Micro USMLE 8-21 (5) Flashcards
(30 cards)
A biotechnology firm is developing a new, small-protein drug designed to prevent the spread of a sexually transmitted infection. Scientists want to block the infectious step of the bacteria’s reproductive cycle. In a patient infected with the targeted pathogen, a Giemsa-stained smear of urethral discharge would look similar to the image below.During which stage of this pathogen’s life cycle is it most infectious?
Extracellular elementary body
Giemsa stain showing intracytoplasmic inclusions in the context of a urethral discharge, potentially due to a sexually transmitted infection, is indicative of Chlamydia trachomatis. Cytoplasmic inclusions can be seen on Giemsa- or fluorescent antibody–stained urethral or cervical smear, but diagnosis of Chlamydia can also be made from a urine sample using nucleic acid amplification techniques. Although it is frequently asymptomatic, C. trachomatis infection can cause urethritis, cervicitis, and pelvic inflammatory disease (PID) in women, as well as conjunctivitis and reactive arthritis (Reiter syndrome). Treatment of Chlamydia infection requires a course of either doxycycline or azithromycin. Chlamydia is infectious when it reaches the developmental stage described as an extracellular elementary body, as this form can attach and enter host cells.
he cytoplasmic inclusions (arrows in image above) are non-infectious as are the intracellular elementary bodies. Similarly, independent reticulate bodies and reticulate bodies that are?
in the process of multiplying are both intracellular, and therefore are not infectious. The stages of Chlamydia development and relationship to infectivity are explained by the figure and table below.
Chlamydia trachomatis, which can cause urethritis, cervicitis, and pelvic inflammatory disease in women, is infectious when it is as an elementary body that can enter host cells from ?
the extracellular domain. While all of the intracellular forms of C. trachomatis are necessary for the reproduction of the organism, only the extracellular form is considered infectious.
This woman presents with a 1- to 2-week history of fatigue, cold intolerance, constipation and neck pain following a likely viral illness. Her examination is significant for a tender thyroid gland. Signs of hypothyroidism with a tender thyroid are most likely to be related to De Quervain thyroiditis, a common cause of transient hypothyroidism seen after viral illnesses. A hyperthyroid stage caused by unregulated T4 and T3 release generally precedes the transient hypothyroid stage.
De Quervain thyroiditis, also known as?
subacute granulomatous thyroiditis, is characterized by an exquisitely tender thyroid gland, elevated erythrocyte sedimentation rate, and other manifestations of hypothyroidism (eg, fatigue, cold intolerance, cool skin, decreased deep tendon reflexes) seen in this patient. Because patients quickly return to a euthyroid state, no treatment is necessary.
Numerous viral agents such as mumps, Epstein-Barr virus, coxsackie virus, flu, and adenovirus have been implicated in De Quervain thyroiditis but the precise cause of the condition is unknown. Graves disease is an autoimmune form of hyperthyroidism caused by ?
production of autoantibodies that activate the thyroid-stimulating hormone receptor. Hashimoto thyroiditis is characterized by antimicrosomal and antithyroglobulin antibodies that lead to hypothyroidism; however, this autoimmune condition typically has a slow course and presents with a nontender thyroid. Postpartum thyroiditis is associated with painless hypothyroidism and would be seen 1 year after pregnancy. Vitamin B12 deficiency leads to a macrocytic anemia and peripheral neuropathy and does not cause elevated thyroid-stimulating hormone levels or thyroid gland tenderness.
De Quervain thyroiditis is a transient hypothyroidism seen after viral illnesses. It is characterized by an exquisitely tender thyroid gland, elevated erythrocyte sedimentation rate, and other manifestations of ?
hypothyroidism, including fatigue, cold intolerance, cool skin, and decreased deep tendon reflexes.
The patient’s presentation is representative of the second stage of subacute sclerosing panencephalitis (SSPE), a sequela of infection with rubeola, or measles virus. SSPE typically presents 7–10 years after initial infection with the virus and results from the failure of mature viral particles to form. This action leads to persistent replication of the virus and nonproductive infection, eventually resulting in demyelination of CNS neurons.
The initial stage of the condition presents with dementia and personality changes and lasts up to 1 year. The second stage of the condition is characterized by severe myoclonus and typically lasts for 3–12 months. The third and fourth stages are characterized by?
worsening dementia and deterioration of the autonomic nervous system, as well as decorticate rigidity or flaccidity. The condition is typically fatal. A diagnosis can be made by the detection of oligoclonal bands in the CSF. High titers of measles antibodies are also often present in the serum of affected patients.
The fact that the patient is from rural India and is unsure of her vaccination status suggests that she may not have received all of her childhood immunizations, including her measles vaccines.
