Atypical mycobacteria have been known to colonize tap water, natural waters, and soil and thus can easily contaminate solutions and disinfectants used in hospital settings. These infections have thus been a source of significant morbidity for patients recovering from laparoscopic surgeries [1]. Erroneous sterilization of laparoscopic instruments is almost always responsible for such outbreaks and

makes it a problem mainly affecting developing countries, such as India. Thus, proper sterilization of such instruments is essential to prevent the occurrence of post laparoscopic wound infections with atypical mycobacteria [2].

Port site infection is a preventable complication of laparoscopic surgery, which nullifies the advantages of this technique over conventional surgery [3]. Despite advances in anti-microbial treatments, sterilisation techniques, and operation theatre environments, surgical wounds are still susceptible to infections. The infection is not associated with the technique of primary port entry [4]. Many species of Mycobacteria, including the fortuitum-chelonae complex, are known to cause diseases in humans and animals[5].

Port Site Infections (PSI) after laparoscopic surgeries is approximately 21/100,000 cases [6]. Immuno-compromised states (diabetes, steroid use, chronic kidney diseases, etc.), pre-operative stay >2 days, operative duration >2 h are the predisposing factors for PSI [7-9]. PSI can be classified into two categories depending upon the timing of their presentations. The First type or Early PSI occurs immediately within seven days of surgery, usually caused by gram negative or positive bacteria acquired during surgery either from the infected organs or the skin. Such infections can be treated by common antibiotics and antiseptic dressings. The second type or Delayed PSI usually presents after few weeks of the laparoscopic surgery. Delayed PSI caused by atypical mycobacteria with an incubation period of 3–4 weeks, and such PSI do not respond to the common antibiotics [10]. PSI due to atypical mycobacteria following laparoscopic surgery differ in terms of clinical manifestations, diagnosis and management. The presentation of atypical mycobacterial infections can be illustrated in five stages.

First stage: A tender nodule appears in the vicinityof the port site, and its usual timing of appearance is around four weeks following the surgery.

Second stage: Increase in the size of the noduleand increased tenderness of the site along with other signs of inflammation with eventual formation of adischarging sinus.

Third stage: Reduced pain sensation following dischargeof the purulent material and necrosis of the skinsurrounding the port site.

Fourth stage: Chronic sinus discharging white or serous fluid.

Fifth stage: Hyper-pigmentation of the skin surrounding the sinus and appearance of multiple nodules at different places.

We retrospectively studied the records of patients who were treated for port site infections in our hospital between1st March 2020 to 30 November February 2024. We divided our patients into two groups depending on the treatment they had received.

Group A constitutes our early port-site excision group. These patients underwent excision of infected port-sites on diagnosis and were put on antimicrobial treatment (Clarithromycin and ciprofloxacin) concurrently (Pic 1a and 1b). All excised port-site tissues were sent for histopathological examinations (pic 3a and 3b).Group B constitutes of patients who were treated with standard medical management using antibiotic regime of Clarithromycin and Ciprofloxacin. Variables like age, sex, type of index surgery, incubation period, size of port site infected and complications for each group were recorded. All patients were followed up for 6 weeks after complete resolution of symptoms/wound healing (Pic 2a and 2b). We compared two groups for demographic and clinical characteristics, infection characteristics and treatment response and complication / outcomes using online software tools.

The variables collected for both the groups are summarized in table 1.

Results of comparative analysis of two groups in different categories are as follows:

Demographic and Clinical Characteristics

The median age of patients was similar across both groups 43.4 years in group A versus 47.2 years in group B, Females constituted the majority of patients in both groups (87.5% in Group A, 78.6% in Group B), with no significant difference in gender distribution (p = 0.47, Chi-square test).

Laparoscopic cholecystectomy was the most commonly associated procedure in both groups (79.2% in Group A vs. 50% in Group B), followed by laparoscopic appendectomy and gynecological surgeries. Though more diverse procedures were present in Group B, the distribution was not statistically significant (p = 0.12, Fisher’s exact test).

Infection Characteristics and Treatment Response

The median incubation period from surgery to symptom onset was 32 days (range: 20–44 days) in Group A and 40.5 days (range: 30–46 days) in Group B. This difference was statistically significant (p = 0.031, Mann–Whitney U test), meaning that surgical excision group had a shorter incubation period. Port site involvement was higher at the 10 mm sites, with 43 sites infected in Group A and 21 in Group B. Involvement of 5 mm sites was minimal in both groups. Group B had a longer average duration of antibiotic therapy (80 days, range: 54–88 days) compared to Group A (43 days, range: 32–54 days), a difference that was statistically significant (p < 0.001, independent T-test).

