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PHAS 6300 Family Practice Infectious Diseases Lyme Disease Most common tick-borne disease in the US and Europe Caused by the spirochete species Borreliella Most common genospecies in the USA is Borrelia burgdorferi B garinii and B afzelii are the dominant genospec...

PHAS 6300 Family Practice Infectious Diseases Lyme Disease Most common tick-borne disease in the US and Europe Caused by the spirochete species Borreliella Most common genospecies in the USA is Borrelia burgdorferi B garinii and B afzelii are the dominant genospecies in Europe and Asia Lyme Disease Most US cases are reported from the mid- Atlantic, northeastern, and north central regions of the country.  Lyme Disease Ixodes scapularis in the northeastern north central, and mid-Atlantic regions of the United States Ixodes pacificus on the West Coast Ixodes ricinus in Europe  Lyme Disease Mice and deer make up the major animal reservoir of B burgdorferi Most human infections occur in the spring and summer Ticks must feed for 24–36 hours or longer to transmit infections. Lyme disease stages Stage 1 (early localized) infection is characterized by erythema migrans Rash begins about 1 week after the tick bite, initially as a flat or only slightly raised lesion. The lesion then then expands over several days About 10–20% of patients either do not have typical skin lesions or the lesions go unnoticed Lyme disease stages Stage 1 (continued) Most patients with erythema migrans will have a concomitant viral- like illness (the “summer flu”) characterized by myalgias, arthralgias, headache, and fatigue. Fever may or may not be present. When present it is typically low grade.  Stage 2 (Early 4-10% will Lyme disseminated) Early experience cardiac disease disseminated symptoms Myopericarditis stages infection Malaise, With arrhythmias fatigue, fever, and heart block headache (sometimes 10-15% will severe), neck experience pain, and Neurological generalized symptoms achiness Meningitis Lyme disease stages Stage 3 (Late stage) infection Chronic arthritis can occurs months to years after develop in about 10% of the initial infection and again patients primarily manifests itself as musculoskeletal, neurologic, Rarely, the nervous system and skin disease. can be involved in late Lyme disease. The classic manifestation of Can be: late disease is a monoarticular Central or oligoarticular arthritis most Encephalopathy commonly affecting the knee or Peripheral other large weight bearing Intermittent paresthesias joints. Radicular pain Lyme disease diagnosis Labs ELISA (antibody testing) False positives if other spirochetal diseases, syphilis, others* Does not distinguish between old and new infections Western blot (immunoblot assay) if ELISA is positive Lyme disease diagnosis Early localized disease Patients with stage 2 Clinical diagnosis on or stage 3 disease the basis of ELISA then Western symptoms and being Blot in an endemic area Patients are often seronegative in this stage so should be treated empirically. Lyme disease treatment Stage 1 (early localized) Prophylaxis for tick and Stage 2 (Early bite with no disseminated) symptoms Doxycycline PO x 10 days Doxycycline 200mg x (first line) 1 dose Amoxicillin or Cefuroxime for patients < 8 y/o or pregnant Tick removal Stage 3 (Late or severe) Use tweezers Arthritis Pull up firmly on tick’s Doxycycline x 28 days mouth part until the CNS or Cardiac symptoms tick releases it’s hold. IV ceftriaxone Syphilis  Syphilis Caused by Treponema pallidum Most frequently transmitted during sexual contact Can also be transmitted from mother to fetus via the placenta Nearly half of all cases of syphilis in the United States occur in men who have sex Primary Syphilis Defined by the presence of a ‘chancre’. A solitary painless ulcer at the site of inoculation. 