Introduction

Toxoplasmosis is caused by the obligate, intracellular protozoan parasite Toxoplasma gondii

-the only Definitive hosts are cats 

-In the majority of infected persons, toxoplasmosis is chronic, asymptomatic, and self-limiting

-it is contracted through the consumption of poorly cooked meat or the ingestion of oocytes in food or water contaminated with cat feces; rarely via blood transfusion or organ transplantation 

-Toxoplasma form oocysts in cats. After ingestion, oocysts become tachyzoites in humans and form tissue cysts mostly in skeletal muscle, eye, brain, placenta,and myocardium 

Symptoms & Signs 

Most individuals are asymptomatic, but severe disease is often seen in the immunocompromised individuals 

-Toxoplasmosis occurs in four major clinical forms: 

Infection in Immunocompetent persons 

-infectious mononucleosis like clinical syndrome 

-self-limiting febrile lymphadenopathy which can be non-tender cervical lymphadenopathy or generalized lymphadenopathy; fever, headache, malaise, fatigue, sore throat and myalgias 

Infection in Immunocompromised persons 

-often secondary to reactivation of latent infection 

-fever, headaches, seizures, mental status changes, encephalopathy, meningoencephalitis, mass lesions, multiple necrotizing brain lesions

-The most common clinical manifestation of toxoplasmosis acquired after birth is asymptomatic localized lymphadenopathy

Congenital infection

-Transplacental transmission highest in third trimester

-Newborns may show low birthweight, hepatosplenomegaly, jaundice, anemia, chorioretinitis, blindness, microcephaly, hydrocephalus, abortion, stillbirth,  tram-track intracerebral calcifications, deafness, mental retardation, blueberry muffin lesions (dermal erythropoiesis), purpura 

Ocular toxoplasmosis

Pain, photophobia, visual changes, uveitis, focal necrotizing retinochoroiditis, chorioretinal scar, glaucoma, blindness  

Diagnosis 

-The primary method of diagnosis is serology 

-Identification of tachyzoites in tissue or body fluids: With Wright or Giemsa stains, tachyzoites are crescent-shaped and have a prominent, centrally placed nucleus. 

-Pregnancy: PCR of amniotic fluid

-Newborns: IgM or IgA antibody tests 

-CT and MRI scans: show multiple ring-enhancing cerebral lesions

Treatment

Immunocompetent patients with only lymphadenopathy: do not require treatment 

Immunocompromised patients: Pyrimethamine plus sulfadiazine; given with leucovorin/folinic acid to limit bone marrow toxicity; Pyrimethamine is not used during the first trimester of pregnancy due to its teratogenicity; trimethoprim-sulfamethoxazole is an effective alternative; Clindamycin can be used in sulfonamide-allergic patients 

Congenital infection: Oral pyrimethamine, sulfadiazine, and folinic acid for 1 year; Spiramycin is used to prevent congenital infection  

Ocular toxoplasmosis: Pyrimethamine and either sulfadiazine or clindamycin for 1 month 

Q. What is the most common clinical manifestation of toxoplasmosis acquired after birth? Asymptomatic localized lymphadenopathy 

Q. What are the most frequently involved lymph nodes in toxoplasmosis? cervical nodes 

Q. What is the most common cause of intracerebral lesions in AIDS patients? Toxoplasmic encephalitis 

Q. What is the most common late presentation of congenital toxoplasmosis? Retinochoroiditis 

Introduction

Babesiosis is a malaria-like disease caused by intraerythrocytic protozoa of the genus Babesia

-similar to malaria, the protozoans invade and lyse the red blood cells 

-it is transmitted by ticks, and occasionally through transfusion of blood products 

 -In the United States, infections occur most frequently in the Northeast and upper Midwest

-Babesia trophozoites appear round or ameboid

-The ring form is most common and lacks the central brownish deposit (hemozoin) typical of Plasmodium falciparum trophozoites

