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Infectious Disease 2
UWORLD + FA Infectious Disease/Micro Review
| Question | Answer |
|---|---|
| Syphilis histopathology description | Proliferative ENDARTERITIS with a surrounding PLASMA CELL infiltrate. |
| Most clinical manifestation of syphilis are due to: | Localized tissue ischemia resulting from ENDARTERITIS |
| What is the clinical manifestation of Syphilis in the Primary Phase? | Painless genital ulcer (chancre) |
| What are some Secondary syphilis manifestations? | - Diffuse rash (palms and soles) - Lymphadenopathy (epitrochlear) - Condylomata lata - Oral lesions, hepatitis |
| What is Condylomata lata? | Painless, wart-like, elevated plaques, on moist areas such as scrotum and perineum, seen in Secondary Syphilis. |
| What are the clinical manifestations of Tertiary Syphilis? | - CNS (tabes dorsalis, dementia), - Cardiovascular (aortic aneurysms, aortic insufficiency), - Cutaneous (gummas) |
| Papillomatous epidermal hyperplasia with cytoplasmic vacuolization. | HPV warts histological description |
| What serotypes of HPV cause warts? | HPV 6 & 11 |
| Septal PANNICULITIS with multinucleated giant cells | Erythema Nodosum |
| Description of Kaposi sarcoma (histo): | Dysplastic spindle-shaped cells surrounding areas of angioproliferative. |
| What is acantholysis? | Detached keratinocytes |
| Acantholysis with superficial dermal infiltrate is seen in? | Pemphigus vulgaris |
| What does a prolonged (over 3-6 months) HBeAg marker indicate? | Chronic HBV infection |
| What marker indicates a decrement in HBV infection infectivity? | The elevated levels of Anti-HBeAg levels. |
| The vanishing or disappearance of _____________________ indicates a low infectivity statues. | HBeAg |
| What HBV marker is indicative of high infectivity status? | HBeAg |
| If infection does not progress into chronic disease, which HBV infection marker is the one to disappear first? How long? | HBsAg should vanish in 3-6 months |
| What is the asymptomatic incubation period of HBsAg? | 6-8 weeks |
| When does Anti-HBcAg appears? | Shortly before symptoms appearance |
| Person vaccinated against HBV is positive for __________________, only. | Anti-HBs antibody |
| What are the two most common SE of Isoniazid therapy in latent TB infections? | 1. Neurological deficits ( prevented with Pyridoxine) 2. Hepatotoxic: 2a --> Mild hepatic dysfunction ( elevated AST/SGOT, ALT/SGPT) 2b --> Frank hepatitis --> fever, anorexia, and possible hepatic failure. |
| What are the Week 1 clinical manifestations of Typhoid Fever? | Rising (progressively) fever, Bacteremia, and Relative-bradycardia (pulse-temperature dissociation) |
| Week 2 of Typhoid Fever is manifested by developing _____________________ and ___________________ on trunk and abdomen. | Abdominal pain; ROSE SPOTS |
| What are the late (Week 3) clinical manifestations of Typhoid fever? | Hepatosplenomegaly and Intestinal bleeding and perforation |
| What is organism that causes Typhoid Fever? | Salmonella typhi or Paratyphi |
| What is the MC mode of transmission of Salmonella Typhi? | Ingestion of contaminated food or water contaminated with feces |
| What are the key characteristics of Salmonella Typhi Fever? | 1. Progressive fever with relative bradycardia 2. Rose spots on abdomen and trunk |
| ESBL stands for: | Extended-Spectrum Beta lactamases |
| ESBL may be produced by ________________________ bacteria. | Gram negative |
| ESBL-bacteria is often resistant to: | Cephalosporins and other beta lactam antibiotics |
| How does ESBL-bacteria acquire resistance to beta-lactam antibiotics? | Plasmid conjugation |
| What is the best treatment for ESBL-producing bacteria? | Carbapenems |
| What are 2 common Echinocandins? | Caspofungin and Micafungin |
| What is the mode of action for Caspofungin? | Inhibit synthesis of polysaccharide glucan (B-glucan), which is essential component of fungal cell wall |
| What antifungals act on the cell wall? | Echinocandins |
| Amphotericin B, Nystatin, and azoles act by disrupting the ___________________. | Cell membrane |
| Flucytosine inhibits fungal _________________ and _____________, halting __________________ and ___________________, respectively. | DNA & RNA; Replication & Protein synthesis |
