Dermoid

Dermoids occur principally in cattle, but they can occur in other food animal species as well (Figure 16.9). The defect in Herefords is genetically transferred, with characteristics of autosomal recessive and polygenic inheritance. In cattle, the site predilection of ocular dermoids is, in decreasing order, the limbus, third eyelid, canthi, eyelid, and conjunctiva. Dermoids rarely appear bilaterally, except in certain lines of Hereford cattle. The clinical manifestation varies from an unsightly blemish to various degrees of visual impairment, keratoconjunctivitis with epiphora, blepharospasm, and corneal ulceration. Surgical removal is recommended if vision is impaired or the eye is painful.

Congenital Porphyria and Protoporphyria

Inherited defects of porphyrin metabolism in cattle and swine are characterized by excessive deposition of porphyrin isomers in the tissues. Congenital porphyria is similar to Gunther’s porphyria in humans and is inherited as an autosomal recessive trait. The incidence is higher in females than in males, but the disease is rare. Even so, it has been recorded in Shorthorn, Holstein, Black and White Danish, Jamaica Red and Black cattle, and Ayrshires. Congenital erythropoietic porphyria in cattle is caused by an inherited deficiency of the enzyme uroporphyrinogen III synthase. Insufficient activity of this enzyme leads to the formation of the metabolites uroporphyrinogen I and coproporphyrinogen I. These porphyrinogens are oxidized to their end products uroporphyrin I and coproporphyrin I, which accumulate in the body. These high levels of porphyrins sensitize the skin and eyes to light.

Protoporphyria is a less common, milder disease than porphyria and is thought to be inherited in cattle. In this disease, there is deficient activity of the enzyme ferrochelatase, resulting in excessive synthesis of protoporphyrin. Ocular clinical signs related to abnormal porphyrin metabolism result from photosensitization. These signs include photophobia, edema, inflammation, and necrosis of the eyelids and the periocular skin. Treatment consists of maintaining affected animals indoors.

Thelazia Species

In North America and Europe, Thelazia spp. are regarded as being nonpathogenic to mildly pathogenic. In contrast, more severe disease, and even blindness, has been reported in other countries. The variability in pathogenicity may result from host, parasite, livestock management, and climatic factors.

Thelazia spp. nematodes are small, slender, white worms that occur in the conjunctival sac and nasolacrimal ducts, and move rapidly in the preocular tear film. Thelazia rhodesi, Thelazia gulosa, Thelazia skrjabini, and Thelazia lacrymalis affect cattle. The worms are more abundant in beef than in dairy breeds.

Unilateral chronic follicular or mucoid conjunctivitis is most common, with irregularities in the lining of the nictitans gland ducts. Other clinical signs include profuse epiphora, photophobia, and ulcerative keratitis. Face flies, especially Musca autumnalis, act as biological vectors and transfer the larvae to the eyes while feeding. Hence, cases are more prevalent in the summer and fall months. The prevalence is lower among cattle grazing short and mid‐size grass pastures than among those grazing transitional or aspen parkland pastures, rough fescue, or woodland‐type pastures. The diagnosis is usually made postmortem by identification of the parasite in the conjunctival sac or nasolacrimal duct. Antemortem diagnosis can be made by careful gross examination of the whole lacrimal apparatus or by demonstration of fully embryonated eggs, larvae, or immature worms using specialized techniques. Often, the clinical diagnosis is made when the eye is being manipulated for unrelated diagnostic or surgical procedures. Treatment includes simple lavage, mechanical removal after topical anesthesia, administration of levamisole (5 mg/kg orally or 1% solution topically) or fenbendazole, and topical administration of ivermectin or echothiophate iodide. Subcutaneous ivermectin (0.2 mg/kg) and doramectin as well as pour‐on ivermectin have been reported to be effective treatments.

Keratomycosis

Fungal infection of the bovine cornea is quite uncommon. A confirmed case of Aspergillus and Fusarium keratitis was reported in a five‐year‐old Holstein cow. Clinical signs included ocular discharge, periorbital swelling, an area of full‐thickness corneal cellular infiltrate, fibrin, hypopyon, diffuse corneal edema, and miosis. The patient was diagnosed with a corneal stromal abscess and secondary anterior uveitis. Response to standard topical antifungal therapy and supportive therapy for uveitis was good.

