ID cases

Case 1

13 year old male with history of pre B cell ALL, currently in relapse and on chemotherapy, admitted with acute onset fever, vomiting and headache.

5 days prior to admission, he had a scheduled neurosurgical procedure of removal of a nonfunctioning VP shunt that was in place for congenital hydrocephalus.

Patient identification

• Patient presented to the ER with a history of fever to 102.9F that began about 4 hours prior to arrival, associated with 6-7 episodes of non-bloody, non-bilious emesis. He also complained of headache and neck pain.

• A CBC done in the ER showed neutropenia and thrombocytopenia. He was given a dose of vancomycin and ceftazidime.

• Although meningitis was suspected, an LP was deferred due to the recent neurosurgical procedure and thrombocytopenia.

• Patient was admitted to the oncology floor for further management.

Brief history

1) Pre B cell ALL diagnosed in December 2005- cancer was in remission after chemotherapy

2) Bone marrow relapse diagnosed in September 2008- started on chemotherapy. Most recent BM biopsy showed persistence of blasts. Chemotherapy was continued to attain remission in preparation for HSCT.

3) History of E. coli sepsis following induction chemotherapy in September 2008. An evaluation at that time showed pulmonary nodules. Due to neutropenic state, he was started on empiric antifungal therapy with voriconazole for suspicion of fungal etiology for the nodules.

Past medical history

4) Congenital hydrocephalus-VP shunt placement at 6 months of age. Most recent evaluation showed a disconnection in the shunt with stable ventricle size. Since the presence of the shunt was a concern for infection following the planned HSCT, shunt was removed 5 days prior to admission. Shunt removal was complicated by adherence to the subdural area that caused a small portion to be broken off. The shunt removal from ventricle also was difficult. However, post op, patient did well and was discharged 3 days prior to admission.

Past medical history (Continued)

5) Herpes simplex virus gingivostomatitis6) Port-a-catheter in place since 2005

Past medical history (Continued)

6-mercaptopurine Voriconazole Inhaled Pentamidine monthly

ALLERGIES: Sulfa drugs Vancomycin-red man syndrome

Medications

Patient had persistent fevers of greater than 400C. Around 12 hours into admission, patient had a generalized tonic clonic seizure. The ID team was consulted for possible herpes simplex virus meningoencephalitis.

Hospital course

No history of illness in other family members. Pet dog at home. No history of travel. No history of consumption of unpasteurized dairy or undercooked meats.

Immunizations are up to date. Father unsure of PPD placement.

Epidemiological history

• T-40.80C, HR-160, Saturation-97% in RA• Mildly responsive to touch, obtunded. No

obvious respiratory distress.• Cracked lips; no obvious oral lesions;

surgical scalp wounds are well healed.• Port-a-catheter in place; heart and lung

exam normal• Abdomen soft with no hepatosplenomegaly• Skin-No rashes, no petechiae or purpura

Physical exam (immediately following seizure episode)

• WBC-500 cells/mm3, Hemoglobin-9.1 g/dl, Platelets-25,000 cells/mm3

• Na-124, K-4.3, Cl-87, CO2-25 mmol/L, BUN-8, Cr-0.8 mg/dl

• Urinalysis-normal• Chest radiograph-normal• CT head-Stable intra-ventricular hemorrhage

(noted immediately post op). No infarction.• LP done one day into admission-CSF WBC-27, RBC-

6625 cells/mm3, N-36%, L-58%, glucose-47, protein-383 mg/dl

Gram stain-pending

Laboratory and Imaging

• Gram positive bacteria-Streptococcus pneumoniae, Staphylococcus aureus, coagulase negative staphyloccus, Enterococcus sp, Listeria monocytogenes

• Gram negative bacteria-Pseudomonas sp., Enterobacter sp., Klebsiella sp., Escherichia coli

• Herpes simplex virus• Cryptococcus neoformans• Toxoplasma gondii

Differential diagnosis

Gram stain-gram positive rods (many were intra-cellular). Culture-Listeria sp

Diagnosis

13 y/o with AMLCSF, Gram stain 1000XIntracytoplasmic gram positive rods

Courtesy by Niaz Banaei, MD Figure 1

13 y/o with AMLBroth culture, Gram stain 1000XGram positive rods

Courtesy by Niaz Banaei, MD Figure 2

Patient , at the time of consult , was empirically started on broad coverage-vancomycin, meropenem, acyclovir, voriconazole.

