Is steroid responsive meningitis in dogs contagious?
The condition is not caused by an infection, and it is not contagious, so your dog can’t pass it on to other pets or people.
There are a number of symptoms associated with steroid responsive meningitis, with the most common being a fever and severe neck pain that often extends into the lower back. The pain will be most severe when your dog tries to touch its chin to its chest.
There are no other neurological issues associated with SRMA, but your pet may:
Your dog’s heart may also fall into an abnormal rhythm as a result of inflammation of the pericardium, which is the sac that covers the heart. They also may suffer from effusion, which is where fluid collects in the abdomen and lungs, though both of these issues are rare.
It’s important that your pet is diagnosed and treated quickly, so your veterinary neurology specialists will work to uncover any other causes that could be contributing to your pet’s symptoms. This includes diseases such as:
Firstly, they will rule out infections or joint disease that can cause spinal pain. As part of this, they will undertake tests, including
If necessary, your dog may also undergo veterinary diagnostic imaging, such as an MRI. However, this isn’t a usual procedure for steroid responsive meningitis, because it is used to rule out any other causes.
In order to confirm a diagnosis of steroid responsive meningitis in dogs, your vet will need to uncover inflammation and evidence of a particular inflammatory cell while examining your pet.
As steroid responsive meningitis in dogs is an autoimmune condition, treatment usually involves flooding the immune system with high doses of prednisolone or other steroid and anti-inflammatory medication, which is either given via injection or orally. This usually continues for between five and seven months.
Where the condition is more severe, your dog may need to stay in hospital for a few days. While here, they may be given dexamethasone sodium phosphate, another anti-inflammatory treatment, intravenously.
It might also be necessary for your pet to take other oral medication, such as azathioprine or cyclosporine, which work to suppress the immune system further and can help prevent the condition returning when used in conjunction with a reduction in the dose of steroids. You should be able to give these to your pet at home.
Where your pet has been given steroids, they will start to improve within a few days, with their symptoms becoming less apparent or even disappearing completely. After a few weeks, their dosage can slowly start to be reduced until the autoimmune response has abated, which will take a few months.
It’s important that you make and keep appointments with your vet during this time, as they will need to check on your pet’s progress and see whether the treatment is having any affect on their organs.
Blood tests may be carried out to assess this, though this will depend on how your pet is responding to its treatment. Visits to your veterinary neurologist might also be needed during treatment, so that they can assess your pet’s progress.
While improvement can be rapid, there are some side effects to steroids, which include:
Your vet will talk through any likely side effects, and will be able to advise you further on what to do should your pet experience any.
Steroid-responsive meningitis-arteritis (SRMA) is a common inflammatory disease of the central nervous system in young dogs. A recently published study (1) examining records from a British veterinary referral hospital found that 48 percent of juvenile dogs that presented with a fever were diagnosed with SRMA.
SRMA is characterized by immune-mediated inflammation of the meninges (the membranes that envelope the brain and spinal cord) and associated blood vessels. The acute form is most common in dogs less than 18 to 24 months old. Clinical signs such as severe neck pain, high fever, and lethargy are experienced intermittently. MRI may be normal, and infectious disease testing will be negative in affected dogs, but cerebrospinal fluid analysis reveals severe neutrophilic inflammation (neutrophils are a type of white blood cell).
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Jeanie Lau, BVSc received a 2017 CHF Clinician-Scientist Fellowship and was awarded funding to study SRMA under the mentorship of Dr. Karen Muñana at N.C. State University. The objectives of CHF Grant 02324-E were to describe the clinical course of SRMA in a population of North American dogs, determine if there were breed differences in the clinical course of the disease, and evaluate owner perception of the quality of life for affected dogs. The study examined records from 61 dogs: 32 cases seen at the N.C. State University Veterinary Teaching Hospital from 2003 to 2017, and 29 cases identified through an owner survey distributed by CHF.
Most of the published literature on this disease describes cases from Europe, but a dedicated group of dog owners and researchers are collaborating with the AKC Canine Health Foundation (CHF) to learn more about the disease in North American dogs.
