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Biomedical subjects

J C Murphy

Publications and source records attributed to J C Murphy.

At least 73 records · Page 4Linked to original sources
PubMed1991

Helicobacter mustelae-induced gastritis and elevated gastric pH in the ferret (Mustela putorius furo).

Helicobacter mustelae has been cultured from the stomachs of ferrets with chronic gastritis; the lesions in the stomach have many of the same histological features seen in H. pylori gastritis in humans. To determine whether H. mustelae-negative ferrets with normal gastric mucosa were susceptible to colonization and whether gastritis developed after infection, four H. mustelae-negative ferrets treated with cimetidine were inoculated orally on two successive days with 3 ml (1.5 x 10(8) CFU) of H. mustelae; eight age-matched H. mustelae-negative ferrets served as controls. All four ferrets became colonized; H. mustelae persisted through week 24 of the study, as determined by positive gastric culture, tissue urease, and Warthin-Starry staining of gastric tissue. Superficial gastritis developed in the oxyntic gastric mucosa, and a full-thickness gastritis, composed primarily of lymphocytes and plasma cells plus small numbers of neutrophils and eosinophils, was present in the antrum. The inflammation was accompanied by an elevation of immunoglobulin G antibody to H. mustelae. At 4 weeks post-inoculation, the four infected (experimental) ferrets developed an elevated gastric pH (4.0 to 5.2) for 2 weeks. The eight control ferrets did not have gastritis; H. mustelae could not be demonstrated in gastric tissue via culture, nor was there an immune response to the bacteria. In ferrets, H. mustelae readily colonizes the stomach and produces a gastritis, a significant immune response, and, like H. pylori infection in humans, a transient elevated gastric pH after Helicobacter infection.

Animals↗
PubMed1991

Group G streptococcal lymphadenitis in rats.

Group G streptococci which have been isolated from the oral flora of rats are also normal inhabitants of the human skin, oropharynx, gastrointestinal tract, and female genital tract. This group of streptococci can cause a wide variety of clinical diseases in humans, including septicemia, pharyngitis, endocarditis, pneumonia, and meningitis. Ten days after oral gavage with 7,12-dimethylbenz[a]anthracene, 12 of 22 two-month-old, female, outbred, viral-antibody-free rats presented with red ocular and nasal discharges and marked swelling of the cervical region. Various degrees of firm, nonpitting edema in the region of the cervical lymph nodes and salivary glands as well as pale mucous membranes and dehydration were observed. Pure cultures of beta-hemolytic streptococci were obtained from the cervical lymph nodes of three rats that were necropsied. A rapid latex test system identified the isolates to have group G-specific antigen. These streptococcal isolates fermented trehalose and lactose but not sorbitol and inulin and did not hydrolize sodium hippurate or bile esculin. A Voges-Proskauer test was negative for all six isolates. Serologic tests to detect the presence of immunoglobulin G antibody to rat viral pathogens and Mycoplasma pulmonis were negative. Histopathologic changes included acute necrotizing inflammation of the cervical lymph nodes with multiple large colonies of coccoid bacteria at the perimeter of the necrotiz zone. To our knowledge, this is the first report of naturally occurring disease attributed to group G streptococci in rats.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1991

Cervical lymphadenitis in guinea pigs: infection via intact ocular and nasal mucosa by Streptococcus zooepidemicus.

The traditional view regarding the pathogenesis of cervical lymphadenitis in guinea pigs is that Lancefield Group C Streptococcus gains access to cervical lymph nodes via an abraded oral mucosa. In this study, it is established that inoculation of intact nasal and conjunctival mucous membranes with Streptococcus zooepidemicus (Lancefield Group C) also can produce the disease. Weanling (SPF) guinea pigs (Cavia porcellus) were divided into two experimental groups of 10 and two control groups of four each. Guinea pigs from each group were individually housed in separate cubicles. Group I was inoculated with 0.05 ml of culture containing 2.8 x 10(7) CFU/ml of S. zooepidemicus into the conjunctiva of the left eye. Group II received a similar inoculum into the left nares. Control groups received 0.05 ml of TSB broth in the same sites. Five of ten guinea pigs in Group II died four to nine days postinoculation. Surviving guinea pigs were euthanatized at intervals between days 4-13 postinoculation. All guinea pigs were necropsied, cultured and examined for evidence of infection. S. zooepidemicus was recovered from 30/50 and 39/46 sites cultured from Groups I and II, respectively. Lymphadenitis was found in cervical lymph nodes from 8/10 guinea pigs in Group I and 10/10 in Group II. The conjunctival and nasal mucosa, therefore, represent potential sites of entry resulting in cervical lymphadenitis in guinea pigs.

