The seasonal variance, global warming, and extraordinary climate conditions around the world change the physiology and behaviors of different animal species. Free ranging birds and mammals harbor some species of potentially pathogenic bacteria; however, these diseases do not result in spontaneous deaths. Being significant individuals of the ecosystem, free living immigrant birds are prone to bacterial diseases. Migratory birds are accommodated in areas located on migration routes to provide rest, food, and water. During this stay, they spread the diseases they bring with them to the poultry in the region and to the poultry farms that do not take adequate biosecurity measures—especially to the free range poultry farms. The migratory birds confront numerous health risks brought on by bacterial species that affect other livestock populace and public health. This chapter provides brief reference on bird-to-bird transmission and general aspects of emerging bacterial zoonoses of migratory birds for wildlife professionals, veterinary practitioners, and students.
- migratory birds
- emerging zoonoses
- bacterial diseases
Numerous wild bird species exist together with people and depend on anthropogenic wellsprings of environment and nutrition. Bird migration is one of the most curious topics in humans about birds’ lifetime period. This behavior is one of the most important and critical turning points for birds throughout their lives. Every year more than 50 billion birds in the world migrate, depending on the seasonal change of food resources, and 5 billion birds of 187 species leave Europe and Asia each year and migrate to Africa. Migratory birds relocate a large number of kilometers all through various mainlands and convey certain pathogens. Sixty-one percent of human pathogens are zoonotic, 60.3% of all developing diseases in people are zoonoses, and 71.8% of these initiate in natural life. The recurrence of free living fowl death occasions and the assortment of irresistible bacterial maladies have expanded extraordinarily amid late decades. Convenient and exact identification of mortality is expected to appropriately guide disease control procedures [1–3]. This review presents brief of emerging bacterial diseases of migratory birds.
2. Emerging bacterial zoonoses in migratory birds
2.1. Avian cholera
Avian cholera is an infectious disease coming about because of contamination by
Acute pasteurellosis infections are common in worldwide and they can cause bird deaths in 12 h, albeit 24–48 h is typical. Vulnerability to contamination and the formation of malady depends on various factors, including gender, age, and hereditary variety . Many birds harbor the organism in nasal clefts. The presence of the bacterium is generally related to severity of upper respiratory infection in the birds. The enzootic focus of infection is healthy nasal carriers . Transmission to vulnerable birds from contaminated wetlands or from direct bird-to-bird contact is the in all probability routes of transmission amid epizootics (Figure 1). Two field cultures were isolated from raccoons that were pathogenic for poultry. Sparrows and pigeons carried organisms without showing clinical signs, but 10% of infected rats developed acute pasteurellosis. The possibility that insects may serve as vectors of FC has been investigated. Transmission by flies, however, is probably not common, as indicated by previous studies. Although FC was maintained in two lots of chickens during the height of the fly season, no spread of the disease occurred to adjoining lots separated only by bird nesting. It was observed that larvae, nymphs, and adult ticks (
2.1.2. Clinical aspects
Birds that survive the initial acute septicemic stage may later succumb to the debilitating effects of emaciation and dehydration, may become chronically infected, or may recover. Female Common Eiders are frequently discovered dead sitting on their clutch . Birds with signs suggestive of neurological involvement (unpredictable ungraceful flight, surrounding while at the same time strolling or swimming, or opisthotonos) have additionally been accounted for .
Similarly as with other bacterial diseases, isolation of the causative agent is required for an authoritative identification. To isolate
2.1.4. Treatment and prevention
Antibacterial chemotherapy has been used extensively in the treatment of FC with varying success, depending to a large extent on the promptness of treatment and drug used. Sensitivity testing is often advantageous, because strains of
Salmonellosis can be transmitted from multiple points of view. The relative contribution of vertical transmission in the two organisms is unclear because it is easy to establish persistent infections and egg transmission with
2.2.2. Clinical aspects
The birds can manifest somnolence, weakness, depressed appetite, poor growth, and adherence of chalky white material to the vent. Death ordinarily follows inside 24 hours. On the off chance that enteritis occurs, there might be diarrhea, making the vent pasted with liquid defecation and urates .
