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A cyclic peptide synthetase gene required for pathogenicity of the fungus Cochliobolus carbonum on maize.

Specificity in many plant-pathogen interactions is determined by single genes in pathogen and host. The single locus for host-selective pathogenicity (TOX2) in the fungus Cochliobolus carbonum governs production of a cyclic tetrapeptide named HC-toxin. We have isolated a chromosomal region, 22 kilobases (kb) long, that contains a 15.7-kb open reading frame (HTS1) encoding a multifunctional cyclic peptide synthetase. The 22-kb chromosomal region is duplicated in toxin-producing isolates of the fungus but is completely absent from the genomes of toxin-nonproducing isolates. Mutants of the fungus with disruptions in both copies of HTS1, at either of two different sites within HTS1, were engineered by DNA-mediated transformation. Disruption of both copies at either site resulted in loss of ability to produce HC-toxin and loss of host-selective pathogenicity, but the mutants displayed different biochemical phenotypes depending on the site of disruption. The results demonstrate that TOX2 encodes, at least in part, a large, multifunctional biosynthetic enzyme and that the evolution of host range in C. carbonum involved the insertion or deletion of a large piece of chromosomal DNA.

Journal Article↗

Identification of multiple structural domains regulating viroid pathogenicity.

To investigate the role of individual structural domains in viroid pathogenicity and replication, a series of interspecific chimeras was constructed by exchanging the terminal left (TL) and/or pathogenicity (P) domains between tomato apical stunt (TASVd) and citrus exocortis (CEVd) viroids. All six chimeras tested were replicated stably in tomato, and the symptoms exhibited by infected plants were intermediate between those induced by the parental viroids. Quantitative comparisons of symptom development and progeny accumulation revealed that: (i) the TL domain of TASVd contains a determinant required for appearance of severe veinal necrosis in tomato, (ii) the severe epinasty and stunting characteristic of TASVd requires the presence of its TL and P domains, and (iii) the variable (V) and terminal right (TR) domains comprising the right side of the native structure also play an important role in viroid pathogenicity. Chimeras containing the right side of TASVd accumulated to higher levels early in infection, and infected plants developed more severe symptoms than those whose right halves were derived from CEVd. Although the individual contributions of the TL and P domains to symptom induction could not be completely separated from that of viroid titer, the TL domain appears to exert a greater effect upon symptom severity than does the P domain. The TL, P, V, and TR domains of TASVd and CEVd contain three discrete regions of sequence and/or structural variability that may correspond to the pathogenicity determinants uncovered by our genetic analysis.

Base Sequence↗

Isolation of phytoalexin-deficient mutants of Arabidopsis thaliana and characterization of their interactions with bacterial pathogens.

A genetic approach was used to assess the extent to which a particular plant defense response, phytoalexin biosynthesis, contributes to Arabidopsis thaliana resistance to Pseudomonas syringae pathogens. The A. thaliana phytoalexin, camalexin, accumulated in response to infection by various P. syringae strains. No correlation between pathogen avirulence and camalexin accumulation was observed. A biochemical screen was used to isolate three mutants of A. thaliana ecotype Columbia that were phytoalexin deficient (pad mutants). The mutations pad1, pad2, and pad3 were found to be recessive alleles of three different genes. pad1 and pad2 were mapped to chromosome IV and pad3 was mapped to chromosome III. Infection of pad mutant plants with strains carrying cloned avirulence genes revealed that the pad mutations did not affect the plants' ability to restrict the growth of these strains. This result strongly suggests that in A. thaliana, phytoalexin biosynthesis is not required for resistance to avirulent P. syringae pathogens. Two of the pad mutants displayed enhanced sensitivity to isogenic virulent P. syringae pathogens, suggesting that camalexin may serve to limit the growth of virulent bacteria.

Arabidopsis↗

Defense activation and enhanced pathogen tolerance induced by H2O2 in transgenic tobacco.

