Historical – There seems to be little doubt that bloedpens has been prevalent in certain parts of the Cape for a considerable time.  According to information obtained by the writer from several old farmers who have grown up in infected localities it would appear that the disease was fairly well known to sheep farmers fifty or sixty years ago.  In 1904 Hutcheon pointed out a reference in the Colesberg Advertiser which shows that bloedpens was very prevalent in the Cape as early as 1888.


Reference to bloedpens as a devastating disease in lambs was made in the agricultural press from time to time, but the disease did not receive the neighbourhood of Steynsburg.  After 1913 the study of this scourge was again neglected until 1921, when the author carried out a series of experiments and succeeded in transmitting the infection to healthy newly-born lambs by feeding the intestinal contents of diseased lambs. Later Neser (1926) also investigated bloedpens.




Constant reference to the existence of a disease known as “lamsiekte”  has been made from time to time by travelers, farmers and others.  During 1780 – 85 le Vaillant (1796) while traveling through the interior of Southern Africa noticed a disease which he described as “lamsiekte” and which he found to be one of the four destructive diseases of the Cape, appearing annually soon after the warm weather had set in.  He states that the affected cattle, although quite healthy in appearance, remain in a lying posture and usually die in about fourteen days.  There was no effective remedy known, so that the sick animals were destroyed as a rule; but their meat was used for human consumption.  Le Vaillant found the malady extensively prevalent in parts of cattle manifesting an abnormal craving for bones when the pasture was poor, but hardly any craving when the veld was good.


While travelling through Southern Africa in 1803-6 Lichtenstein (1812) also observed the existence of “Lamziekte” and referred to it as a sort of “murrain of the most pernicious kind”; he described a case seen by him where the animal kept on eating, although it was unable to stand or rise without assistance.  In the diary of Commissioner de Mist, compiled during his journey in 1805, the prevalence of lamsiekte was recorded in several parts of the Cape.


Hutcheon first refers to “Lam Ziekte” or “Lame-sickness” in 1880, when he noticed the disease in Bredasdorp and in certain Kaffrarian districts.  He took it for an acute form of rheumatism and suggested that the nature of the soil and the veld were predisposing factors.  A detailed description of lamsiekte and styfsiekte, as they occurred in Griqualand West, was given by Hutcheon in his annual report for 1884.  He considered the two diseases as two different manifestations of the same malady and drew attention to the intense craving for bones and other animal matter, shown by stock grazing on affected pastures.  He also remarked on the greater prevalence of both diseases in young, growing stock and cows as compared with oxen and dry cattle; further, he noticed that the sickness was much more prevalent during winter weather and dry seasons, when the pasture was very low in feeding value, than after good rains had fallen and the grass had grown luxuriantly.  It was constantly noticed that the incidence of lamsiekte regularly decreased soon after the first rains of the season.


He correlated the disease with a perverted appetite manifested by phates in the food, grown on soil deficient in lime and phosphates.  He regarded the symptoms as due to a defective form of nutrition of the bones of the affected animals, and maintained that the symptoms could be prevented by feeding the animals on materials like bran and bonemeal, which were rich in phosphates.  This view was strongly supported by the work of Borthwick (1896) in which it was shown that regular feeding of bonemeal greatly reduced the incidence of lamsiekte in cattle.


In his annual report of 1894 Hutcheon reported the presence of “some other immediate and exciting agent” as the cause of the sudden development of the acute form of lamsiekte, and mentioned the presence of an effusion of fluid in the cranial cavity, a lesion which is now known not to exist.  He declared the symptoms of paralysis to be due to these effusions of fluids in the membranes surrounding the brain and the spinal cord, and to the softened and highly congested condition of certain groups of bones, an interpretation which is now known not to represent the truth.  As the lesions described by Hutcheon do not truly correspond with those recorded by later workers, the identity of the various diseases included by him under the term “lamsiekte” is now questioned.  It is particularly difficult to accept his interpretation with regard to styfsiekte, especially when he considers lamsiekte and styfsiekte to be merely two different manifestations of the same disorder.


