https://en.wikivet.net/api.php?action=feedcontributions&user=Clamy&feedformat=atomWikiVet English - User contributions [en]2024-03-29T11:41:46ZUser contributionsMediaWiki 1.35.0https://en.wikivet.net/index.php?title=Ductulo_Vesicular_Urolithiasis_%E2%80%93_Rabbit&diff=91004Ductulo Vesicular Urolithiasis – Rabbit2010-09-07T21:24:07Z<p>Clamy: </p>
<hr />
<div>{{unfinished}}<br />
<br />
Ureterolith is a stone in the ureter (study radiographs very carefully). This can be very painful and the use of Buscopan is useful (spasmolytic and analgesic - relieves spasm and kills pain).<br />
<br />
Vesicular urolith (stone in the bladder) <br />
<br />
The appearance of crystals in the urine. Microscopic examination of the centrifuged sediment helps with the subsequent management of the case. Usually calcium carbonate but often calcium oxalate. Struvite may be seen too.<br />
<br />
Urine sludge is flushed out per catheter and found to contain large amounts of crystals (as described above). Treatment always involves dietary alteration and the use of diuretics to flush out the bladder. I use bendrofluazide (PO q24h in the mornings) and another clinician (William Lewis personal communication 2006) flushes the bladder with saline per urethral catheterisation until the organ is flushed clear of calcium sludge – he tells me that this results in a more rapid improvement than the use of bendrofluazide alone. Catheterisation always involves general anaesthesia and, in does, the use of an endoscope to visualise the urethral orifice. Dietary alteration involves offering Timothy hay and fresh greens and plenty of fresh water. Antibiotics are seldom indicated, except in the presence of infection (Treponema or Pasteurella – the former may be directly associate with anuresis but the latter may be involved in other anatomical systems) and used in conjunction with the anaesthetic.<br />
<br />
Jenkins (2006) differentiates between normal calciuria and micro-urinary calculi (MUC). MUC form in response to cystitis and can cause construction.<br />
<br />
Urine scald occurs as a result of some urine adhering to the fur near the vent (usually due to excessive calcium in the urine (cf. the effect of hard water on your hands). It is a particular problem in obese animals. Management requires pain killers (Buscopan®; Boehringer Ingelheim), neutralising/astringent powders (Cutisan®; Boots Healthcare – available only in pharmacies in France), Rear Guard® (Novartis) to prevent fly strike, and the calcium-sparing diuretic, bendrofluazide, PO q 24 h, every morning. (Note that I use quite a high dose of bendrofluazide in rabbits and rodents).<br />
<br />
Supportive Therapy following medical and surgical treatment of urolithiasis:<br />
*Dietary Fibre<br />
*Prokinetics.<br />
*Fluids (oral, Intraperitoneal)<br />
*Acid environment peat moss as a litter to neutralise ammonia in voided urine.<br />
<br />
Prevention of Urolithiasis:<br />
*Reduce the content of calcium in the diet<br />
<br />
Calcium in New Hay:<br />
*Alfalfa 1.8%<br />
*Clovers approx 1.5%<br />
*Fescue 1.5%<br />
*Timothy 0.66%<br />
*Ryegrass 0.65%<br />
*Orchard Grass 0.27%<br />
*Wheat straw/Oat Hulls 0.15%.<br />
<br />
Ref: Nutrient Requirements of Dairy Cattle VI (1989) NRC Washington DC<br />
<br />
Content of calcium in selected vegetables (in mg per 100g): <br />
*Coriander (16) <br />
*Lettuce (20-102) <br />
*Cauliflower (28) <br />
*Carrots (30) <br />
*Turnips (39) <br />
*Peas (36-42)<br />
*Watercress (40) <br />
*Broccoli (42)<br />
*Spinach (56)<br />
*Parsley (78)<br />
*Kale (94)<br />
Source = www. magpage.com 1997<br />
<br />
For an up-to-date review of urogenital diseases of rabbits see Reusch B (2006)<br />
<br />
<br />
==References==<br />
*Redrobe S (2000): Urogenital system and disorders In Manual of Rabbit Medicine and Surgery ed Paul Flecknell pub BSAVA Cheltenham <br />
*Reusch B (2006) Urogenital System and Disorders in BSAVA Manual of Rabbit Medicine and Surgery eds Meredith A and Flecknell P, 2nd Edition 2006, published by BSAVA Quedgley Glocs<br />
*Jenkins J R (2006) Clinical Pathology in BSAVA Manual of Rabbit Medicine and Surgery eds Meredith A and Flecknell P, 2nd Edition 2006, published by BSAVA Quedgley Glocs <br />
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[[Category:Urogenital_Diseases_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Ductulo_Vesicular_Urolithiasis_%E2%80%93_Rabbit&diff=91002Ductulo Vesicular Urolithiasis – Rabbit2010-09-07T21:21:17Z<p>Clamy: </p>
<hr />
<div>{{unfinished}}<br />
<br />
Ureterolith is a stone in the ureter (study radiographs very carefully). This can be very painful and the use of Buscopan is useful (spasmolytic and analgesic - relieves spasm and kills pain).<br />
<br />
Vesicular urolith (stone in the bladder) <br />
<br />
The appearance of crystals in the urine. Microscopic examination of the centrifuged sediment helps with the subsequent management of the case. Usually calcium carbonate but often calcium oxalate. Struvite may be seen too.<br />
<br />
Urine sludge is flushed out per catheter and found to contain large amounts of crystals (as described above). Treatment always involves dietary alteration and the use of diuretics to flush out the bladder. I use bendrofluazide (PO q24h in the mornings) and another clinician (William Lewis personal communication 2006) flushes the bladder with saline per urethral catheterisation until the organ is flushed clear of calcium sludge – he tells me that this results in a more rapid improvement than the use of bendrofluazide alone. Catheterisation always involves general anaesthesia and, in does, the use of an endoscope to visualise the urethral orifice. Dietary alteration involves offering Timothy hay and fresh greens and plenty of fresh water. Antibiotics are seldom indicated, except in the presence of infection (Treponema or Pasteurella – the former may be directly associate with anuresis but the latter may be involved in other anatomical systems) and used in conjunction with the anaesthetic.<br />
<br />
Jenkins (2006) differentiates between normal calciuria and micro-urinary calculi (MUC). MUC form in response to cystitis and can cause construction.<br />
<br />
Urine scald occurs as a result of some urine adhering to the fur near the vent (usually due to excessive calcium in the urine (cf. the effect of hard water on your hands). It is a particular problem in obese animals. Management requires pain killers (Buscopan®; Boehringer Ingelheim), neutralising/astringent powders (Cutisan®; Boots Healthcare – available only in pharmacies in France), Rear Guard® (Novartis) to prevent fly strike, and the calcium-sparing diuretic, bendrofluazide, PO q 24 h, every morning. (Note that I use quite a high dose of bendrofluazide in rabbits and rodents).<br />
<br />
Supportive Therapy following medical and surgical treatment of urolithiasis:<br />
*Dietary Fibre<br />
*Prokinetics.<br />
*Fluids (oral, Intraperitoneal)<br />
*Acid environment peat moss as a litter to neutralise ammonia in voided urine.<br />
<br />
Prevention of Urolithiasis:<br />
*Reduce the content of calcium in the diet<br />
<br />
Calcium in New Hay:<br />
*Alfalfa 1.8%<br />
*Clovers approx 1.5%<br />
*Fescue 1.5%<br />
*Timothy 0.66%<br />
*Ryegrass 0.65%<br />
*Orchard Grass 0.27%<br />
*Wheat straw/Oat Hulls 0.15%.<br />
<br />
Ref: Nutrient Requirements of Dairy Cattle VI (1989) NRC Washington DC<br />
<br />
Content of calcium in selected vegetables (in mg per 100g): <br />
*Coriander (16) <br />
*Lettuce (20-102) <br />
*Cauliflower (28) <br />
*Carrots (30) <br />
*Turnips (39) <br />
*Peas (36-42)<br />
*Watercress (40) <br />
*Broccoli (42)<br />
*Spinach (56)<br />
*Parsley (78)<br />
*Kale (94)<br />
Source = www. magpage.com 1997<br />
<br />
For an up-to-date review of urogenital diseases of rabbits see Reusch B (2006)<br />
<br />
[[Category:Urogenital_Diseases_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Ductulo_Vesicular_Urolithiasis_%E2%80%93_Rabbit&diff=91001Ductulo Vesicular Urolithiasis – Rabbit2010-09-07T21:12:29Z<p>Clamy: Created page with "{{unfinished}} Ureterolith is a stone in the ureter (study radiographs very carefully). This can be very painful and the use of Buscopan is useful (spasmolytic and analgesic - r..."</p>
<hr />
<div>{{unfinished}}<br />
<br />
Ureterolith is a stone in the ureter (study radiographs very carefully). This can be very painful and the use of Buscopan is useful (spasmolytic and analgesic - relieves spasm and kills pain).<br />
<br />
Vesicular urolith (stone in the bladder) <br />
<br />
The appearance of crystals in the urine. Microscopic examination of the centrifuged sediment helps with the subsequent management of the case. Usually calcium carbonate but often calcium oxalate. Struvite may be seen too.<br />
<br />
Urine sludge is flushed out per catheter and found to contain large amounts of crystals (as described above). Treatment always involves dietary alteration and the use of diuretics to flush out the bladder. I use bendrofluazide (PO q24h in the mornings) and another clinician (William Lewis personal communication 2006) flushes the bladder with saline per urethral catheterisation until the organ is flushed clear of calcium sludge – he tells me that this results in a more rapid improvement than the use of bendrofluazide alone. Catheterisation always involves general anaesthesia and, in does, the use of an endoscope to visualise the urethral orifice. Dietary alteration involves offering Timothy hay and fresh greens and plenty of fresh water. Antibiotics are seldom indicated, except in the presence of infection (Treponema or Pasteurella – the former may be directly associate with anuresis but the latter may be involved in other anatomical systems) and used in conjunction with the anaesthetic.<br />
<br />
Jenkins (2006) differentiates between normal calciuria and micro-urinary calculi (MUC). MUC form in response to cystitis and can cause construction.<br />
<br />
Urine scald occurs as a result of some urine adhering to the fur near the vent (usually due to excessive calcium in the urine (cf. the effect of hard water on your hands). It is a particular problem in obese animals. Management requires pain killers (Buscopan®; Boehringer Ingelheim), neutralising/astringent powders (Cutisan®; Boots Healthcare – available only in pharmacies in France), Rear Guard® (Novartis) to prevent fly strike, and the calcium-sparing diuretic, bendrofluazide, PO q 24 h, every morning. (Note that I use quite a high dose of bendrofluazide in rabbits and rodents).<br />
<br />
Supportive Therapy following medical and surgical treatment of urolithiasis:<br />
*Dietary Fibre<br />
*Prokinetics.<br />
*Fluids (oral, Intraperitoneal)<br />
*Acid environment peat moss as a litter to neutralise ammonia in voided urine.<br />
<br />
Prevention of Urolithiasis:<br />
*Reduce the content of calcium in the diet<br />
<br />
Calcium in New Hay:<br />
*Alfalfa 1.8%<br />
*Clovers approx 1.5%<br />
*Fescue 1.5%<br />
*Timothy 0.66%<br />
*Ryegrass 0.65%<br />
*Orchard Grass 0.27%<br />
*Wheat straw/Oat Hulls 0.15%.<br />
<br />
Ref: Nutrient Requirements of Dairy Cattle VI (1989) NRC Washington DC<br />
<br />
Content of calcium in selected vegetables (in mg per 100g): <br />
*Coriander (16) <br />
*Lettuce (20-102) <br />
*Cauliflower (28) <br />
*Carrots (30) <br />
*Turnips (39) <br />
*Peas (36-42)<br />
*Watercress (40) <br />
*Broccoli (42)<br />
*Spinach (56)<br />
*Parsley (78)<br />
*Kale (94)<br />
Source = www. magpage.com 1997<br />
<br />
For an up-to-date review of urogenital diseases of rabbits see Reusch B (2006)</div>Clamyhttps://en.wikivet.net/index.php?title=Spinal_Disorders_%E2%80%93_Rabbit&diff=89576Spinal Disorders – Rabbit2010-08-31T19:32:04Z<p>Clamy: Created page with "{{unfinished}} Various spinal disorders are encountered in pet rabbits especially those confined in hutches (lack of exercise and sunlight) which then develop deformities due t..."</p>
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<div>{{unfinished}}<br />
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Various spinal disorders are encountered in pet rabbits especially those confined in hutches (lack of exercise and sunlight) which then develop deformities due to the action of the strong lumbar musculature (scoliosis and kyphosis). Disc disease is also encountered. Treatment of these (inevitably chronic) conditions can only be palliative – the use of COX-sparing NSAIDs and physical musculature-stimulating therapies (eg. TENS or similar).<br />
<br />
[[category:Locomotor_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Hind_Limb_Pododermatitis_%E2%80%93_Rabbit&diff=89575Hind Limb Pododermatitis – Rabbit2010-08-31T19:30:26Z<p>Clamy: Created page with "{{unfinished}} ==Description== Hind limb pododermatitis in rabbits is a complex, multifactorial condition involving musculoskeletal as well as integumentary systems. The hind-le..."</p>
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<div>{{unfinished}}<br />
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==Description==<br />
Hind limb pododermatitis in rabbits is a complex, multifactorial condition involving musculoskeletal as well as integumentary systems. The hind-leg stance of the rabbit is naturally digitigrade (ie. plantigarde) except that the metatarsal bones are raised from the ground. Contact with the ground is through the claws and the plantar aspect of the hock. Most of the weight is taken on the hind limb. The superficial digital flexor is constantly under tension (to facilitate immediate response to predators). The animal is therefore well adapted for life on grassland or turf. <br />
<br />
When confined to a caged environment on concrete, wood or even wire mesh the correct stance is not possible and pressure is applied to extra areas of the metatarsus as the claws cannot engage the floor (sliding over hard surfaces or having no weight-bearing at all in the case of wire mesh). This is exacerbated by malnutrition (obesity leads to extra pressure on the plantar metatarsus, emaciation reduces the covering over the bony prominences). The extra pressure causes localised ischaemia, eventual infection and a chronic disease state which may be exacerbated by displacement of the superficial digital tendon. You are referred to Harcourt Brown Textbook of Rabbit Medicine (2002) page 240 for an excellent description of this complex condition. <br />
<br />
==Treatment of ulcerative pododermatitis==<br />
*Address underlying cause – correction of poor husbandry<br />
*Change dirty environment<br />
*Supply companion to increase exercise<br />
*Non-abrasive, soft dry substrate.- peat moss – not wire floors.<br />
*Keep ulcerated areas clean and dry<br />
*Protective bandages – those that are applied to sore areas will be removed by the rabbit so apply around the area<br />
*Liquid bandages like Nu Skin or Germolene can be applied to the affected areas<br />
*Mild clip of hair – leave some fur to take weight<br />
*Systemic antibiosis<br />
*Analgesia (meloxicam) – may help relieve underlying spondylitis/arthritis<br />
*Surgery of non-weight-bearing areas only if absolutely necessary<br />
*Manuka honey<br />
*Euthanasia<br />
<br />
<br />
[[category:Locomotor_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Osteomyelitis_%E2%80%93_Rabbit&diff=89570Osteomyelitis – Rabbit2010-08-31T19:06:09Z<p>Clamy: </p>
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<div>{{unfinished}}<br />
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Osteomyelitis is frequently encountered in pet rabbits. It may occur spontaneously or secondary to trauma. Sites include subcutis, joints, long bones, skull bones, tooth roots, and retrobulbar tissues. Abscesses are often very large and antibiotic therapy, unless aggressive, is therefore unrewarding. They are best treated by adequate surgical excision and prolonged courses of parenteral antibiotics. Rabbit skin heals very rapidly. I always prepare the owner for the administration of very long courses of medication, usually oxytetracycline (Engemycin 5%; Intervet), SC q72hrs for three weeks longer than it takes for the abscess(es) to become clinically undetectable. In severeal cases the animal has been kept on treatment with oxytetracycline parenterally for life will no ill-effects. Topical application of clindamycin by inserting one 25mg Antirobe® capsule Pfizer is recommended and practised by many clinicians in the treatment of cutaneous abscesses in pet rabbits. Clindamycin must not be allowed to enter the gastrointestinal canal. See the note on the treatment of submandibular abscesses [[Submandibular Abscessation – Rabbit|here]].<br />
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[[Category:Locomotor_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Osteomyelitis_%E2%80%93_Rabbit&diff=89569Osteomyelitis – Rabbit2010-08-31T19:05:56Z<p>Clamy: Created page with "{{unfinished}} Osteomyelitis is frequently encountered in pet rabbits. It may occur spontaneously or secondary to trauma. Sites include subcutis, joints, long bones, skull bones..."</p>
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<div>{{unfinished}}<br />
<br />
Osteomyelitis is frequently encountered in pet rabbits. It may occur spontaneously or secondary to trauma. Sites include subcutis, joints, long bones, skull bones, tooth roots, and retrobulbar tissues. Abscesses are often very large and antibiotic therapy, unless aggressive, is therefore unrewarding. They are best treated by adequate surgical excision and prolonged courses of parenteral antibiotics. Rabbit skin heals very rapidly. I always prepare the owner for the administration of very long courses of medication, usually oxytetracycline (Engemycin 5%; Intervet), SC q72hrs for three weeks longer than it takes for the abscess(es) to become clinically undetectable. In severeal cases the animal has been kept on treatment with oxytetracycline parenterally for life will no ill-effects. Topical application of clindamycin by inserting one 25mg Antirobe® capsule Pfizer is recommended and practised by many clinicians in the treatment of cutaneous abscesses in pet rabbits. Clindamycin must not be allowed to enter the gastrointestinal canal. See the note on the treatment of submandibular abscesses [[Submandibular Abscessation – Rabbit|here]].<br />
<br />
[[Category:Locomotor_Disorders_-Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Splay_Leg_%E2%80%93_Rabbit&diff=89568Splay Leg – Rabbit2010-08-31T19:01:10Z<p>Clamy: Created page with "{{unfinished}} "Splay leg" is an affliction involving improper development of the spine, pelvis, hip joint or long bones. Affected animals are unable to adduct the hind legs. Th..."</p>
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<div>{{unfinished}}<br />
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"Splay leg" is an affliction involving improper development of the spine, pelvis, hip joint or long bones. Affected animals are unable to adduct the hind legs. The author has only ever seen this condition in young rabbits (less than three months of age), which tends to support the theory of some authorities. <br />
<br />
It can affect hind limbs only (usually both) or all four legs (ie. one to all four limbs). The condition must be differentiated radiographically from nutritional hyperparathyroidism. Okerman (1994) states that it is a result of several different disorders viz hereditary (sub)luxation of the femur or hereditary nervous disorders such as syringomelia (fluid-filled cavities in the spinal cord). Euthanasia is the usual course of action.<br />
<br />
The author has seen occasional cases of dislocation of the interphalangeal and metatarso-phalangeal joints which have responded to either conservative (cage-rest) or arthrodesive repair. The latter was effected in a New Zealand White using stainless steel laid as a box or mattress suture through the distal end of the metatarsal bone and the proximal end of the phalanx, whereas one four-year-old Netherland Dwarf doe after escape from an urban fox had sustained compound dislocations of both medial (no 2) phalangeo-pedal joints and responded to cage rest and parenteral oxytetracycline, ketoprofen and warmth being the sole other agents used in the initial stages of shock.<br />
<br />
==References==<br />
*Okerman L (1994): Diseases of Domestic Rabbits. Blackwell Scien¬tific Publications ISBN 0-632-03804 -7. 2nd Edition<br />
<br />
[[Category:Locomotor_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Posterior_Paralysis_%E2%80%93_Rabbit&diff=89567Posterior Paralysis – Rabbit2010-08-31T18:58:21Z<p>Clamy: Created page with "{{unfinished}} Posterior paralysis is distressingly common and is nearly always due to a weakness in the caudal lumbar vertebrae and their articulations. Many authors and clinic..."</p>
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<div>{{unfinished}}<br />
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Posterior paralysis is distressingly common and is nearly always due to a weakness in the caudal lumbar vertebrae and their articulations. Many authors and clinicians consider that rabbits have an inherent weakness in this area. Others claim a high incidence of osteoporosis in caged animals. <br />
<br />
Harrenstien et al (1995) cite Harkness (1989) and state that the L6-7 vertebral space is the fulcrum between the major cranial and caudal muscle groups of the rabbit. Lumbar weakness is doubtless a factor contributing to the relatively dispensable nature of the rabbit as a species (see tibial fractures) but it is nevertheless very distressing to the owner, especially if it occurs after a simple veterinary procedure like nail-clipping, and has already proved its "worth" in medico-legal circles in the UK. If there is still "deep pain" response in the hind feet, if there is no faecal or urinary incontinence and if there is no evidence of malalignment of vertebrae on radiography, it is worth attempting treatment with corticosteroids (dexamethasone intravenously followed by intramuscular injection daily and cage rest for two or three weeks, reducing the dose of dexamethasone by 50% every three days or sooner, depending on the response) and oxytetracycline (Engemycin 5%®; Intervet) sc q72hr. Corticosteroids must always be used with extreme caution in rabbits as they may reduce premune responses to organisms like ''Encephalitozoon cuniculi'' and allow the manifestation of other conditions such as hepatic lipidosis. Euthanasia must always be considered as a suitable option for this distressing condition. <br />
<br />
==References==<br />
*Harrenstien L. et al (1995): How to handle respiratory, ophthalmic, neurologic and dermatologic problems in rabbits: Veterinary Medicine 90 (4) 373-380<br />
[[Category:Locomotor_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Septic_Arthritides_%E2%80%93_Rabbit&diff=89563Septic Arthritides – Rabbit2010-08-31T18:52:18Z<p>Clamy: Created page with "{{unfinished}} Septic arthritides are occasionally encountered and are diagnosed radiographically in pet rabbits. Microbiological investigation is very important but Pasteurella..."</p>
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Septic arthritides are occasionally encountered and are diagnosed radiographically in pet rabbits. Microbiological investigation is very important but Pasteurellar organisms often don’t survive the journey through the post to the lab and treatment with antibiotics should cover Pasteurella species in its spectrum so, in the absence of antibiograms, I recommend oxytetracycline (Engemycin 5%®; Intervet) SC q72hrs or procaine penicillin SC q4-7d. <br />
<br />
It is important to note that the use of lincosamides orally or parenterally is contraindicated in rabbits due to the possibility of overgrowth of the large intestine with pathogenic ''Clostridium'' species while these antibiotics are in use. (But see the details of the treatment of abscesses and osteomyelitis).<br />
<br />
Chronic deformative arthroses are occasionally encountered in pet rabbits (Rubel, Isenbugel and Wolvekamp 1991) and are usually treated conservatively or affected animals are humanely destroyed.<br />
<br />
Hyperostotic polyarthropathy is reported in a rabbit fed excess vitamin A in the form of a diet consisting almost exclusively of diets (Frater 2001).<br />
<br />
<br />
==References==<br />
Rubel, Isenbugel and Wolvekamp 1991<br />
<br />
