Microbiology and Immunology 2 Flashcards
Under what conditions does the causative microorganism grow?
Both lepromatous and tuberculoid leprosy are caused by Mycobacterium leprae, an acid-fast bacillus that cannot be grown in vitro. M leprae is an obligate intracellular bacillus that, like other mycobacteria, contains mycolic acid in its cell wall. M leprae grows best in cooler temperatures (eg, skin, peripheral nerves, testes, upper respiratory tract).
How does this patient’s condition differ from a more severe form?
This patient has tuberculoid leprosy, which is largely confined to the skin (hypopigmented macules) and peripheral nerves. Cell-mediated immunity is intact, and patients’ T cells recognize M leprae (positive lepromin skin test). Lepromatous leprosy holds a much worse prognosis because patients have ineffective cell-mediated immunity (negative lepromin skin test). Skin lesions and nerve involvement are much more extensive than in the tuberculoid form, and there may be involvement of the testes, upper respiratory tract, and anterior chamber of the eye.
What is the appropriate treatment for tuberculoid and lepromatous leprosy?
Both tuberculoid and lepromatous leprosy can be treated with a course of oral dapsone. The tuberculoid form is reliably cured by a short course of this medication. Patients with lepromatous leprosy have an exceptionally high bacterial load and may require an extended or even lifelong course of chemotherapy. Alternate therapies for leprosy include rifampin or a combination of clofazimine and dapsone.
What are the side effects of treatment for tuberculoid and lepromatous leprosy?
Dapsone can cause agranulocytosis, so patients should be monitored initially with weekly or biweekly complete blood counts. Rifampin can turn body fluids such as sweat, tears, and urine a red-orange color. Rifampin therefore can be remembered as the “Gatorade drug,” referring to commercials that showed athletes with colored sweat from drinking Gatorade. This can startle patients (and rightly so) if they are not counseled before commencing therapy.
What is the most likely diagnosis?
Meningitis due to Listeria monocytogenes infection. This microorganism, identifiable by its classical tumbling motility, is a gram-positive rod and a common cause of meningitis in newborns and the elderly (Table 3-2).
How is Listeria monocytogenes transmitted?
L monocytogenes is transmitted through ingestion of unpasteurized dairy products such as milk, cheese, and ice cream.
What microorganisms should empiric antibiotic therapy target for this patient?
Group B streptococcus, Escherichia coli, and L monocytogenes are the most common causes of sepsis and bacterial meningitis in infants younger than 1 month of age. Therefore, empiric therapy should be aminopenicillin or vancomycin for gram-positive infection and aminoglycosides, antipseudomonal penicillins, or third- or fourth-generation cephalosporins for gram-negative infection.
How does Listeria monocytogenes evade the host immune response?
L monocytogenes is a facultative intracellular bacterium able to survive in the macrophages of neonates and immunosuppressed patients. In an immunocompetent host, activation of macrophages destroys phagocytosed Listeria.
What other population is at particular risk for developing Listeria monocytogenes infection?
Pregnant patients are at increased risk of developing a serious illness from Listeria known as granulomatosis infantiseptica. It can cause various complications to the mother and baby from premature rupture of membranes and intrauterine fetal demise. The elderly and immunocompromised are also at increased risk for this infection.
What is the most likely diagnosis?
The patient most likely has a hydatid cyst, which is a liver cyst due to Echinococcus infection.
How is Echinococcus transmitted?
Echinococcus is a tapeworm that is transmitted by food or water contaminated with feces containing eggs from the tapeworm. Infection is not endemic to the United States and so is most commonly seen in immigrants or those with a travel history to endemic areas.
What is the typical presentation of Echinococcus infection?
Echinococcus causes slow-growing cysts in the liver. As a result, symptoms are often gradual in onset and include abdominal pain, cough, low-grade fever, a sense of abdominal fullness, hepatomegaly, and obstructive jaundice. Leakage of cysts can cause flushing and urticaria, whereas rupture can cause anaphylaxis and death. Other organs that can be involved include the lungs and the brain. In the lungs, the presentation includes chronic cough, dyspnea, hemoptysis, and pleuritic chest pain. In the brain, presentation includes headache, dizziness, increased intracranial pressure, and hydrocephalus.
