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USMLE Step 2 (Fach) / Infectious disease (Lektion)

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• Adverse effects of drug regiments for Pneumocystis pneumonia Preferred regimen:  Trimethoprim-sulfamethoxazole (IV for acutely ill, oral for non-acutely ill patients)- Rash, neutropenia, hyperkalemia, elevated transaminases- Indications for corticosteroid use include PaO2 ≤ 70 mmHg or an A-a gradient ≥ 35 mmHg on room air. Pentamidine (IV)- Nephrotoxicity, hypotension, hypoglycemia, cardiac arrhythmias, pancreatitis, elevated transaminases Atovaquone (oral)- Gastrointestinal distress, rash Trimethoprim + dapsone (oral)- Dapsone: Hemolytic anemia (check for G6PD deficiency) Clindamycin (IV or oral) + primaquine (oral)- Primaquine: Methemoglobinemia, hemolytic anemia (check for G6PD deficiency)
• Splenic abscess Risk factors:- Infection (eg, infective endocarditis) with hematogenous spread- Hemoglobinopathy (eg, sickle cell disease)- Immunosuppression (eg, HIV)- IV drug use- Trauma Clinical features:- Classic triad of fever, leukocytosis & left upper-quadrant abdominal pain- Left-sided pleuritic chest pain with left pleural effusion commonly seen- Possible splenomegaly- Most commonly due to Staphylococcus, Streptococcus & Salmonella- Usually diagnosed by abdominal CT scan Treatment:- Combination of broad-spectrum antibiotics & splenectomy- Possible percutaneous drainage in poor surgical candidates
• Leprosy Epidemiology:- Mycobacterium leprae- Primarily developing world (eg, Asia, Africa, South America)- Respiratory droplets/nine-banded armadillo- Low infectivity Clinical features:- Macular, anesthetic skin lesions with raised borders- Nodular, painful nearby nerves with loss of sensory/motor function Diagnosis:- Full-thickness biopsy of skin lesion (active edge)- M leprae is not culturable Treatment:- Dapsone + rifampin- Add clofazimine if severe ("multibacillary")
• Shigella gastroenteritis Transmission:- Fecal-oral- Food or waterborne Clinical presentation:- Rapid-onset, high fever- Abdominal pain, watery diarrhea with mucos, ± blood- ± Seizures in children Management:- Fluid & electrolyte replacement- Antibiotics if immunocompromised, bacteremic or severely ill (fluoroquinolones or 3rd generation cephalosporin)
• Prophylaxis criteria for Lyme disease (must meet all 5) - Attached tick is an adult or nymphal Ixodes scapularis (deer tick)- Tick attached for ≥ 36 hours or engorged- Prophylaxis started within 72 hours of tick removal- Local Borrelia burgdorferi infection rate ≥ 20% (eg, New England area)- No contraindications to doxycycline (eg, age < 8, pregnant, or lactating)
• Malaria prophylaxis Mosquito bite prevention:- Mosquito nets- Protective clothing (covering most of the skin, light colors)- Repellant, such as DEET Malaria prophylaxis:- Should be initiated before going to regions with a high-risk of malaria, e.g., tropical Africa, Asia, Latin America- Areas with P falciparum→ If chloroquine-resistant: atovaquone-proguanil, doxycycline, mefloquine→ If chloroquine-sensitive: chloroquine- Areas without P falciparum: primaquine- Agents that are safe during pregnancy: chloroquine, atovaquone-proguanil, mefloquine Standby emergency treatment:- Atovaquone-proguanil- Artemether-lumafantrine
• Babesiosis Epidemiology:- Babesia microti- Ixodes scapularis tick bite (Lyme disease & HGA)- Northeastern United States Clinical features:- Fever, fatigue, myalgias, headache (flu-like symptoms)- If severe: ARDS, CHF, DIC, splenic rupture- Hemolytic anemia with dark urine and icterus: anemia, thrombocytopenia, ↑ bilirubin/LDH/LFTs- Mild splenomegaly and hepatomegaly Diagnosis:- Thin blood smear – intraerythrocytic rings ("Maltese cross") Treatment:- Atovaquone + azithromycin- Quinine + clindamycin (if severe)
• Diphtheria-tetanus-acellular pertussis immunization Components:- Diphtheria toxoid- Tetanus toxoid- Conjugated pertussis antigen (pertactin) Schedule: 5 doses given at ages:- 2, 4 & 6 months- 15-18 months- 4-6 years Contraindications:- Encephalopathy after previous dose- Anaphylaxis to vaccine component
• Chronic osteomyelitis Mechanisms:- Hematogenous seeding- Extension from infection in adjacent structure- Direct inoculation (eg, compound fracture, bite wound) Pathogens:- Staphylococcus aureus (most common)- Coagulase-negative staphylococci- Polymicrobial Risk factures:- Surgical hardware/instrumentation- Diabetes- Impaired circulation or sensation in the limb Clinical features:- Persistent pain, swelling, chronic wound- Sinus tract formation- Nonunion of fracture Diagnosis:- Positive probe-to-bone test- Imaging: lytic lesion with loss of cortical & trabecular bone, surrounding sclerosis, periosteal thickening- Bone biopsy for culture Management:- Surgical debridement- Antibiotics (prolonged course)
