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Infectious Disease and Microbiology
Kawasaki syndrome (Kawasaki disease, KD)
Kawasaki syndrome is an acute, self-limited systemic vasculitis that primarily affects young children, especially those under 5 years of age. It is also known as mucocutaneous lymph node syndrome. Although the disease often resolves on its own, it is clinically significant because it can lead to serious cardiovascular complications, particularly coronary artery aneurysms.
The disease occurs worldwide but is most common in Japan, with most cases seen in children younger than 5 years. It can occur throughout the year, with peaks during winter and spring. Risk factors include recent respiratory infections and environmental exposures such as dust and mites. Genetic susceptibility also plays a role, with involvement of pathways such as caspase-3 and TGF-beta.
Kawasaki syndrome involves inflammation of medium and small blood vessels. In the early stage, there is endothelial swelling and inflammation, which later progresses to widespread systemic inflammation affecting multiple organs, especially the heart. Although the exact cause remains unknown, the condition is believed to be triggered by an infectious agent, possibly through a superantigen-mediated immune response.
Clinically, the diagnosis is based on the presence of fever lasting at least five days along with characteristic features. These include a polymorphous rash, bilateral non-purulent conjunctivitis, oral changes such as cracked lips and strawberry tongue, swelling and redness of the hands and feet followed by peeling, and cervical lymphadenopathy. Incomplete forms of the disease may occur and should still be treated if suspected. Other symptoms may include irritability, joint pain, myocarditis, pericarditis, aseptic meningitis, and gastrointestinal symptoms.
Laboratory findings commonly show anemia, leukocytosis, and thrombocytosis, particularly in later stages. Inflammatory markers such as ESR and CRP are elevated, and hypoalbuminemia and elevated liver enzymes may also be present. Echocardiography is essential to evaluate for coronary artery involvement, while ECG may reveal arrhythmias or other cardiac changes.
Management should be initiated promptly to reduce the risk of complications. The mainstay of treatment is intravenous immunoglobulin (IVIG), given as a single high-dose infusion, with a repeat dose if fever persists. Aspirin is also used, initially at high doses for its anti-inflammatory effect and later at lower doses for its antiplatelet properties. In resistant cases, corticosteroids or agents such as infliximab may be used. Patients with coronary complications may require anticoagulation and specialist cardiac care.
The prognosis is generally good when treated early. Without treatment, a significant proportion of patients develop coronary artery aneurysms, but this risk is markedly reduced with timely therapy. Long-term follow-up with echocardiography is important, especially in those with cardiac involvement.
Complications are mainly cardiovascular and include coronary artery aneurysms, myocardial infarction, myocarditis, and pericarditis, with myocardial infarction being the most common cause of death. Non-cardiac complications may include hearing loss, arthritis, pneumonitis, and macrophage activation syndrome.
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Infectious Disease and Microbiology - Leprosy
Leprosy is a chronic infectious disease caused by Mycobacterium leprae, an acid-fast, slow-growing intracellular organism that primarily affects the skin and peripheral nerves. The disease has a long incubation period, typically ranging from 5 to 7 years, and is transmitted mainly through prolonged close contact, likely via respiratory droplets or direct contact with untreated skin lesions. The organism has a predilection for cooler areas of the body, particularly the skin and peripheral nerves, where it infects Schwann cells and leads to nerve damage.
Leprosy remains a global health concern, although its prevalence has significantly declined over recent decades due to effective multidrug therapy. It is most common in endemic regions such as Brazil, India, Indonesia, and parts of Africa and Southeast Asia. Risk factors include close household contact with infected individuals, extremes of age (children and older adults), and impaired cell-mediated immunity. Genetic susceptibility also plays a role, influencing disease type and severity.
The clinical presentation varies widely depending on the host immune response. Patients typically present with hypopigmented or erythematous skin lesions accompanied by sensory loss, which is a hallmark feature. In tuberculoid disease, lesions are few, well-defined, and associated with localized nerve involvement. In contrast, lepromatous disease is characterized by numerous lesions, nodules, and diffuse skin involvement, often with more extensive nerve damage. Advanced cases may lead to deformities such as loss of eyebrows, hoarseness, and the classic saddle-nose deformity due to cartilage destruction.
