In November 2012, an animal handling center on Hong Kong reported an outbreak of Psittacosis amongst six members of the staff working there. Interestingly, this outbreak was preceded by an outbreak of chlamydiosis amongst the detained Mealy Parrots ( Amazona farinose) held in the facility. Tropical birds are often known to be carriers of Chlamydophila psittaci, the agent responsible for causing psittacosis, an atypical pneumonia associated with bird vectors. It is one of the three commonest zoonotic causes of atypical pneumonia, the others being Francisella tularensis (Tularemia) and Coxiella burnetti (Q Fever). The commonest non-zoonotics agents causing atypical pneumonia include Chlamydia pneumoniae, Mycoplasma pneumoniae, and Legionella pneumophila.
Although Chlamydophila psittaci is often isolated from birds originating in tropical and subtropical regions, it is hardly ever held responsible for large outbreaks in human beings. Even birds are rarely symptomatic. However, the case of the outbreak in Hong Kong is remarkable because researchers have found a novel adenovirus, which they are calling Psittacine Adenovirus HKU1 (to commemorate the Hong Kong University where the isolation was carried out).
Notably Koch's postulates have not been tested out and thus far, it seems to be more of an association/correlation between the presence of the novel adenovirus and the disease. The researchers have found that the virus was absent in the healthy parrots. In the sick parrots, there was a direct correlation between the virus load and bacterial load in the lungs. This is indicated in the following graph published in the PLoS Neglected Tropical Diseases paper which discusses this novel virus:
The hypothesis forwarded by these findings is that the larger the viral load in the lungs of the infected birds, the higher will be the local immunosuppression and hence, will result in a higher bacterial load as well. This higher bacterial load would be represented in a larger likelihood of zoonotic transmission of the bacteria from the sick birds to health humans interacting with them.
There needs to be a lot of scrutiny of this hypothesis, ideally in a natural setting, although that might be difficult to pull off. In an experimental setting we could bring primates in contact with psittacine birds with varying loads of the virus and test whether there is transmission between the species. Alternative, surrogate measures, like looking at viral counts in the lungs and bacterial counts in the bird feces (that is the mode of spread of Chlamydophila psittaci) could be a more humane, albeit indirect way of testing for the effect of the virus on bacterial loads in the birds. The birds would also need to be investigated to test whether the viral infection status and the viral loads are related to the immune status of the birds, since the hypothesis hinges on the fact that a higher viral load would lead to a higher level of immunosuppression in the birds, therefore increasing the likelihood that they would spout the infectious bacteria causing disease in man.
The authors have stressed that this is, to the best of their knowledge, the first report of a confection of psittacine birds with the novel adenovirus and C. psittaci which has translated into a zoonotic outbreak in man. However, C. psittaci has been known to act synergistically with other viruses, causing diseases in animals. Alternatively, some viruses have been known to suppress immune reaction in birds, however, it has never been shown to have caused avian-to-human spread of infection. The authors state in the concluding paragraph:
Virus and bacteria often act synergistically in causing diseases in humans or animals. C. psittaci-avian pneumovirus co-infection has been associated with an outbreak in turkeys [12], C. psittaci-fowlpox virus co-infection with an outbreak in hens [9] and C. psittaci-reovirus with an outbreak in budgerigars [11]. Infectious bursal disease virus and chicken anaemia virus can cause immunosuppression, leading to secondary bacterial infection such as bacterial chondronecrosis with osteomyelitis [43]. However, it is unclear whether co-infection in birds can increase the risk of transmission of avian pathogens to humans. Our investigation suggested that the novel Psittacine adenovirus may have been associated with immunosuppression among infected birds, leading to higher C. psittaci bacterial loads in the lungs of psittacine birds, and hence increasing the risk of infection in exposed humans.
In any case, this is a matter of great interest because this shows that viruses can now, in addition to jumping the species barrier themselves, can actually potentiate and empower other bacteria to do the same. In an era of emergence of antibiotic resistance, this could be, very much, a danger sign we need to be ready to nip in the bud.
