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Zoonoses
Dr. Szekely Annamaria
Zoonoses
any infectious disease that can be transmitted (in some instances, by a vector) from animals to humans
Zoonoses can be listed according to the infectious agent: Parasites protozoa, helminths Fungi Bacteria Viruses Pria
Anthrax
Babesisos
Bartonellosis
Brucellosis
Borrelia (Lyme disease)
Campylobacteriosis
Cat Scratch Disease
Cholera
Echinococcosis
E. Coli
Salmonellosis
Tularemia
Typhus of Rickettsiae
Leptospirosis
Listeriosis
Ornithosis (psittacosis)
Yersiniosis
H1N1 flu
Hantavirus
Helminths
HIV
Q-Fever
Rabies
Dengue fever
Yellow fever
Ebola
West Nile virus
Toxocariasis
Toxoplasmosis
Visceral larva migrans
Cutaneous larva migrans
Chagas disease (parasitic disease)
Creutzfeldt-Jacobs disease
Giardia lamblia
Lyme disease
Is due to systemic infection
the body's immune response to the infection with spirochete Borrelia burgdorferi
the bacteria are inoculated into the skin by a tick bite, from ticks of the genus Ixodes
Lyme disease
First descriptions of the dermatologic manifestations of Lyme disease was in1883 by Alfred Buchwald (acrodermatitis chronica athrophicans)
1912 Swedish dermatologist described the rash which currently is called erythema migrans (EM).
1930 neurologic manifestations and the association with Ixodes ticks were recognized.
1940s several cases of chronic lymphocytic meningitis and polyradiculoneuritis were described, some of which were accompanied by erythematous skin lesions.
Clinical presentation
History of tickbite, epidemiologic context
(patient’s work, woddy, grassy habitats) Season – from May through September The nymphal stage of the tick is responsible for
most infections Incubation 1-2 weeks ( 30 days) Reinfection is not uncommon Relapse is very unusual in patients who have
been treated with appropriate antimicrobials
Clinical presentation
Asymptomatic < 7% 3 stages:
Localized Disseminated Persistent
Early infection
Late infection
Clinical presentation
Stage 1: EM (early localized infection): Isolated erythema migrans (asymptomatic, itch or burn) near the site of the tick bite, the axilla, groin, or popliteal
areas. expanding rash at the site of the tick bite 7-14 days after
the tick is removed. Untreated, the rash may persist for 2-3 weeks. 80% - one episode of erythema migrans, 20% may have
recurrent episodes. Multiple lesions may occur in 20-40% of patients with
Lyme disease and are not the result of multiple tick bites
Clinical presentation
The rash is red, and may be warm, generally painless.
The innermost portion remains dark red and becomes indurated, the outer edge remains red; and the portion in between clears, giving the appearance of a bullseye.
Flu-like symptoms, headache, muscle soreness, fever, and malaise
Clinical presentationStage 2 (weeks-months after the bite):
Disseminated infection – hematologic or lymphatic spread Musculoskeletal and neurologic symptoms are the most common
cardiac disturbances: dizziness, syncope, dyspnea, chest pain, and palpitations; atrioventricular block; fibrinous pericarditis
Intermittent inflammatory arthritis - monoarticular process involving the knee, ankle, and wrist, in decreasing frequency
Polyarticular episodes may also occur. first episode - within 6 months of the erythema migrans lesion. Untreated
it lasts for 1 week.
borrelial lymphocytoma report a bluish red nodular swelling that is almost always on the lobe of the ear or the areola of the nipple
Clinical presentation
Neurologic involvement- Lyme neuroborreliosis - reported in 5-20% of cases.
Meningitis - symptoms occur 2-10 weeks following infection: headache, neck pain or stiffness (rare), and photophobia
Borrelia encephalopathy manifests as a mild confusional state, disturbances in memory, concentration, mood, sleep, personality, and/or language
months to years after the infection - depression and irritability are also common.
Facial paresthesia (progressive), cranial or peripheral radiculoneuropathy.
Clinical presentation
Stage 3 - Chronic Lyme disease (months to years after infection and may occur after a period of latency)
rheumatologic and neurologic manifestation subacute encephalopathy, chronic progressive
encephalomyelitis, and late axonal neuropathies hemiparesis, ataxia, seizures, cognitive impairment,
bladder dysfunction, and hearing loss. Myelitis - 50% of patients with late neuroborreliosis.
Progressive spastic paraparesis or quadriparesis is common.
Clinical presentation- chronic infection
Acrodermatitis chronica atrophicans - especially on the dorsal surfaces of the hands, feet, knees, and elbows.
