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[Morphology and development of the cranium of Felis silvestris f. catus Linné 1758--IV: Visceral skeleton, membrane bones: summary, conclusions and bibliography].

The present last part of the study on morphology and development of the cranium of Felis silvestris f. catus provides a detailed description and discussion of the development of the visceral skeleton and the membrane bones. Finally, there is given a summary with conclusions of the whole investigation. In Felis 2, the Cartilago Meckeli is still in homocontinuous connection with the Malleus. Probably, only the rostral part of the Cartilago will ossify enchondrally, while the caudal part shows some beginning resorption. In this 95 mm Embryo, the Cartilago Reicherti still remains cartilaginous. A small cartilaginous Spence's cartilage lies in dorsolateral position towards the Chorda tympani. All membrane bones of the adult cranium are present in Felis 1. The following development of the osseous skull towards the stage of Felis 2 is characterized by covering the wide fissures of the side wall and by resorption of certain primordial supporting constructions. The interparietal develops from a paired anlage. In Felis 1 and 2, the cartilago within the pterygoid probably serves as a gliding surface for the M. tensor veli palatini. The dental bone contains some largely extended particles of secondary cartilage.

Animals↗

Phagocytic function of equine neutrophils exposed to Mycoplasma felis in vitro and in vivo.

Neutrophils were isolated from the peripheral blood of adult equids (group 1) and were purified on a density gradient of polyvinylpyrrolidone-coated silica gel. A bactericidal assay was developed, using an equine skin isolate of Staphylococcus epidermidis as target bacterium in medium containing pooled fresh equine serum for opsonization. Significant (P less than 0.05) killing was observed after 60 or 120 minutes' incubation. Reduction in bactericidal function of blood neutrophils was not found after incubation with a virulent strain of Mycoplasma felis for 30 or 60 minutes. Similarly, the function of blood and pleural neutrophils of ponies with M felis-induced pleuritis (group 2) was not different from the function of similar neutrophils from sham-inoculated control ponies (group 3). The number of viable M felis organisms was markedly reduced in the presence of fresh equine serum and equine-specific antibodies, but not when the serum was heat inactivated. Equine neutrophils did not phagocytize M felis. Seemingly, M felis did not impair bactericidal activity of equine neutrophils. Therefore, this mechanism does not predispose equids to bacterial pleuritis.

Animals↗

Mycoplasma felis as a cause of pleuritis in horses.

Mycoplasma felis was the only organism recovered from the thoracic cavity of a horse with pleuritis. Large numbers of mildly degenerative neutrophils were in the pleural fluid. The horse developed a serologic response to M felis and recovered during hospitalization. Experimentally, a pony was inoculated in the thoracic cavity with a pure culture of the M felis isolate suspended in the pony's serum. A control pony was inoculated with serum only. Within 48 hours, the principal pony developed fever, increased respiratory rate, pleural effusion, and signs of pain. A highly cellular exudate with nondegenerative neutrophils and large numbers of M felis was recovered from the thoracic cavity. The control pony remained normal. The principal pony developed an antibody response to M felis. The control pony did not. Fourteen days after inoculation, both ponies were euthanatized. Necropsy revealed pleural inflammation in the principal pony. Pleural lesions were not found in the control pony.

Animals↗

Immunoelectrophoretic characterization and cross-reactivity of Rochalimaea henselae, Rochalimaea quintana and Afipia felis.

The soluble antigens of Rochalimaea henselae, Rochalimaea quintana and Afipia felis were characterized by crossed immunoelectrophoresis using bacterial sonicates as antigens against pooled hyperimmune rabbit sera. A precipitin pattern was drawn for each bacterium and shown to be reproducible and stable even when normal or preimmune rabbit serum was incorporated in the intermediate gel. By this technique 56 antigens were identified from R. henselae, 49 from R. quintana, and 39 from A. felis. The serological cross-reaction between R. henselae, R. quintana and A. felis, and between these 3 bacteria and 32 pathogenic bacteria was analysed by rocket-line immunoelectrophoresis, crossed-line immunoelectrophoresis, and tandem-crossed electrophoresis. It was concluded that (i) 4-7 antigens distinguish R. henselae, R. quintana and A. felis from each other, (ii) both Gram-positive and Gram-negative bacteria cross-react with R. henselae, R. quintana and A. felis antisera, (iii) the cross-reacting antigens of Gram-negative bacteria have both precipitating and non-precipitating specificities, whereas Gram-positive bacteria have mainly non-precipitating specificities, (iv) the cross-reacting antigens are common to several species, and (v) fewer cross-reacting antigens are found in phylogenetically disparate species than in more closely related species.

