In: Companion and Exotic Animal Parasitology, Bowman D.D. (Ed.)
Publisher: International Veterinary Information Service (
Respiratory System Parasites of the Dog and Cat (Part II): Trachea andBronchi, and Pulmonary Vessels (20 Apr 2000) D.D. Bowman
Department of Microbiology & Immunology, College of Veterinary Medicine, Cornell University, Ithaca,New York, USA.
This is Part II of a review that covers the majority of parasitic disease of the respiratory system of the dog ancat. Excluded from this review is the canine heartworm which is important and common enough to warrantseparate coverage. Also excluded from this review are the lesions due to Spirocerca lupi, although sometimesincluded as parasite of the respiratory tract, the adults are parasites of the stomach and esophageal wall, andthe lesions produced by the migrating larvae are in the aorta and will be covered under parasites of thevascular system.
Pneumonyssoides caninum [arthropod] Part I: RESPIRATORY PARENCHYMA
Angiostrongylus vasorum [nematode] Aelurostrongylus abstrusus [nematode] Bronchostrongylus subcrenatus [nematode] Troglostrongylus subcrenatus [nematode]Filaroides hirthi [nematode]Paragonimus kellicotti [trematode] Trachea and Bronchi
Crenosoma vulpis
This is a metastrongyloid nematode parasite of bronchi of dogs and other canids. This parasite occurs in dogs
throughout North America and Eurasia [1, 2]. These white worms are characterized by having a crenated
cuticle that is thrown into folds on the anterior end making this portion of the worm appearing superficially
segmented. The males are 4 to 8 mm long and possess a bursa. The females are 12 to 16 mm long and have
the vulva located near mid body. The adults are 0.3 to 0.5 mm in width, and therefore, appear much stockier
than parasites such as Aelurostrongylus which have a similar length. The females lay eggs that develop and
hatch within the respiratory tract. The larvae are then coughed up and swallowed to be passed in the feces
(Fig. 1). Diagnosis can be made by the recovery of the larvae from the feces by the Baermann procedure or by
zinc-sulfate centrifugal flotation. Larvae and adult worms may be found in trachobronchial mucus or
bronchoalveolar lavage samples. The larvae are characterized by possessing a very pointed tail; they measure
250 to 300 microns in length.
Figure 1. Crenosoma vulpis. First-stage larva passed in the feces of a dog. - To view thisimage in full size go to the IVIS website at . - This parasite has been shown to utilize gastropod intermediate hosts [3-5]. Attempts to infect mice with thelarvae from snails were unsuccessful, and it is believed that dogs are probably infected by ingesting thegastropod intermediate host [6]. After dogs ingest the infective-stage larvae from the snail, the larvae migrateto the lungs by way of the visceral lymphatis [4, 5] or via the hepatic portal system [7]. Females deposit larvaeabout 19 days after infection, and the prepatent period is 18 to 21 days. The adult worms probably live eight tonine months or longer.
Infection with this worm typically produces a dry, nonproductive cough that can be elicited by trachealpalpation [8]. In some cases, the cough may be chronic and productive [9]. The worms can be present inconsiderable numbers. Radiographic changes include enhanced definition in the hilus and shoulder regions ofthe bronchial walls; marked bronchial patterns with prominent interstitial markings, and in cases where thecough is productive cardiomegaly with interstitial patterns and tissue densities in the diaphragmatic lobe [2, 8,9]. Bronchoscopy may reveal no reaction of inflammation with moderate mucoid to mucopurulent dischargein the airways [9, 10]. Cytological examination of tracheal wash samples will reveal signs of eosinophiliaindicative of parasitic bronchitis. Stockdale and Hullund [7] showed that the third-stage larvae migratingthrough the liver cause the formation of necrotic foci during the first days of infection, and that the discardedcuticles of these larvae after they reach the lungs cause granulomas to form as centers of interstitialpneumonia.
Treatment of infections with Crenosoma vulpis have been effected with fenbendazole [1, 9, 11]. Doses usedhave included 50 mg per kg body weight once-a-day of three days and 20 mg per kg body weight daily for 14days. Other successful treatments have included the subcutaneous injection of 7.5 mg of levamisole per kgbodyweight followed by as second injection 2 days later [10]. Treatment with febantel as part of Drontal Plus(50 mg praziquantel, 144 mg pyrantel embonate, and 150 mg febantel) once daily for 7 days has also beenshown to clear the infection [8].
