Clinical features of double infection with tick-borne encephalitis and Lyme borreliosis transmitted by tick bite

Background: In Latvia and other endemic regions, a single tick bite has the potential to transmit both tick-borne encephalitis (TBE) and Lyme borreliosis. Objective: To analyse both the clinical features and differential diagnosis of combined tick-borne infection with TBE and Lyme borreliosis, in 51 patients with serological evidence, of whom 69% had tick bites. Results: Biphasic fever suggestive of TBE occurred in 55% of the patients. Meningitis occurred in 92%, with painful radicular symptoms in 39%. Muscle weakness occurred in 41%; in 29% the flaccid paralysis was compatible with TBE. Only two patients presented with the bulbar palsy typical of TBE. Typical Lyme borreliosis facial palsy occurred in three patients. Typical TBE oculomotor disturbances occurred in two. Other features typical of Lyme borreliosis detected in our patients were distal peripheral neuropathy (n = 4), arthralgia (n = 9), local erythema 1-12 days after tick bite (n = 7) and erythema chronicum migrans (n = 1). Echocardiogram abnormalities occurred in 15. Conclusions: Patients with double infection with TBE and Lyme borreliosis fell into three main clinical groups: febrile illness, 3 (6%); meningitis, 15 (30%); central or peripheral neurological deficit (meningoencephalitis, meningomyelitis, meningoradiculitis and polyradiculoneuritis), 33 (65%). Systemic features pointing to Lyme borreliosis were found in 25 patients (49%); immunoglobulin (Ig)M antibodies to borreliosis were present in 18 of them. The clinical occurrence of both Lyme borreliosis and TBE vary after exposure to tick bite, and the neurological manifestations of each disorder vary widely, with considerable overlap. This observational study provides no evidence that co-infection produces unusual manifestations due to unpredicted interaction between the two diseases. Patients with tick exposure presenting with acute neurological symptoms in areas endemic for both Lyme borreliosis and TBE should be investigated for both conditions. The threshold for simultaneous treatment of both conditions should be low, given the possibility of co-occurrence and the difficulty in ascribing individual neurological manifestations to one condition or the other.Peer reviewe

Diphtheritic polyneuropathy: a clinical study and comparison with Guillain-Barré syndrome

OBJECTIVES AND METHODS—Clinical features of 50 adults with diphtheritic polyneuropathy (DP) were studied in Riga, Latvia and compared with 21 patients with Guillain-Barré syndrome (GBS).
RESULTS—Neurological complications occurred in 15% of patients admitted to hospital with diphtheria and usually after severe pharyngeal infection. Bulbar dysfunction occurred in 98% of patients with DP and only 10% of patients with GBS. Limb weakness was mild or absent in 30% of patients with DP. Ventilation dependent respiratory failure occurred in 20% of patients with DP. The first symptoms of DP occurred 2-50 days after the onset of local diphtheria infection. Neurological deterioration in DP continued for a median of 49(range 15-83) days and improvement started 73 (range 20-115) days after onset. In 66% of patients with DP, the neuropathy was biphasic with a secondary worsening after 40 days. By contrast patients with GBS worsened for only 10 days on average (range 2-28 days) and improved after 21 (range 4-49) days. Eight patients with DP died, four from severe cardiomyopathy and four from multiple diphtheritic organ failure. Prolonged distal motor latencies (DMLs) were common to both DP and GBS, and more pronounced than motor conduction slowing. Limb symptoms continued after 1 year in 80% of the patients with DP, 6% were unable to walk independently, but independent respiratory and bulbar function had returned in all survivors. By comparison no patients with GBS died and none were severely disabled after 1 year. No death, in patients with DP occurred after antitoxin on days 1 or 2 after onset of diphtheria symptoms, whereas identical rates of death and peak severity of DP were seen both in those who received antitoxin on days 3-6 and those who did not receive it at all.
CONCLUSION—Diphtheric polyneuropathy is much more likely than GBS to have a bulbar onset, to lead to respiratory failure, to evolve more slowly, to take a biphasic course, and to cause death or long term disability. Antitoxin seems ineffective if administered after the second day of diphtheritic symptoms.


Peripheral neuropathy in chronic occupational inorganic lead exposure: a clinical and electrophysiological study

BACKGROUND AND OBJECTIVES—Traditionally the neuromuscular disorder associated with lead poisoning has been purely motor. This study assessed peripheral nerve function clinically and electrophysiologically in 46 patients with neuropathic features out of a total population of 151 workers with raised blood and/or urinary lead concentrations.
RESULTS—Average duration of occupational exposure for the neuropathic group ranged from 8-47 years (mean 21.7). Their mean blood lead concentration (SD) was 63.9 (18.3) µg/dl (normal <40), urinary lead 8.6 (3.3) µg/dl (normal<5.0), urinary coproporphyrins 66.7(38.4) µg/g creatinine (20-80), urinary aminolaevulinic acid 1.54(0.39) mg/g creatinine (0.5-2.5). All 46 had distal paraesthesiae, pain, impaired pin prick sensation, diminished or absent ankle jerks, and autonomic vasomotor or sudomotor disturbances. Reduced vibration sensation and postural hypotension were present in all 20 studied. None of these 46 patients had motor anormalities. Motor conduction velocity and compound muscle action potential amplitudes were normal, with marginally prolonged distal motor latencies. Sensory nerve action potential amplitudes lay at the lower end of the normal range, and the distal sensory latencies were prolonged. No direct correlation was found between the biochemical variables, and the clinical or electrophysiological data.
CONCLUSIONS—One additional patient was seen with shorter term exposure to lead fumes with subacute development of colicky abdominal pain, severe limb weakness, and only minor sensory symptoms. Unlike the patients chronically exposed to lead, he had massively raised porphyrins (aminolaevulinic acid 21 mg/g creatinine, coproporhyrins 2102 µg/g creatinine). Patients with unusually long term inorganic lead exposure showed mild sensory and autonomic neuropathic features rather than the motor neuropathy classically attributed to lead toxicity. It is proposed that the traditional motor syndrome associated with subacute lead poisoning is more likely to be a form of lead induced porphyria rather than a direct neurotoxic effect of lead.


Diphtheria with polyneuropathy in a closed community despite receiving recent booster vaccination

Introduction and Methods: We report 20 patients aged 18–24 years from Latvia with diphtheritic polyneuropathy. All lived in a closed community and 80% were known to have been fully vaccinated against diphtheria until at least 14 years old. Diphtheria antitoxin had been administered within 3 days of the onset of upper respiratory tract infection in 16 patients and 15 received antibiotics. Results: Neurological symptoms developed after a median of 43 days (range 35–58) compared to only 10 days in previous studies of unvaccinated patients. All showed evidence of mild limb polyneuropathy with electrophysiological evidence of polyneuropathy. Only 30% showed early bulbar abnormalities compared to the usual rate of over 95% in diphtheritic polyneuropathy. However, 45% had later bulbar deterioration coinciding with the limb polyneuropathy. Conclusions: These patients show that an attenuated form of polyneuropathy of later onset, with less prominent early bulbar features, can occur in patients vaccinated against diphtheria according to schedule but living in a closed community in a country where diphtheria remains endemic