Angiomatosis, Bacillary↗

Rapid development of severe hyperplastic gastritis with gastric epithelial dedifferentiation in Helicobacter felis-infected IL-10(-/-) mice.

Interleukin (IL)-10 is a potent anti-inflammatory and immune-regulatory cytokine. Mice deficient in IL-10 production (IL-10(-/-)) develop a spontaneous inflammatory bowel disease, indicating that IL-10 is an important regulator of the mucosal immune response in vivo. To study the role of IL-10 in the host response to gastric Helicobacter infection, stomachs of IL-10(-/-) and wild-type mice were colonized with Helicobacter felis, as a model of human H. pylori infection. Within 4 weeks of H. felis infection, wild-type mice develop a mild, focal chronic gastritis. In contrast, H. felis-infected IL-10(-/-) mice develop a severe hyperplastic gastritis, characterized by a dense, predominantly mononuclear cell inflammation of the mucosa and submucosa and epithelial cell proliferation and dedifferentiation. Within 4 weeks of H. felis infection, there are striking alterations in the character of the gastric epithelium from IL-10(-/-) mice, including a profound loss of parietal and chief cells, focal de novo production of acidic mucins, and marked epithelial proliferation with disordered epithelial architecture. These findings indicate that, in the absence of IL-10, the inflammatory and immunological responses of the murine host to gastric colonization with Helicobacter is a rapidly evolving pathological process with features that mimic those associated with H. pylori infection in humans. H. felis-infected IL-10(-/-) mice may provide a model with which to investigate the cellular and molecular changes that stem from gastric infection with H. pylori.

Animals↗

Molecular, clinical, and pathologic comparison of two distinct strains of Haemobartonella felis in domestic cats.

OBJECTIVE: To characterize 2 strains of Haemobartonella felis by use of molecular techniques. ANIMALS: 35 specific-pathogen-free cats, 6 months to 4 years old. PROCEDURE: Intraperitoneal or IV inoculation with blood containing H felis small form (Hfsm, 18 cats) or H felis large form (Hflg, 11 cats); 6 cats were uninfected controls. Hfsm was evaluated for capability to cross-protect against the more virulent Hflg. Morphology of both strains was compared by light microscopy of Wright-Giemsa-stained blood smears, and the 16S rRNA genes were sequenced. RESULTS: Infection with Hflg induced signs of depression, fever, and severe macrocytic normochromic anemia with nucleated erythrocytes. More than 95% of erythrocytes were parasitized. Inoculation with Hfsm and uninfected control blood induced mild or no clinical signs and no hematologic abnormalities. Anti-H felis IgG was first detected on postinoculation day (PID) 21, and increased to maximal titer of 400 by PID 28. Reactivated infection was observed in 8 of 29 cats (4 Hfsm and 4 Hflg), with 5% parasitized erythrocytes during the later attack. On PID 8, Hflg-inoculated cats had positive results of polymerase chain reaction analysis (PCR) that persisted until cats were treated with doxycycline or oxytetracycline; Hfsm-inoculated cats had positive PCR results that persisted for duration of observation (3 months). CONCLUSIONS: Genetically and morphologically distinct strains of H felis infect cats in the field. The level of genetic difference suggested that these strains may be different species or genera. CLINICAL RELEVANCE: PCR is a critical diagnostic aid to detect occult Haemobartonella spp infection, as well as response to treatment and clearance of the organism.

Anaplasmataceae↗

Peptic ulcer disease associated with Helicobacter felis in a dog owner.

The aim of this study was to investigate the identity of the Helicobacter heilmannii-like bacteria found in the stomach of a human patient suffering from stomach ulcers and her asymptomatic pet dog. An elderly woman was referred for gastroscopy because of right hypochondrial pain, nausea, anorexia and vomiting. Gastric ulcers were observed and histology revealed the presence of multiple H. heilmannii-like bacteria. Multiplex polymerase chain reaction (PCR) identified the bacteria as H. felis. Her pet dog was also examined gastroscopically. Only mild gastric lesions were found but PCR showed the presence of H. felis as well as H. bizzozeronii and Candidatus H. heilmannii. This report associates H. felis infection in humans with severe gastric ulceration. Moreover, the suggestion can be made that the patient contracted H. felis from her dog.

