Fever in a Returning Traveler

Justin Zhang presented a case of a healthy young man presenting with fever after traveling in India for months.

When approaching fever in a returning traveler, there are a number of important considerations that can help guide workup including:

  • is this fever related to travel at all?
  • accompanying ROS (trying to determine if the disease process predominates in a certain organ system)
  • what is endemic in the areas they traveled?
  • what did they do that might put them at risk for certain infections?

Check out this NEJM review for recommendations on approaching fever in a returning traveler.

The patient’s workup was notable for hematologic and LFT abnormalities, which are fairly non-specific, but can be more suggestive of a viral or rickettsial infection. Serologies later returned positive for Dengue, and the patient’s labs and symptoms spontaneously improved with time.

The clinical manifestations of a Dengue infection can range from mild, self-limited febrile illness to hemorrhagic manifestations with shock.

Dengue Fever

  • Fever + 2 of the following: headache, retro-orbital pain, myalgia/arthralgia, rash, leukopenia, hemorrhagic manifestations* *Hemorrhagic manifestations: + Tourniquet test, petechiae/purpura, ecchymoses

Dengue Hemorrhagic Fever *characterized by increased vascular permeability

  • Fever, Thrombocytopenia (Plt <100K), hemorrhagic manifestations PLUS signs of vascular permeability (Hct increase of >20% from baseline, ascites, pleural effusions)

Dengue Shock Syndrome

  • Dengue Hemorrhagic Fever + Shock


As a physical exam pearl: the presence of petechiae and purpura can appear different on different skin tones. It can range from erythematous/violaceous to hyperpigmented lesions.

Anorectal bleeding, Anoscopy, & Anal Paps… Oh my!

Dr. Olivia Harden presented a case of a young cis-gender woman with a history of high-risk HPV + CIN1 s/p multiple colposcopies who presented to clinic with 1 week of painless bright red blood per rectum.

Anorectal bleeding

Anorectal bleeding is a common outpatient concern, and always requires evaluation to identify the etiology. Why? Because serious conditions like colorectal cancer or pre-cancerous polyps can lead to intermittent bleeding. In folks above the age of 50, the risk of colorectal cancer as the cause of rectal bleeding increases substantially and often necessitates evaluation with a colonoscopy. Nevertheless, all patients presenting with rectal bleeding necessitate an evaluation that includes an rectal exam +/- anoscopy (which we can quickly do as PCPs in the outpatient clinic)!


When thinking through the differential diagnosis for rectal bleeding, it is helpful to consider the anatomy of the rectum. Remember, there is a delineation called the “pectinate” or “dentate” line, above which the rectum is innervated by stretch nerve fibers and no pain sensory fibers. Below this line, the rectum is innervated by sensory nerve fibers and is one of the most exquisitely sensitive areas of the body. That’s why when your patient presents with any pathology, growth, infection, or fissure, etc below this line, they are usually quite uncomfortable!

We can use this anatomy to group certain conditions into “painful” and “Painless” etiologies of rectal bleeding (with some overlap, of course).

Another helpful framework involves dividing the differential among “structural,” “vascular,” and “Inflammatory” causes of rectal bleeding


Any patient who presents with new rectal bleeding necessitates, at the very least, a rectal exam +/- anoscopy. This may feel intimidating – never fear, Youtube to the rescue! Check out this fantastic video that reviews an approach to performing a rectal exam and anoscopy in clinic.

An anoscope is a tool that allows you to visualize the rectum. A couple of tips for using this tool during an exam:

  1. Positioning: lateral decubitus
  2. Use lots of lubricant
  3. Use anoscopes that have clear sides so you better visualize the walls of the rectum
  4. When inserting the anoscope, ask the patient to bear down

Anal Pap Smears

Given this patient’s history of high risk HPV, the decision was made to also perform an anal pap smear. Remember, you must perform an anal pap BEFORE anoscopy as lubricant can impact the results.

The guidelines for performing anal paps are in flux and ill-defined – universal screening for anal cancer is not recommended. Those who are at higher risk (anoreceptive sex, HIV+, immunocompromised, history of cervical/vulvar cancer, and some experts add CIN to this list) should undergo screening every ~2 years (though time frame varies).

Here are some best practices for performing an anal pap in clinic:

Till next time!


