Appendiceal actinomycosis presenting as acute appendicitis: A diagnostic and therapeutic challenge
SP Tendulkar1, PA Jain1, MG Mehta1, S George2
Correspondence Address:
Dr. S P Tendulkar
Department of General and Minimal Access Surgery, Sir H.N. Reliance Foundation Hospital and Research Centre, Mumbai, Maharashtra
India
Source of Support: None, Conflict of Interest: None
CheckDOI: 10.4103/jpgm.jpgm_196_22
A 31-year-old female presented with complaints of right lower abdominal pain and vomiting for 2 days. Abdominal examination revealed tenderness at McBurney's point. Laboratory findings were normal, except for a white blood cell count of 18,000/mm3 with a neutrophilic predominance and a C-reactive protein level of 2.5 mg/L. Computed tomography (CT) of the abdomen was suggestive of acute retrocecal appendicitis without any regional lymphadenopathy [Figure 1]a and [Figure 1]b. The patient was posted for an emergency appendectomy. Intra-operatively, the appendix was mildly inflamed with thickened mesoappendix. The cecal pole was especially thickened disproportionate to the extent of surrounding inflammation [Figure 1]c and [Figure 1]d. The rest of the small and large intestine was grossly normal. The right colon was mobilized and appendectomy along with excision of the cecal pole was done. The cecal wall was approximated and reinforced with 3–0 polydioxanone suture in two layers. The patient recovered well postoperatively and was discharged subsequently. Histopathological examination showed acute gangrenous appendicitis with clumps of basophilic filamentous bacteria on the mucosal surface and within the mucosa. Special stains showed gram-positive and acid-fast negative filamentous organisms consistent with actinomycosis [Figure 2]a, [Figure 2]b, [Figure 2]c, [Figure 2]d. Hence, the patient was prescribed intravenous penicillin for 6 weeks followed by oral therapy for 6 months. After 24 months of follow-up, the patient had no postoperative complications or any long-term morbidity.
Figure 1: (a and b) Contrast-enhanced CT Abdomen: Coronal and axial images showing fluid-filled distended [21 mm in diameter] appendix containing two calcific appendicoliths with annular mural thickening and hyperenhancement (arrowed), (c and d) Showing the thickened base of the appendix (arrowed)Figure 2: (a) Focus of actinomycosis with surrounding inflammatory cells (arrowed, H and E stain, original magnification ×10), (b) Gram-positive actinomycotic colony (arrowed, gram stain, original magnification ×10), (c) Acid-fast negative bacteria (acid-fast stain, original magnification ×10), (d) Focus of actinomycosis with surrounding inflammatory cells (arrowed, H and E stain, original magnification ×100Actinomycosis is a subacute–chronic bacterial infection affecting the soft tissues and internal organs of the body. The most common pathogen that causes actinomycosis in humans is Actinomyces israelii. These organisms are indigenous to the oral cavity, gastrointestinal tract, and genital tract.[1],[2],[3] Although A. israelii is a non-pathogenic bacterium, mucosal injuries that disrupt the mucosal barriers, like perforated appendicitis, perforated diverticulitis, Crohn's disease, and intestinal perforation due to bone or fishbone, allow the microorganism to reach deep planes, resulting in actinomycotic infections. Involvement of distant organs is possible via the hematogenous spread, leading to the formation of metastatic abscesses in the liver. However, because of the size of the bacterium, it usually does not spread via the lymphatic system; therefore, regional lymphadenopathy is uncommon or develops late.[1],[2] Actinomycosis commonly occurs in three distinct forms that may occasionally overlap; most clinical disease is cervicofacial (50–55%), followed by 20% occurring in the abdominopelvic form and 15% in the thoracic form.[2],[3],[4] Abdominopelvic actinomycosis is associated with longstanding intrauterine devices, trauma, or any abdominal surgery which is associated with a breach in bowel mucosal integrity.[1],[2],[3] Other known predisposing systemic factors include malnutrition, immunosuppression, and acquired immunodeficiency syndrome. The present case did not have any known local or systemic predisposing factors. Abdominopelvic actinomycosis commonly involves the appendix and the terminal ileum (65% of cases).[3],[4] However, the colon, stomach, liver, gallbladder, pancreas, pelvis, and abdominal wall may also be involved.[2],[5],[6] Appendiceal actinomycosis is one of the rare causes of acute appendicitis with an incidence of 0.02–0.06% of all appendicitis cases. CT features of abdominopelvic actinomycosis are nonspecific, which can range from the bowel wall thickening to an infiltrative mass adjacent to the other involved organs.[1],[2] Definite diagnosis of the disease is often made with the intraoperative or postoperative histopathological examination, like in the present case. Preoperative diagnosis is possible in only 10% of the cases, usually following examination of aspiration or biopsy material obtained under CT guidance.[1],[3] Surgical excision remains the mainstay of therapy. The intense desmoplastic reaction, associated with actinomycosis, limits drug penetration and thereby, warrants high-dose long-term antibiotic therapy.[1],[3] The preferred antibiotic treatment includes intravenous high-dose crystalline penicillin G (2–4 weeks) followed by long-term (6–12 months) oral penicillin or semi-synthetic penicillin derivatives. For patients allergic to penicillin, tetracycline, erythromycin, and clindamycin are accepted and efficient alternatives.[3] Abdominopelvic actinomycosis is associated with a high recurrence rate, increased risk of intestinal fistulization, and localized abscess formation, if not detected or treated inadequately, which can result in significant long-term morbidity and delayed healing. In view of anecdotal evidences with regards to its long-term complications and follow-up, the patient was kept under surveillance for 24 months.
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Conflicts of interest
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