Alopecia areata in a Holstein bull

Alopecia areata in a Holstein bull

Emily Brouwer

Animal Health Laboratory, University of Guelph, Guelph, ON.

AHL Newsletter 2019;23(3):4-5.

A 4-y-old Holstein bull was presented to the herd veterinarian because of multifocal-to-coalescing areas of hair loss. The lesions were localized in black-haired regions, were variably sized (2-10 cm diameter), and would frequently coalesce (Fig. 1). Eventually, the hair would re-grow but would be white where it was previously black (Fig. 2). The lesions were non-pruritic, non-painful, and the underlying skin appeared grossly normal. None of the other animals in the breeding facility were affected, and apart from the skin lesions, the bull was otherwise clinically normal.

The veterinarian collected two 6-mm skin punch biopsies, choosing one from a more recent lesion and one from an older lesion. Histologically, the findings in both sections were similar. Hair follicles were present and comprised of both anagen and telogen follicles. Most hair follicle bulbs contained degenerate matrix cells and abnormally clumped pigment contained within presumptive macrophages and multinucleate cells (Fig. 3). There was frequent peribulbar melanin incontinence, and a subtle increase in perifollicular connective tissue. There were very low numbers of CD3+ T lymphocytes within the follicular bulb and the surrounding dermis (Fig. 4). Superficial dermal vessels were surrounded by moderate numbers of eosinophils.

Adult-onset alopecia with subsequent leukotrichia has been described as the clinical presentation of alopecia areata in Angus, Holstein, and Eringer cattle. This rare condition is a non-scarring, idiopathic dermatosis that is presumed to be caused by autoimmune reaction to hair bulb antigens. In humans, rodents, dogs, and horses with the condition, circulating IgG antibodies directed against trichohyalin have been implicated. For this condition, the gross lesions, pigmentary incontinence, and melanophagia with a lymphocytic mural folliculitis are considered characteristic. Identification of CD3+ T cells within and surrounding the hair bulbs is considered diagnostic.   AHL

Alopecia areata in a Holstein bull.

Figure 1. Alopecia areata in a Holstein bull. Multifocal to coalescing, well-demarcated regions of alopecia and leukotrichia located in regions of pigmented hair.

Focus of alopecia with localized leukotrichia.

Figure 2. Focus of alopecia with localized leukotrichia.

Hair follicle with abnormal pigment distribution and mural lymphocytes. H&E, 20X.

Figure 3. Hair follicle with abnormal pigment distribution and mural lymphocytes. H&E, 20X.

T cells within the hair bulb and the surrounding dermis. CD3 immunohistochemistry, 20X.

Figure 4. T cells within the hair bulb and the surrounding dermis. CD3 immunohistochemistry, 20X.


Timm K, et al. Alopecia areata in Eringer cows. Vet Dermatol 2010;21:545-553.

Valentine BA, et al. Alopecia areata in two black Angus cows. J Vet Diagn Invest 2012;24:405-407.

Slobbering sheep: Bibersteinia trehalosi septicemia in lambs

Slobbering sheep: Bibersteinia trehalosi septicemia in lambs

Jan Shapiro

Animal Health Laboratory, University of Guelph, Kemptville, ON.

AHL Newsletter 2019;23(3):6-7.

In May 2019, three 4-mo-old weaned meat lambs were submitted for postmortem to the Animal Health Laboratory, Kemptville. Of ~100 at risk, 13 had died within 2 wk. Lambs had acute onset of drooling while continuing to try to eat and drink, but over a 24-36 h period became recumbent and died. Neither lameness nor stiffness was observed. Lambs were kept in a multi-age group pen, with no additions to the flock within 6 mo. Only lambs had clinical signs.

Gross postmortem examination revealed multifocal erosion and ulceration of the digestive tract of all 3 lambs, specifically, erosions on the dorsum of the tongue and hard palate of lamb 1, and a jejunal ulcer in lamb 2. Mucosal ulcers covered by plaques of fibrin were in the proximal 1/3 of the esophagus in lambs 1 and 3 (Fig. 1). All 3 lambs had numerous petechiae throughout the lungs, and diffuse hyperplasia of mesenteric, bronchial, and retropharyngeal lymph nodes. There were no gross lesions of the lips, muzzle, dental pad, or hooves, and vesicles were not observed.

Mucosal ulcers covered by plaques of fibrin in the proximal 1/3 of the esophagus (arrows).

Figure 1. Mucosal ulcers covered by plaques of fibrin in the proximal 1/3 of the esophagus (arrows).

