Chapter 12 Infectious diseases

Bovine leukosis (bovine viral leukosis, bovine lymphosarcoma) 242

Calfhood multicentric lymphosarcoma 242

Enzootic (adult) bovine leukosis (EBL), bovine lymphosarcoma 244

Introduction

Infectious diseases are a major limiting factor in cattle production in many parts of the world. In tropical Africa, with its 160 million cattle, the major diseases, i.e., rinderpest, foot-and-mouth disease (FMD), contagious bovine pleuropneumonia, theileriosis, and trypanosomiasis, are all infectious. Such limitations on livestock production lead to shortages of meat, milk, draught animals, and manure, and to the necessity to import from developed countries such as North America and Australia, and the European Union. These imports in turn discourage domestic livestock production, whilst the presence of infectious diseases bars the export of cattle and cattle products to developed countries.

Several infectious diseases have been covered and illustrated in earlier chapters.

Viral diseases

Several major bovine diseases, endemic in many parts of the world, have a viral etiology. They are characterized by their highly contagious nature and the variety of their cloven-footed hosts. Early recognition of suspicious signs and confirmation of the disease in the laboratory, together with prompt and effective control measures, are essential for their eradication.

Foot-and-mouth disease (FMD)

Definition

a highly infectious disease with a short incubation period caused by aphthovirus of the family Picornaviridae with seven serotypes. A transboundary disease of the OIE.

cattle infected with foot-and-mouth disease are dull, off feed, and drool saliva (12.1). Some are lame. On opening the mouth (12.2), large areas of epithelial loss, that are the result of recently ruptured FMD vesicles, are seen on the tongue and hard palate, as in this animal from Zimbabwe. 12.3 also shows recently ruptured tongue vesicles. An unruptured vesicle on the dorsum of the tongue is seen in 12.4.

12.1 FMD drooling

12.2 Foot-and-mouth disease (FMD): extensive loss of epithelium from tongue and gum (Zimbabwe)

12.3 FMD: ruptured vesicles

12.4 FMD: unruptured tongue vesicle (approx. 24 hours)

In a steer infected experimentally, within 2 days initial vesicles have ruptured to reveal ulcers which are seen along the lower gums and inside the lower lip, together with ruptured tongue vesicles (12.5). Two days later the lesions on the tongue, lower lip, and gums have become secondarily infected (12.6). Elsewhere a vesicle on the coronary band and dorsal part of the interdigital space has ruptured. On the seventh day (12.7) the interdigital space shows widespread ulceration along its entire length. A vesicle on the soft skin above the heel has ruptured in another cow (12.8). Lameness may be the first sign of FMD. These interdigital lesions easily become secondarily infected. Multiple teat vesicles are shown in 11.28 (p. 211).

12.5 FMD: ulcers on gums, inside lower lip and tongue (approx. 2 days)

12.6 FMD: secondary infection of oral ulcers (approx. 4 days)

12.7 FMD: interdigital space with widespread ulceration (approx. 7 days)

12.8 FMD: ruptured skin vesicle above heel

Differential diagnosis

includes vesicular stomatitis (4.11), BVD/MD (4.3), bovine papular stomatitis (4.13, 4.14), rinderpest (12.13), digital dermatitis (7.57–7.60), interdigital dermatitis (7.65).

Management

slaughter policy in FMD-free countries, and elsewhere isolation, quarantine, and ring vaccination where disease is endemic.

Rinderpest (“cattle plague”)

Definition

infectious disease caused by a Morbillivirus having variable virulence and a wide ungulate host range.

Clinical features

virgin-soil epizootics (12.9), here in Nigeria, fulminate rapidly and frequently escalate into panzootics, whereas enzootic rinderpest spreads slowly, even inapparently, for months in immature and young adult stock free of maternally-derived antibodies.

12.9 Rinderpest (“cattle plague”): appearance of epizootic (Nigeria)

Clinical diagnosis in fresh epizootics is relatively easy: after a prodromal onset of fever, illness is evident in 48 hours. Affected animals are restless and have dry muzzles and staring coats. Milk yields fall, respirations are shallow and rapid, visible mucous membranes are congested, whilst tears (12.10) and nasal fluids (12.11) flow profusely. The appetite is impaired and constipation develops.

