Prostatitis

Prostatitis is inflammation of the prostate gland, and despite the single name it is not one disease but four genuinely distinct clinical entities grouped under the National Institutes of Health (NIH) consensus classification system.^[1] Getting the category right at the first visit is what actually drives everything downstream — the four categories differ completely in urgency, workup, and treatment duration, and treating one as if it were another is one of the most common ways this condition is mismanaged.

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Almost 9% of Canadian men experience some prostatitis symptoms over the course of a year, and in about 6% those symptoms are a genuine bother; roughly a third experience a remission of symptoms within a year of follow-up.^[1] Men with clinically significant prostatitis symptoms account for about 3% of Canadian male outpatient visits.^[1] In the United States, chronic prostatitis alone accounts for roughly 2 million outpatient visits annually and is the third most commonly diagnosed urologic disease overall, and the single most prevalent urologic diagnosis in men under 50 — about 5% of men aged 20-50 have been affected at some point, though only around 60% of symptomatic men actually seek care.^[2] Less than 10% of all prostatitis is truly bacterial (Categories I and II); the great majority — roughly 90% — is CP/CPPS (Category III), a genuine diagnosis of exclusion rather than an infection.^[1][2]

Prostatitis is neither benign prostatic hyperplasia (BPH) nor a routine urinary tract infection, and it is worth distinguishing all three before treatment starts. BPH is a nonmalignant, androgen-dependent enlargement of prostate tissue that produces gradually progressive voiding symptoms without pain, fever, or a tender gland on examination — see the Lower Urinary Tract Symptoms and Benign Prostatic Hyperplasia chapter for its full workup and treatment. BPH and prostatitis can genuinely coexist (bladder outlet obstruction from BPH is itself a recognized risk factor for ascending infection), but BPH does not, on its own, explain pain, fever, or a tender/boggy prostate.^[1] Isolated cystitis is also genuinely uncommon in men, precisely because the prostate sits along the same anatomic pathway as the lower urinary tract; a febrile urinary tract infection, or one with a recurrent-relapse pattern, in a man should raise real suspicion of prostatic involvement rather than being managed as routine bladder infection (see Assessment & Diagnosis and Choose Initial Treatment).^[1]

Two threads run through this entire chapter because they are where a pharmacist's input is most likely to change what actually happens: the pharmacokinetic reason fluoroquinolones are preferred for prostate infections over agents that otherwise look reasonable on a spectrum-of-activity basis (see Choose Initial Treatment), and the practical counselling point that recent ejaculation or prostatic manipulation can transiently raise a PSA result enough to cause real, avoidable alarm in a man being worked up for something else entirely (see Assessment & Diagnosis and Special Populations).

• Recent urologic instrumentation, catheterization, cystoscopy, or prostate biopsy — a direct-inoculation route specifically for acute bacterial prostatitis.^[3]
• Unprotected intercourse, a new sexual partner, or other sexually transmitted infection risk factors — relevant to STI-likely ABP etiology in younger, sexually active men (see Choose Initial Treatment).^[3]
• Phimosis and intraprostatic ductal reflux.^[3]
• Benign prostatic hyperplasia or another cause of bladder outlet obstruction — predisposes to ascending infection via urinary reflux and is itself part of the differential to keep straight (see Assessment & Diagnosis).^[3]
• Diabetes and other causes of immunosuppression — raise both infection risk and the threshold for hospitalizing a case of ABP.^[3][1]
• An indwelling catheter.^[3]
• Recurrent culture-proven urinary tract infections, especially with the same organism each time — the hallmark risk pattern for chronic bacterial prostatitis.^[1]
• Prostatic calculi — a genuinely important, easily missed contributor to relapsing chronic bacterial prostatitis, since bacterial biofilm on the stone surface resists both antibiotics and host clearance.^[2]
• Psychological stress, anxiety, depression, maladaptive coping (catastrophizing), and poor social support — genuine risk and symptom-severity factors specifically for CP/CPPS, not incidental comorbidities.^[1]
• Pelvic floor myofascial dysfunction and trigger points — a perpetuating factor for the Tenderness domain of CP/CPPS.^[2]
• Smoking — smokers are more likely to have chronic prostatitis than non-smokers.^[2]
• Age under 50 for CP/CPPS specifically, versus any adult age for acute or chronic bacterial prostatitis.^[2]

