Host Defense Part 3

Front 1

Describe the cell wall of mycobacteria.

Back 1

The cell wall is rich in lipids called mycolic acids and is rigid and relatively non-permeable. It has acid-fast property, meaning it is resistant to alcohol decolorization. The cell surface is mannosylated.

Front 2

What cells do myobacterium infect and how does it evade killing?

Back 2

Mycobacterium infect alveolar macrophages by interacting with complement/mannose receptors and blocks phagosome-lysosome fusing.

Front 3

What kind of necrosis is associated with TB?

Back 3

caseating necrosis

Front 4

What occurs during the initial containment phase of TB?

Back 4

T cells (CD4/8) activate macrophages and cause histologic changes (granulomas with multinucleated giant cells). Most bacteria are killed but some survive. This is latency.

Front 5

What cytokines are essential for controlling TB infections?

Back 5

IFN-gamma, IL-12, TNF. People with IFN-gamma and IL-12 defects are susceptible to mycobacterial infections. People taking TNF inhibitors have reactivation of tuberulosis.

Front 6

What is Reactivation TB characterized by?

Back 6

breakdown of granulomas containing organisms allowing growth of latent bacteria.

Front 7

What is Latent TB characterized by?

Back 7

Pathogen has become established in the body but there are no symptoms, no x-ray changes compatible with clinical disease, and bacteriologic studies are negative.

Front 8

What patients tend to get co-infected with TB?

Back 8

HIV patients. TB is the leading killer of HIV patients.

Front 9

Why has TB made a resurgence in the US?

Back 9

Increase in HIV, MDR-TB, Increase in foreign born cases and decrease funding.

Front 10

How is TB transmitted?

Back 10

during active pulmonary TB, transmission is airborne (coughing, talking, sneezing). Spread is enhanced by crowded/poorly ventilated conditions.

Front 11

What is the disease progression of TB?

Back 11

Primary TB occurs after exposure and spontaneously heals within 6 months. The infection is then latent and may progress to Reactivation TB (more common in patients with HIV).

Front 12

A patient gets a required TST and two days later the wheal is 10mm. What could possibly cause a false positive and what further tests are necessary? How should the TST result be interpreted?

Back 12

People who have gotten the BCG vaccine will produce a false positive. To rule out primary TB a chest xray should be obtain on TST positive tests. If the patient is known to have gotten a BCG, the patient should get the Interferon gamma release assay (IGRA) test instead of the TST as this test will differentiate between TB antigens and BCG antigens. Any patient that has received BCG and has a positive TST should be considered to have Latent TB infection (LTBI).

Front 13

What is the proper way to read the TST test?

Back 13

Reading should occur 2-3 days after injection. The induration (wheal) not the erythema should be measure and the reaction recorded in mm.

Front 14

What test should a 3 yr. old child receive if TB is suspected?

Back 14

TST. Recommended for all children under 5 years old. IGRA is recommended when TST doesn't provide good results or if prior BCG. IGRA is a blood test that requires 1 visit versus 2 visits for TST.

Front 15

what test detects rRNA of M. tuberculosis in respiratory specimens that does not distinguish live vs. dead organisms?

Back 15

the Nucleic Acid Amplification Test (NAAT). NAAT can give rapid diagnosis within 4-5 hrs.

Front 16

what symptoms are seen in a TB infections?

Back 16

Patients may present with: fever, malaise/fatigue, SOB/difficulty breathing, hemptysis, night sweats, chills, loss of appetite/anorexia, cough, chest pain.

Front 17

Patient has a positive TST and IGRA. Subsequent chest xray is normal and patient feels fine. What is the diagnosis?

Back 17

Latent TB infection

Front 18

A patient with LTBI is found to be non-compliant with his medications after presenting with lower back pain. If this is a reactivation of his TB, where is the infection and what is it called? What other places can TB cause infection?

Back 18

Pott's disease. Extrapulmonary TB is the spinal column. Can lead to kyphosis due to vertebrae collapse and spinal cord compression. Other extrapulmonary areas of infection is lymphatic system, kidney, CNS and disseminated (miliary TB).

Front 19

How are Mycobacterium tuberculosis identified in culture?

Back 19

Sputum cultures are used and M. tuberculosis is stained acid-fast. M. tuberculosis is slow growing and may take 2-6 weeks to grow

Front 20

What people are at risk of developing a MAC infection?

Back 20

AIDS patients with low CD4 counts (<100), elderly males with COPD, elderly non-smoking females, and cystic fibrosis patients. MAC may also cause hypersensitivity pneumonitis "hot tub lung" and lymphadenitis in children.

In AIDS patients it is usually a disseminated disease (granulomatous) of the liver, spleen or lymph node. Patients are put on a 3 drug therapy: azithromcin/clarithromycin, ethamutol, and rifamycin. Azithromycin is used for prophylaxis in patients with CD4 <50

Front 21

what is the immune reconstitution inflammatory syndrome (IRIS)?

Back 21

typically seen in AIDS patients with a mycobaterium infection. Occurs when the immune system is recovering but then responds to a prior opportunistic infection with an overwhelming inflammatory response that paradoxically makes the symptoms of the infection worse.

Front 22

A asymptomatic patient is found to have a CD4 count of 50. He is diagnosed with AIDS and started on HAART. He subsequently comes down with fever, chills, cough and night sweats. What is the reason behind the onset of the new symptoms? How should this patient be managed?

Back 22

This is a typical IRIS situation. The patient's CD4 count was too low to detect and fight the opportunistic infection (MAC in this case) and once HAART was started the patient's CD4 count increased and allowed the body to fight the infection. Patient should be given NSAIDs or corticosteroids depending on severity.

Front 23

What NTM produces a clinical syndrome similar to M. tuberculosis?

Back 23

Mycobacteria Kansasii. Frequently has positive AFB smear and can infect both HIV-neg and positive patients. In HIV patients can result in disseminated disease.

Front 24

What NTM is associated with fishtanks?

Back 24

Mycobacterium marinum

Front 25

What NTM presents as an ulcerated skin lesion with a necrotic base and is endemic in tropical areas?

Back 25

Mycobacterium ulcerans

Front 26

What are the rapid growing NTM and what type of infections can they cause?

Back 26

M. fortuitum, M. chelonae, M. abscessus. They can cause skin infections with or without bone/joint infections due to IV catheters, contaminated would dressings, prosthetic devices (breast augmentation), tattoos, wound infections following trauma, and patients on steroids.

Front 27

Patient presents with hypopigmented lesions with sensory loss. Patient is diagnosed with Hansen's disease due to acid fast bacilli on Fite stain. Which form of Leprosy does this patient have? What are the characteristics of the second form of leprosy?

Back 27

This patient has tuberculoid leprosy characterized by sensory loss of hypopigmented lesions. On punch biopsy of lesion there would be a strong TH1 response (granulomas) and small amount of bacteria.

The second form is Lepromatous Leprosy characterized by facial deformities (nasal collapse, loss of eyebrows, etc), skin hypopigmentation, motor/sensory loss, and blindness. This form is communicable and punch biopsy would show a TH2 response with a lot of bacteria.

Front 28

What is the treatment for culture positive TB?

Back 28

Treatment is typically for at least 6 months and is broken up into two phases: Initial phase and Continuation Phase. The initial phase is the RIPE drugs (Rifampin, Isoniazid, Pyrazinamide, Ethambutol). These drugs are typically taken daily for 2 months. The continuation phase is typically rifampin and isoniazid for an additional 4-7 months.

Front 29

Why are four drugs used to treat TB initially?

Back 29

Using one drug will lead to pathogenic resistance and initially data will not be available as to what strain is causing the TB and what drugs it is susceptible to because TB is slow growing in culture. Therefore initial treatment is empiric.

Front 30

What is the MOA of Rifampin? How can Mycobacteria obtain resistance to Rifampin?

Back 30

Rifampin inhibits RNA synthesis by inhibiting RNA polymerase. This is bactericidal for mycobacteria. Altering the structure of the RNA polymerase (decreased affinity for rifampin) can lead to drug resistance.

Front 31

A patient taking Rifampin for recent TB infection does not notice her urine turning orange like the doctor said it would. Why would this be the case and what should you tell her?

Back 31

The patient may be taking Rifampin with meals or too close to food intake. Rifampin absorption is decreased by 30% with food (Rifapentine absorption increases with food intake). You should advise her to wait longer between food and Rifampin doses.

Front 32

What are the major side affects of Rifampin?

Back 32

Hepatotoxicity (especially if taken with other drugs that are hepatotoxic) and body fluids turning orange (benign)

Front 33

Why should Rifampin never be taken with HIV protease inhibitors? what other drugs should you avoid with Rifampin?

Back 33

Rifampin is an enzyme inducer (CYP450 3A4 and 2C9) and reduces the levels of HIV protease inhibitors by 90%. Other drugs that react similarly are oral contraceptives, calcium channel blockers, warfarin, and azole antifungals.

Front 34

What is the MOA of Isoniazid? How do bacteria become resistant?

Back 34

Isoniazid interferes with bacterial cell wall synthesis and the exact MOA is uncertain. INH is a prodrug that is activated by a bacterial catalase-peroxidase enzyme called KatG and affects the synthesis of mycolic acid. INH is bactericidal to fast growing bacteria and bacterialstatic to slow growing bacteria. Resistance primarily occurs from decreased uptake of INH or less commonly by alteration of enzymes.

Front 35

How is Isoniazid metabolized?

Back 35

INH is metabolized in the liver via acetylation. The rate of acetylation is determined genetically and broken down into slow acetylaters and rapid acetylaters. Af. Am./Caucasians are typically slow acetylaters and Eskimos/Asian are fast. Slow acetylation causes higher levels in blood and increase in toxic reactions.

Front 36

What are the side effects of Isoniazid?

Back 36

Rash and hepatotoxicity are frequently seen. Of importance is peripheral neuropathy. INH and pyridoxine (vitamin B6) are structural analogs. This leads to pyridoxine being excreted in patients taking INH which leads to peripheral neuritis (numbness, parasthesias, sensitive to touch, etc). Peripheral neuropathy is uncommon but more likely to be seen in the malnourished, diabetics, alcoholics, HIV patients, renal failure, and pregnant/breastfeeding women. Pyridoxine replacement should be given concurrently to prevent.

Front 37

What drug interactions does Isoniazid have?

Back 37

INH inhibits CYP2A6 and CYP2D6 (codeine -> morphine inhibited, tramadol and tamoxifen not converted to active metabolite) moderately and CYP2C19 strongly (increased levels of the SSRI citalopram).

Foods containing histamine and tyramine can also cause symptoms such as sweating, flushing, headache, heart palpitations and low/high blood pressure.

Front 38

What is the MOA of pyrazinamide?

Back 38

the exact MOA is unknown but it disrupts plasma membrane and energy metabolism. PZA is only active at acidic pH and has no benefit after two months of therapy.

Front 39

A patient taking Rifampin, Isoniazid, Pyrazinamide, and Ethambutol is screened for liver damage. The patient's AST/ALT are increased. What drug is most likely to cause this?

Back 39

Pyrazinamide is the most likely culprit. When used in combination with rifampin the hepatotoxic effects are increased.

Pyrazinamide may also lower cyclosporine drug levels.

Front 40

What is the MOA of Ethambutol?

Back 40

Ehambutol inhibits arabinosyl transferase which inhibits synthesis of arabinoglactan which is a component of the cell wall. This results in inhibition of cell wall synthesis.

Front 41

A patient taking Rifampin, Isoniazid, Pyrazinamide, and Ethambutol is screened for liver damage. The patient reports a decrease in acuity and is having visual problems. What drug is most likely to cause this and what other symptoms can it cause?

Back 41

Ethambutol is generally well tolerated and can cause rashes and liver toxicity. It can also cause optic neuropathy causing decreased acuity, color blindness, vertical nystagmus and visual defects. These are reversible with drug discontinuation. Patients should get eye exams after the second month.

Front 42

What are the second line TB agents and when should they be used?

Back 42

Aminoglycosides (Streptomycin, Kanamycin), Capreomycin, Ethionamide, Fluoroquinolones, Cycloserine, and Para-aminosalicyclic Acid (PAS). These second line agents should only be used if there is drug resistance to first line or if patient is intolerant to first line.

Front 43

What is the MOA of the aminoglycosides Streptomycin and Kanamycin and what side effects do they have?

Back 43

MOA is protein sysntesis inhibition that is bacteriocidal. Side effects include ototoxicity, neurotoxicity and nephrotoxicity.

Front 44

What is the MOA of Capreomycin and what are the side effects?

Back 44

MOA is poorly understood but it is active against TB resistant strains. Side effects include auditory, vestibular and renal toxicities. Renal wasting can occur causing hypokalemia and hypomagnesemia.

Front 45

What is the MOA of Ethionamide and what are the side effects?

Back 45

MOA is inhibition of synthesis of oxygenated mycolic acid. Side effects include GI (nausea (do not take on empty stomach) and metallic taste), Neurotoxicity (peripheral neuritis, optic neuritis, anxiety, depression and psychosis - can coadminister pyridoxine to help), Hepatotoxicity (especially with PZA and RIF use) and it is teratogenic so do not use in pregnancy.

Front 46

What is the MOA of cycloserine and what are the side effects?

Back 46

MOA is inhibition of cell wall synthesis. Side effects include CNS adverse effects that are dose related and can worsen underlying disease in seizure patients or mental health disorders. Coadministration of Pyridoxine may help with side effects.

Front 47

What is the MOA of Para-aminosalicylic acid and what are the side effects?

Back 47

MOA is inhibiton of tubercle bacilli growth by impairment of folate synthesis and inhibition of iron uptake. Side effects include GI intolerance, Hepatotoxicity and Hypersensitivity leading to fever, joint pain and rash.

Front 48

What drugs are used to treat Hansen's disease (leprosy)? what are their MOA's and side effects?

Back 48

Dapsone and Clofazamine.

MOA of Dapsone is competitive antagonist of para-aminobenzoic acid (PABA) which prevevents normal bacterial utilization of PABA for folic acid synthesis. Side effects include hypersensitivity reactions (10% mortality) and dose related hemolysis which can lead to hemolytic anemia and methemoglobinemia. Patients with G6PD deficiency are more at risk for hematological reactions. Dapsone is a sulfa drug.

MOA of Clofazamine is unknown but likely interferes with DNA replication. Side effects include pigmentation of skin which can take 4-6 months to occur.

Front 49

What disease does Entamoeba histolytica cause? What is the route of transmission?

Back 49

Amebiasis and is transmitted fecal-oral and consumption of contaminated water. It is commonly seen in settings such as day care, refugee camps, mental health facilities and prisons.

Front 50

What is the clinical syndrome of Amebiasis? How do you diagnosis this disease and what is the treatment.

Back 50

Most patients are asymptomatic and are carriers of Entamoeba histolytica. Symptomatic cases can causes ABD pain, cramping, diarrhea, and bloody stool. Can lead to fever, rigors and leukocytosis. Hepatomegaly and diaphragm elevation are also seen. If E. histolytica gets in the blood stream it likes to form cysts in the liver causing liver abscesses.

Diagnosis involves stool examination for trophs and cysts or using serology. Treatment is metronidazol and iodoquinol.

Front 51

What is seen on histology of Amebic Colitis?

Back 51

There is a flask-like lesion if the GI submucosa is invaded

Front 52

What is the clinical syndrome of Giardiasis? How is it diagnosed and treated?

Back 52

Giardia lamblia is transmitted mainly via consumption of contaminated water or food (commonly seen in people swallowing fresh water from lakes/streams) and fecal-oral. About 50% of people are asymptomatic and those with symptoms have ABD pain, cramping, foul smelling fatty diarrhea and flatulence.

Diagnosis is made from stool exam for trophs and cysts. Treatment is Metronidazole.

Front 53

What is the clinical syndrome of Tichomoniasis? How is it diagnosed and treated?

Back 53

Trichomonas vaginalis can infect both men and women. In men it is mostly asymptomatic but can cause urethritis/prostatitis. In femals it can asymptomatic or cause watery discharge or vaginitis.

Diagnosis is made by examining the discharge for trophs. Treatment is Metronidazole or tinidazole. Must treat partner.

Front 54

What is the clinical syndrome of Cryptosporidiosis? How is it diagnosed and treated?

Back 54

Cryptosporidium infects the brush border of intestinal epiithelium causing enterocolitis with watery diarrhea which resolves spontaneously. Immunocompromised patients can get chronic disease with up to 50 stools/day. Transmission is waterborne and fecal-oral. It is prevalent in day care, among veterinarians, animal handlers and homosexuals.

Diagnosis is acid-fast stool examination or stool antigen detection. Treatment is supportive (spiramycin/paromomycin might help). Male asymptomatic partners should be treated.

Front 55

A patient recently went swimming lake with friends and presents with rapidly progressive meningoencephalitis. What protozoa could cause this presentation? What is the pathophysiology of this disease? What is the treatment?

Back 55

Naegleria fowleri lives in freshwater/brackish water lakes and enters the brain through the cribiform plate (change of smell is a common presenting symptom). Once in the brain it destroys brain tissue and leads to symptoms of encephalitis. Diagnosis can be made by looking for trophs in the CSF. Treatment is Amphotericin B.

Front 56

An AIDS patient is found to have multiple brain granulomatous abscesses. What protozoa can cause this infection? What other non-CNS infections can this protozoa cause? What is the treatment?

Back 56

Can be caused by Acanthamoeba. Acanthamoeba can also cause ocular infections (keratitis/corneal ulceration) through contamination of contact lenses/solutions. Treatment is Pentamidine, ketacondazole and flucytosine.

Front 57

What is the life cycle of Plasmodium species?

Back 57

Plasmodium is transmitted by the Anopheles mosquito and humans are the only reservoir. There are four main species: P. vivax, P. ovale, P. malariae, and P. falciparum. The life cycle in humans is broken down into an exoerythrocytic and erthrocytic stage. Initially after being bitten, the plasmodium sporozoites invade liver parenchymal cells (exoerythrocytic) and replicate (called schizont). The liver cells rupture and allow the Plasmodium merozoites to infect RBCs (erythrocytic stage). They then form schizonts in RBCs and cause rupture.

Front 58

What are the clinical features of a Plasmodium infection?

Back 58

The classical presentation is cyclical occurrence of sudden coldness followed by shivering and then fever and sweating, occuring every two days in P. vivax and P.ovale and three days for P. malariae. P. falciparum can cause recurrent fever every 2 days or a continuous fever as well as neurological symptoms. All species can cause anemia, hypoglycemia, splenomegaly and splenic rupture.

Front 59

What Plasmodium species is highly associated with splenic rupture?

Back 59

P. vivax

Front 60

What Plasmodium species is associated with immune complex disease, nephrotic syndrome and renal failure?

Back 60

P. malariae

Front 61

What type of RBCs do Plasmodium species infect?

Back 61

Depends on the species. P. falciparum invades all erythroid cells, P. vivax/P. ovale invade only reticulocytes, and P. malariae invades only mature RBCs.

Front 62

Which Plasmodium species like to remain in the liver?

Back 62

P. vivax and P. ovale

Front 63

How is Malaria treated?

Back 63

Treatment is based on presence or absence of chloroquine resistance. Resistant strains use mefloquine or atovaquone/proguanil. Life-threatening disease us IV quinidine. For liver stage of P. Vivax/P. ovale add primaquine.

Front 64

What is the clinical syndrome of Babesiosis?

Back 64

Usually asymptomatic but can cause fever, chills, malaise/fatigue, headache, hepatosplenomegaly, anemia and renal failure. Severe/chronic infection occurs in immunocompromised an asplenics.

Front 65

How do you diagnose Babesiosis?

Back 65

Thick and thin blood smear will show intraerythrocytic parasites in tetrads (Maltese cross). Serology for Babesia Ab. Treatment is Clindamycin and quinine if severe.

Front 66

What parasite can be seen in a coinfection with Lyme's disease?

Back 66

Babesia microti which causes Babesiosis because it is transmitted by the same tick, Ixodes. Primarily seen in Northeastern US.

Front 67

What is the clinical syndrome of toxoplasmosis?

Back 67

Toxoplasma gondii causes fever, chills, headache, myalgia, lymphadenopathy in the acute setting. In the chronic setting causes lymphadenopathy, rash, hepatitis, encephalopathy, myocarditis. Can infect the CNS in HIV/immunocompromised patients which can cause ring-enhancing lesions in the brain. Congenital infections present with the classic triad of chorioretinitis, hydrocephalus, and intracranial calcifications.

Front 68

How is Toxoplasma gondii transmitted? How is it treated?