Patient had persistent uncontrolled seizures. Developed cardio-respiratory compromise.

Patient noted to have anisocoria. He had a burr hole in an attempt to decompress.

Eventually support was withdrawn.

Follow up

• Listeriosis is caused by infection by Listeria monocytogenes, a motile, nonsporulating, facultative anaerobic gram positive bacillus. Out of the 6 species of Listeria, L. monocytogenes is the only human pathogen. Infection most often begins after ingestion of the organism in a foodborne source.

• L. monocytogenes can grow in high salt and cold environments, particularly suiting it to survive and grow in processed and refrigerated foods.

• Although bacteremia is a common presentation of listeria infection, the bacterium has tropism for the central nervous system, resulting in meningoencephalitis or cerebritis.

Discussion

• The overall disease prevalence in the US is 0.7 in 100,000, however in infants is 10 in 100,000 and elderly 1.4 in 100,000.

• Patients with abnormalities of T-cell mediated immunity are at particular risk. Hence, listeriosis is an important opportunistic infection in individuals on chronic steroid treatment, hematological malignancy, solid organ transplant and bone marrow transplant recipients, neonates, pregnant women and patients with AIDS.

• The prognosis for cancer patients with listeria bacteremia seems to be better than that for patients with meningoencephalitis.

Discussion (continued)

• Listeria is the fourth most common cause of bacterial meningitis after S. pneumoniae, N. meningitidis and Group B streptococcus. It is one of the 3 major causes of neonatal meningitis and is the most common cause of bacterial meningitis in patients with lymphoma, patients with organ transplants, or those receiving corticosteroid immunosuppressive therapy.

• Trimethoprim-Sulfamethoxazole used primarily for Pneumocystis prophylaxis is also protective against Listeria. However, breakthrough infections are known to occur.

• The preferred agent for treatment of Listeria infection is Ampicillin with Gentamicin added for synergy. Other agents such as Vancomycin and Carbapenems have in vitro activity against Listeria sp..

Discussion (continued)

Case 2

11 yo F presented to the ER with a 2 day history of abdominal pain and vomiting

Pain began at left lower quadrant and progressed to become generalized.

History of nausea and over 20 episodes of nonbloody, nonbilious emesis.

Denies diarrhea, fever, or urinary symptoms.

No medications given at home except Chamomile tea for upset stomach.

HPI

PMH: Previously well. No history of surgeries.

Menarche 1 year back. Last menstrual period was 1 month back.

Meds: None; Allergies: None SH: Immigrated to the US 2 years back from

Mexico. No history of animal exposure. Denies sexual activity.

PMH/Meds/SH

Wt: 44.8Kg/ 70th percentile T- 36.4; HR-100; RR-18; BP-110/64; O2 sat-

99% Non-toxic appearing Abdominal exam: Tenderness at right lower

quadrant. Positive obturator and psoas signs.

Remainder of the exam was normal

Physical Examination

CBC: WBC-19.1 (90%N, 5%L), Hemoglobin-8.9, Platelets-340

Electrolytes-Normal; Liver enzymes-Normal Urinalysis: Sp gr >1.070, 1+ protein,

negative LE and nitrites, 0-2 WBC CT abdomen: Enlarged appendix with

hyperemic mucosa with surrounding periappendiceal inflammatory stranding consistent with acute appendicitis. A calcified mesenteric lymph node was also noted. No lymphedenopathy.

Laboratories/Imaging

Patient taken to OR for laparoscopic appendectomy

Intra-operative findings: acute appendicitis PLUS bilaterally enlarged fallopian tubes left greater than right, chronic adhesions from the omentum to the anterior abdominal wall, adhesions from the anterior surface of the liver to the anterior abdominal wall and some yellow plaques on the liver surface.

Clinical course

Gynecology consultation to perform intra-operative examination.

Findings and management: dilated, hyperemic appearance of the fallopian tubes, with the fluid within the tubes appearing to be less purulent than would be the appearance of a typical pyosalpinx. A pelvic examination revealed copious yellow vaginal discharge, a nulliparous cervix, and fimbriated hymen with no evidence of trauma. Cervical specimens were sent for Gonorrhea and Chlamydia nucleic acid amplification tests (NAAT) and cultures.

