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General Features of
Guinea Pigs
- nervous, will go off
feed with any changes
- long gestation,
dystocia, breed all year, will nurse other infants- good for
rederivation
- precocial birth, wean
early eat solid food at 3-4 days
- few viral infections
- major diseases: scurvy,
respiratory tract infections, and enteric disease
- male dominated
hierarchy, males will groom infants
- bite wounds from
aggressive males, barbering of subordinates
- diurnal, copraphagic,
not cache food, eat frequently, require constant source of water, and
need training on sipper tubes
- indiscriminate
defecation- water bowls, food dishes
- responsive to sound,
startle, freeze, stampede
- vocalize, complex
communication
Anatomic Features
- two inguinal nipples
- intact vaginal closure membrane
- large vesicular glandspubic symphysis under
action of relaxin
- large adrenal glands
- long colon (60% length of rat)
- large tympanic bullae
- intracoronary collateral network
- open inguinal canals
- thick medial walls of pulmonary vessels
- cervical thymus
Hematology
- heterophils
- lymphocytes-large and small predominate
- Kurloff cells
Disease Differential List
- Diarrhea -Tyzzer's, colibacillosis,
salmonella, coccidiosis, Arizona sp, Citrobacter sp, coronavirus,
clostridial typhlitis, clostridial dysbiosis, cryptosporidiosis
- Respiratory -Bordetella, S. pneumonia, S.
zooepidemicus, Klebsiella, Pasteurella multicida, P aeruginosa, C
freudii, S. aureus, heat stress, diaphragmatic hernia, pregnancy
toxemia, gastric torsion
- Ptaylism - Malocclusion, hypovitamin C, heat
stress, flurosis
- SQ Swelling - Abscess-(S. zooepidemicus, S.
aureus, S. moniliformis, Y. pseudotuberulosis), neoplasia (leukemia)
- Dermatitis - Bite wounds, Trixascarus cavia,
cryptococcosis, Staph, dermatophytosis, pediculosis, Chirodiscoides,
Psoroptes.
- Otitis - Otosclerosis, Otitis Media - Often
subclinical - caused by S.pneumoniae, S. zooepidemicus, Bordetella sp,
and Pseudomonas
- Mastitis - Sporadic, early lactation, not
necessarily contagious. Blue breast is characterized by red to purple
enlarged, firm, congested, edematous mammary glands. Lesions can vary
from mild degeneration to necrosis of ductal epithelium with PMN
infiltration in ducts and alveoli. Scattered cells occupy the
interstitium. Chronic mononuclear cell infiltration with interstitial
fibrosis and architectural obliteration will affect future usefulness
of these animals as breeders. Isolates have included E. Coli,
Klebsiella and S, zooepidemicus
- Conjunctivitis - Isolates have includes
Streptococcus, coliforms, Staphlococcus and Pasteurella multocida,
Listeria. Smears should be examined for Chlamydia.
- Infertility - Age, stress, flooring, estrogen
in feed, bedding adherent to genitals, increased temp, nutritional
deficiency, metritis, preputial dermatitis, segmental aplasia of
uterus, cystic ovaries, perinatal death, abortion-stillbirth-(dystocia,
Bordetella, Salmonella, Strep, CMV, birth asphyxiation, pregnancy
toxemia).
- Death - Chilling, overheating, septicemia,
toxemia, Salmonella, cecitis, enteritis, pregnancy toxemia, antibiotic
reaction, pneumonia, volvulus of cecum or stomach, dystocia,
dehydration, stuck foot in grate, fractured limb.
- Anorexia and/or Weight Loss - Neophobia,
water deprivation, temperature, change in food, unpalatable food/improperly
compounded, toxin ingestion, malocclusion, oral laceration, obesity,
metabolic disease, renal failure, Vitamin C deficiency, infection,
neoplasia, loss of cage mate, mechanical failure, territorial
behavior-dominant male, amyloidosis with pododermatitis, protein
deficiency, metabolic calcification, ectoparasitism, Urolithiasis.
- Reluctance to Move - Hypo Vitamin C,
Bordetella, Salmonella, malnutrition, Vitamin E deficiency,
Osteoarthritis, spinal trauma/fracture, dystrophy/myopathy.
I. BACTERIAL INFECTIONS
Bordetella bronchiseptica - A small gram
negative rod, important disease causing organism in the upper respiratory
tract of several species with apparent interspecies transmission. Isolates
do not appear to have differences in virulence. Affects guinea pigs of all
ages, following intranasal inoculation. Severe disease and mortality are
most common in young guinea pigs in the winter. Guinea Pigs may harbor
inapparent infection. The number of subclinical nasal shedders may be
quite high. Rabbits should not be housed with guinea pigs. The organism
has an affinity from ciliated respiratory epithelium. Pregnant sows may
abort, produce stillborn or die. At necropsy, there is mucopurulent to
catarrhal exudate in the nasal passages, and trachea. Pulmonary
consolidation and hemorrhage are usually anteriovental and may involve all
lobes. Mucopurulent exudate in the airways and tympanic bullae may occur.
Pleuritis or pyosalpinx may be seen. Microscopically, acute to chronic
suppurative bronchopheumonia with heterophilic infiltration, obliteration
of the normal architecture and fibrinous exudate may be present. The
organism can be cultured on blood agar from the respiratory tract,
tympanic bullae or affected uterus. Differential diagnoses must include
Streptococcus, Klebsiella, Staphlococcus, or previous Freud's adjuvant
administration (chronic interstitial fibrosis and granulomatous pulmonary
inflammation).
Salmonellosis - S. typhimurium , S.
enteritidis, S. dublin are important and severe sporadic diseases of
guinea pigs. Transmission is by ingestion of contaminated food, water or
bedding. The conjunctiva is a portal of entry in guinea pigs. Salmonella
are frequently in a carrier state and are intermittently shed in the
feces, making elimination of the pathogen difficult. Predisposing factors
include youth or old age, stress of pregnancy or weaning, nutritional
deficiencies, disease, genetics, serotype, environment (winter) and
experimental stress. Salmonellosis may be enteric, systemic, epizootic,
enzootic and zoonotic. Sporadic outbreaks with high mortality in guinea
pigs may approach 100%. Clinical signs are often non-specific: per acute:death,
acute: depression, rapid deterioration, lethargy, dyspnea; in chronic
disease see anorexia, weight loss, and rough hair coat, conjunctivitis,
ocular discharge, general unthriftiness, small litters, abortion, and
sporadic death. Diarrhea is variable, soft feces more common. Lesions of
acute salmonellosis are similar to other animals and involve the liver,
spleen, lymphoid tissues and intestine (enlargement, congestion, focal
necrosis), the spleen may be massive. Increased gas and fluid contents in
the gastrointestinal tract. Pregnant animals may have a purulent metritis.