Back 68

Cysts in undercooked meat of oocysts in cat feces. Can cross the placenta. Treatment is Pyrimethamine + sulfadiazine or clindamycin + pyrimethamine

Front 69

What is the clinical syndrome of Leishmaniasis?

Back 69

Leishmania species can cause a variety of diseases.

Simple Cutaneous leishmaniasis: most common, causes open sore at the bite site which can take up to a year and half to heal.

Diffuse Cutaneous: widespread skin lesions that resemble leprosy and may not heal on own.

Mucocuatneous leishmaniasis: skin and mucosal ulcers which damage primarily the nose and mouth

Visceral Leishmaniasis: most serious form and potentially fatal. Parasite infects internal organs such as liver, spleen, and bone marrow

Front 70

How is Leishmania transmitted? How is it treated?

Back 70

Leishmania parasites are transmitted via female sandfly bites. Treatment is either pentavalen antimony (IV or intralesional), amphotericin B or miltefosine.

Front 71

How do you diagnose Leishmaniasis?

Back 71

Tissue biopsy showing intracellular parasites. Can do serology for visceral form.

Front 72

What is the clinical syndrome of African Sleeping Sickness?

Back 72

Trypanosoma brucei are transmitted via Tsetse fly bites. Parasite grow in infected tissue and are disseminated via blood. Initial symptoms are undulating fever and diffuse LAD (especially on the back of the neck). Later symptoms include cognitive slowing, loss of sensorium, seizures and disruption of sleep cycle (sleep during day, awake at night) when the parasites infect the CNS

Front 73

How do you diagnose and treat African Sleeping Sickness?

Back 73

To diagnose look for parasites in blood or CNS using giemsa stain. Treatment is Pentamidine or suramin for blood stages. Melarsoprol or eflornithine (+nifurtimox) for CNS disease.

Front 74

What is the clinical syndrome of Chagas disease?

Back 74

Trypanosoma cruzi is transmitted by the triatomine bug (kissing bug) which deposit parasite laden urine/feces. Acute symptoms are nonspecific. Chronic infections which can occur a decade later affects the nervous system, digestive system and heart. Can see dilated cardiomyopathy (leads to heart arrhythmias and sudden death), dilation of GI tract due to denervation (megacolon and megaesophagus), achalasia (leads to malnutrition and weight loss)

Front 75

How do you diagnose and treat Chaga's?

Back 75

Diagnosis is by serology. Treat with benznidazole and nifurtimox. Also need to manage heart failure and dysmotility processes.

Front 76

What is the clinical syndrome of the Chinese Liver Fluke?

Back 76

Clonorchis sinensis infection from consumption of raw, smoked or pickled fish causes bile duct invasion with fever, diarrhea, epigastric pain, HSM, and jaundice. Infection is associated with adenocarcinoma of biliary tree (cholangiocarcinoma).

Front 77

How do you diagnose Clonorchis sinensis? What is the treatment?

Back 77

Diagnose by finding eggs in stool or adult worms in biliary tract. There may be eosinophilia. Treatment is with Praziquantel.

Front 78

What is the clinical syndrome of the Lung Fluke?

Back 78

Paragonimus westermani is transmitted via undercooked/raw crabs and crayfish. It migrates from intestine to lungs creating lung cavities. Results in rusty sputum, chest pain and fibrosis. May also migrate to CNS causing cavities and compressive syndromes.

Front 79

How do you diagnose and treat Paragonimiasis (Lung Fluke)?

Back 79

Diagnose by finding eggs in stool and sputum, Radiology can show cavitation and effusion. Eosinophilia is common. Treatment is Thiabendazole and Praziquantel.

Front 80

What is the clinical syndrome of Schistosomiasis?

Back 80

Schistosoma species is transmitted via exposure of water supply that contain infected cercaria and snail hosts. There are three species: S. mansoni, S. hematobium, and S. japonicum. The adult worms live in venous plexuses. SM and SJ live in intrahepatic portal circulation/mesenteric veins. SM/SJ cause portal hypertension, liver/spleen granulomas, HSM, periportal fibrosis, ascites. SH lives in urinary plexuses and can cause bladder cancer (painless hematuria).

Front 81

How do you diagnose and treat Schistosomiasis?

Back 81

Diagnose by finding eggs in stool and urine. S. hematobium has terminal spine on egg, S. mansoni has lateral spine, S. japonicum has blunted spine. Eosinophilia can be present. Treatment is with Praziquantel.

Front 82

What is the clinical syndrome of Pinworms?

Back 82

Enterobius vermicularis can cause intense anal pruritis. Occasionally it causes GU issues and vaginitis. Spread is via person-person. Common in daycare and mental institutions.

Front 83

How do you diagnose and treat a pinworm infection?

Back 83

Diagnose by detecting eggs found in perianal region (scotch-tape test). Treat with Mebendazole or pyrantal pamoate.

Front 84

What is the clinical presentation of Ascariasis?

Back 84

Ascaris lumbricoides is the most common helminth infection. Eggs are ingested from contaminated food/water and larvae penetrate mucosa and migrate to alveloi. This causes irritation, cough, and hypersensitivity pneumonitis. Larva are coughed up and swallowed. These mature to adult worms which can cause GI tract perforation/obstruction and infection of the liver. Ascariasis is prevalent in areas with poor sanitation and where human feces are used as manure.

Front 85

How do you diagnose and treat Ascariasis?

Back 85

Diagnose by finding eggs in stool and/or adult worms in intestinal tract. Eosinophilia can be present. Treatment is Albendazole/mebendazole, pyrantal pamoate.

Front 86

What is the clinical syndrome of Toxocariasis?

Back 86

Caused by three worms Toxocara canis, Toxocara cati and Ancylostoma braziliensis. For Toxocara canis, worm eggs shed by dogs are ingested. Larva penetrate the gut, enter blood, and penetrate tissue to induce inflammation and eosinophilic granulomas. Symptoms include fever, anorexia, cough, wheezing, ABD pain, HSM, arrhythmia or vision loss.

Front 87

How do you diagnose and treat Toxocariasis?

Back 87

Diagnose by serology for Toxocara Abs, tissue biopsy, eosinophilia. Treatment is Albendazole/mebendazole, Steroids for inflammation, antihistamines for itching.

Front 88

What is the clinical syndrome of Hookworms?

Back 88

Caused by Nector americanus (new world) and Ancylostoma duodenale (old world). Larvae transmitted via feces and penetrate skin causing rash and hypersensitivity. They get blood, travel to lungs (pneumonitis and eosinophilia), coughed up and swallowed and mature in GI tract. Attach to gut via biting mouthparts causing chronic blood loss and microcytic anemia. Chronic infection can result in nutritional deficiencies, emaciation and mental/physical retardation in children.

Front 89

How are hookworms diagnosed and treated?

Back 89

Diagnose by finding eggs in stool. Treatment is Albendazole/mebendazole, pyrantal pamoate. Also treat anemia with iron supplementation/transfusion.

Front 90

What is the clinical syndrome of Strongyloidiasis?

Back 90

Infective larvae are found on wet grass and penetrate the skin. Travel to lungs causing pneumonitis. Coughed up and swallowed and mature in GI tract. Can cause ABD pain, diarrhea, vomiting and malabsorption. Can involve pancreatic and biliary systems.

If larvae penetrate the GI tract and get into blood patients can get hyper-infection syndrome. Mortality is high (86%).

Front 91

How do you diagnose and treat Strongyloidiasis?

Back 91

Diagnose by finding larvae or eggs in sputum or stool. Serology and Eosinophilia. Treatment is Ivermectin (first line), albendazole/mebendazole (second line).

Front 92

What three nematodes can cause Filariasis?

Back 92

Wuchereria bancrofti, Onchocerca volvulus and Loa loa

Front 93

What is the clinical syndrome of Filariasis?

Back 93

Transmission of nematode is different depending on which one is causing infection. Mosquitos transmit Wuchereria bancrofti, black flies transmit Onchocerca volvulus, and horse/deer/mango flies transmit Loa loa.

Larvae mature into adults in skin or lymphatics causing chronic inflammation. Chronic fibrosis of lymph nodes and lymphatics lead to elephantiasis in bancroftian filaraisis. In onchocerciasis, microfilaria induce anterior chamber inflammation and blindness (River blindness). In Loiasis, worms can migrate across sclera.

Front 94

What is the clinical syndrome of Dracunculiasis?

Back 94

Dracunculus medinensis is transmitted via infective larvae in fresh water with the microcrustacean host, Cyclops. Larvae invade GI tract and mature in subcutaneous tissue. Adult females migrate to skin creating an ulcer and pain/erythema.

Front 95

How do you diagnose and treat Dracunculiasis?

Back 95

Diagnose by finding worm at site of ulcer. Treatment is removing the worm.

Front 96

What is the clinical syndrome of Cysticercosis?

Back 96

Taenia solium (pork tapeworm) is transmitted by the consumption of undercooked pork. Cysticercosis occurs when cestode invades GI wall, circulates and deposits in tissue to create cysts. These cysts can be asymptomatic or devastating if in CNS (meningitis, hydrocephalus, seizures) or optic tract (vision loss).

Front 97

How do you diagnose and treat Cysticercosis?

Back 97

Diagnose by radiographic/CT finding showing calcified cysticerci, biopsy of cysticerci, serology. Treatment is Praziquantel or abendazole. Co treat with steroids to avoid hyper-reaction to released antigen. Can surgically remove cysts.

Front 98

What is the clinical syndrome of Echinococcosis?

Back 98

Echinococcus granulosis (sheep) and Echinococcus multilocaularis (fox, cat, wolf) release eggs that contaminate soil/water/vegetation. Eggs are ingested and penetrate GI tract and lodge in tissues developing cysts. Expanding cysts (hydatid cysts) cause compressive symptoms and can rupture causing fever, urticaria and anaphylatic shock via release of hydatid sand.

Front 99

How do you diagnose and treat Echinococcosis?

Back 99

Diagnose by radiology or serology. Treatment is surgical resection preteated with albendazole/mebendazole. Inactive hydatid sand before resection with ethanol.

Front 100

What is the clinical syndrome of Diphyllobothriasis?

Back 100

Diphyllobothrium latum (Broad/Fish tapeworm) are transmitted via ingesting cysts in fish tissue. Cysts attach to GI tract and mature. Can cause ABD pain, cramping, nausea/vomiting. Adult worms scavenge vitamin B12 leading to megaloblastic anemia and neurologic sequelae (loss of vibration sense, paresthesia, numbness).

Front 101

How do you diagnose and treat Diphyllobothriasis?

Back 101

Diagnose by finding eggs or parts of worm in stool. Treatment is with Praziquantel, niclosamide or paromomycin. Supplement vitamin B12 if necessary.

Front 102

What is the clinical syndrome of Scabies?

Back 102

Sarcoptes scabiei is transmitted via infected people or fomites. Adults burrow in skin and lay eggs which causes intense itching, secondary excoriation and bacterial superinfection. Norwegian scabies can occur in immunosupressed patients resulting in generalized dermatitis, scaling and crusting due to overgrowth of mites in the skin.

Front 103

How do you diagnose and treat Scabies?

Back 103

Diagnose by analyzing skin scrapings. Treat with Lindane lotion or 5% permethrin cream

Front 104

Fill in the blanks

Back 104

Front 105

What parasites can be identified by using thin and thick blood films? What is the difference between thin and thick?

Back 105

Parasites that reside in the blood such as Plasmodium spp., Babesia spp., Filaria, Leishmania, Toxoplasma, and Trypanosoma spp.

Thin blood films are a single layer of blood cells smeared on a slide. Thick blood films are blood that has been lysed leaving only the WBCs, platelets and parasites

Front 106

What do you see on a blood smear in a patient that has malaria?

Back 106

Blood should be drawn and examined at 6, 12, and 24 hrs after initial sample. This is a thin film sample showing rings in the RBCs. On a thick film you won't see this as the RBCs are lysed. Instead you will see mature parasites.

Front 107

What do you see on blood films for Babesia spp.?

Back 107

"Maltese crosses"

Front 108

What parasite is this and what disease does it cause?

Back 108

Wuchecheria bancrofti. It is one of the agents that causes lymphatic filariasis.

Front 109

What disease state do these two parasites cause?

Back 109

Cause amebic meningoencelphalitis

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Front 116

Fill in the blanks.

Back 116

Front 117

What is the MOA, drug example and clinical indications for the anti-protozoal heavy metals?

Back 117

The inhibition of parasite metabolism is parasticidal. Heavy metal componds are toxic to host as well with greatest toxicity to most metabolically active cells (neuronal, renal tubular, intestinal, and BM stem cells). Their differential toxicity and therapeutic value are largely related to enhanced uptake by the parasite and its intense metabolic activity.

Front 118

What is the MOA, drug example and clinical indications for the anti-protozoal aminoquinoline analogues?

Back 118

Quinine rapidly destroys the erythrocytic stage of malaria and may be used prophylactically to suppress clinical illness or therapeutically to terminate an acute attack. Primaquine accumulates in tissue cells and destroys the extra-erythrocytic (hepatic) staes of malaria, resulting in a cure of the infection. Chloroquine remains the drug of choice for the prophylaxis and treatment of susceptible malaria strains. Chloroquine is active against all five Plasmodium spp. and is well tolerated, inexpensive, and effective orally. Resistance of P. falciparum to chloroquine is widespread. Quinine is used primarily to treat chloroquine-resistant P. falciparum infections. Mefloquine is used for the prophylaxis and treatment of falciparum malaria. Halofantrine is used in the treatment of P. vivax and P. falciparum malaria. It is not recommended for prophylaxis of malaria because of toxicity. Lumafantrine is available only as a fix formulation, combined with artemether.

Front 119

What is the MOA, drug example and clinical indications for the anti-protozoal Folic acid antagonists?

Back 119

The sulfonamides inhibit the conversion of aminobenzoic acid to dihydropteroic acid. The diaminopyrimidines inhibit dihydrofolate reductase, which blocks synthesis of tetrahydrofolate, a percursor for purines, pyrimidines and certain amino acids. Low doses are effective so mammalian cells are unharmed. diaminopryimidine + sulfonamide has a synergistic effect.

Front 120

What is the MOA, drug example and clinical indications for the anti-protozoal protein synthesis inhibitors?

Back 120

Clindamycin and tetracyclines: Plasmodium spp., Babesia spp., and amebae. Clindamycin also useful in CNS toxoplasmosis.

Doxycycline: chemoprophylaxis of chloroquine-resistant P. falciparum.

Spiramycin: Toxoplasmosis, alternative to anti-folates.

Paromomycin: cryptosporidiosis, secondary drug for amebiasis and giardiasis.

Doxycycline: Onchocerca volvulus

Front 121

What is the MOA, drug example and clinical indications for the anti-protozoal diamidines?

Back 121

Pentamidine does not penetrate the CNS and is not useful in the late stages of infection with Trypanosoma brucei gambiense.

Front 122

What is the MOA, drug example and clinical indications for the anti-protozoal nitroimidazoles?

Back 122

The nitroimidazoles have excellent penetration into body tissues and therefore are effective against disseminated amebiasis.

Metronidazole: DOC for trichomoniasis.

Benzndiazole: acute Chaga's.

Tinidazole: amebiasis, giardiasis, and vaginal trichomoniasis.

Front 123

What is the MOA, drug example and clinical indications for the anti-protozoal nitrofurans?

Back 123

Front 124

What is the MOA, drug example and clinical indications for the anti-protozoal Sesquiterpenes?

Back 124

Artemisinin have efficacy against small-ring forms and maturing schizonts of P. vivax and P. falciparum.

Front 125

What is the MOA, drug example and clinical indications for the anti-protozoal Atovaquone + Proguanil combination?

Back 125

Front 126

What is the MOA, drug example and clinical indications for the anti-protozoal Ornithine analogue?

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Front 127

What is the MOA, drug example and clinical indications for the anti-protozoal phosphocholine analogue?

Back 127

Used in visceral Leishmaniasis. Resistance is due to decreased uptake.

Front 128

What is the MOA, drug example and clinical indications for the anti-protozoal Acetanilide?

Back 128

Front 129

What is the MOA, drug example and clinical indications for the anti-protozoal sulfated naphthylamine?

Back 129

Front 130

What is the MOA, drug example and clinical indications for the anti-protozoal thiazolide?

Back 130

Front 131

What is the MOA, drug example and clinical indications for the anti-helminthitic benzimidazoles?

Back 131

Mebendazole: intestinal nematodes and cestodes

Thiabendazole: Strongyloidiasis

Albendazole: Echinococcus species, Giardia spp., filariasis and loiasis

Front 132

What is the MOA, drug example and clinical indications for the anti-helminthitic tetrahydropyrimidine?

Back 132

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What is the MOA, drug example and clinical indications for the anti-helminthitic piperazines?

Back 133

Diethylcarbamazine (DEC): active against filariae that produce river blindness (O. volvulus) and lypathic filariasis (W. bancrofti).

Front 134

What is the MOA, drug example and clinical indications for the anti-helminthitic avermectins?

Back 134

Ivermectin: used primarily to treat ocular and lymphatic filariasis

Front 135

What is the MOA, drug example and clinical indications for the anti-helminthitic Pyrazinoisoquinoline?

Back 135

Praziquantel disrupts the tegument such that antigens are exposed that wouldn't otherwise have been allowing host antibodies to attack the parasite.

Front 136

What is the MOA, drug example and clinical indications for the anti-helminthitic phenol?

Back 136

Front 137

What is the MOA, drug example and clinical indications for the anti-helminthitic quinolone?

Back 137

Front 138

What is the MOA, drug example and clinical indications for the anti-helminthitic organophosphate?

Back 138

Front 139

What is the MOA, drug example and clinical indications for the anti-helminthitic sulfated naphthylamidine?

Back 139

Front 140

What stage of an helminth do antihelminthitic agents work at?

Back 140

They target nonproliferating adult organisms. This is in contrast to antiprotozoans which target younger, more rapidly proliferating cells.

Front 141

What does it mean for fungi to be Dimorphic? Which Fungi are dimorphic?

Back 141

Dimorphism is when fungi adopt two discrete morphological state. Outside of human host they are hyphae and condidia at 25C and inside humans they are yeast at 37C. Histoplasma, Coccidioides, Sporothrix, Blastomyces, Paracoccidioides and Penicillium marnefei are dimorphic. Excluding Sporothrix, these are endemic mycoses and are acquired via inhalation.

Front 142

What is the cellular structure of fungi?

Back 142

They have a plasma membrane and cell wall. They plasma membrane has phospholipids and ergosterol. The cell wall contains chitin and Beta-glucans.

Front 143

Which fungi has a capsule?

Back 143

Cryptococcus

Front 144

What fungal molecules allow for growth in humans?

Back 144

degradative enzymes (breakdown tissues/barriers, obtain nutrients), siderophores (steal sequestered iron), mycotoxins (inhibit immune cells, cause host cell necrosis), and melanins (detoxify phagocyte ROS)

Front 145

What are superficial fungal infections?

Back 145

Limited to surfaces of the skin and hair. They are a cosmetic issue only and are nondestructive and do not evoke an immune response.

Front 146

What are cutaneous fungal infections?

Back 146

Fungal infections that colonize keratinized layers (they secrete keratinase). They are non-invasive but infections may elicit host response (inflammation). Itchy, scaly, and often ring-like patches on the skin.

Front 147

What are subcutaneous fungal infections?

Back 147

Fungal infections of the deeper layers of the skin usually via traumatic inoculation. Evokes immune response and infection remains localized. There may be tissue destruction and epitheliomatous hyperplasia.

Front 148

What are invasive fungal infections? Which pathogens are opportunistic and which ones are primary pathogens?

Back 148

Invasion and establishment of fungal infections in deeper tissues often resulting in prolonged illness and/or systemic spread. Results from immnocompromised host (opportunistic) or primary fungal pathogen that can survive normal immune defenses.

Opportunistic: Pneumocystis, Asperillus, Candida

Primary: Cryptococcus, Histoplasma, Coccidioides

Front 149

What are the risk factors for developing fungal infections?

Back 149

Natural Barrier Defects: indwelling catheters (breach skin barrier), antibacterial treatment (deplete endogenous flora), chemotherapy (disrupt epithelial integrity)

Immune Function Defects: HIV/AIDS, neutropenia, chemotherapy, organ transplantation, cytokine therapies, diabetes

Front 150

How are conidia and hyphae killed by the body?

Back 150

Conidia are taken up and killed by macrophages. Hyphae are too big for macrophages so neutrophils kill them.

Front 151

How does cryptooccus protect itself from ROS killing?

Back 151

Cryptococcus causes cryptococcal meningitis and makes melanin in the brain from L-DOPA. The melanin helps protect against ROS.

Front 152

What virulence factors does Histoplasma have to protect itself?

