Microbiology and Immunology 1 Flashcards
What is the most likely diagnosis?
Keratitis caused by the free-living ameba Acanthamoeba is the most likely diagnosis. Conditions to consider in the differential diagnosis include herpes simplex virus (HSV), herpes zoster virus, and bacterial or fungal infection. However, HSV keratitis would present with photophobia, decreased visual acuity, and dendritic ulcer formation, which are not seen in this patient. Likewise, a bacterial or fungal source would present with accompanying systemic symptoms, and orbital cellulitis would create an ophthalmologic emergency.
What are the risk factors for developing Keratitis caused by the free-living ameba Acanthamoeba?
The number one risk factor for Acanthamoeba infection is extended wearing of contact lenses. Inadequate disinfection of the lenses with homemade saline solution and wearing lenses while swimming or showering can also predispose contact lens wearers to this infection. Acanthamoeba organisms can live in soil, air, and water and are resistant to chlorine.
What are other symptoms and complications of Keratitis caused by the free-living ameba Acanthamoeba?
Unlike bacterial keratitis, keratitis from Acanthamoeba takes days or weeks to cause symptoms. The initial symptoms are usually redness and a feeling of a foreign body in the eye. Blurring of vision may also be present. Over time, this progresses to pain, lid edema, and conjunctival injection. If untreated, increased intraocular pressure, cataracts, and even loss of vision can develop.
How is Keratitis caused by the free-living ameba Acanthamoeba diagnosed?
The diagnosis is made by slit-lamp examination of the eye, which shows thickened epithelium and rough corneal nerves. A characteristic ring on the cornea may also appear approximately 6 weeks after initial infection. Corneal scraping or biopsy reveals irregular polygonal cysts.
What is the appropriate treatment for Keratitis caused by the free-living ameba Acanthamoeba?
Initial treatment consists of topical antimicrobials such as miconazole and neomycin for several months. If the infection has been left untreated (ie, at the corneal ring stage), surgery, such as corneal debridement, is usually required.
What populations are at risk for Keratitis caused by the free-living ameba Acanthamoeba?
Populations include chronic disease patients, such as those with lymphoproliferative disorders, patients on chronic steroids, patients receiving chemotherapy, and patients with AIDS. In these populations, the infection is usually not of the eye but rather of the central nervous system. These patients present with changes in mental status, headache, and stiff neck. They can also develop cranial nerve palsies, ataxia, and hemiparesis (termed granulomatous amebic encephalitis). Treatment is urgent in such cases.
What are the possible bacterial microorganisms found in this sample?
Actinomyces and Nocardia both fit this description. However, although they resemble fungi on Gram stain, they are both bacteria, not fungi. They appear as characteristic gram-positive rods with long, branching filaments.
How are Actinomyces and Nocardia differentiated?
Actinomyces israelii is a non-acid-fast filamentous, anaerobic organism (Figure 3-1) and has characteristic “sulfur granules.” Nocardia, on the other hand, is weakly acid fast and an aerobic organism.
Aside from Actinomyces and Nocardia, what are the other obligate aerobic and anaerobic organisms?
The aerobic organisms are Nocardia, Pseudomonas, Mycobacteria, and Bacillus species (mnemonic: “Nagging Pests Must Breathe”).
The anaerobic organisms are Clostridium, Bacteroides, and Actinomyces species (mnemonic: “Can’t
Breathe Air”).
A pathologist is sent a poorly labeled fluid sample for Gram staining. The test reveals a gram-positive rod that forms long, branching filaments that resemble fungi. After paging the intern, the pathologist learns the sample was drained from an oral abscess. Now which of these two microorganisms is more likely?
Actinomyces is more likely because it is part of the normal oral flora and can cause abscesses in the mouth or gastrointestinal tract after trauma. Nocardia is an opportunistic infection and most often results in pulmonary symptoms due to lung abscesses or, rarely, central nervous system symptoms due to brain abscesses.
If the Nocardia microorganism were found in a sputum sample that stained weakly acid fast, what could be inferred about the patient’s immune status?
