Manifestations of Bacterial Infections

Helicobacter Pylori
Fadi I. Jabr, MD

A 59-year-old woman was evaluated for epigastric discomfort and iron deficiency anemia of 2 months’ duration. Two years earlier, she had undergone left upper lung lobectomy and adjuvant radiation for T2 N0 M0 poorly differentiated adenocarcinoma of the lung.

Laboratory testing. The results of a fecal occult blood test were positive. Esophagogastroduodenoscopy showed gastritis and duodenitis; a Campylobacter-like organism test was positive for Helicobacter pylori. Colonoscopy revealed 3 tubular adenomatous polyps; these were resected. Abdominal and chest CT scans showed only mild hepatomegaly and volume loss in the left lung, consistent with the previous lobectomy.

Treatment. A proton pump inhibitor and an antibiotic were prescribed. However, the anemia persisted and the abdominal pain increased and was now accompanied by melena. There were no symptoms of obstruction. The Figure shown here from the upper GI series revealed a filling mass defect in the jejunum.

Segmental resection of the small bowel showed a 4 cm x 3 cm x 3 cm tumor, 20 cm from the Treitz ligament and about three-fourths the circumference of the small intestine. Microscopic examination revealed a poorly differentiated adenocarcinoma that recapitulated the morphology and pattern of the lung neoplasm resected 2 years earlier. The tumor involved the mucosa, submucosa, and muscularis propria. Adjacent mesenteric lymph nodes and the resection margin were free of tumor. Immunohistochemical studies showed neoplastic cell expression of carcinoembryogenic antigen and cytokeratins. Results of bone scintigraphy were normal.

Discussion. Although jejunal metastasis from adenocarcinoma of the lung is relatively rare, it must be considered in all lung cancer patients who have abdominal pain, GI bleeding, or a positive fecal occult test result. Since most patients are asymptomatic, fecal occult blood testing may provide an early clue to the diagnosis of GI metastases. If upper and lower endoscopies and CT scans of the abdomen are unremarkable, then a conventional study, such as an upper GI series, may reveal the diagnosis.

Outcome of the case. Unfortunately, the prognosis remains poor. Surgical resection provides only palliative treatment of the disease. This patient recovered uneventfully and underwent chemotherapy.

Neisseria Gonorrhoeae
Rahi Kapur, MD, and David Effon, MD

A 22-year-old woman presented to her primary care physician’s office with right lower quadrant and suprapubic abdominal pain. She stated that the pain had begun earlier that day; she had no symptoms on awakening that morning. The pain was dull and constant; the patient rated the intensity at 8 on a scale of 1 to 10. Ibuprofen provided minimal relief. She also reported mild dysuria but denied recent nausea, vomiting, diarrhea, and constipation.

History. The patient had no significant past medical history other than a cesarean delivery for her only pregnancy. She had no known complications as a result of that procedure. She reported no history of sexually transmitted diseases.

Physical examination. On examination, the patient was in mild distress because of the pain. Suprapubic tenderness, right adnexal tenderness, minimal vaginal bleeding, and a thin malodorous vaginal discharge were noted. No adnexal masses were palpated, and no tenderness was elicited over McBurney point. Laboratory studies revealed a white blood cell (WBC) count of 10,000/µL, with a normal differential. 

Laboratory testing. A urine pregnancy test result was negative. Urinalysis revealed a moderate leukocyte esterase level; 5 to 10 WBCs per high-power field (HPF), with 2 to 5 squamous cells per HPF; few bacteria; and occasional trichomonads. The patient was given ibuprofen—without relief of her pain—and metronidazole to cover Trichomonas vaginalis.

A second physical examination revealed significantly more tenderness, including rebound and guarding diffusely throughout the lower abdomen with more specific point tenderness at McBurney point and in the periumbilical area. Because of the change in her condition, the patient was transferred to the local emergency department, where a general surgery consult was obtained.

A CT scan of the abdomen and pelvis with intravenous and oral contrast was ordered to evaluate the patient for appendicitis. The CT scan revealed a thickened tubular structure in the right lower quadrant with a hypodense mass directly adjacent to it. Radiographic interpretation included an adnexal mass, but appendicitis could not be ruled out. There was no abnormality noted in the right upper quadrant. The patient received additional pain medication and antibiotics. The general surgery staff felt that the findings in this patient were consistent with appendicitis, and she was taken to the operating room for emergent laparoscopy.

