Campylobacter Jejuni Infection Research Articles

Epidemiology of Campylobacter jejuni infections in Sweden, November 2011–October 2012: is the severity of infection associated with C. jejuni sequence type?

BackgroundCampylobacter jejuni is among the most frequent causes of bacterial gastroenteritis in Europe. Over 8,000 C. jejuni multilocus sequence typing sequence types (STs) have been described; ST-21 and ST-45 have been identified as the most frequent types in all human studies so far. In contrast to other STs, ST-22 has been associated with the Guillain–Barré syndrome and ST-677 was recently linked to severe systemic infections in Finland. We investigated risk factors associated with hospitalisation in individuals with C. jejuni infections acquired in Sweden.MethodsA total of 1,075 individuals with domestically acquired C. jejuni infection diagnosed between November 2011 and October 2012 in Sweden were included in this retrospective cohort study. Typing data for the isolates as well as clinical data including hospitalisation dates and diagnosis codes for individuals with C. jejuni infection were obtained. Factors associated with hospitalisation and length of hospitalisation were investigated by multivariable analysis.ResultsA total of 289 individuals were hospitalised due to C. jejuni infection (26.8%); those with co-morbidities were over 14 times more likely to become hospitalised than those without (odds ratio [OR]: 14.39, 95% confidence interval [CI]: 6.84–30.26). Those with underlying co-morbidities were also hospitalised longer than those without (4.22 days vs. 2.86 days), although this was not statistically significant. C. jejuni ST-257 (OR: 2.38; CI: 1.08–5.23), but not ST-22 or ST-677, was significantly associated with hospitalisation.ConclusionST-677 was not associated with increased hospitalisation or a longer hospital stay in our study whilst ST-257 was. However, individuals with C. jejuni infections were generally more frequently hospitalised than previously demonstrated; this requires further consideration including possible targeted interventions.

Recurrent Diplopia in a Pediatric Patient with Bickerstaff Brainstem Encephalitis.

Introduction. Acute complete external ophthalmoplegia is a rare finding in clinical practice that is associated with diseases affecting the neuromuscular junction, the oculomotor nerves, or the brainstem. Ophthalmoplegia has been reported with acute ataxia in Miller Fisher syndrome (MFS) and Bickerstaff brainstem encephalitis (BBE). Up to 95% of these cases are associated with anti-GQ1b antibodies. Only a small number of cases of anti-GQ1b negative MFS have been documented in pediatric patients. This is the first case reporting a recurrence of ocular symptoms in an anti-GQ1b antibody negative patient with BBE. Case Presentation. An 8-year-old Caucasian boy presented with complete external ophthalmoplegia without ptosis, cerebellar ataxia, and a disturbance of consciousness. He had recently recovered from a confirmed Campylobacter jejuni infection. On subsequent laboratory testing he was anti-GQ1b antibody negative. He had a recurrence of diplopia at four-week follow-up. Conclusions. This patient's recurrence of diplopia was treated with a five-week course of oral corticosteroids which did not worsen his condition, and this may be a therapeutic option for similar patients. We will discuss the symptoms and treatment of reported pediatric cases of anti-GQ1b antibody negative cases of MFS and the variation between cases representing a spectrum of illness.

Risk factors and clinical implication of superimposed Campylobacter jejuni infection in patients with underlying ulcerative colitis.

