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Infectious Disease and Microbiology – Conjunctivitis
Conjunctivitis is an inflammatory reaction of the conjunctiva characterized by hyperemia (red eye) and discharge. It may be acute or chronic and can be infectious or noninfectious. Important infectious forms include trachoma, caused by Chlamydia trachomatis serotypes A–C; inclusion conjunctivitis, caused by sexually transmitted C. trachomatis serotypes D–K; and ophthalmia neonatorum, an acute mucopurulent conjunctivitis occurring within the first month of life.
The incidence of infectious conjunctivitis in primary care settings is significant. In the Netherlands, rates as high as 13.9 cases per 1000 person-years have been reported. In the United States, Chlamydia species are the most common cause of ophthalmia neonatorum (approximately 6.2 per 1000 live births). The incidence of gonococcal ophthalmia neonatorum has decreased dramatically due to prophylaxis at birth. Trachoma remains a major cause of preventable blindness in parts of northern and sub-Saharan Africa, the Middle East, and Asia. Although global prevalence has declined with improved hygiene, millions worldwide remain visually impaired from trachoma.
Risk factors for trachoma include poverty, overcrowding, poor sanitation, and limited access to clean water and healthcare. Transmission occurs via direct contact (hands, towels) and flies. Viral conjunctivitis is often associated with upper respiratory infections or contact with infected individuals. Adult inclusion conjunctivitis may be associated with a history of urethritis, vaginitis, or cervicitis.
Bacterial conjunctivitis develops when normal ocular defense mechanisms are disrupted, such as in tear film abnormalities, ocular surface damage, or systemic immunosuppression. Infectious causes include bacteria (Staphylococcus, Streptococcus, Haemophilus, Neisseria gonorrhoeae, Chlamydia trachomatis, Treponema pallidum, Bartonella henselae), viruses (adenovirus, enterovirus, HSV, VZV), fungi, and parasites. Viral conjunctivitis may present as epidemic keratoconjunctivitis (EKC), pharyngoconjunctival fever, acute hemorrhagic conjunctivitis, or in association with systemic viral illnesses.
Patients typically report tearing, mucous or mucopurulent discharge, eyelid swelling, redness, and foreign-body sensation. Pain is usually minimal and visual acuity only slightly reduced. Gonococcal conjunctivitis presents rapidly with profuse purulent discharge in sexually active adults or neonates. Viral EKC often begins in one eye and spreads to the other, with watery discharge and photophobia.
On examination, conjunctivitis presents with hyperemia, eyelid edema, and discharge. Viral and chlamydial conjunctivitis commonly show a follicular reaction, whereas bacterial and allergic conjunctivitis typically show a papillary reaction. Bacterial infections produce mucopurulent discharge; gonococcal infection produces thick yellow-green exudate. Preauricular lymphadenopathy is common in viral, HSV, gonococcal, and inclusion conjunctivitis. Trachoma leads to chronic follicular inflammation followed by scarring, entropion, trichiasis, and corneal damage. Parinaud oculoglandular syndrome, associated with Bartonella henselae, presents with granulomatous conjunctivitis and regional lymphadenopathy.
Diagnosis is usually clinical. Microbiologic testing is reserved for hyperacute, severe, chronic, or atypical cases. Gram stain may reveal gram-negative intracellular diplococci in gonococcal infection. Chlamydial infection may be diagnosed by Giemsa staining, culture, ELISA, immunofluorescence, or PCR. Viral pathogens can be identified by PCR. Imaging has no role in routine evaluation.
The differential diagnosis includes dry eye disease, allergic conjunctivitis, Stevens–Johnson syndrome, ocular cicatricial pemphigoid, drug-induced conjunctivitis, tumors, and graft-versus-host disease. In neonates, incubation time helps differentiate gonococcal (1–3 days) from chlamydial (5–14 days) conjunctivitis.
Treatment depends on etiology. Viral conjunctivitis generally requires supportive care with artificial tears and cold compresses. Topical steroids may be used cautiously for membranes or pseudomembranes, but are contraindicated in HSV infection, which requires topical antivirals such as trifluridine. Mild bacterial conjunctivitis is treated empirically with topical broad-spectrum antibiotics such as trimethoprim–polymyxin B or fluoroquinolones for 5–7 days. Haemophilus influenzae infections may require oral amoxicillin–clavulanate if systemic involvement is suspected.
Gonococcal conjunctivitis requires systemic ceftriaxone, with additional topical therapy and coverage for possible chlamydial coinfection using oral azithromycin. Adult inclusion conjunctivitis is treated with oral azithromycin and topical erythromycin or tetracycline ointment. Trachoma is treated with single-dose oral azithromycin and prolonged topical antibiotic therapy. Ophthalmia neonatorum requires systemic treatment based on the organism: ceftriaxone for gonococcal infection, oral erythromycin for chlamydial infection, and intravenous acyclovir for HSV infection.
Most cases of infectious conjunctivitis resolve within three weeks. Exceptions include untreated chlamydial infection, which may become chronic. Trachoma can lead to scarring, entropion, trichiasis, and corneal opacity, resulting in blindness. Viral EKC may cause subepithelial corneal infiltrates requiring prolonged steroid therapy. Neonates are at risk for systemic complications such as sepsis, meningitis, or pneumonia depending on the causative organism.
Preventive measures include hand hygiene, avoidance of sharing personal items, neonatal prophylactic ointment after birth, and treatment of sexual partners in chlamydial conjunctivitis. Public health interventions have significantly reduced the global burden of trachoma, though it remains an important cause of preventable blindness in endemic regions.
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Infectious Disease and Microbiology – Dengue
Dengue is a mosquito-borne viral illness that causes a severe flu-like disease and, in some cases, progresses to life-threatening dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS), with a fatality rate of approximately 1–5% in severe cases. It is caused by the dengue virus, a single-stranded RNA virus of the Flaviviridae family, with four antigenically distinct serotypes (types 1–4). Humans and nonhuman primates serve as reservoirs. Transmission occurs through the bite of infected Aedes aegypti and Aedes albopictus, which are predominantly day-biting mosquitoes.
Globally, about 2.5 billion people—nearly two-fifths of the world’s population—are at risk of infection. An estimated 50–100 million infections occur annually, including approximately 500,000 cases of DHF and hundreds of thousands of deaths worldwide. Transmission increases during the rainy season due to mosquito breeding in stagnant water. Dengue is endemic in around 100 countries across Asia, the Pacific, the Americas, Africa, and the Caribbean, primarily in tropical and subtropical urban and suburban areas.
The principal risk factor is travel to or residence in endemic regions. No genetic predisposition has been clearly identified. Prevention focuses on avoiding mosquito bites and vector control. Measures include using insect repellents containing at least 30% DEET, wearing long-sleeved clothing (preferably treated with permethrin), and eliminating mosquito breeding sites such as stagnant water. Indoor insecticide use and larvicidal agents may reduce mosquito populations. Bed nets are of limited value because Aedes mosquitoes bite during the daytime.
After inoculation, the incubation period ranges from 3 to 14 days, most commonly 4–7 days. The virus initially replicates in dendritic cells and then spreads to reticuloendothelial cells, hepatocytes, and endothelial cells. Immune mediators contribute to the acute febrile illness, which typically lasts 5–7 days, with full recovery within 7–10 days in uncomplicated cases. Prior infection with a different serotype increases the risk of DHF and DSS due to immune-mediated mechanisms.
DHF and DSS usually develop between days 3 and 7 of illness, often at the end of the febrile phase. Increased capillary permeability leads to plasma leakage, hemoconcentration, pleural effusions, and ascites. Thrombocytopenia, capillary fragility, and disseminated intravascular coagulation (DIC) can result in hemorrhage ranging from petechiae to life-threatening gastrointestinal bleeding. Liver involvement may cause hepatitis and coagulopathy, which can be fatal in severe cases. Mother-to-child transmission has been documented.
Clinically, patients present with fever, headache, chills, myalgias, bone pain, rash, nausea, vomiting, abdominal pain, and anorexia. Cutaneous hyperesthesia and changes in taste may occur. Hemorrhagic manifestations include bruising, epistaxis, gum bleeding, menorrhagia, and gastrointestinal bleeding. A careful travel history is essential.
