**13. Fulminant coccal infection without gangrene of the extremities**

Gram-positive cocci occasionally provoke fulminant, lethal systemic infection without gangrene of the extremities. The pathophysiology resembles that of flesheating bacteria infection, accompanying pronounced hypercytokinemia and poor cellular reactions. Streptococcal, pneumococcal, staphylococcal, and enterococcal etiologies are described below.

#### **Figure 42.**

toes. Diabetes-related neutrophilic dysfunction provided him with the vulnerability to infection. Polymicrobial (type I) necrotizing fasciitis resulted in septicemia. Emergency amputation saved his life. The importance of foot care for patients with

*Localized severe burn on the sole of a diabetic male caused by a fan heater, resulting in necrotizing fasciitis (gross appearance). Because of diabetic neuropathy, deep ulcers occurred on the senseless foot. Dry gangrene on the first and second toes (arrowheads) indicates the association of diabetes-related atherosclerosis obliterans.*

An 18-year-old female patient had suffered from anorexia nervosa for 6 years. She happened to develop phlegmonous inflammation on her left lower leg, rapidly progressing to multifocal ulceration and gangrene. In 3 days, she underwent surgical amputation. *Pseudomonas aeruginosa* was cultured from blood and the leg lesion of necrotizing fasciitis. Immunohistochemical identification of the pseudomonal microbe was achieved by using a commercial monoclonal antibody. Representative

Classic pathogens of cellulitis represent group A β-hemolytic *Streptococcus* and

less frequently *Staphylococcus aureus*, but a diverse range of microorganisms, including *Pseudomonas aeruginosa* (as described above), cause cellulitis. Erythematous nodular lesions formed on the leg of neutropenic or leukemic patients were caused by *Stenotrophomonas maltophilia* [121]. Facial cellulitis may result from

**13. Fulminant coccal infection without gangrene of the extremities**

Gram-positive cocci occasionally provoke fulminant, lethal systemic infection without gangrene of the extremities. The pathophysiology resembles that of flesheating bacteria infection, accompanying pronounced hypercytokinemia and poor cellular reactions. Streptococcal, pneumococcal, staphylococcal, and enterococcal

Infrequently, necrotizing fasciitis is caused by *Pseudomonas aeruginosa* [119, 120]. Reportedly, the mortality rate of this type II lesion is 30%, and the infection often happens in the immunocompromised patients. Clinicians should consider empiric pseudomonal antibiotic coverage for preventing the progression of

diabetes mellitus should be emphasized.

*The importance of foot care in diabetic patients should be emphasized.*

features are illustrated in **Figure 42**.

*Haemophilus influenzae* infection [122].

etiologies are described below.

**122**

necrotizing limb infection.

**Figure 41.**

*Pathogenic Bacteria*

Pseudomonas*-related necrotizing fasciitis in a young lady suffering from anorexia nervosa (gross, H&E and immunostain). Her leg with massive necrotic/gangrenous lesions was amputated (left, after sampling of histological specimens). Massive bacterial growth provoked little inflammatory reaction. The bacteria are immunoreactive for* Pseudomonas aeruginosa *antigen detected by a monoclonal antibody (the courtesy by Dr. Takashi Tsuchida, a pathologist in Hamamatsu Medical University Hospital, Hamamatsu, Japan).*

## **13.1 Fulminant streptococcal infection without gangrene of the extremities**

Fulminant infection of group A β-hemolytic *Streptococcus* (*Streptococcus pyogenes*) is typically featured by progressive gangrene in the soft tissue of the extremities, as described above in the Section 10.1. Streptococcal toxic shock syndrome provokes an aggressive lethal condition without predisposing diseases [123, 124]. It should be of note that fulminant group A streptococcal infection is also encountered in cases without gangrenous lesions of the extremities [125]. Streptococcal infection in the internal organs may cause the fatal disease.

