Guinea pig Flashcards
<p>Guinea Pig</p>
<p>Cavia porcellus</p>
<p>models for</p>
<p>anaphylaxis</p>
<p></p>
<p>clasification of GP</p>
<p>hystricomorph</p>
<p>number of digits on fore and hind</p>
<p>four on the front and three on the back</p>
<p>ideal caging for GP</p>
<p>solid bottom cages with bedding</p>
<p>space requirement for GP up to 350g</p>
<p>60in^2</p>
<p>space requirement for GP >350g</p>
<p>101in^2</p>
<p>height requirement for GP cage</p>
<p>7in</p>
<p>ideal temp for GP</p>
<p>68-79F</p>
<p>predominant leukocyte in GP</p>
<p>lymphocyte</p>
<p>name of special leukocytes in peripheral blood</p>
<p>heterophil</p>
<p>where are Kurloff cells found most often and when?</p>
<p>in thymus, spleen, liver, lung during pregnancy</p>
<p>purpose of Kurloff cells</p>
<p>NK cell activity, cancer resistance?</p>
<p>which teeth are open rooted in the GP</p>
<p>all teeth (hyposodontic)</p>
<p>description of oral cavity in GP</p>
<p>small and narrow, soft palate coveres nearly the entire back of the pharynx, only small palatal ostium visible</p>
<p>Stomach of GP</p>
<p>monogastric hind gut fermentor, glandular epithelium all over</p>
<p>describe the Preyer or pinna reflex</p>
<p>cocking of the pinnae in response to a sharp sound.</p>
<p>what are the hormones responsible for growth regulation in GP</p>
<p>Insulin growth factor 1 & 2. (not pituitary growth hormone)</p>
<p>puberty</p>
<p>M: 3-4m</p>
<p>Gestation</p>
<p>59-72d</p>
<p>weaning age</p>
<p>14-28d</p>
<p>special requirement of GP feed</p>
<p>stabilized Vitamin C</p>
<p>how long can stabilized feed be stored</p>
<p>180d post milling</p>
<p>how long can unstabilized feed be stored</p>
<p>90d post milling</p>
<p>describe unique components of female reproductive tract</p>
<p>vaginal closure membrane</p>
<p>at what age does the pubic symphysis fuse?</p>
<p>6-9m</p>
<p>what hormone is responsible for relaxation of the pubic symphysis as parturition nears?</p>
<p>Relaxin</p>
<p>GP are \_\_\_\_\_\_ ovulators</p>
<p>spontaneous</p>
<p>nonseasonally polyestrous</p>
<p>postpartum estrus</p>
<p>highly fertile, 2-10h post delivery</p>
<p>placentation</p>
<p>labryinthine hemomonochorionic</p>
<p>description of Bordatella bronchiseptica</p>
<p>short gram neg rod, non spore forming</p>
<p>clinical signs of Bordatella bronchiseptica</p>
<p>subclinical infections most common but stress may predispose to outbreaks of sepsis resulting in acute death</p>
<p>reservoir of Bordatella bronchiseptica</p>
<p>respiratory tract of many species.</p>
<p></p>
<p>rabbits known to give to GP</p>
<p>necropsy findings of Bordatella bronchiseptica</p>
<p>pulmonary consolidation, exudate in upper and lower respiratory tract</p>
<p>tropism for Bordatella bronchiseptica</p>
<p>cilliated respiratory epitelium</p>
<p>description of Streptococcus equi subsp zooepidemicus</p>
<p>gram +, cocci chain, lancefield group C, B hemolytic, antiphagocytic capsule</p>
<p>clincial signs of Strep equ ssp zooepidemicus</p>
<p>abscess of cervical lymph nodes, abscess basically anywhere,</p>
<p>"thumps"</p>
<p>suppurative or caseous lymphadenitis, acute septicemia, otitis media, mastitis</p>
<p>transmission of Strep equi ssp zooepidemicus</p>
