Purpura Hemorrhagica

Purpura hemorrhagica is a serious immune-mediated vasculitis that affects horses, characterized by widespread inflammation of small blood vessels throughout the body. This condition occurs when the horse's immune system produces antibodies that attack the walls of blood vessels, leading to increased vascular permeability and the leakage of blood and fluid into surrounding tissues. The result is dramatic subcutaneous edema, hemorrhages, and potentially life-threatening complications if left untreated. Purpura hemorrhagica represents one of the most striking and concerning complications that can follow bacterial infections in horses, particularly those caused by Streptococcus equi subspecies equi, the bacterium responsible for strangles.

This condition can affect horses of any age, breed, or discipline, though it most commonly occurs in horses that have recently recovered from strangles or have been exposed to Streptococcus equi bacteria. Horses that have experienced multiple exposures to these bacteria or have received strangles vaccinations while harboring subclinical infections appear to be at increased risk. The condition has also been reported following other bacterial infections, including those caused by Streptococcus equi subspecies zooepidemicus and Corynebacterium pseudotuberculosis, as well as following viral respiratory infections in some cases.

The impact of purpura hemorrhagica on equine health can be devastating without prompt recognition and aggressive treatment. The massive fluid shifts that occur can lead to severe dehydration, electrolyte imbalances, and organ dysfunction. Extensive skin necrosis may develop in areas of severe edema, particularly on the limbs and ventral abdomen, leading to secondary infections and prolonged healing times. In severe cases, the inflammatory process can affect internal organs including the kidneys, gastrointestinal tract, and respiratory system, potentially resulting in fatal outcomes.

Despite its serious nature, purpura hemorrhagica is treatable when identified early and managed aggressively with appropriate immunosuppressive therapy, supportive care, and treatment of any underlying infections. The prognosis varies considerably depending on the severity of clinical signs at presentation, the speed of treatment initiation, and the horse's response to therapy. Early recognition of the characteristic clinical signs, including limb swelling and petechial hemorrhages, is essential for achieving the best possible outcome and preventing the potentially devastating complications associated with this immune-mediated condition.

The primary cause of purpura hemorrhagica is an abnormal immune response, specifically a type III hypersensitivity reaction, in which the horse's immune system produces excessive amounts of antibodies against bacterial antigens. These antigen-antibody complexes, known as immune complexes, deposit in the walls of small blood vessels throughout the body, triggering an inflammatory cascade that damages the vessel walls and increases their permeability. The most common triggering antigen is the M-protein found on Streptococcus equi subspecies equi bacteria, though other bacterial and occasionally viral antigens can initiate this process. The condition typically develops two to four weeks after initial infection or exposure, coinciding with the peak of antibody production.

While no specific genetic predisposition has been definitively identified for purpura hemorrhagica, individual variation in immune response appears to play a role in determining which horses develop this complication following infection. Some horses may have immune systems that are more prone to producing the excessive antibody responses that lead to immune complex formation and deposition. Additionally, horses with compromised immune function or those that have experienced repeated exposure to triggering antigens may be at increased risk for developing this severe complication.

Environmental and management factors significantly influence the risk of purpura hemorrhagica development. Horses housed in facilities where strangles is endemic or where outbreaks occur frequently face repeated exposure to Streptococcus equi, increasing the likelihood of sensitization and subsequent hypersensitivity reactions. Poor biosecurity practices, overcrowding, and stress from transportation or competition can facilitate bacterial transmission and may contribute to immune dysregulation. Vaccination practices also play a role, as administering strangles vaccines to horses that are already infected or have residual bacterial presence can trigger purpura hemorrhagica.

Several risk factors increase the likelihood of a horse developing purpura hemorrhagica following bacterial infection. Horses that have experienced severe or prolonged strangles infections, particularly those with abscessed lymph nodes or metastatic abscess formation, appear to be at higher risk. Incomplete treatment of primary infections, allowing bacteria to persist in the horse's system, may prolong antigen exposure and increase antibody production. Young horses experiencing their first exposure to Streptococcus equi and older horses with waning immunity may both be vulnerable. Concurrent illness, nutritional deficiencies, or other stressors that affect immune function can also predispose horses to developing this complication.

