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Infectious Disease and Microbiology – Botulism
Botulism is a potentially life-threatening neuroparalytic syndrome caused by neurotoxins produced by Clostridium botulinum. Botulinum neurotoxin (BoNT) is among the most potent toxins known. There are five epidemiologic forms of botulism: foodborne, infant botulism, wound botulism, intestinal colonization (adult infectious botulism), and inhalational botulism. Symptoms typically develop 12–36 hours after ingestion of preformed toxin.
Botulism is rare but can occur in small outbreaks, often associated with commercially or home-canned foods. In the United States, most cases occur in infants, approximately one-fourth are foodborne, and a smaller number are related to wounds. Risk factors include improper home canning of low-acid foods such as corn, asparagus, beans, and beets. The fatality rate is higher among patients older than 60 years. Honey ingestion is a well-established risk factor for infant botulism due to gastrointestinal colonization and in situ toxin production. Wound botulism should be suspected in intravenous drug users. Iatrogenic cases have been reported following injection of unlicensed botulinum toxin preparations.
Prevention focuses on proper food preservation techniques. Home-canned foods should be boiled for at least 10 minutes before consumption. Infants under one year of age should not be given honey. Bulging cans should be discarded. Rapid identification of suspected cases is essential to prevent outbreaks.
C. botulinum is an anaerobic, gram-positive, spore-forming rod. It produces toxins classified from types A to G, based on antigenic differences. Human disease is most commonly associated with toxin types A, B, E, and F. Type A is frequently found in the western United States and China, type B in the eastern United States and Europe, and type F worldwide, often linked to fish products. The spores are widely present in soil and marine sediments. While spores are resistant to boiling, they can be destroyed by heating to 120°C. Because of its extreme toxicity, botulinum toxin is considered a potential biological warfare agent.
Clinically, botulism presents with bilateral cranial neuropathies followed by symmetric descending weakness. Patients typically remain afebrile, awake, and alert despite progressive paralysis. Sensory function remains intact. Early manifestations may include diplopia, ptosis, dysarthria, dysphagia, and dry mouth. As paralysis progresses, respiratory failure may occur. Clinical suspicion is critical, as early diagnosis significantly impacts outcomes.
Laboratory confirmation involves detection of toxin in serum, stool, or implicated food samples. The traditional mouse bioassay has limited sensitivity, particularly in wound botulism. However, treatment should not be delayed pending laboratory confirmation when clinical suspicion is high.
The differential diagnosis includes myasthenia gravis, Lambert–Eaton syndrome, tick paralysis, the Miller Fisher variant of Guillain–Barré syndrome, stroke, poliomyelitis, and heavy metal intoxication.
Management is primarily supportive, with close monitoring of respiratory function and mechanical ventilation if required. Equine-derived antitoxin covering toxin types A, B, and E should be administered as early as possible to neutralize circulating toxin. In cases of wound botulism, appropriate antibiotics should be given after antitoxin administration. In infants, intravenous human botulism immune globulin (BIG-IV) is recommended early in the course of illness. Patients often require prolonged rehabilitation. Even after recovery, some individuals may report persistent fatigue, weakness, dizziness, and respiratory difficulty.
Botulism is a potentially life-threatening neuroparalytic syndrome caused by neurotoxins produced by Clostridium botulinum. Botulinum neurotoxin (BoNT) is among the most potent toxins known. There are five epidemiologic forms of botulism: foodborne, infant botulism, wound botulism, intestinal colonization (adult infectious botulism), and inhalational botulism. Symptoms typically develop 12–36 hours after ingestion of preformed toxin.
Botulism is rare but can occur in small outbreaks, often associated with commercially or home-canned foods. In the United States, most cases occur in infants, approximately one-fourth are foodborne, and a smaller number are related to wounds. Risk factors include improper home canning of low-acid foods such as corn, asparagus, beans, and beets. The fatality rate is higher among patients older than 60 years. Honey ingestion is a well-established risk factor for infant botulism due to gastrointestinal colonization and in situ toxin production. Wound botulism should be suspected in intravenous drug users. Iatrogenic cases have been reported following injection of unlicensed botulinum toxin preparations.
Prevention focuses on proper food preservation techniques. Home-canned foods should be boiled for at least 10 minutes before consumption. Infants under one year of age should not be given honey. Bulging cans should be discarded. Rapid identification of suspected cases is essential to prevent outbreaks.
C. botulinum is an anaerobic, gram-positive, spore-forming rod. It produces toxins classified from types A to G, based on antigenic differences. Human disease is most commonly associated with toxin types A, B, E, and F. Type A is frequently found in the western United States and China, type B in the eastern United States and Europe, and type F worldwide, often linked to fish products. The spores are widely present in soil and marine sediments. While spores are resistant to boiling, they can be destroyed by heating to 120°C. Because of its extreme toxicity, botulinum toxin is considered a potential biological warfare agent.
Clinically, botulism presents with bilateral cranial neuropathies followed by symmetric descending weakness. Patients typically remain afebrile, awake, and alert despite progressive paralysis. Sensory function remains intact. Early manifestations may include diplopia, ptosis, dysarthria, dysphagia, and dry mouth. As paralysis progresses, respiratory failure may occur. Clinical suspicion is critical, as early diagnosis significantly impacts outcomes.
Laboratory confirmation involves detection of toxin in serum, stool, or implicated food samples. The traditional mouse bioassay has limited sensitivity, particularly in wound botulism. However, treatment should not be delayed pending laboratory confirmation when clinical suspicion is high.
The differential diagnosis includes myasthenia gravis, Lambert–Eaton syndrome, tick paralysis, the Miller Fisher variant of Guillain–Barré syndrome, stroke, poliomyelitis, and heavy metal intoxication.
Management is primarily supportive, with close monitoring of respiratory function and mechanical ventilation if required. Equine-derived antitoxin covering toxin types A, B, and E should be administered as early as possible to neutralize circulating toxin. In cases of wound botulism, appropriate antibiotics should be given after antitoxin administration. In infants, intravenous human botulism immune globulin (BIG-IV) is recommended early in the course of illness. Patients often require prolonged rehabilitation. Even after recovery, some individuals may report persistent fatigue, weakness, dizziness, and respiratory difficulty.
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Infectious Disease and Microbiology – Blepharitis and Chalazion
Blepharitis is an infection and inflammation of the eyelid margins. It may be classified as anterior (involving inflammation at the base of the eyelashes), posterior (affecting the inner portion of the eyelid and meibomian glands), or granulomatous. Chalazion, in contrast, is a painless granulomatous inflammation of a meibomian gland that produces a localized nodule within the eyelid. Blepharitis is a common condition encountered by both primary care physicians and ophthalmologists. Posterior blepharitis is frequently associated with rosacea and seborrheic dermatitis.
Risk factors include dermatologic conditions such as atopic dermatitis, with more than three-fourths of such patients demonstrating positive cultures for Staphylococcus aureus. However, a positive culture does not always indicate active infection, and clinical correlation is essential. The pathophysiology involves bacterial colonization and inflammation that alter meibomian gland secretions, contributing to gland dysfunction and chronic irritation.
The most common causative organisms are Staphylococcus species, particularly S. aureus. Numerous other pathogens have been reported, including bacteria, fungi, viruses, and parasites, although these are less common. Organisms capable of colonizing adjacent skin areas such as the scalp or nares may spread to the eyelids and contribute to infection. Blepharitis is commonly associated with rosacea and seborrheic dermatitis.
Patients typically report chronic irritation, burning sensation, mild redness, and occasional pruritus of the eyelids. Some may experience blurred vision. On physical examination, acute blepharitis may present with collections of pus and ulceration at the lid margin. Chronic blepharitis often shows misdirected or missing eyelashes, telangiectasia, and a swollen lid margin. Superficial lid involvement usually presents with hyperemia and telangiectasia. Slit-lamp examination by an ophthalmologist may assist in evaluation.
Management focuses primarily on conservative measures. Warm compresses and strict eyelid hygiene are foundational treatments. Gentle massage of the eyelids using a diluted mixture of baby shampoo and water applied with a cotton-tipped applicator helps improve meibomian gland drainage. Topical ophthalmic antibiotics such as bacitracin or erythromycin (twice to four times daily for approximately two weeks) are commonly used for staphylococcal blepharitis. Gentamicin and 1% mercuric oxide preparations may also be used. In chronic or refractory cases, cultures should be obtained, and systemic antibiotics such as dicloxacillin, quinolones, or azithromycin may be considered.
For chalazion, persistent and nontender lesions may require incision and curettage. This involves removal of inflammatory debris via conjunctival incision. If infection is absent, intralesional corticosteroid injection may be considered. In rare cases of necrotizing fasciitis involving the eyelids, urgent surgical debridement is required.
Follow-up is important for nonhealing or ulcerative eyelid lesions, as basal cell carcinoma, squamous cell carcinoma, or meibomian gland carcinoma must be excluded. Complications include the development of hordeolum (stye). An external hordeolum results from staphylococcal infection of the glands of Zeis or Moll at the eyelid margin, whereas an internal hordeolum involves suppurative infection of the meibomian glands within the tarsal plate.
Blepharitis is an infection and inflammation of the eyelid margins. It may be classified as anterior (involving inflammation at the base of the eyelashes), posterior (affecting the inner portion of the eyelid and meibomian glands), or granulomatous. Chalazion, in contrast, is a painless granulomatous inflammation of a meibomian gland that produces a localized nodule within the eyelid. Blepharitis is a common condition encountered by both primary care physicians and ophthalmologists. Posterior blepharitis is frequently associated with rosacea and seborrheic dermatitis.
Risk factors include dermatologic conditions such as atopic dermatitis, with more than three-fourths of such patients demonstrating positive cultures for Staphylococcus aureus. However, a positive culture does not always indicate active infection, and clinical correlation is essential. The pathophysiology involves bacterial colonization and inflammation that alter meibomian gland secretions, contributing to gland dysfunction and chronic irritation.
The most common causative organisms are Staphylococcus species, particularly S. aureus. Numerous other pathogens have been reported, including bacteria, fungi, viruses, and parasites, although these are less common. Organisms capable of colonizing adjacent skin areas such as the scalp or nares may spread to the eyelids and contribute to infection. Blepharitis is commonly associated with rosacea and seborrheic dermatitis.
Patients typically report chronic irritation, burning sensation, mild redness, and occasional pruritus of the eyelids. Some may experience blurred vision. On physical examination, acute blepharitis may present with collections of pus and ulceration at the lid margin. Chronic blepharitis often shows misdirected or missing eyelashes, telangiectasia, and a swollen lid margin. Superficial lid involvement usually presents with hyperemia and telangiectasia. Slit-lamp examination by an ophthalmologist may assist in evaluation.
