Symptoms of Leptospirosis
Symptoms of Leptospirosis
The list of signs and symptoms mentioned in various sources
for Leptospirosis includes the 14
symptoms listed below:
Research symptoms & diagnosis of Leptospirosis:
Leptospirosis: Complications
Review medical complications possibly associated with Leptospirosis:
Leptospirosis Symptoms: Book Excerpts
Diagnostic Testing
Diagnostic testing of medical conditions related to Leptospirosis:
Research More About Leptospirosis
Do I have Leptospirosis?
Wrongly Diagnosed with Leptospirosis?
The list of other diseases or medical conditions
that may be on the differential diagnosis list of alternative diagnoses
for Leptospirosis includes:
See the full list of 11
alternative diagnoses for Leptospirosis
More about symptoms of Leptospirosis:
More information about symptoms of Leptospirosis and related conditions:
Other Possible Causes of these Symptoms
Click on any of the symptoms below to see a full list
of other causes including diseases, medical conditions, toxins, drug interactions,
or drug side effect causes of that symptom.
Medical Books Online about Leptospirosis
Medical Books Excerpts
Excerpts of published medical book chapters related to Leptospirosis
are available from published medical books
for more detailed information about Leptospirosis.
Medical Books Excerpts
- JAUNDICE
- "Algorithmic Diagnosis of Symptoms and Signs" (2003)
- [ read ]
- Fever
- "In a Page: Signs and Symptoms" (2004)
- [ read ]
- FEVER
- "Differential Diagnosis in Primary Care" (2007)
- [ read ]
- JAUNDICE
- "Differential Diagnosis in Primary Care" (2007)
- [ read ]
- Fever
- "Handbook of Signs & Symptoms (Third Edition)" (2006)
- [ read ]
- Jaundice
- "Handbook of Signs & Symptoms (Third Edition)" (2006)
- [ read ]
- Jaundice
- "A Pocket Manual of Differential Diagnosis" (1999)
- [ read ]
- Lassa fever
- "Professional Guide to Diseases (Eighth Edition)" (2005)
- [ read ]
- Fever
- "The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter" (2000)
- [ read ]
- Jaundice
- "The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter" (2000)
- [ read ]
- Fever
- "Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series" (2007)
- [ read ]
- Fever
- "Signs & Symptoms: A 2-in-1 Reference for Nurses" (2007)
- [ read ]
- Jaundice
- "Signs & Symptoms: A 2-in-1 Reference for Nurses" (2007)
- [ read ]
- Fever
- "The Diagnostic Approach to Symptoms and Signs in Pediatrics" (2006)
- [ read ]
- Jaundice
- "The Diagnostic Approach to Symptoms and Signs in Pediatrics" (2006)
- [ read ]
- FEVER
- "Differential Diagnosis in Primary Care" (2007)
- [ read ]
- JAUNDICE
- "Differential Diagnosis in Primary Care" (2007)
- [ read ]
- Fever
- "Pediatric Complaints and Diagnostic Dilemmas" (2003)
- [ read ]
- Jaundice
- "Pediatric Complaints and Diagnostic Dilemmas" (2003)
- [ read ]
Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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Patient Surveys for Leptospirosis
Symptoms of Leptospirosis: Online Medical Books
16 MEDICAL BOOKS ONLINE!
Review excerpts from medical books online, free, without registration,
for more information about the symptoms of Leptospirosis.
Colorado tick fever:
Signs and symptoms
(Professional Guide to Diseases (Eighth Edition))
After a 3- to 6-day incubation period, Colorado tick fever begins abruptly with chills; temperature of 104° F (40° C); severe aching of back, arms, and legs; lethargy; and headache with eye movement such as extraocular movement. Photophobia, abdominal pain, nausea, and vomiting may occur. Rare effects include petechial or maculopapular rashes and central nervous system involvement. Symptoms subside after several days but return within 2 to 3 days and continue for 3 more days before slowly disappearing. Complete recovery usually follows.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Lassa fever:
Signs and symptoms
(Professional Guide to Diseases (Eighth Edition))
After a 7- to 18-day incubation period, this disease produces a fever that persists for 2 to 3 weeks, exudative pharyngitis, oral ulcers, lymphadenopathy with swelling of the face and neck, purpura, conjunctivitis, and bradycardia. Severe infection may also cause hepatitis, myocarditis, pleural infection, encephalitis, and permanent unilateral or bilateral deafness.