Transgenic tobacco deficient in the H2O2-removing enzyme catalase (Cat1AS) was used as an inducible and noninvasive system to study the role of H2O2 as an activator of pathogenesis-related (PR) proteins in plants. Excess H2O2 in Cat1AS plants was generated by simply increasing light intensities. Sustained exposure of Cat1AS plants to excess H2O2 provoked tissue damage, stimulated salicylic acid and ethylene production, and induced the expression of acidic and basic PR proteins with a timing and magnitude similar to the hypersensitive response against pathogens. Salicylic acid production was biphasic, and the first peak of salicylic acid as well as the peak of ethylene occurred within the first hours of high light, which is long before the development of tissue necrosis. Under these conditions, accumulation of acidic PR proteins was also seen in upper leaves that were not exposed to high light, indicating systemic induction of expression. Short exposure of Cat1AS plants to excess H2O2 did not cause damage, induced local expression of acidic and basic PR proteins, and enhanced pathogen tolerance. However, the timing and magnitude of PR protein induction was in this case more similar to that in upper uninfected leaves than to that in hypersensitive-response leaves of pathogen-infected plants. Together, these data demonstrate that sublethal levels of H2O2 activate expression of acidic and basic PR proteins and lead to enhanced pathogen tolerance. However, rapid and strong activation of PR protein expression, as seen during the hypersensitive response, occurs only when excess H2O2 is accompanied by leaf necrosis.

Catalase↗

A role for jasmonate in pathogen defense of Arabidopsis.

To investigate the role of jasmonate in the defense of plants against fungal pathogens, we have studied a mutant of Arabidopsis, fad3-2 fad7-2 fad8, that cannot accumulate jasmonate. Mutant plants were extremely susceptible to root rot caused by the fungal root pathogen Pythium mastophorum (Drechs.), even though neighboring wild-type plants were largely unaffected by this fungus. Application of exogenous methyl jasmonate substantially protected mutant plants, reducing the incidence of disease to a level close to that of wild-type controls. A similar treatment with methyl jasmonate did not protect the jasmonate-insensitive mutant coi1 from infection, showing that protective action of applied jasmonate against P. mastophorum was mediated by the induction of plant defense mechanisms rather than by a direct antifungal action. Transcripts of three jasmonate-responsive defense genes are induced by Pythium challenge in the wild-type but not in the jasmonate-deficient mutant. Pythium species are ubiquitous in soil and root habitats world-wide, but most (including P. mastophorum) are considered to be minor pathogens. Our results indicate that jasmonate is essential for plant defense against Pythium and, because of the high exposure of plant roots to Pythium inoculum in soil, may well be fundamental to survival of plants in nature. Our results further indicate that the fad3-2 fad7-2 fad8 mutant is an appropriate genetic model for studying the role of this important signaling molecule in pathogen defense.

Journal Article↗

Rapid evolution in plant chitinases: molecular targets of selection in plant-pathogen coevolution.

Many pathogen recognition genes, such as plant R-genes, undergo rapid adaptive evolution, providing evidence that these genes play a critical role in plant-pathogen coevolution. Surprisingly, whether rapid adaptive evolution also occurs in genes encoding other kinds of plant defense proteins is unknown. Unlike recognition proteins, plant chitinases attack pathogens directly, conferring disease resistance by degrading chitin, a component of fungal cell walls. Here, we show that nonsynonymous substitution rates in plant class I chitinase often exceed synonymous rates in the plant genus Arabis (Cruciferae) and in other dicots, indicating a succession of adaptively driven amino acid replacements. We identify individual residues that are likely subject to positive selection by using codon substitution models and determine the location of these residues on the three-dimensional structure of class I chitinase. In contrast to primate lysozymes and plant class III chitinases, structural and functional relatives of class I chitinase, the adaptive replacements of class I chitinase occur disproportionately in the active site cleft. This highly unusual pattern of replacements suggests that fungi directly defend against chitinolytic activity through enzymatic inhibition or other forms of chemical resistance and identifies target residues for manipulating chitinolytic activity. These data also provide empirical evidence that plant defense proteins not involved in pathogen recognition also evolve in a manner consistent with rapid coevolutionary interactions.

Amino Acid Sequence↗

HrpZ(Psph) from the plant pathogen Pseudomonas syringae pv. phaseolicola binds to lipid bilayers and forms an ion-conducting pore in vitro.

