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This article describes the clinical and pathological features of an orphan 7-day-old, male Formosan sambar fawn that was hospitalized for treatment of weakness. The fawn had been deprived of colostrum and developed suppurative meningitis that was attributed to Escherichia coli.
Méningite suppurée causée par Escherichia coli chez un cerf sambar de Formose âgé de 7 jours (Cervus unicolor swinhoei). Cet article décrit les caractéristiques cliniques et pathologiques d’un faon de Formose orphelin mâle âgé de 7 jours qui a été hospitalisé pour traitement d’un état de faiblesse. Le faon avait été privé de colostrum et avait développé une méningite suppurée qui a été attribuée à Escherichia coli.
(Traduit par Isabelle Vallières)
A 7-day-old, 6.5-kg, male fawn of farmed Formosan sambar deer (Cervus unicolor swinhoei) was referred to the Veterinary Medicine Teaching Hospital for treatment of weakness of 48-h duration. The primiparous doe had a history of dystocia and failure to nurse the fawn after delivery. Goat’s milk was the only feed for the next few days until diarrhea was noticed by the owner.
At admission, the fawn was permanently recumbent and occasionally showed signs of rigid extension of the limbs and opisthotonos. Abnormal findings during physical examination included an estimated dehydration of 3% to 5%, no suckling reflex, and an elevated respiratory rate (120 breaths/min). The oral mucous membranes were pale and the capillary refill time was >3 s. Laboratory abnormalities included marked leukocytosis (8.2 × 109/L; reference range: 3.2 to 5.2 × 109/L) and neutrophilia (5.9 × 109/L; reference range: 0.9 to 2.8 × 109/L) with left shift (bands, 0.656 × 109/L; reference range: 0 to 0.052 × 109/L). Reference ranges for these values in Formosan sambar deer are for leukocytes, segmented neutrophils, and band neutrophils (1). Differential diagnosis included neonatal septicemia, meningitis, salmonellosis, and malnutrition.
Medical care consisted of maintenance fluid, flunixin meglumine, 1.1 mg/kg body weight (BW), IV, q24h, and florfenicol, 20 mg/kg BW, IM, q48h. Despite supportive treatment and care, the fawn’s condition deteriorated; he developed a fever of 40.8°C and died 6 h after admission. On gross postmortem examination, there were no external lesions on the carcass, the only changes noted were a large quantity of opaque grayish exudate covering the cerebrum (Figure 1A) and a moderate amount of serosanguineous fluid with fibrin in the pericardial sac. Other significant gross changes to the organs were umbilical arterial congestion in the area of the bladder and multifocal intestinal congestion with thinned intestinal walls.
Swab specimens were obtained from the cerebrum and postoccipital cerebrospinal fluid (CSF) for bacterial isolation using blood agar followed by subculture on Eosin-methylene blue (EMB) agar. The isolated colonies were biochemically confirmed to be Escherichia coli using the API 20E system (bioMérieux, Marcy l’Étoile, France), which was consistent with the findings in a smear from the swabs showing clusters of gram-negative rods. The E. coli was negative for Shiga toxin genes as determined by polymerase chain reaction (PCR) as previously described (2). This pathogen was sensitive to ceftiofur, enrofloxacin, and florfenicol and was resistant to amoxicillin, ampicillin, cephalothin, neomycin, and oxytetracycline according to a disc agar diffusion antimicrobial susceptibility test as described by the Clinical and Laboratory Standards Institute (CLSI). No organism was isolated from the pericardium and umbilical arteries.
A sample of CSF containing a large amount of flocculent fibrin clots had a leucocyte count >100 000 cells/μL; a differential cell count revealed 26% bands, 18% segmented neutrophils, 43% monocytes, 12% lymphocytes, and 1% eosinophils. Phagocytosis of rod-shaped bacteria by neutrophils was evident (Figure 2). Histopathologic examination confirmed acute suppurative meningitis with massive infiltration of neutrophils and fibrin deposition in the meninges (Figure 1B). Widespread degenerative lesions of conspicuous vacuolization were observed throughout the superficial cerebral cortex. Numerous inflammatory cells and bacterial clusters were scattered predominantly throughout the pericardium; they were not observed in the myocardium. The umbilical arteries had red blood cells with a mild infiltration of monocytic inflammatory cells, indicative of residual blood in the arteries. There were no significant lesions in the other organs. These results indicated that the Formosan sambar fawn suffered from suppurative meningitis caused by E. coli.
