Common Equine Diseases

Common Equine Diseases

Bacterial Diseases


Anthrax can affect all warm-blooded animals, including humans, and is discussed in Chapter 13.


Botulism is caused by the bacteria Clostridium botulinum. It is a gram positive, spore-forming, anaerobic bacterium that survives in soils, freshwater sediments, and marine sediments. Infection is often the result of ingestion of the toxin through contaminated feed. Toxicoinfectious botulism can be seen in horses and especially foals in the eastern United States. This type of infection, known as “shaker foal syndrome,” results when the horse or foal has the organism growing in its gastrointestinal tract and the organism is producing the toxin. There are eight types of botulism. Large animals are most often infected with types B, C, and D. Horses are not the only large animal that can be infected with C. botulinum. Cattle and sheep can also become infected. The toxin prevents the release of acetylcholine at the neuromuscular junction, resulting in paralysis, especially of the cranial nerves.

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).

Lyme Disease

Lyme disease is caused by at least three strains of Borrelia burgdorferi, a gram-negative, unicellular spirochete with flagellar projections. Borrelia burgdorferi does not live long outside of its host. The bacterium follows a 2-year enzootic life cycle that involves ixodid ticks and mammals (Fig. 9-5). The primary vector for the disease is the deer tick. The female is the most likely competent vector. Other ticks associated with the disease include the black-legged tick and the western black-legged tick. Infection of the horse occurs when a tick attaches to a horse for longer than 24 hours. For successful transmission of the bacteria, the tick must be attached for at least 24 hours and sometimes up to 48 hours. The organism lives in the tick’s gut and is transferred as it feeds on the blood of the horse.

Lyme disease is most prevalent in regions of high humidity and dense vegetation (Fig. 9-6). Although Lyme disease can occur during any time of the year, most cases occur from May through August in the North Central and Pacific coast states.

Clinical signs include low-grade pyrexia, depression, stiffness, lameness, loss of appetite, joint swelling, and eye problems. However, when high fevers and leg edema are present, the condition most often is the result of Anaplasma phagocytophilia, because many ticks are infected with both A. phagocytophilia and Borrelia.

Diagnosis of Lyme disease usually is accomplished with enzyme-linked immunosorbent assay (ELISA) or immunofluorescent antibody testing.

Treatment of Lyme disease includes intravenous (IV) tetracycline and oral doxycycline. Doxycycline cannot be administered intravenously to horses because of the potential side effects. Tetracycline should not be administered orally to horses due to low bioavailability and the risk of active drug reaching the colon and causing diarrhea. Prevention should include use of an insecticide, use of antimicrobials if early exposure to Ixodes is known to have occurred, and vaccination.

Potomac Horse Fever

Potomac horse fever is caused by the bacterium Neorickettsia risticii, formerly known as Ehrlichia risticii. It is a gram-negative obligate intracellular bacterium with an attraction to monocytes.

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.

A definitive diagnosis requires identification of N. risticii in the feces or blood of the infected horse. A polymerase chain reaction (PCR) test is available for detection of N. risticii.

Treatment often involves oxytetracycline if the disease is diagnosed early, most often resolving clinical signs within 3 days. Fluid therapy and nonsteroidal antiinflammatory drugs (NSAIDs) may be provided as supportive treatments.

Rain Rot

Rain rot is caused by Dermatophilus congolensis, a gram-positive, non–acid-fast, facultative anaerobic actinomycete. Dermatophilus congolensis also infects cattle, sheep, goats, pigs, cats, and dogs. Rain rot often presents in areas with high temperatures and high humidity. Animals that are wet for prolonged periods of time often develop the disease.

The condition can affect animals of all ages and presents as crusty scabs or matted tufts of hair. The lesions are usually found on the head, neck, and chest (Fig. 9-9). Yellow or green pus can be found underneath larger scabs. A definitive diagnosis is made from culture and identification of D. congolensis.

Treatment includes antimicrobial therapy. In horses, the lesions should be soaked and removed. In food-producing animals, lime sulfur can be used as a more cost-effective treatment.


Several salmonella serotypes can cause diarrhea in adult horses. Five of the most common serotypes are Salmonella agona, Salmonella newport, Salmonella anatum, Salmonella Krefeld, and possibly the most pathogenic, Salmonella typhimurium.