Symptoms & Signs 

Babesiosis can be asymptomatic 

-Symptomatic babesiosis may show fatigue, fever, headache, arthralgia, myalgia, nausea, vomiting, abdominal pain, anemia, thrombocytopenia, hepatomegaly, splenomegaly, splenic rupture, hemolysis, jaundice, dark urine 

Diagnosis 

Blood smear: identification of intraerythrocytic ring forms resembling malaria on a Giemsa- or Wright-stained peripheral blood smear; merozoites often in tetrads (“Maltese cross”) 

Other methods: PCR, indirect immunofluorescent antibody test

Treatment 

-Most patients have a mild illness and recover without therapy

-Similar to malaria, babesiosis requires the use of antiprotozoals

– Two combination therapies are recommended: atovaquone plus azithromycin or quinine plus clindamycin

-in severe disease: exchange transfusion 

Memory Aid: Babesiosis is a malaria like disease caused by a malaria-like organism and treated with malaria-like drugs 

Introduction

Malaria is a disease caused by Plasmodium parasites 

-it is transmitted by the bite of infected female anopheline mosquitoes

-it is uncommon in temperate climates, but still common in tropical and subtropical countries 

-it is the most significant disease acquired through international travel to the tropics

–approximately half of the world’s population are at risk for malarial infection each year

-Five species of the genus Plasmodium infect humans: Plasmodium vivax, Plasmodium ovale, Plasmodium malariae, Plasmodium falciparum, and Plasmodium knowlesi

-While Plasmodium falciparum is the most common cause of serious malaria, P vivax and P knowlesi can also cause severe and fatal infections

-Plasmodium falciparum is also responsible for cerebral malaria 

-Severe malaria is a medical emergency and requires hospitalization 

Pathophysiology 

Step 1: Infected female Anopheles mosquito bites, infects humans: Sporozoites are released from the mosquito into the human bloodstream 

Step 2: Liver stages: Sporozoites migrate to the liver and start multiplication through asexual reproduction within hepatocytes. The daughter cells are called merozoites. Hepatocytes rupture and release merozoites into the circulation.  

Step 3: Red blood cell stages: Merozoites enter the bloodstream and invade red blood cells. A merozoite enters an erythrocyte, multiples within and forms a schizont. 

Step 4: Invasion of the body: A schizont ruptures to release merozoites which releases pyrogens into the bloodstream causing malaria. Thus, symptomatic malaria is caused only by the erythrocytic stage of infection. 

Step 5: Infection of the mosquito: A portion of the merozoites develop into sexual forms (gametocytes). Feeding on its human host, Anopheles mosquito swallows male and female gametocytes, which undergo sexual reproduction in its gut. They produce sporozoites which travel to the salivary glands waiting to be injected into the next innocent human victim. 

Symptoms & Signs: Fever,chills, myalgia, malaise, headache, cough, chest pain, abdominal pain, nausea, vomiting, diarrhea, arthralgia, tachycardia, tachypnea, and splenomegaly

Fever may follow regular cycles 48-hour (P vivax and P ovale) or 72-hour (P malariae) cycles

Severe complications: Anemia, jaundice, renal failure, metabolic acidosis (pH <7.35), hypoglycemia, shock, disseminated intravascular coagulopathy, pulmonary edema, acute respiratory distress syndrome, impaired consciousness, seizures

Diagnosis 

Thick and thin blood films, Rapid diagnostic tests, PCR based tests 

Treatment 

-no antimalarial drug kills sporozoites, so it is not truly possible to prevent infection using drugs 

-Drugs can prevent symptomatic malaria by inhibiting asexual merozoite production in the hepatocytes 

Artemisinin and derivatives: Artemisinin-based combination therapies (ACTs) achieve the fastest clearance of parasites from the blood; According to the WHO, IV artesunate is the drug of choice for severe malaria, effective against  drug-resistant P falciparum;  Co-Artem (Artemether/ Lumefantrine) may cause hearing loss 

