Bacterial Disease

Avian chlamydiosis is characterized by respiratory, digestive, or systemic infection. Infections are cosmopolitan in distribution and have been identified in at least 460 avian species.Among them poultry, turkeys, ducks, and pigeons are most often affected.  The disease is a significant cause of economic loss and human exposure in many parts of the world.

Etiology

Chlamydia psittaci, formerly renamed Chlamydophila psittaci, is an obligate intracellular bacterium.

Transmission:

Transmission is by the fecal-oral route or by inhalation. Airborne particles and dust spread the organism. Persistence of C psittaci in the nasal glands of chronically infected birds may be an important source of organisms.

Clinical Findings

Clinical signs and symptoms are variable depends upon the virulence of the organism, infectious dose, stress factors, and susceptibility of the bird species; asymptomatic infections are common.

Nasal and ocular discharge, conjunctivitis, sinusitis, green to yellow-green droppings, fever, inactivity, ruffled feathers, weakness, inappetence, and weight loss can be seen in clinically affected birds.

Lesions:

Serofibrinous polyserositis (airsacculitis, pericarditis, perihepatitis, peritonitis), pneumonia, hepatomegaly, and splenomegaly are most often observed. Multiple tan to white to yellow foci and/or petechial hemorrhages can be seen in the liver and spleen. Lesions are usually absent in latently infected birds, even though C psittaci is often being shed.

Diagnosis

Due to difference in the clinical presentations and common occurrence of latently infected carriers, no single diagnostic test can reliably determine infection.

The combination of a serologic and an antigen detection test, especially PCR, or culture, is a practical diagnostic scheme to confirm chlamydiosis. Serologic methods include direct and modified direct complement fixation, elementary body agglutination, antibody ELISA, and indirect immunofluorescence. The elementary body agglutination test detects IgM and is useful to determine recent infection. The complement fixation methods are more sensitive than agglutination methods. High antibody titers may persist after treatment and complicate evaluation of subsequent tests.

Antigen detection methods include immunohistochemistry (eg, immunofluorescence, immunoperoxidase), ELISA, and PCR. ELISA kits developed for detection ofChlamydia trachomatis in people are available commercially and are relatively inexpensive. The organism can also be identified in impression smears of affected tissues (eg, liver, spleen, and lung). Chlamydiae stain purple with Giemsa and red with Macchiavello and Gimenez stains.

Treatment

Avian chlamydiosis is a reportable zoonotic disease. Treatment prevents mortality and shedding but cannot be relied on to eliminate latent infection; shedding may recur. Tetracyclines (chlortetracycline, oxytetracycline, doxycycline) are the antibiotics of choice. Drug resistance to tetracyclines is rare, but reduced sensitivity requiring higher dosages is becoming more common. When tetracyclines are administered orally, additional sources of dietary calcium (eg, mineral block, supplement, cuttle bone) should be reduced to minimize interference with drug absorption.

Doxycycline is the current drug of choice, because it is better absorbed, has less affinity for calcium, better tissue distribution, and a longer half-life than other tetracyclines.

Zoonotic Risk

Avian chlamydiosis is a zoonotic disease that can affect people after exposure to aerosolized organisms shed from the digestive or respiratory tracts of infected live or dead birds or by direct contact with infected birds or tissues.

Some individuals, especially pregnant women and those with impaired immunity, are more susceptible than others. The illness in people is usually respiratory and varies from flu-like symptoms to systemic disease with pneumonia and possibly endocarditis and encephalitis.

Listeriosis is caused by the bacterium Listeria monocytogenes. Although many species of birds, including chickens are susceptible to infection but clinical disease in birds is rare.

Etiology

Caused bya gram-positive, non-spore forming, facultative intracellular, rod-shaped bacterium Listeria monocytogenes . Transmission occurs via ingestion, inhalation, or wound contamination.

Clinical Findings

Clinical signs are not specific in septicemic form but include depression, lethargy, and sudden death. In the encephalitic form, torticollis, leg paddling, opsisthotonos, paresis and paralysis lateral recumbency, ataxia, have been seen.

Lesions:

In septicemic form of listeriosis, extensive degeneration and necrosis of the myocardium along with splenomegaly, necrotic foci in the liver, and pericarditis.

 In the encephalitic form, no gross lesions are seen in the brain, but histopathologic lesions are remarkable and include disseminated microabscesses, extensive fibrinous thrombosis.

Diagnosis

Diagnosis is confirmed by immunohistochemistry to demonstrate L monocytogenes in the tissues or by isolation of the organism, usually from the liver and/or spleen in the septicemic form and brain in the encephalitic form.

