, consolidation of the lung tissue and pneumonia may be present. The nodules tend to break down and may discharge their contents into the bronchioles, resulting in extension of the infection to the upper respiratory tract.
In the cutaneous form (“farcy”), nodules appear along the course of the lymph vessels, particularly of the extremities. These nodules degenerate and form ulcers that discharge a highly infectious, sticky pus. The liver and spleen also may show typical nodular lesions. Histologically, there may be vasculitis, thrombosis, and infiltration of degenerating inflammatory cells.
Diagnosis
The typical nodules, ulcers, scar formation, and debilitated condition may provide sufficient evidence for a clinical diagnosis.
Culture of B mallei from lesions confirms the diagnosis.
A test for delayed hypersensitivity is performed by intrapalpebral inoculation of mallein, a secreted glycoprotein of B mallei found in culture supernatant. Infected hypersensitive horses develop a purulent conjunctivitis within 24 hr and swelling of the eyelid.
Complement fixation is also used to screen for infection.
Competitive ELISA is more sensitive than complement fixation and may become positive as early as 3 days after infection.
PCR based on 16S and 23S rRNA gene sequences may be used for specific identification.
Culture of B mallei from lesions confirms the diagnosis.
A test for delayed hypersensitivity is performed by intrapalpebral inoculation of mallein, a secreted glycoprotein of B mallei found in culture supernatant. Infected hypersensitive horses develop a purulent conjunctivitis within 24 hr and swelling of the eyelid.
Complement fixation is also used to screen for infection.
Competitive ELISA is more sensitive than complement fixation and may become positive as early as 3 days after infection.
PCR based on 16S and 23S rRNA gene sequences may be used for specific identification.
Prevention and Treatment
There is no vaccine. Protective immunity involves T cell responses elicited by live attenuated bacteria. Prevention and control depend on early detection and elimination of affected animals, as well as complete quarantine and rigorous disinfection of the area involved.
Treatment is given only in endemic areas but does not reliably produce a bacteriologic cure. Doxycycline, ceftrazidime, gentamicin, streptomycin, and combinations of sulfazine or sulfamonomethoxine with trimethoprim were effective in the prevention and treatment of experimental glanders.
REFERENCES
www.merckvetmanual.com
Treatment is given only in endemic areas but does not reliably produce a bacteriologic cure. Doxycycline, ceftrazidime, gentamicin, streptomycin, and combinations of sulfazine or sulfamonomethoxine with trimethoprim were effective in the prevention and treatment of experimental glanders.
REFERENCES
www.merckvetmanual.com
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