Fowl Typhoid and Pullorum Disease (Salmonella Gallinarum and Salmonella Pullorum Infection)

Fowl typhoid and pullorum disease are two distinct, yet closely related, septicemic bacterial diseases of poultry caused by the host-specific serovars Salmonella enterica subsp. enterica serovar Gallinarum biovar Gallinarum (S. Gallinarum) and biovar Pullorum (S. Pullorum), respectively. These diseases are of significant economic importance worldwide, particularly in commercial layers, broiler breeders, and backyard flocks, where they cause high morbidity and mortality, decreased egg production, and reduced hatchability. Fowl typhoid primarily affects adult birds, presenting as an acute or chronic septicemia with characteristic necrotic lesions in the liver, spleen, and heart. Pullorum disease predominantly affects young chicks, causing acute septicemia with high mortality, white diarrhea, and characteristic caseous lesions in the liver, lungs, and ceca. Both diseases are transmitted both vertically (through the egg) and horizontally (via fecal-oral route), and they are reportable to the World Organisation for Animal Health (WOAH) in many countries. Control relies on strict biosecurity, serological testing and culling of carriers, and in some regions, vaccination. The diseases are of particular concern in layer and breeder flocks due to their potential for vertical transmission, which can perpetuate infection across generations.

The causative agents are Salmonella enterica subsp. enterica serovar Gallinarum biovar Gallinarum (S. Gallinarum) and biovar Pullorum (S. Pullorum). These are Gram-negative, facultatively anaerobic, non-spore-forming bacilli belonging to the family Enterobacteriaceae. They are host-adapted to poultry, with S. Gallinarum causing fowl typhoid and S. Pullorum causing pullorum disease. Both biovars possess somatic (O) antigens (O1, O9, O12) and flagellar (H) antigens (d, a, etc.), but they are non-motile due to the lack of functional flagella. The bacteria produce endotoxins (lipopolysaccharides) that contribute to the septicemic and toxic effects. They can survive in the environment for extended periods, particularly in feces, litter, and dust, and are resistant to some disinfectants. The infectious dose is relatively low, especially in young birds. The bacteria have the ability to persist in the reproductive tract of carrier hens, leading to vertical transmission via contaminated eggs. The genetic basis for host specificity and virulence is complex, involving multiple virulence factors such as adhesins, invasins, and iron acquisition systems.

Fowl typhoid and pullorum disease are distributed worldwide, with higher prevalence in regions with intensive poultry production and less stringent biosecurity. S. Pullorum is primarily a disease of chickens and turkeys, while S. Gallinarum also affects quail, guinea fowl, and other game birds. The diseases are most commonly seen in commercial layers, broiler breeders, and backyard flocks, but can affect all ages. Pullorum disease is predominantly a disease of young chicks (under 3 weeks of age), with mortality rates often exceeding 50% in untreated flocks. Fowl typhoid typically affects growing and adult birds, with morbidity and mortality varying from 10% to 80% depending on the strain, host susceptibility, and management. In layers, fowl typhoid can cause a sudden drop in egg production of up to 50% and increased mortality. The diseases are transmitted vertically through the egg, as infected hens can shed the bacteria in their ovaries and oviducts, contaminating the egg contents. Horizontal transmission occurs via the fecal-oral route, through contaminated feed, water, litter, equipment, and personnel. Wild birds, rodents, and insects can act as mechanical vectors. The incubation period is typically 4-6 days for pullorum disease and 5-7 days for fowl typhoid. Flocks with poor biosecurity, high stocking density, and inadequate sanitation are at higher risk. The diseases are more severe in young birds and in flocks under stress (e.g., poor nutrition, concurrent infections). Feed conversion ratio (FCR) is adversely affected, with affected flocks showing poor growth and increased feed consumption per unit of weight gain.