• Recommended vaccines for adults Td/Tdap: Tdap once as a substitute for Td booster, then Td every 10 years Influenza: Annually Pneumococcus: Age 19-64- PPSV23 alone→ Chronic heart, lung, or liver disease→ Diabetes, current smokers, alcoholics- Sequential PCV13 + PPSV23 (very high risk patients)→ CSF leaks, cochlear implants→ Sickle cell disease, asplenia→ Immunocompromised (eg, HIV, malignancy)→ Chronic kidney disease Pneumococcus: Age ≥ 65- Sequential PCV13 + PPSV23→ 1 dose of PCV13 followed by PPSV23 at a later time PCV13 = 13-valent pneumococcal conjugate vaccinePPSV23 = 23-valent pneumococcal polysaccharide vaccine
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• Nocardiosis Etiology:- Nocardia species: ubiquitous in soil worldwide- Aerobic, gram-positive rod, partially acid fast- Transmission: inhalation- Risk factors: immunocompromise, advanced age Pulmonary nocardiosis:- Fever, weight loss, anorexia, weight loss- Productive cough, dyspnea, pleuritic chest painMay be mistaken with tuberculosis! Disseminated nocardiosis:- Cuteanous- CNS features (~ 45%): headache, lethargy, confusions, seizures Diagnostics:- Culture: Gram-positive aerobic bacilli, weakly acid-fast, branching filamentous rods- Chest x-ray or CT: pulmonary nodules (with or without cavitation), pulmonary infiltrates (reticulonodular pattern), abscess, empyema- Cranial CT or MRI: brain abscesses Treatment:- Trimethoprim-sulfamethoxazole for at least 6 months- Surgical drainage of abscesses
• Parvovirus B19 infection Clinical features:- Most patients are asymptomatic or have flulike symptoms- Erythema infectiosum (fifth disease): Fever, nausea & "slapped cheek" rash (more common in children)- Acute, symmetric arthralgia/arthritis: Hands, wrists, knees & feet (resembles RA)- Transient pure red cell aplasia; aplastic crisis in patients with underlying hematologic disease (eg, sickle cell) Diagnosis:- B19 IgM antibodies in immunocompetent patients- NAAT for B19 DNA in immunocompromised patients- Reactivation of previous infection: NAAT for B19 DNA
• PPD induration Patients to treat: ≥ 5 mm:- HIV positive patients- Recent contacts of known TB case- Nodular or fibrotic changes on chest x-ray consistent with previously healed TB- Organ transplant recipients & other immunosuppressed patients ≥ 10 mm:- Recent immigrants (< 5 years) from TB-endemic areas- Injection drug users- Residents & employees of high-risk settings (eg, prisons, nursing homes, hospitals, homeless shelters)- Mycobacteriology laboratory personnel- Higher risk for TB reactivation (eg, diabetes, leukemia, end-stage renal disease, chronic malabsorption syndromes)- Children age < 4, or those exposed to adults in high-risk categories ≥ 15 mm:- All of the above plus healthy individuals
• Rabies Pathogenesis: Transmission of rabies virus by bite from infected mammal Reservoir:- United States: bats (most common), raccoons, skunks, foxes- Developing world: dogs Clinical features:- Hydrophobia- Aerophobia- Pharyngeal spasm, spastic paralysis- Agitation- Ascending flaccid paralysis Postexposure prophylaxis: Rabies IG & rabies vaccine immediately after exposure to high-risk wild animal
• Rotavirus vaccine Live vaccine that is given orally. The first dose is given at 2 months, second dose at 4 months, and third dose at 6 months (if needed). Contraindications:- Previous intussusception
• AIDS-defining conditions Variable CD4:- HIV wasting syndrome- Karposi sarcoma- Cervical cancer (invasive)- Lymphoma (Hodgkin) CD4 < 400/mm3:- Reactivation tuberculosis CD4 < 250/mm3:- Coccidioidomycosis CD4 < 200/mm3:- Cryptosporidiosis- HIV-related encephalopathy (AIDS dementia)- Progressive multifocal leukoencephalopathy (PML)- Pneumocystis pneumonia CD4 < 150/mm3:- Histoplasmosis CD4 < 100/mm3:- Cerebral toxoplasmosis- Cryptococcosis- Candidiasis- HSV infections CD4 < 50/mm3:- CMV infections- Tuberculosis-like disease
