Isolated core antibody hepatitis B in sub-Saharan African immigrants.

Chronic hepatitis B virus (HBV) infection is a major health problem in sub-Saharan Africa, where prevalence is > or =8%, and is increasingly seen in African immigrants to developed countries. A retrospective audit of the medical records of 383 immigrants from sub-Saharan Africa attending the infectious diseases clinics at the Royal Melbourne Hospital was performed from 2003 to 2006. The HBV, human immunodeficiency virus (HIV) and hepatitis C virus (HCV) serological results are reported, with a focus on the isolated core antibody HBV pattern (detection of anti-HBc without detection of HBsAg or anti-HBs). Two-thirds (118/174, 68%) of those tested had evidence of HBV infection with detectable anti-HBc. Chronic HBV infection (serum HBsAg detected) was identified in 38/174 (22%) and resolved HBV infection (both serum anti-HBs and anti-HBc detected) in 45/174 (26%). The isolated core antibody pattern was identified in 35/174 (20%), of whom only 1/35 (3%) had detectable serum HBV DNA on PCR testing, indicating occult chronic HBV (OCHB). Only 8/56 (14%) patients with negative anti-HBc had serological evidence of vaccination (serum anti-HBs detected). HIV infection was detected in 26/223 (12%). HCV antibodies were detected in 10/241 (4%), of whom 8 (80%) had detectable HCV RNA. Viral co-infection was detected in only 2/131 (1.5%) patients tested for all three viruses. The isolated core antibody HBV pattern was common among sub-Saharan African patients in our study. These patients require assessment for OCHB infection and monitoring for complications of HBV.

Improving immunization coverage through budgeted microplans and sub-national performance agreements: early experience from Cambodia.

In recent years, Cambodia has demonstrated significant success in specific aspects of immunization with gains through campaign efforts in measles control and polio eradication. In contrast, routine immunization rates have failed to improve over the last five years. In response, the National Immunization Program of the Ministry of Health developed a coverage improvement planning (CIP) process. This paper describes the CIP process in Cambodia, including identified barriers to and strategies for improving coverage. Immunization coverage rose in 8 of 10 pilot districts in the year following the introduction of CIP in 2003. The mean increase in DPT3 coverage across pilot districts on an annual basis was 16%, which provides encouraging early evidence for the effectiveness of the intervention. Factors associated with success in coverage improvement included: (1) development of a needs-based micro-plan, (2) application of performance-based contracting between levels of management, (3) investment in social mobilization, (4) securing finance for health outreach programs and (5) strengthened monitoring systems. Lessons learned will guide program expansion to improve immunization coverage nationally.

Parasitic worms of the central nervous system: an Australian perspective.

The diagnosis and management of parasitic diseases of the central nervous system (CNS) is difficult, even for infectious diseases physicians and neurologists. Furthermore, few overviews of the spectrum of causative helminths and clinical syndromes have been published. In the present study, we review the seven most common parasitic diseases of the CNS: (i) cysticercosis, (ii) neuroschistosomiasis, (iii) paragonimiasis, (iv) angiostrongyliasis, (v) hydatid disease, (vi) sparganosis and (vii) gnathostomiasis. Major syndromes of parasitic disease of the CNS and their differential causes are discussed, including: (i) cystic lesions, (ii) enhancing granulomas (with and without creeping subcutaneous eruptions), (iii) eosinophilic meningoencephalitis and (iv) spinal cord disease. Specific risk factors that predispose to these infections are also discussed and particular attention is drawn to the situation in Australia.

Schistosomiasis in Australian travellers to Africa.

OBJECTIVE: To determine the proportion of Australian travellers to Africa at risk of Schistosoma infection, and the proportion of those infected. DESIGN AND PARTICIPANTS: Retrospective postal survey of 360 patients who had attended Fairfield Hospital travel clinic in 1994 and stated an intention to travel to Malawi, Zimbabwe or Botswana. MAIN OUTCOME MEASURES: Self-reported risk status for Schistosoma infection. For those at risk, results of an indirect haemagglutination assay (IHA). For those with IHA titres > or = 1:32, results of enzyme-linked immunosorbent assay, urine microscopy and eosinophil count. RESULTS: 360 letters were sent; 35 were returned to sender. Of the 325 remaining, 250 (77%) either responded or had an IHA test; 19 of these were still overseas or did not travel. 117/231 (51%) returned travellers considered themselves at risk of infection. Significantly fewer older patients reported exposure (chi 2 = 66.6; P < 0.001). 109/117 (93%) of those at risk had IHA tests and 18 had titres > or = 1:32. Subsequent testing indicated infection in 10/117 travellers (8.5%; 95% CI, 4.2%-15.2%). CONCLUSION: Our findings indicate that a considerable number of Australian travellers to Africa are at risk of schistosomiasis, and some are infected. As complications can be serious, screening is recommended for individuals with any risk of infection, and treatment should be offered to those infected.