Aged↗

Emended description of Rickettsia felis (Bouyer et al. 2001), a temperature-dependent cultured bacterium.

On the basis of phenotypic data obtained on the strain Marseille-URRWFXCal2(T), isolated from the cat flea Ctenocephalides felis, the description of Rickettsia felis (Bouyer et al., 2001) is emended and Marseille-URRWFXCal2(T) is proposed as the type strain of the species. On the basis of polyphasic characterization, especially the inability to grow at temperatures higher than 32 degrees C on Vero cells that allow growth of other Rickettsia to at least 35 degrees C, it is confirmed that this agent, although different from other recognized rickettsial species, is genotypically indistinguishable from bacteria previously detected within cat fleas and provisionally named ELB. Comparison of the phenotypic characteristics previously described for R. felis and those observed for the isolate in this study indicated some differences, although concurrent analysis of the two was not possible as no extant isolates of the first isolate of R. felis exist.

Animals↗

Experimental Helicobacter felis infection in transgenic mice expressing human group IIA phospholipase A2.

BACKGROUND: Both various virulence factors of Helicobacter pylori and host factors influence the clinical outcome of H. pylori infection. In animal experiments with Helicobacter felis, large variations in the severity of disease have been observed between different mouse strains infected with a single isolate of H. felis. C57BL/6 J mouse strain that lacks the expression of group IIA phospholipase A2 has been shown to develop more severe gastric inflammation than other mouse strains. Thus, group IIA phospholipase A2 has been suggested to play a role in regulating inflammation in gastric mucosa. The aim of this study was to examine the possible role of group IIA phospholipase A2 in experimental Helicobacter infection. MATERIALS AND METHODS: Transgenic mice expressing human group IIA phospholipase A2 and their group IIA phospholipase A2 deficient nontransgenic C57BL/6 J littermates were infected with H. felis. The mice were killed 3, 8, and 19 weeks after inoculation of bacteria to determine the histopathological changes in gastric mucosa. RESULTS: The infected mice developed chronic inflammation in gastric mucosa. We found no differences in the colonization of bacteria between transgenic and nontransgenic mice. At 3 and 8 weeks, no difference was found in the severity of inflammation between the two groups. Nineteen weeks after the administration of bacteria the inflammation was more marked in nontransgenic than transgenic mice. Group IIA phospholipase A2 was expressed by in situ hybridization in the neck cells of the glandular stomach in transgenic mice. CONCLUSIONS: The results of the present study suggest that the endogenous expression of group IIA phospholipase A2 diminishes chronic inflammation in gastric mucosa in experimental H. felis infection in mice.

Animals↗

Incidence and distribution pattern of Rickettsia felis in peridomestic fleas from Andalusia, Southeast Spain.

The presence of Rickettsia felis was investigated in three species of pulicid fleas (Ctenocephalides felis, Ctenocephalides canis and Pulex irritans) collected in 38 locales in Andalusia (Spain) over the period 1999-2004. Amplification of a fragment of OmpB gene was positive in 54.17 % of lots of Ct. felis. The identity of the PCR bands was confirmed as R. felis by sequence data obtained directly from the PCR amplicon. No rickettsia was found in Ct. canis nor P. irritans.

Animals↗

Clinical and laboratorial evidence of Rickettsia felis infections in Latin America.

After the discovery and initial characterization of Rickettsia felis in 1992 by Azad and cols, and the subsequent first description of a human case of infection in 1994, there have been two communications of human rickettsiosis cases caused by Rickettsia felis in Latin America. The first one was published in 2000 by Zavala-Velazquez and cols in Mexico. In 2001 Raoult and cols described the occurrence of two human cases of Rickettsia felis rickettsiosis in Brazil. In the present discussion these two articles were compared and after the description of the principal signs and symptoms, it was concluded that more studies are needed with descriptions of a greater number of patients to establish the true frequency of the clinical signs and symptoms present in Rickettsia felis rickettsiosis.

Brazil↗

Detection of a gypsy-like sequence in the genome of the cat flea Ctenocephalides felis (Bouché 1835).

