A Collection of Conditions Related to Bacterial Infection

Syphilitic Aortitis

Sean Cook, DO, and Matthew Marcus, MD
University of South Carolina, Columbia, South Carolina

A 50-year-old man with no significant past medical history presented to the emergency department with a right Achilles tendon rupture following a basketball game. The initial evaluation uncovered new-onset atrial fibrillation with a rapid ventricular response, and the man was admitted to the hospital.
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Diagnostic tests. A nuclear myocardial stress test was performed the following day, the results of which were questionably abnormal.

Contrast-enhanced, electrocardiographic gated computed tomography (CT) coronary angiography showed mild, circumferential aortic wall thickening without calcification (arrow, Figure 1) and an accompanying severe reduction of the ostial luminal diameter of the right and left main coronary arteries (arrow, Figure 2). Left heart catheterization demonstrated 75% concentric stenosis of his proximal left main artery, and 70% stenosis of the right ostial artery. Transthoracic echocardiography revealed no aortic valvular insufficiency.

Given the proximal left main artery aneurysmal dilatation, aortitis was diagnosed. Results of tests for possible causes of aortitis, including autoimmune disease and active bacterial infection, returned negative.

Rapid plasma reagin (RPR) dilution titer was 1:256. Confirmatory syphilis test results also were positive. HIV serology was negative. Lumbar puncture was preformed out of concern for asymptomatic neurosyphilis. The cerebral spinal fluid sample showed lymphocytosis with a normal total protein level and a positive VDRL test result.

Upon further questioning, the patient admitted to an extramarital affair with a coworker 10 years earlier.

The patient was started on continuous infusion of 24 g of intravenous penicillin G for a total of 14 days.

Outcome of the case. Six months after completing treatment, the patient still was asymptomatic, with an RPR titer of 1:16. At 3-year follow-up, he remained asymptomatic, with an RPR titer of 1:2. Thoracic CT angiography showed a moderate improvement in the proximal aortic dilation, with no significant constriction of the right and left coronary arteries.

Discussion. Syphilitic aortitis results from an inflammatory response to an active Treponema pallidum infection. Prior to the antibiotic era, syphilitic aortitis accounted for more than 10% of cardiovascular deaths in the United States.¹ Antibiotics and rapid screening tests have made syphilitic aortitis a rare clinical entity today.

In syphilitic aortitis, chronic inflammation of the ascending aortic lumen results in replacement of healthy tissue with fibrin.^2,3 Active or dead Treponema bacteria have not been found in association with the ongoing inflammatory process. Eventually, fibrin replacement leads to weakening of the aortic lumen, resulting in the characteristic aneurysmal dilation. Additionally, dilation at the aortic valve results in aortic insufficiency with progression to dilated cardiomyopathy.

Large autopsy reviews involving thousands of patients from the early 20th century have shown that the 2 major causes of death from syphilitic aortitis are aneurysmal rupture followed closely by dilated cardiomyopathy caused by aortic insufficiency.^2-4 These later complications of the disease are insidious. The average time from disease exposure to cardiovascular event is between 10 and 40 years.^1,3 Nonspecific symptoms such as midscapular pain, atypical chest pain, and progressive fatigue are the most commonly reported physical symptoms prior to an often fatal event.⁵ Therefore, it is not surprising that at the time of autopsy, 70% of untreated cases of tertiary syphilis and late syphilis have some degree of aortitis present.^1,4

Serologic testing is the primary method of diagnosing syphilitic aortitis. Nonspecific treponemal titers are the quickest and least expensive, making them the initial screening test of choice. Unfortunately, nonspecific treponemal tests have a diagnostic sensitivity of only 70% to 78% in the later stages of syphilitic disease.⁶ Treponema-specific antibodies are sensitive and specific (97%-100%) but are more labor-intensive and more costly. Adding confusion, test results for these specific antibodies remain positive even after successful prior treatment and do not indicate the presence of active disease. Choosing the appropriate serologic test is based on the clinician’s suspicion of syphilitic involvement in suspected aortitis cases. Advanced imaging such as CT or magnetic resonance angiography aid in the diagnosis of aortitis but are nonspecific for syphilitic involvement.