Back 152

They have siderophores to steal iron from body, superoxide dismutase and catalase to degrade ROS, and are able to keep pH of lysosome near neutral which inhibits killing.

Front 153

Patient presents with multiple bumps on hand and recalls being poked by one of her rose bushes when she was gardening the other day. What is the most likely etiology and how should she be treated?

Back 153

Most likely sporotrichosis caused by Sporothrix schenkii. S. schenkii is ubiquitous in soil and lives on plants. Nodules appear to spread proximally from inoculation site along lymphatics. Treatment is with itraconazole.

Front 154

What is seen on histology in a Sporotrichosis infection?

Back 154

"cigar shaped". Thin, septate, dimorphic fungus

Front 155

What symptoms are seen in Histoplasmosis?

Back 155

Most patients are asymptomatic. If symptomatic, may get fever, cough, pulmonary infiltrates and hilar lymphadenopathy (mediastinal lymph nodes). In immunocomproised: bone marrow suppression, diffuse lympadenopathy, oral ulcers, meningitis, and death.

Front 156

What is seen on histology is Histoplasmosis?

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Front 157

How do you diagnose and treat Histoplasmosis?

Back 157

Diagnose by epidemiology, symptoms, and radiographic findings. Serology is useless in immunocompromised. Can look for antigens in urine. Healthy people may not need treatment. Mild disease, use itraconazole. Severe disease, use Amphotericin B. Patients with a CD4<100 should be given itraconazole prophylaxis

Front 158

What is the pathogensis of blastomycosis?

Back 158

There is no characteristic clinical syndrome and should be considered with unusual skin or bone lesions as it has tropism for those two organs. Lesions will have broad-based buds. Treat with itraconazole or amphotericin B.

Front 159

What is the pathogenesis and clinical manifestations of Coccidioidomycosis?

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Caused by Coccidioides immits found in southwest US. the Arthroconidia are inhaled into terminal bronchioles which transform into spherules. These rupture and disseminate the yeast. Most people have self limited febrile respiratory illness. Coccidioidomycosis is deadly if it migrates to the meninges. People that tend to have more severe disease are pregnant women, Af. Am., Native Am., Asian and Hispanics. Treatment is Amphotericin B, Fluconazole and/or Itraconazole for severe disease.

Front 160

What are the most common Candida species to cause Candidiasis? What is there morphology?

Back 160

Candida albicans (most common) and Candida glabrata (increased fluconazole resistance). Candida form pseudohyphae and germ tubes.

Front 161

What clinical syndromes can Candida cause?

Back 161

Mucocutaneous candidiasis: Thrush, esophagitis, vaginitis, diaper rash

Candidemia: Intravascular catheter-related infections, endopthalmitis, endocarditis, hepatosplenic candidiasis.

Front 162

What stains can you use to identify Cryptococcus neoformans?

Back 162

India ink stain of mucicarmine stain

Front 163

What is the clinical manifestations of cryptococcosis? What is the treatment?

Back 163

Cryptococcus neoformans has strong tropism for the meninges so meningitis is most common clinical manifestation. Symptoms of headache, fever, waxing and waning consciousness that can evolve over weeks to months. People most commonly get this through bird droppings such as pigeons.

Treatment is amphotericin B + flucytosine for meningitis, followed by fluconazole.

Front 164

Who is most at risk for developing Cryptococcosis?

Back 164

People with T cell defects such as HIV/AIDS patients, transplantation, and high-dose corticosteroid therapy.

Front 165

Who is at risk for developing Pneumocystis pneumonia? How do you diagnose these patients?

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AIDS patients with CD4 counts below 200. These patients should be put on prophylaxis treatment of TMP/SMX. If allergic use either dapsone, atovaquone, inhaled pentamidine.

Diagnose by finding Penumocystis jiroveci in respiratory secretions. It cannot be grown in culture.

Front 166

What is the clinical manifestations of Pneumocystis pneumonia? What is the treatment?

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Patients often present with a pneumothorax. Symptoms include fever, cough and progressive dyspnea and tends to be subacute. Patients also tend to be tachypneic. Xrays show bilateral pulmonary infiltrates.

Treatment is high dose TMP/SMX (always DOC unless sulfa allergy, in which case use IV pentamidine). Corticosteroids if hypoxic (pO2 < 70 mmHg).

Front 167

What is the main risk factor for developing Aspergillosis?

Back 167

Prolonged neutropenia or neutrophil dysfunction (chronic granulomatous disease)

Front 168

What are the clinical manifestations of Aspergillosis?

Back 168

Aspergillus fumigatus can cause pneumonia (invasive pulmonary aspergillosis), disseminated disease, sinusitis, aspergillomas, and allergic bronchopulmonary aspergillosis (peripheral eosinophilia and elevated IgE levels).

Front 169

What is the arrow pointing to?

Back 169

Aspergilloma - fungal balls/mycetomas. They are non-invasive and can occur in immunocompetent people. May cause hemptysis.

Front 170

How do you diagnose and treat Aspergillosis?

Back 170

Diagnose by finding characteristic hyphae (septate hyphae and 45 degree angle branching). Treatment is voriconazole and amphotericin B.

Front 171

What does Mucormycosis look like on histology?

Back 171

Broad, aseptate hyphae with 90 degree branching.

Front 172

What are the clinical manifestations of Mucormycosis?

Back 172

Caused by multiple species: Rhizopus spp., Absidia spp., Mucor spp. Can cause pulmonary, skin, sinus and rhinocerebral disease. Risk factors are diabetes, acidosis, and severe immunocompromised patients. This mold usually has low virulence but infections are severe and life-threatening.

Front 173

What is the MOA of amphotericin B? What fungi does amphotericin B have activity against?

Back 173

Amphotericin B is a polyene and acts by binding to the ergosterol component of the cell wall of fungi. Thi sleads to disruption of the cell wall integrity, leakage of cellular contents and cell death.

Amphotericin B has a wide range of activity and works against almost all fungi. Typically is only used when patients have life-threatening infections.

Front 174

If Amphotericin B has activity against most fungi, why is it not used in all fungal infections?

Back 174

Amphotericin B has a lot of side effects with nephrotoxicity occurring in 80%. There are also infusion toxicity (phlebitis, hypotension and hemodynamic instability) and electrolyte wasting (potassium and magnesium). Toxicities can be reduced by encapsulating Amphotericin B in lipids such as Abelcet, Amphotec, and AmBisome.

Front 175

What is the MOA of antifungal azoles?

Back 175

Azoles inhibit the synthesis of ergosterol. This leads to membrane instability. Azoles bind to the C-14a demethylase and thus inhibiting the demthylation of lanosterol.

Front 176

What is ergosterol derived from? The anti-fungal class that blocks the synthesis of ergosterol is metabolized what part of the body?

Back 176

Squalene. Azoles block the synthesis of ergosterol and they are metabolized by the liver. Because of this, they can have toxicity to the liver.

Front 177

What infections are fluconazole useful against? What patients should be treated differently when prescribing fluconazole?

Back 177

Fluconazole is almost exclusively used in candidal yeast infections. Also useful in cryptococcus neroformans and coccidiodies immitis infections. Not useful against molds. Patients that have renal insufficiency/failure need to be dosed reduced as this is the only azole to have part of its metabolism in the kidney.

Front 178

Itraconazole is the DOC for which fungal infections?

Back 178

Histoplasmosis, blastomycosis, and sporotrichosis

Front 179

A patient with histoplasmosis and GERD is taking his prescribed medications, but the fungal infection is not clearing. Why? What could help?

Back 179

The DOC for histoplasmosis is Itraconazole. The absorption of itraconazole is pH dependent and absorbs well in acidic conditions. A patient with GERD will be on proton pump inhibitors and thus the gastric pH will be high. Stopping the PPIs and coadministering with an acidic fluid like soda or orange juice will help with the absorption.

Front 180

Which antifungal is useful for the prophylaxis of aspergillosis?

Back 180

Voriconazole. Voriconazole shows an increase survival rate compared to Amphotericin B in patients with invasive aspergillosis.

Front 181

What are the side effects of Voriconazole?

Back 181

visual disturbances (photosensitivity, blurred vision, and hallucinations), neurotoxicity, hepatotoxicity, increased risk of skin cancer and voriconazole resistant pathogens (mucormycosis).

Front 182

What anti-fungal azole drug has the broadest spectrum of activity? What is it mainly used for?

Back 182

Posaconazole has the widest spectrum of use and can be used for Mucormycosis. It is a highly lipophilic drug and must be taken with fatty foods. It is mainly used for the prophylaxis of fungal infections in at risk patients. It is the first anti-fungal drug that has shown reduced mortality as a prophylatic.

Front 183

What is the MOA of griseofulvin? Which fungal infections is griseofulvin used in?

Back 183

Binds to tublin interfering with microtubules and mitosis. Griseofulvin is only used in superficial infections of the skin, hair or nail. Does not treat systemic infections. It is taken orally and after absorption binds to keratin in the epidermal keratin precursor cells. As these cells grow towards the surface, the griseofulvin can then diffuse into the fungus.

Front 184

What is the MOA of the anti-fungal echinocandins? What fungal infections can these be used in?

Back 184

These drugs inhibit the synthesis of B-1,3 glucan impairing cell wall integrity of fungal organism that have B-1,3 glucan. Can be used in the treatment of Candida spp., Aspergilus and PCP.

Front 185

Which drugs are apart of the anti-fungal echinocandins? In what infection are these the DOC?

Back 185

Caspofungin, Micafungin and Anidulafungin. Due to their broad spectrum of activity against Candida and fast activity via IV, they are DOC for candidemia.

Front 186

What is unique about the metabolism of anidulafungin?

Back 186

It is neither metabolized by the liver or kidney, instead undergoes a slow, non-enzymatic metabolism in the body. Thus does not need to be dosed reduced in hepatic/renal failure.

Front 187

What is the MOA of terbinifine? What is the clinical indication for using terbinifine?

Back 187

Inhibits ergosterol synthesis by blocking squalene epoxidase. Terbinifine (Lamisil) is reserved for treating skin, hair, and nail infections. When given orally, there is risk for hepatotoxicity.

Front 188

What is the MOA of Flucytosine (5-FC)? What are the side effects? What infection is it mainly used in?

Back 188

Flucytosine is a fluorinated pyrimidine analogue that forms 5-fluorodeoxyuridylic acid within fungal cells. This is incorporated into DNA synthesis blocking growth. Side effects include diarrhea and bone marrow suppression. It is mainly used in cryptococcal meningitis.

Front 189

strengths and weaknesses?

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Front 190

What is the proper way to collect a TB sample?

Back 190

collect in sterile, leak proof, disposable container (do NOT use waxed container, can result in false positive), refrigerate if transport time is over 1 hr, and don't use swabs.

Front 191

What stains are used in TB diagnosis?

Back 191

Ziehl-Neelsen (hot stain) and Kinyoun (cold stain).

Front 192

What do you do if you suspect TB?

Back 192

Airborne isolation (negative airflow room and N-95 respirator mask), Chest xray, Respiratory AFB smear and culture, TST/IGRA, HIV test, smear and culture from other sites, Nucleic acid amplification test, Drug susceptibility if there is growth.

Front 193

For superficial fungal infections, which test is best for diagnosis?

Back 193

10% KOH skin scrapping test.

Front 194

Which test is best used to detect Cryptococcus neoformans? Why?

Back 194

Indian Ink (collodial carbon) test because it shows the capsule as it doesn't get stained.

Front 195

Are yeast gram positive or negative?

Back 195

gram positive. False results if cell wall is damaged.

Front 196

What staining method will show the presence of most fungi?

Back 196

PAS - fungi are magenta

Front 197

Which staining method is used to look for fungi in peripheral blood smears?

Back 197

Wright-Giemsa stain. Used to detect the fungi PCP, histoplasma, and blastomyces.

Front 198

Which fungi have B-1,3-glucan in their cell wall? Which fungi have mannan?

Back 198

B-1,3-glucan: Aspergillus and Candida

Mannan: Candida

Front 199

What are some potential consequences of bacteremia?

Back 199

sepsis, systemic inflammatory response syndrome (SIRS), multi organ dysfunction, metastatic infection, and death

Front 200

What is the pathogenesis of bacterial endocarditis?

Back 200

First, there must be bacteremia. There then must be an abnormal area on the heart valve where the bacteria can attach (NBTE lesion) and proliferate forming a vegetation.

Front 201

What are the most likely etiologies of endocarditis?

Back 201

typically it is bacterial, casused by coagulase+ staph or staph aureus and by the alpha hemolytic viridans streptococci. Others include Strep. bovis (ALWAYS check for colon cancer), HACEK organisms (Haemophilus aphrophilus, Actinobacillus actinomyceme commitans, Cardiobacter hominis, Eikenella corrodens, and Kingella kingii), Enterococcus spp., and ANYTHING that produces an endocarditis syndrome and is persistently isolated.

Front 202

What is a non-bacterial thrombotic endocarditis (NBTE) lesion and role does it have in endocarditis?

Back 202

A NBTE lesion is when part of the endocardial surface (typically a valve) has exposed subendothelial tissue. This subendothelial tissue acts as a nidus for bacteria which allows the bacteria to attach and grow forming vegetations. A NBTE lesion is an important and necessary first step to develop endocarditis and without it vegetations would not form. The lesions arise from turbulent blood flow usually due to congenital or acquired cardiac valve dysfunction (stenosis/regurgitation). A NBTE lesion has exposed fibrinogen, fibrin, fibronectin, and platelet proteins that allow for binding.

Front 203

Where in the heart are bacterial endocarditis vegetations typically seen?

Back 203

Left sided is more common with mitral valve being most common. Aortic valve is second most common and there can be multiple vegetations with mitral and aortic.

Front 204

What type of patients are more likely to get infective endocarditis?

Back 204

rheumatic heart disease (somewhat rare nowadays), IV drug abuse (right sided endocarditis), mitral valve prolapse, elderly with calcific aortic sclerosis/mitral annular calcification, intravascular devices such as pacers, and those on hemodialysis (they tend to be more bacteremic).

Front 205

What bacterial surface proteins allows for binding to NBTE lesions?

Back 205

Staph, Strep and enterococci have MSCRAMMS (microbial surface component reacting with adhesive matrix molecules) that mediate attachment to NBTE lesion

Front 206

What are the HACEK organisms?

Back 206

Haemophilus aphrophilus, Actinobacillus actinomyceme commitans, Cardiobacter hominis, Eikenella corrodens, and Kingella kingii. They are part of the oral flora and more likely in people with poor oral hygiene. They can cause bacterial endocarditis and produce large vegetations that can occlude large arteries (femoral, brachial, etc.)

Front 207

Name the structures. What is unique about this?

Back 207

This is bacterial endocarditis. There is no PMN or mononuclear cellular infiltrate (which would show blue)

Front 208

When would you want to prophylax for endocarditis?

Back 208

Any kind of surgical or manipulation of oral cavity (give amoxicilin), surgical procedures on the respiratory tract, and surgical procedures of infected skin, skin structures, or MSK tissue.

Front 209

What are the clinical findings of endocarditis?

Back 209

Nonspecific symptoms such as fever, weight loss and fatigue. There may be a new or changing heart murmur, new CHF, conduction block, evidence of embolic event, splenomegaly, and stigmata of endocarditis (osler's nodule, Janeway lesion, Roth spot, splinter hemorrage, petechiae).

Front 210

Fill in the blanks.

Back 210

Front 211

Where are IV drug abusers most likely to get endocarditis? What is a complication of endocarditis at this location?

Back 211

There is a high association with right sided tricuspid valve endocarditis in IVDAs. A complication of this could be pulmonary embolisms. In right sided endocarditis, there may not be a heart murmur and the only symptom could be a fever. Thus a fever of unknown origin in a IVDA should be considered endocarditis until proven otherwise.

Front 212

How do you diagnose endocarditis?

Back 212

blood cultures (almost always positive unless bacteria is fastidious as there is continuous bacterial shedding from vegetation), Trans thoracic echo and trans esophageal echo (gold standard)

Front 213

What is the cause of early prosthetic valve endocarditis? late onset?

Back 213

early infection (<60 days) is usually due to contamination at the time of surgery from coagulase - staph or diphtheroids. Late infection (>60 days) is from the typical pathogens of coagulase+ staph and strep viridans.

Front 214

How is endocarditis treated?

Back 214

4-6 weeks of IV antibiotics (depends on what is the underlying agent) and bactericidal agents are only used. Surgery may be needed if medical treatment isn't curative.

Front 215

Patient presents with honey colored crusts around the mouth that started as vesicles that oozed. What is the diagnosis and treatment?

Back 215

Impetigo. Treatment is warm soaks, topical antibiotics and systemic antibiotics if needed.

Front 216

What are the main causes of imeptigo?

Back 216

Group A strep and S. aureus

Front 217

A neonate presents with diffuse erythema that leads to large bullae and exfoliation. It is noticed that there is only intra-epidermal exfoliation. Nikolsky sign (sloughing of outermost skin with light rubbing) is positive. What is the diagnosis and how is it treated?

Back 217

Staphylococcal Scalded Skin Syndrome. Management is supportive making sure the patient is hydrated and there are dressings on the exfoliated skin. Should also give antibiotics for staph.

Front 218

What is the pathogenesis of Staphylococcal Scalded Skin Syndrome?

Back 218

Caused by a staphylococcal exfoliative toxin that spreads throughout body but localizes to the skin. The toxin breaks down the granulosum and spinosum layers by cleaving desmosomes.

Front 219

What are the common causes of folliculitis? How is it treated?

Back 219

S. aureus usually, pseudomonas (hot tub folliculitis), Candida (in diabetics). Treatment is local care and topical antibiotics. Systemic antibiotics if necessary.

Front 220

A patient on chemotherapy becomes neutropenic due to therapy and develops a superficial skin lesion that has an erythematous base and black eschar center. What is the diagnosis?

Back 220

Ecthyma gangrenosum. Caused by Pseudomonas aeruginosa and seen in immunocompromised from neutropenia.

Front 221

Patient states the area of brown skin has been enlarging and itches. Patient is noted to be obese and has diabetes mellitus. What is the diagnosis and treatment?

Back 221

Diagnosis is Erythrasma caused by Corynebacterium minutissimum. Associated with diabetes, obesity and warm climates. Under Wood's light the brown skin fluoresces red. Treat with topical clindamycin or oral erythromycin.

Front 222

Patient presents with a small mass similar to the image. States that it has drained greenish white pus spontaneously. What is the diagnosis and treatment? What patients are more at risk for developing this?

Back 222

This is a furuncle (boil) most commonly caused by S. aureus and MRSA. Management is warm compression, incision/drainage, and antibiotics. Drainage will show gram + cocci in clusters with neutrophils (staph). Risk factors are diabetes, obesity, IV drug use, and HIV infection.

Front 223

What is a carbuncle? How are they managed?

Back 223

Carbuncles are multiple adjacent furuncles with connective tissue septation given extension into adipose. Management is similar to furuncles: drain and give antigbiotics.

Front 224

Patient presents with multiple subcutaneous nodules on the arm that seems to following a lymphatic pattern. There are some associated red streaks and swelling. What is the diagnosis and what could cause this presentation?

Back 224

This is lymphangitis which is inflammation of lymphatic channels and adjacent tissue representing a spread of infection. Possible etiologies include post cellulitis (strep or staph), filariasis (can result in elephantiasis due to blocked lymphatics), sporotrichosis (commonly seen in rose gardeners), and mycobacterium marinum (people who have or work with aquariums).

Front 225

Patient presents with a diffuse red, swollen leg after being cut out fishing in the ocean. What is the most likely diagnosis? What other etiologies can present similarly?

Back 225

This is cellulitis caused by Vibrio vulnificans (seawater/seashell contact). The most common cause of cellulitis is Group A strep and S. aureus. Other causes include Group B strep in diabetics/chronically ill, Enterobacteriaceae in immunocompromised, Erysipelothrix sp. in fish/meat/hide handlers, Aeromonas hydrophila in fresh water cuts, and anaerobes in traumatic cases.

Front 226

What are risk factors for developing cellulitis?

Back 226

diabetes, obesity, vascular insufficiency, tinea pedis

Front 227

What must be ruled out in a patient with a diffuse red, swollen leg before calling it cellulitis?

Back 227

DVT

Front 228

Patient presents with a bright red well demarcated rash on his face. If this is caused by Group A strep, what is the most likely diagnosis?

Back 228

Erysipelas, which is a special case of cellulits caused by Group A strep. Can also be seen on the legs.

Front 229

Patient presents with a diffuse red, tender rash on his arm. On exam, it feels warm and there is crepitus. X ray also show gas in the tissue. Patient says the pain was worse a few days ago. What is the diagnosis and management?

