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Infectious Disease and Microbiology – Roundworms, Intestinal
Intestinal roundworms are clinically important nematodes that infect humans either after ingestion of eggs from contaminated food, water, or soil, or after infective larvae penetrate the skin. Important intestinal roundworm infections include trichuriasis, enterobiasis, ascariasis, hookworm infection, and strongyloidiasis.
Trichuriasis is caused by Trichuris trichiura, or whipworm, and occurs worldwide, particularly in communities with poor sanitation. Hundreds of millions of people are infected globally. Humans are the principal host, and infection is acquired by ingesting mature eggs from contaminated soil.
After ingestion, whipworm eggs hatch in the intestine, and the larvae migrate to the cecum. Adult worms reside mainly in the cecum and ascending colon and may survive for approximately one year. Diagnosis is made by stool microscopy showing characteristic thick-shelled ova with polar plugs.
Trichuriasis is commonly treated with albendazole 400 mg orally daily for 3 days in mild to moderate infection, with longer courses considered for heavier infection. Mebendazole is another effective option. Heavy worm burdens can cause chronic gastrointestinal symptoms and painful rectal prolapse.
Enterobiasis is caused by Enterobius vermicularis, commonly called pinworm. It occurs worldwide and is especially common among children, households, schools, and other crowded settings. Infection can spread rapidly among family members regardless of socioeconomic status.
Adult pinworms live in the terminal ileum and cecum. At night, female worms migrate to the perianal region to deposit eggs, producing intense itching. Scratching contaminates the hands and fingernails, allowing autoinfection and person-to-person transmission through contaminated clothing, bedding, and surfaces.
Diagnosis of enterobiasis is usually made using the cellophane or Scotch-tape test, which collects the characteristic elongated oval eggs from the perianal region. Stool microscopy is generally less useful because the eggs are deposited outside the intestinal lumen.
Treatment includes a single oral dose of albendazole 400 mg or mebendazole 100 mg, with the dose repeated after 2 weeks to reduce the risk of reinfection. Pyrantel pamoate is an alternative. Household members should generally be treated at the same time, and bedding and clothing should be thoroughly washed.
Complications of enterobiasis include perianal excoriations, secondary bacterial infection, and rarely migration of worms into the female genital tract or abdominal cavity.
Ascariasis is caused by Ascaris lumbricoides and is one of the most common human helminthic infections worldwide. It is especially prevalent in areas with poor sanitation and is commonly seen in children.
Ascaris is the largest human intestinal nematode, with adult worms reaching approximately 35 cm in length. Eggs are passed in feces and become infectious after maturing in soil. They can remain viable in the environment for years.
After infective eggs are swallowed, larvae hatch in the intestine, penetrate the intestinal wall, enter the bloodstream, and migrate to the lungs. They cross into the alveoli, ascend the respiratory tract, are swallowed, and then mature into adult worms in the small intestine. Adult worms may survive for 1–2 years.
Diagnosis is usually established by stool microscopy demonstrating characteristic thick-shelled eggs. Peripheral eosinophilia may develop during the pulmonary migration phase.
Ascariasis is usually treated with albendazole 400 mg orally as a single dose or mebendazole 100 mg twice daily for 3 days. Heavy infection can cause intestinal obstruction, impaired nutrition, and malnutrition, particularly in children.
Hookworm infection is caused predominantly by Necator americanus and Ancylostoma duodenale. It is common in tropical and subtropical regions and affects a substantial proportion of the world’s population.
Infective hookworm larvae in contaminated soil penetrate exposed skin, commonly through bare feet. The larvae enter the bloodstream, migrate to the lungs, penetrate the alveoli, ascend the respiratory tract, and are swallowed. They then attach to the mucosa of the small intestine and feed on blood.
Adult hookworms are approximately 1 cm long and may survive for many years. Chronic intestinal blood loss can result in significant iron deficiency, especially in individuals with poor nutritional reserves.
Diagnosis is made by stool microscopy showing characteristic thin-shelled, colorless eggs. Eosinophilia may occur during larval migration, while chronic disease may produce iron-deficiency anemia.
Treatment generally consists of albendazole 400 mg orally as a single dose or mebendazole for 3 days. Pyrantel pamoate is an alternative. Iron replacement may also be required in patients with significant anemia.
Severe hookworm infection may cause profound iron-deficiency anemia, malabsorption, poor growth, and failure to thrive.
Strongyloidiasis is caused by Strongyloides stercoralis and occurs mainly in tropical and subtropical regions. It is more common in rural communities, institutional settings, and populations with lower socioeconomic conditions.
Infective filariform larvae penetrate the skin following contact with contaminated soil. They enter the circulation, migrate through the lungs, penetrate the alveoli, ascend the respiratory tract, and are swallowed. Adult female worms then live in the upper small intestine.
A distinctive feature of Strongyloides infection is autoinfection. Rhabditiform larvae produced in the intestine can transform into infective filariform larvae before leaving the body. These larvae penetrate the intestinal wall or perianal skin and restart the migration cycle, allowing infection to persist for decades.
Diagnosis is based on demonstration of rhabditiform larvae in stool. Because parasite excretion may be intermittent, repeated stool examinations may be required. Eosinophilia is common in uncomplicated acute and chronic infection. Serologic testing can be useful when stool examinations are negative but clinical suspicion remains high.
Ivermectin is the preferred treatment for strongyloidiasis, usually given at 200 micrograms/kg orally daily for 2 days. A repeat course may be required. Albendazole is an alternative, although generally less effective. Hyperinfection or disseminated strongyloidiasis requires prolonged ivermectin treatment until parasitologic clearance is achieved.
Strongyloides hyperinfection is particularly dangerous in immunocompromised patients, especially those receiving corticosteroids. Large numbers of migrating larvae can cause severe gastrointestinal and pulmonary disease, intestinal microperforation, bacteremia, sepsis, and death.
General prevention of intestinal roundworm infections depends on proper sanitation, safe disposal of human waste, thorough handwashing after defecation and before food preparation, and careful washing, peeling, or cooking of fruits and vegetables. Wearing protective footwear is particularly important for preventing hookworm infection and strongyloidiasis when contact with contaminated soil is possible.
The differential diagnosis includes other intestinal helminthic infections and should be guided by exposure history, clinical manifestations, stool findings, eosinophilia, and geographic risk factors.
Follow-up stool examinations may be useful after treatment to confirm eradication and detect reinfection, particularly in persistent or high-risk infections. Enterobiasis requires attention to household transmission, while strongyloidiasis requires especially careful follow-up in immunocompromised patients.
The overall prognosis is excellent when intestinal roundworm infections are recognized and appropriately treated. However, untreated heavy infection can produce important complications, including rectal prolapse from trichuriasis, intestinal obstruction from ascariasis, severe anemia from hookworm infection, and potentially fatal hyperinfection syndrome from strongyloidiasis.
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Infectious Disease and Microbiology – Rocky Mountain Spotted Fever
Rocky Mountain spotted fever (RMSF) is an acute tick-borne infection caused by the intracellular bacterium Rickettsia rickettsii. Despite its name, most cases in the United States occur outside the Rocky Mountain region. The disease can progress rapidly and may be fatal if treatment is delayed.
RMSF is a reportable disease in the United States, with hundreds to a few thousand cases historically reported each year. Although cases have occurred across most states, a large proportion have been concentrated in North Carolina, Oklahoma, Arkansas, Tennessee, and Missouri. RMSF also occurs in Canada, Mexico, Central America, and South America.
The disease is most common during spring and summer, when tick activity is highest. Children younger than 10 years and adults between 40 and 64 years have historically had high incidence rates. Risk increases with residence or activity in wooded areas, tall grass, and places where dogs and ticks are common. Glucose-6-phosphate dehydrogenase deficiency has been associated with more severe disease in some patients.
Prevention depends on reducing tick exposure. People entering wooded or grassy environments should wear protective clothing, perform frequent tick checks, and consider repellents containing DEET on exposed skin and permethrin on clothing where appropriate. Attached ticks should be removed promptly using fine-tipped forceps, grasping the tick close to the skin and pulling steadily upward without twisting.
