Step Up - Infectious Diseases Flashcards
Nosocomial pneumonia - Definition:
Occurs after the first 72h of hospitalization.
Classic CAP presents with:
- Sudden chill.
- Fever.
- Pleuritic pain.
- Productive cough.
Atypical pneumonia - Presents with:
Often begins with a sore throat and headache followed by a non productive cough and dyspnea.
2 recommended methods of prevention:
- Influenza vaccine - Give yearly to people at incr. risk for complications and to health care workers.
- Pneumococcal vaccine - For patients >65yr and for younger people at high risk (eg those with heart disease, sickle cell disease, pulmonary disease, diabetes, alcoholic cirrhosis, asplenic individuals).
Typical CAP - Common agents:
- S.pneumoniae (60%).
- H.influenza (15%).
- Aerobic gram(-) rods (6-10%) - Klebsiella (and other Enterobacteriaceae).
- S.aureus (2-10%).
Typical CAP - Clinical features - Symptoms:
- Acute onset of fever and shaking chills.
- Cough productive of thick, purulent sputum.
- Pleuritic chest pain (suggest pleural effusion).
- Dyspnea.
Typical CAP - Signs:
- Tachycardia, tachypnea.
- Late inspiratory crackles.
- Bronchial breath sounds
- Incr. tactile vocal fremitus.
- Dullness on percussion.
- Pleural friction rub (associated with a pleural effusion).
Most cases of CAP result from?
Aspiration of oropharyngeal secretions because the majority of organisms that cause CAP are NORMAL INHABITANTS of the pharynx.
CXR - Typical CAP:
- Lobar consolidation.
2. Multilobar consolidation indicates very serious illness.
General approach to diagnosis of CAP - 1st step:
Differentiate lower respiratory tract infection from the other causes of cough and from upper respiratory tract infection.
General approach to diagnosis of CAP - 2nd step - Once lower tract infection is suspected:
Next task is to differentiate between pneumonia and acute bronchitis - Clinical features NOT reliable - CXR the only reasonable method of differentiating between pneumonia and acute bronchitis.
Studies have shown that if VITAL SIGNS are entirely normal, the probability of pneumonia in outpatients is less than?
1%.
Atypical CAP - Common agents:
- Mycoplasma pneumoniae (MC).
- Chlamydia pneumoniae.
- Chlamydia psittaci.
- Coxiella burnetti (Q fever).
- Legionella spp.
- Viruses - Influenza (A, B), adenoviruses, parainfuenza virus, RSV.
Atypical CAP - Clinical features - Symptoms:
- Insidious onset - headache, sore throat, fatigue, myalgia.
- Dry cough (no sputum production).
- Fevers (chills are uncommon).
Atypical CAP - Clinical features - Signs:
- Pulse-Temperature dissociation - normal pulse in the setting of high fever is suggestive of atypical CAP.
- Wheezing, rhonchi, crackles.
Atypical CAP - CXR:
- Diffuse reticulonodular infiltrates.
2. Absent or minimal consolidation.
Sputum culture CAP:
The value of routine sputum collection for Gram stain and culture is controversial. The Infectious Disease Society of America has recently advocated performing sputum Gram stain and culture in ALL patients hospitalized with CAP.
The following steps are appropriate in patients admitted to the hospital with suspected pneumonia:
- CXR (PA and lateral).
- Lab tests - CBC and differential, BUN, Cr, glucose, electrolytes.
- SaO2.
- Two pretreatment blood cultures.
- Gram stain and culture of sputum.
- Antibiotic therapy.
Diagnosis of pneumonia - CXR:
- PA and lateral CXR REQUIRED to confirm the diagnosis.
- Considered sensitive - If CXR findings are NOT suggestive of pneumonia, do not treat the patients with antibiotics.
- After treatment, changes evident on CXR usually lag behind the clinical response (up to 6wks).
- Changes include interstitial infiltrates, lobar consolidation, and/or cavitation.
- False-negative chest radiographs occur with neutropenia, dehydration, infection with PCP, and early disease <24h.
Do radiographic changes and clinical findings help in identifying the causative organism in CAP?
No, they do not help.
Pneumoniae pearls:
- Alcoholics –> Klebsiella.
- Immigrants –> TB.
- Nursing home residents –> Nosocomial pathogen and predilection for the upper lobes (eg Pseudomonas).