Lesions in subacute to chronic cases may demonstrate yellow necrotic foci
in the liver and viscera with hyperemia. Peyer's patch hyperplasia,
hepatomegally, and splenomegally. Microscopically, multifocal
necrogranulomatous hepatitis, splenitis and lymphadenitis with the areas
of necrosis are surrounded by mononuclear cells and neutrophils (paratyphoid
nodules). Diagnosis by culture of mesenteric lymph nodes, conjunctiva,
feces, cecum, or aborted material (SS agar, MacConkey's or others).
Isolation should be serotyped, because non-pathogenic species exist.
Control is depopulation, sanitation and restocking because of the carrier
state. Guinea pigs do not respond to antibiotics well and may develop
enterotoxemia. DDX: clostridium enterotoxemia, yersinosis, Tyzzer's and
pneumococcal septicemia. Zoonotic and interspecies transmission potential
is high.
Cervical Lymphadenitis (Streptococcus
zooepidemicus) - beta-hemolytic, G+, encapsulated, Lancefield Group
C. Asymptomatic inhabitant of the upper respiratory tract-Transmission
through skin wounds,bite wounds, aerosol or genital. Oral cavity abrasions
caused by coarse plant feeds and conjunctiva are commonly implicated.
After penetration, the organism drains to the local lymph nodes. Uni-or
bilateral swelling at angle of jaw is referred to as "lumps" or
cervical lymphadenitis, but may be misleading because other lymph nodes
may be affected and a similar appearance may be caused by agents, such as
Streptobacillus moniliformis, Yersinia pseudotuberculosis, Salmonellae (S.
linate,) other Streptococcus sp., Zygomycetes, and Cavian leukemia.
Grossly, see encapsulated and abscessed ventral and cervical lymph nodes
and abscesses in various organs.The purulent exudate is white to yellow in
color. Septicemia and acute fatal pneumonia occur in the epizootic form.
Torticollis (head tilt) may occur due to otitis media and otitis interna.
Nasal Discharge, ocular discharge, dyspnea and cyanosis may develop.
Chronic infections can be exacerbated by stressors. At necropsy, infection
may vary from an acute fatal septicemia to a chronic suppurative process
in the lymph nodes, thoracic and abdominal viscera, uterus, and ears.
Microscopic evidence of pneumonia, pleuritis, myocarditis, pericarditis,
and peritonitis, otitis media, nephritis, arthritis, and cellulitis will
be seen characterized by necrotizing suppurative inflammation or
fibrinosuppurative inflammation. Chains of gram positive cocci may be seen
in direct smears or tissue sections. Culture on blood agar from abscesses,
heart blood or lungs will yield small beta-hemolytic mucoid colonies.
Systemic antibiotics such as enrofloxacin or chloramphenical are effective.
Abscesses may be drained and flushed. Affected animals should be removed
from the colony until the abscesses have drained and healed. In epizootic
cases, depopulation is advised. Scratch injection with ATCC 12960 (swine)
has provided some immunity. Apparently S. zooepidemicus is strictly an
animal pathogen.
Streptococcus (Diplococcus) pneumoniae -
Caused by a lancet-shaped, gram positive encapsulated coccus in chains and
pairs. Capsular type 19 and less frequently type 4 have been isolated from
guinea pigs. The disease seldom occurs in well-managed facilities, and may
be carried as an inapparent infection in the respiratory tract in up to
50% of animals. Aerosol transmission, mostly during the winter months,
with young and pregnant sows at greatest risk. Other predispositions
include change in environmental temperature, poor husbandry, experimental
procedures and inadequate nutrition. During outbreaks, death, stillbirths
and abortions occur. Pneumococci may activate the alternative complement
cascade, and are protected from phagocytosis due to the polysaccharide
capsules. At necropsy, fibronopurulent pleuropneumonia, pericarditis and
pulmonary consolidation are apparent. Histologically, an acute
fibrinosuppurative bronchopneumonia is present with thrombosis of
pulmonary vessels. Infiltrating cells may be elongate and form palisading
patterns in affected airways. Splenitis, fibrinopurulent meningitis,
metritis, lymphadenitis with focal hepatic and ovarian abscessation have
been reported. Guinea pigs with borderline vitamin C deficiency may
develop S. pneumoniae associated suppurative arthritis and osteomyelitis.
Direct smears will yield G+ alpha- hemolytic, diplococci, blood agar to
culture, and is a little fastidious.(optochin disk on blood agar) DDX:
Bordetella sp., S. zooepidemicus. Serotypes are same as seen in human,
interspecies transmission is suspected.
Staphylococcus sp. - Ulcerative
pododermatitis and acute staphloccocal exfoliative dermatitis are
associated with coagulase positive staphylococcus.
Pododermatitis - Caused by infection
subsequent to trauma, wire cage bottoms and lack of appropriate sanitation.
Bumblefoot may also be caused by obesity, rough cage bottoms, unsanitized
floors. Most lesions are chronic .The contact surface of the forefeet are
swollen, painful and encrusted with necrotic, exudative tissue and clotted
blood and /or crust. Microscopically, lesions are fibrotic
pyogranulomatous inflamation. Amyloidosis has been temporally associated
with advanced cases. Isolated cases of pneumonia, mastitis and
conjunctivitis have been seen.
Dermatitis - Seen in strain 13 guinea pig,
and seen in young pigs born to affected dams. It is characterized by
alopecia, erythema of the ventrum, with exfoliation. Skin lesions regress
in two weeks, with hair re-growth. At necropsy, there is erythema,
scabbing, cracks in the epidermis and hair loss. Histologically, there is
marked epidermal cleavage parakeratotic hyperkeratosis and minimal
inflammatory response. Possible interspecies transmission.