Clinical course

1. Fitz-Hugh-Curtis and pelvic inflammatory disease due to sexually transmitted agent

2. Abdominal/pelvic Mycobacterium disease

3. Peritonitis from ruptured appendicitis4. Acute Yersinia sp. infection5. Inflammatory bowel disease6. Celiac disease

Differential Diagnoses

PPD placed and positive at >25mm at 40 hours.

Quantiferon-Gold positive. Gonorrhea and Chlamydia NAAT negative. Chest x-ray negative for active or past

evidence of tuberculosis. On review of history again, family has a

history of consumption of unpasteurized cheese.

Diagnosis

Endometrial biopsy was eventually obtained for microbiologic diagnosis.

Pathology- proliferative endometrium with granulomatous inflammation and rare acid-fast-bacilli

Microbiology- Cultures confirmed Mycobacterium bovis. Susceptibility testing showed sensitivity to INH, Rifampin and Ethambutol and resistance to Pyrazinamide.

Diagnosis

Proliferative phase endometrium with granulomatous inflammation, H&E stain, at 600X (Courtesy of Lisa Pate, MD)

Pathology slide of the endometrial tissue biopsy

Pathology slide of the endometrial tissue biopsy

Proliferative phase endometrium with rare acid-fast bacilli (arrow), AFB stain, at 1000X (Courtesy of Lisa Pate, MD)

Treated with INH and Rifampin for 1 year. +Ethambutol for first 2 months

Patient did very well throughout therapy. Follow up laparoscopy after 2 months of end

of therapy showed normal fallopian tubes and ovaries with minimal adhesions of cul-de-sac and a few plaques on the liver.

Treatment and follow up

One of the species of the Mycobacterium tuberculosis complex

Tuberculosis due to M. bovis is a zoonosis M. bovis primarily infects cattle and the

pathogen is transmitted to humans by consumption of unpasteurized dairy products.

Mycobacterium bovis

Rare in developed countries due to pasteurization of dairy and testing and culling of infected cattle.

Higher burden in developing world but due to inadequate resources for diagnosis, number of affected humans is unknown.

Accurate diagnosis is important for appropriate choice of anti-tuberculosis medications and length of therapy since M. bovis is intrinsically resistant to pyrazinamide.

Mycobacterium bovis- Epidemiology

Manifests as primary infection and reactivation.

Can cause pulmonary, extrapulmonary and disseminated disease.

Extrapulmonary infection (Gastrointestinal tract, peritoneum, genito-urinary tract) is more common as the infection is usually acquired by ingestion of the bacilli.

Mycobacterium bovis - Clinical aspects

Direct microscopy to visualize granulomatous inflammation and acid-fast bacilli

Isolation in cultures which can take 3-6 weeks and identification of species of the Mycobacterium tuberculosis complex by PCR.

M. bovis is intrinsically resistant to Pyrazinamide.

Therapy for M. bovis is usually longer since pyrazinamide cannot be used (9-12 month regimen)

Mycobacterium bovis- Diagnosis and Treatment

Case 3

GR is a 11 month IM with h/o ‘noisy breathing’ worse when lying supine and difficulty feeding for 3-4 months.

3-4 days PTA had worsening stridor. CXR showed possible mass at trachea. Exposure history significant for visit to India

at 3 months of age and a grandmother with chronic cough.

HPI

Underwent laryngoscopy, bronchoscopy and esophagoscopy.

Failed extubation following procedure and remained intubated for about 10 days.

Underwent Chest/Abdomen CT scan that showed multiple hilar and mediastinal LNs and hypodense lesions in spleen.

HPI cont’d

Differentials included oncological process (such as lymphoma/neuroblastoma) and infectious process.

ID team consulted. PPD placed as TB was high on the differential

PPD positive at 15mm Patient underwent hilar LN biopsy and

cultures grew Mycobacterium tuberculosis.

Hospital course

Culture and sensitivity

CSF studies normal. CT head-normal INH/Rif/Pyr/Etm was started Completed 9 months of treatment for

disseminated Mycobacterium tuberculosis infection.

Management

Case 4

History of Present Illness An 8 year-old girl developed fever ten days

after family camping trip◦ Five days of fever to 102-104 ◦ Diffuse headache, nausea, and two episodes of

non-bloody, non-bilious emesis◦ History of three small “insect bites” on

abdomen, which quickly resolved◦ No photophobia, phonophobia, or neck stiffness◦ No sore throat, cough, conjunctivitis, diarrhea,

arthralgias, or myalgias ◦ Fevers resolved on the fifth day of illness◦ Afebrile for 5 days◦ Recurrent fever prompted outpatient

evaluation.

