Joitakin tutkimuksia aiheesta:
Morphologic, immunohistochemical, and ultrastructural characterization of a distinctive renal lesion in dogs putatively associated with Borrelia burgdorferi infection: 49 cases (1987-1992).
Dambach DM, Smith CA, Lewis RM, Van Winkle TJ.
Vet Pathol, Mar;34(2):85-96. 1997.
A distinctive renal lesion consisting of glomerulonephritis, diffuse tubular necrosis with regeneration, and interstitial inflammation was found in 49 biopsy/necropsy cases obtained from 1987 to 1992. This lesion is manifested clinically as a rapidly progressive glomerular disease that was uniformly fatal. ...Previous reports have associated this lesion with Borrelia burgdorferi exposure. All dogs in this study were from Lyme disease-endemic areas. Of 18 dogs serologically tested, all were positive for exposure. Silver stain examination of kidneys revealed rare spirochetes, suggesting that the presence of spirochetes in the kidney is apparently unrelated to lesion development. The role of vaccination in development of the renal lesion is undetermined. The association of this histologically and clinically unique lesion, Lyme nephritis, with Borrelia burgdorferi infection is significant because it is the only fatal form of canine Lyme borreliosis.
Fetal outcome in murine Lyme disease.
Silver RM, Yang L, Daynes RA, Branch DW, Salafia CM, Weis JJ.
Infect Immun. Jan; 63(1):66-72. 1995. PMID: 7806385
Histologic analysis of gestational tissues from infected animals demonstrated nonspecific pathology consistent with fetal death. These findings indicate an association between murine fetal death and acute infection with B. burgdorferi early in gestation but not with chronic infection. Our data suggest that fetal death is due to a maternal response to infection rather than fetal infection. These findings could provide an explanation for observations in humans in which sporadic cases of fetal death in women infected with B. burgdorferi during pregnancy have been reported, while previous infection has not been associated with fetal death.
Identification of Bartonella henselae in an Aborted Equine Fetus.
Johnson R, Ramos-Vara J, Vemulapalli R
Vet Pathol 2009 Mar; 46(2):277-81.
This report describes the characterization of a Bartonella henselae abortion in an equine fetus by gross, histologic, immunohistochemical, ultrastructural, and molecular methods. Bartonella henselae can cause cat scratch disease, bacillary angiomatosis, bacillary peliosis, and endocarditis in humans and other animals.
The bacterium has been isolated from several mammalian species but only recently from equids; however, it has not been linked to abortion in equids. An aborted equine fetus exhibited necrosis and vasculitis in multiple tissues, with intralesional Gram-negative short-to-spirillar bacteria. Nucleotide sequence analysis of the bacterial 16S rRNA gene amplified from the DNA extracted from fetal tissues revealed 99.9% homology to that of B. henselae.
The presence of B. henselae in the fetal tissues was further confirmed by polymerase chain reaction amplification and nucleotide sequence analysis of other Bartonella species-specific genes. Microorganisms were immunohistochemically labeled with a monoclonal antibody to B. henselae and were ultrastructurally characterized. Attempts to detect known causative agents of equine abortion were unsuccessful. Given the severity of vasculitis and the presence of intralesional bacteria, we concluded that B. henselae infection caused the abortion of this foal.
Aortic Valve Endocarditis in a Dog Due to Bartonella clarridgeiae.
Bruno B. Chomel et al.
J Clin Microbiol. 2001 October; 39(10): 3548?3554.
We report the first documented case of endocarditis associated with Bartonella clarridgeiae in any species. B. clarridgeiae was identified as a possible etiological agent of human cat scratch disease. Infective vegetative valvular aortic endocarditis was diagnosed in a 2.5-year-old male neutered boxer. Historically, the dog had been diagnosed with a systolic murmur at 16 months of age and underwent balloon valvuloplasty for severe valvular aortic stenosis. Six months later, the dog was brought to a veterinary hospital with an acute third-degree atrioventricular block and was diagnosed with infective endocarditis.
The dog died of cardiopulmonary arrest prior to pacemaker implantation. Necropsy confirmed severe aortic vegetative endocarditis. Blood culture grew a fastidious, gram-negative organism 8 days after being plated. Phenotypic and genotypic characterization of the isolate, including partial sequencing of the citrate synthase (gltA) and 16S rRNA genes indicated that this organism was B. clarridgeiae. DNA extraction from the deformed aortic valve and the healthy pulmonic valve revealed the presence of B. clarridgeiae DNA only from the diseased valve. No Borrelia burgdorferi or Ehrlichia sp. DNA could be identified. Using indirect immunofluorescence tests, the dog was seropositive for B. clarridgeiae and had antibodies against Ehrlichia phagocytophila but not against Ehrlichia canis, Ehrlichia ewingii, B. burgdorferi, or Coxiella burnetii.
Development and evaluation of a PCR assay for the detection of Cytauxzoon felis DNA in feline blood samples.
