Mitchell V. Palmer, Carly Kanipe and Paola M. Boggiatto This chapter describes in detail a number of diseases in white-tailed deer (WTD) in the United States. Other chapters describe some of the diseases in detail and the reader should take this into consideration when looking for information about a specific disease entity – see the index for more references, including the formulary in Chapter 34. As a prey species, deer behave in such a manner to avoid predation; consequently, they often do not manifest signs of weakness or vulnerability. This can make recognition of clinical signs difficult, especially in the early stages of disease when behavioural changes may be subtle. Inappetence, separating themselves from others or reluctance to rise or flee when approached can all be signs of ill health. White-tailed deer are subject to many of the same maladies as other deer and domestic ruminants; however, surveys of WTD farmers show that pneumonia and enteritis account for many of the infectious causes of morbidity and mortality. A significant contributor to mortality among farmed WTD is trauma related to handling and restraint. Therefore, it is paramount that producers and veterinarians be familiar with WTD behaviour and trained in proper handling and restraint techniques. White tailed deer are nervous, flighty and more stress-prone than other deer species, such as red deer, elk or fallow deer (Palmer et al. 2017). Decreasing stress through handling system design, handler training, appropriate stocking densities and attention to social hierarchy can mitigate stress-induced illness and injury. Most antibiotic or anti-inflammatory treatments are off-label for use in deer and require a valid veterinarian–client–patient relationship. In the United States, farmed deer are considered a ‘minor species’ by the US Food and Drug Administration. According to the Minor Use Animal Drug Program, the only approved drugs for use in WTD are xylazine (anaesthetic agent) and yohimbine (anaesthesia reversal) (Tell et al. 2023). Bacterial pneumonia is a common cause of morbidity and mortality in farmed WTD (Hattel et al. 2004). Many of the pathogens that cause pneumonia in other ruminants may cause disease in farmed deer, including Mycoplasma spp. (Dyer et al. 2004), Mannheimia haemolytica (Lawrence et al. 2014), Pasteurella spp. and Trueperella pyogenes (Dyer et al. 2004; Palmer et al. 1999). The key to successful treatment is early intervention with antibiotic treatment. The stress of overstocking, handling, transporting and introducing new deer from outside sources, as well as exposure to non-deer ruminants, can increase the risk of disease. Tuberculosis in WTD is caused by the bacterium Mycobacterium bovis, the cause of tuberculosis in cattle and most other mammals. Humans are also susceptible. Deer may become infected through mutual grooming or shared feed. Deer-to-human transmission has been documented and is most commonly seen during field dressing of deer. Superficial cuts on the hands may become infected and cutaneous tuberculosis can result (Wilkins et al. 2003, 2008, 2009). Most deer with tuberculosis show no clinical signs and in a farmed deer setting are identified through testing required for movement, sale or herd certification. However, chronically infected animals may exhibit ill-thrift, weight loss or rough hair coat. Gross findings consist of nodular lesions with a cheesy or abscess-like, gritty appearance in the lymph nodes of the head and/or chest, the lungs or internal surface of the thoracic cavity (Schmitt et al. 1997; Palmer et al. 2000). The medial retropharyngeal lymph nodes are the most common sites for lesions. Unlike cattle, lesions in deer may initially appear as abscesses (Figure 32.1). Figure 32.1 Medial retropharyngeal lymph nodes from Mycobacterium bovis-infected white-tailed deer. Both are representative of lesions associated with bovine tuberculosis. (a) The lesion is composed of whitish caseous material, while (b) is more abscess-like. Source: Mitchell Palmer. Tuberculosis should be on the list of differential diagnoses with any abscess-like lesion in deer. Diagnosis is generally done through tuberculin skin testing by accredited veterinarians. In most countries, tuberculosis is a reportable disease and test-positive animals are generally reported to animal health authorities for official follow-up testing. Although vaccines have been used experimentally (Palmer et al. 2007, 2009, 2014), no vaccine for deer currently exists and antibiotic treatment, although feasible in humans, is generally considered cost-prohibitive in animals. Deer nasal bots have been reported in all areas of the continental United States and Canada (Colwell et al. 2008). Nasal bots are larvae of flies in the genus Cephenemyia and occur in many deer species, including WTD. There are at least five species of Cephenemyia in North America (Colwell et al. 2008). Adult female flies deposit eggs around the nostrils. Larvae migrate up the nasal passages to the posterior pharynx near the base of the tongue and attach to mucosal surfaces. There they feed on blood and mucus. Fully developed larvae move down the nostrils and fall to the ground where they pupate and adult flies emerge. Developing larvae are white; fully developed larvae are yellow-brown and approximately 25–35 mm in length. Recently, it was shown that nasal bots from Chronic Wasting Disease (CWD)-infected deer carry relevant levels of prion infectivity and could be potential vectors of CWD transmission (Soto et al. 2024). Despite their large size, high numbers and location in the posterior pharynx, clinical signs are usually not present and they are generally well tolerated. Occasionally sneezing, snorting or nasal discharge may be noted. Deer less than one year of age are less likely to have nasal bots than adult deer. Diagnosis relies on finding the larvae within the host. Treatment is usually not necessary. An adenovirus has been the cause of sudden death in farmed WTD (Sorden et al. 2000). A similar adenovirus has been the cause of haemorrhagic disease (HD) with high mortality in mule deer (Odocoileus hemionus) and Columbian black-tailed deer (Odocoileus hemionus columbianus; Woods et al. 2018). The disease has been reproduced in WTD experimentally (Woods et al. 2001). The most prominent gross finding is pulmonary oedema. No clinical signs were evident, as most cases were associated with sudden death. Diagnosis is made post-mortem through gross and microscopic tissue evaluation and laboratory testing. Vaccines are not available and treatment has not been attempted. Bovine coronaviruses have been isolated from farmed WTD with diarrhoea and free-ranging WTD and mule deer from Ohio and Wyoming, respectively (Alekseev et al. 2008). However, the most significant coronavirus to infect WTD is the severe acute respiratory disease syndrome coronavirus-2 (SARS-CoV-2). Emerging from China in 2019, SARS-CoV-2 spread through humans widely and evolved rapidly producing many genetic variants (Feng et al. 2023). SARS-CoV-2 infections have been documented in numerous wild, domestic and exotic animal species, such as mink (Munnink et al. 2021), rats (Wang et al. 2022), otters (Padilla-Blanco et al. 2022), ferrets, hamsters (Haagmans et al. 2022), gorillas, cats, dogs, lions, tigers (McAloose et al. 2020) and deer (Hale et al. 2022; Chandler et al. 2021). Most transmission has been from human to animal; however, animal-to-human transmission has been documented in farmed mink (Munnink et al. 2021), domestic cats (Sila et al. 2022), hamsters (Haagmans et al. 2022) and infrequently WTD (Feng et al. 2023; Pickering et al. 2022). Surveys of wild WTD strongly suggest that the virus passes from humans to deer and then spreads between deer (Kuchipudi et al. 2021; Vandegrift et al. 2022a, 2022b; Willgert et al. 2022). Experimental infection studies suggest that transmission from doe to fetus is possible (Cool et al. 2022). Experimental and natural infections with SARS-CoV-2 have shown that gross lesions are unremarkable (Martins et al. 2022; Palmer et al. 2021; Cool et al. 2022). Although WTD are highly susceptible to infection with SARS-CoV-2, they demonstrate no clinical signs (Palmer et al. 2021; Martins et al. 2022; Cool et al. 2022). Infectious virus is shed during the first 5–6 days after infection and the virus is readily transmitted between deer (Martins et al. 2022). Antemortem diagnosis can be made through serological testing, such as virus neutralisation assays or through the detection of virus or viral RNA on nasal or oral swabs. Postmortem diagnosis can be made through the detection of viral RNA by polymerase chain reaction (PCR) or by virus isolation in retropharyngeal lymph nodes. No vaccine is available and treatment is not necessary. Deer acquire the virus from humans (Kuchipudi et al. 2021; Vandegrift