• Progressive multifocal leukoencephalopathy (PML) Etiology:- HIV infection: Usually if CD4 < 200 cells/μL- Hematologic and solid cancers- Inflammatory diseases- Patients treated with immunosuppressants/-modulators (natalizumab, rituximab) Pathophysiology: past subclinical infection with JC virus (most adults are infected)→ event (e.g., immunosuppression) triggers reactivation → infects oligodendrocytes → viral DNA mutation leads to aggressive replication within brain tissue → destruction of infected oligodendrocytes + demyelination Clinical features:- Focal symptoms- Seizures- Impaired vigilance- Cognitive disorders- Behavioral changes Diagnostics:- MRI: disseminated, non-enhancing white matter lesions without mass effect- CSF: detection of JC virus DNA in PCR of cerebrospinal fluid- Brain biopsy and histology : demyelination of axons and intranuclear inclusions Prognosis: high mortality Treatment: supportive therapy and optimization antiretroviral therapy (to improve immune status)
• HIV-associated ocular manifestations HIV retinopathy (CD4 count: variable)- Fundoscopic findings: Small cotton wool spots, microaneurysms, retinal hemorrhages- Tend to self-resolve without progression- Not painful- Vision usually unaffected Herpes simplex keratitis (CD4 count: variable)- Slit-lamp examination: dendritic corneal lesions- Fundoscopic findings are normal- Painful and watery eye(s)- Blurry vision Varicella zoster retinitis (CD4 count: variable)- Fundoscopic findings: retinal necrosis (starting from the periphery)- Painful- Severe loss of vision Toxoplasma retinitis (CD4 count: < 100/μL)- Fundoscopic findings: raised yellow-white cottony lesions (distribution of the lesions not related to vessels)- Painful- Visual impairment Cytomegalovirus retinitis (CD4 count: < 50/μL)- Fundoscopy findings: Hemorrhages (red spots), perivascular white opacities resembling cotton-wool spots (larger than HIV retinopathy!), “pizza pie” appearance: combination of red spots on white opacities, retinal detachment- Not painful- Vision initially unaffected- Vision loss occurs if the retina detaches or the posterior pole (optic nerve or macula) is affected.
• HIV-associated CNS lesions Differential diagnosis of CNS lesions in HIV-positive patients with CD4+ T-cell count < 200/mm3: Cerebral toxoplasmosis- Contrast CT: multiple ring-enhancing lesions predominantly in the basal ganglia- CSF: pleocytosis, elevated protein- Treatment: Pyrimethamine, sulfadiazine, and leucovorin Primary CNS lymphoma (PCNSL)- Contrast CT: solitary ring-enhancing lesion- CSF: EBV positive- Treatment: High dose methotrexate ± whole brain radiotherapy; Oral/IV corticosteroids Cerebral abscess- Contrast CT: focal intraparenchymal lesion with a central hypodense (necrotic) area and peripheral ring enhancement- Biopsy (with CT-guided stereotactic aspiration): best confirmatory test- Treatment: third-generation cephalosporin + metronidazole ± vancomycin Progressive multifocal leukoencephalopathy (PML)- Contrast CT: disseminated, non-enhancing white matter lesions without mass effect HIV-associated encephalopathy (AIDS dementia)- MRI: multiple subcortical hyperintense non-enhancing lesions- Histopathology: giant cells with multiple nuclei (formed through fusion of HIV-infected monocytes)
• Gas gangrene Pathogen: Clostridium perfringens (over 80% of cases): a gram-positive, obligate anaerobic, spore-forming bacilli Path of infection:- Ubiquitous clostridial spores contaminate the wound- Wounds with compromised blood supply create an anaerobic environment → optimal for the proliferation of C. perfringens→ necrosis progresses within 24-36 hours. Such wounds include:→ Deep, penetrating wounds (e.g., knife, gunshot)→ Open fractures→ Septic surgical wounds or procedures (e.g., bowel and biliary tract surgery, septic abortion)  Clinical features:- Excruciating muscle pain- Massive edema with bronze → red-purple → black skin discoloration and overlying bullae- Sweet, foul-smelling, or nonodorous discharge produced by anaerobic metabolic products- Crepitus - Can progress to systemic infection within a few hours- Early signs: fever, tachycardia, altered mental status- Late signs: shock, hemolytic anemia, ARDS, kidney and liver failure, multi-organ failure Diagnostics: - Imaging: radiography, CT, or MRI typically show a characteristic feathering pattern of the soft tissue. - Gram staining: large, gram-positive rods- Surgical exploration Treatment:- Surgical exploration and debridement: If applicable, amputation of the affected extremity may be necessary.- Antibiotic therapy: penicillin plus clindamycin or tetracycline
• Fever + cough – Work-up 1. Everybody gets chest x-ray and SO2 Sputum Production, normal CXR = Bronchitis- Treat: Macrolide or doxycycline Foul Breath, Cavitation CXR = Abscess- Imaging: CT-scan (fungus vs. cancer vs. tuberculosis vs. abscess- Treat: 3rd generation cephalosporin + clindamycin Sputum production, Consolidation on CXR = Pneumonia- Hospital acquired: Pip/taz + vancomycin- Community acquired: Fluoroquinolone or 3rd generation cephalosporin + macrolide Immunocompromised, Hypoxemia, elevated LDH = PCP Myalgias, Arthralgias, body aches = Flu