At the point when the esophagus is cut open, the nodules might be viewed as huge, diffuse plaque-like nodules or as discrete, nodular regions inside the esophagus (Figure 2). Occasional cases of PD can be subclinical, even though the disease may originate by egg transmission. Mortality usually peaks during the second or third week of life. In these situations, the birds exhibit lassitude and an inclination to huddle together under heaters, having droopy wings and distorted body appearance. Labored breathing or gasping may be observed as a result of extensive involvement of the lungs due to PD. Survivors may be greatly retarded in their growth and appear underdeveloped and poorly feathered. In certain instances, a relatively high incidence of infection in the joints, which can produce lameness and obvious joint enlargement, can occur in juveniles. In acute to subacute cases, there is multifocal necrosis of hepatocytes. In chronic cases, especially in cases in which there are large nodules in the heart, the liver will have chronic passive congestion with interstitial fibrosis. The spleen may have severe congestion or fibrin exudation of vascular sinuses in acute stages and severe hyperplasia of the mononuclear phagocytic system cells in later stages. The ceca in young chicks may have extensive necrosis of the mucosa and submucosa, with an accumulation of necrotic debris mixed with fibrin and heterophils in the lumen .
The clinical signs and lesions produced by PD or FT are not pathognomonic. Other
2.2.4. Treatment and prevention
The disinfection must be done daily with hypochlorite-type solutions in feeding points of free-ranging birds in consequence of sudden outbreaks. Reasonably effective prophylactic and therapeutic drugs for poultry production have been developed against PD and FT. Treatment is generally neither feasible nor desired. Sulfonamides, in particular, frequently suppress growth and may interfere with feed and water intake and egg production. Sulfonamides that have been used in the treatment of PD and FT include sulfadiazine, sulfamerazine, sulfathiazole, sulfamethazine, and sulfaquinoxaline. Transmission through shell penetration and feed contamination by
2.3. Avian botulism
Synonyms for botulism are “Limberneck” and “Western duck sickness.” Free-ranging and confinement-reared poultry and feral birds can be affected. Most avian cases are caused by
Laboratory examinations exhibited that decomposing flesh contaminated with botulinum cells or spores can support the production of high amounts of toxin. Waterbirds and different vertebrates unintentionally digest bacteria spores while feeding and convey them in their tissues. Upon death, the subsequent anaerobic condition and rich protein source of cadaver are ideal for vegetation of spores and toxin formation [21, 22].
Avian type C botulism can be caused by ingestion of preformed toxin or by toxico-infection. More than 2000 minimum lethal doses (MLD) of type C toxin/gram of carcass tissue of intoxicated birds have been found. Birds scavenging such carcasses can readily obtain enough toxins to become affected. Fly-blown carcasses may have maggots containing 104–105 MLD of neurotoxin. In aquatic environments, small crustaceans and insect larvae may contain
2.3.2. Clinical aspects
Clinical signs of botulism in chickens, turkeys, pheasants, and ducks are similar. In chickens, flaccid paralysis of legs, wings, neck, and eyelids are predominant features of the disease. Wings droop when paralyzed. Limberneck, the original and common name for botulism, precisely describes the paralysis of the neck. Because of eyelid paralysis, birds appear comatose and may seem dead. Gasping has been reported when birds are handled. Death results from cardiac and respiratory failure. Affected chickens have ruffled feathers, which may fall out with handling. Quivering of certain feather tracts has been observed. Broiler chickens showing signs of botulism may have diarrhea with excess urates in the loose droppings .
2.3.4. Treatment and prevention
Antitoxins can be applied to sick captive birds in early stage of the malady. The most widely recognized strategy for preventing disease is by evacuation of cadavers before development of flies in order to counteract distribution of toxin to different bird populations. In problem areas, removal of contaminated litter and thorough disinfection using calcium hypochlorite or formalin may help reduce spore numbers in the environment. Disinfection of areas around poultry houses has been recommended because spores may be located in the soil outside of the poultry facility and can be transported back into houses. Fly control may be another means of reducing the risk of toxic maggots in the environment. Two cases of type C botulism were reported in commercial broilers and were associated with elevated intake of iron from water and feed sources. However, the relationship between iron and toxicoinfectious type C botulism needs to be experimentally confirmed .