Animals↗
PubMed1991

Juvenile rheumatoid arthritis in a rhesus monkey (Macaca mulatta).

A juvenile rhesus macaque (Macaca mulatta) developed a symmetrical erosive polyarthritis involving both large and small diarthrodial joints. Neither an infectious nor a metabolic etiology could be determined. This case shares many clinical and pathological features with the polyarticular form of human juvenile rheumatoid arthritis.

Animals↗
PubMed1990

Helicobacter mustelae-associated gastritis in ferrets. An animal model of Helicobacter pylori gastritis in humans.

Gastric Helicobacter mustelae was present in 100% of 11 adult female ferrets (Mustela putorius furo). The high immunoglobulin G antibody levels to H. mustelae in all ferrets showed a significant immune response to the organism. Urease mapping of the ferret stomach indicated that the bacteria heavily colonized the proximal duodenum and antrum and, to a lesser extent, the corpus. The histological gastritis observed coincided with presence of H. mustelae. Superficial gastritis was noted in the oxyntic gastric mucosa, whereas in the distal antrum the chronic inflammatory response occupied the full thickness of the mucosa. In the proximal antrum and transitional mucosa, focal glandular atrophy and regeneration were observed. Seven control specific-pathogen-free ferrets were not colonized with the bacteria, did not have detectable levels of immunoglobulin G H. mustelae antibody, and did not have H. mustelae-associated gastritis. The ferret lacks the polymorphonuclear-cell response seen in active chronic gastritis typically described with Helicobacter pylori gastritis in humans. However, the lesion in ferrets does closely resemble the diffuse antral gastritis seen in a subset of adults with H. pylori gastritis as well as children infected with H. pylori. Like H. pylori, H. mustelae adheres tightly to gastric mucosa. The ferret infected with H. mustelae, in addition to specific-pathogen-free uninfected control ferrets, will make longitudinal studies possible, enabling dissection of multiple host and environmental variables that influence the effect of H. mustelae colonization on progression and severity of gastroduodenal disease.

Animals↗
PubMed1989

Treatment of proliferative colitis in ferrets.

Proliferative colitis associated with intracellular Campylobacter sp was diagnosed in 10 ferrets. The ferrets had a history of diarrhea (often blood-tinged or mucoid), dehydration, and chronic weight loss. Additional clinical signs included rectal prolapse, lethargy, fever, and a palpably thick colon. In 5 ferrets, the diagnosis was confirmed by colonic biopsy, via endoscopy. Supportive treatment in 5 ferrets did not alleviate the clinical signs or the proliferative intestinal disorder. oral chloramphenicol treatment (50 mg/kg of body weight, q 12 h for 10 to 21 days) resulted in marked clinical improvement and eradication of proliferative intestinal lesions in 5 ferrets.

Animals↗
PubMed1988

Low friction arthroplasty for old quiescent infection of the hip.

We report the results of low friction arthroplasty in 72 old tuberculous hips and 42 hips with old quiescent septic arthritis. Follow-up was for a minimum of two years. Recrudescence of tuberculosis was seen in only one patient, but deep infection occurred in four of the hips with previous septic arthritis. The reasons for this are discussed. It is recommended that patients with old tuberculous hips should have a course of anti-tuberculous drugs before operation, that patients with previous septic infection should have prophylactic antibiotics and antibiotic-loaded cement and that the operation should be performed by an experienced surgeon.

Adult↗
PubMed1987

Bone grafting for protrusio acetabuli during total hip replacement. A review of the Wrightington method in 61 hips.