et al. 2022a); however, the means of human-to-deer transmission have not been elucidated. The most common lungworms of WTD are Dictyocaulus filaria, Dictyocaulus viviparus, Leptostrongylus alpenae, Muellerius capillaris and Protostrongylus coburni (Prestwood et al. 1971). Of these, D. viviparus is the most common. Transmission is direct with no intermediate host. Low numbers of D. viviparus can be well tolerated (Davidson 1997) but can be a factor in comorbidities and in stressful situations such as malnutrition. The pathology depends on the animal’s immune status, the location of worms in the respiratory tract and the number of infective larvae ingested. Larger numbers of worms may result in bronchopneumonia with fibrinous pleuritis. Bronchioles may be blocked by cellular infiltrate and froth with alveolar collapse. Adult nematodes may be found in airway lumens (Davidson 1997). Clinical signs are those of ill-thrift, anorexia, rough hair coat and weight loss. Increased respiratory rates with increased lung sounds and coughing may be seen, which may be exacerbated by exercise. Diagnosis is based on the presence of clinical signs and faecal analysis using the Baermann technique. Treatment includes the use of common anthelmintics, such as ivermectin, fenbendazole or albendazole. Larval stages of Muellerius may be less responsive to anthelmintics and elevated dosages or more frequent treatment may be necessary. Factors exacerbating lungworm infections include high stocking densities and the presence of other ruminant hosts. Colibacillosis is caused by infection with Escherichia coli, a Gram-negative, rod-shaped, facultative anaerobic bacterium. It is a common causative agent of diarrhoea in neonatal ruminants, including WTD fawns. Escherichia coli colonises the gastrointestinal tract within the first hours of life (Gyles 2010) and while most strains of E. coli are harmless commensals, some strains are capable of causing opportunistic infections. Highly pathogenic E. coli strains can cause intestinal, septicaemic and extraintestinal diseases (Moxley 2022). Strains of E. coli capable of producing disease reside in the lower intestinal tract. In fawns, as with other neonates, the disease is most commonly seen within the first week of life. However, the disease can occur in older fawns, up to one year of age, that are fed inappropriate diets. Lesions are similar to those seen in piglets and calves. The small intestine may contain excess watery fluid and be filled with gas. There may be mild reddening and congestion of the gastrointestinal tract. In cases of septicaemia, fibrinous polyserositis and arthritis may be seen. Clinical signs of colibacillosis can mimic other enteric pathogens. Typically, large amounts of watery or pasty, white-yellow and foul-smelling diarrhoea are present and animals become rapidly dehydrated (Gyles 2010). Additional signs may include lethargy, anorexia, rough coat appearance and cloudy eyes. In severe cases, tremors, hyperesthesia, convulsions, coma and death are possible (Campos Krauer et al. 2020b). Clinical evaluation may also reveal tachycardia, weak pulses and normal to below-normal temperatures. Diagnosis cannot be made solely on clinical presentation, but presumptive diagnosis can be made based on age, history and clinical presentation. Faecal samples can be collected and sent for microbiological analysis; however, as mixed infections are common and as most enteropathogens are also commensals, interpretation may be difficult. Detection of virulence genes from isolated E. coli colonies via PCR is the preferred method for the detection of pathogenic isolates (Moxley 2022). For cases of extraintestinal disease, identification of E. coli from otherwise sterile tissues (i.e. bone marrow, spleen, blood and joints) is diagnostic (Moxley 2022). Identification of affected fawns and early clinical intervention are critical for successful treatment of infected animals. Supportive care, including fluid and electrolyte supplementation to correct dehydration, is important. Fawns should be reared in a warm, clean environment. Additionally, fawns have low energy reserves; therefore, ensuring adequate caloric intake is important. Antimicrobial and anti-inflammatory therapy should be considered depending on the severity of clinical signs. Sick animals should be isolated from healthy ones to prevent disease spread. The best prevention is to ensure fawns