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SAEM Clinical Images Series: Green Foot

The patient is a 59-year-old male with a history of prior DVT, atrial fibrillation, HTN, alcohol use and COPD who presents to the Emergency Department with chest pain, dyspnea, and left lower extremity swelling and pain. He had a prior hospital admission two weeks ago for leg swelling and cellulitis. He was previously prescribed oral gentamicin and topical mupirocin for concerns of foot infection, which he has been compliant with taking. He has been working long hours as a construction worker, but knows of no chemical exposure to his feet and denies walking barefoot. He has had no fever and denies any other complaints at this time.

 

Vitals: BP 151/69; HR 93; R 18; T 97.7°F; O2 sat 95% room air.

General: No acute distress.

Respiratory: Mild wheezes bilaterally.

Extremities: Mild bilateral lower extremity swelling, worse on left compared to right. Left foot discolored as shown in the image – when asked, the patient states the discoloration started initially on the great toenail and progressed to the sole of the foot.

CBC: WBC: 10.2; Hgb: 12.7

Na: 130

ESR: 6

CRP: 0.8

CXR: Mild pulmonary edema.

Foot X-ray: No acute findings, old Lisfranc injury.

Ultrasound: Negative for DVT.

The patient has Green Foot Syndrome.

Pseudomonas aeruginosa

Green foot syndrome is a rarely diagnosed Pseudomonas aeruginosa infection secondary to chronic skin moisture of the feet, identified from the greenish discoloration of skin. The green discoloration is due to pyocyanin and pyoverdine, giving the skin a bluish-green color. Symptoms can also include pruritus, pain, malodor, and paresthesias. Our patient was admitted to the hospital with dermatology consultation, who recommended vinegar soaks, gentamicin cream, and 0.3% ciprofloxacin solution. Other case studies have reported successful treatment by removing the inciting agent and keeping skin dry, acidic soaks such as benzoyl peroxide, and/or oral fluoroquinolones. Green foot syndrome has been reported in soldiers wearing combat boots for long hours and in patients during prolonged cast use. The moist environment of damp skin in boots provides an ideal environment for P. aeruginosa to grow. Our patient often wore construction boots with 2 pairs of socks for long hours at work, which made him susceptible to this infection.

Take-Home Points

  • When patients present with lower extremity complaints, always carefully assess the feet; this patient’s initial complaint was not skin discoloration.

  • Pseudomonas aeruginosa infections can cause a greenish discoloration to feet chronically kept in moist conditions, such as frequent and extended shoe or cast use.

  • García-Martínez FJ, López-Martín I, Castellanos-González M, Segurado-Rodríguez MA. Green foot ulcers. Enferm Infecc Microbiol Clin. 2017 Oct;35(8):536-537. English, Spanish. doi: 10.1016/j.eimc.2015.10.010. Epub 2015 Nov 26. PMID: 26627144.
  • Spernovasilis N, Psichogiou M, Poulakou G. Skin manifestations of Pseudomonas aeruginosa infections. Curr Opin Infect Dis. 2021 Apr 1;34(2):72-79. doi: 10.1097/QCO.0000000000000717. PMID: 33492004.
  • Wu DC, Chan WW, Metelitsa AI, Fiorillo L, Lin AN. Pseudomonas skin infection: clinical features, epidemiology, and management. Am J Clin Dermatol. 2011 Jun 1;12(3):157-69. doi: 10.2165/11539770-000000000-00000. PMID: 21469761.
  • Sloan B, Meffert JJ. “Boot foot” with pseudomonas colonization. J Am Acad Dermatol. 2005;52(6):1109-1110. doi:10.1016/j.jaad.2005.01.105
  • Park, Y., & Bae, J. (2013). Green foot syndrome: A case series of 14 patients from an armed forces hospital. Journal of the American Academy of Dermatology, 69(4), e198-e199. https://doi.org/10.1016/j.jaad.2013.05.012
  • Lee SH, Cho SB. Cast-related green foot syndrome. Clin Exp Dermatol. 2009;34(7):2008-2009. doi:10.1111/j.1365-2230.2009.03317.x
  • Macgregor DM. An unusual presentation of immersion foot. Br J Sports Med. 2004 Aug;38(4):E11. doi: 10.1136/bjsm.2003.007385. PMID: 15273204; PMCID: PMC1724852.