• Complicated UTI - Male patient- Pregnant women- Children or postmenopausal women- Presence of any significant functional or anatomical abnormalities (e.g., BPH, obstruction, stricture)- History of urological pathologies (e.g., neurogenic bladder, kidney cysts, stones)- History of impaired renal function or renal transplantation- Diabetes mellitus- Immunocompromise (e.g., transplant recipients, HIV/AIDS)- Recent history of any instrumentation (e.g., cystoscopy)- Recent placement of any medical devices (e.g., urinary catheter, nephrostomy tubes, or stents)- Infection with a resistant uropathogen or recent antibiotic use- UTI that spreads beyond the bladder (sepsis, pyelonephritis, prostatitis)
• Urethritis Etiology:- Gonococcal urethritis (GU): Neisseria gonorrhoeae - Nongonococcal urethritis (NGU): Chlamydia trachomatis (Most common), Mycoplasma genitalium, Gram-positive cocci, Trichomonas vaginalis, Gardnerella vaginalis Clinical features:- Dysuria- Burning or itching of the urethral meatus- Urethral discharge: purulent, cloudy, blood-tinged, or clear - Initial hematuria- Systemic findings such as fever, chills, or myalgia are absent in urethritis. Urethritis, especially nongonococcal urethritis, may also be asymptomatic! Diagnostics:- Urine dipstick of first-void urine: pyuria (≥ 5-10 WBC per high power field) or positive leukocyte esterase- Urethral smear: ≥ 2 leukocytes per oil immersion field- Gram stain of urethral swab or discharge: Gram-negative diplococci: GU, otherwise NGU- Nucleic acid amplification testing (NAAT) of first-void urine without prior precleaning of the urethra for N. gonorrhea and C. trachomatis Treatment:- Nongonococcal urethritis: single dose azithromycin or doxycycline PO for seven days- Gonococcal urethritis: single dose of ceftriaxone IM and azithromycin PO- If T. vaginalis infection is suspected: metronidazole- Patients should refrain from sexual activity for 1 week after initiation of therapy.- All sexual partners from the 2 months prior to diagnosis should be notified, evaluated for urethritis, and offered empiric treatment.- Repeat NAAT 3-6 months after completion of therapy.
• Endocarditis Pathogens:- Staphylococcus aureus (45-65%): Most common cause of acute IE for all groups (including IV drug users and patients with prosthetic valves or pacemakers/ICDs)- Viridans streptococci (30%): S. sanguinis, S. mutans, S. mitis: Most common cause of subacute IE, especially in predamaged native valves and in prosthetic valves (≥ 60 days after surgery); Common cause of IE following dental procedures- Staphylococcus epidermidis: Common in patients with prosthetic heart valves (most common cause < 60 days following surgery) or pacemakers/ICDs- Enterococcus faecalis (< 10%): Common cause of IE following nosocomial urinary tract infections (UTIs), gastrointestinal or genitourinary procedures- Streptococcus gallolyticus: associated with colorectal cancer; colonoscopy is indicated- Gram-negative HACEK group: In patients with poor dental hygiene and/or periodontal infection Treatment:- Native valves: IV vancomycin 4 weeks- Prosthetic valve < 60 days: vancomycin + gentamycin + cefepime- Prosthetic valve > 60 days: vancomycin + gentamycin- Subacute baterial endocarditis: gentamycin + ceftriaxone- HACEK: IV ceftriaxone- Indications for surgery: congestive heart failure, uncontrolled infection, systemic embolization, prosthetic valve, fungal endocarditis
• African trypanosomiasis (African sleeping sickness) Pathogen: Trypanosoma bruceiRoute of infection: Tsetse fly Stage I:- Trypanosomal chancre- Intermittent fever- Painless lymph node involvement Stage II:- Headache- Behavioral changes: confusion, apathy, psychosis- Daytime somnolence- Ataxia- Coma Diagnostics:- Anemia, granulocytopenia- Stage I: Lymph node aspirate- Stage II: Lumbar puncture and CSF Treatment: Suramin, melarsoprol
• Bacterial meningitis – Treatment Age 2-50: S pneumoniae, Neisseria meningitidis→ Vancomycin + 3rd generation cephalosporin Age > 50: S pneumoniae, N meningitidis, Listeria→ Vancomycin + 3rd generation cephalosporin + ampicillin Immunocompromised: S pneumoniae, N meningitidis, Listeria, gram-negative rods→ Vancomycin + cefepime + ampicillin Neurosurgery/penetrating skull trauma: Gram-negative rods, MRSA, coagulase-negative staphylococci→ Vancomycin + cefepime 3rd generation cephlosporins: ceftriaxone or cefotaximeAlternatives to cefepime: ceftazidime or meropenemAlternative to ampicillin: TMP-SMZ for Listeria