Initially, there is discoloration and inflammation; later, severe atrophy is noted
Clinical presentation- chronic infection
Arthritis: swelling, redness, and pain in one or a few large joints (knee, enkles)- 80% of untreated patients.
acral paresthesias dysesthesias less than 5% of untreated patients have
ophthalmic manifestations such as iritis, keratitis,
retinal vasculitis, or optic neuritis.
Physical examination
EM- usually is flat, liner, round, or oval and monocyclic. neither itching nor pain is present. the rash enlarges a few centimeters per day and fades,
even if untreated, after a few weeks. greater than 5 cm (8 cm) in size axillary or gluteal folds in children, the scalp, face, and hairline are more
common locations.
Laboratory findings CBC, erythrocyte sedimentation rate, and liver function
generally normal (unnecessary) serologic tests can be misleading if performed in the
wrong setting. The patient with solitary, typical EM requires NO
laboratory testing whatsoever. serologic testing is unnecessary during the first several
weeks. A 2-step procedure is recomanded: a screening enzyme-
linked immunoassay (ELISA) and a confirmatory Western blot for specimens that have positive or equivocal results with the ELISA.
Laboratory findings someone with vague symptoms - screening test testing
is also not recommended Large number of false-positive results
viral and bacterial infections, inflammatory diseases, neoplasms) can cause false-positive ELISA results.
confirmatory Western blot testing is recommended.
Seroconversion may take several weeks in patients infected, so early seronegativity is to be expected.
Patients may remain seropositive for long periods; serologic test results cannot be used as a proof or test of cure
Laboratory findings
serum concentrations of immunoglobulin M (IgM) antibodies peak 3-6 weeks after infection and disappear within 4-6 months, levels sometimes remain elevated for several months or years.
Immunoglobulin G (IgG) antibodies are typically detectable within 6-8 weeks after infection, peak within 4-6 months, and remain elevated indefinitely.
In late-stage disease (>4-6 wk after infection), IgG results are more useful than IgM results
Laboratory findings
Spinal fluid should be obtained in patients with neurologic symptoms whose diagnosis is not obvious
in the spinal fluid, Lyme disease produces a pleocytosis characterized by mononuclear cells.
spinal fluid levels of IgM and IgG antibodies to B burgdorferi should be measured, and an index of cerebrospinal fluid (CSF) to serum antibody (immunoglobulin-to-albumin ratio) should be calculated
Treatment
amoxicillin, or cefuroxime axetil for 20 days is indicated for early localized or early disseminated disease associated with erythema migrans, patients with cranial nerve palsy with normal cerebrospinal fluid findings , borrelial lymphocytoma, acrodermatitis chronica atrophicans
Doxycyclin 2x100/ 2x200 mg for 14-21 days doxycycline is contraindicated in patients younger than 8 years and in
pregnant women.
Lyme disease arthritis without neurologic disease may be treated with the above drugs for 28 days, also ceftriaxon 1x2 gr for 14 days
Macrolid (azythromycin) if first-line agents not tolerated
Treatment Neurologic Lyme disease 2-week course (14-28 days) of parenteral
penicillin, ceftriaxone, or cefotaxime
Oral doxycycline is as efficacious as parenteral antibiotics in patients who have Lyme-associated meningitis, facial nerve palsy, or radiculitis
Encephalitis/encephalopathy should be treated with intravenous
antibiotic therapy for 28 days.
Profilaxis ?
the attached tick can be reliably identified as an adult or nymphal I. scapularis tick that is estimated to have been attached for more then 36 h
prophylaxis can be started within 72 h of the time that the tick was removed
Sigle dose of Doxycyclin
Rickettsial infections
Tickborne lymphadenopathy (TIBOLA) An eschar associated with painful cervical lymphadenopathy appears 1
week after a tick bite to the occipital scalp. Fever and rash are seldom present. Patients may develop persistent asthenia and alopecia at the site of the
eschar.
Rocky Mountain spotted fever (RMSF) Onset 1 week following a bite from an infected tick. Fever, headache, maculopapular, petechial rash confusion, and myalgia
are cardinal features Headache is usually persistent, intense, and intractable. Patients usually progresses to mental confusion and delirium. GI symptoms (abdominal pain and diarrhea)-
during early stages of illness. Conjunctival injection may also be seen.
Treatment: Doxycyclin 2x100 mg for 2 weeks
Toxoplasmosis
Caused by the protozoal intracellular parasite Toxoplasma gondii
Cats are the primary hosts Most infections are subclinical
The disease becomes apparent in congenitally acquired infection and in patients with significant immunodeficiency (AIDS).