Other red flags, any category

• An abnormal digital rectal examination — a hard, nodular, or asymmetric prostate — should never be assumed to be prostatitis; it needs the same prostate-cancer workup it would in any other context.^[1]
• Gross or unexplained hematuria needs its own evaluation to exclude bladder or upper-tract pathology rather than being attributed to prostatitis by default.
• Rapidly spreading perineal erythema, crepitus, disproportionate pain, or systemic toxicity out of proportion to the apparent infection — consider Fournier's gangrene, a surgical emergency requiring immediate referral, not outpatient antibiotic escalation.
• Severe depression or suicidal ideation in a man with CP/CPPS — referral to a psychologist or psychiatrist is mandatory, not optional, given the genuine, well-documented psychosocial burden of this condition.^[1]

History

A comprehensive history is mandatory for every patient: pain location, severity, frequency, and duration; lower urinary tract symptoms, both obstructive/voiding and irritative/storage; associated symptoms (fever, other pain syndromes); and impact on activities and quality of life. A full systems review should document past medical and surgical (particularly urologic) history, trauma, medications, and allergies.^[1]

Physical examination

The abdomen, external genitalia, perineum, and prostate must be examined in every category, and the pelvic floor specifically in suspected CBP and CP/CPPS.^[1]

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Urinalysis and culture

Mandatory in acute bacterial prostatitis.^[1] A midstream culture is the starting point for every category and, together with a recurrent-UTI history, decides whether localization testing (below) is needed.

The 4-glass test and 2-glass pre- and post-massage test (PPMT)

A bacterial count at least 10-fold higher in EPS or VB3 than in VB1 or VB2 localizes infection to the prostate and confirms chronic bacterial prostatitis rather than CP/CPPS; the 4-glass test is the diagnostic criterion standard.^[1][2] The simpler 2-glass PPMT, comparing only a pre-massage and a post-massage specimen, offers similar diagnostic accuracy with far less complexity and is a reasonable, more practical default.^[1][2] Microscopy of EPS/urine sediment is optional and adds no proven clinical value on its own.^[1] Semen culture is not recommended — it has not been shown to meaningfully help identify CBP unless it grows the same organism responsible for recurrent UTIs.^[1]

NIH-Chronic Prostatitis Symptom Index (NIH-CPSI)

The internationally standard, validated tool for grading current CP/CPPS symptom severity and tracking response to therapy — a symptom index, not a diagnostic test on its own.^[1]

Total score (0-43) is conventionally categorized as mild (0-14), moderate (15-29), or severe (30-43).^[1][2]

UPOINT phenotyping

Once CP/CPPS is diagnosed, individualized personal therapy directed at a clinically defined phenotype — UPOINT — organizes the entire treatment approach (see Choose Initial Treatment and Pharmacologic Treatment Options); a multimodal approach using specific clinical phenotypes to choose therapies is a genuine, evidence-supported recommendation, since monotherapy provides at best modest efficacy.^[1]

^[1]

Imaging, cystoscopy, urodynamics, and serum PSA

Transrectal ultrasound and CT are not recommended as routine initial workup for any category; TRUS or CT becomes appropriate specifically in ABP refractory to initial therapy, to rule out a prostate abscess.^[1] Cystoscopy is not recommended for routine CP/CPPS evaluation, but is reasonable in selected patients with obstructive voiding symptoms refractory to medical therapy, hematuria, or other suspected lower urinary tract pathology.^[1] Urodynamics/uroflow are optional adjuncts to confirm obstruction, not to differentiate prostatitis categories from each other.^[1] Serum PSA is not recommended in ABP (an elevated result usually just causes confusion and worry) nor routinely in CP/CPPS (it does not help diagnose the condition or direct therapy) — indications for PSA testing in a man with CP/CPPS should be the same as for any other man.^[1]

Psychological assessment

Optional but genuinely relevant: accumulating evidence shows psychosocial parameters — depression, maladaptive coping mechanisms, poor social support — impact both symptoms and treatment results, and screening for them is part of a complete CP/CPPS assessment.^[1] Referral is mandatory, not optional, for severe depression or suicidal ideation.^[1]

