Fever in the Returning Traveler
· freshwater exposure when rafting or swimming in Central and South America => leptospirosis
· speleologists on a caving trip => histoplasmosis or rabies
· zoologists on a field trip => anthrax, brucellosis, plague, tularemia, Q fever, leptospirosis, viral hemorrhagic fever
· health-care worker in a refugee camp => louse-borne typhus, typhoid fever, hepatitis, meningococcus, HIV, relapsing fever, tuberculosis
· military personnel stationed in the Pacific + history of skin eschar + febrile illness with generalized lymphadenopathy/splenomegaly => scrub typhus
· food-borne diseases => typhoid fever (from salmonella typhii, fever, relative bradycardia, relative low WBC, rose spot. Treat c cephalosporin or quinolones) and other enteric fevers, traveler’s diarrhea, shigellosis, salmonellosis, amebiasis, hepatitis A, trichinosis, fascioliasis, and brucellosis
· eating unpasteurized milk products => brucellosis
· promiscuous sexual activities with prostitutes => common sexually transmitted diseases, hepatitis B and C, or acute HIV
· close contact with rodents => plague, leptospirosis, Hantavirus, relapsing fever
· hiking in tick-infested bush in Africa => tick typhus
· camping + tick bite => Rocky Mountain spotted fever, ehrlichiosis, babesiosis, relapsing fever
Back to top
is the most common tropical disease, must always be ruled out before moving on. Then pneumonia, diarrheal (salmonella and shigella), hepatitis, UTI, dengue, typhoid, ricketsial, mono, pharyngitis
Get detailed travel history, bug bites, water, soil, food exposures, sexual encounters, animal handling, tattoos, piercings, pre-exposure vaccinations, pattern of fever
Fever 2-6 weeks post-exposure can be Katayama Fever (acute schistosomiasis) which presents c fever, HA, myalgias, cough, urticaria, hepatosplenomegaly, and eosiniophilia
Generalized lymphadenopathy suggests disease other than malaria
Get CBC, thick/thin q 8 x 2 dasy, UA, blood cxs, LFTs
(Called parasite screen at elmhurst)
Sporozites are injected from female anopheles mosquito, which bites from dusk to dawn. They enter hepatocytes within 30 min. Divides to form merozoites which rupture the hepatocyte and enter the bloodstream to infect RBCs. There they differentiate into trophozoites and then schizonts filled with merozoites which rupture the RBC to infect other RBCs. Periodically, merozoites differentiate to form gametocytes which can infect mosquitoes when they bite infected patients.
Also from airport proximity (runway malaria)
Plasmodium Vivax, Ovale, Malariae, Falciparum
P. Vivax and Ovale are recurrent as they can form hypnozoites which remain dormant in hepatocytes.
Shaking chills to fever. The fever is from RBC rupture as new schiz are released. Clasically, fever is Q72 hrs for malariae (quartan malaria) and Q48 for other species (tertian malaria.) Anemia results from RBC rupture, liver and spleen sequestration of RBCs and depleted iron stores from Hb lost in urine. Renal failure can result from RBC sludging from rigid cells filled with merozoites. Falciparum makes this worse by causing knob-like protuberances on rbcs. Severe hemolysis from falciparum can lead to severe hemoglobinuria (blackwater fever.)
p. falciparum can give Cerebral Malaria from cerebral vasculature sludging. Encephalopathy with normal LP except for elevated protein (no organisms will be in CSF.) Also since it can infect any stage of rbc, large parisitemia load. Not classic paroxysms of fever
Clasically paroxysms of fever and chills followed by exhaustion and sweating
Presents c anemia, bandemia (90%) and thrombocytopenia (50%), also elevated LDH.
Pregnant women will sequester parasites in placenta.
Get thick and thin smears. Draw blood at onset of chills. Get Q8 x 48 hrs
Presents in 8 days in unprotected but can be months to years if pt took proph. Suspect if any travel within the past 2 months
If cloroquine resistant falciparum, need inpt treatment.
