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Hygiene protocols for the prevention and control of diseases (particularly beak and feather disease) in australian birds - chlamydophilosis

Hygiene Protocols for the Prevention and Control of Diseases (Particularly Beak and Feather Disease) in Australian Birds Commonwealth of Australia 2006 Information contained in this publication may be copied or reproduced for study, research, information oreducational purposes, subject to inclusion of an acknowledgment of the source.
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Note
This document describes the disease Chlamydophilosis, and has been developed with the involvement and
cooperation of a broad range of stakeholders, but the making of this document does not necessarily indicate the
commitment of individual stakeholders to undertaking any specific actions. The attainment of objectives and the
provision of funds may be subject to budgetary and other constraints affecting the parties involved. Proposed actions
may be subject to modification over the life of the document due to changes in knowledge.
Chlamydophilosis is also known as parrot fever and psittacosis (psittacine birds), ornithosis (non-psittacine birds) and psittacosis (humans). It is caused by Chlamydophila psittaci, formerly known asChlamydia psittaci. Thus the disease that we currently call chlamydiosis and caused by Chlamydiapsittaci is now chlamydophilosis and caused by Chlamydophila psittaci (Everett et al., 1999). Avian chlamydophilosis is a significant bacterial disease of wild, captive and intensively reared birds. Theagent responsible, Chlamydophila psittaci, is an obligate intracellular parasite. C. psittaci is a significant zoonosis and the term "psittacosis" has been used to describe the disease inhumans to distinguish psittacosis from the venereal disease caused by C. trachomatis. Avianchlamydophilosis (AC) may range from a rapidly fatal peracute disease to a subclinical latent infection,depending on host factors and the strain of C. psittaci involved. The body systems primarily affectedinclude the respiratory and gastrointestinal tracts (including the liver), the cardiovascular system, thespleen and the eyes. Significant mortality and morbidity may occur as a result of the disease, particularlyin parrots and turkeys. Structure and Life Cycle
Chlamydiae are spherical intracytoplasmic organisms 0.2 μm to 1.5 μm in diameter (depending on their
stage of development). They have a cell wall similar to Gram-negative bacteria and they parasitise energy
(ATP from the host's mitochondria. The two major morphological stages in the life cycle of chlamydiae
are termed the elementary body (EB) and the reticulate body (RB). The EB is the smaller infectious form
(0.2-0.3 μm diameter) characterised by a thick, rigid cell wall and very dense cytoplasm. It may be found
outside the host cell. The RB is larger (0.6-1.5 μm), has a thinner cell wall, less dense cytoplasm, and is
the vegetative stage which reproduces by binary fission. Different strains of C psittaci are recognised on
the basis of antigenic and pathogenic differences. Avian strains of C. psittaci are distinct from
mammalian strains (Moulder, 1985)
Epidemiology
All bird species including domestic poultry are susceptible. Turkeys are very susceptible, chickens are
relatively resistant. Surveys of avian chlamydophilosis in feral pigeons have revealed carrier rates of 50 -
90%. High rates of infection are commonly reported in psittacine birds and in some zoos the rate may
reach 100%.
Chlamydophilosis is often introduced into an aviary by infected birds which die several days later (oftenwith uncertain signs) or which infect other birds in the aviary, which die two to three weeks later. Theincubation can be very short, birds may begin shedding chlamydia within a few days of being infectedor it can be very long.
In natural hosts, chlamydial strains are thought to be "host adapted", i.e. the host-parasite relationship hashad time to evolve towards an equilibrium state. Thus, in its "normal" host, a chlamydial strain may berelatively avirulent and remain latent unless the bird is stressed, whereas in an abnormal host the samestrain may be highly virulent and cause epizootic disease. Overt disease in the normal host may beinduced by stress factors such as poor nutrition and hygiene, overcrowding, bacterial or protozoal disease, shipping, racing, migration, breeding, inclement weather or moulting. Prevalence of chlamydophilosisin native birds can rise from a normal value of less than 5% to 100% when they are trapped and crowdedtogether. Chlamydophilosis is common in wild Eastern Rosellas and Crimson Rosellas in NSW and Victoria duringwinter. Periodic outbreaks occur in aviary birds where the disease is endemic and the birds are undergoingtheir first moult (particularly the Neophema species). Often there is a history of stress such as moulting,surgical sexing and overcrowded transport. Young birds are more susceptible to chlamydial infection because they are immunologically immatureand are often exposed to the organism excreted by the parent birds due to the stresses associated withbreeding. In wild and captive flocks with endemic chlamydophilosis the majority of birds carry latent infections.