<p>via aerosol onto epithelium, zoonotic</p>
<p>most common types of Strep pneumoniae</p>
<p>types 4 and 19F</p>
<p>clincial signs of Strep pneumoniae</p>
<p>carrier state common</p>
<p>depression, anorexia, URI, torticolis, abortion, stillbirth</p>
<p></p>
<p>transmission of Strep pneumoniae</p>
<p>aerosol or direct contact with infected animals</p>
<p>necropsy findings of strep pneumoniae</p>
<p>pyogenic processes, fibrinopurulent pleuritis, pericarditis, suppurative pneumonia, otitis media, endometriosis, and arthritis</p>
<p>diagnosis of Strep pneumoniae</p>
<p>observe on gram stained impression smears, serotyping is necessary</p>
<p>treatment of Strep pneumoniae</p>
<p>BAD, more likely to cause a reversion to the subclinical state than eliminate infection</p>
<p>description of Salmonella</p>
<p>gram negative bacillus</p>
<p>most common serovars of Salmonella</p>
<p>enterica sub species enterica, serovars Typhimurium and Enteritidis</p>
<p>Clinical signs of Salmonella</p>
<p>peracute to acute: high morbidity and mortality rough hair coat, weakness, conjunctivitis, abortion, light colored feces, intermittent diarrhea</p>
<p></p>
<p>diarrhea rare in GP (common in rats)</p>
<p>transmission of Salmonella</p>
<p>can be shed by subclinical carriers, fecal-oral, blood-oral, tissue-oral, conjunctiva</p>
<p>gross lesions of Salmonella</p>
<p>hepatomegaly, splenomegaly, small yellow necrotic foci throught the viscera</p>
<p>diagnosis of Salmonella</p>
<p>recover organism, culture on MacConkey or brilliant green agar</p>
<p>treatment of Salmonella</p>
<p>BAD, may lead to subclinical infection</p>
<p>cause of Guinea Pig inclusion conjunctivitis</p>
<p>Chlamydia caviae</p>
<p>clinical signs of Chlamydia</p>
<p>reddening of eyelids, conjunctivitis, purulent exudate, self limiting with recovery in 3-4 weeks</p>
<p>diagnosis of Chlamydia</p>
<p>demonstration of intracytoplasmic inclusion bodies in Giemsa or Macchiavello stained conjunctival epithelial cells</p>
<p>clinical signs of Guinea Pig Adenovirus</p>
<p>subclinical most common, affected animals (stress or immunocompromised) die w/o prior signs</p>
<p>morbidity and mortality of adenovirus</p>
<p>low, high</p>
<p>necropsy of GP Adenovirus</p>
<p>dark red pulmonary consolidation, emphysema, catarrhal exudate, intranuclear inclusion bodies in respiratory epithelial cells</p>
<p>cytomegalovirus is what kind of virus?</p>
<p>caviid herpes virus 2, beta herpes virus</p>
<p>clincial signs of CMV</p>
<p>usually subclinical, may see weight loss, conjunctivitis, and lymphadenopathy</p>
<p>transmission of GPCMV</p>
<p>exposure to saliva carrying the virus, transplacental transmission can also occur</p>
<p>necropsy of GPCMV</p>
<p>karyomegaly of salivary gland epithelium</p>
<p>chronic site of replication of GPCMV</p>
<p>salivary glands</p>
<p>histologic description of GPCMV</p>
<p>eosinophilic intranuclear inclusion bodies in ductal epithelial cells</p>
<p>clinical signs of poliovirus</p>
<p>depression, lameness, flacid paralysis, weight loss, death</p>
<p>transmision of poliovirus</p>
<p>fecal oral, but not definate</p>
<p>necropsy signs of poliovirus</p>
