There has to be a high clinical suspicion for a zoonosis in a patient presenting with nonspecific symptoms, because it can mimic other conditions (such as infections by other agents, noninfectious inflammatory disorders or neoplasia). Imaging plays a crucial role in making the differential diagnosis, but the patient’s history of travelling or home residence, laboratory tests and follow-up after treatment all come together for a complete and correct diagnostic algorithm.
In the following we will review and summarize the radiological appearance of zoonoses, together with their complications.
ASCARIASIS
Ascariasis (Ascaris lumbricoides) represents the most common helminthic disease worldwide.
On Barium examinations (follow-through or enema) a linear filling defect may be seen inside the intestinal lumen of the patient and a dense line representing the barium ingestion by the alimentary tract of the worm. [1]
On US adult roundworm are well recognized: linear or curvilinear, mobile or non-mobile, non-shadowing long echogenic strip with central anechoic area; two echogenic lines that represent the roundworm’s alimentary tract, seen inside and parallel to the two outer echogenic walls of the worm constitutes the ‘‘inner tube sign’’ (Fig. 1); longitudinal section of the worm gives the characteristic “tube within a tube” appearance. Axial orientation of the probe gives the ‘‘target appearance’’ or ‘‘bull’s eye’’ sign. [2]
FASCIOLIASIS
Hepatobiliary fascioliasis (Fasciola hepatica) has two phases which correlate with the radiological findings:
-the acute parenchymal phase: larval migration into the liver -> multiple, small, peripheral, often subcapsular lesions or channels (microabscesses) and/or larger eosinophilic granulomas best seen on CT or MRI (migratory tracts left by the flukes);
-the chronic biliary phase: dilated bile ducts with irregular thick walls (due to hyperplasia); the parasite is best visualized by US (Fig. 2) and ERCP. [1,3]
STRONGYLOIDIASIS
The larva of Strongyloides stercoralis penetrates the skin and via the bloodstream reaches the lungs and the intestine. It can undergo a complete life cycle within the patient (autoinfection) -> endless proliferation. This chronic pathway of continuous autoinfection can lead to a massive and life-threatening parasitic infestation- the hyperinfection syndrome, especially in immunocompromised patients (AIDS or patients who undergo glucocorticoid therapy) where disseminated strongyloidiasis may occur in various organs (liver, lungs- Fig. 3, central nervous system). S. stercoralis is an intestinal parasite, affecting the submucosa and lamina propria of the duodenum and upper jejunum, and the large bowel (not very often). The symptoms are vague (abdominal pain, diarrhea, nausea, and vomiting). Rarely it can manifest as malabsorption syndromes, paralytic ileus, intestinal obstruction (Fig. 4) or gastrointestinal bleeding. [1,4,5]
HYDATID DISEASE (HD)
In humans, HD is caused by Echinococcus tapeworms: E. granulosus, mainly (Fig. 5, Fig. 6, Fig. 7, Fig. 8, Fig. 9) and E. multilocularis (alveolaris), less frequent (Fig. 10).
Based on the stage of cyst growth, they can be classified in 4 types:
Type I: simple cyst with no internal architecture.
Type II: cyst with daughter cyst(s) and matrix.
-IIA: round daughter cysts arranged at the periphery;
-IIB: larger, irregularly shaped daughter cysts that occupy almost the entire volume of the mother cyst;
-IIC: round or oval masses with scattered calcifications and occasional daughter cysts.
Type III: calcified cyst (dead cyst).
Type IV: complicated cyst (ruptured cyst). [6,7]
The most common site of HD is the liver, but local complications (rupture into biliary tree- Fig. 6, peritoneal seeding etc) and secondary involvement due to hematogenous dissemination can be seen in almost any part of the body (lungs Fig. 7, pleura Fig. 7, bones Fig. 7, Fig. 9, muscles Fig. 9 etc). The imaging appearance in other solid organs is similar to hepatic hydatid cyst. [8]
Imaging and serologic findings usually help to establish the diagnosis of HD; unusual location, atypical imaging features or rare species can make the differential diagnosis more complicated.
E. multilocularis infection is less common, but tends to be more invasive, mimicking neoplasms (differential diagnosis with hepatocellular carcinoma, cystic hepatic metastases, biliary cystadenocarcinoma). Imaging findings consist of irregular delineated solid and cystic lesions, typically multiloculated (resembling alveoli hence the alveolar echinococcosis), containing calcifications in the solid portion (punctate, cotton ball appearance) Fig. 10. [1,9]
CYSTICERCOSIS
Eating food or drinking water contaminated by human feces containing Taenia solium eggs leads to extra-intestinal disease- cysticercosis. It is distinct from the “normal” life cycle of the parasite in which the undercooked pork meat containing larval cysts is eaten -> larva mature into adult intestinal tapeworms and the acquired disease is called taeniasis.
In cysticercosis cysts can be present in the brain (69-90% of infected patients, the most common locations are the convexity subarachnoid space, followed by the cisterns, brain parenchyma and the ventricular system Fig. 11), eyes, skeletal muscle (oblong calcific specks parallel to the muscle fibers, giving a characteristic appearance-“rice-grain calcification”) and subcutaneous tissues.
It is classified in five stages according to their evolution from active larvae to dead lesions: non-cystic, vesicular, colloidal vesicular, granular nodular, and calcified nodular Fig. 11. [1,10]
TOXOPLASMOSIS
Infectious diseases can be divided into congenital/perinatal and acquired infections.
Congenital toxoplasmosis is caused by intrauterine infection with Toxoplasma gondii. Manifestations vary from mild symptoms to more severe or even fatal forms in newborns. Scattered parenchymal calcifications, subcortical cysts, porencephaly, ventriculomegaly and lack of cortical malformations are the main imaging findings in congenital toxoplasmosis (Fig. 12). [11]
Acquired infection of Toxoplasma gondii often develops a more aggressive form in immunocompromised patients (AIDS, bone marrow transplanted patients), especially with central nervous system involvement. Low attenuation scattered lesions on CT and on MRI low or high signal on T1 (suggesting hemorrhagic components), high signal on T2 with surrounding edema, peripheral restricted diffusion, homogeneous nodular or “ring enhancement” and the “asymmetric target sign”- a small eccentric nodule along the wall of the enhancing ring, likely representing a thrombosed vein- is highly suggestive for toxoplasmosis (Fig. 13).[12]