C o c c i d i o s i s i n L a r g e an d

S ma ll Rum i n an t s
a, b
Sarah Tammy Nicole Keeton, PhD, MS *, Christine B. Navarre, DVM, MS

KEYWORDS

Coccidia
Coccidiosis
Diarrhea
Ruminants
Cattle
Sheep
Goats

Ionophores

KEY POINTS

Coccidiosis is an important parasitic disease of ruminant livestock caused by the proto-
zoan parasite of the genus Eimeria.

Calves between 6 and 12 months of age and lambs and kids between 1 and 6 months of
age are most susceptible.

Subclinical disease is characterized by poor growth.

Clinical disease is most commonly characterized by diarrhea.

Control of coccidiosis is based on sound management, the use of preventive medications,
and treatment of clinical cases as necessary.

INTRODUCTION: NATURE OF THE PROBLEM

Coccidiosis is a parasitic disease of vertebrate animals, including domestic ruminants.1

It is economically significant, with losses from both clinical and subclinical disease.
Coccidiosis is caused by the protozoan parasite of the genus Eimeria. Eimeria are
host specific, meaning that an Eimeria species that infect goats does not infect sheep
or cattle and vice versa. Certain species of Eimeria are nonpathogenic and do not
cause disease. The pathogenic species and sites of infection are listed in Table 1.
Mixed infections with multiple pathogenic and nonpathogenic species is common.

LIFE CYCLE

Proper treatment and control of coccidiosis requires an understanding of the complex

life cycle and transmission of Eimeria spp (Fig. 1). The life cycle can be divided into

Disclosure: The authors have nothing to disclose.

a
Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State
University, Skip Bertman Drive, Baton Rouge, LA 70803, USA; b LSU AgCenter, School of Animal
Sciences, Louisiana State University, 111 Dalrymple Bldg, 110 LSU Union Square, Baton Rouge,
LA 70803-0106, USA
* Corresponding author. 909 Durnin Drive, Denham Springs, LA 70726.
E-mail address: [email protected]

Vet Clin Food Anim 34 (2018) 201–208

https://doi.org/10.1016/j.cvfa.2017.10.009 vetfood.theclinics.com
0749-0720/18/ª 2017 Elsevier Inc. All rights reserved.
202 Keeton & Navarre

Table 1
Pathogenic species of Eimeria and site of infestation in cattle, sheep, and goats

Species of Eimeria Site of Infestation

Cattle Eimeria zuernii Small and large intestine
Eimeria bovis Small and large intestine
Eimeria alabamensis Small and large intestine
Sheep Eimeria ovinoidalis Cecum and colon
Eimeria crandalis Small and large intestine
Goats Eimeria arloingi Small intestine
Eimeria christenseni Small intestine
Eimeria ninakohlyakimovae Small and large intestine

Data from Taylor MA, Coop RL, Wall RL. Veterinary parasitology. Fourth edition. Chichester (United
Kingdom): Wiley Blackwell; 2016; and Chartier C, Paraud C. Coccidiosis due to Eimeria in sheep and
goats, a review. Small Ruminant Res 2012;103(1):84–92.

2 phases: an exogenous phase (free living in the environment) and an endogenous

phase (parasitic phase within host). The life cycle takes between 2 and 4 weeks to
complete depending on the species of Eimeria and environmental conditions.2
In the exogenous phase of sporogony, unsporulated oocysts are excreted in
feces and undergo sporulation under ideal environmental conditions of oxygen,

Fig. 1. Eimeria life cycle. (From Javier Garza, PhD, USDA-NIFA Fellow, Parasite Immunology,
Division of Animal and Nutritional Sciences, West Virginia University, with permission.)
 Coccidiosis in Large and Small Ruminants 203

moderate temperatures, and high moisture. Sporulation takes 1 to 4 days if envi-

ronmental conditions are ideal but can take several weeks in less favorable
conditions.3
The endogenous phase begins with the animal ingesting sporulated oocysts. Once
ingested, the oocysts undergo excystation, in which the sporozoites are released and
subsequently invade the intestinal cells. The sporozoites then transform into schizonts
and multiply asexually to generate merozoites (merogony). Merozoites may then pene-
trate additional intestinal epithelial cells and multiply further or progress to macroga-
metes or microgametes. During the sexual phase (gametogony), microgametes
(sperm) fertilize macrogametes (ova), producing oocysts. When the oocysts are
mature, they rupture the host cell, are released into the lumen of the intestine, and
are passed in the feces as unsporulated oocysts.4–7 The damage to the gut caused
by this phase is what contributes most to the clinical signs.