The pathophysiology of purpura hemorrhagica involves a complex inflammatory cascade initiated by immune complex deposition. When circulating immune complexes lodge in blood vessel walls, they activate the complement system, a series of proteins that amplify the inflammatory response. Complement activation attracts neutrophils and other inflammatory cells to the vessel walls, where they release destructive enzymes and reactive oxygen species. This inflammatory assault damages the endothelial cells lining the blood vessels, causing gaps to form through which blood and plasma leak into surrounding tissues. The resulting edema, hemorrhage, and tissue hypoxia can progress to skin necrosis in severe cases, particularly in dependent areas where hydrostatic pressure compounds the effects of vascular damage.

Early warning signs of purpura hemorrhagica can be subtle and may initially be attributed to other causes, making vigilant observation essential in horses recovering from strangles or other bacterial infections. The first indications often include mild stiffness or reluctance to move, slight swelling in the lower limbs that may be mistaken for stocking up, and a general sense that the horse is not quite right. A low-grade fever may be present, and horses may show decreased appetite or mild depression. Because horses naturally tend to hide illness as prey animals, these early signs require careful attention, particularly in horses with recent infection history.

The hallmark symptoms of purpura hemorrhagica become dramatically apparent as the condition progresses. Extensive subcutaneous edema develops, typically beginning in the lower limbs and spreading to involve the head, ventral abdomen, and prepuce or udder. This edema is characteristically firm and pitting, meaning that when pressed with a finger, the indentation remains visible for several seconds. The swelling can become so severe that the skin becomes taut and shiny, and the horse may have difficulty moving due to the weight and stiffness of the affected limbs. Petechial and ecchymotic hemorrhages, appearing as small red spots and larger bruises, become visible on the mucous membranes of the gums, nostrils, and conjunctivae.

Behavioral changes in horses with purpura hemorrhagica reflect the discomfort and systemic effects of the condition. Affected horses typically become depressed and lethargic, standing quietly with a lowered head and showing little interest in their surroundings. Appetite decreases significantly, and horses may refuse feed entirely as the condition progresses. The reluctance to move becomes more pronounced as limb swelling increases, and horses may shift weight frequently in an attempt to find comfort. Some horses become anxious or restless, while others become increasingly withdrawn and unresponsive to normal stimuli.

Physical signs of purpura hemorrhagica extend beyond the dramatic edema and hemorrhages. The skin overlying severely swollen areas may develop a blue or purple discoloration, reflecting poor circulation and impending necrosis. Serum may begin to weep through the skin in areas of extreme edema, creating wet, sticky surfaces that attract flies and become susceptible to secondary infection. The horse's pulse and respiratory rate typically increase as the body attempts to compensate for fluid shifts and potential blood loss. Dehydration develops despite the apparent excess of fluid in the tissues, as plasma proteins and fluid are sequestered in extravascular spaces.

Symptom progression in untreated or inadequately treated cases can be rapid and severe. The edema extends from initial sites to involve larger areas of the body, potentially affecting the respiratory tract and causing breathing difficulties. Skin over severely affected areas may begin to slough, revealing raw, painful underlying tissue that requires extensive wound care. Internal organ involvement may manifest as colic signs if the gastrointestinal tract is affected, or as decreased urine production if the kidneys sustain damage. The horse's condition can deteriorate rapidly, with cardiovascular shock developing in severe cases.

Emergency symptoms requiring immediate veterinary care include extreme difficulty breathing or evidence of upper airway obstruction from pharyngeal swelling, collapse or inability to stand, profuse bleeding from any body opening, signs of severe colic, complete refusal of food and water for more than twelve hours, and rapid deterioration despite initial treatment. Horses showing extensive skin sloughing, high fever above 104 degrees Fahrenheit, or signs of cardiovascular compromise such as rapid weak pulse, cold extremities, or prolonged capillary refill time require emergency intervention. Any horse suspected of having purpura hemorrhagica should be evaluated by a veterinarian immediately, as early aggressive treatment significantly improves outcomes.

Physical examination findings in horses with purpura hemorrhagica are often striking enough to suggest the diagnosis immediately. The veterinarian will observe the characteristic pattern of firm, pitting edema affecting the limbs, head, and ventral body regions, along with petechial hemorrhages on visible mucous membranes. Careful palpation of the swollen areas helps differentiate the edema of purpura hemorrhagica from other causes of limb swelling, as the fluid accumulation in this condition tends to be more diffuse and symmetrical than that seen with cellulitis or lymphangitis. The veterinarian will also evaluate the horse's vital parameters, assess hydration status, and examine for evidence of skin necrosis or impending sloughing. A detailed history including recent illness, vaccination, or exposure to sick horses provides crucial context for the diagnosis.