We experienced five cases of fulminant streptococcal infection without gangrene of the extremities (**Table 1**). Four of five cases were young and immunocompetent, and encountered at forensic autopsy. Infectious foci were seen in internal organs such as the tonsil, bronchus, puerperal endometrium, and urinary bladder. The clinical course was very short ranging from 2 to 4 days. Infective and hemorrhagic cystitis with systemic streptococcal dissemination was encountered in an aged female patient with a history of cerebral infarction and femoral neck fracture (**Figure 43**). Necrotizing endometritis in a puerperal lady was the cause of streptococcal toxic shock-like syndrome, as illustrated in **Figure 44**. It can be categorized in so-called puerperal fever. Pregnancy-associated lethal infection should be of particular notice [126]. Group A *Streptococcus* infection was proven by microbial culture in two cases, and immunoreactivities of streptococcal antigens and Strep A were shown on the Gram-positive cocci in all five cases. Strep A is a carbohydrate antigen specific for group A *Streptococcus* [127].

There are two different pathological mechanisms in fulminant streptococcal infection without gangrene of the extremities [125]. One form with overwhelming bacterial growth is characterized by secondary systemic bacterial dissemination accompanying bacterial emboli with poor neutrophilic reaction. Bacterial embolism in the adrenal gland provokes bilateral adrenal hemorrhage (acute adrenocortical insufficiency), being categorized in Waterhouse-Friderichsen syndrome [128] (**Figure 45**). Another form without bacterial embolism was featured by bacterial


*PD—preexisting disease (case 1: cerebral infarct and femoral neck fracture; case 4: Graves' disease), BE—bacterial embolus formation in distant organs and tissues, and MC—microbial culture (ND: not done). \* Negative in the blood but positive from the uterine cervix.*

*a Aspiration of coccal colonies into the alveolar space seen.*

#### **Table 1.**

*Summary of five autopsy cases of fulminant streptococcal infection without gangrene of the extremities [125].*

#### **Figure 43.**

*Fulminant streptococcal infection with hemorrhagic cystitis an 86-year-old female patient (gross, H&E and immunostain). Massive hemorrhagic cystitis is evident. The cocci infected in the eroded bladder wall are immunoreactive for streptococcal antigens.*

> Physicians should keep the possibility of fulminant streptococcal infection in mind, particularly when examining the patient manifesting progressive shock symptoms even without gangrene of the extremities. Autopsy prosecutors (diagnostic and forensic pathologists) must realize the difficulty in making an autopsy diagnosis, particularly when bacterial embolism is not identified under a microscope. The knowledge of these types of fulminant syndrome and the appropriate microscopic recognition of hemophagocytosis in the bone marrow, liver, and spleen are critically important for the autopsy prosecutors. When the association of the hypercytokinemic state was not suspected clinically and microscopically, one can

> *Fulminant streptococcal infection showing septic embolism, Waterhouse-Friderichsen syndrome, and bilateral renal cortical necrosis in the case demonstrated in Figure 43 (adrenal and kidneys; H&E and immunostain). The adrenal glands show massive hemorrhagic necrosis. Septic streptococcal emboli (arrowheads) are seen in capillary vessels of the adrenal. The kidneys show bilateral cortical necrosis with marked fibrin thrombosis in*

*the glomeruli and streptococcal colonization in the renal tubules (streptococcal antigens-positive).*

*Fulminant streptococcal infection with necrotizing endometritis in a 38-year-old female patient (gross, Gram, immunostain). The eroded postpartum endometrium 4 days after delivery is colonized by Gram-positive cocci with positive immunoreactivity for Strep A, a carbohydrate antigen of group A* Streptococcus*. Neutrophilic*

*reaction is limited in the endometrium. This condition is categorized as puerperal fever.*

hardly reach the correct autopsy diagnosis.