Management focuses primarily on conservative measures. Warm compresses and strict eyelid hygiene are foundational treatments. Gentle massage of the eyelids using a diluted mixture of baby shampoo and water applied with a cotton-tipped applicator helps improve meibomian gland drainage. Topical ophthalmic antibiotics such as bacitracin or erythromycin (twice to four times daily for approximately two weeks) are commonly used for staphylococcal blepharitis. Gentamicin and 1% mercuric oxide preparations may also be used. In chronic or refractory cases, cultures should be obtained, and systemic antibiotics such as dicloxacillin, quinolones, or azithromycin may be considered.
For chalazion, persistent and nontender lesions may require incision and curettage. This involves removal of inflammatory debris via conjunctival incision. If infection is absent, intralesional corticosteroid injection may be considered. In rare cases of necrotizing fasciitis involving the eyelids, urgent surgical debridement is required.
Follow-up is important for nonhealing or ulcerative eyelid lesions, as basal cell carcinoma, squamous cell carcinoma, or meibomian gland carcinoma must be excluded. Complications include the development of hordeolum (stye). An external hordeolum results from staphylococcal infection of the glands of Zeis or Moll at the eyelid margin, whereas an internal hordeolum involves suppurative infection of the meibomian glands within the tarsal plate.
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Infectious Disease and Microbiology – Blastomycosis
Blastomycosis is an acute or chronic infection caused by Blastomyces dermatitidis, a dimorphic fungus found in soil. The organism exists as mold in the environment and converts to yeast in human tissue. The annual incidence ranges from 0.3 to 1.8 cases per 100,000 population, with up to 7.4 hospital admissions per 1 million people in endemic regions. The infection is endemic in areas near bodies of water in the southeastern United States and along the Mississippi, Ohio, and St. Lawrence River valleys. It is also found along the Mediterranean coast, in South America, Mexico, and parts of Africa. Although previously thought to affect middle-aged men more commonly, this is likely related to environmental exposure patterns rather than gender predisposition. Immunocompromised individuals are at risk for more severe disease and poorer outcomes. Prevention focuses on minimizing exposure in endemic regions, including the use of respiratory protection for individuals at occupational risk.
Infection occurs through inhalation of conidia from the environment, with potential for hematogenous dissemination to other organs. The immune system more effectively clears the conidial form; however, once inside the host, the organism converts into a broad-based budding yeast form that is less susceptible to immune clearance. Reactivation may occur in immunocompromised patients.
Clinically, blastomycosis most commonly presents as pulmonary disease. Acute pneumonia presents with fever, night sweats, productive cough, dyspnea, and pleuritic chest pain, and may be accompanied by rash. Chronic pneumonia resembles pulmonary tuberculosis, with subacute onset of fever, night sweats, weight loss, mild productive cough, and sometimes hemoptysis. Disseminated disease can involve the skin, bones, genitourinary tract, central nervous system, or other organs. Skin lesions are typically non-tender papules, nodules, or plaques that may become verrucous or ulcerated. Soft tissue swelling may occur and can form draining tracts. CNS involvement may manifest as meningitis or focal neurologic deficits.
Diagnosis relies primarily on culture and direct visualization. Serologic testing is limited due to cross-reactivity with other endemic mycoses. Urine antigen testing is available but also limited by cross-reactivity. Chest radiography may reveal masses, nodules, lobar infiltrates, or cavitary lesions; lymphadenopathy is uncommon. Culture is positive in approximately 86% of sputum samples and 92% of bronchoalveolar lavage specimens. Wet mount preparations using potassium hydroxide or calcofluor white have about 46% sensitivity. The characteristic finding is a large yeast (8–15 μm) with a single broad-based bud. Histopathology shows pyogranulomas, and fungal elements are more easily visualized with methenamine silver or periodic acid–Schiff stains. The differential diagnosis includes atypical pneumonia, lung cancer, mycobacterial disease, and squamous cell carcinoma for cutaneous lesions.
Treatment depends on severity and organ involvement. For pulmonary or disseminated non-CNS disease, amphotericin B (or a lipid/liposomal formulation) is administered for two weeks, followed by itraconazole 200 mg three times daily for three days, then 200 mg twice daily for 6–12 months. Mild to moderate disease may be treated with itraconazole alone for 6–12 months. CNS disease requires lipid/liposomal amphotericin B (3–5 mg/kg IV for 4–6 weeks), followed by at least 12 months of oral azole therapy (itraconazole, fluconazole, or voriconazole). Immunocompromised patients should receive amphotericin B followed by itraconazole for at least 12 months, and lifelong suppressive therapy may be considered. In children with mild disease, itraconazole (10 mg/kg/day) is recommended for 6–12 months; severe disease requires amphotericin followed by itraconazole. In pregnancy, amphotericin B is the treatment of choice, as azoles are contraindicated.
Patients require close monitoring for antifungal toxicity. Therapeutic drug monitoring of itraconazole is recommended after two weeks of therapy, with target levels greater than 1.0 μg/mL and less than 10 μg/mL. Liver function tests should be monitored at least every three months during azole therapy. Itraconazole should be taken with food to enhance absorption. Follow-up for approximately six months after completion of therapy is recommended due to relapse risk.
Prognosis is favorable in immunocompetent individuals, with cure rates of 90–97% when treated appropriately with amphotericin. Mortality approaches 40% in immunocompromised patients, particularly those with bone marrow transplantation or AIDS. Outcomes in pregnant women can be excellent if diagnosed early, though they are at increased risk for severe disease. Complications include respiratory failure (acute respiratory distress syndrome), CNS involvement, and relapse.
Blastomycosis is an acute or chronic infection caused by Blastomyces dermatitidis, a dimorphic fungus found in soil. The organism exists as mold in the environment and converts to yeast in human tissue. The annual incidence ranges from 0.3 to 1.8 cases per 100,000 population, with up to 7.4 hospital admissions per 1 million people in endemic regions. The infection is endemic in areas near bodies of water in the southeastern United States and along the Mississippi, Ohio, and St. Lawrence River valleys. It is also found along the Mediterranean coast, in South America, Mexico, and parts of Africa. Although previously thought to affect middle-aged men more commonly, this is likely related to environmental exposure patterns rather than gender predisposition. Immunocompromised individuals are at risk for more severe disease and poorer outcomes. Prevention focuses on minimizing exposure in endemic regions, including the use of respiratory protection for individuals at occupational risk.
Infection occurs through inhalation of conidia from the environment, with potential for hematogenous dissemination to other organs. The immune system more effectively clears the conidial form; however, once inside the host, the organism converts into a broad-based budding yeast form that is less susceptible to immune clearance. Reactivation may occur in immunocompromised patients.
Clinically, blastomycosis most commonly presents as pulmonary disease. Acute pneumonia presents with fever, night sweats, productive cough, dyspnea, and pleuritic chest pain, and may be accompanied by rash. Chronic pneumonia resembles pulmonary tuberculosis, with subacute onset of fever, night sweats, weight loss, mild productive cough, and sometimes hemoptysis. Disseminated disease can involve the skin, bones, genitourinary tract, central nervous system, or other organs. Skin lesions are typically non-tender papules, nodules, or plaques that may become verrucous or ulcerated. Soft tissue swelling may occur and can form draining tracts. CNS involvement may manifest as meningitis or focal neurologic deficits.
Diagnosis relies primarily on culture and direct visualization. Serologic testing is limited due to cross-reactivity with other endemic mycoses. Urine antigen testing is available but also limited by cross-reactivity. Chest radiography may reveal masses, nodules, lobar infiltrates, or cavitary lesions; lymphadenopathy is uncommon. Culture is positive in approximately 86% of sputum samples and 92% of bronchoalveolar lavage specimens. Wet mount preparations using potassium hydroxide or calcofluor white have about 46% sensitivity. The characteristic finding is a large yeast (8–15 μm) with a single broad-based bud. Histopathology shows pyogranulomas, and fungal elements are more easily visualized with methenamine silver or periodic acid–Schiff stains. The differential diagnosis includes atypical pneumonia, lung cancer, mycobacterial disease, and squamous cell carcinoma for cutaneous lesions.
Treatment depends on severity and organ involvement. For pulmonary or disseminated non-CNS disease, amphotericin B (or a lipid/liposomal formulation) is administered for two weeks, followed by itraconazole 200 mg three times daily for three days, then 200 mg twice daily for 6–12 months. Mild to moderate disease may be treated with itraconazole alone for 6–12 months. CNS disease requires lipid/liposomal amphotericin B (3–5 mg/kg IV for 4–6 weeks), followed by at least 12 months of oral azole therapy (itraconazole, fluconazole, or voriconazole). Immunocompromised patients should receive amphotericin B followed by itraconazole for at least 12 months, and lifelong suppressive therapy may be considered. In children with mild disease, itraconazole (10 mg/kg/day) is recommended for 6–12 months; severe disease requires amphotericin followed by itraconazole. In pregnancy, amphotericin B is the treatment of choice, as azoles are contraindicated.
Patients require close monitoring for antifungal toxicity. Therapeutic drug monitoring of itraconazole is recommended after two weeks of therapy, with target levels greater than 1.0 μg/mL and less than 10 μg/mL. Liver function tests should be monitored at least every three months during azole therapy. Itraconazole should be taken with food to enhance absorption. Follow-up for approximately six months after completion of therapy is recommended due to relapse risk.
Prognosis is favorable in immunocompetent individuals, with cure rates of 90–97% when treated appropriately with amphotericin. Mortality approaches 40% in immunocompromised patients, particularly those with bone marrow transplantation or AIDS. Outcomes in pregnant women can be excellent if diagnosed early, though they are at increased risk for severe disease. Complications include respiratory failure (acute respiratory distress syndrome), CNS involvement, and relapse.
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Infectious Disease and Microbiology – Bell’s Palsy
Bell’s palsy is defined as an acute, idiopathic, unilateral paralysis of the facial nerve (cranial nerve VII). Approximately half of all facial nerve palsies are classified as Bell’s palsy. Bilateral involvement is rare, occurring in about 0.3% of cases. Although termed “idiopathic,” viral etiologies are strongly suspected, particularly herpes simplex virus. Other infectious associations include herpes zoster (including herpes zoster oticus). Rarely, Bell’s palsy has been reported as an adverse event following immunization.
The incidence in the United States ranges from 13 to 34 cases per 100,000 persons annually. The condition most commonly affects individuals aged 20–35 years and those over 70 years of age. Males and females are equally affected. Bell’s palsy is the most common cause of seventh nerve palsy in children. Risk factors include pregnancy, diabetes mellitus, and hypertension in individuals older than 40 years. Currently, there is no known preventive measure.
Clinically, Bell’s palsy presents with acute onset over one to two days and rapid progression to partial or complete unilateral facial paralysis. Patients may experience decreased tear and saliva production on the affected side, hyperacusis (increased sensitivity to sound), dysgeusia (altered taste), and retroauricular pain. The diagnosis is primarily clinical.
