Hepatitis A post-viral encephalitis

Abstract

We report a seven‐year‐old girl who developed a hepatitis A viral infection and encephalitis. The patient developed fever, abdominal pains and jaundice. Five days later she became delirious, combative, and did not respond to verbal commands. Laboratory studies showed elevated liver enzymes and elevated serum immunoglobulin M (IgM) and immunoglobulin G (IgG) antibodies to hepatitis A virus. Cerebrospinal fluid contained IgG antibodies to hepatitis A virus but not IgM antibodies. Polymerase chain reaction, which amplifies a portion of the hepatitis A virus genome, did not demonstrate viral nucleic acid in cerebrospinal fluid. These studies suggest that the patient may have suffered from a post‐viral hepatitis A encephalitis from which she fully recovered.

Evidence of hepatitis A virus infection in the patients with acute encephalitis syndrome in Gorakhpur region, North India

“…Lower glucose (< 50 mg/dl) and relatively higher protein (> 50 mg/dl) levels noted in anti-HAV IgM-positive CSF samples were in agreement with those reported earlier in acute infections with herpes, varicella zoster and mumps viruses (Hammond et al, 1982;Ekmekci et al, 2013). Further, CSF pleocytosis associated with anti-HAV IgM/IgG positivity in the CSF of AES patients was in concurrence with that of the previously reported HAV-associated encephalitis cases (Davis et al, 1993;Lee et al, 2011) and suggested active inflammatory response in this group of patients. A few case reports have been described earlier on the occurrence of encephalitis following the preceding/prodromal stage of hepatitis A (Hammond et al, 1982;Davis et al, 1993;Cam et al, 2005;Lee et al, 2011;Yis et al, 2013).…”

“…Further, CSF pleocytosis associated with anti-HAV IgM/IgG positivity in the CSF of AES patients was in concurrence with that of the previously reported HAV-associated encephalitis cases (Davis et al, 1993;Lee et al, 2011) and suggested active inflammatory response in this group of patients. A few case reports have been described earlier on the occurrence of encephalitis following the preceding/prodromal stage of hepatitis A (Hammond et al, 1982;Davis et al, 1993;Cam et al, 2005;Lee et al, 2011;Yis et al, 2013). This is the first report on the role of hepatitis A demonstrating increase in the severity of the AES, in sizeable group of AES patients.…”

Aseptic Meningitis and Infection-Associated Hemophagocytic Lymphohistiocytosis—Rare Complications of Hepatitis A Virus İnfection

“…9 Associated with HAV infection, Mathew et al 6 reported focal meningoencephalitis in an 11-year-old Indian boy with focal meningeal enhancement in left temporoparietooccipital region, Lee et al 5 reported encephalitis in a 27-year-old Korean male, and Breningstall and Belani 10 reported brainstem encephalitis leading to paraplegia in a 4-year-old boy. Davis et al 11 reported encephalitis in a 7-year-old girl with HAV infection with normal neuroimaging, and PCR did not demonstrate viral nucleic acid in CSF. Yiş et al 1 described a 14-year-old boy with widespread patchy hyperintense lesions in white matter of frontal and temporal lobes, corona radiata, and insular cortex in anicteric phase of hepatitis A. Oleszak et al 7 reported multiphasic disseminated encephalitis following HAV infection in a 7-year-old girl with multiple multifocal hyperintense lesions of various sizes, disseminated throughout cerebral white matter, bilateral thalami, and spinal cord.…”

Neuromuscular complications of hepatitis A virus infection and vaccines

“…To date, there is no proof that HAV enters the CSF [17,18,20]; however, the relatively late collection of CSF after onset of GBS may result in an inability to detect viral RNA [45].…”

“…A variety of neurological syndromes have been reported in serologically confirmed hepatitis A including encephalitis [15][16][17][18][19], meningoencephalitis [20], meningitis [16,18,19], and acute transverse myelitis (ATM) [15,18]. A causal relationship between HAV and neurologic disease has not been established [21], but potential mechanisms of neural injury include: (a) cell-mediated immunity, because lymphocytes from patients with ATM transformed in vitro in response to peripheral nerve protein [22]; (b) possible neurotropism [23], and (c) possible immune complex disease [24].…”