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PATHOGENIC MECHANISMS OF BARTONELLA HENSELAE INFECTIONS

Fumarola, Donato; Giuliani, Giuseppe; Pece, Salvatore

The Pediatric Infectious Disease Journal: April 1996 - Volume 15 - Issue 4 - p 385-386
Letter
Free

Accepted for publication Jan. 5, 1996.

To The Editors:

The article by Abbasi et al.1 prompts us to make so comments concerning the pathogenic mechanisms of extra taneous manifestations in cat-scratch disease, bacillary a omatosis and related disorders.

Virtually nothing is known about the factor(s) responsible for damage production by the major causative agent, Bartonella henselae, in the multiple system organ involvement that includes pulmonary injuries,2 and nongranulomatous lesions such as neurologic disturbances recently described.3, 4 From our point of view it is not unreasonable to speculate that the intimate relationship of the causative agent with the host cells may play a critical role in determining the local tissue pathology in immunocompromised patients or in immunologically intact hosts. With the aim to investigate these interactions we studied the influence of B. henselae on human polymorphonuclear cells in terms of oxidative metabolism (O2- and H2O2 release and luminal-enhanced chemiluminescence assay), degranulation (release of beta-glucuronidase) and chemotaxis (leading front measurement). Our results5 indicated lower biologic activities exhibited by B. henselae compared with a classical Gram-negative organism (Escherichia coli). These findings may explain the survival, the intracellular growth and multiplications of the bacterium within phagocytic cells. In addition as reported preliminarily6B. henselae demonstrated a reduced ability of stimulated human macrophages and human endothelial cells to release some cytokines (tumor necrosis factor-alpha and interleukin 1-alpha), suggesting a possible influence on the nature and the evolution of inflammatory responses in the lesion sites and consequently the variable severity of cat-scratch disease, bacillary angiomatosis and related disorders. Also by an in vivo model of the chick embryo chorioallantoic membrane, assessed in photographic reconstruction by a vascular density index, we found significant neoangiogenesis as a consequence of influence on chorioallantoic membranes vessels by cell-free supernatants of stimulated human mononuclear cells.7 These findings can be regarded as a strategy for the expression of pathologic potency providing new insights into understanding of granulomatous, nongranulomatous and/or angioproliferative host tissue pathology in human infections associated with B. henselae.

The results of these preliminary approaches do not eliminate a role for numerous other factors, including the endotoxic lipopolysaccharide and other constituents of the cell wall of the bacterium, some possibly more important for virulence that have not been identified thus far. The variable severity in clinical presentations and disorder associated with B. henselae infections in people may be attributable to bacterial strain differences8 as well as differences in the cellular inflammatory responses, as most recently suggested also by others.9

Donato Fumarola; Giuseppe Giuliani; Salvatore Pece

Institute of Medical Microbiology

Bari University School of Medicine

Bari, Italy

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REFERENCES

1. Abbasi S, Chesney PJ. Pulmonary manifestations of catscratch disease: a case report and review of the literature. Pediatr Infect Dis J 1995;14:547-8.
2. Caniza MA, Granger DL, Wilson KH, et al. Bartonella henselae: etiology of pulmonary nodules in a patient with depressed cell-immunity. Clin Infect Dis 1995;20:1505-11.
3. Noah DL, Bresee JS, Gorensek MJ, et al. Cluster of five children with acute encephalopathy associated with catscratch disease in South Florida. Pediatr Infect Dis J 1995;14:866-9.
4. Schwartzman WA, Patnaik M, Angulo FJ, Visscher BR, Miller EN, Petel JB. Bartonella (Rochalimaea) antibodies, dementia, and cat ownership among men infected with human immunodeficiency virus. Clin Infect Dis 1995;21:954-9.
5. Fumarola D, Pece S, Fumarulo R, et al. Downregulation of human polymorphonuclear cell activities exerted by microorganisms belonging to the alpha-2 subgroup of proteobacteria (Afipia felis, Rochalimaea henselae). Immunopharmacol Immunotoxicol 1994;16:449-61.
6. Fumarola D, Pece S, Petruzzelli R, et al. Effects of Rochalimaea henselae on human polymorphonuclear and endothelial cells. [Abstract B-367]. Presented at the 94th General Meeting of the American Society for Microbiology, Las Vegas, May 23 to 27, 1994.
7. Fumarola D, Pece S, Ribatti D, Giuliani G, Roncali L, Jirillo E. TNF-alpha secretion by normal human mononuclear cells after exposure to Rochalimaea (Bartonella) henselae and in vitro evaluation of angiogenic responses exerted by cell-free supernatants [Abstract E-10]. Presented at the 95th General Meeting of the American Society for Microbiology, Washington, DC, May 21 to 25, 1995.
8. Kordik DL, Walson KW, Sexton DJ, Hadfield TL, Berkhoff HA, Breitschwerdt EB. Prolonged Bartonella bacteremia in cats associated with cat-scratch disease patients. J Clin Microbiol 1995;33:3245-51.
9. Regnery R, Tappero J. Unraveling mysteries associated with cat-scratch disease, bacillary angiomatosis, and related syndromes. Emerging Infect Dis 1995;1:16-21.
Keywords:

Bartonella henselae infections

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