2.4. Avian tuberculosis
Nontuberculous mycobacteria, including MAC, are ubiquitous in the environment and are commonly isolated from soil and water. Humans become infected by ingestion or inhalation of MAC organisms from the environment. Infected animals and birds commonly shed mycobacteria in their feces, but are not considered to be an important source of human infections. The contaminated environment, especially soil and litter, is the most important source for the transmission of the bacilli to uninfected animals. The longer the premises have been occupied by infected birds and the more concentrated the poultry population, the more prevalent the infection is likely to be [30, 31].
2.4.2. Clinical aspects
The liver (Figure 3A) generally contains similar nodules, but intestines (Figure 3B), spleen (Figure 3C), and lung can present such nodules. Aggregations of these nodules may appear as firm, fleshy, grape-like clusters. Abscesses and nodular growths (Figure 4) have been reported on the skin of birds in the same locations where pox lesions are frequently seen around the eyes, at the wing joints, on the legs, side of the face, and base of the beak .
Demonstration of acid-fast bacilli in smears or histologic sections of liver, spleen, or other organs strengthens the diagnosis and is sufficient for most diagnostic cases. In live, suspected infected birds, fecal smears for culture, staining, and/or PCR may be attempted but these tests are not reliable due to intermittent or no fecal shedding of bacilli . Fecal positivity increases as the disease course progresses . PCR has been used to detect mycobacteria, including
2.4.4. Treatment and prevention
Control of avian tuberculosis in free-living birds is not viewed as plausible on the field since the bacteria perseveres in the field, is resistant to numerous tuberculosis medications and detergents, and it is hard to isolate from sick birds. Treatment with antituberculosis drugs is impractical; however, combinations of isoniazid (30 mg/kg), ethambutol (30 mg/kg), and rifampicin (45 mg/kg) may be applied to captive birds. The recommended duration of therapy is 18 months, provided that there were no adverse side effects .
2.5. Avian chlamydiosis
Chlamydiosis alludes to an infection with microorganisms of the genus
Infection usually occurs with the inhalation of bacteria that are released into the air from birds’ feather patches. Contagion also develops via beak-to-beak feeding from mother bird to juveniles. Since the chlamydia is not completely eliminated, reinfection and damage to host tissues continue. In persistent infections, the inflammatory response increases, chronic inflammatory advances continue in the focal areas, and the etiologic agent is shed from the damaged tissues. Vertical transmission has been demonstrated in ducks, parakeets, seagulls, and snow geese [37, 38].
2.5.2. Clinical aspects
Fowls frequently end up noticeably feeble, quit eating, and create purulent (liquid containing discharge) releases of the eyes and nares. Birds have a tendency to wind up plainly still, stay in a settled position, and crouched up with unsettled feathers . Signs of chlamydiosis in turkeys infected with virulent strains are cachexia, anorexia, elevated body temperature, conjunctivitis, and respiratory distress. Diseased birds excrete yellow-green, gelatinous droppings. Egg production of severely affected hens declines rapidly to 10–20% and may temporarily cease or remain at a very low rate until complete recovery. Disease signs in a flock infected with strains of low virulence are usually anorexia and loose, green droppings in some birds, with less effect on egg production. In overwhelming infections with virulent strains, lungs show diffuse congestion, and the pleural cavity may contain fibrinous exudate. In fatal cases, a dark transudate may fill the thoracic cavity. The pericardial membrane is thickened, congested, and coated with fibrinous exudate. The liver is enlarged and discolored and may be coated with thick fibrin in birds that survive infection with a strain of low virulence, the lungs may not be seriously affected. However, multiplication of organisms on the epicardium may result in the formation of one or more fibrin plaques .
