|
Order: Rodentia
Family: Caviidae
Subfamily: Caviinae
Genus: Cavia
Species: porcellus
ORIGIN: South America
English: short-haired
Abyssinian: short-haired;hair direction in rosettes or whorls
Peruvian: long-haired
Tailless, vocal, gregarious but territorial, generally easy to handle, do not adjust to dietary changes easily, sensitive to gut flora alterations, requires vitamin C in diet, exhibits toxicity to certain antibiotics such as penicillin. Have 1 pair of mammary glands which is inguinal. Lungs have 6 lobes. Forefeet have 4 digits; hindfeet have 3 digits.
Age at puberty:
Minimum breeding age:
Breeding season:
Estrous cycle:
Duration of estrus cycle:
Duration of estrus:
Gestation:
Litter size:
Number of litters:
Ovulation time:
Postpartum return to
estrus:
Chromosome number:
Birth weight:
Weaned:
Weight at maturity:
Breeding life of female:
Life span:
Mating colony:
Recommended (ranges):
Humidity:
Light:
Body temperature:
Mammae:
Chromosome Number:
45-70 days
12 weeks (female averages 450 gms and
male 500 gms)
any time of year
Polyestrus; all year
16-19 days
6-15 hours (when will accept
male)
59-72 days (average is 68) (female
may double weight during pregnancy)
1-8 (average 3)
3-4/female/year
10 hours from onset of estrus
(spontaneous)
6-8 hours (postpartum
estrus)
diploid 64
75-100 gms. NOTE:
Under 50 gms usually die. Young- Very well developed.
Fully haired, eyes open, have teeth
(precocious).
14-21 days. May begin to eat solid
food only a few hours after birth.
700-800 gms - female; 950-1200 gms
-male
3-5 years male: 4-5 years
6 years.
1 male to 3-10 females
(harem)
Temperature: 65-79
degrees
40-70%
10-12 hours/day
1 02.8-103.8 degrees F
2 inguinal
2N - 64
cage: < 350 gms - 60 sq.
inches > 350gms - 101 sq. inches
cage height: 7 inches
Commercial lab chow for guinea pig.
Must have vitamin C source. Keep chow cool and dry to
preserve vitamin C.
Lateral saphenous vein, lingual vein,
marginal ear vein, dorsal vein of the penis, cardiac
puncture.
Ketamine (IM): 44 mg/kg + 2 mg
Acepromazine Meleate
Pentabarbitol (IP): 15-20
mg/Kg
Inhalation: ether, methoxyfluorine,
halothane. Pretreat with atropine.
Do not use Innovar-Vet: causes
sluffing of muscle.
I 1/1 C 0/0 PM 1/1 M 3/3 =
20
Nutrition studies, allergy studies,
radiology, immunology, production of complement,
parasitology, bioassays, diagnosis of infectious diseases by
animal inoculation, tumor inhibitory properties of guinea
pig serum.
RBC: 4.5-7.0 X 106/mm3
HCT: 40%
Hb: 12 gm/100 ml
MCV: 85 Mm3
MCHC: 30%
Ret.: 2%
WBC total:
7,000-10,000/mm3
PMN: 30-50%
Lymph: 40-60%
Mono: 0.9-5%
Eos: 0.01-2%
Bas: 0.1-0.4%
Foa-Kurloff or Kurloff cells or
Kurloff bodies-are specialized mononuclear leukocyte which
contain large mucopolysaccharide, intracytoplasmic inclusion
body. Increased number seem during pregnancy. Origin and
function is not known.
6.6.1 Lymphocytic choriomening Virus (LCMV):
Mice, humans and other animals.
6.6.2 Cytomegalovirus (CMV):
Salivary Gland Disease, species specific
6.6.3 Poliomyelitis virus:
G. pig paralysis; meningomyloencephalitis.
6.6.4 Pneumonia Virus:
Pneumonia
6.6.5 Leukovirus Type C:
Leukemia similar to man.
6.6.6 Myositis:
Possibly virus-swelling of muscles.
