RUMINANTS
Streptococcus gallolyticus subsp. pasteurianus meningoencephalitis and septicemia in goats
Murray Hazlett, Emily Brouwer, Josepha DeLay, Amanda Mansz, Durda Slavic
Formerly belonging to Streptococcus bovis biotype II/2 complex, Streptococcus gallolyticus subsp. pasteurianus is associated with septicemia, meningitis, and endocarditis in humans. It is commonly found in the alimentary tract of ruminants and has been isolated from cases of septicemia in goslings, ducklings, and turkey poults. We have recently seen 4 cases of acute suppurative meningoencephalitis and septicemia associated with this organism in young goats and would like to make practitioners aware of this.
Case 1. A 2-mo-old goat from a farm with several kids with neurologic signs (opisthotonos, ataxia). Postmortem revealed severe neutrophilic meningitis and ventriculitis. S. gallolyticus subsp. pasteurianus was isolated in large numbers and almost pure culture from brain swabs. Moderate numbers were also isolated from lung along with E. coli and Pseudomonas aeruginosa. Listeria monocytogenes was isolated using enrichment procedures from 1 brain swab, however lesions seen were not typical for this organism. A diagnosis of suppurative meningoencephalitis and septicemia associated with S. gallolyticus was made.
Case 2. Two 2-mo-old goats had stiff joints and weak hind or front limbs. About 10% of kids were affected. The major findings in the first kid were severe suppurative arthritis and severe suppurative meningoencephalitis with occasional microabscesses in the perivascular neuropil. The second kid had only arthritis. S. gallolyticus subsp. pasteurianus (3+) was isolated from meninges of kid A as well as in pure culture (1+) in 2 of the affected joints and was considered the significant pathogen here. Tests for CAEV and Listeria were negative.
Case 3. Two 2-4-wk-old meat goats. The kids would go off feed, with some seeming neurologic and star-gazing. An autopsy was performed on the farm on 2 of the goats, and fixed tissues submitted for histology. Both goats had severe neutrophilic meningitis and evidence of septicemia. Although the animals had been treated, because of the similarity to the other cases, brain was submitted from both goats to look for S. gallolyticus subsp. Pasteurianus, which was isolated from the submitted brain sample in one goat (2+), along with Staphylococcus aureus (2+) and Streptococcus pluranimalium (3+). No significant pathogens were isolated from the second brain. This was interpreted as a possible case of S. gallolyticus because of its similarity to cases 1 and 2 (Fig 1).
Case 4 - 32-day-old goat kid displaying neurologic signs and reported as a “herd health problem”. At autopsy there was severe suppurative meningoencephalitis – S. gallolyticus subsp. pasteurianus was isolated (3+) as well as occasional P. aeruginosa.
The clinical presentation and histology seen in these cases is not typical of listeriosis, which is the most common bacterial meningoencephalitis we see in ruminants (Table 1). Although cases of septicemic listeriosis can look similar, these are rare. We strongly suspect involvement of S. gallolyticus subsp. pasteurianus as the cause of septicemia and meningoencephalitis, sometimes with arthritis, in all 4 of these herds. Contaminants and treatment do cause some doubt about interpretation of bacteriology and possibly missed cases due to failure to recover the bacteria.
For an accurate diagnosis when sampling animals with evidence of meningitis, it is important to obtain a clean sample of the meninges or brain. This can be difficult, but if the brain is partially removed so that it is “hanging” from the skull, a sterile swab can usually be worked between the leptomeninges and dura without touching contaminated surfaces. The swab can be submitted for bacterial culture pending histology results. AHL
Table 1. Confirmed and suggested causes of meningitis/encephalitis in 87 goat pathology submissions at the AHL May 2007 to December 2016.
Figure 1. Severe neutrophilic meningitis associated with S. gallolyticus subsp. pasteurianus
Clostridium perfringens type D outbreaks in dairy goats
Maria Spinato, Durda Slavic, Paula Menzies
Outbreaks of enteritis in adult does caused by Clostridium perfringens type D have increased over the past several years, in parallel with the rapid expansion of the dairy goat industry in Ontario. Clinical presentation, postmortem and histologic lesions, and prophylactic strategies often differ in goats, compared to the classical enterotoxemia (“pulpy kidney disease”) syndrome in sheep caused by the same bacterium. The classic presentation of sudden death and nonspecific gross findings of pulmonary edema, glucosuria, and hydropericardium are observed infrequently in goats. More commonly, adult does develop diarrhea of 2-4 days duration while continuing to eat and milk well prior to unexpected death. Severely affected animals are dehydrated, may develop dysentery with fibrinous casts, and exhibit abdominal pain and depression. Case fatality rates can be high.