[[Category:Locomotor_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Cestode_Infestation_%E2%80%93_Rabbit&diff=83226Cestode Infestation – Rabbit2010-08-11T01:42:23Z<p>Clamy: /* References */</p>
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<div>{{unfinished}}<br />
Cestode infestations are not common in pet rabbits except perhaps as the intermediate hosts of ''Taenia pisiformis cystericerci'' and ''Taenia serialis coenuri'' (Goudsward and Thomas 1991). Okerman 1994 states that ''Taenia pisiformis'' is common in backyard rabbits. Intestinal ''Hymenolepis nana'' infestations are difficult to diagnose in the live rabbit as the ova are shed in proglotids in the faeces and flotation techniques are not entirely suitable for their detection (Harkness 1987). <br />
<br />
==Treatment==<br />
They are also difficult to treat as the parasite is known to have a direct life cycle in some situations. The recommended treatment of lumenal infestations in pet rabbits is the use of praziquantel (Droncit; Bayer plc) orally as the plasma levels obtained from the subcutaneous injection of this product is too short-lived to be efficacious. Williams (1979) mentions ''Cittotaenia'' sp and recommends the use of Niclosamide PO to kill the worm.<br />
<br />
<br />
==References==<br />
*Goudsward, M. F. and Thomas, J. A. (1991) Coenurus serialis infection of a white rabbit. Veterinary Record 129 295<br />
*Harkness 1987 ???<br />
*Okerman, L. (1994) Diseases of Domestic Rabbits. Blackwell Scien¬tific Publications ISBN 0-632-03804 -7. 2nd Edition<br />
*Williams, C. S. F. (1979) Guinea Pigs and Rabbits. Veterinary Clinics of North America: Small Animal Practice 9 (3) 487 - 498<br />
<br />
[[Category:Endoparasitism_–_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Encephalitozoon_cuniculi&diff=83225Encephalitozoon cuniculi2010-08-11T01:21:22Z<p>Clamy: /* Transmission of Encephalitozoon cuniculi */</p>
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<div>{{unfinished}}<br />
<br />
==Taxonomy==<br />
*Phylum Microspora; no mitochondria polar tube polar cap<br />
*Class Microsporida<br />
*Order Microsporidia<br />
*May be more related to fungi than to protozoa (Wasson and Peper 2000)<br />
*Obligate intracellular protozoan parasite<br />
*52% normal healthy domestic pet rabbits arte infected (Keeble and Shaw 2006)<br />
*Ubiquitous in other species too<br />
<br />
==The life cycle==<br />
The life cycle of this coccidian is 3 – 4 weeks in total:<br />
*Inhaled, ingested or transplacental – rabbits of 4 – 6 weeks appear most vulnerable<br />
*In utero infections => invasion of foetal lens => => => => => => multiplication and euption of spores later in the rabbit’s life => cataracts, lens rupture and phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
*Invasion of the mucosa per polar tube <br />
*Spiroplasm extruded and multiplication occurs in vacuole<br />
*Distribution by reticulo-endothelial cells => invasion of organs with high blood flow<br />
*Invasion of target organs <br />
*Intracellular multiplication, cell rupture (=> inflammation) and invasion of neighbouring cells or passage to circulation in 3-4 weeks<br />
*Shedding in urine 35 days after initial infection.<br />
<br />
==Presentations of ''Encephalitozoon cuniculi'' in pet rabbits==<br />
*Granulomatous nephritis or interstitial infiltration of lymphocytes and plasma cells <br />
**Usually asymptomatic <br />
**Possibly haematuria <br />
**Incontinence could be neurological in origin <br />
**Treat with benzimidazoles and antibiotics <br />
*Pyogranulomatous phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
**See treatment under [[Iridal Abscesses – Rabbit|iridal abscesses]]<br />
**Use topical ophthalmic preparations, parenteral oxytetracycline and a benzimidazole<br />
*Neurological manifestation of ''E. cuniculi'' infection: granulomatous encephalitis<br />
**Sometimes perivascular infiltration with lymphocytes and plasma <br />
**All areas of the brain<br />
**[[Head Tilt – Rabbit|Torticollis]]<br />
**Treatment<br />
***Initial short-acting corticosteroids, parenteral oxytetracycline and benzimidazoles awaiting lab results <br />
***Vestibular agents<br />
<br />
==Transmission of ''Encephalitozoon cuniculi''==<br />
*Shedding in urine<br />
*Oral and tracheal access<br />
*Neonates can be infected but can also receive immunity from dam.<br />
*[[:Category:Ectoparasites - Rabbit|Ectoparasites]] and [[:Category:Endoparasitism – Rabbit|endoparasites]]? May aid in transmission<br />
*Provision of recently cut short grass gathered from the wild<br />
<br />
==Pathology==<br />
*Principal target organs are kidney, brain, spinal cord<br />
*Other target organs include liver and heart<br />
*Rupture of host cell => invasion of neighbouring cells => chronic, granulomatous inflammation.<br />
*In utero infections => invasion of foetal lens => => => => => => multiplication and eruption of spores later in the rabbit’s life => cataracts, lens rupture and phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
<br />
==Survival of ''Encephalitozoon cuniculi'' in the environment==<br />
*Survives in extreme cold or heat <br />
*At average temperature and in dry conditions it survives 4 weeks<br />
*Easily killed by routine disinfection<br />
<br />
==Diagnosis==<br />
*Urine microscopy (35 days after initial infection)<br />
*Serology – antibodies develop soon after infection but clinical signs take much longer (several weeks)<br />
*Antibodies demonstrated 2 weeks before organisms can be demonstrated intracellularly and 4 weeks before histopathological changes are demonstrated in kidney or organisms demonstrated in urine (Harcourt Brown 2002)<br />
*PCR<br />
*CSF analysis<br />
**Procedure: <br />
***Propofol and intubation<br />
***Head flexed 90º to spine <br />
***38mm 22G spinal needle in cisterna magna<br />
***700-1000μl sample.<br />
***Vestibular signs are accentuated for up to 8hrs post sampling.<br />
**Findings<br />
***Lymphomonocytic pleocytosis 15 cells/μl (n=1.5 /μl) <br />
***Increased protein 0.79g/μl (n= 0.24g/μl) <br />
***Unfortunately other viral, protozoan or immune-mediated encephalitis may induce similar lymphomonocytic pleocytosis<br />
<br />
==Interpretation of ''Encephalitozoon'' antibody tests (Keeble 2007)==<br />
===Single positive result in healthy rabbit===<br />
*Recent infection prior to development of clinical signs<br />
*Chronically infected with no clinical signs<br />
*Previously infected and recovered<br />
*Antibody levels can persist for many years in symptomless animals<br />
<br />
===Single positive result in rabbit with clinical signs of encephalitozoonosis===<br />
*Could be active Encephalitozoon cuniculi infection (or other infection causing signs)<br />
<br />
===Single negative result in healthy rabbit===<br />
*Could be free from infection<br />
*Could be infected less than 2 weeks ago<br />
*Retest in four weeks<br />
<br />
===Single negative result in rabbit with clinical signs of encephalitozoonosis===<br />
*Rules out ''Encephalitozoon cuniculi'' infection as the cause of clinical signs<br />
*Advise further tests<br />
**renal biopsy<br />
**CSF analysis<br />
**mononulear pleocytosis and elevated protein<br />
**MRI/CT scans<br />
<br />
===To establish an ''Encephalitozoon''-free colony===<br />
*Test fortnightly for two months or until all animals are negative for a month, whichever is longer<br />
*Sacrifice any positive cases<br />
<br />
===Treatment=== <br />
*Albendazole q 24 hrs - ?teratogenic (Pollock 2006)<br />
*Fenbendazole q 24 hrs<br />
*Oxytetracycline SC q 72hrs.<br />
*Three possible therapies – my cocktail is albendazole and oxytetracycline as shown above.<br />
*Vestibular-calming agents<br />
*Environmental disinfection<br />
*Corticosteroids<br />
<br />
==References==<br />
[[Category:Neurological_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Encephalitozoon_cuniculi&diff=83224Encephalitozoon cuniculi2010-08-11T01:21:10Z<p>Clamy: /* Transmission of Encephalitozoon cuniculi */</p>
<hr />
<div>{{unfinished}}<br />
<br />
==Taxonomy==<br />
*Phylum Microspora; no mitochondria polar tube polar cap<br />
*Class Microsporida<br />
*Order Microsporidia<br />
*May be more related to fungi than to protozoa (Wasson and Peper 2000)<br />
*Obligate intracellular protozoan parasite<br />
*52% normal healthy domestic pet rabbits arte infected (Keeble and Shaw 2006)<br />
*Ubiquitous in other species too<br />
<br />
==The life cycle==<br />
The life cycle of this coccidian is 3 – 4 weeks in total:<br />
*Inhaled, ingested or transplacental – rabbits of 4 – 6 weeks appear most vulnerable<br />
*In utero infections => invasion of foetal lens => => => => => => multiplication and euption of spores later in the rabbit’s life => cataracts, lens rupture and phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
*Invasion of the mucosa per polar tube <br />
*Spiroplasm extruded and multiplication occurs in vacuole<br />
*Distribution by reticulo-endothelial cells => invasion of organs with high blood flow<br />
*Invasion of target organs <br />
*Intracellular multiplication, cell rupture (=> inflammation) and invasion of neighbouring cells or passage to circulation in 3-4 weeks<br />
*Shedding in urine 35 days after initial infection.<br />
<br />
==Presentations of ''Encephalitozoon cuniculi'' in pet rabbits==<br />
*Granulomatous nephritis or interstitial infiltration of lymphocytes and plasma cells <br />
**Usually asymptomatic <br />
**Possibly haematuria <br />
**Incontinence could be neurological in origin <br />
**Treat with benzimidazoles and antibiotics <br />
*Pyogranulomatous phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
**See treatment under [[Iridal Abscesses – Rabbit|iridal abscesses]]<br />
**Use topical ophthalmic preparations, parenteral oxytetracycline and a benzimidazole<br />
*Neurological manifestation of ''E. cuniculi'' infection: granulomatous encephalitis<br />
**Sometimes perivascular infiltration with lymphocytes and plasma <br />
**All areas of the brain<br />
**[[Head Tilt – Rabbit|Torticollis]]<br />
**Treatment<br />
***Initial short-acting corticosteroids, parenteral oxytetracycline and benzimidazoles awaiting lab results <br />
***Vestibular agents<br />
<br />
==Transmission of ''Encephalitozoon cuniculi''==<br />
*Shedding in urine<br />
*Oral and tracheal access<br />
*Neonates can be infected but can also receive immunity from dam.<br />
*[[:Category:Ectoparasites - Rabbit|Ectoparasites]]- and [[:Category:Endoparasitism – Rabbit|endoparasites]]? May aid in transmission<br />
*Provision of recently cut short grass gathered from the wild<br />
<br />
==Pathology==<br />
*Principal target organs are kidney, brain, spinal cord<br />
*Other target organs include liver and heart<br />
*Rupture of host cell => invasion of neighbouring cells => chronic, granulomatous inflammation.<br />
*In utero infections => invasion of foetal lens => => => => => => multiplication and eruption of spores later in the rabbit’s life => cataracts, lens rupture and phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
<br />
==Survival of ''Encephalitozoon cuniculi'' in the environment==<br />
*Survives in extreme cold or heat <br />
*At average temperature and in dry conditions it survives 4 weeks<br />
*Easily killed by routine disinfection<br />
<br />
==Diagnosis==<br />
*Urine microscopy (35 days after initial infection)<br />
*Serology – antibodies develop soon after infection but clinical signs take much longer (several weeks)<br />
*Antibodies demonstrated 2 weeks before organisms can be demonstrated intracellularly and 4 weeks before histopathological changes are demonstrated in kidney or organisms demonstrated in urine (Harcourt Brown 2002)<br />
*PCR<br />
*CSF analysis<br />
**Procedure: <br />
***Propofol and intubation<br />
***Head flexed 90º to spine <br />
***38mm 22G spinal needle in cisterna magna<br />
***700-1000μl sample.<br />
***Vestibular signs are accentuated for up to 8hrs post sampling.<br />
**Findings<br />
***Lymphomonocytic pleocytosis 15 cells/μl (n=1.5 /μl) <br />
***Increased protein 0.79g/μl (n= 0.24g/μl) <br />
***Unfortunately other viral, protozoan or immune-mediated encephalitis may induce similar lymphomonocytic pleocytosis<br />
<br />
==Interpretation of ''Encephalitozoon'' antibody tests (Keeble 2007)==<br />
===Single positive result in healthy rabbit===<br />
*Recent infection prior to development of clinical signs<br />
*Chronically infected with no clinical signs<br />
*Previously infected and recovered<br />
*Antibody levels can persist for many years in symptomless animals<br />
<br />
===Single positive result in rabbit with clinical signs of encephalitozoonosis===<br />
*Could be active Encephalitozoon cuniculi infection (or other infection causing signs)<br />
<br />
===Single negative result in healthy rabbit===<br />
*Could be free from infection<br />
*Could be infected less than 2 weeks ago<br />
*Retest in four weeks<br />
<br />
===Single negative result in rabbit with clinical signs of encephalitozoonosis===<br />
*Rules out ''Encephalitozoon cuniculi'' infection as the cause of clinical signs<br />
*Advise further tests<br />
**renal biopsy<br />
**CSF analysis<br />
**mononulear pleocytosis and elevated protein<br />
**MRI/CT scans<br />
<br />
===To establish an ''Encephalitozoon''-free colony===<br />
*Test fortnightly for two months or until all animals are negative for a month, whichever is longer<br />
*Sacrifice any positive cases<br />
<br />
===Treatment=== <br />
*Albendazole q 24 hrs - ?teratogenic (Pollock 2006)<br />
*Fenbendazole q 24 hrs<br />
*Oxytetracycline SC q 72hrs.<br />
*Three possible therapies – my cocktail is albendazole and oxytetracycline as shown above.<br />
*Vestibular-calming agents<br />
*Environmental disinfection<br />
*Corticosteroids<br />
<br />
==References==<br />
[[Category:Neurological_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Encephalitozoon_cuniculi&diff=83223Encephalitozoon cuniculi2010-08-11T01:20:15Z<p>Clamy: /* Transmission of Encephalitozoon cuniculi */</p>
<hr />
<div>{{unfinished}}<br />
<br />
==Taxonomy==<br />
*Phylum Microspora; no mitochondria polar tube polar cap<br />
*Class Microsporida<br />
*Order Microsporidia<br />
*May be more related to fungi than to protozoa (Wasson and Peper 2000)<br />
*Obligate intracellular protozoan parasite<br />
*52% normal healthy domestic pet rabbits arte infected (Keeble and Shaw 2006)<br />
*Ubiquitous in other species too<br />
<br />
==The life cycle==<br />
The life cycle of this coccidian is 3 – 4 weeks in total:<br />
*Inhaled, ingested or transplacental – rabbits of 4 – 6 weeks appear most vulnerable<br />
*In utero infections => invasion of foetal lens => => => => => => multiplication and euption of spores later in the rabbit’s life => cataracts, lens rupture and phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
*Invasion of the mucosa per polar tube <br />
*Spiroplasm extruded and multiplication occurs in vacuole<br />
*Distribution by reticulo-endothelial cells => invasion of organs with high blood flow<br />
*Invasion of target organs <br />
*Intracellular multiplication, cell rupture (=> inflammation) and invasion of neighbouring cells or passage to circulation in 3-4 weeks<br />
*Shedding in urine 35 days after initial infection.<br />
<br />
==Presentations of ''Encephalitozoon cuniculi'' in pet rabbits==<br />
*Granulomatous nephritis or interstitial infiltration of lymphocytes and plasma cells <br />
**Usually asymptomatic <br />
**Possibly haematuria <br />
**Incontinence could be neurological in origin <br />
**Treat with benzimidazoles and antibiotics <br />
*Pyogranulomatous phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
**See treatment under [[Iridal Abscesses – Rabbit|iridal abscesses]]<br />
**Use topical ophthalmic preparations, parenteral oxytetracycline and a benzimidazole<br />
*Neurological manifestation of ''E. cuniculi'' infection: granulomatous encephalitis<br />
**Sometimes perivascular infiltration with lymphocytes and plasma <br />
**All areas of the brain<br />
**[[Head Tilt – Rabbit|Torticollis]]<br />
**Treatment<br />
***Initial short-acting corticosteroids, parenteral oxytetracycline and benzimidazoles awaiting lab results <br />
***Vestibular agents<br />
<br />
==Transmission of ''Encephalitozoon cuniculi''==<br />
*Shedding in urine<br />
*Oral and tracheal access<br />
*Neonates can be infected but can also receive immunity from dam.<br />
*[[:Category:Ectoparasites - Rabbit|Ecto]]- and endo-parasites? May aid in transmission<br />
*Provision of recently cut short grass gathered from the wild<br />
<br />
==Pathology==<br />
*Principal target organs are kidney, brain, spinal cord<br />
*Other target organs include liver and heart<br />
*Rupture of host cell => invasion of neighbouring cells => chronic, granulomatous inflammation.<br />
*In utero infections => invasion of foetal lens => => => => => => multiplication and eruption of spores later in the rabbit’s life => cataracts, lens rupture and phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
<br />
==Survival of ''Encephalitozoon cuniculi'' in the environment==<br />
*Survives in extreme cold or heat <br />
*At average temperature and in dry conditions it survives 4 weeks<br />
*Easily killed by routine disinfection<br />
<br />
==Diagnosis==<br />
*Urine microscopy (35 days after initial infection)<br />
*Serology – antibodies develop soon after infection but clinical signs take much longer (several weeks)<br />
*Antibodies demonstrated 2 weeks before organisms can be demonstrated intracellularly and 4 weeks before histopathological changes are demonstrated in kidney or organisms demonstrated in urine (Harcourt Brown 2002)<br />
*PCR<br />
*CSF analysis<br />
**Procedure: <br />
***Propofol and intubation<br />
***Head flexed 90º to spine <br />
***38mm 22G spinal needle in cisterna magna<br />
***700-1000μl sample.<br />
***Vestibular signs are accentuated for up to 8hrs post sampling.<br />
**Findings<br />
***Lymphomonocytic pleocytosis 15 cells/μl (n=1.5 /μl) <br />
***Increased protein 0.79g/μl (n= 0.24g/μl) <br />
***Unfortunately other viral, protozoan or immune-mediated encephalitis may induce similar lymphomonocytic pleocytosis<br />
<br />
==Interpretation of ''Encephalitozoon'' antibody tests (Keeble 2007)==<br />
===Single positive result in healthy rabbit===<br />
*Recent infection prior to development of clinical signs<br />
*Chronically infected with no clinical signs<br />
*Previously infected and recovered<br />
*Antibody levels can persist for many years in symptomless animals<br />
<br />
===Single positive result in rabbit with clinical signs of encephalitozoonosis===<br />
*Could be active Encephalitozoon cuniculi infection (or other infection causing signs)<br />
<br />
===Single negative result in healthy rabbit===<br />
*Could be free from infection<br />
*Could be infected less than 2 weeks ago<br />
*Retest in four weeks<br />
<br />
===Single negative result in rabbit with clinical signs of encephalitozoonosis===<br />
*Rules out ''Encephalitozoon cuniculi'' infection as the cause of clinical signs<br />
*Advise further tests<br />
**renal biopsy<br />
**CSF analysis<br />
**mononulear pleocytosis and elevated protein<br />
**MRI/CT scans<br />
<br />
===To establish an ''Encephalitozoon''-free colony===<br />
*Test fortnightly for two months or until all animals are negative for a month, whichever is longer<br />
*Sacrifice any positive cases<br />
<br />
===Treatment=== <br />
*Albendazole q 24 hrs - ?teratogenic (Pollock 2006)<br />
*Fenbendazole q 24 hrs<br />
*Oxytetracycline SC q 72hrs.<br />
*Three possible therapies – my cocktail is albendazole and oxytetracycline as shown above.<br />
*Vestibular-calming agents<br />
*Environmental disinfection<br />
*Corticosteroids<br />
<br />
==References==<br />
[[Category:Neurological_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Encephalitozoon_cuniculi&diff=83222Encephalitozoon cuniculi2010-08-11T01:19:22Z<p>Clamy: /* Transmission of Encephalitozoon cuniculi */</p>
<hr />
<div>{{unfinished}}<br />
<br />
==Taxonomy==<br />
*Phylum Microspora; no mitochondria polar tube polar cap<br />
*Class Microsporida<br />
*Order Microsporidia<br />
*May be more related to fungi than to protozoa (Wasson and Peper 2000)<br />
*Obligate intracellular protozoan parasite<br />
*52% normal healthy domestic pet rabbits arte infected (Keeble and Shaw 2006)<br />
*Ubiquitous in other species too<br />
<br />
==The life cycle==<br />
The life cycle of this coccidian is 3 – 4 weeks in total:<br />
*Inhaled, ingested or transplacental – rabbits of 4 – 6 weeks appear most vulnerable<br />
*In utero infections => invasion of foetal lens => => => => => => multiplication and euption of spores later in the rabbit’s life => cataracts, lens rupture and phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
*Invasion of the mucosa per polar tube <br />
*Spiroplasm extruded and multiplication occurs in vacuole<br />
*Distribution by reticulo-endothelial cells => invasion of organs with high blood flow<br />
*Invasion of target organs <br />
*Intracellular multiplication, cell rupture (=> inflammation) and invasion of neighbouring cells or passage to circulation in 3-4 weeks<br />
*Shedding in urine 35 days after initial infection.<br />
<br />
==Presentations of ''Encephalitozoon cuniculi'' in pet rabbits==<br />
*Granulomatous nephritis or interstitial infiltration of lymphocytes and plasma cells <br />
**Usually asymptomatic <br />
**Possibly haematuria <br />
**Incontinence could be neurological in origin <br />
**Treat with benzimidazoles and antibiotics <br />
*Pyogranulomatous phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
**See treatment under [[Iridal Abscesses – Rabbit|iridal abscesses]]<br />
**Use topical ophthalmic preparations, parenteral oxytetracycline and a benzimidazole<br />
*Neurological manifestation of ''E. cuniculi'' infection: granulomatous encephalitis<br />
**Sometimes perivascular infiltration with lymphocytes and plasma <br />
**All areas of the brain<br />
**[[Head Tilt – Rabbit|Torticollis]]<br />
**Treatment<br />
***Initial short-acting corticosteroids, parenteral oxytetracycline and benzimidazoles awaiting lab results <br />
***Vestibular agents<br />
<br />
==Transmission of ''Encephalitozoon cuniculi''==<br />
*Shedding in urine<br />
*Oral and tracheal access<br />
*Neonates can be infected but can also receive immunity from dam.<br />
*[[Category:Ectoparasites - Rabbit|Ecto]]- and endo-parasites? May aid in transmission<br />
*Provision of recently cut short grass gathered from the wild<br />
<br />
==Pathology==<br />
*Principal target organs are kidney, brain, spinal cord<br />
*Other target organs include liver and heart<br />
*Rupture of host cell => invasion of neighbouring cells => chronic, granulomatous inflammation.<br />
*In utero infections => invasion of foetal lens => => => => => => multiplication and eruption of spores later in the rabbit’s life => cataracts, lens rupture and phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
<br />
==Survival of ''Encephalitozoon cuniculi'' in the environment==<br />
*Survives in extreme cold or heat <br />
*At average temperature and in dry conditions it survives 4 weeks<br />
*Easily killed by routine disinfection<br />
<br />
==Diagnosis==<br />
*Urine microscopy (35 days after initial infection)<br />
*Serology – antibodies develop soon after infection but clinical signs take much longer (several weeks)<br />
*Antibodies demonstrated 2 weeks before organisms can be demonstrated intracellularly and 4 weeks before histopathological changes are demonstrated in kidney or organisms demonstrated in urine (Harcourt Brown 2002)<br />
*PCR<br />
*CSF analysis<br />
**Procedure: <br />
***Propofol and intubation<br />
***Head flexed 90º to spine <br />
***38mm 22G spinal needle in cisterna magna<br />
***700-1000μl sample.<br />
***Vestibular signs are accentuated for up to 8hrs post sampling.<br />
**Findings<br />
***Lymphomonocytic pleocytosis 15 cells/μl (n=1.5 /μl) <br />
***Increased protein 0.79g/μl (n= 0.24g/μl) <br />
***Unfortunately other viral, protozoan or immune-mediated encephalitis may induce similar lymphomonocytic pleocytosis<br />
<br />
==Interpretation of ''Encephalitozoon'' antibody tests (Keeble 2007)==<br />
===Single positive result in healthy rabbit===<br />
*Recent infection prior to development of clinical signs<br />
*Chronically infected with no clinical signs<br />
*Previously infected and recovered<br />