The primary reason for antimicrobial treatment in syphilitic aortitis is to arrest further inflammatory processes in the aortic lumen. Treatment does not reverse damage that is already present. Treatment consists of 2.4 million units of penicillin formulation, intravenous or intramuscular, weekly for 3 weeks. No significant data exist comparing this recommendation to either shorter or longer courses of penicillin treatment that are recommended in other syphilitic conditions.

As in our patient’s case, all patients with syphilitic aortitis should undergo further evaluation for neurosyphilis with HIV serology tests.

No guidelines exist regarding follow-up of treated syphilitic aortitis cases, although 6- to 12-month intervals seem appropriate during the first several years posttreatment. The decision to reimage patients is left to the provider and should be based on severity at presentation. Otherwise, changes or differences in extremity pulse pressures, unexplained chest discomfort, syncope, and visual disturbances warrant additional investigation.

References:

1. Paulo N, Cascarejo J, Vouga L. Syphilitic aneurysm of the ascending aorta. Interact Cardiovasc Thorac Surg. 2012;14(2):223-225.
2. Roberts WC, Ko JM, Vowels TJ. Natural history of syphilitic aortitis. Am J Cardiol. 2009;104(11):1578-1587.
3. Kampmeier RH, Morgan HJ. The specific treatment of syphilitic aortitis. Circulation. 1952;5(5):771-778.
4. Heggtveit HA. Syphilitic aortitis: a clinicopathologic autopsy study of 100 cases, 1950 to 1960. Circulation. 1964;29(3):346-355.
5. Singh AE, Romanowski B. Syphilis: review with emphasis on clinical, epidemiologic, and some biologic features. Clin Microbiol Rev. 1999;12(2):187-209.
6. Larsen SA, Creighton ET. Rapid plasma reagin (RPR) 18-mm circle card test. In: Larsen SA, Pope V, Johnson RE, Kennedy EJ Jr, eds. A Manual of Tests for Syphilis. 9th ed. Washington, DC: American Public Health Association; 1998:chap 10. https://www.cdc.gov/std/syphilis/manual-1998/chapt10.pdf. Accessed July 15, 2016.

NEXT: Intertrigo of the Foot Caused by Pseudomonas aeruginosa

Intertrigo of the Foot Caused by Pseudomonas aeruginosa

Amar Dave, MD, and Shawna Langley, MD
Riverside County Regional Medical Center,
Moreno Valley, California

A 47-year-old nondiabetic man with a history of hand and foot psoriasis presented to a dermatology clinic with an acute skin infection of the left foot.

History. A recent course of oral terbinafine and trimethoprim-sulfamethoxazole had not improved the infection. Over a 4-year period, he had experienced similar infections on the same foot, which had recurred frequently and often had required hospital admission with the administration of broad-spectrum intravenous antibiotics.

Physical examination. The web spaces and distal foot were severely macerated, with thick, purulent, foul-smelling discharge and pain, requiring the use of crutches for ambulation (Figures 1 and 2).

Diagnostic tests. A Wood lamp examination of the foot was performed and demonstrated the greenish yellow fluorescence pathognomonic of infection with Pseudomonas species (Figures 3 and 4). The man received diagnosis of intertrigo caused by Pseudomonas aeruginosa.

Discussion. P aeruginosa is a gram-negative obligate aerobe. The bacteria produce pyoverdin, a greenish yellow substance that fluoresces under a Wood lamp,¹ sometimes can cause greenish blue staining of clothing that contacts the infected area, and even can discolor the patient’s skin.^2,3 It is a hydrophilic organism with a propensity to grow in moist environments and bodies of water such as swimming pools, hot tubs, and contact lens solution. The bacteria often are found in water reservoirs of hospitals, contributing to carriage of the bacteria on hands of health care workers after washing and subsequent transmission due to skin contact.¹

