A 28-year-old white man was admitted to our hospital because of chronic swelling and redness of the left sub-axillary area. No fever, pruritus, or sweating was reported. His past medical history was unremarkable. The patient reported that, after switching deodorant, he noticed a painful swelling in his left axilla 3 months prior to his admission to our hospital. He was treated by his family physician for postulated hidradenitis suppurativa with antibiotics and anti-inflammatory medications, which did not lead to any improvement. Because of the persistence of the lesion in the axilla, a fine needle aspiration was performed then, which showed "atypical degenerating cells suspicious for malignancy". This finding prompted referral to a major tertiary medical center. At that time there was a flare-up of symptoms in the left axilla in addition to the appearance of a new palpable, tender mass in his left supraclavicular area. This mass was chosen by the attending surgeon to be removed for testing. Culture of a part of the removed specimen grew Propionibacterium acnes. Microscopic examination showed fibrous adipose tissue with acute and chronic inflammation findings consistent with organizing abscess. No lymph node tissue was identifiable. Based on these findings the patient received treatment with levofloxacine 500 mg once a day and metronidazole 500 mg three times a day p.o., which, again, did not lead to any improvement.

Physical examination on admission showed temperature 37,5 degrees C and pulse rate 80/min. His body mass index (BMI) was 35,46 kg/m2 (weight: 128 kg, height: 190 cm). He had gynecomastia and inversion of the nipples. Examination of the chest and neck revealed inflammation of the skin surrounding the left nipple, extending up to the left axilla, and a scar in the left supraclavicular area related to previous biopsy (Figures 1-2). Small, palpable, and tender lymph nodes in the left axilla, left and right cervical areas and left and right inguinal areas were also found. All other systems were examined and found normal.

C-reactive protein level was increased at 2.99 mg/dl (normal less than 0.5 mg/dl). Erythrocyte sedimentation was increased as well at 39 mm/first hr. Complete blood count, blood glucose, aspartate aminotransferase (AST), alanine aminotransferase (ALT), glutamyl transpeptidase, bilirubin, lactate dehydrogenase (LDH), creatine phosphokinase (CPK), serum sodium, potassium, urea, and uric acid were all normal. Tests for cytomegalovirus (CMV), Epstein-Barr (EBV) and human immunodeficiency virus (HIV) were negative. Mantoux test was also negative.

A 23-year-old man presented with one year history of recurrent pyorrhoea from the umbilical area. Specifically, the patient had 5 episodes of omphalitis during the last year prior to his admission to the hospital. All episodes were successfully treated with courses of antimicrobial agents (second generation cephalosporins or amoxicillin/clavulanic acid) by mouth. No fever, abdominal pain or other complaints were reported. His past medical history was significant for dysfunction of the left kidney (79% loss of function in a recent nuclear medicine renal scan), which was attributed to recurrent urinary tract infections during his childhood.

Physical examination on admission showed temperature of 37,4 degrees C, signs of inflammation (redness, tenderness, swelling, and increased temperature) in the umbilical area (Figure 1) as well as purulent umbilical discharge (Figure 2).

Routine laboratory tests including a complete blood count, blood urea, serum creatinine, blood glucose, liver function tests, C-reactive protein, erythrocyte sedimentation rate, and a urinalysis were normal. No growth of microorganisms was found from the culture of the umbilical discharge.

What are the likely underlying causes for the recurrent omphalitis of this young adult?

A 64-year-old male presented to the Emergency Room of the local hospital in a rural area of Greece complaining of fever, shortness of breath, productive cough, and mild low back pain. He had no previous hospitalizations.

The patient's symptoms suggest a lower respiratory tract (LRT) infection as the most likely diagnosis. Streptococcus pneumoniae, Hemophilus influenzae, and Moraxella catarrhalis are common etiologic agents in patients with community acquired LRT infections. In addition, atypical bacteria including Mycoplasma, Chlamydia, Legionella, and Rikketsiae species are the cause of a considerable proportion of lower respiratory tract infections that varies in different age groups. Also, several viruses including influenza, parainfluenza, and adenoviruses may cause LRT infection, especially during the winter session.

The patient was a farmer. His past medical history was significant for a work-related injury in the lower back 10 years ago. He consumed alcohol, about half a liter of wine per day, for 20 years. He did not smoke. He never traveled outside Greece.

The details of the medical history and the habits of the patient suggest additional possible pathogens for his LRT infection, mainly Klebsiella pneumoniae, given the history of alcoholism. Because of his occupation, leptospirosis should be considered in thedifferential diagnosis. In addition, brucellosis should be also considered given that the patient lives in a rural area in Greece where the infection is endemic. It should be noted that brucellosis may cause manifestations from the respiratory system.