Back 229

Necrotizing fasciitis. Patient is in late stage as there is crepitus and anesthesia (pain subsiding). Usually caused by group A strep. If this was biopsied there would be gram positive cocci in chains. Management is surgical debridement without delay and broad spectrum antibiotics initially.

Front 230

Necrotizing fasciitis involving the male genitalia is called?

Back 230

Fournier's Gangrene

Front 231

What M proteins are associated with invasive Group A strep infections and Streptococcal Toxic Shock syndrome?

Back 231

M protein types 1 and 3

Front 232

Patient with a crush injury to his leg develops an ascending necrotic lesion. What is most likely cause of the necrosis and what is the management? What other organism can cause a similar presentation?

Back 232

Gas gangrene caused by Clostridum perfringens. Post-traumatic, devitalized tissue permits anaerobic growth. Alpha toxins are produce which leads to tissue injury and gas development. Management is debridement, leaving the wounds open, and antibiotics.

Group A Streptococcal necrotizing myositis can also present like this.

Front 233

Patient presents with pain upon hyperextending his hip. Patient's CT scan is shown on the left. What can cause this finding and what is the management?

Back 233

This is pyomyositis of the Psoas muscle (Psoas abscess). Can be caused by S. auerus or M. tuberculosis. Patients has a positive Psoas sign (pain on hyperextension of hip). Management is drainage and antibiotics.

Front 234

What is the pathogenesis of osteomyelitis?

Back 234

Hematogenous seeding: occurs mainly in infants/children from minor trauma. Usually due to S. aureus

Contiguous spread: From trauma/surgery, decubitus/diabetic ulcers, or poor circulation.

Psuedomonas in diabetics/IVDA

Salmonella in sickle cell patients

Front 235

What is the clinical presentation of osteomyelitis? How is it managed?

Back 235

Fever, point tenderness, red/swollen around infected bone, loss of range of motion.

Osteomyelitis requires prolonged antibiotic treatment and possibly surgical debridement.

Front 236

What are some potential consequences of chronic osteomyelitis?

Back 236

Many times in chronic osteomyelitis the bacteria are resistant to antibiotics which makes eradication difficult leading to amputation in some cases.

Front 237

How does septic arthritis present?

Back 237

Typically with a single tender, inflamed, swollen, immobile joint. Patients will also have a fever. Joint aspiration will show a purulent fluid with lots of neutrophils.

Front 238

What are the predisposing factors for pyogenic arthritis (septic arthritis)?

Back 238

Chronic joint disease, prosthetic joints, joint trauma, immunosuppressive therapy, any chronic illness

Front 239

What organisms most commonly cause septic arthritis?

Back 239

S. aureus is the most common of any age. N. gonorrhoeae is also another common organism and there may be other skin lesion (as shown to the left) and tenosynovitis (these sites should be cultured).

Front 240

How is septic arthritis managed?

Back 240

Antibiotics, repeated arthrocenteses, open surgical drainage.

Front 241

What is the clinical presentation of a prosthetic joint infection? How is it managed?

Back 241

Patients will present with pain, instability/loosening of the join, +/- fever, +/- drainage. Management is usually removal of the prosthetic joint in a 2 stage surgical process: removal, antibiotics for 6-12 weeks, and then replacement.

Front 242

What microbes commonly cause prosthetic joint infections? How do you diagnose a prosthetic joint infection?

Back 242

Can be caused by Coagulase negative staph, S. aureus, Propionobacterium sp., Diphtheroids, or bacteremia pathogens. Diagnosis is from radiographic evidence of loosening and erosion. Aspiration of the joint will show evidence of bacteria.

Front 243

How do you diagnose tenosynovitis? What is the management?

Back 243

Four cardinal symptoms: flexor tendon sheath tenderness, semi-flexed finger(s), severe pain with finger extension, and symmetrical swelling of whole finger(s). An MRI will show edema involving sheaths. Can do a surgical exploration to identify the bacteria (most commonly S. aureus. Can also be DGI or from etiologies that can cause lymphangitis such as sporotrichosis or mycobacteria).

Management is surgery and antibiotics (vanco for staph and ceftriaxone for DGI)

Front 244

What is necessary for the development of streptococcal toxic shock syndrome and scarlet fever?

Back 244

Streptococcal pyrogenic exotoxins - SPE's. These are superantigens

Front 245

What superantigens does S. aureus produce?

Back 245

S. aureus produces Staphylococcal Toxic Shock Syndrome Toxin 1 and enterotoxins/exotoxins which are all superantigens

Front 246

What are superantigens?

Back 246

Superantigens are molecules that can trigger non-specifi activation and proliferation of Tcells and associated release of cytokines such as IL-2, INFgamma, Interleukine 1 beta and TNF alpha. The superantigen bridges between MHC II receptor and Tcell receptor. It is less specific than normal antigens thus it activates many more Tcells.

Front 247

What kind of response is generated from superantigen binding?

Back 247

CD4 T cells are primarily activated leading to a Th1 helper response (IL-2, IFNgamma, IL-1B and TNFalpha). Since there is a lack of Th2 response, antibody expression is decreased during response to superantigens. This leads patients vulnerable to a recurrence.

Front 248

What people are susceptible to developing Staphylococcal Toxic Shock syndrome?

Back 248

Menstruating women using hyper absorbant tampons, surgical wounds (may not appear hot), Post influenza patients. There is a 5% mortality.

Front 249

What patients are at risk for developing Staphylococcal Toxic Shock Syndrome and what is the mortality rate?

Back 249

Patients with HIV infection, diabetes, cancer, heart/lung disease, chicken pox/shingles, IV drug use, and alcohol abuse are at increased risk. Mortality is almost 50%.

Front 250

What is the clinical presentation of Toxic Shock Syndrome?

Back 250

Patients present with fever, low blood pressure and diffuse sunburn type rash. There may also be confusion, myalgias and diarrhea.

Front 251

When culturing bacteria to diagnose Toxic Shock Syndrome, what is expected difference between a staph infection and a strep infection?

Back 251

Toxic shock due to staph will usually not result in a positive culture whereas in toxic shock due to strep there will usually be a positive culture.

Front 252

What is the management of staph and strep toxic shock syndrome?

Back 252

staph: Supportive care with IV fluids, blood pressure support, etc. Remove the primary infection and give anti-staph antibiotics even if cultures are negative. Consider IVIG if severe

strep: Supportive care same as above, Aggressive surgical debridement of infected area. Anti-strep antibiotics (penicillin + clindamycin, clindamycin blocks protein synthesis leading to lower toxin production), IVIG as cases are more severe with strep.

Front 253

What defines sepsis?

Back 253

Sepsis is infection + systemic inflammatory response (SIRS) as seen by two or more of the following: temp ≥38C or ≤36C, HR≥90, Respirations ≥20/min, WBC count ≥ 12,000 or ≤ 4000 or > 10% immature neutrophils

Front 254

What defines severe sepsis?

Back 254

Sepsis with ≥1 sign of organ failure.

Front 255

What defines septic shock?

Back 255

Sepsis with signs of end organ profusion deficiency as seen by MAP < 65 mmHg and lactate > 4 mmol/L

Front 256

Why is the incidence of severe sepsis cases predicted to increase?

Back 256

increase in invasive procedures, aging population increase use of immunomodulating therapy, longer survival in cancer patients, and increased transplantation (29% of lung transplant patients die from sepsis).

Front 257

What infectious agent causes sepsis in gram positive and gram negative bacteria?

Back 257

gram positive: lipoteichoic acid

gram negative: LPS/endotoxin

Front 258

What receptor binds to endotoxin/LPS?

Back 258

TLR-4

Front 259

How do you treat a septic patient?

Back 259

Antibiotics, IV fluids (lots), give high flow O2, measure lactate/CBC/urine output, get blood cultures, source control (remove infected devices, drain pus, debride, etc), and correct electrolyte imbalances.

Front 260

What are the hemodynamics of a septic patient?

Back 260

Front 261

What patients with sepsis should receive a bicarb drip? Should all patients with sepsis get bicarb?

Back 261

Patients with severe sepsis that have a pH <7.15. Not all septic patients should get bicarb since raising the pH will shift the hemoglobin curve to the left resulting in less oxygen delivery to tissues.

Front 262

What are the three structural genes of HIV and what do they code for?

Back 262

env: makes gp120 and gp41

gag: makes capsid protein

pol: makes reverse transcriptatse, protease and integrase

Front 263

What function does LTR (long terminal repeats) have in the HIV genome?

Back 263

they are involved with the regulation of gene expression and viral replication.

Front 264

Describe the life cycle of HIV.

Back 264

HIV initially infects Langerhan cells found in the skin which express CD4. These Langerhan cells then travel to lymph nodes where the HIV virus replicates and spreads. HIV infects CD4 cells by gp120 binding to CD4 causing a conformational change of gp120 which allows for coreceptor binding of CCR5. Next, gp41 inserts into the membrane which allows for fusion and entry. Once inside, the positive sense RNA is transcribed into double stranded DNA by reverse transcriptase and integrated into the host genome by integrase. Now once the CD4 cell is activated to replicate its genome, protease cuts up the protein so that it can be packaged into viral particles and the life cycle of HIV is complete.

Front 265

How does HIV become resistant to drugs and immune system?

Back 265

HIV reverse transcriptase has a high error rate (1 per 30,000-50,000 base pairs) so every replication there is a mutation somewhere. That is why patients are not infected with just one virus, but many closely related viruses which makes treatment difficult. If the virus mutates a capsid protein, this can cause it to escape the immune response. If the mutation is at an enzymatic site of reverse transcriptase/protease/integrase this can cause drug resistance.

Front 266

Why is it important to put HIV patients on a "cocktail" of drugs?

Back 266

To make sure that drug resistance does not develop, it is important to suppress HIV replication. It has been shown that a cocktail of drugs instead of just one or two has the greatest impact on the number of viral RNA copies in the blood.

Front 267

What can increase the risk of HIV viral entry and infection?

Back 267

STD (causes increase in CD4 cells at site of infection), mucosal injury, and inflammation can increase risk.

Front 268

What people are immune to HIV?

Back 268

People with a homozygous deletion of CCR5 are immune as the HIV cannot enter cells

Front 269

What is the difference between CCR5 and CXCR4?

Back 269

Both are normally chemokine receptors but CCR5 is on macrophages (macrophage tropic) and CXCR4 is on lymphocytes (lymphotropic). HIV binds to CCR5 in early disease and this is how it is acquired. HIV binds to CXCR4 in late disease and this is how it spreads.

Front 270

What initially happens when a person is infected with HIV?

Back 270

There is a viral spike which is the earliest indicator of HIV infection. There will also be a depletion of CD4 cells and about 50% of patients will present with an acute mononucleosis-like syndrome. Patients will be in a window phase where there will not be any antibodies to the HIV present in the serum. This phase lasts for about 4-8 weeks.

Front 271

What occurs during the asymptomatic phase of HIV?

Back 271

During the asymptomatic phase (2-12 yrs) patients will be seroconverted with antibodies to HIV envelope and core proteins. There will be a lower set-point of virus in the plasma than at initial infection. There will also be a continuous depletion of CD4 cells due to viral induced apoptosis from HIV replication and cytotoxic T cells.

Front 272

What is useful about knowing the viral load (viral setpoint) in a patient during their asymptomatic phase?

Back 272

A higher setpoint depicts a worse prognosis and short asymptomatic phase.

Front 273

What role do CD8 and CD4 cells play in cell mediated immunity to HIV?

Back 273

CD8: they can directly kill HIV infected cells and block HIV. There is an initial spike in HIV specific CD8 CTLs and the broader the CTL response the lower the setpoint. However, the function of the CTLs is dependent on CD4 cells.

CD4: HIV specfic CD4 cells are made during an HIV infection but the majority are infected and eliminated soon after being made. Thus, it is difficult to maintain adequate levels of HIV specific CD8 cells. Loss of CD4 cells specific for HIV is distinct to HIV.

Front 274

How can HIV modulate the CD8 CTL response?

Back 274

HIV can evade CTLs by NEF (HIV protein) and induce down regulation of MHC I on CD4 cells.

Front 275

A patient with HIV is seen to have no detectable levels of HIV virus in his plasma. He eventually gets off antiretroviral therapy and a few years later develops symptoms of HIV again. Why?

Back 275

Even when HIV virus is below detectable levels in the plasma, there are latent HIV virus within cells and if antretroviral therapy is stopped the viremia will rebound to high levels.

Front 276

What is conjunctivitis and what causes it?

Back 276

Conjunctivitis is inflammation of conjuctiva (thin clear tissue laying over white part of eye and also lines the lid). Can be infectious or non-infectious in nature.

Infectious: viral (most common) or bacteria (in kids, very contagious)

Non-infectious: Allergic (pollen, etc) or chemical (perfume, cosmetics) and this is not contagious

Front 277

How do you treat non-infectious conjunctivitis?

Back 277

There is no specific treatment and symtopms should resolve on own once the noxious agent is removed. If the conjunctivitis is due to chemicals, this requires prompt washing of eye for 5 mins. Otherwise, compression is key and use clean cloth each time. Can use artificial tears to dilute allergens, decongestants, antihistamines, NSAIDs and corticosteroids.

Front 278

What are the symptoms of conjunctivitis?

Back 278

If it is infectious in nature it will just be one eye, if it is due to allergies it will be both eyes. There will be itching and burning, swollen eyelids, crusty eyelids and light sensitivity.

Front 279

What is the primary cause of viral conjunctivitis?

Back 279

Pinkeye is mainly caused by adenovirus. Patients can present in a few ways.

Pharyngo-conjunctivitis: high fever, pharyngitis, bilateral conjunctivitis and peri-auricular lymph node enlargement.

Epidemic kerato-conjunctivitis: severe, watery discharge, very red, chemosis (swelling of bulbar conjunctiva), lymphadenopathy, and photosensitivity.

Front 280

Patient presents with unilateral conjunctivitis producing a thin watery discharge. There are some vesicular eyelid lesions and an enlarged pre-auricular lymph node. What is the diagnosis and how should this patient be treated?

Back 280

Diagnosis is viral herpes conjunctivitis. Treatment is topical trifluorothymidine drops 9 times/day plus oral acyclovir or valacyclovir.

Front 281

Patient presents with the following rash. What ocular complications can be seen it this type of patient? How should this patient be treated?

Back 281

This is shingles affecting the trigeminal nerve. The most common involvement of the eye is the eyelid and then conjunctiva. Patients can get corneal involvement (keratitis) and Hutchison sign (vesicles at tip of nose) is an indicator for this. VZV can also cause uveitis.

This patient should see ophtho and get oral and topical antivirals.

Front 282

Who normally gets bacterial conunctivitis and how do the clinically present?

Back 282

Kids mostly get bacterial conjunctivits usually due to contaminated fingers (S. aureus). Other ways include oculo-genital spread in the case of Chlamydia, which will have milder symptoms lasting weeks-months.

Should expect bacterial conjunctivitis if there is no itching, no prior history of conjunctivitis, bilateral matting of lids and if there is decreased vision.

Front 283

How should bacterial conjunctivitis be treated?

Back 283

At least 60% resolve on own. Treat if there is a lot of discomfort, the wear contacts, are immunocompromised, or if the cause is gonorrhea/chlamydia. For gonorrhea/chlamydia give IM ceftriaxone. Otherwise, topical antibiotic drops (tobra/gent/cipro/TMPSMX)

Front 284

In the case of conjunctivits, when should you refer to ophtho?

Back 284

If patient has visual loss, moderate to severe pain or pus, corneal involvement, no response to therapy, recurrences, HSV eye disease, wears contacts, on steroids, or has photophobia.

Front 285

Patient presents with conjunctivitis, swollen/painful left knee, painful urination and pus filled sores on soles and palms. What is the primary cause of this syndrome and who mostly gets this? What is the treatment?

Back 285

This is Reiters Syndrome (Reactive Arthritis - can't see, can't pee, can't climb a tree) brought on by a gonorrhea or chlamydia. Men aged 20-40 with HLA-B27 are most susceptible. Treatment is anti-inflammatory drugs.

Front 286

What are the symptoms of keratitis? What can cause keratitis?

Back 286

Symptoms: eye redness, rapid onset of pain, tearing, blurry/decreased vision, photophobia, "sand in eye"

Causes: An injury that scratches the cornea, Contaminated contact lenses (acanthamoeba), viruses (HSV, VZV), contaminated water, and bacterial (strep, pseudomonas, enterobacteriaceae (klebsiella, serratia, proteus), syphilis)

Front 287

What is uveitis and what symptoms are seen?

Back 287

Uveitis is inflammation of the middle layers of the eye (iris, ciliary body, and choroid). Symptoms include: red eye, blurry vision, floaters, pain, and photophobia.

anterior uveitis = iritis

posterior uveitis - vitritis, choroiditis, retinitis, chorioretinitis.

Front 288

What are the main causes of uveitis?

Back 288

bacterial: syphilis, tuberculosis

viral: CMV

Front 289

When should you suspect syphilis as the cause of uveitis?

Back 289

Syphilis can cause eye disease at any stage but its easiest to make the diagnosis in secondary syphilis when there are symptoms such as: rash, headache, lymphadenopathy, alopecia, hepatitis, synovitis, neurologic/ocular abnormalities. Check syphilis antibodies and RPR.

Front 290

How do you diagnose TB as the cause of uveitis?

Back 290

Systemic symptoms may not always be present. A definitive diagnosis can be made if you isolate AFB. Presumptive diagnosis if there are eye findings with a positive result of IGRA/PPD, AFB smear from somewhere else, or abnormal CXR.

Front 291

A patient with AIDS presents with symptoms of visual loss, floaters and photopsia (perceived flashes of light). Eye exam showed fluffy yellow-white lesions close to vessels with hemorrhage. What is the diagnosis and treatment?

Back 291

This is CMV retinitis. Treatment is ganciclovir.

Front 292

What is infetion of the vitreous and aqueous humors called? How does someone get these infections?

Back 292

Called endophthalmitis. Can either be exogenously (trauma, surgery, etc) or endogenously (bacteremic/fungal seeding from endocarditis (40%), meningitis, indwelling catheter, IVDA) acquired.

Acute bacterial endophthalmitis is a medical emergency.

Front 293

What is the clinical presentation of endophthalmitis? How do you diagnose and treat?

Back 293

symptoms include eye ache/pain, decrease in vision/visual acuity. chemosis (conjunctival edema), hypopyon. Diagnose by culturing aqueous/vitreous humor. Give antibiotic injections into vitreous.

Front 294

A patient found to be candidemic should have what additional test done?

Back 294

Any candidemic patient should have a dilated ophtho exam. Up to 6% of fungemic patients will develop endophthalmitis. Patients will have focal white infiltrative lesion described as fluffballs. Start patients on intravitreal and IV antifungals.

Front 295

What are the eyelid infections?

Back 295

Hordeolum/stye: infection of sebaceous gland of Zeis. external.

Chalazion: infection of the Meibomian gland (internal stye)

Blepharitis: Inflammation of lid margin and there is abnormal Meibomian gland secretions. associated with seborrheic dermatitis and rosacea.

Dacrocystadenitis: inflammation of the lacrimal gland. Tender area of erythema/swelling in the lateral part of the upper lid.

Front 296

What is the difference between pre-septal cellulitis and orbital cellulitis?

Back 296

Both can have swollen shut lids with fever and increased WBCs.

Pre-septal: anterior to orbital septum, visual acuity is normal, extra-ocular movements are full, no pain on eye movement, no proptosis.

Orbital (pic): porsterior to orbital septum wit proptosis, ophthalmoplegia and edema of eyelids, pain on eye movement, decreased vision, afferent pupillary defect.

Front 297

Where is the submandibular space? What infection can develop in this space?

Back 297

Ludwig's angina. It is always bilateral and spreads rapidly. The infection begins in the floor of the mouth due to dental infection. Potentially life-threatening as it can obstruct airway.

Front 298

Where is the parapharyngeal space? What can develop in this space?

Back 298

Parapharyngeal abscesses. This is potentially life-threatening due to close proximity of the carotid sheath. Patients will get trismus, induration and swelling below the angle of the mandible, fevors and rigors.

Front 299

Where is the retropharyngeal space? What can develop in this space?

Back 299

Retropharyngeal abscesses. This can be very serious as they can extend into the superior/posterior mediastinum.

Front 300

Pharyngitis caused by Fusobacterium necophorum can potentially cause what syndrome?

Back 300

Lemierre's syndrome. This is an infection of the jugular vein causing clotting. This can result in septic pulmonary emboli. Patients have a persistent fever, rigors, neck pain and respiratory distress.

Front 301

What causes "lumpy jaw"? What would you see on histology?