Pseudomonas skin infections have varied clinical presentations and occur in immunocompromised and immunocompetent hosts. Cutaneous findings in immunocompetent hosts usually are mild and self-limited, including green nail syndrome, hot tub folliculitis, otitis externa, hot foot syndrome, and interdigital infections/foot intertrigo.¹ In contrast, cutaneous infections in immunocompromised hosts can lead to considerable morbidity and mortality and include malignant otitis externa, ecthyma gangrenosum, and even necrotizing fasciitis. An overall increase susceptibility to Pseudomonas is seen in patients with diabetes, who are immunocompromised, who are treated with multiple courses of antibiotics, and with skin breakdown from any cause such as burns and eczema.¹

Foot intertrigo caused by Pseudomonas is common and always should be considered in the differential diagnosis of any patient who presents with maceration, discharge, and inflammation of the web spaces and sole. Pseudomonas sometimes is the single etiologic pathogen in web space infections but more commonly is seen as a concomitant pathogen with dermatophytes and Staphylococcus.⁴

Infection with Pseudomonas should be suspected in any patient not responding to treatment for dermatophytes and gram-positive bacteria. Skin culture will provide a definitive diagnosis, but results can take up to 5 days. In contrast, a Wood lamp provides rapid diagnosis of Pseudomonas via visualization of the classic greenish yellow fluorescence, as seen in our patient’s case.

Treatment options for cutaneous Pseudomonas infections include Castellani paint (carbolfuchsin), topical gentamycin, 5% acetic acid (white vinegar), and 0.5% silver nitrate soaks.⁵ If these measures fail, or if infection is severe enough, oral ciprofloxacin can be used.⁵ P aeruginosa has been developing resistance to ciprofloxacin, however.^6,7

Outcome of the case. Levofloxacin rapidly cleared our patient’s skin infection, but it recurred a few weeks later. Another course of levofloxacin combined with the persistent use of topical silver nitrate resulted in maintained skin clearance.

References:

1. Wu DC, Chan WW, Metelitsa AI, Fiorillo L, Lin AN. Pseudomonas skin infection: clinical features, epidemiology, and management. Am J Clin Dermatol. 2011;12(3):157-169.
2. Kalkan G, Duygu F, Bas Y. Greenish-blue staining of underclothing due to Pseudomonas aeruginosa infection of intertriginous dermatitis. J Pak Med Assoc. 2013;63(9):1192-1194.
3. Bae JM, Park YM. Green foot syndrome: a case series of 14 patients from an armed forces hospital. J Am Acad Dermatol. 2013;69(4):e198-e199.
4. Lin J-Y, Shih Y-L, Ho H-C. Foot bacterial intertrigo mimicking interdigital tinea pedis. Chang Gung Med J. 2011;34(1):44-49.
5. Habif TP. Pseudomonas aeruginosa infection. In: Habif TP. Clinical Dermatology: A Color Guide to Diagnosis and Therapy. 5th ed. Philadelphia, PA: Mosby-Elsevier; 2010:363-370.
6. Obritsch MD, Fish DN, MacLaren R, Jung R. Nosocomial infections due to multidrug-resistant Pseudomonas aeruginosa: epidemiology and treatment options. Pharmacotherapy. 2005;25(10):1353-1364.
7. Su H-C, Ramkissoon K, Doolittle J, et al. The development of ciprofloxacin resistance in Pseudomonas aeruginosa involves multiple response stages and multiple proteins. Antimicrob Agents Chemother. 2010;54(11):4626-4635.

NEXT: Tuberculoid Leprosy

Tuberculoid Leprosy

Madelyn B. King, BS
University of South Alabama College of Medicine, Mobile

Jessica Maglione, MD, and Barbara B. Wilson, MD
University of Virginia, Charlottesville

An 18-year-old woman presented with a 3-month history of a 2-cm, gradually enlarging, asymptomatic skin lesion on her right forearm.

History. The young woman had been treated with terbinafine cream for presumed tinea corporis and clobetasol for the possible presence of granuloma annulare, both without response. She had emigrated from Mozambique within the past year. She was otherwise in excellent health and reported no constitutional symptoms.

Physical examination. Examination revealed a 2-cm, erythematous, papular, annular plaque on her right volar forearm, with decreased central sensation to light touch. The remainder of neurologic examination findings were unremarkable, and no peripheral nerve enlargement was noted.