EPIDEMIOLOGY

Coccidia are highly prolific because each sporulated oocyst has the potential to pro-
duce 23 million oocysts during the endogenous phase after just 21 days.6 This ability
leads to high levels of environmental contamination. Sporulated oocysts are resistant
in the environment and can survive for weeks to months, especially in favorable con-
ditions of moderate heat and moisture.7
Buildup of high levels of contamination are most common in areas where animals
congregate or are crowded and feces are more concentrated in the environment.
Feedlots, drylots, and barns are common types of housing associated with coccidi-
osis. It can also be a problem in heavily stocked pastures, especially around watering
and feeding areas.
Healthy ruminants are generally immune to disease by 1 year of age but serve as a
reservoir to younger animals. The magnitude of infection, clinical signs, and oocyte
shedding are affected by the species of Eimeria involved, level of environmental expo-
sure, and animal immunity. Age, other stressors (weaning, weather, transportation,
other diseases, and so forth), nutrition, and genetic susceptibility all contribute to an-
imal immunity and susceptibility to coccidiosis.7,8

HISTORY AND PHYSICAL EXAMINATION

Calves are most susceptible to infection between 6 and 12 months of age. Lambs and
kids are susceptible from 1 and 6 months of age, but most clinical disease is seen in
lambs and kids between 4 and 8 weeks of age.9,10
There are subclinical and clinical forms coccidiosis. Subclinical infection can cause
depressed appetite as well as decreased feed efficiency from gut damage, which
leads to poor growth rates and weight gains.10,11
The following clinical signs may be associated with clinical coccidiosis:

Diarrhea

Anorexia

Depression

Weakness

Abdominal pain

Dehydration

Pale mucous membranes

Acute weight loss

Straining to defecate and subsequent rectal prolapse
204 Keeton & Navarre

Diarrhea is the most common clinical sign, and it may be bloody or mucoid. The
severity of disease varies from self-limiting, in which animals recover without treat-
ment, to severe cases, in which animals quickly succumb to the infection and die.8,12
Speed and degree of recovery depend on the severity of infection and area of the
gut involved. Animals that recover from more severe infection may become chronic
so-called poor-doers because of permanent scarring of the gut.
Nervous coccidiosis is a condition that occurs in calves after heavy infections with
Eimeria zuernii. Clinical signs include muscle tremors, convulsions, nystagmus, and
other central nervous system signs. Animals may fall to the ground, show neurologic
signs, then recover and have periods of normality. Mortality associated with nervous
coccidiosis can be 80% to 90%. The pathophysiology of this condition is not
known.7,13

DIAGNOSIS

A tentative ante mortem diagnosis of clinical coccidiosis is usually based on flock/

herd history and clinical signs along with observation of coccidia oocysts in feces.
A definitive diagnosis is complicated by the difficulty in interpreting results of fecal ex-
amination for oocytes. Quantitative fecal analysis by sugar or salt flotation techniques
that give results in oocysts per gram of feces are superior to nonquantitative tests.
Low numbers of oocytes are commonly shed in normal animals. Counts of 5000
oocysts per gram or higher in combination with a typical clinical picture are highly
suggestive of coccidiosis. Speciation of the oocysts is important because high
numbers of nonpathogenic species in animals with other diarrheal diseases is
possible. It is also possible to have clinical signs develop in the early stages of the
disease when fecal shedding is low or in animals that are in the chronic stages of
the disease and have intestinal scarring. Fecal examinations on multiple animals dur-
ing a suspected outbreak and over time in the herd or flock are helpful in interpreting
results7,10,14–17
Necropsy may also help confirm coccidiosis in a herd or flock. Intestinal hemor-
rhage and white/gray patches or lines on the mucosa on gross examination are sus-
picious of coccidiosis. Histopathology can help confirm the diagnosis.

PHARMACOLOGIC TREATMENT OPTIONS

Prevention of coccidiosis is superior to treatment because subclinical production los-

ses and potential permanent damage unresponsive to treatment are costly and have
animal welfare implications. Some exposure to the organism is necessary to develop
immunity, but it should be limited. Minimizing stress and other diseases, and opti-
mizing nutrition are important, as is minimizing environmental contamination. Preven-
tion of overcrowding, feeding off the ground, and sanitation of feeding and watering
equipment are important. Exposure to sunlight and desiccation are effective means
of decreasing of oocysts in the environment.
Where environmental control is not adequate, the use of anticoccidial drugs can be
helpful for both treatment and prevention. Anticoccidial drugs work by impeding the
growth and reproduction of coccidian parasites. They have little impact on existing
infection but should help limit both subclinical and clinical disease and environmental
contamination.
There are several anticoccidial drugs available for treatment and prevention of
coccidiosis in ruminants (Table 2). Species and class approval varies and extralabel
use should only be undertaken following the Animal Medicinal Drug Use Clarification
Act (AMDUCA) in the United States. These agents may also be restricted in organic
 Coccidiosis in Large and Small Ruminants 205

Table 2
Anticoccidial agents for use in treatment and prevention of coccidiosis in cattle (C), sheep (S),
and goats (G). Consult product label for specific class restriction within species and
withdrawal times

Agent Treatment Prevention Comments

Amproliuma 10/mg/kg BW for 5 mg/kg BW for Available in multiple forms:
(Corid) 5 d (C) 21 d (C)
9.6% oral solution
25–40 mg/kg BW 50 mg/kg BW for
20% soluble powder
for 5 d 21 d (S, ELDU)
1.25% or 2.5%
(S, G, ELDU) crumbles/pellets
Decoquinate 0.5 mg/kg BW for Feed additive
(Deccox) at least 28 d For prepartum use in sheep
(C, S, G) and goats