Diagnosis is primarily clinical, based on the presence of characteristic skin lesions with sensory loss and thickened peripheral nerves. Skin smears or biopsies may be used to confirm the diagnosis, showing either granulomatous inflammation with few organisms in tuberculoid disease or numerous bacilli in lepromatous disease. The disease is also classified by the World Health Organization into paucibacillary and multibacillary forms based on lesion number and bacterial load.
Treatment involves prolonged multidrug therapy to prevent resistance and ensure cure. Multibacillary disease is treated with a combination of dapsone, rifampin, and clofazimine for an extended duration, while paucibacillary disease requires a shorter regimen with fewer drugs. Alternative agents such as fluoroquinolones, macrolides, and tetracyclines may be used in certain cases. Close monitoring is essential during therapy due to potential drug side effects and immune-mediated reactions.
The prognosis is excellent with appropriate treatment, but complications can arise, particularly involving the immune system. Type I (reversal) reactions involve worsening inflammation and nerve damage, while Type II reactions, known as erythema nodosum leprosum, present with systemic symptoms such as fever and painful nodules. Long-term complications include permanent nerve damage, disability, and deformities if untreated. Early diagnosis and adherence to therapy are crucial in preventing these outcomes.
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Infectious Disease and Microbiology - Leishmaniasis
Leishmaniasis is a parasitic disease caused by protozoa of the genus Leishmania and transmitted through the bite of infected sandflies. It presents in three main clinical forms: cutaneous, mucosal, and visceral, with manifestations depending largely on the host immune response and the infecting species. The disease is widespread, with millions of cases globally and hundreds of millions of people at risk, particularly in tropical and subtropical regions.
Transmission occurs when infected sandflies inoculate promastigotes into the skin. These are taken up by macrophages, where they transform into amastigotes and multiply intracellularly. The parasites preferentially infect cells of the reticuloendothelial system. Disease severity is influenced by parasite burden, species type, and the host’s immune status. Immunocompromised individuals, especially those with HIV, are at increased risk of severe disease.
Cutaneous leishmaniasis typically begins as a papule at the site of the bite, which gradually enlarges, crusts, and ulcerates. The ulcer is usually painless, with raised borders and a granulating base, and may persist for months or even years. Mucosal leishmaniasis, most commonly associated with Leishmania braziliensis, affects the mucous membranes of the nose, mouth, and throat, potentially causing destructive lesions such as nasal septum perforation and voice changes.
Visceral leishmaniasis, also known as kala-azar, is the most severe form and is commonly caused by Leishmania donovani and Leishmania infantum. It presents with prolonged fever, weight loss, hepatosplenomegaly, anemia, and pancytopenia. Without treatment, it carries a high mortality rate. In advanced cases, patients may develop cachexia, edema, and profound immune dysfunction.
Diagnosis is confirmed by demonstrating the parasite in tissue samples such as bone marrow, spleen, liver, or skin lesions. Bone marrow aspiration is commonly used for visceral disease. PCR and serologic tests can support the diagnosis, particularly in visceral leishmaniasis, while skin tests are more useful in epidemiologic studies or cutaneous forms.
Treatment depends on the form and severity of disease. Liposomal amphotericin B is the treatment of choice for visceral leishmaniasis. Other agents include pentavalent antimonials, pentamidine, and newer oral therapies such as miltefosine. Many cases of cutaneous leishmaniasis resolve spontaneously, although treatment may be required for cosmetic reasons or severe disease. Mucosal disease requires systemic therapy due to its destructive nature.
The prognosis varies by form. Cutaneous disease generally has a good outcome, although scarring may occur. Visceral leishmaniasis is life-threatening if untreated but responds well to appropriate therapy. Mucosal disease can lead to significant morbidity and, in some cases, mortality. Complications include relapse, particularly in immunocompromised patients, and adverse effects from treatment such as toxicity from antimonial drugs.