3. Survey and follow‐up data collection
Caregivers were asked to complete an online survey to evaluate the impact of SRMA on QoL, and to provide case follow‐up. The survey comprised a series of closed‐ended questions created with online survey software (©2018 Qualtrics, Provo, Utah) using an interval rating with a Likert‐type scale of 1‐5 or 1‐10 (Supporting Information S1). Although the survey was not formally validated for the study, it was designed to evaluate QoL‐associated themes and questions specific for SRMA in reference to published QoL questionnaires for dogs with other neurological disorders.15, 16, 17, 18
Continuous and ordinal data were reported as mean ± SD, or median and range, respectively. Categorical data were summarized as percentages and fractions. Differences among breeds were analyzed using the 1‐way analysis of variance for continuous variables and the Kruskal‐Wallis test for ordinal outcomes. The Wilcoxon signed rank test was used to compare caregivers rating of QoL over time. For the QoL data, responses relating to adverse effects of corticosteroids (Supporting Information S1, question 4) were adjusted, such that scores from related items (increased appetite and weight gain; increased thirst and urination) were averaged before being combined to generate a composite score of 14 to 56. The ranking analysis of covariance was used to study the effect of breed on response variables, while adjusting for other covariates of relapse frequency and composite corticosteroid adverse effect score. Analyses of correlations between paired variables were performed using the Pearson correlation (r) and Spearman correlation (r s) for continuous and ordinal variables, respectively. Linear regression was applied to study the effect of clinical factors on response variables of QoL, severity of relapse and number of relapse episodes. A P value <.05 was considered significant for all comparisons. Statistical analyses were performed using SAS 9.4 (SAS Institute, Cary, North Carolina).
Ninety‐six cases initially were identified, including 57 cases from the AKC‐CHF survey and 39 cases from the NC State VH. Owners consent to participate in the study was obtained for 37 cases from the AKC‐CHF survey and for all cases from the NC State VH. Eight cases identified through the AKC‐CHF survey were excluded from the study because CSF analysis was not performed (n = 6), residence was outside of North America (1), and CSF findings were not supportive of a diagnosis of the acute form of SRMA (1). Four cases identified at the NC State VH were excluded because of resolution of clinical signs after treatment with antimicrobials in the absence of corticosteroids, and 3 were excluded because of the presence of other neurologic deficits.
Sixty‐one cases met the inclusion criteria (29 cases from the AKC‐CHF survey and 32 cases from the NC State VH). The median age at time of SRMA diagnosis was 8.5 months (range, 2.1‐81.3 months), with 58/61 dogs (95.1%) <24 months of age. There were 34 males (18 sexually intact and 16 neutered), and 27 females (6 sexually intact and 21 spayed). Breeds represented included the Golden Retriever (n = 12), Bernese Mountain Dog (10), Wirehaired Pointing Griffon (9), Boxer (9), Beagle (6), American Staffordshire Terrier (3), German Shepherd Dog (2), Labrador Retriever (2), and 1 each of English Bulldog, Chesapeake Bay Retriever, Pembroke Welsh Corgi, Nova Scotia Duck Tolling Retriever, Giant Schnauzer, Stabyhoun, Weimaraner, and mixed breed. Approximately half of the dogs (31/61) were from North Carolina, with 17 other states represented, including New York (n = 4), Texas (4), California (2), Colorado (2), Illinois (2), Pennsylvania (2), Virginia (2), Connecticut (1), Florida (1), Louisiana (1), Maine (1), Maryland (1), Massachusetts (1), Michigan (1), Minnesota (1), New Jersey (1), and Ohio (1). Two dogs were from Canada; 1 from British Columbia, and 1 from Manitoba.
The median time from onset of clinical signs to diagnosis was 5 days (range, 1‐257 days). The primary presenting complaint in all dogs was neck pain and lethargy. Additional clinical signs included reluctance to rise or walk (52/61, 85.2%), stiff gait (43/61, 70.5%), decreased appetite (39/61, 63.9%), kyphotic posture (16/61, 26.2%), tremors (9/61, 14.8%), diarrhea (9/61, 14.8%), vomiting (4/61, 6.6%), and inappropriate urination (3/61, 4.9%). On initial hospital admission, 40 dogs (65.6%) were febrile, with rectal temperature ≥103°F. The median temperature for all dogs was 103.6°F (range, 100.4°F‐106.2°F). Thoracolumbar pain was elicited on spinal palpation in 21 (34.4%) dogs.
A CBC was available for review in 54 (88.5%) dogs. Of these, neutrophilic leukocytosis was present in 48 dogs (88.9%), with a median neutrophil count of 18.1 × 103/μL (range, 6.6‐48.9 × 103/μL; reference range, 2.8‐9.11 × 103/μL). Cerebrospinal fluid was collected from the cerebellomedullary cistern for analysis in all dogs. The median CSF NCC was 735/μL (range, 4‐7893/μL). The CSF NCC was <50/μL in 11 (18%) dogs, 50‐100/μL in 4 (6.6%) dogs, 101‐1000/μL in 18 (29.5%) dogs, and >1000/μL in 26 (42.6%) dogs. The median CSF protein concentration was 97.7 mg/dL (range, 10.1‐431.6 mg/dL; reference range, 0‐25 mg/dL). The percentage of neutrophils identified on cytologic evaluation was 42%‐97% (median, 81%), with neutrophils reported as nondegenerate and no pathologic organisms noted.