  1. UCSF Anal Neoplasia Clinic: https://analcancerinfo.ucsf.edu/obtaining-specimen-anal-cytology
  2. The ANCHOR Trial: https://www.nejm.org/doi/full/10.1056/NEJMoa2201048
  3. AAFP: Common Anorectal Conditions Part 1 https://www.aafp.org/pubs/afp/issues/2001/0615/p2391.html#afp20010615p2391-t3

VMR 9.9.22 Case of Complete Heart Block

Presenter: Dr. Alana Skovhus

Cardiology Discussants: Dr. Neal Yuan

EP: Dr. Adam Oesterle

CC: Dysuria

HPI: Young woman with history of HTN, mitral valve prolapse, presenting with urinary tract symptoms and CVA tenderness presents to the ED. Started on Ceftriaxone, and incidentally was found to be bradycardic with rates in 30s to 40s.

On further evaluation she had no history of syncopal episodes, no chest pain, no palpitations. In general she is very active and exercises frequently and also is a yoga instructor. She hikes frequently with her dog, though does not recall tick bites or rashes. Had COVID in May 2022.


Found to have complete heart block with junctional escape.

Learning Point #1: What is a “Junctional Escape”?

Notice how p waves are marching out independently of the QRS complexes. The distance or rate our our P waves is about 75bpm and sometimes are buried or hidden in the T waves. Our QRS complexes are marching out at a rate of 36 bpm, and not preceded by a p wave. This rhythm is a “junctional escape” meaning that the pacemaker of the heart is now derived from the junction—the heart’s automaticity has escaped from the sinus node because there is no longer a connection between our sinus node and AV node.

Therefore the intrinsic rhythm of the heart has switched to relying on the conduction system at the junction–> Junctional Escape!

Junctional rhythms can be very stable, over years! However, the progression to syncope (7-10%) is unpredictable, which is dangerous (i.e. with driving). This often drives decision to place a pacemaker even prior to becoming symptomatic. 

As the intrinsic pacer of the heart moves further down the conduction system you will see the QRS devolve into a ventricular QRS (wide) and slower instrinsic rate 20-30bpm. Remember that CO =HR xSV there may not be enough of a HR to ensure adequate cardiac output!

Learning Point #2: Think about ddx for bradycardia drivers intrinsic to the heart or extrinsic to the heart.


Our Patient
Age related generation of the conduction system#1 cause for PPM placementAge did not fit
Ischemia!Would have to be a large MI to knock out your AV nodeNo other clinical signs of ischemia and on exercise treadmill reached 14 METS (marathon runners get to 17 METS)–Would be a challenge with CAD to get to 14 METS.
CardiomyopathiesInfiltrative diseases (Sarcoid, Amyloid, Chagas)

For our patient, given her young age we were suspicious of Cardiac sarcoid which can present without pulmonary symptoms

Cardiac MR and PET-CT were NEGATIVE for infiltrative disease in our patient
RareCongenital diseaseOur team referred her for outpatient genetics evaluation given family history of early CAD and other structural disease. She also had history of MVP.


Our patient
Medications, Medications, Medications!Take a thorough med history: beta blockers, CCB, digoxin, cholinergic toxicity (donepezil)She was taking some supplements, but otherwise no driving medications
ElectrolytesHyperkalemia, hypermagnesiemiaNormal
Hypothemia, Hypoxia
Increased ICP
Normal, Normal Neuro examination
InfectionLyme disease
+History with hiking for lyme, however titer negative, ID was consulted as Lyme disease is a reversible cause of heart block after therapy. Sometimes these patients get a temporary pacer while they finish antibiotics, but nearly all resolve

Negative Blood cultures, no other Duke Criteria or risk factors for endocarditis
OtherHypothyroidism Normal TSH

Learning Point #3: Get your patient walking! (If safe)

When calling Cardiology consult for Bradycardia assess for “Chronotropic response”. Meaning–>when this patient has increased sympathetic tone (walking, bicycle action in bed) does their heart rate augment as it should? Some 2nd degree heart block can be also rate dependent (unlikely with complete heart block like in her case) and will determine whether our EP colleagues place a pacemaker.

Our patient: Treadmill Stress test: Reached 14 METS (marathon runners get to 17METS) and her junctional rhythm was able to augment to 91bpm, and atrial rate also increased, however she remained in complete heart block the entirety of the examination.

Cardiology placed PPM, and she was sent home with genetics referral.