On physical examination, fever is common. Rash may appear in two phases: an initial generalized blanching macular rash followed by a morbilliform maculopapular rash that typically spares the palms and soles. Conjunctival and pharyngeal injection are frequent findings. Signs of shock—tachycardia, hypotension, and delayed capillary refill—indicate severe disease. Hepatomegaly, lymphadenopathy, mucosal bleeding, and altered mental status (suggesting encephalopathy or intracranial hemorrhage) may also be present.
Laboratory evaluation often reveals leukopenia, lymphopenia, elevated hematocrit (reflecting hemoconcentration), and thrombocytopenia. Liver transaminases are commonly elevated, and albumin may be low. Electrolyte disturbances such as hyponatremia and metabolic acidosis may occur. Coagulation studies may show prolonged PT and APTT, low fibrinogen, and elevated fibrin degradation products in DIC. Serologic testing (ELISA for IgM and IgG) is commonly used for diagnosis. Imaging may demonstrate pleural or pericardial effusions and ascites. Head CT is indicated in patients with altered consciousness.
The differential diagnosis includes malaria, yellow fever, rickettsial infections, leptospirosis, typhoid fever, viral hepatitis, meningitis, bacterial sepsis, and other viral illnesses such as influenza or chikungunya.
There is no specific antiviral treatment for dengue, DHF, or DSS. Management is supportive. Aspirin and nonsteroidal anti-inflammatory drugs should be avoided due to bleeding risk. Adequate analgesia, antipyretics (such as acetaminophen), and careful fluid management are essential. In severe cases, aggressive fluid resuscitation using isotonic crystalloids or colloids is required to maintain adequate blood pressure and organ perfusion. Advanced life support protocols should be followed in patients with shock. Blood products may be necessary in cases of severe hemorrhage. Close monitoring of fluid balance, urine output, electrolytes, and coagulation status is critical.
Hospital admission is indicated for patients with hemodynamic instability, DHF, DSS, or significant bleeding. Intensive care is required for hypotension, DIC, or organ failure. Discharge is appropriate once the patient is hemodynamically stable and has recovered clinically.
Prognosis is generally excellent for uncomplicated dengue fever, with most patients recovering fully. Those who survive the critical phase of DHF or DSS usually recover without long-term sequelae. However, complications may include neurological manifestations (encephalopathy, seizures, Guillain–Barré syndrome, transverse myelitis), myocarditis, and liver failure. Cases should be reported to public health authorities, and patients should be informed that infection with a different serotype in the future increases the risk of severe disease.
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Infectious Disease and Microbiology – Cystitis
Cystitis is a lower urinary tract infection (UTI) involving the bladder and occurs in both women and men. It is one of the most common bacterial infections encountered in clinical practice. In the United States, approximately 7 million cases of UTI occur annually. About one-third of women up to 24 years of age will experience at least one episode requiring antibiotic treatment. Furthermore, nearly half of women whose uncomplicated UTIs resolve spontaneously will develop a recurrence within one year. Cystitis is significantly more prevalent in young women than in young men (approximately 20% vs. 0.5% between ages 16–35 years).
Risk factors vary by population. In premenopausal women, risk factors include prior UTI, congenital urinary tract abnormalities, frequent or recent sexual activity, use of spermicides, diaphragm contraception, increasing parity, diabetes mellitus, pregnancy, obesity, neurologic disease, and conditions requiring indwelling or repetitive bladder catheterization. In postmenopausal women, vaginal atrophy, incomplete bladder emptying, pelvic organ prolapse (rectocele, cystocele, urethrocele, uterovaginal prolapse), diabetes, and prior UTIs increase risk. In men, prostatic hypertrophy, urethral obstruction, catheterization, urinary incontinence, and prior urologic surgery are important risk factors.
The most common etiologic agent is Escherichia coli, responsible for more than 80% of cases. Other Enterobacteriaceae include Proteus mirabilis, Klebsiella pneumoniae, Enterobacter species, Citrobacter species, Serratia species, Salmonella species, and Morganella morganii. Non-Enterobacteriaceae such as Pseudomonas aeruginosa may also be involved, particularly in healthcare-associated infections. Among gram-positive organisms, Staphylococcus saprophyticus is a notable cause, especially in young sexually active women. The emergence of extended-spectrum β-lactamase (ESBL)-producing E. coli and other resistant uropathogens is a growing concern in both community and hospital settings.
Clinically, patients typically present with dysuria, urinary frequency, urgency, abrupt onset of symptoms, and sometimes turbid, foul-smelling, or bloody urine. Suprapubic tenderness may be present, and approximately 10% report low back discomfort. Children may present with nonspecific symptoms such as fever, vomiting, or diarrhea. Elderly patients often exhibit minimal or atypical symptoms.
Physical examination may reveal suprapubic tenderness but is otherwise often unremarkable. Diagnosis is supported by laboratory evaluation. Urinary dipstick testing may detect leukocyte esterase and nitrites. Urine microscopy can demonstrate pyuria and bacteriuria. Urine culture confirms the diagnosis and guides antimicrobial therapy. Pregnancy testing should be considered in women of childbearing age. Imaging is generally unnecessary in uncomplicated cases but ultrasonography may be indicated in men, in women who fail to respond to therapy, or in cases of recurrent infection not clearly related to sexual activity.
The differential diagnosis includes infectious conditions such as pyelonephritis (upper UTI), urethritis, vaginitis, and asymptomatic bacteriuria, as well as noninfectious causes including interstitial cystitis, urolithiasis, bladder tumor, and chronic prostatitis or chronic pelvic pain syndrome.
Acute uncomplicated cystitis is treated with short-course antimicrobial therapy. Common regimens include trimethoprim-sulfamethoxazole for three days, trimethoprim alone for three days, fluoroquinolones such as ciprofloxacin or levofloxacin for three days, fosfomycin as a single oral dose, or nitrofurantoin for five to seven days. Selection should be guided by local resistance patterns. In pregnancy, amoxicillin, nitrofurantoin (avoided near term due to risk of neonatal hemolysis), cefpodoxime, or fosfomycin may be used. Recurrent cystitis may be managed with continuous low-dose prophylaxis using agents such as trimethoprim, trimethoprim-sulfamethoxazole, nitrofurantoin, or fluoroquinolones, though this strategy must be individualized due to increasing antimicrobial resistance.
Complementary approaches have been studied. Certain probiotics (e.g., Lactobacillus strains) may reduce recurrence rates. Cranberry products have been suggested to reduce bacterial adherence and may modestly lower recurrence in women with recurrent UTIs. Methenamine salts may be beneficial in short-term prophylaxis in patients without structural urinary abnormalities. Phenazopyridine may relieve dysuria but does not treat infection and carries potential adverse effects such as hemolytic anemia.
The prognosis for acute uncomplicated cystitis is excellent with appropriate antibiotic therapy. However, recurrent episodes are common, especially in patients with underlying risk factors. Complications may include urethritis, progression to pyelonephritis, and psychological distress associated with recurrent infection. Preventive measures include good hygiene, avoidance of spermicides and diaphragms, careful monitoring during pregnancy, and glycemic control in patients with diabetes.
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Infectious Disease and Microbiology – Creutzfeldt–Jakob Disease
Creutzfeldt–Jakob disease (CJD) is a transmissible spongiform encephalopathy, a group of chronic, progressive, and invariably fatal neurodegenerative disorders affecting humans and animals. Animal forms include scrapie in sheep and bovine spongiform encephalopathy (BSE) in cattle. Human prion diseases include CJD, kuru, Gerstmann–Sträussler–Scheinker syndrome, and fatal familial insomnia. CJD is the most common human prion disease and is characterized by rapidly progressive dementia, myoclonus, and motor dysfunction. It occurs in sporadic, familial, iatrogenic, and variant forms, with sporadic CJD (sCJD) accounting for approximately 85% of cases.
The incidence of sporadic CJD is about 1 case per million people per year, typically affecting individuals between 50 and 60 years of age. Familial cases follow an autosomal dominant inheritance pattern and are linked to mutations in the PRNP gene. Higher frequencies of familial CJD have been reported in certain regions, including North Africa, the Middle East, Italy, and Slovakia. Iatrogenic transmission has occurred through corneal transplantation, dural grafts, contaminated neurosurgical instruments, stereotactic electrodes, and cadaveric human growth hormone or gonadotropin therapy. Variant CJD (vCJD), first identified in 1996 during the BSE outbreak in the United Kingdom, represents animal-to-human transmission. A small number of cases have been documented in the United States.