6.6.7 Westing Disease:
Nausea, vomiting
6.6.8 Highly Fatal Diseases:
Infectious agent unidentified;
grows on embryonated egg.
Systemic-rare-Mucormycosis (Absidia spp.)
Dermatophycoses - culture on DTM (Dermatophyte Test Medium). Griseofulvin 15 mg/kg/day for 14-28 days.
6.6.2.1 Scurvy: ( Vitamin C or Ascorbic Acid Deficiency)
Hypovitaminosis C:
Hemorrhage in stifle joints, and lameness. May see bleeding gums.
Treatment:
Use Ascorbic acid 1 mg/100 gm body weight, SubQ: and 0.2-0.5mg/ml drinking water for prevention.
Malocclusion:
Overgrowth of incisors and/or or molars, particularly anterior premolars, "slobbers" or ptyalism
Soft Tissue Calcification:
Imbalance in Mg, Ca, K, P
Antibiotic toxicity:
To narrow-range antibiotics, especially penicillin. Use broad-spectrum such as chloramphenicol.
Cecitis - acute:
May be stress-related, toxic or bacterial (Clostridium perfringens)
Vitamin E deficiency:
Muscular dystrophy, pale muscles
Myositis:
Unknown etiology. Nutritional or viral?
Ketosis:
Commonly pregnancy toxemia - yellow liver disease. Many factors: age, sex, diet, obesity, fasting, fetal load, genetic.
6.6.2.1 Scurvy
A. Etiology:
Guinea pigs lack the hepatic enzyme l-gulonolactone oxidase which is necessary for the conversion of glucose to ascorbic acid (Vitamin C). Vitamin C is involved in many biochemical processes in the body including collagen synthesis and the synthesis of intracellular ground substance. A "rule of thumb" to remember is that a sick guinea pig has scurvy until proven otherwise. If Vitamin C is not supplemented in the diet or if the animals stop eating for any reason they develop scurvy.
B. Clinical Signs:
Scurvy is characterized by weakness, anorexia, diarrhea, skin lesion, limb stiffness and reluctance to move, and death in 3-4 weeks from secondary infection or starvation.
C. Gross Pathology:
On necropsy, affected animals have widespread hemorrhage in muscle and periosteum, especially around the stifle joint and rib cage. Young animals have enlarged costochondral junctions.
D. Diagnosis:
History, gross necropsy findings, serum Vitamin C levels.
E. Treatment:
Severe cases can be treated by giving 50 mg Vitamin C/day orally or parenterally and the disease prevented by making sure Vitamin C is provided in the drinking water it should be mixed fresh each day.
6.6.2.2 Pregnancy Toxmexia:
A. Etiology:
Pregnancy toxemia (ketosis) is similar to the problem seen in ewes. It usually occurs in older obese females. Other predisposing factors include sudden dietary changes, lack of exercise, and environmental stressors. Obese boars may develop a similar toxemia.
B. Clinical Signs:
The condition usually occurs during the last two weeks of gestation or during the first week post-partum. The disease may be asymptomatic, rapidly fatal, or be manifested by depression, reluctance to move, anorexia, dyspnea, convulsions, or abortion. The urine becomes clear, has a pH of 5-6, and contains ketones and protein. The hematologic picture includes hypocalcemia, hyperphosphatemia, increased BUN and hypoglycemia.
C. Gross Pathology:
On necropsy the stomach is empty, the liver and kidneys are fatty, the uterus contains near-term fetuses and some hemorrhage (one theory holds that hemorrhage occurs because the gravid uterus presses the stomach against the liver causing impaired bile drainage, liver dysfunction, and impaired Vitamin K aborsption), ample fat stores are present.
D. Diagnosis:
History, clinical signs, urinalysis, necropsy findings.
E. Treatment:
The condition offers a poor prognosis but treatment with lml 50% dextrose in 3-5 ml sterile saline IV plus a corticosteroid may be attempted.
F. Control:
The condition is best prevented by supplying an adequate amount of digestible energy during late pregnancy and maintaining the animals in a nonobese condition.