At postmortem examination, does are typically in good body condition, dehydrated, and may or may not have external evidence of diarrhea. Lesions in the intestinal tract range from subtle mucosal congestion and edema, to more florid fibrinohemorrhagic enterocolitis that resembles other bacterial enteritides such as salmonellosis (Fig. 1). Sections of mid to distal jejunum and spiral colon are the best samples to submit for histologic examination and bacterial culture to confirm C. perfringens type D.
A recent feed change is commonly reported in goat dairy farms experiencing an outbreak of clostridial enterocolitis. Insufficient adaptation of rumen microflora to the altered ration results in an increased amount of undigested carbohydrate passing through to the intestines, providing a substrate for bacterial proliferation. Recently, it has been identified that a low glucose level, also due to undigested starch, actually stimulates production of the epsilon toxin by C. perfringens type D. It has been suggested that goats develop more severe intestinal lesions compared to sheep because intestinal absorption of epsilon toxin into circulation is slower in goats.
Goats also differ from sheep in their response to clostridial bacterins. Antibody levels tend to drop rapidly in this species, with non-protective titers reported as early as 90 days post-vaccination. This means that a vaccination program should be developed that ensures kids are properly vaccinated (12 and 16 weeks of age, perhaps as young as 8 weeks if a herd is experiencing issues with the other clostridial pathogens), and that does are vaccinated every 4 months as a minimal frequency. However, vaccination alone is likely insufficient to control outbreaks of clostridial enteritis - dietary management is also important. Feeding frequency, access to fiber and avoidance of ruminal acidosis are important management practices to employ for reducing the incidence of C. perfringens type D outbreaks in goat dairies. AHL
Reference
Uzal FA, et al. Diseases produced by Clostridium perfringens type D. In: Uzal FA, et al., eds. Clostridial Diseases of Animals. New
Figure 1. Intestinal tract from a doe diagnosed with C. perfringens type D enterocolitis. Note the opened segments of jejunum and colon with exposed hemorrhagic mucosa.
Update on Cache Valley virus abortions in small ruminants 2016-17
Maria Spinato, Janet Shapiro, Rebecca Egan, Jocelyn Jansen, Paula Menzies
Small ruminant producers and veterinarians have been closely monitoring aborted fetuses and stillborns for deformities that could presage a recurrence of the Cache Valley virus (CVV) outbreak experienced during the 2015-16 lambing period. One caprine fetus with scoliosis, lordosis, domed forehead and prognathism, and one lamb fetus with palatoschisis and a widened asymmetrical face were examined by AHL and OVC pathologists, respectively. No brain deformities were identified grossly in either fetus. Thoracic fluid or heart blood was submitted for CVV antibody determination; both cases tested negative.
Based upon anecdotal reports and the absence of deformed fetuses fitting the case definition of CVV submitted to the AHL between December 2016 - February 2017, this appears to be a quiet season for this arboviral cause of small ruminant abortions. This may be the result of the development of strong maternal herd immunity following the 2015-16 outbreak and/or decreased circulating virus in the fall of 2016. AHL
Anaplasma marginale in a cow in Ontario
Felipe Reggeti, Kristiina Ruotsalo
In December of 2016, the AHL clinical pathology laboratory received EDTA blood and serum from a 3-y-old Holstein cow from Wellington County, with a recent history of abdominal discomfort, scant feces, and nonspecific malaise. The cow was a recent herd addition purchased from the United States. CBC results documented marked anemia (hemoglobin 29 g/L, reference interval 84-120 g/L)., with a marked regenerative response characterized by RBC anisokaryosis, polychromasia, and basophilic stippling. Peripheral blood smear examination revealed erythrocytes containing 1-2, small, round, basophilic, inclusions at the cell periphery, consistent with Anaplasma marginale (Fig. 1). Anaplasmosis was confirmed by Anaplasma antibody cELISA in the AHL virology laboratory, and by PCR (Kansas State VDL). A. marginale had been identified in July, 2013, in a cow in eastern Ontario, by the AHL.
On April 1, 2014, anaplasmosis was removed from the list of federally reportable diseases and placed on the list of provincially immediately notifiable diseases, meaning that only laboratories are required to report suspected or confirmed cases. Cows purchased from infected areas of North America are no longer tested before entering Canada;
Figure 1. Anaplasma marginale in bovine red cells.