Infectious Bovine Rhinotracheitis

Infectious bovine rhinotracheitis (IBR) may cause nonulcerative keratoconjunctivitis. Conjunctivitis is the most common manifestation of IBR and is characterized by raised, white plaques on the bulbar and palpebral conjunctival surfaces (Figure 16.10). Chemosis is also often present. Variable degrees of nonulcerative keratitis can also develop with peripheral edema and vascularization initially. In severe cases, the corneal edema and cellular infiltrate can be quite extensive, resulting in blindness (Figure 16.11).

Listerial Keratoconjunctivitis

The etiological agent is the rod‐shaped, Gram‐positive bacteria Listeria monocytogenes. This condition is also known as silage eye, since the etiological agent is usually found in fermented hay silage. Ocular lesions are frequently observed in the meningoencephalitic form of the disease (also called listeriosis of the central nervous system [CNS]). Neurological signs include vestibular ataxia and unilateral cranial deficits, with reports of facial nerve paralysis and keratoconjunctivitis sicca. Lesions may be located unilaterally or bilaterally, but unilateral presentation is most common. Ocular surface signs include conjunctivitis with excessive lacrimation and photophobia. Keratitis is manifested by punctate abscesses, peripheral clouding (corneal edema), ulceration, and corneal vascularization. Uveitis is also a classic manifestation of this condition with the presence of infiltrative uveal disease, hypopyon, and miosis.

Chlamydial Keratoconjunctivitis

Chlamydiae have been isolated from cattle with conjunctivitis. Incidents of recurrent bilateral keratoconjunctivitis have been reported in different cattle herds. The cases were quite persistent and responded poorly to antibiotic treatment. Chlamydophila spp. DNA was detected in conjunctival swabs by PCR. No other pathogens were detected. Two herdsmen also developed concurrent eye disease, suggesting a possible zoonotic risk.

Malignant Catarrhal Fever

Malignant catarrhal fever (MCF) is a frequently fatal infectious disease that affects cattle, bison, buffalo, deer, and other ruminants. It is caused by several rhabdoviruses belonging to the gamma herpes family. In cattle, it is often transmitted by ovine herpesvirus‐2. Cattle usually do not spread the virus by contact transmission and are considered dead‐end hosts. The “head and eye” form is considered the classical form of the disease, and is accompanied by high fever, inappetence, depression, lesions of the oral cavity and muzzle, profuse mucopurulent nasal discharge, dyspnea, stertor, and diarrhea. The most common ocular sign is corneal edema, which can vary from mild perilimbal to dense complete corneal edema. Other ocular symptoms include exophthalmos, blindness, nystagmus, photophobia, lacrimation and mucopurulent ocular discharge, eyelid edema, and other symptoms of conjunctivitis, keratitis, and anterior uveitis. The degree of corneal edema on first examination does not correlate with prognosis; however, cases that exhibit improvement of the corneal edema may have a better prognosis. Deterioration of uveitis is associated with a poor prognosis; however, improvement of uveitis is not associated with a better prognosis.

Economic Impact

Financial losses from IBK can be profound and occur due to decreased weight gain and decreased milk production, and treatment costs were estimated to be $150 million in the United States in 1993. Less tangible economic losses can also occur, such as a loss of value in show or breeding stock, weight loss and injury from handling animals for treatment, condemnation at slaughter due to ocular lesion detection, and lost productivity during time devoted to treatment. In affected unweaned calves, it was thought that losses associated with IBK were temporary and would recover after weaning and resolution of the condition. However, a study demonstrated that yearlings that had evidence of IBK at weaning had less body weight than cohorts without evidence of IBK, and associations between IBK at weaning and production variables persisted well into the postweaning period.

Incidence

IBK occurs worldwide. In a 1997 report of the US National Animal Health Monitoring System, IBK (1.1% infection rate) was the second‐most prevalent condition affecting unweaned beef calves over three weeks of age (USDA 1997). In the same report, IBK (1.3% infection rate) was the most prevalent condition affecting all beef heifers and cows. In studies at the University of California–Davis field station in Browns Valley, the yearly prevalence of IBK in yearling calves ranges from 57% to 98%.