The CRP concentration was increased in 7 of 9 (77.8%) dogs in which it was measured (median, >60 mg/L; range, <2.5 to >60 mg/L; reference range, 0‐7.6 mg/L). Arthrocentesis was performed in 14 (23.0%) dogs, and indicated suppurative inflammation of multiple joints in the absence of infectious agents in 2 dogs, consistent with immune‐mediated polyarthritis. Fifty‐four (88.5%) dogs underwent infectious disease testing (Table ) that failed to identify a cause for the clinical signs in all dogs.
| Type of test | Samples | Organism | Number |
|---|---|---|---|
| Bacterial culture | Blood | Aerobic bacteria | 16 |
| CSF | Aerobic and anaerobic bacteria | 4 | |
| Urine | Aerobic bacteria | 4 | |
| Indirect fluorescent antibody | Serum | Babesia canis | 37 |
| Babesia gibsoni | 37 | ||
| Bartonella henselae | 37 | ||
| Bartonella vinsoni | 37 | ||
| Ehrlichia canis | 37 | ||
| Rickettsia rickettsii | 37 | ||
| Neospora caninum | 15 | ||
| Toxoplasma gondii | 13 | ||
| Latex cryptococcal antigen agglutination test | Serum or CSF | Cryptococcal neoformans | 16 |
| PCR | Pooled whole blood and CSF | Borrelia burgdorferi | 31 |
| Canine distemper virus | 31 | ||
| Neospora hughesi and caninum | 31 | ||
| Toxoplasma gondii | 31 | ||
| SNAP 4DX Plus | Serum | Anaplasma phagocytophilim | 37 |
| Anaplasma platys | 37 | ||
| Borrelia burgdorferi | 37 | ||
| Dirofilaria immitis | 37 | ||
| Ehrlichia canis or Ehrlichia ewingii | 37 |
Cervical radiographs were performed in 41 (67.2%) dogs, with unremarkable findings. Reports were available for review from 23 (37.8%) dogs that underwent MRI of the cervical spine. A normal study was reported in 6 dogs. Abnormalities included meningeal contrast enhancement in 11 dogs, with this being the sole finding in 6 dogs; signal changes in the cervical paraspinal musculature in 6 dogs, consisting of T2 hyperintensity (n = 1), contrast enhancement (2) or both (3); and, multifocal ill‐defined, T2‐hyperintense lesions within the cervical spinal cord with variable contrast enhancement in 5 dogs.
All dogs were treated initially with corticosteroids after diagnosis. Treatment was initiated with prednisone in all but 2 dogs that were initially treated with dexamethasone and then changed to prednisone. The median time from onset of clinical signs to initiation of treatment was 5 days (range, 1‐257 days). The initial prednisone dosage ranged from .5 to 4.2 mg/kg/d (median, 1.7 mg/kg/d). Of the 28 dogs that were placed on immunosuppressive dosages of prednisone (≥2 mg/kg/d), the duration of immunosuppression ranged from 5 to 111 days (median, 22 days). Five (8.5%) dogs had a second immunomodulatory drug administered concurrently with prednisone at the time of initial diagnosis, whereas an additional 4 (6.5%) dogs started a second immunomodulatory drug at 5 days, 3 weeks, 2 months, and 5 months after commencing initial treatment with prednisone. Drugs administered included azathioprine (n = 4), cytarabine (2), cyclosporine A (1), mycophenolate mofetil (1), and leflunomide (1). Antimicrobials were prescribed in 43 (70.5%) dogs, including doxycycline (n = 30), clindamycin (21), amoxicillin‐clavulanic acid (5), enrofloxacin (4), metronidazole (4), minocycline (3), and trimethoprim‐sulfamethoxazole (2). All dogs were noted to have improvement in clinical signs after initiation of prednisone treatment.
