Chapter 6. Biology and Diseases of Guinea Pigs Flashcards

1
Q

What is the only New World rodent used commonly in research?

A

Guinea pig - Cavia porcellus

  • First domesticated by the Andean Indians of Peru; Dutch introduced to Europe in 16th century & bred by fanciers
  • Colors include white, black, brown, red, brindle, roan; may be mono-, bi-, or tricolored
  • Short regular hair (shorthair or English); longer hair with whorls (Abyssinian), long straight hair (Peruvian), medium-length fine hair (silky)
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2
Q

What stocks of guinea pigs are currently commercially available in the US?

A

Outbred pigmented stocks, albino Hartley stocks, and IAF hairless stocks
-Two inbred strains (strains 2 and 13) no longer available; strain 13 can be obtained from US Army Medical Research Institute of Infectious Dieases (USAMRIID)

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3
Q

What is the taxonomy of the guinea pig?

A

Order Rodentia has 3 suborders Sciuromorpha (squirrel-like rodents), Myomorpha (rat-like rodents), Hystrichomorpha (porcupine-like rodents)

Guinea pigs: Order Rodentia, Suborder Hystrichomorpha (currently controversial), Family Caviidae, Subfamily Caviinae, Genus Cavia

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4
Q

Family Caviidae

A

Five genera and ~23 species of South American rodents
Have 4 digits on forefeet and 3 digits on hind feet
Soles of feet are hairless, nails are short and sharp

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5
Q

Genus Cavia

A

Stocky bodies with a large head, short limbs and ears, single pair of mammae, vestigial tail

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6
Q

Axenic guinea pig

A

Guinea pig was first laboratory animal species maintained in an axenic state

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7
Q

Research uses of guinea pigs

A

Closely model human Vitamin C metabolism and airway reactivity in asthma

  • Anaphylaxis, asthma, delayed hypersensitivity, genetics, gnotobiotics, immunology, infectious disease, nutrition, otology, pharmacology, research in space
  • Pharmaceutical industry use: preclinical testing of cardiac safety of new drugs, hairless G pigs used for development of topical drugs
  • Medical device industry: sensitivity testing, source of serum complement in labs using the complement fixation test to diagnose infx dz
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8
Q

Blood collection in guinea pigs

A

Lack of tail and thick skin make blood collection relatively challenging
Can collect small volumes (~100 µl) from jugular, saphenous, cephalic
Collection of larger volumes from retro-orbital, cranial vena cava, terminal cardiac puncture

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9
Q

Guinea pig intubation & oral dosing

A

Challenging due to their unique pharyngeal anatomy - an elongated soft palate covers the back of the throat, leaving only the small palatial ostium for access to the trachea and esophagus

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10
Q

Guinea pig bedding

A

Solid bottom flooring recommended over wire (only use if necessary experimentally)
Guinea pigs given wood shavings and paper sheets spent sig more time during light cycle in areas of wood shaving, and had slight preference for paper sheets in dark conditions
Some bedding materials will interfere with animal tests involving ascorbic acid depletion because of presence of low levels of Vitamin C - cedar shavings

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11
Q

The Guide cage space requirements for guinea pigs

A

Animals weighing 350g or less: 60 in^2 floor space
Weighing more that 350g: 101 in^2
Height of primary enclosure should be at least 7 inches
Macroenvironmental temp of 20-26 C (68-79 F), relative humidity 30-70%, ventilation of 10-15 fresh air changes per hour with no draft, 12:12 light:dark cycle

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12
Q

Guinea pig feeding and watering

A

Do not adapt readily to changes in how feed and water are presented - need to observe animals often
Feed usually given in J feeder
Water usually given in bottles or by automatic watering system; automatic watering valves used in solid bottom caging should be located outside the cage to minimize wet or flooded cages

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13
Q

Learning in guinea pigs and tonic immobility

A
Positive reinforcement (operant conditioning) recommended
Aversive stimuli that induce anxiety or fear may induce in the guinea pig a profound somatic and autonomic motor inhibition known as TONIC IMMOBILITY behavior - also known as animal hypnosis or feigning death, mediated by periaqueductal gray matter, the limbic forebrain, and spinal areas; should NOT be used as a means of restraint
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14
Q

Circulatory and lymphoreticular system in guinea pigs

A
  • RBC indices (red cell count, hemoglobin, packed cell volume) relatively low compared to other laboratory rodents
  • Historical erythrocyte counts were lower than modern and historical mean white count was higher (subclinical disease)
  • Lymphocytes are predominant leukocyte in peripheral blood
  • Neutrophils (heterophils or pseudoeosinophils) have distinct eosinophilic granules in cytoplasm
  • Foa-Kurloff or Kurloff cell = estradiol-dependent mononuclear leukocyte unique to guinea pigs; found primarily in thymus, sinusoids of spleen, liver, and lung; increased # in circulation during pregnancy; large numbers in placenta - may have role in preventing maternal rejection of fetal placenta; has LARGE MUCOPOLYSACCHARIDE, INTRACYTOPLASMIC INCLUSION BODY - metachromatic and PAS(+), contains proteoglycans and hydrolytic enzymes similar to smaller intracytoplasmic granules in NK cells; has NK cytotoxic activity in vitro and may be part of cancer resistance in guinea pig
  • Guinea pigs, like ferrets and primates, relatively resistant to effects of steroids - thymic and peripheral lymphocytes not markedly reduced by corticosteroid injections
  • Guinea pig is model of genetic control of the histocompatibility-linked immune response
  • Thymus is located in ventral cervical region, easy to remove surgically but accessory thymic islets exist in contiguous fascia, has no apparent afferent lymphatic vessels
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15
Q

Guinea pig dental formula and oral cavity

A

2(I 1/1, C 0/0, PM 1/1, M 3/3) = 20

  • Diastema between incisors and premolars
  • All teeth are open rooted and grow continuously - hypsodontic
  • Incisors normally white (unlike yellow-orange in other rodents); upper incisors shorted than lower
  • Oral cavity small and narrow; soft palate covers nearly entire back of pharynx except for small palatal ostium = guina pig is OBLIGATE NASAL BREATHER
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16
Q

Guinea pig GI system

A

Monogastric hind-gut fermenters

  • Unlike other rodents, stomach is undivided and lined entirely by glandular epithelium
  • Cecum can hold 65% of total GI content
  • Gastric emptying time is ~2 hour
  • Cecal emptying time very slow
  • Total GI emptying time is ~20 hour
  • With coprophagy, entire transit time can be ~60-70 hour
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17
Q

Guinea pig cardiovascular system

A

Both a lower basal coronary blood flow and a lower peak coronary blood flow compared to rat

  • Intercoronary collateral network is well developed = cardiac infarct difficult to produce by acute coronary artery occlusion
  • Myocardiocytes are not as “stiff” compared to rat
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18
Q

Preyer or pinna reflex

A

Cocking of pinnae in response to a sharp sound

-Used in otologic studies as measurement of hearing function

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19
Q

Guinea pig ear

A

Advantages of using guinea pig ear include large bullae, ease of surgical entry to the middle and inner ears, protrusion of the cochlea and blood vessels into the cavity of the middle ear - allows exam of the microcirculation of the inner ear
-Two reported mutations causing inner ear malformation and ‘waltzing’

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20
Q

Guinea pig pituitary gland

A

Pituitary growth hormone is responsible for postnatal growth in vertebrates & removal of pituitary gland in most species alters growth pattern
-Hypophysectomy in guinea pigs does NOT alter growth rate & supplementation with guinea pig pituitary extract fails to alter growth rate of both hypophysectomized and normal guinea pigs

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21
Q

Somatomedins in guinea pigs

A

Somatomedines insulin-like growth factor I (IGF-I) and IGF-II are responsible for growth in guinea pigs

  • Unlike other species, somatomedins in guinea pigs are NOT growth hormone dependent & hypophysectomy does not decrease level of somatomedins
  • What regulates somatomedins in guinea pigs is unknown
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22
Q

Reproductive values for guinea pigs

A
  • First ovulation: 4-5 wks
  • First ejaculation: 8-10 wks
  • Breeding onset in males: 600-700g (3-4 months)
  • Breeding onset in females: 350-450g (2-3 months)
  • Cycle length: 15-17 days
  • Implantation: 6-7 days post ovulation
  • Gestation period: 59-72 days
  • Postpartum estrus: 60-80% fertile
  • Litter size: 2-5
  • Liter interval: 96 days
  • Weaning age: 180g (14-8 days)
  • Breeding life: 18 months-4 years (4-5 litters)
  • Milk composition: 3.9% fat, 8.1% protein, 3.0% lactose
  • Milk yield maximum: 45-65ml/kg body weight/day
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23
Q

Guinea pig diet

A

Feed diet specifically for the species and containing Vitamin C; most feeds now contain stabilized Vitamin C that can be used for 180 days

  • Some cases feed additional high Vit C foods: orange wedges, kale, cabbage
  • Commercial guinea pig pellets are ~18-20% crude protein, 9-18% fiber
  • Metastatic calcification has been assoc w/ diets low in Mg, with incorrect Ca:P ratios, or with extremely high levels of Vit D
  • “Imprint” food types early in life so may not recognize other foods (powdered, additives, vegetable supplements, etc.); placing powder in agar or blending foods for transition can help; guinea pigs scatter food and dribble water so measuring consumption is difficult
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24
Q

Guinea pig hierarchy

A

In mixed-sex groups, a dominant male hierarchy and a less defined female hierarchy develop

  • Scent marking with urine, anal, and supracaudal gland secretions and vocalization and agonistic displays used to assert dominance and defend territory
  • In harem breeding, a dominant female may be apparent by lack of fight wounds or hair loss from barbering
  • Sexually immature males can be housed together, but not recommended for adult males as can fight; shelters placed in group housed male cages reduce aggression
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25
Q

Guinea pig vocalizations

A

Use a dozen or more audible calls for various reasons including calls to increase proximity, greeting, proximity-maintaining calls, proximity-regaining calls, distress calls, alarm calls

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26
Q

Reproductive anatomy in male guinea pigs

A
  • Accessory sex glands include larger, transparent, smooth seminal vesicle (up to 10 cm in length), prostate, coagulating glands, bulbourethral glands, and rudimentary preputial glands
  • Testes remain in inguinal pouches & inguinal canals open for life
  • Os penis present
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27
Q

Reproductive anatomy in female guinea pigs

A
  • Uterus is bicornate & terminates in single os cervix
  • Vagina sealed by vaginal closure membrane - epithelial structure that ruptures just before onset of estrus and reforms after ovulation
  • Sows should be bred first when large enough to bear a litter but before calcification of the fibrocartilaginous pubic symphysis - calcifies and becomes fused between 6-9 months of age - prone to dystocia if first give birth after this fusion
  • Vendors first breed sows when 350-500g (5-13 weeks) and boars when 500-800g (7-13 weeks)
  • Spontaneous ovulators and polyestrous; have postpartum estrus
  • Heavily bred sows may cease hair growth, resulting in patchy alopecia
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28
Q

Estrous cycle in guinea pigs

A

~16 days (13-21 days)

  • Proestrus: 1-1.5 days, characterized by vaginal swelling, rupture of vaginal closure membrane, increased activity, nucleated and cornified epithelial cells on vaginal smear
  • Estrus: 8-11 hours, swollen congested vulva, perforate vaginal membrane, lordosis and rear quarters elevated
  • Metestrus: 3 days
  • Diestrus: 11-12 days
  • Fertile postpartum estrus occurs from 2-10 hour after parturition
  • Estrus can be synchronized with progesterone administered orally or as a SC implant
  • Vaginal impedence measureents can be used to assess stage of estrous cycle
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29
Q

Mating in guinea pigs

A
  • Boar makes one or two intromissions and then ejcaulates
  • Coital completion indicated by grooming, scooting, and perianal marking by the boar
  • Copulatory plug may be found in the female or bedding
  • ~60-85% of matings, including postpartum matings, are fertile
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30
Q

