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Query: UMLS:C0024312 (lymphopenia)
 4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical signs, hematologic changes, serum and fecal virus titers, specific antibody production and the occurrence of histologic lesions were studied in 22 nine-week-old seronegative beagle dogs inoculated by the oral and intravenous route with canine parvovirus. Approximately 30% of the dogs had clinical signs of pyrexia, depression, vomiting, and diarrhea irrespective of the route of inoculation. Events in the dogs inoculated intravenously preceded those in dogs inoculated orally by approximately two days. Only one dog died. Lymphopenia was the most consistent hematologic change. Viremia always preceded the initiation of fecal virus shedding. Viral titers in the serum and feces were significantly greater in symptomatic dogs compared to asymptomatic dogs. Termination of the plasma viremia coincided with the onset of the humoral immune response, but viremia persisted one day longer in symptomatic dogs. The severity of lymphoid tissue and intestinal infection, assessed by tissue immunofluorescence and histology, was also greater in symptomatic dogs. The severity of intestinal disease was highly correlated with the magnitude and duration of viremia.
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PMID:Pathogenesis of canine parvovirus enteritis: the importance of viremia. 298 78

The pathogenesis of canine parvovirus-2 (CPV-2) was studied in orally inoculated conventional dogs using haematological, serological and virological techniques. Virus was first isolated from mesenteric lymph nodes on day 2 after exposure, tonsil on day 3 and small intestine on day 3. Viraemia occurred subsequently and was present in most dogs on days 4 and 5 after exposure. CPV-2 could be isolated from all tissues during viraemia. Relative pyrexia, lymphopenia and neutropenia occurred on days 5, 6 and 7 after exposure, respectively. Virus excretion in faeces began in most dogs on day 4 and continued despite the appearance of neutralising serum antibody. Specific serum antibody, detected in some dogs as early as day 3 and in all dogs by day 7 after exposure, eliminated viraemia and inhibited virus isolation from tissues in cell culture.
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PMID:Pathogenesis of canine parvovirus-2 in dogs: haematology, serology and virus recovery. 298 89

Calves held in isolation showed a progressive decline in maternally derived antibody titres to bovine parvovirus but low concentrations of inhibitors resistant to heat and kaolin treatment persisted as the animals matured. These inhibitors had both haemagglutination inhibition and plaque neutralising activity and were considered to be of non-specific origin. Following oral challenge with bovine parvovirus, calves developed mild to moderate diarrhoea, with lymphopenia and viraemia. Sequential virological and immunofluorescent studies showed that the virus initially infected tonsils and intestinal tract, subsequently spreading to systemic lymphoid tissues. Histological and scanning electron microscopic examinations revealed moderate small intestinal villus atrophy and fusion due to crypt damage, together with lymphoid necrosis predominantly associated with the intestinal tract and thymus. Although the disease was not very severe, this may have been because the low parasite burden in the animals reduced mitotic activity in susceptible tissues.
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PMID:Pathological and virological studies of experimental parvoviral enteritis in calves. 298 93

Healthy adult volunteers were inoculated intranasally with human parvovirus obtained from an asymptomatic blood donor. One week after inoculation, intense viremia was observed in seronegative volunteers, accompanied by a mild illness with pyrexia, malaise, myalgia, itching, and excretion of virus from the respiratory tract. In the following week hematologic studies revealed reticulocytopenia with an associated slight drop in hemoglobin concentration, lymphopenia, neutropenia, and a drop in platelet counts. At 17-18 days after inoculation a second-phase illness with rash and arthralgia lasting three to four days occurred in three of four infected volunteers. This study confirms the etiologic role of human parvovirus in erythematous rash illness, with the second-phase illness being consistent with adult cases of erythema infectiosum. Moreover, the hematologic changes associated with infection support the hypothesis that the same virus is responsible for the temporary arrest of erythropoiesis that leads to aplastic crisis in persons with chronic hemolytic anemia.
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PMID:Experimental parvoviral infection in humans. 299 31

After oral inoculation, the sequential distribution of canine parvovirus was studied in 14 nine-week-old seronegative beagle dogs. Two or three dogs were necropsied on days 1 through 6 after inoculation. Tissues were collected for virus isolation, immunofluorescence testing, and light microscopy. Virus was isolated from, and fluorescent cells were seen in the tonsil, retropharyngeal and mesenteric lymph nodes one and two days after inoculation. Virus infection of systemic and intestinal lymphoid tissues occurred as early as three days after inoculation and was associated with viremia. Intestinal epithelial infection was first seen four days after oral inoculation. All dogs were viremic before intestinal epithelial infection was found. Fecal virus excretion first occurred four days after oral virus inoculation. Intestinal virus infection and lesions became progressively more severe between four and six days after inoculation. The severity of intestinal lesions was variable and related to the severity of systemic lymphoid tissue lesions and the magnitude and duration of viremia. Four littermates of virus-infected dogs were passively immunized against canine parvovirus with convalescent canine serum 24 hours after oral virus inoculation. Neither clinical signs, lymphopenia, nor fecal virus excretion occurred in passively immunized dogs. Intestinal epithelial infection was not demonstrable by immunofluorescence testing when passively immunized dogs were necropsied four, five, and six days after virus inoculation.
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PMID:Pathogenesis of canine parvovirus enteritis: sequential virus distribution and passive immunization studies. 300 96

