Enterococcal antigens inset are immunohistochemically demonstrated in the cocci overwhelmingly growing throughout the destroyed bile duct. Scanning electron microscopy of perforated enterococcal cholangitis. Numerous cocci, 0. Diabetes mellitus had been poorly controlled. Mild obstructive dilatation of the bile duct and gallbladder were associated. Endoscopic retrograde biliary drainage was performed, but the patient soon died of septic shock.
Autopsy demonstrated severe gangrenous and acalculous cholangitis and cholecystitis. Necrotic change with active growth of Gram-negative rods was proven in the biliary tree. Immunostaining using a monoclonal antibody disclosed the Pseudomonas aeruginosa antigen in the invasive bacilli Figure Neutrophilic reaction was relatively mild.
The lower intrapancreatic part of the common bile duct remained intact. The association of diabetes mellitus was evident: the pancreatic islets revealed pronounced deposition of amyloid substances, and the kidney showed diabetic glomerulosclerosis with nodular lesions. Diabetes mellitus accelerated severe necrotizing gangrenous inflammation of the extrahepatic biliary tree.
Neutrophilic reactions are limited. The rods are immunoreactive for a Pseudomonas aeruginosa antigen visualized with a monoclonal antibody.
Acalculous necrotizing cholecystitis was associated. Luminal obstruction of the bile duct by pancreatobiliary malignancy is often associated with bactibilia and provokes secondary ascending bacterial infection.
Enterococci often colonize the cancer tissue, and obstructive cholangitis and liver abscess may follow [ 54 ]. They are responsible for postoperative septic complications. Gram-positive cocci infected the necrotic cancer tissue. Culture of the bile was positive for Enterococcus faecalis. Colonization of culture-proven Enterococcus faecalis is demonstrated in the necrotic cancer tissue arrowheads , provoking acute intrahepatic cholangitis.
Asterisk indicates poorly differentiated adenocarcinoma. Pulmonary gangrene is a rare form of acute and severe necrotizing pneumonia [ 55 , 56 , 57 ]. A necrotic process with cavity formation is observed in a pulmonary segment or lobe. The term pulmonary gangrene is applied when a large amount of lung tissue is sloughed off. The extent of necrosis is far extensive in pulmonary gangrene when compared with usual pulmonary abscess Figure The lesion is often located in the upper lobe of the lung.
Thrombosis of large and small vessels plays a significant role in the ischemic pathogenesis. Klebsiella pneumoniae is often isolated from the gangrenous lesion. Infection of anaerobes should be the cause of foul smell. The anaerobes may secondarily infect the lung slough under the progressively anaerobic environment. Necrotizing cavity-forming pneumonia is noted in bilateral upper lobes of the lung. Foul smell was characteristic.
Gangrenous inflammation is evident histologically. Microbial culture from the lung lesion identified Bacteroides , Pseudomonas aeruginosa and Peptostreptococcus. Pseudomonal infection is indicated by arrowheads, and Gram-positive cocci probably representing Peptostreptococcus are phagocytized by neutrophils. Emphysematous pyelonephritis is a severe, multifocal, necrotizing, and gas-forming form of acute ascending bacterial infection of the renal parenchyma.
Extracapsular extension is common. The disease is most often seen in patients with poorly controlled diabetes mellitus. The common causative pathogens are Enterobacteriaceae , particularly Escherichia coli and Klebsiella pneumoniae [ 58 , 59 , 60 ]. The patient suffering from alcoholic cirrhosis manifested lumbar pain and high fever. Septic shock killed the patient.
The total clinical course was 9 days. At autopsy, both kidneys were enlarged and accompanied multifocal gangrenous changes in association with small foamy bubbles. Foul smell was not associated. Microscopically, gas formation was evident in the necrotic renal parenchyma, in association with diffuse neutrophilic infiltration Figure Numerous Gram-negative rods immunohistochemically expressing E.
Microbial culture confirmed infection of E. The condition can be categorized in non-clostridial gas gangrene. The enlarged kidney shows multifocal gangrenous changes with formation of small bubbles. Gas-forming infection of E. Renal papillary necrosis is another form of lethal renal infection of E.