The hrp gene clusters of plant pathogenic bacteria control pathogenicity on their host plants and ability to elicit the hypersensitive reaction in resistant plants. Some hrp gene products constitute elements of the type III secretion system, by which effector proteins are exported and delivered into plant cells. Here, we show that the hrpZ gene product from the bean halo-blight pathogen, Pseudomonas syringae pv. phaseolicola (HrpZ(Psph)), is secreted in an hrp-dependent manner in P. syringae pv. phaseolicola and exported by the type III secretion system in the mammalian pathogen Yersinia enterocolitica. HrpZ(Psph) was found to associate stably with liposomes and synthetic bilayer membranes. Under symmetric ionic conditions, addition of 2 nM of purified recombinant HrpZ(Psph) to the cis compartment of planar lipid bilayers provoked an ion current with a large unitary conductivity of 207 pS. HrpZ(Psph)-related proteins from P. syringae pv. tomato or syringae triggered ion currents similar to those stimulated by HrpZ(Psph). The HrpZ(Psph)-mediated ion-conducting pore was permeable for cations but did not mediate fluxes of Cl-. Such pore-forming activity may allow nutrient release and/or delivery of virulence factors during bacterial colonization of host plants.

Animals↗

The alpha-helical D1 domain of the tobacco bZIP transcription factor BZI-1 interacts with the ankyrin-repeat protein ANK1 and is important for BZI-1 function, both in auxin signaling and pathogen response.

The tobacco (Nicotiana tabacum) bZIP transcription factor BZI-1 is involved in auxin-mediated growth responses and in establishing pathogen defenses. Transgenic plants expressing a dominant-negative BZI-1-DeltaN derivative, which lacks the N-terminal activation domain, showed altered vegetative growth. In particular auxin-induced rooting and formation of tobacco mosaic virus-induced hypersensitive response lesions are affected. BZI-1-related proteins described in various plant species share the conserved domains D1, D2, BD, and D4. To define those BZI-1 domains involved in transcription factor function, BZI-1 deletion derivatives were expressed in transgenic plants. The domains D1 or BD are crucial for BZI-1-DeltaN function in planta. The basic BD domain is mediating DNA binding of BZI-1. Yeast two-hybrid and in vitro binding studies reveal the ankyrin-repeat protein ANK1, which specifically interacts with a part of the BZI-1 protein (amino acids 73-222) encoding the D1 domain. ANK1 does not bind DNA or act as a co-activator of BZI-1-mediated transcription. Moreover, green fluorescence protein localization studies propose that ANK1 is acting mainly inside the cytosol. Transcription analysis reveals that ANK1 is ubiquitously expressed, but after pathogen attack transcription is transiently down-regulated. Along these lines, ANK1 homologous proteins in Arabidopsis thaliana have been reported to function in pathogen defense. We therefore propose that the D1 domain serves as an interaction surface for ANK1, which appears to regulate BZI-1 function in auxin signaling as well as pathogen response.

Amino Acid Sequence↗

Bacterial persistence within erythrocytes: a unique pathogenic strategy of Bartonella spp.

The genus Bartonella comprises human-specific and zoonotic pathogens responsible for a wide range of clinical manifestations, including Carrion's disease, trench fever, cat scratch disease, bacillary angiomatosis and peliosis, endocarditis and bacteremia. These arthropod-borne pathogens typically parasitise erythrocytes in their mammalian reservoir host(s), resulting in a long-lasting haemotropic infection. We have studied the process of Bartonella erythrocyte parasitism by tracking green fluorescent protein-expressing bacteria in the blood of experimentally infected animals. Following intravenous infection, bacteria colonise a yet enigmatic primary niche, from where they are seeded into the blood stream in regular intervals of approximately five days. Bacteria invade mature erythrocytes, replicate temporarily and persist in this unique intracellular niche for the remaining life span of the infected erythrocytes. A triggered antibody response typically results in an abrogation of bacteremia within 3 months of infection, likely by blocking new waves of bacterial invasion into erythrocytes. The recent establishment of genetic tools for Bartonella spp. permitted us to identify several putative pathogenicity determinants. Application of differential fluorescence induction technology resulted in the isolation of bacterial genes differentially expressed during infection in vitro and in vivo, including an unknown family of autotransporter proteins as well as a novel type IV secretion system homologous to the conjugation system of E. coli plasmid R388. Mutational analysis of a previously described type IV secretion system displaying homology to the virB locus of Agrobacterium tumefaciens provided the first example of an essential pathogenicity locus in Bartonella. Though required for establishing haemotropic infection, it remains to be demonstrated if this type IV secretion system is necessary for colonisation of the primary niche or for the subsequent colonisation of erythrocytes.

Animals↗

Various bacterial pathogens and symbionts infect the amoeba Dictyostelium discoideum.