Atovaquone/proguanil: useful in malaria chemoprophylaxis, it acts at both the liver and the blood stage; can cause oral aphthous ulcers; can enhance warfarin anticoagulation; Contraindications: pregnancy, severe renal insufficiency  

Chloroquine: Chloroquine is the drug of choice for the treatment of sensitive non-falciparum and sensitive falciparum malaria; causes generalized pruritis in black people; Contraindications: Psoriasis, epilepsy 

Mefloquine: first-line drug (taken weekly) given for prophylaxis in all geographical areas with chloroquine resistance; most frequent side effects are vivid dreams, mood changes, insomnia; Contraindications: serious psychiatric disease, seizure disorder 

Primaquine: effective against the liver stages, blood stages and gametocytes; Contraindications: pregnancy, G6PD deficiency, all individuals should have G6PD screening prior to treatment

Quinine: Parenteral quinine is used for severe malaria when parenteral artesunate is not available; it is cardiotoxic; can cause Quinine-induced hyperinsulinemic hypoglycemia; blood glucose concentrations should be monitored; can also cause  hypotension, thrombocytopenia, erythematous rash, increased uterine contractions in pregnant women leading to miscarriage 

Quinidine: a diastereomer of quinine and is more toxic; can cause hypotension and QT prolongation; requires electrocardiographic monitoring 

Doxycycline: effective as chemoprophylaxis and treatment; should be taken daily; Side-effects include photosensitivity, gastrointestinal upset, esophageal ulceration. Contraindications: pregnancy, breast-feeding, and children less than 8 years of age

Clindamycin:  is less effective than doxycycline or atovaquone/proguanil; can be used when other drugs cannot be used (pregnant women, young children)

Pyrimethamine-sulfadoxine: it inhibits folate synthesis in the parasite; of little use due to drug resistance 

Introduction

Leishmaniasis is a complex of diseases caused by the protozoa Leishmania

-it is transmitted by the bite of infected phlebotomine sandflies

Leishmania species are 

-in the sandfly: extracellular, flagellated promastigotes 

-in the humans: obligate intracellular, nonflagellated amastigotes 

Symptoms & Signs 

Three major human diseases: Cutaneous  leishmaniasis, mucocutaneous leishmaniasis, and visceral leishmaniasis 

Cutaneous leishmaniasis

-Lesions start as small papules and develop into nonulcerated dry plaques or large encrusted ulcers with raised and indurated margins 

-Ulcerated nodules look similar to volcanoes seen from above (volcano sign) 

-they are mostly seen over face and ears 

Mucocutaneous leishmaniasis (espundia)

-it is characterized by the chronic and progressive spread of lesions to the nasal, pharyngeal,laryngeal and buccal mucosa

-ulceration of the nasal mucosa and septum, septal perforation, collapse of the nasal bridge and free hanging nose (tapir nose or parrot beak) 

-partial/total naso oropharyngeal mutilating ulceration (espundia)

Visceral leishmaniasis (kala azar)

it most commonly presents with an abrupt onset of moderate- to high-grade persistent, undulating fever associated with rigor and chills

-Splenomegaly, hepatomegaly, lymphadenopathy 

-Anemia, leukopenia, thrombocytopenia, hypergammaglobulinemia  

-Hyperpigmentation of the skin, jaundice, ascites

Diagnosis 

Due to low sensitivity of individual tests, the best approach is to use several diagnostic methods: impression smear, histology, and culture 

Characteristic histological features: tuberculoid granulomatous dermatitis with multinucleated giant cells surrounded by lymphoplasmacytic infiltrate

Treatment 

Local therapy: Excision, laser ablation, cryotherapy, electrotherapy, Paromomycin ointment

Medications: Sodium stibogluconate, Megluminee, Miltefosine, Pentoxifylline, 

Pentamidine, Amphotericin B, Paromomycin, Zinc sulfate 

American Trypanosomiasis

Introduction

American trypanosomiasis (Chagas disease) is caused by Trypanosoma cruzi, a protozoan parasite found only in the Americas

-it is transmitted to humans by blood-sucking triatomine bugs (kissing bugs, assassin bugs, reduviid bugs)

-it  is endemic in many rural areas of Central and South America and Mexico

-In many countries in South America, Chagas disease is the most important cause of heart disease

Symptoms & Signs 

American trypanosomiasis progresses in 3 stages.