1-2cm, clean based, punched out ulcer with a non exudative base and raised, indurated edges. Primary Syphilis Chancre is usually associated with enlargement of the regional lymph nodes Usually described as ‘rubbery, discrete and nontender’  Secondary Syphilis Occurs a few weeks to 6 months after initial symptoms Systemic Sx Fever, headache, malaise anorexia Possibly hepatitis, meningitis or alopecia Generalized lymphadenopathy Rash Diffuse and painless Generally maculopapular or papulosquamous exanthematous lesions Often on the face, trunk, palms and soles Secondary Syphilis Condyloma lata Wart-like moist lesions involving the mucous membranes and other moist areas Common near the chancre site Highly contagious Secondary Syphilis Invasion of Liver- Causing jaundice: Kidneys – Causing nephrotic syndrome Bones – causing periostitis Eyes – Causing uveitis CNS - Causing aseptic meningitis, acute basilar meningitis or cranial nerve palsies Latent Syphilis Occurs if syphilis is Categorized into 2 untreated stages: Defined by Early Latent Syphilis < 1 year since symptoms 1) Lack of symptoms occurred 2) Positive serologic Late latent Syphilis 3) Normal CSF > 1 year since symptoms examination occurred Tertiary Syphilis Can occur at any time after secondary syphilis Rarely seen in developed countries in the modern antibiotic era Symptoms can involve any tissue or organ, but most commonly involves the skin, mucous membranes, skeletal system, eyes, respiratory system, GI system, cardiovascular system and nervous system. Tertiary Syphilis Skin Cutaneous lesions of late syphilis are of two varieties: (1) multiple nodular lesions (2) solitary gummas that start as painless subcutaneous nodules, then enlarge, attach to the overlying skin, and eventually ulcerate Tertiary Syphilis Gummas Localized granuloma with large aggregates of lymphocytes, plasma cells, and multinucleated giant cells – hyperproliferative lesion Grossly, appears as a non-tender nodular lesion with central punched-out necrosis May involve any area or organ of the body but most often affect the Tertiary Syphilis Mucous membranes Gummas Leukoplakia highly destructive to the involved tissue Tertiary Syphilis Skeletal system Bone lesions are destructive, causing periostitis, osteitis, and arthritis with little or no associated redness or swelling but often marked myalgia and myositis of the neighboring muscles  Tertiary Syphilis Eyes Gummatous iritis, chorioretinitis, optic atrophy Cranial nerve palsies Argyll-Robertson pupil Small irregular pupils that constrict with accommodation but doe not constrict when exposed to Tertiary Syphilis Respiratory Gummatous infiltrates into the larynx, trachea, and pulmonary parenchyma, producing discrete pulmonary densities. There may be hoarseness, respiratory distress, and wheezing secondary to the gummatous lesion itself or to subsequent stenosis occurring with healing Tertiary Syphilis GI system Gummas of the liver, often benign but can cause cirrhosis Gastric involvement causing epigastric pain, early satiety, regurgitation, belching, and weight loss are common symptoms.  Tertiary Syphilis Cardiovascular Aortitis Coronary artery stenosis and thrombosis Aneurysms Aortic regurgitation/ Heart failure Tertiary Syphilis Nervous system - Late neurosyphilis Meningitis - headache, irritability, Cranial nerve palsies Vision/ hearing loss Incontinence General paresis Progressive dementia, seizures, psychiatric symptoms, Tertiary Syphilis Nervous system - Late neurosyphilis Tabes dorsalis Demyelination of the posterior columns and spinal nerve roots Causes Areflexia Ataxia Burning pain Weakness Severe unprovoked radicular pain Syphilis Diagnosis Non treponemal tests Treponemal tests RPR VDRL FTA-ABS TPPA Both are prone to false positives and false negatives Initial positive tests should always be confirmed with treponemal tests Syphilis Diagnosis Other options CSF examination Performed when symptoms are suggestive of neurosyphilis Darkfield microscopy Can be used from samples collected from chancres, mucosal lesions or condyloma lata Syphilis treatment Penicillin is the Jarisch-Herxheimer reaction treatment of choice Fever and worsening of symptoms for all stages of in the 1st 24 hours of treatment syphilis Thought to be due to cytokine IM Penicillin G is used for most cases release from killed organisms IV (aqueous) Penicillin Symptoms typically are fever, G is used for chills, headache, myalgias, neurospyphilis hypotension. Doxycycline is second Worsening rash can occur line for penicillin Self limited, can be treated with allergic patients NSAIDs or antipyretics (Tylenol) Syphilis treatment Counsel patients with infectious syphilis to abstain from sexual activity for 7–10 days after treatment. All cases of syphilis must be reported to the appropriate local public health agency to identify and treat sexual contacts. Because treatment failures and reinfection may