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CASE NOTES


OUTBREAK OF HISTOPHILOSIS IN INTRODUCED WEANER CATTLE

Judy Ellem, District Veterinarian, North West Local Land Services, Gunnedah, NSW
Thomas Westermann, Pathology Resident, Elizabeth MacArthur Agricultural Institute, NSW

INTRODUCTION

This case demonstrates a multifactorial disease outbreak of Bovine Respiratory Disease Complex (BRDC) with septicaemic spread of Histophilus somni. Affected animals had immature or compromised immune systems associated with stress due to change of environment, time off feed, transport and commingling, and circulating pathogens. A producer from the Gunnedah region introduced 125 weaner cattle purchased from four different saleyards with multiple PIC origins during April and May 2017. The first sign of a problem was a phone call from a neighbour notifying dead cattle in their paddock next door. Seven steers at varying stages of decomposition were found dead across the paddock. This event occurred three weeks after the weaner steers were introduced.

CASE REPORT

Day 1

The owner initially called a private practitioner who then referred the investigation into multiple deaths to the District Veterinarian. A range of samples were collected, and anthrax, lead toxicity and nitrate poisoning were excluded. One steer was observed to be out on its own, head down and drooling. 

Day 2

The introduced cattle had received a clostridial 5-in-1 vaccination on arrival; a second dose was given on Day 2. Two steers were noted to be unwell, including the steer observed the previous day. They were both pyrexic (40°C), hypersalivating and had bilateral, clear, nasal discharge. The second steer was also tachypnoeic and tachycardic with audible respiratory sounds. Treatment was undertaken in consultation with their private practitioner; oxytetracycline (20mg/Kg IM; Engemycin 100, MSD Animal Health) and tolfenamic acid (1ml/20Kg IM; Tolfedine CS injection, Vetoquinol). 

Day 3

A third steer was observed to be down on Day 3 and reluctant to get up. On examination the steer got up and walked to the yards with a stiff, short stepping hindlimb gait. He was pyrexic (41.2°C), tachypnoeic, depressed, head down and slow to respond to stimuli. He was also treated as above but died overnight. 

Day 4

A post mortem of steer 3 was performed on Day 4 by their private practitioner. Histophilus somni was cultured from both the lung and brain, despite antibiotic treatment and samples being held over the weekend. Consistent with this result was the histopathologic finding of a moderate cerebral vasculitis with intralesional Gram negative bacterial colonies, and mild suppurative encephalitis. In addition, there was evidence of moderate acute bovine pulmonary emphysema and oedema (ABPEE) (syn. atypical interstitial pneumonia, fog fever).

The manager checked the cattle daily with more clinical cases identified the following week. 

Day 6

A fourth steer was found down and treated, only to be found dead the next day.

Day 7

A post mortem was performed on the fourth steer with major findings including fibrinous adhesions within the pericardial sac, multifocal hyperaemia of the meninges, diffusely dark red-purple lungs, mild diffuse hepatomegaly with orange-tan discolouration and a friable consistency, and numerous petechial haemorrhages throughout the carcase. Histopathology confirmed the presence of a suppurative meningoencephalitis and vasculitis, and fibrinonecrotising interstitial pneumonia, with changes typical of ABPEE.

Three clinical cases were identified on Day 7, including a heifer from a mob of 87 in the paddock adjoining the steers. The heifers were introduced the same time as the steers but run as a separate mob. Clinical signs included stiff gaits, pyrexia (40.6°C), tachypnea and tachycardia, mucoid-white or clear nasal discharges, hypersalivation, and raspy lung sounds. One steer had a bilateral ocular discharge and another had raised brown crusty lesions on its dental pad and ulceration of the gingiva. Samples were submitted for exclusion of foot and mouth disease (FMD) and vesicular diseases and were found to be negative.

Day 8

One steer that had been observed ill and treated on Day 2 was recumbent and unable to rise. He had been treated with oxytetracycline (20mg/Kg IM; Engemycin 100, MSD Animal Health) twice in the 6-day course of his illness. The steer was in lateral recumbency, pyrexic (39.9°C), tachypnoeic, tachycardic and had muffled heart sounds. He was also non-responsive to stimuli, and had nystagmus and grazes around the eyes and head.