Birkenheuer AJ, Marr H, Alleman AR, Levy MG, Breitschwerdt EB.
Vet Parasitol. Apr 15;137(1-2):144-9. 2006 Epub Jan 18. 2006 PMID: 16417970
In naturally infected domestic cats the disease is almost always fatal.
Implications of presumptive fatal Rocky Mountain spotted fever in two dogs and their owner.
Elchos BN,Goddard J.
J Am Vet Med Assoc. Nov 15;223(10):1450-2, 1433. 2003 PMID: 14627095
A dog was examined because of petechiation, an inability to stand, pale mucous membranes, a possible seizure, and thrombocytopenia. Tick-borne illness was suspected, but despite treatment, the dog died. Eight days later, a second dog owned by the same individual also died. The dog was not examined by a veterinarian, but Rocky Mountain spotted fever (RMSF) was suspected on the basis of clinical signs. Two weeks after the second dog died, the owner was examined because of severe headache, fever, nausea, vomiting, decreased appetite, lethargy, and a fine rash on the body, face, and trunk. Despite intensive treatment for possible RMSF, the owner died. Although results of an assay for antibodies to Rickettsia rickettsii were negative, results of polymerase chain reaction assays of liver, spleen, and kidney samples collected at autopsy were positive for spotted fever group Rickettsia spp. These cases illustrate how dogs may serve as sentinels for RMSF in humans and point out the need for better communication between physicians and veterinarians when cases of potentially zoonotic diseases are seen.
American canine hepatozoonosis.
Ewing SA, Panciera RJ.
Clin Microbiol Rev. Oct;16(4):688-97. 2003 PMID: 14557294
American canine hepatozoonosis (ACH) is a tick-borne disease that is spreading in the southeastern and south-central United States. Characterized by marked leukocytosis and periosteal bone proliferation, ACH is very debilitating and often fatal.
Fatal cases of Tick-borne fever (TBF) in sheep caused by several 16S rRNA gene variants of Anaplasma phagocytophilum.
Stuen S, Nevland S, Moum T.
Ann N Y Acad Sci. Jun;990:433-4. 2003 PMID: 12860670
A longitudinal study of disease incidence and case-fatality risks on small-holder dairy farms in coastal Kenya.
Maloo SH, Rowlands GJ, Thorpe W, Gettinby G, Perry BD.
Prev Vet Med. Nov 2;52(1):17-29. 2001 PMID: 11566375
Cattle managed in the herded-grazing system had a 60% higher mortality, although not significantly so, than those fed in stalls. Deaths due to ECF accounted for over two-thirds of the deaths.
Animal model of fatal human monocytotropic ehrlichiosis.
Sotomayor EA, Popov VL, Feng HM, Walker DH, Olano JP.
Am J Pathol. Feb;158(2):757-69. 2001 PMID: 11159213
Human monocytotropic ehrlichiosis caused by Ehrlichia chaffeensis is a life-threatening, tick-borne, emerging infectious disease for which no satisfactory animal model has been developed. Strain HF565, an ehrlichial organism closely related to E. chaffeensis isolated from Ixodes ovatus ticks in Japan, causes fatal infection of mice. C57BL/6 mice became ill on day 7 after inoculation and died on day 9.
Spirochetemia caused by Borrelia turicatae infection in 3 dogs in Texas.
Whitney MS, Schwan TG, Sultemeier KB, McDonald PS, Brillhart MN.
Vet Clin Pathol. 2007 Jun;36(2):212-6 PMID: 17523100
Spirochetemia was diagnosed in 2 Siberian Huskies and a Rottweiler from the northwestern region of Texas between June 1999 and October 2001. Clinical findings were nonspecific; tick exposure was documented in 2 of the dogs. Hematologic abnormalities included anemia (n=2), neutrophilia (n=2, including 1 with a left shift), lymphopenia (n=3), eosinopenia (n=3), and thrombocytopenia (n=2). One anemic dog had a positive Coombs' test. In 1 dog, Western blot analysis of serum yielded multiple positive bands with B turicatae lysate, indicating the spirochetemia most likely was due to B turicatae infection. In 2 dogs, spirochetes were cultured from the blood and identified using DNA analysis as Borrelia turicatae; 1 of these dogs also was seropositive for Ehrlichia canis and B burgdorferi. In 2 cases, spirochetemia was more prominent in blood smears prepared immediately after sample collection than in smears prepared from EDTA blood. Two dogs recovered with doxycycline treatment; 1 dog declined clinically despite treatment and was euthanized.
B turicatae is the agent of tick-borne (endemic) relapsing fever in humans and is distinct from B burgdorferi, the agent of Lyme disease; however, serologic cross-reactivity may occur. B turicatae is transmitted by the soft tick, Ornithodoros turicata, and infection should be considered in dogs with spirochetemia and possible exposure to the tick vector.