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1. Learning Objectives
- Be able to recognize and diagnose the major bacterial diseases of pet birds and poultry species
- Appreciate the relationship of mycoplasma or Vitamin A deficiency and the major bacterial diseases.
- Know the common predisposing factors and causative organisms of bumblefoot.
- Understand the significance and be able to diagnose M. avium infections in pet birds and poultry.
- Understand the clinical presentations of Chlamydiosis in both birds and people
- Be able to diagnose and treat chlamydia in pet birds.
- Understand and be able to give advice concerning the public health implications of Chlamydiosis.
2. Introduction
Bacterial diseases of pet birds, poultry and wild birds often involve similar organisms. The key to development of disease relates to the pathogenicity of the organism in combination with a specific constellation of external influences involving stress (immunity), concentration of animals, environmental exposure (sanitation), exposure to other animals and concurrent disease states.
2.1. Normal flora of the psittacine respiratory and gastrointestinal tracts
Understanding the normal flora of the bird you are treating, whether it be a psittacine, a passerine, anseriform, raptor, etc. is important in interpreting culture results and in designing appropriate therapies. Bacterial diseases are common in pet birds and often involve relatively normal flora or environmental pathogens which develop into disease in response to stress and immunosuppression.
3. Bacterial enteritis
3.1. Spontaneous bacterial enteritis in psittacines
Bacterial enteritis is often a spontaneous stress associated disease. Stress factors such as transport/relocation, introduction of a new bird in the household, heavy molting, breeding/egg-laying, and weaning are all capable of initiating diarrhea. Many times however, the stress factor or initiating cause remains elusive.
The most common pathogens involved in psittacine bacterial enteritis are:
- E. coli
- Klebsiella
- Salmonella
- Pasteurella
- Pseudomonas
- Aeromonas
- Citrobacter (also in Finches).
Other less common organisms include:
- Enterobacter
- Proteus
- Serratia
- Mycobacterium
- Chlamydophila
- Candida
- Aspergillus.
3.1.1. Clinical signs
Clinical signs of bacterial enteritis include diarrhea, dehydration, anorexia, weight loss, septicemia, and occasionally sudden death.
3.1.2. Diagnosis
The diagnosis is based on history, clinical signs, fecal gram stain and cloacal culture and sensitivity. The fecal gram stain is used as an in-house quick screen test to determine whether an excessive number of gram negative organisms (>10%, usually of one type) are demonstrable in the feces.
Important differential diagnosis includes dietary indiscretion, and hepatitis, particularly Chlamydiosis.
 Fecal gram stain from a normal psittacine
bird
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3.2. Salmonellosis
Salmonella infections are possible in all types of birds, including pet birds, wild birds and poultry. As with other salmonella diseases, many factors including environmental conditions and specific strain pathogenicity are critical in enabling the organism to cause disease. Salmonella should be considered in the differential diagnosis of any case of enteritis or septicemia.
3.2.1. Paratyphoid Infections (Salmonellosis)
Although there are approximately 200 species of salmonella that have been isolated from poultry only about 10 of these have consistently been linked with disease. Some of the most important are S. typhimurium and S. enteritidis. Most of the enteric salmonellae are motile and classified as paratyphoid organisms and the diseases they produce are termed paratyphoid infections. Enteric salmonellosis in poultry is more of a public health issue than a significant disease entity in chickens or turkeys. Many cases of human salmonellosis have been associated with consumption of improperly cooked poultry meat or eggs. S. enteritidis has been the organism of most recent concern regarding human enteric infection and has been associated with consumption of improperly cooked eggs. Although the carrier state is common with motile salmonella, acute, septicemic, paratyphoid infections are uncommon except in the young fowl or adult birds under the stress of viral disease, inadequate diet or unsanitary environmental conditions.
3.2.1.1. Clinical Signs
Signs are usually seen in chicks under 7-8 weeks of age and consist of somnolence, profuse diarrhea with pasted cloacal opening, dehydration and shivering. Morbidity and mortality are often over 50% during the first two weeks of life.