<p>meningomyeloenchphalitis, perineuronal inflammation, neuronal degeneration</p>
<p>diagnosis of poliovirus</p>
<p>ELISA</p>
<p>Protozoa found in GP</p>
<p>Eimeria caviae</p>
<p>Klossiella cobayae</p>
<p>Cryptosporidium wrairi</p>
<p>Balantidium caviae</p>
<p>nematodes in GP</p>
<p>Paraspidodera uncinata</p>
<p>descriptionof Paraspidodera uncinata</p>
<p>cecal worm</p>
<p>most common helminth in GP</p>
<p>Paraspidodera uncinata</p>
<p>Mites found on GP</p>
<p>Chirodiscoides caviae,</p>
<p>Demodex caviae,</p>
<p>Mycoptes musculinis,</p>
<p>Trixacarus caviae,</p>
<p>Sarcoptes scabiei,</p>
<p>Notoderes muris</p>
<p>pathogenic mites in GP</p>
<p>Chirodiscoides caviae</p>
<p>Trixacarus caviae</p>
<p>Where is Trixacarus found?</p>
<p>burrowing mite, in the skin</p>
<p>Where do lesions occur with Trixacarus</p>
<p>trunk, inner thigs, neck, and shoulders, intense pruritis and alopecia</p>
<p>Where is Chirodiscoides found?</p>
<p>on hair shaft</p>
<p>Where do lesions of Chirodiscoides form?</p>
<p>posterior trunk, causes severe pruritis</p>
<p>lice found on GP</p>
<p>Gliricola porcelli</p>
<p>Gyropus ovalis</p>
<p>Trimenopan hispidum</p>
<p>Trimenopan jenningsi</p>
<p>most common louse found in GP</p>
<p>Gliricola porcelli- chewing louse</p>
<p>location to find lice in GP</p>
<p>ears and nape of neck</p>
<p>fleas found in GP</p>
<p>Ctenocephalides felis</p>
<p>Nosopsyllus fasciatus</p>
<p>Ctenocephalides porcellus</p>
<p>Cause of dermatophytosis in GP</p>
<p>Trichophyton mentagrophytes</p>
<p>spread of Encephalitozoon cuniculi to GP</p>
<p>urine of infected rabbits</p>
<p>clinical signs of Encephalitozoon cuniculi in GP</p>
<p>subclinical infection but may see microscopic lesions in brain and kidney (necrotic foci, microgranulomas, perivascular lymphoplasmacytic cuffs)</p>
<p>clinical signs of marginal vitamin C deficiency</p>
<p>conjunctivitis or upper respiratory disease</p>
<p>hypovitaminosis C, clinical signs</p>
<p>hemorrhage in the subperiosteum, skeletal muscles, joints (stifle, costrocondral junctions) and intestine</p>
<p>reason why GP are susceptible to Vit C deficiency</p>
<p>lack genetic code to produce L-gulonolactone oxidase</p>
<p>histologic changes seen in hypovitaminosis C</p>
<p>epiphyseal growth centers are deranged with reduced osteoid formation, deranged chondrocytes, decreased bony trabeculae in marrow cavity</p>
<p>two forms of toxemia of pregnancy</p>
<p>1) preeclampsia/circulatory form</p>
<p>2) pregnancy ketosis(fasting form)</p>
<p>timeframe of pregnancy for preeclampsia to occur?</p>
<p>last 2 weeks</p>
<p>pathogenesis of preeclampsia</p>
<p>size of uterus interupts blood flow</p>
<p>pathogenesis of fasting ketosis</p>
<p>size of uterus prevents proper intake of food leading to mobilization of muscle and ketones to liver for energy</p>
<p>necropsy of preeclampsia</p>
<p>ecchymotic hemorrhage and focal necrosis</p>
<p>necropsy of fasting ketosis</p>
<p>fatty infiltration of liver, kidney, adrenal glands, vessel walls</p>
<p>minerals involved in urolithiasis</p>
<p>Calcium, phosphourus, magnesium</p>
<p>urolithiasis is most common in what sex?</p>
<p>Females</p>
<p>clinical signsof hypovitaminosis A</p>