Gestation in guinea pigs

A

68 days (59-72 days)

  • Blastocysts implant on day 6 or 7 of gestation
  • Placentation is labyrinthine hemomonochorionic, similar to humans - good model for reproductive toxicology studies
  • Fetuses can be palpated at day 15, 5mm diameter firm swelling
  • Fluid-filled round swellings apparent on U/S at day 16, diagnosis approaches 100% by day 19
  • Pubic symphysis separates to 3 cm during last week of gestation
  • Gestation length generally inversely proportional to litter size
  • Relaxin produced by placenta beginning around day 30 through about day 63 - responsible for loosening of the fibrocartilaginous pelvic symphysis
  • Sows do NOT build nests
  • Pups delivered every 3-7 min; completetion of parturition in 30 min
  • Large litters (3 or more) assoc w/ higher incidence of stillbirths
  • Dystocia can occur in sows bred for the first time after fusion of pubic symphysis, obese sows, sows with large fetuses
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31
Q

Development of newborn guinea pigs

A
  • Born precocious with hair, teeth, open eyes and ears, fully mobile
  • Begin to eat and drink within hours of birth; feeder and sipper tube may be lowered to provide access
  • Average birth weight 45-115g; pups weighing less than 50g at birth generally do not survive
  • Do not nurse for first 24 hr
  • Pup mortality of up to 50% can be seen if pups are undersized or do not receive milk from a sow during first 3-4days of life
  • Voluntary micturition does not occur until 7-14 days of age
  • Can be weaned at 14 days but generally weaned at 21 days
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32
Q

Artifical insemination in guinea pigs

A
  • Electroejaculation produces 0.4-0.8mL of semen; in some electroejaculated boars the ejaculum coagulates in the urethra
  • Sperm can be harvested from the vasa deferentia and epididymides
  • IP insemination has been reported with up to 100% incidence of conception when used in conjunction with estrus synchronization; additional methods include injection of sperm directly into uterine horns following laparotomy, endoscope-guided transcervical insemination
  • AI has been successful up to 16 hr postestrus
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33
Q

Superovulation and embryo transfer in guinea pigs

A
  • Superovulation induced by IP human menopausal gonadotropin (hMG) and by active immunization against the inhibin α-subunit
  • Embryo transfer reported rarely in guinea pigs - a method for rederivation purposes has been described where embryos were harvested from donors at 1.5 and 2.5 days post-coitus and transferred to pseudoprenant females mated to vasectomized males 1.5 to 2.5 days earlier - 59 embryos were transferred & two pups were born at 69 & 71 days gestation
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34
Q

Helicobacter species in guinea pigs

A
  • Naturally occurring Helicobacter spp. in guinea pigs have NOT been reported
  • Experimental infx with Helicobacter pylori results in severe gastritis that can persist for at least 5 months - model for dz in humans
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35
Q

Guinea pigs as respiratory models

A
  • Similar pulmonary system to humans
  • Used to model Legionnaires disease, TB, and other viral and bacterial infx
  • Extremely sensitive to infection with TB and have been used as sentinels in human hospitals; guinea pig model of TB remains gold standard for testing the potency and standardizing PPD use in humans
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36
Q

Bordetella bronchiseptica

A

Commensal in many species including guinea pigs, rats, rabbits, mice, dogs, swine, cats, turkeys, primates

  • Short, G(-) rod or coccobacillus, aerobic, motile, non-sporeforming
  • In vitro growth best at 30 C but slow to poor at 37 C, with minute, circular, pearlescent colonies present at 24 hr and maximum-size colonies at 72 hr; colonies embed in media and surrounded by zone of β-hemolysis
  • There is serotypic variaton within the species, even within one host species
  • Variably dissociates in culture (isogenic mutation) - these isolates vary in hemolysin, dermonecrotoxin, proteases, adenylate cyclase, and hemagglutinin production - may affect host specificity, virulence, and disease manifestation
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37
Q

Bordetella bronchiseptica - clinical signs in guinea pigs

A
  • Subclinical infxs more common
  • Epizootic respiratory or septicemic disease can progress rapidly (often within 24 hr-72 hr) with high mortality
  • All ages and both sexes affected
  • Can see sporadic deaths in enzootically infected colonites
  • Inappetance, depression, upper respiratory discharge, dyspnea, cyanosis, death
  • Genital form with a 5-7 day incubation period causes infertility, stillbirth, abortions
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38
Q

Bordetella bronchiseptica - transmission in guinea pigs

A

Potential for transmission from rabbits to guinea pigs is a primary reason these species are not housed together

  • Transmission: fine particulate aerosol onto the respiratory mucosa, by contaminated fomites, genital contact
  • Many guinea pigs carry as a commensal resident
  • Higher morbidity and mortality occur among young and historically in Strain 2 inbred animals
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39
Q

Bordetella bronchiseptica - necropsy findings in guinea pigs

A
  • Pulmonary consolidation with respiratory exudation, purulent bronchitis, tracheitis, otitis media; consolidated lung areas dark red to red brown to grey
  • Peribronchiolar and perivascular inflammatory cells contribute to fibrinous or fibrinopurulent bronchopneumonia
  • Uterine infections may be pyosalpinx and dead embryos/fetuses
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40
Q

Bordetella bronchiseptica - pathogenesis in guinea pigs

A

Organism attaches to ciliated respiratory epithelium - proliferates rapidly and causes ciliary paralysis, an inflammatory response, antiphagocytic activity, and dermonecrosis - presumably through action of an intracellular heat-labile toxin

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41
Q

Bordetella bronchiseptica - differentials and diagnosis in guinea pigs

A

Bronchopneumonia: Stretococcus pneumoniae, S. zooepidemicus, Klebsiella pneumoniae, adenovirus

  • Definitive diagnosis = swabbing of lumen of bronchi or lower trachea and aerobic culture on sheep blood and MacConkey agar or Smith and Baskerville medium
  • ELISA and IFA more sensitive then culture for detecting, but various Bordetella antigenic variants should be used on serologic testing
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42
Q

Bordetella bronchiseptica - prevention, control, and treatment in guinea pigs

A
  • Reduction or elimination of stressors as clinical dz often arises from preexisting subclinical infx
  • Purchase Bordetella-free stock
  • Commonly carried by dogs and cats; some research facilities restrict pet ownership
  • Control by isolating infected animals and those susceptible and treat or remove the clinically ill
  • Treatment is supportive care and appropriate antibiotics - fluoroquinolones or trimethoprim-sulfonamides
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43
Q

Streptococcus equi subsp. zooepidemicus

A
  • Lancefield’s group C streptococcus; β-hemolytic, G(+), has antiphagocytic capsule (M-like antigen), produces exotoxin including hyaluronidaze, a protease, and a streptokinase
  • Subspecies zooepidemicus survives longer off host than the obligate pathogen S. equi
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44
Q

S. zooepidemicus - clinical signs in guinea pigs

A
  • Pyogenic bacterium assoc w/ suppuration and abscess formation - usually at cervical lymph nodes (cervical lymphadenitis or ‘lumps’)
  • Torticollis, nasal or ocular discharge, dyspnea, cyanosis, hematuria, hemoglobinuria, cyanotic and swollen mammary glands, abortions, stillbirths, unexpected deaths
  • Cervical nodes in otherwise health guinea pig is the usual sign
  • May be inapparent upper respiratory infections
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45
Q

S. zooepidemicus - transmission in guinea pigs

A
  • Zoonotic potential, although transmission from guinea pigs to humans has not been reported
  • All ages affected, may be more common in females
  • Organism inhabits mucosal surfaces
  • Transmission = via aerosol onto respiratory, oropharyngeal, conjunctival, or female genital epithelium
  • Disease is of low contagion
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46
Q

S. zooepidemicus - necropsy findings in guinea pigs

A
  • Most common = Abscessed and encapsulated cervical lymph nodes (node itself may be destroyed) - abscesses contain a nonodorous, yellow-white to red-grey pus
  • Pneumonia, generalized lymphadenitis, septicemia, focal hepatitis, otitis media, pleuritis, peri- and myocarditis, nephritis, mastitis, metritis, arthritis with necrosis and hemorrhage
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47
Q

S. zooepidemicus - differentials and diagnosis in guinea pigs

A
  • Cervical lymphadentitis: Streptobacillus moniliformis - carried by wild rats
  • Upper respiratory lesions & death: S. pneumoniae, B. bronchiseptica, K. pneumoniae, adenovirus
  • Masses in the neck: lipoma, lymphoma in aged guinea pigs
  • Diagnosis: clinical and necropsy signs, isolation of β-hemolytic streptococci from abscess margin or heart blood; chains of streptococci can be seen on Gram stain of exudates
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48
Q

S. zooepidemicus - prevention, control, treatment in guinea pigs

A
  • Prevention: obtain disease free stock, nonabrasive feed (assuming crude fiber may abrade pharyngeal mucosa), trim overgrown or broken teeth, use feeders that do not abrade skin of neck
  • Control: remove affected animals or replace entire colony
  • Treatment: surgically remove abscess and capsule; antibiotics safe for use in guinea pigs (fluoroquinolones, trimethoprim-sulfonamides, gentamicin, or chloramphenicol) may be effective
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49
Q

Streptococcus pneumoniae

A
  • G(+), α-hemolytic, oval to lancet shaped; occurs in culture in paired or chain formation
  • Two serotypes recovered most often from guinea pigs = 4 and 19F; some of which are assumed to be identical to certain human serovars; one study found guinea pigs may be a reservoir for a serotype 19F that had unique allele combination not found in humans
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50
Q

Streptococcus pneumoniae - clinical signs in guinea pigs

A
  • Subclinical upper respiratory tract carrier states common in guinea pigs and humans, often over 50% prevalence in some colonies; may then see sporadic epidemics when animals are stressed or malnourished
  • Clinical signs: high mortality or, in less acute cases, depression, anorexia, nasal and ocular discharge, sneezing and coughing, dyspnea, torticollis, abortions and stillbirths
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51
Q

Streptococcus pneumoniae - transmission in guinea pigs

A
  • Infections rarely reported or detected in research colonies
  • Transmission: respiratory aerosol, direct contact with infected animals (including humans), vertically during birth
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52
Q

Streptococcus pneumoniae - necropsy findings in guinea pigs

A
  • Primarly pyogenic processes: fibrinopurulent pleuritis, pericarditis, peritonitis, suppurative pneumonia, otitis media, endometritis, arthritis
  • Pulmonary lesion is an acute fibrinopurulent bronchopneumonia with thrombosis of pulmonary vessels
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53
Q

Streptococcus pneumoniae - pathogenesis in guinea pigs

A

-Organism becomes established in upper respiratory tract where it is protected by a polysaccharide capsule and can activate an alternative complement pathway which initiates some of the pathologic changes associated with the infection

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54
Q

Streptococcus pneumoniae - differentials and diagnosis in guinea pigs

A
  • S. pneumoniae can usually be observed on Gram-stained impression smears of infected tissue, or can be cultured on blood agar incubated under 5-10% CO2
  • ELISA for streptococci available
  • Definitive dx requires serotyping among the 83 different capsular polysaccharides; serotyping test = Quellung reaction - utilizes a serum pool product or type-specific antisera - bacterial capsule appears opaque and swollen when the antibody reacts with surface antigens
  • Differentials: Bordetella sp, other streptococci, Salmonella sp., Klebsiella sp., adenovirus
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55
Q

Salmonella enterica

A
  • Seen rarely in research guinea pigs
  • Caused by several serovars of the G(-) bacillus Salmonella enterica, subspecies enterica
  • Serovars Typhimurium and Enteritidis are encountered most frequently
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56
Q

Salmonella enterica - clinical signs in guinea pigs

A
  • Peracute or acute infections: only signs may be high morbidity and mortality; mortality may be as high as 50-100% of the population
  • Epizootic outbreaks occur more often in late pregnant, weanling, aged, and malnourished guinea pigs
  • In longer term survivors or in sporadic clinical cases: rough hair coats, weakness, conjunctivitis, abortion of small litters, light-colored feces or intermittent diarrhea
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57
Q

