Definition
Contagious agalactia (CA) of sheep and goats is an infectious
disease of males and females of these species characterized by fever, malaise, and
septicemia followed by arthritis, keratoconjunctivitis, and in the females, mastitis and
agalactia.
Etiology
The etiologic agent of the classical disease is Mycoplasma
agalactiae, which, since its isolation in 1923, has been considered to be the main
cause of the disease. However, it has become evident that the "contagious
agalactia" syndrome (especially in goats) can also be caused by several other
mycoplasmas, notably M. capricolum capricolum and M. putrefasciens (5), M.
mycoides capri (10), and the "large colony" or LC type of M. mycoides
mycoides (1). Some have questioned limiting the term "contagious agalactia"
to the disease caused by M. agalactiae (6). This discussion will focus on CA as
caused by M. agalactiae.
Many of the routinely used disinfectants will effectively
inactivate the organism. Effective disinfectants are sodium hypochlorite (30 ml of
household bleach in 1 gallon of water), cresol, 2 percent sodium hydroxide (lye) (pH
12.4), formalin (1 percent), sodium carbonate (4 percent anhydrous or 10 percent
crystalline with 1 percent detergent), and ionic and nonionic detergents.
Host Range
Goats seem to be more susceptible to the natural disease than are
sheep, but M. agalactiae is an important pathogen of both species. Most outbreaks
occur in the summer months and coincide with the time of births and peak lactation.
Geographic Distribution
Contagious agalactia is an important disease in the Mediterranean
countries of Europe, Asia, and North Africa, in the former Soviet Union, in India and
Pakistan, and in countries of the Near East. It has also been reported from Australia,
South Africa, and South America. Although three isolations of M. agalactiae have
been reported from the United States, it appears that North American strains are of low
virulence and do not cause classical CA.
Transmission
The disease spreads by ingestion of feed, water, or milk
contaminated with infected milk, urine, feces, or nasal and ocular discharges.
Transmission may also be by direct entry to the teat opening at milking or by inhalation
of contaminated dust. Animals with subclinical or chronic infections can carry and shed
the mycoplasmas for months, and the organisms can survive in the supramammary lymph nodes
from one lactation to the next. Contaminated fomites can transmit the organisms between
premises. The disease appears to be less contagious than it was formerly thought to be
(6).
Incubation Period
The incubation period in the natural disease varies between 7 and
56 days.
Clincial Signs
Infection with M. agalactiae occurs in male and female
sheep and goats and can be inapparent or can cause mild, acute, or chronic disease.
Freshening female goats at the beginning of lactation are especially susceptible and often
display the acute form of the disease After an incubation period of from 1 to 8 weeks,
transient fever followed by malaise and inappetance are observed. This is followed by
mastitis, polyarthritis, and keratoconjunctivitis.
The mastitis is characterized by a change in the color of the milk
to greenish-yellow or grayish-blue, and in the texture of the milk to a watery and later
lumpy consistency as lactation decreases and eventually ceases. The udder eventually
becomes flabby, fibrosed, and atrophic.
The polyarthritis, first seen as swelling of the periarticular
tissues, especially of the carpal and tarsal joints, later develops into painful chronic
infection, resulting in lameness and inability to stand or walk. In male goats this may be
the main manifestation of the disease.
The keratoconjunctivitis is usually of short duration and is seen
in about 50 percent of infected animals. It may occasionally develop into a chronic
infection, occasionally resulting in unilateral or bilateral blindness.
Abortion has been described in chronically infected animals, but
its pathogenesis is not understood. Mycoplasma agalactiae has also been associated
with granular vulvovaginitis in goats (13).
Gross Lesions
The principal lesion in female animals is catarrhal mastitis with
primary inflammation of the interstitial tissues followed by secondary acinar involvement.
If the mastitis becomes chronic, progressive fibrosis and eventually parenchymatous
atrophy will be seen.
In males and females dying of the acute disease, congestion of the
musculature and of the spleen and liver may be seen as a result of the septicemia. In both
acute and more chronically affected animals, arthritis with periarticular edema is common
and especially affects the carpal joints. Synovial membranes may be hyperemic, and joint
cavities may be filled with turbid or hemorrhagic fluid. The early eye lesion is usually a
serous and later a mucopurulent conjunctivitis followed by keratitis and occasionally
corneal ulceration.
Morbidity and Mortality
The economic impact of the disease lies in its high morbidity and
resultant loss of milk and meat production rather than in its mortality. The greatest
number of cases develops during those periods when the young are being born and the dams
are in full lactation. In most outbreaks of CA, the mortality is low, seldom exceeding 20
percent, but occasionally secondary bacterial pneumonia may cause a higher mortality.
Diagnosis
Field Diagnosis
The characteristic clinical signs of the disease, namely mastitis
with loss of milk production, keratoconjunctivitis, and arthritis, all occurring at or
soon after parturition, warrant a clinical diagnosis of contagious agalactia. Because
there are several look-alike mycoplasmal and bacterial infections, laboratory confirmation
of field diagnosis is essential.
Specimens for Laboratory
From a live animal, milk, swabs from the eyes, joint fluid, blood,
urine, and feces, all provide good samples for isolation attempts. From a dead animal that
has had severe clinical disease, the best specimens to submit are blood, urine, and
tissues from liver, spleen, and other organs, and joint fluid from those animals with
arthritis. All samples should be collected aseptically and, if possible, placed in
transport medium (heart infusion broth, 20 percent serum, 10 percent yeast extract,
benzylpenicillin at 250 to 1000 IU/ml). Samples should be kept cool and shipped on wet ice
as soon as possible. If transport to the laboratory is delayed (more than a few days),
samples may be frozen (1). Blood should be collected for serum.