Background and aims: Superimposed Campylobacter jejuni infection (CJI) has been described in patients with ulcerative colitis (UC). Its risk factors and impact on the disease course of UC are not known. Our aims were to evaluate the risk factors for CJI in UC patients and the impact of the bacterial infection on outcomes of UC.Methods: Out of a total of 918 UC patients tested, 21 (2.3%) of patients were found to be positive for CJI (the study group). The control group comprised 84 age-matched UC patients who had tested negative for CJI. Risk factors for CJI and UC-related outcomes at 1 year after diagnosis of CJI were compared between the two groups.Results: Ten patients (47.6%) with CJI required hospital admission at the time of diagnosis, including eight for the management of “UC flare”. Treatment with antibiotics resulted in improvement in symptoms in 13 patients (61.9%). On multivariate analysis, hospital admission in the preceding year was found to be an independent risk factor for CJI [odds ratio (OR): 3.9; 95% confidence interval (CI): 1.1–14.1] and there was a trend for chronic liver disease as a strong risk factor (OR: 5.0; 95% CI: 0.9–28.3). At 1-year follow up, there was a trend for higher rates of UC-related colectomy (28.8% vs. 14.3%; P = 0.11), and mortality (9.5% vs. 1.2%; P = 0.096) in the study group.Conclusion: Recent hospitalization within 1 year was found to be associated with increased risk for CJI in UC patients. There was a trend for worse clinical outcomes of UC with in patients with superimposed CJI, which was frequently associated with UC flare requiring hospital admission.

Campylobacter jejuni capsular genotypes are related to Guillain–Barré syndrome

In about one in a thousand cases, a Campylobacter jejuni infection results in the severe polyneuropathy Guillain–Barré syndrome (GBS). It is established that sialylated lipo-oligosaccharides (LOS) of C. jejuni are a crucial virulence factor in GBS development. Frequent detection of C. jejuni with sialylated LOS in stools derived from patients with uncomplicated enteritis implies that additional bacterial factors should be involved. To assess whether the polysaccharide capsule is a marker for GBS, the capsular genotypes of two geographically distinct GBS-associated C. jejuni strain collections and an uncomplicated enteritis control collection were determined. Capsular genotyping of C. jejuni strains from the Netherlands revealed that three capsular genotypes, HS1/44c, HS2 and HS4c, were dominant in GBS-associated strains and capsular types HS1/44c and HS4c were significantly associated with GBS (p 0.05 and p 0.01, respectively) when compared with uncomplicated enteritis. In a GBS-associated strain collection from Bangladesh, capsular types HS23/36c, HS19 and HS41 were most prevalent and the capsular types HS19 and HS41 were associated with GBS (p 0.008 and p 0.02, respectively). Next, specific combinations of the LOS class and capsular genotypes were identified that were related to the occurrence of GBS. Multilocus sequence typing revealed restricted genetic diversity for strain populations with the capsular types HS2, HS19 and HS41. We conclude that capsular types HS1/44c, HS2, HS4c, HS19, HS23/36c and HS41 are markers for GBS. Besides a crucial role for sialylated LOS of C. jejuni in GBS pathogenesis, the identified capsules may contribute to GBS susceptibility.

Campylobacter jejuni infection and IgE sensitization in up to 2-year-old infants.

The "hygiene hypothesis" addresses the correlation between the occurrence of atopy and the frequency of infections in the earliest age, explaining an increase in the incidence of atopic diseases by living in good, infection-free, hygienic conditions. The aim of our study was to determine the conection between atopy and Camplobacter infection, and to analyze the association between serum concentrations of total IgE and Campyobacter infection in relation to atopy in children up to two years. A case control study was conducted with the sample of 98 infants of the average age of 8 months. Total serum IgE and Phadiatop infant multi-test were determined on Immunocap-100 (Phadia AB, Uppsala, Sweden). The presence of atopy was determined by detection of serum-specific IgE > 0.35 kUA/L (Phadiatop infant positive) and serum IgM, IgA, IgG levels against C j uni were determined by a quantitative immuno-enzyme test--SERION ELISA classic. Total IgE cut-off values > 15 kU/L point to atopy in infants, and tIgE cut-off values > or = 8.1 kU/L pointed to a Cj/uni infection in infants. Within the group of atopic children, tIgE levels > 29.8 kU/L point to C. jejuni infection, and within the group of non-atopic children, tIgE levels > or = 5.9 kU/L point to infection. Enteritis is not a predictor of C jejuni infection, because of a high frequency of asymptomatic cases of infection. The risk factors for C. jejuni infection are age and tIgE, and the protective factors are breastfeeding and atopy. C. jejuni infection increases the total serum IgE level, which is pre- dictive of infection, regardless of the presence of atopy. The presence of symptomatic C. jejuni infection reduces the risk of atopy in a child of the age of 5-24 months by the factor of 10.

