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Infectious Disease and Microbiology – Pyelonephritis
Pyelonephritis is a common infection of the upper urinary tract that causes inflammation of the renal pelvis, calyces, and renal parenchyma. It may occur as acute uncomplicated pyelonephritis, acute complicated pyelonephritis, chronic pyelonephritis, or xanthogranulomatous pyelonephritis. Chronic pyelonephritis is characterized by uneven renal scarring and chronic inflammatory changes affecting the renal interstitium and tubules.
The disease is much more common in females than males. Young women, infants, and elderly individuals are the groups most commonly affected. In the United States, more than 250,000 cases occur annually.
Risk factors include pregnancy, urinary tract obstruction caused by prostate disease or urethral narrowing, renal calculi, diabetes mellitus, and recurrent urinary tract infections. In young women, frequent sexual intercourse, spermicide use, stress incontinence, a new sexual partner, and a personal or maternal history of urinary tract infection significantly increase the likelihood of infection. Prevention focuses on prompt recognition and treatment of lower urinary tract infections and reduction of modifiable risk factors.
Most infections occur by ascending spread of organisms from the urethra to the bladder and then through the ureters to the kidneys. Less commonly, hematogenous spread occurs, particularly with gram-positive organisms or fungal infections.
The most common pathogen is Escherichia coli, responsible for approximately 80% of cases. Other important organisms include Proteus species and Klebsiella species. Less common causes include Pseudomonas aeruginosa, enterococci, and Staphylococcus saprophyticus. Isolation of Staphylococcus aureus from urine usually suggests bacteremia. Emphysematous pyelonephritis, a severe gas-forming necrotizing infection of the kidney, is commonly caused by E. coli and Klebsiella species and rarely by Candida species.
Symptoms may develop over several hours or days and commonly include fever, chills, malaise, headache, nausea, vomiting, flank pain, back pain, abdominal pain, dysuria, urgency, and hematuria. Elderly patients may have only minimal symptoms, while children often present with nonspecific findings.
Physical examination frequently demonstrates fever, tachycardia, flank tenderness, dehydration, or signs of sepsis in severe disease.
Diagnosis begins with urinalysis showing pyuria and bacteriuria, although absence of bacteria does not exclude pyelonephritis. Pretreatment urine cultures are essential. Laboratory studies may demonstrate leukocytosis with left shift, elevated inflammatory markers such as ESR and CRP, and abnormalities in renal function tests. Blood cultures may be helpful in severe infections.
Imaging is indicated in recurrent disease, atypical presentations, persistent hematuria, suspected obstruction, or failure to improve after 72 hours of treatment. Plain abdominal radiographs may identify calculi or gas formation. Ultrasonography is preferred initially in recurrent or atypical cases. Contrast-enhanced CT scanning is useful for identifying obstruction, renal or perinephric abscesses, and complicated anatomy. Repeat imaging may be required if clinical deterioration occurs despite treatment.
The differential diagnosis includes cystitis, urethritis, vaginitis, appendicitis, pelvic inflammatory disease, and renal or bladder tumors.
Treatment depends on disease severity and local antimicrobial susceptibility patterns. Outpatient treatment for uncomplicated pyelonephritis may include oral amoxicillin, amoxicillin-clavulanate, trimethoprim-sulfamethoxazole, ciprofloxacin, levofloxacin, norfloxacin, or cefpodoxime. Fluoroquinolones are commonly used because of excellent renal penetration. Therapy usually lasts 10–14 days, although short-course high-dose levofloxacin may be used for 5 days.
Hospitalized patients require intravenous antibiotics such as ciprofloxacin, levofloxacin, ceftriaxone, gentamicin, ampicillin, aztreonam, imipenem-cilastatin, ertapenem, or ticarcillin-clavulanic acid. After clinical improvement and resolution of fever, patients are transitioned to oral therapy to complete treatment.
Supportive care includes rest, analgesics, antiemetics, and adequate hydration. Intravenous fluids are essential in septic or dehydrated patients.
Consultation with a urologist is recommended when obstruction or structural abnormalities are present, since surgical correction may be necessary. Infectious disease consultation is helpful for resistant or unusual organisms such as Pseudomonas aeruginosa or extended-spectrum beta-lactamase–producing bacteria.
Surgical management may be required in emphysematous pyelonephritis, renal or perinephric abscess, renal stones, or xanthogranulomatous pyelonephritis.
Hospital admission is indicated for severe illness, dehydration, inability to tolerate oral medications, pregnancy, or concern for sepsis. Patients can generally be discharged after 24–48 hours of clinical improvement and defervescence.
Follow-up includes post-treatment urine cultures and further imaging or laboratory evaluation in patients with persistent symptoms. Patients should be advised to complete antibiotic therapy exactly as prescribed and maintain adequate hydration.