The pathophysiology involves accumulation of abnormal misfolded prion protein (PrPSc), derived from the normal cellular prion protein encoded by PRNP. These abnormal proteins aggregate in neuronal tissue, leading to neuronal loss, gliosis, and the characteristic spongiform changes—small vacuoles within the neuropil. Inflammation is notably absent. Pathologic changes are most prominent in the cerebral cortex but may also involve basal ganglia, cerebellum, and thalamus. Prion plaques and rods on electron microscopy are pathognomonic.
Clinically, CJD presents with rapidly progressive dementia, myoclonus (present in more than 90% of patients), pyramidal and extrapyramidal signs, and cerebellar dysfunction. Early features include cognitive slowing, impaired concentration, memory loss, mood changes, emotional lability, and hallucinations. As the disease progresses, patients may develop tremor, choreoathetosis, rigidity, hypokinesia, hyperreflexia, spasticity, and extensor plantar responses. Autonomic and endocrine disturbances may occur in certain prion syndromes such as fatal familial insomnia.
Variant CJD typically affects younger patients (19–41 years) and presents initially with behavioral and psychiatric symptoms, followed by ataxia, myoclonus, and dementia. Disease progression leads to death within 7–23 months. Kuru, historically described in Papua New Guinea, is characterized by tremors, ataxia, and later dementia, with incubation periods that may extend up to 50 years.
Definitive diagnosis requires histopathologic examination of brain tissue. Cerebrospinal fluid (CSF) is typically unremarkable, though mild protein elevation may occur. Detection of 14-3-3 protein in CSF may support the diagnosis, but sensitivity and specificity range from 60–90%, and elevations can occur in other neurologic disorders. Genetic testing can identify PRNP mutations in familial cases. Serum S100 protein levels may be elevated. EEG in sporadic CJD often shows periodic sharp-wave complexes, with sensitivity around 64% and specificity 91%, though this pattern is not typical in variant or familial forms. MRI may reveal hyperintense signals in the striatum or other deep brain structures, often disproportionate to visible cortical atrophy. In variant CJD, periodic EEG findings are usually absent.
The differential diagnosis of rapidly progressive dementia with myoclonus includes Alzheimer disease, frontotemporal dementia, Lewy body dementia, HIV-associated dementia, neurosyphilis, tuberculous meningitis, Whipple disease, progressive multifocal leukoencephalopathy, lymphoma, metabolic disorders, autoimmune encephalitis, and paraneoplastic syndromes.
There is currently no effective treatment. CJD is uniformly fatal. Various agents, including amantadine, flupirtine, chlorpromazine, and other experimental therapies targeting prion protein aggregation, have been studied without demonstrated survival benefit. Management is supportive.
Preventive measures in the United States include strict regulations to prevent BSE introduction, control of high-risk bovine materials in the food supply, and adherence to infection control guidelines in medical procedures. The overall risk of transmission is considered minimal under current public health measures.
Prognosis is poor, with progressive neurologic decline leading to death, often within one year of symptom onset in sporadic cases. Serial imaging may demonstrate rapid brain atrophy and ventricular enlargement as the disease advances.
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Infectious Disease and Microbiology – Cryptococcal Infections
Cryptococcal infections are caused by encapsulated yeasts of the genus Cryptococcus. Although more than 50 species exist, the two most clinically important are Cryptococcus neoformans, which primarily affects immunocompromised individuals, and Cryptococcus gattii, which can also infect immunocompetent hosts. These organisms possess a thick polysaccharide capsule that is a major virulence factor. Infection occurs through inhalation of airborne yeast spores into the lungs. While pulmonary disease may remain localized, hematogenous dissemination can occur, particularly in patients with impaired cell-mediated immunity, with a strong predilection for the central nervous system (CNS). Other sites of dissemination include the skin, bones, prostate, and eyes.
In the United States, C. neoformans is more common and is associated with environments contaminated by pigeon droppings, although direct transmission from pigeons to humans has not been documented. C. gattii has traditionally been found in tropical and subtropical regions, particularly around eucalyptus trees, but has emerged in North America, especially in the Pacific Northwest and British Columbia. Respiratory transmission between humans has not been reported. Rare cases of human-to-human transmission have occurred through organ transplantation. Among individuals with HIV infection, the incidence of cryptococcal disease has declined significantly since the widespread use of antiretroviral therapy. In solid-organ transplant recipients, Cryptococcus is the third most common invasive fungal infection and accounts for a substantial proportion of cases in non-HIV patients.
Major risk factors for cryptococcal infection include AIDS (especially in patients with CD4 counts below 100 cells/μL), hematologic malignancies, solid-organ transplantation, and the use of immunosuppressive medications such as glucocorticoids, cyclosporine, and tacrolimus. Additional predisposing conditions include sarcoidosis, splenectomy, chronic obstructive pulmonary disease, diabetes mellitus, and autoimmune disorders such as lupus and rheumatoid arthritis.
After inhalation, yeast organisms deposit in the alveoli. In immunocompetent individuals, infection may remain localized or asymptomatic. In patients with impaired T-cell–mediated immunity, dissemination is more likely. Pulmonary infection represents primary disease, whereas meningitis, skin lesions, or involvement of other organs reflects disseminated infection. The organism’s tropism for the CNS results in cryptococcal meningitis, the most severe and common manifestation of disseminated disease.
Pulmonary cryptococcosis may range from asymptomatic infection to symptomatic pneumonia characterized by cough, dyspnea, fever, pleuritic chest pain, hemoptysis, and, rarely, acute respiratory distress syndrome. CNS infection typically presents with a subacute course over one to three weeks. Headache is the most common symptom and may be accompanied by fever, irritability, confusion, nausea, somnolence, and seizures. Only a minority of patients present with classic signs of meningitis such as neck stiffness and photophobia. On physical examination, nuchal rigidity is often absent. Papilledema is present in approximately one-third of patients due to elevated intracranial pressure. Skin involvement may manifest as painless papules, nodules, or ulcers, sometimes with central umbilication resembling molluscum contagiosum.
Diagnosis is established through laboratory and imaging studies. Serum cryptococcal antigen testing is highly sensitive and useful in both pulmonary and CNS disease. Blood cultures may grow Cryptococcus, particularly when fungal isolator tubes are used. In pulmonary disease, sputum culture or lung biopsy may be required. In CNS infection, cerebrospinal fluid (CSF) analysis is essential. Findings typically include elevated opening pressure (often >200 mm H₂O), elevated protein, low glucose, and lymphocytic pleocytosis. India ink staining may reveal encapsulated yeast, and CSF cryptococcal antigen testing is highly sensitive. Imaging studies such as chest radiography or CT may demonstrate interstitial infiltrates, nodules, cavitation, pleural effusions, lymphadenopathy, or cryptococcomas in pulmonary disease. Brain CT or MRI may reveal nodules, cryptococcomas, or hydrocephalus in CNS infection.
The differential diagnosis includes bacterial pneumonia, Pneumocystis pneumonia, tuberculosis, sarcoidosis, histoplasmosis, coccidioidomycosis, meningoencephalitis of other etiologies, and CNS metastases.
Treatment depends on the site and severity of disease. Mild-to-moderate pulmonary infection is treated with fluconazole 400 mg daily for 6–12 months. CNS infection requires an induction phase of amphotericin B (preferably a lipid formulation in patients at risk for nephrotoxicity) combined with flucytosine for at least 14 days. If there is clinical improvement, consolidation therapy with fluconazole 400 mg daily is given for eight weeks, followed by maintenance therapy with fluconazole 200 mg daily. In HIV-infected patients with prior cryptococcal meningitis, maintenance therapy is continued until immune reconstitution with sustained CD4 counts above 200 cells/μL for more than six months. Elevated intracranial pressure should be managed with serial lumbar punctures, and ventriculoperitoneal shunting may be required in refractory cases.
Complications of cryptococcal infection include persistent elevated intracranial pressure, hydrocephalus, visual impairment, cognitive decline, and death. Close monitoring of renal function during amphotericin and flucytosine therapy, and liver function during fluconazole therapy, is essential. Despite advances in antifungal therapy and HIV management, cryptococcal meningitis remains a major cause of morbidity and mortality worldwide.
