In April, over a period of 2.5 weeks, 6 Holstein heifers from a closed herd died. They had been clinically normal the night before, and were found dead, or moribund less than 12 hours before death. All had received 2 doses of routine respiratory vaccines, but no clostridial vaccines. They were kept in a large free-stall area on sand with about 45 heifers in the group. There was no unusual handling, although some animals were coming into heat periodically and may have been mounting others. There had been some recent excavation in order to expand the milking parlor. Farm management was excellent.
Two animals were submitted to the AHL for autopsy, one that had died (8 months old), and another that was euthanized (12 months). Gross examination was similar in both animals. There was some blood draining from the nares, and one heifer was somewhat bloated. An ELISA for anthrax was performed on both and was negative. On opening the bodies, in the first animal, there was hemorrhage with emphysema involving a 20 x 20 x 6 cm area in front of the right scapula (Fig. 1). A 2 x 2 x 4 cm region of dark hemorrhage was present in the left ventricular free wall papillary muscle. There was marked acute hemorrhage and emphysema with areas of “dry” pallor of the adductor muscles of the right and left hind leg and in tissue dorsal to the udder. Approximately 2,400 cm3 of muscle were involved. In the second animal, there was hemorrhage with some emphysema involving a 10 x 20 x 6 cm area in the brisket region and acute hemorrhage and emphysema of the adductor muscles of the right hind leg – ~1,200 cm3 being affected. Microscopically there was myofiber degeneration with coagulative necrosis. There was marked interstitial edema and emphysema, and in areas a sparse infiltrate of degenerate neutrophils was seen (Fig. 2). Large numbers of gram-positive clostridial-type organisms were present in the section. In the necrotic areas, many myofibers were devoid of nuclei and there were scattered foci of hemorrhage.
Smears done on fresh muscle stained with fluorescein-conjugated antibodies demonstrated Clostridium chauvoei in large numbers in both animals, with no staining for C. novyi, C. septicum, or C. sordelii. No bacterial pathogens were isolated on culture.
Blackleg “outbreaks” have been associated with excavation (1) and spores have been recoverable in contaminated soil at 11 years (2) and perhaps longer. It is also associated with trauma, and assumed to be activation of dormant spores in damaged muscles. In this case, trauma may have been associated with estrus activity, or the “outbreak” may have been due to the recent excavations. The remaining heifers have since been vaccinated for clostridial diseases, and there have been no subsequent losses.
Fig 1. Autopsy photo of Clostridium chauvoei infected muscle showing emphysema, hemorrhage, edema, and necrosis. |
Fig 2. Histology of involved muscle – degenerate myocytes and an infiltrate of degenerate leukocytes in some areas of the lesion are typical. Close of up Gram stain shown in the insert. |
Case 1: In January 2015, a 3-day-old lamb was submitted for postmortem from a flock of 100 in confinement housing. Sixty animals were affected, 2 dead, with a history of swollen joints, non-responsive to a range of treatments including tetracycline in milk, A180® danofloxacin, prednisone, Banamine®, Baytril®, or Liquamycin LA-200®. Lambs were kept with the ewe for 2-3 days, then separated and started on milk replacer. Within 1-2 days, the lambs developed swollen joints. No difference in rate of infection was noted, whether the navels were dipped or not. A 1-week-old lamb posted on-farm a week prior to the current submission had 3+ Streptococcus suis, and E. coli (the latter on enrichment culture only) isolated from a joint swab. The lamb submitted for postmortem at the AHL had a markedly swollen left carpus containing dry, inspissated yellow exudate, and enlarged and edematous left prescapular and axillary lymph nodes. Histology revealed marked fibrinosuppurative synovitis with extension of the inflammation into the adjacent carpal bone. Cultures for Mycoplasma were negative. Bacterial cultures revealed 4+ S. suis from the carpus, and 3+ from the prescapular lymph node. The isolate was sent for serotyping, and typed as S. suis serotype 9.
Case 2: In February 2015, a 7-day-old goat kid was submitted for postmortem from a herd of 800 milking does. Many of the young kids (20/40) were developing lameness with swollen joints, and were unresponsive to antibiotic therapy with tetracycline or lincospectin/isoflupredone acetate. In the affected group, 15% had more than one joint affected. Two kids had concurrent conjunctivitis and 2 kids had pneumonia with pyrexia. Kids at this farm were snatched at birth, given pasteurized cow colostrum, and then fed powdered milk replacer. All navels in affected and non-affected kids were clean and dry. On postmortem examination, the kid was found to have a swollen left carpus, with inspissated fibrin and yellow caseous exudate in the proximal carpal joint. 1+ S. suis was isolated from the carpal swab; cultures for Mycoplasma were negative. The isolate was sent for serotyping, but was untypeable (i.e., not serotypes 1-34). Two weeks after these test results became available, a new group of does on this farm started kidding. Six kids from this cohort of birthing does started to show signs of conjunctivitis and lameness. Before joint swelling was noted, they were treated with florfenicol/flunixin and none progressed to have swollen joints; all recovered normally.
S. suis isolates from cases 1 and 2 were resistant to tetracycline and tilmicosin, with intermediate susceptibility to erythromycin.