Virus multiplication in reticuloendothelial cells causes capillary lesions that lead to erythrocyte and platelet loss; mild to moderate thrombocytopenia (with a tendency toward bleeding); and secondary bacterial infection. These capillary lesions may also cause focal hemorrhage in the stomach, small intestine, kidneys, lungs, and brain and, possibly, hemorrhagic shock and peripheral vascular collapse.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Relapsing fever:
Signs and symptoms
(Professional Guide to Diseases (Eighth Edition))
The incubation period for relapsing fever is 5 to 15 days (the average is 7 days). Clinically, tick- and louse-borne diseases are similar. Both begin suddenly, with a temperature approaching 105° F (40.6° C), prostration, headache, severe myalgia, arthralgia, diarrhea, vomiting, coughing, and eye or chest pains. Splenomegaly is common; hepatomegaly and lymphade-nopathy may occur. During febrile periods, the victim's pulse and respiratory rates rise, and a transient macular rash may develop over his torso.
The first attack usually lasts from 3 to 6 days; then the patient's temperature drops quickly and is accompanied by profuse sweating. A skin rash on the trunk lasting 1 to 2 days is common after the primary febrile episode. The rash may be petechiae, macular, or papular. About 5 to 10 days later, a second febrile, symptomatic period begins. In louse-borne infection, additional relapses are unusual; but, in tick-borne cases, a second or third relapse is common. As the afebrile intervals become longer, relapses become shorter and milder because of antibody accumulation. Relapses are possibly due to antigenic changes in the Borrelia organism.
Complications from relapsing fever include nephritis, bronchitis, pneumonia, endocarditis, seizures, cranial nerve lesions, paralysis, and coma. Death may occur from hyperpyrexia, massive bleeding, circulatory failure, splenic rupture, or a secondary infection.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Rheumatic fever and rheumatic heart disease:
Signs and symptoms
(Professional Guide to Diseases (Eighth Edition))
In 95% of patients, rheumatic fever characteristically follows a streptococcal infection that appeared a few days to 6 weeks earlier. A temperature of at least 100.4° F (38° C) occurs, and most patients complain of migratory joint pain or polyarthritis. Swelling, redness, and signs of effusion usually accompany such pain, which most commonly affects the knees, ankles, elbows, or hips. In 5% of patients (generally those with carditis), rheumatic fever causes skin lesions such as erythema marginatum, a nonpruritic, macular, transient rash that gives rise to red lesions with blanched centers. Rheumatic fever may also produce firm, movable, nontender, subcutaneous nodules about 3 mm to 2 cm in diameter, usually near tendons or bony prominences of joints (especially the elbows, knuckles, wrists, and knees) and less often on the scalp and backs of the hands. These nodules persist for a few days to several weeks and, like erythema marginatum, often accompany carditis.
Later, rheumatic fever may cause transient chorea, which develops up to 6 months after the original streptococcal infection. Mild chorea may produce hyperirritability, a deterioration in handwriting, or an inability to concentrate. Severe chorea (Sydenham’s chorea) causes purposeless, nonrepetitive, involuntary muscle spasms; poor muscle coordination; and weakness. Chorea always resolves without residual neurologic damage.
The most destructive effect of rheumatic fever is carditis, which develops in up to 50% of patients and may affect the endocardium, myocardium, pericardium, or the heart valves. Pericarditis causes a pericardial friction rub and, occasionally, pain and effusion. Myocarditis produces characteristic lesions called Aschoff bodies (in the acute stages) and cellular swelling and fragmentation of interstitial collagen, leading to formation of a progressively fibrotic nodule and interstitial scars. Endocarditis causes valve leaflet swelling, erosion along the lines of leaflet closure, and blood, platelet, and fibrin deposits, which form beadlike vegetations. Endocarditis affects the mitral valve most often in females; the aortic, most often in males. In both females and males, endocarditis affects the tricuspid valves occasionally and the pulmonic only rarely.