**Figure 44.**

*Pathology of Gangrene*

*DOI: http://dx.doi.org/10.5772/intechopen.93505*

**Figure 45.**

**125**

toxin-induced hemophagocytosis by activated macrophages, reflecting a hypercytokinemic state [129] (**Figure 46**). Hypercytokinemia and disseminated intravascular coagulation (DIC) are common phenomena in both forms, and bilateral renal cortical necrosis may be observed as an extreme manifestation of DIC [130]. Hematopoiesis in the bone marrow appear to be normal, but neutrophilic reactions are limited in the primary and disseminated infective foci. Supposedly, neutrophilic functions are acutely suppressed through two different mechanisms during the process of the fulminant disease. The disease is categorized in streptococcal toxic shock-like syndrome mediated by streptococcal superantigens [94, 95].

#### **Figure 44.**

*Fulminant streptococcal infection with necrotizing endometritis in a 38-year-old female patient (gross, Gram, immunostain). The eroded postpartum endometrium 4 days after delivery is colonized by Gram-positive cocci with positive immunoreactivity for Strep A, a carbohydrate antigen of group A* Streptococcus*. Neutrophilic reaction is limited in the endometrium. This condition is categorized as puerperal fever.*

#### **Figure 45.**

*Fulminant streptococcal infection showing septic embolism, Waterhouse-Friderichsen syndrome, and bilateral renal cortical necrosis in the case demonstrated in Figure 43 (adrenal and kidneys; H&E and immunostain). The adrenal glands show massive hemorrhagic necrosis. Septic streptococcal emboli (arrowheads) are seen in capillary vessels of the adrenal. The kidneys show bilateral cortical necrosis with marked fibrin thrombosis in the glomeruli and streptococcal colonization in the renal tubules (streptococcal antigens-positive).*

Physicians should keep the possibility of fulminant streptococcal infection in mind, particularly when examining the patient manifesting progressive shock symptoms even without gangrene of the extremities. Autopsy prosecutors (diagnostic and forensic pathologists) must realize the difficulty in making an autopsy diagnosis, particularly when bacterial embolism is not identified under a microscope. The knowledge of these types of fulminant syndrome and the appropriate microscopic recognition of hemophagocytosis in the bone marrow, liver, and spleen are critically important for the autopsy prosecutors. When the association of the hypercytokinemic state was not suspected clinically and microscopically, one can hardly reach the correct autopsy diagnosis.

toxin-induced hemophagocytosis by activated macrophages, reflecting a

**Case Age/ sex**

*Pathogenic Bacteria*

*a*

**Table 1.**

**Figure 43.**

**124**

*immunoreactive for streptococcal antigens.*

**Clinical course**

1 86 F 3 days + Hemorrhagic

3 38 F 4 days Necrotizing

4 24 F 3 days + Necrotizing

5 35 M 3 days Necrotizing

*Negative in the blood but positive from the uterine cervix.*

*Aspiration of coccal colonies into the alveolar space seen.*

cystitis

endometritis (Puerperal fever)

bronchitis

bronchitis

*embolus formation in distant organs and tissues, and MC—microbial culture (ND: not done). \**

**PD Primary lesion BE MC Autopsy findings**

2 30 M 2 days Acute tonsillitis + Bilateral renal cortical necrosis, bilateral

*PD—preexisting disease (case 1: cerebral infarct and femoral neck fracture; case 4: Graves' disease), BE—bacterial*

*Summary of five autopsy cases of fulminant streptococcal infection without gangrene of the extremities [125].*

+ ND Bilateral renal cortical necrosis, bilateral adrenal hemorrhage, and DIC

adrenal hemorrhage, and DIC

 +\* Hemophagocytic syndrome, bilateral renal cortical necrosis, leukostasis, DIC (microthrombosis), myocardial ischemia,

<sup>a</sup> ND Hemophagocytic syndrome, acute renal tubular necrosis, DIC, myocardial ischemia, pulmonary edema, and tonsillar

 + Hemophagocytic syndrome, acute renal tubular necrosis, DIC, myocardial ischemia, liver congestion, and pulmonary