Complications and Outcomes

Group B showed a higher complication rate. Two cases of incisional hernia were reported exclusively in Group B. Hypertrophic scars were seen in three patients from Group A and one from Group B. One case of keloid formation occurred in Group A. Notably, seven patients in Group B required delayed surgical excision due to persistent symptoms, while no such delays were observed in Group A (p < 0.001, Fisher’s exact test).

Recurrence occurred in one patient in Group A and none in Group B. Though not statistically significant (p = 1.00, Fisher’s exact test), the low recurrence rate in both groups may reflect adequate long-term response once complete treatment was implemented.

Port-site infections are primarily of two types. The first type occurs immediately within a week of surgery. It is caused by gram negative or positive bacteria derived from infection acquired during surgery from the infected gall bladder or from the skin or the surgical procedure itself and can be treated by common antibiotics and local wound dressing. The second type is caused by atypical mycobacteria which includes the group of mycobacterial species that is not part of the M.tuberculosis complex and has an incubation period of 3to 4 weeks and do not respond to common antibiotics [10].Our study is about the second type of infection.

In our study, after laparoscopic surgery the infection started at the 10 mm ports. Umbilical port is the first port to get infected followed by epigastric port. In all laparoscopic Cholecystectomies both umbilical and epigastric ports were infected. Infection was less common in 5mm lateral ports. In laparoscopic procedures, the infection starts at the 10 mm port sites such as the epigastric or umbilical ports after which it spreads sequentially to the other ports [11].Infections with atypical mycobacteria have been primarily reported after laparoscopic procedures [12, 13]. This is because, unlike open surgery, the instruments used here have a layer of insulation that restricts the use of the autoclave in the sterilization process. Contaminated instruments deposit the endospores on to the subcutaneous tissue during the surgical process, which then germinate following which clinical symptoms appear after an incubation period of 3 to4 weeks. The current practice in India is to immerse instruments in 2–2.5% glutaraldehyde solution for 20minutes which achieves disinfection but not sterilization. Furthermore, the source of infection is often the tap water used for cleansing of the instruments after surgery [11].

In our study all patients were started on treatment (port-site excision or medical management) on clinical diagnosis, since culture of the pus collected from the port sites is negative for mycobacterial culture and AFB staining. The only method to obtain microbiological evidence is through tissue culture from the wall of the cavity, which is very difficult to obtain and takes 3 weeks to isolate from culture leading to delayed treatment, which makes clinical diagnosis the best option [11].

All our patients including early excision group received combination therapy with Clarithromycin and Ciprofloxacin. Management of PSIs with atypical mycobacteria lacks consensus. They respond poorly to first lineanti-tubercular drug treatment. Second line ant tubercular drugs including macrolides (clarithromycin), quinolones (ciprofloxacin), tetracyclines (doxycycline) and aminoglycosides (amikacin and tobramycin) in various combinations have been used with promising results [14, 15, 16]. Macrolides including clarithromycin are the only group of antimicrobials active against M.chelonaeand M. abscessus[16]. Mycobacterium fortium-chelonaecomplex has shown resistance to antibiotics because of mutation in the porin channels present in the bacterial wall, which is the site for entry of antibiotic molecules for antimicrobial activity [15, 17]. Linezolid was found to be active against M. chelonaeand has been successfully used for treatment, alone or as combination therapy [18]. We followed the antibiotic combination as given by Chaudhuri et al since the method of diagnosis was same [15].

As summarized in table 1, laparoscopic cholecystectomy was the most common procedure associated with PSI. This is attributed to the fact that this procedure by far is the most common procedure performed at our centre. patients treated with early port-site excision required medical treatment for a smaller number of days (43 Vs80) suggestive of lower morbidity of patients in this group. One patient of TAPP had PSI with AMT and the infection extended to include mesh used which required open re-exploration and mesh removal. One elderly male patient whose infection resolved with antibiotic treatment alone, developed umbilical and epigastric port-site hernia after 6months. This indicates that prolonged ATM infection can be a factor responsible for incisional hernia among others. Not much significant difference was seen about complications. Delayed port-site excision (after 6 weeks of antibiotic treatment) was required in 50% of patients in Group B due to non-resolution of symptoms or progression of disease. In our study results of early port-site excision are promising and may be associated with less morbidity and early return to normal life as seen with other studies [. However, it is imperative that more studies preferably RCTs are done to confirm or refute the same.