How is this condition (a hydatid cyst, which is a liver cyst due to Echinococcus infection) diagnosed?
On x-ray of the abdomen, a rim of calcification around the cyst is able to distinguish hydatid cyst from amebic and pyogenic cysts. However, the diagnosis usually cannot be made with radiology alone and requires an enzyme-linked immunosorbent assay (ELISA). In addition, 25% of patients have eosinophilia.
What is the treatment for Echinococcus infection?
The treatment for Echinococcus infection is usually surgical and involves aspiration of cyst contents followed by excision. However, during drainage, the interventional radiologist or surgeon must be careful not to rupture the cyst as this can lead to anaphylaxis. Therefore, many physicians prefer to inject formalin or ethanol into the cyst to kill the organism before aspirating. In some cases, therapy with a combination of albendazole and mebendazole is sufficient.
What other organisms are classified as cestodes?
Diphyllobothrium latum is a cestode transmitted by ingestion from freshwater fish that causes vitamin B12–deficient macrocytic anemia. D latum is treated with praziquantel. Taenia solium larvae are ingested from undercooked pork and can cause calcified cysts in various organs including the brain (cysticercosis or neurocysticercosis). Cysticercosis is treated with praziquantel, whereas neurocysticercosis is treated with albendazole.
What is the most likely diagnosis?
Malaria due to Plasmodium falciparum. The symptoms give a clue as to the species. The patient’s altered mental status is consistent with a diagnosis of P falciparum malaria, since this is the only strain that commonly has cerebral involvement. This patient’s continuous fever and irregular chills and sweats are also characteristic of P falciparum malaria. Early in infection, irregular fevers are common in all types of malaria, but the fever can become periodic in well-established cases of non-falciparum disease. For example, P vivax and P ovale cause episodes of fever, chills, and sweats every 48 hours. With P malariae, these episodes occur every 72 hours. Splenomegaly is a common finding in malaria due to work hypertrophy from increased RBC breakdown.
What phase of thePlasmodium falciparum life cycle results in the development of anemia?
RBC lysis occurs during the erythrocytic cycle, when the products of asexual replication inside the RBCs (the merozoite form) are released. The immune response to the merozoites, and resulting cytokine release, is responsible for the fever, chills, and sweats.
What are the likely peripheral blood smear (PBS) findings in Malaria due to Plasmodium falciparum?
A PBS is likely to show ring-shaped trophozoites inside the RBCs (see Figure 3-25), and there may be several trophozoites per RBC. Schizonts, the large, multinucleated cells formed from the trophozoite by multiple cycles of nuclear division, may be visible in the erythrocytes in non- falciparum malaria, but are very rarely seen in falciparum disease. Outside the RBCs, oblong gametocytes, diagnostic for P falciparum, may also be visible.
What is the treatment of choice for Malaria due to Plasmodium falciparum?
Chloroquine is the drug of choice in the few areas where there is no resistance. Its major mode of action against Plasmodium is inhibition of the enzyme responsible for polymerizing heme. This results in the accumulation of free heme, which is toxic to the protozoan. Quinidine in combination with doxycycline or pyrimethamine /sulfadoxine is commonly used as first-line treatment for chloroquine-resistant P falciparum. Other effective drugs include mefloquine and atovaquone-proguanil.
What 2 conditions provide protection against malaria?
Sickle cell trait and glucose-6-phosphate dehydrogenase (G6PD) deficiency both protect against malaria. The hypothesis is that increased fragility of the erythrocytes in these diseases does not allow for Plasmodium species to effectively replicate.
What is the most likely diagnosis?
Third-degree atrioventricular (AV) block secondary to Lyme disease. This condition is caused by Borrelia burgdorferi, a gram-negative spirochete that is poorly grown in culture and too small to be seen under regular light microscopy. Fluorescence may be used to visualize the corkscrew-shaped bacterium. However, the diagnosis is usually made clinically, supported by serology. Early local infection may present with a bull’s-eye rash (erythema chronicum migrans) after several days. The early disseminated stage may develop as early as a few days later and presents with cardiac conduction abnormalities (Lyme carditis), cranial nerve palsies (especially cranial nerve VII), and meningitis. Up to 43% of patients with Lyme carditis develop complete heart block.
