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Infectious Diseases and Microbiology: Gonorrhea
Basics
Description
Gonorrhea is caused by Neisseria gonorrhoeae, a gram-negative intracellular diplococcus that infects humans only. Spread occurs through direct mucosal inoculation during sexual contact or childbirth. Transmission is more efficient from men to women, and a single sexual exposure can infect up to half of female partners.
Epidemiology
Gonorrhea remains a major global public health issue and contributes substantially to morbidity, especially in developing regions. Worldwide incidence has been estimated at roughly 62 million new infections annually, with highest rates in sub-Saharan Africa, South and Southeast Asia, the Caribbean, and Latin America. In the United States, hundreds of thousands of cases were reported in 2008 with the highest rates in females aged 15–19 and males aged 20–24; reported rates were higher in African American and Hispanic populations than in White populations.
Risk Factors
Risk is increased by female sex, age under 25, prior gonorrhea or other STIs, new or multiple partners, inconsistent condom use, commercial sex work, drug use, and travel to high-prevalence countries.
General Prevention
Control relies on early detection, immediate treatment at diagnosis, and treatment of sexual partners. Partners within 60 days before symptom onset should be evaluated and treated. Delaying sexual debut, reducing partner number, and consistent condom use decrease transmission.
Etiology
Disease is due to N. gonorrhoeae, a nonmotile, non–spore-forming gram-negative diplococcus.
Commonly Associated Conditions
Coinfection with other STIs is common; Chlamydia coinfection occurs in about one-third of cases. Gonorrhea also increases susceptibility to acquiring HIV.
Diagnosis
Clinical manifestations depend on infection site, bacterial strain, host factors, sex, and coinfections. Many infections are asymptomatic in both sexes. Incubation is typically 2–7 days. In men, urethritis usually begins with dysuria followed by purulent discharge, and acute epididymitis is the most frequent complication. In women, urethritis can cause dysuria, frequency, and urgency, and cervicitis may develop with purulent discharge, cramping, dyspareunia, and postcoital or intermenstrual bleeding; symptoms often intensify around menstruation. Untreated infection can ascend, causing pelvic inflammatory disease with infertility and chronic pelvic pain. Conjunctivitis usually results from autoinoculation and can rapidly threaten vision. In neonates, infection is commonly ophthalmia neonatorum acquired during delivery; ocular prophylaxis with agents such as silver nitrate drops or tetracycline ointment is used for prevention. Disseminated gonococcal infection may present with fever, rash, tenosynovitis, and septic arthritis and can resemble an influenza-like illness without obvious mucosal symptoms, so urethral/cervical, rectal, and pharyngeal sites should be sampled.
Diagnostic Tests and Interpretation
Laboratory Studies
In symptomatic men, Gram stain of urethral discharge can show polymorphonuclear cells and gram-negative intracellular diplococci, but Gram stain performs poorly with endocervical, rectal, and pharyngeal specimens. Culture allows antimicrobial susceptibility testing and should be performed on selective media such as modified Thayer–Martin (or equivalent) with aerobic conditions and increased CO₂; rapid processing is essential because gonococci do not tolerate drying. Strains linked to dissemination may be more fastidious and harder to grow. Nucleic acid–based tests can detect N. gonorrhoeae from swabs or urine with sensitivity and specificity comparable or better than culture, but cost is higher and cross-reactivity with nonpathogenic Neisseria species can occur.
Differential Diagnosis
Urethritis can be nongonococcal due to Chlamydia, Ureaplasma, Mycoplasma genitalium, Haemophilus vaginalis, HSV, adenovirus, and others. Vaginal symptoms may reflect candidiasis, bacterial vaginosis, trichomoniasis, or noninfectious etiologies such as chemical irritation, allergy, fistula, or pregnancy-related leukorrhea. Disseminated gonococcal infection must be distinguished from meningococcemia, ecthyma gangrenosum, other bacteremias, septic arthritis from other bacteria, and reactive arthritis.
Treatment
Medications
CDC-recommended therapy has centered on cephalosporins. For uncomplicated urethral, cervical, or rectal infection, recommended single-dose options include ceftriaxone 125 mg IM, cefixime 400 mg PO, or spectinomycin 2 g IM. Pharyngeal infection is harder to eradicate and is treated with ceftriaxone 125 mg IM as the preferred regimen. Gonococcal conjunctivitis is treated with ceftriaxone 125 mg IM once, with saline eye irrigation as an optional adjunct. Disseminated infection is treated with parenteral cephalosporin-based regimens such as ceftriaxone 1 g IM/IV daily or cefotaxime/ceftizoxime 1 g IV three times daily, or spectinomycin 2 g IM twice daily; continue parenteral therapy for 24–48 hours after clinical improvement, then transition to an oral agent such as cefixime 400 mg PO twice daily to complete a total of one week. If chlamydial infection has not been excluded, provide concurrent chlamydia therapy. Fluoroquinolones are not recommended as first-line therapy in the United States because of widespread resistance.
Additional Treatment
Because Chlamydia coinfection is common, initial management should cover chlamydia (e.g., azithromycin or doxycycline) unless it has been ruled out.
Ongoing Care and Follow-Up
Patient Monitoring
A routine test-of-cure is not required after treating uncomplicated infection. If symptoms persist, obtain culture with susceptibility testing; the most common reason for apparent treatment failure is reinfection from an untreated partner.
Patient Education
Advise consistent condom use and provide instruction on correct condom use.
Complications
The most important complication is pelvic inflammatory disease from ascending infection, which can lead to tubo-ovarian abscess, pelvic peritonitis, and Fitz-Hugh–Curtis syndrome, with long-term infertility and chronic pelvic pain. In men, complications include epididymitis, periurethritis, balanitis, acute or chronic prostatitis, orchitis, seminal vasculitis, and infection of Tyson and Cowper glands. Disseminated gonococcemia is more common in women, with menstruation increasing risk, and typically causes tenosynovitis, migratory arthritis, and peripheral skin lesions that may be maculopapular or pustular; blood cultures are positive in only a minority of cases. Endocarditis and meningitis are rare in the antibiotic era.
Basics
Description
Gonorrhea is caused by Neisseria gonorrhoeae, a gram-negative intracellular diplococcus that infects humans only. Spread occurs through direct mucosal inoculation during sexual contact or childbirth. Transmission is more efficient from men to women, and a single sexual exposure can infect up to half of female partners.
Epidemiology
Gonorrhea remains a major global public health issue and contributes substantially to morbidity, especially in developing regions. Worldwide incidence has been estimated at roughly 62 million new infections annually, with highest rates in sub-Saharan Africa, South and Southeast Asia, the Caribbean, and Latin America. In the United States, hundreds of thousands of cases were reported in 2008 with the highest rates in females aged 15–19 and males aged 20–24; reported rates were higher in African American and Hispanic populations than in White populations.
Risk Factors
Risk is increased by female sex, age under 25, prior gonorrhea or other STIs, new or multiple partners, inconsistent condom use, commercial sex work, drug use, and travel to high-prevalence countries.
General Prevention
Control relies on early detection, immediate treatment at diagnosis, and treatment of sexual partners. Partners within 60 days before symptom onset should be evaluated and treated. Delaying sexual debut, reducing partner number, and consistent condom use decrease transmission.
Etiology
Disease is due to N. gonorrhoeae, a nonmotile, non–spore-forming gram-negative diplococcus.
Commonly Associated Conditions
Coinfection with other STIs is common; Chlamydia coinfection occurs in about one-third of cases. Gonorrhea also increases susceptibility to acquiring HIV.
Diagnosis
Clinical manifestations depend on infection site, bacterial strain, host factors, sex, and coinfections. Many infections are asymptomatic in both sexes. Incubation is typically 2–7 days. In men, urethritis usually begins with dysuria followed by purulent discharge, and acute epididymitis is the most frequent complication. In women, urethritis can cause dysuria, frequency, and urgency, and cervicitis may develop with purulent discharge, cramping, dyspareunia, and postcoital or intermenstrual bleeding; symptoms often intensify around menstruation. Untreated infection can ascend, causing pelvic inflammatory disease with infertility and chronic pelvic pain. Conjunctivitis usually results from autoinoculation and can rapidly threaten vision. In neonates, infection is commonly ophthalmia neonatorum acquired during delivery; ocular prophylaxis with agents such as silver nitrate drops or tetracycline ointment is used for prevention. Disseminated gonococcal infection may present with fever, rash, tenosynovitis, and septic arthritis and can resemble an influenza-like illness without obvious mucosal symptoms, so urethral/cervical, rectal, and pharyngeal sites should be sampled.
Diagnostic Tests and Interpretation
Laboratory Studies
In symptomatic men, Gram stain of urethral discharge can show polymorphonuclear cells and gram-negative intracellular diplococci, but Gram stain performs poorly with endocervical, rectal, and pharyngeal specimens. Culture allows antimicrobial susceptibility testing and should be performed on selective media such as modified Thayer–Martin (or equivalent) with aerobic conditions and increased CO₂; rapid processing is essential because gonococci do not tolerate drying. Strains linked to dissemination may be more fastidious and harder to grow. Nucleic acid–based tests can detect N. gonorrhoeae from swabs or urine with sensitivity and specificity comparable or better than culture, but cost is higher and cross-reactivity with nonpathogenic Neisseria species can occur.
Differential Diagnosis
Urethritis can be nongonococcal due to Chlamydia, Ureaplasma, Mycoplasma genitalium, Haemophilus vaginalis, HSV, adenovirus, and others. Vaginal symptoms may reflect candidiasis, bacterial vaginosis, trichomoniasis, or noninfectious etiologies such as chemical irritation, allergy, fistula, or pregnancy-related leukorrhea. Disseminated gonococcal infection must be distinguished from meningococcemia, ecthyma gangrenosum, other bacteremias, septic arthritis from other bacteria, and reactive arthritis.
Treatment
Medications
CDC-recommended therapy has centered on cephalosporins. For uncomplicated urethral, cervical, or rectal infection, recommended single-dose options include ceftriaxone 125 mg IM, cefixime 400 mg PO, or spectinomycin 2 g IM. Pharyngeal infection is harder to eradicate and is treated with ceftriaxone 125 mg IM as the preferred regimen. Gonococcal conjunctivitis is treated with ceftriaxone 125 mg IM once, with saline eye irrigation as an optional adjunct. Disseminated infection is treated with parenteral cephalosporin-based regimens such as ceftriaxone 1 g IM/IV daily or cefotaxime/ceftizoxime 1 g IV three times daily, or spectinomycin 2 g IM twice daily; continue parenteral therapy for 24–48 hours after clinical improvement, then transition to an oral agent such as cefixime 400 mg PO twice daily to complete a total of one week. If chlamydial infection has not been excluded, provide concurrent chlamydia therapy. Fluoroquinolones are not recommended as first-line therapy in the United States because of widespread resistance.
Additional Treatment
Because Chlamydia coinfection is common, initial management should cover chlamydia (e.g., azithromycin or doxycycline) unless it has been ruled out.
Ongoing Care and Follow-Up
Patient Monitoring
A routine test-of-cure is not required after treating uncomplicated infection. If symptoms persist, obtain culture with susceptibility testing; the most common reason for apparent treatment failure is reinfection from an untreated partner.