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Infectious Disease and Microbiology – Cysticercosis
Cysticercosis is a parasitic infection caused by the larval stage of the pork tapeworm, Taenia solium. Humans develop cysticercosis when they ingest tapeworm eggs, which hatch into larvae (oncospheres) that penetrate the intestinal wall and disseminate hematogenously to tissues. The larvae develop into cysticerci—fluid-filled cysts—within various organs. The central nervous system (CNS) is most commonly affected, a condition known as neurocysticercosis. Other commonly involved sites include skeletal muscle, subcutaneous tissue, heart, and eyes. Many infections remain asymptomatic, but symptomatic disease can result in significant neurologic morbidity.
Cysticercosis occurs worldwide and affects more than 50 million people. It is highly prevalent in Central and South America, sub-Saharan Africa, India, Southeast Asia, and parts of Eastern Europe. In endemic villages, 10% or more of the population may be seropositive, and up to 6% may harbor adult intestinal tapeworms at any time. Neurocysticercosis is the most common parasitic infection of the CNS and is the leading cause of seizures in many developing countries. In Mexico, for example, up to 10% of brain CT scans in some institutions show evidence of neurocysticercosis.
Risk factors include consumption of raw or undercooked pork, poor sanitation, close proximity to pigs (particularly where pigs have access to human feces), and inadequate hand hygiene leading to fecal–oral transmission. Humans are the definitive host for the adult intestinal worm, which resides in the small intestine and sheds eggs or gravid proglottids in stool. Pigs serve as intermediate hosts when they ingest eggs, allowing larvae to encyst in muscle tissue. Humans acquire intestinal tapeworm infection by eating undercooked pork containing cysticerci. In contrast, cysticercosis occurs when humans ingest eggs directly—either through contaminated food or water, poor hygiene, or autoinfection in individuals already infected with the adult worm.
In neurocysticercosis, neurologic symptoms primarily result from the inflammatory response that occurs when cysticerci degenerate. Mass effect may also occur when cysts obstruct cerebrospinal fluid flow, leading to hydrocephalus and increased intracranial pressure. Extraneural disease may involve the eyes (commonly vitreous humor or subretinal space), causing visual disturbance or chronic uveitis. Subcutaneous cysts present as firm nodules that may become inflamed. Skeletal muscle involvement is usually asymptomatic but may produce muscular pseudohypertrophy in heavy infestations. Cardiac involvement can lead to conduction abnormalities.
Clinical manifestations vary widely. Patients may present with chronic headache, seizures, focal neurologic deficits, altered mental status, nausea, vomiting, visual disturbances, insomnia, anorexia, or weight loss. Seizures are the most common presentation. Physical examination often reveals absence of fever, nonfocal neurologic findings, papilledema, hyperreflexia, or visual deficits. Intraocular larvae may be visualized on ophthalmoscopy. Subcutaneous nodules resembling sebaceous cysts may be palpable.
Diagnosis relies on imaging and serologic testing. Brain CT and MRI are key diagnostic tools; MRI is especially useful for detecting brainstem or ventricular cysts. Imaging may show viable cysts, ring-enhancing lesions, or calcified granulomas. Soft tissue radiographs may reveal calcified cysts in muscle. Serologic testing includes enzyme-linked immunoelectrotransfer blot (EITB), which has high sensitivity and specificity in patients with multiple cysts, though sensitivity is lower with single lesions. Stool examination may identify ova and parasites if intestinal infection is present. Lumbar puncture findings are nonspecific but may show lymphocytosis, elevated protein, and decreased glucose in cases with significant inflammation. Biopsy of subcutaneous nodules can confirm the diagnosis.
The differential diagnosis of neurocysticercosis includes brain abscess, neoplasms, tuberculosis, toxoplasmosis, encephalitis, stroke, intracranial hemorrhage, meningitis, and other causes of seizures or focal neurologic deficits.
Treatment includes antiparasitic therapy combined with anti-inflammatory management. First-line therapy consists of praziquantel for two weeks along with corticosteroids (prednisone or dexamethasone) to control inflammation. Albendazole is an effective alternative and is commonly used. Anticonvulsant therapy (e.g., phenytoin, phenobarbital, or benzodiazepines for acute seizures) is required for seizure control. Neurosurgical interventions, such as ventricular shunting or burr hole procedures, may be necessary for obstructive hydrocephalus or elevated intracranial pressure. Ophthalmologic or neurosurgical referral is indicated for ocular or severe CNS involvement.
Prognosis is generally excellent with appropriate diagnosis and treatment, although some patients require long-term anticonvulsant therapy due to persistent calcified lesions. Complications include status epilepticus, stroke, intracranial herniation, hydrocephalus requiring shunt placement, shunt-related complications, and permanent vision loss.
Prevention focuses on improved sanitation, hand hygiene, proper cooking of pork, freezing pork to kill cysticerci, strict meat inspection, treatment of infected individuals, and control of infection in pig populations. Education regarding seizure management and avoidance of high-risk activities after seizures is essential for affected patients.
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Infectious Disease and Microbiology – Septic Bursitis
Bursitis refers to inflammation of a bursa, one of more than 150 sac-like structures in the body that cushion soft tissues over bony prominences. Bursitis may result from infection (pyogenic), crystal deposition due to trauma or gout, or inflammatory arthritis such as rheumatoid arthritis. Septic bursitis most commonly involves superficial bursae and frequently affects the olecranon, prepatellar, subdeltoid, ischial, and trochanteric bursae.
The most important predisposing factor for septic bursitis is trauma, which accounts for approximately 70% of cases. Repetitive microtrauma is common in certain activities and occupations. Specific associations include ischial bursitis in individuals with spinal cord injuries, malleolar bursitis in ice skaters, and subdeltoid bursitis following injections. Additional risk factors include diabetes mellitus, alcohol abuse, chronic skin conditions, intravenous drug use, and invasive procedures such as acupuncture or joint injections, which have been associated with outbreaks of methicillin-resistant Staphylococcus aureus (MRSA).
The most common causative organism is Staphylococcus aureus. Streptococcal species account for 5–30% of cases. Gram-negative bacteria and fungi are rare causes. Prototheca wickerhamii, an environmental algae, has been reported in immunocompromised individuals. In endemic regions, brucellosis should be considered in the differential diagnosis, and tuberculous bursitis may occur as part of disseminated disease.
Clinically, septic bursitis presents with localized painful swelling, erythema, warmth, and tenderness over the affected bursa. Fever may be present. Overlying cellulitis may extend beyond the bursa. Deep bursal infections are more likely to be associated with systemic signs of infection and bacteremia.
Aspiration of bursal fluid is the diagnostic procedure of choice. Fluid analysis typically shows elevated white blood cell counts, often below 20,000 cells/mm³ in septic bursitis. Gram stain positivity varies widely, and culture of aspirated fluid has high sensitivity and specificity. Use of liquid media may improve culture yield. Crystal analysis should be performed, as crystal-induced bursitis can coexist with infection. Laboratory blood tests may show inflammatory markers, but they are nonspecific.
Imaging may support the diagnosis. Plain radiographs can demonstrate soft tissue swelling and subcutaneous edema. Ultrasound is useful in identifying fluid collections and guiding aspiration. MRI may show a fluid-filled bursa with rim enhancement after gadolinium administration, while surrounding structures are typically spared unless there is extension of infection.
The differential diagnosis includes cellulitis, fasciitis, acute monoarthritis, gout, pseudogout, and traumatic injury.
Management includes repeated needle aspiration, often daily, until the bursa is no longer fluctuant. Empiric antibiotic therapy should cover staphylococci and streptococci. For methicillin-sensitive Staphylococcus aureus, intravenous oxacillin or nafcillin is recommended. For MRSA, vancomycin is indicated. Antibiotic therapy is generally continued for at least 14 days, although shorter courses (7 days) may be sufficient in selected non-immunocompromised patients with severe infection requiring hospitalization. The choice between intravenous and oral therapy depends on severity and systemic involvement. Immobilization of the affected joint is advised during acute treatment.
If medical therapy fails, or if there is persistent swelling, pain, or loculated infection, surgical incision and drainage may be necessary. In chronic or recurrent cases, excision of the bursa may be required.
Follow-up care includes rehabilitation to prevent limitation of joint movement and ensure restoration of function.
Bursitis refers to inflammation of a bursa, one of more than 150 sac-like structures in the body that cushion soft tissues over bony prominences. Bursitis may result from infection (pyogenic), crystal deposition due to trauma or gout, or inflammatory arthritis such as rheumatoid arthritis. Septic bursitis most commonly involves superficial bursae and frequently affects the olecranon, prepatellar, subdeltoid, ischial, and trochanteric bursae.