Nocardia is most often found in immunocompromised patients. The clinical presentation and acid-fast sputum sample resembles that of tuberculosis in this high-risk group and is commonly misdiagnosed as such in immunocompromised patients.
What is the appropriate treatment for Nocardia?
What is the appropriate treatment for Actinomyces?
- Nocardia is treated with trimethoprim-sulfamethoxazole.
- Actinomyces is treated with penicillin G.
What is the most likely diagnosis?
Cutaneous anthrax, caused by Bacillus anthracis. The skin lesions are painless and dark or charred ulcerations known as black eschar. Cutaneous anthrax is classically transmitted by contact with the hide of a goat at the site of a minor open wound.
How will the bacillus anthracis microorganism appear on Gram staining?
B anthracis is a gram-positive spore-forming rod. The spores are resistant to many chemical disinfectants, heat, ultraviolet light, and drying and are therefore a feared agent of biological warfare.
Other than bacillus anthracis, what is the other spore-forming microorganism?
Clostridium species are the other gram-positive spore-forming bacteria. Bacillus and Clostridium species can be differentiated by their ability to neutralize oxygen free radicals. Bacillus species (like the other aerobic bacteria) have catalase and superoxide dismutase—enzymes that can neutralize oxygen free radicals and therefore survive in aerobic environments. Clostridium species do not have these enzymes and are therefore obligate anaerobic microorganisms.
What is the other primary manifestation of B anthracis infection?
B anthracis also causes pulmonary anthrax, or woolsorters’ disease. In this condition, inhaled anthrax spores reach the alveoli, where they are taken up by macrophages and carried to mediastinal lymph nodes. This can result in mediastinal hemorrhage and a bloody pleural effusion. X-ray of the chest reveals a widened mediastinum.
What is the most likely diagnosis?
Ascariasis, caused by Ascaris lumbricoides, a nematode (roundworm) found in the southern United States and tropical climates. Ascariasis is the most common helminthic infection worldwide. Eosinophilia is a classic finding in helminth infection and is due to the increased need for eosinophilic release of major basic protein.
What tests can be used to confirm the diagnosis of Ascariasis, caused by Ascaris lumbricoides?
Analysis of a stool sample shows eggs with a knobby, rough surface (Figure 3-3).
What are the appropriate treatments for Ascariasis, caused by Ascaris lumbricoides?
As with many nematode infections, mebendazole or albendazole is the drug of choice. The bendazoles work by disrupting helminthic microtubule synthesis, which weakens cell structure.
What is the most likely diagnosis?
The hemoptysis and pulmonary symptoms, along with the 45-degree septate hyphae found on lavage, indicate Aspergillus infection. Aspergillus is an opportunistic infection, secondary to the patient’s recent immunosuppression from corticosteroid use.
Candida should also be considered but would appear microscopically as pseudohyphae and budding yeasts.
Mucormycosis presents with sinusitis, black nasal discharge, and can progress to hemoptysis, but lavage findings would indicate 90-degree branching nonseptate hyphae. This infection is most common in patients with type 1 diabetes mellitus.
What is x-ray of the chest likely to show in a patient with Aspergillus?
Aspergillus can appear as a “fungus ball” or a circular mobile lung mass within preexisting cavitary lesions in the lungs. This form of Aspergillus infection is called an aspergilloma.
The patient is treated with amphotericin B. What are the drug’s mechanism of action and side effects?
Amphotericin B works by binding to ergosterol, a key component of fungal membranes, thereby disrupting the integrity of the cell membrane. Its side effects can be serious and include fever, chills, kidney damage, hypotension, and arrhythmias. This grave side effect profile has given this powerful drug the nickname “Amphoterrible,” and its use reserved for serious fungal infections.
The patient’s symptoms improve and he is discharged a few days later. However, he returns to the hospital in 3 months with worsened respiratory function, chest pain, and decreased urine output. Could these symptoms be sequelae of the Aspergillus infection that caused his admission?