During surgery, a large ovary, thickened fallopian tube, and adnexal fluid were visualized on the right side. The appendix appeared normal. A significant number of adhesions that involved the liver were noted (Figure). Before the appendectomy was performed, an intraoperative gynecology consult was called, and medical management for likely Fitz-Hugh-Curtis syndrome was recommended. The appendectomy was completed without complication.

Treatment. Metronidazole and doxycycline were prescribed, and the patient did well during her short hospital stay.

Discussion. Fitz-Hugh-Curtis syndrome is not well-known, but it is classified as an emergent condition by the Model of the Clinical Practice of Emergency Medicine.1 As described in multiple case reports, the typical presentation includes right upper-quadrant pain that may be pleuritic in young, sexually active women.2 About 50% to 75% of cases are caused by Chlamydia trachomatis infection, whereas only 10% result from Neisseria gonorrhoeae infection,3,4 as occurred in this patient. Fitz-Hugh-Curtis syndrome has also been implicated as a complication of pelvic inflammatory disease in 5% to 10% of cases.5

In this patient, perihepatitis developed from a gonococcal infection. Instead of the more typical delayed presentation with right upper quadrant pain, her clinical history was consistent with appendicitis. Furthermore, a contrast-enhanced CT scan of the abdomen revealed no abnormalities in the right upper quadrant region.

There is no consensus in the literature regarding the utility and selection of an imaging modality to corroborate the diagnosis of Fitz-Hugh-Curtis syndrome. Although ultrasonography is the preferred imaging study for patients with acute right upper quadrant pain, its diagnostic accuracy is notably poor with respect to hepatic inflammation, capsular abnormalities at the dome of the liver, and small abscesses.6 Furthermore, while a majority of patients with Fitz-Hugh-Curtis syndrome have findings consistent with tubo-ovarian abscess on pelvic ultrasonography, the absence of these findings does not rule out this entity, because rupture may have occurred.

Nishie and colleagues7 found that ultrasonography did not yield any diagnostic clues to the syndrome in 12 patients with confirmed disease; however, retrospective review of enhanced CT scans revealed hepatic capsular enhancement in all 13 patients with Fitz-Hugh-Curtis syndrome. This finding has also been demonstrated in other case reviews, and further research is ongoing.8

Outcome of the case. Unfortunately, the patient did not follow-up after discharge. The final Chlamydia culture was negative, the N gonorrhoeae culture was positive, and peritoneal fluid cultures were negative.

In this patient, retrospective review of the CT scan did not reveal significant hepatic abnormalities, despite the impressive findings in the operating room (Figure). Thus, the absence of either ultrasonographic or CT findings does not rule out Fitz-Hugh-Curtis syndrome. Without a high degree of clinical suspicion, the diagnosis can be missed.9


1.  2005 EM Model Review Task Force, Thomas HA, Binder LS, et al. The 2003 model of the clinical practice of emergency medicine: the 2005 update. Ann Emerg Med. 2006;48(6):e1-e17.

2. Peter NG, Clark LR, Jaeger JR. Fitz-Hugh-Curtis syndrome: a diagnosis to consider in women with right upper quadrant pain. Cleve Clin J Med. 2004;719(3):233-239.

3. Banikarim C, Chacko MR. Pelvic inflammatory disease in adolescents. Adolesc Med Clin. 2004;15(2):273-285, viii.

4. Wattad M, Bishara J, Goldberg N, et al. Thick fits Fitz. Lancet Infect Dis. 2005;5(10):664.

5. Epperly ATA, Viera AJ. Pelvic inflammatory disease. Clin Fam Pract. 2005;7:67-78.

6. Rubens DJ. Hepatobiliary imaging and its pitfalls. Radiol Clin North Am. 2004;42(2):257-278.

7. Nishie A, Yoshimitsu K, Irie H, et al. Fitz-Hugh-Curtis syndrome. Radiologic manifestation. J Comput Assist Tomogr. 2003;27(5):786-791.

8. Hyun JJ, Kim JY, Bak YT, et al. Education and imaging. Gastrointestinal: Fitz-Hugh-Curtis syndrome. J Gastroenterol Hepatol. 2006;

9. Zeger W, Holt K. Gynecologic infections. Emerg Med Clin North Am. 2003;21(3):631-648.

Neisseria Meningitidis
David L. Kaplan, MD

A 49-year-old woman was admitted to the hospital with a high fever of abrupt onset, rigor, headache, myalgias, and profound prostration. Her temperature was 41ºC (105.8ºF), blood pressure, of 60/40 mm Hg, respiration rate of 30 breaths per minute, and pulse rate of 130 beats per minute. 