Oslerus osleri (Nematode)
This is a metastrongyloid nematode parasite causing nodules in the trachea and bronchi of dogs and other
canids. These are very small worms that are found in nodules that tend to be located close to the bifurcation of
the trachea (Fig. 2, Fig. 3). The males are only 4 to 7 mm long and the females are only slightly longer (Fig.
4). The vulva of the female is located just anterior to the anus. The stage passed in the feces is a first-stage
larva (Fig. 5, (Fig. 6) which is virtually indistinguishable from the first-stage larva of Filaroides hirthi, and
larvae are best found in fecal samples by using direct smears or zinc-sulfate centrifugal flotations [12]. The
larva passed in the feces is characterized by having a tail that is characterized by having a constriction just
anterior to its tip, which gives the very tip of the tail a kinked appearance. This parasite has been diagnosed in
dogs from around the world [13-18]. The diagnosis of infection is be confirmed by the viewing of nodules in
the trachea with a bronchoscope, and the presence of the fibrous nodular projections into the lumen of the
trachea and bronchi is diagnostic.
Figure 2. Oslerus osleri. Nodules at the bifurcation of the trachea in a dog. - To view thisimage in full size go to the IVIS website at . - Figure 3. Oslerus osleri. Nodule removed via bronchoscopy from a dog. - To view thisimage in full size go to the IVIS website at . - Figure 4. Oslerus osleri. Adult female worms recovered from a nodule removed from adog. - To view this image in full size go to the IVIS website at . - Figure 5. Oslerus osleri. Large number of eggs containing first-stage larvae followingrupture of a nodule underneath a dissecting microscope. - To view this image in full size go tothe IVIS website at . - Figure 6. Oslerus osleri. First-stage larva recovered from a nodule in the lung of a dog. - Toview this image in full size go to the IVIS website at . - The life cycle of Oslerus osleri has been shown to be direct. Dogs are probably commonly infected as puppiesby the transmission of larvae in sputum by the licking and cleaning of the mother or through regurgitated food[17, 19]. Dunsmore and Spratt [19] found fourth-stage larvae in an experimentally infected Dingo 14 daysafter infection and immature adults one month postinfection. An adult female was found in the trachealmucosa 60 days after the experimental infection of a pup [18]. Dunsmore and Spratt [19] found adults innodules 70 days after infection and nodules in experimentally infected dingos 18 months after infection.
The signs of infection with Oslerus osleri is a dry cough that is precipitated by exercise. Laryngeal or trachealmassage does not tend to elicit a cough as in typical cases of bronchitis. There are usually no signs of seriousdisease until the nodules are enlarged to the point where they cause obstruction of air flow. Some dogs presentwith a persistent cough over a year-long period [14]; while in another case, a 5- to 6-month old Blue Heeler inAustralia was diagnosed as having severe respiratory distress due to Oslerus osleri infection. Cases observedin Yorkshire terriers presented initially as a dry cough that had not responded to antibiotic treatment. Afterdiagnosis, one dog ultimately had to be euthanatized due to the development of severe dyspnea [20]. A7-month-old Pomeranian in Japan presented with a 2-week history of severe dyspnea, and in spite ofsupportive treatment which included the administration of supplemental oxygen, the animal died 5 days afterpresentation [13]. Another presentation has been recurrent pneumothorax, that was cured by the removal ofthe obstructing nodules from the trachea [21]. Nodules are often observed on radiographs , and then therepresence confirmed by endotracheal observation.
Treatment of infections with Oslerus osleri appears to be successful by the subcutaneous administration ofivermectin at 0.2 mg per kg bodyweight [14]. There are three criteria for successful chemotherapy ofinfections with this parasite: disappearance of the signs associated with the infection, resolution of thenodules, and the disappearance of the larvae from the feces of the infected animal. Fenbendazole (50 mg perkg daily for seven days) has been reported to stop coughing in an infected dog [22]. Albendazolethiabendazole, and intravenous thiacetarsemide do not appear to clear all dogs of their infections. Thus, itwould appear that at this time, ivermectin or fenbendazole would be the treatment of choice, but both requirelong-term follow-up to assure that the dog is actually cured of its infection.
Oslerus rostratus (Nematode)
This is a metastrongyloid nematode parasite of felines that occasionally finds its way into the domestic cat.
Oslerus rostratus is a large worm that is closely related to Oslerus osleri. It has been reported from cats in the
United States, Pacific Islands, Southern Europe, and the Middle East [23-26]. The adult males are about 28-37
mm long, and the adult females are 48-64 mm long. The worms are typically found in the bronchial
submucosa. The vulva in the female is located just anterior to the anus. The larvae found in the feces are 335
to 412 micrometer long and have a tail that is similar to the of Oslerus osleri. The life cycle has been described
by Gerichter [23] and Klewer [27] who found that the larvae were capable of development in slugs.