have sufficient colostrum during the first 12 hours of life (Gyles 2010). Colostrum can be ingested directly from the doe or can be supplemented in the case of hand-rearing operations. Vaccination of does prior to fawning is helpful. Several commercial products are available, specifically formulated for fawns. Additionally, E. coli antiserum or monoclonal E. coli antibodies can be administered soon after birth (Campos Krauer et al. 2020b). Mycobacterium avium subspecies paratuberculosis (MAP) is a Gram-positive, acid-fast, facultative intracellular bacterium and the causative agent of paratuberculosis, also known as Johne’s disease in wild and domestic ruminants. Johne’s disease is a chronic, irreversible wasting disease. Transmission is via the faecal-oral route, through exposure of naïve animals to faecal material and/or contaminated feed, water and milk (Sweeney 1996). MAP resides within the intestinal tract and is shed in the faeces from both clinical and subclinical animals. It can also be shed in the colostrum and milk of infected animals. The organism targets the small intestine, particularly affecting the jejunum and ileum where it infects the submucosa and mesenteric lymph nodes (Barletta et al. 2022; Mackintosh et al. 2004). The incubation period is prolonged and may be from months to years. Disease progresses slowly, with the formation of granulomatous lesions and destruction of the intestinal lining. The lesions and damage to the intestine result in malabsorption and protein-losing enteropathy, as animals waste away (Spickler 2017). Gross lesions may include poor body condition with loss of body fat. The gastrointestinal tract may include copious amounts of brown-green liquid faeces (Sleeman et al. 2009). The jejunum, ileum and colon may appear thickened and congested. Mesenteric lymph nodes may be enlarged. In cases of subclinical infection, gross lesions may not be seen (Palmer et al. 2019). Infected animals may be subclinical for years following infection while still shedding MAP in the faeces. Clinical signs of the disease include intractable chronic diarrhoea, weight loss and loss of body condition (Palmer et al. 2019). However, compared to other ruminants, disease in deer appears to exhibit a more acute onset and a range of ages affected, from yearlings to mature breeding stock. Antemortem diagnosis can be made through identification of MAP organism, in faeces via faecal stains or PCR. Culture of faecal samples may also be performed, but due to the slow-growing nature of mycobacteria, results may take several weeks to months. Multiple tests are recommended as shedding can be intermittent or animals may not shed at all, especially during the subclinical stages of the disease (Palmer et al. 2023; Spickler 2017). Serological tests are also available and can be useful in cases of presumptive or confirmatory diagnosis of infected animals. Most serological tests require optimisation for cervid antibody detection (Sleeman et al. 2009). Post-mortem samples, such as ileum, ileocecal valve or mesenteric lymph nodes, can be submitted for culture, PCR and histopathological analysis (Carta et al. 2013). However, all currently available diagnostic methods lack sensitivity and specificity, especially during the early stages of the disease (Roller et al. 2020). There is no treatment for MAP infection. While antimicrobial therapy can be used to improve clinical disease and prolong the animal’s life, relapse will occur and treatment is not curative (Spickler 2017). Control of this disease is based on limiting faecal-oral transmission, obtaining replacement animals from MAP-free sources and management strategies to minimise disease transmission within the herd and to offspring. Deer can be infected with group A rotaviruses (Bayne et al. 2021). Like other rotaviruses, these infect the mature cells of the villus tips of the small intestines leading to rupture and sloughing. Villus blunting and atrophy ultimately results in malabsorptive diarrhoea. Most affected animals are less than two weeks of age. Clinical signs are non-specific and are similar to those associated with other enteric pathogens, including severe diarrhoea, dehydration and lethargy. Antemortem diagnosis can be made using PCR, virus isolation, enzyme-linked immunosorbent assay (ELISA) or electron microscopy of faeces. Postmortem diagnosis can be made using histopathologic examination, immunohistochemistry