Stage 1 Acute Phase: asymptomatic or fever lymphadenopathy, mild hepatosplenomegaly, and morbilliform/urticarial rash,  a painful inflammatory reaction at the site of inoculation (Chagoma); unilateral conjunctivitis with palpebral edema (Romaña sign)

Stage 2 Indeterminate Phase: asymptomatic but infectious stage 

Stage 3 Symptomatic Chronic Phase: 

CNS: Meningoencephalitis 

Heart: Acute myocarditis, Dilated cardiomyopathy, arrhythmias, congestive heart failure 

GI: Dysphagia, regurgitation, aspiration, constipation, megaesophagus, and megacolon

Diagnosis: Demonstration of trypomastigotes in blood, smooth muscle biopsy, xenodiagnosis, serologic testing, PCR 

Treatment

Medications: Benznidazole, nifurtimox  

Introduction

Human African trypanosomiasis (HAT) or African sleeping sickness is a serious infection caused by a protozoan called Trypanosoma 

-the organisms are transmitted by bites of tsetse flies, which are confined to Central Africa  

-the disease is divided into West and East African forms

-Trypanosoma brucei gambiense causes West African sleeping sickness (95% of cases)

-Trypanosoma brucei rhodesiense causes East African sleeping sickness (5% of cases) 

Symptoms & Signs 

-a painful chancre develops at the site of the tsetse bite 

-It consists of a circumscribed, rubbery, indurated, dusky red nodule, often with a central eschar 

-Fever, headache, myalgia, lymphadenopathy, disseminated intravascular coagulopathy, QTc prolongation,pulmonary edema, ARDS, hypotension, and shock

-Involvement of the posterior cervical (Winterbottom sign) and supraclavicular lymph node in Gambian trypanosomiasis

Diagnosis 

Diagnosis is by detection of trypanosomes in blood films, Giemsa-stained thick smears, chancre, lymph node aspirate, bone marrow or CSF 

Treatment 

-Lumbar puncture must always be performed before initiation of therapy for sleeping sickness

-Selection of drugs dependent on whether CNS is involved

-CNS is not invaded: pentamidine, suramin

-CNS is invaded:  eflornithine, nifurtimox, melarsoprol, and fexinidazole 

Prognosis: Without CNS involvement, recovery often complete

Introduction 

Lyme disease is an infection caused by the spirochete Borrelia burgdorferi, which enters the host after a bite by a tick

-Most cases of Lyme disease occur in the northeast United States between April and November

-It is the most common tick-borne illness and the most common vector-borne zoonotic infection in the United States, 

Symptoms & Signs 

Once a human is infected, disease progression is categorized into three stages: Early localized, Early disseminated, and Late persistent

Stage 1: Early Localized Disease

-Characterized by erythema migrans, which is described as “bull’s-eye” eruption. 