Acute uncomplicated pyelonephritis generally has an excellent prognosis, with overall in-hospital mortality below 1–2%. Complications include bacteremia, septic shock, renal abscess, perinephric abscess, and struvite stone formation, particularly in infections caused by Proteus species.
ICD-9 Codes
Escherichia coli and Klebsiella pneumoniae have developed significant resistance to many antibiotic classes. Extended-spectrum beta-lactamase production, often associated with quinolone resistance, presents a major therapeutic challenge. Carbapenems or fosfomycin disodium may be necessary for treatment in resistant infections. Treatment should always be guided by local susceptibility patterns of urinary pathogens. Quinolones and sulfonamides should be avoided during pregnancy and in patients with glucose-6-phosphate dehydrogenase deficiency.
Infectious Disease and Microbiology – Q Fever
Q fever is a globally distributed zoonotic infection caused by Coxiella burnetii. The disease was named “Q” for “query” because its cause was unknown when first described in 1935. It usually presents as an acute febrile illness, atypical pneumonia, or hepatitis, although chronic infection can occur, most commonly as endocarditis.
The primary reservoirs of C. burnetii are cattle, sheep, and goats, though many animals including rodents and cats may be infected. The organism is shed in milk, urine, feces, and particularly amniotic fluid of infected animals. Humans usually acquire infection by inhaling contaminated aerosols. Very few organisms are needed to cause infection, making the bacterium highly infectious. Transmission through blood transfusion is rare.
The disease is often underdiagnosed and underreported worldwide. Many infections are asymptomatic. Cases tend to occur more commonly during lambing and calving seasons, particularly between February and May in some regions. Men are affected more frequently than women.
Prevention includes avoiding unpasteurized milk, proper disposal of infected animal products, isolation of affected animals, and vaccination of high-risk workers in countries where vaccines are available, such as Australia.
Coxiella burnetii is a gram-negative intracellular coccobacillus capable of surviving within host phagolysosomes. Acute infection is characterized by antibodies directed against phase II antigens, while chronic infection is associated with elevated phase I antibody titers. Host immune response, especially T-cell–mediated immunity, plays a major role in determining disease progression.
Approximately half of infected individuals remain asymptomatic. Symptomatic acute Q fever commonly presents as a self-limited febrile illness, influenza-like syndrome, atypical pneumonia, or hepatitis. Symptoms include fever, chills, headache, sweats, nausea, vomiting, diarrhea, and malaise. Pneumonia and hepatitis frequently coexist. Severe infection during pregnancy may result in abortion or neonatal death.
Headache is the most common neurologic symptom. Rare manifestations include epididymitis, erythema nodosum, Guillain-Barré syndrome, hemolytic anemia, optic neuritis, pancreatitis, orchitis, myocarditis, pericarditis, osteomyelitis, meningoencephalitis, and prolonged fever.
Chronic Q fever most commonly manifests as endocarditis, particularly involving the aortic valve. Fever may be absent or low grade. Infection of vascular grafts, aneurysms, and prosthetic material has become increasingly recognized.
Physical examination in acute disease often reveals high fever, occasionally reaching 40°C, with relative bradycardia. Hepatomegaly and splenomegaly may occur. Rash is uncommon compared with other rickettsial diseases.
Diagnosis is primarily serologic. Indirect immunofluorescence is the preferred test. Acute infection is suggested by a fourfold rise in antibody titers between acute and convalescent samples or elevated IgM titers. PCR testing may detect bacterial DNA in blood or tissue specimens. Laboratory abnormalities may include elevated ESR and CRP, thrombocytopenia or thrombocytosis, monocytosis, elevated alkaline phosphatase, and abnormal liver function tests.
Chest imaging in Q fever pneumonia may reveal pleural effusions or infiltrates, and radiographic resolution can take several weeks. Chronic infection should be considered in cases of culture-negative endocarditis.
The differential diagnosis includes other causes of atypical pneumonia, hepatitis of unknown origin, culture-negative endocarditis, and central nervous system infections.
Early treatment improves outcomes. Acute Q fever is usually treated successfully with doxycycline 100 mg twice daily for 14 days. Chronic Q fever, especially endocarditis, is treated with prolonged doxycycline plus hydroxychloroquine therapy, often for 3–4 years or longer. Treatment duration is guided by serial antibody titers. Rifampin or fluoroquinolones may also be used in selected chronic cases.
Most acute infections resolve spontaneously, but chronic Q fever carries significant morbidity and mortality. Mortality from acute disease is approximately 2%, whereas mortality from Q fever endocarditis may reach 25–60%, with frequent relapse.