Salmonella enterica - transmission in guinea pigs

A
  • Inapparent carriers shed the organisms intermittently - continued threat to other animals and humans
  • Transmission: fecal-oral, blood-oral, tissue-oral, via conjunctiva
  • Shed in the feces of wild rodents or other animals, contaminate food (green veggis, hay) intended for guinea pigs
  • Guinea pigs HIGHLY SUSCEPTIBLE to Salmonella; incubation period is 5-7 days
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58
Q

Salmonella enterica - necropsy findings in guinea pigs

A

-Gross lesions may not be present; may see hepatomegaly, splenomegaly, small yellow necrotic foci throughout the viscera

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59
Q

Salmonella enterica- pathogenesis

A

Enter body through GI tract or via conjunctiva & elicit histiocytosis, tissue necrosis, abscess formation

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60
Q

Salmonella enterica - diagnosis in guinea pigs

A
  • Diagnosis: recovery of organism from feces, heart, blood, spleen, or other affected organs through enrichment in a broth such as selenite F or tetrathionate, culture on MackConkey’s or brilliant green agar, and identification of organism
  • Serotyping identifies the serovar
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61
Q

Salmonella enterica - prevention, control, treatment

A
  • Aging, other diseases, malnutrition, and environmental stress are predisposing factors
  • Treatment: NOT recommended; antibitoic use may cause infx to become subclinical and antibiotic resistant
  • Control: euthanize entire colony, sanitize caging and equipment thoroughly, restock with animal known to be free of Salmonella spp.
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62
Q

Clostridium piliforme in guinea pigs

A
  • G(-), curved rod; obligate intracellular anaerobe with subterminal spores that persist for years in the environment
  • Causative agent of Tyzzer’s disease - dz occurs in several species including rodents, rabbits, cats, dogs, horses, some NHP
  • Rare in guinea pigs
  • Clin signs in guinea pigs: emaciation, dehydration, lethargy, diarrhea, death
  • Necrotizing ileitis, typhlitis, and hepatic necrosis in weanling guinea pigs
  • Necropsy: multifocal necrosis and inflammation of ileum, cecum, colon
  • Prevention: avoid stressors and maintain good sanitation
  • Diagnosis: characteristic filamentous bacteria in a Giemsa or Warthin-Starry stained section of enterocytes; organism has not bee directly cultured in vitro
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63
Q

Pasteurella multocida in guinea pigs

A
  • Rare in well-managed colonies; prevalence of infection unknown
  • An epizootic reported in literature involved sporadic, unexpected deaths with pulmonary consolidation, fibrinopurulent serositis, conjunctivitis
  • Diagnosis: culture and identification of characteristic G(-) coccobacillary rods
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64
Q

Pseudomonas aeruginosa in guinea pigs

A
  • Rare in guinea pigs
  • Have been associated with pulmonary lesions involving lung consolidation and severe, focal, necrotizing bronchopneumonia; may also cause conjunctivitis and otitis media; one case study found enlarged, inflamed, fibrous prostate gland with local extension of inflammation
  • Diagnosis: clusters of bacteria surrounded by necrotic debris (‘sulphur granules) in suppurative lesions
  • Pseudomonas is ubiquitous and may be spread in drinking water or in damp bedding or food
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65
Q

Chlamydophila cavia (Chlamydia cavia)

A
  • Formerly Chlamydia psittaci
  • G(-), obligate intracellular bacterium
  • Causes guinea pig inclusion conjunctivitis
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66
Q

Chlamydophila cavia - clinical signs in guinea pigs

A
  • May be subclinical
  • Mild reddening of eyelids up to conjunctivitis with serous to purulent exudate, rhinitis, and genital tract infections; abortions and lower respiratory tract infections
  • Clinical disease is self-limiting with complete recovery in 3-4 weeks
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67
Q

Chlamydophila cavia - differntials and diagnosis in guinea pigs

A
  • Demonstration of intracytoplasmic inclusion bodies in Giemsa- or Macciavello-stained conjunctival epithelial cells
  • PCR
  • Differentials for bacterial conjunctivitis: streptococci, coliforms, S. aureus, Pasteurella multocida
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68
Q

Chlamydophila cavia - control and treatment in guinea pigs

A
  • Self-limiting and typically does not require treatment; Chlamydiophila sp. sensitive to sulfonamide antimicrobials when indicated
  • Conjunctival and genital infections have served as models for human disease; ZOONOTIC POTENTIAL
  • Experimental infx of guinea pig genital tract is good model for human chlamydial genital infx - can be sexually transmitted, similar to children, pups born to infected sows are prone to conjunctivitis
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69
Q

Klebsiella pneumoniae in guinea pigs

A
  • G(-), nonmotile bacillus; causes rare epizootics in guinea pigs of all ages and both sexes
  • Predisposing factors: manutrition, magnitude of exposure, unsanitary environments, genetic predisposition
  • Clinical signs: anorexia, dyspnea, death
  • Necropsy: seropurulent or serofibrinous lesions in the thoracic and abdominal cavities, mastitis, splenomegaly, thrombosis, coagulative necrosis of the liver, granular degeneration of the renal tubular cells, septicemias; pulmonary lesion is acute bronchopneumonia
  • Diagnoses: isolate from blood, liver, spleen, peritoneal exudate, cerebrospinal fluid
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70
Q

Streptobacillus moniliformis in guinea pigs

A
  • Organism of low contagion carried by wild rats and birds; rarely causes disease in research guinea pigs
  • Lesions: cervical adenitis with abscessation like S. zooepidemicus, and a pyogranulmatous bronchopneumonia
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71
Q

Yersinia pseudotuberculosis in guinea pigs

A
  • G(-), nonhemolytic, exotoxin- and enzyme-producing, pleomorphic rod
  • Optimal incubation temperatures are 20-30 C
  • Virulent strains may grow within macrophages
  • Infects both sexes and all ages
  • Clinical signs: 1) Acute, highly fatal septicemia, 2) chronic emaciation, diarrhea, and death within 3-4 weeks, 3) nonfatal lymphadenitis, 4) subclinical carrier state usually following a clinical phase
  • ZOONOTIC
  • Because of persistent carrier state, euthanasia is recommended
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72
Q

Listeria monocytogenes in guinea pigs

A
  • Rare in guinea pigs
  • G(+) rod; widespread in environment including soil and bedding
  • Clinical signs: in hairless guinea pigs unilateral or bilateral keratoconjunctivitis and reproductive disorders
  • Prevention and control involve general precautions
  • Treatment NOT recommended, instead euthanasia because ZOONOTIC
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73
Q

Mycoplasmas in guinea pigs

A

-Mycoplasma caviae, M. pulmonis, etc. and acholeplasmas may occur as latent infections in the reproductive tract, brain, and nasopharynx of guinea pigs

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74
Q

Guinea pig adenovirus (GpAV, GAV)

A
  • Enveloped DNA virus, typical iscosahedral symmetry and 252 capsomers
  • Genetically distinct from adenoviruses infecting other species; is a separate serotype within the genus Mastadenovirus and has the highest homology with other animal Mastadenoviruses and human subgroups A, C, and F
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75
Q

Guinea pig adenovirus - clinical signs

A
  • Subclinical infections may be common - prevalence unknown
  • Clinical disease rare - affected animals usually die without prior signs; may develop dyspnea, tachypnea, dry rales, crepitations, lethargy
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76
Q

Guinea pig adenovirus - transmission

A
  • Infx occurs worldwide and may have a higher prevalence than reported
  • Clinical disease has no age predilection, is sporadic in endemically affected colonies, and is characterized by low morbidity and high mortality
  • Transmission: respiratory route
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77
Q

Guinea pig adenovirus - necropsy findings

A
  • Well-demarcated dark red areas of pulmonary consolidation, compensatory emphysema, sometimes catarrhal exudate in air passages
  • Histology includes necrosis and sloughing of bronchiolar, bronchial, and tracheal epithelial cells - contain large, oval, intranuclear inclusion bodies; surviving epithelium and underlying lamina propria are underlain with a mixed population of inflammatory cells
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78
Q

Guinea pig adenovirus - pathogenesis

A
  • Predisposition factors: stress, immunologically compromised, strain and site of replication of the virus, perhaps anesthetic gas irritation of respiratory tract
  • Virus enters tracheal and bronchial epithelial cells where replication and cell damage occur - followed by epithelial erosion, parenchymal inflammation, exudation in airways
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79
Q

Guinea pig adenovirus - differentials and diagnosis

A
  • Diagnosis: exclusion of other causes and by histologic and electron microscope examination of air passageway epithelial tissue; no specific serologic test - use of mouse adenovirus strain FL antigen produces excessive false (+) reactions; active disease can be detected by PCR from feces or freshly frozen lung
  • Differentials for respiratory disease: B. bronchiseptica, Streptococcus spp., K. pneumoniae, cytomegalovirus, herpesvirus, Sendai, parainfluenza
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80
Q

Guinea pig adenovirus - prevention, control, treatment

A
  • Obtain stocks without history of infection, reduce colony stress, observe immune compromised animals
  • NO treatment
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81
Q

Guinea pig adenovirus - research complications

A
  • Adenoviral vectors used for experimental delivery of aural genes in models of hearing loss; natural infx of study animals did not obviously affect the transfection efficiency of human adenoviral vectors expressing GFP
  • Inapparent pulmonary infections may become clinical problems when animals are stressed
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82
Q

Cytomegalovirus (Caviid herpesvirus 2; guinea pig cytomegalovirus (GPCMV); salivary gland virus)

A
  • Species specific pathogen

- Detected sporadically in lab guinea pigs

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83
Q

Cytomegalovirus - clinical signs

A
  • Usually subclinical
  • Strain of host, pregnancy, and immune compromise may predispose to more serious illness
  • Clinical signs: weight loss, conjunctivitis, lymphadenopathy
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84
Q

Cytomegalovirus - transmission

A
  • Presence likely partially dependent on housing conditions
  • Acute infx followed by chronic, persistent infx
  • Transmission: exposure to saliva carrying the virus, transplacental transmission throughout gestation - preexisting maternal Ab does NOT prevent transmission to fetuses & C-section does NOT interrupt transmission due to transplacental infection
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85
Q

Cytomegalovirus - necropsy findings

A
  • Experimental infection cases more severe signs
  • Natural disease: karyomegaly of salivary gland epithelium (submaxillary gland) to severe interstitial pneumonia, splenomegaly, lymphadenopathy, fetal meningitis
  • Congenital neurological abnormalities and deafness can occur
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86
Q

Cytomegalovirus - pathogenesis

A
  • Viremia within 2 days of exposure - results in widespread, systemic dissemination - salivary gland, hepatic, and renal cells are primary sites of replication
  • Many more organs become infected by 10 days
  • By 12-14 days viremia ceases and virus is more difficult to find in visceral organs
  • By 3 wks postexposure, inclusion bodies are present in salivary glands - chronic, persistent phase contnues in the salivary gland and thymus in adult and in the salivary gland and spleen of fetuses
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87
Q

Cytomegalovirus - diagnosis

A
  • Microscopic identification of large, eosinophilc, usually intranuclear inclusion bodies in the ductal epithelial cells of submaxillary salivary gland - inclusions form at 5 days-3weeks postexposure
  • Inclusion bodies may also be seen in brain, lung, kidney, spleen, pancreas, thymus, liver
  • Indirect fluorescent antibody techniques and histopathology are methods of diagnosis
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88
Q

Cytomegalovirus - prevention, control, treatment

A
  • Prevention and control: select guinea pig stocks known free of GPCMV, screen new arrivals, selective necropsy, serology
  • NO treatment
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89
Q

Cytomegalovirus - research complications

A

-Natural disease may be unapparent (unless detected by serology or necropsy) but could interfere with studies involving tissues harboring virus

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90
Q

Poliovirus in guinea pigs

A

RNA virus; family Picornaviridae; some antigenic cross -reaction with the GDVII strain of Theilovirus