Toxoplasma infection is acquired via eating undercooked meat infected with tissue cysts, via ingestion of food or water contaminated with infected cat feces, or congenitally from mother to fetus
Toxoplasmosis Immunocompetent individuals
Usually asymptomatic, self-limited illness Nonspecific, flulike illness, with prominent, symmetric, isolated
cervical or occipital adenopathy, symmetric, nontender, lasting 4-6 weeks
Infrequently, may cause myocarditis, polymyositis, pneumonitis, hepatitis, encephalitis
Ocular toxoplasmosis (chorioretinitis)
Usually painful Impaired vision, either sudden or gradual, depending on the site
of infection
Toxoplasmosis Immunocompromised individuals
Flulike symptoms, lymphadenopathy CNS toxoplasmosis - seizure, cranial nerve deficits, altered
mental status, focal neurologic deficits, headache Toxoplasmic pneumonitis - Typical symptoms of a pulmonary
infection, including nonproductive cough, dyspnea, chest discomfort, and fever
Congenital toxoplasmosis May have variable symptoms, including petechial rash, jaundice,
developmental delay, and seizure Ventriculomegaly and cerebral calcification may be evident in
CNS imaging Visual defects, blindness
Laboratory findings At least 2 serology tests
IgG indicates past infection
IgM indicates acute infection (particularly in the absence of IgG), IgM in some cases, persist for months or years.
Lack of IgG and IgM may exclude infection.
IgM alone that then transitions to IgG without IgM or both IgG and IgM indicates likely acute infection.
There is a significant rate of IgM false positivity.
Treatment Six-week regimen
Pyrimethamine (100 mg loading dose PO followed by 25-50 mg/d) plus sulfadiazine (2-4 g/d divided qid) or
Pyrimethamine (100 mg loading dose PO followed by 25-50 mg/d) plus clindamycin (300 mg PO qid)
Folinic acid (leucovorin) (10-25 mg/d) should be given to all patients to prevent hematologic toxicity of pyrimethamine.
TMP (10 mg/kg daily) SMX (50 mg/kg/daily) for 4 weeks May substitute sulfadiazine or clindamycin for azithromycin 500 mg daily or
atovaquone 750 mg bid in immunocompetent patients or in patients with history of allergy to the former drugs
Pregnant patients Spiramycin 1 g PO q8h If amniotic fluid test result for T gondii is positive: 3 weeks of pyrimethamine
(50 mg/d PO) and sulfadiazine (3 g/d PO in 2-3 divided doses) alternating with 3-week course of spiramycin 1 g tid for maternal treatmen
Catscratch disease
subacute regional lymphadenitis
a bacterial infection affecting lymph nodes that drain the sites of inoculation
Bartonella henselae, a gram-negative rod
the most common causes of chronic lymphadenopathy in children and adolescents.
history of sustaining a scratch or bite from a cat (typically a kitten).
The initial symptom is formation of a papule at the inoculation site, followed by solitary or regional lymphadenopathy within 1-2 weeks
In most patients, the disease resolves spontaneously within 2-4 months.
Clinical symptoms
Regionaly lymphadenopathy, moderately tender, with erythema and increased warmth of the overlying skin.
Fever Fatigue/ malaise Headache Anorexia Splenomegaly Sore throt Rash, parotide swelling, conjunctivitis Suppuration of the lymphnode – 8-30%
Atypical manifestations
FUO Parinaud oculoglandular syndrome Central nervous system (CNS) involvement encephalitis, seizures, myelitis, peripheral neuropathy, and
neuroretinitis. Hepatosplenic CSD Endocarditis 3% (neg. blood culture, valve replacemnet) Osteomyelitis Joint pain (arthritis, synovitis) Respiratory complaints (atypical pneumonitis) Dermatologic manifestations Treatment: Ciprofloxacin, Gentamicin (iv/im)TMP-SMX,
azythromycin, doxycyclin
Tularemia caused by the gram-negative bacterium, Francisella
tularensis. numerous animals and insects can carry the bacteria,
rabbits and ticks most commonly are implicated in human cases.
Tularemia is divided into 6 forms: Ulceroglandular (70-80%) The organism enters through a scratch,
abrasion, or tick or insect bite and spreads via the proximal lymphatic system. Ulcers at the site of inoculation.
Glandular Oculoglandular (infection of the conjunctiva) Oropharyngeal (eating uncooked rabit meal) Pneumonic (bacteria is inhaled) - dry cough, dypnea, chest pain Typhoidal (septicemic form)
Tularemia
Laboratory test: WBC normal/elevated Hepatic function elevated Serologic testing
Treatment: Streptomycin Gentamicin Fluorquinolones (levoloxacin, ciprofloxacin)
Leptospirosis Leptospirosis, is considered the most common zoonosis in the
world. Often referred to as swamp fever, or mud fever. The most important reservoirs are rodents, and rats are the most
common source worldwide. Infection occurres after animal and rodent bites, after contact with
the animals infected urine, and after ingestion of contaminated food and water.