• Eradicate the infection and prevent progression to urosepsis or abscess in acute bacterial prostatitis.
• Eradicate the infection and prevent relapse in chronic bacterial prostatitis, using a course long enough to actually achieve that (see Choose Initial Treatment).^[1]
• Reduce pain and improve quality of life in CP/CPPS through an individualized, phenotype-directed multimodal approach, since no single agent reliably works and monotherapy provides at best modest efficacy.^[1]
• Correctly differentiate prostatitis from BPH, prostate cancer, and routine UTI before committing to a treatment pathway (see Assessment & Diagnosis).
• Avoid unnecessary or prolonged antibiotic use — particularly repeated empiric courses in CP/CPPS with no documented pathogen.^[1][5]
• Screen for and address the psychosocial contributors to CP/CPPS as an actual treatment target, not an afterthought.^[1]
• Preserve fertility and sexual function where possible, and treat category IV only when a specific, indicated reason exists (elevated PSA, infertility workup, pre-biopsy).^[1]

Why the antibiotic — and the duration — genuinely differs by category: prostate-tissue penetration pharmacokinetics

This is not an arbitrary prescribing preference. The prostate is protected by a blood-prostate barrier, and effective treatment of bacterial prostatitis is fundamentally limited by how well a given antibiotic actually crosses it — a function of the drug's lipophilicity, its degree of plasma protein binding, and, critically, pH-dependent ion trapping.^[7] Prostatic fluid is normally more acidic than plasma; a lipophilic weak base equilibrates across the barrier and becomes proportionally more ionized — and therefore effectively trapped — on the more acidic prostatic side, concentrating there relative to plasma, while a weak acid does the opposite and is comparatively excluded.^[7] Fluoroquinolones are the clearest beneficiary of this chemistry: their zwitterionic structure and lipophilicity give them consistently favourable intraprostatic penetration — prostate tissue-to-serum concentration ratios at or above 1, commonly 2- to 3-fold higher than plasma — which is exactly why the Canadian Urological Association identifies fluoroquinolones as the agents of choice for chronic bacterial prostatitis specifically because of their "unique and favourable pharmacokinetic properties."^[1][7] Trimethoprim-sulfamethoxazole penetrates only moderately, and that penetration is driven almost entirely by the trimethoprim component — sulfamethoxazole itself penetrates poorly, which blunts the synergy the combination normally relies on and is a real part of why it needs a longer course and is reserved as a second choice rather than being interchangeable with a fluoroquinolone.^[7] Most beta-lactams — penicillins and most cephalosporins — penetrate poorly into non-inflamed prostate tissue, since they are ionized weak acids largely excluded by the same pH gradient; selected cephalosporins can still achieve moderate concentrations specifically in the setting of acute inflammation, which disrupts the barrier and increases local permeability.^[7] That last point is exactly why the two bacterial categories are treated so differently: acute bacterial prostatitis is, by definition, an acutely inflamed gland with a genuinely more permeable barrier, which is why empiric IV beta-lactam/aminoglycoside regimens still work well for severe ABP even though those same drugs would be a poor choice for a chronically, non-acutely inflamed gland — and chronic bacterial prostatitis has a comparatively intact barrier and often a biofilm-protected bacterial reservoir on prostatic calculi, which is why CBP specifically needs an agent with genuinely good baseline penetration (a fluoroquinolone) continued for a genuinely long course rather than the shorter 2-4 week course that suffices once the acute inflammatory window of ABP has already improved the drug's access to the tissue.^[7][1]

Acute bacterial prostatitis

• Adequate hydration and antipyretic/analgesic support (see Pharmacologic Treatment Options) while antibiotics take effect.
• A single catheterization with a trial of voiding, or a short-term small-caliber urethral catheter, for severe obstructive voiding symptoms or urinary retention; a suprapubic tube is a reasonable option for a patient who cannot tolerate a urethral catheter.^[1]
• Incision and drainage — most often via a transurethral approach, though perineal, rectal, or transperineal routes are also used — for a confirmed prostatic abscess that does not respond to antibiotics alone.^[1]
• Activity modification and rest during the acute, systemically unwell phase.