• Adults at high risk for influenza complications - Age > 65 - Women who are pregnant & up to 2 weeks postpartum - Underlying chronic medical illness (e.g., COPD, cardiovascular, renal, hepatic) - Immunosuppression - Morbid obesity - Native Americans - Nursing home or chronic care facility residents
• Infectious mononucleosis Etiology: EBV Clinical features:- Fever- Tonsillitis/pharyngitis ± exudates- Posterior or diffuse, tender cervical lymphadenopathy that may become generalized- Significant fatigue- ± Hepatosplenomegaly- ± Rash after amoxicillin Diagnostic findings:- Positive heterophile natibody (Monospot) test (25% false-negative rate during 1st week of illness)- Atypical lymphocytosis- Transient hepatitis Treatment:- Avoid sports for ≥ 3 weeks (contact sports for ≥ 4 weeks) due to the risk of splenic rupture Complications:- Acute airway obstruction- Autoimmune hemolytic anemia & thrombocytopenia- Splenic rupture
• Mycoplasma pneumonia Epidemiology:- Respiratory droplets- Close quarters/young (e.g., school, military)- Fall or winter Clinical features:- Indolent headache, malasie, fever, persistent dry cough- Pharyngitis (nonexudative)- Macular/vesicular rash Diagnostics:- Normal leukocyte count- Subclinical hemolytic anemia (cold agglutinins)- Interstitial infiltrate (chest x-ray) Treatment:- Macrolide or respiratory fluoroquinolone
• Pneumocystis pneumonia Pathogen: P. jirovecii (previously P. carinii); ubiquitous fungus Route of transmission: airborne Risk factors:- HIV Infection; CD4 count: usually < 200/μL- Primary immunodeficiency disorders (e.g., severe combined immunodeficiency disorder) - Malignancy (e.g., leukemia, non-Hodgkin lymphoma)- Immunosuppressive treatment (e.g., chronic glucocorticoid therapy)- Malnutrition Clinical features:- Symptoms typically have a gradual onset (days to weeks) - Low-grade fever and malaise- Dyspnea and non-productive cough- Fatigue, weight loss, chills- May progress to fulminant respiratory failure Diagnostics: - Beta-D-glucan level - Confirmatory test: microscopic identification of P. jirovecii in specimenobtained via bronchoalveolar lavage or induced sputum, with methenamine silver staining and immunofluorescence- CXR - If the CXR is inconclusive, a high-resolution CT scan can be obtained.  Treatment:- High‑dose TMP/SMX for up to 3 weeks- Glucocorticoids: add in the case of severe respiratory insufficiency (either PaO2 < 70 mm or arterial‑alveolar oxygen gradient ≥ 35 Hg). 
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• Jarisch-Herxheimer reaction Acute, transient, systemic reaction to bacterial endotoxinsand pyrogens that are released after initiation of antibiotic therapy  Epidemiology: Commonly seen during treatment of infections with spirochetes (Borrelia, Leptospira).  In syphilis, the Jarisch-Herxheimer reaction is most often seen if treatment begins in the early phases of the secondary stage. Clinical features:- Flu-like symptoms: fever, chills, headache, myalgia- Accompanied by tachypnea, hypotension, and tachycardia- Syphilitic exanthema may flare up- Usually self-limiting within 12–24 hours Treatment:- NSAIDs for symptomatic treatment- May consider meptazinol (= Opioid that has been found to decrease the severity of the reaction)
• Rubella Pathogen: Rubella virus, RNA virus of the family Togaviridae Prodromal phase- Incubation period: 2-3 weeks after infection- Duration: 1–5 days- Post-auricular and suboccipital lymphadenopathy and occasionally splenomegaly- Mild and non-specific symptoms such as low-grade fever, mild sore throat, conjunctivitis, headache, aching joints- Forchheimer sign: enanthem of the soft palate Exanthem phase- Duration: lasts 2-3 days- Non-confluent, pink maculopapular rash - Begins at the head, primarily behind the ears → extends to the trunk and extremities sparing palms and soles- Rash may be itchy in adults- Polyarthritis Diagnostics:- CBC: leukocytopenia with relative lymphocytosis and increased plasma cells- Confirmatory test: serology→ Detection of IgM antibodies → ≥ 4-fold increase in IgG titer
• Cysticercosis Pathogen: Taenia solium (pork tapeworm) Mode of transmission: Fecal-oral ingestion of eggs from feces of humans with intestinal taeniasis Clinical features:- Symptoms caused by cysticerci accumulation in subcutaneous tissue, muscles, brain, spinal cord, and eyes → Palpable subcutaneous cysts→ Myalgia→ Neurocysticercosis: increased intracranial pressure, neurological deficits, seizures→ Ocular cysticercosis: eye pain, loss of visual acuity or vision in one eye Diagnostics:- Initial tests: CBC count may show eosinophilia (in only ∼ 45% of patients)- Imaging: MRI/CT showing multiple, small (< 1 cm) cystic ring-enhancing lesions in the brain with a membranous wall + often an invaginated scolex during earlier stages+ calcified cyst remnants in later stages- Lumbar puncture: ↑ protein, ↓ glucose, mononuclear pleocytosis - Confirmatory test: serum enzyme-linked immunotransfer blot (EITB) assay Treatment: Albendazole + corticosteroids