Patient Education
Advise consistent condom use and provide instruction on correct condom use.
Complications
The most important complication is pelvic inflammatory disease from ascending infection, which can lead to tubo-ovarian abscess, pelvic peritonitis, and Fitz-Hugh–Curtis syndrome, with long-term infertility and chronic pelvic pain. In men, complications include epididymitis, periurethritis, balanitis, acute or chronic prostatitis, orchitis, seminal vasculitis, and infection of Tyson and Cowper glands. Disseminated gonococcemia is more common in women, with menstruation increasing risk, and typically causes tenosynovitis, migratory arthritis, and peripheral skin lesions that may be maculopapular or pustular; blood cultures are positive in only a minority of cases. Endocarditis and meningitis are rare in the antibiotic era.
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Infectious Diseases and Microbiology: Hepatosplenomegaly and Fever
Basics
Description
A midclavicular liver span of at least 12.5 cm supports hepatomegaly. Splenomegaly is defined as a spleen exceeding 250 g or one that is palpable, and on ultrasound is suggested by a cephalocaudal length of 13 cm or more
.
Approach to the Patient
Evaluating Hepatomegaly
Palpate to identify the lower liver edge at the right midclavicular line, then use gentle percussion to define the upper border so liver span can be measured; a span ≥12.5 cm supports hepatomegaly. Because hyperinflated lungs can push the liver downward, the upper border must be assessed to avoid overcalling enlargement.
Evaluating Splenomegaly
Bedside assessment should include both palpation and percussion. Palpation is best done bimanually with the patient supine and in the right lateral position. Percussion methods by Nixon and Castell provide the best diagnostic performance. In Nixon’s method, the patient lies on the right side and percussion begins in the posterior axillary line at the level where lung resonance ends, moving obliquely toward the left anterior costal margin; a dullness span over 8 cm suggests splenomegaly and has moderate sensitivity with high specificity. In Castell’s method, the patient is supine and percussion in the lowest intercostal space at the left anterior axillary line should remain resonant during inspiration if the spleen is normal; this approach has moderate sensitivity and specificity. If missing splenomegaly would change management, confirm with ultrasound or scintigraphy.
Evaluating Fever with Liver and/or Spleen Enlargement
Obtain a comprehensive history emphasizing travel and immigration, occupation, sexual history, intravenous drug use, animal exposure, and family history of malignancy, connective tissue disease, or inherited conditions. Look for associated findings including jaundice, fever duration and pattern, lymphadenopathy, rashes or bite exposures, liver edge texture and tenderness, an enlarged gallbladder or other abdominal mass, and spleen size and consistency. Initial testing commonly includes broad laboratory evaluation, heterophile antibody testing, hepatitis studies, imaging, and in selected cases bone marrow evaluation, endoscopy, and/or liver biopsy.
Epidemiology
In young adults, palpability of the liver and spleen can occur even without disease. In a large sample of healthy military personnel, the liver was not palpable or only at the costal margin in over half, and descended only 1–2 cm below the margin in many others. Studies of healthy college entrants have found a small proportion with unexplained palpable spleens, and palpable spleens have been reported in a notable minority of otherwise normal postpartum women.
Etiology
Hepatomegaly with Fever
Infectious causes include pyogenic or amoebic abscess, ascending cholangitis, chronic granulomatous disease, chronic Q fever, ehrlichiosis, histoplasmosis, HIV, infectious hepatitis, infectious mononucleosis, leptospirosis, syphilis, tuberculosis, and parasitic infections. Malignant causes include diffuse primary hepatic cancer, diffuse metastases, myeloproliferative disorders, lymphoma, and angiosarcoma. Inflammatory causes include sarcoidosis, autoimmune hepatitis, familial Mediterranean fever, and Still’s disease.
Splenomegaly with Fever
Infectious causes include viral infections such as hepatitis, infectious mononucleosis, and HIV; bacterial infections such as endocarditis, pyogenic abscess, salmonellosis, leptospirosis, brucellosis, Bartonella; fungal infections such as histoplasmosis; mycobacterial infections including miliary tuberculosis and nontuberculous mycobacteria; and parasitic infections including malaria, toxoplasmosis, amoebic liver abscess, schistosomiasis with Katayama fever, visceral leishmaniasis, babesiosis, and ehrlichiosis. Inflammatory causes include rheumatoid arthritis, sarcoidosis, systemic lupus erythematosus, and hemophagocytic lymphohistiocytosis. Malignant causes include lymphoma, acute and chronic leukemias, and myelodysplastic or myeloproliferative syndromes. Numerous parasites can enlarge liver and spleen depending on exposure context, including malaria, schistosomiasis, hydatid disease, leishmaniasis, toxocariasis, toxoplasmosis, liver flukes such as Fasciola hepatica, and echinococcal cysts, which can enlarge organs but are rarely febrile. Fever occurs in roughly half of toxoplasmosis and toxocariasis cases.
Diagnosis
History and Clinical Manifestations
In young adults, the combination of fatigue, sore throat, fever, lymphadenopathy, and hepatosplenomegaly is most often infectious mononucleosis. Fever with abdominal pain that may localize to the right upper quadrant, vomiting or anorexia, hepatomegaly, leukocytosis with elevated sedimentation rate, and otherwise unexplained anemia should raise concern for liver abscess. Pyogenic liver abscess most often arises from biliary disease and is commonly due to enteric organisms including Escherichia coli, Klebsiella, enterococci, anginosus group streptococci, and anaerobes, and is most often seen in adults in their fifth and sixth decades. Pyogenic liver abscess with metastatic infection such as endophthalmitis, meningitis, or other focal abscesses suggests Klebsiella pneumoniae, particularly in patients with diabetes and those from East Asia. Amoebic liver abscess is now most often seen in travelers and migrants; men have markedly higher risk of invasive Entamoeba histolytica disease including liver abscess, gastrointestinal symptoms such as nausea, vomiting, or diarrhea occur in a minority, and presentation may occur years after exposure. In HIV with advanced immunosuppression, fever with lymphadenopathy and splenomegaly is often mycobacterial, but lymphoma must be ruled out. Leptospirosis should be considered with compatible exposures and fever with rigors, headache, and myalgias, with severe disease involving pulmonary, hepatic, and renal dysfunction, aseptic meningitis, and bleeding tendencies. In tropical settings, splenomegaly may reflect hyper-reactive malarial splenomegaly, characterized by fever, anemia, weight loss, abdominal discomfort, lassitude, abnormal liver tests, elevated IgM, and hepatic sinusoidal lymphocytosis.
Physical Examination
Beyond confirming fever and organ enlargement, search for diagnostic clues such as lymphadenopathy suggesting lymphoma, infectious mononucleosis, brucellosis, schistosomiasis, HIV, or mycobacterial infection; rashes suggesting schistosomiasis, rickettsial disease, leishmaniasis, mononucleosis, Still’s disease, or syphilis; pharyngeal findings supporting mononucleosis; murmurs or embolic phenomena supporting endocarditis, Bartonella, or brucellosis; jaundice supporting viral hepatitis, cholangitis, or leptospirosis; conjunctival suffusion supporting leptospirosis; and joint findings supporting rheumatoid arthritis, lupus, or Still’s disease.
Diagnostic Tests and Interpretation
Laboratory Studies
Leukocytosis with a left shift supports bacterial infection. Marked lymphocytosis with atypical lymphocytes on smear supports infectious mononucleosis and can be confirmed early with heterophile antibody testing or with EBV viral capsid antigen IgM. Eosinophilia can accompany certain parasitic causes of hepatosplenomegaly but is not typical of amoebic infection. Three sets of blood cultures off antibiotics help exclude most endocarditis, while Bartonella, Brucella, and Q fever are better assessed by serology. Based on exposure history, obtain HIV, syphilis, and viral hepatitis testing, and consider serologies for rickettsial disease, Entamoeba, toxoplasma, schistosomiasis, Q fever, Fasciola, leptospirosis, and ehrlichiosis, along with blood films for malaria and babesiosis. Include biochemistry, autoimmune markers, and ferritin when inflammatory disease is considered. If imaging identifies an abscess, image-guided aspiration can establish diagnosis. Excisional lymph node biopsy or liver biopsy offers the highest yield for lymphoma. Bone marrow biopsy or splenic aspirate can diagnose leishmaniasis, with PCR or serology as alternatives.
Imaging
Ultrasound can confirm enlargement and identify causes such as abscess, hepatocellular carcinoma, or biliary pathology. Contrast-enhanced CT is helpful when ultrasound is nondiagnostic and suspicion remains for focal lesions or lymphoma. MRI is rarely needed but may help distinguish abscess from malignancy.
Treatment
Medications
Therapy is directed by the underlying diagnosis. Confirmed liver abscess requires antibiotics targeting likely organisms; pyogenic abscess is generally managed with percutaneous drainage plus antibiotics, with surgery reserved for failed drainage or complex multiloculated disease. Praziquantel is effective for Schistosoma mansoni in advanced hepatosplenic disease and is preferred when Schistosoma haematobium coinfection is present. Fascioliasis is typically treated with triclabendazole 10 mg/kg for one to two days; bithionol is an alternative, and the role of praziquantel is uncertain.
Ongoing Care and Follow-Up
Advise patients with splenomegaly to avoid contact sports and monitor for spontaneous rupture, which almost always presents with severe upper abdominal pain that often starts in the left upper quadrant, spreads more diffusely, and can radiate to the left shoulder.
Complications
In the United States, spontaneous splenic rupture is most commonly associated with infectious mononucleosis. Although rare, occurring in a small fraction of mononucleosis cases, it is the leading cause of death related to infectious mononucleosis.
Basics
Description
A midclavicular liver span of at least 12.5 cm supports hepatomegaly. Splenomegaly is defined as a spleen exceeding 250 g or one that is palpable, and on ultrasound is suggested by a cephalocaudal length of 13 cm or more
.
Approach to the Patient
Evaluating Hepatomegaly
Palpate to identify the lower liver edge at the right midclavicular line, then use gentle percussion to define the upper border so liver span can be measured; a span ≥12.5 cm supports hepatomegaly. Because hyperinflated lungs can push the liver downward, the upper border must be assessed to avoid overcalling enlargement.
Evaluating Splenomegaly
Bedside assessment should include both palpation and percussion. Palpation is best done bimanually with the patient supine and in the right lateral position. Percussion methods by Nixon and Castell provide the best diagnostic performance. In Nixon’s method, the patient lies on the right side and percussion begins in the posterior axillary line at the level where lung resonance ends, moving obliquely toward the left anterior costal margin; a dullness span over 8 cm suggests splenomegaly and has moderate sensitivity with high specificity. In Castell’s method, the patient is supine and percussion in the lowest intercostal space at the left anterior axillary line should remain resonant during inspiration if the spleen is normal; this approach has moderate sensitivity and specificity. If missing splenomegaly would change management, confirm with ultrasound or scintigraphy.
Evaluating Fever with Liver and/or Spleen Enlargement
Obtain a comprehensive history emphasizing travel and immigration, occupation, sexual history, intravenous drug use, animal exposure, and family history of malignancy, connective tissue disease, or inherited conditions. Look for associated findings including jaundice, fever duration and pattern, lymphadenopathy, rashes or bite exposures, liver edge texture and tenderness, an enlarged gallbladder or other abdominal mass, and spleen size and consistency. Initial testing commonly includes broad laboratory evaluation, heterophile antibody testing, hepatitis studies, imaging, and in selected cases bone marrow evaluation, endoscopy, and/or liver biopsy.