The differential diagnosis is broad and includes infectious causes such as Lyme disease, HIV infection (particularly during seroconversion), otitis media, mastoiditis, tuberculosis, syphilis, infectious meningitis, rubella, tetanus, Mycoplasma infection, and enteroviral infections. Noninfectious causes include sarcoidosis, Sjögren’s syndrome, systemic lupus erythematosus, tumors (parotid gland tumors, melanoma, meningioma), cerebral aneurysm, Guillain-Barré syndrome, trauma, iatrogenic injury, and others. In cases of bilateral facial paralysis, Lyme disease and sarcoidosis should be strongly considered.
Electrodiagnostic studies such as electromyography (EMG) or electroneurography may be useful in selected cases, particularly if recovery is incomplete. Patients with a typical presentation and early recovery usually do not require further testing. Imaging with CT or MRI is indicated if the presentation is atypical, if symptoms progress slowly, or if there is no improvement within six months, to exclude intracranial or middle ear pathology. Recent evidence suggests that ultrasound measurement of the distal facial nerve diameter may help predict recovery at three months.
Early treatment significantly improves outcomes. Prednisolone should be initiated within three days of symptom onset, at a dose of 60–80 mg daily for one week, as it increases the likelihood of complete recovery at three and nine months. Antiviral therapy may be added in severe cases of facial palsy. Eye protection is essential, including artificial tears during the day and lubricating ointment at night, to prevent corneal injury. The role of surgical decompression remains controversial.
Ongoing care focuses on eye protection and psychological support. Complications include incomplete recovery in approximately one-third of patients, keratitis, corneal abrasions, and recurrence in 7–15% of cases.
Bell’s palsy is defined as an acute, idiopathic, unilateral paralysis of the facial nerve (cranial nerve VII). Approximately half of all facial nerve palsies are classified as Bell’s palsy. Bilateral involvement is rare, occurring in about 0.3% of cases. Although termed “idiopathic,” viral etiologies are strongly suspected, particularly herpes simplex virus. Other infectious associations include herpes zoster (including herpes zoster oticus). Rarely, Bell’s palsy has been reported as an adverse event following immunization.
The incidence in the United States ranges from 13 to 34 cases per 100,000 persons annually. The condition most commonly affects individuals aged 20–35 years and those over 70 years of age. Males and females are equally affected. Bell’s palsy is the most common cause of seventh nerve palsy in children. Risk factors include pregnancy, diabetes mellitus, and hypertension in individuals older than 40 years. Currently, there is no known preventive measure.
Clinically, Bell’s palsy presents with acute onset over one to two days and rapid progression to partial or complete unilateral facial paralysis. Patients may experience decreased tear and saliva production on the affected side, hyperacusis (increased sensitivity to sound), dysgeusia (altered taste), and retroauricular pain. The diagnosis is primarily clinical.
The differential diagnosis is broad and includes infectious causes such as Lyme disease, HIV infection (particularly during seroconversion), otitis media, mastoiditis, tuberculosis, syphilis, infectious meningitis, rubella, tetanus, Mycoplasma infection, and enteroviral infections. Noninfectious causes include sarcoidosis, Sjögren’s syndrome, systemic lupus erythematosus, tumors (parotid gland tumors, melanoma, meningioma), cerebral aneurysm, Guillain-Barré syndrome, trauma, iatrogenic injury, and others. In cases of bilateral facial paralysis, Lyme disease and sarcoidosis should be strongly considered.
Electrodiagnostic studies such as electromyography (EMG) or electroneurography may be useful in selected cases, particularly if recovery is incomplete. Patients with a typical presentation and early recovery usually do not require further testing. Imaging with CT or MRI is indicated if the presentation is atypical, if symptoms progress slowly, or if there is no improvement within six months, to exclude intracranial or middle ear pathology. Recent evidence suggests that ultrasound measurement of the distal facial nerve diameter may help predict recovery at three months.
Early treatment significantly improves outcomes. Prednisolone should be initiated within three days of symptom onset, at a dose of 60–80 mg daily for one week, as it increases the likelihood of complete recovery at three and nine months. Antiviral therapy may be added in severe cases of facial palsy. Eye protection is essential, including artificial tears during the day and lubricating ointment at night, to prevent corneal injury. The role of surgical decompression remains controversial.
Ongoing care focuses on eye protection and psychological support. Complications include incomplete recovery in approximately one-third of patients, keratitis, corneal abrasions, and recurrence in 7–15% of cases.
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Infectious Disease and Microbiology – Bartonellosis (Oroya Fever/Verruga Peruana)
Bartonellosis is an infection caused by Bartonella bacilliformis, transmitted by sandflies of the genus Phlebotomus. It occurs in endemic areas and presents in two distinct clinical forms. Nonimmune individuals typically develop an acute febrile illness known as Oroya fever, characterized by profound hemolytic anemia. After recovery from the acute phase, a chronic cutaneous form called verruga peruana may develop, featuring angioproliferative skin lesions that resemble those seen in bacillary angiomatosis caused by other Bartonella species.
The disease is endemic to the Andean river valleys at altitudes between 600 and 2,500 meters in Peru, Ecuador, and Colombia. Oroya fever most commonly affects tourists or visitors who lack prior immunity, whereas verruga peruana is more frequently seen in the native population. Rare imported cases have been reported outside endemic regions. Risk factors include residence in or travel to endemic areas and exposure to the sandfly vector. Prevention focuses on vector control measures such as indoor and outdoor insecticide spraying, use of insect repellents, and bed nets.
Pathophysiologically, B. bacilliformis invades erythrocytes and endothelial cells. The bacteria multiply within intracellular vacuoles inside red blood cells, which are subsequently destroyed by the reticuloendothelial system, resulting in severe hemolytic anemia. The organism is a small, gram-negative bacillus closely related to Bartonella quintana.
The incubation period of Oroya fever averages about three weeks but can extend up to 100 days. The acute illness may begin gradually with low-grade fever, malaise, headache, and anorexia, or abruptly with high fever, chills, diaphoresis, altered mental status, and rapidly progressive anemia. Patients may experience dyspnea, chest discomfort, myalgias, arthralgias, and in severe cases, delirium or coma. Anasarca indicates a poor prognosis. During the convalescent phase, fever subsides and anemia improves.
Physical examination in Oroya fever reveals high fever, signs of profound anemia, generalized nontender lymphadenopathy, and occasionally thrombocytopenic purpura. Splenomegaly is uncommon and may suggest concurrent infection.
Verruga peruana develops weeks to months after recovery from the acute phase. Lesions appear in crops and may be miliary (1–4 mm papular erythematous lesions), nodular, or larger “mular” lesions exceeding 5 mm in diameter. They are typically bright red, bleed easily, and may involve skin, mucous membranes, or internal organs. Lesions are generally nontender unless secondarily infected and may be present at different stages simultaneously.
Diagnosis in the acute phase is made by identifying numerous bacteria attached to red blood cells on Giemsa- or Wright-stained peripheral blood smears or by positive blood or bone marrow cultures. Peripheral smear may also reveal macrocytosis, poikilocytosis, Howell–Jolly bodies, nucleated red blood cells, and immature myeloid cells. Profound anemia with a negative Coombs’ test is typical. In subacute cases, smears may initially be negative, and blood cultures are required. In the chronic phase, organisms can be demonstrated in cultures from skin lesions or bone marrow. Serologic tests such as ELISA or indirect immunofluorescence can support the diagnosis. Skin biopsy may show increased angiogenesis and characteristic endothelial inclusions (Rocha-Lima inclusions).
The acute phase must be differentiated from other endemic febrile illnesses such as malaria, typhoid fever, and leptospirosis. Verruga lesions resemble bacillary angiomatosis, Kaposi’s sarcoma, and certain neoplasms; epidemiologic context is a key diagnostic clue.
Treatment of Oroya fever consists of chloramphenicol (500 mg orally or intravenously every 6 hours) combined with a second antimicrobial, preferably a beta-lactam such as penicillin, for 14 days. Chloramphenicol also provides coverage against salmonellosis, a common secondary infection. Doxycycline is an alternative agent, while fluoroquinolones are generally not recommended due to resistance. Verruga peruana is treated with rifampin (10 mg/kg daily, maximum 600 mg daily) for 10–14 days. Streptomycin is a second-line option. Supportive care, including blood transfusion for severe anemia, is essential in the acute phase. Large or secondarily infected skin lesions may require surgical excision.
Patients with Oroya fever typically require inpatient management, whereas those with verruga peruana can often be managed as outpatients. Monitoring during the acute phase should include hydration status, complete blood counts, and surveillance for secondary infections such as salmonellosis, malaria, or tuberculosis.
Untreated Oroya fever carries a mortality rate of 50–88%. With appropriate therapy, fever usually resolves within 24 hours, though bacteremia may persist longer. Complications include secondary bacterial infections during convalescence and ulceration or bleeding of verruga lesions.
Bartonellosis is an infection caused by Bartonella bacilliformis, transmitted by sandflies of the genus Phlebotomus. It occurs in endemic areas and presents in two distinct clinical forms. Nonimmune individuals typically develop an acute febrile illness known as Oroya fever, characterized by profound hemolytic anemia. After recovery from the acute phase, a chronic cutaneous form called verruga peruana may develop, featuring angioproliferative skin lesions that resemble those seen in bacillary angiomatosis caused by other Bartonella species.
The disease is endemic to the Andean river valleys at altitudes between 600 and 2,500 meters in Peru, Ecuador, and Colombia. Oroya fever most commonly affects tourists or visitors who lack prior immunity, whereas verruga peruana is more frequently seen in the native population. Rare imported cases have been reported outside endemic regions. Risk factors include residence in or travel to endemic areas and exposure to the sandfly vector. Prevention focuses on vector control measures such as indoor and outdoor insecticide spraying, use of insect repellents, and bed nets.
Pathophysiologically, B. bacilliformis invades erythrocytes and endothelial cells. The bacteria multiply within intracellular vacuoles inside red blood cells, which are subsequently destroyed by the reticuloendothelial system, resulting in severe hemolytic anemia. The organism is a small, gram-negative bacillus closely related to Bartonella quintana.
The incubation period of Oroya fever averages about three weeks but can extend up to 100 days. The acute illness may begin gradually with low-grade fever, malaise, headache, and anorexia, or abruptly with high fever, chills, diaphoresis, altered mental status, and rapidly progressive anemia. Patients may experience dyspnea, chest discomfort, myalgias, arthralgias, and in severe cases, delirium or coma. Anasarca indicates a poor prognosis. During the convalescent phase, fever subsides and anemia improves.
Physical examination in Oroya fever reveals high fever, signs of profound anemia, generalized nontender lymphadenopathy, and occasionally thrombocytopenic purpura. Splenomegaly is uncommon and may suggest concurrent infection.