Total hip replacement has been very successful in patients with painful, stiff hips associated with protrusio acetabuli, but the heat of polymerisation of methylmethacrylate cement may cause necrosis of the thin medial wall with consequent danger of migration of the cup. Since 1968 at Wrightington, thin slices of the head of the femur have been used as bone grafts to reinforce the acetabulum. We have reviewed 61 hips in 51 patients at an average of 4 years 3 months after operation. Grading for severity is discussed and the degree of physiological remodelling of the medial wall of the acetabulum after grafting assessed. There was an average of about 4 mm of remodelling, but this varied considerably; most took place within the first year. In no case was there relapse of the protrusio.

Acetabulum↗
PubMed1987

Hematuria in rabbits.

A nine year retrospective study of hematuria in 14 New Zealand White rabbits was conducted to classify possible etiologies of this clinical finding. Physical examination, laboratory tests, radiography and postmortem examination were utilized in most cases to verify the presence of hematuria and to determine its etiology. Uterine adenocarcinoma was diagnosed in two rabbits. Three rabbits had uterine polyps with hemorrhage. Renal infarction with hemorrhage was diagnosed in three rabbits. Urolithiasis with secondary urethral obstruction and hemorrhagic cystitis was identified as the cause of hematuria in four rabbits. Other causes of hematuria included chronic cystitis, disseminated intravascular coagulation, bladder polyps and pyelonephritis. Hematuria of undetermined origin was observed in one rabbit. This last [corrected] case was negative for both blood and porphyrin in the urine, but positive for excess levels of urobilin, the oxidative product of urobilinogen. This case illustrates that hyperpigmented urine should be a rule out in all cases of suspected hematuria in rabbits.

Adenocarcinoma↗
PubMed1987

Comparison of methods to diagnose an epizootic of Corynebacterium kutscheri pneumonia in rats.

An outbreak of Corynebacterium kutscheri pneumonia occurred in a colony of laboratory rats. Diagnostic methods compared on a prospective basis included (1) an enzyme-linked immunosorbent assay (ELISA) for serum antibody to C. kutscheri; (2) C. kutscheri isolation from retrograde nasal wash, cervical lymph nodes, tracheal wash, lung homogenate; and (3) histopathology. C. kutscheri was isolated from one or more of the cultured sites from suspected cases, but no individual rat yielded C. kutscheri from all of the sites. The presence of histological lung lesions was the most frequent indicator of infection (8 of 9 suspected cases), followed by isolation of C. kutscheri from lung homogenate (5 of 6), ELISA for serum antibody (6 of 8), and isolation of C. kutscheri from cervical lymph node (4 of 8). Isolation of C. kutscheri from nasal wash (1 of 9) was the least sensitive indicator of infection. ELISA antibody was not detected in rats which had normal lungs and did not harbor C. kutscheri. It was concluded that ELISA provides noninvasive means for detecting infection and cervical lymph node culture increase the potential for successful isolation of the agent in C. kutscheri infected rats.

Animals↗
PubMed1987

Campylobacter jejuni infection in the ferret: an animal model of human campylobacteriosis.

Campylobacter infection in weanling ferrets (Mustela putorius furo) was studied as an animal model for enteric campylobacteriosis in persons. The screening of fecal cultures on selective campylobacter media showed that Campylobacter jejuni/coli was not present in the normal enteric flora. Intragastric feeding of a mixture of cat feed and 2.5 X 10(8) C jejuni isolated from ferrets with naturally occurring proliferative colitis was accomplished. All ferrets (n = 8) became infected on 3 days after they were inoculated, and at 5 to 7 days, they had bile-tinged, liquid feces with excessive mucus and blood. Ferrets gradually recovered from the diarrhea, and feces were normal 10 to 14 days after inoculation was done. Feces contained C jejuni at 14, 23, 28, 39, 46, 60, 91, 101, 109 and 144 days. In the second experiment, weanling ferrets initially were treated with 10% sodium bicarbonate, and 1 X 10(10) C jejuni organisms were administered in the cat feed. Diarrhea with fecal leukocytes and occult blood with occasional mucus appeared in almost all of the 21 ferrets from days 4 through 7. Campylobacter jejuni was isolated from the blood of 11 ferrets between 3 hours and 14 days after they were inoculated. Campylobacter jejuni bactericidal antibodies were present in serum samples at 14 days, with titers of 1:16 to 1:32. Intestinal lesions including cellular infiltration with mononuclear and polymorphonuclear leukocytes were in the lamina propria of the pyloric mucosa and small intestine of infected and control ferrets. The colon of 3 infected ferrets had small focal infiltrates of neutrophils on the lamina propria; one ferret had perivascular cuffing.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Single-step immunization using a controlled release, biodegradable polymer with sustained adjuvant activity.