Epidemiology
In young adults, palpability of the liver and spleen can occur even without disease. In a large sample of healthy military personnel, the liver was not palpable or only at the costal margin in over half, and descended only 1–2 cm below the margin in many others. Studies of healthy college entrants have found a small proportion with unexplained palpable spleens, and palpable spleens have been reported in a notable minority of otherwise normal postpartum women.
Etiology
Hepatomegaly with Fever
Infectious causes include pyogenic or amoebic abscess, ascending cholangitis, chronic granulomatous disease, chronic Q fever, ehrlichiosis, histoplasmosis, HIV, infectious hepatitis, infectious mononucleosis, leptospirosis, syphilis, tuberculosis, and parasitic infections. Malignant causes include diffuse primary hepatic cancer, diffuse metastases, myeloproliferative disorders, lymphoma, and angiosarcoma. Inflammatory causes include sarcoidosis, autoimmune hepatitis, familial Mediterranean fever, and Still’s disease.
Splenomegaly with Fever
Infectious causes include viral infections such as hepatitis, infectious mononucleosis, and HIV; bacterial infections such as endocarditis, pyogenic abscess, salmonellosis, leptospirosis, brucellosis, Bartonella; fungal infections such as histoplasmosis; mycobacterial infections including miliary tuberculosis and nontuberculous mycobacteria; and parasitic infections including malaria, toxoplasmosis, amoebic liver abscess, schistosomiasis with Katayama fever, visceral leishmaniasis, babesiosis, and ehrlichiosis. Inflammatory causes include rheumatoid arthritis, sarcoidosis, systemic lupus erythematosus, and hemophagocytic lymphohistiocytosis. Malignant causes include lymphoma, acute and chronic leukemias, and myelodysplastic or myeloproliferative syndromes. Numerous parasites can enlarge liver and spleen depending on exposure context, including malaria, schistosomiasis, hydatid disease, leishmaniasis, toxocariasis, toxoplasmosis, liver flukes such as Fasciola hepatica, and echinococcal cysts, which can enlarge organs but are rarely febrile. Fever occurs in roughly half of toxoplasmosis and toxocariasis cases.
Diagnosis
History and Clinical Manifestations
In young adults, the combination of fatigue, sore throat, fever, lymphadenopathy, and hepatosplenomegaly is most often infectious mononucleosis. Fever with abdominal pain that may localize to the right upper quadrant, vomiting or anorexia, hepatomegaly, leukocytosis with elevated sedimentation rate, and otherwise unexplained anemia should raise concern for liver abscess. Pyogenic liver abscess most often arises from biliary disease and is commonly due to enteric organisms including Escherichia coli, Klebsiella, enterococci, anginosus group streptococci, and anaerobes, and is most often seen in adults in their fifth and sixth decades. Pyogenic liver abscess with metastatic infection such as endophthalmitis, meningitis, or other focal abscesses suggests Klebsiella pneumoniae, particularly in patients with diabetes and those from East Asia. Amoebic liver abscess is now most often seen in travelers and migrants; men have markedly higher risk of invasive Entamoeba histolytica disease including liver abscess, gastrointestinal symptoms such as nausea, vomiting, or diarrhea occur in a minority, and presentation may occur years after exposure. In HIV with advanced immunosuppression, fever with lymphadenopathy and splenomegaly is often mycobacterial, but lymphoma must be ruled out. Leptospirosis should be considered with compatible exposures and fever with rigors, headache, and myalgias, with severe disease involving pulmonary, hepatic, and renal dysfunction, aseptic meningitis, and bleeding tendencies. In tropical settings, splenomegaly may reflect hyper-reactive malarial splenomegaly, characterized by fever, anemia, weight loss, abdominal discomfort, lassitude, abnormal liver tests, elevated IgM, and hepatic sinusoidal lymphocytosis.
Physical Examination
Beyond confirming fever and organ enlargement, search for diagnostic clues such as lymphadenopathy suggesting lymphoma, infectious mononucleosis, brucellosis, schistosomiasis, HIV, or mycobacterial infection; rashes suggesting schistosomiasis, rickettsial disease, leishmaniasis, mononucleosis, Still’s disease, or syphilis; pharyngeal findings supporting mononucleosis; murmurs or embolic phenomena supporting endocarditis, Bartonella, or brucellosis; jaundice supporting viral hepatitis, cholangitis, or leptospirosis; conjunctival suffusion supporting leptospirosis; and joint findings supporting rheumatoid arthritis, lupus, or Still’s disease.
Diagnostic Tests and Interpretation
Laboratory Studies
Leukocytosis with a left shift supports bacterial infection. Marked lymphocytosis with atypical lymphocytes on smear supports infectious mononucleosis and can be confirmed early with heterophile antibody testing or with EBV viral capsid antigen IgM. Eosinophilia can accompany certain parasitic causes of hepatosplenomegaly but is not typical of amoebic infection. Three sets of blood cultures off antibiotics help exclude most endocarditis, while Bartonella, Brucella, and Q fever are better assessed by serology. Based on exposure history, obtain HIV, syphilis, and viral hepatitis testing, and consider serologies for rickettsial disease, Entamoeba, toxoplasma, schistosomiasis, Q fever, Fasciola, leptospirosis, and ehrlichiosis, along with blood films for malaria and babesiosis. Include biochemistry, autoimmune markers, and ferritin when inflammatory disease is considered. If imaging identifies an abscess, image-guided aspiration can establish diagnosis. Excisional lymph node biopsy or liver biopsy offers the highest yield for lymphoma. Bone marrow biopsy or splenic aspirate can diagnose leishmaniasis, with PCR or serology as alternatives.
Imaging
Ultrasound can confirm enlargement and identify causes such as abscess, hepatocellular carcinoma, or biliary pathology. Contrast-enhanced CT is helpful when ultrasound is nondiagnostic and suspicion remains for focal lesions or lymphoma. MRI is rarely needed but may help distinguish abscess from malignancy.
Treatment
Medications
Therapy is directed by the underlying diagnosis. Confirmed liver abscess requires antibiotics targeting likely organisms; pyogenic abscess is generally managed with percutaneous drainage plus antibiotics, with surgery reserved for failed drainage or complex multiloculated disease. Praziquantel is effective for Schistosoma mansoni in advanced hepatosplenic disease and is preferred when Schistosoma haematobium coinfection is present. Fascioliasis is typically treated with triclabendazole 10 mg/kg for one to two days; bithionol is an alternative, and the role of praziquantel is uncertain.
Ongoing Care and Follow-Up
Advise patients with splenomegaly to avoid contact sports and monitor for spontaneous rupture, which almost always presents with severe upper abdominal pain that often starts in the left upper quadrant, spreads more diffusely, and can radiate to the left shoulder.
Complications
In the United States, spontaneous splenic rupture is most commonly associated with infectious mononucleosis. Although rare, occurring in a small fraction of mononucleosis cases, it is the leading cause of death related to infectious mononucleosis.
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Infectious Diseases and Microbiology: Insect Bites and Stings
Basics
Description
Zoonoses are infections transmitted from nonhuman animals to humans, and vectors are the animals responsible for transmission. Insect bites and stings can lead to a wide spectrum of infectious diseases with acute, subacute, or highly variable presentations. Noninfectious reactions such as anaphylaxis and inflammatory responses are also common.
Approach to the Patient
Clinical evaluation requires awareness of geographic distribution, vector life cycles, and characteristic clinical syndromes. A detailed history of mosquito or tick exposure and the timing of bites can help narrow the differential diagnosis. Travel history is critical and should include dates, destinations, stopovers, pretravel medical advice, vaccinations, malaria prophylaxis, and preventive measures such as bed nets or repellents. Laboratory confirmation may support the diagnosis but is often unavailable early in illness. Multiple infections can follow a single exposure, as some vectors transmit more than one pathogen simultaneously. Malaria must always be considered in febrile travelers returning from endemic regions and treated as a medical emergency; given the risk of severe outcomes, empiric antimicrobial therapy is often appropriate when suspicion is high.
Epidemiology
Hundreds of thousands of Lyme disease cases have been reported in the United States, with most occurring in the Northeast, Minnesota, and Wisconsin. Rocky Mountain spotted fever occurs throughout the Americas, predominantly in the southern and southeastern United States, with higher incidence in warmer months. West Nile virus has been present in the US since 1999, with tens of thousands of reported cases; most infections are asymptomatic, and true exposure rates are likely much higher. Eastern equine encephalitis is a rare but severe mosquito-borne viral infection found mainly along the East and Gulf coasts, reported sporadically over decades. Malaria remains an important imported infection, with over a thousand cases reported annually in the US.
General Prevention
In areas with tick exposure, preventive strategies include wearing protective clothing and using proper tick-removal techniques with fine tweezers, avoiding crushing or abrupt removal. Insect repellents containing DEET remain the most effective option, particularly when combined with permethrin-treated clothing. Concentrations of 10–30% DEET provide strong protection; higher concentrations do not significantly increase efficacy. Plant-based repellents such as picaridin, PMD, or citronella have some benefit but are less effective than DEET.
Etiology
In the United States, clinicians may encounter both local and imported vector-borne diseases. Mosquitoes transmit malaria, dengue, West Nile virus, yellow fever, chikungunya, and viral encephalitides including eastern equine encephalitis. Ticks transmit Lyme disease, babesiosis, ehrlichiosis, anaplasmosis, Rocky Mountain spotted fever, tularemia, southern tick–associated rash illness, Bartonella infection, tick paralysis, and other rickettsioses. Flies may transmit bartonellosis, African trypanosomiasis, filariasis, onchocerciasis, leishmaniasis, or cause myiasis. Fleas transmit plague, murine typhus, and tungiasis.
Diagnosis
Incubation periods and symptom patterns vary by pathogen. Falciparum malaria typically incubates for about two weeks and presents with fever, chills, headache, abdominal or neck pain, nausea, vomiting, and sometimes jaundice. West Nile virus incubates for up to two weeks; most cases are asymptomatic, while symptomatic illness usually causes short-lived fever, myalgias, headache, and sometimes rash, with possible neurologic involvement. Colorado tick fever presents after several days with biphasic fever, severe headache, photophobia, and myalgias, occasionally with a transient rash. Dengue usually incubates for several days to two weeks and classically causes fever, retro-orbital headache, rash, and marked muscle and joint pain.
Diagnostic Tests and Interpretation
Laboratory evaluation depends on the suspected condition. Blood smears are mandatory in febrile patients returning from malaria-endemic regions. Lyme disease is diagnosed by serology with enzyme immunoassay confirmed by Western blot in compatible cases. Babesiosis is identified on blood smear by intraerythrocytic parasites, with PCR and serology as adjuncts. West Nile virus infection is diagnosed by IgM detection in serum or cerebrospinal fluid. Neuroimaging in eastern equine encephalitis often reveals characteristic thalamic and basal ganglia abnormalities.
Treatment
Management depends on the specific infection and is detailed in disease-specific references. Given the severity of some vector-borne illnesses, prompt empiric therapy is often warranted when clinical suspicion is high.