Monitoring of <i>Campylobacter jejuni</i> Contamination in Different Links of Broiler Production Chain in Qingdao

Microbial monitoring of broiler production can provide an important theoretical basis for the prevention and control of animal diseases and reduce the pollution of the environment. In order to investigate the contamination and spread of Campylobacter jejuni in broiler production chain, we collected samples from the broiler farms, slaughterhouse and market of a big production chain in Qingdao, isolated and identified of Campylobacter jejuni. Then we used genotyping method to subtype the isolates. The result showed that C.jejuni were widespread in broiler pruduction chain, and the strains can spread during the production chain, so strengthen the scientific management of the production chain must be implemented. Control in the feeding, processing and preparation before eating of chicken are the important measures in reducing the Campylobacter jejuni infections caused by chicken.

Autoimmunity Links Vinculin to the Pathophysiology of Chronic Functional Bowel Changes Following Campylobacter jejuni Infection in a Rat Model.

Acute gastroenteritis can precipitate irritable bowel syndrome (IBS) in humans. Cytolethal distending toxin is common to all pathogens causing gastroenteritis. Its active subunit, CdtB, is associated with post-infectious bowel changes in a rat model of Campylobacter jejuni infection, including small intestinal bacterial overgrowth (SIBO). To evaluate the role of host antibodies to CdtB in contributing to post-infectious functional sequelae in this rat model. Ileal tissues from non-IBS human subjects, C. jejuni-infected and control rats were immunostained with antibodies to CdtB, c-Kit, S-100, PGP 9.5 and vinculin. Cytosolic and membrane proteins from mouse enteric neuronal cell lysates were immunoprecipitated with anti-CdtB and analyzed by mass spectrometry. ELISAs were performed on rat cardiac serum using CdtB or vinculin as antigens. Anti-CdtB antibodies bound to a cytosolic protein in interstitial cells of Cajal (ICC) and myenteric ganglia in C. jejuni-infected and naïve rats and human subjects. Mass spectrometry identified vinculin, confirmed by co-localization and ELISAs. Anti-CdtB antibodies were higher in C. jejuni-infected rats (1.27 ± 0.15) than controls (1.76 ± 0.12) (P < 0.05), and rats that developed SIBO (2.01 ± 0.18) vs. rats that did not (1.44 ± 0.11) (P = 0.019). Vinculin expression levels were reduced in C. jejuni-infected rats (0.058 ± 0.053) versus controls (0.087 ± 0.023) (P = 0.0001), with greater reductions in rats with two C. jejuni infections (P = 0.0001) and rats that developed SIBO (P = 0.001). Host anti-CdtB antibodies cross-react with vinculin in ICC and myenteric ganglia, required for normal gut motility. Circulating antibody levels and loss of vinculin expression correlate with number of C. jejuni exposures and SIBO, suggesting that effects on vinculin are important in the effects of C. jejuni infection on the host gut.