Back 301

Cervicofacial actinomycosis is caused by Actinomyces forming an abscess. Histology would show branching gram positive bacteria and sulfur granules.

Front 302

What is Vincent's angina?

Back 302

Acute necrotizing ulcerative gingivits ("trench mouth"). Patients will have horrible breath, blunting of the interdental papilla and ulcerative slouging of the gingiva. Caused by poor oral care, stress, smoking, immunosuppression and malnutrition.

Front 303

What are some potential causes of mediastinitis?

Back 303

Can occur post-operative after cardiac or lung surgery, Histoplama infection (fibrosing mediastinitis), deep neck space infections, and Boerhaave's syndrome (rupture of the esophagus).

Front 304

What are the common etiologies of acute meningitis?

Back 304

S. pneumonia, N. meningitidis, L. monocytogenes, H. influenza, S. agalactiae (GBS), and viral meningitis

Front 305

How does a patient with acute meningitis present?

Back 305

Headache is the prominent early symptom. This is followed by mental status changes (confusion, delirium, lethargy, coma). There will also be fever and nuchal rigidity. Look for triad of fever, nuchal rigidity and mental status change.

Other specific signs are Kernig's sign and Brudzinski sign.

Kernig's: Flex thigh to abdomen and flex knee, then passively extend leg. Patient resists leg extension.

Brudzinski: Passively flexing the neck causes flexion of the hips and knees.

50 % of patients with meningococcemia will have a rash typically on the extremities that is petechial and purpuric.

Front 306

A patient presents with meningismus and rhinorrhea. The rhinorrhea is determined to be CSF fluid. What is the most likely etiology of the meningitis?

Back 306

Patient most likely has a basilar skull fracture allowing S. pneumoniae to cause the meningitis. Patients with head injury and CSF leak are more likely to have recurrent meningitis.

Front 307

A patient presents with meningismus, seizures and other neurological complaints. What bacteria is most likely causing the meningitis?

Back 307

L. monocytogenes

Front 308

What are the typical CSF findings in patients with bacterial meningitis?

Back 308

Low glucose, High protein (>50 is abnormal), high PMNs that are mostly neutrophils, positive gram stain (negative stain doesn't rule out meningitis)

Front 309

What is the treatment for meningitis?

Back 309

Empiric: typically ceftriaxone (3rd gen.), vancomycin and ampicillin.

S. pneumoniae: Penicillin if susceptible. Ceftriaxone +/- vancomycin (if MIC>1 for ceftriaxone) if resistant. Also give dexamethasone.

N. meningitidis: Ceftriaxone. Prophylaxis for contacts (Rifampin/Ciprofloxacin/Ceftriaxone).

L. monocytogenes: Ampicillin or penicillin. Gentamicin for synergy.

H. influenzae: Ceftriaxone and dexamethasone (reduces neurolgic sequelae). Rifampin for household contacts.

S. agalactiae: Ampicillin + Gentamicin initially. Give penicillin-G once you have diagnosis.

Front 310

What patients are at increased risk for getting N. meningitidis?

Back 310

Most commonly seen in children and young adults. People who carry N. meningitidis in their nasopharynx and those with terminal complement deficiencies (C5-C8) have increased risk. Usually seen in overcrowded living quarters (dorms, solider barracks).

Front 311

A Sickle cell patients with petechiae on his extremities and signs of meningismus is unresponsive with poorly perfused extremities, cyanosis, acidosis, and hypoxia. What is going on with this patient. How should he be treated?

Back 311

Patient has meningitis caused by N. meningitidis as evident by the petechiae and meningismus. Sickle cell patients are likely to be asplenic which increases the risk for Waterhouse-Friderichsen syndrome (hemorrhagic adrenalitis) leading to shock. This patient should be given hydrocortisone until patient improves.

Front 312

Who is at risk for getting Listeria monocytogenes? How does Listeria meningitis present?

Back 312

At risk groups include neonates, pregnant women and the elderly. Listeria is a facultative anaerobe that can grow in the cold causing contamination of cold cuts, meats (ex: hotdogs) and raw veggies/milk. Listeria meningitis can present in a variety of ways, from mild symptoms of fever/mental status change to fulminant meningitis with coma

Front 313

What does the CSF analysis show on a person with Listeria meningitis?

Back 313

CSF shows 100% neutrophils to 100% mononuclear cells. Greater than 25% of lymphocytes can be seen. The bacteria may look like "diphtheroids" and should always be considered when that grows in culture.

Front 314

How does meningitis present in a patient with H. influenzae?

Back 314

Usually infects young children with a prior URI. There may be few specific signs and nuchal rigidity may be absent. Seizures/coma are common late manifestations.

Front 315

How is H. influenzae able to cause meningitis after a URI?

Back 315

H. influenzae is encapsulated which enables it to invade the bloodstream following colonization of the respiratory tract.

Front 316

How do neonates present with GBS meningitis?

Back 316

Symptoms are present at or within hours after birth. They include: lethargy, poor feeding, abnormal temperature, grunting respirations, pallor/cyanosis, tachypnea and hypotesnsion.

Front 317

How can GBS meningitis be prevented?

Back 317

Pregnant women should be put on prophylaxis if they have positive vaginal cultures at 35-37 weeks of gestation or if they had a previous infant with GBS meningitis. Prophylaxis is penicillin.

Front 318

What primarily causes aseptic meningitis?

Back 318

Enteroviruses (echoviruses and coxsackieviruses) are the leading causes. HSV accounts for a small portion and is associated with primary genital infection with HSV2.

A chronic form of aseptic meningitis that is causes by HSV2 is Mollaret's meningitis, also called recurrent benign lymphocytic meningitis.

Front 319

Patient complains of headache and nausea for the past 5 weeks. Recently she complains of being more confused and decrease in vision. She is found to have papilledema and lymphadenopathy. A spinal tap was done and the opening pressure was elevated. The CSF was found to be hypoglycorrhachia (low CSF glucose), elevated protein and lymphocytic pleocytosis. What is the most likely diagnosis and etiology? What is the treatment?

Back 319

This is chronic meningitis most likely caused by TB. Should look for TB risk factors: HIV/AIDS, close contact with infected, foreign born or recent travel, etc. Chronic meningitis can be assumed and treated as TB as diagnosis is difficult. CSF will have low glucose and high protein. CXR is abnormal in 50% of patients and will show miliary lesions (multiple small lesions, see pic). Treatment is INH and PZA as they can reach the CSF. Should also give adjunctive corticosteroids.

Front 320

A patient develops a low-grade fever, headache and low-grade CSF pleocytosis after a recent neurosurgery. What is the diagnosis and likely etiology? How is this treated?

Back 320

This is post-neurosurgical meningitis likely caused by S. epidermidis. DOC is vancomycin but this has poor CSF penetration which makes treatment difficult. S. epidermidis likes to form biofilms on foreign bodies so removal of the implanted material may be required for the cure.

Front 321

What are the common causes of brain abscesses?

Back 321

Strepococci (especially S. anginosus): consider oropharyngeal infections, infective endocarditis, recent neurosurgery.

S. aureus: consider cranial trauma or infective endocarditis.

Anaerobes (bacteroides, prevotella)

Gram-negative bacilli: consider otitic foci of infection, neurosurgical procedure, immunocompromised

Actinomyces: consider hematogenous spread from lung, abdomen or contiguous spread from head infection.

Norcardia: consider disseminated infection from lungs or skin. can also be isolated CNS lesion.

Front 322

How does a brain abscess typically present?

Back 322

Headache is the most common presenting symptom. Sudden worsening of the headache with onset of meningismus may signify rupture into the ventricular space. Imaging will show hypodense center with ring enhancement surrounded by a hypodense area of brain edema.

Front 323

How should brain abscesses be treated?

Back 323

Empiric antibiotics should be initiated on the basis of the patient's predisposing conditions and the presumed pathogenesis. For strep, add metronidazole to antibiotic regimen as polymicrobial infections are common. Steroids should be given if there is mass effect with significant edema. Phenytoin should be considered to prevent seizures. Surgical excision is often required.

Front 324

A patient presents with pulmonary nocardia. What CNS disease should this patient be evaluated for?

Back 324

Patients with pulmonary nocardiosis should be evaluated for a possible brain abscess. Immunocompromised patients are more likely to develop nocardiosis. Treatment is sulfonamides.

Front 325

What is a brain abscess?

Back 325

A focal, intracerebral infection that begins as a localized area of cerebritis and develops into a collection of encapsulated pus.

Front 326

What is a subdural empyema? What is the pathogenesis?

Back 326

A collection of pus in the space between the dura and arachnoid.

Pathogenesis: Infection spreads to the subdural space by 1) valveless emissary veins in association with thrombophlebitis 2) extension of osteomyelitis of the skull with accompanying epidural abscess.

Front 327

How does a subdural empyema typically present?

Back 327

Symptoms can be rapidly progressive. Symptoms include increased intracranial pressure (vomiting), meningeal irritation (fever/headache/meningismus), or focal neurologic deficit. If untreated it could lead to cerebral herniation and further increase in intracranial pressure. Diagnose with imaging.

Front 328

How should a subdural empyema be treated?

Back 328

Requires both surgical and medical treatment. Antibiotics are based on gram stain and likely etiology. Metronidazole for anaerobes. Cefepime, ceftazidime, or meropenem for gram-negative.

Front 329

What is a cranial epidural abscess?

Back 329

It is a localized collection of pus between the dura mater and skull/vertebral column. These can give rise to subdural empyemas.

Front 330

How do patients with cranial epidural abscess typically present?

Back 330

The presentation is typically insidious (grows slowly due to how close the dura is to the cranium) and can be masked by the primary infection (sinusitis/otitis media). Fever and headache are common and cranial epidural abscesses can be missed until it is complicated by sudrual empyema, brain abscess, or meningitis. Treatment is medical and surgical.

Front 331

What is the pathogenesis of a spinal epidural abscess? How is it treated?

Back 331

They usually occur from hematogenous dissemination or by local extension from vertebral osteomyelitis. S. aureus is the most common etiology.

Treatment is surgical drainage and long term antibiotics. Vancomycin for staph and cefepime for aerobic gram negatives

Front 332

How do patients with a spinal epidural abscess typically present?

Back 332

They usually progress through 4 stages: 1) backache and focal vertebral pain 2) nerve root pain (radiculopathy or paresthesias) 3) spinal cord dysfunction (defects of motor/sensory/sphincter function) 4) paraplegia. Fever is typically present as well.

Front 333

How does suppurative intracranial thrombophlebitis present?

Back 333

It depends on which vein/sinus has the thrombus. There will typically be a headache and fever. If the cavernous sinus is infected there will be eye findings such as periorbital swelling, diplopia, lateral gaze palsy, etc.

Front 334

What are the clinical manifestations of the common cold?

Back 334

Symptoms usually sore throat followed by nasal obstruction and rhinorrhea. There may also be a cough. Caused by a number of viruses and is a recurrent disease either due to the number of antigenic types or incomplete immunity (parainfluenza, metapneumovirus and RSV).

Front 335

What are the etiologies of pharyngitis and what are their clinical syndromes?

Back 335

Group A strep: Sore throat, odynophagia, fever, anterior cervical LAD and tonsilar exudates. Treatment is PCN or amoxicillin for 10 days. Treatment is effective in preventing acute rheumatic fever.

Group C strep: similar to GAS, can be from contaminated food products.

Arcanbacterium haemolyticum: Similar to GAS but with a scarlatiniform, macular, or maculopapular rash which begins on distal extremities sparing palms and soles. DOC is erythromycin. Rare.

C. diphtheriae: Sore throat, low grade fever, malaise, membrane on tonsilar/pharyngeal surface that bleeds when scraped, bull's neck. Test for toxin and treat with erythromycin or PCN. Consider antitoxin.

N. gonorrhoeae: sore throat in the appropriate sexual history setting. Treatment is Ceftriaxone + Azithromycin or Doxycycline.

EBV: Fever, painful cervical LAD, sore throat, fatigue and headache. Usually diagnosed by rash after giving amoxicillin.

HIV: EBV like syndrome in the acute infection setting called "acute retroviral syndrome"

Enterovirus: Seen in summer/fall. Sore throat with erythema.

Adenovirus: Common cause of pharyngitis. White exudates with throat pain.

Front 336

What is the pathogenesis and clinical symptoms seen in croup?

Back 336

Primarily caused by parainfluenza virus that causes inflammation of the larynx and trachea, particularly at the sublottic level. Subglottic edema leads to stridor and a decrease in tidal volume which can result in tachypnea and respiratory failure.

Symptoms are characterized by a barking cough "seals cough", hoarseness and inspiratory stridor. There is a initial prodrome of rhinorrhea, cough and fever.

Front 337

How do you diagnose Croup? What is the treatment?

Back 337

Based on clinical syndromes and characteristic "steeple sign" see on AP radiograph.

Treatement is dexamethasone and supportive care. If severe can give nebulized racemic epinephrine.

Front 338

How does otitis externa typically present?

Back 338

Patients with otitis externa will have a pruritic and painful outer ear. It will be painful on palpation. Usually caused by P. aeruginosa from swimming or water being trapped in ear canal in hot/humid weather.

Chronic otitis externa is a manifestation of an otitis media infection which is draining through a perforated tympanic membrane leading to irritation. Treat the otitis media.

Invasive otitis externa presents with severe pain and necrotizing infection spreading to adjacent soft tissue. Diabetics and immunocompromised are at risk. Caused by P. aeruginosa. Debride and give antibiotics.

Front 339

How does otitis media typically present? What is the pathogenesis?

Back 339

Diagnosed by fluid in middle ear with symptoms (pain, drainage, fever, etc.). Most commonly seen in children ages 6-24 months.

The pathogenesis is a dysfunction of the eustachian tube. Nasal congestion from an infection or allergies causes blockage of the eustachian tube leading to fluid buildup in the middle ear.

Can be caused by S. pneumoniae, H. influenzae, M. catarrhalis and viruses.

Front 340

What is the treatment for otitis media?

Back 340

Augmentin (Amoxicillin/Clavulanate), IM ceftriaxone or Macrolide for PCN allergy. A tympanostomy tube may be needed to drain the middle ear.

Front 341

How does mastoiditis typically present?

Back 341

Typically in the setting of an acute otitis media. Will see edema, tenderness and erythema over mastoid bone. The pinna will be displaced outward and downward. There may also be purulent discharge. Treatment is the same as acute otitis media. A mastoidectomy may be necessary if prolonged because the infection can spread to the brain causing a brain abscess.

Front 342

What is the pathogenesis and clinical presentation of sinusitis?

Back 342

Pathogenesis: Narrow sinus ostia (mucosal swelling from virus or allergy, mechanical obstruction, or local insult), Cilliary dysfunciton (Kartagener's syndrome causes recurrent sinusitis), or viscous sinus secretions. All of which lead to back of sinus fluid in sinuses.

Clinical syndrome: purulent nasal discharge, nasal obstruction, facial pain/pressure/fullness. Symptoms tend to be persistent for up to 10 days.

Front 343

What is the treatment for sinusitis?

Back 343

Augmentin is first line for both kids and adults. Can also give nasal irrigation and intranasal steroids.

Front 344

Patient presents with fever, tachycardia, sever sore throat and odynophagia. Laryngoscope shows this. What is the diagnosis and treatment?

Back 344

This is epiglottitis which is cellulitis of the epiglottis and adjacent structures. It is most commonly caused by H. influenza type b. This is an airway emergency and patients should be intubated. Treatment is Unasyn (ampicillin/sulbactam) or ceftriaxone + Vancomycin.

Front 345

How does acute bronchitis typically present?

Back 345

Acute bronchitis is inflammation of large and mid-sized airways that is not associated with pneumonia. Usually presents as an URI (nasal congestion, rhinitis, sore throat, malaise, low grade fever) followed by a cough which becomes the dominant symptom. Most bronchitis is viral in nature so treatment is symptomatic. DO NOT give antibiotics as most physicians do. Only give antibiotics in the case of whooping cough (macrolides). Give NA inhibitors for influenza.

Front 346

What is the pathogenesis and clinical presentation of bronchiolitis?

Back 346

Pathogenesis: There is inflammation and luminal narrowing of the bronchioles primarily caused by a virus (RSV most common). Air is inspired through a partial obstruction but can't leave because with expiration there is luminal collapse. This results in obstruction and hyperinflation. This can lead to dyspnea, tachypnea, decreased tidal volume and deacreased ventilation-perfusion ration resulting in arterial hypoxemia. Once infant is no longer to compensate with increased ventilation, then hypercarbia develops.

Clinical presentation: Commonly seen in kids < 2 yrs. Prodromal symptoms of coryza, cough and mild fever. Development of chronic cough and wheezing marks LRT involvement. Patient will also be tachypneic, lethargic and have poor feeding.

Front 347

What signs are suggestive of impending respiratory failure in patients with bronchiolitis?

Back 347

Decreased lung sounds, progressive dyspnea and decreased movement of air.

Front 348

How is bronchiolitis managed?

Back 348

supportive care, supplemental oxygen, inhaled ribavirin (infants with severe RSV), and monoclonal anti-RSV antibody (prevention for high risk infants)

Front 349

What is the pathogenesis and clinical presentation of acute pneumonia?

Back 349

Pathogenesis: Under normal conditions, lung sterility is maintained by the respiratory tract defense mechanisms. Pathogens can enter via 1) macro and micro aspiration of upper airway flora 2) inhalation of contaminated aerosolized material 3) metastatic seeding of lung by hematogenous route.

Clinical presentation: Acute pneumonia is the most common cause of infection related mortality. It presents with fever, chills, fatigue, sweating, headache, nausea, myalgias, cough with sputum production, dyspnea. Those with leukopenia is a poor prognostic indicator. Physical exam shows abnormal vitals, inspiratory rales, dullness on percussion/bronchial breath sounds/E to A change suggestive of consolidation.

Front 350

How is acute pneumonia diagnosed?

Back 350

Diagnose by xray/CT (gold standard), gram staining sputum, doing a fiber optic bronchoscopy, culturing blood/urine, or lung biopsy.

Front 351

When are patients classified as having HAP, VAP, and HCAP?

Back 351

Hospital acquired pneumonia: infection acquireed >48 after hospitalization

Ventilator associated pnemonia: infection acquired >48 hours after endotracheal intubation and mechanical ventilation

Health-care associated pneumonia: Patients who fevelop pneumonia after extensive outpatient contact with the health-care system

Front 352

What microbial agents typically cause chronic pneumonia?

Back 352

Mycobacteria, fungi (histoplasmosis, blastomycosis, etc), invasive molds (aspergillosis), nocardiosis, actinomycosis, melioidosis, worms.

Front 353

What patients are more likely to get chronic pneumonia?

Back 353

Elderly/debilitated patients (aspiration pneumonia), Af. Am. (TB), COPD patients (histo), HCW (TB), archeologisits (cocidioidomycosis), upper mid-West US (histo), SE Asia (meliodosis), HIV (TB), homeless/alcoholics (TB), immunocompromised.

Front 354

How do you diagnose chronic pneumonia?

Back 354

Symptoms are non-specific so epidemiological and exposure history is critical. Chest imaging (CXR and CT) are best.

Front 355

What is the pathogenesis of parapneumonic effusion and empyema?

Back 355

The initial stage (uncomplicated stage) is pulmonary interstitial fluid entering pleural space with increased permeability of capillaries in the pleura.

The second stage (complicated stage) is infection of the plueral effusion with organisms that caused the underlying pneumonia.

The third stage is empyema formation (pus in the pleural space).

Front 356

How do you diagnose a parapneumonic effusion and empyema?

Back 356

Physical exam: decreased breath sounds, dullness to percussion and crackles.

Imaging: CXR will show blunted costo-phrenic angle and free fluid in lateral decubitus. CT is best for emypema and will show "split pluera" sign.

Front 357

How do you differentiate between a transudative and exudative pleural effusion?

Back 357

Front 358

What is the treatment for parapneumonic effusions and empyemas?

Back 358

Uncomplicated parapneumonic effusion: resolves with antibiotics alone for the underlying pneumonia.

Complicated PE and empyema: require drainage. Also antibiotics for most likely pathogen plus anaerobic coverage.

Front 359

What is a lung abscess and what are the risk factors for getting one?

Back 359

They are localized area(s) of pulmonary necrosis caused by infection with cavities > 2cm in diameter. Multiple small cavities < 2cm are called "necrotizing pneumonia". Lung abscesses are usually primary caused by aspiration. Secondary abscesses are due to some underlying condition (cancer, AIDS, etc) or hematogenous seeding (Lemierre syndrome).