After a tick bite, R. rickettsii enters vascular endothelial cells and spreads through the vascular system. Infection produces widespread vasculitis, increasing vascular permeability and activating coagulation pathways. The resulting capillary leak, edema, hypovolemia, and tissue ischemia account for many of the systemic manifestations and complications of RMSF.
Rickettsia rickettsii is an obligate intracellular, gram-negative coccobacillus transmitted through the salivary glands of feeding ticks. Important vectors include Dermacentor variabilis, the American dog tick, in much of the eastern United States, and Dermacentor andersoni, the Rocky Mountain wood tick, in western regions. The brown dog tick, Rhipicephalus sanguineus, can transmit infection in parts of Arizona and Mexico, while Amblyomma species have been important vectors in Central and South America.
The incubation period is generally 2–14 days, averaging about 7 days. Illness usually begins abruptly with fever, severe headache, myalgias, and marked malaise. Nausea, vomiting, and abdominal pain are also common. Neurologic involvement may range from mild confusion to seizures and encephalitis. Importantly, many patients do not recall a tick bite.
The classic triad of fever, rash, and known tick exposure is uncommon early in the disease and should not be required for diagnosis. The rash typically appears 2–5 days after fever begins. It usually starts as small blanching erythematous macules on the wrists and ankles, then spreads to the palms, soles, arms, legs, and trunk. As disease progresses, the lesions may become petechial.
The rash may appear late or may never develop. A minority of patients have so-called spotless RMSF. In addition, the rash may be difficult to recognize in people with darker skin tones. Therefore, absence of rash does not exclude the diagnosis.
Ocular abnormalities may include conjunctivitis, retinal vascular changes, hemorrhages, arterial occlusion, and papilledema. Neurologic findings may include lethargy, photophobia, meningismus, transient hearing loss, amnesia, behavioral changes, seizures, or encephalopathy. Hepatomegaly and pulmonary findings resembling pneumonia can also occur.
Diagnosis requires a high degree of clinical suspicion because laboratory confirmation is often unavailable during the early phase when treatment is most important. Antibodies against R. rickettsii are generally not detectable until approximately 7–10 days after illness begins.
Indirect immunofluorescence antibody testing is the traditional reference serologic method. Diagnosis is supported by a fourfold rise in antibody titer between acute and convalescent specimens. A single positive result may be difficult to interpret because antibodies to other spotted-fever rickettsiae may cross-react and background seropositivity can occur.
Thrombocytopenia is one of the most common laboratory abnormalities. The white blood cell count may be normal, decreased, or elevated and is not sufficiently reliable to exclude the disease. Other abnormalities may include hyponatremia, elevated creatinine, azotemia, increased serum transaminases, bilirubin elevation, and increased creatine kinase.
Chest radiographs may demonstrate focal pulmonary infiltrates or interstitial edema. In patients with encephalopathy, CT or MRI may reveal generalized cerebral edema. Cerebrospinal fluid may show a mild lymphocytic pleocytosis. Electrocardiographic abnormalities may range from nonspecific ST-wave changes to atrial arrhythmias.
Direct immunofluorescence staining of a skin biopsy for R. rickettsii antigens can provide early diagnostic evidence, although it is not routinely available and is generally less practical than clinical diagnosis and serology.
The differential diagnosis is broad and includes viral syndromes, bacterial sepsis, meningococcemia, disseminated gonococcal infection, secondary syphilis, typhoid fever, leptospirosis, ehrlichiosis, anaplasmosis, toxic shock syndrome, drug hypersensitivity reactions, idiopathic thrombocytopenic purpura, thrombotic thrombocytopenic purpura, and bacterial or viral meningoencephalitis.
Treatment should begin immediately when RMSF is suspected and must not be delayed while awaiting laboratory confirmation. Doxycycline is the treatment of choice for both adults and children. Adults are generally treated with doxycycline 100 mg twice daily, while children weighing less than 45 kg receive approximately 2.2 mg/kg per dose twice daily.
Therapy is typically continued for at least 5–7 days and for at least 48 hours after the patient becomes afebrile and shows clear clinical improvement. Oral or intravenous therapy may be used depending on severity and the patient’s ability to tolerate oral medications.
Doxycycline is also recommended for young children despite historical concerns about tooth staining because short courses have not shown the same risk associated with prolonged tetracycline exposure, and delayed effective therapy can be life-threatening.
Chloramphenicol has historically been used as an alternative, particularly when tetracyclines were considered contraindicated. However, outcomes have generally been less favorable than with doxycycline, and treatment decisions in pregnancy or other special circumstances require individualized risk-benefit assessment.
Severely ill patients may require hospitalization and intensive supportive care. Intravenous antibiotics are appropriate for patients with persistent vomiting, unstable vital signs, altered mental status, or other signs of severe disease. Shock, renal failure, respiratory compromise, and neurologic deterioration may require intensive care, hemodynamic support, mechanical ventilation, or renal replacement therapy.
Patients with neurologic symptoms, elevated creatinine, significant vomiting, hypotension, or other unstable vital signs should generally be admitted to the hospital. Approximately one-fourth of suspected cases historically required hospitalization.
The prognosis is strongly influenced by how quickly effective treatment is started. Delay beyond the first several days of illness substantially increases the risk of death and severe complications. Older age, neurologic involvement, renal dysfunction, and failure to receive doxycycline are associated with poorer outcomes.
Most survivors recover fully, but severe disease may produce permanent neurologic deficits, hearing impairment, or tissue ischemia severe enough to cause gangrene and require amputation.
Major complications include meningitis, encephalitis, seizures, acute kidney injury, acute respiratory distress syndrome, shock, disseminated vascular injury, myocarditis, tissue necrosis, and multiorgan failure.
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Infectious Disease and Microbiology – Rheumatic Fever
Rheumatic fever is an inflammatory clinical syndrome that develops following infection of the pharynx with group A Streptococcus. It can produce a wide range of manifestations, including migratory arthritis, characteristic skin lesions, Sydenham chorea, and pancarditis with cardiac valvular dysfunction.
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Rheumatic fever occurs worldwide but has become relatively uncommon in developed countries because of improved living conditions and appropriate antibiotic treatment of streptococcal pharyngitis. It remains an important cause of acquired heart disease in developing countries, historically accounting for approximately 40% of heart disease in some populations. The estimated incidence in the United States has been approximately 0.5 per 100,000 population, with a prevalence of about 2 per 10,000. It primarily affects children between 6 and 15 years of age.
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Approximately one-third of cases may follow subacute or clinically unrecognized group A streptococcal pharyngitis. Historically, the attack rate after untreated streptococcal pharyngitis has ranged from approximately 0.4–3%. Outbreaks may be influenced by the particular circulating strains of Streptococcus.
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Important risk factors include overcrowded living conditions and a previous history of rheumatic fever. Genetic susceptibility has also been proposed, with associations involving certain HLA types, B-cell alloantigens, and immune-response gene polymorphisms, although the precise genetic contribution remains incompletely understood.
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Prevention begins with appropriate diagnosis and treatment of group A streptococcal pharyngitis. A complete course of penicillin therapy can prevent the development of rheumatic fever even when treatment is initiated several days after the onset of sore throat. Patients with a previous episode of rheumatic fever have a substantial risk of recurrence and therefore require secondary antibiotic prophylaxis. Benzathine penicillin G administered intramuscularly at regular intervals is a commonly used regimen, with oral penicillin or certain alternative antibiotics used when appropriate.
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The pathogenesis of rheumatic fever is primarily immune mediated. Molecular mimicry between antigens of group A Streptococcus and human tissues produces an abnormal immune response in which antibodies and immune cells directed against streptococcal components cross-react with host tissues, particularly structures within the heart.
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Group A streptococcal pharyngitis initiates the disease. Rheumatic fever typically develops approximately 1–5 weeks after the infection, with an average interval historically reported at about 19 days. Certain streptococcal strains have been particularly associated with rheumatic fever. Cross-reacting immune responses against streptococcal antigens and cardiac tissues, especially heart valves, contribute to the development of carditis.
