small mammals 5 - Diseases of Rodents and Other Species Flashcards
guinea pig diseases common with rabbits
- Gastrointestinal
Stasis and Dysbiosis - Dental Disease and
Abscesses
Urolithiasis
GP Gastrointestinal
Stasis and Dysbiosis causes
- Dental disease
- Antibiotic-associated enterotoxaemia – G-ve and Clostridium overgrowth
- GDV – rare
GP risk factor for Dental Disease and
Abscesses
- Hypovitaminosis C
Urolithiasis GP surgical outcome
Very poor surgical outcome
Urolithiasis in GPs
- how it arises, what occurs, concurrent issues….
- Urolithiasis is a common problem; etiopathogenesis is unclear.
- Calculi are found in both sexes, usually more than 2 years old.
- 90% of calculi are composed of calcium carbonate.
- Most are in the bladder, urethra (commonly at the urethral orifice in sows), or ureters;
also found in the kidneys and occasionally in the seminal vesicles or vagina. - In males, often lodge at the bladder neck at the seminal colliculus (narrowing at the
urethral mound where the seminal vesicles and prostate gland open into the urethra). - Clinical signs are associated with the size and location of the calculi.
- Bladder or urethral calculi – micturition abnormalities such as hematuria, stranguria, or dysuria and vague clinical signs such as lethargy, reluctance to move, and anorexia.
- If higher in the urinary tract – micturition abnormalities may still be present, but lethargy, anorexia, weight loss, and a hunched posture may be the only clinical signs.
- Concurrent urinary tract infections involving Corynebacterium renale and other bacteria.
urolithiasis in GPs Dx
Diagnosis – clinical signs, physical examination, diagnostic imaging (calcium carbonate is
radio-opaque, contrast urethrogram in males, intravenous pyelograms or contrast CT), urinalysis (hematuria); ultrasound for location and to evaluate anatomic changes in the kidneys or ureters.
urolithiasis in GPs tx, prevention
- Treatment – medical unrewarding; may pass stones smaller than 5 mm; surgical or cystoscopic removal.
- Prevention – increase water intake (nipple drinker), reduce dietary calcium (diets should contain a high percentage of timothy, oat, or grass hays, a lower overall percentage of pellets, and a wide variety of low calcium vegetables; alfalfa hay and pellets and high calcium greens should be avoided); potassium citrate questionable.
- Often reoccurs.
GP Vitamin C Deficiency etiology
- Mutated L-gulonolactone oxidase gene
- Cannot convert L-gulonolactone to L-ascorbic acid
- Require vitaminCPO
- Insufficientifin correct/ poorly stored diet
<><><><> - Guinea pigs are incapable of endogenous vitamin C synthesis because have a mutated gene for L-gulonolactone oxidase, preventing the conversion of L- gulonolactone to L-ascorbic acid.
- Require 10 to 25 mg/kg/day of vitamin C in their diet; pregnant animals require 30 mg/kg/day.
- Young, growing animals more susceptible to scurvy, clinical disease within 2 weeks.
- Inappropriate diet (e.g., rabbit pellets) or poorly stored, lacks vitamin C.
Vitamin C Deficiency result
- Defective type IV collagen, laminin, and elastin
- Compromises blood vessel and joint integrity
<><><><> - Results in defective type IV collagen, laminin, and elastin; compromises blood vessel and joint integrity, resulting in joint and gingival hemorrhages; teeth loosen, and malocclusion develops.
Vitamin C Deficiency clinical signs GP
- Rough hair coat
- Dental disease
- Delayed wound healing
- Lameness, paresis, swollen joints
- Increased susceptibility to bacterial infections
- Pathological fractures
- Generalized hemorrhages
Vitamin C Deficiency Dx
- Serum ascorbic acid level
Vitamin C Deficiency treatment
- Vitamin C parentally then PO
Hyperthyroidism etiology GP
- Common, > 3 years
- Thyroidhyperplasia, adenoma, or carcinoma; non-functional / functional
- If functional→increase in circulating thyroxine and triiodothyronine → increase in metabolic rate
<><><>< - Thyroid hyperplasia, adenoma, and carcinoma; non-functional or functional (leading to hyperthyroidism).
- Most common endocrine disorder; animals older than 3 years.