Severe rheumatic carditis may cause heart failure with dyspnea; right upper quadrant pain; tachycardia; tachypnea; a hacking, nonproductive cough; edema; and significant mitral and aortic murmurs. The most common of such murmurs include:
❑ a systolic murmur of mitral insufficiency (high-pitched, blowing, holosystolic, loudest at apex, possibly radiating to the anterior axillary line)
❑ a midsystolic murmur due to stiffening and swelling of the mitral leaflet
❑ occasionally, a diastolic murmur of aortic insufficiency (low-pitched, rumbling, almost inaudible). Valvular disease may eventually result in chronic valvular stenosis and insufficiency, including mitral stenosis and insufficiency, and aortic insufficiency. In children, mitral insufficiency remains the major sequela of rheumatic heart disease.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Rocky Mountain spotted fever:
Signs and symptoms
(Professional Guide to Diseases (Eighth Edition))
The incubation period is usually about 7 days, but it can range from 2 to 14 days. Generally, the shorter the incubation time, the more severe the infection. Signs and symptoms, which usually begin abruptly, include a persistent temperature of 102° to 104° F (38.9° to 40° C); a generalized, excruciating headache; nausea and vomiting; and aching in the bones, muscles, joints, and back. In addition, the tongue is covered with a thick white coating that gradually turns brown as the fever persists and rises.
Initially, the skin may simply appear flushed. Between days 2 and 5, eruptions begin around the wrists, ankles, or forehead; within 2 days, they cover the entire body, including the scalp, palms, and soles. The rash consists of erythematous macules 1 to 5 mm in diameter that blanch on pressure; if untreated, the rash may become petechial and maculopapular. By the third week, the skin peels off and may become gangrenous over the elbows, fingers, and toes.
The pulse is strong initially, but it gradually becomes rapid (possibly reaching 150 beats/minute) and thready.
Alert A rapid pulse rate and hypotension (systolic pressure less than 90 mm Hg) herald imminent death from complete vascular collapse.
Other signs and symptoms include a bronchial cough, a rapid respiratory rate (as high as 60 breaths/minute), anorexia, constipation, abdominal pain, hepatomegaly, splenomegaly, insomnia, restlessness and, in extreme cases, delirium. Urine output falls to half of the normal level or less, is dark in color, and contains albumin. Complications, although uncommon, include lobar pneumonia, otitis media, pa-rotitis, disseminated intravascular coagulation (DIC) and, possibly, renal failure. In rare cases, RMSF leads to death.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
GI hemorrhage:
Signs and Symptoms
(Professional Guide to Diseases (Eighth Edition))
Bright red blood from rectum or mouth, hypotension, tachycardia, nausea, decreased urine output, decreased level of consciousness, increased respiratory rate, cold, clammy skin
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Rheumatic fever and rheumatic heart disease:
Signs and symptoms
(Handbook of Diseases)
In 95% of patients, rheumatic fever characteristically follows a streptococcal infection that appeared a few days to 6 weeks earlier. A temperature of at least 100.4° F (38° C) occurs.
Joint pain
Most patients complain of migratory joint pain or polyarthritis. Swelling, redness, and signs of effusion usually accompany such pain, which most commonly affects the knees, ankles, elbows, or hips.
Skin lesions and nodules
In 5% of patients (generally those with carditis), rheumatic fever causes skin lesions, such as erythema marginatum. This nonpruritic, macular, transient rash gives rise to red lesions with blanched centers.
Rheumatic fever may also produce firm, movable, nontender, subcutaneous nodules ⅛" to ¾" (0.5 to 2 cm) in diameter, usually near tendons or bony prominences of joints (especially the elbows, knuckles, wrists, and knees) and less commonly on the scalp and backs of the hands. These nodules persist for a few days to several weeks and, like erythema marginatum, often accompany carditis.
Chorea
Later, rheumatic fever may cause transient chorea, which develops up to 6 months after the original streptococcal infection.