Verruga peruana develops weeks to months after recovery from the acute phase. Lesions appear in crops and may be miliary (1–4 mm papular erythematous lesions), nodular, or larger “mular” lesions exceeding 5 mm in diameter. They are typically bright red, bleed easily, and may involve skin, mucous membranes, or internal organs. Lesions are generally nontender unless secondarily infected and may be present at different stages simultaneously.
Diagnosis in the acute phase is made by identifying numerous bacteria attached to red blood cells on Giemsa- or Wright-stained peripheral blood smears or by positive blood or bone marrow cultures. Peripheral smear may also reveal macrocytosis, poikilocytosis, Howell–Jolly bodies, nucleated red blood cells, and immature myeloid cells. Profound anemia with a negative Coombs’ test is typical. In subacute cases, smears may initially be negative, and blood cultures are required. In the chronic phase, organisms can be demonstrated in cultures from skin lesions or bone marrow. Serologic tests such as ELISA or indirect immunofluorescence can support the diagnosis. Skin biopsy may show increased angiogenesis and characteristic endothelial inclusions (Rocha-Lima inclusions).
The acute phase must be differentiated from other endemic febrile illnesses such as malaria, typhoid fever, and leptospirosis. Verruga lesions resemble bacillary angiomatosis, Kaposi’s sarcoma, and certain neoplasms; epidemiologic context is a key diagnostic clue.
Treatment of Oroya fever consists of chloramphenicol (500 mg orally or intravenously every 6 hours) combined with a second antimicrobial, preferably a beta-lactam such as penicillin, for 14 days. Chloramphenicol also provides coverage against salmonellosis, a common secondary infection. Doxycycline is an alternative agent, while fluoroquinolones are generally not recommended due to resistance. Verruga peruana is treated with rifampin (10 mg/kg daily, maximum 600 mg daily) for 10–14 days. Streptomycin is a second-line option. Supportive care, including blood transfusion for severe anemia, is essential in the acute phase. Large or secondarily infected skin lesions may require surgical excision.
Patients with Oroya fever typically require inpatient management, whereas those with verruga peruana can often be managed as outpatients. Monitoring during the acute phase should include hydration status, complete blood counts, and surveillance for secondary infections such as salmonellosis, malaria, or tuberculosis.
Untreated Oroya fever carries a mortality rate of 50–88%. With appropriate therapy, fever usually resolves within 24 hours, though bacteremia may persist longer. Complications include secondary bacterial infections during convalescence and ulceration or bleeding of verruga lesions.
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Infectious Disease and Microbiology – Balanitis
Balanitis refers to inflammation and/or infection of the glans penis, while balanoposthitis involves both the glans and the foreskin. Infectious causes are common and may result from fungal, bacterial, viral, or parasitic pathogens. Sexual exposure plays an important role in transmission, particularly in men whose partners have Candida vaginitis. In young boys, balanitis may occur in association with diaper dermatitis.
Risk factors include being uncircumcised, diabetes mellitus (especially newly diagnosed diabetes), immunodeficiency, poor hygiene, use of broad-spectrum antibiotics, and increasing age in the case of Candida colonization. Circumcision and proper genital hygiene significantly reduce the risk. Treatment of sexual partners is important when Candida or Trichomonas infection is identified.
Infectious etiologies include Candida species (most common), Trichomonas species, anaerobic bacteria such as Bacteroides and Gardnerella vaginalis, Chlamydia, Neisseria gonorrhoeae, human papillomavirus (HPV), herpes simplex virus (HSV), Treponema pallidum, Mycoplasma, Mycobacterium (including Bacillus Calmette–Guérin), group A and B streptococci, Staphylococcus aureus, Borrelia burgdorferi, and Entamoeba histolytica.
Patients typically present with pain, tenderness, erythema, pruritus, edema, erosions, and sometimes pustules on the glans penis. Anaerobic infections may produce a characteristic foul odor.
Diagnosis is largely clinical but may be supported by laboratory testing. Fungal preparations often reveal Candida. Direct impression onto CHROMagar Candida medium has been shown to provide a higher yield than swab sampling. Wet mount examination may detect Trichomonas or Gardnerella. Urethral discharge should be tested for sexually transmitted infections. Serologic or culture testing for HIV, HPV, and HSV may be indicated based on risk factors. Blood glucose testing is recommended to evaluate for underlying diabetes mellitus.
The differential diagnosis includes numerous noninfectious conditions such as irritant dermatitis, trauma, contact dermatitis, lichen sclerosus, lichen planus, Zoon’s balanitis, erythroplasia of Queyrat, pemphigus, pemphigoid, Bowen’s disease, leukoplakia, fixed drug eruption, psoriasis (particularly inverse psoriasis), Paget’s disease, nummular eczema, scabies, and squamous cell carcinoma.
Management begins with good hygiene, including gentle washing of the glans after foreskin retraction. Candida balanitis is typically treated with topical imidazole antifungal agents, and 1% hydrocortisone cream may be added for symptomatic relief. Severe cases may require oral fluconazole. Trichomonas infection responds to metronidazole, and sexual partners should be treated simultaneously. Anaerobic infections may be managed with oral metronidazole, oral amoxicillin–clavulanate, or topical clindamycin cream.
Patients should be monitored for recurrence and evaluated for underlying diabetes if not previously diagnosed. Complications include phimosis, paraphimosis, fissuring of the prepuce, and scarring.
Balanitis refers to inflammation and/or infection of the glans penis, while balanoposthitis involves both the glans and the foreskin. Infectious causes are common and may result from fungal, bacterial, viral, or parasitic pathogens. Sexual exposure plays an important role in transmission, particularly in men whose partners have Candida vaginitis. In young boys, balanitis may occur in association with diaper dermatitis.
Risk factors include being uncircumcised, diabetes mellitus (especially newly diagnosed diabetes), immunodeficiency, poor hygiene, use of broad-spectrum antibiotics, and increasing age in the case of Candida colonization. Circumcision and proper genital hygiene significantly reduce the risk. Treatment of sexual partners is important when Candida or Trichomonas infection is identified.
Infectious etiologies include Candida species (most common), Trichomonas species, anaerobic bacteria such as Bacteroides and Gardnerella vaginalis, Chlamydia, Neisseria gonorrhoeae, human papillomavirus (HPV), herpes simplex virus (HSV), Treponema pallidum, Mycoplasma, Mycobacterium (including Bacillus Calmette–Guérin), group A and B streptococci, Staphylococcus aureus, Borrelia burgdorferi, and Entamoeba histolytica.
Patients typically present with pain, tenderness, erythema, pruritus, edema, erosions, and sometimes pustules on the glans penis. Anaerobic infections may produce a characteristic foul odor.
Diagnosis is largely clinical but may be supported by laboratory testing. Fungal preparations often reveal Candida. Direct impression onto CHROMagar Candida medium has been shown to provide a higher yield than swab sampling. Wet mount examination may detect Trichomonas or Gardnerella. Urethral discharge should be tested for sexually transmitted infections. Serologic or culture testing for HIV, HPV, and HSV may be indicated based on risk factors. Blood glucose testing is recommended to evaluate for underlying diabetes mellitus.
The differential diagnosis includes numerous noninfectious conditions such as irritant dermatitis, trauma, contact dermatitis, lichen sclerosus, lichen planus, Zoon’s balanitis, erythroplasia of Queyrat, pemphigus, pemphigoid, Bowen’s disease, leukoplakia, fixed drug eruption, psoriasis (particularly inverse psoriasis), Paget’s disease, nummular eczema, scabies, and squamous cell carcinoma.
Management begins with good hygiene, including gentle washing of the glans after foreskin retraction. Candida balanitis is typically treated with topical imidazole antifungal agents, and 1% hydrocortisone cream may be added for symptomatic relief. Severe cases may require oral fluconazole. Trichomonas infection responds to metronidazole, and sexual partners should be treated simultaneously. Anaerobic infections may be managed with oral metronidazole, oral amoxicillin–clavulanate, or topical clindamycin cream.
Patients should be monitored for recurrence and evaluated for underlying diabetes if not previously diagnosed. Complications include phimosis, paraphimosis, fissuring of the prepuce, and scarring.
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Infectious Diseases and Microbiology: Postoperative Fever
Basics
Description
Postoperative fever is defined as a body temperature above 38°C (100.4°F) occurring after an invasive procedure. It is classified by timing: immediate (during surgery or within hours), acute (within the first postoperative week), subacute (1–4 weeks after surgery), and delayed (more than one month postoperatively). Most cases result from the inflammatory response to surgery and resolve spontaneously, but fever may signal a serious complication. Evaluation requires careful history, physical examination, and appropriate laboratory and imaging studies, including cultures and Gram stains when indicated. Early postoperative fever is frequently noninfectious; however, fever persisting beyond 96 hours is more likely infectious. Consider that patients may have been incubating community-acquired infection preoperatively. New or persistent fever beyond four days strongly suggests ongoing pathology or a new complication. Surgical wounds, catheter insertion sites, and all dressings must be inspected, and recent interventions such as blood transfusions reviewed.
Epidemiology
Drug fever is the most common noninfectious cause of postoperative fever, most often linked to antimicrobials and heparin. Pneumonia is a common cause after cardiac surgery and occurs in more than 5% of such patients. Sternal wound infections after cardiothoracic surgery occur in up to 5%, typically around postoperative day seven. Postoperative aspergillosis after cardiothoracic procedures carries very high mortality. Fever alone is a poor predictor of infection, with low sensitivity. Postsurgical mediastinitis has high mortality. In obstetrics and gynecology, bacterial vaginosis may increase postoperative infection risk.
General Prevention
Aggressive pulmonary hygiene, including incentive spirometry and mobilization, reduces pulmonary complications such as atelectasis.
Etiology
Common infectious causes include urinary tract infection, pneumonia, sinusitis, suppurative thrombophlebitis, catheter-related infections, and Clostridioides difficile–associated diarrhea. Noninfectious causes include deep venous thrombosis, pulmonary embolism, subarachnoid hemorrhage, gout, and fat embolism. Surgical site infections are uncommon within the first 1–3 days except for aggressive pathogens such as group A streptococci or clostridia, which can present early. Atelectasis is frequently blamed but likely coincidental rather than causal. Other serious causes include transplant rejection. Drug-induced fever is most often associated with beta-lactams, antiepileptics, and heparin. Inflammatory states such as acute myocardial infarction, pancreatitis, or acute respiratory distress syndrome may produce fever without infection. Endocrine emergencies such as adrenal insufficiency or thyrotoxicosis may also present with fever.
Diagnosis
Physical Examination
Drug fever lacks specific features and usually develops days after medication exposure; rash and eosinophilia are uncommon. Malignant hyperthermia typically occurs intraoperatively but may be delayed up to 24 hours and is associated with agents such as succinylcholine or volatile anesthetics. Neuroleptic malignant syndrome is associated with antipsychotics, particularly haloperidol. Withdrawal syndromes from alcohol, opioids, barbiturates, or benzodiazepines may cause fever hours to days after admission, and prior substance use history may not be readily available.
