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Veterinary Infection Biology

Research Focus of the RG „Veterinary Infection Biology“

Research on the mechanisms of Host-Pathogen interactions is the main focus of the research group (RG) Veterinary Infection Biology. We are especially interested in infectious diseases and bacterial pathogens affecting neonates, as neonates are a risk group with particularly high rates of morbidity and mortality and very little is known about the pathophysiology of the neonate compared to the adult host. Our approach is to study such bacterial infections from both the bacterial pathogen as well as the host side of such infections. We therefore examine both bacterial virulence mechanisms and factors as well as the innate immune responses of the infected host. As host-pathogen interactions are very complex, our research and experimental work applies a wide spectrum of techniques from different scientific disciplines, including microbiology, molecular biology, protein biochemistry, and (infection)-immunology. Likewise, our research interests include a broad spectrum of often very different bacterial pathogens. Representatives of Gram-positive pathogens include Streptococcus and Listeria, both of which can cause severe systemic infections (septicemia and/or meningitis) in both humans and animals. In addition, our research also involves members of the Gram-negative Enterobacteriaceae, with a focus on Salmonella Typhimurium. S. Typhimurium is a paradigm for zoonotic, bacterial pathogens, and remains one of the major gastrointestinal pathogens affecting human and animal populations worldwide. Generally causing a self-limiting, gastroenteritis and diarrhea in adults, in the neonate (newborns) and pediatric host, Salmonella infections often lead to systemic and chronic forms of infection. In particular, in Third World countries with poor hygiene standards, Salmonella infections in neonates can show high rates of septicemia and meningitis. An additional focus of research in our group concerns the phenomenon of bacterial persistence. Persistence refers to the ability of sub-populations of bacteria to survive even high concentrations of bactericidal antibiotics, but without acquiring genetically determined resistance. Such persisters therefore survive antibiotic therapies, and can re-emerge to cause relapse and/or chronic, recurring infections. The mechanisms involved in persister formation are complex, and currently poorly understood. Our goal is to contribute to a better understanding of this phenomenon.

Selected publications:

Fulde M*, Rohde M, Hitzmann A, Preissner KT, Nitsche-Schmitz DP, Nerlich A, Chhatwal GS, Bergmann S. SCM, a novel M-like protein from Streptococcus canis, binds (mini)-plasminogen with high affinity and facilitates bacterial transmigration. Biochem J. 2011 Mar 15;434(3):523-35.

Hitzmann A, Bergmann S, Rohde M, Chhatwal GS, Fulde M*. Identification and characterization of the arginine deiminase system of Streptococcus canis. Vet Microbiol. 2013 Feb 22;162(1):270-7

Fulde M*, Rohde M, Polok A, Preissner KT, Chhatwal GS, Bergmann S. Cooperative plasminogen recruitment to the surface of Streptococcus canis via M protein and enolase enhances bacterial survival. MBio. 2013 Mar 12;4(2):e00629-12.

Fulde M1, Bernardo-García N1, Rohde M, Nachtigall N, Frank R, Preissner KT, Klett J, Morreale A, Chhatwal GS, Hermoso JA, Bergmann S. Pneumococcal phosphoglycerate kinase interacts with

Verkühlen GJ, Pägelow D, Valentin-Weigand P, Fulde M*. SCM-positive Streptococcus canis are predominant among pet-associated group G streptococci. Berl Munch Tierarztl Wochenschr. 2016 May-Jun;129(5-6):247-50.

Bergmann S, Eichhorn I, Kohler TP, Hammerschmidt S, Goldmann O, Rohde M, Fulde M*. SCM, the M Protein of Streptococcus canis Binds Immunoglobulin G. Front Cell Infect Microbiol. 2017 Mar 28;7:80. doi: 10.3389/fcimb.2017.00080.

Eichhorn I, Jarek M, van der Linden M, Fulde M*. Draft Genome Sequence of the zoonotic Streptococcus canis isolate G361. Genome Announc. 2017 Sep 21;5(38). pii: e00967-17. doi: 10.1128/genomeA.00967-17.

Zhang K, Dupont A, Torow N, Gohde F, Leschner S, Lienenklaus S, Weiss S, Brinkmann MM, Kühnel M, Hensel M, Fulde M2, Hornef MW2. Age-dependent enterocyte invasion and microcolony formation by salmonella. PLoS Pathog. 2014 Sep 11;10(9):e1004385. doi: 10.1371/journal.ppat.1004385.

Braetz S, Schwerk P, Thompson A, Tedin K, Fulde M. The role of ATP pools in persister cell formation in (fluoro)quinolone-susceptible and -resistant strains of Salmonella enterica ser. Typhimurium. Vet Microbiol. 2017 Oct;210:116-123. doi: 10.1016/j.vetmic.2017.09.007.

Eichhorn I, Tedin K, Fulde M*. Draft Genome Sequence of Salmonella enterica subsp. enterica Serovar Typhimurium Q1. Genome Announc. 2017 Oct 19;5(42). pii: e01151-17. doi: 10.1128/genomeA.01151-17.


Fulde M*, Valentin-Weigand P*. Epidemiology and pathogenicity of zoonotic streptococci. Curr Top Microbiol Immunol. 2013;368:49-81.

Fulde M, Steinert M, Bergmann S. Interaction of streptococcal plasminogen binding proteins with the host fibrinolytic system. Front Cell Infect Microbiol. 2013 Nov 22;3:85.

Fulde M, Hornef M. Maturation of the enteric mucosal innate immune system during the postnatal period. Immunol Rev. 2014 Jul;260(1):21-34. doi: 10.1111/imr.12190.

Hornef MW*, Fulde M*. Ontogeny of mucosal immune responses. Frontiers in Immunology, October 2014, doi: 10.3389/fimmu.2014.00474

Doran KS1, Fulde M1, Gratz N1, Kim BJ1, Nau R1, Prasadarao N1, Schubert-Unkmeir A1, Tuomanen EI1, Valentin-Weigand P. Host-pathogen interactions in bacterial meningitis. Acta Neuropathol. 2016 Feb;131(2):185-209. doi: 10.1007/s00401-015-1531-z.

Book chapters:

Fulde M*, Bergmann S* (2017). Impact of Streptococcal Enolase in Virulence, in: Moonlighting proteins – novel virulence factors in bacterial infections. Ed. Brian Henderson; Wiley Blackwell, pp. 245-259