HIV-1 infection of human macrophages impairs phagocytosis and killing of Toxoplasma gondii.

The susceptibility of patients with AIDS to certain opportunistic infections is due to defective cell-mediated immunity. The contribution of direct infection of macrophages with HIV-1 to this defect is unknown. To address this issue, we infected normal human monocyte-derived macrophages with a monocytotropic strain of HIV-1 and examined their ability to phagocytose and kill the opportunistic pathogen, Toxoplasma gondii. Phagocytosis of heat-killed T. gondii was reduced in HIV-infected macrophages compared with mock-infected controls. Opsonization of heat-killed T. gondii increased phagocytosis by both mock- and HIV-infected macrophages, but phagocytosis in HIV-infected cultures remained lower than in controls. Internalization of live T. gondii by macrophages was unaffected by HIV infection. Intracellular replication of live T. gondii was enhanced by HIV infection, as shown in four experiments, each using monocyte-derived macrophages from a different donor. Treatment of HIV-infected macrophages with IFN-gamma decreased parasite replication but not to control levels. These findings suggest that infection of macrophages by HIV may be a contributing factor to the reactivation of T. gondii infection in patients with AIDS.

Simplified colorimetric analysis of polymerase chain reactions: detection of HIV sequences in AIDS patients.

We have previously described a colorimetric test, designated an amplified DNA assay (ADA), for specific segments of DNA amplified by polymerase chain reactions (PCRs), suited to diagnostic applications. This relied on binding the amplified DNA via a sequence in one oligodeoxyribonucleotide (oligo) to the DNA-binding protein GCN4 coated on the wells of a microtiter dish. Avidin-peroxidase was then bound to biotin at the 5' end of the other oligo and detected colorimetrically. Two successive PCRs with nested oligos were utilized. We describe here several modifications that greatly simplify the ADA. First, we bind the DNA to a glutathione S-transferase-GCN4 fused polypeptide (GST-GCN4) and avidin-peroxidase simultaneously, rather than successively. Second, we carry out the two successive PCRs in the one reaction mixture, using the thermal stabilities of oligos of differing lengths to separate the two reactions. Third, PCRs can be performed in the wells of a microtiter dish and the amplified DNA captured and detected via GST-GCN4 immobilized on beads attached to the lid of the microtiter dish. Hence it is only necessary to pipette the DNA sample once, and up to 96 samples can then be handled simultaneously.

Knob-independent cytoadherence of Plasmodium falciparum to the leukocyte differentiation antigen CD36.

The survival of Plasmodium falciparum-infected erythrocytes is enhanced by the sequestration of mature trophozoites and schizonts from the peripheral circulation. Cytoadherence of infected erythrocytes in vivo is associated with the presence of knobs on the erythrocyte surface, but we and others have shown recently that cytoadherence to C32 melanoma cells may occur in vitro in the absence of knobs. We show here that a knobless clone of P. falciparum adheres to the leukocyte differentiation antigen, CD36, suggesting that binding to CD36 is independent of the presence of knobs on the surface of the infected erythrocyte. This clone showed little cytoadherence to immobilized thrombospondin or to endothelial cells expressing the intercellular adhesion molecule 1. Furthermore, an Mr approximately 300-kD trypsin-sensitive protein doublet was immunoprecipitated from knobless trophozoite-infected erythrocytes. Finding a P. falciparum erythrocyte membrane protein 1 (PfEMP1)-like molecule on these infected erythrocytes is consistent with a role for PfEMP1 in cytoadherence to CD36 and C32 melanoma cells.

Plasmodium falciparum: cytoadherence of a knobless clone.

Sequestration of Plasmodium falciparum-infected erythrocytes is crucial to parasite survival as it prevents destruction in the liver and spleen. Knobs have been considered necessary but not sufficient for cytoadherence to vascular endothelial cells in vivo and to melanoma or umbilical vein endothelial cells in vitro. We describe here a knobless clone that cytoadheres strongly to C32 melanoma cells. This clone cannot express the knob-associated histidine-rich protein (KAHRP) due to the deletion of the KAHRP gene. Our results raise the possibility of an alternative mechanism for in vitro cytoadherence and suggest that the use of long term cultured isolates and melanoma cells as a model for cytoadherence in vivo may be misleading.

AIDS related Kaposi's sarcoma presenting as ulcerative colitis and complicated by toxic megacolon.

Gastrointestinal Kaposi's sarcoma is a well described and usually asymptomatic manifestation of the acquired immune deficiency syndrome. We report a patient who had extensive colonic Kaposi's sarcoma and presented with an ulcerative colitis like illness. Total colectomy was subsequently required as an emergency procedure for toxic megacolon. The patient remains well on maintenance interferon therapy 21 months after surgery.