Treatment and Prevention

Antibiotics may be used successfully to treat the septicemic form of the disease. In vitro, L monocytogenes is susceptible to penicillin, tetracycline, erythromycin, gentamicin, and trimethoprim-sulfamethoxazole. Treatment of the encephalitic form is usually unsuccessful. Prevention should focus on identifying and eliminating potential sources of infection.

Zoonotic Risk

Listeriosis is a serious zoonotic disease. L monocytogenes is recognized as an important food-borne pathogen in people and is of great concern to the public and poultry industry.

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Campylobacteriosis is a significant enterocolitis of people frequently acquired through consumption of undercooked poultry meat contaminated with Campylobacter jejuni. It is the leading bacterial cause of sporadic enteritis in developed countries. Some strains of C jejuni have been reported to cause enteritis and death in newly hatched chicks and poults

Cause:

C jejuni is the predominant species associated with food borne infection derived from poultry. C coli and C lari can also be recovered from the intestinal tract of poultry and have also been implicated in foodborne infection.

Once C jejuni has been introduced into the environment, rapid transmission within the flock occurs, with subsequent colonization of a high proportion of exposed breeders, commercial-meat, or laying-strain poultry. Some strains of Campylobacter can be transmitted vertically, either on the surface of eggs or by trans-ovarian transmission. It has been isolated from the reproductive tracts of hens and roosters.

Clinical Findings and Lesions

Most chicks display no lesions associated with Campylobacter infection. Frequently observed lesions are distention of the jejunum, Disseminated hemorrhagic enteritis, Focal hepatic necrosis.

Microscopic lesions of infected chicks include edema of the mucosa of the ileum and cecum with C jejuni in the brush border of enterocytes. Mononuclear infiltration of the submucosa and villous atrophy occur, with intraluminal accumulation of mucus, erythrocytes, and mononuclear and polymorphonuclear cells.

Diagnosis

Campylobacter can be cultured on many different selective media, but commonly available formulations contain Brucella agar base and bovine blood with as many as seven antibiotics that inhibit overgrowth of Enterobacteriaceae. They also can be cultured on blood agar by selective filtration.

Control and Prevention

Because C jejuni is not found as a specific pathogen under commercial conditions, treatment of poultry flocks is not a consideration. If C jejuni is considered a problem in companion bird aviaries or in exotic species, Antibiotics such as erythromycin can be administered in drinking water. Fluoroquinolones and erythromycins are the classes of antimicrobials used to treat people for campylobacteriosis. Sanition is the key for prevention.

It is a very important wide spread bacterial disease causing great economic loss in the poultry industry. It affects the birds of different age group.

Cause

It is caused by various strains of Escherichia coli.There are various strains which are abundantly present in the environment but all are not pathogenic.Based on antigenic structure are O antigen(154 serotypes),K antigen(88),H antigen(49) and all together 292 serotypes Most common serotypes in poultry are O1,O2,O35 and O78 andin human O157. It is estimated that 15% of the intestinal coliforms are potentially pathogenic. Infection can be primary or secondary after primary host defense damage (eg respiratory viral infections, Mycoplasma infections, parasites, wounds, nutrition).

Transmission

E. coli are normal intestinal inhabitants and are shed via  feces. Egg transmission (via egg surface contamination) is also common and can lead to high chick mortality.The water and droopings are the main source of spread of the disease. Infected cage and incubator act as constant source of infections. Contaminated feed is the frequent source of transmission.

Clinical Signs

Colisepeticemia:Acute infection day to week chicks,characterized by bronchopneumonia,pasty vent with diarrhea,mortality upto 60%.Enteritis:More common in young than adults usually diarrhea.Coligranoloma(Hajares Disease),Omphalitis (Mushy Chick disease), Egg Peritonitis, Arthiritis, Panopthalmitis, Pericarditis

Diagnosis

Isolation and identification of organism, clinical signs with characteristics postmortem lesion(plastic membrane in liver surface,pericardial sac,air sac,pericarditis)

Treatment

Antibiotics based on antibiotic sensitivity test. Drugs like furaltadone,neomycin & doxycyline, chloramphenicol, ampicillin, enrofloxacin, gentamicin and kanamycin have been found to be sensitive.

Control

Biosecurity, proper hatchery management, use of pellet feed,use of probiotics, acidification of gut e.g.citric and fumaric acid @0.5% feed .E.coli vaccination and vaccination against primary causes like respiratory viruses, coccidiosis, IBD, CAV.

It’s a bacterial disease caused by Erysipelothrix rhusiopathiae. This causative organism infect wild rang of birds Disease form is most commonly seen as septicemia but urticarial and endocardial forms also exist.