or fluorescent antibody tests. Preferred diagnostic samples vary by lab but include faeces, intestinal contents and fixed or fresh intestinal tissue. Treatment is supportive and with severe diarrhoea attention to fluid replacement is critical. Enterotoxaemia caused by Clostridium perfringens has been occasionally reported as a cause of illness in farmed deer. As with other ruminant species, the two most commonly implicated clostridial strains are types C & D. Neonatal animals less than 10 days of age lack sufficient intestinal proteolytic enzymes and are unable to degrade the α and β toxins associated with C. perfringens type C; however, older animals may still be affected (Bayne et al. 2021). Disease caused by type D commonly follows overconsumption of high-energy diets and affects young, weaned animals; however, all ages may be affected. Reported cases in farmed WTD are rare; however, due to intense management practices and energy-dense diets, clostridial enteritis should remain a differential diagnosis in cases of acute death. Gross lesions are characterised by multifocal to locally extensive oedematous, necro-haemorrhagic enteritis. Animals, which exhibit neurologic signs, may have petechia or focal encephalomalacia present within nervous tissue. The disease course is most commonly peracute, killing animals within just a few hours. Behavioural signs include colic, depression and teeth grinding. Severe, often haemorrhagic diarrhoea may be present; however, death may occur without diarrhoea. Neurologic signs include seizures, opisthotonos and blindness. Antemortem diagnosis is difficult. C. perfringens is ubiquitous in the environment and commonly found in healthy gastrointestinal tracts. Furthermore, clostridial organisms replicate rapidly after death making it difficult to interpret positive culture results. Identification of the epsilon toxin in intestinal contents can be helpful in identifying type D; however, the toxin degrades within several hours of death. Therefore, its absence does not necessarily rule out disease. Due to its short disease course, treatment is frequently unrewarding. Antibiotics against Gram-positive organisms and supportive therapy may be attempted. While it is recommended to administer C & D antitoxin to at-risk, unaffected herd mates, its use in ill animals is of debatable benefit. Prevention is the most important strategy in preventing clostridial disease. Annual vaccination for types C and D should be provided. Twice-yearly vaccination may also be considered for problem herds. In fawns born to unvaccinated dams, C & D antitoxin administered shortly after birth may provide around two weeks of protection. Finally, feed changes should be made slowly to acclimate rumen and gastrointestinal flora. There are thousands of Salmonella serotypes, which can cause enteric disease in deer of all ages. Salmonella is a zoonotic pathogen. Asymptomatic, latent carriers are possible and these animals may shed Salmonella during times of stress (Bayne et al. 2021). Gross lesions are characterised by dilated intestines filled with gas and yellowish ingesta (Robinson et al. 1970). Mesenteric lymph nodes may be enlarged and oedematous. Salmonellosis should be considered in animals less than one week of age that die acutely. Animals older than one week are more likely to show signs of diarrhoea, which may be accompanied by fever, depression, dehydration and rough hair coat. Diarrhoea may contain blood or fibrin and be associated with tenesmus. Complete blood counts performed on affected animals may show either leukocytosis or leukopenia. Experimental studies have demonstrated a rise in monocytes 3–5 days post-infection as the most reliable indicator of active infection (Robinson et al. 1970). Antemortem diagnosis can be made via faecal culture or PCR. Fresh or frozen intestines and mesenteric lymph nodes collected post-mortem may be cultured or tested using PCR. Treatment largely involves supportive care. The use of antimicrobials is debatable but may prevent septicaemia. Antimicrobial use should be guided by culture and sensitivity results as susceptibility patterns vary widely in Salmonella spp. Isolation of new stock for one month with faecal culture should be considered in closed herds. Currently, vaccination is not routinely practised in deer. Lumpy jaw is a significant cause of morbidity and mortality in farmed WTD and can lead to high rates of death