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
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.