Diagnostic Tests and Interpretation
Laboratory Studies
Urinalysis and urine culture are recommended in patients with indwelling catheters longer than 72 hours. Procalcitonin has uncertain value in distinguishing bacterial causes of postoperative fever.
Imaging
Duplex ultrasonography with Doppler should be considered for new extremity swelling suggestive of deep venous thrombosis. Routine chest radiography is not required within the first 72 postoperative hours if fever is the only indication.
Diagnostic Procedures/Other
Wound swab cultures are rarely useful unless there is clear clinical evidence of infection. Suspected deep intraabdominal abscess may require imaging and, if inconclusive, surgical exploration.
Treatment
Medications
Antibiotics are generally not indicated for early postoperative fever without evidence of infection. Critically ill patients or those with hemodynamic instability should receive empiric broad-spectrum antibiotics after thorough evaluation, but therapy should be discontinued after 48 hours if no infectious source is identified. Atelectasis management includes coughing exercises, incentive spirometry, chest physiotherapy, beta-2 agonists, intermittent positive-pressure breathing, and nebulization. Empiric antifungal therapy is not recommended initially.
Ongoing Care and Follow-Up
Drug fever is diagnosed by exclusion when other causes are ruled out. Surgical wounds and invasive device sites must be repeatedly examined for signs of infection.
Complications
Postoperative infections increase morbidity and mortality, may lead to sepsis, impair wound healing, and cause respiratory failure and other serious outcomes.
Basics
Description
Postoperative fever is defined as a body temperature above 38°C (100.4°F) occurring after an invasive procedure. It is classified by timing: immediate (during surgery or within hours), acute (within the first postoperative week), subacute (1–4 weeks after surgery), and delayed (more than one month postoperatively). Most cases result from the inflammatory response to surgery and resolve spontaneously, but fever may signal a serious complication. Evaluation requires careful history, physical examination, and appropriate laboratory and imaging studies, including cultures and Gram stains when indicated. Early postoperative fever is frequently noninfectious; however, fever persisting beyond 96 hours is more likely infectious. Consider that patients may have been incubating community-acquired infection preoperatively. New or persistent fever beyond four days strongly suggests ongoing pathology or a new complication. Surgical wounds, catheter insertion sites, and all dressings must be inspected, and recent interventions such as blood transfusions reviewed.
Epidemiology
Drug fever is the most common noninfectious cause of postoperative fever, most often linked to antimicrobials and heparin. Pneumonia is a common cause after cardiac surgery and occurs in more than 5% of such patients. Sternal wound infections after cardiothoracic surgery occur in up to 5%, typically around postoperative day seven. Postoperative aspergillosis after cardiothoracic procedures carries very high mortality. Fever alone is a poor predictor of infection, with low sensitivity. Postsurgical mediastinitis has high mortality. In obstetrics and gynecology, bacterial vaginosis may increase postoperative infection risk.
General Prevention
Aggressive pulmonary hygiene, including incentive spirometry and mobilization, reduces pulmonary complications such as atelectasis.
Etiology
Common infectious causes include urinary tract infection, pneumonia, sinusitis, suppurative thrombophlebitis, catheter-related infections, and Clostridioides difficile–associated diarrhea. Noninfectious causes include deep venous thrombosis, pulmonary embolism, subarachnoid hemorrhage, gout, and fat embolism. Surgical site infections are uncommon within the first 1–3 days except for aggressive pathogens such as group A streptococci or clostridia, which can present early. Atelectasis is frequently blamed but likely coincidental rather than causal. Other serious causes include transplant rejection. Drug-induced fever is most often associated with beta-lactams, antiepileptics, and heparin. Inflammatory states such as acute myocardial infarction, pancreatitis, or acute respiratory distress syndrome may produce fever without infection. Endocrine emergencies such as adrenal insufficiency or thyrotoxicosis may also present with fever.
Diagnosis
Physical Examination
Drug fever lacks specific features and usually develops days after medication exposure; rash and eosinophilia are uncommon. Malignant hyperthermia typically occurs intraoperatively but may be delayed up to 24 hours and is associated with agents such as succinylcholine or volatile anesthetics. Neuroleptic malignant syndrome is associated with antipsychotics, particularly haloperidol. Withdrawal syndromes from alcohol, opioids, barbiturates, or benzodiazepines may cause fever hours to days after admission, and prior substance use history may not be readily available.
Diagnostic Tests and Interpretation
Laboratory Studies
Urinalysis and urine culture are recommended in patients with indwelling catheters longer than 72 hours. Procalcitonin has uncertain value in distinguishing bacterial causes of postoperative fever.
Imaging
Duplex ultrasonography with Doppler should be considered for new extremity swelling suggestive of deep venous thrombosis. Routine chest radiography is not required within the first 72 postoperative hours if fever is the only indication.
Diagnostic Procedures/Other
Wound swab cultures are rarely useful unless there is clear clinical evidence of infection. Suspected deep intraabdominal abscess may require imaging and, if inconclusive, surgical exploration.
Treatment
Medications
Antibiotics are generally not indicated for early postoperative fever without evidence of infection. Critically ill patients or those with hemodynamic instability should receive empiric broad-spectrum antibiotics after thorough evaluation, but therapy should be discontinued after 48 hours if no infectious source is identified. Atelectasis management includes coughing exercises, incentive spirometry, chest physiotherapy, beta-2 agonists, intermittent positive-pressure breathing, and nebulization. Empiric antifungal therapy is not recommended initially.
Ongoing Care and Follow-Up
Drug fever is diagnosed by exclusion when other causes are ruled out. Surgical wounds and invasive device sites must be repeatedly examined for signs of infection.
Complications
Postoperative infections increase morbidity and mortality, may lead to sepsis, impair wound healing, and cause respiratory failure and other serious outcomes.
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Infectious Diseases and Microbiology: Sore Throat
Basics
Description
Sore throat refers to painful inflammation of the pharynx, typically worse with swallowing. Common infectious causes are covered elsewhere; the emphasis here is recognizing distinguishing clinical features and considering noninfectious etiologies.
Approach to the Patient
First assess for airway compromise and decide whether the illness is localized or part of a systemic process, most often viral. Clarify symptom type and duration and ask about hoarseness and fever. History should include sick contacts, oral–genital sexual exposure, recent weight loss, and other features suggesting noninfectious causes such as neoplasms. Findings that strongly support streptococcal pharyngitis include fever, marked tonsillar exudate and enlargement, tender anterior cervical nodes, myalgias, and supportive epidemiology such as age, season, and community colonization prevalence. Conjunctivitis points toward viral illness. When clinical and epidemiologic clues suggest gonococcal pharyngitis or diphtheria, use specific microbiologic techniques and begin appropriate therapy promptly. Differentiate laryngitis, croup, and other hoarseness syndromes from epiglottitis. The main practical distinction is group A streptococcal versus nonstreptococcal pharyngitis, confirmed by throat culture or rapid antigen testing.
Epidemiology
Most pharyngitis is viral, accounting for roughly 90% of adult cases and 70% of pediatric cases. Group A beta-hemolytic Streptococcus is more common in children than adults. Antibiotic prescribing is frequent in adults with pharyngitis. In outbreaks involving rheumatogenic strains, untreated group A streptococcal infection can be followed by acute rheumatic fever in a small but meaningful percentage. Lancefield groups C and G streptococci can cause syndromes similar to group A disease and are often opportunistic or healthcare-associated. Arcanobacterium hemolyticum is seen particularly in adolescents and young adults. Parainfluenza infection is most common in children.
General Prevention
Advise patients with streptococcal pharyngitis to avoid close contact with others, and counsel on safer sex practices to reduce sexually transmitted causes.
Etiology
Acute pharyngitis is most often viral, including rhinovirus, coronavirus, influenza A/B, and parainfluenza, and may involve broader respiratory tract symptoms. Acute laryngitis is usually viral and can be caused by rhinovirus, influenza, parainfluenza, coxsackievirus, adenovirus, or respiratory syncytial virus. Some viruses produce characteristic patterns, including herpangina from coxsackie A, infectious mononucleosis from Epstein–Barr virus or cytomegalovirus, HSV gingivostomatitis, and adenoviral pharyngoconjunctival fever. Primary HSV-1 can cause acute pharyngitis, and HSV-2 can cause similar illness after oral–genital exposure. Acute pharyngitis can occur during primary HIV infection. The key bacterial cause is group A Streptococcus, with additional causes including groups C and G streptococci, Arcanobacterium hemolyticum, Neisseria gonorrhoeae, Corynebacterium diphtheriae, Mycoplasma pneumoniae, and Chlamydophila pneumoniae. Sore throat can also occur with systemic infections such as toxoplasmosis, plague, brucellosis, leptospirosis, secondary syphilis, Yersinia infections, and tularemia. Histoplasma and Blastomyces can cause laryngeal nodules with or without ulceration. Candida can cause sore throat with thrush in immunosuppressed patients or those with mucocutaneous candidiasis. West Nile virus can present as a febrile illness with malaise, headache, myalgias, rash, and occasional pharyngitis. Lemierre syndrome can present with sore throat. Deep neck infections include parapharyngeal abscess from spread of tonsillitis, pharyngitis with adenoid involvement, parotitis, mastoiditis, or periodontal infection, and retropharyngeal abscess from spread, lymphatic seeding, trauma, or cervical osteomyelitis extension. Acute necrotizing pharyngeal infections can cause foul breath, fever, and choking sensation, often associated with ulcerative gingivitis. Ludwig angina arises from dental infection near the third molar and causes rapidly spreading bilateral submandibular and sublingual cellulitis with swelling, pain, trismus, drooling, tongue displacement, and progressive dysphagia and sore throat that can lead to airway obstruction. PFAPA syndrome affects young children and causes periodic high fevers lasting several days with aphthous stomatitis, pharyngitis, and cervical adenitis, recurring at regular short intervals without other symptoms.
Diagnosis
Parapharyngeal space infection typically causes toxic appearance, fever, sore throat, dysphagia, and leukocytosis, with possible neck rigidity or contralateral torticollis; advanced disease can produce dyspnea and stridor. Acute necrotizing pharyngeal infection presents with swollen erythematous ulcerated tonsillar pillars covered by a gray membrane that peels easily and is often accompanied by lymphadenopathy. In infectious mononucleosis, pharyngitis is most prominent in the first two weeks. Herpangina presents with fever, sore throat, myalgias, and vesicles on the soft palate between the uvula and tonsils. Tuberculous laryngitis can cause mucosal hyperemia, thickening, nodules, and ulcerations.