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Patients may present with fever, fatigue, joint pain, skin manifestations, involuntary movements, dyspnea, or peripheral edema. Rheumatic fever is fundamentally a clinical diagnosis. Traditionally, diagnosis is based on the Jones criteria together with evidence of a preceding group A streptococcal infection. The clinical manifestations may persist for several months, particularly when carditis is present.
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The major clinical manifestations include migratory polyarthritis, carditis, Sydenham chorea, subcutaneous nodules, and erythema marginatum. Historically, polyarthritis has occurred in approximately 75% of cases, carditis in about 50%, chorea in approximately 15%, and subcutaneous nodules and erythema marginatum in fewer than 10%.
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Polyarthritis commonly occurs early in the disease and is frequently accompanied by fever. The arthritis predominantly involves large joints, particularly the knees, ankles, elbows, and wrists. Several joints may become involved sequentially, producing the characteristic migratory pattern. Joint manifestations generally resolve without permanent damage.
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Carditis may involve the endocardium, myocardium, and pericardium, producing pancarditis. Some cases are clinically subtle, whereas severe disease may present with congestive heart failure. Acute valvular involvement most commonly produces mitral regurgitation, followed by aortic regurgitation. Persistent valvular damage can eventually result in chronic rheumatic heart disease.
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Sydenham chorea consists of irregular, involuntary, purposeless, dance-like movements involving the face and extremities. It may occur together with arthritis and carditis or occasionally appear as the predominant manifestation of rheumatic fever.
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Subcutaneous nodules are painless lesions that usually develop over tendons or near joints. They may reach approximately 2 cm in diameter and are particularly associated with rheumatic carditis.
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Erythema marginatum is an uncommon, transient rash consisting of irregular erythematous lesions, usually involving the trunk and extremities. Because the lesions are evanescent, the rash may be difficult to detect during examination.
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Minor manifestations include fever and arthralgia without objective arthritis. Laboratory or electrocardiographic abnormalities contributing to the traditional minor criteria include elevated inflammatory markers such as erythrocyte sedimentation rate or C-reactive protein and prolongation of the PR interval on electrocardiography.
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Evidence of a preceding group A streptococcal infection should generally be established. This may include a positive throat culture, positive rapid streptococcal antigen testing, or elevated or rising streptococcal antibody titers such as antistreptolysin O, anti-DNase B, or antihyaluronidase antibodies. Exceptions may occur with manifestations such as Sydenham chorea or indolent carditis, which can appear sufficiently late that evidence of the original infection is difficult to demonstrate.
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Echocardiography is an important component of evaluation because it can detect valvular abnormalities and carditis that may not be obvious on physical examination. Serial echocardiography may be required when cardiac involvement progresses or when monitoring established carditis.
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Pathologically, rheumatic fever produces inflammatory lesions within connective tissues. Characteristic Aschoff bodies may be found in the myocardium. Cardiac inflammation can involve all layers of the heart, resulting in pancarditis.
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The differential diagnosis includes juvenile idiopathic arthritis, systemic lupus erythematosus, Lyme disease, gonococcal arthritis, infective endocarditis, viral infections such as rubella and coxsackievirus infection, medication reactions, sickle cell disease, sarcoidosis, inflammatory bowel disease, leukemia, and other causes of inflammatory arthritis or cardiac disease.
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Treatment is directed toward eradication of group A streptococcal infection, suppression of inflammation, management of cardiac complications, and prevention of recurrent disease. Anti-inflammatory therapy with aspirin or other appropriate anti-inflammatory agents has historically been used for arthritis and other inflammatory manifestations. Corticosteroids may be considered in severe carditis, particularly when significant heart failure is present.
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Older treatment regimens used high-dose aspirin, sometimes beginning at approximately 90–100 mg/kg/day and subsequently reducing the dose after clinical improvement. Corticosteroid therapy has historically been used for severe inflammatory cardiac disease. Because aspirin and corticosteroid regimens require careful consideration of toxicity and current clinical recommendations, treatment should be individualized and supervised appropriately.
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Secondary antibiotic prophylaxis is a central component of long-term management because recurrent streptococcal infections can cause additional episodes of rheumatic fever and progressively worsen valvular disease. The required duration depends on whether the initial episode involved carditis and whether residual valvular disease remains.
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Patients with rheumatic fever accompanied by carditis and persistent valvular disease generally require prolonged prophylaxis, historically for at least 10 years or until approximately 40 years of age, whichever is longer. Some individuals at continued high risk of streptococcal exposure or recurrent disease may require lifelong prophylaxis.
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When carditis occurred but no residual cardiac disease remains, prophylaxis has traditionally been continued for approximately 10 years or until at least 21 years of age, whichever period is longer. In rheumatic fever without carditis, prophylaxis is generally continued for at least 5 years or until approximately 21 years of age, whichever is longer. Sydenham chorea as a manifestation of rheumatic fever also warrants secondary prophylaxis.
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Severe valvular disease that fails medical management may require cardiothoracic surgical evaluation. Rheumatic heart disease remains an important indication for valve surgery in regions where rheumatic fever is common. Procedures may include mitral valve repair, commissurotomy, or valve replacement, depending on the type and severity of valvular damage.
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Hospitalization may be necessary for patients with significant carditis, heart failure, severe Sydenham chorea, or other serious manifestations. Discharge is generally appropriate when symptoms are adequately controlled and there is no evidence of uncontrolled heart failure.
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Patients with carditis require long-term clinical and echocardiographic follow-up, often involving both primary care and cardiology specialists. Education regarding adherence to secondary antibiotic prophylaxis is particularly important because recurrent attacks substantially increase the risk of permanent valvular damage.
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The overall prognosis depends largely on the severity of cardiac involvement and the occurrence of recurrent episodes. Many patients recover from the acute illness, but recurrence can occur following subsequent group A streptococcal infections, particularly when secondary prophylaxis is inadequate.
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The most important long-term complication is chronic rheumatic valvular heart disease. Progressive valve dysfunction can eventually result in refractory heart failure, arrhythmias, pulmonary hypertension, and the need for cardiac surgery. Patients with damaged valves may also have an increased risk of infective endocarditis.
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Infectious Disease and Microbiology – Respiratory Syncytial Virus Infection
Respiratory syncytial virus (RSV) is a highly contagious viral infection that causes upper and lower respiratory tract disease in children and adults. It is particularly important in infants, children with congenital heart or chronic lung disease, immunocompromised individuals, and older adults. Acute bronchiolitis is the major clinical manifestation in young children.
RSV is one of the most important causes of lower respiratory tract infection in childhood. In 2005, an estimated 33.8 million episodes of RSV-associated acute lower respiratory tract infection occurred worldwide among children younger than 5 years, with an estimated 66,000–199,000 associated deaths. Severe RSV disease occurs most frequently between 2 and 8 months of age. By 24 months, most children have experienced at least one RSV infection. RSV also causes substantial disease in older adults, with annual attack rates historically estimated at approximately 5–10%.
Important risk factors for severe RSV infection include age younger than 6 months, prematurity, male sex, crowding, lower socioeconomic conditions, exposure to passive cigarette smoke, day-care attendance, older siblings attending day care, and birth during the early part of RSV season. Children with congenital heart disease, chronic lung disease such as bronchopulmonary dysplasia or cystic fibrosis, and individuals who are immunocompromised because of chemotherapy or transplantation are also at increased risk.
Prevention focuses on reducing viral transmission and protecting individuals at high risk of severe disease. Frequent handwashing, avoiding the sharing of contaminated objects, and appropriate infection-control precautions can reduce transmission. Glove and gown precautions are particularly important in healthcare environments. Historically, passive immunization with RSV-specific immunoglobulin and the monoclonal antibody palivizumab has been used for selected high-risk infants. Motavizumab was investigated as a more potent monoclonal antibody against RSV.