3.2.1.2. Diagnosis
Gross lesions are often minimal. Chicks that are only a few days old will often show unabsorbed yolk sac material or foul-smelling yolk sacs suggestive of omphalitis. Tan/grey pinpoint foci may be evident in the liver suggesting focal hepatic necrosis. In more chronic cases hepatic foci are the result of granulomatous inflammation called paratyphoid nodules. Positive diagnosis can be made only with isolation of the organism. Serotyping is necessary to identify species.
3.2.1.3. Prevention
Once established, salmonellae are difficult to eradicate without extreme measures which usually involve slaughtering the entire flock. Sanitation is important especially when the hatching of chicks is part of the operation. Antibiotic treatment can suppress infection but will not eliminate the organisms. Some of the effective antibiotics include furazolidone, sulfaquinoxaline, sulfadiazine and tetracycline.
3.2.2. Pullorum disease and fowl typhoid
(Bacillary white diarrhea, White diarrhea)
Salmonella pullorum and Salmonella gallinarum, are two species-specific salmonellae only found in chickens, causing pullorum disease and fowl typhoid. S. pullorum and S. gallinarum are non-motile.
Pullorum disease is a bacterial infection of chickens and turkeys caused by Salmonella pullorum. The organism can be transmitted in fertile eggs from infected hens. Such passage results in offspring which chronically shed organisms in feces. An agglutination test developed in 1913 has been used to screen and eliminate poultry flocks infected with S. pullorum. This testing has been so effective that by 1945 pullorum disease was no longer of economic importance to the U.S. poultry industry. Today this disease is sporadically seen in small backyard poultry operations.
S. pullorum is a highly host adapted bacterium that is pathogenic in domesticate gallinaceous birds (chickens and turkeys). Although pullorum disease is caused by a salmonella bacterium, the disease rather than being localized to the GI tract results in a diffuse granulomatous process in many organs. In this regard pullorum disease can be considered the avian counterpart of human typhoid fever.
S. gallinarum is another highly host adapted bacterium of chickens and turkeys causing a pullorum-like disease known as fowl typhoid. The lesions of fowl typhoid, for practical purposes, can be considered the same as those of pullorum disease.
3.2.2.1. Clinical Signs
- Adult chickens and turkeys with pullorum disease are usually asymptomatic.
- Fertile eggs from infected hens show reduced hatchability. The chicks that do hatch are often weak and die 4 or 5 days after hatching.
- Chicks appear listless and huddle around the source of heat. Pasty white feces is adherent around the anus. Later, respiratory distress may be evident. Mortality is very high and usually peaks during the second or third week post hatching.
3.2.2.2. Diagnosis
Autopsy findings are variable. Some of the more commonly found lesions consist of nodular, grey/white foci in the lungs and myocardium. The GI tract may also show nodular and often necrotic foci that are especially prominent in the gizzard musculature, cecae and large intestine. The liver may show nodular foci similar to those seen in the myocardium. Microscopic examination of most tissues reveals diffuse, granulomatous inflammation. In some reports caseous abscessation is also present. S.pullorum is easily grown on blood agar. The organism should be positively identified by a laboratory capable of serotyping.
3.3. Avian colibacillosis
(Air sacculitis, Omphalitis, Salpingitis)
As with salmonellosis, all birds are potentially susceptible to enteric and septicemic E.coli infections. In poultry (chickens, turkeys and ducks), most of the outbreaks are associated with poor sanitation, inadequate nutrition or primary infections with viral or mycoplasma agents. Several disease syndromes have consistently been associated with coliform infections. These include: air sacculitis, omphalitis (yolk sac infection) in baby chicks, septicemia in ducks (new duck syndrome) and chickens, enteritis, salpingitis, granulomatous lesions (coligranulomas sometimes referred to as Hjarre's disease), arthritis and synovitis, panophthalmitis and pericarditis. The latter two conditions are complications associated with septicemia. Serotypes commonly associated with poultry disease are O1-K1, O2-K1 and O78-K80. Under some circumstances E. coli can be passed through the pore in the egg shell to infect the embryo during the incubation period. Some of the more important of these conditions are discussed below.