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2025 SAEM Annual Meeting | Copyrighted by SAEM 2025 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.



By |2026-03-04T10:25:32-08:00Mar 13, 2026|Infectious Disease, SAEM Clinical Images|
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SAEM Clinical Images Series: Connect the Dots

The patient is a 39-year-old female with past medical history of polysubstance use disorder and seizures who presents to the Emergency Department complaining of bilateral leg pain, primarily in her joints. She states that she was seen by her PCP today and was given a shot of Toradol, but she reports that her pain has continued to worsen to the point that she has difficulty ambulating. She states that two days ago she developed pruritic blisters on her feet and her feet began to swell. She reports the blisters have worsened and have spread to her hands and forearms as well as her calves and thighs. She denies ever having similar symptoms in the past. She reports some subjective fevers and chills as well as cough and congestion, but denies sore throat, chest pain, abdominal pain, vomiting, diarrhea, dysuria, vaginal bleeding, or vaginal discharge. She denies any recent travel and denies any animal exposure other than her mother’s dog but there are no fleas that she knows of. She denies any recent insect bites. She states that she has been sexually active with one male partner over the last six months and that she has tested negative for STIs in the last two months. She has no other complaints at this time.

 

Vitals: BP 121/77; HR 107; R 22; T 100.8°F; O2 sat 98% room air.

General: Appears mildly uncomfortable but no acute distress.

HEENT: Normal, no signs of pharyngitis.

Respiratory: Clear to auscultation bilaterally.

Cardiovascular: Tachycardia without murmur.

Abdomen: Non-tender, no masses.

Extremities: There are no signs of trauma. Full range of motion but complaints of joint pain with moving her legs and with walking.

Skin: Relevant findings as shown. Discrete, tender, erythematous macules and vesicles on the bilateral feet, calves, forearms and a singular vesicle of the right1st digit

Urinalysis: Small amount of bacteria

This patient has disseminated gonococcal infection.

Disseminated gonococcal infection (DGI) is a serious complication of untreated gonorrhea, potentially leading to severe complications such as septic arthritis, pustular skin lesions, tenosynovitis, and in rare cases, endocarditis or meningitis. DGI is characterized by fevers, polyarticular joint pain, and skin lesions. The diagnosis of disseminated gonorrhea should be considered in any patient presenting with polyarticular joint pain or swelling in the setting of petechial or pustular skin lesions, especially in high risk populations. The skin lesions of disseminated gonorrhea most commonly appear on the distal extremities, and may involve the palms and soles. Patients may also present with acute septic arthritis without an obvious source. Patients with gonoccocal bacteremia may show signs of perihepatitis, meningitis, endocarditis, or osteomyelitis. Disseminated gonococcal infection results from the hematogenous spread of N gonorrhoeae, and typically develops within 3 weeks of primary mucosal infection. Patients with disseminated gonoccocal infection should be admitted for intravenous antibiotics (ceftriaxone). Any sexual partners should be treated as well.

Take-Home Points

  • Consider disseminated gonorrhea when you have a patient with polyarticular joint pain/swelling with pustular skin lesions.

  • Complications of DGI may be severe; admission and aggressive treatment with intravenous antibiotics is warranted.

  • Tang et al. Characterizing the rise of disseminated gonococcal infections in California, July 2020-July 2021. Clin Infect Dis. January 2023;76(2):194-200.
  • Wang CH, Lu CW. Images of the month 2: Disseminated gonococcal infection presenting as the arthritis-dermatitis syndrome. Clin Med (Lond). 2019 Jul;19(4):340-341. doi: 10.7861/clinmedicine.19-4-340. PMID: 31308120; PMCID: PMC6752240.