IBK occurs primarily during the summer months, though winter outbreaks occur. This seasonal fluctuation may result from the increased presence of hemolytic M. bovis, the fly population, and solar radiation during the summer months. The decline through the fall season may result from the lack of susceptible calves, fewer vectors, and decreased intensity of enhancing factors.

Etiology

While M. bovis, a Gram‐negative bacillus, is considered to be the primary cause of IBK, other microbial agents have also been implicated. However, M. bovis is the only organism for which Koch’s postulates have been satisfied. Other infective agents that may play a role in development of IBK include Moraxella ovis (formerly Neisseria/Branhamella ovis), M. bovoculi, IBR virus, Mycoplasma spp., Thelazia spp., and L. monocytogenes. Concurrent infection with IBR causes more severe clinical signs than with IBK alone. Moraxella bovoculi has been isolated from eyes of cattle with clinical signs of IBK; however, the causal role of M. bovoculi and M. ovis in naturally occurring IBK is unclear. Moraxella bovoculi and M. bovis are both more frequently recovered from eyes with IBK lesions than unaffected eyes, which provides weak evidence for a causal role for M. bovoculi in IBK.

Morphology of Moraxella bovis

The morphology of M. bovis colonies is either rough or smooth. Clinical cases of IBK are associated with the rough type, which have cell surface pili, autoagglutinate in distilled water, stain with crystal violet, and hemagglutinate. The β‐hemolytic variants are usually associated with clinical disease.

Electron microscopy has revealed that bacteria from rough colonies of M. bovis are piliated and able to cause disease, whereas those from smooth colonies are nonpiliated and nonpathogenic (Figures 16.12 and 16.13). The capsular pili promote cellular adhesion and enhance the ability to overcome host defenses and maintain an established infection. As a general rule, the piliated, hemolytic form is found in acute cases of IBK, and proportionately more nonpiliated and nonhemolytic isolates are recovered from convalescent and clinically normal carrier cattle.

Transmission

The source of infection is usually a new animal or a carrier animal within the herd. Moraxella bovis can typically be found on the conjunctivae and in the nasal secretions of cattle without any signs or history of infection. Nonhemolytic M. bovis may reside in a herd over the winter months and not cause clinical signs. However, with the onset of spring and increased ultraviolet (UV) radiation, there can be a reversion to the pathogenic, hemolytic form, with subsequent infection of susceptible calves.

Moraxella bovis is transmitted by animal handlers, direct contact with infected animals, contact with fomites, and mechanical vectors, such as flies. The face fly (M. autumnalis) is considered to be the most important vector. However, the house fly (Musca domestica) and stable fly (Stomoxys calcitrans) have also been incriminated as mechanical vectors. These flies may harbor the organism on their legs for as long as three days. Without flies, transmission of IBK throughout a herd may be slow.

Predisposing Factors

The sex of an animal is not a significant factor in development of the disease. All breeds may be affected, but breed‐related differences in susceptibility occur. Bos indicus breeds are more resistant than Bos taurus breeds, and Herefords as well as Hereford crossbreeds appear to have a much higher susceptibility, as do Murray Greys.

The age of cattle affects the persistence and severity of infection with M. bovis. Younger cattle, less than two years, consistently have an increased risk and severity of clinical disease compared with older cattle, even though large numbers of older animals are infected. Developmental immunity is also suggested by observations that infected calves develop disease, whereas their infected dams fail to develop clinical signs. A good correlation exists between the annual peak incidence of IBK and annual peak levels of UV radiation. Increased UV radiation assists in the transformation of M. bovis from nonhemolytic to hemolytic strains. The number of face flies present correlates well with the infection rate and the number of new isolates. Once the number of flies exceeds 10 per animal, IBK spreads from one herd to another. Cattle housed indoors have a higher infection rate of longer duration, but milder clinical disease compared with those housed outdoors. Other environmental factors, such as mechanical irritants to the conjunctiva and cornea and ingestion of aflatoxin, have also been suggested as enhancing factors.