Ongoing Care and Complications
Eastern equine encephalitis carries a high mortality rate, and many survivors have permanent neurologic disability. Delayed diagnosis and treatment of falciparum malaria significantly increase mortality and the risk of permanent neurologic damage. Lyme disease may involve the nervous system or cardiac conduction pathways, leading to neurologic deficits or arrhythmias. Dengue may cause mucosal bleeding and exacerbate preexisting gastrointestinal lesions. Colorado tick fever has been associated with rare but serious complications including encephalitis, meningitis, hemorrhage, myocarditis, orchitis, atypical pneumonia, and hepatitis.
Basics
Description
Zoonoses are infections transmitted from nonhuman animals to humans, and vectors are the animals responsible for transmission. Insect bites and stings can lead to a wide spectrum of infectious diseases with acute, subacute, or highly variable presentations. Noninfectious reactions such as anaphylaxis and inflammatory responses are also common.
Approach to the Patient
Clinical evaluation requires awareness of geographic distribution, vector life cycles, and characteristic clinical syndromes. A detailed history of mosquito or tick exposure and the timing of bites can help narrow the differential diagnosis. Travel history is critical and should include dates, destinations, stopovers, pretravel medical advice, vaccinations, malaria prophylaxis, and preventive measures such as bed nets or repellents. Laboratory confirmation may support the diagnosis but is often unavailable early in illness. Multiple infections can follow a single exposure, as some vectors transmit more than one pathogen simultaneously. Malaria must always be considered in febrile travelers returning from endemic regions and treated as a medical emergency; given the risk of severe outcomes, empiric antimicrobial therapy is often appropriate when suspicion is high.
Epidemiology
Hundreds of thousands of Lyme disease cases have been reported in the United States, with most occurring in the Northeast, Minnesota, and Wisconsin. Rocky Mountain spotted fever occurs throughout the Americas, predominantly in the southern and southeastern United States, with higher incidence in warmer months. West Nile virus has been present in the US since 1999, with tens of thousands of reported cases; most infections are asymptomatic, and true exposure rates are likely much higher. Eastern equine encephalitis is a rare but severe mosquito-borne viral infection found mainly along the East and Gulf coasts, reported sporadically over decades. Malaria remains an important imported infection, with over a thousand cases reported annually in the US.
General Prevention
In areas with tick exposure, preventive strategies include wearing protective clothing and using proper tick-removal techniques with fine tweezers, avoiding crushing or abrupt removal. Insect repellents containing DEET remain the most effective option, particularly when combined with permethrin-treated clothing. Concentrations of 10–30% DEET provide strong protection; higher concentrations do not significantly increase efficacy. Plant-based repellents such as picaridin, PMD, or citronella have some benefit but are less effective than DEET.
Etiology
In the United States, clinicians may encounter both local and imported vector-borne diseases. Mosquitoes transmit malaria, dengue, West Nile virus, yellow fever, chikungunya, and viral encephalitides including eastern equine encephalitis. Ticks transmit Lyme disease, babesiosis, ehrlichiosis, anaplasmosis, Rocky Mountain spotted fever, tularemia, southern tick–associated rash illness, Bartonella infection, tick paralysis, and other rickettsioses. Flies may transmit bartonellosis, African trypanosomiasis, filariasis, onchocerciasis, leishmaniasis, or cause myiasis. Fleas transmit plague, murine typhus, and tungiasis.
Diagnosis
Incubation periods and symptom patterns vary by pathogen. Falciparum malaria typically incubates for about two weeks and presents with fever, chills, headache, abdominal or neck pain, nausea, vomiting, and sometimes jaundice. West Nile virus incubates for up to two weeks; most cases are asymptomatic, while symptomatic illness usually causes short-lived fever, myalgias, headache, and sometimes rash, with possible neurologic involvement. Colorado tick fever presents after several days with biphasic fever, severe headache, photophobia, and myalgias, occasionally with a transient rash. Dengue usually incubates for several days to two weeks and classically causes fever, retro-orbital headache, rash, and marked muscle and joint pain.
Diagnostic Tests and Interpretation
Laboratory evaluation depends on the suspected condition. Blood smears are mandatory in febrile patients returning from malaria-endemic regions. Lyme disease is diagnosed by serology with enzyme immunoassay confirmed by Western blot in compatible cases. Babesiosis is identified on blood smear by intraerythrocytic parasites, with PCR and serology as adjuncts. West Nile virus infection is diagnosed by IgM detection in serum or cerebrospinal fluid. Neuroimaging in eastern equine encephalitis often reveals characteristic thalamic and basal ganglia abnormalities.
Treatment
Management depends on the specific infection and is detailed in disease-specific references. Given the severity of some vector-borne illnesses, prompt empiric therapy is often warranted when clinical suspicion is high.
Ongoing Care and Complications
Eastern equine encephalitis carries a high mortality rate, and many survivors have permanent neurologic disability. Delayed diagnosis and treatment of falciparum malaria significantly increase mortality and the risk of permanent neurologic damage. Lyme disease may involve the nervous system or cardiac conduction pathways, leading to neurologic deficits or arrhythmias. Dengue may cause mucosal bleeding and exacerbate preexisting gastrointestinal lesions. Colorado tick fever has been associated with rare but serious complications including encephalitis, meningitis, hemorrhage, myocarditis, orchitis, atypical pneumonia, and hepatitis.
- Published on
Infectious Diseases and Microbiology: Insect Bites and Stings
Basics
Description
Zoonoses are infections transmitted from nonhuman animals to humans, and vectors are the animals responsible for transmission. Insect bites and stings can lead to a wide spectrum of infectious diseases with acute, subacute, or highly variable presentations. Noninfectious reactions such as anaphylaxis and inflammatory responses are also common.
Approach to the Patient
Clinical evaluation requires awareness of geographic distribution, vector life cycles, and characteristic clinical syndromes. A detailed history of mosquito or tick exposure and the timing of bites can help narrow the differential diagnosis. Travel history is critical and should include dates, destinations, stopovers, pretravel medical advice, vaccinations, malaria prophylaxis, and preventive measures such as bed nets or repellents. Laboratory confirmation may support the diagnosis but is often unavailable early in illness. Multiple infections can follow a single exposure, as some vectors transmit more than one pathogen simultaneously. Malaria must always be considered in febrile travelers returning from endemic regions and treated as a medical emergency; given the risk of severe outcomes, empiric antimicrobial therapy is often appropriate when suspicion is high.
Epidemiology
Hundreds of thousands of Lyme disease cases have been reported in the United States, with most occurring in the Northeast, Minnesota, and Wisconsin. Rocky Mountain spotted fever occurs throughout the Americas, predominantly in the southern and southeastern United States, with higher incidence in warmer months. West Nile virus has been present in the US since 1999, with tens of thousands of reported cases; most infections are asymptomatic, and true exposure rates are likely much higher. Eastern equine encephalitis is a rare but severe mosquito-borne viral infection found mainly along the East and Gulf coasts, reported sporadically over decades. Malaria remains an important imported infection, with over a thousand cases reported annually in the US.
General Prevention
In areas with tick exposure, preventive strategies include wearing protective clothing and using proper tick-removal techniques with fine tweezers, avoiding crushing or abrupt removal. Insect repellents containing DEET remain the most effective option, particularly when combined with permethrin-treated clothing. Concentrations of 10–30% DEET provide strong protection; higher concentrations do not significantly increase efficacy. Plant-based repellents such as picaridin, PMD, or citronella have some benefit but are less effective than DEET.
Etiology
In the United States, clinicians may encounter both local and imported vector-borne diseases. Mosquitoes transmit malaria, dengue, West Nile virus, yellow fever, chikungunya, and viral encephalitides including eastern equine encephalitis. Ticks transmit Lyme disease, babesiosis, ehrlichiosis, anaplasmosis, Rocky Mountain spotted fever, tularemia, southern tick–associated rash illness, Bartonella infection, tick paralysis, and other rickettsioses. Flies may transmit bartonellosis, African trypanosomiasis, filariasis, onchocerciasis, leishmaniasis, or cause myiasis. Fleas transmit plague, murine typhus, and tungiasis.
Diagnosis
Incubation periods and symptom patterns vary by pathogen. Falciparum malaria typically incubates for about two weeks and presents with fever, chills, headache, abdominal or neck pain, nausea, vomiting, and sometimes jaundice. West Nile virus incubates for up to two weeks; most cases are asymptomatic, while symptomatic illness usually causes short-lived fever, myalgias, headache, and sometimes rash, with possible neurologic involvement. Colorado tick fever presents after several days with biphasic fever, severe headache, photophobia, and myalgias, occasionally with a transient rash. Dengue usually incubates for several days to two weeks and classically causes fever, retro-orbital headache, rash, and marked muscle and joint pain. bisnes
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Diagnostic Tests and Interpretation
Laboratory evaluation depends on the suspected condition. Blood smears are mandatory in febrile patients returning from malaria-endemic regions. Lyme disease is diagnosed by serology with enzyme immunoassay confirmed by Western blot in compatible cases. Babesiosis is identified on blood smear by intraerythrocytic parasites, with PCR and serology as adjuncts. West Nile virus infection is diagnosed by IgM detection in serum or cerebrospinal fluid. Neuroimaging in eastern equine encephalitis often reveals characteristic thalamic and basal ganglia abnormalities.
Treatment
Management depends on the specific infection and is detailed in disease-specific references. Given the severity of some vector-borne illnesses, prompt empiric therapy is often warranted when clinical suspicion is high.
Ongoing Care and Complications
Eastern equine encephalitis carries a high mortality rate, and many survivors have permanent neurologic disability. Delayed diagnosis and treatment of falciparum malaria significantly increase mortality and the risk of permanent neurologic damage. Lyme disease may involve the nervous system or cardiac conduction pathways, leading to neurologic deficits or arrhythmias. Dengue may cause mucosal bleeding and exacerbate preexisting gastrointestinal lesions. Colorado tick fever has been associated with rare but serious complications including encephalitis, meningitis, hemorrhage, myocarditis, orchitis, atypical pneumonia, and hepatitis.
Basics
Description
Zoonoses are infections transmitted from nonhuman animals to humans, and vectors are the animals responsible for transmission. Insect bites and stings can lead to a wide spectrum of infectious diseases with acute, subacute, or highly variable presentations. Noninfectious reactions such as anaphylaxis and inflammatory responses are also common.
Approach to the Patient
Clinical evaluation requires awareness of geographic distribution, vector life cycles, and characteristic clinical syndromes. A detailed history of mosquito or tick exposure and the timing of bites can help narrow the differential diagnosis. Travel history is critical and should include dates, destinations, stopovers, pretravel medical advice, vaccinations, malaria prophylaxis, and preventive measures such as bed nets or repellents. Laboratory confirmation may support the diagnosis but is often unavailable early in illness. Multiple infections can follow a single exposure, as some vectors transmit more than one pathogen simultaneously. Malaria must always be considered in febrile travelers returning from endemic regions and treated as a medical emergency; given the risk of severe outcomes, empiric antimicrobial therapy is often appropriate when suspicion is high.