- HIV(+) –> PCP + TB - still more likely to have a TYPICAL infectious agent.
- Legionella –> Organ transplant recipients, renal failure, chronic lung disease, smokers.
Diagnosis of pneumonia - Sputum Gram stain:
Try to obtain in all patients:
- Commonly contaminated with oral secretions.
- A good specimen has a sensitivity of 60% and specificity of 85% for identifying gram(+) cocci in chains (S.pneumoniae).
Diagnosis of pneumonia - Sputum culture:
Try to obtain in all patients REQUIRING hospitalization - Specificity is improved if the predominant organism growing on the culture media correlates with the Gram stain.
Diagnosis of pneumonia - Special stains of the sputum in selected cases:
- Acid-fast stain (Mycobacterium spp.) if TB is suspected.
2. Silver stain (fungi, Pneumocystis carinii) for HIV/immunocompromised.
Diagnosis of pneumonia - Urinary antigen assay for Legionella in selected patients:
- Test is VERY SENSITIVE.
2. Antigen persists in the urine for WEEKS (even after treatment has been started).
Diagnosis of pneumonia - Blood cultures:
Positive in 5%-15% of cases.
Test for microbial diagnosis for outpatients?
NOT required - Empiric treatment is often successful if CAP is suspected.
Treatment of CAP - Decision to hospitalize:
The decision to hospitalize or treat as an outpatient is probably the MOST IMPORTANT decision to be made and is based on severity of disease.
Uncomplicated CAP in patients WITHOUT significant comorbidities - Treat with:
Azithromycin or Clarithromycin (if comorbidities, give a fluoroquinolone).
Treatment of pneumonia - In people younger than 60yrs:
MC organisms are: S.pneumoniae, Mycoplasma, Legionella, Chlamydia.
- -> Macrolides (azithromycin, clarithromycin) or doxycyclin cover ALL of these organisms and are the first-line treatment.
- -> Alternative: Fluoroquinolones.
Treatment of pneumonia - In older adults and patients with comorbidities (more likely to have typical CAP) OR those treated with antibiotics in the last 3 months, treat with:
First-line agent –> Fluoroquinolone (levofloxacin, moxifloxacin).
Treatment of pneumonia - For outpatient, treatment is continued for?
5 days. DO NOT stop treatment until patient has been afebrile for 48h.
Treatment of pneumonia - Hospitalized patients:
A fluoroquinolone alone or a 3rd-gen cephalosporin + macrolide (ceftriaxone + azithromycin) is appropriate.
Treatment of hospital-acquired pneumonia:
Treatment is tailored toward gram(-) rods (any of the following are appropriate):
- Cephalosporins with pseudomonal coverage: ceftazidime, cefepime.
- Carbapenems: imipenem.
- Piperacillin/tazobactam
- -> Macrolides are NOT used - as they are in CAP.
Complications of pneumonia:
- Pleural effusion (“parapneumonic effusions”).
- Pleural empyema occurs in 1%-2% of all cases of CAP (up to 7% of hospitalized patients with CAP).
- Acute respiratory failure may occur if the pneumonia is severe.
Complications of pneumonia - Pleural effusion:
- Can be seen in >50% of patients with CAP on routine CXR. Empyema is infrequent in these patients.
- Most of these effusions have an uncomplicated course and resolve with treatment of the pneumonia with antibiotics.
- Thoracentesis should be performed if the effusion is significant (>1cm on lateral decubitus film) –> Send fluid for Gram stain, culture, pH, cell count, determination of glucose, protein, and LDH.
Ventilator associated pneumonias - Risk:
- Normal mucociliary clearance of the respiratory tract is impaired (cannot cough).
- Also, positive pressure impairs the ability to clear colonization.
Ventilator associated pneumonia - Findings:
- New infiltrate on chest X-ray, purulent secretions from endotracheal tube.
- Fever.
- Rising WBC count.
Ventilator associated pneumonia - Treatment:
Combination of the following 3 different drugs:
- Cephalosporin (ceftazidime or cefepime) OR penicillin (piperacillin/tazobactam) OR carbapenem (imipenem).
- Aminoglycoside OR fluoroquinolone.
- Vancomycin OR linezolid.
Lung abscess Pearls:
- Areas most likely to be infected by aspirated material - POSTERIOR segments of the UPPER lobes and SUPERIOR segments of the LOWER lobes.