Yes; the patient could be suffering from invasive aspergillosis, which is the result of hematogenous spread of his infection to his kidneys, pericardium, and other organs, causing these diffuse symptoms. However, amphotericin B toxicity can also cause nephrotoxicity, dyspnea, and cardiac arrhythmias and therefore should be ruled out.
What patient population is at risk for invasive aspergillosis?
Neutropenic patients (because of hematologic malignancy, chemotherapy, immunosuppressive therapy, solid organ transplant, or HIV infection) are particularly susceptible to invasive aspergillosis.
If, instead of COPD, this patient had a history of severe asthma, to what type of fungal infection would he be most susceptible?
Allergic bronchopulmonary aspergillosis is an IgE-mediated hypersensitivity reaction to Aspergillus spores. The hyperactive inflammatory response in the airways of asthmatics predisposes them to bronchospasm and pneumonitis in response to an otherwise benign inoculation of Aspergillus spores.
What is the most likely diagnosis?
Botulism, resulting from ingestion of the botulinum toxin made by the gram-positive, spore-forming bacteria Clostridium botulinum.
What is the pathophysiology of Botulism toxicity?
Acetylcholine is normally released by motor neurons into the neuromuscular junction, where it binds to muscarinic receptors on the motor endplate of the muscle fiber. This binding depolarizes the membrane and subsequently contracts the muscle. Botulinum toxin binds presynaptically and prevents the release of acetylcholine into the neuromuscular junction. The result is a flaccid paralysis, or inability to contract. The binding is irreversible and it takes approximately 6 months for new synapses to form.
What is the typical course in adult patients with Botulism?
Ingestion of the botulinum toxin in food usually causes symptoms within 12–36 hours. The first symptoms are gastrointestinal distress (eg, cramps and nausea), due to enteric nervous system dysfunction, followed by neurologic symptoms. The first nerves affected are the cranial nerves, causing blurred vision, decreased eye movements, and a decreased gag reflex. The paralysis is symmetric and descending. Autonomic nerves can also be affected, resulting in ileus, urinary retention, and orthostatic hypotension. Respiratory muscles can also be affected, necessitating ventilator support.
Other than botulism, what is the differential diagnosis for this presentation?
The major differential includes Guillain-Barré syndrome, myasthenia gravis, and Lambert-Eaton syndrome. Unlike botulism, the paralysis seen in Guillain-Barré syndrome is due to a postinfectious demyelination of alpha motor neurons and is ascending. The most common infection leading to Guillain-Barré syndrome is Campylobacter jejuni. Myasthenia gravis is an autoimmune condition caused by antibodies created against the muscarinic acetylcholine receptor. Patients with this condition have muscle weakness only after prolonged muscle use, classically at the end of the day. Lambert-Eaton syndrome is a paraneoplastic anti–calcium channel antibody syndrome that causes muscle weakness that improves with prolonged muscle use.
How can botulism toxicity be acquired?
In adults, it is acquired most commonly from ingestion of preformed toxin in contaminated canned foods (usually home canned). In infants, ingestion of bacterial spores found in honey can result in toxicity referred to as “floppy baby syndrome.”
What is the most likely diagnosis?
The fungus Candida albicans can result in systemic or superficial fungal infection (candidiasis). Skinfold infection, vaginitis (yeast infection), and oral thrush are common manifestations of local candidiasis and present as a white, flaky, cheesy exudate on the affected surface.
Where is the microorganism that causes candidiasis normally found?
C albicans is part of the normal flora of mucous membranes of the gastrointestinal tract, respiratory tract, and women’s genital tract. Overgrowth, due to an imbalance in normal flora from women taking antibiotic therapy or patients who are immunocompromised, causes candidiasis.
What laboratory tests can help confirm the diagnosis of candidiasis?
A potassium hydroxide preparation (KOH mount) is used for skin or tissue scrapings. Pseudohyphae and budding yeast (Figure 3-5) are observed in the tissues. Pseudohyphae are seen in culture at 20°C (68°F), and germ tube formation is seen at 37°C (98.6°F). For (rare) systemic disease (eg, invasive candidiasis found primarily in neutropenic patients), blood cultures are positive for the fungus.