• Rabies – Treatment/Prophylaxis Risk evaluation of animal bites:- Administer PEP→ Bite by a known wild reservoir for rabies (e.g., bats, raccoons, foxes), if the animal is not available for testing or if the test comes back positive→ Bite by a domestic carnivore not available for observation or displaying symptoms of rabies- Observe/test animal and possibly administer PEP→ Attack by an unvaccinated domestic carnivore without symptoms of rabies (e.g., dog) → observe animal for a 10-day period→ Animal remains normal: PEP is not necessary→ Animal starts to display symptoms of rabies → Euthanize and study brain samples of the animal → Administer PEP to patient- PEP is not required:→ Bite by a vaccinated domestic carnivore→ Bite by an indoor domestic herbivore Post-exposure prophylaxis:- Cleaning and debridement, as with all bite wounds- Tetanus shot and antibiotic prophylaxis may be indicated- Nonimmunized patient: postexposure prophylaxis→ Rabies immunoglobulin spread in and around the wound→ PLUS rabies vaccine given IM- Prior immunization→ Even patients who have been vaccinated against rabies should be treated after exposure!→ Rabies vaccine IM→ No immunoglobulin→ Check antibody titers
• Amebiasis Amebiasis is an infectious disease caused by the anaerobic protozoan Entamoeba histolytica. Epidemiology:- Occurence: E. histolytica is very common in tropical and subtropical regions (e.g., Mexico, Southeast Asia, India) and affects more than 50 million people worldwide. Amebic infection is relatively rare in the US. - Men and especially immunocompromised individuals have a higher risk of developing liver abscesses. Transmission: Fecal-oral Intestinal amebiasis (dysentery):- Loose stools with mucus and bright red blood- Painful defecation, tenesmus, abdominal pain, cramps, weight loss, and anorexia- Fever in 10-30% of cases and possible systemic symptoms (e.g., fatigue) Extraintestinal amebiasis:- Mostly acute onset of symptoms; subacute courses are rare- In 95% of cases: amebic liver abscess, usually a solitary abscess in the right lobe- Fever in 85-90% of cases (compared to amebic dysentery) - RUQ pain or pressure sensation- Chest pain, pleuralgia- Diarrhea precedes only a third of all cases of amebic liver abscesses.  Diagnostics:- Stool analysis- EIA or copro-antigen ELISA (antigens found in feces) or molecular methods: e.g., PCR- Extraintestinal: Serological antibody detection, LFTs Treatment:- Symptomatic intestinal amebiasis and invasive extraintestinal amebiasis:→ Initial treatment with metronidazole or tinidazole to eradicate invasive trophozoites→ Followed by a luminal agent (e.g., paromomycin or diloxanide) to eradicate intestinal cysts and prevent relapse
• Dengue Epidemiology:- Distribution: tropical regions worldwide, particularly Asia (e.g., Thailand)- Incidence: Most common viral disease affecting tourists in tropical regions- Vector-borne: mosquitoes most commonly from the species Aedes aegypti  Classic dengue fever:- Incubation period: 2-14 days- Children are usually asymptomatic- Starts with fever and malaise that lasts ∼ 1 week- Severe arthralgia and myalgia (often referred to as “break-bone fever”)- Severe headache and retro-orbital pain- Maculopapular, measles-like exanthem (typically appears 2–5 days following fever)- Generalized lymphadenopathyIf symptoms appear more than 2 weeks after returning from a dengue-endemic region, it is very unlikely that dengue is the cause! Dengue hemorrhagic fever (DHF):- Occurs in 1-2% of cases- Generally develops as the initial fever subsides (∼ 1 week after onset)- Temperature change: ranges from hypothermia to a second spike in fever- Abdominal pain, vomiting- Changes in mental status (e.g., confusion)- Hemorrhagic manifestations (e.g., petechiae, epistaxis, gingival bleeding) - Increased vascular permeability → signs of pleural effusion and/or ascites Diagnostics:- Laboratory tests: Leukopenia, thrombocytopenia, ↑ AST, Hct elevated ≥ 20% of normal values if vascular permeability (in DHF) - Best test for confirming infection: serology (IgM, IgG)- Alternatives: PCR, ELISA) Treatment: - Symptomatic treatment: Fluid administration to avoid dehydration, acetaminophen- DHF: Blood transfusions, IV fluids