The steer was euthanised, with major post mortem findings including multifocal coverage of pleural surfaces and pericardium with thick, creamy to fibrinous, pale-yellow material, numerous intrathoracic adhesions, meningeal hyperaemia, petechial haemorrhages in cerebral white matter, endocardium and liver, fibrin strands in lateral ventricles of the brain, and dark red to black abomasal contents. Histopathology identified fibrinosuppurative pleuropneumonia, necrosuppurative myocarditis, suppurative meningoencephalitis with vasculitis and an ulcerative abomasitis.

Day 16 

Owners reported that one further heifer and one steer with clinical signs were treated with oxytetracycline (20mg/Kg IM; Engemycin 100, MSD Animal Health) and tolfenamic acid (1ml/20Kg IM; Tolfedine CS injection, Vetoquinol)

No more cases were identified in these mobs after Day 16.

One month later 

Three heifers from a mob of 50 home-bred and introduced animals were found dead in another paddock. No animals in this group had been observed ill.

One heifer was post-mortemed and major findings included dark purple and consolidated cranioventral lung lobes, dark purple mottling of the caudal lung lobes, an individual laryngeal abscess, white foam in distal trachea and bronchi, fibrinous adhesions on the pleural surface, diffusely reddened abomasal and small intestinal mucosa, and diffuse petechiation of the trachea, lungs, pleura, epicardium, myocardium, endocardium and abomasal and small intestinal mucosa. H. somni was cultured from the lungs. 

A heifer that was first noted ill and treated on day 7, received five repeat treatments oxytetracycline (20mg/Kg IM; Engemycin 100, MSD Animal Health) over the next month. Two weeks after her 5th treatment, owners noted she had an abnormal head carriage with behavioural changes. When yarded, she collapsed in the race. Her neck was outstretched and she had medial strabismus, was tachypnoeic and appeared weak and was unable to raise herself. She was alert and no cranial nerve deficits were detected on examination. She was euthanised and post-mortemed. 

Post mortem findings included massive thickening of the pericardial sac, up to 20 cm in diameter and with numerous scattered fluid-filled spaces, fibrinous adhesions between pericardium and lung, and a moderate volume of dark-yellow, translucent pleural and pericardial fluid. There was also moderate diffuse congestive hepatomegaly which, in association with the fibrinous pericarditis and effusions, is indicative of right and left sided heart failure.

H. somni was cultured from the pericardial sac despite several antibiotic treatments and the chronic nature of the lesions. Sensitivity testing showed that the isolate was susceptible to Ampicillin, Sulphafurazole, Trimethoprim, Tetracyclines, Neomycin and Cefuroxime. 

Other Findings 

Because some animals presented with ulcerations in the buccal cavity and crusty lesions on the muzzle, five animals were tested for pestivirus with four returning an antibody AGID titre >3, and one testing positive to pestivirus antigen capture ELISA. This indicated that pestivirus was active and circulating in the mobs at the time of the outbreak, and that there was at least one persistently infected animal in the group. 

Sporadic bovine encephalomyelitis (SBE) was also considered in this case as some animals had presented with stiff gaits and central nervous system depression consistent with SBE, a disease (occasionally / sometimes / frequently / often?) diagnosed in young cattle in our Gunnedah region. Chlamydia CFT in these animals were either seronegative or yielded low titres, indicating that SBE was not a factor in this case.

One steer, later euthanised, was tested for respiratory viruses and was found negative to PCR for IBR, BRSV and PI3.

Interestingly, one month later there was an episode of sudden death attributed to H. somni infection in another group of heifers, with no subsequent illness or deaths in that group.

DISCUSSION

In its initial stages the speed of this outbreak outpaced our ability to confirm a diagnosis. Monitoring, isolation and early treatment were instigated on suspicion of histophilosis. The cases in the main steer and heifer mobs occurred over a period of 2-3 weeks given that some of the steers found dead could have died up to a week before they were noticed. 

A consistent feature in this case was the isolation of H. somni, both from several different animals and from multiple sites in the same animal. H. somni was cultured despite prior treatment with antibiotics and in one case it was cultured from chronic lesions after the animal had received multiple treatments. Sensitivity testing was requested, as we queried the effectiveness of the antibiotic treatment. The H. somni isolated was still sensitive to tetracycline. 

