UWSA1-4 Flashcards
A 5-year-old boy comes to the office with periorbital edema and rust-colored urine for 2 days. His oral intake has been normal, but his parents are concerned that he is voiding less frequently than usual. Three weeks ago, he had a pustule on his face that subsequently developed an overlying, adherent, honey-crusted layer and resolved with antibiotics. The patient’s blood pressure is mildly elevated. Urinalysis is positive for protein and red blood cell casts. Which of the following characteristics best describes the bacteria involved in this patient’s condition?
This patient’s most likely diagnosis is acute poststreptococcal glomerulonephritis (PSGN). PSGN is an immune complex-mediated disease that occurs 1-3 weeks after a pharyngeal or skin infection (eg, impetigo) by Streptococcus pyogenes (group A Streptococcus or GAS). Deposition of streptococcal nephritogenic antigens within the glomerulus causes immune complex formation, which in turn triggers complement activation and inflammation.
GAS is a gram-positive, beta-hemolytic, bacitracin-sensitive bacterium that grows in chains. Gram-positive bacteria retain the crystal violet stain and appear purple. When GAS is plated on blood agar culture, GAS causes beta hemolysis (complete red cell lysis) and transparency in the normally red agar media. Bacitracin can be used to distinguish GAS from other streptococcal strains, with GAS being sensitive to bacitracin and most non-group A strains resistant.
Symptoms of PSGN typically include edema, gross hematuria, hypertension, and oliguria. The edema is commonly periorbital and can become generalized. Gross hematuria often presents as tea- or cola-colored urine, and urinalysis is positive for protein and blood. Serum abnormalities include a low C3 and mildly elevated creatinine. Antibody titers reflecting a previous GAS infection are helpful in diagnosis (Table). A biopsy is usually not indicated for diagnosis when the presentation is classic.
Strep Pyogenes features
GAS is a gram-positive, beta-hemolytic, bacitracin-sensitive bacterium that grows in chains. Gram-positive bacteria retain the crystal violet stain and appear purple.
When GAS is plated on blood agar culture, GAS causes beta hemolysis (complete red cell lysis) and transparency in the normally red agar media.
Bacitracin can be used to distinguish GAS from other streptococcal strains, with GAS being sensitive to bacitracin and most non-group A strains resistant.
Acute poststreptococcal Glomerulonephritits pathophysiology
PSGN is an immune complex-mediated disease that occurs 1-3 weeks after a pharyngeal or skin infection (eg, impetigo) by Streptococcus pyogenes (group A Streptococcus or GAS)
Deposition of streptococcal nephritogenic antigens within the glomerulus causes immune complex formation, which in turn triggers complement activation and inflammation.
Acute poststreptococcal Glomerulonephritits clinical features
Can be asymptomatic
Symptoms of PSGN typically include edema, gross hematuria, hypertension, and oliguria. The edema is commonly periorbital and can become generalized. Gross hematuria often presents as tea- or cola-colored urine, and urinalysis is positive for protein and blood. Serum abnormalities include a low C3 and mildly elevated creatinine. Antibody titers reflecting a previous GAS infection are helpful in diagnosis (Table). A biopsy is usually not indicated for diagnosis when the presentation is classic.
If symptomatic:
Gross hematuria (tea- or cola-colored urine)
Edema (periorbital, generalized)
Hypertension
Acute poststreptococcal Glomerulonephritits lab findings
Urinalysis: + protein, + blood, ± red blood cell casts
Serum:
↓ C3 & possible ↓ C4
↑ Serum creatinine
↑ Anti-DNase B (antideoxyribonuclease-B) & ↑ AHase (antihyaluronidase)
↑ ASO (antistreptolysin O) & ↑ anti-NAD (from preceding pharyngitis) (antinicotinamide-adenine dinucleotidase)
Staphylococcus aureus features
Staphylococcus aureus is a gram-positive, catalase-positive, coagulase-positive bacterium that grows in clusters.
Differentiating staph from strep
the catalase test is a particularly important test used to determine whether the Gram + cocci is a staphylococci or a streptococci.
Staph is catalase Positive
Strep is catalase Negative
Quelling Reaction
The Quellung reaction refers to capsule swelling that is evident on microscopy after a bacterium is exposed to its capsular antigens. Streptococcus pneumoniae, the most common cause of community-acquired pneumonia, is an example of a Quellung-reaction-positive bacterium.