Risk Factors for Campylobacter jejuni Infection and Impact on the Disease Course in Patients With Ulcerative Colitis

Risk Factors for Campylobacter jejuni Infection and Impact on the Disease Course in Patients With Ulcerative Colitis

Wild-bird feces as a source of Campylobacter jejuni infection in children's playgrounds in Iran

Wild birds are important to public health, and they carry immerging zoonotic pathogens as a reservoir host. They often cause acute gastroenteritis in humans. Many playgrounds in parks are natural habitats for wild birds. Children's behavior, the frequent hand-mouth contact in this age group, is also likely to increase the risk of eating infective material. In this study, we looked into the likelihood that contamination by wild-birds of children's playground is a source of human infection. We did that by estimating the prevalence of Campylobacter spp. in fresh and dried wild-bird fecal samples. From July to August, 2013, we collected 200 samples of fresh and dried feces from 5 publicly accessible children's playgrounds in Mashhad, Iran. Our data by using a cultural method and a test, showed that 17.5% of feces samples contained Campylobacter spp. It was significantly (P < 0.05) more prevalent in the fresh samples (23.85%) than the dried samples (5.7%). We only detected one species of Campylobacter spp. from wild birds in this study. In conclusion, the results of this study showed wild bird species may set up a reservoir for Campylobacter spp. They could be of risk to humans. As far as we are aware, this is the first study in Iran to isolate Campylobacter spp. from children's playgrounds.

Campylobacter jejuni infection suppressed Cl⁻ secretion induced by CFTR activation in T-84 cells.

Campylobacter jejuni causes foodborne disease associated with abdominal pain, gastroenteritis, and diarrhea. These symptoms are induced by bacterial adherence and invasion of host epithelial cells. C.jejuni infection can occur with a low infective dose, suggesting that C.jejuni may have evolved strategies to cope with the bacterial clearance system in the gastrointestinal tract. The mucosa layer is the first line of defense against bacteria. Mucus conditions are maintained by water and anion (especially Cl(-)) movement. Cystic fibrosis transmembrane conductance regulator (CFTR) is the main Cl(-) channel transporting Cl(-) to the lumen. Mutations in CFTR result in dehydrated secreted mucus and bacterial accumulation in the lungs, and recent studies suggest that closely related pathogenic bacteria also may survive in the intestine. However, the relationship between C.jejuni infection and CFTR has been little studied. Here, we used an (125)I(-) efflux assay and measurement of short-circuit current to measure Cl(-) secretion in C.jejuni-infected T-84 human intestinal epithelial cells. The basic state of Cl(-) secretion was unchanged by C.jejuni infection, but CFTR activator was observed to induce Cl(-) secretion suppressed in C.jejuni-infected T-84cells. The suppression of activated Cl(-) secretion was bacterial dose-dependent and duration-dependent. A similar result was observed during infection with other C.jejuni strains. The mechanism of suppression may occur by affecting water movement or mucus condition in the intestinal tract. A failure of mucus barrier function may promote bacterial adhesion or invasion of host intestinal epithelial cells, thereby causing bacterial preservation in the host intestinal tract.

Healthy Baby, Healthy Me food safety curriculum.

Pregnant women are at increased risk for developing certain types of foodborne illness due to hormonal changes necessary during pregnancy to promote the survival of the fetus. Pathogens of special concern to pregnant women and their fetuses include Listeria monocytogenes, Toxoplasma gondii, Salmonella species, and Campylobacter jejuni. 1 Kendall P. Medeiros L. Hillers V. Chen G. DiMascola S. Food handling behaviors of special importance for pregnant women, infants and young children, the elderly, and immune-compromised people. J Am Diet Assoc. 2003; 103: 1646-1649 Abstract Full Text Full Text PDF PubMed Scopus (73) Google Scholar , 2 Smith J.L. Campylobacter jejuni infection during pregnancy: long-term consequences of associated bacteremia, Guillain-Barré Syndrome, and reactive arthritis. J Food Prot. 2002; 65: 696-708 PubMed Google Scholar Nutrition education curricula for pregnant women typically focus on basic food safety concepts, which may not address the pathogen-specific information pregnant women need to understand why they are at higher risk for certain foodborne illnesses, potential health risks to their fetus, and what foods and/or food preparation styles they should avoid to protect themselves and their unborn child. 3 Athearn P.N. Kendall P.A. Hillers V.N. et al. Awareness and acceptance of current food safety recommendations during pregnancy. Matern Child Health J. 2004; 8: 149-162 Crossref PubMed Scopus (58) Google Scholar