RSV spreads from the upper respiratory tract into the lower respiratory tract. Viral infection promotes cell-to-cell fusion, producing characteristic multinucleated structures known as syncytia. Infection and inflammation of the small airways contribute to airway obstruction, mucus production, wheezing, and the characteristic manifestations of bronchiolitis.
Severe RSV bronchiolitis during infancy has been associated with an increased prevalence of recurrent wheezing and asthma later in childhood. Some studies have suggested that RSV prophylaxis may reduce recurrent wheezing in certain nonatopic children, although the relationship between RSV infection, atopy, and subsequent asthma is complex.
The incubation period of RSV is approximately 2–8 days. Transmission occurs through contact with infected respiratory secretions, contaminated hands or surfaces, and respiratory droplets. Infection commonly begins with upper respiratory symptoms and may progress rapidly to cough, coryza, and wheezing. Fever is usually low-grade, although high fever can occur in children.
As the disease progresses, young children may develop a deeper cough, episodes of coughing, wheezing, and manifestations of bronchiolitis. Mild croup may occur, and otitis media is a frequent associated condition. Older adults may develop more significant lower respiratory tract disease, including bronchopneumonia.
Physical examination of infants with RSV lower respiratory tract infection may demonstrate tachypnea, diffuse rales associated with small-airway disease, wheezing, and, in severe cases, cyanosis. Otitis media may also be present. Careful assessment of hydration is particularly important in infants and should include evaluation of skin turgor, capillary refill, and the condition of the mucous membranes.
Laboratory assessment in patients with significant illness may include measurement of oxygen saturation, arterial blood gases, serum electrolytes, and a complete blood count. RSV can be identified from respiratory secretions using rapid diagnostic tests. Other diagnostic techniques include immunofluorescence assays, enzyme-linked immunosorbent assays, and viral culture of nasal washings.
Chest radiographs may demonstrate hyperinflation, focal atelectasis, and pulmonary infiltrates. Expiratory CT imaging may show evidence of small-airway disease, particularly air trapping. Histopathologic examination of lung tissue can demonstrate mononuclear cell and neutrophil infiltration around bronchioles, together with areas of atelectasis and pulmonary infiltrates.
The differential diagnosis includes asthma, acute or chronic bronchitis, bacterial or viral pneumonia, influenza, parainfluenza infection, croup, human metapneumovirus infection, and neonatal sepsis.
Treatment is primarily supportive. Oxygen should be administered when clinically indicated, and adequate hydration should be maintained with oral or intravenous fluids depending on the patient’s condition. Respiratory support, including mechanical ventilation or intubation, may be necessary in severe disease.
Nebulized ribavirin has historically been approved for severe RSV infection. A regimen described is 6 g of lyophilized ribavirin dissolved in 300 mL of distilled water and administered through a small-particle aerosol generator for 12–20 hours per day for 3–7 days. However, evidence supporting substantial clinical benefit has been limited, and concerns include cost and potential occupational exposure of healthcare workers. Its use has therefore generally been reserved for selected severe cases, particularly among profoundly immunocompromised patients.
Various additional approaches have been investigated in high-risk populations. Intravenous palivizumab, alone or in combination with ribavirin, has been studied in severe RSV infection. Combination regimens involving inhaled ribavirin, corticosteroids, intravenous immunoglobulin, and sometimes palivizumab have also been evaluated in transplant recipients. RNA interference therapies have additionally been investigated in lung transplant patients.
Hospitalized patients require careful supportive management. Oxygenation and hydration should be monitored closely, and patients with progressive respiratory failure may require assisted ventilation. Young infants, immunocompromised patients, individuals with significant cardiopulmonary disease, and older adults are at increased risk of severe outcomes.
Most otherwise healthy children hospitalized with RSV infection improve sufficiently for discharge within several days. Follow-up is generally unnecessary after uncomplicated recovery, although patients who subsequently develop persistent or recurrent bronchospasm may require additional evaluation.
The prognosis is generally favorable in healthy children, but RSV can cause substantial morbidity and mortality in young infants, older adults, and individuals with underlying cardiopulmonary disease or immunocompromising conditions. A small but important proportion of infants with RSV infection require intermediate or intensive care.
Potential complications include bacterial pneumonia, otitis media, respiratory failure, and recurrent wheezing. Neurologic complications such as seizures and encephalopathy have also been reported. Severe childhood RSV infection has been associated with subsequent asthma or recurrent wheezing, although the precise causal relationship remains uncertain.
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Relapsing fever is a spirochetal infection characterized by recurrent episodes of fever separated by periods of normal temperature. The disease occurs in two major forms: louse-borne (epidemic) relapsing fever and tick-borne (endemic) relapsing fever.
The epidemiology of relapsing fever varies according to the mode of transmission. Louse-borne relapsing fever, caused by Borrelia recurrentis, is strongly associated with poor socioeconomic conditions, overcrowding, war, famine, and natural disasters, which facilitate the spread of body lice. Although uncommon worldwide today, endemic areas persist in parts of Central and East Africa and the Andes region of South America.
Tick-borne relapsing fever has a worldwide distribution but is particularly common in tropical Africa. In the United States, cases occur mainly west of the Mississippi River. In mountainous regions such as California, Utah, Arizona, New Mexico, Colorado, Oregon, and Washington, Borrelia hermsii is the predominant species, whereas Borrelia turicatae is more common in nonmountainous areas of the Southwest.
Risk factors for louse-borne relapsing fever include homelessness and overcrowding. Tick-borne relapsing fever is associated with recreational or occupational exposure to tick-infested environments. B. hermsii infection is frequently linked to exposure to cabins in pine forests, while B. turicatae infection may follow entry into caves or crawling under houses.
Preventive measures focus on control of lice and ticks. In high-risk settings for tick-borne relapsing fever, postexposure prophylaxis with doxycycline may be recommended. A suggested regimen is doxycycline 200 mg orally on the first day followed by 100 mg daily for four additional days.
The pathophysiology differs according to the vector. In louse-borne disease, crushing infected lice releases Borrelia recurrentis, which enters the body through skin breaks or mucous membranes. Tick-borne disease is transmitted through the saliva of soft-bodied ticks during feeding. Because argasid ticks feed rapidly at night and produce painless bites, many individuals are unaware they were bitten.
Fever corresponds to periods of spirochetemia. During afebrile intervals, spirochetes are sequestered within internal organs. Under immune pressure, the organisms undergo antigenic variation and reappear in the bloodstream, producing recurrent febrile episodes.
Relapsing fever is caused by spirochetes of the genus Borrelia. The human body louse (Pediculus humanus corporis) transmits B. recurrentis, causing epidemic relapsing fever. Tick-borne disease is transmitted by soft-bodied ticks of the genus Ornithodoros, which can carry more than 15 pathogenic Borrelia species.
The incubation period is usually around 8 days, ranging from 5–15 days. Illness begins abruptly with fever accompanied by chills, rigors, headache, malaise, arthralgias, diffuse myalgias, lethargy, cough, jaundice, and photophobia. Some patients develop petechial, macular, or papular rashes. Cardiac and neurologic manifestations may occur, particularly in tick-borne disease.
The febrile episode typically ends suddenly after 3–6 days. After an afebrile period lasting approximately 7–9 days, symptoms recur. Louse-borne relapsing fever usually produces one or two relapses, whereas multiple relapses are common in tick-borne disease.
Physical examination may reveal conjunctival injection and edema, hepatomegaly, splenomegaly, diffuse abdominal tenderness, lymphadenopathy, rales, rhonchi, and neurologic abnormalities. Neurologic complications are more common in tick-borne relapsing fever.
The definitive diagnosis is made by demonstrating Borrelia organisms in peripheral blood obtained during febrile episodes. Thick and thin blood smears stained with Giemsa or Wright stain should be carefully examined. Organisms are rarely detectable during afebrile periods. Dark-field microscopy can also identify spirochetes. Polymerase chain reaction testing may be performed on blood samples. Serologic tests may support the diagnosis but have limited sensitivity and specificity.
The differential diagnosis includes malaria, leptospirosis, dengue fever, babesiosis, tularemia, ehrlichiosis/anaplasmosis, rat-bite fever, and typhus, especially during epidemics of louse-borne relapsing fever.