The gypsy virus of Drosophila melanogaster is the first identified retrovirus of insects. Its infectious properties have been reported, and it is able to cause diverse mutations of the phenotype in the fruit fly. As a typical endogenous retrovirus, it is transmitted vertically as part of the host genome, but horizontal transmission has also been shown for the D. melanogaster gypsy virus. Using polymerase chain reaction with degenerate primers designed from the gypsy element of Drosophila subobscura, a gypsy-like sequence was amplified from the genome of the cat flea Ctenocephalides felis in a pool of laboratory and field strains. High identities with other gypsy-like sequences of Drosophila spp. can be detected. In contrast to some of these gypsy sequences, the 410-bp fragment of C. felis possesses two deletions, which are localised in the env gene region. Because of these deletions and the lack of virus particles in C. felis, the criteria for host infectivity are not fulfilled. Nevertheless, the general detection of a gypsy-like sequence in C. felis and the capability of the ectoparasite to act as transmitter of viral diseases can be of importance for the cat flea's position in the epidemiology of diseases, which are accompanied by a higher rate of mutation.

Animals↗

The importance of local acid production in the distribution of Helicobacter felis in the mouse stomach.

BACKGROUND/AIMS: Helicobacter felis colonizes the gastric mucosa of rodents. Preliminary studies showed differences in the distribution of the organism in different parts of the stomach that seemed related to the secretory capacity of the mucosa. The aim of this study was to determine the localization of H. felis in the mouse stomach and to investigate the influence of acid-suppressive agents. METHODS: Specific-pathogen-free BALB/c mice were infected with H. felis. Colonization was assessed in longitudinal sections of gastric tissue from animals untreated or treated with omeprazole or ranitidine. RESULTS: In untreated H. felis-infected animals, the preferred ecological niche was the antrum and cardia equivalent. The density of colonization correlated with the number of parietal cells per gland. Partial acid suppression with ranitidine produced a slight increase in the colonization of the body but was restricted to the upper portions of the gastric gland. Omeprazole treatment produced a greater colonization of the body with bacteria traversing the entire gland. Some reduction in antral colonization occurred. CONCLUSIONS: These results are consistent with the hypothesis that local acid output is a crucial determinant in the distribution of Helicobacter species in the stomach. Differences in local acid output may explain the different patterns of Helicobacter pylori-induced gastric pathology.

Animals↗

Incidence and significance of isolation of Mycoplasma felis from conjunctival swabs of cats.

Conjunctival swabs taken from 40 cats with conjunctivitis and 65 cats without conjunctivitis were examined for the presence of Mycoplasma felis. The incidence of M. felis in cats with conjunctivitis was 25%. M. felis was not isolated from clinically normal cats. Inoculation of two isolates into the conjunctival sacs of healthy cats induced conjunctival hyperemia, starting 2-3 days after inoculation and disappearing without treatment within 7 days. It is concluded that M. felis plays a role in feline conjunctivitis.

Animals↗

Prevalence of antibodies against feline coronavirus and Chlamydophila felis in Swedish cats.

Serum samples from 214 Swedish cats with no signs of infectious disease were analysed for the presence of antibodies against Chlamydophila felis (Cp felis), while 209 of these were also analysed for feline coronavirus (FCoV) antibodies. The prevalence of antibodies against Cp felis was 11%, with no significant difference between purebred and mixed breed cats. The overall prevalence of antibodies against FCoV was 31%, significantly higher among pure breed cats (65%) than among mixed breed cats (17%). A high proportion of cats with antibodies against FCoV had relatively high antibody titres, and was therefore likely to be shedding FCoV in faeces. For Cp felis, the majority of seropositive animals had relatively low antibody titres, and the risk of these animals infecting others is not known.

Animals↗

Mice lacking secretory phospholipase A2 show altered apoptosis and differentiation with Helicobacter felis infection.