Risk factors: Increased bacterial inoculum (poor dental hygiene), impairment of consciousness (drugs, anesthesia, coma, etc), Impaired cough and epiglottic reflex, impairment of esophageal function, emesis, septic embolization (IVDU and tricuspid valve endocarditis, Lemierre syndrome).

Front 360

List the portions of lung from most likely to least likely to get aspirated material.

Back 360

Posterior segment of right upper lobe > posterior segment of left upper lobe > superior segment of right lower lobe > superior segment of left lower lobe

Front 361

What is the clinical presentation of a lung abscess?

Back 361

Fever, malaise, night sweats, pleuritic pain, cough, purulent "putrid" smelling sputum, weight loss, clubbing of digits, anemia of chronic disease, neutrophilic peripheral leukocytosis.

Front 362

How do you diagnose a lung abscess? How are they managed?

Back 362

CXR and CT showing lung cavity with air-fluid levels. LRT sample for gram stain and culture to determine organism. Blood culture for secondary abscess.

Management is usually just antibiotics targeting specific bacteria. Antibiotic should have anaerobic coverage. Drainage is not typically necessary.

Front 363

What is the difference between gastroenteritis and dysentery?

Back 363

Gastroenteritis: a syndrome consisting of diarrhea and vomiting generally caused by a non-inflammatory infection in the upper small bowel or colon.

Dysentery: frequent small bowel movements with blood and mucous. There is tenesmus and pain on defecation.

Front 364

What are the common pathogens that cause viral gastroenteritis and what are their clinical presentation?

Back 364

Rotavirus: severe watery diarrhea, emesis, fever and abdominal pain that lasts for 3-8 days. Incubation period is 2 days.

Calicivirus (Norovirus): Diarrhea, emesis, nausea and stomach pain that lasts for 1-3 days. Incubation period is 12-48 hrs.

Front 365

What are the common pathogens that cause bacterial gastroenteritis/dysentery and what are their clinical presentation?

Back 365

Shigella: Most common cause of bloody diarrhea in children. Acute bloody dysentery, high fever, systemic symptoms for 7 days.

EHEC: Serotype O157 is most common type of bloody diarrhea caused by EHEC. Abdomical cramps, watery diarrhea that turns into bloody diarrhea, HUS for 2-4 days.

ETEC: Leading cause of travelers diarrhea. Profuse watery diarrhea and abdominal cramping for 3-4 days.

Non-typhodial Salmonella: Foodborne, but can be transmitted via reptiles/amphibians. Fever, cramping abdominal pain, and diarrhea for 3-5 days.

Front 366

How do you diagnose gastroenteritis/dysentery organisms?

Back 366

Front 367

How do you manage viral/bacteria related gastroenteritis/dysentery?

Back 367

Viral: supportive treatment only (oral rehydration)

Bacterial: Dysentery caused by shigella, severe salmonella gastroenteritis, and moderate to severe ETEC give Ciprofloxacin. Do not treat EHEC has this can increase risk for HUS.

Front 368

What pathogen causes profuse vomiting and nausea that is associated with eating fried rice?

Back 368

Bacillus cereus

Front 369

Back 369

Front 370

What antibiotics are associated with C. difficile infection?

Back 370

Penicillins, cephalosporins, clindamycin and fluorquinolones are the most commonly implicated antibiotics.

Front 371

What is the pathogenesis and clinical presentation of C. difficile?

Back 371

Pathogenesis: 1) disruption of normal flora by antibiotics 2) colonization with toxigenic C. difficile 3) toxin production 4) mucosal injury and inflammation.

Clinical presentation: usually occurs 5-10 days after antibiotic exposure with a wide range of severity of diarrhea. There will also be abdominal cramping, fever, and high WBC.

Front 372

How is C. difficile diagnosed and managed?

Back 372

Diagnosis is typically made by looking for toxin production in stools or a C. difficile PCR.

Management includes stopping initial antibiotic causing the C. difficile and treat with metronidazole or oral vancomycin. Stool transplants are becoming a more widely used treatment.

Front 373

What is the pathogenesis and clinical presentation of typhoid fever?

Back 373

Pathogenesis: Salmonella is ingested and penetrates the intestinal epithelium in the small bowel. They multiply in the intestinal lymphoid tissue and then disseminate.

Clinical presentation: Usually from recent travel outside US. Most common symptoms are sustained fever, headache, Diarrhea or constipation, cough, conjunctivitis, abdominal pain, splenomegaly, bradycardia and rose spots.

Front 374

How do you diagnose and manage typhoid fever?Diagn

Back 374

Diagnosis can be made by blood cultures. LFTs may be elevated as well as bilirubin and AP. Clinical presentation and history are important.

Management is ciprofloxacin and make sure to vaccinate prior to travelling to endemic areas.

Front 375

What are the common infectious causes of esophagitis?

Back 375

Candida in HIV patients, CMV in bone marrow transplants, HSV, acute HIV

Front 376

what is the clinical presentation of esophagitis?

Back 376

Patients will have dysphagia, odynophagia, sense of obstruction, not able to tolerate solids, weight loss and anemia.

Front 377

How is esophagitis diagnosed and managed?

Back 377

Diagnosis can be made via endoscopy and biopsy. Presence of yeast and pseudohyphae is consistent with candida. Large shallow ulcers in middle to distal esophagus is CMV. Small superficial ulcers in distal esophagus is HSV.

Management HIV esophagitis (candida) is fluconazole and start HAART. For CMV give ganciclovir or valganciclovir and start HAART. For HSV give acyclovir or valacyclovir.

Front 378

What is the pathogenesis and clinical presentation of Whipple's disease?

Back 378

Pathogenesis: Not completely clear but like transmitted fecal oral or acquired through the environment as it is seen in soil and sewage water. Bacteria invade the small intestine blocking nutrition uptake causing steatorrhea and disseminates throughout the body. There is very little inflammation and patients likely have a defect in cell-mediated immunity.

Clinical presentation: classically weight loss, diarrhea, arthropathies and abdominal pain. There may also be CNS/lung/cardiac symptoms and hyperpigmentation.

Front 379

How do you diagnose and manage Whipple's disease?

Back 379

Diagnose via upper endoscopy with small bowel biopsies looking for PAS-positive macrophages.

Management is Ceftriaxone for 2 weeks and then 1 year of TMP-SMX.

Front 380

What is the pathogenesis and clinical presentation of Tropical Sprue?

Back 380

pathogenesis: occurs after an acute enteric infection in endemic tropical areas. Patient then develops small bowel bacterial overgrowth. These cause small bowel obstruction from toxins and fermentation. Leads to malabsorption of fats, folate and vitamin B12.

clinical presentation: Prolonged diarrhea, abdominal cramping and weight loss with appropriate epidemiology.

Front 381

How is Tropical Sprue diagnosed and managed?

Back 381

Diagnose by upper endoscopy looking at small bowel. It will involve the entire small bowel. Histology will show shortened, blunted vili and elongated crypts. Travel history is important and usually they spend a lot of time in the endemic area.

Management is tetracycline and folate for up to 6 months.

Front 382

What is the pathogenesis and clinical presentation of appendicitis?

Back 382

Pathogenesis: typically caused by obstructing the appendiceal lumen by fecalith. Can also be obstructed due to foreign body, tumor, parasite, etc. Blockage causes mucous buildup -> increase in intraluminal pressure -> impaired vascular and lymphatic drainage -> mucosa ischemia -> microbial invasion -> perforation.

Clinical presentation: 6-24 hrs of colicky, periumbilical pain localized to RLQ. Patient will have mild fever, anorexia, N/V, and guarding.

Front 383

How is appendicitis diagnosed and managed?

Back 383

Diagnosis is made via history and physical exam. Labs will show mild leukocytosis, elevated CRP, and sterile pyuria. CT is highly specific and sensitive (use MRI/ultrasound in pregnancy)

Management is appendectomy and antibiotics.

Front 384

What is the epidemiology of Diverticulosis, Diverticulitis, and Typhlitis?

Back 384

Diverticulosis: Saccular herniations in the colonic wall. They are false diverticula. Attributed to poor diets with low fiber intake. Usually seen in elderly.

Diverticulitis: Inflammation of the diverticula. Seen in patients with diverticulosis.

Typhlitis: "neutropenic enterocolitis" usually in patients with hematologic malinancies getting myelosuppressive chemotherapy.

Front 385

What is the pathogenesis and clinical presentation of diverticulitis?

Back 385

Pathogenesis: similar to appendicitis. There is obstruction of the diverticula, typically by fecalith. Causes mucus buildup and bacterial overgrowth which leads to inflammation of bowel wall and perforation. If perforated, can cause peritonitis and fistula formation.

Clinical presentation: Usually seen in the elderly. They will report LLQ pain with guarding and rebound tenderness. They can also have fever, N/V, change in bowel habits and urinary symptoms.

Front 386

How is diverticulitis diagnosed and managed?

Back 386

Diagnosis is made based on CT findings such as pericolic fat stranding, divertiucla, bowel wall thickening, or abscess formation. Colonoscopy is contraindicated given the risk of perforation.

Management is antibiotics that cover colon bacteria (gram negative and anaerobes) such as fluoroquinolone and metronidazole. If there is an abscess this should be drained percutaneously.

Front 387

What is the pathogenesis and clinical presentation of typhlitis?

Back 387

Pathogenesis: Seen in neutropenic patients. There is mucosal injury and ischemia that allows colonic flora to invade the bowel wall. This causes local destruction and release of endotoxins.

Clinical presentation: Patients tend to have 1-2 weeks of neutropenia. Present with fever, N/V, abdominal pain and tenderness and often bloody diarrhea. There will often be severe stomatitis and pharyngitis. This is rapidily progressive with a high mortality rate.

Front 388

How do you diagnose and manage typhlitis?

Back 388

Diagnosis is made by CT or ultrasound looking for thickening of the bowel wall. If greater than 10mm this has a 60% mortality rate.

Management is usually conservative. Bowel rest, decompression, fluids, nutritional support, and broad spectrum IV antibiotics. Surgery if there is perforation of uncontrolled bleeding.

Front 389

What is the pathogenesis and clinical presentation of spontaneous bacterial peritonitis?

Back 389

Pathogenesis: Not related to intra-abdominal pathology. Enteric bacteria translocate from bowel to mesenteric lymph commonly seen in patients with portal hypertension due to cirrhosis and ascites. These patients have low levels of complement and immunoglobulins which helps the disease progress.

Clinical presentation: fever, abdominal pain, N/V, diarrhea, diffuse abdominal tenderness and rebound. Often leads to decompensation of liver disease (hepatic encephalopathy).

Front 390

How is SBP diagnosed and managed?

Back 390

Diagnosis is made by abdominal paracentesis of the ascites fluid.

Management for SBP is antibiotics. Secondary peritonitis requires surgery. Patients are put on prophylactic antibiotics (cipro or TMP/SMX) as there is a high risk of another episode.

Front 391

What is the pathogenesis and clinical presentation of acute cholecystitis?

Back 391

Pathogenesis: Due to biliary obstruction from a gallstone which increases pressure reduces blood supply and lymphatic drainage. This leads to acute inflammation from normal intestinal flora.

Clinical presentation: RUQ pain with radiation to the infrascapular region. Pain is typically constant and worse after fatty meals. Paitents will have fever and tachycardia. Gallstones are more common in women, > 40 yrs, obese and pregnancy (Fat, Female, Fertile, Forty).

Front 392

How do you diagnose and manage acute cholecystitis?

Back 392

Diagnose by history, physical (Murphy's sign - pain on inspiration when gallbladder is palpated), and imaging (ultrasound or HIDA scan).

Antibiotics may not be necessary in uncomplicated cholecystitis. If there is perforation, gangrene, infection or patients with comorbidities then give antibiotics such as pip-tazo, ampicillin/sulbactam, ertapenem or ceftriaxone + metronidazole. Cholecystectomy should be done with perforation or gangrene.

Front 393

What is the pathogenesis and clinical presentation of acalculous cholecystitis?

Back 393

Pathogenesis: There is some underlying disease that predisposes to gallbladder wall ischemia or stasis of bile. This leads to concentration of bile salts and inflammation/necrosis of gallbladder wall.

Clinical presentation: More subtle symptoms than in acute cholecystitis. May just have fever and RUQ pain. Usually seen in critically ill patients in the ICU. Diagnosis and treatment is the same as acute cholecystitis.

Front 394

What is the pathogenesis and clinical presentation of cholangitis?

Back 394

Pathogenesis: Cholangitis is inflammation or infection of the common bile duct. Bile becomes infected by normal intestinal flora when there is a decrease in the flow of bile due to an obstruction (gall stones, benign stenosis, tumor, complication of stent placement).

Clinical presentation: Charcot's triad of RUQ or epigastric pain, fever or chills, and jaundice. Some patients will also have hypotension and altered mental status in which case it is Reynold's Pentad.

Front 395

How is cholangitis diagnosed and managed?

Back 395

Diagnosis is made by history, physical (Charcot's Triad of Reynold's Pentad), labs (increase in conjugated bilirubin and ALP), blood and bile cultures may be positive, and ultrasound to look for ductal dilation and stones.

Management is ERCP to relieve obstruction with broad spectrum antibiotics initially (pip-tazo, amp-sulbactam, ertapenem)

Front 396

What is the pathogenesis and clinical presentation of a liver abscess?

Back 396

Pathogenesis: Can either be an amebic abscess caused by Entamoeba histolytics (rare in US, but common worldwide) or a pyogenic abscess caused by intestinal flora. Pyogenic abscesses are usually due to an underlying condition such as cholangitis, systemic bacteremia, abdominal infections, etc.

Clinical presentation: Amebic abscesses present with fever, dull aching pain in RUQ. Some will have N/V and diarrhea. Pyogenic abscesses will have fever, malaise, fatigue and anorexia.

Front 397

How are liver abscesses diagnosed and managed?

Back 397

Diagnosis is difficult as there is no specific syndrome. It is a leading cause of fever of unknown origin. Labs will show leukocytosis, elevated ALP and positive blood cultures (pyogenic abscess). CT scan will show abscess.

Management is metronidazole for amebic abscess and drainage + specific antibiotic for pyogenic abscess.

Front 398

How do pancreatic and splenic abscesses present?

Back 398

Pancreatic: usually occurs after pancreatic trauma or pancreatitis caused by intestinal flora. Patients will have fever, abdominal pain and leukocytosis. Diagnose with CT scan and biopsy. Management is drainage, debridement of necrotic areas, and antibiotics specific to organism.

Splenic: Risk factors are IVDU, HIV, and trauma. Caused by Strep, Staph, Salmonellae, E. coli and fungi in immunocompromised. Patients present with fever, LUQ pain, N/V, anorexia, leukocytosis and splenomegaly. Diagnose with CT, ultrasound or plain films. Treatment is antibiotics and drainage. Splenectomy if severe.

Front 399

Why are women more prone to UTIs?

Back 399

1) There is a shorter distance between anus and urethral orifice 2) Shorter length of urethra and 3) There is an absence of antibacterial effects found in prostatic fluid.

Front 400

What is the pathogenesis of UTIs?

Back 400

Most UTIs occur as an ascending infection. Lower UTIs are due to colonization from enteric organisms (E. coli, Proteus mirabilis, etc.) and upper UTIs are typically an extension of a lower UTI.

For infection to occur there is typically a disruption of normal bacterial flora (lactobacilli) and colonization with uropathogens that can result from sex, motility of the bacteria, and mechanical instruments (catheters).

The end result of immune response and bacterial cytotoxins is tissue damage, edema and intense local vasoconstriction.

Front 401

A patient is found to have bacteriuria and pyuria but is not reporting any symptoms. How should this patient be managed? It what situations does management change?

Back 401

Patients with asymptomatic bacteriuria should not be treated even if there is pyuria.

The exceptions to this rule are during pregnancy (increased risk of developing pyelonephritis and increased risk of premature delivery and low birth weight infants), trans-urethral resection of prostate (high incidence of bacteremia following procedure in with ASB) and other urologic procedures with mucosal bleeding.

Front 402

For what patients are screening and treatment of asymptomatic bacteriuria (ASB) not recommended?

Back 402

Pre-menopausal non-pregnant women, diabetic women, elderly patients, patients with spinal cord injuries, and patients on long-term indwelling catheters.

Front 403

What is the clinical presentation of cystitis? How is it diagnosed?

Back 403

Presents with dysuria (hallmark), frequency, urgency, suprapubic pain and WBCs (but no WBC cast) in urine.

Diagnosis is with urinalysis. There will be pyuria, presence of leukocyte esterase and positive urine nitrates (sensitive for enteric gram negatives). Can also do a urine culture.

Front 404

How is cystitis managed?

Back 404

Short course of antibiotics, empiric first and then targeted. Nitrofurantoin or TMP/SMX are commonly given. Fluoroquinolones and B-lactams are second-line.

Front 405

What is the clinical presentation of pyelonephritis?

Back 405

Patients present with progressive flank pain, malaise, fever and chills, prostration, N/V.

Uncomplicated pyelonephritis: healthy non-pregnant women.

Complicated pyelonephritis: everyone other than healthy non-pregnant women.

Front 406

How is pyelonephritis diagnosed and treated?

Back 406

Diagnosis is best seen by a CT with contrast. On urinalysis you will see pyuria, positive nitrates and WBC casts under microscopy.

Management is fluoroquinolones, TMP/SMX, or B-lactams. Also be on the lookout for complications such as calculi, emphysematous pyelonephritis or perinephric abscesses.

Front 407

What is the pathogenesis of emphysematous UTIs? What are the risk factors?

Back 407

Emphysematous UTIs are necrotizing infections of the urinary tract caused by rapid fermentation of glucose by gram negative rods that produce gas within bladder wall, renal pelvis or renal parenchyma.

Risk factors include Diabetes mellitus (most important), urinary tract obstruction, female sex, and >60 yrs old. Mainly caused by E. coli and K. pneumoniae.

Front 408

How do you diagnose and manage emphysematous UTIs?

Back 408

Diagnosis is made based on air in the bladder, renal pelvis, or renal parenchyma. Bacteremia is also seen in up to 50% of cases.

Management is IV antibiotics and urology consultation.

Front 409

A renal abscess found to be caused by S. aureus is most likely due to what?

Back 409

hematogenous seeding, secondary to some other infection like left-sided endocarditis.

Front 410

What is the pathogenesis of CA-ASB and CA-UTI? How should these patients be managed?

Back 410

CA-UTI is the most common health care associated infection world wide and is due to bacteria forming biofilms on catheters and causing infection. The longer the duration of catheterization, the more likely the patient will have an infection (3-10%/day).

Management is the same as ASB and UTI in non catheterized patients. Make sure to limit the unnecessary use of catheters and discontinue them when not needed. Long-term intermittent catherization is favored over indwelling (make sure to change infected indwelling ASAP).

Front 411

What is the clinical presentation of infectious urethritis and how do you diagnose it?

Back 411

Urethritis is inflammation of the urethra with symptoms of muco-purulent or purulent discharge, dysuria and/or urethral pruritus. Mainly caused by the STIs Chlamydia (most common bacterial STI) and Gonorrhea (2nd most). Coinfection of the the two is very common and patients should be treated as being coinfected.

Diagnosis is made based on gram stain of the discharge looking for gram negative diplococci that are in neutrophils which is indicative of gonorrhea. NGU (Chlamydia) will have a negative gram stain. Also look for positive leukocyte esterase on 1st void urine specimen. To determine specific pathogen, do gram stain as above, nucleic acid testing (NABT/NAAT - best sensitivity/specificity) and culture (Thayer Martin Media for Gonorrhea and Diamond's Media for T. vaginalis).

Front 412

How is infectious urethritis treated?

Back 412

Gonococcal urethritis: Ceftriaxone + Azithromycin or Doxycycline

Non-Gonocoocal urethritis: Azithromycin or Doxycycline. Metronidazole if T. vaginalis is suspected.

Sex partners of the last 60 days need to be notified, screened and treated. Reinfection can occur if not treated.

Front 413

What are some complications of infectous urethritis?

Back 413

Urethral strictures, acute epididymitis, prostate involvement, and reactive arthritis.

Front 414

How does acute bacterial prostatitis clinically present, how is it diagnosed and how is it managed?

Back 414

There will be intense pain in the perineum and rectum with fever, dysuria, urinary frequency, difficulty voiding, lower abdominal discomfort, suprapubic pain and sepsis.

Diagnosis is made based UA with microscopy showing pyuria and urine culture showing causative pathogen (most commonly E. coli, can also be gonorrhea/chlamydia in sexually active young men). Rectal exam should not be done as this can trigger bacteremia.

Management is fluoroquinolones (cipro, levo), TMP/SMX, Doxycycline, B-lactams. The acute inflammation enhances penetration of antibiotics into prostate.