Seneviratna [25] has shown that the third-stage larvae from slugs are capable of infecting mice that serve as
paratenic hosts. Similarly, he found that week-old chickens could be infected as paratenic hosts and that the
larvae recovered from these chicks were capable of infecting a cat. Larvae were first observed in the cat 78
days after being given infective-stage larvae. There have been no studies on the signs of infection with thisparasite or on effectiveness of different treatments.
Oslerus pararostratus (Nematode)
This is a metastrongyloid nematode parasite that has been described from nodules found in the trachea of a
dog in Mexico [28]
Eucoleus aerophilus (Nematode)
This is a trichinelloid nematode that like Eucoleus boehi is better known as a capillarid. The worms which are
several mm long are found threaded within the mucosa of the trachea, bronchi, and bronchioles (Fig. 7). The
"capillarid" eggs are 59 to 83 µm long by 26 to 40 µm wide with a surface bearing a net-like ornamentation
(Fig. 8, Fig. 9). The adults are typically seen most commonly in histologic sections. When whole worms are
removed the genus can be recognized by the long, spined spicular sheath of the male.
Figure 7. Eucoleus aerophilus. Section through an adult worm in the tracheal mucosa of acat. - To view this image in full size go to the IVIS website at . - Figure 8. Eucoleus aerophilus. Egg passed in the feces. - To view this image in full size goto the IVIS website at . - Figure 9. Eucoleus aerophilus. Surface of egg showing the fine reticulate markings. - Toview this image in full size go to the IVIS website at . - It is believed that direct ingestion of the egg with an infective larva is the most common route of infection[60]. The prepatent period is between three to five weeks. The eggs deposited by the female within the tractsthey have made in the mucosa slowly work their way to the surface. The freed eggs are then coughed up,swallowed, and passed in the feces. Eggs require a period of development in the soil to become infectious.
The main clinical signs in the cat and dog are coughing and wheezing due to bronchiole disease. A bronchialpattern may be present on chest radiographs. Levamisole has been successfully used to treat infected cats [61,62]. Also, levamisole has successfully been used to treat dog [63]. It is expected that long-term fenbendazoletherapy would also be effective.
Pulmonary Vessels
Cytauxzoon felis
This is an apicomplexam protozoan parasite of wild felids that occasionally finds its way into domestic cats.
This parasite was first reported as a parasite of the domestic cat by Wagner in 1976 [29]. The natural host is
the bobcat [30]. Most of the cases have been reported from the southeastern United States. There is a stage
which circulates in the blood, the merozoites. This is a small blue-staining parasite within the red-blood cell
which has a dark staining nucleus. It is very difficult to distinguish this parasite form Babesia spp. which have
been reported from cats. Due to the typically fulminant presentation of this infection in the domestic cat, the
disease is typically diagnosed at post mortem by the finding of the large schizongonous stages that occur in the
walls of the venous system [31]. These schizonts are commonly found in the venules of the lungs (Fig. 10,Fig. 11).
Figure 10. Cytauxzoon felis. Schizonts developing in vascular system of feline lung in a fatalcase. - To view this image in full size go to the IVIS website at . - Figure 11. Cytauxzoon felis. Schizonts developing in histocytes which are highly increasedin size causing vascular plugging. - To view this image in full size go to the IVIS website . - The life cycle has been only poorly described, and to a great extent has been modeled after what is knownabout the related parasites of the genus Theileria. Merozoites circulate within red blood cells, and are taken upby a feeding tick [32]. It seems that the gametes undergo development and sexual fusion in the stomach of thetick host, and ultimately produce sporozoites that are found in the salivary glands. Once inoculated into a cat,it is not known where the sporozoites first take up residence, but within a few days , schizonts are found inhistiocytes of the veins and venules of the lungs and other tissues. Merozoites appear in the peripheral blood 6to 8 days after inoculation [33].