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2025 SAEM Annual Meeting | Copyrighted by SAEM 2025 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.



By |2026-03-04T10:20:27-08:00Mar 9, 2026|Infectious Disease, SAEM Clinical Images|
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SAEM Clinical Images Series: Pain, Paralysis, and Rash

The patient is an 81-year-old female with a history of asthma and hypertension who presents to the Emergency Department with right-sided abdominal swelling for five days. Five days ago, the right side of her abdomen appeared to protrude more than the left. This protrusion then increased over the next 2-3 days. The patient was diagnosed with shingles to the right lower abdomen earlier that month, but her rash has now nearly resolved. She continues to have “electric” pain in the region of the prior shingles infection. She denies any fevers, abdominal trauma, vomiting, or changes in bowel or bladder habits. She has never had anything like this before.

 

Vitals: All vital signs are normal.

Abdomen: See image provided. There is a firm unilateral distention of the right lower abdomen without shifting dullness or fluid wave. No palpable masses are present. There is moderate tenderness over the protruding region but no rebound or guarding. Bowel sounds are present.

Skin: See image provided. Moderate tenderness to palpation over region.

CBC and CMP are unremarkable.

CT scan of the abdomen and pelvis: No evidence of acute abnormality. Normal appendix. Moderate stool burden.

This patient has a Zoster pseudohernia.

Varicella-Zoster Virus (Shingles).

Zoster pseudohernia (ZP) occurs when the zoster infection infiltrates a posterior thoracic dermatome, affecting the spinal nerve roots responsible for the motor function of the abdominal wall. ZP typically presents with a rapidly progressive unilateral outpouching of the abdomen, giving a hernia-like appearance, but with intact abdominal wall musculature. In most cases, the classic Herpes Zoster rash precedes ZP, however in up to 10% of patients ZP may be the first presenting sign of zoster. Although uncommon, the symptoms are often distressing to patients, with many presenting to emergency departments or surgical offices for initial evaluation. The diagnosis is clinical and is based on a history of zoster infection or classic zoster symptoms and lack of findings suggesting alternate pathology. Abdominal CT or other imaging is recommended to exclude tumors, true hernias, free fluid, or other possible causes of abdominal distention. Electromyography (EMG) can be used to support diagnosis and will typically be abnormal due to the dysfunction of the abdominal wall musculature. Complete recovery occurs in 70-80% of patients within about 4-5 months.

Take-Home Points

  • Zoster Pseudohernia is a rare presentation of herpes zoster infection resulting in dysfunction of the abdominal wall musculature.

  •  There is no specific treatment with most cases fully resolving within several months to one year.

  • Chernev I, Dado D. Segmental zoster abdominal paresis (zoster pseudohernia): a review of the literature. PM R. 2013 Sep;5(9):786-90. doi: 10.1016/j.pmrj.2013.05.013. PMID: 24054853.
  • Yoo J, Koo T, Park E, Jo M, Kim MS, Jue MS. Abdominal pseudohernia caused by herpes zoster: 3 case reports and a review of the literature. JAAD Case Rep. 2019 Aug 5;5(8):729-732. doi: 10.1016/j.jdcr.2019.06.019. PMID: 31440570; PMCID: PMC6698640.

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2025 SAEM Annual Meeting | Copyrighted by SAEM 2025 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.



By |2026-01-25T20:35:10-08:00Jan 26, 2026|Infectious Disease, Neurology, SAEM Clinical Images|
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Gamechanger: Do we really need a lumbar puncture for all febrile infants 0-28 days old?

PECARN febrile infant rule age 0-28 days

A new international pooled analysis challenges the age-old dogma that all febrile infants 0-28 days require a lumbar puncture (LP). Can the PECARN febrile infant prediction rule safely identify a low-risk subset for invasive bacterial illnesses (bacterial meningitis and bacteremia) [1]?