  • Genetic variants among host guinea pigs may affect predisposition to infx and clinical signs
  • Appears more common in pet store than lab guinea pigs, but still a possible diagnosis in guinea pigs with lameness
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91
Q

Poliovirus - clinical signs in guinea pigs

A
  • Clinical signs are rare; within colonies clinical disease is sporadic if it exists at all
  • Clinical signs: depression, lameness in one or more limbs, flaccid paralysis, weight loss, death over 2 weeks
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92
Q

Poliovirus - transmission in guinea pigs

A
  • Transmission route not proven, but fecal-oral common among Picornaviridae
  • In mice and rats the endemic epizootic cycle of Theilovirus is by fecal-oral transmission
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93
Q

Poliovirus - necropsy findings in guinea pigs

A
  • Findings are histologic and include meningomyeloencephalitis, perineuronal inflammation, neuronal degeneration, necrosis of anterior horn cells of the lumbar spinal cord
  • In mice the virus replicates presumably in the grey matter of the cortex and progresses into the white matter and upper motor neuron pathways
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94
Q

Poliovirus - diagnosis in guinea pigs

A

-ELISA using the Theilovirus strain GDVII mouse virus antigen combined with histo findings of CNS and lumbar spinal cord lesions

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95
Q

Poliovirus - treatment and research complications in guinea pigs

A
  • One paper recommended Vitamin C for prevention, control, and treatment, given that Vitamin C contributes to adrenocorticosteroid production and presumably, protection of myelin
  • Infection may complicated investigations of CNS in guinea pigs
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96
Q

Lymphocytic choriomeningitis virus in guinea pigs

A
  • RNA arenavirus
  • Causes lymphocytic choriomeningitis in mice, dogs, primates (including humans) and rarely guinea pigs when contracted iatrogenically via inocluation with contaminated biologicals or possibly through inhalation, ingestion, or through the skin following exposure to biting insects or infected wild mice
  • Clinical signs: CNS dysfunction, hindlimb paralysis
  • Lesions: lymphcytic infiltration in meninges, choroid plexus, ependyma, liver, lungs
  • Diagnosis: IFA - liver is best site for detection; ELISA to detect antibodies
  • ZOONOTIC
  • Has many systemic effects in guinea pigs that would interfere with research projects
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97
Q

Other viral infections in guinea pigs

A
  • Rare and usually clinically inapparent
  • Poxviruses, guinea pig retroviruses, parainflunza viruses, murine pneumonia virus, mammalian orthoreovirus (reovirus 3), simian virus 5, herpesvirus, Sendai virus
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98
Q

Eimeria caviae

A

Protozoan; phylum Apicomplexa; moderately pathogenic
Coccidian with ellipsoidal oocytes without a micropyle
-Infx associated with high populations of Balantidium coli may occur in the proximal colon, with B. coli as a secondary agent producing clinical disease
-Stress is also significant predisposing factor
-Can be commensal without clinical signs

99
Q

Eimeria caviae - transmission

A

Ingestion of sporulated oocysts

  • Oocysts in feces require 2-11 days outside the host to develop to an infective stage; factors impacting maturation include heat, humidity, oxygen
  • Prepatent period = 10 or more days
100
Q

Eimeria caviae - clinical signs

A

In severely infected weanlings: lethargy, anorexia, watery to pasty feces lasting 4-7 days

  • Oocysts may not occur in feces until 10 days post-infx, so may see soiled hair coat, diarrhea, and even death before oocysts detected in feces
  • In survivors constipation may follow diarrhea
101
Q

Eimeria caviae - necropsy findings

A
  • Edema, hyperemia, hemorrhage, white or yellow plaques in the thickened proximal colon and adjacent cecal wall
  • Intestinal contents watery and often contain blood
  • Histo: colonic epithelial cell hyperplasia, intracellular coccidian forms, enterocyte sloughing, edema and congestion of lamina propria
  • Ingested, sporulated cysts invade the mucosal crypts of Liekberkühn in proximal colon and, during schizogony, damage the epithelium
102
Q

Eimeria caviae - diagnosis and differentials

A
  • Oocysts on fecal float, mucosal scraping, stained tissue sections
  • Diff Dx: pantothenic acid or Vitamin C deficiency, cryptosporidiosis, bacterial enteropathies, coronavirus
103
Q

Eimeria caviae - prevention and treatment

A
  • Good sanitation and husbandry, reduction of stress, provision of fresh, appropriate feed
  • Sulfonamides with known anti-Eimeria activity and provision of Vitamin C
104
Q

Cryptosporidium wrairi

A

Coccidium of guinea pigs that has a prolonged phase of endogenous replicaton

105
Q

Cryptosporidium wrairi - clinical signs

A
  • Subclinical infx may be common
  • Clin signs most often seen in young animals (under 300g or up to 16 wks old); may be exacerbated by concomitant E. coli enterotoxemia
  • Weight loss (most common sign), anorexia, potbellied appearance, rectal prolapse, uncommonly diarrhea and death
106
Q

Cryptosporidium wrairi - transmission and necropsy findings

A
  • Transmission: fecal oral; infxs are patent for 2 weeks and cleared by 3-4 wks postingestion in young adults and 1-2 wks in adults
  • Necropsy: diffuse enteritis from duodenum to cecum; intestinal hyperemia, edema, atrophy or necrosis of villus tips, lymphocyte infiltration, hyperplasia of crypt epithelium
107
Q

Cryptosporidium wrairi - diagnosis

A
  • Cryptosporidial bodies intracellularly in brush border epithelium near villus tips and most numerous in anterior ileum
  • Bodies are basophilic, round to oval, 1-4 µm diameter
  • Detect organisms in mucosal scrapings examined on phase contrast microscopy or on stained tissue sections
108
Q

Toxoplasma in guinea pigs

A
  • Acquired when guinea pigs ingest feces from infected cats
  • Infx rare and primarily subclinical
  • Clin signs: vulvar bleeding, abortion; encephalitis
  • Asexual stages of organism, which may survive up to 5 years, are distributed in most tissues - tachyzoites in virtually every organ, bradyzoites in brain, heart, skeletal muscle where they may be detected histologically
  • Moderate immune reponses occur in the host & can identify antibodies to T. gondii
  • Infx of the uterus, placenta, and fetus may be subclinical or cause a blood-filled uterus, fetal deaths, and abortion
109
Q

Balantidium caviae

A
  • Usually nonpathogenic; ciliated protozoan possessing a micro- and macronucleus
  • Transmission: fecal oral
  • Inhabits cecum and colon
  • Its trophozoites may be an opportunistic pathogen in bacterial enteropathies, following mucosal damage, or with E. caviae present in the intestinal wall
  • Identified histologically in intestinal wall (postmortem invasion also possible) and in intestinal contents and feces
110
Q

Klebsiella cobayae - life cycle

A
  • Sporocysts ingested with urine and excyst in gut - sporozoites pass via circulation to renal tubule epithelium, glomerular capillaries, spleen, lungs - maturing schizonts contain 8-12 merozoites, which on host cell rupture pass to the proximal tubular epithelium where second generation schizogony occurs
  • Large schizonts, containing up to 100 merozoites, can cause significant enlargement of infected epithelial cells
  • Gametogonous and sporogonous forms occur in the epithelium of the loop of Henle, and schizogonous stages occur in the epithelial cells of the proximal convoluted tubules and in the glomeruli
  • Merozoits in the loop of Henle produce zygotes, which undergo sporogony
  • Histo: protozoal forms and inflammatory cell infiltrates
111
Q

Klebsiella cobayae - clinical signs, necropsy, prevention

A

Clinical signs and gross necropsy findings are rare except in heavy infestations = renal surface irregular with gray mottling d/t proliferation of interstitial fibroblasts, which may cause some renal impairment
-Prevention: good sanitation, removal of susceptible animals from exposure to the urine of infected animals

112
Q

Other protozoa that may infect guinea pigs

A

Endolimax caviae, Entamoeba caviae, Giardia duodenalis (enteritis), Leishmania enrietti (cutaneous nodules and ulcers), Tritrichomonas caviae, Sarcocystis caviae, Trypanosoma cruzi (chronic myocarditis)

  • Prevention and control are strict sanitation and periodic screening for the organism
  • Sulfonamides are NOT effective treatment
113
Q

Paraspidodera uncinata

A

Cecal worm & only common helminth of guinea pigs

  • Inhabits but does not penetrate the cecal and colonic mucosa
  • Considered non-pathogenic; single report that causes bronchoalveolar eosinophilia
  • Worms mature in 45 days; ellipsoidal egg to egg life cycle is 51-66 days; ova are transmitted in feces and become infective in 3-9 days after shedding
  • Prevention/control: removing fresh feces and maintaining good sanitation
  • Adult male worms: 11-22mm long, females 16-28mm long
114
Q

Bayliascaris procyonis

A

Guinea pig is a paratenic (substitute intermediate) host -Ingest embryonated ascarid eggs present in raccoon feces - larvae migrate via small intestine, other organs, and the bloodstream throughout the host, often including the CNS (cerebral larval migrans), where they may cause damage and inflammation

  • Clin signs: torticollis, ataxia, anorexia, opisthotonos, stupor, hyperexcitability
  • Prevention: exclusion of raccoon feces & removal of ova from environment
  • ZOONOTIC
115
Q

Linguatula serrata

A
  • Pentastome ‘tongue worm’
  • Live in nasopharyngeal region of mammals
  • Nymphs reported in guinea pigs in 1970s
116
Q

Anoplocephala sp. & Monoecolestus sp.

A

Reported in guinea pigs in South America

-Anoplocephala sp. = tapeworms

117
Q

Fasciola hepatica and Fasciola gigantica

A
  • Trematodes; rarely infect guinea pigs - exposed to infectious metacercariae shed from snails
  • Metacercariae move to a vegatation substrate, lose their tails, and encyst on leafy vegetables that guinea pigs may eat
  • Adult flukes mature in host liver and shed eggs into the small intestine and feces
  • Eggs require a snail intermediate host to mature
  • Consequent biliary and hepatic damage may cause anorexia, debilitation, death; infected guinea pigs may become emaciated, anemic, possibly paretic due to aberrant parasite migration
  • Primary lesions in LIVER
118
Q

Mites in guinea pigs

A

listrophorid fur mite: Chirodiscoides caviae, Demodex caviae, Mycoptes musculinus, sarcoptids Trixacarus caviae and Sarcoptes scabiei and Notoedres muris
-Only Chirodiscoides and Trixacarus reported commonly, and usually in pet guinea pigs

119
Q

Chirodiscoides caviae - clinical signs

A
  • Usually subclinical, although a dense population of elongated mites moving on hair shafts is apparent
  • Heaviest infestations on POSTERIOR TRUNK
  • May cause pruritis, self-trauma, alopecia, and dermatitis
  • Heavy infestation: self-mutilation, weight loss, lethargy, in response to pruritis run and bump into objects, convulse, die; stress of disease may cause infertility and abortion
  • Adult males often couple in noncopulatory position with females
120
Q

Trixacarus caviae - clinical signs

A
  • Burrowing, sarcoptidiform mite
  • Asymptomatic or intensely pruritic generalized dermatitis - presence and severity of lesions related to variations in host strain susceptibility and to self-traumatization
  • Secondary infx may contribute to severity and distribution of signs
  • Lesions most common on TRUNK, INNER THIGHS, NECK, SHOULDERS; patchy or generalized; affected skin dry to oily with alopecia and marked hyperkeratosis
  • Heavy infestation: self-mutilation, weight loss, lethargy, in response to pruritis run and bump into objects, convulse, die; stress of disease may cause infertility and abortion
121
Q

Trixacarus caviae - histologic lesions

A

Confined to the stratum corneum and consist of epidermal hyperplasia (or thinning) and orthokeratotic an parakeratotic hyperkeratosis