Chain of reasoning:

Virtual Morning Report: Invasive Fungal Sinusitis

Brandon Yan (MS4) presented a case of an older man with a history of DLBCL currently undergoing chemotherapy who presented with vision loss, initially thought to be temporal arteritis, for which he was treated with high dose prednisone. He unfortunately developed worsening headaches and underwent repeat imaging revealing sinusitis with extension into the orbit and surrounding bone.

He was empirically started on antifungal therapy and underwent debridement with otolaryngology. Intraoperative pathology revealed Aspergillus. He required multiple debridements, retroorbital amphotericin injections and ongoing systemic antifungal therapy, but was able to leave the hospital after 4 weeks of monitoring and treatment.

Fungal Sinusitis: Spectrum of disease

*Presence of a pathogen does NOT equal infection, colonization is common*

  • Fungal ball​
  • Allergic fungal rhinosinusitis​
  • Invasive fungal sinusitis ​
  • Acute/fulminant disease: AspergillusMucoralesFusarium 
  • Chronic/subacute disease: dematiaceous molds (BipolarisCurvularia, and Alternaria)​

Invasive Fungal Sinusitis: Illness Script

  • Time course: acute (days), progressive ​
  • Risk Factors: Hematologic abnormalities, stem cell transplant, chemotherapy-induced neutropenia, advanced HIV disease, diabetes, glucocorticoids ​
  • Pathophysiology: inhalation of spores, angioinvasion > rapid spread​
  • Clinical syndrome: sinus symptoms (fever, facial pain, nasal congestion), neurologic symptoms (change in vision, diplopia, change in mentation, facial numbness)​
  • Workup: imaging (CT is better for bony erosion, MRI is better for soft tissue, intracranial involvement)​, histopathology showing fungal elements

Invasive Fungal Sinusitis: Treatment

  • High mortality (50-80%) due to angioinvasive disease warrants empiric therapy prior to confirmed diagnosis​
  • Medical Therapy: Empiric liposomal Amphotericin B (Ambisome)​
  • Surgical Therapy​ > Aggressive debridement
  • Management of medical comorbidities​ (glycemic control, withdrawal of immunosuppressive agents, treatment of underlying risk factors)


Dr. Sapphire Ear presented a great outpatient case at virtual ambulatory report on August 10th. The discussion focused on the differential diagnosis of testicular swelling, empiric treatment of epididymitis, and when to consider discontinuing a SGLT2-inhibitor.

The case presented was a 74 year old man with HFrEF (EF 40-45%), recurrent DVT/PE on lifelong anticoagulation, and BPH, with a recent E.coli UTI treated with TMP-SMX, who presented to urgent care with recurrent dysuria and new left-sided testicular swelling.

Differential Diagnosis for testicular swelling:

Testicular torsion: Acute onset testicular pain, often associated with high-riding testicle on affected side and absent cremasteric reflex. This is a surgical emergency!

Epididymitis / epididymo-orchitis: Infection of the epididymis that can cause inflammation of the testicle, causing testicular pain with posterior tenderness on exam.

Inguinal hernia: Can become painful if strangulated

Varicocele or hydrocele: Typically manifests as non-painful swelling.

This patient in this case was noted to have a positive UA, a normal cremasteric reflex and a scrotal ultrasound that revealed epididymo-orchitis, along with a large varicocele.

Lastly, we discussed whether to recommend this patient to continue or stop empagliflozin, which had been started a few months before his UTI and subsequent epididymitis. The group was evenly split on this question, since there is a sizable benefit of SLGTi for preventing hospitalization in HFrEF, but it is possible that his UTIs were related to the SLGT2i (theoretical mechanism of increased glucosuria). In the trials of SGLT2i, there was an increased risk of fungal balanitis and other fungal GU infections but not bacterial UTIs.

We also discussed that epididymitis in older men is often due to reflux into ejaculatory ducts secondary to bladder outlet obstruction from BPH. This patient also had his IVC surgically ligated 30 years ago due to recurrent DVTs, which had led to increased venous pressure in lower extremities and a large varicocele in his left testicle, which may also be risk factors for developing epididymitis.

Digging into a Cavitary Lesion – Virtual Morning Report – August 5, 2022

Dr. Daniel Boctor presented a fascinating case at virtual morning report on August 5th. The discussion highlighted many important themes including the differential diagnosis and management of hemoptysis, the differential diagnosis for a cavitary diagnosis, and *spoiler alert* the diagnosis of a Rasmussen Aneurysm.