Mortality and morbidity is highest amongst the young, however, losses generally don't exceed 20%. Incontrast, where infective organisms are introduced to disease-free flocks, mortality may approach 90%.
The latter scenario occurs most commonly where wild infected birds are able to mingle with naivedomestic poultry flocks or where new birds are introduced to existing stock without adequate prophylaxis.
C. psittaci is excreted in the faeces and nasal discharges of infected birds. The organism is resistant todrying and can remain infectious for several months. Some infected birds can appear healthy and shedthe organism intermittently. Shedding can be activated by stress factors, including relocation, shipping,crowding, chilling, and breeding. Pathogenesis
Transmission of C. psittaci occurs most commonly by inhalation (less often by ingestion) of infective EBs
shed in faeces, lacrimal and nasal secretions and respiratory exudates. Infected birds may transmit
chlamydia by regurgitative feeding of their young. Transmission may occur via consumption of infected
carcasses by predatory birds. Arthropod vectors such as lice, mites and simulid flies can transmit
chlamydia (Eddie et al., 1962).
Dissemination is favoured during periods of stress (e.g. poor nutrition, overcrowding, concurrent disease,shipping, racing and migration) due to activation of latent infection followed by excretion of largenumbers of infective organisms - with or without the development of disease. Behavioural traits which favour or enhance transmission include: colonial nesting, e.g. amongst herons, egrets, cormorants, pigeons and sparrows.
regurgitation feeding of young by parents certain natural feeding strategies which promote aggregations of birds in a potentiallycontaminated environment.
Chlamydophila psittaci has a predilection for cells of the respiratory tract, serous cavities andreticuloendothelial system, especially mononuclear phagocytes. Multiplication of chlamydiae results incell lysis and this combined with the host's inflammatory response causes the clinical manifestations ofavian chlamydophilosis - conjunctivitis, rhinitis, airsacculitis, pericarditis, hepatic and splenic necrosisand arteritis. Enteric infections are common in most avian species. Excretion of infective EBs occurs infaeces and diarrhoea is a common clinical sign.
Chlamydial infections elicit both humoral and cell mediated immune responses. Acute fatal disease andrecurrent subacute attacks occur, but there is a tendency toward chronic latent infections. The acuteinflammatory reaction evoked by chlamydial invasion probably contributes to the pathogenesis of disease by producing secondary injury to tissues. Latency is an equilibrium between the host's immune defences and the pathogen's intracellularpersistence. The pathogen is quiescent - present but not multiplying, while the host remains infected andsusceptible to future episodes of disease should its immune defences be impaired. Differences in pathogenicity of certain strains for certain species of bird may be related to the degree andmode of exposure, the route of infection and the hosts innate resistance which in itself is subject tophysiological and environmental influences. After aerosol inoculation the organism multiplies in thelung, air sacs and pericardial membrane. By 48 hours organisms can be detected in blood, liver, spleenand kidney cells and after 72 hours there is excretion of organisms in the faeces and nasal secretions. Clinical Signs
The clinical signs of chlamydophilosis may be indistinguishable from several other febrile septicaemic
diseases of birds and differential diagnoses should include salmonellosis, tuberculosis, erysipelas,
mycoplasmosis, pasteurellosis, E. coli, and aspergillosis. The usual time between exposure to C. psittaci
and onset of illness ranges from 3 days to several weeks. However, active disease can appear years after
exposure. Affected psittacine birds often have distended sinuses, blepharitis, sneezing, serous oculonasal
discharge, dyspnoea, tail-bobbing, green diarrhoea, depression. Sudden death may be the only history
(Vanrompay, 1995; Johnston et al., 1999)
In affected turkey flocks, birds may be thin and anorexic, pyrexic and have yellow-green diarrhoea.