·Clostridium piliforme, Bacillus piliformis
- Tyzzer's lesions are usually confined to the gastrointestinal tract in
young guinea pigs. Multifocal gray foci on the liver, rough hair coat,
lethargy, watery diarrhea, death. Large numbers of spirochetes were
associated with clostridial organisms near lesions. Experimental
inoculation of young animals produced lesions in intestine and liver by
four days. Edematous, hemorrhagic, ulcerative, or necrotizing ileitis and
typhlitis with transmural involvement and fluid contents. Hepatic lesions
when present are characterized by focal coagulative necrosis in periportal
regions with variable numbers of PMN's. Warthin-Starry and Giemsa stains
will demonstrate the organism. Interspecies transmission.A carrier state
seems to be suggested by outbreaks appearing after stress.
Clostridium difficile (Antibiotic toxicity and
dysbacteriosis) - A fatal enterocolitis caused by clostridial toxin
after administration of narrow spectrum drugs. Clindomycin, lincomycin,
erythromycin, penicillin, bacitracin, dihydrostreptomycin, and ampicillin
cause disease 1-5 days after administration. Profuse diarrhea with high
mortality, after rapid kill-off of gram positive normal flora. For example,
after IM injection of 50,000 IU penicillin there was a 100X decrease of G+
within 12 hours, followed by a 10,000,000X increase in G- bacteremia due
to E. coli. In addition, some AB are excreted in the bile. This can be
prevented by using a broader spectrum antibiotic. Oddly, C. difficile is
usually susceptible to Penicillin in vitro. At necropsy, the cecal mucosa
is edematous, hemorrhagic and distended by gas and bloody fluid. The
terminal ileum demonstrates hyperplasia of the mucosa, with mononuclear
cell infiltrates in the lamina propria. Cecal epithelial degeneration with
sloughing, edema of the lamina propria, and leucocytic infiltration. Assay
of cecal contents for C. difficile, this syndrome may occur in the absence
of history of AB administration. Safer AB: chloramphenicol, enrofloxicin,
trimethoprim-sulfa, and aminogycosides. Rule out other common causes of
GIT disease.
Klebsiella pneumoniae - Patterns of
epizootic septicemia and pneumonia with pleuritis, pericarditis and
splenic hyperplasia are reported. Culture of Klebsiella sp . is diagnostic.
Citrobacter freundii - An epizootic of
Citrobacter septicemia with pneumonia, pleuritis, enteritis with isolation
of the organism was reported.
Clostridium perfringens - Acute fatal
typhlitis, sporadic. The cecum contains fluid, gas and ingesta.
Micro-degeneration and sloughing of enterocytes, necrosis of adjacent
submucosa, C. perfringens, spirochetes and other bacteria have been
isolated and causally associated.
CAR Bacillus - "Cilia associated
respiratory bacilli", "gliding bacteria", filamentous,
0.2u-6-8u long trilaminar cell wall, exacerbates other respiratory disease.
Guinea pigs are not very susceptible. Direct contact. No gross lesions
with rat origin bacteria.
Campylobacter-like Organism - Segmental
epithelial hyperplasia of the duodenum was seen in steroid treaded guinea
pigs. An outbreak with diarrhea, weight loss and mortality, yielded
affected animals with adenomatous hyperplasia in the ileum and jejunum.
Similar to the changes seen in hamster Campylobacter-associated disease
with organisms in the immature crypt epithelium on EM.
Pseudomonas aeruginosa - Pulmonary
botryomycosis with sulfur granules present in the focal suppurative
lesions was reported.
Corynebacterium sp. - C. kutcheri, one
report, mostly a disease of mice and rats, possibly an interspecies
exposure. Has caused chorioamnionitis in man.
Yersinia pseudotuberculosis - Experimental
disease can be produced, but spontaneous disease is rare. In the acute
form, small cream colored nodules are seen in the terminal ileum and cecal
intestinal wall with enteritis and ulceration of the mucosa. In the
subacute to chronic forms, miliary to caseous lesions may be present in
the mesenteric lymph nodes, spleen, liver and lung. Culture is diagnostic.
Streptobacillus moniliformis - Similar to
Streptococcal infections, suppurative creamy to caseous exudate, lesions
culture positive for S. moniliformis include cervical lymphadenitis,
abscessation, and pyogranulomatous pneumonia.
·Listeriosis (Listeria monocytogenes ) -
Unilateral or bilateral conjunctivitis with serous lacrimation to purulent
ulcerative keratoconjunctivitis with neovascularization. Diffuse moderate
to severe inflammatory infiltrate composed of neutrophils and few
lymphocytes and monocytes expand the cornea and present in the superficial
bulbar and palpebral conjunctiva. Lacrimal gland necrosis and inflammation,
no other lesions noted. Listeria is a gram+ aerobic nonspore-forming
bacterium widely distributed in silage and hay.
II. RICKETTSIAL/CHLAMYDIAL INFECTIONS
Chlamydia psittici-Guinea Pig Inclusion Disease (GPIC)
- Spontaneously occurring conjunctival infection due to Chlamydia psittici
(member of the psitticosis-lymphogranuloma-trachoma group). It is
widespread among conventional colonies, frequently asymptomatic, but may
be demonstrated with conjunctival smear stained with Giemsa. Young, 4-12
week old animals, are most susceptible with most adults seopositive. May
also see rhinitis or genital tract infection, photophobia. There may be
abortions or respiratory tract infections with concurrent
immunosuppression and/or Streptococcus or Bordetella. Transmission by
direct contact to feces, saliva, nasal secretions, and cervically by
pregnant sows. Grossly, the conjunctiva may be erythematous with serous or
exudative ocular discharge. Conjunctival scrapings and smears contain
sloughed cells, heterophils and lymphocytes. Antigen is demonstrable with
specific antibody and IFA.and stained smears with identification of
inclusion bodies Self-limiting disease (three-to-four weeks) with no
residual damage. DDX: Streptococcus zooepidemicus, Coliforms, Staph,
Pasteurella, Listeria. Not proven to be contagious to humans.
III. VIRAL INFECTIONS
Cytomegalovirus (Herpesvirus) - Species
specific. Natural infection in humans, primates, mice, rats and guinea
pigs. Cells produce characteristic large intranuclear and intracytoplamic
inclusion bodies. The infection may be subclinical,latent or persistent.
