Drug Resistant Urinary Isolates of Pseudomonas Aeruginosa and Acinetobacter Species

A 22-year-old male, labourer by occupation, presented with a 2-day history of fever. The fever was abrupt in onset and was associated with chills and rigors. The patient had also developed a purpuric rash and altered sensorium for 1 day. There was no history of any seizures. At the time of presentation, the patient was unconscious and in hypotension (blood pressure of 70/48 mmHg). He had tachycardia (pulse 118/min, regular) and was tachypneic (RR 28/min). He had a purpuric rash over his extremities [Figure 1]. He also had neck rigidity, but moved all limbs to pain, and his plantars were flexor. Fundus revealed no papilledema. In view of the presentation, a working diagnosis of meningococcemia with meningitis was made and the patient was managed with volume resuscitation, intravenous ceftriaxone and hydrocortisone. His blood pressure improved initially. Noncontrast computed tomography (CT) of the head was unremarkable. A lumbar puncture was performed and the cerebrospinal fluid revealed protein of 112 mg/dL, sugar of 12 mg/ dL, cells 2,300 with 95% polymorphs and gram stain showing gram-negative diplococcici. Latex agglutination test was positive for Group A meningococcal infection. Over his stay, his urine output was low (100 mL over 12 h) and urine dipstick showed presence of blood. His renal functions were deranged (serum creatinine 4.3 ng/ mL, blood urea 242 mg/dL, serum Na+ 134, serum K 5.5 meq/L). Serum creatine kinase was 32,220 U/L. Other investigations revealed Hb 11.8 gm%, TLC 23,000, platelet count 48,000/μL, serum bilirubin 1.9, SGPT 96 U/L. Urine myoglobin was not performed. Although the patient was planned for hemodialysis, he developed hypotension and, in spite of all measures, including vasopressor support, the patient died.


Sir,
We read with interest the article on rhabdomyolysis secondary to staphylococcal endocarditis. [1] We would like to share our experience with a case of severe rhabdomyolysis secondary to meningococcemia.
A 22-year-old male, labourer by occupation, presented with a 2-day history of fever. The fever was abrupt in onset and was associated with chills and rigors. The patient had also developed a purpuric rash and altered sensorium for 1 day. There was no history of any seizures. At the time of presentation, the patient was unconscious and in hypotension (blood pressure of 70/48 mmHg). He had tachycardia (pulse 118/min, regular) and was tachypneic (RR 28/min). He had a purpuric rash over his extremities [ Figure 1]. He also had neck rigidity, but moved all limbs to pain, and his plantars were flexor. Fundus revealed no papilledema. In view of the presentation, a working diagnosis of meningococcemia with meningitis was made and the patient was managed with volume resuscitation, intravenous ceftriaxone and hydrocortisone. His blood pressure improved initially. Noncontrast computed tomography (CT) of the head was unremarkable. A lumbar puncture was performed and the cerebrospinal fluid revealed protein of 112 mg/dL, sugar of 12 mg/ dL, cells 2,300 with 95% polymorphs and gram stain showing gram-negative diplococcici. Latex agglutination test was positive for Group A meningococcal infection.
Over his stay, his urine output was low (100 mL over 12 h) and urine dipstick showed presence of blood. His renal functions were deranged (serum creatinine 4.3 ng/ mL, blood urea 242 mg/dL, serum Na+ 134, serum K 5.5 meq/L). Serum creatine kinase was 32,220 U/L. Other investigations revealed Hb 11.8 gm%, TLC 23,000, platelet count 48,000/µL, serum bilirubin 1.9, SGPT 96 U/L. Urine myoglobin was not performed. Although the patient was planned for hemodialysis, he developed hypotension and, in spite of all measures, including vasopressor support, the patient died.
The above case highlights the presence of severe rhabdomyolysis in case of bacterial septicaemia secondary to meningococcal infection. Although rhabdomyolysis has been reported with meningococcal infection, we are not aware of any report of renal failure secondary to rhabdomyolysis with meningococcemia . [2,3] Rhabdomyolysis can therefore be another cause of acute renal shutdown in sepsis apart from septic acute tubular necrosis. Clinicians should be aware of this possibility and appropriate management, including renal replacement, should be initiated when indicated. Sir, The emergence of antibiotic resistance and its spread has been a serious challenge to the clinicians. Penicillinase Letters to Editor represents the infancy of antibiotic resistance, which was followed by penicillin-inactivating enzymes. Recently the focus of clinicians has shifted to non-lactosefermenting gram-negative pathogens responsible for hospital-acquired infections (HAI). [1] Further, if we talk about intensive care units (ICUs), Acinetobacter sp. and Pseudomonas sp. are frequently encountered. [2] Acinetobacter has emerged as an important and problematic human pathogen as it is the causative agent of several types of infections, including pneumonia, meningitis, septicemia and urinary tract infections (UTI). It is ranked second after Pseudomonas among the nosocomial, aerobic, nonfermentative, gram-negative bacilli pathogens. Isolates from both the genera are multidrug resistant and sometimes also exhibit pan resistance. The aim of our study was to find the prevalence of multidrug resistance and pan-drug resistance among gram-negative uropathogens.