Pathogenesis

In clinical outbreaks of IBK, M. bovis can be isolated from most affected cattle. The initial corneal lesions probably result from bacterial cytotoxicity, whereas advanced lesions may be associated with bacterial/host inflammatory interaction. While M. bovis does not produce collagenase, the pathophysiology of IBK is likely associated with collagenase release from damaged epithelial cells, fibroblasts, and neutrophils. In addition, gelatinase and DNase have been detected in whole cultures, while dermonecrotoxins and cytotoxins for BHK 21 cell line monolayers and soluble factors that cause reversible detachment of cultured corneal epithelial cells have been detected in M. bovis culture filtrates. Both hemolytic and cytotoxic activities of neutrophils and corneal epithelial cells are important in the pathogenesis of IBK. Additionally, pathogenic factors of M. bovis, including pilin and cytotoxin (hemolysin, cytolysin), contribute to the pathogenesis of clinical disease. Pilin facilitates attachment to the corneal surface. Cytotoxin lyses bovine neutrophils, erythrocytes, lymphocytes, and corneal epithelial cells

Clinical Signs

The earliest clinical signs are varying degrees of epiphora, blepharospasm, and photophobia; conjunctival hyperemia and chemosis also occur. Often, this stage may be missed clinically because of an inability to carefully observe affected animals. Within 24–48 h after the onset of clinical signs, the axial cornea may develop small epithelial defects. Small corneal vesicles may precede ulceration. A small, pale, yellow to white raised abscess may appear near the center of the cornea, and over the following 24–48 h, the corneal opacity may increase in size or slough, leaving a shallow, round to oval, superficial ulcer with perilesional edema (Figures 16.14 and 16.15). During the next few days, the corneal ulcer may expand and deepen (Figure 16.16).

There is marked perilimbal conjunctival vascular hyperemia and initiation of superficial corneal vascularization. Blepharospasm, mild to moderate aqueous flare, and iridocyclitis are present. The conjunctival exudate becomes mucopurulent, with matting of the eyelashes. Vascularization of the cornea proceeds rapidly toward the primary central lesion. By seven to nine days postinfection, an area of inflammation and corneal vascularization surrounds the well‐delineated corneal ulcer (Figure 16.17). As the vascularization reaches the ulceration, the corneal opacity clears from the periphery toward the center. The ulcer epithelializes, and the facet gradually reduces by stromal regeneration, leaving a slightly raised, dense scar. Corneal healing is well advanced in two to three weeks and in one to two months only a faint localized central corneal opacity may remain.

The keratoconjunctivitis may result in secondary iridocyclitis, with hypopyon, synechiae, and even panophthalmitis. Occasionally, perforation of the corneal ulcer results in iris prolapse (Figure 16.18), in which case blindness may result. The eye may also become hypotensive and phthisical or buphthalmic from secondary glaucoma (Figure 16.19). In 75% of cases, ocular involvement is unilateral, but bilateral involvement may also occur. Affected animals are reluctant to compete for food, milk production is reduced, and weight gain is suppressed, usually in direct relation to the severity of the lesion. In young cattle, the disease process is usually more severe than in older animals.

Medical Treatment

Antibiotic treatment has been shown to be successful in reducing healing times of IBK‐associated corneal lesions. However, few reports directly compare different antibiotic classes, so it is difficult to evaluate comparative antibiotic efficacy. Currently, oxytetracycline formulations such as Liquamycin/LA‐200™ (Zoetis Animal Health, Parsippany, NJ, USA), Bio‐Mycin 200™ (Boehringer Ingelheim Vetmedica Inc., St. Joseph, MO, USA), and Noromycin 300 LA™ (Norbrook Inc., Overland Park, KS, USA), and the tulathromycin formulation Draxxin™ (Zoetis Animal Health) are the only parenteral antibiotics labeled for IBK in cattle. Topical medications approved for IBK include the oxytetracycline formulation Terramycin™ (Zoetis Animal Health) and Vetericyn Pink Eye Spray™ (Innovacyn Inc., Rialto, CA, USA). Veterinarians are encouraged to consult current online publications for up‐to‐date information on IBK labeled drugs. Other treatment options require extralabel drug use in food animals, which is very carefully regulated by the US Food and Drug Administration and by the American Veterinary Medical Association via the Animal Medicinal Drug Use Clarification Act. Therefore, other treatment options should only be used if currently labeled drug have been shown ineffective, and as long as the drugs are not prohibited for extralabel use in food animals (AVMA 2007).

