Signalment:  

2-year-old, male, mixed breed, bovine (Bos taurus)This bovine belonged to a herd of 2-year-old cattle that were placed in a pasture highly infested with bracken fern (Pteridium aquilinum). Five cattle (including the one of this report) died after presenting clinical signs that included high fever, hemorrhages through the nose, petechiae in mucous membrane and hematuria. The 12 cattle had been placed in the bracken fern infested pasture in mid-October (spring) and the deaths occurred from late December to early January (summer). When examined for the first time, the bovine of this report was depressed and had a rough hair coat, few petechiae in the ocular mucosae, slightly red discolored urine, soft stools with small blood clots and rectal temperature of 40.2°C. In the following days the rectal temperature peaked to 42.2°C and the clinical signs got worse with frank hematuria, hemorrhages through the nose, depression, and foul smelling black soft stools with blood clots. This bovine died after a 6-day clinical course (the other 4 affected cattle died after clinical courses that varied from 25 days). In the terminal phase of the disease the rectal temperature dropped to 39°C.


Gross Description:  

Large hemorrhages were seen in the subcutaneous tissue of the trunk and abdominal cavity, mainly in the areas of attrition. Multiple 0.5 cm diameter subepicardial hemorrhagic foci were observed in both ventricles. The natural and cut surfaces of lymph nodes and spleen were hemorrhagic. Petechiae, ecchymosis and hematomas were observed in the omentum and mesentery (Fig. 1-1), in the intestine at its junction with the mesentery and in the serosa of the fore stomachs. Several small ulcers were observed in the abomasal mucosa and a large (17x4 cm) cylindrical blood clot was observed in the lumen of the abomasum, near the pylorus. There were ulcers covered with blood in the intestinal mucosa mainly over the Peyers patches. Partial blood was admixed with the contents of the large intestine and a large cylindrical clot (15x3 cm) was observed in the lumen of the cecum. The mucosa of the ureters were markedly edematous and hemorrhagic. The bladder contained approximately 200 ml of urine and blood, and the bladder mucosa was swollen and hemorrhagic. There was partially clotted blood in the joint cavities of the pelvic limbs.


Histopathologic Description:

The hemorrhages observed grossly were confirmed on histopathological examination. Sections of the bone marrow of the sternum were prepared from the affected bovine (Fig. 1-2) and from a normal age matched control (Fig. 1-3). Both sections are arranged in the same glass histoslide submitted. There was severe aplasia of the bone marrow of the affected bovine as compared to the control. The sinusoids of the marrow are distended due to the lack of pressure usually posed by the large numbers of hematopetic cells. There is paucity or absence of nucleated cells, including megacariocytes, which can be observed in normal regular numbers in the control section.


Morphologic Diagnosis:  


Bovine, bone marrow, sternum, aplasia, severe,
Etiologic diagnosis: toxic bone marrow aplasia
Etiology: toxic substance(s) in Pteridium aquilinum
Condition: acute poisoning by Pteridium aquilinum


Lab Results:  

Severe thrombocytopenia and neutropenia were seen. Below are results of blood tests performed on the day before the bovine of this report died. 
Blood coagulation test
Parameter Unity Reference Values Affected Bovine
Partial time of activated thromboplastin seg25-4549.3
Prothrombin time seg   20.2

Complete blood cell count
Parameter Unity Reference Values Affected Bovine
Red blood cells (x106/mm3)(5.0-10.0)5.1
Hemoglobin (g/dl)(8.0-15.0)79
Packed cell volume (%)(24-46)23
Mean corpuscular volume (fl)(40.0-60.0)45.1
Mean corpuscular hemoglobin concentration (%)(30.0-36.0)34.3
Leucocytes (/mm3)(4,000-12,000)5100
Neutrophils (%)(15%-45%)0
  (/mm3)(600-4,000)0
Lymphocytes (%)(45%-75%)100
  (/mm3)(2,500-7,500)5100
Monocytes (%)(2%-7%)0
  (/mm3)(25-840)0
Eosinophils (%)(0%-20%)0
  (/mm3)(0-2,400)0
Basophils (%)(0%-2%)0
  (/mm3)(0-200)0
Platelets (x103/mm3) 100-800 3


Condition:  

Aplastic anemia, bracken fern toxicosis


Contributor Comment:  