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Infectious Disease and Microbiology - Legionnaires disease
Legionnaires’ disease is a form of pneumonia caused by gram-negative bacteria of the Legionellaceae family, most notably Legionella pneumophila. It was first identified in 1976 following an outbreak among attendees of an American Legion convention. A milder, non-pneumonic illness caused by the same organism is known as Pontiac fever. Together, these conditions are referred to as legionellosis.
The disease is relatively common among atypical pneumonias, accounting for a proportion of community-acquired pneumonia cases requiring hospitalization. It is associated with outbreaks linked to contaminated water systems such as cooling towers, air conditioning units, spas, and fountains. Cases occur more frequently in warmer months when such systems are widely used. Risk factors include older age, smoking, chronic lung disease, immunosuppression, and recent exposure to contaminated water sources or travel.
Legionella organisms are aerobic, intracellular bacteria that thrive in aquatic environments. They can proliferate in man-made water systems and are transmitted primarily through inhalation of aerosolized contaminated water. Once inhaled, the bacteria infect alveolar macrophages, where they replicate intracellularly. The immune response involves activation of T cells, which enhance macrophage-mediated killing.
Clinically, Legionnaires’ disease presents with high fever, malaise, myalgias, and headache, followed by respiratory symptoms such as cough, which may become productive, and chest pain. Gastrointestinal symptoms, including diarrhea and vomiting, are common and can help distinguish it from other pneumonias. Neurological symptoms such as confusion or encephalopathy may occur in severe cases. The incubation period is typically 2 to 10 days. In contrast, Pontiac fever presents as a self-limited febrile illness without pneumonia.
On physical examination, patients may have fever, tachypnea, and signs of lung consolidation such as rales. Relative bradycardia, hypotension, and altered mental status may also be present. Laboratory findings often include hyponatremia, elevated liver enzymes, and inflammatory markers. Diagnosis is supported by detection of Legionella antigen in urine, which is particularly useful early in the disease but mainly detects serogroup 1. Culture on specialized media and PCR testing may also be used.
Chest imaging typically shows patchy or lobar infiltrates, often involving the lower lobes, and pleural effusions may be present. Radiographic resolution can be slow and may lag behind clinical improvement.
Treatment involves prompt initiation of appropriate antibiotics. First-line therapy includes macrolides such as azithromycin or fluoroquinolones, with the latter preferred in severe cases. Intravenous therapy is used initially in hospitalized patients, followed by oral therapy once clinical improvement occurs. Treatment duration is generally 10–14 days, but longer courses may be required in immunocompromised individuals.
The prognosis depends on the patient’s overall health and comorbidities, with mortality rates ranging from 5% to 30%. Complications may include respiratory failure, multiorgan dysfunction, and extrapulmonary involvement such as myocarditis or renal failure. Early recognition and treatment are critical to improving outcomes.
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Infectious Disease and Microbiology - Laryngitis/Laryngotracheobronchitis (Croup)
Laryngitis refers to inflammation of the laryngeal mucosa, while laryngotracheobronchitis, commonly known as croup, involves inflammation of the subglottic airway, trachea, and bronchi. These conditions are most often caused by viral infections and typically present as part of an upper respiratory tract illness. Croup is particularly common in young children, especially between 3 months and 3 years of age, and tends to occur more frequently in boys.
The epidemiology reflects seasonal viral patterns. Laryngitis commonly occurs during winter in association with respiratory infections. Croup is most frequently caused by Parainfluenza virus type 1, especially in the fall, while Influenza virus and Respiratory syncytial virus contribute during winter and early spring. Other pathogens such as adenovirus, rhinovirus, enterovirus, and Mycoplasma pneumoniae may also be involved.
Risk factors for laryngitis include smoking, alcohol use, immunosuppression, and close contact with infected individuals. In croup, young age and possible variations in immune response play a major role. Prevention is mainly through avoidance of infected individuals and proper hand hygiene.
The underlying pathophysiology involves viral infection leading to inflammation, edema, and narrowing of the airway. In croup, subglottic swelling leads to airway obstruction, which is more pronounced in children due to their smaller airway diameter. This results in the characteristic stridor and respiratory distress.