What populations other than immunocompromised patients are at risk for serious forms of candidiasis?
Intravenous drug users are at higher risk for candidal endocarditis.
What are the appropriate treatments for candidiasis?
Fluconazole or nystatin is used for superficial infections, and amphotericin B or fluconazole can be used for systemic infections.
What is the most likely diagnosis?
Chagas disease, or American trypanosomiasis, caused by the protozoan Trypanosoma cruzi.
What is the vector of the responsible protozoan in Chagas disease?
The vector is the reduviid bug, also known as the “kissing bug” because the bite is painless.
What is the classic sign associated with the acute form of Chagas disease?
The Romaña sign is painless, unilateral periorbital edema and conjunctivitis that results from acute Chagas disease. This sign is specific but not sensitive for acute T cruzi infection (Figure 3-6).
Where in the world is Chagas disease commonly found?
Chagas disease is commonly found in the southern United States, Mexico, and Central and South America (ie, only in the Western hemisphere).
What is the pathophysiology of Chagas disease?
This woman is experiencing chronic Chagas disease, which is most often characterized by heart block, ventricular tachycardia, and dilated cardiomyopathy. Dilatation of the esophagus and colon (megaesophagus and megacolon) can cause difficulty swallowing and constipation. The acute phase of the disease can be characterized by a hard red area called a chagoma at the parasite’s site of entry into the host, accompanied by fever and meningoencephalitis. In endemic areas, the acute phase is seen more frequently in children.
What is the appropriate treatment for Chagas disease?
Nifurtimox and benznidazole are used to treat acute cases. However, there is no effective treatment for chronic Chagas disease. For chronic heart disease, supportive measures for congestive heart failure, antiarrhythmics to prevent recurrent ventricular tachycardia, and pacemaker implantation for heart block are used. For gastrointestinal disease, dilation of the esophageal sphincter, changes in diet, the use of laxatives and/or enemas, and in some cases eventual resection of the megacolon are used.
What other disease is caused by the protozoan species that causes Chagas disease?
The protozoa Trypanosoma gambiense and Trypanosoma rhodesiense cause African sleeping sickness. This illness is characterized by lymphadenopathy, recurrent fevers due to antigenic variation, somnolence, and possibly coma. It is transmitted by the tsetse fly, whose bite is painful.
What is the most likely diagnosis?
This patient has cholera, a potentially fatal dehydrating illness caused by Vibrio cholerae. This microorganism is a gram-negative, curved, motile, polar flagellated rod (Figure 3-7) that resembles “shooting stars” on Gram stain. Symptomatic cholera usually manifests in epidemics, and it is endemic to developing regions in Africa, Asia, South and Latin America, and recently the Middle East.
What is the primary differential diagnosis of cholera?
Watery diarrhea induced during travel within a foreign country makes the noninvasive enterotoxigenic Escherichia coli (ETEC) infection the primary differential diagnosis (“traveler’s diarrhea”). However, ETEC diarrhea is not associated with white mucous flecks and generally is not as voluminous as the diarrhea induced by cholera.
How does the microorganism involved in cholera exert its effect on the gastrointestinal tract?
V cholerae is ingested through fecally contaminated water. It secretes an exotoxin (cholera toxin) that binds to the surface of intestinal epithelium. This toxin ADP-ribosylates adenylyl cyclase, thus increasing levels of cyclic adenosine monophosphate (cAMP) within the intestinal mucosa. This causes increased chloride secretion and decreased sodium absorption, leading to a massive secretory loss of fluids and electrolytes.
What are the clinical manifestations of cholera?
The hallmark of cholera is rice-water stools, so described because the small white flecks of mucus resemble grains of rice. The onset of this diarrhea typically occurs 1–3 days after infection. Vomiting and abdominal cramping is common, but fever is rare because V cholerae itself is noninvasive and thus remains in the gastrointestinal tract. Many infections are asymptomatic, but severe cholera can lead to extreme dehydration that can cause death within hours due to the excretion of electrolytes leading to renal failure, arrhythmias from hypokalemia, and metabolic acidosis from bicarbonate loss.