Treatment depends on the type of disease. Louse-borne relapsing fever is treated with a single oral dose of tetracycline 500 mg or doxycycline 100 mg. Tick-borne relapsing fever requires a longer course, typically tetracycline 500 mg orally every 6 hours or doxycycline 100 mg orally twice daily for 7 days.
Patients with meningitis or encephalitis should receive parenteral antibiotics such as penicillin G or ceftriaxone for 10–14 days. Erythromycin may serve as an alternative regimen, particularly for patients unable to take tetracyclines.
A Jarisch-Herxheimer reaction may occur shortly after initiation of antibiotic therapy, especially with penicillin treatment. This reaction results from rapid destruction of spirochetes and may present with fever, hypotension, chills, and worsening symptoms.
Careful follow-up is necessary because relapses are common. Untreated louse-borne relapsing fever has a mortality rate ranging from 4–40%, while untreated tick-borne disease carries a mortality rate of 2–5%.
Major complications include myocarditis with arrhythmias, liver damage, cerebral hemorrhage, acute respiratory distress syndrome, meningitis, meningoencephalitis, cranial neuritis, aphasia, hemiplegia, iridocyclitis, and panophthalmitis.
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Rabies is a fatal viral infection caused by a bullet-shaped, single-stranded RNA virus belonging to the family Rhabdoviridae. The disease primarily affects the central nervous system and is almost universally fatal once clinical symptoms develop.
Rabies remains a major global public health problem. Approximately 15 million people receive postexposure prophylaxis annually worldwide. According to the World Health Organization, many cases are underreported, and annual deaths may exceed 55,000. The disease is more common in developing countries and occurs worldwide except in Antarctica and a few isolated island nations. In developing nations, dog bites are the most common mode of transmission, whereas in developed countries transmission more commonly occurs through raccoons, bats, foxes, and skunks.
Individuals at increased risk include laboratory workers involved in rabies research or vaccine production, veterinarians, wildlife officers, and people frequently exposed to wild animals. Exposure in caves may result from inhalation of aerosolized bat excreta. There is no known genetic predisposition.
The most effective preventive measure is mass vaccination of animals, especially dogs. Individuals with occupational or travel-related risk should receive preexposure vaccination. Preexposure prophylaxis consists of rabies vaccine administered intramuscularly on days 0, 7, and 21 or 28. Antibody titers should be periodically checked in high-risk individuals such as laboratory workers and wildlife officers.
The rabies virus enters the body through broken skin or mucous membranes, most commonly after an animal bite. The incubation period usually ranges from 20–90 days but may vary considerably. After entry, the virus travels centripetally through peripheral nerves by axonal transport to the central nervous system, where viral replication occurs with formation of characteristic Negri bodies. The virus then spreads centrifugally to tissues including the salivary and lacrimal glands.
Human infection usually results from bites of rabid animals, especially dogs. Because the virus is present in high concentrations in saliva, scratches or licks on broken skin may also transmit infection.
History is crucial for diagnosis. Multiple bites, bites involving the face, and deep penetrating injuries carry greater risk than superficial bites through clothing or bites to extremities. Early symptoms include paresthesias or pain at the bite site, fever, malaise, sore throat, nausea, and vomiting. This prodromal phase generally lasts 2–10 days.
Following the prodrome, encephalitis develops. Patients may exhibit fever, personality changes, agitation, hyperactivity, hallucinations, biting behavior, and autonomic instability. Characteristic findings of furious rabies include hydrophobia, in which attempts to drink or even the sight of water provoke painful pharyngeal spasms, and aerophobia, in which airflow or sensory stimuli trigger spasms. Seizures may occur, sometimes precipitated by tactile stimuli. Periods of agitation alternate with intervals of lucidity. Rapid progression to coma commonly follows. Paralysis may develop later in the disease.
Paralytic rabies presents differently and may resemble Guillain-Barré syndrome, with progressive weakness and paralysis.
Laboratory diagnosis is difficult and often secondary to clinical suspicion and exposure history. Direct fluorescent antibody testing of a skin biopsy taken from the nape of the neck remains the standard diagnostic method. RT-PCR testing of saliva, cerebrospinal fluid, or tissue specimens may also be used. Cerebrospinal fluid findings are nonspecific and may show pleocytosis. MRI may demonstrate increased T2 signal intensity in the hippocampi, hypothalamus, or brainstem, although imaging findings are not specific.
Pathologic examination reveals Negri bodies, especially in hippocampal pyramidal cells. Paralytic rabies may also show segmental demyelination resembling Guillain-Barré syndrome.
The differential diagnosis includes tetanus, viral encephalitis, acute disseminated encephalomyelitis, poliomyelitis, Guillain-Barré syndrome, and acute demyelinating polyneuropathy.
Management after exposure is critical because established rabies is almost universally fatal. Immediate wound cleansing with soap and water and irrigation with iodine-containing solutions can reduce transmission risk by approximately 90%.
For previously unvaccinated individuals, postexposure prophylaxis includes human rabies immunoglobulin at 20 units/kg administered once on day 0. As much of the dose as possible should be infiltrated around the wound, with the remainder injected intramuscularly at a site distant from vaccine administration. Rabies vaccine is administered intramuscularly in the deltoid region on days 0, 3, 7, 14, and 28.
Previously vaccinated individuals do not require rabies immunoglobulin and instead receive booster vaccine doses on days 0 and 3.
Immunocompromised patients may have inadequate vaccine responses and should undergo antibody testing 2–4 weeks after vaccination.
Hospital admission is recommended for patients with deep or multiple wounds, altered behavior, or neurologic symptoms. Supportive care, including intravenous fluids and careful nursing management, is essential in symptomatic rabies. Environmental stimuli should be minimized to reduce provocation of spasms and seizures.
Patients should be advised to observe the biting dog or animal for 10 days if possible. If the animal dies, disappears, or develops abnormal behavior during this period, health authorities should be notified immediately.
The prognosis of clinical rabies is extremely poor, with nearly 100% mortality in unvaccinated individuals once symptoms develop. In contrast, individuals who receive prompt postexposure prophylaxis after exposure generally have an excellent prognosis.
Complications include encephalomyelitis, intractable seizures, Guillain-Barré syndrome, myocarditis, arrhythmias, respiratory failure, vascular collapse, and death.
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Pyelonephritis is a common infection of the upper urinary tract that causes inflammation of the renal pelvis, calyces, and renal parenchyma. It may occur as acute uncomplicated pyelonephritis, acute complicated pyelonephritis, chronic pyelonephritis, or xanthogranulomatous pyelonephritis. Chronic pyelonephritis is characterized by uneven renal scarring and chronic inflammatory changes affecting the renal interstitium and tubules.
The disease is much more common in females than males. Young women, infants, and elderly individuals are the groups most commonly affected. In the United States, more than 250,000 cases occur annually.
Risk factors include pregnancy, urinary tract obstruction caused by prostate disease or urethral narrowing, renal calculi, diabetes mellitus, and recurrent urinary tract infections. In young women, frequent sexual intercourse, spermicide use, stress incontinence, a new sexual partner, and a personal or maternal history of urinary tract infection significantly increase the likelihood of infection. Prevention focuses on prompt recognition and treatment of lower urinary tract infections and reduction of modifiable risk factors.
Most infections occur by ascending spread of organisms from the urethra to the bladder and then through the ureters to the kidneys. Less commonly, hematogenous spread occurs, particularly with gram-positive organisms or fungal infections.
The most common pathogen is Escherichia coli, responsible for approximately 80% of cases. Other important organisms include Proteus species and Klebsiella species. Less common causes include Pseudomonas aeruginosa, enterococci, and Staphylococcus saprophyticus. Isolation of Staphylococcus aureus from urine usually suggests bacteremia. Emphysematous pyelonephritis, a severe gas-forming necrotizing infection of the kidney, is commonly caused by E. coli and Klebsiella species and rarely by Candida species.