The typical presentation is a severely ill cat with signs that included anemia and depression. These signs maybe accompanied by fever, dehydration, icterus, splenomegaly, and hepatomegaly. Packed cell volumesdecrease markedly, but the reticulocyte counts and mean cell volumes remain normal [33]. Platelets aredecreased in number. Lymphocyte and eosinophil counts become decrease near the time of death, about 8days after infection. Bone marrow aspirates are a good place to recover the large, diagnostic schizonts. Almostall cats die between 9 and 15 days after being infected. Typically, between 1 to 4% of blood cells haveorganisms, but up to 25% of red blood cells may be parasitized. Attempts have been made to treatexperimentally induced cytauxzoonosis with parvaquone (Clexon) and buparvaquone (Butalex); both drugshave been shown to be successful in treating theileriosis in cattle [34]. In the regimen employed, the diseasestill proved a fatal one. Over a 24-h period, a cat that presented with a 2-day history of lethargy and anorexiabecame seriously icteric and had dark brown urine [35]. The cat was treated with a 10-day course ofenrofloxacin followed by a 5-day course of tetracycline. Organisms were present in the cat after the 10-daycourse of enrofloxacin, but were not present in blood samples collected 6 and 15 weeks after discharge. It isnot known why this cat survived; enrofloxacin is not known to be effective against protozoa.
Angiostrongylus vasorum (Nematode)
This is a meatastrongyloid nematode parasite of the pulmonary arteries of the dog and other canids. The
parasite is most commonly seen in dogs in southern Europe, but it has also been reported from the United
Kingdom and northern Europe, South America (Brazil and Colombia), and Uganda in Africa [36-39]. This
worm has also been reported in naturally infected animals in the Canadian provinces on the Atlantic coast.
The adult females are about 18 to 25 mm long, and the males are 14 to 18 mm long. The spicules of the males
are 300 to 400 micrometer long, and the vulva of the female is located just anteriad to the anus. When seen in
necropsy (Fig. 12), the worms appear red to dark brown in color with the white ovaries and uteri coiled around
the intestine giving the worm a 'barber pole' appearance. The females lay eggs that contain a single cell, and
the eggs are carried to the pulmonary capillaries where they lodge and develop. The larvae that hatch from the
eggs, penetrate the alveoli, and are carried up the respiratory escalator, are swallowed, and passed in the feces.
The larvae of Angiostrongylus vasorum are apparently indistinguishable from those of Aelurostrongylus
[12] and have a recognizable kink to the tip of the tail. The larvae passed in the feces are very active
larvae which are easy to recover in the feces using a Baermann apparatus. The larva is approximately 310-400
micrometer long and has a characteristic dorsal spine on the tail.
Figure 12. Angiostrongylus vasorum. Lungs of a dog at necropsy showing the dark redworms in the open artery. - To view this image in full size go to the IVIS website . - The life cycle of Angiostrongylus vasorum has been shown to involve a required snail intermediate host[40-42]. When infective larvae are ingested by a dog, they migrate to the mesenteric lymph nodes where theyundergo two molts and become immature adults by five days after infection [43]. These larvae then migrate tothe right ventricle and pulmonary artery by days nine and ten postinfection (Fig. 13). The adults are mature byabout a month after infection. Larvae appear in the feces about 49 to 57 days after the dog is infected [41, 44].
Following experimental infection, rodents will occasionally maintain larvae in their mesenteric lymph nodes[41], and these rodents could perhaps serve as paratenic hosts. Frogs have recently been shown to possibly actas intermediate hosts for this parasite [45]. Dogs probably maintain the infection for life [37]; anexperimentally infected dog shed larvae for five years after infection [42].
Figure 13. Angiostrongylus vasorum. Histologic section showing transverse sections throughseveral adult worms. - To view this image in full size go to the IVIS website at - Older dogs with chronic angiostrongylosis will typically present with clinical signs of gradually progressingpulmonary disease and cardiac failure [37]. These dogs will show signs including depression, stunted growth,weight loss, decreased activity tolerance, coughing, dyspnea, and perhaps edema. Occasionally, chronicinfections can be accompanied by asthmatic respiratory distress [46]. On other occasions, chronic infectionshave been associated with coagulopathies [47]. This condition can be associated with anemia, hemoptysis,melena, and subcutaneous hematomas. A dog with a history of bleeding episodes and a severe regenerativeanemia was found to have a coagulopathy that consisted of a consumptive intramuscular process thatresembled disseminated intravascular coagulation and later a diagnosis of angiostrongylosis was made [48].
Clinical signs are very rarely associated with acute infections with Angiostrongylus vasorum, althoughpulmonary changes, which can be quite severe, can occur quite soon after the infection is initiated [37, 44].
