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Zoonotic diseases

Last updated: November 17, 2020

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
- Worldwide occurrence
- In 2017, 153 cases of acute Q fever and 40 cases of chronic Q fever in the US ^[1]
- 70% of cases occur in men ^[2]
- Peak incidence in April and May ^[1]
Pathogen: Coxiella burnetii (gram-negative, intracellular)
- Morphological similarities to Rickettsia
- Can survive in harsh environments in endospore form
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
Pathophysiology: development of antigens
- Phase I antigens: seen when C. burnetii is highly infectious
- Phase II antigens: seen when C. burnetii is less infectious
  - Antigenic shift essential to differentiating acute Q fever from the chronic variant (see below)
- Virulence factors of C. burnetii
  - C. burnetii escapes macrophage phagocytosis by:
    - Producing superoxide dismutase to inactive phagolysosomal enzymes
    - Inhibiting cathepsin fusion
- 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
		Acute Q fever	Chronic Q fever
Incubation period ^[3]		2–6 weeks	Months to years
Clinical features		Often asymptomatic. Sudden onset of flu-like symptoms, which last for 1–2 weeks High-grade fever, chills, malaise, myalgia Headache, retroorbital pain, photophobia Rhinitis, pharyngitis, laryngitis Nausea, vomiting, diarrhea Atypical pneumonia: generally mild with nonproductive cough and fever Hepatitis, possibly hepatomegaly without jaundice Rare manifestations: meningoencephalitis, acute endocarditis associated with antiphospholipid syndrome, and immunosuppression Post-Q fever fatigue syndrome: fatigue, headache, night sweats, arthralgia, myalgia, blurred vision, fasciculations, painful lymphadenopathy Pregnancy: ↑ risk of spontaneous abortion, intrauterine growth retardation, intrauterine fetal death, and premature delivery	Low-grade fever Endocarditis: Q-fever is the most common cause of culture-negative endocarditis. Culture-negative osteomyelitis
Diagnostics	Serology via IFA (best initial test)	Anti-phase II antibody IgG titers ≥ 200 and IgM titers ≥ 50 In cases of negative IFA but high clinical suspicion, perform PCR on serum or tissue samples before administering antibiotics. IgM antibody titers to phase II antigens much higher than titers to phase I antigens	Anti-phase I antibody IgG titers > 800 or persistently high levels of anti-phase I antibody 6 months after completing therapy Antibodies with titers to phase I antigens are much higher than the titers to phase II antigens.
Diagnostics	Additional findings	↑ Liver enzymes , leukocytosis, thrombocytopenia Blood cultures are often negative. Chest x-ray: round opacities in patients with atypical pneumonia
Treatment		First-line: doxycycline for 2 weeks Second-line: macrolides (e.g., azithromycin) Among pregnant women or children < 8 years with mild disease: trimethoprim-sulfamethoxazole	First-line: doxycycline PLUS hydroxychloroquine for ≥ 18 months Second-line: rifampin and doxycycline/ciprofloxacin Valve repair may be required in the case of endocarditis.
Prevention		Avoid consuming unpasteurized milk products

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
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
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.

Rocky Mountain spotted fever rash

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)
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
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
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
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
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
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.

Monocytic inclusion bodies in ehrlichiosis

Babesiosis

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)
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)
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
- 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.
Diagnostics
- 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
Treatment
- Atovaquone PLUS azithromycin for mild disease
- Quinine PLUS clindamycin for severe infections

Babesia microti (blood smear) Babesia

Plague

Epidemiology: western US (as scattered cases in rural areas)
Pathogen: Yersinia pestis
Reservoir: prairie dogs, squirrels, rodents
Route of transmission: flea bites
Clinical features
- 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
Diagnostics
- Culture
- Microscopy with Wayson stain taken from buboes, blood, or sputum show bipolar staining of bacteria (appearance of “closed safety pin”)
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

Acral gangrene due to bubonic plague Yersinia pestis

References

Vannier EG, Diuk-Wasser MA, Ben Mamoun C, Krause PJ. Babesiosis.. Infect Dis Clin North Am. 2015; 29 (2): p.357-70. doi: 10.1016/j.idc.2015.02.008 . | Open in Read by QxMD
Wormser GP, Villafuerte P, Nolan SM, et al. Neutropenia in Congenital and Adult Babesiosis. Am J Clin Pathol. 2015; 144 (1): p.94-96. doi: 10.1309/ajcp2phh4hbvhzfs . | Open in Read by QxMD
Plague - Resources for Clinicians. https://www.cdc.gov/plague/index.html. Updated: September 10, 2015. Accessed: March 24, 2017.
CDC - Q fever. https://www.cdc.gov/qfever/stats/index.html. Updated: June 27, 2019. Accessed: November 17, 2020.
Leone M, Honstettre A, Lepidi H, et al. Effect of Sex onCoxiella burnetiiInfection: Protective Role of 17β‐Estradiol. J Infect Dis. 2004; 189 (2): p.339-345. doi: 10.1086/380798 . | Open in Read by QxMD
CDC - Travelers' Health. https://wwwnc.cdc.gov/travel/yellowbook/2020/travel-related-infectious-diseases/q-fever. Updated: June 24, 2019. Accessed: November 17, 2020.
Ostergaard L, Huniche B, Andersen PL. Relative bradycardia in infectious diseases. J Infect. 1996; 33 (3): p.185-91.
Newby JG. The Weil-Felix Test Is Archaic and Misleading. JAMA: The Journal of the American Medical Association. 1986; 255 (8): p.1020. doi: 10.1001/jama.1986.03370080042021 . | Open in Read by QxMD
Rocky Mountain Spotted Fever (RMSF) - Information for Health Care Providers. https://www.cdc.gov/rmsf/healthcare-providers/index.html. Updated: May 18, 2017. Accessed: March 28, 2018.
Rocky Mountain Spotted Fever (RMSF) - Information for Healthcare Providers. https://www.cdc.gov/rmsf/healthcare-providers/index.html. . Accessed: September 8, 2020.
Herold G. Internal Medicine. Herold G ; 2014