The haploid soil amoeba Dictyostelium discoideum is a suitable model organism to study host-pathogen interactions with Legionella pneumophila. In this study we show that D. discoideum AX2 is also susceptible to infection with other important human pathogens and obligate intracellular symbionts. Infection assays demonstrated that Legionella-like amoebal pathogens (LLAP K62), Mycobacterium avium and the obligate intracellular endosymbionts of Acanthamoeba sp. strains TUME1, UWE25 and UWC6 were able to multiply within Dictyostelium. Salmonella typhimurium and Pseudomonas aeruginosa also invaded Dictyostelium, however were degraded shortly after uptake. Comitin-minus host cells were more permissive to infections with L. pneumophila and LLAP K62. Furthermore, this mutation significantly delayed the degradation of S. typhimurium. Accompanying electron and fluorescence microscopy of infected AX2 cells revealed that L. pneumophila and M. avium replicate within vacuoles, while LLAP K62, TUME1 and UWE25 were tightly enclosed by membranous structures within the cytoplasm. The beta-proteobacterium UWC6 was found to persist in the cytoplasm. The observed subcellular locations which correspond to the locations within the respective natural hosts suggest that D. discoideum is a representative model system for these pathogens and symbionts.

Acanthamoeba↗

Delivery of dangerous goods: type III secretion in enteric pathogens.

Type III secretion systems (TTSSs) of Gram-negative pathogens are molecular syringes that inject bacterial virulence factors directly into host cells. These virulence factors manipulate host cell pathways to aid bacterial survival within the host. Four important enteric pathogens use TTSSs to colonize and persist within the intestinal environment. The following is a brief review of the way in which TTSSs and their effectors contribute to the pathogenic nature of the prototypic diarrheal pathogens Salmonella, Shigella, Yersinia and enteropathogenic Escherichia coli (EPEC).

Dysentery, Bacillary↗

Recent pre-harvest supplementation strategies to reduce carriage and shedding of zoonotic enteric bacterial pathogens in food animals.

Food-borne bacterial illnesses strike more than 76 million North Americans each year. Many of these illnesses are caused by animal-derived foodstuffs. Slaughter and processing plants do an outstanding job in reducing bacterial contamination after slaughter and during further processing, yet food-borne illnesses still occur at an unacceptable frequency. Thus, it is imperative to widen the window of action against pathogenic bacteria. Attacking pathogens on the farm or in the feedlot will improve food safety all the way to the consumer's fork. Because of the potential improvement in overall food safety that pre-harvest intervention strategies can provide, a broad range of preslaughter intervention strategies are currently under investigation. Potential interventions include direct anti-pathogen strategies, competitive enhancement strategies and animal management strategies. Included in these strategies are competitive exclusion, probiotics, prebiotics, antibiotics, antibacterial proteins, vaccination, bacteriophage, diet, and water trough interventions. The parallel and simultaneous application of one or more preslaughter strategies has the potential to synergistically reduce the incidence of human food-borne illnesses by erecting multiple hurdles, thus preventing entry of pathogens into the food chain. This review emphasizes work with Escherichia coli O157:H7 to illustrate the various strategies.

Animal Feed↗

Gordon Memorial Lecture. Poultry mycoplasmas: sophisticated pathogens in simple guise.

Mycoplasmas are a genus within the class Mollicutes (trivial name mollicutes), which are the smallest known prokaryotes capable of self-replication. They have a very small genome, and have evolved to this 'minimalist' status by losing non-essential genes, including those involved in cell wall synthesis. The mollicutes exploit their limited genetic material to the maximum and many are successful pathogens in man, animals, birds and plants. Most of those of veterinary importance are in the genus Mycoplasma and include 4 poultry pathogens of economic importance: Mycoplasma gallisepticum, Mycoplasma synoviae, Mycoplasma meleagridis and Mycoplasma iowae. The pathogenetic mechanisms of mycoplasmas are not fully understood, but they are successful pathogens because they can enter the host and multiply, evade the defence mechanisms, cause damage and escape to infect new hosts. M. gallisepticum is one of several motile species and possesses a terminal tip structure that mediates adherence to its target tissues. For some species, including M. gallisepticum, some of the organisms may become intracellular. Some Mycoplasma species, including the pathogenic poultry species, have a remarkable ability to vary their major surface antigens, a mechanism that is thought to help them to persist in their host by evading the immune response. The molecular and cellular events that lead to the development of lesions and clinical disease are still obscure. Some lesions appear to be the result of indirect damage from the host's inflammatory and cellular responses. Despite short survival times in the environment, mycoplasmas are able to transmit successfully to new hosts. In poultry flocks there is both horizontal and vertical transmission, the former being encouraged by intensive husbandry and stress factors. Establishing the pathways of transmission and the possible role of other birds, such as game and wild birds, as intermediate vectors between poultry flocks is now greatly aided by the availability of modern molecular methods for strain typing.