Chronic bacterial prostatitis

• Adherence counselling is genuinely the single highest-yield non-drug intervention here — the entire rationale for a 4- to 12-week course is incomplete tissue penetration, and stopping early once symptoms improve is the most common reason for relapse (see Common Errors to Avoid).
• Identify and address underlying risk factors that perpetuate infection: bladder outlet obstruction, phimosis, and — genuinely important and easy to miss — prostatic calculi, which harbour bacterial biofilm and can require surgical management (radical TURP or open/simple prostatectomy) as a genuine last resort when every other option has failed.^[1][2]

Chronic prostatitis/chronic pelvic pain syndrome

• Hot sitz baths — about 10 minutes is usually sufficient, and most patients find several a day genuinely helpful for symptomatic relief.^[2]
• A soft cushion or inflatable "donut," avoiding prolonged bicycle riding, and avoiding sitting on cold, hard surfaces — all reduce direct perineal pressure that can aggravate pelvic floor and prostatic pain.^[2]
• Dietary trigger identification — caffeine reduction is close to a universal recommendation, and reducing alcohol, spicy food, and citrus is reasonable to trial; frame this the same way this platform's Interstitial Cystitis chapter does — as an individualized elimination-and-reintroduction exercise to find a given patient's own triggers, not a rigid universal diet.^[2]
• Manual pelvic floor physical therapy — myofascial trigger-point release and paradoxical relaxation techniques — is most useful specifically for men with a positive Tenderness (T) domain on UPOINT phenotyping (palpable pelvic floor tenderness, spasm, or trigger points).^[2]
• Regular, scheduled ejaculation — commonly advised at least once every 3 days — is thought to reduce prostatic fluid stasis and ductal buildup; prostatic massage as a treatment in its own right remains genuinely controversial with conflicting evidence, so scheduled ejaculation is the more practical, better-tolerated alternative to advise.^[2]
• Smoking cessation — smokers are more likely to have chronic prostatitis than non-smokers.^[2]
• Regular exercise has shown symptom improvement in at least one randomized study, and stress reduction and sleep optimization are reasonable general measures given the strong link between CP/CPPS symptom severity and psychological stress.^[2]
• Psychological support, ideally including a cognitive behavioural therapy component, should be considered for the Psychosocial (P) UPOINT domain; referral to a psychologist or psychiatrist is mandatory, not optional, for a patient with severe depression or suicidal ideation.^[1]
• Acupuncture has shown good efficacy for CP/CPPS symptoms in several studies, particularly when combined with other treatment modalities.^[2]

Younger, sexually active men

STI-likely acute bacterial prostatitis is managed the same way this platform's Epididymitis chapter manages STI-likely epididymitis — ceftriaxone plus doxycycline, with partner notification and empiric partner treatment for the 60 days preceding symptom onset, abstinence until treatment is complete and symptoms have resolved, and reinfection screening at 6 months. See that chapter for the full partner-management protocol; the same underlying ascending-STI logic applies here.^[3]

Men over 50

CP/CPPS Category IIIA in an older man with a demonstrably enlarged prostate is one of the few situations where a 5-alpha-reductase inhibitor has a genuine, if secondary, role — not as primary monotherapy, but as part of a multimodal plan, given at least 6 months before judging effect.^[1] An episode of acute or chronic bacterial prostatitis in this age group should also prompt evaluation for underlying bladder outlet obstruction from BPH once the acute infection has resolved — see the Lower Urinary Tract Symptoms and Benign Prostatic Hyperplasia chapter for that workup.

Men with recurrent instrumentation, indwelling catheters, or nursing-home residence

These men carry a materially higher risk of resistant organisms — Pseudomonas aeruginosa and Enterococcus species show a poorer response to standard antimicrobial therapy than E. coli and other Enterobacteriaceae — so culture-directed rather than purely empiric therapy, and a broader initial empiric regimen while cultures are pending, are both reasonable.^[1]

Men undergoing or considering PSA-based evaluation

Serum PSA is not recommended as a routine part of the prostatitis workup itself — an elevated PSA in ABP usually just causes confusion and worry, and PSA does not help diagnose or direct therapy in CP/CPPS.^[1] But when a PSA result is genuinely needed — for an unrelated, appropriately indicated prostate-cancer risk discussion happening around the same time — two confounders specifically need to be accounted for: recent ejaculation (advise at least 48 hours of abstinence beforehand) and active or recent prostatic infection/inflammation (wait at least 6 weeks after resolution before interpreting a result).^[4][2] See Assessment & Diagnosis for the full counselling point, and the Lower Urinary Tract Symptoms and Benign Prostatic Hyperplasia chapter for the separate PSA-interpretation nuance created by 5-alpha-reductase inhibitor therapy.

