Human bite wounds as a portal of entry for infective endocarditis and purulent pericarditis: a very rare association

Abstract

Human bites are an infrequent cause of emergency department visits and hospital admissions. There are rarely published cases of complicated infection, such as infective endocarditis. We present a rare case of a patient with acute infective endocarditis in a healthy native valve and purulent pericarditis from a human bite. A 40-year-old man with obesity suffered deep human bites by an adult woman, with two deep lesions in the anterior thorax and one superficial lesion in the upper abdomen and admitted in intensive care unit with septic shock and a persistent aortic murmur. Echocardiography described evidence of vegetation, perforation and severe regurgitation of aortic valve. Scanner described moderate pericardial effusion. Cardiac surgery was performed, with evidence of purulent pericardial effusion after pericardiotomy, and subsequently aortic valve replacement with a 25 mm bioprosthesis. The patient showed positive progress.

Background

Human bites are an infrequent cause of emergency department visits and hospital admissions.^{1 2} The reason for consultation is mainly in the context of wound finding lesions.³ A higher frequency of consultation is found in men, and there is a wide age range between 18 and 78 years (mean 28 years). Lesions more frequently affect the hands (50.3%), extremities (23.5%) and head-neck (17.8%).² They can be divided into an occlusive human bite or a closed fist lesion on the oral cavity, which are generally secondary to fighting and are usually underestimated.¹

Saliva has been found to contain more than 50 species of bacteria and a high microbial load, which explains the high rate of infection associated with bites. A range of secondary infections have been seen in the range of 2%–25% depending on different factors, some of them being a longer delay in emergency room consultation, a bite from an adult, depth, injuries in the upper limbs and hands and bites in relatively avascular areas (such as auricular cartilage).^{1 4} Regarding infectious agents, 54% of wounds have aerobic and anaerobic bacteria, 44% only have aerobes and 2% only have anaerobes.⁵ The most frequent germs described are aerobic, especially Streptococcus sp with 84% (mainly Streptococcus anginosus), Staphylococcus sp with 54% (mainly Staphylococcus aureus) and Eikenella corrodens with 30% of cases.⁵ Infections with hepatitis viruses, herpes, tetanus, actinomycetes, Treponema pallidum and acquired immunodeficiency virus are rare.^{1 6–8}

Wound infection can be superficial (cellulitis with or without abscess) or deep (abscess, septic arthritis, osteomyelitis, tenosynovitis or necrotising fasciitis). There are rarely published cases of complicated infection, such as infective endocarditis (IE), meningitis or brain abscess.^{9 10} We present a rare case of a patient with acute IE in a healthy native valve and purulent pericarditis from a human bite.

Case presentation

A 40-year-old man with obesity suffered deep human bites by an adult woman, with two deep lesions in the anterior thorax and one superficial lesion in the upper abdomen (figure 1A, B). Subsequently, a progressive condition began, characterised by general compromise, headache and fever, to which dyspnoea with minimal effort and orthopnea were added. After 14 days, the patient received consultation in the emergency room and was in poor general condition attributed to septic shock with arterial hypotension, sinus tachycardia of 112 bpm, fever of 39°C, poor peripheral perfusion and deep skin lesions due to the human bites. Initial laboratory work revealed leukocytosis 13 300 × mm³, thrombocytopenia 36 000 × mm³, C reactive protein 357 mg/dL (normal value [NV]<10 mg/dL), creatinine 2.32 mg/dL, urea nitrogen 34 mg/dL and lactate 34 mg/dL (NV <18.4 mg/dL). ECG showed sinus tachycardia and nonspecific alterations causing repolarisation in the inferolateral wall. Chest X-ray showed a few interstitial infiltrates and a slight increase in the cardiothoracic index. Two peripheral blood cultures were taken, and empirical antibiotics with vancomycin, imipenen and amikacin were started in parallel with advanced haemodynamic resuscitation with fluids plus vasopressors (norepinephrine up to 0.1 µg/kg/min), with good clinical response. The patient was admitted to the critical unit, and a persistent aortic systolic murmur and a decreasing diastolic component were observed.

Figure 1.

(A) Evolved lesion after cardiac surgery on the right delto-pectoral region. (B) Evolved lesion after cardiac surgery on the left delto-pectoral region. (C) Transoesophageal echocardiogram showing noncoronary veil vegetation. (D) Colour Doppler shows severity of aortic regurgitation. (E) Chest level CT to show pericardial effusion (yellow arrow). (F) Abdominal CT to show splenic infarction (yellow arrow).

Investigations

A transthoracic and transesophageal echocardiographic study was performed, highlighting a mildly dilated left ventricle with preserved systolic function (left ventricular ejection fraction [LVEF] 57%), three-leaflet aortic valve and left coronary veil with a 9.4 mm vegetation and rupture that caused severe insufficiency (figure 1C, D), mitral valve without vegetation and moderate functional insufficiency, without pericardial effusion or other significant findings. Microbiological study was performed with two positive aerobic blood cultures for oxacillin-sensitive S. aureus and a minimum inhibitory concentration of vancomycin of 1 µg/mL, for which the antimicrobials were adjusted to cloxacillin and clindamycin. Forty-eight hours after hospital admission, an imaging dissemination study was performed:

• Brain CT: small hypodense foci in frontolateral subcortical and left corticosubcortical at occipital and parasagittal levels.

• Chest–abdomen–pelvis CT: moderate pericardial effusion associated with signs of pericarditis (figure 1E). Bilateral pleural effusion associated with passive atelectasis. Splenic focal lesions (figure 1F). Bilateral focal renal lesions, with a greater magnitude in the left kidney.