Symptoms may develop over several hours or days and commonly include fever, chills, malaise, headache, nausea, vomiting, flank pain, back pain, abdominal pain, dysuria, urgency, and hematuria. Elderly patients may have only minimal symptoms, while children often present with nonspecific findings.
Physical examination frequently demonstrates fever, tachycardia, flank tenderness, dehydration, or signs of sepsis in severe disease.
Diagnosis begins with urinalysis showing pyuria and bacteriuria, although absence of bacteria does not exclude pyelonephritis. Pretreatment urine cultures are essential. Laboratory studies may demonstrate leukocytosis with left shift, elevated inflammatory markers such as ESR and CRP, and abnormalities in renal function tests. Blood cultures may be helpful in severe infections.
Imaging is indicated in recurrent disease, atypical presentations, persistent hematuria, suspected obstruction, or failure to improve after 72 hours of treatment. Plain abdominal radiographs may identify calculi or gas formation. Ultrasonography is preferred initially in recurrent or atypical cases. Contrast-enhanced CT scanning is useful for identifying obstruction, renal or perinephric abscesses, and complicated anatomy. Repeat imaging may be required if clinical deterioration occurs despite treatment.
The differential diagnosis includes cystitis, urethritis, vaginitis, appendicitis, pelvic inflammatory disease, and renal or bladder tumors.
Treatment depends on disease severity and local antimicrobial susceptibility patterns. Outpatient treatment for uncomplicated pyelonephritis may include oral amoxicillin, amoxicillin-clavulanate, trimethoprim-sulfamethoxazole, ciprofloxacin, levofloxacin, norfloxacin, or cefpodoxime. Fluoroquinolones are commonly used because of excellent renal penetration. Therapy usually lasts 10–14 days, although short-course high-dose levofloxacin may be used for 5 days.
Hospitalized patients require intravenous antibiotics such as ciprofloxacin, levofloxacin, ceftriaxone, gentamicin, ampicillin, aztreonam, imipenem-cilastatin, ertapenem, or ticarcillin-clavulanic acid. After clinical improvement and resolution of fever, patients are transitioned to oral therapy to complete treatment.
Supportive care includes rest, analgesics, antiemetics, and adequate hydration. Intravenous fluids are essential in septic or dehydrated patients.
Consultation with a urologist is recommended when obstruction or structural abnormalities are present, since surgical correction may be necessary. Infectious disease consultation is helpful for resistant or unusual organisms such as Pseudomonas aeruginosa or extended-spectrum beta-lactamase–producing bacteria.
Surgical management may be required in emphysematous pyelonephritis, renal or perinephric abscess, renal stones, or xanthogranulomatous pyelonephritis.
Hospital admission is indicated for severe illness, dehydration, inability to tolerate oral medications, pregnancy, or concern for sepsis. Patients can generally be discharged after 24–48 hours of clinical improvement and defervescence.
Follow-up includes post-treatment urine cultures and further imaging or laboratory evaluation in patients with persistent symptoms. Patients should be advised to complete antibiotic therapy exactly as prescribed and maintain adequate hydration.
Acute uncomplicated pyelonephritis generally has an excellent prognosis, with overall in-hospital mortality below 1–2%. Complications include bacteremia, septic shock, renal abscess, perinephric abscess, and struvite stone formation, particularly in infections caused by Proteus species.
ICD-9 Codes
- 590.00 – Chronic pyelonephritis without lesion of renal medullary necrosis
- 590.10 – Acute pyelonephritis without lesion of renal medullary necrosis
- 590.80 – Pyelonephritis, unspecified
Escherichia coli and Klebsiella pneumoniae have developed significant resistance to many antibiotic classes. Extended-spectrum beta-lactamase production, often associated with quinolone resistance, presents a major therapeutic challenge. Carbapenems or fosfomycin disodium may be necessary for treatment in resistant infections. Treatment should always be guided by local susceptibility patterns of urinary pathogens. Quinolones and sulfonamides should be avoided during pregnancy and in patients with glucose-6-phosphate dehydrogenase deficiency.
Infectious Disease and Microbiology – Q Fever
Q fever is a globally distributed zoonotic infection caused by Coxiella burnetii. The disease was named “Q” for “query” because its cause was unknown when first described in 1935. It usually presents as an acute febrile illness, atypical pneumonia, or hepatitis, although chronic infection can occur, most commonly as endocarditis.
The primary reservoirs of C. burnetii are cattle, sheep, and goats, though many animals including rodents and cats may be infected. The organism is shed in milk, urine, feces, and particularly amniotic fluid of infected animals. Humans usually acquire infection by inhaling contaminated aerosols. Very few organisms are needed to cause infection, making the bacterium highly infectious. Transmission through blood transfusion is rare.
The disease is often underdiagnosed and underreported worldwide. Many infections are asymptomatic. Cases tend to occur more commonly during lambing and calving seasons, particularly between February and May in some regions. Men are affected more frequently than women.
Prevention includes avoiding unpasteurized milk, proper disposal of infected animal products, isolation of affected animals, and vaccination of high-risk workers in countries where vaccines are available, such as Australia.
Coxiella burnetii is a gram-negative intracellular coccobacillus capable of surviving within host phagolysosomes. Acute infection is characterized by antibodies directed against phase II antigens, while chronic infection is associated with elevated phase I antibody titers. Host immune response, especially T-cell–mediated immunity, plays a major role in determining disease progression.
Approximately half of infected individuals remain asymptomatic. Symptomatic acute Q fever commonly presents as a self-limited febrile illness, influenza-like syndrome, atypical pneumonia, or hepatitis. Symptoms include fever, chills, headache, sweats, nausea, vomiting, diarrhea, and malaise. Pneumonia and hepatitis frequently coexist. Severe infection during pregnancy may result in abortion or neonatal death.
Headache is the most common neurologic symptom. Rare manifestations include epididymitis, erythema nodosum, Guillain-Barré syndrome, hemolytic anemia, optic neuritis, pancreatitis, orchitis, myocarditis, pericarditis, osteomyelitis, meningoencephalitis, and prolonged fever.
Chronic Q fever most commonly manifests as endocarditis, particularly involving the aortic valve. Fever may be absent or low grade. Infection of vascular grafts, aneurysms, and prosthetic material has become increasingly recognized.
Physical examination in acute disease often reveals high fever, occasionally reaching 40°C, with relative bradycardia. Hepatomegaly and splenomegaly may occur. Rash is uncommon compared with other rickettsial diseases.
Diagnosis is primarily serologic. Indirect immunofluorescence is the preferred test. Acute infection is suggested by a fourfold rise in antibody titers between acute and convalescent samples or elevated IgM titers. PCR testing may detect bacterial DNA in blood or tissue specimens. Laboratory abnormalities may include elevated ESR and CRP, thrombocytopenia or thrombocytosis, monocytosis, elevated alkaline phosphatase, and abnormal liver function tests.
Chest imaging in Q fever pneumonia may reveal pleural effusions or infiltrates, and radiographic resolution can take several weeks. Chronic infection should be considered in cases of culture-negative endocarditis.
The differential diagnosis includes other causes of atypical pneumonia, hepatitis of unknown origin, culture-negative endocarditis, and central nervous system infections.
Early treatment improves outcomes. Acute Q fever is usually treated successfully with doxycycline 100 mg twice daily for 14 days. Chronic Q fever, especially endocarditis, is treated with prolonged doxycycline plus hydroxychloroquine therapy, often for 3–4 years or longer. Treatment duration is guided by serial antibody titers. Rifampin or fluoroquinolones may also be used in selected chronic cases.
Most acute infections resolve spontaneously, but chronic Q fever carries significant morbidity and mortality. Mortality from acute disease is approximately 2%, whereas mortality from Q fever endocarditis may reach 25–60%, with frequent relapse.
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Pyelonephritis is a common infection of the upper urinary tract that causes inflammation of the renal pelvis, calyces, and renal parenchyma. It may present as acute uncomplicated pyelonephritis, acute complicated pyelonephritis, chronic pyelonephritis, or xanthogranulomatous pyelonephritis. Chronic pyelonephritis is characterized by uneven renal scarring and chronic inflammatory changes involving the renal interstitium and tubules.