Streptococcus suis is an important pathogen of swine, causing sudden death, meningitis, septicemia, arthritis, endocarditis, and pneumonia. It has also been increasingly isolated from a range of other animal species including ruminants, horses, dogs, and cats. A recent case report from the Atlantic Veterinary College documents S. suis arthritis in 2 lambs from a single premises (1). S. suis (particularly serotype 2 but also other serotypes) (2), is also a potential zoonotic pathogen.
The AHL database from May 2007-February 2015 was queried (Table 1). Arthritis, pulmonary abscessation, and abscesses in various locations were the most frequent diagnoses in juvenile sheep and goats < 6 months of age. Joints involved included carpal, tarsal, and stifle joints. One lamb had a concurrent umbilical infection with S. suis.
Table 1: Streptococcus suis infections in sheep and goats, May 2007-May 2015
Diagnoses |
Sheep (n=13) |
Goats (n=14) |
Arthritis , < 3 months old |
6 (1* with Ureaplasma; 1* with E. coli) |
3 |
Pneumonia/pulmonary abscesses, < 3 months old |
2 (1 with Mannheimia and mycoplasma) |
3 * (1 with myocarditis) |
Meningitis, 2 weeks old |
|
1 |
Conjunctivitis, 4 days old |
|
1* |
Vertebral abscess, 6 months old |
1 |
|
Pharyngeal abscess, 2 months old |
1* |
|
Thyroid abscess, 1 month old |
1* |
|
Abscess, cheek/jaw/site unknown, adult or age unknown |
1* |
3* |
Mastitis/milk samples, adult animals |
1 |
3* (2 bulk tank samples) |
* = in mixed culture |
|
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Two bovine fetuses submitted to the AHL for postmortem examination had unusual joint lesions attributed to in utero Ureaplasma diversum infection.
Case 1 involved a Holstein heifer fetus aborted at approximately 8 months gestation. The abortion was an isolated case within the herd and the cow was healthy. At postmortem examination, the fetus had severe arthritis affecting multiple joints including the hips, shoulders, carpi, and hock joints. The affected joints contained thick exudates, erosion of the articular cartilage, and hyperemia of the synovial lining. The lungs of the fetus were aerated, indicating that it was alive at the time of abortion. Histologically, the joints exhibited marked arthritis with fibrin exudates, hyperplasia of the synovium, and infiltrates of neutrophils, lymphocytes, and plasma cells (Fig. 1). The fetus also had mild encephalitis and hepatitis. Ureaplasma diversum was isolated from an affected joint and lung.
Case 2 involved a Holstein bull calf that was born 28 days prematurely. The animal had difficulty standing after birth, and was noted to have a swollen left foreleg. At one week of age, the calf developed diarrhea and neurologic signs and subsequently died. At postmortem examination, the animal was noted to be small, weighing only 26 kg. Thickened joint capsules and fibrotic periarticular tissue were noted in the left carpal, right stifle (Fig.2), and atlantoaxial joints. Affected cartilage appeared yellow, pitted and fibrillated. Abundant fibrinopurulent exudate filled the foramen magnum and surrounded C1 spinal cord. The caudal aspect of vertebra C1 and the cranial aspect of C2 had extensive irregular erosion of articular cartilage, and the dens appeared collapsed and deformed (Fig.3). Histologically, sections of thickened synovium had prominent villus hyperplasia and lymphoplasmacytic infiltrates with focal effusion of fibrin into the joint space. Affected appendicular bone sections revealed irregular thinning of articular cartilage with loss of matrix and chondrocytes. Vertebra C1 contained several concentrically oriented clusters of degenerate neutrophils and macrophages surrounded by irregular deposits of mature fibrovascular stroma. Cervical spinal cord segments had mild Wallerian degeneration of ventral white matter tracts, consistent with compressive myelopathy. A section of eyelid revealed mild conjunctival epithelial hyperplasia and mucous metaplasia with dispersed subconjunctival lymphoplasmacytic infiltrates. Cultures of lung and right hock synovium were negative for pathogenic bacteria and Ureaplasma spp. in this calf.
A recent case series of 5 aborted bovine fetuses described destructive polyarthropathy attributed to in utero Ureaplasma diversum infection which was identified by PCR or culture in 4 of the 5 fetuses (1). Gross and histologic lesions in this paper are similar to those described in these 2 affected calves. Cows infected with Ureaplasma diversum typically abort in the 3rd trimester; premature or weak term calves may also occur. This organism is part of the normal genital tract flora of cattle, and is believed to be transmitted during breeding. Ureaplasma has also been isolated from artificial insemination and embryo transfer fluids. Common histologic lesions are amnionitis and chorioallantoic vasculitis in the placenta, and lymphoplasmacytic conjunctivitis with goblet cell metaplasia and non-suppurative interstitial pneumonia in fetal tissues (2). Joints are rarely examined closely when performing postmortems on bovine fetuses, and it is possible that this lesion has been overlooked in some cases of abortion caused by Ureaplasma diversum.
Figure 1. Histologic section of joint containing hyperplastic synovium, fibrin exudate, and inflammatory cell infiltrates (case 1).
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Figure 2. Thickened and pitted articular cartilage over right lateral tibial plateau compared to left (case 2)
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Figure 3. Thickened joint capsule, deformed dens, and fibrinosuppurative exudate in atlantoaxial joint (case 2).
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