The most important predisposing factor for septic bursitis is trauma, which accounts for approximately 70% of cases. Repetitive microtrauma is common in certain activities and occupations. Specific associations include ischial bursitis in individuals with spinal cord injuries, malleolar bursitis in ice skaters, and subdeltoid bursitis following injections. Additional risk factors include diabetes mellitus, alcohol abuse, chronic skin conditions, intravenous drug use, and invasive procedures such as acupuncture or joint injections, which have been associated with outbreaks of methicillin-resistant Staphylococcus aureus (MRSA).
The most common causative organism is Staphylococcus aureus. Streptococcal species account for 5–30% of cases. Gram-negative bacteria and fungi are rare causes. Prototheca wickerhamii, an environmental algae, has been reported in immunocompromised individuals. In endemic regions, brucellosis should be considered in the differential diagnosis, and tuberculous bursitis may occur as part of disseminated disease.
Clinically, septic bursitis presents with localized painful swelling, erythema, warmth, and tenderness over the affected bursa. Fever may be present. Overlying cellulitis may extend beyond the bursa. Deep bursal infections are more likely to be associated with systemic signs of infection and bacteremia.
Aspiration of bursal fluid is the diagnostic procedure of choice. Fluid analysis typically shows elevated white blood cell counts, often below 20,000 cells/mm³ in septic bursitis. Gram stain positivity varies widely, and culture of aspirated fluid has high sensitivity and specificity. Use of liquid media may improve culture yield. Crystal analysis should be performed, as crystal-induced bursitis can coexist with infection. Laboratory blood tests may show inflammatory markers, but they are nonspecific.
Imaging may support the diagnosis. Plain radiographs can demonstrate soft tissue swelling and subcutaneous edema. Ultrasound is useful in identifying fluid collections and guiding aspiration. MRI may show a fluid-filled bursa with rim enhancement after gadolinium administration, while surrounding structures are typically spared unless there is extension of infection.
The differential diagnosis includes cellulitis, fasciitis, acute monoarthritis, gout, pseudogout, and traumatic injury.
Management includes repeated needle aspiration, often daily, until the bursa is no longer fluctuant. Empiric antibiotic therapy should cover staphylococci and streptococci. For methicillin-sensitive Staphylococcus aureus, intravenous oxacillin or nafcillin is recommended. For MRSA, vancomycin is indicated. Antibiotic therapy is generally continued for at least 14 days, although shorter courses (7 days) may be sufficient in selected non-immunocompromised patients with severe infection requiring hospitalization. The choice between intravenous and oral therapy depends on severity and systemic involvement. Immobilization of the affected joint is advised during acute treatment.
If medical therapy fails, or if there is persistent swelling, pain, or loculated infection, surgical incision and drainage may be necessary. In chronic or recurrent cases, excision of the bursa may be required.
Follow-up care includes rehabilitation to prevent limitation of joint movement and ensure restoration of function.
- Published on
Infectious Diseases and Microbiology: Trauma-Related Infections
Basics
Description
Trauma-related infections broadly include infections that arise directly or indirectly from wounds or injuries. A recently recognized high-risk group is patients needing emergency operations for non-trauma causes such as gastrointestinal perforation, obstruction, bleeding, or acute inflammation, which is associated with increased infection-related mortality.
Epidemiology
Incidence
Millions of wounds are treated annually in U.S. emergency departments, including large numbers of burns and lacerations, and cutting or piercing injuries generate substantial outpatient visits. Reported infection rates among trauma patients vary widely across studies. Sepsis contributes to a significant proportion of deaths in hospitalized trauma patients.
Risk Factors
Higher risk is linked to heavily contaminated wounds, impaired blood supply from injury, emergent splenectomy, glucocorticoid exposure, delayed treatment, obesity, and greater injury severity.
General Prevention
Thorough cleaning and irrigation with water or normal saline is essential. Topical antibiotics and occlusive dressings reduce infection rates in traumatic lacerations. Confirm tetanus immunization status and vaccinate patients who are overdue or uncertain. Highly contaminated wounds may require secondary intention healing or delayed primary closure. In open limb fractures, prophylactic antibiotics lower early infection risk. Although high-quality placebo-controlled trials are limited for severely injured contaminated patients, empiric antibiotics are commonly used for penetrating chest or abdominal injuries and severe head wounds. Short prophylactic courses are generally as effective as longer courses, supported by evidence in penetrating abdominal trauma showing no major outcome difference between 24-hour and 5-day regimens. Antibiotic levels can be altered by fluid shifts and hyperdynamic physiology, and data support higher doses for shorter durations, especially in trauma laparotomy patients. Short prophylaxis reduces infection in compound mandibular fractures. After traumatic splenectomy, the risk of early serious infection is low in isolated splenic injury but rises with greater injury and associated trauma; encapsulated organisms are key pathogens early and late. Administer pneumococcal and meningococcal vaccines once clinically stable after splenectomy. Strict infection control practices reduce hospital-acquired infections in severely injured patients.
Etiology
Trauma increases infection risk through vascular disruption and microcirculatory damage causing ischemia, edema, compartment syndromes, and necrosis; contamination of wounds and sterile spaces by soil or water exposure; post-shock immune dysfunction; reduced IgM responses after splenectomy compared with nonsplenectomized infected posttrauma patients; and additional immune suppression from corticosteroids used for head injury. Common infections in multiply injured patients include pneumonia and empyema, bacteremia or fungemia (including catheter-related), surgical site infection, intraabdominal infection, meningitis, urinary tract infection, sinus infection, wound infection, and Clostridioides difficile colitis after prior antibiotic exposure. Acinetobacter baumannii infections have been reported in injured military personnel from conflict regions, with some isolates susceptible only to carbapenems such as imipenem.
Diagnosis
History
Diagnosis is challenging because fever may be noninfectious after trauma, patients may be unable to provide history, examinations may be limited, and usual infection signs are less reliable in critically ill, multiply traumatized patients.
Physical Examination
Fever, tachycardia, and hypotension can occur after severe injury without infection. In critically ill patients, track ventilator requirements, sputum volume and character, and urine and stool output. In hospitalized trauma patients, perform a complete exam emphasizing indwelling devices, skin, operative wounds, abdomen, and respiratory findings. Inspect injured sites for local infection signs including pain, foul odor, erythema, swelling, purulent drainage, and delayed healing.
Diagnostic Tests and Interpretation
Laboratory Studies
Obtain CBC with differential, electrolytes, and kidney and liver function tests, recognizing leukocytosis may reflect trauma alone. Whenever possible, collect cultures from suspected sites before antibiotics, including blood, sputum, urine, cerebrospinal fluid studies and culture when penetrating head injury or CNS drains are present, wound cultures, and abscess cultures. With watery diarrhea and prior antibiotic exposure, test stool for C. difficile.
Imaging
Use chest radiography to assess pneumonia, especially in mechanically ventilated patients. Chest CT is more sensitive for thoracic infection in septic trauma patients and can guide correction of malpositioned or blocked thoracostomy tubes, though concurrent thoracic injuries can reduce test accuracy. Abdominal CT can identify intraabdominal infection such as perforation, colitis, cholecystitis, or abscess. For suspected extremity infection, ultrasound, CT, or MRI can help exclude abscess.
Diagnostic Procedures/Other
Image-guided or operative drainage of abscesses is diagnostic and therapeutic; send fluid for Gram stain, aerobic and anaerobic cultures, add fungal studies for abdominal or pelvic collections, and consider acid-fast bacilli smear and mycobacterial culture based on epidemiologic risk.
Differential Diagnosis
In severely injured patients, infection mimics include atelectasis, deep vein thrombosis, drug fever, allergic reactions or anaphylaxis, hypovolemia, large hematoma, sterile inflammation, pulmonary contusion, transfusion reactions, and central fever from brain injury.
Treatment
Medications
Correcting local anatomic problems such as open fractures or perforated abdominal organs is often more important than antibiotics alone. In trauma patients, unexplained hemodynamic instability not due to hypovolemia should prompt empiric antibiotics even if other infection signs are absent. Choose antibiotics based on suspected source, local resistance, trauma context (bites, water exposure, soil contamination), hospitalization duration and risk of resistant organisms, local MRSA prevalence, and allergies. If no source is identified, start broad-spectrum therapy including antistaphylococcal coverage plus broad gram-negative and anaerobic activity
.
