Nigel Gillan, District Veterinarian, Mudgee

Posted Flock & Herd June 2018


District Veterinarians often receive reports of neurological disease in livestock. Investigation of these cases is necessary because of the possibility of notifiable/exotic diseases, or those with food safety implications. Examples include lead toxicity or, in older animals, transmissible spongiform encephalopathies (scrapie in sheep and ‘mad cow disease’ in cattle). Other possible causes of neurological disease in livestock include metabolic disorders (e.g. hypomagnesaemia, pregnancy toxaemia), toxicities (e.g. nitrate/nitrite poisoning), or infectious disease (e.g. listeriosis, bacterial meningitis). Histophilus somni is a commensal organism of bovine mucous membranes which has the potential to cause a range of diseases, including meningoencephalitis. In this case, meningoencephalitis due to H somni was found to be the cause of neurological disease in a mob of weaner cattle.



In late May 2017 a beef producer near Mudgee, NSW observed a recently weaned heifer with a slow, stiff gait. Two days later, a second animal was seen with an unsteady gait and, when recumbent, reluctant to rise. The following day, this animal was recumbent and did not rise, and mentation was markedly depressed. Clinical signs in the animal originally observed with a stiff gait were unchanged. The owner consulted a private veterinarian, and both animals were treated with oxytetracycline (20mg/kg SC; Bivatop 200; Boehringer Ingelheim) and meloxicam (0.5mg/kg SC; Metacam 20mg/mL; Boehringer Ingelheim).

The following morning the recumbent animal was found dead, while the animal with a stiff gait had improved slightly. The District Veterinarian attended the property on this morning.

These animals were from a herd consisting of 28 cows, 13 joined heifers, and 28 weaners (born July/August 2016). The herd was grazing mixed pasture with no supplementary feed. 

The weaners had been yard weaned for 13 days (fed oaten hay and calf pellets) then held in a separate paddock for a further 10 days. Following this period of separation (23 days in total) the weaners were returned to the main herd. The two cases occurred around 10 days after this introduction.

Clinical Exam

The heifer originally observed with a slow, stiff gait was examined briefly in the yards. The gait appeared only very mildly ataxic – consistent with the owner’s assessment of general improvement following treatment with oxytetracycline and meloxicam.

Necropsy Findings

The second animal, which had been found dead, was necropsied. Mild, patchy areas of petechial haemorrhage were present throughout subcutaneous tissues and muscle. Moderate, petechial epicardial haemorrhages were also present. Multifocal, circular, 3-10mm red lesions were visible on the surface of the cerebrum (Figure 1). These lesions had a relatively well-demarcated but slightly ‘fuzzy’ border, and extended 5-10mm below the cerebral surface into deeper cerebral tissue (Figure 2). In deeper tissues the lesions were dark red and friable (Figure 3).

Aqueous humour, fresh kidney, a swab from one of the cerebral lesions (in AMIES transport media), and a range of formalin-fixed tissues (including the entire brain) were collected for laboratory testing.

Multifocal lesions on cerebral surface
Figure 1: Multifocal, circular red lesions on the cerebral surface.
Lesions on cerebral surface
Figure 2: One of the larger cerebral lesions, showing the slightly ‘fuzzy’ appearance of the lesion’s border.
Cut surface of lesion
Figure 3: Cut surface of a cerebral lesion, showing the dark red, friable appearance.

Laboratory Testing

Analysis of aqueous humour revealed levels within normal ranges (Table 1):

Table 1: Aqueous humour analysis
Test Result Normal range
Urea 6.7 mmol/L 2.1-10.7 mmol/L
Glucose 0.0 mmol/L <4.2 mmol/L
BHB 0.12 mmol/L 0.00-0.80 mmol/L
Calcium 1.30 mmol/L 1.00-2.40 mmol/L
Magnesium 1.03 mmol/L 0.48-1.50 mmol/L
Nitrate <10 mg/L <10 mg/L
Nitrite <1 mg/L <1 mgl/L

Two sections of brain tissue were examined histologically, revealing severe, multifocal, necrosupparative and haemorrhagic meningoencephalitis.

