Role of infection due to Campylobacter jejuni in the initiation of Guillain-Barré syndrome.

Recent reports suggest that infection with Campylobacter jejuni, a common enteric pathogen, may cause Guillain-Barré syndrome (GBS) by triggering demyelination of peripheral nerves. GBS is preceded by an acute infectious illness (due to a variety of agents) in 50%-75% of cases; the onset of neurological symptoms is preceded by diarrhea in 10%-30% of cases. In the last decade, more than 20 published anecdotal reports and case series have described patients with C. jejuni infection documented 1-3 weeks before onset of GBS. Cultures of fecal samples obtained at the onset of neurological symptoms from patients with GBS have yielded C. jejuni in more than 25% of cases. A relatively rare serotype, Penner type O19, is overrepresented among isolates of C. jejuni from Japanese patients with GBS. Serological studies suggest that 20%-40% of patients with GBS have evidence of recent C. jejuni infection. In summary, infection with C. jejuni is a common antecedent to GBS and probably plays a role in initiating demyelination; although several pathogenic mechanisms are possible, none has been proven.

Serum antibodies to GM1, GD1b, peripheral nerve myelin, and Campylobacter jejuni in patients with Guillain-Barré syndrome and controls: correlation and prognosis.

Serum antibodies to monosialoganglioside (GM1), disialoganglioside (GD1b), and Campylobacter jejuni, measured by enzyme-linked immunosorbent assay and serum antibodies to peripheral nerve myelin, measured by the C1 fixation and transfer assay, were studied in 58 acute-phase patients with Guillain-Barré syndrome (GBS), 42 disease controls, and 29 normal controls. Anti-peripheral nerve myelin antibodies were elevated in 57 of 58 patients with GBS compared with controls, whereas only 8.6% had increased antibody titers to GM1 and 10.3% to GD1b. Only low antibody titers (GM1) or no antibodies (GD1b) were found in controls. More GBS patients (17.2%) than controls (7%) had antibodies to C jejuni. Poor recovery with inability to walk at 1 year after onset of symptoms was seen in 3 (5%) of the patients with GBS. All 3 patients had serological evidence of recent C jejuni infection but no antibodies to GM1 or GD1b. GBS patients with antibodies to GM1 or GD1b had excellent recovery. Our data indicate that antibodies to GM1 or GD1b do not necessarily mediate the extensive axonal damage seen in these severely affected patients.

A surgeon with AIDS. Lack of evidence of transmission to patients.

In January 1989 [corrected], the media reported the identity of a surgeon who was recently diagnosed with the acquired immunodeficiency syndrome (AIDS). Concern about surgeon-to-patient transmission of human immunodeficiency virus (HIV) persisted despite reassurances from health authorities. Therefore, HIV antibody testing was offered to the surgeon's patients. We identified 2160 patients operated on since 1982; none had been reported to Tennessee's AIDS registry. A total of 264 had already died; none were reported to have died of AIDS or other HIV-related diseases. Of the 1896 patients remaining, we contacted 1652; 616 (37%) were tested. Only one (an intravenous drug user) was HIV antibody positive, and his medical history suggested that he may already have had AIDS at the time of his surgery. These results support the concept that the risks to patients operated on by HIV-infected surgeons are most likely quite low and support recommendations for the individualized assessment of HIV-infected health care workers.

KIE: The authors attempted to notify and to offer HIV antibody testing to all patients who had been operated on by a Tennessee surgeon with AIDS during the seven years prior to his diagnosis. They found no evidence of HIV transmission to patients from the surgeon. Six hundred and sixteen former patients were screened for HIV; only one, an intravenous drug user, tested positive for HIV antibody. None of 2,160 former patients appeared on the Tennessee AIDS registry. None of 264 deceased patients were reported to have died of AIDS or of AIDS-related diseases. Mishu, et al. argue that their findings support the conclusion that risks to patients operated on by HIV-positive surgeons are probably quite low, and that each instance of a HIV-infected health worker should be assessed individually.

Foodborne hepatitis A: evidence that microwaving reduces risk?

