Renal effects of Dirofilaria immitis in experimentally and naturally infected cats

Canine heartworm infection has been associated with glomerular disease and proteinuria. We hypothesized that proteinuria, likely due to glomerular damage, would also be found in cats experimentally and naturally infected with Dirofilaria immitis. Two populations of cats were evaluated, including 80 that were each experimentally infected with 60 infective heartworm larvae as part of a drug safety study, and 31 that were naturally infected with D. immitis. Each had a control population with which to be compared. In the experimentally infected group, we evaluated urine from 64 cats. Ten of these cats were shown to have microalbuminuria 8 months post infection. No cat refractory to infection with larvae and no cats from the control group demonstrated microalbuminuria. All 10 microalbuminuric cats were shown to have significant proteinuria, as measured by the urine protein:creatinine ratio. There was a subtle, but significant, association between worm burden and proteinuria, and although the presence of adult heartworms was required for the development of proteinuria, both microfilaremic and amicrofilaremic cats were affected. Neither the presence of circulating heartworm antibodies and antigen nor the presence of antigenuria predicted the development of proteinuria. Both heavily infected cats (5-25 adult heartworms) and cats with worm burdens compatible with natural infections (1-4 adult heartworms) developed proteinuria, and the relative numbers of cats so affected were similar between heavily and more lightly infected cats. Naturally infected cats, for which only dipstick protein determinations were available, were shown to have a significantly greater incidence of proteinuria (90% vs 35%) than did those in an age- and gender-matched control population. Additionally, the proteinuria in heartworm-infected cats was 3- to 5-fold greater in severity. We conclude that cats infected with mature adult heartworms are at risk for developing proteinuria and that this is recognized relatively soon after infection. While heavier infections may predispose cats to developing proteinuria, this complication is seen in naturally infected cats and experimental cats with worm burdens similar to those seen in natural infections (i.e., "clinically appropriate" worm burdens). The clinical relevance of heartworm-associated proteinuria is yet to be determined.     

Infection of Rrs1 barley by an incompatible race of the fungus Rhynchosporium secalis expressing the green fluorescent protein

Scald disease of barley, caused by the fungal pathogen Rhynchosporium secalis, is one of the most serious diseases of this crop worldwide. Disease control is achieved in part by deployment of major resistance (Rrs) genes in barley. However, in both susceptible and resistant barley plants, R. secalis is able to complete a symptomless infection cycle. To examine the R. secalis infection cycle, Agrobacterium tumefaciens‐mediated transformation was used to generate R. secalis isolates expressing the green fluorescent protein or DsRed fluorescent protein, and that were virulent on an Rrs2 plant (cv. Atlas), but avirulent on an Rrs1 plant (cv. Atlas 46). Confocal laser scanning microscopy revealed that R. secalis infected the susceptible cultivar and formed an extensive hyphal network that followed the anticlinal cell walls of epidermal cells. In the resistant cultivar, hyphal development was more restricted and random in direction of growth. In contrast to earlier models of R. secalis infection, epidermal collapse was not observed until approximately 10 days post‐inoculation in both cultivars. Sporulation of R. secalis was observed in both susceptible and resistant interactions. Observations made using the GFP‐expressing isolate were complemented and confirmed using a combination of the fluorescent probes 5‐chloromethylfluorescein diacetate and propidium iodide, in the non‐transformed wild‐type isolate. The findings will enable the different Rrs genes to be better characterized in the effect they exert on pathogen growth and may aid in identification of the most effective resistance.     

Measurement of Parity Nonconservation and an Anapole Moment in Cesium

The amplitude of the parity-nonconserving transition between the 6S and 7S states of cesium was precisely measured with the use of a spin-polarized atomic beam. This measurement gives Im(E1pnc)/beta = -1.5935(56) millivolts per centimeter and provides an improved test of the standard model at low energy, including a value for the S parameter of -1.3(3)exp (11)theory. The nuclear spin-dependent contribution was 0.077(11) millivolts per centimeter; this contribution is a manifestation of parity violation in atomic nuclei and is a measurement of the long-sought anapole moment.     