- Excessive circulating thyroid hormones (thyroxine and triiodothyronine) result in
an increase in metabolic rate and exacerbate effects on the sympathetic nervous system.
Hyperthyroidism clinical signs GP
If functional
* Increased appetite
* PU/PD
* Weight loss
* Hyperactivity, nervousness
* Soft feces or diarrhea
* Palpable subcutaneous masses on the ventral neck
* Tachycardia, heart murmur, arrhythmia
* Hyperesthesia
<><><><>
Clinical signs – progressive weight loss, reduced body condition, normal or increased appetite, polydipsia and polyuria, hyperactivity, nervousness, and soft feces or diarrhea; palpable subcutaneous masses on the ventral neck, tachycardia, heart murmur, arrhythmia, and hyperesthesia.
Hyperthyroidism GP Dx
- Thyroid panel
- US, FNA
- Diagnosis – blood sample for full thyroid panel; diagnostic imaging (fine-needle aspirate).
Hyperthyroidism treatment GP
- Radioactive I131 best
- Surgical removal difficult
- Life-long methimazole or carbimazole
<><><> - Treatment – radioactive iodine-131 gold-standard; drugs that inhibit thyroid hormone synthesis, such as methimazole or carbimazole, not curative and life-long treatment; surgical removal difficult.
Ovarian Cysts GP
* Etiology and Result
- Ovarian cysts are common in guinea pigs, older animals.
- Two types occur: serous cysts (cystic rete ovarii, non-functional cysts) and
hormone-producing follicular cysts. - Problems reported concurrently include leiomyomas of the uterine structures,
granulosa cell tumors, cystic endometrial hyperplasia, and endometritis. - Serous Cysts
- Develop spontaneously throughout the estrous cycle, not LH responsive, not hormone-producing; single / multilocular, clear fluid; 0.5-7 cm diameter, increase with age; only space-occupying signs.
- Diagnosis by ultrasound.
- Palliative draining but can quickly reoccur; ovariohysterectomy.
- Follicular Cysts
- Usually coincide with serous cysts; derived from preovulatory follicles that fail to ovulate; alters normal ovarian cyclicity.
- Associated with bilaterally symmetric nonpruritic flank alopecia and mammary hyperkeratosis.
- May respond to gonadotropin-releasing hormone (GnRH) and human chorionic gonadotropin (hCG) by inducing a surge of luteinizing hormone (LH), resulting in luteinization of cysts.
- Sustained-release GnRH formulations (e.g., deslorelin implants) not effective, can lead to vaginal infections.
Ovarian Cysts Dx GP
US
Ovarian Cysts Tx GP
- Serous
- Drain, ovariohysterectomy
<><><><> - Follicular
- GnRH, hCG → LH surge → luteinization
- Not sustained-release GnRH formulations
GP ectoparasites etiology
- Fur mite – Chirodiscoides caviae
- Sarcoptic mite – Trixacarus caviae, zoonotic
- Lice and, rarely, Demodex
- Secondary bacterial / fungal
infections
Trixacarus caviae cause what in GP
severe pruritis
Ectoparasites GP treatment
- Ivermectin / selamectin
- Antihistamine, NSAIDs
- Environment
GP ectoparasites summary
- The fur mite Chirodiscoides caviae is most common; subclinical to severe.
- The sarcoptic mite Trixacarus caviae is the most severe; scratch so intensely,
appear to be having a seizure; zoonotic. - Infection with lice (Gliricola porcelli, Gyropus ovalis) and, rarely, Demodex caviae
also occurs. - Secondary fungal or bacterial infections.
- Diagnosed by microscopic examination and direct visualization of the mites or
their eggs. - Treatment with ivermectin or selamectin effective; often repeat.
- Treat severe pruritus with antihistamines (diphenhydramine, hydroxyzine), and
NSAIDs. - Disinfect the environment.
Dermatophytosis in GP organisms
- Trichophyton mentagrophytes and T. benhamiae
- Microsporum canis
GP pneumonia pathogen
- Bordetella bronchiseptica * Rabbits → GP
GP enteritis etiology
- Tyzzer’s disease * Salmonellosis
GP cervical lymphadenitits pathogen
Streptococcus equi, subsp. zooepidemicus