3.3.1. Air sacculitis
This condition is most common in 5-6 week old broiler chickens and is usually the result of an underlying mycoplasma infections of the air sacs. Newcastle virus, infectious bronchitis virus and laryngotracheitis virus have also been linked to this condition. The abdominal air sacs are thickened with a loss of normal transparency with flecks of yellow material on the inner walls. Fibrinous exudate is usually also evident on the surface of the liver and pericardial sac. This is really the most common manifestation of the disease known as chronic respiratory disease or CRD.
3.3.2. Omphalitis
E. coli is often isolated in pure culture form the unabsorbed yolk sac of recently hatched chicks which clinically show depression, and variable mortality during the first few days of life. On gross examination the yolk sac contains a foul-smelling, pasty, yellow/brown yolk material. In additions the navel is swollen with moist exudate on the surrounding skin surface. Other common bacterial organisms have been associated with omphalitis including Proteus, Aerobacter, Salmonella, Staphylococcus, Streptococcus, and Bacillus.
3.3.3. Salpingitis
This is a relatively common condition in older laying hens. It is thought to result from and ascending coliform infection of the lower oviduct which subsequently prevents normal motility and resultant impaction with partially calcified yolks. The oviduct is markedly distended with yolk material which sometimes has a fetid odor if sepsis is extensive. Affected birds can live for long periods (6 months and longer).
4. Bacterial Respiratory Disease
4.1. Spontaneous bacterial respiratory diseases in psittacines
As with bacterial enteritis, bacterial respiratory disease is also often a stress associated phenomenon, including environmental stress (cold). Bacterial disease also commonly develops secondarily to an underlying Vitamin A deficiency.
The most common pathogens involved in psittacine bacterial respiratory diseases are:
- Klebsiella
- E. coli
- Enterobacter
- Pseudomonas
- Pasteurella
- Mycoplasma
Others encountered include:
- Salmonella
- Proteus
- Serratia
- Hemophilus
- Actinobacillus
- Chlamydia
- Aspergillus
4.1.1. Clinical signs
Clinical signs of respiratory disease may include sneezing, nasal discharge, dyspnea, lethargy, anorexia, exercise intolerance, wasting and rarely coughing. The clinical signs will vary according to the location of the infection, from the sinuses (upper respiratory), to the air sacs, or the lungs themselves.
4.1.2. Diagnosis
The diagnosis is based on clinical signs, choanal culture and sensitivity, and radiographs. Radiographs are extremely important in locating and characterizing the infection. Important differential diagnosis includes viral respiratory diseases (Amazon tracheitis virus), chlamydia, toxic inhalants (Teflon, smoke), allergies, fungal disease and dyspnea caused by abdominal distention (non-respiratory cause).
4.2. Avian Mycoplasmosis
Avian mycoplasmosis represents the most ubiquitous, economically devastating respiratory poultry disease in the United States. A conservative estimate of the annual loss to the commercial poultry industry would be well over 100 million dollars. Similar to mycoplasma infections in mammalian species, once established in a group of animals it is impossible to eradicate the infection unless the entire population is destroyed. Mycoplasma organisms are easily spread by aerosols and it is also possible to transmit the organism in fertilized egg. Although of high importance in poultry, mycoplasma infections in pet bird species are rarely diagnosed.
Respiratory mycoplasma infections in chickens and turkeys result in clinical signs and gross lesions that are remarkably similar to those caused by C. psittaci however avian mycoplasma infections are of no consequence to humans.
 Chronic respiratory disease in poultry
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4.2.1. Mycoplasma gallisepticum
(MG, Chronic respiratory disease, CRD, Air sacculitis, Infectious sinusitis of turkeys, PPLO infection)
This organism is widespread in the bird population. In addition to the chicken and turkey, natural infections have been documented in pheasants, peafowl, Coturnix and bob white quail, wild turkeys and housefinches. One source claims to have isolated the organism from a yellow-naped Amazon parrot.