Histologically, mucosal erosions and ulcers were covered with fibrin, enmeshed neutrophils, caseous debris, and large numbers of intralesional bacteria. Lamina propria was congested and some blood vessels had thrombi. In lung, lymph nodes, liver, spleen, and brain, bacterial colonies and fibrin thrombi were seen in blood vessels, and bacterial colonies were in parenchyma, sometimes accompanied by caseous necrosis. The diagnosis of acute bacterial septicemia was supported by isolation of Bibersteinia trehalosi from lung, liver, and spleen.

Bibersteinia trehalosi is a sporadic cause of septicemia in sheep, usually occurring in weaned lambs. B. trehalosi normally resides in the tonsils and nasopharynx of apparently healthy animals, but can progress from the tonsils to the lungs and bloodstream to cause systemic disease under exposure to various stresses, such as inclement weather, change of pasture or feed, overcrowding, poor ventilation, handling, and transport. Clinical signs may include fever, anorexia, lethargy, or sudden death with no signs. Common postmortem lesions are petechial and ecchymotic hemorrhages in subcutis, intermuscular fascia, pleura, lungs, epicardium, and mesentery, and swollen lymph nodes. Pneumonia is also frequently seen, and in many cases B. trehalosi is isolated in mixed culture with Mannheimia haemolytica, Pasteurella multocida, or Trueperella pyogenes.

Erosion and ulceration of the oral cavity, tongue and esophagus are not consistent lesions of Bibersteinia trehalosi septicemia, but when they occur, some owners report drooling as the prominent clinical sign. Observation of these lesions prompted consultation with CFIA regarding reportable disease differential diagnoses such as foot-and-mouth disease, bluetongue, peste des petits ruminants, and vesicular stomatitis. More common etiologies include parapoxvirus infection (orf), oral trauma, and bacterial infections.

Ovine herpesvirus type 2 (OHV-2) was also detected in lamb tissues by PCR. OHV-2 is believed to be endemic, and usually asymptomatic, in Ontario sheep flocks. However, experimentally, it may cause MCF-like mucosal disease in sheep. The possibility that OHV-2 could cause similar disease under field conditions, and the significance of OHV-2 in this case is unknown.   AHL


Caswell JL, Williams KJ. Respiratory system. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals, 6th ed. Elsevier, 2016, vol 2:562-563.

Constable PD, et al. Systemic and multi-organ diseases. In: Veterinary Medicine, 11th ed, vol 2. Elsevier, 2017:2042-2043.

Bovine herpesvirus 4-associated ulcerative mammary dermatitis

Bovine herpesvirus 4-associated ulcerative mammary dermatitis

Josepha DeLay, Kalie Bernardo, Cynthia Miltenburg, Betsy Elsmo

Animal Health Laboratory, University of Guelph, Guelph, ON (DeLay); Tavistock Veterinary Services, Tavistock, ON (Bernardo); Ontario Ministry of Agriculture, Food and Rural Affairs, Guelph, ON (Miltenburg); Wisconsin Veterinary Diagnostic Laboratory, Madison, WI (Elsmo).

AHL Newsletter 2019;23(3):7-8.

Two lactating cows in a 200-cow free-stall Holstein dairy herd developed ulcerative, exudative teat skin lesions that spread over a period of several days to other teats (Fig. 1). Skin biopsies taken at the margin of affected and unaffected skin demonstrated segmentally ulcerated epidermis covered by thick plaques of necrotic cellular debris and clusters of bacterial cocci. Eosinophilic intranuclear inclusions were evident in a few epithelial cells of intact epidermis adjacent to the cutaneous ulcers (Fig. 2).

The intranuclear inclusions were suspicious for viral involvement (specifically herpesviruses), and other histologic lesions indicated secondary bacterial dermatitis. Bovine herpesvirus 2 (BoHV-2), the agent of bovine herpes mammilitis, was the main etiologic differential diagnosis, however the virus was not detected in skin biopsies by PCR. Subsequent PCR testing identified bovine herpesvirus 4 (BoHV-4) nucleic acid in the samples. This virus also produces intranuclear inclusions in infected epithelial and other cells.

BoHV-4 is gammaherpesvirus. The virus has been associated with many disease conditions in cattle including pneumonia, metritis, abortion, and dermatitis, although direct causation of these diseases by the virus has not been confirmed. BoHV-4 has also been associated with ulcerative dermatitis with vasculitis and pyrexia in haired, non-mammary skin of cattle. A potentially synergistic effect of bovine leukemia virus infection with BoHV-4-associated disease has been suggested. Further research is required to confirm BoHV-4 causation of mammary dermatitis and potentially of other diseases in cattle, and to determine the pathogenesis of skin lesions.