The median follow‐up for all dogs was 2 years (range, 10 days to 12.5 years). Three dogs had <1 month of follow‐up at the time of data collection, all of which were in clinical remission. Twenty‐nine (47.5%) dogs suffered at least 1 relapse during the follow‐up period. Nine dogs (14.8%) had 1 relapse, 7 dogs (11.5%) had 2 relapses, 6 dogs (9.8%) had 3 relapses, 2 dogs (3.3%) had 4 relapses, and 5 dogs (8.2%) had ≥5 relapses. Five dogs had repeat CSF analysis performed at the time of clinical relapse. Results were normal in 1 dog (1/μL NCC, 17 mg/dL protein), whereas the remaining 4 dogs had neutrophilic pleocytosis with NCC of 8, 30, 2530, and 2830/μL, and neutrophil percentages on cytology of 50, 73, 77, and 95, respectively. All relapses were treated with prednisone at a median dosage of 2.0 mg/kg/d (range, .2‐6.0 mg/kg/d). A second immunomodulatory drug was commenced in 13/29 (44.8%) dogs, including 4/5 (80%) dogs treated with <1.0 mg/kg/d of prednisone during relapse. Drugs utilized included cyclosporine A (n = 7), azathioprine (5), and mycophenolate mofetil (1).
Twenty‐two (75.9%) dogs had their first relapse after treatment for SRMA was discontinued, occurring a median of 139.5 days after cessation of prednisone treatment (range, 12‐2176 days). The time between completion of prednisone treatment and first relapse was <3 months in 4 dogs, 3‐6 months in 8 dogs, and >6 months in 10 dogs. In 7/29 (24.1%) dogs, relapse occurred while the prednisone dosage was being tapered, with a median time period of 7 days (range, 3‐15 days) from the previous dosage reduction. The median age at first relapse was 19.2 months (range, 3.3‐84.4 months).
Analysis was performed to identify factors associated with frequency and caregivers assessment of severity of relapse in the 29 dogs. The variables evaluated included age at onset of clinical signs, CSF NCC, CSF neutrophil percentage, CSF protein concentration, prednisone dosage, prednisone treatment duration, treatment with a second immunomodulatory drug at initial diagnosis, and duration between onset of clinical signs and initiation of treatment. A relationship was found between CSF NCC and frequency of disease relapse (P = .003). No other associations were identified.
Twenty‐nine (47.5%) dogs were reported to have resolution of clinical signs after completing the prescribed course of corticosteroids at the time of last follow‐up, with a median duration of resolution of clinical signs of 37 months (range, 1‐143 months) and a median total duration of prednisone treatment of 247 days (range, 45‐1419 days). Two (3.3%) dogs achieved clinical resolution for 64 and 139 days, but were reported to have relapsed at last communication and were lost to follow‐up. Twenty‐five (41.0%) dogs were in remission and undergoing a tapering schedule of prednisone administration at follow‐up, with a median duration of prednisone treatment of 435 days (range, 10‐2174 days). Overall, 5 (8.2%) dogs died during the follow‐up period, of which 4 (80%) died because of reasons unrelated to SRMA. One dog (1.6%) was euthanized because of relapse and development of neurologic deficits.
Fifty‐two (85.2%) caregivers completed the online survey. Caregivers were asked to assess the severity of neck pain at onset, and the majority of respondents (76.9%) noted improvement in clinical signs within 1‐2 days of starting prednisone. Adverse effects of prednisone reported by the caregiver included polydipsia (n = 47, 90.4%), polyuria (46, 88.5%), polyphagia (45, 86.5%), panting (39, 75.0%), weight gain (39, 75.0%), thinning of the hair coat (36, 69.2%), restlessness (29, 55.8%), sleeping more than usual (29, 55.8%), inappropriate urination (25, 48.1%), “pot belly” appearance (25, 48.1%), development of nondermatological infections (20, 38.5%), diarrhea (19, 36.5%), dermatitis (18, 34.6%), and vomiting (7, 13.5%). Adverse effects that were reported by caregivers as being severe included polyphagia (23, 44.3%), polydipsia (22, 42.3%), polyuria (20, 38.5%), and thinning of the hair coat (13, 25.0%). Forty‐eight percent (25/52) of respondents reported that their dogs core vaccinations were not up‐to‐date since being diagnosed with SRMA.
Caregivers were asked to rate their dogs QoL on a scale of 1‐10, with 1 being poor and 10 being excellent. The mean QoL for dogs during treatment (5.3, SD .4) was significantly worse than the QoL during clinical resolution (8.8, SD 1.8; P < .001) and since diagnosis of SRMA (8.2, SD 1.2; P < .001). The QoL during treatment was associated with the severity of prednisone adverse effects (r s = −.52, P = .03; Figure ). This association persisted when adverse effects were evaluated separately based on the following categories: polyphagia and weight gain (r s = .68, P < .0001), polyuria and polydipsia (r s = .65, P < .0001), urination in inappropriate places (r s = .84, P < .0001), sleeping more (r s = .78, P < .0001), restlessness and pacing (r s = .82, P < .0001), increased panting (r s = 0.83, P < .0001), and change in appearance (r s = .59, P < .0001). A higher prednisone dosage was associated with more severe adverse effects (r = .24, P = .02), but neither the duration of immunosuppression nor the duration of prednisone treatment was associated with the severity of adverse effects.