Bottom Line

For more than  four decades, the standard of care for febrile infants in the first month of life has been aggressive: full sepsis workup (including an LP), admission, and IV antibiotics. A new study in JAMA suggests this paradigm may be shifting [2, 3].

  • In an international pooled analysis of more than  1,500 febrile infants aged ≤28 days, the updated PECARN febrile infant prediction rule missed zero cases of bacterial meningitis.
  • Inclusion Criteria: Non-ill-appearing, full time (≥37 weeks) infants aged 0–28 days with fever (≥38.0°C), who underwent blood and urine testing including procalcitonin (PCT).
  • Exclusion Criteria: Critically ill appearance, prematurity, comorbidities, or antibiotic use in preceding days.
  • Implication: Cerebrospinal fluid analysis is unnecessary for a subset of non-ill-appearing febrile infants ≤28 days old.
  • What now? The current data provides a solid, practice-changing, evidence-based foundation for a shared decision-making conversation that wasn’t possible before.

Study

To answer this question, the authors performed 2 distinct analyses:

  1. Primary Analysis (The “External” Test): To test the rule’s validity in new, diverse populations, the primary analysis pooled data from 4 prospective international cohort studies (Canada, Spain, Europe, UK/Ireland).
    • Population: 1,537 non-ill-appearing, full-term (≥37 weeks) infants aged 0–28 days with fever (≥38C)
    • Why no US data? This was done to validate the PECARN rule externally, avoiding the bias of testing it on the same US population from which it was derived.
  1. Secondary Analysis (The “Maximize Power” Test): To generate the most precise safety estimates possible, the authors then pooled the 4 international cohorts PLUS the 2 original US-based PECARN cohorts.
    • Population: 2,531 infants total
    • Result: Even with the added US data, the rule missed zero cases of bacterial meningitis.

What is the updated PECARN febrile infant prediction?

An infant ≤28 days old is low risk if they meet all 3 criteria:

  1. Urinalysis: Negative
  2. Absolute neutrophil count (ANC): ≤4,000/mm3
  3. Serum procalcitonin: ≤0.5 ng/mL

The Findings

The prevalence of Invasive Bacterial Infections (IBI) in all studied patients was 4.5%.

  • 3.8% bacteremia
  • 0.7% meningitis

Performance of the PECARN Rule

MetricPrimary Analysis of 4 International Cohorts (95% CI)Secondary Analysis of 4 International + 2 US PECARN Cohorts (95% CI)
Total Infants1,5372,531
Classified as “Low Risk”632 (41.1%)1,079 (42.6%)
Sensitivity94.2%
(85.6–97.8%)		94.8%
(88.1–97.8%)
Specificity41.6%
(36.7–46.7%)		43.3%
(38.7–48.0%)
Negative Predictive Value (NPV)99.4%
(98.1–99.8%)		99.6%
(98.7–99.9%)
Positive Predictive Value (PPV)6.9% ( 4.8–9.9%)6.1%
(4.5–8.2%)
Missed Meningitis Cases0 (out of 11 cases)0 (out of 22 cases)
Missed Bacteremia Cases4 (5.8% of IBI cases)5 (5.3% of IBI cases)

Number needed to tap calculation

One of the most compelling arguments for using this rule is the statistical trade-off required to find a single missed case. The authors provide estimated Negative Predictive Values (NPV) across a range of disease prevalences.

If we assume a 1.00% prevalence of bacterial meningitis (which is conservative; the study observed 0.7%), the NPV for bacterial meningitis is 99.95% [2].

This means that for every 10,000 PECARN low-risk infants, 9,995 do not have bacterial meningitis, and 5 might. We can translate this into a “Number Needed to Tap” (NNT) to find one missed case:

  • Risk of Missed Case = 1 – 0.9995 = 0.0005
  • NNT = 1 / 0.0005 = 2000

Bottom Line: You would hypothetically need to perform 2,000 lumbar punctures on low-risk infants to find ONE case of bacterial meningitis that the rule missed.