4.2.1.1. Clinical Signs
4.2.1.1.1. Adult chickens
Signs are often non-specific consisting of decreased feed intake and a loss of normal growth rate. Laying chickens will show a variable drop in egg production. Signs of respiratory disease include: ocular and nasal discharge and mild dyspnea.
 Mycoplasmal sinusitis in a chicken
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4.2.1.2. Diagnosis
Air sacs are almost always affected but may vary in appearance from a mild cloudiness to severe thickening with floccular tan/yellow exudate on the inner lining. In severe cases there is extensive caseous material within the air sacs. Mucoid or mucopurulent exudate is often present in the nasal sinuses, choanae, and trachea. The pericardial sac is often thickened and cloudy. Turkeys may only show swelling of the infraorbital sinuses. However, they may also show air sac and upper airway lesions similar to chickens. A positive diagnosis of MG is usually made with a plate or tube agglutination test. Since this disease is almost always chronic, serum samples from several birds in an involved flock are used for this test. Isolation and identification of the organism is also possible.
4.2.1.3. Differential Diagnosis
Chlamydiosis, fowl cholera, colibacillosis, influenza and aspergillosis can resemble MG infections in the turkey and chicken.
4.2.1.4. Prevention
The most practical means of controlling M. gallisepticum is through the depopulation of infected flocks with subsequent effort to use stock derived for mycoplasma free breeders. This is often economically unfeasible. A method of immunization by controlled exposure has been practiced in some farms. Vaccine strains of mycoplasma are administered in the drinking water. There are no antibiotics that can be administered to chickens producing meat or eggs for human consumption that will eliminate M. gallisepticum or prevent the transmission of this organism in fertilized eggs.
4.2.2. Mycoplasma meleagridis (MM)
MM is a mycoplasma disease which only infects domestic turkeys. All age groups are affected. The pathogenesis and transmission are similar to that described above for M. gallisepticum. Although aerosols and egg transmission are the most common means of infection MM has also been shown to be transmissible to humans who handle poults during sex determination by the cloacal examination method. Semen has also been show to harbor the organism and MM can be venereally transmitted.
4.2.2.1. Clinical Signs
Young poults will often show a mild sinusitis however respiratory signs are rarely observed.
4.2.2.2. Diagnosis
Young poults show thickened air sacs, often with small amounts of flocculent, yellow material on the inner lining. Sinusitis and synovitis have also been seen in adults with MM infection. A plate agglutination test can be used to serologically confirm an outbreak.
4.2.2.3. Differential Diagnosis
MG and chlamydial infection must be considered in a provisional diagnosis of MM
4.2.2.4. Prevention
This disease is controlled in a similar manner as MG. However, the MM organism is somewhat more sensitive to antibiotic therapy and tylosin and tetracycline have been used to control and limit the signs of infection in poults. Lincomycin (spectinomysin) at the rate of 2gm/gal of drinking water has been used for the first 5-10 days of life to reduce the incidence of air sacculitis.
4.2.3. Mycoplasma synoviae
(Synovitis, Enlarged hock disease, MS, Tenovaginitis)
MS is not a respiratory mycoplasma infection but is included here for organizational purposes only. The disease is characterized by swollen hocks with exudates in the hock joints and Achilles tendon sheaths. Chickens and turkeys 4-12 weeks of age are most commonly affected. Guinea fowl are also susceptible. Infection is by aerosols and infected fertile eggs.
4.2.3.2. Diagnosis
The hock joints and tendon sheaths contain excessive, creamy to caseous, gray/yellow exudate in the joints and tendon sheaths. The sternal bursa may be filled with caseous material as a result of the birds resting on the keel and being unable to walk. This lesion is sometimes referred to as a "breast blister". Abscesses are sometime seen in the pads on the plantar surfaces of the feet. This lesion is sometime called "bumblefoot".