Signs from acute infections seem to occur mainly in younger dogs that present with dyspnea, coughing fits,bronchopneumonia, and dilation of the right heart, and on rare occasions the acute course can lead to deathtwo weeks after presentation [49]. It is believed that this acute type of presentation is due to the ingestion of alarge number of infective larvae on a single occasion. The experimental infection of 4-month-old puppies with150 larvae induced significant pneumonic changes but little in the way of clinical signs [44]. The first changeswere observed in the lungs prior to egg production, and it has been suggested that the worms may elaboratesome substance that provoked the observed eosinophilic response associated with nodules of poorlycircumscribed foci of interstitial pneumonia and thickened alveolar wall. The most sever changes in the lungwere noted to occur at the time of patency. At 60 days postinfection, there were numerous granulomascontaining viable and necrotic parasite eggs and irregular areas of fibroplasia that obliterated alveoli and wereinterpreted as resolving granulomas. At this time in the infection, there are vascular changes that includethrombi and intimate proliferation of the vascular walls. Radiographs taken at this time reveal an alveolarpattern associate with the hemorrhage into the alveolar spaces at the time of patency [50]. As the infectionsprogressed, the alveolar patter regressed and left an interstitial pattern. Treatment of dogs infected withAngiostrongylus vasorum has been performed using ivermectin at 200 mcg per kg [51, 52]. Fenbendazole at20 mg per kg once or twice daily for 2 to 3 weeks has also proven successful [51, 53]. The drug that hashistorically been utilized to treat this infection has been levamisole. The levamisole is given at 7.5 mg per kgfor 2 consecutive days, followed by 2 days at 10 mg per kg, and if the infection is not cleared, the regimen isrepeated [37]. Problems encountered with levamisole therapy have been problems with dosing due to itsapparent unpleasant taste, failure of some infections to respond, temporary neurologic disturbances in somedogs, and anaphylactic reactions that are believed due to large numbers of rapidly dying worms.
Toxocara spp. (Nematode)
Toxocara canis and Toxocara cati are mainly considered to be of importance because of their potential to
cause intestinal disease in their respective canine and feline hosts. Also, both of these worms have importance
in that both have the potential to cause visceral larval toxocariasis in humans. Less well recognized is the fact
that both of these parasites are capable of causing pulmonary disease in dogs and cats.
Toxocara canis is capable of causing pulmonary disease in both the dog and the cat. In the dog, the larvae ofToxocara canis regularly make a liver-lung migration before the larvae take up residence in either theintestinal tract as adults or within somatic tissues as arrested larvae. As the worms migrate through the lungs,they cause petechial hemorrhages, and larvae are found in the pleural cavity and diaphragm [54]. Also,Toxocara canis larvae have been reported on rare occasions to cause myocarditis with associated pulmonaryarterial thrombi in the canine host [55]. In the cat, Toxocara canis has been shown to cause significantchanges in the pulmonary arteries [56, 57]. The work of Pankavitch [56] carefully describes how the medialhypertrophy of the pulmonary arteries that occurs with larval migration through the lungs is markedly greaterwith Toxocara canis than it is with either Toxocara cati and Aelurostrongylus abstrusus. As of this time, therehave been no cases where the pulmonary effects of these infections have been diagnosed and treatedantemortum.
Figure 14. Toxocara canis. Medial hypertrophy of the pulmonary arteries in a cat infectedwith Toxocara canis (transverse section stained with Verhoff’s Van Giesen stain). - To viewthis image in full size go to the IVIS website at . - Toxocara cati is known to cause pulmonary changes in cats, and it appears that there has been no examinationof its effects on the lungs of dogs. The work of Pankavitch [56] showed that the histopathologic effects of themigrating larvae of Toxocara cati were minimal changes in the lungs of cats, especially when compared to thechanges induced by Toxocara canis and Aelurostrongylus abstrusus. Jonas et al. [58] found similar resultsalthough using other methods. These authors examined the hemodynamic changes in cats experimentallyinfected with Toxocara cati and Aelurostrongylus abstrussus. Seven of 10 cats with Aelurostrongylusabstrusus had increased pulmonary artery pressures or pulmonary vascular resistance indices. Only 6 of the 16cats infected with Toxocara cati became moderately hypertensive. Weatherley and Hamilton [59] reportedthat in kittens inoculated with eggs of Toxocara cati, that there was a cellular inflammatory activity thatprogressively increased up to 4 weeks after infection. By 6 weeks after infection,. there was a gross thickeningof the arterial walls with pronounced intimate proliferation. By 8 weeks after infection, there was completeocclusion of some vessels. Thus, it would seem that in the case of Toxocara cati, it is not yet resolved as to theseverity of the lesions induced in the lungs of cats by migrating larvae. Also, as with Toxocara canis, there hasbeen no examination of the effects of different treatments on reducing the pathology caused by thesemigrations.
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