Subsequently, numerous alternative theories were formulated with regard to the cause of lamsiekte.  In 1907 Spreull and Robertson (Robertson, 1907) incriminated a pasteurella as the causal organism of the disease.  Two years later Keeling Roberts (1910), in support of this view, tried to reproduce lamsiekte experimentally by means of inoculations with cultures of a bacterium obtained from the intestines of sick animals and also by the oral administration of carcass material or ingesta procured from affected animals.  He undoubtedly produced lamsiekte but he failed to give the correct explanation of his own results.


A view frequently expressed by farmers was that the disease could be contracted by cattle as a result of the ingestion of stomach contents, skins and carcass material of animals which had succumbed from lamsiekte.  In order to test this conception together with various theories held with regard to the cause of the malady, Walker (1913) and Mitchell (1913) carried out a series of experiments.  They failed entirely to find any evidence in support of the pasteurella theory and demonstrated beyond doubt that lamsiekte was neither infectious nor contagious in the ordinary sense.  They succeeded in reproducing symptoms resembling those of the disease under review, by administering carcass material and crushed bones in various stages of putrefaction.  Both investigators, however, were puzzled by what was thought to be an irregularity of their results and guardedly declared the symptoms to be due to a “non-specific form of toxemia” following the absorption of septic material.  Moreover, Mitchell showed that muzzled animals were unable to pick up the disease when allowed to run about on “infected” veld in contact with other cattle, some of which contracted lamsiekte.


Accordingly, it was concluded that the transmission of the causal agent was effected by ingestion, and the possibility presented itself that plant poisons might produce the disease.  But, on account of the negative results obtained from a number of feeding experiments carried out by Burtt-Davy (1913) and Theiler (1913), Theiler advanced an “accumulated vegetable poison theory”.  This suggested that a toxin was produced in the grass under certain climatic conditions.  It was thought that the toxin accumulated in the muscles of the animals, and that it could be eliminated under certain conditions.


Stead (1913) formulated “a vitamin deficiency theory”, but this was promptly dismissed by Theiler, Viljoen and Green (1915).  Likewise, the view expressed by Hedinger (1915) that lamsiekte was a form of sarcosporidiosis was readily discarded by Theiler and Viljoen (Viljoen, 1918).  Theiler also considered the remote possibility that the disease might be caused by an ultra-visible virus transmitted through the accidental ingestion of insects by cattle, but he soon dismissed this theory also.  However, during the course of his experiments, he actually produced symptoms like those of lamsiekte by drenching cattle with blow-fly pupae collected in the vicinity of a lamsiekte carcass in an “infected” area, though he failed to provoke similar symptoms when he used blow-fly pupae obtained from diseased cadavers in non-lamsiekte areas.


In 1919 Theiler (Theiler, 1920) and his collaborators proved beyond doubt that lamsiekte was normally produced in cattle that displayed a perverted appetite, by the ingestion of carcass material picked up from the veld.  The disease was transmitted experimentally to healthy animals by drenching them with decomposed carcass debris, collected at random from lamsiekte veld.  The causal agent was believed to be a toxin present in putrefying animal matter in certain localities.


It was subsequently established that the toxin is elaborated by a specific anaerobic bacterium which grows luxuriantly in carcass debris.  This anaerobe is distinetly different from ordinary putrefactive organisms that are not able to produce an analogous toxin.  Toxin is, therefore, not present in all carcass debris, but only in dead animal matter in which the specific toxicogenic organism has multiplied.  Robinson finally identified the bacterium as a member of the botulinus group (Theiler and Robinson, 1927; Robinson, 1930).


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Lamsiekte.  Posterior paralysis.  (Onderstepoort collection).


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Lamsiekte, showing paralysed tongue.  (Onderstepoort collection).


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Tetanus.  Horse.  (Onderstepoort collection).




Although early records of tetanus in South Africa are few (Hutcheon, 1901, 1904) sporadic cases both in animals and man are reported from time to time in different parts of the Union, but the disease has never yet assumed serious proportions.  The author has studied the disease in horses, cattle and sheep; in horses the seat of infection was usually a wound in the foot; in cattle the infection followed parturition; and in the sheep the primary seat of disease was a wound at the root of the horns of a ram.


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Tetanus.  Horse.  (Onderstepoort collection).