4.2.4. Mycoplasmosis in pet birds
Mycoplasma infections may be an undiagnosed component of respiratory disease in pet birds since it is difficult to isolate and culture. Although the pathogenesis of M.gallisepticum, M. synoviae, and M. meleagridis are well understood in chickens, these organisms are infrequenlty associated with disease in pet birds.
Close contact is required for successful transmission consequently, mycoplasmosis is most likely to be a problem in aviaries. When described, signs of mycoplasmosis in pet birds include chronic conjunctivitis, rhinitis, sinusitis, tracheitis, and arthritis. Infection may also contribute to decreased fertility and embryo or early chick mortality.
Tentative diagnosis is made on the basis of characteristic microscopic lesions and ruling out other causes of respiratory disease.
4.2.5. Mycoplasmosis in wild birds
Mycoplasmal organisms are likely very prevalent in many wild birds species. An emerging disease in house finches has involved a new strain of Mycoplasma, related to M. gallisepticum which has been spreading from the mid-Atlantic region across the US since 1994. Affected birds show clinical signs of conjunctivitis, rhinitis, and sinusitis, which can lead to anorexia, weight loss and increased susceptibility to predation. Bird feeders have been found to act as fomites and a place where birds congregate, leading to the spread of the disease. Treatment consists of tetracycline ophthalmic ointment and tylosin in drinking water. (see EID article and supplemental reading links at end of chapter for more information).
4.3. Infectious Coryza
(Coryza, Croup)
Infectious coryza is an upper respiratory diseases of chickens, pheasants and Guinea fowl. The disease is characterized by conjunctivitis, occulonasal discharge and swelling of the infraorbital sinuses. The causative organism is Hemophilus paragallinarum (formerly H. gallinarum) however it is likely that this organism becomes established in the upper respiratory tract and nasal sinuses as a result of a synergistic relation with M. gallisepticum. H. paragallinarum is transmitted by aerosol and has low survivability in the environment. Clinically healthy carriers of this organism are common.
4.3.1. Clinical Signs
Chronic occulonasal discharge with adhered eyelid margins in addition to swollen infraorbital sinuses in the absence of more severe respiratory signs are the typical presenting signs.
4.3.2. Diagnosis
The infraorbital sinuses are usually filled with a caseous, yellow exudate. In chronic cases the infraorbital abscesses may communicate with the choana. Gram stained smears of the exudate reveal small, Gram (-), bipolar, filamentous rods. H. paragallinarum can be grown on blood agar but, similar to all hemophilus organisms, requires the presence of a Staphylococcus aureus nurse colony to produce factor-V necessary for growth.
4.4. Turkey Coryza
(Turkey rhinotracheitis, Bordetellosis, Infectious sinusitis of turkeys)
Turkey coryza is clinically similar to coryza in chickens but the etiologic agent is Bordetella avium. The presence of Mycoplasma gallisepticum appears to enhance this disease and in all likelihood plays a role in the pathogenesis of this disease similar to that as described for coryza in chickens.
5. Pododermititis in Captive Wild Birds
A potential problem seen with captive raptors and many waterfowl species is a condition called bumblefoot. Certain higher stress species, such as falcons and accipiters, are predisposed to this problem. Bumblefoot usually results from a combination of factors, including inappropriate or dirty perching surfaces, conditions which force one foot to bear more weight than another, or immune suppression. Microscopic lesions develop on the plantar surfaces of the feet, allowing penetration of bacteria, most often Staphylococcus aureus. The resulting infection can range from a superficial dermatitis to a severe, deep lesion resulting in osteomyelitis. Treatment consists of correcting predisposing factors, appropriate antibiotic therapy based on culture and sensitivity, possible surgical intervention in severe cases, and therapeutic topical medications and bandages.
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6. Systemic Bacterial diseases
6.1. Mycobacteriosis
(M. avium, M. genevense, M. tuberculosis)
Mycobacterium avium is by far the most commonly encountered organism in this group. It is an "atypical" mycobacterium recently discovered to be genetically identical to M. paratuberculosis (Johne's in cattle). In addition to birds it has been known to infect pigs, guinea pigs, rabbits, and rarely humans (the zoonotic potential is slight unless immunosuppression is present in the human). In birds, both captive and wild, the presence of this mycobacterium is probably much greater than we realize. Disease is less common however.