The original 2 affected cows were euthanized or culled given the severity and persistence of teat lesions. A third cow in the herd subsequently developed teat lesions that were successfully treated with topical antibiotic preparations targeting presumed secondary bacterial dermatitis. Other measures were also taken to reduce any potential effects of teat trauma, including proper milking machine function.   AHL

Ulcerative, exudative skin lesions involving multiple teats.

Figure 1. Ulcerative, exudative skin lesions involving multiple teats.

Intact epithelial cells with eosinophilic intranuclear inclusion bodies and peripheralized nuclear chromatin (arrows) in teat epidermis adjacent to ulcer.

Figure 2. Intact epithelial cells with eosinophilic intranuclear inclusion bodies and peripheralized nuclear chromatin (arrows) in teat epidermis adjacent to ulcer.


Bellino C et al. Potential pathogenic role of bovine herpesivurs 4 in two dairy cows with dermatitis-pyrexia-hemorrhagic syndrome. J Clin Microbiol 2015;53:2763-2767.

Lyman D. BHV-4 contributes to udder lesions. Bovine Vet. January 2019

Acute nitrate toxicosis in Holstein heifers

Acute nitrate toxicosis in Holstein heifers

Margaret Stalker, Clark Sinclair, Felipe Reggeti, Nick Schrier, Kalie Bernardo

Animal Health Laboratory, University of Guelph, Guelph, ON (Stalker, Reggeti, Schrier); Tavistock Veterinarians, Tavistock, ON (Sinclair, Bernardo).

AHL Newsletter 2019;23(3):9.

Three 12-15 mo-old Holstein heifers were found dead overnight in 2 adjacent pens in a freestall barn. A recent feed change to sorghum silage had occurred one week ago, and 60 heifers were being fed the silage as the main source of roughage along with a small amount of corn and access to a protein lick tank. Feed intake was considered normal. No clinical signs were observed the previous evening. The animals were found dead in lateral recumbency in the morning. One heifer was sent to the AHL for postmortem examination. The animal was in good body condition, oral mucous membranes were slightly pale, and ocular mucous membranes were slightly dusky. No significant gross abnormalities were found on postmortem examination. The rumen was full of silage, with a small gas cap, and rumen pH was 6.5-7.0. Based on the history of multiple animals affected following a recent feed change to sorghum silage, the silage was removed and replaced with corn silage. A silage sample, as well as postmortem ocular fluid from the heifer, was submitted to the AHL Toxicology laboratory for nitrate analysis.

The sorghum silage nitrate analysis was 40,000 mg/kg dry weight (40,000 ppm or 4%). In general, feed with <5,000 ppm nitrate is considered safe to feed under all conditions, 5,000-9,999 ppm is considered safe for non-pregnant animals but should be limited to 50% of the ration for bred cows, 10,000-17,000 ppm should be limited to 35-40% of the total dry matter in the ration and should not be fed to pregnant animals; feeds >17,000 ppm nitrate are considered to be toxic and should not be fed to cattle.1 Ocular fluid nitrate analysis was 52 mg/l. Nitrate values in excess of 10 ppm are suspicious for, and in excess of 20 ppm are considered indicative of toxicity2.

Fast-growing forage crops such as sorghum may accumulate toxic levels of nitrates under stressful growing conditions, for example periods of dry weather followed by a rain, or after heavy applications of nitrogen fertilizers. Although ensiling can reduce nitrate levels by 25-65%, the crop must be at the correct moisture level for proper fermentation to occur. Baleage is generally too dry to ferment completely, and nitrate levels are stable in dry hay.3

Nitrates in forage are reduced to nitrite in the rumen, then quickly converted by rumen bacteria to ammonia, which is absorbed and excreted into urine. High levels of nitrate ingestion and subsequent nitrite production overwhelm conversion to ammonia, and nitrite is absorbed directly, oxidizing hemoglobin to methemoglobin (MHb) which is incapable of oxygen transport. Clinical signs of hypoxia can be subtle, and include increased respiratory rate, apprehension, weakness, depression and recumbency. Pregnant animals may abort. If MHb reaches 75-80%, animals begin to die. If the accumulation is not lethal, MHb is slowly reduced back to Hb over a 12-24 hour period. At autopsy, few distinctive lesions are evident. Blood and tissues may be dark or “chocolate brown” colored, but this is not a consistent feature. Forage testing of composite samples is the only method to evaluate risk for nitrate toxicosis, prior to feeding.   AHL


1. Niles G. As livestock producers dip into low-quality forages, beware nitrate. Colorado State University VDL

2. Burrows and Tyrl. Toxic Plants of North America, 2nd ed. Wiley-Blackwell, 2013.

3. Crop Report – August 1, 2019, OMAFRA Field Crop News .