During July 1988, 68 persons in Chattanooga, Tennessee, developed serologically confirmed hepatitis A. Between 15 June and 3 July, 93% of case-patients ate at a specific restaurant compared with only 3% of the local community. An intravenous drug user who worked as a cook was identified as the source. A case-control study was done to identify the vehicle of transmission. Case-patients were more likely than controls to have eaten hamburger buns and pickles, the only foods routinely handled after cooking. Of the restaurant patrons included in the study, 12 microwaved their food before consumption; none developed clinical illness despite eating large amounts of food handled after cooking. Sandwiches that were not microwaved were significantly associated with illness (odds ratio = 9.6; P less than .02). This epidemiologic evidence suggests that microwaves inactivate hepatitis A virus in food.

Salmonella enteritidis gastroenteritis transmitted by intact chicken eggs.

OBJECTIVE: To determine the source and to describe the clinical importance of a large outbreak of Salmonella enteritidis gastroenteritis in Tennessee, which is outside the geographic focus of the S. enteritidis pandemic. DESIGN: A case-control study and tracing of the source eggs. SETTING: A Tennessee community and a large layer farm in Indiana. PATIENTS: Case patients ate at the implicated restaurant and subsequently developed S. enteritidis gastroenteritis; controls ate with the case patients, but did not develop gastroenteritis. MEASUREMENTS: Eighty-one case patients were identified; 73 (90%) had eaten egg-containing sauces at a local restaurant on a given evening. The eggs were traced to their farm of origin in Indiana. The farm was inspected 5 weeks after the outbreak. MAIN RESULTS: Of 24 patients with culture-proved cases, 11 were hospitalized. Hollandaise and bernaise sauces prepared with intact, extra-large, grade-A eggs were strongly associated with illness (P less than 0.001). Salmonella enteritidis was isolated from specimens collected from chickens and the farm. Antimicrobial susceptibility patterns, phage typing, and plasmid profiles of isolates from the farm and from patients were indistinguishable. CONCLUSIONS: Salmonella enteritidis infection is a large and growing public health problem that is spreading beyond the northeastern United States. This study shows a direct link between infected poultry flocks and an outbreak of human illness.

Outbreaks of Salmonella enteritidis infections in the United States, 1985-1991.

The spread of Salmonella enteritidis infections in the United States was tracked to identify potential risk factors and preventive measures. Isolation rates and information regarding outbreaks of S. enteritidis from 1985 through 1991 were determined by reports to the national Salmonella surveillance system and through the foodborne disease outbreak surveillance system. From 1985 through 1991, 380 outbreaks were reported involving 13,056 ill persons and 50 deaths. The proportion of Northeast outbreaks fell from 81% in 1985 to 55% in 1991 as the number of outbreaks in other areas increased. Grade A shell eggs were implicated in 82% of outbreaks. Case-fatality rates in nursing homes and hospitals were 70 times higher than in other settings. Cultures of environmental or animal specimens from all farms tested yielded S. enteritidis. Eggborne S. enteritidis infections are a major public health problem. Preventive measures, including educating consumers about proper handling of eggs, using pasteurized eggs, and controlling infections on egg farms, may stem the impact of this disease.

Salmonella enteritidis outbreak in a restaurant chain: the continuing challenges of prevention.

In 1990, a Salmonella enteritidis (SE) outbreak occurred in a restaurant chain in Pennsylvania. To determine its cause(s), we conducted a case-control study and a cohort study at one restaurant, and a survey of restaurants. Egg dishes were associated with illness (P = 0.03). Guests from one hotel eating at the restaurant had a diarrhoeal attack rate of 14%, 4.7-fold higher than among those not eating there (P = 0.04). There were no differences in egg handling between affected and unaffected restaurants. Eggs supplied to affected restaurants were medium grade AA eggs from a single farm, and were reportedly refrigerated during distribution. Human and hen SE isolates were phage type 8 and had similar plasmid profiles and antibiograms. We estimate the prevalence of infected eggs during the outbreak to be as high as 1 in 12. Typical restaurant egg-handling practices and refrigeration during distribution appear to be insufficient by themselves to prevent similar outbreaks.

Guillain-Barré syndrome in northern China. The spectrum of neuropathological changes in clinically defined cases.