Diagnostic testing helps confirm the diagnosis and assess the severity of the condition. Complete blood count often reveals evidence of an inflammatory response, including elevated white blood cell count with increased neutrophils, though these findings are not specific to purpura hemorrhagica. More characteristically, the blood work may show decreased platelets (thrombocytopenia) and evidence of anemia if significant hemorrhage has occurred. Serum biochemistry panels help evaluate kidney and liver function, which may be compromised in severe cases. Urinalysis may reveal protein or blood in the urine, indicating kidney involvement. Measurement of serum M-protein antibody titers can support the diagnosis and help identify the triggering infection, with elevated titers against Streptococcus equi being particularly significant.

Advanced diagnostic procedures may be employed in cases where the diagnosis is uncertain or to assess the extent of organ involvement. Skin biopsy from affected areas can confirm the presence of vasculitis and immune complex deposition, providing definitive histopathological evidence of the condition. Ultrasound examination may be used to evaluate internal organs, assess the extent of subcutaneous fluid accumulation, and identify any abscesses or other complications. In horses with respiratory signs, endoscopy of the upper airway can assess the degree of pharyngeal and laryngeal swelling. Guttural pouch endoscopy may be performed to check for persistent Streptococcus equi infection, particularly if the horse has a history of strangles.

Differential diagnosis is important because several other conditions can cause similar clinical signs. Severe cellulitis or lymphangitis may produce limb swelling but typically affects one limb predominantly and is associated with more localized heat and pain. Equine viral arteritis can cause edema and hemorrhages but is accompanied by different systemic signs and has a distinct epidemiological pattern. Clostridial infections can cause rapidly progressive swelling but are typically associated with wounds and produce gas in tissues. Severe allergic reactions or anaphylaxis may cause sudden swelling but usually affect the face and airways more prominently. African horse sickness, in endemic areas, must be considered as it causes edema and hemorrhages. Heart failure or severe hypoproteinemia can cause dependent edema but without the hemorrhagic component. A thorough clinical evaluation combined with appropriate diagnostic testing allows the veterinarian to distinguish purpura hemorrhagica from these other conditions and institute appropriate treatment.

Emergency and immediate treatment of purpura hemorrhagica focuses on halting the destructive immune response and stabilizing the horse's condition. The cornerstone of therapy is high-dose corticosteroid administration, typically dexamethasone given intravenously at doses ranging from 0.05 to 0.2 milligrams per kilogram body weight once or twice daily. These immunosuppressive medications work by dampening the excessive immune response, reducing antibody production, and decreasing inflammation in blood vessel walls. Treatment should begin as soon as the diagnosis is suspected, as delays allow continued vascular damage and increase the risk of complications. Intravenous fluid therapy is often necessary to combat dehydration and support circulation, as significant fluid volume is lost from the vascular space into tissues.

Medical management extends beyond corticosteroids to address the multiple aspects of this complex condition. Antimicrobial therapy is essential to eliminate any residual bacterial infection that may be providing ongoing antigenic stimulation. Penicillin-based antibiotics are typically chosen for their efficacy against Streptococcus species, though treatment courses may need to be extended for several weeks to ensure complete bacterial clearance. Non-steroidal anti-inflammatory drugs such as flunixin meglumine may be used cautiously for their anti-inflammatory and analgesic effects, though they should not replace corticosteroids as the primary treatment. Plasma transfusions may be beneficial in severely affected horses, providing both volume support and replacement of depleted clotting factors and albumin.

Surgical intervention is rarely required in purpura hemorrhagica but may become necessary to manage complications. If extensive skin necrosis develops, debridement of dead tissue may be required to promote healing and prevent secondary infection. Escharotomy, the surgical release of constrictive necrotic tissue, may be necessary if circumferential skin sloughing threatens limb circulation. In rare cases where upper airway obstruction becomes severe enough to threaten life, emergency tracheotomy may be required to establish an airway below the level of obstruction. These surgical interventions are supportive measures rather than treatments for the underlying condition.