Natural infection of guinea pigs is characterized by swelling of and
lesions in the salivary glands, kidneys, and liver. Most will seroconvert
within a few months. It is transmitted by exposure to infected saliva,
urine or transplacentally. Replicaton and transmission of virus in
salivary glands and secretions.Pregnant guinea pigs and immunosuppressed
or inoculated animals develop more extensive lesions. Lymphoproliferative
(lymphoid hyperplasia), mononucleosis-like syndromes and lymphadenopathy
occurs in experimentally infected animals. Lesions are often found as
incidental lesions at necropsy. Primarily seen in the submaxillary
salivary duct epithelium. Large eosinophilic intranuclear inclusions with
marked karyomegaly and margination of nuclear chromatin in affected cells.
Occasional small intracytoplasmic inclusions are seen in ductal epithelial
cells. There may be a concurrent periductal mononuclear cell infiltrate
around infected ducts. In acute systemic infections, interstitial
pneumonia with necrosis and inclusions can be seen in the liver, kidney,
lung, spleen and lymph node. Useful animal model.
Guinea Pig Adenovirus Infection - Seen in the
United States and Europe. Low morbidity but high mortality in infected
animals. Usually related to experimental manipulation with impairment of
the immune system. Grossly, consolidation of the cranial lobes of the lung
are seen. Necrotizing bronchitis, bronchiolitis with desquamation of the
epithelial lining and inflammatory cell infiltration. Some airways will be
obliterated by cell debris, WBC's and fibrin.Pneumonia and necrotizing
tracheitis may be present. Nuclei of respiratory epithelial cells often
contain distinctive basophilic to amphophilic inclusions 7-15u in
diameter. Electron microscopy reveals classic arrays. This virus has not
been isolated, however, disease has been reproduced with cell-free
filtrates.
Coronavirus-like Infection in Young Guinea Pigs
- Characterized by wasting, anorexia, diarrhea seen after arrival from
vendor. Low morbidity and mortality. Acute to subacute necrotizing
enteritis involving the distal ileum. Copious amounts of mucoid material
present throughout the gastrointestinal tract. Blunting and fusion of the
affected villi with synctial giant cells in the intestinal mucosa. Viral
particles consistent with coronavirus seen on EM.
·Guinea Pig Herpes-like Virus (Herpesvirus) (Caviid
Herpesvirus 2) - Isolated from primary kidney cell culture - does
not produce disease in the natural host.
·Guinea Pig X-Virus (GPXV) (Herpesvirus) (Caviid
Herpesvirus 3) - Originally isolated from leukocytes of Strain 2
pigs - experimental inoculation into Hartley Strain caused, viremia, focal
hepatic necrosis and mortality - a possible complicating factor for
research.
·Lymphocytic Choriomeningitis (LCM) (Arenavirus)
- Mostly experimental disease in guinea pigs. Posterior paresis, liver and
splen enlargement Lymphocytic infiltrates in meninges, choroid plexus,
ependyma, liver, adrenal, kidney and lungs. Wide host range, exposure by
inhalation, ingestion,intrauterine or through intact skin. DX viral
antigen in tissue or section, by IFA, ELISA, MAP, Complicates research and
is transmissible to humans, causing mild to moderate illness. Wild mice
are a reservoir.
Cavian Leukemia (Retroviridae, Type C
Oncovirus Group, Mammalian Group) - Widespread, spontaneous disease
in inbred and outbred strains. Seen in young adults. Lymphadenopathy,
rough hair coat, weight loss, ascending paralysis seen in clinical disease.Leukocytes
vary from 50,000-250,000. Can be produced with transplanted cells and cell
free extracts. Preponderance of cells are lymphoblastic in blood smear.
Large lymph nodes in the cervical axillary and inguinal areas are seen
with splenomegally and hepatomegally, affected tissues are swollen and
pale. There is a moderate infiltration with obliteration of the normal
architecture with lymphoblastic-type leukemic cells in the spleen, liver,
bone marrow, lung, thymus, GIT-GALT, heart, eyes and adrenals. Model of
viral associated Neoplasia.
Other viruses: Serologic evidence of
subclinical exposure: Sendai, Murine Poliovirus, Reovirus3, Pneumonia
virus of mice, SV5
IV. MYCOTIC INFECTIONS
Dermatomycoses are most common; usually caused by T. mentagrophytes.
Systemic mycoses relatively rare with only a few reports.
Trichophyton mentagrophytes - Strain
related susceptibility. Mortality rate in neonates approaches 100%.
Spontaneous regression in adults, recurrence in sows at parturition.
Related to environmental conditions: heat, humidity, spores in hair
bedding and soil. Cutaneous lesions may first appear on the nose, other
regions of the head and then on the sides and back. On gross examination,
the lesions are circumscribed, erythematous, edematous, scaly with
alopecia. Pustules are usually due to secondary bacteria. On microscopic
exam, there is hyperkeratosis, epidermal hyperplasia, PMN infiltration,
pustules in the epidermis and hair follicles. Arthrospores anf hyphae are
seen in H&E, PAS or GMS. Wet preps with 10% KOH. Culture in
Sabouraud's dextrose. Very zoonotic. Cull and slaughter is advisable.
Systemic griseofulvin may cause teratogenesis. Useful animal model.
Zygomycetes sp.
Aspergillus sp.
Histoplasma capsulatum.
Cryptococcus neoformans.
Torulopsis pintolopesii- gastric yeast, normal flora, unaffected by
ketoconazole
V. PROTOZOAN PARASITES
·Toxoplasma gondii - Naturally occurring
disease rare under current housing practice. Infections are asymptomatic,
multifocal hepatitis and pneumonitis, cysts in the myocardium, CNS. Can be
passed in the milk. Infected through ingestion of Felid oocysts in food or
bedding need to differentiate from E. cunculi.
·Encephalitozoon cuniculi - Infectious, are
usually asymptomatic. Similar to E. cuniculi infections in other animals,
multifocal granulomatous encephalitis and interstitial nephritis. Glial
nodules, perivascular lymphoplasmacytic cuffing in the neuropil and
meninges. Obligate intracellular protozoa, incidence varies from 25-95%.
Becomes clinical with stress or immunosuppression. Hematogenously spread
via macrophages, selectively parasitizing vascular endothelium, especially
brain and kidney life cycle 3-5 days. Gross-Kidney - variably severe
multiple white pinpoint foci, indented gray area over cortical surface.