Spirometra erinacei / S. erinaceieuropaei in a feral cat in Manawatu with chronic intermittent diarrhoea

CASE HISTORY: A feral cat captured in the Manawatu region of New Zealand was treated for worms and fleas, and kept confined in a metabolic cage. It showed good appetite and weight gain but had intermittent watery, yellow diarrhoea.

CLINICAL FINDINGS: Clinical examination under sedation was unremarkable and routine blood tests showed no significant abnormalities. The cat was negative for feline immunodeficiency virus (FIV) and feline leukaemia virus (FeLV). Different canned cat foods did not alter the course of the diarrhoea, and the cat was euthanised 6 months after capture. At necropsy, two sections of adult Spirometra tapeworms were found in the jejunum and typical Spirometra eggs were found in colonic contents. Molecular identification of the parasite was undertaken, using the cytochrome- c oxidase subunit-1 gene (cox1) sequence.

DIAGNOSIS: Chronic intermittent diarrhoea associated with Spirometra erinacei / S. erinaceieuropaei infection.

CLINICAL RELEVANCE: Spirometra has not been reported in New Zealand before but has been associated with gastrointestinal disease in cats in other parts of the world. It requires speciestargeted treatment to be eliminated effectively, and is zoonotic. Diagnosis could be diffi cult for clinicians who are not familiar with the parasite and its life cycle.     

Understanding feline heartworm infection: disease, diagnosis, and treatment

Feline heartworm disease is a very different clinical entity from canine heartworm disease. In cats, the arrival and death of immature heartworms in the pulmonary arteries can cause coughing and dyspnea as early as 3 months postinfection. Adult heartworms suppress the function of pulmonary intravascular macrophages and thus reduce clinical disease in chronic feline heartworm infection. Approximately 80% of asymptomatic cats self-cure. Median survival time for symptomatic cats is 1.5 years, or 4 years if only cats living beyond the day of presentation are considered. Aberrant worm migration is more frequent than it is in dogs, and sudden death can occur with no prior clinical signs. The bacterial endosymbiont Wolbachia likely contributes to the inflammatory pathology of heartworm disease, but its role is not yet fully clear. Unfortunately, the diagnosis, treatment, and management of feline heartworm disease are far from simple. Antemortem diagnosis is hampered by low worm burdens, the frequency of all-male infections, and nonspecific radiographic lesions. It is up to the veterinarian to determine the correct index of suspicion and choose the right combination of diagnostic tests to achieve an answer. Treatment is symptomatic because adulticide therapy is risky and does not increase survival time. Despite the dangers of feline heartworm disease, less than 5% of cats in the United States are on chemoprophylaxis. It is important for veterinarians to take a proactive preventive stance because heartworm infection in cats is a multisystemic disease that has no easy cure.     

Thyroid function tests in euthyroid dogs treated with L-thyroxine

The effects of treatment with L-thyroxine (1 mg/m2 of body surface/d, PO, for 8 weeks) on the thyroxine (T4) and triiodothyronine (T3) responses to thyrotropin (TSH) and thyrotropin-releasing hormone (TRH) administration were determined in 10 euthyroid Beagles; 4 other dogs acted as controls. The TSH response test was performed before treatment and at weeks 2, 4, and 8 of treatment in all dogs and at 2 and 4 weeks after cessation of treatment in 6 dogs. The TRH response test was performed before treatment and at week 6 of treatment in all dogs and at 5 weeks after cessation of treatment in 6 dogs. Suppression of the T3 response to TSH was evident at treatment week 2, whereas the T4 response was suppressed at week 4 and remained suppressed for the duration of the study. Four weeks after stopping treatment, T4 and T3 responses to TSH in 2 dogs were within the hypothyroid range. The T4 response to TRH was completely suppressed after 6 weeks of thyroxine treatment, but returned to pretreatment values by 5 weeks after cessation of treatment. Suppression of thyroid and pituitary function is evident after administration of a replacement dose of L-thyroxine to euthyroid dogs.     

Diabetes mellitus in the juvenile dog: a report of four cases.

In four cases of diabetes mellitus in juvenile dogs, clinical and clinicopathologic findings were similar to those of juvenile onset diabetes mellitus in man. However, histopathologic findings varied from the usual findings in the human disease, and lack of plasma insulin was not proved in the canine cases.