From the moment a newborn foal exits the warm fluid environment of its gestation and draws a first postpartum breath of air, it is exposed to millions of would-be invaders that would do it harm if not for the components of the foal's immune system, which are myriad in number and elegant in their complex yet coordinated interactions. Foals are born precocious, meaning that they are designed and equipped to become ambulatory and travel in the protective custody of a herd within hours of being born (contrast this with the situation in humans, in which newborn infants are helpless and completely dependent on adult care for years). In many ways a foal's immune system is similar to the foal itself, in that it is capable of recognizing and initiating protective responses against pathogens from the time of birth. In fact, equine fetuses can mount an immune response while still in utero. Nevertheless, some aspects of immunity in foals are not mature and fully operant in the neonatal period, and certain pathogens are particularly adept at finding loopholes in a neonatal foal's protective mechanisms and causing disease despite all the cells and circulating antibodies that exist to prevent infection.

One such pathogen is Rhodococcus equi, a bacterium that is ubiquitous in environments where horses reside, that adult horses have no reason to fear, but which can cause a lethal abscess-forming infection in the lungs and other tissues in young foals.

What is It?

Rhodococcus equi is a facultative intracellular bacterium, meaning that it prefers to live inside of cells. But R. equi won't select just any cell: what makes R. equi distinctive is that the cells it targets to infect are the very cells that exist to destroy it.

The bacteria invade one of the most ferocious types of killing cell in the body, the macrophage. Macrophages engulf and destroy foreign agents like bacteria; they are large cells that circulate among tissues while conducting immune surveillance.

A specialized population of macrophages lives in the alveolar sacs of the lungs--a good arrangement because potential pathogens are inhaled and impact the alveolar surfaces with every breath. The bold infective scheme employed by Rhodococcus works, and this is why: Although the macrophages will recognize and engulf the bacteria, R. equi prevents fusion of the sacs in which it resides with other tiny sacs in the macrophage cytoplasm that contain a potent and poisonous mixture of hydrogen peroxide and other compounds lethal to bacteria. By preventing fusion of the poison-bearing sacs with the sacs in which they are enclosed, the bacteria continue to divide and thrive inside the very cells that should destroy them.

Eventually, the macrophage itself is destroyed, a process that frees the engulfed bacteria and leads to recruitment of ever- increasing numbers of other inflammatory cells. As this battle between immune elements and foreign invaders continues, large areas of lung are replaced by abscesses.

In the lungs of infected foals, a number of abscesses develop and sometimes turn into very large masses. In essence, R. equi doesn't infect the foal's tissue cells so much as it infects the foal's immune cells, rendering the foal's immune response ineffective.

Foals are exposed to R. equi cells at or very near the time of birth, likely in the first few days after parturition, but pneumonia typically is not recognized until foals are one to five months old (this varies by region). Foals in the two- to three-month age range are in an "antibody valley," meaning the maternally derived antibodies that the foal obtained passively via ingesting colostrum at birth have waned in concentration.

During this time, the foal's native immune mechanisms are maturing and becoming fully protective, but there is a period in this transition stage from passive to active immune predominance when foals are immunologically vulnerable to pathogens. This concept is well known, but researchers also have learned that certain cytokines (molecules generated by immune cells that foment and target the immune response) are necessary for the foal's immune cells to fight off an R. equi challenge, but those cytokines are not present in young foals.

R. equi infection has been the focus of intense research efforts. The foal, the bacterium, and the environment are the three key elements in any situation involving an infected foal. The foal's defenses, the bacterium's invasive mechanisms, components of the environment that might lead to compromise in the foal (like a concurrent parasite load or poor nutrition), or a high load of the organism (like poor manure-removal programs and dusty areas with high concentrations of horses) are in constant interplay and balance. These factors have been extensively evaluated on R. equi- endemic farms, and results suggest that the good husbandry practices enjoined by most horse owners do not, unfortunately, protect foals from infection.

A vaccine for bolstering a foal's defenses is not currently available, so augmenting the foal's immune mechanisms in other ways might be the only way of controlling the infection, at least on large farms with numerous mares and foals.

Administration of hyperimmune plasma (rich in anti-rhodococcal antibodies) in the first week to month of a foal's life is known to decrease the prevalence of foal R. equi pneumonia on a given premise, and ongoing research suggests that certain elements of the foal's cell-mediated immunity are lacking, and these elements are prime candidates for bolstering in the future.

Also, scientists have conducted extensive research to answer the question of why some foals become infected and others do not on farms on which infection is endemic. Although the jury is still out on many particulars of that point, it is clear that foals reared on farms with large acreage, high numbers of mares and foals, and a population of transient mares and foals (meaning mare-foal pairs that might only reside on the premises long enough for breeding or that come and leave for other reasons) are at higher risk of contracting R. equi pneumonia. Even intensely managed farms with strict health care protocols in place can have R. equi problems.

Surprisingly, the chief source of R. equi on a farm is the gastrointestinal tracts of adult horses and infected foals. In adult horses, R. equi is a component of normal bowel flora and causes no harm. Its ticket to the lungs of susceptible foals appears to be dust. After the organism is passed into the environment by way of the manure, when dust is swirled up in areas of high horse traffic (like around pasture gates, waterers, or feed troughs, and inside poorly ventilated stalls, especially those with dirt floors), foals inspire the bacteria in air.