| What are the functions of DNA pol I: | 1. Remove RNA primers via 5' to 3' exonuclease activity 2. Replace RNA primers with DNA, via 5' to 3' polymerase activity |
| What function or characteristic is unique to DNA polymerase I? | 5' to 3' exonuclease activity |
| What is the role or function of Primase? | To create RNA primers |
| Who removes RNA primers? | DNA pol I |
| What is the "proofreading" activity of DNA pol I and III? | 3' to 5' exonuclease activity |
| Autoimmune inflammation of Exocrine glands (lacrimal, salivary, and vaginal) | Sjogren syndrome |
| Immune-destruction of the lacrimal and salivary glands | Sjogren syndrome |
| Sjogren patients are positive for what antibodies? | anti-Ro (SSA) and anti-La (SSB) |
| Term used to describe severe dry mouth? Common pathology associated. | Sjogren syndrome is characterized by XEROSTOMIA |
| What is a complication of the Xerostomia seen in Sjogren's syndrome? | The decrease salivary flow leads to increased rate of dental caries and other oral infections (thrush). |
| What is the histopathological description of Sjogren syndrome tissue? | Lymphocytic infiltrate, wth germinal centers |
| Keratoconjunctivitis sicca | Sjogren syndrome |
| Sjogren syndrome is presents with __________________, ______________, and bilateral _________________ enlargement | Keratoconjunctivitis sicca, Xerostomia; Parotid |
| Enteroviral infection may cause: | Hand-Foot-and-Mouth Disease and Herpangina |
| What is a rare, but severe, complication of Coxsackievirus type A infection? | Myocarditis |
| What is Herpangina? Seen in? | Oral ulcerations seen in Enteroviral infection with Coxsackie A virus. |
| Oval-shaped vesicles on palms and soles A; vesicles and ulcers in oral mucosa | Coxsackie A virus infection |
| What is a dinguiguehing difference between C. perfringens and C. Septicum? | C. perfringens gas gangrene is caused by a previous trauma, whichle C. Septicum is not associated with traumatic lesion. |
| What is the main risk factor for C. septicum infection? | Underlying COLONIC MALIGNANCY |
| Spore-forming, exotoxin-producing, gram + bacterium | C. perfringens and C. septicum |
| What is the leading cause of foodborne gastroenteritis? | Non-typhoidal salmonella |
| What are some common complications of Non-Typhoid salmonella infection? | Osteomyelitis --> spread to long bones Mycotic aneurysm --> spread to vasculature Endocarditis --> spread to Heart |
| What kind of food is often associated with Salmonella contamination? | Poultry (chicken) products |
| Invasion of enterocytes, lead to massive neutrophil-mediated inflammatory response in lamina propria/ Peyer's Patches --> control infection. | Non-Typhoid Salmonella pathogenesis |
| Typhoidal Salmonella pathogenesis is described as: | Invasion of enterocytes causes a BLUNTED neutrophil response due to CAPSULAR ANTIGEN Vi --> extensive intracellular replication in macrophages leading to the spread through lymphatics and RES. |
| What are the most important manifestations of Entameba Histolytica infection? | 1. Colitis (diarrhea, bloody-stool with mucus) 2. Liver abscess (RUQ pain, fever) |
| What possible organism is indicated by Flask-shaped colonic ulcers during Colonoscopy? | Entameba Histolytica |
| 1. Microcephaly, craniofacial disproportion 2. Neurological abnormalities (Spasticity and seizures) 3. Ocular abnormalities | Congenital ZIKA syndrome |
| What are common findings in neuroimaging of Zika-infected patient? | Calcifications, VENTRICULOMEGALY, Cortical thinning |
| How are atypical (reactive) lymphocytes activated? | Acticarted by cytotoxic T-cells and NK cells |
| What intracellular infections are manifested with Reactive lymphocytes? | HIV, CMV, Toxoplasmosis, EBV-mononucleosis (MC) |
| What is contained in reactive lymphocytes? | Cytotoxic granules, made of Perforin and granzymes |
| Required growth factors for H. influenzae culture | X (hematin) and V (NAD+) |
| Co-culture of __________________ and __________________, produces the _______________________. | H. influenzae and S. aureus; Satellite phenomenon. |