The patient's condition deteriorated despite the administration of antimicrobial treatment (ceftriaxone 1 g every 12 hours i.v. and clarithromycin 500 mg every 12 hours p.o.) at the local hospital. He was transferred to a tertiary hospital in Athens, two days after his admission at the local hospital. He presented with temperature 38.5 oC, heart rate 108/min, and tachypnea (45 breaths/min). Physical examination on admission revealed crackles in the base of the left lung and the upper right lung. Routine laboratory testing showed white blood cell count 8,800/mm 3, neutrophils 88%, erythrocyte sedimentation rate 104 mm/1st hour, serum urea 57 mg/dl and creatinine 1.4mg/dl. Gram stain of a sputum specimen showed about 20 neutrophils per optic field. Chest x-rays on admission showed infiltrates in the left lower and the right upper lobe (figure 1). Arterial gas testing showed PaO2/FiO2=240, arterial pH = 7.48, and PCO2=28 mmHg.

The patient's worsening condition despite the use of appropriate antimicrobial treatment for community-acquired pneumonia suggests several possibilities. First, that the pathogen responsible for his pneumonia was indeed one of the most commonly implicated micro-organisms in LRT infections, namely Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, or an atypical pathogen that was however resistant to the administered agents. There is an increasing proportion of pneumococcal isolates with full resistance to penicillin in several countries during the last years. Although still a controversial issue, it seems that the majority of evidence supports that the outcome of patients who receive treatment with ceftriaxone for pneumonia due to Streptococcus pneumoniae with full resistance to penicillin is worse than with vancomycin or other agents with activity against this pathogen. Second, the pathogen may be one not included in the above list of microorganisms. Someone should also consider other etiologic agents such as staphylococci, streptococci other than Streptococcus pneumoniae, anaerobes, and Gram-negative bacteria other than Klebsiella pneumoniae. In addition, mycobacteria, mainly Mycobacterium tuberculosis, should be always considered in the differential diagnosis in patients with LRT infection. It should be also noted that antibacterial agents would not influence the natural history of a viral LRT infection, except if a secondary bacterial infection had already developed. Non-infectious causes of lung infiltrates should also be included in the differential diagnosis at this stage.

Because of deterioration of his condition, antimicrobial treatment with vancomycin 1 gr every 12 hours i.v. and ciprofloxacin 400 mg every 12 hours i.v. was started. Treatment with ceftriaxone continued, while clarithromycin was stopped. Despite the change of the regimen of antibiotics, the patient's condition continued to deteriorate and he was transferred to the intensive care unit (ICU), after a three-day hospitalization in the medical ward. On admission to the ICU, he was intubated due to severe respiratory failure (PaO2/FiO2 ratio 175, arterial pH 7.21, PaCO2=59 mm Hg). Laboratory testing showed white blood cell count =11,100/mm3 (polymorphonuclear cells = 89%), hemoglobin = 9.9 g/dl, hematocrit = 32%, platelets = 103,000/ mm3, serum urea 131 mg/dl, serum creatinine 1.7 mg/dl, C-reactive protein = 16.4 mg/dl, fibrinogen 935 mg/dl, and D-dimmer 544 ìg/l. A CT-scan of the chest showed extensive infiltrates in both lungs with pneumoceles (figure 2).

What's your diagnosis? (Please click below for the response)

A 58-year-old man was admitted to the hospital complaining of a 3-day history of fever, malaise and a painful swelling of the right parotid gland. For 2 days before his admission, he had been taking amoxicillin and metronidazole, as the swelling was thought to be related to dental infection, by his general practitioner. His medical history was unremarkable. The patient did not suffer from any immune or endocrine disease and has not taken any other medication in the past. He did not mention any history of diarrhea, vomiting, abdominal pain, joint pain or joint swelling. He was living in Athens suburbs, working as a civil servant.

As the symptoms seemed to persist, the patient was referred to our Hospital's ENT department for evaluation. At physical examination, a firm mass was palpable at the right parotid, and the patient was admitted for further investigation. No evidence of palpable regional lymph nodes was noted and no other clinical findings could be revealed. The chest X-ray showed no abnormalities. His white blood count was 9,250/mm3 (69.7% neutrophils, 17.2% lymphocytes, and 6.8% monocytes), haematocrit 48.5%, haemoglobin level 16.1 g/dl, platelet count 267,000/mm3, C - reactive protein 8.3 mg/dl (normal values up to 0.5 mg/dl) and erythrocyte sedimentation rate 70 mmHg/1st hour. A CT scan of the face was performed (Figure).

What is your diagnosis?