Supportive care plays a crucial role in the successful management of purpura hemorrhagica. Affected horses should be maintained in a clean, dry, well-bedded stall to minimize contamination of weeping skin lesions. Limb bandaging with padded wraps can help reduce edema and protect damaged skin, though bandages must be changed frequently to prevent maceration. Topical wound care with appropriate antimicrobial preparations helps manage skin lesions and prevent secondary infection. Hydrotherapy, if available and tolerated, can help reduce limb swelling and promote circulation. Nutritional support is important, and horses that cannot or will not eat may require nasogastric tube feeding or intravenous nutritional supplementation.

Rehabilitation and return to work must be approached gradually as the horse recovers from purpura hemorrhagica. Initial activity should be limited to short periods of hand-walking as the edema resolves and the horse's strength returns. The duration and intensity of exercise are increased progressively based on the horse's response and the veterinarian's assessment. Complete resolution of clinical signs may take several weeks to months, and horses should not return to full work until all symptoms have resolved and the corticosteroid taper is complete. Some horses may experience residual effects such as scarring from skin lesions or prolonged limb swelling that require ongoing management.

Treatment decisions must consider multiple factors including the severity of clinical signs, the horse's response to initial therapy, financial constraints, and the intended use of the horse. Mild cases caught early may respond well to oral corticosteroids and supportive care managed on an outpatient basis. Severe cases typically require hospitalization for intensive monitoring and intravenous treatment. The presence of complications such as extensive skin necrosis or internal organ involvement worsens the prognosis and increases treatment costs. Competition horses face additional considerations regarding drug withdrawal times, as corticosteroids are prohibited or restricted in most equine sports. Open communication between the veterinarian and owner about prognosis, costs, and realistic expectations helps guide appropriate treatment decisions.

Recovery timeline for purpura hemorrhagica varies considerably depending on the severity of the initial presentation and the horse's response to treatment. Horses with mild to moderate cases that receive prompt treatment may show significant improvement within the first week, with visible reduction in edema and resolution of hemorrhages. However, complete recovery typically requires four to eight weeks of treatment, including a gradual tapering of corticosteroid doses to prevent relapse. Severe cases with extensive skin necrosis may require months of wound care and healing before the horse returns to normal function. Throughout this period, regular veterinary monitoring is essential to assess progress and adjust treatment as needed.

Post-treatment care and monitoring continue well beyond the resolution of obvious clinical signs. The corticosteroid taper must be managed carefully, typically reducing the dose by approximately twenty-five percent every five to seven days once clinical improvement is established. Attempting to reduce doses too quickly often results in relapse, requiring a return to higher doses and extended treatment. During the recovery period, horses should be monitored closely for any return of swelling, hemorrhages, or other symptoms. Regular blood work may be performed to assess the resolution of inflammatory markers and ensure that kidney and liver function remain normal.

Prognosis factors significantly influence the likelihood of full recovery and return to previous function. Horses that receive treatment early in the disease course, before extensive tissue damage has occurred, generally have better outcomes than those with advanced cases. The presence of complications such as laminitis, which can develop secondary to the inflammatory state, significantly worsens the prognosis. Horses that respond promptly to corticosteroid therapy, showing measurable improvement within the first forty-eight to seventy-two hours, typically have more favorable outcomes than those requiring escalating doses or alternative treatments. The horse's overall health status, age, and any concurrent conditions also influence recovery potential.

Long-term soundness outlook for horses recovering from purpura hemorrhagica is generally favorable for those that survive the acute phase without major complications. Most horses that recover fully can return to their previous level of work and performance. However, some horses may have residual effects including areas of scarring from skin necrosis, chronic mild limb swelling or lymphedema, or increased sensitivity to future bacterial infections. Horses that experienced laminitis as a complication may have permanent hoof damage affecting soundness. There is also a risk of recurrence, particularly if the horse is re-exposed to the triggering bacterial antigen, making ongoing management and prevention strategies important for long-term health.

Management practices that reduce exposure to triggering pathogens form the foundation of purpura hemorrhagica prevention. Implementing strict biosecurity protocols helps prevent the introduction and spread of Streptococcus equi and other bacteria that can trigger this immune-mediated condition. New horses should be quarantined for a minimum of three weeks before introduction to the resident herd, and ideally should be tested for strangles carrier status. Facilities should have established protocols for handling outbreaks of respiratory disease, including isolation of affected horses and designation of separate equipment and personnel for healthy and sick horses. Regular cleaning and disinfection of shared equipment, water sources, and high-traffic areas helps reduce environmental bacterial loads.