What other conditions can cause Third-degree atrioventricular (AV) block?
Damage to the heart’s conduction system by fibrosis, ischemia, cardiomyopathy, myocarditis, or iatrogenic damage (eg, after valve replacement) may cause complete heart block. Digitalis, calcium channel blockers, and β-blockers may produce a temporary conduction abnormality.
What is the route of infection in Lyme disease?
Lyme disease is an arthropod-borne infection. The Ixodes tick transmits B burgdorferi. Mice and deer are reservoirs for the disease.
What is the prognosis for a patient with Lyme disease?
The prognosis is good. The conduction abnormalities secondary to Lyme carditis are self-limited and short lived and often resolve within days to weeks. It is uncommon for residual conduction abnormalities to persist after the infection has been cleared.
What is the appropriate immediate treatment for a patient with Lyme disease?
The patient’s ECG demonstrates bradycardia at a rate of 40/min. The episode of syncope indicates that cerebral perfusion is inadequate at this heart rate. Consequently, transvenous pacing may be initiated, but a permanent pacemaker is not needed. Antibiotic treatment for Lyme carditis consists of intravenous ceftriaxone until the PR interval is < 300 ms, at which point oral antibiotics may be initiated. The same regimen applies to Lyme disease with neurological features. Doxycycline or amoxicillin is used for primary infection and Lyme arthritis only.
What is the most likely diagnosis?
This child has measles, one of the most transmissible viral infections. Measles is caused by an RNA virus that is a member of the genus Morbillivirus and the family Paramyxoviridae. Transmission occurs by respiratory droplets and the incubation period is approximately 10 days. Two of this patient’s symptoms are typical of measles: Koplik spots and blanching rash with cephalocaudal spread.
What should be considered in the differential diagnosis other than measles?
Flulike symptoms may also be caused by infection with rhinoviruses, parainfluenza or influenza, adenovirus, or respiratory syncytial virus. Common causes of rash include Mycoplasma pneumoniae, human herpesvirus-6, rubella, Rocky Mountain spotted fever, scarlet fever, or a drug reaction. However, none of these rashes have cephalocaudal spread and none feature Koplik spots.
What are potential neurologic sequelae of measles?
Approximately 1:1000 patients with measles develop encephalitis, which is rapidly fatal in 15% of cases and leads to permanent neurological damage in 25% of patients. Infection with Morbillivirus can trigger acute disseminating encephalomyelitis, an autoimmune attack on the central nervous system, which is lethal in up to 20% of cases. Survivors often suffer mental retardation and epilepsy. Approximately 7–10 years after a measles infection, subacute sclerosing panencephalitis may develop; this infection, although rare, is almost always fatal.
What tests can confirm the diagnosis of measles?
Anti-measles IgM is seen in patient serum approximately 48 hours after the onset of the rash. A mucosal biopsy may demonstrate Warthin-Finkeldey cells (multinucleated giant cells with inclusion bodies in the nucleus and cytoplasm).
What is the appropriate treatment for measles?
There is no treatment for active infection; care is limited to supportive measures. Measles is a reportable disease and the patient must be placed in isolation. If other children in the family have not received the measles-mumps-rubella vaccine, it is likely that they will develop measles as this virus is highly transmissible.
What is the most likely diagnosis?
Infectious mononucleosis is most frequently caused by Epstein-Barr virus (EBV), a member of the Herpesviridae family.
Other than infectious mononucleosis, What should be considered in the differential diagnosis?
Several diseases present with symptoms similar to mononucleosis. However, streptococcal infection of the oropharynx is usually not associated with splenomegaly, and cytomegalovirus pharyngitis tends to be mild if clinically apparent at all. Low-grade fever, lymphadenopathy, and splenomegaly may also be seen in lymphoma. Lymphoproliferative disorders generally do not present with tonsillar exudate.
What are the peripheral blood smear (PBS) findings in infectious mononucleosis?