Rx c cloroquine, if vivax or ovale also give primaquine b/c they hang out in the liver (not to be given in G6PD)
Falciparum: doxy+quinine+clinda (bactrim)
(JEM 23:1, 2002)
Severe falciparum associated with acidosis from vascular parasite sludging and erythrocyte rigidity. Severe anemia also contributes to hypoxia. Decreased hepatic clearance of lactate. Small amount of parasite production of lactate. May induce renal fx in adults further contributing to acidosis.
The lactate in falciparum may be from the parasites themselves and fluid resus just to get the lactate down may lead to volume overload (CCM 2013;41:972)
African Sleeping Sickness
TseTse fly-posterior cervical nodes
Chagas-Treponema Cruzi. Edema of face with preauricular node enlargement.
(EMR 24, 5)
Caused by infection with the larval stage of the pork tapeworm Taenia Solium.
They may effect any organ system. Most commonly they encyst in subcutanous or muscle tissue; this is generally asymptomatic.
Intestinal Tape Worm Disease
spread by consumption of undercooked pork infected with t. solium. Ingested cysticerci (fluid filled vesicles containing larvae) decyst in the intestines, attach to the bowel wall, and mature into a tapeworm that releases eggs into the stool.
spread by person to person contact as a result of fecal contamination of water or food
Eggs are ingested that hatch into larvae in the intestine. These penetrate the bowel wall and disseminate to various organs. If they infect the central nervous system, the disorder is known as neurocysticercosis (NCC). It is the most common parasitic infection of the central nervous system. Most prevalent in Hispanic countries. It is the leading cause of adult-onset epilepsy in these nations. The cysts in the brain may be solitary or multiple. The cysts have a fibrous outer layer which allow them to avoid immunologic response for years, thereby remaining asymptomatic. In 2-5 years, the cysts undergo spontaneous degeneration and calcify; this causes an inflammatory response with local edema.
The most common presentation is epilepsy. Usually not associated with Neurologic symptoms, but HA, motor or sensory deficits, cerebellar ataxia, and involuntary movements can occur. Cysts have been known to produce enough inflammation to cause lacunar or large artery strokes. Ventricular cysts can result in hydrocephalus and increased ICP. Massive infection can cause cysticercotic encephalitis.
Dx with CT and serologic tests. MRI is even more sensitive.
Patients with only calcifications do not need drug treatment, though this is controversial.
Patients who are to be treated should probably be admitted to monitor for decompensation.
Praziquantel 50 mg/kg/day for 15 days or
Albendazole 15 mg/kg/day for 8 days.
Steroids should probably be preadministered before antiparasitics. Dexamethasone 10 mg QD should be sufficient.
Antiparasitics should be withheld in cysticercotic encephalitis as could cause herniation.
Anti-seizure meds should also be started. Many patients can be weaned off after treatment is complete.
(EMR 24, 5)
Caused by the protozoa entamoeba histolytica. Spread person to person via the fecal oral route. 10% of the world population is infected. Endemic throughout Mexico, Central and South America, India, and Africa. In the US, the disease is primarily from Mexico and Latin America. Male homosexuals also have high rates of entamoeba, but this is entamoeba dispar, a non pathogenic strain.
Amoebic liver abscesses classically occur in males age 20-40. The Zulu word for the disease, isigwebedhla, means disease of strong, young men. Alcohol probably plays a role in decreased immune response to the amoeba.
Infection begins with the ingestion of cysts from contaminated food/water. The cysts hatch, releasing trophozoites which attach to colonic mucosa. Some parasites may ascend the portal venous system to the liver. There they cause multiple small abscesses which coalesce to form one large abscess. Amebic colitis and hepatic abscess are by far the most common manifestations of the disease.
Administration of steroids can cause toxic megacolon in those suffering from amoebic colitis.
Must differentiate between amoebic and pyogenic liver abscess. Can dx by CT or UTS. There are also antibody tests, but these remain positive for life.