6.6.2.3 Diabetes Mellitus
Probably has a viral etiology. Type C-viral particle was isolated. Abyssinian guinea pig 6 weeks to 3 months of age are mostly affected.
6.6.2.4 Torsion of uterus or stomach:
Pregnant guinea pigs are more susceptible to this disease.
6.6.2.5 Duodenal Hyperplasia:Soft Tissue Mineralization:
Single case in a 3 1/2 month old female is reported. There was mucosal hyperplasia of proximal duodenum.
Guinea pigs use cations rather than NH3 to neutralize excess acid excreted by the kidney. Thus this species is particularly susceptible to abnormal dietary levels of and imbalances (eg. high P low Mg) between Ca, P, Mg and K. This is thought to be the reason why guinea pigs are more susceptible to soft tissue mineralization than other rodent species.
6.6.3.1 Antibiotic Induced Enterotoxemia
A. Etiology:
Guinea pigs have a gram positive intestinal flora which is easily upset and overcome by gram negatives, leading to an enterocolitis, bacteremia, and death. Antibiotics which have been implicated in upsetting the flora include penicillin, erythromycin, lincomycin, chlortetracycline, oxytetracycline, strepto-mycin, and bacitracin. An overgrowth of Clostridium difficile and resulting toxemia may occur following antibiotic therapy.
B. Clinical Signs:
Signs of enteritis may include anorexia, weight loss, depression, conjunctivitis, or acute death. Diarrhea or soft feces may or may not be present.
C. Gross Pathology:
A large distended hemorrhagic cecum containing bloody liquid contents may be observed.
D. Histopathology:
Extensive vascular congestion, submucosal hemorrhage and edema and sloughing of the mucosal epithelium have been reported.
E. Diagnosis:
History of antibiotic therapy, necropsy findings, isolation of Clostridium difficile or its toxin from cecal contents.
F. Treatment:
None; supportive fluid therapy if diagnosed prior to death.
G. Control:
Discriminate use of antibiotics.
6.6.3.2 Salmonellosis
A. Etiology:
Salmonella enteritidis var. typhimurium is the major species isolated but Salmonella dublin also have been involved.
B. Transmission:
Transmission usually occurs orally, either via the feces of infected or carrier animals or by contaminated greens. The organism may also invade via the conjunctiva.
C. Clinical Signs:
The infection is usually latent, but very old or very young animals, and animals stressed from nutritional deficiencies, concomitant disease of nonspecific factors may break with the disease. Clinical signs may include lethargy, anorexia, rough coat, and conjunctivitis. Diarrhea is not usually seen. Acute deaths occur primarily in young, weanling guinea pigs or sows close to parturition. Abortions frequently occur. Mortality may range from 50-l00%.
D. Gross Pathology:
No lesions are usually found in acute cases. Enlargement of the spleen, liver, and mesenteric lymph nodes occur in subacute to chronic disease. White foci and/or nodules may occur throughout the spleen and liver. Secondary pleuritis, pericarditis, and peritonitis may occur.
E. Histopathology:
Granuloma formation and/or foci of necrosis in liver, spleen, mesenteric lymph nodes, or Peyer's patches.
F. Diagnosis:
Culture and isolation of Salmonella spp. on selective media (Brilliant green, MacConkey's, Selenite broth).
G. Treatment:
Animals in affected colonies are usually euthanized, but pet animals may be treated orally with 20-55 mg chloramphenicol/kg body weight every 8 hours or 6.5 mg/kg IM every l2 hours. Guinea pigs should be treated with antibiotics only when benefits outweigh the risks.
H. Control:
Do not feed greens as part of diet or if owner insists make sure the greens are washed first. You can use diluted clorax to wash greens and then rinse thoroughly prior to feeding. Remove infected animals from colony.
I. Public Health Significance:
Salmonella typhimurium can cause a transient diarrhea in humans.
6.6.3.3 Bordetella Pneumonia or Bordetellosis
A. Etiology:
Bordetella bronchiseptica - small gm (-),B-hemolytic, non-fermenting rod.
B. Transmission:
The organism can be carried by rats, rabbits, dogs, cats, and primates and is transmitted by direct contact, by contaminated fomites, or by respiratory aerosol.