Micro mild to moderate granulation to chronic interstitial nephritis and
tubular dilation. The granulomas are principally in the epithelial cells
of collecting tubules. Organisms are most abundant in early stages of
disease which complicates research.
Klossiella cobayae - "non-pathogenic"-Infects
kidneys of guinea pigs. Organisms form schizonts in glomerular endothelial
cells that are 8-12u and multinucleated. Within the tubular epithelium at
the corticomedullary junction and medulla are variably sized, irregularly
round 12-75u diameter vacuoles that enlarge the cells and compromise the
tubular lumen. Microgametes and macrogametes, sporoblasts and sporocysts
are seen. Generally an incidental finding, tubular epithelial cell
regeneration with variable amounts of lymphocytes and plasma cells in the
interstitium.
Giardia caviae - A flagellate in the small
intestine. Adheres to surface of epithelium and apparently causes no
clinical signs or lesions.
Cryptosporidium wrairi - A recognized
pathogen, may be subclinical. In small intestine, clinical infection
occurs in juveniles. Infection rate of 30-40% are typical. Causes greazy
rough hair coat, lethargy, diarrhea, weight loss, emaciation, morbidity
may range from 0-50%. At necropsy, animals are thin and potbellied, with
perineal fecal staining. Small intestine will be hyperemic and will
contain watery material and little food. Acute edematous lesions seen in
the jejunum, anterior ileum and cecum. Hyperplasia of the crypt epithelium,
edema of the lamina propria and leucocytic infiltration. Necrosis and
sloughing of enterocytes occur at the villar tips. In emaciated animals
with chronic lesions, there is villar atrophy and fusion, metaplasia and
flattening of villar enterocytes. Eosinophilic inflammation may be
present.Organisms are very small, round, intracellular, but
extracytoplasmic with hold fasts, present within the brush border of
enterocytes. They can be seen inmucosal scraping or paraffin embedded
tissue with H&E but PAS is popular. Transmission by oocysts in water,
food, fomites. E. coli has been associated with clinical cases of C.
wrairi.
Eimeria caviae - Typical Eimerian life cycle.
Should not be a problem in a well-managed colony. Following ingestion of
sporulated oocysts, sporozoites penetrate the intestinal mucosa,
schizogeny detectable in seven days, diarrhea at 10-13 days, severely
affected will have diarrhea before oocytes sporulate. Weaning and seasonal
fluctuation. At necropsy the colonic wall is hyperemic, the mucosa
congested and edematous, with petechial hemorrhages, and gray-white
nodules. Ingesta may be flecked with blood. Chronically, colonic
hyperplasia, edema of the lamina probria, infiltration with PMN's and
mononuclear cells, microgametes and macrogametes in large numbers. DX see
organisms in mucosal scraping, fecal float, histology. Rx: coccidiostats.
Balantidium caviae - Ordinarily
non-pathogenic but can be a secondary invader. Organisms are large, have
cilia in variable number of rows, have a large ovoid to ellipsoid
macronucleus, have a smaller micronucleus, have one contractile vacuole,
and have a bean-shaped cytostome. Seen in fecal smears or in histo
sections.
Entamoeba caviae is non-pathogenic, however
experimental infection with Entamoeba histolytica provides an appropriate
animal model. Produces liver abcesses, bloody diarrhea, intestinal pain,
fever. Presence of trophozoites containing erythrocytes indicative of
pathogenic strains. Amoeba mimic macrophages and heptocytes in histology
sections. Lesions are flask shaped ulcers progressing to transmural
abcesses. Liver abcesses have minimal inflamitory reaction.
Tritrichomonas species are incidental common
findings-oval pear shaped eosinophilic flagellates, non pathogenic.
VI. HELMINTH PARASITES
Nematodes Paraspidodera uncinata (Cecal Worm) -
Found in cecum and colon; rarely produces clinical disease. Is not common.
Is 2-5mm long and has a direct life cycle of 65 days, with no migration
beyond the intestinal mucosa.Shed eggs in fece, thick wall ascarid type
egg.
Trematodes Fasciola sp. - Has been reported
several times and produced severe liver damage. Infection associated with
feeding greens contaminated with metacercariae.
VII. ARTHROPOD PARASITES
Mallophagia - Large biting, chewing lice
cause pediculosis, pruritis, rough hair coat, alopecia in heavy infections.
Gyropus ovalis - The oval guinea pig louse (uncommon)
wide head -1.0-1.2mm long.
Gliricola porcelli.- The slender guinea pig
louse (common) thin head -1.0-1.5mm long.
Chirodiscoides caviae - Relatively common in
commercial supplies, lab facilities and pet animals; can bee seen moving
around especially in the lumbar region. Non-burrowing, pretty harmless.
Usually seen in a group of 3-2 immature males and one more mature female
easily overlooked unless heavy infestation (>200/cm3) pruritus with
alopecia. Magnification exam for diagnosis.
Trixacarus caviae - Burrowing sarcoptic mange,
intense pruritus, widespread alopecia, and hyperkeratosis. Severe dry,
scaling, crusting, dermatitis, especially near neck and shoulders, inner
thighs, abdomen. Probably some historical confusion with Sarcoptes and
Notodres. Self-mutilation, some mortality. Hematological changes
associated with intense marked pruritis, include heterophilia, monocytosis,
eosinophilia and basophilia. Flaccid paralysis and convulsions have been
noted, vigorous scratching has lead to seizures. Microscopically-paraffin
embedded specimen see epidermal hyperplasia, orthokeratosis, parakeratosis,
irregular burrows in stratum corneum contains mites and eggs. Spongiosus,
PMN infiltration, hair follicles not usual. 10% KOH mites and eggs. Human
contacts may experience urticaria. TX: ivermectin.
Psoroptes cuniculi - Rabbit ear mites may
affect guinea pigs.
Demodex caviae - One report; no clinical
signs.
Mycoptes musculi and Notodres muris -
probable interspecies infection, not common.
VIII. METABOLIC/ AGE-RELATED DISEASES
Scurvy (Vitamin C Deficiency) - Only
primates, guinea pigs, red vented bulbul birds, channel catfish and Indian
fruit-eating bats are known to require a dietary exogenous ascorbic acid.