The use of a biodegradable polymer for antigen delivery based on poly(CTTH-iminocarbonate) (IUPAC nomenclature: poly[oxyimidocarbonyloxy-p-phenylene [2-(hexyloxycarbonyl)ethylene]imino[2-[1-(benzyloxy)formamido]- 1-oxotrimethylene]-p-phenylene]) was investigated. This polymer was selected since its primary degradation product, N-benzyloxycarbonyl-L-tyrosyl-L-tyrosine hexyl ester (CTTH) was found to be as potent an adjuvant as complete Freund's adjuvant and muramyl dipeptide, when measuring the serum antibody response to bovine serum albumin (BSA) in male CD-1 mice over 56 weeks. BSA released from subcutaneously implanted polymeric antigen delivery devices made of poly(CTTH-iminocarbonate) resulted in significantly higher (P less than 0.006) anti-BSA antibody titers than devices made of poly(bisphenol A-iminocarbonate).

Adjuvants, Immunologic↗
PubMed1986

Surveillance of mice for antibodies to murine cytomegalovirus.

The sera of 256 mice from nine commercial sources were screened for antibodies to murine cytomegalovirus (MCMV) because a surveillance of this virus has not been reported in the literature for over a decade. Although no evidence of antibodies to MCMV were detected by complement fixation or nuclear anticomplement immunofluorescence, 54.7% of these sera did have antibodies that were detected by enzyme-linked immunosorbent assay. These data emphasize the need for proper containment of laboratory mice to prevent the potential outbreak of acute MCMV infection. Including MCMV antibody surveillance by enzyme-linked immunosorbent assay in routine health monitoring of mice and imparting these findings in an analysis of the role of MCMV on interpretation of experimental results is advised.

Animals↗
PubMed1986

Therapy with cyclosporine in experimental murine myocarditis with encephalomyocarditis virus.

To explain the progression from infectious viral myocarditis to congestive cardiomyopathy an infection/immune hypothesis has been proposed stating that the primary viral process incites an excessive or disordered immunologic response against the myocardium. To test whether one form of immunosuppressive therapy might ameliorate this process, we used cyclosporine in a murine preparation of infectious myocarditis (encephalomyocarditis [EMC] virus), which has been shown to result in a congestive cardiomyopathy pathologically similar to that seen in man. Eight-week-old male DBA-2 mice were infected with EMC virus and randomized to a treatment or control group. Cyclosporine (25 mg/kg/day) was administered subcutaneously for 3 weeks, starting (1) at 1 week after infection during viral replication, and (2) at 3 weeks after infection, after the period of active viral replication. In mice treated during viral replication there was a significantly higher mortality rate compared with that of control mice (15/21 vs 9/29, p = .01). There was no evident reduction in myocardial pathology (inflammation, necrosis, or calcification) in the treated compared with the control groups. In mice treated after the period of viral replication, there was no improvement in mortality (8/22 vs 2/19, NS) compared with control. Treated mice showed no reduction in myocardial histopathologic lesions. Furthermore, treated mice had significantly greater heart weight/body weight ratios (1.3 +/- 0.4% vs 1.0 +/- 0.3%, p less than .005), lung weight/body weight ratios (1.1 +/- 0.5% vs 0.8 +/- 0.3%, p less than .05), and liver weight/body weight ratios (6.0 +/- 0.8% vs 5.4 +/- 0.6%, p less than .005) than control mice, suggesting more severe myocardial failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