Laboratory Diagnosis
Diagnosis of CA must be confirmed by isolation and serological
identification of the causative agent. Serology, (the complement fixation [CF] test,
indirect hemagglutination test, enzyme-linked immunosorbent assay [ELISA][11]) for the
detection of antibodies is useful on a herd basis after the presence of the disease has
been confirmed by isolation of the organism.
Differential Diagnosis
As stated in the section on etiology, several other mycoplasmas
(especially of goats) can cause syndromes resembling contagious agalactia. Pneumonia,
mastitis, and arthritis can also be caused by Pasturella haemolytica; mastitis can
also be caused by streptococci, staphylococci, or other bacteria; and arthritis can also
be caused by both caprine arthritis encephalitis virus and the bacteria Erysipelothrix
rhusiopathiae.
Treatment
With early antibiotic (tetracyclines, tylosin, erythomycin, and
tiamulin fumarate) treatment the prognosis is good, and only in those animals developing
chronic arthritis or keratoconjunctivitis is recovery unlikely. Oxyteracycline does not
prevent subsequent shedding of the organisms, and with the other drugs this still needs to
be determined.
Vaccination
Both live and inactivated vaccines have been used in the
prevention of CA. A live-attenuated vaccine for goats (7) and vaccine prepared from a
naturally avirulent strain of mycoplasma are effective in goats. Formalin-inactivated
aluminum hydroxide precipitated vaccines have been extensively used in Eastern Europe.
Because there seems to be some strain variation, the use of autogenous vaccines
incorporating local strains of mycoplasma is recommended. The efficacy of inactivated
vaccines is low. Two concerns about the use of live vaccines are that the vaccine organism
may be shed in the milk and that although the vaccines may prevent the development of
clinical disease, they do not prevent infection and shedding of virulent organisms.
Control and Eradication
Prevention
Because CA is a chronic disease that may exist subclinically in
carrier animals, it is important to maintain sufficient regulatory restrictions to prevent
its introduction in apparently healthy animals.
Control and Eradication
In endemic areas, normal sanitary precautions of separating
affected animals from healthy animals, separating milking animals from younger animals,
cleaning and disinfection of milking utensils, practicing good hygienic principles when
milking, cleaning and disinfection of stalls, and eliminating litter will reduce the
incidence of disease in a flock. If possible, newborn animals should be removed from the
dam immediately after birth and fed only pasteurized colostrum and then pasteurized milk.
Eradication can be accomplished by slaughter of all infected and
contact flocks.
Public Health
There is no evidence that humans are susceptible to M. agalactiae.
GUIDE TO THE LITERATURE
1. BANGA, H.S., and GUPTA, P.P. 1988. Pathogenicity of Mycoplasma
mycoides subsp. mycoides (large colony type) for sheep udder. Austr. Vet. J., 65:361-362.
2. BRIDRE, J., and DONATIEN, A. 1923. Le microbe de l'agalazie
contagieuse et sa culture in vitro. C.R. Acad. Sci. (D) (Paris), 177:841-843.
3. COTTEW, G.S. 1984. Overview of mycoplasmoses of sheep and
goats. Isr. J. Med. Sci., 20:962-964.
4. DaMASSA, A. J,. 1983. Recovery of Mycoplasma agalactiae from
mastitic goat milk. J. Am. Vet. Med. Assoc., 183:548-549.
5. DaMASSA, A.J., BROOKS, D.L., and HOLMBERG, C.A. 1987.
Comparison of caprine mycoplasmosis caused by Mycoplasma capricolum, Mycoplasma mycoides
subsp. mycoides, and Mycoplasma putrefasciens. Isr. J. Med. Sci., 23:636-640.
6. DaMASSA, A.J., WAKENELL, P.S., and BROOKS, D.L. 1992.
Mycoplasmas of goats and sheep. J. Diagn. Invest., 4:101-113.
7. FOGGIE, A., ETHERIDGE, J.R., ERDAG, O., and ARISOY, F. 1970.
Contagious agalactia of sheep and goats: Preliminary studies on vaccines. J. Comp.
Pathol., 80:345-350.
8. JASPER, D.E., and DELLINGER, J.D. 1979. Isolation of exotic
mycoplasma from goats. Proc. 22nd Ann. Mtng. Am Assoc. Vet. Lab. Diagn., pp 119-124.
9. JONES, G.E. 1985. The pathogenicity of some ovine or caprine
mycoplasmas in the lactating mammary gland of sheep and goats. J. Comp. Pathol.,
95:305-318.
10. MISRI, J., GUPTA, P.P. and SOOD, N. 1988. Experimental
Mycoplasma capri mastitis in goats. Austr. Vet. J., 65:33-35.
11. SCHAEREN, W., and NICOLET, J. 1982. Micro-ELISA for detecting
contagious agalactia in goats. Schweiz. Arch. Tierheilkd., 124:163-177.
12. SINGH, A., GUPTA, P.P. and BANGA, H.S. 1990. Pathogenicity of
Acholeplasma laidlawii for the goat udder. Austr. Vet. J., 67:155-156.
13. SINGH, A., RAJYA, B,S,, and MOHANTY,G,C, 1974. Granular
vulvovaginitis (GVV) in goats associated with Mycoplasma agalactiae. Corn. Vet.
64:435-442.
14. YEDLOUTSCHNIG, R.J. 1978. Mycoplasma mycoides subsp. capri and
Mycoplasma agalactiae Isolation from goats in the United States: A Review Including
Unpublished Findings. Proc. 82nd Ann. Mtng. U.S. Anim. Hlth. Assoc., pp 272-276.
C. John Maré, B.V.Sc., Ph.D., Veterinary
Science/Microbiology, University ot Arizona, Tucson, Arizona 85721
|