The disease is characterized by coagulation necrosis of the renal medullary pyramid: the renal papillae are anatomically vulnerable to ischemic changes [ 61 ]. The patient manifested symptoms of acute pyelonephritis and died of acute renal failure.
At autopsy, the renal papillae are necrotic and demarcated with yellowish zones. Ascending infection of E. Endophthalmitis represents bacterial or fungal infection of the eyeball, as an acute illness medical emergency having up to a few days duration [ 62 , 63 , 64 ].
Patients complain of blurred vision, red eye, pain, and lid swelling. Due to progressive vitritis, hypopyon can be seen at the time of presentation. Exogenous organisms invade the eyeball via trauma, surgery, or corneal infection. When infection spreads to the adjacent orbital soft tissue, it is called as panophthalmitis. Endophthalmitis is localized to the eye, and it does not result in bacteremia or fungemia.
Streptococcal infection may be proven in the surgical specimen. Prolonged inflammation results in ophthalmophthisis Figure Gram-positive cocci, including Staphylococcus epidermidis and Streptococcus viridans , are commonly isolated after surgery for cataract or intravitreal injection. Gram-negative bacteria such as Pseudomonas aeruginosa , Hemophilus influenzae , and Moraxella catarrhalis infrequently cause endophthalmitis.
Bacillus cereus and fungi, particularly Fusarium spp. Figure 30 illustrates a surgical specimen of a Fusarium -infected eyeball. Traumatic corneal infection extended to the surrounding tissues such as the lens, palpebra, and orbit to provoke panophthalmitis. The fungal colonies on the surface microscopically reveal several-celled chained or beaded , fusiform to sickle-shaped macroconidia hyphae. The eyeball is totally collapsed and deteriorated.
Traumatic infection resulted in ophthalmophthisis. Gram-positive cocci inside the eyeball are immunoreactive for streptococcal antigens. Black melanin pigment in the iris is shown in the right bottom corner.
The corneal fungal infection extended to the lens, palpebra and orbital connective tissue. Chained or beaded several-celled appearance of hyphae is characteristic of Fusarium spp. Endocarditis-associated endogenous endophthalmitis is usually caused by Staphylococcus aureus and streptococci.
Klebsiella pneumoniae is another important pathogen for endogenous endophthalmitis. Hyperalimentation may lead to endophthalmitis caused by Candida albicans.
Most cases are categorized in the non-clostridial etiology. Clostridial infection is seen in the gastrointestinal tract and pancreas, including emphysematous pancreatitis [ 28 ], as described in the Section 6.
Vincent angina, named after the French physician Jean H. Vincent — , represents acute necrotizing ulcerative gingivitis caused by fusiform bacteria and spirochetes [ 84 , 85 ]. It is also called as trench mouth or fusospirochetosis. The patients complain of progressive painful swelling and hemorrhagic ulceration of the gum.
The punched-out ulcer, 2—4 mm in size, is seen in the interdental papilla, and is covered with white pseudomembranes. Bad breath is associated. The infection can effectively be treated with penicillin. Infrequently, Vincent angina may spread to involve the mouth and throat to be diagnosed as acute necrotizing periodontitis. Noma is a rapidly progressive and necrotizing infection of the soft and hard tissues around the oral cavity, as an advanced clinical form of Vincent angina [ 86 , 87 ].
It is also called as fusospirochetal gangrene. It represents gangrenous stomatitis or necrotizing fasciitis of the oral cavity. The preferred age of the patients is below 10 years, and the disease mostly occurs in malnourished children of African poverty. The prognosis is poor. In developed countries, severely immunosuppressed patients including acquired immunodeficiency syndrome with poor oral hygiene may suffer from this critical condition.
It begins in the form of Vincent angina, and is rapidly followed by painless and extensive necrosis of the oral cavity. Eventually, the extensive involvement of the cheek, nose, palate, and maxillary bones results in serious facial destruction.