Front 415

How does chronic bacterial prostatitis clinically present, how is it diagnosed and how is it managed?

Back 415

Patients with CBP will have recurrent bacterial UTIs by same organism (most likely E. coli). They will also be asymptomatic between episodes of bladder bacteriuria and have a normal prostate on exam.

Diagnosis is more difficult than acute prostatitis. It is solely based on symptoms and number of WBC in expressed prostatic secretions or prostate biopsy.

Management is more difficult than ABP as there is no inflammation to help drive the antibiotics into the prostate. Fluoroquinolones are used for 4-6 weeks.

Front 416

How does a prostatic abscess clinically present?

Back 416

A prostatic abscess is a rare complication of acute bacterial prostatitis. Symptoms can mimic those of ABP: fever, obstructive voiding symptoms, sepsis. Management requires abscess drainage and antibiotics.

Front 417

How does epididymitis clinically present?

Back 417

Epididymitis occurs via sexual transmission or on the backdrop of an underlying urologic pathology. Patients will have dysuria, urethral discharge, irritative symptoms, unilateral tender swelling and erythema in posterior scrotum, and hydrocele.

Non-specific Bacterial Epididymitis is more common in men >35 yrs. and is caused by enteric gram negatives, pseudomonas, gram positive cocci, or TB (TB is rare but most common manifestation of GU tract TB). Risk factors include catheters, ABP/CBP.

Sexually Transmitted Epididymitis is more common in men < 35 yrs. and is due to Chlamydia and gonorrhea. Requires same treatment as typical Chlamydia/gonorrhea infections.

Front 418

What is the clinical presentation of orchitis?

Back 418

Orchitis is inflammation of the testicle and can caused by either virusus (major cause) or bacteria.

The major cause of orchitis is mumps due to hematogenous seeding. There will be testicular pain and swelling 4-6 days after parotitis. Most cases are unilateral. It has been associated with infertility (rare), but more likely in bilateral cases. Other viruses include Coxsackie B viruse and LCMV.

Bacterial orchitis is usually the result for an adjacent infection such as epididymitis. Patients will have high fevers, pain radiating to inguinal canal, testicular swelling, N/V, hydrocele and erythema. Surgery and antibiotics are usually required.

Front 419

What are the most common infectious causes of vulvovaginitis? How do they present?

Back 419

In order of frequency: Bacterial vaginosis, Vulvovaginal candidiasis, and trichomoniasis.

Bacterial vaginosis: Most common cause in women of child-bearing age usually due to an overgrowth of mixed complex anaerobic flora. Patients present with vaginal discharge as major complaint.

Vulvovaginal Candidiasis: Caused by Candida albicans. Patients will present with pruritus, vaginal soreness, dyspaneuria, external dysuria and white vaginal discharge "cottage cheese".

Trichomoniasis: Caused by Trichomonas vaginalis. Will present with diffuse malodorous yellow-green vaginal discharge with vulvar irriation and vaginal pH of 5-6.

Front 420

How do you diagnose and manage Bacterial Vaginosis?

Back 420

Based on Amsel's criteria of 3 or more of the following: 1) Homogenous, thin, grey-white and malodorous discharge that coats the vaginal walls 2) Presence of "clue" cells on microscopy (gram stain is gold standard) 3) pH of vaginal fluid >4.5 and 4) Positive amine ("Whiff") test (Fishy odor on 10% KOH prep).

Management is to only treat women with symptoms (most women are asymptomatic). Treat with Metronidazole and Clindamycin. Recurrence is very common.

Front 421

How do you diagnose and manage Trichomoniasis?

Back 421

Diagnosis is made by microscopy of vaginal secretions "wet prep", NABT (nucleic acid based testing), and culture (Diamond's media). There is a strong association with HIV transmission.

Management is with Mentronidazole or Tinidazole and to notify, screen, and treat all sex partners.

Front 422

How do you diagnose and manage Vulvovaginal Candidiasis?

Back 422

Diagnosis is made by symptoms of vaginitis but with a normal pH (<4.5), a wet prep of 10% KOH or gram stain showing yeast/pseudohyphae, and a culture showing candida.

Management is OTC anti-fungal (Clotrimazole, etc), oral fluconazole or other antifungals if resistant.

Front 423

What are the common causes of cervicitis? How do they present?

Back 423

Cervicitis can either be endo- or ecto-cervicitis. Endo-cervicitis is due to STIs such as N. gonorrhoeae, C. trachomatis, M. genitalium and T. vaginalis. Ecto-cervicitis is typically non-infectious, except due to HIV.

There will be mucopurulent or purulent vaginal discharge. If it is endo-cervicitis, this will emanate from the endocervical canal. Patients will report dysuria, abnormal uterine bleeding, lower abdominal pain or pelvic dyspaneuria. Of note there is no vulvar discomfort or dyspaneuria.

Cervicitis due to T. vaginalis will present as a "strawberry cervix"

Front 424

How do you diagnose and manage cervicitis?

Back 424

Diagnose by examining the cervix and gram staining the discharge, NABT/NAAT, culture (N. gonorrhoeae - Thayer Martin, T. vaginalis - Diamond's), and "wet prep" for T. vaginalis.

Management is Azithromycin or Doxycycline for chlamydia (add ceftriaxone if Gonorrhea) and metrondiazole if T. vaginalis.

Front 425

What potential complications can result from cervicitis?

Back 425

Pelvic Inflammatory disease including endometritis, salpingitis, tubo-ovarian abscess and pelvic peritonitis.

Front 426

What patients are at increased risk of developing PID?

Back 426

Young sexually active women between 15-24 (3x the likelihood), patients attending STD clinics, and patients living in areas with high prevalence of CT/GC (account for up to 40% of cases).

Front 427

How do you diagnose and manage PID?

Back 427

diagnose by having ≥1 of the following: cervical motion tenderness, uterine tenderness, and adnexal tenderness. More specific criteria involves more invasive testing such as endometiral biopsy, transvaginal US and laparoscopy.

Management is empiric treatment for sexually active young women and those at risk for STIs if they have signs and symptoms of PID. Treat with Ceftriaxone + Doxycycline + Metronidazole.

Front 428

What are the complications of PID?

Back 428

Risk of ectopic pregnancy increases 7x after one episode of PID. Risk of infertility increases with each episode (1 = 13%, 2 = 25-35%, ≥3 = 50-75%).

Front 429

What is the clinical presentation of post-partum endometritis?

Back 429

Post-partum endometritis is an infection of the uterus following Cesarean delivery after ROM and is the most common cause of puerperal fever. Patients will present with fever on 1st or 2nd post partum day, lower abdominal pain, uterine tenderness, and peripheral leukocytosis.

The microbial etiology is typically polymicrobial (GBS, enterococcus, G. vaginalis, E. coli, anaerobes, urogenital mycoplasmas). If onset is late (2d-6w) it is C. trachomatis. Hospital outbreaks are due to GAS from HCWs during delivery.

Front 430

How is post-partum endometritis managed?

Back 430

Early onset give clindamycin +gentamicin. Late onset give azithromycin or doxycycline + metronidazole. Continue therapy until afebrile for 24 hrs, pain free, and leukocytosis resolves.

Front 431

If post-partum endrometritis does not respond to antibiotics, what should be suspected?

Back 431

septic pelvic vein thrombosis

Front 432

How is must HIV be treated?

Back 432

HIV must be treated with combination therapy for life. Most HIV regimens contain 2 NRTIs with Truvada most commonly used.

Front 433

What is the side effects of older NRTIs?

Back 433

Older NRTIs such as didanosine, zalcitabine, and stavudine can cause peripheral neuropathy, pancreatitis, lactic acidosis and lipoatrophy. Older protease inhibitors also are associated with lipdystrophy.

Front 434

What is the mechanism of action for NRTIs and NNRTIs?

Back 434

NRTI/NtRTIs: These are structural analogs of deoxynucleotides that lack 3'-hydroxyl group and the necessary bond group needed to extend the chain. These are incorporated into growing chain and halt synthesis. Are competitive substrated inhibitors.

NNRTI: Block RT by binding at different site on enzyme and is not incorporated into viral DNA. It is a non-competitive inhibitor. These are not effective against HIV-2 (Most of HIV in US is HIV-1).

Front 435

What should be tested for prior to using abacavir?

Back 435

HLA-B57. A positive test indicates strong likelihood of hypersensitivity reaction to abacavir.

Front 436

A HIV patient has a CrCl of 40 and is taking tenofovir. How should this patient be managed? What side effects is this patient at risk for being that he is taking tenofovir?

Back 436

Tenofovir should be dose reduced in patients with a CrCl <50.

Tenofovir is part of Truvada (other drug is emtricitabine). Side effects include renal and bone toxicities. Fanconi sydrome is a proximal renal disease in which patients don't reabsorb glucose, amino acids, uric acid, phosphate and bicarb and is a side effet of tenofovir.

Front 437

What is considered a complete HIV therapy?

Back 437

a NNRTI + 2 NRTIs. The gold standard is Atripla, which is Efavirenz (NNRTI) + Truvada (Tenofovir + emtricitabine).

Front 438

Which NNRTI drug should not be given in patients with high CD4 counts?

Back 438

Nevirapine. "Healthy" HIV patients get severe liver problems when given this drug.

Nevirapine is also associated with Steven-Johnson syndrome and is the most often used drug for mother to child prevention

Front 439

What side effects are seen with Efavirenz?

Back 439

CNS issues with abnormal dreams being common, taking Efavirenz on an empty stomach decreases absorption (high absorption with fatty meals) and decreases CNS effects. There are also concerns about drug interactions (inducer) and it is teratogenic in first trimester.

Front 440

Which HIV drug should not be taken with protein drinks or be given to patients taking PPIs?

Back 440

Rilpivirine. Protein drinks decrease absorption by 50%. PPIs are contraindicated.

Of note, caution should be taken in giving Rilpivirine to patients with high viral loads and low CD4 counts.

Front 441

How does HIV become resistant to reverse transcripase inhibitors?

Back 441

Not known for sure but involves development of mutations. Mutations can be at or near the drug binding site of RT gene. The important aspect is that a mutation to one RTI can confer resistance to others of the same class.

Front 442

What is the MOA of protease inhibitors?

Back 442

They bind directly to the active site of protease causing the enzyme to lock and prevent cleavage of natural substrate. Drug resistance is conferred by a mutation that reduces the binding affinity of the drug. Drug resistance is hard to develop as it is a multi-step process and this is why protease inhibitors are credited with HIV being a chronic disease rather than a fatal one.

Front 443

What are the most commonly used protease inhibitors?

Back 443

atazanavir and darunavir and both are part of "recommended" regimens with Truvada for initial therapy.

Atazanavir: caution with PPI use, can be used in pregnancy, must be taken with food. Can cause hyperbilirubinemia

Darunavir: requires boosting, is a sulfa drug.

Front 444

What is the only co-formulated PI with boosting agent?

Back 444

Lopinavir/ritonavir. Ritonavir is the boosting agent used for most PIs and causes many drug interactions.

Front 445

What is unique about tipranavir?

Back 445

It acts as a CYP3A inducer and induces its own metabolism. Requires a large amount of ritonavir for boosting.

Front 446

What is the MOA of HIV entry inhibitors?

Back 446

There are two drugs in this class, Enfuvirtide and Maraviroc.

Enfuvirtide: Targets gp41 to block fusion. Most patients will develop an injection site reaction.

Maraviroc: targets the CCR5 co-receptor protein. Not useful against CXCR4 co-receptor. Must know the HIV tropism (whether CCR5 or CXCR4 HIV).

Front 447

What is the MOA of integrase inhibitors?

Back 447

Integrase inhibitors block the HIV DNA from integrating into the host DNA. There are three drugs: Raltegravir, Doutegravir, and Elvitegravir

Front 448

What are the pros and cons of the integrase inhibitors?

Back 448

Raltegravir - Pro: no drug interactions. Con: BID dosing.

Dolutegravir - Pro: no drug interactions, Qday dosing for naive patients, useful for raltegravir resistant virus

Elvitegravit - Pro: available in a single tablet complete regimen. Con: requires boosting.

Front 449

How is HIV transmitted perinatally?

Back 449

20% of cases are due to intrauterine infection and 80% are due to peripartum causes such as onset of placental separation, mother-to-fetus microtransfusions, and labor/ROM.

Front 450

What are the risk factors for MTCT transmission of HIV?

Back 450

Maternal factors: serum/genital viral load, AIDS diagnosis/CD4 count, Co-infection with HSV/TB/syphilis, substance abuse

Peripartum factors: prolonged ROM, placental abruption, preterm, chorioamnionitis, mastitis during breastfeeding

Infant factors: duration of breastfeeding, use of anti-retrovirals.

Front 451

What was learned through the various MTCT HIV trials?

Back 451

Front 452

What are some public health strategies for decreasing HIV MTCT?

Back 452

Increased aces to ART for HIV infected mothers,

HIV testing in 1st and 3rd trimesters, Access to contraception, breastfeeding with ART therapy or replacement feeding with safe water supplies, and better access to healthcare.

Front 453

Why must infants born to HIV mothers be tested multiple times to see if they are infected?

Back 453

Maternal antibodies to HIV can cross the placenta and infants will initially be tested positive. Repeat testing is necessary to determine HIV status.

Front 454

What are the health disparities associated with HIV?

Back 454

HIV rates in impoverished areas in the US are similar to those in sub-Saharan Africa, prevalence of HIV infection increases as annual income decreases and is higher in those with less education, recently homeless, who live below the poverty threshold and who are disabled.

The highest HIV prevalence is in Af. Am. women.

Front 455

What is selective IgA Deficiency? How do patients with sIgAD present?

Back 455

sIgAD is the most common primary immunodeficiency disorder (1:600). It is defined as having IgA levels < 7 mg/dL with normal IgG, IgM and presence of B cells. IgA levels between 7-19 is considered partial sIgAD.

The majority of patients with sIgAD do not have increased rate of infections. Those that do develop recurrent upper/lower respiratory tract infections and giardia (IgA is concentrated in linin of respiratory and GI tracts).

Front 456

sIgAD patients are at increased risk for what diseases?

Back 456

They are at increased risk for autoimmune disease (common) and malignancy.

Autoimmune: RA,SLE, ITP, HSP, Addison's, DM1, IBD, etc.

Malignancy: adenocarcinoma, Hodgkin's lymphoma, ALL, etc

Front 457

What is the treatment for sIgAD?

Back 457

In those with recurrent infections, prophylactic antibiotics is helpful. IgG replacement is not indiciated as their levels are normal.

sIgAD patients are at risk of anaphylaxis when given blood transufions as they make IgE anti-IgA antibodies. To reduce risk, RBCs should be washed.

Front 458

What is Common Variable Immunodeficiency (CVID)? What infections are these patients at risk for?

Back 458

It is an immune disorder characterized by low immunoglobulin levels (IgG and typically IgA/IgM also). This results in poor specific Ab response with increased infection rate. CVID usually presents in adolescence/adulthood and is uncommon under 2 years old. Only a minority of patients have a genetic mutation (TACI, ICOS, BAFF, APRIL).

Patients present with infections commonly involving the sino-pulmonary tract, blood, GI tract (giardia), and other systems.

Front 459

What diseases are CVID patients at risk for?

Back 459

Autoimmunity: cytopenias, IBD, diabetes

Non-caseating granulomatous disease: GLILD - can mimic sarcoidosis

Lymphoreticular disorders: splenomegaly, adenopathy, lymphoma, Good's syndrome (CVID with thymoma)

Front 460

What is the treatment for CVID?

Back 460

Lifelong IVIG or SCIG as they are deficient in IgG.

Front 461

In which patients should a Complement deficiency be suspected? How should they be tested?

Back 461

Complement deficiencies are rare and lead to increased susceptibility to infection.

Patients with recurrent disseminated pyogenic infections (S. pneumoniae, H. influenzae) should be tested for C3 deficiency as opsonization (C3b) is critical for controlling encapsulated bacteria.

Patients with recurrent neisserial infections should be tested for C5-C9 deficiency (screening is recommended with meningococcal sepsis/meningitis).

Screening is done through the CH50 lab test

Front 462

What is Job syndrome (Hyper IgE)/STAT 3 Deficiency? How do patients present?

Back 462

There is a mutation of STAT3 that results in a syndrome characterized by recurrent skin and lung bacterial infections, mucocutaneous candidiasis, eczema and numerous connective tissue abnormalities.

Patients will have recurrent staph abscesses of skin/lung/joints, pneumatoceles, pruritis dermatitis, elevated IgE, eosinophilia, coarse facial feature, recurrent fractures and failure of permanent teeth to erupt.

Front 463

What is the treatment for Job syndrome/STAT 3 deficiency?

Back 463

Lifelong anti-staph antibotics, lobectomy for persistent pneumatoceles, and IVIG/SCIG.

Front 464

How do patients with IL-12/IFN-gamma axis defects present? How should they be treated?

Back 464

Defects in IL-12/IFN-gamma results in increased susceptibility to mycobacterial and salmonella infections. Treatment is lifelong mycobacterial prophylaxis with macrolides.

Front 465

What is Bruton's X-linked Agammaglobulinemia (XLA)? How do patients present and what is the treatment?

Back 465

This is a X-linked mutation in Bruton's Tyrosine Kinase (BTK) that results in a lack of B cell production. This increases susceptibility to bacterial infections.

Patients will get pneumonias, recurrent sinusitis/otitis media, bacteremia/sepsis, septic joints, bronchiectasis, enterovirus meningoencephalitis, etc.

Patients are put on IVIG/SCIG and prophylatic antibiotics.

Front 466

How does selective IgG deficiency differ from CVID? When does sIgGD occur?

Back 466

They both have deficient IgG levels but IgA/IgM are normal with normal specific Ab responses in selective IgG deficiency. Also, IgG replacement is rarely indicated in selective IgG deficiency.

Selective IgG deficiency can occur in a number of situations: Transient Hypogammaglobulinemia of Infancy (there is a delay of adequate levels of IgG during infancy), Protein losing enteropathy (there is a loss of protein, including IgG, in the stool), and medication effects (steroids suppress immune system).

Front 467

What is the pathogenesis of Chronic Granulomatous Disease?

Back 467

CGD is a X-linked recessive (severe)/autosomal recessive defect in NADPH oxidase resulting in neutrophils to be unable to make ROS/peroxide which are important for the respiratory burst and microbe killing. Patients with CGD are unable to kill catalase positive organisms because those organisms break down ROS that they make so there is no ROS for the neutrophil to use. CGD patients can still fight off catalase negative species as they produce ROS which the neutrophil can use to kill the bacteria.

Front 468

Which organisms are CGD patients at risk for getting?

Back 468

Catalase positive organisms: S. aureus, Burkholderia cepacia, Serratia marcescens, Norcardia spp., Aspergillus spp.

Front 469

In children that present with a Staph liver abscess, which disease should screened for?

Back 469

Chronic Granulomatous Disease. Staph liver abscess in a child/young adult is almost pathognomonic.

Patients can also get recurrent lymphadenitis, pulmonary abscess (norcardia), fungal pneumonia (aspergillus) and recurrent osteomyelitis (S. aureus).

Front 470

What treatment should CGD patients receive?

Back 470

Prophylactic TMX/SMX and itraconazole, IFN-gamama injections, and consider BMT

Front 471

What is the pathogenesis of leukocyte adhesion deficiency (LAD) and how do these patients present? What is the treatment?

Back 471

LAD patients have a mutation of CD18 which normally interacts with ICAMs to allow neutrophils to move from the bloodstream to tissues.

Patients will present with persistent leukocytosis, inability to form pus (necrotic abscess), impaired wound healing, recurrent skin infections, severe periodontal disease and delayed umbilical cord separation with omphalitis.

Treatment is antibiotics and BMT.

Front 472

What is Severe Combined Immune Deficiency (SCID)?

Back 472

SCID is a rare genetic syndrome resulting in a severe deficiency of lympocytes (T and B cell, +/- NK cells). It is usually diagnosed at birth and is a pediatric emergency. Patients have extreme susceptibility during there first 6 months of life and is fatal before age 1 without BMT.

Front 473

How do undiagnosed SCID patients present? What is the treatment?

Back 473

Infants will fail to thrive, wil get oral candidiasis, prolonged infections (bronchiolitis, otitis media), diarrhea, PCP, severe varicella, mycobacterial infection fro BCG vaccine. Infections will often be unresponsive to therapy.

Treatment involves isolation (bubble boy), IVIG/SCIG, TMP/SMX prophylaxis, blood products that are CMV negative/irradiated/leuko-reduced. BMT for cure.

Patients should not get live vaccines as it could be fatal.

Front 474

What is DiGeorge/22q11 Deletion Syndrome?