Mild chorea may produce hyperirritability, a deterioration in handwriting, or an inability to concentrate. Severe chorea causes purposeless, nonrepetitive, involuntary muscle spasms; poor muscle coordination; and weakness. Chorea always resolves without residual neurologic damage.
Carditis
The most destructive effect of rheumatic fever is carditis, which develops in up to 50% of patients. It may affect the endocardium, myocardium, pericardium, or the heart valves.
Pericarditis causes a pericardial friction rub and, occasionally, pain and effusion. Myocarditis produces characteristic lesions called Aschoff bodies (in the acute stages) and cellular swelling and fragmentation of interstitial collagen, leading to formation of a progressively fibrotic nodule and interstitial scars.
Endocarditis causes valve leaflet swelling, erosion along the lines of leaflet closure, and blood, platelet, and fibrin deposits, which form beadlike vegetations. Endocarditis usually affects the mitral valve in females and the aortic valve in males. In both sexes, endocarditis affects the tricuspid valves occasionally and the pulmonic valve only rarely.
Severe rheumatic carditis may cause heart failure with dyspnea, right-upper-quadrant pain, tachycardia, tachypnea, significant mitral and aortic murmurs, and a hacking, nonproductive cough.
The most common murmurs include:
❑ a systolic murmur of mitral insufficiency (high-pitched, blowing, holo-systolic, loudest at apex, possibly radiating to the anterior axillary line)
❑ a midsystolic murmur caused by stiffening and swelling of the mitral leaflet
❑ occasionally, a diastolic murmur of aortic insufficiency. Valvular disease may eventually result in chronic valvular stenosis and insufficiency, including mitral stenosis and insufficiency and aortic insufficiency. In children, mitral insufficiency remains the major after-effect of rheumatic heart disease.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Fever - Case 11-1: 18-Month-Old Girl:
IV. Clinical Presentation
(Pediatric Complaints and Diagnostic Dilemmas)
Despite advances in our understanding of the molecular basis for NF1, the
diagnosis remains one that is largely based on clinical criteria. Clinical
diagnosis of NF1 requires the presence of at least two of the seven consensus
criteria stipulated by the National Institutes of Health (NIH) (Table 11-3).
Children with sporadic rather than inherited cases may not meet the NIH
diagnostic criteria until later in life. At 1 year of age, approximately 50% of
individuals with sporadic disease lack two or more of the cardinal clinical
features permitting diagnosis, but by age 8 years, 95% meet NIH criteria.
The most visible features of NF1 are flat, evenly pigmented macules known as café-au-lait spots. These macules, often present at birth, increase in both number
and size over the first few years of life. One or two caf
é-au-lait macules are present in up to 25% of the normal population, but the
presence of six or more macules should raise suspicion for NF1. These macules
are easier to visualize with the use of a Wood
's lamp. Skinfold freckling, another pigmentary change associated with NF1,
usually occurs in the axillae, groin, nape of the neck, or under the chin. By 6
years of age, approximately 80% of children with NF1 demonstrate axillary or
inguinal freckling.
Lisch nodules are benign pigmented hamartomas of the iris that occur in patients
with NF1. These nodules do not interfere with vision. Lisch nodules may not be
apparent in young children, but they are present in more than 95% of adolescent
and adult patients. Detection of Lisch nodules on bedside examination is
challenging, and diagnosis frequently requires a slit-lamp examination by an
experienced ophthalmologist. In contrast to Lisch nodules, optic nerve tumors,
such as optic nerve gliomas, occur primarily in younger children. They are
often associated with asymmetric, noncorrectable vision loss, diminished
peripheral vision and color discrimination, and proptosis.
Subcutaneous or cutaneous (dermal) neurofibromas are rarely seen in young
children but appear during or just before adolescence. Neurofibromas are
present in 48% of 10-year-old patients and 84% of 20-year-old patients.
Cutaneous lesions frequently begin as small papules on the face, scalp, trunk,
and extremities. Deep lesions may be detected only through palpation. These
lesions represent a major cosmetic problem but do not transform into malignant
tumors. In contrast, plexiform neurofibromas surround soft tissue and bone,
causing aberrant growth. Plexiform neurofibromas, present in 30% of patients,
are locally invasive and may undergo malignant transformation. They may be
accompanied by overlying hyperpigmentation or hypertrichosis. Other tumors that
occur with higher frequency in patients with NF1 include pheochromocytomas,
juvenile chronic myeloid leukemia, and rhabdomyosarcomas.