Diagnostic tests. Potassium hydroxide preparation test results were negative for fungal hyphae. A 4-mm punch biopsy was performed, and pathology tests revealed granulomatous dermatitis, suspicious for tuberculoid leprosy. Results of special stains for acid-fast bacilli were negative. Nevertheless, due to high clinical suspicion, the sample was sent to the National Hansen’s Disease Laboratory Research Program for polymerase chain-reaction (PCR) testing. PCR results were weakly positive for Mycobacterium leprae, and the sequencing for other mycobacteria was notably negative.

These findings, combined with the histologic and clinical presentation, confirmed the diagnosis of tuberculoid leprosy. The patient was started on a 6-month multidrug treatment regimen of daily dapsone 100 mg and rifampin 600 mg.

Discussion. Leprosy, also known as Hansen disease, is a progressive, granulomatous disease that predominantly affects the skin and nervous system. Because of its debilitating nature, it remains a significant global public health concern. Delayed diagnosis can result in increased morbidity.

On average, 150 to 250 cases are reported annually in the United States, with the predominant incidence (85%-95%) in immigrants from endemic regions such as Asia, Africa, and South America.¹ In 2003, 9 countries, including Mozambique, accounted for 84% of leprosy’s global prevalence.¹ However, endemic cases have been reported in Hawaii, Puerto Rico, and on the US mainland in the region of the western Gulf of Mexico and California.²

The disease is caused by infection with M leprae, an aerobic, acid-fast, rod-shaped bacterium. Humans serve as the primary reservoir for M leprae, but the nine-banded armadillo, found in the southern United States and Mexico, also can serve as a natural host.^3,4 Although the precise mode of transmission remains unclear, M leprae is thought to be transmitted through aerosol spread of nasal secretions.⁵ The organism’s incubation period can range from several months to 20 to 50 years.⁶

A timely diagnosis of leprosy is critical, given that without prompt treatment, symptoms can become irreversible. M leprae infection manifests clinically as a heterogeneous spectrum of symptoms ranging from mild skin lesions in tuberculoid leprosy to severe systemic involvement in multibacillary lepromatous leprosy. Patients can present with skin lesions, paresthesias, weakness, and visual disturbances. The granulomatous skin lesions in tuberculoid leprosy classically present as erythematous macules or papules exhibiting characteristic central anesthesia. Painful peripheral nerve enlargement also is associated with this form.⁷

The clinical phenotype of leprosy is largely dictated by the host’s immune response. Skin and peripheral nerve lesions in paucibacillary tuberculoid leprosy are more consistent with a robust helper T cell type 1 cell-mediated response. In addition, few acid-fast bacilli are present.⁸ Conversely, multibacillary lepromatous leprosy is composed primarily of a humoral helper T cell type 2 response and is associated with a greater acid-fast bacilli burden.^8,9 Clinically, it presents with more-severe, progressive symptoms such as extensive symmetric cutaneous involvement, nasal septal perforation, and leonine facies.

Due to the inability to culture M leprae, the diagnosis depends on both the clinical presentation and the presence of acid-fast bacilli detected with Ziehl-Neelson carbolfuchsin staining or the presence of M leprae DNA detected with PCR testing.^10-12

Treatment of leprosy depends on the clinical presentation and the number of acid-fast bacilli. Multidrug therapy remains the cornerstone of all leprosy treatment regimens. Paucibacillary single lesions can be treated with 6 to 12 months of daily dapsone and rifampin to prevent resistance. Multibacillary forms require the addition of clofazimine and the extension of the treatment regimen to 24 months.^7,13

References:

