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This article was published in 1955
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INSTITUTE OF INSPECTORS OF STOCK OF N.S.W. YEAR BOOK.
Bovine Malignant Catarrh
I. G. PEARSON, B.V.Sc., Veterinary Research Officer, Glenfield.
This acute, highly fatal, infectious viral disease of cattle has now been definitely diagnosed in New South Wales. It causes a croupous inflammatory oedema of the upper respiratory tract, and a profuse ropey, yellow, muco-purulent nasal discharge is characteristic. There is frequent eye involvement with watery or purulent discharge and corneal opacity. Often the C.N.S. also is involved; stupor or excitement, and the animals may charge. Lymph nodes, especially those draining the head and neck, frequently are enlarged and oedematous. There is a high fever. Diarrhoea may or may not be present, Some authors record papular and vesicular dermatitis, especially pronounced on withers, forearms, scrotum and teats; leaving parchment-like crusts in the hair. They also speak of stomatitis, pharyngitis and vaginitis as well as rhinitis,
This disease has been known in Europe for over one hundred years, and is present also in Africa, U.S.A. and Indonesia. With their usual picturesque phrasing, the Africans call it "Snotsiekte". Insanitary conditions, low altitude and moisture are listed as predisposing causes.
It usually occurs sporadically, mostly not in winter, but herd outbreaks are recorded overseas. It does not spread rapidly and so is not as economically important as some other diseases. However, at least one valuable animal has been lost in this State. The incubation period varies from two weeks to ten months, with two to eight weeks common after inoculation. The disease usually is fatal in four to ten days, although some animals recover. The method of natural spread is obscure and experimental transmission is difficult with most strains. Wildebeest and sheep are suspected as reservoirs of infection, although the disease does not affect them very severely, if at all. Buffaloes are susceptible.
The following photograph, though naturally lacking much that is provided with a coloured slide, will serve to illustrate the general appearance of an advanced case of this disease:
POST-MORTEM lesions are referable to the upper respiratory tract symptoms, Sometimes hyperaemia and haemorrhages are seen in abomasum, duodenum, caecum and rectum. Small round white foci 2 mm. in diameter slightly raised above the mucosa and with distinct black crater-like depressions in the centre, may be found in the fundus and folds of the abomasum, The liver may appear to be finely cirrhosed.
DIAGNOSIS: This depends on sporadic incidence, symptoms and attempted transmission, but as success with this seems to depend on the strain of virus involved, confirmation usually rests on the histopathology. The primary results of infection are seen in the lymphoid-macrophage system. There is a rapid depletion of small lymphocytes from spleen and lymph nodes, followed by an intense proliferative activity throughout the body by all potentially lymphocytogenous elements. This explains the predominantly perivascular distribution of lesions outside lymphopoietic tissues. Some authors have found inclusion bodies.
The following specimens should be submitted:
A. For transmission experiment.
1. 200 mls. citrated blood, using 12.6 ccs. of a saturated solution of sodium citrate.
2. Unpreserved lymph node or nodes draining the head or neck, 2 oz. of liver and/or spleen collected as aseptically as possible. These specimens should be forwarded in an ice-box.
B. For histopathology.
3. Sections of liver, kidney and adrenalin 10 per cent, formal saline; together with any abomasal lesions.
4. Nasal mucosa and pieces of brain, especially the cerebellar end, in Zenker's fixative for 12 hours, washed in running water for 24 hours, then transferred to 70 per cent. iodised alcohol. If specimens can reach the laboratory early the following day they may be sent in the fixative solution. The motoric vagoglossopharyngeal nucleus is the site of choice for inclusion bodies, and this is found lateroventrally on the medulla oblongata, about half to three-quarters of an inch caudal to the pons, (Zenker's fixative will be available from the District Veterinary Officer).
DIFFERENTIAL DIAGNOSIS:
Nasal granuloma: dyspnoea, loud snuffling noise (summer snuffles) mostly muco-purulent, bilateral nasal discharge sometimes blood-stained, may be rapid loss of condition and mild; thickening of nasal mucosa evident, particularly over turbinate bones, with formation of small nodules and sometimes ulceration of mucos membranes, which are mostly inflamed. Usually no fever, may be several animals affected and for long period, occurs in warmer weather with symptoms abating as winter approaches; very few deaths.
Photosensitisation: general swelling of head; all exposed mucosae and skin may be affected: swelling, crusts, discharges, salivation.
Infectious Ophthalmia: keratitis with "pointing", ocular discharge, no nasal discharge. Also may see keratitis following treatment with phenothiazine.
Sinusitis: very tender to percussion over sinuses, may be nasal discharge, often unilateral, sometimes evidence of injury.
EXOTIC INFECTIOUS DISEASES:
Details obtainable from Service Publication Division of Veterinary Hygiene) No. 4.
Foot and Mouth disease: vesicular eruption over mucosae and skin, especially buccal cavity and hoof clefts, drooling, fever; very rapid spread in herd; not usually fatal; no nasal or ocular discharge.
Vesicular stomatitis: very similar to F & M.
Rinderpest: High fever; congestion of vaginal or preputial mucosae; papules, vesicles, ulcers in mouth with yellowish-grey necrotic material; salivation, ocular and maybe nasal discharge; diarrhoea; rapid spread.
CONTROL:
There is no effective treatment, although palliative measures probably should be adopted. Attempts have been made to develop a vaccine but this has not shown marked success to date. It did, however, cut short a herd outbreak in Kenya. Even if efficient, it hardly would be economical where the disease occurs only sporadically.