Clinical signs
A rabid cats with typical clinical signs of encephalitis: Seizures, salivation, pupil dilatation (Courtesy Dr Veera Tepsumethanon).
Aggressive behaviour towards humans is unusual in healthy cats, so any unjustified aggressive behaviour in cats must be considered highly suspicious.
Rabies should be suspected not only when there has been a recent history of a bite by or exposure to a rabid animal but also where an unvaccinated cat may have been in contact with potentially infected wildlife, such as bats. Indeed, only recently (November 2007), a cat in France died of rabies as a result of infection with bat lyssavirus. However, although rabid bats having been reported in the UK [Johnson et al, 2003; Fooks 2003; Harris et al, 2007] and the Mammal Society estimates that British cats could be killing 230, 000 bats a year [Fooks, personal communication], no cases of cat rabies have been documented in the UK. These findings indicate that the risk of cats becoming infected with rabies from bats may be low.
Two disease forms can be identified in cats: the furious and the paralytic one. The furious form of rabies has three clinical phases (prodromal, furious or psychotic and paralytic or dumb) but they are not always clearly distinct in cats. The other has only two phases: prodromal and paralytic. During the very short prodromal phase (12-48 hours) of both forms, a wide range of quite non-specific clinical signs (fever, anorexia, vomiting, diarrhoea) may occur, sometimes accompanied by neurological signs. Marked behavioural changes may be noticed at first, such as unusually friendly or shy or irritated behaviour or increased vocalization. Altered behaviour depends on forebrain involvement and may be associated with other neurological signs reflecting the inoculation site. If the bite occurs in the face, clinical signs reflect cranial nerve and forebrain involvement: the former may produce depressed or absent reflexes (palpebral, corneal, pupillary, etc.), strabismus, dropped jaw, inability to move whiskers forward, dysphagia, laryngeal paralysis, voice change, tongue paralysis. Forebrain involvement is responsible for seizures, muscular twitching or tremors, aimless pacing, exaggerated emotional responses (irritability, rage, fearfulness, photophobia, attacking inanimate objects, etc). The tendency to bite may be the consequence of the loss of inhibitory control by cortical neurons over the subcortical bite reflex whereby dogs and cats turn and snap at anything that touches them around the mouth [O’Brien and Axlund, 2005]. If this is the case, the animal snaps without warning or showing any emotion when doing it. Pruritus at the bite site can be observed. If the infecting bite was on the limbs, neurological signs start from the spinal cord and an ascending lower motor neuron (LMN) paralysis occurs before the brain signs. The encephalitis rapidly spreads throughout the CNS producing severe ataxia, disorientation, paralysis, seizures, status epilepticus eventually followed by coma and death from respiratory arrest.
The furious phase is more consistently developed in cats showing behaviour abnormalities (described above) [Fogelman et al, 1993]. The paralytic phase (paraparesis, incoordination, generalized paralysis, coma and death) usually begins after five days of starting first clinical signs.
Isolated reports of survival after a confirmed clinical disease are available in cats, dogs and humans [Bernard 1985, Fekadu 1991], but death usually occurs after a clinical course of 1-10 days. Cats often die in 3-4 days [Rupprecht and Childs, 1996] and according to a more recent report, 25% of deaths occur in cats within 4 days of clinical course, while in dogs within 2 days only [Tepsumethanon et al, 2004].
Atypical forms with chronic course have been described after experimental infection in cats [Murphy et al, 1980].
The severe public health risk (veterinarians included!) requires that differential diagnosis of CNS diseases characterized by sudden onset and rapidly evolving clinical signs, always includes rabies for free roaming, unvaccinated cats living in endemic areas or travelling there. In this case, the clinical approach must make safety the priority because the manipulation and restraint of the cat easily may provoke biting at the time when salivary glands are usually already infected and rabies virus is shed in saliva. Guidelines indicating that a clinical diagnosis of rabies should be included in the differential diagnosis in live cats with suspected encephalitis based on history and observation of the cat inside the carrier would help to reduce the risk of exposure for the veterinary team (see the flow chart below that was adapted for cats from Tepsumethanon et al, 2003). Vaccine-induced rabies in cats was observed in the past when modified-live vaccines were available. Neurological signs occurred several weeks after vaccination and were characterized mostly by progressive upper motor neuron (UMN) limb paralysis and cranial nerve deficits.
Box 1. Clinical signs of rabid cats infected by classical rabies virus (Genotype I)
History and clinical signs by the owner:
1. Dramatic changes from normal behaviour.2. Very aggressive, biting human and/or animal with no apparent reason.
http://www.oie.int/eng/normes/mmanual/A_summary.htm
General appearance and clinical signs at observation:
1. 90% of rabid cats show clinical signs of the furious form.2. Thin (the cat cannot eat)
3. Ruffled and dirty coat. (the cat cannot clean itself)
4. Mucous membranes, tongue, nose and footpads are reddish pink, high fever.
5. The chin and front legs are wet from saliva (salivation).
6. Permanent movement and excitement (restlessness).
7. Imbalanced gait due to paresis of the hind legs.
8. Pupil dilatation unresponsive to light.
9. Abnormal water uptake (water runs back out of mouth).
(Courtesy Dr Veera Tepsumethanon)