Seizures occur in approximately 4% to 5% of patients with NF1. Seizures may be
generalized or partial. In a study by Korf et al., 22 of 359 NF1 patients
developed seizures. The seizures were most often characterized as
complex-partial (9 patients), febrile (6 patients), or generalized epilepsy (3
patients). Other manifestations of NF1 include learning disabilities, pain,
scoliosis, headaches, stroke, and bowel or bladder complications (secondary to
pelvic plexiform neurofibromas).
» READ BOOK EXCERPT ONLINE »
Source: Pediatric Complaints and Diagnostic Dilemmas, 2003
Fever - Case 11-4: 7-Month-Old Girl:
IV. Clinical Presentation
(Pediatric Complaints and Diagnostic Dilemmas)
Most patients with AIN in infancy suffer from mild infections such as otitis
media, gastroenteritis, lymphadenitis, superficial skin infections, or upper
respiratory tract infections. In one series, 6 (23%) of 26 girls developed
cellulitis of the labia majora, and 3 of these 6 infections were caused by
P. aeruginosa. Approximately 10% to 15% of patients have serious infections, including
pneumonia, sepsis, or meningitis. In approximately 10% of children, the
diagnosis is suspected only after a routine complete blood count reveals
neutropenia.
» READ BOOK EXCERPT ONLINE »
Source: Pediatric Complaints and Diagnostic Dilemmas, 2003
Jaundice - Case 15-1: 14-Day-Old Boy:
IV. Clinical Presentation
(Pediatric Complaints and Diagnostic Dilemmas)
Classic galactosemia is an autosomal recessive disease. If not recognized and
treated, it can be fatal in the neonatal period. Some of the more common
presenting clinical signs have already been discussed (jaundice, hepatomegaly,
vomiting, and encephalopathy); more fulminant clinical courses may represent
superimposed bacterial sepsis. Among the laboratory findings seen with classic
galactosemia are conjugated (or combined) hyperbilirubinemia, liver function
test and coagulation study abnormalities, elevations of serum and urine amino
acids, and a renal tubulopathy with galactosuria, glycosuria, proteinuria, and
metabolic acidosis. Not surprisingly, plasma galactose and erythrocyte
galactose-1-phosphate levels are also elevated.
Disappointingly, even galactosemic children whose diets were restricted very
early are at increased risk for developmental delays and learning disabilities,
compared with their healthy counterparts. Although many children have IQs in
the normal range, cognitive, speech, and motor impairments are, nevertheless,
more common. Longer delays before initial diagnosis and treatment of
galactosemia correlate with worse neurodevelopmental sequelae.
Hypergonadotropic hypogonadism is often observed in girls with galactosemia, and
most are infertile as adults. Galactosemic males demonstrate normal puberty and
fertility.
The gene for the galactose-1-phosphate uridyl transferase enzyme has been
localized to chromosome 9, and multiple variations at that locus have been
described. Some African-Americans with galactosemia have a milder clinical
course because of a different transferase variant. Still another variant, known
as the Duarte variant, is usually clinically insignificant. Prenatal diagnosis
of galactosemia is available.
» READ BOOK EXCERPT ONLINE »
Source: Pediatric Complaints and Diagnostic Dilemmas, 2003
Jaundice - Case 15-3: 2-Month-Old Boy:
IV. Clinical Presentation
(Pediatric Complaints and Diagnostic Dilemmas)
Prolonged neonatal jaundice may be the first sign of congenital hypothyroidism
and hypopituitarism. Feeding difficulties, apnea, noisy breathing, and overall
sluggishness are other common manifestations. Physical findings specifically
attributable to hypothyroidism can include a relatively large head, anterior
fontanel, tongue, and abdomen; umbilical hernia; edema; and a
lower-than-expected pulse and temperature. Mental and physical development
become increasingly retarded over time when hypothyroidism goes undetected and
uncorrected.