| The ____________ of S. aureus provides the ___________________ growth factors required by H. influenzae. | B-hemolysis; X (hematin) and V (NAD+) |
| Prolonged use of tampons and/or wound packing, leads to development of _______________________________. | Toxic Shock Syndrome |
| What organism is usually involved in Toxic Shock Syndrome? | Staph aureus |
| The superantigen in Staph aureus infection | TSST-1 |
| ______________ (superantigen) binds to ________ on __________ WITHOUT processing and ___________________ activate T-cells, leading to massive release of _________________________, leading to clinical symptoms of S. aureus TSS. | TSST-1; MHC-II on APCs; NON-specifically; inflammatory cytokines (TNF-a, IL-6, INF-g, etc). |
| Activation of TLRs is often seen in gram_________________ bacteria, leading to rapid onset of __________________ and fever. | Gram negative; Hypotension |
| Gentamicin is a common _____________________. | Aminoglycoside |
| What is the MC mode of resistance to aminoglycosides? | Antibiotic (aminoglycoside)-modifying enzymes |
| What is the role or function of antibiotic-modifying enzymes? | Add chemical groups to antibiotics, leading to diminished ability to bind to the 16S ribosomal RNA within the 30S ribosomal subunit. |
| Acetyl, adenyl. and phosphate | Antibiotic-modifying enzyme groups |
| Penicillins most common way of resistance is: | Beta-lactamase, ESBL |
| Vancomycin MC resistance is due to: | Mutated peptidoglycan cell wall (D-ala-D-lac) |
| Mutated DNA gyrase | MC mode of fluoroquinolone resistance |
| Tetracyclines most commonly acquired resistance via: | Impaired influx / Increased efflux |
| Decreased uptake or Increased efflux out of bacterial cells by plasmid-encoded transport pumps | Mechanism of Tetracycline resistance |
| What kind of antibiotics' mechanism of resistance is produced by a mutated RNA polymerase? | Rifamycins |
| Universal HBV vaccination would lead to -----> | Decline in HCC cases |
| DHFR is: | Dihydrofolate reductase |
| DHFR is inhibited by these drugs: | 1. TMP (bacteria) 2. MTX (humans) 3. Pyrimethamine (Protozoa) |
| Inhibition of DHFR prevents the conversion of _______________ acid into _______________. | Dihydrofolic acid into THF |
| The sulfonamides work a step ______________ the action of TMP, MTX and Pyrimethamine. | before |
| TMP is paired with ____________ ( ___________-___________) creating a "______________________" | SMX; (TMP-SMX); Sequential blockade |
| Pyrimethamine inhibits _________________ in ________________, thus making excellent for treatment of __________________ and ___________. | Parasitic DHFR in protozoa; Malaria and Toxoplasmosis |
| CCR5 inhibitor | Maraviroc |
| Enfuvirtide is a __________________________ used in HIV replication antiviral panel. | Fusion inhibitor |
| What are some common Protease Inhibitor in the HIV antiviral drugs? | Saquinavir, Ritonavir |
| What suffix is associated with HIV Protease inhibitors? | --navir |
| Common NRTI and NNRTIs? | Efavirenz, Tenofovir, lamudivine |
| Suffix seen in HIV Integrase inhibitors? | --gravir |
| ---__________________, suffix of _______________ inhibitors, and _--________, suffix in __________________ Inhibitors. | --gravir --------> Integrase inhibitors --navir ---------> Protease inhibitors |
| Raltegravir is a : | HIV integrase inhibitor |
| MoA of Raltegravir | Disrupts HIV genome integration, preventing synthesis of viral mRNA. |
| What kind of HIV antiviral drugs prevent the synthesis of viral (HIV) mRNA? | Integrase inhibitors |
| Adverse effect of all HIV Integrase inhibitors | Increased level of Creatine Kinase (CK) |
| What medication is this HIV patient most likely taking, if blood serum shows elevated levels of creatine kinase? | Raltegravir |
| Methylation of the aminoglycoside-binding portion of the ribosome | Common way of Aminoglycoside mechanism of resistance |
| Non-sterile gloves, gowns, and private room | Contact precautions |
| Contact precautions are needed in what infections? | Methicillin-RESISTANT Staph aureus (MRSA), VRE, and other parasitic infections |
| What kind of meaures is required to prevent MSSA (nosocomial) transmission? | Hand hygiene is sufficient |