-it is a flat, nonpruritic, erythematous, maculopapular lesion near the site of infection

– Erythema progresses with central clearing 

-it can be accompanied by fever, chills, fatigue, myalgias, arthralgias, and lymphadenopathy

Stage 2: Early Disseminated Disease

-it occurs within a few days to months of the initial infection

-it can involve multiple organs

Fatigue: persistent fatigue is a hallmark of untreated disseminated Lyme disease 

Joints: Asymmetric oligoarticular arthritis of the large joints, particularly the knees; Migratory pains in muscles, joints, and periarticular structures 

Nervous system: it can produce both central and peripheral nervous system disease, acute as well as chronic 

CNS: meningitis or meningoencephalitis, headache, dementia, depression

Cranial nerves:  unilateral or bilateral facial nerve palsy

PNS: painful peripheral radiculopathy 

Heart: Conduction system abnormalities, myocarditis, pericarditis, AV block 

-the most common cardiac manifestation: Atrioventricular blockade

Stage 3: Late Persistent Disease 

-Less than 10% of patients with acute Lyme disease develop chronic manifestations of the disorder

-It can manifest as chronic arthritis, diffuse musculoskeletal pains, myocarditis, subacute encephalopathy, axonal polyneuropathy, chronic insomnia, and leukoencephalopathy

Diagnosis 

Enzyme-linked immunosorbent assay (ELISA), Western blot (immunoglobulin IgM and IgG for B. burgdorferi), CSF analysis (the mononuclear pleocytosis typical of Lyme infection)

Treatment 

Antibiotic treatment is indicated for all stages of Lyme disease

Doxycycline, Amoxicillin, Cefuroxime, Ceftriaxone, Cefotaxime, Penicillin G, erythromycin 

Do not use doxycycline in children under 9 years of age 

Prognosis 

Most manifestations resolve over time even without therapy

Q. What is the most common neurologic manifestation of Lyme disease? Bell palsy (seventh cranial nerve)

Q. What is the hallmark skin lesion of early Lyme disease? Erythema migrans

Introduction 

-Leptospirosis is a waterborne zoonosis of worldwide distribution, caused by spirochetes of the genus Leptospira

-it is excreted in urine of reservoir animals, especially rodents

-it is spread by animal urine contaminating lakes and streams

-Hawaii has the highest incidence in the United States

-Leptospira are tightly coiled, thin, flexible spirochetes, with very fine spirals, one end is often bent, forming a hook

-Human infection usually occurs often in bodies of water, entering the body through mucous membranes (mouth, nose, conjunctivae) and breaks in the skin (cuts and abrasions) 

Symptoms & Signs 

-Most human infections are asymptomatic and self-limited

-In symptomatic patients, Leptospirosis is a biphasic illness

Leptospiremic phase:  fever,severe headache, chills, myalgias, hepatitis (with or without jaundice), nausea, vomiting, conjunctival injection without purulent discharge 

Severe leptospirosis (Weil’s syndrome): hemorrhage, jaundice, acute renal injury, aseptic meningitis,uveitis, hepatic failure, renal failure, uveitis, rash, and circulatory collapse

Diagnosis 

Serum agglutination tests are the primary diagnostic method 

Other diagnostic aids: Dark-field examination, whole blood or urine culture

Treatment 

Mild leptospirosis: Oral doxycycline, ampicillin or amoxicillin 

Moderate or severe leptospirosis: intravenous penicillin, ampicillin, or ceftriaxone

Introduction

Rat-bite fever consists of two similar febrile zoonoses caused by the treponeme Spirillum minus (Asia), or the bacteria Streptobacillus moniliformis (North America)

-Streptobacillus moniliformis is a pleomorphic Gram-negative rod

-Spirillum minus is a Gram-negative spirochete

-it is transmitted to humans by the bites from rats, mice, squirrels or gerbils 

-it can also result from exposure to rat feces or urine and ingestion of infected food or drink 

Symptoms & Signs 

-A flu-like illness: Fever, chills, headache, stiff neck, myalgia, nausea and vomiting 

-A rash: macular, morbilliform or petechial rash resembling measles 

-A desquamation: over the palms and soles 

-Arthritis: mostly involving large joints 

Diagnosis 

Gram stains of S. moniliformis:  Gram-negative filamentous branching chains, interspersed with bead-like swellings giving “necklace-shaped” colonies 

Dark field examination reveals Gram-negative spirochete Spirillum minus 

Treatment 

Treatment of choice: Penicillins; amoxicillin-clavulanic acid, Penicillin G

Alternative: Doxycycline

Introduction

Relapsing fever is a bacterial infection caused by the spiral-shaped Borrelia species (excluding Borrelia burgdorferi, the causative organism of Lyme disease) transmitted by lice or tick bites.