Additional Treatment
Monitor clinical response and narrow therapy to culture and susceptibility results. If diagnostic evaluation is negative and the patient is stable, consider stopping antibiotics. Duration depends on infection site and clinical course. Remove central venous and urinary catheters as soon as they are no longer needed.
Issues for Referral
Severe injuries require urgent evaluation at experienced trauma centers with surgical and critical care capability. Infectious diseases consultation is useful when the patient is critically ill, not improving on therapy, or diagnosis remains uncertain.
Surgery/Other Procedures
Drain collections, debride necrotic tissue, and repair fractures or perforations promptly, and implement measures to mobilize respiratory secretions.
In-Patient Considerations
Initial Stabilization
Stabilize airway and circulation, provide rapid fluid resuscitation, and document all injuries.
Admission Criteria
Admit patients with penetrating injuries, fractures needing urgent repair, abnormal vital signs, impaired mental status, uncontrolled pain, or severe injuries. Burns meeting moderate to major thresholds require admission to specialized burn care centers.
Discharge Criteria
Discharge when fever has been absent for more than 24 hours, vital signs are stable, and follow-up for antibiotics and wound care is arranged.
Ongoing Care and Follow-Up
Patient Monitoring
Monitor closely for wound infection and healthcare-associated infections, which occur in a meaningful minority of hospitalized trauma patients.
Diet
Provide adequate nutritional support and consider nutrition consultation in severely injured hospitalized patients.
Patient Education
Teach warning signs of wound infection and provide clear instructions for wound care, including packing and dressing-change schedules.
Prognosis
Trauma-related infection increases mortality risk and is associated with worse functional outcomes during the year after injury compared with trauma patients without infection.
Complications
Serious outcomes include septic shock, respiratory failure, peritonitis and abdominal abscess, osteomyelitis, brain abscess, and acute acalculous cholecystitis.
Basics
Description
Trauma-related infections broadly include infections that arise directly or indirectly from wounds or injuries. A recently recognized high-risk group is patients needing emergency operations for non-trauma causes such as gastrointestinal perforation, obstruction, bleeding, or acute inflammation, which is associated with increased infection-related mortality.
Epidemiology
Incidence
Millions of wounds are treated annually in U.S. emergency departments, including large numbers of burns and lacerations, and cutting or piercing injuries generate substantial outpatient visits. Reported infection rates among trauma patients vary widely across studies. Sepsis contributes to a significant proportion of deaths in hospitalized trauma patients.
Risk Factors
Higher risk is linked to heavily contaminated wounds, impaired blood supply from injury, emergent splenectomy, glucocorticoid exposure, delayed treatment, obesity, and greater injury severity.
General Prevention
Thorough cleaning and irrigation with water or normal saline is essential. Topical antibiotics and occlusive dressings reduce infection rates in traumatic lacerations. Confirm tetanus immunization status and vaccinate patients who are overdue or uncertain. Highly contaminated wounds may require secondary intention healing or delayed primary closure. In open limb fractures, prophylactic antibiotics lower early infection risk. Although high-quality placebo-controlled trials are limited for severely injured contaminated patients, empiric antibiotics are commonly used for penetrating chest or abdominal injuries and severe head wounds. Short prophylactic courses are generally as effective as longer courses, supported by evidence in penetrating abdominal trauma showing no major outcome difference between 24-hour and 5-day regimens. Antibiotic levels can be altered by fluid shifts and hyperdynamic physiology, and data support higher doses for shorter durations, especially in trauma laparotomy patients. Short prophylaxis reduces infection in compound mandibular fractures. After traumatic splenectomy, the risk of early serious infection is low in isolated splenic injury but rises with greater injury and associated trauma; encapsulated organisms are key pathogens early and late. Administer pneumococcal and meningococcal vaccines once clinically stable after splenectomy. Strict infection control practices reduce hospital-acquired infections in severely injured patients.
Etiology
Trauma increases infection risk through vascular disruption and microcirculatory damage causing ischemia, edema, compartment syndromes, and necrosis; contamination of wounds and sterile spaces by soil or water exposure; post-shock immune dysfunction; reduced IgM responses after splenectomy compared with nonsplenectomized infected posttrauma patients; and additional immune suppression from corticosteroids used for head injury. Common infections in multiply injured patients include pneumonia and empyema, bacteremia or fungemia (including catheter-related), surgical site infection, intraabdominal infection, meningitis, urinary tract infection, sinus infection, wound infection, and Clostridioides difficile colitis after prior antibiotic exposure. Acinetobacter baumannii infections have been reported in injured military personnel from conflict regions, with some isolates susceptible only to carbapenems such as imipenem.
Diagnosis
History
Diagnosis is challenging because fever may be noninfectious after trauma, patients may be unable to provide history, examinations may be limited, and usual infection signs are less reliable in critically ill, multiply traumatized patients.
Physical Examination
Fever, tachycardia, and hypotension can occur after severe injury without infection. In critically ill patients, track ventilator requirements, sputum volume and character, and urine and stool output. In hospitalized trauma patients, perform a complete exam emphasizing indwelling devices, skin, operative wounds, abdomen, and respiratory findings. Inspect injured sites for local infection signs including pain, foul odor, erythema, swelling, purulent drainage, and delayed healing.
Diagnostic Tests and Interpretation
Laboratory Studies
Obtain CBC with differential, electrolytes, and kidney and liver function tests, recognizing leukocytosis may reflect trauma alone. Whenever possible, collect cultures from suspected sites before antibiotics, including blood, sputum, urine, cerebrospinal fluid studies and culture when penetrating head injury or CNS drains are present, wound cultures, and abscess cultures. With watery diarrhea and prior antibiotic exposure, test stool for C. difficile.
Imaging
Use chest radiography to assess pneumonia, especially in mechanically ventilated patients. Chest CT is more sensitive for thoracic infection in septic trauma patients and can guide correction of malpositioned or blocked thoracostomy tubes, though concurrent thoracic injuries can reduce test accuracy. Abdominal CT can identify intraabdominal infection such as perforation, colitis, cholecystitis, or abscess. For suspected extremity infection, ultrasound, CT, or MRI can help exclude abscess.
Diagnostic Procedures/Other
Image-guided or operative drainage of abscesses is diagnostic and therapeutic; send fluid for Gram stain, aerobic and anaerobic cultures, add fungal studies for abdominal or pelvic collections, and consider acid-fast bacilli smear and mycobacterial culture based on epidemiologic risk.
Differential Diagnosis
In severely injured patients, infection mimics include atelectasis, deep vein thrombosis, drug fever, allergic reactions or anaphylaxis, hypovolemia, large hematoma, sterile inflammation, pulmonary contusion, transfusion reactions, and central fever from brain injury.
Treatment
Medications
Correcting local anatomic problems such as open fractures or perforated abdominal organs is often more important than antibiotics alone. In trauma patients, unexplained hemodynamic instability not due to hypovolemia should prompt empiric antibiotics even if other infection signs are absent. Choose antibiotics based on suspected source, local resistance, trauma context (bites, water exposure, soil contamination), hospitalization duration and risk of resistant organisms, local MRSA prevalence, and allergies. If no source is identified, start broad-spectrum therapy including antistaphylococcal coverage plus broad gram-negative and anaerobic activity
.
Additional Treatment
Monitor clinical response and narrow therapy to culture and susceptibility results. If diagnostic evaluation is negative and the patient is stable, consider stopping antibiotics. Duration depends on infection site and clinical course. Remove central venous and urinary catheters as soon as they are no longer needed.
Issues for Referral
Severe injuries require urgent evaluation at experienced trauma centers with surgical and critical care capability. Infectious diseases consultation is useful when the patient is critically ill, not improving on therapy, or diagnosis remains uncertain.
Surgery/Other Procedures
Drain collections, debride necrotic tissue, and repair fractures or perforations promptly, and implement measures to mobilize respiratory secretions.
In-Patient Considerations
Initial Stabilization
Stabilize airway and circulation, provide rapid fluid resuscitation, and document all injuries.
Admission Criteria
Admit patients with penetrating injuries, fractures needing urgent repair, abnormal vital signs, impaired mental status, uncontrolled pain, or severe injuries. Burns meeting moderate to major thresholds require admission to specialized burn care centers.
Discharge Criteria
Discharge when fever has been absent for more than 24 hours, vital signs are stable, and follow-up for antibiotics and wound care is arranged.
