Laboratory diagnosis of viral and other infectious diseases.
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Rats were infected with H. muris from the first to the second week of their life. Four weeks later 20 of the infected rats were inoculated with 1.5 x 10(5) T. cruzi. Control animals were given the same number of parasites. In both experimental groups no hemoflagellate could be seen in blood smears four weeks after infection. The comparison of the course of infection of T. cruzi in rats with and without H. muris was made using t- and Wilcoxon-Test for Pair Differences. Rats with H. muris infections showed a low development of T. cruzi up to the 16th day of infection with this flagellate (P less than 0.0005). This difference in the development of the trypanosomes is lost from the 17th to the 27th day after infection.
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A method is described for preparation of an antigen from E. ovis-infected blood first lysed by freezing and thawing, and then followed by sonic disruption of the centrifuged deposit. It was then used in a complement fixation test to demonstrate antibodies in sheep infected with E. ovis. The antigen was not anti-complementary and it retained its potency for long periods when stored concentrated, at about -20 degrees C. Repeated freezing and thawing also has had no effect on the potency of the concentrated antigen. The testing of 668 serums from commercial flocks where E. ovis infection has been diagnosed microscopically has shown the CFT to be a valuable diagnostic aid mainly on a flock sample basis, though the test could be of value on an individual sample basis if the sample were taken from a recently infected sheep.
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An agent morphologically similar to Haemobartonella muris was isolated from the blood of rats infected with a strain of Trypanosoma lewisi kept at this Department. It caused acute hemolytic anemia, splenomegaly, glomerulonephritis, and death within 5 to 8 days in mature Sprague-Dawley rats. The disease was less severe in weanling rats which usually recovered within 3 to 4 wk. The anemia was accompanied by phagocytosis of erythrocytes by monocytes of the spleen and bone marrow, by high titers of cold-active hemagglutinin, high titers of antibody to the third component of fixed complement (immunoconglutinin), and antibody to fibrinogen/fibrin related products. Filtrates of blood from anemic rats passing a 0.20-micron filter did not produce disease or signs of infections, but filtrate from a 0.45-micron filter was infective. Attempts to grow the agent on rat embryo fibroblast cultures and in embryonated chicken eggs were successful. Tests for bacteria, mycoplasma, and spirochetes gave negative results. Blood of infected rats did not produce signs of infections when inoculated into laboratory mice, and normal rats housed in cages with acutely infected rats did not develop signs of infection or disease. Morphological similarity did not allow differentiation of the agent from H. muris. However, its virulence for mature rats differs markedly from that usually seen in H. muris infection.
Hemotropic mycoplasmas represent an important cause of anemia in cats worldwide. Previously known as Haemobartonella species, sequencing of the 16S rRNA genes of these organisms has led to their reclassification as mycoplasmas. Two species have been identified in cats, M haemofelis and "Candidatus M haemominutum." The latter organism alone has not been associated with disease in naturally infected cats but may cause anemia in FeLV-infected cats and accelerate development of FeLV-induced myeloproliferative disease. The mode of transmission of these organisms remains enigmatic. Nevertheless, development of sensitive DNA-based tests for these unculturable organisms has improved the understanding of the epidemiology and pathogenesis of FHM. Cats with clinical signs and laboratory abnormalities consistent with FHM should be treated with doxycycline; enrofloxacin may represent an effective alternative. Transfusion with packed red blood cells after cross-matching may be required for severely anemia cats, and addition of prednisone may be required if the diagnosis of FHM is uncertain, or response to antimicrobials alone is insufficient. Affected cats should be tested for FeLV, the most common concurrent infection in cats with FHM.
H. felis is a rickettsial parasite that causes hemolysis and sequestration of feline erythrocytes. It should be considered as a potential primary pathogen or opportunist in any cat presented with signs ranging from episodic malaise to acute anemic collapse. Diagnosis requires visualization of the organism in properly prepared blood smears. Treatment uses antirickettsial drugs, corticosteroids, and supportive measures. Clinical recovery requires immune containment of the organism. Treatment does not eliminate the organism from the host. Carrier cats may relapse when their immunity is severely compromised by other diseases such as FeLV. Transmission is presumed to be by blood-sucking parasites and possibly bite wounds between cats. Prevention requires prudent health management of cats. Future advances in the knowledge of the disease will relate mainly to the development of a diagnostic technique that will allow identification of all infected cats.
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A survey of the blood parasites of 20 Liomys salvini revealed 3 types of parasites. Sixty percent of the mice harbored Trypanosoma zeledoni, 5% an unnamed species of Hepatozoon, and 20% of the mice were infected with a species of Haemobartonella.
Two cases of clinical feline hemobartonellosis with dramatic hematological changes are reported. One cat succumbed to an acute, severe hemolytic anemia accompanied by markedly increased numbers of nucleated erythrocytes. The second cat presented with a remarkably elevated leukocyte count and responded well to treatment with tetracycline. In both instances, the initial hematological data was very unusual for feline hemobartonellosis. These cases further exemplify the greatly variable and sometimes misleading hematological changes seen with Hemobartonella felis infection.
Human and animal infections by Anaplasmataceae are increasingly recognized as important and potentially fatal arthropod-transmitted diseases. Since the first recognition and implementation of diagnostic methods for human infection by Ehrlichia chaffeensis and Anaplasma phagocytophilum, the incidence of infections has linearly increased. Moreover, diagnostic and epidemiological testing indicates that "ehrlichia" infections are globally distributed and suggests that additional agents of human and veterinary "ehrlichiosis" will be identified. With increasing disease identification has come recognition that the infections can be severe, with approximately one-half of patients requiring hospitalization for complications including respiratory distress, myocarditis, neurological complications, hepatitis, a septic or toxic shock-like disease, opportunistic infections, and death in 0.5 to 3.0%. An understanding of the diseases, pathophysiology, pathogenesis, control, and management will best be developed through fundamental investigations. Advances in comprehension as to the separate contributions of bacteria and host are crucial since most data now suggest that alterations in host neutrophil function and protection from innate and adaptive immunity also contribute to disease manifestations. It is reasonable to operate from the hypothesis that these host cell functional changes ultimately benefit bacterial survival while inadvertently eliciting clinical disease in poorly adapted hosts. A firmer basis for the scientific understanding of Anaplasmataceae biology will allow logical and rational approaches toward infection control, prevention, and treatment.
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An 11-year-old male domestic shorthaired cat was presented with behavioural disturbances and abdominal distension of two days' duration. Haemobartonella felis was found on routine haematology and serum biochemistry showed mild azotaemia. Abdominocentesis revealed a transudate. Bilateral perinephric fluid accumulations were observed on ultrasonography and chronic nephrosclerosis was diagnosed on needle biopsies of the kidney. A celiotomy with resection of the major portion of both cyst walls was performed. The omentum was extended along the floor of the abdomen, across the ventral aspect of both kidneys and attached to the remnants of the pseudocyst wall. Ongoing physiological drainage was secured and cyst recurrence was prevented. Perirenal fluid was not detected at clinical and ultrasound follow-up examinations 14 days and seven months postoperatively. Mild azotaemia and refractory Haemobartonella infection were, however, still present.
Pleuromutilins have an aegyptianellicidal efficacy. A significant chemotherapeutic influence on the course of the infection in chickens could only be achieved after repeated oral and intramuscular applications of at least 150 mg and 75 mg/kg body weight respectively. However, even at these concentrations the infections were not cleared.