Preceeding infections of Reactive Arthritis
Genitourinary infection: Chlamydia trachomatis
Enteritis: Salmonella, Shigella, Yersinia, Campylobacter, Clostridioides (formerly Clostridium) difficile
Reactive Arthritis symptoms
Asymmetric oligoarthritis
Enthesitis
Dactylitis
Ocular: conjunctivitis, anterior uveitis
Genital: urethritis, cervicitis, prostatitis
Dermal: keratoderma blennorrhagicum, circinate balanitis
Oral ulcers
Reactive arthritis risk factor
HLA B27
Reactive arthritis Pathophysiology
Genitourinary or gastrointestinal infection typically precedes the onset of symptoms by 2-6 weeks. The manifestations are caused by immune-complexes involving bacterial antigens. However, it does not represent disseminated infection, and joint aspirates are sterile (ie, it is a reactive, not infectious, arthritis).
Ankylosing Spondylitis description
Ankylosing spondylitis is a chronic disease affecting the axial skeleton and causes progressive stiffness and pain.
It is associated with HLA B27, but extra-articular symptoms are not prominent.
Disseminated gonococcal infection description
Disseminated gonococcal infection presents as
purulent arthritis (eg, knee, wrist, ankle)
or
as the triad of tenosynovitis, dermatitis, and non-purulent polyarthralgias.
Hypersensitivity Vasculitis
Hypersensitivity vasculitis is a drug reaction characterized by a purpuric rash.
Viral Arthritis description
Viral arthritis causes symmetric, polyarticular disease. It is most common following parvovirus, hepatitis B, hepatitis C, rubella, and alphavirus infection.
Chromosome 15 genomic imprinting disorders
- Prader-Willi Syndrome
- Angelman Syndrome
Pathophysiology of Prader-Willi Syndrome
This child has Prader-Willi syndrome (PWS), a genomic imprinting disorder caused by the loss of paternally inherited alleles on chromosome 15q11-13. Within this region, certain genes are differentially imprinted and silenced depending on the parent of origin. Alleles that are maternally imprinted cannot be actively expressed unless there is a functional paternal copy. PWS can be caused by any genetic defect that results in the absence of this paternal contribution, most commonly microdeletions of the paternal 15q11-13 region or maternal uniparental disomy (ie, both chromosome 15s are inherited from the mother). This patient’s normal fluorescence in-situ hybridization (FISH) findings indicate that his condition is most likely due to maternal uniparental disomy.
Causes of prader-willi syndrome
Loss of paternally inherited allele from chromosome 15:
Paternal microdeletion
or
Maternal uniparental disomy
Clinical Features of Prader-Willi syndrome
Neonatal hypotonia
Hyperphagia/obesity
Short stature
Small hands & feet
Hypogonadism
Dysmorphic facies
Intellectual disability
Causes of Angelman Syndrome
Loss of maternally inherited allele from chromosome 15
Maternal microdeletion
Paternal uniparental disomy
S&S of Angelman syndrome
Epilepsy/seizures
Ataxic gait/tremors
Poor motor & language development
Inappropriate laughter/smiling
Intellectual disability
Celiac disease genetic implications
Celiac disease has a genetic component and is associated with the human leukocyte antigen
(HLA) DQ2 and DQ8 genotypes.
Celiac Disease Pathophysiology
Celiac disease (celiac sprue, gluten-sensitive enteropathy) is caused by dietary exposure to gliadins (a component of gluten) in wheat and related grains in susceptible individuals. This sensitivity to gluten can trigger autoimmune reactions in the gastrointestinal tract. In the small bowel, celiac disease causes marked villous atrophy in a background of diffuse enteritis. CD8+ T-cell lymphocytes infiltrate the small intestine surface epithelium, and a wide range of inflammatory cells (CD4+ T-cell lymphocytes, plasma cells, macrophages, eosinophils, and mast cells) take up residence in the lamina propria. Celiac disease has a genetic component and is associated with the human leukocyte antigen (HLA) DQ2 and DQ8 genotypes.
Celiac Disease S&S
This patient, with persistent diarrhea, bloating, and weight loss, has typical symptoms of celiac disease.
Celiac disease is often associated with dermatitis herpetiformis, which causes grouped vesicles, papules, and urticaria on the extensor surfaces of the elbows, knees, sacrum, and buttocks. The lesions are extremely pruritic and are caused by cross-reactivity of anti-gliadin IgA antibodies with transglutaminase at the dermal basement membrane. Skin biopsy will show microabscesses at the dermal papillary tips, which coalesce to form subepidermal blisters. Immunofluorescence staining for IgA confirms the diagnosis.
