J Vet Diagn Invest 1: 195-200 (1989)
REVIEW ARTICLE
Ostertagiasis in cattle
Gilbert H. Myers, R. Flint Taylor
Ostertagiasis, a parasitic gastritis caused by the
nematode Ostertagia ostertagi, is the most important
of the gastrointestinal helminth infections of cattle in
temperate climates.2 It is also important in some sub-
tropical regions with winter rainfall. Ostertagiasis is
manifested as several patterns of clinical disease based
on a complex and variable epidemiology. In addition,
huge financial losses are incurred annually by produc-
ers due to undiagnosed subclinical disease resulting in
lowered production. The annual cost of gastrointestinal
nematodiasis in the United States has conservatively
been estimated in excess of $250 million.2,10 Osterta-
giasis accounts for a major portion of that loss.
Life cycle
Ostertagia has a direct life cycle. Eggs passed in the
feces develop into first-stage larvae (L,), which hatch,
develop, and moult to become second-stage larvae (L2),
which in turn develop and moult to the third and in-
fective stage (L3). All of this occurs in the fetal pat, and
the L3 then migrates under moist conditions onto the
herbage. The L3 retains the outer sheath of the L3 and
is the most resistant of the free-living stages. Following
ingestion, the parasitic cycle involves development
through the L3 and L3 stages in the gastric glands. This
usually takes 21 days, by which time the adult parasite
emerges from the glands onto the surface of the aboma-
sal mucosa.2
Epidemiology
Northern US and Canada. The seasonal occurrence
of ostertagiasis in the northern US and Canada is il-
lustrated (Fig. 1). Additional epidemiological consid-
erations include
1. Infective third-stage L3 larvae will survive over
winter and for up to 1 year on pasture. This over-
From the Department of Technical Services (Myers) and the De-
partment of Research and Development (Taylor), Hoechst-Roussel
Agri-Vet Company, Somerville, NJ 08876.
Presented as a poster at the 30th Annual Meeting of the AAVLD,
Salt Lake City, UT, October 26-27, 1987.
Received for publication October 26, 1987.
195
wintered contamination poses a risk of infection to
cattle grazing spring pasture in the northern states.9,20
2. Pasture contamination (numbers of infective L3 lar-
vae per unit of forage) increases abruptly beginning
in mid-summer. High levels of pasture contami-
nation continue through late summer and fall, with
production losses and possible clinical type I disease
as outcomes that may occur at this time of year.
3. The incidence of type I disease is high in young
cattle compared to the relatively uncommon oc-
currence of type II ostertagiasis in yearlings and
older animals. The actual incidence of type I infec-
tions is probably underreported.
Southern US. The seasonal occurrence of osterta-
giasis in the southern US is illustrated in Fig. 2. Ad-
ditional epidemiological considerations are
1. The cool, wet winters common in the South are
ideal for the development and survival of infective
L 3 larvae on pasture. As a result, contamination
accumulates during the winter months, with pro-
duction losses and possible clinical type I disease.
2. The incidence of type I disease is high in young
cattle compared to the relatively uncommon oc-
currence of type II ostertagiasis in yearlings and
older animals. The actual incidence of type I infec-
tions is probably underreported.28
3. The occurrence of type II disease is uncommon,
and clinical signs may be found only in a small
percentage of an affected herd. These 2 aspects of
type II disease complicate recognition and diag-
nosis. 28
Clinical disease
Ostertagiasis has several forms of clinical disease.
These clinically distinct conditions are type I, pre-type
II, and type II.
Type I disease. This is a disease of young susceptible
cattle (suckling beef calves, dairy heifers, and stocker
cattle) in the summer and fall months (northern cli-
mate) or in winter and spring (southern climate). It
corresponds to the classical form of ostertagiasis de-
scribed in the literature for several decades. Infective
larvae are ingested daily by young growing cattle on
196
TYPE I
Figure 1. Generalized seasonal pattern of 0. ostertagi in the
northern US and Canada. (Adapted from Williams JC: 1986, Vet
Clin North Am [Food Anim Pract] 2:251.)
pasture; the larvae migrate to the gastric glands of the
abomasum, grow, and become adults in about 3 weeks.
These young adult worms then break out of the glands,
creating substantial damage during this exodus.2 The
disease process is continuous and cumulative during
this emergence phase.
Depending on the severity of infection, clinical signs
may vary from reduced growth or production to full-
blown clinical disease. Fulminating clinical osterta-
giasis includes profuse diarrhea, rapid weight loss, sub-
mandibular edema (“bottle jaw”), increased mortality,
anemia, and generally poor condition with a rough hair
coat. 2 Less severely affected animals may exhibit
marked appetite suppression, although other signs of
disease may be mild or absent.