Past Medical History:◦ Seasonal allergic rhinosinusitis◦ History of obstructive sleep apnea, status-post

tonsillectomy and adenoidectomy

Medications:◦ Fexofenadine◦ Montelukast

Allergies:◦NKDA

Social History: ◦ Lives in Menlo Park, CA

Parents and a healthy 6 year-old brother No pets

◦ Recently returned from a trip to national parks throughout southern Utah and Northern Arizona Stayed in hotels with the exception of an “upscale”

lodge at Bryce Canyon National Park Did not recall any indoor or outdoor animal

exposures

◦ No sick contacts

Physical Examination: ◦ T 100.4 F (38 C), pulse 104 bpm, BP 110/58 mm

Hg, R 20 breaths per minute◦ Complete physical examination unremarkable

Labs:◦ Chemistries, liver function tests, and creatinine

normal ◦ White blood cell count 12,400/uL (range 4,500-

13,500/uL) 67% neutrophils (>20% bands), 12% lymphocytes, and

20% monocytes. ◦ Hemoglobin was 11.7g/dL (11.5-15.5g/dL)◦ Platelets were normal◦ Erythrocyte sedimentation rate was 90 mm/hr

(range 0-10mm/hr)◦ C-reactive protein was 6.9 mg/dL (range 0-0.9

mg/dL)◦ Heterophile antibody positive

Differential Diagnosis?

1. Lyme disease (Borrelia burgdorferi)

2. Leptospirosis (e.g. Leptospira interrogans)

3. Epstein-Barr virus

4. Colorado tick fever

5. Tick-borne relapsing fever (e.g. Borrelia hermsii)

6. Rat-bite fever (e.g. Streptobacillus moniliformis)

Incidentally noted…

Peripheral blood, Giemsa stain, 1000x (Courtesy of Niaz Banaei, M.D.)

Differential Diagnosis?1. Lyme disease (Borrelia

burgdorferi)

2. Leptospirosis (e.g. Leptospira interrogans)

3. Tick-borne relapsing fever (e.g. Borrelia hermsii)

4. Syphilis (Treponema pallidum)

Peripheral blood, Giemsa stain, 1000x (Courtesy of Niaz Banaei, M.D.)

Clinical Course Prior to Diagnosis: ◦ Admitted to Lucile Packard Children’s Hospital for

observation

Treatment/Follow-up:◦ A presumptive diagnosis of TBRF was made◦ After first dose of doxycycline

T 39.5 deg C, pulse 156 bpm, SBP 90 mmHg Emesis, rigors, and myalgias

◦ Received acetaminophen and a 20ml/kg normal saline bolus, with subsequent resolution of symptoms and normalization of vital signs

◦ Discharged home, completed a 10 day course of doxycycline without complications

◦ Borrelia hermsii serologies subsequently became available: IgM 1:64 (range <1:16) IgG 1:64 (range <1:64)

Epidemiology 25 documented cases per

year in the United States

Spring/summertime predominance

Associated with sleeping in rustic cabins

Clusters of cases of B. hermsii described at the north rim of the Grand Canyon, Big Bear Lake in southern California, and Lake Tahoe near the California-Nevada border. Centers for Disease Control and Prevention: National Center for Zoonotic,

Vector-borne and Enteric Diseases (NCZVED) Division of Vector-Borne Infectious Diseases (DVBID)

Epidemiology United States - tick-borne relapsing

fever is caused by:◦ Borrelia hermsii (mountainous

western states)◦ B. turicatae (Texas) ◦ B. parkeri

Rodents are natural hosts

Transmitted by the soft-bodied tick Ornithodoros (e.g. O. hermsii)

Nocturnal feeder Drawn to exhaled breath Painless bite Remains attached for 5-30

minutes.

History of tick bite is often not elicitedRed Book Online Visual Library, 2009. Image 018_07. Available at: ttp://aapredbook.aappublications.org/visual.

