Summary
Zoonotic diseases are infections that are transmitted from animals to humans. While animals may transmit infection directly, they usually serve as hosts for a pathogen that is then transmitted to humans by a vector (e.g., ticks, fleas). Zoonoses are usually endemic to certain geographical regions, and peaks in incidence often correlate with the life cycle of the transmitting vector. Common diseases include Q fever, Rocky Mountain spotted fever, endemic typhus, ehrlichiosis, and babesiosis. Although these conditions differ in their exact presentation, symptomatic cases typically present with fever, flulike symptoms, and possibly skin rashes. In some cases of fulminant disease, there may be complications such as disseminated intravascular coagulation, shock, and organ failure. Most zoonoses are treated with antibiotics and respond well to treatment.
For information on some other zoonotic diseases such as anaplasmosis and epidemic typhus, see “Tick-borne diseases” and “Louse-borne diseases.”
Q fever
- Definition: a notifiable zoonotic disease with cattle, sheep, and goats as the primary reservoir
- Epidemiology
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Pathogen: Coxiella burnetii (gram-negative, intracellular)
- Morphological similarities to Rickettsia
- Can survive in harsh environments in endospore form
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Route of transmission
- Direct infection (no vector transmission)
- Inhalation of spore-containing aerosols from the amniotic fluid or secretions of infected livestock
- Ingestion of raw milk produced by infected animals
- Risk groups: slaughterhouse workers, farmers, shepherds, veterinarians
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Pathophysiology: development of antigens
- Phase I antigens: seen when C. burnetii is highly infectious
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Phase II antigens: seen when C. burnetii is less infectious
- Antigenic shift essential to differentiating acute Q fever from the chronic variant (see below)
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Virulence factors of C. burnetii
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C. burnetii escapes macrophage phagocytosis by:
- Producing superoxide dismutase to inactive phagolysosomal enzymes
- Inhibiting cathepsin fusion
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C. burnetii escapes macrophage phagocytosis by:
- C. burnetii infection induces a range of immune responses, ranging from autoantibody production to immunosuppression
- One of two syndromes develop depending on the host's immune response:
- Acute Q fever: few C. burnetii organisms and stronger cell response to the pathogen
- Chronic Q fever
- Multiple C. burnetii organisms and weaker cell response
- C. burnetii survives in monocytes and macrophages
Type of Q fever | |||
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Acute Q fever | Chronic Q fever | ||
Incubation period [3] |
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Clinical features |
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Diagnostics | Serology via IFA (best initial test) | ||
Additional findings |
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Treatment |
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Prevention |
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Rocky Mountain spotted fever (RMSF)
- Epidemiology: endemic in the South (especially North Carolina, Tennesse, Oklahoma, and Arkansas) and Midwest (especially Missouri) [4]
- Pathogen: Rickettsia rickettsii; (aerobic, gram-negative, obligate intracellular bacteria )
- Reservoir: dogs, rodents, ticks
- Route of transmission: bite of Dermacentor variabilis (dog tick)
- Pathophysiology: : infection of endothelial cells → vasculitis and subsequent endothelial dysfunction → SIRS → shock, peripheral and/or pulmonary edema, DIC, renal failure
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Clinical features (incubation period ∼ 7 days, or 3–12 days) [4]
- Fever, headache, myalgia, malaise, conjunctivitis, nausea, and abdominal pain
- Blanching macular rash; (90% of cases): begins on wrists and ankles → spreads to the trunk, palms, and soles → becomes petechial and/or hemorrhagic in 50% of cases
- Hepatomegaly, splenomegaly
- Noncardiogenic pulmonary edema with ARDS
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Diagnostics: integration of clinical presentation and laboratory confirmation [5]
- Serology: preferably indirect immunofluorescence assay for IgG
- PCR: possible using whole blood
- Culture isolation: difficult since routine blood cultures are not able to cultivate the organism
- Treatment: doxycycline in children and adults [4]
The Rash of Rocky Mountain spotted fever starts at the wRists.
“Palms and soles are crucial for driving CARSS:” the typical infectious causes of a rash of palms and soles include Coxsackie A infection, RMSF, and Secondary Syphilis.
Typhus
Endemic typhus (also known as murine typhus)
- Definition: an exanthematous typhus fever caused by Rickettsia typhi
- Epidemiology: occurs worldwide, mainly in warm coastal regions, southern US
- Pathogen: Rickettsia typhi
- Transmission: : via vector (rat and cat fleas)
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Clinical features
- Incubation period: 8–16 days
- Fever, severe headache, malaise
- Maculopapular or petechial rash erupts on the trunk → spread to extremities (palms and soles are spared)
- No eschar (scab at site of flea bite)
- Relative bradycardia [6]
- Brill-Zinsser disease: exacerbated recurrence many years after the primary episode
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Diagnostics
- Indirect immunofluorescence (four-fold rise in antibodies)
- Positive Weil-Felix reaction: a diagnostic test for rickettsial infections, whereby suspensions of proteus antigens (OX 19, OX 2, or OX K) are mixed with a patient's serum [7]
- Agglutination occurs in the serum of patients infected with Rickettsia.