(microthrombosis)

and liver congestion

hyperplasia

edema

hypercytokinemic state [129] (**Figure 46**). Hypercytokinemia and disseminated intravascular coagulation (DIC) are common phenomena in both forms, and bilateral renal cortical necrosis may be observed as an extreme manifestation of DIC [130]. Hematopoiesis in the bone marrow appear to be normal, but neutrophilic reactions are limited in the primary and disseminated infective foci. Supposedly, neutrophilic functions are acutely suppressed through two different mechanisms during the process of the fulminant disease. The disease is categorized in streptococcal toxic shock-like syndrome mediated by streptococcal superantigens [94, 95].

*Fulminant streptococcal infection with hemorrhagic cystitis an 86-year-old female patient (gross, H&E and immunostain). Massive hemorrhagic cystitis is evident. The cocci infected in the eroded bladder wall are*

#### **Figure 46.**

*Fulminant streptococcal infection without septic embolism caused by erosive bronchitis (bronchus: Gram, bone marrow and kidney: H&E). Local infection of Gram-positive cocci on the bronchus provoked hypercytokinemia and disseminated intravascular coagulation. Activated hemophagocytic macrophages (arrowheads) are distributed in the bone marrow. The kidney shows acute tubular necrosis.*

#### **13.2 Fulminant pneumococcal infection**

*Streptococcus pneumoniae* (so-called *Pneumococcus*), a capsule-forming Grampositive coccus, is a leading cause of community-acquired pneumonia. Fulminant pneumococcal infection is a life-threatening disease, resulting in DIC and multiorgan failure [131, 132]. "Purpura fulminans" represents an extreme skin manifestation of DIC and Waterhouse-Friderichsen syndrome (caused by bilateral adrenal hemorrhage). The disease is often seen in splenectomized or immunosuppressed patients [133–135], while it is also observed in healthy patients without a history of splenectomy [136].

A pregnant woman aged 20's manifested high fever and systemic skin rash. She had a history of splenectomy 10 years earlier. The total clinical course was as short as 2 days: septic shock provoked DIC and generalized petechiae. The disease represented puerperal fever. At autopsy, the uterus contained a dead fetus. The placenta contained small abscesses with infection of Gram-positive cocci with immunoreactivity of pneumococcal antigens (**Figure 47**). In the blood, α-hemolytic *Streptococcus* was isolated. Cytokine storm-related hemophagocytosis was observed in the bone marrow and spleen. Neither gangrene of the extremity nor pneumonia was associated. The final diagnosis was fulminant pneumococcal infection as a form of overwhelming postsplenectomy infection.

Another case (a 60-year-old male patient) of fulminant pneumococcal infection is displayed in **Figure 48**. Total clinical course was 3 days. The small-sized spleen was observed. Neither limb gangrene nor pneumonia was observed. The entry of *S. pneumoniae* was unclear. The glomeruli showed bacterial embolism by capsuleforming Gram-positive cocci immunohistochemically expressing pneumolysin (a pneumococcal hemolytic exotoxin). The capsule formation is visualized with the colloidal iron method that stains the acidic substances blue.

#### **13.3 Fulminant staphylococcal infection**

Community-acquired methicillin-resistant *Staphylococcus aureus* (CA-MRSA) often infects the skin and soft tissue of healthy young people. Severe invasive CA-MRSA infections include necrotizing pneumonia, necrotizing fasciitis, "purpura

fulminans" (Waterhouse-Friderichsen syndrome) and disseminated infection with septic emboli [137–139]. The severe life-threatening infection may be caused by CA-MRSA, bearing the staphylococcal cassette chromosome mec gene type IV and

*Fulminant pneumococcal infection (H&E, Gram, colloidal iron and immunostain). Systemic spread of capsule-forming Gram-positive cocci drastically killed the patient. The glomeruli show septic embolism by cocci*

