**3. Wet gangrene**

In the present review article, pathologic features of varied gangrenous lesions are illustrated. In addition to gross findings, microscopic features are presented mainly with hematoxylin and eosin (H&E) and Gram stains. When needed, immunohistochemical approach is combined [1, 2]. Immunostaining using rabbit antisera raised against *Bacillus* Calmette-Guérin (BCG; *Mycobacterium bovis*), *Bacillus cereus*, *Treponema pallidum*, and *Escherichia coli* is employed. These low-specificity (widely cross-reactive) antimicrobial antisera effectively yield clear high-sensitivity signals with a low background [3, 4]. Please visit the author's Website at https://pathos223.

Dry gangrene represents coagulative necrosis of ischemic tissue, caused by inadequate blood supply due to peripheral artery disorders. The term dry gangrene is used only for necrosis of the acral limb [6, 7]. Patients with atherosclerosis, hypercholesterolemia, and diabetes mellitus are susceptible to dry gangrene, particularly when they smoke. The low local oxygen level provokes putrefaction without bacterial growth. The affected portions become dry, solidified, and reddish black (**Figure 1**). Once gangrene has developed, the affected tissue is no longer salvageable. The boundary of the dried lesion is sharply demarcated from the nonischemic skin so that autoamputation may follow [8]. Because of the lack of infection, dry gangrene is not so emergent as wet gangrene and gas gangrene. However, dry gangrene may develop to wet gangrene when the secondary infection happens. Diabetes mellitus is a serious and the most important risk factor for

*Dry gangrene (gross appearance of two cases). Atherosclerosis-induced dry gangrene is seen in the foot (left). The border of necrotic lesion is relatively sharp. In the right panel, the toes of a diabetic patient are dry and blackcolored, and wet gangrene with red swelling and epidermal blister formation followed (the courtesy of Drs. Mitsuhiro Tachibana and Yasuhito Kaneko at Department of Diagnostic Pathology and Dermatology, Shimada*

com/en/ [5].

*Pathogenic Bacteria*

**Figure 1.**

**96**

*Municipal Hospital, Shimada, Japan).*

**2. Dry gangrene**

developing both dry and wet gangrenes.

Wet or infected gangrene is featured by bacterial infection of the necrotic tissue, and secondary sepsis accompanies a poor prognosis when compared with dry gangrene [9–11]. The affected part becomes markedly edematous, soft, rotten, and dark. Blisters filled with turbid fluid are formed on the discolored and cold-ontouch skin (**Figure 2**). Secondary infection of Gram-positive cocci is common. Infection of saprogenic (anaerobic) bacteria causes a foul smell. Gas formation is often associated, eliciting crepitation on touch. Causative bacteria are polymicrobial or monobacterial. In case of monobacterial infection by *Clostridium perfringens*, we call the status as clostridial gas gangrene. Wet gangrene rapidly progresses via the blockage of blood flow, and the hypoxic stagnant blood promotes rapid growth of anaerobic bacteria that often release exotoxins. The mortality rate of wet gangrene is high so that emergency salvage amputation is often necessary. Disseminated infection (sepsis) eventually leads the patient to death. The predisposing disorders for developing wet gangrene include diabetes mellitus, arteriosclerosis obliterans (atherosclerotic arterial obstruction), and calciphylaxis/calcific uremic arteriolopathy or "gray scale" (painful and intractable ulcers caused by arteriolar wall calcification in patients with chronic renal failure under dialysis).

Several lethal conditions described below are encompassed in the category of wet gangrene. These include polymicrobial necrotizing fasciitis, gas gangrene, Fournier's gangrene, fulminant streptococcal infection, *Vibrio vulnificu*s infection, and *Aeromonas hydrophila* infection.