• Unilateral cervical lymphadenopathy Epidemiology:- Age: most common in children < 5 years Etiology:- Bacterial infections (up to > 80% of cases): S. aureus, Group A Streptococcus, Oral anaerobes, Group B Streptococcus (GBS), Francisella tularensis- Subacute or chronic: Nontuberculous mycobacteria, Mycobacterium tuberculosis, Bartonella henselae, Toxoplasma gondii- Kawasaki disease, PFAPA syndrome- Malignancy: leukemia, lymphoma, metastasis of oral mucosa cancers - Connective tissue disorders (e.g., juvenile rheumatoid arthritis, systemic lupus erythematosus) Clinical features:- Usually child appears healthy; possibly history of preceding upper respiratory tract infection or dental conditions- May have symptoms of an underlying infection (e.g., fever, malaise, tachycardia)- Most common: submandibular or deep cervical nodes (> 80% of cases)- 3-6 cm large, tender, warm, possibly erythematous skin over the node- Lymph nodes may become fluctuant and form an abscess over time or become indurated. Diagnostics:- Laboratory tests: CBC, ESR, CRP- Serology: if tularemia or cat-scratch disease is suspected- Tuberculin test in chronic cases- Bacterial culture: Blood culture, throat swab and oral swab, gram stain and culture of material obtained from fine needle aspiration- Histopathological evaluation of sample obtained by excisional biopsy- Imaging: ultrasound exam or CT scanning Treatment:- Conservative management by active observation for disease regression may be recommendable for children with no fever and non-tender lymphadenopathy.- All other cases are treated empirically with oral antibiotics for 10-14 days (e.g., clindamycin)- Surgical measures: incision and drainage of large abscesses
• Zika virus infection Epidemiology:- Since 2015, epidemic outbreaks have been reported in South America (especially Brazil). Route of transmission:- Vector-borne transmission by the mosquito Aedes aegypti (common) - Transplacental transmission from the mother to the fetus- Sexual transmission Clinical features:- Incubation time: 2-14 days- Approx. 80% of cases remain asymptomatic- In symptomatic patients, the manifestations are usually mild and last for 2-7 days- Fever- Flu-like symptoms: headache, arthralgia, myalgia, non-purulent conjunctivitis, malaise- Maculopapular, pruritic rash During pregnancy:- Microcephaly (craniofacial disproportion) - Spasticity (contractures), hyperreflexia, ocular abnormalities (e.g., pigmentary retinal mottling), and sensorineural hearing loss Diagnosis:- First 7 days of the infection: PCR detects Zika virus RNA in blood and/or urine samples- During days 7-28: PCR and/or serology- After 28 days: serology confirms Zika virus antibodies
• Lemierre syndrome Life-threatening infection that affects young immunocompetent patients. Etiology: - Gram-negative anaerobic bacillus Fusobacterium necrophorum (part of the normal oral flora) Clinical features:- Begins with tonsillitis- Invades lateral pharyngeal space through the lymphatic system → internal jugular vein thrombosis- Sore throat, high fevers, rigors, dysphagia, neck pain and swelling- Septic thromboemboli can seed the lungs, causing respiratory symptoms and leading to nodules on chest x-ray Diagnostics:- Culture from blood or pus Treatment:- Supportive (e.g., airway management)- Antibiotics- Surgery (eg., incision and drainage)
• Clostridium septicum Gram-positive, spore-forming colonic bacterium - The risk is increased in those with colonic malignancy
• Yersiniosis Pathogen: Yersinia enterocolitica- Gram-negative, rod-shaped, pleomorphic bacterium; obligate pathogen Transmission:- Foodborne (e.g., raw/undercooked pork)- Contaminated water- Direct/indirect contact with infected animal (e.g., dogs, pigs, rodents, and their feces)  Clinical features:- Duration: 1–46 days- Low-grade fever, vomiting- Inflammatory diarrhea (may be bloody in severe cases)- Pseudoappendicitis → mesenteric lymphadenitis, particularly in the ileum, with typical signs of appendicitis  Diagnosis: direct pathogen detection in culture or cold enrichment  Treatment: in severe cases, antibiotic therapy with fluoroquinolones or 3rd generation cephalosporins (depends on susceptibility to the drug)  Complications: particularly in patients with HLA-B27- Reactive arthritis- Erythema nodosum- Acute abdomen: appendicitis, bowel perforation, toxic megacolon, cholangitis- Bacteremia
