Silent Bite: Capnocytophaga meningitis with bilateral sensorineural hearing loss in splenectomized patient

doi:10.21203/rs.3.rs-4114497/v1

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Silent Bite: Capnocytophaga meningitis with bilateral sensorineural hearing loss in splenectomized patient

https://doi.org/10.21203/rs.3.rs-4114497/v1

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Splenectomized patients are at increased risk for infection with encapsulated bacteria including Capnocytophaga canimorsus found in canine oral flora. We report the clinical course, diagnostic workup, and treatment outcome of an asplenic woman who developed meningitis with bilateral sensorineural hearing loss after a dog bite. To limit the significant morbidity and mortality associated with this bacterium, it is imperative that providers consider Capnocytophaga canimorsus as the cause of infection and for the immunocompromised and symptomatic patient to seek prompt medical attention in the context of canine exposure.

Capnocytophaga meningitis

sensorineural hearing loss

asplenia

dog bite

Capnocytophaga canimorsus is a gram-negative, rod-shaped commensal bacterium found in the oral flora of dogs and cats [1, 2]. Immunocompromised individuals including the splenectomized, functionally asplenic, cirrhotic, alcoholic, and those with neoplasms or on corticotherapy are at an increased risk of infection with C. canimorsus. Infected patients often present with a history of contact with a dog or cat and may report being bitten, scratched, or licking of pre-existing lesions. A wide range of morbidities have been reported with C. canimorsus infection including pain at the site of injury, purulent discharge, localized cellulitis, lymphangitis, osteomyelitis, eye infections, high-grade bacteremia, meningitis, endocarditis, disseminated intravascular coagulation, complicated pneumonia, renal failure, hemolytic uremic syndrome, gangrene of the digits or extremities, and fulminant sepsis [2, 3]. There are also case reports that describe hearing loss in patients with C. canimorsus infection [4–7]. Mortality from C. canimorsus sepsis and bacteremia ranges from 25–60% [3]. In the United States, an estimated 2 million dog bites occur annually and approximately 25,000 splenectomies are performed each year [8, 9]. Given its potential for significant morbidity and mortality, it is prudent to consider C. canimorsus infection as a culprit for the immunocompromised patient presenting with infectious signs and symptoms and a history of canine exposure.

A 62-year-old female presented with a 1 week-history of malaise, joint aches, diarrhea, and headaches which were managed with increasing use of ibuprofen. Additionally, she noted a 1-day history of epistaxis, bleeding gums, and bilateral hearing loss with tinnitus and vertigo. Of note, the patient suffered a dog bite a few days before the symptoms started and had returned from a 2-night stay in a cabin in the woods of the Mississippi river valley region a day before. Medical history is significant for splenectomy due to trauma, gastroesophageal reflux disease on omeprazole, and osteoporosis. Physical exam revealed bilateral lower extremity petechial rash. Initial chemistry profile significant for potassium 2.6, creatinine 4.16 (baseline 0.8-1), glomerular filtration rate (GFR) 11 (baseline > 60). Initial blood counts showed thrombocytopenia with a platelet count of 8 without leukopenia or anemia. The coagulation profile revealed elevated fibrinogen, but prothrombin (PT) and partial thromboplastin time (PTT) were within normal limits.

Computed tomography (CT) of the head showed no acute intracranial abnormality and stable previously known prominent pituitary gland. Initial workup for acute kidney injury (AKI) included urinalysis which was significant for trace proteinuria and hyaline casts. Urine eosinophils negative. Renal ultrasound showed no cystic or solid lesions or hydronephrosis. On admission, blood and urine cultures were collected and the patient was started on broad-spectrum antibiotics. Blood cultures were significant for Capnocytophaga canimorsus. With concerns for meningitis given her acute neurological symptoms, the patient was started on meropenem. MRI (magnetic resonance imaging) brain revealed no intracranial abnormality or abscess but was significant for mildly prominent pituitary measuring 10 mm.

Initial workup for thrombocytopenia included a blood smear which was negative for schistocytes, lactate dehydrogenase (LDH) elevated at 474, haptoglobin within normal limits. Infectious causes including respiratory pathogen array, gastrointestinal pathogen array, hepatitis-C, clostridium difficile, and HIV (Human immunodeficiency virus) were all negative. Plasmic score was high and the follow-up test for ADAMTS13 activity was reduced but did not meet the cutoff for TTP (thrombotic thrombocytopenic purpura). Complement-mediated microangiopathic anemia was ruled out as serum ANA, C4 and C3 complement were within normal limits and UPEP (urine protein electrophoresis) and SPEP (serum protein electrophoresis) unremarkable. Suspecting possible immune thrombocytopenia, she was started on IV (intravenous) steroids. Lumbar puncture was performed, and CSF (cerebrospinal fluid) glucose, protein, and cell diff were within normal limits. CSF bacterial and VDRL (venereal disease research laboratory) were negative. Initial audiology evaluation showed poor word recognition score with hearing sensitivity of 250–8000 Hz, confirming moderate to severe sensorineural hearing loss bilaterally.