Physical examination. Extensive purpuric patches and large ecchymoses were noted on the lower extremities and the buttocks. Signs of meningeal irritation were absent. 

Analysis of a specimen of cerebrospinal fluid was unremarkable; blood cultures revealed an infection caused by Neisseria meningitidis

Discussion. Patients with meningococcemia may not demonstrate meningeal signs; however, 50% to 80% will present with petechiae and purpuric skin lesions.1 Thus, a careful examination of the skin and mucosal surfaces is warranted in the acutely ill febrile patient.

Outcome of the case. The patient was given ceftriaxone (2 g bid), and penicillin, 24 million U/d; she was discharged from the hospital after 10 days. 


1. Rosenstein NE, Perkins BA, Stephens DS, et al. Meningococcal disease. N Engl J Med. 2001;344(18):1378-1388. 

Morganella Morganii
Melver L. Anderson, MD, FACP, and Nassrene Y. Elmadhun, MD

A 69-year-old man with stage II chronic kidney disease due to hypertension fell from his bicycle and presented to the emergency department (ED) with abrasions, ecchymoses, and a 3-cm laceration on his right leg. The patient was an avid cyclist. His wounds were cleaned and the laceration sutured. There were no fractures, and the patient was discharged home.

Two days later, the patient returned to the ED with septic shock and multiple tense hemorrhagic bullae over the right leg. The previously sutured laceration showed no signs of inflammation. There was tenderness and swelling in the right knee.

Laboratory testing. He was admitted to the ICU, where empiric intravenous vancomycin and piperacillin/tazobactam were given. Right knee aspirate was consistent with hemarthrosis; a Gram stain and culture were negative. Within 12 hours, gram-negative rods identified as Morganella morganii were growing in all 4 blood culture bottles, sensitive to ertapenem. An MRI scan of the patient’s right leg showed extensive cellulitis but normal-appearing deeper structures. The bullae enlarged and ruptured within a few days, and central eschars developed.

Treatment. Over the next 10 days, the patient was intermittently febrile and new, flaccid opaque bullae developed with surrounding erythema and expressible purulence. Culture of these ecthyma gangrenosum–like eruptions were positive for M morganii, despite ongoing therapy with intravenous ertapenem. Findings on MRI scans of the lower extremities were unchanged. Daily fevers persisted for another 10 days and then trended slowly downward. 

Discussion. M morganii is an increasingly common cause of nosocomial infection that presents as a life-threatening, community-acquired disease with severe dermatological manifestations. This case highlights the potential for M morganii to affect nonimmunocompromised hosts through what would otherwise be viewed as a mild inoculum. M morganii may be resistant to β-lactam antibiotics commonly selected for the empiric treatment of skin and soft tissue infections. It is a gram-negative rod found in soil and water and is present in normal fecal flora in humans and other mammals and in reptiles.

Although a rare human pathogen, M morganii has been reported as a cause of urinary tract infections (UTIs), nosocomial surgical wound infections, peritonitis, CNS infection, endophthalmitis, pneumonia, chorioamnionitis, neonatal sepsis, pyomyositis, necrotizing fasciitis, and arthritis. 

Numerous cases of nosocomial infection have been described, usually as post-surgical wound infections or UTIs. Patients in whom bacteremia develops are typically immunocompromised, diabetic, or elderly or have at least 1 serious underlying disease.1 The overall mortality associated with M morganii bacteremia is as high as 38%.2 Two dermatological observations reported with M morganii bacteremia include hemorrhagic bullae and ecthyma gangrenosum–like eruptions.3,4

This patient was seronegative for HIV and had no evidence of malignancy or serious chronic illness other than mild chronic kidney disease. He had received no corticosteroids recently. Our infection control records reported only 9 cases of cultures positive for M morganii in the preceding 6 months, and the only case of bacteremia during that time was in our patient. It does not appear that this was a nosocomial transmission of M morganii. His wounds were likely contaminated during the bicycle accident. We did not find another reported case of severe community-acquired M morganii sepsis with multiple dermatological manifestations in an immunocompetent host.

Therefore, Morganella should be considered a possible causative agent in cases of community-acquired trauma followed by septic shock and skin manifestations of bullae or ecthyma gangrenosum. Because M morganii can be resistant to β-lactam antibiotics, isolation of this organism may mandate an alteration in antimicrobial treatment.