Ascorbic acid is essential in the hydrolase reaction for formation of
hydroxyproline and hydroxylysine in the collagen molecule. Lack of
l-gulonolactone oxidase in the glucose to Vitamin C pathway. Connective
tissue cells don't produce collagen at a normal rate, with deficient or
defective production of interosseous matrix. Vitamin C is also necessary
for the catabolism of cholesterol to bile acids. In scurvy, epiphyseal
cartilage persists, bone formation is suppressed. The cartilage lattice
lengthens but is not replaced by bone. The resultant structure is very
susceptible to trauma, resulting in multiple microfractures. Increased
capillary fragility results from increased intercellular space between
endothelial cells, vacuolar degeneration of endothelia and depletion of
subendothelial collagen. Increased Prothrombin time, increased
susceptibility to bacterial infection (especially Strep pneumonae)
impaired macrophage migration, decreased phagocytosis of PMN's. Clinically,
guinea pigs have swollen hind limbs, and move with great difficulty.
Increased vocalization (due to pain when moving). Anorexia, weight loss,
delayed healing of wounds. Death in 2-3 wks due to starvation or secondary
bacterial infection. At necropsy, there is enlargement of the
osteochondral junctions with hemorrhage into the soft tissues. Especially
in periarticular regions of hind limbs. Animals are thin and unkempt, with
variable diarrhea. Variable blood in feces, ecchymosis in the urinary
bladder and adrenals enlarged. Microscopically persistence of irregular
epiphyseal cartilage evident in young animals, microfractures of
cartilaginous spicules and hemorrhage. Proliferation of mesenchymal cells
in periosteal regions and medullary cavity with displacement of BM
hematopoeitic cells. May be aggregates of pink material between cells.
Dental abnormalities occur: fibrosis of the pulp and derangement of
odontoblasts. Subclinical hemosiderin laden macrophages in the lamina
propria of the intestine. Severe skeletal abnormalities create a locomotor
problem. Requires 5-10mg/kg daily, pregnant sows require six times that.
Myopathies
Myopathy/Myositis - Necrotizing with necrosis
of myofibers and leucocytic infiltration, loss of cross striation,
multinucleated strap cell formation, variable mononuclear cells.
Nutritional Muscular Dystrophy - Associated
with Vitamin E and Selenium deficiency. Depression, conjunctivitis,
spontaneous hind limb weakness, marked decrease in fertility. May die
within one week of onset. Elevation of CPK. Marked pathology - coagulative
necrosis, hyalinization of myofibers, fragmentation, increased basophilia,
rowing of nuclei (regeneration) not mineralization, testicular
degeneration later with Vitamin E deficiency. RX: tocopherol.
Myocardial/Skeletal Muscular Dystrophy with
Mineralization - Poorly understood, multifocal mineralization, may
be seen as an incidental finding, especially in hind legs. May be
asymptomatic, multifocal mineral with minimal inflammatory response,
myocardial degeneration with mineral occasionally seen. In chronic lesions,
will get mineral and fibrosis. There may be a genetic component.
Metastatic Calcification - Seen most often in
guinea pigs over one year of age. Muscle stiffness, untriftiness, renal
insuffiency, mineral deposition may be confined to soft tissues around
elbows and ribs, or may be widespread and include mineralization of lungs,
trachea, heart, aorta, liver, kidney, stomach, uterus, and sclera. Dietary
factors, possibly low magnesium and high phosphorus High Ca/PO4 appear to
interfere with Mg absorption. Rabbit food contains an excess of Vitamin D.
Guinea pigs require more folic acid than rabbits. Use von Kossa or
Alizarin stain for mineral in tissues. May be seen as an incidental
finding in soft tissues.
Pregnancy Toxemia-Two different forms with similar clinical presentations.
Both occur in advanced pregnancy with depression, acidosis, ketosis,
proteinuria, ketonuria, and lowered urinary pH to 5-6. Pregnancy in guinea
pigs has been referred to as a "parasitism of staggering proportions".
Fasting Metabolic Pregnancy Toxemia -
Nutritional - OBESE sows, last two weeks of pregnancy, especially second
pregnancy. Uterine contents are frequently 50% of non-pregnant weight.
Stress factors: shipping, change in feeding, cabbage deprivation. Low
blood sugar, ketosis, hyperlipemia, comatose and die in 5-6 days. Necropsy:
animals have abundant fat with marked fatty infiltration in the liver,
kidneys, adrenals, even in vessels stained with fat stains. Caused by
reduced carbohydrate intake and mobilization of fat as an energy source.
Circulatory/Toxic Pregnancy Toxemia (pre-eclampsia) -
Uteroplacental ischemia occurs due to compression of the aorta caudal to
the renal vessels by the gravid uterus. This results in a significant
reduction of blood pressure in the uterine vessels, with placental
hemorrhage, necrosis, thrombocytopenia, ketosis, and death. On micro,
there will be leucocytic infiltration, multifocal periportal liver
necrosis, nephrosis, and adrenocortical hemorrhage. This has been
reproduced experimentally. Animal model.
Diabetes Mellitus - Spontaneous disease with
no clinical signs early in the disease. Onset three months, hyperglycemia,
glucouria, rarely ketonuria, reduced fertility. Frequently, animals
introduced into the colony will become diabetic, suggesting an infectious
agent, not identified. Micro, there is vacuolation and degeneration of the
beta cells in the islets of Langerhan's with fatty infiltration of the
exocrine pancreas and fibrosis of the vascular stroma. Glomerular tufts
demonstrate thickened basement membranes with sclerosis in advanced cases.
Segmental Nephrosclerosis - Common in aged
(>1yr) guinea pigs, characterized by small lumpy kidneys with clinical
signs of renal failure. Weight loss, edema, polyuria, polydipsia, and
proteinuria. Irregular, pitted renal cortices. Possibly related to
autoimmune disease, infectious agents and vascular disease. Resulting from
focal ischemia and fibrosis. Spontaneous deposits of IgG and complement
(C3) were demonstrated along the mesenchymal and peripheral glomerular
basement membrane. Accelerated disease is seen in animals fed high protein
diets. Elevated blood pressure and renal hypertension has been noted. At
necropsy there are multiple granular pitted areas on the renal surface.
Pale streaks extend down the cortex to the medulla in advanced cases.
