Genetic characterization and epidemiology of Helicobacters in non-domestic animals.

BACKGROUND: Novel helicobacter infections and associated disease are being recognized with increasing frequency in animals and people. Yet, the pervasiveness of infection in distantly related animal taxa, genetic diversity of helicobacters, and their transmissability are not known. AIM: To better understand the ecology of helicobacters, we did a PCR survey and epidemiologic analysis of 154 captive or wild vertebrate taxa originating from 6 continents. MATERIALS AND METHODS: One hundred twenty nine helicobacter 16s rRNA gene segments were amplified by PCR and sequenced from ninety-three mammalian, reptilian, avian, or amphibian host species. Prevalence estimates were generated, and univariate logistic regression analyses were used to explore relationships between infection status and the health and characteristics of the 220 individual animals. RESULTS: One hundred and nineteen novel helicobacter DNA sequences were found. No significant relationship between infection and host health was found; however, multi-infection or infections with particular genotypes were associated with mild clinical signs. Phylogenetic and genetic comparisons of helicobacters suggested prolonged co-adaptation and niche-associated divergence as well as periodic inter-species transmission. CONCLUSION: The genus Helicobacter should accordingly be viewed as a collection of hundreds of organisms that have colonized most tetrapod taxa and have the potential to expand into new hosts as contact among animals and between animals and people increases.

New hosts for equine herpesvirus 9.

Equine herpesvirus 9 was detected in a polar bear with progressive encephalitis; the source was traced to 2 members of a potential equid reservoir species, Grevy's zebras. The virus was also found in an aborted Persian onager. Thus, the natural host range is extended to 6 species in 3 mammalian orders.

Evolution of mammals and their gut microbes.

Mammals are metagenomic in that they are composed of not only their own gene complements but also those of all of their associated microbes. To understand the coevolution of the mammals and their indigenous microbial communities, we conducted a network-based analysis of bacterial 16S ribosomal RNA gene sequences from the fecal microbiota of humans and 59 other mammalian species living in two zoos and in the wild. The results indicate that host diet and phylogeny both influence bacterial diversity, which increases from carnivory to omnivory to herbivory; that bacterial communities codiversified with their hosts; and that the gut microbiota of humans living a modern life-style is typical of omnivorous primates.

Hepatic hemorrhage, hemocoelom, and sudden death due to Haemoproteus infection in passerine birds: eleven cases.

Haemoproteus spp. are ancient apicomplexan hemoparasites that have undergone extensive coevolution with their natural hosts and are typically species specific, with inapparent or minimal pathogenicity. A promiscuous genotype of Haemoproteus capable of undergoing host switching on a familial level was identified. This protozoan caused severe disease with high mortality in 6 species of exotic passerine birds housed in California at the San Diego Zoo's Wild Animal Park: Surinam crested oropendola (Psarocolius decumanus decumanus), Guianan turquoise tanager (Tangara mexicana mexicana), blue-necked tanager (Tangara cyanicollis caeruleocephala, Guianan red-capped cardinal (Paroaria gularis gularis), magnificent bird of paradise (Diphyllodes magnificus hunsteini), and superb bird of paradise (Lophorina superba). The birds had few or no clinical signs. Necropsy findings consisted of hemocoelom and irregularly scattered areas of hemorrhage and hepatocellular necrosis. Affected areas of liver contained solitary protozoal megaloschizonts in varied states of degeneration and peripheral nonsuppurative inflammation. No other parasite life stages were found in parenchymal organs or blood smears. Polymerase chain reaction using consensus primers for an avian malarial mitochondrial cytochrome B gene segment was positive in all cases. Sequencing and BLAST analysis identified the protozoan as a Haemoproteus sp. related to Haemoproteus spp. found in asymptomatic passerine birds native to North America. In situ hybridization was performed in 3 animals with a mitochondrial cytochrome B probe and was positive only in megaloschizonts. These findings suggest the recognition of a genotype of Haemoproteus that exhibits high levels of host infidelity and causes severe disease in captive birds exotic to North America.