The pathology of the Guillain-Barré syndrome remains controversial, and autopsied cases available for study by contemporary techniques are uncommon. Large numbers of cases clinically diagnosed as Guillain-Barré syndrome occur in northern China. In this study we examined the neuropathological changes in 12 autopsied cases from Hebei Province, China. Eleven died early in the course of their disease. In all cases tissue was specially handled and fixed for electron microscopy and for immunocytochemistry. Three of these 12 cases had typical acute inflammatory demyelinating polyneuropathy (AIDP) with lymphocytic infiltration and macrophage-mediated demyelination, reproducing the pathological picture most often reported in Guillain-Barré syndrome in North America, Europe, and Australia. Six cases had predominantly axonal involvement, characterized by Wallerian-like degeneration of nerve fibres, with only minimal demyelination and with minimal inflammation in five. Three cases, even though paralysed at the time of death, had only very mild changes in the spinal roots and sciatic nerves. Within the group of six predominantly axonal cases, there were important differences both in the severity of the abnormalities and in the classes of fibres involved. Three cases had extensive Wallerian-like degeneration of sensory as well as motor fibres [acute motor-sensory axonal neuropathy (AMSAN)], while in the other three cases the fibre degeneration affected the motor nerve fibres almost exclusively. These latter cases establish a structural basis for the clinical and electrophysiological picture termed the acute motor axonal neuropathy (AMAN) pattern. In both the AMAN and the AMSAN patterns, a prominent feature was the presence of macrophages within the periaxonal space, surrounding or displacing the axon, and surrounded by an intact myelin sheath. These studies show that the early pathological changes in cases clinically diagnosed as the Guillain-Barré syndrome are diverse and not restricted to the well-known pattern of AIDP, and that the predominant pathological patterns may differ in different parts of the world. The differences in pathological findings between acute inflammatory demyelinating polyneuropathy and the axonal patterns are likely to reflect differences in the pathogenetic mechanisms. The periaxonal macrophages in the axonal patterns suggest that an important epitope may be localized to the axolemma or periaxonal space. The mild cases indicate that severe paralysis can occur early in Guillain-Barré syndrome without prominent structural changes along the nerve, suggesting that physiological block or nerve terminal changes may be implicated.

Serologic evidence of previous Campylobacter jejuni infection in patients with the Guillain-Barré syndrome.

OBJECTIVE: To determine if patients with the Guillain-Barré syndrome are likely to have had Campylobacter jejuni infection before onset of neurologic symptoms. DESIGN: A case-control study. SETTING: Several university medical centers. PATIENTS: Case patients met clinical criteria for the Guillain-Barré syndrome between 1983 and 1990 and had a serum sample collected and frozen within 3 weeks after onset of neurologic symptoms (n = 118). Disease controls were patients with other neurologic illnesses (n = 56); healthy controls were hospital employees or healthy family members of patients (n = 47). MEASUREMENTS: Serum IgA, IgG, and IgM antibodies to C. jejuni were determined by enzyme-linked immunosorbent assays. Assays were done in a blinded manner. RESULTS: Optical density ratios > or = 2 in two or more immunoglobulin classes were seen in 43 (36%) of patients with the Guillain-Barré syndrome and in 10 (10%) of controls (odds ratio, 5.3; 95% CI, 2.4 to 12.5; P < 0.001). Increasing the optical density ratio or the number of immunoglobulin classes necessary to yield a positive result increased the strength of the association. The number of patients with the Guillain-Barré syndrome who had positive serologic responses was greatest from September to November (P = 0.02). Male patients were three times more likely to have serologic evidence of C. jejuni infection (P = 0.009); the proportion of patients with the syndrome who had a positive serologic response increased with age. CONCLUSIONS: Patients with the Guillain-Barré syndrome are more likely than controls to have serologic evidence of C. jejuni infection in the weeks before onset of neurologic symptoms. Campylobacter jejuni may play a role in the initiation of the Guillain-Barré syndrome in many patients.

Guillain-Barré syndrome in northern China. Relationship to Campylobacter jejuni infection and anti-glycolipid antibodies.