Diagnostic Tests and Interpretation
Laboratory Studies
Throat culture is the reference standard for streptococcal diagnosis but takes 24–72 hours. Rapid antigen tests are highly specific but have variable sensitivity.
Imaging
Retropharyngeal infection may be suggested by lateral neck soft-tissue radiography, while CT or MRI best defines source and extent.
Diagnostic Procedures/Other
In suspected tuberculous laryngitis, biopsy may show granulomas with acid-fast bacilli, with cultures needed for confirmation and susceptibility testing.
Differential Diagnosis
Viral pharyngitis commonly includes sore throat with coryza and cough, an inflamed edematous pharynx, and usually no exudate, though adenovirus and mononucleosis can be exudative. Fever, tender anterior cervical nodes, erythematous pharynx with or without tonsillar enlargement or exudate, and absence of cough support streptococcal pharyngitis in children and adults. Mycoplasma-related sore throat typically occurs in young healthy patients with mild pharyngitis and prominent tracheobronchitis symptoms.
Treatment
Medications
Patients at high risk of complications from streptococcal infection, such as those with prior rheumatic carditis or valvular disease, should receive immediate antibiotics while awaiting culture confirmation. Parapharyngeal space infection management includes airway protection, operative drainage, and intravenous antibiotics targeting streptococci and oral anaerobes, using regimens such as penicillin plus metronidazole, cefoxitin, or ampicillin-sulbactam. For streptococcal pharyngitis, a single intramuscular dose of benzathine penicillin may be slightly more effective than oral penicillin VK and ensures adherence.
Ongoing Care and Follow-Up
Post-viral chronic fatigue syndrome can include fatigue, fever, sore throat, painful lymph nodes, myalgias, arthralgias, sleep disturbance, and headache. Appropriate treatment and monitoring of group A streptococcal infection aims to prevent nonsuppurative complications such as acute rheumatic fever and glomerulonephritis, reduce toxic complications and local suppurative spread, limit transmission, and shorten illness duration. Sore throat can also precede broader constitutional symptoms that culminate in viral encephalitis.
Complications
Peritonsillar abscess can follow untreated streptococcal pharyngitis and presents with unilateral swelling and erythema and uvular deviation. Parapharyngeal infections can lead to airway obstruction, aspiration after intraoral rupture, jugular vein thrombophlebitis with pulmonary emboli, carotid artery erosion, and mediastinitis.
Basics
Description
Sore throat refers to painful inflammation of the pharynx, typically worse with swallowing. Common infectious causes are covered elsewhere; the emphasis here is recognizing distinguishing clinical features and considering noninfectious etiologies.
Approach to the Patient
First assess for airway compromise and decide whether the illness is localized or part of a systemic process, most often viral. Clarify symptom type and duration and ask about hoarseness and fever. History should include sick contacts, oral–genital sexual exposure, recent weight loss, and other features suggesting noninfectious causes such as neoplasms. Findings that strongly support streptococcal pharyngitis include fever, marked tonsillar exudate and enlargement, tender anterior cervical nodes, myalgias, and supportive epidemiology such as age, season, and community colonization prevalence. Conjunctivitis points toward viral illness. When clinical and epidemiologic clues suggest gonococcal pharyngitis or diphtheria, use specific microbiologic techniques and begin appropriate therapy promptly. Differentiate laryngitis, croup, and other hoarseness syndromes from epiglottitis. The main practical distinction is group A streptococcal versus nonstreptococcal pharyngitis, confirmed by throat culture or rapid antigen testing.
Epidemiology
Most pharyngitis is viral, accounting for roughly 90% of adult cases and 70% of pediatric cases. Group A beta-hemolytic Streptococcus is more common in children than adults. Antibiotic prescribing is frequent in adults with pharyngitis. In outbreaks involving rheumatogenic strains, untreated group A streptococcal infection can be followed by acute rheumatic fever in a small but meaningful percentage. Lancefield groups C and G streptococci can cause syndromes similar to group A disease and are often opportunistic or healthcare-associated. Arcanobacterium hemolyticum is seen particularly in adolescents and young adults. Parainfluenza infection is most common in children.
General Prevention
Advise patients with streptococcal pharyngitis to avoid close contact with others, and counsel on safer sex practices to reduce sexually transmitted causes.
Etiology
Acute pharyngitis is most often viral, including rhinovirus, coronavirus, influenza A/B, and parainfluenza, and may involve broader respiratory tract symptoms. Acute laryngitis is usually viral and can be caused by rhinovirus, influenza, parainfluenza, coxsackievirus, adenovirus, or respiratory syncytial virus. Some viruses produce characteristic patterns, including herpangina from coxsackie A, infectious mononucleosis from Epstein–Barr virus or cytomegalovirus, HSV gingivostomatitis, and adenoviral pharyngoconjunctival fever. Primary HSV-1 can cause acute pharyngitis, and HSV-2 can cause similar illness after oral–genital exposure. Acute pharyngitis can occur during primary HIV infection. The key bacterial cause is group A Streptococcus, with additional causes including groups C and G streptococci, Arcanobacterium hemolyticum, Neisseria gonorrhoeae, Corynebacterium diphtheriae, Mycoplasma pneumoniae, and Chlamydophila pneumoniae. Sore throat can also occur with systemic infections such as toxoplasmosis, plague, brucellosis, leptospirosis, secondary syphilis, Yersinia infections, and tularemia. Histoplasma and Blastomyces can cause laryngeal nodules with or without ulceration. Candida can cause sore throat with thrush in immunosuppressed patients or those with mucocutaneous candidiasis. West Nile virus can present as a febrile illness with malaise, headache, myalgias, rash, and occasional pharyngitis. Lemierre syndrome can present with sore throat. Deep neck infections include parapharyngeal abscess from spread of tonsillitis, pharyngitis with adenoid involvement, parotitis, mastoiditis, or periodontal infection, and retropharyngeal abscess from spread, lymphatic seeding, trauma, or cervical osteomyelitis extension. Acute necrotizing pharyngeal infections can cause foul breath, fever, and choking sensation, often associated with ulcerative gingivitis. Ludwig angina arises from dental infection near the third molar and causes rapidly spreading bilateral submandibular and sublingual cellulitis with swelling, pain, trismus, drooling, tongue displacement, and progressive dysphagia and sore throat that can lead to airway obstruction. PFAPA syndrome affects young children and causes periodic high fevers lasting several days with aphthous stomatitis, pharyngitis, and cervical adenitis, recurring at regular short intervals without other symptoms.
Diagnosis
Parapharyngeal space infection typically causes toxic appearance, fever, sore throat, dysphagia, and leukocytosis, with possible neck rigidity or contralateral torticollis; advanced disease can produce dyspnea and stridor. Acute necrotizing pharyngeal infection presents with swollen erythematous ulcerated tonsillar pillars covered by a gray membrane that peels easily and is often accompanied by lymphadenopathy. In infectious mononucleosis, pharyngitis is most prominent in the first two weeks. Herpangina presents with fever, sore throat, myalgias, and vesicles on the soft palate between the uvula and tonsils. Tuberculous laryngitis can cause mucosal hyperemia, thickening, nodules, and ulcerations.
Diagnostic Tests and Interpretation
Laboratory Studies
Throat culture is the reference standard for streptococcal diagnosis but takes 24–72 hours. Rapid antigen tests are highly specific but have variable sensitivity.
Imaging
Retropharyngeal infection may be suggested by lateral neck soft-tissue radiography, while CT or MRI best defines source and extent.
Diagnostic Procedures/Other
In suspected tuberculous laryngitis, biopsy may show granulomas with acid-fast bacilli, with cultures needed for confirmation and susceptibility testing.
Differential Diagnosis
Viral pharyngitis commonly includes sore throat with coryza and cough, an inflamed edematous pharynx, and usually no exudate, though adenovirus and mononucleosis can be exudative. Fever, tender anterior cervical nodes, erythematous pharynx with or without tonsillar enlargement or exudate, and absence of cough support streptococcal pharyngitis in children and adults. Mycoplasma-related sore throat typically occurs in young healthy patients with mild pharyngitis and prominent tracheobronchitis symptoms.
Treatment
Medications
Patients at high risk of complications from streptococcal infection, such as those with prior rheumatic carditis or valvular disease, should receive immediate antibiotics while awaiting culture confirmation. Parapharyngeal space infection management includes airway protection, operative drainage, and intravenous antibiotics targeting streptococci and oral anaerobes, using regimens such as penicillin plus metronidazole, cefoxitin, or ampicillin-sulbactam. For streptococcal pharyngitis, a single intramuscular dose of benzathine penicillin may be slightly more effective than oral penicillin VK and ensures adherence.
Ongoing Care and Follow-Up
Post-viral chronic fatigue syndrome can include fatigue, fever, sore throat, painful lymph nodes, myalgias, arthralgias, sleep disturbance, and headache. Appropriate treatment and monitoring of group A streptococcal infection aims to prevent nonsuppurative complications such as acute rheumatic fever and glomerulonephritis, reduce toxic complications and local suppurative spread, limit transmission, and shorten illness duration. Sore throat can also precede broader constitutional symptoms that culminate in viral encephalitis.
Complications
Peritonsillar abscess can follow untreated streptococcal pharyngitis and presents with unilateral swelling and erythema and uvular deviation. Parapharyngeal infections can lead to airway obstruction, aspiration after intraoral rupture, jugular vein thrombophlebitis with pulmonary emboli, carotid artery erosion, and mediastinitis.
- Published on
Infectious Diseases and Microbiology: Red Eye
Basics
Description
Red eye may result from sight-threatening conditions such as uveitis, endophthalmitis, acute angle-closure glaucoma, or scleritis, which typically produce ciliary injection. More commonly, redness is due to conjunctival hyperemia associated with conjunctivitis, keratitis, dry eye disease, foreign body irritation (including contact lenses), blepharitis, or environmental irritants. Ocular trauma may cause subconjunctival hemorrhage. Not all causes are infectious. Uveitis involves intraocular inflammation and may be anterior, posterior, or pan-uveitis. Endophthalmitis is a severe intraocular infection involving the vitreous cavity. Acute angle-closure glaucoma is an ophthalmic emergency caused by obstruction of aqueous outflow and elevated intraocular pressure. Episcleritis affects superficial scleral tissues, while scleritis is a deeper, more severe inflammatory process that may occur with keratitis or uveitis. Conjunctivitis is the most common cause of red eye and usually includes discharge. Keratitis primarily affects the cornea.
Epidemiology
Primary acute angle closure occurs more frequently in Asian populations than in Caucasians. Incidence rates for conjunctivitis, keratitis, and uveitis vary and are addressed in their respective discussions.