Dermatitis Herpetiformis
Celiac disease is often associated with dermatitis herpetiformis, which causes grouped vesicles, papules, and urticaria on the extensor surfaces of the elbows, knees, sacrum, and buttocks. The lesions are extremely pruritic and are caused by cross-reactivity of anti-gliadin IgA antibodies with transglutaminase at the dermal basement membrane. Skin biopsy will show microabscesses at the dermal papillary tips, which coalesce to form subepidermal blisters. Immunofluorescence staining for IgA confirms the diagnosis.
Celiac disease histology
In the small bowel, celiac disease causes marked villous atrophy in a background of diffuse enteritis. CD8+ T-cell lymphocytes infiltrate the small intestine surface epithelium, and a wide range of inflammatory cells (CD4+ T-cell lymphocytes, plasma cells, macrophages, eosinophils, and mast cells) take up residence in the lamina propria.
“Cobblestone mucosa and transmural inflammation” are characteristic of
Crohn disease
Identify
Polycystic Ovarian Syndrome Pathophysiology
polycystic ovary syndrome (PCOS), a common endocrine disorder in women that is associated with an elevated LH/FSH ratio and ovarian hyperresponsiveness to LH.
Because LH stimulates the ovarian theca cells to produce androgens, patients with PCOS usually have hyperandrogenism, which can be diagnosed clinically (eg, acne, hirsutism) or biochemically (ie, high testosterone level)
Elevated androgen levels and an unbalanced LH/FSH ratio both inhibit the maturation and release of a single dominant ovarian follicle (ie, ovulation). Therefore, patients with PCOS are typically anovulatory and develop multiple, smaller follicles that arrest in development. These follicles eventually degenerate and accumulate fluid, causing the classic appearance of bilaterally enlarged, polycystic ovaries.
Lesch-Nyhan Syndrome pathophysiology
Lesch-Nyhan syndrome caused by an X-linked recessive defect in hypoxanthine-guanine phosphoribosyltransferase (HGPRT). The HGPRT enzyme participates in the purine salvage pathway by catalyzing the conversion of hypoxanthine and guanine to inosine monophosphate and guanosine monophosphate, respectively. Deficiency of this enzyme causes decreased purine salvage, increased purine synthesis, hyperuricemia, and hyperuricuria.
Lesch-Nyhan Syndrome S&S
Characteristic features include self-mutilating behavior (eg, finger and lip biting), mild intellectual disability, involuntary movements (eg, dystonia), delayed motor development, nephrolithiasis, and gout. Parents may also report a “frost” on the skin under the affected child’s diaper due to hyperuricuria. Treatment with allopurinol decreases uric acid levels and therefore relieves symptoms related to gout and urolithiasis, but this treatment has little effect on neurological symptoms.
Antibiotics that inhibit prokaryotic protein synthesis at the 30s ribosomal subunit
tetracyclines (eg, doxycycline) and the aminoglycosides (eg, streptomycin)
Macrolide MOA
macrolide antibiotic that binds to the 50s prokaryotic ribosomal subunit and blocks the translocation step by preventing tRNA release from the donor site after peptide bond formation.
Chloramphenicol MOA
Chloramphenicol binds to the 50s prokaryotic ribosomal subunit and blocks peptidyltransferase action, thereby preventing new peptide bond formation.
Rifampin MOA
Rifampin blocks prokaryotic mRNA synthesis by bacterial RNA polymerase.
Typically used in combination with other antibiotics to minimize bacterial resistance, rifampin treats active tuberculosis and prevents meningitis caused by Neisseria meningitidis or Haemophilus influenzae.
Puromycin MOA
Puromycin is an aminonucleoside antibiotic that has a structure analogous to aminoacyl-tRNA. In prokaryotes, it leads to the premature release of unfinished polypeptide chains as polypeptidyl-puromycin derivatives.
Pilocarpine MOA
Muscarinic agonist
Atropine MOA
Muscarinic antagonist
Physostigmine moa
Acetylcholinesterase inhibitor
Phenylephrine MOA
alpha-adrenergic receptor agonist (α1 > α2)
What’s This?
peripheral blood smear shows macrocytosis and a hypersegmented neutrophil.