*with colloidal iron-positivity (stained blue) and pneumolysin immunoreactivity (stained brown).*

*Fulminant pneumococcal infection (H&E and immunostain). In this young lady with a history of splenectomy, the placenta was the entry of Gram-positive cocci. The bacteria with immunoreactivity of pneumococcal antigens are identified in the cytoplasm of neutrophils in a small abscess among placental villi.*

**Figure 47.**

*Pathology of Gangrene*

*DOI: http://dx.doi.org/10.5772/intechopen.93505*

**Figure 48.**

**127**

#### **Figure 47.**

**13.2 Fulminant pneumococcal infection**

*distributed in the bone marrow. The kidney shows acute tubular necrosis.*

**Figure 46.**

*Pathogenic Bacteria*

without a history of splenectomy [136].

of overwhelming postsplenectomy infection.

**13.3 Fulminant staphylococcal infection**

**126**

colloidal iron method that stains the acidic substances blue.

*Streptococcus pneumoniae* (so-called *Pneumococcus*), a capsule-forming Grampositive coccus, is a leading cause of community-acquired pneumonia. Fulminant

*Fulminant streptococcal infection without septic embolism caused by erosive bronchitis (bronchus: Gram, bone marrow and kidney: H&E). Local infection of Gram-positive cocci on the bronchus provoked hypercytokinemia and disseminated intravascular coagulation. Activated hemophagocytic macrophages (arrowheads) are*

immunosuppressed patients [133–135], while it is also observed in healthy patients

A pregnant woman aged 20's manifested high fever and systemic skin rash. She had a history of splenectomy 10 years earlier. The total clinical course was as short as 2 days: septic shock provoked DIC and generalized petechiae. The disease represented puerperal fever. At autopsy, the uterus contained a dead fetus. The placenta contained small abscesses with infection of Gram-positive cocci with immunoreactivity of pneumococcal antigens (**Figure 47**). In the blood, α-hemolytic *Streptococcus* was isolated. Cytokine storm-related hemophagocytosis was observed in the bone marrow and spleen. Neither gangrene of the extremity nor pneumonia was associated. The final diagnosis was fulminant pneumococcal infection as a form

Another case (a 60-year-old male patient) of fulminant pneumococcal infection is displayed in **Figure 48**. Total clinical course was 3 days. The small-sized spleen was observed. Neither limb gangrene nor pneumonia was observed. The entry of *S. pneumoniae* was unclear. The glomeruli showed bacterial embolism by capsuleforming Gram-positive cocci immunohistochemically expressing pneumolysin (a pneumococcal hemolytic exotoxin). The capsule formation is visualized with the

Community-acquired methicillin-resistant *Staphylococcus aureus* (CA-MRSA) often infects the skin and soft tissue of healthy young people. Severe invasive CA-MRSA infections include necrotizing pneumonia, necrotizing fasciitis, "purpura

pneumococcal infection is a life-threatening disease, resulting in DIC and multiorgan failure [131, 132]. "Purpura fulminans" represents an extreme skin manifestation of DIC and Waterhouse-Friderichsen syndrome (caused by bilateral

adrenal hemorrhage). The disease is often seen in splenectomized or

*Fulminant pneumococcal infection (H&E and immunostain). In this young lady with a history of splenectomy, the placenta was the entry of Gram-positive cocci. The bacteria with immunoreactivity of pneumococcal antigens are identified in the cytoplasm of neutrophils in a small abscess among placental villi.*

#### **Figure 48.**

*Fulminant pneumococcal infection (H&E, Gram, colloidal iron and immunostain). Systemic spread of capsule-forming Gram-positive cocci drastically killed the patient. The glomeruli show septic embolism by cocci with colloidal iron-positivity (stained blue) and pneumolysin immunoreactivity (stained brown).*

fulminans" (Waterhouse-Friderichsen syndrome) and disseminated infection with septic emboli [137–139]. The severe life-threatening infection may be caused by CA-MRSA, bearing the staphylococcal cassette chromosome mec gene type IV and expressing Panton-Valentine leucocidin, an exotoxin lethal to leukocytes [140]. CA-MRSA has emerged as an important pathogen in the community worldwide.

