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Campylobacter jejuni infection is an important trigger of Guillain-Barré syndrome (GBS), and serotype HS:19 strains are over-represented among GBS-associated isolates. Structures in C. jejuni lipooligosaccharide (LOS) resemble human gangliosides, suggesting that molecular mimicry could be important in triggering the neural injury. We assessed the genetic diversity among 36 C. jejuni serotype HS:19 and non-HS:19 strains by analysis of PCR-based restriction fragment length polymorphism (RFLP) patterns of 12 LOS biosynthesis-related genes (wla cluster). PCR amplification revealed that the size, order, and direction of each wla gene was identical among all strains tested. However, an additional ORF, located between wlaI and wlaK, was detected in 28 of the 36 isolates examined, and nucleotide sequence analysis revealed that the gene was identical to orfE in C. jejuni strain NCTC 11168. An inverted repeat motif was found downstream of the wlaI stop codon and upstream of the orfE stop codon, an organization allowing pairing of repeated sequences that could lead to deletion of the internal segment. Digestion of the PCR products with restriction endonuclease DdeI or AluI and cluster analysis of RFLP banding patterns showed that all HS:19 strains were closely related and distinct from non-HS:19 strains, consistent with earlier analyses, suggesting that HS:19 strains represent a highly clonal population. RFLP analysis of wla genes also may be useful for epidemiological studies.

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Infection with Campylobacter jejuni is one of the most common causes of gastroenteritis worldwide; it occurs more frequently than do infections caused by Salmonella species, Shigella species, or Escherichia coli O157:H7. In developed countries, the incidence of Campylobacter jejuni infections peaks during infancy and again during early adulthood. Most infections are acquired by the consumption and handling of poultry. A typical case is characterized by diarrhea, fever, and abdominal cramps. Obtaining cultures of the organism from stool samples remains the best way to diagnose this infection. An alarming recent trend is the rapid emergence of antimicrobial agent--resistant Campylobacter strains all over the world. Use of antibiotics in animals used for food has accelerated this trend. It is fortunate that complications of C. jejuni infections are rare, and most patients do not require antibiotics. Guillain-Barré syndrome is now recognized as a post-infectious complication of C. jejuni infection, but its incidence is <1 per 1000 infections. Careful food preparation and cooking practices may prevent some Campylobacter infections.

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Guillain-Barré syndrome (GBS), a neurologic disease characterized by acute paralysis, is frequently preceded by Campylobacter jejuni infection. Serotype O19 strains are overrepresented among GBS-associated C. jejuni isolates. We previously showed that all O19 strains tested were closely related to one another by randomly amplified polymorphic DNA (RAPD) and restriction fragment length polymorphism analyses. RAPD analysis demonstrated a 1.4-kb band in all O19 strains tested but in no non-O19 strains. We cloned this O19-specific band; nucleotide sequence analysis revealed a truncated open reading frame with significant homology to DNA gyrase subunit B (gyrB) of Helicobacter pylori. PCR using the random primer and a primer specific for gyrB showed that in non-O19 strains, the random primer did not recognize the downstream gyrB binding site. The regions flanking each of the random primer binding sites were amplified by degenerate PCR for further sequencing. Although the random primer had several mismatches with the downstream gyrB binding site, a single nucleotide polymorphism 6 bp upstream from the 3' terminus was found to distinguish O19 and non-O19 strains. PCR using 3'-mismatched primers based on this polymorphism was designed to differentiate O19 strains from non-O19 strains. When a total of 42 (18 O19 and 24 non-O19) strains from five different countries were examined, O19 strains were distinguishable from non-O19 strains in each case. This PCR method should permit identification of O19 C. jejuni strains.

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Since the eradication of polio in most parts of the world, Guillain-Barré syndrome (GBS) has become the most common cause of acute flaccid paralysis. GBS is an autoimmune disorder of the peripheral nervous system characterized by weakness, usually symmetrical, evolving over a period of several days or more. Since laboratories began to isolate Campylobacter species from stool specimens some 20 years ago, there have been many reports of GBS following Campylobacter infection. Only during the past few years has strong evidence supporting this association developed. Campylobacter infection is now known as the single most identifiable antecedent infection associated with the development of GBS. Campylobacter is thought to cause this autoimmune disease through a mechanism called molecular mimicry, whereby Campylobacter contains ganglioside-like epitopes in the lipopolysaccharide moiety that elicit autoantibodies reacting with peripheral nerve targets. Campylobacter is associated with several pathologic forms of GBS, including the demyelinating (acute inflammatory demyelinating polyneuropathy) and axonal (acute motor axonal neuropathy) forms. Different strains of Campylobacter as well as host factors likely play an important role in determining who develops GBS as well as the nerve targets for the host immune attack of peripheral nerves. The purpose of this review is to summarize our current knowledge about the clinical, epidemiological, pathogenetic, and laboratory aspects of campylobacter-associated GBS.