Animals↗

Non-pathogenic bacteria modulate colonic epithelial gene expression in germ-free mice.

BACKGROUND: We established a bacterial reconstitution model to investigate epithelial cell-luminal bacteria interaction. The aim of the study was to identify the known genes directly or indirectly modulated by non-pathologic bacterial flora in the colonic epithelia of germ-free mice. METHODS: Germ-free mice were orally given a bacterial suspension prepared from specific pathogen-free counterparts (bacterial reconstitution). Colonic epithelial cells were isolated, then total and poly (A) RNA were extracted. We investigated differential gene expression in colonic epithelial cells among germ-free, bacteria-reconstituted, and specific pathogen-free mice by DNA microarray. Finally, differential expression was confirmed by Northern blot or quantitative RT-PCR. RESULTS: Thirty genes were initially selected as differentially expressed genes in DNA microarray analysis. We confirmed that genes associated with growth (Reg IIIbeta, Reg IIIgamma, guanylate nucleotide binding protein 2), apoptosis (Bcl-associated death promotor), cytoskeleton (tubulin alpha4, erythrocyte protein band 7.2), and immune response (lymphocyte antigen complex 6) were induced by bacterial reconstitution. In contrast, genes possibly participating in extracellular oxidant defence (selenoprotein P, metallothionein 1) and cellular metabolism (cytochrome P450, HMGCoA synthase 2, alcohol dehydrogenase 1 complex, aldehyde dehydrogenase family 1, carbonic anhydrase 1, glycoprotein galactosyltransferase alpha1,3) were down-regulated by bacterial challenge. CONCLUSION: Non-pathogenic bacteria modulated colonic gene expression in germ-free mice, suggesting that non-pathogenic bacteria possibly initiate epithelial change in genetically normal and/or abnormal hosts. The present study provides a basis for the functional study of each molecule in symbiosis with luminal bacteria in healthy and diseased colon.

Animals↗

Mastitis pathogens present in bulk tank milk from seven dairy herds in the Waikato region, New Zealand.

AIM: To identify and enumerate colony forming units (cfu) of mastitis pathogens in bulk tank milk (BTM) from pasture-fed New Zealand dairy cows in the Waikato region. METHODS: BTM samples from seven seasonal-calving dairy herds in the Waikato region were collected monthly from August to December 2004 (cows calved during July-September). Milk samples were cultured on blood aesculin and MacConkey agar plates for 24 h, and the number of mastitis pathogens identified and counted. RESULTS: Colonies identified in BTM included aesculin-positive streptococci, Staphylococcus aureus, coagulase-negative staphylococci (CNS), and coliforms; counts ranged from zero to >1,000 cfu/ml. Counts>1,000 cfu/ml for total aesculin-positive streptococci, CNS and coliforms were present in 48%, 51% and 11% of BTM samples, respectively. Counts of Staph. aureus ranged from zero to 1,000 cfu/ml, but first appeared in BTM samples only in October. Staphylococcus aureus was repeatedly isolated in BTM from 4/7 farms during the testing period. CONCLUSIONS: Counts of mastitis pathogens in this study appeared high relative to interpretive criteria set by other workers, which may indicate a high prevalence of mastitis risk factors on these farms. Interpretation of results is difficult as aesculin-positive streptococci, CNS and coliforms can be isolated from the environment as well as from cows with clinical or subclinical mastitis. Furthermore, Staph. aureus is inconsistently excreted from infected bovine mammary glands. More extensive study of this method is required in New Zealand to attempt to further validate the interpretation of results of bacterial culture of BTM. CLINICAL RELEVANCE: This method may be used to monitor challenge from mastitis pathogens over time as part of milk quality control programmes. The technique may be of use as a screening test to provide information to veterinarians, affording them the opportunity to have an input into mastitis control on dairy farms in New Zealand.

Animals↗

Hereditary non-polyposis colorectal cancer: identification of mutation carriers and assessing pathogenicity of mutations.