Clinically, laryngitis presents with hoarseness, reduced voice pitch, and sometimes aphonia. In severe cases, airway obstruction may lead to stridor. Croup typically begins with fever followed by hoarseness and a distinctive “barking” cough. Inspiratory stridor, tachypnea, and chest wall retractions are common findings. In more severe cases, both inspiratory and expiratory stridor, wheezing, and signs of respiratory distress such as tachycardia and fatigue may develop.
Diagnosis is primarily clinical. Laboratory findings are usually normal, although hypoxemia may occur in severe cases. Imaging is not routinely required but may support the diagnosis. A classic anterior–posterior neck x-ray in croup shows subglottic narrowing known as the “steeple sign.”
Management depends on severity. Mild laryngitis is usually treated with supportive care such as humidified air, and medications are not required unless bacterial infection is suspected. In croup, corticosteroids such as dexamethasone are the mainstay of treatment and significantly improve symptoms. Nebulized epinephrine may be used in moderate to severe cases for temporary relief of airway obstruction, but patients require observation due to possible rebound symptoms. Supplemental oxygen is used in cases of hypoxemia, and severe cases may require intubation and mechanical ventilation.
The overall prognosis is excellent, with most cases resolving within a few days, although cough may persist longer. Complications are uncommon but may include airway obstruction and respiratory failure in severe croup. Rare complications include pneumothorax, pulmonary edema, and secondary infections. Long-term effects such as airway hyperreactivity or subglottic stenosis may occur in severe or recurrent cases.
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Infectious Disease and Microbiology - Larva migrans syndromes
Larva migrans syndromes represent a group of conditions caused by the migration of helminth larvae through human tissues, affecting the skin, internal organs, or eyes. These syndromes include cutaneous, visceral, and ocular forms, depending on where the larvae migrate. Humans are accidental hosts, and the parasites are unable to complete their life cycle, leading instead to tissue inflammation and damage.
The condition is seen worldwide but is more common in tropical and subtropical regions. Infections are particularly frequent in children, especially those under 6 years old. Cutaneous larva migrans is the most common tropical dermatosis, often acquired from contaminated beaches or soil. Visceral and ocular forms are most commonly caused by Toxocara canis and, less frequently, Toxocara cati, with a significant proportion of the population showing evidence of past infection.
Risk factors include contact with soil contaminated by dog or cat feces, poor hand hygiene, and geophagia. Children who play in contaminated environments are particularly at risk. Prevention focuses on avoiding direct contact with contaminated soil, wearing protective footwear, maintaining good hygiene, and regular deworming of pets.
The pathophysiology varies by form. In visceral larva migrans, eggs are ingested and hatch in the intestine, after which larvae migrate via the bloodstream to organs such as the liver, lungs, and central nervous system. These larvae may persist for years, causing chronic inflammation. In cutaneous larva migrans, larvae penetrate the skin but remain confined to the epidermis, migrating and forming characteristic tracks.
Cutaneous larva migrans, commonly caused by Ancylostoma braziliense, presents with intensely itchy, serpiginous, erythematous skin lesions that slowly advance over time. These lesions are most often found on the feet, legs, or areas exposed to contaminated ground. Visceral larva migrans may present with fever, fatigue, abdominal pain, cough, and hepatomegaly, while ocular larva migrans may cause visual disturbances, floaters, or even unilateral blindness due to retinal inflammation.
Physical examination findings vary with the syndrome. Cutaneous disease shows a creeping eruption on the skin, while visceral disease may show hepatomegaly, wheezing, or lymphadenopathy. Ocular disease may reveal retinal granulomas, uveitis, or optic nerve involvement on funduscopic examination.
Laboratory findings in visceral disease often include marked eosinophilia, leukocytosis, and elevated IgE levels. Serologic testing such as ELISA can support the diagnosis. Imaging studies may reveal hepatic or pulmonary lesions, while ocular disease is diagnosed primarily through ophthalmologic examination. Larvae are rarely identified directly in tissue samples.