1. World Health Organization. Global leprosy situation, 2005. Wkly Epidemiol Rec. 2005;80(34):289-295.
2. A Summary of Hansen’s Disease in the United States-2014. Baton Rouge, LA: National Hansen’s Disease Program, Health Resources and Services Administration, US Dept of Health and Human Services; 2015. http://www.hrsa.gov/hansensdisease/pdfs/hansens2014report.pdf. Accessed July 18, 2016.
3. Monot M, Honoré N, Garnier T, et al. On the origin of leprosy. Science. 2005;​308(5724):1040-1042.
4. Truman R. Armadillos as a source of infection for leprosy. South Med J. 2008;​101(6):581-582.
5. Scollard DM, Adams LB, Gillis TP, Krahenbuhl JL, Truman RW, Williams DL. The continuing challenges of leprosy. Clin Microbiol Rev. 2006;19(2):338-381.
6. Davey TF, Rees RJW. The nasal discharge in leprosy: clinical and bacteriological aspects. Lepr Rev. 1974;45(2):121-134.
7. Legendre DP, Muzny CA, Swiatlo E. Hansen’s disease (leprosy): current and future pharmacotherapy and treatment of disease-related immunologic reactions. Pharmacotherapy. 2012;32(1):27-37.
8. Britton WJ, Lockwood DNJ. Leprosy. Lancet. 2004;363(9416):1209-1219.
9. Misra N, Murtaza A, Walker B, et al. Cytokine profile of circulating T cells of leprosy patients reflects both indiscriminate and polarized T-helper subsets: T-helper phenotype is stable and uninfluenced by related antigens of Mycobacterium leprae. Immunology. 1995;86(1):97-103.
10. Anderson H, Stryjewska B, Boyanton BL Jr, Schwartz ML. Hansen disease in the United States in the 21st century: a review of the literature. Arch Pathol Lab Med. 2007;131(6):982-986.
11. Truman RW, Andrews PK, Robbins NY, Adams LB, Krahenbuhl JL, Gillis TP. Enumeration of Mycobacterium leprae using real-time PCR. PLoS Negl Trop Dis. 2008;2(11):e328.
12. Lini N, Shankernarayan NP, Dharmalingam K. Quantitative real-time PCR analysis of Mycobacterium leprae DNA and mRNA in human biopsy material from leprosy and reactional cases. J Med Microbiol. 2009;58(pt 6):753-759.
13. Recommended treatment regimens. National Hansen’s Disease Program, Health Resources and Services Administration, US Dept of Health and Human Services. http://www.hrsa.gov/hansensdisease/diagnosis/recommendedtreatment.html. Accessed July 18, 2016.

NEXT: Multisystem Streptococcal Abscesses in Immunocompetent Individuals

Multisystem Streptococcal Abscesses in Immunocompetent Individuals

Robert K. Mannel, MD, and Fahed A. Saada, MD
University of Florida College of Medicine, Jacksonville

In case 1, a 54-year-old man with no past medical history presented to the emergency department (ED) after having had a witnessed episode of seizure and urinary incontinence.

History and physical examination. The patient had a social history of alcohol abuse, a 35-pack-year cigarette smoking history, and chronic odontogenic infections consisting primarily of dental caries that had required multiple tooth extractions in the past year.

On admission, his Glasgow Coma Scale (GCS) score was 15/15. He was febrile, at 39°C. Physical examination findings were unremarkable.

Figure 1. In case 1, noncontrast CT (top row) demonstrated scattered, rounded, hypodense lesions and surrounding edema. CT with contrast (bottom row) demonstrated multiple ring-enhancing lesions with surrounding vasogenic edema, primarily in the frontal lobes and left parietal lobe.

Figure 2. In case 1, T2-weighted axial (top row) and T1-weighted axial (bottom left and middle) and sagittal (bottom right) MRI of the head with contrast demonstrated relatively uniform characteristics of low signal-rim T2 with more heterogeneous internal components, as well as moderate surrounding edema. The lesions demonstrated identical marginal ring enhancement following contrast.

Figure 3. In case 1, a chest radiograph (top left) demonstrated pulmonary opacity on the right lobe. Chest CT with contrast (axial, top right and bottom left; coronal, bottom right) demonstrated multiple confluent linear densities involving the right upper and lower lobes with air bronchograms.

Diagnostic tests. His white blood cell count was 16,400/µL (reference range, 4500-11,000/µL). Cranial computed tomography (CT) (Figure 1) and magnetic resonance imaging (MRI) (Figure 2) demonstrated multiple supratentorial contrast ring-enhancing lesions and surrounding vasogenic edema with a slight midline shift. Chest radiography and CT (Figure 3) revealed multiple confluent linear densities involving the right lung with air bronchograms.

