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Lyme borreliosis is an infectious disease, caused by the spirochaete Borrelia burgdorferi and transmitted by ticks, in our regions by the tick Ixodes ricinus. The disease mainly affects skin, nervous system, joints and heart. Lyme borreliosis develops in three stages, and the various clinical manifestations may assigned to the respective stages. As far as skin is concerned, in stage I typically appears erythema chronicum migrans, very often accompanied by flu-like symptoms; in stage III, months to years after the manifestations of the early phase, acrodermatitis chronica atrophicans, may be encountered. Among the neurological manifestations, in stage II, meningoradiculoneuritis (Bannwarth's syndrome) develops as the most frequent disease, characterized by pheripheral paresis at the lower extremities and bilateral facial nerve palsy. Lyme arthritis mainly affects the knee. To assure the diagnosis of Lyme borreliosis, a number of serological tests is performed as the direct detection of the causative agent is rather difficult and time consuming. Possibly, the use of the polymerase chain reaction to detect B. burgdorferi DNA may improve the diagnostic tools.
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PMID:[Diagnosis of Lyme borreliosis]. 761 May 28

A 4-year-old boy showed two episodes of encephalitis/encephalopathy involving disturbed consciousness, convulsion, and paresis associated with the elevated levels of protein and myelin basic protein of the cerebrospinal fluid. MRI studies of the brain revealed symmetrical lesions in the brain stem and thalami at the first episode, and additional lesions were found in the cerebellum involving both the gray and white matter in the second episode. The intensities of MRI lesions were low in T I and high in T2. These episodes were followed by an elevation of the anti-viral antibody titers, for influenza A virus during the first episode and for adenovirus during the second. In the second episode, intravenous methylprednisolone therapy resulted in rapid improvement of his neurological signs.
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PMID:Acute relapsing encephalopathy mimicking acute necrotizing encephalopathy in a 4-year-old boy. 1059 58

The primary HIV infection is the period of time following HIV inoculation. Its manifestations are diverse. We present here some clinical cases: a mononucleosis-like syndrome with fever, angina, lymphadenopathy and skin rash, a frequent picture, with among other signs, flu-like symptoms, lymphocytic meningitis and facial paresis. In presence of those nonspecific clinical pictures, it is important for the primary health care physician to consider primary HIV infection, detect a history of exposure and order HIV-tests including p24-antigenemia. On one side, an early treatment blocks replication and dissemination of HIV in the body and brings an amelioration of prognosis. On the other side, the patient is particularly infectious during this phase and should take appropriate preventive measures.
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PMID:[Primary HIV infection, how to recognize it?]. 1068 11

The scientific literature of the past century is reviewed on fowl plague (presently termed highly pathogenic avian influenza, HPAI) in pigeons. HPAI viruses cause epidemic disease outbreaks with high rates of losses in many avian species, particularily in chickens and turkeys. Also susceptible to disease are quails, guinea fowl, ducks, geese, ostriches, passerine birds, and birds of prey whereas conflicting reports on the susceptibility of the domestic pigeon exist. Based on literature reports and on own experiments, and applying as criteria for judgements clinically overt forms of disease, virus multiplication plus shedding and seroconversion, it is concluded that domestic pigeons are only partially susceptible to influenza A viruses of the haemagglutinin subtype H7. Infection of pigeons with H7 viruses results only in some of them in signs, virus shedding and seroconversion. Using the same criteria, pigeons appear to be even less susceptible to infection with influenza A viruses of the H5 subtype. Only one of five publications describe in 1/19 pigeons exposed to H5 influenza A virus depression one day before death, and only 2/19 multiplied and excreted virus, and 1/19 developed circulating antibodies. Consequently, pigeons play only a minor role in the epidemiology of H5 influenza viruses. In contrast, following infection with influenza A virus of the subtype H7 clinical signs in pigeons consist of conjunctivitis, tremor, paresis of wings and legs, and wet droppings. H7-infected pigeons multiply and excrete H7 viruses and develop circulating antibodies. Albeit of the status of infection, free-flying domestic pigeons can act as mechanical vectors and vehicles for long-distance transmission of any influenza A virus if plumage or feet were contaminated.
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PMID:Review of the literature on avian influenza A viruses in pigeons and experimental studies on the susceptibility of domestic pigeons to influenza A viruses of the haemagglutinin subtype H7. 1564 16