Treatment depends on the clinical form. Cutaneous larva migrans is treated with antiparasitic agents such as albendazole or ivermectin, and symptoms usually resolve as the larvae die. Visceral larva migrans may not require treatment in mild cases, but severe disease is managed with albendazole or mebendazole. Ocular disease may also require antiparasitic therapy, often combined with corticosteroids to reduce inflammation, although treatment must be carefully managed to avoid worsening ocular damage.
Prognosis is generally good for cutaneous and most visceral cases, with spontaneous resolution common. However, ocular larva migrans carries a risk of permanent vision loss. Complications may include secondary bacterial infection in cutaneous disease, and in severe visceral cases, involvement of the brain, heart, or lungs.
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Infectious Disease and Microbiology: Intraabdominal Abscess
An intraabdominal abscess is a localized collection of microorganisms, inflammatory cells, and pus enclosed within a fibrous capsule in the abdominal cavity. These abscesses may form within the peritoneal cavity, inside abdominal organs such as the liver or spleen, or in retroperitoneal spaces. They can also extend into adjacent areas like the pelvis or psoas muscle. Based on location, intraabdominal abscesses are classified as intraperitoneal, visceral, or retroperitoneal.
Epidemiologically, intraabdominal abscesses are more common in men and typically occur between the third and fifth decades of life. Most abscesses are located in intraperitoneal or retroperitoneal spaces rather than within organs. Common causes vary by age group and condition; for example, appendicitis is a major cause in children, while postoperative complications are more common in adults. Patients with diabetes, immunosuppression, malignancy, or conditions like pancreatitis are at increased risk. Certain infections, including fungal infections such as Candida, may occur more frequently in immunocompromised individuals.
The pathophysiology usually involves the دخول of enteric organisms into the peritoneal cavity through disruption of the gastrointestinal tract, such as perforation, inflammation, trauma, or surgery. This leads to localized infection, inflammation, and abscess formation. Both aerobic and anaerobic bacteria often act synergistically. Common causative organisms include Bacteroides fragilis, Enterobacteriaceae (such as Escherichia coli), streptococci, enterococci, and sometimes fungi like Candida. The exact pathogens depend on the source and location of the infection.
Clinically, patients often present with nonspecific symptoms such as fever, abdominal pain, nausea, vomiting, malaise, and sometimes signs of sepsis. The presentation varies depending on the location of the abscess. Liver abscesses may cause right upper quadrant pain and systemic symptoms, while splenic abscesses may present with left upper quadrant pain. Perinephric abscesses often cause flank pain that may radiate to the groin. In elderly patients, fever of unknown origin may be the only presenting sign, making diagnosis challenging.
Diagnosis relies on a high index of suspicion and appropriate investigations. Laboratory findings may include leukocytosis, abnormal liver function tests, anemia, and sometimes bacteremia. Imaging plays a crucial role, with computed tomography (CT) scan being the most sensitive and widely used modality. Ultrasound is also useful, especially for liver and kidney abscesses. Definitive diagnosis is often achieved by aspiration of abscess contents for microbiological analysis, which helps guide targeted antimicrobial therapy.
Management of intraabdominal abscesses involves three key components: control of the source of infection, administration of appropriate antimicrobial therapy, and drainage of the abscess. Broad-spectrum antibiotics are initiated empirically and later tailored based on culture results. Common regimens include combinations that cover both aerobic and anaerobic organisms, such as cephalosporins with metronidazole, carbapenems, or beta-lactam/beta-lactamase inhibitor combinations. Antifungal therapy is indicated when fungal pathogens are identified.
Drainage of the abscess is essential and can be achieved either percutaneously under imaging guidance or surgically. Percutaneous drainage is preferred when feasible, but surgical intervention is required in cases where drainage is not possible, the abscess is multiloculated, or there is failure to respond to conservative treatment. Some cases, such as small or specific types of abscesses, may be managed medically under close monitoring.
Patients with severe infection may require hospitalization, fluid resuscitation, and intensive care support if septic shock develops. Ongoing care includes close monitoring, follow-up imaging, and addressing underlying conditions such as biliary disease, malignancy, or urinary tract abnormalities. Preventive strategies focus on early diagnosis and management of intraabdominal infections and prompt treatment of conditions like appendicitis or diverticulitis.