Bracken fern (Pteridium aquilinum) is the second most important plant poisoning in southern Brazil and responsible for 12% of all cattle deaths caused by poisonous plants in this region.(11) The ingestion of bracken fern results in three forms of clinical disease in cattle (two of those are chronic and characterized by development of neoplasms): 1) squamous cell carcinomas in the upper digestive tract (base of tongue, esophagous and entrance of the rumen) (13); 2) several types of the neoplasms in the urinary bladder.(14) This latter condition is associated with bleeding from the urinary bladder and universally known as enzootic hematuria. The cocarcinogenesis of bracken fern with bovine papillomavirus-4 (BPV-4) and BPV-2 is implicated respectively in the pathogenesis of upper digestive tract squamous cell carcinomas and bladder tumors (11, 12). 3) A third condition caused by the ingestion of the plant is characterized by bone marrow aplasia and generalized bleeding tendency (17) and is the one affecting the bovine of this report. This condition is generally referred to as the acute form of bracken fern poisoning. It is mostly a disease of cattle but has been occasionally reported in sheep. Acute bracken fern poisoning in cattle was originally reported in England at the end of 19th century as an acute disease characterized by high fever, hemorrhages and high lethality rates.(16) During this time the etiology was only suspected but it was confirmed in the following year (1) and in later years by successive experiments in cattle being fed with large amounts of the plant for prolonged periods.(4,5,9,15) The same disease was observed during the autumn of 1917-1920 in cattle from the state of New York (2) but only confirmed later as being caused by the ingestion of bracken fern.(5) Since then the disease has been reported from several other countries.(17,18)

Clinical signs associated with acute form of bracken fern poisoning in cattle include high fever (up to 42.5°C), severe hemorrhages in various tissues and organs, neutropenia and thrombocytopenia.(4,8,10,15,16) High fever appears to be the first clinical sign of the disease, and some believe (14) the intensity of fever that occurs in acute bracken fern poisoning is not duplicated by any other diseases in cattle. Fever is followed by hemorrhage through nasal cavity and depression. In the advanced stages of the disease the fever may subside.(4,9,10,12)

Acute bracken fern poisoning in cattle has been subdivided by some (10, 12) into two types: 11) enteric, which is the most common and characterized mainly by depression, anorexia, high fever, and weak pulse, blood clots in the feces and foul smelling feces, pale mucous membranes and bleeding from mucous membranes of the nose, eyes, vagina, and anus; and 2) laryngeal-�-�with clinical signs including high fever, roaring, laborious breathing and edema of the larynx. In our experience, however, it is not uncommon to observe signs of both types overlapping in the same animal, as is the case of the bovine of this report. Hemorrhages from venipunctures, from insect bites and in the milk are commonly observed. Death ensues usually 2-3 days after the first clinical signs; however peracute cases of 4-10 hours and cases of recovery are also reported.(4,17) In our region (unpublished data) acute bracken fern poisoning generally occurs in spring and summer months, in hill camps where the ecology is conducive of fern growth, with morbidity rates of 12.5%-21.5% and high lethality rates.

The primary lesion in the acute bracken fern poisoning in cattle is a severe suppression (aplasia) of the bone marrow (as observed in the bovine of this report) which results in thrombocytopenia and neutropenia. No changes are observed in red blood cells (9) and any deficit in RBCs numbers are due more to the hemorrhaging than to the bone marrow suppression since the RBC half-life in cattle is considerably greater (157-162 days) than that of platelets (5-10 days) and neutrophils (12 hours). Usually death due to bleeding related to thrombocytopenia occurs when the numbers of platelets are lower than 10,000/mm3 of blood. In these cases fatal bleeding within body cavities occurs. In the case of this report platelets were 3,000/mm3 one day before death.

There is usually bacteremia related to the almost complete lack of neutrophils in the peripheral blood.(4,9) If after the onset of the bacteremia the bovine survives for several days, infarcts may occur in the liver, lung, kidney and spleen. Death occurs because of internal hemorrhage or septicemia.(10,12)

The most remarkable necropsy findings are hemorrhages of almost any size in almost any organ.(10,12,15) Petechiae and ecchymosis occur in the subcutaneous tissue and there is edema and hemorrhages in lymph nodes; petechiae and paint-brush hemorrhages are observed on serosal surfaces of several organs from abdominal and thoracic cavities. Abundant collections of partially clotted blood can be found in the peritoneal cavity. Mucosal ulcerations and blood clots in the lumen of fore stomachs, abomasum, small and gross intestine are observed. Pale necrotic areas of necrosis can usually be observed in the liver but also in the heart, kidney and spleen. These areas are usually referred to as infarcts but probably are caused by toxins of bacteria and not really by ischemia due to compromise of the vasculature. Pharyngeal and laryngeal edema can be marked.(10,12,16)

The hemorrhages observed grossly can be confirmed histologically. Additionally, foci of coagulative necrosis associated with clusters of bacteria can be found in the liver, heart, kidney and spleen. The most striking histological change is the severe aplasia of the bone marrow.(4,9)

The norsesquiterpene glucoside ptaquiloside is the toxin in P. aquilinum responsible for the bone marrow suppression in acute disease (6); this toxin has cumulative properties and the time elapsed from the beginning of the ingestion of the plant and the development of the clinical signs will depend of the amount of ingested plant.(4,12) Usually the ingestion of daily amounts equal to or above than 10 g/kg/bw during 2-11 weeks are necessary to produce the disease.(4,9)

The list of differential diagnosis for acute bracken fern poisoning in cattle should include anaplasmosis, pneumonic mannheimiosis (differential for the laryngeal form), septicemia pasteurellosis, leptospirosis, sweet clover poisoning, bacillary hemoglobinuria.(12) A similar disease caused by bone marrow suppression is reported in cattle from Australia and is caused by the ingestion of an yet different poisonous plant (Cheilanthes sieberi).(3)