The patient commenced broad-spectrum intravenous antibiotics (meropenem/doripenem, trimethoprim-sulfamethoxazole, and amikacin) and dexamethasone. Blood cultures were negative for bacteria, while bronchoalveolar lavage revealed mixed flora. A lung biopsy was negative for malignancy. HIV, toxoplasmosis, and cryptococcal test results were negative. Transesophageal echocardiography was performed and ruled out vegetation. The antibiotic regimen was changed to ceftriaxone, metronidazole, vancomycin, and trimethoprim-sulfamethoxazole.

One week after admission, the patient experienced fluctuating consciousness and neurologic deterioration to a GCS score of 3/15. A follow-up head CT scan revealed an increase in the size of the masses and new enhancing lesions, with worsening midline shift. The patient was intubated and transferred to the neurointensive care unit. An urgent left craniotomy was performed, followed by stereotactic aspiration of the abscesses, which grew Streptococcus anginosus.

The infectious disease consultant recommended further evaluation for gastrointestinal (GI) tract pathology. A CT of the abdomen and pelvis demonstrated multiple areas of haustral thickening involving the sigmoid colon and multiple subcentimeter hypodensities within the left hepatic lobe; however, the patient refused further testing, including a colonoscopy.

Outcome of the case. After sensitivities test results returned, the antibiotic regimen was switched to penicillin for 6 weeks of treatment. The patient improved over several weeks to a GCS score of 15/15. Five weeks after admission, head CT scans revealed persistent ring-enhancing masses with a moderate decrease in lesion size. He was discharged to an inpatient rehabilitation facility.

In case 2, a 30-year-old man with an unremarkable past medical history presented to the ED after having experienced 3 days of unrelenting headaches.

History and physical examination. The patient described gradual-onset headaches with photophobia and intermittent scotomata. On admission, his GCS score was 15/15. He was afebrile, and vital signs were stable. Physical examination findings, including of the oropharynx, were unremarkable.

Diagnostic tests. His initial laboratory test results, including a complete blood cell count, chemistry panel, and blood cultures, were unremarkable. Head CT without contrast demonstrated multifocal areas of mixed attenuations involving the bilateral occipital and frontal lobes. A stat contrast-enhanced brain MRI (Figure 4) revealed additional right corpus callosum and left cerebellar involvement, with mass effect on the fourth ventricle. Chest radiography and CT (Figure 5) showed a cavitary lesion within the left lung base.

Figure 4. In case 2, fluid attenuation inversion recovery MRI showed multifocal lesions and associated vasogenic edema (left), gradient echo with areas of susceptibility (middle), and a left cerebellar T2 lesion (right).

Figure 5. In case 2, chest CT showed a left lung base cavity.

On day 2, the patient was taken emergently to the operating room for posterior fossa craniectomy with removal of the left cerebellar lesion. Aspiration and culture of the abscess revealed S anginosus, and based on the recommendation of an infectious disease specialist, he was placed on ceftriaxone, metronidazole, and vancomycin.

In the neurointensive care unit, his intracerebral pressures remained elevated, so an additional burr hole was placed in the right occipital region, and the bilateral frontal lobe lesions were drained. Soon thereafter, the patient developed compartment syndrome of his left leg and was found to have extensive popliteal vein clotting, with thrombosis of the distal arterial tree.

Outcome of the case. He died after his course worsened, with refractory hypotension, hypoxemia, severe lactic acidosis, and acute renal failure.

Discussion. S anginosus is a species in the Streptococcus milleri group (SMG) of viridans streptococci, along with Streptococcus intermedius and Streptococcus constellatus. These organisms were first described in 1956 by Guthof¹ after having been isolated from dental abscesses and are now acknowledged to be normal flora of the oropharynx and the GI tract. The distinguishing feature of SMG organisms is their propensity to form abscesses and cause invasive pyogenic infections, including head and neck infection, brain abscesses, and intrathoracic and intra-abdominal infections.² This characteristic differentiates SMG bacteria from other pathogenic streptococci such as Streptococcus agalactiae and Streptococcus pyogenes.