A sick foal functions as a multiplier for R. equi because as the infection silently burgeons in the lungs, the foal coughs up and swallows increasingly bacteria-laden mucus. After passing through the foal's intestines, the organisms are deposited back in the environment, where they contribute to the environmental load of the pathogen that will infect other foals.

However, as the bacteria in the gastrointestinal tract, they might give rise to some of the other rhodococcal infections, including colitis and enlargement of the mesenteric lymph nodes. A relatively common complication of R. equi infection is development of a single large abscess in the abdomen. Other foals develop joint swelling, skin lesions, or bone infections. All of these manifestations of infection decrease the prognosis for survival. While lung infections in most foals respond favorably to antimicrobial treatment, abdominal abscesses and bone infections don't respond as well, and foals that do survive might be smaller in size than their peers.

Clinical signs of R. equi pneumonia can range from a slightly high resting respiratory rate and a fever in a normal-appearing foal, to respiratory distress in an obviously ill youngster. Foals in the latter state will have flared nostrils, noticeable contraction of the abdominal muscles during breathing, and severe exercise intolerance. Some foals will have purulent nasal discharge and a cough; in other foals these signs can be surprisingly subtle, given the severity of the disease.

Visibly ill foals infected with R. equi will have a high rectal temperature--which arises partly from fever and partly from difficulty breathing--and a increased heart rate. Results of blood work typically reveal inflammatory changes such as a high white cell count and high fibrinogen (a plasma protein) concentration. Foals often have an unthrifty appearance because as it becomes more difficult for them to breathe, they nurse less. Also, bacteria swallowed in infected mucus can infect portions of the gastrointestinal tract, leading to diarrhea and poor absorption of ingested nutrients.

One of the most frightening aspects of R. equi pneumonia is that foals can appear normal one day, but appear extremely ill the next. In some foals the disease progresses so quickly that the foals are simply found dead without ever exhibiting any obvious external signs. Because most foals reach the susceptible age for R. equi pneumonia in the summer months, their survival can be further challenged by extreme heat, which can be lethal.

Although a veterinarian might note the typical pattern of R. equi lung abscess formation with ultrasound or radiography, certain diagnosis of R. equi infection requires that he collect a sample of airway fluid through an endoscope or by means of a transtracheal aspirate. Fluid obtained from the lower airways is cultured and undergoes susceptibility testing or a polymerase chain reaction (PCR) assay. Many veterinarians prefer the former because that technique reveals other bacteria besides R. equi that might also be infecting the foal, and it yields information about the best antimicrobial choices.

Identifying R. equi is important because the drug combination used to treat this infection might not be the best choice for other types of infections. In addition, treatment for rhodococcal pneumonia typically continues for four to eight weeks or longer in foals with abdominal abscesses or other extrapulmonary infections. An important component of the cost involved in treating a foal with rhodococcal pneumonia is the monitoring that takes the form of recheck examinations, serial blood work, and sonographic or radiographic imaging.

Treatment of R. equi pneumonia typically involves administration of a drug combination that includes rifampin plus erythromycin, azithromycin, or clarithromycin.

These combinations are effective in part because they can penetrate macrophage membranes and reach the sequestered bacteria. Owners should be aware of two occasional--but important--drawbacks associated with the treatment regimen: development of diarrhea and hyperthermia.

Foals that are receiving erythromycin, azithromycin, or clarithromycin during the summer should be monitored carefully for overheating, as these medications have been associated with hyperthermia severe enough to cause death. Hyperthermia differs from fever in that it's a derangement of thermoregulation that arises from excessive and abnormal muscular activity, as opposed to a physiologic reaction to the presence of pathogens. Rectal temperatures exceeding 105.5°F should make the veterinarian suspicious of hyperthermia. Foals with high rectal temperature (for any reason) should be kept cool; protection from heat stress is an important component of treatment.

Prevention Aids

Although a vaccine is not available at present to help horse owners control R. equi infection, owners and veterinarians can establish some preventive measures. Administration of plasma to foals in the first week to the first month of life reduces the prevalence of the disease on a premise. Dust control and keeping the stocking density as low as possible can help. Transient mare-foal pairs should always be housed on a different part of the farm than the resident herd members, and movement of farm help between the two groups should be minimized. Manure from foals with R. equi pneumonia should be removed and not spread on fields, unless they are fields where no young foals are confined.

Take-Home Message

R. equi is a pathogen that has developed sophisticated mechanisms for evading immune destruction.

Foals can and do respond favorably to treatment and survive to become athletic adults, but the microbe remains a foe to respect because of its unique biology and the fact that infection is typically far ahead of human detection.

About the Author

Kim A. Sprayberry, DVM, Dipl. ACVIM

Dr. Kim A. Sprayberry, DVM, Dipl. ACVIM, is an internal medicine specialist at Hagyard Equine Medical Institute in Lexington, Ky. When not working with horses, she enjoys pursuits in medical journalism and editing as well as kayaking and American southwest archaeology.

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