Gas formation may be associated. In noma neonatorum, the disease manifests massive orofacial mucocutaneous gangrene in the neonate [ 88 ]. A similar disorder may be encountered in the genitalia and is called as noma pudendi. The polymicrobial etiology is known in both conditions. Gram stain smeared from the ulcer easily identifies both fusiform bacteria and long spiral-shaped spirochetes Figure The key players are anaerobic, Gram-negative fusiform pathogens, Fusobacterium nucleatum older term: Bacillus fusiformis and Prevotella intermedia.
The spiral microbes are identified as Borrelia vincentii. Many other bacteria have been co-isolated, including Porphyromonas gingivalis an anaerobic, Gram-negative, porphyrin-producing bacillary pathogen of periodontitis , Tannerella forsynthesis , Treponema denticola , Staphylococcus aureus , and nonhemolytic streptococci. Vincent angina Gram. Gram-stained smear prepared from a painful gingival ulcer demonstrates mixed bacterial infection, including Gram-negative fusiform bacilli and filamentous spiral microbes.
Gram-positive cocci and long rods are also intermingled. Numerous bacilli accompanying gas formation and immunoreactive with E. Colonies of filamentous bacteria, representing anaerobic Actinomyces spp. A gas-forming, necrotizing lesion is observed in the biopsied maxillary bone. Grocott methenamine silver stain identifies colonies of filamentous bacteria in the lesion, probably representing Actinomyces colonization.
The Gram-negative bacteria around the gas bubble are immunoreactive with a commercial antiserum against Escherichia coli , which shows wide cross-reactivity to Gram-negative bacteria the courtesy by Dr. A variety of microbes cause progressive and often lethal gangrenous lesions in the soft tissue, particularly on the extremities.
The disease affects persons of any age. In some cases, protein S deficiency may be responsible for the necrotizing inflammation. It has been reported that vimentin, an intracellular intermediate filament of nonepithelial cells, is upregulated in the injured skeletal muscle cells and functions as the major skeletal-muscle protein binding to streptococci [ 93 ].
The life-threatening gangrene follows the subacute form of necrotizing fasciitis or occurs suddenly without preexisting ulceration.
As shown in Figure 5 , an advanced, deep pocket-forming decubitus in the sacral region may cause the lethal gangrenous lesion categorized in non-clostridial gas gangrene [ 18 ]. Clinically, high fever, pain at the site of infection, and skin necrosis gangrene with hemorrhagic bulla formation are associated.
Scarlatiniform rash may be noted. Finally, massive gangrenous necrosis involves the extremity. Microscopically, pronounced myonecrosis with foci of infection of Gram-positive cocci is observed. Gram-positive cocci grow within the lesion of advancing gangrenous necrosis of soft tissue.
Cellular reactions are minimal, because of the ischemic anaerobic state with poor blood flow. In the cultured blood, short chains of Gram-positive cocci, morphologically typical of Streptococcus , are seen Figure Streptococcal septicemia provokes streptococcal toxic shock-like syndrome [ 94 ].
The bacterial exotoxins superantigens such as streptococcal pyrogenic exotoxins-A, B, C, F, and streptococcal superantigen provoke a severe cytokine storm. Hypercytokinemia activates hemophagocytosis by macrophages. Activation of NLRP3 inflammasome may be an essential event for the cytokine storm in streptococcal toxic shock-like syndrome [ 95 ].
Numerous chained cocci are demonstrated in the cultured blood. Vessels are thrombosed, and the striated muscle fibers show coagulation necrosis. Colonies of Gram-positive cocci are scattered in the ischemic tissue.
The bacteria are commonly sensitive to penicillin and its derivatives, but the intravenous antibiotics administration is clinically ineffective, principally because of the absence of blood flow. The drug can hardly reach the site of infection. Progressive gangrene of the extremities caused by infection of Vibrio vulnificus is characteristically seen in patients with liver cirrhosis or hemochromatosis [ 96 , 97 , 98 , 99 ].
High iron concentration in the serum is essential for the bacteria to grow in the body. In contrast to V. The bacteria proliferate in the gut of the sea creature when the temperature is high. Two transmission pathways of the pathogen are known: transenteric infection and traumatic skin infection.