  • Folds in stratum corneum contain mites and eggs; adult mites found in short tunnels
  • Spongiosis and leukocytic/monocytic infiltration occur in dermis
  • CBC may show heterophilia, eosinophilia, basophilia
122
Q

Demodex caviae - clinical signs

A
  • Reported rarely

- May localize to CONJUNCTIVAE, FOREQUARTERS - alopecia and crust and papule formation

123
Q

Myocoptes, Sarcoptes, Notoedres - clinical signs in guinea pigs

A

May cause pruritic dermatitis

124
Q

Chirodiscoides caviae & Trixacarus caviae - transmission

A
  • Both widely distributed in North America and Europe & probably occur worldwide
  • Transmission: direct contact, via pelage, cage debris, fomites, bedding
  • Trixacarus has 10-14 day life cycle
  • Sows pass mites to weanlings, naive adults; cool carcasses pass mite to warm living guinea pigs
125
Q

Chirodiscoides caviae - necropsy findings & pathogenesis

A
  • No abnormal necropsy findings, except mite and ova on hair shafts
  • Attach to hair shafts and do not burrow in skin
126
Q

Trixacarus caviae - necropsy findings & pathogenesis

A
  • Severe cutaneous lesions, associated loss of body fat, pale liver, subcutaneous signs of secondary bacterial infx (e.g., staphylococcal pyoderma)
  • Burrow into stratum corneum; pruritic response apparently due to initial allergic response to mite antigen and consequent inflammation
127
Q

Chirodiscoides caviae - differentials

A
  • Ovoid and elongated with a triangular anterior; paired male and female nymphs also characteristic
  • Lice, other mites
128
Q

Trixacarus caviae - differentials

A
  • Indicated by clinical signs, especially pruritis & mites on skin scraping or biopsy
  • Shorter than S. scabiei (200-450 µm); skin and hair may have to be dissolved in 10% potassium hydroxide and then filtered to retain the mites
  • Mites often on lumbar region and lateral aspects of rear legs
  • Pediculosis, dermatophytosis, barbering, sarcoptic and notoedric mange
129
Q

Chirodiscoides caviae & Trixacarus caviae - prevention and control

A
  • More likely to occur when maintained in unsanitary conditions with inadequate veterinary care
  • Trixacarus lesions seem to occur in some strains more than others and in stressed animals
  • Control is by repeated treatment of all animals & thorough cleaning and sanitization of environment; larvae and nymphs in environment may establish new infestations
130
Q

Chirodiscoides caviae - treatment

A

Application at 2 week interval of a diluted (water and propylene glycol) spray of ivermection, selamectin, or pyrethrin

131
Q

Trixacarus caviae - treatment

A
  • Ivermection 0.2-0.5 mg/kg SC or orally 3x at 7-10 day intervals
  • Treated guinea pigs may be shaved or bathed in medicated shampoo to loosen and remove cutaneous debris
  • Infestation may persist despite ivermectin tx
132
Q

Chirodiscoides caviae & Trixacarus caviae - research complications

A
  • T. caviae can cause transient, pruritic papulovesicular lesions in humans
  • G pigs with untreated, severe acariasis are not useful in research, especially if study involves cutaneous responses
133
Q

Lice in guinea pigs

A

Suborder Mallophaga (chewing or bitiing lice) - abrade the skin and ingest fluids

  • Gliricola porcelli = slender louse
  • Gyropus ovalis = ovoid
  • Trimenopan hispidum & Trimenopan jenningsi
134
Q

Lice - clinical signs & transmission in guinea pigs

A
  • 1.0-1.5 mm adult lice attached to hair shafts
  • Sometimes asymptomatic
  • Heavy infestations: erythema, scratching, alopecia, scabbing around the ears and nape of neck
  • Transmisson: direct contact with infected host or via contaminated bedding
  • Gliricola porcelli seen more often than Gyropus ovalis; infx rare in laboratory guinea pigs
  • On death of host, lice migrate away from cooling body along hair shafts
135
Q

Lice - diagnosis, prevention/control, treatment in guinea pigs

A
  • Diagnosis: viewing adult or immature lice with hand lens
  • Gliricola = narrow head and body (0.3 mm wide)
  • Gyropus = ovoid and broader (0.5 mm wide)
  • Prevention: obtaining clean stock, maintaining good sanitation
  • Control: isolation, treatment with dust, dip, or ivermectin, medicated shampoos and shaving, and cleaning the environment
136
Q

Fleas and ticks in guinea pigs

A
  • Ctenocephalides felis (cats [and dog] flea) & Nosophyllus fasciatus (northern rat flea) reported to be able to infest guinea pigs
  • Occurrence in laboratory guinea pigs rare
  • Clin signs: pruritis, skin crusts, anemia
  • C. felis is intermediate host for cestode Dipylidium caninum, & N. fasciatus for hymenolepid tapeworms
  • Some tick genera (Dermacentor) could possibly affect guinea pigs
137
Q

Dermatophytosis in guinea pigs

A
  • Primarily caused by Trichophyton mentagrophytes (zoophilic, filamentous dermatophyte; aerobic, ubiquitous, saprophytic, keratinophilic fungus)
  • Also reported in guinea pigs: Arthroderma benhamiae (teleomorph derived from mating strains of T. mentagrophytes complex), Microsporum spp., Scopulariopsis brevicaulis
  • Fungi live in soil, on other animals, in straw, wood, food
138
Q

Dermatophytosis - clinical signs in guinea pigs

A
  • Lesions begin on the muzzle and head, hair, nails
  • Lesions occur most often in young guinea pigs or guinea pigs genetically predisposed, stressed, pregnant, malnourished, diseased, or living in unsanitary conditions
  • Subclinical infx possible
  • Lesions in ‘hairless’ guinea pigs resemble humans lesions more closely
  • Irregularly shaped areas of alopecia, scaling, crusing, reddening may extend to back and sides but rarely to limbs
  • May see associated vesicles, pustules, abscesses d/t secondary bacterial infx
  • Lesions sometimes pruritic, often self-limiting, can last up to 30 or more days
  • Severely affected young may die
139
Q

Dermatophytosis - epizootiology and transmission in guinea pigs

A
  • Dermatophytoses occur in many warm-blooded species, especially younger animals in close contact; primates, dogs, cats, horses, swine, ruminants, rodents, and birds
  • Transmission: direct contact with spores either on animal itself or fomites like bedding
  • ZOONOTIC
  • Incubation period of 9-12 days
140
Q

Dermatophytosis - necropsy findings in guinea pigs

A
  • Changes in skin confined to superficial keratin layers and structures of the skin and hair follicles
  • UV light may cause M. CANIS to fluoresce yellow green, but false positive and false negative possible
141
Q

Dermatophytosis - pathogenesis in guinea pigs

A

-Fungi solubilize keratin with proteases - produces scale accumulation on and around the lesion and loosening and weakening of the hair shafts - dermatophyte penetrates the stratum corneum or invades hair follicles - growth continues down the hair shaft to the keratogenous one until the growth inwards equals the outward growth rate

142
Q

Dermatophytosis - diagnosis & differentials in guinea pigs

A
  • Hair loss: protein and caloric deficiency, chewing and barbering, bacterial dermatopathies (Staph and Strep), cystic ovary effects, acariasis, continuous breeding
  • Diagnosis: observation of irregularly shaped, nonpruritic, flaky-skin lesions on the head; recovery of organism from hair and epithelial debris on Sabourand’s dextrose agar or dermatophyte test media; observation of species-characteristic morphologic features and macroconidia in Microsporum or microconidia in Trichophyton
  • Epithelial cells and debris best obtained by vigourous brushing with a toothbrush
  • Most reliable diagnostic method: fungal culture; growth usually occurs within 10 days
143
Q

Dermatophytosis - prevention in guinea pigs

A

Selection of nonsusceptible animals, good husbandry including appropriate feed and clean environment, alleviation of stress
-Dark, moist environments support survival and replication of dermatophytes

144
Q

Dermatophytosis - control in guinea pigs

A

Improved sanitation and husbandry, reduction of stressors, removal of infected animals and environmental control

  • Infected hairs MUST be removed from environment
  • Disease is usually self-limiting bu full resolution may take months
145
Q

Dermatophytosis - treatment in guinea pigs

A
  • Griseofulvin 25 mg/kg PO Q24hr for 2 weeks past resolution of clinical signs; oral griseofulvin absorbed poorly in the intestine unless given with a high fat meal & is teratogenic
  • Topical griseofulvin in dimethyl sulfoxide solution for 5-7 days
  • 1% tolnaftate topically
  • Butenafine topically for 10 days
  • Thiabendazole, ketoconazoe (hair clipped), itraconazole, terbinafine hydrochloride
146
Q

Encephalitozoon cuniculi

A

Single-cell, intracellular microsporidian (and true fungus) affecting canids, rabbits, rats, NHPs, guinea pigs, and other species

  • In guinea pigs no know clinical signs & few if any necropsy findings
  • True prevalence in guinea pigs unknown due to subclinical infx and infrequent serologic screening
147
Q

Encephalitozoon cuniculi - transmission

A
  • Infective spores disseminated in urine and then ingested or inhaled; transplacental transmission suspected in several species
  • Guinea pigs relatively resistant to infx (source of spores may be rabbit urine)
148
Q

Encephalitozoon cuniculi - histologic lesions in guinea pigs

A
  • Microscopic lesions occur primarily in the brain and kidney
  • Infected brain: may have randomly distributed necrotic foci, microgranulomas, perivascular lymphoplasmacytic cuffs, lymphocytic meningitis
  • Renal lesions: may or may not occur; multiple, 2-4mm grey to white granulomatous foci seen as indentations or plaques just beneath the renal capsule (could confuse with nephrosis in older guinea pigs)
  • Interstitial, mononuclear nephritis
  • Lesions may also occur in liver and lungs
149
Q

Encephalitozoon cuniculi - life cycle

A
  • Ingested organism undergoes merogony and then sporogony in cytoplasm of endothelial cells, peritoneal macrophages, renal tubular epithelium, and oligodendrocytes
  • Spores are found intracellularly and, after cell rupture, extracellularly
150
Q

Encephalitozoon cuniculi - diagnosis and differentials in guinea pigs

A
  • Characteristic histo lesions, birefringence of organisms under polarized light, staining with periodic acid-Schiff or Goodpasture-carbol fuchsin stain, indirect ELISA, fluorescent immunoassay, Western blot
  • Serologic screening is preferred method
  • Diff dx: toxoplasmosis - distinguish by Gram stain
151
Q

Encephalitozoon cuniculi - prevention and control in guinea pigs

A

Purchase and breed seronegative animals, house away from seropositive rabbits, regular program of serologic screening and removal of seropositive animals, strict sanitation

152
Q

Encephalitozoon cuniculi - treatment in guinea pigs

A

No treatment reported for guinea pigs, but fenbendazole and albendazole have been used with variable results in rabbits

153
Q

Histoplasma capsulatum in guinea pigs

A
  • Spontaneous infections have occurred

- Emaciation, lameness, gastroenteritis, lymphadenopathy

154
Q

Candida albicans in guinea pigs

A

-Spontaneous infections have occurred - was associated with occlusive capillary embolism and tissue infarction

155
Q

Other mycoses to which guinea pigs are experimentally susceptible

A
  • Cryptococcus neoformans, Coccidioides immitis, Blastomyces dermatitidis, Aspergillus fumigatus
  • A normal stomach inhabitant, Torulopsis pintolopesii, may cause enteritis
  • Scopulariopsis sp., Aspergillus sp., Penicillium sp. may be part of fungal microbiota of guinea pig haircoat
156
Q

Signs of marginal nutritional deficiencies in guinea pigs

A
  • Increased susceptibility to infectious dz, esp streptococcal infx and enteropathies
  • Signs of conjunctivitis or upper respiratory dz should always suggest a marginal Vitamin C deficiency and treatment should include Vitamin C supplementation
  • In group housing, larger guinea pigs can bully smaller or younger guinea pigs, resulting in nutritional deficiencies
157
Q