The recommended medium for chlamydiae consists of SPG buffer. For isolation, the following samples should be preferably collected: pharyngeal/choanal slit swabs in live birds. Cloacal swabs or fresh feces are less optimal because chlamydial shedding is intermittent. In dead birds, lungs, spleen, and liver can be sampled. The specimen should be stored at −80°C if it will not be sent to laboratory immediately . This methodology would be the same or comparative for migratory birds.
2.5.4. Treatment and prevention
Chlamydiosis treatment for poultry has not changed over the years. The drug of choice varies from country to country. Among tetracylines, which are the drugs of choice, chlortetracycline and doxycycline are most often used. Enrofloxacin (fluoroquinolone antibiotic) can also be used. Contact with potential reservoirs or vectors such as pet birds, rodents, arthropods, and wild and feral birds should also be prevented. General sanitation must be practiced diligently. Movement of people should be restricted so that visitors do not have free access to premises holding birds. This is easier to accomplish if birds are confined in houses and if the “all-in-all-out” principle is used on the farm .
Mycoplasma phylogeny and taxonomy continue to be re-examined by the application of molecular tools such as DNADNA hybridization DNA sequence analysis of the 16S rRNA gene, 16S rRNA PCR and denaturing gradient gel electrophoresis, and tRNA gene PCR. The complete genome sequence has been determined for MG strains Rlow, Rhigh, and F , and a database dedicated to the comparative genomics of Mollicutes, including MG, has been established .
Experimental intra-crop inoculation of house finches resulted in infection, disease, and a serological response .
2.6.2. Clinical aspects
In house finches, MG causes mild-to-severe eyelid swelling, conjunctivitis, and watery discharge from one or both eyes as well as nares. Air sacs frequently contain caseous exudate that may be focal, multifocal, or diffused. Conjunctivitis with periocular swelling and inflammation are characteristics of MG in house finches and other songbirds .
The gold standard for MG diagnosis is isolation and identification of the organism. In some cases, the isolation of MG in culture is impaired by the overgrowth of saprophytic mycoplasmas that inhabit the upper respiratory tract of avian species and contaminant bacteria and fungi that may not be successfully inhibited by mycoplasma-selective media. To culture MG, fluid sinus exudate should be inoculated directly to mycoplasma broth and/or agar media . Swabs can also be taken from the trachea or choanal cleft (palatine fissure) for MG culture.
2.6.4. Treatment and prevention
Tularemia is essentially a malady of mammals, yet normal diseases by
There are no reports of the clinical course in normally infected birds, and clinical signs in wild animals are inadequately archived, principally because of the acute character of tularemia in many species .
The bacteria can also be identified in culture or specimens by hybridization with probes specific to the 16S rRNA gene of
Avian cholera has become the most important emerging bacterial disease of waterbirds and geese. The vast majority of the geographic extension and expanded recurrence of outbreaks of avian cholera has happened since 1970. The high prevalence of avian tuberculosis disease that has happened since 1982 has challenged the survival of crane populations. Salmonellosis has turned into a noteworthy source of mortality at poultry breeders all through the world, and mycoplasmosis in house finches has turned into the most quickly spreading infection at any point found in free living birds. Avian botulism has likewise extended in geographic circulation and has increased expanded noticeable prominence as a disease of waterbirds. It is, without a doubt, the most critical malady of waterbirds around the world. The geographic expansion of avian botulism has mostly occurred during the past quarter century. Of the diseases addressed in this section, chlamydiosis and tick-borne pathogens pose the greatest risk to public health and other livestock, especially poultry production. Avian tuberculosis can be a significant risk for humans who are immunocompromised. Salmonellosis is a common, but seldom fatal, human infection that can be acquired from infected wild birds. Convenient and exact identification of mortality is expected to appropriately guide disease control procedures. Keeping in mind the main scope to precisely identify which diseases are emerging and zoonotic in the field, specimen should be sent to avian research laboratories, which know about the wide assortment of conceivable diseases that may infect wild birds and domestic livestock.