Important guardrails: Who is this rule for?

Before applying these findings, we need to understand the strict inclusion criteria. This study—and the PECARN rule itself—was only validated on a specific population.

The “Must-Have” Checklist:

  • ✅ Non-ill-Appearing: The infant cannot appear ill. The study defined this strictly, excluding infants with abnormal appearance, work of breathing, or circulation findings (often using the Pediatric Assessment Triangle or other illness indicators). If the baby looks sick, the rule does not apply.
  • ✅ Full-Term: Infants must be ≥37 weeks gestation. Preterm infants have different immunological risks and were excluded.
  • ✅ Age 0–28 Days: This specific analysis focused exclusively on the first 28 days of life.
  • ✅ Proven Fever: Documented temperature ≥38C

The SBI vs. IBI distinction

If you are already using the PECARN rule for older infants (29–60 days), you likely use it to rule out Serious Bacterial Infections (SBIs), which includes urinary tract infections (UTIs) [1].

This study is different – it focused purely on invasive bacterial infections (IBIs), which is defined as bacteremia and/or bacterial meningitis.

What did the PECARN rule miss?

The rule had perfect sensitivity for bacterial meningitis, but it did miss 5 cases of bacteremia out of more than 2,500 infants ≤28 days old despite a low-risk stratification. Let’s look at the 5 cases classified as “missed bacteremia:

  • 1 case: H. influenzae bacteremia
  • 1 case: E. coli bacteremia (without UTI)
  • 1 case: E. coli bacteremia (with E. coli UTI)
  • 2 cases: S. aureus bacteremia (One of these also had a concurrent E. coli UTI).

The authors note that S. aureus in blood cultures can be a contaminant rather than a true pathogen. If these S. aureus cases were indeed contaminants, the true sensitivity of the rule would be even higher than reported.

Notably, all 5 cases of missed bacteremia occurred in infants aged 8-21 days. There were 0 missed bacteremia cases in the 22-28 day age group.

How do we reconcile this with the most current 2021 AAP guidelines?

To understand why this study is a big deal, we have to look at what the American Academy of Pediatrics (AAP) guidelines currently tells us to do. The new data exposes a potential practice shift specifically for infants in the third week of life (8–21 days).

Age GroupCurrent AAP Guidelines (2021)New PECARN Data (2025)Bottom Line for Practice
0–7 Days

Excluded

Standard of care is full sepsis workup (including LP), IV antibiotics, and admission.

Technically Included

Rule missed 0 cases of IBI in this age group, but sample size was smaller (~15% of cohort).

No Change

Due to perinatal risks and smaller sample sizes, the full sepsis workup remains a safe standard of care.

8–21 Days

• Action: Routine LP required

• Strategy: Full sepsis workup (including LP), IV antibiotics, and admission

• Reasoning: Previously considered insufficient data

Potential to Defer LP

• Meningitis: 0 missed cases

• Bacteremia: 5 missed cases (all occurred in the 8–21 day window).

• Nuance: High sensitivity for meningitis challenges the mandatory LP rule, but missed bacteremia warrants caution.

Proceed with Caution

While you might safely skip the LP (since 0 infants with bacterial meningitis were missed), the risk of missed bacteremia suggests these infants still require close monitoring. A reasonable approach for a well-appearing infant with normal inflammatory markers and urinalysis might be to skip the LP, give no antibiotics, but still hospitalize for observation.

22–28 Days

• Action: Risk stratify

• Strategy: Defer LP if inflammatory markers are normal.

• Reasoning: Biomarkers considered reliable risk stratification tools for meningitis.

Evidence to Defer LP

• Meningitis: 0 missed cases

• Bacteremia: 0 missed cases

Strong Validation

This study supports the AAP’s existing recommendation: Skip the LP if all the PECARN criteria (UA, ANC, PCT) are negative, but admit for observation.