Pre-type II disease. This form of ostertagiasis is
usually clinically mild or silent. It is characterized by
ingestion of infective L3 larvae, which enter the gastric
glands as in type I disease; however, once they develop
into fourth-stage larvae their development is arrested.
This cessation of development is termed “hypobiosis”
or larval inhibition. This type of disease occurs in fall
and early winter (northern climate) or in the period
between February and September (southern climate).
Larval arrest, inhibition, or hypobiosis is evidently
triggered by harsh climatic conditions of either cold
(northern) or hot and dry (southern) regions.28 The
period of hypobiosis may last 4-7 months.
Infections may involve 100,000 or more arrested or
inhibited larvae, with no overt clinical disease. How-
ever, these mild or absent signs of clinical disease may
lead to a false sense of security for the producer, cli-
nician, or diagnostician; once climatic conditions im-
prove, a massive eruption may occur, leading to type
II ostertagiasis. 2,10,26 Diagnosis is made by epidemio-
logic knowledge of the region and parasite identifica-
tion with history of management practices.
Myers, Taylor
Figure 2. Generalized seasonal pattern of 0. ostertagi in the
southern US. (Adapted from Williams JC: 1986, Vet Clin North
Am [Food Anim Pract] 2:250.)
Type II disease. Type II disease occurs primarily
in yearling (or older) cattle. After cattle have acquired
large numbers of inhibition-prone larvae, type II dis-
ease may occur when weather conditions favoring sur-
vival of their progeny on pasture improve. Inhibited
larvae are then signaled to begin the remainder of their
maturation sequence; this may occur gradually or in
bursts. In northern climates, this maturation and erup-
tion occurs during early spring; in the southern regions,
it occurs in the fall months.26 Louisiana workers have
observed type II outbreaks almost exclusively after
unusually hot and dry summers.28 The clinical signs
are identical to type I disease in severely affected cattle
and may vary in severity depending upon the magni-
tude of the eruptions. If emergence of parasites from
abomasal glands is gradual, a protracted disease occurs;
if a massive maturation occurs, the clinical signs are
severe, rapid, and usually catastrophic. In less severely
infected animals appetite suppression may be the pri-
mary clinical sign, with growth retardation or produc-
tion losses being the end result.
Pathology
The primary gross lesions of both type I and type II
ostertagiasis are multiple white, raised, umbilicated
nodules on the mucosal surface of the abomasum, fre-
quently accompanied by mucosal reddening and ede-
ma. In severe infections these nodules may be so
frequent that coalescence occurs, resulting in a “Mo-
rocco-leather” appearance.2
Histologically, abomasal glands contain larvae in
varying stages of development. Accompanying the
parasitic glandular invasion is hyperplasia and disten-
tion of gastric glands with flattening of glandular epi-
thelium. These distended glands lack differentiated
acid-producing parietal and pepsinogen-producing chief
 Review article: Ostertagiasis in cattle 197
22
cells. Adjacent glands unoccupied by larvae have a systemic changes is a depression of host appetite;l,8
degeneration of chief and parietal cells as well. Inflam-this relatively constant feature of 0. ostertagi infection
mation is minimal during early and middle phases of (as well as virtually all other gastrointestinal nema-
larval encystment and development, including hypo- todes) results in lowered weight gain and reductions in
biosis; however, during the emergence of young adults all other areas of productivity. The mechanism of ap-
in either type I or type II disease, there may be exten- petite depression is not clearly understood; speculative
sive mixed inflammatory infiltrate. Calves experimen- theories involving increased gut hormone production
tally infected with inhibited strains of larvae have beenas an aberrent response to the presence of worms have
reported to have increased numbers of globule leuco- been proposed but not definitively proven.8,24
cytes, eosinophils, and focal aggregates of lympho- Ostertagia ostertagi-infected cattle also have other
plasmocytic cells when compared with calves infected pathophysiologic changes of the digestive system that
with noninhibited strains.l,8 This histologic feature, alter protein metabolism. Work conducted by several
coupled with the presence of gross lesions and the cor- investigators has shown that although there is little
rect season, may provide a diagnosis of inhibited os- actual effect on protein digestion and absorption, there
tertagiasis. Such diagnostic differentiation becomes of is a major impairment of postabsorptive protein me-
paramount importance when mixed type I and type II tabolism in infected animals, even in a subclinical or
infections occur (or type II alone), as the verification clinically silent form of the disease. 1,17,18 This physio-
of presence of inhibited larvae will affect choice or logic feature will, of course, lead to reduced rate-of-
dosage of an appropriate anthelmintic. gain and lowered feed efficiency; hence, low-grade in-
Electron microscopy studies on distended glands have fections produce subclinical infections that result in
shown that there are gaps between cells in the hyper- significant “economic disease” for the producer.