Epidemiology
Hundreds of thousands of Lyme disease cases have been reported in the United States, with most occurring in the Northeast, Minnesota, and Wisconsin. Rocky Mountain spotted fever occurs throughout the Americas, predominantly in the southern and southeastern United States, with higher incidence in warmer months. West Nile virus has been present in the US since 1999, with tens of thousands of reported cases; most infections are asymptomatic, and true exposure rates are likely much higher. Eastern equine encephalitis is a rare but severe mosquito-borne viral infection found mainly along the East and Gulf coasts, reported sporadically over decades. Malaria remains an important imported infection, with over a thousand cases reported annually in the US.
General Prevention
In areas with tick exposure, preventive strategies include wearing protective clothing and using proper tick-removal techniques with fine tweezers, avoiding crushing or abrupt removal. Insect repellents containing DEET remain the most effective option, particularly when combined with permethrin-treated clothing. Concentrations of 10–30% DEET provide strong protection; higher concentrations do not significantly increase efficacy. Plant-based repellents such as picaridin, PMD, or citronella have some benefit but are less effective than DEET.
Etiology
In the United States, clinicians may encounter both local and imported vector-borne diseases. Mosquitoes transmit malaria, dengue, West Nile virus, yellow fever, chikungunya, and viral encephalitides including eastern equine encephalitis. Ticks transmit Lyme disease, babesiosis, ehrlichiosis, anaplasmosis, Rocky Mountain spotted fever, tularemia, southern tick–associated rash illness, Bartonella infection, tick paralysis, and other rickettsioses. Flies may transmit bartonellosis, African trypanosomiasis, filariasis, onchocerciasis, leishmaniasis, or cause myiasis. Fleas transmit plague, murine typhus, and tungiasis.
Diagnosis
Incubation periods and symptom patterns vary by pathogen. Falciparum malaria typically incubates for about two weeks and presents with fever, chills, headache, abdominal or neck pain, nausea, vomiting, and sometimes jaundice. West Nile virus incubates for up to two weeks; most cases are asymptomatic, while symptomatic illness usually causes short-lived fever, myalgias, headache, and sometimes rash, with possible neurologic involvement. Colorado tick fever presents after several days with biphasic fever, severe headache, photophobia, and myalgias, occasionally with a transient rash. Dengue usually incubates for several days to two weeks and classically causes fever, retro-orbital headache, rash, and marked muscle and joint pain. bisnes
Nenek dia
Diagnostic Tests and Interpretation
Laboratory evaluation depends on the suspected condition. Blood smears are mandatory in febrile patients returning from malaria-endemic regions. Lyme disease is diagnosed by serology with enzyme immunoassay confirmed by Western blot in compatible cases. Babesiosis is identified on blood smear by intraerythrocytic parasites, with PCR and serology as adjuncts. West Nile virus infection is diagnosed by IgM detection in serum or cerebrospinal fluid. Neuroimaging in eastern equine encephalitis often reveals characteristic thalamic and basal ganglia abnormalities.
Treatment
Management depends on the specific infection and is detailed in disease-specific references. Given the severity of some vector-borne illnesses, prompt empiric therapy is often warranted when clinical suspicion is high.
Ongoing Care and Complications
Eastern equine encephalitis carries a high mortality rate, and many survivors have permanent neurologic disability. Delayed diagnosis and treatment of falciparum malaria significantly increase mortality and the risk of permanent neurologic damage. Lyme disease may involve the nervous system or cardiac conduction pathways, leading to neurologic deficits or arrhythmias. Dengue may cause mucosal bleeding and exacerbate preexisting gastrointestinal lesions. Colorado tick fever has been associated with rare but serious complications including encephalitis, meningitis, hemorrhage, myocarditis, orchitis, atypical pneumonia, and hepatitis.
- Published on
Emergency and Acute Medicine – Joint Pain and Fever
Overview and Definitions
Joint pain accompanied by fever suggests an inflammatory or infectious process and requires prompt evaluation. Joint involvement may be monoarticular, oligoarticular, or polyarticular and may be symmetric or asymmetric. Arthritis refers to inflammation of a joint and is a clinical finding rather than a diagnosis, whereas arthralgia denotes joint pain without objective inflammation. Acute joint disorders last less than six weeks, while chronic disorders persist beyond this duration.
Clinical Approach
The presence of fever narrows the differential diagnosis toward infectious, crystal-induced, immune-mediated, or reactive etiologies. Noninflammatory disorders such as osteoarthritis or fibromyalgia are rarely associated with fever. History should focus on onset and tempo of symptoms, recent infections, travel, trauma, sexual exposure, immunosuppression, and prior joint disease. Physical examination should assess for warmth, erythema, swelling, effusion, and limitation of motion, as well as extra-articular features such as rash, cardiac murmurs, or enthesitis. Synovial fluid aspiration and analysis are mandatory in acute monoarthritis or when infection or crystal disease is suspected.
Epidemiology
Septic arthritis is usually monoarticular, with polyarticular involvement occurring in 10–20% of adults. Risk factors include diabetes mellitus, chronic kidney disease, malignancy, immunosuppression, intravenous drug use, trauma, prosthetic joints, and underlying joint disease. Musculoskeletal manifestations occur in up to 45% of patients with infective endocarditis. Viral outbreaks, particularly chikungunya, have caused large numbers of cases of acute febrile polyarthritis, especially among travelers.
Etiology and Pathophysiology
Septic arthritis is the most important diagnosis to exclude and is most commonly caused by Staphylococcus aureus. Other infectious causes include disseminated gonococcal infection, endocarditis, Lyme disease, Whipple’s disease, secondary syphilis, and mycobacterial or fungal infections. Viral etiologies include parvovirus B19, acute HIV infection, hepatitis B, dengue virus, and chikungunya. Noninfectious causes include gout, pseudogout, acute rheumatic fever, adult-onset Still’s disease, systemic lupus erythematosus, vasculitis, and rarely malignancy.
Diagnostic Evaluation
Synovial fluid analysis is central to diagnosis. Bacterial arthritis is suggested by leukocyte counts greater than 50,000 cells/µL with polymorphonuclear predominance, turbid appearance, and low viscosity. Gram stain and culture should always be performed, and blood cultures obtained in acute presentations. Gonococcal arthritis frequently yields negative synovial cultures, requiring sampling of mucosal sites. Elevated ESR and CRP favor bacterial infection, while markedly elevated ferritin levels suggest adult-onset Still’s disease.
Management
Suspected septic arthritis requires immediate empiric antimicrobial therapy after appropriate cultures are obtained. Most cases of nongonococcal septic arthritis require surgical drainage or joint washout. Gonococcal arthritis is usually managed medically with ceftriaxone. NSAIDs provide symptomatic relief in viral and reactive arthritis. Early joint immobilization followed by gradual mobilization is recommended once infection is controlled.
Complications
Delayed or inadequate treatment of septic arthritis may result in irreversible joint destruction, osteomyelitis, bacteremia, and systemic sepsis.
- Published on
Emergency and Acute Medicine – Lymphadenopathy and Fever
Overview and Definitions
Lymphadenitis refers to inflammation of one or more lymph nodes, while lymphangitis involves inflammation of lymphatic channels; both may occur in acute or chronic disease. Mesenteric lymphadenitis results from inflammation of mesenteric nodes and may clinically mimic acute appendicitis. In most regions, lymph nodes larger than 1 cm are abnormal; epitrochlear nodes greater than 0.5 cm and inguinal nodes greater than 1.5–2 cm are considered enlarged, although palpable inguinal nodes are common in healthy adults. Generalized lymphadenopathy is defined as involvement of two or more noncontiguous nodal regions.
Clinical Approach
Fever commonly accompanies lymphadenopathy, with infection being the leading cause. Lymph node enlargement may be incidental or the primary presenting feature, and clinicians must determine whether observation or further investigation is required. A detailed history and comprehensive physical examination are essential. Duration is informative, as suppurative infections usually present within one week, whereas chronic lymphadenopathy suggests infections such as HIV or tuberculosis, malignancy, inflammatory, or autoimmune disease. Epidemiologic factors including travel, sick contacts, and animal exposure should be assessed. Associated symptoms include weight loss, fever, night sweats, sore throat, cough, pruritus, fatigue, lymph node pain, and myalgia or arthralgia. Examination should include all nodal regions to determine whether disease is localized or generalized, along with abdominal assessment for hepatosplenomegaly. Findings such as anemia, petechiae, or bleeding suggest bone marrow infiltration. While many infections cause fever with lymphadenopathy, pathogens such as Francisella tularensis, Bartonella henselae, and mycobacteria often present with a single prominent lymph node and fever.
Epidemiology
More than two-thirds of patients presenting to primary care with lymphadenopathy have nonspecific or upper respiratory causes. The likelihood of malignancy increases with age, particularly over 50 years. In primary care, approximately 1% of patients with lymphadenopathy have an underlying malignancy. Acute mesenteric lymphadenitis is more common in children. In developed countries, mycobacterial lymphadenopathy is more often due to nontuberculous species.
Etiology
Infectious causes include viral infections such as Epstein–Barr virus, cytomegalovirus, herpes simplex virus, dengue, rubella, measles, HIV, and West Nile virus; bacterial infections including streptococci, Staphylococcus aureus, Bartonella henselae, brucellosis, tularemia, plague, melioidosis, tuberculosis, nontuberculous mycobacteria, listeriosis, leptospirosis, secondary syphilis, diphtheria, typhoid fever, and lymphogranuloma venereum; fungal infections such as histoplasmosis, coccidioidomycosis, paracoccidioidomycosis, and cryptococcosis; parasitic infections including toxoplasmosis, leishmaniasis, trypanosomiasis, and filariasis; and rickettsial diseases. Immunologic causes include systemic lupus erythematosus, rheumatoid arthritis, vasculitides, Still’s disease, dermatomyositis, graft-versus-host disease, juvenile idiopathic arthritis, mixed connective tissue disease, serum sickness, and Sjögren’s syndrome. Malignant causes include Hodgkin and non-Hodgkin lymphomas, acute and chronic leukemias, hairy cell leukemia, amyloidosis, sarcomas, and metastatic disease. Other causes include lipid storage disorders, endocrine diseases such as hyperthyroidism and Addison disease, Castleman disease, Kikuchi disease, drug reactions, familial Mediterranean fever, and Kawasaki disease. In HIV infection, lymphadenopathy ranges from early follicular hyperplasia to opportunistic infections and malignancies, with common causes including lymphoma, mycobacterial infection, toxoplasmosis, systemic fungal infection, and bacillary angiomatosis.
Diagnostic Evaluation
Assessment of lymph nodes should document size, shape, consistency, mobility, and tenderness. Hard nodes suggest carcinoma, rubbery firm non-tender nodes are typical of lymphoma, and tender mobile nodes usually indicate reactive infection. Some malignancies, such as acute leukemia, may cause rapid enlargement with pain. Initial laboratory evaluation should be guided by risk factors and may include blood cultures, HIV testing, syphilis serology, heterophile antibody testing, toxoplasma, CMV, EBV serologies, Bartonella serology, urine histoplasma antigen, autoimmune markers, and other targeted tests. Fine-needle aspiration can be useful, but excisional biopsy provides superior diagnostic yield, particularly for lymphoma. Lymph node specimens should be evaluated with cultures, mycobacterial and fungal stains, cytology, and molecular diagnostics. Chest radiography may reveal pulmonary or mediastinal involvement. Ultrasonography is useful for superficial nodes, while CT or MRI better evaluate deep nodal disease and guide biopsy. PET imaging identifies metabolically active nodes. In the absence of high-risk features, observation for 2–4 weeks is appropriate, with biopsy indicated if lymphadenopathy persists.