The former septicemic condition is often fatal, initiating a painful skin lesion on the arm or leg resembling honeybee bite. Gangrenous changes of the extremity progress rapidly. Gas formation is not associated. The traumatic infection of V. The prognosis is better than the former. In a biopsy specimen sampled in an emergency suite, perivascular cuffing by infected microbes is observed around small vessels and sweat glands arrowhead in the deep dermis through subcutis.
Inflammatory reaction is sparse. Gram stain showed negativity. Lethal gangrene of the extremities or face is also caused by Aeromonas hydrophila in patients under an immunocompromised condition, with diabetes mellitus or on hemodialysis, as a form of opportunistic infection [ , , , , ]. The bacteria invade the skin via a minor trauma. Figure 35 illustrates gross features of lethal gangrene of the right upper arm caused by A.
Vesicles are formed on the necrotic skin. An outbreak of A. There were many infected scratches and pustules distributed over the bodies. Lethal gangrene is observed on the right upper arm. Vesicular skin change is evident. Autopsy confirmed that septicemia caused multiorgan abscess formation see Figure Microscopically, the lesion shows clusters of Gram-negative rods around necrotic subcutaneous tissue.
Cellular reaction is poor. In the case as shown in Figure 36 , necrotizing foci of infection were disseminated in the rectum, epididymis, prostate, liver, and kidneys. Septic embolism is noted in the rectum, while Gram-negative rods are clustered around the dilated and thrombosed vascular structure in the epididymis, where inflammatory reaction is sparse. The necrotizing change rapidly progresses to the surrounding soft tissue, eventually resulting in septicemia.
The scrotum is markedly swollen and becomes reddish-black in color Figure The penis is either involved or spared. The physiological lack of subcutaneous fat tissue in the scrotum and penis accelerates the bacterial spread. Gas production and malodor may be associated. It belongs to non-clostridial gas gangrene when gas production is noted. The preferred age ranges from 50 to 80 years.
Immunocompromised condition also accelerates the disease. Perianal abscess should be a risk factor of the disease. Masturbation-related minor penile skin injury may cause the disease in younger age [ ]. Massive hemorrhagic necrosis started from the scrotum and extended to the left hip and leg left. Marked black swelling of the scrotum is serious, and necrotizing change extends toward the perianal region right.
The rapidly progressive gangrene caused death in both patients. The penis is spared in the left case, but massively involved in the right case. Microscopically, massive necrosis of the skin tissue is evident. Mixed bacterial infection, including Streptococcus and anaerobic bacteria, is often proven. When streptococci are isolated, it is categorized in fulminant streptococcal infection Figure Secondary surface infection of Trichosporon spp. Debridement specimen discloses massive transmural necrosis of the scrotal tissue.
Gas bubbles are scattered in the heavily infected necrotic tissue. Gram-positive cocci are immunoreactive for streptococcal antigens. This case represents fulminant streptococcal infection with gas formation non-clostridial gas gangrene.
As illustrated in Figure 39 , fulminant necrotizing inflammation involved the lower part of the rectum in a female patient suffering from myelodysplastic syndrome. Emergency surgery disclosed transmural gangrenous necrosis of the rectal wall with massive mixed bacterial infection, including E. Gram-negative rods are immunoreactive for E. Necrotizing fasciitis represents clinically severe pyogenic infection cellulitis of the skin and underlying soft tissue [ , , , , ].
Deep, painful, and intractable ulceration subacutely progresses predominantly on the extremities Figure Minor trauma may provide the entry for pathogens. The condition uncommonly follows surgical procedures. Diabetes mellitus, immunosuppression, alcoholism, drug abuse, atherosclerosis-related ischemia, and malnutrition may be prodromal to this troublesome condition.
It may be seen in healthy persons [ ]. Necrotizing fasciitis is categorized into two types: type I polymicrobial infection and type II monobacterial infection. Deep and painful ulceration is caused by local and invasive bacterial infection.
This aged male diabetic case had a history of arterial replacement therapy for atherosclerosis obliterans. In order to relieve pain and to avoid septicemic spread of infection, amputation surgery was performed. Necrotizing inflammation extends to the striated muscle layer. In Figure 41 , necrotizing fasciitis seen in a poorly controlled diabetic male patient is presented. In the wintertime, a fan heater gave the patient a severe burn on his sole, because he did not feel pain sensation due to diabetic peripheral neuropathy.