*Antibody levels can persist for many years in symptomless animals<br />
<br />
===Single positive result in rabbit with clinical signs of encephalitozoonosis===<br />
*Could be active Encephalitozoon cuniculi infection (or other infection causing signs)<br />
<br />
===Single negative result in healthy rabbit===<br />
*Could be free from infection<br />
*Could be infected less than 2 weeks ago<br />
*Retest in four weeks<br />
<br />
===Single negative result in rabbit with clinical signs of encephalitozoonosis===<br />
*Rules out ''Encephalitozoon cuniculi'' infection as the cause of clinical signs<br />
*Advise further tests<br />
**renal biopsy<br />
**CSF analysis<br />
**mononulear pleocytosis and elevated protein<br />
**MRI/CT scans<br />
<br />
===To establish an ''Encephalitozoon''-free colony===<br />
*Test fortnightly for two months or until all animals are negative for a month, whichever is longer<br />
*Sacrifice any positive cases<br />
<br />
===Treatment=== <br />
*Albendazole q 24 hrs - ?teratogenic (Pollock 2006)<br />
*Fenbendazole q 24 hrs<br />
*Oxytetracycline SC q 72hrs.<br />
*Three possible therapies – my cocktail is albendazole and oxytetracycline as shown above.<br />
*Vestibular-calming agents<br />
*Environmental disinfection<br />
*Corticosteroids<br />
<br />
==References==<br />
[[Category:Neurological_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Encephalitozoon_cuniculi&diff=83221Encephalitozoon cuniculi2010-08-11T01:17:58Z<p>Clamy: /* To establish an Encephalitozoon-free colony */</p>
<hr />
<div>{{unfinished}}<br />
<br />
==Taxonomy==<br />
*Phylum Microspora; no mitochondria polar tube polar cap<br />
*Class Microsporida<br />
*Order Microsporidia<br />
*May be more related to fungi than to protozoa (Wasson and Peper 2000)<br />
*Obligate intracellular protozoan parasite<br />
*52% normal healthy domestic pet rabbits arte infected (Keeble and Shaw 2006)<br />
*Ubiquitous in other species too<br />
<br />
==The life cycle==<br />
The life cycle of this coccidian is 3 – 4 weeks in total:<br />
*Inhaled, ingested or transplacental – rabbits of 4 – 6 weeks appear most vulnerable<br />
*In utero infections => invasion of foetal lens => => => => => => multiplication and euption of spores later in the rabbit’s life => cataracts, lens rupture and phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
*Invasion of the mucosa per polar tube <br />
*Spiroplasm extruded and multiplication occurs in vacuole<br />
*Distribution by reticulo-endothelial cells => invasion of organs with high blood flow<br />
*Invasion of target organs <br />
*Intracellular multiplication, cell rupture (=> inflammation) and invasion of neighbouring cells or passage to circulation in 3-4 weeks<br />
*Shedding in urine 35 days after initial infection.<br />
<br />
==Presentations of ''Encephalitozoon cuniculi'' in pet rabbits==<br />
*Granulomatous nephritis or interstitial infiltration of lymphocytes and plasma cells <br />
**Usually asymptomatic <br />
**Possibly haematuria <br />
**Incontinence could be neurological in origin <br />
**Treat with benzimidazoles and antibiotics <br />
*Pyogranulomatous phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
**See treatment under [[Iridal Abscesses – Rabbit|iridal abscesses]]<br />
**Use topical ophthalmic preparations, parenteral oxytetracycline and a benzimidazole<br />
*Neurological manifestation of ''E. cuniculi'' infection: granulomatous encephalitis<br />
**Sometimes perivascular infiltration with lymphocytes and plasma <br />
**All areas of the brain<br />
**[[Head Tilt – Rabbit|Torticollis]]<br />
**Treatment<br />
***Initial short-acting corticosteroids, parenteral oxytetracycline and benzimidazoles awaiting lab results <br />
***Vestibular agents<br />
<br />
==Transmission of ''Encephalitozoon cuniculi''==<br />
*Shedding in urine<br />
*Oral and tracheal access<br />
*Neonates can be infected but can also receive immunity from dam.<br />
*Ecto- and endo-parasites? May aid in transmission<br />
*Provision of recently cut short grass gathered from the wild<br />
<br />
==Pathology==<br />
*Principal target organs are kidney, brain, spinal cord<br />
*Other target organs include liver and heart<br />
*Rupture of host cell => invasion of neighbouring cells => chronic, granulomatous inflammation.<br />
*In utero infections => invasion of foetal lens => => => => => => multiplication and eruption of spores later in the rabbit’s life => cataracts, lens rupture and phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
<br />
==Survival of ''Encephalitozoon cuniculi'' in the environment==<br />
*Survives in extreme cold or heat <br />
*At average temperature and in dry conditions it survives 4 weeks<br />
*Easily killed by routine disinfection<br />
<br />
==Diagnosis==<br />
*Urine microscopy (35 days after initial infection)<br />
*Serology – antibodies develop soon after infection but clinical signs take much longer (several weeks)<br />
*Antibodies demonstrated 2 weeks before organisms can be demonstrated intracellularly and 4 weeks before histopathological changes are demonstrated in kidney or organisms demonstrated in urine (Harcourt Brown 2002)<br />
*PCR<br />
*CSF analysis<br />
**Procedure: <br />
***Propofol and intubation<br />
***Head flexed 90º to spine <br />
***38mm 22G spinal needle in cisterna magna<br />
***700-1000μl sample.<br />
***Vestibular signs are accentuated for up to 8hrs post sampling.<br />
**Findings<br />
***Lymphomonocytic pleocytosis 15 cells/μl (n=1.5 /μl) <br />
***Increased protein 0.79g/μl (n= 0.24g/μl) <br />
***Unfortunately other viral, protozoan or immune-mediated encephalitis may induce similar lymphomonocytic pleocytosis<br />
<br />
==Interpretation of ''Encephalitozoon'' antibody tests (Keeble 2007)==<br />
===Single positive result in healthy rabbit===<br />
*Recent infection prior to development of clinical signs<br />
*Chronically infected with no clinical signs<br />
*Previously infected and recovered<br />
*Antibody levels can persist for many years in symptomless animals<br />
<br />
===Single positive result in rabbit with clinical signs of encephalitozoonosis===<br />
*Could be active Encephalitozoon cuniculi infection (or other infection causing signs)<br />
<br />
===Single negative result in healthy rabbit===<br />
*Could be free from infection<br />
*Could be infected less than 2 weeks ago<br />
*Retest in four weeks<br />
<br />
===Single negative result in rabbit with clinical signs of encephalitozoonosis===<br />
*Rules out ''Encephalitozoon cuniculi'' infection as the cause of clinical signs<br />
*Advise further tests<br />
**renal biopsy<br />
**CSF analysis<br />
**mononulear pleocytosis and elevated protein<br />
**MRI/CT scans<br />
<br />
===To establish an ''Encephalitozoon''-free colony===<br />
*Test fortnightly for two months or until all animals are negative for a month, whichever is longer<br />
*Sacrifice any positive cases<br />
<br />
===Treatment=== <br />
*Albendazole q 24 hrs - ?teratogenic (Pollock 2006)<br />
*Fenbendazole q 24 hrs<br />
*Oxytetracycline SC q 72hrs.<br />
*Three possible therapies – my cocktail is albendazole and oxytetracycline as shown above.<br />
*Vestibular-calming agents<br />
*Environmental disinfection<br />
*Corticosteroids<br />
<br />
==References==<br />
[[Category:Neurological_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Encephalitozoon_cuniculi&diff=83220Encephalitozoon cuniculi2010-08-11T01:17:43Z<p>Clamy: /* Interpretation of Encephalitozoon antibody tests (Keeble 2007) */</p>
<hr />
<div>{{unfinished}}<br />
<br />
==Taxonomy==<br />
*Phylum Microspora; no mitochondria polar tube polar cap<br />
*Class Microsporida<br />
*Order Microsporidia<br />
*May be more related to fungi than to protozoa (Wasson and Peper 2000)<br />
*Obligate intracellular protozoan parasite<br />
*52% normal healthy domestic pet rabbits arte infected (Keeble and Shaw 2006)<br />
*Ubiquitous in other species too<br />
<br />
==The life cycle==<br />
The life cycle of this coccidian is 3 – 4 weeks in total:<br />
*Inhaled, ingested or transplacental – rabbits of 4 – 6 weeks appear most vulnerable<br />
*In utero infections => invasion of foetal lens => => => => => => multiplication and euption of spores later in the rabbit’s life => cataracts, lens rupture and phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
*Invasion of the mucosa per polar tube <br />
*Spiroplasm extruded and multiplication occurs in vacuole<br />
*Distribution by reticulo-endothelial cells => invasion of organs with high blood flow<br />
*Invasion of target organs <br />
*Intracellular multiplication, cell rupture (=> inflammation) and invasion of neighbouring cells or passage to circulation in 3-4 weeks<br />
*Shedding in urine 35 days after initial infection.<br />
<br />
==Presentations of ''Encephalitozoon cuniculi'' in pet rabbits==<br />
*Granulomatous nephritis or interstitial infiltration of lymphocytes and plasma cells <br />
**Usually asymptomatic <br />
**Possibly haematuria <br />
**Incontinence could be neurological in origin <br />
**Treat with benzimidazoles and antibiotics <br />
*Pyogranulomatous phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
**See treatment under [[Iridal Abscesses – Rabbit|iridal abscesses]]<br />
**Use topical ophthalmic preparations, parenteral oxytetracycline and a benzimidazole<br />
*Neurological manifestation of ''E. cuniculi'' infection: granulomatous encephalitis<br />
**Sometimes perivascular infiltration with lymphocytes and plasma <br />
**All areas of the brain<br />
**[[Head Tilt – Rabbit|Torticollis]]<br />
**Treatment<br />
***Initial short-acting corticosteroids, parenteral oxytetracycline and benzimidazoles awaiting lab results <br />
***Vestibular agents<br />
<br />
==Transmission of ''Encephalitozoon cuniculi''==<br />
*Shedding in urine<br />
*Oral and tracheal access<br />
*Neonates can be infected but can also receive immunity from dam.<br />
*Ecto- and endo-parasites? May aid in transmission<br />
*Provision of recently cut short grass gathered from the wild<br />
<br />
==Pathology==<br />
*Principal target organs are kidney, brain, spinal cord<br />
*Other target organs include liver and heart<br />
*Rupture of host cell => invasion of neighbouring cells => chronic, granulomatous inflammation.<br />
*In utero infections => invasion of foetal lens => => => => => => multiplication and eruption of spores later in the rabbit’s life => cataracts, lens rupture and phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
<br />
==Survival of ''Encephalitozoon cuniculi'' in the environment==<br />
*Survives in extreme cold or heat <br />
*At average temperature and in dry conditions it survives 4 weeks<br />
*Easily killed by routine disinfection<br />
<br />
==Diagnosis==<br />
*Urine microscopy (35 days after initial infection)<br />
*Serology – antibodies develop soon after infection but clinical signs take much longer (several weeks)<br />
*Antibodies demonstrated 2 weeks before organisms can be demonstrated intracellularly and 4 weeks before histopathological changes are demonstrated in kidney or organisms demonstrated in urine (Harcourt Brown 2002)<br />
*PCR<br />
*CSF analysis<br />
**Procedure: <br />
***Propofol and intubation<br />
***Head flexed 90º to spine <br />
***38mm 22G spinal needle in cisterna magna<br />
***700-1000μl sample.<br />
***Vestibular signs are accentuated for up to 8hrs post sampling.<br />
**Findings<br />
***Lymphomonocytic pleocytosis 15 cells/μl (n=1.5 /μl) <br />
***Increased protein 0.79g/μl (n= 0.24g/μl) <br />
***Unfortunately other viral, protozoan or immune-mediated encephalitis may induce similar lymphomonocytic pleocytosis<br />
<br />
==Interpretation of ''Encephalitozoon'' antibody tests (Keeble 2007)==<br />
===Single positive result in healthy rabbit===<br />
*Recent infection prior to development of clinical signs<br />
*Chronically infected with no clinical signs<br />
*Previously infected and recovered<br />
*Antibody levels can persist for many years in symptomless animals<br />
<br />
===Single positive result in rabbit with clinical signs of encephalitozoonosis===<br />
*Could be active Encephalitozoon cuniculi infection (or other infection causing signs)<br />
<br />
===Single negative result in healthy rabbit===<br />
*Could be free from infection<br />
*Could be infected less than 2 weeks ago<br />
*Retest in four weeks<br />
<br />
===Single negative result in rabbit with clinical signs of encephalitozoonosis===<br />
*Rules out ''Encephalitozoon cuniculi'' infection as the cause of clinical signs<br />
*Advise further tests<br />
**renal biopsy<br />
**CSF analysis<br />
**mononulear pleocytosis and elevated protein<br />
**MRI/CT scans<br />
<br />
===To establish an Encephalitozoon-free colony===<br />
*Test fortnightly for two months or until all animals are negative for a month, whichever is longer<br />
*Sacrifice any positive cases<br />
<br />
===Treatment=== <br />
*Albendazole q 24 hrs - ?teratogenic (Pollock 2006)<br />
*Fenbendazole q 24 hrs<br />
*Oxytetracycline SC q 72hrs.<br />
*Three possible therapies – my cocktail is albendazole and oxytetracycline as shown above.<br />
*Vestibular-calming agents<br />
*Environmental disinfection<br />
*Corticosteroids<br />
<br />
==References==<br />
[[Category:Neurological_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Encephalitozoon_cuniculi&diff=83219Encephalitozoon cuniculi2010-08-11T01:17:07Z<p>Clamy: </p>
<hr />
<div>{{unfinished}}<br />
<br />
==Taxonomy==<br />
*Phylum Microspora; no mitochondria polar tube polar cap<br />
*Class Microsporida<br />
*Order Microsporidia<br />
*May be more related to fungi than to protozoa (Wasson and Peper 2000)<br />
*Obligate intracellular protozoan parasite<br />
*52% normal healthy domestic pet rabbits arte infected (Keeble and Shaw 2006)<br />
*Ubiquitous in other species too<br />
<br />
==The life cycle==<br />
The life cycle of this coccidian is 3 – 4 weeks in total:<br />
*Inhaled, ingested or transplacental – rabbits of 4 – 6 weeks appear most vulnerable<br />
*In utero infections => invasion of foetal lens => => => => => => multiplication and euption of spores later in the rabbit’s life => cataracts, lens rupture and phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
*Invasion of the mucosa per polar tube <br />
*Spiroplasm extruded and multiplication occurs in vacuole<br />
*Distribution by reticulo-endothelial cells => invasion of organs with high blood flow<br />
*Invasion of target organs <br />
*Intracellular multiplication, cell rupture (=> inflammation) and invasion of neighbouring cells or passage to circulation in 3-4 weeks<br />
*Shedding in urine 35 days after initial infection.<br />
<br />
==Presentations of ''Encephalitozoon cuniculi'' in pet rabbits==<br />
*Granulomatous nephritis or interstitial infiltration of lymphocytes and plasma cells <br />
**Usually asymptomatic <br />
**Possibly haematuria <br />
**Incontinence could be neurological in origin <br />
**Treat with benzimidazoles and antibiotics <br />
*Pyogranulomatous phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
**See treatment under [[Iridal Abscesses – Rabbit|iridal abscesses]]<br />
**Use topical ophthalmic preparations, parenteral oxytetracycline and a benzimidazole<br />
*Neurological manifestation of ''E. cuniculi'' infection: granulomatous encephalitis<br />
**Sometimes perivascular infiltration with lymphocytes and plasma <br />
**All areas of the brain<br />
**[[Head Tilt – Rabbit|Torticollis]]<br />
**Treatment<br />
***Initial short-acting corticosteroids, parenteral oxytetracycline and benzimidazoles awaiting lab results <br />
***Vestibular agents<br />
<br />
==Transmission of ''Encephalitozoon cuniculi''==<br />
*Shedding in urine<br />
*Oral and tracheal access<br />
*Neonates can be infected but can also receive immunity from dam.<br />
*Ecto- and endo-parasites? May aid in transmission<br />
*Provision of recently cut short grass gathered from the wild<br />
<br />
==Pathology==<br />
*Principal target organs are kidney, brain, spinal cord<br />
*Other target organs include liver and heart<br />
*Rupture of host cell => invasion of neighbouring cells => chronic, granulomatous inflammation.<br />
*In utero infections => invasion of foetal lens => => => => => => multiplication and eruption of spores later in the rabbit’s life => cataracts, lens rupture and phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
<br />
==Survival of ''Encephalitozoon cuniculi'' in the environment==<br />
*Survives in extreme cold or heat <br />
*At average temperature and in dry conditions it survives 4 weeks<br />
*Easily killed by routine disinfection<br />
<br />
==Diagnosis==<br />
*Urine microscopy (35 days after initial infection)<br />
*Serology – antibodies develop soon after infection but clinical signs take much longer (several weeks)<br />
*Antibodies demonstrated 2 weeks before organisms can be demonstrated intracellularly and 4 weeks before histopathological changes are demonstrated in kidney or organisms demonstrated in urine (Harcourt Brown 2002)<br />
*PCR<br />
*CSF analysis<br />
**Procedure: <br />
***Propofol and intubation<br />
***Head flexed 90º to spine <br />
***38mm 22G spinal needle in cisterna magna<br />
***700-1000μl sample.<br />
***Vestibular signs are accentuated for up to 8hrs post sampling.<br />
**Findings<br />
***Lymphomonocytic pleocytosis 15 cells/μl (n=1.5 /μl) <br />
***Increased protein 0.79g/μl (n= 0.24g/μl) <br />
***Unfortunately other viral, protozoan or immune-mediated encephalitis may induce similar lymphomonocytic pleocytosis<br />
<br />
==Interpretation of Encephalitozoon antibody tests (Keeble 2007)==<br />
===Single positive result in healthy rabbit===<br />
*Recent infection prior to development of clinical signs<br />
*Chronically infected with no clinical signs<br />
*Previously infected and recovered<br />
*Antibody levels can persist for many years in symptomless animals<br />
<br />
===Single positive result in rabbit with clinical signs of encephalitozoonosis===<br />
*Could be active Encephalitozoon cuniculi infection (or other infection causing signs)<br />
<br />
===Single negative result in healthy rabbit===<br />
*Could be free from infection<br />
*Could be infected less than 2 weeks ago<br />
*Retest in four weeks<br />
<br />
===Single negative result in rabbit with clinical signs of encephalitozoonosis===<br />
*Rules out ''Encephalitozoon cuniculi'' infection as the cause of clinical signs<br />
*Advise further tests<br />
**renal biopsy<br />
**CSF analysis<br />
**mononulear pleocytosis and elevated protein<br />
**MRI/CT scans<br />
<br />
===To establish an Encephalitozoon-free colony===<br />
*Test fortnightly for two months or until all animals are negative for a month, whichever is longer<br />
*Sacrifice any positive cases<br />
<br />
===Treatment=== <br />
*Albendazole q 24 hrs - ?teratogenic (Pollock 2006)<br />
*Fenbendazole q 24 hrs<br />
*Oxytetracycline SC q 72hrs.<br />
*Three possible therapies – my cocktail is albendazole and oxytetracycline as shown above.<br />
*Vestibular-calming agents<br />
*Environmental disinfection<br />
*Corticosteroids<br />
<br />
==References==<br />
[[Category:Neurological_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Encephalitozoon_cuniculi&diff=83218Encephalitozoon cuniculi2010-08-11T01:15:45Z<p>Clamy: /* Interpretation of Encephalitozoon antibody tests (Keeble 2007) */</p>
<hr />
<div>{{unfinished}}<br />
<br />
==Taxonomy==<br />
*Phylum Microspora; no mitochondria polar tube polar cap<br />
*Class Microsporida<br />
*Order Microsporidia<br />
*May be more related to fungi than to protozoa (Wasson and Peper 2000)<br />
*Obligate intracellular protozoan parasite<br />
*52% normal healthy domestic pet rabbits arte infected (Keeble and Shaw 2006)<br />
*Ubiquitous in other species too<br />
<br />
==The life cycle==<br />
The life cycle of this coccidian is 3 – 4 weeks in total:<br />
*Inhaled, ingested or transplacental – rabbits of 4 – 6 weeks appear most vulnerable<br />
*In utero infections => invasion of foetal lens => => => => => => multiplication and euption of spores later in the rabbit’s life => cataracts, lens rupture and phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
*Invasion of the mucosa per polar tube <br />
*Spiroplasm extruded and multiplication occurs in vacuole<br />
*Distribution by reticulo-endothelial cells => invasion of organs with high blood flow<br />
*Invasion of target organs <br />
*Intracellular multiplication, cell rupture (=> inflammation) and invasion of neighbouring cells or passage to circulation in 3-4 weeks<br />
*Shedding in urine 35 days after initial infection.<br />
<br />
==Presentations of ''Encephalitozoon cuniculi'' in pet rabbits==<br />
*Granulomatous nephritis or interstitial infiltration of lymphocytes and plasma cells <br />
**Usually asymptomatic <br />
**Possibly haematuria <br />
**Incontinence could be neurological in origin <br />
**Treat with benzimidazoles and antibiotics <br />
*Pyogranulomatous phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
**See treatment under [[Iridal Abscesses – Rabbit|iridal abscesses]]<br />
**Use topical ophthalmic preparations, parenteral oxytetracycline and a benzimidazole<br />
*Neurological manifestation of ''E. cuniculi'' infection: granulomatous encephalitis<br />
**Sometimes perivascular infiltration with lymphocytes and plasma <br />
**All areas of the brain<br />
**[[Head Tilt – Rabbit|Torticollis]]<br />
**Treatment<br />
***Initial short-acting corticosteroids, parenteral oxytetracycline and benzimidazoles awaiting lab results <br />
***Vestibular agents<br />
<br />
==Transmission of ''Encephalitozoon cuniculi''==<br />
*Shedding in urine<br />
*Oral and tracheal access<br />
*Neonates can be infected but can also receive immunity from dam.<br />
*Ecto- and endo-parasites? May aid in transmission<br />
*Provision of recently cut short grass gathered from the wild<br />
<br />
==Pathology==<br />
*Principal target organs are kidney, brain, spinal cord<br />
*Other target organs include liver and heart<br />
*Rupture of host cell => invasion of neighbouring cells => chronic, granulomatous inflammation.<br />
*In utero infections => invasion of foetal lens => => => => => => multiplication and eruption of spores later in the rabbit’s life => cataracts, lens rupture and phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
<br />
==Survival of ''Encephalitozoon cuniculi'' in the environment==<br />
*Survives in extreme cold or heat <br />
*At average temperature and in dry conditions it survives 4 weeks<br />
*Easily killed by routine disinfection<br />
<br />
==Diagnosis==<br />
*Urine microscopy (35 days after initial infection)<br />
*Serology – antibodies develop soon after infection but clinical signs take much longer (several weeks)<br />
*Antibodies demonstrated 2 weeks before organisms can be demonstrated intracellularly and 4 weeks before histopathological changes are demonstrated in kidney or organisms demonstrated in urine (Harcourt Brown 2002)<br />
*PCR<br />
*CSF analysis<br />
**Procedure: <br />
***Propofol and intubation<br />
***Head flexed 90º to spine <br />
***38mm 22G spinal needle in cisterna magna<br />
***700-1000μl sample.<br />
***Vestibular signs are accentuated for up to 8hrs post sampling.<br />
**Findings<br />
***Lymphomonocytic pleocytosis 15 cells/μl (n=1.5 /μl) <br />
***Increased protein 0.79g/μl (n= 0.24g/μl) <br />
***Unfortunately other viral, protozoan or immune-mediated encephalitis may induce similar lymphomonocytic pleocytosis<br />
<br />
==Interpretation of Encephalitozoon antibody tests (Keeble 2007)==<br />
===Single positive result in healthy rabbit===<br />
*Recent infection prior to development of clinical signs<br />
*Chronically infected with no clinical signs<br />
*Previously infected and recovered<br />
*Antibody levels can persist for many years in symptomless animals<br />
<br />
===Single positive result in rabbit with clinical signs of encephalitozoonosis===<br />
*Could be active Encephalitozoon cuniculi infection (or other infection causing signs)<br />
<br />
===Single negative result in healthy rabbit===<br />
*Could be free from infection<br />
*Could be infected less than 2 weeks ago<br />
*Retest in four weeks<br />
<br />
===Single negative result in rabbit with clinical signs of encephalitozoonosis===<br />
*Rules out ''Encephalitozoon cuniculi'' infection as the cause of clinical signs<br />