Infectious mononucleosis leads to lymphocytosis. The WBC count is often elevated (12,000–18,000/ mm3) with more than 50% lymphocytes. Up to 10% “atypical” lymphocytes containing large amounts of cytoplasm may be seen. However, these findings may also be seen in other infections (eg, cytomegalovirus, rubella, and toxoplasmosis), in some malignancies, and as a result of drug reactions.
Which malignancies are associated with EBV infection?
Burkitt lymphoma is endemic to Africa and primarily affects children. The disease is a B-cell lymphoma and often presents with a tumor of the jaw. This tumor often has a “starry sky” appearance under light microscope. Nasopharyngeal carcinoma is one of the most common cancers in southern China, and evidence supports EBV as its primary causative agent.
What treatments are available for Infectious mononucleosis?
Symptomatic treatment, usually with nonsteroidal anti-inflammatory drugs, is usually used. Although EBV might be expected to be susceptible to acyclovir since it is a herpesvirus, studies have shown that acyclovir produces reduction of oral shedding of the virus but no other significant clinical benefit. Ampicillin should be avoided, not just because it is ineffective against viruses but because it can precipitate a rash.
What is the most likely diagnosis?
Mucormycosis.
What is the microscopic appearance of the fungus involved in Mucormycosis?
The zygomycetes are nonseptate, branching fungi, with wide (> 90-degree) branch angles and large hyphae. By contrast, Aspergillus tends to have narrow, septated hyphae and branches in acute angles.
What patient populations are at increased risk for Mucormycosis?
The fungus is ubiquitous in nature and spores can be transmitted in air. Most patients are exposed to these spores several times per year, but an intact immune system is usually sufficient protection. Therefore, mucormycosis is typically seen in diabetic patients with poor glucose control or those with ketoacidosis. Neutropenic patients, burn victims, and patients treated with iron-chelating drugs are also at risk.
What patient populations are at increased risk for Mucormycosis?
The fungus is ubiquitous in nature and spores can be transmitted in air. Most patients are exposed to these spores several times per year, but an intact immune system is usually sufficient protection. Therefore, mucormycosis is typically seen in diabetic patients with poor glucose control or those with ketoacidosis. Neutropenic patients, burn victims, and patients treated with iron-chelating drugs are also at risk.
What is the pathogenesis of Mucormycosis?
The fungi grow along blood vessels and invade their walls. Protruding hyphae are highly thrombogenic, resulting in ischemia and necrosis of distal tissues, which, in turn, provide nutrients for continued fungal growth. Necrosis compromises the integrity of the bony walls of the sinuses and the cribriform plate, allowing fungal growth into paranasal sinuses, the bony orbit around the eye, or the brain. This rhinocephalic form of infection is rapidly progressive and carries a high mortality rate. Other forms include pulmonary, gastrointestinal, cutaneous, and disseminated infection.
What is the appropriate management for Mucormycosis?
Surgical debridement of infected and necrotic tissue is paramount. Reversal of the permissive condition (in this case ketoacidosis) should be initiated in conjunction with potent antifungal therapy with amphotericin B. However, despite optimal management, this condition still carries a high mortality rate.
What is the most likely diagnosis?
Orchitis secondary to mumps. In rare instances, orchitis can affect both testes and lead to sterility.
How is the mumps virus transmitted?
The mumps virus is a member of the Paramyxoviridae family of single-stranded RNA viruses. It is not stable enough to be aerosolized but can be transmitted by droplets (eg, sneeze). The virus has a 2- to 3-week incubation period, after which the infection results in painful inflammation and edema of glandular tissues including the parotid gland, testes, and ovaries.
What other clinical syndrome can result from infection with the mumps virus?
How is mumps diagnosed?
For the most part, the diagnosis of mumps can be made clinically. Supportive laboratory values include elevated amylase due to infection in the parotid glands. In uncertain cases, viral polymerase chain reaction assay may also be used.
What is the appropriate treatment for mumps?
The treatment is supportive and directed at reducing pain. Analgesics, compression, and icing of the parotid gland can be useful. In children, aspirin should be avoided as it has been linked to Reye syndrome. Vaccination with live attenuated mumps virus as part of the measles-mumps-rubella vaccine is used to prevent disease.
What is the most likely diagnosis?
This patient likely has Neisseria meningitidis meningitis, a gram-negative, kidney-shaped diplococci infection.