Additional Considerations

  1. Procalcitonin is mandatory: This rule relies on serum procalcitonin. If your facility only uses CRP and WBC, you cannot use this reduction strategy safely.
  1. Consider herpes simplex virus (HSV) meningoencephalitis: This PECARN rule is to identify young febrile infants with bacterial infections and not HSV. You thus must still risk-stratify for HSV separately (seizures, vesicles, maternal history, etc) and perform a LP if HSV is suspected, independent of the PECARN prediction rule.

Summary

For the first time, we have high-quality, multi-national data suggesting that a routine LP may not be necessary for every febrile infant ≤28 days old. While guidelines have not officially changed, this study provides the evidence needed to support shared decision-making with caregivers.

We can now honestly tell parents: “Based on these blood and urine tests, the chance of your baby having bacterial meningitis is extremely low—likely less than 1 in 2,000. We can safely hold off on the spinal tap and antibiotics right now and admit for observation.”

That is a conversation we couldn’t have yesterday.

References

  1. Kuppermann N, Dayan PS, Levine DA, et al; Febrile Infant Working Group of the Pediatric Emergency Care Applied Research Network (PECARN). A clinical prediction rule to identify febrile infants 60 days and younger at low risk for serious bacterial infections. JAMA Pediatr. 2019;173(4):342-351. doi:10.1001/jamapediatrics.2018.5501. PMID 30776077
  2. Burstein B, Waterfield T, Umana E, Xie J, Kuppermann N. Prediction of Bacteremia and Bacterial Meningitis Among Febrile Infants Aged 28 Days or Younger. JAMA. Published online December 8, 2025. doi: 10.1001/jama.2025.21454
  3. Searns JB, O’Leary ST. Moving the Field Forward to Safely Do Less With Febrile Neonates. JAMA. Published online December 8, 2025. doi: 10.1001/jama.2025.23133
  4. Pantell RH, Roberts KB, Adams WG, et al; Subcommittee on Febrile Infants. Evaluation and management of well-appearing febrile infants 8 to 60 days old. Pediatrics. 2021;148(2):e2021052228. PMID 34281996
By |2026-01-09T03:36:22-08:00Dec 24, 2025|Expert Peer Reviewed (Clinical), Infectious Disease, Pediatrics|
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SAEM Clinical Images Series: Strawberry Tongue

A 7-year-old male with no significant past medical history presented to the Emergency Department complaining of a sore throat. The parents stated that he had been running fevers for two days along with a worsening sore throat. The patient had been able to swallow, but had decreased oral intake secondary to pain. There are no other complaints at the time.

 

strawberry tongue

Vitals: BP 110/70; HR 111; R 17; T 101°F; O2 sat: 99% on room air.

General: Well appearing, no acute distress, normal voice.

HEENT: There is no sign of conjunctivitis. Oropharyngeal exam is remarkable for exudative pharyngitis with tonsillar swelling. There is no sign of peritonsillar abscess or airway compromise. Uvula midline and normal. Tongue as shown. Anterior cervical lymphadenopathy is present.

Respiratory: Clear to auscultation bilaterally.

Cardiovascular: Tachycardia without murmur.

Abdomen: Non-tender, no organomegaly.

Skin: Relevant findings as shown.

Non-contributory

Strawberry tongue and sandpaper rash.

Scarlet fever

Scarlet fever is caused by Group A Streptococcus (S. pyogenes), and most commonly occurs in children aged 5-15 years. The illness typically begins with a prodrome of fever, sore throat, headache, and abdominal pain, followed 1-2 days later by a distinctive coarse rash with a texture that resembles sandpaper. Exudative pharyngitis is usually present. The tongue may initially have a white coating which fades by day 4-5, revealing a bright red, “strawberry tongue” as seen in this case. The rash usually starts on the neck, axillae, and groin, and then spreads to the trunk and extremities. Pastia lines, which are linear petechial eruptions, may be present in the antecubital and axillary folds. Facial flushing with a pale area around the mouth is also common. Desquamation of the skin may occur about two weeks after the rash appears. A rapid strep test can quickly confirm the diagnosis. If scarlet fever is left untreated, it can lead to serious complications such as rheumatic fever or post-streptococcal glomerulonephritis. Early diagnosis and treatment with antibiotics, usually penicillin or amoxicillin, are effective in preventing sequelae.