Fault bars and bacterial infection

Fault bars are conspicuous malformations on bird feathers that are produced during feather growth. The causes of fault bars are poorly understood. In our study, we used the presence of Campylobacter jejuni infection in 302 urban feral pigeons (Columba livia) as a proxy of physiological stress and correlated this stress with fault bar abundance. The overall prevalence of Campylobacter infection in these birds was 24.5 %. Bacterial infection was equally prevalent in young birds and adults, but males showed a slightly higher prevalence than females. Fault bars were more abundant in young birds than in adults, particularly among young males. Pigeons with Campylobacter infection had more fault bars than uninfected birds. These results suggest that the physiological state of the individual bird could be as important as external stressors in determining the occurrence of fault bars and that parasites may play a role in fault bar formation.

The role of serine protease HtrA in acute ulcerative enterocolitis and extra-intestinal immune responses during Campylobacter jejuni infection of gnotobiotic IL-10 deficient mice.

Campylobacter jejuni infections have a high prevalence worldwide and represent a significant socioeconomic burden. C. jejuni can cross the intestinal epithelial barrier as visualized in biopsies derived from human patients and animal models, however, the underlying molecular mechanisms and associated immunopathology are still not well understood. We have recently shown that the secreted serine protease HtrA (high temperature requirement A) plays a key role in C. jejuni cellular invasion and transmigration across polarized epithelial cells in vitro. In the present in vivo study we investigated the role of HtrA during C. jejuni infection of mice. We used the gnotobiotic IL-10−/− mouse model to study campylobacteriosis following peroral infection with the C. jejuni wild-type (WT) strain NCTC11168 and the isogenic, non-polar NCTC11168ΔhtrA deletion mutant. Six days post infection (p.i.) with either strain mice harbored comparable intestinal C. jejuni loads, whereas ulcerative enterocolitis was less pronounced in mice infected with the ΔhtrA mutant strain. Moreover, ΔhtrA mutant infected mice displayed lower apoptotic cell numbers in the large intestinal mucosa, less colonic accumulation of neutrophils, macrophages and monocytes, lower large intestinal nitric oxide, IFN-γ, and IL-6 as well as lower TNF-α and IL-6 serum concentrations as compared to WT strain infected mice at day 6 p.i. Notably, immunopathological responses were not restricted to the intestinal tract given that liver and kidneys exhibited mild histopathological changes 6 days p.i. with either C. jejuni strain. We also found that hepatic and renal nitric oxide levels or renal TNF-α concentrations were lower in the ΔhtrA mutant as compared to WT strain infected mice. In conclusion, we show here that the C. jejuni HtrA protein plays a pivotal role in inducing host cell apoptosis and immunopathology during murine campylobacteriosis in the gut in vivo.

Acute Motor-Sensory Axonal Neuropathy With Hyperreflexia in Guillain-Barré Syndrome

Guillain-Barré syndrome is an acute inflammatory autoimmune polyradiculoneuritis. Progressive motor weakness and areflexia are essential for its diagnosis. Hyperreflexia has rarely been reported in the early healing period of Guillain-Barré syndrome following Campylobacter jejuni infection in patients with acute motor axonal neuropathy with antiganglioside antibody positivity. In this study, we report a 12-year-old girl presenting with complaints of inability to walk, numbness in hands and feet, and hyperactive deep tendon reflexes since the onset of the clinical picture, diagnosed with acute motor-sensory axonal neuropathy type of Guillain-Barré syndrome.