Therapy for IBK is recommended to relieve pain and maintain productivity. Combined parenteral (20 mg/kg) and oral (alfalfa pellets containing 1 g/0.45 kg of pellet administered daily for 10 days at a dosage of 2 g/calf/day) administration of oxytetracycline appears to be an effective method of reducing the severity of herd outbreaks of IBK. Oxytetracycline therapy appears to be superior to penicillin G. Calves treated with oxytetracycline had fewer recurrences and less shedding of M. bovis compared with those treated with penicillin G. Long‐acting oxytetracycline formulations (LA‐200, LA‐300, and Bio‐Mycin 200) are currently approved for treatment of IBK in the United States. While parenteral long‐acting oxytetracycline formulations can be used in lactating dairy cattle, alfalfa pellets containing oxytetracycline cannot. The duration of the carrier stage (i.e., a normal eye with hemolytic M. bovis) is reduced by two injections of long‐acting oxytetracycline at 20 mg/kg each. In addition to shortening the carrier stage, treatment reduces the progression of lesions and shortens healing times in affected animals.

Other antibiotics demonstrating efficacy against M. bovis include tilmicosin (one dose of 5–10 mg/kg subcutaneously), long‐acting ceftiofur crystalline‐free acid (one dose of 6.6 mg of ceftiofur equivalents/kg subcutaneously into the posterior aspect of the pinna), florfenicol (two injections of 20 mg/kg intramuscularly q 48 h or a single dose of 40 mg/kg subcutaneously), tulathromycin (2.5 mg/kg subcutaneously), and clindamycin (150 mg subconjunctivally q 24 h for three days). Other drugs recommended by various authors include penicillin, ampicillin, ormetoprim–sulfadimethoxine (prohibited for extralabel use in lactating dairy cattle in the United States), furazolidone (prohibited for use in food animals in the United States), gentamicin, and neomycin.

Moraxella bovis is usually resistant to tylosin, lincomycin, and erythromycin, and has variable susceptibility to cloxacillin. Some M. bovis strains, however, may be sulfa‐resistant. While M. bovis is sensitive to many antibiotics, regional and strain differences may necessitate culture and sensitivity tests to select a specific antibiotic, especially during a severe outbreak. The treatment selected is influenced by the management practice of the affected animals. Dairy operations usually have daily access to the animals, but milk withdrawal times become important issues. Dairy operations therefore may choose procaine penicillin because of the short milk withdrawal times. Because beef cattle are infrequently handled, beef practitioners may opt for long‐lasting parenteral medications such as oxytetracycline. As antibiotic drug residues vary according to the drug formulation, dose, frequency, route of administration, and weight of the animal, the Food Animal Residue Avoidance Database should be contacted to determine withdrawal times and legality of use of a particular drug in an extralabel fashion. Other medical treatments for IBK include topical atropine and nonsteroidal anti‐inflammatory drugs (NSAIDs). These medications assist in relief of intraocular pain and decrease the incidence of inflammatory‐induced ocular lesions. Some reports detail use of local corticosteroids in IBK‐affected eyes without any detrimental effect. The lack of evidence‐based medicine indicating corticosteroids is beneficial in IBK cases, and the possibility of potentiating collagenases and prolonging healing times must be considered. Therefore, corticosteroids are best avoided in IBK.

Regardless of the therapy chosen, additional treatment steps should be taken to control the herd infection and minimize the economic effects. Critical measures include use of insecticides to control face flies, segregation of affected animals, personal disinfection between treatments of affected and noninfected animals, and frequent mowing of pastures.

Vaccination

In herds severely affected by IBK, vaccination may be worthwhile. Recommendations are to vaccinate six weeks before onset of the expected disease season. Calves should be vaccinated at 21–30 days of age, with a second vaccination occurring 21 days later. Vaccine administration should be at least 21 days before the fly season. It is not known whether colostral antibodies will interfere with the vaccines. Adult cattle should receive two initial vaccinations, followed by yearly boosters near the beginning of the vector season.