*Advise further tests<br />
**renal biopsy<br />
**CSF analysis<br />
**mononulear pleocytosis and elevated protein<br />
**MRI/CT scans<br />
<br />
===To establish an Encephalitozoon-free colony===<br />
*Test fortnightly for two months or until all animals are negative for a month, whichever is longer<br />
*Sacrifice any positive cases<br />
<br />
===Treatment=== <br />
*Albendazole q 24 hrs - ?teratogenic (Pollock 2006)<br />
*Fenbendazole q 24 hrs<br />
*Oxytetracycline SC q 72hrs.<br />
*Three possible therapies – my cocktail is albendazole and oxytetracycline as shown above.<br />
*Vestibular-calming agents<br />
*Environmental disinfection<br />
*Corticosteroids</div>Clamyhttps://en.wikivet.net/index.php?title=Encephalitozoon_cuniculi&diff=83217Encephalitozoon cuniculi2010-08-11T01:14:11Z<p>Clamy: /* Presentations of Encephalitozoon cuniculi in pet rabbits */</p>
<hr />
<div>{{unfinished}}<br />
<br />
==Taxonomy==<br />
*Phylum Microspora; no mitochondria polar tube polar cap<br />
*Class Microsporida<br />
*Order Microsporidia<br />
*May be more related to fungi than to protozoa (Wasson and Peper 2000)<br />
*Obligate intracellular protozoan parasite<br />
*52% normal healthy domestic pet rabbits arte infected (Keeble and Shaw 2006)<br />
*Ubiquitous in other species too<br />
<br />
==The life cycle==<br />
The life cycle of this coccidian is 3 – 4 weeks in total:<br />
*Inhaled, ingested or transplacental – rabbits of 4 – 6 weeks appear most vulnerable<br />
*In utero infections => invasion of foetal lens => => => => => => multiplication and euption of spores later in the rabbit’s life => cataracts, lens rupture and phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
*Invasion of the mucosa per polar tube <br />
*Spiroplasm extruded and multiplication occurs in vacuole<br />
*Distribution by reticulo-endothelial cells => invasion of organs with high blood flow<br />
*Invasion of target organs <br />
*Intracellular multiplication, cell rupture (=> inflammation) and invasion of neighbouring cells or passage to circulation in 3-4 weeks<br />
*Shedding in urine 35 days after initial infection.<br />
<br />
==Presentations of ''Encephalitozoon cuniculi'' in pet rabbits==<br />
*Granulomatous nephritis or interstitial infiltration of lymphocytes and plasma cells <br />
**Usually asymptomatic <br />
**Possibly haematuria <br />
**Incontinence could be neurological in origin <br />
**Treat with benzimidazoles and antibiotics <br />
*Pyogranulomatous phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
**See treatment under [[Iridal Abscesses – Rabbit|iridal abscesses]]<br />
**Use topical ophthalmic preparations, parenteral oxytetracycline and a benzimidazole<br />
*Neurological manifestation of ''E. cuniculi'' infection: granulomatous encephalitis<br />
**Sometimes perivascular infiltration with lymphocytes and plasma <br />
**All areas of the brain<br />
**[[Head Tilt – Rabbit|Torticollis]]<br />
**Treatment<br />
***Initial short-acting corticosteroids, parenteral oxytetracycline and benzimidazoles awaiting lab results <br />
***Vestibular agents<br />
<br />
==Transmission of ''Encephalitozoon cuniculi''==<br />
*Shedding in urine<br />
*Oral and tracheal access<br />
*Neonates can be infected but can also receive immunity from dam.<br />
*Ecto- and endo-parasites? May aid in transmission<br />
*Provision of recently cut short grass gathered from the wild<br />
<br />
==Pathology==<br />
*Principal target organs are kidney, brain, spinal cord<br />
*Other target organs include liver and heart<br />
*Rupture of host cell => invasion of neighbouring cells => chronic, granulomatous inflammation.<br />
*In utero infections => invasion of foetal lens => => => => => => multiplication and eruption of spores later in the rabbit’s life => cataracts, lens rupture and phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
<br />
==Survival of ''Encephalitozoon cuniculi'' in the environment==<br />
*Survives in extreme cold or heat <br />
*At average temperature and in dry conditions it survives 4 weeks<br />
*Easily killed by routine disinfection<br />
<br />
==Diagnosis==<br />
*Urine microscopy (35 days after initial infection)<br />
*Serology – antibodies develop soon after infection but clinical signs take much longer (several weeks)<br />
*Antibodies demonstrated 2 weeks before organisms can be demonstrated intracellularly and 4 weeks before histopathological changes are demonstrated in kidney or organisms demonstrated in urine (Harcourt Brown 2002)<br />
*PCR<br />
*CSF analysis<br />
**Procedure: <br />
***Propofol and intubation<br />
***Head flexed 90º to spine <br />
***38mm 22G spinal needle in cisterna magna<br />
***700-1000μl sample.<br />
***Vestibular signs are accentuated for up to 8hrs post sampling.<br />
**Findings<br />
***Lymphomonocytic pleocytosis 15 cells/μl (n=1.5 /μl) <br />
***Increased protein 0.79g/μl (n= 0.24g/μl) <br />
***Unfortunately other viral, protozoan or immune-mediated encephalitis may induce similar lymphomonocytic pleocytosis<br />
<br />
==Interpretation of Encephalitozoon antibody tests (Keeble 2007)==<br />
Single positive result in healthy rabbit<br />
*Recent infection prior to development of clinical signs<br />
*Chronically infected with no clinical signs<br />
*Previously infected and recovered<br />
*Antibody levels can persist for many years in symptomless animals<br />
<br />
Single positive result in rabbit with clinical signs of encephalitozoonosis<br />
*Could be active Encephalitozoon cuniculi infection (or other infection causing signs)<br />
<br />
Single negative result in healthy rabbit<br />
*Could be free from infection<br />
*Could be infected less than 2 weeks ago<br />
*Retest in four weeks<br />
<br />
Single negative result in rabbit with clinical signs of encephalitozoonosis<br />
*Rules out Encephalitozoon cuniculi infection as the cause of clinical signs<br />
*Advise further tests<br />
**renal biopsy<br />
**CSF analysis<br />
**mononulear pleocytosis and elevated protein<br />
**MRI/CT scans<br />
<br />
To establish an Encephalitozoon-free colony:<br />
*Test fortnightly for two months or until all animals are negative for a month, whichever is longer<br />
*Sacrifice any positive cases<br />
<br />
Treatment <br />
*Albendazole 10 mg/kg q 24 hrs - ?teratogenic (Pollock 2006)<br />
*Fenbendazole 20 mg/kg q 24 hrs<br />
*Oxytetracycline 30 mg/kg SC q 72hrs.<br />
*Three possible therapies – my cocktail is albendazole and oxytetracycline as shown above.<br />
*Vestibular-calming agents<br />
*Environmental disinfection<br />
*Corticosteroids</div>Clamyhttps://en.wikivet.net/index.php?title=Encephalitozoon_cuniculi&diff=83216Encephalitozoon cuniculi2010-08-11T01:10:20Z<p>Clamy: Created page with "{{unfinished}} ==Taxonomy== *Phylum Microspora; no mitochondria polar tube polar cap *Class Microsporida *Order Microsporidia *May be more related to fungi than to protozoa (Was..."</p>
<hr />
<div>{{unfinished}}<br />
<br />
==Taxonomy==<br />
*Phylum Microspora; no mitochondria polar tube polar cap<br />
*Class Microsporida<br />
*Order Microsporidia<br />
*May be more related to fungi than to protozoa (Wasson and Peper 2000)<br />
*Obligate intracellular protozoan parasite<br />
*52% normal healthy domestic pet rabbits arte infected (Keeble and Shaw 2006)<br />
*Ubiquitous in other species too<br />
<br />
==The life cycle==<br />
The life cycle of this coccidian is 3 – 4 weeks in total:<br />
*Inhaled, ingested or transplacental – rabbits of 4 – 6 weeks appear most vulnerable<br />
*In utero infections => invasion of foetal lens => => => => => => multiplication and euption of spores later in the rabbit’s life => cataracts, lens rupture and phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
*Invasion of the mucosa per polar tube <br />
*Spiroplasm extruded and multiplication occurs in vacuole<br />
*Distribution by reticulo-endothelial cells => invasion of organs with high blood flow<br />
*Invasion of target organs <br />
*Intracellular multiplication, cell rupture (=> inflammation) and invasion of neighbouring cells or passage to circulation in 3-4 weeks<br />
*Shedding in urine 35 days after initial infection.<br />
<br />
==Presentations of ''Encephalitozoon cuniculi'' in pet rabbits==<br />
*Granulomatous encephalitis, sometimes perivascular infiltration with lymphocytes and plasma cells in all areas of the brain<br />
*Granulomatous nephritis or interstitial infiltration of lymphocytes and plasma cells <br />
**Usually asymptomatic <br />
**Possibly haematuria <br />
**Incontinence could be neurological in origin <br />
**Treat with benzimidazoles and antibiotics <br />
*Pyogranulomatous phacoclastic uveitis<br />
<br />
==Transmission of ''Encephalitozoon cuniculi''==<br />
*Shedding in urine<br />
*Oral and tracheal access<br />
*Neonates can be infected but can also receive immunity from dam.<br />
*Ecto- and endo-parasites? May aid in transmission<br />
*Provision of recently cut short grass gathered from the wild<br />
<br />
==Pathology==<br />
*Principal target organs are kidney, brain, spinal cord<br />
*Other target organs include liver and heart<br />
*Rupture of host cell => invasion of neighbouring cells => chronic, granulomatous inflammation.<br />
*In utero infections => invasion of foetal lens => => => => => => multiplication and eruption of spores later in the rabbit’s life => cataracts, lens rupture and phacoclastic [[Uveitis – Rabbit|uveitis]]<br />
<br />
==Survival of ''Encephalitozoon cuniculi'' in the environment==<br />
*Survives in extreme cold or heat <br />
*At average temperature and in dry conditions it survives 4 weeks<br />
*Easily killed by routine disinfection<br />
<br />
==Diagnosis==<br />
*Urine microscopy (35 days after initial infection)<br />
*Serology – antibodies develop soon after infection but clinical signs take much longer (several weeks)<br />
*Antibodies demonstrated 2 weeks before organisms can be demonstrated intracellularly and 4 weeks before histopathological changes are demonstrated in kidney or organisms demonstrated in urine (Harcourt Brown 2002)<br />
*PCR<br />
*CSF analysis<br />
**Procedure: <br />
***Propofol and intubation<br />
***Head flexed 90º to spine <br />
***38mm 22G spinal needle in cisterna magna<br />
***700-1000μl sample.<br />
***Vestibular signs are accentuated for up to 8hrs post sampling.<br />
**Findings<br />
***Lymphomonocytic pleocytosis 15 cells/μl (n=1.5 /μl) <br />
***Increased protein 0.79g/μl (n= 0.24g/μl) <br />
***Unfortunately other viral, protozoan or immune-mediated encephalitis may induce similar lymphomonocytic pleocytosis<br />
<br />
==Interpretation of Encephalitozoon antibody tests (Keeble 2007)==<br />
Single positive result in healthy rabbit<br />
*Recent infection prior to development of clinical signs<br />
*Chronically infected with no clinical signs<br />
*Previously infected and recovered<br />
*Antibody levels can persist for many years in symptomless animals<br />
<br />
Single positive result in rabbit with clinical signs of encephalitozoonosis<br />
*Could be active Encephalitozoon cuniculi infection (or other infection causing signs)<br />
<br />
Single negative result in healthy rabbit<br />
*Could be free from infection<br />
*Could be infected less than 2 weeks ago<br />
*Retest in four weeks<br />
<br />
Single negative result in rabbit with clinical signs of encephalitozoonosis<br />
*Rules out Encephalitozoon cuniculi infection as the cause of clinical signs<br />
*Advise further tests<br />
**renal biopsy<br />
**CSF analysis<br />
**mononulear pleocytosis and elevated protein<br />
**MRI/CT scans<br />
<br />
To establish an Encephalitozoon-free colony:<br />
*Test fortnightly for two months or until all animals are negative for a month, whichever is longer<br />
*Sacrifice any positive cases<br />
<br />
Treatment <br />
*Albendazole 10 mg/kg q 24 hrs - ?teratogenic (Pollock 2006)<br />
*Fenbendazole 20 mg/kg q 24 hrs<br />
*Oxytetracycline 30 mg/kg SC q 72hrs.<br />
*Three possible therapies – my cocktail is albendazole and oxytetracycline as shown above.<br />
*Vestibular-calming agents<br />
*Environmental disinfection<br />
*Corticosteroids</div>Clamyhttps://en.wikivet.net/index.php?title=Head_Tilt_%E2%80%93_Rabbit&diff=83215Head Tilt – Rabbit2010-08-11T00:58:26Z<p>Clamy: </p>
<hr />
<div>{{unfinished}}<br />
{| cellpadding="10" cellspacing="0" border="1" <br />
| Also known as:<br />
| '''Torticollis<br />
|-<br />
|}<br />
<br />
The main common neurological disorder of rabbits is head tilt or torticollis; there are several causes.<br />
<br />
==Aetiology==<br />
===Peripheral vestibular disease=== <br />
Peripheral vestibular diseases corresponds to an extension of otitis externa or from the nasal cavity to the middle or inner ear via the Eustachian tube, the trigeminal nerve or by a haematogenous route so it is often associated with respiratory infections. <br />
<br />
The causative organisms include ''P. multocida'', ''Staphylococcus'' spp., ''Bordetella bronchiseptica'', ''E. coli'', ''Pseudomonas aeruginosa''. Psoroptiasis should also be considered. <br />
<br />
Treatment includes antibiotics for ''Pasteurella'' (also see The Pasteurellar Syndrome) and/or acaricides for psoroptiasis (see chapter on skin disorders). <br />
<br />
Various pharmacotherapeutic approaches have been suggested to alleviate the clinical signs:<br />
*Meclozine (Sea-Legs®; SSL International) PO q6–8hrs is suggested to control spinning of affected rabbits (Saunders 2002; Keeble 2006). <br />
*Prochlorperazine (Stemetil®; Distriphar) – PO q8-12hr – oral suspension. If the case is so bad that you can’t manage oral medication, I suppose it might be worth trying a SC dose but the outer pack is 10 ampoules of 12.5mg each and you have the Cascade to consider)<br />
*Personally I’d try cinnarizine (Stugeron®; Janssen Cilag) – I found it useful in dogs with head tilt or idiopathic trigeminal neuropathy so it might help to stabilise a rabbit a bit during the early stages of a head tilt disorder – untested in this species – you have been warned!<br />
<br />
===Organisms causative of central vestibular or cerebellar disease=== <br />
These include the bacteria listed above as causing peripheral vestibular disease (with the addition of ''Listeria monocytogenes'')and also protozoan diseases (eg. ''Encephalitozoon cuniculi'' and ''Toxoplasma gondii''). ''Encephalitozoon'' is not found in the inner ear tissue, only in the CNS where it causes a non-suppurative meningitis and a granulomatous encephalitis, sometimes accompanied by perivascular infiltration with lymphocytes and plasma cells. All areas of the brain are affected.<br />
<br />
''E. cuniculi'' may yield biochemical test results indicative of renal disorder and positive serology for ''E. cuniculi'' antibodies. Note that ''E. cuniculi'' also causes ophthalmic lesions (capsular rupture, cataract development and phacoclastic [[Uveitis – Rabbit|uveitis]]). <br />
<br />
Treatment of ''E. cuniculi'' is described [[Encephalitozoon cuniculi – Rabbit|here]]. For treatment of toxoplasmosis consider sulphonamides and be aware that clindamycin is extremely toxic in this species.<br />
<br />
===Miscellaneous causes of head tilt in rabbits===<br />
Cerebral larva migrans (''Baylisascaris procyonis'') has also been incriminated. Neoplasia has been diagnosed on MRI or CT scans. Cerebrovascular accidents may also be diagnosed on MRI and propentofylline or nicergoline are suggested as treatments. Another possible cause is trauma, including bites to the back of the neck: supportive treatment should rely on antibiosis and analgesics.<br />
<br />
Cerebral mycoses are unlikely to be encountered in the UK. I’d try itraconazole but I would be very dubious of success, given the time take from initial infection to onset of signs and the slow build up of itraconazole to therapeutically effective plasma levels.<br />
<br />
Toxicoses: <br />
*Lead – house rabbits which nibble wires etc. Signs include depression lethargy inappetance and “subtle neurologic changes” (Hillyer 1994). Calcium EDTA: q6hrs (Richardson 2000). Saunders (2002) suggests metoclopramide or cisapride (if it ever becomes available), to promote gastrointestinal motility and decreasing the absorption of the heavy metal.<br />
*Woolly milk pod contamination of hay in the USA.<br />
<br />
==Clinical signs of central and peripheral vestibular disease==<br />
Differentiate between central (eg. Encephalitoonosis) and peripheral (eg. Pasteurellosis) vestibular disease in rabbits (Harcourt Brown 2002). Both show: <br />
*Loss of balance<br />
*Head tilt<br />
*Falling<br />
*Horizontal nystagmus<br />
*Rotary nystagmus<br />
*Ventrolateral strabismus<br />
*Signs shown in central but not in peripheral vestibular disease<br />
*Rolling<br />
*Vertical nystagmus<br />
*Positional nystagmus<br />
*Signs shown sometimes in central but never in peripheral vestibular disease <br />
**Intention tremor (cerebellar) <br />
**Hemiparesis with ipsilateral postural reaction deficits<br />
*Mentation<br />
**Central vestibular cases are possibly depressed whereas peripheral cases are probably not<br />
<br />
===Diagnostics to differentiate between Encephalitoonosis and Pasteurellosis===<br />
*Radiographic changes seen in tympanic bulla in pasteurellosis<br />
*Serology<br />
*Haematology – neutrophilia and a shift to the left might indicate bacterial infection<br />
<br />
==Therapeutic approach to head tilt in rabbits==<br />
*Oxytetracycline IM and low dose + corticosteroid IM + benzimidazoles<br />
*Diazepam IM<br />
*Meclozine PO q6–8hrs <br />
*Prochlorperazine PO q8-12hr – oral suspension. <br />
*Cinnarizine q 12–24 h<br />
<br />
===Corticosteroids in rabbits===<br />
*Consider absorption from topical applications<br />
*Compromisation of premunity <br />
*In anorexia, mobilizes free fatty acids from adipose tissue => hepatic lipidosis<br />
*Increased populations of intestinal coliforms<br />
*Ratio of aerobes to anaerobes alters<br />
*Reserve for acute cases<br />
<br />
'''Note: Chronic pruritic seborroeic otitis is usually associated with yeasts (''Candida'' sp.) whereas purulent otitis, especially where the discharge is tacky and sticky, may show ''E. coli'' and ''Pseudomonas'' sp on culture.'''<br />
<br />
==References==<br />
*Hillyer, E. V. (1994) Pet Rabbits. Veterinary Clinics of North America: Small Animal Practice. 24 (1) 25-65. <br />
*Keeble, E. (2006) Nervous and Musculoskeletal Disorders in BSAVA Manual of Rabbit Medicine and Surgery eds Meredith A and Flecknell P, 2nd Edition 2006, published by BSAVA Quedgley Glocs<br />
*Richardson, V. (2000) Rabbits: Health, husbandry and disease. Blackwell Science, Oxford<br />
*Saunders, R. (2002) Understanding Head Tilt in Rabbits "New Directions": Small Animal Eyes and Ears (from the publishers of Veterinary Times) Issue 1, Volume 1, Feb 2002 pages 4-5 <br />
<br />
[[Category:Neurological_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Head_Tilt_%E2%80%93_Rabbit&diff=83214Head Tilt – Rabbit2010-08-11T00:55:01Z<p>Clamy: </p>
<hr />
<div>{{unfinished}}<br />
{| cellpadding="10" cellspacing="0" border="1" <br />
| Also known as:<br />
| '''Torticollis<br />
|-<br />
|}<br />
<br />
The main common neurological disorder of rabbits is head tilt or torticollis. <br />
There are several causes<br />
<br />
==Aetiology==<br />
===Peripheral vestibular disease=== <br />
Peripheral vestibular diseases corresponds to an extension of otitis externa or from the nasal cavity to the middle or inner ear via the Eustachian tube, the trigeminal nerve or by a haematogenous route so it is often associated with respiratory infections. <br />
<br />
The causative organisms include ''P. multocida'', ''Staphylococcus'' spp., ''Bordetella bronchiseptica'', ''E. coli'', ''Pseudomonas aeruginosa''. Psoroptiasis should also be considered. <br />
<br />
Treatment includes antibiotics for ''Pasteurella'' (also see The Pasteurellar Syndrome) and/or acaricides for psoroptiasis (see chapter on skin disorders). <br />
<br />
Various pharmacotherapeutic approaches have been suggested to alleviate the clinical signs:<br />
*Meclozine (Sea-Legs®; SSL International) PO q6–8hrs is suggested to control spinning of affected rabbits (Saunders 2002; Keeble 2006). <br />
*Prochlorperazine (Stemetil®; Distriphar) – PO q8-12hr – oral suspension. If the case is so bad that you can’t manage oral medication, I suppose it might be worth trying a SC dose but the outer pack is 10 ampoules of 12.5mg each and you have the Cascade to consider)<br />
*Personally I’d try cinnarizine (Stugeron®; Janssen Cilag) – I found it useful in dogs with head tilt or idiopathic trigeminal neuropathy so it might help to stabilise a rabbit a bit during the early stages of a head tilt disorder – untested in this species – you have been warned!<br />
<br />
===Organisms causative of central vestibular or cerebellar disease=== <br />
These include the bacteria listed above as causing peripheral vestibular disease (with the addition of ''Listeria monocytogenes'')and also protozoan diseases (eg. ''Encephalitozoon cuniculi'' and ''Toxoplasma gondii''). ''Encephalitozoon'' is not found in the inner ear tissue, only in the CNS where it causes a non-suppurative meningitis and a granulomatous encephalitis, sometimes accompanied by perivascular infiltration with lymphocytes and plasma cells. All areas of the brain are affected.<br />
<br />
E cuniculi may yield biochemical test results indicative of renal disorder and positive serology for E cuniculi antibodies. Note E cuniculi also causes ophthalmic lesions (capsular rupture, cataract development and phacoclastic [[Uveitis – Rabbit|uveitis]]). <br />
<br />
Treatment of ''E. cuniculi'' is described [[Encephalitozoon cuniculi – Rabbit|here]]. For treatment of toxoplasmosis consider sulphonamides and be aware that clindamycin is extremely toxic in this species.<br />
<br />
===Miscellaneous causes of head tilt in rabbits===<br />
Cerebral larva migrans (''Baylisascaris procyonis'') has also been incriminated. Neoplasia has been diagnosed on MRI or CT scans. Cerebrovascular accidents may also be diagnosed on MRI and propentofylline or nicergoline are suggested as treatments. Another possible cause is trauma, including bites to the back of the neck: supportive treatment should rely on antibiosis and analgesics.<br />
<br />
Cerebral mycoses are unlikely to be encountered in the UK. I’d try itraconazole but I would be very dubious of success, given the time take from initial infection to onset of signs and the slow build up of itraconazole to therapeutically effective plasma levels.<br />
<br />
Toxicoses: <br />
*Lead – house rabbits which nibble wires etc. Signs include depression lethargy inappetance and “subtle neurologic changes” (Hillyer 1994). Calcium EDTA: q6hrs (Richardson 2000). Saunders (2002) suggests metoclopramide or cisapride (if it ever becomes available), to promote gastrointestinal motility and decreasing the absorption of the heavy metal.<br />
*Woolly milk pod contamination of hay in the USA.<br />
<br />
==Clinical signs of central and peripheral vestibular disease==<br />
Differentiate between central (eg. Encephalitoonosis) and peripheral (eg. Pasteurellosis) vestibular disease in rabbits (Harcourt Brown 2002). Both show: <br />
*Loss of balance<br />
*Head tilt<br />
*Falling<br />
*Horizontal nystagmus<br />
*Rotary nystagmus<br />
*Ventrolateral strabismus<br />
*Signs shown in central but not in peripheral vestibular disease<br />
*Rolling<br />
*Vertical nystagmus<br />
*Positional nystagmus<br />
*Signs shown sometimes in central but never in peripheral vestibular disease <br />
**Intention tremor (cerebellar) <br />
**Hemiparesis with ipsilateral postural reaction deficits<br />
*Mentation<br />
**Central vestibular cases are possibly depressed whereas peripheral cases are probably not<br />
<br />
===Diagnostics to differentiate between Encephalitoonosis and Pasteurellosis===<br />
*Radiographic changes seen in tympanic bulla in pasteurellosis<br />
*Serology<br />
*Haematology – neutrophilia and a shift to the left might indicate bacterial infection<br />
<br />
==Therapeutic approach to head tilt in rabbits==<br />
*Oxytetracycline IM and low dose + corticosteroid IM + benzimidazoles<br />
*Diazepam IM<br />
*Meclozine PO q6–8hrs <br />
*Prochlorperazine PO q8-12hr – oral suspension. <br />
*Cinnarizine q 12–24 h<br />
<br />
===Corticosteroids in rabbits===<br />