12.10 Rinderpest: affected eye in epizootic outbreak

12.11 Rinderpest: nose with foul discharge in epizootic outbreak

The emergence of mucosal erosions 2–5 days later is the first sign suggestive of rinderpest: raised pinheads of necrotic epithelium reminiscent of oatmeal coat all visible mucous membranes, for example tongue and lips (12.12). They are readily abraded to reveal shallow erosions with a hemorrhagic layer of intact basal cells (12.13). The erosions enlarge and coalesce throughout the alimentary tract from the mouth and esophagus (12.14) to the rectum. Salivation is profuse. The affected cattle are now obviously sick, drink excessively, and pass soft feces. In 2–3 days the fever regresses and diarrhea starts. The brown, fluid feces contain necrotic debris streaked with blood. Dehydration is rapid and the frequent straining reveals the capillary stasis in the rectum known as zebra stripes (12.15). Breathing is labored and painful. Most cattle die within 6–12 days of the onset of overt illness. Pregnant cows abort during convalescence that lasts for months. In contrast, enzootic rinderpest is difficult to diagnose clinically. Adult cows are immune and passively immunize their sucking progeny, protecting them for up to 9 months; thereafter they are at risk. The clinical signs are muted, and often one or more of the cardinal features of the classic epizootic syndrome such as fever, erosions, mucopurulent nasal and ocular discharges, and diarrhea are absent. Most affected animals survive and suspicions of rinderpest are not roused. The illustrations are from Saudi Arabia, Yemen, and Nigeria.

12.12 Rinderpest: raised pinheads of necrotic epithelium (“oatmeal”) on tongue and lips

12.13 Rinderpest: abraded erosive lesions on dental pad, tongue, and gum

12.14 Rinderpest: extensive erosion in esophagus

12.15 Rinderpest: capillary stasis in rectum (“zebra stripes”)

Differential diagnosis

lesions are indistinguishable from those in BVD (4.3). Other similar diseases are FMD (12.1–12.8), IBR (5.2), and malignant catarrhal fever (12.20–12.22).

Management

the incidence of rinderpest has declined spectacularly following massive international vaccination campaigns financed by Europe and the USA, and organized in Africa and Asia by the Food and Agricultural Organization of the United Nations (FAO) and the Office International des Épizooties (OIE). Today, rinderpest has been eradicated from the whole world, apart from a residual focus in southern Somalia, where serosurveillance and vaccination are difficult, due to the lawless state of the country. Previously infected countries are actively following OIE regulations (it is a transboundary disease), maintaining eradication of rinderpest. Early recognition and notification of new outbreaks are vital.

while endemic on the African continent, where it is characterized mainly by inapparent infections, bluetongue is sporadic in many other parts of the world, including Eastern Europe and the Mediterranean basin. Spread of BTV to Western European countries (including the UK, the Netherlands, and Germany) occurred in 2007. In North America it is a mild clinical condition and differential diagnosis is difficult. Infection is more common than disease, which presents as a hyperemic, inappetant animal. Bluetongue causes initial hyperemia of the muzzle and lips, followed by inflammatory and erosive lesions. This Dutch Holstein animal (12.16) shows a mucopurulent nasal discharge, hyperemia of the muzzle, and early gum erosions. Necrotic areas may be seen in the gums in a 2-year-old heifer (12.17) where the mucosa behind the incisor teeth has either sloughed or shows white diphtheritic plaques. Note the excessive salivation, a result of discomfort and a reluctance to close the jaws. Changes in the hard palate (12.18) include extensive areas of ulceration which extend onto the dental pad. Some clinical cases of BTV show irregular superficial teat erosions (12.19). Stiffness and laminitis, with distal edema of all limbs, may sometimes be seen. Clinical lesions in cattle are allegedly mediated by an IgE hypersensitivity reaction. Diagnosis is by PCR and AGID assay and by virus isolation.

12.16 Bluetongue: mucopurulent nasal discharge, gum erosions (Netherlands)

12.17 Bluetongue: sloughed oral mucosa (Netherlands)

12.18 Bluetongue: necrosis of hard palate (USA)

12.19 Bluetongue: superficial teat erosions

malignant catarrhal fever causes marked pyrexia, anorexia, and profound depression, with catarrhal and mucopurulent inflammation of the upper respiratory and alimentary epithelia, keratoconjunctivitis following a characteristic initial peripheral keratitis, and lymphadenopathy. Typically, a clinical case has a foul, pungent oral odor. MCF herd outbreaks are seasonal and occur predominantly in Africa. Elsewhere (North America and Europe), only sporadic cases are seen. The “head and eye” syndrome of the Devon cow in 12.20 includes a purulent oculonasal discharge, mild keratitis, and hyperemia of the nostrils. Note the almost pathognomonic hypopyon in the crossbred Charolais suckler cow in 12.21. There is a marked ocular discharge and pus is settling toward the base of the anterior chamber. Iridocyclitis may lead to photophobia. The nasal discharge is, unusually, not particularly severe. Areas of dry necrosis and ulceration are seen on the gums and dental pad of 12.22. Similar changes are commonly seen on the nostrils. Clinical cases in cattle are not infectious, but if they survive they are infected for life and may infect their calves in utero.

12.20 Malignant catarrhal fever (MCF): head and eye syndrome in cow (Devon)

12.21 Malignant catarrhal fever: characteristic hypopyon in cow (Charolais cross)

12.22 Malignant catarrhal fever: dry necrosis and ulceration on gums and dental pad

despite occasional reports of success with cortisone and antibiotics, most cases are best culled as soon as the diagnosis is confirmed. Inactivated wildebeest-associated MCF vaccine is available in some countries. Some Western European countries have recently introduced voluntary vaccination programs. It is a transboundary disease of the OIE.