Take-Home Points

  • Scarlet fever is characterized by strawberry tongue, sandpaper rash, and exudative pharyngitis. The cause is Group A Streptococcus.

  • Early diagnosis and antibiotic treatment are crucial to prevent the serious potential complications of untreated scarlet fever, such as rheumatic fever and post-streptococcal glomerulonephritis.

  • The Sanford Guide to Antimicrobial Therapy. Dallas, TX :Antimicrobial Therapy, Inc., 1995.

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Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2025 SAEM Annual Meeting | Copyrighted by SAEM 2025 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.



By |2025-11-09T21:20:57-08:00Nov 14, 2025|Infectious Disease, Pediatrics, SAEM Clinical Images|
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SAEM Clinical Images Series: Tangled in the Toilet

An otherwise healthy 46-year-old male presented to the Emergency Department with 18 months of diarrhea and intermittent abdominal cramping that has acutely worsened in the past week. On the morning of presentation, he noticed a worm-like object in his stool, which he brought to the ED (See images), prompting his visit. Throughout these 18 months, he experienced 4-10 loose bowel movements per day. He tried dietary modifications, including the removal of dairy, gluten, and soy, all without relief. The patient frequently travels for work, mainly to the US, Europe, and intermittently to Asia. His diet includes all forms of meat, fish, and shellfish. He denied fevers, chills, headaches, chest pain, shortness of breath, unexpected weight loss or gain, nausea, vomiting, or changes in his urinary habits. His stool has been non- greasy and has not contained any blood or mucous.

Vitals: BP 136/85; HR 70; R 18; T 98.2°F; O2 sat; 97% room air.

General: Well appearing, no acute distress.

Abdomen: There is mild tenderness to palpation in bilateral lower quadrants. Bowel sounds present in all quadrants. No rebound tenderness or guarding. No organomegaly.

Lymph: No lymphadenopathy present.

Skin: No rashes.

WBC: 5.4

Hgb: 14.4

Dibothriocephalus (Diphyllobothrium) latus: a tapeworm.

Stool ova and parasites.

This patient is infected with Dibothriocephalus (Diphyllobothrium) latus, a tapeworm distinctive for its proglottids with central hyperpigmented reproductive organs, as shown in the images. Patients rarely visualize the tapeworm in their stool, so diagnosis is usually made with a stool ova and parasite study. Diphyllobothrium latus infection is commonly caused by eating raw, undercooked, or lightly pickled seafood contaminated with tapeworm eggs. Tapeworm eggs are also occasionally used as weight loss supplements. The market for these supplements is not regulated; thus, the eggs may be from other parasites, leading to more severe manifestations of infection in different body areas, such as the brain, lungs, or muscles. Diphyllobothrium latus infection can cause pernicious anemia, as 80% of Vitamin B12 intake may be absorbed by the worm. Treatment for Diphyllobothrium latus is a single dose of praziquantel. Due to fecal-oral transmission, patients who engage in high risk transmission-prone behaviors should consider having their partners tested and treated as well.

Take-Home Points

  • Diphyllobothrium latus infection may cause Vitamin B12 deficiency and resultant anemia as the worm may absorb up to 80% of B12 intake.

  •  A single dose of praziquantel is generally sufficient to eradicate tapeworm infection.