Hereditary non-polyposis colorectal cancer (HNPCC), also referred to as Lynch syndrome, is an autosomal dominantly inherited disorder that is characterized by susceptibility to colorectal cancer and extracolonic malignancies, in particular endometrial cancer. HNPCC is caused by pathogenic mutations in the mismatch repair (MMR) genes, which play an important role in maintaining genomic stability during DNA replication. Identification of MMR gene mutation carriers is important as this enables them to enrol in surveillance programmes, thus reducing their risk of cancer and increasing survival. Clinical criteria as well as non-clinical criteria have been formulated to select patients for mutation analysis. In this paper we review the approaches used to select patients for mutation analysis. Mutation analysis in the MMR genes may yield mutations of which the pathogenic nature is unclear. Criteria to determine the pathogenicity of such variants are discussed, as well as differences in design of functional assays to assess pathogenicity.

Base Pair Mismatch↗

The prevalence of potential pathogenic bacteria in nasopharyngeal samples from healthy children and adults.

OBJECTIVE: To elucidate the prevalence of potential pathogenic bacteria in nasopharyngeal samples from healthy individuals, and the influence on the carrier rate of age, season of the year, and type of child day care. DESIGN: Nasopharyngeal swab samples obtained in routine medical care from individuals with no sign of infection were studied in 159 pre-school children aged below 7 years, 198 schoolchildren aged 7-15 years, and 261 adults (.16 years). RESULTS: The prevalence of pathogenic bacteria in healthy individuals decreased with age. The overall isolation frequencies for pre-schoolchildren, schoolchildren, and adults, respectively, were: Moraxella catarrhalis (27%, 4% and 2%); Streptococcus pneumoniae (19%, 6% and 0.8%); Haemophilus influenzae (13%, 6% and 3%). The prevalence of S. pneumoniae in children 7-15 years was higher during the summer than in the winter. We could not confirm any variation in the carrier rate due to the type of child day care. CONCLUSION: Potentially pathogenic bacteria are often present in nasopharyngeal samples taken from healthy pre-school children, but rarely from people > or = 16 years of age. This means that the use of nasopharyngeal samples to discriminate between bacterial and viral respiratory tract infection needs to be evaluated further in patients < 16 years. The importance of the seasonal variation in the prevalence of potential pathogenic bacteria in the nasopharynx needs further study.

Adolescent↗

Prevalence of Fusobacterium necrophorum and other upper respiratory tract pathogens isolated from throat swabs.

Fusobacterium necrophorum, an anaerobic, Gram-negative rod, has been identified recently as a significant cause of persistent sore throat syndrome (PSTS). This disease is characterised by chronic, recurrent or persistent sore throat, which is believed to respond poorly to penicillin in vivo. The aim of this study is to examine the prevalence of F. necrophorum in all throat swabs received in our diagnostic microbiology department and to compare the results with those for other recognised respiratory pathogens. All throat swabs received in the laboratory over a four-week period were cultured for beta-haemolytic streptococcus groups A, C and G, Corynebacterium diphtheriae, Arcanobacterium haemolyticum and F. necrophorum. Latex agglutination techniques, phenotypic reactions and antibiograms are used to identify these organisms. The age of the patient and the clinical details as stated on the request form were noted. Among a total of 248 samples, 27 were positive for beta-haemolytic streptococcus group A, two were positive for beta-haemolytic streptococcus group C, five were positive for beta-haemolytic streptococcus group G and 24 were positive for F. necrophorum. The most common isolate in the under 20 age group was beta-haemolytic streptococcus group A. In the over 20 age group, F. necrophorum was the pathogen most frequently isolated. A clinical diagnosis of 'sore throat' was most likely to be positive for beta-haemolytic streptococcus group A, a clinical diagnosis of PSTS was most likely to be positive for F. necrophorum and a clinical diagnosis of 'tonsillitis' was equally likely to be caused by beta-haemolytic streptococcus group A or F. necrophorum. beta-haemolytic streptococcus group A was present in 11% of the samples and F. necrophorum was present in 10% of the samples. In total, these two pathogens accounted for 18.5% of throat infections in the sampled group. The results show that F. necrophorum is as significant a cause of throat infection as is beta-haemolytic streptococcus group A. Examination of this provisional data suggests that targeting culture towards these two pathogens may be possible in certain cohorts of patients if more precise clinical data are received from medical staff. However, based on the clinical symptoms routinely provided by clinicians requesting microscopy, culture and sensitivity on throat swabs, F. necrophorum culture is required on all throat swabs received in the laboratory.

Actinomycetaceae↗