The organism enters the body when mucous membranes or abraded skin come in contact with contaminated environmental sources.
Often leads to renal and hepatic dysfunction.
Clinical simptoms
The incubation period is usually 7-12 days, with a range of 2-20 days.
90% of patients manifest a mild anicteric form of the disease
5-10% have the severe form with jaundice, otherwise known as Weil disease.
First stage: septicemic stage (bacteria can be isolated fom the blood culture) fever; flu like symptoms, sore throat; splenomegaly;
hepatomegaly; mild jaundice; muscle tenderness; lymphadenopathy; and a macular, maculopapular, erythematous, urticarial, or hemorrhagic rash.
Clinical simptoms
Second stage (antibodys can be detected): General - Adenopathy, rash, fever, bleeding, signs of
hypovolemia/cardiogenic shock Icteric - Jaundice, hepatomegaly, abdominal tenderness, signs of
coagulopathy Pulmonary - Cough, hemoptysis, dyspnea, respiratory distress Neurologic - signs of meningitis Ocular - Subconjunctival hemorrhage, uveitis, signs of
iridocyclitis or chorioretinitis Hematologic - Bleeding, petechiae, purpura, ecchymosis,
splenomegaly, abdominal tenderness Cardiac - Signs of congestive heart failure, pericarditis
Treatment
Supportive therapy and careful management of renal, hepatic, hematologic, and CNS complications are important
Antibiotic th.: Mild leptospirosis: doxycycline, ampicillin, or amoxicillin. For severe leptospirosis: primary therapy is penicillin G
Alternative regimens are ampicillin, amoxicillin, or erythromycin, cephalosporins.
Echinococcosis
Infection with the larval form of Echinococcus multilocularis causes alveolar echinococcosis
cystic echinococcosis resulting from Echinococcus granulosus infection (rare)
Initially, it is located in the liver and then may spread to any other organ through metastases
E multilocularis eggs, are dispersed in the environment via the feces of carnivores.
The eggs may contaminate various types of food, including fruits and vegetables collected from gardens or infected meadows, and drinking water.
Hepatic localization and extrahepatic involvement
Echinococcosis-clinical symptoms
Jaundice Vague abdominal (right upper quadrant) pain is the most
common symptom Hepatomegaly is observed in 16% of cases. In the presence of bacterial superinfection, fever and
chills may accompany gallstonelike symptoms. Various symptoms: dyspnea and bile sputum, seizures
and stroke, bone pain or skin tumor - symptoms of a secondary location or metastasis of the parasitic lesions
Laboratory findings
Blood cell count Hypereosinophilia is a rare feature of disease (< 10%). Lymphopenia develops in 45% of cases.
Increase in levels immunglobulin IgG levels Increased CRP Hepatic function normal or ↑ GGT, AP Serologic testing (ELISA, WB) Imaging studies: ultrasound (pseudoneoplastic intrahepatic mass with a
heterogeneous ultrasonographic structure ), CT, MRI, colangiography Chest ray Avoid needle biopsy (risk of dissemination) Surgycal biopsy, hystological examination
Treatment
Antiparasitic th.: mebendazole, albendazole in high doses
Long term chemotherapy (several years)
Surgical procedures (radical, palliative, liver transplant)
Toxocariasis
is an illness of humans caused by a larvae (immature worms) of either the dog roundworm (Toxocara canis), the cat roundworm (Toxocara cati) or the fox (Toxocara canis)
is often called visceral larva migrans The illness is caused by the ingestion of the egs is a major cause of blindness and may
provoke rheumatic, neurologic, or asthmatic symptoms Dg.: pneumonia, bronchospasms, chronic pulmonary
inflammation, hypereosinophilia, hepatomegaly, hypergammaglobulinaemia (IgM, IgG, and IgE classes)
Toxocariasis- clinical presentation
Most cases are asymptomatic Symptoms depend of the organ affected:
coughing, fever, abdominal pain, headaches, and changes in behavior and ability to sleep wheezing, hepatomegaly, and lymphadenitis
Patients can present with pallor, fatigue, weight loss, anorexia, asthma, chest tightness, increased irritability, nausea, and vomiting.
Ocular larva migrans: red eye, white pupil, fixed pupil, retinal fibrosis, retinal detachment, inflammation of the eye tissues, retinal granulomas, and strabismus
Diagnosis, treatment
Leukocytosis Eosinophilia Serological testing (ELISA) CT, MRI (visceral granuloma)
Treatment: Often resolves by itself Albendazole, mebendazole Steroids for OLM Granulomas-surgical removal