Intestinal Bacterial Changes in Chlamydia‐induced Primary Enteritis of Newborn Calves*

Storz, J.; Collier, Justine; Eugster, Anne; Altera, K. P.

doi:10.1111/j.1749-6632.1971.tb35002.x

Cited by 15 publications

(5 citation statements)

References 14 publications

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“…One explanation may be malabsorption of nutrients due to the local inflammatory response to intestinal mucosal chlamydial infection. While it is clear that C. pecorum resides in the intestinal tract of calves [9] , [15] , [24] , clinical symptoms would have been evident in our study if C. pecorum had caused enteritis and/or malabsorption syndrome. In the absence of such symptoms, a more likely explanation is a systemic effect of the sum total of inflammatory mediators released in response to the inapparent C. pecorum infection of virtually all mucosal membranes.…”

Section: Discussionmentioning

confidence: 63%

Asymptomatic Endemic Chlamydia pecorum Infections Reduce Growth Rates in Calves by up to 48 Percent

et al. 2012

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Intracellular Chlamydia (C.) bacteria cause in cattle some acute but rare diseases such as abortion, sporadic bovine encephalomyelitis, kerato-conjunctivitis, pneumonia, enteritis and polyarthritis. More frequent, essentially ubiquitous worldwide, are low-level, asymptomatic chlamydial infections in cattle. We investigated the impact of these naturally acquired infections in a cohort of 51 female Holstein and Jersey calves from birth to 15 weeks of age. In biweekly sampling, we measured blood/plasma markers of health and infection and analyzed their association with clinical appearance and growth in dependence of chlamydial infection intensity as determined by mucosal chlamydial burden or contemporaneous anti-chlamydial plasma IgM. Chlamydia 23S rRNA gene PCR and ompA genotyping identified only C. pecorum (strains 1710S, Maeda, and novel strain Smith3v8) in conjunctival and vaginal swabs. All calves acquired the infection but remained clinically asymptomatic. High chlamydial infection associated with reduction of body weight gains by up to 48% and increased conjunctival reddening (P<10−4). Simultaneously decreased plasma albumin and increased globulin (P<10−4) suggested liver injury by inflammatory mediators as mechanisms for the growth inhibition. This was confirmed by the reduction of plasma insulin like growth factor-1 at high chlamydial infection intensity (P<10−4). High anti-C. pecorum IgM associated eight weeks later with 66% increased growth (P = 0.027), indicating a potential for immune protection from C. pecorum-mediated growth depression. The worldwide prevalence of chlamydiae in livestock and their high susceptibility to common feed-additive antibiotics suggests the possibility that suppression of chlamydial infections may be a major contributor to the growth promoting effect of feed-additive antibiotics.

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Section: Discussionmentioning

confidence: 63%

Asymptomatic Endemic Chlamydia pecorum Infections Reduce Growth Rates in Calves by up to 48 Percent

et al. 2012

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“…In addition, Storz et al . [37] have experimentally confirmed this genetic differentiation in virulence long ago by experimental oral inoculation of calves, the original host, with C. pecorum isolates LW613 or 66P130. Highly virulent strain LW613 caused severe hemorrhagic diarrhea and polyarthritis with predominantly lethal outcome.…”

Section: Discussionmentioning

confidence: 75%

Host Adaptation of Chlamydia pecorum towards Low Virulence Evident in Co-Evolution of the ompA, incA, and ORF663 Loci

et al. 2014

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Chlamydia (C.) pecorum, an obligate intracellular bacterium, may cause severe diseases in ruminants, swine and koalas, although asymptomatic infections are the norm. Recently, we identified genetic polymorphisms in the ompA, incA and ORF663 genes that potentially differentiate between high-virulence C. pecorum isolates from diseased animals and low-virulence isolates from asymptomatic animals. Here, we expand these findings by including additional ruminant, swine, and koala strains. Coding tandem repeats (CTRs) at the incA locus encoded a variable number of repeats of APA or AGA amino acid motifs. Addition of any non-APA/AGA repeat motif, such as APEVPA, APAVPA, APE, or APAPE, associated with low virulence (P<10−4), as did a high number of amino acids in all incA CTRs (P = 0.0028). In ORF663, high numbers of 15-mer CTRs correlated with low virulence (P = 0.0001). Correction for ompA phylogram position in ORF663 and incA abolished the correlation between genetic changes and virulence, demonstrating co-evolution of ompA, incA, and ORF663 towards low virulence. Pairwise divergence of ompA, incA, and ORF663 among isolates from healthy animals was significantly higher than among strains isolated from diseased animals (P≤10−5), confirming the longer evolutionary path traversed by low-virulence strains. All three markers combined identified 43 unique strains and 4 pairs of identical strains among all 57 isolates tested, demonstrating the suitability of these markers for epidemiological investigations.

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“…27 Diseases caused by these agents include abortion, pneumonia, gastroenteritis, encephalomyelitis, conjunctivitis, arthritis, and/or sexually transmitted diseases. 18,27,34…”

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confidence: 99%

Chlamydia pecorum

et al. 2016

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Chlamydial abortion in small ruminants is usually associated with Chlamydia abortus infection. Although Chlamydia pecorum has been detected in aborted ruminants and epidemiological data suggests that C. pecorum is abortigenic in these species, published descriptions of lesions in fetuses are lacking. This work describes fetoplacental lesions in a caprine abortion with C. pecorum infection, and further supports the abortigenic role of C. pecorum in ruminants. A 16-month-old Boer goat aborted twin fetuses at ~130 days of gestation. Both fetuses (A and B) and the placenta of fetus A were submitted for postmortem examination and diagnostic workup. At autopsy, the fetuses had moderate anasarca, intermuscular edema in the hindquarters (A), and brachygnathia and palatoschisis (B). In the placenta, the cotyledons were covered by yellow fibrinosuppurative exudate that extended into the adjacent intercotyledonary areas. Histologically, there was severe suppurative and necrotizing placentitis with vasculitis (arteriolitis) and thrombosis, multifocal lymphohistiocytic and neutrophilic hepatitis (A), and fibrinosuppurative enteritis in both fetuses. Chlamydia antigen was detected in the placenta by the direct fluorescent antibody test and in fetal intestines by immunohistochemistry. Nested polymerase chain reaction of DNA extracted from formalin-fixed, paraffin-embedded sections of placenta and intestine amplified 400 bp of the Chlamydia 16S rRNA gene that was sequenced and found to be 99% identical to C. pecorum by BLAST analysis. Other known abortigenic infectious agents were ruled out by specific testing. It is concluded that C. pecorum infection is associated with fetoplacental lesions and sporadic abortion in goats.

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Intestinal Bacterial Changes in Chlamydia‐induced Primary Enteritis of Newborn Calves*

Cited by 15 publications

References 14 publications

Asymptomatic Endemic Chlamydia pecorum Infections Reduce Growth Rates in Calves by up to 48 Percent

Asymptomatic Endemic Chlamydia pecorum Infections Reduce Growth Rates in Calves by up to 48 Percent

Host Adaptation of Chlamydia pecorum towards Low Virulence Evident in Co-Evolution of the ompA, incA, and ORF663 Loci

Chlamydia pecorum

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