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This article was published in 1998
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A disease was commonly reported in Cuba in the 1970's where it was known as "Borrachera" (molasses drunkenness).


This is a report of the death of about 200 cattle showing classical symptoms of PE (Polioencephalomalacia) in a herd of 6,300, of which 3,500 were being fed an ab lib diet of molasses and high protein concentrate, with a limited amount of roughage.


PE essentially refers to softening of the cerebrocortical gray matter, distributed in a laminar pattern (also known as cerebrocortical necrosis, CCN). Full pathological description is given in Jubb Kennedy & Palmer 1993, and will not be described any further here.

The disease is classically described in sheep, and less commonly cattle. In cattle it is commonest 9-12 months of age when animals are introduced into a feedlot. Unlike sheep, field reports of the condition in cattle in Australia are uncommon (OR Coverdale pers comm), with the highest incidence in coastal areas. (G Fraser pers comm).

Some specific situations in which the disease have been associated are water deprivation (as occurs with pigs), specific dietary components (eg high sulphate levels) and with various plant poisons (eg. bracken fern).

It can be experimentally be reproduced by anti-thiamine agents (eg amprolium). The cause remains unknown, but it is associated with increased thiaminase levels, and thiaminase producing bacteria in the rumen have been implicated. This is fully discussed in Blood, Radostits and Gay.

I will discuss details of some aspects of the disease directly.


The property concerned has an area of 6,200 HA, with rainfall of about 32-35 inches (average). Rainfall is mainly summer, with a tendency to be later in summer when the Dorrigo easterly 'mists' occur. Pastures are highly improved mostly perennial rye and clover with other species (eg paspalum etc). The property is close to the gorge country, and some parts are steep with flat pasture flats descending into valleys.

The property runs mostly cattle and is part of a 3 property complex The operation is mostly breeding cattle (Beefmaker and crosses) and large steer operation. Young stock are sold as store (pre-feedlot) cattle.

Disease occurrence was late 94 early 95 which was in a severe period of a general 4 year drought. The division of the Board where the property was drought declared 1.4.94 to 1.11.95, as well as most 1993.

As feed supplies deteriorated cattle mobs were progressively being introduced onto feed, with the movement of cattle onto the property from other properties, as well as within property movements.

The feeding regime varied with prices and supply but essentially was:

(1) molasses ab lib.
(2) high protein concentrate mix feed separately. This was based on a commercial soybean / copra meal with mineral / vitamin added.
(3) roughage - this was whatever was cheapest and included failed crops, usually in large round bales sourced from Victoria, NSW and Queensland.

The amounts of concentrate and roughage being fed varied depending amount and type of pasture feed left in the paddock, and type of stock being fed. In general steers were approaching feedlot conditions, heifers were on basic maintenance ration, and cows and calves were given paddocks with most roughage.

First call - 7 steers had died in a week and owner was worried about acute pneumonia and IBR etc going through mob. Clinical signs as reported included heavy breathing, reluctant to move, not feeding and a range of non-specific nervous signs.

Clinical signs in a sick animal examined were a lot of frothy discharge, wandering about with wobbly gait and convulsions prior to death PM of same animal - nothing significant but brain was not examined.

Second call (2 weeks later) - deaths occurring in other mobs including cows (about 30). It should be noted that odd deaths from other causes were occurring eg old cows with various problems, various feeding problems in younger stock especially as roughage cut out in paddocks, plus the usual found dead bogged in river edge etc.

Clinical signs in cow examined were various nervous signs ie twitching, exaggerated movements when moved, convulsive fit and down paddling PM - gross nothing, histo - mild cerebral oedema in brain.

After discussions with Bob Rhimberger Vet Clinician, Sydney University, the most likely diagnosis was considered to be PE. All sick animals given B1 injections and Thiamine concentrate levels increased in feed. Roughage levels increased.

