By Dr. Chris Cebra, Oregon State University
I am writing this editorial to describe Eimeria
macusaniensis infection, which I believe to be one of the most important emerging diseases in camelids. The
causative organism is the largest of the camelid coccidia, 100 microns in length, thick-walled, and
watermelon seed-shaped. It has longer prepatent (32 to 43 days) and patent (up to 40 days) periods than other
species of coccidia, and also is as commonly associated with disease and death in adults as in
crias. It is not a new organism. Dr. Jarvinen's work from 1999 suggested that it was present in most herds,
and my recent experiences support that. It is "emerging" because of greater awareness, better
detection methods, and possibly higher case attack rates. It is my belief that the extreme environmental
stability of this organism has allowed it to build up
over the 20+ years of popular camelid farming in the U.S., and that together with certain management
practices including overcrowding, co-housing of crias and adults, overuse of certain pastures, and mixing
stressed camelids from different locations, has lead to a real increase in clinical cases.
Eimeria macusaniensis follows the typical coccidian lifecycle, requiring 13 to 21 days on the ground for
oocysts to sporulate, having multiple rounds of replication within the host, and primarily damaging
the intestinal epithelium. The severity of clinical disease relates to host immunity and infective dose.
Lightly infected, immunocompetent camelids may transiently shed small numbers of organisms, but will
show no signs. Immunocompromised or immunonaive camelids, such as stressed adults or all
crias, confronted with a large or overwhelming dose, may succumb to fatal disease in as little as 3 weeks, or
as long as 2 weeks before oocysts appear in the feces. Adults within an infected herd appear to be less
susceptible than ones introduced later, for example for breeding. The major signs of severe disease are
those of weakness and wasting. Unless the camelid is weighed frequently, the owner frequently notices
nothing wrong until the camelid collapses. Diarrhea is uncommon, except in crias. Hypoproteinemia is the
major blood abnormality. Clinical abnormalities will be more comprehensively described in a
soon-to-appear scientific report.
The combination of lack of specific GI signs and a negative fecal examination makes the infection easy to
miss. We consider all ill-thrift camelids to be suspect, and either treat empirically or perform
multiple fecal examinations over at least a 2 week period. Even then, shedding is often light (<100
oocysts/g) for the first week of patency, even in camelids with overwhelming infections. Considering
that most of the anticoccidial medications available in the U.S. are most efficacious against the earlier
stages of the organism, delaying treatment in suspect camelids is unlikely to be advantageous. It is more
difficult to decide what to do with non-clinical shedders and their herdmates. As with other internal
parasites, in general we acknowledge their presence and try to control them, not eliminate them. The long
prepatent period, together with the pelleted camelid feces, offers the potential for timely manure removal
to decrease pasture contamination. We believe the thick wall of the organisms imparts extreme
environmental resistance, so leaving paddocks and pastures empty is of less benefit than with other GI
parasites. Radical soil treatments including burning and topsoil removal have been tried, but such
approaches should only be considered in extreme circumstances. As with other parasites, a good
management approach decreasing stocking density, avoiding admixtures of stressed camelids, encouraging
eating from above-ground feeders, avoiding excess cohabitation of crias and adults, conducting fecal
parasite surveillance, timely antiparasitical treatments, and frequently checking demeanor and body
condition of camelids should decrease the number of affected camelids and allow early identification of
those that require treatment.
I have only lightly addressed fecal detection. This will also be the subject of an upcoming scientific
report. The high density of the oocyst makes it more likely to float in denser float solutions and also
slower to rise. The low numbers at the onset of patency dictate that very sensitive techniques should
be used. These factors should be considered when choosing the method of fecal analysis.
Primary Reference:
Cebra CK, Valentine BA, Schlipf Jr. JW, Bildfell RJ,
McKenzie E, Waitt LH, Heidel JR, Cooper BJ, Lohr CV,
Bird KE, Saulez MN, Firshman AM. "Eimeria
macusaniensis infection in 15 llamas and 34 alpacas".
J Am Vet Med Assoc. 2007 Jan 1;230(1):94-100.
Reprinted from Wool & Wattles: The AASRP Newsletter,
vol. 34, #4; pp. 10-11, Oct.-Dec. 2006 with
permission from Dr. Chris Cebra and the American
Assoc. of Small Ruminant Practitioners. Permission to
reprint this article is granted to participants in the
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