- Aspirated material is more likely to affect the RIGHT lobe due to angle of the right main stem bronchus from the trachea.
Lung abscess - Typical case:
The typical case is aspiration of a large volume of oropharyngeal contents or food, with resulting pneumonia and necrosis when adequate treatment is NOT administered.
By definition, a lung abscess is formed by?
One or more cavities, each >2cm in diameter.
Lung abscesses can be complications of the following:
- Aspiration of organisms.
- Acute necrotizing pneumonia.
- Hematogenous spread of infection from distant site.
- Direct inoculation with contiguous spread.
Lung abscess - Causative organisms:
Bacteria that colonize the oropharynx:
- Oral anaerobes: Prevotella, Peptostreptococcus, Fusobacterium, Bacteroids spp.
- Other: S.aureus, S.pneumoniae, and aerobic gram(-) bacilli.
Lung abscesses - Epidemiology/risk factors:
- Main risk factor is predisposition to aspiration.
- Poor dental hygiene.
- Edentulous patients are less likely to aspirate oropharyngeal secretions.
Lung abscesses - Clinical features:
- Majority –> Indolent course. Some present more acutely.
- Cough - Foul-smelling sputum is consistent with ANAEROBIC infection - Sometimes blood-tinged.
- Fever, chills.
- Constitutional symptoms: Fatigue, malaise, weight loss.
Lung abscess - Diagnosis - CXR:
Reveals thick-walled cavitation with air-fluid levels.
–> Look for abscess in dependent, poorly ventilated lobes.
Lung abscess - Diagnosis - CT:
May be necessary to differentiate between abscess and empyema.
Lung abscess - Diagnosis - Culture:
Consider obtaining cultures via bronchoscopy or transtracheal aspiration rather than simple expectoration to avoid contamination with oral flora.
Lung abscess - Treatment:
- Hospitalization is often required if lung abscess is found. Postural drainage should be performed.
- Antimicrobial therapy.
Lung abscess - Antimicrobial therapy:
- Antibiotic regimens include coverage for the following:
a. Gram(+) cocci - ampicillin or amoxicillin/clavulanic acid, ampicillin/sulbactam, or vancomycin for S.aureus.
b. Anaerobes - Clindamycin or metronidazole.
c. If Gram(-) are suspected - Add fluoroquinolone or ceftazidime. - CONTINUE antibiotics until the cavity is gone or until CXR findings have improved considerably.
Lung abscess - Antimicrobial therapy - How long may it take?
This may take months!
TB - Transmission:
- Occurs via inhalation of aerosolized droplets containing active organism.
- Only those with active TB are contagious (eg by coughing, sneezing).
- People with primary TB are NOT contagious.
Percentage of people with primary TB that will develop active disease in their lifetime?
Only 5-10%.
TB - Risk factors:
- HIV(+)
- Recent immigrants (within past 5yrs).
- Prisoners
- Health care workers
- Close contacts of someone with TB.
- Alcoholics
- Diabetics
- Glucocorticoid use
- Hematologic malignancy
- Injection drug users.
Primary TB - Clinical features:
- Asymptomatic.
- Pleural effusion may develop.
- If the immune response is incomplete, the pulmonary and constitutional symptoms of TB may develop. This is known as progressive primary TB.
Primary TB - Radiographic findings:
- Ghon’s complex - calcified primary focus with an associated lymph node.
- Ranke’s complex - when Ghon’s complex undergoes fibrosis and calcification.
Extrapulmonary TB - Sites:
- Lymph nodes.
- Pleura.
- GUT.
- Spine
- Intestine.
- Meninges.
Diagnosis of TB is challenging in HIV patients because:
- PPD skin test result is negative.
- Patients have “atypical” CXR findings.
- Sputum smears are more likely to be negative.
- Granuloma formation may NOT be present in the late stages.
Diagnosis of TB - CXR:
- Classic –> Upper lobe infiltrates with cavitations.
- Other possible findings:
a. Pleural effusion.
b. Ghon’s complex and Ranke’s complex - evidence of healed primary TB.
c. Atypical findings common in immunocompromised patients.
Diagnosis of TB - Sputum studies:
- DEFINITIVE diagnosis is made by sputum culture - growth of M.tuberculosis.