| Patient with active TB requires ______________________ precautions. | Isolation |
| Group A Streptococcus is ___________________________. | Strep pyogenes |
| What kind of conditions are precipitated by a Strep pyogenes infection? | 1. Strep Skin Infection (IMPETIGO) 2. Streptococcal pharyngitis |
| Streptococcal impetigo may lead to the development of ___________ and _____________. | ARF (acute Rheumatic fever); PSGN |
| Streptococcal pharyngitis only develops ___________________. | ARF (acute Rheumatic fever) |
| Methylation of 23S rRNA-binding site prevents binding of drug. | Mechanism of Resistance in Macrolides |
| Bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation. | Mechanism of Resistance in Aminoglycosides |
| Chloramphenicol mode of resistance: | Plasmid-encoded acetyltransferase inactivates the drug. |
| What enzyme is inhibited by Sulfonamides and Dapsone? | Bacterial dihydropteroate synthase |
| Mutated or altered bacterial Dihydropteroate synthase. | Mechanism of Resistance in Sulfonamides |
| Clinical presentation of Non-bullous impetigo | PAINFULL, non-itchy pustules and honey-crusted lesions |
| What are the most common organisms that cause Non-bullous impetigo? | Staph aureus and Strep pyogenes |
| HSV-6 infection is known as _____________________. | Roseola |
| Fever for 3-5 days, and once subsided, apparition of erythematous, blanching, maculopapular truncal rash. | Roseola (HSV-6 infection) |
| What is MCC of febrile seizures? | HSV-6 infection |
| Pattern seen in roseola rash | Neck and Trunk ------> Face and extremities |
| How is the rash spread pattern in Rubella and Measles? | Cephalocaudal spread (Starts at forehead and goes down) |
| Unique spots in Rubella? | Forchheimer spots in Soft Palate |
| Distinguishing and pathognomic spots in Measles? | Koplik spots in buccal mucosa |
| What does a CENTRIPETAL rash pattern means? | Rash starts EXTREMITIES and moves to the TRUNK |
| A CENTRIFUGAL rash spread is the one starting at the ____________ and extending to the __________________. | Trunk -------> Extremities |
| What conditions/disorder display a centripetal rash? | 1. Coxsackie A (Hand-Foot-Mouth Disease) 2. RMSF (Rocky Mountain Spotty Fever) (only rickessi) 3. Syphilis |
| Which bacterial family and species display a centrifugal rash pattern? | Rickettsial (prowazekii, typhi, tsunamushi) |
| RMSF rash involves the ______________ and ____________. Rickettsial _______________ is the causative organism of RSMF. | Wrist and ankles. Rickettsii |
| Mnemonic CARS is used for? | Centripetal rash conditions (Coxsackie A, RMSF, and Secondary Syphilis). Involves wrist, soles, and palms. Remember you drive CARS with PALMS and SOLES |
| MC organisms that cause Atypical pneumonia? | Mycoplasma and Chlamydia infectections |
| Mycoplasma has __________________, while Chlamydia has a _____________________. | Mycoplasma ------No cell wall Chlamydia ---------> Modified cell wall |
| Effects of Mycoplasma lack of cell wall? | 1. Not able to gram stain 2. Ineffective to the treatment with Beta-lactam antibiotics |
| What is the most proper treatment for Atypical Pneumonia? | Macrolides and Tetracyclines (Protein synthesis inhibitors) |
| CXR with Bilateral PATCHY infiltrates | Atypical Pneumonia |
| __________________ pneumonia has a CXR ________________ infiltrate finding. | Legionella |
| What are the main two Atypical Pneumonia causative organism? What other is much less common? | Main two are Mycoplasma and Chlamydia; Legionella is rarely seen causing atypical pneumonia. |
| CXR of fungal pneumonias | Lobar, nodular, or cavitary infiltrates |
| Curved, gram negative, free-living bacterium that grows in marine environments | Vibrio vulnificus |
| Mode of transmission of V. vulnificus? | 1. Ingestion of raw seafood (oysters) 2. Wound contamination |
| What type of people is at increased risk of developing a serious complication by V. vulnificus infection? | Liver disease patients or those with Iron overload |
| What are serious complications seen in V. vulnificus infection? | Sepsis and NECROTIZING FASCIITIS |
| What is the treatment for Gardnerella (bacterial) vaginosis? | Metronidazole or Clindamycin |