6.1.1. Clinical signs
Clinical signs include cutaneous nodules/lesions, diarrhea, chronic wasting, anemia (bone marrow disease), arthritis, and sudden death. This disease is very insidious and typically involves a very prolonged course before clinical signs are apparent.
6.1.2. Diagnosis
Antemortem diagnosis is difficult. Possible testing can include biopsy (liver, spleen, intestine, etc.), fecal culture (takes several months), tuberculin testing (very unreliable in birds), CBC (marked leukocytosis, monocytosis), serum chemistry (elevated liver enzymes and bile acids), radiology, and exploratory laparoscopy. Serology is currently being developed and shows promise (see reference). Postmortem diagnosis is made through demonstration of the organism in multiple organs and most often in the intestinal tract (miliary lesions). These lesions are not always visible grossly and special acid fast stains must be requested in order to visualize microscopically. With proper staining, foamy macrophages filled with organisms will be seen. Mycobacterial species identification can be made only through culture and ID. A PCR test for M. avium and M. TB is available for biopsy or necropsy specimens
 Acid fast organisms in the liver of a toucan with
TB
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6.1.3. Treatment
Treatment for mycobacterial infections can be attempted with isoniazid, rifampin, ethambutol, streptomycin, clofazimine, cycloserine, etc. and has been avidly supported by certain avian veterinarians (Rosskopf). This position is controversial. Treatment must be continued for 18 months or more, is very expensive, and involves constant exposure to a very infectious organism. Control of an outbreak in an aviary can only be obtained through elimination of carriers and thorough cleaning of the environment (difficult). Contagion to other birds is very high and the organism will live in the soil for a very long time and is resistant to many disinfectants.
M. tuberculosis is very rare but can occur. It is most often contracted from an infected human caretaker. In birds this disease is usually a cutaneous disease with lesions around the face. Treatment is not recommended and positive diagnosis is REPORTABLE.
6.1.4. Tuberculosis in Poultry
Compared with pet birds the incidence in poultry is quite low. When encountered in poultry it is usually seen in small, backyard flocks. Mycobacterium avium is the most common species.
6.1.4.1. Clinical Signs
As in pet birds, signs are often non-specific and usually associated with progressive wasting and emaciation. Flocks that consist of older birds (more than 2 years of age) are most likely to be infected. Chronic diarrhea is sometimes present.
6.1.4.2. Diagnosis
At autopsy birds with tuberculosis will show nodular foci in the liver, spleen and intestinal serosa. Less frequently the spleen and bone marrow will show involvement. Acid fast stains of imprints of these nodules will show numerous, large, pleomorphic, acid fast bacilli. A tuberculin test is available using the avian strain of the organism and can be used to detect exposure to other members of the flock or colony. Chickens are usually tested by inoculation into the wattle. Other birds are inoculated in the wing web.
 Nodular lesions from TB in the liver
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6.2. Fowl Cholera
(Avian pasteurellosis, Avian hemorrhagic septicemia)
Fowl cholera is an acute, septicemic disease caused by Pasteurella multocida that effects chickens, turkeys, ducks, geese and many species of waterfowl. The disease occurs worldwide and is relatively common. A similar disease has been described in domestic ducks and is known as New Duck Disease, the causative organism is P. anatipestifer.
Fowl cholera almost always seen as an acute, rapidly fatal disease in poultry with a mortality that approaches 100%. The disease is more common in the late summer and fall with mature birds more susceptible than chicks. Recovered birds harbor the organism in the upper respiratory tract and nasopharynx. Wild birds and many mammalian species (cats and cattle ) harbor the organism in the nasopharyngeal region. These species are thought to spread the organism to susceptible birds. Birds that die in acute septicemia have the organism in all tissues and cannibalism is a common means of spreading an infection within the flock.
6.2.1. Clinical signs
- Acute fowl cholera is dramatic.