Renal function recovered up to 1.3 mg/dL creatinine; negative aerobic blood cultures were obtained on the fourth day of evolution along with negative serologies for HIV and hepatitis B and C, but leukocytosis and elevated C reactive protein levels were persistent.

Differential diagnosis

Analysing this clinical case with intensivists, members of Heart Team and infectologists, was considered as an acute IE in the native valve, caused by S. aureus, with severe aortic insufficiency, embolic-type lesions at the cerebral, splenic and renal organs, associated with pericarditis and moderate pericardial effusion.

Treatement

After discussion with cardiovascular team, surgical resolution was pursued, with cardiac surgery performed on the sixth day of hospital admission. Issues addressed included an anterior thoracic skin lesion that drained pus, sternotomy and pericardiotomy with abundant pericardial fluid discharge and purulent and serohematic appearance, and a 3-leaflet aortic valve with 0.5×1 cm of vegetation in the noncoronary veil and another 1×1.5 cm with perforation in the left coronary veil. Subsequently, aortic valve replacement was performed with a 25 mm bioprosthesis, without incident. Pericardial fluid and valve cultures were negative.

Outcome and follow-up

The patient showed a successful progress, a decrease in inflammatory parameters and control of the condition. Transthoracic echocardiogram, highlighting the normally functioning aortic valve prosthesis, normal-sized left ventricle and preserved systolic function (LVEF 60%), without pericardial effusion. Six weeks of anti-staphylococcal treatment was completed, and the patient was discharged from the hospital. In outpatient check-ups, he was in normal functional capacity and without late surgical complications.

Discussion

Identifying the infection gateway for IE is of crucial importance, since this is the route through which the usual or frequently isolated causal germs are in blood cultures associated with this specific route enter. This allows a better clinical approach to each case and more appropriate surgical and medical management. In our case, it is highly probable that this patient, after suffering the human bite (cutaneous gateway), had the signs and symptoms of a serious infection in the approximate period of 14 days, evolving to septic shock. Later acute aortic regurgitation in a healthy valve, with rupture of the left coronary veil, 9 mm of vegetation, and severe regurgitation was developed. Two blood cultures taken at admission revealed oxacillin-sensitive S. aureus. The clinical definition of acute IE includes S. aureus infection, according to the Duke-Li criteria.¹¹

Acute IE was observed in 36.9% of episodes, and S. aureus predominated in 29% of all cases reported in the National Cooperative Study of IE in Chile (ECNEI-2), which included 506 consecutive patients prospectively studied between 1998 and 2008.¹² In most cases, it was difficult to pin down the entry route. In a recent study with 318 prospectively studied patients designed to determine the entry route in IE, the most frequent entry route was the cutaneous route (40%), and approximately 2/3 of these patients were observed in relation to healthcare centres and intravenous drug addiction.¹³ The most frequently isolated organism in this series was Staphylococcus in 78% of cases (S. aureus in 55% and coagulase-negative Staphylococcus in 23% of cases).

Only a small proportion of the patients with S. aureus bacteremia present IE: 6% in an Australian study and 10.1% in another research, in a series partially studied with TEE.^{14 15} On the other hand, the proportions were 25% and 31.7% in those patients systematically studied with TEE, respectively.^{16 17}

Acute staphylococcal IE, according to its virulence, can have a mean duration of 3 days prior to hospitalisation.¹⁸ Because it is a primarily invasive pathogen, these patients often develop a disseminated disease with embolic metastatic infection in the skin, soft tissues, bones, joints and eyes, with some images compatible with embolisations, in this case being observed in the CT images of the brain, chest, abdomen and pelvis.¹⁹

As a rare complication, we recorded in this patient, during surgery, the presence of purulent pericarditis, which was even a rare complication in the preantibiotic era, with high mortality.^{20 21} In a prospective study on IE and acute coronary syndrome, in 586 consecutive episodes between 1995 and 2005, clinical manifestations of pericarditis were reported in only five cases (0.85%).²² In another clinical series, the degree of pericardial involvement was 8.5%.²³ This may be due to (sterile) immunological processes or direct infection by the causative microbial agent.²⁴

Diagnosis is difficult, as clinically, IE can present insidiously with fever, dyspnoea, chest pain and leukocytosis.²⁵ Acute cardiac tamponade without a clear aetiology should make the treating physician suspect underlying IE; a study with TTE and TEE is imperative for IE diagnosis and management.²⁴

When pericarditis is purulent, it may be due to erosion of a fungal aneurysm of the sinus of Valsalva or complications from coronary septic embolisation, with or without acute coronary syndrome.²⁶ As previously mentioned, acute purulent pericarditis is rare, and subxiphoid pericardiotomy and pericardial sac lavage should be considered and may require surgical drainage.^{21 24 27} In our patient, the origin of this purulent pericarditis could have been embolic.

Aforementioned, relation between purulent pericarditis and endocarditis is exceptional and with few reports, but its association with human bites as a port of entry has not been described previously; to our knowledge, this would be the first case described in English medical literature. Early surgical treatment in complicated IE is recommended, according to recent guidelines.^28–30 In this case, acute valve disfunction, heart failure, purulent pericarditis and septic infection was mandatory to decide the early surgery. Early diagnosis and intervention of the heart team were crucial, in indication of surgical drainage of purulent pericarditis and valve replacement with a biological prosthesis and specific antibiotic treatment, all of which were decisive in its subsequent favourable clinical evolution.

Learning points.

• Suspect infective endocarditis in serious evolution of injuries by human bite.

• Evaluate extracardiac injuries.

• Team work leads to better treatment.

• Detection and early treatment of cardiovascular complication towards a good clinical outcomes.