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Guillain-Barré syndrome (GBS), an acute demyelinating peripheral neuropathy, may be triggered by an acute infectious illness; infection with Campylobacter jejuni is the most frequently reported antecedent event. In Japan, O:19 is the most common serotype among GBS-associated C. jejuni strains. To determine whether serotype O:19 occurs among GBS-associated strains in the United States and Europe, we serotyped seven such strains and found that two (29%) of seven GBS-associated strains from patients in the United States and Germany were serotype O:19. To determine whether GBS-associated strains may be resistant to killing by normal human serum (NHS), we studied the serum susceptibility of 17 GBS- and 27 enteritis-associated strains (including many O:19 and non-O:19 strains) using C. jejuni antibody positive (pool 1) or negative (pool 2) human serum. Using pool 1 serum we found that one (6%) of 18 serotype O:19 strains compared with 11 (42%) of 26 non-O:19 strains were killed; results using pool 2 serum were nearly identical. Finally, 8 O:19 and 8 non-O:19 strains were not significantly different in their ability to bind complement component C3. Serotype O:19 C. jejuni strains were overrepresented among GBS-associated strains in the United States and Germany and were significantly more serum-resistant than non-O:19 strains. The mechanism of this resistance appears unrelated to C3 binding.

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A previously unrecognized sequelum of infection with Campylobacter jejuni, a common cause of gastroenteritis, is Guillain-Barré syndrome (GBS). GBS is the most common cause of acute neuromuscular paralysis; 30% to 40% of cases are preceded by C. jejuni infection. Both patient and bacterial characteristics likely play a role in the pathogenesis of C. jejuni-induced GBS. Molecular mimicry between the LPS of some campylobacters and structures present on the gangliosides of the peripheral nerve may explain how this acute infectious diarrheal illness triggers GBS.

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Guillain-Barré syndrome (GBS), a neurologic disease that produces ascending paralysis, affects people all over the world. Acute infectious illnesses precede 50%-75% of the GBS cases. Although many infectious agents have been associated with GBS, the strongest documented association is with Campylobacter infection. The first line of evidence supporting Campylobacter infection as a trigger of GBS is anecdotal reports. The second line of evidence is serologic surveys, which have demonstrated that sera from GBS patients contain anti-Campylobacter jejuni antibodies, consistent with recent infection. Finally, culture studies have proven that a high proportion of GBS patients have C. jejuni in their stools at the time of onset of neurologic symptoms. Neurologic symptoms are more severe and more likely to be irreversible when GBS is preceded by C. jejuni infection. One of every 1058 Campylobacter infections results in GBS, and 1 of 158 Campylobacter type O:19 infections results in GBS.

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Guillain-Barré syndrome (GBS) is an autoimmune disease characterized by acute neuromuscular paralysis. Of an estimated annual number of 2628-9575 US cases, 526-3830 are triggered by Campylobacter infection. Research objectives were to identify the lifetime consequences of GBS and, when possible, to quantify their economic burden. The cost-of-illness method was used to calculate annual societal resources spent on medical care and lost productivity due to illness or premature death from Campylobacter-associated GBS. Estimated total costs (in US$) of Campylobacter-associated GBS ($0.2-$1.8 billion) were added to previously estimated costs of campylobacteriosis ($1.3-$6.2 billion) for a total annual cost from Campylobacter of $1.5-$8.0 billion (1995 dollars). It is concluded that up to $8.0 billion in US human illness costs are spent annually because of Campylobacter infection. Economic evaluation of the other costs associated with GBS, such as physical and psychological costs, would increase these estimates.