Molecular epidemiology of Mycobacterium avium subsp. avium and Mycobacterium intracellulare in captive birds.

Mycobacterium avium subsp. avium and Mycobacterium intracellulare are primary causes of mycobacteriosis in captive birds throughout the world, but little is known about how they are transmitted. To define the local epidemiology of infection, we strain-typed 70 M. avium subsp. avium and 15 M. intracellulare culture isolates obtained over a 4-year period from captive birds. Typing was performed using randomly amplified polymorphic DNA (RAPD) PCR, amplified fragment length polymorphic (AFLP) fragment analyses, and for a subset of isolates, DNA sequencing of a segment of the 16S-23S rRNA internal transcribed spacer region. Six strain clusters comprising 43 M. avium subsp. avium, isolates were identified; 42 isolates had unique typing patterns, including all M. intracellulare isolates. Phylo-geographical analyses using RAPD and AFLP fingerprints and animal confinement histories showed no correlation between housing of infected birds and mycobacterial strain-type, except for two animals. The diversity of M. avium subsp. avium and M. intracellulare isolates and minimal evidence for bird-to-bird transmission suggest that environmental reservoirs may be important sources of infection in captivity.

Extraneural prion neuroinvasion without lymphoreticular system infection.

While prion infection of the lymphoreticular system (LRS) is necessary for neuroinvasion in many prion diseases, in bovine spongiform encephalopathy and atypical cases of sheep scrapie there is evidence to challenge that LRS infection is required for neuroinvasion. Here we investigated the role of prion infection of LRS tissues in neuroinvasion following extraneural inoculation with the HY and DY strains of the transmissible mink encephalopathy (TME) agent. DY TME agent infectivity was not detected in spleen or lymph nodes following intraperitoneal inoculation and clinical disease was not observed following inoculation into the peritoneum or lymph nodes, or after oral ingestion. In contrast, inoculation of the HY TME agent by each of these peripheral routes resulted in replication in the spleen and lymph nodes and induced clinical disease. To clarify the role of the LRS in neuroinvasion, the HY and DY TME agents were also inoculated into the tongue because it is densely innervated and lesions on the tongue, which are common in ruminants, increase the susceptibility of hamsters to experimental prion disease. Following intratongue inoculation, the DY TME agent caused prion disease and was detected in both the tongue and brainstem nuclei that innervate the tongue, but the prion protein PrP(Sc) was not detected in the spleen or lymph nodes. These findings indicate that the DY TME agent can spread from the tongue to the brain along cranial nerves and neuroinvasion does not require agent replication in the LRS. These studies provide support for prion neuroinvasion from highly innervated peripheral tissues in the absence of LRS infection in natural prion diseases of livestock.

Reproductive and neurological Quaking(viable) phenotypes in a severe combined immune deficient mouse background.

The quaking(viable) (qkv) mutation, a spontaneous deletion of a multigenic region encompassing roughly 1 Mb at 5.9 cM on the proximal end of mouse chromosome 17, causes severe trembling in all homozygous animals and infertility in all homozygous males. Physiologically, quaking mice exhibit dysmyelination and postmeiotic spermatogenic arrest. Molecular defects in Qkv mice occur in the affected tissues, indicating the primary causes of these pathologies are cell autonomous. However, because both the reproductive and neurological defects are in immune-privileged sites and because some similar pathologies at both sites have been shown to be immune mediated, we tested whether the immune system participates secondarily in manifestation of Qkv phenotypes. The qkv mutation was bred into a severe combined immune-deficient mouse line (SCID; devoid of mature B and T cells) and penetrance of the neurological and the male sterile phenotypes was measured. Results showed that neither defect was ameliorated in the immune-deficient background. We conclude that the Qkv pathologies do not likely involve a B- or T-cell-dependent response against these immune-privileged sites.