Definition
Epizootic lymphangitis is a chronic infectious granulomatous
disease of the skin, lymph vessels, and lymph nodes of the neck and legs of horses caused
by Histoplasma farciminosum.
Etiology
Epizootic lymphangitis is caused by a dimorphic fungus, Histoplasma
farciminosum, formerly known as Cryptococcus farciminosis, Zymonema
farciminosa, Saccharomyces farciminosus, or H. capsulatum var. farciminosum. In tissue, the organism is present in a yeast form; it forms mycelia in
the environment, has a saprophytic phase in the soil, and is relatively resistant to
ambient conditions, which allows it to persist many months in warm, moist conditions (3).
Host Range
The natural host range seems to be limited to horses, donkeys, and
occasionally mules. Rare cases of human infection have been reported, but identification
of the causative organism has not been substantiated.
Geographic Distribution
Currently the disease is endemic in west, north, and north-east
Africa, the Middle East, India, and the Far East. The disease earned its designation of
epizootic during the international conflicts of the first half of the twentieth century in
which large numbers of horses were congregated and moved. Many outbreaks occurred in
military animals.
Transmission
H. farciminosum is introduced via open wounds. Transmission
generally involves infection of wounds by flies contaminated by feeding on the open wounds
of infected animals (1,7). (The organism has been isolated from the gastrointestinal tract
of flies [1]).
Incubation Period
The incubation period is variable and is usually several weeks.
Clinical Signs
There is no breed, sex, or age predilection in epizootic
lymphangitis. This disease most typically involves the skin and associated lymph vessels
and nodes. In addition, the conjunctiva and nictitating membrane may be involved.
Occasionally there is involvement of the respiratory tract (1,3,7,8). The body temperature
and general demeanor of the animal are not changed. The initial lesion is a painless
cutaneous nodule about 2 cm in diameter. This nodule is intradermal and is freely moveable
over the subcutis. Lesions are most commonly found on the skin of the face, forelimbs,
thorax, and neck or the (less often) medial aspect of the rear limbs. The subcutaneous
tissue surrounding the nodule becomes diffusely edematous. The nodule gradually enlarges
and ultimately bursts. Some cases do not progress beyond small, inconspicuous lesions that
heal spontaneously. More typically, resultant ulcers increase in size and undergo cycles
of granulation and partial healing followed by renewed eruption. The surrounding tissues
become hard, variably painful, and swollen. The infection spreads along lymph vessels and
causes cord-like lesions, leading to diffuse and irregular involvement of an area of skin.
After, a lesion initially increases in size, additional cycles of eruption and granulation
lead to progressively smaller areas of ulceration until eventually only a (usually
stellate) scar remains. The development and regression of a lesion takes about 3 months
(1,3,7,8). Where lesions overlie joints, involvement may extend to synovial structures and
produce severe arthritis.
Conjunctivitis or keratoconjunctivitis may occur — usually in
conjunction with skin lesions (1). A serous or purulent nasal discharge containing
abundant organisms may be observed. Although respiratory lesions are described as common
in older literature (3), this form of the disease appears to be rare in more recent
outbreaks (1)
Gross Lesions
The affected skin and subcutaneous tissue is thickened, fibrous,
and firm. Several purulent foci may be apparent on cut section. Lymphatic vessels are
distended with pus. Regional lymph nodes are swollen, soft, and reddened and may contain
purulent foci. Arthritis, periarthritis, and periostitis have been described. The nasal
mucosa may have multiple, small gray-white nodules or ulcers with raised borders and
granulating bases. Nodules and abscess may occur in internal organs, including the lungs,
spleen, liver, and testes (3).
Morbidity and Mortality
The incidence of disease is high only when large numbers of
animals are collected together (as in military situations, for racing, or on village
commonages). Mortality is low.
Diagnosis
Field Diagnosis
Although the clinical presentation of the disease may lead to a
presumptive diagnosis of epizootic lymphangitis, the similarity of this disease to
glanders makes laboratory confirmation essential.
Specimens for Laboratory
A whole or section of a lesion and a serum sample should be
collected aseptically. The samples should be kept cool and shipped on wet ice as soon as
possible. Sections of lesions in 10 percent buffered formalin and air-dried smears of
exudate on glass slides should be submitted for microscopic examination.
Laboratory Diagnosis
Demonstration of the yeast in tissue sections or smears of lesions
is considered the most reliable means of diagnosis. Attempts to culture the organism fail
in up to half of cases (1,2,8). The organism in the tissues is in its yeast form. It may
be stained with Giemsa, Diff-Quik, or Gomori methenamine silver (2,8). In addition, an
indirect fluorescent antibody technique for demonstration of the organism has been
developed (4).