1 kg of 13% premix in 22 kg
of trace mineralized salt
Lasalocid 1 mg/kg BW Feed additive
(Bovatec) continuously For prepartum use in sheep
(C, S) G 5 ELDU) and goats

1 kg of 6% premix in 22 kg
of trace mineralized salt
Monensin 20 g/ton of feed (G) Feed additive
(Rumensin) (S 5 ELDU) May be best choice for goats
Cattle doses vary by
class-see specific
labels
Sulfaquinoxaline 10–20 mg/kg As a 0.015% solution in water
BW for 3–7 d (C)
(S, G 5 ELDU)

Abbreviations: BW, body weight; ELDU, extralabel drug use.

a
Amprolium is a thiamine analog and can cause polioencephalomalacia, especially at high
doses.
Data from Refs.15–17

and natural programs. Anticoccidial agents used in other species, such as poultry,
may be toxic to ruminants.15
The most commonly used anticoccidial drugs from those listed in Table 2 are the
ionophores (decoquinate, lasalocid, and monensin). They are feed additives classified
as antibiotics. By altering the rumen bacteria, they also improve feed efficiency and
control bloat and acidosis.18 Sulfa drugs are commonly used to treat coccidiosis in
many species but the exact mechanism is not known. Their clinical effectiveness
may be more related to control of secondary bacterial enteritis than to a direct effect
on coccidia. Sulfaquinoxaline is the only sulfa drug approved for control of coccidiosis
and only in cattle.
When using anticoccidial drugs for prevention or treatment of weaned young stock,
all animals in the group should be medicated. Resistance to coccidiostats can occur,
and is common in poultry.7 To minimize this potential, longer-term preventive uses
should be limited to high risk-situations. Although resistance is possible, evidence
that it occurs in ruminant Eimeria spp is mostly circumstantial at this time. Treatment
success of clinical coccidiosis is frequently unrewarding, and no drug has ever been
documented to be highly efficacious for treatment.19 Once clinical signs appear, dam-
age to the intestines has already occurred. What seems to be lack of efficacy of a
treatment (continued diarrhea), is most likely caused by a damaged gut.20 Use of
206 Keeton & Navarre

drugs such as amprolium and sulfas for treatment may help prevent worsening of
clinical signs by limiting reinfection in animals that cannot be removed from a contam-
inated environment and for which addition of ionophores to feed is impractical.
As mentioned before, the degree of oocyst shedding is affected by many factors,
including initial dose, stage of the infections, age of the animal, and individual suscep-
tibility. Therefore, using oocyst counts to determine drug efficacy/resistance in 1 or a
small number of animals is difficult. The use of products not approved for food animal
species, such as ponazuril (Marquis), for clinical cases that seem to be refractory to
approved treatments is not recommended. It is unlikely to be any more clinically effec-
tive once clinical signs appear, and the meat withdrawal time is more than 120 days
(contact FARAD.org for exact withdrawal times).21 Use of ponazuril for convenience
(1 dose compared with multiple doses of approved products) is illegal under
AMDUCA.
Coccidiosis prevention is usually reserved for calves after weaning, when they are
most susceptible, and in drylot or crowded condition. If problems occur in nursing
calves, an anticoccidial drugs in creep feed may be necessary. Because lambs and
kids are most at risk while still on the dam, coccidiostats can be provided to the
dams for 30 days before lambing/kidding to reduce environmental contamination.
An added benefit to the use of ionophores prepartum in sheep and goats is a potential
decrease in the incidence pregnancy toxemia.16

NONPHARMACOLOGIC TREATMENT OPTIONS

Coccidiosis vaccines are commercially available for poultry. Despite ongoing

research, a commercially available product in ruminants has not been developed.
Sericea lespedeza, a leguminous plant containing condensed tannins with anti-
parasitic properties, has been shown to be successful in preventing and controlling
coccidiosis and gastrointestinal nematode infections in lambs. In a study conducted
by the Louisiana State University Agricultural Center, sericea lespedeza was fed to
experimentally infected lambs to evaluate efficacy. The increase, peak, and decline
of fecal egg counts observed in the control lambs indicated a typical patent infec-
tion. The comparatively unchanged fecal egg count in the treatment lambs indicated
that sericea lespedeza effectively controlled infection compared with the control
lambs.21 In addition, fecal egg count remained lower than in control lambs, which
is in agreement with other reports of reduced fecal egg count in sericea lespe-
deza–fed animals.21–23 Under the conditions of this study, sericea lespedeza effec-
tively controlled Eimeria spp infection, as well as reducing nematode infections. The
use of this plant could be beneficial in weaning management to control
coccidiosis.24

SUMMARY

Coccidiosis is an important parasitic disease of ruminant livestock. Control of coccid-

iosis in cattle, sheep, and goats is based on sound management, the use of preventive
medications, and treatment of clinical cases as necessary.

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208 Keeton & Navarre

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