The doctor-shy patient did not visit a hospital for 1 week, and this allowed the lesion far progressed. Severe atherosclerosis had provoked dry gangrene in his 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 diabetes mellitus should be emphasized. 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. The importance of foot care in diabetic patients should be emphasized. Infrequently, necrotizing fasciitis is caused by Pseudomonas aeruginosa [ , ].
Clinicians should consider empiric pseudomonal antibiotic coverage for preventing the progression of necrotizing limb infection. An 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 features are illustrated in Figure Massive bacterial growth provoked little inflammatory reaction. The bacteria are immunoreactive for Pseudomonas aeruginosa antigen detected by a monoclonal antibody the courtesy by Dr.
Erythematous nodular lesions formed on the leg of neutropenic or leukemic patients were caused by Stenotrophomonas maltophilia [ ]. Facial cellulitis may result from Haemophilus influenzae infection [ ].
Gram-positive cocci occasionally provoke fulminant, lethal systemic infection without gangrene of the extremities. The pathophysiology resembles that of flesh-eating bacteria infection, accompanying pronounced hypercytokinemia and poor cellular reactions. Streptococcal, pneumococcal, staphylococcal, and enterococcal etiologies are described below.
Streptococcal toxic shock syndrome provokes an aggressive lethal condition without predisposing diseases [ , ].
It should be of note that fulminant group A streptococcal infection is also encountered in cases without gangrenous lesions of the extremities [ ]. 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 Necrotizing endometritis in a puerperal lady was the cause of streptococcal toxic shock-like syndrome, as illustrated in Figure It can be categorized in so-called puerperal fever.
Pregnancy-associated lethal infection should be of particular notice [ ]. 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 [ ]. Summary of five autopsy cases of fulminant streptococcal infection without gangrene of the extremities [ ]. Massive hemorrhagic cystitis is evident.
The cocci infected in the eroded bladder wall are immunoreactive for streptococcal antigens. Fulminant streptococcal infection with necrotizing endometritis in a 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. There are two different pathological mechanisms in fulminant streptococcal infection without gangrene of the extremities [ ].
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 [ ] Figure Another form without bacterial embolism was featured by bacterial toxin-induced hemophagocytosis by activated macrophages, reflecting a hypercytokinemic state [ ] Figure 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 [ ].
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 ]. 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.
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. 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. Streptococcus pneumoniae so-called Pneumococcus , a capsule-forming Gram-positive coccus, is a leading cause of community-acquired pneumonia.
Fulminant pneumococcal infection is a life-threatening disease, resulting in DIC and multiorgan failure [ , ]. The disease is often seen in splenectomized or immunosuppressed patients [ , , ], while it is also observed in healthy patients without a history of splenectomy [ ]. 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 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. 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. Another case a year-old male patient of fulminant pneumococcal infection is displayed in Figure Total clinical course was 3 days.
The small-sized spleen was observed. Neither limb gangrene nor pneumonia was observed. The entry of S. The glomeruli showed bacterial embolism by capsule-forming 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.
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. 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 [ ].
A 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. 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 Disseminated intravascular coagulation was associated. Hypercytokinemia activated hemophagocytosis by macrophages. No gangrene of the extremities was observed. Bacterial entry was unclear. Septic emboli of Gram-positive cocci are pronounced in the pulmonary artery branches. Microabscess is formed in the heart muscles. The next day, he manifested high fever and hematemesis.
He died of DIC and septic shock in 2 days. Figure 50 demonstrates glomerular septic emboli of MRSA and massive adrenal hemorrhage. Marked adrenal hemorrhage right panel indicated an extreme form of DIC or Waterhouse-Friderichsen syndrome.
Enterococci may rarely cause a fulminant form of systemic infection [ , , ]. Enterococcal gangrenous inflammation in the bile duct was already described in the Section 8. Opportunistic, necrotizing, and lethal enterococcal enteritis may be encountered in immunocompromised patients. 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.
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. As abovementioned repeatedly, diabetes mellitus predisposes gangrenous inflammation, particularly when the disease is poorly controlled.