C. Clinical Signs:
May be none; sneezing, nasal discharge, conjunctivitis, dyspnea, death. Stillbirths and abortions may occur.
D. Gross Pathology:
Lesions seen on necropsy include a mucopurulent rhinitis, tracheitis, and pulmonary consolidation. Portions of the lungs are dark red or grayish and firm. Consolidation often follows a bronchial pattern.
E. Histopathology:
Purulent bronchitis, fibrinous broncho-pneumonia.
F. Diagnosis:
Smear and gram stain exudate, culture.
G. Treatment:
Chloramphenicol at 40-60 mg/animal/day PO or l0-30 mg/kg b.i.d. IM (chloramphenicol will also penetrate the inner ear), sulfamethazine - 4 ml of 12.5% solution/500 ml water for 1-2 weeks, or cephaloridine -l0 mg/animal/day IM. An autogenous bacterin can be made to help prevent Bordetella bronhiseptica infections.
H. Control:
Prevention includes good sanitation and housing guinea pigs separately from other species which may harbor the causative organisms.
6.6.3.4 Streptococcal Pneumonia
A. Etiology:
Streptococcus pneumoniae (Diplococcus pneumoniae). Predisposing factors include pregnancy, sudden temperature changes, shipment, subclinical Vitamin C deficiency, poor husbandry, and experimental procedures.
B. Transmission:
Direct contact; aerosol. Humans may carry.
C. Clinical Signs:
Nasal discharge; rhinitis, conjunctivitis, otitis media, dyspnea, and death. Guinea pigs may be lethargic, anorexic, and have a ruffled hair coat. Pregnant dams may abort. With otitis media, torticollis, incoordination, and circling may be observed.
D. Gross Pathology:
Fibrinous pleuritis and pericarditis; fibrinopurulent bronchopneumonia with consolidation, frothy, serosanguinous fluid in trachea, otitis media, and metritis.
E. Diagnosis:
Culture of affected tissues; gross pathology; tissue smear. Gram stain revealing gram positive lancet shaped bacteria in pairs; histopathological examination of lungs (a fibrinopurulent bronchopneumonia); tissue gram stain showing typical organisms.
F. Treatment:
Chloramphenicol at 40-60 mg/animal/day PO or l0-30 mg/kg b.i.d IM (chloramphenicol will also penetrate the inner ear), sulfamethazine - 4 ml of 12.5% solution/500 ml water for l-2 weeks, or cephaloridine - l0 mg/animal/day IM. No autogenous vaccine used.
G. Control:
Good husbandry, elimination of carriers; reduction of environmental stress.
6.6.3.5 Streptococeal Lymphadenitis or Cervical Adenitis
A. Etiology:
Streptococcus zooepidemicus Lancefield
Group C. Streptobacillus moniliformis has occasionally been implicated.
B. Transmission:
Streptococcus zooepidemicus may be transmitted by bite wound or respiratory aerosols and may invade the conjunctiva or genital or oral musoca. The infection may spread to also involve the respiratory tract and middle ear.
C. Clinical Signs:
The organisms infect cervical lymph nodes which swell and become abscessed. These abscesses may spontaneously rupture.
D. Diagnosis:
Clinical signs: culture.
E. Treatment:
The affected animal should be isolated from the rest of the colony. If the abscess is soft, it can be lanced and flushed t.i.d for 5 days with a tamed iodine solution. If the abscess is hard it should be left alone and the animal treated with cephaloridine at the level of l0 mg/animal/day for 5-l0 days.
6.6.3.6 Mastitis
Mastitis is a fairly common problem in lactating quinea pigs. The affected gland becomes diffusely or focally enlarged, hyperemic and warm, and later becomes cyanotic and cold. Depression ensues and the animal dies from septicemia or toxemia. Mastitis can be caused by a variety of organisms including Pasturella, Klebsiella, coliforms, streptococci, and staphylococci. Treatment consists of hot packs and systemic antibiotics.
