History and exam
Key diagnostic factors
common
fever
Cat-scratch disease (CSD) - prolonged fever, usually in excess of 2 weeks' duration.
Trench fever - fever with chills, sweating, malaise, anorexia occur after an average incubation period of 8 days (range 5 to 20 days) of exposure to the body louse (Pediculus humanus humanus). Fever is classically maintained for 5 to 7 days, followed by recurrences every 3 to 5 days (hence the names "quintana" or "5-day fever”), but the pattern is variable and fever may occur only once.[17]
Carrion disease (Oroya fever) - associated with chills, malaise, generalized weakness, and headache. Average incubation period is 60 days (range 10 to 210 days).[5][31][49]
Night sweats are common in CSD.
skin manifestations (cat-scratch disease [CSD])
A papular or pustular lesion appears at the site of inoculation, about 3 to 10 days after exposure. It progresses into a crusted lesion.
Lesions may occur as maculopapular and urticaria eruptions, granuloma annulare, erythema nodosum, erythema marginatum, or leukocytoclastic vasculitis.
In immunocompromised patients with bacillary angiomatosis, reddish-brown papules similar to Kaposi sarcoma lesions are present.
lymphadenopathy (CSD, Oroya fever)
Ipsilateral regional lymphadenopathy affecting a single lymph node occurs in 85% of typical CSD patients. About 10% of the nodes suppurate.
Also a manifestation of Oroya fever.
Mediastinal lymphadenopathy may rarely occur in some cases and a mediastinal mass may be noted.
episodic abdominal pain (CSD)
Many patients with systemic symptoms present with right upper quadrant pain or periumbilical abdominal pain as a result of liver involvement.
headache, post-orbital (trench fever)
Generalized headaches with post-orbital pain may occur.
maculopapular rash (trench fever)
Several crops of erythematous maculopapular rash are present on the abdomen, chest, and back.
nodular skin lesions (verruga peruana, Peruvian wart)
After weeks to months of a prolonged bacteremic prodromal phase (Oroya fever), patients develop nodular lesions on the face and trunk.
Initially these are in the miliary form: red papules <3 mm in size. The second stage of lesions is the mular form, characterized by sessile, red, nodular tumors of about 5 mm diameter. The third-stage lesions are larger, painless, subcutaneous nodules, located mostly on the extensor surfaces of the extremities, and are prone to bleeding, ulceration, and infection.
Other diagnostic factors
common
gastrointestinal symptoms
Nausea, vomiting, and weight loss may occur.
bone and joint pain (trench fever)
Myalgia, arthralgia, and severe pain in the neck, back, and legs including tibia occurs; therefore, the disorder is sometimes known as shinbone fever.
severe pallor (Oroya fever)
Severe anemia is a predominant clinical feature in Oroya fever, leading to the manifestations of dyspnea, jaundice, and generalized edema.
hepatosplenomegaly (Oroya fever)
Manifestation of Oroya fever.
uncommon
dyspnea, heart murmur, and signs of cardiac failure (CSD, trench fever)
Clinical features of endocarditis and subsequent heart failure may be present.
mental state changes (CSD, Oroya fever)
Mental status change occurs as a result of encephalopathy in CSD, which is the most common neurologic manifestation of Bartonella henselae. Neurologic complications occur only in 2% of the infections.
Neurologic manifestation of Oroya fever. May range from somnolence and delirium to coma. May be associated with seizures.
nuchal rigidity (CSD)
CSD can cause aseptic meningitis (cerebrospinal fluid typically yields normal results, although pleocytosis and elevated protein may be present).
red eye (CSD, trench fever)
Parinaud syndrome (fever, regional lymphadenopathy, and follicular conjunctivitis) may occur in about 5% of the patients with CSD.
Marked conjunctival injection occurs in about 95% of cases of trench fever.
painless visual loss, with unilateral, abrupt onset (CSD)
This is a classic presentation of neuroretinitis, for which Bartonella henselae is the most commonly identified etiologic agent.
Neuroretinitis is a form of optic neuropathy with optic disk swelling and macular stellate exudates. This is the most common posterior segment ocular complication of B henselae.
bone pain (CSD)
Osteomyelitis secondary to Bartonella henselae infection may present with bone pain, tenderness, and fever.
mastoiditis (CSD)
Mastoiditis, with breakdown of the osseous septa of the mastoid, may occur and requires mastoidectomy. Tissue diagnosis of CSD is made from granulation tissue and infected lymph nodes adjacent to the mastoid cortex.[43]
Janeway lesions, Osler nodes, or splinter hemorrhages (CSD, trench fever)
Physical exam may reveal classic findings of endocarditis such as Roth spots, Janeway lesions, Osler nodes, or splinter hemorrhages.
chest pain
Chest pain secondary to pleurisy may occur in patients with lung involvement.
photophobia
May occur in patients with central nervous system involvement.
gastrointestinal bleeding
Disseminated bartonellosis in an immunocompromised patient may lead to bacillary angiomatosis of the gastrointestinal tract, which may manifest as gastrointestinal bleeding.
Risk factors
strong
cat scratches and bites
Contact with cats has been reported in 87% to 99% of patients, and >50% of patients have had a definite history of a cat scratch or bite.[24] The risk is increased if the cat was aged ≤12 months and had fleas.[24]
Seasonal breeding of domestic cats and close proximity to family pets most likely contribute to the disease occurring mainly between September and March in temperate zones.[4]
exposure to arthropod vectors
Cats infested with the cat flea (Ctenocephalides felis), which is responsible for the transmission of Bartonella henselae between cats, indirectly increase the risk of human exposure to infection.[4]
The human body louse (Pediculus humanus humanus) can transmit B quintana to a new host 5 to 6 days after feeding on an infected person. Infected lice excrete the organism for life.[26][27]
The sand fly Lutzomyia verrucarum, which transmits B bacilliformis, is found only in the valleys of the Andes Mountains in Peru, Ecuador, Columbia, Chile, and Bolivia. Travelers to these areas of South America, where the disease is endemic, may also become infected.[32]
Various arthropods that may transmit B vinsonii include biting flies, fleas, keds, lice, and sandflies.[13]
The Centers for Disease Control and Prevention (CDC) states that there is no evidence that ticks spread Bartonella infection to people.[33] Polymerase chain reaction studies have demonstrated DNA of Bartonella species in ticks and some believe that B henselae is transmissible by the Ixodes scapularis tick. After review, experts have concluded that transmission of any Bartonella species by ticks does not occur to animals or humans.[25]
homelessness or poor living conditions
There is an independent correlation between homelessness, poor living conditions, and alcohol misuse with B quintana infections. Outbreaks have been reported among homeless people in the US, Europe, and Japan.[21][22][23]
In Seattle, homeless patients had a 20% seropositivity of B quintana compared with only 2% in blood donors.[34] In France, the incidence of seropositivity of B quintana was 30% among homeless people compared with none in a control group.[6][35]
weak
immunosuppression
Although Bartonella infections do occur in immunocompetent individuals, they can become systemic, chronic, and increasingly life threatening in immunocompromised patients, such as those with AIDS, alcohol-use disorder, other compromising health problems, or those on immunosuppressive medication.[4]
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