| ____________________ vaginitis is treated with ___________________, and also the partner. | Trichomonas; Metronidazole |
| What is the treatment (drug) used for Candida vaginitis? | Fluconazole |
| Bacterial vaginosis (Gardnerella): | White discharge + clue cells + "fishy odor" + ph >4.5 |
| Green-yellow vaginal discharge + Malodorous discharge + elevated vaginal pH (>4.5) and treated with Metronidazole. Dx? | Trichomoniasis |
| "Cottage-cheese" like vaginal discharge is seen in? | Candida vaginitis |
| What is the normal pH range for the vagina? | 3.8 -- 4.5 |
| INH inhibits _______________________ synthesis, in the treatment of _____. it is known it has to be processed by mycobacterial __________________. | mycolic acid; TB; CATALASE PEROXIDASE |
| What RIPE drug is involved with Catalase Peroxidase? | Isoniazid |
| What are the main side effects of Ganciclovir therapy? | Neutropenia, Anemia, and Thrombocytopenia |
| What are the main clinical uses for Ganciclovir? | CMV colitis and CMV retinitis |
| MoA seen in ganciclovir? | Inhibits viral DNA synthesis by blocking CMV DNA polymerase |
| What is the treatment of Gonorrhea? | Azithromycin + Ceftriaxone |
| Staphylococcal foodborne illness are due to: | Preformed Enterotoxin |
| Washing hands prior to preparing food helps to___________________ | Prevent contamination |
| How does ensuring proper refrigeration storage for food help to prevent a Staphylococcal entero illness? | Prevents bacterial proliferation/ enterotoxin production |
| How quickly are GI symptoms of Staphylococcal foodborne illness presented? | 3-4 hours |
| Undercooked beef is often associated with: | EHEC infection ---> bloody diarrhea and HUS |
| Shiga-toxin | Seen in Shigella and EHEC |
| Time elapsed for initial symptoms of an EHEC infection? | 3-4 days |
| What drugs are used in the treatment of MRSA? | 1. Vancomycin 2. Daptomycin 3. Linezolid |
| Daptomycin mechanism of action | 1. Causes the DEPOLARIZATION of bacterial cellular membrane and, 2. Inhibition of DNA, RNA, and protein synthesis. |
| What are the main side effects of Daptomycin therapy for MRSA? | 1. Elevated levels of Creatine phosphokinase (CPK) 2. Increased incidence of myopathy |
| Vancomycin is usually the 1st line of treatment of _____________, Vancomycin is seen with increased risk of developing ______________ and _________________. | MRSA; Nephrotoxicity ; Red Man Syndrome |
| What can inactivate Daptomycin? | Pulmonary surfactant |
| Binding to bacterial 23S ribosomal RNA of the 50S subunit, leading to the prevention of forming the 70S initiation complex, required for proper bacterial protein translation. | Linezolid mode of action |
| What are the main side effects seen with Linezolid? | 1. Thrombocytopenia 2. Optic Neuritis 3. Increased risk of Serotonin syndrome if co-administered with a Serotonin agonist such as Citalopram. |
| Common 3 NNRTIs? | Nevirapine, Efavirenz, and Delavirdine |
| What NNRTis are contraindicated in pregnant women? | Delavirdine and Efavirenz |
| NNRTI do not require ___________________________ and are considered ________________________ inhibitors of the HIV RT. | Intracellular phosphorylation; Allosteric |
| Efavirenz is associated with development of ____________________ and ______ symptoms. | Vivid dreams and CNS symptoms |
| What diseases are associated with IXODES tick? | Lyme Disease (Borrelia burgdorferi) and Babebiosis (babesia microti) |
| Key clue of Babebiosis | Intraerythrocytic pleomorphic ring forms (Maltese crosses) seen in PBS |
| Maltese crosses | Babebiosis |
| AEDES mosquito transmits __________________ and _______________. | Dengue and Malaria |
| What area of the USA is associated with dense Ixodes tick population? | Northeastern USA |
| What are other names for Inactivated vaccines? | Killed or Component Vaccines |
| What is generated by a killed vaccine? | Humoral response (only) against extracellular viral antigens, preventing viral entry to the cell. |
| Inactivated vaccines prevent the ____________________ to the cell. | Viral entry |
| Contrary killed vaccines, the Live-Attenuated vaccines produce: | Strong cell-mediated immune response that KILL VIRAL CELLS, in addition to providing a humoral response. |