Neonatal meningitis is thought to be a sequel to the hematogenous spread of microorganisms from a primary source of infection, such as bacteremia, diarrhea, septic arthritis, omphalophlebitis, or uveitis (3). The disease is often caused by E. coli, and occasionally by Streptococcus pneumoniae, Streptococcus bovis, or Klebsiella oxytoca in calves under 2 weeks of age (4,5). A similar disease process with coliform meningitis has been recognized in compromised neonatal llamas and alpacas (6,7), but there is little information as to a similar syndrome in captive or farmed deer (8,9). Lack of information is probably not due to the absence of similar diseases in deer, but rather due to minimal attention by the owners.
Intracranial abscessation/suppurative meningoencephalitis occurs infrequently in deer; 2 studies of white-tailed deer (Odocoileus virginianus) in North America reported this disease in only 0.6% of 359 fawns and 2.2% to 4% of adults (10,11). Arcanobacterium pyogenes was isolated in a greater proportion of brain specimens (29.2% to 61%) compared with E. coli (8.3% to 10%) (10,11). In one study, 87% of cases of intracranial abscessation occurred in males, mostly in males >1 y, and mostly in September to April (10). These findings are consistent with a predisposition based on the cycle of antler development and behavioral traits associated with reproduction (10,11). The present study appears to be the first report of coliform meningitis in a fawn.
In a study of calves with coliform septicemia, 23 (43%) had meningitis, and 5 of the 23 had diarrhea (12). The fact that the clinical signs were perceived soon after the diarrhea suggests that the septicemia resulted from the enteric infection. However, it has also been demonstrated experimentally that septicemia can occur without enteritis (12). In the present case, even though bacterial examination confirmed a brain infection caused by E. coli in the fawn, the pathological findings enabled an exact diagnosis of suppurative meningitis and the associated pericarditis. Nevertheless, there was not sufficient histopathologic evidence to identify the possible route of infection.
There is little placental transfer of antibody in the ruminants prior to birth (7,13), thus, failure to ingest sufficient colostrum increases the risk of infection during the neonatal period (7,13,14). High mortality, primarily resulting from diarrhea, septicemia, or pneumonia, often occurs in hand-reared mule deer fawns. The high prevalence of such diseases and failure to respond to therapy suggest a lack of adequate passive immunity from colostrum in these fawns (13). In the case described herein, deprivation of colostrum may have contributed to disease in this fawn.
Suppurative meningitis is a common ailment in ruminants that is associated with high mortality and is generally difficult to treat. Once the diagnosis has been made, the infectious process is often well-advanced in the brain and other organs, resulting in a poor prognosis, even with appropriate antimicrobial therapy (5,7). Successful treatment of meningitis requires that effective antibiotics penetrate the blood-brain barrier (6). Although the E. coli was susceptible in vitro to florfenicol, ceftiofur, and enrofloxacin, only florfenicol could achieve therapeutic concentrations in the CSF (14). Failure to absorb colostral antibodies, malnourishment and poor sanitation may increase the risk of neonatal mortality (7). In the present case, caprine milk was the source of feed for the fawn due to the absence of maternal colostrum. The E. coli may have been transmitted to the fawn during artificial nursing. It is advisable to store deer colostrum for future cases, especially on a commercial sambar deer farm. As soon as a doe’s failure to nurse is detected, the only recourse is to administer stocked doe or bovine colostrum within 18 h after birth, giving 400 mL during 4 h (100 mL/h) (13). Appropriate hygienic procedures should also be observed when nursing orphan fawns. CVJ
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