6.6.3.7 Pododermatitis or Staphylococcosis
Pododermatitis is most often seen in guinea pigs housed on rough, unsanitized wire floors. Lesions consist of chronic, fibrous granulomas with or without a necrotic, hemorrhagic crust on the ventral surface of the feet. Coagulase positive Staphylococci have often been isolated from the lesions. The best treatment is to transfer the affected animal(s) to a solid-floored cage with clean soft, dry bedding.
6.6.3.8 Mycoplasmal Infection - M. caviae
A nonpathogenic species has been isolated from nasopharynx and vagina. M. pulmonis has been isolated from vagina but is nonpathogenic for guinea pigs.
6.6.4.1 Inclusion Conjunctivitis or Guinea Pig Inclusion Conjunctivitis
Chlamydia psittaci is enzootic in some guinea pig colonies and may cause conjunctivitis in l-3 week old guinea pigs. Infected animal may exhibit reddened eyelids or there may be no clinical signs. Diagnosis is made by demonstrating initial and elementary bodies in epithelial cells from conjunctival scrapping, by staining with Machiavello or Giemsa stains. The infection clears spontaneously by the time the animals are 4 weeks old.
6.6.4.2 Lymphocytic Choriomeningitis (LCM)
Low incidence in guinea pigs when infection occurs, viral infection is usually latent. Transmission is via inhalation or ingestion of infected urine or feces or by viral penetration through the skin. Occasionally, neurological signs are seen. These consist of hind leg paralysis and signs of meningitis. Gross lesions may be absent or pneumonia, pulmonary edema, pleural exuade, fatty liver, and splenomegaly may be seen.
6.6.4.3 Guinea Pig Cytomegalovirus (GPCMV): Herpesvirus-Herpesviridae
Not very common. Infect salivary gland, cervical lymph nodes and kidney. Intranuclear and less frequently intracytoplasmic inclusion body may be used to identify infection. May cause necrosis of many organs, e.g., spleen, liver, kidney and lung.
6.6.4.4 Guinea Pig Herpes-Like Virus (GPHLV):
Significance unknown
6.6.4.5 Guinea Pig X Virus ( GPXV): Hepesvirus type 3
Significance unknown. Experimental inoculation caused mortality of 50% within 11 weeks. Lesion observed was focal hepatic necrosis.
6.6.4.6 Guinea Pig Retrovirus:
Causes guinea pig L2C leukemia. It is an acute lymphocytic leukemia of B lymphocytes.In natural disease - enlarged lymph nodes , dull hair coat, sluggish, high WBC count is reported.
6.6.4.7 Adeno virus - not common
Clinical signs include dyspnea.
6.6.4.8 Paramyxoviruses isolated from Guinea Pigs:
- A. Sendai or Parainfluenza type l - Frequently serologically positive. Sendai virus has not been isolated from guinea pigs.
- B. Guinea pig parainfluenza virus-5 (Parainfluenza Type 5) - not known to produce disease
6.6.4.9 Possible virus infection of Guinea Pigs
Serologic evidence only.
- A. Parainfluenza 2
- B. " " 3
- C. Pneumonia virus of mice
- D. Reovirus 3
- E. Theilers virus
Neoplasms are not common in guinea pigs. Spontaneous tumors of special interest as research models are the lymphosarcomas and leukemias.
Lice (Gliricola porcelli, Gyropus ovalis) and mites (Chirodiscoides caviae) may cause partial alopecia, epidermal scaling, and pruritus. These may be seen by the naked eye about the head. The lice will leave the body of a dead animal as it cools to seek a new host. Ectoparasites are easily treated by dusting the animal with a cat flea powder or by hanging a dichlorvos strip in the room.
Trixicarus caviae - Sarcoptid mite which is pathogenic for guinea pigs; causes intense pruritus.
A. Cryptosporidiosis
1. Etiology:
Cryptosporidium wrari, a protozoan, measures 3.4-4.4 mm as a mature schizont, 4.0-7.0 mm macrogamete.
2. Clinical Signs:
May be none, weight loss in older guinea pigs, diarrhea in weanlings.