- Sudden deaths: laying hens are often found dead in the nest box, wild birds in large numbers are found in a given area..
- Toxicity is often suspected in outbreaks of acute fowl cholera.
- Sick birds are anorexic and depressed.
- Cyanosis of comb with respiratory rales and nasal and oral mucus discharge.
- White, watery or green-mucoid diarrhea is sometimes evident.
- Chronic fowl cholera results in birds with swollen joints, wattles, foot pad and tendon sheaths. Cheesy exudate may also be present in the conjunctival sac, and infraorbital sinuses.
6.2.2. Diagnosis
Gross lesions may be absent in birds that die peracutely. The most common findings are petechia or ecchymoses on the pericardium and serosal surfaces of the gizzard, small intestine, and abdominal fat. Numerous pinpoint grey/white foci may be present on naturnl ud cut surfaces of the liver. The lungs may be dark red with wet cut surfaces. A gram stained blood smear or imprint of the liver usually reveals numerous, gram-negative, bipolar bacilli characteristic of P. multocida. The organism is easily grown on blood agar.
 Pasteurellosis may produce epicardial petechiae
and/or multifocal hepatic necrosis
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6.2.3. Differential Diagnosis
Erysipelas and acute colibacillosis in turkeys are clinically similar to fowl cholera.
6.2.4. Prevention
Bactrins are available but are not always effective. A live oral vaccine is available for chickens and turkeys using the CU strain of P. multocida. Many antibiotics and sulfa drugs are available to treat fowl cholera. Culture and sensitivity tests are important since widespread resistance is common with this organism.
6.3. Erysipelas
Fowl erysipelas is usually an acute septicemic disease in turkeys caused by Erysipelothrix rhusiopathiae. The disease has also been reported in geese, ducks, pen-reared pheasants and other game birds. Male turkeys are more often affected than females but this is probably due to introduction of the organism through skin lesions of the snood which occur during fighting among male turkeys as they reach sexual maturity.
E. rhusiopathiae is shed in the feces of recovered turkeys in addition to infected lambs and swine. The organism can persist for years in the soil, however, disease outbreaks are most common in the late fall and early winter months. The oral route of infection is the most common portal of entry. Hen turkeys have been infected from artificial insemination suggesting that the organism may be shed in semen.
6.3.1. Clinical Signs
- Signs are sudden and usually consist of acute deaths with no other clinical signs.
- Morbidity and mortality increase suddenly during the next few days.
- Male turkeys will often show a swollen snood in addition to areas of cutaneous erythema reminiscent of the diamond skin lesion seen in swine with erysipelas.
6.3.2. Diagnosis
Gross lesions are typical of acute septicemia and similar to those described for fowl cholera. Petechia are common on the epicardium, intestinal serosa and abdominal adipose tissue. Splenomegaly is common. Suppurative arthritis may be present in birds that live a few days after showing clinical signs. Tan, friable, vegetative lesions may be present on the AV valves. Gram stained impression smears from cut surfaces of the liver, spleen or bone marrow will usually reveal numerous, pleomorphic, gram positive, thin bacilli.
7. Chlamydiosis
(Chlamydiosis, ornithosis, psittacosis, parrot fever)
| Family Chlamydiaceae | |
| Genus Chlamydia | |
| Chlamydia trachomatis | human ocular and venereal infections |
| Chlamydia suis | swine |
| Chlamydia muridarum sp. nov. | hamsters and mice |
| Genus Chlamydophila | |
| Chlamydophila psittaci | 6 avian serovars and 2 mammalian serovars: birds, humans, separate serovars for pigeons, turkeys |
| Chlamydophila pneumoniae | humans, horses, koalas, other mammals |
| Chlamydophila pecorum | mammals, incl. koalas |
| Chlamydophila felis | cats |
| Chlamydophila caviae | guinea pigs |
| Chlamydophila abortus | ruminants |
7.1. Introduction/Historical perspective
Avian chlamydiosis is an important disease from two aspects: it is a significant disease in most avian species (150 species documented), and it can become a zoonotic disease with potential to spread to humans. The classification of Chlamydial organisms has recently changed considerably (see references www.chlamydiae.com). Previously, most of the chlamydia were identified as Chlamydia psittaci. The avian chlamydia is now called Chlamydophila psittaci. The current complement of chlamydial organisms are listed in the table above.