Following ingestion or inhalation, the bacteria colonize the intestinal tract and invade the intestinal epithelium, particularly in the lower small intestine and ceca. They then disseminate via the bloodstream to internal organs, including the liver, spleen, bone marrow, and reproductive tract. The bacteria multiply intracellularly in macrophages and hepatocytes, causing bacteremia and septicemia. The endotoxin released from the bacteria triggers a systemic inflammatory response, leading to fever, depression, and vascular damage. In acute cases, there is widespread necrosis and inflammation in the liver, spleen, and heart, with characteristic grayish-white necrotic foci. In the liver, there is hepatocellular necrosis and infiltration of heterophils and mononuclear cells. The spleen shows lymphoid depletion and necrosis. In the lungs, there may be interstitial pneumonia and caseous exudate. In the ceca, there is caseous core formation due to necrosis and inflammation of the cecal mucosa. In adult birds, the bacteria can localize in the ovary and oviduct, leading to oophoritis, salpingitis, and peritonitis, with resultant egg production drops and vertical transmission. In chicks, the disease is often peracute, with death occurring before significant lesion development. The immune response involves both humoral and cell-mediated immunity, but the bacteria can evade the immune system by surviving within macrophages, leading to a chronic carrier state.

Intrinsic factors include age (young chicks are highly susceptible to pullorum disease, while fowl typhoid affects older birds), genetic susceptibility (some breeds are more resistant), immune status (immunosuppression due to stress or concurrent diseases increases susceptibility), and high production stress in layers. Extrinsic factors include poor biosecurity (allowing introduction of infected birds or contaminated equipment), high stocking density, poor ventilation leading to ammonia accumulation, wet litter, contaminated feed or water, and inadequate cleaning and disinfection of facilities. Vaccination failure or lack of vaccination can also predispose to disease. Concurrent infections with other pathogens (e.g., Mycoplasma gallisepticum, infectious bursal disease virus) can exacerbate the severity of salmonellosis. Nutritional deficiencies, such as vitamin A or E deficiency, can impair mucosal immunity and increase susceptibility.

Clinical signs vary with the age of the bird and the biovar. In pullorum disease (chicks under 3 weeks), signs include depression, huddling, anorexia, white diarrhea (which may be pasty and adhere to the vent), labored breathing, and high mortality. Chicks may show nervous signs such as ataxia and opisthotonos. In older birds, pullorum disease may be subclinical, with carriers showing no signs. Fowl typhoid in growing and adult birds presents with acute onset of depression, anorexia, increased thirst, fever, and a drop in egg production. Birds may have pale combs and wattles, diarrhea (yellow-green), and dehydration. In chronic cases, birds may become emaciated and show lameness due to arthritis. Mortality can be high, especially in acute outbreaks. In layers, there may be a sudden drop in egg production of up to 50%, with eggs showing shell abnormalities (thin shells, rough shells). In broilers, there may be poor growth and increased FCR. Neurological signs are less common but can occur in severe septicemia.

Differential diagnoses include other bacterial septicemias such as colibacillosis (Escherichia coli infection), fowl cholera (Pasteurella multocida), and erysipelas (Erysipelothrix rhusiopathiae). Viral diseases such as Newcastle disease, avian influenza, and infectious bursal disease can also present with similar signs. Mycoplasmosis (Mycoplasma gallisepticum) can cause respiratory signs and egg production drops. Coccidiosis can cause diarrhea and mortality in chicks. Aspergillosis can cause respiratory signs and mortality in young birds. Key differentiating features: Colibacillosis often presents with perihepatitis and airsacculitis, and E. coli can be isolated on MacConkey agar. Fowl cholera causes sudden death in older birds with septicemia and petechial hemorrhages on the heart, and P. multocida is a bipolar staining organism. Newcastle disease and avian influenza cause respiratory and neurological signs, with characteristic lesions in the trachea and proventriculus, and are diagnosed by virus isolation and serology. Infectious bursal disease causes bursal atrophy and is diagnosed by bursal lesions and PCR. Mycoplasmosis causes respiratory rales and airsacculitis, and is diagnosed by serology and PCR. Coccidiosis is diagnosed by intestinal lesions and oocysts in feces. Aspergillosis causes granulomatous lesions in the lungs and air sacs, and fungal hyphae are seen on histopathology.