The disease is much more common in females than males. Young women, infants, and elderly individuals are the most commonly affected groups. In the United States, more than 250,000 cases occur annually.
Risk factors include pregnancy, urinary obstruction due to prostate disease or urethral narrowing, renal stones, diabetes mellitus, and recurrent lower urinary tract infections. In young women, frequent sexual intercourse, spermicide use, stress incontinence, a new sexual partner, and a personal or maternal history of urinary tract infection significantly increase risk. Prevention focuses on early diagnosis and treatment of lower urinary tract infections and reduction of modifiable risk factors such as spermicide use.
Most infections occur by ascending spread of pathogens from the urethra to the bladder and then through the ureters to the kidneys. Less commonly, hematogenous spread occurs, especially with gram-positive organisms or fungal infections.
The most common causative organism is Escherichia coli, responsible for approximately 80% of cases. Other pathogens include Proteus species and Klebsiella species. Less common causes include Pseudomonas aeruginosa, enterococci, and Staphylococcus saprophyticus. Isolation of Staphylococcus aureus from urine often suggests bacteremia. Emphysematous pyelonephritis, a severe gas-forming necrotizing infection, is commonly caused by E. coli and Klebsiella species and occasionally by Candida species.
Symptoms may develop over several hours or days. Patients commonly experience fever, chills, nausea, vomiting, malaise, headache, flank pain, back pain, abdominal pain, and symptoms of lower urinary tract infection such as dysuria, urgency, and hematuria. Elderly patients may present with few symptoms, while children often present nonspecifically.
Physical examination commonly reveals fever, tachycardia, flank tenderness, and sometimes signs of sepsis or dehydration. Toxic appearance may indicate severe infection.
Diagnosis begins with urinalysis demonstrating pyuria and bacteriuria, although absence of bacteria does not exclude pyelonephritis. Pretreatment urine cultures are essential. Laboratory studies may show leukocytosis with left shift, elevated ESR and CRP, and abnormal renal function tests. Blood cultures may be helpful in severe cases.
Imaging is reserved for atypical presentations, recurrent disease, suspected obstruction, or failure to improve within 72 hours of therapy. Plain abdominal radiographs may identify calculi or gas formation in emphysematous pyelonephritis. Ultrasonography is preferred initially for recurrent or atypical disease. Contrast-enhanced CT scanning provides better evaluation of obstruction, abscesses, or complicated anatomy. Repeat ultrasonography may be necessary if deterioration occurs despite treatment.
The differential diagnosis includes cystitis, urethritis, vaginitis, appendicitis, pelvic inflammatory disease, and tumors of the kidney or bladder.
Treatment depends on disease severity and whether the infection is complicated. Outpatient therapy for uncomplicated acute pyelonephritis may include oral amoxicillin, amoxicillin-clavulanate, trimethoprim-sulfamethoxazole, ciprofloxacin, levofloxacin, norfloxacin, or cefpodoxime. Fluoroquinolones are commonly used because of their excellent renal tissue penetration. Treatment generally lasts 10–14 days, although high-dose levofloxacin may be given for 5 days.
Hospitalized patients require intravenous therapy with agents such as ciprofloxacin, levofloxacin, ceftriaxone, gentamicin, ampicillin, aztreonam, imipenem-cilastatin, ertapenem, or ticarcillin-clavulanic acid. Once fever resolves and clinical improvement occurs, patients are transitioned to oral therapy to complete the course.
Supportive care includes rest, analgesics, antiemetics, and adequate hydration. Intravenous fluids are especially important in septic or dehydrated patients.
Consultation with a urologist is indicated when urinary obstruction or structural abnormalities are present, as surgical correction may be necessary. Infectious disease consultation is helpful for unusual or resistant organisms such as Pseudomonas aeruginosa or extended-spectrum beta-lactamase–producing bacteria.
Surgical intervention may be necessary in emphysematous pyelonephritis, renal or perinephric abscess, renal calculi, or xanthogranulomatous pyelonephritis.
Hospital admission is recommended for severe illness, high fever, significant pain, dehydration, inability to tolerate oral medications, poor compliance, or pregnancy. Patients may be discharged after 24–48 hours of clinical improvement and defervescence.
Follow-up includes post-treatment urine cultures and further imaging or laboratory testing in patients with persistent symptoms. Patients should be advised to complete prescribed antibiotic courses and maintain adequate fluid intake.
Acute uncomplicated pyelonephritis generally carries an excellent prognosis, with overall in-hospital mortality below 1–2%. Complications include bacteremia, septic shock, renal abscess, perinephric abscess, and formation of struvite stones, particularly with Proteus infections.
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Psittacosis, also called parrot fever or ornithosis, is a systemic zoonotic infection caused by Chlamydophila psittaci. It is transmitted from infected birds to humans and most often affects the lungs, producing an atypical pneumonia. Although the name comes from the Greek word for parrot, almost any bird can act as a source of infection.
The disease is uncommon in the United States, with only a small number of reported cases each year, but it is likely underdiagnosed because many infections are mild or self-limited. C. psittaci is estimated to cause a small percentage of community-acquired pneumonia cases. People at higher risk include bird owners, pet shop workers, poultry workers, veterinarians, pigeon fanciers, taxidermists, zoo workers, and people who handle birds or bird tissues.
Transmission occurs mainly through inhalation of contaminated bird secretions, dried feces, feathers, or tissues. Infected birds may appear healthy or may show signs such as ruffled feathers, respiratory symptoms, conjunctivitis, or diarrhea. Shedding increases when birds are stressed. Prevention includes proper bird quarantine, treatment of infected birds by veterinarians, protective clothing, gloves, eye protection, and fitted respirators when handling potentially infected birds or cleaning cages.
After an incubation period of about 5–21 days, psittacosis usually begins suddenly with fever, chills, headache, muscle aches, sweating, and a dry cough. Respiratory symptoms may be mild early in illness. Severe headache is common, and some patients develop confusion, agitation, lethargy, or meningoencephalitis. Gastrointestinal symptoms such as nausea, vomiting, abdominal pain, and diarrhea may occur. Rarely, psittacosis can involve the heart, kidneys, liver, eyes, joints, blood, or central nervous system. Severe cases can progress to respiratory failure, septic shock, kidney failure, liver failure, disseminated intravascular coagulation, or hemophagocytic syndrome.
On examination, patients may have fever, pharyngitis, hepatomegaly, and abnormal lung findings such as fine rales, rhonchi, egophony, or bronchial breath sounds. Neck stiffness, photophobia, altered mental status, and splenomegaly may occur in some cases.
Diagnosis can be difficult because laboratory findings are nonspecific. Testing may include complete blood count, electrolytes, kidney and liver function tests, coagulation studies, urinalysis, blood cultures, and specific testing for psittacosis. White blood cell counts may be low, normal, or elevated, and inflammatory markers may rise. Mild liver enzyme elevation is common. Diagnosis is usually made by serology, showing a fourfold rise in IgG titers between acute and convalescent samples. PCR testing of respiratory specimens may also help, although culture is rarely performed because it requires specialized facilities.
Chest radiographs are abnormal in most patients and may show interstitial infiltrates, nodules, a miliary pattern, or lobar consolidation. Radiographic findings may appear more severe than the physical examination suggests. Bronchoscopy with bronchoalveolar lavage may be useful when PCR testing is needed.
The differential diagnosis includes other causes of atypical or community-acquired pneumonia, such as Chlamydia pneumoniae, Mycoplasma pneumoniae, Coxiella burnetii, Legionella pneumophila, viral pneumonia, influenza, histoplasmosis, coccidioidomycosis, and obstructive lung cancer.
Doxycycline is the first-line treatment. Mild to moderate disease is treated with doxycycline 100 mg orally twice daily, while severe cases may require intravenous doxycycline. Tetracycline is an alternative. Symptoms and fever usually improve within 24–48 hours after treatment begins. Therapy should continue for at least 10 days and generally for 10–14 days after fever resolves. Macrolides such as azithromycin or erythromycin may be used in children, pregnancy, or patients unable to tolerate doxycycline.