- Obtain 3 morning sputum specimens - culture takes 4-8wks.
- PCR can detect more rapidly.
- Diagnosis sometimes made by finding AFB on microscopic exam, but this is NOT definitive because other mycobacteria may colonize airways.
If PPD test is positive, what should be done?
A CXR to rule out active disease. Once active disease is EXCLUDED, 9 months of INH treatment is initiated (!).
A patient with a positive PPD test has how much lifetime risk of TB?
A 10% lifetime risk of TB –> This risk is reduced to 1% after 9months of INH treatment.
If patient has been BCG vaccinated, and we find positive PPD, do we give INH?
Yes, for 9 months, REGARDLESS of the BCG vaccination.
TB Treatment - Patients with active TB must be ISOLATED until sputum is negative for AFB. First-line therapy:
4-drug regimen: 1. INH 2. Rifampin 3. Pyrazinamide 4. Ethambutol or streptomycin FOR 2 MONTHS!
TB Treatment - After the initial 2 month phase?
A phase of 4 MONTHS is recommended using INH and rifampin.
Prophylactic treatment for latent (primary) TB:
Consists of 9 months of INH after active TB has been excluded (negative CXR, sputum, or both).
ALL TB medications can cause?
Hepatotoxicity. Discontinue treatment only if liver transaminases rise to 3-5times the upper limit or normal.
Influenza - Transmission:
Orthomyxovirus –> Transmitted via respiratory droplets, typically occurring in winter months.
Influenza - Clinical findings:
Rapid onset of:
- Fever
- Chills
- Malaise
- Headache
- Non productive cough
- Sore throat
- Nausea may also be present
Meningitis - Pathophysiology:
- Infectious agents –> Frequently colonize the nasopharynx and respiratory tract.
- These pathogens enter the CNS.
Meningitis - How do pathogens enter the CNS?
- Invasion of the bloodstream, which leads to hematogenous seeding of the CNS.
- Retrograde transport along cranial (eg olfatory) or peripheral nerves.
- Contiguous spread from sinusitis, otitis media, surgery, or trauma.
Acute meningitis:
Onset within hrs to days.
Chronic meningitis:
Onset within weeks to months - commonly caused by mycobacteria, fungi, Lyme, or parasites.
Acute bacterial meningitis - Complications:
- Seizures
- Coma
- Brain abscess
- Subdural empyema
- DIC
- Respiratory arrest
Acute bacterial meningitis - Complications - Permanent sequelae:
- Deafness
- Brain damage
- Hydrocephalus
Aseptic meningitis - Etiology:
- Enteroviruses
- HSV
- Also by certain bacteria, parasites, fungi
Acute bacterial meningitis is a…?
MEDICAL EMERGENCY! Frequently fatal, even with appropriate treatment.
Acute bacterial meningitis - clinical features:
Characteristic triad:
- Fever
- Nuchal rigidity
- Change in mental status
Meningitis - Symptoms:
- Headache (may be more severe when lying down).
- Fevers.
- Nausea and vomiting.
- Stiff, painful neck.
- Malaise.
- Photophobia.
- Alteration in mental status (confusion, lethargy, even coma).
Meningitis - Signs:
- Nuchal rigidity (may be ABSENT).
- Rashes - Maculopapular with petechiae –> PURPURA is classic for N.meningitidis/ Vesicular lesions in varicella or HSV.
- Incr. ICP and its manifestations - papilledema, seizures.
- Cranial nerve palsies.
- Kernig (only in 50%) and Brudzinki (only in 50%).
Diagnosis of meningitis - LP or CT first?
CT of the head, first –> If there are focal neurologic signs or if there is evidence of a space-occupying lesion with elevations in ICP.
Meningitis - Prophylaxis:
- Rifampin
- Ceftriaxone
for all close contacts of patients with meningococcus, give 1 dose of IM ceftriaxone.
Meningitis Treatment - Infants:
Cefotaxime + ampicillin + vanco (aminoglycoside if <4weeks).
Meningitis Treatment - 3mo to 50yrs:
Ceftriaxone or cefotaxime + Vancomycin.
Meningitis Treatment - >50yrs:
Ceftriaxone or cefotaxime + vancomycin + ampicillin.
Meningitis Treatment - Impaired cellular immunity (eg HIV):
Ceftazidime + Ampicillin + Vancomycin.
