After studying this chapter, you will be able to • Describe and recognize clinical signs associated with specific diseases • Understand the etiology of the diseases • Understand and describe common treatments for disease • Know the common scientific names of parasites associated with this species • Know the common vaccinations and their schedules associated with this species Anthrax can affect all warm-blooded animals, including humans, and is discussed in Chapter 13. Clinical signs include a creeping paralysis that usually begins at the head and moves caudally (Fig. 9-1). Veterinarians diagnose botulism with identification of C. botulinum in the feces, blood, or feed that was ingested. Treatment is generally supportive but may include attempts to flush the toxin from the gastrointestinal tract using gastric lavage or purgatives. Mortality is often high due to respiratory paralysis (Fig. 9-2). Equine canker is a chronic hypertrophic, moist pododermatitis of the epidermal tissues of the foot (Fig. 9-3). The most commonly isolated agents include Fusobacterium necrophorum and one or more Bacteroides spp. The disease is often seen in the southern states and the Midwest. The exact cause of canker is unknown, but most horses affected by canker have a history of being housed in wet areas year round. Lameness usually does not present until the corium is involved. Equine canker has a characteristic odor. The frog usually is very friable and has a cottage cheese–like appearance. Treatment often involves superficial debridement and topical antimicrobial agents (Fig. 9-4). Neorickettsia risticii lives inside trematodes (flukes) that infect snails. When the trematodes release their larvae and enter a water environment, the larvae are infected with N. risticii. The larvae of the caddis and mayfly, which also live in water, consume the infected trematode larvae and become infected with N. risticii themselves. When the caddis and mayfly larvae hatch, they are infected with N. risticii. If a horse then accidentally eats one of the flies, the horse becomes infected (Figs. 9-7 and 9-8). The bacteria will begin to replicate inside the gastrointestinal tract of the horse, causing the clinical signs of depression, diarrhea, fever, toxemia, abortion in pregnant mares, and sometimes laminitis. Salmonella infections, both the mild clinical and acute clinical forms, should be treated with IV fluid and electrolyte replacement. The use of gastrointestinal protectants and antibiotics is controversial. NSAIDs are given to help counteract the effects of endotoxins and to control pain. In severe causes, administration of equine plasma may be indicated to correct hypoproteinemia. The plasma may also provide specific antibodies to the endotoxin and provide coagulation factors. Due to the zoonotic risk and contamination of other horses with Salmonella, clients and other facility staff must be educated on the importance of quarantine. Prevention of Salmonella can be difficult because Salmonella is present in the environment (Figs. 9-11 and 9-12). A horse with strangles often presents with a sudden fever, mucopurulent nasal discharge (Fig. 9-13), and abscessation of the submandibular and retropharyngeal lymph nodes (Figs. 9-14 and 9-15). Younger horses are more likely to develop more severe lymph node abscessation, which extends the recovery period. The submandibular and retropharyngeal abscesses may make it difficult for the horse to swallow. Some horses may become listless or anorexic. Clinical findings of EPM vary greatly depending on the localization of the parasite. Asymmetric muscle atrophy is a common clinical sign of EPM that often affects the quadriceps and gluteal muscles (Fig. 9-21). The horse may show signs of cranial nerve abnormalities, such as atrophy of the tongue, self-mutilation of the tongue, and recumbency (Fig. 9-22). The life cycle of B. caballi begins when an infected tick feeds on a naive horse. The most common tick for transmittal of B. caballi is Dermacentor nitens. The sporozoites immediately invade the erythrocytes, and within the erythrocytes the parasites develop from a small anaplasmoid body (trophozoites) into a large pyriform body (merozoites). The cycle then continues when a naive tick feeds on the horse and ingests the infected erythrocytes. Most of the trophozoites are destroyed in the midgut of the tick but the merozoites survive, allowing the new tick to infect another horse. The life cycle of B. equi is similar to B. caballi except for transovarial transmission within the tick and the possible addition of a preerythrocytic stage within lymphocytes (Figs. 9-23 and 9-24). Dermatophytosis is also known as ringworm. It is a common superficial cutaneous fungal infection caused by keratinophilic fungi that invade the stratum corneum of the skin and other keratinized structures. Trichophyton equinum is the most common agent that causes ringworm in horses (Fig. 9-27). Other agents include Trichophyton verrucosum, Trichophyton mentagrophytes, Microsporum canis, Microsporum equinum, and Microsporum gypseum. Ringworm is highly contagious and is spread by direct or indirect contact. Indirect contact includes sharing tack, stalls, feed and water containers, and insects. The fungus can survive on these items for up to 12 months. Clinical signs include small round lesions covered with small scales (Fig. 9-28). The hair often breaks off just above the skin level. Older lesions may heal in the center, but the edges are quite active. Identification of ringworm can be made with a Wood lamp or by culture or histology (Fig. 9-29). White line disease is caused by the invasion of bacteria, fungus, or yeast into the inner horn. When the infection results from fungus, it is also called “onychomycosis.” The affected area of the hoof fills with a cheesy material and air pockets that are often packed with debris (Figs. 9-30 and 9-31). The infection starts at the ground and, if left untreated, can migrate to the coronary band. Clinical signs are often similar to those of laminitis. The horse may be lame, or its sole may be warm to the touch. Sometimes the pockets are filled with a black, foul-smelling substance similar to thrush. Treatment involves resection of the underlying hoof wall and topical application of an antiseptic. Clinical signs of EIA vary depending on the virus strain and the susceptibility of the horse. Acute EIA is caused by a virulent strain of EIA. The incubation period ranges from 5 to 30 days. When clinical signs present, the horse often develops a fever, becomes lethargic, and is anorexic (Fig. 9-34). The mucous membranes appear pale and may have petechiae. The animal may be icteric, and neurologic signs may develop (Fig. 9-35). Blood analysis reveals thrombocytopenia and anemia.
Common Equine Diseases
Bacterial Diseases
Anthrax
Botulism
Canker
Potomac Horse Fever
Salmonella
Strangles
Other Microbial Diseases
Equine Protozoal Myeloencephalitis
Piroplasmosis
Dermatophytosis
White Line Disease
Viral Diseases
Encephalomyelitis
Equine Infectious Anemia
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Common Equine Diseases
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