Ongoing Care and Follow-Up
Patient Monitoring
Monitor closely for wound infection and healthcare-associated infections, which occur in a meaningful minority of hospitalized trauma patients.
Diet
Provide adequate nutritional support and consider nutrition consultation in severely injured hospitalized patients.
Patient Education
Teach warning signs of wound infection and provide clear instructions for wound care, including packing and dressing-change schedules.
Prognosis
Trauma-related infection increases mortality risk and is associated with worse functional outcomes during the year after injury compared with trauma patients without infection.
Complications
Serious outcomes include septic shock, respiratory failure, peritonitis and abdominal abscess, osteomyelitis, brain abscess, and acute acalculous cholecystitis.
- Published on
Infectious Disease and Microbiology – Adenovirus Infections
Adenovirus infections are caused by nonenveloped, double-stranded DNA viruses measuring approximately 70–80 nm in diameter. Human adenoviruses belong to the genus Mastadenovirus and include more than 50 serotypes. These viruses possess an icosahedral capsid composed of 20 triangular faces and 12 vertices. The genome consists of linear double-stranded DNA encoding structural and nonstructural proteins. Infection may result in either lytic replication or latent persistence, and certain serotypes have demonstrated oncogenic potential in animal models.
Adenoviruses contribute to a proportion of viral respiratory illnesses. Although rhinoviruses are the most common cause of acute respiratory infections, adenoviruses account for up to 5% of respiratory infections in children and fewer than 2% in adults. Infections occur most frequently from fall through spring. Transmission occurs via inhalation of aerosolized particles, direct inoculation of conjunctival mucosa, and possibly via the fecal–oral route. Outbreaks of acute respiratory disease due to specific serotypes are well documented among military recruits, particularly in winter and spring. Following infection, type-specific antibodies develop and provide protection against reinfection with the same serotype. Severe or disseminated disease may occur in immunocompromised individuals, including patients with AIDS, solid-organ or bone marrow transplant recipients, and children with congenital immunodeficiencies.
In children, adenovirus commonly causes acute upper respiratory tract infection characterized by prominent rhinitis. Lower respiratory involvement, including bronchiolitis and pneumonia, may occur. Pharyngoconjunctival fever is a distinctive syndrome seen in outbreaks, particularly in summer camps, presenting with low-grade fever for 3–5 days followed by rhinitis, sore throat, cervical lymphadenopathy, and conjunctivitis, typically resolving within 1–2 weeks. Adenovirus also causes pharyngitis and, in young children, acute diarrheal illness. Other manifestations include hemorrhagic cystitis and epidemic keratoconjunctivitis. In adults, acute respiratory disease presents with sore throat, gradual onset of fever that may reach 39°C, cough, coryza, and lymphadenopathy. In immunocompromised patients, adenovirus pneumonia may present abruptly with fever, rigors, malaise, nonproductive cough, gastrointestinal symptoms, headache, and arthralgia.
Physical examination may reveal pharyngeal edema, injection, and tonsillar enlargement with minimal exudate. Ocular involvement presents with conjunctival injection and discharge. In immunocompromised hosts, localizing findings may be minimal despite severe disease.
Definitive diagnosis is established by viral culture or detection of adenovirus from conjunctival, oropharyngeal, sputum, urine, or stool specimens. Viral cytopathic effects in tissue culture can be confirmed by immunofluorescence or other immunologic assays. Certain enteric adenovirus types require specialized cell lines or direct ELISA testing of stool. Serologic diagnosis may demonstrate rising antibody titers using complement fixation, neutralization assays, ELISA, or radioimmunoassay. In adenovirus pneumonia, chest radiography often shows bilateral diffuse interstitial infiltrates and occasionally pleural effusions. The clinical presentation is frequently indistinguishable from other viral respiratory infections or Mycoplasma pneumoniae.
Management is primarily supportive, as no specific antiviral therapy is routinely indicated for immunocompetent patients. Live oral vaccines targeting adenovirus types 4 and 7 are used in military settings to prevent outbreaks. In immunocompromised individuals with severe infection, treatment with cidofovir and intravenous immunoglobulin has shown benefit in some cases. Intravenous gamma globulin and type-specific antibodies may also be helpful. Ribavirin and ganciclovir have been used in selected cases, although evidence remains limited.
In transplant recipients and other immunocompromised patients, adenovirus pneumonia carries significant morbidity and mortality, which may exceed 60%, underscoring the importance of early recognition and supportive management.
Adenovirus infections are caused by nonenveloped, double-stranded DNA viruses measuring approximately 70–80 nm in diameter. Human adenoviruses belong to the genus Mastadenovirus and include more than 50 serotypes. These viruses possess an icosahedral capsid composed of 20 triangular faces and 12 vertices. The genome consists of linear double-stranded DNA encoding structural and nonstructural proteins. Infection may result in either lytic replication or latent persistence, and certain serotypes have demonstrated oncogenic potential in animal models.
Adenoviruses contribute to a proportion of viral respiratory illnesses. Although rhinoviruses are the most common cause of acute respiratory infections, adenoviruses account for up to 5% of respiratory infections in children and fewer than 2% in adults. Infections occur most frequently from fall through spring. Transmission occurs via inhalation of aerosolized particles, direct inoculation of conjunctival mucosa, and possibly via the fecal–oral route. Outbreaks of acute respiratory disease due to specific serotypes are well documented among military recruits, particularly in winter and spring. Following infection, type-specific antibodies develop and provide protection against reinfection with the same serotype. Severe or disseminated disease may occur in immunocompromised individuals, including patients with AIDS, solid-organ or bone marrow transplant recipients, and children with congenital immunodeficiencies.
In children, adenovirus commonly causes acute upper respiratory tract infection characterized by prominent rhinitis. Lower respiratory involvement, including bronchiolitis and pneumonia, may occur. Pharyngoconjunctival fever is a distinctive syndrome seen in outbreaks, particularly in summer camps, presenting with low-grade fever for 3–5 days followed by rhinitis, sore throat, cervical lymphadenopathy, and conjunctivitis, typically resolving within 1–2 weeks. Adenovirus also causes pharyngitis and, in young children, acute diarrheal illness. Other manifestations include hemorrhagic cystitis and epidemic keratoconjunctivitis. In adults, acute respiratory disease presents with sore throat, gradual onset of fever that may reach 39°C, cough, coryza, and lymphadenopathy. In immunocompromised patients, adenovirus pneumonia may present abruptly with fever, rigors, malaise, nonproductive cough, gastrointestinal symptoms, headache, and arthralgia.
Physical examination may reveal pharyngeal edema, injection, and tonsillar enlargement with minimal exudate. Ocular involvement presents with conjunctival injection and discharge. In immunocompromised hosts, localizing findings may be minimal despite severe disease.
Definitive diagnosis is established by viral culture or detection of adenovirus from conjunctival, oropharyngeal, sputum, urine, or stool specimens. Viral cytopathic effects in tissue culture can be confirmed by immunofluorescence or other immunologic assays. Certain enteric adenovirus types require specialized cell lines or direct ELISA testing of stool. Serologic diagnosis may demonstrate rising antibody titers using complement fixation, neutralization assays, ELISA, or radioimmunoassay. In adenovirus pneumonia, chest radiography often shows bilateral diffuse interstitial infiltrates and occasionally pleural effusions. The clinical presentation is frequently indistinguishable from other viral respiratory infections or Mycoplasma pneumoniae.
Management is primarily supportive, as no specific antiviral therapy is routinely indicated for immunocompetent patients. Live oral vaccines targeting adenovirus types 4 and 7 are used in military settings to prevent outbreaks. In immunocompromised individuals with severe infection, treatment with cidofovir and intravenous immunoglobulin has shown benefit in some cases. Intravenous gamma globulin and type-specific antibodies may also be helpful. Ribavirin and ganciclovir have been used in selected cases, although evidence remains limited.
In transplant recipients and other immunocompromised patients, adenovirus pneumonia carries significant morbidity and mortality, which may exceed 60%, underscoring the importance of early recognition and supportive management.
- Published on
Infectious Disease and Microbiology – Actinomycosis
Actinomycosis is a chronic, slowly progressive, suppurative, and tissue-destructive infection characterized by mass-like lesions and sinus tract formation. It most commonly affects the head and neck region but may also involve the thorax, abdomen, pelvis, central nervous system, bones, and soft tissues. The disease is indolent and often mimics malignancy or other chronic infections.