Horses infected with salmonella can have one of three types: carrier, mild clinical, or acute clinical. Carrier horses are subclinical carriers that intermittently shed the organism. If a carrier horse is stressed, the horse may develop clinical signs. Horses that develop the mild clinical form of the disease develop pyrexia, anorexia, depression, and a soft watery diarrhea (Fig. 9-10). Horses with this form of salmonella infection often display clinical signs for 4 to 5 days but shed the organism in their feces for days to months after the infection. The third form of the disease, acute clinical, causes a watery, foul-smelling diarrhea, abdominal pain, severe depression, anorexia, and a pronounced neutropenia. Horses with this form of infection often dehydrate quickly, causing electrolyte imbalances and, with prolonged diarrhea, enterocolopathy and bacteremia. Horses left untreated with the acute clinical form of the disease have increased likelihood of death.

Diagnosis of the disease is based on clinical signs, neutropenia, and fecal cultures. Salmonella cannot be consistently cultured from fecal material because it requires multiple fecal samples to be collected and cultured throughout the day. Culturing a rectal biopsy can increase the chances of identifying the organism but is not without risk to the patient. Another alternative to culture is the polymerase chain test available for Salmonella identification. Horses that are subclinical carriers can be very difficult to identify due to the intermittent shedding.

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).


Strangles (distemper) is caused by the bacterium Streptococcus equi. Streptococcus equi is gram-positive coccoid often transmitted through the nasal discharge produced from an infected horse. The transmission can occur via direct contact or indirect contact.

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.

If the disease spreads throughout the body, the disease is often re-termed “metastatic strangles” or “bastard strangles.” The fatality rate of horses with bastard strangles increases greatly. Common sites of abscessation include the kidney, spleen, liver, mesentery, lung, and brain.

Diagnosis of strangles is performed with culture of nasal swabs, pus from an abscess (Fig. 9-16), or nasal washes. Other forms of diagnosis can include polymerase chain reaction (PCR) and serology.

Veterinarians are divided on the form of therapy to use. Some veterinarians think antibiotic therapy should be performed, and others think it should not. When drug therapy is used, penicillin is often the drug of choice. Most horses will recover from the disease with rest and palatable food. Warm compresses can be used to mature the abscesses. Once the abscesses have ruptured or been lanced, they should be flushed daily with povidone-iodine solution. Prevention of the disease includes vaccination.


Tetanus is caused by endotoxins produced by the bacterium Clostridium tetani. Clostridium tetani is a motile, anaerobic, gram-positive bacillus. The most common cause of infection is contamination of wounds (Fig. 9-17). Puncture wounds that contain rusty metal, dirt, or manure are particularly likely to cause infection. Contaminated surgical incisions and umbilical structures may also lead to tetanus infections.

The incubation period of tetanus ranges from 1 to 60 days but usually averages between 7 and 10 days. The disease begins with generalized stiffness. With mild infections the stiffness may remain localized in the head and neck. Stiffness leads to the characteristic stance known as the “sawhorse appearance” (Fig. 9-18), in which the head, neck, back, and legs are stiff and the tail head is elevated. In some more severe cases, the horse may even be recumbent, and dyspnea may be seen. Diagnosis is often based on clinical signs.

Treatment should include placing the horse in a quiet dark area. Water and feed should be placed high in the stall so that the horse does not have to lower its head to eat and drink. Some horses may need body support to prevent them from falling. The wound should be cleaned, and tetanus antitoxin can be infiltrated around the wound. Sedatives and muscle relaxants can be used to control the muscle stiffness. Mortality is often 50%. Horses that survive the disease usually will stabilize within 2 to 7 days, with gradual recovery over a few weeks.

Other Microbial Diseases

Equine Protozoal Myeloencephalitis

Equine protozoal myeloencephalitis (EPM) is most commonly caused by the protozoan Sarcocystis neurona, but it also can be caused by the protozoan Neospora hughesi. Sarcocystis neurona is the most common cause of EPM. In the United States the only definitive host for S. neurona is the opossum, although armadillos, raccoons, cats, and skunks have been identified as natural intermediate hosts. Transmission of the disease occurs when horses consume sporocysts in opossum feces (Fig. 9-20).

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).