Pyelonephritis is a common infection of the upper urinary tract that causes inflammation of the renal pelvis, calyces, and renal parenchyma. It may occur as acute uncomplicated pyelonephritis, acute complicated pyelonephritis, chronic pyelonephritis, or xanthogranulomatous pyelonephritis. Chronic pyelonephritis is characterized by uneven renal scarring and chronic inflammatory changes affecting the renal interstitium and tubules.
The disease is much more common in females than males. Young women, infants, and elderly individuals are the groups most commonly affected. In the United States, more than 250,000 cases occur annually.
Risk factors include pregnancy, urinary tract obstruction caused by prostate disease or urethral narrowing, renal calculi, diabetes mellitus, and recurrent urinary tract infections. In young women, frequent sexual intercourse, spermicide use, stress incontinence, a new sexual partner, and a personal or maternal history of urinary tract infection significantly increase the likelihood of infection. Prevention focuses on prompt recognition and treatment of lower urinary tract infections and reduction of modifiable risk factors.
Most infections occur by ascending spread of organisms from the urethra to the bladder and then through the ureters to the kidneys. Less commonly, hematogenous spread occurs, particularly with gram-positive organisms or fungal infections.
The most common pathogen is Escherichia coli, responsible for approximately 80% of cases. Other important organisms include Proteus species and Klebsiella species. Less common causes include Pseudomonas aeruginosa, enterococci, and Staphylococcus saprophyticus. Isolation of Staphylococcus aureus from urine usually suggests bacteremia. Emphysematous pyelonephritis, a severe gas-forming necrotizing infection of the kidney, is commonly caused by E. coli and Klebsiella species and rarely by Candida species.
Symptoms may develop over several hours or days and commonly include fever, chills, malaise, headache, nausea, vomiting, flank pain, back pain, abdominal pain, dysuria, urgency, and hematuria. Elderly patients may have only minimal symptoms, while children often present with nonspecific findings.
Physical examination frequently demonstrates fever, tachycardia, flank tenderness, dehydration, or signs of sepsis in severe disease.
Diagnosis begins with urinalysis showing pyuria and bacteriuria, although absence of bacteria does not exclude pyelonephritis. Pretreatment urine cultures are essential. Laboratory studies may demonstrate leukocytosis with left shift, elevated inflammatory markers such as ESR and CRP, and abnormalities in renal function tests. Blood cultures may be helpful in severe infections.
Imaging is indicated in recurrent disease, atypical presentations, persistent hematuria, suspected obstruction, or failure to improve after 72 hours of treatment. Plain abdominal radiographs may identify calculi or gas formation. Ultrasonography is preferred initially in recurrent or atypical cases. Contrast-enhanced CT scanning is useful for identifying obstruction, renal or perinephric abscesses, and complicated anatomy. Repeat imaging may be required if clinical deterioration occurs despite treatment.
The differential diagnosis includes cystitis, urethritis, vaginitis, appendicitis, pelvic inflammatory disease, and renal or bladder tumors.
Treatment depends on disease severity and local antimicrobial susceptibility patterns. Outpatient treatment for uncomplicated pyelonephritis may include oral amoxicillin, amoxicillin-clavulanate, trimethoprim-sulfamethoxazole, ciprofloxacin, levofloxacin, norfloxacin, or cefpodoxime. Fluoroquinolones are commonly used because of excellent renal penetration. Therapy usually lasts 10–14 days, although short-course high-dose levofloxacin may be used for 5 days.
Hospitalized patients require intravenous antibiotics such as ciprofloxacin, levofloxacin, ceftriaxone, gentamicin, ampicillin, aztreonam, imipenem-cilastatin, ertapenem, or ticarcillin-clavulanic acid. After clinical improvement and resolution of fever, patients are transitioned to oral therapy to complete treatment.
Supportive care includes rest, analgesics, antiemetics, and adequate hydration. Intravenous fluids are essential in septic or dehydrated patients.
Consultation with a urologist is recommended when obstruction or structural abnormalities are present, since surgical correction may be necessary. Infectious disease consultation is helpful for resistant or unusual organisms such as Pseudomonas aeruginosa or extended-spectrum beta-lactamase–producing bacteria.
Surgical management may be required in emphysematous pyelonephritis, renal or perinephric abscess, renal stones, or xanthogranulomatous pyelonephritis.
Hospital admission is indicated for severe illness, dehydration, inability to tolerate oral medications, pregnancy, or concern for sepsis. Patients can generally be discharged after 24–48 hours of clinical improvement and defervescence.
Follow-up includes post-treatment urine cultures and further imaging or laboratory evaluation in patients with persistent symptoms. Patients should be advised to complete antibiotic therapy exactly as prescribed and maintain adequate hydration.