- No longer recommended in routine practice due to low sensitivity and specificity
- Still valuable test in resource-limited areas where indirect immunofluorescence is not available
- Treatment: doxycycline OR chloramphenicol
The rash of Typhus starts on the Trunk.
Scrub typhus
- Definition: an exanthematous typhus fever caused by Orientia tsutsugamushi. Not to be confused with epidemic typhus, which is caused by Rickettsia prowazekii
- Epidemiology: occurs mainly in central, eastern, and southeast Asia, as well as northern Australia and South Pacific
- Pathogen: Orientia tsutsugamushi
- Transmission: via vector: Trombicula mites larvae (chiggers) from rodents
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Clinical features
- Incubation period: 7–10 days
- Fever, severe headache, myalgias, arthralgia, cough
- Maculopapular rash
- Eschar at site of mite attachment
- Lymphadenopathy
- Relative bradycardia despite fever
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Diagnostics
- Serology (four-fold rise in antibodies)
- Positive Weil-Felix reaction
- Treatment: doxycycline OR chloramphenicol
Ehrlichiosis
- Epidemiology: southeastern and south-central US, mid-Atlantic States
- Pathogen: Ehrlichia chaffeensis; , Ehrlichia ewingii (intracellular, gram-negative bacteria)
- Reservoir: whitetail deer
- Route of transmission: bite of the lone star tick (Amblyomma americanum) → infection of monocytes and macrophages
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Clinical infection (incubation period of 1–2 weeks)
- Fever, headaches, malaise, myalgias
- Similar to RMSF, but usually without a rash (“spotless RMSF”)
- Possibly neurologic symptoms (altered mental status, stiff neck, clonus)
- May cause renal failure and GI bleeding
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Diagnostics
- Leukopenia, thrombocytopenia, elevated serum transaminases
- Wright-Giemsa stain of blood smear: detection of morulae (intracytoplasmic mulberry-like inclusion bodies) inside the infected monocytes
- Serology via IFA: IgG Ehrlichia titer
- Treatment: : PO doxycycline OR tetracycline
“ANother GRANd day starts with an EaRLI CoFFEE in the MOrNing:” in ANaplasmosis, morulae are formed in GRANulocytes and ehrlichiosis is caused by EhRLIchia CHaFFEEnsis in MONocytes.
Babesiosis
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Epidemiology
- Worldwide occurrence
- Endemic in the Northeast, Northwest, and upper Midwest of the US
- Seasonal distribution: most cases in July and August when tick populations reach their peak
- Pathogen: Babesia species, especially Babesia microti (protozoan parasites)
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Route of transmission
- Natural reservoir: wild animals (especially rodents), cattle
- Transmission to humans via tick bites: Ixodes scapularis (also transmits Borrelia burgdorferi, responsible for Lyme disease, and Anaplasma phagocytophilum, responsible for human granulocytic anaplasmosis)
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Clinical features (incubation period of 1–6 weeks) [8]
- Most cases asymptomatic or mild, but may be severe or even fatal
- Flulike symptoms (e.g., fever, malaise, myalgia, headache)
- Hemolytic anemia with dark urine and icterus
- Mild splenomegaly and hepatomegaly
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Severe infection
- May lead to DIC, ARDS, congestive heart failure, splenic rupture, and death
- Individuals with asplenia are at increased risk of severe babesiosis
- Clinical features are similar to malaria infections.
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Diagnostics
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Laboratory findings
- Hemolytic anemia
- Thrombocytopenia
- Lymphocytopenia, neutropenia [9]
- ↑ Transaminases
- ↑ Alkaline phosphatase
- Thin blood smear (confirmatory test): ring shapes and maltese cross formations within the RBCs
- PCR, serology
- Coinfection with other tick-borne pathogens (e.g., Borrelia, A. phagocytophilum) should be considered
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Laboratory findings
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Treatment
- Atovaquone PLUS azithromycin for mild disease
- Quinine PLUS clindamycin for severe infections
Plague
- Epidemiology: western US (as scattered cases in rural areas)
- Pathogen: Yersinia pestis
- Reservoir: prairie dogs, squirrels, rodents
- Route of transmission: flea bites
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Clinical features
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Bubonic plague (most common):
- Sudden onset of fever, headache, myalgias, chills, and painful swollen lymph nodes (buboes)
- May progress to sepsis, pneumonia, and meningitis
- Septicemic plague: signs and symptoms of sepsis, abdominal pain, possible shock, DIC
- Pneumonic plague : rapidly progressing pneumonia with possible respiratory failure and shock
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Bubonic plague (most common):
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Diagnostics
- Culture
- Microscopy with Wayson stain taken from buboes, blood, or sputum show bipolar staining of bacteria (appearance of “closed safety pin”)
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Treatment: Do not delay treatment for diagnosis. [10]
- Isolation with droplet precautions until pneumonic plague is ruled out
- First-line: IV gentamicin OR fluoroquinolones for 10–14 days
- Second-line: doxycycline OR tetracycline