A definitive diagnosis requires identification of characteristic lesions and parasites within the central nervous system upon necropsy. Antemortem tests include evaluation of serum and cerebrospinal fluid but are not considered definitive.

Treatment involves antiprotozoal drugs and supportive therapy such as NSAIDs, and many veterinarians think horses should be supplemented with vitamin E as an antioxidant. Prevention should involve reducing opossum access to horse feeds and pastures.


Piroplasmosis is a tick-borne protozoal disease caused by one of two protozoans that invade red blood cells: Babesia equi and Babesia caballi. They are transmitted primarily by ixodid ticks. The ticks are found worldwide, but the disease is most common in areas of tropical, subtropical, and temperate regions.

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).

Clinical signs include pyrexia, depression, anemia, thirst, and eye problems (Fig. 9-25). The urine is yellow to reddish in color. Mortality is 10% to 15%. Prevention involves tick control and sterilization of needles and medical instruments between uses.

Diagnosis of piroplasmosis can be accomplished with blood smears, complement fixation tests, indirect immunofluorescent antibody tests, ELISA, PCR, or in vitro organism cultivation.

Treatment of adult horses with acute clinical signs involves administration of imidocarb dipropionate, diminazene, amicarbalide, euflavine, and/or tetracyclines. Prevention of the disease should include restriction of movement of infected horses and tick feeding prevention (Fig. 9-26).


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).

Treatment of ringworm can be accomplished with povidone-iodine, thiabendazole ointment, sulfur dip, miconazole, ketoconazole, fluconazole, or captan. The environment can be treated with diluted bleach (1 : 40) and by elimination of infected tack.

White Line Disease

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.

Viral Diseases


Eastern equine encephalomyelitis, western equine encephalomyelitis, and Venezuelan equine encephalomyelitis are caused by equine alphaviruses.

Eastern equine encephalomyelitis and Western equine encephalomyelitis both are found throughout North America. Venezuelan equine encephalomyelitis is most commonly found in the southern United States and in countries further south. Encephalomyelitis is transmitted by the mosquito. Common clinical signs include fever, ataxia, anorexia, paralysis, circling, head pressing, and hyperexcitability (Fig. 9-32).

Diagnosis is presumptive before death. There are no known treatments for encephalomyelitis. Treatment should be supportive. Prevention should include vaccination.

Equine Arteritis

Equine viral arteritis is caused by equine arteritis virus (EAV). EAV causes flu-like symptoms, abortion, and, in very young horses, pneumonia. The disease is transmitted through either respiratory particles or venereal routes (Fig. 9-33). Even though horses can transmit the disease through bodily fluids (e.g., urine), aborted fetuses, and aerosol, infected semen is the primary source of infection. Semen from infected stallions can be chronically or acutely infected with the virus. The stallion is the natural reservoir for the virus. The incubation period is 2 to 14 days.

Horses are often subclinical carriers of the virus. Clinical signs that present in adults often include abortion, respiratory signs, and fever. In foals, clinical signs can include pneumonia and enteritis.

Because the disease has many possible differential diagnoses, the diagnosis should never be made based on clinical signs. To confirm a case of equine arteritis, virus isolation, paired serum samples, viral antigen, or viral nucleic acid detection should be used.

Treatment of horses with severe infections includes NSAIDs, fever-reducing drugs, diuretics, and rest. Most adult horses recover uneventfully. There is no effective treatment for foals with pneumonia or for carrier stallions. Stallions that carry the virus should be surgically castrated. Prevention of the disease includes vaccination.

Equine Infectious Anemia

Equine infectious anemia (EIA; swamp fever) is caused by equine infectious anemia virus (EIAV). EIAV is a lentivirus of the Retroviridae family. The disease is transmitted through blood-sucking insects.

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.

Diagnosis of the disease is made by serologic testing. Four serological tests are accepted by the United States Food and Drug Administration: the agar gel immunodiffusion test (AGID), cELISA, Vira-CHECK ELISA, and the synthetic antigen ELISA.

There is no specific therapy for horses diagnosed with EIA. The disease is reportable in the United States. Most often the horse is recommended for euthanasia. If the owner elects not to euthanize, the animal must be quarantined from other horses, the horse cannot undergo travel interstate, and supportive therapy is recommended (Fig. 9-36).

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Aug 11, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on Common Equine Diseases

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