Management
Treatment depends on the underlying etiology and should be directed at the identified cause. Empiric therapy may be required in severe infection, while malignancy or autoimmune disease requires disease-specific management.
Follow-Up and Prognosis
In patients without features concerning for malignancy or severe infection, clinical observation for 2–4 weeks after initial evaluation is appropriate before proceeding to biopsy.
Complications
Delayed diagnosis or treatment of infectious lymphadenopathy may lead to disseminated or severe infection.
Overview and Definitions
Lymphadenitis refers to inflammation of one or more lymph nodes, while lymphangitis involves inflammation of lymphatic channels; both may occur in acute or chronic disease. Mesenteric lymphadenitis results from inflammation of mesenteric nodes and may clinically mimic acute appendicitis. In most regions, lymph nodes larger than 1 cm are abnormal; epitrochlear nodes greater than 0.5 cm and inguinal nodes greater than 1.5–2 cm are considered enlarged, although palpable inguinal nodes are common in healthy adults. Generalized lymphadenopathy is defined as involvement of two or more noncontiguous nodal regions.
Clinical Approach
Fever commonly accompanies lymphadenopathy, with infection being the leading cause. Lymph node enlargement may be incidental or the primary presenting feature, and clinicians must determine whether observation or further investigation is required. A detailed history and comprehensive physical examination are essential. Duration is informative, as suppurative infections usually present within one week, whereas chronic lymphadenopathy suggests infections such as HIV or tuberculosis, malignancy, inflammatory, or autoimmune disease. Epidemiologic factors including travel, sick contacts, and animal exposure should be assessed. Associated symptoms include weight loss, fever, night sweats, sore throat, cough, pruritus, fatigue, lymph node pain, and myalgia or arthralgia. Examination should include all nodal regions to determine whether disease is localized or generalized, along with abdominal assessment for hepatosplenomegaly. Findings such as anemia, petechiae, or bleeding suggest bone marrow infiltration. While many infections cause fever with lymphadenopathy, pathogens such as Francisella tularensis, Bartonella henselae, and mycobacteria often present with a single prominent lymph node and fever.
Epidemiology
More than two-thirds of patients presenting to primary care with lymphadenopathy have nonspecific or upper respiratory causes. The likelihood of malignancy increases with age, particularly over 50 years. In primary care, approximately 1% of patients with lymphadenopathy have an underlying malignancy. Acute mesenteric lymphadenitis is more common in children. In developed countries, mycobacterial lymphadenopathy is more often due to nontuberculous species.
Etiology
Infectious causes include viral infections such as Epstein–Barr virus, cytomegalovirus, herpes simplex virus, dengue, rubella, measles, HIV, and West Nile virus; bacterial infections including streptococci, Staphylococcus aureus, Bartonella henselae, brucellosis, tularemia, plague, melioidosis, tuberculosis, nontuberculous mycobacteria, listeriosis, leptospirosis, secondary syphilis, diphtheria, typhoid fever, and lymphogranuloma venereum; fungal infections such as histoplasmosis, coccidioidomycosis, paracoccidioidomycosis, and cryptococcosis; parasitic infections including toxoplasmosis, leishmaniasis, trypanosomiasis, and filariasis; and rickettsial diseases. Immunologic causes include systemic lupus erythematosus, rheumatoid arthritis, vasculitides, Still’s disease, dermatomyositis, graft-versus-host disease, juvenile idiopathic arthritis, mixed connective tissue disease, serum sickness, and Sjögren’s syndrome. Malignant causes include Hodgkin and non-Hodgkin lymphomas, acute and chronic leukemias, hairy cell leukemia, amyloidosis, sarcomas, and metastatic disease. Other causes include lipid storage disorders, endocrine diseases such as hyperthyroidism and Addison disease, Castleman disease, Kikuchi disease, drug reactions, familial Mediterranean fever, and Kawasaki disease. In HIV infection, lymphadenopathy ranges from early follicular hyperplasia to opportunistic infections and malignancies, with common causes including lymphoma, mycobacterial infection, toxoplasmosis, systemic fungal infection, and bacillary angiomatosis.
Diagnostic Evaluation
Assessment of lymph nodes should document size, shape, consistency, mobility, and tenderness. Hard nodes suggest carcinoma, rubbery firm non-tender nodes are typical of lymphoma, and tender mobile nodes usually indicate reactive infection. Some malignancies, such as acute leukemia, may cause rapid enlargement with pain. Initial laboratory evaluation should be guided by risk factors and may include blood cultures, HIV testing, syphilis serology, heterophile antibody testing, toxoplasma, CMV, EBV serologies, Bartonella serology, urine histoplasma antigen, autoimmune markers, and other targeted tests. Fine-needle aspiration can be useful, but excisional biopsy provides superior diagnostic yield, particularly for lymphoma. Lymph node specimens should be evaluated with cultures, mycobacterial and fungal stains, cytology, and molecular diagnostics. Chest radiography may reveal pulmonary or mediastinal involvement. Ultrasonography is useful for superficial nodes, while CT or MRI better evaluate deep nodal disease and guide biopsy. PET imaging identifies metabolically active nodes. In the absence of high-risk features, observation for 2–4 weeks is appropriate, with biopsy indicated if lymphadenopathy persists.
Management
Treatment depends on the underlying etiology and should be directed at the identified cause. Empiric therapy may be required in severe infection, while malignancy or autoimmune disease requires disease-specific management.
Follow-Up and Prognosis
In patients without features concerning for malignancy or severe infection, clinical observation for 2–4 weeks after initial evaluation is appropriate before proceeding to biopsy.
Complications
Delayed diagnosis or treatment of infectious lymphadenopathy may lead to disseminated or severe infection.
- Published on
Emergency and Acute Medicine – Lung Nodules
Overview and Definitions
Pulmonary nodules are rounded opacities surrounded by lung parenchyma and are typically less than 3–4 cm in diameter; larger lesions are classified as lung masses. Pathologically, a pulmonary nodule is a small, approximately spherical, circumscribed focus of abnormal tissue, while radiologically it is defined as a round opacity, at least moderately well marginated, and no more than 3 cm in maximum diameter. Linear or planar opacities are not considered nodules. Chest imaging may reveal a solitary pulmonary nodule, often referred to as a coin lesion, or multiple pulmonary nodules.
Clinical Approach
The primary objective is to distinguish benign from malignant nodules. Evaluation begins with a thorough history, as the probability of malignancy increases with age and is rare in patients younger than 35 years. Important malignancy risk factors include prior lung cancer, family history of lung cancer, cigarette smoking, second-hand smoke exposure, occupational carcinogen exposure such as asbestos or radon, pulmonary fibrosis, chronic obstructive pulmonary disease, and alpha-1 antitrypsin deficiency. A higher cumulative smoking burden is associated with increased cancer risk. If malignancy is suspected, it is essential to determine whether the lesion represents a primary lung cancer or metastatic disease. Fever suggests an infectious etiology, and immunocompromised patients are at risk for opportunistic infections presenting as solitary or multiple nodules. Physical examination may reveal signs of malignancy including cachexia, anemia, jaundice, clubbing, bone pain, abdominal masses, or superior vena cava syndrome. Radiologic features such as size, distribution, shape, calcification pattern, cavitation, lymphadenopathy, pleural effusion, and clustering provide diagnostic clues. Low-risk nodules may be followed with serial CT imaging, whereas larger or suspicious nodules warrant biopsy, PET imaging, or video-assisted thoracoscopic surgery. Empiric antimicrobial therapy should be initiated in immunocompromised patients or those at risk for rapid deterioration.
Epidemiology
Pulmonary nodules are common, with up to 51% of smokers aged 50 years or older having nodules detected on CT. Fewer than 1% of nodules smaller than 5 mm are malignant in patients without a history of cancer. The likelihood of malignancy increases with size: approximately 0.2% for nodules under 3 mm, 0.9% for 4–7 mm, 18% for 8–20 mm, and greater than 50% for nodules larger than 20 mm. Male smokers have a tenfold increased risk of lung cancer compared with nonsmokers, rising to 15–35 times higher in heavy smokers. Paragonimus westermani infection can present as a lung nodule in endemic regions of East and Southeast Asia. Tuberculosis commonly presents with hilar lymphadenopathy, and histoplasmosis is the most frequent cause of hospitalization from endemic mycoses in the United States.
Etiology and Pathophysiology
Solitary pulmonary nodules may be caused by primary lung malignancies including adenocarcinoma, squamous cell carcinoma, large cell carcinoma, and small cell carcinoma, as well as metastatic disease from breast, head and neck, thyroid, melanoma, colon, kidney, sarcoma, and germ cell tumors. Other causes include carcinoid tumors, infections such as bacterial abscesses, tuberculosis, atypical mycobacteria, histoplasmosis, blastomycosis, coccidioidomycosis, cryptococcosis, aspergilloma, nocardiosis, Pneumocystis infection, and parasitic infections including echinococcosis, dirofilariasis, ascariasis, and paragonimiasis. Benign neoplasms include hamartoma, lipoma, and fibroma. Non-neoplastic causes include arteriovenous malformations, bronchogenic cysts, granulomatosis with polyangiitis, sarcoidosis, rheumatoid nodules, amyloidoma, rounded atelectasis, intrapulmonary lymph nodes, hematoma, pulmonary infarction, and mucoid impaction. Multiple pulmonary nodules are more often benign when less than 1 cm, but in patients with known malignancy, nodules larger than 0.5 cm are more likely metastatic. Infectious causes of multiple nodules include septic emboli, fungal infections, tuberculosis, atypical mycobacteria, and paragonimiasis, while inflammatory conditions such as sarcoidosis, rheumatoid arthritis, and vasculitis are also common causes.
Diagnostic Evaluation
History should assess for tuberculosis risk factors, immunosuppression, aspiration risk, and exposure to endemic fungi. Lung abscesses may arise from aspiration, tricuspid valve endocarditis, or septic thrombophlebitis such as Lemierre syndrome, often in patients with poor dentition or prolonged recumbency. Symptoms include cough, sputum production, dyspnea, fever, night sweats, weight loss, and anorexia. Laboratory evaluation may include blood cultures, sputum Gram stain and culture, fungal cultures, acid-fast bacilli staining and mycobacterial cultures, cryptococcal antigen testing, galactomannan and beta-D-glucan assays, and serologic testing for endemic fungi. Imaging with high-resolution CT can detect nodules as small as 1–2 mm. Benign calcification patterns include homogeneous, central, concentric, and popcorn calcifications, while malignant features include eccentric or amorphous calcification and spiculated borders. Ground-glass halos suggest invasive fungal infection, particularly aspergillosis. PET imaging identifies metabolically active lesions. Transthoracic echocardiography is indicated when septic emboli are suspected, and CT of the neck should be performed if Lemierre syndrome is considered. Percutaneous biopsy or VATS is indicated when malignancy risk is high.