3mm

Clinical Manifestations Fever, headache, myalgias, arthralgias,

nausea Hepatomegaly (17%), splenomegaly

(41%), and rash (28%) Initial febrile episode lasts 2-7 days Afebrile period lasts days to weeks During initial febrile episode, organisms

can exceed 100,000/mm3

Alteration of surface proteins allows escape from recognition by antibodies, causing recurrent spirochetemia

Febrile episodes shorter, less frequent over time

Diagnosis Giemsa- or Wright-stained thin and

thick peripheral blood smears◦Thicker than other spirochetes◦Higher avidity for routine stains◦Present in higher number

Sensitivity ~70% during the febrile phase

Higher sensitivity with acridine orange/fluorescence microscopy

Specific for relapsing fever

Red Book Online Visual Library, 2009. Image 128_43. Available at:

http://aapredbook.aappublications.org/visual.

Peripheral blood, Giemsa stain, 1000x (Courtesy of Niaz Banaei, M.D.)

T. pallidum L. interrogans

B. hermsii

Diagnosis Serology

◦ cross reaction occurs with Borrelia burgdorferi, Leptospira spp, and Treponema pallidum.

Blood culture◦ Barbour-Stoenner-Kelly medium

Mouse inoculation

Treatment Children > 8 years:

◦ Doxycycline x 5-10 days Children < 8 years and pregnant women:

◦ Penicillin or erythromycin can be used. Therapy can cause Jarisch-Herxheimer

reaction:◦ Close monitoring, especially during the first 4

hours◦ Acute febrile response, headache, myalgia◦ Occasional hypotension◦ Resolves in hours with supportive care

Case 5

History of Present Illness 5 y/o boy from northern California

presented with a 6 weeks of fevers and a 3 week history of progressive frontal headache waking him from sleep and emesis following a 5-day flulike illness. Developed diplopia and decreased hearing from left ear, then brought to ER for acute slurring of speech.

• PMHx: born at term via vaginal delivery• SHx: two pet dogs. No other pets or

contact with other animals. No pica. Yearly travel to Phoenix, AZ for 7 days – returned 2 months prior to current illness. No exposure to known or suspected tuberculosis. No dietary risk factors.

• Meds: had received amoxicillin/clavulanate (two courses), azithromycin, cefdinir over 6 weeks preceding admission

Physical Examination:◦ T 38.6 deg C, P 82, BP 104/56, R 22, SpO2 97% on

room air◦ Alert, awake, interactive. No alterations in

mentation.◦ Neuro: L-sided esotropia; decreased hearing L ear

by finger rub. No other focal deficits.◦ Remainder of exam normal

• Studies:• White blood cell count 18,700/μL (normal 5,000-

10,000/μL) – 81% neutrophils, 16% lymphocytes, 2% monocytes, and no

eosinophils. • The hemoglobin and platelet counts normal• C-reactive protein was 19.4mg/dL (normal <0.2mg/dL).• Sodium 129mmol/L (normal 135-145mmol/L); other

routine chemistries were unremarkable. • Liver function tests normal. • CSF white blood cell count was 195 cells/μL (normal

<10/ μL ) – 1% neutrophils, 61% lymphocytes, 12% monocytes, and 26%

eosinophils• CSF protein 49 mg/dL, CSF glucose of 39mg/dL.

CSF with abundant eosinophilsPermission obtained from Lezlee Pasche, M.D., Dept. of Pathology, Stanford University

Studies:◦ PPD neg◦ Gastric aspirates neg for AFB x3◦ Blood cultures and CSF bacterial cultures negative◦ HIV ELISA negative

Imaging:◦ Chest film: left lower lobe nodule with hilar

adenopathy◦ Brain MRI: left-sided subependymal leukomalacia

Left lower lobe pulmonary nodule with L hilar prominence

Differential Diagnosis Coccidioides spp. Baylisascaris procyonis Mycobacterium tuberculosis Angiostrongylus cantonensis Balamuthia mandrillaris

Diagnosis Serum Coccidioides immunodiffusion (IgM)

positive Serum Coccidioides quantitative

immunodiffusion (IgG) 1:16 (nl negative) CSF Coccidioides quantitative

immunodiffusion positive 1:1 (nl negative) Fungal cultures from CSF were negative