Port-site infections caused by atypical mycobacteria (ATM) present a significant post-laparoscopic complication, characterized by delayed onset, resistance to standard antibiotics, and potential for prolonged morbidity. In this study of 38 patients, early surgical excision of infected port sites (Group A) led to faster resolution and fewer severe complications compared to those initially managed with antibiotics alone (Group B). Group B patients experienced longer disease duration, higher complication rates, and a 50% need for delayed surgical intervention. These findings highlight that early surgical management of ATM-related port-site infections shows faster healing and less complications than the conventional medical management which in turn helps to improve outcomes and preserve the advantages of minimally invasive surgery

1. Gayathri Devi DR, Sridharan D, Indumathi VA, Babu PRS, SandhyaBelwadi MR, Swamy ACV (2004) Isolation of mycobacterium Chelonae from wound infection following laparoscopy: a case report. Indian J Tuberc 51:149–151.
2. VeenaKumariHB, Nagarathna S, ChandramouliBA,UmamaheshwaraRao GS, Chandramukhi A (2008) Investigation of an outbreak of device-related postoperative ventriculitis: a lesson learnt. Indian J PatholMicrobiol 51(2):301–303.
3. Sasmal PK, Mishra TS, Rath S, Meher S, Mohapatra D. Port site infection in laparoscopic surgery: A review of its management. World Journal of Clinical Cases. 2015;3(10):864-71.
4. Molloy D, Kaloo PD, Cooper M, Nguyen TV. Laparoscopic entry: A literature [8] review and analysis of techniques and complications of primary port entry. Aust N Z J ObstetGynaecol. 2002;42(3):246-54.
5. Muthusami JC, Vyas PL, Mukundan U, Jesudason MR, Govil S, Jesudason SR. [9] Mycobacterium fortuitum: An iatrogenic cause of soft tissue injury in surgery. ANZ J Surg. 2004;74(8):662-66.
6. Aziz R. Practical manual of operative laparoscopy. New York: Springer-Verlag; 1992. p. 1–8.
7. Lilani SP, Jangale N, Chowdhary A, Daver GB. Surgical site infection in clean and clean-contaminated cases. Indian J Med Microbiol 2005;23:249–52.
8. Owens CD, Stoessel K. Surgical site infections: epidemiology, microbiology and prevention. J Hosp Infect 2008;70(Suppl 2):3–10.
9. Boni L, Benevento A, Rovera F, Dionigi G, Di Giuseppe M, Bertoglio C, et al. Infective complications in laparoscopic surgery. Surg Infect (Larchmt) 2006;7 (Suppl2):S109–11.
10. Falkinham JO. Epidemiology of infection by nontuberculous mycobacteria. ClinMicrobiol Rev 1996;9:177–215.
11. SumitChaudhuri&DebojyotiSarkar&ReshmiMukerji. Diagnosis and Management of Atypical Mycobacterial Infection after Laparoscopic Surgery. Indian J Surg 2010; 72(6):438–442.
12. Muthusami JC, Vyas FL, Mukundan U, Jesudason MR, Govil S Jesudason SR (2004) Mycobacterium fortuitum: an iatrogenic cause of soft tissue infection in surgery. ANZ J Surg 74(8):662–666
13. Chauhan A, Gupta AK, Satyanarayan S, Jena J (2007) A case of nosocomical atypical mycobacterial infection. MJFAI 63:201–202.
14. Verghese S, Agrawal P, Benjamin S. Mycobacterium chelonae causing chronic wound infection and abdominal incisional hernia. Indian J PatholMicrobiol 2014; 57: 335-337
15. Chaudhuri S, Sarkar D, Mukerji R. Diagnosis and management of atypical mycobacterial infection after laparoscopic surgery. Indian J Surg 2010; 72: 438-442.
16. Wallace RJ, Meier A, Brown BA, Zhang Y, Sander P, OnyiGO, Böttger EC. Genetic basis for clarithromycin resistance among isolates of Mycobacterium chelonae and Mycobacterium abscessus. Antimicrob Agents Chemother 1996; 40: 1676-1681
17. Svetlíková Z, Skovierová H, Niederweis M, Gaillard JL, McDonnell G, Jackson M. Role of porins in the susceptibility of Mycobacterium smegmatis and Mycobacterium chelonaeto aldehyde-based disinfectants and drugs. Antimicrob Agents Chemother 2009; 53:4015-4018
18. Wallace RJ, Brown-Elliott BA, Ward SC, Crist CJ, Mann LB, Wilson RW. Activities of linezolid against rapidly growing mycobacteria. Antimicrob Agents Chemother 2001; 45: 764-767.
19. Vikas Kumar Heer, SuhailKhuroo, Ajaz Ahmed Wani, Sonia Nagyal c, BeenaJad. Outcomes of surgical management of post laparoscopy atypical myco-bacterial port site infections: Is early surgery a better alternative?Surgery in Practice and Science 8 (2022) 100054