Although a study of antimicrobial susceptibility of H. somni isolated from clinically affected cattle in Australia6 found that most isolates from cattle in QLD and NSW were susceptible to antimicrobial agents most frequently used to treat BRD, they identified one isolate with resistance to tetracyclines. The authors suggested this highlighted the importance of continued surveillance to detect emerging resistance to antimicrobials.6

Another important feature of this outbreak was the number of different clinical manifestations of Histophilus infection including septicaemia, pneumonia, pleuritis, pericarditis, myocarditis, abomasitis, enteritis and meningoencephalitis. There was acute disease with death, as well as severe, chronic disease that necessitated euthanasia. Others recovered; one of these was later noted to be lame with swollen carpi. Twelve animals were treated and survived. Two were treated and later euthanised. In some cases the course of the disease was so acute that they were found dead and two died within 24 hours despite treatment. In total, 14 animals died. 

Virulence factors enable H. somni to adhere to vascular endothelium, accounting for its propensity to cause multi-organ infection. This adhesion causes activation of platelets and thrombus formation, leading to infarction and necrosis.5,8,9 Lipooligosaccharides produced by the bacteria can induce apoptosis of endothelial cells,7 contributing to the vasculitis observed with H. somni septicaemia.9 

Secretions of immunoglobulin Fc-binding proteins assist H. somni in the evasion of complement-mediated killing mechanisms.7,9 Transferrin-binding proteins allow the bacteria to utilize iron for growth.7,9 The formation of a biofilm, which is an aggregate of bacteria connected by an extracellular matrix, enables the bacteria to colonize and persist at sites. This biofilm formation may contribute to its ability to evade host defence mechanisms and withstand antimicrobial treatment.5,7 H. somni can also impair the phagocytic function of neutrophils and macrophages, destroy macrophages and induce apoptosis of neutrophils, thus increasing its own survival.7,9

Interestingly, other bacteria that also act as opportunistic pathogens in bovine respiratory disease complex (BRDC), such as Mannheimia haemolytica and Pasteurella multocida, were not isolated in any of these cases. 

There were several other suspect or confirmed cases of histophilosis in New South Wales submitted to the Elizabeth Macarthur Agricultural Institute in 2017. Six outbreaks had positive H. somni culture results with consistent histopathology, despite prior antimicrobial therapy in three cases. Additional disease outbreaks had histories, clinical signs, gross findings and histopathology consistent with histophilosis, but did not have fresh material available for culture. These cases were submitted between May and December from properties in various LLS regions, including Northern Tablelands, Central Tablelands, North West, Central West, Riverina and Hunter. Mortalities in each outbreak ranged from 1-23 animals, and all were beef cattle either in feedlots or pasture-based systems, both male and female, and affecting both calves and animals up to 20 months of age. Many outbreaks had histories involving weaning, purchase from saleyards, transportation and/or recent introduction to a feedlot, 3-5 weeks prior. 

In two of the cases in this outbreak there was histopathologic evidence of ABPEE, which is characterised by alveolar oedema and emphysema, necrosis of bronchiolar epithelium and necrosis of type I pneumocytes (required for gas exchange) observed as hyaline membranes lining alveoli, with consequent type II pneumocyte hyperplasia. This disease typically affects only a few animals, occurring 4-14 days following movement of cattle from dry pasture to lush pasture and is associated with metabolism of L-tryptophan to 3-Methylindole (3-MI) by rumen flora, causing cell membrane damage and the aforementioned histopathologic lesions. 

Affected animals will often be tachypnoeic and dyspnoeic, with increased expiratory effort. Grossly, the trachea is filled with foam and lungs are heavy, wet, fail to collapse and have striking interlobular oedema. The two cases of ABPEE in this outbreak occurred two and four days after movement from a paddock of dry, seeded grasses, predominantly liver grass, to green ryegrass. It is likely that both ABPEE and histophilosis contributed to mortality. The two diseases may have occurred independently or APBEE may have predisposed to the development of, or exacerbated pre-existing, histophilosis. 