What is the appropriate treatment for cholera?
Oral rehydration solution (ORS), which has reduced mortality rates from 50% to < 1%. A typical preparation of ORS contains glucose, potassium chloride, sodium chloride, and sodium bicarbonate. Glucose facilitates sodium absorption from the gut, which allows for the concurrent absorption of water. Antibiotics are of limited use in stopping the diarrhea, although early use of doxycycline can reduce the volume of diarrhea and decrease the duration of bacteria excretion by 1 day.
What is the most likely diagnosis?
The most likely diagnosis is chronic granulomatous disease (CGD), an X-linked inherited immunodeficiency syndrome. This patient is predisposed to bacterial and fungal infections. The normal thymic shadow suggests normal T-cell maturation, which effectively rules out a diagnosis of severe combined immunodeficiency or DiGeorge syndrome. The strong family history of male involvement on the maternal side indicates an X-linked hereditary condition and suggests CGD as the likely diagnosis in this patient.
Infections with which organisms could be particularly severe and problematic in a patient with chronic granulomatous disease (CGD)?
Patients with CGD are at risk for serious infections with catalase-positive bacteria, including Staphylococcus aureus, Aspergillus species, and Burkholderia cepacia.
Why are patients with chronic granulomatous disease (CGD) especially susceptible to catalase- positive organisms?
Reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, which is required for production of reactive oxygen species, is deficient in patients with CGD. The radicals are used by neutrophils during the oxidative burst to kill engulfed organisms. Many bacterial species make free radicals as by-products of their metabolism. These free radicals contribute to the toxic environment in the neutrophil lysosomes. However, catalase-positive bacteria such as S aureus can neutralize these free radicals, leaving the patient unprotected against these organisms. The primary method of host immunity is containment of the offending organism, leading to numerous granulomatous formations (Figure 3-8).
What laboratory test can confirm a diagnosis of chronic granulomatous disease (CGD)?
The nitroblue tetrazolium test can detect the presence of a respiratory burst in neutrophils. In normal individuals the test is positive, but in patients with CGD the test is negative because the superoxide free radical is not produced.
What medical treatments are available for chronic granulomatous disease (CGD)?
Infections must be treated aggressively with appropriate antimicrobials. Trimethoprim-sulfamethoxazole can be used as long-term prophylaxis. In addition, interferon-α, an immunomodulator, is used in patients with CGD.
What therapy or procedure provides a definitive cure for chronic granulomatous disease (CGD)?
Bone marrow transplantation provides a source of functional neutrophils with the ability to create oxygen free radicals to effectively kill organisms engulfed by phagocytosis.
What is the most likely diagnosis?
Antibiotic-associated colitis or pseudomembranous colitis caused by Clostridium difficile superinfection (or overgrowth). C difficile is a gram-positive, spore-forming anaerobe. It should be noted that most antibiotic- associated diarrhea (without fever) is osmotic, resulting from decreased carbohydrate digestion secondary to a loss of gut flora. However, C difficile infection will present with fever and leukocytosis, and can be a very serious complication of prolonged antibiotic use.
What are the manifestations of C difficile?
Approximately 20% of hospitalized patients are asymptomatically colonized with Clostridium difficile and then become carriers. Patients with symptoms upon colonization usually present with a low-grade fever, watery diarrhea, lower abdominal pain, leukocytosis, and a recent history (within 10 weeks) of antibiotic use. In severe cases, inflammation of the peritoneum can result from microperforation in the diseased colon. These patients present with signs of peritonitis such as rebound tenderness and involuntary guarding. On colonoscopy, they likely have pseudomembranes on the colon, which are raised yellow-white plaques created by the C difficile toxins (Figure 3-9). Risks include ileus and toxic megacolon, which can grossly perforate and cause death. Emergent colectomy is indicated and can be a lifesaving procedure if performed in a timely manner.
What population of patients is susceptible to C difficile?
