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.