Difficulties in distinguishing SMG organisms have caused ambiguity in determining their pathogenic potentials.³ S constellatus and S intermedius are well-recognized causes of central nervous system (CNS) abscesses. Cases of other CNS infections such as meningitis and lateral or cavernous sinus thrombosis also have been described.⁴ Intracranial abscesses may develop following additional odontogenic, thoracic, or GI tract sites of infection.

There are few recent reports in the medical literature of multiple intracranial abscesses due to SMG pathogens. One case reported a previously well 39-year-old man who had clinical and radiographic findings that were very similar to those of our patients, although no underlying cause was discovered.⁵ That patient responded very well and returned to baseline after treatment with 3 months of intravenous antibiotics. Another case report described S intermedius as a cause of lobar pneumonia with meningitis and brain abscesses in a 55-year-old man with history of alcohol abuse.⁶ Both of these case reports isolated the exact SMG organism using further microbiologic testing (16S ribosomal RNA sequencing).

Our patients presented with abscesses of the lung and CNS, along with possible GI tract infection. The origin of the infection in our patients was unknown, although in case 1, the patient’s history of multiple tooth extractions, poor dental hygiene, and oral and endodontic infections likely was the cause. Infections with SMG bacteria range from minor oral infections such as pharyngitis or dental abscesses to life-threatening invasive infection with bacteremia and metastatic abscess formation. The SMG bacteria have been isolated mostly from dental caries and periodontal disease.⁷

Furthermore, recent research into the concentration of SMG bacteria presenting in the saliva of alcoholic patients compared with nonalcoholic patients showed elevated levels.⁸ This finding suggests that persons with alcoholism have a higher than average risk for SMG bacterial infection; therefore, aspiration of the normal flora is more likely to cause metastatic spread of the pathogen to the thoracic cavity.

If clinical suspicion of SMG bacterial infection arises, a possible role of a coinfecting organism or the need to search for occult abscess should be investigated. Timely diagnosis with appropriate treatment is key, since these virulent bacteria can rapidly cause severe illness and death.

References:

1. Guthof O. Pathogenic strains of Streptococcus viridans: streptococci found in dental abscesses and infiltrates in the region of the oral cavity [in German]. Zentralbl Bakteriol Orig. 1956;166(7-8):553-564.
2. Gossling J. Occurrence and pathogenicity of the Streptococcus milleri group. Rev Infect Dis. 1988;10(2):257-285.
3. Claridge JE III, Attorri S, Musher DM, Hebert J, Dunbar S. Streptococcus intermedius, Streptococcus constellatus, and Streptococcus anginosus (“Streptococcus milleri group”) are of different clinical importance and are not equally associated with abscess. Clin Infect Dis. 2001;32(10):1511-1515.
4. Petti CA, Simmon KE, Bender J, et al. Culture-negative intracerebral abscesses in children and adolescents from Streptococcus anginosus group infection: a case series. Clin Infect Dis. 2008;46(10):1578-1580.
5. Kirkman MA, Donaldson H, O’Neill K. Neurological pictures: multiple intracranial abscesses due to Streptococcus anginosus in a previously well individual. J Neurol Neurosurg Psychiatry. 2012;83(12):1231-1232.
6. Khatib R, Ramanathan J, Baran J Jr. Streptococcus intermedius: a cause of lobar pneumonia with meningitis and brain abscesses. Clin Infect Dis. 2000;​30(2):396-397.
7. Whiley RA, Beighton D, Winstanley TG, Fraser HY, Hardie JM. Streptococcus intermedius, Streptococcus constellatus, and Streptococcus anginosus (the Streptococcus milleri group): association with different body sites and clinical infections. J Clin Microbiol. 1992;30(1):243-244.
8. Morita E, Narikiyo M, Yokoyama A, et al. Predominant presence of Streptococcus anginosus in the saliva of alcoholics. Oral Microbiol Immunol. 2005;​20(6):362-365.