Encephalitis is often seen together with…?
Meningitis
Encephalitis - Viral causes:
- HSV-1
- Arbovirus - Eastern equine encephalitis, West Nile virus.
- Enterovirus - polio.
- Less common causes - Measles, mumps, EBV, CMV, VZV, rabies, prion diseases such as Creutzfeldt-Jakob.
Encephalitis - NON viral infectious causes:
- Toxoplasmosis.
2. Cerebral aspergillosis
Encephalitis - Non infectious causes:
- Metabolic encephalopathies.
2. T-cell lymphoma.
Encephalitis - Risk factors:
- AIDS - toxoplasmosis when CD4 is <200.
- Other forms of immunosuppression.
- Travel in underdeveloped countries.
- Exposure to insect (eg mosquito) vector in endemic areas.
- Exposure to certain wild animals (bats) in an endemic area for rabies.
Encephalitis - Overall mortality:
About 10%.
Encephalitis - Clinical features:
- Patients often have a prodrome of headache, malaise, and myalgias.
- Within hours to days, patients become more acutely ill.
- Patients frequently have signs and symptoms of meningitis (headache, fever, photophobia, nuchal rigidity).
- Altered sensorium, possibly including confusion, delirium, disorientation, and behavior abnormalities.
- Focal neurologic findings - Hemiparesis, aphasia, cranial nerve lesions, seizures.
Encephalitis - Diagnosis:
- Routine lab tests - to rule out viral causes. Include CXR, urine and blood cultures, urine tox screen, and serum chemistries.
- Perform LP –> Examine CSF.
- MRI of the brain –> IMAGING STUDY OF CHOICE.
- EEG –> Helpful in diagnosing HSV-1.
- Brain biopsy –> In an acutely ill patient with a focal, enhancing lesion on MRI without a clear diagnosis.
Encephalitis - Management of possible complications:
- Seizures - require anticonvulsant therapy.
2. Cerebral edema - Treatment may include hyperventilation, osmotic diuresis, and steroids.
DDX in patients with fever + altered mental status:
- Infection –> Sepsis, UTI/urosepsis, pneumonia, bacterial meningitis, intracranial abscess, subdural empyema.
- Medication/drugs –> Neuroleptic malignant syndrome (haloperidol, phenothiazines).
- Delirium tremens.
- Metabolic –> Thyroid storm.
Hepatitis in immunosuppressed:
By CMV, EBV, HSV.
Hep B is associated with…?
PAN
Hep C is associated with…?
Cryoglobulinemia
Course of hep B - Acute infection subclinical in?
70%.
Course of hep B:
Resolution –> 90%.
Chronic hep –> 5-10%.
Chronic carrier –> <1%.
Course of CHRONIC hep B:
Cirrhosis –> In 25%, 10-30yrs after onset.
HCC from hep B infection:
- Chronic hep (5-10%).
2. Chronic carrier (<5%).
Course of hep C - Acute infection subclinical in?
75%
Course of hep C:
Chronic hep –> 85-90%.
Resolution –> 10-15%.
Fulminant –> <1%.
Course of CHRONIC hep C:
Cirrhosis –> In 10-20% of all patients - 20-30yrs after onset.
Hep E is particularly prevalent in:
- India
- Pakistan
- Southeast Asia
- Parts of Africa.
If transaminases are markedly elevated (>500), think:
- Acute viral hepatitis.
- Shock liver.
- Drug-induced hepatitis.
Risk of developing cirrhosis or HCC in chronic hep B:
25-40%.
Risk of developing cirrhosis or HCC in chronic HCV:
10-25%.
In acute hep or in drug-induced hep is ALT more elevated?
In acute hep.
In chronic HBV or in chronic HCV is ALT higher?
In chronic HBV, but it varies.
Hep and Hep B treatment:
Active (vaccine) and passive (Ig) immunization are available for BOTH.
Chronic hep B Treatment:
- IFN-alpha.
2. Lamivudine (nucleoside analog).
Chronic HCV treatment:
- IFN-alpha.
2. Ribavirin
Botulism - General:
- Ingestion of PREFORMED TOXINS (!!!!).
- Toxins can be inactivated by cooking food at high temperatures.
- Wound contamination is another source for botulism.
Botulism - Severity of illness:
Varies widely, from mild, self-limiting symptoms, to rapidly fatal disease.