*Consider absorption from topical applications<br />
*Compromisation of premunity <br />
*In anorexia, mobilizes free fatty acids from adipose tissue =>hepatic lipidosis<br />
*Increased populations of intestinal coliforms<br />
*Ratio of aerobes to anaerobes alters<br />
*Reserve for acute cases<br />
<br />
'''Note: Chronic pruritic seborroeic otitis is usually associated with yeasts (''Candida'' sp.) whereas purulent otitis, especially where the discharge is tacky and sticky, may show ''E. coli'' and ''Pseudomonas'' sp on culture.'''<br />
<br />
[[Category:Neurological_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Head_Tilt_%E2%80%93_Rabbit&diff=83212Head Tilt – Rabbit2010-08-11T00:53:11Z<p>Clamy: </p>
<hr />
<div>{{unfinished}}<br />
The main common neurological disorder of rabbits is head tilt or torticollis. <br />
There are several causes<br />
<br />
==Aetiology==<br />
===Peripheral vestibular disease=== <br />
Peripheral vestibular diseases corresponds to an extension of otitis externa or from the nasal cavity to the middle or inner ear via the Eustachian tube, the trigeminal nerve or by a haematogenous route so it is often associated with respiratory infections. <br />
<br />
The causative organisms include ''P. multocida'', ''Staphylococcus'' spp., ''Bordetella bronchiseptica'', ''E. coli'', ''Pseudomonas aeruginosa''. Psoroptiasis should also be considered. <br />
<br />
Treatment includes antibiotics for ''Pasteurella'' (also see The Pasteurellar Syndrome) and/or acaricides for psoroptiasis (see chapter on skin disorders). <br />
<br />
Various pharmacotherapeutic approaches have been suggested to alleviate the clinical signs:<br />
*Meclozine (Sea-Legs®; SSL International) PO q6–8hrs is suggested to control spinning of affected rabbits (Saunders 2002; Keeble 2006). <br />
*Prochlorperazine (Stemetil®; Distriphar) – PO q8-12hr – oral suspension. If the case is so bad that you can’t manage oral medication, I suppose it might be worth trying a SC dose but the outer pack is 10 ampoules of 12.5mg each and you have the Cascade to consider)<br />
*Personally I’d try cinnarizine (Stugeron®; Janssen Cilag) – I found it useful in dogs with head tilt or idiopathic trigeminal neuropathy so it might help to stabilise a rabbit a bit during the early stages of a head tilt disorder – untested in this species – you have been warned!<br />
<br />
===Organisms causative of central vestibular or cerebellar disease=== <br />
These include the bacteria listed above as causing peripheral vestibular disease (with the addition of ''Listeria monocytogenes'')and also protozoan diseases (eg. ''Encephalitozoon cuniculi'' and ''Toxoplasma gondii''). ''Encephalitozoon'' is not found in the inner ear tissue, only in the CNS where it causes a non-suppurative meningitis and a granulomatous encephalitis, sometimes accompanied by perivascular infiltration with lymphocytes and plasma cells. All areas of the brain are affected.<br />
<br />
E cuniculi may yield biochemical test results indicative of renal disorder and positive serology for E cuniculi antibodies. Note E cuniculi also causes ophthalmic lesions (capsular rupture, cataract development and phacoclastic [[Uveitis – Rabbit|uveitis]]). <br />
<br />
Treatment of ''E. cuniculi'' is described [[Encephalitozoon cuniculi – Rabbit|here]]. For treatment of toxoplasmosis consider sulphonamides and be aware that clindamycin is extremely toxic in this species.<br />
<br />
===Miscellaneous causes of head tilt in rabbits===<br />
Cerebral larva migrans (''Baylisascaris procyonis'') has also been incriminated. Neoplasia has been diagnosed on MRI or CT scans. Cerebrovascular accidents may also be diagnosed on MRI and propentofylline or nicergoline are suggested as treatments. Another possible cause is trauma, including bites to the back of the neck: supportive treatment should rely on antibiosis and analgesics.<br />
<br />
Cerebral mycoses are unlikely to be encountered in the UK. I’d try itraconazole but I would be very dubious of success, given the time take from initial infection to onset of signs and the slow build up of itraconazole to therapeutically effective plasma levels.<br />
<br />
Toxicoses: <br />
*Lead – house rabbits which nibble wires etc. Signs include depression lethargy inappetance and “subtle neurologic changes” (Hillyer 1994). Calcium EDTA: q6hrs (Richardson 2000). Saunders (2002) suggests metoclopramide or cisapride (if it ever becomes available), to promote gastrointestinal motility and decreasing the absorption of the heavy metal.<br />
*Woolly milk pod contamination of hay in the USA.<br />
<br />
==Clinical signs of central and peripheral vestibular disease==<br />
Differentiate between central (eg. Encephalitoonosis) and peripheral (eg. Pasteurellosis) vestibular disease in rabbits (Harcourt Brown 2002). Both show: <br />
*Loss of balance<br />
*Head tilt<br />
*Falling<br />
*Horizontal nystagmus<br />
*Rotary nystagmus<br />
*Ventrolateral strabismus<br />
*Signs shown in central but not in peripheral vestibular disease<br />
*Rolling<br />
*Vertical nystagmus<br />
*Positional nystagmus<br />
*Signs shown sometimes in central but never in peripheral vestibular disease <br />
**Intention tremor (cerebellar) <br />
**Hemiparesis with ipsilateral postural reaction deficits<br />
*Mentation<br />
**Central vestibular cases are possibly depressed whereas peripheral cases are probably not<br />
<br />
===Diagnostics to differentiate between Encephalitoonosis and Pasteurellosis===<br />
*Radiographic changes seen in tympanic bulla in pasteurellosis<br />
*Serology<br />
*Haematology – neutrophilia and a shift to the left might indicate bacterial infection<br />
<br />
==Therapeutic approach to head tilt in rabbits==<br />
*Oxytetracycline IM and low dose + corticosteroid IM + benzimidazoles<br />
*Diazepam IM<br />
*Meclozine PO q6–8hrs <br />
*Prochlorperazine PO q8-12hr – oral suspension. <br />
*Cinnarizine q 12–24 h<br />
<br />
===Corticosteroids in rabbits===<br />
*Consider absorption from topical applications<br />
*Compromisation of premunity <br />
*In anorexia, mobilizes free fatty acids from adipose tissue =>hepatic lipidosis<br />
*Increased populations of intestinal coliforms<br />
*Ratio of aerobes to anaerobes alters<br />
*Reserve for acute cases<br />
<br />
'''Note: Chronic pruritic seborroeic otitis is usually associated with yeasts (''Candida'' sp.) whereas purulent otitis, especially where the discharge is tacky and sticky, may show ''E. coli'' and ''Pseudomonas'' sp on culture.'''<br />
<br />
[[Category:Neurological_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Head_Tilt_%E2%80%93_Rabbit&diff=83211Head Tilt – Rabbit2010-08-11T00:51:39Z<p>Clamy: /* Organisms causative of central vestibular or cerebellar disease */</p>
<hr />
<div>{{unfinished}}<br />
The main common neurological disorder of rabbits is head tilt or torticollis. <br />
There are several causes<br />
<br />
==Aetiology==<br />
===Peripheral vestibular disease=== <br />
Peripheral vestibular diseases corresponds to an extension of otitis externa or from the nasal cavity to the middle or inner ear via the Eustachian tube, the trigeminal nerve or by a haematogenous route so it is often associated with respiratory infections. <br />
<br />
The causative organisms include ''P. multocida'', ''Staphylococcus'' spp., ''Bordetella bronchiseptica'', ''E. coli'', ''Pseudomonas aeruginosa''. Psoroptiasis should also be considered. <br />
<br />
Treatment includes antibiotics for ''Pasteurella'' (also see The Pasteurellar Syndrome) and/or acaricides for psoroptiasis (see chapter on skin disorders). <br />
<br />
Various pharmacotherapeutic approaches have been suggested to alleviate the clinical signs:<br />
*Meclozine (Sea-Legs®; SSL International) PO q6–8hrs is suggested to control spinning of affected rabbits (Saunders 2002; Keeble 2006). <br />
*Prochlorperazine (Stemetil®; Distriphar) – PO q8-12hr – oral suspension. If the case is so bad that you can’t manage oral medication, I suppose it might be worth trying a SC dose but the outer pack is 10 ampoules of 12.5mg each and you have the Cascade to consider)<br />
*Personally I’d try cinnarizine (Stugeron®; Janssen Cilag) – I found it useful in dogs with head tilt or idiopathic trigeminal neuropathy so it might help to stabilise a rabbit a bit during the early stages of a head tilt disorder – untested in this species – you have been warned!<br />
<br />
===Organisms causative of central vestibular or cerebellar disease=== <br />
These include the bacteria listed above as causing peripheral vestibular disease (with the addition of ''Listeria monocytogenes'')and also protozoan diseases (eg. ''Encephalitozoon cuniculi'' and ''Toxoplasma gondii''). ''Encephalitozoon'' is not found in the inner ear tissue, only in the CNS where it causes a non-suppurative meningitis and a granulomatous encephalitis, sometimes accompanied by perivascular infiltration with lymphocytes and plasma cells. All areas of the brain are affected.<br />
<br />
E cuniculi may yield biochemical test results indicative of renal disorder and positive serology for E cuniculi antibodies. Note E cuniculi also causes ophthalmic lesions (capsular rupture, cataract development and phacoclastic [[Uveitis – Rabbit|uveitis]]). <br />
<br />
Treatment of ''E. cuniculi'' is described [[Encephalitozoon cuniculi – Rabbit|here]]. For treatment of toxoplasmosis consider sulphonamides and be aware that clindamycin is extremely toxic in this species.<br />
<br />
===Miscellaneous causes of head tilt in rabbits===<br />
Cerebral larva migrans (''Baylisascaris procyonis'') has also been incriminated. Neoplasia has been diagnosed on MRI or CT scans. Cerebrovascular accidents may also be diagnosed on MRI and propentofylline or nicergoline are suggested as treatments. Another possible cause is trauma, including bites to the back of the neck: supportive treatment should rely on antibiosis and analgesics.<br />
<br />
Cerebral mycoses are unlikely to be encountered in the UK. I’d try itraconazole but I would be very dubious of success, given the time take from initial infection to onset of signs and the slow build up of itraconazole to therapeutically effective plasma levels.<br />
<br />
Toxicoses: <br />
*Lead – house rabbits which nibble wires etc. Signs include depression lethargy inappetance and “subtle neurologic changes” (Hillyer 1994). Calcium EDTA: q6hrs (Richardson 2000). Saunders (2002) suggests metoclopramide or cisapride (if it ever becomes available), to promote gastrointestinal motility and decreasing the absorption of the heavy metal.<br />
*Woolly milk pod contamination of hay in the USA.<br />
<br />
==Clinical signs of central and peripheral vestibular disease==<br />
Differentiate between central (eg. Encephalitoonosis) and peripheral (eg. Pasteurellosis) vestibular disease in rabbits (Harcourt Brown 2002). Both show: <br />
*Loss of balance<br />
*Head tilt<br />
*Falling<br />
*Horizontal nystagmus<br />
*Rotary nystagmus<br />
*Ventrolateral strabismus<br />
*Signs shown in central but not in peripheral vestibular disease<br />
*Rolling<br />
*Vertical nystagmus<br />
*Positional nystagmus<br />
*Signs shown sometimes in central but never in peripheral vestibular disease <br />
**Intention tremor (cerebellar) <br />
**Hemiparesis with ipsilateral postural reaction deficits<br />
*Mentation<br />
**Central vestibular cases are possibly depressed whereas peripheral cases are probably not<br />
<br />
===Diagnostics to differentiate between Encephalitoonosis and Pasteurellosis===<br />
*Radiographic changes seen in tympanic bulla in pasteurellosis<br />
*Serology<br />
*Haematology – neutrophilia and a shift to the left might indicate bacterial infection<br />
<br />
==Therapeutic approach to head tilt in rabbits==<br />
*Oxytetracycline IM and low dose + corticosteroid IM + benzimidazoles<br />
*Diazepam IM<br />
*Meclozine PO q6–8hrs <br />
*Prochlorperazine PO q8-12hr – oral suspension. <br />
*Cinnarizine q 12–24 h<br />
<br />
===Corticosteroids in rabbits===<br />
*Consider absorption from topical applications<br />
*Compromisation of premunity <br />
*In anorexia, mobilizes free fatty acids from adipose tissue =>hepatic lipidosis<br />
*Increased populations of intestinal coliforms<br />
*Ratio of aerobes to anaerobes alters<br />
*Reserve for acute cases<br />
<br />
'''Note: Chronic pruritic seborroeic otitis is usually associated with yeasts (''Candida'' sp.) whereas purulent otitis, especially where the discharge is tacky and sticky, may show ''E. coli'' and ''Pseudomonas'' sp on culture.'''</div>Clamyhttps://en.wikivet.net/index.php?title=Head_Tilt_%E2%80%93_Rabbit&diff=83210Head Tilt – Rabbit2010-08-11T00:50:20Z<p>Clamy: </p>
<hr />
<div>{{unfinished}}<br />
The main common neurological disorder of rabbits is head tilt or torticollis. <br />
There are several causes<br />
<br />
==Aetiology==<br />
===Peripheral vestibular disease=== <br />
Peripheral vestibular diseases corresponds to an extension of otitis externa or from the nasal cavity to the middle or inner ear via the Eustachian tube, the trigeminal nerve or by a haematogenous route so it is often associated with respiratory infections. <br />
<br />
The causative organisms include ''P. multocida'', ''Staphylococcus'' spp., ''Bordetella bronchiseptica'', ''E. coli'', ''Pseudomonas aeruginosa''. Psoroptiasis should also be considered. <br />
<br />
Treatment includes antibiotics for ''Pasteurella'' (also see The Pasteurellar Syndrome) and/or acaricides for psoroptiasis (see chapter on skin disorders). <br />
<br />
Various pharmacotherapeutic approaches have been suggested to alleviate the clinical signs:<br />
*Meclozine (Sea-Legs®; SSL International) PO q6–8hrs is suggested to control spinning of affected rabbits (Saunders 2002; Keeble 2006). <br />
*Prochlorperazine (Stemetil®; Distriphar) – PO q8-12hr – oral suspension. If the case is so bad that you can’t manage oral medication, I suppose it might be worth trying a SC dose but the outer pack is 10 ampoules of 12.5mg each and you have the Cascade to consider)<br />
*Personally I’d try cinnarizine (Stugeron®; Janssen Cilag) – I found it useful in dogs with head tilt or idiopathic trigeminal neuropathy so it might help to stabilise a rabbit a bit during the early stages of a head tilt disorder – untested in this species – you have been warned!<br />
<br />
===Organisms causative of central vestibular or cerebellar disease=== <br />
These include the bacteria listed above as causing peripheral vestibular disease (with the addition of ''Listeria monocytogenes'')and also protozoan diseases (eg. ''Encephalitozoon cuniculi'' and ''Toxoplasma gondii''). ''Encephalitozoon'' is not found in the inner ear tissue, only in the CNS where it causes a non-suppurative meningitis and a granulomatous encephalitis, sometimes accompanied by perivascular infiltration with lymphocytes and plasma cells. All areas of the brain are affected.<br />
<br />
E cuniculi may yield biochemical test results indicative of renal disorder and positive serology for E cuniculi antibodies. Note E cuniculi also causes ophthalmic lesions (capsular rupture, cataract development and phacoclastic [[Uveitis – Rabbit|uveitis]]). <br />
<br />
Treatment of ''E. cuniculi'' is described here. For treatment of toxoplasmosis consider sulphonamides and be aware that clindamycin is extremely toxic in this species.<br />
<br />
===Miscellaneous causes of head tilt in rabbits===<br />
Cerebral larva migrans (''Baylisascaris procyonis'') has also been incriminated. Neoplasia has been diagnosed on MRI or CT scans. Cerebrovascular accidents may also be diagnosed on MRI and propentofylline or nicergoline are suggested as treatments. Another possible cause is trauma, including bites to the back of the neck: supportive treatment should rely on antibiosis and analgesics.<br />
<br />
Cerebral mycoses are unlikely to be encountered in the UK. I’d try itraconazole but I would be very dubious of success, given the time take from initial infection to onset of signs and the slow build up of itraconazole to therapeutically effective plasma levels.<br />
<br />
Toxicoses: <br />
*Lead – house rabbits which nibble wires etc. Signs include depression lethargy inappetance and “subtle neurologic changes” (Hillyer 1994). Calcium EDTA: q6hrs (Richardson 2000). Saunders (2002) suggests metoclopramide or cisapride (if it ever becomes available), to promote gastrointestinal motility and decreasing the absorption of the heavy metal.<br />
*Woolly milk pod contamination of hay in the USA.<br />
<br />
==Clinical signs of central and peripheral vestibular disease==<br />
Differentiate between central (eg. Encephalitoonosis) and peripheral (eg. Pasteurellosis) vestibular disease in rabbits (Harcourt Brown 2002). Both show: <br />
*Loss of balance<br />
*Head tilt<br />
*Falling<br />
*Horizontal nystagmus<br />
*Rotary nystagmus<br />
*Ventrolateral strabismus<br />
*Signs shown in central but not in peripheral vestibular disease<br />
*Rolling<br />
*Vertical nystagmus<br />
*Positional nystagmus<br />
*Signs shown sometimes in central but never in peripheral vestibular disease <br />
**Intention tremor (cerebellar) <br />
**Hemiparesis with ipsilateral postural reaction deficits<br />
*Mentation<br />
**Central vestibular cases are possibly depressed whereas peripheral cases are probably not<br />
<br />
===Diagnostics to differentiate between Encephalitoonosis and Pasteurellosis===<br />
*Radiographic changes seen in tympanic bulla in pasteurellosis<br />
*Serology<br />
*Haematology – neutrophilia and a shift to the left might indicate bacterial infection<br />
<br />
==Therapeutic approach to head tilt in rabbits==<br />
*Oxytetracycline IM and low dose + corticosteroid IM + benzimidazoles<br />
*Diazepam IM<br />
*Meclozine PO q6–8hrs <br />
*Prochlorperazine PO q8-12hr – oral suspension. <br />
*Cinnarizine q 12–24 h<br />
<br />
===Corticosteroids in rabbits===<br />
*Consider absorption from topical applications<br />
*Compromisation of premunity <br />
*In anorexia, mobilizes free fatty acids from adipose tissue =>hepatic lipidosis<br />
*Increased populations of intestinal coliforms<br />
*Ratio of aerobes to anaerobes alters<br />
*Reserve for acute cases<br />
<br />
'''Note: Chronic pruritic seborroeic otitis is usually associated with yeasts (''Candida'' sp.) whereas purulent otitis, especially where the discharge is tacky and sticky, may show ''E. coli'' and ''Pseudomonas'' sp on culture.'''</div>Clamyhttps://en.wikivet.net/index.php?title=Head_Tilt_%E2%80%93_Rabbit&diff=83209Head Tilt – Rabbit2010-08-11T00:49:52Z<p>Clamy: /* Therapeutic approach to head tilt in rabbits */</p>
<hr />
<div>{{unfinished}}<br />
The main common neurological disorder of rabbits is head tilt or torticollis. <br />
There are several causes<br />
<br />
==Aetiology==<br />
===Peripheral vestibular disease=== <br />
Peripheral vestibular diseases corresponds to an extension of otitis externa or from the nasal cavity to the middle or inner ear via the Eustachian tube, the trigeminal nerve or by a haematogenous route so it is often associated with respiratory infections. <br />
<br />
The causative organisms include ''P. multocida'', ''Staphylococcus'' spp., ''Bordetella bronchiseptica'', ''E. coli'', ''Pseudomonas aeruginosa''. Psoroptiasis should also be considered. <br />
<br />
Treatment includes antibiotics for ''Pasteurella'' (also see The Pasteurellar Syndrome) and/or acaricides for psoroptiasis (see chapter on skin disorders). <br />
<br />
Various pharmacotherapeutic approaches have been suggested to alleviate the clinical signs:<br />
*Meclozine (Sea-Legs®; SSL International) PO q6–8hrs is suggested to control spinning of affected rabbits (Saunders 2002; Keeble 2006). <br />
*Prochlorperazine (Stemetil®; Distriphar) – PO q8-12hr – oral suspension. If the case is so bad that you can’t manage oral medication, I suppose it might be worth trying a SC dose but the outer pack is 10 ampoules of 12.5mg each and you have the Cascade to consider)<br />
*Personally I’d try cinnarizine (Stugeron®; Janssen Cilag) – I found it useful in dogs with head tilt or idiopathic trigeminal neuropathy so it might help to stabilise a rabbit a bit during the early stages of a head tilt disorder – untested in this species – you have been warned!<br />
<br />
===Organisms causative of central vestibular or cerebellar disease=== <br />
These include the bacteria listed above as causing peripheral vestibular disease (with the addition of ''Listeria monocytogenes'')and also protozoan diseases (eg. ''Encephalitozoon cuniculi'' and ''Toxoplasma gondii''). ''Encephalitozoon'' is not found in the inner ear tissue, only in the CNS where it causes a non-suppurative meningitis and a granulomatous encephalitis, sometimes accompanied by perivascular infiltration with lymphocytes and plasma cells. All areas of the brain are affected.<br />
<br />
E cuniculi may yield biochemical test results indicative of renal disorder and positive serology for E cuniculi antibodies. Note E cuniculi also causes ophthalmic lesions (capsular rupture, cataract development and phacoclastic [[Uveitis – Rabbit|uveitis]]). <br />
<br />
Treatment of ''E. cuniculi'' is described here. For treatment of toxoplasmosis consider sulphonamides and be aware that clindamycin is extremely toxic in this species.<br />
<br />
===Miscellaneous causes of head tilt in rabbits===<br />
Cerebral larva migrans (''Baylisascaris procyonis'') has also been incriminated. Neoplasia has been diagnosed on MRI or CT scans. Cerebrovascular accidents may also be diagnosed on MRI and propentofylline or nicergoline are suggested as treatments. Another possible cause is trauma, including bites to the back of the neck: supportive treatment should rely on antibiosis and analgesics.<br />
<br />
Cerebral mycoses are unlikely to be encountered in the UK. I’d try itraconazole but I would be very dubious of success, given the time take from initial infection to onset of signs and the slow build up of itraconazole to therapeutically effective plasma levels.<br />
<br />
Toxicoses: <br />
*Lead – house rabbits which nibble wires etc. Signs include depression lethargy inappetance and “subtle neurologic changes” (Hillyer 1994). Calcium EDTA: q6hrs (Richardson 2000). Saunders (2002) suggests metoclopramide or cisapride (if it ever becomes available), to promote gastrointestinal motility and decreasing the absorption of the heavy metal.<br />
*Woolly milk pod contamination of hay in the USA.<br />
<br />
==Clinical signs of central and peripheral vestibular disease==<br />
Differentiate between central (eg. Encephalitoonosis) and peripheral (eg. Pasteurellosis) vestibular disease in rabbits (Harcourt Brown 2002). Both show: <br />
*Loss of balance<br />
*Head tilt<br />
*Falling<br />
*Horizontal nystagmus<br />
*Rotary nystagmus<br />
*Ventrolateral strabismus<br />
*Signs shown in central but not in peripheral vestibular disease<br />
*Rolling<br />
*Vertical nystagmus<br />
*Positional nystagmus<br />
*Signs shown sometimes in central but never in peripheral vestibular disease <br />
**Intention tremor (cerebellar) <br />
**Hemiparesis with ipsilateral postural reaction deficits<br />
*Mentation<br />
**Central vestibular cases are possibly depressed whereas peripheral cases are probably not<br />
<br />
===Diagnostics to differentiate between Encephalitoonosis and Pasteurellosis===<br />
*Radiographic changes seen in tympanic bulla in pasteurellosis<br />
*Serology<br />
*Haematology – neutrophilia and a shift to the left might indicate bacterial infection<br />
<br />
==Therapeutic approach to head tilt in rabbits==<br />
*Oxytetracycline IM and low dose + corticosteroid IM + benzimidazoles<br />
*Diazepam IM<br />
*Meclozine PO q6–8hrs <br />
*Prochlorperazine PO q8-12hr – oral suspension. <br />
*Cinnarizine q 12–24 h<br />
<br />
==Corticosteroids in rabbits==<br />
*Consider absorption from topical applications<br />
*Compromisation of premunity <br />
*In anorexia, mobilizes free fatty acids from adipose tissue =>hepatic lipidosis<br />
*Increased populations of intestinal coliforms<br />
*Ratio of aerobes to anaerobes alters<br />
*Reserve for acute cases<br />
<br />
'''Note: Chronic pruritic seborroeic otitis is usually associated with yeasts (''Candida'' sp.) whereas purulent otitis, especially where the discharge is tacky and sticky, may show ''E. coli'' and ''Pseudomonas'' sp on culture.'''</div>Clamyhttps://en.wikivet.net/index.php?title=Head_Tilt_%E2%80%93_Rabbit&diff=83208Head Tilt – Rabbit2010-08-11T00:49:22Z<p>Clamy: </p>
