An Intriguing Case of Meningitis. Tiffany Mylius MLS (ASCP)

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1 An Intriguing Case of Meningitis { Tiffany Mylius MLS (ASCP)

2 A 4yo male presents with 2wk history of URI symptoms. On the day of admission, the patient woke up with a HA in the morning, took a nap later that day and FOC couldn t wake him. EMS was called and upon arrival noted altered mental status, jaw stiffening, increased HR, and left eye gaze. At OSH ED, due to acute respiratory failure the patient was intubated, an LP was performed, a blood culture was obtained, and antibiotics started. The patient was then transferred to Children s for further care. Initial concern was a sinusitis that tracked intracranial, or a questionable injury. PT has a past medical history of febrile seizures, otherwise normal. An EEG was placed to monitor any seizure activity by request of Neurology. Infectious Disease consultation included antibiotic treatment along with additional laboratory testing.

3 Initial Testing performed at OSH ED: Hematology 3/11/17: WBC 57.1 H K/MM3 SEGS % CSF CELL COUNT 3/11/17: Color - Pale Yellow Character - Cloudy WBC Count / 4444 / 0-10mm3 RBC Count / 1489 / 0-1 mm3 Polynuclear Cells / 99 / % Mononuclear Cells / 1 / % Glucose / <1 / mg/dl Protien / 320 / mg/dl Chemistry 3/11/17: Glucose / 156 / mg/dl Lactic Acid / 7.2 / mmol/l C Reactive Protien / 5.19 / <=0.90 mg/dl

4 CHCO Testing admission date compared with discharge date: Hematology 3/11/17: WBC H ^3/uL SEGS 79.0 % Chemistry 3/11/17: Glucose 118 H mg/dl LACTATE WB 3.30 H mmol/l C Reactive Protein 5.3 H mg/dl Procalcitonin *H ng/ml HEMATOLOGY 3/20/17 WBC ^3/uL SEGS 20.6 % CHEMISTRY 3/20/17 Glucose / 92 / mg/dl C Reactive Protein / <0.5 / mg/dl Procalcitonin / / ng/ml

5 Additional Scans: EEG monitoring was negative at 24 hrs. for seizure activity MRI results: Brain MRI demonstrates multiple areas of enhancement and cytotoxic edema. -left parietal and bilateral temporal cortices -speckled foci of enhanced of the left parietal lobe -no mass or midline shift

6 Dural enhancement seen most over left frontal and bilateral parietal areas Small area of cortical inflammation with cytotoxic edema

7 Microbiology Results: CSF Microbiology 3/11/17: -Large number Segmented neutrophils (polys) observed -Moderate number Gram Positive Cocci -Rare {Streptococcus agalactiae} (Group B Streptococcus) -MIC: - Amplicillin 0.12 mcg/ml Susceptible - Vancomycin 1 mcg/ml Susceptible Respiratory culture / Negative Blood Culture / Negative Respiratory Pathogen Panel / Negative Meningitis Encephalitis Panel / [Group B Streptococcus] BLOOD CULTURE CENTRAL LINE 3/11/17: - {Streptococcus agalactiae} MIC: - Ampicillin 0.12 mcg/dl Susceptible - Cefotaxime <=0.25 mcg/dl Susceptible - Clindamycin <=0.06 mcg/dl Susceptible - Erythromycin <=0.06 mcg/dl Susceptible - Penicillin <=0.03 mcg/dl Susceptible - Vancomycin 1 mcg/dl Susceptible

8 Microbiology:

9 The D-test is used to look for inducible clindamycin resistance in organisms like Group B strep. If the D-test is positive, there will be a characteristic blunting or D- formation in between the disks. This is where resistance to Clindamycin was induced by erythromycin.

10 What made this interesting? What are common causes of bacterial meningitis? What kind of infections does GBS usually cause? What kind of patients usually get GBS infections?

11 What are common causes of bacterial meningitis? The three most common organisms causing acute bacterial meningitis in children are SPN, NMG, and HFLU. GBS is a common cause of bacterial meningitis in neonates, but not schoolaged children. Underlying conditions can be associated with increased risk of meningitis or particular bacterial species or both.

