Coccidiosis in new world camelids (Proceedings)

A variety of parasites affect the gastrointestinal tract of New World camelids. Some of these are unique to camelids, but many also infest or infect ruminants, other domestic animals, cervids, or other wildlife as well. As a rule, parasitic infections are more associated with ill thrift than more specific and overt signs of GI disease, such as diarrhea or colic, but as such, they are among the most common causes of poor-doing in domestic camelids. Awareness of the importance of protozoal enteritis has been growing steadily. This is reflected both in the number of scientific publications, and the overall recognition that parasite control strategies must extend beyond anthelmintics. Also, once considered diseases of crias, certain protozoal enteritides are now widely recognized as important disorders of all ages of camelids.

New World camelids appear to be susceptible to at least 5 species of Eimeria. These appear to be camelid-specific, unlike many worms, Giardia, and Cryptosporidium. Thus, transmission from ruminants or wildlife is not thought to be important. Camelid coccidia do, however, affect all species of New World camelid, and whether they also affect Old World camels is an open question. Whereas coccidiosis is primarily thought to be a disease of the young in many species, and is well publicized as a cause of illness and death in crias in South America, it is becoming more commonly recognized worldwide as a cause of adult morbidity and mortality as well.

Camelid coccidia can be lumped into categories of small and large. The small coccidia are relatively conventional in appearance and life cycle, and will be familiar to anyone acquainted with coccidial disease in domestic poultry or ruminants. The large coccidia of camelids are relatively unique. The small coccidia include, by increasing size of oocysts, Eimeria punoensis (17 to 22μ in length), E. alpacae (22 to 26μ), and E. lamae (30 to 40μ). Oocysts become more ovoid as they get larger, so that E. punoensis is about 16% longer than it is wide without a clearly visible polar cap (by standard light microscopy), whereas E. lamae is about 60% longer than it is wide and has an obvious cap. These follow the same general lifecycle as Cryptosporidium with a few notable exceptions. Eimeria oocysts are not thin-walled and are not capable of autoinfection. They do not sporulate and become infective until they have spent 4 to 12 days (for E. lamae) or more outside of the host. After ingestion, sporulated oocysts usually release 8 sporozoites, which penetrate epithelial cells. The host cell nucleus and organelles are marginalized and the cell ruptures with maturation of each parasitic stage. Thus, mucosal loss can be widespread, particularly during the early, multiplicative stages of infection. The prepatent periods are approximately 10 days for E. punoensis, 15-16 days for E. lamae, and 16-18 days for E. alpacae.

The small coccidia are best associated with hemorrhagic, watery diarrhea progressing to weakness, lethargy, weight loss or poor weight gain, feed refusal, dehydration, and eventually shock, coma, and death. Colic, respiratory distress, and cerebral signs are uncommon or late findings. The gut, particularly the terminal jejunum and ileum, is occasional hemorrhagic or markedly edematous, and may have areas of mucosal hemorrhage, fibrinonecrotic pseudomembranes, or punctate white lesions, but is more commonly grossly non-remarkable. Histologically, lesions are most pronounced in the villi. There is mucosal loss and villus shortening. Immature and mature forms of the coccidia may be present. The submucosa is often filled with hemorrhagic or eosinophilic infiltrates. In severe cases, the mucosa is lost to the basement membrane. Protein loss is considerable, and hypoproteinemia is the most consistent blood abnormality. Anemia, hyponatremia, and hypochloremia are other common abnormalities.

The small coccidia primarily cause clinical disease in crias up to around 8 months of age. South American crias are usually shedding by around 23 days of age, with earliest shedding by 15 days, meaning they become infected shortly after birth. Shedding increases until 40 to 50 days of age, then gradually tapers off. Illness usually occurs in those first 2 months. Under rare circumstances, clinical disease is seen in older crias or adults. This usually reflects overwhelming exposure or a poor immune response.

The large Eimeria of New World camelids are E. macusanensis and E. ivitaensis. These are 3 to 4 times larger than small coccidia, and are approximately 80 to 100μ in length. As such, they resemble E. leukarti of horses, E. camelli of camels, and other large Eimeria. E. ivitanensis oocysts are elongated ellipses, whereas E. macusaniensis is ovoid and pyriform, resembling a cut avocado or watermelon seed in shape. Both have an obvious polar cap. There is some heterogeneity in size and shape of E. macusanensis, and it is possible that future research will reveal that distinct species exist. E. macusanensis also has a thick wall (approximately 8.5 to 11μ), which makes the cyst extremely durable; identifiable cysts have survived approximately 10,000 years in mummies.

