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Category: Clinical Microbiology
Atrophic Rhinitis, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555817947/9781555812447_Chap10-1.gif /docserver/preview/fulltext/10.1128/9781555817947/9781555812447_Chap10-2.gifAbstract:
Atrophic rhinitis is a contagious respiratory disease of pigs that is highly prevalent throughout the world where modern pig husbandry is practiced. Several agents were suspected to be etiological agents in the early studies. These included bacteria (Pseudomonas, Actinomyces, Sphaerophorus, Corynebacterium, or Mycoplasma), a virus (cytomegalovirus), and trichomonads. However, only certain defined strains of Bordetella bronchiseptica and Pasteurella multocida proved to be able to constantly reproduce marked turbinate atrophy, the most characteristic lesion of atrophic rhinitis. A productive P. multocida infection needs predisposing factors among which B. bronchiseptica preinfection is the most commonly recognized one. This interaction between the two pathogens classifies atrophic rhinitis as a member of the family of polymicrobial infections, and the disease are reviewed with special attention to this aspect. The dominant pathological lesion of atrophic rhinitis is an atrophy of the nasal turbinate bones as assessed by transverse section of the nasal cavity at the level of the first/second upper premolar teeth where the dorsal and ventral conchae are maximally developed in the normal pig. Atrophic rhinitis is thought to reduce growth rates, which makes it an economically important disease for pig producers. Vaccination is widely used to try to reduce the prevalence of atrophic rhinitis in herds affected by the disease. The specific synergistic interactions between B. bronchiseptica and P. multocida support the notion that it is a genuine polymicrobial disease, which in addition may serve as a useful model system for more complex mixed infections.
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Cross-sections of snouts of 6-week-old pigs. (a) Uninfected pig showing normal anatomy of nasal structures. (b) Pig after infection with B. bronchiseptica and toxigenic P. multocida. The left dorsal turbinate is absent, and only a band of connective tissue remains from the left ventral turbinate. The right dorsal turbinate is slightly shrunken, and both scrolls of the right ventral turbinate show moderate atrophy. (c) Pig after infection with B. bronchiseptica and toxigenic P. multocida. There is complete absence of all turbinate structures accompanied with slight lateral deviation of the nasal septum.
Cross-sections of snouts of 6-week-old pigs. (a) Uninfected pig showing normal anatomy of nasal structures. (b) Pig after infection with B. bronchiseptica and toxigenic P. multocida. The left dorsal turbinate is absent, and only a band of connective tissue remains from the left ventral turbinate. The right dorsal turbinate is slightly shrunken, and both scrolls of the right ventral turbinate show moderate atrophy. (c) Pig after infection with B. bronchiseptica and toxigenic P. multocida. There is complete absence of all turbinate structures accompanied with slight lateral deviation of the nasal septum.
Diagram of some of the signal transduction pathways affected by the dermonecrotic (DNT) and adenylate cyclase (Ad cyclase) toxins from B. bronchiseptica and by the P. multocida toxin (PMT). Targets modified by the toxins are shown by open arrows. Direct interaction between molecules is shown by solid arrows, and interactions where the intervening components are either not shown or not known are indicated by dotted arrows. Abbreviations: GPCR, G-protein-coupled receptor; Gq α and G12/13 α, the alpha subunits of the respective heterotrimeric G proteins; PKA, protein kinase A; cAMP, cyclic AMP; MEK, MAP kinase/extracellular signal-regulated kinase kinase; ERK, extracellular signal-regulated kinase.
Diagram of some of the signal transduction pathways affected by the dermonecrotic (DNT) and adenylate cyclase (Ad cyclase) toxins from B. bronchiseptica and by the P. multocida toxin (PMT). Targets modified by the toxins are shown by open arrows. Direct interaction between molecules is shown by solid arrows, and interactions where the intervening components are either not shown or not known are indicated by dotted arrows. Abbreviations: GPCR, G-protein-coupled receptor; Gq α and G12/13 α, the alpha subunits of the respective heterotrimeric G proteins; PKA, protein kinase A; cAMP, cyclic AMP; MEK, MAP kinase/extracellular signal-regulated kinase kinase; ERK, extracellular signal-regulated kinase.
Diagram of some of the potential virulence determinants regulated by the bvg genes in Bordetella species. Abbreviations: bvg, Bordetella virulence gene; vrg, vir (bvg)- repressed gene; FHA, filamentous hemagglutinin. Tibor Magyar, Veterinary Medical Research Institute, Hungarian Academy of Sciences, H-1143 Budapest, Hungary. Alistair J. Lax, Oral Microbiology, Guy's King's and St. Thomas' Dental Institute, King's College London, London SE1 9RT, United Kingdom.
Diagram of some of the potential virulence determinants regulated by the bvg genes in Bordetella species. Abbreviations: bvg, Bordetella virulence gene; vrg, vir (bvg)- repressed gene; FHA, filamentous hemagglutinin. Tibor Magyar, Veterinary Medical Research Institute, Hungarian Academy of Sciences, H-1143 Budapest, Hungary. Alistair J. Lax, Oral Microbiology, Guy's King's and St. Thomas' Dental Institute, King's College London, London SE1 9RT, United Kingdom.