By the end of December 2000, the epidemiological system 'Alert' of the Public Health Institute in Tirane reported an outbreak of acute gastroenteritis. The outbreak involved children in Tirane and in the rural area. In total, 2722 children were seen in Tirane Hospital and 982 (56.4%) were treated for acute gastroenteritis. The age group with the highest morbidity was 0-5 years (89.7%), followed by the 6-9 (6.2%) and 10-15 years age groups (4.1%). The distribution of acute gastroenteritis cases, which occurred along the same water distribution system, suggests a waterborne origin. The nucleic acid amplification confirmed the co-circulation of different genotypes of rotavirus, mainly P[8]G9 and P[8]G3, responsible for the outbreak. Other enteric viruses such as astrovirus serotype 1, adenovirus and Norovirus, genogroups I and II were detected. Co-infections with different rotavirus genotypes and even with different enteric viruses were detected in several samples.

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The objectives of the present study were to assess the occurrence of human adenoviruses (HAdVs) in paediatric patients with gastroenteritis in Albania and to characterize HAdV strains. Faecal specimens from children admitted with acute gastroenteritis to the Paediatric Hospital in Tirana were screened for HAdV, using broad-range primers targeting the hexon gene, in combination with species-specific primers targeting the fiber gene. Phylogenetic analysis was then performed to assess the genetic relationships among the different sequences and between the sequences of the samples and those of the prototype strains. Adenovirus DNA was detected in 33/142 samples (23.2%); 14 belonged to species F (13 HAdV-41 and 1 HAdV-40), 13 to species C (1 HAdV-1, 8 HAdV-2, and 4 HAdV-5), 5 to species B (HAdV-3), and 1 to species A (HAdV-12). Rotavirus coinfection was present in 9/33 (27.2%) positive samples. In the remaining 24 positive samples (12 enteric—F species; 12 nonenteric—A, B, or C species), HAdVs were detected as unique viral pathogens, suggesting that HAdV may be an important cause of diarrhoea in children requiring hospitalization. This is the first study investigating the presence of human adenoviruses (species A–G) as etiologic agents of viral gastroenteritis in children in Albania.

Human Bocavirus (HBoV) has been recently identified in association with acute viral gastroenteritis (AGE). The objective of this work was to investigate the prevalence of HBoV in children with AGE in Albania. Stool specimens collected from 142 children were analyzed by amplification of partial NP1 and Vp1/Vp2 genes. HBoV was detected in 13 samples (9.1%), 12 HBoV-1 and one HBoV-2. All HBoV-positive patients were co-infected with rotavirus and/or adenovirus, a finding which might indicate that there is no clear causal association of this agent with diarrhea. Further investigation is needed to assess the pathogenic role of HBoV in childhood diarrhea.

Three different studies are reported concerning the environmental pollution caused by viruses in Albania. The first study describes an outbreak of gastroenteritis in the capital city, involving 2,722 children attending the Paediatric Unit of Tirana Hospital. The age group with the highest morbidity was 0-5 years, with 89.5%; no fatalities were recorded during the outbreak. Rotavirus was detected in 26/28 faecal samples by RT-PCR, although astrovirus, adenovirus and calicivirus were also present. The second study describes an outbreak of hepatitis A virus involving the city of Lac. Two hundred cases were recorded, with the highest incidence in the age-group 5-9 years. Phylogenetic analysis of the VP1/2A region showed the presence of a unique sequence: genotype IA. Rotavirus was identified in drinking-water samples collected during the outbreak. The third study describes the prevalence of HAV and HEV in 202 sera randomly collected from 12 different cities in Albania. HAV showed a high incidence (66.2%), whereas none was positive for HEV. The genomic analysis of the VP1/2A junction revealed the presence of only one genotype (IA) with few point mutations and just two amino acid substitutions at codons 22 and 34. Additionally, two potential antigenic variants were detected, the first at position 46 of VP3 and the second at position 23 of VP1.