Lumpy-skin disease (LSD)

Definition

a capripoxvirus disease of cattle first reported in Northern Rhodesia (Zambia) in 1929, now widespread in Africa, including Egypt, with recent spread into the Middle East. LSD affects European breeds of cattle most severely. Biting flies are the main vectors.

Clinical features

initially a fluctuating fever, lacrimation, and inappetance for 2 weeks, during which circumscribed nodules appear in the skin over the whole body (12.23) and mucous membranes of the mouth and respiratory tract, genitalia (orchitis), and conjunctiva. These nodules (12.24) are discrete, firm, raised, and painful, and contain hard gray-yellow material. Regional nodes are enlarged (prescapular in 12.24). Edema of the lower limb is common in severely affected animals. Some nodules resolve rapidly, whilst others become firm necrotic sitfasts (12.23 body and 12.25 head and neck) that heal slowly and drop out, leaving a scar. Secondary infection can lead to suppurating ulcers and abscesses. A few nodules may persist for years. Subclinical cases develop isolated nodules which are often missed.

12.23 Lumpy-skin disease (LSD): multiple skin nodules over trunk

12.24 Lumpy-skin disease: discrete nodules and enlarged prescapular nodules in cow (Jersey)

12.25 Lumpy-skin disease: resolution of some nodules with sitfast on face (Ethiopia)

Mortality rates in endemic areas are 1–3%, but in virgin soil epizootics may approach 100%. In South Africa lumpy-skin disease is the most serious cause of economic loss in cattle, due to prolonged debility, milk loss, infertility in both cows and bulls, abortion, and hide damage.

Differential diagnosis

ulcerative lymphangitis (pseudotuberculosis) (3.48), pseudo-lumpy-skin disease (Allerton herpes virus infection) (12.26, 12.27), dermatophilosis (streptothricosis) (3.42).

12.26 Pseudo-lumpy-skin disease: irregular cutaneous plaques over cheek and neck

12.27 Pseudo-lumpy-skin disease: multiple plagues, some brown and crusty in perineum and on udder skin (Charolais)

Management

good nursing, sulfonamides or antibiotics for secondary infections, use of attenuated virus vaccine (Neethling strain). Slaughter policy of affected and contact cattle, coupled with vaccination of at-risk cattle before likely disease spread into a previously free area or country. It is a transboundary disease of the OIE.

Pseudo-lumpy-skin disease (LSD), (Allerton virus infection)

Definition

one of two bovine herpesvirus-2 syndromes (see also bovine herpes mammillitis, p. 208), pseudo (false)-lumpy-skin disease is characterized by transient moderate fever and exudative cutaneous plaques. Disease occurs primarily in southern Africa, and very occasionally in the USA, Australia, and the UK.

Clinical features

initial fever and mild lymphadenopathy are followed within a few days by emergence of numerous circular or oval superficial cutaneous plaques about 1–2 cm diameter. These are hard, firm, have a red margin, and enlarge to 3–5 cm, becoming umbilicated. The centers are depressed and exude to form brown crusts (12.26). The skin beneath the crusts dies within 2 weeks to reveal smooth new skin, and fresh hair grows within 2 months. Lesions are frequently on the face, neck, back, and perineum (12.27), as in this pedigree Charolais heifer in the UK. Clinical recovery is uncomplicated.

Diagnosis depends on clinical appearance and demonstration of herpesvirus-2 from peripheral lesions (skin scraping or punch biopsy). Biopsy will also reveal eosinophilic intranuclear inclusion bodies.

acute febrile disease of cattle and sheep readily communicable to humans, and caused by a mosquito-borne phlebovirus (Bunyaviridae). Previously confined to Africa, including Egypt (1977–78), a major epidemic (2000) in Saudi Arabia and Yemen resulted in severe cattle losses and numerous human deaths.

Clinical features

calves usually die after a short peracute illness with high fever, severe dyspnea, and terminally lateral recumbency with extended legs and neck. Cows, following a transient fever, icterus, leucopenia, and incoordination, abort and may die. Nonpregnant adults experience a low-grade fever. Epidemics of RVF are linked to wet years in which hatching of larger numbers of infected mosquito eggs occurs (Aedes linneatopennis).

Autopsy changes in calves and fetuses include a spectacular bright orange-yellow and diffusely necrotic liver (12.28), whilst adult cattle show discrete focal necrotic hepatic lesions (12.29). Widespread hemorrhages are evident in the subcutaneous tissues, musculature, and serosa of the intestine (12.30). Diagnosis depends on viral isolation from aborted fetuses or blood. Veterinarians are at particular risk when handling infected tissues.