-it occurs in two forms linked to the mode of transmission and the Borrelia species involved

Louse-borne relapsing fever (LBRF): epidemic; caused by Borrelia recurrentis, transmitted by the body louse 

Tick-borne relapsing fever (TBRF): endemic; caused by multiple Borrelia species, transmitted by ticks 

Symptoms & Signs 

After a louse or tick bite, Borrelia enters the body, multiplies and produces endotoxins which affect the liver, spleen, and capillaries. 

-Abrupt onset of fever, chills, nausea, vomiting, arthralgia, headaches

rashes, hepatomegaly, splenomegaly 

-Delirium, neurologic and psychological abnormalities

-Attacks terminates abruptly after 3-10 days 

-Relapse occurs after an interval of 1-2 weeks 

-Three to ten relapses may occur before recovery

Diagnosis 

Thin or thick blood smears stained with Wright or Giemsa stain reveal large, loosely coiled spirochetes; PCR techniques, serology 

Treatment 

Procaine Penicillin G, tetracyclines, erythromycin

Congenital syphilis is a transplacental fetal infection with T.pallidum 

Symptoms & Signs: 

Early symptoms (within 2 years of life): flu-like syndrome associated with nasal discharge (snuffles), maculopapular rash, anemia, jaundice, hepatosplenomegaly,hydrocephalus, lymphadenopathy, chorioretinitis 

Late symptoms (after 2 years of life): Saddle nose, saber shins, short maxilla, frontal bossing, high palatal arch, eighth nerve deafness, interstitial keratitis, triangular or peglike teeth (Hutchinson teeth)

-The most common eye lesion in congenital syphilis: interstitial keratitis

-treatment of the mother during pregnancy prevents congenital syphilis 

-All infants born to mothers with positive syphilis tests should have RPR or VDRL test 

Neurosyphilis, infection of the CNS by T.pallidum can occur at any stage of infection 

Symptoms & Signs 

Fever,  eye pain, redness, photophobia, vision loss, uveitis, iritis, hearing loss,  cranial nerve abnormalities (especially cranial nerves II, III, IV, VI, VII, and VIII), meningismus 

Tabes dorsalis: It results from damage to the posterior columns of the spinal cord 

It presents with sensory ataxia, impairment of proprioception and vibration sense, a wide-based gait with impaired balance that is exacerbated by eye closure (the Romberg sign), muscular hypotonia, hyporeflexia, paresthesias, analgesia, or sharp, agonizing,  (‘shooting’/ ‘lightning) pains in the muscles of the leg, painful bladder spasms, urinary incontinence, impotence,  footdrop, and loss of reflexes.

-It can be accompanied by an Argyll Robertson pupil (which accommodates, but does not react to, light, light-near disassociation phenomenon) and optic atrophy 

-Painless trophic ulcers may develop over pressure points on the feet. 

-Sensory loss and hypotonicity can lead to the occurrence of hypertrophic (Charcot) joints. 