Third call (few days later) - about 45 died. Property inspection - clearly roughage was running out in most paddocks (at this stage feeding 800 cows with calves, 300 steers and 800 heifers, about 100 tonne week). Whilst many cattle were showing signs classically described for PE (most of the clinical symptoms mentioned in Blood Radostits and Gay and Hungerford were present), some others had signs suggesting pneumonic conditions eg heavy difficult breathing, dehydrated looking with dry crusty nose, nasal discharge as well as frothy salivation (as may be seen in PE) and no obvious nervous signs.

One bull examined; showing pneumonic and nervous signs (gross congestion and lung inflammation). PM - gross nothing, histo - brain - oedema, vascular congestion and some necrotic neurons.

Sample herd blood testing - calcium levels normal, magnesium levels normal 4 ex 10 had Chlamydia CFT levels of 16/32.
Feed sample - only minute traces of Aspergillus riger and A flavus - concluded not aflatoxicosis.

Fourth call (a week later) - 20 cows in mob of 110 died over about week, many over 3 days. Manager worried about certain load of hay from Walgett (which came with the usual clods of black soil, kangaroo and wild pig carcases etc).

At this stage the manager estimated deaths from this condition was 68 cows, 3 heifers, 4 bulls and 8 steers.

One animal with pneumonic and nervous signs examined. PM - lung - amount of lobular pneumonia, brain - mild congestion, mild oedema of cerebral cortex with some neuronal necrosis suggestive of PE.

Serology on two sick animals - Chlamydia CFT - 2 x 16.

Serology test of normal stock 2 ex 20, 16 CFT Chlamydia, 4 ex 20, 8 CFT Chlamydia.


Diagnosis in live animals

A New Zealand summary article (Rammel & Hill, 1986) mentions as follows:

The differential diagnosis for nervous signs given Blood Radostits and Gay also includes:

In this case the RVL and Veterinary practitioner suspected SBE - but it didn't resemble any of the SBE I had seen at Narrabri (of which there is plenty!!)

Blood, Radostits and Gay refers in the table to diagnosis using biochemical tests in text.

The text is more up front ie "None of the biochemical tests described are practical under usual practice conditions.... A diagnosis is reached after careful consideration of the epidemiological data."

This case was confused by the fact that a variable degree of pulmonary congestion was present and in some animals the only clinical signs appear to be from this cause.

PM Diagnosis

Brain lesions The brains submitted were from animals that had short clinical episodes - JK & P describe that early severe lesions are less obvious than longer standing cases.

I don't now recall if ultra violet light illumination which reflects fluorescence indicating brain necrosis was carried out (Jackman 1983).


"In Cuba, molasses toxicity occurs in cattle fed on a liquid molasses-urea feeding system with limited forage. The clinical and necropsy findings are identical to poliocncephalomalacia. However, molasses toxicity is not thiamin responsive and can be reversed by feeding forage." (BR & G)

I can find very few recent references to this ie PE specifically related to molasses feeding. Certainly in this case the diet was molasses based, and there was no response to thiamine so maybe it was PE induced by molasses toxicity.

Bulk molasses feeding is now common in NE for winter feeding of cattle. It is a major source of energy and fed with urea supplements or by-pass protein supplements will greatly assist cattle through the winter as quality pasture becomes less available, and cattle turn to dried off roughage from excess summer growth.

This is the only property where PE was reported, but enquiries with other persons feeding molasses suggests they fed molasses to utilise dry feed and did not feed molasses when roughage sources were low, or supplemented adequately with hay.


  1. Blood DC, Radostits OM and Gay CC (1996), Veterinary Medicine 9th Edition Bailliere Tindall
  2. Jackman R (1983) Cerebral autofluorescence and thiamine deficiency in cerebrocortical necrosis Vet Rec. 112:548-550
  3. Jubb KVF, Kennedy, PC and Palmer, NC (1993) [Pathology of Domestic Animals] Vol 1 pp 1340-1343, Academic Press, California USA
  4. Rammel CG & Hill JH (1986), A review of Thiamine deficiency and its diagnosis, especially in ruminants NZ Vet. J 34:202-204


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