Infection is most often seen in elderly hospitalized patients. C difficile produces resistant spores, which are commonly found on hospital objects and on the hands of health care workers. Common alcohol-based hand sanitizers are ineffective at eliminating C difficile spores. C difficile colonizes the gastrointestinal (GI) tract (usually the colon) after the normal gut flora is killed or altered by antibiotics. The antibiotics most commonly associated with this disease are the penicillins, cephalosporins, and clindamycin. Once it has colonized the GI tract, C difficile releases toxins (toxins A and B) that permeate and destroy intestinal epithelial cells, respectively. A new, more virulent strain of this bacterium that produces a binary toxin is associated with the use of fluoroquinolones.
How is C difficile diagnosed and treated?
Definitive diagnosis can be made with a cytotoxicity assay, an enzyme-linked immunosorbent assay for C difficile toxin A, or polymerase chain reaction. First-line treatment is with oral metronidazole or vancomycin. Fecal transplantation is an emerging therapy that aims to replenish the missing gut flora in patients with C difficile overgrowth by introducing normal fecal bacteria from a healthy patient. Pilot studies reveal a high success rate of this procedure, but further testing is needed before it becomes standard of care.
What is the most likely diagnosis?
Congenital syphilis. This infection is one of the so-called ToRCHeS infections (Toxoplasmosis, other infections, Rubella, Cytomegalovirus, Herpes simplex virus, Syphilis), the most common causes of congenital infection.
What is the most likely diagnosis?
Congenital syphilis. This infection is one of the so-called ToRCHeS infections (Toxoplasmosis, other infections, Rubella, Cytomegalovirus, Herpes simplex virus, Syphilis), the most common causes of congenital infection.
What is the causative microorganism in Congenital syphilis?
Treponema pallidum.
What symptoms are commonly found in patients with Congenital syphilis?
Congenital syphilis is a cause of hydrops fetalis, or stillbirth due to fluid accumulation in the fetus. If the newborn survives, it can develop various abnormalities, including the classic facial anomalies (tooth abnormalities known as Hutchinson incisors and mulberry molars, saddle nose, frontal bossing, and short maxilla), as well as recurrent ear infections and interstitial keratitis, leading to vision problems.
In the newborn, what tests can help confirm the diagnosis of congenital syphilis?
Serum rapid plasma reagin (RPR) test: Umbilical cord blood may show false-positive results because of maternal titers but remains the best screening tool for detecting syphilis infection.
Serum analysis and lumbar puncture can be performed for Venereal Disease Research Laboratory (VDRL) testing. VDRL testing detects anticardiolipin antibodies that are produced by patients with syphilis. The serum VDRL is used for screening purposes. VDRL testing from cerebrospinal fluid (CSF) samples is used to detect central nervous system involvement of the disease, known as neurosyphilis. Other CSF findings such as pleocytosis (increased number of cells) and elevated protein levels also suggest infection. The presence of anticardiolipin antibodies is not specific to syphilis and can return false-positive results in patients with Epstein-Barr virus, systemic lupus erythematosus, rheumatoid arthritis, and other autoimmune or inflammatory conditions.
What are the appropriate treatments for syphilis?
Benzathine penicillin G for 10–14 days is the first-line treatment for syphilis.
What is the most likely diagnosis?
Creutzfeldt-Jakob disease (CJD) is a prion disease characterized by rapidly progressive dementia with ataxia, myoclonus, and death within 1 year.
What are the classic brain histology findings in Creutzfeldt-Jakob disease (CJD)?
On histology, prion disease presents with dramatic neuronal loss with numerous vacuoles in the gray matter resembling a porous sponge. This is therefore known as spongiform encephalopathy.
What is the most likely diagnosis?
What microorganism causes this disease?
Cryptococcal meningitis is the most common fungal cause of meningitis and is prevalent among patients with AIDS.
Cryptococcus neoformans is heavily encap- sulated yeast. It is found only as a yeast; it is not a dimorphic microorganism.
What cerebrospinal fluid findings are expected in Cryptococcal meningitis?