The reported incidence is approximately 1 per 300,000 population in the United States and about 1 per 100,000 in Europe. It occurs at all ages, with peak frequency in middle-aged adults, and has a male-to-female ratio of about 3:1. Risk factors include poor oral hygiene, dental manipulation, oral trauma, intrauterine contraceptive device (especially when used for more than 2 years), abdominal surgery, appendicitis, diverticulitis, foreign bodies, malnutrition, and immunodeficiency such as HIV infection, chronic granulomatous disease, or prolonged corticosteroid therapy. Cases have also been described in osteoradionecrosis and bisphosphonate-related mandibular osteonecrosis. Prevention includes maintaining good oral hygiene and, in women with long-term intrauterine devices and suspicious symptoms, device removal with short-term antibiotic therapy. Patient isolation is not required.
Humans are the natural reservoir. The organisms colonize the oral cavity, particularly dental plaque and tonsillar crypts, as commensals. Infection typically follows disruption of the mucosal barrier due to trauma or surgery, allowing invasion into deeper tissues. The disease spreads contiguously and occasionally hematogenously. Aspiration may lead to thoracic involvement, while abdominal and pelvic disease often follows bowel perforation, appendicitis, or diverticulitis. Although incubation is unclear, diagnosis is usually delayed because of the chronic course. Clinical forms include cervicofacial, thoracic, abdominal, pelvic, central nervous system, and disseminated disease.
Actinomyces species are microaerophilic or anaerobic, filamentous, branched, Gram-positive, non–acid-fast rods. Actinomyces israelii is the most frequently identified species, although A. naeslundii, A. meyeri, A. odontolyticus, and Propionibacterium propionica have also been implicated. These organisms are normal flora of the oral cavity and female genital tract. Most infections are polymicrobial, often involving anaerobic oral flora that may act as copathogens.
Clinical presentation varies by site. Patients may have low-grade fever, weight loss, and pain. Cervicofacial disease often presents with perimandibular swelling, trismus, and purplish discoloration of overlying skin, with sinus tract formation draining characteristic yellow “sulfur granules.” Thoracic disease presents with cough, chest pain, dyspnea, mass-like lesions, pleural thickening, empyema, chest wall invasion, and possible mediastinal or spinal involvement. Abdominal disease typically manifests as a firm mass, often in the right iliac fossa following appendicitis, or in the left lower quadrant after diverticulitis, sometimes with chronic perianal abscesses and fistulae. Pelvic disease may present as abscesses or a “frozen pelvis.” Central nervous system involvement causes focal neurologic deficits or chronic meningitis.
Diagnosis requires high suspicion, especially when mass lesions coexist with draining sinuses and sulfur granules. Specimens should be obtained before antibiotic therapy. Gram stain of pus or tissue from sterile sites demonstrating filamentous, Gram-positive, non–acid-fast organisms is more sensitive than culture. Swab cultures are not recommended, and specimens must be processed anaerobically. Direct immunofluorescence may assist in specific cases. Imaging with CT or MRI helps determine disease extent. Lung disease may show the “open bronchus sign.” Bone involvement may demonstrate a saw-toothed appearance, and CNS disease often appears as single or multiloculated lesions with surrounding edema. Differential diagnosis includes malignancy, nocardiosis, tuberculosis, botryomycosis, and endemic fungal infections.
Treatment consists of prolonged high-dose penicillin therapy. Recommended first-line therapy includes intravenous penicillin G (10–24 million units daily in divided doses) for 2–6 weeks, followed by oral penicillin V for 6–12 months, or intravenous ampicillin followed by oral amoxicillin for similar duration. Mild cervicofacial disease may be treated with oral therapy alone. Alternatives for penicillin-allergic patients include tetracyclines, erythromycin, or clindamycin. Surgical intervention, including abscess drainage or excision of fibrotic tissue, is often necessary.
Prognosis is generally excellent with appropriate prolonged therapy, as resistance among Actinomyces species is rare. Treatment failure usually suggests an undrained abscess or presence of resistant copathogens. Potential complications include disseminated disease and bowel obstruction in extensive abdominal or pelvic involvement.
Actinomycosis is a chronic, slowly progressive, suppurative, and tissue-destructive infection characterized by mass-like lesions and sinus tract formation. It most commonly affects the head and neck region but may also involve the thorax, abdomen, pelvis, central nervous system, bones, and soft tissues. The disease is indolent and often mimics malignancy or other chronic infections.
The reported incidence is approximately 1 per 300,000 population in the United States and about 1 per 100,000 in Europe. It occurs at all ages, with peak frequency in middle-aged adults, and has a male-to-female ratio of about 3:1. Risk factors include poor oral hygiene, dental manipulation, oral trauma, intrauterine contraceptive device (especially when used for more than 2 years), abdominal surgery, appendicitis, diverticulitis, foreign bodies, malnutrition, and immunodeficiency such as HIV infection, chronic granulomatous disease, or prolonged corticosteroid therapy. Cases have also been described in osteoradionecrosis and bisphosphonate-related mandibular osteonecrosis. Prevention includes maintaining good oral hygiene and, in women with long-term intrauterine devices and suspicious symptoms, device removal with short-term antibiotic therapy. Patient isolation is not required.
Humans are the natural reservoir. The organisms colonize the oral cavity, particularly dental plaque and tonsillar crypts, as commensals. Infection typically follows disruption of the mucosal barrier due to trauma or surgery, allowing invasion into deeper tissues. The disease spreads contiguously and occasionally hematogenously. Aspiration may lead to thoracic involvement, while abdominal and pelvic disease often follows bowel perforation, appendicitis, or diverticulitis. Although incubation is unclear, diagnosis is usually delayed because of the chronic course. Clinical forms include cervicofacial, thoracic, abdominal, pelvic, central nervous system, and disseminated disease.
Actinomyces species are microaerophilic or anaerobic, filamentous, branched, Gram-positive, non–acid-fast rods. Actinomyces israelii is the most frequently identified species, although A. naeslundii, A. meyeri, A. odontolyticus, and Propionibacterium propionica have also been implicated. These organisms are normal flora of the oral cavity and female genital tract. Most infections are polymicrobial, often involving anaerobic oral flora that may act as copathogens.
Clinical presentation varies by site. Patients may have low-grade fever, weight loss, and pain. Cervicofacial disease often presents with perimandibular swelling, trismus, and purplish discoloration of overlying skin, with sinus tract formation draining characteristic yellow “sulfur granules.” Thoracic disease presents with cough, chest pain, dyspnea, mass-like lesions, pleural thickening, empyema, chest wall invasion, and possible mediastinal or spinal involvement. Abdominal disease typically manifests as a firm mass, often in the right iliac fossa following appendicitis, or in the left lower quadrant after diverticulitis, sometimes with chronic perianal abscesses and fistulae. Pelvic disease may present as abscesses or a “frozen pelvis.” Central nervous system involvement causes focal neurologic deficits or chronic meningitis.
Diagnosis requires high suspicion, especially when mass lesions coexist with draining sinuses and sulfur granules. Specimens should be obtained before antibiotic therapy. Gram stain of pus or tissue from sterile sites demonstrating filamentous, Gram-positive, non–acid-fast organisms is more sensitive than culture. Swab cultures are not recommended, and specimens must be processed anaerobically. Direct immunofluorescence may assist in specific cases. Imaging with CT or MRI helps determine disease extent. Lung disease may show the “open bronchus sign.” Bone involvement may demonstrate a saw-toothed appearance, and CNS disease often appears as single or multiloculated lesions with surrounding edema. Differential diagnosis includes malignancy, nocardiosis, tuberculosis, botryomycosis, and endemic fungal infections.
Treatment consists of prolonged high-dose penicillin therapy. Recommended first-line therapy includes intravenous penicillin G (10–24 million units daily in divided doses) for 2–6 weeks, followed by oral penicillin V for 6–12 months, or intravenous ampicillin followed by oral amoxicillin for similar duration. Mild cervicofacial disease may be treated with oral therapy alone. Alternatives for penicillin-allergic patients include tetracyclines, erythromycin, or clindamycin. Surgical intervention, including abscess drainage or excision of fibrotic tissue, is often necessary.
Prognosis is generally excellent with appropriate prolonged therapy, as resistance among Actinomyces species is rare. Treatment failure usually suggests an undrained abscess or presence of resistant copathogens. Potential complications include disseminated disease and bowel obstruction in extensive abdominal or pelvic involvement.
