A liver, heart, iliac vessel, and two kidneys were recovered from a 39-year-old man who died of traumatic head injury and were transplanted into five recipients. The liver recipient eighteen days post-transplantation presented with headache, ataxia and fever, followed by rapid neurologic decline and death. Diagnosis of granulomatous amebic encephalitis (GAE) was made on autopsy. Balamuthia mandrillaris infection was confirmed with immunohistochemical and PCR assays. Donor and recipients' sera were tested for B. mandrillaris antibodies. Donor brain was negative for Balamuthia by immunohistochemistry and PCR; donor serum Balamuthia antibody titer was positive (1:64). Antibody titers in all recipients were positive (range, 1:64 to 1:512). Recipients received a 4- to 5-drug combination of miltefosine or pentamidine, azithromycin, albendazole, sulfadiazine, and fluconazole. Nausea, vomiting, elevated liver transaminases and renal insufficiency was common. All other recipients survived and have remained asymptomatic 24-months post-transplant. This is the third donor-derived Balamuthia infection cluster described in solid organ transplant recipients in the U.S. As Balamuthia serologic testing is only available through a national reference laboratory, it is not feasible for donor screening, but may be useful to determine exposure status in recipients and to help guide chemotherapy.

In a study to compare the prophylactic efficacy of passive and passive-active immunization against hepatitis B virus (HBV) among newborn infants of HBV carrier mothers positive for hepatitis B e in Korea, both regimens resulted in effective protection against development of hepatitis B surface antigen (HBsAg): 10 of 12 recipients of hepatitis B immune globulin (HBIG) and 25 of 29 recipients of HBIG and vaccine during nine months of follow-up. Among untreated controls in the same population just before the present study, 12 of 16 developed HBsAg within nine months of birth. Seven recipients of HBIG and vaccine and four untreated infants who had HBsAg in their blood at birth were excluded. The declining antibody levels in infants who received only HBIG as compared with the rising antibody levels in infants who received HBIG followed by three doses of HBV vaccine suggest that long-term protection will be seen only in the latter group.

Liver biopsies from 52 patients with chronic hepatitis B were investigated for the presence and distribution of HBcAg and the results were compared with the status of hepatitis B virus deoxyribonucleic acid (HBV-DNA). The patients consisted of 37 men and 15 women, aged 16-55 years (mean = 34 years). Serum alanine aminotransferase (ALT) was elevated in 50 patients (range: 18-969 U/L; mean = 290 U/L). Serological testing showed HBsAg in all, HBeAg in 45 (87%), and HBV-DNA in 28 (54%). Liver biopsies demonstrated HBcAg in 35 (67%) patients. HBcAg was not only present in 31 of 45 (69%) patients who were seropositive for HBeAg, but also in four of seven (57%) with antibody to HBeAg (anti-HBe). In 28 of 35 (80%) patients with HBcAg in the liver, serum HBV-DNA was detected. However, no serum HBV-DNA was detected in 17 patients who had no detectable HBcAg in the liver. The distribution of HBcAg in the liver was rather cytoplasmic and nuclear than nuclear alone. Among 33 patients with cytoplasmic HBcAg in the liver, 15 (45%) had an evidence of acute exacerbation of hepatitis with marked ALT elevation (range: 168-894 U/L; mean = 385 U/L) and nine patients showed severe chronic active hepatitis and confluent necrosis, histologically. These results indicate that the presence of HBcAg in the liver correlates with the amount of circulating hepatitis B virus as quantified by serum level of HBV-DNA. The predominant cytoplasmic HBcAg in the liver may suggest the possibility of multiple episodes of acute exacerbation and more severe ongoing hepatitis during the clinical course.

Serological evidence of hepatitis B virus (HBV) infection and serum alphafetoprotein (AFP) were assayed in sera from 112 Korean patients with primary hepatocellular carcinoma (PHC) and from 63 age- and sex-matched controls. Serological evidence of HBV infection was found in 100% of PHC patients and in 97% of controls. The majority of PHC patients (87%) were positive for hepatitis B surface antigen (HBsAg). In contrast, only 14% of control individuals were positive for HBsAg, but 82% were positive for antibody to HBsAg (anti-HBs). Hepatitis B e antigen (HBeAg) was detected in a high percentage (38%) of HBsAg-positive PHC patients, but in none of the nine HBsAg-positive control individuals. Serum AFP was detectable in 83% of PHC patients but in only one of 63 controls (1.5%). These results document that HBV infection may be the major factor in the development of PHC in this country.