Histophilus somni was isolated from a routine bacterial culture of the cerebral swab.

Lead toxicity was considered an important differential diagnosis in this case. Lead testing was not performed on the fresh kidney sample because an alternate diagnosis could be established.


H somni is a gram-negative coccobacillus, and is considered a commensal of bovine mucous membranes. Pathogenic and non-pathogenic strains may be shed in nasal or urogenital secretions, and it is thought that inhalational exposure can lead to colonisation of the respiratory tract and subsequent haematogenous spread (Janzen, n.d.).

When infection of cattle with H somni was first described in 1956, thromboembolic meningoencephalitis (TEME) was the most common form (Radostits et al, 2000). Since then, however, a range of other clinical forms have been described, including septicaemia, polysynovitis, pleuritis, suppurative bronchopneumonia, myocarditis, otitis media, mastitis, and reproductive tract diseases (Radostits et al, 2000). In an Australian context, it has been suggested that Bovine Respiratory Disease (in feedlot cattle or post-transport) is the most common manifestation of the H somni disease complex, but that there may be an increasing prevalence of other presentations of the disease (Read and Slattery, 2011).

The histological findings in this case were consistent with the neurological form of the Histophilus somni disease complex. This aetiology was confirmed by bacterial culture. 

Previous antimicrobial treatment can prevent recovery of the organism (Janzen, n.d.), but, in this case, H somni was cultured in spite of the fact that the animal had been treated with oxytetracycline the day prior to death. Around the time of this case, staff at the State Veterinary Diagnostic Laboratory reported several cases of disease due to H somni in which a positive culture was obtained despite recent antimicrobial therapy (T Westermann, pers. comm.). For this reason, attempting culture in suspect cases should not necessarily be ruled out on the basis of recent antimicrobial treatment.

There are several historical and clinical features of this case which are consistent with typical reports of the disease. Recently weaned calves (the age group affected in this case) are known to be at a higher risk of illness and death due to H somni (Janzen, n.d.). Clinically, the marked depression and the low morbidity/high mortality are consistent with other reported cases of TEME (Janzen, n.d.; Perez et al, 2010). 

The fact that disease occurred in extensively grazed animals is not typical of the H somni disease complex, which is more commonly reported in feedlot animals (Perez et al, 2010). However, TEME has previously been described in grazing cattle (Perez et al, 2010).

It is possible that the mixing of recently weaned cattle with a mob of older animals contributed to the development of disease in this case. Older animals may have been more likely to be carriers of the organism, while the younger stock may have been unexposed, and also immunocompromised following the recent stress of weaning. It is possible that other diseases (e.g. common viral agents such as BVDV) also contributed to an immunocompromised state, but serology to determine herd exposure was not performed in this case. It was suggested to the owner that focussing on low-stress weaning and avoiding mixing recently weaned animals with older cattle might reduce the risk of disease occurring. However, it is difficult to predict the likelihood of cases in future years, since animal husbandry in this herd was already of a high standard.

In this case, the owner administered oxytetracycline and meloxicam to the ataxic heifer five days after the initial dose, and stiffness continued to improve. No further suspect cases were observed.


Particular thanks to the owner for generously providing a detailed history and management notes, and to Tom Westermann (Elizabeth Macarthur Agricultural Institute) for comments on H somni culture and diagnosis.


  1. Janzen ED (n.d.) Overview of Histophilosis, accessed 20/11/17,
  2. Perez DS, Perez FA, Bretschneider G (2010) ‘Histophilus somni: pathogenicity in cattle. An update’, Anales de Veterinaria de Murcia, Vol. 26, pp. 5-21
  3. Radostits OM, Gay CC, Blood DC, Hinchcliff KW (2000) Veterinary Medicine: A Textbook of the Diseases of Cattle, Sheep, Pigs, Goats and Horses. 9th Edition, WB Saunders, London
  4. Read L, Slattery S (2011) Bovine Histophilus Cases in the North West LHPA, accessed 8/1/18,


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