Back 474

This is a congenital immunodeficiency due to a deletion at 22q11. The severity depends on the size of the deletion. It affects the development of the thymus gland, which is responsible for T cell development.

Patients will classically have unusual faces, with small, low-set ears, bulbous nose and small mouth.

Front 475

What embryotic pounch is affected in DiGeorge's syndrome?

Back 475

The 3rd and 4th pouch are affected as they give rise to the Thymus.

The 3rd pouch also gives rise to the parathyroid glands and hypocalcemia is a common symptom due to less PTH.

The 4th pouch also gives rise to the aortic arch which can give rise to congenital heart disease (seen in 75% of patients) such as interrupted aortic arch type B, pulmonary atresia, aberrant subclavian, and Tetralogy of Fallot.

Front 476

How should patients with complete DiGeorge's syndrome be treated?

Back 476

Less than 1% of DiGeorge patients have complete DiGeorge, meaning thymic aplasia. In this case patients should be put on PCP prophylaxis (TMP/SMX), IgG replacement, reverse isolation, and thymic transplant.

Front 477

What is Wiscott-Aldrich Syndrome (WAS)?

Back 477

WAS is a triad of Eczema, Thrombocytopenia and Recurrent Infections.

It is a X-linked defect in Wiscott-Aldrich Syndrome Protein that affects cell signaling and actin filament assembly.

The most common cause of death is EBV-induces lymphoma.

Treatment is BMT

Front 478

What is Chediak-Higashi Syndrome?

Back 478

A rare autosomal recessive disorder in the lysosomal trafficking regulator protein LYST. This impairs transport into lysosomes which ultimately affects destruction of intracellular bacteria. Patients get frequent/recurrent pyogenic infections and periodontal disease.

Patients will also have oculocutaneous albinism (hypopigmentation of skin, eyes and hair) and progressive neuropathy (CN palsy, seizures, etc).

Front 479

What is Ataxia Telangiectasia?

Back 479

AT is a autosomal recessive syndrome of the ATM gene that codes for a protein that recognizes damaged dsDNA breaks. Thus patients have an increased sensitivity to radiation.

Patients present with recurrent upper/lower respiratory tract infections, decreased IgA, lymphopenia, variable IgG deficiency, and telangiectasias of the eye and face.

Patients are at risk for progressive neurodegenerative disease, lymphoreticular malignancies and progeria (premature aging).

Front 480

Describe how specific non-transplant related immune deficits predispose to specific types of infections.

Back 480

Patients with Chronic lymphocytic leukemia (CLL) and Multiple myeloma both produce monoclonal lymphocytes that results in hypogammaglobulinemia. This defect increases the chance of bacterial, encapsulated organisms.

In patients with acute leukemia, they tend to be neutropenic and predisposes them to severe gram-negative infections and candida/fungal infections.

Lymphoma patients have T cell dysfunction which results in fungal/viral infections.

Front 481

Describe the most common sources through which non-transplant related immunosuppressed individuals acquire infections.

Back 481

Most cytotoxic chemotherapy causes neutropenia (<500 cells/mm^3). This is commonly seen in induction therapy for acute leukemia. There is low risk for this in solid tumors.

Front 482

Describe the role of anti-bacterial, anti-viral and anti-fungal prophylaxis in cancer patients.

Back 482

Antibacterial: Need to cover for Pseudomonas aeruginosa (FQs)

Antiviral: HSV 1/2 and VZV reactivation is common (Acyclovir/Valacyclovir)

Antifungal: Candida is more common than molds. Fluconazole for Candida and Posaconazole/Voriconazole for molds.

PCP: give TMP/SMX prophylaxis for patients on high dose steroids/ALL induction.

Front 483

Define febrile neutropenia and compare/contrast low risk and high risk febrile neutropenic patients

Back 483

febrile neutropenia is neutropenia plus a single temperature ≥ 38.3C or temp ≥38C for ≥1 hr or temp ≥ 38 twice in a 12hr period.

High risk febrile neutropenia patients will have a MASCC score < 21. Patients are at higher risk if they are going to neutropenic for longer and have co-morbid problems like hemodynamic instability, mucositis, mental status changes, infection, etc.

Front 484

Describe the role of empiric antimicrobial therapy in the setting of febrile neutropenia.

Back 484

Initial regimen should cover gram negative organisms including Pseudomonas and oral flora. Monotherapy can include piperacillin/tazobactam, cefepime, ceftazidime. If penicillin allergy: vancomycin + astreonam.

Additional gram positive coverage (vancomycin, linezolid or daptomycin) should be added if patient becomes unstable/septic, gets pneumonia, severe mucositis, if there is an infection due to a catheter or skin infection.

Front 485

Describe how hematopoietic cell transplant related immune deficits predispose to certain types of infections.

Back 485

Hematopoietic Stem Cell Transplantation carries a significant morbidity and mortality with infection accounting for 20% of deaths. After HSCT, all components of the immune system are dysfunctional. There is damaged epithelial barriers/mucosal surfaces, pancytopenia with severe neutropenia, and there is a risk of GvHD (biggest contributor to infectious morbidity/mortality).

Front 486

Describe the timeline for specific infections after hematopoietic cell transplantation.

Back 486

Pre-engraftment (0-30 days): There is severe neutropenia and break down of mucosal surface which can lead to mucositis. This increases the risk for infection from GI flora or gram + organisms from central lines. HSV reactivation can occur as well as Candida infection.

Early post-engraftment (up to day 100): There is weakened cellular/humoral immunity with the possibility of GvHD. Opportunistic infections are most likely. Aspergillus, Candida, Pneumocystis, CMV reactivation and EBV can be seen

Late infections (after 1 yr): B and T cells are beginning to recover and patients are most at risk for opportunistic/community acquired bacteria. Can get Aspergillus, PCP, VZV, CMV, EBV, and encapsulated bacteria.

Front 487

Describe the role of anti-bacterial/viral/fungal prophylaxis in hematopoietic cell transplant patients.

Back 487

Front 488

Describe how solid organ transplant related immune deficits predispose to certain types of infections.

Back 488

Solid organ transplant patients are required to be immunosuppressed for life to prevent rejection. They are typically on calcineurin inhibitors (tacrolimus), antimetabolite agents (Mycophenolate), and mTOR inhibitors (Sirolimus) for immunosuppression maintenance. Patients therefore may have low neutrophils, lymphocytes or CD4 count which will predispose the patient to infection.

Front 489

Describe the timeline for specific infections after solid organ transplantation.

Back 489

<4 weeks: patients with infections <4 weeks post transplant typically have a a nosocomial infection (MRSA,VRE, etc) or donor derived (Aspergillus, Pseduomonas)

1-6 months: These patients typically have a reactivation of a latent disease (BK polyomavirus, CMV, HSV, etc) of an opportunistic infection (Cryptococcus, TB, etc).

>6 months: These patients typically have a community acquired infection such as pneumonia or UTI.

Front 490

Describe the role of anti-bacterial/viral/fungal prophylaxis in solid organ transplant patients.

Back 490

Antiviral: Risk for CMV and HSV. Patients at high risk for CMV (seronegative recipient receiving a seropositive donor) is put on valanciclovir for 3-6 months. If patient is not on valganciclovir for CMV, should consider valacyclovir for HSV for 3 months.

Antibacterial: All solid organ transplant recipients should be put on PCP prophylaxis with TMP/SMX. Duration is anywhere from 6 months to life.

Antifungal: Lung transplants are at highest risk of fungal infection and should be put on anti-mold agents (voriconazole) for at least 6 months and up to life. Other transplants are unlikely to need coverage but it depends on patient's risk.

Front 491

How is AIDS defined?

Back 491

Presence/history of an AIDS-defining illness OR CD4 lymphocyte count <200 cells/mm^3 OR CD4 lymphocytes less than 14% of total lymphocytes.

Front 492

A patient with HIV presents with a brain abscess. What is the most likely diagnosis? How should patients be managed for this disease?

Back 492

Most likely Toxoplasma gondii from raw/undercooked meat or cat litter. Primarily causes brain abcesses. Patients can be treated with Pyrimethamine/sulfadiazine and all patients with a CD4<200 should be put on TMP/SMX prophylaxis.

Front 493

An AIDS patient presents with the following brain lesion. It was biopsied and determined to be a lymphoma. What is the causative agent of this lymphoma, particularly in AIDS patients? How should the patient be managed?

Back 493

This is a lymphoma caused by EBV. EBV has the ability to transform B cells into immortalized cells and thus cancer. This patient should be put on chemo + HAART

Front 494

How does an AIDS patient with PML typically present? What is the causative agent and how is it diagnosed?

Back 494

PML patients with have varying degrees of encephalitis (asymptomatic to comatose) and this is caused by reactivation of the JC virus. Diagnosis can be made by MRI by finding demylination of the white matter at multiple locations.

Front 495

If this was seen on fundoscopy in an AIDS patient, what would be the causitive agent? How should would a patient like this be treated? What other diseases can this agent cause in an AIDS patient?

Back 495

This is CMV retinitis showing the "ketchup and mayo" presentation. This patient can be treated with valganciclovir or foscarnet.

Other CMV diseases in AIDS patients include CNS disease (encephalitis/meningitis) or end-organ disease (GI, kidney, lung)

Front 496

A patient with AIDS presents with meningitis and a high opening pressure on spinal tap. What is the most likely etiology? How do you diagnose and treat this patient?

Back 496

This is Cryptococcus neoformans, which is an encapsulated yeast spread by bird droppings. To diagnose, do India Ink stain on CSF to look for lack of staining of the capsule. This patient should be given Amphotericin B and 5FC. Fluconazole can be given for prophylaxis.

Front 497

When should AIDS patients be put on prphylaxis for PCP? What is the typical treatment for PCP?

Back 497

Patients with a CD4 < 200 or a CD4 % <14 should be put on prophylaxis with TMP/SMX.

Typically treatment for PCP is TMP/SMX and prednisone for severe cases.

Front 498

How does Kaposi Sarcoma typically present in AIDS patients?

Back 498

Kaposi Sarcoma is caused by HHV-8 (KSHV) and causes sarcomas of the skin, mouth, GI, and lungs. Diagnosis is made by biopsy and treatment is chemo.

Front 499

Define and describe the term "Fever of Unknown Origin (FUO)".

Back 499

Front 500

What are some common infectious and non-infectious etiologies of FUO?

Back 500

Infectious: unrecognized abscess, Endocarditis (HACEK organisms or other fastidious bugs), TB, Histoplasmosis, Osteomyelitis.

Connective tissue disroders: Adult Still's disease (fever, rash, arthritis), RA, SLE, Temporal Arteritis, polmyalgia rheumatica.

Malignancies: Lymphoma (most common), Leukemia, metastatic liver tumor, Renal cell carcinoma.

Miscellaneous: Factitious, Drug fever, Familiar fever syndromes, PE (6%), IBD, TTP, Pheochromocytoma.

Front 501

How do you work-up a patient with an infectious or non-infectious FUO?

Back 501

Workup should be directed by patient's symptoms and most likely diagnosis. Get a comprehensive history and verify fevers and establish pattern. Most should get the following: CBC with differential, serum chemistries, LFTs, UA, blood culture (for selected causes based on exposure history), HIV antibiody, CXR. Consider bone marrow biopsy in patients with dissemiated granulomatous disease with abnormal CBC checking for disseminated histoplasmosis.

Physical exam: check temporal artery in elderly, sinus tenderness, listen for murmur, look for endocarditis stigmata, lymphadenopathy, thryomegaly, HSM, perirectal abscess in neutropenia, DVT, and check skin/mucous membranes/teeth.

Imaging can help make the diagnosis with CT for abscesses, Venous duplex imaging for DVT and PET for malignancy.

Front 502

What is the pathogenesis of Measles/rubeola?

Back 502

Measles is caused by the rubeola virus (Paramyxoviridae family) which is a helical, enveloped, negative sense ssRNA. Measles is transmitted by aerosolized particles from infectious persons (most infectious during prodromal period - 4th day after rash). Measles is highly contagious and 100% of susceptible people will get it. During the 8-10 day incubation period, measles virus replicates and lyses respiratory epithelial cells, leading to infection and lysis of reticuloendothelial cells and viremia.

Front 503

What are the clinical manifestations of Measles/rubeola?

Back 503

After the 8-10 day incubation period there is a prodromal phase of fever, cough, conjuctivitits and coryza. 2-3 days later there will be Koplik spots (grayish-white lesions on an erythematous base) on the buccal mucosa, which are pathognomonic for Measles. The next day the maculopapular rash develops, starting from the face and spreads to the trunk and extremities. The rash is typically more confluent on the face, neck and upper chest. The rash resolves and fades from the head down 2-3 days later.

Front 504

What are the lab findings and how do you treat Measles/rubeola?

Back 504

Lab studies will show leukopenia/lymphopenia. Can test for IgG antibodies or do PCR.

There is no specific treatment available. In malnourished patients, then vitamin A is recommended. Ribavirin can be used in immunocompromised patients.

Front 505

What are the complications of Measles/rubeola?

Back 505

The most common complication is otitis media (7-9%). Respiratory complications can also occur (bronchiolitis, bronchitis, pneumonia, reactivated TB). The most life threatening complication is subacute sclerosing panenchepahlitis which is fatal and occurs a few years after illness.

Front 506

What is the pathogenesis of Rubella?

Back 506

Rubella (Togavirus family) is a icosohedral, enveloped, positive ssRNA virus. It is transmitted by aerosolized particles from infectious patients (5 days before - 6 days after rash). It is more common in late winter and spring.

Front 507

What are the clinical manifestations of Rubella?

Back 507

There is a prodromal period 1-5 days before rash that includes fever, eye pain, arthralgia, sore throat and GI complaints. There may also be posterior auricular lymphadenopathy. The maculopapular rash is similar to Measles as it starts on the face and spreads to the rest of the body. The rash lasts for 3 days and is why Rubella is called "3-day measles".

Front 508

What are the lab finding and how do you treat rubella?

Back 508

Lab studies show leukopenia. Can look for IgG in a culture from nose/throat/urine.

Treatment is supportive.

Front 509

What is the pathogenesis of Parvovirus B 19?

Back 509

Parvovirus B19 is a icosohedral, nonenveloped, linear ssDNA that replicates in erythrocyte precursors. Virus-induced cytotoxicity causes reticulocytopenia due to lack of RBC production in BM. Infection is most common during spring. It can be transmitted via respiratory droplets, blood transfusion, and mother-to-fetus.

Front 510

What are the clinical manifestations of Parvovirus B19?

Back 510

Patients can get erythema infectiousum (Also called Fifth disease: low grade fever, slapped cheeks, lacy rash on extremities), seronegative arthritis in adults that resolves on own (especially women), transient aplastic crisis in sickle cell patients, persistent anemia in immunocompromised and hydrops fetalis in fetus due to fetal anemia.

Front 511

What are some complications of a pregnant women getting Parvovirus B19?

Back 511

Abortion in the first 20 weeks or hydrops fetalis.

Front 512

What are live attenuated vaccines?

Back 512

They are derived from the wild strain of the pathogen. They are capable of infecting host cells, but they are less virulent than the normal wild strain. They are the most effective at developing protective immunity. They induce the same immune mechanism as natural infection and thus provide B and T cell memory.

Front 513

What are inactivated vaccines?

Back 513

Pathogens in the vaccine are inactivated or killed by heat/chemicals. Thus they cannot infect host cells or replicate (no replication means not as many pathogens and less immune response). This means that CD8 T cells are not generated effectively and immunity is primarily mediated by antibodies. Booster immunizations are required to maintain immunity.

Front 514

On the cellular level, what does booster immunizations do?

Back 514

Booster immunizations allow for re-exposure of the B cell to the killed virus. This allows B cells to undergo somatic hypermutation of the B cell receptor which can allow for higher affinity antibodies. This process is called affinity maturation. In addition, it helps establish a memory B cell population and enhance the magnitude of the Ig antibody response.

Front 515

What are subunit vaccines?

Back 515

These are vaccines that contain a single component from a pathogen, like in the Hep B vaccine that contains HBsAg or inactive toxins for diphtheria and tetanus. Protetive immunity is mediated by antibody production as Cellular immunity requires cell infection.

The advantages of subunit vaccines are: No risk of infection, immune response is directed against the antigen most relevant in clearing the pathogen, and large amounts of the vaccine can be produced.

Disadvantage is that some people may not have the MHC II molecule that effectively binds the peptide in the vaccine.

Front 516

What are conjugate vaccines?

Back 516

They are a type of subunit vaccine that contains two components, one from the pathogen and the second is to enhance the immune response.

Some pathogens, like H. influenza, have polysaccharides that are immunogenic, but just injecting the polysaccharides would not elicit the production of antibodies because only proteins present via MHC II and effector CD4 cells are required to activate B cells. So the polysaccharide are bound to toxins that will activate the B cells that recognize the polysaccharide.

Front 517

What are some new vaccine strategies?

Back 517

Live attenuated vaccines strains generated by recombinant DNA technology (virulence factors are rendered inactive) and DNA vaccines (makes pathogenic proteins and activates both cellular and humoral immunity).

Front 518

What are vaccine adjuvants?

Back 518

Adjuvants are substances used in vaccines to enhance the adaptive immune response. They are important for killed and subunit vaccines as these do no infect cells. The adjuvants activate APCs vial TLRs, promote phagocytosis, and allow longer half-life of vaccine in the skin (depot effect). Alum and MF59 are common adjuvants.

The DTaP vaccine is an example of an adjuvant. This vaccine has diphtheriae and tetanus toxin with a killed whole pertussis bacterium. The pertussis bacterium provides adjuvant effect since the bacterium can engage receptors to activate APCs.

Front 519

How are vaccines being used to treat cancer patients?

Back 519

The idea of using vaccines in cancer patients is to immunize patients with tumor cell lysates to induce or amplify the tumor-specific T and B cells. Tumors are immunoprivileged and directly inoculating the patient with tumor antigens will activate the host's immune response to the tumor cells. This can be achieved by just injecting the antigen or loading the antigen onto patient's dendritic cells.

Front 520

What is passive and active immunization?

Back 520

Passive: Is temporary immunization by administering preform antibodies which allows for immediate protection. This is IVIG. Used in preventing Hep B, tetanus, varicella, rabies, and CMV in transplant patients.

Active: This is basis of vaccines. Administration of immunogens to stimulate protective anitbody response. This provides longer lasting immunity but takes time to be effective (about 2 weeks).

Front 521

What are some contraindications for ALL vacines?

Back 521

An allergy to a vaccine component, a previous anaphylactic event to vaccine, or a patient with moderate or severe acute illness.

Front 522

Which bacteria/viruses are characterized as "high priority agents" in terms of potential use by bioterrorists?

Back 522

Bacillus anthracis, Variola major, Yersinia pestis, Clostridium botulinum toxin, Franciella tularensis, Filoviruses (Ebola/Marbug hemorrhagic fevers) and Arenaviruses (Lassa virus)

Front 523

What features make an infectious agent "high priority"?

Back 523

A "high priority" infectious agent will have high disease/infectivity ratio with high mortality, A long shelf-life that maintains viability and infectivity, can be delivered via aerosol and person-to-person, and one that requires a vaccine for the attacker.

Front 524

What are the three clinical presentations of anthrax?

Back 524

Inhalational Antrhax: Most deadly form with abrupt onset of respiratory distress, shock and death within 1-2 days. Will see mediastinal widening on CXR (get CT to confirm).

Cutaneous Anthrax: Associated with sheep's wool. Starts as painless papule with surrounding edema. Then turns into a vesicle and finally an eschar which is necrotic.

Gastrointestinal Anthrax: This is a consequence of eating contaminated meat is never seen in US. Symptoms of nausea, vomiting, fever, bloody diarrhea and hematemesis. Progresses to sepsis and almost universally fatal.

Front 525

What are the key components of the smallpox rash?

Back 525

Maculopapular rash that starts in the oropharynx/face/extremities and spreads to the trunk. Lesions are in the same stage of development. There will be a central umbillication of the lesions. Patients are not infectious until they have the lesions in their mouth.

Patients with smallpox will have a prodrome, in contrast to VZV which has no prodrome.

Front 526

What antibiotics have activity against B. anthracis and Y. pestis?

Back 526

Ciprofloxacin or Doxycycline.

Front 527

How can you limit person-to-person spread of smallpox and the plague?

Back 527

Isolate patient and contacts. Smallpox contacts and HCW should be vaccinated. Use proper PPE (Y. petis: Droplet isolation with a regular surgical mask, B. anthracis: Airborne and Contact so use gowns, gloves, N-95 mask, negative airflow and dedicated equipment/clothing/bed linens etc.).