Like viral meningitis, fungal meningitis has an elevated WBC count with a lymphocytic predominance. However, all other laboratory results mimic those of bacterial meningitis: increased opening pressure, increased protein, and decreased glucose in cerebrospinal fluid (Table 3-1).
What is the most likely diagnosis?
Cysticercosis, caused by Taenia solium (pork tapeworm), is a cestode (tapeworm) infection. When the tapeworm invades the brain, it forms small nonpurulent abscesses that can later calcify. The disease then becomes known as neurocysticercosis and is responsible for the majority of adult-onset seizures in developing nations.
What is the most likely diagnosis?
Infectious mononucleosis syndrome resulting from cytomegalovirus (CMV) infection. CMV is a double- stranded linear virus in the family Herpesviridae. Infected cells have intranuclear inclusions, and on histology have an “owl’s-eye” appearance, as seen in the center of Figure 3-13.
What is the most likely diagnosis?
This woman is likely experiencing dengue fever, also known as “breakbone fever” because of the severe joint and muscle pain associated with it.
What is the most likely diagnosis?
The child most likely has diphtheria caused by the toxin-producing, gram-positive Corynebacterium diphtheriae. The pathognomonic findings are the gray pharyngeal pseudomembranes on physical exam.
How does the Corynebacterium diphtheriae microorganism cause this presentation?
Exotoxin A is an enzyme that blocks protein synthesis by inactivating elongation factor EF-2 by ribosylating adenosine phosphate. This results in decreased mRNA translation and protein synthesis. (Pseudomonas toxin has a similar mechanism.)
What is the most likely diagnosis?
Elephantiasis is caused by the nematode (roundworm) Wuchereria bancrofti.
What is the most likely diagnosis?
Giardiasis due to Giardia lamblia infection. Giardia appears as both a flagellated, motile, denucleated trophozoite and as a round cyst. Flatulence, foul-smelling stools, and chronic watery diarrhea in a patient with a recent travel history or exposure to well water is characteristic of Giardia infection. The ova and parasite test that reveals “smiley face” trophozoites are diagnostic.
What is the differential diagnosis for Giardiasis?
Entamoeba histolytica can cause a similar spectrum of symptoms but would present with bloody diarrhea instead of watery diarrhea. Infections with enterotoxigenic Escherichia coli, Vibrio cholerae, and Campylobacter jejuni can also cause watery diarrhea, but the onset in these cases is generally acute and will resolve within a few days.
What is the likely causative organism of this condition?
Neisseria gonorrhoeae through sexual contact with an infected partner. The vaginal infection can cause discharge and dysuria. If the bacteria disseminate, skin lesions, tenosynovitis, or septic arthritis can develop. Septic arthritis is a serious condition that must be treated aggressively to prevent permanent damage to the joint.
In this patient, what is Gram stain of a cervical swab likely to show?
Neisseria gonorrhoeae - Gram-negative kidney-shaped cocci in pairs. However, the endocervical Gram stain is insensitive and nonspecific and is best diagnosed by nucleic acid testing.
What infectious agents are most frequently responsible for neonatal sepsis?
Group B streptococci (GBS), Escherichia coli, and Listeria monocytogenes are common causes of sepsis, pneumonia, and meningitis in newborns. GBS often colonizes the vaginal flora of women and can be transmitted vertically during vaginal delivery. This patient’s lack of prenatal care, primiparous vaginal delivery, and onset soon after birth make GBS sepsis a likely diagnosis.
What is the next step in identifying the causative agent?
In Gram staining of a blood sample, GBS appear as gram-positive cocci, L monocytogenes appears as motile gram-positive rods, and E coli appears as gram-negative rods.
How did the infant become infected?
These bacteria can spread through the placenta or be acquired from the birth canal during delivery. The mother may be infected or colonized but asymptomatic. However, pregnant and postpartum women are also at risk for GBS urinary tract infection or chorioamnionitis.
What is the most likely diagnosis?