Nutritional considerations play a supporting role in maintaining immune system health and reducing the risk of abnormal immune responses. A balanced diet providing adequate protein, vitamins, and minerals supports optimal immune function without overstimulation. Particular attention should be paid to vitamin E and selenium status, as deficiencies in these nutrients can impair immune regulation. Avoiding sudden dietary changes and maintaining consistent feeding practices reduces stress that might compromise immune function. Horses recovering from bacterial infections should receive optimal nutrition to support healing without pushing for rapid return to work.

Exercise and conditioning practices should be managed to avoid immunosuppression while maintaining fitness. Overtraining and excessive physical stress can temporarily impair immune function, potentially increasing susceptibility to infection or abnormal immune responses. Horses should be allowed adequate rest and recovery following illness before returning to full training programs. Maintaining horses in good body condition, neither too thin nor too fat, supports overall health and immune function. Regular exercise promotes circulation and lymphatic drainage, which may help reduce the risk of severe edema if exposure to triggering pathogens does occur.

Environmental factors in the horse's living situation significantly influence disease risk. Reducing overcrowding decreases stress and limits pathogen transmission between horses. Ensuring adequate ventilation in barns and stables minimizes respiratory irritation and bacterial aerosol concentrations. Maintaining clean, dry footing reduces environmental bacterial loads and skin damage that might provide entry points for infection. Separating horses by age group or use can help limit exposure of naive individuals to endemic pathogens. Facilities housing large numbers of transient horses, such as show grounds or training centers, present particular challenges requiring enhanced biosecurity measures.

Vaccination strategies for strangles must be carefully considered in the context of purpura hemorrhagica prevention. While strangles vaccines can help reduce the severity of infection and shedding of bacteria, improper vaccination can actually trigger purpura hemorrhagica in sensitized horses. Vaccination should never be administered to horses during or immediately after strangles outbreaks, or to horses that have been recently exposed to infected animals. Horses that have previously experienced purpura hemorrhagica should generally not receive strangles vaccines. When vaccination is appropriate, intranasal modified-live vaccines may carry lower risk than intramuscular products in some situations. Consultation with a veterinarian regarding the specific circumstances and disease risk helps guide appropriate vaccination decisions.

Daily management adjustments are essential for horses diagnosed with or recovering from purpura hemorrhagica. During the acute phase, affected horses require intensive monitoring including twice-daily assessment of vital parameters, measurement of limb circumferences to track edema, and careful observation for signs of deterioration or improvement. Medication schedules must be followed precisely, with corticosteroids given at consistent times to maintain therapeutic blood levels. Clean water should be available at all times, with intake monitored to ensure adequate hydration. Feed should be offered in easily accessible locations, with hay placed at ground level to avoid the increased head swelling that can occur when horses eat from elevated hay nets.

Housing and turnout considerations must be modified during recovery from purpura hemorrhagica. The ideal environment is a clean, deeply bedded stall with good drainage that allows the horse to rest comfortably while minimizing contamination of skin lesions. Straw bedding may be preferable to shavings in horses with open wounds, as shavings can adhere to weeping skin and irritate healing tissue. The stall should be kept dry, with wet areas cleaned promptly to prevent bacterial proliferation. Once the acute phase has resolved and the horse is stable on medication, limited turnout in a small, clean paddock may be beneficial for promoting circulation and maintaining mental health, but horses should be protected from extreme weather conditions.

Exercise modifications during recovery must balance the benefits of movement for reducing edema against the risks of overexertion and stress. During the acute phase, horses should be kept quiet with activity limited to gentle walking within the stall or short periods of hand-grazing. As recovery progresses and edema resolves, hand-walking can be gradually increased in duration and distance. Horses should not be turned out with other horses during recovery, as the risk of injury and the stress of social interactions could trigger relapse. Return to ridden work should only occur after veterinary clearance and should progress slowly, with careful monitoring for any return of symptoms.

Monitoring and ongoing care requirements extend throughout the recovery period and beyond. Daily visual inspection of the horse should include checking mucous membrane color and refill time, assessing the degree of limb and body swelling, and examining any skin lesions for signs of infection or healing. Temperature should be recorded at least once daily, as fever may indicate infection or inflammation. Body weight should be monitored weekly if scales are available, as fluid shifts and appetite changes can cause significant weight fluctuations. A detailed log of medications, clinical observations, and any concerns helps track progress and provides valuable information for veterinary consultations.

