**8.6 Endophthalmitis**

Endophthalmitis represents bacterial or fungal infection of the eyeball, as an acute illness (medical emergency) having up to a few days duration [62–64]. 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. Patients with Hansen's disease (leprosy) are highly susceptible to traumatic eyeball infection. Streptococcal infection may be proven in the surgical specimen. Prolonged inflammation results in ophthalmophthisis (**Figure 29**). Grampositive cocci, including *Staphylococcus epidermidis* and *Streptococcus viridans*, are commonly isolated after surgery for cataract or intravitreal injection. Gramnegative bacteria such as *Pseudomonas aeruginosa*, *Hemophilus influenzae*, and *Moraxella catarrhalis* infrequently cause endophthalmitis. *Bacillus cereus* and fungi, particularly *Fusarium* spp., are the major cause of post-traumatic endophthalmitis [65]. **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).

Endocarditis-associated endogenous endophthalmitis is usually caused by *Staphylococcus aureus* and streptococci. *Klebsiella pneumoniae* is another important

#### **Figure 28.**

*Renal papillary necrosis in a male patient aged 60's with uncontrolled diabetes mellitus (gross and H&E). 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. coli *was associated.*

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 27**). Numerous Gram-negative rods immunohistochemically expressing *E. coli* antigens are clustered within the necrotic renal tubules and around gas-filled bubbles. Microbial culture confirmed infection of *E. coli*. The condition can be categorized in

E. coli*-infected emphysematous pyelonephritis in a diabetic male patient aged 70's (gross, H&E and immunostain for* E. coli *antigens). The enlarged kidney shows multifocal gangrenous changes with formation of small bubbles. Gas-forming infection of* E. coli *is evident both histologically and immunohistochemically in*

*Pulmonary gangrene (gross, H&E, Gram). 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*

non-clostridial gas gangrene.

Peptostreptococcus*) are phagocytized by neutrophils.*

**Figure 26.**

*Pathogenic Bacteria*

**Figure 27.**

**112**

*severe acute purulent pyelonephritis.*

**9. Vincent angina and noma (cancrum oris, gangrenous stomatitis)**

periodontitis.

*Pathology of Gangrene*

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

**Figure 31.**

**115**

*cocci and long rods are also intermingled.*

Vincent angina, named after the French physician Jean H. Vincent (1862–1950), 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

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. Hence, the name of "cancrum oris" (meaning oral cancer). Gas formation may be associated. In noma neonatorum, the disease manifests massive orofacial (mucocutaneous) gangrene in the neonate [88]. A similar disorder

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 31**). 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*

may be encountered in the genitalia and is called as noma pudendi.

#### **Figure 29.**

*Endophthalmitis in a leprosy patient (gross, H&E and immunostain). 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.*

#### **Figure 30.**

*Traumatic ophthalmitis caused by* Fusarium *infection in a Cambodian teenager (gross and H&E). 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. (the courtesy of Dr. Chhut Vanthana, a pathologist at Sihanouk Hospital Center of HOPE, Phnom Penh, Cambodia).*

pathogen for endogenous endophthalmitis. Hyperalimentation may lead to endophthalmitis caused by *Candida albicans*.

### **8.7 Gangrenous/emphysematous inflammation in other organs**

Gangrenous/emphysematous inflammation may occur in the stomach [33, 66] (see **Figures 16** and **17**), esophagus [67], colorectum [68] (see **Figures 15** and **18**), urinary bladder [69, 70], ureter [71], urethra [72], penis [73], epididymis/testis [74, 75], endometrium [76], vagina [77], breast [78], bone [79], striated muscle [80], aorta [81], mediastinum [82], and endocardium [83]. Most cases are categorized in the nonclostridial etiology. Clostridial infection is seen in the gastrointestinal tract and pancreas, including emphysematous pancreatitis [28], as described in the Section 6.2.