A 56-year-old woman comes to the office due to a 3-month history of excessive fatigue, along with progressive numbness in both feet. Her sleep is adequate, and she eats a normal diet. The patient has a history of hypothyroidism that was diagnosed following pregnancy 20 years ago. Her only current medication is levothyroxine, and she does not use alcohol. Physical examination shows mucosal pallor with a flat, shiny tongue. Neurologic examination finds diminished vibratory sensation in both feet. TSH level is normal. Peripheral blood smear is shown in the image below.
This patient has fatigue, peripheral neuropathy, and atrophic glossitis. The peripheral blood smear shows macrocytosis and a hypersegmented neutrophil. In addition, she has a history of autoimmune thyroiditis (the most common cause of hypothyroidism in developed countries). In light of her current symptoms, this patient most likely has pernicious anemia due to autoimmune destruction of gastric mucosa.
Over time, this damage results in chronic atrophic gastritis, causing profound hypochlorhydria and leading to a compensatory increase in serum gastrin levels (antral G cell gastrin secretion is inhibited by hydrochloric acid). In addition, the loss of intrinsic factor-secreting parietal cells leads to depletion of vitamin B12 stores and eventual deficiency.
Vitamin B12 deficiency causes hematologic (eg, macrocytic anemia) and neurologic (eg, peripheral neuropathy, combined degeneration of ascending and descending spinal tracts) manifestations. Pernicious anemia occurs most commonly in patients age >50, but it can be seen more frequently in younger patients with other autoimmune disorders.
Vitamin B12 Deficiency S&S
Vitamin B12 deficiency causes hematologic (eg, macrocytic anemia)
fatigue, peripheral neuropathy, and atrophic glossitis
and neurologic (eg, peripheral neuropathy, combined degeneration of ascending and descending spinal tracts) manifestations.
Pernicious Anemia Pathophysiology
Pernicious anemia is due to autoimmune destruction of gastric mucosa (parietal cells). Production of gastric acid is diminished, leading to a compensatory increase in gastrin release. Secretion of gastric intrinsic factor is also lost, leading to vitamin B12 deficiency.
Over time, this damage results in chronic atrophic gastritis, causing profound hypochlorhydria and leading to a compensatory increase in serum gastrin levels (antral G cell gastrin secretion is inhibited by hydrochloric acid).
In addition, the loss of intrinsic factor-secreting parietal cells leads to depletion of vitamin B12 stores and eventual deficiency. Vitamin B12 deficiency causes hematologic (eg, macrocytic anemia) and neurologic (eg, peripheral neuropathy, combined degeneration of ascending and descending spinal tracts) manifestations.
Pernicious anemia occurs most commonly in patients age >50, but it can be seen more frequently in younger patients with other autoimmune disorders.
Secretin mechanism of secretion
Secretin is produced by S cells of the duodenal mucosa in response to passage of gastric acid through the pylorus.
A 26-year-old man comes to the office due to a scrotal mass. He first noticed a painless mass in the scrotum 4 weeks ago while in the shower and thinks it may be getting larger. The patient has no history of abdominal or genital trauma. On examination, he has a left-sided scrotal mass that is palpable when he stands but disappears when he lies down. Light does not shine through the mass when a penlight is held behind it. Which of the following is the most likely diagnosis?
Varicoceles are dilations of the spermatic vein pampiniform plexus that are common in adults. They tend to arise on the left side as the left gonadal vein is one of the longest veins in the body and drains into the left renal vein at a perpendicular angle. The pressure within the left renal vein is also higher due to compression between the aorta and the superior mesenteric artery (“nutcracker effect”). This increased pressure in the left gonadal vein results in valve leaflet failure and retrograde blood flow toward the testis on standing. When the patient is recumbent, much of the blood returns to systemic circulation and the varicocele diminishes in size.
A varicocele can present as a vague fullness or as a large, compressible mass likened to a “bag of worms.” It does not transilluminate light. Some individuals are asymptomatic; others experience aching pain relieved with recumbency, testicular atrophy, or reduced fertility (due to blood stasis and/or increased scrotal temperature).
Varicocele Pathophysiology
Varicoceles are dilations of the spermatic vein pampiniform plexus that are common in adults. They tend to arise on the left side as the left gonadal vein is one of the longest veins in the body and drains into the left renal vein at a perpendicular angle. The pressure within the left renal vein is also higher due to compression between the aorta and the superior mesenteric artery (“nutcracker effect”). This increased pressure in the left gonadal vein results in valve leaflet failure and retrograde blood flow toward the testis on standing. When the patient is recumbent, much of the blood returns to systemic circulation and the varicocele diminishes in size.