<hr />
<div>{{unfinished}}<br />
The main common neurological disorder of rabbits is head tilt or torticollis. <br />
There are several causes<br />
<br />
==Aetiology==<br />
===Peripheral vestibular disease=== <br />
Peripheral vestibular diseases corresponds to an extension of otitis externa or from the nasal cavity to the middle or inner ear via the Eustachian tube, the trigeminal nerve or by a haematogenous route so it is often associated with respiratory infections. <br />
<br />
The causative organisms include ''P. multocida'', ''Staphylococcus'' spp., ''Bordetella bronchiseptica'', ''E. coli'', ''Pseudomonas aeruginosa''. Psoroptiasis should also be considered. <br />
<br />
Treatment includes antibiotics for ''Pasteurella'' (also see The Pasteurellar Syndrome) and/or acaricides for psoroptiasis (see chapter on skin disorders). <br />
<br />
Various pharmacotherapeutic approaches have been suggested to alleviate the clinical signs:<br />
*Meclozine (Sea-Legs®; SSL International) PO q6–8hrs is suggested to control spinning of affected rabbits (Saunders 2002; Keeble 2006). <br />
*Prochlorperazine (Stemetil®; Distriphar) – PO q8-12hr – oral suspension. If the case is so bad that you can’t manage oral medication, I suppose it might be worth trying a SC dose but the outer pack is 10 ampoules of 12.5mg each and you have the Cascade to consider)<br />
*Personally I’d try cinnarizine (Stugeron®; Janssen Cilag) – I found it useful in dogs with head tilt or idiopathic trigeminal neuropathy so it might help to stabilise a rabbit a bit during the early stages of a head tilt disorder – untested in this species – you have been warned!<br />
<br />
===Organisms causative of central vestibular or cerebellar disease=== <br />
These include the bacteria listed above as causing peripheral vestibular disease (with the addition of ''Listeria monocytogenes'')and also protozoan diseases (eg. ''Encephalitozoon cuniculi'' and ''Toxoplasma gondii''). ''Encephalitozoon'' is not found in the inner ear tissue, only in the CNS where it causes a non-suppurative meningitis and a granulomatous encephalitis, sometimes accompanied by perivascular infiltration with lymphocytes and plasma cells. All areas of the brain are affected.<br />
<br />
E cuniculi may yield biochemical test results indicative of renal disorder and positive serology for E cuniculi antibodies. Note E cuniculi also causes ophthalmic lesions (capsular rupture, cataract development and phacoclastic [[Uveitis – Rabbit|uveitis]]). <br />
<br />
Treatment of ''E. cuniculi'' is described here. For treatment of toxoplasmosis consider sulphonamides and be aware that clindamycin is extremely toxic in this species.<br />
<br />
===Miscellaneous causes of head tilt in rabbits===<br />
Cerebral larva migrans (''Baylisascaris procyonis'') has also been incriminated. Neoplasia has been diagnosed on MRI or CT scans. Cerebrovascular accidents may also be diagnosed on MRI and propentofylline or nicergoline are suggested as treatments. Another possible cause is trauma, including bites to the back of the neck: supportive treatment should rely on antibiosis and analgesics.<br />
<br />
Cerebral mycoses are unlikely to be encountered in the UK. I’d try itraconazole but I would be very dubious of success, given the time take from initial infection to onset of signs and the slow build up of itraconazole to therapeutically effective plasma levels.<br />
<br />
Toxicoses: <br />
*Lead – house rabbits which nibble wires etc. Signs include depression lethargy inappetance and “subtle neurologic changes” (Hillyer 1994). Calcium EDTA: q6hrs (Richardson 2000). Saunders (2002) suggests metoclopramide or cisapride (if it ever becomes available), to promote gastrointestinal motility and decreasing the absorption of the heavy metal.<br />
*Woolly milk pod contamination of hay in the USA.<br />
<br />
==Clinical signs of central and peripheral vestibular disease==<br />
Differentiate between central (eg. Encephalitoonosis) and peripheral (eg. Pasteurellosis) vestibular disease in rabbits (Harcourt Brown 2002). Both show: <br />
*Loss of balance<br />
*Head tilt<br />
*Falling<br />
*Horizontal nystagmus<br />
*Rotary nystagmus<br />
*Ventrolateral strabismus<br />
*Signs shown in central but not in peripheral vestibular disease<br />
*Rolling<br />
*Vertical nystagmus<br />
*Positional nystagmus<br />
*Signs shown sometimes in central but never in peripheral vestibular disease <br />
**Intention tremor (cerebellar) <br />
**Hemiparesis with ipsilateral postural reaction deficits<br />
*Mentation<br />
**Central vestibular cases are possibly depressed whereas peripheral cases are probably not<br />
<br />
===Diagnostics to differentiate between Encephalitoonosis and Pasteurellosis===<br />
*Radiographic changes seen in tympanic bulla in pasteurellosis<br />
*Serology<br />
*Haematology – neutrophilia and a shift to the left might indicate bacterial infection<br />
<br />
==Therapeutic approach to head tilt in rabbits==<br />
*Oxytetracycline IM and low dose + corticosteroid eg 0.1-0.5mg/kg IM + benzimidazoles<br />
*Diazepam IM<br />
*Meclozine PO q6–8hrs <br />
*Prochlorperazine PO q8-12hr – oral suspension. <br />
*Cinnarizine q 12–24 h<br />
<br />
==Corticosteroids in rabbits==<br />
*Consider absorption from topical applications<br />
*Compromisation of premunity <br />
*In anorexia, mobilizes free fatty acids from adipose tissue =>hepatic lipidosis<br />
*Increased populations of intestinal coliforms<br />
*Ratio of aerobes to anaerobes alters<br />
*Reserve for acute cases<br />
<br />
'''Note: Chronic pruritic seborroeic otitis is usually associated with yeasts (''Candida'' sp.) whereas purulent otitis, especially where the discharge is tacky and sticky, may show ''E. coli'' and ''Pseudomonas'' sp on culture.'''</div>Clamyhttps://en.wikivet.net/index.php?title=Head_Tilt_%E2%80%93_Rabbit&diff=83207Head Tilt – Rabbit2010-08-11T00:48:33Z<p>Clamy: Created page with "{{unfinished}} The main common neurological disorder of rabbits is head tilt or torticollis. There are several causes ==Aetiology== ===Peripheral vestibular disease=== Periphe..."</p>
<hr />
<div>{{unfinished}}<br />
The main common neurological disorder of rabbits is head tilt or torticollis. <br />
There are several causes<br />
<br />
==Aetiology==<br />
===Peripheral vestibular disease=== <br />
Peripheral vestibular diseases corresponds to an extension of otitis externa or from the nasal cavity to the middle or inner ear via the Eustachian tube, the trigeminal nerve or by a haematogenous route so it is often associated with respiratory infections. <br />
<br />
The causative organisms include ''P. multocida'', ''Staphylococcus'' spp., ''Bordetella bronchiseptica'', ''E. coli'', ''Pseudomonas aeruginosa''. Psoroptiasis should also be considered. <br />
<br />
Treatment includes antibiotics for ''Pasteurella'' (also see The Pasteurellar Syndrome) and/or acaricides for psoroptiasis (see chapter on skin disorders). <br />
<br />
Various pharmacotherapeutic approaches have been suggested to alleviate the clinical signs:<br />
*Meclozine (Sea-Legs®; SSL International) PO q6–8hrs is suggested to control spinning of affected rabbits (Saunders 2002; Keeble 2006). <br />
*Prochlorperazine (Stemetil®; Distriphar) – PO q8-12hr – oral suspension. If the case is so bad that you can’t manage oral medication, I suppose it might be worth trying a SC dose but the outer pack is 10 ampoules of 12.5mg each and you have the Cascade to consider)<br />
*Personally I’d try cinnarizine (Stugeron®; Janssen Cilag) – I found it useful in dogs with head tilt or idiopathic trigeminal neuropathy so it might help to stabilise a rabbit a bit during the early stages of a head tilt disorder – untested in this species – you have been warned!<br />
<br />
===Organisms causative of central vestibular or cerebellar disease=== <br />
These include the bacteria listed above as causing peripheral vestibular disease (with the addition of ''Listeria monocytogenes'')and also protozoan diseases (eg. ''Encephalitozoon cuniculi'' and ''Toxoplasma gondii''). ''Encephalitozoon'' is not found in the inner ear tissue, only in the CNS where it causes a non-suppurative meningitis and a granulomatous encephalitis, sometimes accompanied by perivascular infiltration with lymphocytes and plasma cells. All areas of the brain are affected.<br />
<br />
E cuniculi may yield biochemical test results indicative of renal disorder and positive serology for E cuniculi antibodies. Note E cuniculi also causes ophthalmic lesions (capsular rupture, cataract development and phacoclastic [[Uveitis – Rabbit|uveitis]]). <br />
<br />
Treatment of ''E. cuniculi'' is described here. For treatment of toxoplasmosis consider sulphonamides and be aware that clindamycin is extremely toxic in this species.<br />
<br />
===Miscellaneous causes of head tilt in rabbits===<br />
Cerebral larva migrans (''Baylisascaris procyonis'') has also been incriminated. Neoplasia has been diagnosed on MRI or CT scans. Cerebrovascular accidents may also be diagnosed on MRI and propentofylline or nicergoline are suggested as treatments. Another possible cause is trauma, including bites to the back of the neck: supportive treatment should rely on antibiosis and analgesics.<br />
<br />
Cerebral mycoses are unlikely to be encountered in the UK. I’d try itraconazole but I would be very dubious of success, given the time take from initial infection to onset of signs and the slow build up of itraconazole to therapeutically effective plasma levels.<br />
<br />
Toxicoses: <br />
*Lead – house rabbits which nibble wires etc. Signs include depression lethargy inappetance and “subtle neurologic changes” (Hillyer 1994). Calcium EDTA: q6hrs (Richardson 2000). Saunders (2002) suggests metoclopramide or cisapride (if it ever becomes available), to promote gastrointestinal motility and decreasing the absorption of the heavy metal.<br />
*Woolly milk pod contamination of hay in the USA.<br />
<br />
==Clinical signs of central and peripheral vestibular disease==<br />
Differentiate between central (eg. Encephalitoonosis) and peripheral (eg. Pasteurellosis) vestibular disease in rabbits (Harcourt Brown 2002). Both show: <br />
*Loss of balance<br />
*Head tilt<br />
*Falling<br />
*Horizontal nystagmus<br />
*Rotary nystagmus<br />
*Ventrolateral strabismus<br />
*Signs shown in central but not in peripheral vestibular disease<br />
*Rolling<br />
*Vertical nystagmus<br />
*Positional nystagmus<br />
*Signs shown sometimes in central but never in peripheral vestibular disease <br />
**Intention tremor (cerebellar) <br />
**Hemiparesis with ipsilateral postural reaction deficits<br />
*Mentation<br />
**Central vestibular cases are possibly depressed whereas peripheral cases are probably not<br />
<br />
===Diagnostics to differentiate between Encephalitoonosis and Pasteurellosis==<br />
*Radiographic changes seen in tympanic bulla in pasteurellosis<br />
*Serology<br />
*Haematology – neutrophilia and a shift to the left might indicate bacterial infection<br />
<br />
==Therapeutic approach to head tilt in rabbits==<br />
*Oxytetracycline IM and low dose + corticosteroid eg 0.1-0.5mg/kg IM + benzimidazoles<br />
*Diazepam IM<br />
*Meclozine PO q6–8hrs <br />
*Prochlorperazine PO q8-12hr – oral suspension. <br />
*Cinnarizine q 12–24 h<br />
<br />
==Corticosteroids in rabbits==<br />
*Consider absorption from topical applications<br />
*Compromisation of premunity <br />
*In anorexia, mobilizes free fatty acids from adipose tissue =>hepatic lipidosis<br />
*Increased populations of intestinal coliforms<br />
*Ratio of aerobes to anaerobes alters<br />
*Reserve for acute cases<br />
<br />
'''Note: Chronic pruritic seborroeic otitis is usually associated with yeasts (''Candida'' sp.) whereas purulent otitis, especially where the discharge is tacky and sticky, may show ''E. coli'' and ''Pseudomonas'' sp on culture.'''</div>Clamyhttps://en.wikivet.net/index.php?title=Keratopathy_%E2%80%93_Rabbit&diff=82769Keratopathy – Rabbit2010-08-10T01:37:16Z<p>Clamy: </p>
<hr />
<div>{{unfinished}}<br />
<br />
Walden (1990) reports signs of vitamin A deficiency in adult rabbits to include a dull whitish patch developing on the axial cornea and spreading centrifugally to the limbus where pigmentation may develop. The recommended dose of vitamin A is based on the daily requirement which is 60 IU per kilogram of bodyweight. In the absence of treatment, [[Keratitis and Conjunctivitis – Rabbit|keratitis]] and [[Blindness – Rabbit|blindness]] may ensue.<br />
<br />
Ulcerative keratitis may not always be due to external factors in rabbits. Williams (2006) describes persistent superficial epithelial erosion “similar to corneal basement membrane dystrophy of boxer dogs” and recommends fairlyaggressive treatment including grid, and superficial, keratectomy.<br />
<br />
Keratoconjunctivitis sicca may be difficult to diagnose in rabbits – see notes on the use of the Schirmer 1 tear test.<br />
<br />
==References==<br />
*Walden (1990)<br />
*Williams D L (2006) Ophthalmology in BSAVA Manual of Rabbit Medicine and Surgery eds Meredith A and Flecknell P, 2nd Edition 2006, published by BSAVA Quedgley Glocs<br />
<br />
[[Category:Ophthalmological_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Blindness_%E2%80%93_Rabbit&diff=82768Blindness – Rabbit2010-08-10T01:36:35Z<p>Clamy: Created page with "{{unfinished}} Okerman (1994) lists the causes of blindness as: *Inherited glaucoma; glaucoma is seen as an inherited condition in rabbits carrying the r..."</p>
<hr />
<div>{{unfinished}}<br />
<br />
Okerman (1994) lists the causes of blindness as:<br />
*Inherited glaucoma; [[Glaucoma – Rabbit|glaucoma]] is seen as an inherited condition in rabbits carrying the recessive bu gene.<br />
*Disturbances of the CNS <br />
*[[Myxomatosis – Rabbit|Myxomatosis]]. <br />
*Cataracts<br />
*Panophthalmitis <br />
<br />
<br />
==References==<br />
*Okerman L (1994): Diseases of Domestic Rabbits. Blackwell Scien¬tific Publications ISBN 0-632-03804 -7. 2nd Edition<br />
<br />
[[Category:Ophthalmological_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Glaucoma_%E2%80%93_Rabbit&diff=82767Glaucoma – Rabbit2010-08-10T01:34:13Z<p>Clamy: Created page with "{{unfinished}} ==Description== The bu gene is common in New Zealand White rabbits, causing a dysplastic iridocorneal angle where drainage is very poor. A useful paper on the con..."</p>
<hr />
<div>{{unfinished}}<br />
<br />
==Description==<br />
The bu gene is common in New Zealand White rabbits, causing a dysplastic iridocorneal angle where drainage is very poor. A useful paper on the condition is Ueno and colleagues report on histopathological changes in iridocorneal angle of inherited glaucoma in rabbits (Graefes Arch Clin Exp Ophthalmol. 1999; 237: 654 - 660)<br />
<br />
==Clinical Signs==<br />
Clinical signs include scleral congestion. A tonometer may be used in rabbits but rabbits have to be restrained in true lateral recumbency to obtain an accurate reading and the thin nature of the cornea means that if the Tonopen XL is used the flowing corrective formula must be applied:<br />
<br />
True IOP (mmHg) = 1.12(Tomopen value) + 3.07<br />
<br />
Normal intraocular pressures are between 15 and 23 mmHg whereas those of between 26-48 mmHg are diagnostic of glaucoma (Williams 2006). The dilated pupil that accompanies glaucoma may not be so obvious if [[Uveitis – Rabbit|uveitis]] is present and in any case may be difficult to assess as corneal oedema may be present. Buphthalmos and exposure keratitis are apparently a sequel to glaucoma in rabbits.<br />
<br />
An emerging clinical precursor of glaucoma in rabbits is ''Encephalitozoon cuniculi'' infection leading to the formation of a white mass within the iris. It is important to assess the condition very carefully and to rule out the presence of [[Uveitis – Rabbit|uveitis]].<br />
<br />
==Treatment==<br />
Lawton (1993) says that the use of Daranide® should be avoided, whereas Williams (2006) says that medical treatment is rarely effective or necessary. The treatment recommended by Lawton involves the injection of gentamycin into the vitreous as it destroys the ciliary body and the retina and stops vitreous production.<br />
<br />
==References==<br />
*Lawton M P C (1993) Procs BVZS Autumn Meeting ZSL 4/12/93 <br />
*Ueno et al (Graefes Arch Clin Exp Ophthalmol. 1999; 237: 654 - 660)<br />
*Williams D L (2006) Ophthalmology in BSAVA Manual of Rabbit Medicine and Surgery eds Meredith A and Flecknell P, 2nd Edition 2006, published by BSAVA Quedgley Glocs<br />
<br />
[[Category:Ophthalmological_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Aberrant_Conjunctival_Overgrowth_%E2%80%93_Rabbit&diff=82766Aberrant Conjunctival Overgrowth – Rabbit2010-08-10T01:29:09Z<p>Clamy: Created page with "{{unfinished}} Aberrant conjunctival overgrowth occurs uniquely in the rabbit and is manifested by the production (growth) of conjunctive from the limbus over the cornea but not..."</p>
<hr />
<div>{{unfinished}}<br />
<br />
Aberrant conjunctival overgrowth occurs uniquely in the rabbit and is manifested by the production (growth) of conjunctive from the limbus over the cornea but not adhering to it (cf. [[Symblepharon – Rabbit|symblepharon]] in which the tissue does adhere to the cornea). Treatment of aberrant conjunctival overgrowth is usually unrewarding as the condition is prone to recur but the surgical approach of resection of the aberrant tissue and suturing it to the limbus is advocated, perhaps followed by topical application of cyclosporin (Williams 2006)<br />
<br />
==References==<br />
*Williams D L (2006) Ophthalmology in BSAVA Manual of Rabbit Medicine and Surgery eds Meredith A and Flecknell P, 2nd Edition 2006, published by BSAVA Quedgley Glocs<br />
[[Category:Ophthalmological_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Uveitis_%E2%80%93_Rabbit&diff=82765Uveitis – Rabbit2010-08-10T01:27:29Z<p>Clamy: Created page with "{{unfinished}} Uveitis is usually considered to be bacterial and haematogenous in origin (Williams 2000); ''Pasteurella'' is usually the culprit. Treatment should include system..."</p>
<hr />
<div>{{unfinished}}<br />
<br />
Uveitis is usually considered to be bacterial and haematogenous in origin (Williams 2000); ''Pasteurella'' is usually the culprit. Treatment should include systemic antibiosis (oxytetracycline SC q 72hrs) and a mydriatic to reduce intraocular pain. The effect of pain on the gastrointestinal system may need to be addressed with the use of analgesics and prokinetics.<br />
<br />
==References==<br />
*Williams, 2000<br />
<br />
[[Category:Ophthalmological_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Iridal_Abscesses_%E2%80%93_Rabbit&diff=82764Iridal Abscesses – Rabbit2010-08-10T01:25:02Z<p>Clamy: Created page with "{{unfinished}} Iridal abscesses require the use of parenteral oxytetracycline or enrofloxacin and topical tobramycin. This can also be one of the manifestations of ''Encephalito..."</p>
<hr />
<div>{{unfinished}}<br />
<br />
Iridal abscesses require the use of parenteral oxytetracycline or enrofloxacin and topical tobramycin. This can also be one of the manifestations of ''Encephalitozoon cuniculi'' infection. See notes in Urogenital and Nervous Systems. Note ''E. cuniculi'' also causes other ophthalmic lesions; capsular rupture, cataract development and pyogranulomatous phacoclastic uveitis. Serological testing to differentiate the cause (between ''Pasteurella'' and ''Encephailitozoon'') may be helpful. Phacoclastic uveitis can develop to such an extent that lens removal by phacofragmentation may be necessary, but the rabbit has an ability to regenerate the lens after this procedure (van der Woerdt 2005).<br />
<br />
==References==<br />
*van der Woerdt 2005<br />
<br />
<br />
[[Category:Ophthalmological_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Exophthalmos_%E2%80%93_Rabbit&diff=82763Exophthalmos – Rabbit2010-08-10T01:22:23Z<p>Clamy: </p>
<hr />
<div>{{unfinished}}<br />
<br />
Unilateral exophthalmos (Wagner F et al 2005) may be caused by:<br />
*Orbital abscesses (is this the same as retrobulbar abscesses)<br />
*Orbital cellulites<br />
*Orbital cysts<br />
*Retrobulbar fat prolapse<br />
*Salivary mucocoele<br />
*Orbital neoplasia<br />
*''Taenia serialis'' - coenurosis<br />
<br />
Bilateral exophthalmos may be caused by, I assume, the above occurring bilaterally and also by: <br />
*Thymoma (Vernaue et al 1995)<br />
*Mediastinal lymphoma (Wagner F et al 2005)<br />
<br />
==References==<br />
*Vernaue et al (1995): Thymoma in a geriatric rabbit with hypercalcaemia and periodic exophthalmia J Am Vet Med Assoc 206 820-822<br />
*Wagner F et al (2005): Recurrent bilateral exophthalmos associated with metastatic carcinoma in a pet rabbit. Journal of Small Animal Practice 46, 393-397<br />
<br />
[[Category:Ophthalmological_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Exophthalmos_%E2%80%93_Rabbit&diff=82762Exophthalmos – Rabbit2010-08-10T01:22:07Z<p>Clamy: Created page with "{{unfinished}} Unilateral exophthalmos (Wagner F et al 2005) may be caused by: *Orbital abscesses (is this the same as retrobulbar abscesses) *Orbital cellulites *Orbital cysts ..."</p>
<hr />
<div>{{unfinished}}<br />
<br />
Unilateral exophthalmos (Wagner F et al 2005) may be caused by:<br />
*Orbital abscesses (is this the same as retrobulbar abscesses)<br />
*Orbital cellulites<br />
*Orbital cysts<br />
*Retrobulbar fat prolapse<br />
*Salivary mucocoele<br />
*Orbital neoplasia<br />
*''Taenia serialis'' - coenurosis<br />
<br />
Bilateral exophthalmos may be caused by, I assume, the above occurring bilaterally and also by: <br />
*Thymoma (Vernaue et al 1995)<br />
*Mediastinal lymphoma (Wagner F et al 2005)<br />
<br />
==References==<br />
*Vernaue et al (1995): Thymoma in a geriatric rabbit with hypercalcaemia and periodic exophthalmia J Am Vet Med Assoc 206 820-822<br />
*Wagner F et al (2005): Recurrent bilateral exophthalmos associated with metastatic carcinoma in a pet rabbit. Journal of Small Animal Practice 46, 393-397</div>Clamyhttps://en.wikivet.net/index.php?title=Corneal_Lipidosis_%E2%80%93_Rabbit&diff=82761Corneal Lipidosis – Rabbit2010-08-10T01:19:27Z<p>Clamy: Created page with "{{unfinished}} Corneal lipidosis has been observed by myself in rabbits and presents the same clinical appearance as in dogs and cats. Other than to assess the liver function o..."</p>
<hr />
<div>{{unfinished}}<br />
<br />
Corneal lipidosis has been observed by myself in rabbits and presents the same clinical appearance as in dogs and cats. Other than to assess the liver function of the subject and alter the diet accordingly, I regret that I can offer no clinical advice. Lawton (1993) reported the occurrence of corneal dystrophy due to cholesterol clefts which he asserted are both dietary and hereditary (clinical work-up includes blood testing for cholesterol and triglycerides and the treatment involves dietary adjustment).<br />
<br />
Corneal oedema can occur with glaucoma and indolent ulceration. If thermal keratoplasty is required, Williams (2006) warns that the thin nature of the rabbit cornea makes this a delicate procedure.<br />
<br />
Corneal dystropies are reported (Williams 2006).<br />
<br />
==References==<br />
*Lawton M P C (1993) Procs BVZS Autumn Meeting ZSL 4/12/93 <br />
*Williams 2006<br />
<br />
[[Category:Ophthalmological_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Keratopathy_%E2%80%93_Rabbit&diff=82759Keratopathy – Rabbit2010-08-10T01:15:32Z<p>Clamy: </p>
<hr />
<div>{{unfinished}}<br />
<br />
Walden (1990) reports signs of vitamin A deficiency in adult rabbits to include a dull whitish patch developing on the axial cornea and spreading centrifugally to the limbus where pigmentation may develop. The recommended dose of vitamin A is based on the daily requirement which is 60 IU per kilogram of bodyweight. In the absence of treatment, [[Keratitis and Conjunctivitis – Rabbit|keratitis]] and blindness may ensue.<br />
<br />
Ulcerative keratitis may not always be due to external factors in rabbits. Williams (2006) describes persistent superficial epithelial erosion “similar to corneal basement membrane dystrophy of boxer dogs” and recommends fairlyaggressive treatment including grid, and superficial, keratectomy.<br />
<br />