| Foscarnet is used for ____________ and ___________ infections. | HIV and HSV |
| Pyrophosphate analogue | Foscarnet |
| Foscarnet is _______________________ analogue, used in __________ and __________ viruses. | Pyrophosphate; HIV and HSV. |
| What are the 2 main clinical uses for Foscarnet? | 1. CMV retinitis/colitis when Ganciclovir fails in AIDS patients 2. Acyclovir-resistant HSV |
| Mode of action seen with Foscarnet? | Binds and inhibits to: 1. Reverse transcriptase in HIV 2. DNA polymerase in Acyclovir-resistant HSV infection |
| What side effects are presented with Foscarnet? | Nephrotoxicity, and electrolyte imbalances leading to Seizures |
| What electrolyte imbalances are developed in Foscarnet antiviral therapy? | Hypo/Hypercalcemia, Hypo/Hyperphosphatemia, Hypokalemia, and Hypomagnesemia ==> SEIZURES |
| What is the best way to prevent vertical HIV transmission to the fetus? | Antiviral therapy to all HIV pregnat women |
| Broad, NON-septate hyphae with right-angle branching | Mucor spp histological description |
| Mucormycosis is presented as: | Facial pain, headache, and black necrotic eschar in diabetic patient with DKA |
| How is the best way to confirm dx of Mucormycosis? | Histological examination of affected tissue (mucosa) |
| 45 degree angle branching-------> 90 degree angle branching -----> | Aspergillus fumigatus Mucor specie |
| The hyphae in Mucormycosis is _________________________, while the one describe in Aspergillosis is ____________________. | NON-septate; Septate |
| What virus is causative of Progressive Multifocal Leukoencephalopathy? | JC virus |
| What is seen in CT of brain in a patient with Progressive Multifocal Leukoencephalopathy? | White matter lesions with NO ENHANCEMENT/Edema |
| T2-weighted MRI with white matter lesions and no associated edema or enhancement. Dx? | PML by JC virus |
| Pt presents with confusion, paresis, ataxia, seizures, all progressed slowly over several years. Patient is HIV positive, with inconsistent antiviral therapy. | PML by JC virus |
| Brain imaging of EBV infection: | Single-enhancing lesion, seen in Primary Lymphoma |
| Toxoplasmosis brain imaging shows: | Multiple-ring enhancing lesions with surrounding edema |
| What are the two main brain enhancing lesions? | Toxoplasmosis (multiple) and Primary solitary Lymphoma (single + EBV) |
| Persistence of HBsAg over 6 months | Chronic HBV infection |
| HBV surface glycoproteins | HBsAg |
| What HBV serologic markers are present in acute infection? | HBsAg, HBeAg, and anti-HBc IgM |
| HBV polypeptide | HBeAg |
| Increased viral replication and infectivity of HBV infection is indicated with increased levels of ____________________ serologic marker. | HBeAg |
| Anti-HBc IgM: | - First sign of acute HBV infection - Only serologic marker present in the WINDOW PHASE |
| Presence of Anti-HBs indicates: | 1. Cleared infection or immunity 2. Confers long-term immunity |
| Cleared infection of HBV is indicated by presence of ____________. | Anti-HBs antibody |
| The increase presence of Anti-HBe antibody indicates? | Decreased viral replication and infectivity |
| What antibody is not present after vaccination for HBV? | Anti-HBc IgG |
| Large, sporulating, gram positive rod, encased by antiphagocytic polypeptide capsule | Bacillus anthrasis |
| What is the main component of the capsule in B. anthracis? | D-glutamic acid |
| What is caused by B. anthracis? | Pulmonary anthrax |
| Clinical manifestations of Pulmonary anthrax: | Hemorrhagic MEDIASTINITIS, shock and death, caused by B. anthracis infection. |
| What are the MC ways of Ascaris Lumbricoides infection: | Transmission via contaminated food and water |
| The__________________ travels from the _____________ all the way to the _________________. | Ascaris lumbricoides; Small intestine ; Pulmonary alveoli |
| What is the collection of pulmonary symptoms called in Ascaris lumbricoides? | Loeffler syndrome |
| Transient, eosinophilic pneumonitis with pulmonary symptoms | Loeffler syndrome |
| What is the most common treatment for A. lumbricoides infection? | Albendazole |
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rakomi
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