Follow-up Had been started on fluconazole 12mg/kg

empirically, which was continued. Had been started on dexamethasone, which

was continued Completed a course of albendazole Had complete resolution of neurologic

deficits and was discharged home

Follow Up

Re-admitted one week later with L-sided weakness and aphasia

Despite aggressive antifungal therapy, eventually became quadraparatic

Later, developed hydrocephalus

Diffusion-restricted lesions in bilateral basal ganglia (not seen – lesions in bilateral frontal lobes), consistent with vasculitic infarctions

Coccidioidomycosis Dimorphic fungus

Two species◦ Coccidioides immitis (CA, AZ)

◦ Coccidioides posadasii (AZ, TX, Mexico, S. America) Described in 2002

◦ No clinical difference between species

Clinical Manifestations Acute pneumonia Chronic or progressive pneumonia Pulmonary nodules/cavities Extrapulmonary, non-meningeal disease CNS disease Cutaneous disease

CNS Disease◦ Found in 50% of patients with dissemination◦ Occurs weeks to months after initial infection◦ Symptoms: fever variable; HA, altered mental

status, personality changes, nausea, vomiting, neurologic deficits

◦ Signs: meningismus (50%), gait abnormalities, focal neuro findings

◦ Hydrocephalus can occur early or late (30-50%)◦ Vascultic infarcts can occur early or late (15-20%)

CNS Disease Diagnosis:

◦ Cerebrospinal fluid wbcs low double-digits to >10000

Lymphocytic predominance most common Neutrophil predominance can occur Eosinophils uncommon, but highly suggestive

Protein usually >150mg

Glucose usually low

CNS Disease

Histopathology: not directly applicable◦ identification in other body sites useful

Fungal culture: rarely positive◦ More likely positive with VP shunt in place◦ Mycelial forms occasionally seen

CSF serology◦ Low sensitivity, high specificity◦ High-titer IgG diagnostic (complement fixation)

“spill-over” can cause low-titer positivity◦ CSF IgG is followed

CNS Disease

Therapy:◦ Winn, 1946: intrathecal amphotericin-B deoxycholate◦ Einstein, 1961: IT ampho-B became gold standard

Direct cisternal injection, via Ommaya, or lumbar injection Therapy 2-8 years Complications common (bacterial infection, arachnoiditis – back

pain, paraplegia, quadriplegia, urinary retention, sexual dysfxn)

◦ Classen, 1988: fluconazole for meningitis described◦ Galgiani, 1993: fluconazole new gold standard (400mg)

Higher-dose fluconazole now preferred Therapy is lifelong

◦ Case reports for voriconazole, caspofungin, posaconazole

CNS Disease Long-term management

◦Periodic LPs to follow IgG◦Monitoring for hydrocephalus, shunt if

needed◦Monitor for drug toxicity

Prognosis◦Mortality 100% prior to antifungals◦Mortality ~30% with intrathecal ampho-B◦Mortality ~30% with fluconazole

CNS vasculitis◦ No consensus on management

Case 6

Case 6 6yo female in USOGH until 17 PTA when she

developed Sx of N/V x 24 hours and fever (103oF) which were persistent, nightly and associated w/ chills and sweats. She had fatigue/wt. loss (~6 lbs.) and decreased appetite

Sibling w/ GAS-pt. placed on amox. w/o improvement

See on multiple occasions

Outpatient Work-up

WBC 9600; 45 segs 15 bands ESR 60 then 77 GSP including LFTs nl CXR nl SXR nl U/A and Cx: NG PPD: neg Bone scan: uptake in R mandible AUS: multiple small lesions throughout the

liver and spleen

Exposure History Lives on a farm in Half Moon Bay 2 yr. old cat, several dogs, chickens, rabbits,

horses. Farm worker recently PPD converter H/O tick bites

Physical Exam Well appearing VSS w/ 38.7oC 1 cm L axillary node No HSM Otherwise nl

Lab. Studies WBC 8300; 59S 28L AST 26: ALT 18 CXR: Interstitial infiltrate R lung: viral

pneumonia ACT: Multiple tiny low attenuation foci in

parenchyma of liver and spleen: DDX: fungal vs. bacterial abscess vs. lymphoproliferative dis.

Echo. Nl PPD: neg

Hospital Course Naficillin, gentamycin, flagyl initiated Pt. febrile for first 5 days By day 5 she became asymptomatic and

was eating well D/C to home on antibiotics Repeat ACT at day 10 showed foci smaller

in size Cat scratch serology: 1:512 PT changed to po rifampin and completed

3 week course AUS after 2 months nl