Severe cases may require hospitalization, respiratory support, and intensive care. Patients with altered mental status, hypoxemia, cardiac dysfunction, or kidney impairment should be admitted. Droplet precautions and standard infection control practices should be used.
Follow-up includes completion of antimicrobial therapy and public health reporting. Health departments may investigate possible bird sources and additional cases. Patients should be educated about symptoms in birds and humans, transmission routes, and prevention strategies.
With appropriate doxycycline therapy, prognosis is usually excellent and death is rare. Complications can include fulminant multisystem disease, hepatitis, anemia, reactive arthritis, meningoencephalitis, keratoconjunctivitis, myocarditis, pericarditis, nephritis, thrombophlebitis, and pulmonary infarction.
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Members of the genus Pseudomonas are motile, gram-negative, aerobic bacteria associated with a broad range of infections. Burkholderia pseudomallei (formerly Pseudomonas pseudomallei) causes melioidosis, also known as Whitmore’s disease or Nightcliff gardener’s disease. Burkholderia mallei (formerly Pseudomonas mallei) causes glanders, a zoonotic disease primarily affecting horses, mules, and donkeys but also capable of infecting humans. Both B. pseudomallei and B. mallei are considered potential bioterrorism agents.
Pseudomonas aeruginosa is one of the leading causes of hospital-acquired urinary tract infections, pneumonia, and bacteremia. It accounts for approximately 10% of all nosocomial infections and is especially common among patients hospitalized for more than one week. Melioidosis is endemic in tropical regions, particularly Southeast Asia, while glanders remains endemic in parts of Africa, Asia, the Middle East, Central America, and South America. Person-to-person transmission of melioidosis is rare.
Risk factors for P. aeruginosa infection include disruption of normal host barriers through endotracheal intubation or urinary catheterization, immunosuppression, and prior broad-spectrum antibiotic therapy. Patients with cystic fibrosis are especially susceptible to chronic lower respiratory tract colonization and infection. P. aeruginosa is also a major cause of ventilator-associated pneumonia. Central nervous system infections are associated with neurosurgical procedures, indwelling devices, cerebrospinal fluid leaks, penetrating trauma, and bacteremia. Bone and joint infections may occur after surgery, intravenous drug use, or penetrating trauma. Malignant external otitis is a severe invasive infection seen primarily in diabetic or immunocompromised patients and may extend into the central nervous system. Ocular infections, gastrointestinal infections in neutropenic patients, and burn wound infections are also common manifestations.
Risk factors for melioidosis include diabetes mellitus, thalassemia, chronic kidney disease, and occupational or environmental exposure to contaminated soil or water. There is no available vaccine against Pseudomonas infections, and prevention mainly relies on minimizing risk factors and limiting healthcare-associated exposures.
The pathogenesis of Pseudomonas infections begins with bacterial attachment and colonization of surfaces such as catheters, respirators, and damaged tissue. This may lead to localized infection followed by hematogenous dissemination and systemic disease.
P. aeruginosa is the most important human pathogen within this group. Other clinically relevant species include Burkholderia cepacia, associated with respiratory infections in cystic fibrosis patients and various nosocomial infections; Burkholderia pickettii, implicated in hospital outbreaks; Comamonas acidovorans, a rare cause of endocarditis; Pseudomonas fluorescens, linked to contaminated blood products; Pseudomonas putida, which may cause sepsis in immunocompromised hosts; and Stenotrophomonas maltophilia, associated with pneumonia, bacteremia, endocarditis, meningitis, urinary tract infections, and wound infections.
Clinical manifestations depend on the organ system involved. In early cystic fibrosis, P. aeruginosa causes recurrent upper respiratory symptoms, while advanced disease leads to chronic productive cough, recurrent pneumonia, respiratory compromise, weakness, and weight loss. Corneal ulcers due to P. aeruginosa may progress rapidly and threaten vision. Malignant external otitis presents with severe otalgia and otorrhea, and physical examination typically reveals erythema, swelling, purulent discharge, granulation tissue, and debris in the external auditory canal.
Characteristic skin lesions known as ecthyma gangrenosum may occur in P. aeruginosa bacteremia. These lesions begin as hemorrhagic vesicles with surrounding erythema and progress to central necrosis and ulceration. Exposure to contaminated hot tubs or pools may result in diffuse pruritic maculopapular or vesiculopustular eruptions. Osteomyelitis of the foot often follows penetrating injury, while sternoclavicular septic arthritis is associated with intravenous drug use.
Melioidosis most commonly involves the lungs and presents with fever, productive cough, and tachypnea. It may also produce acute or chronic suppurative infections of the skin and internal organs. Glanders may manifest as chronic suppurative abscesses, mucopurulent infection of mucous membranes with granulomatous ulcers, or systemic disease with fever, pleuritic chest pain, diarrhea, headache, and myalgia. Lymphadenopathy and splenomegaly may also occur.
Diagnosis requires appropriate cultures from blood, urine, sputum, bronchoalveolar lavage fluid, wounds, or other affected sites, followed by antimicrobial susceptibility testing. Imaging studies depend on the site of infection. In malignant external otitis, CT and MRI often demonstrate bony erosion and new bone formation. Melioidosis may produce upper lobe infiltrates or thin-walled cavities resembling tuberculosis on chest imaging. MRI is useful in suspected osteomyelitis, while echocardiography is indicated when endocarditis is suspected in bacteremic patients. Bronchoalveolar lavage or endotracheal aspirates are useful for confirming respiratory infections in intubated patients.
Differential diagnosis varies according to the clinical presentation. In cases of pneumonia, alternatives include bacterial pneumonias, viral infections, and Pneumocystis jiroveci pneumonia.
Most P. aeruginosa infections are treated with one or two antibiotics to which the organism is susceptible. Common antipseudomonal agents include aminoglycosides, carbapenems, extended-spectrum penicillins such as piperacillin, third-generation cephalosporins such as ceftazidime, fluoroquinolones such as ciprofloxacin, and monobactams. Increasing resistance to ciprofloxacin necessitates caution when selecting empiric therapy.
Bacteremia is commonly treated with agents such as ceftazidime, cefepime, meropenem, imipenem-cilastatin, piperacillin-tazobactam, or aztreonam in beta-lactam-allergic patients. Addition of an aminoglycoside may be appropriate in settings with high resistance rates. Pneumonia is managed similarly, though inhaled tobramycin may also be used. Osteomyelitis requires prolonged high-dose antipseudomonal beta-lactam or fluoroquinolone therapy, often combined with surgical intervention. Central nervous system infections are treated primarily with ceftazidime, cefepime, or meropenem, while imipenem is generally avoided because of neurotoxicity and rapid resistance development.
Ocular infections require topical, subconjunctival, intravitreal, and sometimes systemic antibiotics depending on severity. Malignant external otitis is treated with beta-lactam antibiotics or ciprofloxacin, although relapse may occur even after prolonged therapy. Urinary tract infections are managed with antipseudomonal beta-lactams, fluoroquinolones, or aminoglycosides. Burn wound infections often require topical therapy and careful antibiotic selection because resistance can develop rapidly.
Treatment of melioidosis depends on disease severity and often requires prolonged therapy. Glanders is initially treated with agents such as imipenem, ceftazidime, or meropenem combined with ciprofloxacin and doxycycline, followed by extended oral therapy to reduce relapse risk.
Surgical intervention is frequently necessary in osteomyelitis and may be required in malignant otitis externa for debridement. Infectious disease consultation is strongly recommended, particularly in cases of melioidosis or glanders.
Close follow-up is essential because of the risk of relapse and emergence of multidrug-resistant organisms. Resistance mechanisms include chromosomal beta-lactamases and extended-spectrum beta-lactamases. Prognosis depends on the site of infection, severity of illness, host immune status, and timeliness of therapy. Complications include septic shock, respiratory failure, metastatic infection, brain abscesses, septic emboli, cranial nerve involvement, meningitis, and death.