Risk Factors
Risk factors for angle-closure glaucoma include advanced age, hyperopia, cataract, female sex, prior angle closure in the fellow eye, and Asian ethnicity; prophylactic laser iridotomy is often performed in the unaffected eye. Contact lens use increases the risk of bacterial keratitis. Subconjunctival hemorrhage may occur spontaneously or with bleeding disorders, minor trauma, or increased venous pressure from coughing or sneezing. Autoimmune connective tissue disorders are associated with ocular inflammation, and uveitis may be an initial manifestation.
General Prevention
Proper contact lens hygiene reduces infectious and inflammatory complications. Screening with gonioscopy and preventive laser iridotomy can prevent acute angle closure in high-risk individuals.
Pathophysiology
Ciliary injection involves deeper vascular branches and indicates inflammation of the cornea, iris, ciliary body, or sclera. Conjunctival injection is superficial, mobile with the conjunctiva, and improves with topical vasoconstrictors. Acute angle closure usually results from pupillary block, causing pressure differential between the posterior and anterior chambers, forward bowing of the iris, and obstruction of aqueous outflow through the trabecular meshwork.
Etiology
Conjunctivitis, keratitis, uveitis, and endophthalmitis have infectious and noninfectious causes. Acute angle-closure glaucoma and subconjunctival hemorrhage are noninfectious. Episcleritis is usually idiopathic, though immunologic reactions to herpes simplex or varicella zoster may occur. Scleritis is rarely infectious but may result from systemic infections or extension from keratitis; reported pathogens include fungi (Aspergillus, Fusarium), herpes viruses, mycobacteria, Nocardia, Pseudomonas, Proteus (after scleral buckle procedures), syphilis, leprosy, Lyme disease, and tuberculosis.
Commonly Associated Conditions
Endophthalmitis most commonly follows intraocular surgery. Contact lens wear strongly predisposes to bacterial keratitis.
Diagnosis
History
Subconjunctival hemorrhage is unilateral, painless, and vision is unaffected. Conjunctivitis often begins in one eye but is commonly bilateral and features discharge with minimal visual change. Keratitis is usually unilateral and associated with redness, foreign body sensation, tearing, and decreased vision. Uveitis presents with reduced vision, photophobia, and ocular pain. Acute angle-closure glaucoma presents with severe unilateral pain, decreased vision, nausea, and vomiting. Anterior scleritis causes severe pain and tenderness; posterior scleritis may cause significant visual impairment with less obvious redness. Episcleritis resembles conjunctivitis but has mild discomfort and no discharge. Endophthalmitis presents with pain and significant vision loss.
Physical Examination
Slit-lamp examination is essential. Subconjunctival hemorrhage appears as a sharply demarcated red patch under the conjunctiva. Conjunctivitis shows hyperemia, discharge, membranes or pseudomembranes, papillary or follicular reaction, and possibly preauricular lymphadenopathy. Keratitis reveals epithelial defects, stromal opacities, discharge, and anterior chamber inflammation. Anterior uveitis is diagnosed by inflammatory cells in the anterior chamber and keratic precipitates. Acute angle closure presents with a mid-dilated poorly reactive pupil, corneal edema, and elevated intraocular pressure.
Diagnostic Tests and Interpretation
Laboratory Studies
Routine cultures are unnecessary in typical conjunctivitis except in hyperacute cases suggestive of Neisseria gonorrhoeae. Keratitis lesions are sampled for Gram stain and culture.
Imaging
Confocal microscopy assists in diagnosing Acanthamoeba keratitis. Neuroimaging may identify vascular abnormalities such as carotid-cavernous fistulas or arteriovenous malformations associated with red eye.
Diagnostic Procedures/Other
Corneal biopsy may be needed for refractory keratitis. Vitreous sampling during vitrectomy can assist in diagnosing uveitis or endophthalmitis via cytology, culture, and PCR.
Differential Diagnosis
Key distinguishing features include:
Visual acuity is typically preserved in conjunctivitis and subconjunctival hemorrhage but reduced in uveitis, keratitis, and acute angle closure. Discharge is common in conjunctivitis and keratitis but absent in subconjunctival hemorrhage, uveitis, and acute angle closure. Pain is absent in conjunctivitis and subconjunctival hemorrhage but present in uveitis, keratitis, and acute angle closure. Photophobia is typical of uveitis and sometimes keratitis. Pruritus suggests allergic conjunctivitis.
Treatment
Medications
Viral conjunctivitis is managed supportively with artificial tears and cold compresses; topical steroids are rarely required. Mild bacterial conjunctivitis is treated with topical antibiotics such as trimethoprim-polymyxin B or a fluoroquinolone for several days. Bacterial keratitis requires intensive fortified topical antibiotics administered hourly. Acute bacterial endophthalmitis is treated with intravitreal antibiotics targeting gram-positive and gram-negative organisms. Anterior uveitis is treated with topical corticosteroids and cycloplegic agents; infectious causes require specific antimicrobial therapy. Acute angle-closure glaucoma requires urgent reduction of intraocular pressure with systemic acetazolamide, intravenous mannitol, topical beta-blockers, and pilocarpine, followed by laser iridotomy. Episcleritis is treated with artificial tears, topical steroids, and oral NSAIDs. Scleritis often requires systemic corticosteroids and may necessitate immunomodulatory therapy depending on associated systemic disease.
Additional Treatment / Surgery
Laser iridotomy is definitive for angle closure after stabilization. Severe infectious keratitis or scleritis causing tissue thinning may require surgical grafting.
Prognosis
Outcome depends on etiology, ranging from benign in subconjunctival hemorrhage to guarded in endophthalmitis.
Complications
Chronic inflammation may lead to cataract formation, secondary glaucoma, and cystoid macular edema.
Basics
Description
Red eye may result from sight-threatening conditions such as uveitis, endophthalmitis, acute angle-closure glaucoma, or scleritis, which typically produce ciliary injection. More commonly, redness is due to conjunctival hyperemia associated with conjunctivitis, keratitis, dry eye disease, foreign body irritation (including contact lenses), blepharitis, or environmental irritants. Ocular trauma may cause subconjunctival hemorrhage. Not all causes are infectious. Uveitis involves intraocular inflammation and may be anterior, posterior, or pan-uveitis. Endophthalmitis is a severe intraocular infection involving the vitreous cavity. Acute angle-closure glaucoma is an ophthalmic emergency caused by obstruction of aqueous outflow and elevated intraocular pressure. Episcleritis affects superficial scleral tissues, while scleritis is a deeper, more severe inflammatory process that may occur with keratitis or uveitis. Conjunctivitis is the most common cause of red eye and usually includes discharge. Keratitis primarily affects the cornea.
Epidemiology
Primary acute angle closure occurs more frequently in Asian populations than in Caucasians. Incidence rates for conjunctivitis, keratitis, and uveitis vary and are addressed in their respective discussions.
Risk Factors
Risk factors for angle-closure glaucoma include advanced age, hyperopia, cataract, female sex, prior angle closure in the fellow eye, and Asian ethnicity; prophylactic laser iridotomy is often performed in the unaffected eye. Contact lens use increases the risk of bacterial keratitis. Subconjunctival hemorrhage may occur spontaneously or with bleeding disorders, minor trauma, or increased venous pressure from coughing or sneezing. Autoimmune connective tissue disorders are associated with ocular inflammation, and uveitis may be an initial manifestation.
General Prevention
Proper contact lens hygiene reduces infectious and inflammatory complications. Screening with gonioscopy and preventive laser iridotomy can prevent acute angle closure in high-risk individuals.
Pathophysiology
Ciliary injection involves deeper vascular branches and indicates inflammation of the cornea, iris, ciliary body, or sclera. Conjunctival injection is superficial, mobile with the conjunctiva, and improves with topical vasoconstrictors. Acute angle closure usually results from pupillary block, causing pressure differential between the posterior and anterior chambers, forward bowing of the iris, and obstruction of aqueous outflow through the trabecular meshwork.
Etiology
Conjunctivitis, keratitis, uveitis, and endophthalmitis have infectious and noninfectious causes. Acute angle-closure glaucoma and subconjunctival hemorrhage are noninfectious. Episcleritis is usually idiopathic, though immunologic reactions to herpes simplex or varicella zoster may occur. Scleritis is rarely infectious but may result from systemic infections or extension from keratitis; reported pathogens include fungi (Aspergillus, Fusarium), herpes viruses, mycobacteria, Nocardia, Pseudomonas, Proteus (after scleral buckle procedures), syphilis, leprosy, Lyme disease, and tuberculosis.
Commonly Associated Conditions
Endophthalmitis most commonly follows intraocular surgery. Contact lens wear strongly predisposes to bacterial keratitis.
Diagnosis
History
Subconjunctival hemorrhage is unilateral, painless, and vision is unaffected. Conjunctivitis often begins in one eye but is commonly bilateral and features discharge with minimal visual change. Keratitis is usually unilateral and associated with redness, foreign body sensation, tearing, and decreased vision. Uveitis presents with reduced vision, photophobia, and ocular pain. Acute angle-closure glaucoma presents with severe unilateral pain, decreased vision, nausea, and vomiting. Anterior scleritis causes severe pain and tenderness; posterior scleritis may cause significant visual impairment with less obvious redness. Episcleritis resembles conjunctivitis but has mild discomfort and no discharge. Endophthalmitis presents with pain and significant vision loss.
Physical Examination
Slit-lamp examination is essential. Subconjunctival hemorrhage appears as a sharply demarcated red patch under the conjunctiva. Conjunctivitis shows hyperemia, discharge, membranes or pseudomembranes, papillary or follicular reaction, and possibly preauricular lymphadenopathy. Keratitis reveals epithelial defects, stromal opacities, discharge, and anterior chamber inflammation. Anterior uveitis is diagnosed by inflammatory cells in the anterior chamber and keratic precipitates. Acute angle closure presents with a mid-dilated poorly reactive pupil, corneal edema, and elevated intraocular pressure.
Diagnostic Tests and Interpretation
Laboratory Studies
Routine cultures are unnecessary in typical conjunctivitis except in hyperacute cases suggestive of Neisseria gonorrhoeae. Keratitis lesions are sampled for Gram stain and culture.
Imaging
Confocal microscopy assists in diagnosing Acanthamoeba keratitis. Neuroimaging may identify vascular abnormalities such as carotid-cavernous fistulas or arteriovenous malformations associated with red eye.
Diagnostic Procedures/Other
Corneal biopsy may be needed for refractory keratitis. Vitreous sampling during vitrectomy can assist in diagnosing uveitis or endophthalmitis via cytology, culture, and PCR.
Differential Diagnosis
Key distinguishing features include:
Visual acuity is typically preserved in conjunctivitis and subconjunctival hemorrhage but reduced in uveitis, keratitis, and acute angle closure. Discharge is common in conjunctivitis and keratitis but absent in subconjunctival hemorrhage, uveitis, and acute angle closure. Pain is absent in conjunctivitis and subconjunctival hemorrhage but present in uveitis, keratitis, and acute angle closure. Photophobia is typical of uveitis and sometimes keratitis. Pruritus suggests allergic conjunctivitis.