Keratoconjunctivitis sicca may be difficult to diagnose in rabbits – see notes on the use of the Schirmer 1 tear test.<br />
<br />
==References==<br />
*Walden (1990)<br />
*Williams D L (2006) Ophthalmology in BSAVA Manual of Rabbit Medicine and Surgery eds Meredith A and Flecknell P, 2nd Edition 2006, published by BSAVA Quedgley Glocs<br />
<br />
[[Category:Ophthalmological_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Keratopathy_%E2%80%93_Rabbit&diff=82758Keratopathy – Rabbit2010-08-10T01:15:15Z<p>Clamy: Created page with "{{unfinished}} Walden (1990) reports signs of vitamin A deficiency in adult rabbits to include a dull whitish patch developing on the axial cornea and spreading centrifugally to..."</p>
<hr />
<div>{{unfinished}}<br />
<br />
Walden (1990) reports signs of vitamin A deficiency in adult rabbits to include a dull whitish patch developing on the axial cornea and spreading centrifugally to the limbus where pigmentation may develop. The recommended dose of vitamin A is based on the daily requirement which is 60 IU per kilogram of bodyweight. In the absence of treatment, [[Keratitis and Conjunctivitis – Rabbit|keratitis]] and blindness may ensue.<br />
<br />
Ulcerative keratitis may not always be due to external factors in rabbits. Williams (2006) describes persistent superficial epithelial erosion “similar to corneal basement membrane dystrophy of boxer dogs” and recommends fairlyaggressive treatment including grid, and superficial, keratectomy.<br />
<br />
Keratoconjunctivitis sicca may be difficult to diagnose in rabbits – see notes on the use of the Schirmer 1 tear test.<br />
<br />
==References==<br />
*Walden (1990)<br />
*Williams D L (2006) Ophthalmology in BSAVA Manual of Rabbit Medicine and Surgery eds Meredith A and Flecknell P, 2nd Edition 2006, published by BSAVA Quedgley Glocs</div>Clamyhttps://en.wikivet.net/index.php?title=Corneal_Abrasions_%E2%80%93_Rabbit&diff=82757Corneal Abrasions – Rabbit2010-08-10T01:11:58Z<p>Clamy: Created page with "{{unfinished}} Corneal abrasions are occasionally encountered in pet rabbits usually as a result of injury on straw bedding (barley awns) or from injuries sustained from being c..."</p>
<hr />
<div>{{unfinished}}<br />
<br />
Corneal abrasions are occasionally encountered in pet rabbits usually as a result of injury on straw bedding (barley awns) or from injuries sustained from being chased by dogs or children. These can be confirmed by the instillation of fluorescein drops followed by examination with and without a cobalt blue filter over the light source after the excess fluorescein has been flushed away. Treatment is as for other mammals - repeated topical applications of antibiotics following sensitivity testing or, in the event of antibiotic sensitivity testing not being available, utilising an agent known to include ''Pasteurella multocida'' in its spectrum of activity. From clinical experience I prefer aqueous ophthalmic solutions preferably those containing hydroxypropylmethylcellulose (hypromellose), to ointments for the treatment of corneal injuries and abrasions and I recommend that applications should be repeated hourly or more frequently, but care must be taken not to cause stress with such frequent handling. Refractory cases can be treated surgically by surgical debridement of the ulcer margin and temporary tarsorrhapy or a nictitans flap (I prefer to place sutures through the cartilage of the membrana nictitans rather than attempt to pick up the very fine conjunctival epithelium of the membrana which tends to tear very easily in this species).<br />
<br />
[[Category:Ophthalmological_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Symblepharon_%E2%80%93_Rabbit&diff=82754Symblepharon – Rabbit2010-08-10T01:07:35Z<p>Clamy: </p>
<hr />
<div>{{unfinished}}<br />
<br />
Symblepharon can follow chronic blepharo-conjunctivitis and may have to be addressed aggressively using surgery in an attempt to prevent the formation of adhesions. I have seen one case of symblepharon in a rabbit with severe pasteurellar infection. This was treated with long-term procaine penicillin <br />
SC q72hrs and topical antibiotics as indicated by microbiological investigation. Initially scarring was relieved by incision into the tarsal plate, parallel to the skin surface. Subsequent adhesions were excised under topical analgesia (Proxymetacaine Minims®; Alcon) and NSAID’s (Acular®: Allergan) and topical corticosteroids and cyclosporin were used as indicated on frequent (monthly) examinations. The rabbit and the owner were both very compliant with this prolonged course of treatment, but the case was lost to follow-up after I retired.<br />
<br />
[[Category:Ophthalmological_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Symblepharon_%E2%80%93_Rabbit&diff=82753Symblepharon – Rabbit2010-08-10T01:06:36Z<p>Clamy: Created page with "{{unfinished}} Symblepharon can follow chronic blepharo-conjunctivitis and may have to be addressed aggressively using surgery in an attempt to prevent the formation of adhesion..."</p>
<hr />
<div>{{unfinished}}<br />
<br />
Symblepharon can follow chronic blepharo-conjunctivitis and may have to be addressed aggressively using surgery in an attempt to prevent the formation of adhesions. I have seen one case of symblepharon in a rabbit with severe pasteurellar infection. This was treated with long-term procaine penicillin <br />
SC q72hrs and topical antibiotics as indicated by microbiological investigation. Initially scarring was relieved by incision into the tarsal plate, parallel to the skin surface. Subsequent adhesions were excised under topical analgesia (Proxymetacaine Minims®; Alcon) and NSAID’s (Acular®: Allergan) and topical corticosteroids and cyclosporin were used as indicated on frequent (monthly) examinations. The rabbit and the owner were both very compliant with this prolonged course of treatment, but the case was lost to follow-up after I retired.</div>Clamyhttps://en.wikivet.net/index.php?title=Dacryocystitis_%E2%80%93_Rabbit&diff=82751Dacryocystitis – Rabbit2010-08-10T00:57:00Z<p>Clamy: </p>
<hr />
<div> <br />
{{unfinished}}<br />
==Description==<br />
Dacryocystitis is one of the most common conditions encountered in practice and can be one of the most difficult to treat due to the persistence of the organism involved and the tendency of the condition to recur. It is very important to examine the teeth and both nasolacrimal ducts of every rabbit irrespective of the reason for which the animal is presented for clinical examination. <br />
<br />
==Clinical Signs==<br />
Clinical signs of dacryocystitis include a milky discolouration of the precorneal tear film, epiphora, crust formation along the affected eyelid margins and a caseous discharge from the nostril. The condition can be unilateral or bilateral. The clinician may have to apply digital pressure on the lacrimal sac to observe a milky discharge from the lacrimal punctum. Keratitis and conjunctivitis are sometimes observed. A white crust on medial canthus is a frequent early clinical sign.<br />
<br />
==Aetiology==<br />
<br />
The prime agent of aetiological significance is [[Cheek Teeth Malocclusion – Rabbit|dental malocclusion]]. The constant growth of the teeth combined with the low bone density of the rabbit skull results in the migration of the roots of the teeth leading to:<br />
<br />
#Occlusion of the naso-lacrimal duct by the roots of the incisors (welling of the milky discharge up the lacrimal apparatus results in epiphora). <br />
#Invasion of the eye socket by the roots of the molars leading to retrobulbar infection, buphthalmos or simply ocular irritation and epiphora.<br />
<br />
<br />
Microbiological investigation yields profuse growth of many organisms, usually ''Pasteurella multocida'' (Petersen-Jones and Carrington 1988), but ''Staphylococcus'' species and ''Streptococcus'' species, can also be frequently involved. Dacryocystitis can be due to an ascending infection from the nasal cavity via the nasolacrimal duct and is a constituent part of the syndrome of Pasteurella infection in rabbits (Whittaker 1989).<br />
<br />
A survey conducted by Leo Laboratories in 1994 yielded:<br />
<br />
#''Staphyloccus'' spp. - non-haemolytic, 17 isolates; haemolytic coagulase -ve, 10 isolates; haemolytic coagulase +ve, 5 isolates.<br />
<br />
#''Streptococcus'' spp. - non-haemolytic, 4 isolates; alpha-haemolytic, 2 isolates <br />
<br />
#''Pasteurella'' spp. - Pasteurella aerogenes 2 isolates, ''Pasteurella multocida'' 3 isolates, unidentified ''Pasteurella'' spp. 2 isolates, <br />
<br />
#''Bacillus'' spp. - 7 isolates, <br />
<br />
#''Corynebacterium'' spp. - 5 isolates, <br />
<br />
#''Enterobacter'' spp. - 3 isolates<br />
<br />
#''E coli'' - (non-haemolytic) 3 isolates <br />
<br />
#''Pseudomonas'' spp. - ''Pseudomonas vesicularis'' 2 isolates, unidentified ''Pseudomonas'' spp. 1 isolate, <br />
<br />
#''Branhamella'' spp. - one isolate<br />
<br />
#''Proteus'' spp. - one isolate<br />
<br />
#''Acinetobacter junii'' - one isolate<br />
<br />
#No isolates were detected in 12 specimens. <br />
<br />
As well as dental disorders, a triggering factor for the establishment and persistence of infection is thought to be the ammonia produced either by the degeneration of urinary urea in a poorly absorptive litter (Okerman 1988) or from a pet maintained on an imbalanced (high protein) diet (Jenkins 1991). I always counsel the owners of affected animals to attend to hygiene and diet simultaneously. Peat moss /Turf mould is recommended as hutch litter due to its ability to absorb the ammonia produced by the decomposition of urinary urea.<br />
<br />
==Treatment==<br />
<br />
The condition is very difficult to treat as tooth roots are an important factor in the persistent eye infections of rabbits and the distal naso-lacrimal duct may become involved with periapical abscessation of the maxillary incisors (overlong incisor root with thinning or periosteal proliferation of the palatial bone). Dental conditions do not, generally speaking, resolve quickly in rabbits, if at all. Also the causative organism, particularly if it is the ubiquitous ''Pasteurella multocida'', seems to be well adapted to the conjunctival microclimate and local immunity appears to be suppressed. In addition, cannulation of the entire course of the lacrimal duct is impossible due to the tortuous course and varying diameter of the duct although flushing from the lacrimal punctum is possible (Burling et al 1991). Even if the condition is discovered only co-incidentally when the rabbit is presented for some other reason, the following approach should be undertaken: <br />
<br />
*Make sure that the dental disease is thoroughly addressed.<br />
<br />
*Under local analgesia using proxymetacaine hydrochloride BP (Minims; Alcon), I canulate the lacrimal duct as described by Petersen-Jones and Carrington (1988) and flush the apparatus (irrigating canula reference AS85 from Arnolds Veterinary Products, or iv cannula) with sterile saline until the fluid runs clear from the the nares. The bevelled end of the Surflo intravenous canula makes it an easier instrument for this purpose. The apparatus is then irrigated diluted ophthalmic preparations of antibiotics, ideally following microbial cultures and sensitivity testing. <br />
<br />
*In some cases it is impossible to effect drainage of the tenacious purulent material. I once had success with a solution of trypsin is infused into the duct and the procedure is reattempted after twenty-four to forty-eight hours. <br />
<br />
*Follow-up treatment comprises systemic and topical antibiosis, usually with oxytetracyline (Engemycin® 5%; Intervet) and tetracycline ophthalmic ointment (Fucithalmic®; Leo) or gentamicin (Tiacil®; Virbac) applied to the conjunctival fornix q 6-8 hrs, or antibiotics are selected after sensitivity testing. In the absence of antibiotic sensitivities. I have noticed that topical applications of ophthalmic preparations containing neomycin are frequently not effective in the treatment of this condition.<br />
<br />
==Prognosis==<br />
Prognosis the favourability of the prognosis is inversely proportional to the dental health and to the length of time taken for any response to treatment. Poor response is an indication for withdrawal of treatment and microbiological investigation, including antibiotic sensitivity testing. Long-term, repeated irrigation may result in permanent stenosis or obstruction. <br />
<br />
In young animals in a collective situation (eg. pet shops) a simple conjunctivitis in which the teeth are not involved may be encountered. Cytology may be useful in identifying the causative organism(s). Chlamydophila psittaci may be involved (scrapings from the back of the membrana nictitans may be helpful) and should respond to ciporofloxacin eye drops (Ciloxan®; Alcon Labs).<br />
<br />
==References==<br />
*Burling et al (1991): Anatomy of the rabbit nasolacrimal duct and its clinical implications in Progress in Veterinary Comparative Ophthalmology Vol 1 No 1 pp 33 to 40.<br />
*Jenkins (1991)<br />
*Okerman L (1994): Diseases of Domestic Rabbits. Blackwell Scien¬tific Publications ISBN 0-632-03804 -7. 2nd Edition<br />
*Petersen-Jones S.M. and Carrington S.D. (1988): Pasteurellar dacryocystitis in rabbits: Veterinary Record 122 514 to 515<br />
*Whittaker (1989)<br />
<br />
[[Category:Ophthalmological_Disorders_-_Rabbit]]</div>Clamyhttps://en.wikivet.net/index.php?title=Dacryocystitis_%E2%80%93_Rabbit&diff=82750Dacryocystitis – Rabbit2010-08-10T00:54:06Z<p>Clamy: </p>
<hr />
<div> <br />
{{unfinished}}<br />
==Description==<br />
Dacryocystitis is one of the most common conditions encountered in practice and can be one of the most difficult to treat due to the persistence of the organism involved and the tendency of the condition to recur. It is very important to examine the teeth and both nasolacrimal ducts of every rabbit irrespective of the reason for which the animal is presented for clinical examination. <br />
<br />
==Clinical Signs==<br />
Clinical signs of dacryocystitis include a milky discolouration of the precorneal tear film, epiphora, crust formation along the affected eyelid margins and a caseous discharge from the nostril. The condition can be unilateral or bilateral. The clinician may have to apply digital pressure on the lacrimal sac to observe a milky discharge from the lacrimal punctum. Keratitis and conjunctivitis are sometimes observed. A white crust on medial canthus is a frequent early clinical sign.<br />
<br />
==Aetiology==<br />
<br />
The prime agent of aetiological significance is [[Cheek Teeth Malocclusion – Rabbit|dental malocclusion]]. The constant growth of the teeth combined with the low bone density of the rabbit skull results in the migration of the roots of the teeth leading to:<br />
<br />
#Occlusion of the naso-lacrimal duct by the roots of the incisors (welling of the milky discharge up the lacrimal apparatus results in epiphora). <br />
#Invasion of the eye socket by the roots of the molars leading to retrobulbar infection, buphthalmos or simply ocular irritation and epiphora.<br />
<br />
<br />
Microbiological investigation yields profuse growth of many organisms, usually ''Pasteurella multocida'' (Petersen-Jones and Carrington 1988), but ''Staphylococcus'' species and ''Streptococcus'' species, can also be frequently involved. Dacryocystitis can be due to an ascending infection from the nasal cavity via the nasolacrimal duct and is a constituent part of the syndrome of Pasteurella infection in rabbits (Whittaker 1989).<br />
<br />
A survey conducted by Leo Laboratories in 1994 yielded:<br />
<br />
#''Staphyloccus'' spp. - non-haemolytic, 17 isolates; haemolytic coagulase -ve, 10 isolates; haemolytic coagulase +ve, 5 isolates.<br />
<br />
#''Streptococcus'' spp. - non-haemolytic, 4 isolates; alpha-haemolytic, 2 isolates <br />
<br />
#''Pasteurella'' spp. - Pasteurella aerogenes 2 isolates, ''Pasteurella multocida'' 3 isolates, unidentified ''Pasteurella'' spp. 2 isolates, <br />
<br />
#''Bacillus'' spp. - 7 isolates, <br />
<br />
#''Corynebacterium'' spp. - 5 isolates, <br />
<br />
#''Enterobacter'' spp. - 3 isolates<br />
<br />
#''E coli'' - (non-haemolytic) 3 isolates <br />
<br />
#''Pseudomonas'' spp. - ''Pseudomonas vesicularis'' 2 isolates, unidentified ''Pseudomonas'' spp. 1 isolate, <br />
<br />
#''Branhamella'' spp. - one isolate<br />
<br />
#''Proteus'' spp. - one isolate<br />
<br />
#''Acinetobacter junii'' - one isolate<br />
<br />
#No isolates were detected in 12 specimens. <br />
<br />
As well as dental disorders, a triggering factor for the establishment and persistence of infection is thought to be the ammonia produced either by the degeneration of urinary urea in a poorly absorptive litter (Okerman 1988) or from a pet maintained on an imbalanced (high protein) diet (Jenkins 1991). I always counsel the owners of affected animals to attend to hygiene and diet simultaneously. Peat moss /Turf mould is recommended as hutch litter due to its ability to absorb the ammonia produced by the decomposition of urinary urea.<br />
<br />
==Treatment==<br />
<br />
The condition is very difficult to treat as tooth roots are an important factor in the persistent eye infections of rabbits and the distal naso-lacrimal duct may become involved with periapical abscessation of the maxillary incisors (overlong incisor root with thinning or periosteal proliferation of the palatial bone). Dental conditions do not, generally speaking, resolve quickly in rabbits, if at all. Also the causative organism, particularly if it is the ubiquitous ''Pasteurella multocida'', seems to be well adapted to the conjunctival microclimate and local immunity appears to be suppressed. In addition, cannulation of the entire course of the lacrimal duct is impossible due to the tortuous course and varying diameter of the duct although flushing from the lacrimal punctum is possible (Burling et al 1991). Even if the condition is discovered only co-incidentally when the rabbit is presented for some other reason, the following approach should be undertaken: <br />
<br />
*Make sure that the dental disease is thoroughly addressed.<br />
<br />
*Under local analgesia using proxymetacaine hydrochloride BP (Minims; Alcon), I canulate the lacrimal duct as described by Petersen-Jones and Carrington (1988) and flush the apparatus (irrigating canula reference AS85 from Arnolds Veterinary Products, or iv cannula) with sterile saline until the fluid runs clear from the the nares. The bevelled end of the Surflo intravenous canula makes it an easier instrument for this purpose. The apparatus is then irrigated diluted ophthalmic preparations of antibiotics, ideally following microbial cultures and sensitivity testing. <br />
<br />
*In some cases it is impossible to effect drainage of the tenacious purulent material. I once had success with a solution of trypsin is infused into the duct and the procedure is reattempted after twenty-four to forty-eight hours. <br />
<br />
*Follow-up treatment comprises systemic and topical antibiosis, usually with oxytetracyline (Engemycin® 5%; Intervet) and tetracycline ophthalmic ointment (Fucithalmic®; Leo) or gentamicin (Tiacil®; Virbac) applied to the conjunctival fornix q 6-8 hrs, or antibiotics are selected after sensitivity testing. In the absence of antibiotic sensitivities. I have noticed that topical applications of ophthalmic preparations containing neomycin are frequently not effective in the treatment of this condition.<br />
<br />
==Prognosis==<br />
Prognosis the favourability of the prognosis is inversely proportional to the dental health and to the length of time taken for any response to treatment. Poor response is an indication for withdrawal of treatment and microbiological investigation, including antibiotic sensitivity testing. Long-term, repeated irrigation may result in permanent stenosis or obstruction. <br />
<br />
In young animals in a collective situation (eg. pet shops) a simple conjunctivitis in which the teeth are not involved may be encountered. Cytology may be useful in identifying the causative organism(s). Chlamydophila psittaci may be involved (scrapings from the back of the membrana nictitans may be helpful) and should respond to ciporofloxacin eye drops (Ciloxan®; Alcon Labs).<br />
<br />
==References==<br />
*Burling et al (1991): Anatomy of the rabbit nasolacrimal duct and its clinical implications in Progress in Veterinary Comparative Ophthalmology Vol 1 No 1 pp 33 to 40.<br />
*Jenkins (1991)<br />
*Okerman L (1994): Diseases of Domestic Rabbits. Blackwell Scien¬tific Publications ISBN 0-632-03804 -7. 2nd Edition<br />
*Petersen-Jones S.M. and Carrington S.D. (1988): Pasteurellar dacryocystitis in rabbits: Veterinary Record 122 514 to 515<br />
*Whittaker (1989)</div>Clamyhttps://en.wikivet.net/index.php?title=Dacryocystitis_%E2%80%93_Rabbit&diff=82749Dacryocystitis – Rabbit2010-08-10T00:50:55Z<p>Clamy: /* Treatment */</p>
<hr />
<div> <br />
{{unfinished}}<br />
==Description==<br />
Dacryocystitis is one of the most common conditions encountered in practice and can be one of the most difficult to treat due to the persistence of the organism involved and the tendency of the condition to recur. It is very important to examine the teeth and both nasolacrimal ducts of every rabbit irrespective of the reason for which the animal is presented for clinical examination. <br />
<br />
==Clinical Signs==<br />
Clinical signs of dacryocystitis include a milky discolouration of the precorneal tear film, epiphora, crust formation along the affected eyelid margins and a caseous discharge from the nostril. The condition can be unilateral or bilateral. The clinician may have to apply digital pressure on the lacrimal sac to observe a milky discharge from the lacrimal punctum. Keratitis and conjunctivitis are sometimes observed. A white crust on medial canthus is a frequent early clinical sign.<br />
<br />
==Aetiology==<br />
<br />
The prime agent of aetiological significance is [[Cheek Teeth Malocclusion – Rabbit|dental malocclusion]]. The constant growth of the teeth combined with the low bone density of the rabbit skull results in the migration of the roots of the teeth leading to:<br />
<br />
#Occlusion of the naso-lacrimal duct by the roots of the incisors (welling of the milky discharge up the lacrimal apparatus results in epiphora). <br />
#Invasion of the eye socket by the roots of the molars leading to retrobulbar infection, buphthalmos or simply ocular irritation and epiphora.<br />
<br />
<br />
Microbiological investigation yields profuse growth of many organisms, usually ''Pasteurella multocida'' (Petersen-Jones and Carrington 1988), but ''Staphylococcus'' species and ''Streptococcus'' species, can also be frequently involved. Dacryocystitis can be due to an ascending infection from the nasal cavity via the nasolacrimal duct and is a constituent part of the syndrome of Pasteurella infection in rabbits (Whittaker 1989).<br />
<br />
A survey conducted by Leo Laboratories in 1994 yielded:<br />
<br />
#''Staphyloccus'' spp. - non-haemolytic, 17 isolates; haemolytic coagulase -ve, 10 isolates; haemolytic coagulase +ve, 5 isolates.<br />
<br />
#''Streptococcus'' spp. - non-haemolytic, 4 isolates; alpha-haemolytic, 2 isolates <br />
<br />
#''Pasteurella'' spp. - Pasteurella aerogenes 2 isolates, ''Pasteurella multocida'' 3 isolates, unidentified ''Pasteurella'' spp. 2 isolates, <br />
<br />
#''Bacillus'' spp. - 7 isolates, <br />
<br />
#''Corynebacterium'' spp. - 5 isolates, <br />
<br />
#''Enterobacter'' spp. - 3 isolates<br />
<br />
#''E coli'' - (non-haemolytic) 3 isolates <br />
<br />
#''Pseudomonas'' spp. - ''Pseudomonas vesicularis'' 2 isolates, unidentified ''Pseudomonas'' spp. 1 isolate, <br />
<br />
#''Branhamella'' spp. - one isolate<br />
<br />
#''Proteus'' spp. - one isolate<br />
<br />
#''Acinetobacter junii'' - one isolate<br />
<br />
#No isolates were detected in 12 specimens. <br />
<br />
As well as dental disorders, a triggering factor for the establishment and persistence of infection is thought to be the ammonia produced either by the degeneration of urinary urea in a poorly absorptive litter (Okerman 1988) or from a pet maintained on an imbalanced (high protein) diet (Jenkins 1991). I always counsel the owners of affected animals to attend to hygiene and diet simultaneously. Peat moss /Turf mould is recommended as hutch litter due to its ability to absorb the ammonia produced by the decomposition of urinary urea.<br />
<br />