The prognosis depends on early recognition and effective management. Mortality rates remain significant, particularly for splenic and hepatic abscesses, especially if diagnosis is delayed. Prompt treatment with antibiotics and adequate drainage significantly improves outcomes.
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Infectious Disease and Microbiology: Influenza
Influenza is an acute viral respiratory infection caused by influenza viruses, typically presenting as a self-limited illness but capable of causing severe or life-threatening complications in vulnerable populations. While most healthy individuals recover fully, high-risk groups—including the elderly, young children, pregnant women, and those with chronic medical conditions—are more likely to develop complications such as pneumonia, respiratory failure, or death.
Influenza is highly prevalent worldwide, affecting approximately 5–20% of the population annually. Seasonal outbreaks occur predominantly during the winter months, often referred to as “flu season.” In the United States, influenza is responsible for tens of thousands of deaths and hundreds of thousands of hospitalizations each year. Occasionally, pandemics arise when new subtypes of influenza A viruses emerge, often due to major genetic changes, allowing rapid global spread with little preexisting immunity in the population.
Transmission occurs through respiratory droplets, direct contact with infected individuals, or contaminated surfaces. Viral shedding begins early—often within the first day of infection—and continues for about 5–10 days, though children may shed the virus longer. Preventive measures include good hand hygiene, respiratory etiquette, and especially annual vaccination. Vaccination is recommended for all individuals older than 6 months, with particular emphasis on high-risk groups. Two main vaccine types are available: inactivated vaccines given intramuscularly and live attenuated vaccines administered intranasally.
Influenza viruses are RNA viruses belonging to the Orthomyxoviridae family and are classified into types A, B, and C. Types A and B are responsible for most seasonal epidemics, while type C typically causes mild disease. Influenza A viruses are further subtyped based on hemagglutinin (HA) and neuraminidase (NA) surface proteins. Antigenic drift (small mutations) leads to seasonal variation, whereas antigenic shift (major genetic reassortment) can result in pandemics. The virus infects respiratory epithelial cells, and symptoms are largely due to the host immune response, including the release of proinflammatory cytokines, which may lead to severe complications such as cytokine storm and multiorgan failure.
Clinically, influenza is characterized by abrupt onset of fever, cough, nasal congestion, myalgia, headache, and malaise. The sudden onset of fever and cough during influenza season is highly suggestive of the disease. In some cases, especially in high-risk individuals, complications such as bacterial pneumonia may develop several days after initial symptoms, often indicated by recurrence of fever and worsening respiratory symptoms. Severe cases may involve exacerbation of underlying conditions like asthma or heart failure, as well as rare complications such as encephalitis, myocarditis, rhabdomyolysis, or shock.
Diagnosis is confirmed through laboratory testing of respiratory specimens. Reverse transcription polymerase chain reaction (RT-PCR) is the most sensitive and specific test and provides rapid results. Rapid antigen tests are also available but are less sensitive, especially in adults. Imaging such as chest X-ray may be necessary in severe cases to assess for pneumonia or other complications.
Treatment includes antiviral medications and supportive care. Neuraminidase inhibitors such as Oseltamivir and Zanamivir are effective against both influenza A and B and are most beneficial when started within 48 hours of symptom onset. They are especially recommended for high-risk patients or those with severe disease. Older drugs such as amantadine and rimantadine are less commonly used due to resistance. Supportive care includes rest, hydration, and management of symptoms.
In hospitalized patients, severe influenza may require intensive care support, including oxygen therapy, mechanical ventilation, or extracorporeal membrane oxygenation in cases of respiratory failure. Early antiviral treatment is recommended for hospitalized patients regardless of the duration of symptoms.
The prognosis for most individuals is good, with complete recovery expected. However, influenza can lead to serious complications, particularly in high-risk groups. These include bacterial pneumonia (commonly due to Streptococcus pneumoniae), acute respiratory distress syndrome (ARDS), myocarditis, and neurologic complications such as encephalopathy or Guillain–Barré syndrome. Vaccination and early treatment remain key strategies in reducing morbidity and mortality associated with influenza.