Men with infertility

Chronic bacterial prostatitis and CP/CPPS are both associated with impaired sperm concentration, motility, and morphology.^[2] Category IV found incidentally during an infertility workup is one of the specific situations where antimicrobial therapy is a reasonable, optional consideration despite the complete absence of symptoms.^[1]

Severe psychiatric comorbidity

Referral to a psychologist or psychiatrist is mandatory, not optional, for any CP/CPPS patient with severe depression or suicidal ideation — this reflects genuine, evidence-based psychosocial modelling of the syndrome, not a generic add-on recommendation.^[1]

• Acute bacterial prostatitis: expect defervescence and clear clinical improvement within 48-72 hours of appropriate antibiotics; if this does not occur, image (TRUS or CT) to rule out a prostatic abscess rather than simply extending the same regimen.^[1] Complete the full 2-4 week course even once symptoms resolve, and consider evaluating for underlying bladder outlet obstruction once the acute episode has resolved, particularly in a man over 50.
• Chronic bacterial prostatitis: clinical improvement is typically seen within the first 1-2 weeks, but the full 4- to 12-week course (depending on the agent and organism) must be completed regardless — this is genuinely the single most important adherence message in this chapter, since premature discontinuation is the leading cause of relapse.^[1] For a treatment-refractory patient with a confirmed uropathogen still localized to the prostate, reasonable strategies include intermittent antimicrobial treatment of acute symptomatic recurrences, low-dose antimicrobial suppression, or — genuinely a last resort, and only if every other option has failed — radical TURP or open/simple prostatectomy.^[1]
• CP/CPPS: reassess the NIH-CPSI periodically to track objective response rather than relying on unprompted recall, and revisit the UPOINT phenotype at follow-up, since a patient's dominant domain — and therefore the most useful next therapy — can shift over time.^[1] Reconsider the diagnosis itself — including a repeat localization culture to exclude a missed chronic bacterial component — if a patient fails to improve despite multiple, adequately trialled multimodal approaches, rather than continuing to escalate indefinitely against a diagnosis that may need revisiting.^[2]
• Any category: re-screen for depression, anxiety, and suicidal ideation at follow-up in a patient with persistent symptoms, given how strongly psychosocial burden and symptom severity are linked in this condition.^[1][2]

1. Acute bacterial prostatitis not defervescing within 48-72 hours of appropriate antibiotics: image (TRUS or CT) to rule out a prostatic abscess; broaden or adjust the antibiotic based on culture and sensitivity results; drain any confirmed abscess.^[1]
2. Chronic bacterial prostatitis relapsing after an apparently complete course: first confirm the full course was actually completed and adherence was genuine before assuming true antimicrobial failure; repeat localization culture to confirm the organism and its susceptibility; switch to sulfamethoxazole-trimethoprim (fluoroquinolone-resistant organism, 8-12 weeks) or fosfomycin (multidrug-resistant E. coli, 6-12 weeks).^[1][6]
3. Chronic bacterial prostatitis genuinely refractory despite an adequately long, susceptibility-directed course: intermittent antimicrobial treatment of acute symptomatic recurrences, or low-dose antimicrobial suppression, are reasonable next steps; radical TURP or open/simple prostatectomy is a genuine last resort, reserved for when every other option has failed.^[1]
4. CP/CPPS not responding to an initial single-domain intervention (for example, an alpha-blocker alone): do not simply escalate that one drug's dose — move to genuinely multimodal, UPOINT-directed combination therapy across every positive domain, since monotherapy provides at best modest efficacy in this category.^[1][5]
5. CP/CPPS refractory despite an adequate multimodal trial: refer to a pain management specialist and/or a multidisciplinary team (urology, pelvic floor physical therapy, psychology); reconsider the diagnosis itself, including a repeat localization culture to exclude a missed chronic bacterial component and reassessment for interstitial cystitis or pelvic floor myalgia as the dominant driver.^[2]
6. Any new red flag at any point — urosepsis, an abnormal/hard/nodular DRE, gross hematuria, or suicidal ideation — escalate or refer immediately rather than continuing the current management plan.^[1]