65M w/ IDDM presenting with acute onset hemoptysis.
Chest X-Ray

Differential Diagnosis for Hemoptysis

There is a broad differential for hemoptysis, including but not limited to the following list:

  • Pseudo-hemoptysis
    • Upper Airway Bleeding
    • Upper GI Bleed
    • Serratia pneumonia
  • Primary Vascular
    • AV Malformation
    • Pulmonary Embolism
    • PA Rupture
  • Parenchymal Abnormality
    • Pneumonia
    • Tuberculosis
    • Lung Abscess
    • GPA
  • Tracheobronchial Abnormality
    • Bronchiectasis
    • Neoplasm
    • Bronchitis
    • Airway Trauma
  • Other
    • Coagulopathy

Remember, when managing hemoptysis, your first job is to triage.

  1. Triage: Is this massive hemoptysis (>150cc/24 hour or >100cc/1 hour)? Is there impaired gas exchange or hemodynamic instability attributable to hemoptysis?
  2. ABCs: Always start here! Does your patient require urgent intubation? (Remember, always position your patient with the “bad lung down” when concerned for massive hemoptysis to prevent blood pooling in the unaffected lung)
  3. IV Access and Resuscitation: make sure you have sufficient access, resuscitate appropriately, and correct any bleeding diathesis
  4. Imaging: Start CXR, then CT chest, then bronchoscopy if needed

This patient was found to have a cavitary lung lesion infiltrating the left pulmonary artery – the likely culprit for the bleed! So what cavitates?

Our spectacular ID consultant, Dr. Jen Babik, and Rheumatology consultant, Dr. Sarah Goglin discussed bacterial (nocardia, TB), fungal (yeast, endemic fungi, molds), and autoimmune (GPA) causes.

Dr. Boctor taught us about the final diagnosis in this case – a rare diagnosis called the Rasmussen Aneurysm. These aneurysms can cause massive hemoptysis, with mortality associated with pulmonary artery rupture. Whereas tuberculosis can often cause hemoptysis via bronchial artery hypertrophy and weak bronchopulmonary communications, a Rasmussen’s Aneurysm leads to the formation of granulation tissue in place of the tunica media and adventitia of the pulmonary artery, ultimately leading to pseudoaneurysm formation and rupture. These aneurysms will likely ultimately need embolization or coiling, in addition to long term treatment of active pulmonary tuberculosis with RIPE therapy.

Stay tuned for more fascinating cases from morning report across the three hospital sites: Zuckerberg San Francisco General Hospital, UCSF – Parnassus campus, and the San Francisco VA Medical Center.

VMR: 7.29.22 Image Negative Myelopathy

VA case presented by student doctor Joseph Replogle.

CC: ”My legs are not working”​

HPI: 72 yo man h/o Afib on AC, prior CAD, HFrEF, T2DM (c/b neuropathy), hypothyroidism, B12 deficiency (treated), recent COVID and prostate cancer presenting progressive with LE weakness and falls​.

This patient had progressive lower extremity weakness starting one month prior to presentation which gradually worsened. The patient’s initial examination demonstrated

CN II-XII intact, motor 5/5 strength in upper bilateral extremities, 4/5 strength in lower extremities, normal bulk, tone, no cogwheel rigidity, diminished sensation in lower extremities to upper shins to light touch, Babinski NEG bilaterally, 2+ in all reflexes, Intact coordination.

On second presentation, 3 weeks later was wheelchair bound:

CN II-XII intact, 3/5 LE strength, paresthesias up to trunk, proprioception of toes diminished, cold/temp intact. +Babinski bilaterally, hyperreflexia in LE

His exam with upper motor neuron features without Cranial Nerve involvement localizes to the spinal cord.