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Infectious Disease and Microbiology: Infectious Mononucleosis
Infectious mononucleosis (IM), also known as glandular fever, is a common self-limiting clinical syndrome caused primarily by Epstein–Barr virus. It is characterized by acute onset of fever, sore throat, lymphadenopathy, and atypical lymphocytosis. EBV is transmitted mainly through saliva, which is why the illness is often called the “kissing disease.” After infection, the virus persists lifelong in the host.
IM is common worldwide. In industrialized countries, EBV infection often occurs either in early childhood, when it is usually asymptomatic, or in late adolescence, when it is more likely to cause symptomatic mononucleosis. By adulthood, 90–95% of people have evidence of prior EBV infection. Risk factors include close contact with an infected person and immunosuppression, especially in transplant recipients. In rare cases, certain inherited immune defects can lead to severe, even life-threatening EBV infection.
The pathophysiology begins when EBV infects the oropharyngeal epithelium and then B lymphocytes. The immune response, especially proliferation of cytotoxic CD8+ T lymphocytes, is responsible for much of the clinical syndrome. These activated lymphocytes appear as atypical lymphocytes on the blood smear. Although the immune response controls the primary infection, EBV remains latent for life.
Clinically, young children are often asymptomatic or have only mild illness. In adolescents and young adults, the disease usually begins with fatigue, malaise, and myalgias, followed by fever and sore throat. Common symptoms include fever, sore throat, malaise, headache, anorexia, myalgias, and sometimes abdominal pain, nausea, or vomiting. On examination, patients commonly have cervical lymphadenopathy, pharyngitis or tonsillitis, splenomegaly, and sometimes hepatomegaly. Less common findings include palatal petechiae, periorbital edema, rash, and jaundice. A maculopapular rash may occur, especially after exposure to ampicillin or amoxicillin.
Diagnosis is usually supported by laboratory findings. Atypical lymphocytosis and relative or absolute lymphocytosis are common. Mild thrombocytopenia and elevated liver enzymes may also be present. Heterophile antibody tests such as the Monospot are widely used and are fairly sensitive and specific in symptomatic patients, although they may be negative early in illness or in young children. EBV-specific serology, including viral capsid antigen and EBV nuclear antigen antibodies, can help confirm the diagnosis when needed. Ultrasound may be used to assess splenomegaly, especially in athletes.
Treatment is mainly supportive. Most patients only need rest, fluids, and symptom relief with acetaminophen or nonsteroidal anti-inflammatory drugs. Corticosteroids are reserved for severe complications such as impending airway obstruction, severe thrombocytopenia, hemolytic anemia, myocarditis, pericarditis, or neurologic complications. Patients should avoid contact sports and strenuous physical activity for at least 3–4 weeks, or longer if splenomegaly persists, because of the risk of splenic rupture. Beta-lactam antibiotics such as ampicillin and amoxicillin should be avoided unless clearly indicated for another reason.
The prognosis is generally excellent, and most cases resolve within 1–2 weeks. However, fatigue may persist for weeks or even months in some patients. Complications are uncommon but may include autoimmune hemolytic anemia, thrombocytopenia, airway obstruction, hepatitis, myocarditis, pericarditis, neurologic syndromes, pneumonia, splenic rupture, and lymphoproliferative disorders in susceptible individuals.
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Infectious Disease and Microbiology: HIV Infection
Human immunodeficiency virus (HIV) infection is a chronic viral disease that progressively impairs the immune system, primarily through destruction and dysfunction of CD4+ T lymphocytes. Without treatment, it can lead to acquired immunodeficiency syndrome (AIDS), the advanced stage of infection characterized by severe immunosuppression, opportunistic infections, malignancies, and death. HIV-1 is the predominant type worldwide, while HIV-2 is found mainly in West Africa and generally causes slower disease progression.