plastic mucosa; these gaps may partially or totally Another feature of altered protein metabolism in
separate adjacent cell membranes of the zonulae oc- infected animals is a consistent hypoproteinemia; this
cludentes. 15 Junctions between postcapillary venule condition leads to generalized tissue edema (i.e., ‘“bot-
endothelial cells are also separated. Both type I and tle jaw”), which adversely affects carcass quality.7,23
type II diseases produce these cellular and ultrastruc- Animals severely affected in this manner may have up
tural changes.2 to 16% less total body solids.
The actual mechanism of the diarrhea induced by
Pathophysiology 0. ostertagi infection is not understood. Bacterial over-
Structural and ultrastructural changes are associated growth resulting from increased abomasal pH is one
with major functional changes in abomasal digestive contributing factor.2 The interrelationships of all the
physiology. These changes include pathophysiologic events are complex and not clearly
defined. The results, however, are identical to those
1. Decrease in acid production due to loss of parietal
seen in animals suffering from bacterial enteritis
cell function; this leads to abomasal pH values of
2 (“scours”), i.e., loss of sodium and water, peripheral
>2.6, often reaching the pH 5-7 range.
circulatory collapse, cardiovascular shock, and death.
2. Absence of proteolytic pepsin because, in the ab-
Speculation has persisted about nematode-produced
sence of low abomasal pH, pepsinogen is not acti-
enteric toxins, immune-mediated or allergic-type diar-
vated. Digestion eventually ceases at pH 5, and
rhea initiated by the parasite, and other theories; how-
bacterial overgrowth may occur; this is contribu-
2 ever, to date, no definitive work has clarified the mech-
tory to diarrhea as a sequel.
anism of 0. ostertagi- induced diarrhea.
3. Movement of serum proteins (especially albumin)
and sodium from circulating blood into the aboma-
sal lumen because of the compromised intercellular
junctions in the hyperplastic mucosal epithelial Diagnosis
2
cells. Although diagnosis of fulminating type I osterta-
giasis is very straightforward, the complexity of the life
As a result of these changes, both structural and func-
cycle, epidemiology, geographic and climatic varia-
tional changes found in types I and II disease are ba-
tion, and gradations or severity of 0. ostertagi infection
sically the same and occur mainly from the time of
can make accurate diagnosis of type II disease difficult.
worm emergence onward. Age differences in affected
The following parameters are useful in addressing this
cattle between types I and II may produce some clinical
diagnostic problem:
variations, however.
Generalized pathophysiologic changes occur as a re- 1. History, including details of previous parasite prob-
sult of ostertagiasis in addition to those localized in lems (on farm or in vicinity), control measures,
the abomasum. One of the most pronounced and costly animal population density, previous grazing history
198
Pasture contamination in
temperate climates of treated
stocker cattle and dairy heifers
Figure 3. Pasture contamination in temperate climates: treated
stocker cattle and dairy heifers.
and pasture management, and age of affected ani-
mals.
2. Knowledge of regional 0. ostertagi epidemiology,
location where infection occurred (northern or
southern disease pattern), and unusual weather con-
ditions (several months prior) that may lead to in-
creased hypobiosis, etc.
3. Routine examination of abomasum of all cattle sub-
mitted for necropsy (both gross and histopatho-
logic). Laboratory diagnosticians routinely exam-
ining sections of abomasum histologically will soon
develop an awareness of the incidence of type II
disease or pre-type II infection. This information,
coupled with history and local epidemiology can
then enable more accurate prognostication and
treatment recommendations.
4. Routine parasitologic examination of all cattle sub-
mitted for necropsy.
5. Plasma pepsinogen determinations. These may be
useful in establishing the degree of abomasal dam-
age. Values of over 3,000 mU are indicative of
clinical disease.6,25
6. Abomasal pH values. In infected animals they will
be > 2.6.2,25
Treatment and control
Presently cattle producers attempt to control gas-
trointestinal nematode parasites including 0. ostertagi
by administering 1 or more anthelmintic treatments
during a production cycle. Herds are treated when han-
dled for other purposes. Thus, treatment is given when
convenient and generally not in relation to basic epi-
demiological criteria such as potential contamination
Myers, Taylor
buildup, larval inhibition, or risk of reinfection. For
example, in many areas spring and fall treatment of
beef herds is a common practice. This traditional ap-
proach, ifconsistently followed, has definite merit and
can minimize the risk of ostertagiasis through reduc-
tion of pasture contamination.27
Practical management options alone do not provide
useful levels of control. Total eradication of parasites
is unlikely, due to the immense number of eggs shed
and the long survival time of the infective stages in
the environment. Likewise, pasture rotation by itself
cannot be relied on. Rotation of pastures actually may
increase levels of contamination and worm infection
compared with continuously grazed pastures.6,13 This
fact can become critical when pasture rotation is com-
bined with high stocking rates, an increasingly popular
management practice known as “intensive grazing.”