Botulism - Clinical features:
- Abdominal cramps.
- Nausea.
- Vomiting.
- Diarrhea.
Botulism - Hallmark:
Symmetric, DESCENDING flaccid paralysis.
Starts with dry mouth, diplopia, and/or dysarthria. Paralysis of limb musculature occurs later.
Botulism - Diagnosis:
- DEFINITIVE diagnosis is IDENTIFICATION of toxin in serum, stool, or gastric contents (bioassay).
- Identifying C.botulinum alone in food is NOT a reliable diagnostic indicator.
Botulism - Treatment:
- Admit patient and observe respiratory status closely. Gastric laavge is helpful only within several hrs after ingestion of suspected food.
- If suspicion is high, administer antitoxin (toxoid) as soon as lab specimens are obtained (do NOT WAIT for the results).
- For contaminated wounds - Wound cleansing and penicillin.
DDX of food-borne botulism:
- Guillain-Barre syndrome - Characteristically ASCENDING paralysis, but ONE VARIETY (Fischer) can be DESCENDING.
- Eaton-Lambert syndrome.
- Myasthenia gravis - EMG studies differentiate.
- Diphtheria.
- Tick paralysis.
Intra-abdominal abscess - Etiology:
- Spontaneous bacterial peritonitis.
- Pelvic infection (eg tubo-ovarian abscess).
- Pancreatitis
- Perforation of the GI.
- Osteomyelitis of the vertebral bodies with extension into the retroperitoneal cavity.
Intra-abdominal abscess - Diagnosis:
CT or US.
Intra-abdominal abscess - Treatment:
- Typically involves DRAINAGE of the abscess.
2. Antibiotic regimen should include broad coverage against Gram(-) rods, enterococci, and anaerobes.
Non infectious causes of cystitis or cystitis-like symptoms:
- Cytotoxic agents (eg cyclophosphamide).
- Radiation to pelvis.
- Dysfunctional voiding.
- Interstitial cystitis.
Host-dependent factors - Incr. risk for recurrent or complicated UTIs:
- DM - Incr. risk for recurrent UTIs.
- Patients with spinal cord injury.
- Immunocompromised.
- Any structural/functional abnormality that impedes urinary flow (eg incomplete voiding, neurogenic bladder, BPH, vesicourethral reflux, calculi).
Male risk factors - UTIs:
- Uncircumsized males are at higher risk due to bacterial colonization of the foreskin.
- Anal intercourse.
- Vaginal intercourse with a female colonized with uropathogens.
Lower UTIs - When to obtain cultures:
- Age >65.
- Diabetes.
- Recurrent UTIs.
- Presence of symptoms for 7days or more.
- Use of a diaphragm.
Major clinical feature to remember about LOWER UTIs:
In LOWER UTIs, fever is characteristically ABSENT.
Asymptomatic bacteriuria - Diagnosis:
2 successive positive cultures (>10^5CFU/mL) must be present.
Asymptomatic bacteriuria - Treat when?
Only in pregnancy or before urologic surgery.
Lower UTIs - Diagnosis - Dipstick analysis:
- Leukocyte esterase test (+) –> Pyuria.
2. Positive nitrite test for presence of bacteria (gram(-)) –> Sensitive for Enterobacteriaceae.
Urinalysis - Most important finding:
Presence of WBCs.
Urinalysis - Adequacy of collection:
- Presence of epithelial (squamous) cells indicates vulvar or urethral contamination.
- If contamination is suspected, perform a straight catheterization of the bladder.
Urinalysis - Criteria for UTI - Bacteriuria:
> 1 organism per oil-immersion field.
Bacteriuria without WBCs may reflect contamination and is NOT a reliable indicator of infection.
Urinalysis - Criteria for UTI - Pyuria:
It is the most valuable finding for diagnosis: Greater than or equal to 10 leukocytes/μL is ABNORMAL.
Urinalysis - Other findings:
Hematuria and mild proteinuria may be present. Hematuria in and of itself does NOT require extended therapy.
Lower UTIs - Diagnosis - Urine culture:
- Confirms the diagnosis (high specificity).
- Traditional criteria –> >10^5 CFU/mL –> misses up to 1/3 of UTIs.
- Colony counts as low as 10^2 to 10^4 CFU/mL are adequate for diagnosis if clinical symptoms are present.