  • CBC: nl
  • BMP: normal, TSH normal​
  • ESR normal​
  • HbA1c 7​
  • HIV neg​
  • RPR, B12, homocysteine, vit E, zinc neg, copper 56 (slightly low)
  • LP: normal except protein 57 with oligoclonal bands
  • Imaging
  • MRI spine: moderate DDD without cord signal changes​
  • PET-CT: negative​
  • EMG: non-specific weakness without clear pattern

DX: Image Negative Myleopathy, cause remains undiagnosed

Teaching Pearls

Expert Discussant: Dr. Aaron Berkowitz

We discussed an approach to falls with the first branch point in our schema being related to 1) Neuroaxis or 2) Environment

Once entering the Neuro axis we turned to our trusty CP Solvers for a schema thinking about the different components of the Neuro axis. For this patient without LOC and falls and weakness

CSF Studies with Oligoclonal bands: Sign of immunoglobulin production in the CSF. It is important to compare serum immunoglobulin testing at the same time to ensure the process is isolated to the CSF. Classically oligoclonal bands are seen in MS, however others to consider include Lyme disease, Autoimmune processes, Brain Tumor.

Myelopathy with normal spinal MRI is not uncommon.​

​Given the wide differential, many clinical features help narrow the picture: speed of onset, pattern of progression, bladder/bowel dysfunction, age, family history, etc.​

​Reference: “Myelopathy but normal MRI: where next?”​https://pubmed.ncbi.nlm.nih.gov/18344379/​

​Post-COVID, MRI-negative myelopathies have been described but pathophysiology is unclear:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8186350/

Chain of reasoning for our case

SFGH inpatient/outpatient report: Cushing syndrome

Last week, Dr. Joanie Addington-White saw a woman in clinic with new profound weakness and edema, and directly admitted her for expedited workup of possible Cushing syndrome. We discussed this case both in RFPC preclinic conference and in inpatient morning report, where Dr. Rob Weber and Dr. Julia Wagner presented the patient’s course.

This patient surprisingly turned out to have extremely low cortisol levels. Both Dr. Addington-White and the inpatient team noted that she was using an herbal supplement from Mexico daily for arthritis pains (Artri Ajo King), which a Google search suggested may contain dexamethasone and methylprednisolone! A very important plug for asking patients about non-prescribed medications and supplements. (There may also be NSAIDs in this supplement, and the patient had also recently been diagnosed with a gastric ulcer!)

In clinic, we discussed the physical exam findings of Cushing syndrome, all of which were present in this patient to varying degrees.

  • Sudden-onset weight gain — this patient noted >20 pound weight gain in a few months.
  • Round “moon facies” with a plethoric appearance due to telangiectasias — Joanie had the patient pull up an old picture on her phone to compare to her current appearance (below).
  • Thin skin, striae and ecchymoses
  • A dorsocervical fat pad (formerly known as “buffalo hump” and supraclavicular fat pads
  • Hypertension
  • Muscle wasting causing weakness — the patient was newly using a wheelchair due to profound weakness
  • Hirsutism/acne

We also discussed the diagnostic approach to Cushing syndrome, both inpatient and outpatient.

  • First, diagnose a high cortisol state:
    • Late night cortisol: remember, cortisol has a diurnal secretion, and should be at its lowest late at night. (Save your AM cortisol tests for AI testing!) If you are in the hospital, you can draw a late night serum cortisol, but as an outpatient, it is easier for patients to collect a salivary sample and bring it to the lab the next day. Check in with the lab about best practices around collection, but you can be assured that cortisol is stable in saliva for several days.
    • 24-hour urine cortisol: very reliable and feasible to do from clinic. Patients need close counseling on how to complete a 24-hour urine collection correctly — their first void on day 1 should not be collected.
    • Low-dose dexamethasone suppression test: this testing modality makes use of the fact that labs are usually open at 8AM! You have your patient take 1mg dexamethasone between 11PM and midnight and go to the lab to get a serum cortisol at 8AM. If cortisol is high, you have your diagnosis. No need to do this in the hospital if you can measure cortisol in another way, like a late night cortisol or 24hr urine cortisol. A note: this may be less accurate in obese patients.
  • If your cortisol is high, then find the source of the elevation.
    • Plasma ACTH: Your go to next test! This will be suppressed if the extra cortisol is coming from the adrenals (or exogenously!) If ACTH is high, it suggests a pituitary or ectopic source.
      • High-dose dexamethasone suppression test: If ACTH is high, a high-dose dexamethasone suppression test can suggest the source. A pituitary source should be suppressed, but an ectopic source may not.
      • If ACTH is high, you can also get imaging (MRI, CT) to try to determine its source.

And of course, all that said, don’t be fooled by a low cortisol if you suspect Cushing! Make sure to do a thorough review for exogenous steroid exposure, as the team did in this case.