Erysipelas in poultry is seen worldwide and, although considered a sporadic disease, endemic areas exist.

Etiology:

E rhusiopathiae is a facultative, anaerobic bacterium. Two additional genomic species have been described: E tonsillarum, and most recently E inopinata, but neither is considered pathogenic for poultry. The organism is small, non-acid fast, nonmotile, does not form spores, and produces no known toxins. There is no flagellum, but a capsule has been demonstrated.

Epidemiology

Erysipelas occurs sporadically in poultry of all ages. It is ubiquitous in nature and found where nitrogenous substances decompose.

In nonvaccinated flocks, morbidity and mortality rates may reach 40%–50%, but mortality is usually <15%. In vaccinated flocks, some birds may be depressed for a short period and recover. Mortality in vaccinated and nonvaccinated poultry is influenced by the virulence of the organism.

Clinical Findings:

– Droopy, with an unsteady gait

– Cutaneous lesions and swollen hocks

– Decrease in Egg production and conjunctival edema can be seen in organic, cage-free flocks.

– Egg production may drop markedly

Lesions

Gross lesions such as peritonitis, pericarditis, petechiation of the heart, catarrhal exudate in the GI tract, and degeneration of fat associated with the thigh and heart may be noted. Vascular damage and fibrin thrombi are common findings on microscopic examination.

Diagnosis

A presumptive diagnosis can be based on an impression smear of the liver or spleen or on a smear of cardiac blood or bone marrow that shows gram-positive, slender, pleomorphic rods. Bone marrow is the tissue of choice in partially decomposed specimens. Isolation and identification of E rhusiopathiae is necessary for definitive diagnosis. Identification can be made by fluorescent antibody staining and PCR

Treatment

The antibiotic of choice is a rapid-acting penicillin such as potassium or sodium penicillin. As soon as a presumptive diagnosis is made, penicillin should be administered IM at 22,000 U/kg body wt, simultaneously with a full dose of erysipelas bacterin.

Vaccination will control erysipelas. Both inactivated and live vaccines are available for use in turkeys; only vaccines approved for use in turkeys should be used.

Fowl Cholera ( Avian Cholera, Pasteurellosis, Avian Haemorrhagic Septicaemia)

Cause

Pasteurella mulotocida, a gram negative bacterium that casuses fowl cholera

Transmission

It takes place by ingestion of contaminated feed or water. It is not transmitted vertically through eggs. The flies and red mite act like carriers while the rodents (rats and mice) can contaminate the feed and water.

Species affected

It can affect turkeys, chickens, ducks, geese, etc.

Clinical signs and lesions

There is depression and decrease in appetite in the birds. There is fall in egg production by 5-15%. In case of acute infection, there is bluish combs and wattles while there is swollen wattles in chronic infection. Mortality is higher in acute infection than chronic infection.

The lesions in acute phase include vascular changes in abdominal viscera, haemorrhages, liver swollen with focal necrosis, flaccid and haemorrhagic ovaries and ruptured yolks. The lesions in chronic phase include localized infections in conjunctiva and facial odema. The lesions can also be seen in infection in middle ear which causes torticollis and infection in meninges.

Diagnosis

It is diagnosed on the basis of clinical signs. Virus can be isolated from the affected internal organs.

Treatment and Control

It is treated by use of antibiotics after antibiotic sensitivity test. The proper management of hygiene and control of rodents are to applied for prevention. The live and inactivated vaccines can be given in the endemic areas.

Disease is characterized by rapid onset of acute mortality.  Birds succumbing to the infection have necrosis of the skin and subcutaneous tissue, usually involving the breast, abdomen, wing, or thigh.

Etiology:

It’s the disease of turkeys and chickens caused by Clostridium septicumC perfringens type A, and Staphylococcus aureus, either singly or in combination.

Clinical Findings

clinical findings are generally includes  depression, incoordination, inappetence, leg weakness, ataxia, and high fever.

Lesions:

Gross lesions consist of dark reddish purple to green, weepy areas of the skin. Affected areas usually include abdomen, breast, wings, or legs. Areas of affected dermis and subcutis are characterized by extensive blood-tinged edema, with or without gas (crepitus). Infection may extend into underlying musculature, which may be discolored and contain edema and gas.

Diagnosis

Tentative diagnosis is based on the history, lesions and clinical findings. Diagnostic confirmation is based on the presence of lesions and isolation of the causative agent(s) from affected tissue.