• Performing a vigorous prostatic massage or DRE in a patient with suspected acute bacterial prostatitis — this can precipitate bacteremia and worsen the patient's condition; gentle examination only, and reserve prostatic massage for localization testing once ABP has been excluded.^[1][3]
• Ordering or over-interpreting a PSA during active acute bacterial prostatitis, or without asking about recent ejaculation or prostatic manipulation — both are common, avoidable sources of a falsely alarming result (see Assessment & Diagnosis).^[1][4][2]
• Defaulting to sulfamethoxazole-trimethoprim as first-line empiric therapy for acute bacterial prostatitis without knowing local E. coli resistance patterns.^[1]
• Stopping chronic bacterial prostatitis antibiotics once symptoms improve rather than completing the full 4- to 12-week course — the entire rationale for that duration is incomplete tissue penetration, and early discontinuation is the single most common, and most avoidable, cause of relapse.^[1]
• Prescribing repeated or prolonged antibiotic courses for CP/CPPS in a patient with a negative culture and no documented pathogen — current AUA guidance explicitly cautions against this, and it is not supported for men who have already failed a prior antibiotic trial.^[1][5]
• Choosing moxifloxacin for a urinary tract or prostate infection — despite generally good tissue penetration, it achieves clinically inadequate urinary and prostatic fluid concentrations due to minimal renal excretion, and is not an appropriate substitute for levofloxacin in this indication.
• Treating Category IV (asymptomatic inflammatory prostatitis) — by definition an incidental, symptom-free finding — as something that needs definitive antibiotic therapy.^[1]
• Ordering a semen culture to try to "confirm" chronic bacterial prostatitis — it is not recommended, and a negative result does not rule CBP out.^[1]
• Missing the psychosocial dimension of CP/CPPS and treating only the physical symptoms, rather than screening for depression, maladaptive coping, and social dysfunction as an actual UPOINT domain in its own right.^[1]
• Confusing prostatitis, BPH, and a routine UTI without applying the actual distinguishing features — onset pattern, DRE findings, and systemic symptoms — rather than treating any pelvic/voiding complaint in a man as interchangeable with the other two (see Assessment & Diagnosis).^[1]

How to use this table: Doses are adult doses and require patient-specific confirmation (renal/hepatic function, weight, allergy history). Pediatric dosing is weight-based per the current product monograph unless stated. Drug pricing is intentionally omitted. Select any drug name to open its complete Pharmasist Drug Database page.

Acute Bacterial Prostatitis — Severe Illness or Urosepsis (Initial Parenteral Therapy)

Continue IV therapy until defervescence and resolution of urosepsis, then step down to an oral fluoroquinolone to complete 2-4 weeks total. Hospitalization is mandatory for hyperpyrexia, prolonged vomiting, severe dehydration, tachycardia, tachypnea, or hypotension, and recommended for high-risk patients (diabetes, immunosuppression, older age, prostatic abscess, severe voiding disorder).

Acute Bacterial Prostatitis — Outpatient, Mild-to-Moderate Illness

For patients who are not severely ill and are tolerating oral intake.

Acute Bacterial Prostatitis — Likely Sexually Transmitted Etiology (Younger, Sexually Active Men)

Mirrors this platform's Epididymitis chapter regimen and partner-management protocol — the same ascending-STI logic applies when the infection has reached the prostate itself.

Chronic Bacterial Prostatitis

Because of their unique, favourable pharmacokinetic properties, fluoroquinolones are the agents of choice; treatment-refractory patients with a confirmed, prostate-localized uropathogen may need intermittent treatment of recurrences or low-dose suppressive therapy (see Treatment Failure / Next Step).

Auxiliary Therapy for Acute and Chronic Bacterial Prostatitis

Alpha-blockers do not treat the infection itself but reduce urinary retention risk and improve voiding comfort; NSAIDs address pain and, in ABP, fever.

Chronic Prostatitis/Chronic Pelvic Pain Syndrome — UPOINT-Directed Multimodal Therapy

Organized by the UPOINT domain each agent targets — direct therapy to a patient's actual positive domains simultaneously rather than trialling one drug class after another in sequence (see Choose Initial Treatment and Assessment & Diagnosis).