Treat with metronidazole 750 mg TID x 10 days; has a 90% cure rate. Alternatively, oral chloroquine 600 mg OD x 2 days, then 300 mg OD x 3 weeks. Following treatment with one of these agents, a luminal agent should be given. Use iodoquinol, paromomycin, or diloxanide furoate.
(EMR 24, 5)
Caused by protozoan flagellate, Trypanosoma Cruzi. African sleeping sickness is caused by similar T. Brucei. Endemic in Latin America. The insect vector (reduviid bug) resides in cracks and holes of mud, stone, or wood houses.
Acute Chagas’ disease often has a mild clinical course. Chagomas, inflammatory reactions to insect bite, may form after infection. The Romana sign, consisting of painless, palpebral and periocular edema, is pathonogmonic. Invasion of the CNS can occur, rarely causing life threatening meningoencephalitis. A small number of patients also go on to develop acute myocarditis with death secondary to congestive heart failure. Most acute illness resolves in 4-6 weeks.
After the acute phase, most patients enter the indeterminate phase of the disease. 1/3 of these patients will go on to develop chronic Chagas’ disease. Myocardial damage causes thinning of ventricular walls, apical aneurysms, biventricular enlargement, and conduction abnormalities. EKG may show RBBB, LAFB, or complete AV block. Patients go on to develop dysrhythmias, cardiomyopathy, or thromboembolism.
GI involvement is also possible with dysphagia, odynophagia, regurgitation, aspiration, abdominal pain, chronic constipation, or even chagasic megacolon or volvulus.
Diagnosis of the chronic form is by antibody to T. Cruzi, an IgG ELISA test.
Treatment options are scarce. Benznidazole 5 mg/kg/day for 60 days and Nifurtimox 8-10 mg/kg/day for 90-120 days shorten the acute phase of the disease. Chronic sufferers are still treated with the above regimen, but it is much less effective. Transplant is ineffective as the graft gets infected.
Found in more than 100 countries, including the US
Caused by single stranded RNA virus in the flavivirus family. Relative to yellow fever, St. Louis Encephalitis, and Japanese Encephalitis.
Breakbone fever (severe bone pain)
Mosquito bites during the day. Female Aedes Aegypti. Four serotypes; after infection with one, patient has lifelong immunity to that type but not the other three.
3-14 day incubation
Non-specific febrile illness is often seen in young children.
Older children and adults often have Classic Dengue: high fevers, severe frontal and retro-orbital headache, myalgias, arthralgias, prostration, and anorexia. On the third day of illness, a maculopapular rash appears on the chest, face, and flexor surfaces. Rash classically consists of white islands in a sea of red. The febrile period usually lasts 5-7 days. At this time, patients may report itching of palmar and plantar surfaces. Petechiae, purpura, epistaxis, and GI bleeding can occur during this time.
Dengue hemorrhagic fever (DHF) is seen in individuals who have had prior infection with one of the other serotypes. High fever with thrombocytopenia and hemoconcentration (from capillary leakage) are seen. Hemorrhagic manifestations are also present. Test by inflating BP cuff to 5 less than systolic for 5 minutes, pos. if >3 ptechiae per cm. DIC picture can also develop.
Dengue Septic Shock (DSS) -DHF c shock. Fluid therapy can be life saving.
IgM and IgG antibody tests are available. IgM usually will turn positive 5 days after infection. Treatment for all types is supportive. Massive amounts of fluid may be needed.
From trematode worms endemic in the Far East.
Invade the biliary tree causing chronic hepatic fibrotic changes. From eating contaminated fish. Predisposes to both gallstone disease as well as acalcoulous cholecystitis. Signs of chronic biliary disease accompanied by O&P in the stool. Use praziquantel 25 mg/kg TID for 2 days or Albendazole 10 mg/kg BID for 7 days.