-About one-third of patients with untreated latent syphilis progress to tertiary syphilis 

Manifestations: 

Gummas: granulomatous, erosive, nodular lesions with central necrosis which most commonly affect the skin and bones

-they affect the palate, nasal mucosa, tongue, tonsils, pharynx

-Ulceration of gummas can cause saddle-nose deformity due to erosion of cartilage 

CNS lesions: meningovascular syphilis, paresis, tabes dorsalis 

Cardiovascular lesions: aortitis, aortic valve insufficiency, coronary ostial stenosis, and saccular aneurysm 

Latent syphilis is defined as the asymptomatic period more than 1 year after primary infection with no clinical manifestations but positive serologic tests 

-it is a diagnosis of exclusion after primary, secondary, tertiary and neurosyphilis have been ruled out 

-Patient can be infectious during this period 

-Secondary syphilis relapses often interrupt latent syphilis 

-it can last 20-30 years 

-It should be treated with benzathine penicillin or doxycycline 

Primary Syphilis 

Introduction 

Syphilis is a sexually transmitted, systemic disease caused by the spirochete Treponema pallidum 

-It occurs in multiple overlapping stages: Primary, Secondary, Tertiary, and Latent syphilis. 

-Neurosyphilis can occur at any stage.

-It is contracted through direct sexual contact with primary or secondary lesions 

-Congenital syphilis can be contracted across the placenta.

Symptoms & Signs 

Syphilis passes through 4 distinct clinical phases:

• Primary stage: one or more, usually painless chancres 
• Secondary stage: rash, condylomata lata, with or without lymphadenopathy, and organ disease
• Latent syphilis: absence of signs or symptoms of disease, with only reactive serologic tests as evidence of infection
• Tertiary stage: cutaneous, neurologic, or cardiovascular manifestations.

-Infectious lesions of syphilis can be present anywhere on the body but are typically located in or around the genital, anal, or oral area

-Chancre: Dusky red macule which evolves into a papule, then an ulcer 

Diagnosis 

A diagnosis of syphilis of any stage should be confirmed through the use of two-stage serologic tests

Serologic tests are either nontreponemal, which measure anticardiolipin antibodies, or treponemal , which measure antibodies to T. pallidum

Nontreponemal tests:

• VDRL—Venereal Disease Research Laboratory.
• RPR—Rapid plasma reagin.

Treponemal tests:

• EIA—Enzyme immunoassay.
• TP-PA—T. pallidum particle agglutination.
• FTA-ABS—Fluorescent treponemal antibody absorption.
• MHA-TP—Microhemagglutination assay for T. pallidum.

– Lyme disease may cause a false-positive treponemal test but rarely causes a false-positive nontreponemal test.

-Test all patients with syphilis for HIV.

-Traditionally, a diagnosis of syphilis of any stage should be confirmed through the use of two-stage serologic tests.

-Dark-field microscopy is useful in evaluating moist cutaneous lesions

Treatment 

-Treatment of choice for all stages of syphilis: Benzathine penicillin

-The dose and duration depend on the stage 

-Penicillin allergy: Doxycycline, Ceftriaxone, Azithromycin

-Counsel patients to abstain from sexual activity for 7–10 days after treatment-The Jarisch–Herxheimer reaction: Fever and aggravation of the existing clinical picture in the hours following treatment. The reaction resolves spontaneously within 24 hours

-Tuberculous meningitis occurs in persons of all ages

-After primary infection in the lungs, blood-borne bacilli travel to the meninges 

Symptoms & Signs 

-Gradual onset with headache, fever, irritability, vomiting, nuchal rigidity, neck stiffness, cranial nerve palsies 

-Meningeal involvement is prominent at the base of the brain, affecting the pons and optic chiasm, leading to cranial nerve (especially III, IV, and VI) palsies, which results in visual impairment and diplopia 

Diagnosis 

-Cornerstone of diagnosis: Lumbar puncture 

-CSF obeys the ‘500 rule’: Lymphocytic pleocytosis fewer than 500, protein less than 500 mg/dL; glucose less than 45 mg/dL 

-Pathology: Basal meningeal, white gelatinous exudate containing mononuclear cells  

Treatment 

Treatment with isoniazid, rifampin, and pyrazinamide

All three penetrate the cerebrospinal fluid wall 

Add corticosteroids for hydrocephalus.