Guillain-Barré syndrome has been considered to be primarily an acute inflammatory demyelinating polyneuropathy (AIDP). Our experience with Guillain-Barré syndrome in northern China differs from the traditional concept. Electrophysiologically and pathologically, most of our patients have motor axonal degeneration with minimal cellular inflammation, which we have termed 'acute motor axonal neuropathy' (AMAN). The current studies were undertaken to characterize prospectively the clinical, electrophysiological, and serological features of Guillain-Barré syndrome, defined clinically, in northern China. In 1991 and 1992, we characterized by electrodiagnostic criteria 129 Chinese patients with Guillain-Barré syndrome. The AMAN form was present in 65% of patients, the AIDP form in 24% and 11% were unclassifiable. For the 38 patients who presented from January to October, 1992, we performed serological assays for antibodies to Campylobacter jejuni and to glycolipids. Of these 38 patients, 55% had AMAN, 32% had AIDP and 13% were unclassifiable. Sixty-six percent of the 38 had serological evidence of recent C. jejuni infection as compared with 16% of village controls (P = 0.001). Seventy-six percent of AMAN patients and 42% of AIDP patients were seropositive. IgG anti-GM1 antibodies were more frequent in Guillain-Barré syndrome patients compared with village controls (42% versus 6%; P < 0.01). However, no statistically significant correlations were found between the pattern of disease, AMAN or AIDP, anti-glycolipid antibodies, or C. jejuni antibodies. Based on electrophysiological criteria, Guillain-Barré syndrome in northern China can be divided into two predominant forms: AIDP and AMAN. The AMAN form is more common and predominates in the yearly summer outbreaks of Guillain-Barré syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

A massive outbreak of type E botulism associated with traditional salted fish in Cairo.

In April 1991, 91 hospitalized patients in Cairo were reported to the Egyptian Ministry of Health with botulism intoxication. To define the spectrum of illness and identify a food vehicle, 45 patients were interviewed and a case-control investigation was conducted among families of 5 hospitalized patients. Clinical specimens and specimens of implicated food were tested for toxin and cultured for Clostridium botulinum. Hospitalized patients had symptoms consistent with botulism; 18 (20%) of 91 reported patients died. Illness was associated with eating faseikh (uneviscerated, salted mullet fish; lower 95% confidence limit of odds ratio = 6.6, P < .001). All 5 case-families purchased faseikh from one shop. Very high levels of type E botulinal toxin were detected in faseikh reported to be purchased from the implicated shop; C. botulinum type E was isolated from cultures of clinical specimens and from the faseikh. This is the first documented outbreak of botulism in Egypt and the largest type E outbreak ever reported.

Pathology of the motor-sensory axonal Guillain-Barré syndrome.

The concept of a severe motor-sensory neuropathy of acute onset caused by an immune attack on the axon ("axonal" Guillain-Barré syndrome) has been advanced primarily based on electrodiagnostic and limited pathological data, but remains controversial. At autopsy some cases demonstrate unusually severe inflammatory demyelinating neuropathy. There are conflicting data about whether antecedent Campylobacter jejuni infection is associated with "axonal" Guillain-Barré syndrome. We report 4 individuals from Hebei Province, China, who died 7, 7, 18, and 60 days after onset of a syndrome diagnosed clinically as Guillain-Barré syndrome. High titers of antibodies recognizing C. jejuni, consistent with recent infection, were found in the 2 patients tested. At autopsy the 3 with early disease had ongoing wallerian-like degeneration of fibers in the ventral and dorsal roots and in the peripheral nerves, with only minimal demyelination or lymphocytic infiltration. All 3 had numerous macrophages in the periaxonal space of myelinated internodes, and rare intraaxonal macrophages as well. Examination of the patient having the syndrome for 60 days confirmed the extensive loss of large fibers in the spinal roots and nerves, and the paucity of demyelination and remyelination. These observations confirm predictions that some patients with severe motor-sensory Guillain-Barré syndrome, as defined clinically, have predominantly axonal lesions of both motor and sensory fibers, even in the early stages of the disease, and that axonal Guillain-Barré syndrome can follow C. jejuni infection. The pathology supports the possibility that such cases of motor-sensory axonal Guillain-Barré syndrome represent the most severe end of a spectrum of immune attack directed toward epitopes on the axon.