Lower UTIs - Diagnosis - Blood culture:
Only indicated if patient is ill and urosepsis is suspected.
Complicated UTI:
- Any UTI that spreads beyond the bladder (eg pyelonephritis, prostatitis, urosepsis) –> Risk factors for upper UTI: pregnancy, diabetes, and vesicoureteral reflux.
- Any UTI caused by structural abnormalities, metabolic disorder, or neurologic dysfunction.
Complications - UTI during pregnancy:
Incr. risk of preterm labor, low birth weight, and other complications, especially in advanced pregnancy.
Complications - Recurrent infections:
- Usually due to infection with new organism, but sometimes is a relapse due to unsuccessful treatment of the original organism.
- Risk factors include impaired host defenses, pregnancy, vesicourethral reflux, and sexual intercourse in women.
- Generally the consequences are not significant unless the patient is at risk for upper UTI.
The following groups are considered to have complicated UTI:
- Men
- Diabetics
- Renal failure
- Pregnancy
- History of pyelonephritis in last year
- UT obstruction, indwelling catheter, stent, nephrostomy tube.
- Antibiotic resistant organism .
- Immunocompromised patients (HIV, transplant patients).
UTIs treatment - For uncomplicated UTI:
Empiric treatment is appropriate - do NOT wait for culture results.
If complicated EXTEND TREATMENT TO 7DAYS.
UTI treatment - Pregnant women with UTI:
- Treat with ampicillin, amoxicillin, or oral cephalosporins for 7-10days.
- Avoid fluoroquinolones (can cause fetal arthropathy(!)).
UTI treatment - UTIs in men:
- Treat as uncomplicated cystitis in women, but for 7 days.
2. Perform a urologic workup if there are complications or recurrences, or if initial treatment fails.
UTI treatment - Recurrent infections:
- If a relapse occurs within 2 weeks of cessation of treatment, continue treatment for 2 more weeks and obtain a urine culture.
- Otherwise treat as for uncomplicated cystitis. If the patient has more than two UTIs per year, give chemoprophylaxis.
Pyelonephritis - Complications (unusual):
- Sepsis occurs in 10-25% of patients with pyelonephritis. May lead to shock(!).
- Emphysematous pyelonephritis - caused by gas-producing bacteria in diabetic patients.
- Chronic pyelonephritis and scarring of the kidneys - rare unless underlying renal disease exists.
Pyelonephritis - Diagnosis - Urinalysis:
- Look for pyuria, bacteriuria, and leukocyte casts.
2. As in cystitis, hematuria and mild proteinuria may be present.
Pyelonephritis - Diagnosis - Blood/urine cultures:
Blood cultures –> Obtain in ill-appearing patients and ALL hospitalized patients.
Urine cultures –> Obtain in ALL patients with suspected pyelonephritis.
Pyelonephritis - Diagnosis - CBC:
Leukocytosis with left shift.
Pyelonephritis - Diagnosis - Renal function:
This is usually preserved. Impairment is usually reversible, especially with IV fluids.
Pyelonephritis - Diagnosis - Imaging studies:
Perform these if treatment fails or in any patient with complicated pyelonephritis. Consider renal US, CT, IVP, or retrograde ureterogram.
Treatment for uncomplicated pyelonephritis:
- Use outpatient treatment if the patient can take ORAL antibiotics. Treat based on gram stain.
- Repeat urine culture 2-4 days after cessation of therapy.
- If symptoms fail to resolve within 48hr, adjust treatment based on urine culture.
- Further failure to respond –> Urologic investigation.
For recurrent pyelonephritis:
- If relapse is due to the same organism despite appropriate treatment, treat for 6 weeks.
- If relapse is due to a new organism, treat with appropriate therapy for 2 weeks.
Prostatitis - Acute or chronic bacterial is more common?
Chronic bacterial is more common.
Acute bacterial prostatitis occurs more commonly in?
Younger men.
Prostatitis - Pathophysiology:
- Ascending infection.
- May occur after catheterization.
- Other causes - direct/lymphatic spread from the rectum.
- Hematogenous spread (rare).
Acute bacterial prostatitis - Causative organisms:
Gram(-) organisms predominate - E.coli, Klebsiella, Proteus, Pseudomonas, Enterobacter, Serratia spp.