The diagnostic approach begins with a thorough flock history, including clinical signs, mortality patterns, egg production data, and vaccination status. A complete necropsy of several affected birds is essential to observe characteristic gross lesions. Based on necropsy findings, samples should be collected for bacteriology (liver, spleen, heart blood, bone marrow, and in layers, ovary and oviduct). For serology, serum samples should be collected for rapid serum agglutination (RSA) test, which is a quick screening test for both S. Pullorum and S. Gallinarum. Positive RSA results should be confirmed by ELISA or tube agglutination. For molecular diagnosis, PCR assays targeting specific genes (e.g., fliC, speC) can differentiate between the two biovars. Bacterial isolation and identification are the gold standard, with biochemical tests and serotyping confirming the serovar. Histopathology can support the diagnosis by showing characteristic lesions. In cases of vertical transmission, egg and hatchery samples (fluff, meconium) can be cultured. The diagnostic algorithm should follow a stepwise approach: 1) Flock history and clinical signs; 2) Necropsy and gross lesion assessment; 3) Bacterial culture and isolation; 4) Serotyping and biotyping; 5) Molecular confirmation (PCR); 6) Serological screening (RSA, ELISA); 7) Histopathology for confirmation; 8) Differential diagnosis rule-out.

Serology: Rapid serum agglutination (RSA) test is commonly used for screening; positive samples are confirmed by tube agglutination or ELISA. ELISA can quantify antibody titers, with a positive result indicating exposure. Molecular diagnostics: PCR assays targeting the rfbS gene or other specific sequences can differentiate S. Gallinarum from S. Pullorum. Real-time PCR is rapid and sensitive. Microbiology: Isolation on selective media such as MacConkey agar, brilliant green agar, or XLT4 agar. Colonies are non-lactose fermenting on MacConkey. Biochemical tests (e.g., triple sugar iron, urea, indole) and serotyping with specific antisera confirm the serovar. Blood chemistry: In affected birds, there may be leukocytosis with heterophilia, and elevated liver enzymes (AST, ALT) due to hepatic necrosis. Coccidiosis lesion scoring is not applicable, but if concurrent coccidiosis is suspected, intestinal lesion scoring (0-4 scale) can be performed. Mycotoxin feed assays may be indicated if feed contamination is suspected, but are not specific for salmonellosis.

Imaging is not commonly used in the diagnosis of fowl typhoid and pullorum disease. Radiography may be used to detect bone lesions in chronic cases (e.g., osteomyelitis), but is not specific. Ultrasonography is not practical in poultry. Gross necropsy photography is essential for documentation and can be used for teaching and diagnostic reference. Characteristic lesions include hepatomegaly with grayish-white necrotic foci, splenomegaly, and caseous cecal cores in pullorum disease. In fowl typhoid, there may be pericarditis, perihepatitis, and oophoritis in layers.

Gross necropsy lesions: In pullorum disease, chicks show caseous lesions in the liver, lungs, and ceca. The liver may be enlarged with multiple grayish-white necrotic foci. The spleen is enlarged and mottled. The ceca may contain caseous cores. In fowl typhoid, adult birds show hepatomegaly with bronze discoloration and necrotic foci, splenomegaly, and sometimes pericarditis and peritonitis. In layers, there may be oophoritis with misshapen, discolored follicles. Microscopic histopathology: In the liver, there are multifocal areas of coagulative necrosis with infiltration of heterophils and mononuclear cells. The spleen shows lymphoid depletion and necrosis. In the lungs, there is interstitial pneumonia with caseous exudate. In the ceca, there is mucosal necrosis and inflammation with caseous core formation. In the ovary, there is follicular degeneration and inflammation. No inclusion bodies are seen, as this is a bacterial disease.

Treatment of fowl typhoid and pullorum disease is challenging due to the intracellular nature of the bacteria and the potential for carrier states. Antibiotic therapy can reduce mortality and clinical signs but may not eliminate the carrier state. Commonly used antibiotics include amoxicillin (10-20 mg/kg body weight orally, or 250-500 mg/L drinking water for 3-5 days), oxytetracycline (10-20 mg/kg, or 200-400 mg/L drinking water for 5-7 days), enrofloxacin (10 mg/kg, or 50-100 mg/L drinking water for 3-5 days, where legal), and florfenicol (10-20 mg/kg, or 200-400 mg/L drinking water for 3-5 days). However, antibiotic resistance is a growing concern, and treatment should be based on culture and sensitivity testing. Supportive therapy with vitamins (A, D3, E, C, K) and electrolytes in drinking water can help reduce stress and mortality. In severe outbreaks, depopulation may be recommended to eliminate the source of infection. Vaccination is used in some countries as a control measure, with live attenuated vaccines (e.g., S. Gallinarum 9R strain) available for fowl typhoid. However, vaccination is not a substitute for biosecurity and eradication programs.