==Treatment==<br />
<br />
The condition is very difficult to treat as tooth roots are an important factor in the persistent eye infections of rabbits and the distal naso-lacrimal duct may become involved with periapical abscessation of the maxillary incisors (overlong incisor root with thinning or periosteal proliferation of the palatial bone). Dental conditions do not, generally speaking, resolve quickly in rabbits, if at all. Also the causative organism, particularly if it is the ubiquitous ''Pasteurella multocida'', seems to be well adapted to the conjunctival microclimate and local immunity appears to be suppressed. In addition, cannulation of the entire course of the lacrimal duct is impossible due to the tortuous course and varying diameter of the duct although flushing from the lacrimal punctum is possible (Burling et al 1991). Even if the condition is discovered only co-incidentally when the rabbit is presented for some other reason, the following approach should be undertaken: <br />
<br />
*Make sure that the dental disease is thoroughly addressed.<br />
<br />
*Under local analgesia using proxymetacaine hydrochloride BP (Minims; Alcon), I canulate the lacrimal duct as described by Petersen-Jones and Carrington (1988) and flush the apparatus (irrigating canula reference AS85 from Arnolds Veterinary Products, or iv cannula) with sterile saline until the fluid runs clear from the the nares. The bevelled end of the Surflo intravenous canula makes it an easier instrument for this purpose. The apparatus is then irrigated diluted ophthalmic preparations of antibiotics, ideally following microbial cultures and sensitivity testing. <br />
<br />
*In some cases it is impossible to effect drainage of the tenacious purulent material. I once had success with a solution of trypsin is infused into the duct and the procedure is reattempted after twenty-four to forty-eight hours. <br />
<br />
*Follow-up treatment comprises systemic and topical antibiosis, usually with oxytetracyline (Engemycin® 5%; Intervet) and tetracycline ophthalmic ointment (Fucithalmic®; Leo) or gentamicin (Tiacil®; Virbac) applied to the conjunctival fornix q 6-8 hrs, or antibiotics are selected after sensitivity testing. In the absence of antibiotic sensitivities. I have noticed that topical applications of ophthalmic preparations containing neomycin are frequently not effective in the treatment of this condition.<br />
<br />
==Prognosis==<br />
Prognosis the favourability of the prognosis is inversely proportional to the dental health and to the length of time taken for any response to treatment. Poor response is an indication for withdrawal of treatment and microbiological investigation, including antibiotic sensitivity testing. Long-term, repeated irrigation may result in permanent stenosis or obstruction. <br />
<br />
In young animals in a collective situation (eg. pet shops) a simple conjunctivitis in which the teeth are not involved may be encountered. Cytology may be useful in identifying the causative organism(s). Chlamydophila psittaci may be involved (scrapings from the back of the membrana nictitans may be helpful) and should respond to ciporofloxacin eye drops (Ciloxan®; Alcon Labs).<br />
<br />
==References==</div>Clamyhttps://en.wikivet.net/index.php?title=Dacryocystitis_%E2%80%93_Rabbit&diff=82748Dacryocystitis – Rabbit2010-08-10T00:49:01Z<p>Clamy: /* Aetiology */</p>
<hr />
<div> <br />
{{unfinished}}<br />
==Description==<br />
Dacryocystitis is one of the most common conditions encountered in practice and can be one of the most difficult to treat due to the persistence of the organism involved and the tendency of the condition to recur. It is very important to examine the teeth and both nasolacrimal ducts of every rabbit irrespective of the reason for which the animal is presented for clinical examination. <br />
<br />
==Clinical Signs==<br />
Clinical signs of dacryocystitis include a milky discolouration of the precorneal tear film, epiphora, crust formation along the affected eyelid margins and a caseous discharge from the nostril. The condition can be unilateral or bilateral. The clinician may have to apply digital pressure on the lacrimal sac to observe a milky discharge from the lacrimal punctum. Keratitis and conjunctivitis are sometimes observed. A white crust on medial canthus is a frequent early clinical sign.<br />
<br />
==Aetiology==<br />
<br />
The prime agent of aetiological significance is [[Cheek Teeth Malocclusion – Rabbit|dental malocclusion]]. The constant growth of the teeth combined with the low bone density of the rabbit skull results in the migration of the roots of the teeth leading to:<br />
<br />
#Occlusion of the naso-lacrimal duct by the roots of the incisors (welling of the milky discharge up the lacrimal apparatus results in epiphora). <br />
#Invasion of the eye socket by the roots of the molars leading to retrobulbar infection, buphthalmos or simply ocular irritation and epiphora.<br />
<br />
<br />
Microbiological investigation yields profuse growth of many organisms, usually ''Pasteurella multocida'' (Petersen-Jones and Carrington 1988), but ''Staphylococcus'' species and ''Streptococcus'' species, can also be frequently involved. Dacryocystitis can be due to an ascending infection from the nasal cavity via the nasolacrimal duct and is a constituent part of the syndrome of Pasteurella infection in rabbits (Whittaker 1989).<br />
<br />
A survey conducted by Leo Laboratories in 1994 yielded:<br />
<br />
#''Staphyloccus'' spp. - non-haemolytic, 17 isolates; haemolytic coagulase -ve, 10 isolates; haemolytic coagulase +ve, 5 isolates.<br />
<br />
#''Streptococcus'' spp. - non-haemolytic, 4 isolates; alpha-haemolytic, 2 isolates <br />
<br />
#''Pasteurella'' spp. - Pasteurella aerogenes 2 isolates, ''Pasteurella multocida'' 3 isolates, unidentified ''Pasteurella'' spp. 2 isolates, <br />
<br />
#''Bacillus'' spp. - 7 isolates, <br />
<br />
#''Corynebacterium'' spp. - 5 isolates, <br />
<br />
#''Enterobacter'' spp. - 3 isolates<br />
<br />
#''E coli'' - (non-haemolytic) 3 isolates <br />
<br />
#''Pseudomonas'' spp. - ''Pseudomonas vesicularis'' 2 isolates, unidentified ''Pseudomonas'' spp. 1 isolate, <br />
<br />
#''Branhamella'' spp. - one isolate<br />
<br />
#''Proteus'' spp. - one isolate<br />
<br />
#''Acinetobacter junii'' - one isolate<br />
<br />
#No isolates were detected in 12 specimens. <br />
<br />
As well as dental disorders, a triggering factor for the establishment and persistence of infection is thought to be the ammonia produced either by the degeneration of urinary urea in a poorly absorptive litter (Okerman 1988) or from a pet maintained on an imbalanced (high protein) diet (Jenkins 1991). I always counsel the owners of affected animals to attend to hygiene and diet simultaneously. Peat moss /Turf mould is recommended as hutch litter due to its ability to absorb the ammonia produced by the decomposition of urinary urea.<br />
<br />
==Treatment==<br />
<br />
The condition is very difficult to treat as tooth roots are an important factor in the persistent eye infections of rabbits and the distal naso-lacrimal duct may become involved with periapical abscessation of the maxillary incisors (overlong incisor root with thinning or periosteal proliferation of the palatial bone). Dental conditions do not, generally speaking, resolve quickly in rabbits, if at all. Also the causative organism, particularly if it is the ubiquitous Pasteurella multocida, seems to be well adapted to the conjunctival microclimate and local immunity appears to be suppressed. In addition, cannulation of the entire course of the lacrimal duct is impossible due to the tortuous course and varying diameter of the duct although flushing from the lacrimal punctum is possible (Burling et al 1991). Even if the condition is discovered only co-incidentally when the rabbit is presented for some other reason, the following approach should be undertaken: <br />
<br />
*Make sure that the dental disease is thoroughly addressed.<br />
<br />
*Under local analgesia using proxymetacaine hydrochloride BP 0.5% (Minims; Alcon), I canulate the lacrimal duct as described by Petersen-Jones and Carrington (1988) and flush the apparatus (irrigating canula reference AS85 from Arnolds Veterinary Products, or iv cannula) with sterile saline until the fluid runs clear from the the nares. The bevelled end of the Surflo intravenous canula makes it an easier instrument for this purpose. The apparatus is then irrigated diluted ophthalmic preparations of antibiotics, ideally following microbial cultures and sensitivity testing. <br />
<br />
*In some cases it is impossible to effect drainage of the tenacious purulent material. I once had success with a solution of trypsin is infused into the duct and the procedure is reattempted after twenty-four to forty-eight hours. <br />
<br />
*Follow-up treatment comprises systemic and topical antibiosis, usually with oxytetracyline (Engemycin® 5%; Intervet) and tetracycline ophthalmic ointment (Fucithalmic®; Leo) or gentamicin (Tiacil®; Virbac) applied to the conjunctival fornix q 6-8 hrs, or antibiotics are selected after sensitivity testing. In the absence of antibiotic sensitivities. I have noticed that topical applications of ophthalmic preparations containing neomycin are frequently not effective in the treatment of this condition.<br />
<br />
==Prognosis==<br />
Prognosis the favourability of the prognosis is inversely proportional to the dental health and to the length of time taken for any response to treatment. Poor response is an indication for withdrawal of treatment and microbiological investigation, including antibiotic sensitivity testing. Long-term, repeated irrigation may result in permanent stenosis or obstruction. <br />
<br />
In young animals in a collective situation (eg. pet shops) a simple conjunctivitis in which the teeth are not involved may be encountered. Cytology may be useful in identifying the causative organism(s). Chlamydophila psittaci may be involved (scrapings from the back of the membrana nictitans may be helpful) and should respond to ciporofloxacin eye drops (Ciloxan®; Alcon Labs).<br />
<br />
==References==</div>Clamyhttps://en.wikivet.net/index.php?title=Dacryocystitis_%E2%80%93_Rabbit&diff=82343Dacryocystitis – Rabbit2010-08-08T01:56:08Z<p>Clamy: </p>
<hr />
<div> <br />
{{unfinished}}<br />
==Description==<br />
Dacryocystitis is one of the most common conditions encountered in practice and can be one of the most difficult to treat due to the persistence of the organism involved and the tendency of the condition to recur. It is very important to examine the teeth and both nasolacrimal ducts of every rabbit irrespective of the reason for which the animal is presented for clinical examination. <br />
<br />
==Clinical Signs==<br />
Clinical signs of dacryocystitis include a milky discolouration of the precorneal tear film, epiphora, crust formation along the affected eyelid margins and a caseous discharge from the nostril. The condition can be unilateral or bilateral. The clinician may have to apply digital pressure on the lacrimal sac to observe a milky discharge from the lacrimal punctum. Keratitis and conjunctivitis are sometimes observed. A white crust on medial canthus is a frequent early clinical sign.<br />
<br />
==Aetiology==<br />
<br />
The prime agent of aetiological significance is [[Cheek Teeth Malocclusion – Rabbit|dental malocclusion]]. The constant growth of the teeth combined with the low bone density of the rabbit skull results in the migration of the roots of the teeth leading to:<br />
<br />
#Occlusion of the naso-lacrimal duct by the roots of the incisors (welling of the milky discharge up the lacrimal apparatus results in epiphora). <br />
#Invasion of the eye socket by the roots of the molars leading to retrobulbar infection, buphthalmos or simply ocular irritation and epiphora.<br />
<br />
<br />
Microbiological investigation yields profuse growth of many organisms, usually Pasteurella multocida (Petersen-Jones and Carrington 1988), but Staphylococcus species and Streptococcus species, can also be frequently involved. Dacryocystitis can be due to an ascending infection from the nasal cavity via the nasolacrimal duct and is a constituent part of the syndrome of Pasteurella infection in rabbits (Whittaker 1989).<br />
<br />
A survey conducted by Leo Laboratories in 1994 yielded:<br />
<br />
#''Staphyloccus'' spp. - non-haemolytic, 17 isolates; haemolytic coagulase -ve, 10 isolates; haemolytic coagulase +ve, 5 isolates.<br />
<br />
#''Streptococcus'' spp. - non-haemolytic, 4 isolates; alpha-haemolytic, 2 isolates <br />
<br />
#''Pasteurella'' spp. - Pasteurella aerogenes 2 isolates, Pasteurella multocida 3 isolates, unidentified Pasteurella spp. 2 isolates, <br />
<br />
#''Bacillus'' spp. - 7 isolates, <br />
<br />
#''Corynebacterium'' spp. - 5 isolates, <br />
<br />
#''Enterobacter'' spp. - 3 isolates<br />
<br />
#''E coli'' - (non-haemolytic) 3 isolates <br />
<br />
#''Pseudomonas'' spp. - Pseudomonas vesicularis 2 isolates, unidentified Pseudomonas spp. 1 isolate, <br />
<br />
#''Branhamella'' spp. - one isolate<br />
<br />
#''Proteus'' spp. - one isolate<br />
<br />
#''Acinetobacter junii'' - one isolate<br />
<br />
#No isolates were detected in 12 specimens. <br />
<br />
As well as dental disorders, a triggering factor for the establishment and persistence of infection is thought to be the ammonia produced either by the degeneration of urinary urea in a poorly absorptive litter (Okerman 1988) or from a pet maintained on an imbalanced (high protein) diet (Jenkins 1991). I always counsel the owners of affected animals to attend to hygiene and diet simultaneously. Peat moss /Turf mould is recommended as hutch litter due to its ability to absorb the ammonia produced by the decomposition of urinary urea.<br />
<br />
==Treatment==<br />
<br />
The condition is very difficult to treat as tooth roots are an important factor in the persistent eye infections of rabbits and the distal naso-lacrimal duct may become involved with periapical abscessation of the maxillary incisors (overlong incisor root with thinning or periosteal proliferation of the palatial bone). Dental conditions do not, generally speaking, resolve quickly in rabbits, if at all. Also the causative organism, particularly if it is the ubiquitous Pasteurella multocida, seems to be well adapted to the conjunctival microclimate and local immunity appears to be suppressed. In addition, cannulation of the entire course of the lacrimal duct is impossible due to the tortuous course and varying diameter of the duct although flushing from the lacrimal punctum is possible (Burling et al 1991). Even if the condition is discovered only co-incidentally when the rabbit is presented for some other reason, the following approach should be undertaken: <br />
<br />
*Make sure that the dental disease is thoroughly addressed.<br />
<br />
*Under local analgesia using proxymetacaine hydrochloride BP 0.5% (Minims; Alcon), I canulate the lacrimal duct as described by Petersen-Jones and Carrington (1988) and flush the apparatus (irrigating canula reference AS85 from Arnolds Veterinary Products, or iv cannula) with sterile saline until the fluid runs clear from the the nares. The bevelled end of the Surflo intravenous canula makes it an easier instrument for this purpose. The apparatus is then irrigated diluted ophthalmic preparations of antibiotics, ideally following microbial cultures and sensitivity testing. <br />
<br />
*In some cases it is impossible to effect drainage of the tenacious purulent material. I once had success with a solution of trypsin is infused into the duct and the procedure is reattempted after twenty-four to forty-eight hours. <br />
<br />
*Follow-up treatment comprises systemic and topical antibiosis, usually with oxytetracyline (Engemycin® 5%; Intervet) and tetracycline ophthalmic ointment (Fucithalmic®; Leo) or gentamicin (Tiacil®; Virbac) applied to the conjunctival fornix q 6-8 hrs, or antibiotics are selected after sensitivity testing. In the absence of antibiotic sensitivities. I have noticed that topical applications of ophthalmic preparations containing neomycin are frequently not effective in the treatment of this condition.<br />
<br />
==Prognosis==<br />
Prognosis the favourability of the prognosis is inversely proportional to the dental health and to the length of time taken for any response to treatment. Poor response is an indication for withdrawal of treatment and microbiological investigation, including antibiotic sensitivity testing. Long-term, repeated irrigation may result in permanent stenosis or obstruction. <br />
<br />
In young animals in a collective situation (eg. pet shops) a simple conjunctivitis in which the teeth are not involved may be encountered. Cytology may be useful in identifying the causative organism(s). Chlamydophila psittaci may be involved (scrapings from the back of the membrana nictitans may be helpful) and should respond to ciporofloxacin eye drops (Ciloxan®; Alcon Labs).<br />
<br />
==References==</div>Clamyhttps://en.wikivet.net/index.php?title=Dacryocystitis_%E2%80%93_Rabbit&diff=82342Dacryocystitis – Rabbit2010-08-08T01:52:27Z<p>Clamy: /* Aetiology */</p>
<hr />
<div> <br />
{{unfinished}}<br />
==Description==<br />
Dacryocystitis is one of the most common conditions encountered in practice and can be one of the most difficult to treat due to the persistence of the organism involved and the tendency of the condition to recur. It is very important to examine the teeth and both nasolacrimal ducts of every rabbit irrespective of the reason for which the animal is presented for clinical examination. <br />
<br />
==Clinical Signs==<br />
Clinical signs of dacryocystitis include a milky discolouration of the precorneal tear film, epiphora, crust formation along the affected eyelid margins and a caseous discharge from the nostril. The condition can be unilateral or bilateral. The clinician may have to apply digital pressure on the lacrimal sac to observe a milky discharge from the lacrimal punctum. Keratitis and conjunctivitis are sometimes observed. A white crust on medial canthus is a frequent early clinical sign.<br />
<br />
==Aetiology==<br />
<br />
The prime agent of aetiological significance is [[Cheek Teeth Malocclusion – Rabbit|dental malocclusion]]. The constant growth of the teeth combined with the low bone density of the rabbit skull results in the migration of the roots of the teeth leading to:<br />
<br />
#Occlusion of the naso-lacrimal duct by the roots of the incisors (welling of the milky discharge up the lacrimal apparatus results in epiphora). <br />
#Invasion of the eye socket by the roots of the molars leading to retrobulbar infection, buphthalmos or simply ocular irritation and epiphora.<br />
<br />
<br />
Microbiological investigation yields profuse growth of many organisms, usually Pasteurella multocida (Petersen-Jones and Carrington 1988), but Staphylococcus species and Streptococcus species, can also be frequently involved. Dacryocystitis can be due to an ascending infection from the nasal cavity via the nasolacrimal duct and is a constituent part of the syndrome of Pasteurella infection in rabbits (Whittaker 1989).<br />
<br />
A survey conducted by Leo Laboratories in 1994 yielded:<br />
<br />
#''Staphyloccus'' spp. - non-haemolytic, 17 isolates; haemolytic coagulase -ve, 10 isolates; haemolytic coagulase +ve, 5 isolates.<br />
<br />
#''Streptococcus'' spp. - non-haemolytic, 4 isolates; alpha-haemolytic, 2 isolates <br />
<br />
#''Pasteurella'' spp. - Pasteurella aerogenes 2 isolates, Pasteurella multocida 3 isolates, unidentified Pasteurella spp. 2 isolates, <br />
<br />
#''Bacillus'' spp. - 7 isolates, <br />
<br />
#''Corynebacterium'' spp. - 5 isolates, <br />
<br />
#''Enterobacter'' spp. - 3 isolates<br />
<br />
#''E coli'' - (non-haemolytic) 3 isolates <br />
<br />
#''Pseudomonas'' spp. - Pseudomonas vesicularis 2 isolates, unidentified Pseudomonas spp. 1 isolate, <br />
<br />
#''Branhamella'' spp. - one isolate<br />
<br />
#''Proteus'' spp. - one isolate<br />
<br />
#''Acinetobacter junii'' - one isolate<br />
<br />
#No isolates were detected in 12 specimens. <br />
<br />
As well as dental disorders, a triggering factor for the establishment and persistence of infection is thought to be the ammonia produced either by the degeneration of urinary urea in a poorly absorptive litter (Okerman 1988) or from a pet maintained on an imbalanced (high protein) diet (Jenkins 1991). I always counsel the owners of affected animals to attend to hygiene and diet simultaneously. Peat moss /Turf mould is recommended as hutch litter due to its ability to absorb the ammonia produced by the decomposition of urinary urea.</div>Clamyhttps://en.wikivet.net/index.php?title=Dacryocystitis_%E2%80%93_Rabbit&diff=82341Dacryocystitis – Rabbit2010-08-08T01:51:53Z<p>Clamy: /* Clinical Signs */</p>
<hr />
<div> <br />
{{unfinished}}<br />
==Description==<br />
Dacryocystitis is one of the most common conditions encountered in practice and can be one of the most difficult to treat due to the persistence of the organism involved and the tendency of the condition to recur. It is very important to examine the teeth and both nasolacrimal ducts of every rabbit irrespective of the reason for which the animal is presented for clinical examination. <br />
<br />
==Clinical Signs==<br />
Clinical signs of dacryocystitis include a milky discolouration of the precorneal tear film, epiphora, crust formation along the affected eyelid margins and a caseous discharge from the nostril. The condition can be unilateral or bilateral. The clinician may have to apply digital pressure on the lacrimal sac to observe a milky discharge from the lacrimal punctum. Keratitis and conjunctivitis are sometimes observed. A white crust on medial canthus is a frequent early clinical sign.<br />
<br />
==Aetiology==<br />
<br />
The prime agent of aetiological significance is [[Cheek Teeth Malocclusion – Rabbit|dental malocclusion]]. The constant growth of the teeth combined with the low bone density of the rabbit skull results in the migration of the roots of the teeth leading to:<br />
<br />
#Occlusion of the naso-lacrimal duct by the roots of the incisors (welling of the milky discharge up the lacrimal apparatus results in epiphora). <br />
#Invasion of the eye socket by the roots of the molars leading to retrobulbar infection, buphthalmos or simply ocular irritation and epiphora.<br />
<br />
<br />
Microbiological investigation yields profuse growth of many organisms, usually Pasteurella multocida (Petersen-Jones and Carrington 1988), but Staphylococcus species and Streptococcus species, can also be frequently involved. Dacryocystitis can be due to an ascending infection from the nasal cavity via the nasolacrimal duct and is a constituent part of the syndrome of Pasteurella infection in rabbits (Whittaker 1989).<br />
<br />
A survey conducted by Leo Laboratories in 1994 yielded:<br />
<br />
#''Staphyloccus'' spp. - non-haemolytic, 17 isolates; haemolytic coagulase -ve, 10 isolates; haemolytic coagulase +ve, 5 isolates.<br />
#''Streptococcus'' spp. - non-haemolytic, 4 isolates; alpha-haemolytic, 2 isolates <br />
<br />
#''Pasteurella'' spp. - Pasteurella aerogenes 2 isolates, Pasteurella multocida 3 isolates, unidentified Pasteurella spp. 2 isolates, <br />
<br />
#''Bacillus'' spp. - 7 isolates, <br />
<br />
#''Corynebacterium'' spp. - 5 isolates, <br />
<br />
#''Enterobacter'' spp. - 3 isolates<br />
<br />
#''E coli'' - (non-haemolytic) 3 isolates <br />
<br />
#''Pseudomonas'' spp. - Pseudomonas vesicularis 2 isolates, unidentified Pseudomonas spp. 1 isolate, <br />
<br />
#''Branhamella'' spp. - one isolate<br />
<br />
#''Proteus'' spp. - one isolate<br />
<br />
#''Acinetobacter junii'' - one isolate<br />
<br />
#No isolates were detected in 12 specimens. <br />
<br />
As well as dental disorders, a triggering factor for the establishment and persistence of infection is thought to be the ammonia produced either by the degeneration of urinary urea in a poorly absorptive litter (Okerman 1988) or from a pet maintained on an imbalanced (high protein) diet (Jenkins 1991). I always counsel the owners of affected animals to attend to hygiene and diet simultaneously. Peat moss /Turf mould is recommended as hutch litter due to its ability to absorb the ammonia produced by the decomposition of urinary urea.</div>Clamy