A rare cause of acute flaccid paralysis: Human coronaviruses

Abstract

Acute flaccid paralysis (AFP) is a life-threatening clinical entity characterized by weakness in the whole body muscles often accompanied by respiratory and bulbar paralysis. The most common cause is Gullian–Barre syndrome, but infections, spinal cord diseases, neuromuscular diseases such as myasthenia gravis, drugs and toxins, periodic hypokalemic paralysis, electrolyte disturbances, and botulism should be considered as in the differential diagnosis. Human coronaviruses (HCoVs) cause common cold, upper and lower respiratory tract disease, but in the literature presentation with the lower respiratory tract infection and AFP has not been reported previously. In this study, pediatric case admitted with lower respiratory tract infection and AFP, who detected for HCoV 229E and OC43 co-infection by the real-time polymerase chain reaction, has been reported for the first time.

Introduction

Acute flaccid paralysis (AFP) is a clinical entity characterized by areflexia and/or hyporeflexia and weakness which reaches a maximum within days or weeks.[1] Polioviruses, enterovirus 71, flavivirus, herpes virus, and rabies virus are well-known as viral etiologic agents.[2] In this article, who presented with lower respiratory tract infection and AFP, and was detected to have co-infection of human coronavirus (HCoV) 229E and OC43 is reported. AFP associated with HCoV infections has not been reported previously in the literature, and has been reported for the first time in this article.

Case Report

A 3-year-old girl hospitalized due to the development of shortness of breath and inability to walk 1-day after the beginning of fever, rhinorrhea, cough, and weakness. On the same day, respiratory distress increased, she was intubated, and mechanical ventilation started. On physical examination, she was conscious but swallowing, chewing and speech functions damaged, muscle strength was 0/5 and deep tendon reflexes (DTRs) were absent, the plantar response was flexor. Physical examination of other systems was normal. Complete blood count, electrolytes and blood biochemistry and urinalysis were normal, C-reactive protein was negative and erythrocyte sedimentation rate was 20 mm/h. Chest radiography was normal. Cerebrospinal fluid (CSF) pressure, glucose, and protein were normal. Blood, urine, and CSF cultures were negative. Stool and nasal swab cultures were taken. Electroneuromyography (ENMG) revealed no pathological findings. No abnormalities in the brain and spinal cord magnetic resonance imaging were detected - so intracranial and spinal pathologies were excluded.

Intravenous antibiotherapy was given for 10 days. After 48 h of hospitalization, a total of 2 g/kg intravenous immunoglobulin (IVIG) in 3 days was given. Mechanical ventilation lasted 7 days. At the end of this period, muscle strength improved to 2–3/5, DTR became norm active, bulbar paralysis and respiratory distress had regressed. At the end of the 2^nd week, she could mobilize and walk with a guide. Lumbar puncture and ENMG repeated in the 3^rd week did not reveal any pathological findings and Gullian–Barre syndrome (GBS) was completely excluded. Real-time polymerase chain reaction (PCR) analysis of nasal swab samples was reported to be positive for HCoV 229E and OC43 and HCoV co-infection was diagnosed.

Discussion

Flaccid paralysis occurs by the damage of lower motor neurons in the anterior horn of the spinal cord or peripheral nerves either by direct invasion or parainfectious and/or postinfectious immune-mediated mechanisms.[2] Besides GBS, differential diagnosis of AFP includes: Compressive and inflammatory diseases of spinal cord, the anterior horn motor neurons involvement by infectious (poliomyelitis vaccine-associated poliomyelitis, other enteroviral myelitis, a Japanese encephalitis, and West Nile virus as agents) and vascular pathology, myasthenia gravis, drug and toxins affecting neuromuscular junction (aminoglycosides, organophosphates, snake venom and botulism, etc.), muscle disease such as viral myositis or inflammatory myopathy, hypokalemic periodic paralysis and electrolyte disorders (hypermagnesemia and hypokalemia).[3]

Preliminary diagnosis was GBS for this case; however, CSF and ENMG findings in the 1^st week of paralysis did not support this diagnosis. During the period of mechanical ventilation muscle strength increased and in this short time DTR normalized, as well as after 3 weeks paralysis started no pathologic findings observed by repeating lumbar puncture and ENMG so GBS was excluded. History, clinical presentation, physical examination, and laboratory tests were totally normal that ruled out toxicological etiology, polio, and botulismus.

Members of coronaviridae can cause respiratory, intestinal, hepatic and neurological diseases of various severities in humans and animals.[4] In particular, HCoV OC43 is a neurotrophic, neuroinvasive and neuroinflammatory virus. Experimental animal studies reported that HCoV OC43 causes flaccid paralysis and demyelination.[5] HCoVs can cause neurological symptoms such as seizures and meningoencephalitis in children[6] but AFP has not been reported until now.

HCoVs may cause more serious respiratory disease in case of immune suppression and with various respiratory agents rather than single infection.[7] In addition HCoV, 229 and OC43 co-infection causing more severe respiratory disease has been demonstrated by a study.[8] We have reported case of co-infection with HCoV 229E and OC43 detected by real-time PCR analysis of nasal swab samples, and additional different respiratory pathogen has not been demonstrated, it suggests that co-infection caused lower respiratory tract infection and AFP.

We believe that HCoV 229E and OC43 co-infection may cause respiratory failure and AFP. Whether IVIG have a role in the treatment needs to be supported by more data from the literature.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.