Microscopically, segmental to diffuse interstitial fibrosis with
distortion of the normal architecture are seen. Mostly, the convoluted
tubules and loops of Henle are involved. Tubules are lined by poorly
differentiated cuboidal to squamous epithelium. Scattered tubules contain
variable degrees of proteinaceous material and cell debris. There is
senescence of individual glomeruli with fibrosis which may become
extensive. There may be scattered foci of lymphoplasmacytic inflammation,
medial hypertrophy of the renal vessels and endothelial hyperplasia. There
may be increased BUN and creatinine values with non-regenerative anemia
and low urine specific gravity.
Osteoarthritis/ osteoarthrosis - Spontaneous
and induced by surgical partial medial meniscectomy. Lameness unilateral
and bilateral, reluctant to move, joint enlargement. Moderate to severe
changes of the tibial plateau, more severe medial, characterized by
chondrocyte and proteoglycan loss in the superficial and middle zone of
the articular cartilage and proliferation of subjacent chondrocytes to
form clones with fibrillation of hypocellular matrix. Also affects medial
femoral condyle and meniscus, with tibial and femoral osteophytes.
Synovial changes are characterized by increased mature fibrous connective
tissue, mild synoviocyte hyperplasia with occasional papillary projections.
Inflammatory cell infiltrate may not be present despite marked
degenerative changes. Bone marrow may get replaced by fibroblasts, adipose
tissue, and foci of metaplastic cartilage may be present. Animals normal
may be normal at 61 days of age, severe arthrosis by 18 months. Hartley
strain.
IX. NEOPLASIA
True neoplastic lesions are rare, usually found in animals over three
years of age. A serum factor, possibly asparaginase, has been demonstrated
to have anti-tumor activity. Foa Kurloff cells inhibit transformed human
epithelial cells in vitro.
Lung-Pulmonary/bronchogenic papillary adenoma : (35%)
small white circumscribed, visible - papillary structures lined by a
single layer of hyperchromatic cuboidal epithelium. Malignancy is rare.
Skin and subcutis: trichofolliculoma,
sebaceous adenoma, penile papilloma, lipoma, fibrosarcoma, fibroma,
carconoma.
Uterus: leiomyoma (25%), fibroma, myxosarcoma,
leiomyosarcoma.
Ovaries: cystic rete ovarii (hormonal
imbalance associated with leiomyosarcoma), teratoma.
Endocrine: adrenocortical adenoma.
Mammary: fibroadenoma, adenocarcinoma in
males and females with mets to lymph nodes.
X . UNIQUE AND MISCELLANEOUS CONDITIONS
Kurloff Body - A cytoplasmic inclusion
found in a mononuclear leukocyte called a Kurloff cell. It is unique to
guinea pigs. In the non-pregnant guinea pig, the cells are located
primarily in the sinusoids of the spleen, and in the stromal tissues of
the bone marrow and thymus, and not normally in lymph nodes. The cells are
rare in fetuses and neonates, but are common in adults, especially females.
Their numbers increase during pregnancy and after exogenous estrogen
treatment in both sexes. The bodies are round to oval, usually 1-8 microns
in diameter, and are initially granular and later more finely fibrillar to
homogeneous within a vacuole. They are PAS-positive, stain positive for
fibrinoid material by the Lendrum stain and are thought to be secreted by
the cell itself. It is interpreted to be composed primarily of
mucopolysaccharides and glycoprotein associated with a protein
polysaccharide material. On ultrastructure, the inclusions are membrane
bound, and other cytoplasmic organelles in these cells are consistent with
secretory activity. Large numbers of cells may be present in the placental
labyrinth of pregnant sows. Kurloff cells have been shown to release
inclusion material into the fetal endothelium and trophoblast. In vitro,
the material has a toxic effect on macrophages. Kurloff cells may have a
role in preventing maternal rejection of the fetal placenta, creating a
barrier separating fetal antigens from immunologically competent maternal
cells. These cells have been misinterpreted as lupus cells.
Rhabdomyomatosis (Nodular Glycogen Infiltration)
- Occasionally observed as an incidental finding in guinea pigs of various
ages. In the past it was considered a degenerative lesion or a "blastemoid"
tissue malformation. However, it is now considered to be a congenital
disease related to a disorder of glycogen metabolism. Occasionally, larger
lesions may appear grossly as pale pink, poorly defined foci or streaks.
Rhabdomyomatosis may be seen most frequently in the left ventricle, but
has been reported in any region. The lesion consists of a spongy network
of enlarged, vacuolated myocardial cells supported by a loose network of
delicate fibrils. The myocyte cytoplasm is abundant. The nucleus is
central or peripheral. The cytoplasm may consist of pink fibrillar to
granular material radiating from the nucleus (spider cells) or may have an
abortive striated appearance. Vacuoles are round to polygonal and contain
abundant glycogen (PAS positive) that is washed out during processing.
Glycogen can be demonstrated in alcohol fixed specimens. There may be
displacement and flattening of myocyte nuclei in affected fibers. It is
considered an incidental finding and normally does not compromise cardiac
function. This occurs also in swine, cattle, dogs, and man.
Perivascular Lymphoid Nodules in Lung -
Aggregates of lymphocytes in the adventitia of pulmonary vessel may be
seen in a variety of stains and can be seen in young guinea pigs as early
as five days. Very common. Usually seen around smaller branches of
pulmonary arteries and veins. They appear to enlarge with age. Germ-free
animals usually do not have these, at least up to three months of age. May
be grossly visible as circumscribed pale, pinpoint up to 0.5mm subpleural
foci. May be mistaken for granulomas created after SQ injection of Freud's
adjuvant.
Osseous Metaplasia - Occasionally seen in
guinea pigs, hamsters and rats. No clinical significance. May occur
anywhere, but lung is common site and less so in kidney. Have seen plates
of bone with bone marrow in the eye. Spicules are composed of dense
lamellar bone with varying degrees of calcification. There is usually no
reaction in adjacent alveoli. Large numbers of foci with bone marrow have
been seen in X-irradiated guinea pig. On microscopic, concentric to
eccentric aggregates of small arteries and veins. There may be focal to
diffuse infiltrates in the alveolar septa of some animals. Most animals
are free of these lesions. Airways and alveoli are clear. On electron
microscopy, the lymphocytes have normal morphology and no virus.
Alopecia - Frequently see thinning of hair in
young animals at time of weaning; is associated with the period of
transition between loss of baby fur and appearance of more coarse guard
hairs. May be due to hairpulling, barbering,nutritional stress, hormones.