<p>keratitis, squamous metaplasia, crusty eyelids</p>
<p>cause of hypervitaminosis A</p>
<p>giving multivitamin supplement instead of just vit c</p>
<p>clinical signs of hypervitaminosis A</p>
<p>degeneration of cartilaginous epiphyseal plates, abnormal bone repair, teratogenic effects</p>
<p>are guinea pigs susceptible to Rickets?</p>
<p>dont see in GP</p>
<p>location of metastatic calcification?</p>
<p>skeletal and cardiac muscle fibers</p>
<p>diabetes mellitus is found in what inbred strains</p>
<p>Abyssinian Hartley colonies</p>
<p>GP response to Freund's complete adjuvant</p>
<p>pulmonary granulomas</p>
<p>frequently bred sows often show</p>
<p>hair thinning</p>
<p>cause of ulcerative pododermatitis or bumblefoot</p>
<p>Staph aureus, enters through abrasions/injury to feet, most often from wire floors</p>
<p>antibiotics associated with typhlocolitis</p>
<p>aminopenicillins, cephalosporins, clindamycin, streptomycin, lincomycin</p>
<p>organism associated with antibiotic associated typhlocolitis</p>
<p>Clostridium difficile</p>
<p>pathogenesis of antibiotic associated typhlocolitis</p>
<p>1) antibiodic induced suppression of resident microflora</p>
<p>fffmost common neoplasia in GP</p>
<p>lymphosarcoma</p>
<p>gastric ulcers can occur secondary to</p>
<p>uremia, ketosis, excessive stress, Citrobacter infection</p>
<p>cause of Rhabdomyomatosis</p>
<p>congenital abnormality of glycogen metabolism</p>
<p>causes of nephrosclerosis</p>
<p>autoimmune, infectious, vascular disorders, high protein diet</p>
<p>anatomical part of the ovary that is responsible for cyst formation</p>
<p>rete ovarii</p>
<p>description of retina of GP</p>
<p>paurangiotic (few vessels near optic disk)</p>
<p>amyloidosis can be seen secondary to what clinical conditions</p>
<p>staphylococcal pododermatitis and osteoarthritis</p>
<p>what is unique about the GP cardiovascular system?</p>
<p>good collateral circulation, difficult to cause infarcts</p>
<p>what is unique about the dentition of GP</p>
<p>they are the only rodent to have premolars</p>
<p></p>
<p>all teeth are open rooted and grow continuisly</p>
<p>what is the shock organ of the GP</p>
<p>lung</p>
<p>4 things to know about Yersinia pseudotuberculosis</p>
<p>1. zoonotic</p>
<p>2. 4 clinical states, acute disease, chronic disease, nonfatal lymphanepitis, or subclinical carrier state</p>
<p>3. antibiotic tx leads to carrier state</p>
<p>4. culture at cold temps 20-30C</p>
<p>things to know about antibiotic induced enterotoxemia- hemorrhagic typhilitis</p>
<p>Clostridium difficile is causative agent</p>
<p>caused by antibiotics or dietary change</p>
<p></p>
<p>things to know about Clostridium piliforme- Tyzzers disease</p>
<p>wide host range</p>
<p>rare in GP</p>
<p>triad of lesions, heart-liver-GI</p>
<p>causative agents of mastitis in GP</p>
<p>pasturella</p>
<p>klebsiella</p>
<p>strep</p>
<p>staph</p>
<p>coliforms</p>
<p>clinical condition caused by Cryptosporidium wrairi</p>
<p>greasy coat</p>
<p>kidney protozoa of GP</p>
<p>Klossiella cobayae</p>
<p>asymptomatic infecteion, incidental on necropsy</p>
<p>what antibiotics are safe for GP</p>
<p>fluoroquinolones</p>
<p>gentamicin</p>
<p>TMS</p>
<p>chloramphenicol</p>