JPC Diagnosis:  

Bone marrow: Hypoplasia, trilineage, diffuse, severe


Conference Comment:  

Bracken fern toxicosis occurs in several domestic species including pigs, horses, sheep and cattle. Susceptibility depends on the species affected, with cattle and horses being highly susceptible. Sheep rarely eat this plant and are thus affected less often, and pigs are rarely affected.(7,8,19) The plant is most toxic when it is green and actively growing. This plant is not very palatable, so it is often only eaten in large quantities during drought conditions. In monogastrics, bracken fern poisoning leads to a thiamine deficiency. This results in neurologic and cardiac disease most commonly reported in pigs and horses.(7,8,19)

There are numerous toxins within bracken fern including quercetin, ptaquiloside, shikimic acid, aquilide A, and prunasin.(7,8,19) The two major syndromes commonly seen in cattle are aplastic anemia and enzootic hematuria. The severity of disease depends upon how much of the plant is ingested. There is a cumulative affect with this poison. Morbidity is low and mortality is high with this disease. If enough of the toxin is ingested over weeks to months, death via thrombocytopenic hemorrhage or septicemia secondary to neutropenia is often the result.(7,8,19)

In cattle and sheep, bracken fern poisoning results in an irreversible trilineage marrow hypoplasia and resultant aplastic pancytopenia. The chronic form is usually from long term, low level ingestion of bracken fern resulting in persistent hematuria and alimentary tract neoplasia.(7,8,19) Bracken fern toxicity also commonly causes neoplasia within the urinary bladder.(7,8,19) Papillomas, fibromas, and hemagiomas are most common in the urinary bladder. 

Hemorrhages can be found in almost any tissue with bracken fern poisoning, but they are usually most numerous in the stomach and small intestine. Multiple neoplasms of the bladder wall or esophagus and forestomachs may also been seen at necropsy. Marrow cellularity is often markedly diminished and the marrow appears pink and soft.(7,8,19)


References:

1. Anonymous: Fern Poisoning. J. Comp Path Therap 7:165-167,1984
2. Bosshart JK, Hagan WA: A fatal unidentified disease of cattle in New York State. Cornell Vet 10:102-13,1920
3. Clark IA, Dimmock CK: The toxicity of Cheilanthes sieberi to cattle and sheep. Aust Vet J 47:149-152, 1971
4. Evans WC, Evans ET, Hughes LE: Studies on bracken poisoning. Part III. Field outbreaks of bovine bracken poisoning. Brit Vet J 110:426-442, 1954
5. Hagan WA, Zeissig A: Experimental bracken poisoning of cattle. Cornell Vet 17:194-208, 1927
6. Hirono I, Kono Y, Takahashi K, Yamada K, Niwa H, Ojika M, Kigoshi H, Hiiyama K, Uosaki Y: Reproduction of acute bracken poisoning in a calf with ptaquiloside, a bracken constituent. Vet. Rec. 115:375-378, 1984
7. Maxie MG, Youssef S: Nervous system. In: Jubb, Kennedy, and Palmers Pathology of Domestic Animals, ed. Maxie MG, 5th ed., vol 1, pp. 354-357. Saunders Elsevier, Philadelphia, PA, 2007
8. Maxie MG, Newman SJ: Urinary system: In: Jubb, Kennedy, and Palmers Pathology of Domestic Animals, ed. Maxie MG, 5th ed., vol 2, pp. 518-520. Saunders Elsevier, Philadelphia, PA, 2007
9. Naftalin JM, Cushnie GH: Pathology of bracken fern poisoning in cattle. J. Comp. Path Therap 64:54-74, 1954
10. Osebold JW: An approach to the pathogenesis of fern poisoning in the bovine species. J Am Vet Med Assoc 121:440-441, 1951
11. Rissi DR, Rech RR, Pierezan F, Gabriel AL, Trost ME, Brum JS, Kommers GD, Barros CSL: Plant and plant-associated mycotoxins poisoning in cattle in Rio Grande do Sul, Brazil: 461 cases. [Intoxica+�-�+�-�o por plantas e micotoxinas associadas a plantas em bovinos no Rio Grande do Sul]. Pesq Vet Bras 27:261-268, 2007. (In Portuguese, Abstract in English)
12. Sippel WL: Bracken fern poisoning. J Am Vet Med Assoc 121:9-13, 1952
13. Souto MAM, Kommers GD, Barros CSL, Piazer JVM, Rech RR, Riet-Correa F & Schild AL: Neoplasms of the upper digestive tract of cattle associated with spontaneous ingestion of bracken fern (Pteridium aquilinum). [Neoplasias do trato alimentar superior de bovinos associadas ao consumo


Click the slide to view.


1-1 Omentum, mesentery, and small intestine, ox


1-2 Bone marrow, ox


1-3


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