Nutrition is no substitute for a sound parasite pro-
gram. Available evidence suggests that higher levels of
protein in the diet may ameliorate, but not reverse, the
dramatic effect that nematode infections can have on
nitrogen retention and turnover.1l
Recent work suggests that late turnout onto per-
manent pasture in the spring provides some measure
of parasite control. Late turnout prevents exposure of
animals to the overwintered larval population present
on herbage at the start of the grazing season. Harvest
and storage of early-season forage would allow utili-
zation of the forage without risking early-season in-
fections. l6 Seasonal variation in the pattern of pasture
contamination serves as the basis of modem control
approaches for 0. ostertagi and other gastrointestinal
parasites.
Control methods should be preventive in nature in-
stead of curative. Control measures will vary according
to local climatic conditions, livestock management
system, and epidemiology throughout the United States.
Broad recommendations regarding timing of preven-
tive treatment can only be made on a regional or cli-
matic basis. Ostertagiasis is a herd disease. To be ef-
fective, control through preventive treatment should
include all cattle sharing the same pastures. Beef cows
may serve as important sources of pasture contami-
nation due to the large volume of manure (and large
numbers of worm eggs) passed daily onto pastures
grazed by young susceptible animals.l6
The risk of clinical ostertagiasis can be greatly re-
duced if serious pasture contamination is prevented.21
Prevention of serious contamination is the goal of pre-
ventive treatment programs. Timing of treatment is
crucial to the success of such programs. Several an-
thelmintic treatments administered at 3-week intervals
have been shown to provide seasonal control for dairy
heifers and stocker cattle (Fig. 3). The goal of these
treatment programs is prevention of significant pasture
 Review article: Ostertagiasis in cattle 199

erably more effective against inhibited and developing

fourth-stage (L4) larvae than older compounds are. 14,29,30
Proper timing of treatment is crucial to successful
implementation of preventive treatment programs.
Products are not a substitute for a planned, carefully
implemented program, monitored through use of fecal
egg counts. An inexpensive and practical fecal egg count
method designed to monitor parasite infections in herds
of livestock has been described.4 Use of such a method
allows practitioners and clinical laboratories to gain
information on herd infection levels and more effec-
tively monitor control programs.
Acknowledgements
We express our gratitude and appreciation to Mrs. Olivia
Messmer and Mrs. Carol Lutz for their secretarial support
in the typi ng, editing, and other preparation of this document.

March July October Sources and manufacturers

Figure 4. Worm infections in suckling beef calves during the
summer grazing season. Values on the ordinate are fecal egg counts
per 2-g sample. Rx = treatment. (Adapted from Bumgamer SD,
Brauer MA, Corwin RM, et al.: 1986, J Am Vet Med Assoc 198:
429.)
contamination at critical times during the production
cycle. l3
Options available to accomplish preventive treat-
ment programs have expanded in recent years with the
introduction of sustained release technology available
in Canada and a pour-on formulation.19 Anthelmintic
medicated feeds and a molasses block containing fen-
bendazole a are also available.3 New formulations such
as these allow herds to be treated at strategic times
without individual animal handling, thus making stra-
tegic treatment programs flexible and more practical.
Currently, strategically timed treatment programs are
being incorporated into herd management for stocker
12,13,16
cattle and dairy heifers. Routine use of products
effective against inhibited 0. ostertagi (fenbendazole a
and ivermectinb) has been recommended during pre-
type II ostertagiasis. The goal of such treatment is to
prevent clinical type II ostertagiasis and resulting pas-
ture contamination. Mid-summer treatment is begin-
ning to be practiced in Midwestern cow/calf herds. This
treatment prevents the buildup of pasture contami-
nation that would normally occur during late-season
grazing (Fig. 4)5,7
After a diagnosis of clinical ostertagiasis is obtained,
herd treatment may prevent further deaths, but will
not reverse lost weight gain. Nevertheless, product se-
lection is important in treatment of type I and type II
ostertagiasis; the newest available therapeutic anthel-
mintics (fenbendazolea and ivermectinb) are consid-
a. Hoechst-Roussel Agri-Vet Company, Somerville, NJ.
b. MSD-AGVET, Rahway, NJ.
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