3. Gross Pathology:
In weanlings, an acute enteritis may be found. In older animals, infection may cause a chronic enteritis with the ileum most severely affected.
4. Histopathology:
Cryptosporidia are most numerous in the ileum and are usually distributed over the surface of the villi, being most numerous at the tips, infected villi are short, broad, sometimes flattened and irregular. An infiltrate of monocytes and eosinophils occur in the lamina propria and may transmigrate through the epithelium.
5. Diagnosis:
Examination of fresh mucosal scrapings with phase-contrast microscopy is the best method.
6. Control:
Infections can be eliminated by the addition of 0.2% sulfaquinoxiline or sulfamthmazine to the water.
There are several other endoparasites in the guinea pig; however, they rarely are associated with disease. A few of the more frequently found parasites are:
6.6.7.1 Malocclusion
Guinea pigs, like other rodents, have open rooted teeth which keep growing throughout the animals' life. Unlike other rodents, however, it is the anterior cheek teeth of the mandible (premolar and first molar) which tend to malocclude. The teeth grow inward toward the tongue. Animals with malocclusion exhibit chronic weight loss and may slobber (ptyalism). There may be secondary malocclusion of the incisors. The overgrown teeth should be clipped or filed back. The cause of the condition is unknown but may involve dietary factors. Therefore, the nutritional adequacy of the diet should always be reviewed. Also, since the condition may be hereditary, affected animals should not be used for breeding stock.
6.6.7.2 Dystocia
Dystocia may be caused by abnormally large or malformed fetuses and may occur in animals bred after 6 months of age due to fusion of the pubic symphysis. The only remedy for this is cesarian section. If the problem is uterine inertia, l unit of oxytocin may be administered to initiate uterine contraction.
6.6.7.3 Barbering
Alopecia may result from dominant animals barbering or pulling hair from submissive animals. Self barbering also occurs and may be recognized by location of the areas of hair loss (head, neck, and shoulders are spared). Feeding hay decreases the incidence of barbering.
6.6.7.4 Vaginitis/Scrotal Plugs
Wood chips may cause vaginitis in female guinea pigs by becoming jammed across the vulva and causing a foreign body reaction. Male guinea pigs may accumulate a plug of sebaceous material and bedding in the skin fold between the two halves of the scrotum. Both conditions may be treated by washing the affected areas with mild soap and water and carefully pulling the debris out bit by bit. Animals should be placed on different bedding until the area heals. Scrotal plugs can be prevented from recurring by periodic washing.
6.6.7.5 Iatrogenic Muscle Necrosis
Intramuscular use of Innovar-VetR in guinea pigs will cause marked necrosis at the site of injection and may lead to the loss of the limb.
6.6.7.6 Trauma Due to Caging
Young guinea pigs kept on wire mesh floors may catch their feet and legs in the wire. Often the limb swells and the animal is unable to free itself or the animal fractures the limb trying to remove it, and has to be destroyed. The problem is avoided by the use of solid bottom cages with contact bedding.
6.6.8.1 Dermatophytosis
A. Etiology:
Trichophyton mentagrophytes
B. Transmission:
Spores, direct contact.
C. Clinical Signs:
Young, aged, pregnant, and stressed animals are most susceptible to the disease. Most infections are inapparent, but if lesions occur they consist of irregular hairless areas which may be scabby or crusty. The lesions usually begin at the tip of the nose and spread to the rest of the head, limb, and, back. They may become abscessed if secondary bacterial
infections sets in.
D. Diagnosis:
Dermatophytosis may be diagnosed by taking a skin scraping from the margin of the lesion, placing it in a drop of l0% KOH, and gently heating for l5-20 seconds. A drop of blue ink in the preparation will help stain the fungal elements, consisting of arthrospores surrounding the hairshaft. A portion of the scraping should also be placed on dermatophytes test media. The media will turn red in 4-5 days if a dermatophyte is present.
E. Treatment:
Grieseofulvin (l5 mg/kg body weight orally for l4-28 days) or a topical antifungal cream applied b.i.d. for a minimum of 4 weeks may be used for treatment.
|