Treatment and Control

Total cleanout and disinfection of affected houses has reduced or eliminated gangrenous dermatitis infection on farms with historical problems. Salting of floors has also reduced bacterial challenge in subsequent flocks.

Gangrenous dermatitis can be treated effectively with administration of many broad-spectrum and gram-positive antibiotics. Water acidifiers have been used in cases to reduce, but not eliminate, mortality where mortality rates are low or antibiotic efficacy has been poor.

It is an acute respiratory disease of chicken caused by gram negative bacterium Haemophilus  paragalinarum. Three serotypes (A,B,C) have been reported among them serotype B is confined only to certain geographical areas.It occurs in growing chicks and layers.Great economic loss is due to increased culls and marked decrease in egg production 10-40%.Economical impact of IC in multi-stage farm is enormous.

Transmission

Transmit from bird to bird through air borne,farm to farm by contaminated feed,water,equipments and personnels,transport cages and truck.

Clinical signs and lesions

Signs are like CRD,the most prominent features of disease are facial edema,swollen wattles,cyanosis with cherry exudates in sinus,drop in egg production upto 10-40% sometimes total loss. Morbidity is very high, mortality is variable,but can reach in same flock ,a percentage as high as 20-30%.Acute catarrhal-fibrinous rhinitis and sinusitis are the specific lesions, Mouth and nostril have peculiar fowl odour.

Diagnosis

Diagnosis can be done on the basis of rapid spread of the disease and characteristic clinal signs but conformation can only be done by the isolation. In field condition Gram’s staining of the nasal or infraorbital exudates  revealing bipolarly stained gram negative organism will be very helpful. Besides these above method serological test like haemaggluination test, haemagglutination Inhibition test and dot blotting test are reliable method for diagnosis.

Treatment

Potentiated sulphonamide is a combination of choice.Treatment of the disease done effectively by administering antibiotics like amoxicillin, macrolides,erythromycin, tetracyclines &quinolones in drinking water.

Prevention and control

Bio-security and proper disinfection are most important.Since there is the problem of carrier bird among the treated the affected bird should be depopulated and equipment and premises be disinfected properly and kept vacant for 30-60 days before reuse.There should be adequate flock density and regular ,timely vaccination of the bird against the infectious coryza.

Necrotic Enteritis is an acute enterotoxemia. The disease primarily affects broiler chiken ( 2-5 weeks old) and turkeys (7- 12 weesk old) raised on litter but can also affect commercial layer pullets raised in cages.

Etiology

It is caused by gram positive obligatory anaerobic bacteria Clostridium perfringes, C. pergringens type A and type c are associated with necrotic enteritis in poultry. Toxins produced by the bacteria cause damage to the small intestine, liver lesions and mortality.

Transmission

 C. perfringes is a nearly ubiquitous bacteria readily found in soil, dust, feces feed and used poultry litter. It is a normal inhabitant of the intestine of healthy chickens. It causes necrotic enteritis if there is alternation in intestinal microflora or damage to intestinal mucos due to Coccidiosis, Mycotoxcosis, Salmonellosis.

Clinical symptoms

The disease is mostly characterized by sudden increase in mortality with severely depressed and anorectic birds. However birds reluctant to move and diarrhea may also be seen.

Lesions

Lesion are found in small intestine which may be ballooned, friable, and contain a foul smelling, brown fluid. The mucosa is often referred to as a Turkish towel appearance as it is covered with a tan to yellow pseudomembrane.

Diagnosis

History, clinical sign and lesions help in diagnosis. Isolation of large numbers of C. perfringes from intestinal contents confirms the diagnosis. Differential media specially designated for isolation of C. perfringens  can be used.

NE must be deferentially diagnosed with Intestinal Coccidiosis and Ulcerative Enteritis.

Treatment and control

It is essential to prevent the coccidiosis as coccidial damage is mainly responsible for NE. Avoiding drastic changes in feed and minimizing level of fishmeal, wheat, barley or rye in feed helps in prevention.

Antibiotic are given through drinking water for treating NE. bacitracin and Lincomycin are commonly used. The medicated drinking water should be the sole source of water.

It’s acute febrile bacterial disease that affects wide range of birds.

Etiology:

The causal organism, Borrelia anserina, is an actively motile spirochete, ~0.2–0.3 μm × 8–20 μm, and consists of 5–8 loosely arranged coils. Cultivation in vitro is difficult. Borrelia will grow on Barbour-Stoenner-Kelly medium but loses virulence after 12 passages.

Generally, an infected Argas tick can transmit the bacteria at every feeding and maintains the infection throughout larval, nymphal, and adult stages. The ticks also transmit the infection transovarially.