A case of septic cavernous sinus thrombosis in 41 year old men is described. One week prior to hospitalisation he had an influenza infection. During influenza nose furunculus, labial herpes and viral left otitis media with facial nerve paresis occurred. Patient manipulated furunculus nasi. On admission to hospital he complained of severe hedeache, left ear pain and left visual loss. He had left orbital cellulitis with immobile eyeball, the left part of the face, neck and throat were swollen. Lumbar puncture showed cerebrospinal fluid containing protein 156 mg/dl, glucose 94 mg/dl, and 5888 polymorphonuclear cells. Cranial CT scan showed left exophatlmos with periorbital swelling, left ethmoid sinusitis, and probable thrombosis of cerebral vessels. Involvement of the right eye appeared after two days. He was treated with high dose of antibiotics, steroids and anticoagulants. After four days in the control cranial CT scan two focus of intracerebral hemorrhage were found in the frontal lobe. We excluded anticoagulants from the therapy. The patients improved slowly and he was discharged after 22 days of hospitalisation with the left abducent and facial nerve paresis.
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PMID:[Septic thrombosis of the cavernous sinus complicated by intracerebral hemorrhage]. 1652 56

One week after a flu-like prodrome, an 18-month-old boy developed acute severe, symmetrical, painless weakness and wasting of the shoulder girdle and upper limbs, drooling, dysphagia, dysarthria, atrophy and fasciculations of the tongue. Milder paresis involved the mimic muscles and the neck extensors. The legs were intact with brisk reflexes. The flail immobile upper limbs produced the appearance that the boy was restrained in a narrow barrel. Electrodiagnostic findings suggested demyelinating motor neuropathy sparing the legs. CSF (45 days after onset) was normal. Initial recovery was observed but 70 days after onset the child suffered severe relapse and died from respiratory arrest. This is another rare case of the pharyngeal-cervical-brachial variant of Guillain-Barre syndrome in infancy with an unusual relapsing course leading to a fatal outcome.
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PMID:The "Child in the Barrel syndrome"--severe pharyngeal-cervical-brachial variant of Guillain-Barre Syndrome in a toddler. 1956 2

A clinical-electroneuromyographical study of 40 children (32 (80%) of them aged from 12 to 17 years, mean age 13,9+/-1,8 years, and 8 (20%) - from 1 to 8 years, mean age 4,4+/-2,1 years) were studied in the acute period of facial nerve paralysis (FNP). Six (15%) children had FNP in the anamnesis. Among precipitating factors were the cold exposure the day before disease onset (20 (50%) patients), symptoms of flu (13 (32,5%) patients) and psycho-emotional tension (3 (7,5%) patients). No precipitation was noted in 4 (10%) children. The degree of muscle paresis was 81,9+/-7% that corresponded to clinical stages III-IV according to K. Rosler. An electroneuromyographical analysis of motor ortho- and antidromic response to the facial nerve stimulation on the side of paresis and on the contralateral side in patients and controls revealed the presence of proximal axon- and myelinopathy of facial nerve with the involvement of its own motorneurons and brain stem interneurons. The maintenance of wink reflex and F-wave blocks in the period over 3 weeks are prognostically unfavorable factors for restoration of mimic muscle function in the early stage of disease.
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PMID:[Clinical-electroneuromyographical characteristics of facial nerve paralysis in children]. 2003 48

A 73-year-old man was admitted to our hospital with a high fever and left paresis. A rapid diagnosis test was positive for influenza A was positive by rapid diagnosis test and diffusion-weighted MRI imaging of the brain showed a high intensity lesion of the right cerebral peduncle. The patient was therefore diagnosed as having influenza A virus infection complicated with lacunar infarction. In spite of initial treatment with oseltamivir and anticoagulant therapy, he lost consciousness eight hours after admission. The high intensity lesion of the cerebral peduncle enlarged and new lesions in the thalamus, hippocampus and calcarine cortex were detected with brain MRI. Additionally, an electroencephalographic study showed an entire slow wave and as the other causative pathogens of central nerve system infection were not detected, the likely diagnosis was influenza-associated encephalitis. We administered a high dose of intravenous immunoglobulin since the low-grade fever and mild unconscious state had continued in spite of the treatment with methylprednisolone pulse therapy. His consciousness was restored and body temperature became normal immediately. We could confirm the efficacy of our treatment by measurement of IL-6 levels in the serum and cerebrospinal fluid during the entire clinical course. In conclusion, a high dose of intravenous immunoglobulin therapy might be one of the effective treatments for influenza-associated encephalitis.
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PMID:[An adult case of influenza-associated encephalitis successfully treated with high dose intravenous immunoglobulins]. 2274 53