Tuberculosis is a bacterial infection caused by Mycobacterium tuberculosis 

-M.tuberculosis is an obligate intracellular bacteria that is aerobic, acid fast, and nonencapsulated

-One-third of the world’s population is infected with TB

-TB usually affects the lung, but virtually all other organ systems may be involved

-Infection is transmitted by aerosolized respiratory droplet nuclei

Symptoms & Signs

Pulmonary tuberculosis: Fatigue, weight loss, fever, cough and night sweats; Primary tuberculosis may coalesce into a small granuloma in the upper lobe (Ghon complex) 

Spinal tuberculosis ( Pott disease):  Pain, deformity, the most common sites involved are the thoracic and lumbar vertebrae 

Lymph nodes(Scrofula): painless swelling of cervical and supraclavicular nodes

TB of the skin (Scrofuloderma): Skin ulcerations in the inguinal or cervical region with lymphadenopathy 

Urinary tract: urethral stricture, nephritis, hematuria, “sterile” pyuria 

Diagnosis 

Tuberculin skin test (TST)

Interferon gamma release assays (IGRAs): QuantiFERON, T-SPOT test

Culture of the sputum, urine, tissue, bone 

Biopsy: Granulomas with caseating necrosis 

Chest X-ray: Diagnostic test of choice; shows upper lobe infiltrates with cavitation and/or lymphadenopathy 

Treatment 

-Treatment is with standard multidrug regimens

-Antimicrobial therapy should be administered for 6–9 months

-Isoniazid, rifampin,Rifapentine, pyrazinamide,streptomycin and ethambutol 

-Pyridoxine should be given to patients taking isoniazid to reduce nervous system side effects 

-Test Visual acuity and red-green color vision before initiating ethambutol

-Perform audiometry before initiating streptomycin 

Prevention: BCG vaccine can prevent up to 50% of TB cases 

-Yersinia pestis is a nonmotile, non-spore forming, bipolar staining Gram-negative bacillus 

-Plague is a systemic zoonosis (infections in humans acquired by contact with animals) caused by Yersinia pestis, a gram-negative bacillus 

-It is a disease of rodents transmitted to humans by flea bites 

Symptoms & Signs 

Plague occurs in three common forms: 

Bubonic plague: sudden onset of fever, chills, prostration,headache, delirium,ulcer at the site of inoculation; regional lymphadenitis with suppuration of nodes (bubo) is the initial lesion

Pneumonic plague (Black Death): Cough, dyspnea, cyanosis, hemoptysis 

Septicemic plague: hemorrhage into skin and mucous membranes, shock

Diagnosis 

Aspirate from a bubo; culture of pus, sputum and blood; serologic testing 

Cultures show bipolar staining, Gram-negative coccobaccili (short rods with rounded ends with a ‘closed safety pin’ appearance) 

Treatment 

Doxycycline, ciprofloxacin,  levofloxacin, moxifloxacin, streptomycin, gentamicin, TMP-SMX

Salmonellosis Typhoid fever 

-Typhoid fever is caused by Salmonella typhi 

-Salmonella is a facultative gram-negative rod

-it is transmitted by the fecal-oral route and by contamination of food or water 

Symptoms & Signs

-Headache, nausea, vomiting, abdominal pain, abdominal distension, “pea soup” diarrhea, erythematous maculopapular lesions that blanch on pressure (Rose spots), slow rise of fever to maximum and then slow return to normal (stepladder fever), relative bradycardia, splenomegaly, temperature pulse dissociation (bradycardia relative to fever)

Diagnosis 

Labs: leukopenia 

Culture: Culture of bacteria from blood, stool, urine, and bone marrow 

Treatment 

Ciprofloxacin, levofloxacin, chloramphenicol, azithromycin

Prevention

-Oral and intramuscular vaccines are available for travelers to endemic areas

-Vaccine repeated after 5 years 

Q. What are the most serious complications of typhoid fever? gastrointestinal hemorrhage and perforation