BACKGROUND & AIMS: Infection with Helicobacter pylori uniformly leads to a chronic superficial gastritis that may progress to atrophic gastritis, a premalignant process. A mouse model of Helicobacter felis infection was used to study possible genetic determinants of the response to infection. METHODS: Three inbred mouse strains with known secretory phospholipase A2 (sPLA2) genotypes [BALB/c (+/+), C3H/HeJ (+/+), and C57BL/6 (-/-)] were orally infected with H. felis and examined longitudinally using routine histology, immunocytochemistry, electron microscopy, proliferating cell nuclear antigen, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling, and Northern and Western blot studies. RESULTS: Only the C57BL/6 strain showed increased gastric fundic proliferation and apoptosis in response to infection. In addition, the C57BL/6 mouse showed a marked loss of parietal and chief cells, along with a marked expansion of an aberrant gastric mucous cell lineage that stained positive for spasmolytic polypeptide. In contrast, no significant change in these cell types was observed in BALB/c and C3H/HeJ strains. Increased expression of sPLA2 was observed in BALB/c and C3H/HeJ after H. felis infection, whereas sPLA2 expression was absent in C57BL/6 mice. CONCLUSIONS: H. felis infection leads to increased apoptosis and altered cellular differentiation in the C57BL/6 mouse, a strain that lacks gastric sPLA2 expression. Because sPLA2 has been identified recently as the MOM1 (modifier of MIN) locus that influences polyp formation in the colon, these studies suggest that sPLA2 may also influence the gastric epithelial response to Helicobacter infection.

Animals↗

Oral immunization with recombinant Helicobacter pylori urease confers long-lasting immunity against Helicobacter felis infection.

Recombinant Helicobacter pylori urease (rUre) has been shown to confer protection against challenge with Helicobacter felis in mice. The purpose of the present study was to examine duration of the immune response and long-term protective efficacy of immunization with rUre. Swiss Webster mice were orally immunized four times at weekly intervals with 100 microg rUre plus 5 microg heat-labile enterotoxin of Escherichia coli (LT) adjuvant, or with LT only. At 4, 10, 20 or 40 weeks post immunization, 25 rUre-immunized mice and control mice were challenged with H. felis and sacrificed at 2 or 10 weeks post-challenge. H. felis infection was assessed by gastric urease assay and by histology. Anti-H. pylori urease specific antibody levels were measured in serum and saliva both pre- and post-challenge. Over the 40 week time period, the infection rates in rUre-immunized mice were significantly lower than those in controls (p < 0.05) as assessed by gastric urease activity. Protection ranged from 79 100% at 2 weeks post-challenge and 63-78% at 10 weeks post-challenge. Gastric bacterial density in rUre-immunized mice was significantly lower than that of controls (p < 0.03) as determined by histologic assessment. Anti-urease antibody levels remained elevated in the serum and mucosal compartments at 39 weeks following immunization. This study shows that immunization with rUre plus LT results in long-lasting protective immunity against challenge with H. felis.

Adjuvants, Immunologic↗

mRNA expression of cytokines and chemokines in the normal gastric surface mucous epithelial cell line GSM06 during bacterial infection with Helicobacter felis.

BACKGROUND AND AIM: A group of the proinflammatory and chemotactic cytokines (chemokines) has been considered as an important factor in the pathomechanism of different bacterial diseases, among them the common Helicobacter pylori infection. Experimental results obtained with gastric biopsy samples of H. pylori positive patients, and with H. pylori infected tumor originated gastric cell lines indicated that these cytokines have essential roles in the development and maintenance of the immune response and inflammation of the gastric mucosa during H. pylori infection. Although the mRNA expression was shown in these biopsy samples and cell lines, it is not yet proved that the normal gastric mucosal epithelial cells themselves express these cytokines. The establishment of a gastric surface mucous cell line with non-tumor origin (GSM06), and the usage of Helicobacter felis as a model of the classic H. pylori infection gave us the possibility to check this question. MATERIALS AND METHODS: in this study GSM06 cells were infected with different numbers (10(5), 10(6), 10(7), 10(8), 10(9) bacterium/ml medium) of H. felis for two different time periods (2, 4 h). Cells treated with medium only were used as control. Then the mRNA expression of the following cytokines was measured by RT-PCR method in the GSM06 cells: proinflammatory cytokine IL1-beta, and chemokine RANTES, eotaxin, MCP-1, MIP1-alpha and MIP1-beta. RESULTS: we found that neither mRNA of the investigated cytokines was expressed constitutively, however the GSM06 cells expressed the mRNA of each cytokine during H. felis infection. CONCLUSION: our results prove that normal gastric surface mucous epithelial cells express immunologically active peptides during H. felis infection. We may suppose that the epithelial cells of the gastric mucosa contribute to the immune response and inflammation by expressing proinflammatory (IL1-beta) and chemotactic (RANTES, eotaxin, MCP-1, MIP1-alpha and beta) cytokines during H. pylori infection in human.

Animals↗