The life cycles of the large coccidia resemble those of small coccidia, except that everything generally takes longer. The prepatent period for E. macusaniensis is from 32-43 days; that from E. ivitaensis has not been reported. Sporulation times for E. macusaniensis range from 2 to 3 weeks, with faster times under warmer conditions. Sporulation appears to arrest at 7°C or below. Sporulation times for E. ivitaensis has not been reported, but appears to be in the 7 to 10 day range in our laboratory. The longer lifecycle means that patent infections appear later than with small coccidia, but not necessarily that disease occurs later. Severe disease and death appear to be able to occur within 3 weeks of initial exposure and 2 weeks before establishment of patency. There is growing evidence that crias shedding small Eimeria oocysts or showing signs of enterotoxemia, may actually be dying of prepatent E. macusaniensis infection. Additionally, there are increasing reports of prepatent or patent disease in adult camelids. Some of these are long-time herd residents, but most have a history of transportation and mixing with new groups of animals. Whereas shows, sales, and movement for breeding may cause stress and inhibit the immune response, the simplest explanation may lie in eating habits: new entrants in a herd are more likely to eat off the ground than out of feeders, or more likely to eat in the less desirable areas of pasture. Thus, they may ingest larger doses of the parasite and be more likely to show disease signs.

The characteristics of clinical disease associated with E. macusaniensis have been studied and reported more extensively than any other parasitic gastroenteritis in camelids. It is likely that much of this information pertains to other coccidial infections and to parasitic gastroenteritis in general. In younger camelids, gastroenteritis is more likely to result in clinical diarrhea, whereas in older camelids, diarrhea is often absent or easy to miss. In fact, in adults, it is frequently counterintuitive to directly link the presenting signs to GI illness. In addition to or instead of diarrhea, general signs include weight loss or poor weight gain, ill-thrift, and increasing lethargy, weakness, and loss of appetite. It is one of the most common causes for weakness, weight loss, hypoproteinemia, or ill thrift in our area. Some animals show colic signs, probably more with E. macusaniensis than with any other parasitic gastroenteritis. As the disease progresses, hypoproteinemia worsens without commensurate anemia; mild anemia is common, but hypoproteinemia and hypoalbuminemia often become severe (such as 3.8 to 2.2 mg/dl for serum total protein and 1.8 to 0.6 mg/dl for serum albumin concentrations). There is also often some reduction in serum sodium and chloride concentrations, and hypokalemia become more marked with anorexia. With worsening disease, the animal becomes susceptible to translocation of bacteria or toxins through the damaged mucosa, the effects of hypoproteinemia, and circulatory shock. Signs of other organ systems are seen: camelids may develop ascites, hydrothorax, hydropericardium, pharyngeal edema, and cerebral edema, with ensuing abdominal distention, increased respiratory effort, lethargy, tachycardia, hypothermia, dysphagia, salivary loss, and cerebral signs. Eventually, there is also clinicopathologic evidence of the systemic disease including azotemia, metabolic (usually lactic) acidosis, high liver enzymes, hyperbilirubinemia, and increases in fat fractions. Abdominocentesis usually yields a transudate. Abdominal imaging is also inconclusive: colicky camelids may have ileus and fluid-distended intestine, though usually to a lesser degree than camelids with GI obstruction. Thickened bowel walls are rare (<10% of cases). In some cases, signs are insidious, and the animal is simply found dead.

Light microscopic examination of fecal samples is also the standard method of detecting coccidia. There are a number of pitfalls, namely prepatent or peripatent disease, intermittent shedding, and oocysts with a range of densities. Prepatent disease is more common in the coccidia with longer life cycles, namely E. macusaniensis. For E. macusaniensis, clinical disease and death can occur up to 2 weeks before the appearance of oocysts in the feces. For small coccidia, clinical disease usually appears around the same time as fecal cysts passage, but may precede it by a day or two. If prepatent disease is suspected, serial fecal analyses at two to four day intervals may be used to confirm the organism; presumptive treatments may be instituted in the interim. When looking for prepatent or peripatent shedding of protozoan parasites, it is important to keep the shedding curve in mind; Eimeria oocyst passage resembles a bell-shaped curve, with few at the earliest stages, peaking in 1 to 2 weeks before tapering off.

Small Eimeria and E. ivitaensis oocyst appear to float readily in flotation solutions with a specific gravity of 1.18 (saturated saline, 33% ZnSO4). E. macusaniensis requires denser solution (S.G. >1.025?)

The most commonly used anticoccidial medications for camelids in North America are amprolium (10 mg/kg at the label dilution, PO, q24h for 5 days) and sulfa antibiotics. Both are more effective against the immature forms of the parasite in ruminants and should not be expected to immediately reduce fecal shedding. Efficacy in camelids remains empirical, and pharmacokinetic trials on sulfa antibiotics suggests that uptake (and therefore efficacy) is negligible once the forestomach develops. Likewise, amprolium put in the water supply is often not drunk in sufficient quantities to be effective; individual animal dosing is preferred. Treatment with amprolium during the prepatent period does appear to reduce subsequent shedding, and also decrease the viability of oocysts. There has been some concern that protracted treatment with amprolium may cause polioencephalomalacia, but I have not seen that with the 5-day course. Milling decoquinate (0.5 mg/kg for 28 days) into pelleted feeds may also be helpful, if the crias are old enough to eat the pellets.

Benzeacetonitrile compounds have been gaining popularity as a coccidia treatment in the U.S. and are in heavy use in other countries. Ponazuril and toltrazuril (5 to 20 mg/kg, PO, q24h for up to 3 days) are effective against multiple stages of the parasite and rapidly stop shedding. The higher doses and longer courses are for treatment of individuals; the lower doses may be used for control.