• Blastomycosis Epidemiology:- South/south-central states, Mississippi & Ohio River valleys, Upper Midwest staes, Great Lakes states & Canadian provinces- Disseminated disease may occur even in immunocompetent patients- Generally more severe in immunocomprimised patients Clinical features:- Lung: Acute & chronic pneumonia (usually mild to moderate but may be severe)- Skin: Wartlike lesions, violaceous nodules, skin ulcers- Bone: Osteomyelitis- Genitourinary: Prostatitis, epididymo-orchitis- Central nervous system: Meningitis, epidural or brain abscesses Diagnosis:- Culture (blood, sputum, tissue specimens)- Microscopy (body fluids, sputum, tissue specimens)- Antigen testing (urine, blood) Treatment:- Mild pulmonary disease in immunocompetent patients: May consider not treating- Mild-to-moderate pulmonary disease, mild disseminated disease: Oral itraconazole- Severe pulmonary disease, moderately severe to severe dissemintated disease, immunocompromised patients: Intravenous amphotericin B
• Meningococcal vaccination Regular schedule (vaccinate at age 11-18):- Primary vaccination preferably at age 11-12- Booster at age 16-21 (if primary vaccination at age < 16) High-risk patients (vaccinate even if age > 18)- Complement deficiency, asplenia- College students in residential housing (age ≤ 21) military recruits- Travel to endemic area, exposure to community outbreaks
• Rubella (German measles) Congenital:- Sensorineural hearing loss- Cataracts- Patent ductus arteriosus Children: - Mild- Low-grade fver- Lymphadenopathy: Suboccipital, posterior auricular, posterior cervical- Cephalocaudal spread of maculopapular rash- ± Petechiae or Forchheimer spots on the soft palate Adolescents/Adults:- Same as children + arthralgias/arthritis Diagnosis: Serology
• Acute bacterial rhinosinusitis Pathogen: Nontypeable Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis Clinical features:- Cough, nasal discharge- Fever- Face pain/headache Diagnostic criteria:- Persistent symptoms ≥ 10 days without improvement- Severe onset (fever ≥ 39° C + drainage) ≥ 3 days- Worsening symptoms following initial improvement Treatment: Amoxicillin ± clavulanate
• Hepatitis A Risk population:- International travelers- Men who have sex with men- Illicit drug users- Those with household or sexual contact with infected persons Postexposure prophylaxis:- Close personal contacts (e.g., sexual contacts, household contacts) of hepatitis A-infected patients- Child care center contacts (e.g., staff and children) where staff, children, or household contacts of attendees have been infected- Food preparation workers whose coworkers have been infected Prophylaxis should be given within 2 weeks of exposure; in general, younger patients (age ≤ 40) should receive hepatitis A vaccine, whereas older patients (age ≥ 41) should receive hepatitis A immune globulin
• Sporotrichosis Epidemiology:- Sporothrix schenckii (dimorphic fungus)- Decaying plant matter/soil- Gardeners & landscapers Clinical features:- Subacute/chronic- Skin papule → ulceration with nonpurulent, odorless drainage- Proximal lesions along lymphatic chain- Lymphadenopathy, deeper spread & systemic symptoms are rare Diagnosis: Cultures (aspirate fluid or biopsy) Treatment: 3-6 months of oral itraconazole
• Acute cervical adenitis in children Unilateral:- Staph aureus, Strep pyogenes → Pronounced erythema, tenderness- Anaerobic bacteria (e.g., Prevotella buccae) → Dental caries, periodontal disease- Bartonella henselae → Papular nodular at site of cat scratch or bite- Myocbacterium avium → Gradual onset, nontender Bilateral:- Adenovirus → Pharyngoconjunctivitis- EBV/CMV → Mononucleosis
• Meningitis - Work-up Start on empirical antibiotic therapy immediately if meningitis is suspected and any of the following features are present: - Immunocompromise- Focal neurological deficits- Abnormal level of consciousness- Seizure at initial presentation- History of CNS disease. If none of these features are present, the patient should first undergo lumbar puncture and then immediately receive empirical therapy.
• Septic arthritis Risk factors:- Abnormal joint: Osteoarthritis, rheumatoid arthritis, prosthetic joint, gout- Age > 80- Diabetes- IV drug abuse, alcoholism- Intra-articular glucocorticoid injections Clinical features:- Acute monoarthritis: hot, swollen, decreased range of movement- Fever- Elevated ESR & CRP Diagnosis:- Blood cultures- Synovial fluid analysis: leukocytosis (> 50,000/mm3), Gram stain, culture Initial treatment:- Gram-positive cocci: vancomycin- Gram-negative rod: 3rd-generation cephlosporin- Negative microscopy: vancomycin (+ 3rd-generation cephalosporin if immunocompromised)

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