Splenectomies are performed for patients with traumatic injuries, idiopathic thrombocytopenic purpura, thalassemia, hereditary spherocytosis, sickle cell anemia, and lymphoma. Although humans can survive without a spleen, there is an increased risk of overwhelming post-splenectomy infection (OPSI), and the estimated mortality rate has been reported up to 70% [10]. This significant risk for overwhelming infection can be explained by the absence of important host defense mechanisms provided by the spleen. The spleen is an intraperitoneal lymphoid organ that filters immune complexes from circulation thus protecting the body from microbial infection [11, 12]. It holds B-lymphocytes and mononuclear phagocytes that directly attack bacteria in addition to generating IgM that is responsible for eliminating encapsulated organisms including C. canimorsus.

C. canimorsus requires specific culture media for growth and has an incubation period of 1 to 14 days, with an average of 6 days, thus prolonging the ability to make a definitive microbiological diagnosis [1, 2]. Successful growth has been achieved with standard chocolate agar or Columbia agar with 5% sheep’s blood and aerobic 5–10% CO₂-enriched atmosphere at a temperature of 35℃ to 37℃. It does not grow on MacConkey agar [13]. In 11 patients with C. canimorsus meningitis, lumbar puncture revealed an elevated protein level in 9 patients with 8 labs below < 2.0 g/L, a decreased CSF glucose level (< 0.4 g/L) for most of the patients, and WBC count range of 0-6000 cells/µL and a neutrophilic predominance in 8 patients [13]. C. canimorsus can also be identified with a Gram stain that will test positive for Gram-negative rods.

Penicillin is regarded as the drug of choice for C. canimorsus infection [2]. C. canimorsus is also susceptible to imipenem, erythromycin, clindamycin, vancomycin, chloramphenicol, third generation cephalosporins, fluoroquinolones, rifampin, metronidazole, and doxycycline [2, 13]. Resistance has been reported with aztreonam, fosfomycin, polymyxin, and trimethoprim/sulfamethoxazole.

Sensorineural hearing loss (SNHL) is a known complication of acute meningitis and appears to be described often as a complication of capnocytophaga meningitis [4, 5, 14]. Even though our patient did not experience all the typical symptoms of meningitis, her SNHL was bilateral, acute, and coincided strongly with the development of this bacteremia. AKI was likely secondary to excessive use of NSAIDs during the viral prodrome and improved with aggressive IV hydration. The platelet count normalized with steroids, but in retrospect was likely secondary thrombocytopenia from bacteremia. Although a lumbar puncture was done and CSF profile/cultures/bacterial PCR were negative, they were taken almost a week after initiation of antibiotics with CNS (central nervous system) penetration. After otolaryngology evaluation, repeat MRI and lumbar puncture, no clear alternate cause has been determined thus far. Overall, the most likely scenario remains that her acute SNHL was related to a capnocytophaga meningitis complicating the bacteremia. Our patient has completed antimicrobial therapy. With audiology rehabilitation, she was able to improve her word recognition abilities, though she now requires hearing aids.

A thorough clinical history combined with collaboration between the clinical team and microbiologists is essential for a correct and prompt diagnosis. High-risk patients should be counseled on the risk of keeping pets and the importance of promptly seeking medical attention in the setting of a dog bite or scratch. Early recognition and treatment can limit the morbidity and mortality associated with C. canimorsus infection.

AKI

Acute kidney injury

ANA

Antinuclear antibody

CNS

Central nervous system

CO₂

carbon dioxide

Computed tomography

GFR

Glomerular filtration rate

HIV

Human immunodeficiency virus

Hertz

Intravenous

MRI

Magnetic resonance imaging

NSAID

Nonsteroidal anti-inflammatory drug

OPSI

Overwhelming post-splenectomy infection

PCR

Polymerase chain reaction

Prothrombin time

PTT

Partial thromboplastin time

SNHL

Sensorineural hearing loss

SPEP

Serum protein electrophoresis

TTP

Thrombotic thrombocytopenic purpura

UPEP

Urine protein electrophoresis

VDRL

Venereal disease research laboratory

Conflict of interest Statement: The authors have no personal or institutional interest in the authorship and/or publication of this manuscript.

IRB compliance statement and ethical adherence: This work was performed in accordance with The Code of Ethics of the World Medical Association and Declaration in Helsinki, as well as the guidelines enforced by our local Institutional Review Board regarding patient consent.

Funding Disclosures: The authors declare that no funds, grants, or other support were received during the preparation of this manuscript.

Competing interests: The authors have no relevant financial or non-financial interests to disclose.

Author contributions: All authors contributed to the study conception and design. Material preparation, data collection and analysis were performed by Sonia Pulido and Mehwish Kishore. The first draft of the manuscript was written by Sonia Pulido and Mehwish Kishore and all authors commented on previous versions of the manuscript. All authors read and approved the final manuscript.

Ethics approval: This work was performed in accordance with The Code of Ethics of the World Medical Association and Declaration in Helsinki, as well as the guidelines enforced by our local Institutional Review Board at the University of Illinois College of Medicine in Peoria regarding patient consent.

Consent to participate: Informed consent was obtained from the patient included in the study.

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No competing interests reported.

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Silent Bite: Capnocytophaga meningitis with bilateral sensorineural hearing loss in splenectomized patient

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