Impact of Campylobacter jejuni cj0268c Knockout Mutation on Intestinal Colonization, Translocation, and Induction of Immunopathology in Gnotobiotic IL-10 Deficient Mice

BackgroundAlthough Campylobacter jejuni infections have a high prevalence worldwide and represent a significant socioeconomic burden, the underlying molecular mechanisms of induced intestinal immunopathology are still not well understood. We have recently generated a C. jejuni mutant strain NCTC11168::cj0268c, which has been shown to be involved in cellular adhesion and invasion. The immunopathological impact of this gene, however, has not been investigated in vivo so far.Methodology/Principal FindingsGnotobiotic IL-10 deficient mice were generated by quintuple antibiotic treatment and perorally infected with C. jejuni mutant strain NCTC11168::cj0268c, its complemented version (NCTC11168::cj0268c-comp-cj0268c), or the parental strain NCTC11168. Kinetic analyses of fecal pathogen loads until day 6 post infection (p.i.) revealed that knockout of cj0268c did not compromise intestinal C. jejuni colonization capacities. Whereas animals irrespective of the analysed C. jejuni strain developed similar clinical symptoms of campylobacteriosis (i.e. enteritis), mice infected with the NCTC11168::cj0268c mutant strain displayed significant longer small as well as large intestinal lengths indicative for less distinct C. jejuni induced pathology when compared to infected control groups at day 6 p.i. This was further supported by significantly lower apoptotic and T cell numbers in the colonic mucosa and lamina propria, which were paralleled by lower intestinal IFN-γ and IL-6 concentrations at day 6 following knockout mutant NCTC11168::cj0268c as compared to parental strain infection. Remarkably, less intestinal immunopathology was accompanied by lower IFN-γ secretion in ex vivo biopsies taken from mesenteric lymphnodes of NCTC11168::cj0268c infected mice versus controls.Conclusion/SignificanceWe here for the first time show that the cj0268c gene is involved in mediating C. jejuni induced immunopathogenesis in vivo. Future studies will provide further deep insights into the immunological and molecular interplays between C. jejuni and innate immunity in human campylobacteriosis.

Automatic Evaluation of Test Strips for Anti-Ganglioside Antibodies in Patients with Guillain-Barr&amp;#233; Syndrome Using EUROLineScan Software

Campylobacter jejuni infection has been implicated in the pathogenesis of Guillain-Barré syndrome (GBS) due to production of humoral immune response against neural antigens. A case-control study was performed in a tertiary care teaching hospital for the estimation of anti-ganglioside antibodies in GBS patients and their controls. Blood samples were collected from 59 GBS cases, 58 neurological controls (NC) and 60 non-neurological control (NNC) patients for automatic estimation of IgG and IgM antibodies to seven gangliosides using EUROLineScan software. Antibodies of IgG class for GM1 were highly significant in GBS (p = 0.000) and NC (p = 0.031) compared to NNC. However GBS group was not significant (p = 0.413) compared to NC. For GM2 ganglioside, GBS and NC groups were significant (p = 0.000) compared to NNC, but GBS group was not significant (p = 0.999) compared to NC. For GM3 ganglioside, GBS and NC groups were significant (p = 0.000) compared to NNC; but GBS group was insignificant (p = 0.858) compared to NC with similar trend for all other ganglioside antibodies. When IgM class of antibodies was evaluated for GM1, GBS group was not significant (p = 0.604) whereas NC group was significant (p = 0.000) compared to NNC. GBS group was not significant compared to NC (p = 0.011). The trend was the same for GM2 antibodies. For GM3, GBS group was significant (p = 0.010) and NC was near significant (p = 0.055) compared to NNC. However GBS group was not significant (p = 0.808) compared to NC. No groups were significant (p > 0.05) in relation to the remaining gangliosides except for GQ1b where GBS group (p = 0.001) and NC group were significant (p = 0.000) compared to NNC. GBS group was also significant (p = 0.001) compared to NC and NNC. Anti-gangliosides antibodies were present in highly significant levels in the GBS group, though they were also present in the non-paralytic neurological control patients compared to the non-neurological control group.

The impact of serine protease HtrA in apoptosis, intestinal immune responses and extra-intestinal histopathology during Campylobacter jejuni infection of infant mice.