Affected animals do mount a humoral immune response to the
infection, and an enzyme-linked immunosorbent assay (ELISA) for the diagnosis of epizootic
lymphangitis has been developed (5,6). Attempts have also been made to utilize intradermal
skin testing (with histoplasmin or histofarcin) with encouraging results (5,10).
Differential Diagnosis
Epizootic lymphangitis must be differentiated from glanders
(mallein test and serology, absence of yeasts in the pus), strangles (which usually occurs
in outbreak form, affects mainly young animals, is always acute and febrile, and is not
associated with cutaneous nodules, buds and ulcers), and ulcerative lymphangitis (which is
more acute and caused by Corynebacterium pseudotuberculosis).
Treatment
Successful treatment with intravenous administration or sodium
iodide, oral administration of potassium iodide, and surgical excision of lesions where
possible has been reported, but recurrences of clinical signs months later is possible
(3,7). In vitro sensitivity of the organism to amphotericin B, nystatin, and clotrimazole
has been reported (7,8). In most areas, epizootic Iymphangitis is a reportable disease,
and treatment is not allowed. Affected animals must be destroyed (1).
Vaccination
Horses that recover from clinical infection are immune to
reinfection. Although promising results have been obtained with experimental vaccines, a
vaccine is not commercially available.
Control and Eradication
Strict hygienic precautions are essential to prevent spread of
epizootic Iymphangitis. Great care should be taken to prevent spread by grooming or
harness equipment. Contaminated bedding should be burned. The organism may persist in the
environment for many months.
Epizootic lymphangitis is a chronic disease. Many mildly affected
horses recover. Those that do are reputedly immune for life — a belief that has led
to a premium being placed in endemic areas on horses with characteristic scars (3). In
most areas of the world, however, this is a reportable disease; treatment of clinical
cases is not permitted, and destruction of affected horses is usually mandatory. In most
areas, epizootic lymphangitis has been eradicated by a strict policy of slaughter of
infected animals.
Public Health
Although rare cases of human infection have been reported, they
have not been substantiated by unequivocal identification of the causative organism.
GUIDE TO THE LITERATURE
1. AL-ANI, F.K., and AL-DELAIMI, A.K. 1986. Epizootic lymphangitis
in horses: Clinical, epidemiological and haematological studies. Pakistan Vet. J.,
6:96-100.
2. CHANDLER, F.W., KAPLAN, W., and AJELLO, L. 1980. Color Atlas
and Text of the Histopathology of Mycotic Diseases. Chicago:Year Book Medical
Publishers, pp.70-72, 216-217.
3. HENNING, M.W. 1956. Animal Diseases in South Africa, 3d
ed, Johannesburg, South Africa: Central News Agency, pp.194-203.
4. GABAL, M.A., BANNA, A.A., and GENDI, M.E. 1983. The fluorescent
antibody technique for diagnosis of equine histoplasmosis (epizootic lymphangitis).
Zbl.Vet. Med. (B), 30:283-287.
5. GABAL, M.A., and KHALIFA, K. 1983. Study on the immune response
and serological diagnosis of equine histoplasmosis (epizootic lymphangitis). Zbl. Vet.
Med. (B), 30:317-321.
6. GABAL, M.A., and MOHAMMED, K.A. 1985. Use of
enzyme-linkedimmunosorbent assay for the diagnosis of equine histoplasmosis farciminosi
(epizootic lymphangitis). Mycopathologia, 91:35-37.
7. MORROW, A. N., and SEWELL, M. M .H .1990. Epizootic
Lymphangitis, in Handbook on Animal Diseases in the Tropics 4th ed, Sewell, M.M.H.
and Brocklesby, D.W. eds, London: Bailliere Tindall, pp.364-367.
8. SCOTT, D.W. 1988. Large Animal Dermatology.
Philadelphia:W.B. Saunders Co., pp.192-193.
9. SELIM, S.A., SOLIMAN, R., OSMAN, K., PADHYE, A.A., and AJELLO,
L. 1985. Studies on histoplasmosis farciminosi (epizootic lymphangitis) in Egypt.
Isolation of Histoplasma farciminosum from cases of histplasmosis farciminosi in horses
and its morphological characteristics. Eur. J. Epidemiol., 1:84-89.
10. SOLIMAN, R., SAAD, M.A., and REFAI, M. 1985. Studies on
histoplasmosis farciminosi (epizootic lymphangitis) in Egypt. 111. Application of a skin
test ("Histofarcin") in the diagnosis of epizootic lymphangitis in horses.
Mykosen, 28:457-461.
R.O. Gilbert, B.V.Sc., M.Med.Vet., College of Veterinary Medicine,
Cornell University, Ithaca, N Y 14853-6401
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