Johnes Disease (Paratuberculosis) in Cattle

Clinical Signs.

Affected cattle, sheep and goats develop progressive emaciation. Typical age of onset of obvious clinical signs: 2-7 yrs. Cattle develop profuse, chronic, nonfetid diarrhea (no blood or fibrin), progressive weight loss, and submandibular and brisket edema. Chronic weight loss is the most common clinical sign in small ruminants; they do not commonly develop diarrhea but pasty unpelleted feces are occasionally noted. Appetite and rectal temperatures are normal in most cases.

Guernsey cow with clinical signs of Johne's disease

Guernsey cow with clinical signs of Johne’s disease

Guernsey cow with clinical signs of Johne’s disease


Subclinical disease exists for years before the affected animal shows typical the clinical signs of weight loss ± diarrhea. Subclinically affected dairy animals economically impact the herd by producing less milk than unaffected herdmates. Subclinical animals shed less organisms than clinically apparent cases, but still provide a source of infective organisms to other animals in the herd.

Typical clin path findings: decreased serum total protein and albumin, elevated CK and ALP, and hyperphosphatemia (reason unclear).

Pathogenesis. The disease is caused by Mycobacterium paratuberculosis, a Gram positive, acid fast bacterial rod. The organism was isolated in 1826 by Drs. Johne (pronounced “yoney”) and Frothingham. Transmission is primarily by the oral-fecal route. The majority of infections occur shortly after birth when the animals are most susceptible. After 6 months of age, cattle become more resistant to infection, and a much higher dose is needed to cause infection. At least 25% of heavily infected cows spread the disease transplacentally to their fetuses, and shed organisms in their milk. Infected bulls shed organisms in their semen, but sexual transmission has not been proven.

Once ingested, organisms invade the lamina propria of the ileum, cecum and colon, and slowly multiply. The organisms incite a granulomatous reaction (macrophages, lymphocytes) in the bowel, and spread to regional lymph nodes via infected macrophages. The progressive inflammatory response distorts the lamina propria, causing leakage of protein-rich fluid into the intestinal lumen and malabsorption of nutrients. The ileal, cecal, and colonic mucosa becomes grossly thickened and corrugated in appearance as the disease advances in most cattle breeds (not always evident in bos indicus and small ruminants). Subclinically affected animals shed low numbers of organisms (<100/gram of feces) compared to clinically affected animals (100,000 to 6 million/gram of feces).

Three Disease Stages

  1. Stage 1: preclinical/prepatent
  2. Stage 2: preclinical/patent
  3. Stage 3: clinical and patent



Currently, there is not a reliable method of detecting subclinical infections in animals, so eradication of this disease is very difficult to accomplish.

1) fecal culture. 2-5 gms feces needed. Specificity 100%. Sensitivity: 50% in late subclinical and clinically affected animals. Subclinical animals shed intermittently or at levels below detection (more false negatives). It takes 8-16 weeks to obtain results of the fecal culture! Note: the cattle strain will grow on culture but the sheep strain will not grow in medium.

2) Tissue morphology. Demonstration of acid-fast Gram positive organisms in the ileum, cecum, colon, and regional lymph nodes (taken by laporatomy or at necropsy) is very supportive of the diagnosis. Although rectal scrapings can be used as supportive evidence of infection, occasional false positives can arise because saprophytic (nonpathogenic) mycobacterium are occasionally present in this area. False negatives also can occur if the disease is not advanced enough to involve the rectal mucosa.

3) Serologic Tests (detects antibodies)



Agar gel immunodiffusion

Approx 100% specific but lacks sensitivity in subclinical cases (only 26% detected). In clinically affected cases, sensitivity is improved to 60-80%.

Complement fixation

Sensitivity and specificity similar to AGID. This test is used for international import/export testing.


Approved in 1992 by USDA. This new ELISA is superior to AGID and CF tests for detecting subclinical cases, and its specificity is excellent (99.7%). Sensitivity for detecting subclinical cases (stages 1 and 2):46%. Sensitivity for detecting clinical (stage 3) cases :88%. This test is currently being recommended for screening herds and replacement heifers and cows prior to purchase (JAVMA 1993; 203:1456).

The most rapid way to facilitate eradication of Johnes animals from the herd is to use fecal culture and the ELISA in combination on an annual basis. However, use of the ELISA alone is more cost effective, but eradication will take longer.


There is no practical and effective treatment, and infected animals should be culled for slaughter purposes. The progeny of infected cows are very likely to be infected. In rare instances, very valuable cows have been treated with clofazimine. Clinical signs regress but treated animals continue to shed organisms. This treatment is cost-prohibitive in most situations.


1) Test and cull program. Test cattle 2 years old and older annually with ELISA test and/or fecal culture. Cull positive cows and their offspring.

2) Only purchase cattle from herds that test routinely for Johnes, and maintain a low herd prevalence (<2% positive). Test cattle prior to purchase. Note: in Wisconsin, there is an implied warranty that cattle sold in the State are Johnes-free.

3) Use semen only from Johnes-free bulls.

4) In problem herds, dairy calves can be removed from cows at birth, fed colostrum and milk from Johnes-negative cows, and housed in a separate facility away from the milking herd for at least the first 6 months of life. (This tactic will fail if calves were infected in utero)

5) Areas that remain wet and swampy must be drained, and feces removed in order to reduce the number of organisms in the environment (organism can survive 9-11 mos in feces and soil).

6) Vaccine. The vaccine is not a substitute for sanitation and test/removal practices. It’s use is severely restricted, and highly regulated by State authorities. A State Veterinarian will authorize it’s use only in herds that have already complied with other control measures. Only a few states currently allow its use: Wisconsin and Pennsylvania. Neonates between the age of 1-35 days are vaccinated with the bacterin in the brisket. Granulomas commonly form at the injection site, and vaccinates will have a positive TB test (the main reason for the tight regulation). Vaccinates still shed organisms but are less likely to become clinically ill. People handling the vaccine must avoid accidental self-injection (causes persistent granuloma formation).