Hypovitaminosis C - etiology

A
  • Also known as scorbutus or scurvy
  • Occurs in a small number of species - notably humans, some other primates, guinea pigs, bats - that lack the genetic code to produce the hepatic enzyme L-gulonolactone oxidase - this enzyme converts L-gulonolactone into the isomers L-ascorbate (AH) & L-dehydroascorbic acid (DHA)
  • Probable primary roles of vitamin C are acting as a cofactor in hydroxylation and amidation reactions by transferring elections to enzymes that provide reducing equivalents (i.e., protons) and scavenging both intracellular and extracellular superoxide radicals and singlet oxygen, whose activity results in tissue damage
  • Lack of vitamin C results in defective cross-linking of collagen fibrils characterized by defective wound healing and fragile capillaries
158
Q

Hypovitaminosis C - clinical signs in guinea pigs

A
  • May be subclinical, accompanied by overt signs of infectious dz (e.g., diarrhea, upper resp infx), or a primary vitamin C deficiency
  • Marginal deficiencies particularly impt in laboratory guinea pigs d/t increased susceptbility to infectious disease
  • Signs of secondary (usually bacterial) infx include unexpected death, diarrhea, weight loss, swollen and reddened orbital margins, dehydration, dyspnea
  • Most obvious clinical signs of Vit C deficiency = fragility of small blood vessels - rupture causing bruises, reluctance to move, screaming when restrained, swollen joints
159
Q

Hypovitaminosis C - necropsy findings in guinea pigs

A
  • Hemorrhage in the subperiosteum, adrenal cortex, skeletal muscle, joints (especially stifles and costochondral junctions), and intestine; gut may be atonic and hyperemic
  • Histology: changes related in many cases to absence of hydroxyproline and hydroxylysine elements in connective tissue; epiphyseal growth centers of long bones are deranged w/ greatly reduced osteoid formation, degenerating and deranged chondrocytes, decreased bony trabeculae in the marrow cavity, reduced osteoclastic and increased osteoblastic activity, multiple microfractures; myofilaments fragmented and mitochondria swollen; hemorrhage in many tissues
160
Q

Hypovitaminosis C - pathogenesis

A
  • With defects in amino acid metabolism (including tyrosine and phenylalanine), fibroblasts and osteoprogenitor cells produce defective intracellular architecture and the products dentin, collagen, and osteoid
  • Junctional defects and cytoplasmic disruption occur between endothelial cells; in muscle, liver, connective tissue cells; in pericapillary fibrous tissue; and in arterial intimae
  • Subendothelial cholesterol deposition increases, as does lipid peroxidation of cardiac muscle
  • Iron absorption in the gut and steroidgenesis in the adrenal gland decrease - may be related to increased macrophage cytotoxicity
  • Macrophage migration and heterophil phagocytosis are decreased
  • Cholesterol catabolism slowed, reducing bile acid production and consequently fat-soluble vitamin assimilation, and cholesterol accumulates in the liver
161
Q

Hypovitaminosis C - differentials and diagnosis in guinea pigs

A
  • Weakness, pain, and death in young guinea pigs: infectious disease, osteoarthritis, heat stress, toxemias
  • History of inappropriate feed, decreased prothrombin time, and serum Vitamin C level below 0.55 mg/dL (normal around 2.01 mg/dL) indicate hypovitaminosis C
162
Q

Hypovitaminosis C - control and prevention in guinea pigs

A
  • Foods providing at least 6 mg Vitamin C per day are adequate
  • Vitamin C level of 250-500 mg/L in drinking water also provides adequate levels if the water is replenished daily
  • Vitamin C ‘half-life’ in glass bottles is ~24 hr
  • In food stored at 72 F, vitamin C has only 33% of original activity at 30 days postmilling and 14% at 90 days; most commercial guinea pig chows now use a stabilized vitamin C guaranteeing a shelf life of at least 180 days
  • Guinea pigs on alcohol consumption studies have an increased need for vitamin C
  • Lesions develop in 7-10 days with NO vitamin C & in ~3 weeks with marginally deficient diets
  • Improper compounding and storage, autoclaving, and feeding food formulated for other species are common errors
  • Pregnant guinea pigs may require up to 30 mg/kg daily. but the levels given commonly (10 mg/kg daily) probably exceed requirements
163
Q

Hypovitaminosis C - treatment in guinea pigs

A

Parenteral or oral administration of Vitamin C daily at levels up to 30 mg/kg
-Recovery occurs rapidly over 1-2 weeks

164
Q

Hypovitaminosis C - research complications in guinea pigs

A

Research with scorbutic guinea pigs is compromised in several ways due to profound and extensive changes, including decreased disease resistance

165
Q

Pregnancy toxemias of guinea pigs

A

1) Preeclampsia, eclamptogenic toxemia, or the circulatory form
- Arises from abnormal vascular changes that lead to ischemia of the uteroplacental unit
2) Fasting ketosis, of the metabolic-nutritional form
- Progresses from hypoglycemia and hyperlipidemia

166
Q

Preeclampsia pregnancy toxemia - clinical signs in guinea pigs

A
  • Occurs in late pregnancy (last 2 weeks) and immediately postpartum
  • Occurs more often in obese, multiparous, stressed sows
  • Affected animals may die without clinical signs or may be dehydrated, depressed, anorexic, underweight
  • Proteinuria, acidic urine (pH 5-6; normal pH 8), ketonuria, elevated serum creatinine, increased or decreased plasma triglyceride levels
  • UNLIKE preeclampsia in humans (who also have labyrinthine hemomonochorionic placentation), guinea pigs exhibit hypertension variably and edema rarely
  • Guinea pig placentation = hemomonochorial with maternal blood circulating around a single trophoblastic layer over fetal capillaries
167
Q

Fasting ketosis pregnancy toxemia - clinical signs in guinea pigs

A
  • Occurs in last trimester (after 45 days), but most often in the last 1-2 weeks
  • Weakness, depression, dehydration, may die following a 1 to 3 day fast
  • Acidic urine, ketonuria, variable plasma glucose levels, hyperlipidemia, elevated alkaline phosphatase and ornithine carbamyl transferase serum levels
168
Q

Pregnancy toxemia epizootiology

A

Many mammals, including humans, NHPs, rabbits, dogs, ruminants, and guinea pigs, exhibit similar conditions in late pregnancy or early lactation but characteristics vary

169
Q

Pregnancy toxemia - necropsy findings in guinea pigs

A
  • Preeclamptic animals usually exhibit more severe changes
  • Preeclamptic/circulatory form: uterus, placenta and adrenal cortices show petechial and ecchymotic hemorrhage and focal necrosis; placental attachment sites, which detach easily, are also affected; fetuses are dead and decomposing; enlarged, yellow-tan liver with necrotic foci, subcapsular hemorrhage of kidneys,
  • Fasting ketosis/metabolic-nutritional form: gastric ulcers; fatty infiltration of liver, kidney, adrenal glands, and vessel walls; uterus and placentae have petechial and ecchymotic hemorrhages but NOT as severe as preeclampsia form; livers develop fewer necrotic areas, if any
170
Q

Pregnancy toxemia - pathogenesis in guinea pigs

A
  • Preeclampsia has been induced experimentally in guinea pigs by constricting the abdominal aorta or severing or ligating arteries supplying the pregnant uterus
  • Pathogenesis behind uteroplacental ischemia poorly defined; proposed course in guinea pigs involves thrombocytopenia, thromoplastin release, alterations in the renin-angiotensin aldosterone system, vasoconstriction, deposition of fibrin, and disseminated intravascular coagulation
  • Initial causes of preeclampsia IN HUMANS multifactorial and involve reduced placental perfusion d/t insufficient valvular dilation (uterine vessels in late pregnancy only 40% of normal size) and defective trophoblastic replacement of vascular endothelium accompanied by fibrinoid accumulation in and around vessels - proceeds to generalized endothelial dysfunction through a maternal response to trophoblast antigens or vasoconstriction and activation of a clotting cascade initiated by oxygen-free radicals, lipid peroxides, and proteases; triglyceride levels increase within endothelial cells; apparently a genetic predisposition
171
Q

Pregnancy toxemias - differentials and diagnosis in guinea pigs

A
  • Depression and death in late pregnancy suggest pregnancy ketosis
  • Acidic urine, absence of acute septicemic disease (e.g., salmoellosis, bordetellosis), and poor response to treatment support this diagnosis
172
Q

Pregnancy toxemias - prevention in guinea pigs

A
  • Pregnant guinea pigs should be fed nutritious and balanced diet continuously without changes
  • Guinea pig breeding stock with no history of obesity or deaths during pregnancy should be selected and housed in a reduced stress environment
173
Q

Pregnancy toxemias - treatment in guinea pigs

A
  • Rare success with treatment
  • Administration of electrolyte fluids, glucose, calcium gluconate, coticosteroids, and various combintions of fruits and veggies provide no certain disease reversal
174
Q

Pregnancy toxemias - research complications in guinea pigs

A

Any research project involving breeding or obese guinea pigs, particularly in a stressful environment, can have many sudden animal deaths

175
Q

Urolithiasis and cystitis etiology in guinea pigs

A
  • Specific cause of uroliths unknown, but probably involves genetic factors, diets with calcium, magnesium, and phosphorus imbalances, cystitis, nephritis, or urinary tract environmental factors
  • Decreased urine flow, elevated urine pH, and the uroliths themselves may predispose to cystitis
  • Proteinaceous urethral plugs fund occasionally in older male guinea pigs probably originate from seminal vesicle content
  • Bacteria assoc w/ cystitis in guinea pigs include E. coli, Staphylococcus sp., Streptococcus pyogenes
  • Cystitis often accompanies urolithiasis, lower urinary tract infection, immunosuppression, estrogenic stimulation, diabetes; may be mild to severe, and acute, subacute ulcerative, or chronic
176
Q

Urolithiasis and cystitis - clinical signs in guinea pigs

A
  • Urolithiasis usualy subclinical and occurs in older sows
  • When urinary blockage or infx occurs, can see weakness, weight loss, pain on palpation, vocalization, straining, anuria or dysuria, anorexia, a small thickened bladder, hematuria
  • Signs may progress over several weeks; untreated animals may die
  • Urine sediment may contain crystals, erythrocytes, and epithelial cells
177
Q

Urolithiasis and cystitis - epizootiology in guinea pigs

A
  • Occurs most often in aged (over 30 months) females

- Urinary tract blockage by proteinaceous plugs occurs in aged males

178
Q

Urolithiasis and cystitis - necropsy findings in guinea pigs

A
  • Unilateral or bilateral uroliths in the bladder, kidneys, ureters, urethra, vagina, or passed in the urine; concretions of up to 2 cm in diameter may occur in the bladder or urethra
  • With concurrent cystitis, bladder may be distended with urine and have thickened, hemorrhagic walls with calculi adherent to the mucosa
  • Proteinaceous plugs occur in the male urethra or bladder
  • Hydroureter, hydrourethra, hydronephrosis d/t continued occlusion of urinary output with fluid containing white to brown mineral sediment or solid masses
179
Q

List the most common types of uroliths found in guinea pigs

A

In order of frequency: calcium carbonate, calcium phosphate, magnesium ammonium phosphate hexohydrate, calcium oxalate
-Individual uroliths may contain a mixture of these crystal types

180
Q

Urolithiasis and cystitis - pathogenesis in guinea pigs

A
  • Progression of ionic saturation, supersaturation, nucleation, crystallization, and crystal growth in urolith formation
  • In urinary bladder, protein may provide a nucleus for crystal formation
181
Q

Urolithiasis and cystitis - differentials and diagnosis in guinea pigs

A
  • Diagnosis: based on clinical signs of cystitis, detection of uroliths on radiographs or U/S
  • Diff dx: infection, neoplasia, trauma to genitalia
182
Q