What test can confirm the diagnosis of Neisseria meningitidis meningitis?
Culture of meningococcus from cerebrospinal fluid (CSF) or blood. Lumbar puncture shows an elevated WBC count (with mainly polymorphonuclear cells), decreased glucose levels, and normal to high protein levels. Bacteria are visible on Gram stain. This pathogen can also be cultured on Thayer-Martin media (chocolate agar with antibiotics to kill competing bacteria). N meningitidis is oxidase positive and ferments both maltose and glucose.
What are Kernig and Brudzinski signs?
Kernig sign is considered positive when the patient resists straightening of the knee joint while the hip is flexed. Brudzinski sign is considered positive when the patient, while supine, lifts his legs when the neck is flexed by the examiner. Neither test is very sensitive, but a positive result is suggestive of meningeal irritation either by blood or inflammation.
What are the most important virulence factors and toxins of Neisseria meningitidis?
N meningitidis has thin protrusions called pili that help it attach to nasopharyngeal epithelial cells. Once attached to the nasopharynx, the pathogen secretes IgA protease to neutralize the predominant antibody idiotype found on mucous membranes. N meningitidis also features a capsule that protects it from other host defenses such as complement and phagocytosis. As with all gram-negative bacteria, N meningitidis has lipopolysaccharide, a potent endotoxin, in its cell wall.
What is the appropriate treatment for Neisseria meningitidis meningitis?
Intravenous penicillin G or ceftriaxone must be administered immediately. Bacterial meningitis can be fatal within hours, so empiric antimicrobial treatment must be started before culture results or other confirmatory tests become available. Rifampin is recommended as prophylactic treatment for contacts of the patient, especially if they are immunocompromised or have not been vaccinated.
What is the most likely diagnosis?
Onchocerciasis (river blindness) is caused by Onchocerca volvulus, a nematode (roundworm) found near rivers. Onchocerciasis is the leading cause of blindness in the developing world. Of the 18 million people infected worldwide, 99% of cases are in Zaire and Nigeria.
How is Onchocerca volvulus transmitted?
The bite of a female black fly transmits larvae (microfilariae) into the host’s skin. Humans are the only known definitive host of this parasite.
What is the pathogenesis of the Onchocerca volvulus?
The larvae become adults within 6–12 months, and subsequent fibrosis around the adult worms results in subcutaneous nodules, which protect the parasite from the host’s immune system. The parasites mate in the tissue, releasing microfilariae that can migrate to the eye where they cause keratitis and subsequent sclerosis.
What tests can help confirm the diagnosis of Onchocerciasis?
A skin biopsy may show larvae under the microscope, whereas nodules contain the adult filariae. The microfilariae in the eye may be visible on slit-lamp examination. Serologic tests such as enzyme-linked immunosorbent assay, polymerase chain reaction assay, and direct antigen testing are also available but require a laboratory, which is often not available to physicians treating the primary patient population.
What are the appropriate treatments for Onchocerciasis?
Ivermectin is effective against the larvae (microfilariae). It must be given every 6–12 months until the patient is asymptomatic. The subcutaneous nodules containing adult worms can be surgically removed.
What is the most likely diagnosis?
Osteomyelitis. Staphylococcus aureus is responsible for approximately 90% of pyogenic osteomyelitis cases. S aureus expresses receptors for the bone matrix, thus allowing it to adhere to bone and produce a focus of infection. Many affected adults have a history of compound fracture or surgery.
What patient populations are susceptible to osteomyelitis?
Osteomyelitis can be a sequela of trauma, as is the case in this patient, but is also often found in intravenous drug abusers (direct injection of bacteria) and patients with diabetes who have poorly controlled blood glucose. Bacteremic patients (typically children) may develop osteomyelitis as a consequence of hematogenous spread.
How does a subperiosteal abscess lead to accelerated bone necrosis?
A subperiosteal abscess separates the bone from its blood supply in the periosteum, leading to ischemic injury and necrosis.
A history of sickle cell disease would increase a patient with osteomyelitis’s risk of infection from which pathogen?
Patients with sickle cell disease have an increased risk of developing Salmonella osteomyelitis because of the reduced immune clearance of this pathogen.