Acute uncomplicated pyelonephritis generally has an excellent prognosis, with overall in-hospital mortality below 1–2%. Complications include bacteremia, septic shock, renal abscess, perinephric abscess, and struvite stone formation, particularly in infections caused by Proteus species.
ICD-9 Codes
- 590.00 – Chronic pyelonephritis without lesion of renal medullary necrosis
- 590.10 – Acute pyelonephritis without lesion of renal medullary necrosis
- 590.80 – Pyelonephritis, unspecified
Escherichia coli and Klebsiella pneumoniae have developed significant resistance to many antibiotic classes. Extended-spectrum beta-lactamase production, often associated with quinolone resistance, presents a major therapeutic challenge. Carbapenems or fosfomycin disodium may be necessary for treatment in resistant infections. Treatment should always be guided by local susceptibility patterns of urinary pathogens. Quinolones and sulfonamides should be avoided during pregnancy and in patients with glucose-6-phosphate dehydrogenase deficiency.
Infectious Disease and Microbiology – Q Fever
Q fever is a globally distributed zoonotic infection caused by Coxiella burnetii. The disease was named “Q” for “query” because its cause was unknown when first described in 1935. It usually presents as an acute febrile illness, atypical pneumonia, or hepatitis, although chronic infection can occur, most commonly as endocarditis.
The primary reservoirs of C. burnetii are cattle, sheep, and goats, though many animals including rodents and cats may be infected. The organism is shed in milk, urine, feces, and particularly amniotic fluid of infected animals. Humans usually acquire infection by inhaling contaminated aerosols. Very few organisms are needed to cause infection, making the bacterium highly infectious. Transmission through blood transfusion is rare.
The disease is often underdiagnosed and underreported worldwide. Many infections are asymptomatic. Cases tend to occur more commonly during lambing and calving seasons, particularly between February and May in some regions. Men are affected more frequently than women.
Prevention includes avoiding unpasteurized milk, proper disposal of infected animal products, isolation of affected animals, and vaccination of high-risk workers in countries where vaccines are available, such as Australia.
Coxiella burnetii is a gram-negative intracellular coccobacillus capable of surviving within host phagolysosomes. Acute infection is characterized by antibodies directed against phase II antigens, while chronic infection is associated with elevated phase I antibody titers. Host immune response, especially T-cell–mediated immunity, plays a major role in determining disease progression.
Approximately half of infected individuals remain asymptomatic. Symptomatic acute Q fever commonly presents as a self-limited febrile illness, influenza-like syndrome, atypical pneumonia, or hepatitis. Symptoms include fever, chills, headache, sweats, nausea, vomiting, diarrhea, and malaise. Pneumonia and hepatitis frequently coexist. Severe infection during pregnancy may result in abortion or neonatal death.
Headache is the most common neurologic symptom. Rare manifestations include epididymitis, erythema nodosum, Guillain-Barré syndrome, hemolytic anemia, optic neuritis, pancreatitis, orchitis, myocarditis, pericarditis, osteomyelitis, meningoencephalitis, and prolonged fever.
Chronic Q fever most commonly manifests as endocarditis, particularly involving the aortic valve. Fever may be absent or low grade. Infection of vascular grafts, aneurysms, and prosthetic material has become increasingly recognized.
Physical examination in acute disease often reveals high fever, occasionally reaching 40°C, with relative bradycardia. Hepatomegaly and splenomegaly may occur. Rash is uncommon compared with other rickettsial diseases.
Diagnosis is primarily serologic. Indirect immunofluorescence is the preferred test. Acute infection is suggested by a fourfold rise in antibody titers between acute and convalescent samples or elevated IgM titers. PCR testing may detect bacterial DNA in blood or tissue specimens. Laboratory abnormalities may include elevated ESR and CRP, thrombocytopenia or thrombocytosis, monocytosis, elevated alkaline phosphatase, and abnormal liver function tests.
Chest imaging in Q fever pneumonia may reveal pleural effusions or infiltrates, and radiographic resolution can take several weeks. Chronic infection should be considered in cases of culture-negative endocarditis.
The differential diagnosis includes other causes of atypical pneumonia, hepatitis of unknown origin, culture-negative endocarditis, and central nervous system infections.
Early treatment improves outcomes. Acute Q fever is usually treated successfully with doxycycline 100 mg twice daily for 14 days. Chronic Q fever, especially endocarditis, is treated with prolonged doxycycline plus hydroxychloroquine therapy, often for 3–4 years or longer. Treatment duration is guided by serial antibody titers. Rifampin or fluoroquinolones may also be used in selected chronic cases.
Most acute infections resolve spontaneously, but chronic Q fever carries significant morbidity and mortality. Mortality from acute disease is approximately 2%, whereas mortality from Q fever endocarditis may reach 25–60%, with frequent relapse.
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