JC virus causes progressive multifocal leukoencephalopathy and manifests in altered mental status, motor deficits, and visual symptoms. It rarely affects immunocompetent persons. Poliovirus infection is characterized by flaccid paralysis and muscular atrophy. Rabies virus spreads from the site of the initial bite from an infected animal to motor and sensory neurons and can lead to ?
convulsions, paresthesias, cognitive effects, and flaccid paralysis; the time course of this patient’s illness is extremely slow for rabies. The rubella virus, if acquired antenatally, can lead to congenital rubella syndrome, which is characterized by ophthalmologic and cardiac defects and fetal mortality.
Subacute sclerosing panencephalitis (SSPE) is a sequela of rubeola, or measles virus, and can be detected by the presence of oligoclonal bands in CSF. High titers of measles antibodies are often present in the serum of affected patients. Be suspicious of SSPE in a patient who has an unknown vaccination history, is from an endemic area, and presents with ?
myoclonus and worsening dementia.
The patient received a renal transplant 10 years ago and takes immunosuppressant drugs as a result. When he is not working, he likes to garden or take his children to a local park, activities that would put him in regular contact with soil and pigeon droppings, and therefore with Cryptococcus neoformans.
In immunosuppressed individuals, C. neoformans can lead to cryptococcal pneumonia. This is the second most common clinical manifestation of cryptococcal infection. Symptoms can include fever, fatigue, cough, and pleuritic chest pain. Other less common findings may include ?
hemoptysis, auscultatory rales, or a pleural rub. C. neoformans is visualized via India ink stain and detected by serum cryptococcal antigen.
Board review guides often emphasize that this species is a causative agent of fungal meningitis in immunocompromised patients (with Blastomyces, Coccidioides, and Histoplasma as causes of fungal pneumonia). Students should note, however, that these are oversimplifications. All the systemic mycoses can cause infection in a number of sites. Although meningoencephalitis is the most common clinical manifestation of cryptococcal disease, it is not the only one. In fact, the initial site of inoculation with Cryptococcus is? t
he lung; meningitis can ensue only after the yeasts have disseminated from this site. Patients present more often with cryptococcal meningitis, in large part because many cryptococcal lung infections are asymptomatic.
Other organs, such as the abdomen, bones, skin, and genitourinary tract, may be affected in disseminated disease; however, these are not the initial site of infection and are therefore rarer manifestations of cryptococcal infection.
This means that diffuse abdominal pain with rebound tenderness is not likely to found in this patient. Peritonitis is a rare manifestation of infection with C. neoformans. Likewise, dull bone pain that worsens on movement is not a symptom that this patient would likely experience. Osteolytic bone lesions are? another less common manifestation of disseminated cryptococcal infection. Clinical presentation can vary (acute or chronic, and generally nonspecific occur symptoms first); however, bony involvement is not likely in the initial presentation of the disease.
Cutaneous lesions are found in 10%–15% of cases of disseminated disease involving C. neoformans, and they are often signs of ?
a particularly severe disease. Although the patient is immunosuppressed, it is unlikely that the microorganism was disseminated from the initial infection site in the lung.
And finally prostatitis can occur in cases of disseminated cryptococcal infection. It is seen occasionally in cryptococcal pneumonia. But it is unlikely that this patient would first present with symptoms of prostatitis (urinary frequency and urgency).
Cryptococcus neoformans, visualized via India ink stain and detected by serum cryptococcal antigen, is carried by pigeons. The most common disease caused by?
this microorganism is meningoencephalitis, followed by cryptococcal pneumonia
The child presents with asymptomatic, flesh-colored papules that show central umbilication, which is characteristic of molluscum contagiosum. Molluscum contagiosum is a member of the poxvirus family that causes a localized infection consisting of nonerythematous, pearly, dome-shaped papules on the skin. However, this infection frequently leads to localized dermatitis, causing the surrounding skin to become pink, dry, and pruritic. As the papules resolve, the skin may become inflamed and crust over for a week or two.
Molluscum contagiosum is a common disease of childhood and often spreads via?
direct skin-to-skin contact or via indirect contact such as with the sharing of bath towels. An association with use of swimming pools has been reported and is likely where this patient became infected. The lesions may appear anywhere on the body except the palms and soles, and are usually self-limited in immunocompetent people. If the lesions appear on the genitalia of sexually active people, it is considered a sexually transmitted disease. In immunocompromised patients, particularly those with HIV-positive status, lesions can be quite large (eg, giant molluscum) and widespread.
Molluscum contagiosum is not caused by adenovirus, hepadnavirus, herpesvirus, papillomavirus, or polyomavirus. Adenovirus commonly presents with pharyngitis and coryza, and hepadnavirus causes hepatitis B. Herpesviruses are responsible for genital herpes and cold sores (HSV-1 and -2) as well as chickenpox and shingles (varicella zoster). Papillomavirus causes ?
the common wart in children, and reactivation of the polyomavirus results in progressive multifocal leukoencephalopathy (PML) in immunosuppressed patients.