The prognosis for affected flocks is guarded to poor, depending on the age of the birds, the biovar involved, and the speed of intervention. In pullorum disease, mortality in chicks can be high (up to 80-100%) if untreated, but with prompt antibiotic therapy, mortality can be reduced to 10-20%. In fowl typhoid, mortality in adult birds can range from 10% to 50%, and egg production may take several weeks to recover. Chronic carriers may remain in the flock, leading to recurring outbreaks and vertical transmission. The long-term prognosis for the flock is poor if carriers persist, as they can perpetuate the infection. In many countries, the presence of S. Pullorum or S. Gallinarum in breeding flocks necessitates depopulation to prevent vertical transmission. The economic impact includes mortality, reduced egg production, increased FCR, and costs of treatment and biosecurity measures.

After an outbreak, a structured monitoring program should be implemented. This includes serial serological testing (RSA or ELISA) of all birds at regular intervals (e.g., every 2-4 weeks) until negative results are obtained. Any positive birds should be culled immediately. Environmental sampling (litter, dust, water) should be conducted to assess contamination levels. Cleaning and disinfection of the facility should be performed with effective disinfectants (e.g., phenolic compounds, formaldehyde) after removal of all birds. Litter should be removed and disposed of properly. A downtime of at least 2-4 weeks is recommended before restocking. In breeding flocks, hatchery hygiene should be reviewed, and eggs should be fumigated or treated with antibiotics (e.g., gentamicin) to reduce vertical transmission. Regular audits of biosecurity protocols should be conducted to prevent re-introduction.

Pearls: 1) In pullorum disease, the presence of caseous cecal cores in chicks is highly suggestive. 2) In fowl typhoid, the liver may have a bronze discoloration, which is a classic finding. 3) The rapid serum agglutination test is a quick and inexpensive screening tool, but false positives can occur; confirm with ELISA or culture. 4) In layers, a sudden drop in egg production with increased mortality should always raise suspicion for fowl typhoid. 5) Both diseases are vertically transmitted, so testing of breeding flocks is critical. Pitfalls: 1) Do not rely solely on clinical signs, as they can be similar to other diseases. 2) Antibiotic treatment may suppress clinical signs but not eliminate carriers, leading to recurrence. 3) Do not use live vaccines in flocks that are already infected, as they can cause disease. 4) Failure to implement strict biosecurity can lead to rapid spread. 5) Misdiagnosis as colibacillosis or fowl cholera can lead to inappropriate treatment and continued spread.

Antibiotics: Amoxicillin: 10-20 mg/kg body weight orally once daily for 3-5 days, or 250-500 mg/L drinking water for 3-5 days. Oxytetracycline: 10-20 mg/kg body weight, or 200-400 mg/L drinking water for 5-7 days. Enrofloxacin: 10 mg/kg body weight, or 50-100 mg/L drinking water for 3-5 days (not approved in some countries for poultry). Florfenicol: 10-20 mg/kg body weight, or 200-400 mg/L drinking water for 3-5 days. Withdrawal times vary by country and drug; typically 5-7 days for meat and 0-3 days for eggs. Supportive therapy: Vitamins A, D3, E, C, and K in drinking water at label doses for 3-5 days. Electrolytes and glucose can be added to drinking water to reduce dehydration. Vaccines: Live attenuated S. Gallinarum 9R vaccine is available for fowl typhoid; administered via drinking water or subcutaneous injection at 8-12 weeks of age, with a booster at 16-18 weeks. Inactivated vaccines are also available. For pullorum disease, no commercial vaccine is widely available; control is based on testing and culling.

Landmark studies have demonstrated the efficacy of serological testing and culling in eradicating pullorum disease from commercial flocks (e.g., the National Poultry Improvement Plan in the USA). Research by Barrow and colleagues has characterized the virulence mechanisms of S. Gallinarum and S. Pullorum, including the role of lipopolysaccharides and iron acquisition systems. Field trials have shown that live vaccines can reduce mortality and egg production losses in fowl typhoid outbreaks. A meta-analysis of antibiotic treatments for salmonellosis in poultry found that fluoroquinolones and third-generation cephalosporins are most effective, but resistance is emerging. The AAAP and WOAH provide guidelines for the control and prevention of these diseases, emphasizing biosecurity, testing, and depopulation of infected breeding flocks. Recent studies have focused on the development of rapid molecular diagnostic tools, such as real-time PCR, for early detection and differentiation of the two biovars.