Quality of life and use considerations become important as horses recover from purpura hemorrhagica and owners plan for the future. Most horses that recover fully can return to their previous activities without long-term restrictions. However, owners should be prepared for an extended recovery period that may span several months, during which the horse cannot be worked or shown. The financial commitment of prolonged treatment and rehabilitation should be realistically assessed early in the process. For horses with complications or incomplete recovery, modifications to intended use may be necessary. Some horses with residual limb swelling may be comfortable in lighter work but unable to return to high-level competition. Breeding animals should not be bred during recovery, and discussion with a veterinarian about the advisability of future breeding is appropriate given the immune-mediated nature of the condition.

Purpura hemorrhagica can affect horses of any breed, as the condition results from an immune response to bacterial infection rather than from inherited genetic factors. However, certain populations may face increased risk based on their likelihood of exposure to triggering pathogens, particularly Streptococcus equi. Young horses experiencing their first exposure to strangles are at risk for developing post-infectious purpura hemorrhagica, making yearlings and young horses in training programs particularly vulnerable populations. Conversely, older horses with repeated exposures over their lifetimes may develop hypersensitivity, and senior horses with waning immune regulation may also be at increased risk for aberrant immune responses.

Use and discipline considerations significantly influence risk for purpura hemorrhagica. Horses that travel frequently to shows, competitions, or breeding facilities face repeated exposure to respiratory pathogens including Streptococcus equi. Racehorses, particularly young Thoroughbreds in training, often live in high-density environments where respiratory diseases spread readily. Horses used in lesson programs or therapeutic riding face exposure to many different people and may be housed with horses from various backgrounds. Breeding stallions with numerous mare contacts, and mares shipped to breeding farms, also face increased exposure risk. These use patterns do not cause purpura hemorrhagica directly but increase the likelihood of the bacterial infections that can trigger the condition.

While no genetic test exists for purpura hemorrhagica susceptibility, breeding recommendations should consider the general immune health of prospective breeding animals. Horses that have experienced purpura hemorrhagica may have an underlying tendency toward immune dysregulation that could potentially be passed to offspring, though this has not been definitively established. More practically, the risk of spreading strangles during the breeding process is a concern, and horses recovering from recent infections should not participate in breeding activities until fully cleared. Maintaining complete health records, including any history of strangles or purpura hemorrhagica, helps inform breeding and purchasing decisions and supports management of disease risk in equine populations.

Strangles, caused by Streptococcus equi subspecies equi, is the condition most commonly associated with subsequent development of purpura hemorrhagica. This highly contagious upper respiratory infection typically precedes purpura hemorrhagica by two to four weeks, and horses with a history of severe or complicated strangles are at greatest risk. Other complications of strangles that may co-occur with purpura hemorrhagica include guttural pouch empyema, metastatic abscess formation (bastard strangles), and chronic carrier status. Understanding this relationship is essential for recognizing at-risk horses and implementing appropriate monitoring following strangles outbreaks.

Several conditions may present with clinical signs similar to purpura hemorrhagica, requiring careful differentiation. Severe cellulitis or lymphangitis causes limb swelling but typically affects one limb predominantly and is associated with fever, pain, and lameness more pronounced than the systemic signs seen with purpura hemorrhagica. Equine viral arteritis can cause edema and petechial hemorrhages along with respiratory signs and abortion in pregnant mares. Clostridial myonecrosis causes rapidly progressive swelling but is typically associated with wounds and produces gas in tissues. Severe systemic allergic reactions may cause facial and limb swelling but develop acutely rather than over days. Anasarca from heart failure or hypoproteinemia causes dependent edema without the hemorrhagic component.

Potential complications of purpura hemorrhagica extend beyond the immediate vascular damage. Laminitis can develop secondary to the severe systemic inflammation, and the risk may be increased by the high-dose corticosteroid therapy required for treatment. Extensive skin necrosis leads to prolonged wound healing, scarring, and risk of secondary bacterial infection. Kidney damage from immune complex deposition or cardiovascular compromise can result in acute or chronic renal dysfunction. Pharyngeal and laryngeal swelling may cause upper airway obstruction requiring emergency intervention. Internal organ involvement can cause gastrointestinal dysfunction, including colic or protein-losing enteropathy. Thrombophlebitis may develop at intravenous catheter sites in hospitalized horses, complicating fluid therapy and medication administration.