Clinical Findings

Signs include listlessness, depression, somnolence, moderate to marked shivering, and increased thirst. Ruffled feathers, anemia, and pale combs can be noticed as well, and in appetence can lead to reduced weight. Young birds are affected more severely than older ones. Egg production in layers or breeders may be reduced by 5%–10%, with a higher number of small eggs.

Lesions:

The spleen is enlarged, with petechial or ecchymotic hemorrhages, appearing dark or mottled. However, a contrasting situation may be seen in Mongolian pheasants, in which the spleen is reported to be small and pale. Occasionally, the liver may be swollen and contain focal areas of necrosis. Kidneys may be enlarged and pale. Green, catarrhal enteritis is common.

Diagnosis

Diagnosis depends on demonstration of Borrelia in the blood, either as actively motile during darkfield microscopy, as stained spirochetes in Giemsa-stained blood smears, or by PCR. In young birds, theBorrelia may reach vast numbers per oil-immersion field and persist for several days. Older birds usually have low numbers of Borrelia that are detected only with difficulty, or not at all, and that persist for only 1–2 days. Increased numbers of immature RBCs are noticed due to the anemia. Silver staining can be used to demonstrate the bacteria in tissues.

Treatment and Control

Several antibacterial agents are effective. The most widely used are penicillin derivatives, but streptomycins, tetracycline and tylosin is also effective.

Control must be directed against the biologic vector. Argas ticks are notable for their long lifespan, ability to survive for extended periods without a blood meal, efficiency in transmitting the spirochete, and ability to remain securely hidden in cracks and crevices often beyond the effective reach of pesticides. Accordingly, control is difficult. A combination of tick eradication and immunization is the most effective means of control.

 

Staphylococcosis is a bacterial disease that can affect a wide range of avian species, including poultry, and is seen worldwide. Economic losses may result from decreased weight gain, decreased egg production, lameness, mortality, and condemnation at slaughter.

Etiology

Caused by gram positive bacteria staphylococcus aureus. S aureus is a gram-positive, catalase-positive, coccoid bacterium that appears in grape-like clusters on stained smears. Staphylococcus toxins can enhance the pathogenicity of a strain.

Clinical Findings

Common clinical finding includes ruffled feathers and reluctant to walk, Depression, swollen joints in chronic cases along with gangrenous dermatitis.

Lesions:

Common lesion includes osteomylitis and fragile bones, femoral head necrosis, arthritis and synovitis. In most of the cases dark moist areas under skin is observed.

In addition, septicemia can result in green livers or livers with multifocal necrosis and/or granulomas. In acute infections, a sudden increase in mortality may be noted.

Diagnosis

Although some lesions may be suggestive of a Staphylococcus infection, diagnosis is confirmed by isolation and identification of causative organism.

Treatment and Prevention

Antibiotics used to treat Staphylococcus infections include penicillin, erythromycin, lincomycin, and spectinomycin. Proper management to prevent injury and immune compromised poultry helps prevent staphylococcosis. Beak and toe trimming procedures in young chickens and turkeys could result in a staphylococcal septicemia.

It’s a bacterial disease caused by gram positive streptococcus species.

Etiology

Streptococci are non spore forming, non-motile, gram-positive, catalase-negative coccoid bacteria that occur singly, in pairs, or in short chains when observed on stained smears.

 Transmission is via oral or aerosol routes as well as through skin injuries.

Clinical Findings

Streptococcal infections show septicemia, depression, lethargy, ruffled feathers, pale comb and wattles. In affected layers, egg production may drop by 15%. Acute fibrino-purulent conjunctivitis has been noted in infections caused by other Streptococcus spp.

Lesions:

Lesions in the acute septicemic form include splenomegaly, hepatomegaly (with or without reddish tan to white multifocal necrotic foci), and enlarged kidneys, congestion of subcutaneous tissue with or without sero-sanguinous fluid. Omphalitis in chicks. Blood stained feathers around the mouth and head due to blood from the oral cavity have been reported occasionally.

Chronic streptococcal infections result in arthritis and/or tenosynovitis, osteomyelitis, pericarditis, myocarditis ,salpingitis and valvular endocarditis. Lesions on the heart valves appear as small yellowish white or tan raised areas on the valvular surface.

Diagnosis

Diagnosis is made on the basis of history, clinical signs, and lesions. Isolation of Streptococcus spp from lesions confirms the diagnosis. Streptococci can be cultured easily on blood agar.

Treatment and Control

Antibiotics, including penicillin, erythromycin, novobiocin, oxytetracycline, chlortetracycline, and tetracycline, have been used to treat acute and sub acute infections.

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