Incidence

Actual incidence in the general cattle population of the United States is often difficult to assess. In herds of live cattle, the incidence of OSCC has shown to vary from 4.4% to 5.6%. However, many of these studies considered herds of Hereford or Hereford cross cattle only and hence it is difficult to extrapolate.

Geographic Distribution

Bovine OSCC occurs worldwide, but there is an association between the occurrence of OSCC and an increased level of solar radiation. The incidence of OSCC increased significantly with decreases in latitude, increases in altitude, and mean annual hours of sunlight.

Signalment

The onset of OSCC is age related, with older cattle having a significantly greater risk. The average age of cattle with OSCC is 8.1 years. The incidence of OSCC is significantly higher in B. taurus than in B. indicus breeds. Though other cattle breeds are affected, the Hereford is overrepresented. This association is partially related to the typical periocular depigmentation. Age and lack of corneoconjunctival pigmentation were significant risk factors. Ayrshires are the most susceptible dairy breed and have a corresponding predilection for SCC of the vulva. There is no true sex difference in the incidence of OSCC. The higher incidence observed in females results from the males having been marketed before the age of peak incidence.

Genetic Predisposition

There is considerable evidence suggestive of a genetic basis for OSCC, such as variable morbidity rates among various breeds of cattle, lines of sires, and increased rates in the progeny of affected compared with those of unaffected parents. Lesion development is not heritable directly, but the genetic effect on periocular pigmentation determines to a large extent the degree to which the eye is susceptible.

A negative association exists between eyelid pigmentation and the occurrence of OSCC. Eyelid margin pigmentation clearly has an inhibitory effect on eyelid lesions but seems to have little effect on development of the much more frequent, conjunctival OSCC.

Corneoscleral (i.e., limbal) and bulbar conjunctival pigment have a local inhibitory effect on the development of OSCC.

Etiology of OSCC

A specific carcinogen has not been identified. A number of factors, including age, gender, breed, periocular and corneoscleral pigmentation, exposure to sunlight, viral infection, and nutrition, likely contribute to development of OSCC.

Exposure to sunlight plays a significant causal role in the development of OSCC. In cattle, all measures of solar radiation indicate a significant association between increasing risks of OSCC and increasing levels of radiation. Associations are evident whether affliction is defined as the occurrence of any type of tumor (i.e., plaque, papilloma, and carcinoma) or as the occurrence of only papilloma or carcinoma. Average ages of affected cattle are lower at high levels than at low levels of radiation.

Viral cofactors have been suggested in the etiology of OSCC, but there is no definite evidence. IBR virus has been isolated from ocular carcinoma and one of its precursor lesions, and “IBR‐type” inclusion bodies have been consistently observed in all types of OSCC lesions. It is not known whether IBR virus has a predilection for the epithelial tissue in ocular tumors. In addition, because IBR virus can be frequently isolated from early plaque lesions, it apparently exists early in the course of the disease among many animals. Whether IBR has a part in initiating tumor growth is only speculative. The role of bovine papilloma virus (BPV) in OSCC has also been examined. Neither the use of papilloma virus‐specific antibodies nor that of DNA hybridization assays for all six known types of BPV could demonstrate a direct association with OSCC. While not needed for tumor maintenance, BPV may play a role initially in tumor formation. Nutritional status affects the development of OSCC from six to nine years of age. Cattle with high nutritional levels have an occurrence of OSCC of 14%, whereas cattle on lower feed intakes have an occurrence of 1.5%. Animals on a high nutritional plane also have increased severity and number of tumors and reduced five‐year survival rates compared with those in animals at a low level of nutrition.

Clinical Signs

Approximately 75% of OSCC and precursor lesions affect the bulbar conjunctiva and cornea, and of these, 90% involve the limbus and 10% involve the cornea. The remaining 25% of OSCC lesions are distributed in the palpebral conjunctiva, nictitating membrane, and eyelids. Bovine OSCC has a characteristic progression through a series of benign stages and then, possibly, to a malignant stage. On the globe and third eyelid, the initial lesion is a plaque. Plaques may progress to a papilloma, then to a noninvasive carcinoma (i.e., carcinoma in situ

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