Pig Colony Research Articles

A reproductive study of Weiser-Maples guinea pigs

The Weiser-Maples (WE) guinea pig strain was introduced by Backshire Co., Ltd. (USA) in 1977. We have been breeding WE strain guinea pigs for skin melanization research. The WE guinea pig colony produced 1271 pups in 417 litters from May 1978 through December 1983. Breeding date are shown below. The mean litter size was 3.05, the stillborn rate was 15.2%, the weaning rate for live-born pups was 93.5% and the sex ratio was 1.01. The average age at first vaginal membrane rupture was 31.4 days at which time body weight was 290.5g. The mean length of the first 7 estrous cycles was about 17 days, with no cyclical variation in length. The mean duration of gestation was 67.9 days. Duration of pregnancy varied with litter size. There was an inverse relationship between litter size and duration of pregnancy. Most of the pups were delivered alive in mid-pregnancy with a parturition range of 56 to 76 days. The probability of pup death depends on gestational length: the lowest incidence of mortality was seen in litters born at 70 days. The mortalities were related to litter size but not to parity. There was an inverse relationship between birth weight and litter size. In WE guinea pigs, the mean weight for a litter of 1 was 120 g; for a litter of 5, the mean body weight was 58g. Male body weights were slightly heavier than female at birth and at weaning age. The mean body weights are shown below, date of birth: female 88.3g, male 93.3g, weaning age (2 weeks): female 181.1g, male 198.8g and 30 weeks: female 758.7g, male 1018.0g. These date for WE guinea pigs are comparable to those of other strains.

Outbreak of keratoconjunctivitis due to Salmonella weltevreden in a guinea pig colony

The purpose of this report is to demonstrate that the ability to produce keratoconjunctivitis (KC) is a property found in Salmonella weltevreden. This observation is contrary to previous reports that Salmonella spp. do not produce KC. An outbreak of KC due to S. weltevreden occurred in a guinea pig colony, and the animals carried the organism in the intestinal tract. The same Salmonella serotype that caused an epidemic of diarrhea in humans and a routine laboratory isolate also possessed the ability to induce KC. Unlike Shigella spp. (the prototype organisms positive for KC), S. weltevreden induced KC and bound Congo red dye even when grown at 30 degrees C. It invaded HeLa cells in culture but did not hybridize with a DNA probe for invasiveness of Shigella spp. and enteroinvasive Escherichia coli even though it harbored plasmids. It was susceptible to all the antibiotics tested, was hydrophobic, and showed mannose-sensitive hemagglutination. It did not have enterotoxic or cytotoxic activities.

Platelet Interaction with Vessel Wall and Collagen in Pigs with Homozygous von Willebrand’s Disease Associated with Abnormal Collagen Aggregation

A subgroup of pigs with von Willebrand's disease from the Mayo Clinic stock shows abnormal platelet aggregation in response to collagen [vWD-Homo(-)], in contrast to the normal aggregation responses observed in the main colony of pigs with homozygous vWD [vWD-Homo(+)]. This subgroup has been characterized at Mayo as a storage pool deficiency due to the reduced levels of ADP and Serotonin in the platelet dense granules. In the present studies, an ex-vivo perfusion chamber was utilized to investigate the deposition of 111In-labeled platelets on aortic subendothelium and collagen type I exposed to blood from vWD-Homo(-), vWD-Homo(+) and normal animals. Both non-anticoagulated and heparinized blood were exposed for wall shear rates ranging from 212 sec-1 to 3380 sec-1 and exposure times as long as 30 min. An enhanced decrease in platelet deposition in the vWD-Homo(-) animals was observed compared to vWD-Homo(+) animals. The decrease was observed primarily at the higher shear rates and was more pronounced in the absence of heparin and on the collagenous substrate. Thus, the abnormality in collagen-induced aggregation, which has been characterized as a storage-pool type defect, results in a decreased platelet deposition compared with that produced by severe vWD alone.

Serological evidence of rotavirus infection in a guinea pig colony.

Antibodies reacting with simian rotavirus SA11 were detected by enzyme immunoassay (EIA) and Western blot assay (WBA) in sera from guinea pigs bred for experimental use at the Fundação Oswaldo Cruz, Rio de Janeiro, Brazil. The proportion of antibody-positive animals and the antibody titres rose sharply in 1985, were maintained at a high levels in 1986 and declined in 1987. There were no obvious signs of disease coinciding with serological evidence of infection. Results of WBA suggest that the virus involved belongs to subgroup 1 of group A rotaviruses.