Outcome of the case. By day 23, there was significant improvement in the appearance of the lower extremities and leukocytosis had normalized.


1. McDermott C, Mylotte JM. Morganella morganii: epidemiology of bacteremic disease. Infect Control. 1984;5:131-137.

2. Lee IK, Liu JW. Clinical characteristics and risk factors for mortality in Morganella morganii bacteremia. J Microbiol Immunol Infect. 2006;39:328-334.

3. Bagel J, Grossman ME. Hemorrhagic bullae associated with Morganella morganii septicemia. J Am Acad Dermatol. 1985;12:575-576.

4. Del Pozo J, García-Silva J, Almagro M, et al. Ecthyma gangrenosum-like eruption associated with Morganella morganii infection. Br J Dermatol. 1998;139:520-521.

Staphylococcus Aureus
David Effron, MD, and Jeffrey Pennington, MD

A 15-day-old boy was brought for evaluation after his mother noted a “lump” in his left breast that morning. There was no history of illness or trauma. The infant's appetite and activities were normal, and he had no constitutional symptoms. He was delivered vaginally at full term and did not require a prolonged nursery stay or antibiotic therapy. Results of standard maternal screens were negative.

Physical examination. The infant was afebrile and had normal vital signs. His left breast was erythematous, warm, tense, and tender. No fluctuance or pustules are noted, and no discharge can be expressed. The remainder of the examination results were unremarkable

Discussion. The patient was diagnosed with a breast abscess, a condition more common in neonates than in older children. Abscesses usually develop in full-term infants during the first 6 weeks of life; about 84% develop during the first 3 weeks. Boys and girls are equally affected initially; after 2 weeks, the incidence is higher in girls. This is probably a result of the physiologic breast enlargement that is more common in girls after the age of 2 weeks. Breast abscess rarely affects premature infants, because the breast tissue is underdeveloped.

Neonatal breast abscesses are usually caused by Staphylococcus aureus, but infections with group B streptococci, Escherichia coli, Salmonella, Proteus mirabilis, and Pseudomonas aeruginosa have been reported.

In infants with S aureus breast abscess, the nasal or pharyngeal mucous membranes are usually colonized. S aureus may spread from the nasopharynx to the skin of the nipple and move from there up the ducts of the physiologically enlarged breast to infect deeper tissues. Other sites that may be colonized are areas of intact skin, including the perineum, hands, and umbilicus.

In most cases, treatment involves incision, drainage, and parenteral antibiotic therapy. Once neonatal abscess is diagnosed, empiric therapy with clindamycin or vancomycin is initiated. Therapy is adjusted when the susceptibility of the organism has been determined.

Treatment. This patient was admitted to the pediatric hospital. Intravenous vancomycin therapy was started, and the abscess was drained by needle-guided ultrasonography. The left pectoralis region was scanned with a linear high-frequency probe in transverse and sagittal orientations (Figures 1 and 2). A 1.08 cm x 1.06 cm hypoechoic spherical mass was noted below the left areola, with some hyperechoic debris posteriorly. The surrounding subcutaneous tissue appeared edematous.

Cultures of the abscess grew methicillin-resistant S aureus. The infection resolved after a 21-day course of intravenous vancomycin. 

Breast abnormalities are common in neonates. Bilateral breast hypertrophy results from elevated estrogen levels in women during the last trimester of pregnancy. Breast hypertrophy is sometimes associated with galactorrhea (“witch’s milk”). Parents or grandparents may squeeze the neonate’s breast to express this milk, which can lead to mastitis, a staphylococcal infection that requires antibiotic therapy. It is prudent to counsel parents about neonatal breast hypertrophy and galactorrhea to prevent mastitis.

Outcome of the case. The patient was discharged home and recovered uneventfully.


1. Bratu S, Eramo A, Kopec R, et al. Community-associated methicillin-resistant Staphylococcus aureus in hospital nursery and maternity units. Emerg Infect Dis. 2005;11(6):808-813. 

2. Brook I. The aerobic and anaerobic microbiology of neonatal breast abscess. Pediatr Infect Dis J. 1991;10(10):785-786.

3. Lee MC, Rios AM, Aten MF, et al. Management and outcome of children with skin and soft tissue abscesses caused by community-acquired methicillin-resistant Staphylococcus aureus. Pediatr Infect Dis J. 2004;23(2):123-127.

4. Rudoy RC, Nelson JD. Breast abscess during the neonatal period. A review. Am J Dis Child. 1975;129:1031-1034.