There may be a rapid drop in egg production (up to 40%).
Young ducks with acute chlamydophilosis are depressed, anorexic, ataxic, and have diarrhoea and aserous to purulent oculonasal discharge. There may be terminal convulsions. Ducks with chronicchlamydophilosis may just appear emaciated and in poor health. Acute cases in chickens involve mainly cardiovascular and gastrointestinal signs, with low mortalitiesand only in young. Acute disease in pigeons presents as anorexia, ill-thrift, diarrhoea, weakness, conjunctivitis, blepharitis,rhinitis, creaking and rattling respiratory sounds. Chronic disease - weak, thin, emaciated. May havetransient diarrhoea with mild infections.
Lesions
Most birds which die of acute chlamydophilosis have marked splenomegaly and hepatomegaly but the
presence of fibrinous or fibrino-purulent exudates on serosal surfaces, as well as congested organs such
as liver and spleen is sufficient to initiate confirmatory diagnostic tests. These include cytological
examination of smears; culture; and immunological tests. Histopathology is unreliable for confirming a
diagnosis. Cytology is often more reliable. Elementary bodies may be visualised in liver and spleen
smears with appropriate stains (Macchiavello, Giemsa, Giminez, Castenada) within macrophages in
affected tissues. Fluorescent antibody stains are a rapid diagnostic test (the smear should be dried and
then fixed in acetone).
Tentative diagnoses can be made on the basis of seeing EBs in stained tissues but because of theirsimilarity to some other bacteria e.g. mycoplasmas, diagnosis should be confirmed by demonstration ofchlamydial growth in experimental hosts after inoculation, demonstration of chlamydial antigen orsignificantly rising titres of antibody. There is no single test or combination of tests which will determine that a bird is free of chlamydiae. Methods for diagnosing chlamydophilosis
Diagnosis is by clinical signs supported by tests such as the Clearview® test (Oxoid) which detect
chlamydial group specific antigen (designed for C. trachoma). The Clearview® test has limitations for
antemortem use. These tests have a high sensitivity and lower specificity particularly if used on faecal
or cloacal swabs due to cross-reactions with other antigens (Fudge, 1997). Other methods of diagnosis
include histochemical staining, tissue culture and serology such as the Immunocomb® test (Flammer,
1997).
Combining a PCR test with a serologic titre offers the most thorough diagnostic plan (Tully, 2001).
Treatment
Doxycycline, is highly recommended for the treatment of acutely ill birds and has produced the most
consistent therapeutic results in most birds. It is lipophilic which results in tissue concentrations higher
than other tetracyclines. Its half life is 22 hours as opposed to 8 hours for tetracycline, and absorption
from the gut is rapid, almost complete (95% vs 25% -80% for other tetracyclines) and subject to less
interference from calcium. A major advantage of this drug is that it has less of an adverse effect on normal
gut flora than other tetracyclines due to its rapid absorption and excretion as an inactive conjugate in the
faeces. The incidence of secondary infections while on medication is reduced. Intravenous dose route
of 10-100 mg/kg body weight for 1 to 2 doses, followed by oral administration (5-25 mg/kg, per os BID)
for 45 days.
Psittavet (Vetafarm) - doxycycline hydrochloride 40 mg/g green powder). Dose: for parrots 10 g/ldrinking water.; for pigeons 5 g/l drinking water for 45 days. Add citric acid125 ppm for potentiation.
The Australian Pigeon Company. Doxycycline hydrochloride 120mg/g. Dose1.5 g/L in DW for birds.
Supportive and adjunctive therapy Elimination of concurrent parasitic, bacterial and fungal infections. Candidiasis can be treatedwith nystatin. Supplementary lactobacillus can be fed (psittacine isolate).