Molecular Genetic Analysis of Porcine von Willebrand Disease: Tight Linkage to the von Willebrand Factor Locus

von Willebrand disease (vWD), one of the most common bleeding disorders in humans, is manifested as a quantitative or qualitative defect in von Willebrand factor (vWF), an adhesive glycoprotein (GP) with critical hemostatic functions. Except for the rare severely affected patient with a gene deletion as etiology of the disease, the molecular basis for vWD is not known. We studied the molecular basis for vWD in a breeding colony of pigs with a disease closely resembling the human disorder. The porcine vWF gene is similar in size and complexity to its human counterpart, and no gross gene deletion or rearrangement was evident as the pathogenesis of porcine vWD. A restriction fragment-length polymorphism (RFLP) within the porcine vWF gene was identified with the restriction endonuclease HindIII, and 22/35 members of the pedigree were analyzed for the polymorphic site. Linkage between the vWF locus and the vWD phenotype was established with a calculated LOD score of 5.3 (1/200,000 probability by chance alone), with no crossovers identified. These findings indicate that porcine vWD is due to a molecular defect within (or near) the vWF locus, most likely representing a point mutation or small insertion/deletion within the vWF gene.

Molecular genetic analysis of porcine von Willebrand disease: tight linkage to the von Willebrand factor locus

von Willebrand disease (vWD), one of the most common bleeding disorders in humans, is manifested as a quantitative or qualitative defect in von Willebrand factor (vWF), an adhesive glycoprotein (GP) with critical hemostatic functions. Except for the rare severely affected patient with a gene deletion as etiology of the disease, the molecular basis for vWD is not known. We studied the molecular basis for vWD in a breeding colony of pigs with a disease closely resembling the human disorder. The porcine vWF gene is similar in size and complexity to its human counterpart, and no gross gene deletion or rearrangement was evident as the pathogenesis of porcine vWD. A restriction fragment- length polymorphism (RFLP) within the porcine vWF gene was identified with the restriction endonuclease HindIII, and 22/35 members of the pedigree were analyzed for the polymorphic site. Linkage between the vWF locus and the vWD phenotype was established with a calculated LOD score of 5.3 (1/200,000 probability by chance alone), with no crossovers identified. These findings indicate that porcine vWD is due to a molecular defect within (or near) the vWF locus, most likely representing a point mutation or small insertion/deletion within the vWF gene.

Malignant Hyperthermia-Reply

In Reply.— The mechanism of MH that was proposed in the MEDICAL NEWS & PERSPECTIVES article is the one commonly cited in the literature 1,2 and in anesthesiology textbooks. 3,4 It is the product of the research of several investigators who have worked with colonies of pigs in which the MH syndrome includes muscle rigidity. This porcine syndrome more closely parallels the clinical course of the disease than does the syndrome evidenced in Dr Williams' pig colony.

わが国のモルモットコロニーにおける肺炎球菌, 溶血レンサ球菌, サルモネラ, 気管支敗血症菌およびセンダイウイルスの汚染状況

S. pneumoniae, S. zooepidemicus, Salmonella spp., B. bronchiseptica and Sendai virus were examined in a total of 45 guinea pig colonies (17 institutional and 28 breeder's colonies) of Hartley strain, and found to be positive in 6, 3, 5, 20 and 14 colonies, respectively. Sendai virus was highly prevalent among guinea pigs, showing so high rates positive as 80 to 100% of animals obtained from 11 of the 14 contaminated colonies. B. bronchiseptica was also shown to be prevalent within contaminated colonies by indication of rates positive more than 40% of animals examined in 14 of the 20 colonies. Infection rates of other 3 pathogens, however, ranged from lower than 20% to higher than 80% according to colonies. All strains of Salmonella isolated in this survey were identified as S. typhimurium and those of S. pneumoniae as serotype 19F.

Clinical salmonellosis in a guinea pig colony caused by a new Salmonella serotype, Salmonella ochiogu.

During a severe outbreak of clinical salmonellosis in an experimental guinea pig colony, a new strain of Salmonella was isolated and identified. The new serotype, with the antigenic structure 1,3,19 : Z38 : e, n, Z15, for which the name Salmonella ochiogu has been suggested, caused both enteric and systemic infection in the animal colony. During the outbreak a total of 127 animals died (26.9%). All ages of animal were affected. Treatment with oral tetracycline was successful when combined with strict hygienic measures.

An epizootic of pneumococcal infection occurred in inbred guinea pig colonies.