A varicocele can present as a vague fullness or as a large, compressible mass likened to a “bag of worms.” It does not transilluminate light. Some individuals are asymptomatic; others experience aching pain relieved with recumbency, testicular atrophy, or reduced fertility (due to blood stasis and/or increased scrotal temperature)
“nutcracker effect”
The pressure within the left renal vein is also higher due to compression between the aorta and the superior mesenteric artery
Varicocele S&S
A varicocele can present as a vague fullness or as a large, compressible mass likened to a “bag of worms.” It does not transilluminate light. Some individuals are asymptomatic; others experience aching pain relieved with recumbency, testicular atrophy, or reduced fertility (due to blood stasis and/or increased scrotal temperature).
What is a hydrocele?
Hydroceles are peritoneal fluid collections that accumulate between the parietal and visceral layers of the tunica vaginalis. Hydroceles can be small or quite large, with pain increasing with the mass size. Although communicating hydroceles can change in size with positional changes, the fluid within a hydrocele is easily transilluminated
Varicocele description
Varicoceles are dilations of the spermatic vein pampiniform plexus that enlarge with standing and regress with lying down. Patients may be asymptomatic or experience aching pain relieved with recumbency, testicular atrophy, or reduced fertility.
Acanthosis nigracans
acanthosis nigricans, a reactive skin condition characterized by brown to black, velvety thickened plaques that tend to arise in flexural regions such as the axillae or back of the neck.
Acanthosis nigricans is most commonly associated with benign conditions such as insulin resistance or obesity. However, it can also signal the presence of malignancy within the gastrointestinal (GI) tract (eg, stomach, liver) or lungs. When acanthosis nigricans appears suddenly, spreads quickly, or involves the mucous membranes or palms and soles, the likelihood of malignancy increases. It has been postulated that malignancy and hyperinsulinemia cause acanthosis nigricans by influencing growth factor production.
Adrenal insufficiency presentation
Adrenal insufficiency can present with fatigue and weight loss, and it is associated with hyperpigmentation due to increased secretion of ACTH and melanocyte-stimulating hormone in response to inadequate cortisol levels.
Antiandrogen therapies
A pediatric cardiologist is consulted about a 2-week-old boy with a suspected congenital heart defect. The patient struggles while feeding, developing tachypnea, tachycardia, and transient cyanosis. The boy’s postnatal course was complicated by a seizure during the first week. Physical examination shows low-set ears and increased distance between the eyes. Karyotype analysis reveals a partial deletion on chromosome 22. Disturbed development of which of the following cardiac structures most likely occurred in utero?
Conotruncal (outflow tract) defects are common in infants with DGS and include persistent truncus arteriosus, tetralogy of Fallot, and interrupted aortic arch. In utero, a wall normally divides the single truncal root into a separate pulmonary artery and ascending aorta. Persistent truncus arteriosus occurs when this septum does not form, leading to branching of the aorta, pulmonary arteries, and coronary arteries from a single arterial trunk. This defect can lead to cyanosis and heart failure if it is not surgically corrected.
Hyper IgM syndrome
An error in CD40 signaling from t cells to b cells
The 5 major types of immunoglobulin are distinguished by different amino acid sequences in their heavy chain (alpha, delta, epsilon, gamma, mu). Unstimulated B cells constitutively express mu and delta heavy chains and generate only IgM and IgD. In order to generate other immunoglobulin types, B cells must undergo costimulation by CD40 ligand (CD40L), which is expressed on the surface of activated CD4 cells.
Binding of CD40L to CD40 triggers activated B cells to undergo class-switch recombination, which replaces the mu heavy chain with alpha, epsilon, or gamma depending on concurrent cytokines released by the activated CD4 cell. This leads to the production of IgA (alpha heavy chain), IgE (epsilon heavy chain), or IgG (gamma heavy chain).
DNA Methylation
DNA methylation refers to the addition of methyl groups to nucleotide residues (often adenine and cytosine) by the enzyme DNA methyltransferase. In eukaryotes, cytosine-guanine dinucleotide repeats (CpGs) in the promoter region of genes are preferentially methylated as part of the epigenetic code – a heritable form of gene regulation not reliant on changes in the genetic code itself. The methylation of cytosine residues in CpGs prevents transcription factors from binding to the promoter, effectively silencing transcription of genes not required by terminally differentiated somatic cells. It can also be pathologic; an example includes malignancies in which selective methylation downregulates tumor suppressor genes.