Fluid and electrolyte therapy is advised for depressed and dehydrated birds. Warmed lactatedRingers administered subcutaneously at 5 - 10 mls/100 g BW is effective.
Hypoglycaemic birds should be supported with intramuscular dextrose.
Anorectic birds will require tube feeding. New birds should not be introduced to the aviary/flock without first being isolated and put on a45 day course of prophylactic medication Sick birds should be isolated in a small enough cage to prevent excessive flying, kept warm anduncrowded (preferably 1 or 2 birds to a cage) in surroundings that are cleaned and disinfecteddaily. All surfaces with which infective organisms may come in contact should be cleaned anddisinfected with 2% Virkon S solution. Prevention and Control
Prevention and control of avian chlamydophilosis is reliant on isolation and treatment of affected birds,
quarantine and prophylactic treatment of potentially infected birds and detection of carriers of the disease.
The source of infection of a flock should be identified where possible and further contact with infectiveorganisms prevented. Contact between potentially infected wild birds and their droppings and poultryshould be prevented.
Affected birds should be isolated and treated with doxycycline under sanitary conditions with minimumstress to the birds. The rest of the flock should be periodically monitored for several months after anoutbreak to determine if infection has spread. It is wise to treat the rest of the flock prophylactically, asdiagnosis of subclinical carriers is not very efficient. Quarantine and treatment of new birds prior to introduction to a flock should last at least 45 days,depending on the treatment regime for the species involved. Provided there is no direct or indirect contactwith wild birds, aviculturists should be able to maintain chlamydia free premises by instituting a singleyearly 45 day course of CTC in the feed for all resident birds. Stress associated with handling, transport,housing and nutrition should be avoided and bird owners are advised to buy birds directly from breederswith known healthy stock. Anti-chlamydial prophylaxis pre- and post-shipment should be mandatory.
Doxycycline doses of 50 mg/kg may cause regurgitation in some psittacine birds (Carpenter, 2001). Owners should be counselled that introduction of new birds can reinfect the original stock and theyshould be advised on appropriate preventative measures. Owners that present sick birds should beadvised to seek referral to an infectious disease expert. Humans should not be treated prophylactically.
Breeders and dealers should be acquainted with the clinical signs. Carpenter JW, Mashima TY and Rupiper DJ (2001). Exotic Animal Formulary, 2nd Ed. WBSaunders Company. Pp 118-119.
Eddie B, Meyer KF, Lambrecht FL and Furman DP. 1962. Isolation of ornithosis bedsoniae frommites collected at turkey quarters and from chicken lice. J Infect Dis. 110: 231-237 Everett KDE, Bush RM, Anderson AA. 1999. Emended description of the order Chlamydiales,proposal of Parachlamydiaceae fam. nov. and Simkaniaceae fam. nov., each containing onemonotypic genus, revised taxonomy of the family Chlamydiaceae, including a new genus andfive new species, and standards for the identification of organisms. Int J Syst Bacteriol.
49:415–440.
Flammer K. Chlamydia. 1997. In: Altman RB, Clubb SL, Dorrestine GM, Quesenberry K, eds.
Avian Medicine and Surgery. Philadelphia, PA: WB Saunders, pp 364–379.
Fudge AM. 1997. A review of methods to detect Chlamydia psittaci in avian patients. J AvianMed Surg. 11:153–165.
Moulder JW. 1985. Comparative biology of intra-cellular parasitism. Microbiol Rev 49: 298-337.
Tully TN Jr. 2001. Update on Chlamydophila psittaci on avian patients. Semin Avian Exotic PetMed. 10: 20-24. Vanrompay D, Ducatelle R, Haesebrouck F. 1995. Chlamydia psittaci infections - a review withemphasis on avian chlamydiosis. Vet Microbiol. 45: 93-119.

Source: https://www.environment.gov.au/system/files/pages/ecc30ec4-f63e-4ef7-8662-35d9ddcb4a36/files/chlamydophilosis.pdf