The effect of oral infection of puppies, eight and 10 weeks old, with canine parvovirus of faecal origin was studied. Clinical signs of enteric disease were first apparent at five days after inoculation and persisted during days 6 and 7 after inoculation. The severity of clinical signs varied from transient dullness and anorexia to emesis, dysentery and death. Changes in haematological parameters were first found at day 3 after inoculation when a relative lymphopenia was observed. A profound neutropenia developed in severely affected dogs after the appearance of clinical enteric disease. Post mortem examination revealed thymic atrophy in all dogs killed on day 4 after inoculation. Macroscopic changes in the small intestine were apparent only in animals examined during the phase of severe enteric disease and consisted of thickening, rigidity and congestion of the small intestines. Microscopically there was lymphocytolysis in the thymic cortex and the germinal centres of the lymph nodes from days 2 and 3 after inoculation respectively and this rapidly resulted in depletion of these tissues. There was repopulation of lymph nodes from day 7 after inoculation but significant thymic regeneration was not apparent during the course of this study. In the small intestine, necrosis of crypt epithelium, atrophy of villi and, in some areas, complete collapse of mucosal architecture were found but the extent of these changes varied along the length of the small intestine and between individuals. Regenerative intestinal changes were observed in those animals surviving the acute phase of enteric dysfunction. The variable severity of clinical and enteric lesions, together with the factors which may affect the expression of clinical disease, are discussed.
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PMID:Canine parvovirus enteritis 1: Clinical, haematological and pathological features of experimental infection. 609 17

In specific pathogen-free dogs, clinical signs of experimental canine parvovirus infection were mild, inconsistent and transient. Clinical signs were more pronounced in conventionally-raised dogs, but the severe disease reported in field cases was not reproduced in either group. A pronounced plasma viremia occurred on the 2nd to 4th day post-infection (d.p.i.) in dogs challenged oronasally. Antibody was detectable on the 5th d.p.i. Marked pyrexia was rare, but a significant temperature rise usually coincided with the appearance of antibody and the cessation of viremia. Significant lymphopenia, but not leukopenia, occurred on the 3rd to 7th d.p.i. Virus could be readily isolated from fecal matter on the 3rd to 8th d.p.i.; a few dogs continued to shed virus for up to 12 days. In dogs challenged parenterally, the onset of elevated temperatures, viral shed and antibody production occurred 24-48 hours sooner. Convalescent dogs were no longer contagious for susceptible contact animals 25 days or longer after challenge, although infectious virus persisted in feces for more than 6 months at room temperature. Active giardiasis seemed to exacerbate the clinical syndrome, although treatment with corticosteroids or anti-thymocyte serum did not.
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PMID:Experimental canine parvovirus infection in dogs. 621 33

Withholding food from dogs for 24 hours prior to, and for 48 hours following oral challenge with a gut mucosal homogenate of canine parvovirus-2, was a successful means of reproducing gastroenteric signs of canine parvovirus-2 infection. Twenty-one of 24 dogs, which had previously received various vaccine preparations of mink enteritis virus or were unvaccinated, and which were starved at challenge, developed soft or liquid feces with large or without large clots of mucus. Altered feces were most frequent on postexposure day 11. Seven dogs passed frank blood in their stools on one or more occasions and seven dogs vomited sporadically. Pyrexia was noted in 71.6% of the dogs on postexposure day 6 and lymphopenia was detected on postexposure day 5 or 6 in 50% of the dogs monitored. In contrast, four dogs not starved at the time of challenge remained free of gastrointestinal signs apart from one dog which passed a soft stool with scant mucus on one day, postexposure day 6. Also four dogs vaccinated with a killed canine parvovirus-2 vaccine preparation and subsequently starved at the time of challenge, remained clinically healthy. Apart from these last mentioned four dogs, all others shed canine parvovirus-2 in their feces following challenge.
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PMID:Successful experimental challenge of dogs with canine parvovirus-2. 628 Aug 19

Dogs and cats respond to many diseases by changes in leukocyte numbers. Infectious diseases often cause leukocytosis due to neutrophilia. Left shift may accompany the leukocytosis, indicating that the marrow is mounting a response to the disease. Left shift also indicates that the marrow has fallen somewhat behind the needs of the animal. Degenerative left shift is considered a poor sign. Lymphopenia and eosinopenia also are found in infectious diseases. Lymphocytosis may occur during the recovery or if the disease becomes chronic. The nature and duration of the infection determine the magnitude of the monocyte response. It is erroneous to consider a disease chronic based only upon monocytosis. Trauma, autoimmunity, or any disease with significant tissue destruction can evoke a monocyte response. Leukopenias are relatively common in cats and are found with moderate frequency in dogs. Drugs, viral diseases (such as FeLV, feline enteritis, parvovirus), ehrlichiosis, and hereditary conditions may cause panleukopenias or single leukopenias. Occasionally leukocyte examination provides evidence of a specific etiology (such as with ehrlichiosis). Sometimes changes occur which, although not specific for a disease, may provide a strong evidence of a particular disease (such as in salmon poisoning). Leukocyte evaluation should include not only total count and differential count (with calculation of absolute numbers of the different cells) but also morphologic examination of the cells by qualified people. In many practices the only qualified person is the veterinarian.
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PMID:The leukocytes. 703 46

Five eight week old dogs were inoculated orally and intranasally with cell culture origin canine parvovirus. Three dogs became depressed and anorectic and developed a mild (one dog) to severe diarrhea five days postinfection. The remaining dogs had subclinical infections but developed a lymphopenia followed by a transient lymphocytosis. The ill dogs developed mild (one dog) to severe neutropenia and a moderate lymphopenia. One died nine days postinfection. Recovery was associated with cessation of viral excretion and with lymphocytosis and antibody production. Two of three dogs challenged intragastrically developed mild clinical signs and a moderate panleukopenia four to eight days postinfection. The pathological changes of the experimental disease were very similar to that of spontaneous disease. Bone marrow changes included a severe granulocytic and mild erythroid depletion. The pathogenesis of canine parvovirus infection is discussed.
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PMID:Experimental parvovirus infection in dogs. 734 Sep 6


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