Paratuberculosis is a chronic debilitating disease affecting ruminant livestock and is caused by Mycobacterium avium subsp. paratuberculosis (MAP). It has a huge impact on animal welfare causing both direct and indirect economic losses and also arouses a serious public health concern causing Johne’s disease in humans. Disease control becomes challenging in many countries where there is large population of ruminants and various husbandry systems.
MAP is known to occur in both domestic and free-ranging wild ruminants as well as omnivores and carnivores and non-human primates. Dairy cattle have the highest reported prevalence, with 20 %- 90 % of herds infected in most major dairy-producing countries. The disease has a significant economic impact on the goat and sheep industries in India.
Infected animals excrete substantial amounts of Mycobacterium avium subspecies paratuberculosis (MAP) in their stools, but only small amounts in their colostrum and milk. It is resistant to environmental variables and can live for more than a year on pasture; life in water is longer than survival in soil. The infection is mainly spread by feces to the mouth; the dose required to infect an animal is unknown. The introduction of sub-clinically infected carriers infects herds or flocks, causing them to become MAP-infected.
Although infection occurs early in life i.e. shortly often after birth—clinical indications do not appear until the animals are sexually mature. Slowly, but steadily, the condition progresses to clinical illness. Infection resistance improves with age, although it never reaches 100%. Infection is caused through absorption of the organism during suckling on infected teats, consumption of MAP-contaminated milk, solid feed, or water, or licking and grooming in a contaminated environment. Intrauterine infections are seen in the later, bacteremic phases of illness.
This intracellular pathogen infects macrophages in the GI tract and related lymph nodes after ingestion and uptake in the Peyer’s patches of the lower small intestine. Some animals may be able to remove infection by a cell-mediated immune response, although the frequency with which this happens is unknown. In most cases, the organisms grow and cause chronic granulomatous enteritis, which prevents nutrients from being absorbed, resulting in the cachexia seen in advanced infections. This can take months or years to manifest, and it’s frequently accompanied by a drop in cell-mediated immunity, an increase in serum antibody, and bacteremia, as well as infection spreading outside the GI tract. Fecal shedding occurs before clinical indications appear, and animals that are infected at this “silent” stage are key sources of transmission.
Clinical Findings and lesions
Weight loss and diarrhea are common symptoms of tuberculosis in cattle in the late stages of illness, but infected animals might appear healthy for months or years. Diarrhea in cattle can be chronic or intermittent, while diarrhea in sheep, goats, and other ruminants is rare. It is passed without tenesmus and usually contains no blood, mucus, or epithelial debris. Due to a protein-losing enteropathy, the diarrhoea grows more severe over time, weight loss continues, coat color fades, and ventral and submandibular edema develops.
Milk yield in dairy cattle and goats may decline or fail to meet expectations. The temperature and appetite of the animals are normal. The condition progresses, eventually leading to emaciation and death. The herd cull rate grows in tandem with the prevalence of MAP infection within the herd, whereas dairy herd milk production falls. Although the disease is similar in sheep and goats, diarrhea is not a common symptom, and advanced cases may shed wool easily. Infected animals can show a wide range of pathologies, from a lack of visible lesions to a thickened and corrugated colon with swollen and edematous surrounding lymph nodes. Clinical symptoms and the severity of lesions frequently do not correlate. In advanced cachectic situations, carcasses may be emaciated, with loss of pericardial and peri-renal fat. The distal small-intestinal wall is often diffusely thickened with a non-ulcerated mucosa thrown into noticeable transverse folds; however the lesions can be moderate. The jejunum and colon may be affected both proximally and distally by lesions. In most cases, serosal lymphangitis and enlargement of the mesenteric and other regional lymph nodes can be seen.
Control and Treatment
Main control measures include prevention of exposure of young animals to MAP and Identification, culling or segregations of infectious adult animals
There is no recognized treatment that is effective. Control necessitates proper sanitation and management procedures aimed at limiting the organism’s exposure to young animals. Calves, kids, or lambs should be born in manure-free locations, removed from the dam as soon as possible after delivery in the case of dairy cattle, bottle-fed pasteurized colostrum or procured from dams that test negative, and reared as far away from adults and their manure as feasible until >1 year old. Unless the waste milk has been pasteurized, milk replacer should be used instead of waste milk.
Adults can benefit from a regular testing programme to help focus their efforts on illness control. For commercial dairy herds that have been confirmed infected by culture or PCR, low-cost diagnostics (e.g., ELISA) have the greatest cost benefit. Animals that test positive, especially large shedders or those with strong-positive ELISA results should be slaughtered as soon as possible.
Retesting should be done at least once a year until herd tests show low infection prevalence (less than 5%). Because the disease can induce intrauterine infection, more active management efforts involve culling calves from dams that have or develop symptoms of the disease. Replacements for the herd should be recruited from herds that are thought to be disease-free, and the replacements should be checked before being introduced to the new herd. More basic farm techniques, such as raising food and water troughs, using piped water instead of ponds, and harrowing periodically to distribute excrement on pasture, can also assist reduce fecal pollution. Vaccinating calves under one month old can lower illness incidence, but it does not prevent shedding or new infections in the herd. As a result, vaccination does not negate the necessity for proper management and cleanliness. Vaccination has increased the productive life of goat herds in Spain and Australia. Cattle treated with an inactivated whole-cell mineral-oil vaccine produce granulomas ranging in size from one to several inches in diameter at the inoculation site (brisket) and may test positive for tuberculin. Self-inoculation by accident can cause severe acute reactions, such as sloughing and persistent sinusitis and tendinitis.
Sanmeet Kour, Sheza Farooq, Harpreet KourPhD Scholar, Division of Veterinary Microbiology, Guru Angad Dev Veterinary and Animal Sciences University, Ludhiana, India
PhD Scholar, Division of Animal Biotechnology, Guru Angad Dev Veterinary and Animal Sciences University, Ludhiana, India
PhD Scholar, Division of Veterinary Pharmacology and Toxicology, Guru Angad Dev Veterinary and Animal Sciences University, Ludhiana, India