Urolithiasis and cystitis - prevention and control in guinea pigs

A
  • Selection of animals known free of urolithiasis, provision of appropriate food and ample water, immediate clinical care of guinea pigs with cystitis
  • Alfalfa hay and some of the dark leafy veggies are high in calcium
  • Grass hay and other sources of Vitamin C are preferable in order to avoid stone formation
183
Q

Urolithiasis and cystitis - treatment in guinea pigs

A

-Provision of fluids and appropriate systemic antibiotics based on C&S (fluoroquinolones), proper diet, if indicated cystoscopic or surgical removal of uroliths

184
Q

Protein, caloric deficiencies in guinea pigs

A
  • Occur occasionally when feeding is restricted or neglected, or due to malocclusion
  • Usual consequences are reproductive impairment, both infertility and death of low weight (<50g) neonates, hair loss
  • Pregnancy and lactation may cause a negative energy balance and subsequent hair loss
185
Q

Limiting amino acids for guinea pigs

A

Arginine, Methionine, Tryptophan

-Guinea pigs can produce niacin from tryptophan - tryptophan-deficient diets can produce cataract formation

186
Q

Essential fatty acid deficiencies in guinea pigs

A

Weight loss, ulcerative dermatitis, hair loss, visceral abnormalities

187
Q

Hypovitaminosis A in guinea pigs

A
  • Rare in herbivores

- Poor growth, keratitis, squamous metaplasia, crust eyelids and pinnae, loss of organization in tooth forming elements

188
Q

Hypervitaminosis A in guinea pigs

A
  • Can be caused by giving a multivitamin supplement
  • -Degeneration of cartilaginous epiphyseal plates in long bones, abnormal bone repair, teratogenic effects during organogenesis at 14-20 days
189
Q

Vitamin K in guinea pigs

A
  • Effects of vitamin K in guinea pigs not well defined

- May synthesize sufficient vitamin K (and most B vitamins) to prevent overt abnormalities

190
Q

Vitamin D in guinea pigs

A
  • Experimental deficiency produces wider epiphyseal cartilage plates, enamel hypoplasia, weight loss
  • Rickets is NOT a spontaneous disease in guines pigs
  • Hypervitaminosis D caused by diet misformulation reported to cause anorexia, weight loss, death
191
Q

Thiamine (B1) deficiency in guinea pigs

A
  • CNS disorders, including tremors and imbalance

- In B-deficient scorbutic animals, increased muscle weakness occurs

192
Q

Riboflavin (B2) deficiency in guinea pigs

A

-Corneal vascularization, skin lesions, myocardial hemorrhage, decreased growth and failure to thrive

193
Q

Niacin (nicotinic acid) deficiency in guinea pigs

A

-In young guinea pigs causes anemia and diarrhea

194
Q

Pyridoxine (B6) deficiency in guinea pigs

A

-In young animals causes depression in phagocytic activity of myeloid cells

195
Q

Folic acid deficiency in guinea pigs

A

-In young animals causes general signs as well as profuse salivations and terminal convulsions

196
Q

Pantothenic acid (B5) deficiency in guinea pigs

A

-Anorexia, weight loss, and - if deficient in weeks 9-10 of gestation, causes abortion and sometimes death of dams

197
Q

Choline deficiency in guinea pigs

A

-Poor growth and fatty liver

198
Q

Vitamin E and selenium deficiencies in guinea pigs

A
  • Major signs: Hindlimb weakness through myasthenia or muscular dystrophy, reduced reproductive performance, paralysis, death
  • Associated signs: coagulative necrosis of muscle, testicular degeneration, degenerative changes in seminiferous tubules, reduction of spermatozoa and spermatids. elevated creatine phosphokinase
  • Mucular dystrophy precedes testicular degeneration
  • Lethargy and conjunctivitis seen in debilitated animals
  • Iatrogenic deficiency of selenium and Vitamin C reported to cause skeletal muscle cell death
199
Q

Calcium and phosphate imbalances in guinea pigs

A
  • Excess increases the requirement for magnesium, which contributes to metastatic mineralization
  • Guinea pigs use cation exchange and phosphate anions for removing excess hydrogen ions rather than removing protons by excretion of ammonium ions
  • Calcium turnover is rapid in guinea pigs
  • Phosphate ions are critical component of metastatic mineralization; magnesium supplementation essential to offset hyperphosphatemia; high phosphate levels lower plasma pH
  • Potassium will counteract adverse effects of excess phosphate by providing an exchange cation to remove excess hydrogen ions
200
Q

Manganese deficiency in guinea pigs

A

-Reproductive disorders, pancreatic hypoplasia

201
Q

Copper deficiency in guinea pigs

A

-Slow growth and myelination failure

202
Q

Magnesium deficiency in guinea pigs

A

-Poor weight gain, hair loss, hindlimb weakness

203
Q

Metastatic calcification or mineralization in guinea pigs

A
  • May occur in guinea pigs over 1 year of age
  • Usually subclinical
  • Occurs on skeletal and cardiac muscle fibers; renal collecting tubules, interstitium, convoluted tubules, Bowman’s capsule; in other soft tissue esp around elbows and ribs; in lungs, trachea, aorta, liver, stomach, uterus, sclera
  • Gross lesions: irregular, grey patches on tissue surfaces that grate when cut with a blade
  • Histo changes: notable in hindlimb muscles; mononuclear cell infiltration, mineralization, fibrosis
  • Clinical signs: if present, poor growth, hair loss, muscle stiffness, bone deformities, nephrosis, death
  • Probable causes: diets with calcium, phosphate, magnesium, and Vitamin D imbalances
  • Mineral deposits are usually calcium, phosphates, or carbonates combined with other minerals
  • May have local low tissue pH
  • Prevention: don’t feed diets for other species to guinea pigs
204
Q

Diabetes mellitus in guinea pigs

A
  • Uncommon in guinea pigs, except for certain inbred colonies or male Abyssinian-Hartley colonies with a genetic predisposition or a yet unidentified infectious agent
  • Clinical signs evident at 3-6 months of age, affect both sexes; polyuria, weight loss, infertility, cataract formation, variable glycemia, hyperlipemia, glycosuria, (over 100-2000 mg/dl), rare ketouria
  • Resembles Type I diabetes mellitus in humans = islet hyperplasia, degranulation of beta cells, thickening of basement membranes of peripheral capillaries, fatty infiltration of exocrine cells, glomerulosclerosis
  • Spontaneous remissions accelerated by feeding hay and leafy greens occur; injected insulin not needed to maintain animals but insulin or an oral hypoglycemia agent has decreased glucosuria
205
Q

Anorexia in guinea pigs

A
  • Common, especially if feeders or waterers or food (odor, taste, density, texture, form) or water (flavor) has changed
  • Guinea pigs are neophobic & by 4 days old develop food preferences & then may not recognize as food other diets (powders, veggies, supplements, etc.)
  • Other factors: postsurgical stress, ketosis, malocclusion, drafts, illness, water deprivation
  • Treatment: provide preferred or sweetened foods, changing feeder or waterer, treating existing disease, reducing crowding, reducing obesity
206
Q

Heat stress in guinea pigs

A
  • Sensitive to sudden or extreme environmental changes; such changes are predisposing factors for respiratory disease and stress-precipitated illnesses
  • Guinea pigs’ ancestors lived at high, cooler altitudes = heat stressed easily, even when in direct sunlight at temps as low as 70 F.
  • Clinical signs: shallow, rapid respiration; weakness, hyperthermia, coma, death
  • Treatment: cool water baths, corticosteroids, parenteral fluids
207
Q

Barbering and skin biting in guinea pigs

A
  • Pulling and ingestion (trichotillomania) of cage mates’ hair occurs primarily in group-housed females; may be precipitated by stressors or need to displace another guinea pig from food/water source
  • Chewing of hair (trichophagia) may occur without wounds; self-barbering occurs caudal to the anterior shoulders; dominance-associated or agonistic trichophagia by conspecifics usually on rump, back, and around eyes and ears
  • Barbering and skin damage most often occur among status seeking adult males with or without a sow present, when parents groom young, or weanlings chew sow’s hair
  • Self-barbering may be ameliorated by feeding hay and dark, leafy greens
  • Biting may cause alopecia, scratches, lacerations, deep wounds; perineal wounds contaminated with bedding or food can become infected, extend to prepuce, cause urine retention & bleeding, pain during mating, reduced reproductive performance; some boars scoot around cage and push bedding into prepuce causing similar signs
  • Prevention: reduce environmental stressors, early weaning, separation of boars to single housing or provision of shelters, perhaps hay feeding
  • Treatment: cleaning of wound and placing in clean cage; few topical antimicrobials are effective and, if ingested, may precipitate enterotoxemia
208
Q

Ear chewing in guinea pigs

A
  • Aggressive behavior

- Severe damage can results in infections and partial or complete loss of pinnae

209
Q

Other traumatic injuries in guinea pigs

A
  • Limbs caught and injured in wire cage walls or flooring
  • Bone fractures from improper handling or dropping
  • Diaphragmatic hernia
  • Broken or luxated vertebral column
  • Fracture of liver capsule
  • Broken teeth
210
Q

Adjuvant-induced pulmonary granulomas in guinea pigs

A
  • Guinea pigs injected SC with Freud’s complete adjuvant may develop pulmonary granulomas
  • Lesions are similar to perivascular lymphoid nodules or focal pneumonia caused by other conditions
211
Q

Alopecia in guinea pigs

A
  • Frequently bred sows show hair thinning - d/t high metabolic demands or pregnancy and probable genetic and metabolic factors
  • Hair loss in breeding groups may be d/t trichophagia
  • Hair regrows when breeding stops or social dynamic changes
  • Alopecia may also occur in young animals at weaning, when the hair coat changes character, and when guinea pigs are on low-protein or low-calorie diets
212
Q

Dystocia in guinea pigs

A
  • Common in guinea pigs
  • May be d/t uterine inertia, pregnancy toxemia, fetuses too large to pass through pelvic canal, os coxae failed to separate - despite relaxin release, to the 2.5-3 cm needed to allow fetuses to pass
  • Failure or fibrocartilaginous pelvic joint to separate occurs most frequently in sows bred for the first time over 7 months of age b/c symphysis usually fuses and becomes resistant to relaxin
  • Clinical signs: still narrow symphysis near 73 days gestation, straining, depression, vaginal discharge
  • Prevention: first breeding before 7 months of age, prevent obesity and fasting while pregnant, remove animals with known family history or dystocia
  • Young guinea pigs involved in dystocia experience hypoxia, which is often fatal
  • Treatment: digital removal of fetus; calcium, glucose, 1-3 mg/kg oxytocin (ONLY if pubic symphysis confirmed open); C-section
213
Q

Ulcerative pododermatitis (bumblefoot) in guinea pigs

A
  • Occurs on volar surfaces of one or more feet and presents with enlarged, firm, ulcerated wounds
  • Chronic, ulcerative lesions may have Staphylococcus involvement
  • Can be associated with amyloid accumulation in the liver, adrenals, spleen, pancreatic islets
  • Prevention and treatment: provide smooth wire or solid-bottom flooring with bedding, good sanitation, reduction of obesity; severe cases antibiotic treatment, softening with lotion, surgical debriding
  • S. aureus can cause pneumonia, mastitis, conjunctivitis, cheilitis, osteoarthritis; has been assoc w/ exfoliative dermatitis with alopecia, erythema, scabs, epidermal cracks
  • Staph enter skin through abrasions
  • Histology: parakeratosis with minimal inflammation
  • Pododermatitis rapidly progresses to osteomyelitis is not treated
  • Amputation NOT an option due to body weight distribution
214
Q