Molluscum contagiosum is caused by a poxvirus and is characterized by pink papules, which may be umbilicated. Itching may be present or absent. Molluscum contagiosum is commonly transmitted by skin-skin contact in children, but is associated with ?
sexual transmission in adults.
The syndrome described in the vignette is consistent with Guillain-Barré syndrome (GBS), which is a common cause of acute peripheral neuropathy. Two-thirds of patients have preceding viral or gastrointestinal illness. Campylobacter jejuni, a curved, oxidase-positive, gram-negative bacterium that causes gastroenteritis, has been associated with GBS. The pathogenesis is thought to involve generation of antiganglioside antibodies induced by C. jejuni exposure.
GBS manifests as?
an ascending paralysis with diminished reflexes and progresses over a period of days. Findings include elevated γ-globulin, decreased nerve conduction velocity indicative of demyelination, and albuminocytologic dissociation in the CSF (increased protein, normal WBC). Nerve biopsy (which is rarely done) would show segmental demyelination with an endoneurial inflammatory infiltration.
Streptococcus pneumoniae (α-hemolytic, encapsulated, gram-positive cocci that produces an IgA protease) that results in bacteremia, meningitis, osteomyelitis, or septic arthritis Pseudomonas aeruginosa (non-lactose-fermenting, oxidase-positive, gram-negative, aerobic bacilli) that causes otitis externa, urinary tract infection, pneumonia, and sepsis in immunocompromised hosts Clostridium botulinum (rod-shaped, gram-positive, spore-forming anaerobe that produces a heat-labile toxin) inhibits ?
acetylcholine release at the neuromuscular junction and causes flaccid paralysis Treponema pallidum (spiral-shaped bacteria with axial filaments) is the cause of syphilis and causes tabes dorsalis, which manifests as loss of fine touch and proprioception
Guillain-Barré syndrome may be preceded by Campylobacter jejuni infection and is characterized by an ascending paralysis that evolves ?
over days to weeks with the loss of deep tendon reflexes. CSF analysis shows albuminocytologic dissociation, elevated γ-globulin, and decreased nerve conduction velocity indicative of demyelination.
This patient presents with nausea, abdominal cramping, bloating, and watery diarrhea. Although a number of bacterial and viral infections can manifest with such symptoms, the patient’s recent camping trip suggests that he has been infected with Giardia lamblia. Colonization of the gut by Giardia trophozoites results in small bowel inflammation and villous atrophy, which reduces absorptive capability. The image of the duodenal aspirate reveals?
a pear-shaped trophozoite.
Giardia may be diagnosed by microscopic detection of the organism in stool, antigen detection, or nucleic acid amplification. Trophozoites have four pairs of flagella and two nuclei. They attach to epithelial cells in duodenal and jejunal crypts through a sucking disk on their ventral surface. The trophozoites absorb nutrients from the host and cause inflammation and malabsorption, but they do not invade the intestinal cells.
Activation of enteral adenylate cyclase is associated with bacterial organisms and is likely to cause a secretory diarrhea, which is a separate mechanism from that of diarrhea caused by Giardia lamblia. In addition, enzyme depletion that can occur at the intestinal brush border could lead to reduced digestion and absorption, seen in conditions such as lactose intolerance. Invasion of the intestinal lining is more likely to manifest as a ?
bloody diarrhea, and viral infection of the cells of the small intestinal villi would not result in the presence of a microorganism in the duodenal aspirate.
Giardia trophozoites can lead to small bowel inflammation and villous atrophy, resulting in ?
reduced absorptive capability and malabsorption. Giardia infection is diagnosed by duodenal aspiration.
This patient presents with a nonproductive cough, low-grade fever, and malaise. These symptoms, in association with patchy areas of congestion without consolidation, are suggestive of atypical pneumonia.
In patients who present with insidious onset of dry cough, low-grade fever, headache, myalgias, and nausea or emesis, an atypical pneumonia should be considered. X-ray of the chest is often more impressive than clinical examination findings and is characterized by a patchy interstitial infiltrate (see image). Treatment consists of ?
antibiotic therapy with a macrolide, usually azithromycin, for 5 days.
Mycoplasma pneumoniae is the most common cause of atypical pneumonia. Alhough Mycoplasma pneumonia is largely a clinical diagnosis, multiplex polymerase chain reaction (PCR) from a nasopharyngeal sample can be used to detect Mycoplasma and is now the diagnostic test of choice for suspected Mycoplasma infections because of its high specificity and sensitivity.
Eosinophil cationic protein (ECP) levels are nonspecific in the diagnosis of Mycoplasma pneumonia, since ECP can also be elevated in asthma. Giemsa stain is the gold standard for diagnosis of malaria, not Mycoplasma pneumonia. Mycoplasma is pleomorphic and contains sterols, which do not Gram stain. Mycoplasma can be detected by the cold agglutinin test, but this is not the preferred method of detection because it has? .
low sensitivity and specificity; PCR is much more reliable