SFGH Morning Report – RA and HLH

On Tuesday, rheumatology fellow and former UCSF IM resident Dr. Nathan Karp presented a case of a woman with a history of RA who presented with 3 weeks of constitutional symptoms and was found to have HLH from a possible hematologic malignancy.

Rheumatoid Arthritis Pearls

  • Important features that can help frame the severity of a patient’s rheumatoid arthritis include:
    • Serologies: RA and CCP. Patient with positive CCP are more likely to have erosive disease.
    • Any extraarticular symptoms?
    • Joint involvement: rheumatologists often quantify disease activity with a scale, the CDAI.
    • Medication regimen
  • Ask about tobacco use, since that can portend worse prognosis in RA!

Very High Ferritin

This patient’s ferritin was 26,000! While high ferritin can be nonspecific (remember it is an acute phase reactant!), there is a more limited differential for extremely high ferritin, like >1-2,000. This includes:

  • HLH
  • Hemachromatosis
  • Adult-Onset Still’s disease
  • Hematologic malignancy

HLH Pearls

  • HLH, or hemophagocytic lymphohistiocytosis, is a rare syndrome of macrophage overactivation. You will see cytopenias from hemophagocytosis (consumption of hematopoetic cells by macrophages), as well as other symptoms and lab abnormalities related to immune system overactivation and cytokine storm. In this case, the bone marrow biopsy (below) clearly showed a macrophage consuming a erythrocyte! Pretty cool!
  • If you would like to review the diagnostic criteria for HLH, click here.
  • We don’t usually think of RA as a predisposing factor for HLH, but it can predispose patients to lymphoproliferative disorders or other malignancies, which can trigger HLH. It also may predispose patients to infections, which could also be a trigger. In this case, the patient is undergoing workup for a possible hematologic malignancy.
Patient’s bone marrow biopsy. See the macrophage eating the RBC in the middle of the screen? That’s hemophagocytosis!!


  1. HLH Review: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4062561/
  2. RA and Malignancy: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5696277/#:~:text=Malignancy%20is%20a%20major%20comorbidity,and%20breast%20cancer%20is%20lower.

Middle age man with a lung mass

Today Dr. Sherry Chao presented an amazing case in intern report of a middle-aged man with no past medical history that presented with subacute worsening dyspnea on exertion and fatigue who was found to have a new large mass that crossed tissue planes.

The discussion was amazing and her we highlight some key teaching points.

Red arrow points to the mass, the image on the left is located at the level of the lungs while the image on the right is located in the abdominal region.

Approach to Lung Mass: The approach to many pulmonary complaints including masses, nodules and cavitation is the same and includes three main buckets. Malignancy: Adenocarcionoma, Small cell, Squamous cell. Lymphomas. Mesothelioma should be considered in this case given how close the mass looks to the pleura and biggest risk factor of asbestos exposure should be explored. As a side note asbestos related pulmonary disease ranges from pleural calcifications, pleural mass and mesothelioma. Infection: mycobacteria, endemic fungi, nocardia, and actinomyces, crypto, bacterial empyema, and mucor in very immunocompromised patients. Autoimmune: GPA and igG4 related diseases.

Mass that is crossing tissue planes: The crossing of tissue planes in this case allows for narrowing of differential diagnosis particularly within the infectious disease bucket. It is unusual for most bacterial infections to cross planes and this finding should increase concerns for TB, mucor, fusobacterium and actinomyces. We can also consider the endemic fungi such as blastomycosis (blasts through tissues).

Biopsy lung mass location: In general, if mass is in the periphery consult IR but if it is more centrally located close to airways consult pulm.

Core biopsy of right middle thorax mass. Shows sheets of histiocytes and sulfur granules with associated neutrophilic inflammation.

Sulfur Granules in Path: These are granules composed of bacteria, calcium and pus which give a yellow color that looks like sulfur granules, there is no actual sulfur in the slide. The path also shows a eosinophilic ring called the splendore-hoeppli. This is a classic finding seen in actinomyces.

Actinomyces: Most often missed diagnosis that can affect immunocompetent hosts. RF: poor dentition and IUDs. It usually looks like a mass and it is a great mimic for cancer. Lives in GI tract and lungs and can present with massess in these organ systems. I can also colonize IUDs. Actinomyces often presents as a growing mass and the treatment of choice is IV PCN.