Highly pathogenic avian influenza A (HPAI), subtype H5N1, remains an emergent threat to the human population. While respiratory disease is a hallmark of influenza infection, H5N1 has a high incidence of neurological sequelae in many animal species and sporadically in humans. We elucidate the temporal/spatial infection of H5N1 in the brain of ferrets following a low dose, intranasal infection of two HPAI strains of varying neurovirulence and lethality. A/Vietnam/1203/2004 (VN1203) induced mortality in 100% of infected ferrets while A/Hong Kong/483/1997 (HK483) induced lethality in only 20% of ferrets, with death occurring significantly later following infection. Neurological signs were prominent in VN1203 infection, but not HK483, with seizures observed three days post challenge and torticollis or paresis at later time points. VN1203 and HK483 replication kinetics were similar in primary differentiated ferret nasal turbinate cells, and similar viral titers were measured in the nasal turbinates of infected ferrets. Pulmonary viral titers were not different between strains and pathological findings in the lungs were similar in severity. VN1203 replicated to high titers in the olfactory bulb, cerebral cortex, and brain stem; whereas HK483 was not recovered in these tissues. VN1203 was identified adjacent to and within the olfactory nerve tract, and multifocal infection was observed throughout the frontal cortex and cerebrum. VN1203 was also detected throughout the cerebellum, specifically in Purkinje cells and regions that coordinate voluntary movements. These findings suggest the increased lethality of VN1203 in ferrets is due to increased replication in brain regions important in higher order function and explains the neurological signs observed during H5N1 neurovirulence.
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PMID:Neurovirulence of H5N1 infection in ferrets is mediated by multifocal replication in distinct permissive neuronal cell regions. 2305 66

Clinical trials have shown that AS03-adjuvanted H5N1 and A(H1N1)pdm09 vaccines are highly immunogenic, although with an increased reactogenicity profile relative to non-adjuvanted vaccines in terms of the incidence of common injection site and systemic adverse events (AEs). We evaluated pooled safety data from 22,521 adults who had received an AS03-adjuvanted H5N1 or A(H1N1)pdm09 influenza or control vaccine with the purpose to identify medically-attended AEs (MAEs), including subsets of serious AEs (SAEs), potentially immune-mediated diseases (pIMDs), and AEs of special interest (AESI), and to explore a potential association of these AEs with the administration of an AS03-adjuvanted influenza vaccine. For participants who had received an AS03-adjuvanted vaccine, the relative risks (RRs) for experiencing a MAE or a SAE compared to control group (participants who had received a non-adjuvanted vaccine or saline placebo) were 1.0 (95% confidence interval [CI]: 0.9; 1.1) and 1.1 (95% CI: 0.9; 1.4), respectively. The overall RRs for experiencing an AESI or a pIMD (AS03-adjuvanted vaccine/control) were 1.2 (95% CI: 0.9; 1.6) and 1.7 (95% CI: 0.8; 3.8), respectively. Thirty-8 participants in the AS03-adjuvanted vaccine group had a pIMD reported after vaccine administration, yielding an incidence rate (IR) of 351.9 (95% CI: 249.1; 483.1) per 100,000 person-years. The estimated IRs in the AS03-adjuvanted vaccine group were greater than the literature reported rates for: facial paresis/VIIth nerve paralysis, celiac disease, thrombocytopenia and ulcerative colitis. These results do not support an association between AS03-adjuvanted H5N1 and A(H1N1)pdm09 vaccines and the AEs collected in the trials included in the analysis.
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PMID:Safety of AS03-adjuvanted inactivated split virion A(H1N1)pdm09 and H5N1 influenza virus vaccines administered to adults: pooled analysis of 28 clinical trials. 2548 67


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