Seen in sows in late pregnancy; is thought to be due to reduced anabolism
of maternal skin associated with the rapid increase in fetal growth. The
condition worsens with subsequent pregnancies. Nutritional (protein
deficient <15% Crude Protein) and genetic factors are also involved and
affect degree of alopecia. May also be caused by barbering, rough surfaces
in cages or infections. Culling the most severely affected breeders
reduces severity of alopecia.
Cystitis and Urolithiasis (urinary calculi) -
Stones occur anywhere in urinary tract and vary in size from sand to
stones. Usually are calcium and magnesium carbonates and phosphates. Age,
sex and immunosuppresion are related to development. E. coli cystitis in
breeding females causes a thickening of the bladder mucosa, congestion,
intramural/intralumenal hemorrhage, leukocytic infiltration in the
submucosa, occasionally with desmoplasia, ulceration, PMN's. May be the
initiating factor or secondary to uroliths in the urinary bladder.
Cystic Ovaries(cystic rete ovarii, serous cysts) -
Usually seen in sows over one year old. Thin walled, fluid filled,
fluctuant cysts up to 2cm in diameter and contain clear fluid. Variable
size, lined by low cuboidal to columnar epithelial cells. Solitary cilia
or tufts of cilia are present on the lumenal surface . There may be marked
compression of ovarian tissue. Associated with cystic endometrial
hyperplasia, mucometra, endometritis and fibroleiomyomas.
Trophoblastic Giant Cells - Derived from the
outermost layer of the fetal placenta (trophoblast) which is in direct
contact with the maternal blood supply. (The guinea pig has a labyrinthine
hemomonochorial placenta in which there is a single trophoblast layer
forming a continuous syncytial layer.) These cells have remarkable
migratory activity and can migrate out into the myometrium.
Embryonic Placentoma (deciduoma): A
multi-layered transitory growth of parthenogenic origin that occurs within
the ovary of the young female, the placentoma is resolved by fibrosis.
Regresses after 12-21 days of pseudopregnancy. Contins 6 regions. The
mesometrial region (decidua basalis) consists of both spiny mesometrial
cells and granulated metrial gland cells. A typical GMG cells are large
(40u), frequently binucleate, with eosinophilic, intracytoplasmic granules
(PAS+, diastase resistant), suspected to be bone marrow derived.
Gastric Dilation- Acute, occurs sporadically,
frequently affected animals are found dead with no previous indication of
illness. Gastric volvulus will demonstrate 180 degree.
Cecal Torsion - Acute death, displaced cecum
distended with fluid and gas, wall may demonstrate edema and hemorrhage.
Colonic Intussusception - Stress, dehydration,
straining, hemorrhage protrusion of colon prolapsed through rectum.
Reduction is unsuccessful.
Focal Hepatic Necrosis - Multifocal
coagulative necrosis, frequently subcapsular, with minimal or no
inflammation. May be a terminal event due to portal blood flow changes.
Chronic Hepatopathy - Characterized by
variably severe periportal and interstitial fibrosis, hepatocellular
degeneration, bile duct proliferation suggestive or an anoxic change.
Liver Contusion - Fracture of the capsule of
the liver with hemorrhage into the peritoneum. Caused by trauma,
mishandling, falls.
Foreign Body Pneumonitis - Pneumoconiosis -
focal pulmonary lesions associated with inhalation of food or bedding
materials. Incidental finding with animals on wood chips or rice straw. At
necropsy there may be areas of atelectasis, or circumscribed nodules in
the parenchyma of the lung, usually not visible grossly. Recent lesions
will have plant fiber lodged in small airways with PMN's and macrophages,
lesions of longer duration will exhibit focal granulomatous bronchiolitis
and alveolitis with macrophages and multinucleated giant cells. Plant
fibers are birefringent, an incidental finding that may complicate
research.
·Freund's Adjuvant Granuloma - After
subcutaneous injection of Freund's, multifocal granulomatous response in
lung.
Cataracts - Autosomal dominant, possibly
associated with IDDM or L-tryptophan deficiency. Will get lens desiccation
with long-term anesthesia.
Pea Eye - Hyperplastic nodule of lacrimal or
zygomatic gland origin on inferior conjunctival sac.
Fatty Infiltration of the Pancreas - The
proportion of exocrine pancreas decreases with age with no apparent
impairment of function. Histologically, there are large areas of adipose
tissue between normal pancreatic tissue.
Thymus - Degenerating thymocytes are
frequently observed in close association with Hassell's corpuscles,
especially in younger animals. They may evolve into thymic cysts.
Germfree Animals - Germfree animals have a
disproportionately large cecum. In conventional animals the cecum
comprises about 10% of the body weight; whereas, in germfree it comprises
about 25-30%. Predisposes animals to rupture, herniation, torsion,
volvulus and uterine prolapse; Germfree animals also have hypoplastic
lymph nodes and lymphatics along the gastrointestinal tract, lower WBC's,
changes in WBC differentials, and serum protein concentration.
Hairless - Euthymic strain available, useful
in dermal research. Hair follicles form and produce rudimentary hair. Hair
present on face and feet. Non pigmented. Fragile.
Malocclusion of Teeth - Open rooted maxillary
premolar and molar teeth overgrow laterally to the labial mucosa.
Mandibular premolar and molar teeth overgrow to the lingual side and
occasionally incarcerate the tongue. Will see weight loss, anorexia,
salivation, wasting. May see secondary malocclusion of the incisors. Cause
varied; may be improper diet, a genetic predisposition (e.g., high
incidence in strain 13 involving more than one gene with incomplete
penetrance), one report of flurosis (caused impairment of dentin and
enamel formation). Guinea pig teeth grow continuously throughout life, at
necropsy food particles will be trapped around cheek teeth. Cheek teeth
will have irregular contours and sharp edges.
Neuritis- Sciatic inflammation and muscle
necrosis due topoorly placed IM injection of ketamine. May see swelling
and lameness, or on more severe cases self mulilation of foot and leg.
Microscopic will see muscle necrosis, regeneration and degeneration, sub
acute to chronic perineural inflammation, perivascular inflammation.
Heat Stress- excessive salivation, rapid
shallow breathing, hyperemia of extremities, elevated body temperature.
Tissues congested, and serosal surfaces tacky at necropsy.
Fracture - Animals not familiar with grids
may fracture legs after stepping into holes.
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