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Campylobacter jejuni serotype O19 strains associated with the Guillain-Barré syndrome (GBS) and other strains were examined by restriction fragment length polymorphism (RFLP) analysis of polymerase chain reaction products of the flaA genes and by random amplified polymorphic DNA (RAPD) analysis. RFLP analysis showed that regardless of LIO serotype, geographic origins, or association with GBS, the O19 isolates shared an identical digestion pattern by each of four restriction endonucleases, DdeI, MboI, MseI, and AluI. In contrast, among C. jejuni O1 or O2 strains, RFLP patterns were different even among strains of the same LIO serotype. The results of the RAPD analysis were consistent with the flaA RFLP data. These data indicate that all of the O19 strains that were tested were closely related to one another whether they were or were not associated with GBS.

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During an outbreak of type E foodborne botulism in Cairo in 1991, an investigational equine F(ab')2 "despeciated" heptavalent botulism immune globulin (dBIG) was provided to the Egyptian Ministry of Health by the U.S. Army. Of 54 patients known to have been treated with antitoxins, 4 received commercially available trivalent antitoxins, 45 received dBIG, and 5 received both commercial antitoxin and dBIG. Physicians recorded side effects in 10 (22%) of 45 patients who received dBIG; in nine cases, reactions were considered "mild," and in one case they were believed to be serum sickness. In contrast, possible serum sickness during hospitalization was recorded for two of four patients who were receiving commercial antitoxins. No complications of therapy were noted for any patient who was receiving both antitoxin types. In a separate study, 31 patients were contacted about their reactions to the antitoxin by telephone after discharge from the hospital. Seven (54%) of 13 patients attributed symptoms that they experienced while they were hospitalized to receipt of dBIG, while four (44%) of nine patients who indicated that they had received commercial antitoxins and one (20%) of five who received both commercial antitoxin and dBIG reported side effects before discharge. Data on the efficacy of the antitoxins were not obtained. In our experience, equine dBIG was at least as safe as commercially available antitoxins in treating type E foodborne botulism.

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OBJECTIVE: To investigate an outbreak of tuberculosis, determine the number of active cases and infections, and examine efforts to control the spread of disease. SETTING: A small town in Maine, in which no cases of tuberculosis had been reported in the previous 3 years. DESIGN: Epidemiologic investigation of an outbreak of tuberculosis infection and disease. MEASUREMENTS: A patient with an active case of tuberculosis was defined as a resident of the town or the surrounding area or an employee of the local shipyard who had a culture of sputum or tissue that was positive for Mycobacterium tuberculosis between June 1989 and May 1992. A case of tuberculous infection was defined as a positive tuberculin skin test result in a person with no previous positive test result. RESULTS: 21 active cases of tuberculosis occurred among shipyard workers and persons residing in the affected community between 1989 and 1992. One patient was the source of the outbreak; 8 months lapsed between the onset of this patient's illness and appropriate diagnosis and treatment. The M. tuberculosis strains isolated from this patient and from six other patients belonged to phage type I, auxiliary 14. All isolates were susceptible to drug treatment. Of 9898 persons who were tested, 697 (7%) were newly infected. Because isoniazid prophylaxis was not routinely offered to infected persons older than 35 years of age, only 341 (49%) infected persons completed isoniazid prophylaxis. CONCLUSIONS: Many secondary cases of tuberculosis occurred throughout this small Maine community because of delayed diagnosis and treatment of the source patient, delayed outbreak investigation, and failure to promote isoniazid prophylaxis to all persons infected during the outbreak. Aggressive efforts to identify persons with new infection are of limited value in controlling tuberculosis unless they are accompanied by an equally aggressive use of isoniazid prophylaxis.

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Between 19 March 1990 and 24 December 1992, six persons in Nova Scotia presented with a unique neurological illness. A prodrome of fever and headache was followed by neurogenic bladder, transverse myelitis, and encephalopathy in association with mononuclear pleocytosis of the CSF and nerve-conduction study findings consistent with polyradiculopathy. The spinal cords of three of the patients appeared abnormal on myelograms or magnetic resonance imaging studies. No microbial agent was isolated or demonstrated serologically. All of the patients were treated with antimicrobial agents and corticosteroids. Three recovered completely, but neurogenic bladder persisted in the remaining three. We suggest that this group of patients manifested an encephalomyeloradiculopathy that is likely a new clinical entity of infectious or parainfectious etiology.

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