Among the physical findings that may be detected in patients with congenital
hypopituitarism are micropenis, midline craniofacial defects (e.g., cleft lip
or palate), a single central incisor, and signs of hypoglycemia or
hypocortisolism, such as lethargy or apnea. The possibility of septo-optic
dysplasia should be considered whenever congenital hypopituitarism is
diagnosed. In addition to the neuroendocrine deficiency, these patients have
optic nerve hypoplasia and agenesis of the septum pellucidum.
» READ BOOK EXCERPT ONLINE »
Source: Pediatric Complaints and Diagnostic Dilemmas, 2003
Jaundice - Case 15-4: 6-Week-Old Girl:
IV. Clinical Presentation
(Pediatric Complaints and Diagnostic Dilemmas)
Infants with biliary atresia often present in the first 2 to 6 weeks of life
with acholic stools, hepatomegaly, and jaundice. Over time the urine darkens,
the jaundice persists, the liver grows (as bile stasis worsens), and even the
spleen may enlarge. In the early weeks and months, these children often appear
well and have unremarkable medical histories. If the disease goes untreated,
malnutrition, growth retardation, and liver dysfunction emerge. Portal
hypertension, coagulopathy, and hypersplenism may develop. In untreated
patients, average expected survival time is about 1 year.
In this case, the baby presented with a direct hyperbilirubinemia but also a
mild elevation of liver enzymes suggestive of hepatocellular injury. This is
common in EHBA, although these findings may also be seen with neonatal
hepatitis or other disease entities, and indeed there can be considerable
overlap in clinical and laboratory findings among the various etiologies of
conjugated hyperbilirubinemia. The complete blood count was not suggestive of
acute infection, and the urinalysis appeared benign. The absence of
urobilinogen is actually consistent with an obstructive cholestasis, because
its formation requires entry of conjugated bilirubin into the intestine for
degradation by gut bacteria. The presentation of a jaundiced but otherwise
well-appearing 6-week-old infant with conjugated hyperbilirubinemia prompted an
immediate search for an obstructive process, and hepatic scintigraphy strongly
suggested the diagnosis that was confirmed by intraoperative cholangiogram.
» READ BOOK EXCERPT ONLINE »
Source: Pediatric Complaints and Diagnostic Dilemmas, 2003
Jaundice - Case 15-6: 5-Week-Old Girl:
IV. Clinical Presentation
(Pediatric Complaints and Diagnostic Dilemmas)
Alagille syndrome typically manifests as cholestasis in the first months of
life. Clinical and laboratory findings of the liver disease include jaundice,
acholic stools, pruritus, growth failure, conjugated hyperbilirubinemia, and
elevations of hepatic enzymes. Most patients with Alagille syndrome also have
heart murmurs, and the underlying heart conditions range in severity from
benign (e.g., mild peripheral pulmonary stenosis) to complex disease requiring
surgery (e.g. tetralogy of Fallot). The most common ocular finding in Alagille
syndrome is posterior embryotoxon, a dysgenesis of the anterior chamber of the
eye (best seen on slit-lamp examination) in which there is prominence of
Schwalbe
's ring, a ridge of collagenous fibers surrounding the periphery of Descemet's membrane.
Patients with Alagille syndrome often have a distinctive facies that may be
detectable as early as infancy. Features can include a triangular face with a
broad forehead and pointed chin, deeply set eyes, and a long nose with a
bulbous tip. Xanthomas are another physical finding common to patients with
Alagille syndrome.
Other problems associated with Alagille syndrome include renal anomalies (both
structural and functional), pancreatic insufficiency, intracranial hemorrhage,
and cognitive impairments. Assessments of renal function and anatomy (i.e.,
ultrasonography) should be performed. The patient presented in this case, for
example, demonstrated slow but spontaneous improvement in her renal function
and never required alkali supplementation.
» READ BOOK EXCERPT ONLINE »
Source: Pediatric Complaints and Diagnostic Dilemmas, 2003
Fever and Neutropenia:
Presentation
(Pediatric Infectious Disease)
Fever in the neutropenic patient is usually defined as a single temperature
greater than 38.3
°C, (101.3°F) or a sustained temperature of 38°C (100.4°F) temperature for more than 1 hour.