12 What kind of infections does GBS usually cause? GBS causes invasive disease in young infants, pregnant women and older adults. GBS lives in GI tract and GU tract GBS in infants: To prevent early-onset (babies <1 week old) GBS: Test all pregnant women for GBS late in pregnancy (35-37 weeks) Give antibiotics during labor to women who test positive for GBS Early-onset GBS: sepsis (infection of the blood), pneumonia (infection in the lungs), and sometimes meningitis (infection of the fluid and lining around the brain). Late-onset GBS (1wk-3mos): similar diseases, but meningitis is more common

13 What kind of patients usually get GBS infections? Our patient is not a neonate, pregnant woman, or older adult. Could his infection have come from GI or GU tract? He had a dental cleaning the week before getting sick. Maybe had oral infection or trauma? Most cases of GBS in adults are people with medical conditions that put them at increased risk, such as: Diabetes mellitus Cardiovascular disease Congestive heart failure History of cancer Obesity Immunosuppression or underlying condition

14 What further made this Interesting? *cluster differential deficient in BCell receptors Immunology consulted to evaluate for hypogammaglobulinem ia or other related immunodeficiency as a cause for his bacterial meningitis. He was found to have decreased immunoglobulins (G, A, M) on immune workup, suggesting a likely humoral immunodeficiency (circulating deficiency) as a possible setup to this unusual infection. B-CELL PHENO 3/20/17 CD45 LYMPH CT thou/mcl % CD3 (T CELLS) 95 H % % CD19 B CELLS 0 L % % CD16+CD56 NK % % CD4 (HELPER) 74 H % % CD8 SUPP'R % CD3 (T CELLS) cells/mcl CD19 (BCELLS)* 3 L cells/mcl CD16 + CD56 NK cells/mcl CD4 HELPER CELL cells/mcl CD8 SUPPRESSOR cells/mcl H/S RATIO 3.8 >=1.0 SURFACE MARKER T&B PANEL 3/20/17 CD3 (T3) 97 H % CD3 ABS /ul CD4 (T4) 75 H % T4 ABS 2791 H /ul CD8 (T8) % T8 ABS /ul CD4/CD8 RATIO 3.84 H RATIO CD19 (B4) LESS THAN 1 L % CD19 ABS LESS THAN 37 L /ul CD16/CD56 3 L 4-17 % CD16/CD56 ABS 102 L /ul

15 Treatment: Meningitis in general: Supportive care If seizure present, consider antiepileptic therapy Rehabilitation Antibiotics and Medications: -IV Vancomycin and Ceftriaxone at a meningitis dose (8 to 10 fold greater than in vitro) -Decadron (to decrease hearing loss associated with certain organisms with meningitis) -Rifampin (to increase antibiotic penetration) Our patient Patient was discharged with Ceftriaxone 2,000 mg IV every 24 hours for the next 3 weeks through a placed PICC line. He will also take IVIg 500 mg/kg to treat his immune deficiency

16 Meningitis Medications: DRUGS Neonates 0-7 DAYS 8-28 DAYS INFANTS AND CHILDREN Amikacin divided q12h 30 divided q8h divided q8h Ampicillin 150 divided q8h 200 divided q6h or q8h 300 divided q6h Cefotaxime divided q8h or q12h divided q6h or q8h divided q6h or q8h Ceftriaxone 100 divided q12h or q24h Ceftazidime divided q8h or q12h 150 divided q8h 150 divided q8h Gentamicin 5 divided q12h 7.5 divided q8h 7.5 divided q8h Meropenem 120 divided q8h Nafcillin 75 divided q8h or q12h divided q6h or q8h 200 divided q6h Penicillin G 150,000 divided q8h or q12h 200,000 divided q6h or q8h 300,000 divided q4h or q6h Rifampin divided q12h divided q12h or q24h Tobramycin 5 divided q12h 7.5 divided q8h 7.5 divided q8h Vancomycin divided q8h or q12h divided q6h or q8h 60 divided q6h

17 What was the final diagnosis? During his work-up he was found to have decreased immunoglobulin's (G, A, M) on immune workup, suggesting a likely humoral immunodeficiency as a possible setup to this unusual infection. This would make sense due to his reoccurring otitis media infections. Given his immunoglobulin findings he did subsequently receive IVIg as an inpatient and thus will need to start immunoglobin therapy thru Immunology going forward, they will work on getting his subcutaneous IG ordered etc.

18 What was the final diagnosis? Repeat T and B cell testing showed undetectably low CD19 B cells and low immunoglobulins Tests for antibody response to vaccines were all undetectable: Strep pneumo, diphtheria, tetanus

19 Bruton agammaglobulinemia (x-linked alpha gammaglobulinemia) GOKEY BTK BRUTON TYROSINE KINASE PROTEIN EXPRESSION FLOW CYTOMETRY BLOOD Btk protein is normally present intracellular in B cells and monocytes and detected by flow cytometry. CD19 B cells are close to absent in this male patient. The decreased Btk protein raises the possibility of a diagnosis of X-linked agammaglobulinemia (XLA) in this male patient but it has to be verified by gene sequencing since the flow data, which is dependent on antibody specificity, may not always provide an accurate diagnosis, unless completely absent. Recommend correlation with clinical and family history.

20 THANK YOU

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