Treatment
Medications
Viral conjunctivitis is managed supportively with artificial tears and cold compresses; topical steroids are rarely required. Mild bacterial conjunctivitis is treated with topical antibiotics such as trimethoprim-polymyxin B or a fluoroquinolone for several days. Bacterial keratitis requires intensive fortified topical antibiotics administered hourly. Acute bacterial endophthalmitis is treated with intravitreal antibiotics targeting gram-positive and gram-negative organisms. Anterior uveitis is treated with topical corticosteroids and cycloplegic agents; infectious causes require specific antimicrobial therapy. Acute angle-closure glaucoma requires urgent reduction of intraocular pressure with systemic acetazolamide, intravenous mannitol, topical beta-blockers, and pilocarpine, followed by laser iridotomy. Episcleritis is treated with artificial tears, topical steroids, and oral NSAIDs. Scleritis often requires systemic corticosteroids and may necessitate immunomodulatory therapy depending on associated systemic disease.
Additional Treatment / Surgery
Laser iridotomy is definitive for angle closure after stabilization. Severe infectious keratitis or scleritis causing tissue thinning may require surgical grafting.
Prognosis
Outcome depends on etiology, ranging from benign in subconjunctival hemorrhage to guarded in endophthalmitis.
Complications
Chronic inflammation may lead to cataract formation, secondary glaucoma, and cystoid macular edema.
- Published on
Infectious Diseases and Microbiology: Rash and Fever
Basics
Description
Rash refers to temporary skin eruptions that accompany localized or generalized infectious diseases. This topic emphasizes the differential diagnosis and early recognition of potentially life-threatening generalized eruptions.
Approach to the Patient
A detailed history should assess immune status, full medication list, travel history, immunization record, exposure to pets or animals, arthropod bites, cardiac abnormalities, prosthetic material, recent contact with ill persons, and possible sexually transmitted infections. Clarify the initial site of rash, pruritus or pain, and speed and direction of spread. Document associated symptoms including prodrome, fever, and itching. Physical examination should define lesion morphology (macules, papules, vesicles, plaques, nodules), configuration (annular, target), arrangement, and distribution (central versus peripheral).
Epidemiology
Infectious mononucleosis may present with generalized maculopapular, petechial, or urticarial rash, often after antibiotic exposure. Approximately one-fifth of erythema infectiosum cases occur in adults, though rash may resemble rubella. Up to half of patients with primary HIV infection develop a maculopapular rash within days of fever onset, typically involving the upper trunk and face. Rubella has been declared eliminated in the United States. Cutaneous leishmaniasis affects up to 1.5 million individuals annually worldwide. Rash occurs in about half of dengue cases. In early Lyme disease, erythema migrans develops at the tick bite site in most patients.
General Prevention
Women of reproductive age should be immunized against rubella. Pregnant women diagnosed with early rubella infection should receive counseling regarding fetal risks and management options.
Etiology
Common adult rash patterns include centrally distributed maculopapular eruptions (such as dengue, infectious mononucleosis, leptospirosis, Lyme disease, primary HIV infection, rubella, measles, typhoid fever, systemic lupus erythematosus, and various rickettsial infections), peripheral eruptions (including bacterial endocarditis, chronic meningococcemia, disseminated gonococcal infection, erythema multiforme, Rocky Mountain spotted fever, and secondary syphilis), confluent desquamative erythemas (graft-versus-host disease, Kawasaki disease, scarlet fever, staphylococcal and streptococcal toxic shock syndromes), vesiculobullous eruptions (disseminated Vibrio vulnificus infection, ecthyma gangrenosum, rickettsialpox), nodular eruptions (disseminated fungal or mycobacterial infections, erythema nodosum, Sweet syndrome), and purpuric eruptions (acute or chronic meningococcemia, disseminated gonococcal infection, enteroviral petechiae, Rocky Mountain spotted fever, thrombotic thrombocytopenic purpura).
Diagnosis
Rocky Mountain spotted fever (RMSF) typically presents with rash around day four of illness, beginning as blanching macules that may progress to purpura and necrosis; genital involvement may be suggestive. Rash may be absent in some cases and is associated with worse prognosis. Meningococcal disease often produces petechiae that evolve into palpable purpura, though other lesion types can occur. Fulminant meningococcemia with disseminated intravascular coagulation constitutes Waterhouse–Friderichsen syndrome. Cutaneous findings in infective endocarditis include vascular phenomena such as petechiae, splinter hemorrhages, and Janeway lesions, and immunologic signs such as Osler nodes and Roth spots. Lyme disease progresses from erythema migrans to neurologic or cardiac involvement and later arthritis or chronic skin changes. Ehrlichiosis often features headache and high fever, with variable rash. Staphylococcal toxic shock syndrome presents with diffuse erythematous rash resembling sunburn, followed by desquamation within two weeks, along with conjunctival injection, mucosal hyperemia, and strawberry tongue. Streptococcal toxic shock syndrome often arises from invasive soft-tissue infection. Dengue rash is typically maculopapular and appears within several days of illness onset.
Diagnostic Tests and Interpretation
Laboratory Studies
Gram stain and culture of pustular or bullous lesions should be performed when infection is suspected. Antibodies to Rickettsia rickettsii become detectable after the first week of RMSF. Meningococcal disease is confirmed by Gram stain and culture of blood or cerebrospinal fluid; skin biopsy may assist. Streptococcal toxic shock syndrome more commonly involves bacteremia than staphylococcal toxic shock syndrome.
Diagnostic Procedures/Other
Skin biopsy with culture and histopathologic examination may establish diagnosis in unclear cases.
Differential Diagnosis
Desquamating erythroderma is more common in staphylococcal than streptococcal toxic shock syndrome. Gonococcemia frequently causes a pustular hemorrhagic rash but may present with diverse lesion types.
Treatment
Management depends on the underlying etiology and may require urgent antimicrobial or supportive therapy.
Ongoing Care and Follow-Up
Serial documentation of rash progression with photography or ink demarcation can assist monitoring.
Complications
Untreated Rocky Mountain spotted fever carries high mortality, underscoring the importance of early recognition and treatment.
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Basics
Description
Rash refers to temporary skin eruptions that accompany localized or generalized infectious diseases. This topic emphasizes the differential diagnosis and early recognition of potentially life-threatening generalized eruptions.
Approach to the Patient
A detailed history should assess immune status, full medication list, travel history, immunization record, exposure to pets or animals, arthropod bites, cardiac abnormalities, prosthetic material, recent contact with ill persons, and possible sexually transmitted infections. Clarify the initial site of rash, pruritus or pain, and speed and direction of spread. Document associated symptoms including prodrome, fever, and itching. Physical examination should define lesion morphology (macules, papules, vesicles, plaques, nodules), configuration (annular, target), arrangement, and distribution (central versus peripheral).
Epidemiology
Infectious mononucleosis may present with generalized maculopapular, petechial, or urticarial rash, often after antibiotic exposure. Approximately one-fifth of erythema infectiosum cases occur in adults, though rash may resemble rubella. Up to half of patients with primary HIV infection develop a maculopapular rash within days of fever onset, typically involving the upper trunk and face. Rubella has been declared eliminated in the United States. Cutaneous leishmaniasis affects up to 1.5 million individuals annually worldwide. Rash occurs in about half of dengue cases. In early Lyme disease, erythema migrans develops at the tick bite site in most patients.
General Prevention
Women of reproductive age should be immunized against rubella. Pregnant women diagnosed with early rubella infection should receive counseling regarding fetal risks and management options.
Etiology
Common adult rash patterns include centrally distributed maculopapular eruptions (such as dengue, infectious mononucleosis, leptospirosis, Lyme disease, primary HIV infection, rubella, measles, typhoid fever, systemic lupus erythematosus, and various rickettsial infections), peripheral eruptions (including bacterial endocarditis, chronic meningococcemia, disseminated gonococcal infection, erythema multiforme, Rocky Mountain spotted fever, and secondary syphilis), confluent desquamative erythemas (graft-versus-host disease, Kawasaki disease, scarlet fever, staphylococcal and streptococcal toxic shock syndromes), vesiculobullous eruptions (disseminated Vibrio vulnificus infection, ecthyma gangrenosum, rickettsialpox), nodular eruptions (disseminated fungal or mycobacterial infections, erythema nodosum, Sweet syndrome), and purpuric eruptions (acute or chronic meningococcemia, disseminated gonococcal infection, enteroviral petechiae, Rocky Mountain spotted fever, thrombotic thrombocytopenic purpura).
Diagnosis
Rocky Mountain spotted fever (RMSF) typically presents with rash around day four of illness, beginning as blanching macules that may progress to purpura and necrosis; genital involvement may be suggestive. Rash may be absent in some cases and is associated with worse prognosis. Meningococcal disease often produces petechiae that evolve into palpable purpura, though other lesion types can occur. Fulminant meningococcemia with disseminated intravascular coagulation constitutes Waterhouse–Friderichsen syndrome. Cutaneous findings in infective endocarditis include vascular phenomena such as petechiae, splinter hemorrhages, and Janeway lesions, and immunologic signs such as Osler nodes and Roth spots. Lyme disease progresses from erythema migrans to neurologic or cardiac involvement and later arthritis or chronic skin changes. Ehrlichiosis often features headache and high fever, with variable rash. Staphylococcal toxic shock syndrome presents with diffuse erythematous rash resembling sunburn, followed by desquamation within two weeks, along with conjunctival injection, mucosal hyperemia, and strawberry tongue. Streptococcal toxic shock syndrome often arises from invasive soft-tissue infection. Dengue rash is typically maculopapular and appears within several days of illness onset.
Diagnostic Tests and Interpretation
Laboratory Studies
Gram stain and culture of pustular or bullous lesions should be performed when infection is suspected. Antibodies to Rickettsia rickettsii become detectable after the first week of RMSF. Meningococcal disease is confirmed by Gram stain and culture of blood or cerebrospinal fluid; skin biopsy may assist. Streptococcal toxic shock syndrome more commonly involves bacteremia than staphylococcal toxic shock syndrome.
Diagnostic Procedures/Other
Skin biopsy with culture and histopathologic examination may establish diagnosis in unclear cases.
Differential Diagnosis
Desquamating erythroderma is more common in staphylococcal than streptococcal toxic shock syndrome. Gonococcemia frequently causes a pustular hemorrhagic rash but may present with diverse lesion types.
Treatment
Management depends on the underlying etiology and may require urgent antimicrobial or supportive therapy.
Ongoing Care and Follow-Up
Serial documentation of rash progression with photography or ink demarcation can assist monitoring.
Complications
Untreated Rocky Mountain spotted fever carries high mortality, underscoring the importance of early recognition and treatment.
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