Management
Empiric antibiotics should be initiated in patients with fever or systemic toxicity after obtaining blood cultures. Suspected tuberculosis requires differentiation between latent and active disease using clinical assessment, imaging, and sputum studies. Mild pulmonary histoplasmosis may not require treatment, but persistent or moderate-to-severe disease is treated with itraconazole or amphotericin B followed by itraconazole. Lung abscesses are typically polymicrobial and treated with beta-lactam/beta-lactamase inhibitors or clindamycin. Voriconazole is first-line therapy for invasive aspergillosis, with surgical debridement considered when feasible. Paragonimiasis is treated with praziquantel or triclabendazole.
Follow-Up and Prognosis
Malignant solitary pulmonary nodules typically double in volume over 20–400 days. Low-risk nodules smaller than 1 cm may be monitored with serial CT imaging, while high-risk nodules should be surgically excised. PET scanning is most useful for nodules larger than 1 cm with intermediate malignancy risk to guide management decisions.
Complications
Untreated lung abscesses may progress to respiratory failure requiring mechanical ventilation. Cavitation may occur in infectious, malignant, and inflammatory nodules, and cavitary lesions are frequently complicated by secondary Aspergillus infection.
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KembaraXtra-Medicine: 22q11.2 Deletion Syndrome
22q11.2 deletion syndrome (22q11.2 DS) is a contiguous gene deletion syndrome caused by a heterozygous deletion on the long arm of chromosome 22 at position q11.2. This deletion typically involves approximately 50 genes, including TBX1, a critical developmental gene involved in cardiac and thymic formation. The syndrome is characterized by a broad and highly variable phenotype, most commonly including congenital heart disease, hypocalcemia, immune dysfunction, palatal abnormalities, renal and skeletal anomalies, gastrointestinal issues, learning difficulties, and psychiatric disorders. It is the most common microdeletion syndrome and most often arises as a de novo event, though it may also be inherited in an autosomal dominant pattern.
The condition has been described under several synonymous diagnoses, including DiGeorge syndrome, velocardiofacial syndrome (VCFS), conotruncal anomaly face syndrome, Cayler cardiofacial syndrome, and autosomal dominant Opitz G/BBB syndrome. From a coding perspective, it is classified under ICD-10-CM codes Q93.59, Q93.81, Q93.88, and Q93.89, reflecting various chromosomal deletion categories.
Epidemiologically, 22q11.2 deletion syndrome has an estimated incidence and prevalence of approximately 1 in 2,148 individuals. It affects males and females equally and is present at birth, although diagnosis may be delayed or missed in individuals with milder manifestations. Diagnosis tends to occur earlier in patients with congenital heart disease. While it appears more prevalent among individuals of European descent, it occurs across all populations.
Genetically, approximately 85% of affected individuals have the classic 3 Mb deletion at 22q11.2, while around 10% have a smaller nested 1.5 Mb deletion. Because smaller deletions may be missed by fluorescence in situ hybridization (FISH), chromosomal microarray or MLPA is the preferred diagnostic method. About 94% of cases occur de novo due to nonallelic homologous recombination, but when a parent is affected, there is a 50% recurrence risk in each pregnancy. The condition is not associated with advanced maternal age.
Clinically, congenital heart disease is one of the most common and serious manifestations, occurring in approximately 69% of individuals, with about one-third requiring surgical repair. Endocrine abnormalities are present in over half of patients, most notably hypocalcemia due to hypoparathyroidism, as well as thyroid dysfunction, vitamin D deficiency, hypoglycemia, and occasional growth hormone deficiency. Immune dysfunction is seen in the majority of individuals and may include T-cell lymphopenia from thymic hypoplasia, humoral immune deficiencies, recurrent infections, allergies, asthma, and autoimmune conditions.
Otolaryngologic and craniofacial manifestations are frequent and include velopharyngeal insufficiency, submucous cleft palate, bifid uvula, and, less commonly, overt cleft palate or cleft lip. Chronic otitis media, hearing loss, airway abnormalities, obstructive sleep apnea, and characteristic facial features such as hooded eyelids, bulbous nasal tip, and micrognathia are commonly observed. Gastrointestinal involvement often presents as feeding difficulties, dysphagia, gastroesophageal reflux, constipation, and the need for tube feeding in infancy, with occasional structural anomalies such as malrotation or imperforate anus.
Skeletal anomalies occur in roughly half of affected individuals and most commonly involve the cervical spine, sometimes with instability, as well as scoliosis, clubfoot, craniosynostosis, and limb anomalies. Genitourinary findings include renal anomalies, hypospadias, cryptorchidism, and absent or malformed reproductive organs in some patients. Neurologic and developmental manifestations are prominent, with most individuals experiencing learning difficulties, speech and language delay, and mild motor delay. Psychiatric conditions such as ADHD, anxiety, autism spectrum disorder, mood disorders, psychosis, and sleep disturbances are common, particularly in adolescence and adulthood.
Hematologic abnormalities may occur due to deletion of the GP1BB gene, leading to platelet dysfunction and bleeding tendencies. Although malignancy remains uncommon overall, individuals with 22q11.2 deletion syndrome have an increased risk compared with the general population, including leukemias and solid tumors such as Wilms tumor and thyroid carcinoma.
Diagnosis is confirmed by chromosomal microarray or MLPA, with additional baseline evaluation guided by age and clinical findings. Recommended assessments include echocardiography, renal ultrasound, immune studies, calcium and thyroid monitoring, developmental evaluations, and neuropsychological testing. Brain imaging and spinal imaging are reserved for specific clinical indications.
Management is multidisciplinary and lifelong, focusing on early intervention and surveillance. Nonpharmacologic therapy includes early speech therapy beginning in infancy, as well as physical, occupational, educational, and behavioral supports. Medical management may involve calcium and vitamin D supplementation, cardiac medications, endocrine replacement therapy, treatment of immune dysfunction with antibiotics or IVIG, gastrointestinal support, and psychiatric medications when indicated. Surgical interventions may be required for cardiac defects, airway anomalies, gastrointestinal malformations, or palatal abnormalities.
Prognosis varies widely depending on the severity of organ involvement. Most individuals attend mainstream school with additional support, and many achieve varying degrees of independence in adulthood. Morbidity and mortality are increased compared with the general population, with congenital heart disease being the leading cause of death. Long-term follow-up at a specialized 22q center, genetic counseling, and comprehensive family education are essential components of care.
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KembaraXtra-Medicine: Abdominal Aortic Aneurysm
An abdominal aortic aneurysm (AAA) is a segmental, full-thickness dilation of the abdominal aorta that measures at least 50% larger than the normal vessel diameter. Because the average infrarenal aortic diameter in adults is about 2 cm, an aortic diameter of 3.0 cm or greater is commonly used as the threshold for defining an AAA. The relevant ICD-10-CM codes include I71.4 for abdominal aortic aneurysm without rupture and I71.3 for abdominal aortic aneurysm with rupture.
AAA is primarily a disease of older adults and occurs far more often in men than women, with men affected about four times as frequently. In the United States, roughly 13,000 deaths per year are attributed to AAA. Among men older than 60 years, the prevalence is estimated at about 1.2% to 3.3%, which is lower than older reports, likely reflecting reductions in smoking rates. Importantly, men with a subaneurysmal aorta (about 2.6-2.9 cm) have a meaningful risk of progression, with more than half developing an AAA (>3.0 cm) within 5 years, and a notable proportion eventually reaching larger sizes over longer follow-up.
Most AAAs develop in the infrarenal aorta and tend to enlarge progressively over time, with faster expansion as diameter increases. Aneurysm size is the strongest predictor of rupture, and because larger aneurysms grow more quickly, surveillance intervals shorten as size increases. Typical monitoring intervals include imaging every 3 years for AAAs 3.0–3.9 cm, every 12 months for 4.0–4.9 cm, and every 6 months for 5.0–5.4 cm. Rupture is often catastrophic, especially outside the hospital setting, where mortality is commonly 80–90%. Female sex, older age, and especially current smoking are associated with higher rupture risk, and rupture risk rises steeply as aneurysm diameter increases, particularly once the AAA exceeds 5.5 cm.
Screening is designed to detect AAAs before rupture. The USPSTF recommends one-time screening ultrasound for men aged 65–75 who have ever smoked and suggests selective screening for older men who never smoked but have risk factors such as a first-degree family history. Repeat screening after a negative scan is generally not considered beneficial, and men older than 75 are unlikely to benefit. Evidence is currently insufficient to clearly define the balance of benefits and harms of screening women aged 65–75 who have smoked or have a family history. The Society for Vascular Surgery recommends one-time ultrasound screening for men and women aged 65–75 with tobacco history, for men and women aged 65–75 with a first-degree relative with AAA, and for selected patients older than 75 who are otherwise in good health and have smoking history or a first-degree relative with AAA.
Most AAAs are asymptomatic and discovered incidentally on imaging. Physical examination may reveal a pulsatile abdominal mass, but exam sensitivity is only moderate and becomes less reliable with larger abdominal girth; importantly, palpation does not increase rupture risk. When symptoms occur, they may include abdominal, back, flank, or groin pain, or symptoms caused by compression of nearby structures such as early satiety, nausea, vomiting, venous thrombosis from venous compression, ureteral obstruction with hydronephrosis, or distal thromboembolization causing leg pain and discoloration. A ruptured AAA can present with the classic triad of abdominal/back pain, hypotension, and a pulsatile mass, though this full triad is seen in only about half of cases, and rupture rapidly progresses to hemorrhagic shock requiring emergent repair.
AAA formation is driven by degenerative and inflammatory processes within the aortic wall, including smooth muscle cell loss, thinning of the media, infiltration by inflammatory cells, and breakdown of extracellular matrix components such as elastin, leading to progressive dilation and risk of rupture. Age is a major nonmodifiable risk factor, with markedly increased risk after 65 years. Smoking is the strongest modifiable risk factor, strongly linked to aneurysm formation, enlargement, and rupture. Family history also increases risk and may reflect inherited connective tissue susceptibility. Other associated conditions include hyperlipidemia, obesity, peripheral arterial disease, cerebrovascular disease, coronary artery disease, hypertension, and the presence of aneurysms elsewhere. Healthier dietary patterns and regular moderate exercise are associated with lower AAA risk, and moderate exercise does not appear to increase expansion or rupture risk.
Diagnosis is most often made by imaging rather than labs. AAA should be considered in the differential for patients with abdominal, back, or flank pain—especially older adults and smokers—and in those with a pulsatile abdominal mass. Important alternative diagnoses include aortic dissection, ulcerated aortic plaque, renal colic, mesenteric ischemia, pancreatitis, diverticulitis, peptic ulcer disease, and biliary disease. Laboratory testing is not routinely needed, but inflammatory markers and blood cultures may be considered if an inflammatory or infected aneurysm is suspected.
Ultrasound is the preferred screening and surveillance tool because it is noninvasive, widely available, and highly accurate. CT is typically used for preoperative planning and is the imaging modality of choice for symptomatic AAA or suspected rupture because it better defines anatomy, involvement near renal arteries, and signs of wall instability or rupture. MRA may also be used and can be highly accurate. Traditional diagnostic angiography has largely been replaced by noninvasive imaging, though angiographic techniques remain relevant in procedural planning and intraoperative decision-making.
