Transcript ID cases - Pediatrics House Staff

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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.
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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 nonbloody, 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.
1) Pre B cell ALL diagnosed in December 2005cancer 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.
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.
5) Herpes simplex virus gingivostomatitis
6) Port-a-catheter in place since 2005
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6-mercaptopurine
Voriconazole
Inhaled Pentamidine monthly
ALLERGIES:
 Sulfa drugs
 Vancomycin-red man syndrome
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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.
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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.
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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
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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%, glucose47, protein-383 mg/dl
Gram stain-pending
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Gram positive bacteria-Streptococcus
pneumoniae, Staphylococcus aureus,
coagulase negative staphyloccus,
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Enterococcus sp, Listeria monocytogenes
Gram negative bacteria-Pseudomonas sp.,
Enterobacter sp., Klebsiella sp., Escherichia
coli
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Herpes simplex virus
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Cryptococcus neoformans
Toxoplasma gondii
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Gram stain-gram positive rods (many were
intra-cellular). Culture-Listeria sp
13 y/o with AML
CSF, Gram stain 1000X
Intracytoplasmic gram positive rods
Courtesy by Niaz
Banaei, MD Figure 1
13 y/o with AML
Broth culture, Gram stain 1000X
Gram positive rods
Courtesy by Niaz Banaei,
MD Figure 2
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Patient , at the time of consult , was
empirically started on broad coveragevancomycin, 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.
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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.
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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.
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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..
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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.
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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.
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Wt: 44.8Kg/ 70th percentile
T- 36.4; HR-100; RR-18; BP-110/64; O2 sat99%
Non-toxic appearing
Abdominal exam: Tenderness at right lower
quadrant. Positive obturator and psoas signs.
Remainder of the exam was normal
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CBC: WBC-19.1 (90%N, 5%L), Hemoglobin8.9, 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.
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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.
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Gynecology consultation to perform intraoperative 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.
1. Fitz-Hugh-Curtis and pelvic inflammatory
disease due to sexually transmitted agent
2. Abdominal/pelvic Mycobacterium disease
3. Peritonitis from ruptured appendicitis
4. Acute Yersinia sp. infection
5. Inflammatory bowel disease
6. Celiac disease
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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.
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Endometrial biopsy was eventually obtained
for microbiologic diagnosis.
Pathology- proliferative endometrium with
granulomatous inflammation and rare acidfast-bacilli
Microbiology- Cultures confirmed
Mycobacterium bovis. Susceptibility testing
showed sensitivity to INH, Rifampin and
Ethambutol and resistance to Pyrazinamide.
Pathology slide of the endometrial tissue biopsy
Proliferative phase endometrium with granulomatous inflammation, H&E
stain, at 600X (Courtesy of Lisa Pate, MD)
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)
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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.
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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.
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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.
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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.
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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)
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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.
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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.
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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.
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CSF studies normal. CT head-normal
INH/Rif/Pyr/Etm was started
Completed 9 months of treatment for
disseminated Mycobacterium tuberculosis
infection.
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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.
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Past Medical History:
◦ Seasonal allergic rhinosinusitis
◦ History of obstructive sleep apnea, status-post
tonsillectomy and adenoidectomy
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Medications:
◦ Fexofenadine
◦ Montelukast
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Allergies:
◦ NKDA
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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
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Physical Examination:
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Labs:
◦ T 100.4 F (38 C), pulse 104 bpm, BP 110/58 mm
Hg, R 20 breaths per minute
◦ Complete physical examination unremarkable
◦ Chemistries, liver function tests, and creatinine
normal
◦ White blood cell count 12,400/uL (range 4,50013,500/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
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Lyme disease (Borrelia burgdorferi)
2.
Leptospirosis (e.g. Leptospira interrogans)
3.
Epstein-Barr virus
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Colorado tick fever
5.
Tick-borne relapsing fever (e.g. Borrelia
hermsii)
6.
Rat-bite fever (e.g. Streptobacillus
moniliformis)
Peripheral blood, Giemsa stain, 1000x (Courtesy of Niaz Banaei, M.D.)
1.
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4.
Lyme disease (Borrelia
burgdorferi)
Leptospirosis (e.g.
Leptospira interrogans)
Tick-borne relapsing fever
(e.g. Borrelia hermsii)
Syphilis (Treponema
pallidum)
Peripheral blood, Giemsa stain, 1000x
(Courtesy of Niaz Banaei, M.D.)
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Clinical Course Prior to Diagnosis:
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Treatment/Follow-up:
◦ Admitted to Lucile Packard Children’s Hospital for
observation
◦ 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)
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25 documented cases per year
in the United States
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Spring/summertime
predominance
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Associated with sleeping in
rustic cabins
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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)
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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 elicited
3mm
Red Book Online Visual Library, 2009. Image 018_07.
Available at: ttp://aapredbook.aappublications.org/visual.
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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
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Giemsa- or Wright-stained thin and thick
peripheral blood smears
◦ Thicker than other spirochetes
◦ Higher avidity for routine stains
◦ Present in higher number
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Sensitivity ~70% during the febrile phase
 Higher sensitivity with acridine orange/fluorescence
microscopy
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Specific for relapsing fever
B. hermsii
Peripheral blood, Giemsa stain, 1000x (Courtesy of Niaz Banaei, M.D.)
L. interrogans
T. pallidum
Red Book Online Visual Library, 2009. Image 128_43. Available at:
http://aapredbook.aappublications.org/visual
.
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Serology
◦ cross reaction occurs with Borrelia burgdorferi,
Leptospira spp, and Treponema pallidum.
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Blood culture
◦ Barbour-Stoenner-Kelly medium
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Mouse inoculation
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Children > 8 years:
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Children < 8 years and pregnant women:
◦ Doxycycline x 5-10 days
◦ Penicillin or erythromycin can be used.
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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
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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.
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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
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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
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Studies:
White blood cell count 18,700/μL (normal 5,00010,000/μL)
– 81% neutrophils, 16% lymphocytes, 2% monocytes, and no
eosinophils.
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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
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CSF protein 49 mg/dL, CSF glucose of 39mg/dL.
CSF with abundant eosinophils
Permission obtained from Lezlee Pasche, M.D., Dept. of
Pathology, Stanford University
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Studies:
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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
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Coccidioides spp.
Baylisascaris procyonis
Mycobacterium tuberculosis
Angiostrongylus cantonensis
Balamuthia mandrillaris
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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
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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
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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
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Dimorphic fungus
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Two species
◦ Coccidioides immitis (CA, AZ)
◦ Coccidioides posadasii (AZ, TX, Mexico, S. America)
 Described in 2002
◦ No clinical difference between species
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Acute pneumonia
Chronic or progressive pneumonia
Pulmonary nodules/cavities
Extrapulmonary, non-meningeal disease
CNS disease
Cutaneous 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%)
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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
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Histopathology: not directly applicable
◦ identification in other body sites useful
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Fungal culture: rarely positive
◦ More likely positive with VP shunt in place
◦ Mycelial forms occasionally seen
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CSF serology
◦ Low sensitivity, high specificity
◦ High-titer IgG diagnostic (complement fixation)
 “spill-over” can cause low-titer positivity
◦ CSF IgG is followed
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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
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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
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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
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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
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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
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Well appearing
VSS w/ 38.7oC
1 cm L axillary node
No HSM
Otherwise nl
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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
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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