Caused by trematode blood flukes from a snail. Eggs are excreted by a human carrier into fresh water. There, they hatch and invade snails where they mature into the larval form. The larvae enter the water and must find a human within 72 hours. The larvae penetrate exposed skin and migrate to the lungs through the venous system. They transit through the heart until they reach the portal hepatic circulation. Eventually the larvae mature to schistosomes and lay eggs which are passed through the intestines or bladder into the stool or urine. Some eggs lodge in the portal vein. It is the eggs and not the adult forms which produce immune response by the body. Katayama fever occurs 4-6 weeks after infection, coinciding with egg deposition. Peripheral eosinophilia will usually be present, along with signs of systemic disease. Schistosomal serological assays will be positive at this point. Most presentations in the US will be for the manisfestations of chronic disease. Hematuria, ureteral obstruction, and bacterial superinfection are common. May also be associated with squamous cell bladder cancer. Intestinal schistosomiasis is usually milder causing bloody, mucoid diarrhea. Hepatosplenic disease is caused by periportal fibrosis causing megaly, increased LFTs, ascites and variceal bleeding. Treat with praziquantel 20 mg/kg BID (higher doses for S. Japonicum infections)
Typhoid (Enteric Fever)
Fever, HA, abd pain, possible organomegaly, later pea soup diarrhea.
Usually from contaminat
Dx by blood, stool, or bone marrow cultures
Mimicked by plague, intestinal anthrax, melioidosis, bartonellosis, leptosirosis, typhus, tularemia, brucellosis
Mary Mallon=Typhoid Mary
Bandemia with low WBC
hyperplasia of Peyer’s patches
get blood cultures
Chloramphenicol 15 mg/kg Q6
Bactrim can also be used
if the patient has altered mental status, give Dexamethasone
From contaminated water (animal urine)
Can enter through intact waterlogged skin
5-30 days incubation
flu-like illness c aseptic meningitis
The main occupational groups at risk include farm workers, veterinarians, pet shop owners, field agricultural workers, abattoir workers, plumbers, meat handlers and slaughterhouse workers, coal miners, workers in the fishing industry, military troops, milkers, and sewer workers. Studies in sewer workers show greater prevalence of leptospira antibodies than in controls. Infected rats may contaminate sewer water. Partial or total immersion in mud and water plays a role in facilitating infection in sewer workers and rice-field workers. Milkers may be splattered in the face, causing subsequent infection via the conjunctivae. Infection of military troops occurs as a result of direct exposure to infected urine or indirect contact with contaminated soil and water. Seroprevalence surveys of livestock workers have shown ranges of positive antibody titers at 8-29%. Leptospirosis is caused by pathogenic spiral bacteria belonging to the genus Leptospira, the family Leptospiraceae, and the order Spirochaetales. These spirochetes are finely coiled, thin, motile, obligate, slow-growing anaerobes. Their flagella allow them to burrow into tissue. The genus Leptospira was originally thought to comprise only 2 species, L interrogans, which is pathogenic, and L biflexa, which is saprophytic. More recent work has identified 7 distinct species of pathogenic leptospires, which appear as more than 250 serologic variants (serovars). First stage: This stage is called the septicemic or leptospiremic stage because the organism may be isolated from blood cultures, cerebrospinal fluid (CSF), and most tissues. During this stage, which lasts about 4-7 days, the patient develops a nonspecific flulike illness of varying severity. It is characterized by fever, chills, weakness, and myalgias, primarily affecting the calves, back, and abdomen. Other symptoms are sore throat, cough, chest pain, hemoptysis, rash, frontal headache, photophobia, mental confusion, and other symptoms of meningitis. Because of the abrupt nature of the onset, the patient can often tell exactly when the symptoms started. During the 1-3 day period of improvement that follows the first stage, the temperature curve falls and the patient may become afebrile and relatively asymptomatic. The fever then recurs, indicating the onset of the second stage when clinical or subclinical meningitis appears. Second stage: This stage is called the immune or leptospiruric stage because circulating antibodies may be detected or the organism may be isolated