**7. Non-clostridial gas gangrene**

Gas gangrene is commonly caused by clostridial infection, but non-clostridial bacteria may also provoke gas gangrene mostly in the extremities [36–38]. Early diagnosis and therapy are required, because the disease rapidly progresses to fatal toxemia. This unique dermatologic emergency is featured by the detection of nontraumatic subcutaneous emphysema of the leg with or without association of

#### **Figure 17.**

Clostridium butyricum*-induced lethal gastric gas gangrene (gross, H&E and Gram). The gastric wall demonstrates formation of gas bubbles both grossly and microscopically. The growing Gram-positive rods exhibit distinct spore formation in rugby ball-shaped bacterial bodies, morphologically consistent with* C. butyricum *(the courtesy of Dr. Mayu Fukushima, a pathologist at Hamamatsu Medical University Hospital, Hamamatsu, Japan).*

and peritonism occur. Acute appendicitis is caused by the blockage of the

*liver are immunoreactive with a monoclonal antibody against* E. coli *antigen (inset).*

displayed in **Figure 19**.

**107**

**Figure 18.**

*Pathology of Gangrene*

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

**8.2 Gangrenous and emphysematous cholecystitis**

appendiceal lumen (most commonly by fecalith impaction). The blockage results in increased luminal pressure, impaired blood flow, and invasive infection of bacterial flora. When the gangrenous process proceeds, rupture of the appendix can result [44–46]. Mixed bacterial infection is proven. Causative pathogens include

E. coli*-induced non-clostridial gas gangrene accompanying foamy liver seen in a diabetic male patient aged 70's with advanced rectal adenocarcinoma (gross and H&E, inset: immunostain). Transportal infection of* E. coli *provoked foamy liver due to gas formation by the infected bacteria. The rods embolic in capillary vessels of the*

*Escherichia coli*, *Bacteroides fragilis*, *B. splanchnicus*, *B. intermedius*, *Peptostreptococcus*, *Pseudomonas*, *Lactobacillus*, *Bilophila wadsworthia*, *Fusobacterium nucleatum*, *Eggerthella lent*a, and *Streptococcus anginosus* (or *milleri*) group. An average of 10.2 different microorganisms have been isolated from the infected lesion. Microscopically, the appendiceal wall reveals marked transmural collection of neutrophils and massive necrosis with the disappearance of the proper muscle layer. Colonization of cocci and rods is easily observed within the gangrenous lesion. Fibrinopurulent peritonitis is associated. Medium-sized blood vessels are thrombosed, accelerating the gangrenous change. Representative findings are

Gangrenous cholecystitis is defined as infection-associated transmural necrosis and perforation of the gallbladder wall, as a result of secondary ischemia due to vascular thrombosis. Mural necrosis (infarction) provokes perforation in 25% of cases. Gangrenous cholecystitis represents a form of acute acalculous cholecystitis (**Figure 20**), and the pathology and epidemiology differ from chronic cholecystitis induced by gallstones [47–49]. *Enterobacteriaceae* and anaerobic bacteria are frequently cultured from the bile. The mortality rate is high between 15 and 50%. Risk factors for the development of gangrenous cholecystitis include male sex, advanced

Emphysematous cholecystitis is a fulminant and sinister form of acute gangrenous cholecystitis, and it is characterized by the presence of gas both in the lumen (pneumobilia) and wall of the gallbladder. Gas may be extended to the biliary tree or adjacent structures. Either clostridial or non-clostridial etiology is encountered [50]. In case of non-clostridial infection, mixed infection of rods and cocci is often proven microscopically (**Figure 21**). Emphysematous cholecystitis, a form of gas

age, delayed surgery, cardiovascular diseases, and diabetes mellitus.

erythema, tenderness, or bullous lesions. Non-clostridial gas gangrene most often results from polymicrobial infection of mixed kinds of microbes, and it is mainly seen in diabetic patients [39–41]. The causative gas-producing bacteria include *Escherichia coli*, *Klebsiella pneumoniae*, *Enterobacter cloacae*, *Pseudomonas aeruginosa*, *Aeromonas hydrophila*, *Bacteroides* spp., and *Streptococcus anginosus* group (former *S. milleri* group) [42]. Groups A, B, and G streptococci also cause gas gangrene, as a form of fulminant streptococcal infection [43], as described in the Section 10.1. **Figure 5** illustrates the gas-forming fulminant group A β-hemolytic streptococcal infection, caused by a deeply ulcerated (pocket-forming) decubitus at the sacral region of a 72-year-old diabetic woman. Another diabetic male patient aged 70's with advanced rectal adenocarcinoma suddenly manifested nontraumatic and nonclostridial gas gangrene in the abdominal cavity. Massive transportal infection of gas-forming *E. coli* resulted in the formation of foamy liver (**Figure 18**). Intrahepatic vascular-invasive growth of Gram-negative rods was observed under a microscope, and infection of *E. coli* was immunohistochemically confirmed.

Emphysematous (gas-producing) inflammation may be encountered in a variety of organs and tissues, as described in the next section.