BackgroundCampylobacter jejuni has emerged as a leading cause of bacterial enterocolitis. The serine protease HtrA has been shown to be a pivotal, novel C. jejuni virulence factor involved in cell invasion and transmigration across polarised epithelial cells in vitro. However, the functional relevance of the htrA gene for the interaction of C. jejuni with the host immune system in the infant mouse infection model has not been investigated so far.ResultsHere we studied the role of C. jejuni htrA during infection of 3-weeks-old infant mice. Immediately after weaning, conventional wild-type mice were perorally infected with the NCTC11168∆htrA mutant (∆htrA) or the parental wild-type strain. Approximately one third of infected infant mice suffered from bloody diarrhea until day 7 post infection (p.i.), whereas colonic histopathological changes were rather moderate but comparable between the two strains. Interestingly, parental, but not ∆htrA mutant infected mice, displayed a multifold increase of apoptotic cells in the colonic mucosa at day 7 p.i., which was paralleled by higher colonic levels of pro-inflammatory cytokines such as TNF-α and IFN-γ and the matrix-degrading enzyme matrixmetalloproteinase-2 (MMP-2). Furthermore, higher numbers of proliferating cells could be observed in the colon of ∆htrA infected mice as compared to the parental wild-type strain. Remarkably, as early as 7 days p.i. infant mice also exhibited inflammatory changes in extra-intestinal compartments such as liver, kidneys and lungs, which were less distinct in kidneys and lungs following ∆htrA versus parental strain infection. However, live C. jejuni bacteria could not be found in these organs, suggesting the induction of systemic effects during intestinal infection.ConclusionUpon C. jejuni ∆htrA strain infection of infant mice, intestinal and extra-intestinal pro-inflammatory immune responses were ameliorated in the infant mouse model system. Future studies will shed further light onto the molecular mechanisms of host-pathogen interactions.

Paraparetic Guillain‐Barré syndrome: Extending the axonal spectrum

AbstractThere are few reports of the paraparetic variant of Guillain‐Barré syndrome, and its pathophysiology is not well understood. We report a patient presenting with acute paraparesis following diarrhea. Serial nerve conduction studies suggested primary axonal injury, and not demyelination, predominantly in the lower limbs compared with the upper limbs. There was serological evidence of recent Campylobacter jejuni infection and strongly positive immunoglobulin G anti‐GD1a antibodies. Paraparetic Guillain‐Barré syndrome is likely to represent a regional form of Guillain‐Barré syndrome, with a nosological position within the axonal subtype.

SEASONAL VARIATION, SUB–TYPE AND PRODROMAL ILLNESSES IN GUILLAIN–BARRE SYNDROME

BackgroundStudies have produced contradictory evidence for seasonal variation in the incidence of Guillain–Barre Syndrome (GBS), possibly due to the potentially confounding factor of the prodromal illness, for example peaks in...

Campylobacter Jejuni and Cytopenias

BackgroundLeukopenia and thrombocytopenia in a febrile patient are not uncommon and may be a diagnostic clue in patients without an alternative explanation for cytopenias. This has not been reported in Campylobacter jejuni infections. MethodsA healthy patient with fever, rigors, and an acute diarrheal illness was noted to have a white blood cell count of 2.65 × 109/L and platelet level of 125 × 109/L. Retrospective chart review of all adult C. jejuni stool-positive cases admitted over 1 year revealed leukopenia in 6 of 20 (30%), thrombocytopenia in 5 of 20 (25%), and both in 1 of 20 (5%). ResultsCytopenias were mild, transient, and not associated with prolonged hospital stay or complications. ConclusionsAcute C. jejuni infections should be added to the differential diagnosis of acute febrile illnesses that may be associated with leukopenia or thrombocytopenia. Cytopenias can be an important diagnostic clue in febrile illnesses, and their differential is presented.