A 70-year-old man suffering from hepatitis virus C-related liver cirrhosis complained of fever and sudden abdominal pain. He soon became septicemic and skin eruptions appeared. Blood microbial culture identified CA-MRSA. The patient died of septic shock 5 days after onset. Autopsy revealed massive septic emboli of Gram-positive cocci in systemic organs and tissues (**Figure 49**). Disseminated intravascular coagulation was associated. Hypercytokinemia activated hemophagocytosis by macrophages. No gangrene of the extremities was observed. Bacterial entry was unclear. The pathophysiological process resembled that of staphylococcal toxic shock syndrome: the bacteria secrete toxic shock syndrome toxin-1 to activate Vβ2-positive T-lymphocytes secreting cytokines [141].

Another male inpatient aged 60's suffering from liver cirrhosis received endoscopic ligation therapy for esophageal varices. The next day, he manifested high fever and hematemesis. He died of DIC and septic shock in 2 days. The entry of hospital-acquired MRSA (HA-MRSA) was the esophagus, and disseminated septic emboli provoked bilateral adrenal hemorrhage (Waterhouse-Friderichsen syndrome) and hemophagocytosis. **Figure 50** demonstrates glomerular septic emboli of MRSA and massive adrenal hemorrhage.

## **13.4 Fulminant enterococcal infection**

Enterococci may rarely cause a fulminant form of systemic infection [142–144]. Enterococcal gangrenous inflammation in the bile duct was already described in the Section 8.3. Opportunistic, necrotizing, and lethal enterococcal enteritis may be encountered in immunocompromised patients. A diabetic male patient aged 80's with acute thrombosis of the superior mesenteric artery is presented. In the surgical specimen, the transmurally necrotic small bowel wall was heavily colonized by Gram-positive and enterococcal antigens-positive cocci (**Figure 51**), and *Enterococcus faecalis* was identified by microbial culture. Formation of capsules (biofilm), rich in acidic substances, was evident with colloidal iron stain. Septic dissemination of enterococci followed to kill the patient.

**14. Gangrenous inflammation associated with uncontrolled diabetes**

*Fulminant enterococcal infection (H&E, colloidal iron, and immunostain). Enterococcal necrotizing enteritis followed acute thrombosis of superior mesenteric artery in a diabetic male patient aged 80's. In the surgical specimen, the transmurally necrotic small bowel wall is heavily colonized by Gram-positive cocci with colloidal iron-stained thick acidic capsules. Enterococcal antigens are proven. Microbial culture identified* Enterococcus

*Fulminant HA-MRSA infection (kidney: H&E, Gram, immunostain for staphylococcal antigen and PBP2*<sup>0</sup>

*septicemia (see also Figure 10). Marked adrenal hemorrhage (right panel) indicated an extreme form of DIC*

*and adrenal: H&E). Septic emboli in the glomerulus represent Gram-positive cocci with positivity for*

*staphylococcal antigens and penicillin-binding protein 2*<sup>0</sup> *(PBP2*<sup>0</sup>

*or Waterhouse-Friderichsen syndrome.*

*;*

*), immunohistochemically confirming MRSA*

As abovementioned repeatedly, diabetes mellitus predisposes gangrenous inflammation, particularly when the disease is poorly controlled. Here, three special

The external ear canal guards against infection by producing a protective layer of cerumen that creates an acidic and lysozyme-rich environment. Malignant otitis externa is a type of life-threatening infection in the aged and poorly controlled

disease situations as severe complications of diabetes mellitus are described.