occur, patients treated for syphilis should be monitored clinically and serologically with nontreponemal titers every 3–6 months. Chancroid Causative agent Haemophilus ducreyi Clinical manifestations Genital ulcers at the inoculation site Painful, enlarged inguinal lymphadenopathy which can liquify and become fluctuant (bubo formation)  Chancroid Diagnosis Usually clinical on the basis of having ruled out Syphilis and HSV PCR and immunochromatograp hy are possible but not commonly performed Treatment Azithromycin or Ceftriaxone Chancroid Syphilis Chancroid Pain Painless Painful Borders of ulcer ‘punched out’ Indurated, Irregular, undermined raised Base of ulcer Hard, clean, non-exudative Erythematous, sometimes with grey or yellow purulent exudate Lymphadenopathy Non-tender, sometimes Tender, usually unilateral, bilateral overlying erythema and possibly buboes Parasitic Diseases  Malari a Causative agent Plasmodium genus Plasmodium falciparum Plasmodium vivax Plasmodium ovale Plasmodium malariae Plasmodium knowlesi Epidemiology  Malaria Pathophysiology Malaria is transmitted by the bite of infected female anopheline mosquitoes. During feeding, mosquitoes inject an immature form of the Plasmodium, which circulates to the liver and rapidly infects hepatocytes, causing Malaria Pathophysiology After maturing in the liver, they are subsequently released and rapidly infect erythrocytes (red blood cells) This causes RBC Lysis which in turn causes cyclical fever that typifies malaria. Malaria Plasmodium falciparum is responsible for nearly all severe disease, since it uniquely infects erythrocytes of all ages and mediates the sequestration of infected erythrocytes in small blood vessels, thereby evading clearance by the spleen Malaria Symptoms Prodrome Severe symptoms (P. Headache, fatigue falciparum usually) Cyclical fever Cerebral malaria Cold stage (chills) Altered mental status Hot stage (fever) Delirium Diaphoretic stage (sweats) Seizures Occurs every 48 hours or Coma 72 hours depending on the Blackwater fever type of plasmodium Severe hemolysis Hemoglobinuria (dark urine) Renal failure Malaria Morbidity In highly endemic regions, where people are infected repeatedly, antimalarial immunity prevents severe disease in most older children and adults. However, young children, who are relatively nonimmune, are at high risk for severe disease from P falciparum infection, and this population is responsible for most deaths from malaria, usually from cerebral malaria and severe anemia. Malaria Diagnosis Clinical diagnosis: Patients with fever who traveled to endemic area Labs: Giemsa stained blood smear Rapid antibody or antigen tests CBC – various abnormalities Malaria treatment Treatment Prevention P falciparum Bed nets Artemisinin- based Permethrin containing combination therapies insecticides (ACTs) Malaria vaccine (coming) Chemoprophylaxis Chloroquine Non- P falciparum Malarone Chloroquine in most areas Mefloquine Primaquine or tafenoquine Doxycycline should be added if P vivax or P ovale Amoebas (Amebas) Amebas are unicellular organisms common in the environment: many are parasites of vertebrates and invertebrates  Amebiasi s Causative agent Entamoeba histolytica Symptoms/ Signs Most infections are asymptomatic GI symptoms range from mild diarrhea to severe dysentery Can cause liver abscesses causing RUQ pain, tender hepatomegaly, fever, anorexia and weight loss  Amebiasis Diagnosis Stool antigen test Stool PCR Ova and parasites exam Abscesses can be detected on ultrasound, CT or MRI Treatment Metronidazole or tinidazole Plus an intraluminal agent* If live abscesses are present Chloroquine should also be added.  Giardiasis Causative agent Giardia lablia, a flagellate protozoan AKA Giardia intestinalis and Giardia duodenalis Risk factors Travel to endemic areas Recreation or wilderness travel (Backpacker’s diarrhea): common in rivers, lakes, etc Local outbreaks Contaminated drinking water Daycare centers  Giardiasis Symptoms/ signs 50% will have no symptoms When present, symptoms could include: Abdominal cramps, bloating, flatulence Steatorrhea, frothy, greasy foul smelling diarrhea Occasionally malabsorption and weight loss Diarrhea can become chronic Giardiasis Diagnosis Stool antigen test (preferred) Stool microscopy Treatment Oral rehydration Tinidazole is preferred if > 3 y/o Nitazonaxide if 1-3 y/o Metronidazole if