Epizootiological observations were made on an outbreak of pneumococcal infection occurred in 14 inbred guinea pig colonies during January to October, 1981. Monthly incidences of diseased animals ranged from 16.6 to 0%, showing the highest rate in the first month of the occurrence. Affection rates were remarkably different according to guinea pig strains, being 75% in JY-1 but 0% in JYG and Strain 2. Affected animals showed ruffled fur, dry-dirty noses, emaciated abdomen and dyspnea, and some of them were resulted in death. At necropsy, the fibrinopurulent pneumonia, pleuropneumonia and pleuritis were found as the major pathological features, and in addition, the fibrinopurulent pericarditis and peritonitis with a large amount of exudate were also observed in some cases. Streptococcus pneumoniae was isolated from nearly all the affected organs, and also from the external nares and trachea. Isolation rate from the external nares was especially high, thus 97.1% of infected guinea pigs including healthy carriers were detected by cultivation of nasal swab samples. Carrier rates of healthy animals were gradually increased from 17.2% in April to 36.5% in October, but the organism was not detected from JYG strain at all. During the observation period, vaccination, advance of weaning age of animals and administration of high vitamin C dose were taken as preventive measures of the epizootic, but no remarkable effect was obtained. The same diseased conditions were successfully produced in Hartley guinea pigs by experimental nasal infection of a pneumococcal strain isolated from this epizootic.

Susceptibility of inbred and outbred mouse strains to Sendai virus and prevalence of infection in laboratory rodents

Sendai virus is one of the more prevalent and serious virus infections of rodents. Infection was found in 66% of the mouse, 63% of the rat, 83% of the hamster, and 44% of the guinea pig colonies examined. Twenty-four inbred and outbred strains of mice were tested for their sensitivity to lethal Sendai virus infection. The 129/J mice tested were approximately 25,000-fold more sensitive than SJL/J mice; however, both mouse strains were similarly permissive in support of viral replication in their lung tissues. Histopathological studies revealed that whereas lesions in both sensitive and resistant mice were qualitatively similar, the lesions in the more sensitive 129/J mice appeared earlier, were much more extensive, and persisted longer than in the resistant SJL/J mice. These results suggest that the observed variance in sensitivity is not the result of a genetic restriction on virus infection and replication but rather is the result of a physiological factor(s) possibly related to some aberration of strain difference in the humoral or cell-mediated immune response.

Spontaneous tumors in the Dunkin-Hartley guinea pig.

Seventy-nine spontaneous neoplasms in Dunkin-Hartley guinea pigs were observed over a 9-year period in the Fort Detrick guinea pig colony. Sixty-three of the neoplasms were found during approximately 8,500 necropsies performed on animals under 27 months of age. The remaining 16 tumors were in 34 breeders maintained after 27 months of age on a natural life-span study. Of this group, 10 (29.4%) developed neoplasms by the termination of the study, when the animals were 80 months of age. The skin tumor, trichofolliculoma, of which there were 29, comprised the largest tumor classification.

Housing Guinea pig colony

Summary A description is given of a system of managing a guinea pig colony so as to use labour and foodstuffs as efficiently as possible.

Chlortetracycline in the nutrition of guines pigs.

SummaryChlortetracycline hydrochloride has been included in various diets of a guinea pig colony for 3 years without evidence of toxicity. It had no effect on growth rate and caused no mortality when added to a purified diet at levels from 25 to 200 mg/kg. At the routine level of 25 mg/kg, the antibiotic decreased abortions and adult mortality and eliminated cervical lymphadenitis from the breeding colony. Although chlortetracycline may be toxic to guinea pigs under some conditions, in our laboratory it has been beneficial in the maintenance of a breeding colony and has been used routinely in purified experimental diets for growth studies.

A Highly Fatal Disease of Guinea Pigs

Our guinea pig colony is carefully watched for infectious diseases and every attempt is made to eliminate any that appear. For several years deaths have been few and the common guinea-pig pathogens have not been observed. This year, in a group of apparently normal guinea pigs removed for observation, a few young animals were found to have elevated temperatures. Inoculations of organ-suspensions were made into other animals and an agent was secured that is highly fatal for guinea pigs.When injected subcutaneously, intraperitoneally, intracerebrally, or intranasally, guinea pigs show an elevated temperature in from 2 to 5 days, which persists for approximately 5 days and then drops to normal or below. Leucocyte counts show from 3000 to 5000 cells, while the red corpuscles are normal in number and volume. The infection can be transmitted by contact, but so far attempts to infect by feeding have been unsuccessful. Guinea pigs die in about 2 weeks after inoculation, and to date not a single animal has survived...