This is a case of hand-foot-mouth disease, caused by coxsackie A virus. This syndrome presents with a tender rash on the palms, soles, and often the buttocks and painful vesicles on the oral mucosa. This patient’s avoidance of solid food strongly suggests involvement of the oral mucosa.
What is the most likely diagnosis?
Herpes simplex virus type 2 (HSV-2). The pathognomonic findings for herpes infections are painful vesicles. Both HSV-1 and HSV-2 can cause genital herpes, but more than 80% of genital lesions are due to HSV-2.
What is the most likely diagnosis?
Hookworm, or nematode, infection. The findings of eosinophilia and microcytic anemia with recent immigration from an endemic area are highly suggestive of this condition.
What is the most likely diagnosis?
Infection with influenza virus.
The patient has had a similar infection in the past. Why is her immune system not protecting her from this illness with influenza virus?
The isotype of hemagglutinin and neuraminidase is constantly changing because of a phenomenon known as antigenic drift. This is the result of random small mutations that cause changes in the antigenic structure of the virus. These mutations result in antigen structures that are only partially recognized by the host immune system.
What is the likely cause of this patient’s repeated infections and allergic reaction to the blood transfusion? What is the next step in management of this condition?
This patient is having an anaphylactic reaction. IgA is a common component in blood products. This patient likely has hereditary IgA deficiency, and therefore has developed IgG antibodies against IgA. He is particularly susceptible to gastrointestinal infections, especially giardiasis, for which secretory IgA plays an important protective role. IgA deficiency can occur as an isolated syndrome or may involve concurrent IgG deficiency, which increases the risk of sinopulmonary infections.
Because of the patient’s severe anaphylactic reaction to the transfused blood products, it is imperative to discontinue transfusion and administer epinephrine injection. Epinephrine counteracts the bronchospasm and vasodilation that is causing his respiratory difficulty and decreasing blood pressure.
What is the cause of the patient’s milk allergy?
In the absence of intestinal IgA, large proteins are more likely to enter the bloodstream whole. An IgG antibody reaction to these proteins can then cause an allergic reaction. (This is different from lactose intolerance, which is not a true allergy and involves a deficiency of lactase.) For the same reasons, patients with IgA deficiency are at increased risk of developing antibodies against wheat proteins and thus celiac disease.
What is the most likely diagnosis?
This is Kaposi sarcoma, an angiogenic neoplasm prevalent in HIV-positive patients. Kaposi sarcoma is caused by human herpesvirus-8 (HHV-8), a member of the Herpesviridae family. Members of this family are DNA viruses with a double-stranded, linear genome in an enveloped, icosahedral capsid.
What important alternative diagnosis must be ruled out?
An important alternative diagnosis for such skin lesions in HIV patients is bacillary angiomatosis (BA), which typically presents with systemic symptoms such as fever, chills, and malaise. However, because BA is caused by Bartonella henselae it is nonneoplastic and can readily be treated with antibiotics.
How does the human herpesvirus-8 (HHV-8), cause the characteristic discolored skin lesions seen in Kaposi sarcoma?
HHV-8 has a tropism for endothelium cells and is thought to induce vascular endothelial growth factor, which causes irregular vascular channels to develop in the skin. RBCs extravasate into these spaces, causing the characteristic purple-red skin lesions as seen in Figure 3-21.
What is the most likely diagnosis?
This patient is suffering from kala azar, or visceral leishmaniasis. Visceral leishmaniasis is caused by the protozoan Leishmania donovani and is characterized by spiking fevers, hepatosplenomegaly, and pancytopenia.
What is the most likely diagnosis?
Legionnaire’s disease, an infection caused by the gram-negative rod Legionella pneumophila. Any patient presenting with diarrhea and pneumonia-like symptoms has Legionella until proven otherwise. This patient has evidence of interstitial, or atypical, pneumonia, which makes the diagnosis even more likely.
What risk factors does the patient have for developing Legionella?
The patient’s history of diabetes and smoking predisposes him to Legionella infection. Given his occupation as a maintenance man, he likely works with air conditioning systems. As this microorganism grows in infected water sources, the patient’s occupation places him at risk.