Here, three special disease situations as severe complications of diabetes mellitus are described. 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 diabetic patients. Those immunocompromised patients who suffer from acquired immunodeficiency syndrome, undergo chemotherapy, and take immunosuppressant medications such as glucocorticoids may also be vulnerable to this serious disease [ , , , , ].
Once infection becomes established in the external meatus of the susceptible patient, the bacteria invade the underlying structures of the soft tissue and destroy the temporal bone, and finally resulting in septicemia. Pseudomonas aeruginosa is the inciting organism in the vast majority of cases. Features of biofilm infection by Gram-negative rods are characteristic.
The biopsy histology is illustrated in Figure Fungal etiology is also known, and Aspergillus and Candida can be the causative microbes. Myxoid matrix of the colony indicates biofilm infection. Gram-negative rods are demonstrated in the smear preparation. Mucormycosis zygomycosis is infection by the class Zygomycetes , mainly Mucor ramosissimus, Rhizomucor pusillus and Rhizopus oryzae.
Sixteen species of Zygomycetes infect the human. Zygomycetes mucoral fungi are common molds growing in a moist environment. Fungi commonly have chitin as structural polysaccharide, but Zygomycetes synthesize chitosan, a deacetylated homopolymer of chitin. The main sites of localized mucormycosis are the lung and paranasal cavity. Formation of conidiophores is rarely encountered in case of paranasal cavity infection. The gross features of systemic mucormycosis represent hemorrhagic infarction of the involved tissues and organs [ ].
Microscopically, faintly basophilic and wide hyphae, showing the lack of septum formation and wide angle of lamification, are seen in the mycotic thrombus. Stamp smear preparations Figure 53 reveal typical microscopic morphology of mucormycosis. Infection of Zygomycetes is microscopically featured by angioinvasiveness and weak reactivity with Grocott staining, as illustrated in Figure However, some lesions of mucormycosis reveal clear basophilia with strong Grocott reactivity refer to Figure 57 , displaying neonatal intestinal mucormycosis.
Formation of conidiophores in the paranasal cavity and stamp cytology preparation of cerebral mucormycosis in a pediatric acute leukemia case. It needs urgent treatment to halt the spread of tissue death as rapidly as possible. Diabetes is linked to gangrene. Diabetic neuropathy , or nerve death, can mean that a person has an injury and does not notice it.
Diabetes also affects the small arterial vessels and they become insufficient to supply the extremity. Dry gangrene is sometimes called mummification.
It starts more slowly than wet gangrene, and it is most commonly associated with chronic disease, including diabetes. The skin becomes dry, shriveled, and usually dark in color, ranging from brown to purplish-blue and feels cool or cold to touch.
Blood vessel diseases such as atherosclerosis commonly cause dry gangrene. In wet or moist gangrene, the skin swells and blisters form and may rupture. Pus may appear. It is generally associated with infection of the dead tissue. Wet gangrene can develop following a severe burn or frostbite. This type of gangrene can occur in people with diabetes who have an injury but do not notice or attend to it due to diabetic neuropathy.
Gas gangrene, also called clostridial myonecrosis, is a particularly virulent form of wet gangrene. It is associated with poorly cleansed wounds. It sometimes results from surgery in which the blood supply has become damaged. Dry forms result from a progressive loss of blood supply to tissues. Dry forms can become wet forms if they develop a bacterial infection. All forms of gangrene happen because of a loss of blood supply to a certain area.
This deprives tissue of oxygen and nutrients, causing the tissue to die. Wet forms can develop from :. Risk factors for gangrene include :. The part will be cold to the touch, and there will be a loss of pulse in the arteries. There may not be any external signs of internal gangrene, but the following may occur as a result of septic shock and other complications:. Gas gangrene can produce all of these symptoms, and others.
The infected area of skin can quickly extend, with some changes visible within minutes. In gas gangrene, the skin may :. This is known as subcutaneous emphysema. The gas is produced by the infectious bacteria and is highly toxic, causing the necrosis to spread quickly.
A doctor will carry out a physical examination and take a medical history, to find out about symptoms and potential exposure to infection or trauma.
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