The documentation of human respiratory infection as a result of association with birds has been known for more than a hundred years. However, knowledge of the clinical aspects of the disease was elucidated in the pandemic of 1929 -1930 when it was thought that only psittacines could transmit the disease. Prior to the development of tetracycline antibiotics, psittacosis was a serious human disease associated with a 20% mortality. Since that time it has been shown that virtually all avian species can be infected with C. psittaci and that a wide range of pathogenicity exists. This is true for the disease produced in birds and in humans. Turkeys and ducks are the chief source of human infections from industry.
Chlamydial infections are endemic in avian and mammalian populations. At least 159 wild avian species have been shown to be infected. In most birds infection is inapparent and the shedding of organisms is common.
Government intervention and current quarantine practices for pet birds were set up in 1974. This quarantine procedure is really designed for the detection of VVND, and is only carried out for 30 days. Psittacosis is not considered an exotic disease since it is well established in wild and captive bird populations in North America. Prophylactic treatment for psittacosis during quarantine is often practiced, but this policy is no longer mandatory. Treatment with chlortetracycline is often less than optimal. Because of the zoonotic potential, chlamydiosis in birds is considered a REPORTABLE disease and specific quarantine and treatment regimens must be carried out for those cases that arise. These practices will be discussed below.
7.2. Pathogenesis of chlamydiosis
7.2.1. Characteristics of the organism
The organism was not completely characterized or understood until the mid 1960's! It was previously felt to be a "large virus".
Chlamydial species are obligate intracellular bacteria similar to mycoplasma and rickettsia. They can multiply only within the cytoplasm of living cells. The organism has a spherical shape 0.2 - 1.5 m in diameter. It forms an elementary body as the infectious form of the organism, which grows into the reticulate body (the vegetative phase). The reticulate body replicates by fission and produces daughter cells.
The organism is shed intermittently in feces and respiratory secretions. It can be visualized in infected tissue preparations using Giemsa, Castaneda, Maccievellos, or Gimenez staining techniques. It is Gram negative. Isolation requires growth in cell culture of murine, avian, or human cell origin. It can also be propagated in chicken embryos, mice and guinea pigs.
The organism can survive in the environment for several months. It is destroyed by quaternary ammonium compounds and lipid solvents. Common disinfectants that are effective include benzalkonium chloride (Roccal or Zephiran), 70% alcoholic iodine solution in ethanol, 3% hydrogen peroxide, and silver nitrate. Chlorhexidine is not effective against chlamydia. Freezing does not kill the organism (need 6 freeze-thaw cycles).
7.2.2. Characteristics of the disease in poultry and wild birds
Chickens rarely become clinically ill with ornithosis. Mild outbreaks may be so insignificant as to go unnoticed. In some instances mild respiratory signs and/or diarrhea may be seen. Young birds may develop acute fibrinous pericarditis and hepatitis.
More severe outbreaks in turkeys, ducks, geese or pigeons will show severe depression, anorexia, respiratory distress and nasal discharge. Yellow-green diarrhea may also be evident in addition to vague neurologic signs suggestive of ataxia or paresis. In pigeons, the asymptomatic carrier state may be important as a wild reservoir and continuing source of infection for more susceptible species.
Most often, wild birds are asymptomatic carriers. Some of these strains however may be extremely pathogenic for people, other mammals, and other birds.
7.2.2.1. Chlamydia Outbreak in Turkeys - an example
In a 1986 Minnesota outbreak, 12 flocks were suspected, and the disease was confirmed in 10. The original source of infection was felt to be from wild birds. The turkeys showed clinical signs of malaise, anorexia, 6% mortality, mild diarrhea, weight loss, and many with no
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