For analysis of breed differences, breeds represented by ≥6 dogs were included separately, with dogs grouped into the following categories: Beagle, Bernese Mountain Dog, Boxer, Golden Retriever, Wirehaired Pointing Griffon, and others. Variables that were evaluated for differences among breeds are summarized in Table . No differences were identified with respect to clinical presentation, CSF findings, treatment response, and relapse. However, a significant difference in the number of reported prednisone adverse effects among breeds was identified (P = .04). Analysis of the difference in least squares means among breeds identified Wirehaired Pointing Griffons as having a significantly higher number of total observed adverse effects compared with other breeds (P = .04). The difference in the severity of prednisone adverse effects among breeds was not statistically significant (P = .06). A significant difference also was identified in the maximal prednisone dosage among breeds (P = .001), with the prednisone dosage administered to Wirehaired Pointing Griffons (mean ± SD, 2.38 ± .46 mg/kg/d) being significantly higher compared to the dosage administered to Beagles (mean ± SD, 1.88 ± .13 mg/kg/d; P = .04), Bernese Mountain Dogs (mean ± SD, 1.55 ± 1.10 mg/kg/d; P = .01), and Golden Retrievers (mean ± SD, 1.86 ± .23 mg/kg/d; P = .005). Boxers (mean ± SD, 3.11 ± 1.07 mg/kg/d) also were treated with a significantly higher prednisone dosage compared to Beagles (P = .02), Bernese Mountain Dogs (P = .008), Golden Retrievers (P = .002), and other breeds (P = .03).
| Category | Specific variable | Statistical test | P value |
|---|---|---|---|
| Clinical presentation | Severity of neck pain | Kruskal‐Wallis | .71 |
| Age of onset of clinical signs | Kruskal‐Wallis | .12 | |
| CSF findings | NCC | ANOVA | .69 |
| Neutrophil percentage | ANOVA | .53 | |
| Protein concentration | ANOVA | .20 | |
| Treatment | Prednisone dosage | Kruskal‐Wallis | .001 |
| Time to clinical improvement | Kruskal‐Wallis | .44 | |
| Time to return to normal | Kruskal‐Wallis | .71 | |
| Number of adverse effects | ANOVA | .04 | |
| Combined prednisone score | ANOVA | .06 | |
| Relapse | Time to relapse | Kruskal‐Wallis | .86 |
| Relapse frequency | Kruskal‐Wallis | .61 | |
| Severity of clinical signs at relapse | Kruskal‐Wallis | .64 | |
| Quality of life | Before diagnosis | Kruskal‐Wallis | .22 |
| During treatmenta | |||
| • Combined prednisone score | Linear regression | .03 | |
| • Relapse frequency | Linear regression | .84 | |
| During remissiona | |||
| • Combined prednisone score | Linear regression | .24 | |
| • Relapse frequency | Linear regression | .66 | |
| Since diagnosisa | |||
| • Combined prednisone score | Linear regression | .24 | |
| • Relapse frequency | Linear regression | .34 |
To the best of our knowledge, this report is the first study of SRMA involving client‐owned dogs in North America. The breeds represented most often, contributing ≥10% to the study population, were the Golden Retriever, Bernese Mountain Dog, Wirehaired Pointing Griffon, Boxer, and Beagle. Beagles, Bernese Mountain Dogs, and Boxers have been overrepresented in previous studies of SRMA.2, 3, 7, 19 Our findings suggest that Golden Retrievers and Wirehaired Pointing Griffons also should be included among the breeds recognized to develop SRMA. Golden Retrievers have been included in the population of affected dogs in a previous study of SRMA,14 whereas SRMA has not been described previously in the Wirehaired Pointing Griffon. A recent retrospective case control study also identified the Border Collie, Jack Russell Terrier, and Whippet as having increased odds of developing SRMA.3 These newly recognized breeds may have a genetic predisposition to develop SRMA, and provide the opportunity for further investigation into the pathogenesis of the disorder.
Study findings regarding clinical presentation and response to treatment were in agreement with published information on SRMA. The median age of onset was 8.5 months, with 95% of dogs <2 years old at the time of diagnosis, consistent with the previously reported age of onset of 6‐18 months.1, 2 Approximately two thirds of dogs in our study were pyrexic on presentation, with temperature ≥103.0°F. A recent retrospective study of pyrexia in dogs aged 1‐18 months identified SRMA as the most common diagnosis, suggesting that SRMA should be considered in the differential diagnosis o