In contrast to eukaryotes, the methylation of adenine and cytosine residues in prokaryotic DNA helps the cell distinguish its DNA from foreign DNA. Unmethylated foreign DNA is destroyed as part of a cellular defense mechanism. Adenine residues may also be methylated shortly after DNA replication, allowing mismatch repair enzymes to distinguish between old and new strands.
Cox-1 vs Cox-2
A newborn boy is in the neonatal intensive care unit for management of prematurity. He was delivered vaginally at 26 weeks gestation due to premature labor and preterm rupture of membranes. The patient is intubated and has an umbilical arterial catheter in place. The medical team is preparing to place another catheter through the umbilical vein. To reach the inferior vena cava and right atrial junction, the umbilical venous catheter most likely passes through which of the following structures?
Ductus venosus
Describe fetal blood flow
In utero, blood flows from the placenta into the fetus via the umbilical vein. The blood then flows to the fetal liver, where it may be diverted into the inferior vena cava (IVC) via the ductus venosus. The ligamentum teres and ligamentum venosum are the remnants of the umbilical vein and ductus venosus in adults, respectively.
The umbilical vessels are commonly used for central vascular access and resuscitation of a critically ill neonate. These procedures take advantage of the fact that complete closure of the ductus venosus does not occur until approximately 1 week after birth, although this structure is closed functionally within hours of birth. An umbilical venous catheter passes through the umbilical vein and ductus venosus until the tip reaches the IVC at the junction of the right atrium.
Umbilical vessel structure
Azygous vein
Foramen ovale
In the fetus, the foramen ovale allows blood to pass from the right atrium directly into the left atrium, bypassing the lungs. Lung inflation at the time of birth decreases right heart pressure relative to left heart pressure, causing closure of the foramen ovale. The foramen ovale is obliterated in most adults, with the fossa ovale as its remnant.
Identify
A 53-year-old man who recently emigrated from Russia comes to the office due to several months of productive cough with occasional hemoptysis. Medical history is significant for tuberculosis and chronic bronchitis. The patient has smoked a pack of cigarettes per day for the past 20 years. Tuberculin skin testing yields 15 mm of indurated erythema. Bronchoalveolar lavage fluid is cultured, and microscopic examination of the cultured organism is shown in the image below:
Culture of this patient’s bronchoalveolar lavage fluid shows a conidial head consistent with Aspergillus fumigatus, a fungus ubiquitous in the environment (eg, soil) worldwide.
In culture, Aspergillus has a characteristic microscopic morphology, with conidial heads (fruiting structures) that project from septate hyphae on exposure to air. The conidial head is composed of a supportive conidiophore (hyphal stalk) and terminal vesicle with radiating phialides that bear infectious conidia (spores). The conidia disseminate in the air and spread the organism.
Inhalation of conidia may lead to pulmonary disease in certain individuals. In patients with a history of tuberculosis, Aspergillus can colonize preexisting lung cavities. Multiplication of fungal elements within these cavities can lead to formation of an aspergilloma (ie, fungus ball), which may cause chronic cough and occasional hemoptysis (due to eroded blood vessels). Treatment includes antifungal therapy and surgical excision.
Candida albicans description
Candida albicans is a yeast that typically causes mucocutaneous infections in immunocompetent hosts. Widespread disease occurs only in immunocompromised patients, and microscopic examination would show budding yeast and pseudohyphae
Mycobacterium histology
Reactivation of latent Mycobacterium tuberculosis infection may cause cough and hemoptysis, but culture would grow acid-fast bacilli (appear pink-purple with acid-fast stain).
Pneumocystis jiroveci
Pneumocystis jirovecii is a ubiquitous fungal organism that causes opportunistic pneumonia in HIV-positive patients with CD4 counts < 200/mm3. Microscopic examination of sputum or bronchoalveolar lavage fluid shows cup- or disc-shaped organisms; it cannot be cultured.
A colony of bacteria resistant to gentamicin and a colony resistant to ampicillin are mixed on an agar plate containing both antibiotics. Bacterial growth is noted after incubation for 24 hours. The same experiment is then repeated with the addition of deoxyribonuclease (DNAse) to the agar plate. The enzyme is functional in the culture medium but is not able to penetrate the bacterial cell membrane. During this second experiment, no bacterial growth is observed. Which of the following is the most likely mechanism of bacterial survival in the first experiment?
Transformation