  • Schantz, P. M. (1996). Tapeworms (cestodiasis). Gastroenterology Clinics of North America., 25(3), 637–653. https://doi.org/10.1016/s0889-8553(05)70267-3
  • Craig P, Ito A. Intestinal cestodes. Curr Opin Infect Dis. 2007 Oct;20(5):524-32. doi: 10.1097/QCO.0b013e3282ef579e. PMID: 17762788
  • Scholz T, Garcia HH, Kuchta R, Wicht B. Update on the human broad tapeworm (genus Diphyllobothrium), including clinical relevance. Clin Microbiol Rev. 2009; 22:146–160

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2025 SAEM Annual Meeting | Copyrighted by SAEM 2025 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2025-10-26T13:38:34-07:00Oct 31, 2025|Infectious Disease, SAEM Clinical Images|
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SAEM Clinical Images Series: Painful Great Toe

great toe

A 63-year-old-male with a past history of hypertension, renal failure with dialysis three times per week, and prior infective endocarditis appropriately treated with a regimen that ended four weeks ago presented with left great toe pain that started three weeks ago. The toe began swelling two weeks ago with continued pain and tenderness, becoming discolored approximately one week ago. He noted subjective fever and chills, but had no other complaints.

 

Vitals: Heart Rate 104, BP 111/69 mmHg, Temperature oral 38.1°C, Respiratory Rate 16; SpO2: 99% on room air

Skin: The plantar surface of the left great toe has violaceous discoloration extending to the dorsum of the distal phalanx around the nail. It is tender to touch at the plantar surface only. There is dark brown to black discoloration 16 mm x 8 mm at the distal medial aspect of the toe without ulceration.

Musculoskeletal: Good range of motion at all joints without pain.

Cardiovascular: 3/6 systolic murmur noted at the right sternal border.

The rest of the examination is normal.

BMP: BUN 19 mg/dL, Creatinine  5.21 mg/dL

Hemoglobin: 12.3 g/dL

WBC: 12.28 x 10^9/L

Imaging: X-ray of the left foot is unremarkable

Osler node

Yes, the patient should be admitted; an Osler node or Janeway lesion is indicative of active endocarditis. An Osler node is a painful, tender, nodular lesion that is bluish-purple and is located on the distal phalanx of the fingers or toes. Classically, pain precedes any swelling, with subsequent discoloration occurring with skin pigmentation being described as reddish, cyanotic, bluish-purple, vivid pink, or erythematous. The skin may desquamate or darken, but ulceration is rare. Histologic evaluation reveals necrotizing vasculitis and inflammatory infiltration of the vascular channels. Aspiration and culture of the lesions typically yields no organisms, though several case reports note positive bacterial growth with organisms that match the underlying endocarditis bacteria. Whether an Osler node is caused by micro-septic emboli or by an immune response is a controversy that has not yet been settled. Janeway lesions, also seen in endocarditis, are similar discolored macules on the palms or soles. However, Janeway lesions are normally painless, which is a key factor that differentiates them from Osler nodes. Osler nodes or Janeway lesions are indicative of active endocarditis. Patients with these lesions, such as the patient in this case, should be admitted for blood cultures, echocardiography, and intravenous antibiotics. This patient was admitted, and his echo confirmed multiple vegetative lesions with severe aortic valvular disease. The patient was subsequently transferred for valve replacement surgery after three weeks of intravenous antibiotics.

Take-Home Points

  • Osler nodes are tender, violaceous nodules located on the finger or toe pads.

  • Janeway lesions, located on the palms or soles, have similar discoloration but are not tender.

  • Osler nodes and Janeway lesions are uncommon but important manifestations of infective endocarditis.

  • Farrior JB, Silverman ME. A consideration of the differences between a Janeway’s lesion and an Osler’s node in infectious endocarditis. Chest. 1976 Aug;70(2):239-43. doi: 10.1378/chest.70.2.239. PMID: 947688.

  • Philip J, Bond MC. Emergency Considerations of Infective Endocarditis. Emerg Med Clin North Am. 2022 Nov;40(4):793-808. doi: 10.1016/j.emc.2022.07.001. Epub 2022 Oct 7. PMID: 36396222.

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2023 SAEM Annual Meeting | Copyrighted by SAEM 2023 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2025-04-23T10:53:56-07:00Apr 25, 2025|Cardiovascular, Infectious Disease, SAEM Clinical Images|
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