from urine; it may not be recoverable from blood or CSF. This stage occurs as a consequence of the body’s immunologic response to infection and lasts 0-30 days or more. Disease referable to specific organs is seen. These organs include the meninges, liver, eyes, and kidney. Nonspecific symptoms, such as fever and myalgia, may be less severe than in the first stage and last a few days to a few weeks. Many patients (77%) experience headache that is intense and poorly controlled by analgesics; this often heralds the onset of meningitis. Anicteric disease: Aseptic meningitis is the most important clinical syndrome observed in the immune anicteric stage. Meningeal symptoms develop in 50% of patients. Cranial nerve palsies, encephalitis, and changes in consciousness are less common. Mild delirium may also be seen. Symptoms may be nonspecific, and a viral etiology may be suspected. Meningitis usually lasts a few days, but occasionally it can last 1-2 weeks. Death is extremely rare in the anicteric cases. Icteric disease: Leptospires may be isolated from the blood for 24-48 hours after jaundice appears. Abdominal pain with diarrhea or constipation (30%), hepatosplenomegaly, nausea, vomiting, and anorexia also are seen. Uveitis (2-10%) can develop early or late in the disease and has been reported to occur as late as 1 year after initial illness. Iridocyclitis and chorioretinitis are other late complications that may persist for years. These symptoms first manifest 3 weeks to 1 month after exposure. Subconjunctival hemorrhage is the most common ocular complication of leptospirosis, occurring in as many as 92% of patients. Leptospires may be present in the aqueous humor. Renal symptoms such as azotemia, pyuria, hematuria, proteinuria, and oliguria are seen in 50% of patients with leptospirosis. Leptospires may be present in the kidney. Pulmonary manifestations occur in 20-70% of patients. Adenopathy, rashes, and muscular pain also are seen.
Weil syndrome This severe form of leptospirosis primarily manifests as profound jaundice, renal dysfunction, hepatic necrosis, pulmonary dysfunction, and hemorrhagic diathesis. It occurs at the end of the first stage and peaks in the second stage, but the patient’s condition can deteriorate suddenly at any time. Often the transition between the stages is obscured. Fever may be marked during the second stage. Criteria to determine who will develop Weil disease are not well defined. Pulmonary manifestations include cough, dyspnea, chest pain, bloodstained sputum, hemoptysis, and respiratory failure. Vascular and renal dysfunction accompanied by jaundice develop 4-9 days after onset of disease, and jaundice may persist for weeks. Patients with severe jaundice are more likely to develop renal failure, hemorrhage, and cardiovascular collapse. Hepatomegaly and tenderness in the right upper quadrant may be present. Oliguric or anuric acute tubular necrosis may occur during the second week due to hypovolemia and decreased renal perfusion. Multi-organ failure, rhabdomyolysis, adult respiratory distress syndrome, hemolysis, splenomegaly (20%), congestive heart failure, myocarditis, and pericarditis also may occur. Weil syndrome carries a mortality rate of 5-10%. The most severe cases of Weil syndrome, with hepatorenal involvement and jaundice, carry a case-fatality rate of 20-40%. Mortality rate is usually higher for older patients.
Rx c Pcn or tetracycline
Most prevalent parasitic infection in the world (25% of world population)
Eggs are ingested, Larvae penetrate intestinal wall, migrate to lungs, ascend tracea to pharynx where they are swallowed, reach small intestines and mature into worms.
Obstruction of intestines by worms, worm in hepatobiliary treem or inflamm. Rxn from migration of worms
Biliary or pancreatic ascariasis can mimic normal causes (Worms can also act as a nidus for stone formation)
Loefflers syndrome-Cough, dyspnea, wheezing, fever from larvae in lungs. Will see fleeting pulmonary infiltrates c peripheral eosinophilia. Can also get bacterial pneumonia from feces on larvae.
Appendiceal Ascariasis-worms get stuck in appendix, can cause appendicitis and periappendiceal abcess after rupture
Single Dose Mebendazole (500 mg) or Albendazole (400 mg). If obstructed Oiperazine Citrate 150 mg/kg followed by six doses 65 mg/kg.
Back to top
Joint Swelling in Traveler/Immigrant
swollen extremity in traveller/immigrant=filariasis, parasitic mosquito spread infection which blocks the lymphatics
Back to top
| | |Back to top