» READ BOOK EXCERPT ONLINE »
Source: Pediatric Infectious Disease, 2004
Outpatient Evaluation of Fever:
Presentation
(Pediatric Infectious Disease)
The history, physical exam, and even complete laboratory evaluations do not
separate these infants into
“high-risk” (high statistical likelihood to have a serious bacterial infection) and “low-risk” categories.
» READ BOOK EXCERPT ONLINE »
Source: Pediatric Infectious Disease, 2004
Article Excerpts About Symptoms of Leptospirosis:
Leptospirosis (General): DBMD (Excerpt)
In
humans it causes a wide range of symptoms, and some infected persons
may have no symptoms at all. Symptoms of leptospirosis include
high fever, severe headache, chills, muscle aches, and vomiting,
and may include jaundice (yellow skin and eyes), red eyes, abdominal
pain, diarrhea, or a rash. If the disease is not treated, the
patient could develop kidney damage, meningitis (inflammation
of the membrane around the brain and spinal cord), liver failure,
and respiratory distress. In rare cases death occurs. (Source: excerpt from Leptospirosis (General): DBMD)
Leptospirosis (General): DBMD (Excerpt)
Illness usually begins
abruptly with fever and other symptoms. Leptospirosis may occur
in two phases; after the first phase, with fever, chills, headache,
muscle aches, vomiting, or diarrhea, the patient may recover for
a time but become ill again. If a second phase occurs, it is more
severe; the person may have kidney or liver failure or meningitis.
This phase is also called Weil's disease. (Source: excerpt from Leptospirosis (General): DBMD)
Leptospirosis and Your Pet: DBMD (Excerpt)
What are the
signs of leptospirosis in pets?
The clinical signs of leptospirosis vary and are nonspecific.
Sometimes pets do not have any symptoms. Common clinical signs
reported in dogs include fever, vomiting, abdominal pain, diarrhea,
refusal to eat, severe weakness and depression, stiffness, severe
muscle pain, or inability to have puppies. Generally younger animals
are more seriously affected than older animals. (Source: excerpt from Leptospirosis and Your Pet: DBMD)
Leptospirosis: DBMD (Excerpt)
Symptoms include fever, headache,
chills, muscle aches, vomiting, jaundice, anemia, and sometimes
a rash. (Source: excerpt from Leptospirosis: DBMD)
Leptospirosis as a Cause of Symptoms or Medical Conditions
When considering symptoms of Leptospirosis, it is also important to consider Leptospirosis as a possible cause of other medical conditions.
The Disease Database lists the following medical conditions that Leptospirosis may cause:
- (Source - Diseases Database)
Leptospirosis as a symptom:
For a more detailed analysis of Leptospirosis as a symptom, including causes, drug side effect causes, and drug interaction causes, please see our Symptom Center information for Leptospirosis.
Leptospirosis: Onset and Incubation
Incubation period for Leptospirosis: 7 to 14 days
Incubation period for Leptospirosis: The time between a person's exposure to a contaminated source
and becoming sick is 2 days to 4 weeks. (Source: excerpt from Leptospirosis (General): DBMD)
Medical articles and books on symptoms:
These general reference articles may be of interest
in relation to medical signs and symptoms of disease in general:
Full list of premium articles on symptoms and diagnosis
About signs and symptoms of Leptospirosis:
The symptom information on this page
attempts to provide a list of some possible signs and symptoms of Leptospirosis.
This signs and symptoms information for Leptospirosis has been gathered from various sources,
may not be fully accurate,
and may not be the full list of Leptospirosis signs or Leptospirosis symptoms.
Furthermore, signs and symptoms of Leptospirosis may vary on an individual basis for each patient.
Only your doctor can provide adequate diagnosis of any signs or symptoms and whether they
are indeed Leptospirosis symptoms.
What is an allergy and what is it that causes some people to suffer from them? Why do allergies flare up during certain times of the year? Learn...
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» Next page:
Diagnostic Tests for Leptospirosis
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