**mellitus**

**Figure 51.**

**129**

**Figure 50.**

*Pathology of Gangrene*

*DOI: http://dx.doi.org/10.5772/intechopen.93505*

**14.1 Malignant otitis externa**

faecalis*. Septic systemic dissemination killed the patient.*

#### **Figure 49.**

*Fulminant CA-MRSA infection (lung and heart: H&E). Septic emboli of Gram-positive cocci are pronounced in the pulmonary artery branches. Microabscess is formed in the heart muscles.*

#### **Figure 50.**

expressing Panton-Valentine leucocidin, an exotoxin lethal to leukocytes [140]. CA-MRSA has emerged as an important pathogen in the community worldwide. A 70-year-old man suffering from hepatitis virus C-related liver cirrhosis complained of fever and sudden abdominal pain. He soon became septicemic and skin eruptions appeared. Blood microbial culture identified CA-MRSA. The patient died of septic shock 5 days after onset. Autopsy revealed massive septic emboli of Gram-positive cocci in systemic organs and tissues (**Figure 49**). Disseminated

hemophagocytosis by macrophages. No gangrene of the extremities was observed. Bacterial entry was unclear. The pathophysiological process resembled that of staphylococcal toxic shock syndrome: the bacteria secrete toxic shock syndrome toxin-1 to activate Vβ2-positive T-lymphocytes secreting cytokines [141].

Another male inpatient aged 60's suffering from liver cirrhosis received endoscopic ligation therapy for esophageal varices. The next day, he manifested high fever and hematemesis. He died of DIC and septic shock in 2 days. The entry of hospital-acquired MRSA (HA-MRSA) was the esophagus, and disseminated septic emboli provoked bilateral adrenal hemorrhage (Waterhouse-Friderichsen syndrome) and hemophagocytosis. **Figure 50** demonstrates glomerular septic emboli of

Enterococci may rarely cause a fulminant form of systemic infection [142–144]. Enterococcal gangrenous inflammation in the bile duct was already described in the Section 8.3. Opportunistic, necrotizing, and lethal enterococcal enteritis may be encountered in immunocompromised patients. A diabetic male patient aged 80's with acute thrombosis of the superior mesenteric artery is presented. In the surgical specimen, the transmurally necrotic small bowel wall was heavily colonized by Gram-positive and enterococcal antigens-positive cocci (**Figure 51**), and *Enterococcus faecalis* was identified by microbial culture. Formation of capsules (biofilm), rich in acidic substances, was evident with colloidal iron stain. Septic

*Fulminant CA-MRSA infection (lung and heart: H&E). Septic emboli of Gram-positive cocci are pronounced*

*in the pulmonary artery branches. Microabscess is formed in the heart muscles.*

intravascular coagulation was associated. Hypercytokinemia activated

MRSA and massive adrenal hemorrhage.

*Pathogenic Bacteria*

**13.4 Fulminant enterococcal infection**

**Figure 49.**

**128**

dissemination of enterococci followed to kill the patient.

*Fulminant HA-MRSA infection (kidney: H&E, Gram, immunostain for staphylococcal antigen and PBP2*<sup>0</sup> *; and adrenal: H&E). Septic emboli in the glomerulus represent Gram-positive cocci with positivity for staphylococcal antigens and penicillin-binding protein 2*<sup>0</sup> *(PBP2*<sup>0</sup> *), immunohistochemically confirming MRSA septicemia (see also Figure 10). Marked adrenal hemorrhage (right panel) indicated an extreme form of DIC or Waterhouse-Friderichsen syndrome.*

#### **Figure 51.**

*Fulminant enterococcal infection (H&E, colloidal iron, and immunostain). Enterococcal necrotizing enteritis followed acute thrombosis of superior mesenteric artery in a diabetic male patient aged 80's. In the surgical specimen, the transmurally necrotic small bowel wall is heavily colonized by Gram-positive cocci with colloidal iron-stained thick acidic capsules. Enterococcal antigens are proven. Microbial culture identified* Enterococcus faecalis*. Septic systemic dissemination killed the patient.*