Antibiotic-associated typhlocolitis in guinea pigs

A
  • Enteropathies and deaths in guinea pigs occurring w/in 1-5 days of administration of certain antibiotics assumed to result from 1) antibiotic-induced suppression of resident microflora, perhaps Bacteroides; 2) loss of cecal colonization resistance; 3) colonization, proliferation, and toxin production by transiting or resident commensals, usually one or more strains of C. difficile
  • E. coli is NOT a normal intestinal inhabitant in guinea pigs; may proliferate in antibiotic-caused dysbiosis
  • Antibiotics most often implicated: AMINOPENICILLINS, CEPHALOSPORINS, CLINDAMYCIN, STREPTOMYCIN, LINCOMYCIN (penicillin dose as low as 2000 U or ampicillin over 6 mg/kg Q8hr for 8 days known to cause death)
  • Clinical signs: vary with drug dose and strain of opportunisitic pathogen; rapidly progressive lethargy, rough hair coat, diarrhea, death
  • Necropsy: hemorrhagic typhlitis, cecum distended with bloody liquid feces; severe inflammatory rxn in the lamina propria and microulceration of the mucosa with inflammatory cell infiltration
  • Treatment: supportive fluids, highly palatable food, heat
215
Q

Clostridium difficile in guinea pigs

A
  • Common, fecal-borne, anaerobic, G(+), commensal whose large subterminal spores persist in the environment
  • Some strains produce protein exotoxins (cytotoxins) A & B - bind to epithelial cell membrane receptors
  • Toxin B is more cytotoxic but requires Toxin A (enterotoxin) to access mucosal cells
  • Toxin A causes fluid secretion, mucosal damage, inflammation - results in cell death
  • Cause of antibiotic-associated typhlocolitis
  • Drug prophylaxis NOT recommended: treatment of choice in humans, metronidazole, may exacerbate toxicosis in guinea pigs
  • Treatment: supportive fluids, highly palatable food, heat
216
Q

Quinolones and fluoroquinolones in guinea pigs

A
  • Use cautiously in immature guinea pigs
  • Report showed single SC dose of 350 mg/kg quinolone nalidixic acid in 6 week old guinea pigs cause severe degeneration of middle-zone chondrocytes
217
Q

Streptomycin adverse effects in guinea pigs

A
  • Otoconial (inner ear cell) loss in the striola region of both utricle and saccule in adult, mixed-sex guinea pigs following seven IP injections of 250 mg/kg streptomycin
  • Recovery often occurred in 8-10 weeks
218
Q

Aminoglycoside adverse effects in guinea pigs

A

-Interfere with calcium uptake into otoconia (inner ear cells)

219
Q

Neoplasia in guinea pigs

A
  • Most common in animals over 3 years of age
  • Most common type are those of hemolymphopoietic system, followed by respiratory system, integument, reproductive tract, mammary gland, hemopoietic system, cardiovascular system, endocrine glands
220
Q

Ma;occlusion in guinea pigs

A
  • Elodontic and hypsodontic teeth
  • Maocclusion may occur because of shortness of maxilla, abnormally narrow mandibular separation (anaesognathism), nutritional deficiency, broken or deviated teeth d/t trauma or periodontal infx
  • Root abscesses may extend into mandible or maxillary sinus & cause exophthalmos
  • Premolars and molars involved most often, but incisors can also be maloccluded
  • Clinical Signs: weight loss, inappetance, drooling (‘slobbers’), oral laceration and bleeding, gaping mouth, death
  • Necropsy: periodontal dz and overgrown teeth, often with sharp edges and POINTS ON LABIAL SIDE OF MAXILLARY & LINGUAL SIDE OF ROSTRAL MANDIBULAR MANDIBULAR CHEEK TEETH; elongated coronal surfaces may arch, inhibit tongue movement, and force open the mouth
  • Diagnosis: clinical signs and oral exam
  • Differentials: drooling can also be d/t folic acid deficiency, chronic fluorosis, heat stress, hypovitaminosis C, dental abscesses
  • Treatment: trim overgrown teeth to 2-3 mm above the gingiva & file sharp points (dental bur or rongeurs; only in anesthetized animals); remove infected teeth, drain abscess, antibiotics
  • Tooth extraction via bucotomy is complicated b/c of difficulty in access and relative paucity of alveolar bone in mandible
  • INHERITED, esp in 2/N and 13/N inbred strains = don’t breed
221
Q

Gastric ulcers in guinea pigs

A

-Probably secondary to uremia, ketosis, excessive stress, Citrobacter infection

222
Q

Acute gastric volvulus in guinea pigs

A

Reported in 6 breeder guinea pigs aged up to 26 months

  • Found dead or with dyspnea, cyanosis, tachycardia, distended stomachs containing fluid and gas rotated 180 degrees on mesenteric axis; diaphragm displaced anteriorly
  • Cause of volvulus not apparent
223
Q

Acute typhlitis and typhlocolitis in guinea pigs

A
  • All ages; Strain 13 more commonly involved
  • May be due to manipulation, antibiotic use, corticosteroid injection, fasting, torsion, advanced pregnancy
  • May be no clinical signs except death
224
Q

Cecal impaction in guinea pigs

A

Caused by wood shavings, hair, inspissated digesta

225
Q

Other GI conditions in guinea pigs

A

Colonic stricture, dilation, cecal torsion, cecal and rectal impactions, rectal prolapse, circumanal sebaceous accumulations

226
Q

Hepatic conditions in guinea pigs

A

Contusion, focal coagulative necrosis (maybe d/t agonal hypoxia), idiopathic cholangiofibrosis

227
Q

Rhabdomyomatosis in guinea pigs

A
  • Cardiac rhabdomyoma
  • Pale, pink foci or streaks with indistinct margins in the myocardium, usually the left ventricle
  • Relatively common in guinea pigs; similar lesions occur in dogs, swine, humans
  • Streaks = glycogen accumulation in myofibers or Purkinje fibers d/t congenital abnormality of glycogen metabolism
  • Diagnosis: alcohol-fixed specimens stained with periodic acid-Schiff stain
  • No apparent cardiac impairment caused by the lesions
228
Q

Perivascular and peribronchiolar lymphoid nodules in guinea pigs

A
  • May begin at early age and continue as common occurrence in older animals
  • Primary cause for nodules unknown; may be antigenic stimulation and are less common in SPF guinea pigs
  • Perivascular lymphoid nodules, consisting of normal lymphocytes, may be in the adventitia of the pulmonary arteries and veins
  • In older guinea pigs, aggregations reach 0.5mm diameter & visible grossly as pinpoint-sized subpleural foci
229
Q

Other respiratory abnormalities in guinea pigs

A
  • Rarely reported

- Thickened pulmonary artery musculature, osseous metaplasia in alveolar septa, foreign body pneumonia

230
Q

Nephrosclerosis in guinea pigs

A
  • Incidental findings in aged guinea pigs
  • Characterized by weakness, anemia, dilute urine, increased BUN and creatinine
  • Autoimmune, infectious, and vascular diseases may contribute
  • Necropsy: pitted subcapsular renal surface with pale streaks extending into the cortex and even medulla; segmental to diffuse interstitial fibrosis causes kidney to have irregular surface
  • Histo: most glomeruli remain normal, but immune complex deposition occurs in basement membrane
  • Chronic renal failure may predispose to cochlear dysfunction, especially in the hair cells
231
Q

Ovarian cysts in guinea pigs

A
  • Normal guinea pig: ovaries lie caudo-lateral to kidneys, 6-8mm long & 4-5mm diameter; rete ovarii are derived from the mesonephric tubules & occur in the hilus of the ovary
  • Cysts of the rete ovarii are common in sows 1.5-5 yrs of age
  • Cause of cysts unknown; both androgens and estrogens may be involved in the pathogenesis
  • Incidence may range from 76-90% in older sows
  • Clinical signs: anorexia, depression, abdominal distension, bilateral symmetric hair loss over flanks and rump, reproductive failure
  • Diagnosis: careful clinical exam (avoid rupturing cyst), radiography, U/S imaging using a 6.0 or 10.0 MHz mechanical sector transducer
  • Cysts are up to 7 cm or more in diameter, singular or multilocular, unilateral or bilateral (R more often than L), may be assoc w/ leiomyomas of the uterine body or horn, cystic endometrial hyperplasia, or endometritis; larger cysts may cause pressure atrophy in adjacent ovarian tissue
  • Treatment: surgical removal
232
Q

Osteoarthritis in guinea pigs

A
  • Report noted spontaneous, progressive osteoarthritis in stifle and other joints of male Dunkin Hartley guinea pigs
  • Noted as early as 3 months of age; became severe by 22 months
  • Changes in cartilage included increased levels of proteoglycans and decreased collagen
  • Histo: osteophytse, calcification of collateral ligaments of the joint, degeneration of weight-bearing, articular surfaces
  • Hypovitaminosis C, obesity, joint injury may contribute to joint degeneration
  • Mechanical load and stiffness are significant pathogenic mechanisms
233
Q

Other musculoskeletal abnormalities in guinea pigs

A

-Scorbutus lesions, osteodystrophy, nutritional myopathy, consequences of injections and bites

234
Q

Eye exam in guinea pigs

A
  • Paurangiotic retina - retinal blood vessels are minute and restricted to the direct neighbourhood of the optic disc - and NO tapetum
  • Pupil dilation by using 1% tropicamide drops or, in pigmented animals, one drop each of 1% atropine and 10% phenylephrine 3-4x within 15 min
  • Exam best accomplished using a 20-diopter (D) or 30-D indirect condensing lens
  • Fluorescein dye use, exfoliative conjunctival exam, and culture are diagnostic methods
235
Q

Blepharitis in guinea pigs

A
  • Blepharitis with epithelial flaking, crusting, alopecia, swelling, reddening of lids = ‘dull eyes’
  • Usually seen in guinea pigs with marginal hypovitaminosis C, with subclinical infx - usually of upper respiratory tract, or with malocclusion or renal disease
236
Q

Conjunctivitis in guinea pigs

A

-Caused by chlamydophilae, streptococci, staphylococci, Pasteurella spp., physical or chemical irritants

237
Q

Exophthalmos in guinea pigs

A

-Upper molar root abscess extending into maxillary sinus and orbit, orbital trauma, foreign bodies, sialocele, lacrimal gland cysts or inflammation, neoplasia (lymphosarcoma)

238
Q

Nodules at conjunctival sac (‘pea eye’) in guinea pigs

A

-May be a portion of a lacrimal gland, or a yellow subconjunctival fat deposit

239
Q

Cataracts in guinea pigs

A
  • May result from feeding a diet low in L-tryptophan (under 0.1%). diabetes
  • Heritable cataracts have been reported in strain 13/N d/t a single, autosomal, gene deletion of 34 residues that produces a novel zeta-crystallin lens protein; homozygous = lenses completely opaque; heterozygous = lenses have a well-demarcated opaque nucleus with a normal cortex
240
Q

Other ocular abnormalities in guinea pigs

A

Dermatophytosis of the lids, common bacterial infections, herpesvirus conjunctivitis, listerial keratoconjunctivitis, ophthalmitis, ocular dermoid, microphthalmia, corneal dryness, optotoxicity from toxin ingestion, ulceration, osseous metaplasia, osseous choristoma of the ciliary body

241
Q

Treatment of ocular disorders in guinea pigs

A

-Topical or systemic antibiotics; known safe and effective = fluoroquinolones, chloramphenicol, trimethoprim-sulfonamide

242
Q

Endocrine disorders in guinea pigs

A

Hyperthyroidism, hyperparathyoidism, and hyperadrenocorticism have been reported, but incidence of these is low

243
Q

Amyloidosis in guinea pigs

A
  • Deposition of amyloid A (AA) in the kidney, liver, spleen, adrenal glands
  • Associated with aging or chronic inflammatory conditions, such as staphylococcal pododermatitis and osteoarthritis, or with multiple casein injections
  • Amyloid = extracellular deposition of polymerized serum protein subunits that have a role in inflammation
  • Condition is slowly progressive, begins in the renal mesangium, and extends into subendothelial portions of capillary basement membranes
244
Q

Claviceps purpura in guinea pigs

A
  • Guinea pigs that eat grasses contamined with hyphal masses (sclerotia) of Claviceps purpura - which produces alkaloids ergotamine and ergometrine - may develop dry gangrene of feet
  • Toxins damage the capillary epithelium and lead to thrombosis and necrosis