Amaurosis

Amaurosis is blindness without any externally detectable defect in the visual system. The cornea, lens, and uveal tract appear to be normal. If the lesion is limited to the cer­ebral cortex, and optic nerve and nuclei are intact, the pupillary reflexes are also normal.

BLindnessversus Failure to Blink

It is common but inaccurate to equate the ability to blink in response to a menacing hand gesture with the ability to see; this is because the entire visual pathway, from the ret­ina to the cerebral cortex, must be intact for the reflex to function (deLahunta et al. 2015). Because it is a learned response, very young kids may not menace, even though they have no trouble seeing and following a moving bottle or other item of interest. Goat kids develop a menace response by about 2 weeks of age, with males being delayed relative to female kids (Raoof et al. 2011). A goat with nor­mal vision also fails to blink if facial nerve paralysis is pre­sent. This possibility is investigated by actually touching the medial or lateral canthus. Even a blind animal should then blink, unless either sensory or motor function is disturbed.

Blindness versus Severe Depression or Toxemia

Severely obtunded or semi-comatose goats respond mini­mally to stimuli routinely applied to evaluate cranial nerve function. If the animal is severely depressed, a metabolic disease (hypoglycemia, hypocalcemia, pregnancy toxemia, rumen acidosis, water deprivation/sodium ion toxicosis), liver disease (see Chapter 11), or terminal septicemic or toxemic condition (Boermans et al. 1988), rather than a lesion specifically involving visual pathways or cerebral cortex, may be present. It is inappropriate, then, to limit diagnostic consideration to those diseases with blindness as a leading sign.

Polioencephalomalacia

Blindness is almost always present in advanced cases of polioencephalomalacia. Thus, thiamine administration, as discussed in Chapter 5, is indicated (at least initially) for every goat with amaurosis.

Enterotoxemia

Blindness is one sign of focal symmetrical encephalomala- cia, an uncommon disease reportedly caused by exotoxins of Clostridium perfringens, in sheep. The condition has been reported only rarely in goats (Oliveira et al. 2010); see Chapter 5.

Lead Poisoning

Although blindness is a prominent sign of lead poisoning in cattle, this is not the case in goats. Anorexia and diarrhea or abortion, not blindness and convulsions, are reported with experimental lead poisoning in goats (Dollahite et al. 1975; Davis et al. 1976).

Hydrocephalus

A young kid that has a good suckle reflex and a normal gait may become separated from its dam or stuck in corners. Hydrocephalus or other congenital malformation of the brain may be responsible for this abnormal behavior asso­ciated with blindness. Sometimes the skull is domed, which increases the suspicion of hydrocephalus. Other kids have no outward conformational changes even though very little brain is in fact present. In the United States, in utero Cache Valley virus infection is an important cause of hydrocephalus and hydranencephaly in kids (see Chapter 13).

Vitamin A Deficiency

Maternal deficiency of vitamin A produces atrophy of the optic nerves in calves. This is because the optic canals have not grown to accommodate the optic nerves, resulting in pressure atrophy and demyelination of the nerves. In the case of acquired avitaminosis A in cattle, there is an initial, often reversible night blindness caused by deficient forma­tion of rhodopsin. If the deficiency continues, the retina degenerates and eventually constriction of the optic nerve can occur in growing calves. Papilledema is an important sign of vitamin A deficiency and is secondary to increased cerebrospinal fluid (CSF) pressure.

Severe vitamin A deficiency, as occurs during the dry season or droughts in semiarid regions, causes night blind­ness that is not always accompanied by corneal opacity and ulceration. These ocular problems are documented in sheep (Eveleth et al. 1949; Ghanem and Farid 1982) and have been reproduced experimentally in goats (Schmidt 1941).

Coenurosis

Coenurus cerebralis is the larval stage of the tapeworm Taenia multiceps. It can form a cyst in the cerebral hemi­spheres or median fissure. A common clinical sign is par­tial or total blindness in one eye (Sharma 1965; Tirgari et al. 1987; Nooruddin et al. 1996). The head is held in the direction away from the blind eye and the animal circles in that direction; that is, toward the cerebral lesion. Pupillary reflexes generally remain normal, but papilledema may be noted because of increased intracra­nial pressure (Sharma and Tyagi 1975). In some cases, the skull overlying the cyst is softened and deformed, and pressure on the affected bone elicits signs of pain (loud bleating). Vision usually returns within one day after sur­gical removal of the cyst. The disease has not been reported in recent years in the United States (Kimberling 1988), but might be the explanation for Ormilo (head disease), seen in small ruminants kept by the Maasai in Kenya and Tanzania (ProMED 2017).

Miscellaneous Causes of Central Blindness

Several other diseases may cause blindness in sheep, and perhaps in goats. Melioidosis is a fatal septicemic disease caused by Burkholderia (Pseudomonas) pseudomallei and occurs mainly in Southeast Asia and Australia. A central blindness can accompany other neurologic signs. Likewise, scrapie can cause blindness, but will probably be recog­nized by other neurologic signs.

Chronic poisoning with some forms of arsenic, in some species, can cause blindness. Acute blindness in cattle and sheep has been associated with consumption of rape (Brassica napus), but documentation is meager. In some instances of poisoning with Brassica spp., the actual cause of blindness may be polioencephalomalacia (Wikse et al. 1987). Ironwood (Erythrophleum chlorostachys), a tree from tropical Australia, has been reported to poison goats and cause, among other signs, a staring-eyed demea­nor, with vision apparently affected (Hall 1964). Overdosage with hexachlorophene, rafoxanide, and closantel can cause degeneration of the optic nerve, optic tract, or retina (Button et al. 1987). The pathologic changes (Gill et al. 1999; Ecco et al. 2006) resemble those caused by Stypandra spp., but pigment epithelium hypertrophy has not been described.

Residual Blindness

Blindness may persist for days, weeks, or even the life of a goat that did not receive thiamine early in the course of polioencephalomalacia. Other traumatic or metabolic insults to the cerebral cortex (prolonged application of a disbudding iron, pregnancy toxemia) could also result in amaurosis. Usually there is a history of partial recovery from a previous severe illness.