Drug Resistant Urinary Isolates of Pseudomonas Aeruginosa and Acinetobacter Species
The isolates isolated from hospitalized patients at Government Medical College and Hospital, Chandigarh, were collected in the Department of Microbiology from January 2007 to June 2007. The isolates were identified using routine conventional methods based upon microscopic findings, colony morphology and enzymatic characters. Routine antibiotic sensitivity testing was done by disc-diffusion method according to the recommendations of Clinical and Laboratory Standard Institute (CLSI). [3] The isolates were defined as multidrug-resistant (MDR) phenotypes if they were resistant to more than two classes of antibiotics, cephamycin, aminoglycoside, carbapenem and fluoroquinolones. [4] The isolates were considered to be pan-drug-resistant (PDR) phenotypes if they showed diminished susceptibility to almost all the antibiotics recommended for empirical therapy. [4] A total of 4912 urine samples were received in the department within the period of 6 months. Out of these, 1409 samples grew pathogens. The details of different bacterial species encountered in urine samples are given in Table 1. The most frequent organism was E. coli, followed by K. pneumoniae. Candida sp. was the commonest fungal isolate. Table 2 depicts the distribution of MDR and PDR isolates amongst gram-negative urinary pathogens. Maximum numbers of MDR and PDR isolates were observed in P. aeruginosa (72%); followed by Acinetobacter sp., where the value reached up to 62%. The frequency of multidrug resistance and pan-drug resistance in K. pneumoniae was 49%; and in E. coli, 28%.
Amongst all isolates, MDR and PDR isolates were mainly distributed amongst gram-negative bacteria, specifically focused at P. aeruginosa followed by Acinetobacter (71.7% and 62.6%, respectively). P. aeruginosa and Acinetobacter have in some cases expressed resistance to all clinically available compounds. P. aeruginosa possesses more tools for defying the activity of antimicrobial agents than virtually any other microorganism. [5] Like P. aeruginosa, Acinetobacter has been found to express a variety of different resistance mechanisms, including production of aminoglycosidemodifying enzymes, ESBLs and carbapenemases, as well as through changes in outer membrane proteins, penicillinbinding proteins and topoisomerases. [6] During the last decade, efforts to combat multidrugresistant microorganisms mainly focused on gram-positive bacteria. Since the number of reports on infections caused by gram-negative microorganisms, for which no adequate therapeutic options exist, is increasing, it is time to intensify attention towards gram-negative resistance.
We must remain mindful that indiscriminate use of any antibacterial agent will inevitably lead to resistance. As such, continued emphasis on effective infectioncontrol measures and judicious and parsimonious use of available antimicrobial agents will remain mainstays in any reasonable strategy to maximize the usefulness of available antimicrobial agents.  Sir, Recently, a report of mycotic giant cell epitheliomatous inverted papilloma appeared in your journal. [1] We present here the histopathological evidence of a mycoplasmotic giant cell epitheliomatous inverted papillary carcinoma.
A 45-year-old female with history of chronic asthma, chest X-ray report of interstitial changes in lungs, high resolution computerized tomography (HRCT) thorax report of soft tissue density lesions in the lung presented with ear problem, clinically diagnosed as "right aural polyp." A small biopsy tissue from the polyp was submitted for histopathological diagnosis.
The biopsy section [ Figure 1] revealed that the thickness of the keratinocytic strata decreased and hyperchromasia increased from right to the left (A). On the right plank, marked by intense eosinophil cell infiltrate, the basal layer presented discrete foci of hyperchromatic basal cells showing surface attached-elongate mycoplasma and protoplastic inclusions in the nucleus and cytoplasm (B). Occasionally, the basal cell displayed enlarged, intensely hyperchromatic, cleaved nucleus impending cell proliferation (Inset C). Parabasal epitheliomatous proliferation in the ret-e-pegs formed inverted papillae without a keratinocytic core (C Under high-power lens, the periodic acid Schiff (PAS)stained section through deep invading papillae showed PASpositive inclusions suspicious of histoplasma [ Figure 2]. Oil immersion lens revealed PAS+ve replicate mycoplasma in the intercellular clefts, cytoplasm and nucleus of the infested and disrupted carcinoma cells (Inset A), showing protoplastic spheroid, oval, coccoid, balloon, disc, ring, star, granule and filament forms. Nuclear inclusions merged with the host cell chromatin inducing protoplastic character of forming nourishment vacuoles (Inset B). The inclusionladen cytoplasm depicted (amoeboid) pseudopodia. Hybrid chromatin with its vacuole increased at the expense of infested-cell cytoplasm (inset C). The vacuole disappeared with increase of chromatin transformed into protoplastic (mycoplasmoid) spheroids of 1-2 microns, giving rise to mega mononucleate giant cells (inset D). The nuclear protospheroids enlarged, cleaving the nuclear membrane, to get released into the cytoplasm (inset E), giving rise to multinucleate giant cell awaiting fission.
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