Management depends on aneurysm size, symptoms, and overall surgical risk. Smoking cessation is essential because it reduces AAA expansion and rupture risk, and patients should be offered structured cessation support. Blood pressure and lipid control should follow standard cardiovascular prevention guidance, though medications such as statins or beta blockers are not used solely to prevent AAA expansion. Definitive treatment is aneurysm repair, performed either as open surgical repair (OSR) or endovascular aneurysm repair (EVAR). EVAR is generally favored when anatomy is suitable because it reduces short-term morbidity, but it requires lifelong surveillance for complications such as endoleaks, graft migration, fractures, infection, and aneurysm sac enlargement. CTA is commonly used early in follow-up, with ultrasound increasingly used for ongoing surveillance to reduce radiation and contrast exposure.
Elective repair is generally recommended for infrarenal or juxtarenal AAAs at about 5.5 cm or larger, for AAAs growing more than 0.5 cm in 6 months, and for any AAA that is symptomatic, regardless of size. For women, repair may be considered at slightly smaller diameters (often around 5.0 cm) depending on guideline and risk context. Ruptured AAA requires emergent repair, and symptomatic AAA usually requires urgent intervention. For small asymptomatic AAAs, studies show no clear advantage to early repair compared with careful imaging surveillance.
Referral to vascular surgery is recommended at the time an AAA is diagnosed so that surveillance, risk reduction, and timing of repair can be individualized. At the same time, it is important to optimize comorbidities—particularly coronary artery disease, pulmonary disease, and renal dysfunction—because these conditions increase operative risk and influence whether EVAR or open repair is appropriate.
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Infectious Disease and Microbiology – Neurological Symptoms and Signs with Fever
Overview and Definitions
Clouding of consciousness refers to mild inattentiveness and slightly reduced wakefulness. Obtundation describes slowed responses to external stimuli with decreased alertness and increased sleepiness. Coma is a state of unarousable unconsciousness with no purposeful response to pain. Encephalitis is inflammation of the brain associated with neurologic or mental status changes. Meningitis is inflammation of the meninges surrounding the central nervous system and may be acute, presenting over hours, or chronic, lasting longer than four weeks.
Clinical Approach
Fever with neurologic symptoms requires urgent evaluation for central nervous system infection, systemic infection, or noninfectious neurologic pathology. History should include onset and progression of neurologic symptoms, medication and substance use, trauma, travel, animal exposures, immunocompromised states, and past medical history, with collateral history when available. A complete physical examination should be performed with emphasis on dermatologic, head and neck, cardiopulmonary, and a comprehensive neurologic assessment including mental status, cranial nerves, funduscopy, gait, tone, power, reflexes, sensation, and cerebellar function. Level of consciousness should be documented using the Glasgow Coma Scale. Examination for meningitis includes assessment of neck stiffness, Kernig and Brudzinski signs, and jolt accentuation of headache. Funduscopic examination is important to detect papilledema, subarachnoid hemorrhage, or hypertensive encephalopathy.
Epidemiology
Herpes simplex virus type 1 accounts for approximately 10% of encephalitis cases. In regions where tuberculosis is endemic, tuberculomas are a frequent cause of intracranial mass lesions. The annual incidence of bacterial meningitis in the United States is approximately 1.5 per 100,000 population. In adults, the most common pathogens are Streptococcus pneumoniae, Neisseria meningitidis, and Listeria monocytogenes, with Staphylococcus aureus, including methicillin-resistant strains, increasingly recognized.
Etiology
Acute fever with neurologic signs suggests bacterial meningitis, encephalitis, or infectious intracranial lesions, all of which are medical emergencies. CNS granulomas may be caused by syphilis, cysticercosis, tuberculoma, fungal infections, or sarcoidosis. Enteroviruses are the most common cause of aseptic meningitis. Opportunistic infections are common in advanced HIV infection. Listeria rhombencephalitis presents with brainstem and cranial nerve involvement and is best identified on MRI. Parasitic causes include Echinococcus granulosus, schistosomiasis, amebiasis, and paragonimiasis. Fungal causes include Cryptococcus neoformans, Histoplasma, Coccidioides, Blastomyces, Aspergillus, mucormycosis, and Pseudallescheria. Viral cerebellar encephalitis may follow measles, varicella, Lyme disease, rabies, or legionellosis. Free-living amoebae such as Naegleria fowleri cause acute fulminant meningitis, while Acanthamoeba and Balamuthia cause chronic meningoencephalitis. Noninfectious causes include drug intoxication or withdrawal, malignancy, and subarachnoid hemorrhage.
Clinical Features
Bacterial meningitis typically presents with acute onset of fever, headache, neck stiffness, photophobia, nausea, and vomiting. Absence of headache and jolt accentuation makes bacterial meningitis unlikely, although individual clinical features lack sensitivity. Central nervous system tuberculosis is commonly associated with fever. Brucellosis may cause chronic granulomatous meningitis with constitutional symptoms and relevant animal exposure.
Diagnostic Evaluation
Initial investigations include complete blood count, electrolytes, renal and liver function tests, and blood cultures. Lumbar puncture is essential unless contraindicated by raised intracranial pressure or coagulopathy and should include opening pressure, cell count with differential, protein, glucose, Gram stain, culture, mycobacterial and fungal studies, cryptococcal antigen, syphilis testing, and PCR for herpes simplex or varicella zoster virus. Neuroimaging with CT or MRI is required to exclude space-occupying lesions, with MRI offering superior sensitivity for encephalitis and brainstem disease. In bacterial meningitis, cerebrospinal fluid typically shows elevated opening pressure, neutrophilic pleocytosis, high protein, and low or normal glucose. Viral meningitis usually demonstrates lower white cell counts with lymphocytic predominance and moderately elevated protein.
Management
Empiric treatment for suspected bacterial meningitis includes a third- or fourth-generation cephalosporin combined with vancomycin, with ampicillin added in patients over 50 years of age or immunocompromised to cover Listeria. Dexamethasone should be administered early when pneumococcal meningitis is suspected. Acyclovir should be initiated if herpes simplex encephalitis is a consideration. Antimicrobial therapy must not be delayed for imaging or lumbar puncture when meningitis is suspected.
Additional Care
Management often requires a multidisciplinary approach, with involvement of physiotherapy, occupational therapy, and speech and language pathology during recovery.
Follow-Up and Prognosis
Early recognition and prompt treatment are critical to reducing morbidity and mortality associated with infectious neurologic syndromes.
Complications
Complications include death, deafness, visual impairment, seizures, stroke, cognitive impairment, and increased intracranial pressure.
Overview and Definitions
Clouding of consciousness refers to mild inattentiveness and slightly reduced wakefulness. Obtundation describes slowed responses to external stimuli with decreased alertness and increased sleepiness. Coma is a state of unarousable unconsciousness with no purposeful response to pain. Encephalitis is inflammation of the brain associated with neurologic or mental status changes. Meningitis is inflammation of the meninges surrounding the central nervous system and may be acute, presenting over hours, or chronic, lasting longer than four weeks.
Clinical Approach
Fever with neurologic symptoms requires urgent evaluation for central nervous system infection, systemic infection, or noninfectious neurologic pathology. History should include onset and progression of neurologic symptoms, medication and substance use, trauma, travel, animal exposures, immunocompromised states, and past medical history, with collateral history when available. A complete physical examination should be performed with emphasis on dermatologic, head and neck, cardiopulmonary, and a comprehensive neurologic assessment including mental status, cranial nerves, funduscopy, gait, tone, power, reflexes, sensation, and cerebellar function. Level of consciousness should be documented using the Glasgow Coma Scale. Examination for meningitis includes assessment of neck stiffness, Kernig and Brudzinski signs, and jolt accentuation of headache. Funduscopic examination is important to detect papilledema, subarachnoid hemorrhage, or hypertensive encephalopathy.
Epidemiology
Herpes simplex virus type 1 accounts for approximately 10% of encephalitis cases. In regions where tuberculosis is endemic, tuberculomas are a frequent cause of intracranial mass lesions. The annual incidence of bacterial meningitis in the United States is approximately 1.5 per 100,000 population. In adults, the most common pathogens are Streptococcus pneumoniae, Neisseria meningitidis, and Listeria monocytogenes, with Staphylococcus aureus, including methicillin-resistant strains, increasingly recognized.
Etiology
Acute fever with neurologic signs suggests bacterial meningitis, encephalitis, or infectious intracranial lesions, all of which are medical emergencies. CNS granulomas may be caused by syphilis, cysticercosis, tuberculoma, fungal infections, or sarcoidosis. Enteroviruses are the most common cause of aseptic meningitis. Opportunistic infections are common in advanced HIV infection. Listeria rhombencephalitis presents with brainstem and cranial nerve involvement and is best identified on MRI. Parasitic causes include Echinococcus granulosus, schistosomiasis, amebiasis, and paragonimiasis. Fungal causes include Cryptococcus neoformans, Histoplasma, Coccidioides, Blastomyces, Aspergillus, mucormycosis, and Pseudallescheria. Viral cerebellar encephalitis may follow measles, varicella, Lyme disease, rabies, or legionellosis. Free-living amoebae such as Naegleria fowleri cause acute fulminant meningitis, while Acanthamoeba and Balamuthia cause chronic meningoencephalitis. Noninfectious causes include drug intoxication or withdrawal, malignancy, and subarachnoid hemorrhage.
Clinical Features
Bacterial meningitis typically presents with acute onset of fever, headache, neck stiffness, photophobia, nausea, and vomiting. Absence of headache and jolt accentuation makes bacterial meningitis unlikely, although individual clinical features lack sensitivity. Central nervous system tuberculosis is commonly associated with fever. Brucellosis may cause chronic granulomatous meningitis with constitutional symptoms and relevant animal exposure.
Diagnostic Evaluation
Initial investigations include complete blood count, electrolytes, renal and liver function tests, and blood cultures. Lumbar puncture is essential unless contraindicated by raised intracranial pressure or coagulopathy and should include opening pressure, cell count with differential, protein, glucose, Gram stain, culture, mycobacterial and fungal studies, cryptococcal antigen, syphilis testing, and PCR for herpes simplex or varicella zoster virus. Neuroimaging with CT or MRI is required to exclude space-occupying lesions, with MRI offering superior sensitivity for encephalitis and brainstem disease. In bacterial meningitis, cerebrospinal fluid typically shows elevated opening pressure, neutrophilic pleocytosis, high protein, and low or normal glucose. Viral meningitis usually demonstrates lower white cell counts with lymphocytic predominance and moderately elevated protein.
Management
Empiric treatment for suspected bacterial meningitis includes a third- or fourth-generation cephalosporin combined with vancomycin, with ampicillin added in patients over 50 years of age or immunocompromised to cover Listeria. Dexamethasone should be administered early when pneumococcal meningitis is suspected. Acyclovir should be initiated if herpes simplex encephalitis is a consideration. Antimicrobial therapy must not be delayed for imaging or lumbar puncture when meningitis is suspected.
Additional Care
Management often requires a multidisciplinary approach, with involvement of physiotherapy, occupational therapy, and speech and language pathology during recovery.
Follow-Up and Prognosis
Early recognition and prompt treatment are critical to reducing morbidity and mortality associated with infectious neurologic syndromes.
Complications
Complications include death, deafness, visual impairment, seizures, stroke, cognitive impairment, and increased intracranial pressure.