HIV remains a major global health problem, affecting millions of individuals worldwide. In the United States alone, more than one million people are living with HIV, with tens of thousands of new infections occurring annually. Transmission occurs through sexual contact, blood exposure such as needle-sharing or occupational exposure, and mother-to-child transmission during pregnancy, delivery, or breastfeeding. The risk of transmission varies by route, with blood exposure and receptive anal intercourse carrying higher risks than other exposures. Advances in antiretroviral therapy (ART) and perinatal management have markedly reduced maternal–fetal transmission.
The virus is a retrovirus of the lentivirus family. It binds to CD4 receptors and co-receptors on host lymphocytes, enters the cell, and uses reverse transcriptase to convert viral RNA into DNA. This viral DNA integrates into the host genome, allowing lifelong infection. Subsequent activation of infected cells leads to production of new viral particles, which destroy CD4 cells and gradually weaken cellular immunity. This immune dysfunction predisposes patients to a wide range of infectious and noninfectious complications.
Clinically, HIV infection progresses through several stages. Acute HIV infection may occur within weeks of transmission and often presents with a nonspecific viral syndrome including fever, pharyngitis, rash, myalgias, lymphadenopathy, diarrhea, and headache. This is followed by an asymptomatic phase that may last many years, during which viral replication continues and CD4 counts slowly decline. Symptomatic HIV infection develops as immunosuppression worsens and may include recurrent mucocutaneous infections, weight loss, fevers, and eventually opportunistic infections such as Pneumocystis jirovecii pneumonia, cryptococcal meningitis, toxoplasmosis, cytomegalovirus disease, and Mycobacterium avium complex infection. HIV is also associated with malignancies such as Kaposi sarcoma, lymphoma, cervical cancer, and neurologic complications including HIV-associated neurocognitive disorder.
Diagnosis begins with screening using highly sensitive HIV antibody tests, followed by confirmatory testing. In suspected acute HIV infection, HIV RNA testing is essential because antibody tests may still be negative during early infection. Once diagnosis is confirmed, baseline evaluation includes CD4 count, HIV viral load, resistance genotype, complete blood count, renal and liver function tests, and screening for co-infections such as hepatitis A, B, and C, syphilis, tuberculosis, toxoplasmosis, cytomegalovirus, and varicella zoster. These tests help assess disease stage, identify treatment needs, and detect concurrent infections.
Treatment with antiretroviral therapy is the cornerstone of HIV management. The goals of ART are to suppress plasma HIV RNA to undetectable levels, preserve or restore immune function, reduce HIV-related complications, and prevent transmission. Standard treatment consists of combination therapy using multiple drug classes, commonly two nucleos(t)ide reverse transcriptase inhibitors together with either a non-nucleoside reverse transcriptase inhibitor, a protease inhibitor, or an integrase strand transfer inhibitor. Choice of regimen depends on drug resistance, side effects, pill burden, co-morbidities, pregnancy considerations, and potential drug interactions. ART is generally lifelong, and adherence is critical to prevent virologic failure and resistance.
Prevention of HIV includes condom use, safe blood practices, clean needle access, screening of blood products, and routine testing, especially in pregnancy and high-risk populations. Post-exposure prophylaxis should be started as soon as possible after significant occupational or non-occupational exposure, ideally within hours and no later than 72 hours, and continued for four weeks. Pre-exposure prophylaxis has also become an important preventive strategy for individuals at substantial risk.
Ongoing care requires regular monitoring of viral load, CD4 count, medication toxicity, cardiovascular risk factors, and co-infections. Patients with advanced immunosuppression require prophylaxis against opportunistic infections, such as trimethoprim-sulfamethoxazole for Pneumocystis and toxoplasmosis, and azithromycin for Mycobacterium avium complex when indicated. Vaccination, cancer screening, and management of long-term complications are also essential parts of care.
The prognosis of HIV infection has improved dramatically with effective ART. Many patients who are diagnosed early and remain adherent to treatment can achieve near-normal life expectancy. However, treatment failure may occur due to poor adherence or drug resistance, leading to virologic, immunologic, and clinical decline. Without treatment, HIV infection remains a progressive and often fatal disease.