among fawns (Haigh et al. 2005; Campos Krauer et al. 2020a). Lumpy jaw represents a bacterial osteomyelitis and overlying cellulitis of soft tissues of the oral cavity. Most often associated with Fusobacterium spp., the causal agent of necrobacillosis, other bacterial agents such as T. pyogenes and Actinomyces bovis may also be involved (Chirino-Trejo et al. 2003). Infection often begins with cuts or punctures within the mouth caused by coarse feed or tooth eruption. Fusobacterium spp. and other oral bacteria then penetrate and colonise the damaged gingiva. The organism does not cross intact epidermal surfaces. Areas of necrosis with fibrinopurulent exudate may be present on the gingiva, tongue, pharynx, periodontal surfaces or buccal surfaces of the cheek. Tooth loss and large defects in bone may occur. Lumpy jaw is usually characterised by firm, swollen jaws or cheeks due to swelling of the jaw and surrounding tissue. Drooling and weight loss may be seen. Diagnosis is based on clinical signs and the presence of regions of necrosis in the oral cavity. Confirmatory diagnosis is made through isolation of causative organism through anaerobic culture. Treatment is most successful when initiated early and involves antimicrobials, including penicillin, florfenicol and oxytetracycline (Chirino-Trejo et al. 2003). Commercial Fusobacterium bacterins for cattle or sheep can be used, but efficacy in deer has not been proven. Management practices such as avoiding the accumulation of faeces in pens, keeping feeding and drinking areas clean, reducing stress by avoiding overcrowding, overhandling and social instability are beneficial. Soil contamination is an important source of infection (Mainar-Jaime et al. 2007). Wet muddy soil with high manure content should be avoided or replaced with limestone. Coccidiosis is caused by infection with a single-celled protozoan parasite. In ruminants, species of the genus Eimeria are responsible for causing disease. In WTD, four different species of coccidia (E. odocoilei, E. virginianus, E. mccordocki and E. madisonensis) have been found to cause disease (Cottingham et al. 2022). Coccidia infect epithelial cells lining the intestinal tract resulting in malabsorption and diarrhoea. Transmission is faecal-oral, with infection occurring through ingestion of sporulated oocysts. Coccidiosis is typically a disease of young animals, 1–2 months of age and up to one year. Infection with one species does not provide cross-protection or immunity against infection with another. Clinical signs of coccidiosis include watery diarrhoea with little or no blood; however, in severe cases, fawns can develop bloody, mucoid diarrhoea, with clots of blood and shreds of epithelium and tenesmus. Severely affected animals can also develop a fever, anorexia, dehydration, loss of body condition and can be fatal (Cottingham et al. 2022). Diagnosis consists of identifying oocysts using faecal flotation methods. Multiple samples should be collected as diarrhoea may precede shedding of oocysts. The number of oocysts present in faecal samples varies and is determined by the size of the ingested inoculum, the replication potential of the species, the stage of infection and the age and health status of the affected animals (Andrews 2022).
Chapter 32
An Overview of Diseases of Farmed White-tailed Deer
Introduction
Respiratory Diseases
Bronchopneumonia
Tuberculosis
Background
Clinical Signs
Pathology
Diagnosis
Treatment/Prevention
Nasal Bots
Background
Clinical Signs
Diagnosis/Treatment/Prevention
Adenovirus
Background
Pathology and Clinical Signs
Diagnosis/Treatment/Prevention
Coronavirus
Background
Pathology
Clinical Signs
Diagnosis/Treatment/Prevention
Lungworm
Background
Pathology
Clinical Signs
Diagnosis
Treatment/Prevention
Gastrointestinal Diseases
Colibacillosis
Background
Pathology
Clinical Signs
Diagnosis
Treatment/Prevention
Mycobacterium avium subspecies paratuberculosis
Background
Pathology
Clinical Signs
Diagnosis
Treatment/Prevention
Rotavirus
Background
Clinical Signs
Diagnosis
Treatment/Prevention
Clostridial Enterotoxaemia
Background
Pathology
Clinical Signs
Diagnosis
Treatment/Prevention
Salmonellosis
Background
Pathology
Clinical Signs
Diagnosis
Treatment/Prevention
Lumpy Jaw
Background
Pathology
Clinical Signs
Diagnosis
Treatment/Prevention
Coccidiosis
Background
Clinical Signs
Diagnosis
Treatment/Prevention
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