ABPEE is one of several forms of interstitial lung disease. A very similar syndrome occurring in feedlot cattle, acute interstitial lung disease (AILD), presents with the same clinical signs and causes similar gross and histopathological changes. The pathogenesis of AILD is unknown, with suspect causes including 3-MI, melengestrol acetate, dusty and hot conditions, and concurrent bacterial or viral infections, such as BRSV. Some other causes of interstitial lung disease in cattle include, but are not limited to, Dictyocaulus viviparus, anaphylaxis and other form of toxic lung injury, including various plants, such as stinkwood (Zieria arborescens), and chemicals, such as Paraquat herbicide.1,9

The importance of effective biosecurity management and regular monitoring of livestock that have been recently introduced is a lesson from this case. Once the owner instigated daily monitoring of the cattle, they were able to identify, treat, manage and isolate affected animals.

Previous Flock and Herd articles2,3 discuss risk factors involved in grass-fed cattle cases. This case has similar risk factors.

PCR testing of one actively infected steer was negative for IBR, PI3 and BRSV. Testing of the group, either by pooled PCR or paired serum sampling to test for a rise in antibody titres, would have been useful in assessing exposure to these respiratory viruses. 

Histophilus is considered an opportunistic pathogen and environmental stress contributes to the development of clinical disease.1 This case is an example of what can happen with a combination of risk factors and concurrent diseases in young cattle being introduced by producers to rebuild their herds.

ACKNOWLEDGEMENTS

Dr. Pedro Pinczowski, Pathologist, Coordinator of Biosecurity (Elizabeth MacArthur Agricultural Institute), NSW

REFERENCES

  1. TJ Parkinson, JJ Vermunt and J Malmo.  The Histophilus somni disease complex Diseases of Cattle in Australasia A Comprehensive Textbook 2011; p189-190, p207-208
  2. Libby Read and Shaun Slattery, North West LHPA, Narrabri. Bovine Histophilosis Cases in the North West LHPA  Flock & Herd Case Notes March 2011
  3. Bill Johnson, Tablelands LHPA, Goulburn. Investigating Risk Factors For Two Histophilosis Outbreaks in Grass-Fed Cattle Flock & Herd Case Notes April 2013
  4. Phillip Kemsley, Casino. Histophilus in Feeder Cattle Flock & Herd Case Notes March 2012
  5. Eugene D Janzen, DVM, MVS, Professor, Production Animal Health, Faculty of Veterinary Medicine, University of Calgary. Overview of Histophilosis MSD Veterinary Manual www.msdvetmanual.com
  6. Lauren K Goldspink, Joanne L Mollinger, Tamsin S Barnes, Mitchell Groves, Timothy J Mahoney, Justine S Gibson.  Antimicrobial susceptibility of Histophilus somni isolated from clinically affected cattle in Australia. The Veterinary Journal 203 (2015) 239-243
  7. Gerard M Murray, Ronan G O’Neill, Simon J More, Maire C McElry, Bernadette Earley, Joseph P Cassidy. Evolving views on bovine respiratory disease: An appraisal of selected key pathogens – Part 1.The Veterinary Journal 217 (2016) 95-102
  8. M Donald McGavin, James F Zachary. Pathologic Basis of Veterinary Disease, Fourth Edition pp 525-529; 880-881
  9. J Caswell & K Williams. Respiratory system. In: Maxie MG, ed. Jubb, Kennedy and Palmer’s Pathology of Domestic Animals. Vol 2. 6th ed. Philadelphia, PA: Elsevier Saunders; 2016: Vol 1. pp 408-411, Vol 2. pp 513-520, 602
  10. KE Hay, TS Barnes, JM Morton, ACA Clements, TJ Mahoney. Risk Factors for bovine respiratory disease in Australian feedlot cattle: Use of a causal diagram-informed approach to estimate effects of animal mixing and movements before feedlot entry. Preventative Veterinary Medicine 117(2014) 160-169
  11. KE Hay, RCK Ambrose, JM Morton, PF Horwood, JL Gravel, S Waldron, MA Commins, EV Fowler, ACA Clements, TS Barnes, TJ Mahoney. Effects of exposure to Bovine viral diarrhoea virus 1 on risk of bovine respiratory disease in Australian feedlot cattle. Preventative Veterinary Medicine 126 (2016) 159-169
  12. KE Hay, TS Barnes, JM Morten, JL Gravel, MA Commins, PF Horwood, RC Ambrose, ACA Clements, TJ Mahoney. Associations between exposure to viruses and bovine respiratory disease in Australian feedlot cattle. Preventative Veterinary Medicine 127(2016) 121-133

 


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